horse state part C - internal diseases

Swallowing and Oesophageal Disorders

Main disorders:

1⃣ Dysphagia = abnormal swallowing
2⃣ Esophageal obstruction / choke
3⃣ Megaesophagus
4⃣ Esophageal stricture / stenosis
5⃣ Other disorders:

• Rupture / perforation / laceration

• Esophagitis

• Esophageal diverticulum

• Esophageal cysts

1⃣ DYSPHAGIA

Dysphagia = abnormality/difficulty in swallowing.

⚠ It is a clinical sign, NOT a specific disease.

The causes can be divided according to where the problem occurs:

• Oral, Pharyngeal, Esophageal, Systemic

1. ORAL CAUSES

Problem occurs before food is properly transferred into the pharynx.

Causes:

• Facial paralysis, Lip lesions, Temporomandibular joint disorders, Hyoid disorders, OA → pain

• Lingual abnormalities

  • Inability to move ingesta

• Dental disorders

• Congenital/acquired palatal defects

• Foreign bodies, Neoplasia

🧠 Think: MOUTH cannot prepare/move food → ORAL dysphagia

2. PHARYNGEAL CAUSES

Pharyngeal paralysis

Can result from:

• Glossopharyngeal nerve damage, Guttural pouch mycosis, Botulism, Heavy-metal poisoning

Other causes:

• Pharyngeal compression

  • e.g. strangles

• Pharyngeal cysts, Epiglottic lesions, Laryngeal abnormalities

3. ESOPHAGEAL CAUSES

• Megaesophagus, Choke, Stenosis/stricture, Cysts, Rupture, Neoplasia

4. SYSTEMIC CAUSES

• Nutritional myodegeneration

• Equine grass sickness

• Tetanus

🩺 CLINICAL SIGNS OF DYSPHAGIA

• Slow and Messy eating

• Halitosis (bad breath)

• Quidding

• Productive cough

• Nasal reflux of: Saliva, Ingesta, Fluids

• Weight loss

🌾 What is QUIDDING?

Horse chews food → Forms a partially chewed bolus → Cannot process/swallow it properly → Drops/spits it from mouth

➡ Quidding = rejection/dropping of semi-masticated food

Often associated with:
➡ Dental/oral disease.

⭐ ORAL vs NASAL REFLUX

👄 Food/reflux from MOUTH

➡ Think oral cavity

👃 Food/fluid from NOSE

➡ Think pharyngeal or esophageal problem

🔎 DIAGNOSIS OF DYSPHAGIA

• History, Clinical signs

• Physical examination, Oral examination

• Nasal endoscopy

• X-ray

• Fluoroscopy

Treatment ➡ Treat the underlying cause

2⃣ 🚨 ESOPHAGEAL OBSTRUCTION – CHOKE

Choke = acute obstruction of the esophagus.

⚠ Important in horses: CHOKE ≠ tracheal obstruction

→ The horse can usually still breathe because the obstruction is in esophagus, not trachea

🔍 COMMON CAUSE

Typically caused by:

• 🌾 Dry fibrous material

→ Dry food enters esophagus → Absorbs saliva → Swells → Bolus expands → Blocks esophageal lumen → CHOKE!!🚨

📍 PREDISPOSED SITES

Three important narrow regions:

1⃣ Cranial cervical esophagus

2⃣ Apertura thoracica cranialis
= thoracic inlet

3⃣ Diaphragmatic esophageal hiatus

🧠 NECK → CHEST ENTRANCE → DIAPHRAGM

🩺 CLINICAL SIGNS – CHOKE

• Dysphagia, Distress, Reflux, Saliva from nose and mouth, Ingesta from nostrils, Extended neck, Dehydration

Typical picture:

Horse eats → Suddenly distressed → Stretches neck → Tries repeatedly to swallow → SALIVA + FOOD FROM NOSE (green frothy nasal discharge)

🚨 MAJOR COMPLICATION

Aspiration pneumonia

Refluxed material → Enters respiratory tract → Aspiration → Pneumonia

Clinical sign: Cough

🔎 DIAGNOSIS – CHOKE

Nasogastric tube ⭐

• Try to pass tube. Tube reaches obstruction → Cannot pass into stomach

→ Supports diagnosis of esophageal obstruction

Also:

➡ Distension of cervical esophagus may be visible/palpable!

💊 TREATMENT – CHOKE ⭐⭐⭐

1. Sedation

➡ Alpha-2 agonist + butorphanol

Sedation also helps lower the head, reducing aspiration risk.

2. Spasmoanalgesia (Buscopan)

Purpose:

➡ Relax esophageal muscle
➡ Reduce pain/inflammation

Can include NSAIDs

3. Massage

If obstruction is accessible in cervical esophagus:
➡ Gentle external massage may help.

4. LAVAGE THROUGH NASOGASTRIC TUBE ⭐

Use: Saline/water

Repeated gentle lavage helps soften and remove obstruction.

🚫 DO NOT use oil for lavage

Why?

Oil → Can be aspirated → Enters lungs → Cannot be cleared effectively → Severe lipoid/granulomatous pneumonia

5. IV FLUIDS

Choke can cause:

• Dehydration

• Electrolyte abnormalities

Therefore:
➡ IV rehydration
➡ Electrolyte supplementation

Also supports tissue perfusion.

6. SURGERY

If conservative treatment fails:

➡ Esophagotomy

Used only when necessary because esophageal surgery has a relatively high complication risk.

3⃣ MEGAESOPHAGUS

Megaesophagus = dilation/distension of the esophagus associated with loss/reduction of normal motility.

Esophageal motility ↓ → Food cannot move efficiently toward stomach → Food + fluid accumulate → Esophagus stretches → MEGAESOPHAGUS

🔍 ETIOLOGY

Congenital:

Especially described in Friesian horses, associated with developmental/connective-tissue abnormalities

Acquired

Can be associated with:

• Vascular ring abnormalities/strictures

• Herpesvirus

• Myeloencephalitis

• Nerve damage

• Chronic esophageal obstruction

🩺 CLINICAL SIGNS

• Coughing, Nasal reflux of ingesta, Distension of cervical esophagus

Potential consequence:
🚨 Aspiration pneumonia

🔎 DIAGNOSIS

⭐ Contrast radiography

Contrast enters esophagus → X-ray → Dilated esophagus becomes visible

💊 TREATMENT

Feeding management is important:

• Feed food and water from an elevated position

• Example: Step-up/elevated feeding station

• Goal: Use gravity to assist passage of food toward stomach.

4⃣ ESOPHAGEAL STRICTURE / STENOSIS

Stricture/stenosis = narrowing of the esophageal lumen.

Frequently occurs around: Thoracic inlet

3 types

• adventitia and muscularis

• mucosa and submucosa

• annular stenosis.

🔍 ETIOLOGY

Most commonly:
➡ Sequel to choke/esophageal obstruction

Why?

Choke → Pressure/inflammation damages esophageal wall → Healing → Fibrosis/scar tissue → Scar contracts → LUMEN NARROWS

Can also be:

• Congenital, Acquired, Parasitic

🪱 GASTEROPHILUS INERMIS

Migrating bot-fly larvae can cause:

➡ Esophageal inflammation → Stenosis → Secondary dilation of esophagus cranial to obstruction

Diagnosis: Endoscopy

Treatment: Ivermectin

🔎 DIAGNOSIS – STRICTURE

⭐ Contrast radiography

Can demonstrate:
➡ Narrowed segment
➡ Dilation proximal to narrowing

💊 TREATMENT

Conservative:

• Antibiotics if indicated, NSAIDs

• Feeding management

• Balloon Dilatation: Balloon placed into narrowed segment → Inflated → Stretches stenotic area → Lumen becomes wider

Surgical

Possible procedures:

• Esophagomyotomy, Esophagopexy, Partial resection

5⃣ ESOPHAGEAL RUPTURE / PERFORATION / LACERATION 🚨

Esophageal wall is damaged.

Causes:

• External trauma, Kicks, Stick wounds

• Misuse/trauma from nasogastric tube

⚠ Why is it dangerous?

Esophagus ruptures → Saliva + ingesta leak into neck tissues → Massive bacterial contamination → Severe inflammation/infection → PHLEGMON + subcut emphysema

Phlegmon = diffuse spreading infection/inflammation of soft tissues.

6⃣ ESOPHAGITIS

= Inflammation of the esophagus

Causes:

• Choke, Reflux, Pyloric stenosis / delayed gastric emptying

💊 Treatment

• Feeding management

• Antibiotics if bacterial infection is involved

• NSAIDs

• Treatment of delayed gastric emptying/underlying disease

7⃣ ESOPHAGEAL DIVERTICULUM

= pouch/outpouching of esophageal wall. (almost always cercical region)

TRUE ➡ Involves all layers

FALSE ➡ Does not involve all layers; involvement of the muscular layer.

Traction arises from fibrotic contraction of all tissue layers, whereas pulsion involves mucosal protrusion through a muscular defect.

8⃣ ESOPHAGEAL CYSTS

Two types:

• Intramural Inclusion cyst ➡ Squamous epithelial lining, youngs and yearlings, congenital

• Esophageal Duplication cyst

🩺 Clinical Signs

• Dysphagia, Regurgitation/reflux

🔎 Diagnosis

• Endoscopy, USG, X-ray

Therapy

• surgical technique recommended for managing congenital intramural esophageal cysts → MARSUPIALIZATION (The cyst wall is incised, and its edges are sutured to the horse's neck skin, creating an open pouch (stoma). Complete resection is HIGH complication risk.

9. Equine grass sickness → toxicoinfection with clostridium botulinum. affecting the enteric nervous stsrem - neuropathy. acute, subacute, chronic. Clostridium tetani causes spastic paralysis, while Clostridium botulinum causes flaccid paralysis.

🧠 QUICK COMPARISON ⭐⭐⭐

Disorder	Main problem	Key clue
Dysphagia	Abnormal swallowing	Clinical sign, many causes
Choke	Acute obstruction	👃 Food/saliva from nose + NG tube won't pass
Megaesophagus	↓ Motility + dilation	Dilated esophagus + reflux
Stricture	Narrowed lumen	Often after previous choke
Rupture	Hole/tear	Saliva + food enter tissues → phlegmon
Esophagitis	Inflammation	Often after choke/reflux
Diverticulum	Esophageal pouch	Food can accumulate
Cyst	Mass/cyst	Dysphagia + regurgitation

• What is choke? → Acute obstruction of the esophagus, usually by impacted feed material.

• What is the typical sign the owner notices? → ⭐ Feed, saliva and/or fluid coming from the nostrils shortly after attempting to eat or drink.

• Which horses were specifically mentioned as predisposed to choke? → Friesian horses.

• How can you diagnose choke in the field? → Pass a nasogastric tube; it cannot be advanced beyond the obstruction. Cervical esophageal distension may also be palpable.

• What spasmolytic drug can you use? → Buscopan (hyoscine butylbromide).

• What reproductive drug did Zert say can also help relax the esophagus? → Oxytocin, particularly for certain esophageal obstructions.

• How do you treat choke conservatively? → Sedate → keep the head low → carefully lavage through a nasogastric tube → massage a palpable cervical obstruction → repeat attempts if necessary.

• Why should the horse's head be kept low during lavage? → To allow lavage fluid/feed material to drain from the nose and reduce aspiration into the lungs.

• If lavage is unsuccessful, should you immediately operate? → No. Continue conservative treatment and repeated careful lavage when appropriate; surgery is generally a last resort.

• If the horse needs fluids, where should they be given? → ⭐ IV, not orally/nasogastrically while the esophagus is obstructed.

• What important complication can occur during choke/treatment? → ⭐ Aspiration pneumonia.

• How do you diagnose aspiration pneumonia? → Clinical respiratory examination plus thoracic ultrasound; pulmonary consolidation/fluid-related changes may be detected, with B-lines/comet-tail artifacts depending on pulmonary involvement.

• How do you treat aspiration pneumonia? → Broad-spectrum antimicrobial therapy + NSAIDs/supportive care, with additional respiratory support depending on severity.

Stomach Diseases and Verminous Chronic Gastritis

Main conditions:

1⃣ Equine grass sickness
2⃣ Equine Gastric Ulcer Syndrome – EGUS
3⃣ Gastric impaction
4⃣ Verminous chronic gastritis

• Gasterophilosis

• Habronemiasis

• Trichostrongylosis
  5⃣ Gastric neoplasia – SCC

1⃣ 🌱 EQUINE GRASS SICKNESS

Equine Dysautonomia/Equine grass sickness = highly fatal neuropathy of grazing horses linked to neurotoxic enzymes

Main lesion: ➡ Degeneration of neurons of the autonomic nervous system

Especially:
⭐ Enteric nervous system

Therefore:

Autonomic/enteric neurons degenerate → GIT cannot function normally → Severe ↓ gastrointestinal motility → Mainly GIT signs

🔍 Etiology

The exact cause is not completely established.

Your notes suggest:

➡ Possible toxicoinfection associated with Clostridium botulinum

Intestinal infection → Toxin production → Damage to autonomic neurons → Loss of GIT motility

🩺 THREE CLINICAL FORMS ⭐⭐⭐

🔴 ACUTE

Severe disease.

• Colic, Severe ↓ gut motility, Dysphagia, Gastric distension, Gastric reflux, Muscle tremors

Outcome: ☠ Death usually in <4 days

🟠 SUBACUTE

• Similar to acute form, but less severe/slower progression

🟡 CHRONIC

More prolonged disease.

• Dullness, ↓ GIT motility, Severe/progressive weight loss, Hard, dry feces, Tachycardia, Crusty nasal discharge

🔎 Diagnosis

Presumptive:

• based on: Clinical signs, History, Physical examination

Definitive:

• ⭐ Histopathology / biopsy → Looking for characteristic neuronal degeneration.

Post-Mortem:

May find:

• Gastric distension, Colon containing hard + dry feces

Why?

↓ Enteric nervous function → decreased Motility → GI contents stagnate → Water absorbed → Hard/dry feces

💊 Treatment

No specific curative treatment.

➡ Supportive treatment only

Due to poor prognosis:
➡ Euthanasia often recommended

2⃣ 🔥 EQUINE GASTRIC ULCER SYNDROME – EGUS

Gastric ulcer = an open sore/defect in the stomach mucosa

🧪 NORMAL STOMACH

Glandular epithelium continuously secretes:HCl – hydrochloric acid

The stomach therefore needs protection against its own acid.

Protective mechanisms include:

🛡 Mucus/bicarbonate barrier
💧 Alkaline saliva
🩸 Normal mucosal blood flow and epithelial defenses

If protection fails → Acid damages mucosa → ULCERATION

📍 TWO REGIONS

• Squamous mucosa: Most commonly affected, Approximately 80%

• Glandular mucosa: Approximately 20%

🧠 WHY IS SQUAMOUS MUCOSA VULNERABLE?

Glandular stomach is designed to secrete and resist acid, while the squamous mucosa has much less acid protection.

Especially during exercise → Acidic gastric contents → splash upward → Contact squamous mucosa → Damage

🔍 ETIOLOGY / RISK FACTORS

Diet

• High concentrate and Low roughage

Why? Less roughage → Less chewing → Less alkaline saliva → Less buffering of acid → Increased ulcer risk

• Other factors: Stress, Other GIT disease, Systemic illness, Anorexia, withholding food, NSAID therapy

• 🏇 INTENSE EXERCISE ⭐

Very common in:

• Racehorses, Performance horses >90%

Exercise → Increased abdominal pressure / acid movement → Acid contacts squamous mucosa → Ulceration

💊 WHY NSAIDs CAN CAUSE ULCERS?

NSAIDs → ↓ Prostaglandins → ↓ Mucosal protection/blood flow/bicarbonate → Glandular defenses weaken → Ulceration

🩺 Clinical Signs

• Can range from no clinical signs to Anorexia, Colic, Depression, Weight loss, Diarrhea

🔎 Diagnosis

⭐ Gastroscopy / endoscopy

➡ Direct visualization of gastric mucosa, and the response to treatment

💊 TREATMENT – EGUS ⭐⭐⭐

1. Management

• Decrease/stop ulcerogenic NSAIDs where possible

• ↓ Concentrate feeding, ↑ Roughage

• Avoid prolonged fasting

2. GASTRIC ACID SUPPRESSION

• ⭐ Omeprazole (Proton-pump inhibitor – PPI). Blocks gastric proton pumps → ↓ HCl secretion → ↑ Gastric pH → Allows ulcer healing

3. Histamine H₂ receptor antagonists. Example Cimetidine → ↓ Histamine stimulation of acid secretion → ↓ HCl

🛡 OTHER TREATMENT

• Antacids, Mucosal protectants

3⃣ 🥕 GASTRIC IMPACTION

= Persistent and progressive accumulation of ingesta in the stomach.

Food accumulates → Cannot leave normally → Stomach becomes progressively full → Risk of gastric rupture

🔍 Etiology

1. Dry feed that swells/forms a mass, Example: Beet pulp

2. Other causes:

• Dental disease → poor mastication, Inadequate water supply, Rapid food intake, Pyloric outflow obstruction, Bezoars

3. Liver Disease → may cause secondary gastric impaction. Example: Ragwort poisoning

🩺 Clinical Signs

• Colic, Abdominal distension, Anorexia, Lethargy, Recumbency

🔎 Diagnosis

⚠ Definitive diagnosis can be difficult.

• May only be diagnosed during Exploratory celiotomy

• Rectal Examination: May detect displacement of spleen

• Ultrasound: May show abnormally large/distended stomach

💊 TREATMENT

🚨 Main concern = GASTRIC RUPTURE

• Therefore: Withhold feed and Limit/control water intake

• Gastric Lavage via Nasogastric tube → Soften/remove accumulated ingesta.

• 💧 IV Therapy → Correct dehydration/electrolytes

• 💊Analgesia for Pain/colic

• Surgery ➡ Gastrotomy: Incision into stomach → Remove impaction (Often unsuccessful / poor prognosis)

4⃣ 🪱 VERMINOUS CHRONIC GASTRITIS

Three important parasites:

🪰 Gasterophilus = BOT FLY

🪱 Habronema = STOMACH WORM + SUMMER SORES

🪱 Trichostrongylus axei = STOMACH HAIR WORM

A. 🪰 GASTEROPHILOSIS

Very common gastric parasite of horses.

Caused by:
➡ Bot-fly larvae

• Gasterophilus haemorrhoidalis, G. intestinalis, G. nasalis

🔄 LIFE CYCLE ⭐⭐⭐

Adult bot fly → Eggs deposited on horse's hair (Face, Lips, Intermandibular region, Forelegs) → Horse licks itself → Eggs enter mouth → Hatch to L1 → L1 burrows into oral mucosa → Molt → L2 → Migrate toward pharynx → Enter stomach → Molt → L3 → Attach/remain in GIT for approximately 10–12 months⭐ → L3 passed in feces
→ Pupate in soil → Adult fly emerges after approximately 3–9 weeks⭐

🔄 Cycle repeats

⚙ Pathogenesis

Larvae attach to gastric mucosa → Local irritation/inflammation → Mucosal damage → Bleeding → Ulceration → Possible secondary infection
➡ possible release of Hemolytic toxin

🩺 Clinical Signs

Oral larval migration may cause:

• Pus pockets in gums, Salivation, Head shaking, Loss of appetite, Chewing problems

Gastric infection can contribute to → Gastritis/ulceration

🔎 Diagnosis

Coprology

Larvae may be found seasonally, especially: April / beginning of May

⭐ Best: Gastroscopy/endoscopy: Directly visualize larvae attached to stomach.

💊 Treatment:⭐ Ivermectin

B. 🪱 HABRONEMIASIS

Important because it has 3 forms:

1⃣ Gastric
2⃣ Cutaneous
3⃣ Conjunctival

🦠 Etiology

Nematodes:

Habronema muscae, Habronema microstoma

➡ Adults live in gastric mucosa.

Draschia megastoma

➡ Produces large nodules in stomach wall.

🐴 FINAL HOST

➡ Horse and other equids

Adult worms normally live in Stomach

🪰 INTERMEDIATE HOST

⭐ Muscid flies – Musca

🔄 LIFE CYCLE ⭐⭐⭐

Adults in stomach → Eggs/L1 passed in feces → Fly larvae ingest eggs/L1 → Develop to infective L3 → Adult fly feeds on moist areas of horse (Eyes, Genitalia, Nostrils, Lips/wounds) → L3 leave fly → Horse swallows L3 → L3 reach stomach → Develop into adults → GASTRIC HABRONEMIASIS

🫃 GASTRIC FORM ⭐Most common

Causes:
➡ Gastritis and Sometimes granuloma formation

H. muscae + H. microstoma

➡ Gastritis, Usually without large granulomas

Draschia megastoma ⭐ → Causes: Large (up to 10cm) granulomatous nodules in gastric mucosa. Contain Worms and Necrotic material.

🧠 DRASCHIA = DRAMATIC BIG NODULE

🪰 ABERRANT HABRONEMIASIS

What if larvae deposited by flies do NOT reach the stomach?

L3 deposited in:
👁 Eye
🩹 Skin/wound
👃 Nostrils
🍆 Genitalia

⬇

Cannot complete normal life cycle → Remain in tissue → Strong local hypersensitivity → Granulomatous inflammation ➡ ABERRANT FORM

👁 CONJUNCTIVAL FORM

Can cause:

• Conjunctivitis, Eyelid thickening, Granulomatous lesions

🩹 CUTANEOUS FORM

Causes:

• Non-healing wounds, Ulceration, Severe itching, Granulomatous skin lesions, Granular dermatitis

⭐ Called: 🌞 SUMMER SORES

Why summer? 🪰 More flies → More larvae deposited in wounds → Habronema lesions

🔎 Diagnosis

• Endoscopy

• ELISA

• Identify non-healing reddish granulomas

• Larvae may be identified in lesions

💩 FECAL EXAM

⚠ Eggs are difficult to detect!!

➡ Eggs are very dense and may not float in standard flotation solutions

💊 Treatment

⭐ Ivermectin

➡ Especially against adult worms/systemic parasitic burden.

Local aberrant lesions may additionally require:
➡ Local wound/inflammation management.

C. 🪱 TRICHOSTRONGYLOSIS

Etiology:

⭐ Trichostrongylus axei

Also called: Stomach hair worm

Common in horses grazing on pasture shared or previously used by infected ruminants!

🔄 Life Cycle

Infective L3 → Horse ingests L3 while grazing→ Larvae penetrate gastric mucosa → Molt/develop → Adults emerge into gastric lumen

⚙ Pathogenesis

Causes: Catarrhal gastritis

🔎 Diagnosis

⭐ Coproculture

💊 Treatment

⭐ Ivermectin

🧠 THREE GASTRIC PARASITES ⭐⭐⭐

Parasite	What is it?	Key feature	Diagnosis	Treatment
Gasterophilus	🪰 Bot-fly larvae	Larvae attached to stomach	Endoscopy	Ivermectin
Habronema/Draschia	🪱 Nematodes	Gastritis + summer sores; Draschia → huge nodules	Endoscopy/ELISA	Ivermectin
Trichostrongylus axei	🪱 Stomach hair worm	Catarrhal gastritis	Coproculture	Ivermectin

5⃣ 🧬 GASTRIC NEOPLASIA

• Squamous Cell Carcinoma – SCC

• Important gastric neoplasia in horses.

🩺 Clinical Sign

Most characteristic:
➡ Chronic progressive weight loss

Can also eventually cause nonspecific GI signs.

🔎 Diagnosis

⭐ Biopsy

💊 Treatment

Generally:
❌ Not attempted

➡ Usually advanced when diagnosed + Poor prognosis

⭐ EXAM ESSENTIALS

🌱 GRASS SICKNESS

➡ Highly fatal autonomic neuropathy
➡ Especially enteric nervous system
➡ Severe ↓ GIT motility
➡ Possible C. botulinum toxicoinfection association
➡ Acute: colic + dysphagia + reflux + tremors → death <4d
➡ Chronic: dull + thin + hard/dry feces
➡ Definitive Dx = histopathology/biopsy
➡ Supportive only / euthanasia often recommended

🔥 EGUS

➡ Acid damages insufficiently protected gastric mucosa
➡ Squamous mucosa especially affected
➡ High concentrate + low roughage + fasting + stress + NSAIDs + intense exercise
➡ Gastroscopy ⭐
➡ Omeprazole
➡ More roughage / less concentrate

🥕 GASTRIC IMPACTION

➡ Progressive accumulation of ingesta
➡ Dry/swelling feed + poor mastication/water + outflow obstruction
➡ Risk = gastric rupture 🚨
➡ Difficult diagnosis
➡ Withhold feed + NG lavage + IV fluids
➡ Gastrotomy possible but difficult/poor success

🪱 VERMINOUS CHRONIC GASTRITIS

GASTEROPHILUS

BOT FLY
➡ Eggs on HAIR
➡ Horse LICKS
➡ Mouth → stomach
➡ Larvae remain 10–12 months
➡ Endoscopy
➡ Ivermectin

HABRONEMA

STOMACH WORM + SUMMER SORES
➡ Musca = intermediate host
➡ Swallowed L3 → gastric form
➡ Skin/eye L3 → aberrant form
➡ Draschia → 10 cm gastric granulomas
➡ Ivermectin

TRICHOSTRONGYLUS AXEI

STOMACH HAIR WORM
➡ L3 ingested
➡ Penetrates gastric mucosa
➡ Catarrhal gastritis
➡ Coproculture
➡ Ivermectin

Small Intestine Diseases and Verminous Enteritis

Main groups:

1⃣ Chronic inflammatory bowel disease – CIBD
2⃣ Idiopathic chronic diarrhea
3⃣ Intestinal obstruction
4⃣ Ulcerative duodenitis
5⃣ Small intestinal volvulus
6⃣ Intussusception
7⃣ Verminous/parasitic enteritis
8⃣ Alimentary lymphoma
9⃣ Bacterial diseases
🔟 Viral diseases

1⃣ CHRONIC INFLAMMATORY BOWEL DISEASE – CIBD

CIBD = collective term for a group of chronic enteropathies with similar clinical signs.

➡ Chronic inflammation/infiltration of intestinal wall → Poor intestinal function → Malabsorption → Weight loss ± diarrhea

Etiology: Often uncertain.

Possible causes: Immune-mediated disease or Infectious agents (Parasites, Bacteria)

🩺 Clinical Signs

• ⭐ Weight loss, Diarrhea, Colic, Fever

🔎 Diagnosis

• ⭐ Definitive diagnosis ➡ Histopathology

• USG, Blood samples

💊 Treatment

First: ➡ Corticosteroids, Examples: Dexamethasone, Prednisolone

Purpose: → Suppress intestinal inflammation / immune reaction

If ineffective: ➡ Combine with azathioprine (immunosuppressive drug)

2⃣ 💩 IDIOPATHIC CHRONIC DIARRHEA

Idiopathic = cause unknown

In horses, the exact cause of chronic diarrhea often remains undiagnosed.

Possible Causes/Associations:

• Previous intestinal infection, Dietary change

• Especially seen in Foals and Yearlings

🩺 Clinical Signs

• Chronic diarrhea and Weight loss

🔎 Diagnosis

⭐ Diagnosis of exclusion

Meaning:

Rule out parasites → Rule out infection → Rule out inflammatory disease → Rule out other causes
⬇
No cause identified
⬇
➡ Idiopathic chronic diarrhea

💊 Treatment

Symptomatic:

• Antidiarrheal therapy (Codeine phosphatase), Probiotics, Activated charcoal

3⃣ 🚧 INTESTINAL OBSTRUCTION

Two major types:

A. SIMPLE OBSTRUCTION ➡ Blood supply is maintained

B. STRANGULATING OBSTRUCTION ➡ Blood supply is compromised ⭐ This difference is extremely important.

🟡 SIMPLE OBSTRUCTION

• The lumen becomes blocked, but the vascular supply remains intact initially.

• Causes: Feed material, Parasites, Extraluminal mass

🔴 STRANGULATING OBSTRUCTION 🚨

Obstruction + vascular compromise → Intestine strangulated →↓ Venous drainage → ↓ Arterial perfusion → Ischemia → Necrosis → Loss of intestinal barrier →
🔥 ENDOTOXEMIA

🩺 Clinical Signs – Strangulation

• Usually much more severe: Severe pain, ↑ Heart rate, Abnormal mucous membrane color, Progressive systemic deterioration

• 🚨 Surgical emergency.

4⃣ 🔥 ULCERATIVE DUODENITIS

More common in foals than adults.

🔍 Etiology

• Excess HCl + pepsin reaching the duodenum

🩺 Clinical Signs

• Nonspecific: Fever, Mild–moderate colic, Dullness, Diarrhea

🔎 Diagnosis

• ⭐ Duodenoscopy = most specific.

• Long endoscope: Approximately 2 meters, can be performed in: Foals up to approximately 6 months

• Also: X-ray, Bloodwork

💊 Treatment

Goal: Reduce acid + protect mucosa

H₂ antagonist (Cimetidine) or Proton-pump inhibitor (Pantoprazole) + Mucosal protector (Sucralfate)

5⃣ 🔄 SMALL INTESTINAL VOLVULUS

= A segment of small intestine twists: ➡ >180° around the axis of its mesentery

⚙ What Happens?

• SI twists → Mesenteric vessels twist → Blood flow compromised → Ischemia → Necrosis → Severe acute colic

• Therefore:
  ➡ Strangulating obstruction

🔍 Cause:

• Can be associated with altered/local abnormal peristalsis

• More commonly affects foals

🩺 Clinical Sign

• ⭐ Acute, severe colic

💊 Treatment / Prognosis

• Requires rapid surgical assessment/treatment.

• Prognosis depends strongly on Duration + Degree of ischemia

• The longer it is twisted → the more bowel dies → worse prognosis.

6⃣ INTUSSUSCEPTION

= One segment of intestine invaginates into the adjacent segment

One segment slides inside another → Obstruction + Possible vascular compromise

7⃣ 🪱 VERMINOUS / PARASITIC ENTERITIS

Important parasites:

A. Anoplocephala

B. Parascaris equorum

C. Strongyloides westeri

D. Eimeria leuckarti

A. 🪱 ANOPLOCEPHALA

• Equine Tapeworms ➡ Cestodes

• All live in different intestinal locations and:
  ➡ Can occur simultaneously

• They attach to: Intestinal mucosa

⭐ THREE SPECIES

Species	Location	Size	Importance
A. perfoliata	⭐ Ileocecal junction	~20 cm	Most pathogenic
A. magna	Jejunum	~80 cm	Largest
Paranoplocephala mamillana	Duodenum	~5 cm	Smallest

⭐ A. PERFOLIATA

Most important/pathogenic:

• Ileocecal junction is narrow → Many tapeworms accumulate → Inflammation + obstruction → Colic → Potential intestinal damage/rupture → Peritonitis

🔄 LIFE CYCLE – ANOPLOCEPHALA ⭐⭐⭐

Final host: Horse

Intermediate host: Oribatid pasture mite

Infective stage: ⭐ Cysticercoid

Adult tapeworm in horse → Eggs passed in feces → Pasture mite eats eggs → Egg develops into cysticercoid → Horse grazes → Accidentally eats infected mite → Cysticercoid released → Develops into adult → Attaches to intestinal wall

⚙ Pathogenesis

Can cause:

• Catarrhal and Hemorrhagic enteritis, Mucosal ulceration, Intestinal obstruction, Intestinal rupture, Peritonitis

• 81% of constipations and 22% of spastic colic’s are caused by tapeworms!!

🩺 Clinical Signs

• Constipation, Colic, Diarrhea, Weight loss, Anemia, Dull coat

🔎 Diagnosis

• ⭐ ELISA / PCR. ELISA can help assess: Exposure/infection burden

• Coprology is difficult as egg shedding is low and intermittent/discontinuous. Therefore: Negative fecal examination does not reliably exclude infection.

💊 Treatment

• ⭐ Praziquantel, can be used alone or in combination with: Moxidectin, Ivermectin

B. 🪱 PARASCARIOSIS

• Etiology:⭐ Parascaris equorum

• Nematode / ascarid, ca. 40 cm, in Small intestine

• Especially common in: ⭐Foals and young horses

🔄 LIFE CYCLE – PARASCARIS ⭐⭐⭐

Direct life cycle ➡ NO intermediate host

Eggs passed in feces → Develop to infective stage in environment → Horse ingests infective eggs → larva hatch in stomach → intestine → penetrate intestinal wall → LIVER → parenchyma → bloodstream → LUNGS → molting to L4 → Trachea → cough → Swallows → stomach → small intestine → Develop into adults

⚙ Pathogenesis

Migration/adults can cause:

• Pneumonia, Chronic intestinal inflammation, Colic, Intestinal obstruction with heavy burdens

• Toxin release with affinity for nervous system → Possible neurological signs such as convulsions

🩺 Clinical Signs

• Inappetence, Fever, Diarrhea, Coughing, Colic, Poor condition. GREEN nasal discharge (Alicia said 90% of foals with this has parascariosis)

🔎 Diagnosis

➡ Coprology (flotation method)

💊 Treatment: ⚠ Resistance is an important problem for this parasite. it is one of the hardest to kill!

