Larval migration of the ascarid nematode Toxocara canis following infection and re-infection in the gerbil Meriones unguiculatus.

A morphological and immunohistochemical study of larval migration patterns was performed in gerbils that were infected once (primary infected group) or twice (secondary infected group) with 1500 eggs of Toxocara canis. Animals from the primary infected and the re-infected group were killed at different times after infection, and larvae were counted in the intestines, liver, lungs and brain. Fragments of all organs were formalin fixed and paraffin embedded for histology and immunohistochemistry analyses (using polyclonal anti-Toxocara serum raised in rabbits infected with T. canis). In the primary infected group, larvae were more abundant in the intestine at 24 h, in the liver and lungs between 24 and 72 h and in the brain after 96 h; larvae predominated in the brain for up to 60 days after infection. In the re-infected group, an increase in the number of larvae in the liver and a reduction in the number of larvae in the brain was observed up to 60 days after re-infection. Inflammatory reactions were absent or limited. Eosinophils and loose granulomata were observed around the larvae and their antigens in the primary infected group and were more severe. Many eosinophils and typical epithelioid granulomata were observed around larvae in the re-infected group. These results demonstrate that the migration pattern of T. canis larvae in gerbils is similar to that in mice and rats, exhibiting a late neurotropic stage. In the re-infected group, there was histological evidence of an adaptive T-helper 2 (Th-2) response, and larvae were apparently retained within granulomata in the liver, without obvious signs of destruction.

PCR-RFLP genotyping of Toxoplasma gondii from chickens from Espírito Santo state, Southeast region, Brazil: new genotypes and a new SAG3 marker allele.

Brazil is one of the regions with the highest prevalences of Toxoplasma gondii in humans and animals. Because free-range chickens become infected by feeding from ground contaminated with oocysts, the prevalence of T. gondii in this host has been widely used as an indicator of the strains prevalent in the environment. The genetic variability among T. gondii isolates from different healthy and sick hosts all over the world has been recently studied. Three clonal genetic lineages (Types I, II and III) were initially recognised as predominant in Western Europe and the United States. T. gondii strains are genetically diverse in South America. In Brazil, recombination plays an important role in strain diversification. The objective of this study was to genetically characterise T. gondii isolates from free-range chickens from Espírito Santo state, Southeast region, Brazil, using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). A total of 44 isolates among 47 previously described isolates (TgCkBr234-281) from free-range chickens were included in this study. Strain typing was performed using 12 PCR-RFLP markers: SAG1, SAG2, alt. SAG2, SAG3, BTUB, GRA6, c22-8, c29-2, L358, PK1, Apico and CS3. Eleven genotypes were identified. Ten isolates (23%) were grouped into four novel genotypes. Four isolates, distributed in four counties, corresponded to the Type BrI lineage, the genotype found most frequently in Brazil. No clonal Types I, II or III lineages were found. Two novel genotypes were represented by single isolates. Unique alleles were identified for the markers SAG1, c22-8 and CS3, and for the first time, a unique allele was found for the marker SAG3. Although a large number of T. gondii genotypes have already been identified from a variety of animal hosts in Brazil, new genotypes are continuously identified from different animal species. This study confirmed the diversity of T. gondii in Brazil and demonstrates clonal Type I, II and III lineages are rare in this country.

Carbamazepine inhibits angiotensin I-converting enzyme, linking it to the pathogenesis of temporal lobe epilepsy.

We find that a common mutation that increases angiotensin I-converting enzyme activity occurs with higher frequency in male patients suffering from refractory temporal lobe epilepsy. However, in their brains, the activity of the enzyme is downregulated. As an explanation, we surprisingly find that carbamazepine, commonly used to treat epilepsy, is an inhibitor of the enzyme, thus providing a direct link between epilepsy and the renin-angiotensin and kallikrein-kinin systems.

Seroprevalence and isolation of Toxoplasma gondii from free-range chickens from Espírito Santo state, southeastern Brazil.

