PRIORITY This presentation created by :

Group 1
DISEASES OF
AVIAN BASED ON
BAI AND DA MEMO

Memorandum Circular 30: List

of BAI priority animal diseases
 Objectives

Identify the BAI Identify the commonly

priority diseases used diagnostic
focused on Poultry procedures in identifying
disease
Identify the
Identify the Common
common signs and
Treatment and
clinical findings of
Management Practices
the stated diseases
What is the List
of BAI Priority
Animal Refers to those identified diseases by BAI
Diseases? based on relevance and established
weighte criteria, such as zoonotic disease
or/with public health concern, socio-
economic impact, notifiable or
reportable animal disease, food safety
concerns, and laboratory capacity.
Name of Diseases
Avian Infectious Laryngotracheitis (ILT)

Common Name of Diseases

Avian Infectious Laryngotracheitis (ILT)

Etiologic Agent / Causative Agent:

Laryngotracheitis Virus (ILTV),

Epidemiology
• Geographic Areas: ILT is prevalent globally
• Outbreaks: Farms with poor biosecurity
Avian Infectious
Laryngotracheitis
measures, occurs yea round, but occurs
more frequently on colder months
• Risk Factors: High-density poultry farming,
poor ventilation, stress, and lack of
vaccination
 Mode of Transmission
The ILTV is primarily transmitted aerosol via respiratory secretions :

• Direct contact: Infected birds can transmit the virus through nasal or ocular
secretions.

• Aerosol transmission: The virus can spread through the air over short distances
in crowded, poorly ventilated environments.

• Fomites: Contaminated equipment, clothing, shoes, and feed can contribute to

the indirect spread of the virus between flocks.

• Vertical transmission: In rare cases, the virus can be transmitted from infected
hens to their offspring via eggs.
 Clinical Signs/ Lesions
The clinical signs of ILT can range from mild to severe, with the
severity depending on the virulence of the virus and the health
status of the flock. The main clinical signs include:
• Respiratory distress
• Gasping
• Serous to mucopurulent nasal discharge
• Head shaking
• Swelling of the head, neck, and sinuses
• Conjunctivitis
• Ocular discharge
• Reduced feed and water intake
• Depression and lethargy
soiling of back and wing feathers with mucus and blood
Clinical Signs/ Lesions
 Lesions
• The trachea often shows congestion, edema, and hemorrhagic
lesions. The tracheal mucosa may appear thickened and
inflamed.
• The larynx and pharynx can become swollen, and there may be
the presence of necrotic plaques or ulcerations.
 Differential Diagnosis
Diagnosis of ILT is based on clinical signs, post-mortem lesions, and laboratory testing.
· Clinical examination: The characteristic clinical signs of respiratory distress and nasal
discharge are highly suggestive of ILT.
· Necropsy and histopathology: Gross lesions in the trachea and larynx, as well as
histopathological examination, can reveal characteristic intranuclear inclusion bodies
in affected tissues.
· Polymerase Chain Reaction (PCR): PCR testing is the most reliable and specific method
to confirm the presence of ILTV DNA in respiratory samples, tissues, or swabs.
· Serology: Enzyme-linked immunosorbent assays (ELISA) or virus neutralization tests
can be used to detect antibodies against ILTV in the serum, although these are more
useful for monitoring immunity rather than acute diagnosis.
· Virus isolation: The virus can be isolated from infected tissues in cell culture, though
this method is labor-intensive and less commonly used today due to the availability of
PCR.
 Differential Diagnosis
Differentiation from FF
Disease Key Clinical Signs Lesions Differentiation from ILT
Disease

AI causes systemic
involvement (swelling, AI presents with systemic
Respiratory distress,
Hemorrhages in multiple edema) and often sudden signs (edema, cyanosis),
sudden death, swelling of
Avian Influenza (AI) organs, edema in death, while ILT primarily unlike FF, which causes
the head, leg edema,
head/neck, cyanosis affects the respiratory proliferative skin and
diarrhea
tract with hemorrhagic mucosal lesions
tracheitis

ND has neurological
Respiratory distress, ND causes systemic and
Hemorrhages in trachea, involvement, while ILT is
neurological signs neurological signs,
Newcastle Disease (ND) intestines, and brain, air strictly respiratory with
(tremors, paralysis), whereas FF mainly affects
sacculitis characteristic
greenish diarrhea the skin and oral cavity
hemorrhagic tracheitis

CRD has no skin lesions,

CRD lacks severe tracheal
Mild respiratory distress, while FF presents with
Chronic Respiratory Air sacculitis, caseous hemorrhage seen in ILT
nasal discharge, reduced wart-like growths on the
Disease (CRD) exudate in air sacs and has chronic
egg production skin and mucous
progression
membranes
 Differential Diagnosis

Aspergillosis is
fungal, non-
Aspergillosis
contagious, and
Dyspnea, lacks the
Yellow nodules presents with
gasping, silent cutaneous and
Aspergillosis in lungs, fungal granulomatous
respiratory mucosal lesions
plaques in air sacs lung lesions
distress characteristic of
rather than
FF disease
hemorrhagic
tracheitis
 Differential Diagnosis

Chronic Respiratory Aspergillosis

Avian Influenza Newcastle Disease
Disease
 Treatment/Control/Prevention

1. Supportive care:
• Antibiotics: used to control secondary bacterial infections (e.g.,
oxytetracycline or tylosin may be prescribed).
• Anti-inflammatory drugs: Drugs like flunixin meglumine may be used to
reduce inflammation and pain associated with respiratory distress.
 Treatment/Control/Prevention
2. Vaccination: Vaccination is the primary method of prevention
and control of ILT.
• Live vaccines: These vaccines are often used in areas with high
risk of ILT outbreaks. Live attenuated vaccines (e.g., Herpesvirus of
Turkeys, HVT, and attenuated ILTV vaccine) are commonly used,
and they are typically administered by eye-drop or spray.
• Dose: A single dose of the vaccine is typically administered at 1
day of age via eye-drop or spray.
• Killed vaccines: Killed vaccines may be used in some cases,
particularly when live vaccines are contraindicated or in breeder
flocks.
 Treatment/Control/Prevention

3. Biosecurity measures:
• Preventing contact with infected birds or fomites is crucial.
• Ensuring good ventilation, reducing overcrowding, and
isolating new or sick birds from healthy ones can help limit the
spread of the virus.
Treatment/Control/Prevention
• Disinfecting equipment, clothing, and vehicles that come into contact with
infected birds is essential.
• Culling: In severe outbreaks, culling infected birds may be necessary to
prevent further spread of the virus.
• Quarantine and Monitoring: Monitoring the flock for clinical signs and
isolating any suspect cases early can prevent widespread outbreaks.
Name of Diseases
Avian Mycoplasmosis (Mycoplasma gallesepticum
&Mycoplasma synoviae)

Common Name of Diseases

Avian Mycoplasmosis (commonly referred to as CRD or Chronic
Respiratory Disease in poultry)

Etiologic Agent / Causative Agent:

Mycoplasma gallisepticum (MG) and Mycoplasma synoviae
(MS

Epidemiology
Mycoplasma gallisepticum (MG) and Mycoplasma
synoviae (MS) affect poultry worldwide, especially
in areas with poor biosecurity or intensive farming.
Avian
Outbreaks are common in high-density flocks and
stressful conditions. MG affects chickens, turkeys,
and game birds, while MS also impacts ducks.
Mycoplasmosis
Mycoplasmosis is chronic, causing production
losses, reduced growth, and increased
susceptibility to secondary infections.
 Mode of Transmission
• Horizontal transmission (bird-to-bird): The primary route of transmission is through
respiratory secretions, including nasal discharge, saliva, and feces.
• Vertical transmission: Mycoplasma gallisepticum can also be transmitted from infected
hens to their offspring via eggs, making it difficult to eradicate in flocks.
• Indirect transmission: The bacteria can be spread through contaminated equipment,
clothing, feed, water, and transport vehicles. This is a common route in crowded or poorly
managed farms.

Clinical Signs/ Lesions

The clinical signs of Mycoplasmosis depend on the age of the bird,
the specific strain of Mycoplasma, and the presence of secondary
infections (such as viral or bacterial co-infections).
 Clinical Signs/ Lesions
Mycoplasma gallisepticum (MG):
Respiratory issues: Nasal discharge, coughing, sneezing, ocular discharge,
and labored breathing.
Swelling: Head and neck swelling due to sinusitis.
Eye inflammation: Conjunctivitis.
Production losses: Reduced egg production and quality.
Secondary infections: Increased susceptibility to bacterial infections like E.
coli.
 Clinical Signs/ Lesions
Lesions: Inflammation and thickening in the trachea, bronchi, lungs, and air
sacs.
Mycoplasma synoviae (MS):
Respiratory symptoms: Mild signs like sneezing and nasal discharge.
Joint problems: Arthritis, synovitis, swollen hocks, joint deformities, and
lameness.
Lesions: Joint swelling, synovial membrane inflammation, and increased synovial
fluid.
Clinical Signs/ Lesions
Diagnosis of avian mycoplasmosis involves a combination of clinical signs, post-
mortem examination, and laboratory testing:
· Clinical signs: Observing respiratory distress, nasal discharge, and lameness in
flocks, especially when secondary infections are present, can suggest
Mycoplasmosis.
· Necropsy: Gross lesions such as congestion and inflammation in the respiratory
tract (trachea, lungs, and air sacs) are characteristic of MG infections, while MS is
associated with joint swelling and inflammation.
· Culture: Mycoplasma bacteria can be cultured from respiratory exudates,
synovial fluid, or other tissues. However, this can be time-consuming and
difficult due to the slow growth of Mycoplasma species.
 Diagnosis

· Polymerase Chain Reaction (PCR): PCR testing is the most sensitive and specific
method for detecting Mycoplasma gallisepticum and Mycoplasma synoviae DNA
in clinical samples such as tracheal swabs, blood, or tissue samples.
· Serology: Enzyme-linked immunosorbent assays (ELISA) or serum agglutination
tests can detect antibodies against MG and MS and can be used for herd-level
diagnosis, especially in asymptomatic carriers.
 Differential Diagnosis
Disease Key Clinical Signs Lesions Differentiation from Others

Mycoplasmosis Unlike AI and ND, Mycoplasmosis lacks

Mild respiratory distress, nasal discharge, Air sacculitis, caseous
(Chronic sudden death and systemic involvement.
coughing, swollen sinuses, decreased egg exudate in air sacs, swollen
Respiratory Unlike Aspergillosis, it is bacterial and
production sinuses
Disease - CRD) contagious

AI causes systemic involvement (edema,

Hemorrhages in multiple
Respiratory distress, sudden death, hemorrhages), whereas Mycoplasmosis is
Avian Influenza (AI) organs, edema in head/neck,
swelling of the head, cyanosis, diarrhea mainly chronic respiratory. ND also has
cyanosis
neurological signs

ND has neurological symptoms absent in

Respiratory distress, neurological signs Hemorrhages in trachea,
Newcastle Disease Mycoplasmosis and Aspergillosis. AI can also
(tremors, paralysis, twisted neck), greenish intestines, brain; air
(ND) cause hemorrhages but lacks neurological
diarrhea sacculitis
signs

Aspergillosis is fungal, non-contagious, and

Dyspnea, gasping, silent respiratory Yellow nodules in lungs,
Aspergillosis has granulomatous lung lesions, unlike viral
distress fungal plaques in air sacs
and bacterial infections
 Differential Diagnosis
Disease

Mycoplasmosis (Chronic Respiratory Disease -

CRD)

Avian Influenza (AI)

Newcastle Disease (ND)

Aspergillosis
 Differential Diagnosis
• Infectious Laryngotracheitis (ILT)
• Avian Influenza (AI)
• Newcastle Disease
• Aspergillosis

Treatment/Control/Prevention
1. Antibiotics
Antibiotics like tetracyclines (e.g., oxytetracycline) and macrolides (e.g., tylosin) are
commonly used to treat Mycoplasma infections in poultry, with typical doses
administered via drinking water for 5–7 days. Joint inflammation caused by
Mycoplasma synoviae may require NSAIDs like flunixin meglumine for pain and
swelling. While treatment manages symptoms, it does not eradicate the infection,
which can persist and cause chronic issues.
 Treatment/Control/Prevention

2. Vaccination:
Vaccines, particularly for Mycoplasma gallisepticum (MG), are a key
preventive measure.
Live attenuated vaccines like the F-strain are commonly used, administered
via drinking water, eye-drop, or spray at 1–2 weeks of age, with a booster at 6–
8 weeks.
There is no effective vaccine for Mycoplasma synoviae yet, though
inactivated vaccines are under development for high-risk areas.
 Treatment/Control/Prevention
3. Biosecurity:
Prevent infections by isolating new birds, disinfecting equipment, and
controlling movement between farms.
Quarantine new birds for 3 weeks and test for Mycoplasma before introducing
them to the flock.
Minimize stress through proper ventilation, nutrition, and avoiding
overcrowding.
In severe cases, culling infected or high-risk birds may be necessary to limit
disease spread.
Name of Diseases
Fowl Typhoid & Pullorum Disease

Common Name of Diseases

Salmonellosis

Etiologic Agent / Causative Agent:

Salmonella Gallinarum, a specific serovar of Salmonella
enterica. Pullorum Disease (PD) is caused by Salmonella
Pullorum, another serovar of Salmonella enterica.

Epidemiology
Fowl Typhoid and Pullorum Disease
Fowl Typhoid &
Pullorum Disease
are serious infectious diseases of
poultry, with historical significance
due to their role in reducing poultry
productivity and trade.
 Epidemiology
Fowl Typhoid: Primarily affects adult chickens but can also infect turkeys,
game birds, and other poultry. It is globally prevalent but less common in
developed countries due to strict control measures.
Pullorum Disease: Mainly affects chicks under three weeks old but can
occur in older birds. Historically a major issue in hatcheries, it is now rare
in developed countries due to control programs.
Outbreak Triggers: Both diseases are more likely in crowded conditions,
poor biosecurity environments, and regions with inadequate veterinary
surveillance. Pullorum Disease has been largely controlled through strict
screening and testing protocols.
 Mode of Transmission
Fowl Typhoid (FT):
Horizontal transmission: Bacteria are shed in feces, contaminating food, water,
and surfaces, which other birds ingest.
Vertical transmission: Rarely, bacteria pass from infected hens to chicks through
eggs, leading to infected hatchlings.
Pullorum Disease (PD):
Horizontal transmission: Similar to FT, spread occurs via fecal-oral routes
through contaminated food, water, or surfaces.
Vertical transmission: More common than in FT, with bacteria frequently passed
through infected eggs. Chicks from these eggs are born infected and may show
signs shortly after hatching.
 Clinical Signs/ Lesions

Fowl Typhoid (FT):

Acute symptoms: Sudden death, lethargy, depression, respiratory
distress (coughing, sneezing, nasal discharge), and
greenish/yellowish diarrhea.
Chronic cases: Poor weight gain, reduced egg production, and
reproductive issues in hens.
Lesions: Enlarged, congested liver, spleen, and kidneys; intestinal
inflammation or ulcers observed on necropsy.
 Clinical Signs/ Lesions

Pullorum Disease (PD):

Acute symptoms: In chicks, lethargy, diarrhea, reduced appetite,
and sudden death. Older birds may show respiratory distress.
Chronic cases: Stunted growth, poor feed conversion, and
abnormal feathering in surviving chicks.
Lesions: Pale, swollen liver, enlarged spleen, necrotic liver foci,
and intestinal inflammation or hemorrhage seen during necropsy.
Clinical Signs/ Lesions
 Diagnosis
·Clinical examination: The presence of sudden death, diarrhea, and respiratory
signs, particularly in young chicks or adult birds, can raise suspicion of Fowl
Typhoid or Pullorum Disease.
·Necropsy: Examination of internal organs (liver, spleen, intestines) can provide
clues to the diagnosis, such as swelling, necrosis, or hemorrhage.
·Bacterial culture: The definitive diagnosis is typically made by isolating Salmonella
Gallinarum or Salmonella Pullorum from fecal samples, blood, or tissues.
·Polymerase Chain Reaction (PCR): PCR is highly sensitive and specific for detecting
the DNA of Salmonella species, including S. Gallinarum and S. Pullorum.
·Serological tests: Serum agglutination or enzyme-linked immunosorbent assays
(ELISA) can detect antibodies against Salmonella Gallinarum and Salmonella
Pullorum, useful for monitoring flock exposure or screening for carriers.
 Differential Diagnosis
Disease Key Clinical Signs Lesions Differentiation from Others

Lethargy, greenish-yellow diarrhea, Unlike Colibacillosis, Fowl Typhoid mainly

Fowl Typhoid Enlarged, bronze-colored liver,
reduced egg production, pale affects the liver and spleen. Coccidiosis
(Salmonella swollen spleen, enteritis, necrotic
combs, high mortality in severe causes bloody diarrhea, while
Gallinarum) foci in organs
cases Mycoplasmosis is mainly respiratory

