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Toxocara canis induces a predominantly Th2 type response with enhanced amounts of interleukin (IL)-4 and reduced amounts of interferon (IFN)-gamma in infected mice. In this study, we investigated the macrophage function of T. canis-infected mice from the standpoint of cytokine production. C3H/HeN mice were infected with T. canis by oral administration of embryonated eggs. Ten days after infection, macrophages were obtained from spleen and peritoneal cavity, were cultured with lipopolysaccharide, and cytokines in the culture supernatant were evaluated with enzyme-linked immunosorbent assay. Macrophages from T. canis-infected mice produced IL-1 and IL-6 equivalent to macrophages from normal mice. The production of IL-10 and tumour growth factor (TGF)-beta was enhanced, but IL-12 and tumour necrosis factor (TNF)-alpha production was diminished. The addition of IFN-gamma, anti-IL-10 antibody, anti-TGF-beta antibody or indomethacin did not restore the production of IL-12 and TNF-alpha by macrophages from T. canis-infected mice. Furthermore, the stimulation of normal macrophages with T. canis antigen in vitro induced IL-1alpha, IL-6, IL-10 and TGF-beta, but not IL-12 and TNF-alpha. These results indicate that cytokine producing pattern of macrophages is altered by T. canis-infection, and this altered macrophage function may play an important role in the modification of the immune response to T. canis.
Toxocara canis, commonly known as the dog ascrid, is a frequent parasite of the domestic dog. If the eggs of an adult worm are accidentally ingested by a human host, usually a child, a larval form of the worm develops that can survive for a limited period in various human tissues. The retina is one of these tissues and upon the death of this organism a granulomatous reaction occurs and a fibrotic mass is formed in the retina. This unusual ophthalmoscopic appearance is demonstrated by the presentation of three fundus photographs of patients with suspected Toxocara lesions. A knowledge of this parasite and its life cycle will aid in its recognition, treatment, and possible prevention.
Toxocara canis larvae, infective to Man, secrete a number of antigenic macromolecules into culture medium over prolonged periods of time. These antigens have been collected and characterised with respect to molecular weight by sodium dodecyl sulphate-polyacrylamide gel electrophoresis following extrinsic and intrinsic radiolabelling, or electrophoresis followed by gel staining or immunoblotting. Panels of enzymes and lectins have been applied to examine protease sensitivity and carbohydrate composition, respectively, and a number of other biochemical data have been noted. Taken together, the excretory-secretory molecules contain more than 40% carbohydrate of which the majority is N-acetylgalactosamine and galactose. The individual antigens may readily be separated by gel filtration on a Sepharose 6B column, and it is shown that the major excretory-secretory macromolecules are all glycoproteins which differ in essential characteristics. For example, the 32 kDa antigen (TES-32) binds concanavalin A, is sensitive to a range of proteases and is the band most readily stained by silver and Coomassie blue. Both TES-120 and TES-400 components are resistant to tryptic or peptic cleavage, bind to Helix pomatia lectin and stain with periodic acid-Schiff, yet unlike TES-120, TES-400 does not incorporate radioactive methionine nor can it be stained by silver stain techniques. Finally, one protease, staphylococcal V8, reveals cleavage sites only in the TES-70 and TES-400 molecules.
Toxocara canis infection of abnormal hosts results in a condition in which infective larvae migrate through the soft tissues of the body, exclusive of the skin. This condition is known as visceral larva migrans (VLM) and causes a syndrome characterized by hepatosplenomegaly, hyperglobulinemia, hypereosinophilia, and transient pulmonary infiltrates. Because of the known association between hypereosinophilia and eosinophilic heart disease, we have been studying the hearts of mice infected with T. canis for evidence of myocardial damage and have previously described a severe eosinophilic myocarditis that leads to a marked myocardial fibrosis. We have measured eosinophil peroxidase (EPO) levels (a marker enzyme for specific granules of eosinophils) in homogenized lungs, homogenized hearts, and eosinophils recovered from the lungs of mice infected with T. canis over a 6-wk period. A marked accumulation of EPO was observed in the lungs of infected mice from day 14 postinfection (PI) to at least 6 wk of infection. Most of the EPO was associated with eosinophils that comprise the bulk of the pulmonary infiltrates associated with the VLM syndrome. However, following bronchoalveolar lavage, cytochemical localization of EPO activity in lungs from infected mice suggested that eosinophil degranulation had resulted in this marker enzyme being deposited within the pulmonary parenchyma. Peak levels of EPO were found in the myocardium by day 14 PI and declined over the 6-wk period. These levels equaled about 1/3 of the levels seen in the lungs of the same mice. These studies suggest that in mice infected with T. canis, the presence of increased numbers of eosinophils may lead to marked peroxidatic cardiopulmonary damage.