• Resistant to: Benzimidazoles, Ivermectin, Pyrantel (require higher doses)

• Can use: tiabendazol, mebendazol, fenbendazol

C. 🪱 STRONGYLOIDES WESTERI

• Threadworm present in Duodenum, mainly in Foals

• Important: One of the first nematodes to infect young foals!

👩 Adult Worms in Horse

Inside horse: Parasitic females

They reproduce: Parthenogenetically/asexually

Males and free-living females occur: In environment

🔄 LIFE CYCLE ⭐⭐⭐

Embryonated eggs/L1 passed in feces.

In environment there are 2 pathways:

A. HOMOGONIC DEVELOPMENT:

L1 → Molts → Infective L3 → Enters horse by Skin penetration OR Ingestion

B. HETEROGONIC DEVELOPMENT:

L1 → Free-living male + female adults → Sexual reproduction → Larvae → Develop into infective L3 → Enter horse

🐴 MIGRATION IN HORSE

🫁 Tracheal Route

• L3 penetrates skin → Subcutaneous tissues → Lymphatic/blood circulation → Lungs → Pharynx → Cough → Swallow → Duodenum → Adult female

• Peroral infection may also ultimately lead to intestinal establishment.

🐴 MARE → FOAL TRANSMISSION ⭐

• Lactogenic/transmammary transmission: Dormant larvae in mare → Activated around parturition/lactation → Larvae passed in milk → Foal infected

• This explains why very young foals can become infected early!

🩺 Clinical Signs

Especially: Enteritis in young foals

Can cause → Severe watery diarrhea

🔎 Diagnosis ➡ Coprology? (Alicia said sedimentation of the milk from the mother, and observe the parasite)

💊 Treatment

• Tiabendazole, Fenbendazole

• NEVER use ivermectin in foals (→ intoxication and death), only in adult horses!

D. 🦠 EIMERIA LEUCKARTI

• Protozoa/coccidia, in the small intestine

• Affected: Young horses/foals, particularly up to approximately 1½ years

⚙ Pathogenesis

Parasite enters → Intestinal epithelial cells → Reproduces intracellularly → Numbers increase →💥 Cell ruptures → Intestinal epithelial damage

Can cause: Catarrhal enteritis and Hemorrhagic inflammation

🩺 Clinical Signs

• Mild/light watery diarrhea, Jaundice, Anorexia, Fever, Weight loss, Emaciation

🔎 Diagnosis: Coprology

💊 Treatment
⭐ Symptomatic/supportive therapy only (atb, hydration)

Recovery:
➡ Approximately 2–3 weeks

🧠 PARASITE COMPARISON ⭐⭐⭐

Parasite	Type	Location	Key clue
Anoplocephala perfoliata	Cestode	Ileocecal junction	🕷 Mite IH + colic
Parascaris equorum	Nematode	SI	🫀 Liver → 🫁 lung migration
Strongyloides westeri	Nematode	Duodenum	Foal + 🥛 transmammary + diarrhea
Eimeria leuckarti	Protozoa	SI	Young horse + epithelial cell destruction

8⃣ 🧬 ALIMENTARY LYMPHOMA

Neoplastic disease involving intestinal/GI lymphoid tissue.

🩺 Clinical Signs

• Weight loss ⭐, Malabsorption, Colic, Diarrhea

🔎 Diagnosis: ⭐ Histopathology = definitive

💊 Treatment / Prognosis:

➡ Extremely poor prognosis, Euthanasia generally recommended

9⃣ 🦠 BACTERIAL DISEASES OF SMALL INTESTINE

A. ANTERIOR ENTERITIS

• Proximal enteritis / duodenitis-proximal jejunitis

• Possible agents: Salmonella Typhimurium, Clostridium perfringens

🩺 Clinical Signs

• Abdominal pain, Ileus, Large-volume gastric reflux may occur, Hypovolemia, Endotoxemia, Shock

🔎 Diagnosis

• Cultivation/culture

• Clinical diagnosis also relies heavily on examination and GI findings.

💊 Treatment

🚨 Aggressive supportive therapy

• Nasogastric decompression, IV fluids, Antibiotics when indicated

• Manage endotoxemia/pain

B. 🌊 POTOMAC HORSE FEVER

Acute enterocolitis syndrome.

• Etiology: Neorickettsia risticii

• Geographically important especially: USA / Canada

• Affects: Small + large intestine

⚙ Pathogenesis

Enterocolitis → Severe intestinal inflammation → Endotoxemia → Systemic disease

🩺 Clinical Signs ⭐

• Acute fever, Profuse watery diarrhea, Edema, Abortion, 🚨 Acute laminitis, Death

🔎 Diagnosis

⭐ PCR, blood testing

💊 Treatment:

• Tetracyclines

• Vaccination is available in endemic regions.

C. 🦠 EQUINE PROLIFERATIVE ENTEROPATHY – EPE

• Etiology: ⭐ Lawsonia intracellularis

Mainly affects:
➡ Foals / weanlings

⚙ What Happens?

Lawsonia infects intestinal cells → Causes proliferation/thickening of intestinal mucosa → Poor absorption → Protein loss → Weight loss + edema

🩺 Clinical Signs

• Diarrhea, Lethargy, Fever, Peripheral edema ⭐, Colic, Weight loss

🔎 Diagnosis

• ELISA, IFAT, USG (USG may demonstrate: Thickened intestinal wall)

💊 Treatment

Supportive therapy + Antibiotics such as:

• Erythromycin, Rifampin, Doxycycline

🔟 🦠 VIRAL DISEASES

A. ROTAVIRUS

Family: Reoviridae

Important cause of Diarrhea in young foals, Especially: <2 months, but can be a few days to several months.

⚙ Pathogenesis ⭐

Rotavirus damages INTESTINAL VILLI → ↓ Absorptive surface → Malabsorption → Maldigestion → Watery diarrhea

🩺 Clinical Signs

• Fever, Depression, Watery diarrhea, Dehydration

📊 Epidemiology

⭐ High morbidity: Many foals affected

⭐ Low mortality: Most survive with appropriate supportive care

🔎 Diagnosis

• Rapid antigen tests, ELISA

🛡 Prevention

• Vaccination strategies, including vaccination of pregnant mares where appropriate

• Hygiene, Reduce stress, Support colostral immunity

B. CORONAVIRUS
➡ Can cause intestinal disease

⚠ The line “high mortality in youngs” should not be your main exam definition for equine coronavirus without additional course context.

🧠 BIG PICTURE – HOW TO ORGANIZE QUESTION 3

               SMALL INTESTINE DISEASE
                         │
       ┌─────────────────┼──────────────────┐
       │                 │                  │
 INFLAMMATORY        MECHANICAL         INFECTIOUS
       │                 │                  │
     CIBD            Obstruction         Parasites
 Duodenitis           Volvulus           Bacteria
                      Intussusception      Viruses
       │                                    │
       │                             ┌──────┴──────┐
       │                             │             │
 MALABSORPTION                     FOALS        ADULTS
       │
 WEIGHT LOSS

⭐ PARASITES – EXAM ESSENTIALS

🪱 ANOPLOCEPHALA

➡️ Tapeworm
➡️ A. perfoliata = ileocecal junction = most pathogenic
➡️ Intermediate host = mite
➡️ Infective stage = cysticercoid
➡️ Colic/obstruction/intestinal damage
➡️ ELISA/PCR
➡️ Praziquantel

🪱 PARASCARIS

➡️ Young horses
➡️ Small intestine
➡️ Direct life cycle
➡️ GUT → LIVER → LUNG → TRACHEA → SWALLOW → GUT
➡ Cough + colic ± obstruction
➡ Coprology

🪱 STRONGYLOIDES WESTERI

➡ Young foals
➡ Duodenum
➡ Parasitic females in horse
➡ Free-living generation possible
➡ Important transmammary/lactogenic transmission
➡ Severe watery diarrhea
➡ Benzimidazole / ivermectin

🦠 EIMERIA LEUCKARTI

➡ Coccidia
➡ Young horses
➡ Reproduces in intestinal epithelial cells
➡ Cell rupture → enteritis
➡ Coprology
➡ Supportive treatment

⭐ OTHER EXAM ESSENTIALS

CIBD

Chronic weight loss + diarrhea → histopathology → corticosteroids

Simple obstruction

Lumen blocked, blood flow intact

Strangulation

Lumen + blood flow blocked → ischemia/endotoxemia

Volvulus

SI twists >180° around mesentery → severe acute colic

Intussusception

One intestine telescopes into another

Ulcerative duodenitis

Foal + HCl/pepsin → ulcer → acid suppression + sucralfate

Anterior enteritis

Proximal SI inflammation → ileus/reflux → hypovolemia/endotoxemia

Potomac horse fever

Neorickettsia → fever + watery diarrhea + laminitis → tetracycline

EPE

Lawsonia → foal + intestinal thickening + weight loss + peripheral edema

Rotavirus

Foal → villous damage → malabsorption → watery diarrhea

4. Large Intestine Diseases, Equine Strongylidosis & Cyathostomosis

Main topics:

1⃣ Large-intestine anatomy
2⃣ Colic
3⃣ Intestinal obstruction
4⃣ Pelvic flexure impaction
5⃣ Left dorsal displacement
6⃣ Right dorsal displacement
7⃣ Acute colitis
8⃣ Cecal tympany
9⃣ Large strongyles
🔟 Small strongyles – cyathostomosis
1⃣1⃣ Pinworms – oxyurosis

LARGE-INTESTINE ANATOMY

The large intestine begins at the: CECUM, and ends with: DESCENDING/SMALL COLON

CECUM: Located mainly on: Right side of abdominal cavity

Parts:

• Base/basis, Body/corpus, Apex, Taeniae, Haustra

LARGE COLON: ⭐⭐⭐

Learn the pathway:

RIGHT VENTRAL COLON → STERNAL FLEXURE → LEFT VENTRAL COLON → PELVIC FLEXURE⭐ → LEFT DORSAL COLON → DIAPHRAGMATIC FLEXURE —> RIGHT DORSAL COLON → TRANSVERSE COLON → SMALL / DESCENDING COLON

🧠 Think of it as a double layered horse shoe!

1. 🐴 COLIC

Colic = acute abdominal pain.

⚠ Colic is NOT a disease.

It is a: CLINICAL SIGN / SYNDROME indicating abdominal pain

🔍 Causes

Usually associated with disruption of normal gastrointestinal function/motility.

Predisposing factors include:

• Diet, Management, Parasites

Pain may result from:

• Distension, with accumulation of Gas, Fluid, Ingesta

• Obstruction

• Mesenteric tension (Torsion, Hernias, Intussusception)

• Ischemia (Vascular occlusion / strangulation)

• Inflammation (Mucosal inflammation, Irritation, Ulceration)

🩺 Clinical Signs

• Horse may: Paw the ground, look toward flanks, Kick abdomen, lie down more than normal, Roll, Sweat

⚠ FALSE COLIC:

• Not every horse showing colic behavior has primary GI disease.

• Other painful diseases can mimic colic: → Uterine torsion, Rhabdomyolysis (monday morning disease), Severe bladder distension, Laminitis

2. LARGE-INTESTINE OBSTRUCTION

Important sites according to your notes:

⭐ Pelvic flexure
⭐ Left dorsal colon
⭐ Right dorsal colon

🟢 SIMPLE OBSTRUCTION

Blood supply remains normal initially.

Causes:

• Impaction, Enteroliths, Trichobezoars, Foreign bodies (Sand, Nylon)

• Strictures, Adhesions/fibrous bands, Large-colon displacement

🟡 INCOMPLETE OBSTRUCTION

• Some ingesta and gas can still pass.

🔴 COMPLETE OBSTRUCTION

• Nothing passes → Ingesta + gas accumulate rapidly → Severe intestinal distension → Abdominal distension → Pressure on Diaphragm and Vena cava → Respiratory + cardiovascular compromise can develop.

🚨 STRANGULATING OBSTRUCTION

• Most dangerous. = Obstruction + compromised vascular supply

• Causes: Volvulus, Intussusception, Strangulating lipoma

⚙ Pathogenesis

• Strangulation → Blood supply compromised → Intestinal ischemia → Necrosis → Loss of mucosal barrier → Bacteria + endotoxins cross intestinal wall → ENDOTOXEMIA

• Also: Fluid sequestration → HYPOVOLEMIA

🩺 Clinical Signs

• Severe colic, Hypovolemia

• Pale → congested/cyanotic abnormal mucous membranes

• Tachycardia, Rapid deterioration, Endotoxemia

🚨 EMERGENCY

3. 🌾 PELVIC FLEXURE IMPACTION

One of the classic sites of large-colon impaction.

📍 Anatomy

• Pelvic flexure connects: LEFT VENTRAL COLON → PELVIC FLEXURE → LEFT DORSAL COLON

• Important: There is a marked reduction in lumen diameter here → Natural site for obstruction.

🔍 Etiology

Dry / inadequately digested feed → Moves through large colon → Reaches narrow pelvic flexure → Fails to pass → IMPACTION (forstoppelse)

🩺 Clinical Signs

Usually relatively mild:

• Mild abdominal pain, Slight ↑ heart rate, Usually no severe toxemia initially

🔎 Diagnosis

• Clinical signs, Auscultation of intestinal sounds, Rectal examination is also important clinically

💊 Treatment

• Oral fluids, IV fluids, Mild analgesics, Laxatives, Withhold feed until resolved

If medical treatment fails: ➡ Surgery

4. 🔄 LEFT DORSAL DISPLACEMENT

• Nephrosplenic / Renosplenic Entrapment

• The large colon moves dorsally on the LEFT side, and becomes trapped around/between Spleen, Nephrosplenic/renosplenic ligament, Left kidney region

⚙ What Happens?

Colon moves dorsally → Passes over/around spleen → Becomes entrapped in nephrosplenic region → Colon may rotate → Ventral colon becomes positioned dorsally
+Dorsal colon becomes positioned ventrally

The spleen may be:
➡ Displaced ventrally, Congested/engorged

🩺 Clinical Signs

➡ Abdominal pain / colic. Severity varies.

🔎 Diagnosis

• Rectal examination ⭐ ➡ Abnormal colon position

• USG ➡ Useful for assessing spleen/kidney/colon relationship

• Abdominocentesis may yield splenic blood if the displaced spleen is inadvertently entered.

💊 Treatment

Conservative techniques may include:

• Feed restriction, Short-term anesthesia

• Positioning/rolling ➡ Right lateral recumbency and Roll over the back

• If unsuccessful/severe: Surgery

5. 🔄 RIGHT DORSAL DISPLACEMENT

Colon is displaced: Between cecum and right body wall

⚙ Development:

• Pelvic flexure impaction → Pelvic flexure moves cranially toward diaphragm → Gas distends sternal + diaphragmatic flexures → Colon migrates caudally along ventral abdominal wall → Colon may twist along long axis around caecocolic attachment → Colon becomes edematous

• Usually: Not initially severely ischemic

🩺 Clinical Signs

• Abdominal pain, Gas distension

🔎 Diagnosis

• Rectal examination

• Important clue: ❌ Cannot identify normal: Cecum, Pelvic flexure, because anatomy has been displaced.

💊 Treatment

Medical

• Analgesics, Fluids

Surgical

• Remove/decompress intestinal contents, Reposition colon

• good prognosis and low reoccurrence

6. ACUTE COLITIS

= Acute inflammation of the large intestine/colon.

Etiology:

• Salmonellosis, Clostridial infection, Antibiotics, NSAIDs, Contaminated feed

⚙ Pathogenesis ⭐

• Inflammation damages mucosa → Intestinal barrier is lost → Luminal bacteria + toxins penetrate mucosa → Systemic inflammation → ENDOTOXEMIA

• Also: Severe fluid loss into intestine → Diarrhea and Dehydration

🩺 Clinical Signs

• Fever, Inappetence, Colic, Diarrhea

• Bloody diarrhea can occur especially with: Salmonella, Clostridial disease

• Signs of: Endotoxemia

🔎 Diagnosis

• Clinical signs, Dehydration

• Blood: ↑ PCV ➡ Hemoconcentration from dehydration

• Metabolic acidosis

• Leukopenia

💊 Treatment

• Aggressive IV fluids, Flunixin meglumine

• Intestinal adsorbents/supportive therapy

• Antibiotics when specifically indicated, including selected bacterial infections such as clostridial disease

7. 🎈 CECAL TYMPANY

= Gaseous distension of the cecum

🔍 Etiology

• Rapid fermentation, Colonic displacement, Obstruction

🩺 Clinical Signs

• Distended abdomen, Abdominal pain

🔎 Diagnosis

• Auscultation + percussion

→ ⭐ Characteristic: High-pitched “PING”

• Also: Rectal examination

💊 Treatment

➡ Remove/decompress gas, for example by catheter/trocarization when clinically indicated AND Correct underlying cause

9⃣ 🪱 EQUINE STRONGYLIDOSIS

LARGE STRONGYLES

Location of adults: Cecum + colon (Proximal ventral colon)

🪱 TWO GROUPS

1. Genus STRONGYLUS

• ⭐ Larvae migrate through organs

S. vulgaris ➡ Cranial/anterior mesenteric artery

S. edentatus ➡ Liver

S. equinus ➡ Liver + pancreas

2. Genus TRIodontophorus

Examples:

• T. serratus

• T. tenuicollis

• T. brevicauda

• T. minor

➡ No major extraintestinal larval migration like Strongylus spp.

🪱 LARGE STRONGYLES – STRONGYLUS spp. ⭐⭐⭐

Large strongyles are located as adults in the:

➡ Cecum and colon

They have a direct life cycle:

Eggs in feces → Develop in environment → Infective L3 → Horse ingests L3 while grazing → Larvae penetrate intestinal mucosa→ Larval migration differs between species → Larvae eventually return to large intestine → Adults attach to intestinal mucosa using their large buccal capsule → Suck tissue/blood → many small bleeding ulcers

1⃣ 🩸 STRONGYLUS VULGARIS ➡ Arteritis parasitaria ⭐⭐⭐

🔄 MIGRATION

Infective L3 → Enters large intestine → Remains there for maximum approximately 10 days → Penetrates intestinal mucosa → develops/migrates as L4
→ Migrates through arteries toward → A. mesenterica cranialis, Abdominal aorta and Thoracic aorta → Larvae form small nodules in arterial walls → PARASITIC ARTERITIS → Damage to vessel wall → Aneurysm + thrombus formation → nodules/lesions release larvae → Larvae migrate back toward large intestine → Develop into adults

🚨 WHY DOES S. VULGARIS CAUSE COLIC?

The important lesion is:

Arteritis → Thrombus → Thromboembolism / impaired intestinal blood supply → ISCHEMIA → INFARCTION → NECROSIS of intestinal wall → Severe colic

🩸 ADULT WORMS

Adults return to large intestine, they have a Large buccal capsule, in which attaches strongly to the intestinal mucosa and draws mucosal tissue into the buccal capsule → Bleeding mucosal ulcers

2⃣ 🫀 STRONGYLUS EQUINUS

Larvae penetrate intestine → Migrate across the abdominal cavity → LIVER → Migrate to PANCREAS → Eventually return to large intestine → Develop into adults

Migration period according to Alica: ⭐ 8–9 months

⚙ Consequences

Larval migration through soft tissues causes:

• Tissue injury, Inflammation, Nodules, Fibrosis

• Even after deworming: Parasite dies/is eliminated, But damaged tissue heals with FIBROTIC TISSUE → Can cause later problems

3⃣ 🫀 STRONGYLUS EDENTATUS ⭐⭐⭐

⚠ You MUST explain the migration and how it can lead to PERITONITIS.

🔄 MIGRATION

Larvae penetrate intestinal wall → Migrate to LIVER → Form small nodules in liver → Migrate from liver toward FLANK / abdominal wall region → Larvae migrate through abdominal tissues/peritoneal region → Cause tissue damage + inflammation → PERITONITIS

Migration period: 9–11 months

🧠 THREE SPECIES – DO NOT MIX THEM UP ⭐⭐⭐

Species	Main migration	Major consequence	Time from lecture
S. vulgaris	🩸 Cranial mesenteric artery → aorta	Arteritis parasitaria → thrombus → ischemia/infarction	L3 initially SI/LI mucosa max ~10 d before migration
S. equinus	🫀 Liver → pancreas	Tissue damage + fibrosis	8–9 months
S. edentatus	🫀 Liver → flank/peritoneal region	⭐ Severe peritonitis + hepatic fibrosis	9–11 months

🩺 Clinical Signs – Strongylidosis

• Anemia, Colic, Poor condition, Diarrhea, Fever, Anorexia, Weight loss

🔎 Diagnosis

• Coprology, Necropsy

• ⭐ Larval culture for species differentiation. Strongyle eggs look very similar on routine fecal examination.

💊 Treatment

• Fenbendazole (kills migrating larva, small strongyle is resistant)

• Moxidectin (kills both adults and encysted larva)

🔟 🪱 SMALL STRONGYLES - CYATHOSTOMOSIS

Also called: Cyathostomins

• Genus Trichonema

• Cyathostomes

• More than 50 species

Location of adults:

➡ Cecum + colon

Small strongyles are very common in horses.

⭐ BIG DIFFERENCE FROM LARGE STRONGYLESLARGE STRONGYLES

➡ Larvae MIGRATE to organs/vessels

SMALL STRONGYLES

➡ Larvae DO NOT perform major extraintestinal migration
➡ Instead, they ENCYST in the mucosa of the cecum and colon

🧠 LARGE = LEAVE, SMALL = STAY

🔄 LIFE CYCLE – CYATHOSTOMINS ⭐⭐⭐

Direct life cycle

➡ No intermediate host

Eggs shed in feces → Develop in environment → Infective L3 → Horse ingests L3 while grazing → L3 reach cecum + colon → Invade the large-intestinal mucosa → Form encysted/nodular stages → Develop toward L4 → Larvae emerge from mucosa back into intestinal lumen → Develop into adult worms → Adults produce eggs
→ Eggs passed in feces 🔄

😴 HYPOBIOSIS ⭐

The encysted larvae can:

➡ ARREST THEIR DEVELOPMENT

They remain dormant in the intestinal mucosa.
➡ They may remain encysted for up to ~3 years

⚙ PATHOGENESIS

Small strongyles are generally considered less individually pathogenic than the large Strongylus spp., but:

⚠ Heavy infections can cause severe disease.

1⃣ ENCYSTMENT

Larvae invade intestinal mucosa → Form nodules → Damage mucosa →Cause:

• Inflammatory reaction, Edema, Mucosal bleeding, Thickening/damage of intestinal wall

2⃣ MASS EMERGENCE ⭐⭐⭐

Large numbers of encysted larvae can reactivate and emerge from the mucosa at approximately the same time.

Thousands of larvae emerge → Large areas of mucosa are damaged → Severe inflammation → Loss of intestinal barrier/function → Protein/fluid loss → Severe watery diarrhea

This clinical syndrome is:

⭐ LARVAL CYATHOSTOMINOSIS

So remember:

The dangerous part is not only having encysted larvae — it is especially when MANY emerge simultaneously.

🩺 CLINICAL SIGNS

• ⭐ Weight loss, Rough/dull coat

• ⭐ Watery diarrhea

• Colic, Fever, Anemia, Poor condition

With severe larval cyathostominosis:
➡ Severe enteritis/colitis
➡ Protein loss may occur
➡ Rapid deterioration can occur

🔎 DIAGNOSIS

• Coprology / fecal egg count

• Necropsy

• Larval culture for species identification

⚠ IMPORTANT LIMITATION

Encysted larvae may not be detected by fecal egg counts.

❗ Low fecal egg count does NOT necessarily mean there are few encysted cyathostomin larvae.

💊 TREATMENT

⭐ MOXIDECTIN

Important because it has activity against:

• Adult cyathostomins

• Larval stages

• ⭐ Encysted larvae

⭐ LARGE vs SMALL STRONGYLES

	LARGE STRONGYLES	SMALL STRONGYLES
Adults	Cecum + colon	Cecum + colon
Infective stage	L3	L3
Intermediate host	None	None
Life cycle	Direct	Direct
Larval behavior	⭐ Migrate outside intestine	⭐ Encyst in intestinal mucosa
Main danger	Organ/vessel damage	Mucosal damage
Important syndrome	S. vulgaris arteritis	Larval cyathostominosis
Hypobiosis	Not key feature	⭐ Very important
Severe disease mechanism	Migration	⭐ Mass larval emergence
Key treatment in notes	Moxidectin	⭐ Moxidectin

1⃣1⃣ 🪱 PINWORMS – OXYUROSIS

Etiology: ⭐ Oxyuris equi

Type:
➡ Nematode

Location:
➡ Cecum + colon

🔄 LIFE CYCLE

Adult females in colon → Pregnant female migrates toward anus → Deposits eggs in sticky fluid around anus → Severe irritation/pruritus → Horse rubs tail/perineum against objects → Eggs enter environment → Develop to eggs with infective stage L3 → Horse ingests infective eggs → small intestine → large intestine → L4 with large buccal capsule ingests on wall → destroy wall → L5 → adult in colon

🩺 Clinical Signs ⭐

Main sign:

🍑 INTENSE PERIANAL ITCHING

• Horse rubs rear end → Hair breaks/falls out → Focal alopecia around tail/perianal area → Skin trauma → Possible secondary infection

🔎 Diagnosis

⭐ Perianal tape/swab test

Why not rely on ordinary fecal exam?

Because:
➡ Female deposits eggs around anus, not primarily into feces.

💊 Treatment

1⃣ Anthelmintic:

• Moxidectin

• Ivermectin orally

2⃣ Very important:
➡ Clean eggs from perianal skin/environment

🧠 WHOLE QUESTION IN ONE MAP

              LARGE INTESTINE
                    │
       ┌────────────┴────────────┐
       │                         │
    DISEASES                 PARASITES
       │                         │
       ├─ Colic                  ├─ LARGE STRONGYLES
       ├─ Obstruction            │      ↓
       ├─ Pelvic impaction       │    MIGRATE
       ├─ Left displacement      │      ↓
       ├─ Right displacement     │  S. vulgaris → artery
       ├─ Acute colitis          │  S. edentatus → liver
       └─ Cecal tympany          │  S. equinus → liver/pancreas
                                 │
                                 ├─ SMALL STRONGYLES
                                 │      ↓
                                 │   ENCYST
                                 │      ↓
                                 │  Cyathostomosis
                                 │
                                 └─ OXYURIS
                                        ↓
                                   PERIANAL ITCH

Principles of Treatment and Prevention of Parasitic Infections in Horses

MAIN PRINCIPLE

Treatment and prevention of equine parasitic infections have TWO main components:

1⃣ MANAGEMENT

➡ Decrease the number of infective parasite stages in the environment

2⃣ THERAPEUTIC CONTROL

➡ Deworming with anthelmintics at appropriate intervals / according to parasite burden

⭐ GOAL = BREAK THE PARASITE LIFE CYCLE

Horse has parasites → Eggs/larvae contaminate environment → Develop into infective stages → Horse becomes reinfected
⬇
🔄 Cycle continues

Therefore:

MANAGEMENT + ANTHELMINTICS → Reduce environmental contamination → Reduce reinfection → BREAK LIFE CYCLE

⚠ ANTHELMINTIC RESISTANCE

• Traditionally, parasite control relied heavily on repeated anthelmintic treatment.

• Anthelmintics → Kill intestinal worms → ↓ Egg production → ↓ Environmental contamination

BUT:

Frequent/inappropriate deworming → Selection pressure → Resistant parasites survive → Reproduce
⬇
💊 ANTHELMINTIC RESISTANCE

Therefore:

❌ Deworming alone is NOT sustainable

We need:

⭐ MANAGEMENT + MONITORING + TARGETED/APPROPRIATE TREATMENT

1⃣ 🌱 MANAGEMENT

1.💩 MANURE REMOVAL ⭐

Remove manure regularly from:

• Pasture, Paddocks, Stables, Every 24–72 hours!

Strongyle eggs are passed in feces → Eggs hatch → Larvae develop → Infective L3 develop in environment within approximately 5–7 days

Therefore → 💩 Remove feces BEFORE larvae become infective

2.💧 DECREASE HUMIDITY

• Many free-living parasite stages survive/develop better in moist conditions

3.♨ COMPOST MANURE ⭐

• Many parasite eggs have resistant shells and survive adverse environmental conditions

• Proper composting → Heat generated → Eggs/larvae devitalized → ↓ Environmental contamination

4.🚜 PASTURE MANAGEMENT

Can include:

• Deep plowing, Reseeding, Manure removal, Pasture rotation

5.🍽 FEEDING MANAGEMENT

• ❌ Do not feed directly from contaminated ground. Instead: Use elevated feeders

6.🆕 QUARANTINE NEW HORSES ⭐

• New arrivals may introduce resistant or unfamiliar parasite populations.

Therefore:

• New horse → QUARANTINE → Fecal examination → Appropriate parasite treatment if indicated → Only then introduce to herd/pasture
  → Larvicidal treatment before turnout of new arrivals.

7.🌱 PASTURE ROTATION

• Move horses from Contaminated pasture → Pasture with lower parasite contamination
  ➡ Deworming appropriately before moving animals!

• Most important: Cleanest pasture → foals + young horses

• Young horses:
  ➡ Less developed immunity, and more susceptible to important parasites such as Parascaris

8.🪰 INSECT CONTROL

Important because flies act as ➡ Intermediate hosts/vectors for some parasites.

• Habronema:🪰 Muscid flies transmit L3

• Gasterophilus: Adult bot flies deposit eggs on horse

• Therefore:
  ➡ Implement fly-control programs.

9. FOALS

Foals are especially susceptible to:

• Parascaris, Strongyloides westeri, Other nematodes

• Tapeworms during the first year

Recommendations:

➡ Regular deworming approximately every 60 days/2months

with drugs:
➡ Safe and effective against ascarids

Protocols during first year should account for:
➡ Nematodes and Cestodes

⚠ For your exam, remember this as the course protocol; modern parasite-control programs may adjust treatment based on local resistance and monitoring.

2⃣ 🔬 MONITORING ENDOPARASITES

Why monitor?

➡ Identify parasite burden
➡ Decide whether treatment is needed
➡ Assess effectiveness
➡ Reduce unnecessary drug use
➡ Slow resistance

💩 BASIC FECAL FLOTATION

• Detects: Parasite eggs

• Problem: ⚠ Some parasites shed eggs intermittently

• Therefore: A negative fecal sample does not always exclude infection!

• Also, encysted/larval stages may not produce eggs.

🔬 DIRECT MICROSCOPY

• Feces can be examined directly for: Eggs/larvae/other parasite stages.

🔢 McMASTER METHOD ⭐

• A quantitative fecal egg-count technique.

• → Eggs per gram (EPG)

• Therefore helps estimate the intensity of egg shedding/infection

• If 200 EPG → start deworming

• If 600 EPG → HEAVY infestation

🧫 LARVAL CULTURE

• Useful especially because: Strongyle eggs can look very similar

• Culture larvae → Examine larvae → Help differentiate strongyle groups/species

☠ POST-MORTEM EXAMINATION

Can identify:

• Adult worms, Larvae, tissue migration, Nodules, Intestinal lesions

3⃣ 💊 ANTHELMINTICS

Four major chemical families of equine anthelmintics:

Chemical family	Important drug/example	Main association
Macrocyclic lactones	Ivermectin, moxidectin	Strongyles, bots, several nematodes
Acylated quinoline pyrazines	Praziquantel	Tapeworms/Anoplocephala
Tetrahydropyrimidines	Pyrantel	Luminal nematodes ± tapeworm activity depending dose
Benzimidazoles	Fenbendazole, mebendazole, oxibendazole, thiabendazole	Broad nematode activity

A. 💊 MACROCYCLIC LACTONES ⭐⭐⭐

• Ivermectin, Moxidectin

• Very important broad-spectrum equine anthelmintics.

⭐ MOXIDECTIN:

Important against:

• Adult AND Larval strongyles

• ⭐ Encysted cyathostomin larvae

• Migrating large strongyle larvae

⭐ IVERMECTIN:

Important against:

• Large strongyles

• Luminal nematodes

• Strongyloides

• Habronema

• ⭐ Gasterophilus larvae

• Some ectoparasites such as mites

B. 💊 PRAZIQUANTEL (Acylated quinoline pyrazines)⭐⭐⭐

Main thing to remember:

🪱 PRAZIQUANTEL = TAPEWORMS

Especially:

• Anoplocephala perfoliata, A. magna

• Paranoplocephala mamillana

Often available combined with Ivermectin or Moxidectin

Why important?

If horse repeatedly receives only nematocidal drugs without effective cestocidal treatment:

➡ Tapeworm infection can persist.

C. 💊 PYRANTEL (Tetrahydropyrimidine)

Effective mainly against luminal stages including:

• Adult large strongyles

• Small strongyles – resistance can occur

• Ascarids

• Pinworms

• Also: Anoplocephala perfoliata at appropriate tapeworm dosing.

