Poultry exam

part 2

17. Non-infectious, infectious and parasitic diseases of the beak, beak cavity and crop - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

Non-infectious:

• Beak deformities (congenital, rickets)

• Beak necrosis (fine feed accumulation)

• Vitamin A deficiency → metaplasia

• Foreign bodies → crop impaction

• Chemicals, trauma

Infectious:

• Bacteria: Pasteurella, Pseudomonas, Klebsiella

• Viruses: fowl pox

• Fungi: Candida albicans (candidiasis)

Parasitic:

• Trichomonas gallinae

• Capillaria spp.

1. Beak disorders

• Congenital deformities: brachygnathia superior/inferior

• Acquired deformities: rickets / osteomalacia

• 👉 Key mechanism: Ca + P + Vit D3 imbalance → poor bone mineralisation

• Necrosis: due to fine feed accumulation (Finely ground feed → accumulation → pressure necrosis)

2. Stomatitis

• Inflammation of oral mucosa

• Causes: infectious + chemical

  • fowl pox

  • Candida

  • Trichomonas

  • bacteria (Pseudomonas, Klebsiella)

• CS: swelling, lesions, reduced feed intake, weight loss, lethargy

3. Ingluvitis (crop inflammation)

• Causes: feed (high fiber), chemicals, infections (pasteruella, candida, pox, trichomonas, Capillaria anulata, C. Contorta (flubendazole), Gongylonema ingluvicola.)

• Types: catarrhal, hemorrhagic, necrotic

• CS: anorexia, weight loss, foul regurgitation

4. Crop disorders

• Impaction: foreign material → obstruction

• Pendulous crop: enlarged, fluid-filled caused by nerve/muscle damage

• Metaplasia → Vit A deficiency

5. Candidiasis (yeast)

• Opportunistic (Candida albicans)

• Often after antibiotics, dysbiosis and poor hygiene

• CS:

  • Young: anorexia, crop stasis →regurgitation, white plaques

  • Adults: mild signs

• Lesions: white pseudomembranes/plaques in crop → “sour crop”

• Dx: cytology from crop swab (smears)

• Tx: antifungals (nystatin)

6. Trichomoniasis

• Protozoa (Trichomonas gallinae)

• Transmission: contaminated water

• CS:

  • yellow caseous plaques (‘yellow buttons’) in oral cavity

  • can block esophagus → starvation

  • Rapid weight loss, death

• Tx: metronidazole

• Diagnosis: crop swab → cytology

• Prevention: hygiene, clean water

Clinical Signs (general):

• Anorexia

• Weight loss

• Regurgitation

• Oral plaques/lesions

• Dysphagia

Diagnostics:

• Clinical signs

• Oral/crop examination

• Cytology (Candida)

• Detection of parasites

👉 Key line: diagnosis based on lesions + cytology/parasitology

Differential Diagnosis:

• Vitamin deficiencies (A)

• Infectious diseases (pox, bacterial infections)

• Foreign body/obstruction

Therapy:

• Cause-specific:

  • Antifungals (Candida)

  • Antiprotozoals (Trichomonas)

• Supportive care

Prevention:

• Good hygiene

• Proper nutrition (Vit. A!)

• Clean water

• Avoid overcrowding

💡 Exam high-yield lines:

• Candidiasis = white plaques in crop/oral cavity

• Trichomoniasis = yellow caseous lesions blocking esophagus

• Vit A deficiency = metaplasia

• Crop disorders = regurgitation + foul smell

18. Non-infectious, infectious and parasitic diseases of the proventriculus and gizzard - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

Diseases of the proventriculus

1. Proventriculitis (inflammation)

Infectious cause:

• Proventriculitis can be caused by viral infections (e.g. Newcastle disease), fungi, bacteria, and mycotoxins

• Infectious: Candida, Newcastle disease

• Fungal-like organism: Macrorhabdus ornithogaster (mainly pet birds, rare in poultry)

• Toxic: mycotoxins (Fusarium, Aspergillus metabolites)

CS:

• Weight loss

• Regurgitation

• Diarrhea

• Poor feed conversion

Non-infectious cause:

• Intoxocation (Mycotoxicosis)

• Fusarium toxins → necorsis and ulceration of oral mucosa, GI reddening, visceral hemorrhages, lymphoid and spleen atrophy

• Cyclopiazonic acid (Aspergillus flavus) → lesions in proventriculus, gizzard, liver, spleen, proventricular dilation + ulceration and thickend mucosa

• PM: Enlarged, mottled proventriculus with thickened mucosa

• CS: imparied feed conversion, decreased weight, mortality

3. Proventricular dilation syndrome

• Cause: poor diet (high fiber, mash feed)

• CS: enlarged proventriculus, thin wall, gizzard atrophy due to lack of food

4. Parasite: Tetrameres americana

• Located in proventricular glands and visible as red spots on serosa

• CS: anemia, weight loss, thickened proventriculus

• Heavy infection: thick, edematous proventriculus + possible partial obstruction

Diseases of the gizzard

1. Impaction

• Cause: litter ingestion (turkeys), indigestible material

• CS: sudden death in young birds

2. Dilation of the gizzard

• Cause: soft feed, lack of grit

• → inflammation + dysfunction

• 👉 “Lack of grit → poor mechanical digestion → dilation and dysfunction”

3. Parasite: Amidostomum anseris

• Located under keratin layer of gizzard, proventriculus or esophagus in waterfowl

• Causes hemorrhage + necrosis

• Severe infections → anemia, blood loss

4. Clostridiosis

• Clostridium spp. can cause necrosis in the proventriculus–gizzard junction

5. Macrorhabdus (megabacteria)

   • rare, mainly in companion birds, causes weight loss

🧠 Clinical Signs (general):

• Weight loss

• Regurgitation

• Diarrhea

• Poor growth

• Anemia (parasites)

• Sudden death (impaction)

🔬 Diagnostics:

• Post-mortem examination (key!)

• Detection of parasites in proventriculus/gizzard

• Lesions: dilation, hemorrhages, thickening

❌ Differential Diagnosis:

• Candidiasis (crop involvement)

• Infectious enteritis

• Mycotoxicosis vs bacterial enteritis

• Foreign body obstruction

💊 Therapy:

• Anthelmintics (parasites)

• Supportive care

• No specific treatment for toxicosis (remove feed source)

🛡 Prevention:

• Good feed quality (no mold)

• Provide grit

• Proper litter management

• Biosecurity

• Deworming in free-range systems

💡 EXAM HIGH-YIELD POINTS:

• Proventriculus diseases → toxins + parasites + diet problems

• Gizzard impaction → turkeys + litter ingestion

• Tetrameres → red spots in proventriculus

• Amidostomum → gizzard hemorrhage in waterfowl

19. Non infectious and infectious diseases of the intestines and cloaca - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

Enteritis = inflammation of the intestines
- Main etiological groups: Bacteria, Viruses, Parasites, Intoxications, Non-specific causes (management, nutrition, stress)

🦠 1. INFECTIOUS DISEASES

A. Bacterial diseases

1. Necrotic enteritis

• Etiology: Clostridium perfringens (toxins)

• Predisposition: gut damage, coccidiosis, diet changes

• Symptoms:

  • Sudden death, Depression, ruffled feathers, Diarrhea

• Lesions:

  • Necrosis of small intestine (“Turkish towel” mucosa), Liver lesions

• Diagnostics:

  • Necropsy + bacteriology

• Differential diagnosis:

  • Coccidiosis

  • Salmonellosis

• Therapy:

  • Antibiotics (penicillin, bacitracin)

• Prevention:

  • Good hygiene, Control of coccidiosis, Feed management

2. Pullorum disease

• Etiology: Salmonella pullorum

• Transmission: vertical + horizontal

• Symptoms:

  • High mortality in chicks, Weakness, diarrhea

• Lesions:

  • Unabsorbed yolk sac, White nodules in organs, Cecal cores

• Diagnostics:

  • Serology, bacteriology

• Differential diagnosis:

  • Fowl typhoid

  • Colibacillosis

• Therapy:

  • Usually not treated (eradication programs)

• Prevention:

  • Testing breeder flocks, Biosecurity

3. Fowl typhoid

• Etiology: Salmonella gallinarum

• Symptoms:

  • Depression, diarrhea, Pale comb, dehydration

• Lesions:

  • Similar to pullorum, but in older birds

• Diagnostics:

  • Culture, serology

• Differential diagnosis:

  • Pullorum disease

• Therapy:

  • Antibiotics (limited use)

• Prevention:

  • Vaccination + eradication

4. Colibacillosis (E. coli)

• Etiology: Escherichia coli

• Predisposition: poor hygiene

• Forms:

  • Enterocolitis

    • Diarrhea, dehydration

  • Coligranuloma (Hjarre’s disease)

    • Granulomas in intestine, liver, mesentery

• Diagnostics:

  • Culture

• Differential diagnosis:

  • Tuberculosis

• Therapy:

  • Antibiotics

• Prevention:

  • Hygiene, ventilation

5. Avian tuberculosis

• Etiology: Mycobacterium avium

• Course: chronic

• Symptoms:

  • Weight loss, emaciation, Lameness (bone involvement)

• Lesions:

  • Granulomas in the intestine, liver

• Diagnostics:

  • Necropsy, histology

• Differential diagnosis:

  • Coligranuloma

• Therapy:

  • Not practical → culling

• Prevention:

  • Biosecurity, remove infected birds

Other bacteria

• Pasteurella multocida (fowl cholera)

• Campylobacter spp.

• Yersinia enterocolitica (usually non-pathogenic)

B. Parasitic diseases (important examples)

• Eimeria spp. → coccidiosis (bloody diarrhea)

• Ascaridia spp. → obstruction, poor growth

• Capillaria spp. → enteritis

• Histomonas meleagridis → blackhead disease

• Trichomonas spp. → upper GIT, sometimes intestines

Key signs:

• Diarrhea, Weight loss, Poor performance

Diagnostics:

• Fecal exam (oocysts, eggs)

Therapy:

• Antiparasitics (coccidiostats, anthelmintics)

Prevention:

• Hygiene, Litter management

C. Viral enteritis (brief)

• Rotavirus, coronavirus, adenovirus, parvovirus

• Symptoms: diarrhea, poor growth, mortality in young birds

• Diagnosis: PCR, histopathology

• Prevention: biosecurity, vaccination (when available)

• Newcastle disease

• Causes enteric + respiratory + neurological signs

• Highly contagious, high mortality

2. NON-INFECTIOUS DISEASES

A. Intoxications

Heavy metals

• Copper (CuSO₄ overdose):

  • Catarrhal enteritis

  • Mucous exudate

• Mercury:

  • Caustic burns, ulcers

• Phosphorus:

  • Diarrhea, weakness, anorexia

General signs:

• Diarrhea, Depression, Weight loss

Diagnostics:

• History + toxicology

Therapy:

• Remove toxin, Supportive care

Prevention:

• Proper dosing, Avoid contaminated feed/water

B. Non-specific causes

• Poor nutrition

• Sudden feed change → enteritis

• Stress

• Dysbiosis

C. Hypomotility - nervous origin

D. Volvulus – due to gas → obstruction

CLOACAL DISEASES

1. Cloacitis

• Etiology:

  • Infection, irritation, enteritis

• Symptoms:

  • Dirty vent, Foul odor. Ulceration, Stop laying eggs

• Therapy:

  • Clean area, Antibiotics (if bacterial)

• Prevention:

  • Hygiene

2. Cloacal prolapse

• Causes:

  • Enteritis (straining)

  • Egg-laying problems

• Symptoms:

  • Protruding cloaca

• Therapy:

  • Reposition + supportive care

• Prevention:

  • Proper nutrition (Ca, fiber)

  • Avoid obesity

🧠 Differential diagnosis (important exam part)

• Coccidiosis vs necrotic enteritis

• Salmonellosis vs colibacillosis

• Tuberculosis vs coligranuloma

• Intoxication vs infectious enteritis

✅ Key prevention principles

• Biosecurity

• Hygiene & litter management

• Proper nutrition

• Vaccination (Salmonella, others)

• Parasite control

20. Protozoan diseases of the GIT - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

1. COCCIDIOSIS (most important)

Etiology

• Eimeria spp. (intracellular protozoa)

• Very common → disease occurs only with high infection dose

Important species (chickens)

• Eimeria tenella → ceca (bloody diarrhea) ⭐

• Eimeria necatrix → small intestine (severe hemorrhage) ⭐

• Eimeria acervulina → mild, poor growth

• Eimeria brunetti → lower intestine, necrosis

👉 Most pathogenic: E. tenella & E. necatrix (deep tissue schizogony → hemorrhage)

Pathogenesis

• Ingestion of sporulated oocysts

• Destruction of intestinal epithelium → hemorrhage

Symptoms

• Diarrhea (often bloody), Dehydration, Weight loss, High mortality

• Predisposes to secondary infections (e.g. Clostridium)

Lesions

• Hemorrhagic enteritis, Thickened intestinal wall, Cecal cores (E. tenella)

Diagnostics

• Fecal flotation (oocysts)

• Necropsy

Differential diagnosis

• Necrotic enteritis

• Salmonellosis

Therapy

• Toltrazuril, sulfonamides

• Ionophores (in feed)

Prevention

• Hygiene, Anticoccidials in feed, Vaccination

2. HISTOMONIASIS (Blackhead disease)

• Histomonas meleagridis

• Transmitted via Heterakis gallinarum eggs

Pathogenesis

• Affects ceca + liver

Symptoms

• Depression, anorexia, Yellow diarrhea, Cyanotic head (“blackhead”), High mortality (especially turkeys)

Lesions (pathognomonic ⭐)

• Ceca: thickened wall, ulcers, cheesy core

• Liver: round necrotic lesions

👉 Severe cases → perforation → peritonitis

Diagnostics

• Necropsy (very characteristic lesions)

Differential diagnosis

• Trichomoniasis

Therapy

• No effective protozoal treatment

• Control of Heterakis (e.g. flubendazole)

Prevention

• Deworming, Hygiene, Separation of turkeys and chickens

3. TRICHOMONIASIS

• Trichomonas gallinae

Location

• Upper GIT (crop, esophagus, pharynx)

Symptoms

• Dysphagia, Weight loss, Weakness, Death (especially pigeons), Death within 8–10 days (severe cases)

Lesions

• “Yellow buttons” (caseous plaques)

Diagnostics

• Microscopy (crop swab)

Differential diagnosis

• Histomoniasis

• Vitamin A deficiency

Therapy

• Nitroimidazoles (non-food birds only)

Prevention

• Clean water, Avoid bird-to-bird transmission

🧠 General clinical signs (important summary)

• Diarrhea, Weight loss, Dehydration, Reduced growth, Mortality

🔍 Diagnostics (general)

• Fecal examination (oocysts), Microscopy, Necropsy lesions

⚖ Differential diagnosis (exam favorite)

• Bacterial enteritis (Clostridium, Salmonella)

• Viral enteritis

• Helminths

💊 Therapy (general)

• Antiprotozoals (toltrazuril, sulfonamides), Supportive care

🛡 Prevention

• Hygiene and sanitation, Dry litter, Anticoccidials in feed, Control of intermediate hosts

🧠 KEY EXAM TIPS

• ⭐ Coccidiosis = most important

• ⭐ Histomoniasis = pathognomonic liver lesions

• ⭐ Trichomoniasis = yellow plaques in upper GIT

• ⭐ Always mention:

  • fecal exam

  • biosecurity

• ⭐ E. tenella → bloody cecal diarrhea

• ⭐ Histomoniasis → liver + cecal lesions (pathognomonic)

• ⭐ Transmission via Heterakis = classic question

• ⭐ Secondary Clostridium infection → very important link

21. Helminthoses of the GIT - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

🪱 Etiology

Nematodes (most important)

• Ascaridia galli

• Capillaria spp.

