Poultry exam part 3

35. Infectious and non-infectious diseases of the central nervous system in poultry - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

Non-infectious disease

1. Encephalomalacia (Crazy chick syndrome)

Etiology

• Deficiency of vitamin E (often also linked to selenium imbalance)

• Rancid feed (oxidized fats → destroys vitamin E)

Pathogenesis

• Vitamin E = antioxidant → protects neuronal membranes

• Deficiency → lipid peroxidation → neuronal damage

• Lesions:

  • Cerebellar edema, Hemorrhages, Liquefactive (colliquative) necrosis

Clinical signs

• Ataxia, imbalance, Falling over, rolling, Tremors, Paralysis

Diagnosis

• Feed history (poor-quality fats)

• Clinical signs + necropsy (cerebellar lesions)

Differential diagnosis

• Avian encephalomyelitis, Newcastle disease, Toxicities

Therapy

• Vitamin E ± selenium supplementation, Correct feed quality

Prevention

• Proper feed storage, Antioxidants in feed, Balanced nutrition

2. Thiamine deficiency (Vit B1)

Etiology

• Vitamin B1 deficiency

Pathogenesis

• Impaired carbohydrate metabolism → ↓ ATP in neurons → brain dysfunction

Clinical signs

• Incoordination, Opisthotonus (“stargazing”), Paralysis, Blue comb

Diagnosis

• Clinical signs + feed analysis

Therapy

• Vitamin B1 (injection or feed)

Prevention

• Balanced diet

3. Aflatoxicosis

Etiology: Aspergillus flavus

Signs

• Depression, Incoordination, Paralysis

Prevention

• Feed quality control (important!)

4. Lead intoxication

Signs

• “Stargazing”

• CNS disturbances

Infectious diseases

1. Botulism

Etiology

• Toxin from Clostridium botulinum

• Not contagious (intoxication, not infection)

Source

• Decaying organic matter

• Maggots (important in waterfowl)

Pathogenesis

• Neurotoxin blocks acetylcholine release → flaccid paralysis

Clinical signs

• Progressive paralysis, Unable to walk or fly, “Limber neck” (flaccid neck), Drowning in waterfowl, Mydriasis

Diagnosis

• Detection of toxin (serum, crop, GIT), Neutralization test

Differential diagnosis

• Newcastle disease. Marek’s disease, Trauma

Therapy

• Remove toxin source, Supportive care, Antitoxin (rarely used in poultry practice)

Prevention

• Proper carcass disposal, Clean water sources, Control of decaying material

2. Newcastle disease (ND)

Etiology

• Newcastle disease virus (Paramyxovirus)

Strains

• Velogenic (highly virulent)

• Mesogenic (moderate)

• Lentogenic (low virulence)

Transmission

• Direct contact (respiratory secretions, feces)

• Inhalation, ingestion

Pathogenesis

• Respiratory + nervous + digestive involvement

Clinical signs

• Velogenic

  • Severe respiratory distress

  • CNS signs: tremors, paralysis, torticollis

  • High mortality

  • Drop in egg production

• Mesogenic

  • Respiratory signs

  • ↓ egg production

• Lentogenic

  • Mild respiratory disease

Diagnosis

• Serology:

  • HA (hemagglutination), HI test, ELISA

Differential diagnosis

• Avian influenza, Infectious bronchitis, Avian encephalomyelitis

Therapy

• ❌ No treatment

Prevention

• Vaccination, Biosecurity

3. West Nile fever

Etiology

• West Nile virus

Transmission

• Mosquito vectors

Pathogenesis

• Neurotropic → encephalitis

Clinical signs

• Often subclinical in birds, but may include:

  • Tremors, Weakness, Paralysis, Convulsions, Death

Diagnosis

• Serology, PCR

Differential diagnosis

• Newcastle disease, Avian encephalomyelitis

Therapy

• ❌ No specific treatment

Prevention

• Mosquito control, Biosecurity

3. Avian encephalomyelitis (AE)

Etiology

• Avian encephalomyelitis virus

Transmission

• Vertical (egg), Horizontal

Pathogenesis

• Virus affects CNS → neuronal degeneration

Clinical signs

• Ataxia, Tremors (especially head/neck), Leg weakness, Recumbency → paralysis

• ↓ egg production in adults

Diagnosis

• Clinical signs (young chicks!), Histopathology (brain/spinal cord lesions), Virus isolation

Differential diagnosis

• Encephalomalacia, Newcastle disease, Marek’s disease

Therapy

• ❌ No treatment

Prevention

• Vaccination of breeders, Prevent vertical transmission

4. Fowl cholera (only partially relevant)

Etiology: Pasteurella multocida

• It can cause torticollis (CNS sign) due to otitis interna

But don’t overfocus—this is mainly systemic disease, not CNS.

🧾 Quick comparison (high-yield)

Disease	Type	Key sign	Special clue
Encephalomalacia	Non-infectious	Ataxia, falling	Vitamin E deficiency
Botulism	Toxin	Flaccid paralysis	Limber neck
Newcastle disease	Viral	Respiratory + CNS	High mortality (velogenic)
West Nile fever	Viral	Encephalitis	Mosquito transmission
Avian encephalomyelitis	Viral	Tremors in chicks	Vertical transmission

36. Infectious and non-infectious diseases of the peripheral nervous system in poultry - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

Non-infectious diseases

Curled-toe paralysis

Etiology

• Riboflavin (vitamin B2) deficiency

Pathogenesis

• Riboflavin → essential for oxidative metabolism

• Deficiency → degeneration of peripheral nerves (especially sciatic nerve)

Clinical signs

• Reduced growth rate, Weakness, reluctance to move, Diarrhea, Characteristic: inward curling of toes, Progressive symmetrical paresis

Diagnosis

• Clinical signs, Feed analysis

Differential diagnosis

• Marek’s disease, Toxic neuropathies

Therapy

• Vitamin B2 supplementation, Reversible if treated early

Prevention

• Balanced diet

Pantothenic acid deficiency (Vit B5)

• Causes peripheral neuropathy

• Classic DDx with riboflavin deficiency and Marek’s

• Etiology: Vit B5 deficiency

• Pathology: degeneration of myelinated peripheral nerves

• Clinical signs:

  • Ataxia

  • “Goose-stepping gait” ⭐

• Diagnosis: feed + signs

• Treatment: vitamin B complex

Organophosphate poisoning

Key mechanism

• Inhibits acetylcholinesterase → overstimulation of PNS + CNS

Clinical signs

• SLUD signs:

  • Salivation

  • Lacrimation

  • Urination

  • Defecation

• tremors, paralysis

Treatment

• Atropine!

