Dr. drh. Maxs U.E. Sanam, M.Sc. PASTEURELLACEAE.

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Presentation transcript:

Dr. drh. Maxs U.E. Sanam, M.Sc. PASTEURELLACEAE

Haemorrhagic Septicaemia

Introduction Haemorrhagic septicaemia (HS), also known as Septicaemia epizooticae (SE) is a major disease of cattle and buffaloes occurring as catastrophic epizootics in many Asian and African countries, resulting in high mortality and morbidity. The disease has been recorded in wild mammals in several Asian and European countries. In many Asian countries disease outbreaks mostly occur during the climatic conditions typical of monsoon (high humidity and high temperatures).

The disease is caused by Pasteurella multocida, a Gram-negative coccobacillus residing mostly as a commensal in the upper respiratory tract of animals. The Asian serotype B:2 and the African serotype E:2 (Carter and Heddleston system), corresponding to 6:B and 6:E (Namioka- carter system), are mainly responsible for the disease. In wild animals, serotype B:2,5 is predominantly present. The association of other serotypes, namely A:1, A:3 with a HS-like condition in cattle and buffaloes in India has been recorded.

HS has been erroneously and widely used as a synonym for shipping fever and other infections. The result has been that the disease has been mistakenly reported in South America and elsewhere. There was similar confusion in the 1940s and the differences between the diseases have been clarified. HS and shipping fever are two separate conditions caused by different bacteria (Pasteurella multocida vs Mannheimia haemolytica). Unlike HS, shipping fever is not septicaemic nor does it cause multisystemic petechial haemorrhages.

Clinical signs Most cases in cattle and water buffalo are acute or peracute. Although the disease is very similar in both species, buffalo tend to have more severe clinical signs and a shorter course of disease. A fever, dullness and reluctance to move may be the first signs. Salivation and a profuse serous nasal discharge develop, and edematous swellings become apparent in the submandibular region. Theseswellings spread to the neck and brisket. In calves, hemorrhagic gastroenteritis has also been reported. Respiratory distress occurs, with frothing at the mouth, and the animal usually collapses and dies 6 to 48 hours after the initial clinical signs. Either sudden death or a protracted course up to a few days is also possible. Animals with clinical signs, particularly buffalo, rarely recover. Chronic cases have not been reported

The clinical manifestations of the typical disease caused by B:2 or E:2 strains include a rise in temperature, respiratory distress with nasal discharge, and frothing from the mouth, and leads to recumbency and death. Infection with serotypes A:1 and A:3 predominantly involves pneumonia resulting in mortality. Septicaemia is the characteristic feature in all the disease conditions The incubation period varies from 3 to 5 days. In peracute cases, sudden death with observable clinical signs may be observed

Buffaloes are generally more susceptible to HS than cattle and show more severe forms of disease with profound clinical signs. Subcutaneous oedema from the mandible to the brisket is one distinctive feature of the disease in endemic areas Most deaths are confined to older calves and young adults.

Massive epizootics may occur in endemic as well as non-endemic areas. In the recent past, HS has been identified as a secondary complication in cattle and buffalos following outbreaks of foot and mouth disease (FMD). Case fatality approaches 100% if treatment is not followed at the initial stage of infection. The diagnosis of the disease is based on the clinical signs, gross pathological lesions, morbidity and mortality patterns, and confirmation by isolation of the pathogens and their conventional and molecular characterisation.

DIAGNOSTIC TECHNIQUES Post-mortem lesions Most animals succumbing to HS typically show swelling of the neck due to severe blood-tinge oedema. There are abundant petechial haemorrhages involving many tissues, and particularly serosal membranes. The thoracic, pericardial and abdominal cavities may contain serosanguinolent fluid. The lungs are congested and notably oedematous. Microscopically, there is interstitial pneumonia as well as focal infiltrates of neutrophils and macrophages in many tissues. These lesions are similar to those observed in severe sepsis.

Isolation and identification of the agent Cultural and biochemical methods The septicaemia in HS occurs at the terminal stage of the disease. Therefore, blood samples taken from sick animals before death may not always contain P. multocida organisms. The latter are also not consistently present in the nasal secretions of sick animals. A blood sample or swab collected from the heart is satisfactory if it is taken within a few hours of death. If the animal has been dead for a long time, a long bone, free of tissue, can be taken. If there is no facility for postmortem examination, blood can be collected from the jugular vein by incision or aspiration. Blood samples in any standard transport medium should be dispatched on ice and well packed to avoid any leakage. (Serotyping & molecular methods please see OIE Terresterial Manual 2008)

Post mortem lesions Bovine, submandibular region. There is severe subcutaneous/fascial edema and multifocal hemorrhage. The parotid gland exhibits interlobular edema.

Bovine, heart. There are numerous often coalescing petechiae on the epicardium.

Bovine, head and neck. Marked subcutaneous edema.