Fowl cholera is a contagious, bacterial disease of birds caused by Pasteurella multocida. Chronically, it causes lameness, swollen wattles (in chickens), pneumonia (in turkeys), and torticollis, but it can also be asymptomatic. Both attenuated live vaccines and adjuvanted bacterins are available to aid in prevention, and it is sensitive to some antibiotics. Clinical Findings
exhibit pleomorphism a
fter repeated subculture. P multocida is considered a single species although it includes three subspecies: multocida, septica, and gallicida. Subspecies multocida is the most common cause of disease, but septica and gallicida may also cause cholera-like disease. In freshly isolated cultures or in tissues, the bacteria have a bipolar appearance when stained with Wright’s stain. Although P multocida may infect a wide variety of animals, strains isolated from nonavian hosts generally do not produce fowl cholera. Strains that cause fowl cholera represent a number of immunotypes (or serotypes). P multocida can be subgrouped by capsule serogroup antigens into five capsular types (A, B, C, D, and F) and into 16 somatic serotypes. Turkeys and waterfowl are more susceptible than chickens, older chickens are more susceptible than young ones, and some breeds of chickens are more susceptible than others. Chronically infected birds and asymptomatic carriers are considered to be major sources of infection. Wild birds may introduce the organism into a poultry flock, but mammals (including rodents, pigs, dogs, and cats) may also carry the infection. However, the role of these as a reservoir has not been thoroughly investigated. Dissemination of P multocida within a flock and between houses is primarily by excretions from the mouth, nose, and conjunctiva of diseased birds that contaminate their environment. In addition, P multocida survives long enough to be spread by contaminated crates, feed bags, shoes, and other equipment. The infection does not seem to be egg-transmitted. Clinical findings from fowl cholera vary greatly depending on the course of disease. 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. 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 lameness, as well as exudative conjunctivitis and pharyngitis. Torticollis may result when the meninges, middle ear, or cranial bones are infected. 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 disseminated throughout the liver and spleen. In chronic forms of fowl cholera, suppurative lesions may be widely distributed, often involving the respiratory tract, the conjunctiva, and adjacent tissues of the head. Caseous arthritis and productive inflammation of the peritoneal cavity and the oviduct are common in chronic infections. A fibrinonecrotic dermatitis that includes caudal parts of the dorsum, abdomen, and breast and involves the cutis, subcutis, and underlying muscle has been observed in turkeys and broilers. Sequestered necrotic lung lesions in poultry should always raise suspicion of cholera. Diagnosis
Confirmed by bacterial culture
Although the history, signs, and lesions may aid field diagnosis, P multocida should be isolated, characterized, and identified for confirmation. Primary isolation can be accomplished using media such as blood agar, dextrose starch agar, or trypticase soy agar. Isolation may be improved by the addition of 5% heat-inactivated serum. P multocida can be readily isolated from viscera of birds dying from peracute/acute fowl cholera, whereas isolation from suppurative lesions of chronic cholera may be more difficult. At necropsy, bipolar microorganisms may be demonstrated by the use of Wright’s or Giemsa stain of impression smears obtained from the liver in the case of acute cholera. In addition, immunofluorescent microscopy and in situ hybridization have been used to identify P multocida in infected tissues and exudates. PCR has been used for the detection of P multocida in pure and mixed cultures and clinical samples. This method may help identify carrier animals within flocks. However, the specificity and sensitivity of the PCR must be improved. Conventional serotyping suffers from problems with reproducibility and reliability, and the methods are quite laborious. A multiplex PCR has been developed that can differentiate between different somatic serotypes and may enable more efficient vaccine development. Serologic testing can be done by rapid whole blood agglutination, serum plate agglutination, agar diffusion tests, and ELISA. Serology may be used to evaluate vaccine responses but has very limited value for diagnostic purposes. Several bacterial infections may be confused with fowl cholera based solely on the gross lesions. Escherichia coli, Salmonella enterica, Ornithobacterium rhinotracheale, gram-positive cocci, and Erysipelothrix rhusiopathiae (erysipelas) may all produce lesions indistinguishable from those caused by P multocida. Prevention
Good management practices, including a high level of biosecurity, are essential to prevention. Rodents, wild birds, pets, and other animals that may be carriers of P multocida must be excluded from poultry houses. The organism is susceptible to ordinary disinfectants, sunlight, drying, and heat. Adjuvant bacterins are widely used and generally effective. Because bacterins are only effective in preventing disease caused by the same serotypes included in the vaccine, somatic serotyping is important. Thus, it is important to know the most prevalent serotypes within an area. Autogenous bacterins are recommended when polyvalent bacterins are found to be ineffective. Attenuated live vaccines are available for administration in drinking water to turkeys and by wing-web inoculation to chickens. These live vaccines can effectively induce immunity against different serotypes of P multocida. They are recommended for use in healthy flocks only. Treatment