Colibacillosis causes more generalized

Air sacculitis, pericarditis,
Colibacillosis (E. Respiratory distress, septicemia, infections and often follows other diseases.
perihepatitis, caseous exudate in
coli infection) diarrhea, decreased growth rate Unlike Fowl Typhoid, it does not specifically
organs
target the liver and spleen

Intestinal hemorrhages, thickened Coccidiosis is protozoal, not bacterial, and

Bloody or mucoid diarrhea, weight
Coccidiosis intestinal walls, cecal cores (in primarily affects the intestines, unlike Fowl
loss, ruffled feathers, weakness
Eimeria tenella) Typhoid and Colibacillosis

Mycoplasmosis primarily affects the

Mild respiratory distress, nasal
Mycoplasmosis Air sacculitis, caseous exudate in respiratory system, whereas Fowl Typhoid,
discharge, swollen sinuses, reduced
(CRD) air sacs Colibacillosis, and Coccidiosis have
egg production
systemic or intestinal involvement
Differential Diagnosis
Disease

Fowl Typhoid
(Salmonella
Gallinarum)

Colibacillosis (E.
coli infection)

Coccidiosis

Mycoplasmosis
(CRD)
 Treatment/Control/Prevention
1. Antibiotic Treatment:
Common antibiotics for Salmonella in poultry include
chlortetracycline, sulfonamides (e.g., sulfadimethoxine), and
neomycin, given via drinking water for 5–7 days.
Antibiotics control symptoms and secondary infections but do not
cure the disease, especially in cases of vertical transmission.
2. Control and Prevention:
Culling: Infected or exposed birds should be culled to prevent the
spread.
Egg Testing: Eggs from infected birds should be tested and
discarded to prevent vertical transmission, with strict sanitation in
hatcheries.
 Treatment/Control/Prevention
3. Vaccination:
Vaccines for Salmonella Gallinarum (Fowl Typhoid) and Salmonella
Pullorum are used to prevent outbreaks, typically administered in
breeder flocks.
Fowl Typhoid vaccine: Live attenuated vaccine given at 6-8 weeks via
injection.
Pullorum Disease vaccine: Inactivated vaccine given to chicks at 1 day
of age.
 Treatment/Control/Prevention
4. Biosecurity:
Hygiene: Regular cleaning and disinfecting, testing new birds,
and managing the movement of people and equipment are
essential.
Rodent Control: Prevent transmission by controlling rodents,
which can carry Salmonella.
Monitoring and Testing: Regular flock testing for Salmonella
Gallinarum and Salmonella Pullorum helps detect carriers.
Environmental Control: Proper ventilation, avoiding
overcrowding, and ensuring adequate nutrition help minimize
disease impact.
Name of Diseases
Avian Influenza

Common Name of Diseases

Bird Flu

Etiologic Agent / Causative Agent:

Avian Influenza is caused by Influenza A viruses,
which belong to the family Orthomyxoviridae

Epidemiology
Avian Influenza can occur globally,
Avian
Influenza
with different regions experiencing
outbreaks at different times. The virus
is commonly found in wild waterfowl
(e.g., ducks, geese) which serve as
natural reservoirs for the virus.
 Epidemiology
• Outbreaks of Avian Influenza are often seasonal, with a higher incidence occurring during the
cooler months (fall and winter). However, outbreaks can happen year-round depending on
environmental factors and migration patterns.
• Epidemiology of H5N1 and H7N9:
• H5N1: This strain gained global attention in the early 2000s due to its high pathogenicity and
ability to cross species barriers. It primarily affected poultry but has also caused human
infections with high mortality rates.
• H7N9: First identified in China in 2013, H7N9 is associated with human infections and has
resulted in significant outbreaks in poultry.
• H5N8: Recently, H5N8 has caused widespread outbreaks in poultry worldwide, especially in
Europe and Asia, with infections in wild birds as well.
 Mode of Transmission
Direct Transmission: Avian Influenza spreads primarily through direct contact
between infected and healthy birds, mainly via respiratory secretions (nasal
discharge, saliva, feces). Infected birds shed the virus in these secretions, and
healthy birds can ingest or inhale the virus from contaminated environments,
food, water, or surfaces.
Indirect Transmission: The virus can spread via contaminated equipment,
clothing, footwear, vehicles, feed, and water, making biosecurity crucial to
prevent outbreaks.
Wild Bird Migration: Migratory wild birds, particularly waterfowl, can carry the
virus without showing symptoms, facilitating its spread to domestic poultry.
Human Transmission: Rare human transmission occurs, especially with
strains like H5N1 and H7N9, typically through close contact with infected
poultry or contaminated environments. Human-to-human transmission is
uncommon but possible with highly pathogenic strains.
 Clinical Signs/ Lesions
Highly Pathogenic Avian Influenza (HPAI) (e.g., H5N1, H7N9):
Acute sudden death: Birds may die suddenly, often without prior
clinical signs.
Severe respiratory distress: Symptoms include sneezing, coughing,
nasal discharge, and gasping.
Neurological symptoms: Tremors, incoordination, paralysis, drooping
of wings and head.
Swelling: Edema in the head, neck, and eyes, sometimes with
hemorrhagic or bluish discoloration of comb and wattle.
Diarrhea: Greenish, watery feces.
Lesions: Necrotic foci in the liver, spleen, and kidneys, hemorrhages in
internal organs, gastrointestinal tract, and skin.
 Clinical Signs/ Lesions

Low Pathogenic Avian Influenza (LPAI):

Mild respiratory signs: Sneezing, coughing, and nasal discharge, but
less severe than HPAI.
Digestive signs: Mild diarrhea or changes in feces appearance.
Reproductive signs: Decreased egg production, soft-shelled or
deformed eggs in laying hens.
Lesions: Mild congestion in the respiratory tract, minor inflammation,
and slight changes in the gastrointestinal tract.
Clinical Signs/ Lesions
 Diagnosis

Diagnosis
• Clinical Signs: The sudden onset of disease, high mortality, and a
combination of respiratory and neurological symptoms should raise
suspicion of Avian Influenza, particularly in high-risk flocks or during
known outbreaks.
• Post-mortem Examination: Lesions such as hemorrhages in internal
organs, edema in the head and neck, and necrosis in the liver and
spleen are suggestive of HPAI.
 Differential Diagnosis
• Laboratory Diagnosis:
o RT-PCR (Reverse Transcription Polymerase Chain Reaction): The
most reliable and rapid method to detect Avian Influenza virus in
clinical samples (e.g., oropharyngeal or cloacal swabs, tissue samples).
o Virus Isolation: The virus can be cultured from swabs or tissues, but
this method is time-consuming and requires a high-level biosafety
containment.
o Serology: ELISA or Hemagglutination Inhibition (HI) tests can detect
antibodies against the virus, useful for identifying exposure or
infection in flocks.
 Differential Diagnosis
Disease Key Clinical Signs Lesions Differentiation from Others

Respiratory distress, sudden death, AI causes systemic involvement with high

Hemorrhages in multiple
Avian Influenza (Bird swelling of the head, cyanosis, mortality. Unlike ND, it may lack neurological
organs, edema in head/neck,
Flu - AI) diarrhea, neurological signs (in signs. Unlike Fowl Cholera, it often causes
cyanosis
some cases) cyanosis and widespread hemorrhages

ND has distinct neurological symptoms,

Respiratory distress, neurological Hemorrhages in trachea,
Newcastle Disease absent in Fowl Cholera and Aspergillosis. AI
signs (tremors, paralysis, twisted intestines, and brain; air
(ND) can also cause hemorrhages but lacks
neck), greenish diarrhea sacculitis
consistent neurological signs

Fowl Cholera differs from AI and ND by

Fowl Cholera Swollen wattles, greenish diarrhea, Hemorrhages in heart, liver,
causing swollen wattles and liver lesions. It
(Pasteurella fever, lameness, sudden death in intestines, swollen liver with
lacks AI's cyanosis and ND's neurological
multocida) peracute cases necrotic foci
signs

Aspergillosis is fungal, non-contagious, and

Dyspnea, gasping, silent respiratory Yellow nodules in lungs, has granulomatous lung lesions, unlike viral
Aspergillosis
distress, weight loss fungal plaques in air sacs and bacterial infections that cause systemic
disease
 Differential Diagnosis
Disease

Mycoplasmosis (Chronic Respiratory Disease -

CRD)

Avian Influenza (AI)

Newcastle Disease (ND)

Aspergillosis
Differential Diagnosis

Disease

Avian Influenza (Bird

Flu - AI)

Newcastle Disease (ND)

Fowl Cholera
(Pasteurella multocida)

Aspergillosis
Differential Diagnosis
• Newcastle Disease
• Fowl Cholera
• Aspergillosis

Treatment/Control/Prevention

1. Treatment:
No specific antiviral treatment for Avian Influenza in poultry,
particularly for highly pathogenic strains.
Supportive care (e.g., clean water, feed) and management of
secondary infections are used in less severe cases.
Antiviral agents like oseltamivir are used experimentally in humans
but are not approved for poultry.

2. Control and Prevention:

Culling: Affected and exposed birds are culled to prevent the virus
from spreading. This is the primary control measure.
 Treatment/Control/Prevention
3. Vaccination:
Vaccination against strains like H5N1 and H5N8 is used in
some countries, particularly in regions with endemic risks.
H5N1 vaccine: Administered at 0.5 mL per bird, typically at
4-6 weeks, with boosters as needed in high-risk areas.

4. Biosecurity:
Strict biosecurity measures are crucial, including
controlling access to farms, disinfecting equipment and
vehicles, and quarantining new birds.
Isolation of infected flocks: Infected flocks should be
isolated to prevent contact with healthy birds and wildlife.
Name of Diseases
Newcastle Disease (ND)

Common Name of Diseases

avian paramyxovirus type 1 (APMV-1) infection/
Poultry Plague

Etiologic Agent / Causative Agent:

Newcastle Disease virus (NDV), a paramyxovirus
classified as Avian Paramyxovirus 1 (APMV-1

Epidemiology
Global Distribution: Newcastle Disease
Newcastle
Disease (ND)
affects both domestic poultry and wild
birds, with a higher prevalence in regions
with poor biosecurity and limited
vaccination coverage. It can occur
anywhere worldwide.
 Epidemiology

Outbreaks: Major outbreaks are often linked to poor flock management,

failure to vaccinate, or the introduction of infected birds from endemic
regions.
Endemic Areas: NDV is endemic in parts of Africa, Asia, and Europe. In
developed countries, strict vaccination programs help control the disease,
but occasional outbreaks still occur in wild birds or poultry exposed to
infected environments.
Seasonality: While outbreaks can occur year-round, they are more common
in winter and early spring, often due to biosecurity lapses, overcrowding, and
poor ventilation in poultry houses.
 Mode of Transmission
Direct Contact:
The virus spreads primarily through direct contact with infected birds' secretions, such
as feces, saliva, and nasal discharge. Infected birds shed the virus, especially during
the acute phase of infection.
Indirect Transmission:
The virus can survive in the environment for extended periods and be spread through
contaminated equipment, feed, water, clothing, vehicles, and people. It can also
spread via airborne droplets over short distances.
Wild Bird Reservoirs:
Wild birds, including pigeons, waterfowl, and migratory birds, can carry NDV
asymptomatically, acting as reservoirs. These birds can transmit the virus to domestic
poultry, especially where wild birds and poultry interact.
Vertical Transmission:
Infected hens can lay infected eggs, transmitting the virus to chicks. This mode of
transmission is more common with velogenic strains of NDV.
 Clinical Signs/ Lesions
Velogenic (High Pathogenic) Newcastle Disease (most severe):
Sudden death: Often the first sign, particularly in young poultry.
Severe respiratory distress: Gasping, coughing, sneezing, and
nasal discharge.
Neurological signs: Incoordination, paralysis, torticollis (neck
twisting), tremors, and "star-gazing" posture.
Gastrointestinal signs: Watery, greenish diarrhea.
Edema and swelling: Swelling of the head, neck, and eyes, with
bluish discoloration of the comb and wattle.
Lesions: Hemorrhages in internal organs, thickened trachea, and
necrosis in the gizzard.
 Clinical Signs/ Lesions
Velogenic infection clinical signs of
Newcastle disease of chickens:
(a) Misshappen eggs (Piller, 2010);
(b) internal and external
hemorrhage (Herenda and
Chamber, 1994);
(c) green watery diarhhea (Lucas
and Jamroz, 1961);
(d) comb cyanosis (Admin, 2017).

ResearchGate. (n.d.). ResearchGate - Temporarily Unavailable.

https://www.researchgate.net/figure/elogenic-infection-clinical-signs-of-Newcastle-disease-of-
chickens-a-Misshappen-eggs_fig3_323658575
 Clinical Signs/ Lesions
Clinical signs and lesions observed:

(a) Torticollis

(b) proventriculitis,

(c) tracheitis.

ResearchGate. (n.d.). ResearchGate - Temporarily Unavailable.

https://www.researchgate.net/figure/Figure-2-Clinical-signs-and-lesions-observed-a-Torticollis-b-
proventriculitis-c_fig2_334192419
 Clinical Signs/ Lesions

Mesogenic (Moderate Pathogenic) Newcastle Disease:

Milder respiratory signs: Coughing, sneezing, and nasal
discharge.
Milder neurological signs: Incoordination and mild
paralysis.
Reduced egg production: Soft-shelled eggs and
decreased production in laying hens.
Lesions: Mild hemorrhages in the gastrointestinal tract
and slight swelling of the head.
 Clinical Signs/ Lesions

Lentogenic (Low Pathogenic) Newcastle Disease:

Mild respiratory signs: Sneezing, nasal discharge, and
mild coughing.
Mild or no neurological signs: Occasionally slight
incoordination or tremors in chicks.
Reduced egg production: Mild drop in egg production
or quality in adult hens.
Lesions: Mild congestion in the respiratory tract and
slight swelling of the head, with generally minimal
lesions.
 Clinical Signs/ Lesions
(a) nervous signs as torticolis
(b) congested pectoral muscle
(c) Congestion of trachea
(d) Mucoid discharges in trachea
(e) Haemorrhage on tips of
proventriculus
(f) Ulcer in small intestine
(g) Haemorrhage of iliocaecal tonsils
(h) Congested brain tissue.

https://www.sciencedirect.com/science/article/pii/S0032579119300483
 Diagnosis
1. Clinical Signs:
o Clinical suspicion is based on sudden deaths, neurological symptoms, respiratory distress,
and gastrointestinal signs. Affected birds may show the characteristic torticollis (twisted
neck) and "star-gazing" posture.
2. Laboratory Diagnosis:
o Reverse Transcription Polymerase Chain Reaction (RT-PCR): The most reliable method for
detecting NDV RNA in clinical samples (e.g., swabs, blood, tissues).
o Virus Isolation: NDV can be cultured in embryonated eggs or cell cultures. The virus
typically causes a characteristic embryo death or hemagglutination in red blood cells.
o Serological tests: The Hemagglutination Inhibition (HI) test can be used to detect
antibodies against NDV, especially useful for detecting exposure in non-symptomatic birds.
Enzyme-linked immunosorbent assays (ELISA) can also be used for routine surveillance.
Differential Diagnosis

Similarities with Differences from

Disease Clinical Signs Lesions
Newcastle Disease Newcastle Disease

Hemorrhages in
Respiratory distress,
trachea, proventriculus, Severe edema, comb
Avian cyanosis, decreased egg Respiratory signs,
and discoloration, and more
Influenza production, diarrhea, high mortality
intestines; swollen hemorrhagic lesions
high mortality
combs and wattles

Fibrinous pneumonia,
Greenish diarrhea, caseous exudate in Respiratory signs
Fowl Presence of purulent and
nasal discharge, swollen sinuses, and nervous
Cholera fibrinous exudates
wattles, lameness pericarditis, involvement
hepatomegaly
Differential Diagnosis

Sudden death,
Liver and kidney
neurological signs, Neurological No infectious
necrosis, hemorrhages,
Toxicology diarrhea signs and sudden cause; rapid
sometimes
(depending on mortality onset of signs
no gross lesions
toxin)

Respiratory Caseous nodules in Fungal plaques

distress, weight loss, lungs and air sacs, Respiratory and chronic
Aspergillosis open-mouth yellow or involvement disease pattern
breathing green fungal plaques
 Treatment/Control/Prevention
1. Treatment:
No antiviral treatment: There is no specific antiviral
treatment for ND, especially in severe outbreaks. The
focus is on controlling secondary infections and
providing supportive care.
Antibiotics: These may be used to manage secondary
bacterial infections but do not affect the virus itself.
Supportive care: Ensuring adequate hydration,
warmth, and nutrition can aid recovery in less severe
cases.
 Treatment/Control/Prevention
Control and Prevention:
Vaccination: The primary method of controlling ND, particularly in high-risk
areas.
Live attenuated vaccines: Commonly used, administered via drinking water,
spray, or intramuscular injection. These provide long-lasting immunity.
Inactivated vaccines: Used for controlled vaccination, especially for specific
strains or high-risk areas.
Dosing:
Live vaccines (e.g., Hitchner B1, LaSota strain) are administered to chicks at 1-2
days old via drinking water, with boosters at 4-6 weeks and again before
production.
Inactivated vaccines: Administered intramuscularly, 0.5 mL for adult birds, and
0.2-0.5 mL for chicks.
 Treatment/Control/Prevention
Biosecurity:
Strict biosecurity measures are essential to prevent virus introduction. This
includes controlling access, disinfecting equipment, maintaining
sanitation, and ensuring workers avoid contact with infected or wild birds.
Quarantine new birds: Test and quarantine new birds before they are
introduced to a flock.
Surveillance:
Regular testing using serology or RT-PCR can detect early signs of
infection, even in asymptomatic carriers.
Culling:
Infected and exposed birds should be culled to prevent the virus from
spreading. Depopulating affected flocks is crucial to limit transmission.
 Treatment/Control/Prevention

Environmental Management:

Ventilation and overcrowding: Proper ventilation and

managing crowding can reduce stress and help limit virus
spread.