D. 💊 BENZIMIDAZOLES – BZs

Examples:

• Fenbendazole, Mebendazole, Oxibendazole, Thiabendazole

• Broad-spectrum activity.

Can target:

• Large strongyles

• Cyathostomins ⚠ resistance common

• Parascaris

• Oxyuris

Other:

💊 PIPERAZINE

• Parascaris, Pinworms, Some small strongyles
  ❌ Poor/not effective for large strongyles.

4⃣ 🪰 PYRETHROIDS

External / environmental parasite control

Examples:

• Cypermethrin

• Permethrin

• Pyrethrum

Used particularly for:
➡ Insect/ectoparasite control: lice, ticks, insects (dipteran, fleas, lice)

⚙ Mechanism

• Synthetic pyrethroids such as cypermethrin/permethrin: ➡ Affect/modulate sodium channels in parasite/insect nerves → Prolonged neuronal excitation → Paralysis/death

• Pyrethrum: → Contact insecticidal action

⭐ WHICH DRUG FOR WHICH PARASITE? ⭐⭐⭐

Parasite	Main treatment
🪱 Small strongyles / cyathostomins	⭐ Moxidectin; fenbendazole depending resistance
🩸 Large/migratory strongyles	Ivermectin / moxidectin⭐
🪱 Parascaris	Depends strongly on resistance; BZ/pyrantel/ML according to susceptibility
🪱 Tapeworm – Anoplocephala	⭐ Praziquantel
🪰 Gasterophilus / bots	⭐ Ivermectin / ML
🪱 Strongyloides westeri	Ivermectin or fenbendazole
🍑 Oxyuris equi	ML or BZ + environmental/perianal cleaning
🪰 Habronema	Ivermectin + local lesion/fly management

1⃣ SMALL STRONGYLES

Cyathostomins ➡ Moxidectin or Fenbendazole where effective

Why moxidectin important?

⭐ Activity against encysted larvae

2⃣ LARGE STRONGYLES

Treatment:

➡ Ivermectin
➡ Moxidectin

Important because:
➡ Activity against adults + important migrating larval stages.

3⃣ 🪱 PARASCARIS

Especially important in:
➡ Foals/young horses

⚠ Anthelmintic resistance is a major consideration.

Your notes mention resistance to:

• Macrocyclic lactones

• Benzimidazoles

• Pyrantel

Therefore:

➡ Drug choice should depend on known/local efficacy

Possible classes:

• BZs: tiabendazol, mebendazol, fenbendazol

• Pyrantel

• MLs where still effective

⚠ Heavy Parascaris infections in foals need particular care because rapid killing of a very large worm burden can contribute to intestinal obstruction.

4⃣ 🪱 TAPEWORMS

• Anoplocephala perfoliata

• A. magna

• Paranoplocephala mamillana

⭐ Drug of choice:

PRAZIQUANTEL

Often combined with:
➡ Ivermectin/moxidectin

5⃣ 🪰 BOT FLIES

Gasterophilus spp.

Larval stages are susceptible to:

➡ Macrocyclic lactones

Especially:
⭐ Ivermectin

Yellowish eggs may be visible with naked eye on horse hair.

6⃣ 🪱 STRONGYLOIDES WESTERI

Threadworm

➡ Ivermectin or Fenbendazole

Fenbendazole:
➡ 50 mg/kg

compared with standard:
➡ 7.5 mg/kg

⭐ those numbers are lecturer-specific.

7⃣ 🍑 OXYURIS EQUI

Pinworm

Treatment:

• Macrocyclic lactones

• Benzimidazoles

• Pyrantel has variable efficacy according to notes

BUT:

Remember management too:

Female lays sticky eggs around anus → Environment/perineum contaminated → Reinfection

Therefore:

⭐ Clean perianal area + environment

⚠ ANTHELMINTIC RESISTANCE ⭐⭐⭐

This is a major part of modern parasite control.

Repeated unnecessary treatment → Susceptible worms die → Resistant worms survive → Resistant worms reproduce → Population becomes increasingly resistant

Therefore:

❌ Do not rely only on frequent blind deworming.

Instead:

➡ Fecal monitoring
➡ Appropriate drug choice
➡ Treat strategically/appropriately
➡ Environmental management
➡ Avoid unnecessary treatment
➡ Monitor treatment efficacy

🧪 HOW CAN WE CHECK IF A DEWORMER WORKS?

Conceptually:

Fecal egg count before treatment → Deworm → Repeat fecal egg count after treatment → Compare egg counts

If expected reduction does not occur:
➡ Suspect anthelmintic resistance / treatment failure

This is the principle of the:
⭐ Fecal Egg Count Reduction Test – FECRT

🧠 WHOLE QUESTION IN ONE MAP

         PARASITE CONTROL
                │
      ┌─────────┴─────────┐
      │                   │
 MANAGEMENT           THERAPY
      │                   │
 manure removal       anthelmintics
 composting               │
 pasture rotation         ├─ ML
 clean feeding            ├─ BZ
 quarantine               ├─ pyrantel
 fly control              └─ praziquantel
      │
      └─────────┬─────────┘
                │
           MONITORING
                │
         FECAL EGG COUNT
                │
       TARGETED TREATMENT
                │
      ↓ DRUG RESISTANCE

⭐ EXAM ESSENTIALS

If you need to answer this quickly:

“The goal of parasite control is to break the parasite life cycle by combining environmental management with appropriate anthelmintic treatment. Management includes frequent manure removal, composting, pasture rotation, reducing humidity, avoiding feeding directly from contaminated ground, quarantine and fecal examination of new horses, use of the cleanest pasture for young horses, and insect control. Parasite burden is monitored by fecal examination, especially quantitative methods such as McMaster. Anthelmintic treatment should be selected according to the parasite and resistance situation rather than relying only on frequent routine treatment. Important drugs include ivermectin and moxidectin for strongyles, moxidectin especially for encysted cyathostomins, praziquantel for tapeworms, and ivermectin for Gasterophilus and Habronema. Anthelmintic resistance is an important problem, so management, monitoring and appropriate treatment must be combined.”

🧠 FINAL MEMORY

M-M-M

🌱 MANAGEMENT

Reduce parasites in environment

🔬 MONITORING

Know what/how much is present

💊 MEDICATION

Treat appropriately

⬇

🔨 BREAK THE LIFE CYCLE

And remember the three strongest drug associations:

PRAZIQUANTEL → TAPEWORM 🪱

MOXIDECTIN → ENCYSTED CYATHOSTOMINS 😴

IVERMECTIN → BOTS 🪰

PERITONITIS

Peritonitis = inflammation of the peritoneum → tissue lining the abdominal cavity and organs.

Normal peritoneum:

• Secretes fluid → lubricates abdominal cavity

• Minimizes adhesion formation

• Has antibacterial properties

ETIOLOGY

May occur primary or secondary.

🦠 Infectious / septic:

• Surgical complications, Intestinal perforation, Uterine perforation, Metritis, Post-castration, Enteritis, Septicemia

⚪ Non-septic:

• Ruptured bladder/ureter / kidney, Bile, gastric or pancreatic juice, Foreign body, Neoplasia, Uroliths, Hepatitis, Gastric rupture

🪱 Parasitic:

• Larval migration

🩸 Traumatic:

• Uterine artery hemorrhage, Penetrating abdominal wound, Blunt abdominal wound, Ruptured diaphragm

PATHOGENESIS

1⃣ Fibrin + adhesions

Peritonitis → ↓ fibrinolytic activity → precipitation/deposition of fibrin → adhesions + pain

2⃣ Fluid loss + shock

Inflammatory response → activation of leukocytes + immunoglobulins
→ proteins + fluid + electrolytes move from plasma into abdominal cavity → hypovolemia + hypoproteinemia → cardiovascular collapse / shock

🧠 Remember:
FIBRIN → ADHESIONS
FLUID/PROTEIN LOSS → HYPOVOLEMIA → SHOCK

CLINICAL SIGNS

🚨 Peracute peritonitis

• E.g. gastric rupture, May be found dead, Profound toxemia, Rapid circulatory failure, Death within 4–12 h

🔥 Acute peritonitis

• Tachycardia, Tachypnoea

• Congested → cyanotic mucous membranes

• Cold extremities, Dehydration, Depression, Sweating, Immobility, Sensitivity to pressure / abdominal pain

⏳ Subacute / chronic peritonitis

• Dullness, ↓ Appetite, Progressive weight loss

• Abdominal pain → low-grade, intermittent or absent

• Intermittent fever, Variable bowel sounds, Chronic diarrhea in some cases

DIAGNOSIS

⭐ Peritonitis is characterized by:

• ↑ amount of peritoneal fluid

• ↑ cellular content

• ↑ protein content

💉 Abdominocentesis → examine peritoneal fluid

• Cytology of peritoneal fluid = definitive diagnosis

• Biochemistry:

  • ↑ Lactate

  • ↑ WBC

  • ↑ Albumin/globulin ratio

Appearance of peritoneal fluid:

• Turbid + off-white → haemoperitoneum / intestinal infarction

• Turbid + brown/green → contamination with intestinal contents

Other diagnostics:

• USG, X-ray, Laparoscopy

🔹 TREATMENT

1. Treat the underlying cause

2. Medical treatment

• 💧 IV fluid therapy

• 💊 NSAIDs

• 💉 Antibiotics → Penicillin = first choice

3. Correct

• Cardiovascular shock

• Endotoxic shock

4. Fibrinolytic medications

• Heparin

• Fragmented heparin

→ ↓ fibrin/adhesion formation

5. Abdominal drainage + lavage

• Drain peritoneal fluid

• Lavage with sterile solution

• Via cannula or Foley catheter

🪱 PARASITIC PERITONITIS ⭐

1⃣ Strongylus edentatus

• Larval migration → can cause peritonitis

2⃣ Setariosis
Caused by:

• Setaria equina

• Setaria labiato-papillosa

• Setaria cervi

Transmission: 🦟 Mosquitoes

Pathogenesis:
Mosquito infection
→ adult worms 10–15 cm long in abdominal cavity
→ produce microfilariae in blood
→ larvae may migrate to eyes + other organs

Clinical consequences:

• Peritonitis, CNS signs, Visual impairment

Diagnosis:

• 🔬 Microfilarial larvae in blood

• ELISA → antibodies

Treatment:

• 💉 Ivermectin

🧠 EXAM SEQUENCE

PERITONITIS = inflammation of peritoneum

E:
Septic / non-septic / parasitic / traumatic

⬇

P:
↓ fibrinolysis → fibrin → adhesions + pain
Fluid + protein + electrolytes leave plasma → hypovolemia + hypoproteinemia → shock

⬇

CS:
Peracute: toxemia → circulatory failure → death
Acute: tachycardia + tachypnoea + dehydration + abdominal pain
Chronic: dullness + ↓ appetite + weight loss + intermittent pain/fever

⬇

Dx:
⭐ Abdominocentesis + cytology
↑ fluid + ↑ cells + ↑ protein

⬇

Tx:
⭐ Underlying cause + IV fluids + NSAIDs + ATB + shock treatment + heparin ± abdominal drainage/lavage

Parasitic peritonitis = Strongylus edentatus migration + Setaria.

SETARIA:
🦟 Mosquito → abdominal worms → microfilariae in blood → eyes/CNS/peritoneum → Dx blood/ELISA → Tx ivermectin

Asthma

EQUINE ASTHMA / RECURRENT AIRWAY OBSTRUCTION (RAO)
= common condition characterized by laboured breathing due to obstruction of the bronchioles.

• Pulmonary hypersensitivity associated with stabling + feeding hay

• Usually reversible with environmental dust control

🧠 Think: Dust/hay → hypersensitivity → small airway obstruction

ETIOLOGY

Hypersensitivity to inhaled dust → inflammation of small airways.

Important inhaled triggers:

• Dust, Mould spores, Fungi, Actinomycetes, Gases

⭐ Associated with stabling and hay feeding

⭐ Tends to increase with age → commonly >7 years

PATHOGENESIS ⭐

Allergen exposure

⬇

Hypersensitivity + airway inflammation

⬇

3 important effects:

1. Bronchospasm → smooth muscle contraction of bronchi
2. Mucus hypersecretion
3. Inflammatory bronchitis

⬇

Reduced airway lumen

⬇

↓ Expiratory airflow → laboured expiration / dyspnoea

Chronic cases:

Persistent inflammation → structural changes:

• Metaplasia, Hyperplasia, Emphysema

🧠 Remember the 3:
SPASM + MUCUS + INFLAMMATION → narrowed airway → ↓ expiration

CLINICAL SIGNS

Severity ranges from subclinical → mild → severe.

🟢 Subclinical

• Mainly performance horses

• Exercise intolerance

🟡 Mild

• Occasional/sporadic cough

  • During feeding and During exercise

• Slight nasal discharge

🔴 Severe

• Chronic cough, Dyspnoea, Bilateral nasal discharge, ↑ Respiratory rate

• Exercise intolerance, Increased expiratory effort

⭐ Classic severe sign = double expiratory effort

DIAGNOSIS

1⃣ History + clinical signs ⭐

Typical:

• Horse >7 years, Chronic cough >3 months, Double expiratory effort, Dilated nostrils

2⃣ Cough reflex + auscultation

• ↑ Susceptibility to cough reflex

• Crackles, Wheezing

3⃣ Endoscopy

May show:

• Mucopurulent discharge in trachea + bronchi

• Congestion of airway mucosa

• Thickening of airway mucosa

Severe cases:

• Collapse of trachea + bronchi during expiration/coughing

4⃣ Additional tests

• Tracheal aspirate

• BAL / cytology

• X-ray

5⃣ Inhalation challenge test

Expose horse to mouldy hay/straw

→ worsening of clinical signs
and/or
→ changes in tracheal aspirate/BAL cytology

6⃣ Response to treatment

Improvement following:

• Corticosteroids

• Bronchodilators

⚠ Corticosteroids when respiratory infection is unlikely.

TREATMENT⭐⭐⭐

1⃣ ENVIRONMENTAL MANAGEMENT — MOST IMPORTANT

Reduce allergen/dust exposure:

• “Dust-free” environment

• Pasture + fresh grass

• Wet hay before feeding

• Avoid straw bedding

• Good ventilation

🧠 Without environmental control → drugs alone are not enough.

2⃣ Corticosteroids

→ ↓ pulmonary inflammation

• Systemic: Dexamethasone

• Inhaled: Beclomethasone

3⃣ Bronchodilators

→ rapid relief of bronchospasm

Rapid, relatively short-lived action:

• Albuterol, Clenbuterol

4⃣ Mucolytics

→ ↓ viscosity of respiratory secretions

• Acetylcysteine

5⃣ Mucokinetic agents

→ aid clearance of respiratory secretions

PROGNOSIS

Changes associated with RAO are mostly reversible with appropriate environmental management and treatment.

⚠ Once structural damage / emphysema develops → changes may become irreversible!

➡ Generally favourable prognosis if managed before permanent structural damage.

CIZEK'S LIST — RESPIRATORY PATHOGENS

🦠 VIRAL

• Equine rhinopneumonitis — EHV-1

• Equine herpesvirus 2 — EHV-2

• Equine herpesvirus 5 — EHV-5

  • → Interstitial pneumonia

• Adenovirus

• Equine influenza virus

• African horse sickness virus

• Morbillivirus

• Reovirus

• Equine rhinovirus

🦠 BACTERIAL

• Clostridium tetani → lockjaw / tetanus

• Streptococcus equi → strangles

• Burkholderia mallei → glanders

• Rhodococcus equi → pneumonia in foals ⭐

For Rhodococcus equi, I would say pyogranulomatous/abscessing bronchopneumonia in foals rather than simply “interstitial pneumonia.”

🧠 EXAM SEQUENCE

EQUINE ASTHMA / RAO

E:
Dust/hay/mould hypersensitivity, especially stabled horses >7 years

⬇

P:
Allergen exposure
→ bronchospasm + mucus hypersecretion + inflammatory bronchitis
→ ↓ airway lumen
→ ↓ expiratory airflow

Chronic → metaplasia + hyperplasia + emphysema

⬇

CS:
Exercise intolerance → cough → nasal discharge → dyspnoea + double expiratory effort

⬇

Dx:
History + CS → auscultation → endoscopy → tracheal aspirate/BAL ± X-ray ± challenge test

⬇

Tx:
⭐ ENVIRONMENT FIRST
Dust control + pasture/wet hay + ventilation

• corticosteroids

• bronchodilators

• mucolytics/mucokinetics

⬇

Prognosis:
Favourable and mostly reversible → until structural damage/emphysema occurs.

Pleuropneumonia and Verminous pneumonia

A. PLEUROPNEUMONIA

Pleuropneumonia = infection/inflammation of the lung AND pleural space.

⭐ You know the pleura is involved when there is fluid around the lungs → PLEURAL EFFUSION.

Pleural effusion = excess fluid around the lungs.

ETIOLOGY

Usually secondary to factors that lower respiratory defence → secondary bacterial infection.

1⃣ Stress / long-distance transport ⭐⭐⭐

• “Transit fever”

• Long-distance travel
  → prolonged head elevation → prevents normal drainage of respiratory secretions → secretions + bacteria descend into lower airways → pleuropneumonia

• ⭐ Very common cause!

2⃣ Viral respiratory disease

Predisposes to secondary bacterial infection:

• EHV-1, EHV-2, EHV-4, EHV-5

• Equine influenza

3⃣ Bacterial infection

• Streptococcus equi → strangles

• Rhodococcus equi

• Burkholderia mallei → glanders

• Pseudomonas

• Bordetella bronchiseptica

4⃣ Immunosuppression

• Corticosteroid therapy

• Cushing's disease

5⃣ Aspiration / inhalation pneumonia

Due to:

• Dysphagia, Esophageal obstruction, Pharyngeal paralysis, Choke, Inhaled foreign bodies

6⃣ Trauma

• Direct thoracic trauma, Penetrating chest wounds

7⃣ Pulmonary emboli/infarction

• E.g. secondary to: jugular phlebitis + thrombosis

PATHOGENESIS ⭐⭐⭐

1⃣ EXUDATIVE PHASE

Initial bacterial colonization of lung tissue
→ inflammatory response
→ protein-rich inflammatory exudate

⬇

2⃣ FIBRINOPURULENT PHASE

Bacterial infection progresses
→ large amount of septic fibrinopurulent exudate
→ accumulates in pleural cavity

⬇

3⃣ ORGANIZATION PHASE

Fibrin becomes organized
→ fibrous tissue
→ thick “pleural peel”

CLINICAL SIGNS

• Fever, Reluctance to move

• Abduction of elbows, Tachypnoea

• Dyspnoea → inspiratory + expiratory

• Cough, Nasal discharge

• Sternal edema, Stilted gait, Reluctance to lie down

🧠 Think: A very painful horse that doesn't want to move or lie down + respiratory disease.

DIAGNOSIS

1⃣ History + clinical signs

⭐ Ask: Has the horse recently travelled a long distance?

2⃣ Thoracic auscultation ⭐

Ventral lung field:
→ muffled / absent sounds due to pleural fluid

Dorsal lung field:
→ abnormal lung sounds

Heart sounds audible over larger-than-normal area
→ suggests pleural effusion

🧠 Fluid sinks → ventral sounds disappear.

3⃣ Percussion

• Reduced/dull ventrally
  → pleural effusion

4⃣ X-ray

• Fluid line → pleural effusion

• Consolidated lung

5⃣ Ultrasound ⭐

Shows:

• Pleural effusion, Consolidated lung, Abscesses, Fibrin, Adhesions

• ⭐ USG gives more detail than X-ray.

6⃣ Blood

Early/severe bacterial sepsis or toxemia:

• Leukopenia, Neutropenia + left shift, Hemoconcentration, Azotemia

Later stage:

• Leukocytosis, Mature neutrophilia, Hyperfibrinogenemia, Hyperglobulinemia, Hypoalbuminemia

7⃣ Thoracocentesis ⭐

Collect pleural fluid for:

• Cytology, Bacterial culture

• ⚠ Include anaerobic culture

8⃣ Respiratory sampling

• TTW = transtracheal wash

• BAL = bronchoalveolar lavage

🔹 TREATMENT

• 💉 Systemic antibiotics → treat bacterial infection

• 💊 NSAIDs → analgesic + anti-inflammatory

• Supportive care: Pleural drainage + lavage ⭐ → remove infected pleural fluid. If large quantities of thick, organized fibrinopurulent material cannot be adequately drained → Thoracotomy

🪱 B. VERMINOUS PNEUMONIA

Important parasites:

⭐ 1. Dictyocaulus arnfieldi

⭐ 2. Migrating larvae of Parascaris equorum

⭐ 3. Echinococcus equinus → equine cystic echinococcosis

🪱 1. DICTYOCAULUS ARNFIELDI ⭐⭐

Nematode / lungworm = Dictyocaulus arnfieldi

Predilection site:
→ Bronchi + bronchioles

Adults develop/live in the lungs.

Life cycle — DIRECT ⭐

Infective larvae are ingested during grazing → Migrate from intestine → Reach lungs → Adults develop in bronchi/bronchioles → Eggs + larvae carried up to trachea

→ Coughed up + swallowed → Released with feces onto pasture → Infect new host

🔹 Pathogenesis

Larvae/adults irritate respiratory mucosa

→ inflammation of bronchi, chronic bronchitis, pneumonia

Severe cases:

→ airway damage/obstruction

→ compensatory emphysema

🔹 Clinical signs ⭐

• Severe paroxysmal/productive cough

• Dyspnoea

• Mucopurulent nasal discharge, Fever

🔹 Diagnosis

• Larvoscopy / detection of larvae in feces

• 20 larvae / 1 g feces → high-intensity infection

🔹 Treatment ⭐

• Ivermectin, Moxidectin, Macrocyclic lactones

• Pasture management, Change pasture during season, Reduce reinfection.

🪱 2. PARASCARIS EQUORUM

Nematode = Parascaris equorum

• Large worm → about 40 cm, adults located in small intestine

• Very common in older foals

• ⭐ Verminous pneumonia occurs because of MIGRATING LARVAE.

Life cycle — DIRECT ⭐

Eggs passed in feces → Develop to infective stage in environment → Eggs ingested → Larvae penetrate intestinal wall → Liver

→ Lungs → Trachea → Irritation → horse coughs → Larvae swallowed → Return to small intestine → Become adults

Pathogenesis

Migrating larvae cause:

• Focal eosinophilic inflammation, Bleeding, Calcified subpleural nodules, Pneumonia

In liver:

• “Milk spots” = scar tissue

Intestinal infection:

• Chronic intestinal inflammation, Colic

• Release of toxins with affinity for the nervous system

🔹 Clinical signs

• Cough, Fever, Inappetence, Pneumonia, ± Colic / GI signs

🔹 Diagnosis

• Coprology / fecal examination

🔹 Treatment

⚠ Parascaris equorum has important anthelmintic resistance.

Resistance can occur to:

• Benzimidazoles, Ivermectin / macrocyclic lactones, Pyrantel

→ treatment choice should account for local resistance and efficacy.

🪱 3. ECHINOCOCCUS EQUINUS — EQUINE CYSTIC ECHINOCOCCOSIS

🔹 Etiology

Cestode / tapeworm

Echinococcus equinus
→ causes equine cystic echinococcosis
→ produces fertile hydatid cysts

🔹 Hosts ⭐

Definitive hosts (DH):

• Dog, Red fox, Arctic fox, cats

Intermediate hosts (IH):

• ⭐ Horse / donkey (also sheep, goat, cattle, pig)

🧠 DOG = definitive host → HORSE = intermediate host

🔹 Life cycle + Pathogenesis

Horse ingests Echinococcus eggs from contaminated environment/grass → Larvae migrate into tissues → Formation of hydatid cysts → Cysts + surrounding inflammation

→ If pulmonary involvement is extensive → respiratory impairment / pneumonia-like signs

🔹 Clinical signs

Usually related to the number and size of cysts.

If many cysts:

• Shortness of breath, Cough, Respiratory disease

🔹 Diagnosis

• Imaging, including X-ray when pulmonary cysts are suspected

🔹 Treatment / prognosis

Single cyst → may cause little clinical problem

Many cysts → no practical treatment for the cyst burden → poor prognosis / euthanasia may be considered

🧠 VERMINOUS PNEUMONIA — EXAM MEMORY

3 PARASITES:

1⃣ Dictyocaulus arnfieldi ⭐⭐⭐
→ LUNGWORM
→ bronchi/bronchioles
→ chronic bronchitis
→ severe paroxysmal cough + dyspnoea
→ severe = compensatory emphysema
→ Dx larvae in feces
→ Tx IVERMECTIN

2⃣ Parascaris equorum ⭐⭐
→ mainly foals
→ larvae migrate INTESTINE → LIVER → LUNGS → TRACHEA → swallowed → INTESTINE
→ coughing + pneumonia
→ Dx coprology

3⃣ Echinococcus equinus ⭐
→ cystic echinococcosis / hydatid cysts
→ dog = DH, horse = IH
→ multiple pulmonary cysts → cough + dyspnoea
→ imaging/X-ray.

Exercise intolerance associated with upper respiratory tract diseases and nasopharyngeal myiasis

General concept

Upper respiratory tract diseases can cause partial airway obstruction → reduced airflow during exercise → respiratory noise + exercise intolerance / poor performance.

🐴 1. HYPERTROPHY OF ALAR FOLDS

• Vibrating sound during inspiration

• Characteristic “high blowing” noise

Dx

• Place sutures from the skin to the dorsal opening of the false nostrils

• Compare respiratory noise before vs after

Tx

• Resection of the alar folds

🩸 2. PROGRESSIVE ETHMOIDAL HEMATOMA (PEH) ⭐

Etiology

• Unknown

• Expanding submucosal hemorrhages on the surface of the ethmoidal turbinate labyrinth

• Mucosal capsule may split → bloody discharge

• More common in horses >4 years

CS

• ⭐ Low-grade recurrent hemorrhage/epistaxis from nostril

• Dirty nasal discharge, Nasal obstruction, Facial swelling

• Rarely: Nervous signs, Blindness

Dx

• History + physical examination

• ⭐ Endoscopy

• X-ray, CT

Tx

• Chemical ablation → 10% formalin

🦠 3. PRIMARY & SECONDARY SINUSITIS / EMPYEMA

Empyema = collection of pus.

Primary sinusitis

Usually starts with URT viral infection → impaired mucociliary clearance → stagnation of mucus → opportunistic bacterial infection → hyperplasia of sinus lining → narrowing of ostia → inspissation/thickening of pus

Secondary sinusitis ⭐

Usually associated with dental periapical suppuration.

Especially roots of 4th–6th maxillary cheek teeth

→ fracture/necrosis/devitalization → infection spreads into sinus.

CS

• Initially mucoid unilateral nasal discharge → Later purulent + malodorous

• Facial swelling, Nasal obstruction

Dx

• History + CS, Physical examination

• Percussion

• ⭐ Oral/dental examination

• Endoscopy

• X-ray

Tx

Conservative:

• Systemic antibiotics, Steam inhalation, Light exercise

Surgical:

• Catheter placement/drainage, Radical surgery if required

🟡 4. SINUS CYSTS

Etiology

• Unknown

• Some features similar to PEH

• Arise around drainage ostium

• Contain yellow fluid → blood pigment degradation

CS

• Nasal obstruction, Facial swelling, Rarely ocular proptosis

• Mucoid nasal discharge

Dx

• CS + physical examination

• Endoscopy, X-ray

Tx

• ⭐ Fronto-nasal flap surgery

🍄 5. MYCOTIC RHINITIS & SINUSITIS

Etiology

• Opportunistic fungal infection secondary to other predisposing/supportive conditions.

CS

• Low-grade unilateral purulent nasal discharge

• ± Epistaxis

Dx

• ⭐ Endoscopy

Tx

• Topical antifungal treatment

• Benzimidazole

• Foley balloon catheter

🔴 6. NEOPLASIA & POLYPS

Etiology

True tumors are uncommon:

• Squamous cell carcinoma

• Adenocarcinoma

• Osteoma

Polyps:

• Pedunculated inflammatory proliferations

• Covered by mucous membrane

• May be associated with dental periapical disease

CS

• Putrid nasal discharge mixed with blood

• Ocular proptosis

Dx

• Physical examination, Endoscopy, X-ray, CT

Tx

• Fronto-nasal flap surgery

🟢 7. CHRONIC GUTTURAL POUCH EMPYEMA + CHONDROIDS

⭐Pathogenesis

Failure of drainage

→ accumulation of pus/mucus in guttural pouch → pus becomes inspissated → solid concretions form → CHONDROIDS

⭐ Important association: Streptococcus equi → strangles

CS

• Bilateral purulent nasal discharge

• Swelling of parotid region

Dx

• Clinical signs, X-ray, Endoscopy is also useful

Tx

• Drainage, Foley balloon catheter, Lavage

🐴 8. LARYNGEAL HEMIPLEGIA / RECURRENT LARYNGEAL NEUROPATHY

⭐⭐⭐Pathogenesis

Progressive functional loss of recurrent laryngeal nerve → permanent dysfunction of intrinsic laryngeal muscles → inadequate arytenoid movement → partial airway obstruction → exercise intolerance.

CS

• ⭐ Exercise intolerance

• ⭐ Inspiratory noise

• Often asymptomatic at rest

• May have an unusual whinny

Dx

• Palpation of larynx:

  • Atrophy of intrinsic laryngeal musculature

  • Arytenoid depression

• “Grunt-to-the-stick” test

• ⭐ Endoscopy

Tx

• ⭐ Prosthetic laryngoplasty (“tie-back”)

  • Mimics function of the CAD muscle

• Tracheotomy/intubation when indicated

• Permanent tracheostomy in selected severe cases

🧠 RLN → inspiratory noise + poor performance → endoscopy → tie-back

🪰 9. NASOPHARYNGEAL MYIASIS ⭐⭐⭐

Definition

Myiasis = parasitic infestation of a living mammal by larval stages (maggots) of dipterous flies.

Etiology

⭐ Rhinoestrus purpureus “Horse nose bot”

• Botfly

• Larvae/maggots affect nasal/nasopharyngeal region

Other parasites causing rhinitis:

• Habronema muscae

• Draschia megastoma

Life cycle ⭐

Adult fly deposits larvae in horse's nostrils → Larvae migrate through nasal mucosa + sinuses → Feed/develop within host → Develop to L3 → L3 migrate back toward nostrils → Fall onto ground → Pupate

⬇

After approximately 15–30 days → adult flies emerge

Pathogenesis

Larvae migrate and feed within nasal tissues

→ irritation + mucosal damage → rhinitis/sinusitis → may predispose to secondary bacterial infection

Severe disease may involve deeper respiratory structures.

Clinical signs⭐

Initially:

• Serous nasal discharge

As mucosa is damaged:

• Bloody nasal discharge

Also:

• Rubbing nose, Head shaking, Sneezing, Wheezing, Snorting

• Mild fever

• Secondary bacterial infection

Diagnosis

⭐ Endoscopy → visualize larvae

Treatment

Few larvae (e.g. 1–10): → may be self-limiting/self-healing

Many larvae (e.g. 20–50): → ⭐ Ivermectin (Macrocyclic lactones)

Prevention:
→ preventive treatment in August

🧠 RHINOESTRUS → nose/sinuses → bloody discharge + head shaking → endoscopy → IVERMECTIN

⚠ OTHER IMPORTANT CONDITIONS previously asked on state:

1. Glanders (Burkholderia mallei), 3 forms: Nasal, Pulmonary, Cutaneous

2. Equine rhinitis → deformed face (?)

🧠 CAUSES OF POOR PERFORMANCE / EXERCISE INTOLERANCE ⭐⭐⭐

Know this list:

• Laryngeal hemiplegia / recurrent laryngeal neuropathy

• Epiglottic entrapment (EE)

• Arytenoid chondritis

• Guttural pouch infection

• Aryepiglottic fold entrapment

• Tracheal stenosis / stricture / collapse

• Arytenoid chondroma

• Ethmoidal hematoma

• Nasal polyps

• Pharyngeal and subepiglottic cysts

• Rhinitis

• Nasal granuloma

🧠 EXAM MEMORY — QUESTION 9

If you draw this question, start with:

“Upper respiratory tract diseases can cause airway obstruction, abnormal respiratory noise and exercise intolerance.”

