Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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1- Necrotic Enteritis
Definition
Disease of young chickens caused by toxins produced by Clostridium
perfringens type A and type C characterized by sudden onset of high mortality
and necrosis of the mucous membrane of the small intestine, the disease is also
known as clostridial enteritis, enterotoxemia and rot gut.
Etiology
The etiologic agent is a Gram-positive, spore-forming anaerobe; C.
perfringens type A and type C, both of these strains are capable of producing
various toxins and enzymes which are responsible for the associated lesions and
clinical signs. Specifically, alpha-toxin produced by C. perfringens types A and
C and beta-toxin produced by C. perfringens type C.
Influencing factors
1- The risk of necrotic enteritis is low when birds are kept on wire floors or other
types of housing that minimizes their contact with feces.
2- Low-level maternal immunity against C. perfringens is associated with an
increased risk of necrotic enteritis in broiler chickens.
Pathogenesis
The presence of C. perfringens in intestine alone is not sufficient to induce
necrotic enteritis, but the (1) predisposing factor causing damage to the intestinal
mucosa, and (2) the presence of higher than normal numbers of intestinal C.
perfringens organisms.
Bacterial cells adhere to damaged epithelium where they proliferate and
induce coagulative necrosis. Attraction and lysis of heterophil as well as tissue
necrosis and bacterial proliferation. The alpha toxin (a necrotizing toxin)
produced which destroys cell membranes. Toxins may also enter the blood stream
or bile duct causing systemic effects as in cholangiohepatitis.
Clinical signs
necrotic enteritis is characterized by increased mortality depression,
decreased feed intake, reluctance to move, ruffled feathers, diarrhea with
temporarily reduced weight gain.
Lesions
Gross lesions: lesions confined to the small intestine, primarily the jejunum,
ileum and cecum. The intestines are friable and distended with gas. The
mucosa is lined by a loosely to tightly adherent yellow too green
pseudomembrane that is often described as having a “Turkish towel”
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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appearance. Hepatitis characterized by swollen, tan colored livers with necrotic
foci with cholecystitis.
Microscopic lesions: Characterized by severe necrosis of the intestinal mucosa
with an abundance of fibrin admixed with cellular debris adherent to the
necrotic mucosa. Colonization of organisms in necrotic tissues and lamina
propria with fibrin and cellular debris are present in the lumen which
represented the lesions of Turkish towel. in liver bile duct hyperplasia,
fibrinoid necrosis, cholangitis and focal granulomatous inflammation.
Differential Diagnosis
1- Eimeria brunetti or Eimeria maxima infection.
2- Ulcerative enteritis is caused by C. colinum.
Treatment
Necrotic enteritis effectively treated with the administration of lincomycin,
bacitracin, oxytetracycline, penicillin, and tylosin tartrate when used in the water.
Bacitracin, lincomycin, virginiamycin, penicillin, avoparcin, nitrovin and
tylosin have been shown to be effective in preventing and controlling NE when
placed in the feed.
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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2- Ulcerative Enteritis
Definition
an acute bacterial infection in young chickens, turkeys, and game birds
characterized by sudden onset and rapidly increasing mortality with present of
ulcerative enteritis and yellow to gray necrotic foci in liver and spleen.
Etiology
Clostridium colinum is the etiologic agent, anaerobic, fastidious to culture,
gram-positive, spore-forming, with subterminal, oval spores.
Predisposing Factors
stress, coccidiosis, infectious bursal disease, immunosuppression considered
as predisposing factor to occurrence the infection.
Pathogenesis
Infection can be introduced by feeding on contaminated fecal material by
spores or by recovered carrier birds. After oral infection, the bacterium adheres
to the intestinal villi, producing enteritis and ulcers in portions of the small
intestine and upper large intestine. Bacilli migrate to the liver via portal
circulation, producing necrotic foci that later coalesce into extensive hepatic
necrosis.
