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 eating

• Messy eating

• Halitosis = bad breath

• Quidding

• Productive cough

• Nasal reflux of: Saliva, Ingesta, Fluids

• Weight loss

🌾 What is QUIDDING?

Horse chews food → Forms 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

Why can esophageal disease cause nasal reflux?

Esophagus obstructed → Food + saliva cannot move toward stomach → Material returns cranially → Reaches pharynx → Enters nasopharynx → Comes from nostrils

🔎 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

🚨 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

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

🔍 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

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.

TRUE ➡ Involves all layers

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

8⃣ ESOPHAGEAL CYSTS

Two types:

• Inclusion cyst ➡ Squamous epithelial lining

• Duplication cyst

🩺 Clinical Signs

• Dysphagia, Regurgitation/reflux

🔎 Diagnosis

• Endoscopy, USG, X-ray

🧠 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

⭐ EXAM ESSENTIALS

Dysphagia

➡ Abnormal swallowing = clinical sign, not disease
➡ Causes: oral / pharyngeal / esophageal / systemic
➡️ Quidding = dropping/rejection of semi-chewed food
➡ Nasal reflux → think pharyngeal/esophageal dysfunction

Choke ⭐

➡ Acute esophageal obstruction
➡ Dry fibrous food absorbs saliva and expands
➡ Predisposed: cervical esophagus → thoracic inlet → diaphragmatic hiatus
➡ Food/saliva from nose + extended neck
➡ NG tube cannot pass
➡ Major complication = aspiration pneumonia
➡ Sedate alpha-2 + butorphanol
➡ Massage + lavage with water/saline
➡ ❌ NO OIL → aspiration → lipoid/granulomatous pneumonia
➡ IV fluids
➡ Esophagotomy if necessary

Megaesophagus

➡ ↓ Motility → dilation → food accumulation
➡ Friesian association
➡ Contrast X-ray
➡ Elevated feeding

Stricture

➡ Narrow lumen
➡ Often sequel to choke
➡ Inflammation → fibrosis → narrowing
➡ Contrast X-ray
➡ Balloon dilation / surgery

Rupture

➡ Saliva + food into neck tissues
➡ Severe infection/phlegmon

Diverticulum

➡ True = all wall layers

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-5EHV-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

Your lecture lists:

• H7N7

• H3N8

CS

Classic:

• Pyrexia

• Nasal discharge

• ⭐ Harsh, dry cough

• Weakness

Dx

• PCR

• ELISA

• Virus isolation

Tx

• Supportive

Prevention

💉 Vaccination

Your lecture: 2×/year

🧠 INFLUENZA = FEVER + HARSH DRY COUGH

---

🦠 6. EQUINE RHINOVIRUSEtiology

Picornaviridae → equine rhinovirus

Transmission

• Respiratory route

• Your lecture also lists 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

Your lecture: 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 infection

→ 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

Your lecture:

• CFT = complement fixation test

Tx

Your notes list antibiotics such as:

• 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

Your lecture lists:

• 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 / TETANUSEtiology

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

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.