Mycoplasma Disease in Bison
Murray Woodbury DVM, MSc.
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Mycoplasma bovis is a small bacteria-like organism lacking a cell wall. There are other members of the Mycoplasma genus that cause diseases in various species of livestock but M. bovis is the most pathogenic and most economically important of those infecting North American bovines. It was first noted as a cattle pathogen in the 1960’s, mostly causing mastitis in dairy cows. It has since increased its range of disease expression in individual animals as well as its overall impact to livestock health, welfare and productivity. In cattle it causes middle ear infections, arthritis, conjunctivitis, mastitis, arthritis, reproductive disorders, and respiratory disease. It plays a major role in the chronic pneumonia and polyarthritis syndrome (CPPS) seen in feedlot cattle, making the treatment of animals with this syndrome expensive and unrewarding to treat successfully. By the early 2000’s, M. bovis infection in cattle was common, especially in feedlot cattle. In a 2006 study M. bovis was present in 85% of cattle with acute fibrinous pneumonia and 98 % of cattle with chronic pneumonia (Gagea et al., 2006).
Not surprisingly, at about the same time M. bovis was emerging in the cattle population, outbreaks of polyarthritis and pneumonia were noted in bison herds. In 2002, an outbreak of severe M. bovis-associated pneumonia with arthritis was diagnosed in a Saskatchewan herd (but unreported in the literature). During this period there were also anecdotal reports of mycoplasma pneumonia with high morbidity and mortality with subsequent decreases in herd fertility in large Midwestern American bison herds (Dave Hunter, Turner Enterprises, pers. communication). In 1999, there was an outbreak of mycoplasma pneumonia recorded in yearling bison on pasture. In 2004, the problem struck a mixed age herd in New Mexico, affecting mostly older cows, 8-12 years of age. In 2009, an outbreak occurred in a herd in Nebraska, affecting breeding age animals but apparently sparing the calves and in 2011 a Montana herd also suffered significant losses in breeding age bison. In 2008, a CPPS-like syndrome was reported in feedlot bison from North Dakota (Dyer et al., 2008). This became the first published record of M. bovis pneumonia and arthritis in bison. An outbreak of CPPS in a Kansas bison herd was published in 2010 by Kyathanahalli et al., 2010, this time establishing with molecular laboratory identification techniques that the causative organisms were nearly identical to the M. bovis strains known to cause disease in cattle. It is reasonable to suspect that these published and unpublished reports represent the tip of the proverbial iceberg representing mycoplasma disease in bison herds.
M. bovis organisms colonize the mucosal surfaces, or the lining, of the respiratory tract but, at least in cattle, during active infection can be isolated from multiple body sites such as the upper airways, conjunctiva and urogenital tract (Maunsell et al., 2011). These locations also represent sites where shedding of organisms takes place. Shedding can be intermittent in animals with no clinical signs of disease, or heavy and persistent in obviously sick animals. In cattle, stressful events such as mixing of unfamiliar animals (social stress), entry into a feedlot, shipping, cold or heat stress are associated with increased rates of nasal shedding (Boothby et al., 1983). Chronic asymptomatic infection with occasional shedding of organisms is possible. This appears to be important to the transmission of M. bovis organisms between individuals, and especially to the maintenance of infection within a herd and exposure of naïve populations (Maunsell et al., 2011).
Mycoplasma organisms are susceptible to the effects of drying and sunlight but they can survive for relatively long periods outside the host in cool, humid conditions. M. bovis can persist for months in recycled sand bedding and has been found in cooling ponds and dirt lots on dairies (Bray et al., 1997). There is a lack of information about the role of environmental reservoirs and fomites (inanimate objects or material that is capable of transmitting infectious organisms from one individual to another) in maintaining or spreading infection among or between herds.
Bison herds are most likely infected by the introduction of asymptomatic carriers of M. bovis organisms. It is probable that the stress of transportation, introduction or mixing of new animals in the herd, and other stress related factors causes carrier animals to shed organisms in respiratory secretions, resulting in transmission via aerosols, nose-to-nose contact, or indirectly through contamination of feed, water or farm equipment.
