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Overview of Pasteurellosis of Sheep and Goats

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Pasteurella and Mannheimia organisms are β-hemolytic, gram-negative, aerobic, nonmotile, nonsporeforming coccobacilli in the family Pasteurellaceae. This family tends to inhabit the mucosal surfaces of the GI, respiratory, and genital tract of mammals. Many are known as opportunistic secondary invaders. Some species show preferences for specific surfaces and hosts. Updating of phylogenetic data has resulted in renaming based on gene sequence analysis. As a result, P haemolytica biotypes A and T were reclassified as M haemolytica (biotype A) and P trehalosi (biotype T). More recently, P trehalosi has been reclassified as Bibersteinia trehalosi. Each isolate of M haemolytica and B trehalosi is designated with a biotype and serotype. M haemolytica A2 is the most common strain isolated from sheep and goat respiratory pasteurellosis, although A6, A13, and Ant have been reported in sheep and Ant in goats. M haemolytica A2 is routinely reported from cases of mastitis in sheep. B trehalosi T3, T4, T10, and T15 have been most often associated with the systemic or septicemic form of pasteurellosis affecting lambs. These serotypes have been regrouped to B trehalosi biotype 2, and a new biotype 4 has been added. B trehalosi is often isolated from the lungs of sheep, goats, and cattle, but pathogenicity is variable and may be incidental. P multocida has also been reported as a cause of pneumonic pasteurellosis in sheep and goats and has been isolated in herd outbreaks of septic arthritis. M haemolytica is the most commonly isolated bacteria in clinical cases, followed closely by B trehalosi, with P multocida seen less frequently.

M haemolytica and B trehalosi are distributed worldwide, and diseases caused by them are common in sheep and goats of all ages, although the prevalence of serotypes may vary by region and flock. M haemolytica, B trehalosi, and P multocida are common commensal organisms of the tonsils and nasopharynx of healthy sheep and goats. The presence of multiple Pasteurella spp may serve to keep the bacterial populations in check, because there appears to be some interference with growth when multiple species are present. For these organisms to cause infection, a combination of stressors, including heat, overcrowding, exposure to inclement weather, poor ventilation, handling, and transportation, leaves sheep and goats susceptible to respiratory viral infections. Parainfluenza 3, adenovirus type 6, respiratory syncytial virus, possibly bovine adenovirus type 2, ovine adenovirus types 1 and 5, and reovirus type 1 cause primary respiratory infections that are rarely life threatening but predispose to secondary M haemolytica infections. Respiratory infections with Mycoplasma ovipneumoniae and Bordetella parapertussis have also been reported to be associated with secondary M haemolytica infections. The combination of stressors and primary infections are thought to break down the mucosal barrier integrity of the lower respiratory tract, allowing M haemolytica to colonize, proliferate, and induce significant tissue damage.

The virulence of M haemolytica and B trehalosi is mediated by the action of several factors, including endotoxin, leukotoxin, and capsular polysaccharide, that afford the bacteria advantages over host immunity. The leukotoxin is particularly important in the pathogenesis, because it is specifically toxic to ruminant leukocytes, resulting in fibrin deposition in lungs and on pleural surfaces. The lipopolysaccharide endotoxin contributes to adverse reactions in the lungs and also leads to systemic circulatory failure and shock. The capsular polysaccharide prevents the phagocytosis of the bacteria and assists in attachment to the alveolar epithelial surface. Survival of the acute phase of pneumonic pasteurellosis depends on the extent of lung involvement and damage in the lower respiratory tract. Sheep and goats that recover may have chronic respiratory problems, including reduced lung capacity and weight gain efficiency if ≥20% of the lung was damaged. In one review, there was no association between virulence and the presence of hemolysis on blood agar culture plates.

B trehalosi mainly causes septicemia and systemic pasteurellosis in sheep <2 mo old. The systemic form of pasteurellosis caused by B trehalosi is characterized by fever, listlessness, poor appetite, and sudden death in young sheep. The organism is thought to move from the tonsils to the lungs and pass into the blood. This results in septicemia and localization of the infection in one or more tissues such as the joints, udder, meninges, or lungs. P multocida has been reported to be isolated from polyarthritis in young lambs. M haemolytica has been reported from cases of mastitis, especially in sheep. All of these bacteria can cause a severe fibrinonecrotic pneumonia in sheep and goats. The disease is characterized by acute onset of illness, very high fevers, dyspnea, anorexia, and often death.

The differentiation of pasteurellosis from other causes of respiratory disease is based on the high mortality and rapid progression to death. Diagnosis of pneumonic and septicemic forms of pasteurellosis is based on necropsy examination, gross and histopathologic findings, and isolation of organisms from a range of tissues. Lesions include subcutaneous hemorrhage; epithelial necrosis of the tongue, pharynx, esophagus, or occasionally the abomasum and intestine; enlargement of tonsils and retropharyngeal lymph nodes; and peracute, multifocal, embolic, necrotizing lesions in the lung and liver. There is better correlation with PCR analysis of lung tissue than with microbial culture in identifying the presence of M haemolytica, B trehalosi, and P multicoda.

Early identification of respiratory disease and introduction of effective antibiotic therapy is necessary. Death losses are high in severely affected animals. Antimicrobial susceptibility patterns of M haemolytica, B trehalosi, and P multicoda have shown resistance to penicillins (all three organisms), sulfadimethoxine (P multocida), and tetracyclines (B trehalosi). Ampicillin, ceftiofur, danofloxacin, enrofloxacin, florfenicol, trimethoprim-sulfamethoxazole, and tulathromycin would be expected to have good efficacy, although extra-label use of fluoroquinolones is prohibited in the USA. Treatment is frequently unrewarding unless begun very early in the disease process because of rapid progression of lung damage and endotoxin release. Parenteral fluids and anti-inflammatory agents are important adjuncts to antibiotic therapy. Although septicemic pasteurellosis has favorable antimicrobial susceptibility, response to therapy is often disappointing. Administering prophylactic antibiotics to at-risk lambs may be beneficial.

Pasteurellosis prevention would be desirable given the economic costs of treatment, losses, and reduction of weight gains in survivors. Commercial vaccines are available for cattle but unfortunately are specific for M haemolytica A1, and there is little or no cross-protection against M haemolytica A2 experimentally. Commercial vaccines for M haemolytica A2 are available in the UK and have been reported to be beneficial in reducing death losses and decreased weight gains from both septicemic and pneumonic forms of pasteurellosis. An intranasal recombinant vaccine has protected lambs challenged with P multocida, but this vaccine is not commercially available. There are no commercial vaccines in the USA, but producers can get autogenous bacterins for their flocks; however, evidence that these are efficacious is anecdotal. Prevention of respiratory viruses by using a vaccination program would be expected to decrease respiratory pasteurellosis by preventing the initial insult that allows colonization. Inclusion of prophylactic antibiotics, mainly tetracycline, in the feed during the months of the year with the highest incidence is a common management practice. Avoidance or reduction of known stressors such as heat, overcrowding, exposure to inclement weather, poor ventilation, handling, and transportation should also be considered.

Last full review/revision September 2015 by Sherrill A. Fleming, DVM, DACVIM, DABVP

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