Eradication of infection requires depopulation, followed by thorough cleaning and disinfection
Antibiotics may reduce mortality but won't eliminate P multocida from a flock
A number of drugs will lower mortality from fowl cholera; however, deaths may resume when treatment is discontinued, showing that treatment does not eliminate P multocida from a flock. Eradication of infection requires depopulation and cleaning and disinfection of buildings and equipment. The premise should then be kept free of poultry for a few weeks. When antibiotics are used, early treatment and adequate dosages are important. Sensitivity testing often aids in drug selection and is important because of the emergence of multiresistant strains. Sulfamethazine or sulfadimethoxine in feed or water usually controls mortality. Sulfas should be used with caution in breeders because of potential toxicity and cannot be used in hens laying eggs for human consumption. High levels of tetracycline antibiotics in the feed (0.04%), drinking water, or administered parenterally may be useful. Penicillin in turkeys is often effective for sulfa-resistant infections. In ducks, a combined injection of streptomycin and dihydrostreptomycin can be effective. Respiratory disorders
Fowl cholera is a contagious respiratory disease of birds caused by bacterium P. It is another bacterial disease that can be hosted by multiple bird species. It causes acute mortality and chronic suppurative necrosis. Because of these symptoms and because eradication of infection requires depopulation, followed by thorough cleaning and disinfection, it can be a costly operation for the farmer (Sander, 2019). Financial costs of fowl cholera are amplified by high mortality. Mortality rates of 5%–20% can occur in the early stages of disease. Mortality may even reach much higher rates (see e.g. Pilatti et al., 2016). As the disease becomes chronic, mortality may drop to 2%–5% a month. Chronically infected birds may die, remain infected for long periods, or recover. Costs usually occur in birds over 16 weeks of age. In addition, fowl cholera causes economic costs in chicken and turkey breeders, especially in broiler breeders, due to low production of hatching eggs and reduction of fertility (Huberman and Terzolo, 2016). Based on the literature (e.g. Morris and Fletcher, 1988), Fasina et al. (2012) assumed that income loss associated with fowl cholera was $0.015 (€0.012) per kg meat and mortality was 25%–35% (on average 18%). The few studies that exist on economic impacts of fowl cholera focused on outbreaks in turkeys, but these estimates are also outdated, mostly originating from the 1980s. In a retrospective study, Carpenter et al. (1988) found that the relative mortality rates of turkeys were 52% higher in fowl cholera outbreak toms and 26% higher in hens than in their controls, medication costs were nearly tripled, and the relative condemnation rate was 60% higher in fowl cholera outbreak flocks than in control flocks. The average costs of fowl cholera were nearly $0.40 (€0.33) per bird in an outbreak flock of 50,000 birds and $0.12 (€0.10) per bird in nonoutbreak flocks vaccinated against fowl cholera. Moreover, Christiansen (1990) found that production losses and treatment costs associated with fowl cholera were estimated at $0.51 (€0.452) per bird placed in a fowl cholera outbreak flock in 1985–86. The total cost of vaccination against fowl cholera was about half of the costs of outbreak. Overall, 0.5% of total turkey meat production in California in 1985–86 was lost because of fowl cholera. gallisepticum is causing chronic respiratory disease in chickens and infectious sinusitis in turkeys. gallisepticum is the most pathogenic and economically significant mycoplasmal pathogen of poultry. Airsacculitis in chickens or turkeys resulting from M. gallisepticum infections, with or without complicating pathogens, causes increased condemnations at processing. Economic costs from condemnations or downgrading of carcasses, reduced feed and egg production efficiency, and increased medication costs are additional factors that make this one of the costliest disease problems confronting commercial poultry production. Prevention and control programmes, which may include surveillance (serology, culture, isolation, and identification) and vaccination, account for additional costs (Ley, 2003). The financial costs of M. gallisepticum however have not been assessed recently. Mohammed et al. (1987) estimated that the costs of M. gallisepticum in commercial layer flocks in California were approximately $0.25 (about €0.20) per layer in the study region, or $0.23 to $0.55 (€0.19 to €0.46) per infected bird. The costs were mainly associated with losses in egg yield because M. gallisepticum-infected flock produced 12 and 5 fewer eggs per hen than an uninfected flock. Flocks that became infected with M. gallisepticum after vaccination produced 6 eggs per hen more than unvaccinated infected flocks in the first cycle, but no significant difference was observed between such groups in the second cycle (Mohammed et al., 1987).
