V-NOW! Symposium on genetic variation of malaria parasites: implications for selection of adequate control strategies. Leiden, The Netherlands, November 14-16, 1990.
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An integrated system for the control of the major human helminth parasites.
Disease due to virtually all of the human helminth parasites can be prevented simultaneously by a simple system based on the following premises: 1) helminths do not multiply within their definitive hosts, and their distribution in host populations is overdispersed; 2) disease manifestations occur largely in the small proportion of hosts, often school children, with heavy worm burdens; and 3) a few single-dose, broad-spectrum anthelmintics given in low doses at prolonged intervals can maintain worm burdens below pathogenic levels for almost all of the major human helminth parasites. The three drugs might be albendazole or one of the other benzimidazoles for hookworm, ascaris and trichuris; ivermectin for the filaria, including onchocerca and many other nematodes such as strongyloides; and praziquantel for virtually all trematodes and cestodes. The target group would be school children treated at intervals set to maintain worm burdens below the disease-inducing threshold. It is possible that all three drugs could be administered in low doses simultaneously at yearly intervals. Studies will be necessary to examine drug interactions, development of drug resistance, optimal dosages and timing, and effects on morbidity.
Animals↗
The delivery of exoerythrocytic parasites of Plasmodium berghei: a hormone controlled process.
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The worm parasites of cattle and buffalo and their control in Thailand.
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Three conserved cis-acting sequences in the core promoter control gene expression in the protozoan parasite Entamoeba histolytica.
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Animals↗
The chequered history of malaria control: are new and better tools the ultimate answer?
Following Ronald Ross' demonstration in 1897 that mosquitoes transmit malarial parasites, efforts to control malaria were naturally focussed on attacking the mosquito vector by various measures, mainly directed against the aquatic stages. Although the results were spectacular in some areas, there was a growing realisation that effective control of malaria depended on other factors, including the availability of better drugs than quinine and a greater understanding of the epidemiology of the disease under various environmental conditions. With the discovery of DDT, an all-out effort was made to eradicate malaria by attacking adult mosquitoes. Eradication was not achieved in many countries, mainly because of inadequate health infrastructures. With the emergence of chloroquine-resistant parasites, the search for more effective drug regimens intensified, various drugs and drug combinations were assessed, and methods were developed to monitor and assess degrees of resistance. Since resistance to drugs can develop very quickly, the use of drug combinations, especially those containing artemisinin derivatives, is now recommended. Insecticide-impregnated bednets have become the preferred method of vector control. Although the search for better tools must continue, the events of the past century emphasise the need to strengthen health systems to ensure that they are capable of delivering effective interventions and of assessing their effectiveness in controlling malaria.
Animals↗
Deficient control of Trypanosoma cruzi infection in C57BL/6 mice is related to a delayed specific IgG response and increased macrophage production of pro-inflammatory cytokines.
Earlier work in Trypanosoma cruzi-infected C57BL/6 and BALB/c mice revealed an acute disease, of lethal outcome in the former group and lesser severity in BALB/c mice. Fatal course was not accompanied by an increased parasite load, but by a substantial imbalance between pro- and anti-inflammatory cytokine serum levels. To better characterise the mechanisms allowing the host to restrain the infection, we have now studied the specific IgG production and in vitro behaviour of peritoneal macrophages (PMs) when exposed to T. cruzi. BALC/c mice displayed higher serum levels of specific immunoglobulins in the first weeks of acute infection. In vitro infected PMs showed no between-group differences in the number of intracellular parasites, although TNFalpha levels were significantly higher in culture supernatants from C57BL/6 mice. Because an LPS-based pretreatment (desensitisation protocol followed by a sublethal LPS dose) reduced disease severity of C57BL/6 mice, we next explored the features of the in vitro infection in PMs from mice subjected to such protocol. PMs from LPS-pretreated mice had a decreased production of TNFalpha and IL-1beta, becoming more permissive to parasite replication. It is concluded that deficient control of T. cruzi infection in C57BL/6 mice may also involve a less satisfactory specific IgG response and increased TNFalpha production by PMs. Improved disease outcome in LPS-pretreated mice may be associated with the reduced inflammatory cytokine production by PMs, but the impaired ability of these cells to control parasite growth suggests that compensatory mechanisms are operating in the in vivo situation.
