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PubMed2000

Serodiagnosis of recently acquired Toxoplasma gondii infection with a recombinant antigen.

A portion of a cDNA encoding a 35-kDa antigen from Toxoplasma gondii was cloned into the CKS expression vector and expressed in Escherichia coli. By using the enzyme-linked immunosorbent assay (ELISA), the recombinant protein (rP35 antigen) was examined for reactivity with immunoglobulin G (IgG) antibodies in the sera of pregnant women. Of these women, 41 had a toxoplasma serologic profile suggestive of recently acquired T. gondii infection (Sabin-Feldman dye test [DT] titers from 1:256 to 1:32,000, positive IgM ELISA titers from 2.3 to 9.7, positive IgA ELISA from 1 to >28, and acute patterns in the differential agglutination [AC/HS] test) (group I), and 50 women had a toxoplasma serologic profile suggestive of infection acquired in the distant past (low DT titers from 1:16 to 1:512, negative IgM ELISA titers from 0 to 0.8, and chronic patterns in the AC/HS test) (group II). The classification of acute or chronic profile was based on the individual's clinical history as well as the combination of the results of the toxoplasma serological profile. An additional group (group III) was composed of sera from 50 women who were seronegative for T. gondii antibodies in the DT. The results revealed that whereas 85.3% of women in group I had IgG antibodies that reacted with the rP35 antigen, only 8% of women in group II had IgG antibodies that reacted with the same antigen. In immunoblots, the rP35 antigen was recognized by IgG antibodies in a pool of sera from individuals with a toxoplasma serologic profile compatible with acute infection but not in a pool of sera from individuals with a serologic profile characteristic of a chronic infection. These results reveal that IgG antibodies against the P35 antigen are produced during the acute stage of the infection but are uncommon in the latent or chronic phase of the infection. Thus, the rP35 antigen may be a useful serologic marker to differentiate between recently acquired infection and that acquired in the more distant past.

Antibodies, Protozoan↗

PubMed2006

Symptomatic toxoplasma infection due to congenital and postnatally acquired infection.

AIMS: To determine the incidence and severity of symptomatic toxoplasma infection presenting during childhood due to congenital or postnatally acquired infection. METHODS: Between 2002 and 2004, newly diagnosed children (<16 years) with signs or symptoms of congenital or ocular toxoplasmosis were reported by clinicians to the British Paediatric and Ophthalmic Surveillance Units or by toxoplasma referral laboratories. Confirmed cases were estimated to have a greater than 50% probability of congenital and/or ocular toxoplasmosis, based on clinical and serological findings. RESULTS: Thirty eight children had confirmed toxoplasma infection. Twenty two (58%) were classified with congenital infection (cumulative incidence for England and Wales 1.62[corrected]/100,000 live births; 95% CI 0.85[corrected] to 2.83[corrected]), of whom 2 (9%) were stillborn, 7 (32%) live births had intracranial abnormalities and/or developmental delay (5 of whom had retinochoroiditis), and 10 (45%) had retinochoroiditis with no other abnormalities reported. A further 16 (42%) children were classified as infected after birth; all had retinochoroiditis. CONCLUSIONS: The low burden of symptomatic congenital toxoplasmosis combined with the lack of evidence of an effective treatment support current policy not to offer prenatal or neonatal screening for toxoplasma infection. Primary prevention strategies need to address acquisition of infection in childhood which accounts for half the ocular disease due to toxoplasma infection in children in the UK and Ireland.

Abortion, Spontaneous↗

PubMed2002

Reliability of expert interpretation of retinal photographs for the diagnosis of toxoplasma retinochoroiditis.

AIMS: To measure agreement and estimate sensitivity and specificity of uveitis experts' interpretation of retinal photographs for the diagnosis of toxoplasma retinochoroiditis. METHODS: The authors collated 96 retinal photographs from patients presenting with symptomatic posterior uveitis to ophthalmology clinics within a defined geographical area. Five uveitis experts independently ranked each photograph as definite, probable, possible, or not toxoplasma retinochoroiditis. They measured interobserver agreement based on an intraclass correlation coefficient and estimated sensitivity and specificity for each observer using a maximum likelihood model. RESULTS: The intraclass correlation coefficient for all five observers was 0.62 (95% CI: 0.54 to 0.69). Estimates of sensitivity and specificity for individual observers ranged from 71% to 96% and 58% to 100% respectively when appearances were dichotomised as definite or probable toxoplasma retinochoroiditis, versus possible or not. CONCLUSION: Agreement between uveitis experts on the interpretation of retinal photographs was moderate to good, but the estimates of sensitivity and specificity of their interpretation for the diagnosis of toxoplasma retinochoroiditis were highly variable. Assuming that interpretation of photographs is similar to real time ophthalmoscopy, clinicians need to beware that treatment decisions made on the basis of a single assessment will include patients without toxoplasma retinochoroiditis and will miss patients with the disease.

