Mycoplasma synoviae
A Microbial Biorealm page on the genus Mycoplasma synoviae
Classification
Higher order taxa
Bacteria; Firmicutes; Mollicutes; Mycoplasmataceae; mycoplasma; synoviae (2)
Species
Mycoplasma synoviae
Description and significance
Mycoplasma synoviae is a Gram-negative parasitic bacteria responsible for causing respiratory tract disease and synovitis (inflammation in the lining of the joints) in turkeys and chickens, although other types of birds are susceptible as well. Naturally, this causes significant economic problems in the poultry industry. The primary habitat is the mucous membranes of the respiratory tract of the birds that are infected, although the joints are also affected. Infection occurs primarily through attachment of the bacteria to the host cell by means of specialized surface proteins and adhesins that results in prolonged intracellular persistence that may cause lethality if combined with a secondary virus. (1) (2)
Genome structure
Mycoplasma synoviae has one circular chromosome that is made up of 799, 476 bp with a total of 694 ORFs and a G+C content of 28.5mol%. There are 672 protein genes and 41 RNA genes. This information is based on Mycoplasma synoviae strand 53, which was isolated from a broiler breeder chicken from Brazil. (1)
The phylogeny of mollicutes is interesting as regards the degeneration of the genome. During their evolutionary history multiple reductions in genome size have occurred, the usual genetic code has been altered, and the overall rate of evolution uncharacteristically high. One suggested reason for the reduction in genome size is the evolution of mollicutes into strict parasites making much of their metabolic machinery obsolete. (7)
Cell structure and metabolism
Like all mycoplasma, Mycoplasma synoviae is phenotypically distinguishable by its small size (0.3-0.8 microns in diameter) as well as its lack of a cell wall. The cell membrane is rich in protein components that consists of adaptive lipoproteins that work to attach the cell to a host and invade their immune system. It is also non-motile due to the lack of flagella. Over the many years of evolutionary development, Mycoplasma synoviae has lost all genes required for amino acid and cofactor synthesis as well as synthesis of the cell wall and lipid metabolism. It also does not have a urea cycle. As a result, the substrates and cofactors needed must be taken from the host or artificial culture. Examples include nicotinamide adenine dinucleotide (NAD) and amino acids. It has also lost many genes required for other cellular processes, such as signal transduction, transcription factors, regulatory genes, and cell division. It is also lacking genes coding for components of energy metabolism so it is mostly dependent on glycolysis in order to produce ATP. (1) (9)
Ecology
Mycoplasma synoviae can be transmitted by the respiratory route or by egg transmission and colonize primarily in the respiratory systems of birds such as chickens and turkeys. It has been determined that chickens are more susceptible than turkeys to the pathogen. Other birds cannot acquire the pathogen by natural means, though intravenous inoculation can cause pheasants and geese to be affected. Ducks and other specimens of birds seem to be unaffected by the pathogen. (8)
This pathogen is significant because it reduces optimal production, raises food conversion rates, and leads to downgrading of carcasses in poultry. There is also reason to believe that it can lead to a reduced egg production and a lowered rate of viable hatching chicks, though evidence is sketchy at best for now. This is because egg transmission occurs at a low rate and many factors modify its transmission. (9)
Pathology
Mycoplasma synoviae does not cause any lethal diseases alone. What it does do though is contribute to the destabilization of the immune system to allow secondary infections such as infectious bronchitis or Newcastle disease to develop respiratory syndromes of severe impact such as respiratory lesions. In other words, Mycoplasma synoviae acts as an initiating agent to soften up the immune system so that a virus can take effect more prominently. The infection appears to be worldwide, though it is only prevalent in chickens and turkeys, although other types of birds can contract it under experimental conditions. Symptoms include swollen feet, paleness in the face, ruffled feathers, and inappetance. Rarer symptoms include diarrhea, emaciation, and acute anemia. It is also very likely that there are no noticable symptoms at all, in which case the only possible way to detect the pathogen is via a blood sample. Mortality is low unless another virus is present as well, in which case recovery may be impossible. (3) (5) (8)