Animals↗
Water-related vector-borne diseases.
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Communicable Disease Control↗
Shared control of epidemiological traits in a coevolutionary model of host-parasite interactions.
Most models concerning the evolution of a parasite's virulence and its host's resistance assume that each component of the relationship (transmission, virulence, recovery, etc.) is controlled by either the host or the parasite but not by both. We present a model that describes the coevolution of host and parasite, assuming that the rate of transmission or the virulence depends on both genotypes. The evolution of these traits is constrained by trade-offs that account for costs of defense and attack strategies, in line with previous studies on the separate evolution of the host and the parasite. Considering shared control by the host and the parasite in determining the traits of the relationship leads to several novel predictions. First, the host should evolve maximal investment in defense against parasites with an intermediate replication rate. Second, the evolution of the parasite strongly depends on the way the host's defense is described. Third, the coevolutionary process may lead to decreasing the parasite's virulence as a response to a rise in the host's background mortality, contrary to classical predictions.
Adaptation, Physiological↗
Marginal zinc deficiency has no effect on primary or challenge infections in mice with Heligmosomoides polygyrus (Nematoda).
The effect of low dietary zinc on the survival of an intestinal nematode (Heligmosomoides polygyrus) was investigated in two experiments. In experiment 1 (primary infection), outbred CD1 mice were infected once only with 100 H. polygyrus larvae. In Experiment 2 (challenge infection), mice were given a primary infection that was terminated after 9 d using an anthelmintic drug; the mice were reinfected 5 d later. This protocol stimulates host immunity to the second parasitic infection. Three dietary treatments (control, 60 mg Zn/kg diet; zinc-restricted, 5 mg Zn/kg diet; and energy-restricted, 60 mg Zn/kg diet) were used for both experiments. Both infected and uninfected mice were included within each dietary treatment to control for the effect of parasitic infection on host nutritional status. Plasma zinc concentrations were significantly lower in mice fed the zinc-restricted diet, compared with mice fed the control or energy-restricted diets in both experiments; there were no significant differences in plasma alkaline phosphatase activity or tissue zinc concentration. The significant reduction in plasma zinc had no significant effect on worm burden or egg production of H. polygyrus in either experiment, indicating that the 30-40% reduction in plasma zinc was not sufficient to modify parasite numbers. However, the parasite did affect host nutritional status. Spleen weight was significantly higher in infected mice in both experiments. Following the challenge infection, both liver and spleen copper concentrations were significantly higher, and spleen iron concentration significantly lower, in the infected compared with the noninfected mice.
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Initiating malaria control programs in the third world: directives for short- and long-term solutions.
Although malaria is a growing problem affecting several hundred million people each year, many malarial countries lack successful disease control programs. Worldwide malaria incidence rates are dramatically increasing, generating fear among many people who are witnessing malaria control initiatives fail. In this paper, we explore two options for malaria control in poor countries: (1) the production and distribution of a malaria vaccine and (2) the control of mosquitoes that harbor the malaria parasite. We first demonstrate that the development of a malaria vaccine is indeed likely, although it will take several years to produce because of both biological obstacles and insufficient research support. The distribution of such a vaccine, as suggested by some economists, will require that wealthy states promise a market to pharmaceutical companies who have traditionally failed to investigate diseases affecting the poorest of nations. But prior to the development of a malaria vaccine, we recommend the implementation of vector control pro- grams, such as those using Bti toxin, in regions with low vector capacity. Our analysis indicates that both endogenous programs in malarial regions and molecular approaches to parasite control will provide pragmatic solutions to the malaria problem. But the successful control of malaria will require sustained support from wealthy nations, without whom vaccine development and vector control programs will likely fail.
