The pathogenesis and treatment of mycoplasmal infections

Nicolson, Garth L.; Nasralla, Marwan Y.; Nicolson, Nancy L.

doi:10.1016/s1069-417x(00)88885-8

Cited by 18 publications

(29 citation statements)

References 39 publications

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“…Changes in culture conditions for mESCs could lead to the loss of the ability for self-renewal, induction of differentiation and finally loss of the ability to contribute to the germline (Nagy et al 2003;Buehr et al 2003;Tielens et al 2006). Mycoplasma-infected mESCs at passage P13?6, where approximately 580 mycoplasmas were associated with each mESC, showed severely reduced expression of POU5F1 and SSEA-1 markers (46.3%).…”

Section: Discussionmentioning

confidence: 99%

“…At passages P13?5, P13?10, P13?15 and P13?20, 15 to 20 mESCs were injected into each d3.5 blastocyst and embryo transfers with seven blastocysts per uterine horn were performed as described (Nagy et al 2003). Control mESCs were injected and transferred first.…”

Section: Production Of Chimeric Progeny and Germline Transmissionmentioning

confidence: 99%

“…Under optimal culture conditions, they maintain pluripotent properties (Nagy et al 2003) and express characteristic markers, including the stage specific embryonic antigen-1 (SSEA-1) and the POU5F1 (also known as OCT-4) transcription factor (Knowles et al 1978;Scholer et al 1990). When introduced into pre-implantative host embryos they can contribute to somatic tissues and the germline (Bradley et al 1984;Gossler et al 1986).…”

Section: Introductionmentioning

confidence: 99%

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Mycoplasma contamination of murine embryonic stem cells affects cell parameters, germline transmission and chimeric progeny

et al. 2008

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Murine embryonic stem cells (mESCs) inoculated at passage P13 with the mycoplasma species M. hominis, M. fermentans and M. orale and cultured over 20 passages showed reduced growth rate and viability (P < 0.0001) compared to control mESCs. Spectral karyotypic analysis of mycoplasma-infected mESCs showed a number of non-clonal chromosomal aberrations which increased with the duration of infection. The differentiation status of the infected mESCs was most affected at passage P13+6 where the infection was strongest and 46.3% of the mESCs expressed both POU5F1 and SSEA-1 markers whereas 84.8% of control mESCs expressed both markers. The percentage of germline chimeras from mycoplasma-infected mESCs was examined after blastocyst injection and embryo transfer to suitable recipients at different passages and, compared to the respective control group, was most affected at passage P13+5 (50% vs. 90%; P < 0.07). Further reductions were obtained at the same passage in the percentage of litters born (50% vs. 100%; P < 0.07) and in the percentage of pups born (22% vs. 45%; P < 0.001). Thirty three chimeras (39.8%) obtained from blastocyst injection with mycoplasma-infected mESCs showed reduced body weight (P < 0.0001), nasal discharge, osteoarthropathia, and cachexia. Flow cytometric analysis of plasma from chimeras produced with mycoplasma-infected mESCs revealed statistically significant differences in the proportions of T-cells and increased levels of IgG1 (P < 0.001), IgG2a (P < 0.05) and IgM (P < 0.05), anti-DNA antibodies (P < 0.05) and rheumatoid factor (P < 0.01). The present data indicate that mycoplasma contamination of mESCs affects various cell parameters, germline transmission, and postnatal development of the resulting chimeras.

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Section: Discussionmentioning

confidence: 99%

Section: Production Of Chimeric Progeny and Germline Transmissionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mycoplasma contamination of murine embryonic stem cells affects cell parameters, germline transmission and chimeric progeny

et al. 2008

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“…Despite the growing awareness of the previously widely neglected significance of mycoplasmas in classical but also newly emerging clinical manifestations, little is known about the interference with the host cell metabolism and the immune response during infection (7,10). We recently identified the nonmevalonate, 2-C-methyl-D-erythritol-4-phosphate (MEP) pathway of isoprenoid biosynthesis in a wide range of microbial infectious agents and were able to correlate the presence of this pathway with the pathogen's ability to stimulate human V␥9/V␦2 T cells (6).…”