Differences between cattle and bison outbreaks
The above information about transmission of M. bovis has been derived from cattle sources but seems relevant to bison if only because commercial bison and beef producers use similar and sometimes identical management techniques. However, much less is known about the actual relationship between M. bovis and the individual bison and it would be prudent not to carry assumptions or extrapolations about similarities between cattle and bison regarding transmission or pathogenesis of disease too far.
Much has been made about the role of other bacterial or viral organisms in clinical disease of cattle involving M. bovis. Some cattle studies have made an association between M. bovis and bovine virus diarrhea infection (BVD), infectious bovine rhinotracheituis (IBR) and bovine respiratory syncytial virus (BRSV) in cases of complicated pneumonia. M. bovis is commonly isolated from chronic pneumonias due to Manheimia hemolytica, Histophilus somni and Pasteurella multocida (Maunsell et al., 2011). Although M. bovis can be the sole infectious agent isolated from outbreaks of bovine respiratory disease they are often considered by many to be secondary or tertiary invaders in bovine pneumonia, making acute cases into chronic ones that are difficult and expensive to treat.
On the other hand, there is plenty of anecdotal evidence supported by laboratory testing, that M. bovis acts as a primary pathogen more frequently in bison. There are several instances of laboratory identification of pure cultures of M. bovis from herd outbreaks of respiratory disease, with no other apparent respiratory pathogens present. (Dave Hunter, Turner Enterprises; Shelagh Copeland, Pathology Services, Manitoba Agriculture; Jennifer Davies, Clinical and Diagnostic Services, UCVM, personal communication). Research is ongoing to further verify this information in bison.
It is understood that M. bovis causes disease in cattle of all ages but appears to be most common in calves and young feedlot stock. This is perhaps partly because of susceptibility and partly because of increased opportunity for infection in these young animals. In bison, there is evidence that older, breeding age animals on pasture are at risk. There are unpublished reports of grazing bison herds in New Mexico (2004), Nebraska (2009), South Dakota (2010), Montana (2011) and Alberta (2011) suffering outbreaks of mycoplasma-associated pneumonia and polyarthritis. Calves at foot are apparently unaffected by mycoplasma but often die from starvation and disease related to the lack of maternal care. Mature bulls are not spared and suffer the same fate as the cows. Mortality rates in these have been as high as 25% or more, causing significant economic losses to individual producers.
The clinical signs common to most types of pneumonia are coughing and an increased respiratory rate. A low grade fever, mild depression and runny eyes are often observed in affected animals but most of these signs are often too subtle to be of any use when observing bison. Mycoplasmas do not produce toxins like other pneumonia-causing pathogens so affected animals remain alert and usually eat with their cohorts. Producers who have experienced range epidemics in their herds often say that the first sign of illness is reluctance to move or intolerance to exercise. The usual flight distance or comfort zone of bison will shrink and the animal will remain in place on approach until it grudgingly moves off, often with a stiff gait, presumably from the early effects of arthritis. In cattle it has been observed that it can take 7-14 days after infection before dramatic clinical signs are evident. Similarly, bison producers will often notice a loss of body condition before pneumonic signs become obvious. The chronic nature of mycoplasma pneumonia and the pain associated with arthritis (won’t forage for food) combine to create emaciated and weak bison that are often euthanized for welfare reasons before they die on their own.
Arthritis appears to be an inconsistent feature of mycoplasma disease in bison. In cattle, it is rare to have arthritis without lung involvement and pneumonia usually precedes joint involvement by 2-4 weeks. Also in cattle, the carpus or front knees and the stifles or hind knees are the most commonly affected joints. Although joints are extremely painful, the articular surfaces are relatively unaffected with most of the inflammation occurring in the joint capsule and surrounding tissues. This means that if treatment of infection were established there is a good chance that the animal will return to soundness with minimal residual joint damage. This information needs to be confirmed and documented for bison arthritis.