Vertical starch gel electrophoresis was used to resolve proteins encoded by 18 gene loci in ascaridoid nematodes. Estimates of genetic variability were made from population samples of the dog ascarid (Toxocara canis), cat ascarid (Toxocara cati), and the horse ascarid (Parascaris equorum). Levels of polymorphism and mean heterozygosity were high, which is not consistent with the hypothesis that the intestinal environment selects for monomorphism among endoparasites. Most observed allele frequencies conformed to Hardy-Weinberg equilibrium expectations as tested by chi2 goodness-of-fit, suggesting that the proteins evaluated are inherited in a Mendelian fashion and that these nematodes are mating at random. Subunit structures of the following enzymes, deduced from electrophoretic phenotypes of heterozygotes, corresponded to those of vertebrates: lactate dehydrogenase; malate dehydrogenase; 6-phosphogluconate dehydrogenase; phosphoglucomutase; esterase D; peptidase B; peptidase D; and mannose-6-phosphate isomerase. This observation substantiates the conservative nature of polypeptide subunit number across phylogenetically diverse groups of organisms.
The effect of 5-2,500 infective Toxocara canis and 5-1,000 T. cati eggs on the humoral immune response and on the distribution of larvae in the organism was studied in paratenic hosts--inbred C57BL6/J mice. With each dose of T. canis eggs the maximal antibody level was recorded on day 56 post infection and was followed by a moderate decline that lasted until day 154 of the experiment. A correlation between the antibody level and the egg count was observed only with the infective dose of 5-50 eggs. A more rapid occurrence of antibodies was recorded in mice infected with a high dose of eggs. In those given 5 and 7 T. cati eggs the antibody level exceeded the extinction threshold value only from day 21 to day 84. Low doses of T. canis (n = 5) and T. cati (n = 7) eggs caused a comparable distribution of larvae in mice, and the larval recoveries on day 70 post infection ranged between 10.00% and 25.74%. Following a dose of 500 T. cati eggs, 22.28% of the larvae were recovered, although only 1.08% were localized in the brain. A dose of 1,000 T. canis eggs yielded 36.37% of the larvae, with as much as 28.13% being found in the brain.
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Toxocara canis causes the visceral larva migrans syndrome in which central nervous involvement is rare. We report the case of a 40-year-old woman presenting with a subacute weakness of the right leg and dysaesthesiae in the right Th8-Th10 dermatomas. Spinal magnetic resonance imaging examination showed abnormal hyperintensity within the spinal cord. Cerebrospinal fluid analysis revealed eosinophilic pleocytosis. Antibody titres to Toxocara canis were higher in the cerebrospinal fluid than in the serum. Treatment using mebendazole led to a complete clinical recovery, normalization of cerebrospinal fluid parameters and improvement in spinal magnetic resonance imaging abnormalities.
Toxocara canis is a commun ascarid of dogs worldwide. The ingestion of helminths eggs by humans may cause visceral larva. Knowing the prevalence of T. canis in domestic dogs from Havana City (17.9%), it was decided to study for the first time the contamination of soil in the city with canine nematode ova, and thus, understand the magnitude of the rich for our population, thus, mainly children, for developing the disease three soil samples were taken in different residential areas from 15 municipalities of Havana City, and they were processed by Willis flotation technique (1921). Nineteen out of 45 samples were positive to T. canis eggs accounting for 42.2% of prevalence. Only 3 municipalities were found to have negative results. 38.2% of egg were embryonate. Findings are discussed.
