Trypanosoma evansi (Kinetoplastida: Trypanosomatidae) in capybaras (Hydrochoerus hydrochaeris, Rodentia: Hydrochoeridae): prevalence, effect and sexual selection.

Parasites play a crucial role in the ecology of animals. They also appear to be important in mechanisms underlying sexual selection processes. In this article we study the prevalence, effect and potential role in sexual selection of the protozoon Trypanosoma evansi in capybaras, Hydrochoerus hydrochaeris. We collected our samples from the annual capybara cull of a ranch in Venezuela, using the volume of the snout scent gland as an indicator of dominance; the residuals of body weight as indicators of condition; and the residuals of the spleen mass as indicators of immune function. Overall prevalence was 30.9% (N=97) with no difference between males and females and no relation between infection with T. evansi and condition. However, we found that infected animals had larger spleens (residuals), indicating an immunological cost of the infection. Further, males with larger snout scent glands (more dominant) were less likely to be infected than males with smaller glands (less dominant) suggesting that by choosing males with a large gland, females may be using the gland as an indicator of health, which is consistent with the "good genes" view of sexual selection.

Relationship between behavioral alterations and activities of adenylate kinase and creatine kinase in brain of rats infected by Trypanosoma evansi.

The aim of this study was to investigate the behavioral assessment and activities of important enzymes involved in the phosphoryl transfer network in rat brains that were experimentally infected with Trypanosoma evansi. Behavioral assessment (cognitive performance), pro-inflammatory cytokines in serum and activities of adenylate kinase (AK), pyruvate kinase (PK), and creatine kinase (CK) in brain were evaluated at 5 and 15 days post-infection (PI). Here we demonstrate a cognitive impairment in the rats infected with T. evansi. At 5 and 15 days PI, a memory deficit and a depressant activity were demonstrated by an inhibition avoidance test and increase in the immobility time in a tail suspension test, respectively. On day 5 PI, a decrease in the CK activity and an increase in the AK activity were observed. On day 15 PI, an increase in the CK activity and a decrease in the AK activity were observed. Considering the importance of energy metabolism for brain functioning, it is possible that the changes in the activity of enzymes involved in the cerebral phosphotransfer network and an increase in the proinflammatory cytokines (TNF and IFN) may be involved at least in part in the cognitive impairment in infected rats with T. evansi.

Biology of human pathogenic trypanosomatids: epidemiology, lifecycle and ultrastructure.

Leishmania and Trypanosoma belong to the Trypanosomatidae family and cause important human infections such as leishmaniasis, Chagas disease, and sleeping sickness. Leishmaniasis, caused by protozoa belonging to Leishmania, affects about 12 million people worldwide and can present different clinical manifestations, i.e., visceral leishmaniasis (VL), cutaneous leishmaniasis (CL), mucocutaneous leishmaniasis (MCL), diffuse cutaneous leishmaniasis (DCL), and post-kala-azar dermal leishmaniasis (PKDL). Chagas disease, also known as American trypanosomiasis, is caused by Trypanosoma cruzi and is mainly prevalent in Latin America but is increasingly occurring in the United States, Canada, and Europe. Sleeping sickness or human African trypanosomiasis (HAT), caused by two sub-species of Trypanosoma brucei (i.e., T. b. rhodesiense and T. b. gambiense), occurs only in sub-Saharan Africa countries. These pathogenic trypanosomatids alternate between invertebrate and vertebrate hosts throughout their lifecycles, and different developmental stages can live inside the host cells and circulate in the bloodstream or in the insect gut. Trypanosomatids have a classical eukaryotic ultrastructural organization with some of the same main organelles found in mammalian host cells, while also containing special structures and organelles that are absent in other eukaryotic organisms. For example, the mitochondrion is ramified and contains a region known as the kinetoplast, which houses the mitochondrial DNA. Also, the glycosomes are specialized peroxisomes containing glycolytic pathway enzymes. Moreover, a layer of subpellicular microtubules confers mechanic rigidity to the cell. Some of these structures have been investigated to determine their function and identify potential enzymes and metabolic pathways that may constitute targets for new chemotherapeutic drugs.

Relationship between testicular lesion and hormone levels in male rats infected with Trypanosoma evansi.

