The relative importance of these sources in any country varies according to the conditions during the adverse period for larval survival. The sources of pasture contamination are again the ewes during the PPR and the lambs following ingestion of larvae, which have survived the summer. This coincides with conditions which are favourable to the development of the free-living stages of Teladorsagia and so infective larvae accumulate during the winter to cause clinical problems or production loss in the second half of the winter arrested larval development occurs at the end of the winter or early spring. In many of these areas lambing is geared to an increase in the growth of pasture, which occurs with the onset of rain in late autumn or winter. The epidemiology in subtropical areas is basically similar to that in temperate zones, except that the seasonal timing of events is different. Subsequently, adult ewes harbour only very low populations of Teladorsagia except during the annual periparturient rise (PPR). Immunity is acquired slowly and usually requires exposure over two grazing seasons before a significant resistance to infection develops. If ingested prior to October, the majority of these larvae mature in 3 weeks thereafter, many become arrested in development for several months and may precipitate type II disease when they mature. It is these eggs deposited in the first half of the grazing season from April to June which give rise to the potentially dangerous populations of L 3 from July to October. Eggs passed by lambs, from worm burdens which have accrued from the ingestion of overwintered larvae, also contribute to the pasture contamination. These larvae are derived mainly from eggs passed in the faeces of ewes during the periparturient period, from about 2 weeks prior to lambing until about 6 weeks post-lambing. circumcincta L 3 increase markedly from mid-summer onwards and this is when most disease appears. In subtropical areas with winter rainfall outbreaks of disease occurs primarily in late winter. In Europe a clinical syndrome analogous to type I bovine ostertagiosis occurs from August to October thereafter arrested development of many ingested larvae occurs and a type II syndrome has been occasionally reported in late winter and early spring, especially in young adults. trifurcata are responsible for outbreaks of clinical disease, particularly in lambs. In heavy infections these nodules coalesce and the abomasal folds are often very oedematous and hyperaemic.Įpidemiology: In sheep, T. The developing parasites cause distension of parasitised gastric glands, leading to a thickened hyperplastic gastric mucosa similar to that seen in cattle (see Fig. Pathology: The pathology is similar to that described for O. Plasma pepsinogen levels are above the normal of about 0.8 IU tyrosine and usually exceed 2.0 IU in sheep with heavy infections. Diarrhoea is intermittent and although stained hindquarters are common, the fluid faeces, that characterise bovine ostertagiosis, are less frequently seen.ĭiagnosis: This is based on clinical signs, seasonality of infection and faecal egg counts and, if possible, postmortem examination, when the characteristic lesions can be seen in the abomasum. Skeletal growth can also be impaired.Ĭlinical signs: The most frequent clinical sign is a marked loss of weight. circumcincta carcase evaluation can show poor protein and fat deposition. circumcincta causes a marked depression in appetite and this, together with losses of plasma protein into the gastrointestinal tract and sloughed intestinal epithelium, results in interference with the post-absorptive metabolism of protein. In subclinical infections, it has been shown under both experimental and natural conditions that T. Pathogenesis: In clinical infections, this resembles the situation in cattle and similar lesions are present at necropsy, although the morocco leather appearance of the abomasal surface seen in cattle is not common in sheep and goats.

Life cycle: Both the free-living and parasitic phases of the life cycle are similar to those of the bovine species, O.

Caprine strongyles treatment