• Heterakis gallinarum

Others (less common)

• Davainea proglottina (cestode)

• Prosthogonimus spp.

• Trichostrongylus tenuis

• Amidostomum spp.

🪱 Nematodes

1. ASCARIDIOSIS

• Ascaridia galli

• Affects the small intestine

• Direct life cycle

Pathogenesis

• Mechanical irritation

• Obstruction of intestine (duodenum/jejunum)

• Migration → cloaca

Clinical signs

(depend on worm burden)

• Weight loss, Decreased egg production, Diarrhea, Anemia, Depression (drooping wings, ruffled feathers) Mortality (severe cases)

Diagnostics

• Fecal examination (eggs), Necropsy (adult worms)

Differential diagnosis

• Coccidiosis, Bacterial enteritis, Malnutrition

Therapy

• Anthelmintics:

  • Piperazine, Flubendazole, Ivermectin, Tetramisole

Prevention

• Hygiene and sanitation, Litter management, Rotation of pasture

2. CAPILLARIOSIS

• Capillaria spp.

• Location:

  • Crop: C. annulata, C. contorta

  • Small intestine: C. obsignata, C. bursata, C. caudinflata

  • Ceca: C. anatis

Life cycle

• Direct or indirect

• Some species require earthworms as intermediate hosts

Pathogenesis

• Inflammation of mucosa, Thickening of intestinal wall

• Severe cases → catarrhal/croupous enteritis

Clinical signs (similar to ascaridiosis)

• Weight loss, Diarrhea, Anemia, Poor production, Mortality (heavy infections)

Diagnostics / Therapy / Prevention

👉 Same as Ascaridia

3. HETERAKIOSIS

• Heterakis gallinarum

• Located in ceca

• Direct life cycle (Earthworms = transport hosts)

Pathogenesis

• Cecal inflammation, Thickened mucosa, Petechial hemorrhages

⭐ VERY IMPORTANT:

• Vector for Histomonas meleagridis (blackhead disease)

Clinical signs

• Usually mild:

  • Poor growth, Depression

• Severe cases → death

Diagnostics

• Fecal exam, Necropsy

Therapy

• Anthelmintics (flubendazole, etc.)

Prevention

• Deworming, Hygiene, Control of earthworms

🪱 Cestodes (tapeworms)

• Examples:

  • Davainea proglottina → hemorrhagic enteritis (duodenum)

  • Raillietina tetragona → ileum

• Indirect life cycle (snails, slugs, ants)

• Clinical signs:

  • Diarrhea, Poor growth

• Therapy:

  • Praziquantel

• Prevention:

  • Control intermediate hosts

🪱 Trematodes (flukes)

• Example:

  • Prosthogonimus spp.

• Life cycle: snail + dragonfly

• Location:

  • Intestine → can migrate to oviduct

• Clinical importance:

  • ↓ egg production

  • Peritonitis (rupture)

👉 Prevention:

• Avoid wet environments (snails!)

🧠 OTHER HELMINTHS (brief mention)

• Trichostrongylus tenuis
  → affects ceca/intestine → causes weight loss, anemia, enteritis

• Amidostomum spp. (gizzard worms)
  → affect gizzard → cause gizzard erosion, anemia, poor growth

🧠 GENERAL CLINICAL SIGNS (important summary)

• Weight loss, Diarrhea, Anemia, Reduced egg production, Poor growth, Mortality (heavy infections)

🔍 DIAGNOSTICS

• Fecal examination (eggs), Necropsy

⚖ DIFFERENTIAL DIAGNOSIS

• Coccidiosis, Bacterial enteritis, Viral enteritis, Nutritional deficiencies

💊 THERAPY

• Anthelmintics (flubendazole, ivermectin, piperazine)

• Supportive care

🛡 PREVENTION

• Hygiene & sanitation

• Dry litter

• Pasture rotation

• Control of intermediate hosts

🎯 KEY EXAM POINTS

• ⭐ Ascaridia galli → intestinal obstruction

• ⭐ Capillaria → thin worms, severe mucosal damage

• ⭐ Heterakis gallinarum → vector of histomoniasis

• ⭐ Always mention:

  • fecal exam, deworming, hygiene

22. Diseases of bursa of Fabricius - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

The Bursa of Fabricius:

• Primary lymphoid organ in birds

• Located dorsal to cloaca

• Responsible for B-cell (humoral) immunity

• Atrophies around 6 months of age

🦠 1. Infectious bursal disease (IBD, Gumboro) ⭐ MOST IMPORTANTE

• Birnavirus

• Serotype 1 → pathogenic (chickens)

• Serotype 2 → non-pathogenic (no disease/immunosuppression)

• Highly contagious: Fecal-oral + fomites (equipment, clothes, vehicles)

Pathogenesis

• Destruction of B lymphocytes
  → severe immunosuppression

Clinical signs

Subclinical (age < 3 weeks)

• No obvious signs

• Poor vaccine response → Severe immunosuppression → Secondary infections

Clinical (age 3–6 weeks)

• Depression, prostration, Watery diarrhea, Soiled vent, Cloacal inflammation, Incoordination

Lesions

• Acute: enlarged, edematous, hemorrhagic bursa

• Chronic: bursal atrophy

Diagnostics

• PCR, Necropsy findings

Differential diagnosis

• Marek’s disease

• Lymphoid leukosis

• Coccidiosis (diarrhea cases)

Therapy

• ❌ No specific treatment

• Supportive care

Prevention

• Vaccination (core vaccine), Biosecurity

2. Lymphoid leukosis

• Avian leukosis virus (retrovirus)

Key features

• Bursal-dependent tumor disease

• Affects birds >14–16 weeks (slow tumor development)

Pathogenesis

• Infection of B cells → tumor formation

• Organs affected:

  • Liver, Spleen, Bursa

Clinical signs

• Non-specific:

  • Weakness, Weight loss, Diarrhea

• Tumors develop later

Diagnostics

• PCR, Necropsy (tumors)

Differential diagnosis

• Marek’s disease ⭐ important (No neurological signs (unlike Marek’s disease)

Prevention

• Eradication programs

• Control vertical transmission

3. Marek’s disease

• Gallid herpesvirus (MDV)

Key features

• Highly contagious - Spread via feather dander (very resistant in environment)

• Causes:

  • Tumors, Nerve lesions (very important difference!)

• Pathogenesis: Virus infects T-lymphocytes → lymphoma formation

Clinical signs

• Paralysis (legs, wings) ⭐, Weight loss, Ocular changes, Skin lesions

Bursa involvement

• Usually atrophy, not tumors

Diagnostics

• Clinical signs + PCR

Differential diagnosis

• Lymphoid leukosis (NO nerve signs there!)

Prevention

• Vaccination (very important)

Prosthogonimus

• May affect bursa (young) and oviduct (older birds)

• Causes ↓ egg production, cloacal issues

🧠 SUMMARY TABLE (very useful for exam)

Disease	Age	Bursa	Key sign
IBD	3–6 weeks	Enlarged → atrophy	Immunosuppression
Leukosis	>14 weeks	Tumors	Neoplasia
Marek	Any (often young)	Atrophy	Paralysis

🔍 Diagnostics (general)

• PCR, Necropsy

• Histopathology

⚖ Differential diagnosis (important!)

• Marek vs Leukosis:

  • Marek → nerve lesions

  • Leukosis → bursal tumors

💊 Therapy

• Mostly no specific treatment

• Supportive care

🛡 Prevention

• Vaccination (IBD, Marek), Biosecurity, Breeding control

🎯 KEY EXAM POINTS

• ⭐ IBD = most important (immunosuppression!)