Then remember the major diseases:

ALAR FOLD
→ high blowing → resection

ETHMOID HEMATOMA
→ recurrent epistaxis → endoscopy → 10% formalin

SINUSITIS
→ primary = respiratory infection
→ secondary = dental disease

SINUS CYST
→ facial swelling → fronto-nasal flap

MYCOTIC
→ unilateral purulent discharge → topical antifungal

NEOPLASIA/POLYPS
→ bloody/putrid discharge → surgery

GUTTURAL POUCH EMPYEMA
→ S. equi → chondroids → lavage

LARYNGEAL HEMIPLEGIA ⭐
→ inspiratory noise + exercise intolerance → endoscopy → tie-back

NASOPHARYNGEAL MYIASIS ⭐
→ Rhinoestrus purpureus
→ larvae in nose/sinuses
→ serous → bloody discharge + head shaking
→ endoscopy → ivermectin

Infectious diseases of the respiratory tract

Viral

• Equine rhinotracheitis / rhinopneumonitis — EHV-1 + EHV-4

• EHV-2 + EHV-5

• Equine influenza

• African horse sickness

• Equine viral arteritis

• Equine rhinovirus

• Equine adenovirus

• Reovirus

• Equine morbillivirus / Hendra virus

Bacterial

• Strangles — Streptococcus equi

• Glanders — Burkholderia mallei

• Rhodococcus equi

• Lockjaw / tetanus — Clostridium tetani

Parasitic

• Dictyocaulus arnfieldi, Parascaris equorum, Cystic echinococcosis, Rhinoestrus purpureus

🦠 1. EQUINE RHINOTRACHEITIS / RHINOPNEUMONITIS ⭐⭐⭐

Etiology

Alphaherpesviridae

• EHV-1, EHV-4

EHV-1 ⭐

Associated with:

• Respiratory disease, Abortion, Neonatal disease, CNS/neurological disease

Transmission

Direct or indirect contact with:

• Nasal secretions

• Aborted fetus, Fetal membranes, Fetal fluids

CS

• Fever, Serous nasal discharge, Cough, Submandibular lymphadenopathy

Dx

• Nasopharyngeal swab

• PCR

• Virus isolation, ELISA, IFA

Tx

• Supportive treatment

• Antibiotics → secondary bacterial infection

• Respiratory disease often self-limiting

Prevention

💉 Vaccination

According to your lecture:

• Adults → once/year

• Foals → 3 doses starting at 4–6 months

• Breeding animals → before breeding season

• Pregnant mares → 5th + 7th + 9th month

🧠 EHV-1 = RESPIRATORY + ABORTION + NEONATAL + CNS

🦠 2. EHV-2 & EHV-5

EHV-2

→ respiratory infection:

• Fever, Watery nasal discharge, Enlarged mandibular LN, Cough

EHV-5 ⭐

→ associated with equine multinodular pulmonary fibrosis (EMPF)

🦟 3. AFRICAN HORSE SICKNESS ⭐⭐

Etiology

• Reoviridae → Orbivirus

• Severe disease with very high mortality.

Transmission ⭐

• 🦟 Culicoides midges

• ❌ No direct horse-to-horse transmission

Clinical forms

🫁 Pulmonary form

• Pulmonary edema, Cough, Lung congestion, Severe respiratory disease

❤ Cardiac form

• Pyrexia, Edema of head + neck

Dx

• PCR, ELISA, VNT

Prevention

💉 Vaccination in endemic areas

🧠 AHS = CULICOIDES → LUNG EDEMA or HEAD/NECK EDEMA

🦠 4. EQUINE VIRAL ARTERITIS (EVA) ⭐⭐

Etiology

Arteriviridae → Equine arteritis virus

Transmission

• Aerosol, In utero, ⭐ Venereal,

• ⭐ Long-term carrier state in stallions

Pathogenesis

• Virus causes vasculitis of small vessels

CS

• Fever, Cough, Respiratory distress, Abortion, including late gestation

Dx

• Nasopharyngeal swab, PCR

• ELISA

Tx

• Supportive

Prevention

• Vaccination

🧠 EVA = VASCULITIS + VENEREAL + CARRIER STALLION + ABORTION

🦠 5. EQUINE INFLUENZA ⭐⭐⭐

Etiology

Orthomyxoviridae → Influenza A

• H7N7, H3N8

CS

Classic:

• Pyrexia, Nasal discharge

• ⭐ Harsh, dry cough

• Weakness

Dx

• PCR, ELISA, Virus isolation

Tx

• Supportive

Prevention

💉 Vaccination, 2×/year

🧠 INFLUENZA = FEVER + HARSH DRY COUGH

🦠 6. EQUINE RHINOVIRUS

Etiology

• Picornaviridae → equine rhinovirus

Transmission

• Respiratory route

• venereal transmission

CS

• Pneumonia in young foals

• Often subclinical in adults

Dx

• ELISA, VNT

🦠 7. EQUINE ADENOVIRUS

Can cause:

• Acute upper respiratory disease

• Conjunctivitis

• Bronchopneumonia

• GIT infection

🦠 8. MORBILLIVIRUS / HENDRA VIRUS ⭐

Important: ⚠ ZOONOTIC

CS

• Bloody nasal discharge

• Pyrexia, Pneumonia, Severe respiratory disease

• High mortality! Death may occur within 1–3 days

🧠 HENDRA = ZOONOTIC + BLOODY NOSE + PNEUMONIA

🧫 9. STRANGLES / EQUINE DISTEMPER ⭐⭐⭐

Etiology

• Streptococcus equi

• Common, especially in young horses.

Pathogenesis

• S.equi → swelling + abscessation of submandibular/retropharyngeal lymph nodes → may compress upper respiratory structures → respiratory obstruction → “strangles”

• Immune-mediated complication: ⭐ → After infection, some horses can develop excessive immune-complex formation → deposition in blood vessel walls → vasculitis → purpura hemorrhagica

CS

• Fever, Anorexia, nasal discharge, Productive cough, Dyspnoea, Difficulty swallowing

• ⭐ Enlarged + painful lymph nodes, Abscess formation

• Edema may occur with purpura hemorrhagica

Dx

• Culture

• PCR

  • Nasopharyngeal sample

  • Guttural pouch lavage

• ELISA/serology where indicated

Tx

Depending on disease stage:

• Penicillin, NSAIDs

• Soft food

• Hot packs on superficial LN/abscesses

• Drain mature abscesses

• Tracheotomy if severe airway obstruction

• Guttural pouch lavage → empyema/chondroids

• Surgical removal when necessary

Prevention

💉 Vaccination

🧠 STRANGLES = S. EQUI → LN ABSCESSES → AIRWAY COMPRESSION

☠ 10. GLANDERS ⭐⭐⭐

Etiology

• Burkholderia mallei

• ⚠ ZOONOTIC

Pathogenesis

• Causes ulcerating nodules in: Upper respiratory tract, Lungs, Skin

• Acute: may rapidly be fatal

• Chronic: recurrent abscessation/nodular disease

3 FORMS ⭐⭐⭐

👃 1. Nasal form

• Catarrhal → purulent nasal discharge

• Nodules → Nodules ulcerate → Heal with characteristic stellate scars

🫁 2. Pulmonary form

• Small tubercle-like nodules in lungs

• Nodules break down → Contents enter bronchioles

• Infection may extend into URT

• Lung consolidation

• Pneumonia

🦵 3. Cutaneous form = FARCY

• Nodules along lymphatic vessels

• Especially extremities

• Ulceration

• Sticky, highly infectious pus

Dx

• CFT = complement fixation test

Tx

• Doxycycline, Trimethoprim, Streptomycin

⚠ But for the exam, emphasize that in eradication programs such as in Europe, infected horses are generally not treated → euthanasia/culling according to official disease-control measures.

Prevention

• ❌ No vaccine

🧠 GLANDERS = B. MALLEI + ZOONOTIC + 3 FORMS:
NASAL – PULMONARY – FARCY

🫁 11. RHODOCOCCUS EQUI ⭐⭐⭐

Etiology

• Rhodococcus equi

• ⭐ Major cause of severe pneumonia in foals, especially around 1–4 months

• Can have significant mortality.

Pathogenesis

• ⭐ Pyogranulomatous pneumonia / lung abscesses

• May also cause polysynovitis

CS

• Lethargy, Fever, Cough, Nasal discharge, Tachypnoea, Respiratory distress, Dyspnoea

Dx

⭐ Transtracheal wash + culture/PCR

Plus:

• USG, X-ray

Tx

• Azithromycin, Erythromycin

• Long treatment → around 2 months

• Penicillin + streptomycin as another listed protocol

Supportive respiratory treatment:

• Expectorants

• Bronchodilators → e.g. salbutamol

• Mucolytics

• NSAIDs

🧠 RHODOCOCCUS = FOAL 1–4 MONTHS + LUNG ABSCESSES + TTW

🧫 12. LOCKJAW / TETANUS

Etiology

• Clostridium tetani → produces neurotoxins

Respiratory relevance:

Neurotoxin → spastic paralysis → respiratory muscle involvement → hypoxia/hypoxemia → death from:

• Respiratory failure/hypoxemia

• ± aspiration pneumonia

Prevention ⭐

• 💉 Vaccination

🪱 PARASITIC RESPIRATORY DISEASES (Alica said no parasites on this question)

From your previous questions:

1. Dictyocaulus arnfieldi
→ lungworm
→ bronchi/bronchioles
→ chronic bronchitis + severe cough + dyspnoea
→ ivermectin

2. Migrating Parascaris equorum larvae
→ liver → lungs → trachea → swallowed

3. Cystic echinococcosis
→ hydatid cysts, potentially involving lungs

4. Rhinoestrus purpureus
→ nasopharyngeal myiasis
→ larvae in nose/sinuses
→ nasal discharge + head shaking
→ ivermectin

🧠 EXAM MEMORY — QUESTION 10

If you need to quickly structure the answer:

VIRAL

EHV-1/4 → respiratory + abortion/CNS with EHV-1
EHV-5 → multinodular pulmonary fibrosis
Influenza → harsh dry cough
AHS → Culicoides + pulmonary edema/head edema
EVA → vasculitis + carrier stallion + abortion
Hendra → zoonotic + severe pneumonia

BACTERIAL

Strangles → S. equi + LN abscesses
Glanders → B. mallei + zoonotic + nasal/pulmonary/farcy
Rhodococcus → foals 1–4 months + lung abscesses
Tetanus → spastic paralysis → respiratory failure

PARASITIC

Dictyocaulus* + Parascaris + Echinococcus + *Rhinoestrus

⭐ The 6 I would know in the most detail

EHV-1/4 → Influenza → African horse sickness → Strangles → Glanders → Rhodococcus equi

Those give you enough material to build a substantial oral answer even if you don't remember every detail of the smaller diseases.

Heart rhythm disorders

Arrhythmia = disturbance of the rate, regularity, or site of formation of cardiac electrical impulses.

Two main groups:

• 🐢 Bradyarrhythmia → <24 BPM

• 🏃 Tachyarrhythmia → >50 BPM

❤ NORMAL CARDIAC CONDUCTION SYSTEM

1⃣ SA node → starts the heartbeat

• Primary pacemaker

• Determines heart rate

• Produces electrical impulse

• → both atria contract → blood moves into ventricles

2⃣ AV node → delays the impulse

• Receives impulse from SA node

• ⭐ Delays conduction

• Allows atria to finish emptying and ventricles to fill

3⃣ Bundle of His

• Continuation of AV node

• Conducts impulse down interventricular septum

• Divides into:

  • Right and Left bundle branch

4⃣ Purkinje fibers

• Spread impulse through ventricular myocardium

• → ventricular contraction

• → blood ejected into pulmonary artery + aorta

🧠 SA → AV → BUNDLE OF HIS → PURKINJE → VENTRICULAR CONTRACTION

🐢 BRADYARRHYTHMIAS <24 BPM

1. THIRD-DEGREE AV BLOCK ⭐⭐⭐

= Complete AV block

⚠ Your notes say “slow conduction,” but the important concept is:

⭐ NO communication/conduction between atria and ventricles.

Etiology

• Inflammation, Degenerative changes

Pathogenesis

• SA node continues to depolarize atria, BUT → impulses do not reach ventricles

• Atria + ventricles beat independently!

• Ventricles are activated by a subsidiary pacemaker (Junctional, Ventricular)

CS

• Severe exercise intolerance

• Frequent syncope (fainting)

Dx

Auscultation:

• Very slow ventricular rate, often <20 BPM

ECG:
⭐ P waves and QRS complexes have NO relationship

Tx:

Improve conduction/rate:

• Vagolytic → atropine, glycopyrrolate

• Sympathomimetic → isoproterenol

• Corticosteroid → dexamethasone

Definitive option:

• ⭐ Cardiac pacemaker

🧠 3rd DEGREE = P AND QRS DIVORCED → SYNCOPE → PACEMAKER

2. SECOND-DEGREE AV BLOCK ⭐⭐⭐

Not all SA/sinus impulses are conducted through the AV node to the ventricles.

→ some atrial contractions occur without ventricular contraction

⭐ This is important in horses because some forms of second-degree AV block can occur physiologically at rest due to high vagal tone and disappear with exercise.

Etiology

Your notes include:

• Electrolyte imbalance, e.g. hypercalcemia

• AV node disease

• High vagal tone can cause physiological block

CS

Physiological → often no clinical signs

Pathological/severe:

• Exercise intolerance, Collapse

Dx

Auscultation:

• Slow/irregular heart rate

• Periodically dropped beat

ECG:
⭐ P wave NOT followed by QRS complex

Can range from:

• Occasional blocked P wave to Most P waves being blocked

Tx

• Physiological → no treatment required (Exercise should abolish vagally mediated block)

• Persistent/pathological cases → investigate underlying cause

🧠 2nd DEGREE = SOME P WAVES HAVE NO QRS

3. SINUS BRADYCARDIA / SINUS ARRHYTHMIA / SA BLOCK

Sinus bradycardia

→ SA node fires normally but too slowly

Sinus arrhythmia

→ variation in intervals between sinus impulses

SA block

→ impulse from SA node fails to reach atrial myocardium

Dx

SA block — auscultation:

• Regular systolic/diastolic intervals

• Then a pause

Sinus bradycardia/arrhythmia:

• Rhythmic variation in diastolic intervals

Tx

• Exercise

• Vagolytic → atropine

• Sympathomimetic → isoproterenol

4. SINUS ARREST

SA node fails to fire

→ pause lasting ≥2 normal P–P intervals

• Uncommon in horses!

Etiology

• Inflammatory changes, Degenerative changes, Sinus node disease

• Conditions causing high vagal tone

Dx

Auscultation:

• Prolonged pause

ECG:

• ⭐ Irregular/prolonged P–P interval

Tx

• High-dose dexamethasone

🧠 SINUS ARREST = SA NODE DOESN'T FIRE → LONG PAUSE

🏃 TACHYARRHYTHMIAS >50 BPM

5. ATRIAL FIBRILLATION ⭐⭐⭐

• Very important equine arrhythmia.

Pathogenesis

Chaotic electrical activity within atria

→ atria do not contract normally

→ irregular impulses reach AV node

→ irregular ventricular rhythm

Can be associated with:

• Cardiac disease/heart failure, Systemic illness, Electrolyte abnormalities, Colic and other conditions

CS

⭐ Exercise intolerance, May have poor performance.

Dx

Auscultation:
⭐ Irregularly irregular rhythm

ECG:

• ❌ No P waves

• ⭐ Fibrillation (f) waves

• Irregular R–R intervals

• Usually normal QRS morphology

Tx

⭐ Quinidine → oral or IV according to protocol

Your lecture also lists:

• Digitoxin/digoxin, Furosemide, Vasodilators such as acepromazine in selected cardiac cases

🧠 ATRIAL FIBRILLATION = NO P WAVES + f WAVES + IRREGULARLY IRREGULAR

6. SUPRAVENTRICULAR TACHYCARDIA

= Rapid rhythm originating above the ventricles.

• Uncommon in horses!

Important:

• If HR becomes extremely high, e.g. >150 BPM → ↓ ventricular filling → ↓ cardiac output → cardiovascular collapse

Dx

Auscultation:

• ⭐ Rapid, regular rhythm

ECG:

• Increased HR

• Usually narrow/normal-looking QRS complexes

Tx

Drugs that slow AV nodal conduction:

• Calcium-channel blockers

• β-blockers

• Digoxin in selected cases

🧠 SVT = FAST + REGULAR + SUPRAVENTRICULAR

7. VENTRICULAR TACHYCARDIA ⭐⭐⭐

Etiology

• Congenital/cardiac disease, Electrolyte imbalance, Acid-base imbalance, Hypoxia, Ischemia, Toxins, Drugs, CNS disease

Pathogenesis

• Rapid impulses originate in ventricular myocardium

• Ventricles contract rapidly/inefficiently → ↓ cardiac output → potentially life-threatening arrhythmia

CS

Can cause signs of cardiovascular compromise/CHF:

• Weakness, Syncope, Jugular pulsations/distension, Peripheral/ventral edema, Pleural effusion, Pericardial effusion, Pulmonary edema, Ascites

Dx

Auscultation:

• Rapid regular rhythm

ECG:

• ⭐ >60 beats/min

• P waves may be normal

• P waves may occur before, during or after the QRS complex

• ⭐ Bizarre/abnormal QRS complexes

Treatment

Treatment is indicated when:

• Horse shows clinical signs at rest

• Ventricular rate is excessively high

Antiarrhythmic drugs:

• ⭐ Lidocaine WITHOUT epinephrine

• Quinidine, Procainamide, MgSO₄, Amiodarone

🧠 VENTRICULAR TACHYCARDIA = >60 BPM + BIZARRE QRS + P WAVES UNRELATED → LIDOCAINE WITHOUT EPINEPHRINE

🩺 CARDIAC AUSCULTATION — FIRDA

Remember:

F – Frequency → heart rate

I – Intensity → loudness

R – Rhythm → regular/irregular

D – Demarcation → distinction between heart sounds

A – Adventitious sounds → murmurs/additional abnormal sounds

🫀 VALVE AUSCULTATION

LEFT side

• Pulmonary valve

• Aortic valve

• Mitral valve

RIGHT side

• Tricuspid valve

🧠 LEFT = PAM
Pulmonary – Aortic – Mitral

RIGHT = Tricuspid

💊 GENERAL THERAPY OF ARRHYTHMIAS ⭐⭐⭐

FIRST:

⭐ Rule out extracardiac causes before giving anti-arrhythmic drugs.

For example:

• Electrolyte disturbances, Acid-base abnormalities, Hypoxia, Systemic disease, Drugs/toxins

Goals is to Prevent:

• Weakness, Syncope, Seizures, CHF

• Progression to lethal arrhythmia

Bradycardia:

⭐ Atropine trial
→ determines whether high vagal tone is responsible.

Lecture also lists:

• Clenbuterol, Terbutaline, Propantheline bromide

Tachycardia:

Acute:

• Diltiazem, ⭐ Lidocaine

Long-term:

• Digoxin, Atenolol, Propranolol

🧠 EXAM MEMORY

The easiest way to separate the important ECG findings:

Arrhythmia	⭐ ECG clue
2nd-degree AV block	P wave → NO QRS sometimes
3rd-degree AV block	P and QRS completely unrelated
Sinus arrest	Long P–P pause
Atrial fibrillation	NO P waves + f waves + irregular rhythm
SVT	Very fast, usually narrow QRS
Ventricular tachycardia	Fast + abnormal/wide QRS

🔥 Five sentences to know perfectly

2nd-degree AV block: Some P waves are not followed by QRS complexes.

3rd-degree AV block: There is complete AV dissociation, so P waves and QRS complexes have no relationship.

Sinus arrest: The SA node fails to fire, producing a prolonged pause.

Atrial fibrillation: There are no P waves, fibrillation waves are present, and the rhythm is irregularly irregular.

Ventricular tachycardia: Rapid ventricular impulses produce a fast rhythm with abnormal/wide QRS complexes.

Valvular and septal heart disorders

Two main groups:

Congenital

• Ventricular septal defect (VSD), Patent ductus arteriosus (PDA), Tetralogy of Fallot, Patent foramen ovale (PFO)

Acquired

• Mitral regurgitation, Aortic regurgitation, Tricuspid regurgitation, Pulmonic valve insufficiency, Endocarditis

🫀 CONGENITAL DISORDERS

1. VENTRICULAR SEPTAL DEFECT — VSD ⭐⭐⭐

⭐ Most common congenital heart defect in foals

= hole in the interventricular septum

Pathogenesis

• Because pressure is higher in the left ventricle: LEFT → RIGHT SHUNT

• Blood moves from LV → RV → increased blood flow/volume overload → cardiac dilation + hypertrophy

CS

• Failure to thrive. Exercise intolerance, Pale mucous membranes, Heart murmur

Dx

• Auscultation → murmur

• ECG

• ⭐ Echocardiography/Doppler → visualize defect + blood shunting

Tx

Depends on severity:

• Small/restrictive VSD → may have normal life

• Exercise restriction when indicated

• vasodilators → acepromazine

🧠 VSD = HOLE BETWEEN VENTRICLES → HIGH PRESSURE LEFT → LOW PRESSURE RIGHT

2. PATENT DUCTUS ARTERIOSUS — PDA ⭐⭐

Normal fetal circulation:

• Ductus arteriosus connects Pulmonary artery ↔ aorta → allows fetal blood to bypass the non-functioning lungs

After birth:

• normally closes within the first days → becomes ligamentum arteriosum

PDA

• Patent = open, → ductus arteriosus fails to close

• After birth, systemic pressure is higher:

AORTA → PULMONARY ARTERY → excessive pulmonary blood flow → blood returns to left heart → ⭐ left-sided volume overload

CS

• Cough, Exercise intolerance

• Pale MM, Dyspnea

• ⭐ Prominent continuous “machinery-like” murmur

Dx

• ⭐ Echocardiography

• Left ventricular enlargement

• ECG

• Doppler → abnormal blood flow

Tx

• Furosemide

• ACE inhibitors

🧠 PDA = DUCTUS STAYS OPEN → CONTINUOUS MACHINERY MURMUR → LEFT-SIDED VOLUME OVERLOAD

3. TETRALOGY OF FALLOT ⭐⭐⭐

Congenital disorder consisting of 4 abnormalities:

P-V-R-A

1. Pulmonic stenosis

2. Ventricular septal defect

3. Right ventricular hypertrophy

4. Aorta displaced/overriding (The displaced aorta receives blood from both ventricles)

4. PATENT FORAMEN OVALE — PFO

• Normal fetal circulation: The foramen ovale allows: RIGHT ATRIUM → LEFT ATRIUM → fetal blood bypasses the lungs.

• After birth → should close.

PFO

• Failure of the foramen ovale to close → persistent communication between atria → abnormal shunting may occur.

• ⚠ In foals, anatomical closure may take several weeks, so persistence shortly after birth does not necessarily mean permanent disease.

🧠 FORAMEN OVALE = ATRIUM ↔ ATRIUM

Compare:

VSD = VENTRICLE ↔ VENTRICLE
PFO = ATRIUM ↔ ATRIUM
PDA = AORTA ↔ PULMONARY ARTERY

❤ ACQUIRED VALVULAR DISEASE

5. MITRAL REGURGITATION / INSUFFICIENCY ⭐⭐⭐

Mitral valve fails to close properly during systole

→ blood leaks:

LEFT VENTRICLE → LEFT ATRIUM

→ LA volume overload/enlargement → increased pulmonary venous pressure → pulmonary congestion/hypertension → can predispose to atrial fibrillation

Etiology

• Chronic degeneration, Fibrotic lesions, Bacterial endocarditis, Valvulitis

• ⭐ Rupture of chordae tendineae

CS

• Exercise intolerance, Heart murmur, Pulmonary congestion, Edema

• Jugular distension if advanced heart failure develops

Dx

• Auscultation → murmur

• Echocardiography: Valve thickening, Prolapse, Calcification, Cardiac chamber enlargement

• ⭐ Doppler → demonstrates regurgitant blood flow

Tx

• ACE inhibitor → enalapril

• Arterial vasodilator → acepromazine

🧠 MITRAL = LV → LA BACKFLOW → PULMONARY CONGESTION + AF

6. AORTIC REGURGITATION / INSUFFICIENCY ⭐⭐⭐

• Aortic valve fails to close properly during diastole → blood flows backward: AORTA → LEFT VENTRICLE → LV volume overload → LV dilation

Important:

• ⭐ Common cause of a diastolic murmur in middle-aged/older horses

Etiology

• Degenerative valve disease, Valve/cusp lesions, Bacterial endocarditis

CS

• Often asymptomatic initially

Later:

• Poor performance, Murmur, Tachycardia

Dx

• Auscultation, ECG

• ⭐ Doppler → regurgitant flow

Tx

• ACE inhibitor → enalapril

• Arterial vasodilator → acepromazine

🧠 AORTIC REGURGITATION = AORTA → LV DURING DIASTOLE → LV DILATION

7. TRICUSPID REGURGITATION ⭐⭐

Important

• Common in racehorses in training

• Incidence increases with age + training

Pathogenesis

• Tricuspid valve does not close properly

→ backflow: RIGHT VENTRICLE → RIGHT ATRIUM

Etiology

• Degeneration, Valvulitis

• Secondary to pulmonary hypertension

CS

• Usually asymptomatic

Rarely:

• Exercise intolerance, Signs of right-sided CHF if severe

Dx

• Auscultation, ECG

• ⭐ Doppler

Tx

Usually no treatment necessary

If CHF:
→ treat heart failure + primary etiology

🧠 TRICUSPID = RIGHT SIDE + COMMON IN TRAINING RACEHORSES

8. PULMONIC VALVE INSUFFICIENCY

⭐ Least clinically significant of the valvular diseases

Usually associated with other cardiac lesions.

Etiology

• Pulmonary hypertension, Bacterial endocarditis

CS

• Heart murmur

• Often few/no clinical signs

🧠 PULMONIC INSUFFICIENCY = usually secondary + least significant

🦠 9. ENDOCARDITIS ⭐⭐⭐

Inflammation/infection of the cardiac endothelium

→ commonly affects heart valves → may extend to the heart wall

Etiology

• Usually follows bacteremia

• Streptococcus, Pasteurella, Actinobacillus

→ bacteria reach valves → colonization/inflammation → valvular lesions/vegetations → valve dysfunction

CS

Think SYSTEMIC INFECTION + HEART DISEASE

• ⭐ Fever, Depression, Anorexia, Weight loss, Tachycardia

Dx

• ECG

• ⭐ Echocardiography/USG → thickened/abnormal valves or vegetative lesions

• ⭐ Blood culture

Tx

⭐ Long-term antibiotics based on culture/sensitivity

Supportive:

• Furosemide → decrease edema/congestion

• NSAIDs

• Lecture: heparin

🧠 ENDOCARDITIS = BACTEREMIA → INFECTED VALVE → FEVER + MURMUR/HEART DISEASE → ECHO + CULTURE → LONG-TERM ATB

🧠 EXAM MEMORY — BACKFLOW DIRECTION ⭐⭐⭐

This is the easiest way to understand the valve diseases:

Disorder	Abnormal blood flow	Main consequence
Mitral regurgitation	LV → LA	LA/pulmonary congestion
Aortic regurgitation	Aorta → LV	LV overload + dilation
Tricuspid regurgitation	RV → RA	Right-sided volume overload
Pulmonic insufficiency	Pulmonary artery → RV	Usually less significant

🔥 Congenital one-line memory

VSD → LV → RV shunt; most common congenital defect

PDA → ductus fails to close; continuous machinery murmur

Tetralogy of Fallot → Pulmonic stenosis + VSD + RV hypertrophy + overriding aorta

PFO → persistent opening between atria

🔥 Acquired one-line memory

Mitral → LV → LA → pulmonary congestion

Aortic → Aorta → LV → diastolic murmur in older horse

Tricuspid → RV → RA → common in racehorses in training

Pulmonic → least significant

Endocarditis → bacteremia → infected valves → fever → long-term antibiotics

Diseases of blood vessels and veins, and arteritis parasitaria

Vascular disorders

• Thrombophlebitis

• Aortoiliac thrombosis

Parasitic/vector-borne diseases

• ⭐ Strongylus vulgaris → “arteritis parasitaria”

• ⭐ Babesiosis

• ⭐ Theileriosis

• Filariosis — Setaria equina

• Parafilariosis

Viral diseases affecting blood/vessels

• African horse sickness

• Equine viral arteritis

• Equine infectious anemia

🩸 1. THROMBOPHLEBITIS ⭐⭐⭐

= Inflammation of a vein associated with thrombus formation

→ thrombus can partially or completely obstruct the vein.

⭐ In horses, the jugular vein is most commonly affected.

Etiology

• IV catheterization

• IV injections

• Severe systemic disease, especially endotoxemia → hypercoagulability → predisposes to thrombosis

CS

• ⭐ Distended vein, Pain on palpation, Local subcutaneous edema

• Fever, Neutrophilia

Dx

• Clinical signs

• ⭐ Ultrasound + Doppler

  • Determines size of thrombus, Degree of obstruction, Abnormal/absent blood flow, Inflamed vein → thickened wall, Thrombus → hyperechoic structure

Tx

Local + systemic treatment:

• Broad-spectrum antibiotics when septic thrombophlebitis is suspected

• NSAIDs → flunixin meglumine

• Antithrombotic → heparin

Severe cases:

• Surgical removal/resection of affected vein

• Drain adjacent abscesses

🧠 THROMBOPHLEBITIS = IV CATHETER → JUGULAR → INFLAMMATION + THROMBUS → USG/DOPPLER

🦵 2. AORTOILIAC THROMBOSIS ⭐⭐⭐

= A thrombus partially or completely obstructs the:

Terminal aorta → iliac arteries

→ reduced blood supply to the hindlimbs → ⭐ exercise-induced hindlimb lameness

Etiology

Associated with:

• Strongylus vulgaris migration → Damage to the vessel wall

CS

The important clue is that signs occur during exercise but may be absent at rest:

• Hindlimb lameness, Ataxia, Stiff gait, Weak peripheral/digital arterial pulses, Edema of affected limb

Dx

• Clinical signs

• ⭐ Rectal ultrasonography + Doppler
  → detects thrombosis
  → evaluates abnormal blood flow

Tx

⭐ Early treatment is essential

• NSAIDs

• Long-term antithrombotic treatment:

  • Heparin

  • Warfarin

• Larvicidal deworming if parasite-associated

Prognosis

⚠ Guarded

🧠 AORTOILIAC THROMBOSIS = HINDLIMB SIGNS DURING EXERCISE + ABSENT/BETTER AT REST

🪱 BABESIOSIS ⭐⭐⭐

Etiology

• Babesia caballi, Babesia equi

Host/vector

• Horse = vertebrate host

• 🕷 Ticks = vector

Life cycle:

In horse: → asexual reproduction in RBCs

In tick: → sexual development/sporogony

Pathogenesis

• Parasites invade RBCs → RBC destruction → ⭐ hemolytic anemia

• Blood stasis → clogged vessels → degeneration/damage of capillary endothelial cells → anoxia → accumulation of toxic metabolites

• Macroscopic hemorrhages

Clinical signs

• ⭐ High fever, Hemolytic anemia, Icterus, ⭐ Hemoglobinuria

• Macroscopic hemorrhages

Diagnosis

• Blood smear → piroplasms in RBCs

Treatment

• ⭐ Imidocarb dipropionate

• Symptomatic/supportive treatment

🧠 BABESIA = RBC DESTRUCTION → HEMOLYTIC ANEMIA + ICTERUS + HEMOGLOBINURIA → IMIDOCARB

THEILERIOSIS ⭐⭐⭐

Etiology

• Theileria equi

Pathogenesis

• Tick-borne protozoan

• T. equi has stages involving leukocytes before erythrocytic infection.

• ⭐ Formation of Koch's blue bodies

• Also invades RBCs → piroplasms → RBC destruction → hemolytic anemia

Clinical signs

• Fever, Hemolytic anemia, Icterus may occur

• Abortion

Diagnosis

• ⭐ Blood smear

• Koch's blue bodies / piroplasms

Treatment

• ⭐ Imidocarb

🧠 THEILERIA EQUI = WBC + RBC → KOCH'S BLUE BODIES + HEMOLYTIC ANEMIA → IMIDOCARB

🪱 STRONGYLUS VULGARIS — ARTERITIS PARASITARIA ⭐⭐⭐

Etiology

• Strongylus vulgaris (= large strongyle)

Adults:
→ cecum + colon

Larvae:
→ migrate through arteries, especially the ⭐ cranial mesenteric artery

Life cycle ⭐⭐⭐

Eggs shed in feces → Develop in environment → infective L3 → Horse ingests L3 while grazing → L3 penetrate intestinal mucosa → Larvae migrate in arteries, especially Cranial mesenteric artery (May also involve: Jejunal artery, Ileocolic artery, Caudal mesenteric artery) → Develop/molt toward L5 → Return to large intestine → Form nodules → Nodules rupture → adults emerge into intestinal lumen

Pathogenesis ⭐⭐⭐

Adults:

Large buccal capsule → attach to intestinal mucosa → blood feeding → bleeding ulcers

Migrating larvae:

Migration in arterial walls → inflammation → ⭐ THROMBOARTERITIS → thrombosis → arterial wall damage → aneurysm → reduced/interrupted intestinal blood supply → ischemia/infarction → colic

🧠 S. VULGARIS → CRANIAL MESENTERIC ARTERY → THROMBOARTERITIS → ↓ BLOOD TO INTESTINE → COLIC

CS

• Colic

• Anemia, Poor body condition, Diarrhea, Fever, Anorexia, Weight loss

Dx

• Coprology - flotation method

• Larval culture → species determination

• Necropsy

Tx

• Fenbendazole

• ⭐ Moxidectin → adults + migrating larvae

⚠ Problematic as resistance for pyrantel, ivermectin and benzimidazoles!

