Nematode infections

Microscopically, toxocara granulomas consist of a central mass of karyorrhectic nuclear debris, and eosinophilic structureless and often fibrinoid-like material (Spencer 1973. In less severe tissue reactions the centres of the lesions are occupied by a mass of eosinophils without cellular necrosis. In a minority of lesions a portion of the causative larva may be identified near the centre of the lesion and cross sections may show the characteristic alar ridges projecting from the exterior of the cuticle. Around the central necrotic area the lesions consist of masses of eosinophil cells, plasma cells, lymphocytes and histiocytic cells, the latter often arranged in a characteristic pallisaded fashion. 

Escape of the larva into the posterior eye chamber results in an endophthalmitis and the formation of a retinal granuloma (Ashton 1960). 

In the mouse, a monoclonal antibody (IgM isotype) against Brugia malayi microfilariae induces resistance against the lymph-dwelling nematode para- 

Specific antibodies to the cuticule of microfilariae of Brugia pahangi were detected in infected, amic-rofilaraemic cats (Ponnudurai et al. 1974). 

A 34-year-old woman resident in the city of Colombo, Sri Lanka, with tropical pulmonary eosino-philia a few days after starting diethylcarbamazine 

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Nematode infections Nematode resistance Nematodes Nemaworm capsules Nembutal (sodium)... 

Anthelmintic agents have been utilized to treat a multimde of nematode infections. These include roundworms, tapeworms, and lungworms in cattle and swine. Two classes of compounds included as anthelmintic agents will be discussed here, lev-amisole and thiabendazoles (thiabendazoles can also act as pesticides). Thiabendazoles can cause nephrotoxicity, teratogenesis, and immunosuppression and can disrupt endocrine balance. Because of these toxicides, residues of these compounds in food animals are of food safety concern. 

The rate of progression of signs and symptoms varies depending on the infecting organism. A differential diagnosis for keratitis must include viral, fungal, and nematodal infections in addition to bacterial causes.19... 

JR Egerton, D Suhayda, CH Eary. Prophylaxis of nematode infections in cattle with an indwelling, ruminoreticular ivermectin sustained release bolus. Vet Parasitol 74 614-617, 1986. 

Table 2.1. Filarial nematodes infected with intracellular bacteria. The method of detection is shown. Neither electron microscopy nor the immuno-histochemical staining techniques used are to be regarded as Wolbachia specific (see note). Positive identification of intracellular bacteria as Wolbachia is shown only where PCR amplified products of rRNA or ftsZ genes have been sequenced. ...

Trichinellosis is caused by the parasitic nematode Trichinella spiralis. This parasite has a complex life cycle that alternates between intestinal and muscle cell compartments of the host. This nematode infection is unusual because 7. spiralis is an intracellular parasite of mammalian cells. In addition, the broad host range of this parasite includes most mammals. The disease in humans has intrigued parasitologists, other biologists and public health workers for over a century (Cambell, 1983). The attraction to trichinellosis pardy stems from the debilitating and sometimes fatal effects that characterize this disease. 

Dropkin, V.H. (1969) Cellular responses of plants to nematode infections. Annual Review of Phytopathology 7, 101-122. 

T Helper Cell Cytokine Responses During Intestinal Nematode Infection Induction, Regulation and Effector Function... 

The in vivo manipulation of specific type 2 cytokines using anticytokine monoclonal antibodies, or mouse strains with targeted deletions in cytokine and/or cytokine receptor genes, has proved a fruitful approach in identifying the importance of individual cytokines and the responses that they control in contributing to host resistance. These studies have identified important roles for IL-4, IL-9 and IL-13 in host protection against nematode infection, though the relative importance of each cytokine appears to be nematode-species dependent. 

A cardinal role for IL-4 in host protection against intestinal nematode infection was first shown in the H. polygyrus challenge model. Worm expulsion was delayed following treatment with anti-IL-4 or anti-IL-4 receptor monoclonal antibodies, while control treated animals successfully cleared infection (Urban et al., 1991b). Blockade of the IL-4 receptor effectively prevents the in vivo function of IL-4 and IL-13, as these two cytokines share the IL-4 receptor a-chain for signalling functions (Lin et al, 1995). In... 

It is clear that the type 2 cytokines IL-4, IL-9 and IL-13 play an obligatory role in host resistance to nematode infection whereas type 1 responses promote host susceptibility. Therefore, given that susceptibility to nematode infection is not due to a lack of responsiveness perse, but rather the development of an inappropriate response, it is important to understand the factors that influence the induction and expansion of Th subset responses and so control infection outcome. Studies in nematode models and other systems have addressed these questions and identified the importance of host genetic factors, the nature of the antigen and the antigen presenting cell, co-stimulatory molecules on these cells, and the cytokine and chemokine environment immediately following induction of the response. 

As mentioned above, yS T cells are numerous in the gut and can produce cytokines in the absence of conventionally presented antigen (Kaufmann, 1996). These cells have been shown to produce IL-4 or IFN-y (Ferrick el al., 1995) and are potentially an important source of these cytokines in the intestinal microenvironment following nematode infection. Supporting this suggestion, IL-4 mRNA has been found in y8 T cells from the caecum of resistant mice immediately following T. muris infection (Lukaszewski and R.K. Grencis, unpublished observations). 

Given that epithelial cells have been shown to be a source of chemokines at mucosal sites (Li et al., 1999 Santy et al, 1999 Song et al, 1999), it will be important to define the expression and function of chemokines and their receptors in the intestinal microenvironment during nematode infection, and to determine what effects, if any, these have on the polarization or regulation of anti-nematode responses. 

As mentioned above, a prototypic type 2 response is mounted against nematode infection in most cases (consisting of elevated IgE, eosinophilia and intestinal mastocytosis), with a number of coexisting variables likely to... 

A variety of type 2 cytokines and the non-lymphoid cell-derived growth factor, stem cell factor (SCF) (Hiiltner et al., 1989 Copeland et al., 1990 Huang et al., 1990 Thompson-Snipes et al., 1991 reviewed in Befus, 1995), are known to be important in the development of intestinal mast cell responses associated with nematode infection but the contribution of this population to host protection depends on the nematode species in question. 

The involvement of mast cells in host protection against nematode infection is well characterized in T. spiralis infection. W/Wv mice exhibited a significant delay in worm expulsion, and treatment with either anti-SCF or anti-SCF receptor monoclonal antibody dramatically inhibited mast cell responses and expulsion of T. spiralis for the duration of treatment (Donaldson et al., 1996). W/Wv mice also lack interstitial cells of cajal and intraepithelial y T cells (Maeda et al., 1992 Puddington et al., 1994), which may contribute to the impaired response in these animals (see below). However, supporting evidence of a role for mast cells in protection against T. spiralis comes from studies in which overexpression of IL-9 in mice (which is known to influence the mast cell responses see above) resulted in an extremely rapid mast cell-dependent expulsion of T. spiralis (Faulkner et al., 1997). 

Eosinophilia is a hallmark of intestinal nematode infection and is known to be under the control of IL-5 (Finkelman et al., 1992). As discussed above, treatment with anti-IL-5 monoclonal antibody (and so ablation of eosinophilia) had no effect on expulsion of T. muris, 77. polygyms, N. brasiliensis or T. spiralis infections, suggesting that either redundant mechanisms operate under these circumstances or that eosinophils are not a critical component of effector responses operating against most murine... 

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