Disinfection: After outbreaks, disinfect farms—especially

egg-laying flocks—to ensure the virus does not persist in the
environment.
Name of Diseases
Escherichia coli Infection

Common Name of Diseases

Collibacillosis

Etiologic Agent / Causative Agent:

Escherichia coli (E. coli), a gram-negative,
facultative anaerobic bacterium

Epidemiology
• Global Distribution: E. coli infections are found
Escherichia coli
worldwide and can affect both commercial and
backyard poultry. Colibacillosis is particularly
prevalent in poultry farms with poor management,
Infection
inadequate hygiene, or overcrowding, which
facilitates the spread of the bacteria
 Epidemiology
• Outbreaks: E. coli infections tend to occur more frequently in young poultry,
particularly chicks and poults, which have immature immune systems.
However, older birds can also become infected under stressful conditions.

• Seasonality: E. coli infections are common year-round but may be more

prevalent during the warmer months when environmental conditions favor the
survival and proliferation of the bacteria, and birds are more susceptible to
stress factors.

• Risk Factors: Poor air quality, poor sanitation, poor nutrition, overcrowding,
and inadequate vaccination programs increase the risk of outbreaks. High
levels of environmental ammonia, poor ventilation, and inadequate bedding
can exacerbate the spread of E. coli.
Mode of Transmission
1. Fecal-Oral Transmission:
E. coli is primarily transmitted through contaminated feed, water, and bedding. Infected birds shed
the bacteria in their feces, and healthy birds can ingest the bacteria by consuming contaminated
materials.

2. Direct Contact:
Direct contact with infected birds or contaminated equipment, such as feeders and drinkers, can
facilitate transmission. The bacteria can also spread through contact with farm workers or vehicles
that have been exposed to contaminated environments.

3. Environmental Contamination:
E. coli can persist in the environment for extended periods, particularly in moist conditions. It can
colonize surfaces, bedding, and water sources, making control challenging in poultry houses with
poor hygiene practices.

4. Secondary Infections:
E. coli is often a secondary pathogen, taking advantage of an initial viral or bacterial infection, or
stressful conditions that compromise the immune system of the bird.
 Clinical Signs/ Lesions
Colibacillosis can present in several forms, depending on the strain of E. coli and the organs affected.
The clinical signs range from mild respiratory symptoms to severe systemic infections.

1. Respiratory Form (most common in young birds):

o Air sacculitis: Inflammation of the air sacs, which may lead to difficulty breathing, lethargy, and
increased mortality. This is often characterized by yellowish-green exudates in the respiratory system.
o Coughing and sneezing are often present, sometimes with nasal discharge and congestion.
o Gasping and open-mouth breathing can be seen in severe cases due to impaired respiratory function.

2. Systemic Form:
o Septicemia: E. coli can spread to the bloodstream, leading to systemic infection, characterized by
fever, anorexia, and depression.
o Peritonitis: Inflammation of the abdominal cavity, often with accumulation of yellowish fluid.
o Hepatitis and splenitis: In severe cases, E. coli can infect the liver and spleen, causing tissue necrosis
and the formation of abscesses.
o Synovitis and arthritis: E. coli can also cause infections in the joints, leading to lameness and swelling.
 Clinical Signs/ Lesions
3. Local Infection:
o Enteritis: Inflammation of the intestines can result in diarrhea, which is
often greenish or watery in appearance.
o Oophoritis: In female birds, E. coli can infect the ovaries, causing a
decrease in egg production, with eggs appearing soft-shelled or misshapen.
4. Post-mortem Lesions:
o Air sacculitis (cloudy, yellowish exudates in air sacs)
o Peritonitis (yellow, purulent fluid in the abdominal cavity)
o Liver and spleen enlargement (with necrotic areas or abscesses)
o Pneumonia (with consolidation in lung tissue)
 Clinical Signs/ Lesions
(A) Yolk sac infection in a 4‐day‐old leghorn chick. Yolk
sac is distended, hyperemic (note prominent vessels),
and filled with abnormal brown, watery contents.
(B) Omphalitis and yolk sac infection in a group of 3‐day‐
old leghorn chicks. Navels are inflamed and yolk sacs are
distended with abnormal contents.
(C) Advanced air sac disease in a 20‐day‐broiler chicken.
Polyserositis (pericarditis, perihepatitis, peritonitis,
airsacculitis) has occurred as a result of systemic spread
of E. coli.
(D) Pleuropneumonia and airsacculitis in a broiler chicken
caused by E. coli infection.

https://vemedim.com/en/1/specialized-in-livestock-and-
poultry/technical/1105/escherichia-coli-infection-in-poultry
 Clinical Signs/ Lesions
(1) Gross and microscopical findings of natural infection by scherichia
coli in poultry birds of Mozambique.
(2) Heart. Areas of pericardial adherence characterized by severe
fibrin deposits.
(3) Liver. Enlarged, with multifocal areas covered by fibrin deposits.
(4) Heart. Severe thickening of the pericardium with multiple intact
and degenerate heterophils, macrophages, lymphocytes, and plasma
cells intermixed by fibrin.
(5) Liver. Moderate infiltrate of macrophages, lymphocytes, and
plasma cells predominantly at the periportal spaces.
(6) Spleen. Fibrinoid necrosis of follicular centers and blood vessels
(splenic arteriole).
(7) Liver. Multifocal immunolabeling for E. coli in a periportal area and
in sinusoids.

https://www.scielo.br/j/pvb/a/JPmVD9RWHjRLwch9HJZ4RQc/
 Diagnosis
1. Clinical Signs:
o The combination of respiratory symptoms (such as coughing, sneezing, and nasal
discharge), lethargy, and systemic signs (like diarrhea, anorexia, and swelling of the
abdomen) often raises suspicion of an E. coli infection.
o Necropsy findings (air sacculitis, peritonitis, and abscesses) help support the
diagnosis.
2. Laboratory Diagnosis:
o Bacterial culture: E. coli can be isolated from feces, respiratory samples, blood, or
tissues (e.g., liver, spleen) in infected birds. The bacterium can be cultured on standard
media such as MacConkey agar.
o PCR (Polymerase Chain Reaction): A more specific method for identifying pathogenic
strains of E. coli, including APEC and ExPEC.
o Serology: Serological tests like ELISA or hemagglutination inhibition (HI) tests can
detect antibodies in the blood, indicating prior exposure to E. coli.
Differential Diagnosis

Similarities with Differences from

Disease Clinical Signs Lesions
Newcastle Disease Newcastle Disease

Respiratory distress,
Perihepatitis,
lethargy, decreased
pericarditis, air Respiratory signs, Bacterial-specific
Escherichi egg
sacculitis, systemic infection fibrinous exudates
a coli production, greenish
fibrinous exudate
diarrhea

Respiratory distress, Mucosal thickening

Respiratory distress
coughing, sneezing, in the trachea, kidney No fibrinous exudate
Infectious and egg production
decreased egg swelling, misshapen or systemic lesions
Bronchitis issues
production eggs
Differential Diagnosis
Sudden death,
Fibrinous pericarditis, Slower disease onset;
greenish diarrhea, Respiratory and
Mycoplasmosis hepatitis, pneumonia, no severe fibrinous
swollen wattles, systemic involvement
joint exudates pericarditis
lameness

Respiratory Caseous nodules in More severe and

distress, weight lungs and air sacs, Respiratory sudden onset; more
Fowl Cholera
loss, open-mouth yellow or involvement suppurative
breathing green fungal plaques exudate

Hemorrhages in
Respiratory
trachea, proventriculus,
distress, cyanosis, Comb cyanosis and
swollen Respiratory signs,
Avian Influenza diarrhea, more hemorrhagic
combs, fibrinous systemic lesions
decreased egg lesions
exudate in multiple
production
organs
 Treatment/Control/Prevention
1. Treatment:
o Antibiotics: Treatment with antibiotics is common, particularly when secondary
bacterial infections occur. Common antibiotics used include:
 Amoxicillin or amoxicillin-clavulanate (dosage: 10-15 mg/kg body weight, orally
or in drinking water)
 Tetracyclines (e.g., Oxytetracycline): 20-30 mg/kg, orally or in drinking water
 Fluoroquinolones (e.g., Enrofloxacin): 10 mg/kg body weight, administered orally
or via drinking water, although their use is restricted in some countries due to
concerns about antimicrobial resistance.
o Supportive Care: Providing adequate hydration, electrolytes, and nutritional
support is important for recovery in mild cases.
o Anti-inflammatory drugs (e.g., NSAIDs) may be used to reduce inflammation in
affected organs, such as the respiratory system and joints.
 Treatment/Control/Prevention
2. Control and Prevention:
o Good Biosecurity Practices: Implement strict biosecurity measures to prevent the
introduction and spread of E. coli in poultry farms. This includes proper cleaning and
disinfection of facilities, equipment, and feed and water sources.
o Vaccination: Vaccines against E. coli are available and can be used to reduce the incidence
of air sacculitis and septicemia. Vaccines are typically administered subcutaneously or
intramuscularly in the early stages of life (e.g., at 1-2 weeks of age) and may require booster
doses in high-risk populations.
o Environmental Management:
 Improved ventilation and reducing overcrowding can reduce stress, which is a major
predisposing factor for E. coli infections.
 Proper management of feed and water (e.g., ensuring clean water and preventing
contamination) is crucial in reducing infection risks.
o Antibiotic Stewardship: To prevent resistance, antibiotics should be used cautiously,
following the advice of a veterinarian and only when necessary.
Name of Diseases
Fowl Cholera

Common Name of Diseases

Pasteurellosis

Etiologic Agent / Causative Agent:

Pasteurella multocida, a gram-negative,
facultative anaerobic bacterium.

Epidemiology
• Global Distribution: Fowl Cholera is Fowl Cholera
widespread worldwide and can affect both
commercial poultry and wild birds. It is
endemic in many parts of the world,
particularly in regions with high poultry
density and insufficient biosecurity
measures.
 Epidemiology
• Outbreaks: Fowl Cholera outbreaks are more common in wet, warm
climates, especially in areas with inadequate sanitation and overcrowded
poultry facilities. Outbreaks often occur in intensively managed poultry
farms, but can also affect free-range and backyard poultry. The disease can
also affect wild birds and mammals, particularly in areas where poultry and
wildlife intermingle.
• Seasonality: While the disease can occur year-round, it is more frequent
during rainy seasons or times of high environmental stress, such as during
extreme temperature fluctuations or overcrowding.
• Risk Factors: Poor sanitation, overcrowding, and stress due to
environmental factors (e.g., extreme weather or poor ventilation) increase
the risk of outbreaks. Transmission is also facilitated when birds are in close
contact with wild birds or rodents, which can carry the bacteria
asymptomatically.
 Mode of Transmission
1. Direct Contact:
Pasteurella multocida is primarily transmitted through direct contact with infected birds or their
secretions, including feces, nasal discharge, saliva, and wounds.
2. Fecal-Oral Route:
The bacteria can be shed in the feces of infected birds and contaminate the environment, including
feed, water, and bedding. Healthy birds may ingest contaminated food or water, leading to
infection.
3. Indirect Transmission:
o The bacteria can be transmitted indirectly through contaminated equipment, vehicles, clothing,
and farm workers who come into contact with infected birds or contaminated materials.
o Rodents, wild birds, and insects can also act as vectors, transmitting the bacteria from infected
areas to healthy birds.
4. Vertical Transmission:
Though rare, Pasteurella multocida can occasionally be transmitted from hen to egg, leading to
infection in chicks.
 Clinical Signs/ Lesions
In acute fowl cholera, finding a large number of dead birds without
previous signs is usually the first indication of disease.

Mortality often increases rapidly.

In more protracted cases, depression, anorexia, mucoid discharge from

the mouth, ruffled feathers, diarrhea, and increased respiratory rate are
usually seen.

Pneumonia is particularly common in turkeys.

 Clinical Signs/ Lesions

In chronic fowl cholera, signs and lesions are generally related

to localized infections of the sternal bursae, wattles, joints,
tendon sheaths, and footpads, which often are swollen
because of accumulated fibrinosuppurative exudate.

There may be exudative conjunctivitis and pharyngitis.

Torticollis may result when the meninges, middle ear, or

cranial bones are infected.
 Clinical Signs/ Lesions
Lesions observed in peracute and acute forms of the disease are primarily
vascular disturbances. These include general passive hyperemia and
congestion throughout the carcass, accompanied by enlargement of the liver
and spleen.

Petechial and ecchymotic hemorrhages are common, particularly in

subepicardial and subserosal locations. Increased amounts of peritoneal and
pericardial fluids are frequently seen.

In addition, acute oophoritis with hyperemic follicles may be observed.

In subacute cases, multiple, small, necrotic foci may be dissentinated

throughout the liver and spleen.
 Clinical Signs/ Lesions
This photo shows two chickens
suffering from an acute case of
fowl cholera. The rooster on the
left is depressed and sleepy (A).
The hen on the right shows
cyanotic comb and wattles (B).

Maini, S. (2016, April 15). Fowl cholera in poultry. Engormix. https://en.engormix.com/poultry-

industry/poultry-diseases/fowl-cholera-poultry_a36625/
 Clinical Signs/ Lesions

Maini, S. (2016, April 15). Fowl cholera in poultry. Engormix. https://en.engormix.com/poultry-

industry/poultry-diseases/fowl-cholera-poultry_a36625/

This photo shows a chronic clinical case of fowl cholera in a rooster.

Note the severe swelling of the comb and both wattles. The incision
of the wattles displays abundant yellow caseum material from
which oozes a purulent fluid.
 Clinical Signs/ Lesions

Two lumps of yellow

caseum material are
found in the peritoneal
omentum.

Maini, S. (2016, April 15). Fowl cholera in poultry. Engormix. https://en.engormix.com/poultry-

industry/poultry-diseases/fowl-cholera-poultry_a36625/
 Clinical Signs/ Lesions
Subserous petechial or
ecchymosed haemorrhages in
the anterior part of the small
intestine, the gizzard or the
abdominal fat are discovered.

FOWL cholera - Diseases of poultry - The poultry site | The poultry site. (n.d.). The Poultry Site.
https://www.thepoultrysite.com/publications/diseases-of-poultry/181/fowl-cholera
 Diagnosis
1. Clinical Signs:
o Fowl Cholera can be suspected based on the rapid onset of mortality,
particularly in young birds, with clinical signs such as sudden death, fever,
diarrhea, and respiratory distress. Necropsy findings of hemorrhagic lesions in
internal organs (liver, spleen, lungs) and pericardial effusion are strong indicators.

