The mycoplasma – a wolf in sheep’s clothing?

Janet M. Bradbury

Department of Veterinary Pathology

University of Liverpool

 

Proceedings of the 24th Technical Turkey Conference p5

 

Introduction

Mycoplasmas are the smallest known bacteria that are capable of replicating outside cells. They are highly evolved organisms and possess only a minimal set of genes

and yet, despite this, they are able to cause diseases of significant economic impact in both mammals and birds. Major efforts made by the poultry industry some years ago resulted in the production of mycoplasma-free primary breeding stock and it then seemed possible that the incidence and impact of the avian mycoplasmas might diminish into insignificance. Certainly the majority of poultry production in the European Community maintains a mycoplasma-free status. M. meleagridis (Mm) and M. iowae (Mi), which are classed as turkey pathogens, are now rarely encountered in Europe. However infections with the pathogenic species M. gallisepticum (Mg) and M. synoviae(Ms) still occur in turkeys and chickens, with Ms being more prevalent than Mg. At present Ms is particularly common in laying chickens but both  infections occur sporadically in breeders, even in flocks maintained with apparently good biosecurity. Methods for the detection of mycoplasmas have  improved and PCR techniques are now available for rapid diagnosis, but despite this it would seem that these simple little microorganisms are still able to outwit us in our attempts to detect, control and eradicate them. Some of the possible reasons for this will be discussed in the light of current knowledge.

 

Mycoplasma control at international and national level

Within the European Community there is legislation (Directive 90/539/EEC) which governs the control of Mg and Mm in respect of intra-Community trade in poultry and hatching eggs. The legislation also applies to imports from third countries. However there is no such legislation for Ms, which may, as a result, reduce local incentive to control this mycoplasma and may explain its increased prevalence. In the UK the Poultry Health Scheme reflects the EU Directive in laying down control measures for Mg and Mm but not Ms. In contrast to this the United States Department of Agriculture’s National Poultry Improvement Plan encompasses all three of these mycoplasma species.

 

Control at the local level

Poultry production tends to be concentrated into certain areas which provides a very large susceptible population of birds and probably increases the risk of exposure to mycoplasmas. It is well recognised that continuous production sites are especially difficult to rid of infection and in some areas the close proximity of a number of poultry farms may in fact not be very different to a continuous production site.

At the University of Liverpool we are completing a three year industry-sponsored case:control study into the risk factors associated with unexplained Mg and Ms ‘breaks’ in broiler and turkey breeders. All plausible routes of spread are being addressed including farm locations and management practices.

 

Widening host range?

Mycoplasmas are traditionally thought to be rather host specific but recent findings have weakened this dogma, suggesting that some mycoplasmas infect an increasing

number of hosts. An example among the avian mycoplasmas is Mm, which was for years thought to be host-specific for turkeys, but has now also been found in

raptors (Lierz et al., 2000). Mg and Ms are recognised to have a wider host range

than Mm. In addition to infecting chickens and turkeys, Mg infections have been reported in geese, ducks, peafowl, pheasant, red-legged partridge, quail and an

Amazon parrot. It appears to be a primary pathogen in game birds (McMartin et al., 1996; Ganapathy and Bradbury 1998) and is frequently detected in cases of

upper respiratory disease in UK pheasants and red-legged partridges (Bradbury et al., 2001b). It may also be pertinent to note that the population of game birds in the

UK has shown a considerable expansion recently but there is no evidence as yet that links game birds with spread of Mg to commercial poultry. Wild birds may also be

implicated in Mg infections. For example it was isolated from two peregrine falcons at a recovery centre in Spain (Poveda et al., 1990) and since 1994 Mg has emerged as a

major pathogen in North American finches (Ley et al., 1996; Luttrell et al., 1996) although there is little evidence of spread to poultry. In our laboratory we have recently found PCR evidence of Mg in wild UK corvids (Bradbury et al., 2000).

Ms has been isolated from natural infections in a number of hosts other than chickens and turkeys. These include guinea fowl, geese, ducks, red-legged partridge, quail, racing pigeons and in Spain it was also isolated from three house sparrows captured on a commercial poultry farm (Poveda et al., 1990). The prevalence of Ms in game birds is unclear as there are very few confirmed reports. We have isolated it, albeit very infrequently, from clinically normal pheasants (Bradbury et al., 2001a), but it did not appear to be involved in the upper respiratory disease incidents investigated in our laboratory.

 

Persistence in the environment

Earlier studies indicated that Mg and Ms could potentially survive for several days on materials such as feathers, human hair and cotton clothing (Christensen et al., 1994). One Mg strain also survived for 24 hours in the human nose. However we still do not know the relevance of these laboratory studies to the farm situation where survival might be prolonged due to protection by organic matter or exudates.