Prevalence of Toxoplasma gondii infection in 510 free-range (FR) chickens (380 from 33 small farms, and 130 from a slaughter house for FR chickens) from Espírito Santo state, southeastern Brazil, was investigated. Antibodies to T. gondii were sought using commercial indirect haemagglutination (IHAT, Imuno-HAI Toxo(®), Wama Diagnóstica, São Paulo, Brazil, cut-off 1:16) and the modified agglutination test (MAT, cut-off 1:25) tests. Attempts were made to isolate viable T. gondii from seropositive chickens by bioassay in mice. Pooled samples of brain, heart and quadriceps muscle of one thigh (total 40 g) from 64 chickens with IHAT titers of ≥ 1:16 were minced, digested in pepsin and bioassayed in mice. Antibodies to T. gondii were found in 40.4% (206/510) FR chickens by IHAT (titer ≥ 1:16) and 38.8% (198/510) by MAT (titer ≥ 1:25); concordance between IHAT and MAT was 81.6% (kappa index=0.614). Viable T. gondii was isolated (designated TgCkBr234-281) from 48 of 64 (75%) seropositive (IHAT titers ≥ 1:32) FR chickens. Most isolates of T. gondii were virulent for mice; 100% of mice inoculated with 44 of 48 isolates died of toxoplasmosis within 30 days post inoculation (p.i). An epidemiological investigation revealed that people living in rural areas have little knowledge about the parasite and about the risk of acquiring it from raw meat. Results indicated that the locally available IHAT was useful for screening of chicken sera for T. gondii antibodies.

Transferable SAFT-VR models for the calculation of the fluid phase equilibria in reactive mixtures of carbon dioxide, water, and n-alkylamines in the context of carbon capture.

The amine functional groups are fundamental building blocks of many molecules that are central to life, such as the amino acids, and to industrial processes, such as the alkanolamines, which are used extensively for gas absorption. The modeling of amines and of mixtures of amines with water (H(2)O) and carbon dioxide (CO(2)) is thus relevant to a number of applications. In this contribution, we use the statistical associating fluid theory for potentials of variable range (SAFT-VR) to describe the fluid phase behavior of ammonia + H(2)O + CO(2) and n-alkyl-1-amine + H(2)O + CO(2) mixtures. Models are developed for ammonia (NH(3)) and n-alkyl-1-amines up to n-hexyl-1-amine (CH(3)NH(2) to C(6)H(13)NH(2)). The amines are modeled as homonuclear chain molecules formed from spherical segments with additional association sites incorporated to mediate the effect of hydrogen-bonding interactions. The SAFT-VR approach provides a representation of the pure component fluid phase equilibria, on average, to within 1.48% of the experimental data in relative terms for the saturated liquid densities and vapor pressures. A simple empirical correlation is derived for the SAFT-VR parameters of the n -alkylamine series as a function of molecular weight. Aqueous mixtures of the amines are modeled using a model of water taken from previous work. The models developed for the mixtures are of high fidelity and can be used to calculate the binary fluid phase equilibrium of these systems to within 2.28% in relative terms for the temperature or pressure and 0.027 in absolute terms for the mole fraction. Regions of both vapor-liquid and liquid-liquid equilibria are considered. We also consider the reactive mixtures of amines and CO(2) in aqueous solution. To model the reaction of CO(2) with the amine, an additional site is included on the otherwise nonassociating CO(2) model. The unlike interaction parameters for the NH(3) + H(2)O + CO(2) ternary mixture are obtained by comparison to the experimental data available for this system. The resulting model is found to correlate and predict the liquid-phase loading (moles of CO(2) per mole of amine) to within 0.091 of experimental data in absolute terms. The parameters describing the NH(3)-CO(2) interaction are then transferred to other n-alkyl-1-amines, and sample predictions of the fluid phase equilibria for the n-propyl-1-amine + H(2)O + CO(2), n-butyl-1-amine + H(2)O + CO(2), and n-hexyl-1-amine + H(2)O + CO(2) mixtures are presented. The latter mixture is found to exhibit regions of liquid-liquid immiscibility.

Presence of intestinal helminths decreases T helper type 1 responses in tuberculoid leprosy patients and may increase the risk for multi-bacillary leprosy.