2. Laboratory Diagnosis:
o Bacterial culture: The definitive diagnosis is made by isolating Pasteurella
multocida from blood, feces, swabs from infected tissues, or necropsy specimens
(e.g., liver, heart, spleen). Culturing on blood agar often reveals the characteristic
hemolytic colonies.
o PCR (Polymerase Chain Reaction): PCR can be used to detect Pasteurella
multocida DNA and confirm the diagnosis in cases where culture is difficult or
time-consuming.
Diagnosis
o PCR (Polymerase Chain Reaction): PCR can be used to
detect Pasteurella multocida DNA and confirm the diagnosis
in cases where culture is difficult or time-consuming.

o Serology: The Rapid Plate Agglutination Test (RPA) can be

used for detecting antibodies to Pasteurella multocida in the
blood, but this is typically more useful in detecting exposure
rather than diagnosing active infection.
Differential Diagnosis

Differences from Fowl

Disease Clinical Signs Lesions Similarities with
Cholera
Fowl Cholera

Sudden death, Fibrinous

Respiratory signs,
greenish diarrhea, pericarditis,
systemic infection, Acute onset with purulent
Fowl Cholera nasal discharge, pneumonia,
fibrinous and fibrinous exudates
swollen wattles, hepatitis,
exudates
lameness swollen joints

Perihepatitis,
Respiratory Respiratory and
pericarditis, air E. coli often lacks joint
distress, weight loss, systemic signs,
Colibacillosis sacculitis, swelling and comb
lethargy, fibrinous
fibrinous involvement
diarrhea exudates
exudate
Differential Diagnosis
Respiratory distress, Caseous nodules in lungs
Respiratory signs and chronic
Aspergillosis weight loss, open-mouth and air sacs, yellow or Fungal plaques and slower
lesions
breathing green fungal plaques disease

Nasal discharge, facial Catarrhal inflammation

Respiratory signs and facial Absence of systemic
Infectious Coryza swelling, conjunctivitis, of nasal passages and
swelling fibrinous lesions
sneezing sinuses

Respiratory distress, Hemorrhages in trachea

Newcastle Respiratory signs and sudden Absence of systemic
neurological signs, and digestive tract;
Disease mortality fibrinous lesions
greenish diarrhea swollen spleen

Hemorrhages in trachea,
Respiratory distress, Respiratory signs, systemic Severe comb discoloration
proventriculus, and
Avian Influenza cyanosis, diarrhea, infection, fibrinous and more hemorrhagic
multiple organs; swollen
decreased egg production lesions lesions
combs
Treatment/Control/Prevention
1. Treatment:
o Antibiotics: Fowl Cholera is treated with systemic antibiotics, although the use of antibiotics should
be based on sensitivity testing to ensure effectiveness against Pasteurella multocida strains. Common
antibiotics include:
 Enrofloxacin (Baytril®): 10 mg/kg body weight, administered via drinking water or injection.
 Tetracycline (Oxytetracycline): 20 mg/kg body weight, administered orally or in drinking water.
 Penicillin: 5-10 mg/kg body weight, injected intramuscularly (although penicillin resistance is
increasing).
o Supportive care: Providing proper hydration, electrolytes, and nutrition is important in treating
affected birds.
2. Control and Prevention:
o Vaccination:
 Inactivated vaccines are available and can be used to control Fowl Cholera, particularly in high-risk
areas. These vaccines are typically administered to chicks or adult birds via intramuscular or
subcutaneous injection.
 The typical vaccination schedule involves vaccinating birds at 2-3 weeks of age and boosting them
every 6-12 months depending on the risk of exposure
 Treatment/Control/Prevention
o Biosecurity:
 Implementing strict biosecurity measures is crucial to preventing the spread of Fowl
Cholera. This includes controlling the movement of people, equipment, and animals on
and off the farm, disinfecting contaminated surfaces, and limiting contact with wild
birds and rodents.
 Isolation of infected birds and quarantine of new birds is important to prevent
outbreaks.
o Environmental Management: Ensuring clean feed, water, and housing conditions is
essential to prevent bacterial contamination. Proper ventilation and reducing
overcrowding can reduce stress and the spread of disease.
o Rodent and Wild Bird Control: Preventing exposure to wild birds and controlling
rodents are important steps in reducing the risk of transmission, as these animals can
act as asymptomatic carriers.
Name of Diseases
Fowl Pox

Common Name of Diseases

Avian Fowl Pox

Etiologic Agent / Causative Agent:

Fowl Pox virus (FPV), which belongs to the
Avipoxvirus genus in the Poxviridae family

Epidemiology
• Global Distribution: Fowl Pox is widespread Fowl Pox
globally and affects poultry industries in both
commercial and backyard settings. It is
particularly common in regions where
biosecurity measures are poor or in free-range
farming systems where birds are exposed to wild
fowl or other animals that may carry the virus.
 Epidemiology
• Outbreaks: Outbreaks of Fowl Pox can occur throughout the year,
but they are more common in warmer climates, especially in areas
with high humidity. The disease tends to spread more quickly in
overcrowded and poorly managed poultry flocks.

• Risk Factors: Poor hygiene, high stocking density, and contact with
wild birds or mosquitoes are significant risk factors for the
transmission of Fowl Pox. The disease often becomes more prevalent
during periods of environmental stress, such as extreme weather
conditions or poor nutrition.
 Mode of Transmission
1. Direct Contact:
Fowl Pox is primarily transmitted through direct contact with infected birds or contaminated
surfaces. The virus is shed in lesions, nasal discharge, and feces of infected birds. Birds can
become infected by coming into contact with these materials.
2. Indirect Transmission:
The virus can be spread indirectly through contaminated equipment, such as feeders, drinkers,
egg trays, or farm workers' clothing. Since the virus can persist in the environment for extended
periods, it can be transmitted via aerosols or contaminated surfaces.
3. Insect Vectors:
Mosquitoes and other biting insects (e.g., sandflies) can serve as vectors of Fowl Pox, particularly
the cutaneous form of the disease. Mosquitoes become infected when they feed on the blood of
infected birds, and can transmit the virus to healthy birds during subsequent feedings.
4. Vertical Transmission:
Though rare, Fowl Pox can be transmitted vertically from hen to egg, leading to infection in newly
hatched chicks. This form of transmission is more common in chronic infections.
 Clinical Signs/ Lesions
1. Cutaneous Form:
The classic clinical signs of the cutaneous form of Fowl Pox include:
o Lesions: These typically appear on unfeathered areas, such as the comb,
wattles, eyelids, and legs. The lesions are usually yellowish or scabby, and they
may begin as small raised pustules that eventually form crusty scabs.
o Swelling: The affected areas may become swollen, red, and inflamed,
particularly around the eyes and face.
o Lesion Development: The scabs eventually dry and fall off, leaving behind
scars.
o Weight loss and decreased egg production may be seen, especially in laying
hens with severe lesions on their combs and wattles.
 Clinical Signs/ Lesions
2. Diphtheritic Form:
The diphtheritic form of Fowl Pox affects the mucosal surfaces of the respiratory
system, such as the mouth, trachea, and esophagus.
o Lesions in the throat and mouth: These lesions are often yellowish or grayish, forming
membranous plaques. The lesions can obstruct the respiratory passages, leading to
difficulty breathing, coughing, and gasping.
o Severe infections can cause death by suffocation due to airway blockage or secondary
bacterial infections.

3. Systemic Infections:
In severe cases, Fowl Pox can lead to systemic infection, affecting internal organs such
as the liver and spleen. This can lead to fever, lethargy, and secondary infections,
though these severe cases are less common than the cutaneous form.
 Clinical Signs/ Lesions
(A) Fibrinous polyserositis (asterisks); (B)
trachea, severe tracheitis and congestion
(arrow);
(C) skin and eyelid, dermatitis and serous
blepharoconjunctivitis;
(D) oral cavity, necrotic stomatitis
(arrow);
(E) lung, congestion and severe edema
(arrow);
(F) lung, extensive areas of pneumonia
with necrosis (arrow).
ResearchGate. (n.d.). ResearchGate - Temporarily Unavailable.
https://www.researchgate.net/figure/Macroscopic-lesions-of-systemic-avian-pox-in-canaries-A-
Fibrinous-polyserositis_fig1_336211389
 Diagnosis
1. Clinical Diagnosis:
o The diagnosis is often suspected based on clinical signs, particularly the characteristic skin
lesions, especially in unfeathered areas of the bird.
o Diphtheritic lesions in the mouth and trachea can also indicate the diphtheritic form of the
disease.

2. Laboratory Diagnosis:
o PCR (Polymerase Chain Reaction): PCR can be used to detect the DNA of the Avipoxvirus in
samples from lesions or swabs from the affected respiratory tract.
o Histopathology: Microscopic examination of tissue samples from lesions can reveal
characteristic intracytoplasmic inclusion bodies, which are typical of Poxvirus infections.
o Virus Isolation: The virus can be isolated from lesion scrapings or tissues in cell culture.
o Serology: Serum tests can detect antibodies against the virus, indicating exposure, though
they are not helpful for diagnosing active infection.
Differential Diagnosis

Differences from Fowl

Disease Clinical Signs Lesions Similarities with Fowl Pox
Pox

Nodular, wart-like
Skin nodules, scabs on
skin lesions; yellow Presence of scabs and
combs, wattles, eyelids; Respiratory involvement
Fowl Pox diphtheritic plaques plaques; slower
respiratory distress in (diphtheritic form)
in the mouth and disease onset
diphtheritic form
trachea

Respiratory distress, Hemorrhages in Cyanosis,

Avian cyanosis, diarrhea, trachea, Respiratory signs and comb hemorrhagic lesions,
Influenza decreased egg proventriculus, involvement and systemic
production swollen combs involvement

Respiratory distress, Hemorrhages in Neurological signs and

Newcastle
neurological signs, trachea, intestines, Respiratory involvement more hemorrhagic
Disease
greenish diarrhea and other organs lesions
Differential Diagnosis
Sudden death,
greenish Fibrinous
Respiratory signs
diarrhea, nasal pericarditis, Acute onset,
Fowl Cholera and comb
discharge, pneumonia, fibrinous exudates
involvement
swollen wattles, swollen joints
lameness

Nasal discharge,
Catarrhal Respiratory signs
Infectious facial swelling, No skin or
inflammation of and facial
Coryza conjunctivitis, diphtheritic lesions
nasal passages involvement
sneezing

Caseous nodules
Respiratory
Fungal in lungs and air Presence of fungal
distress, weight Respiratory
Infection sacs; yellow or plaques, no skin
loss, open-mouth involvement
(Aspergillosis) green fungal scabs
breathing
plaques
 Treatment/Control/Prevention
o Biosecurity:
 Strict biosecurity measures are essential in preventing the introduction and spread of
Fowl Pox. These measures include controlling access to the farm, disinfecting equipment
and vehicles, and preventing contact with wild birds or mosquitoes.
 Controlling insect vectors, such as mosquitoes and sandflies, can significantly reduce
the risk of transmission. This may involve the use of insect repellents or mosquito nets
around poultry houses.
o Quarantine: Newly introduced birds should be quarantined for at least 2-3 weeks to
ensure they do not bring in infections like Fowl Pox.
o Isolation of infected birds: Infected birds should be isolated to prevent the virus from
spreading to healthy individuals.
o Environmental Management: Reducing overcrowding, maintaining good sanitation, and
ensuring proper ventilation can help reduce the environmental stress that predisposes
birds to viral infections.
Name of Diseases
Gapeworm Infection

Common Name of Diseases

Syngamiasis

Etiologic Agent / Causative Agent:

Syngamus trachea

Epidemiology
• Global Distribution: Gapeworm infection is Gapeworm
found worldwide, particularly in regions with
large poultry industries or where wild birds
(especially waterfowl) and poultry intermingle.
Infection
The disease can affect domestic poultry
(chickens, turkeys, ducks, geese) and wild birds.
 Epidemiology

• Outbreaks: Outbreaks of Gapeworm infection are more common in free-range

poultry or areas where birds have access to infected soil or contaminated
environments. The infection is more frequently observed in young birds that are
more susceptible.
• Seasonality: It is often more common during wet and warm seasons, as these
conditions are favorable for the survival of the eggs and larvae of Syngamus
trachea. Infected wild birds, especially ducks and geese, can serve as a source of
contamination for domestic flocks.
 Mode of Transmission
1. Ingestion of Infective Eggs:
Birds typically become infected with Gapeworm when they ingest infective eggs that
are shed in the feces of infected birds. These eggs hatch into larvae, which migrate to
the trachea and mature into adult worms.
2. Paratenic Hosts:
Earthworms, insects, and other small animals may act as paratenic hosts for the
larvae of the gapeworm. Birds that ingest these infected intermediate hosts can
become infected as well.
3. Direct Transmission via Contaminated Environment:
The eggs of Syngamus trachea can be passed into the environment through fecal
contamination. Birds can ingest these eggs while pecking at the ground or feeding
from contaminated water sources or feed.
4. Vertical Transmission:
While rare, vertical transmission from hen to egg has been reported, particularly in
cases of chronic or heavily infected flocks.
 Clinical Signs/ Lesions
Gapeworm infection primarily affects the respiratory system,
and clinical signs depend on the severity of the infestation. The
presence of the worms in the trachea leads to breathing
difficulties and other noticeable symptoms.
1. Classic Gaping Behavior:
A characteristic symptom of Gapeworm infection is the gaping
behavior, where infected birds stretch their necks and open
their mouths in an effort to breathe better due to airway
obstruction.
2. Respiratory Distress:
Infected birds exhibit labored breathing, wheezing, and
coughing. The trachea can become obstructed, leading to
difficulty breathing, gasping for air, and visible nasal discharge.
3. Neck Twisting:
Neck extension and twisting may also occur in severe cases. This
is due to the irritation caused by the presence of the worms in
the trachea.
 Clinical Signs/ Lesions
4. Lethargy and Weight Loss:
Infected birds may become lethargic, stop eating, and show
signs of weight loss as a result of decreased feeding.
5. Death:
In severe cases, the airway obstruction and secondary
bacterial infections can lead to suffocation and sudden
death, particularly in young birds with high parasite loads.
6. Lesions:
On necropsy, the trachea of affected birds may show signs of
inflammation, with mucosal swelling and necrosis. The worms
themselves can be visible within the trachea and bronchi.
Adult worms are bright red and are often visible to the naked
eye.
 Diagnosis
1. Clinical Signs:
The primary diagnostic clue is the classic gaping behavior, where birds stretch
their necks and breathe with open mouths. If there is a history of free-range or
outdoor access, this raises suspicion for a gapeworm infection.
2. Laboratory Diagnosis:
o Fecal Examination: A fecal flotation test can identify Syngamus trachea eggs.
The eggs are distinctive, oval, and bipolar (with plugs at both ends).
o Endoscopy: In more severe cases, an endoscopic examination of the trachea
may reveal the presence of the adult worms.
o Necropsy: Necropsy can confirm the diagnosis by revealing adult worms in the
trachea and associated lesions such as mucosal swelling and necrosis.
o PCR and Histopathology: PCR testing and histopathological examination of
tracheal tissue can also be used to detect the parasite.
Differential Diagnosis

Similarities with
Disease clinical signs lesions Differences with Gapeworm infection
Gapeworm infection

Gapeworm involves worms obstructing

the respiratory tract, ILT causes swollen
Coughing, sneezing,
and hemorrhagic tracheal membranes.
Infectious snicking, gasping for Swollen and hemorrhagic Both diseases cause
Gapeworm is more likely to cause a
Laryngotrachei breath, and mucous membranes of respiratory distress,
gurgling sound from the trachea or
tis (ILT) discharge from the the trachea. including gasping for air
throat, and ILT is more likely to cause
eyes and nostrils
sneezing and nasal discharge

Respiratory
Hemorrhages in the
problems, but also
digestive tract, lesions in ND can cause nervous system signs
Newcastle nervous system Respiratory problems like
lymphoid tissue, (tremors, paralysis) and green diarrhea,
Disease issues like tremors, caughing and gasping
congestion/hemorrhage which are not typical of gapeworm
paralysis and green
in trachea and lungs
diarrhea.
 Similarities with
Disease clinical signs lesions Gapeworm Differences with Gapeworm infection
infection

congestion and
inflammation of the
Respiratory signs, trachea and lungs,
Both diseases
conjunctivitis, diarrhea, Greenish diarrhea,
cause respiratory conjunctivitis, purple discoloration &
Avian Influenza sudden death, lack of hemorrhages in the
signs, including sudden death in severe AI.
energy/appetite/coordinatio gut. Swollen face,
coughing
n, purple discoloration easily removed
gizzard lining.

Both cause
respiratory
White mucous
distress, affect
congestion of the
the trachea,
lungs and air sacs,
Labored breathing, open- bronchi, and
nodules in the
mouth breathing, tail lungs. Both can
lungs, inflammation Aspergillosis involves fungal plaques
Aspergillosis bobbing, elevated lead to loss of
of the air sacs, and granulomas
respiratory rate, appetite and
fungal granulomas
inappetence, lethargy. lethargy. Both
in the lungs and air
can be more
sacs
severe in young
birds.
Treatment/Control/Prevention

o Deworming Programs: Regular deworming with anthelmintic medications is

important in areas where Gapeworm is common. This helps to reduce the worm burden
in poultry flocks.
o Environmental Management:
 Reducing exposure to contaminated environments can help minimize the risk. This
includes proper cleaning and disinfection of poultry houses and equipment to reduce
the presence of Syngamus trachea eggs in the environment.
o Vector Control: Since earthworms and insects can serve as intermediate hosts for the
gapeworm larvae, controlling these vectors in free-range systems is crucial.
o Minimize Wild Bird Exposure: Flocks should be kept away from areas with high
concentrations of wild birds, particularly waterfowl, which may act as reservoirs for
the parasite. Ensuring proper fencing and preventing contact with wild bird droppings
is key.
o Vaccination: While there is no vaccine for Gapeworm, keeping birds healthy through
proper nutrition and biosecurity practices reduces the risk of secondary infections and
complications from the worm infestation.
Name of Diseases
Infectious Bronchitis

Common Name of Diseases

Chicken Bronchitis or Avian Infectious Bronchitis
(IBV)

Etiologic Agent / Causative Agent:

Infectious Bronchitis Virus (IBV), a coronavirus that
specifically targets the respiratory system in
poultry.

