Innovations from the Integrated Family Planning and Parasite Control Project: PDA experience.
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Suckling Merino lambs on lucerne pasture, demonstrated no appreciable mass gain when compared with untreated controls, despite regular treatment with anthelmintics. This was ascribed to severe parasitic challenge. After weaning and transfer to wheat stubble fields with no parasitic challenge, however, the live mass of the untreated lambs, still harbouring a residual burden of nematodes, was depressed. Control sheep produced 1.2 kg less wool than regularly-treated sheep, but produced finer wool which had a higher market value. Regularly-treated ewes (F1) produced 12.1% more lambs, but their mean live mass was 2.6 kg lower than that of ewes treated less frequently. The overall financial benefit was in favour of the group which received fewer anthelmintic treatments and was due mainly to the higher market value of the finer wool produced by these apparently stressed animals.
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Models of the population biology and transmission of helminth parasites of domestic ruminants do not generally include any explicit reference to production because that would require the identification of a systematic relationship between parasitism and production loss. This is difficult because (1) the relationship between parasitism and production loss (in so far as we can identify one) is non-linear, (2) it is by no means clear which index of parasitism we should use in defining the nature of the relationship and (3) time delays in the system and the multicausal nature of production losses make it difficult to tease out those components of the loss that are attributable to parasitism.
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TNF is involved in host resistance to several pathogens. Recently it was found that mice lacking the p55 receptor for TNF (TNFRp55 -/-) do not control growth of the intracellular bacteria, Listeria monocytogenes and Mycobacterium tuberculosis. Here we report that the course of infection in TNFRp55 -/- mice with another intracellular pathogen, the protozoan parasite Leishmania major, is also quite different from normal mice. TNFRp55 -/- mice developed larger lesions than control mice and failed to resolve these lesions. However, they were able to eliminate parasites within the lesions. Histologic analysis indicated that at late stages lesions from TNFRp55 -/- mice appeared similar to lesions associated with cutaneous graft-vs-host disease. Both TNFRp55 -/- and control mice developed a normal Th1-type response during infection. We also found that IFN-gamma-activated macrophages from TNFRp55 -/- mice produced nitric oxide and killed L. major in vitro, which correlated with the ability of TNFRp55 -/- mice to eliminate the parasites in vivo. The production of nitric oxide by macrophages from TNFRp55 -/- mice required the presence of the parasites, however, since in their absence TNF could only synergize with IFN-gamma for nitric oxide production when added to normal, but not TNFRp55 -/-, macrophages. These results indicate that neither macrophage microbicidal activity nor nitric oxide production is absolutely dependent on the p55 receptor for TNF. Furthermore, they uncover a previously undefined role for TNFRp55 in resolution of parasite-induced inflammatory lesions.
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The effects of horn fly and gastrointestinal nematode control on body weight gain of yearling Angus-Brangus cross heifers were evaluated in three separate studies during the years 1999, 2000 and 2002. In each year, the studies started in late May and lasted for 150, 148 and 123 days, respectively. In all three studies, the tag treatment (10% lambdacyhalothrin+13% piperonyl butoxide impregnated ear tags) provided excellent horn fly control. In the three studies, the average weekly horn fly counts for tagged heifers were 1, 3, and 0 flies per side while the average on untreated heifers was 52, 163 and 90 flies per side. In studies 1 and 2, there was no difference (P>0.1) in weight gain between tagged and untreated heifers, but in study 3, tagged heifers gained 50% more weight (P<0.001) than the untreated heifers. For gastrointestinal nematode control, ivermectin (IVM) was administered on Day 0 in studies 1 and 3 using a sustained release bolus and on Day 0 and subsequent 56-day intervals in study 2 using either the injectable or pour-on formulation. Heifers treated with IVM in studies 1 and 3 had significantly lower (P<0.05) GI nematode fecal egg counts compared to control heifers. In study 2, IVM treated heifers also had significantly lower GI nematode fecal egg counts compared to control heifers, except for Day 90 when no differences in fecal egg counts were observed between IVM pour-on treated and control heifers. Weight gain of heifers that received IVM was significantly greater (P<0.005) than untreated heifers in each of the three studies. IVM treated heifers gained 45, 61 and 184% more weight than the untreated heifers during the three studies. There was no interaction (P>0.1) between the main treatment effects of fly control and gastrointestinal nematode control.
It is clear from both laboratory and clinical studies that the blood-stage malaria parasite does not itself directly cause most of the serious complications of the disease, with the possible exception of anaemia. For example, T cell- deprived mice with lethal infections survive longer and mice can be protected against early death by vaccines that appear not to affect parasitaemia. In certain cases antibodies to TNF have the same effect. Clinically it has been known for over 50 years that children in endemic areas develop immunity to the serious toxic aspects of malaria several years before their parasitaemias start to fall. Recent work on the induction of cytokines such as tumour necrosis factor (TNF) by exoantigens of the blood-stage parasite and on the role of cytokines in this and other toxic diseases suggests that an appropriate vaccine might induce antibody that blocks the effect of the exoantigens, thus conferring on young children the anti-disease immunity that normally takes years to appear. Such vaccines might be less hampered by the antigenic variation that makes anti-parasite immunity slow to develop. Characterisation of the molecules involved is a high priority.
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