Resistance to intracellular pathogens such as Mycobacterium leprae is dependent upon an effective T helper type 1 (Th1)-type immune response. On the other hand, intestinal helminths are known to subvert the host's immune response towards to either a Th2-type immune response or a regulatory T cell up-regulation, which may affect the host's ability to mount an effective response to mycobacteria. Here, we report a significant association between intestinal helminth infections and lepromatous leprosy [odds ratio (OR), 10.88; confidence interval (CI) 95%: 4.02-29.4; P<0.001]. We also observed that the frequency of intestinal helminths correlated strongly with the mycobacterial index (r=0.982, P<0.01). Corroborating with our hypothesis, intracellular levels of interferon-gamma were decreased significantly in leprosy patients co-infected with intestinal helminths when compared to leprosy patients without worms. Conversely, lepromatous leprosy patients with intestinal worms produced higher levels of both interleukin (IL)-4 and IL-10. Our results suggest that a pre-existing infection by intestinal helminths may facilitate the establishment of M. leprae infection or its progression to more severe forms of leprosy.

The effect of buserelin acetate on the uterus of adult rats: morphological aspects.

PURPOSE OF INVESTIGATION: To evaluate the effect of buserelin acetate on the morphology of the endometrium of adult, non-castrated, female Wistar rats. METHODS: Female Wistar rats at estrus or diestrus (assessed by vaginal cytology) received daily subcutaneous injections of 20 mg buserelin acetate for four, eight or 12 days. Rats were sacrificed 24 hours or five days following final dosage. A control group received diluent for 12 days. RESULTS: Progressive tissue hypotrophy occurred during treatment and was followed by estrogenic hyperactivity five days after the end of treatment. Vaginal cytology and endometrial histology revealed intense, vacuolized lining and glandular epithelia, brush borders and endometrial stroma densely infiltrated with eosinophils. CONCLUSIONS: Buserelin acetate appears to cause a progressive blockade of gonadotrophin secretion when administered to female rats for four, eight or 12 days, and an important rebound effect, with accentuated estrogen release already apparent in the first estrous cycle following treatment.

Bcl-2 expression and apoptosis induction in human HL60 leukaemic cells treated with a novel organotellurium(IV) compound RT-04.

Organotellurium(IV) compounds have been reported to have multiple biological activities including cysteine protease-inhibitory activity, mainly cathepsin B. As cathepsin B is a highly predictive indicator for prognosis and diagnosis of cancer, a possible antitumor potential for these new compounds is expected. In this work, it was investigated the effectiveness of organotellurium(IV) RT-04 to produce lethal effects in the human promyelocytic leukaemia cell line HL60. Using the MTT tetrazolium reduction test, and trypan blue exclusion assay, the IC50 for the compound after 24 h incubation was 6.8 and 0.35 microM, respectively. Moreover, the compound was found to trigger apoptosis in HL60 cells, inducing DNA fragmentation and caspase-3, -6, and -9 activations. The apoptsosis-induced by RT-04 is probably related to the diminished Bcl-2 expression, observed by RT-PCR, in HL60-treated cells. In vivo studies demonstrated that the RT-04 treatment (2.76 mg/kg given for three consecutive days) produces no significant toxic effects for bone marrow and spleen CFU-GM. However, higher doses (5.0 and 10 mg/kg) produced a dose-dependent reduction in the number of CFU-GM of RT-04-treated mice. These results suggest that RT-04 is able to induce apoptosis in HL60 cells by Bcl-2 expression down-modulation. Further studies are necessary to better clarify the effects of this compound on bone marrow normal cells.

Effects of simultaneous treatment with estrogen and testosterone on the uterus of female adult rats.

BACKGROUND: Testosterone (T) associated with estrogen (E) has been used in hormonal replacement therapy in postmenopause women and the effects of this hormonal association on the uterus are not known. OBJECTIVE: To study the effect of long-term simultaneous exposure to testosterone and estrogen on the uterus of non-castrated adult female rats. METHODS: Groups of ten adult noncastrated female Wistar rats were treated with non-esterified testosterone and beta estradiol (subcutaneous implants with 50 mg of each hormone) or with testosterone cipionate and estradiol valerate (weekly intramuscularly or by subcutaneous injection of respectively, 2.85 mg/kg and 0.166 mg/kg). Control groups received no treatment (10 rats) or injections of diluents (6 rats). All animals were killed six months after hormonal exposure. RESULTS: All rats treated with T+E developed hyperplasia and hyperkeratosis of the vaginal and cervical epithelium and focal metaplasia with keratinization of the endocervical and endometrial epithelium. Ascending pelvic inflammatory disease with pyometra and tuboovarian abscesses were frequent (25% mortality until the end of the experiment). CONCLUSIONS: Testosterone associated with estrogen induced metaplasia of the genital epithelium but did not induce neoplastic lesions. The metaplasic lesions reduced the mucosal defense mechanisms enhancing ascending genital inflammatory disease. Although metaplasia of the cervical and endometrial epithelium has been observed after estrogen exposure in rats, testosterone does not appear to inhibit these estrogen effects.