🦟🪱 FILARIOSIS — SETARIA EQUINA ⭐⭐

Etiology

Setaria equina

Hosts

• Final host = horse

• Intermediate host/vector = mosquito

Location

Adult worms:
→ abdominal/peritoneal cavity

Microfilariae:
→ circulate in blood

Life cycle

Adults in abdominal cavity

→ release microfilariae into blood → mosquito takes blood meal → ingests microfilariae → develop to infective L3 → mosquito transmits L3 to another horse

CS

• Anemia, Hemorrhages, Skin edema

• CNS signs → your lecture associates these with toxic metabolites/aberrant migration

Dx

⭐ Blood smear → microfilariae

Tx

⭐ Ivermectin

🧠 SETARIA = MOSQUITO → ADULTS ABDOMEN → MICROFILARIAE IN BLOOD → IVERMECTIN

🩸🪱 PARAFILARIOSIS ⭐⭐

Etiology

Parafilaria multipapillosa

Location

Adults:
→ subcutaneous tissue

Especially:

• Neck, Chest

Transmission

🪰 Blood-feeding flies act as vectors.

CS

⭐ “SUMMER BLEEDING” / parasitic dermatorrhagia

• Subcutaneous nodules

• Spontaneously bleeding skin lesions

• Most obvious during warm/fly season

Dx

• Microfilariae/parasite stages in blood or lesion material

Tx

• ⭐ Ivermectin

• Fly control

🧠 PARAFILARIA = SUBCUTANEOUS → SUMMER BLEEDING

🦠 VIRAL DISEASES OF BLOOD/VESSELS

AFRICAN HORSE SICKNESS ⭐⭐

Etiology

Reoviridae → Orbivirus

Severe disease with high mortality.

Transmission

⭐ Culicoides midges

❌ No direct horse-to-horse transmission

CS

🫁 Pulmonary form

• Pulmonary edema

• Cough

• Lung congestion

❤ Cardiac form

• Pyrexia

• ⭐ Edema of head + neck

Dx

• PCR

• ELISA

• VNT

Prevention

💉 Vaccination in endemic areas

🧠 AHS = CULICOIDES → PULMONARY EDEMA / HEAD-NECK EDEMA

9. EQUINE VIRAL ARTERITIS — EVA ⭐⭐⭐

Etiology

Arteriviridae → Equine arteritis virus

Transmission

• Aerosol

• In utero

• ⭐ Venereal

• ⭐ Long-term carrier stallions

Pathogenesis

⭐ Vasculitis of small blood vessels

CS

• Fever

• Cough

• Respiratory distress

• Edema may occur

• Abortion

Dx

• Nasopharyngeal swab

• PCR

• ELISA

Tx

• Supportive

Prevention

💉 Vaccination

🧠 EVA = VASCULITIS + VENEREAL + CARRIER STALLION + ABORTION

EQUINE INFECTIOUS ANEMIA — EIA ⭐⭐⭐

Etiology

• Retroviridae → Lentivirus, equine infectious anemia virus

Transmission:

Mainly through infected blood, particularly:

• Blood-feeding insects

• Contaminated blood/equipment

• Transplacental

Pathogenesis:

Persistent infection

→ immune-mediated destruction of RBCs/platelets → anemia + thrombocytopenia

CS

Disease can be acute, chronic or inapparent:

• Recurrent fever, Anemia, Arrhythmia

• Weakness, Weight loss

• Edema of lower chest, abdomen and legs

• Petechial hemorrhages of mm

Dx

⭐ Serology:

• AGID / Coggins test

• ELISA, PCR

Tx

❌ No curative treatment

Infected horses remain lifelong carriers, so management depends on official disease-control requirements. Euthanise!

🧠 EIA = LENTIVIRUS → BLOOD TRANSMISSION → FEVER + ANEMIA → COGGINS → LIFELONG INFECTION

🧠 EXAM MEMORY — QUESTION 13

For recall, think of the question as three blocks:

Vascular
→ Thrombophlebitis + Aortoiliac thrombosis

Parasites
→ Strongylus vulgaris + Babesia/Theileria + Setaria + Parafilaria

Viruses
→ AHS + EVA + EIA

⭐ Key associations

Thrombophlebitis → IV CATHETER + JUGULAR THROMBUS

Aortoiliac thrombosis → HINDLIMB LAMENESS DURING EXERCISE

Strongylus vulgaris → CRANIAL MESENTERIC ARTERY → THROMBOARTERITIS → COLIC

Babesia → RBC → HEMOLYTIC ANEMIA

Theileria → WBC/RBC + KOCH’S BLUE BODIES

Setaria → MOSQUITO + ABDOMINAL CAVITY + MICROFILARIAE

Parafilaria → SUMMER BLEEDING

AHS → CULICOIDES

EVA → VASCULITIS + STALLION + ABORTION

EIA → LENTIVIRUS + ANEMIA + COGGINS

For the actual oral answer, I’d put the most emphasis on thrombophlebitis, aortoiliac thrombosis, and especially Strongylus vulgaris, because S. vulgaris is the direct link to the “arteritis parasitaria” part of the question.

Equine dermatitis - infectious and parasitic origin

Main groups

Infectious:

• 🦠 Bacterial → Glanders, Staphylococcal dermatitis, Dermatophilosis

• 🧬 Viral → Papillomatosis, Vesicular stomatitis, Horsepox

• 🍄 Fungal → Dermatophytosis / ringworm

• 🦠 Protozoal → Besnoitiosis, Trypanosomosis/Dourine

Parasitic:

• 🕷 Mites → Sarcoptes, Psoroptes, Chorioptes

• 🪲 Lice → biting + sucking

• 🪰 Biting flies + ticks

• 🪱 Nematodes → Onchocerciasis, Habronemiasis, Parafilariosis

🦠 BACTERIAL

1. GLANDERS ⭐⭐⭐

Etiology

Burkholderia mallei

• ⚠ ZOONOTIC

• Notifiable/regulated disease

Pathogenesis

→ Ulcerating nodules in URT, lungs + skin

Acute: rapid severe disease/death
Chronic: recurrent abscessation

3 forms

👃 Nasal: catarrhal → purulent discharge → nodules ulcerate → characteristic stellate scars

🫁 Pulmonary: tubercle-like lung nodules → break down into bronchioles → spread → lung consolidation + pneumonia

🦵 Cutaneous = FARCY ⭐
→ nodules along lymphatic vessels, especially extremities
→ ulceration
→ sticky, highly infectious dark-honey pus

Dx

• CFT — complement fixation test

• Intradermal mallein test

Tx

• Doxycycline, Trimethoprim, Streptomycin

⭐ In Europe/control programs → mandatory culling/euthanasia rather than treatment

Prevention

• ❌ No vaccine

🧠 GLANDERS = B. mallei → ZOONOTIC → NASAL + PULMONARY + FARCY

🦠 2. FOLLICULITIS & FURUNCULOSIS / STAPHYLOCOCCAL DERMATITIS

Etiology

• Staphylococcus aureus

CS

Inflammation of:

• Hair follicles → folliculitis

• Surrounding dermis/subcutis → deeper furunculosis

→ warm + painful skin

Common sites:

• Saddle area, Pastern, Tail

Dx

• Bacterial culture

Tx

• Antiseptic shampoo:

  • Iodophor, Chlorhexidine

• Antibiotics when indicated for bacterial infection

• autovaccine

🧠 STAPH → HAIR FOLLICLES → warm painful saddle-area lesions

🌧 3. DERMATOPHILOSIS — “RAIN SCALD/RAIN ROT” ⭐⭐⭐

Etiology

• Dermatophilus congolensis

Pathogenesis

• Prolonged rain/moisture/sweat → weakens skin protective barrier → release/spread of dormant bacterium living in the skin → skin infection

CS

• Papules + pustules → Exudative lesions → ⭐ Crusty lesions with hairs in

Sites:

• Dorsal trunk, Muzzle, Distal limbs (areas exposed to rain, and sweaty regions)

Dx

• Culture, Impression smear, Skin biopsy

Tx

• Soak lesions in chlorhexidine soap and remove crusts

• Topical antibacterial/antiseptic treatment

• ATB spray/solution once daily × 1 week

🧠 RAIN + D. CONGOLENSIS → PAPULE → EXUDATE → CRUST

🧬 VIRAL SKIN DISEASES

4. EQUINE PAPILLOMATOSIS ⭐

Etiology

• Papillomaviridae → Equine papillomavirus

• Highly contagious amoung young horses by direct contact or shared items

Common:

• ⭐ Young horses below 3 years (immune system still developing)

• Older immunosuppressed horses

CS

• Warts on Muzzle, Lips, Inner surface of ear

Dx

• Clinical signs, Biopsy, Histopathology

Tx

• Usually self-limiting
  → spontaneously disappears after several months

• Autogenous vaccine may be used in selected cases

🧠 YOUNG HORSE + WARTS → PAPILLOMAVIRUS → usually SELF-LIMITING

🦠 5. VESICULAR STOMATITIS

Etiology

• Rhabdoviridae → vesiculovirus

Transmission

• Insect transmitted: Sand flies, Black flies

CS

• ⭐ Excessive salivation

• Vesicles on Mouth, Tongue, Lips

• Lesions may occur around hooves

Dx

Samples:

• Vesicle fluid, Epithelium

Tests:

• PCR, ELISA, CFT

Tx/control

• No specific antiviral treatment

• Isolation/quarantine + official control measures

🧠 VESICULAR = VESICLES IN MOUTH + SALIVATION + HOOF LESIONS

🦠 6. HORSEPOX - Extinct or nearly absent??

Etiology

• Poxviridae → Horsepox virus

CS

• Vesicles → rapidly ulcerate → progressively crust

Mainly:

• Muzzle, Face

Dx

• Virus isolation/cultivation

Tx

• Usually spontaneous resolution in approximately 4 weeks

🍄 7. DERMATOPHYTOSIS / RINGWORM

⭐⭐⭐Etiology

• Trichophyton equinum

Transmission

• Direct contact

• Fomites ⭐

CS

• Red, Itchy, Scaly, ⭐ Circular lesions

• Alopecia

Common sites:

• Saddle area, Neck, Face

Dx

• Fungal culture → Sabouraud agar

• Skin scraping + hair → microscopy

• Wood's lamp may be used, although it is not reliable for all equine dermatophytes

Tx

Often spontaneously resolves, BUT treatment:
→ speeds recovery
→ decreases spread/transmission

Topical antifungal treatment:

• Thiabendazole

• Lime sulfur

• Other appropriate antifungals

⭐ Disinfect environment + equipment

Vaccination for prevention/treatment.

🧠 RINGWORM = CIRCULAR ALOPECIA + FOMITES → FUNGAL CULTURE

PARASITE ORIGIN

NB! Mention this list first, then she will ask to explain 2/3 of them:

PROTOZOA:

• Besnoitiosis — Besnoitia bennetti

• Trypanosomosis / Dourine — Trypanosoma equiperdum

NEMATODES:

• Habronemiasis — Habronema spp.

• Parafilariosis — Parafilaria multipapillosa

• Onchocerciasis

  • Onchocerca cervicalis, O. gutturosa, O. reticulata

ECTOPARASITES:

Acarinosis = mites/mange

• Sarcoptes scabiei var. equi, Psoroptes equi, Chorioptes equi

Entomosis:

• Pediculosis / lice

• Hippoboscidosis (Hippobosca equina),

• Dermatitis caused by biting Diptera

• Simuliotoxicosis

🦠 PROTOZOA

8. BESNOITIOSIS ⭐⭐

Etiology

• Besnoitia bennetti, a cyst-forming coccidian parasite

• FH: cats, IH: horse

• Vector: flies 

Life cycle

Cat sheds oocysts → contaminate grazing/water → horse ingests → tissue cyst formation of skin over nostrils etc.

Especially:

• Skin, Nostrils, Eyes/sclera

Pathogenesis

Cysts cause:

• Skin edema, Hyperkeratosis, Alopecia

Eye involvement:
→ small visible cysts on sclera
→ ⭐ “scleral pearls”

CS

• Fever, Nasal discharge, Ocular discharge, Salivation

• Stiff gait, Orchitis, Subcutaneous edema

• ⭐ Multifocal pinpoint cysts:

  • Nostrils, Ears, Face, Body

  • crusty and hard skin lesions

• ⭐ Scleral pearls

Dx

• Skin biopsy - gold standard

• Endoscopy of nasal cavity

• ELISA

Tx

⚠ Difficult/problematic

• No reliable treatment to eliminate established tissue cysts → life long carriers

• Early infection → lecture suggests trimethoprim

• Trimetoprim + sulfamethoxazole (Bactrim) stops cyst formation but not kill the parasite or already formed cysts, it is mainly symptomatic/supportive

🧠 BESNOITIA = SKIN CYSTS + SCLERAL PEARLS

2⃣ TRYPANOSOMOSIS / DOURINE ⭐⭐⭐

Etiology

• Trypanosoma equiperdum

Transmission ⭐

• Coitus / venereal transmission

CS

Initially:

• Vaginal/genital discharge, Genital edema, Perineal edema

Characteristic skin lesion:

⭐ “SILVER DOLLAR PLAQUES”

→ transient cutaneous plaques, last maximum ~7 days, then it migrates to blood and release neurotoxins

Disease progresses to neurological involvement:

→ weakness, ataxia, neurological dysfunction, may progress to death

🧠 DOURINE = SEX → GENITAL EDEMA → SILVER DOLLAR PLAQUES → NEURO SIGNS

ECTOPARASITES — MITES

9. SARCOPTIC MANGE ⭐

Etiology

• Sarcoptes scabiei var. equi

• Burrowing mite → forms tunnels in skin

• Very uncommon in horses

• Transmission → direct contact

CS

• ⭐ Severe pruritus

• Hard/thickened skin, Papules, Crusts, Alopecia

Dx

⭐ DEEP skin scraping (border between healthy and affected skin)

Tx

• Pyrethroid dip/spray

• Repeat every 7–10 days, ≥3 treatments

• Macrocyclic lactones orally (ivermectin)

• ± ATB for secondary infection

• Minerals + vitamin E to support skin healing

10. PSOROPTIC MANGE

Etiology

• Psoroptes equi

• NON-BURROWING

CS

• Crusting, Serous exudation, Erythema, strong Pruritus, Alopecia

Dx

⭐ SUPERFICIAL skin scraping

Tx

• Topical Pyrethroids, Ivermectin

11. CHORIOPTIC MANGE ⭐⭐

Etiology

• Chorioptes equi

• Non-burrowing

⭐ “LEG MANGE”

CS

• Sticky scales, Strong pruritus, Restlessness, self mutilation, Lesions especially on distal limbs

• Severe infestation → lameness

Skin lesions can progress through:

1. Eczema crustosum

• dry scales, small nodules/pustules → dry → crusts/scales

⬇

2. Eczema madidans

→ loss of superficial skin layers → exposed corium / moist-weeping dermatitis

⬇

3. Eczema verrucosum

→ chronic proliferative skin → multiple wart-like lesions → ⭐ “cauliflower” appearance

🧠 CRUSTOSUM → MADIDANS → VERRUCOSUM
DRY → WET/RAW → CAULIFLOWER

Dx

• Superficial skin scraping + microscopy

Tx

• Clip hair, Remove scabs, Scrub/shampoo

• Treat horse AND in-contact animals

• Topical treatment is the main method → Selenium sulfide shampoo → appropriate topical acaricide

• Oral ivermectin paste, Fipronil spray

• Ivermectin, Topical synthetic pyrethroids

🧠 CHORIOPTES = LEG MANGE

9⃣ HORSE LICE — PEDICULOSIS

Biting louse: Werneckiella equi equi

Sucking louse: Haematopinus asini

CS

• Pruritus, Rubbing, Hair loss, Skin sores

• Loss of condition

• Heavy sucking-lice infestation → anemia

Dx

→ lice/nits visible on hair + microscopy

Tx

→ ectoparasitic treatment, including synthetic pyrethroids

🪰 13. BITING FLIES/DIPTERA

Important examples:

• Horse flies

• Deer flies

• Culicoides → biting midges

• Simulium → black flies

Pathogenesis

⭐ Only females blood-feed/bite in many important biting-fly groups.

Blood feeding → saliva/anticoagulants injected → local skin injury → secondary bacterial infection possible→ saliva can cause allergic/hypersensitivity reactions → pruritus + dermatitis

Can also act as vectors, depending on species/pathogen.

Examples

• African horse sickness, Equine infectious anemia, Equine onchocerciasis

Tx/prevention

• Mainly Supportive

• Fly control/repellents: ⭐ Synthetic pyrethroids

• Treat secondary bacterial dermatitis if significant

1⃣1⃣ HIPPOBOSCIDOSIS

Etiology

H- ippobosca equina = forest fly / horse louse fly

Important

• Blood-feeding ectoparasite, Mainly affects horses, Can also feed on cattle

CS

Bites can cause:

• Irritation, Restlessness, Pruritus, Local dermatitis

🧠 HIPPOBOSCA EQUINA = FOREST FLY → BLOOD FEEDING

🪱 NEMATODES AFFECTING SKIN

14. CUTANEOUS ONCHOCERCIASIS ⭐⭐

Etiology

• Onchocerca cervicalis, O. gutturosa, O. reticulata

• Adult O. cervicalis live especially in ligamentous/connective tissue adjacent to the nuchal ligament

• Migrating microfilariae affect the skin + eyes

Pathogenesis

• Microfilariae migrate into the skin → hypersensitivity → dermatitis

• Migration to the eyes → keratoconjunctivitis

Clinical signs

• Alopecia, scaling and crusting, especially on the face + neck

• Pruritus/dermatitis

• Subcutaneous masses

• Edema

• Lameness

• Eye problems

Diagnosis

• Clinical signs

• Skin biopsy → demonstration of microfilariae

Treatment

• ⭐ Ivermectin → very effective against microfilariae

• Corticosteroids → inflammatory/hypersensitivity reaction when appropriate

🧠 ONCHOCERCA = NUCHAL LIGAMENT → MICROFILARIAE → SKIN + EYES → IVERMECTIN

15. HABRONEMIASIS ⭐⭐⭐

Etiology

• Habronema muscae, Habronema microstoma → adults in stomach mucosa

• Draschia megastoma → nodules in stomach wall

• Final host = horse/equids

• Intermediate host/vector = muscid flies

Life cycle ⭐

• Eggs/L1 shed in feces → fly ingests eggs/L1 → develop to L3 inside fly → fly feeds around horse's eyes, genitalia, nostrils, lips or wounds → deposits L3 onto horse

• Normal route: horse swallows L3 → adults develop in stomach

• Aberrant route: larvae remain in skin/eyes → cannot complete life cycle → inflammation + hypersensitivity

🧠 FECES → FLY → L3 → HORSE → SWALLOW → STOMACH

3 Forms ⭐⭐⭐

1⃣ Gastric form — most common

• Adults in stomach → gastritis

• Large granulomas in gastric mucosa

2⃣ Cutaneous form — aberrant

• Larvae deposited in skin/wounds → cannot complete life cycle

• Local hypersensitivity

• Non-healing ulcerative/granulomatous skin lesions

• ⭐ “SUMMER SORES”

3⃣ Conjunctival form — aberrant

• Larvae around eyes → conjunctivitis

• Thickened eyelids + granulomatous lesions

• Aberrant lesions may also involve nostrils and genitalia

Diagnosis

• Characteristic non-healing reddish cutaneous granulomas

• Larvae may be demonstrated

• Endoscopy → gastric form

• ELISA

• Eggs are difficult to detect by routine fecal flotation because they do not float well in standard flotation solutions

Treatment

• ⭐ Ivermectin

• Moxidectin mentioned in lecture

• Wound management + fly control

🧠 HABRONEMA = MUSCID FLY → GASTRIC / CONJUNCTIVAL / CUTANEOUS → SUMMER SORES ⭐⭐⭐

16. PARAFILARIOSIS ⭐⭐⭐

Etiology

• Parafilaria multipapillosa

Location

• Adults live in subcutaneous tissue

• Form small nodules, especially on the neck and chest

Transmission

• 🪰 Blood-feeding flies act as vectors

Life cycle

• Fly feeds on horse → transmits infective larvae → parasites develop in subcutaneous tissue → skin nodules/lesions develop → lesions bleed → flies acquire parasite stages while feeding → transmission continues

Clinical signs

• Subcutaneous nodules

• Spontaneously bleeding skin lesions

• More common/prominent during the warm/fly season

• Characteristically called:

  • ⭐ “SUMMER BLEEDING”

  • ⭐ “PARASITIC DERMATORRHAGIA”

Diagnosis

• Demonstration of parasite stages/microfilariae in lesion or blood material

• Lecture: microfilariae in blood smear

Treatment

• Ivermectin

• ⭐ Fly control

🧠 PARAFILARIA = SUBCUTANEOUS TISSUE → BLOOD-FEEDING FLIES → SUMMER BLEEDING

🧠 EXAM MEMORY — QUESTION 14

You have a lot of diseases in this question, so learn them by groups:

🦠 BACTERIAL

Glanders → B. mallei → FARCY → dark sticky pus → CFT/mallein → euthanasia

Staph → S. aureus → folliculitis/furunculosis → warm painful skin

Dermatophilosis → D. congolensis → RAIN SCALD → crusts

🧬 VIRAL

Papilloma → young horse + warts + self-limiting

Vesicular stomatitis → mouth vesicles + salivation

Horsepox → vesicles → ulcers → crusts

🍄 FUNGAL

Ringworm → T. equinum → circular alopecia + fomites

🦠 PROTOZOA

Besnoitia → skin cysts + SCLERAL PEARLS

🕷 MITES

Sarcoptes → BURROWING → DEEP scraping

Psoroptes → NON-BURROWING → SUPERFICIAL scraping

Chorioptes → LEG MANGE

🪲 LICE

Biting + sucking → pruritus/hair loss; sucking → anemia

🪱 NEMATODES ⭐⭐⭐

Onchocerca → NUCHAL LIGAMENT → SKIN + EYES

Habronema → FLY → SUMMER SORES

Parafilaria → SUMMER BLEEDING

🔥 Three “summer” associations to separate

Habronema → SUMMER SORES
Parafilaria → SUMMER BLEEDING
Culicoides → insect-bite hypersensitivity / summer-associated pruritus

That distinction is particularly useful for an oral exam.

Equine skin tumors

Main skin tumours to know:

1. ⭐ Sarcoid — most common equine skin neoplasm

2. ⭐ Melanoma — especially older grey/white horses

3. ⭐ Squamous cell carcinoma (SCC) — non-pigmented/mucocutaneous areas

4. Mastocytoma

5. Lymphoma

6. Lymphosarcoma

1. SARCOIDS ⭐⭐⭐

• Tumour of fibroblastic cell origin

• Unique to equids

• ⭐ Most common equine skin neoplasm

• Most commonly affects young to middle-aged horses

Etiology

• Associated with bovine papillomavirus (BPV)

• Insects may contribute to transmission

• Possible genetic predisposition

Clinical signs

Can have several appearances:

• Verrucous → scaly, wart-like

• Fibroblastic → fleshy, often ulcerated

• Occult → flat lesion

Common locations:

• Head, Legs, Ventrum

Dx

• Appearance

• Biopsy + histopathology

⚠ Sarcoids can be difficult because trauma/biopsy may sometimes stimulate aggressive growth, so biopsy should be planned carefully.

Tx

⭐ Difficult to treat + recurrence is common

Options:

• Wide surgical excision

  • Location may make complete excision difficult, Recurrence can occur

• Cryotherapy

• BCG immunotherapy

• Autogenous vaccines

• Intralesional radiation/brachytherapy → e.g. iridium

• Chemotherapy:

  • 5-fluorouracil, Cisplatin, Topical/intralesional depending on protocol

🧠 SARCOID = MOST COMMON → BPV → YOUNGER HORSE → MANY FORMS → HIGH RECURRENCE

2. MELANOMA ⭐⭐⭐

• Tumour arising from: Melanocytes, Melanoblasts

• Can be benign or malignant.

• ⭐ Very common in older grey horses

• Especially horses that become progressively: dappled grey → white with age

Pathogenesis

• Abnormal proliferation of melanocytic cells and melanin production

• Often slow-growing

• May remain localized for years, But some become locally invasive or metastatic

CS

⭐ Pigmented nodules

• Single or multiple, Dermal or subcutaneous, May ulcerate

Typical locations:

• ⭐ Under/around tail and perineum

• Around anus/rectum, Genitalia

• Around mouth, Around eyes

• Distal limbs

Dx

• Characteristic appearance

• FNA → cytology

• ⭐ Biopsy + histopathology = definitive

Tx

If:

• Few lesions, Small, Not growing, Not causing problems → monitor/observe

Treatment options:

• Surgical excision

• Laser, Cryotherapy

• Intralesional chemotherapy → cisplatin

• Therapeutic melanoma vaccine → canine melanoma vaccine has been used off-label

• High-frequency irreversible electroporation
  → electrical pulses create pores in tumour cell membranes
  → irreversible cell damage/death

🧠 MELANOMA = OLD GREY HORSE → BLACK NODULES → TAIL/PERINEUM → OFTEN SLOW-GROWING

3. SQUAMOUS CELL CARCINOMA — SCC ⭐⭐⭐

Common epithelial neoplasm affecting:

• Head, Mucocutaneous junctions, Genitalia

Predisposition

• ⭐ Older horses, Light-coloured horses, Particularly non-pigmented skin

Etiology

⭐ UV light-associated neoplasia

Pathogenesis

• Tumour cells invade through the dermis as cords/islands of neoplastic cells.

Important:

• ⭐ Often locally aggressive/invasive

• Metastasis is less common, particularly early in the disease

CS

• Wart-like papules

• Ulcerated nodules/masses

• Usually solitary

• May have pigment/colour changes depending on location

Typical sites:

• Eyelids/ocular region, Mucocutaneous junctions, Genitalia

Dx

• Location + appearance

• ⭐ Biopsy + histopathology

Tx

• Surgical excision

• Cryotherapy

• Laser

⚠ Complete removal is important because:
→ incomplete excision → recurrence

Prognosis depends strongly on location, size, invasiveness and ability to completely remove the tumour.

🧠 SCC = OLD + LIGHT/NON-PIGMENTED + UV → ULCERATIVE/WART-LIKE → LOCALLY AGGRESSIVE

4. MASTOCYTOMA

= Mast cell tumour

Tx

⭐ Surgical resection

Generally:

• Good outcome after complete excision, Low recurrence rate

🧠 MASTOCYTOMA = MAST CELLS → SURGERY → LOW RECURRENCE

5. LYMPHOMA

= Tumour arising from lymphoid cells/lymphocytes.

• Cutaneous involvement can occur as part of lymphoid neoplasia.

Tx / Prognosis

• Treatment generally not recommended

• Poor prognosis

🧠 LYMPHOMA = LYMPHOCYTES → POOR PROGNOSIS

6. LYMPHOSARCOMA

• Uncommon in horses

• Usually affects middle-aged to older horses

CS

⭐ Typically:

• Multiple subcutaneous nodules

• Especially on the trunk

🧠 LYMPHOSARCOMA = OLDER HORSE → MULTIPLE SUBCUTANEOUS NODULES ON TRUNK

🧠 EXAM DIFFERENTIATION ⭐⭐⭐

Tumour	Typical horse	Typical appearance/location	Key fact
Sarcoid	Young–middle-aged	Variable: flat, wart-like, fibroblastic	⭐ Most common; BPV; recurrence
Melanoma	Older grey horse	Pigmented nodules, especially tail/perineum	Often slow-growing
SCC	Older, light-coloured	Non-pigmented/mucocutaneous areas	⭐ UV; locally aggressive
Mastocytoma	—	Cutaneous mass	Surgery → low recurrence
Lymphoma	—	Lymphoid tumour	Poor prognosis
Lymphosarcoma	Middle-aged/older	Multiple subcutaneous trunk nodules	Uncommon

🔥 Three major tumours

SARCOID
→ Most common + BPV + younger horse + high recurrence

MELANOMA
→ Older GREY horse + pigmented nodules + tail/perineum

SCC
→ Older LIGHT horse + non-pigmented skin + UV + locally aggressive

If you can immediately distinguish those three, you have the core of this question.

Equine cystitis and hematuria

1. CYSTITIS ⭐⭐⭐

Cystitis = inflammation of the urinary bladder.

→ More common in mares because of the shorter urethra, which facilitates ascending infection.

Etiology

1. Cystic calculi

• ⭐ Mainly calcium carbonate stones

2. Ascending bacterial infection

• E. coli, Proteus, Klebsiella, Enterococcus, Streptococcus, Staphylococcus, Pseudomonas

3. Neurological/viral disorders causing bladder dysfunction

• Herpesvirus

• Equine herpesvirus myeloencephalopathy

• Polyneuritis equi

→ impaired bladder emptying → urine retention → predisposition to cystitis.

🧠 CYSTITIS = CALCULI + ASCENDING BACTERIA + NEUROLOGICAL BLADDER DYSFUNCTION

Clinical signs ⭐⭐⭐

• Dysuria = difficult/painful urination

• ⭐ Pollakiuria = abnormally frequent urination

  • In mares, may resemble signs of oestrus

• Urine dribbling

• Haematuria, Pyuria

• Perineal scalding in mares

• Soiling of hindlegs in males

🧠 DYSURIA + POLLAKIURIA + DRIBBLING + BLOOD/PUS IN URINE

Diagnosis

• Rectal palpation
  → assess bladder

• Ultrasonography
  → ⭐ thickened bladder wall
  → may detect calculi

• Endoscopy/cystoscopy
  Mucosa may be:

• Thickened, Hyperaemic, Ulcerated

• Urinalysis + sediment examination
  May find:

→ ⭐ RBC → haematuria

→ WBC/leukocytes → inflammation/pyuria

→ Bacteria, Crystals

• Bacterial culture
  → identify bacteria and guide antibiotic treatment.

🧪 Normal equine urine:

Important because horse urine normally looks unusual:

• Often cloudy and thick

• Contains microscopic calcium carbonate crystals

• Alkaline

⭐ Normal pH approximately 7.5–8.5

So → Cloudy urine ≠ automatically cystitis in a horse!!

Blood analysis

May show increased:

• Creatinine

• BUN — blood urea nitrogen

Particularly if there is concurrent renal dysfunction/urinary obstruction.

Treatment

⭐ Treat/correct the underlying cause

Bacterial cystitis
→ antibiotics based preferably on culture + sensitivity

Lecture lists drugs excreted through kidneys/urinary tract:

• Aminoglycosides

• Trimethoprim/sulfadiazine

• Fluoroquinolones

• Penicillins

• Cephalosporins

Cystic calculi
→ ⭐ surgical removal

🧠 CYSTITIS Tx = CORRECT CAUSE → CULTURE-BASED ATB → REMOVE CALCULI IF PRESENT

🩸 2. HAEMATURIA ⭐⭐⭐

Haematuria = presence of intact RBCs/blood in urine.

Blood can originate from:

• Kidneys, Ureters, Bladder, Urethra

• Reproductive tract contamination

Etiology

Important causes include:

• ⭐ Urinary tract infection / cystitis

• Urolithiasis

• Trauma, Neoplasia, Drug toxicity

• Systemic disease, Exercise-induced haematuria

• Urethral defects, Urethral rents

• Idiopathic renal haemorrhage

• ⭐ Verminous nephritis → Halicephalobus gingivalis

Urethral rent

= tear in the urethra that communicates with the corpus spongiosum of the penis

→ blood enters the urethra → haematuria/urethral bleeding.

🧠 URETHRAL RENT = TEAR → CORPUS SPONGIOSUM ↔ URETHRA → BLOOD IN URINE

Clinical signs

Main sign:

⭐ Red/discoloured urine

Other signs depend on underlying cause:

• Dysuria, Pollakiuria

• Colic/discomfort

• Urinary obstruction

Diagnosis

⭐ Urinalysis

Urine sediment:
→ presence of RBCs confirms haematuria

Then investigate source with:

• USG

• Cystoscopy/endoscopy

• Rectal examination

• Culture if infection suspected

• Blood examination when indicated

Treatment

Depends entirely on the cause:

• Bacterial infection → antibiotics

• Dehydration/renal compromise → IV fluids when indicated

• Urolithiasis → surgical removal

• Trauma → appropriate management

• Treat underlying renal/systemic disease

🧠 HAEMATURIA IS A SIGN → FIND WHERE THE BLOOD COMES FROM → TREAT THE CAUSE

🧪 HAEMATURIA vs HAEMOGLOBINURIA ⭐⭐⭐

This is probably one of the most important distinctions for the oral exam.