Toxic neuropathies

• Lead, mercury, arsenic

Signs

• Weakness, Paralysis

Trauma/Neoplasia (non-viral)

• Tumors compressing peripheral nerves

2. Infectious diseases

Marek’s disease

Etiology

• Gallid alphaherpesvirus 2

Pathogenesis

• Virus infects lymphocytes → tumor formation

• Infiltration of peripheral nerves → enlargement + dysfunction

Clinical forms (important!)

1. Classical (neurolymphomatosis) ⭐

   • Asymmetrical paralysis (legs/wings) → split legs posture

   • Nerve enlargement (especially sciatic)

   • Crop dilation (vagus nerve involvement)

2. Acute form

   • Depression, paralysis, high mortality

3. Ocular form

   • Grey iris, Unequal pupils, Blindness

4. Cutaneous form

   • Nodules at feather follicles

5. Immunosuppression

   • T-cell damage → ↓ immunity

Clinical signs

• Asymmetrical paralysis ⭐, Weight loss, Tumors in organs

Diagnosis

• Enlarged peripheral nerves (especially sciatic)

• Lymphoid tumors in viscera

Differential diagnosis

• Lymphoid leukosis (older birds >14 weeks)

• Nutritional neuropathies (B2 deficiency)

Therapy

• ❌ No treatment

Prevention

• Vaccination (key control method)

Newcastle disease

Caused by Newcastle disease virus

• Mainly CNS, but can also cause paralysis affecting peripheral nerves

Botulism

Caused by Clostridium botulinum

• Toxin blocks neuromuscular transmission → flaccid paralysis (PNS effect)

🧾 Updated comparison table (PNS focus)

Disease	Type	Key signs	Distinguishing feature
Curled-toe paralysis	Nutritional	Symmetrical paresis, curled toes	Vit B2 deficiency
Pantothenic acid deficiency	Nutritional	Ataxia, goose-step gait	Demyelination
Marek’s disease	Viral	Asymmetrical paralysis	Enlarged sciatic nerve, tumors
Botulism	Toxic	Flaccid paralysis	Limber neck
Newcastle disease	Viral	Paralysis + systemic signs	Respiratory involvement
Organophosphate poisoning	Toxic	Tremors, paralysis, SLUD signs	AChE inhibition
Heavy metal toxicity	Toxic	Ataxia, neuropathy	Feed contamination
Trauma / neoplasia	Non-inf.	Nerve dysfunction	Mechanical damage

🎯 Key exam contrasts (VERY important)

• Symmetrical paralysis → nutritional (B2 deficiency)

• Asymmetrical paralysis → Marek’s disease ⭐

• Flaccid paralysis → botulism

• “Goose-stepping → pantothenic acid deficiency”

• “Cholinesterase inhibition → organophosphates”

37. Mycotoxicoses

🍄 Mycotoxicoses = disease caused by toxins produced by fungi growing in feed (especially grains).

👉 Important:

• Not infectious

• Often chronic + production losses (↓ weight gain, ↓ egg production, ↓ immunity)

🔹 Etiology (main fungi)

• Aspergillus flavus

• Penicillium viridicatum

• Fusarium species

• Claviceps species

Mechanism of action

Mycotoxins cause oxidative stress and lipid peroxidation → membrane damage and cell death.

• Inhibition of protein/DNA synthesis

• Disruption of cellular metabolism

General systemic effects:

• Immunosuppression ⭐

• Hepatotoxicity (liver damage)

• Nephrotoxicity

• Hematopoietic damage

• GIT disturbances

• Nervous signs

Main types of mycotoxicoses

1. Aflatoxicosis ⭐

Source

• Aspergillus, Penicillium

Target organ

• Liver (primary)

Pathogenesis

• Hepatotoxic + immunosuppressive

Clinical signs

• Depression, Inappetence, Ataxia, Convulsions, Opisthotonus, Death

Effects

• ↓ growth, ↓ egg production, Immunosuppression

2. Fusariotoxicosis

Toxins

• Trichothecenes

• Fumonisins

• Zearalenone

Target

• Digestive system + immune system

• Zearalenone → estrogenic effects

  • Reproductive disorders

  • ↓ hatchability

Clinical signs

• Feed refusal ⭐, Oral lesions (caustic effect), Dermatitis, Bone marrow suppression

3. Ochratoxicosis

Target organ

• Kidneys (nephrotoxic) ⭐

Clinical signs

• Poor growth, ↓ production, Immunosuppression, Hypothermia

4. Ergotism

Source

• Claviceps spp. (infected grains)

Effects

• Nervous system → convulsions

• Vascular system → vasoconstriction, gangrene

• Endocrine disruption

Pathogenesis (general)

• Toxins absorbed from GIT

• Cause:

  • Liver damage, Kidney damage, Immunosuppression, Nervous signs (in some toxins)

Clinical signs (general)

• Reduced growth, Poor feed efficiency, ↓ egg production, Immunosuppression, Neurological signs (ataxia, convulsions), Increased mortality

Diagnosis

Based on:

• History (moldy feed!) ⭐, Clinical signs, Necropsy

Confirmation:

• Detection of toxins (chromatography, lab tests)

Sampling sites

• Feed storage, Feeders, Recently dead birds

🔹 Differential diagnosis

• Nutritional deficiencies (Vit E, B1), Infectious diseases (e.g. Newcastle disease virus), Toxicities (heavy metals, pesticides)

🔹 Therapy

• ❗ Remove contaminated feed (most important), Replace with clean feed, Activated charcoal (limited use in practice), Supportive care

🔹 Prevention ⭐ (very important)

• Proper feed storage (dry, cool conditions), Avoid mold contamination, Good ventilation, Regular feed inspection

• Use of mycotoxin binders (adsorbents)

🧾 Quick comparison table

Toxin	Main target	Key sign
Aflatoxin	Liver	Immunosuppression, CNS signs
Fusariotoxins	GIT, immune	Feed refusal, oral lesions
Ochratoxin	Kidney	Poor growth
Ergot alkaloids	Nervous/vascular	Convulsions, gangrene

🎯 Exam tips

• “Most important = aflatoxicosis (liver + immunosuppression)”

• “Feed refusal → Fusarium toxins”

