Harold L. Watson

Ureaplasma urealyticum intrauterine infection: role in prematurity and disease in newborns.

Ureaplasma urealyticum, a common commensal of the urogenital tract of sexually mature humans, is gaining recognition as an important opportunistic pathogen during pregnancy. While its etiologic significance in many aspects of adverse pregnancy remains controversial, recent evidence indicates that U. urealyticum in the absence of other organisms is a cause of chorioamnionitis. Furthermore, ureaplasmal infection of the chorioamnion is significantly associated with premature spontaneous labor and delivery. In at least some cases, it appears to be causal. Present evidence indicates that U. urealyticum is a cause of septicemia, meningitis, and pneumonia in newborn infants, particularly those born prematurely. There is strong but not definitive evidence that ureaplasmal infection of the lower respiratory tract can lead to development of chronic lung disease in very low-birth-weight infants. Although risk factors for colonization of the lower genitourinary tract have been identified, little information is available concerning risk factors for intrauterine infection and host immune responses to invasive infection. Recent establishment of animal models of respiratory and central nervous system diseases should provide an opportunity to evaluate risk factors, pathogenic mechanisms, and operative immune mechanisms. However, the most critical need is additional information concerning indications for diagnosis and treatment as well as efficacy of treatment. Images

Gender Is a Major Factor in Determining the Severity of Mycoplasma Respiratory Disease in Mice

ABSTRACT Gender is a significant factor in determining the susceptibility to and severity of pulmonary diseases in both humans and animals. Murine respiratory mycoplasmosis (MRM), due to Mycoplasma pulmonisinfection, is an excellent animal model for evaluation of the role of various host factors on the development of acute or chronic inflammatory lung diseases. MRM has many similarities to mycoplasma respiratory disease in humans. The purpose of the present study was to determine whether gender has a significant impact on lung disease due to M. pulmonis infection in mice. It was demonstrated that male mice consistently developed more severe disease in the lung parenchyma than did female mice. There was no gender difference in disease severity along the airways or any difference in mycoplasma numbers in lungs of male and female mice. Furthermore, surgical removal of reproductive organs reduced the severity of mycoplasma disease and the numbers of mycoplasma organisms recovered from lungs. Thus, gender plays a significant role in determining the severity of M. pulmonis disease. In fact, the gender of the host was a major factor in determining whether an acute or chronic inflammatory lung disease developed after infection with M. pulmonis.

Mycoplasma penetrans bacteremia and primary antiphospholipid syndrome.

Mycoplasma penetrans, a rare bacterium so far only found in HIV-infected persons, was isolated in the blood and throat of a non-HIV-infected patient with primary antiphospholipid syndrome (whose etiology and pathogenesis are unknown).

Mycoplasma pulmonis V-1 surface protein variation: occurrence in vivo and association with lung lesions☆

The V-1 antigen of Mycoplasma pulmonis is exposed to the surface of the mycoplasma and has an immunoblot banding pattern that varies in vitro between and within strains. To determine if V-1 variation occurs in vivo, we infected C3H/HeNCr mice intranasally with 5 X 10(8) colony-forming units of M. pulmonis strain 5782C. We isolated M. pulmonis clones from the respiratory tracts of mice up to 28 days post-infection, then used anti-V-1 monoclonal antibody P39 to visualize their V-1 immunoblot banding patterns. By the 28th day following infection, 92% of the recovered clones had variant V-1 banding patterns. Additionally, there was a significant correlation between the severity of lung lesions and the percentage of V-1 variant clones recovered from the respiratory tracts of individual mice. These studies prove that V-1 variation does occur in vivo, and suggest that mice with more severe pulmonary lesions tend to have more V-1 variant clones as a percentage of the M. pulmonis population. Thus, variation in the V-1 protein may be a mechanism by which M. pulmonis persists in the in vivo environment, possibly by evasion of host immune surveillance or by alteration of its surface membrane to take better advantage of its environmental niche in the host.

Two genomic clusters among 14 serovars of Ureaplasma urealyticum

Summary Fourteen established serovars of Ureaplasma urealyticum were examined by restriction endonuclease cleavage patterns of genomic DNA, Southern blot hybridization and DNA-DNA hybridization. The restriction endonuclease cleavage patterns and the Southern blot hybridization both revealed that the 14 serovars are divided into two clusters. The DNA-DNA hybridization data further confirmed that these two clusters are genetically distinct of each other.

Nystatin induces secretion of interleukin (IL)-1β, IL-8, and tumor necrosis factor alpha by a toll-like receptor-dependent mechanism

ABSTRACT Nystatin is an antifungal compound with potent proinflammatory properties. Herein, we demonstrate that nystatin induces interleukin (IL)-1β, IL-8, and tumor necrosis factor alpha secretion through its activation of toll-like receptor 1 (TLR1) and TLR2. Hence, a TLR-dependent mechanism could serve as the molecular basis for the proinflammatory properties of nystatin.

Research letterCharacterization of a major Mycoplasma penetrans lipoprotein and of its gene

A novel mycoplasmal species designated as Mycoplasma penetrans has been isolated recently from patients infected with human immunodeficiency virus. p35, a major antigen extracted from the membrane of this mycoplasma using Triton X-114 has been found to be a lipoprotein. After proteolytic treatment of p35, the sequence of one of the resulting peptides was determined and a corresponding oligonucleotide was deduced. Using this oligonucleotide as a probe the p35 gene was cloned and sequenced. Sequence analysis revealed an amino-terminal signal peptide with a potential acylation site which would result in a 35.3 kDa mature product. In addition, the p35 gene was followed by an open reading frame with a corresponding polypeptide partially homologous to p35, in particular to the N-terminus region.