A prominent difference between Mycoplasma synoviae and the similar pathogen Mycoplasma gallisepticum is that the first tends to infiltrate other organs of the bird's body, while the latter does not. Examples include the heart, liver, and spleen. Another prominent difference is the symptom of arthritis, which rarely occurs in Mycoplasma gallisepticum. Additionally, Mycoplasma synoviae acts together with other viruses to also cause air sacculitis in chickens and turkeys, which causes inflammation of the air sacs that all birds have. However, subclinical respiratory tract infection remains as the most common form of infection. (7) (8)
Application to Biotechnology
Thus far, it seems that the only benefit of Mycoplasma synoviae is that those birds that recover from infection seem to be resistant to foot pad challenge, meaning that their legs had become stronger than before. (7)
Current Research
1) The first study was done to analyse the indirect transmission properties of Mycoplasma synoviae. Chickens were introduced to an insolated area that was previously contaminated by Mycoplasma synoviae broth culture. 34 days later, these birds were eliminated and replaced by healthy chicks without disinfecting. Chicks were also placed in an isolated area containing food, feathers, and dust that came from an infected laying hen flock. In all three situations, the chicks contracted the pathogen but it took longer for the chicks that were in the habitat containing infected food, feathers, and dust. It was determined that Mycoplasma synoviae could be transferred indirectly and contaminated materials, such as feathers, food, and dust, that can infect chicks even after remarkably long silent periods. (4)
2) A quick, qualitative test to determine the presence of Mycoplasma synoviae was found by means of the Rapid Slide Agglutination (RPA) Test. This test is used to determine the presence of antibodies in serum of the blood from potentaially infected birds that react with the Mycoplasma synoviae antigens. "Briefly, the test consists of mixing a drop of test anitsera with a commercially produced stained mycoplasma antigen on an agglutination tile for 2-3 minutes. The presence of agglutination when compared with appropriate controls is indicative of a positive result, indicating that the sample contains antibodies to Mycoplasma synoviae. " If the antibodies are present in the serum sample, then it confirms that the source animal has been challenged by Mycoplasma synoviae antigens or was recently vaccinated. (5)
3) In order to determine the range of its pathogenicity, scientists used intravenous inoculations to inject Mycoplasma synoviae into various other birds aside from chickens and turkeys to determine whether any other bird could concievably contract any symptoms. Pheasants, guinea fowl, and geese suffered from joint pain and respiratory infection, though the effects of the respiratory infection were minor. Ducks and other kinds of birds tested, including British wild fowl and exotic birds found in zoos, were unaffected. (8)
References
(1)Vasconcelos, AT. "Genome Project - Mycoplasma Synoviae 53 Project At LNCC - Laboratorio Nacional De Computacao Cientifica." NCBI. 18 Aug. 2005. PubMed. 2 May 2007 <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=genomeprj&cmd=Retrieve&dopt=Overview&list_uids=10676>.
(2)Gattiker, Alexandre. "HAMAP: Mycoplasma Synoviae (Strain 53) Complete Proteome." ExPASy. 7 Nov. 2002. Swiss Institute of Bioinformatics. 2 May 2007 <http://expasy.org/sprot/hamap/MYCS5.html>.
(3)McMullin, Paul. "Mycoplasma Synoviae Infection, M.S. Infectious Synovitis." ThePoultrySite.Com. 1 Jan. 2004. 5M Enterprises Ltd. 2 May 2007 <http://www.thepoultrysite.com/diseaseinfo/99/mycoplasma-synoviae-infection-ms-infectious-synovitis>.
(4)Picault, JP, C Marois, M Kobisch, and I Kempf. "Experimental Evidence of Indirect Transmission of Mycoplasma Synoviae." NCBI. Winter 2005. PubMed. 2 May 2007 <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16120251&dopt=Abstract>.
(5)Bell, M. "TC0308 Mycoplasma Synoviae Rapid Slide Agglutination (RSA) Test." TDS. Dec. 2004. OIE Manual of standards for Diagnostic Tests and Vaccines 2000. 2 May 2007 <http://www.defra.gov.uk/corporate/vla/lab-test/surv/ltd-tc0308.pdf>.
(6)Salisch, H, M Ryll, R Leise, and U Neumann. "Use of an Alkaline Phosphatase-Labelled Probe for the Detection of Mycoplasma Synoviae in Chickens." Blackwell Synergy. Feb. 2000. Journal of Veterinary Medicine Series B. 2 May 2007 <http://www.blackwell-synergy.com/links/doi/10.1046/j.1439-0450.2000.00312.x/full/>.
(7)Chan, Voon L., Philip M. Sherman, and Billy Bourke, eds. "Bacterial Genomes and Infectious Diseases". Totawa: Humana P, 2006. 177-186.
(8)Tully, J G., and R F. Whitcomb, eds. "The Mycoplasmas-Human and Animal Mycoplasmas". Vol. II. New York: Academic P, 1979. 17-21.
(9)Razin, S, and M F. Barile, eds. "The Mycoplasmas-Mycoplasma Pathogenicity". Vol. IV. Orlando: Academic P, Inc., 1985. 124-128.
Edited by Robert Rishwain, student of Rachel Larsen and Kit Pogliano
KMG
