In new pulmonary tuberculosis (TB) patients, the World Health Organization previously recommended performing sputum smear examination at the end of the second month of therapy and, if positive, to extend the intensive phase. We performed a systematic review and metaanalysis to evaluate the accuracy of a positive sputum smear or culture during treatment for predicting failure or relapse in pulmonary TB. We searched PubMed, EMBASE, and the Cochrane Library for studies published in English through December 2009. We included randomized controlled trials, cohort, and case-control studies of previously untreated pulmonary TB patients who had received a standardized regimen with rifampin in the initial phase. Accuracy results were summarized in forest plots and pooled using a hierarchical regression approach. Fifteen papers met inclusion criteria. The pooled sensitivities for both the 2 month smear (24%, 95% CI 12-42, 6 studies) and culture (40%, 95% CI 25-56, 4 studies) to predict relapse were low. Corresponding specificities (85%, 95% CI 72-90) and (85%, 95% CI 77-91) were higher, but modest. For failure, the 2 month smear (7 studies) had low sensitivity (57%, 95% CI 41-73) and higher, though modest, specificity (81%, 95% CI 72-87). Both sputum smear microscopy and mycobacterial culture during TB treatment have low sensitivity and modest specificity for predicting failure and relapse. Although we pooled a diverse group of patients, the individual studies had similar performance characteristics. Better predictive markers are needed.

Proteinuria and an elevated creatinine level were associated with an increased risk of death and development of ADI. These associations may reflect the direct role of the kidney in modulating HIV disease, or they may act as markers of greater comorbidity.

Antigenic variation of infectious organisms is a major factor in evasion of the host immune response. However, there has been no definitive demonstration of this phenomenon in the malaria parasite Plasmodium falciparum. In this study, cloned parasites were examined serologically and biochemically for the expression of erythrocyte surface antigens. A cloned line of P. fakciparum gave rise to progeny that expressed antigenically distinct forms of an erythrocyte surface antigen but were otherwise identical. This demonstrates that antigenic differences on the surface of P. fakiparum-infected erythrocytes can arise by antigenic variation of clonal parasite populations. The antigenic differences were shown to result from antigenic variation of the parasite-encoded protein, the P. falciparum erythrocyte membrane protein 1.

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The survival of Plasmodium falciparum-infected erythrocytes is enhanced by the sequestration of mature trophozoites and schizonts from the peripheral circulation. Cytoadherence of infected erythrocytes in vivo is associated with the presence of knobs on the erythrocyte surface, but we and others have shown recently that cytoadherence to C32 melanoma cells may occur in vitro in the absence of knobs. We show here that a knobless clone of P. falciparum adheres to the leukocyte differentiation antigen, CD36, suggesting that binding to CD36 is independent of the presence of knobs on the surface of the infected erythrocyte. This clone showed little cytoadherence to immobilized thrombospondin or to endothelial cells expressing the intercellular adhesion molecule 1. Furthermore, an Mr approximately 300-kD trypsin-sensitive protein doublet was immunoprecipitated from knobless trophozoite-infected erythrocytes. Finding a P. falciparum erythrocyte membrane protein 1 (PfEMP1)-like molecule on these infected erythrocytes is consistent with a role for PfEMP1 in cytoadherence to CD36 and C32 melanoma cells.

Foscarnet may be an effective treatment for severe mucocutaneous disease due to acyclovir-resistant, TK-negative strains of HSV-2.

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