Laboratory-acquired parasitic infections from accidental exposures.
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Parasitic diseases are receiving increasing attention in developed countries in part because of their importance in travelers, immigrants, and immunocompromised persons. The main purpose of this review is to educate laboratorians, the primary readership, and health care workers, the secondary readership, about the potential hazards of handling specimens that contain viable parasites and about the diseases that can result. This is accomplished partly through discussion of the occupationally acquired cases of parasitic infections that have been reported, focusing for each case on the type of accident that resulted in infection, the length of the incubation period, the clinical manifestations that developed, and the means by which infection was detected. The article focuses on the cases of infection with the protozoa that cause leishmaniasis, malaria, toxoplasmosis, Chagas' disease (American trypanosomiasis), and African trypanosomiasis. Data about 164 such cases are discussed, as are data about cases caused by intestinal protozoa and by helminths. Of the 105 case-patients infected with blood and tissue protozoa who either recalled an accident or for whom the likely route of transmission could be presumed, 47 (44.8%) had percutaneous exposure via a contaminated needle or other sharp object. Some accidents were directly linked to poor laboratory practices (e.g., recapping a needle or working barehanded). To decrease the likelihood of accidental exposures, persons who could be exposed to pathogenic parasites must be thoroughly instructed in safety precautions before they begin to work and through ongoing training programs. Protocols should be provided for handling specimens that could contain viable organisms, using protective clothing and equipment, dealing with spills of infectious organisms, and responding to accidents. Special care should be exercised when using needles and other sharp objects. (+info)
Unraveling immunology.
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A report on the 11th International Congress of Immunology, Stockholm, Sweden, 22-27 July 2001. (+info)
Growth status and related medical conditions among refugee children in Massachusetts, 1995-1998.
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OBJECTIVES: This study analyzed growth and identified related medical conditions among refugee children in Massachusetts. METHODS: Between July 1995 and June 1998, 1825 refugee children were screened. Variables included positive tuberculin (purified protein derivative; PPD) test; dental abnormalities; pathogenic parasites; weight-for-age, height-for-age, and weight-for-height z scores; and body mass index greater than the 84th percentile. RESULTS: Of all the children, 21% had parasites, 62% had caries, and 25% had a positive PPD reaction. Twelve percent overall and 28% younger than 2 years had anemia. Eight percent had height-for-age z scores less than -2, and 6% had weight-for-age z scores greater than +2. Of those aged 1 to 9 years, 7% had weight-for-height z scores greater than +2. Weight-for-height z scores less than -2 were concentrated among Africans and East Asians (both 8%). Height-for-age z scores less than -2 were seen among African (13%), Near Eastern (19%), and East Asian (30%) children. Weight-for-height z scores greater than +2 and body mass index greater than the 84th percentile were concentrated among children from the former Yugoslavia (8% and 15%) and the former Soviet Union (8% and 14%). CONCLUSIONS: Recently arrived refugee children have significant growth abnormalities. European refugees were overweight; those from developing countries had growth retardation. (+info)
Biochemical and molecular mechanisms of drug resistance in parasites.
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Drug resistance is complicating the treatment of parasitic diseases. We review here the basic mechanisms of parasite resistance in malaria, sleeping sickness, leishmaniasis and common helminthiases. Parasites resort to multiple biochemical means to achieve resistance and we have begun to isolate and characterize the genes/proteins implicated in resistance. Understanding drug resistance is essential for the control of parasitic diseases. (+info)
Modelling parasite drug resistance: lessons for management and control strategies.
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Mathematical models of the evolution of drug resistance in infectious diseases are predominantly concentrated in three main areas: antimalarial, antibiotic and anthelmintic resistance. There appears to be little or no cross-reference between them. This literature was examined to identify factors that influence the evolution of drug resistance irrespective of the species and drug under study. The aim is to provide non-technical readers with a basic qualitative understanding of the issues and pitfalls involved in designing drug treatment regimens to minimize the evolution of resistance. The principal factors determining the rate at which resistance evolves appear to be (i) the starting frequency of resistance, (ii) the level and pattern of drug use, (iii) the drug's pharmacokinetic properties, (iv) the number of genes required to encode resistance, (v) the level of sexual recombination in the parasite population, (vi) intrahost dynamics and, in particular, whether 'crowding' effects are present, (vii) the genetic basis of resistance and (viii) the number of individual parasites in an infection. The relative importance of these factors depends on the biology of the organisms under consideration and external factors such as the extent to which the infrastructure of health care delivery constrains the practicalities of drug regimens. (+info)
Interactions between sources of mortality and the evolution of parasite virulence.