Acute Disease↗

PubMed1993

Prevalence of toxoplasma myocarditis in patients with the acquired immunodeficiency syndrome.

OBJECTIVE: To evaluate the prevalence of cardiac toxoplasmosis in a series of 182 necropsies performed between 1987 and 1991 on patients infected with the human immunodeficiency virus (HIV), to correlate this prevalence with the ante mortem diagnosis of cardiac involvement, and to assess the role of such cardiac lesions in the immediate cause of death. PATIENTS AND METHODS: Complete necropsies of 182 HIV-infected patients (48 women, 134 men) were performed consecutively between 1987 and 1991. Risk factors, identified in 174 cases, included drug abuse (111/182), homosexuality (51/182), and blood transfusions (12/182). 16 samples were systematically obtained from each heart for histological study. If trophozoites or lymphocytic myocarditis were seen, immunohistochemical investigations were carried out with polyclonal antibodies for Toxoplasma gondii. An ultrastructural study was performed in four patients with toxoplasma myocarditis. Myocardial lesions were defined by the Dallas classification. Clinical data (and information on electrocardiograms and echocardiograms) were obtained from medical records. RESULTS: Cardiac toxoplasmosis was diagnosed at necropsy in 21 (12%) patients. Cardiac lesions were associated with toxoplasmic encephalitis in 18 patients and were solitary in three patients. Acute diffuse myocarditis was present in 6/21, rare foci of myocarditis were seen in 8/21, and intramyocytic toxoplasmic cysts without any inflammatory reaction or necrosis were seen in 4/21. Anti-toxoplasma immunolabelling showed cardiac toxoplasmosis in three patients with lymphocytic myocarditis. Particles with the ultrastructural characteristics of Toxoplasma gondii trophozoites were seen in four cases. Six patients had presented with cardiac symptoms, confirmed by electrocardiographic and echocardiographic abnormalities during their disease course, and their cardiac lesions were directly responsible for the death. CONCLUSION: Cardiac toxoplasmosis was common in this necropsy series of HIV-infected patients. Cardiac toxoplasmosis had been suspected clinically in four patients. Myocardial lesions were generally asymptomatic and were not discovered until necropsy. Solitary cardiac involvement was not uncommon reflecting parasite reactivation at a myocardial site. The incidence of cardiac toxoplasmosis in this group of immunodepressed subjects from an area with a high prevalence of this parasitic disease justifies regular follow up of such patients by electrocardiography and echocardiography as well as immediate administration of anti-toxoplasma treatment should sudden heart failure occur.

Acquired Immunodeficiency Syndrome↗

PubMed1994

Importance of early gamma interferon production in Propionibacterium acnes-induced resistance to Toxoplasma gondii infection in mice.

Treatment of mice with heat-killed Propionibacterium (P.) acnes conferred transient protection against Toxoplasma infection. To investigate the mechanism of this nonspecific resistance, the production of gamma interferon (IFN-gamma) by P. acnes-injected mice was evaluated in comparison with that by noninjected controls upon infection with Toxoplasma. Mice pretreated with this bacterium produced significantly more IFN-gamma than that produced by control mice up to 24 hr of infection. A single injection of anti-IFN-gamma MAb on day 0 but not later than day 3 of infection resulted in a total abrogation of the resistance conferred by P. acnes. Likewise, daily injection of cyclosporin A (Cs-A), a potent inhibitor of T cell function, during the first 3 days of Toxoplasma infection severely exacerbated the infection, in accordance with a marked suppression of the early IFN-gamma production. In contrast, the administration of Cs-A for 3 consecutive days starting at day 4 had no significant consequence on P. acnes-induced anti-toxoplasma resistance, while it reduced greatly the ability of P. acnes-injected mice to produce IFN-gamma in the later phase of infection. Moreover, no significant increase in mortality and suppression of IFN-gamma production was noted in mice receiving anti-asialo GM1 antibody. These results suggest that the early IFN-gamma production by T cells is an essential event for the establishment of P. acnes-induced anti-toxoplasma resistance in mice.

