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Query: UMLS:C0024530 (malaria)
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Avian malaria (Plasmodium relictum) caused significant mortality in wild-caught Magellanic penguins (Spheniscus magellanicus) in 1986 at the Blank Park Zoo in Des Moines, Iowa (USA). In early winter, wild birds were captured off the southern coast of Chile and flown to Detroit, Michigan for a 38 day quarantine. After quarantine, 18 birds were dispersed to Lansing, Michigan, six to a facility in Maine, and 46 to Des Moines, Iowa. Upon arrival in Des Moines, several penguins became weak and inactive, had to be force-fed, and died after 2 days. Gross lesions at postmortem included splenomegaly, hepatomegaly, and pulmonary edema. Histopathological examination revealed numerous intraendothelial schizonts in spleen, lung, liver, heart and kidney. Schizonts were generally 16 to 28 micron by 11 to 16 micron and contained merozoites of two distinct sized (macromerozoites, nuclei 1.0 micron; micromerozoites, nuclei 0.5 micron). Based on the morphology of the abundant exoerythrocytic forms, a tentative diagnosis of avian malaria (Plasmodium sp.) was made. Subsequent transmission electron microscopic examination of schizonts in formalized tissue revealed merozoites with tear-shaped rhoptries. Antimalarial therapy was initiated early but deaths continued for 5 mo. Mortality, which eventually totaled 83%, occurred in three distinct waves, each separated by a hiatus of approximately 1 mo. Despite examinations of repeated blood smears, intraerythrocytic Plasmodium relictum was not detected until late in the outbreak. Diagnosis was based on morphologic characteristics including schizonts with eight to 12 merozoites/segmenter and round gametocytes that displaced and turned the infected erythrocyte nucleus. In addition to malaria, penguins showed evidence of aspergillosis, bacterial enteritis (Escherichia coli; Proteus sp.; and Edwardsiella sp.), and helminthiasis (Contracaecum sp. and Tetrabothrius sp.). Based on gross and histological lesions, disease prevalence in this group of penguins was malaria 58%, aspergillosis 61%, enteritis 60%, helminthiasis 26%. Epidemiologic investigation including group transport history, disease prevalence in co-quarantined birds not sent to Des Moines and climatological data implicated Des Moines as the likely site for initial exposure, although information is not conclusive. Stress and concurrent disease certainly contributed to the severe mortality in this group of penguins infected with P. relictum.
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PMID:Plasmodium relictum as a cause of avian malaria in wild-caught magellanic penguins (Spheniscus magellanicus). 319 55

A model for the prediction of IgG titres in females of the Jackass penguin (Spheniscus demersus) was developed, based on IgG which was maternally transmitted to the yolk of unembryonated eggs produced by these females. However, prediction of the female titre based on the titre of embryonated eggs may be inadequate. Blood samples from 10 S. demersus females and their corresponding embryonated (n = 10) and unembryonated (n = 49) eggs were analysed by indirect ELISA for avian malaria (Plasmodium relictum, P. elongatum) IgG and Aspergillus spp. IgG. There was no correlation between humoral responses to avian malaria and Aspergillus spp. in females or in their eggs. Avian malaria and Aspergillus spp. titres were significantly higher (P < 0.05) in the eggs than in the corresponding females and were significantly correlated (P < 0.01) with the blood titres, r = 0.84, r = 0.89, respectively. No correlation was found between titres of embryo yolk-sac (embryonated eggs) and the blood of their female parent; however, the embryo blood and the corresponding female titres were significantly (P < 0.05) correlated (avian malaria, r = 0.74; Aspergillus spp., r = 0.69). Blood and the corresponding egg-yolk (unembryonated eggs) IgG titres regressed significantly (P < 0.01). Female IgG titre (y) is related to (unembryonated) egg-yolk IgG titre by the significant (P < 0.05) regression y = -0.61 + 1.46X for avian malaria, and y = -0.02 + 0.85X for Aspergillus spp., with +/- 95% prediction limits of +/- 0.15 and +/- 0.12, respectively. This model provides access to serological information on the remote free-ranging Jackass penguins and captive Jackass-penguin colonies without the necessity of stressful blood collection.
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PMID:A model for the prediction of relative titres of avian malaria and Aspergillus spp. IgG in Jackass penguin (Spheniscus demersus) females based on maternal IgG in egg-yolk. 889 66