The aim of this study was to evaluate the relationship between testicular lesions and hormone levels in rats experimentally infected with Trypanosoma evansi. For that, the measurement of reproductive hormones, histopathology and biomarkers of cellular injury were carried out in twenty-four animals, which were divided into two groups with 12 animals each. Group A was the negative control, or uninfected, while group B was composed by animals infected with T. evansi. Both groups were divided again into two other subgroups (n=6), from which serum and testicular fragments were collected on days 5 (A1 and B1) and 15 (A2 and B2) post-infection (PI). The morphological analysis showed increased alterations of head and tail of sperm in infected rats when compared with those of the control group. A significant reduction (P<0.01) in the levels of LH, FSH, testosterone and estradiol, associated with an increase in cortisol, was observed in serum of group B when compared with negative control. Additionally, NOx, lipid peroxidation and protein oxidation were enhanced in testicles, indicating the occurrence of cellular lesion. On histopathology, it was possible to observe testicular degeneration, among other disorders in infected animals. Therefore, based on these results, it is possible to conclude that the experimental infection with T. evansi caused changes in the levels of the main hormones of male rats associated with cellular injury.

Clinico-haematobiochemical and cardiac alterations in Trypanosoma evansi infected buffaloes of Andhra Pradesh, India.

The present research aimed to document the incidence, clinical signs, haematological, and serum biochemical alterations, as well as electrocardiography and echocardiography findings in 62 buffaloes (selected from a total of 240) infected with Trypanosoma evansi. The study spanned one year, from January 2022 to December 2022. Morphological identification of Trypanosoma evansi was done by the presence of a centrally positioned nucleus with a small sub-terminal kinetoplast at the posterior position through microscopic examination of Giemsa stained peripheral blood smears. The incidence of trypanosomosis were determined to be 26% (62/240) using stained blood smear examination and 41% (98/240) through polymerase chain reaction assay. Clinical signs exhibited by buffaloes with trypanosomosis included the lack of rumination (94%; 58/62), anorexia (90%; 56/62), emaciation (87%; 54/62), loss of milk yield (84%; 52/62), ocular discharges (82%; 51/62), depressed demeanour (81%; 50/62), sunken eye balls (61%; 38/62), fever (60%; 37/62), scleral congestion (56%; 35/62) and intermittent fever (42%; 26/62). Cardiovascular clinical findings in affected buffaloes included tachycardia (44%; 27/62), cardiac arrhythmia (24%; 15/62), cardiac murmurs (19%; 12/62) and muffled heart sounds (18%; 11/62). In the present study, buffaloes with trypanosomosis exhibited significant reduction in haemoglobin (p = 0.008), packed cell volume (p = 0.004), total erythrocyte count (p = 0.003), mean corpuscular volume (p = 0.042), total leucocyte count (p = 0.048) and absolute neutrophil count (p = 0.012); a significant increase in absolute eosinophil count (p = 0.011) and absolute monocyte count (p = 0.008) compared to the apparently healthy buffaloes. Additionally significant decrease in albumin (p = 0.001), A/G ratio (p = 0.007), calcium (p = 0.008), glucose (p = 0.007), phosphorous (p = 0.048), sodium (p = 0.008), potassium (p = 0.041) and chloride (p = 0.046) were observed in buffaloes with trypanosomosis compared to healthy ones. Buffaloes with trypanosomosis also showed significant increase in globulin (p = 0.004), aspartate aminotransferase (p = 0.008), bilirubin (p = 0.034), blood urea nitrogen (p = 0.071), creatinine (p = 0.029), cholesterol (p = 0.046), lactate dehydrogenase (p = 0.009), gamma-glutamyl transferase (p = 0.004) and creatine kinase-myoglobin binding levels (p = 0.005). Electrocardiography explorations in buffaloes with trypanosomosis revealed sinus tachycardia, low voltage QRS complex, ST segment elevation, wide QRS complex, sinus arrhythmia, sinus bradycardia, wandering pace maker, first degree atrio ventricular block, biphasic T wave and tall T wave. Echocardiography examination unveiled cardiac chamber dilatation, ventricular wall thickening and indications of pericarditis/cardiac tamponade. Necropsy was carried on the dead buffaloes during the study period disclosed severely congested blood vessels on epicardial surface, endocardial haemorrhages, and presence of pericardial fluid. Histopathological examination of the heart revealed hyaline degeneration, haemorrhages in the cardiac muscles and varying degrees of degenerative changes. Additionally, the pericardium displayed increased thickness due to presence of more elastic fibres, fibroblast cells in the myocardium, discontinuity of muscle layers, vascular congestion, perivascular mono nuclear cell infiltration and augmented thickness of the endocardium with fibroblast cell proliferation. The study's conclusion highlights cardiac alterations as secondary complications in buffaloes infected with Trypanosoma evansi. Further investigations are recommended to elucidate therapeutic modifications and refine the treatment paradigm.

