Definition
Classical hemorrhagic septicemia is a particular form of
pasteurellosis caused by Pasteurella multocida and manifested by an acute and
highly fatal septicemia mainly in susceptible cattle and water buffaloes.
The name hemorrhagic septicemia is used rather loosely in some
countries to include pneumonic pasteurellosis (shipping or transport fever), a disease
caused mainly by P. haemolytica, although various serotypes of P. multocida are occasionally involved. Although the morbidity of pneumonic pasteurellosis of cattle
can be high, the mortality rate is much less than that of hemorrhagic septicemia.
Etiology
Hemorrhagic septicemia is caused by two serotypes of P.
multocida; namely, B:2 and E:2. The letter denotes the capsular antigen as determined
originally by the indirect hemagglutination test of Carter (5), and the numeral 2 stands
for the somatic or O antigen as determined by the agar gel diffusion precipitin test
developed by Heddelston and associates (17). This somatic antigen 2 is the equivalent to
the 6 in the classification of Namioka and associates. In a new classification, Pasteurella
multocida strains causing most pasteurella infections, including hemorrhagic
septicemia, are called P. multocida subspecies multocida.
Host Range
Cattle and water buffaloes are the principal hosts of hemorrhagic
septicemia, and it is widely considered that buffaloes are the more susceptible. The
disease is thought to be endemic in one large herd of North American range bison; however,
epidemics appear to be rare. In the United States, the disease has been confirmed only in
American bison in 1912, 1922, and 1965. The P. multocida isolant from the 1922
outbreak, a serotype B:2, is maintained in the USDA culture collection as a reference
strain. Although outbreaks of hemorrhagic septicemia have been reported in sheep and
swine, it is not a frequent or significant disease. Cases have been reported in deer,
elephants and yaks. There is as yet no evidence of a reservoir of infection outside the
principal hosts: cattle, water buffaloes, and bison.
Geographic Distribution
Hemorrhagic septicemia in epidemic form is a disease mainly of
cattle and water buffaloes either maintained separately or together. Radical changes in
weather, including the advent of monsoons, debility caused by seasonal levels of low
nutrition, and the pressure of work (draft animals) are related to the explosive
occurrences of the disease in certain parts of the world. Southeast Asia, where such
conditions often coincide, is the area of highest incidence. The disease occurs in the
Middle East and Africa where the environmental circumstances and predisposing conditions
are not as clearly defined as in Southeast Asia. As in Asia, the disease is frequently
associated with the rainy season and poor physical condition.
Hemorrhagic septicemia was recognized in Japan as a specific
disease of cattle caused by particular strains of Pasteurelia as early as 1923.
Since 1926, the disease has been controlled, and the last recorded case in cattle in Japan
occurred in 1952.
The B:2 serotype has been recovered from hemorrhagic septicemia in
countries of Southern Europe, the Middle East, and Southeast Asia, including China. This
same serotype has been reported from Egypt and the Sudan. The E:2 serotype has been
recovered from hemorrhagic septicemia occurring in Egypt, the Sudan, the Republic of South
Africa, and several other African countries. There is no report of either serotype being
recovered from Australia, New Zealand, and countries of South and Central America.
There is no evidence that the disease has spread from carrier
bison in the Western United States to neighboring cattle. Given the conditions in which
hemorrhagic septicemia occurs in endemic areas (e.g., primitive husbandry practices, low
country plains, and well-defined dry and wet seasons), it seems unlikely that the disease
will reach epidemic proportions in the United States.
Transmission
The disease is spread by direct and indirect contact (fomites).
The source of the infection is infected animals or carriers. The carrier state may be
greater than 20 percent shortly after an outbreak, but within 6 weeks the rate is usually
less than 5 percent. The causal agent does not survive for more than 2 to 3 weeks in the
soil or on pastures. Close herding and wetness, as occurs during the rainy season, appear
to contribute to spread. There is no evidence that biting arthropods are significant
vectors.
Incubation Period
The influence of extrinsic factors in the development of the
clinical pasteurelloses, and particularly in hemorrhagic septicemia, has been noted by
many workers. When favorable circumstances for the growth and multiplication of P.
multocida in the animal body occur, severe septicemia develops within a few hours.
However, the organisms may be harbored for varying periods in a small percentage of
carrier animals without any clinical sign. The perpetuation of the disease from year to
year or season to season is generally attributed to the carrier state. The immune status
of the animal is thought to influence the severity of the disease.
Cattle or buffalo artificially inoculated subcutaneously with
lethal doses (approximately 20,000 bacilli) show clinical signs within a few hours and
succumb within 18 to 30 hours.