Toxocara infection is not associated with viral or bacterial central nervous system infection in children.

BACKGROUND: Helminth infections with larvae that migrate through the tissues have been considered risk factors for CNS infections. OBJECTIVES: The present work was designed to investigate the prevalence of anti- TOXOCARA antibodies in the serum and/or in the cerebrospinal fluid (CSF) of children with infectious meningitis or meningoencephalitis and of a control group, without meningitis, admitted at the Children's Hospital NS Glória, Vitória, ES, Brazil. PATIENTS AND METHODS: After adsorption with ASCARIS LUMBRICOIDES antigen, serum and/or cerebrospinal fluid of 381 inpatients (201 with meningitis and 180 without meningitis) were submitted to an ELISA IgG, for anti- TOXOCARA antibodies using secretion/excretion antigens of third stage larvae of T. CANIS. RESULTS: No significant differences between the meningitis and the control groups were observed in the frequencies of positive tests for anti- TOXOCARA antibodies in the serum or CSF (respectively for the meningitis and control group: 33/103 or 32 % and 52/152 or 34.2 % for the serum, p = 0.821; 48/184 or 26.1 % and 23/121 or 19.0 % for the CSF; p = 0.196. CONCLUSION: The results demonstrated that TOXOCARA infection, evaluated by detection of anti- TOXOCARA antibodies in serum or CSF, is not associated with viral or bacterial meningitis or meningoencephalitis in children in our country.

Morphological changes induced by testosterone in the mammary glands of female Wistar rats.

Increased levels of androgens in postmenopausal women are considered to be a risk factor for breast cancer. Testosterone, alone or in combination with estrogen, induces epithelial dysplasia and mammary tumors in Noble rats. Since this model of hormone-induced neoplasia has not been reported in other rat strains, we studied the effect of testosterone on the mammary gland morphology of female Wistar rats. Sixty adult, non-castrated, female Wistar rats were implanted in the dorsum midline with a silicone tube containing 50 mg testosterone (testosterone propionate in 30 animals and non-esterified testosterone in the remaining 30 animals) and 20 additional animals were implanted with empty tubes and used as control. Five animals per group were killed 30, 60, 90, 120, 150, and 180 days after implantation, and the mammary glands were dissected, fixed and embedded in paraffin. Histological sections were then stained with hematoxylin and eosin and picrosyrius red for collagen visualization. Morphological and morphometric analysis demonstrated ductal proliferation and acinotubular differentiation with secretory activity in all treated animals, peaking at 90 days of androgen exposure. After 90 days the proliferation of acinar epithelial cells was evident, but there was a progressive reduction of secretory differentiation and an increase in intralobular collagen fibers. There was no morphological evidence of dysplastic changes or other pre-neoplastic lesions. Testosterone treatment applied to adult, non-castrated female Wistar rats induced a mammary gland hyperplasia resembling the lactating differentiation, with progressive reduction in secretory differentiation.