 

Properties of the organism

It is known that mycoplasmas, including Mg and Ms, can persist for long periods in the host in the face of a seemingly good immune response. Research studies are now beginning to provide explanations for this. For example, mycoplasmas were  traditionally considered to be surface pathogens but evidence is accumulating to suggest that some may become intracellular and thus have a means of avoiding the effects of antibodies and antibiotics. This has been shown to occur in vitro with Mg (Winner et al., 2000) and may well occur in birds. Variation among Mg ans Ms strains has been well recorded in the literature, with some ‘atypical’ strains proving difficult to detect in the field by serological testing. It has emerged more recently that several mycoplasmas, including Mg and Ms, have sophisticated mechanisms which result in variation (phenotypic switching) of their surface antigens. Such alterations are presumed to allow subpopulations of mycoplasmas to avoid the immune response during the course of infection (Levisohn et al., 1995). Despite the very small number  of genes in mycoplasmas, the proportion dedicated to antigenic cell surface variation is impressively large and with Mg can represent up to 16% of the genome (Bassegio et al., 1996). This suggests that evasion of the host’s immune system by varying its surface components at high frequency is very important to the success of Mg as a  pathogen and could explain how it is able to persist in the host. A similar situation seems to exist in Ms where a multigene family is responsible for variation in the size and expression of certain important membrane antigens (Noormohammadi et al., 1998).

 

Conclusions

The mycoplasma tends to be a subtle pathogen, often appearing to be relatively harmless. The infections do not make news headlines like Newcastle disease or salmonella infections but a mycoplasma break in a valuable breeding flock can have serious consequences. In view of this and the fact that the organism can change its surface ‘appearance’ to avoid recognition by its host, the mycoplasma may justifiably be likened to ‘a wolf in sheep’s clothing’.

 

References

Baseggio, N., Glew, M.D., Markham, P.F., Whithear, K.G. and Browning, G.F. (1996). Size and genomic location of the pMGA multigene family of Mycoplasma gallisepticum. Microbiology, 142, 1429-1435.

 

Bradbury, J.M., Dare, C. M., Yavari, C.A. and Forrester, A. (2000). Evidence of Mycoplasma gallisepticum in British wild birds. Abstracts of the 13th Congress of the International Organization for

Mycoplasmology, Fukuoka, Japan, p 253.

 

Bradbury, J.M., Yavari, C.A. and Dare, C.M. (2001a). Detection of Mycoplasma synoviae in clinically normal pheasants. Veterinary Record, 184, 72-74.

 

Bradbury, J.M., Yavari, C.A. and Dare, C.M. (2001b). Mycoplasmas and respiratory disease in pheasants and partridges in Great Britain. Avian Pathology, 30, in press.

 

Christensen N. H., Yavari C. A., McBain A.J. and Bradbury J.M. (1994). Investigations into the survival of Mycoplasma gallisepticum, Mycoplasma synoviae and Mycoplasma iowae on materials found in the poultry house environment. Avian Pathology, 23, 127-143.

 

Ganapathy, K. and Bradbury, J.M. (1998). Pathogenicity of Mycoplasma gallisepticum and Mycoplasma imitans in red-legged partridges (Alectoris rufa). Avian Pathology, 27, 455-463.

 

Levisohn, S., Rosengarten, R. and Yogev, D. (1995). In vivo variation of Mycoplasma gallisepticum antigen expression in experimentally infected chickens. Veterinary Microbiology, 45, 219-231.

 

Ley, D.H., Berkhoff, J.E. and Mclaren, J.M. (1996). Mycoplasma gallisepticum isolated from house finches (Carpodacus mexicanus) with conjunctivitis. Avian Diseases, 40, 480-483.

 

Lierz, M., Schmidt, R., Brunnberg, L. and Runge, M. (2000). Isolation of Mycoplasma meleagridis from free-ranging birds of prey in Germany. Journal of Veterinary Medicine Series B, 47, 63-67.

 

Luttrell, M.P., Fischer, J.R., Stallknecht, D.E. and Kleven, S.H. (1996) Field investigation of Mycoplasma gallisepticum infections in house finches (Carpodacus mexicanus) from Maryland and Georgia. Avian

Diseases, 40, 335-341.

 

McMartin, D A., DaMassa, A.J., McKeen, W.D., Read, D., Daft, B. and Lam, K.M.(1996). Experimental reproduction of Mycoplasma gallisepticum disease in chukar partridges (Alectoris graeca). Avian

Diseases, 40, 408-416.

 

Noormohammadi, A.H., Markham, P.F., Duffy, M.F., Whithear, K.G., and Browning, G.F. (1998). Multigene families encoding the major haemagglutinins in phylogenetically distinct mycoplasmas. Infection and Immunity, 66, 3470-3475.

 

Poveda, J.B., Carranza, J., Miranda, A., Garrido, A., Hermoso, M. Fernandez, A. and Domenech, J. (1990). An epizootiological study of avian mycoplasmas in southern Spain. Avian Pathology, 19, 627-633.

 

Winner, F., Rosengarten, R. and Citti, C. (2000). In vitro cell invasion by Mycoplasma gallisepticum. Infection and Immunity, 68, 4238-4244.

 

JANET M. BRADBURY The mycoplasma – a wolf in sheep’s clothing? 6 Proceedings of the 24th Technical Turkey Conference