Clinical Signs
The majority of cases in cattle and buffalo are acute or peracute
with death occurring from 6 to 24 hours after the first recognized signs. In a few
outbreaks, animals may survive as long as 72 hours. Dullness, reluctance to move, and
elevated temperature are the first signs. Following these signs, salivation and nasal
discharge appear, and edematous swellings are seen in the pharyngeal region and then
spread to the ventral cervical region and brisket. Visible mucous membranes are congested,
and respiratory distress is soon followed by collapse and death. Recovery, particularly in
buffaloes, is rare. Chronic manifestations of hemorrhagic septicemia do not appear to
occur.
Gross Lesions
Widely distributed hemorrhages, edema, and general hyperemia are
the most obvious tissue changes observed in infected animals. In almost all cases there is
an edematous swelling of the head, neck, and brisket region (Fig. 63). Incision of the edematous swellings reveals a coagulated
serofibrinous mass with straw-colored or blood-stained fluid. This edema, which distends
tissue spaces, is also found in the musculature (Fig. 64). There are subserosal petechial hemorrhages throughout
the animal, and blood-tinged fluid is frequently found in the thoracic and abdominal
cavities. Petechiae may be found scattered throughout some tissues and lymph nodes,
particularly the pharyngeal and cervical nodes, which are also swollen and often
hemorrhagic. Pneumonia is not usually extensive nor is gastroenteritis. Cases that are
atypical in regard to throat swelling (absent) and pneumonia (extensive) are occasionally
seen.
Morbidity and Mortality
Husbandry, weather and immunity affect morbidity. In endemic
areas, from 10 to 50 percent of the cattle or buffalo populations acquire solid immunity
through exposure or subclinical infection. Close herding and wetness predispose to an
increased morbidity. Most animals that develop clinical signs die.
Diagnosis
Field Diagnosis
In countries where hemorrhagic septicemia is endemic, it is
usually readily diagnosed — particularly if there is a history of previous outbreaks
and a failure to vaccinate. When a small number of animals are affected, diagnosis may be
more difficult. This could be the case if hemorrhagic septicemia were to occur in the
United States. In endemic areas, the rapid course, usual high herd incidence, and the
appearance of edematous swellings in the throat, cervical, and parotid regions is highly
suggestive.
Specimen for Laboratory
From an animal with typical signs, the organism can be isolated
from heparinized blood, affected tissue, liver, lung, kidney, and spleen. All samples
should be collected aseptically. Samples should be kept cool and shipped on wet ice as
soon as possible. Swabs in transport media, ribs, and tips of ears are sometimes submitted
from remote areas in developing countries.
Laboratory Diagnosis
Isolation of a small gram-negative rod or coccobacillus in pure or
nearly pure culture with the general colonial appearance of a Pasteurella species
from an animal with typical signs is grounds to suspect hemorrhagic septicemia. If there
has been postmortem decomposition with the presence of extraneous bacteria, the
inoculation of mice and rabbits with blood or suspensions of tissues will facilitate
recovery of the pasteurellae of hemorrhagic septicemia in pure or nearly pure culture.
Both mice and rabbits are highly susceptible to the two serotypes B:2 and E:2. Definitive
diagnosis depends upon the identification of the cultures as P. multocida and the
subsequent identification of serotype B:2 or E:2. Because several different serotypes of P.
multocida that do not produce classical hemorrhagic septicemia occur in cattle, it is
necessary to serotype the isolate. The National Veterinary Services Laboratories, Ames, IA
should be contacted regarding the serotyping of suspected hemorrhagic septicemia strains
of P. multocida.
Serologic procedures for the detection of specific antibody are
not used in diagnosis.
Differential Diagnosis
The sudden death seen with peracute and acute hemorrhagic
septicemia must be differentiated from that due to lightning, snakebites, blackleg,
rinderpest, and anthrax.
Treatment
The onset and course of the disease are generally rapid and leave
little time for antimicrobial therapy. However, several of the sulfonamides and
antibiotics such as penicillin and the tetracyclines can be used successfully in the early
stages. In some outbreaks in Southeast Asia, animals with elevated temperatures are
isolated and treated intravenously with a soluble sulfonamide.
Vaccination
The most efficacious immunizing agent has been the oil-adjuvant
vaccine prepared from the appropriate serotype. Vaccine of this type is more slowly
absorbed and produces a longer-lasting immunity than do regular and alum-precipitated-type
bacterins. The oil-adjuvant bacterin has the advantage of requiring only one dose
annually, but it has the disadvantages of being difficult to syringe and occasionally
produces a marked local reaction. A live vaccine prepared from a fallow deer strain of P.
multocida has shown considerable promise with protection for as long as a year. This
strain, serotype B:3,4, is closely related immunologically to serotype B:2 but is less
virulent.
Control and Eradication
In endemic areas the only practical ways to protect animals are by
an organized program of vaccination and maintenance of animals in as good a condition as
possible. When favorable conditions for outbreaks are known to recur periodically, such
preventive measures can be carried out in advance, and the potential consequences of the
disease will thus be lessened.
