Infection with Trypanosoma lewisi or Trypanosoma musculi may promote the spread of Toxoplasma gondii.

Toxoplasma gondii can infect almost all warm-blooded vertebrates with pathogensis being largely influenced by the host immune status. As important epidemiological hosts, rodents are globally distributed and are also commonly found infected with haemoflagellates, such as those in the genus Trypanosoma. We here address whether and how co-infection with trypanosomes can influence T. gondii infection in laboratory models. Rats of five strains, co-infected with T. lewisi and mice of four strains, co-infected with T. musculi, were found to be more or less susceptible to T. gondii infection, respectively, with corresponding increased or decreased brain cyst burdens. Downregulation of iNOS expression and decreased NO production or reverse were observed in the peritoneal macrophages of rats or mice, infected with trypanosomes, respectively. Trypanosoma lewisi and T. musculi can modulate host immune responses, either by enhancement or suppression and influence the outcome of Toxoplasma infection.

Effects of iron supplementation on blood adenine deaminase activity and oxidative stress in Trypanosoma evansi infection of rats.

The aim of this study was to assess the effects of iron supplementation on oxidative stress and on the activity of the adenosine deaminase (ADA) in rats experimentally infected by Trypanosoma evansi. For this purpose, 20 rats were divided into four experimental groups with five animals each as follows: groups A and B were composed by healthy animals, while animals from groups C and D were infected by T. evansi. Additionally, groups B and D received two subcutaneous doses of iron (60 mg kg(-1)) within an interval of 5 days. Blood samples were drawn on day 8 post infection in order to assess hematological and biochemical variables. Among the main results are: (1) animals from group C showed reduced erythrogram (with tendency to anemia); however the same results were not observed for group D; this might be a direct effect of free iron on trypanosomes which helped to reduce the parasitemia and the damage to erythrocytes caused by the infection; (2) iron supplementation was able to reduce NOx levels by inhibiting iNOS, and thus, providing an antioxidant action and, indirectly, reducing the ALT levels in groups Band D; (3) increase FRAP levels in group D; (4) reduce ADA activity in serum and erythrocytes in group C; however, this supplementation (5) increased the protein oxidation in groups B and D, as well as group C (positive control). Therefore, iron showed antioxidant and oxidant effects on animals that received supplementation; and it maintained the activity of E-ADA stable in infected/supplemented animals.

Iron metabolism and its relationship to anemia and immune system in Trypanosoma evansi infected rats.

The aim of this study was to evaluate biochemical parameters of iron metabolism in rats experimentally infected with Trypanosoma evansi. To this end, 20 rats (Wistar) were intraperitoneally inoculated with blood containing trypomastigotes 10(6) (Group T) and 12 animals were used as negative control (Group C) and received saline (0.2 mL) through same route. Blood samples were collected by cardiac puncture on day 5 (C5, T5) and 30 (C30, T30) post-inoculation (pi) to perform complete blood count and determination of serum iron, transferrin, ferritin, total and latent iron fixation capacity, transferrin saturation and prohepcidin concentration. Also, bone marrow samples were collected, to perform Pearls staining reaction. Levels of iron, total and latent iron binding capacity and prohepcidin concentration were lower (P<0.05) in infected rats (T5 and T30 groups) compared to controls. On the other hand, levels of transferrin and ferritin were higher when compared to controls (P<0.05). The transferrin saturation increased on day 5 pi, but decreased on day 30 pi. The Pearls reaction showed a higher accumulation of iron in the bone marrow of infected animals in day 5 pi (P<0.01). Infection with T. evansi in rats caused anemia and changes in iron metabolism associated to the peaks of parasitemia. These results suggest that changes in iron metabolism may be related to the host immune response to infection and anemic status of infected animals.

Livestock trypanosomosis in Uganda: parasite heterogeneity and anaemia status of naturally infected cattle, goats and pigs.

