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Fowl cholera is an infectious avian disease caused by the bacterium, Pasteurella multocida. A wide variety of wild and domestic birds are susceptible, and outbreaks of fowl cholera are not uncommon among wild waterfowl. Fowl cholera can be acute or chronic, generalized, or local and is characterized by sudden onset with high morbidity and high mortality. Fowl cholera is said to be a disease of overcrowding, spread by contact between healthy and ill birds, in an environment contaminated with Pasteurella organisms. Stress appears to be an important factor in breaking down the bird's resistance. Cold, damp weather predisposes birds to this disease and outbreaks are generally seen during the winter months in overwintering waterfowl flocks.
The only existing enzootic areas of fowl cholera in the world are the Muleshoe National Refuge in Texas, in north central California and in the rainwater basin in Nebraska where periodic winter outbreaks occur. Sporadic outbreaks have occurred in other areas of the U.S. during the winter months, with Wisconsin and Illinois being the states closest to Michigan with fowl cholera cases.
Fowl cholera has occurred only once in Michigan and that was in a green heron.
The mechanism of spread of avian cholera among waterfowl is unknown. In domestic fowl the means of disease spread is believed to be via ingestion, mechanically by arthropod vectors or by inhalation. Inhalation appears to be the most likely route of transmission but there is also evidence of oral transmission from diseased carcasses to predators and scavenger birds. During fowl cholera outbreaks in waterfowl, owls, hawks and eagles may become infected after feeding on diseased carcasses. Another means of transmission involves the inhalation or ingestion of infective water aerosols created as the birds land and wing flap. Water from contaminated areas can remain infective for long periods of time even after removal of dead birds. There is some evidence that gulls and rodents, as well as previously exposed and surviving birds may act as chronic carriers of the Pasteurella organism.
Clinical signs of fowl cholera following infection may be manifested peracutely of acutely, with previously healthy birds suddenly being found dead or profoundly ill. Before death, the birds may exhibit convulsions, uncoordinated fluttering, stiffness, and rapid breathing. Birds which do not die acutely, may show signs of listlessness, shivering and huddling. Respiratory sound, sneezing and sticky nasal discharges are sometimes observed. The feathers surrounding the vent, eyes and beak may become matted with secretion. The droppings which may start out as pasty and yellow, may become bloodstained due to intestinal ulceration. Birds chronically affected with fowl cholera show weight loss, abdominal distention, lameness and joint enlargement.
Acute death as a result of P. multocida infection is due to release of endotoxins by the bacteria following invasion of the systemic circulation. The most prominent gross lesions are petechial hemorrhages on the epicardium and myocardium and occasionally on the surface of the gizzard. Focal necrosis of the liver as well as hemorrhagic consolidation of the lungs is often seen. With respiratory involvement, there is evidence of a catarrhal exudate which is most prominent in the upper trachea. The intestinal tract is usually empty or contains a thin greenish fluid and hemorrhages may be present on the serosal surface.
Presumptive diagnosis can be made based on the necropsy findings of petechial hemorrhages in the epicardial adipose tissue and myocardium with focal necrosis in the liver. Sudden death of large numbers of waterfowl during the winter months is further support for a diagnosis of fowl cholera. Definitive diagnosis is based on the isolation and identification of P. multocida from the heart blood of a fresh specimen.
Treatment of fowl cholera outbreaks in waterfowl is not practical, but when individual treatment is applicable, chlortetracycline, oxytetracycline and sulfaquinoxaline in the feed or water have been
shown to be effective.
In the face of an outbreak, control is directed at attempts to limit transmission of the disease. All carcasses should be collected and burned. Dead birds floating on the water not only serve as a source of contamination but also act as decoys and lure more waterfowl into infectious water. Contaminated pools can be drained and cultivated or flushed by flooding with pumped or flood waters.
Artificial maintenance of open water after the end of hunting season by pumping operations should be discouraged as this acts to concentrate and hold birds north of their normal wintering areas. In severe outbreaks, it is occasionally recommended that attempts be made to limit the scavenging activities of gulls, as they can act as transmitters of fowl cholera, due to their resistance to the disease.
Fowl cholera does not appear to be a problem in Michigan at this time, but due to the close proximity of other states where the problem has existed, there is a potential for die-offs in overwintering waterfowl in overcrowded areas. Game farm pheasants are also susceptible to the disease and large die-offs can occur. It is important to be aware of this disease, as early detection, diagnosis, and cleanup are the best means of control.