Animals↗

PubMed1975

[Serological studies on rabbits inoculated with Toxoplasma gondii]

Serological studies on toxoplasmosis were conducted with rabbits sera that were immunized with RH strain or infected with Beverley strain of Toxoplasma gondii. Complement fixation tests, agar-gel double diffusion tests and agar-gel immunoelectrophoresis were performed. Toxoplasma crude antigen was prepared from the organisms in mice peritoneal fluids, which were infected with RH strain of Toxoplasma gondii. The organisms were suspended in saline volume originally exudated and counted in hemocytometer for purity of the organisms over 99%. These suspended organisms were prepared by sonication, and the solution was centrifuged for 30 min. at 10,000 rpm in 4 degrees C. These supernatant fluids were used as crude antigen. On the other hand, purified antigens were fractionated on Sephadex G-200 gel filtration. A Sephadex G-200 column, 80 by 4 cm, equilibrated with Tris-HCl-(0.1M)-NaCl (1.0M) buffer, pH 8.0 was used. The eluate fractions were collected in 3 ml per hour and the absorbance at 280 nm was measured with a Beckman Du-2 spectrophotometer. Each tube is pooled into 6 fractions by protein density graph. For immunization of rabbits, crude antigen of RH strain was emulsified with an equal amount of incomplete Freund's adjuvant and l ml of mixture was injected subcutaneously into them once a week for 5 successive weeks. Antisera were obtained at an interval of a week, beginning the first week after the last immunization, while several rabbits were infected with Beverley strain of Toxoplasma gondii by inoculating about 200 cysts and antisera were obtained from them serially at a week interval. The results were as follows: 1. The sera from the rabbits immunized with the RH strain or infected with Beverley strain of Toxoplasma gondii againist the crude antigen showed the first positive reactions in 2 or 3 weeks after the administration or immunization in complement fixation tests. Maximum titers appeared in 4 or 5 weeks after immunization with RH strain and in 7 or 9 weeks after infection with Beverley strain respectively. 2. Complement fixation tests showed the positive reactions in the rabbits sera immunized with RH strain against the purified antigens II, III, IV, V and VI: moreover, antigen IV fraction showed the highest titer. On the other hand in the rabbits sera infected with Beverley strain against the purifed antigens II, III and IV fractions showed the positive reaction; especially, antigen fraction IV showed the highest titer. 3. In immuno-diffusion tests, the sera from the rabbits immunized with RH strain and infected with Beverley strain, against the crude antigen appeared the precipitin bands 2 weeks after the immunization or infection. And the former showed the 2 or 5 precipitin bands after 5-8 weeks and the latter showed the l or 2 precipitin bands after 6 weeks. 4. The sera from the rabbits immunized with RH strain against the purified antigens II, III, IV,V and VI showed the precipitin bands, and the sera from the rabbits infected with Beverley strain against the purified antigens II, III and IV showed the precipitin bands in the immuno-diffusion tests. Especially antigen IV was the strongest reaction against the sera from RH strain and Beverley strain. 5. In agar-gel immunoelectrophoresis, the immunized sera against the crude antigen showed 8 arcs. But the infected sera against the crude antigen showed 4 or 5 arcs. 6. The immunized sera against the fractionated antigens II, III, IV, V, VI showed arcs, but against the fractionated antigen IV showed 6 arcs and in the antigens II, III, V, VI showed l or 2 arcs only. On the other hand, the infected sera against the fractionated antigens IV showed 4 arcs, II and III showed the l arcs, which was the most weak of all.

Journal Article↗

PubMed1987

Serological cross-reactivity between Sarcocystis and Toxoplasma in pigs.

The development of antibody titers and cross reation between Sarcocystis and Toxoplasma were investigated by means of IFA test and ELISA in pigs experimentally infected with 1.5 x 10(6) S. suicanis sporocysts and 10,000 T. gondii oocysts, respectively. The intact and soluble Sarcocystis antigens were prepared from the bradyzoites harvested by peptic digestion of infected pork. The intact and soluble Toxoplasma, antigens were prepared from the tachyzoites in mouse peritoneal cavity. IgG antibodies in pigs infeded with Sarcocystis and Toxoplasma, respectively were detected first at 2 weeks post infection on both IFA test and ELISA. The antibody titer to Toxoplasma reached its maximum at 6 weeks post infection and decreased thereafter. The antibody titer to Sarcocystis reached its maximum terminally. The cross-reaction titer in pigs infected with Toxoplasma against Sarcocystis antigen was up to 1:16 in IFA test and up to 1:32 in ELISA. The titer in control group was below 1:4 in both reactions.