• ⭐ Age matters (very exam-relevant)

• ⭐ Marek = paralysis

• ⭐ Leukosis = tumors in older birds

• ⭐ Bursa = B-cell immunity

23. Non-infectious and parasitic diseases associated with changes in the liver - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

1. Non-infectious

• Metabolic:

  • Fatty liver hemorrhagic syndrome (FLHS)

• Intoxications

  • Mycotoxins (aflatoxicosis)

  • Heavy metals (lead, mercury)

  • Arsenic, cobalt, phosphorus

2. Parasitic / infectious affecting liver

• Protozoa:

  • Histomoniasis (Histomonas meleagridis) ⭐

  • Trichomoniasis (Trichomonas gallinae)

• Fungal:

  • Aspergillosis (Aspergillus fumigatus)

🟡 1. Fatty liver hemorrhagic syndrome (FLHS)

• High-energy diet + low exercise

• Diet should contain ~0.3 ppm selenium

• Seen in caged laying hens (especially summer)

Pathogenesis

• Excess fat accumulation → fragile liver → rupture → hemorrhage

Clinical signs

• Obesity, ↓ egg production, Sudden death, Pale comb

Lesions

• Enlarged, yellow, friable liver, Hemorrhages, Abdominal fat deposits

Diagnostics

• History + necropsy

Differential diagnosis

• Aflatoxicosis

• Infectious liver diseases

Therapy

• Not practical (often sudden death)

Prevention

• Diet control, Weight management, Reduce energy intake

2. Aflatoxicosis

• Mycotoxins from fungi:

  • Aspergillus

  • Penicillium

• Aflatoxicosis is one of the most important causes of liver damage in poultry production!

Clinical signs

• Depression, Inappetence, Neurological signs (ataxia, convulsions), Death

Lesions

• Liver = enlarged, yellow, sometimes necrotic

Diagnostics

• Feed analysis, History

Therapy

• Remove contaminated feed, Supportive care

Prevention

• Proper feed storage, Avoid mold contamination

3. Heavy metals

Lead

• Liver degeneration, atrophy

Mercury

• Fatty degeneration

3. Histomoniasis (important parasitic cause)

• Histomonas meleagridis

• Transmission via Heterakis gallinarum eggs

Pathogenesis

• Cecum → liver spread

• Severe necrosis

Clinical signs

• Depression, Sulfur-yellow diarrhea (very characteristic), Cyanotic head (black head disease), High mortality

Lesions (pathognomonic ⭐)

• Liver: round necrotic lesions

• Ceca: caseous cores

Diagnostics

• Necropsy

Differential diagnosis

• Coccidiosis, Bacterial hepatitis

Therapy

• No effective treatment

Prevention

• Deworming (Heterakis), Biosecurity, Separate turkeys and chickens

4. Trichomoniasis

• Trichomonas gallinae

Liver involvement

• Can cause necrotic lesions in liver

Clinical signs:

• Weight loss, Weakness, Upper GIT lesions

Diagnostics

• Microscopy

Therapy

• Nitroimidazoles (non-food birds)

Prevention

• Hygiene, Clean water

🍄 5. Aspergillosis

• Aspergillus fumigatus

Pathogenesis

• Primarily respiratory

• May spread → liver granulomas

Clinical signs

• Respiratory signs, Weakness

Lesions

• Granulomas in:

  • Air sacs, Lungs, Liver

Diagnostics

• Culture, histology

Therapy

• Antifungals (limited success)

Prevention

• Good ventilation, Dry litter

🧠 GENERAL CLINICAL SIGNS

• Weight loss,Decreased production, Depression, Mortality

• Liver enlargement

🔍 DIAGNOSTICS

• Necropsy, Feed analysis

• Microscopy/PCR

⚖ DIFFERENTIAL DIAGNOSIS

• Infectious hepatitis

• Coccidiosis

• Septicemia

• Nutritional disorders

💊 THERAPY

• Often supportive

• Remove cause (toxins, parasites)

🛡 PREVENTION

• Proper nutrition

• Good feed storage

• Biosecurity

• Parasite control

🎯 KEY EXAM POINTS

• ⭐ FLHS = metabolic, high-energy diet, sudden death

• ⭐ Aflatoxicosis = most important toxin

• ⭐ Histomoniasis = liver necrosis (classic lesions)

• ⭐ Always mention:

  • feed quality

  • management

  • parasite control

24. Infectious diseases associated with changes in the liver - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

🦠 1. SALMONELLOSIS

I. Pullorum disease

• Salmonella pullorum

• Vertical + horizontal transmission

Clinical signs

• High mortality in chicks (acute), Weakness, diarrhea

Lesions

• Unabsorbed yolk sac

• White-gray nodules (necrotic foci) in liver and organs ⭐

Diagnostics

• Culture, PCR

II. Fowl typhoid

• Salmonella gallinarum

Clinical signs

• Affects older birds, Depression, diarrhea, Pale, dehydrated birds

Pathogenesis:

• After ingestion, bacteria invade intestinal epithelium → septicemia → spread to liver, spleen, kidneys

Lesions

• Similar to pullorum

• Hepatomegaly, congestion ± necrosis

• may have hemorrhages and granulomatous peritonitis

Diagnosis:

• PCR / ELISA needed to differentiate from pullorum disease

Differential diagnosis (for both)

• Colibacillosis, Coccidiosis, Necrotic enteritis

Therapy

• No effective treatment; eradication (depopulation) due to carrier state

Prevention

• Biosecurity, Testing breeder flocks, Hygiene

III. Salmonella typhimurium

• Causes paratyphoid infections

• Similar lesions (liver congestion, necrosis)

🦠 2. AVIAN TUBERCULOSIS

• Mycobacterium avium

Clinical signs

• Chronic course, Weight loss, emaciation, Lameness

Lesions

• Granulomas in liver, spleen, intestine ⭐

Diagnostics

• Tuberculin test, Histology (Ziehl–Neelsen staining)

Differential diagnosis

• Coligranuloma, Neoplasia

Therapy

• ❌ Not practical

Prevention

• Culling, Sanitation

🦠 3. DUCK VIRAL HEPATITIS

• Picornavirus (Avihepatovirus)

Clinical signs

• Young ducklings (<7 weeks), Sudden death, Neurological signs (opisthotonos)

Lesions

• Enlarged liver with hemorrhages ⭐

Diagnostics

• PCR, Necropsy

Differential diagnosis

• Aflatoxicosis

• Septicemia

• Duck viral enteritis

• Septicemia

• Mycotoxicosis

Therapy

• ❌ No treatment

Prevention

• Vaccination of breeders

• Biosecurity

🦠 4. INCLUSION BODY HEPATITIS (IBH)

• Avian adenovirus

Pathogenesis

• Liver damage with intranuclear inclusion bodies ⭐

Clinical signs

• Sudden mortality, Depression, Pale comb, Sometimes jaundice

Lesions

• Pale, enlarged, friable liver, Hemorrhages

Diagnostics

• Histology (inclusions), PCR

Differential diagnosis

• IBD (immunosuppression link)

• Aflatoxicosis

Therapy

• ❌ No effective treatment

Prevention

• Control immunosuppressive diseases:

  • Infectious bursal disease

  • Chicken infectious anemia

🧠 GENERAL CLINICAL SIGNS

• Depression, Diarrhea, Weight loss, Sudden death, ↓ production

🔍 DIAGNOSTICS

• Necropsy (very important), PCR, Culture

⚖ DIFFERENTIAL DIAGNOSIS (important)

• Aflatoxicosis, Fatty liver syndrome, Histomoniasis, Septicemia

💊 THERAPY

• Limited, Often supportive or culling

🛡 PREVENTION

• Biosecurity

• Vaccination (where available)

• Good management

• Control of immunosuppression

🎯 KEY EXAM POINTS

• ⭐ Salmonella → necrotic foci in liver

• ⭐ TB → granulomas (chronic)

• ⭐ Duck hepatitis → acute, high mortality, hemorrhagic liver

• ⭐ IBH → inclusion bodies in hepatocytes

• ⭐ Many have no treatment → prevention is key

25. Non-infectious and infectious diseases of the female reproductive organs - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

In birds, only the left ovary and oviduct are functional.