Animals↗
The potential of nematophagous fungi to control the free-living stages of nematode parasites of sheep: studies with Duddingtonia flagrans.
The nematophagous fungus, Duddingtonia flagrans, isolated from a fresh sheep faecal sample obtained from a farm in northern New South Wales, Australia, was subjected to a number of in vivo investigations in both surgically modified and normal sheep to determine its capacity to survive passage through the gastrointestinal tract. Single and sustained dosing experiments established that between 5 x 10(5) and 10(6) chlamydospores/day resulted in a substantial (> 80%) reduction in the number of infective larvae derived from nematode eggs in faeces. This effect can be maintained if dosing continues. These results demonstrate for the first time the potential of nematophagous fungi to be deployed by means of sustained release technology in the biological control of nematode parasites of livestock.
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Control strategies for ostertagiasis.
There are currently four major options for control of ostertagiasis and other ruminant gastrointestinal parasites. These are the traditional, suppressive, integrated and strategic approaches. Strategic dosing is the most realistic and beneficial approach for most regions of the world, including the U.S.A. It is effective, practical, labor-saving and can yield big economic returns. Today this approach is even more appropriate because of important advances in the technology of controlled release and pulse-release devices. Top priority in worm control programs should be given to dairy replacement heifers in their first year at pasture and to beef calves in the immediate post-weaning period. This is preferable to recommendations for blanket treatment of all beef and dairy cattle, regardless of age, immune status or pasture infectivity. An anthelmintic overkill is both wasteful and potentially harmful in that it increases the selection pressure for drug resistance. It is suggested that better dissemination of information is needed to make producers aware of the benefits of strategic dosing programs. This would eliminate much of the confusion about parasite control and focus attention on simple and effective programs that could significantly reduce current losses to the livestock industries.
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Serologic diagnosis of Oestrus ovis (Diptera:Oestridae) in naturally infested sheep.
Sera from eighteen control sheep supposed to be free from parasitism by Oestrus ovis Linnaeus, 1761, and from 100 sheep raised in an enzootic area of O.ovis infestations were tested to detect anti-Oestrus antibodies by double immunodiffusion (DD) and indirect haemagglutination (IH) tests with somatic crude antigens from first (L1), second (L2) and third (L3) instar of O.ovis larvae. At necropsy, eighty-eight out of 100 sheep from the O.ovis infested area were found to be parasitized while the eighteen control ovines did not show Oestrus larvae. Examination of the sera from the parasitized sheep by DD showed positive results of 42% for L1, 59% for L2 and 18% for L3. Screening the sera with IH gave sensitivities of 100% for L1, 100% for L2 and 97.7% for L3. Sheep, naturally parasitized by gastrointestinal nematodes, presented no cross immune reactions in DD tests with the three larval stages of O.ovis or with L2 larvae in IH tests.
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Mechanism of resistance to lysis by the alternative complement pathway in Trypanosoma cruzi trypomastigotes: effect of specific monoclonal antibody.
Trypanosoma cruzi G strain epimastigotes were lysed by normal human serum (NHS) through activation of the alternative complement pathway (ACP), whereas metacyclic trypomastigotes were resistant to lysis. Epimastigotes and metacyclics with equivalent amounts of C3b deposited on their surface bound factor B with similar affinities. In contrast, factor H bound with higher affinity to metacyclics than to epimastigotes. Both T. cruzi forms with bound C3b were extensively (60 to 80%) lysed after formation of surface C3-convertase and the addition of a C3-C9 complement source. In the presence of factors H and I, or incubation with NHS with EDTA, the percentage of lysis of metacyclics decreased faster than that of epimastigotes with increasing incubation times. These data suggest, as a possible mechanism of resistance to lysis in metacyclic trypomastigotes, the higher binding affinity of factor H to C3b and the inactivation of the latter by serum regulatory proteins. Metacyclics were lysed by NHS, through ACP, in the presence of human immune serum to T. cruzi or anti-T. cruzi monoclonal antibody, but not with the Fab fragment of the latter, which recognizes a 90,000 m.w. antigen from T. cruzi metacyclics. Protection of parasite-bound C3b from serum control proteins was observed when parasites were incubated, before C3 deposition, with the lytic monoclonal antibody but not with its Fab fragment or a nonrelated IgG control. When C3b was deposited on metacyclics before antibody binding, C3b inactivation occurred. In the lysis of metacyclics, through ACP activation, binding of antibody apparently creates new acceptor sites which prevent the activity of serum regulatory proteins.