Clinical signs
Increased mortality without any obvious signs, in other cases signs may
include depression, depressed, listless birds with humped backs, ruffled feathers,
diarrhea, and sometimes bloody or watery white droppings, chickens recover
within 2–3 week, and mortality rarely exceeds 10%.
Lesions
Gross lesions: The most important lesions are found in the intestine, liver and
spleen. There are small, circular to lenticular mucosal ulcers affecting the small
intestine, caeca and upper large intestine, these ulcers may coalesce to form
large ulcer that penetrate as deep as the serosa, which may become perforated
and result in peritonitis. The ulcers may coalesce to form large areas with a
pseudomembrane. In liver there is yellow to gray necrotic foci are the
predominant lesions in the hepatic parenchyma. Splenomegaly with
hemorrhages and necrotic areas may be present.
Microscopic lesions: Intestinal ulcers consist of small haemorrhagic and necrotic
areas, often with clumps of Gram positive bacteria. The ulcers involve villi and
extend into the submucosa. The ulcers sometimes reach as deep as the muscular
layer and serosa. Affected tissue is surrounded by granulocytes and
mononuclear inflammatory cells. Liver lesions consist of multifocal foci of
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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coagulative necrosis that are often poorly demarcated and with inflammatory
reaction with present of Gram-positive bacteria in these necrotic foci.
Differential Diagnosis
1- Coccidiosis.
2- Necrotic enteritis.
3- Histomoniasis.
Diagnosis
Gross postmortem lesions, isolation of causative agents
Treatment
Streptomycin (0.006%) and furazolidone (0.02%) in the feed are effective
to treat the disease. Bacitracin at 200 g/ton is used for prevention.
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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3- GANGRENOUS DERMATITIS
Definition
Contagious disease of chickens and turkeys caused by Clostridium
perfringens type A, C. septicum and Staphylococcus aureus. The disease is
characterized by a sudden onset of acute mortality with necrosis of the skin and
subcutaneous tissue, usually involving the breast, abdomen, wing or thigh.
Gangrenous dermatitis has also been referred to as necrotic dermatitis,
gangrenous cellulitis, gangrenous dermatomyositis, avian malignant edema, gas
edema disease, wing rot, and, in some instances, blue wing disease.
Etiology
C. septicum and C. perfringens type A. with Staphylococcus aureus
involved and rarely C. novyi, when S. aureus is present with a clostridial pathogen
the disease is more severe than either alone.
Hosts
Gangrenous dermatitis affects chickens and turkeys and is most commonly
seen in broilers of about 4–7 weeks.
Contributing Factors
In many instances, it is believed to occur as a sequela to other diseases which
produce immunosuppressive effects such as infectious bursal disease (IBD) virus,
chicken infectious anemia virus, reticuloendotheliosis virus, and avian
adenovirus infections, including inclusion body hepatitis virus.
Clinical signs
The clinical signs include increased mortality, marked depression,
incoordination of movement and death within a few hours. The carcasses
decompose rapidly with a foul odor. Mortality varies from low to very high.
Lesions
Gross lesions: consist of dark reddish-purple, weepy areas of the skin, usually
devoid of feathers. Affected areas usually include wings, breast, abdomen, or
legs. Extensive blood-tinged edema, with or without gas (emphysema), is
present beneath the affected skin. Underlying musculature is discolored gray
or tan and may contain edema and gas between muscle bundles. The kidney
and liver are often congested and in some birds the lungs are congested and
oedematous and can resemble a mass of dark-red jelly.
Microscopic changes: are characterized by edema and emphysema with
numerous large, basophilic bacilli or small cocci within subcutaneous tissues.
Severe congestion, hemorrhage and necrosis of underlying skeletal muscle are
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/ Dr. Saevan S. Al-Mahmood
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often present. Liver, if affected, contains small, randomly scattered, discrete
areas of coagulation necrosis with bacteria.
DIAGNOSIS
Diagnosis is based on the presence of gross lesions and the demonstration
of the pathogens.