Journal Article↗

PubMed1997

Detection of Toxoplasma gondii Antigen in Cerebrospinal Fluid Samples Using a Dot-Enzyme-Linked Immunosorbent Assay.

Toxoplasma encephalitis (TE) is the most common manifestation of a recurrent Toxoplasma gondii infection in immunocompromised individuals, especially in AIDS patients. The infection is associated with considerable morbidity and mortality, even with improved diagnostic procedures and adequate treatment. The diagnosis of TE is difficult to establish by the demonstration of the parasite in the central nervous system or in cerebrospinal fluid (CSF). In order to diagnose TE we have developed a TGA-Dot-ELISA for antigen detection using rabbit anti-toxoplasma antiserum. We have applied this test to specimens of cerebrospinal fluid from patients with toxoplasma encephalitis (180 patients), neurocysticercosis (15), or bacterial meningitis (15). The relative sensitivity and specificity obtained for the TGA-Dot-ELISA were 0.930 and 0.730, respectively. TGA-Dot-ELISA is a promising method for the rapid diagnosis and effective prophylaxis of toxoplasma encephalitis.

Journal Article↗

PubMed1989

[Toxoplasma gondii infections and oocyst shedding in domestic cats and the significance of this for the epidemiology and epizootiology of toxoplasmosis].

Because of the dissemination of oocysts the cat and other felines have a central position within Toxoplasma gondii epidemiology and epizootiology. From 1984 to 1986, 267 cats between 2 months and 15 years old were serologically examined (SFT) for Toxoplasma antibodies. The rate of infection was 59.9 per cent. The infection rate of stray cats (72.5%) was significantly higher than that of domestic cats (40%). The high infection rate of herbivores results from behaviour of stray cats. In faeces of 264 animals Toxoplasma oocysts could not be proved by flotation technique. But in 39 samples of faeces Toxocara mystax eggs were found, in one sample Toxascaris leonina eggs. Coproscopical examinations did not reflect the real degree of parasitization of cats. The rate of disseminators of oocysts is drainable by Toxoplasma gondii infection found serologically. About 40% of the animals at the age of up to one year were found to excrete Toxoplasma oocysts.

Animals↗

PubMed2000

Demonstration of parasites in toxoplasma lymphadenitis by fine-needle aspiration cytology: report of two cases.

Two cases of toxoplasma lymphadenitis diagnosed by fine-needle aspiration (FNA) cytology, in which the microorganisms were identified in the cytologic preparations, are presented. The first case was that of an 8-yr-old boy with bilateral cervical lymphadenopathy of 2-mo duration, in which an FNA specimen of one of the lymph nodes in a Papanicolaou-stained smear disclosed a toxoplasma cyst, and in Wright-Giemsa preparation, dispersed tachyzoites and a pseudocyst. The second case was that of a 52-yr-old man with enlargement of a single lymph node in the neck, of 3-mo duration, FNA of which in Wright-Giemsa preparation disclosed numerous tachyzoites dispersed free in exudate, and also within cells, forming pseudocysts. In both cases, immunocytochemistry by the peroxidase method for Toxoplasma gondii antigen was positive. The tachyzoites seen in Wright-Giemsa preparations, when subjected to fluorescence microscopy, emitted autofluorescence, facilitating their identification. While the presence of parasites in toxoplasma lymphadenitis is quite unusual, having been reported occasionally in histologic preparations and only rarely in cytologic FNA materials, our 2 cases suggest that in active disease, tachyzoites may not be so uncommon in FNA specimens. Besides the use of immunocytochemistry in the diagnosis of the disease, air-dried preparations stained by the Wright-Giemsa method are valuable for the demonstration of such parasites through careful search, along with the possible use of fluorescence microscopy.

Animals↗

PubMed1979

Increased toxoplasma antibodies in idiopathic inflammatory muscle disease. A case-controlled study.

Antibodies to Toxoplasma gondii were measured in sera from 69 patients with polymyositis, dermatomyositis, and myositis associated with other connective tissue diseases and compared to 69 age-, race-, and sex-matched controls with unrelated diseases. Complement fixation toxoplasma antibodies were significantly more frequent in polymyositis and correlated with high IgM levels. Other distinguishing clinical or laboratory features of these patients were not found. The high toxoplasma antibodies were not associated with generally hyperactive humoral immunity. The serologic data suggested that inflammatory muscle disease was associated with recent active toxoplasma infection in certain patients. The pathogenetic role of the microorganism remains uncertain.