Morphological changes induced by testosterone in the mammary glands of female Wistar rats

Increased levels of androgens in postmenopausal women are considered to be a risk factor for breast cancer. Testosterone, alone or in combination with estrogen, induces epithelial dysplasia and mammary tumors in Noble rats. Since this model of hormone-induced neoplasia has not been reported in other rat strains, we studied the effect of testosterone on the mammary gland morphology of female Wistar rats. Sixty adult, non-castrated, female Wistar rats were implanted in the dorsum midline with a silicone tube containing 50 mg testosterone (testosterone propionate in 30 animals and non-esterified testosterone in the remaining 30 animals) and 20 additional animals were implanted with empty tubes and used as control. Five animals per group were killed 30, 60, 90, 120, 150, and 180 days after implantation, and the mammary glands were dissected, fixed and embedded in paraffin. Histological sections were then stained with hematoxylin and eosin and picrosyrius red for collagen visualization. Morphological and morphometric analysis demonstrated ductal proliferation and acinotubular differentiation with secretory activity in all treated animals, peaking at 90 days of androgen exposure. After 90 days the proliferation of acinar epithelial cells was evident, but there was a progressive reduction of secretory differentiation and an increase in intralobular collagen fibers. There was no morphological evidence of dysplastic changes or other pre-neoplastic lesions. Testosterone treatment applied to adult, non-castrated female Wistar rats induced a mammary gland hyperplasia resembling the lactating differentiation, with progressive reduction in secretory differentiation.

Short report: do intestinal nematodes increase the risk for multibacillary leprosy?

Intestinal helminths are known to subvert the host's immune response towards a Th2 response, which in turn may lead to both eosinophilia and high immunoglobulin E titers often associated with these parasites. Mycobacterium leprae infection may lead to different clinical and pathological forms. Multibacillary forms are associated with Th2 cytokines, whereas paucibacillary forms are associated with Th1 cytokines. We report a significantly higher frequency of intestinal helminthic infections in patients with the lepromatous form, a multibacillary form of leprosy (odds ratio, 2.99; 95% confidence interval, 1.82-4.95; P = 0.006) when compared with patients with paucibacillary leprosy or to a control group without leprosy. A direct correlation was also found between mycobacterial index and the frequency of intestinal helminths. Our results suggest that the presence of intestinal helminths may facilitate the establishment of M. leprae infection or the progression to more severe forms of leprosy.

Intestinal nematodes, Toxocara infection, and pyogenic liver abscess in children: a possible association.

Eosinophilia and intestinal helminths are frequent in children with pyogenic liver abscess (PLA) diagnosed in Vitória (Brazil). For these reasons we hypothesized that nematode infection with larvae migrating through the tissues (Ascaris, Strongyloides, Ancylostoma, Necator and Toxocara) may be a predisposing factor for PLA in children. We compared the prevalence of intestinal helminth and Toxocara infection between children with PLA and a control group of children with no evidence of PLA at the Children's Hospital N.S. da Glória in Vitória. From October 1996 to February 1998, 13 children with PLA and 110 children with diseases other than PLA provided five stool samples (Hoffman, Baerman and Kato-Katz methods) and one blood sample for anti-Toxocara antibodies (ELISA IgG, with previous adsorption with Ascaris suum antigen). All PLA and comparison children belonged to a low socioeconomic class and lived in similar conditions. The frequency of intestinal nematodes and anti-Toxocara antibodies were significantly higher in PLA patients than in controls (intestinal helminths: 10/13 or 76.9 per cent in PLA cases and 31/110 or 28.1 per cent in controls; OR = 8.94; 95 per cent confidence interval (CI): 1.97 < OR < 50.06; anti-Toxocara antibodies: 9/13 or 69.2 per cent in PLA and 31/110 or 28.1 per cent in controls; OR = 6.59; 95 per cent CI: 1.65 < OR < 31.05). Moreover, the degree of eosinophilia was higher in PLA patients. Malnutrition was present in both groups. Hemoglobin was 9.5 g/dl in PLA patients and 9.7 g/dl in controls; p = 0.900. Serum levels of IgA and IgM were normal or above normal, with no difference between the two groups, but the levels of IgG and IgE were higher in PLA patients. Although there is some missing data in respect to some socioeconomic parameters in affected and comparison groups. these results support the hypothesis that helminth infection with larvae migrating through tissues may be a predisposing factor for PLA in children. Th2 cell activation and downregulation of Th1 cells, induced by helminths, thus reducing the microbicidal activity of phagocytes, as well as the granulomatous reaction around the larvae (mainly of Toxocara sp.) causing the trapping of bacteria in liver, may be possible explanations for the increased risk for PLA in children with intestinal nematodes and/or Toxocara infection.

Pathology of pyogenic liver abscess in children.

