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Molecular epidemiology of Pneumocystis carinii pneumonia.

C. B. Beard,T. Navin

Published 1996 in Emerging Infectious Diseases

ABSTRACT

Although reactivation of latent infections has long been considered the primary explanation for PCP in immunosuppressed patients, over the years a steady flow of reports has described clusters of PCP cases (2). In addition, recent studies have suggested that the duration of latency is very limited, i.e., usually less than 1 year (3,4). Still other studies have demonstrated genetic variation in PCR-amplified P. carinii DNA from the lungs of patients during subsequent PCP episodes (5). Together, these observations provide strong circumstantial evidence of person-to-person transmission of P. carinii. Consequently, establishing the role that person-to-person transmission plays in the epidemiology of PCP is urgent. Another important area of PCP epidemiology is determining the predisposing factors for disease. The most frequently discussed predictor of disease is CD4+ cell count, specifically as it relates to care and management of AIDS patients (6); however, it has long been known that malnutrition can be an important contributor (7). The degree to which other factors such as viral infections or pneumonitis of other causes, may come into play, is yet to be shown. Much can also be learned regarding the epidemiology of PCP in HIV-infected infants. Recent studies report that primary infections in these infants often develop when the child is 3 to 6 months old (8,9). The source of these patients’ P. carinii infections (i.e., the hospital setting, their mothers, other children, or an environmental source) is not known. Clinicians working with AIDS patients need a sensitive, reliable, and noninvasive tool for early detection and diagnosis of PCP infections (10,11). Besides the standard procedures of bronchoalveolar lavage (BAL) and induced sputum (IS) sampling, recent studies indicate that it is possible to amplify P. carinii DNA sequences by polymerase chain reaction (PCR) directly from blood or serum samples and from nasopharyngeal aspirates of PCP patients (11,12). Further studies are needed to confirm that a PCR-based diagnostic tool superior to microscopy can be adapted for use in clinical settings. A serologic tool that will distinguish recent PCP infections from those past is also needed. Prophylaxis failures have been reported for both trimethoprim-sulfamethoxazole (TMP-SMX) and pentamidine (13-16). Studies evaluating these cases, however, are frequently complicated by the difficulties in assessing and confirming patient compliance with the prophylaxis regimen. The only factor that has a significant correlation with failure in most cases, however, is the patient’s CD4+ T lymphocyte count (14). Although this correlation would be expected because of the general increased risk for PCP associated with CD4+ cell depletion (6) and the increase in prophylaxis complications in HIV-infected patients (17), these drugs may not eliminate all organisms, and some degree of patient immunity may be required to clear or control the infection. What role, if any, specific antimicrobial resistance mechanisms play in the reported treatment failures has not been shown; however, the emergence of resistance is always a threat. Likewise, long-term TMP-SMX prophylaxis increases the possibility for the selection of antimicrobial resistance in bacterial pathogens, some of which are important potential causes of pneumonia in HIV-infected patients (18). Identifying potential antimicrobial resistance mechanisms in P. carinii is difficult because of the lack of an established culture system for human P. carinii that would allow traditional antimicrobial sensitivity testing. At least three separate lines of data suggest that P. carinii is a commonly encountered organism: the high seroprevalence rates reported in normal populations (19), the rapid rate at which infants acquire primary infections (8) and AIDS patients become reinfected after successful treatment (20), and the amplification of P. carinii-specific DNA from ambient air sampled from the environment (e.g., an apple orchard) (21) and from rooms of animals and patients with PCP (22). Airborne transmission has been demonstrated for PCP in rats (23-26) and is by far the most likely mechanism proposed for natural exposure to P. carinii in humans (2,22). Given the similarities Commentary

PUBLICATION RECORD

  • Publication year

    1996

  • Venue

    Emerging Infectious Diseases

  • Publication date

    Unknown publication date

  • Fields of study

    Biology, Medicine

  • Identifiers
    PMID 8903219PMCID 2639819
  • External record

    Open on Semantic Scholar

  • Source metadata

    Semantic Scholar, PubMed

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