Tuberculosis and other mycobacterial Infections

Kali PB, Gray GE, et al. Combining PMTCT with active case finding for tuberculosis. J Acquir Immune Defic Syndr 2006 Apr 24 [Epub ahead of print]. http://gateway.ut.ovid.com/gw2/ovidweb.cgi

Tuberculosis (TB) has become a leading cause of maternal mortality and morbidity in high HIV prevalence settings. Active TB in pregnant women has potentially serious consequences for foetuses and newborns. In Soweto (South Africa) there is more than 90% uptake of voluntary counselling and HIV testing during routine antenatal care, and almost one third of pregnant women are found to have HIV- infection. The post-test counselling session in the prevention of mother-to-child transmission programme provides an opportunity to screen HIV-infected pregnant women for TB. In this study, 370 HIV-infected pregnant women were screened for symptoms of active TB by lay counsellors at the post-test counselling session. If symptomatic, they were referred to nurses who investigated them further. Eight women were found to have previously undiagnosed, smear-negative, culture-confirmed TB (that is an incidence of 21.6/1000). The mean CD4 count in those with active TB was significantly lower than in those without TB. Symptoms most associated with active TB were haemoptysis and fever. The authors conclude that the incidence of TB in HIV-infected pregnant women is high, and screening for TB during routine antenatal care should be implemented in high HIV prevalence settings.

 


Ustianowski AP, Lawn SD, Lockwood DN. Interactions between HIV infection and leprosy: a paradox. Lancet Infect Dis 2006;6:350-360.http://www.thelancet.com/journals/laninf/article/PIIS1473309906704935/fulltextEarly in the HIV epidemic it was feared that HIV would undermine leprosy control, as has occurred with TB. It was predicted that patients with leprosy and HIV co-infection would have an increased risk of lepromatous disease and a faster clinical evolution, and that the leprosy would be more difficult to treat. None of these concerns have materialised and the interaction between HIV and Mycobacterium leprae seems to be far more subtle than that between HIV and TB. Ustianowski and colleagues reviewed the epidemiological, clinical, and pathological data relating to leprosy/HIV co-infection. The published epidemiological data are limited in quality but show neither an increased HIV prevalence among leprosy cases nor an alteration in clinical spectrum of leprosy among co-infected patients. Some data suggest that immune-mediated reactions that complicate leprosy occur at a higher frequency in co-infected patients. Leprosy has now been reported presenting as immune reconstitution disease among patients commencing HAART. Histopathological observations reveal a normal spectrum of appearances in biopsies of leprosy lesions from co-infected patients, even among those with advanced immunodeficiency. These observations suggest that cell-mediated immune responses to Mycobacterium leprae are preserved at the site of disease despite evidence that these responses are abrogated systemically, in contrast to TB where host granulomatous responses are impaired by HIV co-infection. The authors speculate that this paradox may relate to differences within leprosy and TB granulomas between the activation state and rates of cell turnover that differentially affect the susceptibility of granulomas to HIV. The authors conclude that the interactions between leprosy and HIV have been little studied and further research on the clinical, pathological, and management aspects of this co-infection is warranted.

 

Comorbidity
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