Resistance of mice to <i>Toxocara canis</i>: effect of prechallenge infections and injections of worm extracts

Izzat, N. N.; Olson, L. J.

doi:10.1139/z70-188

Cited by 12 publications

(6 citation statements)

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“…Published reports differ in whether protection against reinfection was obtained in such experiments (Olson, 1962) or not (Schmunis andPacheco. 1970: Izzat andOlson, 1970), but any such protection was limited, if it occurred at all. Extracts from worms gave better protection (Izzat and Olson, 1970).…”

Section: Discussionmentioning

confidence: 99%

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ANTIBODY RESPONSES TO TOXOCARA CANIS USING SERA FROM PARASITE‐INFECTED MICE AND PROTECTION FROM TOXOCARIASIS BY IMMUNISATION WITH ES ANTIGENS

Nicholas

Stewart

1984

Aust J Exp Biol Med

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Summary. Evidence for serological cross-reactions between To.xocara cants and related nematode parasites has been sought using sera from infecled mice and the immunodiagaoslic excretory/secretory (ES) antigen of T. canis larvae. Sera from mice experimentally infected with either T. cani.i. T, caii. T. ptcropodis, Toxascaris leonino or Ascaris suum were tested for the presence of antibodies to T. canis ES antigen by solid-phase radioimmunoassay (RIA) or enzyme-linked immunosorbent assay (ELISA) using anti-mouse IgG. 7". canis ES antigen was obtained from the medium used to culture T. canis larvae, this being the same source of antigen as has been used in a highly satisfactory immunodiagnostic lest for human toxocariasis (viscera! larva migrans). Sera from mice infected with cither A. .tui/m, T. cati or T. pteropodis showed definile cross-react ions with T. cam's ES antigen in one or other of the two essays used. No reaction between anti-r. teonina sera and T. canis ES antigen was demonstrated, although infection levels with this parasite were low in mice. Concerning biological activity of ES antigen, it is of some interest that mice hyperimmunised with 7". canis ES antigen in adjuvant were shown to be significantly resistant to infection by 7". canis.

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Section: Discussionmentioning

confidence: 99%

“…1970: Izzat andOlson, 1970), but any such protection was limited, if it occurred at all. Extracts from worms gave better protection (Izzat and Olson, 1970). As in our experiments, immunisation delays migrating larvae in the liver (Olson, 1962).…”

Section: Discussionmentioning

confidence: 99%

ANTIBODY RESPONSES TO TOXOCARA CANIS USING SERA FROM PARASITE‐INFECTED MICE AND PROTECTION FROM TOXOCARIASIS BY IMMUNISATION WITH ES ANTIGENS

Nicholas

Stewart

1984

Aust J Exp Biol Med

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“…To date, attempts to generate protective anti-larval immunity in laboratory rodents have had mixed results. While an early report noted that immunisation with somatic extracts of eggs or adult worms resulted in approximately half the number of surviving challenge larvae (Izzat and Olson, 1970), susceptibility to larval infection was unaltered in mice immunised with UV-irradiated eggs or larval ES antigens (Abo-Shehada et al, 1991). Likewise, a more recent study found no evidence of protection by administering a second challenge of larvae to previously infected mice, other than they were more likely to sequester in the brain (Kolbeková et al, 2011).…”

Section: Immunity In the Definitive Hostmentioning

confidence: 99%

Toxocara canis: Molecular basis of immune recognition and evasion

Maizels

2013

Veterinary Parasitology

126

105

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Toxocara canis has extraordinary abilities to survive for many years in the tissues of diverse vertebrate species, as well as to develop to maturity in the intestinal tract of its definitive canid host. Human disease is caused by larval stages invading musculature, brain and the eye, and immune mechanisms appear to be ineffective at eliminating the infection. Survival of T. canis larvae can be attributed to two molecular strategies evolved by the parasite. Firstly, it releases quantities of ‘excretory–secretory’ products which include lectins, mucins and enzymes that interact with and modulate host immunity. For example, one lectin (CTL-1) is very similar to mammalian lectins, required for tissue inflammation, suggesting that T. canis may interfere with leucocyte extravasation into infected sites. The second strategy is the elaboration of a specialised mucin-rich surface coat; this is loosely attached to the parasite epicuticle in a fashion that permits rapid escape when host antibodies and cells adhere, resulting in an inflammatory reaction around a newly vacated focus. The mucins have been characterised as bearing multiple glycan side-chains, consisting of a blood-group-like trisaccharide with one or two O-methylation modifications. Both the lectins and these trisaccharides are targeted by host antibodies, with anti-lectin antibodies showing particular diagnostic promise. Antibodies to the mono-methylated trisaccharide appear to be T. canis-specific, as this epitope is not found in the closely related Toxocara cati, but all other antigenic determinants are very similar between the two species. This distinction may be important in designing new and more accurate diagnostic tests. Further tools to control toxocariasis could also arise from understanding the molecular cues and steps involved in larval development. In vitro-cultivated larvae express high levels of four mRNAs that are translationally silenced, as the proteins they encode are not detectable in cultured larvae. However, these appear to be produced once the parasite has entered the mammalian host, as they are recognised by specific antibodies in infected patients. Elucidating the function of these genes, or analysing if micro-RNA translational silencing suppresses production of the proteins, may point towards new drug targets for tissue-phase parasites in humans.

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“…Recently we examined the impact of single versus multiple exposures to T. canis (4). In this situation, we anticipated a more heightened and sustained host immune reaction to secondary and subsequent infections of the parasite (44)(45)(46)(47)(48)(49)(50). Prior work had noted that the pattern of larval distribution in various organ systems is different in rodents given single versus multiple doses of T. canis (51)(52)(53).…”

Section: Immunological Considerationmentioning

confidence: 99%

The consequences of parasitic infection for the behavior of the mammalian host.

Donovick

Burright

1987

Environ Health Perspect

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As many as one billion people may be infected with animal parasites. The behavioral consequences of such infection, or of illness in general, is poorly understood. This issue is discussed using as an example infection of mice with Toxocara canis, the common roundworm of dogs. Current literature suggests that two-thirds of all dogs have been infected with this parasite, and 7% of all humans have antibodies to T. canis. T. canis completes its life cycle in dogs, but when it infects aberrant mammalian hosts (e.g., humans or mice), larvae migrate through various organ systems including the brain, where they can remain viable and mobile for extended periods of time. Changes in motor activity, sensory reactivity, and learning of mice infected with T. canis have been observed. The pattern of behavioral changes is influenced by the infection regime and exposure to other toxicants such as lead.

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Resistance of mice to Toxocara canis: effect of prechallenge infections and injections of worm extracts

Cited by 12 publications

References 0 publications

ANTIBODY RESPONSES TO TOXOCARA CANIS USING SERA FROM PARASITE‐INFECTED MICE AND PROTECTION FROM TOXOCARIASIS BY IMMUNISATION WITH ES ANTIGENS

ANTIBODY RESPONSES TO TOXOCARA CANIS USING SERA FROM PARASITE‐INFECTED MICE AND PROTECTION FROM TOXOCARIASIS BY IMMUNISATION WITH ES ANTIGENS

Toxocara canis: Molecular basis of immune recognition and evasion

The consequences of parasitic infection for the behavior of the mammalian host.

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