140. Fowl cholera.

Question 1

Occurence ethiology and epidemiology?

Answer 1

OCCURRENCE

• More common in warmer climate, summer or late autumn and in water fowl,
• sporadic in moderate climate

Ethiology

• Caused by P. multocida A (D, F)
• capsule: polysaccharide, outermost layer
• hyaluronic acid capsule
• (not regarded as antigen as it is normally present in animals, helps spread of bacterium)
• Serotypes, different frequency, facultative pathogen
• Virulence variants
• High: acute fowl cholera;
• Low: mild, chronic or asymptomatic

Ethiology

• Susceptibility: turkey, duck, goose, hen (lower susc.), wild living birds, Increasing with age
• Resistance is low (inactivate with heat or disinfectants), survives in water
• Differences depending on virulence
• Virulent strains ʹ cause acute fowl cholera, introduction to the farm is necessary
• o Less virulent strains ʹ chronic forms, asymptomatic carriage (can be present in the farm normally)
• Source of infection: discharge from carrier animals, instruments, water, other hosts, humans
• No germinative infection!
• Convalescent animals remain carriers
• Bacterium is present on mucous membrane of resp. tract or lymphoid tissues of the gut
• Predisposing factors (Primary pasteurellosis)
• Stress, feather pecking, force feeding, transport, grouping, other stress, warm weather, temperature
• fluctuations
• In acute fowl cholera: High morbidity and high mortality (if no treatment - exponential mortality)
• Occurs in grower and adults

Question 2

Pathogenesis?

Answer 2

PATHOGENESIS

• Airborne or oral infection ʹ colonization of the upper respiratory epithelium
• Disease is influenced by virulence of the agent, resistance of the host and nature & severity of predisp. factors
• If predisposing effects ʹ see clinical signs
• Acute Septicemia
• Endotoxin effect (from endotoxins released from the lysed bacteria): damage of blood vessels (increased
• permeability = hemorrhages) and will activate the coagulation cascade
• thrombocyte aggregation,
• release of procoagulants,
• formation of thrombi (focal necrosis ʹ result of both bacterium & thrombi)
• Elevation of corticosteroids, endotoxin shock (reason for death)
• Chronic: arthritis, tendosynovitis, bursitis, inflammation of the upper respiratory tract and infl. of the comb and wattles
• Cell number of bacteria in the blood is not as high as in acute case, and bacteria will be withdrawn into
• the joints (where antibodies cannot get to the bacterium and destroy it)

Question 3

Clinical signs?

Answer 3

CLINICAL SIGNS

• Incubation period of 1-5 days (depend on predisposing Factors)
• Peracute: very short incubation time, don’t see clinical signs, only depression and death
• Acute: Fever, anorexia, depression, diarrhea (sometimes with blood), nasal discharge, sneezing, drop of egg
• production, conjunctivitis
• Chronic ʹ weight loss, arthritis, bursitis, tenosynovitis, upper respiratory signs, nasal discharge, diarrhea, otitis
• media (CNS signs ʹ ataxia, stargazing), cranial pasteurellosis, inflammation of the wattle (enlarged, warm and hyperemic

Question 4

Pathology?

Answer 4

PATHOLOGY

Peracute: don’t see too much maybe a few hemorrhages

Acute

• Hemorrhages (serous membrane),
• hemorrhagic enteritis,
• fibrin in the gut,
• focal inflammation and necrosis in the liver (later also in the spleen and other parenchymal organs),
• peritoneal fluid in the abdomen,
• fibrinous pneumonia, spleen is generally normal (sometimes enlarged)

Chronic

• Focal inflammation and necrosis in the liver with fibrinous perihepatitis,
• salpingitis,
• fibrinous inflammation of the skull bones (cranial pasteurellosis),
• arthritis, tenosynovitis and bursitis

Question 5

Diagnosis and differential diagnosis?

Answer 5

DIAGNOSIS

• Due to exponential death curve
• fast diagnosis is crucial
• Epidemiology, clinical signs and pathology
• Detection of the agent
• isolation, microscopic examination
• direct smear from blood or parenchymal organs ʹ
• see large amount of gram negative bipolar bacteria), PCR (detection of carriage)

Differential diagnosis

• Toxicoses
• Other septicemic disease
• (Erysipelothrix, salmonella, E. coli etc.), respiratory diseases
• Diseases with focal inflammation and necrotic lesions in the liver ʹ campylobacter hepatitis, chronic fowl
• typhoid, paratyphoid, yersiniosis, borreliosis

Question 6

Treatment and prevention?

Answer 6

TREATMENT & PREVENTION

• Immediate Antibiotic treatment ʹ Potentiated sulfonamides, Tetracyclines, Macrolides, Fluoroquinolones
• Mainly per os (septicemic!, if parenteral treatment Æ can transmit infection)
• Elimination of the predisposing effects
• increase efficacy of antibiotic treatment
• Prevention of introduction of a virulent strain isolation, closed herd, rodent control, give tap water!
• Movement restriction in the case of fowl cholera,
• risk of keeping convalescent animals
• Prevention of predisposing effects
• Vaccines
• Inactivated vaccines (Europe ʹ only inactive) ʹ multivalent => contain most frequent serotypes present in an area
• At 6-8 weeks of age 2x (two weeks apart), type specific, relative protection
• Attenuated vaccines in drinking water, US