Non-infectious

• Cysts, Degeneration (toxins, vitamin A deficiency), Hypoplasia (genetic), Neoplasia

Infectious

• Bacterial: Salmonella, E. coli, Mycoplasma, Pasteurella

• Viral: Infectious bronchitis, egg drop syndrome

• Parasitic: Prosthogonimus spp.

DISEASES OF THE OVARY

1. Non-infectious

I. Cysts

• Fluid-filled structures

• Etiology: Endocrine imbalance, Chronic inflammation

• Usually incidental finding

• ❗ Minimal effect on production

II. Degeneration

• Causes:

  • Toxins, Vitamin A deficiency, Infections (e.g. Fowl typhoid)

• Lesions:

  • Misshapen, dark follicles

III. Hypoplasia

• Congenital

• Small, underdeveloped ovary

• ↓ egg production

IV. Neoplasia

• Adenocarcinoma

• Lymphosarcoma (e.g. Marek's disease)

2. Infectious ovarian diseases

I. Salmonellosis

• Misshapen follicles

• Caseous content

II. Fowl cholera

• Oophoritis (ovarian inflammation)

III. Infectious bronchitis

• ↓ egg production (up to 70%)

• Poor egg quality:

  • thin shell, soft shell, watery albumen

DISEASES OF THE OVIDUCT

Salpingitis ⭐ (VERY IMPORTANT)

• Multifactorial:

  • Trauma, ascending infection from cloaca, Spread from air sacs

• Common agents:

  • E. coli, Mycoplasma gallisepticum, Salmonella, Pasteurella multocida

Clinical signs

• Abnormal eggs (soft, misshapen, shell-less), ↓ egg production, Cloacal discharge, “Penguin posture” ⭐

Lesions

• fibrin + caseous exudate, hyperemia, edema in the oviduct, Oviduct dilation, Secondary ovarian atrophy

Diagnostics

• Necropsy, Bacteriology

Differential diagnosis

• Egg retention, Egg drop syndrome, Cloacitis

Therapy

• Antibiotics (early stages only)

Prevention

• Hygiene, Reduce trauma, Control respiratory infections

Egg peritonitis

• Etiology:

  • Reverse flow of egg material + bacteria (often E. coli)

• Clinical signs:

  • Distended abdomen, Penguin posture, ↓ egg production

• Lesions:

  • Fibrin / “cooked egg” material in abdomen

• Diagnosis:

  • Necropsy

• Therapy:

  • Poor prognosis

II. Egg retention (egg binding)

• Etiology: Large/deformed egg, Nutritional deficiency (Ca!) Oviduct dysfunction

Clinical signs

• Straining, Depression, Distended abdomen, Swollen vent

Complications

• Oviduct rupture → peritonitis

Therapy

• Lubrication, Massage, Surgery

Prevention

• Proper nutrition (Ca, vitamins)

III. Egg drop syndrome (EDS)

• Adenovirus

Clinical signs

• Sudden drop in egg production, Soft or shell-less eggs

Diagnostics

• History + production data

Differential diagnosis:

• Newcastle disease, Avian influenza, Vitamin D₃ deficiency

Prevention

• Vaccination, Avoid contaminated vaccines

IV. Prolapse

• Egg retention, Salpingitis, Cloacal inflammation

Clinical signs

• Visible prolapse, Cannibalism risk

Therapy

• Clean, Disinfect, Reposition

Prevention

• Good management, Prevent egg binding

V. Prosthogonimus spp.

• Trematodes

• Indirect life cycle (snails, insects)

Clinical signs

• ↓ egg production, Soft-shelled eggs

• Severe: oviduct rupture → peritonitis

Diagnostics

• Eggs in feces, Necropsy

Therapy

• Limited

Prevention

• Control intermediate hosts, Dry environment

Other:

• Mycoplasma meleagridis – low hatchability

• IBD – cystic dilation of oviduct - Birnavirus

• NCD – low egg production

• Fungi – Aspergillosis, F2 → estrogenic → cystic degeneration of ovary

• Prolapse – cannibalism, other parts might be pulled from abdominal cavity.

🧠 GENERAL DIAGNOSTICS

• History (egg production!), Clinical signs, Necropsy, Microbiology

⚖ DIFFERENTIAL DIAGNOSIS (IMPORTANT)

• Infectious bronchitis

• Egg drop syndrome

• Nutritional deficiencies

• Cloacitis

🛡 PREVENTION (KEY POINTS)

• Biosecurity

• Vaccination (IB, EDS)

• Proper nutrition (Ca, vitamin A)

• Hygiene

🎯 WHAT YOU SHOULD ADD (from your original notes)

✔ Mention:

• “Penguin posture” (salpingitis) ⭐

• Ascending vs descending infection

• Vitamin A deficiency (degeneration)

• Ca deficiency (egg binding)

❗ FINAL TIP

“Salpingitis is the most important oviduct disease and is usually multifactorial, involving bacterial infection combined with mucosal damage.”

In birds, only the left ovary is functional, and the most important reproductive disorders include salpingitis, egg retention, and egg peritonitis, often associated with bacterial infections such as E. coli.

26. Non-infectious and infectious diseases of the male reproductive organs - etiology, symptoms, diagnostics, dif. dg, therapy and prevention. Artificial insemination in poultry.

Non-infectious

• Atrophy, Hypoplasia, Hyperplasia (physiological in breeding season), Neoplasia (rare)

Infectious

• Orchitis, Epididymitis

• Bacterial: E. coli, Salmonella, Staph, Strep

• Viral: Newcastle disease, Marek's disease

• Fungal: Aspergillus

• Protozoa: Trichomonas

• Venereal infections

DISEASES OF TESTICLES

1. Orchitis (inflammation) ⭐

• Bacterial (especially Salmonella, E. coli)

Clinical signs

• Testicular enlargement or later:

  • Orchitis may lead to testicular atrophy, fibrosis, and calcification

Diagnostics

• Clinical exam, Necropsy

• complete blood count:

  • leukocytosis, heterophilia (neutrophilia in mammals)

Differential diagnosis

• Neoplasia, Degeneration

Therapy

• Antibiotics (based on sensitivity)

Prevention

• Hygiene, Control systemic infections

2. Atrophy

• etiology: Age, Malnutrition, Chronic disease, Vitamin deficiency

Signs

• ↓ fertility, Reduced testicle size

3. Hypoplasia

• Congenital, Small, non-functional testes

4. Hyperplasia

• Physiological during breeding season

5. Neoplasia

• Rare, Mostly in older birds

DISEASES OF PENIS (phallus – present in waterfowl only) ⭐

Etiology

• Trauma during mating (especially on land)
  → secondary infection

Clinical signs

• Hyperemia, Edema, Prolapse, Necrosis (if severe)

Therapy

• Cleaning (e.g. KMnO₄), Antibiotics, Reposition if prolapsed

VENEREAL DISEASES

Etiology

• Bacteria: Neisseria, Pasteurella, Mycoplasma

• Fungi: Candida, Aspergillus

• Protozoa: Trichomonas

• Venereal diseases are infections transmitted during mating, caused by bacteria (e.g. Mycoplasma, Salmonella), fungi (Candida), and protozoa (Trichomonas), leading to inflammation (catarrhal, crupous, necrotic) of the reproductive tract in males and females

• High morbidity, low mortality

Clinical signs

• Apathy, Weight loss, Cloacal inflammation

Diagnostics

• Clinical exam, Necropsy

Therapy

• Antibiotics/antimicrobials

Prevention

• Hygiene, Health control, Artificial insemination (reduces spread)

🧠 GENERAL DIAGNOSTICS

• Clinical exam, Necropsy, Microbiology

⚖ DIFFERENTIAL DIAGNOSIS

• Tumors, Nutritional infertility, Systemic infections

💊 THERAPY

• Mainly antimicrobial

• Often limited success

🛡 PREVENTION

• Biosecurity, Good nutrition, Disease control

🧪 ARTIFICIAL INSEMINATION (AI) ⭐

Why used

• Common in turkeys (heavy males can’t mate efficiently)

Collection

• Massage abdomen and back

• Apply pressure → semen release

Important fact ⭐

• Semen loses fertilizing ability quickly (~1 hour)
  → extenders used

Insemination

• Cloaca everted, Semen deposited into oviduct

Frequency

• About once per week

Advantages

• Improves fertility, Controls genetics, Reduces venereal disease spread

🎯 FINAL EXAM SENTENCE

“Male reproductive diseases in poultry are less common and mainly include orchitis, testicular atrophy, and venereal infections, while artificial insemination is widely used in turkeys to improve fertility and reduce disease transmission.”

