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IgE antibody production in rats against multiple components of excretory-secretory products of the nematode Nippostrongylus brasiliensis.

Infection with the nematode Nippostrongylus brasiliensis (NB) induces the intense production of specific and non-specific immunoglobulin E (IgE) in rats. In the present study, we analysed NB-derived allergenic substances and the variability of IgE antibody production in response to these allergens in outbred Sprague-Dawley rats. Two kinds of crude allergens were used: the excretory-secretory products (ES) of adult NB, and an extract of homogenized adult worms (AW). ELISA showed that IgE antibody titres to ES were more than five times higher than the titres to AW. In the homologous passive cutaneous anaphylaxis (PCA) reaction using serum from infected rats, as little as 50 micrograms of ES had a maximal PCA activity, while even 1 mg of AW still gave a slightly lower PCA titre. Thus, it appeared that ES contained more allergen than AW at the same amount of total proteins. By immunoblot analysis, at least six components were recognized by IgE antibodies from infected animals, and these components were exactly the same in both ES and AW. The results indicated that the allergenic components in ES and AW were the same molecules, and that only those molecules which could be excreted or secreted from living worms were allergenic. Among the array of allergens, 130,000 and 70,000 molecular weight (mw) molecules were commonly recognized by IgE from all serum samples examined, while other components of the allergens were recognized variably by IgE antibodies from individual animals. These findings suggested that individual animals varied considerably in their IgE antibody production to the different constituents of the nematode allergens.

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Epidemiology of sheep nematodes in sub-arctic Greenland: sources of infection on rangeland grazing.

Sources of nematode infection on the rangelands of a southern Greenlandic sheep farm were investigated as a part of a study of the epidemiology of Ostertagia and Nematodirus infections in a sub-arctic climate. Herbage larval counts were performed on samples collected from selected localities on the rangeland and post mortem worm-counts made on tracer lambs that had grazed these areas for the latter part of the summer season. Relatively high concentrations of larvae were found in good quality native grasses at sea-level and in grasses growing beneath canopies of willow-shrub at higher altitudes. In general, however, the infectivity of the vegetation was very low and the pick-up of infection by the tracer lambs was correspondingly small.

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Anorexia in rats infected with the nematode, Nippostrongylus brasiliensis: experimental manipulations.

Nippostrongylus brasiliensis induces a biphasic anorexia in laboratory rats, the first phase coincident with lung invasion (ca day 2) and the second when the worms mature in the intestine (ca day 8). Using the anthelminthic, mebendazole (MBZ), N. brasiliensis infections of the rat were eliminated between the first and second anorexic episodes. This intervention prevented the expression of the second phase of anorexia. Rats exposed to a second infection with N. brasiliensis, 3 weeks after the primary infection, exhibited only a first phase anorexic response which was not influenced by MBZ termination of the primary infection. The lower cumulative food intake and weight gain of all infected rats after 8 days of infection were accompanied by elevated plasma insulin and, in some individuals, by elevated plasma leptin, compared with uninfected controls and previously-infected MBZ-treated rats. Messenger RNA levels for neuropeptide Y were higher in the hypothalamic arcuate nucleus of 8-day infected rats than in recovering MBZ-treated animals. Inoculation of rats with heat-killed N. brasiliensis larvae failed to induce anorexia and did not alter the severity of biphasic anorexia on subsequent injection of viable larvae. The first anorexic episode is therefore dependent upon viable migrating larvae. The second phase of anorexia clearly requires the continuing presence of the parasite beyond the lung phase. Viable migrating larvae are also required to confer 'resistance' to reinfection.

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Biphasic hypothermia in mice infected with a parasitic nematode, Trichinella spiralis.

In BALB/c mice infected with Trichinella spiralis, changes in body temperature (Tb) were observed over 35 days after the infection. T. spiralis infection induced hypothermia two times at 7 and 28 days after infection. The initial decrease persisted for about one week with a peak (37.1 +/- 0.62 degrees C) around 10 days after the infection, while the later phase persisted for at least one week. Both 10 and 35 days after the infection, there were remarkable decreases in Tb. The serum glucose level of infected mice at 10 days was significantly (p < 0.01) decreased compared with that of control mice at the same number of days, while the level in infected mice at 35 days was not decreased. Moreover, the later phase of hypothermia was prevented by the cyclooxygenase inhibitor indomethacin (10 mg/kg i.p.), while the initial phase was not. We conclude that hypothermia was caused by two different mechanisms, involving the effects of hypoglycemia and prostaglandins.

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Use of an ivermectin bolus against gastrointestinal nematode and lungworm infections in first-year grazing calves.

Two groups of first-year grazing cattle each were either left untreated as controls (group 1) or treated with an ivermectin bolus at turnout (group 2). Whereas group 1 suffered from dictyocaulosis, the bolus treated calves remained healthy. Shedding of lungworm larvae was completed prevented and gastrointestinal nematode egg output effectively reduced. During the 154 day grazing season the ivermectin bolus provided a season-long protection against parasitic gastroenteritis and bronchitis.

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Parasite-induced anorexia: leptin, insulin and corticosterone responses to infection with the nematode, Nippostrongylus brasiliensis.