Epidemiology
• Global Distribution: Infectious Bronchitis Infectious
occurs worldwide and is one of the most
common respiratory diseases in poultry. It is a
major concern in the poultry industry, leading to Bronchitis
substantial economic losses.
Epidemiology

• Outbreaks: IB outbreaks can occur throughout the year, but they are
more common during wet and cooler seasons when the virus can be
transmitted more easily. Outbreaks tend to be frequent in regions with
dense poultry populations or poor biosecurity measures.
• Strains: There are many serotypes or strains of IBV, some of which are
geographically specific. For example, Massachusetts, H120, and D274
strains are common in North America and Europe, while QX and 4/91
strains are prevalent in Asia. Different strains can affect chickens in
various ways, leading to variations in clinical signs and severity.
Mode of Transmission

1. Aerosol Transmission:
IBV is primarily spread through the aerosol route. Infected birds release the virus in their
nasal discharge, saliva, feces, and airborne droplets, which can be inhaled by healthy birds.
The virus can remain viable in the environment for several hours, especially in humid
conditions.
2. Fecal-Oral Route:
While the virus is mainly spread through aerosol droplets, it can also be transmitted via the
fecal-oral route. Feces from infected birds may contaminate water, feed, or environmental
surfaces, where it can be ingested by healthy birds.
3. Direct Contact:
Direct contact with infected birds or contaminated equipment (e.g., feeders, drinkers,
housing facilities) can also lead to the transmission of the virus.
4. Vertical Transmission:
IBV can also be transmitted vertically from infected hens to eggs, leading to infected chicks
after hatching, although this is less common than horizontal transmission.
Clinical Signs/ Lesions

Infectious Bronchitis affects the respiratory and

sometimes the renal and reproductive systems,
depending on the strain of IBV. Clinical signs can
range from mild to severe and are typically more
pronounced in young chicks.
1. Respiratory Signs:
o Sneezing
o Nasal discharge (clear or mucous-like)
o Coughing and gasping for air
o Rales or wheezing (abnormal respiratory sounds)
o Tracheal inflammation and swelling
2. Reduced Egg Production:
In layers, IBV can lead to a significant drop in egg
production. The eggs may be soft-shelled, misshapen,
or have thin or rough shells. Affected hens often stop
laying temporarily or lay fewer eggs.
Clinical Signs/ Lesions
3. Renal Lesions:
Some strains of IBV can infect the kidneys,
leading to renal lesions and kidney enlargement.
This is typically seen in severe infections,
particularly with QX strain, which causes white
urates and kidney damage.
4. Ovary and Oviduct Damage:
In some cases, IBV can affect the reproductive
system, causing lesions on the ovary or oviduct,
leading to impaired egg production and
decreased fertility.
5. Other Signs:
o Decreased feed intake and weight loss in
affected flocks
o Chick mortality can be high if the infection is
severe, especially in young chicks that cannot
cope with respiratory distress.
Diagnosis
1. Clinical Signs:
o Diagnosis of IB is often suspected based on characteristic respiratory signs and a history of
exposure to poultry with similar symptoms in nearby farms.
o The virus often causes sudden onset of respiratory distress, with a high rate of coughing
and sneezing.
2. Laboratory Diagnosis:
o PCR (Polymerase Chain Reaction): PCR tests are the most definitive way to identify IBV, as
they can detect the virus's genetic material in swabs taken from the trachea, nasal cavity, or
feces.
o Virus Isolation: The virus can be isolated from swabs or tissues and grown in cell culture,
although this method is more time-consuming.
o Serology: ELISA or Hemagglutination Inhibition (HI) tests can detect antibodies to IBV in
blood samples, indicating past infection or exposure.
o Histopathology: Examination of tissues (e.g., tracheal or renal tissues) can reveal
characteristic inflammatory lesions and evidence of viral infection.
Differential Diagnosis

Similarities with
Disease clinical signs lesions Gapeworm Differences with Gapeworm infection
infection

dullness, loss of
congestion and
appetite, coughing,
inflammation of the
nasal and ocular respiratory sudden death and may involve cyanosis and
Avian trachea and lungs.
discharge, facial distress, coughing, edema of the comb and wattles, which are
Influenza dehydration and
swelling, paralysis, and sneezing less common in other respiratory diseases
congestion of viscera and
and sometimes
muscles
greenish diarrhea

watery eyes, swollen

Infectious eyelids, oral and edema of the conjunctiva,
Difficult breathing Lesions include inflamed trachea containing
Laryngotrachei nasal discharge, nasal turbinates, sinuses,
and coughing cheesy plugs
tis inflamed sinuses, larynx, and trachea
rales, and coughing
Differential Diagnosis

Similarities with
Disease clinical signs lesions Gapeworm Differences with Gapeworm infection
infection

dullness, loss of
congestion and
appetite, coughing,
inflammation of the
nasal and ocular respiratory issues,
Mycoplasmosi trachea and lungs. inflammation of the trachea and frothy
discharge, facial coughing, and
s dehydration and exudate in the air sacs
swelling, paralysis, sneezing
congestion of viscera and
and sometimes
muscles
greenish diarrhea

watery eyes, swollen

Infectious eyelids, oral and edema of the conjunctiva,
Difficult breathing Lesions include inflamed trachea containing
Laryngotrachei nasal discharge, nasal turbinates, sinuses,
and coughing cheesy plugs
tis inflamed sinuses, larynx, and trachea
rales, and coughing
Treatment/Control/Prevention
1. Treatment:
o Supportive Care: There is no specific antiviral treatment for IBV. However, supportive care can be provided,
including:
 Antibiotics: For secondary bacterial infections (e.g., Tylosin or Oxytetracycline) that may complicate the viral
infection.
 Anti-inflammatory drugs: Drugs such as NSAIDs (e.g., Flunixin meglumine) can be used to alleviate inflammation
and discomfort.
 Electrolyte supplementation and improved nutritional support to aid recovery and help with dehydration.
2. Vaccination:
o Live attenuated vaccines: These vaccines are often used to control IBV outbreaks in poultry. They can be
administered via drinking water, spray, or injection depending on the vaccine strain.
 Massachusetts and H120 strains are commonly used in the poultry industry, but the choice of vaccine depends
on the local virus strain.
 Vaccination dosage:
 In drinking water: Typically, a dose of 1,000 doses per liter of water, depending on the product and manufacturer
recommendations.
 Spray vaccination: Can be used in cases where drinking water is not feasible, with doses of 1,000 doses per 200
ml of water.
 Booster doses: Regular booster vaccinations are often required, especially in areas with high exposure to the
virus.
Treatment/Control/Prevention

3. Biosecurity Measures:
o Isolation of infected birds: Infected flocks should be isolated to prevent the spread of the
virus to healthy birds.
o Disinfection: Thorough cleaning and disinfection of poultry houses, equipment, and vehicles
can help reduce the risk of transmission. The use of quaternary ammonium compounds or
virucidal disinfectants is recommended.
o Control of Wild Birds: Wild birds can act as reservoirs for the virus, so preventing contact
between wild birds and domestic poultry is crucial.
o Good management practices: Ensuring that poultry houses are well-ventilated, with adequate
space and clean bedding, helps to reduce the spread of the virus.
4. Quarantine and Surveillance:
o Quarantine newly introduced birds for at least 2-3 weeks to prevent the introduction of IBV or
other diseases.
o Surveillance through regular testing of flocks for IBV is important to monitor the presence of
the virus in the region.
Name of Diseases
Infectious Coryza

Common Name of Diseases

Avian Coryza

Etiologic Agent / Causative Agent:

Avibacterium paragallinarum

Epidemiology
• Geographic Distribution: Infectious Coryza is Infectious
found worldwide, but it is more common in areas
with high-density poultry farming and poor
biosecurity measures. It has been reported in
Coryza
both commercial poultry farms and backyard
flocks.
Epidemiology

• Outbreaks: The disease is more likely to occur in intensive poultry systems where birds
are housed in close quarters. Outbreaks can happen at any time of the year, but they are
more frequent during cooler, damp seasons when environmental stressors weaken the
birds' immune systems.
• Age and Species Affected: Although older birds can be affected, young chickens
(especially chicks and pullets) are more susceptible to the disease. The disease primarily
affects chickens, but turkeys and other poultry species can also be infected.
• Strains: There are several serotypes of Avibacterium paragallinarum. These serotypes
can vary in their virulence, and specific strains may be more common in different
geographic regions.
Mode of Transmission
1. Direct Contact:
o The bacteria are primarily transmitted via direct contact between infected and healthy birds.
o Sick birds shed the bacteria through their nasal discharge, saliva, and feces, which can then be
spread to other birds through physical contact or by coming into contact with contaminated feed,
water, or bedding.
2. Aerosol Transmission:
o Aerosolization of the bacteria occurs when infected birds cough or sneeze, releasing bacteria
into the air. Healthy birds inhale these particles, leading to respiratory infections.
3. Fomites and Contaminated Equipment:
o The bacteria can be transmitted via contaminated equipment, such as feeders, drinkers,
vehicles, and personnel that move between infected and uninfected areas. It is common in poorly
cleaned or overcrowded environments.
4. Vertical Transmission:
o Although rare, the bacteria can sometimes be transmitted from infected hens to eggs, leading to
infections in newly hatched chicks.
Clinical Signs/ Lesions

Infectious Coryza primarily affects the respiratory system and is

characterized by the following clinical signs:
1. Respiratory Distress:
o Nasal discharge (which may be serous or purulent)
o Swelling around the eyes (periorbital swelling), which may lead to closed
eyes due to the swelling.
o Coughing and sneezing
o Rales or wheezing, indicating respiratory distress
o Labored breathing and snicking sounds
o Conjunctivitis and redness around the eyes
2. Facial Swelling:
o Edema around the eyes, wattles, and neck, caused by bacterial infection
and inflammation.
Clinical Signs/ Lesions
3. Decreased Feed and Water Intake:
o Infected birds often reduce their food and water intake due to difficulty
breathing and general discomfort.
4. Decreased Egg Production:
o In layer hens, a significant reduction in egg production is often noted due to
the stress of infection and respiratory distress.
5. Mortality:
o Mortality can occur in severe cases or in cases where secondary bacterial
infections (e.g., E. coli) or complications arise, such as pneumonia.
6. Lesions:
o Necrotic lesions in the upper respiratory tract, including the sinuses, larynx,
and trachea.
o In severe cases, congestion and hemorrhage in the nasal passages and sinus
tissues may be observed. Secondary bacterial infections may cause further
tissue damage.
Treatment/Control/Prevention

1. Treatment:
o Antibiotics:
The primary treatment for Infectious Coryza involves the use of antibiotics to control the bacterial
infection and prevent secondary bacterial complications. Common antibiotics include:
 Tetracyclines (e.g., Oxytetracycline)
Dosage: Typically, 0.5–1 g/L of drinking water for 5-7 days.
 Sulfonamides (e.g., Sulfadimethoxine)
Dosage: 125 mg/L of drinking water for 5 days.
 Penicillin (in case of secondary bacterial infections like E. coli or Pasteurella)
 Neomycin or Chlortetracycline may also be used for respiratory secondary infections.
o Anti-inflammatory drugs such as Flunixin meglumine can be used to reduce inflammation and
discomfort.
o Supportive Care: Providing warmth, adequate hydration, and nutritional support is essential for
recovery. In severe cases, birds may need antioxidants, electrolytes, and vitamins to support the
immune system.
Treatment/Control/Prevention

2. Control and Prevention:

o Vaccination:
There are inactivated and live attenuated vaccines available for Avibacterium
paragallinarum. Vaccination can be used to control outbreaks and to protect flocks in
endemic areas.
 Live vaccines are typically administered to day-old chicks or pullets.
 Inactivated vaccines are used for booster vaccination in adult flocks.
 Vaccine Dosage: The specific dose depends on the product used, but typically, 0.5 ml
per bird is given by intramuscular or subcutaneous injection.
Treatment/Control/Prevention

o Biosecurity Measures:
 Isolation of infected birds to prevent the spread to healthy flocks.
 Disinfection of equipment, vehicles, and housing areas with appropriate
disinfectants (e.g., quaternary ammonium compounds or virucidal disinfectants).
 Avoiding crowding and maintaining proper ventilation to reduce stress on the
birds.
o Quarantine New Birds: All new birds should be quarantined for at least 2-3 weeks
before being introduced to the flock to ensure they are not carrying Infectious
Coryza or other diseases.
o Environmental Control:
 Clean water sources, feeders, and bedding regularly to prevent the buildup of
bacteria and reduce the chances of contamination.
Treatment/Control/Prevention

1. Clinical Signs:
The characteristic symptoms of nasal discharge, facial swelling, and respiratory
distress strongly suggest Infectious Coryza. However, these signs can overlap with
other respiratory diseases, so laboratory confirmation is necessary.
2. Laboratory Diagnosis:
o Bacterial Culture: The definitive diagnosis is often made by culturing the
bacterium from nasal swabs, sinus swabs, or tracheal exudates. The bacterium grows
readily on simple media and can be identified based on its gram-negative staining
and oxidase-positive reaction.
o PCR: PCR (Polymerase Chain Reaction) testing is highly sensitive for detecting
Avibacterium paragallinarum from swab samples.
o Serology: Serological tests, such as ELISA (Enzyme-Linked Immunosorbent Assay),
can detect antibodies to the bacteria in blood samples, which can confirm past or
present infection.
Differential Diagnosis

Similarities with
Disease clinical signs lesions Differences with infectious coryza
infectious coryza

Respiratory signs
Slower Onset; Serous to
Catarrhal inflammation (nasal discharge,
mucoid nasal discharge
of nasal sneezing, coughing); IC: Rapid onset, foul odor, marked
Mycoplasmosi (less profuse/odor than
passages/sinuses/trach Reduced feed/water facial swelling. MG: Slower onset, less
s (Mycoplasma IC); Mild facial swelling;
ea; Airsacculitis (cloudy intake; Drop in egg odor, mild facial swelling, potential
gallisepticum) Watery to mucoid ocular
or cheesy exudate in air production. for chronic course.
discharge;
sacs) Inflammation of the
Sneezing/Coughing
upper respiratory tract

Rapid Onset; Coughing, Catarrhal inflammation

sneezing, tracheal rales; of trachea/bronchi; Respiratory signs IC: Foul odor, marked facial swelling,
Nasal discharge (usually Possible airsacculitis; (nasal discharge, less respiratory distress. IB: More
Infectious serous, less profuse/foul Kidney lesions (swollen, sneezing, coughing); pronounced respiratory distress
Bronchitis than IC); Ocular discharge; pale kidneys with urate Reduced feed/water (gasping), potential kidney
Respiratory distress deposits); Oviduct intake; Can cause involvement, eggshell abnormalities,
(gasping); Possible kidney lesions in young chicks economic losses nephrosis
lesions (cystic oviduct)
Differential Diagnosis

Similarities with
Disease clinical signs lesions Gapeworm Differences with Gapeworm infection
infection

dullness, loss of
congestion and
appetite, coughing,
inflammation of the
nasal and ocular respiratory issues,
Newcastle trachea and lungs. inflammation of the trachea and frothy
discharge, facial coughing, and
Disease dehydration and exudate in the air sacs
swelling, paralysis, sneezing
congestion of viscera and
and sometimes
muscles
greenish diarrhea

watery eyes, swollen

eyelids, oral and edema of the conjunctiva,
Avian Difficult breathing Lesions include inflamed trachea containing
nasal discharge, nasal turbinates, sinuses,
Influenza and coughing cheesy plugs
inflamed sinuses, larynx, and trachea
rales, and coughing
Differential Diagnosis

Similarities with
Disease clinical signs lesions Gapeworm Differences with Gapeworm infection
infection

dullness, loss of
congestion and
appetite, coughing,
inflammation of the
nasal and ocular respiratory issues,
trachea and lungs. inflammation of the trachea and frothy
Fowl pox discharge, facial coughing, and
dehydration and exudate in the air sacs
swelling, paralysis, sneezing
congestion of viscera and
and sometimes
muscles
greenish diarrhea
3. Differential Diagnosis:
o Both Mycoplasmosis and Infectious Coryza cause similar respiratory signs, including nasal
discharge and coughing. However, Mycoplasma infections tend to have a chronic course and
are associated with sinusitis and conjunctivitis. PCR testing can differentiate between these
two pathogens.
o (IB): IBV causes similar respiratory distress but also affects egg production more severely in
layers and can cause kidney lesions in some strains. IBV is typically confirmed through PCR or
virus isolation.
o (ND): ND causes respiratory symptoms but also leads to neurological signs (e.g., torticollis
or twisted neck) and greenish diarrhea, which is not seen in Infectious Coryza.
o (AI): AI can cause similar respiratory signs but is often associated with systemic illness,
fever, and neurological signs, unlike Infectious Coryza.
o Fowl Pox: Poxvirus infections cause cutaneous lesions (not respiratory distress), which
distinguishes them from Coryza.
01

AVIANTUBERCULOSIS
Common Name:
Avian Tuberculosis (also known as Mycobacteriosis)

Etiological Agent:
· Mycobacterium avium complex (MAC), primarily
Mycobacterium avium and occasionally Mycobacterium
genavense.
 EPIDEMIOLOGY
· Avian tuberculosis is primarily a disease of wild birds, poultry, and pet
birds.
· It is more commonly observed in poultry operations, particularly in
chickens, turkeys, ducks, and waterfowl.
· Mycobacterium avium is widely distributed in the environment, and the
disease is primarily zoonotic, meaning it can potentially be transmitted
to humans (especially in immunocompromised individuals).
· Outbreaks are more frequent in areas with poor sanitation, high bird
density, or poor biosecurity practices. Birds in backyard flocks or those
in free-range systems are also at risk of exposure.
MODE OF TRANSMISSION
· Ingestion environmental materials such as soil or litter can spread the
bacteria.