27. Egg-output disorders, the factors and diseases influencing egg-output, management of egg -output disorders in poultry farming.

Egg-output disorders are conditions that lead to a reduction in egg production or egg quality in laying hens. Because egg production depends on the normal function of the whole organism, almost any systemic disease, metabolic imbalance, or stress condition can result in decreased laying performance.

1. Egg-output abnormalities

Eggs may show different quality defects such as:

• soft-shelled or shell-less eggs → rapid passage through uterus (shell gland)

• thin or poorly calcified shells → nutritional / viral / genetic causes

• small or misshapen eggs

• double-yolk eggs→ ovulation of 2 follicles simultaneously (common at onset of lay)

These abnormalities can be caused by infectious agents, nutritional deficiencies, genetic factors, or toxins. For example, bacteria such as E. coli, Proteus, Micrococcus, and Pseudomonas can contaminate the reproductive tract and affect egg quality. Fungi such as Aspergillus and Penicillium may penetrate the shell and cause mould contamination.

• E. coli, Proteus, Pseudomonas → penetrate and multiply inside egg

• Aspergillus, Penicillium → mouldy eggs via pores

2. Bird-related (reproductive system) causes

Any disease affecting the female reproductive organs can lead to decreased egg output. These include:

• salpingitis and oophoritis (often E. coli, Mycoplasma, Salmonella, Prosthogonimus)

• ovarian cysts, degeneration, hypoplasia

• prolapse and rupture of oviduct

• neoplasia

• egg peritonitis

• Venereal infections transmitted during mating may also contribute to reproductive tract inflammation and reduced fertility.

• CS: “penguin posture”, abdominal distension, cloacal discharge, decreased production and body condition

3. Factors influencing egg production

I. Age and genetics

Hens start laying at around 18–22 weeks (5months ish), reach peak production early, and then gradually decline with age. Produce eggs from 5 months of age, peak in the first 8 weeks, and decline to 65% after 12 months. When moulting (feather shedding) they do not produce eggs

II. Nutrition

Proper nutrition is essential:

• Energy-protein balance is critical

• Calcium and vitamin D are essential for shell formation

• Methionine and lysine support egg protein synthesis

• Vitamin E and selenium support reproductive and antioxidant function

• Water intake directly influences feed intake and production

III. Light

Photoperiod strongly regulates reproduction. Increasing day length stimulates laying, and commercial flocks are usually kept at about 14–16 hours of light daily.

IV. Stress

Stress is a major cause of production drop and includes:

• heat stress

• overcrowding

• transport and handling

• sudden feed changes

• vaccination or management stress

4. Infectious diseases affecting egg output

Egg production can be significantly reduced by:

• Bacteria: Salmonella spp., Streptococcus, E. coli

• Viruses: Infectious bronchitis, Newcastle disease, Marek’s disease, lymphoid leukosis, avian influenza, egg drop syndrome

• Fungi: Aspergillus spp. (mycotoxicoses may also impair production)

5. Important production diseases

• Egg drop syndrome (adenovirus): sudden drop in production with soft-shelled and shell-less eggs in otherwise healthy birds

• Caged layer fatigue: metabolic disease due to calcium depletion at peak laying → causing thin shells, weakness, anorexia and bone fragility

• Fatty liver haemorrhagic syndrome: occurs in overfed, inactive hens with high-energy diets, leading to liver fat accumulation and possible fatal haemorrhage

6. Management and prevention

Control of egg-output disorders is based on:

• balanced nutrition and correct body condition

• proper lighting programs - (22h, 30-40lux, first 3days, gradually decrease to 10lux at 15days)

• heat stress management - temperature (30* young, 25* adult),

  - Relative Humidity (60%)

  - Good ventilation

• strict biosecurity and hygiene

• vaccination against key diseases (IB, ND, EDS)

• all-in all-out production systems

• continuous monitoring of production performance

Conclusion

In summary, egg-output disorders are multifactorial, involving nutrition, environment, stress, and infectious diseases. Effective prevention relies mainly on good management, disease control, and maintaining physiological balance of the laying hen.

28. Hatching of eggs in poultry and its control.

Egg hatching in poultry = the process by which a fertilized egg develops into a viable chick under controlled environmental conditions.

1. Egg formation

The egg is formed in the reproductive tract of the hen. The yolk is produced in the ovary and released when mature. It is captured by the infundibulum, where fertilization occurs if sperm is present.

The egg then passes through:

• magnum – deposition of albumen

• isthmus – formation of shell membranes

• uterus (shell gland) – formation of shell and pigmentation

• vagina – oviposition

2. Veterinary control of hatching

The goal of veterinary control is to ensure high fertility, high hatchability, and production of healthy chicks. This includes control of hygiene, incubation conditions, and prevention of microbial contamination.

• Fertility = fertilization success

• Hatchability = ability of fertile eggs to produce chicks

• Hatchability is influenced by egg quality, storage duration, ventilation, and breeder nutrition, especially vitamin E and selenium levels.

• Deficiency of vitamin E and selenium in breeder diets can impair embryo development and reduce hatchability due to muscular weakness (myodystrophy).

3. Handling and storage of hatching eggs

Hatching eggs are easily contaminated and should be collected frequently and kept clean. Dirty eggs should not be used for hatching due to high risk of contamination. Very large or very small eggs reduce hatchability — large eggs may result in navel defects, while small eggs provide insufficient nutrients for embryo development.

• eggs are collected several times daily

• fumigated with formaldehyde gas to reduce microbial load (reduces bacterial contamination by Salmonella, E. coli and improves hatchability and chick quality)

• stored at 10–12°C and 70–75% humidity

• before incubation, eggs are equilibrated at room temperature (~18–22°C)

Long storage reduces hatchability due to embryo aging and quality deterioration. (too long storage → reduced hatchability. embryo aging before incubation → mortality increases)

Hatchability decreases if eggs are stored for more than 7 days or if temperature changes too rapidly, leading to condensation and increased microbial contamination

4. Incubation conditions

Optimal incubation conditions are critical:

• Eggs are incubated with the blunt end up to ensure correct air cell positioning, which is essential for the chick’s first breath during internal pipping.

• temperature: 37.8°C

• relative humidity: 50–60%

• CO₂ and oxygen exchange must be ensured

• Proper ventilation is essential to supply oxygen and remove CO₂; inadequate ventilation can lead to embryo suffocation and mortality.

• eggs are turned every 2–3 hours to prevent embryo adhesion and ensure normal development

Turning is essential especially during early embryogenesis. prevents embryo adhesion to membranes and supports normal development of extraembryonic structures.

Critical incubation phases:

• early phase = organogenesis (very sensitive)

• late phase = respiratory transition (air cell use)

5. Candling and monitoring

Eggs are examined by candling:

• day 5–6: (white eggs): fertility check (viability of embryo)

• day 7-8 (brown eggs)

• day 18: embryo development and viability (check if it moves)

This allows removal of infertile or dead embryos.

6. Hatching phase

On day 19, eggs are transferred to the hatcher:

• temperature slightly reduced to ~37°C

• humidity increased to 70–75%

• chicks hatch around day 21

After hatching, chick quality is evaluated, and weak chicks are removed.

Very important to evaluate:

• hatchability %

• chick quality scoring

• culling weak chicks

7. Sexing and management

Chicks may be sexed, especially in commercial layer production. Cloacal sexing (Japanese method) is commonly used. In broiler systems, sex separation may also be performed for management efficiency.