• 🩸 Haematuria = intact RBCs in urine

• Centrifuge urine: → RBCs sediment at the bottom → supernatant becomes yellow/clear

• ⭐ RBCs visible in urine sediment

🔴 Haemoglobinuria

• = free haemoglobin in urine due to intravascular haemolysis

Centrifuge urine:

→ no RBC pellet explaining the colour, → ⭐ supernatant remains red

	Haematuria	Haemoglobinuria
What is present?	Intact RBCs	Free haemoglobin
Sediment microscopy	⭐ RBCs	No/very few RBCs
After centrifugation	RBCs settle → supernatant clears	⭐ Supernatant stays red
Think	Urinary tract bleeding	Intravascular haemolysis

🧠 CENTRIFUGE IT:

HAEMATURIA → RED CELLS GO DOWN ⬇ → SUPERNATANT CLEARS

HAEMOGLOBINURIA → RED COLOUR STAYS 🔴

Equine acute and chronic renal failure

1. ⭐ Acute renal failure (ARF)

2. ⭐ Chronic renal failure (CRF)

3. Renal parasites

   • Klossiella equi

   • Halicephalobus gingivalis

4. Leptospirosis

1. ACUTE RENAL FAILURE — ARF ⭐⭐⭐

= Rapid deterioration of renal function

→ ↓ filtration/excretion → accumulation of nitrogenous waste products → azotemia ± uremia

Often associated with:

→ ↓ urine production = oliguria

→ disturbances in:

• Fluid balance, Electrolytes, Acid-base balance

🧠 ARF = RAPID LOSS OF RENAL FUNCTION → AZOTEMIA + OLIGURIA

Etiology ⭐⭐⭐

1. Endotoxemia

Especially associated with:

• Colic

• Acute diarrhea/colitis

→ renal hypoperfusion/ischemia

2. Acute septic pyelonephritis

• Leptospira spp.

3. Nephrotoxins

🌱 Plants

• Red maple, Oak, Onion, White snakeroot

⚙ Heavy metals

• Mercury, Lead, Arsenic

💊 Antibiotics

• ⭐ Gentamicin

• Neomycin, Tetracyclines, Sulfonamides, Cephalosporins

💊 NSAIDs

• ⭐ Flunixin meglumine

🩸 Pigments

• Myoglobin, Hemoglobin

🧠 ARF = ENDOTOXEMIA + INFECTION + NEPHROTOXINS

Pathogenesis

Different etiological agents can cause:

→ renal tubular injury/necrosis

→ renal ischemia

→ inflammatory response

→ direct nephron damage

Examples:

• NSAIDs
  → ↓ renal prostaglandins → ↓ renal perfusion → ischemic injury

• Nephrotoxic antibiotics
  → tubular damage/necrosis

• Myoglobin/hemoglobin
  → pigment-associated renal tubular injury

Result:

↓ GFR → azotemia → fluid/electrolyte/acid-base disturbances

Clinical signs

• ⭐ Anorexia

• Oliguria

• Depression, Colic

• May occur with: Colitis, Myositis

⚠ Nephrotoxins are often not kidney-specific, so clinical signs from damage to other organs may predominate.

Diagnosis ⭐⭐⭐

Rectal palpation

• Kidney may be enlarged/irregular

• ⭐ In the horse, only the caudal pole of the LEFT kidney is normally accessible rectally

Ultrasonography

Acute injury may show:

• Enlarged/swollen kidney

• Edema

• Altered echogenicity

Laboratory

⭐ Most important:

• ↑ Creatinine, Azotemia

• Inappropriately low specific gravity (= poorly concentrated urine)

Other abnormalities from your lecture:

• ↑ Globulins, ↑ Calcium

• ↓ Phosphorus, ↓ Albumin

• Urinary casts

• Enzymes

• Glucosuria

Urine dipstick → measure pH, Protein, Glucose, Ketones, Bilirubin, Urobilinogen, Blood

Treatment ⭐⭐⭐

1. Treat the primary cause

2. Remove nephrotoxins

⭐ Stop suspected nephrotoxic drugs/toxins.

3. Correct fluid/electrolyte abnormalities

• IV fluid therapy

• Correct:

  • Dehydration, Electrolyte abnormalities, Acid-base abnormalities

Monitor carefully for:
⚠ Edema/fluid overload, especially if oliguria persists.

Your lecture lists methods to stimulate urine production:

• Dextrose, Mannitol, Furosemide, Dopamine

4. Pyelonephritis

Use appropriate antimicrobials, ideally based on culture/sensitivity.

Lecture lists:

• Aminoglycosides, Trimethoprim/sulfadiazine (equibactim oral powder)

• Fluoroquinolones, Penicillins, Cephalosporins

⚠ Remember that aminoglycosides themselves can be nephrotoxic, so renal function matters when selecting treatment.

5. Leptospiral infection

• Tetracycline, Streptomycin, Penicillin

Prognosis

Better prognosis when:

• ⭐ Underlying cause can be corrected

• Creatinine stabilizes/decreases after treatment

• Horse becomes polyuric

🧠 ARF Tx = REMOVE CAUSE → FLUIDS/ELECTROLYTES → MONITOR URINE + CREATININE

2. CHRONIC RENAL FAILURE — CRF ⭐⭐⭐

= Slow, progressive and irreversible loss of functional nephrons

→ progressively reduced renal function.

Important cause to consider in horses presented with: ⭐ WEIGHT LOSS + ANOREXIA

Etiology

Two main groups:

A. Tubulointerstitial causes

• Toxins, Obstruction, Pyelonephritis, Neoplasia, Infiltrative disease

• Chronic septic pyelonephritis → usually associated with ascending urinary tract infection

• Renal neoplasia → SCC, Adenocarcinoma, Primary renal cell carcinoma

• Chronic interstitial nephritis → Associated with: Toxins, Hemodynamic injury

B. Glomerular causes

• Glomerulonephritis

• Renal hypoplasia

• Amyloidosis

• Glomerulosclerosis

• Chronic glomerulonephritis → Can be associated with: Immune-mediated injury, Ischemia, Infarction

Clinical signs ⭐⭐⭐

Think of a thin horse that drinks and urinates a lot:

• ⭐ Weight loss, Anorexia, Cachexia, Depression, Dehydration

• ⭐ Polyuria

• ⭐ Polydipsia

• Edema, Fever

• Oral ulceration

🧠 CRF = WEIGHT LOSS + PU/PD + DEHYDRATION

Diagnosis

• Ultrasound: Chronic kidneys may become: ⭐ Small/shrunken + irregular with chronic structural changes.

• Endoscopy: May demonstrate ureteral discharge: Blood, Pus (Especially with pyelonephritis)

• Renal biopsy: ⭐ Provides definitive histopathological diagnosis of the underlying renal lesion.

Laboratory:

• Anemia, Leukocytosis, Proteinuria, Hypochloremia, Hyponatremia, Hematuria

• Renal function testing commonly demonstrates: ↑ Creatinine, ↑ BUN/azotemia, Poor urine concentrating ability (low specific gravity)

Treatment

⚠ CRF is progressive, so treatment is primarily supportive and aimed at maintaining quality of life/prolonging survival.

Nutritional/supportive management:

• Supplement carbohydrates

• Fat

• Electrolytes:

  • Sodium, Potassium, Calcium, Bicarbonate

Diet:

• Low-protein diet (<10%)

Also:
→ maintain hydration
→ treat underlying infection/other correctable causes where possible.

🧠 CRF Tx = SUPPORTIVE → HYDRATION + NUTRITION/ELECTROLYTES + MANAGE CAUSE

🪱 3. RENAL PARASITES

A. KLOSSIELLOSIS ⭐⭐

Etiology

• Protozoan apicomplexa/coccidian: Klossiella equi → renal coccidiosis

Pathogenesis

• Develops within renal tissue → lesions/granules in renal cortex → may impair renal function.

• Meronts in endothelial cells of glomerular capsule. LC not understood.

Dx

⭐ Oocysts in urine

Tx

❌ No known effective treatment that reliably eliminates Klossiella.

🧠 KLOSSIELLA EQUI = RENAL COCCIDIA → KIDNEY CORTEX → OOCYSTS IN URINE → NO SPECIFIC Tx

B. HALICEPHALOBUS GINGIVALIS

Etiology

• Free-living opportunistic nematode.

• During abnormal migration: → may disseminate to kidneys (BUT it is very rare!)

• It may also affect other tissues, particularly CNS and other organs.

🧠 HALICEPHALOBUS = ABERRANT MIGRATION → KIDNEY POSSIBLE BUT RARE

🦠 4. LEPTOSPIROSIS ⭐⭐⭐

Etiology

• Bacterium: Leptospira interrogans

In horses, leptospirosis is especially associated with:

• ⭐ Uveitis

• ⭐ Abortion

Renal disease can also occur, particularly in affected foals.

Pathogenesis

Organism enters bloodstream

→ spreads hematogenously

→ affinity for:

• Kidneys, Liver, Pregnant uterus

Kidney

→ colonization of renal tubules/nephrons → renal damage → possible renal failure

Liver

→ hepatitis/necrosis

Pregnant uterus

→ crosses placenta → fetal infection → ⭐ abortion

🧠 LEPTO = BLOOD → KIDNEY + LIVER + PREGNANT UTERUS

Clinical signs

• ⭐ Polydipsia

• ⭐ Polyuria

• Fever, Dehydration

• Icterus/jaundice

Depending on manifestation:

• Uveitis, Abortion, Renal disease

Diagnosis

• ELISA

• ⭐ MAT (microscopic agglutination test) (gold standard!!!)

Treatment

Antibiotics:

• Tetracycline, Streptomycin, Penicillin

🧠 LEPTO = UVEITIS + ABORTION ± KIDNEY → MAT → ANTIBIOTICS

🔥 ARF vs CRF — KNOW THIS

	ACUTE RENAL FAILURE	CHRONIC RENAL FAILURE
Onset	⭐ Rapid	⭐ Slow/progressive
Urination	Often oliguria initially	⭐ Polyuria/polydipsia
Kidney	Often swollen/enlarged	Often small/shrunken/irregular
Common causes	Endotoxemia, nephrotoxins, infection	Chronic nephritis, pyelonephritis, glomerular disease
Creatinine	↑	↑
Main approach	⭐ Remove cause + restore fluid/electrolyte balance	⭐ Long-term supportive management
Reversibility	Can be reversible	Usually irreversible/progressive

🧠 Final memory

ACUTE = BIG/WET KIDNEY + OLIGURIA → REMOVE CAUSE + FLUID THERAPY

CHRONIC = SMALL/IRREGULAR KIDNEY + WEIGHT LOSS + PU/PD → SUPPORTIVE CARE

KLOSSIELLA = OOCYSTS IN URINE

HALICEPHALOBUS = RARE ABERRANT KIDNEY MIGRATION

LEPTOSPIRA = UVEITIS + ABORTION + POSSIBLE RENAL FAILURE

Disorders of horse consciousness

The nervous system is divided into:

• Brain, Spinal cord, Peripheral nerves

Clinical signs depend on which part of the nervous system is affected.

The neurological examination aims to:

1. Determine whether neurological dysfunction is present

2. Determine its severity

3. ⭐ Localize the lesion

🧠 1. GENERAL NEUROLOGICAL EXAMINATION

A. History

Ask about:

• Age, Breed

• Duration of signs, Progression

• History of trauma

• Previous/current diseases

• Medication, Vaccination status

• Recent travel

• Environment

B. Physical + neurological examination ⭐⭐⭐

1. Behaviour

Look for:

• Seizures, Head pressing, Circling, Aggressiveness, Abnormal behaviour

2. Mental status/consciousness ⭐⭐⭐

Evaluate level of consciousness and awareness:

• Normal/alert

• Depression

• Somnolence → abnormally sleepy

• Semicoma/stupor → responds only to strong stimuli

• Coma → unconscious, does not respond appropriately to stimuli

🧠 DEPRESSION → SOMNOLENCE → STUPOR/SEMICOMA → COMA

3. Head posture + coordination

Look for:

• Head tilt, Head swaying

• Abnormal position/movement

→ Head tilt especially suggests vestibular dysfunction!

4. Cranial nerves

• Examine CN I–XII.

5. Gait + posture ⭐⭐⭐

Observe:

• Ataxia → incoordination

• Paresis → weakness

• Spasticity

• Hypermetria → exaggerated limb movement

• Stumbling

Observe the horse:

• Walking, Turning/circling, Backing

• If appropriate, with additional gait challenges

6. Neck + forelimbs

Evaluate:

• Symmetry, Malformations, Muscle atrophy, Patchy sweating

• Strength of voluntary movement, Skin sensation, Spinal reflexes

7. Trunk + hindlimbs

Evaluate:

• Symmetry, Muscle mass, Sensation, Strength, Coordination

8. Tail + anus

Evaluate:

• ⭐ Perineal reflex

• Tail tone

• Anal tone

• Asymmetry

9. PROPRIOCEPTION ⭐⭐⭐

Proprioception = horse's awareness of the position of its limbs/body.

Test:

Make the horse walk in tight circles.

• Normal horse → mildly crosses limbs appropriately.

• Neurological horse → may Cross excessively, Step on itself, Swing/reach the outside limb too far, Misplace limbs

🧠 PROPRIOCEPTION = “DOES THE HORSE KNOW WHERE ITS LEGS ARE?”

10. LIMB STRENGTH

Forelimbs

• Push the horse at the shoulder toward the opposite limb.

• Normal → resists displacement → does not collapse.

Hindlimbs

⭐ Tail-pull test

Pull the tail laterally while horse:

• Stands

• Walks forward

Normal → resists → maintains balance and supports body weight.

Neurological weakness → easily displaced → difficulty recovering balance.

Also look for:

• Stumbling

🧠 PUSH SHOULDER = FORELIMBS; PULL TAIL = HINDLIMBS

🐴 2. NEUROLOGICAL EXAMINATION OF FOALS ⭐⭐

Be careful because some findings that would be abnormal in adults can be normal in young foals.

Normal/possible in foals:

• Menace response reduced or absent

• Jerky head movements

• Mild dysmetria

• Mild incoordination

• Slap-test response can be variable up to approximately 1 month

🧠 FOAL ≠ SMALL ADULT — immature neurological responses can be normal

👋 3. SLAP TEST — TLAR ⭐⭐⭐

= Thoracolaryngeal adductor reflex (TLAR)

Procedure:

→ Slap the saddle/thoracic region on one side

→ observe movement of the contralateral arytenoid cartilage using transnasal endoscopy.

• ⭐ the expected reflex is arytenoid adduction (moves inward)

Used to assess neurological pathways involving:

• Cervical spinal cord and Brainstem/vagal-recurrent laryngeal pathways

• Can help detect neurological dysfunction/lesions affecting these pathways.

🧠 SLAP BACK → WATCH ARYTENOID ADDUCT

🔬 4. DIAGNOSTIC TESTS

1. Cerebrospinal fluid (CSF)

• Can be collected from: Atlanto-occipital space, and Lumbosacral region

Imaging

• Radiography, CT

• MRI → particularly useful for intracranial disease

Other

• Needle electromyography (EMG)

• Necropsy

🧠 5. DISORDERS OF CONSCIOUSNESS

EPILEPSY ⭐⭐⭐

= recurrent seizures

• A seizure results from abnormal electrical activity in the brain.

Etiology

• Idiopathic

OR secondary to cerebral cortical damage caused by:

• Ischemia, Trauma, Infectious disease, Neoplasia

Clinical signs

• ⭐ Loss/alteration of consciousness

• Tonic-clonic seizures

• Abnormal movements, Paddling, Urination, Defecation, Salivation

Treatment

• Acute seizure:
  ⭐ Diazepam

• Idiopathic/recurrent cases: phenytoin

🧠 EPILEPSY = RECURRENT SEIZURES → LOSS OF CONSCIOUSNESS + TONIC/CLONIC MOVEMENTS → DIAZEPAM ACUTELY

🦠 6. CIZEK'S INFECTIOUS DISEASES OF THE NERVOUS SYSTEM

Know the list:

Equine encephalomyelitis ⭐⭐⭐

• Eastern equine encephalomyelitis — EEE

• Western equine encephalomyelitis — WEE

• Venezuelan equine encephalomyelitis — VEE

Transmission:

• Mosquitoes

• Rodent/bird reservoir cycles depending on virus

Pathogenesis:
→ inflammation of brain/CNS

Dx:

• Lecture: ELISA

Tx:

• Supportive

Other infectious neurological diseases:

• Getah virus — Alphavirus

• Borna disease — Bornavirus

• Pseudorabies/Aujeszky disease — Suid alphaherpesvirus 1

• Louping ill — Flavivirus

• ⭐ Rabies — Lyssavirus

🧠 EEE/WEE/VEE + GETAH + BORNA + AUJESZKY + LOUPING ILL + RABIES

👁 7. CRANIAL NERVES I–XII ⭐⭐⭐

This part is much easier if you learn function + how to test it.

CN I — OLFACTORY

Function: smell

Test: → response to familiar/non-irritating odours

🧠 I = SMELL

CN II — OPTIC ⭐⭐⭐

Function:

• Vision

• Afferent component of menace response and pupillary light reflex

Test: Menace response → threatening hand gesture toward eye → horse should blink.

Pathway involves:

• ⭐ CN II → sees threat

• ⭐ CN VII → closes eyelid

Obstacle course → evaluates vision.

🧠 II SEES, VII BLINKS

CN III — OCULOMOTOR ⭐⭐⭐

Function:

• Eye movement, Pupil constriction

Test: Observe Pupil size, Symmetry

Pupillary light reflex — PLR → shine bright light into eye → immediate pupil constriction

🧠 III = CONSTRICT PUPIL

CN IV — TROCHLEAR

Function:

• Eye position/movement

• Innervates dorsal oblique muscle

Assess normal eye position and movement.

🧠 IV = EYE POSITION

CN V — TRIGEMINAL ⭐⭐⭐

Three branches:

1. Ophthalmic

2. Maxillary

3. Mandibular

Function

⭐ Major sensory nerve of the face

Also motor function to muscles of mastication.

Test

Facial sensation/reflexes:

• Touch/prick face, Corneal/palpebral region, Nostrils, Lips

Look for:

• Ear movement, Eyelid closure, Nostril movement, Withdrawal of lip/labial commissure

🧠 V = FEEL THE FACE + CHEW

CN VI — ABDUCENS

Function:

• Eye position/movement

Important for lateral movement of eye.

🧠 VI = ABDUCT EYE

CN VII — FACIAL ⭐⭐⭐

Branches include:

• Auricular, Palpebral, Buccal

Function

Controls facial muscles.

Test

Observe ability to:

• Move ears, ⭐ Blink eyelids, Move lips, Move nostrils, Eat normally

Remember:

CN V = sensory input from face
CN VII = facial motor response

🧠 VII = FACIAL MOVEMENT + BLINK

CN VIII — VESTIBULOCOCHLEAR ⭐⭐⭐

Two functions:

Cochlear → hearing

Vestibular → balance

Abnormality may produce:

• Head tilt, Ataxia, Nystagmus

🧠 VIII = HEARING + BALANCE

CN IX — GLOSSOPHARYNGEAL

Function:

• Pharynx, Swallowing, Component of gag/pharyngeal reflex

🧠 IX = PHARYNX + SWALLOW

CN X — VAGUS ⭐⭐⭐

Functions include:

• Pharynx/larynx, Swallowing, Laryngeal function

• Parasympathetic visceral functions

Your lecture particularly associates it with:

⭐ SLAP TEST / TLAR

🧠 X = VAGUS → LARYNX → SLAP TEST

CN XI — ACCESSORY

Function:
Motor function to muscles of:

• Neck, Shoulder region

🧠 XI = NECK/SHOULDER MUSCLES

CN XII — HYPOGLOSSAL ⭐⭐

Function:
⭐ Tongue movement

Test

• Inspect tongue size/symmetry, Pull tongue from mouth → Horse should provide resistance

• Observe tongue movement

🧠 XII = TONGUE

🔥 CRANIAL NERVES — RAPID EXAM TABLE

CN	Nerve	Main thing to remember
I	Olfactory	Smell
II	Optic	Vision
III	Oculomotor	Pupil constriction
IV	Trochlear	Eye position
V	Trigeminal	Facial sensation + chewing
VI	Abducens	Eye position/abduction
VII	Facial	Facial movement + blink
VIII	Vestibulocochlear	Hearing + balance
IX	Glossopharyngeal	Swallow/pharynx
X	Vagus	Larynx + slap test
XI	Accessory	Neck muscles
XII	Hypoglossal	Tongue

🧠 The highest-yield associations

II + VII → MENACE:
II sees → VII blinks

II + III → PLR:
II detects light → III constricts pupil

V + VII → FACIAL REFLEX:
V feels → VII moves

VIII → HEAD TILT/BALANCE

IX + X → SWALLOWING/PHARYNX

X → SLAP TEST

XII → TONGUE

Vestibular syndrome and brainstem disorders

🧠 Vestibular system

Responsible for:

• ⭐ Balance

• Posture

• ⭐ Eye movements

It has two major parts:

1. Peripheral vestibular system
   → inner/middle ear + vestibular nerve

2. Central vestibular system
   → vestibular structures/pathways in the brainstem/CNS

Dysfunction causes:
→ loss of normal posture and balance
→ ataxia
→ abnormal eye movements/nystagmus

1. VESTIBULAR SYNDROME ⭐⭐⭐

Vestibular syndrome = group of diseases affecting the vestibular system.

Main question:

⭐ Is it PERIPHERAL or CENTRAL?

🦻 2. PERIPHERAL VESTIBULAR DISEASE ⭐⭐⭐

The lesion is associated with the inner/middle ear or peripheral vestibular nerve.

Etiology

• Otitis media/interna ⭐

• Other aural diseases → Polyps, Granulomas, Neoplasia

• Trauma → Blunt trauma

• Polyneuritis equi: Neurological inflammatory disease, Also associated with cauda equina syndrome

• ⭐ Temporohyoid osteoarthropathy (THO), Very important equine cause.

🦴 TEMPOROHYOID OSTEOARTHROPATHY — THO ⭐⭐⭐

Pathogenesis

• The stylohyoid bone becomes pathologically fused/ankylosed to the petrous temporal bone.

Normally the hyoid apparatus moves during:

• Chewing, Swallowing

If fused:

→ normal movement creates excessive stress → pathological fracture can occur in:

• Stylohyoid bone and Petrous temporal bone

→ nearby cranial nerves/vestibular structures can be damaged → vestibular signs ± facial paralysis.

Tx

⭐ Ceratohyoidectomy

→ removes part of the ceratohyoid bone
→ reduces mechanical forces transmitted through the hyoid apparatus.

🧠 THO = STYLOHYOID FUSES TO TEMPORAL BONE → FRACTURE/NERVE DAMAGE → VESTIBULAR SIGNS → CERATOHYOIDECTOMY

Clinical signs — PERIPHERAL ⭐⭐⭐

• ⭐ Head tilt

• ⭐ Circling toward the side of the lesion

• Ataxia, Imbalance, Recumbency

• ⭐ Horizontal or rotatory nystagmus

• Facial nerve paralysis (CN VII) may occur

Mental status is generally normal with a purely peripheral lesion.

🧠 PERIPHERAL = HEAD TILT + HORIZONTAL/ROTATORY NYSTAGMUS + NORMAL MENTATION

🧠 3. CENTRAL VESTIBULAR DISEASE ⭐⭐⭐

Lesion is within the CNS/brainstem.

• Occurs less frequently than peripheral vestibular disease.

Etiology

🦠 Infectious diseases

Viral/protozoal

• Equine protozoal myeloencephalitis — EPM

• Eastern equine encephalomyelitis — EEE

• Western equine encephalomyelitis — WEE

• West Nile virus — WNV

• Rabies

• Equine herpesvirus-1 — EHV-1

⚠ EPM is protozoal, not viral.

Bacterial

• Listeria, Salmonella

• Streptococcus equi → strangles

• Burkholderia mallei → glanders

• Clostridium botulinum

Other

• Trauma, Neoplasia, Brain abscess

Clinical signs — CENTRAL ⭐⭐⭐

• ⭐ Vertical nystagmus

• Circling, Imbalance, Ataxia

• ⭐ Altered mentation

• Other cranial nerve deficits

Because the lesion is in the brainstem/CNS, other neurological abnormalities are more likely.

🧠 CENTRAL = VERTICAL NYSTAGMUS + ALTERED MENTATION + MULTIPLE CN DEFICITS

🔥 PERIPHERAL vs CENTRAL

	Peripheral	Central
Lesion	Inner/middle ear, CN VIII	Brainstem/CNS
Head tilt	⭐ Common	Can occur
Circling	Toward lesion	Can occur
Nystagmus	⭐ Horizontal/rotatory	⭐ Vertical possible
Mentation	⭐ Normal	⭐ Altered
CN deficits	VII/VIII commonly	Multiple CNs possible
Examples	Otitis, THO	Encephalitis, EPM, trauma, neoplasia

🧠 Easiest distinction

PERIPHERAL → EARS + HORIZONTAL/ROTATORY + NORMAL BRAIN

CENTRAL → BRAINSTEM + VERTICAL + ABNORMAL MENTATION

🔬 4. DIAGNOSIS ⭐⭐⭐

1.Full neurological examination

Use the examination from Q18:

• Behaviour

• Mental status

• Head posture

• Cranial nerves

• Gait

• Ataxia

• Proprioception

• Limb strength

• Tail/perineal reflexes

Goal:
⭐ Localize lesion as peripheral or central.

2.Endoscopy

• Guttural pouch endoscopy

Can help evaluate structures around:

• Stylohyoid bone, Temporohyoid joint

• Especially useful with suspected THO.

3.Imaging

X-ray:

Look for:

• ⭐ THO, Otitis, Masses, Fractures

CT

Very useful for:

• Skull, Temporohyoid region, Middle/inner ear

MRI

Useful for:

• Brain, Brainstem, Soft tissues

4.💉 CSF ANALYSIS

Collect and examine cerebrospinal fluid.

May demonstrate:

• Inflammatory/cytological abnormalities

• Changes associated with neurological disease

Your lecture specifically mentions:

• Polyneuritis equi

• Immunological testing for EPM

EPM can sometimes mimic peripheral vestibular disease.

5.🦠 INFECTIOUS DISEASE TESTING

Serology/PCR/specific testing depending on suspicion:

• EPM

• EEE

• WEE

• WNV

• EHV-1

💊 TREATMENT

Treatment depends on the underlying cause.

• Otitis media/interna →⭐ Prolonged antibiotic therapy

• THO → ⭐ Ceratohyoidectomy

• Infectious central vestibular disease → specific antimicrobial/antiprotozoal treatment when available, → supportive care

• Trauma/inflammation → supportive treatment according to cause and severity.

🧠 EXAM MEMORY

First say:

“The vestibular system controls balance, posture and eye movements and can be divided into peripheral and central components.”

Then differentiate:

🦻 PERIPHERAL

OTITIS + THO

→ head tilt
→ circles toward lesion
→ horizontal/rotatory nystagmus
→ facial paralysis
→ normal mentation

🧠 CENTRAL

ENCEPHALITIS + EPM + TRAUMA + NEOPLASIA

→ vertical nystagmus
→ altered mentation
→ multiple cranial nerve deficits
→ imbalance/ataxia

⭐ THO

STYLOHYOID ↔ PETROUS TEMPORAL BONE FUSION → FRACTURE → VESTIBULAR SIGNS → CERATOHYOIDECTOMY

Spinal ataxia and equine protozoal myeloencephalitis

1. ATAXIA ⭐⭐⭐

Ataxia = incoordination caused by impaired proprioception (sense of body/limb position), often accompanied by some degree of weakness/paresis.

Types of ataxia

• Cerebellar ataxia

• Cerebral ataxia

• Vestibular ataxia

• Sensory/proprioceptive ataxia

• ⭐ Spinal ataxia → motor dysfunction with incoordination of the limbs and/or trunk

🧠 ATAXIA = INCOORDINATION; PARESIS = WEAKNESS

🧠 2. SPINAL ATAXIA

Etiology

Spinal cord dysfunction can result from:

• Trauma, Myelopathy, Inflammation

• Infectious disease:

  • EHV-1

  • Protozoal disease → EPM

• Degenerative disease, Neoplasia, Toxins

• Compression, e.g., Wobbler syndrome

Clinical signs

• Motor dysfunction

• ⭐ Incoordination of extremities

• Trunk instability

• Paresis

• Proprioceptive deficits

📍 3. SPINAL CORD LESION LOCALIZATION ⭐⭐⭐

This is the important pattern to understand rather than memorize randomly.

First remember:

UMN lesion
→ normal/increased tone and reflexes
→ spastic/strong-looking but poorly coordinated movement

LMN lesion
→ ⭐ weakness
→ decreased tone/reflexes
→ possible muscle atrophy

C1–C5

Lesion is above the limb LMNs.

Thoracic limbs → UMN
Pelvic limbs → UMN

→ all four limbs can be affected.

🧠 C1–C5 = UMN ALL 4

C6–T2

This region contains LMNs supplying the thoracic limbs.

Therefore:

Thoracic limbs → LMN
Pelvic limbs → UMN

🧠 C6–T2 = LMN FRONT + UMN BACK

T3–L3

Below the thoracic limb innervation:

Thoracic limbs → NORMAL
Pelvic limbs → UMN

🧠 T3–L3 = FRONT NORMAL + BACK UMN

L4–S1

Contains LMNs supplying pelvic limbs:

Thoracic limbs → NORMAL
Pelvic limbs → LMN

🧠 L4–S1 = FRONT NORMAL + BACK LMN

Sacral–caudal

Thoracic limbs → normal

Pelvic limbs → normal or LMN, depending on exact lesion.

May produce ⭐ cauda equina signs:

• Urinary incontinence/dysfunction

• Rectal/fecal incontinence

• Reduced tail/anal tone

🔥 Localization table

Lesion	Thoracic limbs	Pelvic limbs
C1–C5	UMN	UMN
C6–T2	⭐ LMN	UMN
T3–L3	Normal	UMN
L4–S1	Normal	⭐ LMN
Sacral/caudal	Normal	Normal/LMN + cauda equina signs

🧠 C6–T2 controls FRONT LMN; L4–S1 controls BACK LMN

📊 4. GRADING OF ATAXIA — 0–5 ⭐⭐⭐

Grade 0

→ No neurological deficit detected

Grade 1

→ Very mild deficit
→ not readily detected during normal gait/posture
→ may become apparent with challenging manoeuvres

Grade 2

→ ⭐ Deficit easily detected
→ Exaggerated when challenging the horse

Grade 3

→ ⭐ Deficit prominent at normal gait

Grade 4

→ Severe

• Stumbling

• Tripping

• Spontaneously falling

Grade 5

→ ⭐ Recumbent
→ unable to stand/get up without assistance

🧠 0 NONE → 1 SUBTLE → 2 OBVIOUS WHEN CHALLENGED → 3 OBVIOUS NORMALLY → 4 FALLS → 5 RECUMBENT

🔬 5. DIAGNOSIS OF SPINAL ATAXIA

1. Neurological examination

• Assess: Gait, Proprioception, Paresis, UMN/LMN signs, Tail/anal tone, Cranial nerves where relevant

2. Radiography

• Especially cervical spine: C1–T1

• Lateral, Oblique, Neutral, Flexed, Extended views

3. Myelography

• → evaluates spinal cord compression

4. Slap test

• → evaluates thoracolaryngeal reflex

• As discussed in Q18: ⭐ normal response = brief contralateral laryngeal/arytenoid adduction

5. Laboratory

• CSF, Hematology, Biochemistry, Serology

🦴 6. WOBBLER SYNDROME ⭐⭐⭐

Cervical vertebral stenotic myelopathy — CVSM

= Compression of the cervical spinal cord

Etiology

Can result from:

• Vertebral malformation, Malarticulation, Abnormal vertebral development, Displacement, Vertebral canal stenosis

• Synovial cysts/other compressive lesions → spinal cord compression → proprioceptive/UMN dysfunction.

Clinical signs

⭐ Usually pelvic limbs affected more severely initially:

• Hindlimb ataxia

• Paresis, Wide-based stance, Incoordination

• As disease progresses → forelimbs may also become affected

🧠 WOBBLER = CERVICAL CORD COMPRESSION → HINDLIMBS WORSE THAN FORELIMBS

Diagnosis

• Neurological examination

• Cervical radiographs

• ⭐ Myelography

• Advanced imaging where available

• Abnormal slap test

Treatment

• Glucocorticoids

• Neck braces

• ⭐ Surgical treatment/decompression/stabilization in selected cases

🐴 7. OCCIPITO-ATLANTO-AXIAL MALFORMATION — OAAM ⭐⭐⭐

= Congenital developmental abnormality particularly associated with Arabian horses.

• Affects: Occipital bone, Atlas C1 and Axis C2

Typical abnormality:

• ⭐ Atlas is fused to the occipital bone → abnormal upper cervical anatomy → compression/damage of the cranial cervical spinal cord.