· Direct contact: Contact with infected birds (especially through droppings)

can also spread the disease.

· Environmental contamination: Mycobacterium avium is persistent in the

environment, especially in moist, organic material. Birds that peck or forage
in contaminated environments are at risk.

· Vertical transmission: There is some evidence that infection can be passed

from infected hens to their eggs, although this is less common.
 CLINICAL SIGNS
o Chronic weight loss and poor growth in young birds or failure to thrive in infected adults.

o Loss of appetite, lethargy, and depression.

o Diarrhea in some cases, often with undigested food in the droppings.

o Respiratory distress: Although less common, labored breathing or wheezing can be

observed if the lungs are affected.

o Swelling of the abdominal area due to the formation of granulomas in the liver, spleen, or
intestines.

o Changes in feather quality or feather loss in some cases.

 LESIONS
o Granulomas: The hallmark lesion of avian tuberculosis is the formation of granulomatous
lesions (nodules) in internal organs, particularly the liver, spleen, and intestines.

o Caseous or necrotic tissue: The granulomas can contain caseous (cheese-like) material or
necrotic tissue, particularly in advanced stages of infection.

o Lung lesions: Although less common, granulomas can also form in the lungs and air sacs,
leading to respiratory issues.

o Enlarged liver and spleen: Often palpable during physical examination.

o Intestinal lesions: Lesions may be found in the gastrointestinal tract, leading to impaired
digestion and absorption.
In severe or chronic cases, systemic infection can lead to cachexia (wasting) and death
 CASEOUS OR
NECROTIC
TISSUE

https://www.thepoultrysite.com/publications/dis
eases-of-poultry/188/avian-tuberculosis
 DIAGNOSIS
o Clinical signs: Chronic weight loss, lethargy, and organomegaly (especially of
the liver and spleen) in the presence of a known exposure risk for
Mycobacterium avium.

o Histopathology: Granulomas with caseous necrosis are characteristic of avian

tuberculosis. Tissue samples (liver, spleen, intestine) can be examined
microscopically for granulomatous inflammation.

o Acid-fast staining: The presence of acid-fast bacilli (which retain the stain
despite acid washing) in tissues or feces is a key diagnostic feature.
 DIAGNOSIS
o PCR (Polymerase Chain Reaction): Molecular testing can detect
Mycobacterium avium DNA in tissues, feces, or other samples, providing a
rapid and sensitive diagnostic method.

o Culture: Isolation of the bacteria from tissues or feces (though it is slow and
requires special media) can confirm the diagnosis. Cultures often take weeks
to grow, so PCR or histology is preferred for quick diagnosis.

o Serology: There are serological tests available for Mycobacterium avium,

but they are typically used for screening rather than confirming the disease.
DIFFERENTIAL DIAGNOSIS
o Aspergillosis: This fungal infection can cause similar granulomatous
lesions, especially in the respiratory tract.

o Chronic bacterial infections such as Salmonella or Escherichia coli

infections can also cause granulomatous lesions in the liver and spleen.

o Avian tuberculosis can be confused with infectious coryza,

Mycoplasmosis, or other chronic wasting diseases, especially in birds with
gastrointestinal or respiratory symptoms.
 TREATMENT
· No specific treatment: There is no effective treatment or cure for avian
tuberculosis. The disease is often chronic and progressive, and treatment is usually
not practical for large flocks.

· Antibiotics: In some cases, antimicrobial therapy with rifampin or isoniazid

(commonly used for tuberculosis in humans) can be attempted, but the treatment is
not always effective in birds. Treatment is often not feasible due to the chronic
nature of the disease and its environmental persistence.
 TREATMENT
· Supportive care: Providing supportive care (e.g., improving diet and
hydration, managing secondary infections) can help the bird cope with the
disease but does not cure it.

· Culling: In the case of infected flocks, particularly in commercial poultry,

culling infected birds may be necessary to prevent further spread. Infected
birds should be euthanized humanely to control the outbreak.
CONTROL AND PREVENTION
· Biosecurity:

o Prevent introduction of infected birds by quarantining new stock and ensuring that
any incoming birds are disease-free.
o Maintain good biosecurity practices, including disinfecting equipment and clothing,
to reduce cross-contamination between infected and healthy flocks.
o Regularly test and monitor birds for the presence of the disease, particularly in
high-risk settings like poultry farms.

· Environmental management:
o Clean and disinfect poultry houses and bird enclosures regularly. Mycobacterium
avium can persist in the environment, particularly in moist conditions.
o Control rodents and other animals that can serve as vectors for the disease.
CONTROL AND PREVENTION
Vaccination:

· Currently, there is no commercial vaccine for avian

tuberculosis available, although research is ongoing into
vaccine development.

· Avoid contact with wildlife: Wild birds can serve as reservoirs

for Mycobacterium avium and can introduce the bacteria into
poultry flocks. Preventing wild bird access to poultry houses or
enclosures is important for preventing infection.
02

PIGEONPARAMYXOVIRUS
Common Name:

· Pigeon Paramyxovirus (PPMV-1), also referred to as Pigeon

Paramyxovirus Disease.

Etiological Agent:

· Pigeon Paramyxovirus 1 (PPMV-1), a strain of the

Paramyxoviridae family, specifically in the Avulavirus
genus, which is genetically related to Newcastle disease
virus (NDV).
.
 EPIDEMIOLOGY
· Pigeon Paramyxovirus primarily affects pigeons (especially homing
pigeons), though it can occasionally infect other avian species.
· The disease is more common in areas where there is high-density pigeon
populations or where pigeons are bred or kept for racing and other purposes.

· Outbreaks are reported in various parts of the world, particularly in Europe,

Asia, and North America. It is more frequently seen in pigeons that are in
close contact with other birds or in environments with poor biosecurity.
· The virus can be spread among pigeons through contact with infected birds,
contaminated equipment, or fecal droppings.
MODE OF TRANSMISSION
· Direct contact: Infected pigeons shed the virus in their saliva, feces, and nasal
secretions, leading to transmission via direct contact with these fluids.

· Aerosol transmission: The virus can be transmitted through aerosolized droplets

when infected birds sneeze or cough.

· Indirect transmission: The virus can also spread via contaminated feed, water,
equipment, and environmental surfaces.

· Vertical transmission: It is possible for the virus to be passed from infected parent
birds to their offspring (in eggs or through direct contact).
 CLINICAL SIGNS
Sudden death: In some cases, infected pigeons may die suddenly, especially in acute
infections.

Neurological signs: These include head tremors, twisting of the neck (torticollis), and paralysis
(typically affecting the wings and legs).

Respiratory signs: Sneezing, nasal discharge, and difficulty breathing may be observed in
affected birds.

Digestive signs: Diarrhea or wet droppings (often greenish) are common.

Lethargy: Infected birds may appear weak, inactive, and depressed.

Feather loss: Affected birds may show signs of feather deterioration or loss due to illness or
poor health.

Dehydration: Loss of fluid due to diarrhea and poor feeding behavior.

TWISTING
OF THE NECK

https://pigeondoctors.com/paramyxovirus/
DIARRHEA OR
WET DROPPINGS
(OFTEN
GREENISH)

https://pigeondoctors.com/paramyxovirus/
 LESIONS
Lesions in the digestive tract: Swelling and inflammation of the gastrointestinal
tract may be present, leading to watery diarrhea and other digestive issues.

Neurological lesions: Lesions in the brain (encephalitis) or other parts of the

nervous system can cause paralysis and the characteristic neurological signs.

Inflammation of the air sacs and trachea: Can result in respiratory distress and
abnormal respiratory sounds.

Pericardial inflammation: In some cases, inflammation of the heart and

surrounding tissue may be observed.
 DIAGNOSIS
Clinical signs: The presence of neurological and respiratory symptoms,
particularly head tremors, torticollis, and diarrhea, is suggestive of PPMV-1
infection.
PCR (Polymerase Chain Reaction): PCR tests are highly sensitive and can
detect the presence of Pigeon Paramyxovirus 1 in various tissue samples (e.g.,
swabs, feces, or tissues).
Virus isolation: Virus isolation in cell cultures can be used to confirm the
diagnosis, although it is a time-consuming process.
Serology: Detection of antibodies to Newcastle disease virus or PPMV-1 using
ELISA or hemagglutination inhibition tests can indicate exposure or infection.
Histopathology: Tissue samples, especially from the nervous system or
digestive system, may show characteristic lesions like encephalitis and
gastrointestinal inflammation.
DIFFERENTIAL DIAGNOSIS
Avian Encephalomyelitis (AE) Newcastle Disease (ND) Avian Influenza (AI)

Respiratory symptoms, diarrhea,

Ataxia, tremors (head/neck), Neuro/resp signs, diarrhea,
Clinical Signs sudden death, potentially severe
paralysis. sudden death.
systemic signs.

respiratory tract lesions and systemic

Microscopic brain lesions, no Nonsuppurative encephalitis,
Lesions involvement; specific lesions depend
gross lesions, pancreas foci. respiratory lesions, necrosis.
on the strain of AI.

All can cause neurological signs; Shares neuro signs with AE; both Can cause sudden death and high
Similarities
high morbidity/mortality possible. can cause sudden death. morbidity in affected birds.

AI involves more systemic signs

ND can be caused by virulent APMV (beyond respiratory/neuro), has high
Picornavirus; tremors of head/neck; strains across various avian species, mortality in severe strains, and is less
Differences
no resp signs; lower mortality. with combined respiratory and tied to pigeons specifically. Caused by
neurological signs. an orthomyxovirus rather than a
paramyxovirus.
 TREATMENT
Supportive care:
Hydration: Ensure that infected birds remain hydrated, especially if they have
diarrhea or respiratory distress.

Antibiotics: Secondary bacterial infections are common in birds with

respiratory symptoms, so broad-spectrum antibiotics such as enrofloxacin or
oxytetracycline may be used to prevent further complications.
Anti-inflammatory drugs: NSAIDs (e.g., flunixin meglumine) may help reduce
inflammation and ease discomfort.
No specific antiviral treatment: There is no specific antiviral medication for
PPMV-1, and treatment is largely supportive. Most birds with acute PPMV-1
infection do not survive, especially in the absence of early intervention.
CONTROL AND PREVENTION
Vaccination:
Vaccination against Newcastle disease virus (which includes PPMV-1) is a key
preventive measure for pigeons. Vaccines designed for Newcastle disease may
provide protection against Pigeon Paramyxovirus as well, as they are genetically
similar.
Live attenuated vaccines are commonly used in pigeons and can be given orally or
injected.

Biosecurity:
Quarantine new birds: Ensure that newly introduced birds are kept in isolation for at
least 2-3 weeks to monitor for signs of PPMV-1 and other potential diseases.
Limit exposure to wild birds: Prevent direct contact between domestic pigeons and
wild birds, as wild pigeons can be carriers of the virus.
Disinfection: Regularly disinfect cages, aviaries, and any equipment that may come
in contact with the birds, especially when moving birds between different areas.
CONTROL AND PREVENTION
Control of infected flocks:

Culling: Infected birds, particularly those showing severe symptoms or sudden

death, should be culled to prevent further spread.
Disposal of carcasses: Proper disposal of infected carcasses is crucial to prevent
environmental contamination and reduce the risk of transmission.

Environmental management:

Ensure proper ventilation and cleanliness in aviaries and enclosures to reduce

stress and improve overall bird health.
Implement regular cleaning protocols and monitor hygiene in pigeon lofts and other
bird housing systems.
03

MYCOTIC PNEUMONIA
Common Name:

Mycotic pneumonia is often referred to simply as fungal

pneumonia. It refers to a lung infection in poultry caused
by fungal organisms. Although rare compared to bacterial
or viral infections, mycotic pneumonia can still cause
significant health issues in poultry.
 ETIOLOGIC AGENT
Mycotic pneumonia is caused by various fungal pathogens, with the most common
being:

1. Aspergillus species (especially Aspergillus fumigatus), which is the most frequent

cause of fungal pneumonia in poultry.

2. Candida albicans and Cryptococcus neoformans can also cause pneumonia, though
less frequently.
Among these, Aspergillus fumigatus is the most common fungal agent responsible for
causing respiratory problems in poultry, particularly in young birds. Aspergillus spores
are widely present in the environment, especially in feed and litter.
 EPIDEMIOLOGY
· Geographic Distribution: Aspergillus infections are common worldwide, especially in
poultry operations with poor environmental control. They have been reported in
intensive poultry farms, particularly in humid and poorly ventilated environments.
· Outbreak Timing: Mycotic pneumonia can occur year-round but is more prevalent in
warm, damp environments that promote fungal growth. Fungal outbreaks are more
likely when feed or litter is contaminated, or poor ventilation is present.
· Age and Species Affected: Young birds (chicks and poults) are most susceptible to
fungal pneumonia due to their immature immune systems. However, older birds can
also develop the disease, particularly if they are exposed to high levels of fungal spores
or other immunosuppressive conditions.
· Fungal Growth Conditions: Aspergillus fumigatus thrives in warm, humid conditions,
making poorly stored feed, humid litter, and poorly ventilated housing ideal
environments for fungal growth.
 MODE OF TRANSMISSION
Control of infected flocks:Mycotic pneumonia, particularly due to Aspergillus species, is
primarily transmitted through aerosolized spores. The key routes of transmission are:
1. Inhalation of Fungal Spores:
o Aspergillus spores are ubiquitous in the environment, especially in dust or moldy
feed. Birds inhale these spores, which can lead to infection when they reach the lungs.
o Spores may also be present in litter, water, or feed if they are contaminated by moldy
conditions.
2. Contaminated Feed or Bedding:
o Aspergillus spores can be found in moldy feed and contaminated bedding material.
Inhalation of spores from these sources can lead to respiratory infections in birds.
3. Secondary Infections:
Mycotic pneumonia can also be aggravated by secondary bacterial infections due to the
impaired immune system caused by the fungal infection. Escherichia coli and
Salmonella are examples of bacteria that may complicate mycotic pneumonia
 Clinical Signs
1. Respiratory Distress:
Gasping, coughing, sneezing, and nasal discharge are common signs of
pneumonia.
Labored breathing and wheezing are often seen as the infection worsens.
2. Depression and Lethargy:
Infected birds are often lethargic and appear weak or disoriented due to the
general effects of the infection on their overall health.
3. Reduced Appetite and Growth:
Infected birds may have reduced feed intake and poor growth due to the energy
expended in combating the infection and due to reduced ability to breathe
effectively.
4. Swelling of the Head and Neck:
Swelling in the sinus and periorbital regions (around the eyes) can sometimes be
observed due to the infection spreading to the sinuses.
Clinical Signs

Lethargy

Swelling of the Head and Neck.

 Lesions
5. Lesions at Necropsy:
Granulomatous lesions in the lungs, characterized by focal nodules or
pale, grayish areas in the lung tissue.

Congested and inflamed air sacs, which may have yellow or greenish
exudates.

In severe cases, the infection may cause extensive tissue damage in the
lungs, leading to pneumonia and necrosis.

6. Secondary Bacterial Infections:

As the fungal infection weakens the bird’s immune system, secondary
bacterial infections like E. coli or Pasteurella multocida may exacerbate
respiratory distress and lead to septicaemia, enteritis, or other
complications.
 DIAGNOSIS
1. Clinical Signs:
o The signs of respiratory distress, nasal discharge, and labored breathing may suggest
mycotic pneumonia, but these signs overlap with several other respiratory diseases in
poultry.
2. Laboratory Diagnosis:
o Fungal Culture: The gold standard for diagnosis is fungal culture. Tissue samples or
respiratory tract swabs can be cultured on specific fungal media (e.g., Sabouraud agar)
to isolate and identify the fungus, usually Aspergillus fumigatus.
o PCR (Polymerase Chain Reaction): PCR can be used to rapidly detect Aspergillus DNA
in samples, especially when fungal culture is not readily available.
o Histopathology: Tissue samples from the lungs and air sacs can be examined
microscopically for the presence of fungal hyphae or granulomatous lesions indicative
of fungal infection.
DIFFERENTIAL DIAGNOSIS
Bacterial Pneumonia Mycoplasma Infections Chronic Respiratory Disease (CRD)

Respiratory distress (coughing,

Respiratory distress (rales, coughing,
sneezing, nasal discharge,
sneezing, difficulty breathing), nasal
Clinical Signs Similar respiratory symptoms wheezing), conjunctivitis, swollen
discharge, conjunctivitis. Reduced feed
eyes and sinusitis, reduced egg
efficiency and weight gain
production.

Mild catarrhal sinusitis, tracheitis, and

airsacculitis in uncomplicated M.
No characteristic fungal Mild catarrhal sinusitis, tracheitis, and
Lesions gallisepticum infections in chickens.
lesions. airsacculitis.
Turkeys develop severe mucopurulent
sinusitis, tracheitis, and airsacculitis.

Can cause similar respiratory Can cause similar respiratory

Similarities Can cause similar respiratory distress
symptoms. distress.