The prevalence and pathogenic effects of trypanosomosis were determined in cattle, goats and pigs reared in Kasese, Jinja and Rakai districts, Uganda; presence of trypanosomes was detected by buffy coat technique (BCT). The overall prevalence of trypanosomosis in cattle was 7.6% (144/1,891), 0.7% in goats (4/573) and 2.3% in pigs (9/386). Internal transcribed spacer 1 (ITS1) of ribosomal DNA polymerase chain reaction was utilised to identify trypanosomes to species level and revealed infections in 108 of the 144 trypanosome-positive cattle while all infected goats and pigs gave amplicons. Trypanosoma vivax was the most prevalent trypanosome species in cattle in single and mixed infections compared to infections involving Trypanosoma congolense and Trypanosoma brucei; in pigs, eight were mixed infections with one single T. vivax infection. No predominant trypanosome species was detected in goats. Anaemia, the main trypanosomosis pathological feature, was investigated by determining packed cell volume (PCV). Mean PCV values by t test in infected individuals were significantly lower than non-infected individuals (P<0.05) for all animal species. However, the proportion of anaemic animals was not significantly different in infected and non-infected individuals. In addition, the percent of infected animals by Fisher's exact test depended on district of origin and species but not sex. These findings show that trypanosomosis is a major cause of anaemia in livestock in endemic areas. Cattle were the major animal species affected by trypanosomosis; similar genotypes of trypanosomes were detected in the three animal species. BCT was more effective than ITS1 rDNA detecting trypanosomes in naturally infected cattle.

Hyperlipidaemia in trypanosomiasis of naturally infected horses: possible cachexia-anorexia syndrome?

Trypanosomiasis caused by Trypanosoma evansi commonly produces wasting disease with signs of emaciation and cachexia mainly at the end stage. The present study was conducted to explore the possible hyperlipaemia or hyperlipidaemia and its association with cachexia-anorexia in equine trypanosomiasis. Out of the fifteen confirmed animals, none of the plasma sample was opaque. There was a significant increase in plasma triglyceride, total cholesterol and blood urea nitrogen and a highly significant increase in low-density lipoprotein (LDL) levels. A mild increase in high-density lipoprotein (HDL) and very low-density lipoprotein levels were observed, while the relative percentage of HDL and LDL was altered with high significance. A moderate increase in triglyceride and highly significant increase in LDL might be the reasons for retention of appetite and lipolysis. Possible protein breakdown and presence of lipolysis might be the reasons for cachexia in equine trypanosomiasis.

Detection of cross infections by Leishmania spp. and Trypanosoma spp. in dogs using indirect immunoenzyme assay, indirect fluorescent antibody test and polymerase chain reaction.

The aim of this study was to detect cross infections by Leishmania spp. and Trypanosoma spp. using enzyme-linked immunosorbent assay (ELISA), indirect fluorescent antibody test (IFAT) and polymerase chain reaction (PCR). Thus, 408 blood samples were collected from dogs domiciled in Araçatuba Municipality, São Paulo State, Brazil; the dogs were of both sexes, of several breeds and aged 6 months. For Leishmania spp., 14.95% (61 out of 408) of dogs were reactive using IFAT. Positivity was 20.10% (82 out of 408) using ELISA and 29.66% (121 out of 408) using PCR, with significant differences for the sex and age of these animals (p < 0.05). For Trypanosoma spp., antibody occurrence using ELISA was 10.54% (43 out of 408), while PCR indicated 2.45% (10 out of 408) positive dogs. Using IFAT, 10.29% (42 out of 408) of animals were considered positive and only sex showed a significant difference (p < 0.05). In this study, 10.54% (43 out of 408) of animals were seropositive according to ELISA for Trypanosoma spp., of which 79.07% (34 out of 43) showed positive results in the molecular diagnosis for Leishmania spp., while of the 10.29% (42 out of 408) positive dogs according to IFAT, 95.24 % (40 out of 42) had confirmed infection by this parasite. The obtained results demonstrate evidence of cross infections by both protozoa in the animals analysed in this study.

Delta-aminolevulinate dehydratase activity in red blood cells of rats infected with Trypanosoma evansi.