• “Kidney damage → ochratoxin”

• Always mention moldy feed + prevention

38. Aflatoxicosis, ochratoxicosis - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

AFLATOXICOSIS

Etiology

• Aspergillus flavus

• Aspergillus parasiticus

• Occurs in poorly stored feed (high moisture + temperature)

• Most susceptible: ducks, turkeys ⭐ highly sensitive

Pathogenesis

• Primary target: liver ⭐

• Effects:

  • Inhibition of protein synthesis

  • Immunosuppression

  • Mutagenic, carcinogenic, teratogenic

• Outcomes:

  • High dose → acute hepatocellular necrosis

  • Low dose → chronic liver damage + poor growth

• Acute → hepatocellular necrosis, death

• Chronic → ↓ growth, immunosuppression, hepatomegaly

Clinical signs

• ↓ feed intake, ↓ growth rate, ↓ egg production & hatchability, Depression, weakness, Hemorrhages

• In severe cases:

  • Ataxia, convulsions, Sudden death

👉 Note: vomiting is not typical in poultry (birds cannot vomit)

Lesions (important for diagnosis)

• Enlarged, pale or fatty liver, Hepatic necrosis, Visceral hemorrhages

Diagnosis

• History (moldy feed!) ⭐, Clinical signs, Necropsy findings

• Confirmation: toxin detection (chromatography)

Differential diagnosis

• Other mycotoxicoses

• Nutritional deficiencies (Vit E, B1)

• Infectious diseases (e.g. Newcastle disease virus)

• Heavy metal toxicity

Therapy

• ❗ Remove contaminated feed (most important), Replace with clean feed

• Mycotoxin binders (adsorbents)

• Supportive care

⚠ Amphotericin B is NOT standard for mycotoxicosis → don’t emphasize it in exams

Prevention ⭐

• Proper feed storage (dry, cool), Avoid mold growth, Feed inspection, Use of toxin binders, Good ventilation

OCHRATOXICOSIS

Etiology

• Caused by ochratoxin A (OTA)

• Produced by:

  • Penicillium viridicatum

  • Aspergillus ochraceus

Pathogenesis

• Primary target: kidney (nephrotoxic) ⭐

• Also affects:

  • Liver, Immune system, Bone marrow

  • Chronic cases → anemia

Mechanisms

• Inhibits protein synthesis, Causes oxidative damage, Alters calcium balance, Immunosuppression

Clinical signs

• ↓ growth and feed efficiency, ↓ egg production

• Hypothermia, Diarrhea, Weakness, depression

• Severe cases → death

Lesions

• Enlarged, pale kidneys ⭐, Possible liver changes, General poor condition

Diagnosis

• History (contaminated feed), Clinical signs, Necropsy

• Confirmation: toxin detection

Differential diagnosis

• Aflatoxicosis, Other nephrotoxic agents, Infectious diseases

Therapy

• Remove contaminated feed ⭐, Supportive therapy, Mycotoxin binders

👉 L-carnitine, vitamins, probiotics = supportive only

Prevention

• Same as aflatoxicosis:

  • Feed quality control, Proper storage, Ventilation, Use of adsorbents

Feed sources:

• Contaminated grains (corn, rice) ⭐

• Oil-rich feeds (e.g. peanuts)

🧾 🔥 High-yield comparison table

Feature	Aflatoxicosis	Ochratoxicosis
Main organ	Liver ⭐	Kidney ⭐
Key effect	Immunosuppression	Nephrotoxicity
Fungi	Aspergillus spp.	Aspergillus + Penicillium
Signs	↓ growth, hemorrhage	↓ growth, weakness
Special note	Carcinogenic	Affects coagulation

🎯 EXAM GOLD LINES

• “Aflatoxin primarily affects the liver and causes immunosuppression.” ⭐

• “Ochratoxin is mainly nephrotoxic.” ⭐

• “Diagnosis is based on history of moldy feed and toxin detection.”

• “Treatment = remove contaminated feed.”

previously asked questions:

• Aflatoxicosis sign: immunosuppression, hepatomegaly, fatty liver, poor growth, decreased production, haemorrhages. Biochemistry:↓ total protein, ↓ albumin, ↓ cholesterol

• Avoidance of aflatoxins in the field: cannot fully prevent, only control (storage, rapid drying, limits)

• Unit of mycotoxins in feed: ppb (parts per billion)

39. Other mycotoxicoses (fusariotoxicosis, F2- toxicosis, T2 - toxicosis) - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

Fusariotoxicosis

Caused by fungi of the genus Fusarium species producing several important toxins

🔬 Main toxin groups

1. Trichothecenes (T-2 toxin, DON) ⭐

Mechanism

• Inhibit protein synthesis

• Strong cytotoxic + immunosuppressive effect

Clinical signs

• Feed refusal ⭐, Oral necrosis and ulceration ⭐

• Dermatitis (skin lesions), Diarrhea, ↓ egg production, Immunosuppression (bone marrow damage)

2. Zearalenone (F-2 toxin) ⭐

Type

• Estrogenic mycotoxin

Effects

• Reproductive disorders ⭐, Oviduct enlargement, ↓ egg production, Infertility, Poor eggshell quality

3. Fumonisins

• Poor feed conversion

• No clear lesions in poultry

• High doses → skeletal disorders (turkeys)

4. Moniliformin

• Cardiotoxic + nephrotoxic

• Sudden death possible in severe cases

🧠 General clinical signs (Fusariotoxicosis)

• Feed refusal ⭐

• Oral lesions ⭐

• Poor growth

• Immunosuppression

• ↓ production

🔬 Diagnosis

• History: moldy grain/feed ⭐

• Clinical signs

• Feed toxin analysis (chromatography)

• Necropsy: oral/GIT lesions, lymphoid atrophy

⚖ Differential diagnosis

• Aflatoxicosis

• Viral diseases (Newcastle disease)

• Bacterial enteritis

• Nutritional deficiencies

💊 Therapy

• Remove contaminated feed ⭐, Supportive care, Mycotoxin binders (adsorbents), Vitamin supplementation

🛡 Prevention

• Proper feed storage (dry, cool) ⭐, Prevent mold growth, Regular feed inspection, Use of toxin binders

Other mycotoxicoses:

1. Ergotism

Caused by Claviceps species

Mechanism

• Vasoconstriction → ischemia

• Neuro + endocrine effects

Clinical signs

• Cyanosis of comb/wattles ⭐

• Necrosis of extremities (toes)

• Decreased egg production

• Lameness

2. Rubratoxicosis (rare but mentionable)

Produced by Penicillium species.