Bacterial etiology; lacks fungal Mycoplasma etiology; often

lacks granulomatous lesions; often
granulomas; may have other polymicrobial; mild catarrhal
Differences involves conjunctivitis and sinusitis,
systemic signs depending on the
especially in turkeys.
inflammation; can be chronic; reduced
bacteria involved. egg production.
 TREATMENT
Antifungal Treatment:
Itraconazole or Fluconazole are commonly used antifungal drugs to treat
Aspergillus fumigatus infections.
Itraconazole dosage: 10–20 mg/kg of body weight orally once daily for 7–
14 days, depending on the severity of the infection.
Amphotericin B: In severe cases, Amphotericin B can be used intravenously or in
nebulized form.
Amphotericin B dosage: Typically, 0.5–1 mg/kg body weight, depending
on veterinary advice.
Antibiotics for Secondary Bacterial Infections:
If secondary bacterial infections are present, antibiotics such as Tetracyclines
(e.g., Oxytetracycline) or Sulfonamides (e.g., Sulfadimethoxine) can be
administered.
Oxytetracycline dosage: 1-2 g/L of drinking water for 5–7 days.
CONTROL AND PREVENTION
Environmental Management:

Improving ventilation: Adequate airflow and humidity control in poultry houses are
crucial in preventing the proliferation of fungal spores.

Controlling moisture: Ensuring that feed and litter do not become wet or moldy
helps reduce the risk of fungal contamination.

Regular cleaning and disinfection of poultry houses, feeders, and water sources to
reduce fungal buildup.
CONTROL AND PREVENTION
Biosecurity Measures:
Restricting the movement of contaminated equipment or personnel between
infected and healthy flocks to avoid spreading fungal spores.
Quarantining new birds and ensuring that they are free from fungal infections before
introducing them to healthy flocks.

Fungal-Free Feed:
Ensuring proper storage of feed and preventing it from becoming contaminated with
mold is critical. Moldy feed is a primary source of fungal spores, including
Aspergillus.

Vaccination:
There is no vaccine available for mycotic pneumonia caused by Aspergillus
fumigatus, so prevention relies heavily on environmental control and biosecurity
measures.
 AVIAN
RHEOVIRUS
Common Name:Avian
reovirus (ARV)
 ETIOLOGICAL AGENT
Avian rheovirus is a viral infection caused by the avian
reovirus (ARV), which is a member of the Reoviridae family
and the Orthoreovirus genus. This virus primarily affects
poultry, including chickens, turkeys, and other avian
species, causing a range of symptoms that can impact the
respiratory, digestive, and musculoskeletal systems.
 EPIDEMIOLOGY

Avian Rheovirus primarily affects poultry, including

chickens, turkeys, and ducks, though it has also been
observed in other avian species.
The disease has been reported worldwide, with
outbreaks occurring in countries with intensive poultry
farming, such as the United States, Europe, and parts
of Asia.
 EPIDEMIOLOGY
The disease is especially common in broiler chickens and
has been associated with poor growth and joint issues in
affected flocks.
Infected birds can carry the virus asymptomatically,
making it difficult to control once introduced into a
flock.
MODE OF TRANSMISSION
Fecal-oral transmission
Direct contact
Vertical transmission.
Environmental contamination
 CLINICAL SIGNS
Lameness and swollen joints (particularly in the legs,
hocks, and tendons), often referred to as "viral arthritis".
Difficulty walking, stiffness, and reluctance to move.
Respiratory signs: Mild sneezing, coughing, and nasal
discharge.
Reduced growth rates and poor weight gain in affected
birds.
Depression, lethargy, and poor feed conversion.
CLINICAL SIGNS
 LESIONS
Swollen joints with inflammation, particularly in the hock joints.
Synovial fluid accumulation in affected joints.
Inflammation and fibrosis in the tendons and surrounding
tissues.
Mild respiratory tract inflammation may be present.
Subcutaneous edema (fluid accumulation under the skin),
especially around joints.
Lesions in muscles, tendons, and ligaments may also be
observed.
LESIONS
 DIAGNOSIS
Clinical signs: History of lameness, swollen joints, and
poor growth in affected flocks, particularly in broilers.
PCR (Polymerase Chain Reaction)
Virus isolation
Serology
Histopathology
DIFFERENTIAL
DIAGNOSIS
 Mycoplasmosis (M. synoviae or M. Rheumatoid Arthritis or other bacterial
Infectious Laryngotracheitis (ILT)
gallisepticum) infections (like Salmonella)

Lameness, swollen joints (especially M.

synoviae), respiratory distress Respiratory distress (coughing,
Lameness, swollen joints, difficulty walking.
(especially M. gallisepticum), reduced gasping, conjunctivitis), blood-tinged
Clinical Signs Salmonella can cause joint lesions with
egg production. Disease is generally tracheal exudate, mortality. ILT affects
synovitis and bursitis
more severe in turkeys, with swelling of only chickens, pheasants, and peafowl
the infraorbital sinuses.

Mild catarrhal sinusitis, tracheitis, and

airsacculitis in uncomplicated M.
Intranuclear inclusions in conjunctival Joint lesions with synovitis and bursitis
Lesions gallisepticum infections in chickens.
scrapings. Blood-tinged tracheal exudate caused by other bacteria or viruses
Turkeys develop severe mucopurulent
sinusitis, tracheitis, and airsacculitis.

Can cause lameness or difficulty walking, and Can cause difficulty walking and are can cause lameness, swollen joints and
Similarities
reduced growth/weight gain. associated with poor health. difficulty walking

Mycoplasma etiology; may have respiratory Rheumatoid arthritis is immune-mediated

Herpesvirus etiology; primarily respiratory
Differences signs and reduced egg production; lesions are (non-infectious); bacterial arthritis has a
with blood-tinged exudate; limited host range.
milder than in Reovirus. specific bacterial cause (Salmonella)
 TREATMENT

No specific antiviral treatment exists for avian rheovirus, so

management focuses on reducing secondary bacterial infections
and supporting affected birds.
Supportive care:
Antibiotics: To prevent or treat secondary bacterial infections
that might arise due to joint inflammation, such as Tylosin,
Enrofloxacin, or Oxytetracycline.
 TREATMENT

Anti-inflammatory drugs: Non-steroidal anti-inflammatory

drugs (NSAIDs) such as Flunixin meglumine or Meloxicam can be
used to reduce pain and inflammation in the joints.
Hydration and proper nutrition: Ensure the birds have access to
clean water and high-quality feed to help maintain their
strength and promote recovery.
 CONTROL AND PREVENTION

Vaccination: Currently, there are no commercial vaccines available for

avian rheovirus, but attenuated or inactivated vaccines may be
developed in the future.
Biosecurity measures:
Quarantine new birds before introducing them to a flock.
Limit access to contaminated equipment, feed, and water that
may carry the virus.
 CONTROL AND PREVENTION

Disinfect equipment, cages, and facilities regularly to

minimize environmental contamination.
Maintain good sanitation and ventilation in poultry
houses to prevent the spread of the virus.
Management:
Culling
Good husbandry practices
Veterinary intervention
HISTOPLASMOSIS
Common Name:
Darlings disease
 ETIOLOGICAL AGENT
Histoplasmosis in birds is a fungal infection caused by the organism
Histoplasma capsulatum. This pathogen is a dimorphic fungus that
typically affects the respiratory system, but it can also have
systemic involvement, depending on the severity of the infection.
 EPIDEMIOLOGY
• Histoplasmosis is a fungal infection caused by the organism Histoplasma
capsulatum.
• It primarily affects wild birds (particularly pigeons, doves, and waterfowl) but
can also affect domestic poultry, such as chickens, turkeys, and ducks.
• Outbreaks are most common in regions with high humidity and abundant bird
droppings, particularly in North America, South America, and parts of Asia.
• The disease is often associated with exposure to contaminated environments,
such as pigeon roosts, bird aviaries, or poultry houses where feces accumulate and
become a source of infection.
 MODE OF TRANSMISSION
• Inhalation of fungal spores: Birds inhale Histoplasma spores present in
dust particles from contaminated bedding, feces, or soil. Spores are often
found in areas where bird droppings accumulate and decompose.
• Fecal contamination: The fungus can also be spread through the
ingestion of contaminated feed or water, although inhalation is the primary
route of transmission.
 CLINICAL SIGNS
Clinical Signs in birds:
Respiratory distress: Sneezing, coughing, nasal discharge, and
difficulty breathing.
Lethargy and reduced activity.
Poor weight gains or failure to thrive.
Diarrhea and loss of appetite.
Swollen joints or lameness in some cases, especially if the infection
spreads.
Convulsions or neurological signs can occur in severe cases.
 CLINICAL SIGNS

SWELLING OF HOCK JOINTS

 LESIONS

Granulomatous lesions in the lungs, air sacs, and sometimes the liver or
spleen.
Lung consolidation: Thickening of lung tissue due to chronic inflammation.
Visceral involvement: Organs like the liver, spleen, and intestines may show
signs of granuloma formation or inflammation.
Air sac lesions: In severe cases, fungal growth can lead to fibrosis and
thickening of the air sacs.
LESIONS
 DIAGNOSIS

Clinical signs combined with a history of exposure to bird droppings

or contaminated environments can suggest histoplasmosis.
Fungal culture: Isolation of Histoplasma capsulatum from
respiratory secretions, feces, or tissue samples.
PCR (Polymerase Chain Reaction): Specific and sensitive for
detecting Histoplasma DNA in tissue samples.
 DIAGNOSIS

Histopathology: Microscopic examination of tissues (e.g., lungs,

liver, spleen) to identify typical granulomatous lesions containing
fungal organisms.
Serology: Detection of antibodies to Histoplasma in blood samples,
though this may be less reliable for definitive diagnosis in birds.
 DIFFERENTIAL DIAGNOSIS

Avian tuberculosis (by Mycobacterium avium)

Aspergillosis
Chlamydiosis (Psittacosis)
Mycobacteriosis or other bacterial infections that can lead to
granulomatous inflammation.
Avian influenza or Newcastle disease
 Avian Tuberculosis (Mycobacterium avium) Aspergillosis Chlamydiosis (Psittacosis)

Variable; respiratory signs (coughing,

Weight loss, sluggishness, lameness, Resp. distress, lethargy, reduced sneezing), ocular discharge, diarrhea,
Clinical Signs
diarrhea, resp. signs. appetite. lethargy, weight loss, ruffled feathers,
sometimes neurological signs.

Granulomas: liver, spleen, intestine, Inflammation and lesions in the respiratory

Lesions Granulomas: lungs, air sacs.
bone marrow. tract, liver, spleen, air sacs, and heart.

Fungal; resp. disease; granulomas in Can cause respiratory signs, lethargy, and
Similarities Weight loss, lethargy, respiratory signs.
lungs/air sacs. weight loss.

Bacterial etiology (Chlamydia psittaci);

Differences Fungal; birds source of infection. Fungal; primary resp. disease.
zoonotic; can cause a wide range of signs.
 DIFFERENTIAL DIAGNOSIS

Avian tuberculosis (by Mycobacterium avium)

Aspergillosis
Chlamydiosis (Psittacosis)
Mycobacteriosis or other bacterial infections that can lead to
granulomatous inflammation.
Avian influenza or Newcastle disease
 TREATMENT
Antifungal treatment:
Itraconazole or Fluconazole are commonly used antifungal drugs for
treating histoplasmosis. The recommended dosage is based on
veterinary advice, but typical dosing for birds may range from 5-10
mg/kg daily.
Amphotericin B can be used in severe cases but is more toxic and
generally reserved for life-threatening infections.
 SUPPORTIVE CARE
Hydration: Ensure that infected birds are well-hydrated, especially
if they are suffering from respiratory distress or diarrhea.
Good nutrition: Provide high-quality feed to support immune
function and recovery.
Antibiotics: If secondary bacterial infections occur, broad-spectrum
antibiotics such as enrofloxacin or oxytetracycline may be used.
Improved environmental conditions: Reducing dust and fungal spore
exposure by improving ventilation and removing contaminated bedding
is crucial.
 CONTROL AND PREVENTION
Environmental management:
Reduce exposure to contaminated areas: Limit the movement of
birds into areas where large amounts of feces have accumulated.
Proper disposal of feces: Regular cleaning and removal of bird
droppings from aviaries, poultry houses, and outdoor areas.
Improve ventilation: Ensure that poultry houses or aviaries have
adequate airflow to reduce the accumulation of fungal spores in the
air.
 CONTROL AND PREVENTION
Biosecurity:
Quarantine new birds: Prevent introducing potentially infected birds
into clean flocks by implementing quarantine protocols.
Use of protective equipment: When handling infected birds or
cleaning contaminated areas, personal protective equipment (PPE) such
as masks, gloves, and eye protection can reduce the risk of exposure to
fungal spores.
Culling:
In severe outbreaks, particularly in high-risk environments like aviaries
or poultry farms, culling of severely affected birds may be necessary to
prevent the spread of the infection.
TRICHOMONIASIS
Common Name:Canker or
Frounce
 ETIOLOGICAL AGENT

Trichomoniasis in avian species is primarily caused by the

protozoan parasite Trichomonas gallinae. This parasite
infects various bird species, especially pigeons, doves, and
other columbids, though it can affect other birds as well.
 EPIDEMIOLOGY
Trichomoniasis is a parasitic infection caused by the protozoan
Trichomonas gallinae.
It commonly affects pigeons (Columbidae), doves, raptors (e.g.,
falcons and hawks), and other wild birds, but can also affect domestic
poultry like chickens, turkeys, and ducks.
Outbreaks have been documented worldwide, but the disease is
especially prevalent in areas with high densities of pigeons and doves.
Trichomoniasis is often seen in wild bird populations, and poultry can
occasionally become infected through contact with wild birds or their
contaminated environment.
 MODE OF TRANSMISSION
Direct contact: The disease is primarily transmitted through the
ingestion of contaminated feed, water, or direct contact with infected
birds' oral or nasal secretions.
Fecal-oral transmission: Trichomonas trophozoites can be present in
bird droppings, contaminating the environment where healthy birds
might ingest them.
Mechanical transmission: The parasite can also be spread indirectly
through contaminated feeders, water sources, or equipment that has
been exposed to infected droppings.
Vertical transmission: Infected parents can transmit the parasite to
their offspring through feeding (i.e., "crop milk" in pigeons and doves).
 CLINICAL SIGNS
Oral lesions: Yellowish or white caseous (cheese-like) lesions can
develop in the crop, esophagus, and sometimes the tongue or pharynx.
Difficulty swallowing (dysphagia), leading to drooling or the
regurgitation of food.
Lethargy and loss of appetite.
Weight loss due to difficulty in eating and drinking.
Respiratory distress may develop if the infection extends into the
trachea or lungs.
Nasal discharge and swollen neck in some cases if the infection
spreads.
 LESIONS

Yellowish plaques or nodules in the mouth, throat, crop, and

esophagus.
Lesions may extend into the trachea and larynx in severe cases.
Inflammation and ulceration of the affected mucosal surfaces.
In severe or chronic cases, secondary bacterial infections may result
in pneumonia or abscess formation.
 FIGURE A: MILD LESION IN A BONELLI’S
EAGLE

B: MULTIFOCAL MODERATE LESION IN A

LONG-EARED OWL

C AND D: SEVERE LESIONS INVADING THE

EYE AND OROPHARYNGEAL CAVITY IN A
COMMON KESTREL

E: SEVERE LESION IN A EURASIAN

COLLARED DOVE

F: SEVERE LESION IN A ROCK PIGEON

(MARTÍNEZ-HERRERO ET AL., 2020).

