Bibersteinia trehalosi infections
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Top of pageOriginally described as biotype T (trehalose fermenting) of the [Pasteurella] haemolytica complex, Bibersteinia trehalosi was recognized as a separate species (named Pasteurella trehalosi) in 1990 (Sneath and Stevens, 1990). The organism was reclassified as Bibersteinia trehalosi in 2007 on the basis of phylogenetic studies (Blackall et al., 2007).
B. trehalosi is an important pathogen of sheep, primarily associated with septicaemia in older lambs (Gilmour, 1978; Sneath and Stevens, 1990; Donachie, 2007), and less commonly with respiratory disease (Miller et al., 2011; Gonzalez et al., 2013). B. trehalosi has also been isolated from bighorn sheep with pneumonia (Rudolph et al., 2007; Wolfe et al., 2010; Drew et al., 2014) and from goats with pasteurellosis (Sanchis and Abadie, 1992; Guillou, 2004; Abadie and Thiery, 2006).
B. trehalosi has been isolated from cases of bovine respiratory disease (Collins, 2011; Cortese et al., 2012) but its role as a primary pathogen in cattle is uncertain.
Hosts/Species Affected
Top of pageBibersteinia trehalosi is a common inhabitant of the upper respiratory tracts and tonsils of healthy sheep (Al-Sultan and Aitken, 1985). B. trehalosi can cause ovine systemic pasteurellosis and/or septicaemia in feeding lambs, most commonly following a period of stress or management change (Sanchis et al., 1991; Sanchis and Abadie, 1992; Davies et al., 1997). Some B. trehalosi strains have also been found to be involved in wild ruminant pneumonia (Villard et al., 2006; Dassanayake et al., 2013).
B. trehalosi is considered normal flora in the tonsils of bison (Bison bison) (Ward et al., 1999; Dyer et al., 2001) and has been isolated from both healthy and diseased cattle (Nakaya et al., 1995; Blackall et al., 2007; Collins, 2011; Cortese et al., 2012), roe deer (Blackall et al., 2007), goats (Ward et al., 2002) and from adult chamois (Rupicapra rupicapra) with interstitial pneumonia (Richard et al., 1992).
Distribution Table
Top of pageThe distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
| Continent/Country/Region | Distribution | Last Reported | Origin | First Reported | Invasive | Reference | Notes | |
|---|---|---|---|---|---|---|---|---|
Asia | ||||||||
| Japan | Present | Nakaya et al., 1995 | ||||||
| Turkey | Present | Güler et al., 1996; Kaya and Kirkan, 1999 | ||||||
Africa | ||||||||
| Ethiopia | Present | Sisay and Zerihun, 2003 | ||||||
| Kenya | Present | Mwangota et al., 1978 | ||||||
| Sudan | Present | Elsheikh and Hassan, 2012 | ||||||
North America | ||||||||
| USA | Present | Present based on regional distribution. | ||||||
| -California | Present | Tomassini et al., 2009 | ||||||
| -Colorado | Present | Wolfe et al., 2010 | ||||||
| -Idaho | Present | Dunbar et al., 1990; Drew et al., 2014 | ||||||
| -Oregon | Present | Miller et al., 2012 | ||||||
| -Wyoming | Present | Miller et al., 2012 | ||||||
Europe | ||||||||
| France | Present | Abadie and Thiery, 2006; Villard et al., 2006 | ||||||
| Hungary | Present | |||||||
| Spain | Present | Gonzalez et al., 2013 | ||||||
| UK | Present | Watson and Scholes, 2010; Collins, 2011 | ||||||
Oceania | ||||||||
| Australia | Present | Present based on regional distribution. | ||||||
| -New South Wales | Present | Mackie et al., 1995 | ||||||
| New Zealand | Present | Black, 1997 | ||||||
Pathology
Top of pageThe 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 septicaemia and localization of the infection in one or more tissues such as the joints, udder, meninges, or lungs.
Postmortem examinations sometimes reveal subcutaneous haemorrhages over the neck and thorax, with superficial haemorrhages on the pleura, diaphragm and epicardium. The lungs may be swollen with widespread haemorrhages, and bloodstained froth in the airways, but no evidence of consolidation. Necrotic erosions are sometimes seen in the pharynx around the tonsils, nasal mucosa, oesophagus and abomasum. The tonsils and retropharyngeal lymph nodes are enlarged. The abdominal viscera are often congested; in some cases, necrotic infarcts may also be present in the liver, spleen and kidney, visible as small grey foci (Sargison, 2009).
