Babesia bovis: adhesion of parasitized red blood cells to bovine umbilical vein endothelial cells in vitro does not select for virulence

Molloy, J.B.; Bowles, Pamela M.; Jorgensen, W.K.; Cooke, Brian M.

doi:10.1016/s0014-4894(03)00095-x

Cited by 9 publications

(7 citation statements)

References 17 publications

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“…As mentioned above, the objective of the study was fulfilled when the virulence of the strains was assessed; nevertheless, the hypothesis originally established could not be tested as all clones studied showed a similar virulence regardless of their adhesive or nonadhesive phenotype. In this sense, similar results were recently reported in that animals inoculated with erythrocytes infected with B. bovis adherent in vitro to endothelial cells from bovine umbilical chord did not show an exacerbation of clinical signs when compared to animals inoculated with the nonadhesive mother strain 9 . In conclusion, through in vitro selection and enrichment, it is possible to obtain endothelial cell‐adhesive and nonadhesive populations from originally pathogenic and nonpathogenic populations of B. bovis .…”

Section: Discussionsupporting

confidence: 87%

Evaluation of Cattle Inoculated with Babesia bovis Clones Adhesive In Vitro to Bovine Brain Endothelial Cells

Canto

Millán

Ramos

et al. 2006

Annals of the New York Academy of Sciences

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A comparative assessment of the virulence of Babesia bovis clones that adhere or not to bovine brain endothelial cells was done using two clones of B. bovis: (1) a clone phenotypically characterized as virulent (2F8) and (2) a clone of reduced virulence (RAD). Of these subpopulations, we selected those that had adhesive characteristics (a) or nonadhesive characteristics (na) in cultured endothelial cells. Twenty Holstein cattle, 12 months of age or older, were used in this study, and these cattle were randomly assigned to five groups of four animals each. The clones and their respective subpopulations were inoculated via intramuscular injection at a 0.5 x 10(7) infected erythrocyte dosage. Group A was inoculated with aRAD, group B with naRAD, group C with a2F8, group D with na2F8, and group E remained as a control. All inoculated animals showed a decrease in the packed cell volume (PCV), with group D showing the largest decrease (39.53%) and longest time (7 days) with rectal temperature above 39.5 degrees C. Babesia was observed in stained blood smears from only six cattle. While the four parasite subpopulations were pathogenic, significant differences were not noted among them, despite that the subpopulations considered to be virulent caused the greatest reduction in PCV per individual.

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Section: Discussionsupporting

confidence: 87%

Evaluation of Cattle Inoculated with Babesia bovis Clones Adhesive In Vitro to Bovine Brain Endothelial Cells

Canto

Millán

Ramos

et al. 2006

Annals of the New York Academy of Sciences

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“…Unlike human malaria, babesia has the advantage of being a natural host‐parasite system in which such a relationship can be determined. Interestingly, two previous studies have failed to detect differences in the adhesive properties between B. bovis parasites that cause mild or severe infections in vivo when adhesion was tested in static adhesion assays (Molloy et al ., 2003; Canto et al ., 2006). Our observations suggest that it would be clearly worthwhile to revisit these earlier studies and infect cattle with PRBCs that had been selected for adhesion under flow conditions to monitor the severity of the resulting disease.…”

Section: Discussionmentioning

confidence: 99%

New insights into the altered adhesive and mechanical properties of red blood cells parasitized by Babesia bovis

Hutchings

Fernandez

et al. 2007

Molecular Microbiology

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SummarySequestration of parasite-infected red blood cells (RBCs) in the microvasculature is an important pathological feature of both bovine babesiosis caused by Babesia bovis and human malaria caused by Plasmodium falciparum. Surprisingly, when compared with malaria, the cellular and molecular mechanisms that underlie this abnormal circulatory behaviour for RBCs infected with B. bovis have been relatively ignored. Here, we present some novel insights into the adhesive and mechanical changes that occur in B. bovis-infected bovine RBCs and compare them with the alterations that occur in human RBCs infected with P. falciparum. After infection with B. bovis, bovine RBCs become rigid and adhere to vascular endothelial cells under conditions of physiologically relevant flow. These alterations are accompanied by the appearance of ridge-like structures on the RBC surface that are analogous, but morphologically and biochemically different, to the knob-like structures on the surface of human RBCs infected with P. falciparum. Importantly, albeit for a limited number of parasite lines examined here, the extent of these cellular and rheological changes appear to be related to parasite virulence. Future investigations to identify the precise molecular composition of ridges and the proteins that mediate adhesion will provide important insight into the pathogenesis of both babesiosis and malaria.

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“…The implications, from this single case study (a splenectomised individual, but the pathology can be equally complex in intact and asplenic patients [ 308 , 309 ]), implies that another mechanism, such as high cytokines [ 310 ], must be the cause of the falciparum-like pathology of this disease. It is also appropriate to note here that selection for degree of sequestration of Babesia bovis , widely regarded as a parallel for the vaso-occlusive model of falciparum malaria, did not produce parasites that generated more virulent infections in cattle [ 311 ].…”

Section: Practical Consequences Of These Changesmentioning

confidence: 99%

Human malarial disease: a consequence of inflammatory cytokine release

Clark

Budd

Alleva

et al. 2006

Malar J

262

190

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Malaria causes an acute systemic human disease that bears many similarities, both clinically and mechanistically, to those caused by bacteria, rickettsia, and viruses. Over the past few decades, a literature has emerged that argues for most of the pathology seen in all of these infectious diseases being explained by activation of the inflammatory system, with the balance between the pro and anti-inflammatory cytokines being tipped towards the onset of systemic inflammation. Although not often expressed in energy terms, there is, when reduced to biochemical essentials, wide agreement that infection with falciparum malaria is often fatal because mitochondria are unable to generate enough ATP to maintain normal cellular function. Most, however, would contend that this largely occurs because sequestered parasitized red cells prevent sufficient oxygen getting to where it is needed. This review considers the evidence that an equally or more important way ATP deficency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen. This activity of these cytokines, plus their capacity to control the pathways through which oxygen supply to mitochondria are restricted (particularly through directing sequestration and driving anaemia), combine to make falciparum malaria primarily an inflammatory cytokine-driven disease.

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Babesia bovis: adhesion of parasitized red blood cells to bovine umbilical vein endothelial cells in vitro does not select for virulence

Cited by 9 publications

References 17 publications

Evaluation of Cattle Inoculated with Babesia bovis Clones Adhesive In Vitro to Bovine Brain Endothelial Cells

Evaluation of Cattle Inoculated with Babesia bovis Clones Adhesive In Vitro to Bovine Brain Endothelial Cells

New insights into the altered adhesive and mechanical properties of red blood cells parasitized by Babesia bovis

Human malarial disease: a consequence of inflammatory cytokine release

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