Avian malaria has had a profound impact on the demographics and behaviour of Hawaiian forest birds since its vector, Culex quinquefasciatus the southern house mosquito, was first introduced to Hawaii around 1830. In order to understand the dynamics of the disease in Hawaii and gain insights into the evolution of vector-mediated parasite-host interactions in general we studied the population genetics of Cx. quinquefasciatus in the Hawaiian Islands. We used both microsatellite and mitochondrial loci. Not surprisingly we found that mosquitoes in Midway, a small island in the Western group, are quite distinct from the populations in the main Hawaiian Islands. However, we also found that in general mosquito populations are relatively isolated even among the main islands, in particular between Hawaii (the Big Island) and the remaining Hawaiian Islands. We found evidence of bottlenecks among populations within the Big Island and an excess of alleles in Maui, the site of the original introduction. The mitochondrial diversity was typically low but higher than expected. The current distribution of mitochondrial haplotypes combined with the microsatellite information lead us to conclude that there have been several introductions and to speculate on some processes that may be responsible for the current population genetics of vectors of avian malaria in Hawaii.
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PMID:Bottlenecks and multiple introductions: population genetics of the vector of avian malaria in Hawaii. 1109 16

Avian malaria is caused by a diverse community of genetically differentiated parasites of the genera Plasmodium and Haemoproteus. Rapid seasonal and annual antigenic allele turnover resulting from selection by host immune systems, as observed in some parasite populations infecting humans, may extend analogously to dynamic species compositions within communities of avian malarial parasites. To address this issue, we examined the stability of avian malarial parasite lineages across multiple time-scales within two insular host communities. Parasite communities in Puerto Rico and St Lucia included 20 and 14 genetically distinct parasite lineages, respectively. Lineage composition of the parasite community in Puerto Rico did not vary seasonally or over a 1 year interval. However, over intervals approaching a decade, the avian communities of both islands experienced an apparent loss or gain of one malarial parasite lineage, indicating the potential for relatively frequent lineage turnover. Patterns of temporal variation of parasite lineages in this study suggest periodic colonization and extinction events driven by a combination of host-specific immune responses, competition between lineages and drift. However, the occasional and ecologically dynamic lineage turnover exhibited by insular avian parasite communities is not as rapid as antigenic allele turnover within populations of human malaria.
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PMID:Temporal stability of insular avian malarial parasite communities. 1512 59

The southern house mosquito, Culex quinquefasciatus, is a widespread tropical and subtropical disease vector. In the Hawaiian Islands, where it was introduced accidentally almost two centuries ago, it is considered the primary vector of avian malaria and pox. Avian malaria in particular has contributed to the extinction and endangerment of Hawaii's native avifauna, and has altered the altitudinal distribution of native bird populations. We examined the population genetic structure of Cx. quinquefasciatus on the island of Hawaii at a smaller spatial scale than has previously been attempted, with particular emphasis on the effects of elevation on population genetic structure. We found significant genetic differentiation among populations and patterns of isolation by distance within the island. Elevation per se did not have a limiting effect on gene flow; however, there was significantly lower genetic diversity among populations at mid elevations compared to those at low elevations. A recent sample taken from just above the predicted upper altitudinal distribution of Cx. quinquefasciatus on the island of Hawaii was confirmed as being a temporary summer population and appeared to consist of individuals from more than one source population. Our results indicate effects of elevation gradients on genetic structure that are consistent with known effects of elevation on population dynamics of this disease vector.
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PMID:Fine-scale population genetic structure of a wildlife disease vector: the southern house mosquito on the island of Hawaii. 1705 93

1. Seasonal variation in environmental conditions is ubiquitous and can affect the spread of infectious diseases. Understanding seasonal patterns of disease incidence can help to identify mechanisms, such as the demography of hosts and vectors, which influence parasite transmission dynamics. 2. We examined seasonal variation in Plasmodium infection in a blue tit Cyanistes caeruleus population over 3 years using sensitive molecular diagnostic techniques, in light of Beaudoin et al.'s (1971; Journal of Wildlife Diseases, 7, 5-13) model of seasonal variation in avian malaria prevalence in temperate areas. This model predicts a within-year bimodal pattern of spring and autumn peaks with a winter absence of infection. 3. Avian malaria infections were mostly Plasmodium (24.4%) with occasional Haemoproteus infections (0.8%). Statistical nonlinear smoothing techniques applied to longitudinal presence/absence data revealed marked temporal variation in Plasmodium prevalence, which apparently showed a within-year bimodal pattern similar to Beaudoin et al.'s model. However, of the two Plasmodium morphospecies accounting for most infections, only the seasonal pattern of Plasmodium circumflexum supported Beaudoin et al.'s model. On closer examination there was also considerable age structure in infection: Beaudoin et al.'s seasonal pattern was observed only in first year and not older birds. Plasmodium relictum prevalence was less seasonally variable. 4. For these two Plasmodium morphospecies, we reject Beaudoin et al.'s model as it does not survive closer scrutiny of the complexities of seasonal variation among Plasmodium morphospecies and host age classes. Studies of host-parasite interactions should consider seasonal variation whenever possible. We discuss the ecological and evolutionary implications of seasonal variation in disease prevalence.
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PMID:Seasonal variation in Plasmodium prevalence in a population of blue tits Cyanistes caeruleus. 1831 39

