Mycoplasma penetrans

Classification

Higher order taxa

Bacteria; Firmicutes; Mollicutes; Mycoplasmatales; Mycoplasmataceae; Mycoplasma; Mycoplasma penetrans

Species

NCBI: [1]

Mycoplasma penetrans, Mycoplasma penetrans HF-2 strain

Description and significance

Mycoplasma penetrans looks like an elongated flask and has a tip-like structure at one pole of the cell which facilitates it to penetrate into the eukaryotic cell (3). Mycoplasma penetrans are parasitic bacteria and inhabit humans specifically in the urogenital and respiratory tracts (1). Because the Mycoplasma penetrans genome sequence, ~1.3Mb, is larger than those of Mycoplasma pneumoniae, Mycoplasma genitalium, Mycoplasma pulmonis and Ureaplasma urealyticum, which range from 0.57 to 0.95 Mb, it is important to have its genome sequenced because this contrast suggests that this organism may possess additional genetic information involved in its unique infection process (1). The first time Mycoplasma penetrans was isolated was from a urine sample from a human immunodeficiency virus (HIV)-infected patient (2). In addition, Mycoplasma penetrans was also isolated from a patient with a case of primary antiphospholipid syndrome and not infected with HIV (3). This suggests that Mycoplasma penetrans can be pathogenic to humans without HIV (3).

Genome structure

Shotgun sequencing was used to sequence this organism. The genome size of Mycoplasma penetrans HF-2 strain was sequenced to be approximately 1,358,633 bp (3). Mycoplasma penetrans has a single circular chromosome which contains 1038 predicted coding sequences (CDSs) (3). Within the 1038 CDSs, 463 are specific to Mycoplasma penetrans (3). Mycoplasma penetrans have the minimum range of genome sizes that are necessary for self-replication (4). In general, Mycoplasmas are the simplest self-replicating bacteria (3).

Cell structure and metabolism

Mycoplasmas penetrans, like the other Mycoplasma species do not have a cell wall (4). They also do not have most of the necessary genes for nutrient metabolism and thus adopt a lifestyle of a parasitic nature in host organisms (4). They have an elongated flask-like structure with a tip-like structure at one pole of the cell which may be what allows the mycoplasma to adhere to and invade the host cells (5).

Mycoplasma penetrans lacks uridine kinase, which is an essential cellular gene that is involved in pyrimidine metabolism (1). The phosphotransferase, uridine kinase, mediates phosphorylation of uridine and cytidin to make uridine and cytidine monophosphate (UMP/CMP) (1). In addition to uridine kinase, Mycoplasma penetrans also lacks the 5'-nucleotidase that metabolizes UMP and CMP to uridine and cytidine (1). Mycoplasma penetrans contains the uracil phosphoribosyltransferase (Upp) genethat is used to convert uracil to UMP, thus this Upp-dependent uracil conversion might be the main pathway for the production of UMP in the Mycoplasma penetrans (1). Mycoplasma penetrans also has another pathway that converts carbamoyl-phosphate to UMP via orotate-related metabolism (1).

Mycoplasma penetrans has a set of genes that code for enzymes which are involved in orotate-related metabolism (1). These include: aspartate carbamoyltransferase, dihydroorotase, dihydoorotate oxidase, orotate phosphoribosyltransferase, orotidine-5'-phosphate decarboxylase, and the pyrimidine operon regulatory protein (1). Orotate-related metabolism is related to an ATP synthesis system called the arginine dihydrolase pathway (1). The enzymes that participate in this pathway include: arginine deaminase, ornithine carbomoyltransferase, and carbamate kinase (1). Mycoplasma penetrans is the only species of Mycoplasmataceae to have a orotate-related metabolism that is related to the arginine dihydrolase pathway and pyrimidine metabolism (1).

Ecology

Describe any interactions with other organisms (included eukaryotes), contributions to the environment, effect on environment, etc.

Mycoplasma penetrans is an intracellular bacterial pathogen (1). Thus its interaction with humans is of a parasitic sort.

Pathology

How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.

So far found only in humans, Mycoplasma penetrans is an intracellular bacterial pathogen. It typically penetrates into human cells and infects humans in the urogenital and respiratory tracts. It attaches to host epithelial cells with its tip structure, the attachment organelle. Mycoplasma penetrans is particularly associated with HIV-1 infection. There are Anti-M. penetrans antibodies found in patients in the process of developing AIDS, as well as, asymptomatic HIV carriers. There is a rapid decline in CD4-positive lymphocyte counts in M.penetrans-seropositive HIV-infected individuals. There is also mitogenic effects of M. penetrans on lymphocytes. This implies that infection of Mycoplasma penetrans will deteriorate the immune system in HIV infection. Mycoplasma penetrans has also been suggested to be a cause of non-HIV related urethritis and respiratory disease. Mycoplasma penetrans was also isolated in a healthy HIV- negative patient in the form of the HF-2 strain.