Section: While Most Mycoplasma Species Appear To Have Evolutionarily mentioning

confidence: 99%

Mycoplasma penetrans Is Capable of Activating Vγ9/Vδ2 T Cells While Other Human Pathogenic Mycoplasmas Fail To Do So

et al. 2004

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“…Broad-range bacterial PCR uses primers to recognize conserved sequences of bacterial chromosomal genes encoding rRNA (Dicuonzo et al, 1999). This method is now considered a reliable clinical test for identifying the specific causative species of endocarditis when resected heart valve material is available (Nicolson et al, 1998;Millar et al, 2001;Houpikian & Raoult, 2005).…”

Section: Discussionmentioning

confidence: 99%

Late-onset prosthetic valve endocarditis caused by Mycoplasma hominis, diagnosed using broad-range bacterial PCR

Jamil

Sandoe

Gascoyne-Binzi

et al. 2012

Journal of Medical Microbiology

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We report what is believed to be the first case of late-onset prosthetic valve endocarditis caused by Mycoplasma hominis in a case of blood culture-negative endocarditis. The objective of this report is to emphasize the use of a broad-range PCR technique for bacterial 16S rRNA genes in identifying the causative pathogen, thus enabling targeted antimicrobial treatment. Case reportA 40-year-old male had undergone aortic (19 mm Sorin Bicarbon) and mitral (25 mm Sorin Bicarbon) valve replacement surgery for rheumatic valvular disease 9 years previously. He was slow to recover from his initial surgery, suffering from fever and lethargy post operation. Blood cultures were negative but echocardiography showed a mitral valve vegetation. The patient was treated for culture-negative endocarditis with intravenous antibiotics (gentamicin 3 mg kg 21 once daily for 2 weeks and vancomycin 1 g daily for 6 weeks), with resolution of his symptoms and the vegetation at follow-up examination.Nine years later, the patient presented with abdominal pain, dark urine, melaena, jaundice, epistaxis and intermittent pyrexia. Examination revealed a murmur of mitral regurgitation but no peripheral stigmata of endocarditis. Blood tests confirmed haemolytic anaemia. Trans-oesophageal echocardiography revealed partial mitral prosthesis dehiscence with severe paraprosthetic regurgitation, but no vegetations were seen. The aortic prosthesis was functioning normally, but there was significant tricuspid regurgitation. The patient underwent urgent mitral valve re-replacement and tricuspid valve repair. During surgery, vegetations were noted to be present on the mitral prosthesis. Microscopy and Gram staining of the explanted valve tissue showed no microorganisms, and valve bacterial culture was initially negative.DNA was extracted from the resected valve using the tissue protocol of the QIAamp DNA mini extraction kit (Qiagen). Amplification of the 16S rRNA gene was performed using the primers FD1, 59-AGAGTTTGATCCTG-GCTCAG-39 (Weisburg et al., 1991), and UR, 59-CTAC-GCATTTCACCGCTACAC-39 (Hendolin et al., 2000), with Brilliant SYBR QPCR MasterMix (Stratagene). The PCR was performed using the MX3000P QPCR platform (Stratagene) using the following programme: activation at 95 u C for 10 min followed by 40 cycles of 95 u C for 30 s, 62 u C for 1 min and 72 u C for 1 min 30 s and a final extension step at 72 u C for 10 min. The amplicons were purified using a MinElute PCR purification kit (Qiagen) and the nucleic acid sequence was determined at Lark Technologies, Essex, UK. PCR amplification and nucleotide sequencing of the bacterial 16S rRNA gene identified the organism as M. hominis from the excised tissue. The nucleotide sequences were compared with those available through the NCBI database using BLAST (http://blast.ncbi. nlm.nih.gov/Blast.cgi). The nucleotide sequence showed 99.8 % (669/670 bp) 16S rRNA gene sequence similarity to that of M. hominis.An active infection was subsequently confirmed when M. hominis was cultured from valve tissue and detect...

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The pathogenesis and treatment of mycoplasmal infections

Cited by 18 publications

References 39 publications

Mycoplasma contamination of murine embryonic stem cells affects cell parameters, germline transmission and chimeric progeny

Mycoplasma contamination of murine embryonic stem cells affects cell parameters, germline transmission and chimeric progeny

Mycoplasma penetrans Is Capable of Activating Vγ9/Vδ2 T Cells While Other Human Pathogenic Mycoplasmas Fail To Do So

Late-onset prosthetic valve endocarditis caused by Mycoplasma hominis, diagnosed using broad-range bacterial PCR

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