Trypanosoma evansi: Adenosine deaminase activity in the brain of infected rats

The study was undertaken to evaluate changes in the activity of adenosine deaminase (ADA) in brains of rats infected by Trypanosoma evansi. Each rat was intraperitoneally infected with 10⁶ trypomastigotes either suspended in fresh (group A; n = 13) and cryopreserved blood (group B; n = 13). Thirteen animals were used as control (group C). ADA activity was estimated in the cerebellum, cerebral cortex, striatum and hippocampus. No differences (P > 0.05) in ADA activity were observed in the cerebellum between infected and non-infected animals. Significant (P < 0.05) reductions in ADA activity occurred in cerebral cortex in acutely (day 4 post-infection; PI) and chronically (day 20 PI) infected rats. ADA activity was significantly (P < 0.05) decreased in the hippocampus in acutely infected rats, but significantly (P < 0.05) increased in the chronically infected rats. Significant (P < 0.05) reductions in ADA activity occurred in the striatum of chronically infected rats. Parasites could be found in peripheral blood and brain tissue through microscopic examination and PCR assay, respectively, in acutely and chronically infected rats. The reduction of ADA activity in the brain was associated with high levels of parasitemia and anemia in acute infections. Alterations in ADA activity of the brain in T. evansi-infected rats may have implications for pathogenesis of the disease.     

Oxidative Stress in the Heart of Rats Infected with Trypanosoma evansi

This study was conducted to investigate the occurrence of oxidative stress in the heart tissue of rats infected with Trypanosoma evansi. Rats were divided into 2 groups (A and B) with 12 animals each, and further subdivided into 4 subgroups (A1 and A2, 6 animals/each; and B1 and B2, 6 animals/each). Animals in the groups B1 and B2 were subcutaneously inoculated with T. evansi. Thiobarbituric acid reactive substances (TBARS), superoxide dismutase activity (SOD), glutathione S-transferase activity (GST), reduced glutathione activity (GSH), and non-protein thiols (NPSH) in the heart tissue were evaluated. At day 5 and 15 post-infection (PI), an increase in the TBARS levels and a decrease in the SOD activity (P<0.05) were observed. GSH and GST activities were decreased in infected animals at day 15 PI (P<0.05). Considering the proper functioning of the heart, it is possible that the changes in the activity of these enzymes involved in the oxidative stress may be related, at least in part, in the pathophysiology of rats infected with T. evansi.     

Trypanosoma evansi: Cholinesterase activity in acutely infected Wistar rats

The aim of this study was to evaluate cholinesterase activity during the early acute phase of Trypanosoma evansi infection in rats. Fifteen male Wistar rats were randomly distributed into three groups (n = 5 animals per group): two trypanosome-infected groups (T3 and T5) and uninfected controls (C). The animals were inoculated intraperitoneally with 10⁶ trypanosomes. The blood was collected by cardiac puncture on the 3rd (T3) or 5th day post-infection (T5 and C). Cerebrum and cerebellum were removed for the evaluation of acetylcholinesterase (AChE) activity. AChE activity was also evaluated in whole blood and butyrylcholinesterase activity (BUChE) in plasma samples. Parasitemia were progressive increase and parasites were observed in the peripheral blood of all infected animals one day post-inoculation. AChE activity was not altered in cerebrum and cerebellum tissues. AChE activity in blood significantly decreased in the T3 and T5 groups (26.63 and 25.86 mU/l mol Hb) compared with the control (37.84 mU/l mol Hb). In addition BUChE activity in plasma was lower in the T3 (7.01 μmol BTC hydrolyzed/h/mL) than the T5 and C groups (9.84 and 12.00 μmol BTC hydrolyzed/h/mL). This study therefore, shows that reductions in the activity of cholinesterase occur in acute infection by T. evansi in rats and this demonstrates an important change occurring in animals infected by the protozoan and may indicate a potential role the enzymes play in the mechanism of disease.     

Expression of murine adenosine deaminase (ADA) in transgenic maize

A murine adenosine deaminase (ADA) gene, driven by the maize ubi-1 promoter and intron region, was transformed into embryogenic maize callus, along with a bar and gusA gene-containing plasmid, using microparticle bombardment. Selection in the presence of either the herbicide Basta® or the adenosine analogue 2-deoxyadenosine resulted in transgenic cultures that expressed GUS and accumulated a 41kD protein that immunoprecipated with an ADA-specific polyclonal antibody. ADA enzyme activity was observed in extracts from transgenic callus as well as regenerated plants and progeny. Cultures expressing ADA grew in the presence of 200mg/l 2-deoxyadenosine, a concentration which completely inhibited the growth of non-transgenic cultures. ADA activity appeared to segregate in progeny of regenerated plants as a single, dominant Mendelian trait. These results suggest that ADA, in combination with adenosine analogue selection, represents a potentially viable selectable marker system for transgenic maize production.     