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A well-known result from the theory of the evolution of virulence is the prediction that the virulence of a pathogen (i.e. the rate of parasite-induced host mortality) always evolves to higher levels when host background mortality rates increase. This prediction, however, is derived from models that assume that host mortality sources combine additively to determine the overall host mortality rate. In this paper, we suggest that such additivity is probably rare for many host-pathogen systems, and explore how the predictions for the evolution of virulence are altered when interactions between host mortality sources are incorporated into the theory. Our results indicate that if mortality-source interactions are sufficiently strong then the evolutionarily stable level of virulence can actually decrease as the background mortality rate increases. Consequently, a detailed mechanistic description of how parasites and other mortality sources combine to cause host mortality is required before reliable predictions about virulence evolution can be made. Moreover, mortality-source interactions make empirical comparisons of the virulence of different parasites a much more subtle issue. (+info)
Determinants of low birth weight among HIV-infected pregnant women in Tanzania.
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BACKGROUND: Low birth weight (LBW) increases the risk of infant death, but little is known about its causes among HIV-infected populations in sub-Saharan Africa. OBJECTIVE: We assessed sociodemographic, nutritional, immunologic, parasitic, and infant risk factors for birth weight, LBW, and small-for-gestational-age (SGA) status in a cohort of 822 HIV-positive women enrolled in a clinical trial of vitamin supplementation and pregnancy outcomes in Dar es Salaam, Tanzania. DESIGN: Women were enrolled at prenatal care clinics during their second trimester, at which time blood, stool, urine, and genital specimens were collected, and anthropometric measurements and sociodemographic data were recorded. Birth weight was measured at hospital delivery. RESULTS: The mean (+/-SD) birth weight was 3015 +/- 508 g, 11.1% of newborns weighed <2500 g (LBW), and 11.5% were SGA. In multivariate analyses, maternal weight at enrollment and a low CD8 cell count were inversely associated with LBW. Advanced-stage HIV disease, previous history of preterm birth, Plasmodium falciparum malaria, and any helmintic infection were associated with higher risk of LBW. The intestinal parasites Entamoeba histolytica and Strongyloides stercoralis were predictors of LBW despite their low prevalence in the cohort. In a multivariate-adjusted linear regression model, BMI, midupper arm circumference, a CD4 cell count <200 x 10(6) cells/L (200 cells/mm(3)), primiparity, maternal literacy, and infant HIV infection at birth were significantly associated with birth weight in addition to risk factors included in the LBW model. Determinants of SGA included maternal weight, low serum vitamin E concentration, candidiasis, malaria, and infant HIV infection at birth. CONCLUSION: Prevention of HIV disease progression and vertical transmission, improved nutritional status, and better management of malaria and intestinal parasitic infections are likely to reduce the incidence of LBW in Tanzania. (+info)
An unlikely partnership: parasites, concomitant immunity and host defence.
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Concomitant immunity (CI) against macroparasites describes a state of effective anti-larval immunity coupled with persistent adult infection. Experimental studies indicate that immunologically concealed adult worms might promote anti-larval immunity via the release of cross-reactive antigens, thus creating a barrier against continual infection and restricting burden size within the host. CI offers an important potential benefit to established worms by preventing overcrowding within the host. Thus, CI may be interpreted as akin to vaccination; relatively long-lived adult worms 'vaccinate' their host with larval surface antigens and so benefit from reduced conspecific competition. The shared responsibility for host vaccination among adult worms leads to a problem of collective action. Here, we build on earlier analytical findings about the evolutionary forces that shape cooperation among parasites in order to produce a stochastic simulation model of macroparasite social evolution. First, we theoretically investigate a parasite adaptation hypothesis of CI and demonstrate its plausibility under defined conditions, despite the possibility of evolutionary 'cheats'. Then we derive a set of predictions for testing the hypothesis that CI is partly a host-manipulative parasite adaptation. Evidence in support of this model would present an unusual case of adaptive population regulation. (+info)