Public Health
There is as yet no authenticated report of human infections due to
serotypes B:2 and E:2. However, because other serotypes of P. multocida can cause a
variety of human infections, precautions should be taken to minimize exposure to the
hemorrhagic septicemia varieties of P. multocida.
GUIDE TO THE LITERATURE
1. ANONYMOUS. 1991. Proceedings of the Fourth International
Workshop on Haemorrhagic Septicaemia, Kandy, Sri Lanka. Bangkok, Thailand:FAO/APHCA
Publication. Food and Agricultural Organization of the United Nations.
2. BAIN, R.V.S., De ALWIS, M.C.L., CARTER, G.R., and GUPTA, B.K.
1982. Haemorrhagic septicemia, FAO Animal Production and Health Paper 33, Food and
Agriculture Organization of the United Nations, Rome.
3. CARTER, G.R. 1967. Pasteurellosis: Pasteurelia multocida and
Pasteurella hemolytica. Adv. Vet. Sci., 11:321-379.
4. CARTER, G.R., and CHENGAPPA, M.M. 1981. Identification of types
B and E Pasteurella multocide by counter-immunoelectrophoresis. Vet. Rec., 108:145-146.
5. CARTER, G.R. 1984. Serotyping Pasteurelia multocida. Methods in
Microbiol., 16:247-258.
6. CARTER, G.R., and De ALWIS, M.C.L. 1989. Haemorrhagic
Septicaemia. In Pasteurella and Pasteurellosis, C. Adlam, and J.M. Rutter,eds.,
London:Academic Press, pp. 131-160.
7. CARTER, G.R., and CHENGAPPA, M.M. 1991. Rapid presumptive
identification of type B Pasteurella multocida from haemorrhagic septicaemia. Vet. Rec.,
128:526.
8. CARTER, G.R., MYINT, A., VAN KHAR, R., and KHIN, A. 1991.
Immunization of cattle and buffaloes with live haemorrhagic septicaemia vaccine. Vet.
Rec., 128:203.
9. De ALWIS, M.C.L. 1981. Mortality among cattle and buffaloes in
Sri Lanka due to haemorrhagic septicemia. Trop. Anim. Hlth. Prod., 13:195-202.
10. De ALWIS, M.C.L. 1984. Haemorrhagic septicaemia in cattle and
buffaloes. Rev. Sd. Tech. Off. Int. Epiz., 3:707-730.
11. GOUCHENOUR, W.S. 1924. Haemorrhagic septicemic studies. J. Am.
Vet. Med. Assoc., 65:433-445.
12. HEDDLESTON, K.L., and GALLAGHER, J.E. 1969. Septicemic
pasteurellosis (Hemorrhagic septicemia) in the American bison. A serologic survey. Bull.
Wildl. Dis. Assoc., 5:207-207.
13. HEDDLESTON, K.L., GALLAGHER, J.E., and REBERS, P.A. 1972. Fowl
Cholera: Gel diffusion precipitin test for serotyping Pasteurelia multocida from avian
species. Avian Dis., 16:925-936.
14. HEDDLESTON, K.L., RHOADES, D.R., and REBERS, P.A. 1967.
Experimental pasteurellosis; Comparative studies on Pasteurella multocida from Asia,
Africa, and North America. Am. J. Vet. Res., 28:1003-1012.
15. HIRAMUNE, T., and De ALWIS, M.C.L. 1982. Haemorrhagic
septicemia carrier status of cattle and buffaloes in Sri Lanka. Trop. Hlth. Prod.,
14:91-92.
16. MYINT, A., CARTER G.R., and JONES, T.O. 1987. Prevention of
haemorrhagic septicaemia with a live vaccine. Vet. Rec., 120:500-502.
17. NAMIOKA, S., and BRUNER, D. W. 1963. Serological studies on
Pasteurelia multocida., IV. Type distribution of the organisms on the basis of their
capsule and O groups. Cornell Vet., 53:41-53.
18. PERREAU, P. 1961. Contribution a 1'etude immunologique de
Pasteurella multocida. Rev. D'Elevage et de Med. Vet. Des Pays Tropicaux., 14:245-256.
19. RHOADES, K.R., HEDDLESTON, K.L., and REBERS, P.A. 1967.
Experimental hemorrhagic septicemia: Gross and microscopic lesions resulting from acute
infections and from endotoxin administration. Can. J. Comp. Med., 31:226-233.
20. RIMLER, R.B. 1978. Coagglutination test for identification of
Pasteurella multocida associated with hemorrhagic septicemia. J. Clin. Microbiol., 8:214
R.G.R. Carter, D.V.M., D.V.Sc., Professor Emeritus, Department of
Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech,
Blacksburg. VA.
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