There is growing evidence that M. bovis may cause abortion and infertility in bison. A recent abortion outbreak in a bison herd in Alberta has been attributed to M. bovis, confirmed with laboratory evidence (unpublished). Several herds in the US have had infertility that lasted several sequential breeding seasons following an epidemic of mycoplasma associated pneumonia (Dave Hunter, Turner Enterprises).
In the past, accurate diagnosis of clinical M. bovis infection in cattle was difficult because the initial or primary pneumonia was often caused by other respiratory pathogens. The contribution of M. bovis to the clinical problem in a living animal could prove difficult to assess because the organism is often found in the nasal secretions and upper airways of normal animals. Information about how or whether M. bovis inhabits the respiratory tract of normal bison is lacking. If it is indeed part of the normal flora of bison airways, then we do not understand the circumstances that lead to clinical disease in bison.
Isolation of M. bovis from culture of upper airways in live animals or from diseased tissue on post mortem requires careful sampling, special media, and time to allow the organism to form identifiable colonies. Transtracheal washes are superior to nasal or tonsil swabs for sampling organisms for the diagnosis of M. bovis pneumonia in live cattle but it is difficult to imagine that these would be easily performed in bison in most situations (Maunsell et al., 2011).
M. bovis-specific antibodies can be detected in serum from experimentally infected cattle using an indirect ELISA test. However in natural infections antibody levels in individual animals are poorly correlated with disease status (Maunsell et al., 2011). Not all animals develop high titres and maternal antibody (from colostrum) can cause high levels in calves. Serology is best used to determine exposure status of the herd in surveillance or biosecurity applications. However, there is currently no validated ELISA test for bison and we can only assume that the cattle test is useful in bison.
Polymerase chain reaction (PCR) testing is valuable in identifying M. bovis in tissues from clinical cases and can also identify various strains or types of M. bovis. Strain identification is important to transmission studies and understanding the epidemiology of mycoplasma infection in bison. Immunohistochemistry (IHC) can be used to identify M. bovis organisms associated with lesions from post mortem specimens.
Interestingly, the postmortem lung lesions of M. bovis in bison sometimes resemble those of Mycoplasma mycoides subspecies mycoides, the causative agent of Contagious Bovine Pleuropneumonia (CBPP), an OIE-notifiable disease. Mycoplasma organisms isolated during the investigation of outbreaks in bison in Alberta, Montana, and Nebraska were determined to not be M. mycoides. However, the apparent similarity of the lesions brings the question of whether the bison strains isolated differ from the cattle counterparts or are more related to M. mycoides than to M. bovis.
On post mortem, there is severe, sometimes unilateral, fibrinonecrotizing pneumonia, sometimes pleuropneumonia wth prominent pulmonary sequestra formation. Widespread dissemination of the infection, typified by areas of caseous necrosis (abscessation) is common, but sites of the lesions are inconsistent (Gagea et al., 2006). See figures 1 and 2 below. Microscopically, there is a subacute to chronic necrotizing bronchopneumonia with suppuration (pus formation). IHC staining shows large amounts of the M. bovis antigen present. As noted above, in bison, M. bovis can be the sole pathogen isolated, indicating that unlike the case with cattle, it may be capable of causing primary disease. Arthritic joints contain fibrinous or caseous exudates and the surrounding tendons, synovial sheaths, connective tissue, and muscle contain foci of caseous necrosis and extensive fibrosis (Gagea et al., 2006).