The aim of this study was to evaluate the activity of delta-aminolevulinate dehydratase (δ-ALA-D) in red blood cells of rats infected with Trypanosoma evansi and establish its association with haematocrit, serum levels of iron and zinc and lipid peroxidation. Thirty-six male rats (Wistar) were divided into 2 groups with 18 animals each. Group A was non-infected while Group B was intraperitoneally infected, receiving 7·5×106 trypomastigotes per animal. Each group was divided into 3 subgroups of 6 rats and blood was collected during different periods post-infection (p.i.) as follows: day 5 (A1 and B1), day 15 (A2 and B2) and day 30 PI (A3 and B3). Blood samples were collected by cardiac puncture to estimate red blood cell parameters (RBC), δ-ALA-D activity and serum levels of iron, zinc and thiobarbituric acid reactive substances (TBARS). Rats in group B showed a significant (P<0·05) reduction of RBC count, haemoglobin concentration and haematocrit at days 5 and 15 p.i. The activity of δ-ALA-D in blood was significantly (P<0·001) increased at days 15 and 30 p.i. δ-ALA-D activity in blood had a significant (P<0·05) negative correlation with haematocrit (r=-0·61) and haemoglobin (r=-0·70) at day 15 p.i. There was a significant (P<0·05) decrease in serum iron and zinc levels and an increase in TBARS levels (P<0·05) during infection. The δ-ALA-D activity in blood was negatively correlated with the levels of iron (r=-0·68) and zinc (r=-0·57) on day 30 p.i. It was concluded that the increased activity of δ-ALA-D in blood might have occurred in response to the anaemia in remission as heme synthesis was enhanced.

Malnutrition as the cause of recumbency in suckler cows associated with Trypanosoma theileri infection.

BACKGROUND: Recumbent cows are a diagnostic challenge because of a wide range of differential diagnoses, which include trauma, neurological and metabolic disorders, malnutrition and mineral deficiencies. This case report describes recumbent suckler cows that presented as a herd problem. In addition to weakness due to inanition, Cu and Se deficiencies were considered as possible aetiologies of the recumbency. Furthermore, Trypanosoma (T.) theileri, a blood parasite of unknown importance in Germany, was detected in the blood of some cows. CASE PRESENTATION: Three recumbent cows were referred to the Clinic for Ruminants and Swine, Faculty of Veterinary Medicine of the University of Leipzig. They were unable to rise and had low body condition scores and rough hair coats. Haematological and serum biochemical analyses showed neutrophilia, electrolyte imbalances, increased activities of muscle and liver enzymes and decreased concentrations of trace elements, especially Copper (Cu) and Selenium (Se). T. theileri was detected in a routine blood smear from one cow. The cows did not respond to an intensive care protocol, which included intravenous fluids and electrolytes, mineral substitution, non-steroidal anti-inflammatories and antibiotics, and were therefore euthanized or died. Postmortem examination showed cachexia, subcutaneous and scleral oedema and muscular dystrophy, especially in the hind limbs. Follow-up examination of the herd of origin produced similar findings including the detection of T. theileri in a large proportion of the herd. Ration analysis revealed considerable undersupply of several nutrients. CONCLUSIONS: Based on all findings, an aetiological diagnosis of trace mineral and nutrient deficiency with possible involvement of T. theileri was made.

Immune responses to haemorrhagic septicaemia (HS) vaccination in Trypanosoma evansi infected buffalo-calves.

To assess the immunosuppressive effect of Trypanosoma evansi infection in buffalo-calves on immune responses to heterologous antigen, the study was planned to examine the responses of haemorrhagic septicaemia vaccination in simultaneously and previously (80 days before vaccination) T. evansi-infected buffalo-calves. Eight buffalo-calves were divided into three groups. Buffalo-calves of group A (n = 3) were previously (80 days before primary vaccination with haemorrhagic septicaemia [HS] vaccine) infected with T. evansi (1 x 10(7) tryps.calf(-1); sc) and that of group B (n = 3) were infected with T. evansi (1 x 10(7) tryps.calf(-1); sc) on the day of primary vaccination with HS vaccine. Two healthy uninfected control calves given only HS vaccine were kept in group C. All the buffalo-calves were given a booster dose of vaccine 21 days post-primary vaccination (PPV). Twenty eight days PPV, animals of group A were given trypanocidal quinapyramine prosalt at 6.66 mg kg(-1). Immunosuppressive effect of T. evansi infection was evident from day 7 PPV with HS vaccine. The effect was more pronounced in previously T. evansi-infected buffalo-calves as compared with simultaneously infected buffalo-calves. Group A buffalo-calves appeared to have recovered from the immunosuppressive effect after 28 days post-trypanocidal treatment as observed by humoral and cell-mediated immune responses. Immunosuppressive effect to HS vaccination was observed in T. evansi-infected buffalo-calves, and trypanocidal therapy enabled the calves to mount the responses similar to uninfected controls.