Trypanosoma evansi: Levels of copper, iron and zinc in the bloodstream of infected cats

The aim of this study was to evaluate the concentrations of copper, iron and zinc in blood serum of cats experimentally infected with Trypanosoma evansi. Animals were divided into two groups: control and infected with T. evansi. The animals were infected with 10⁸ trypomastigotes each and parasitemia was estimated daily for 56 days by microscopic examination of smears. Hematological and biochemical parameters were evaluated for monitoring of the disease. Serum metal levels were determined in blood samples collected at days 7, 28 and 56 of the experiment. Inductively coupled plasma optical emission spectrometry was used to measure the levels of copper, iron and zinc. Significant differences were observed among groups (P < 0.05). Increased levels of copper and decreased iron and zinc levels were observed. A decrease in the number of red blood cells was also observed 7 days after inoculation. Biochemical parameters were not altered. Therefore, the infection by T. evansi might alter the serum metal levels, causing metabolic disturbances in cats.     

Pre-treatment with curcumin modulates acetylcholinesterase activity and proinflammatory cytokines in rats infected with Trypanosoma evansi

The potent activity against Trypanosomes and health beneficial effects of curcumin (Cur) has been demonstrated in various experimental models. In this study, we evaluated the in vivo effect of Cur as trypanocide and as potential anti-inflammatory agent, through the evaluation of immunomodulatory mechanisms in rats infected with Trypanosoma evansi. Daily oral Cur was administered at doses of 0, 20 or 60 mg/kg as preventive treatment (30 and 15 days pre infection) and as treatment (post infection). The treatment of the groups continued until the day of euthanasia. Fifteen days after inoculation, parasitemia, plasma proinflammatory cytokines (IFN-γ, TNF-α, IL-1, IL-6), anti-inflammatory cytokines (IL-10) and blood acetylcholinesterase activity (AChE) were analyzed. Pretreatment with Cur reduced parasitemia and lethality. Cur inhibited AChE activity and improved immunological response by cytokines proinflammatory, fundamental during T. evansi infection. We found that Cur is not so important as an antitrypanosomal activity but as immunomodulator agent. These findings reveal that the preventive use of Cur stimulates anti-inflammatory mechanisms, reducing an excessive inflammatory response.     

Diminazene aceturate associated with sodium selenite and vitamin E in the treatment of Trypanosoma evansi infection in rats

The aim of this study was to evaluate the utilization of a standard treatment with diminazene aceturate against the infection caused by Trypanosoma evansi, associated to sodium selenite and vitamin E. In vitro tests showed trypanocidal effect related to the treatment with diminazene aceturate and sodium selenite, but vitamin E had no harmful effect on the trypanosomes. In vivo experiments utilized a total of 72 adult outbreed females rats, separated into 9 groups (A, B, C, D, E, F, G, H and I), 8 animals each. Group A was the uninfected group; groups B to I were infected with 0.2 mL of blood containing 10⁶ trypanosomes. Parasitemia was estimated daily by microscopic examination of blood smears. Group B served as positive control; group C was treated with diminazene aceturate; group D with sodium selenite; group E with vitamin E; group F received an association of diminazene aceturate and sodium selenite; group G received an association of diminazene aceturate and vitamin E; group H received an association of diminazene aceturate, sodium selenite and vitamin E, and group I received an association of sodium selenite and vitamin E. Diminazene aceturate was administrated in a single dose on the 3rd day post infection (PI). Sodium selenite and vitamin E were administered at the 3rd and 23rd day PI. In vivo tests showed increase of longevity in groups treated with diminazene aceturate associated with sodium selenite (groups F and H). No difference was found between groups C and E, thus the vitamin E did not increase the efficacy of treatment against T. evansi when associated to diminazene aceturate. The curative efficacy of treatments was 37.5, 87.7, 37.7 and 75% to the groups C, F, G and H, respectively. Other treatments showed no efficacy. The sodium selenite when combined with chemotherapy may represent an alternative in the treatment of trypanosomosis.     