Little is known about preexisting lesions in livers of children with pyogenic liver abscess (PLA). Study of these lesions may elucidate possible predisposing factors for the disease. In Vitória, state of Espirito Santo, Brazil, PLA in children is frequently associated with helminthic infections and eosinophilia. We hypothesize that nematode infection with larvae migrating through the liver is a predisposing factor for PLA, because the infection induces immunomodulation and likely trapping of bacteria in liver granulomas. In this report, we describe observations of 22 cases of PLA in children studied at autopsy (16 cases) or in surgical biopsies (6 cases), including 17 boys and 5 girls ranging in age from 1 to 13 years (mean 4.6 years, median 3.5 years). Multiple abscesses in both lobes were found in 13 cases and a single abscess was found in the right lobe in 10 cases. All cases showed histologically classical pyogenic inflammation without morphological evidence of amoebiasis. In six cases there were granulomas similar to those caused by larva migrans visceralis (from Toxocara or other nematodes) in liver tissue not affected by the abscess. Nematode antigens in central areas of necrosis of granuloma in all six cases and fragments of a larva, possibly of Toxocara, were found on samples immunohistochemically stained with polyclonal anti-Toxocara antibodies. There were numerous eosinophils in abscesses with Charcot-Leyden crystals. Eosinophils were found frequently in portal triads far from the abscess wall. In four cases, in which bile duct ascariasis was found, worms were noted in the bile ducts, and eggs were found in liver parenchyma surrounding the abscess in two cases. Foreign-body granulomas were found in one case in which penetrating trauma was the cause of abscess. In one case there was one histiocytic granuloma whose origin was not determined. The observation of six cases of granuloma similar to larva migrans visceralis (or produced by other nematode larva) in liver tissue not directly affected by the abscess supports the hypothesis that helminth infections with larva migrating through the liver are a predisposing factor for pyogenic hepatic abscess in children.

Frequency of myocarditis in cases of fatal meningococcal infection in children: observations on 31 cases studied at autopsy.

The frequency of myocarditis associated with meningococcal disease in children was reported only in two autopsied series (United States and South Africa). Here we report the frequency of associated myocarditis in 31 children who died of meningococcal infection at Hospital Infantile N.S. da Glória in Vitória, Espirito Santo State, Brazil. The diagnosis was confirmed by isolation of Neisseria meningitidis. At least three sections of fragments of both atria and ventricles were studied using the Dallas Criteria for the morphologic diagnosis of myocarditis. The mean age was 47.6 +/- 39.8 months and the mean survival time after the onset of symptoms was 46.1 +/- 26.5 h (12-112 h). Myocarditis was present in 13 (41.9%) patients, being of minimal severity in 11 cases and of moderate severity in 2 cases. There were no cases with severe diffuse myocarditis. The frequency of myocarditis was not influenced by sex, presence of meningitis, survival time after the onset of symptoms or use of vasoactive drugs. The frequency of myocarditis reported here was intermediate between the values reported in the only two case series published in the literature (57% in the United States and 27% in South Africa). Although our data confirm the high frequency of myocarditis in meningococcal disease, further investigations are necessary to elucidate the contribution of myocarditis to myocardial dysfunction observed in cases of meningococcal infection in children.

Increased sleeping time after pentobarbital anesthesia in rats treated with intravenous injection of BCG.

Intravenous injection of BCG in rats induces protection against liver cell necrosis produced by CCl4. Impairment of hepatic mixed function oxidases by cytokines produced by activated Kupffer cells is the mechanism proposed to explain that protection. To verify the function of hepatic mixed function oxidases after Kupffer activation, the sleeping time after sodium pentobarbital anesthesia was evaluated in rats after intravenous injection of BCG. Male adult albino rats received BCG (50 micrograms, intravenous) and 48 h or 6 days after were anestethized with sodium pentobarbital (33 or 66 mg/g i.p.). The sleeping time was measured from the beginning of sleep until the animal started having spontaneous movement and stand up on the forepaws. The results showed that the animals treated with BCG presented a significative increase in the sleeping time, indicating reduced inactivation of the pentobarbital, an indirect evidence of inhibition of mixed function oxidase system. BCG treated rats showed hepatic and splenomegaly, both 48 and 6 days after treatment. Histology showed an increase in number of mononuclear cells in the sinusoids in the liver and in the red pulp of the spleen 48 h after injection. Small epitheliod granulomas scattered in the hepatic lobules and in the red pulp were observed in rats killed six days after the BCG injection. Hepatocyte injury, induced by activated macrophages, would be not responsible for the reduced pentobarbital inactivation, because at six days there were several granulomas scattered in lobules, but the increase of sleep time in this group was similar to that observed in rats 48 h after injection of BCG. These results demonstrate that activation of Kupffer cells with BCG induces impairment of mixed function oxidase system soon as 48 h after injection of activator, probably due to production of IL-1, IL-6 and TNF alpha by activated Kupffer cells and other mononuclear cells migrated to the liver.