CONTROL
Important management measures include a high standard of hygiene,
avoiding overcrowding of stock and the protection of the birds against
immunosuppressive agents.
Treatment
Treatment effectively with the administration of chlortetracycline,
oxytetracycline, erythromycin, penicillin, or copper sulfate in the water.
Chlortetracycline or furoxone in the feed.
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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4- BOTULISM
Definition
Botulism is an intoxication caused by exotoxins of Clostridium botulinum.
Synonyms are “limberneck” and “Western duck sickness.” can affect a variety of
birds, including broiler chickens, and mammals, including humans.
Etiology
C. botulinum is a gram-positive, spore-forming bacterium capable of
elaborating potent exotoxins under appropriate environmental conditions.
Clinical signs
Clinical signs of botulism in chickens, turkeys, pheasants, and ducks are
similar included flaccid paralysis of legs, wings, neck, and eyelids are
predominant features of the disease. Paralytic signs progress cranially from the
legs to include wings, neck, and eyelids. Initially, affected birds are found sitting
and are reluctant to move. Limberneck, the original and common name for
botulism, precisely describes the paralysis of the neck. Because of eyelid
paralysis, birds appear comatose and may seem dead. Gasping has been reported
when birds are handled. Death results from cardiac and respiratory failure.
Affected chickens have ruffled feathers, which may fall out with handling.
Lesions
There are no specific gross or microscopic lesions.
Diagnosis
Clinical signs and isolation the causative agent and toxins.
Treatment
Antibiotics including bacitracin (100 g/ton in feed), streptomycin (1g/L in
water), or periodic chlortetracycline treatments also reduced mortality. Penicillin
was ineffective in controlling outbreak.
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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5- FOWL CHOLERA
Fowl cholera is acute or chronic contagious disease affecting domesticated
and wild birds caused by Pasteurella
multocida appears as a septicemic disease
associated with high morbidity and mortality with economic significance losses
to most types of poultry, it’s also known as avian cholera, avian pasteurellosis, or
avian hemorrhagic septicemia.
Pathogenesis
the organism enters the host through cutaneous wounds. Following
colonization of the upper respiratory tract pathogenic P. multocida strains spread
to the lungs, followed by invasion, bacteremia and septicemia. It has been
suggested that some of the differences in host susceptibility to P. multocida
infection may be due to differences in the host response expressed in the lung
during the early phase of infection.
Clinical signs
In acute form there is unexpected deaths of a large number of birds in a flock
are often observed with anorexia, ruffled feathers, mucous discharge from the
mouth and nose, diarrhea, cyanosis and general depression may be seen.
In chronic form signs are mainly due to localized infections of joints,
abscesses of the head at comb and wattles, oviduct and the respiratory tract
(dyspnea and rales). The chronic infection may follow an acute infection or
caused by infection with an organism of low virulence.
Lesions
In acute forms general septicemic lesions with congestion throughout the
carcass accompanied by pinpoint necrotic areas with enlargement of the liver and
spleen. Often there are petechial and ecchymotic hemorrhages at sites such as the
subepicardial fat of the heart, in mucous membranes, on the gizzard and in
abdominal fat. Acute lesions develop as a result of disseminated intravascular
coagulation.
In chronic forms there is suppurative lesions widely distributed involving
respiratory tract appear as pneumonia, th3e conjunctiva and adjacent tissues of
the head. Caseous arthritis, peritonitis and oophoritis are common in chronic form
in adult. Lung lesions are fibrinonecrotic pneumonia and fibrinopurulent pleuritis.
Diagnosis
A diagnosis made from clinical observations, clinical signs, necropsy
findings, and isolation of P. multocida.
Treatment
Sodium sulfamerazine 150 mg/kg/b.w. orally or 0.2% in drinking water for
3 days effectively reduced mortality.