Biochemical detection of adenosine deaminase in Trypanosoma evansi

Biochemical and molecular research on parasites has increased considerably in trypanosomes in the recent years. Many of them have the purpose of identify areas, proteins and structures of the parasite which are vulnerable and could be used in therapy against the protozoan. Based on this hypothesis this study aimed to detect biochemically the enzyme adenosine deaminase (ADA) in Trypanosoma evansi, and to adapt an assay to the measurement of its activity in trypomastigotes. Firstly, the parasites were separated from the blood of mice experimentally infected with a DEAE-cellulose column. The ADA activity in trypomastigotes was evaluated at concentrations of 0.1, 0.2, 0.5, 0.6 and 0.8 mg of protein by spectrophotometry. ADA activity was observed in the parasites at all concentrations tested and its activity was proportional to the concentration of protein, ranging between 0.64 and 2.24 U/L in the lowest and highest concentration of protein, respectively. Therefore, it is possible to detect biochemically ADA in T. evansi, an enzyme that may be associated with vital functions of the parasite, similar to what occurs in mammals. This knowledge may be useful in the association of the chemotherapic treatment with specific inhibitors of the enzyme, in future studies.     

Purification and characterization of intestinal adenosine deaminase from mice

Adenosine deaminase (ADA) was isolated from small intestine of mice and purified to utmost homogeneity. SDS-PAGE of purified ADA gave a molecular weight of 41 kDa. Western blot analyses gave a single reactive band at 41 kDa and the other band was an associated ADA binding protein. The purified enzyme was more stable in the alkaline pH. The optimum pH and the pI values were about 7.0 and 4.96, respectively. Km values of the small intestinal ADA for adenosine and 2-deoxyadenosine were 23 and 16M, respectively. Purine riboside was a competitive inhibitor with Ki of 5 M, whereas 2-3-o-isopropylidene adenosine acted as an uncompetitive inhibitor (Ki 66 M). Activity of ADA was inhibited by the presence of theophylline (-40%), caffeine (-30%), and L-cysteine (-50%). Significantly, Hg²⁺ (100 M) inhibited 98% of the initial ADA activity. In addition, various purine analogs such as inosine, purine, -adenosine and adenine showed variable inhibitions on the activity of ADA. Relative ADA activity towards 3-deoxyadenosine and 6-chloropurine riboside was lower by 30% and 40%, respectively. However, the activity towards 2-o-methyl adenosine was higher (30%) compared to the activity obtained using adenosine.     

Indigofera oblongifolia as a fight against hepatic injury caused by murine trypanosomiasis

Trypanosoma evansi is a hazardous pathogenic parasite infecting a broad variety of livestock and affects wildlife worldwide. Trypanosoma evansi has gained resistance to most drugs used; therefore, it requires alternative medicines. The objective of this research was to investigate the impact of Indigofera oblongifolia leaf extract (IE) on T. evansi-induced hepatic injury.Mice were once infected with 1000 T. evansi. The treated group was gavaged with 100 mg/Kg IE after infection. Histological and biochemical changes in mice hepatic tissue were studied. Also, the oxidative damage in the liver was evaluated through determining the level of glutathione (GSH), Malondialdehyde (MDA), nitric oxide (NO) and catalase (CAT) markers. IE was able to suppress the induced parasitemia due to infection. Also, IE improved the histological liver architecture. Furthermore, the liver enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) activity were improved after IE mice were treated. IE protects against hepatic damage caused by trypanosomiasis in mice. Further studies are needed to isolate the active compounds in IE and to monitor these compunds’ ameliorative function.     

CpG-ODN Class C Mediated Immunostimulation in Rabbit Model of Trypanosoma evansi Infection

CpG oligodeoxynucleotides (CpG-ODN) stimulate immune cells from a wide spectrum of mammalian species. Class C CpG-ODN is relatively stable and has the combined immune effects of both A and B classes of CpG-ODN. Trypanosoma evansi produces the state of immuno-suppression in the infected hosts. The current chemotherapeutic agents against this parasite are limited in number and usually associated with severe side effects. The present work aimed to determine the immunostimulatory effects of CpG-ODN class C in T. evansi infected rabbits. Rabbits inoculated with CpG C and challenged with T. evansi resulted in delayed onset of clinical signs with reduced severity in comparison to that of T. evansi infected rabbits. The treatment also enhanced humoral immune responses. Histopathological findings in liver and spleen revealed enhancement of mononuclear cell infiltration and secondary B cell follicles. These results demonstrate that CpG-ODN class C, has immunostimulatory properties in rabbit model of trypanosomosis. The use of booster doses or sustained delivery of CpG-ODN will further elucidate the prolonged CpG-ODN generated immune responses.     