Clinical signs

Foals may:

• Be stillborn

• Be ⭐ ataxic from birth

• Develop progressive ataxia during first months of life

Characteristic posture:

• Extended neck

• Reduced ability to flex the atlanto-occipital joint

Dx

• ⭐ X-ray

• Genetic testing

Tx

❌ No effective treatment

🧠 OAAM = ARABIAN FOAL → OCCIPUT + C1 + C2 MALFORMATION → ATAXIA FROM BIRTH

🦠 8. EQUINE PROTOZOAL MYELOENCEPHALITIS — EPM ⭐⭐⭐

Etiology

Protozoan:

⭐ Sarcocystis neurona

Mainly important in:
🇺🇸 North America

Hosts

Definitive host (FH):
⭐ Opossum

Intermediate hosts can include:

• Raccoons

• Other wildlife

Horse:
⭐ Aberrant/dead-end host

🧠 EPM = SARCOCYSTIS NEURONA → OPOSSUM → HORSE = ABERRANT HOST

🔄 Life cycle

Opossum sheds sporocysts in feces → Contaminates Pasture, Feed, Water → Horse ingests sporocysts → Sporozoites released → Parasite disseminates and can enter the CNS → Lesions develop in:

• Brain

• Brainstem

• Spinal cord

→ neurological signs depend on location of CNS lesions

⚠ For your exam, I would avoid saying that S. neurona routinely “forms cysts in the horse brain.” The key point is multifocal inflammatory lesions/meronts in the CNS; horses are aberrant hosts.

🧠 Pathogenesis

• Parasite reaches CNS → inflammation + neuronal/tissue damage → multifocal neurological dysfunction.

• Because lesions can occur in different places: ⭐ Clinical signs are highly variable and often asymmetric.

🚨 Clinical signs ⭐⭐⭐

Very important characteristic:

⭐ ASYMMETRIC NEUROLOGICAL SIGNS

Can include:

• Asymmetric ataxia, Weakness, Incoordination

• ⭐ Muscle atrophy

• Facial sensory deficits, Lameness, Urinary incontinence, Cranial nerve deficits depending on lesion, Other signs depending on CNS localization

• incoordination, gait abn, head tilt, facial nerve paralysis, diffic swallowing, loss of sensation,  seizures, lameness, blindness, muscle atrophy of gluteus muscle etc.

🧠 EPM = ASYMMETRIC ATAXIA + FOCAL MUSCLE ATROPHY

🔬 Diagnosis

Diagnosis can be difficult because exposure does not necessarily mean neurological disease.

Your lecture lists:

• Serology, PCR, Western blot

For the exam, remember:

⭐ Serum + CSF antibody testing can support diagnosis when interpreted together with neurological findings.

So:
neurological examination + compatible signs + laboratory testing

💊 Treatment

Your lecture lists:

Antiprotozoal

• Trimethoprim-sulfadiazine

• Toltrazuril

Supportive

• NSAIDs

• ⭐ Vitamin E

• Vitamin B complex

🧠 EPM Tx = ANTIPROTOZOAL + ANTI-INFLAMMATORY/SUPPORTIVE CARE

🔥 EXAM STRUCTURE FOR Q20

If you draw this question, I would answer it in this order:

1. Define ataxia
→ incoordination + loss of proprioception ± paresis

2. Name types
→ cerebral, cerebellar, vestibular, sensory, spinal

3. Localize spinal lesion
→ C1–5 = UMN/UMN
→ C6–T2 = LMN/UMN
→ T3–L3 = normal/UMN
→ L4–S1 = normal/LMN

4. Grade 0–5
→ 0 normal → 5 recumbent

5. Important spinal disease
→ Wobbler = cervical spinal cord compression

6. Congenital disease
→ OAAM = Arabian foal + C1/C2/occiput

7. EPM
→ S. neurona → opossum → horse aberrant host → asymmetric ataxia + muscle atrophy

🧠 Final memory line

SPINAL ATAXIA = PROPRIOCEPTIVE INCOORDINATION ± PARESIS

WOBBLER = CERVICAL COMPRESSION

OAAM = ARABIAN FOAL

EPM = OPOSSUM → S. NEURONA → ASYMMETRIC ATAXIA + MUSCLE ATROPHY

Peripheral nerve disorders

Peripheral nerve disorders in horses can result from:

• ⭐ Trauma

• Compression/ischemia during anaesthesia

• Fractures, Deep injections, Infection/inflammation

• Neuromuscular junction disorders, Neurotoxins

⭐ Nerves commonly affected during anaesthesia

• Facial nerve, Radial nerve, Suprascapular nerve

🧠 1. PERIPHERAL NERVE INJURIES

Peripheral nerve injuries are common after trauma or prolonged compression.

Main nerves to know:

• Ischiatic/sciatic, Femoral, Suprascapular, Radial, Tibial, Facial

🦵 ISCHIATIC / SCIATIC NERVE

Anatomy/function:

• Origin → approximately L5–S1 region

• Runs from lower back/pelvis into the hindlimb.

• Provides major motor and sensory innervation to the pelvic limb and divides into:

→ Tibial nerve and Common fibular/peroneal nerve (n.peroneus communis)

Causes of damage

• ⭐ Deep IM injections, Pelvic fractures, Femoral fractures, Trauma

Clinical signs

• weakness/paresis or partial paralysis of affected hindlimb

• Severity depends on the location and extent of nerve damage.

🧠 SCIATIC = DEEP INJECTION + PELVIC/FEMORAL TRAUMA → HINDLIMB PARESIS

🦵 FEMORAL NERVE ⭐⭐

Function:

• Innervates the:⭐ Quadriceps

• Quadriceps: → extends the stifle

Causes

• Dystocia/birth trauma, Prolonged tissue pressure, Anaesthesia in dorsal recumbency, Pelvic trauma

Clinical signs

Damage → quadriceps dysfunction

→ inability to properly extend/fix the stifle

→ limb may collapse/flex during weight bearing

→ difficulty supporting weight.

🧠 FEMORAL → QUADRICEPS → EXTENDS STIFLE

🦴 SUPRASCAPULAR NERVE ⭐⭐⭐

Very important because it produces:

⭐ SWEENEY SHOULDER

Causes:

• Kicks, Collision/trauma, Compression/injury, Connective tissue/scar formation after injury

Muscles affected:

• Suprascapular nerve supplies: M. supraspinatus, M. infraspinatus → These muscles stabilize the shoulder joint.

Clinical signs:

Early:

→ loss of shoulder stabilization → ⭐ lateral shoulder subluxation / “popping” during weight-bearing

After approximately 2–4 weeks:

→ obvious atrophy of Supraspinatus and Infraspinatus muscles

→ scapular spine (spina scapulae) becomes very prominent = ⭐ Sweeney shoulder

Treatment:

• Stall rest, Physiotherapy, Long recovery period

• Severe/chronic compression → surgery may be performed to Remove scar tissue, Decompress/reduce tension on nerve

🧠 SUPRASCAPULAR → SUPRA + INFRA ATROPHY → PROMINENT SCAPULAR SPINE = SWEENEY SHOULDER

🦵 RADIAL NERVE ⭐⭐⭐

Function

Innervates muscles involved in:

• Elbow extension, Carpal extension, Digital extension

• It also contributes to movement around the shoulder.

Causes

• ⭐ Ischemic/compressive injury during anaesthesia in lateral recumbency

• Humeral fractures, Trauma

Clinical signs

• ⭐ Dropped elbow

• Failure/inability to extend the limb, Carpus/digit remain flexed

• Difficulty advancing/positioning limb normally. ⭐ Unable to properly bear weight

🧠 RADIAL = EXTENSOR NERVE → DAMAGE = DROPPED ELBOW + CANNOT EXTEND/BEAR WEIGHT

🦵 TIBIAL NERVE

• Major terminal branch/continuation of the sciatic nerve.

• Innervates → Gastrocnemius, Digital flexors, Other caudal crus muscles

• Gastrocnemius contributes strongly to: → ⭐ hock extension

• Damage → gastrocnemius weakness/atrophy → inability to maintain normal hock extension → hock flexion/dropped hock

🧠 TIBIAL → GASTROCNEMIUS → EXTENDS HOCK → DAMAGE = FLEXED/DROPPED HOCK

🙂 2. FACIAL NERVE PARALYSIS ⭐⭐⭐

CN VII — Facial nerve

• A relatively common peripheral nerve injury.

Etiology

Most classically:

⭐ Horse lies for prolonged period with pressure on side of face

Especially:

• Anaesthesia

• Halter left on during recumbency

Other causes:

• Facial surgery, Rough handling, Otitis media, Trauma, Guttural pouch infection

Clinical signs

A unilateral proximal facial nerve lesion causes paresis/paralysis of facial muscles.

Affected side may show:

• ⭐ Drooping eyelid

• Drooping ear, drooping lip, drooping nostril

• Facial asymmetry

• ⭐ Inability to blink

Auriculopalpebral branch

If only the auriculopalpebral branch is damaged:

→ primarily affects: Ear movement, Eyelid movement/blinking

🧠 FACIAL NERVE = MOVE FACE → DAMAGE = DROOPING EAR/EYELID/LIP/NOSTRIL

Diagnosis

Electromyography — EMG

Can help determine:

• Location, Severity, Extent of nerve damage

Treatment

Supportive methods from your lecture:

• Acupuncture, Massage, Heat to affected muscles, Laser therapy, Electrotherapy

• Peripheral nerves regenerate slowly.

• ⚠ Protect the eye if the horse cannot blink → risk of corneal damage.

Prognosis → Poor prognosis if there is no improvement within 6 months.

💪 3. MYASTHENIA GRAVIS ⭐⭐⭐

= Disorder of neuromuscular transmission → nerve signal cannot efficiently activate skeletal muscle.

Pathogenesis

Autoantibodies are directed against Acetylcholine receptors — AChR at the neuromuscular junction.

→ ↓ number/function of ACh receptors → impaired neuromuscular transmission → muscle weakness.

🧠 MG = ANTIBODIES AGAINST ACh RECEPTORS

Clinical signs

Characteristic: ⭐ Muscle weakness worsens with exercise and improves with rest

Can also cause:

• Megaesophagus, Dysphagia

Megaesophagus:

→ food/material may be aspirated → secondary aspiration pneumonia

🧠 MG = EXERCISE → WORSE; REST → BETTER

Diagnosis

• AChR antibodies

Lecture:

• IFAT for circulating antibodies against AChR

• Tensilon test: Administration of a short-acting anticholinesterase → transient improvement in muscle strength supports neuromuscular transmission dysfunction.

Treatment
⭐ Prednisolone → immunosuppressive treatment.

🦠 4. TETANUS ⭐⭐⭐

• Clostridium tetani

→ produces a powerful neurotoxin → ⭐ SPASTIC PARALYSIS

🧠 TETANUS = TIGHT/STIFF

Transmission

• C. tetani spores are found in soil.

• Enter through wounds, especially where anaerobic conditions develop.

Examples:

• Castration

• Skin wounds/lesions

• Surgical wounds

• Other deep contaminated wounds

→ bacteria proliferate under anaerobic conditions → produce neurotoxin → toxin affects nervous system.

Clinical signs ⭐⭐⭐

• Initial stiffness/lameness, Progressive generalized muscle stiffness

• ⭐ Lockjaw — trismus

• Elevated/stiff ears, Elevated/stiff tail, Hyperresponsiveness, Arched back

• Generalized spastic paralysis

• Later → lateral recumbency → legs held rigidly extended

• Death may occur due to: ⭐ respiratory muscle spasm/paralysis

Diagnosis

Often sufficient:

• Clinical signs

• History of recent wound/trauma

Gram stain

• C. tetani has characteristic: ⭐ “Tennis-racket” appearance due to terminal spores. G+ → purple color in gram stain

• Toxin may also be demonstrated, although diagnosis is usually clinical.

Treatment ⭐⭐⭐

• Wound treatment

Very important:

→ open/aerate wound → remove necrotic tissue → clean/debride → your lecture mentions hydrogen peroxide → local antimicrobial management

Antibiotics

• Penicillin (kills G+ bacteria)

Tetanus antitoxin

→ neutralizes unbound circulating toxin

⚠ Cannot reverse toxin already bound to nervous tissue.

Supportive

• Sedatives, Muscle relaxants, Quiet/dark environment, Supportive nursing

Prevention ⭐⭐⭐

⭐ VACCINATION

🧠 TETANUS = WOUND → TOXIN → SPASTIC PARALYSIS + LOCKJAW → ANTITOXIN + WOUND CARE + ATB → VACCINATE

☠ 5. BOTULISM ⭐⭐⭐

Etiology: Clostridium botulinum

Exposure can be associated with:

• ⭐ Decaying/contaminated hay, Silage, Contaminated feed

• Neurotoxin interferes with neuromuscular transmission → ⭐ FLACCID PARALYSIS

Clinical signs

• Incoordination, Muscle tremors, Progressive weakness

• ⭐ Flaccid paralysis, Drooling, Dysphagia, Recumbency, Colic

🧠 TETANUS = SPASTIC 🔒 vs BOTULISM = FLACCID 🫠

🌱 6. EQUINE GRASS SICKNESS ⭐⭐⭐

= Highly fatal neuropathy of horses.

→ Causes degeneration of neurons of the:

⭐ Autonomic nervous system, especially the⭐ Enteric nervous system

Therefore, the disease is predominantly manifested by GIT signs.

Etiology

• The exact cause is not fully established.

• Your lecture mentions a proposed association with: Clostridium botulinum type C/toxicoinfection → intestinal toxin production → neuronal damage.

For the exam, phrase it as:

“The exact cause is unknown, but clostridial toxicoinfection has been proposed.”

Clinical consequences:

Autonomic/enteric neuronal degeneration → severe gastrointestinal dysfunction.

Can result in:

• Dysphagia, Reduced/absent intestinal motility, Colic, Gastric distension, Constipation, Weight loss depending on form

Diagnosis

Presumptive

• Clinical signs, History, Physical examination

Definitive

⭐ Histopathology/biopsy

Post-mortem findings may include:

• Gastric distension, Colon containing hard, dry feces

Treatment

Primarily: Supportive care

Severe/acute cases: → poor prognosis → euthanasia often recommended.

🧠 GRASS SICKNESS = AUTONOMIC/ENTERIC NEURON DEGENERATION → GIT FAILURE

☠ 7. ORGANOPHOSPHATE POISONING ⭐⭐⭐

Etiology

Exposure to:

• Insecticides, Contaminated food, Contaminated water

• Overdosing of antiparasitic/insecticidal preparations

Pathogenesis

Organophosphates → ⭐ INHIBIT ACETYLCHOLINESTERASE

Normally:

• ACh (acetylcholine) released → signal → acetylcholinesterase breaks down ACh.

With organophosphate:

❌ AChE inhibited → acetylcholine accumulates → continuous cholinergic stimulation → excessive:

• Autonomic activity

• Neuromuscular activity

🧠 ORGANOPHOSPHATE = ↓ AChE → ↑ ACh → TOO MUCH CHOLINERGIC ACTIVITY

Clinical signs

• Anxiety, ⭐ Salivation, Bradycardia, Stiff gait, Muscle tremors, Incoordination, Ataxia, Respiratory dysfunction/failure

Treatment

⭐ Atropine → blocks muscarinic effects of excess acetylcholine.

Plus:

⭐ Oximes, e.g. pralidoxime → can reactivate acetylcholinesterase if administered appropriately/early.

🧠 ORGANOPHOSPHATE → AChE INHIBITION → ATROPINE + OXIME

🔥 EXAM SUMMARY — KNOW THESE ASSOCIATIONS

Disorder/nerve	Key association
Sciatic nerve	Deep injection / pelvic trauma → hindlimb paresis
Femoral nerve	⭐ Quadriceps → cannot extend/stabilize stifle
Suprascapular nerve	⭐ Sweeney shoulder
Radial nerve	⭐ Dropped elbow + cannot extend limb
Tibial nerve	Gastrocnemius → flexed/dropped hock
Facial nerve	⭐ Drooping face + inability to blink
Myasthenia gravis	⭐ AChR antibodies → exercise-induced weakness
Tetanus	⭐ Spastic paralysis + lockjaw
Botulism	⭐ Flaccid paralysis
Grass sickness	⭐ Autonomic/enteric neuron degeneration
Organophosphate	⭐ AChE inhibition → cholinergic overstimulation

🧠 Final memory line

SWEENEY = SUPRASCAPULAR

DROPPED ELBOW = RADIAL

CAN'T EXTEND STIFLE = FEMORAL

DROPPING FACE = FACIAL

MG = AChR ANTIBODIES

TETANUS = SPASTIC

BOTULISM = FLACCID

GRASS SICKNESS = AUTONOMIC GUT

ORGANOPHOSPHATE = AChE ↓ → ACh ↑

Equine endocrinopathies

The main endocrinopathies to know:

1. ⭐ PPID / Equine Cushing's disease

2. ⭐ Insulin resistance / insulin dysregulation

3. ⭐ Equine metabolic syndrome — EMS

4. Diabetes mellitus — rare

5. Hypoadrenocorticism

6. Hypothyroidism

🧠 1. PPID — PITUITARY PARS INTERMEDIA DYSFUNCTION ⭐⭐⭐

• Also called: Equine Cushing's disease — ECD

Epidemiology

• ⭐ Most common endocrinopathy of older horses, Especially horses >10 years (Prevalence increases with age)

Etiology + pathogenesis

→ tumor/enlargement of the pars intermedia of the pituitary gland → excessive production of ACTH → adrenal stimulation → ↑ cortisol → Cushing-like clinical signs.

• Loss of dopaminergic inhibition of the pars intermedia → hyperplasia/adenoma → excessive production of POMC-derived hormones, including ACTH.

• This explains why: ⭐ Pergolide = dopamine agonist works.

🧠 PPID = OLD HORSE + PARS INTERMEDIA + ↑ ACTH

Clinical signs ⭐⭐⭐

1. Abnormal hair coat

Your lecture calls this: ⭐ HIRSUTISM

→ More modern term: Hypertrichosis

• Retention of winter coat, Abnormally long hair, Delayed/incomplete shedding

• This is a highly characteristic sign of advanced PPID!!

🧠 OLD HORSE THAT DOESN'T SHED → THINK PPID

2. Laminitis ⭐⭐⭐

PPID horses have increased risk of → endocrinopathic laminitis

• This is one of the most clinically important complications.

3. Abnormal fat distribution

Fat can accumulate:

• ⭐ Neck → cresty neck

• Around tail head

May also have muscle wasting despite regional fat deposition.

4. PU/PD

• Polyuria, Polydipsia

5. Recurrent/chronic infections

Increased susceptibility to:

• Tooth root infections, Sinusitis, Sole abscesses, Other infections

Also:
⭐ Delayed wound healing

Other signs

• Lethargy, Muscle weakness/wasting, ⭐ Excessive sweating, Abnormal body condition

🔬 Diagnosis

Clinical signs

• An older horse with: ⭐ hypertrichosis + laminitis + muscle wasting/abnormal fat distribution → strongly suggests PPID.

• Resting plasma ACTH ⭐⭐⭐ Measure: plasma ACTH concentration (>35pg/ml → positive)

⚠ For understanding: ACTH varies substantially with season, so modern interpretation uses seasonally adjusted reference intervals rather than one fixed cutoff throughout the year.

CBC

Lecture abnormalities:

• Neutrophilia, Lymphopenia, Monocytosis

• Glucose: May show Hyperglycemia, Glucosuria, Especially when insulin dysregulation is also present.

Endocrine tests

• ⭐ Resting ACTH

• TRH stimulation test

• Dexamethasone suppression test — in your lecture

• ACTH stimulation test — in your lecture

💊 Treatment

1. ⭐ Pergolide mesylate

Pergolide = dopamine agonist

→ restores dopaminergic inhibition of pars intermedia activity → reduces excessive hormone production.

🧠 PPID → PERGOLIDE

2. Trilostane

→ inhibits adrenal steroid synthesis → ↓ cortisol production.

But pergolide is the key PPID treatment to know!

Management

Very important: ⭐ Prevent/manage laminitis

Also:

• Appropriate diet, Hoof care, Treat infections, Dental care, Clip excessive hair if necessary, Monitor body condition

🍬 2. INSULIN RESISTANCE / INSULIN DYSREGULATION ⭐⭐⭐

Insulin resistance = decreased tissue response to circulating insulin.

Therefore insulin is less effective at promoting normal glucose metabolism in:

• Skeletal muscle, Adipose tissue, Liver

Important distinction:

⭐ Horses with EMS (equine metabolic syndrome) commonly have insulin dysregulation, but insulin resistance/dysregulation can occur without the full EMS phenotype.

Etiology/mechanisms

• ↓ density of insulin receptors

• Malfunction of insulin receptors

• Problems with glucose transporter translocation/function

Result: → tissues respond poorly to insulin.

Pathogenesis

Compensated insulin resistance ⭐⭐⭐

Most common situation:

Tissues respond poorly to insulin → Pancreas produces MORE insulin → ⭐ Hyperinsulinemia → Blood glucose may initially remain relatively normal.

🧠 COMPENSATED IR = ↑ INSULIN TO KEEP GLUCOSE CONTROLLED

Uncompensated IR / β-cell exhaustion

Eventually: → pancreatic β-cells cannot compensate adequately → insulin secretion becomes insufficient relative to need → persistent hyperglycemia → possible type 2 diabetes mellitus

🍬 Diabetes mellitus

• Very rare in horses.

• More likely in horses with severe/advanced endocrine disease such as PPID with insulin dysregulation.

• When hyperglycemia becomes severe → glucose exceeds renal threshold → glucosuria → osmotic diuresis → ⭐ polyuria → polydipsia.

🧠 DIABETES = HYPERGLYCEMIA → GLUCOSURIA → OSMOTIC DIURESIS → PU/PD

🐴 3. EQUINE METABOLIC SYNDROME — EMS ⭐⭐⭐

EMS is an endocrine/metabolic disorder characterized principally by:

⭐ Insulin dysregulation
⭐ Regional/generalized adiposity in many affected horses
⭐ High risk of endocrinopathic laminitis

Predisposed horses:

Often affects “thrifty” equids:

• ⭐ Ponies, Donkeys, Arabians, Mustangs

• These animals are genetically/metabolically efficient at storing energy.

Pathogenesis

Adipose tissue → production of adipokines → hormonal/metabolic disturbance → impaired normal insulin response → hyperinsulinemia ± altered glucose metabolism.

The key exam concept is:

EMS triad

ADIPOSITY + INSULIN DYSREGULATION/HYPERINSULINEMIA + LAMINITIS RISK

🚨 Laminitis ⭐⭐⭐

This is the major clinical consequence.

Insulin dysregulation → prolonged/excessive hyperinsulinemia → lamellar dysfunction → ⭐ endocrinopathic laminitis

⚠ Your notes say hyperglycemia causes the lamellar damage. For the exam, if you want the more accurate key association, remember: HYPERINSULINEMIA → LAMINITIS

rather than hyperglycemia itself being the main mechanism.

🧠 EMS → HIGH INSULIN → HIGH LAMINITIS RISK

Clinical signs

• Adiposity: Can be Generalized obesity or ⭐ Regional adiposity. Typical locations:

→ Cresty neck: fat along neck crest

→ Tail head: abnormal fat deposits

Other: Prepuce, Under skin of trunk, Other regional deposits

• ⭐ LAMINITIS

Some horses may have insulin dysregulation without being generally obese.

🔬 Diagnosis

• Resting serum insulin: ⭐ Important screening test.

• Dynamic testing: Combined glucose-insulin test → assesses insulin/glucose regulation.

💊 Treatment of EMS ⭐⭐⭐

1. MANAGEMENT — MOST IMPORTANT

Weight loss

For obese horses: → controlled reduction of body condition.

Diet

• ⭐ Restrict pasture access

• Low sugar, Low starch, Reduce non-structural carbohydrates

• Appropriate forage management

Exercise

⭐ Regular exercise when safe.

⚠ Do not exercise a horse with active painful laminitis until appropriately managed.

🧠 EMS Tx = DIET + WEIGHT LOSS + EXERCISE

2. Medical treatment

For selected horses not responding adequately to management:

• Metformin

→ lowers blood glucose
→ improves insulin sensitivity/metabolic control.

Levothyroxine sodium

→ promotes weight loss
→ can improve insulin sensitivity in obese horses.

But remember:

⭐ Medication does not replace dietary/management changes.

🔥 PPID vs EMS — VERY IMPORTANT

	PPID	EMS
Typical horse	⭐ Older horse	Often younger/middle-aged “thrifty” horse
Main problem	Pituitary pars intermedia dysfunction	⭐ Insulin dysregulation
Hair coat	⭐ Hypertrichosis	Usually normal
Body condition	Muscle wasting ± abnormal fat	⭐ Obesity/regional adiposity common
Cresty neck	Can occur	⭐ Common
Laminitis	⭐ Common	⭐ Common
PU/PD	Common	Not classic unless marked metabolic disturbance
Main diagnostic test	⭐ ACTH / TRH stimulation	⭐ Insulin testing
Main treatment	⭐ Pergolide	⭐ Diet + weight loss + exercise

🧠 Easy distinction

OLD + HAIRY → PPID

FAT/CRESTY + HIGH INSULIN → EMS

BOTH → LAMINITIS

🟠 4. HYPOADRENOCORTICISM

Also called:

• Adrenal insufficiency → “Steroid let-down syndrome” → insufficient adrenal corticosteroid activity.

Treatment

⭐ Prednisolone

🧠 HYPOADRENOCORTICISM → CORTICOSTEROID REPLACEMENT

🦋 5. HYPOTHYROIDISM

True primary hypothyroidism is uncommon in adult horses.

Clinical sign from your lecture

⭐ Goitre

Treatment

⭐ Levothyroxine sodium → thyroid hormone supplementation.

🧠 HYPOTHYROIDISM → GOITRE → LEVOTHYROXINE

🔥 EXAM STRUCTURE FOR Q22

Start with the two important diseases:

1⃣ PPID

Old horse → pars intermedia → ↑ ACTH → hypertrichosis + laminitis + PU/PD → ACTH/TRH → PERGOLIDE

2⃣ INSULIN RESISTANCE

↓ tissue response to insulin → compensatory hyperinsulinemia

3⃣ EMS

Thrifty horse → regional adiposity + insulin dysregulation → LAMINITIS → insulin testing → DIET + WEIGHT LOSS + EXERCISE

Then briefly mention:

Diabetes → rare → hyperglycemia + glucosuria + PU/PD

Hypoadrenocorticism → prednisolone

Hypothyroidism → goitre → levothyroxine

🧠 Final memory line

PPID = OLD + HAIRY → ACTH → PERGOLIDE

EMS = CRESTY/FAT + HIGH INSULIN → LAMINITIS → DIET/EXERCISE

DIABETES = RARE

HYPOADRENOCORTICISM = PREDNISOLONE

HYPOTHYROIDISM = GOITRE → LEVOTHYROXINE

Equine myopathies

Main conditions:

1. ⭐ Exertional rhabdomyolysis — “Monday morning disease”

2. ⭐ Polysaccharide storage myopathy — PSSM

3. ⭐ Hyperkalemic periodic paralysis — HYPP

4. Post-anesthetic myopathy/myoneuropathy

5. Nutritional myopathy — Vit E/Se deficiency

6. Sweeney shoulder — suprascapular nerve damage

🔬 1. DIAGNOSTIC APPROACH TO THE MUSCULAR SYSTEM

Physical examination

1. Inspection

• Symmetry, Size, Shape of muscle groups, Muscle wasting/atrophy

2. Palpation

• Muscle tone, Sensitivity/pain, Asymmetry, Atrophy, Swelling, heat

3. Gait

• Walk the horse and look for: Lameness, Weakness, Stiffness, Pain, Reluctance to move

🩸 Clinical pathology ⭐⭐⭐

Three important muscle enzymes:

1. ⭐ CK — Creatine kinase/creatine phosphokinase/CPK.

Found mainly in:

• Skeletal muscle, Cardiac muscle

Muscle damage → ↑ CK

⚠ Training, transport and exercise can cause mild increases.

🧠 CK = sensitive indicator of RECENT muscle damage

2. LDH — Lactate dehydrogenase

• Not tissue-specific, Found in: Muscle, Liver, Erythrocytes

• → can increase with muscle damage, but not specific.

3. AST — Aspartate aminotransferase

• High activity in Skeletal muscle, Liver, Erythrocytes

• → ↑ with muscle damage but also other tissue injury.

🧠 MYOPATHY BLOODWORK = CK + AST + LDH

🔬 Muscle biopsy

Percutaneous biopsy commonly from:

• ⭐ Gluteus medius

• Semitendinosus
  → sample normal and abnormal muscle where appropriate.

• Useful for diagnosing structural/metabolic myopathies.

⚡ Electromyography — EMG

• Used to investigate: ⭐ Neuromuscular disease

🏇 2. EXERTIONAL RHABDOMYOLYSIS ⭐⭐⭐

Also called:

• Paralytic myoglobinuria

• Monday morning disease

• “Tying-up”

Classical presentation:

Horse in training → rested for >1 day, BUT continues receiving a full/high-carbohydrate diet → returned to exercise → develops painful muscle disease.

🧠 REST + FULL GRAIN → EXERCISE → TYING-UP

Etiology

• ⭐ Dietary imbalance

• Overexertion

• Defects in intracellular Ca²⁺ regulation

• Breed predisposition

Different underlying myopathies can produce exertional rhabdomyolysis.

Pathogenesis

• During rest + high carbohydrate feeding → ↑ glycogen storage in muscles

• During exercise → increased energy demand → muscle metabolic dysfunction/injury → muscle fiber damage → intracellular contents released.

• One very important product: ⭐ MYOGLOBIN

• Muscle damage → myoglobin enters blood → filtered by kidneys → myoglobinuria → urine can become dark/red-brown.

• Severe muscle damage/dehydration: → risk of acute kidney injury

• Your lecture also describes accumulation of lactic acid causing muscle irritation, pain and damage.

For the exam, the safest core pathway is:

• Exercise → muscle fiber injury/rhabdomyolysis → CK/AST ↑ + myoglobin release → myoglobinuria ± renal injury

Clinical signs ⭐⭐⭐

Severity is variable:

• ⭐ Stiff gait, Reluctance to move, Painful muscles, Sweating

• Tachycardia, Tachypnea

• Pyrexia

• Muscle cramping,

• Dark urine/myoglobinuria in severe cases

🧠 TYING-UP = PAINFUL + STIFF AFTER EXERCISE

Diagnosis

• Clinical signs/history

• ⭐ ↑ CK, ↑ AST, ↑ LDH

• ⭐ Myoglobinuria

• Fluid abnormalities

• Electrolyte abnormalities

💊 Treatment

Goals:

1. ⭐ Limit further muscle damage

2. Maintain fluid balance

3. Correct electrolytes

4. ⭐ Prevent renal damage/failure

5. Control pain

Mild cases:

• Phenylbutazone OR flunixin meglumine

• Acepromazine

• Rest

• Vitamin E + Selenium

Acepromazine:
→ sedation + vasodilation → may help reduce anxiety/stiffness.

Severe cases:

• ⭐ IV fluids

• Corticosteroids, Phenylbutazone

• Xylazine

• Rest — 6–8 weeks

⚠ Return to exercise should depend on the cause and clinical/biochemical recovery rather than automatically applying the same 6–8 week period to every rhabdomyolysis case.

Prevention ⭐⭐⭐

• Appropriate exercise management

• Avoid sudden exercise after prolonged rest

• ⭐ High-fat, low-starch diet

• Adapt carbohydrate intake to workload

🧠 RHABDO PREVENTION = REGULAR EXERCISE + ↓ STARCH + ↑ FAT

🧬 3. POLYSACCHARIDE STORAGE MYOPATHY — PSSM ⭐⭐⭐

PSSM is an important cause of:

• ⭐ Exertional rhabdomyolysis

Predisposed breeds:

• ⭐ Quarter Horses, Draft horses, Warmbloods

Pathogenesis

Abnormal muscle carbohydrate/glycogen metabolism/storage → abnormal accumulation of glycogen/polysaccharide in skeletal muscle → predisposition to muscle dysfunction → exertional rhabdomyolysis.

Clinical signs

Similar to exertional rhabdomyolysis:

• Muscle stiffness, Pain, Reluctance to move

• Exercise intolerance, Episodes of tying-up

Treatment/management ⭐⭐⭐

Key nutritional principle:

⭐ SUPPLEMENT FAT — NOT SUGAR

→ reduce starch/sugar intake
→ use fat as alternative energy source
→ regular controlled exercise.

🧠 PSSM = POLYSACCHARIDE STORAGE → TYING-UP → LOW STARCH + HIGH FAT

⚡ 4. HYPERKALEMIC PERIODIC PARALYSIS — HYPP ⭐⭐⭐

• Inherited muscle disorder particularly associated with: ⭐ Quarter Horses

Characterized by intermittent episodes of:

• Muscle tremors, Weakness, Possible collapse

Pathogenesis ⭐⭐⭐

HYPP is a disorder of skeletal muscle sodium channels (Na+)

Abnormal ion movement → excessive/persistent sodium influx → abnormal membrane depolarization → muscle fiber excitability → fasciculations/tremors, followed by:
→ weakness ± paralysis.

🧠 HYPP = Na⁺ CHANNEL DEFECT → ABNORMAL DEPOLARIZATION → TREMOR + WEAKNESS

Clinical signs

Often begins in relatively young horses.