Trypanosoma evansi infection impairs memory, increases anxiety behaviour and alters neurochemical parameters in rats.

The aim of this study was to investigate neurochemical and enzymatic changes in rats infected with Trypanosoma evansi, and their interference in the cognitive parameters. Behavioural assessment (assessment of cognitive performance), evaluation of cerebral L-[3H]glutamate uptake, acetylcholinesterase (AChE) activity and Ca+2 and Na+, K+-ATPase activity were evaluated at 5 and 30 days post infection (dpi). This study demonstrates a cognitive impairment in rats infected with T. evansi. At 5 dpi memory deficit was demonstrated by an inhibitory avoidance test. With the chronicity of the disease (30 dpi) animals showed anxiety symptoms. It is possible the inhibition of cerebral Na+, K+-ATPase activity, AChE and synaptosomal glutamate uptake are involved in cognitive impairment in infected rats by T. evansi. The understanding of cerebral host­parasite relationship may shed some light on the cryptic symptoms of animals and possibly human infection where patients often present with other central nervous system (CNS) disorders.

Variation in disease phenotype is marked in equine trypanosomiasis.

BACKGROUND: Equine trypanosomiasis is a severe and prevalent disease that has the greatest impact globally upon working equids due to its distribution across lower income countries. Morbidity and mortality rates are high; disease management strategies in endemic regions are ineffective and cost prohibitive. Individual variation in disease phenotype in other species suggests host factors could reveal novel treatment and control targets but has not been investigated in equids. METHODS: A prospective clinical evaluation of equines presenting for a free veterinary examination was performed in hyperendemic villages in The Gambia. Age, body condition score and body weight were estimated by validated methods, and haematocrit and total protein concentration measured. Animals fulfilling 2 out of 5 clinical inclusion criteria (anaemia, poor body condition, pyrexia, history of abortion, oedema) for a diagnosis of trypanosomiasis received trypanocidal treatment with follow-up at 1 and 2 weeks. Blood samples underwent PCR analysis with specific Trypanosoma spp. primers and results were compared to the subject's clinical and clinicopathological features. A mixed effects generalised linear model was generated to evaluate the association of infection status with degree of pyrexia and anaemia. RESULTS: Morbidity was high within examined (n = 641) and selected (n = 247) study populations. PCR status was not associated with a defined disease phenotype; there was intra- and inter-species variability. Donkeys were more frequently Trypanosoma spp.-positive (P < 0.001) and febrile (P < 0.001) than horses, but infected horses were more anaemic (P < 0.001), and in poorer body condition (P < 0.001) than donkeys. Sex was correlated to disease phenotype: males were more anaemic (P = 0.03) and febrile (P < 0.001). Haemoparasite co-infections were more common than a single infection. CONCLUSIONS: There was evidence of diversity in trypanosomiasis clinical signs plus variable disease phenotypes within equid subpopulations that warrant further investigation. The complex co-infection profile of field cases requires greater consideration to optimise disease management.

Lipid peroxidation in cats experimentally infected with Trypanosoma evansi.

The objective of this study was to evaluate the lipid peroxidation and the susceptibility of erythrocytes to in vitro peroxidation as indicators of oxidative damage in erythrocytes and their roles in the pathogenesis of anemia during experimental Trypanosoma evansi infection in cats. Animals were divided into two groups: control and infected with T. evansi. Seven cats were infected with 10(8) trypomastigotes each, and parasitemia was estimated daily for 49 days by microscopic examination of smears. Hematological and biochemical parameters were evaluated for monitoring of the disease. Plasma lipid peroxidation (Thiobarbituric Acid Reactive Substances (TBARS)) and the susceptibility of erythrocytes to in vitro peroxidation were evaluated. Blood samples for analysis were collected at days 21 and 49 post-inoculation. TBARS level, indicated by MDA concentration, was higher in the infected group than in the control group in both analyzed periods, as well as the in vitro erythrocyte peroxidation (P < 0.001). The infected cats had variable degrees of regenerative anemia, which could be explained by the damage in erythrocyte membrane caused by lipid peroxidation.

Trypanosoma evansi induces detrimental immuno-catabolic alterations and condition like type-2 diabetes in buffaloes.