Conclusion

Successful hatching depends on proper egg handling, strict environmental control during incubation, and effective veterinary hygiene measures to ensure high fertility and hatchability and production of healthy chicks.

29. The causes of embryonal mortality & growth disorders in poultry & water fowl.

Embryonal mortality is an important economic factor in poultry production because it directly affects hatchability. It typically occurs in two critical phases during incubation:

• Early mortality (around day 4) – associated with metabolic changes, especially peak lactic acid production and CO₂ exchange

• Late mortality (around day 19) – when oxygen demand increases significantly before hatching

• Two mortality peaks: day 4 & day 19

• Embryo development and mortality are monitored by candling, usually at days 5–7 and again around day 16, where we can observe blood vessels and embryo viability.

Causes of embryonal mortality

The causes can be grouped into four main categories:

1. Nutritional factors

• Deficiencies of vitamins (A, B-complex, E) and minerals (Ca, P, Mn, Zn)

• Protein and lipid deficiencies

• Vitamin E and selenium deficiency → muscle weakness and poor hatchability

2. Management factors

• Incorrect temperature, humidity, and ventilation

• Poor egg handling or storage (e.g. long storage, contamination)

• Inadequate turning of eggs

• Cracked shells or improper incubation conditions

3. Infectious diseases

• Bacterial: Salmonella, Streptococcus

• Viral: Newcastle disease, infectious bronchitis, Marek’s disease, IBD

• Fungal: Aspergillus

4. Genetic factors

• Lethal genes causing embryonic death

Age-related causes

• Early (0–7 days): poor hygiene, trauma, vitamin deficiencies, toxicosis

• Mid (7–14 days): malnutrition, infectious diseases

• Late (14–21 days): malposition, oxygen deficiency, improper incubation

Growth disorders in poultry

These are mainly divided into metabolic and infectious causes, especially in fast-growing broilers.

1. Metabolic diseases

Metabolic growth disorders mainly affect the cardiovascular system, causing mortality, and the musculoskeletal system, causing lameness and poor growth.

a) Sudden death syndrome

• Seen in fast-growing broilers

• Due to metabolic imbalance and cardiac arrhythmias

• Birds appear healthy → sudden collapse and death

b) Muscular dystrophy

• Caused by selenium and vitamin E deficiency

• Leads to muscle degeneration

• Clinical signs:

  • Skeletal muscle → weakness, inability to stand

  • Cardiac muscle → sudden death

c) Rickets

• Caused by imbalance of Ca, P, and vitamin D₃

• Leads to soft, deformed bones and poor growth

2. Infectious growth disorders

Malabsorption syndrome

• Multifactorial disease (viruses like reovirus, enterovirus + toxins)

• Affects intestinal absorption

• Clinical signs:

  • Poor growth and uneven flock

  • Diarrhea, undigested feed

  • Poor feathering (“helicopter wings”)

Short conclusion

So overall, embryonal mortality and growth disorders are multifactorial problems involving nutrition, management, infections, and genetics, and proper control requires good biosecurity, balanced nutrition, and optimal incubation conditions.

30. Metabolic diseases of bones - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

Metabolic bone diseases are mainly caused by disturbances in calcium, phosphorus, and vitamin D₃ metabolism, leading to defective bone formation, mineralisation, or maintenance.

1. Rickets (young birds)

Rickets is a disease of growing animals, characterized by defective mineralisation of bone and cartilage. There is a disorder of endochondral ossification in growing bones

Etiology

• Deficiency of calcium, phosphorus, or vitamin D₃

• Incorrect Ca:P ratio

• Lack of sunlight (↓ vitamin D synthesis)

• Renal or gastrointestinal disorders

Clinical signs

• Enlarged joints and epiphyses, Soft, pliable beak and claws, Bone deformities, lameness, stiff gait, Poor growth and weakness

Diagnosis

• Clinical signs + history (nutrition), Radiology: poor mineralisation

• Post-mortem shows poorly mineralised, soft and deformed bones

• Biochemically, we may see decreased calcium and phosphorus and increased alkaline phosphatase

Differential diagnosis: perosis, Marek’s disease, and vitamin deficiencies

Treatment & prevention

• Correct diet (balanced Ca:P ratio)

• Vitamin D₃ supplementation

• Proper management and sunlight exposure

2. Osteomalacia (adult birds)

Osteomalacia is the adult form of rickets, affecting bone remodelling.

Etiology

• Vitamin D₃, Ca, or P deficiency

• Renal disease → phosphorus imbalance

Clinical signs

• Fragile bones, fractures, Spinal deformities, Thin or soft eggshells

Key point

→ Same mechanism as rickets, but in mature skeleton

3. Osteoporosis (cage layer fatigue)

Osteoporosis is a reduction of total bone mass (both organic and inorganic components).

Etiology

• High calcium demand during egg production

• Inadequate calcium or vitamin D₃ intake

• Protein deficiency (matrix formation)

Clinical signs

• Lameness, reluctance to move, Fragile bones, fractures, Drop in egg production, Soft-shelled eggs

4. Cage layer fatigue (important clinical form)

This is a severe form of osteoporosis seen in high-producing layers.

Pathogenesis

• Calcium is mobilized from bones for eggshell production

• → depletion of medullary bone → cortical bone thinning

Clinical signs

• Birds unable to stand (“cage paralysis”), Very fragile bones (tibia, femur fractures), Reduced feed intake

Differential diagnosis

• Infectious causes of lameness (e.g. arthritis, osteomyelitis)

• Trauma

• Mycotoxicosis

Treatment & prevention (general principle)

• Balanced nutrition (Ca, P, vitamin D₃)

• Proper Ca:P ratio

• Adequate protein supply

• Good management (exercise, housing)

• Supplementation in high-risk periods (laying phase)

Osteopetrosis

“Osteopetrosis is the opposite condition, with thickened bones, often associated with viral diseases like leukosis.”

Strong closing sentence

So overall, metabolic bone diseases in poultry are primarily nutritional disorders, and prevention through correct diet and management is far more effective than treatment.

• Clear distinction: rickets vs osteomalacia vs osteoporosis

• Mention of cage layer fatigue = clinical form

• Good inclusion of Ca:P imbalance + vitamin D₃

31. Infectious diseases of bones - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

Infectious bone diseases in poultry are mainly caused by viral and bacterial agents, leading to deformities, lameness, and reduced productivity.

1. Osteopetrosis (“marble bone disease”)

Osteopetrosis is a viral neoplastic disease caused by a strain of the avian leukosis virus. (retrovirus)

Pathogenesis

• The virus alters osteoblast activity → excessive bone formation → thickened, dense bones → exostosis and often anemia (bone marrow compression)

Lesions

• Bilateral, symmetrical thickening of long bones

• Especially tibiotarsus and tarsometatarsus

Clinical signs

• Lameness, difficulty moving, Emaciation (can’t reach feed/water), Weakness, recumbency

Key point

→ Bone is thick but abnormal and non-functional

2. Osteomyelitis

Osteomyelitis is a bacterial infection of bone (epiphyseal region common), often secondary to septicaemia.

Etiology

• Staphylococcus aureus (most common)

• E. coli, Salmonella, Streptococcus, Mycoplasma synoviae

Pathology

• Bone lysis, necrosis

• Replacement by caseous exudate

• Chronic → sclerosis and deformity

Clinical signs

• Lameness, Swollen joints, Reduced mobility

Treatment

• Antibiotics, but the response is often poor

3. Femoral head necrosis (FHN)

Also called femoral head separation in fast-growing broilers.

Pathogenesis

• Mechanical stress + bacterial infection → Separation of growth plate → necrosis

• vascular damage → thrombosis → necrosis

• Primary event is usually:

  • Mechanical stress + rapid growth in broilers
    → this leads to weakness at the growth plate (epiphysis)
    → separation of the growth plate = femoral head separation (FHS)

• After separation:

  • Blood supply is compromised

  • The area becomes susceptible to bacterial colonization (e.g. E. coli, Staph, Strep)

• Then:

  • Thrombosis can occur in damaged vessels

  • This contributes to ischemia → necrosis of the femoral head

Etiology

• E. coli, Staphylococcus, Streptococcus

Clinical signs

• Severe lameness, Birds may use wings for support

Prevention

• Good hygiene, Proper management of fast-growing birds. ATB not recommended.

