Pneumocystis carinii Infection Linked to Sudden Infant Death Syndrome

WESTPORT, Jan 11 (Reuters Health) - Pneumocystis carinii infection is associated with sudden infant death syndrome (SIDS), researchers report in the December 1999 issue of Clinical Infectious Diseases.

Dr. Sergio L. Vargas, of the University of Chile in Santiago, and multinational colleagues point out that there is well-documented serological evidence that primary P. carinii infection is common in very young immunocompetent children. To determine whether there is histological support for that assumption, they evaluated lung autopsy samples from 534 consecutive pediatric patients at Santiago hospitals who did not have AIDS or malignancies.

The researchers detected P. carinii infection in 25% of 16 children aged 5 days to 1 year who had died of SIDS, compared with only 2.9% of 342 children in the same age group who had died of other causes. The difference was statistically significant, they report.

In further study of an additional 161 cases of SIDS, Dr. Vargas and colleagues found that 35.1% of 134 infants from Chile and 14.8% of 27 infants from Oxford, UK, tested positive for P. carinii infection.

The researchers categorized 88.1% of 42 cases of P. carinii-associated SIDS as stage 1 or 2. This suggests, they say, that "...primary infection was asymptomatic in most SIDS cases." In support of this idea, the authors note that "...the load of P. carinii organisms in SIDS cases was mild, and clusters were difficult to find histologically. Therefore, the terminal event of SIDS cannot be explained by these findings under the current understanding of P. carinii disease."

Dr. Vargas' group suggests that "[a] possible explanation for the pathogenic role of P. carinii in some infants with SIDS is that it reduces the level of pulmonary surfactant," noting that previous studies have found decreased levels of surfactant in infants with SIDS. The higher frequency of P. carinii infection in these infants could also be an indication of an underlying immune defect, they note.

Clin Infect Dis 1999;29:1489-1493.