Fever of unknown origin in an infant with an unexpected blood film report: a case report.

INTRODUCTION: Fever of unknown origin (FUO) can be defined as a rectal temperature higher than 38.3 degrees C on several occasions over more than 3 weeks, the diagnosis of which remains uncertain after initial investigations. Identification of the causes and management of FUO in children is an important role of rural primary care physicians, and is guided by thorough history-taking and repeated physical examinations combined with standard laboratory tests and simple imaging procedures. This can be difficult in rural practice due to poor availability and reliability of laboratory and imaging procedures, and the cost and misuse of antibiotics. Dependence on clinical and laboratory examinations may fail in diseases presenting in non-endemic areas. Trypanosomiasis is a known cause of fever; however, it is an unusual cause of FUO considering the place of residence of this patient. CASE REPORT: This report describes a case of trypanosomiasis presenting as FUO. The patient was a one-year-old Nigerian female who had been managed for malaria and bronchopneumonia for 2 weeks in a private clinic and was finally referred for further management to Eku Baptist Hospital, a rural mission hospital in the Niger Delta of Nigeria. Results of her laboratory tests showed nothing of significance apart from anaemia and trypanosomes discovered unexpectedly in the blood film. This was confirmed after a cervical lymph node biopsy and microscopic examination of the glandular fluid. Treatment with eflornithine was effective. CONCLUSION: The diagnosis of trypanosomiasis in this patient highlights that when a patient is not obviously exposed to the causative factors of a disease, possible occurrences may present a diagnostic problem.

Trypanosoma evansi: hematologic changes in experimentally infected cats.

This study aimed at evaluating hemogram and erythropoietic changes in cats experimentally infected with Trypanosoma evansi. Thirteen adult female non-breeding Felix catus were separated into two groups: seven animals were infected with 10(8) trypomastigotes each, and six animals were used as negative controls. Animals were kept in air-conditioned rooms and blood smears were performed daily for 49 days. Blood samples were collected from the jugular vein at days 0, 7, 21, 35 and 49 and stored in blood-collecting tubes containing anticoagulant. Bone marrow was collected from the proximal epiphysis of the right femur at days 14 and 42 post-inoculation (PI). Total erythrocyte count, hematocrit and hemoglobin showed statistical differences among groups from the seventh day PI onwards (P<0.05). The mean corpuscular volume and the mean corpuscular hemoglobin concentration remained normal, characterizing a normocytic-normochromic anemia. Reticulocyte count increased in the infected group from the 21st day onwards, but remained near normal values suggesting a mild regenerative anemia. Moreover, the myeloid:erythroid ratio significantly reduced at day 42 PI, evidencing a bone marrow hematopoietic response. Based on these results we conclude that cats infected with T. evansi have normocytic, normochromic, regenerative anemia.

Indigofera oblongifolia protects against trypanosomiasis-induced spleen injury.

BACKGROUND: Trypanosomiasis is a neglected tropical disease, transmitted by blood-sucking insects and can affect humans and animals, depending on the species of Trypanosoma parasite. Trypanosoma has acquired resistance to the majority of drugs used; hence, alternative medicines are required. Indigofera oblongifolia leaf extract (IOE) has been shown to treat blood stage malaria. Here, IOE was used to demonstrate its effect on Trypanosoma evansi-infected mice. METHODS: Analysis of IOE by gas chromatography-mass spectrometry showed the presence of many active components like flavonoids and phenolics. The mice were divided into three groups as follows: vehicle control, T. evansi-infected mice and T. evansi-infected-treated mice. RESULTS: The findings demonstrate a significant effect of IOE treatment on T. evansi-infected mice. Parasitemia was decreased by 70%, weight loss was reduced, and splenomegaly was significantly decreased. Additionally, IOE improved the histological architecture of the spleen, as shown by the improved histological injury score post-treatment. Anemia was apparent during the course of infection in T. evansi-infected mice; this was reversed upon treatment with IOE to almost the normal level of hemoglobin and erythrocytes. Reduced glutathione and catalase were also ameliorated upon IOE treatment compared to T. evansi-infected mice. CONCLUSION: Overall, this study shows the ameliorative role of IOE against T. evansi-induced spleen injury in mice.

