Fowl typhoid

Fowl typhoid

Article Originally written by Kajol Dahal…..B.V.Sc and AH..IAAS,Paklihawa

Introduction:

Fowl typhoid is an economically important disease of poultry and other birds, with high mortality. It is characterized by septicemia and yellow diarrhea. It is primarily a disease of mature and growing chickens but also appears in ducks, pheasants, turkeys, guinea fowl and other birds.

 Fowl typhoid infection still occurs worldwide in non-commercial poultry but has been eradicated from commercially raised poultry in the United States and many other developed countries.

Etiology:

FT is caused by Salmonella gallinarum, a gram negative, rod shaped bacteria of Enterobacteriaceae family.

Transmission:

The infected bird (reactor and carrier) is the most means important of perpetuation and spread of organism. Transmission may be horizontal through feco-oral route. It may occur within a flock as a result of cannibalism of infected birds, eating of infected eggs, through wounds on skin, feces contaminated feed and water. Egg transmission is also seen from contamination of ovum following ovulation but localization of S. gallinarum in the ovules before ovulation is the chief mode of transovarian or vertical transmission.

Pathogenesis:

The probable mode of pathogenesis is that, following ingestion, the organism localize in the intestinal epithelial cells. It invade the epithelial cell and is phagocytized by the mononuclear cell inside which the bacteria multiply. Through the mononuclear cell it gains entrance to blood stream giving rise to bacteremia. Then it localized in various organs like spleen, liver, lungs and reproductive organs. Bacteremia may lead to death or partial clearance of bacteria may lead to subclinical carrier state.

Incubation period:

 The incubation period is usually 4 to 6 days.

Clinical signs:

FT is primarily the disease of growing and adult chickens however the young chicks and poults are also infected as a result of transovarian transmission.

Chicks and poulets: The birds hatched from S. gallinarum infected eggs can manifest somnolescence, weakness, depressed appetite, poor growth and adherence of chalky white material to the vent, death may soon follow.

Growing and mature: Acute outbreaks of FT in chickens may begin by a sudden drop in feed consumption, with birds being droopy, greenish yellow diarrhea, showing ruffled feathers and pale and shrunken combs. Other signs, such as a drop in egg production, decreased fertility, and diminished hatchability, can sometimes be observed depending upon the severity of infection. Death may occur within 4 days of exposure.

Gross lesions:

Chicks:

In peracute cases of  FT, birds that die suddenly in the early stages of brooding may show no gross lesions. In acute cases, enlarged and congested liver, spleen, and kidneys may be seen . Livers may have white foci of 2–4 mm in diameter. The yolk sac and its contents may or may not reveal any abnormalities, but in protracted cases, interference with yolk absorption may occur. In such cases, the yolk sac contents may be of creamy or caseous consistency. Occasionally, those birds with respiratory signs may have white nodules in the lung and white nodules, resembling Marek’s disease tumors, may be present in the cardiac muscle.

Fig: Salmonella affected ovarian follicles of chickens

Fig : enlarged liver with necrotic foci and bronze colour

Fig: spleenomegaly

Growing and mature:

Hepatomegaly is seen with characteristic copper colour of the liver and small white necrotic foci. In some cases, the pericardium exhibits only a slight translucency, and the pericardial fluid may be increased in volume and turbid. In the more advanced stages, the pericardial sac is thickened and opaque. In chronic carrier hens with FT there are a few misshapen, discolored cystic or nodular ova among a few normal-appearing ovules. The involved ova may contain oily and caseous material enclosed in a thickened capsule. Spleenomegaly and Catarrhal enteritis with or without ulcers is seen. In the male, testes may have white foci or nodules.

Microscopic lesions:

In peracute cases of FT, only severe vascular congestion in various organs, especially liver, spleen, and kidney, can be identified. In acute to subacute cases, there is multifocal necrosis of hepatocytes with accumulation of fibrin and infiltration of neutrophils in the hepatic parenchyma. In chronic cases, the liver will have chronic passive congestion with interstitial fibrosis and necrosis of myocardium with some fibrosis in heart. The spleen may have severe congestion. And marked depletion of lymphocytes from bursa occurs.

Diagnosis:

A definitive diagnosis of FT requires the isolation and identification of S. Gallinarum. A tentative diagnosis, however, can be made based on flock history, clinical signs, mortality, and lesions. FT is characteristically systemic infection and causative organisms can be isolated from most internal organs. The liver, spleen and ceaca usually are involved and are the preferred organs to culture.

Differential Diagnosis:

The clinical signs and lesions produced by FT is not pathognomonic. Other Salmonella infections may produce similar lesions in the liver, spleen, and intestine, which cannot be distinguished grossly or microscopically from those produced by FT. Aspergillus or other fungi may produce similar lesions

in the lungs. S. Gallinarum can localize in major joints and tendon sheaths of chicks. Such signs and lesions resemble those produced by organisms such as Mycoplasma synoviae, Staphylococcus aureus, Pasteurella multocida. Sometimes the white nodules in the heart of young chicks may resemble Marek’s disease tumors.

Fig:Ovary

References:

Saif, Y.M (2008) Diseases of poultry. Garsington Road, UK: Blackwell publishing ltd.(12th edition)

Davison,Sherrill.FowlTyphoid.https://www.msdvetmanual.com/poultry/salmonelloses/fowl-typhoid

Calnek, B.W., H.J. Barnes and C.W. Beard. 1995. Disease of poultry, Iowa State University Press, USA (9th Edition)

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