Shared features in the pathobiology of babesiosis and malaria

Krause, Peter J.; Daily, Johanna P.; Telford, Sam R.; Vannier, Edouard; Lantos, Paul M.; Spielman, Andrew

doi:10.1016/j.pt.2007.09.005

Cited by 96 publications

(92 citation statements)

References 74 publications

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“…cynomolgi-induced anemia is not prevented in doubly infected monkeys. Babesia and Plasmodium are protozoan parasites that infect erythrocytes and result in comparable clinical features, including induction of anemia (25,37). The hematocrit level, hemoglobin level, erythrocyte count, and percentage of reticulocytes (Fig.…”

Section: B Microti Infection In Rhesus Macaquesmentioning

confidence: 99%

“…A typical pathological feature of both Plasmodium and Babesia infections is the presence of marked erythro-and hemosiderophagocytosis and excessive deposition of pigment due to the extreme lysis of erythrocytes and enzymatic transformation of released hemoglobin (1,25). At the end of this study organs and tissues were collected from all monkeys and examined for pathology.…”

Section: B Microti Infection In Rhesus Macaquesmentioning

confidence: 99%

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Suppression ofPlasmodium cynomolgiin Rhesus Macaques by Coinfection withBabesia microti

Duivenvoorde¹,

Wel²,

Werff³

et al. 2010

Infect Immun

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Both Plasmodium and Babesia species are intraerythrocytic protozoans that infect a wide range of hosts, including humans, and they elicit similar inflammatory responses and clinical manifestations that differ markedly in severity. We recently reported that a rhesus macaque that was chronically infected with Babesia microti was able to control infection with Plasmodium cynomolgi (a parasite of macaques with characteristics very similar to those of Plasmodium vivax) better than naïve monkeys. To confirm this and to investigate the underlying immunopathology, six naïve rhesus monkeys were infected with B. microti. After 24 days, four of these monkeys and four naïve rhesus monkeys were challenged with P. cynomolgi blood-stage parasites. B. microti persisted at low levels in all monkeys, and the clinical parameters were comparable to those of noninfected controls. There was a significant decrease in P. cynomolgi parasitemia in animals coinfected with B. microti compared to the parasitemia in animals infected with P. cynomolgi alone. This decrease in P. cynomolgi parasitemia correlated with increases in the levels of proinflammatory monocytes at the time of P. cynomolgi infection and with higher C-reactive protein (CRP) serum levels 1 week after malaria infection. Therefore, we conclude that ongoing infection with B. microti parasites leads to suppression of malaria infection.

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Section: B Microti Infection In Rhesus Macaquesmentioning

confidence: 99%

Section: B Microti Infection In Rhesus Macaquesmentioning

confidence: 99%

Suppression ofPlasmodium cynomolgiin Rhesus Macaques by Coinfection withBabesia microti

Duivenvoorde¹,

Wel²,

Werff³

et al. 2010

Infect Immun

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“…B. microti infections in young and healthy adults generally cause a mild virus-like infection but may be asymptomatic. More-severe disease occurs primarily in neonates, the elderly, and those who are immunocompromised, with mortality rates as high as 20% (8,9).…”

mentioning

confidence: 99%

Expression, Purification, and Biological Characterization of Babesia microti Apical Membrane Antigen 1

et al. 2015

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eThe intraerythrocytic apicomplexan Babesia microti, the primary causative agent of human babesiosis, is a major public health concern in the United States and elsewhere. Apicomplexans utilize a multiprotein complex that includes a type I membrane protein called apical membrane antigen 1 (AMA1) to invade host cells. We have isolated the full-length B. microti AMA1 (BmAMA1) gene and determined its nucleotide sequence, as well as the amino acid sequence of the AMA1 protein. This protein contains an N-terminal signal sequence, an extracellular region, a transmembrane region, and a short conserved cytoplasmic tail. It shows the same domain organization as the AMA1 orthologs from piroplasm, coccidian, and haemosporidian apicomplexans but differs from all other currently known piroplasmida, including other Babesia and Theileria species, in lacking two conserved cysteines in highly variable domain III of the extracellular region. Minimal polymorphism was detected in BmAMA1 gene sequences of parasite isolates from six babesiosis patients from Nantucket. Immunofluorescence microscopy studies showed that BmAMA1 is localized on the cell surface and cytoplasm near the apical end of the parasite. Native BmAMA1 from parasite lysate and refolded recombinant BmAMA1 (rBmAMA1) expressed in Escherichia coli reacted with a mouse anti-BmAMA1 antibody using Western blotting. In vitro binding studies showed that both native BmAMA1 and rBmAMA1 bind to human red blood cells (RBCs). This binding is trypsin and chymotrypsin treatment sensitive but neuraminidase independent. Incubation of B. microti parasites in human RBCs with a mouse anti-BmAMA1 antibody inhibited parasite growth by 80% in a 24-h assay. Based on its antigenically conserved nature and potential role in RBC invasion, BmAMA1 should be evaluated as a vaccine candidate.

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“…More research has been done on the consequences of the similar malarial parasites, Plasmodium falciparum and Plasmodium vivax, which are very similar to Babesia spp., but which are a much more significant cause of serious disease and mortality in humans [80,81]. Research has shown that humans born to malarial mothers have lower birth weights owing to inter-uterine growth retardation.…”

Section: Discussionmentioning

confidence: 99%

Infection before pregnancy affects immunity and response to social challenge in the next generation

Curno

Reader

McElligott

et al. 2011

Phil. Trans. R. Soc. B

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Natural selection should favour parents that are able to adjust their offspring's life-history strategy and resource allocation in response to changing environmental and social conditions. Pathogens impose particularly strong and variable selective pressure on host life histories, and parental genes will benefit if offspring are appropriately primed to meet the immunological challenges ahead. Here, we investigated transgenerational immune priming by examining reproductive resource allocation by female mice in response to direct infection with Babesia microti prior to pregnancy. Female mice previously infected with B. microti gained more weight over pregnancy, and spent more time nursing their offspring. These offspring generated an accelerated response to B. microti as adults, clearing the infection sooner and losing less weight as a result of infection. They also showed an altered hormonal response to novel social environments, decreasing instead of increasing testosterone production upon social housing. These results suggest that a dominance-resistance trade-off can be mediated by cues from the previous generation. We suggest that strategic maternal investment in response to an infection leads to increased disease resistance in the following generation. Offspring from previously infected mothers downregulate investment in acquisition of social dominance, which in natural systems would reduce access to mating opportunities. In doing so, however, they avoid the reduced disease resistance associated with increased testosterone and dominance. The benefits of accelerated clearance of infection and reduced weight loss during infection may outweigh costs associated with reduced social dominance in an environment where the risk of disease is high.

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Shared features in the pathobiology of babesiosis and malaria

Cited by 96 publications

References 74 publications

Suppression ofPlasmodium cynomolgiin Rhesus Macaques by Coinfection withBabesia microti

Suppression ofPlasmodium cynomolgiin Rhesus Macaques by Coinfection withBabesia microti

Expression, Purification, and Biological Characterization of Babesia microti Apical Membrane Antigen 1

Infection before pregnancy affects immunity and response to social challenge in the next generation

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