Increased Trypanosoma spp. richness and prevalence of haemoparasite co-infection following translocation.

BACKGROUND: Understanding how fauna translocation and antiparasitic drug treatment impact parasite community structure within a host is vital for optimising translocation outcomes. Trypanosoma spp. and piroplasms (Babesia and Theileria spp.) are known to infect Australian marsupials, including the woylie (Bettongia penicillata). However relatively little is known about these haemoparasites, or how they respond to management practices such as translocation. We monitored haemoparasites infecting woylies for up to 12 months during two fauna translocations to supplement existing woylie populations in three different sites (Dryandra, Walcott and Warrup East) within south-western Australia between 2014 and 2016, with the aim of investigating (i) how haemoparasite prevalence, Trypanosoma spp. richness and Trypanosoma spp. community composition varied over time and between different sites following translocation; and (ii) whether ivermectin treatment indirectly impacts haemoparasite prevalence. Using molecular methods, 1211 blood samples were screened for the presence of trypanosomes, and a subset of these samples (n = 264) were also tested for piroplasms. RESULTS: Trypanosomes and piroplasms were identified in 55% and 94% of blood samples, respectively. We identified five Trypanosoma species, two Theileria species, a single species of Babesia and a novel Bodo species. Trypanosoma spp. richness and the prevalence of haemoparasite co-infection increased after translocation. Prior to translocation, Trypanosoma spp. community composition differed significantly between translocated and resident woylies within Walcott and Warrup East, but not Dryandra. Six months later, there was a significant difference between translocated and resident woylies within Dryandra, but not Walcott or Warrup East. The response of haemoparasites to translocation was highly site-specific, with predominant changes to the haemoparasite community in translocated woylies occurring within the first few months following translocation. Ivermectin treatment had no significant effect on haemoparasite prevalence. CONCLUSIONS: This study contributes to our understanding of haemoparasite dynamics in woylies following translocation. The highly site-specific and rapid response of haemoparasites to translocation highlights the need to better understand what drives these effects. Given that haemoparasite prevalence and composition of translocated and resident animals changed significantly following translocation, we propose that parasite monitoring should form an essential component of translocation protocols, and such protocols should endeavour to monitor translocated hosts and cohabiting species.

Rationale and design of a randomized placebo-controlled trial assessing the effects of etiologic treatment in Chagas' cardiomyopathy: the BENznidazole Evaluation For Interrupting Trypanosomiasis (BENEFIT).

BACKGROUND: Benznidazole is effective for treating acute and chronic (recently acquired) Trypanosoma cruzi infection (Chagas' disease). Recent data indicate that parasite persistence plays a pivotal role in the pathogenesis of chronic Chagas' cardiomyopathy. However, the efficacy of trypanocidal therapy in preventing clinical complications in patients with preexisting cardiac disease is unknown. STUDY DESIGN: BENEFIT is a multicenter, randomized, double-blind, placebo-controlled clinical trial of 3,000 patients with Chagas' cardiomyopathy in Latin America. Patients are randomized to receive benznidazole (5 mg/kg per day) or matched placebo, for 60 days. The primary outcome is the composite of death; resuscitated cardiac arrest; sustained ventricular tachycardia; insertion of pacemaker or cardiac defibrillator; cardiac transplantation; and development of new heart failure, stroke, or systemic or pulmonary thromboembolic events. The average follow-up time will be 5 years, and the trial has a 90% power to detect a 25% relative risk reduction. The BENEFIT program also comprises a substudy evaluating the effects of benznidazole on parasite clearance and an echo substudy exploring the impact of etiologic treatment on left ventricular function. Recruitment started in November 2004, and >1,000 patients have been enrolled in 35 centers from Argentina, Brazil, and Colombia to date. CONCLUSION: This is the largest trial yet conducted in Chagas' disease. BENEFIT will clarify the role of trypanocidal therapy in preventing cardiac disease progression and death.

