A prospective study was carried out at the University Hospital, Kuala Lumpur to determine the cervical carriage rate of Ureaplasma urealyticum and Mycoplasma hominis among healthy pregnant women at delivery and the incidence of nasopharyngeal colonisation among their infants.
Congenital pneumonia is one of the common causes of respiratory distress at birth with significant morbidity and mortality in infants. Estimates show that neonatal pneumonia including congenital pneumonia contributes to between 750 000 and 1.2 million neonatal deaths every year which accounts for 10% global child mortality. Etiological agents are many and vary but atypical bacterial causes are few. The commonest cause for atypical bacteria is Ureaplasma urealyticum. Congenital pneumonia is often clinically difficult to diagnose owing to poor specificity of clinical signs, with similarities in radiologic presentation with other respiratory conditions of the newborn. Isolation of causative organism (s) by culture from nasopharyngeal aspirates or tracheal aspirates obtained within 8 hours of life is the gold standard of its diagnosis. However, this technique is elaborate and time consuming in identifying atypical bacteria. Development of a more sensitive modality such as polymerase chain reaction (PCR) has dramatically altered the microbiological diagnosis of congenital pneumonia.
Ureaplasma parvum colonizes human mucosal surfaces, primarily in the respiratory and urogenital tracts, causing a wide spectrum of diseases, from non-gonococcal urethritis to pneumonitis in immunocompromised hosts. Although the basis for these diverse clinical outcomes is not yet understood, more severe disease may be associated with strains harboring a certain set of strain-specific genes. To investigate this, whole genome DNA macroarrays were constructed and used to assess genomic diversity in 10 U. parvum clinical strains. We found that 7.6% of U. parvum genes were dispersed into one or more strains, thus defining a minimal functional core of 538 U. parvum genes. Most of the strain-specific genes (79%) were of unknown function and were unique to U. parvum. Four hypervariable plasticity regions were identified in the genome containing 93% of the variability in the gene pool (UU32-UU33, UU145-UU170, UU440-UU447 and UU527-UU529). We hypothesized that one of them (UU145-UU170) was a pathogenicity island in U. parvum and we characterized it. Thus, we propose that the clinical outcome of U. parvum infection is probably associated with this newly identified pathogenicity island.