Parasitic infection Flashcards
(40 cards)
What are the potential consequences of large strongyle infections in horses?
Migration through mesenteric arteries, causing thrombosis, infarctions, necrosis, and arteritis lesions
How is larvicidal treatment hypothesized to impact large strongyle infections?
Larvicidal treatment may release antigenic factors from larvae, exacerbating arterial and intestinal lesions and colic.
What is the role of immune serum in arteritis lesions caused by large strongyles?
Immune serum reduces the severity of arteritis, suggesting the immune response modulates and potentiates pathogenicity.
What is a significant concern with Parascaris spp. infections in foals?
Colic related to intestinal impaction and rupture, with potential hypersensitivity in mature horses responding to low-level infections.
What gastrointestinal issues are associated with Anoplocephala perfoliata infections?
Case reports describe cecal ruptures, intussusceptions, and ileal region colics.
Why are cyathostomins generally not considered major colic agents?
Efficacious anthelmintic treatments significantly reduce colic incidence, but they are implicated in Uhlinger’s field studies.
What are the clinical signs of larval cyathostominaisis?
Sudden onset diarrhea, weight loss, hypoproteinaemia, and a 50% fatality rate.
What mechanisms induce changes in gastrointestinal function by parasitic organisms?
Mechanical disruption of tissues, release of factors altering cell function, and induction of immune responses.
How do helminth parasites disrupt gastrointestinal function in terms of smooth muscle and epithelial alterations?
They stimulate intestinal smooth muscle hyperplasia and alter the myoelectric activity of the equine small intestine and colon.
What type of cytokine response is induced by gastrointestinal nematodes in mouse models?
Type 2 T-helper cell cytokine response, including interleukins IL-4, IL-5, IL-9, and IL-13.
What are the major effectors involved in the responses to helminths in mouse models?
Goblet cells, enteric nervous system, epithelial cells, and alternately activated macrophages.
What are the clinical manifestations of Onchocerca cervicalis infections in horses?
Focal, alopecic, depigmented, and pruritic lesions, often with seasonal variability.
What is the role of eosinophils in the skin response to Onchocerca microfilariae?
Eosinophils’ toxic enzymes and proteins are implicated in lesion development.
What are the mechanisms of protective resistance against equine parasites?
Innate and acquired resistance, including age-related and acquired resistance.
What is age-related resistance, and which parasites show it?
Older individuals show resistance to most equine helminth parasites, except for parasites with broader host ranges.
What is partial resistance to S. vulgaris, and what does it allow?
Partial resistance allows arterial larvae to reside within the horse despite acquired resistance against infective stages.
What is the self-cure phenomenon observed in sheep?
Ingestion of a large number of infective larvae induces expulsion of existing adult parasites.
What is the speculated contribution of rapid expulsion mechanisms to resistance to reinfection in equines with cyathostomins?
These reactions may contribute to resistance by preventing reinfection with viable and undamaged larvae.
What is the role of T cells in protective resistance against nematodes?
T-cell responses are essential for the induction of protective resistance, likely due to T-cell dependency of antibody response and mediation of secondary effector cell responses.
How is rapid expulsion at the epithelial surface distinct from self-cure?
Rapid expulsion involves immediate expulsion or immune exclusion, while self-cure is the expulsion of existing adult parasites.
How is equine resistance to reinfection with cyathostomins acquired?
Over time with continued exposure to pasture L3, and it appears genetically regulated.
What are the immune evasion strategies of helminth parasites?
Production and secretion of molecules disrupting host effector responses, mimicking host immune regulatory factors, and downregulating protective responses.
How can helminth parasites induce a regulatory immune response?
By stimulating dendritic cells, activating regulatory T cells, and alternately activated macrophages, leading to the production of TGF-β and IL-10.
What is the potential application of helminth therapy in human diseases?
Treatment of inflammatory bowel disease and ulcerative colitis, where infection with certain helminths impedes type 1 inflammatory responses.