Diagnosis
Top of pageClinical disease usually follows within a few days of exposure to predisposing factors; sudden death often occurs in the absence of premonitory clinical signs (Gilmour, 1978; Ellis, 1984). Occasionally, affected animals show a fever, reluctance to move, dyspnoea, blood-stained frothy discharge from the nose and mouth, and recumbency followed by death (Gilmour, 1978). The mortality rate seldom exceeds 5 percent.
Diagnosis of pneumonic and septicaemic forms of pasteurellosis is based on necropsy examination, gross and histopathologic findings, and isolation of organisms from a range of tissues, including lungs, liver and spleen (Ellis, 1984). Lesions include subcutaneous haemorrhage; epithelial necrosis of the tongue, pharynx, oesophagus, or occasionally the abomasum and intestine; enlargement of tonsils and retropharyngeal lymph nodes; and peracute, multifocal, embolic, necrotizing lesions in the lung and liver.
Disease Course
Top of pageBibersteinia trehalosi is a common inhabitant of the upper respiratory tract and tonsils of healthy sheep. Local mucosal invasion and systemic spread are thought to follow a period of stress or management change (Dyson et al., 1981; Suàrez-Güémes et al., 1985). Stress is thought to result in corticosteroid-dependent bacterial proliferation in the tonsillar region, and injury to the alimentary tract, with consequent ulceration (Suàrez-Güémes et al., 1985). The injured pharyngeal, abomasal and duodenal mucosa serve as portals of entry for B. trehalosi derived from the tonsils. From these sites bacteria gain access to the blood as emboli, most of which impact in the capillary bed of the lungs (Dyson et al., 1981), whilst bacterial invasion of the lower alimentary tract results in primary embolization of the hepatic sinusoids (Suàrez-Güémes et al., 1985). Rapid multiplication of bacteria in these sites results in embolic dissemination to other organs and tissue. Death is attributed to endotoxaemia (Dyson et al., 1981; Suàrez-Güémes et al., 1985; Hodgson et al., 1993).
The virulence of B. trehalosi is mediated by the action of several factors, including endotoxin, adhesins, leukotoxin, and capsular polysaccharide, that afford the bacteria advantages over host immunity. The leukotoxin is particularly important in pathogenesis (Subramaniam et al., 2014). Typically, domestic sheep carry leukotoxin-positive Mannheimia haemolytica and/or B. trehalosi as commensal bacteria in their nasopharynx. In contrast, most bighorn sheep do not carry leukotoxin-positive M. haemolytica or B. trehalosi, or carry leukotoxin-negative strains in their nasopharynx (Subramaniam et al., 2014).
Dassanayake et al. (2010) describe the interaction between B. trehalosi and M. haemolytica. The authors point out that although B. trehalosi is commonly isolated from cases of pneumonia in bighorn sheep, M. haemolytica is the only pathogen that has consistently been shown to cause bronchopneumonia and death under experimental conditions. Other studies show that only leukotoxin-producing strains of B. trehalosi can cause pneumonia (Dassanayake et al., 2013). As a result, there is some question as to whether or not B. trehalosi is likely to be a major cause of pneumonia in bighorn sheep. Research by the authors shows that B. trehalosi replicates at almost twice the rate of M. haemolytica and is able to inhibit and overgrow M. haemolytica. This data would lead to speculation that, in many cases, M. haemolytica might be the initial cause of pneumonia but is then overgrown by B. trehalosi, which is the organism subsequently isolated.
Although B. trehalosi infections are considered rare in cattle, B. trehalosi is sometimes isolated from cattle with respiratory disease and reports seem to be increasing (Collins, 2011). Cortese et al. (2012) reported severe non-responsive bovine respiratory disease (BRD) outbreaks associated with multidrug-resistant B. trehalosi.
To evaluate the role of B. trehalosi in BRD, Hanthorn et al. (2014) used an intra-tracheal inoculation model in calves. They found that B. trehalosi-inoculated calves did not have increased lung involvement compared to control calves and concluded that B. trehalosi may not be a primary pathogen of respiratory disease in cattle. Culture of B. trehalosi from diagnostic submissions should not be immediately identified as a primary cause of respiratory disease, they say. They speculate that the main role of B. trehalosi in BRD may be as secondary and perhaps opportunistic bacteria.