Purification and characterization of Plasmodium yoelii adenosine deaminase

Plasmodium lacks the de novo pathway for purine biosynthesis and relies exclusively on the salvage pathway. Adenosine deaminase (ADA), first enzyme of the pathway, was purified and characterized from Plasmodium yoelii, a rodent malarial species, using ion exchange and gel exclusion chromatography. The purified enzyme is a 41 kDa monomer. The enzyme showed K_m values of 41 μM and 34 μM for adenosine and 2′-deoxyadenosine, respectively. Erythro-9-(2-hydroxy-3-nonyl) adenine competitively inhibited P. yoelii ADA with K_i value of 0.5 μM. The enzyme was inhibited by DEPC and protein denaturing agents, urea and GdmCl. Purine analogues significantly inhibited ADA activity. Inhibition by p-chloromercuribenzoate (pCMB) and N-ethylmaleimide (NEM) indicated the presence of functional –SH groups. Tryptophan fluorescence maxima of ADA shifted from 339 nm to 357 nm in presence of GdmCl. Refolding studies showed that higher GdmCl concentration irreversibly denatured the purified ADA. Fluorescence quenchers (KI and acrylamide) quenched the ADA fluorescence intensity to the varied degree. The observed differences in kinetic properties of P. yoelii ADA as compared to the erythrocyte enzyme may facilitate in designing specific inhibitors against ADA.     

Diphenyl diselenide modulates nucleotidases,reducing inflammatory responses in the liver of <Emphasis Type="Italic">Toxoplasma gondii</Emphasis>-infected mice

The aim of this study was to verify the effect of diphenyl diselenide (PhSe)₂ on hepatic nucleotidases and on the concentration of purines in mice infected by Toxoplasma gondii. The animals were divided into four groups: Group A (uninfected), Group B (uninfected and treated with (PhSe)₂), Group C (infected), and Group D (infected and treated with (PhSe)₂). The inoculation (groups C and D) was performed with 50 cysts of T. gondii (ME-49 strain). Mice from groups B and D were treated with 5 μmol kg^?1 of (PhSe)₂. Liver tissue from infected mice showed less severe inflammation, elevated ATP/ADO ratio, elevated NTPDase, 5′nucleotidase, and ADA activities compared to the uninfected group (Group A; P < 0.05). However, infected and treated mice showed decreased ATP levels and elevated ADO levels, as well as higher NTPDase and 5′nucleotidase activities and decreased ADA activity in the hepatic tissue compared to the infected group (P < 0.05). Moreover, the (PhSe)₂ treatment of infected mice reduced the hepatic inflammation and showed an immunomodulatory effect on ectonucleotidases of hepatic lymphocytes, which it returned to basal levels. Therefore, chronic infection by T. gondii induces hepatic inflammation in mice, and it is possible that purine levels and nucleotidase activities in hepatic tissue are related to the pathogenesis of the infection in this tissue. The treatment with (PhSe)₂ was able to reverse the hepatic inflammation in mice chronically infected, possibly due to the modulation of purinergic enzymes that produce an anti-inflammatory profile through the purinergic system in the liver tissue.     

Ubiquinone systems of the genus Cladosporium and morphologically similar taxa

Abstract We measured adenosine deaminase (ADA) activity in a guinea pig model of Legionella pneumophila infection. Female Hartley guinea pigs were inoculated intraperitoneally with one-quarter of the LD₅₀ dose of L. pneumophila Philadelphia-1 strain. Control groups were inoculated with clinical isolates of Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae or Klebsiella pneumoniae . Each group consisted of 5 animals. ADA activity in plasma was assayed calorimetrically before and at various intervals after infection by measuring the amount of ammonia produced after adnosine was added to plasma samples. ADA activity before inoculation was 25.6±6.0 IU/1, it reached 174.4±60.0 IU/1 on day 3 after inoculation of L. pneumophila . ADA activity returned to normal levels on day 14. ADA activity did not increase significantly in guinea pigs infected with the other types of bacteria. These findings suggest that measurement of plasma ADA activity may be useful for the diagnosis of Legionella infection.     