FIGURE A: LESIONS IN A GOSHAWK PRESENTING COINFECTION WITH T. GALLINAE AND CAPILLARIDS. THE ARROWHEAD
SHOWS A NEMATODE;
B: CAPILLARID EGGS FROM A SMEAR (FORZÁN ET AL., 2010)
 DIAGNOSIS
Clinical signs: Observing typical oral lesions and difficulty
swallowing, along with a history of contact with infected birds or
environments.
Microscopic examination: Fresh swabs from the oral cavity, crop, or
esophagus can be examined under a microscope to identify Trichomonas
trophozoites.
Culture: The organism can be cultured from infected lesions or oral
swabs to confirm the diagnosis.
PCR (Polymerase Chain Reaction): A more sensitive method for
detecting Trichomonas DNA in tissues or swabs.
 DIFFERENTIAL DIAGNOSIS
Disease Cause Lesions Clinical Signs Diagnosis

Microscopy (wet
Trichomonas White, caseous (cheese-like) lesions in the crop and Crop swelling, difficulty swallowing, regurgitation, weight
Trichomoniasis mount, Giemsa
gallinae (Protozoan) esophagus, inflammation of the mucosa loss, lesions in the crop and esophagus
stain), PCR

Canker (Avian White, nodular lesions in the crop, esophagus, and Similar to trichomoniasis: crop swelling, difficulty Fungal culture,
Candida spp. (Fungal)
Candidiasis) oropharynx swallowing, regurgitation, weight loss Histopathology

PCR, Virus
Avian Influenza Edema and congestion in the digestive tract, Respiratory distress, diarrhea, edema, nervous signs,
Avian influenza virus isolation,
(AI) gastrointestinal hemorrhages in severe cases digestive tract lesions (sometimes crop involvement)
Serology

Yellowish to brown nodules or ulcerated lesions on Pox lesions on skin and mucous membranes (oral cavity Histopathology,
Avian Pox Avian poxvirus
oral mucosa, skin lesions (wart-like) involvement), can cause crop lesions PCR

Histomonas
Histomoniasis Liver necrosis, cecal lesions, yellowish discoloration in Yellow droppings, liver and cecal lesions, lethargy, not Histopathology,
meleagridis (Protozo
(Blackhead) the ceca and liver typically oral/crop lesions PCR
an)
 TREATMENT

Antiprotozoal drugs:
Dimetridazole is the most commonly used treatment for
trichomoniasis in birds. The typical dosage for pigeons and other avian
species is 50-100 mg per liter of drinking water for 5-7 days.
Ronidazole is another effective treatment, often used at a dose of
25 mg per kg of body weight orally for 5-7 days.
Metronidazole can also be used, but it is less commonly employed in
avian species.
 SUPPORTIVE CARE

Fluid therapy to maintain hydration, especially if the bird is

dehydrated due to difficulty swallowing.
Antibiotics may be used if there is a secondary bacterial infection,
though they are not effective against the parasite itself. Common
antibiotics for secondary infections include Tylosin or Enrofloxacin.
Improved nutrition: Providing easily accessible, nutritious food and
water to affected birds to aid in recovery.
 CONTROL & PREVENTION
Isolation of infected birds: Infected birds should be isolated to
prevent the spread of the disease to healthy birds, especially in captive
or domestic situations.
Good hygiene: Regularly clean and disinfect bird housing, feeding
equipment, and water containers to minimize the spread of the
parasite.
Control of wild bird populations: Preventing contact with wild
pigeons, doves, and other infected species is critical in preventing
outbreaks, especially in poultry farms.
 CONTROL & PREVENTION

Treatment of affected flocks: All birds in a flock should be treated,

even if only some birds are showing symptoms, to prevent further
spread.
Quarantine new birds: Isolate newly introduced birds from the main
flock until they are confirmed healthy and free from infection.
 CONTROL & PREVENTION

Treatment of affected flocks: All birds in a flock should be treated,

even if only some birds are showing symptoms, to prevent further
spread.
Quarantine new birds: Isolate newly introduced birds from the main
flock until they are confirmed healthy and free from infection.
CRYPTOCOCCOSIS
Common Name:
Cryptococcosis
 ETIOLOGICAL AGENT

Cryptococcosis is caused by Cryptococcus

neoformans, a fungal infection that
typically affects the lungs and central
nervous system in mammals and birds.
 EPIDEMIOLOGY
Cryptococcosis is an opportunistic fungal infection and is primarily a
disease of immunocompromised animals and humans. However, it can
also affect healthy birds, especially those in environments with high
fungal spore loads, such as areas with pigeon droppings or decaying
organic matter.
The disease is worldwide but more commonly reported in urban areas
where pigeons are abundant and where Cryptococcus neoformans is
found in their droppings.
It is more common in pigeons, doves, and occasionally chickens or
waterfowl.
MODE OF TRANSMISSION

Inhalation of fungal spores

Environmental exposure

Vertical transmission
 CLINICAL SIGNS

Respiratory distress: Difficulty breathing, nasal discharge, coughing, or

sneezing.
Lethargy and poor appetite.
Neurological symptoms: In severe cases, birds may exhibit head
tremors, paralysis, lack of coordination, and circling behavior.
Swelling of the head and neck due to localized fungal growth.
Sudden death can occur in some birds, particularly if the infection
progresses rapidly to the central nervous system or lungs.
 LESIONS

Granulomatous inflammation in the lungs, air sacs, and sinuses.

Masses or nodules in the brain or central nervous system can occur,
leading to neurological signs.
Inflammation and abscess formation in affected organs, such as the
lungs, liver, or kidneys.
Lung consolidation with fungal growth and tissue necrosis.
Enlargement of the head or neck due to infected sinuses or cranial
lesions.
 DIAGNOSIS

Clinical signs: The presence of respiratory and neurological signs in

birds with a history of exposure to pigeons or contaminated
environments should raise suspicion of cryptococcosis.
Fungal culture
Microscopic examination
PCR (Polymerase Chain Reaction)
Serology
 DIFFERENTIAL DIAGNOSIS
Disease Cause Clinical Signs Lesion Diagnosis Differentiation from Cryptococcosis

species Respiratory
distress, nasal Histopathology, culture, Aspergillosis causes granulomatous lesions in the respiratory system, with
Aspergillosis Aspergillus species Granulomas in lungs, air sacs, and sinuses.
discharge, coughing, PCR no skin or CNS involvement like cryptococcosis.
lethargy.

Coughing, nasal
Mycoplasma Mycoplasmosis usually causes mild to moderate inflammation of the
discharge, Typically no significant gross lesions; some
Mycoplasmosis gallisepticum, M. PCR, serology, culture respiratory tract without granulomas or skin lesions seen in
conjunctivitis, respiratory tract inflammation
synoviae cryptococcosis.
respiratory distress

Neurological signs:
Avian
Avian ataxia, tremors, Lesions in the brain: neuronal degeneration Histopathology, virus AE affects the nervous system with brain lesions, but lacks the
encephalomyelitis
Encephalomyelitis (AE) paralysis, and lymphocytic infiltration. isolation, PCR granulomatous or skin involvement seen in cryptococcosis.
virus
incoordination.

Neurological signs
(paralysis, torticollis),
Avian paramyxovirus Lesions in various organs: encephalitis, PCR, virus isolation, ND causes more acute systemic involvement, often with hemorrhagic
Newcastle Disease (ND) respiratory distress,
serotype 1 hemorrhages in internal organs. serology lesions, unlike the slow, granulomatous progression of cryptococcosis.
gastrointestinal
symptoms.

Bacterial Septicemia Salmonella spp., E. Lethargy, inappetence, Septicemia; lesions in internal organs, Blood cultures, PCR, Bacterial infections cause widespread organ enlargement and necrosis
(e.g., Salmonellosis) coli diarrhea, sudden death. especially the liver, spleen, and heart. bacteriological isolation without the distinctive granulomas or skin lesions of cryptococcosis.
 TREATMENT

Antifungal therapy:
Fluconazole or Itraconazole are commonly used to treat cryptococcosis
in birds. Typical doses for birds range from 5-10 mg/kg orally once a
day for 3-4 weeks, depending on the severity of the infection.

Amphotericin B may be used in severe cases, though it is more toxic and

typically reserved for critical infections. Dosing varies, but it is usually
given in a diluted form via injection (e.g., 0.1-0.2 mg/kg every 2-3
days).
 CONTROL AND PREVENTION

Environmental management:
Cleanliness: Regular cleaning and disinfection of aviaries, poultry
houses, and other bird enclosures to reduce fungal spore exposure.
Avoid exposure to contaminated areas
Improved ventilation
Pigeon control
Quarantine new birds
Protective equipment
 AVIAN
ASPERGILLOSIS
Common Name: Air Sac
Disease or Aspergillosis of
Birds
 ETIOLOGICAL AGENT

Caused by Aspergillus species, primarily Aspergillus

fumigatus, Aspergillus flavus, and Aspergillus niger.
 EPIDEMIOLOGY
Avian Aspergillosis is a fungal infection that can affect various bird
species, particularly poultry, pet birds, wild birds, and waterfowl.

The disease is worldwide but more commonly observed in environments

with poor ventilation, high humidity, and high spore loads (such as bird
aviaries, poultry houses, or areas with contaminated feed).

Aspergillosis is more common in immunocompromised birds or those

under stress, such as birds that are malnourished, overcrowded, or
exposed to contaminated bedding, litter, or poor air quality.
MODE OF TRANSMISSION

Inhalation of fungal spores

Environmental contamination

Contaminated equipment
 CLINICAL SIGNS

Respiratory distress: Labored breathing, wheezing, and nasal discharge.

Open-mouth breathing and dyspnea (difficulty breathing).
Lethargy and reduced activity.
Decreased appetite and weight loss.
Depression and failure to thrive in young or stressed birds.
Coughing or sneezing may be observed in some cases.
 LESIONS

Air sac infections

Lung consolidation
Sinusitis and laryngeal lesions
Fungal plaques
Cerebral aspergillosis
Systemic spread
 DIAGNOSIS

Clinical signs: Respiratory distress, lethargy, and failure to thrive in

the presence of a history of exposure to a contaminated environment
should raise suspicion for aspergillosis.
Microscopic examination
Fungal culture
PCR (Polymerase Chain Reaction)
Radiographs (X-rays)
Serology
 DIFFERENTIAL DIAGNOSIS
Disease Cause Clinical Signs Lesions Differentiating Factors

Cryptococcus species Aspergillosis causes granulomatous lesions in the

Respiratory distress, neurological signs,
Cryptococcosis (e.g., C. neoformans, Granulomatous lesions in skin, brain, lungs. respiratory system, with no skin or CNS involvement
skin nodules.
C. gattii) like cryptococcosis.

Mycoplasma Mycoplasmosis usually causes mild to moderate

Coughing, nasal discharge, conjunctivitis, Typically no significant gross lesions; some
Mycoplasmosis gallisepticum, M. inflammation of the respiratory tract without
respiratory distress respiratory tract inflammation
synoviae granulomas or skin lesions seen in cryptococcosis.

Avian Avian AE affects the nervous system with brain lesions, but
Neurological signs: ataxia, tremors, Lesions in the brain: neuronal degeneration
Encephalomyeliti encephalomyelitis lacks the granulomatous or skin involvement seen in
paralysis, incoordination. and lymphocytic infiltration.
s (AE) virus cryptococcosis.

Neurological signs (paralysis, torticollis), ND causes more acute systemic involvement, often
Newcastle Disease Avian paramyxovirus Lesions in various organs: encephalitis,
respiratory distress, gastrointestinal with hemorrhagic lesions, unlike the slow,
(ND) serotype 1 hemorrhages in internal organs.
symptoms. granulomatous progression of cryptococcosis.

Bacterial Bacterial infections cause widespread organ

Salmonella spp., E. Lethargy, inappetence, diarrhea, sudden Septicemia; lesions in internal organs,
Septicemia (e.g., enlargement and necrosis without the distinctive
coli death. especially the liver, spleen, and heart.
Salmonellosis) granulomas or skin lesions of cryptococcosis.
 TREATMENT

Antifungal medications:
Itraconazole is the most commonly used treatment for avian
aspergillosis, with doses ranging from 5-10 mg/kg orally once a day for
3-4 weeks, depending on the severity of the disease.
Fluconazole can also be used, typically at a dose of 5-10 mg/kg orally
once a day.
Amphotericin B is reserved for severe cases, particularly when the
infection is systemic. It can be administered intravenously or
subcutaneously at a dose of 0.1-0.2 mg/kg every 2-3 days.
 CONTROL AND PREVENTION
Environmental management:
Good ventilation
Regular cleaning
Reduce moisture
Biosecurity:
Limit exposure to contaminated environments
Quarantine new birds
Management:
Treat affected flocks
Culling
 AVIAN
SINUSITIS
Common Name: Sinus
Infection in birds
 ETIOLOGICAL AGENTS
Sinusitis in birds can be caused by bacterial, fungal, or viral infections,
as well as by foreign bodies or trauma.

Common pathogens associated with bacterial sinusitis include

Escherichia coli, Mycoplasma gallisepticum, Chlamydia psittaci, and
Streptococcus species. Fungal sinusitis is often caused by Aspergillus
species.

Viral infections such as avian influenza, Newcastle disease, or

infectious laryngotracheitis (ILT) can also cause secondary sinusitis.
 EPIDEMIOLOGY
Sinusitis is relatively common in pet birds, poultry, and wild birds,
particularly in environments with poor ventilation, high humidity, or
overcrowding.

It is more common in poultry, pet birds, and parrots due to their

anatomy and susceptibility to upper respiratory infections.

Sinusitis can be seen in flocks or individual birds that are stressed or

immunocompromised, making them more prone to infection. Poor
sanitation and inadequate environmental conditions (e.g., high ammonia
levels, dusty or wet environments) can increase the risk.
 MODE OF TRANSMISSION
Direct contact: Sinusitis can spread from bird to bird through
aerosolized droplets, especially in closed environments such as aviaries
or poultry houses.

Indirect transmission: Contaminated equipment, cages, food, or water

can spread bacteria or viruses that lead to sinus infections.

Environmental factors: Exposure to mold, dust, and ammonia fumes in

poorly ventilated environments can contribute to the development of
sinusitis in birds.
 CLINICAL SIGNS

Nasal discharge
Facial swelling and swollen sinuses
Respiratory distress
Sneezing and coughing
Eye discharge
Loss of appetite and lethargy
In chronic cases, birds may have persistent nasal discharge and facial
deformities from the thickening of the sinuses.
 CLINICAL SIGNS

https://www.researchgate.net/figure/Figure-1-A-layer-bird-showing-ocular-
discharge-and-infra-orbital-sinus-swelling_fig1_276301779
MACROSCOPIC AND MICROSCOPIC LESIONS:

(A) SWOLLEN HEAD, SUBMANDIBULAR EDEMA AND STICKY EYES;

(B) PURULENT NASAL DISCHARGE;

(C) HEMORRHAGIC INFLAMMATION OF THE SINUS INFRAORBITALIS ALONG WITH FIBRINOUS MASS;

(D) CONJUNCTIVITIS, FACIAL TISSUE EDEMA AND HEMORRHAGES ALONG WITH GELATINOUS AND CHEESE-LIKE MATERIAL;

(E) HYPEREMIA, WIDESPREAD AND DIFFUSE PLASMATIC EDEMA WITH FIBRIN FILAMENTS AND INFILTRATION OF
INFLAMMATORY CELLS (STARS). HE. BAR: 100 ΜM;

(F) PREDOMINANT PRESENCE OF HETEROPHILS (ARROWS) AS COMPARED TO MONONUCLEAR CELLS (TRIANGLE). HE. BAR: 20
ΜM;

(G) HYPERPLASTIC TRACHEITIS, LOSS OF CILIA, PAPILLARY PROLIFERATION OF THE EPITHELIUM. HE. BAR: 200 ΜM;

(H) MAGNIFIED VIEW OF THE TRACHEA SHOWING HYPERPLASTIC TRACHEITIS CHARACTERIZED BY PAPILLARY
PROLIFERATION OF THE EPITHELIUM, MONONUCLEAR CELL INFILTRATION IN THE LAMINA PROPRIA AND CONGESTIVE
VESSELS. HE. BAR: 50 ΜM
 LESIONS
Swollen sinuses: The sinuses, especially around the eyes and beak, may
be visibly enlarged or asymmetrical.
Purulent or caseous material in the sinuses.
Inflammation and congestion in the nasal cavity and air sacs.
Granulomas or polyps in chronic or fungal infections.
In severe cases, the infection can spread to the brain or orbits, causing
neurological signs or blindness.
 DIAGNOSIS

Clinical signs
Physical examination
Radiographs (X-rays)
Endoscopy
Microbiological culture
PCR
Serology
 DIFFERENTIAL DIAGNOSIS
Disease Cause Lesions Clinical Signs Differentiating Factors

Thick, yellow to green nasal exudates,

Bacterial Escherichia coli, Purulent nasal discharge, localized swelling, Often secondary to poor management
possible swelling or abscesses around
Sinusitis Staphylococcus lethargy conditions or immune compromise.
the sinuses.

Fungal plaques in the nasal cavity,

Aspergillosis Chronic yellow/green nasal discharge, facial Often in immunocompromised birds;
Aspergillus species sinuses, or air sacs; granulomatous
(Fungal Sinusitis) swelling, respiratory distress. chronic signs, sometimes systemic.
lesions.

Chronic
Mycoplasma Mild to moderate sinus inflammation, Sneezing, nasal discharge, conjunctivitis, Chronic with flare-ups in high-stress
Respiratory
gallisepticum catarrhal exudates. coughing. conditions, primarily in poultry.
Disease (CRD)

Swelling of the head and neck, Rapid onset, systemic involvement

Avian Influenza Sudden onset of respiratory signs (dyspnea,
Viral (Influenza A) hemorrhagic lesions in the sinuses or (fever, abdominal swelling), high
(Bird Flu) nasal discharge), lethargy.
respiratory tract. mortality.

Mild to moderate nasal discharge,

Psittacosis Chlamydia psittaci. Nasal discharge, conjunctivitis, lethargy, History of exposure to infected birds,
occasionally mucopurulent material in
(Chlamydiosis coli respiratory distress, diarrhea. often affects parrots.
sinuses.
 TREATMENT

Antibiotics:
Enrofloxacin
Doxycycline
Trimethoprim-sulfamethoxazole
Antifungal treatment:
Itraconazole or fluconazole may be used. In
severe cases, amphotericin B may be considered.
 CONTROL AND PREVENTION
Environmental management:
Improve ventilation
Maintain clean environments
Control humidity
Biosecurity:
Quarantine new birds
Avoid overcrowding
Vaccination
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