Toxocara canis infective stage larvae continually produce excretory-secretory (TES) glycoproteins in long-term in vitro culture. The kinetics of synthesis and secretion were studied by metabolic labelling with radioactive [35S]methionine, [14C]serine and [14C]threonine. Maximal incorporation rates required overnight pre-incubation of parasites in medium depleted of the appropriate amino acid. Larvae rapidly incorporated isotope into their somatic tissues, but there was a minimum delay of 10 h before secretion of labelled antigens. Labelling with [14C]serine and [14C]threonine demonstrated a relative abundance of these amino acids in the major surface/secreted glycoproteins of this nematode (TES-32 and 120). Pulse-chase experiments suggested that TES-120 may be derived from a 58 kDa precursor, reflecting extensive posttranslational glycosylation. Inhibition of N-glycosylation with tunicamycin and digestion with N-glycanase provided evidence of N-glycosylation in the lower molecular weight ES components (TES-32, 55 and 70). These agents had no effect on the higher molecular weight components (TES-120 and 400) implying that for these molecules glycosylation is predominantly O-linked. The largest ES component (TES-400) was unusual, in incorporating serine and threonine but not methionine, and by exhibiting increased apparent molecular weight following pronase digestion; it is suggested that this molecule is a proteoglycan.
Toxocara canis larvae were cultured in vitro in medium containing [35S-]methionine for six days. The medium and the larval tissues were analysed for biosynthetically labelled polypeptides by sodium dodecyl sulphate polyacrylamide gel electrophoresis and autoradiography. Immunoprecipitates with positive and negative human antiserum were similarly analysed, using Staphylococcus aureus to absorb immunocomplexes. The larvae secrete biosynthetically labelled polypeptides into the medium, with three major polypeptides of molecular weights between 99 and 110 X 10(3) the major constituents. Both of these react strongly with human IgG in human positive sera. Many polypeptides become labelled in the larval tissue, but only one polypeptide with similar molecular weight to the ES antigens, strongly reacted with human IgG.
Toxocara canis infective larvae are known to produce abundant glycosylated molecules which may be found associated with the surface or secreted into their environment. Using a range of fluorescein-conjugated and gold-conjugated lectins, the localization of particular carbohydrates was defined on the surface of live parasites, and internally at the ultrastructural level. Surface exposure of N-acetyl galactosamine and N-acetyl glucosamine was deduced by binding of FITC-conjugated Helix pomatia (HPA) and wheat-germ agglutinins (WGA). These sugars appear to be associated with a densely staining surface coat as conventional immuno-electron microscopy procedures dissipate this coat and reveal no surface binding site for these lectins. However, by using cryo-immuno-electron microscopical (C-IEM) techniques, the surface coat is retained and can be shown to bind WGA. The fluorescent lectins also revealed strong WGA binding to the secretory and amphidial pores, while the buccal opening and the cuticular alae bound HPA. Corresponding results were obtained at the ultra-structural level. Thus, HPA bound to the electron-dense area of the cuticle, areas of local cuticular thickening such as the alae and buccal labia, as well as to the oesophageal lumen. WGA also bound to the thickened cuticle of the alae and the buccal opening, but showed no reaction to either the electron-dense layer of the cuticle or the oesophageal lumen. Unlike HPA, WGA did bind specifically to the secretory column contents and the electron-dense regions of the lips associated with the chemosensory amphids. The compartmentalization of the sugars N-acetyl galactosamine and N-acetyl glucosamine, their sources and routes of surface expression and the possible association with the TES glycoprotein antigens are discussed.
Toxocara canis, the parasitic roundworm of the dog may infect aberrant hosts including mice and humans. The present study examined the behavioral and pathological changes at each of three postintubation periods (Period 1: 8-10 days, 2: 49-51 days, and 3: 84-86 days postintubation, respectively) in independent groups of mice intubated with 1000 eggs of T. canis. Eight-ten days after intubation Toxocara infected animals typically showed depressed levels of activity relative to saline-intubated controls. The scope and severity of behavioral changes were attenuated when different mice were tested 49-51 days after infection, and then became more severe when the third set of animals was tested 84-86 days after intubation. While brain pathology increased over the three periods, visceral organs showed marked pathology 8-10 days after intubation followed by a decrease in severity. These data suggest that Toxocara associated pathological changes in visceral organs and in the brain have behavioral consequences in mice. Given the similarity in migratory pathways of this parasite in rodents and humans, and the findings of T. canis larvae in human brain tissue, the results of this animal study may have implications concerning the possible etiology of behavioral disorders for children who have a known history of pica for dirt.