M. penetransis an intracellular bacterial pathogen to humans. As its name indicating, penetration into human cells is a typical feature of M. penetrans. In human diseases, M. penetrans mainly associates with the human immunodeficiency virus (HIV)-1 infection. In adult, 20-40% of HIV-positive homosexual population in Europe and the U. S. A. are infected with M. penetrans. Among both homosexual and heterosexual male population are infected with M. penetrans in South America. Anti-M. penetrans antibodies are developed even in asymptomatic HIV carriers and in patients in the process of developing AIDS. Rapid declaration of CD4-positive lymphocyte counts in M. penetrans-seropositive HIV-infected individuals was reported. Since M. penetrans has mitogenic activity to lymphocytes from HIV-infected individuals, it may be suggested that persistent M. penetrans infection may contribute to the deterioration of the immune system in HIV-infection. On the other hand, M. penetrans infection has also been suggested to be a primary cause of human disease in non-HIV-related urethritis and respiratory disease (Emerging Infect. Dis. 5: 164-167, 1999). In this case, the patient had acute onset of arthritis, fever, progressive asthenia, hemplytic anemia and severe respiratory distress. On day 4 of admission to hspital, the patient required a ventilator and was admitted to the intensive care unit. With the development of anticardiolipin antibodies, the patient was diagnosed as anti-phospholipid syndrome. No virus and bacteria except M. penetrans was isolated from the patient. Three strains were isolated from this patient, HF-1 from blood, HF-2 from tracheal aspirate and HF-3 from throat. The patient was cured rapidly by treatment with clindamycin, to which the clinical isplate of M. penetrans is sensitive.
In order to investigate bacterial pathogenicity of this new agent to humans, whole genome sequence of M. penetrans HF-2 strain was determined.
Shotgun libraries inserted with hydrodynamically shared genomic DNA with 1-2 kbp and 4-5 kbps lengths were sequenced. Sequence data were assembled by using the Phred/Phrap/Consed package of base-calling, sequence-assembly and automated finishing software. The assembled data were confirmed by the pattern of pulse-field gel electrophoresis after digestion with restriction enzymes. Coding sequences (CDSs) were predicted by using the program GLIMMER which trained with CDSs of M. genitalium, M. pneumoniae and Ureaplasma urealyticum and then confirmed by using the program FramePlot (FEMS Microbiol. Lett. 174:251-253), which was modified for Mycoplasma genome.