Effects

• Hemorrhagic syndrome ⭐

• Liver damage

• Neurological signs (secondary to metabolic disturbance)

👉 Usually low importance in poultry exams, just name it.

🧾 FINAL HIGH-YIELD SUMMARY TABLE

Toxin	Main effect	Key sign
Trichothecenes (T-2, DON)	Cytotoxic	Oral necrosis + feed refusal ⭐
Zearalenone (F-2)	Estrogenic	Reproductive disorders ⭐
Fumonisins	Metabolic	Poor feed conversion
Moniliformin	Cardiotoxic	Sudden death
Ergot alkaloids	Vascular	Gangrene, cyanosis

---

🎯 EXAM GOLD LINES

• “Trichothecenes cause oral necrosis and immunosuppression.” ⭐

• “Zearalenone is an estrogenic mycotoxin causing reproductive disorders.” ⭐

• “Fusariotoxicosis often presents as feed refusal and poor growth.”

• “Diagnosis is based on moldy feed history and toxin detection.”

40. Intoxications caused by drugs - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

Drug toxicosis occurs due to:

• Overdose

• Wrong route of administration

• Prolonged use

• Drug combinations (interactions)

• Species sensitivity differences

Toxicosis caused by ionophores is relatively common in poultry, because these compounds are commonly

administered for the prevention and treatment of coccidiosis and are subject to overdosing and mixing

errors. Ionophores have a broad spectrum of activity but a narrow range of safety in poultry.

💊 1. Ionophore toxicity (MOST IMPORTANT)

Common drugs:

• Monensin

• Salinomycin

• Narasin ionophores

🔬 Mechanism

• Disrupt ion transport (Na⁺, K⁺, Ca²⁺) across membranes

• → ↑ intracellular Ca²⁺

• → muscle degeneration + cell death

🐔 Clinical signs ⭐

• Weakness, ataxia, Dyspnea, Diarrhea, ↓ feed intake, Growth depression

Specific signs:

• Monensin → backward leg paralysis

• Salinomycin → paralysis, ↓ egg production

• Narasin → flaccid paralysis (wings + legs),

Turkeys = most sensitive ⭐, Chickens less sensitive. Dose errors common in mixed feeding systems!

⚠ Important interaction

• Toxicity ↑ with:

  • tiamulin ⭐

  • macrolides (erytrhomycin)

  • chloramphenicol

💊 Treatment

• Remove drug immediately, Supportive therapy

• No specific antidote

🛡 Prevention

• Correct dosing

• Avoid drug incompatibility

• Species-specific feed control (turkeys!)

2. Sulfonamide toxicity

🔬 Mechanism

• Folate metabolism inhibition

• Bone marrow suppression

🐔 Clinical signs ⭐

• Anemia, Hemorrhages, Weakness, Poor clotting

🧠 Key point

• Often occurs in hot weather → ↑ water intake → overdose

💊 Treatment

• Vitamin K ⭐ (very important), Supportive care

🔵 3. Nitrofurans (historical/less relevant)

Effects

• Neurotoxicity

• Hyperexcitability

• Convulsions

👉 Note: banned in many countries

🟣 4. Hypervitaminosis A

• Excess vitamin A

• Eye lesions:

  • crusts, edema, blindness

🧠 5. General toxic substances (mention briefly)

• Selenium

• Salt (NaCl)

• Copper sulfate

👉 “All substances are toxic in high doses”

⚖ Differential diagnosis (important upgrade)

Drug intoxications must be distinguished from:

• Infectious CNS diseases (Newcastle disease, Marek’s disease)

• Mycotoxicoses

• Nutritional deficiencies

• Heavy metal poisoning

🎯 EXAM ONE-LINER SUMMARY

👉 “Drug intoxications in poultry are mainly caused by ionophores and sulfonamides due to overdose, interactions, or species sensitivity, leading to neuromuscular and hematopoietic disorders.”

41. Intoxications caused by chemical compounds and toxic gases - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

General causes

• Accidental exposure

• Improper storage of chemicals

• Contaminated feed/water

• Poor ventilation (gases)

• Overdose or misuse of disinfectants/rodenticides

🧪 1. Anticoagulant rodenticides (VERY IMPORTANT)

🔬 Mechanism

• Inhibit vitamin K recycling in liver

• ↓ synthesis of clotting factors II, VII, IX, X

• → coagulopathy and hemorrhages

🐔 Clinical signs ⭐

• Sudden weakness, Pale comb and mucosa, Dyspnea (lung hemorrhage), Bloody droppings, Sudden death

🔬 Diagnosis

• Prolonged clotting time ⭐

• Reduced prothrombin time (PT) ⭐

• Necropsy: internal hemorrhages (lungs, intestine, body cavity)

💊 Treatment ⭐

• Vitamin K1 ⭐ (key antidote), Activated charcoal, Plasma/blood transfusion (severe cases)

🛡 Prevention

• Secure bait placement, Avoid access of poultry to rodent poison, Proper farm biosecurity

2. Heavy metals

a. Lead poisoning

Sources

• Paint, Batteries, Contaminated soil/feed

Mechanism

• Enzyme inhibition

• Neurotoxicity + nephrotoxicity

Clinical signs ⭐

• Depression, Weakness, Green droppings, Ataxia, paralysis

b. Mercury poisoning

Effects

• GIT irritation, Nervous signs, Diarrhea, Weakness

Other chemical intoxications

• Zinc: cage wire ingestion → neurological signs, green droppings; treatment Ca-EDTA

• Nitrates/nitrites → methemoglobinemia → cyanosis, hypoxia ⭐

• Copper sulfate → GIT irritation and enteritis

• Salt excess (NaCl) → neurological signs, edema, seizures

3. Toxic gases (VERY IMPORTANT)

Ammonia (MOST COMMON IN POULTRY)

Source

• Decomposition of uric acid in litter

• Poor ventilation

Effects ⭐

• Respiratory tract damage, Keratoconjunctivitis, Corneal ulcers, Blindness (high levels)

Clinical signs

• Eye irritation, Swollen eyelids, Growth depression, Blindness → starvation risk

Carbon monoxide

Mechanism

• Forms carboxyhemoglobin → blocks oxygen transport → hypoxia

Signs ⭐

• Sudden death, Cyanosis, Weakness

Necropsy

• Bright red/pink tissues ⭐ (classic sign)