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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6- PULLORUM DISEASE
Infectious poultry disease caused by the bacterium Salmonella pullorum that
affects mainly young chicks of 2 to 3 weeks of age, characterized by white
diarrhea and decrease in hatching ratio and transmitted via ovary, these diseases
had been previously known as bacillary white diarrhea.
Etiology
Salmonella pullorum is Gram negative, nonmotile, facultating anaerobe.
Spread
The most important method by which pullorum disease infects birds is from
an infected parent bird via the ovary to the newly hatched chick.
Clinical signs
Young chicks: birds hatched from infected eggs dead in the incubator shortly after
hatching, other signs include characteristic white diarrhea with excessive
numbers of dead-in-shell chicks and deaths shortly after hatching.
Adult chickens: adults are less severely
affected by pullorum disease and may
simply become carriers with lameness and swollen hock joints may be seen in
growing birds and result in poor growth rates. Reduced egg production with
lowered fertility and hatchability.
Lesions
In Chicks die shortly after hatching with peritonitis and unabsorbed yolk sac. The
lungs may be congested and the liver dark and swollen with hemorrhages visible
on the surface. In chicks that die after showing typhlitis: the caeca are enlarged
and distended with hard, dry, necrotic material. Discrete, small, white, necrotic
foci are also often found in the liver, lungs, myocardium and gizzard wall.
In growers affected with arthritis, the hock and wing joints are usually enlarged
because of the presence of excess lemon- or orange-colored gelatinous material
around the joints.
In adult birds the characteristic lesion is an abnormal ovary with the ova irregular,
cystic, misshapen, with peritonitis, arthritis and pericarditis. In some infected
adult hens, the ovary is inactive with the ova small, pale and undeveloped.
Treatment
Sulfonamides, nitrofurans, chloramphenicol, tetracyclines shown to reduce
the mortality but not eliminating the infection.
Differential Diagnosis
Mycoplasma, Staphylococcus, Pasteurella.
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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7- PARATYPHOID
Is a contagious disease caused by gram – negative bacterium Salmonella
spp. Affected birds, with human health significant.
Cause
The most important species that because disease are Salmonella enteritis and
Salmonella typhimurium.
Clinical Signs:
Paratyphoid associated with disease only in very young birds. Signs include
closed eye, drooping wings and ruffled feathers, anorexia and emaciation. Profuse
watery diarrhea, pasting of the vent area. In adult birds reduced egg production.
Gross and Histopathology changes
Sever enteritis is often accompanied by focal necrotic lesions in the mucosa
of the small intestine, cheesy cecal cores are often observed. Spleen and livers
and commonly swollen and congested, with evident hemorrhagic streaks or
necrotic foci. Slight inflammatory processes with heterophile infiltration.
Unabsorbed, coagulated yolk material may be present in the yolk sac. Other
lesions included panophthalmitis, sever typhlitis, airsacculitis.
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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8- FOWL TYPHOID
Is a septicemic disease affecting primarily young chickens and turkeys, but
other birds such as quail, pheasants, ducks, peacocks and Guinea fowler also
susceptible, caused by gram negative bacteria Salmonella gallinarum.
Etiology
Gram negative bacteria Salmonella gallinarum.
Transmission
By direct contact with other infected birds, or by feeding contaminated feed
and water, or by cannibalism of infected carcasses.
Clinical Signs
Chicks and adult revealed weakness, depressed appetite, poor growth and
adherence of chalky white material to the vent due to chalky or yellow diarrhea.
Flocks that have passed through serious outbreak usually have a high percentage
of carriers at maturity. Blindness and synovitis may be appeared. Infected mature
birds show sudden drop in feed consumption, with birds being droopy, showing
ruffled feathers and pale and shrunken combs, drop in egg production, decreased
fertility and diminished hatchability. Increase body temperature. Morbidity and
mortality same as pullorum disease.
