A comparative study showed that 5 laboratory strains of Trypanosoma cruzi could be divided into a non-responsive group (Sonya clone and Colombiana) and a responsive group (Tulahuén, Y and Peru), based on long-term treatment of mouse infections with nifurtimox and benznidazole. In vitro sensitivity of epimastigotes and blood-stream trypomastigotes in macrophage cultures did not distinguish the strains, nor did the rate of development of nifurtimox resistance by epimastigote cultures. 7 novel anti-T. cruzi compounds also behaved similarly with respect to the 2 groups. A small decrease in sensitivity was observed in vitro by non-responsive strains of T. cruzi after re-isolation from treated mice. It is postulated that there could be an immunological component involved in successful treatment of T. cruzi infection.
Following previous studies of verapamil reversal of chloroquine resistance in malaria and multi-drug resistance in cancer cells, the effect of verapamil was investigated on nifurtimox-resistant Trypanosoma cruzi in vitro and antimony-resistant Leishmania donovani in vitro and in vivo. Verapamil alone was not active against either parasite, but in combination with nifurtimox it reversed the drug resistance of T. cruzi and in combination with sodium stibogluconate reversed the drug resistance of L. donovani.
Cell-free and cell-associated human immunodeficiency virus cultures suspended in 10% serum remained infectious for several weeks at room temperature. The stability was further increased when cell-associated virus was suspended in neat serum. When dried onto a glass coverslip, virus remained infectious for several days, although cell-associated virus lost infectivity more rapidly than cell-free virus. Many parameters influence the capacity of a virus to survive in the environment, including the concentration of virus, the temperature, the humidity, and the nature of the surrounding medium. The rate at which infectivity is lost is an important determinant of the potential risk of transmission.
The efficacy of sodium hypochlorite was assessed against human immunodeficiency virus type 1 suspended in low (8% v/v) or high (80% v/v) concentrations of serum or in a high (80%) concentration of blood. In the presence of 8% serum, 100 p.p.m. available chlorine in the disinfectant test mixture inactivated 3.75 log TCID50 HIV/ml within 30 s. When the test mixture contained 80% serum, 500 p.p.m. available chlorine inactivated more than 4 log TCID50 HIV/ml in 1-2 min. Lower concentrations of available chlorine were unable to inactivate the virus completely. In the presence of 80% blood, 1000 p.p.m. available chlorine in the disinfectant test mixture was unable to inactivate 3.75 log TCID50 HIV/ml, although 2500 p.p.m. available chlorine was able to inactivate at least 1.5 log TCID50 HIV/ml. In all test mixtures, the chlorine rapidly became combined and thus less active. Our results emphasise the importance of cleaning prior to disinfection with sodium hypochlorite since it may prove to be ineffective in the presence of high levels of organic matter. In cases where prior cleaning is impossible, care must be taken to use the higher recommended concentration (a minimum of 10,000 p.p.m. available chlorine).
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