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In the global effort to eliminate lymphatic filariasis, annual mass treatments are conducted with diethylcarbamazine (DEC) or ivermectin, combined with albendazole. The success of this strategy depends on achieving high levels of drug coverage, which reduces the number of persons with circulating microfilariae so that transmission of the parasite is interrupted. Because resources are often limited, a simple, inexpensive, and reliable method to estimate drug coverage is needed. During the period December 2000 to February 2001, three methods were used to assess drug coverage in Leogane Commune, Haiti: a probability survey using a cluster sample design (n = 1421 persons); a distribution-point survey based on a convenience sample of houses near the distribution points (n = 4341 persons); and a survey based on a convenience sample of primary schools (n = 5036 children). The coverage estimations were 71.3% (95% CI 66.7-75.9), 73.6% (95% CI 70.1-77.0), and 77.8% (95% CI 73.5-82.1), respectively. Survey costs for the probability, distribution point, and school surveys were US$2217, US$979, and US$312, respectively. The 2 convenience sampling methods provided point estimates of drug coverage that were similar to those of the probability survey. These methods may have a role for monitoring drug treatment coverage between less frequent, but more costly, probability sample surveys.

Background: In August 1999, a prison inmate infected with the human immunodeficiency virus (HIV) was diagnosed with pulmonary tuberculosis (TB). This source patient lived in a prison dormitory housing over 300 HIV-infected men, and was symptomatic for at least 2 months prior to diagnosis. We report a large outbreak of TB in HIV-infected prison inmates with subsequent transmission of Mycobacterium tuberculosis outside the prison., Methods: Exposed inmates were screened by symptom review, chest radiograph and tuberculin skin test (TST) in September and December 1999. We recorded CD4 cell counts, viral loads and receipt of highly active antiretroviral therapy (HAART)., Results: The source patient lived on the right side of a two-sided dormitory exclusively housing HIV-infected men. Of 114 men tested from the right side, 75 (66%) had documented TST conversions. Of 96 converters overall, 82 (85%) had TSTs measuring > or = 15 mm. Within 6 months of diagnosis of TB in the source patient, 30 additional inmates and a healthcare worker who cared for the source patient developed TB disease. Two other inmates developed TB disease in spring of 2001., Conclusions: We describe extensive transmission of M. tuberculosis in a group of HIV-infected prison inmates with high TST conversion rates and subsequent transmission in the community. In settings where HIV-infected persons are congregated, the consequences of TB outbreaks are magnified.

In October 2000, 71,187 persons were treated for lymphatic filariasis using albendazole and diethylcarbamazine (DEC) or DEC alone in Leogane, Haiti. We documented the frequency of adverse reactions, severity and cost of treatment. Adverse reactions were classified as minor, moderate, or severe. Overall, 24% (17,421) of the treated persons reported one or more adverse reactions. There were 15,916 (91%) minor and 1502 (9%) moderate adverse reaction reports. Men outnumbered women 2:1 in reporting moderate problems. Three patients, representing roughly one in 25,000 persons treated, were hospitalized with severe adverse reactions judged to be treatment-associated by physician review. The cost per person treated for adverse reactions was more than twice the cost per person treated for lymphatic filariasis (dollar 1.60 versus dollar 0.71). Severe adverse reactions to lymphatic filariasis treatment using DEC with or without albendazole are uncommon. Minor and moderate reactions are more commonly reported and their management represents a challenge to lymphatic filariasis elimination programs.

The capacity of reduced glutathione (GSH) to protect lung tissue against ozone-induced pulmonary fibrosis was investigated. Male B6C3F1 mice were exposed to 0, 0.2, 0.5, and 1.0 ppm ozone for 23 hr/day for 14 days. During exposures and/or for a period of 90 days after exposures, subgroups of mice at each exposure level were given drinking water containing 30 mM L-buthionine-S,R-sulfoximine (BSO) to lower in vivo levels of GSH. These BSO treatments reduced blood glutamylcysteine synthetase (GCS) activity (regulatory enzyme for GSH biosynthesis) and lung nonprotein sulfhydryl (NPSH) levels in nonexposed animals by approximately half. In contrast, ozone exposures increased blood GCS activity and lung NPSH levels in a concentration-dependent manner, with smaller increases in the BSO-treated mice. Immediately after exposures, an ozone-related inflammatory response was seen in lungs, but no histopathological signs of developing fibrosis were evident. Ninety days later, mice exposed to 1 ppm ozone and not treated with BSO had modest evidence of pulmonary fibrosis. Mice exposed to 1 ppm ozone and treated with BSO during this post-exposure period (regardless of BSO treatment during exposures) showed histopathological evidence of exacerbated pulmonary fibrosis, compared to similarly exposed mice not treated with BSO postexposure. These results indicated that interference with the body's normal defense mechanisms against oxidant damage, including suppression of GSH biosynthesis, exacerbates the subsequent development of pulmonary fibrosis.