Gross Lesions
Birds that die suddenly in the early stage of brooding may show no gross
lesions. In acute cases, enlargement livers are seen. Livers have white foci of 2-4
mm in diameter. In such cases, the yolk sac may be contents of creamy caseous
consistency. Occasionally these birds with respiratory signs may have white
nodules in the lung, these nodules resembling Mark’s disease tumors and may be
present in the cardiac muscle or pancreases. The pericardium may be thickened
and the pericardial sac may contain yellow serous or fibrinous exudate. Some bird
with swollen of joints. The ceca may contain caseous cores. Splenomegaly with
gray necrotic foci. Enteritis. Adult chickens show few misshapen, discolored
cystic ova among a few normal appearing ovules. The involved ova may contain
oily and caseous material enclosed in a thickened capsule. Fibrinous peritonitis
and peri hepatitis.
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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9- ARIZONOSIS
Arizona infection or avian arizonosis (AA) is an acute or chronic egg-
transmitted disease of primarily of young turkey poults characterized by
septicemia and neurological signs and blindness and increased mortality caused
by Salmonella enterica serovar arizonae
Clinical signs
The signs shown by adult with arizonosis are similar to those shown by
chicks with salmonellosis but eye abnormalities are seen more frequently and
nervous signs are a regular additional feature. Various nervous signs, including
ataxia, trembling, leg paralysis, torticollis and convulsions, have been described.
A characteristic finding is visual impairment, with a white opacity that can be
seen deep in the eye when looking directly into the pupil.
Gross lesions
Adult dying of arizonosis are likely to have a septicemic carcass with
generalized peritonitis. The yolk sacs are frequently inflamed and the air sacs
thickened with opaque white to yellow, cheesy, caseous deposits adhering. The
livers may be swollen and discolored (yellow) and discrete necrotic foci are
sometimes found throughout the substance of the liver. Commonly there is an
enteritis and a distinctive finding.
Eye lesions are a characteristic feature, with retinitis and a thick exudate
covering the back inner surface of the eyeball. Sometimes this varies and appears
as a hard, circular white disc of inspissated caseous material.
Histopathology
There is moderate to severe fibrinosuppurative inflammation associated
with Gram-negative bacteria in the yolk sac and yolk stalk. In the brain, there is
severe meningitis with in infiltration of heterophiles mixed with fibrin and
bacterial colonies. Otitis interna with bacteria and neuritis and ganglionitis of the
vestibulocochlear nerve most likely due to spread of S. enterica arizonae from
brain meninges have been seen.
Treatment
Chemotherapy may reduce losses in acute outbreaks and may be
recommended to prevent spread of the disease. injectable antibiotic such as
gentamicin and spectinomycin. These injectable, given at the hatchery, have
dramatically controlled the acute losses and morbidity that may occur during the
first three week of age.
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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10- INFECTIOUS CORYZA
Definition:
An acute or chronic, highly infectious disease of chickens, characterized by
catarrhal inflammation of the upper respiratory tract, especially nasal and sinus
mucosae caused by bacterium Haemophilus paragallinarum and is seen in many
countries especially in multi-age farms. Morbidity is high but mortality low if
uncomplicated although it may be up to 20%.
Pathogenesis:
The route of infection is conjunctival or nasal with an incubation period of
1-3 days followed by rapid onset of disease over a 2-3-day period with the whole
flock affected within 10 days. The disease reported in two forms:
1- The uncomplicated form (produced by H. paragallinarum only) results in
rapid onset of clinical signs, usually 1 to 3 days after exposure. These signs
persist from 7 to 14 days on the average.
2- The complicated disease is usually more severe and may take a chronic
course, depending on the complicating agent; Escherichia coli, Pasteurellae,
fowl poxvirus, infectious bronchitis virus, and laryngotracheitis virus may be
complicating agents.
Clinical Signs:
Facial swelling, Purulent ocular and nasal discharge, Swollen wattles,
Sneezing, Dyspnea, Loss in condition, Drop in egg production of 10-40% and
Inappetence. The chief sign is a serous to mucoid exudate from one or both
nostrils. This may be the only sign in chickens. The nasal exudate from chickens
with recent infection is usually clear exudate.
