parasitemia/phosphatase

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Evaluation of clinical signs, parasitemia, hematologic and biochemical changes in cattle experimentally infected with Trypanosoma vivax.

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Infections by Trypanosoma vivax cause great losses to livestock in Africa and Central and South Americas. Outbreaks due this parasite have been occurred with increasing frequency in Brazil. Knowledge of changes caused by T. vivax during the course of this disease can be of great diagnostic value.

Effect of copper on growth and serum constituents of immunized and non-immunized rabbits infected with Trypanosoma brucei.

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Seventy-two five-week-old New Zealand White rabbits were divided into three groups and fed a basal diet containing 0, 125 or 250 ppm supplemental Cu for 4 weeks before each Cu-group was further subdivided into three lots of 8 rabbits each. One subgroup was immunized with Trypanosoma brucei before

Direct exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increases infectivity of human erythrocytes to a malarial parasite.

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Direct exposure to 10 nM 2,3,7,8-TCDD caused a 75% increase and a 2-fold increase in the infectivity of isolated human erythrocytes to P. falciparum after 48 hours when the parasites were in an unsynchronized or synchronized state of growth, respectively. Treatment of human erythrocytes with 10

Levamisole inhibits sequestration of infected red blood cells in patients with falciparum malaria.

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BACKGROUND Sequestration of infected red blood cells (iRBCs) in the microcirculation is central to the pathophysiology of falciparum malaria. It is caused by cytoadhesion of iRBCs to vascular endothelium, mediated through the binding of Plasmodium falciparum erythrocyte membrane protein-1 to several

Clinical chemistry of anaplasmosis: blood chemical changes in infected mature cows.

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The clinical chemical changes induced by Anaplasma marginale infection were determined in 16 adult, intact cows infected with either of 2 virulent isolates and in 8 others treated with a live sheep-attenuated A marginale vaccine and were compared with the clinical chemical analyses in 7 noninfected

Testosterone responsiveness of spleen and liver in female lymphotoxin beta receptor-deficient mice resistant to blood-stage malaria.

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Disrupted signaling through lymphotoxin beta receptor (LTbetaR) results in severe defects of the spleen and even loss of all other secondary lymphoid tissues, making mice susceptible to diverse infectious agents. Surprisingly, however, we find that female LTbetaR-deficient mice are even more

Transfusion-Transmitted Babesiosis During Total Hip Arthroplasty.

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Babesiosis is a potentially life-threatening zoonotic disease that is endemic to the northeastern United States and increasing in prevalence worldwide. Transmitted by the same Ixodes tick responsible for Lyme disease, the intraerythrocytic parasite Babesia causes a wide range of clinical

Umbilical cord-blood infections with Plasmodium falciparum malaria are acquired antenatally in Kenya.

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BACKGROUND It is unknown whether the presence of Plasmodium falciparum malaria parasites in umbilical cord blood denotes infection acquired antenatally or contamination with infected maternal blood at delivery. METHODS Parasites were quantified by real-time quantitative polymerase chain reaction

Infection by the Protozoan Parasite Toxoplasma gondii Inhibits Host MNK1/2-eIF4E Axis to Promote Its Survival

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The obligate intracellular parasite Toxoplasma gondii reprograms host gene expression through multiple mechanisms that promote infection, including the up-regulation of mTOR-dependent host mRNA translation. In addition to the mTOR-4E-BP1/2 axis, MAPK-interacting kinases 1 and 2 (MNK1/2)

Characterization of Plasmodium falciparum protein kinase 2.

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A sustained elevation of free Ca(2+) is observed on the rupture and release of merozoites of Plasmodium falciparum from the erythrocytes. The immunoelectron micrographs demonstrate that calmodulin is localized in merozoites. To elucidate the Ca(2+) signal of P. falciparum invasion, we attempted to

DNA hybridization for assessment of response of Plasmodium falciparum to chloroquine therapy.

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We studied the accuracy of PFR1-AP, a synthetic DNA hybridization probe conjugated to alkaline phosphatase, in monitoring Plasmodium falciparum parasitemia during in vivo drug susceptibility surveys. Duplicate blood samples were collected from six children enrolled in a 14-day in vivo chloroquine

Retrospective case-control study of hepatozoonosis in dogs in Israel.

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Signalment, clinical signs, and physical examination and clinicopathologic findings in dogs diagnosed with Hepatozoon canis parasitemia (n = 100) were compared with those in Hepatozoon-negative dogs (n = 180). A subset (n = 15) of Hepatozoon-positive dogs with unusually high (> 800 H canis

Serum transcobalamin II levels in patients with malaria infection.

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Serum transcobalamin II (TCII) levels were determined in 56 patients with P. falciparum malaria infection. They were divided into 3 groups: severe (malarial parasite > 5% or patients with cerebral malaria or renal insufficiency), moderate (1-5% infection without complications) and mild (1%

Competitive antibody binding inhibition ELISA for the detection of Plasmodium falciparum antigen.

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A competitive antibody binding inhibition ELISA to detect Plasmodium falciparum-infected cells in clinical specimens was developed. Optimum conditions developed included: 12.5 micrograms/ml of P. falciparum antigen for plate coating, 25 micrograms/ml of polyclonal rabbit anti-P. falciparum IgG, 30

Detection of Anaplasma marginale DNA in bovine erythrocytes by slot-blot and in situ hybridization with a PCR-mediated digoxigenin-labeled DNA probe.

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A 409-base pair (bp) DNA fragment derived from the msp-1 beta gene of Anaplasma marginale was amplified and simultaneously labeled with digoxigenin-11-dUTP by a polymerase chain reaction (PCR) assay. The resulting digoxigenin-labeled 409-bp PCR product was used as a probe for slot-blot and in situ

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