Trypanosoma evansi: Activities of adenine nucleotide degradation enzymes in cerebral cortex of infected rats

This study aimed to evaluate the activities of the ectoenzymes NTPDase and 5′-nucleotidase in synaptosomes from cerebral cortex of rats experimentally infected with Trypanosoma evansi. The animals were divided in four groups (n = 10) according to the time and degree of parasitemia (groups A, B, C and D). The animals from group A were euthanized on day 3 (low parasitemia), group B on day 5 (high parasitemia) and group C on day 15 (low parasitemia). Group D consisted of healthy rats (not-infected, n = 15) and were divided in three periods (n = 5) in order to compare with the infected groups. After euthanasia, cerebral cortex was removed for the preparation of synaptosomes and enzymatic assays. Group A showed no changes in enzymatic activities compared with control. The hydrolysis of ATP, ADP and AMP by the enzymes NTPDase and 5′-nucleotidase were increased (P < 0.05) in group B (38%, 140% and 61%, respectively) when compared with control. In the group C it was observed a decreased (22%) hydrolysis of ATP when compared with control group. The activities of NTPDase and 5′-nucleotidase in synaptosomes alters the acute phase of the disease when the number of circulating parasites is high, thus the change observed is probably due to the parasitemia.     

The effect of host plants on Tetranychus evansi, Tetranychus urticae (Acari: Tetranychidae) and on their fungal pathogen Neozygites floridana (Entomophthorales: Neozygitaceae)

In a series of tritrophic-level interaction experiments, the effect of selected host plants of the spider mites, Tetranychus evansi and Tetranychus urticae, on Neozygites floridana was studied by evaluating the attachment of capilliconidia, presence of hyphal bodies in the infected mites, mortality from fungal infection, mummification and sporulation from fungus-killed mite cadavers. Host plants tested for T. evansi were tomato, cherry tomato, eggplant, nightshade, and pepper while host plants tested for T. urticae were strawberry, jack bean, cotton and Gerbera. Oviposition rate of the mites on each plant was determined to infer host plant suitability while host-switching determined antibiosis effect on fungal activity. T. evansi had a high oviposition on eggplant, tomato and nightshade but not on cherry tomato and pepper. T. urticae on jack bean resulted in a higher oviposition than on strawberry, cotton and Gerbera. Attachment of capilliconidia to the T. evansi body, presence of hyphal bodies in infected T. evansi and mortality from fungal infection were significantly higher on pepper, nightshade and tomato. The highest level of T. evansi mummification was observed on tomato. T. evansi cadavers from tomato and eggplant produced more primary conidia than those from cherry tomato, nightshade and pepper. Switching N. floridana infected T. evansi from one of five Solanaceous host plants to tomato had no prominent effect on N. floridana performance. For T. urticae, strawberry and jack bean provided the best N. floridana performance when considering all measured parameters. Strawberry also had the highest primary conidia production. This study shows that performance of N. floridana can vary with host plants and may be an important factor for the development of N. floridana epizootics.     

Evaluation of Nisin F in the Treatment of Subcutaneous Skin Infections, as Monitored by Using a Bioluminescent Strain of Staphylococcus aureus

The potential of nisin F as an antimicrobial agent in treating subcutaneous skin infections was tested in vivo by infecting C57BL/6 mice with a bioluminescent strain of Staphylococcus aureus (Xen 36). Strain Xen 36 has the luxABCDE operon located on a native plasmid. Mice were grouped into four groups: Infected with strain Xen 36 and treated with nisin F, infected with strain Xen 36 and treated with saline (placebo), not infected and treated with nisin (control) and not infected and not treated (control). The immune systems of the mice were suppressed with deksamethasone. Mice were treated with either nisin F or sterile physiological saline 24 and 48 h after infection with subcutaneously injected S. aureus Xen 36 (4 × 10⁶ CFU). Histology and bioluminescent flux measurements revealed no significant difference between infected mice treated with nisin and saline, respectively. However, infected mice treated with nisin F had an increased number of polymorphonuclear cells when compared with infected mice treated with saline. Also, not infected mice treated with nisin F had an influx of polymorphonuclear cells. Nisin F is thus ineffective in combating deep dermal staphylococcal infections. The apparent immune modulation of nisin when subcutaneously injected has to be investigated.     

