Hemorrhagic septicemia

Haemorrhagic septicaemia is one of the most economically important pasteurelloses.^[1][2] Haemorrhagic septicaemia in cattle and buffaloes was previously known to be associated with one of two serotypes of P. multocida: Asian B:2 and African E:2 according to the Carter-Heddleston system, or 6:B and 6:E using the Namioka-Carter system.^[2]

The disease occurs mainly in cattle and buffaloes.^[2] However, some cases of infection in other animals have been reported. Sporadic cases in goats (Capra aegagrus hircus) have been reported in Malaysia and India.^[3][4][5] Kasali^[6] presented evidence for the disease in the African buffalo (Syncerus nanus). In Sudan, HS was reported in camels.^[7] However, it is interesting to note that Awad et al.^[8] reported that camels are resistant to experimental infection with doses that are lethal to buffaloes. Pigs have been infected by serogroup B in Malaysia and India.^[3][9][10] In Sri Lanka, some cases of HS have been reported in wild elephants (Elephas maximus) during simultaneous outbreaks among cattle and buffaloes in the same locality.^[11][12][13] Serotypes B:1 and B:3,4 have been responsible for a septicaemic disease in the USA in antelope (Antilocapra americana) and elk (Cervus canadensis), respectively. Serotype B:4 was reported in Canada to be associated with a septicaemic disease in bison (Bison bison).^[14] Cases in horses and donkeys (Equus africanus asinus) have been reported in India.^[15]

Serotypes E:2 and B:2 were formerly associated with HS outbreaks in Africa and Asia respectively. Serotype E:2 was reported in Senegal, Mali, Guinea, Ivory Coast, Nigeria, Cameroon, the Central African Republic and Zambia.^[2][16] However, it is now inaccurate to associate outbreaks in Africa with serotype E:2 as many outbreaks of HS in Africa have now been associated with serogroup B.^[17] In the same manner, serogroup E has been associated with outbreaks in Asia.^[17] For instance, one record of "Asian serotype" (B:2) was reported in Cameroon.^[18] Some reports showed that serotype B:2 may be present in some East African countries.^[19] Both serogroups B and E have been reported in Egypt and Sudan.^[20] Natural routes of infection are inhalation and/or ingestion.^[2] Experimental transmission has succeeded using intranasal aerosol spray or oral drenching.^[2] When subcutaneous inoculation is used experimentally, it results in rapid onset of the disease, a shorter clinical course and less marked pathological lesions compared to the longer course of disease and more profound lesions of oral drenching and the intranasal infection by aerosols.^[21]

When HS was introduced for the first time into a geographic area, morbidity and mortality rates were high.^[22] In fact, when the clinical disease first appeared and clinical signs started, the case fatality rate approached 100% unless animals were treated in the very early stages of disease.^[19]

Clinical signs

A wide variety of clinical signs have been described for HS in cattle and buffaloes.^[2] In Sri Lanka, some descriptions of the disease were derived from experimental transmission studies.^[21][23] The incubation periods (the time between exposure and observable disease) for buffalo calves 4–10 months of age varied according to the route of infection.^[21] The incubation period was 12–14 hours, approximately 30 hours and 46–80 hours for subcutaneous infection, oral infection and natural exposure, respectively.

There is also variability in the duration of the clinical course of the disease. In the case of experimental subcutaneous infection, the clinical course lasted only a few hours, while it persisted for 2–5 days following oral infection and in buffaloes and cattle that had been exposed to naturally-infected animals.^[21] It has also been recorded from field observations of five HS outbreaks in Malaysia that the clinical courses of per-acute and acute cases were 4–12 hours and 2–3 days, respectively.^[24]

Generally, progression of the disease in buffaloes and cattle is divided into three phases. Phase one is characterised by temperature elevation (rectal temperature 40-41 °C), loss of appetite and depression. Phase two is typified by increased respiration rate (40-50/minute), laboured breathing, clear nasal discharge (turns opaque and mucopurulent as the disease progresses), salivation and submandibular oedema spreading to the pectoral (brisket) region and even to the forelegs. Finally, in phase three, there is typically recumbency, continued acute respiratory distress and terminal septicaemia.^[23] The three phases overlap when the course is short. In general, buffaloes have a more acute onset of disease than cattle, and furthermore, the disease typically has a shorter duration.^[25]

Pathology and pathogenesis

When investigating the carcass of an animal that died from HS, the most obvious gross lesion is subcutaneous oedema in the submandibular and pectoral (brisket) regions.^[21] Petechial haemorrhages are found subcutaneously and in the thoracic cavity. In addition, congestion and various degrees of consolidation of the lung may occur.^[21] It was shown that animals that died within 24–36 hours, had only few petechial haemorrhages on the heart and generalised congestion of the lung, while in animals that died after 72 hours, petechial and ecchymotic haemorrhages were more evident and lung consolidation was more extensive.^[26]

Epidemiology

Three factors affect the global distribution of HS: climatic conditions, husbandry practices and the species of animal.^[27] For example, in 1981, Sri Lanka was a good example of different distribution patterns because it had a variety of agroclimatic regions and different husbandry practices. Consequently, Sri Lanka had distinct endemic and non-endemic areas for HS.^[2] The disease was almost non-existent where there was a predominance of hills. Here, the climatic conditions were mild and also temperate dairy breeds were reared. In contrast to this, in the warmer dry plains, where there were seasonal heavy rains and indigenous cattle, buffaloes and zebu cattle, the disease was endemic. Occasional sporadic outbreaks happened in areas with topography, climate and animals that were between these extremes.^[2]

Generally, South Asia is the area of highest prevalence and incidence of HS.^[7] This is attributed to radical changes in weather between seasons, animal debilitation caused by seasonal scarcities of fodder and the pressures of the work that animals do e.g. draught animals.^[28] The disease also occurs, but to a lesser extent, in the Middle East and Africa. Predisposing conditions are not as clearly defined as in South Asia.^[28]

In India from 1974-1986, HS was responsible for the highest mortality rate of infectious diseases in buffaloes and cattle, and was second in its morbidity rate in the same animals. When compared to foot and mouth disease, rinderpest, anthrax and black leg,^[29] HS accounted for 58.7% of the deaths due to these five endemic diseases.^[29][30]

It has been reported as the most important bacterial disease of cattle and buffaloes in Pakistan.^[31] In Pakistan, HS is considered as a disease of great economic importance. In the Punjab province alone, the financial losses due to HS were estimated to be more than 2.17 billion Pakistani rupees (equivalent to 58 million USD) in 1996.^[32][33] According to farmers’ opinions in a participatory disease surveillance (PDS) done in Karachi, HS is more important than foot and mouth disease (FMD) and this is due to the higher mortality rate and the greater economic impact of HS.^[34]

See also

• Sepsis (presence of microorganisms in the blood)
• Viral hemorrhagic septicemia (unrelated viral infection of fish)

References

External links

• Current status of Hemorrhagic septicemia worldwide at OIE. WAHID Interface - OIE World Animal Health Information Database
• Disease card
• Moustafa, Ahmed (2014) A molecular epidemiological study on Haemorrhagic septicaemia disease in Pakistan. PhD thesis, Murdoch University at http://researchrepository.murdoch.edu.au/27595/