Thrombocytopenia in experimental trypanosomiasis.

The effect of experimental trypanosomiasis on coagulation was studied because a patient in this hospital with Rhodesian trypanosomiasis developed thrombocytopenia with disseminated intravascular coagulation. Rats injected intraperitoneally with this strain of Trypanosoma rhodesiense consistently developed trypanosomiasis and severe thrombocytopenia without changes in hematocrit or concentration of fibrinogen or fibrin split products. At the time of 50% mortality (4-5 days) mean platelet counts per cubic millimeter of infected rats were 18,000+/-9,000 (+/-2 SEM) compared to 1,091,000+/-128,000 in uninfected controls. In vitro, concentrated trypanosomes and trypanosomefree supernates of disrupted organisms added to normal rat, rabbit, or human blood produced platelet aggregation within 30 min. This platelet aggregation was not blocked by inhibitors of ADP, kinins, or early or late components of complement. In vivo thrombocytopenia also occurred in infected rabbits congenitally deficient in C6 and in infected, splenectomized rats. Although the aggregating substance obtained from disrupted trypanosomes is heat-labile, it is active in the presence of complement inhibitors, suggesting that this trypanosomal product may be a protein enzyme or toxin. Since the phenomenon is independent of immune complexes, complement, ADP, and kinins, it appears to represent a new mechanism of microbial injury of platelets and the induction of thrombocytopenia.

[Strokes caused by infection in the tropics]. / Ictus de causa infecciosa en el trópico.

INTRODUCTION: Almost three out of every four people in the world who suffer a fatal stroke live in developing countries. A number of different tropical diseases may appear in Europe in the coming years as a consequence of the demographic change that is being brought about by migratory flows. We review the main infectious causes of strokes in the tropics. DEVELOPMENT: There are estimated to be 500 million cases of malaria every year. Cerebral malaria can cause cerebral oedema, diffuse or focal compromise of the subcortical white matter and cortical, cerebellar and pontine infarctions. Chagas disease is an independent risk factor for stroke in South America. At least 20 million people have the chronic form of Chagas disease. The main prognostic factors for Chagas-related stroke are the presence of apical aneurysms, arrhythmia and heart failure. Vascular complications of neurocysticercosis include transient ischemic attacks, ischemic strokes due to angiitis and intracranial haemorrhages. The frequency of cerebral infarction associated with neurocysticercosis varies between 2% and 12%. Gnathostomiasis is a cause of subarachnoid haemorrhage in south-east Asia. Other less common causes of stroke are viral haemorrhagic fevers due to arenavirus and flavivirus. CONCLUSIONS: Several diseases that are endemic in the tropics can be responsible for up to 10% of the cases of strokes in adults.

Potential association of reduced cholinesterase activity with Trypanosoma evansi pathogenesis in buffaloes.

The present study aimed to investigate the association of cholinesterase activity with trypanosomosis in buffaloes. Thirty-three clinical cases of trypanosomosis in water buffaloes, found positive for trypomastigotes of T. evansi on blood smear examination, were divided into two groups based on clinical manifestations. Twenty diseased buffaloes revealing only common clinical signs were allocated to Group I, while the remaining 13 buffaloes showing common clinical manifestations along with neurological disturbances were allocated to Group II. Twelve clinically healthy buffaloes, free from any haemoprotozoa infection, were kept as healthy control (Group III). Blood samples were collected from buffaloes of all three groups to determine serum cholinesterase activity. Compared to buffaloes of healthy control group, cholinesterase activity in T. evansi-infected buffaloes of Group I and II was significantly (P<0.001) lower. However, no significant difference was observed in cholinesterase activity between the T. evansi-infected buffaloes exhibiting neurological disorders and no neurological disorders. Summing up, reduced cholinesterase activity seems to be associated with the pathogenesis of natural T. evansi infection and its clinical manifestations in buffaloes possibly by evading immune response. Further studies are warranted on association of cholinesterase activity in T. evansi-infected buffaloes with neurological disorders.