🧠 1. Organophosphates (VERY IMPORTANT)

organophosphates

🔬 Mechanism

• Inhibit acetylcholinesterase

• → accumulation of acetylcholine

• → continuous stimulation of cholinergic system

🐔 Clinical signs ⭐

• Salivation, lacrimation, Diarrhea, Dyspnea, Tremors, seizures, Paralysis → death

🔬 Diagnosis

• History of exposure (pesticides/feed contamination)

• Clinical signs

• Response to therapy

💊 Treatment ⭐

• Atropine sulfate ⭐ (antidote)

• Supportive care

🛡 Prevention

• Avoid contaminated feed

• Proper pesticide use

🧠 2. Ionophores (VERY IMPORTANT)

ionophores

🔬 Mechanism

• Disrupt Na⁺ / K⁺ / Ca²⁺ transport

• → ↑ intracellular Ca²⁺

• → muscle cell death

🐔 Clinical signs ⭐

• Weakness, ataxia

• Dyspnea

• ↓ feed intake

• Growth depression

• Paralysis (species-dependent)

Specific:

• Monensin → backward leg paralysis

• Salinomycin → ↓ production

• Narasin → flaccid paralysis (turkeys especially)

⚠ Key interaction ⭐

• Toxicity ↑ with:

  • tiamulin

  • macrolides

🛡 Prevention

• Correct dosing in feed

• Avoid drug combinations

• Species safety (turkeys!)

🧪 4. Other chemical intoxications (mention briefly)

• Fertilizers → methemoglobinemia

• Salt excess → neurological signs, edema, seizures

• Copper sulfate → GIT irritation, enteritis

• Household chemicals (chlorine, disinfectants), petroleum products, toxic plants, and fumes such as Teflon pyrolysis products

⚖ Differential diagnosis

• Infectious diseases (Newcastle disease, botulism), Mycotoxicosis, Nutritional deficiencies, Heat stress (for respiratory signs)

🎯 EXAM ONE-LINER

👉 “Chemical and gas intoxications in poultry are mainly caused by rodenticides, heavy metals, and toxic gases, leading to coagulation disorders, organ damage, and respiratory or neurological signs depending on the agent.”

42. Metabolic and mycotic diseases in pigeons - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

🐦 Metabolic and mycotic diseases in pigeons

1. Fatty liver (hepatic lipidosis)

• Excess energy intake + low activity

• Obesity → fat accumulation in liver

• Liver dysfunction and hemorrhage risk

• Signs: obesity, ↓ egg production, weakness, sudden death

• PM: enlarged yellow friable liver

• Tx: vitamin E, choline, diet correction

2. Gout

• Uric acid metabolism disorder (kidney dysfunction, high protein, dehydration)

• Multifactorial cause: overfeeding with proteins, kidney impairment, chronic renal failure, Vitamin A imbalance

• Visceral and articular forms

• Signs: weakness, anorexia, joint swelling

• PM: urate deposits on organs

3. Rickets

• Ca/P/Vit D3 imbalance

• Soft bones, deformities, lameness

4. Vitamin A deficiency

• Epithelial keratinization

• Eye lesions, blindness, poor growth

5. 🍄 Candidiasis

• crop and GI infection

• white plaques, regurgitation

• treated with antifungals + hygiene

• Diagnosis: cytology of feces and crop

• Clinical signs in adult birds are typically mild and may include mild weight loss, lethargy, and dull plumage.

  Clinical signs in juvenile birds include anorexia, crop stasis, white plaques in the oral cavity, regurgitation,

  and weight loss. With severe infections, there may be complete crop and GI stasis.

6. 🍄 Aspergillosis

Aspergillus fumigatus

• Air sac and lung granulomas

• Dyspnea, high mortality in young birds

• antifungal therapy, ventilation

• Transmission is by inhalation of fungus spores from contaminated litter, or contaminated feed. Hatcheries may also contribute to infection of chicks.

• Diagnosis: endoscopy

• • Acute: high morbidity and mortality, gasping, sleepiness, anorexia, convulsions, and death

  • Chronic: gasping, coughing, loss of body weight, dyspnea, tail bobbing, exercise intolerance

43. Parasitic diseases of the feathers and skin in pigeons - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

Lice (Phthiraptera)

1. Columbicola columbae🪶

• Host-specific

• Found only in:

  • pale-backed pigeons, speckled pigeons, rock pigeons, stock pigeons

• Localization:

  • undersides of feathers, upper wing feathers

• Feeding:

  • feathers (keratin), NOT blood

• Pathogenicity:

  • low, not fatal, no significant damage, not a vector of diseases, no major economic losses

• CS: Usually minimal signs, Mild feather damage

• Transmission: direct contact

• Diagnosis: visual exam

• Treatment: pyrethrins

Mites

1. Dermanyssus gallinae - Red mite

• Most common mite in pigeons

• Blood-sucking parasite, Nocturnal feeder

• CS: Feather picking, Skin irritation, Pruritus, Anemia (important!)

• Leaves host during the day!!

• Lives in:

  • cracks, crevices, environment (lofts, nests)

• Can survive long periods without feeding

• Diagnosis: inspect cracks/perches at night (flashlight, white paper)

• Treatment:

  • pyrethroids

  • carbamates / organophosphates (classic)

• Prevention: cleaning, nest rotation

2. Knemidocoptes spp.

• Only genus of burrowing mites in birds

• Important species:

  • K. mutans → scaly leg

  • K. gallinae → causes depluming itch

  • K. pilae → scaly face/beak

• Localization:

  • burrow into:

    • feather shafts, skin

• CS: Severe pruritus and pain, Self-trauma: birds pull out feathers, Depression, Constant preoccupation with feather pulling, Reduced feed intake, Weight loss

• Diagnosis: skin scraping

• Treatment: ivermectin + repeat 7–10 days

Fleas

1. Ceratophyllus columbae

• Common ectoparasite of feral pigeons

• Blood-feeding

• CS: Irritation, Stress, Blood loss → anemia (high numbers)

• Diagnosis: skin/feather exam

• Treatment: ivermectin + environment control

Other ectoparasites

Cimex lectularius - Bed bug

• Blood-sucking parasite (bed bug, primarily feed on humans)

• Affects:

  • pigeons, poultry, mammals

• CS: Irritability, Anemia (heavy infestations), Bite reactions: swelling and itching (due to saliva injection)

