Pasteurella multocida type B

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Haemorrhagic septicaemia (or pasteurellosis) is a peracute to acute, highly fatal bacterial disease, principally of cattle and water buffaloes (Bubalus bubalis), in which the Gram-negative Pasteurella multocida serotypes B:2 (Asian) or E:2 (African) are the usual causal organisms. It is endemic throughout south-east Asia, India, and many regions of Africa. Normally the Asian form is caused by serotype B and the African form (East African haemorrhagic fever) primarily by serotype E[1]. Various other serotypes have also been isolated from individual cases[2], and type B has been isolated from cattle in Egypt and Sudan[3], and from African buffaloes (Syncerus caffer) in South Africa.

By means of an indirect haemagglutination test (Carter procedure) P. multocida strains are characterized according to their capsular antigens into five capsular groups (A, B, D, E, and F) and, using a gel diffusion test, into 16 somatic types (1 to 16) (Heddlestone procedure). Traditionally haemorrhagic septicaemia has been regarded as being caused only by serotype B:2 or E:2 but other strains are recognized as causing it, in particular types B:1 and B:3,4. Both of the latter types have been linked to outbreaks of haemorrhagic septicaemia in the USA whilst B:3,4 was involved in disease among reindeer (Rangifer tarandus) in Lapland and fallow deer (Dama dama) in Denmark and the UK, and serotype B:2 has been implicated in an outbreak in cattle in Zimbabwe[1].

African wildlife

Disease due to this bacterium has been diagnosed in a number of wildlife species including hippopotami, elephants, and lions[3]

Infection with P. multocida type B has recently been diagnosed in South Africa in African buffaloes (Syncerus caffer) kept under intensive, or semi-intensive conditions [4]. In African buffaloes, this septicaemic condition is rapidly fatal, and death is seldom preceded by overt clinical signs except, perhaps, for anorexia. Outbreaks are often associated with stress and adverse environmental conditions such as high temperatures, excessive rain, or other inclemental weather conditions.


Outbreaks of the disease may occur throughout the year and they are independent of season. The distribution and frequency of the disease have been associated with climatic conditions, specific husbandry practices, and type of animals reared[2].

The natural infection is usually by inhalation or ingestion of infective material produced by the presence of clinically infected or carrier animals with which they come into contact[2]

Shed bacteria do not survive outside the host for long periods, although their persistence may be enhanced by moist soil, and infected animal tissues in the environment.

Naturally acquired immunity has been documented in water buffaloes and it has been suggested that morbidity and mortality rates in endemic and non-endemic areas are dependent on the proportion of naturally acquired immune to non-immune animals. H. multocida may also occur in the nasopharynx and tonsils of healthy cattle and buffaloes where they may be present for several months. Intermittent shedding occurs from these sites. Infection in these latent carriers may, under unknown circumstances, be re-activated with the development of full-blown, clinical disease [2]


Haemorrhagic septicaemia, in contrast to many other Pasteurella infections, is a primary pasteurellosis with a 100% mortality rate [2]. Their pathogenicity is determined by a cluster of numerous virulence factors including the capsular antigens, fimbriae and adhesins, OMPs, endo- and exotoxins, multocidin and siderophores, extracellular enzymes, and plasmids[2].

The onset of clinical signs is associated with a high rate of bacterial proliferation. Strain differences and the genetic composition of the host, are known to be related to differences in lesion severity and duration of the disease before death. The role of the intrinsic bacterial properties determining mucosal invasion, evasion of innate immunity, persistence in the host, and the sudden onset of bacterial multiplication are known[2]

Clinical signs and pathology

African buffaloes

Fig. 1. Blood smear from a live animal; Diff Quik stain; Note the marked bacteraemia
Fig. 2. Marked congestion and cyanosis of peritracheal tissues. The perilaryngeal oedema is typical, and in many cases the only obvious lesion present
Fig. 3. Marked acute fibrinous pleuritis, multifocal pulmonary haemorrhages, and splenomegaly in a buffalo that died of haemorrhagic septicaemia
Fig. 4. Lymphoid hyperplasia, oedema and cortical petechial haemorrhages
Retropharyngeal lymph node with marked lymphoid hyperplasia, marked congestion, petechial haemorrhage and oedema

