Inhibited fourth-stage larvae (L4) of Ostertagia ostertagi were described by Anderson et al (1965). This hypobiosis was an important factor in the development of clinical ostertagiasis of cattle in southern Australia before the development of anthelmintics effective against the larvae embedded in the abomasal mucosa.
Hypobiosis is not a well-recognised feature of the epidemiology of Teladorsagia circumcincta in sheep. There have been some references to them from time to time, but I am not aware of any published data.
During a trial investigating the epidemiology of gastrointestinal parasites in lambs grazing pastures in the Riverina which were irrigated during the summer, tracer lambs were grazed with a group of ram lambs for one month. After being removed from the trial mob, the tracers were kept on raised slatted floors and hand-fed for a month. The lambs were then slaughtered and total worm counts performed on their gastrointestinal tract, including differentiation between adult worms and fourth-stage larvae.
The total worm counts and the number of fourth-stage larvae are shown in Table 1
Charts 1 and 2 show the proportion of Teladorsagia which remained as L4 four weeks after ingestion by month and also in relation to the daily larval intake of the tracers. The daily intake was calculated by dividing the total number of parasites by the number of days in the trial mob. The daily intakes were allocated to months based on the number of days in a particular month in each grazing period.
Chart 3 shows the percentage of larvae which remained arrested at L4 plotted against the logarithm of the average daily pickup
Soulsby (1982) considered that ingested Teladorsagia larvae developed into adults in 18-21 days after infection unless hypobiosis had occurred. This would seem to be the case in this trial.
Clinically this hypobiosis would appear to be the reason why faecal egg counts for Teladorsagia often have little relationship to the total worm count rendering faecal egg counts unreliable as a diagnostic tool for clinical parasitiasis.
The cause of hypobiosis is not well described. In cattle, Armour and Bruce (1974) considered that the primary stimulus for hypobiosis was decreasing temperature. This does not seem to be the case here. If anything the level of hypobiosis seems to follow the rate of larval pickup in which case it may be a result of the immune response of the host rather than a feature of the parasite's epidemiology.