Hemorrhagic septicemia (HS) is an acute, highly fatal disease caused by particular serotypes of Pasteurella multocida. It principally affects cattle and water buffaloes; the latter are thought to be more susceptible. HS is seen infrequently in swine and even less commonly in sheep and goats. It has been reported in bison, camels, elephants, horses, and donkeys, and there is evidence of its occurrence in yak. An acute pasteurellosis indistinguishable from HS is seen infrequently in deer, elk, and probably other feral ruminants. Laboratory rabbits and mice are highly susceptible to experimental infection.
HS is a major disease of cattle and water buffalo in Asia, Africa, and some countries of southern Europe and the Middle East. The disease causes severe economic losses through morbidity and mortality. It is ranked as the most important contagious disease of cattle and water buffaloes by countries in South and Southeast Asia. Although HS may be seen at any time of year, the worst epidemics occur during the rainy season. It is most common in the river valleys and deltas of southeast Asia among buffaloes used in rice cultivation. The only true outbreaks in North America have occurred in bison in Yellowstone National Park in 1965. Occurrence in Central and South America has not been confirmed.
Epidemic HS is caused by 1 of 2 serotypes of P multocida, designated B:2 and E:2. Serotype E:2 has been recovered only in Africa; B:2 causes the disease elsewhere and also has been recovered from cases in Egypt and the Sudan. Serotypes closely related antigenically to serotype B:2 have been implicated in limited outbreaks of a disease indistinguishable from HS in deer and elk. P multocida is an extracellular bacterium, and immunity is primarily humoral.
Transmission, Epidemiology, and Pathogenesis
Animals are infected by direct or indirect contact. The source of infective bacteria is thought to be saliva or nasal discharges from normal carriers or clinically ill animals. As many as 5% of cattle and water buffaloes may be carriers in endemic regions.
It is hypothesized that animals become susceptible as a result of various stresses, eg, the inanition seen in cattle and water buffalo at the beginning of the rainy season. Natural infection is acquired by ingestion or inhalation. The initial site of proliferation is thought to be the tonsillar region. Endotoxin appears to be the major virulence factor responsible for clinical signs and death. In susceptible animals, a septicemia develops rapidly, and death ensues within 8–24 hr after the first signs develop. Type B P multocida from cases of HS produce hyaluronidase, but not type E P multocida. Significance of this enzyme in the disease process is not known. Exotoxins have not been demonstrated in the B and E strains.
The mortality rate is high when the agent is introduced to virgin or nonendemic regions. Losses vary widely in endemic areas. The heaviest losses occur during the monsoon rains in southeast Asia, and it is thought that the organisms, which can survive for hours and probably days in the moist soil and water, are transmitted widely at this time.
Most cases are acute or peracute, resulting in death within 8–24 hr after onset. Because the course is so short, clinical signs may easily be overlooked. Animals first evince dullness, then reluctance to move, high fever, profuse salivation, and serous nasal discharge. Edematous swelling is frequently seen, beginning in the throat region and spreading to the parotid region, neck, brisket, and perineum. Mucous membranes are congested. There is respiratory distress, and usually the animal goes down and dies within hours. Occasional cases linger for several days. Recovery is rare. There appears to be no chronic form.
The most obvious changes in affected animals are the edema, cellulitis, widely distributed hemorrhages, and general hyperemia. Endotoxin-induced coagulopathy combined with endothelial cell damage is believed to be responsible for the hemorrhages noted in field cases of HS. In most cases, there is edematous swelling of the head, neck, and brisket region; incision of these swellings reveals a clear or straw-colored serous fluid. The edema is also found in the musculature, and the subserous petechial hemorrhages, which are found throughout the animal, are particularly characteristic. Blood-tinged fluid is often found in the pericardial sac and in the thoracic and abdominal cavities. Petechial hemorrhages are particularly prominent in the pharyngeal and cervical lymph nodes. Gastroenteritis is seen only occasionally and, unlike in pneumonic pasteurellosis, pneumonia usually is not extensive.
Some characteristic epidemiologic and clinical features aid in the recognition of HS. Of particular significance is a history of earlier outbreaks and a recent failure to vaccinate. Sporadic cases are more difficult to diagnose clinically. The season of the year, rapid course, and high herd incidence, with fever and edematous swellings indicate typical HS. Characteristic necropsy lesions support the diagnosis. Although typical outbreaks are not difficult to recognize clinically, particularly in endemic regions, acute salmonellosis, anthrax, pneumonic pasteurellosis, and rinderpest should be considered.
A presumptive diagnosis is based on the isolation of P multocida from the blood and vital organs of an animal with typical signs. Definitive diagnosis depends on identifying the serotype as B:2 (or closely related serotypes) or E:2. Other serotypes cause various infections in cattle and buffalo but not typical HS. The passive mouse protection test using specific B:2 and E:2 immune rabbit sera is used in Asia and Africa to identify these serotypes. More precise tests, such as indirect hemagglutination, coagglutination, and counterimmunoelectrophoresis and immunodiffusion tests, are available in some laboratories.
If postmortem decomposition has occurred, the causative agent may be obscured by overgrowth of extraneous bacteria. In such cases, the subcutaneous inoculation of mice or rabbits with small amounts of blood and tissue suspensions facilitates the recovery of the pasteurellae in pure or nearly pure culture.
Serologic tests are of no value in diagnosis. However, the indirect hemagglutination procedure and passive mouse protection test are of value in determining the immune status of animals.
Treatment and Prevention
Various sulfonamides, tetracyclines, penicillin, and chloramphenicol (where its use is permitted) are effective if administered early. Because of the rapid course of the disease and the frequent difficulty of access to animals, antimicrobial therapy often is not practicable. However, it is essential that bactericidal concentrations of antimicrobial agents be reached in the blood as soon as possible. Therefore, initial IV administration of drugs followed by SC or IM dosing is recommended. Although multiple antibiotic resistance has been reported for some strains of P multocida, it has not been described for the HS serotypes.
The principal means of prevention is by vaccination. Three kinds of vaccine are widely used: plain bacterin, alum-type precipitated bacterin, and oil-adjuvant bacterin. The most effective bacterin is the oil-adjuvant—one dose given SC provides protection for 9–12 mo; it should be admi-nistered annually. The alum-precipitated-type bacterin is given at 6-mo intervals. Maternal antibody interferes with vaccine efficacy in calves. The oil-adjuvant vaccine has not been popular because of difficulty in syringing and occasional adverse tissue reactions. A live intranasal vaccine prepared from a B:3,4 serotype of deer origin is being used with reported success in southeast Asia. Attempts to elicit longterm immunity with live streptomycin-dependent P multocida vaccine has given variable results in cattle and buffaloes. More recently, a live attenuated Type B P multocida vaccine given IM appeared to give adequate protection in calves against experimental challenges. Animals that survive natural infection usually develop strong immunity to future exposure to homologous and often heterologous strains.
The HS serotypes of P multocida have not been recovered from human infections. However, because many serotypes of P multocida have the potential to infect humans, appropriate precautions should be taken.
Last full review/revision March 2012 by M. M. Chengappa, DVM, PhD, DACVM