• Climate:

  • temperate & subtropical

• Behavior:

  • feeds at night, hides during day in cracks/crevices

• Loft infestations can be heavy

• Diagnosis: inspection of nests + fecal spots

• Treatment: environmental control + pyrethroids

• Re-treatment after 7–10 days

• Ixodes ticks

  • blood sucking → anemia

  • vector: borrelia

• Pseudolynchia canariensis (louse fly)

→ Vector of Haemoproteus columbae

→ Causes weakness, anemia-like signs in young birds

• Harpyrhynchus

  • located at the feather base

  • may cause:

    • hyperkeratotic epithelial cysts

• Cheyletiella

  • rare in pigeons

  • burrowing mange-like disease

  • burrows may become infected with mould

  • feeds on debris

  • CS: dermatitis + secondary fungal infection

Diagnosis

• Clinical signs (pruritus, feather loss, anemia)

• Direct detection:

  • lice on feathers

  • mites (skin scraping, feather exam)

• Environmental inspection:

  • cracks, nests, lofts (critical for Dermanyssus & Cimex)

• History:

  • hygiene status, infestation in flock

Differential diagnosis

• Nutritional deficiencies, Behavioral feather picking, Bacterial dermatitis, Fungal infections, Viral feather diseases, Toxicities

Therapy

Insecticides / acaricides

• Pyrethrin

  • Columbicola

  • Dermanyssus

  • fleas

• Carbamates

  • mites

• Organophosphates

  • mites

  • environmental treatment

• Pyrethroids = good for surface/on-host parasites

• Environment parasites = treat environment

• Burrowing mites = ivermectin works better

Important principles

• Repeat treatments (life cycles!)

• Treat environment, not just birds:

  • especially for:

    • Dermanyssus gallinae

    • Cimex lectularius

Prevention

• Thorough cleaning of pigeon houses

• Reduce hiding places (cracks, crevices)

• Environmental treatment:

  • organophosphates

  • pyrethroids (residual effect)

• Good hygiene, Regular monitoring

🔑 Key high-yield distinctions (don’t skip these in oral exams)

• Columbicola = feather feeder, LOW pathogenicity

• Dermanyssus = nocturnal, lives OFF host, causes anemia

• Knemidocoptes = burrowing → severe pruritus + self-trauma

• Cimex = environmental parasite → night feeding + itching

• Fleas/ticks = blood loss → anemia

Parasite	Type	Feeding	Main problem	Key feature
Columbicola columbae	Louse	Feathers	Mild irritation	Host-specific, non-blood sucking
Dermanyssus gallinae	Mite	Blood	Pruritus, anemia	Nocturnal, lives in environment
Knemidocoptes spp.	Mite	Tissue	Severe pruritus, feather loss	Burrowing → depluming itch
Ceratophyllus columbae	Flea	Blood	Irritation, anemia	Common in feral pigeons
Cimex lectularius	Insect	Blood	Itching, anemia	Hides in cracks, night feeder

44. Protozoan diseases in pigeons - etiology, symptoms, diagnostics, dif. dg, therapy and prevention

1. Trichomoniasis (Canker)

• Caused by Trichomonas gallinae

• Flagellated protozoa

• Localization:

  • oral cavity, pharynx, esophagus, crop, liver (systemic cases)

Transmission

• Direct transmission Via “pigeon milk” from infected adults to chicks (very important!)

• Carriers common

Clinical signs

• Young birds most affected

• Early:

  • small white-yellow lesions in oral cavity (soft palate)

• Progression:

  • ulceration and inflammation, lesions extend to esophagus, crop, proventriculus, formation of large necrotic masses → obstruction

• Severe cases:

  • spread to liver and organs

• General signs:

  • rapid weight loss, weakness, listlessness, death in 8–10 days

Diagnosis

• Clinical signs + typical lesions

• Microscopy (wet mount)

Differential diagnosis

• Avian pox (diphtheritic form)

  • key difference: removal → bleeding

Therapy

• Metronidazole

Prevention

• Hygiene, Prevent contact between infected and healthy birds, Control carriers

2. Coccidiosis

• Family: Eimeriidae

• Species:

  • Eimeria columbanum

  • Eimeria labbeana

• Localization: intestine → catarrhal enteritis

Epidemiology

• Mainly young birds

• Risk factors:

  • warm, damp conditions, poor hygiene, poor ventilation

Clinical signs

• Non-specific:

  • ruffled feathers, hunched posture, weight loss

• Digestive:

  • bloody or mucoid diarrhea

• Severe:

  • paralysis, death

Diagnosis

• Fecal examination (oocysts)

Therapy

• Sulfonamides

Prevention

• Toltrazuril, Ionophores, Hygiene management

3. Toxoplasma gondii

• Final host: cats (felids)

• Birds = intermediate hosts

Pathogenesis

• Cell damage → necrosis, Cyst formation in organs, Inflammatory lesions

Clinical signs

• Anorexia, Conjunctivitis, Neurological signs

Diagnosis

• Serology / histopathology (if needed)

Prevention

• Avoid contact with cat feces

4. Haemoproteus columbae

• Related to malaria parasites

Transmission

• Vector:

  • Pseudolynchia canariensis

Clinical signs

• Anemia, Weakness

Diagnosis

• Blood smear (Giemsa stain)

Therapy

• Sulfonamides (limited effect)

5. Leucocytozoon spp.

Transmission

• Vector:

  • blackflies (Simuliidae)

Pathogenesis

• Liver invasion → cell destruction

Clinical signs

• Apathy, Anemia, Leucocytosis, Diarrhea, CNS signs, Emaciation

• Death in 7–10 days or survival with organ damage

Diagnosis

• Blood smear (Giemsa)

Therapy

• ❌ No effective treatment

🎯 High-yield summary (for oral exam ending)

• Trichomonas → oral lesions + necrotic masses, transmission via pigeon milk

• Eimeria → intestinal disease, diarrhea, young birds

• Toxoplasma → systemic + neurological, cats involved

• Haemoproteus / Leucocytozoon → blood parasites → anemia, vector-borne

45. Helminthoses in pigeons - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

1. Cestodes (tapeworms)

Hymenolepis columbae

• Cestode of pigeons and gallinaceous birds

• Indirect life cycle

• Intermediate hosts: earthworms, snails, slugs, insects

Clinical signs

• Usually asymptomatic

• Heavy infections:

