Search for Primary Infection by Pneumocystis carinii in a Cohort of Normal, Healthy Infants

Abstract

To determine whether Pneumocystis carinii is associated with clinical illness in the competent host, 107 normal, healthy infants were enrolled in a 2-year prospective cohort study in Chile. P. carinii was identified by specific stains and nested--deoxyribonucleic acid (DNA) amplification of the large subunit mitochondrial ribosomal ribonucleic acid gene of P. carinii f. sp. hominis, and seroconversion was assessed by enzyme-linked immunosorbent assay of serum samples drawn every 2 months. P. carinii DNA was identified in nasopharyngeal aspirates obtained during episodes of mild respiratory infection in 24 (32%) of 74 infants from whom specimens were available for testing. Three (12.5%) of those 24 infants versus 0 of 50 infants who tested negative for P. carinii had apnea episodes. Seroconversion developed in 67 (85%) of 79 infants who remained in the study by 20 months of age and occurred in the absence of any symptoms of disease in 14 (20.8%). The study indicates that P. carinii DNA can be frequently detected in healthy infants, and it raises the hypothesis that they may be an infectious reservoir of P. carinii in the community. Further investigation is needed to identify whether P. carinii causes overt respiratory disease in infants.

Molecular typing of Pneumocystis jirovecii found in formalin-fixed paraffin-embedded lung tissue sections from sudden infant death victims

“…These results reinforce the idea that infants could constitute an important part of the P. jirovecii reservoir (Durand-Joly et al, 2003;Nevez et al, 2001;Totet et al, 2003a;Vargas et al, 2001).…”

“…An association between Pneumocystis primary infection and sudden infant death syndrome (SIDS) has been reported in autopsy studies (Morgan et al, 2001;Vargas et al, 1999Vargas et al, , 2001. Pneumocystis has also been reported in noncomparative studies in infants from Oxford, UK or Rochester and Yale, USA (Morgan et al, 2001;Vargas et al, 1999).…”

“…Seroepidemiological data, obtained using several antigens, indicate that primary infection by Pneumocystis organisms is one of the most frequent infections in humans, affecting more than 90 % of normal healthy children during the first 2 years of life (Meuwissen et al, 1977;Peglow et al, 1990;Pifer et al, 1978;Vargas et al, 2001;Wakefield et al, 1990a). However, only a small amount of information is available about the infection source and the clinical or pathological changes associated with this first contact with the fungus.…”

NosocomialPneumocystis jiroveciiinfections

“…Indeed, several populations have been identified as being colonized by the fungus. Low burden of P. jirovecii organisms have been detected using PCR assays in patients with various levels of immunodeficiency (Nevez et al, 1999a;Nevez et al, 1999b), with acute or chronic pulmonary diseases (Calderon et al, 1996;Armbruster et al, 1997;Sing et al, 1999b;Nevez et al, 2002), immunonaive infants with P. jirovecii primary infection (Nevez et al, 2001a, Vargas et al, 2001, pregnant women with physiological immunity changes (Vargas et al, 2003), and health care workers in contact with patients with PCP (Miller et al, 2001, Durand-Joly et al, 2003, reviewed in Peterson et al, 2005. In fact, Pneumocystis infections can have a large spectrum of presentations, of which PCP in immunocompromised patients may represent only a part, while mild infections such as colonization may constitute the major part.…”

Contribution of T cell subsets to the pathophysiology ofPneumocystis-related immunorestitution disease

“…Although exposure to P. carinii is nearly universal, as demonstrated by the appearance of anti-P. carinii antibody in 85% of children by the age of 20 mo (35), a period of immunosuppression is essential for the development of clinical disease (15,34). Several studies have demonstrated a positive correlation between the degree of inflammation and the severity of disease (4,23,36), suggesting that the pathogenesis of Pneumocystis pneumonia (PcP) is primarily inflammatory in nature, in that infection with P. carinii is necessary to cause pneumonia, but certain aspects of the immune response against P. carinii are responsible for the associated pathophysiology (30,39).…”