The present study aimed to investigate the perturbations in immuno-metabolic and redox status of buffaloes with trypanosomosis. Thirteen buffaloes suffering from clinical trypanosomosis and eight apparently healthy buffaloes were included in the present study. Buffaloes with trypanosomosis found to have markedly elevated levels of interleukin-10 (IL-10), nonesterified fatty acids (NEFA) and beta-hydroxybutyrate (BHBA) in comparison with healthy controls. Whereas, total antioxidant capacity (TAC) and haemoglobin levels of buffaloes with trypanosomosis were significantly lower than the healthy controls. Remarkable elevation in malondialdehyde (MDA) and protein carbonyls (PC) levels were also observed in the diseased buffaloes. Moreover, buffaloes with trypanosomosis were found to have markedly elevated levels of serum glucose, total proteins, globulins, urea and aspartate aminotransferase (AST) and markedly lowered levels of serum calcium, total cholesterol levels and albumin/globulin (A/G) ratio as compared to the controls. Findings of our study evidently suggest that Trypanosoma evansi induces remarkable immunosuppressive and pro-oxidative status with an increased catabolic activity and hyperglycemic condition like type-2 diabetes in naturally infected buffaloes. Therefore, immuno-metabolic and pro-oxidative predicaments should be addressed by the veterinary clinician while managing the clinical cases of trypanosomosis in buffaloes.

[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.

Hematological and biochemical changes in water buffalo calves (Bubalus bubalis) infected with Trypanosoma evansi.

Four water buffalo calves (Bubalus bubalis) were each inoculated intravenously with 10(6)T. evansi (camel isolate) and the fifth calf kept as non-infected control. The blood and sera of all calves were examined every 4 days during the first month post-inoculation (pi) and then once weekly until the end of the experiment (88 days pi). They were examined for hematological and biochemical changes, liver and kidney function tests. Hemoglobin concentration (Hb%), packed cell volume (PCV) and red blood cell count were significantly decreased. Total leucocytic count, lymphocytes and monocytes showed significant increase. Liver function tests revealed significant elevation in the activity of lactate dehydrogenase enzyme (LDH), globulin, total biliruben and indirect biliruben while alkaline phosphatase enzyme showed significant decrease. Kidney function tests revealed significant decrease of both creatinine and urea.

Semen characteristics and reaction time of Yankasa rams experimentally infected with Trypanosoma evansi infection.

Trypanosomosis is a serious, often fatal disease of domestic animals and humans, and a major constraint to livestock productivity and agricultural development in areas of Africa, Latin America, the Middle East, and Asia. It is caused by hemoflagelate protozoan of the genus Trypanosoma. Several species of Trypanosoma such as Trypanosoma congolense, Trypanosoma vivax, Trypanosoma brucei, and Trypanosoma evansi are known to infect domestic animals. Trypanosoma evansi is one of the most widespread pathogenic trypanosomes in the world causing disease known as "Surra" in animals. The effects of experimental T evansi infection on some aspects of reproduction in Yankasa rams were investigated over a 108-day period. Rams in the infected group A (n = 7) were each inoculated with 1 × 10(6) trypanosomes in 1 mL of donor blood via the jugular vein, whereas the control group B (n = 5) were administered 1 mL of normal saline. Semen volume, gross motility, live and/or dead sperm ratio, sperm morphologic abnormalities, and concentration as well as reaction time of infected and control rams were evaluated on a weekly basis. The results showed a nonsignificant (P > 0.05) decrease in semen volume and a significant (P < 0.05) decrease in concentration compared to the control rams. Reaction time showed considerable significant (P < 0.05) increase from preinfection values 26.7 ± 4.54 to 94.7 ± 7.54 seconds compared to control 32.9 ± 2.64 to 33.4 ± 4.78 seconds. Furthermore, semen gross motility for infected rams differed significantly (P < 0.05) from those of the control. There was a significant surge (P < 0.05) in the total sperm morphologic abnormalities in the infected rams to 90.75 ± 2.73% by week 20 (14 weeks after infection), compared to preinfection value of 20.9 ± 0.52%. The outcome of this study suggests that infection with T evansi in Yankasa rams has far reaching severe effects on their reproductive performance.

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.

Co-infection with Plasmodium berghei and Trypanosoma brucei increases severity of malaria and trypanosomiasis in mice.