  • ↓ performance, diarrhea

Diagnosis

• Detection at necropsy (adult worms)

Therapy

• Praziquantel

• Flubendazole

Davainea proglottina

• Very small cestode

• Intermediate host: molluscs

Pathogenesis

• Scolex penetrates deeply into duodenal villi

• Causes:

  • necrosis, hemorrhagic inflammation

Clinical signs

• Light infection:

  • poor growth, weakness, ↓ egg production

• Heavy infection:

  • hemorrhagic enteritis, emaciation, dyspnea, death

Diagnosis

• Post-mortem:

  • microscopic scraping of duodenum

2. Nematodes (roundworms)

Syngamus trachea

• Respiratory nematode

• Adults in permanent copulation (Y-shape)

• Localization: trachea

Life cycle

• Direct, Facultative intermediate hosts:

  • earthworms, snails, insects

Pathogenesis

• Tracheal irritation, mucus production, airway obstruction

Clinical signs

• Coughing, sneezing, Respiratory distress, Gasping (“gapes”), open-mouth breathing, Head shaking, Anorexia, apathy

Diagnosis

• Visual exam:

  • trachea under light → worms visible

• Fecal flotation: eggs

Therapy

• Flubendazole

Ascaridia columbae

• Common intestinal nematode

Pathogenesis

• Intestinal epithelial damage. May cause hemorrhagic enteritis

Clinical signs

• ↓ feed intake, weight loss, poor growth

Diagnosis: fecal flotation

Capillaria spp.

• Capillaria caudinflata

• Capillaria obsignata

Pathogenesis

• Light infection:

  • inflammation, thickening

• Heavy infection:

  • severe thickening of GIT, catarrhal / croupous enteritis

Clinical signs

• anorexia, drooping wings, ruffled feathers, weight loss, ↓ egg production, anemia, diarrhea, mortality

• Diagnosis: fecal flotation

3. Other helminths

• Echinostoma revolutum (trematode)

  • causes hemorrhagic enteritis

• Raillietina tetragona (cestode)

  • causes enteritis

4. Diagnosis (general)

• Fecal examination (eggs)

• Necropsy (adult worms)

• Clinical signs (GI or respiratory)

5. Differential diagnosis

• Bacterial enteritis

• Coccidiosis

• Nutritional deficiencies

• Toxicities

6. Therapy (general)

• Anthelmintics:

  • praziquantel → cestodes

  • flubendazole → nematodes

7. Prevention

• Hygiene, Control of intermediate hosts

• Clean food and water, Avoid damp environments

• Regular deworming

🎯 High-yield summary

• Cestodes → indirect life cycle, often mild (Hymenolepis), but can be severe (Davainea)

• Nematodes → GI or respiratory disease

  • Syngamus → gasping (very characteristic)

  • Ascaridia / Capillaria → enteritis, weight loss

• Treatment = praziquantel (tapeworms) + flubendazole (roundworms)

46. Bacterial diseases in pigeons - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

1. Chlamydiosis (Ornithosis / Psittacosis)

• Caused by Chlamydia psittaci

• Obligate intracellular bacterium

• Infects many bird species including pigeons

Pathogenesis / tropism

• Upper respiratory tract:

  • sinuses, conjunctiva, trachea

• Systemic spread possible (liver, spleen)

Clinical signs

• Asymptomatic carriers OR severe disease

• Ocular/nasal discharge, Anorexia, depression

• Dyspnea, Dehydration, Diarrhea

• Biliverdinuria (green urates), ↓ performance / egg production

Diagnostics

• PCR

• Serology:

  • ELISA, complement fixation, indirect/direct fluorescent antibody

• Radiology:

  • hepatomegaly, splenomegaly, airsacculitis

Therapy

• Doxycycline, Reduce dietary calcium (important for absorption)

Prevention

• Quarantine new birds, Biosecurity, Hygiene

2. Mycoplasmosis

• M. columbinum (respiratory)

Pathogenesis

• Colonization of upper respiratory tract early in life

• Disease appears with immunosuppression → Secondary infections common

Clinical signs

• Racing pigeons:

  • fatigue, increased panting

• Respiratory:

  • rhinitis, tracheitis, sinusitis

Diagnosis

• PCR, ELISA, Serology

• Post-mortem lesions

Therapy

• Antibiotics (supportive, not always curative)

• Vaccination (where available)

Mycobacterium avium

• intestinal granulomas, weight loss

• Diagnosis: necropsy findings of granulomatous lesions in liver and spleen, confirmed by acid-fast staining or PCR

• Treatment: generally not effective, and control relies on culling and strict biosecurity

3. Pasteurellosis (Fowl cholera)

• Caused by Pasteurella multocida

Clinical forms

Peracute

• sudden death

Acute

• fever, depression, anorexia, respiratory signs, diarrhea, cyanosis, death

Chronic

• joint swelling, tendonitis, wattle/footpad swellings, respiratory disease

Diagnostics

• PCR, culture, serology, necropsy (typical lesions)

Therapy

• Sulfonamides, Antibiotics (variable success)

Prevention

• Vaccination, Hygiene, Biosecurity, Eradication in outbreaks

4. Other important bacterial diseases

Salmonellosis

• Mainly affects joints and internal organs

• Signs:

  • lameness (arthritis common in pigeons), diarrhea, torticollis

• Prevention:

  • vaccination, hygiene

Colibacillosis

• Avian colibacillosis

• Causes:

  • septicemia, enteritis, toxemia

• Signs:

  • diarrhea, weakness, dehydration

• Treatment:

  • antibiotics (often resistance problem)

Clostridiosis

• Clostridial necrotic enteritis in birds

Clinical signs

• sudden death, depression, diarrhea

Pathology

• necrotic enteritis, foul-smelling intestinal contents, pseudomembranes

Therapy

• penicillin / antibiotics in water

Prevention

• probiotics, hygiene, avoid contaminated feed

5. (Important vector-borne bacterial disease)

Avian spirochetosis

• Vector: ticks (Argas spp.)