Figures 1 and 2
Figure 1 - Pulmonary sequestra Figure 2 - Fibrinous pleuritis
Mycoplasma organisms do not have a cell wall so antimicrobial drugs whose action is directed at the bacterial cell wall are not effective (eg. penicillins or cephalsporins) nor are they affected by drugs that interfere with folic acid metabolism (eg. sulfonamides). They are generally susceptible to drugs that interfere with protein synthesis such as tetracyclines, macrolides (Zactran etc., except erythromycin), fluoroquinolones (ciprofloxacin) and florfenicol (Nuflor). In cattle, tulathromycin (Draxxin), florfenicol (Nuflor), oxytetracycline (Liquamycin), tilmicosin (Micotil) and tylosin (Tylan) are approved in the US for treating respiratory disease associated with M. bovis. Enrofloxacin (Baytril) is only approved in the US for use in pneumonias due to Pasteuella sp, Manheimia sp or Histophilus sp and off label use is not permitted. If you are in doubt about the uses for which an antibiotic is approved, read the label. The truly bad news is that there are no antimicrobial drugs in the US or Canada that are approved for use in bison and there are no food safety related residue limits attached to their use in bison.
In cattle, antimicrobial treatment for M. bovis infection is generally only effective when treatment is initiated in the early stages of the disease and only when continued for an extended period of time. In bison this principle also applies, but the nature of bison and the difficulty handling bison both on pasture and in the feedlot can make regular treatment impractical. Draxxin is convenient to use in bison because, at least in cattle, one dose provides 7-14 days of therapeutic drug levels against mycoplasma and other bacterial causes of respiratory disease. Empirical evidence with bison shows that treatment is often rewarding at first but relapses are common and treatment must be sustained over a period of several weeks if any success is to be expected. Cattle with arthritis have an especially poor response to treatment (Maunsell et al., 2011) and bison are likely no different. Bison with M. bovis pneumonia will frequently, if not usually, go on to die despite treatment.
Vaccination is an obvious strategy in infectious disease control but in cattle vaccination against M. bovis associated disease has not been very successful. There are commercial vaccines available and autogenous vaccines have also been used but there is little actual proof that these products have been effective in anything other than experimental situations.
In experiments meant to demonstrate their effectiveness some vaccines were counterproductive, actually increasing the severity of disease in vaccinated animals exposed to M. bovis (Maunsell et al., 2011). In view of their doubtful usefulness in cattle, vaccines are not a suitable preventative strategy in bison, especially those products designed for use in cattle.
The best way to prevent M. bovis infections is to maintain a closed herd or at least to test and quarantine new additions before introducing them into the herd. Serology (ELISA) can also be used to identify uninfected herds from which to purchase replacement animals in cow calf operations. Bulls should be screened as well. On the other hand purchased bison that are naive to M. bovis should not be placed in seropositive herds as this practice places the introduced animals at risk from mycoplasma disease.
In feedlot situations this kind of biosecurity is not practical or possible. Instead, preventative strategies should focus on maximizing respiratory system health and immune function as opposed to M. bovis specific measures. Minimize handling, decrease stocking densities and reduce other sources of stress. There is anecdotal evidence that vaccination with modified live BVD cattle vaccine depresses immune function in bison. Metaphylactic treatment of new animals with Draxxin has been suggested in high risk situations (Maunsell et al., 2011). Segregation of sick animals and other general hygiene practices when treating sick bison should be employed. M. bovis can survive rather well in the environment but it is susceptible to chlorhexidine, chlorine, or iodine based disinfectants and all implements and instruments used for treatment should be suitably disinfected (Maunsell et al., 2011).
There are large knowledge gaps in the subject of M. bovis infections in cattle and even less is known about this organism and its relationship to bison. Throughout this article the authors have used empirical and anecdotal evidence to support ideas about M. bovis in bison. Personal communication is used in place of published literature to establish “facts” about mycoplasma disease in bison. Research into suitable, bison-specific diagnostic and screening tests for bison is needed. Epidemiological research is needed to establish risk factors for M. bovis pneumonia and arthritis especially when they occur in large herd outbreaks of severe clinical disease. The bison industry needs evidence based treatment and prevention strategies to deal with extremely expensive outbreaks showing high morbidity and high mortality rates. Mycoplasma infection could be the most important newly emerging disease the bison industry has ever had to deal with.
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