The lesions in buffaloes are characteristically those of a haemorrhagic septicaemia. The carcass is severely congested and cyanotic. Submandibular and peritracheal oedema Fig. 2. are often the only lesions seen in buffaloes that died of the infection. The macroscopic lesions include severe, diffuse, fibrinous pleuritis in more advanced cases Fig. 3., a moderate to severe serofibrinous perilaryngitis and tracheitis. The lymph nodes reflect severe lymphoid hyperplasia, oedema, haemorrhage Fig. 4 and Fig. 5, and occasionally, a multifocal, necrotic lymphadenitis. There is often a severe, diffuse, fibrinous peritonitis. Multiple petechial haemorrhages may occur in many tissues and organs including the myocardium, trachea, diaphragm, and subcutaneous tissues of the head, neck and thorax. The spleen is enlarged following a moderate white pulp hyperplasia[4].

Blood smears from animals suffering from the disease reveal numerous Gram-negative, pleomorphic bacteria that occur either singly, in pairs, or in short chains Fig. 1. These bacteria are also visible in tissue smears made from the tonsils, lungs, and brain[4]. In histological sections bacteria are seen singly or as bacterial thrombi and/or emboli in blood vessels and lymphatics, and in lymph nodes. In the lymph nodes the bacterial emboli occur in the red pulp and the sinusoids of the follicular marginal zones[4].


The lesions seen at necropsy (also in African buffaloes) are indicative of a septicaemic disease. On blood smear (stained with Gram's, Leishman's, or Methyline Blue stains) there are marked leukopenia and a monopopulation of innumerable small, bacterial cocco-bacilli in the background, typical in appearance of Pasteurella sp.. Impression smears (lymph node, tonsil, and perilaryngeal oedema) reveal the same bacteria (see Fig. 1). The bacteria are pleomorphic, their appearance depending on the growth stage in which they are in, and they occur singly, in pairs, or in short chains. They are Gram-negative and non-endospore-forming [2].

The diagnosis should be confirmed by culture and typing of the organism from representative samples collected at necropsy. These samples should include blood and nasal secretions in live animals, and from necropsies blood, liver, spleen, lung and bone marrow collected form a long bone [2]. The diagnosis by culturing should be made according to OIE methodology.

The diagnosis in live animals should be made on the basis of the history, clinical signs, lesions seen at necropsy, morbidity and mortality patterns, species susceptibility, and age group.

PCR assays may be used for confirming the presence of the bacteria in clinical specimens collected from diseased animals, and for rapid screening to select specimens submitted for culture. The use of molecular techniques is complex and its detail is beyond the scope of this section[2].


Antibiotic treatment of animals manifesting clinical signs is usually of little use. Treatment of cases in the early stages (those with an elevated body temperature) of the disease may benefit form antibiotic treatment keeping in mind that there is an increasing prevalence of multiple drug-resistant strains of Pasteurella multocida. All in-contact animals should be treated immediately following the initial diagnosis. Generally cases are treated with oxytetracycline, co-trimoxazole, or a combination of penicillin and streptomycin or sulphaquinoxaline[2]

Vaccination of susceptible animals is the only way in which to prevent outbreaks of haemorrhagic septicaemia[2]. There are numerous variables affecting the efficacy of vaccination. These, in South Africa, when dealing with African buffaloes, are not known. The precise mechanisms for immunity and the specific antigens responsible for immunity, are not known, particularly as they apply to African buffaloes.


  1. 1.0 1.1 Bastianello SS & Henton , MM, 2004. In: JAW Coetzer, GR Thomson, RC Tustin (Eds.), Infectious Diseases of Livestock, with Special Reference to Southern Africa (second ed.), Oxford University Press Southern Africa, Cape Town, South Africa
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 Shivachandra, S. B., Viswas, K. N., & Kumar, A. A., 2011. A review of hemorrhagic septicemia in cattle and buffalo. Animal Health Research Reviews,12(01), 67-82.
  3. 3.0 3.1 De Alwis, M. C. L., 1992. Haemorrhagic septicaemia — a general review. British Veterinary Journal, 148(2), 99-112.
  4. 4.0 4.1 4.2 4.3 Pathology Reports, Section of Pathology, Faculty of Veterinary Science, University of Pretoria. South Africa. Reports no. S02623-15; S01908-15; and S01335-15