• Signs:

  • fever, weakness, sudden death, green/yellow feces

• Diagnosis:

  • blood smear (Giemsa, dark-field microscopy)

• Treatment:

  • tetracyclines

• Prevention:

  • tick control

🎯 High-yield exam summary

• Chlamydia → respiratory + systemic + doxycycline

• Mycoplasma → chronic respiratory + performance loss

• Pasteurella → septicemia + acute death + chronic joint disease

• Salmonella → joints + diarrhea

• E. coli → septicemia/enteritis (secondary)

• Clostridium → necrotic enteritis + sudden death

• Borrelia → tick-borne septicemic disease

47. Viral diseases in pigeons - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

1. Avian pox

• Family: Poxviridae (Avipoxvirus)

Clinical forms

1. Cutaneous form

• Nodular lesions on unfeathered skin

• Common sites: eyelids, beak, legs

• Eyelid lesions → possible eye closure

2. Diphtheritic (wet) form

• Lesions on mucosa:

  • mouth, pharynx, larynx, trachea

• Caseous, firmly adherent plaques

• Interferes with:

  • feeding, respiration

3. Mixed form

• Combination of both

Diagnosis

• Clinical lesions (typical), PCR, ELISA / histopathology

Therapy

• No specific antiviral treatment, Supportive care only

• Secondary infection control

Prevention

• Vaccination (attenuated vaccine) in high-risk areas

• Vector control (mosquitoes)

• Biosecurity

2. Newcastle disease

• Paramyxovirus (Avian avulavirus 1)

Forms

• Velogenic (highly virulent) → high mortality

• Mesogenic → moderate disease

• Lentogenic → mild respiratory disease

Clinical signs

Velogenic

• severe respiratory + nervous signs, lethargy, dyspnea, tremors, paralysis, torticollis

Mesogenic

• coughing, ↓ egg production

Lentogenic

• mild respiratory signs (sneezing, coughing)

Diagnosis

• Serology:

  • hemagglutination (HA), hemagglutination inhibition (HI), ELISA

Therapy

• ❌ No treatment

Prevention

• Vaccination, Strict biosecurity

3. Avian influenza

• orthomyxovirus, subtype H5N1

Types

• Low pathogenic (LPAI)

• High pathogenic (HPAI)

Clinical signs

LPAI

• respiratory signs, sinusitis, green diarrhea, mild depression

HPAI

• systemic disease, edema of head, cyanosis, hemorrhages, organ necrosis, high mortality

Diagnosis

• PCR, Serology

Therapy

• ❌ No treatment

Prevention

• Biosecurity (most important), Vaccination (limited use depending region)

4. Pigeon herpesvirus

Pathogenesis

• Transmission during feeding (regurgitation)

• Replication in oropharynx

• Systemic spread (viraemia)

Clinical signs

• depression, anorexia, conjunctivitis, oral + pharyngeal ulcers, dyspnea, diarrhea

5. Inclusion body hepatitis

• Adenovirus

Pathology

• Liver is:

  • pale, swollen, friable, hemorrhagic

Clinical signs

• sudden death (most typical), depression shortly before death, pale comb/wattles, sometimes icterus

Diagnosis

• necropsy (liver lesions), histopathology (inclusion bodies)

Therapy

• ❌ No effective treatment

• ❌ No vaccine (generally)

6. Circovirus

• Pigeon circovirus

• Pathogenesis: immunosuppression by destroying lymphoid tissue, leading to chronic wasting and increased susceptibility to secondary infections

• CS: Chronic wasting, poor growth, immunosuppression, secondary infections

• there is no specific treatment and control relies on biosecurity and prevention

🎯 High-yield summary

• Pox → skin + diphtheritic plaques

• Newcastle → neuro + respiratory + high mortality

• Influenza → systemic hemorrhagic disease

• Herpesvirus → oral ulcers + respiratory + diarrhea

• Adenovirus → liver necrosis + sudden death

48. The tasks of the field practitioner in the poultry farming

1. Preparation of the poultry house before arrival

a) Cleaning, disinfection.

• Before new chickens arrive, the hall must undergo proper disinfection (to remove mealworms).

• Disinfection consists of two steps:

  • mechanical cleaning

  • chemical disinfection

• The efficacy of disinfection can be controlled by bacterial swabs.

b) Deep litter management

• Deep litter should also be disinfected.

• Types of bedding include:

  • hay, special pellets, wood shavings

• An aerosolator using Virkon S is used for disinfection of bedding.

c) Environmental conditions

• Temperature: around 30°C

• Relative humidity: around 50%

2. Arrival of chicks

• When chicks arrive:

  • random samples from a few animals should be performed

  • purpose: confirm health status

  • includes checking antibody titers (Ab titers)

• During the first days:

  • probiotics are added

  • plant extracts are added

  • purpose:

    • increase appetite, increase water intake

3. Feed control

• Check the composition of food:

  • adherence to recommended dietary levels

• Check for:

  • presence of mycotoxins

• Coccidiostatic drugs can be added:

  • to control coccidian parasites

4. Vaccination program

• Take blood to evaluate maternal antibody titers

• Maternal antibodies can last up to 3 weeks

• Vaccination timing is chosen based on antibody level

Infectious bronchitis

• Vaccination occurs in hatcheries

• Often combined with Newcastle disease vaccination

• Depending on epizootiological situation:

  • revaccination at 2 weeks of age

Newcastle disease

• Revaccination at 20 days of age

5. Regular veterinary visits and monitoring

• During first 3 weeks of production:

  • vet should visit farm 2× per week

• Activities:

  • collect carcasses

  • check protocols/records

Monitoring health status

• Daily mortality rate:

  • max 3%

• Signs of disease:

  • changes in feed intake

  • changes in weight
    → indicate malabsorption or disease

Handling sick or dead birds

• If dead chicken is found:

  • perform necropsy

• If sick animal is found:

  • take samples

  • start treatment:

    • antibiotics

    • supportive therapy

    • antifungals

    • anticoccidials

6. Salmonella monitoring

• Salmonella sampling performed 3 weeks before birds leave

• Shoe cover sampling system:

  • vet walks through halls

  • fecal samples collected on shoe covers

  • detection of Salmonella types:

    • Pullorum

    • fowl typhoid

    • S. copenhagen

7. Blood sampling in poultryMain vein puncture sites:

a) ulnar vein (wing vein)
b) medial metatarsal vein

• rarely in older birds due to thick scales
  c) jugular vein

• right one is larger and more visible

Important notes

• Blood sampling almost always causes hematoma

• Birds have very thin skin:

  • do NOT apply pressure through skin onto vein

  • pressure can remove blood from vessel

• After a few days:

  • blue-green discoloration (bruising) may appear

8. Main health problems in broilers

• Main problems:

  • locomotor disorders

  • respiratory disorders

• Most common bacterial infections:

  • E. coli

  • Enterococcus