Pasteurellosis of sheep and goats commonly refers to bacterial infections of the lower respiratory tract. Mannheimia haemolytica (formerly Pasteurella haemolytica), Pasteurella multocida, and Bibersteinia trehalosi are the primary pathogens and may occur as a mixed-pathogen infection. Mannheimia haemolytica is the most commonly isolated bacterium in clinical cases, followed closely by B trehalosi, with P multocida occurring less frequently.
Bibersteinia trehalosi is often isolated from the lungs of sheep, goats, and cattle; however, pathogenicity is variable and may be incidental. Pasteurella 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.
Etiology and Pathogenesis of Pasteurellosis of Sheep and Goats
Pasteurella and Mannheimia organisms are beta-hemolytic, gram-negative, aerobic, nonmotile, non–spore-forming coccobacilli in the family Pasteurellaceae. This family tends to inhabit the mucosal surfaces of the GI, respiratory, and genital tracts 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, Pasteurella haemolytica biotypes A and T have been reclassified as Mannheimia haemolytica (biotype A) and Pasteurella 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. The most common strain isolated from sheep and goat respiratory pasteurellosis is M haemolytica A2, although A6, A13, and Ant have been reported in sheep, as has Ant in goats. Additionally, M haemolytica A2 is routinely reported from cases of mastitis in sheep. Bibersteinia 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.
Both M haemolytica and B trehalosi are distributed worldwide, and the diseases they cause are common in sheep and goats of all ages, although the prevalence of serotypes may vary by region and flock. Mannheimia 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, given that 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 sheep and goats 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 is thought to break down the mucosal barrier integrity of the lower respiratory tract, allowing M haemolytica to colonize, proliferate, and induce tissue damage.
The virulence of M haemolytica and B trehalosi is mediated by the action of several factors, including endotoxin, leukotoxin, and capsular polysaccharide, which 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 decreased 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.
Clinical Findings and Lesions of Pasteurellosis of Sheep and Goats
Bibersteinia trehalosi mainly causes septicemia and systemic pasteurellosis in sheep < 2 months 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.
Pasteurella multocida has been reported to be isolated from polyarthritis in young lambs.
Mannheimia haemolytica has been reported from cases of mastitis, especially in sheep.
All of these bacteria can cause severe fibrinonecrotic pneumonia in sheep and goats. The disease is characterized by acute onset of illness, high fever, dyspnea, anorexia, and often death.
Death losses are high in severely affected animals.
Diagnosis of Pasteurellosis of Sheep and Goats
Clinical evaluation, history, and clinical signs
Transtracheal wash or bronchoalveolar lavage
Diagnosis of pasteurellosis of sheep and goats is made based on clinical evaluation, including history of stressors or preceding viral respiratory insult, and clinical signs of acute bronchopneumonia and endotoxemia (eg, dyspnea, fever, depression, anorexia, coughing, oronasal discharge, and increased or abnormal lung sounds). Pneumonia may be observed in conjunction with increased observations of septicemia, polyarthritis, meningitis, and mastitis in the herd.
Differentiation of pasteurellosis from other causes of respiratory disease is based on the high mortality rate and rapid progression to death.
Pulmonary auscultation is poorly correlated with the distribution of lung lesions; thoracic ultrasonography can be used to identify pleuritis and superficial parenchymal lesions.
The blood leukogram, fibrinogen concentration, and acute phase protein concentrations may indicate a nonspecifc inflammatory response.
Pulmonary samples may be collected antemortem via transtracheal wash or bronchoalveolar lavage or at necropsy; there is better correlation with PCR assay of lung tissue than with microbial culture in identifying the presence of P multocida, M haemolytica, or B trehalosi. Confirmation of P multocida, M haemolytica, or B trehalosi in antemortem transtracheal wash or bronchoalveolar lavage samples or postmortem lung lesions provides definitive diagnosis.
Gross necropsy finding are consistent with bronchopneumonia including pneumonitis, focal fibrinopurulent lesions, coagulative necrosis, and fibrinous pleuritis. Diagnosis of pneumonic and septicemic forms of pasteurellosis is based on necropsy, 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.
Treatment of Pasteurellosis of Sheep and Goats
Ancillary anti-inflammatory treatments
Metaphylaxis of high-risk populations
Early identification of respiratory disease and introduction of effective antimicrobial treatment is necessary. Antimicrobial treatment typically consists of long-acting tetracyclines, broad-spectrum beta-lactam antimicrobials, macrolides, or florfenicol. Bacteriologic culture and antimicrobial susceptibility testing of clinical isolates may be indicated to direct antimicrobial treatment. Antimicrobial susceptibility patterns of M haemolytica, B trehalosi, and P multocida have shown resistance to penicillins (all three organisms), sulfadimethoxine (P multocida), and tetracyclines (B trehalosi and occasionally M haemolytica), although tetracycline resistance is less prevalent in small ruminant disease than that in cattle. Ampicillin, ceftiofur, danofloxacin, florfenicol, trimethoprim-sulfamethoxazole, tilmicosin (in sheep), and tulathromycin would be expected to have good efficacy. Although enrofloxacin is likely efficacious, in the US it is not labeled for use in small ruminants, and fluoroquinolones are expressly prohibited from extralabel use.
Treatment is frequently unrewarding unless begun early in the disease process because of rapid progression of lung damage and endotoxin release.
Parenteral fluids and anti-inflammatory agents are potential adjuncts to antimicrobial treatment. Ancillary anti-inflammatory treatments (eg, flunixin or dexamethasone) are often used but not well supported by the literature. Although NSAIDs specifically are appropriate in the face of endotoxemia, there is no consensus on efficacy for improved clinical outcomes in small ruminant pasteurellosis and little positive evidence when used for bovine respiratory disease. Corticosteroids are not indicated in small ruminant pasteurellosis. Although septicemic pasteurellosis has favorable antimicrobial susceptibility, response to treatment is often disappointing.
Administering antimicrobials to at-risk lambs prophylactically may be beneficial.
Prevention of Pasteurellosis of Sheep and Goats
Pasteurellosis prevention would be desirable given the economic costs of treatment, losses, and reduction of weight gain in survivors. Avoidance or reduction of known stressors such as heat, overcrowding, exposure to inclement weather, poor ventilation, handling, nutritional problems, transportation, and commingling is a primary consideration for prevention of disease. Inclusion of metaphylactic antimicrobial treatment, mainly with tetracycline, during the months of the year with the highest incidence of pasteurellosis is a common management practice.
A vaccination program to prevent respiratory virus infection would be expected to decrease the incidence of respiratory pasteurellosis by avoiding the initial insult that allows colonization.
There are no commercial vaccines against pasteurellosis organisms in the US; producers can obtain autogenous bacterins for their flocks, but evidence that these are efficacious is anecdotal. 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 increasing weight gains from both septicemic and pneumonic forms of pasteurellosis. An intranasal recombinant vaccine has protected lambs challenged with P multocida; however, this vaccine is not commercially available.
Pasteurellosis typically causes bacterial bronchopneumonia of small ruminants secondary to viral pneumonia or other respiratory insult, potentially in conjunction with increased observations of other systemic disease processes.
Pasteurella multocida, Mannheimia haemolytica, and Bibersteinia trehalosi are the primary pathogens and may occur as a mixed-pathogen infection.
Treatment is based on early intervention with appropriate antimicrobials.
Prevention includes management practices to decrease stressors and prophylactic treatment where appropriate. There are no commercially available vaccines for small ruminant pasteurellosis in the US.