Trypanosoma vivax in water buffalo of the Venezuelan Llanos: An unusual outbreak of wasting disease in an endemic area of typically asymptomatic infections.

Trypanosoma vivax has been associated with asymptomatic infections in African and South American buffalo. In this study, T. vivax was analyzed in water buffalo (Bubalus bubalis) from Venezuela in a molecular survey involving 293 blood samples collected from 2006 to 2015 across the Llanos region. Results demonstrated constant infections (average 23%) during the years analyzed. In general, animals were healthy carriers of T. vivax with low levels of parasitemia and were diagnosed exclusively by TviCATL-PCR. However, an outbreak of severe acute infections mostly in dairy animals was reported during a prolonged drought affecting 30.4% of a buffalo herd (115 animals examined). During the outbreak, animals exhibiting anemia and neurological disorders developed fatal infections, and 7% of the herd died within nine months before treatment against trypanosomosis. Microsatellite locus genotyping (MLG) of T. vivax samples before and during the outbreak revealed similar genotypes, but outbreak isolates exhibited the most divergent MLG. Venezuelan samples from symptomless and sick buffalo did not share the MLGs previously detected in asymptomatic Brazilian buffalo. Trypanosoma evansi was not detected in the herd examined during the outbreak. However, as expected Babesia sp. (62.6%) and Anaplasma sp. (55.6%) infections were highly prevalent in asymptomatic buffalo in the studied areas. This is the first South American outbreak of highly lethal acute T. vivax infections in water buffalo. Our results suggest that chronically infected and asymptomatic buffalo living in areas of enzootic equilibrium can develop symptomatic/lethal disease triggered by stressful scarcity of green forage and water during long droughts, inappropriate management of herds and likely concomitant anaplasmosis and babesiosis. Altogether, these factors weaken buffalo immune defenses, allowing T. vivax to proliferate and, consequently, allowing for progression to wasting disease.

Development of a pHrodo-based assay for the assessment of in vitro and in vivo erythrophagocytosis during experimental trypanosomosis.

Extracellular trypanosomes can cause a wide range of diseases and pathological complications in a broad range of mammalian hosts. One common feature of trypanosomosis is the occurrence of anemia, caused by an imbalance between erythropoiesis and red blood cell clearance of aging erythrocytes. In murine models for T. brucei trypanosomosis, anemia is marked by a very sudden non-hemolytic loss of RBCs during the first-peak parasitemia control, followed by a short recovery phase and the subsequent gradual occurrence of an ever-increasing level of anemia. Using a newly developed quantitative pHrodo based in vitro erythrophagocytosis assay, combined with FACS-based ex vivo and in vivo results, we show that activated liver monocytic cells and neutrophils as well as activated splenic macrophages are the main cells involved in the occurrence of the early-stage acute anemia. In addition, we show that trypanosomosis itself leads to a rapid alteration of RBC membrane stability, priming the cells for accelerated phagocytosis.

Neuropsychiatric manifestations of some tropical diseases.

Some tropical diseases are the direct cause of severe disturbances of cerebral function while others affect only finer cerebral systems controlling fears, anxiety and personality traits. The mechanisms by which psychiatric symptoms are produced in tropical disorders are not any different from the mechanisms that relate to any physical disorders. Neuropsychiatric symptoms may be caused by a number of different mechanisms including bacterial toxins, release of cytokines, hyperthermia, shock (poor perfusion), acute renal insufficiency, pulmonary failure (shock lung), coagulopathy, disruption of the blood-brain barrier, and/or the nest of pathogens into the central nervous system. The following tropical illnesses can be associated with neuropsychiatric symptoms: neurocysticercosis, malaria, trypanosomiasis, dengue, and schistosomiasis. Neurological and psychiatric impairments induced by tropical diseases both represent a major category of invalidating disorders, which cause profound changes in the nervous system functions, often associated with severe sequels or late-onset disturbances. It is therefore important to disseminate knowledge of the neuropsychiatric symptoms accompanying tropical diseases in order to increase the awareness of these problems and challenges.