Gross lesions:
Catarrhal inflammation of mucous membranes of nasal passages and
sinuses. Catarrhal conjunctivitis and edema of face and wattles occur frequently.
Edema may occur on one or both sides of face and may be so extensive that vision
is obscured.
Histopathological lesions:
Most often observed in the upper respiratory tract. Affected areas of
epithelium in the nasal cavity, infraorbital sinuses, and trachea undergo
Treatment:
Sulfonamides, Erythromycin, oxytetracycline.
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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11- AVIAN CHLAMYDIOSIS (PSITTACOSIS, ORNITHOSIS)
Definition:
Contagious disease characterized by hyperthermia, nasal and ocular
discharges, with reduced egg production caused by Chlamydia psittaci.
psittacosis or parrot fever in birds and humans, Ornithosis in domestic and wild
fowl.
Etiology:
Avian chlamydiosis is caused by the bacterium Chlamydia psittaci.
Clinical signs:
Signs of chlamydiosis are anorexia, elevated body temperature,
conjunctivitis, and respiratory distress. The birds excrete yellow-green,
gelatinous droppings. Egg production of severely affected hens declines rapidly
to 10—20%.
P.M. Lesions:
Lungs show diffuse congestion, and pleural cavity may contain fibrinous
exudate. Air sacs are thickened and heavily coated with fibrinous exudate. The
pericardial membrane is thickened, congested, and coated with fibrinous exudate.
The heart may be enlarged, and its surface may be covered with thick fibrin
plaques with yellowish, flaky exudate.
Histopathological changes:
Trachitis characterized by extensive infiltration of mononuclear cells,
lymphocytes, and heterophils in the lamina propria and submucosa. Lungs of
severely affected birds were congested and had extensive infiltration with
mononuclear cells and fibrin. The pericardium and epicardium were thickened by
swelling of congested vessels and an inflammatory exudate containing fibrin.
Diagnosis:
Clinical signs, gross lesions, isolation the causative agent.
Treatment:
Chlortetracycline.
Poultry diseases /
2016 – 2017
/ Dr. Saevan S. Al-Mahmood
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12- AVIAN TUBERCULOSIS
Definition:
Contagious disease caused by Mycobacterium avium. Avian tuberculosis is
a chronic infection persistence in a flock once established induces decreased egg
production, and finally causes death.
Etiology:
Mycobacterium avium acid fast bacterium.
Clinical Signs:
Good appetite with progressive loss of weight evident as atrophy of breast
muscles, feathers assume a dull and ruffled appearance, comb and wattles have a
bluish discoloration with icterus, temperature of affected bird remains normal.
Gross lesions:
Pinpoint to several centimeters, irregular grayish yellow or grayish white
nodules in spleen, liver, and intestine. Involvement of liver and spleen results in
enlargement, which can result in fatal hemorrhage from rupture. Large nodules
have an irregular knobby appearance, smaller nodules present over capsular
surface of affected organs. On cross section, nodule contain variable number of
small yellowish foci or a single soft yellowish caseous center surrounded by a
fibrous capsule. Granuloma formation within bone marrow.
Microscopic lesions:
The basic lesion of M. avium infection consists of multiple granulomas with
a central caseous necrosis. Granulomas consist of accumulation of large number
of macrophages and epithelioid which fuse near periphery to form multinucleate
giant cells. A fibrous capsule consisting of fibrocytes and blood vessels occurs
near outer portion of peripheral area. Acid fast bacilli are numerous in necrotic
zone of tubercle but can be found adjacent giant cells. Calcification of tubercle
rarely occurs in fowl.
Diagnosis:
Lesions and tuberculin test.
Treatment:
Isoniazid (30 mg/kg), ethambutol (30 mg/kg), and rifampicin (45 mg/kg),
recommended duration of therapy was 18 months, provided that there were no
adverse side effects.