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Control of malaria and filariasis vectors in South India.
Community participation is increasingly seen as a major component of successful control programmes against parasitic diseases. One of the strongest exponents of this has been the Vector Control Research Centre (VCRC) in Pondicherry, South India (Fig. 1), who have successfully motivated and involved village communities in vector control activities with considerable success against malaria and filariasis vectors. Their largest single programme, the Filariasis Control Demonstration Project in Pondicherry Town, has now been handed to the Pondicherry State Government, while the VCRC's work on malaria and filariasis control is now expanding throughout other parts of India. As this article shows, much has been learnt from these projects, not just about control techniques but also about education, administration and decision-making.
Journal Article↗
Quantifying genetic and nongenetic contributions to malarial infection in a Sri Lankan population.
Explaining the causes of variation in the severity of malarial disease remains a major challenge in the treatment and control of malaria. Many factors are known to contribute to this variation, including parasite genetics, host genetics, acquired immunity, and exposure levels. However, the relative importance of each of these to the overall burden of malarial disease in human populations has not been assessed. Here, we have partitioned variation in the incidence of malarial infection and the clinical intensity of malarial disease in a rural population in Sri Lanka into its component causes by pedigree analysis of longitudinal data. We found that human genetics, housing, and predisposing systematic effects (e. g., sex, age, occupation, history of infections, village) each explained approximately 15% of the variation in the frequency of malarial infection. For clinical intensity of illness, 20% of the variation was explained by repeatable differences between patients, about half of which was attributable to host genetics. The other half was attributable to semipermanent differences among patients, most of which could be explained by known predisposing factors. Three percent of variation in clinical intensity was explained by housing, and an additional 7% was explained by current influences relating to infection status (e.g., parasitemia, parasite species). Genetic control of Plasmodium falciparum infections appeared to modulate the frequency and intensity of infections, whereas genetic control of Plasmodium vivax infections appeared to confer absolute susceptibility or refractoriness but not intensity of disease. Overall, the data show consistent, repeatable differences among hosts in their susceptibility to clinical disease, about half of which are attributable to host genes.
Age Factors↗
Multinucleate host cells induced by Vittaforma corneae (Microsporidia).
The microsporidium Vittaforma corneae develops within the target cell cytoplasm. In the present study, green monkey kidney (E6) cells infected at 30 degrees C, 35 degrees C or 37 degrees C with V. corneae developed enlarged multinucleate structures of up to 200 microm in any horizontal dimension made up either of a single cell or of multiple fused cells. A number of epithelial cell types (SW-480, HT-29, Caco-2 and HCT-8) were infected with V. corneae but did not induce the same highly organized structures, suggesting that for the structure to develop, the host cell must be capable of continued mitosis, and not be differentiated or be detaching from the surface matrix. Live cell imaging of infected E6 cells revealed large, multinucleate infected cells characterized by a central focus from which radiated parasite stages and host cell mitochondria. Immunocytochemistry identifying gamma and alpha tubulin suggested that a single centrally-located microtubule organizing centre governed the distribution of parasite stages and host cell organelles, with mitochondria and parasites being eventually transported towards the periphery of the structure. Whole cell patch clamp analysis of infected cells indicated an average five-fold increase in total membrane capacitance, consistent with an enlarged single cell. Scanning electron microscopy revealed cell-like protrusions around the periphery of the structure with the intervening space being made up of parasites and cell debris. Clearly in the case of V. corneae-infected E6 cells the parasite-host cell relationship involves subverting the host cell cytoskeleton and cell volume control, providing the parasite with the same protected niche as does a xenoma.
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