Individuals in natural populations may be infected with multiple different parasites at a time. These parasites may interact with each other or act independently in the host, and this may result to varying outcomes on host health and survival. This study therefore aimed at investigating the health impact of co-infection of mice with Plasmodium berghei and Trypanosoma brucei. Forty Swiss albino mice (14-17g) were divided into four groups of ten. Mice in groups A and B received 10(6)P. berghei and groups B and C 10(5)T. brucei, while group D were uninfected. The co-infected mice had higher P. berghei and T. brucei parasitaemia, compared with the mono-infected mice. The co-infected mice had significantly (p<0.05) lower survival rate compared with the mono-infected mice. Co-infection of mice with P. berghei and T. brucei resulted in rapid P. berghei and T. brucei development and increased parasitaemia. The leukocyte numbers significantly (p<0.05) reduced on days 12 and 15 post infection among P. berghei infected mice, in the presence or absence of T. brucei. Anaemia and hypoglycaemia was more severe in the co-infected mice. Therefore, co-infection of mice with P. berghei and T. brucei may increase pathologic impact to the host by increasing parasitaemia.

Experimental Trypanosoma evansi infection in the goat. I. Clinical signs and clinical pathology.

A strain of Trypanosoma evansi isolated from an equine case of surra in Mindanao, Philippines was used to infect intravenously two groups (A and B) of five male goats aged 8-10 months. Animals of groups A and B received 5000 and 50 000 trypanosomes, respectively, and five further animals (group C) served as uninfected controls. Four of the 10 infected goats died 8-78 days after inoculation. Group C goats gained weight (mean 22.8 g/day) while infected goats in groups A and B lost weight (means of 21.4 and 45.0 g/day, respectively). Parasitaemia fluctuated regularly between peaks and troughs, with repeated periods of about 6 days during which no trypanosomes were detected in the blood. Clinical signs and clinico-pathological changes in infected goats were not pathognomonic in the absence of parasites in the blood, and leucocytosis was not a reliable indicator of infection. It was concluded that in endemic areas fluctuating fever, progressive emaciation, anaemia, coughing, testicular enlargement and diarrhoea are suggestive of surra; confirmation, however, may necessitate examination of blood every few days for trypanosomes, and possibly other diagnostic tests.

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.

Chemokines in host-protozoan-parasite interactions.

Here, we review the interactions between parasites and chemokines and chemokine receptors in toxoplasmosis, trypanosomiasis, leishmaniasis, malaria and other diseases caused by protozoan parasites. The potential roles of chemokines after infection by these intracellular pathogens include host defence functions such as leukocyte recruitment, participation in cell-mediated immunity and antiprotozoal activity. However, these interactions can also help the parasite in, for example, the penetration of host cells.

VSG-GPI anchors of African trypanosomes: their role in macrophage activation and induction of infection-associated immunopathology.

African trypanosomes express a glycosylphosphatidyl inositol (GPI)-anchored variant-specific surface glycoprotein (VSG) as a protective coat. During infection, large amounts of VSG molecules are released into the circulation. Their interaction with various cells of the immune system underlies the severe infection-associated pathology. Recent results have shown that anti-GPI vaccination can prevent the occurrence of this pathology.

Hypotension in rabbits infected with Trypanosoma brucei.

1 Blood pressures and heart rates of 12 anaesthetized rabbits chronically infected with T.brucei were measured (average infection time 39 days (range 25-67). The systolic BP was 31.4 +/- 5.7 mmHg, the diastolic BP 25.0 +/- 7.2 mmHg, and the heart rate 120.5 +/- 24.2 beats/minute. Two rabbits were already hypotensive 10 days after infection. In 12 anaesthetized control rabbits, the systolic BP was 66.2 +/- 7.3 mmHg (mean +/- s.e.), the diastolic BP 60.2 +/- 7.3 mmHg, and the heart rate 116.3 +/- 15.9 beats/minute. 2 The intravenous injection of 3 X 10(8) disintegrated trypanosomes into infected rabbits lowered the blood pressure by 41.4 +/- 22.0%. Pretreatment of two rabbits with aprotinin prior to administration of parasites prevented the fall in blood pressure. 3 Injection of 3 X 10(8) live trypanosomes complexed with hyperimmune sera produced a fall of 68.3 +/- 38.4% in the systolic BP of normal rabbits. Disintegrated or live trypanosomes, or hyperimmune sera alone had no effect. Pretreatment of animals with aprotinin prior to administration of the immune complex abolished the fall in BP. 4 The results suggest that the profound hypotension in chronic trypanosomiasis is caused by complex formation of trypanosomes with antibody. Since it can be prevented by pretreatment with aprotinin, it is likely that activation of plasma kallikrein with a subsequent release of plasma kinins contributes to this effect.