• ⭐ Recurrent episodes

• Muscle fasciculations/tremors, Weakness, Collapse, Possible recumbency

• Between attacks: → horse may appear normal.

Diagnosis ⭐⭐⭐

• DNA test: ⭐ Genetic test for HYPP mutation. Very important.

• Clinical signs, Signalment/history

• Potassium chloride challenge test: → administer KCl → provoke clinical signs.

⚠ This is historical and potentially dangerous; genetic testing is the key diagnostic method to remember!

Treatment

Mild attack

Horse trembling but not recumbent:

• Light exercise, Feed grain, ⭐ Acetazolamide

Severe attack

Recumbency:

• IV catheter/access

• ⭐ Calcium gluconate

If insufficient response, lecture lists:

• Sodium bicarbonate, Dextrose

These help stabilize membrane excitability and/or shift potassium intracellularly.

🧠 HYPP Dx = DNA; Tx = ACETAZOLAMIDE / severe → IV therapy

🛏 5. POST-ANESTHETIC MYOPATHY / MYONEUROPATHY ⭐⭐⭐

Pathogenesis

• During prolonged anesthesia: Body weight + immobility → prolonged muscle compression → ↓ blood flow → ⭐ ischemia + hypoperfusion → muscle injury/necrosis.

• Large, heavy, well-muscled horses are especially susceptible.

🧠 ANAESTHESIA → PRESSURE → ISCHEMIA → MUSCLE DAMAGE

Muscles commonly affected

• Triceps, Quadriceps, Hindlimb extensors, Longissimus, Masseter, Gluteal muscles

Position matters ⭐⭐⭐

• Lateral recumbency → Triceps, Deltoid, Dependent hindlimb muscles

• Dorsal recumbency → Longissimus, Gluteal muscles

Clinical signs

1. Localized

• Affected muscle may be ⭐ Hard OR flaccid, Hot, Painful, Swollen

Horse may:

• Be weak, Have difficulty standing, Be unable to stand

2. Generalized

• Weakness, Paresis, Restlessness, Anxiety, Sweating, Colic-like signs

Diagnosis

• Important history: ⭐ Recent/prolonged general anesthesia

Plus:

• Clinical signs

• ↑ CK, ↑ AST, ↑ LDH

Treatment

Mild

• Phenylbutazone OR flunixin

• Dimethyl sulfoxide — DMSO

Severe

• NSAIDs, Xylazine, Butorphanol, Acepromazine

• ⭐ Fluid therapy

• Mannitol

Also supportive nursing and assistance with standing where appropriate.

🍃 6. NUTRITIONAL MYOPATHY

⭐ Vitamin E + selenium deficiency

These are important antioxidant nutrients.

Deficiency:

→ oxidative muscle damage → myopathy.

🧠 NUTRITIONAL MYOPATHY = ↓ VIT E + ↓ Se

🦴 7. SWEENEY SHOULDER

This was also covered in Q21 — peripheral nerve disorders.

Cause

Damage to:

⭐ SUPRASCAPULAR NERVE

→ denervation/atrophy of:

• M. supraspinatus

• M. infraspinatus

→ prominent scapular spine

= ⭐ Sweeney shoulder

🧠 SWEENEY = SUPRASCAPULAR NERVE → SUPRA + INFRA ATROPHY

🔥 EXAM DIFFERENTIATION

Disease	Key association
Exertional rhabdomyolysis	⭐ Exercise → painful stiff muscles + ↑ CK ± myoglobinuria
PSSM	⭐ Abnormal glycogen/polysaccharide storage → tying-up
HYPP	⭐ Quarter Horse + Na⁺ channel defect → episodic tremor/weakness
Post-anesthetic myopathy	⭐ Compression/ischemia after GA
Nutritional myopathy	⭐ Vitamin E + Se deficiency
Sweeney shoulder	⭐ Suprascapular nerve → supra/infraspinatus atrophy

🧠 Final memory

RHABDO = EXERCISE → MUSCLE BREAKDOWN → CK ↑ + MYOGLOBINURIA

PSSM = GLYCOGEN/POLYSACCHARIDE → LOW STARCH + HIGH FAT

HYPP = QUARTER HORSE + Na⁺ CHANNEL → TREMORS/WEAKNESS → DNA TEST

POST-ANAESTHETIC = PRESSURE → ISCHEMIA

NUTRITIONAL = VIT E + Se DEFICIENCY

SWEENEY = SUPRASCAPULAR NERVE

Hepatopathies and intoxications

Main parts:

1. ⭐ Diagnostic approach to liver disease

2. General treatment of liver failure

3. Theiler's disease

4. Chronic active hepatitis

5. Cirrhosis/fibrosis

6. Cholangiohepatitis + biliary calculi

7. Tyzzer's disease

8. Liver flukes

9. ⭐ Important intoxications

🔬 1. DIAGNOSTIC APPROACH TO HEPATOPATHIES

History

• Age

  • Foals → congenital/neonatal diseases

  • Older horses → chronic/fibrotic disease

• Single vs multiple animals affected

  • Multiple → think toxicosis/feed problem or infectious/parasitic disease

• Duration, Progression, Feed/pasture, Drugs/treatments, Exposure to toxic plants

🩸 Laboratory diagnosis ⭐⭐⭐

A. Hepatocellular damage

Enzymes associated with hepatocellular injury:

• ⭐ GLDH — glutamate dehydrogenase

• SDH — sorbitol dehydrogenase

• LDH — lactate dehydrogenase

• AST — aspartate aminotransferase

🧠 HEPATOCYTES → GLDH + SDH

B. Biliary tract damage / cholestasis

Important enzymes:

• ⭐ GGT — gamma-glutamyl transferase

• ALP/AP — alkaline phosphatase

🧠 BILE DUCT → GGT + ALP

C. Liver function

With impaired liver function:

• ⭐ ↑ Direct/conjugated bilirubin

• ⭐ ↑ Serum bile acids

• ↑ Blood ammonia

• ↓ Albumin

• ↓ Urea production

• Hypoglycemia can occur

• ↑ Triglycerides/cholesterol may occur

⚠ Your notes have both “decreased blood urea” and “increased BUN.” With true severe hepatic insufficiency, urea synthesis can decrease, while BUN can vary with hydration, renal function, protein metabolism, etc. For the exam, remember ↓ urea synthesis as the direct liver-function concept.

🩸 Clotting function

The liver synthesizes many clotting factors.

Liver failure:

→ impaired coagulation

→ ⭐ prolonged prothrombin time — PT

🔬 Liver biopsy ⭐⭐⭐

Used to determine:

• Fibrosis, Inflammation, Type of lesion, Distribution/location of disease, Severity/prognosis

🧠 BIOPSY = WHAT TYPE + HOW MUCH FIBROSIS?

💻 Ultrasound

Liver can be examined mainly on the right side, caudal/ventral to the lung field, approximately: 6th–15th intercostal spaces

Can identify:

• Abscesses, Masses, ⭐ Choleliths, Biliary sludge, Dilated bile ducts, Chronic fibrosis, Hepatomegaly

2. GENERAL TREATMENT OF LIVER FAILURE

Treatment is primarily:

⭐ SUPPORTIVE + TREAT UNDERLYING CAUSE

• Fluid therapy

• IV balanced electrolyte solutions as appropriate.

Correct:

• Dehydration, Electrolyte abnormalities, Glucose abnormalities, Acid-base disturbances

🧠 Hepatic encephalopathy

Liver failure → inadequate detoxification of ammonia → ↑ blood ammonia → CNS dysfunction → hepatic encephalopathy

Methods to reduce intestinal ammonia production/absorption:

• Lactulose, Neomycin, Mineral oil, Vinegar/acidification in older lecture protocols

🧠 LIVER FAILURE → ↑ NH₃ → BRAIN → HEPATIC ENCEPHALOPATHY

🟠 3. ACUTE HEPATIC NECROSIS — THEILER'S DISEASE ⭐⭐⭐

• Theiler´s disease = Acute/peracute severe hepatic necrosis resulting in ⭐ Acute liver failure

• Historically also called serum hepatitis.

Etiology

• Unknown

• Classically, there may be a history of ⭐ Tetanus antitoxin 4–10 weeks previously

So the exam association is:

HORSE + TETANUS ANTITOXIN WEEKS AGO + ACUTE LIVER FAILURE → THEILER'S DISEASE

Clinical signs

Peracute liver failure:

• ⭐ Hepatic encephalopathy

• Icterus, Depression/neurological signs, Red/discolored urine, Rapid deterioration

Diagnosis

• History, Acute onset

• ⭐ ↑ liver enzymes, Liver function abnormalities

• Histopathology

🧠 THEILER = ANTITOXIN HISTORY → PERACUTE NECROSIS → ICTERUS + ENCEPHALOPATHY

🟠 4. CHRONIC ACTIVE HEPATITIS ⭐⭐⭐

= Chronic, active, progressive inflammatory liver disease

• Can eventually progress to → fibrosis, liver failure, major CNS involvement/hepatic encephalopathy, death.

• Lesion location: ⭐ Often periportal

Etiology

• Not fully determined. Possible: ⭐ Immune-mediated/autoimmune mechanism

Clinical signs

Often intermittent/nonspecific:

• Depression, ⭐ Weight loss, variable icterus, Recurrent/intermittent signs

Diagnosis

Laboratory

• ⭐ ↑ GGT, ↑ ALP, ↑ Bilirubin

• Bilirubin in urine — from your lecture

• Leukocytosis, Monocytosis, ↑ Total plasma protein

Liver biopsy

Important to assess:

• Inflammation, Fibrosis, Distribution

Treatment

• Supportive care, Plus lecture corticosteroid protocol:

• Dexamethasone
  → approximately 5 days → gradually reduce over ~10 days → change to oral prednisolone for ~5 weeks.

🧠 CHRONIC ACTIVE HEPATITIS = PROGRESSIVE INFLAMMATION → PERIPORTAL → SUPPORT + CORTICOSTEROIDS

🟤 5. CIRRHOSIS / HEPATIC FIBROSIS

End-stage consequence of:

→ hepatocyte death, chronic inflammation, ⭐ extensive fibrosis.

Liver architecture becomes distorted:

• Depressed fibrous bands, Alternating regenerative nodules of parenchyma

Clinical signs

Most characteristic:

⭐ Chronic progressive weight loss

Later:

• Icterus, Hepatic encephalopathy, Other signs of liver failure

Diagnosis

⭐ Liver biopsy → determines degree of fibrosis.

Treatment

❌ Fibrosis cannot generally be reversed once advanced, → supportive treatment only.

Prognosis

🔴 Poor

🧠 CIRRHOSIS = END-STAGE FIBROSIS → BIOPSY → POOR PROGNOSIS

🦠 6. CHOLANGIOHEPATITIS + BILIARY CALCULI ⭐⭐⭐

Importance

• ⭐ One of the most important/common biliary tract diseases in horses.

Pathogenesis:

• Probably starts as Cholangitis ( inflammation/infection of bile ducts) → extends into liver → Cholangiohepatitis

Chronic disease may be associated with:

• ⭐ Intrahepatic biliary calculi

• ⭐ Extrahepatic biliary calculi

Severe cases:

→ suppurative inflammation, → bridging fibrosis.

Clinical signs

Nonspecific:

• Fever, ⭐ Icterus, Weight loss, Hepatic encephalopathy

Diagnosis

Ultrasound

Look for:

• Choleliths, Dilated bile ducts, Biliary abnormalities

Laboratory

• ⭐ ↑ GGT, ↑ ALP, ↑ Bilirubin

• Hematological inflammatory changes

Treatment

⭐ Long-term antibiotics

Preferably: → based on bacterial culture + sensitivity

🧠 CHOLANGIOHEPATITIS = BILE DUCT INFECTION → GGT ↑ + ICTERUS → LONG-TERM ATB

🐴 7. TYZZER'S DISEASE ⭐⭐⭐

= ⭐ Acute, highly fatal hepatitis of foals

Etiology

Correct key organism: ⭐ Clostridium piliforme
(now commonly called Clostridium piliforme; historically Bacillus piliformis)

⚠ Your notes also list Clostridium perfringens, but Tyzzer's disease specifically = C. piliforme.

Transmission

Spores in environment → fecal-oral → infection → severe hepatic disease/necrosis.

Clinical signs

Acute onset:

• Depression, Anorexia, Recumbency, Ataxia, ⭐ Icterus, Fever, Often rapid death

Diagnosis

• ⭐ Liver biopsy/histopathology

• PCR

Treatment

• Lecture: IV penicillin

But: ⚠ Disease progresses rapidly, so treatment is often unsuccessful.

🧠 TYZZER = FOAL + C. PILIFORME + ACUTE FATAL HEPATITIS

🪱 8. LIVER FLUKE

Rare in horses.

Etiology

Trematodes:

• ⭐ Fasciola hepatica, Fasciola gigantica

• IH: ⭐ Snail

🔄 Life cycle

• Adult flukes in bile ducts → eggs passed in feces → miracidium develops/hatches → penetrates snail → develops through larval stages → cercariae leave snail → attach to vegetation and become metacercariae → horse eats contaminated vegetation → larvae released in intestine → penetrate/migrate to liver → young flukes tunnel through liver tissue → after approximately 8 weeks, enter bile ducts → mature adults.

🧠 FASCIOLA = SNAIL → GRASS/METACERCARIA → INTESTINE → LIVER → BILE DUCT

Clinical signs

• Fever, ⭐ Icterus, Weight loss

Diagnosis

• Coprology:⭐ Sedimentation, because trematode eggs are heavy.

• Blood: May have increased: SDH, AST, ALP, LDH

• Serology → ELISA

Treatment

Your lecture lists:

• ⭐ Triclabendazole

• Praziquantel

• Snail control

For your exam, triclabendazole is the drug I would strongly associate with Fasciola.

🧠 LIVER FLUKE → SEDIMENTATION → TRICLABENDAZOLE

☠ 9. INTOXICATIONS

Important groups:

1. ⭐ Pyrrolizidine alkaloids

2. Castor bean

3. Maple

4. Cyanogenic plants

5. Organophosphates/carbamates

6. ⭐ Mycotoxins

🌿 A. PYRROLIZIDINE ALKALOID TOXICITY ⭐⭐⭐

Plants

Lecture lists:

• ⭐ Ragwort, Fiddleneck, Rattleweed, Hound's tongue, “Salivation Jane” in your notes

Pathogenesis

Repeated ingestion over: ⭐ weeks → months

→ cumulative hepatotoxicity → progressive hepatocyte damage → fibrosis/liver failure → hepatic encephalopathy.

Clinical signs

• ⭐ Weight loss, Inappetence, Liver failure, ⭐ Hepatic encephalopathy

🧠 PYRROLIZIDINE = CHRONIC PLANT INGESTION → LIVER DAMAGE → ENCEPHALOPATHY

🌱 B. CASTOR BEAN

Seeds contain ⭐ RICIN, Highly toxic.

Clinical signs

• Incoordination, Sweating, Muscle spasms, Tachycardia, Tachypnea

• Diarrhea, Colic, Convulsions, Shock

Severe poisoning → rapid death, potentially within approximately 35 hours according to your lecture.

🧠 CASTOR BEAN = RICIN → SEVERE GI + SYSTEMIC TOXICITY/SHOCK

🍁 C. MAPLE TOXICITY ⭐⭐⭐

Certain maple exposure can cause severe oxidative damage to RBCs.

→ ⭐ Methemoglobinemia
→ Heinz body formation
→ hemolysis

Clinical signs

• Icterus, ⭐ Cyanosis, Respiratory distress, Weakness

Treatment

Your lecture:

⭐ Methylene blue

🧠 MAPLE → RBC OXIDATION → METHEMOGLOBIN + HEINZ BODIES

☠ D. CYANOGENIC GLYCOSIDES ⭐⭐⭐

Plants

Lecture:

• Hydrangea, Flax, Cherry, Sudan grass

Contain cyanogenic glycosides.

Pathogenesis

Glycosides → release hydrogen cyanide (HCN) → ⭐ inhibits cytochrome c oxidase → cells cannot effectively utilize oxygen → histotoxic hypoxia → rapid respiratory/cellular failure.

Clinical signs

• ⭐ Dyspnea, Ataxia, Trembling, Recumbency, Rapid death, Respiratory arrest

Treatment

Lecture:

⭐ IV sodium nitrite + sodium thiosulfate

🧠 CYANIDE = BLOCKS CYTOCHROME OXIDASE → TISSUES CAN'T USE O₂

🧪 E. ORGANOPHOSPHATES + CARBAMATES ⭐⭐⭐

• AChE — acetylcholinesterase inhibitors

Pathogenesis

Inhibit:

⭐ ACETYLCHOLINESTERASE → acetylcholine accumulates → excessive cholinergic stimulation → muscarinic + nicotinic signs.

Clinical signs

• Colic, Diarrhea, Dyspnea, Convulsions

• ⭐ Hypersalivation

• Sweating, Muscle tremors

• ⭐ Miosis, Weakness

Your lecture also associates carbamates with methemoglobinemia/cyanosis.

Diagnosis

• EDTA blood

• ⭐ Measure cholinesterase activity

• Examine:

  • GI contents, Liver, Feed

Treatment

⭐ Atropine sulfate

Lecture says “alloxine”; this almost certainly refers to an oxime, such as:

⭐ Pralidoxime (2-PAM)

particularly relevant for organophosphate poisoning.

🧠 ORGANOPHOSPHATE = AChE ↓ → ACh ↑ → CHOLINERGIC SIGNS → ATROPINE + OXIME

🍄 F. MYCOTOXICOSIS ⭐⭐⭐

= Toxicity caused by toxins produced during fungal/mould growth

Etiology

• Ingestion of: Contaminated grains, Contaminated forage containing fungal toxic metabolites.

Effects

• Damage liver

• Impair metabolism

• Impair nutrition

• Affect endocrine/exocrine systems

• ↓ Growth, ↓ Feed efficiency

• ⭐ Suppress immunity

• Alter microorganisms

• Irritate/ulcerate mucous membranes and skin

  • Stomatitis, Hyperkeratosis

🍄 FUMONISIN ⭐⭐⭐

Very important in horses. Neurotoxic

Clinical signs:

• Anorexia, ⭐ Ataxia, Blindness, ⭐ Head pressing, Depression, Seizures

🧠 FUMONISIN = BRAIN → ATAXIA + BLINDNESS + HEAD PRESSING

🍄 AFLATOXIN

Mainly:

⭐ Hepatotoxic

Can cause:

• Liver dysfunction, Icterus, Neurological signs secondary to severe hepatic dysfunction.

🧠 AFLATOXIN = LIVER

Diagnosis of mycotoxicosis

Often nonspecific.

Use:

• Clinical signs, History

• ⭐ Analysis of feed

• Removal/change of suspect feed, Improvement after feed change supports suspicion

Treatment

• ⭐ Remove ALL contaminated feed

• Supportive therapy, Replace with safe feed

• Lecture: add adsorbent/binding agents to feed

🔥 EXAM SUMMARY

Disease/toxin	⭐ Key association
Theiler's disease	Tetanus antitoxin weeks earlier → acute hepatic necrosis
Chronic active hepatitis	Progressive inflammation → periportal disease
Cirrhosis	End-stage fibrosis → poor prognosis
Cholangiohepatitis	GGT ↑ + biliary inflammation/calculi
Tyzzer's	Foal + C. piliforme + fatal hepatitis
Fasciola	Snail → liver → sedimentation → triclabendazole
Pyrrolizidine	Chronic plant ingestion → liver failure
Castor bean	Ricin
Maple	Methemoglobin + Heinz bodies
Cyanide	Cytochrome oxidase inhibition
Organophosphate	AChE inhibition → atropine + oxime
Fumonisin	⭐ Neurological disease
Aflatoxin	⭐ Hepatotoxicity

🧠 Final memory line

GLDH/SDH = HEPATOCYTES; GGT/ALP = BILE DUCTS

THEILER = ACUTE NECROSIS

CIRRHOSIS = FIBROSIS

TYZZER = FOAL

FASCIOLA = SNAIL

PYRROLIZIDINE + AFLATOXIN = LIVER

FUMONISIN = BRAIN

CYANIDE = CELLS CAN'T USE O₂

ORGANOPHOSPHATE = TOO MUCH ACh

Foal diseases: infectious and parasitic

For the exam, divide them into:

1. Bacterial

• ⭐ Rhodococcus equi

• Neonatal salmonellosis

• Septic arthritis + osteomyelitis

• Bacterial pneumonia

• ⭐ Tyzzer's disease

• Bacterial causes of diarrhea

2. Viral

• Adenovirus

• EHV-1

• EVA

• ⭐ Rotavirus

• Coronavirus / parvovirus

3. Parasitic

• ⭐ Parascaris equorum

• ⭐ Strongyloides westeri

• Eimeria leuckarti

🦠 1. BACTERIAL DISEASES

A. RHODOCOCCUS EQUI ⭐⭐⭐

• One of the most important causes of severe pneumonia in foals!

• Typical age: ⭐ 1–4 months

Pathogenesis

• Primarily causes:→ pyogranulomatous pneumonia → ⭐ lung abscesses

• Can disseminate and cause extrapulmonary disease, including:

→ ⭐ Polysynovitis

→ Diarrhea/intestinal lesions

→ Other abscesses

🧠 R. EQUI = 1–4 MONTH FOAL + PNEUMONIA + LUNG ABSCESSES

Clinical signs

• Lethargy, Fever, ⭐ Cough, Nasal discharge, Tachypnea, Dyspnea, Diarrhea, Colic, Weight loss

• Severe disease: → high mortality if untreated.

Diagnosis ⭐⭐⭐

• Tracheal aspirate / transtracheal wash → bacterial culture/PCR

• Ultrasound → detects peripheral pulmonary abscesses/consolidation.

• X-ray → pulmonary lesions/abscesses.

🧠 R. EQUI Dx = TRACHEAL SAMPLE + USG/X-RAY

Treatment

• Requires prolonged antimicrobial therapy.

Your lecture lists:

• ⭐ Azithromycin, Erythromycin

• Treatment may last ~2 months

• Penicillin + streptomycin — lecture alternative

Supportive:

• Expectorants, Bronchodilators, e.g. salbutamol, Mucolytics, NSAIDs

🧠 R. EQUI = LONG-TERM ANTIBIOTIC THERAPY

B. NEONATAL SALMONELLOSIS ⭐⭐⭐

Etiology/transmission

Mare may be an asymptomatic carrier

→ sheds Salmonella in feces → contaminates environment → foal exposed around birth.

Clinical signs

Your lecture emphasizes very early onset:

⭐ 12–72 hours after birth

• Severe watery diarrhea, Fever, Dehydration, Limb edema, Septicemia, Possible death

🧠 SALMONELLA = NEONATAL FOAL + EARLY WATERY DIARRHEA + SEPSIS

Diagnosis

• History, Clinical signs, CBC

• ⭐ Fecal culture/PCR as appropriate

• Blood culture if septicemia suspected

Treatment

• ⭐ IV fluids

• Antibiotics for septicemic foals, based on culture where possible

• Lecture: trimethoprim/sulfadiazine

• NSAIDs/supportive treatment

Prevention

⭐ Adequate colostrum / passive transfer

Plus:

• Clean mare, Clean foaling environment, Identify/manage carrier animals, Good hygiene

🦴 C. SEPTIC ARTHRITIS + OSTEOMYELITIS ⭐⭐⭐

• Joint and/or bone infection.

• Especially in: ⭐ Neonatal foals <30 days

• Often secondary to: Bacteremia/septicemia

Etiology

• E. coli, Actinobacillus, Klebsiella, Salmonella

Entry can occur through:

• ⭐ Intestine, Umbilicus, Lungs, Penetrating wounds → bacteremia → organisms localize in joints/bones.

Clinical signs

⭐ Sudden severe lameness

• Swollen joint, Pain, Fever, Depression, Anorexia

• Diarrhea/systemic septic signs

Diagnosis

Ultrasound

→ synovial effusion, → synovial membrane proliferation.

⭐ Joint aspiration

• Synovial fluid: Cloudy/turbid, ↓ viscosity, ↑ WBC, Fibrin/clots, Culture

Blood culture

→ especially septic foals.

X-ray

May demonstrate:

• Osteolysis, Sclerosis, Soft-tissue swelling

Treatment ⭐⭐⭐

⚠ EMERGENCY — rapid aggressive treatment is required to prevent irreversible cartilage/bone damage.

• Systemic antibiotics

  • Lecture: ampicillin

• Intra-articular antibiotics

  • Lecture: gentamicin

• ⭐ Regional limb perfusion with gentamicin

• Joint drainage/lavage

• Analgesia

🧠 FOAL + HOT SWOLLEN JOINT + LAMENESS = SEPTIC ARTHRITIS UNTIL PROVEN OTHERWISE

🫁 D. BACTERIAL PNEUMONIA

Etiology

• Often mixed infection.

• E. coli, Salmonella, Klebsiella, Citrobacter, Actinobacillus, Pasteurella, Streptococcus, Rhodococcus

Routes of infection

• Placenta/in utero, Aspiration during birth

• Umbilical infection → hematogenous spread

• ⭐ Inhalation

Clinical signs

• ⭐ Increased respiratory rate

• Fever, Cough, Nasal discharge, Depression, Dyspnea in severe cases

Diagnosis

• Auscultation → abnormal lung sounds

• ⭐ Ultrasound

• X-ray

• ⭐ Transtracheal aspirate/wash → cytology + culture

Treatment

⭐ Antibiotics based on culture/sensitivity

• supportive treatment.

🟡 E. TYZZER'S DISEASE ⭐⭐⭐

Definition

• Acute, highly fatal hepatitis of foals

Etiology

⭐ Clostridium piliforme

Spores in environment.

Transmission: → fecal-oral

⚠ As in Q24: C. perfringens can cause foal enterocolitis, but Tyzzer's disease specifically = C. piliforme.

Clinical signs

• Acute depression, Anorexia, Recumbency, Ataxia, ⭐ Icterus, Fever, Rapid deterioration/death

Diagnosis

• Liver biopsy/histopathology

• ⭐ PCR

Treatment

Lecture:

• IV penicillin

But treatment is often unsuccessful because disease progresses rapidly.

🧠 TYZZER = FOAL + C. PILIFORME + ACUTE FATAL HEPATITIS

💩 BACTERIAL CAUSES OF FOAL DIARRHEA

Know the list from your lecture:

• ⭐ E. coli

• Lawsonia intracellularis

• Salmonella

• Clostridium perfringens

• Rhodococcus equi

• Actinobacillus equi

🧠 FOAL DIARRHEA → E. COLI + SALMONELLA + CLOSTRIDIUM + LAWSONIA + RHODOCOCCUS + ACTINOBACILLUS

🦠 2. VIRAL DISEASES

A. ADENOVIRUS

Generally opportunistic.

Especially associated with:

• Foals, ⭐ Immunocompromised animals

Uncommon in normal healthy horses.

B. EHV-1

⭐ Important herpesvirus in foals.

Can cause:

• Respiratory disease, Abortion in mares, Neonatal disease, Neurological disease

→ See your Q10B for complete EHV notes.

C. EQUINE VIRAL ARTERITIS — EVA

Foals can become infected:

⭐ In utero

→ severe neonatal disease → high mortality.

See Q10B for complete EVA.

💩 D. ROTAVIRUS ⭐⭐⭐

Important cause of foal diarrhea.

Your lecture: ⭐ 2–5 months old

Clinical signs

• Fever, ⭐ Watery diarrhea, Dehydration

Diagnosis

• Rota test / fecal antigen testing

🧠 ROTAVIRUS = YOUNG FOAL + WATERY DIARRHEA + DEHYDRATION

Other viruses causing diarrhea

• Coronavirus

• Adenovirus

• Parvovirus

🪱 3. PARASITIC DISEASES

A. PARASCARIOSIS ⭐⭐⭐

Etiology

• Nematode: Parascaris equorum

• Large roundworm: → up to approximately 40 cm

• Location of adults:
  ⭐ Small intestine

Very common particularly in foals and young horses.

🔄 Life cycle

⭐ DIRECT

Important:

ENTERIC → HEPATIC → PULMONARY MIGRATION

Horse ingests infective egg → larvae hatch in intestine → penetrate intestinal wall → liver → lungs → migrate up respiratory tract → swallowed → return to small intestine → mature adults.

🧠 PARASCARIS = GUT → LIVER → LUNG → GUT

Clinical signs

During migration/adult infection:

• Inappetence, Poor growth, Fever

• ⭐ Cough

• Respiratory signs

• Pot-bellied appearance possible

• Severe burdens → intestinal obstruction/colic

Diagnosis

⭐ Coprology/fecal egg examination

Treatment

Your lecture emphasizes:

⚠ Anthelmintic resistance is important in Parascaris.

Resistance can occur particularly to:

• Macrocyclic lactones such as ivermectin

• Benzimidazoles in some populations

• Pyrantel in some populations

Treatment should therefore be based on appropriate parasite-control strategy and known efficacy.

⚠ I would not learn “require larger doses” as the solution to resistance. Increasing the dose is not the general answer to anthelmintic resistance.

🧠 PARASCARIS = YOUNG HORSE + LIVER/LUNG MIGRATION + RESISTANCE

🪱 B. STRONGYLOIDES WESTERI ⭐⭐⭐

Etiology

• Nematode: Strongyloides westeri

Location:
⭐ Duodenum/small intestine

Important association:

⭐ One of the earliest parasites to infect foals

Adult biology

Interesting exam point:

Only parasitic females occur in the horse.

In the environment:
→ free-living males + females can occur.

🔄 Life cycle

Can involve several routes.

1. Percutaneous / tracheal route

Infective L3 → penetrate skin → subcutaneous tissues → lymphatics/blood → ⭐ lungs → pharynx → coughed up + swallowed → intestine → adult female → eggs passed.

🧠 SKIN → LUNG → SWALLOW → GUT

2. Peroral infection

L3 ingested → penetrate GI mucosa → migrate → eventually reach intestine and mature.

3. Somatic/lactogenic route ⭐⭐⭐

Larvae can become arrested/hypobiotic in tissues of mare.

During pregnancy/lactation:

→ larvae reactivate → ⭐ transmammary/lactogenic infection → foal infected through milk.

Your lecture also mentions transplacental infection.

Most important association:

⭐ Lactogenic transmission from mare → foal

Clinical signs

Young foals:

• ⭐ Enteritis, Watery diarrhea

• Particularly early in life

• Weakness/dehydration if severe

🧠 STRONGYLOIDES = VERY YOUNG FOAL + MILK + WATERY DIARRHEA

Diagnosis

⭐ Coprology

Treatment

• Benzimidazoles, Ivermectin

🦠 C. EIMERIA LEUCKARTI

Etiology

Protozoan/coccidian: ⭐ Eimeria leuckarti

• Location: Small intestine

Primarily affects:
→ young horses/foals, generally up to around 1–1.5 years

Pathogenesis

Parasite develops/reproduces in intestinal epithelial cells

→ multiplication → cell destruction → intestinal inflammation.

Can cause:

• Catarrhal enteritis

• More severe/hemorrhagic inflammation of small intestine

Clinical signs

Often mild/subclinical, but your lecture lists:

• ⭐ Mild, watery diarrhea

• Anorexia

• Fever

• Weight loss

• Emaciation

• Jaundice

Diagnosis

⭐ Coprology

→ characteristic large coccidial oocysts.

Treatment

Your lecture:

❌ No established specific treatment

→ symptomatic/supportive therapy.

Lecture states:
→ recovery/healing may occur after 2–3 weeks.

🧠 EIMERIA LEUCKARTI = COCCIDIA + YOUNG HORSE + SMALL INTESTINE + OOCYSTS IN FECES

---

🔥 VERY IMPORTANT DIFFERENTIATION

Disease	Age/association	⭐ Key sign
Rhodococcus equi	1–4 months	Lung abscesses + pneumonia
Neonatal Salmonella	12–72 h in lecture	Severe watery diarrhea/sepsis
Septic arthritis	<30 days	Sudden lameness + swollen joint
Tyzzer's	Young foal	Acute fatal hepatitis + icterus
Rotavirus	Young foal	Watery diarrhea + dehydration
Parascaris	Older foals/young horses	Liver-lung migration + cough
Strongyloides	⭐ Very young foal	Early watery diarrhea + lactogenic transmission
Eimeria leuckarti	Up to ~1–1.5 yr	Usually mild intestinal coccidiosis

🧠 FINAL EXAM MEMORY

RHODOCOCCUS = 1–4 MONTHS → LUNG ABSCESSES

SALMONELLA = NEONATE → DIARRHEA + SEPSIS

SEPTIC ARTHRITIS = <30 DAYS → SWOLLEN JOINT

TYZZER = C. PILIFORME → FATAL HEPATITIS

ROTAVIRUS = WATERY DIARRHEA

PARASCARIS = GUT → LIVER → LUNG → GUT

STRONGYLOIDES = MILK → VERY YOUNG FOAL → DIARRHEA

EIMERIA = COCCIDIA → SMALL INTESTINE