B. trehalosi has been identified as the cause of necrotizing hepatitis/sudden death in an adult cow (Watson and Scholes, 2010). Spagnoli et al. (2011) describe a case of subcutaneous botryomycosis caused by B. trehalosi in a Texas Longhorn steer.
Epidemiology
Top of pageAlthough sheep of any age are susceptible to systemic pasteurellosis, animals five to 12 months old are at greatest risk (Dyson et al., 1981; Ellis, 1984). Prevalence increases in cold, wet weather conditions (Dyson et al., 1981). Stress associated with weaning, transportation, vaccination and shearing, as well as a change in diet, are thought to be predisposing factors (Suarez-Guemes, 1983; Suàrez-Güémes et al., 1985; Mackie et al., 1995). Concurrent diseases such as cobalt deficiency or tickborne fever (caused by Anaplasma phagocytophilum) may also predispose to outbreaks of the disease (Sargison, 2009; Daniel et al., 2015).
Disease Treatment
Top of pageAntimicrobials effective against gram-negative bacteria, such as ampicillin, amoxicillin-clavulinic acid, ceftiofur, oxytetracycline and florfenicol, can potentially be used to treat B. trehalosi infections, although strains vary in their susceptibility (Richard et al., 1992; Sanchis and Abadie, 1992; Weiser et al., 2009; Scott, 2011). However, sheep are rarely seen in the early stages of the disease and treatment is only successful if begun very early in the disease process due to rapid progression of lung damage and endotoxin release. Parenteral fluids and anti-inflammatory agents are important adjuncts to antibiotic therapy (Scott, 2011).
The presence of antimicrobial resistance genes in B. trehalosi was first reported by Kehrenberg et al. (2006) in a florfenicol-resistant isolate from a calf. They found that resistance to chloramphenicol and florfenicol were associated with a plasmid which also carried functionally active genes for resistance to sulphonamides.
Prevention and Control
Top of pageImmunization and Vaccines
In some countries, vaccines are available for small ruminants that offer some degree of immunity to Pasteurella haemolytica/Pasteurella trehalosi; most are combined with clostridial disease vaccines (Duncanson, 2012). The vaccine that is solely for pasteurellosis has to be given as two doses separated by 4-6 weeks. If there is an early threat to younger lambs, the first dose should be given at 2 weeks of age and the second at 6 weeks of age. Otherwise the timing should be adjusted so that the second dose is given a few days before the time of greatest threat. The Pasteurella component is much more expensive than the clostridial component of the combined vaccine, and so should only be given if there is a real need (Duncanson, 2012).
Bowersock et al. (2014) reported that a multivalent modified-live virus (MLV) vaccine containing M. haemolytica toxoid protected calves against challenge exposure with virulent B. trehalosi by reducing the mortality rate, lung lesion scores, and clinical scores for respiratory disease.
Husbandry methods and good practice
While vaccines offer the best means of disease control, stress likely plays a part in predisposing to disease. Flock management should be designed to minimize the stress involved in changes of environment and nutrition (Dyson et al., 1981; Suàrez-Güémes et al., 1985).
References
Top of pageDonachie W, 2007. Pasteurellosis. In: Diseases of Sheep, 4th edition [ed. by Aitken, I.]. Ames, Iowa, USA: Blackwell Publishing, 224-231.
Dyer NW; Ward ACS; Weiser GC; White DG, 2001. Seasonal incidence and antibiotic susceptibility patterns of Pasteurellaceae isolated from American bison (Bison bison). Canadian Journal of Veterinary Research, 65(1):7-14.
Gilmour NJL, 1978. Pasteurellosis in sheep. Veterinary Record, 102(5):100-102.
Sisay T; Zerihun A, 2003. Diversity of Mannheimia haemolytica and Pasteurella trehalosi serotypes from apparently healthy sheep and abattoir specimens in the highlands of Wollo, North East Ethiopia. Veterinary Research Communications, 27(1):3-14.
Sneath PH; Stevens M, 1990. Actinobacillus rossii sp. nov., Actinobacillus seminis sp. nov., nom. rev., Pasteurella bettii sp. nov., Pasteurella lymphangitidis sp. nov., Pasteurella mairi sp. nov., and Pasteurella trehalosi sp. nov. International Journal of Systematic Bacteriology, 40(2):148-153.
Distribution Maps
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