Human trypanosome infection and the presence of intradomicile Rhodnius pallescens in the western border of the Panama Canal, Panama.

An entomologic search was carried out to collect intradomicile triatomines in dwellings from rural communities in the western border of the Panama Canal, Panama. Sixty-nine triatomines were collected inside 20 houses of 67 houses investigated. Rhodnius pallescens was the only triatomine species found and included adults of both sexes and nymphs. A significantly high Trypanosoma cruzi (72.7%) and T. rangeli (40%) vector infection rate was detected. Blood meal analysis showed that 68% of R. pallescens had fed on humans. Human serologic analysis and hemoculture performed on inhabitants from triatomine-infested houses showed that 32.1% (18 of 56) of the samples were trypanosome infected. Thirteen samples (23.2%) had antibodies against T. cruzi. Six of these seropositive samples were from children less than 15 years old. Trypanosoma rangeli was isolated in five hemoculture samples, all from children less than 11 years old. The epidemiologic implications of these findings in terms of human infection are discussed.

Laboratory-acquired malaria, leishmaniasis, trypanosomiasis, and toxoplasmosis.

Because of renewed interest in parasitic diseases, increasing numbers of persons in clinical and research laboratories have the potential for exposure to parasites and therefore are at risk for acquiring parasitic infections. In this review of laboratory-acquired parasitic infections, we concentrate on protozoan diseases that frequently have been reported to be laboratory acquired: malaria, leishmaniasis, trypanosomiasis (American and African), and toxoplasmosis. These diseases can be severe, even fatal, and may be difficult to diagnose. Many laboratorians who have acquired these diseases did not recall having had an accident. Of those with recognized accidents, needlestick injuries were the most common. Laboratories should have established protocols for handling specimens that may contain viable organisms and for responding to laboratory accidents.

Ultrastructural alterations in the adrenal gland cortex of mice experimentally infected with a Venezuelan isolate of Trypanosoma evansi.

The ultrastructural study of adrenal gland from mice experimentally infected with Trypanosoma evansi, in addition to intravascular and intracellular trypanosomes, showed different degrees of cortical cell alterations and capillary wall modifications. Beside its biological scope, these results suggest a role for the adrenal cortex to partake in Surra's etiopathogenesis and describe for the very first time a T. evansi intracellular stage.

Animal-level risk factors for Trypanosoma evansi infection in camels in eastern and central parts of Kenya.

Point prevalences and animal-level risk factors for Trypanosoma evansi infection were investigated in a cross-sectional study that involved 2227 camels from eastern and central parts of Kenya. The screening tests used were haematocrit centrifugation technique (HCT), mouse inoculation and latex agglutination (Suratex). All camels were screened with HCT, while 396 and 961 of them were, in addition, screened with mouse inoculation and Suratex tests, respectively. Parasitological and Suratex test results were used in parallel to determine the number of camels exposed to T. evansi infections. Statistical analyses were conducted using Statistical Analysis Systems. Parasitological and Suratex test results in parallel were dependent variables in multivariable logistic regression models that determined risk factors for T. evansi infection. Herd-level clustering was corrected with general estimation equations. The prevalences were 2.3% and 19.6%, using parasitological and Suratex tests, respectively, and 21.7% when both tests were used in parallel. There was a positive association between the screening tests (McNemar's test = 104.8, P = 0.001) although the strength of association was low (Kappa = 0.2; 95% CI: 0.1-0.3). Before accounting for herd-level clustering, dry season (OR = 1.5; 95% CI: 1.0, 2.1) and nomadic pastoralism (OR = 1.8; 95% CI: 1.1, 3.2) were associated with increased odds of a camel being exposed to T. evansi infection compared to wet season and ranching, respectively. Following this correction, only nomadic pastoralism was significantly associated (OR = 3.1; 95% CI = 1.0, 14.4) with T. evansi infection compared to ranching. It is concluded that camels managed under nomadic pastoralism had higher risk of being exposed to T. evansi infections than camels from ranching systems of management.

Post eclosion age predicts the prevalence of midgut trypanosome infections in Glossina.