4. Avian tuberculosis

A chronic granulomatous infection caused by Mycobacterium avium.

Pathology

• Granulomas in:

  • Liver, Spleen, Bone marrow

Clinical signs

• Chronic weight loss, Lethargy, Sometimes lameness

Diagnosis

• Tuberculin test, PCR, histopathology

Treatment & prevention

• No treatment → culling

• Prevention: hygiene, flock turnover

Differential diagnosis

• Metabolic bone diseases (rickets, osteoporosis), Trauma, Nutritional deficiencies

General prevention

• Biosecurity and hygiene

• Good management

• Control of systemic infections

Strong closing sentence

So overall, infectious bone diseases in poultry are mainly secondary to systemic infections or viral tumors, and prevention relies primarily on biosecurity, hygiene, and proper flock management.

32. Muscle disorders in poultry - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

Muscle disorders in poultry include atrophy, muscular dystrophy, and myopathies, caused by nutritional deficiencies, metabolic disturbances, mechanical damage, stress, or toxins.

1. Atrophy

• Definition: ↓ size and function of the muscle after normal development

• Etiology: malnutrition, decreased body weight, chronic systemic diseases (e.g. Marek’s disease)

• CS: muscle wasting

• Dx: clinical + history

• Tx: treat underlying disease, improve nutrition

2. Muscular dystrophy (nutritional myopathy)

• Etiology: deficiency of vitamin E and selenium

• Pathogenesis:

  • Se (glutathione peroxidase) + Vit E protect membranes from oxidative damage

  • Deficiency → lipoperoxidation → degeneration + calcification of muscle cells

• CS:

  • Skeletal muscle → weakness, stiffness, trembling, inability to stand

  • Cardiac muscle → acute heart failure, sudden death

• Dx: history + lesions

• Tx/Prevention: supplementation of Vit E + Se

3. Myopathies (non-inflammatory muscle degeneration)

a) Deep pectoral myopathy (“green muscle disease”)

• Seen in heavy broilers/turkeys

• Etiology: excessive wing flapping → muscle overuse

• compartment-like syndrome due to rigid fascia

• Pathogenesis:

  • muscle swelling inside tight fascia → vascular compression → ↓ blood flow → ischemia → hypoxia → necrosis

• PM: early pale, swollen muscle → later green → fibrous capsule

• Prevention: careful handling, genetic selection

b) Capture myopathy

• Rare in poultry

• Etiology: stress, struggle, transport. predisposed by stress + selenium deficiency

• Pathogenesis: anaerobic glycolysis → lactic acidosis + hyperthermia

• Lesions: pale skeletal muscle (especially legs), sometimes cardiac muscle

• Peracute cases: no visible lesions

• Prevention: minimize stress and handling

c) Toxic myopathy (ionophore toxicity)

• Agents: monensin, salinomycin, narasin

• they are ionophore anticoccidial drugs that disrupt ion transport in parasites, but in overdose they increase intracellular calcium in muscle cells, causing toxic myopathy.

• Pathogenesis:

  • ↑ cation transport → ↑ intracellular Ca²⁺ → disruption of ionic balance → muscle cell death

• CS: incoordination, leg weakness, diarrhea, dyspnea, ↓ feed intake, weight loss

• Ionophore toxicity is increased by ATB (tiamulin, macrolides (erythromycin), chloramphenicol)

• Prevention: correct dosing, avoid drug interactions

d) Pododermatitis
Even though it is skin/joint-related, it often appears in locomotor questions:

• Multi-factorial disease in broilers/breeders

• Predisposing factors:

  • wet litter, obesity

• Lesion: plantar skin erosion → ulcer → abscess → fibrosis

• Leads to:

  • lameness + reduced fertility

• Prevention:

  • dry litter, ammonia control, feed restriction in breeders

e) Aflatoxins → ONLY mention if examiner expands to systemic myopathies

Not necessary for muscle disorders, but if you want extra:

• Aflatoxins cause neuromuscular signs (torticollis, paralysis, seizures) via liver damage → toxin effect

🔑Key exam sentence:

“Muscle disorders in poultry result from nutritional deficiencies (Vit E/Se), ischemic damage due to muscle overuse, stress-induced metabolic acidosis, or ionophore toxicity, leading to degeneration, necrosis, and impaired locomotion or sudden death.”

33. Diseases of the joints - etiology, symptoms, diagnostics, dif. dg, therapy and prevention.

Joint diseases in poultry include developmental, metabolic, and infectious disorders, affecting cartilage, growth plates, and synovial structures, leading to lameness and reduced performance.

1. Chondrodystrophy

• Etiology: genetic disorder of cartilage development

• Types:

  • Lethal chondrodystrophy → inherited → shortened cartilaginous bones

  • Embryonal form → skull deformity (brachycephaly), parrot beak

• Pathogenesis: abnormal cartilage development → skeletal malformation

• CS: deformities, non-viable chicks (severe cases)

• Dx: post-mortem, congenital abnormalities

• Tx: none

• Prevention: breeding selection

2. Dyschondroplasia (Tibial dyschondroplasia)

• Etiology:

  • rapid growth (broilers)

  • genetic predisposition

  • Vit D metabolism disorders

  • Ca:P imbalance

  • mycotoxins

• Pathogenesis:

  • failure of chondrocyte maturation → avascular cartilage plug in growth plate

• Most affected: proximal tibiotarsus

• CS: lameness, reluctance to move, fractures

• Dx: necropsy (cartilage plug in growth plate)

• DDx: rickets

• Tx: none specific

• Prevention: balanced nutrition, genetic selection

3. Gout

• Etiology:

  • hyperuricemia due to renal dysfunction

  • high protein diet

  • dehydration

  • Vit A deficiency

• Pathogenesis: uric acid deposition in tissues → crystal formation

• Types:

  • Visceral gout → organs (heart, liver, kidneys)

  • Articular gout → joints (swelling, inflammation)

• CS:

  • anorexia, weight loss, diarrhea, ↓ egg production

  • lameness (articular form)

• Dx: necropsy (urate deposits)

• Tx: supportive (e.g. alkalization of water with sodium bicarbonate)

• Prevention: proper nutrition, kidney protection, hydration

4. Infectious synovitis

• Agent: Mycoplasma synoviae infection

• Pathogenesis: respiratory infection → systemic spread → synovitis, tendinitis

• CS:

  • lameness

  • swollen hocks, footpads

  • depression, recumbency

  • sternal bursitis

• Dx:

  • ELISA, PCR, serology

  • clinical signs + lesions

• Tx: antibiotics (variable response)

• Prevention: biosecurity, vaccination, monitoring

5. Leg deformities (valgus/varus)

• Etiology:

  • rickets (poor mineralization)

  • chondrodystrophy

  • rapid growth

• Pathogenesis: weak bones → mechanical stress → angular deformities

• CS: valgus (lateral), varus (medial) deviation, lameness

• Dx: clinical observation

• Tx: none once developed

• Prevention: nutrition (Ca, P, Vit D3), growth control

6. Spondylolisthesis (“kinky back”)

• Etiology:

  • rapid growth

  • conformation defects

  • possible bacterial involvement in breeders

• Pathogenesis: vertebral displacement → spinal cord compression

• CS:

  • posterior paralysis

  • inability to stand

  • abnormal posture

• Dx: clinical signs + post-mortem

• Tx: none

• Prevention: genetic selection, growth control

🔑 Key exam summary

“Joint diseases in poultry are mainly caused by developmental cartilage defects (chondrodystrophy, dyschondroplasia), metabolic disorders (gout), and infectious agents (Mycoplasma synoviae), leading to lameness, deformities, and reduced locomotion performance.”