Avian malaria parasites are supposed to exert negative effects on host fitness because these intracellular parasites affect host metabolism. Recent advances in molecular genotyping and microscopy have revealed that coinfections with multiple parasites are frequent in bird-malaria parasite systems. However, studies of the fitness consequences of such double infections are scarce and inconclusive. We tested if the infection with two malaria parasite lineages has more negative effects than single infection using 6 years of data from a natural population of house martins. Survival was negatively affected by both types of infections. We found an additive cost from single to double infection in body condition, but not in reproductive parameters (double-infected had higher reproductive success). These results demonstrate that malaria infections decrease survival, but also have different consequences on the breeding performance of single- and double-infected wild birds.
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PMID:Effects of malaria double infection in birds: one plus one is not two. 1846 16

Pantothenate, a precursor of the fundamental enzyme cofactor coenzyme A (CoA), is essential for growth of the intraerythrocytic stage of human and avian malaria parasites. Avian malaria parasites have been reported to be incapable of de novo CoA synthesis and instead salvage CoA from the host erythrocyte; hence, pantothenate is required for CoA biosynthesis within the host cell and not the parasite itself. Whether the same is true of the intraerythrocytic stage of the human malaria parasite, Plasmodium falciparum, remained to be established. In this study we investigated the metabolic fate of [(14)C]pantothenate within uninfected and P. falciparum-infected human erythrocytes. We provide evidence consistent with normal human erythrocytes, unlike rat erythrocytes (which have been reported to possess an incomplete CoA biosynthesis pathway), being capable of CoA biosynthesis from pantothenate. We also show that CoA biosynthesis is substantially higher in P. falciparum-infected erythrocytes and that P. falciparum, unlike its avian counterpart, generates most of the CoA synthesized in the infected erythrocyte, presumably necessitated by insufficient CoA biosynthesis in the host erythrocyte. Our data raise the possibility that malaria parasites rationalize their biosynthetic activity depending on the capacity of their host cell to synthesize the metabolites they require.
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PMID:The human malaria parasite Plasmodium falciparum is not dependent on host coenzyme A biosynthesis. 1958 50

Assessing parasite specificity to vector is crucial to understanding the emergence of vector-borne diseases and the evolution of parasite diversity. Avian malaria parasites have a cosmopolitan distribution and broad avian host range, which together predict they are vector generalists, but little is known about parasite-vector associations in the wild. We tested this prediction by asking if 5 different mosquito species, known to feed on birds and abundant in the northeastern United States, were naturally infected in the field with identical avian Plasmodium spp. lineages. Mosquitoes were not pooled but rather analyzed individually, and, possibly as a result, lineage diversity was higher than reported in previous avian malaria vector studies. Plasmodium spp. lineages were rare in Aedes canadensis and absent in Aedes aurifer and Culiseta melanura. We sequenced a standard Plasmodium cytochrome b marker from Culex pipiens pipiens, Culex restuans, and Ae. canadensis. Most Plasmodium clades were shared by Cx. pipiens and Cx. restuans. In addition, 4 individual lineages were shared by both mosquito species, including the most common lineage. One Plasmodium clade, however, was only found in Cx. restuans. We therefore found limited support for our prediction that avian Plasmodium spp. vector breadth accompanies host breadth. The association of both Culex species with most Plasmodium clades, and the presence of a single parasite lineage in 3 mosquito species representing 2 genera, suggests that avian Plasmodium species are not tightly coevolved with vector species.
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PMID:Avian malaria parasites share congeneric mosquito vectors. 1969 68

Avian malaria parasites (Plasmodium) occur commonly in wild birds and are an increasingly popular model system for understanding host-parasite co-evolution. However, whether these parasites have fitness consequences for hosts in endemic areas is much debated, particularly since wild-caught individuals almost always harbour chronic infections of very low parasite density. We used the anti-malarial drug Malarone to test experimentally for fitness effects of chronic malaria infection in a wild population of breeding blue tits (Cyanistes caeruleus). Medication caused a pronounced reduction in Plasmodium infection intensity, usually resulting in complete clearance of these parasites from the blood, as revealed by quantitative PCR. Positive effects of medication on malaria-infected birds were found at multiple stages during breeding, with medicated females showing higher hatching success, provisioning rates and fledging success compared to controls. Most strikingly, we found that treatment of maternal malaria infections strongly altered within-family differences, with reduced inequality in hatching probability and fledging mass within broods reared by medicated females. These within-brood effects appear to explain higher fledging success among medicated females and are consistent with a model of parental optimism in which smaller (marginal) offspring can be successfully raised to independence if additional resources become available during the breeding attempt. Overall, these results demonstrate that chronic avian malaria infections, far from being benign, can have significant effects on host fitness and may thus constitute an important selection pressure in wild bird populations.
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PMID:Chronic malaria infections increase family inequalities and reduce parental fitness: experimental evidence from a wild bird population. 2007 Apr 58


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