The teneral phenomenon, as observed in Glossina sp., refers to the increased susceptibility of the fly to trypanosome infection when the first bloodmeal taken is trypanosome-infected. In recent years, the term teneral has gradually become synonymous with unfed, and thus fails to consider the age of the newly emerged fly at the time the first bloodmeal is taken. Furthermore, conflicting evidence exists of the effect of the age of the teneral fly post eclosion when it is given the infected first bloodmeal in determining the infection prevalence. This study demonstrates that it is not the feeding history of the fly but rather the age (hours after eclosion of the fly from the puparium) of the fly when it takes the first (infective) bloodmeal that determines the level of fly susceptibility to trypanosome infection. We examine this phenomenon in male and female flies from two distinct tsetse clades (Glossina morsitans morsitans and Glossina palpalis palpalis) infected with two salivarian trypanosome species, Trypanosoma (Trypanozoon) brucei brucei and Trypanosoma (Nannomonas) congolense using Fisher's exact test to examine differences in infection rates. Teneral tsetse aged less than 24 hours post-eclosion (h.p.e.) are twice as susceptible to trypanosome infection as flies aged 48 h.p.e. This trend is conserved across sex, vector clade and parasite species. The life cycle stage of the parasite fed to the fly (mammalian versus insect form trypanosomes) does not alter this age-related bias in infection. Reducing the numbers of parasites fed to 48 h.p.e., but not to 24 h.p.e. flies, increases teneral refractoriness. The importance of this phenomenon in disease biology in the field as well as the necessity of employing flies of consistent age in laboratory-based infection studies is discussed.

Proteomics of trypanosomatids of human medical importance.

Leishmania spp., Trypanosoma cruzi, and Trypanosoma brucei are protozoan parasites that cause a spectrum of fatal human diseases around the world. Recent completion of the genomic sequencing of these parasites has enormous relevance to the study of their biology and the pathogenesis of the diseases they cause because it opens the door to high-throughput proteomic technologies. This review encompasses studies using diverse proteomic approaches with these organisms to describe and catalogue global protein profiles, reveal changes in protein expression during development, elucidate the subcellular localisation of gene products, and evaluate host-parasite interactions.

Oligopeptidase B from Trypanosoma evansi. A parasite peptidase that inactivates atrial natriuretic factor in the bloodstream of infected hosts.

Serine oligopeptidases of trypanosomatids are emerging as important virulence factors and therapeutic targets in trypanosome infections. We report here the isolation and characterization of oligopeptidase B (OpdB) and its corresponding gene from Trypanosoma evansi, a pathogen of significant veterinary importance. The T. evansi opdB gene was present as a single copy per haploid genome containing an open reading frame of 2148 bp encoding a protein of 80.664 kDa. Purified OpdB hydrolyzed substrates with basic residues in P1 (k(cat)/K(m) for carbobenzyloxy-L-arginyl-L-arginyl-7-amido-4-methylcoumarin, 337 s(-1) x microm(-1)) and exhibited potent arginyl carboxypeptidase activity (k(cat)/K(m) for Val-Lys-Arg Arg-OH, 231 s(-1) x mM(-1)). While not secreted, T. evansi released OpdB into the plasma of infected hosts where it retained catalytic activity. Plasma OpdB levels correlated with blood parasitemia. In vitro, OpdB cleaved the peptide hormone atrial natriuretic factor (ANF) at four sites: Arg3 Arg4, Arg4 Ser5, Arg11 Ile12, and Arg27 Tyr28, thereby abrogating smooth muscle relaxant and prohypotensive properties of ANF. Circulating plasma ANF levels in T. evansi-infected rats were depressed from 130 to 8 pg x ml(-1), and plasma ANF levels inversely correlated with plasma OpdB activity. The in vitro half-life of ANF in rat plasma was reduced 300-fold in plasma from T. evansi-infected rodents, which contains high levels of OpdB activity. Addition of OpdB inhibitors to cell-free plasma from infected rodents significantly abrogated this ANF hydrolysis. Furthermore the in vivo ANF half-life was reduced 5-fold in T. evansi-infected rats. Thus, we propose a role for OpdB in peptide hormone dysregulation in trypanosomiasis, specifically in generating the depressed plasma levels of ANF in mammals infected with T. evansi.

In vitro production of metacyclic forms of Trypanosoma musculi and their infectivity in CBA mice.

Bloodstream forms of Trypanosoma musculi, cultured in Schneider's drosophila medium at room temperature, multiply and differentiate through a series of developmental stages into infective metacyclic trypomastigotes in 10 days. Oral inoculation with these culture forms into CBA mice produced a parasitemia similar to that produced by intraperitoneal infection with bloodstream forms except for a three-day longer prepatent period. Attempts to induce parasitemia with bloodstream forms given orally were unsuccessful.

Effect of malnutrition on susceptibility of mice to Trypanosoma musculi: vitamin A-deficiency.

Vitamin A-deficiency was studied in mice infected with Trypanosoma musculi. Irrespective of diet, trypomastigotes (trypanosomes) appeared in peripheral tail blood of all inoculated mice after 6-day incubation periods. On the average, vitamin A-deficient mice had parasitemias about 10 times greater than animals fed a complete diet and 8 times pair-fed controls. Parasitemias lasted longer in vitamin-deficient hosts, and reached a maximum five days later than those from control hosts.