Adolescent↗

PubMed1997

Cytokine responses induced by Toxoplasma gondii in astrocytes and microglial cells.

To investigate the role of astroglia in intracerebral immune response to Toxoplasma gondii, astrocytes cultured from mouse brain were inoculated with mouse-virulent or -avirulent toxoplasma strains. In comparison to microglia/ brain macrophages, astrocytes as host cells allowed stronger proliferation of avirulent parasites. Toxoplasma infection of astroglia was accompanied by release of interleukin- (IL)1 alpha, IL-6, and granulocyte/macrophage colony-stimulating factor (GM-CSF) activity, whereas alternative challenge by lipopolysaccharide (LPS) evoked no IL-1 response and significantly higher titers of IL-6 and GM-CSF. At the mRNA level, both stimuli induced transcription of all three cytokines in astrocytes. Secretion of IL-1 and IL-6 upon infection was triggered by T. gondii brady- and tachyzoites in a time- and dose-dependent manner. Heat killing of parasites, but not an exposure to polymyxin B, abrogated their cytokine-inducing activity, thus indicating that an LPS-independent stimulus is provided by T. gondii. When administered in combination, LPS synergistically augmented the IL-1-inducing effect of toxoplasma infection. In comparison, T. gondii-induced, but not an LPS-triggered, IL-6 response of astrocytes resisted to antagonization with IL-10. The IL-6 response of parasitized astroglia was up-regulated by external tumor necrosis factor (TNF)-alpha and transforming growth factor (TGF)-beta 1, with only TNF-alpha enhancing simultaneous release of IL-1. Substantial secretion of IL-10 and TNF-alpha was detected in T. gondii-infected microglia, but not in astrocyte cultures. A possibly autocrine stimulation of infected astroglia via IL-1 was found to be unlikely, since addition of IL-1 receptor antagonist did not affect the release of IL-6 and GM-CSF while inhibiting these responses in IL-1-treated cells. The findings substantiate a separate, T. gondii-induced pathway of astroglia activation characterized by the release of IL-1 which may drive local inflammatory reaction both at initial infection of the brain and during reactivating toxoplasmosis.

Animals↗

PubMed1995

Toxoplasma gondii: stable complementation of sag1 (p30) mutants using SAG1 transfection and fluorescence-activated cell sorting.

Toxoplasma gondii and the related Apicomplexan protozoan pathogens, Plasmodium, Cryptosporidium, and Eimeria, are obligate intracellular parasites which cause severe disease in their hosts. The recent development of transient transfection of Toxoplasma permits the development of strategies utilizing "reverse genetics" to identify molecules critical to parasite survival within the host. We have utilized transfection of Toxoplasma tachyzoites to stably complement a sag1 (or p30) mutant that does not make detectable SAG1. Transfection of mutants with the wild-type SAG1 gene resulted in transient expression of SAG1 in approximately 15-20% of the transfected population. Stable transformants were enriched by repeated sorting of live parasites using a fluorescein-labeled monoclonal antibody specific for SAG1. Cloned recombinant parasites expressed SAG1 at wild-type levels and maintained expression for over 5 months after transfection (approximately 300 divisions). Cloned transformants (which proved to be siblings) carried both the mutated gene and one copy of the transfected gene which had inserted randomly into the Toxoplasma genome.

Animals↗

PubMed1999

Toxoplasma gondii resides in a vacuole that avoids fusion with host cell endocytic and exocytic vesicular trafficking pathways.

Toxoplasma gondii actively penetrates its vertebrate host cell to establish a nonfusigenic compartment called the parasitophorous vacuole (PV) that has previously been characterized primarily in phagocytic cells. To determine the fate of this unique compartment in nonphagocytic cells, we examined the trafficking of host cell proteins and lipids in Toxoplasma-infected fibroblasts using quantitative immunofluorescence and immunoelectron microscopy. Toxoplasma-containing vacuoles remained segregated from all levels of the endocytic pathway, as shown by the absence of delivery of transferrin receptors, mannose phosphate receptors, and the lysosomal-associated protein LAMP1 to the vacuole. The PV was also inaccessible to lipids (DiIC16, and GM1) that were internalized from the plasma membrane via the endocytic system. In contrast, vacuoles containing dead parasites or zymosan sequentially acquired both endosomal and lysosomal protein markers and host lipids, reflecting the competency of fibroblasts to process phagocytic vacuoles. The mature PV often lies adjacent to the host cell Golgi, suggesting that it may intersect with vesicles from the exocytic pathway. Despite this proximity, the PV was inaccessible to nitrobenzadiazole-labeled sphingolipids exported from the Golgi and did not contain the host protein markers AP1 or beta-COP. Our results demonstrate that Toxoplasma resides in a compartment that excludes delivery of protein and lipid components from the host cell endocytic and exocytic pathways.