Prevalence of anti-Toxocara antibodies in a random sample of inpatients at a children's hospital in Vitória, Espírito Santo, Brazil.

In the streets of Vitória, in the State of Espírito Santo, Brazil, are large number of stray dogs, many of which are infected with Toxocara canis, suggesting a high risk for human infection. In order to investigate the prevalence of Toxocara infection in children in Espírito Santo we studied the prevalence of anti-Toxocara antibodies in 100 random inpatients over one year of age, at the Children's Hospital N.S. da Glória, the reference children's hospital for the State. All the sera were collected during the period between October 1996 and January 1997. The mean age was 6.6 +/- 4.1 yrs. (1 to 14 yrs., median 6 yrs.) and there were patients from all of the different wards of the hospital. Sixty-eight patients came from the metropolitan area of Vitória and the other 32 from 17 other municipalities. The anti-Toxocara antibodies were investigated by ELISA-IgG using a secretory-excretory antigen obtained from second stage larvae. All sera were adsorbed with Ascaris suum antigen before the test. Thirty-nine sera (39%) were positive, predominantly from boys, but the gender difference was not statistically significant (boys: 25/56 or 44.6%; girls: 14/44 or 31.8%; p = 0.311). The prevalence of positive sera was higher, but not statistically significant, in children from the urban periphery of metropolitan Vitória (formed by the cities of Vitória, Cariacica, Vila Velha, Serra and Viana) than in children from 17 other municipalities (44.1% and 28.1% respectively, p = 0.190). Although the samples studied do not represent all children living in the State of Espírito Santo, since the Children's Hospital N.S. da Glória admits only patients from the state health system, it is probable that these results indicate a high frequency of Toxocara infection in children living in Espírito Santo. Further studies of population samples are necessary to ascertain the prevalence of Toxocara infection in our country.

Kupffer cell activation with BCG. Corynebacterium parvum or zymosan protects against acute liver injury induced by carbon tetrachloride in rats.

Kupffer cells have been implicated in the pathogenesis of liver injury, but there is controversy about the effects of activation of these cells on the hepatotoxicity of chemicals and endotoxin. It has been shown that injection of Corynebacterium parvum in rats induces macrophage activation that protects against toxic effects of carbon tetrachloride and acetaminophen, five days after injection, and this protection is due to inhibition of microsomal oxidizing enzymes and increased production of glutathion. To verify if the protective effect occurs soon after Kupffer cell activation, with different activators, male albino rats were treated with intravenous injection of BCG (0.5 ml with 7.5.10(8) bacilli), Corynebacterium parvum (30 mg/kg) or zymosan (7.5.10(6) yeast cells). Fourty-eight hours after the injection of one of the macrophage activators, the animals and rats treated with intravenous injection of saline (controls) received carbon tetrachloride by subcutaneous route (1 ml/kg of CCl4, 3:1 in soybean oil). Fourty-eight hours after the animals were killed after ether anesthesia and fragments of the liver were fixed, paraffin embedded and the sections stained with hematoxylin and eosin. A Weibel grid with 168 points was used to estimate the percent volume of necrosis and severe hydropic degeneration. The results showed that the volume density of necrosis and severe hydropic degeneration were significatively lesser in rats treated with the three Kupffer cells activators. The protection was greater with BCG and Corynebacterium parvum than with zymosan. These results confirm that activation of Kupffer cell with three different activators can induce protection against liver cell injury produced by carbon tetrachloride in rats soon as 48 h after injection of activators.