Cytokines in rats experimentally infected with Trypanosoma evansi

The aim of this study was to measure the levels of interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), interleukin 1 (IL-1) and interleukin 6 (IL-6) in the serum of rats experimentally infected with Trypanosoma evansi and to correlate these levels with hematological parameters. Initially, 48 rats (group T) were intraperitoneally inoculated with cryopreserved blood containing 1 × 10⁶ trypomastigotes per animal. Twenty-eight animals (group C) were used as negative controls and received 0.2 mL of saline by the same route. The experimental groups were formed according to the time after infection and the degree of parasitemia as follows: four control subgroups (C3, C5, C10 and C20) with seven non-inoculated animals each and four test subgroups (T3, T5, T10 and T20) with 10 animals each inoculated with T. evansi. The blood samples were collected by cardiac puncture at days 3 (C3, T3), 5 (C5, T5), 10 (C10, T10) and 20 (C20, T20) post-infection (PI) to perform the complete blood count and the determination of IFN-γ, TNF-α, IL-1 and IL-6 levels using an ELISA quantitative sandwich. Infected rats showed normocytic normochromic anemia during the experimental period. T. evansi infection in rats caused a serum increase (P < 0.01) of IFN-γ, TNF-α, IL-1 and IL-6 levels at days 3, 5, 10 and 20 PI compared to the controls. The multiple linear regressions showed a reduction of 24% in the hematocrit as a consequence of the increased IFN-γ, TNF-α and IL-1. Therefore, we conclude that the infection caused by T. evansi causes an increase in the pro-inflammatory cytokines. These results suggest a synergism among IL-1, TNF-α and IFN-γ contributing to the development of anemia. This increase is associated with the regulation of immune responses against the parasite.     

Trypanosoma evansi: Ca(2+) ATPase activity and lipid peroxidation in skeletal muscle from rats experimentally infected

The aim of this study was to evaluate Ca²⁺ ATPase activity and the lipid peroxidation in muscles from rats experimentally infected by Trypanosoma evansi and its roles in the muscle pathogenesis in trypanosomosis. Thirty-six rats were divided in two groups. Group A was infected with an isolate from T. evansi and group B was used as a negative control. Group A was divided into three subgroups (A1, A2 and A3), three animals each group, as well as group B (B1, B2 and B3). The collection of samples were performed at days 5 (A1 and B1), 15 (A2 and B2) and 30 (A3 and B3) post-infection (PI) with the purpose of comparison between healthy and infected rats in the course of the disease. The Ca²⁺ ATPase enzyme activity was determined in skeletal muscle samples. Muscle tissue lipid peroxidation was determined by TBARS levels, and histopathologically it was investigated a possible damage to the muscle tissue of rats infected with T. evansi. It was observed a significant decrease of Ca²⁺ ATPase activity in infected rats compared to not-infected. This enzymatic inhibition was observed at days 5, 15 and 30 PI. A significant increase was observed for TBARS levels in the muscles of infected rats at days 5, 15 and 30 PI. It was not identified any histological alterations for gastrocnemius in rats infected by T. evansi at days 5 and 15 PI. Nevertheless, at day 30 PI it was verified inflammatory infiltrate with mononuclear cells between muscle fibers in three infected rats (50%). T. evansi infections in rats showed a negative correlation between Ca²⁺ ATPase and TBARS levels. Based on these results we suggest that the leg weakness and muscle injuries common in infected animals with T. evansi may be related to a reduced activity of Ca²⁺ ATPase and oxidative stress.     

Immunological studies of the mechanism of anaemia in experimental Trypanosama evansi infection in rats

Pathological changes in the blood of rats acutely infected with Trypanosoma evansi and the probable mechanism of the accompanying anaemia, were investigated. A severe anaemia, together with rreticulocytosis and hepato-splenomegaly, were regularly observed. Histological examination of the liver, spleen and bone-marrow confirmed the increasedin erythropoietic activity that the observed anaemia was due to increasedextravascular destruction of erythrocytes rather than by inhibition of haemopoietic activity. All the infected rats showed significant immune responses to the infecting trypanosome peak agglutinin titres occurring 10–12 days after injection, coincidentally with maximun destruction of erythrocytes. Serological examination of sera and erythrocytes from all infected and control rats did not reveal the presence of either circulating or adsorbed erythrocyte auto--antibodies. Furthermore, there was no in vivo trypanosomal antigen coating of the erythrocytes from either infected or multiple antigen-injected rats. Repeated intraveoous injections into rats of more than 100 μg per g body weight of soluble T. evansi antigen resulted in moderately severe, probably antibody-mediated, haemolytic anaemia. It is considered that an immunologically-mediated mechanism may be responsible for the development of the anaemia accompanying T. evansi infection.