The nematode parasite, Nippostrongylus brasiliensis, induces a biphasic anorexia in its rat host. The mechanisms, underlying this anorexia and its possible advantages to the host or parasite are unknown. We have investigated the effect of acute (12-24 h) and chronic (2-17 days) infections on plasma concentrations of leptin, insulin and corticosterone, and on hypothalamic expression of neuropeptide Y, galanin and corticotrophin-releasing factor genes. Plasma leptin was elevated in infected rats relative to uninfected ad libitum-fed controls and pair-fed controls in 12 h infections initiated at dark onset and in infections of 2 days' duration. At other times prior to parasite expulsion, plasma leptin in infected and pair-fed rats was lower than that of uninfected ad libitum-fed controls, reflecting the existing state of negative energy balance. Elevated plasma leptin concentrations in infected rats at day 2 post-infection were accompanied by reduced neuropeptide Y gene expression in the hypothalamic arcuate nucleus compared with both ad libitum control and pair-fed animals, and by lowered corticotrophin-releasing factor gene expression in the paraventricular nucleus relative to pair-feds. Twelve hour infections were characterized by a substantial increase in plasma corticosterone that was independent of reduced food intake, and in 12 h infections initiated at dark onset, where plasma leptin was elevated, there was also increased plasma insulin concentration in infected rats. In longer infections, differences between the groups in plasma insulin and corticosterone concentration were only observed at day 4 post-infection. In summary, perturbations to leptin, insulin and corticosterone signals early in infection may have a causative role and might feed back onto hypothalamic gene expression, whereas subsequent changes in these parameters are more likely to be secondary to negative energy balance.

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Studies on the effect of treatment with anthelmintics on weight gain in calves, naturally infected with gastrointestinal nematodes.

To avoid disease outbreaks caused by gastro-intestinal nematodes different prophylactic measures are recommended. In this connection pasture hygienic achievements and anthelmintics are used. In practice it is often difficult to realize pasture hygienic steps as move the animals to parasite free areas and to avoid that they come back to the infected. In many cases the parasite control is limited to routine deworming. Our intention was to study if anthelmintic treatment without other measures had any effect on weight gain and number of eggs in faeces in calves naturally infected with Ostertagia ostertagi. The studies were done during two stable seasons 1975/76 and 1976/77 when the calves were treated two weeks after stabling, and during two grazing seasons 1976 and 1977 when the calves were treated 20 days or 15 and 20 days after turning out. In none of the trials any obvious influence on the weight gain and number of eggs was observed. The failing effect during the stable season might depend on the fact that the parasites to more than 90% were in inhibited L4-stage, and the failing effect during grazing, is surely an effect of reinfection when the calves remain on the infected pastures. As prophylactic measure anthelmintic treatment is of very little value if not the calves at the same time are protected against reinfection by moving to clean pastures.

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B-cell activation in the mesenteric lymph nodes of resistant BALB/c mice infected with the murine nematode parasite Trichuris muris.

Immune responses in resistant BALB/c mice infected with the murine nematode parasite Trichuris muris were examined. Following the establishment of infection, worm burdens of T. muris were expelled by BALB/c mice by day 21 postinfection (p.i.). Specific immunoglobulin G1 (IgG1) antibodies to T. muris excretory/secretory (E/S) antigens were detected in sera from infected mice, though specific IgG2a antibodies were not observed during infection. Ig-producing cells increased in the mesenteric lymph nodes (MLN) of infected mice on days 7, 14, and 21 p.i., with the greatest increase in numbers of IgG- and IgA-producing cells occurring on day 14. Marked increases in the relative percentages of B220+ and surface Ig+ (sIg+) cells were observed in the MLN of infected mice on days 14 and 21 p.i. Furthermore, cellular expansion of the MLN in infected mice resulted in an increase in the absolute numbers of B220+ and sIg+ cells. The levels of interleukin 2 (IL-2), IL-4, and interferon-gamma (IFN-gamma) detected in the supernatants from concanavalin A-stimulated MLN cells of infected mice were higher than those found in normal mice. Consequently, the expulsion of T. muris in resistant BALB/c mice was concomitant with cytokine production and B-cell activation in the MLN of infected mice. These results suggest the involvement of B-cell responses in protective immunity to T. muris infection.

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Development and survival of infective larvae of nematode parasites of sheep on pasture in a cool tropical environment.

The development and survival of nematode parasites of sheep were studied in a cool tropical environment of the highlands of Ethiopia on 24 plots serially contaminated with Haemonchus contortus, Longistrongylus elongata and Trichostrongylus colubriformis eggs over a period of 2 consecutive years from June 1993 to May 1995. The availability of infective larvae was monitored by monthly pasture sampling and larvae recovery. Infective larvae were recovered from the herbage collected from the plots contaminated in June, July, August, September and October of both years. The longevity of infective larvae varied between two and six weeks when eggs were deposited on pasture in June and October, respectively. During the dry and short rainy season (November through May), eggs failed to develop into L3 stage. It is suggested that the long period (7 to 8 months) of lack of development of trichostrongylid infective larvae on the pasture can be efficiently used in a strategic treatment programme to interrupt transmission of H. contortus, L. elongata and T. colubriformis in sheep in this environment.

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