As parasitic bacteria, mycoplasmas can continue to colonize the host even in the presence of a specific immune response. This property of mycoplasmas may explain the slowly progressive chronic manifestations of mycoplasma-associated diseases. The mechanisms for evasion of host immune responses in mycoplasmas are poorly understood. However, a number of recent studies have demonstrated that many mycoplasma species can modify their surface antigenic molecules with high frequency (31, 32), which might play a key role in circumventing the host immune system. The rapid change of surface antigenic molecules may generate phenotypic heterogeneity in the propagating mycoplasma population and provide advantages not only for evasion of host immune responses but also for other aspects of mycoplasma survival, such as adaptation to environmental changes. (4)

Application to Biotechnology

Does this organism produce any useful compounds or enzymes? What are they and how are they used?

Current Research

The complete nucleotide sequence of Mycoplasma penetrans HF-2 strain was determined. In the analysis of the genomic sequence, it was revealed that Mycoplasma penetrans possesses a large number of paralogous gene repertoires with chromosomal structures that allow for antigenic variation. This influences how persistent they are at infecting human hosts (1).

Enter summaries of the most recent research here--at least three required

References

1 Sasaki, Y., J. Ishikawa, A. Yamashita, K. Oshima, T. Kenri, K. Furuya, C. Yoshino, A. Horino, T. Shiba, T. Sasaki and M. Hattori. “The complete genomic sequence of Mycoplasma penetrans, an intracellular bacterial pathogen in humans.” Nucleic Acids Research. 2002. Volume 30 No. 23. p. 293-5300.

2 Lo, S.C., Hayes, M.M., Tully, J.G., Wang, R.Y., Kotani, H., Pierce, P.F., Rose, D.L., and Shih, J.W. "Mycoplasma penetrans sp. nov., from the urogenital tract of patients with AIDS." Int. J. Syst. Bacteriol. 1992. Volume 42. p. 357-364.

3 Ferrer-Navarro M, Gomez A, Yanes O, Planell R, Aviles FX, Pinol J, Perez Pons JA, Querol E. “Proteome of the Bacterium Mycoplasma penetrans.” J. Proteome Res. 2006. Volume 5 No 3. p.688 -694.

4 A. Horino, Y. Sasaki, T. Sasaki, and T. Kenri. “Multiple promoter inversions generate surface antigenic variation in Mycoplasma penetrans.” Journal of Bacteriology. 2003. Volume 185. No 1. p. 231-242

5 Röske K, Blanchard A, Chambaud I, Citti C, Helbig JH, Prevost MC, Rosengarten R, Jacobs E. “Phase variation among major surface antigens of Mycoplasma penetrans.” Infection and immunity. 2001. Volume 69. No 12. p. 7642-51.

6 Bendjennat M, Blanchard A, Loutfi M, Montagnier L, Bahraoui E. “Role of Mycoplasma penetrans Endonuclease P40 as a Potential Pathogenic Determinant.” Infection and Immunity. 1999. Vol 67. No 9. p. 4456-62.

7 Hussain AI, Robson WL, Kelley R, Reid T, Gangemi JD. “Mycoplasma penetrans and Other Mycoplasmas in Urine of Human Immunodeficiency Virus-Positive Children.” 1999. Vol 37. No 5. p. 1518-1523.

8 M. Tarshis, A. Yavlovich, A. Katzenell, I. Ginsburg, and S. Rottem. “Intracellular Location and Survival of Mycoplasma penetrans Within HeLa Cells.” Current Microbiology. 2004. Vol 49. No 2. p. 136-140.

9 [http://www.liebertonline.com/doi/pdf/10.1089/hyb.2006.046?cookieSet=1. Ferraz AS, Belo EF, Coutinho LM, Oliveira AP, De Gaspari EN. “Rapid and efficient preparation of monoclonal antibodies against 35 kDa lipoprotein of Mycoplasma penetrans.” Hybridoma. 2007. Vol 26. No 2. p. 92-97.

Edited by Ling Tsay, student of Rachel Larsen and Kit Pogliano