3T3 Cells↗

PubMed1975

[Cellular immune reactions of the white mouse after superinfection with Toxoplasma gondii (author's transl)].

After superinfection of immunized mice with a virulent strain of Toxoplasma (BK) these mice don't die. There is formation of a cellrich exudate with only very few toxoplasmas. The number of the different exudate-cells (macrophages, big, middlesized and small lymphocytes and heterophils) turn in direction of the lymphocytes in that way, that after the 3rd day of infection 70% of all exudate-cells belong to the group of lymphocytes. They seem to cause the death of the toxoplasmas. After in vitro incubation of trophozoites and exudate-cells of immune mice for 2 hours at 37 degrees C nearly 80% of the added toxoplasmas are killed. Electronmicroscopical pictures show, that this killing is produced by a process of lysis.

Animals↗

PubMed1986

The immunocytochemical demonstration of Toxoplasma antigen in the brains of congenitally infected mice.

The peroxidase anti-peroxidase immunocytochemical staining method was used to identify Toxoplasma antigen in paraffin embedded sections of the brains of 22 mice congenitally infected with the parasite. Intact Toxoplasma tissue cysts were readily demonstrated in the brain in all cases. In 4 of the 22 infected mice there was evidence of rupture of the cyst wall and/or presence of extra-cystic Toxoplasma antigen. Further support for the extra-cystic location of Toxoplasma antigen was obtained by electron microscopy of reprocessed tissue which revealed endozoites in the area immediately surrounding a ruptured cyst. The possible implications of these findings in relation to the pathogenesis of congenital toxoplasmic meningo-encephalitis are discussed.

Animals↗

PubMed1979

Learning capacity and memory of normal and Toxoplasma-infected laboratory rats and mice.

An experimental Toxoplasma-infection affects the learning performance and the memory of laboratory rats and mice. The investigations yielded the following results: 1. Maze experiments with rats showed that infection significantly reduces the learning performance of the infected animals. However, no significant differences were found between infected rats inoculated at varying times prior to training. In contrast to the learning capacity, memory does not seem to be impaired at all by infection. 2. Compared to rats, the learning capacity of mice is much more conspicuously retarded by a Toxoplasma-infection. In the memory test, the infected animals remained significantly below the performance level of the controls on all days, indicating that their memory was severely affected. 3. A significant correlation was established between the learning performance of the mice and the number of brain cysts. It is assumed that the cysts contribute to the impairment of learning ability. The fact that animals infected for a longer period usually show improved test performances further supports this assumption. This coincides with the decrease in brain cysts. Nevertheless, the clusters of necrosis developing together with the cysts in the nervous tissue might also cause learning retardation. 4. In mice, infection with an avirulent Toxoplasma-strain does not always take a wholly asymptomatic course. When observing the animals closely, a few of them could be seen to run in 'circles' with their heads bent to one side when moving and sitting, which might be interpreted as an impairment of the sense of balance. 5. Another effect of the Toxoplasma-infection in the animal species used is the significantly reduced activity observed on many days of training.

Animals↗

PubMed1989

Aminopeptidase activity in the brains of mice with chronic Toxoplasma gondii infections.

Aminopeptidase activity on beta-naphthylamide (NA) substrates was assayed in brain extracts from normal and Toxoplasma gondii-infected mice at 4 months postinfection. Correlations of levels of aminopeptidase activity, Toxoplasma-specific antibody production, and the number of brain cysts were studied in normal and Toxoplasma-infected mice. The Toxoplasma-specific antibody and the formation of cysts were markedly enhanced in the parasite-infected mice. The highest levels of activity for the NA substrates tested were observed in normal mice. In contrast, the activity levels were significantly lower in T. gondii-infected mice than in the corresponding normal mice. These results suggest an association between chronic toxoplasmosis and aminopeptidase activity in the parasite-infected host brain.

Aminopeptidases↗