Ostertagiasis in the cow and weaned calf in the northeastern USA

Abstract

Most gastrointestinal nematode infections of cattle in the northeast USA are combinations of Ostertagia ostertagi and Cooperia oncophora. These infections are usually of little consequence in adult cattle because of immunity and consequent low levels of infection. Some work has been done on the effects of infection on milk production but the results are equivocal. Clinical ostertagiasis in calves can lead to mortality. Such outbreaks are often associated with situations where calves are pastured at an early age onto special calf pastures that are used consistently for this purpose. Subclinical ostertagiasis is more usual in this region where light infections become established in calves with no obvious clinical signs. Such infections exact a toll on productivity in the form of decreased weight gains, decreased carcass quality, reduced nitrogen balance and negative effects on post-absorptive protein metabolism. Subclinical infections can also cause transient suppression of cell-mediated immune responses in calves. Increases in fecal worm egg counts of cows have been shown to occur during the spring months and these may contribute to increased contamination of pastures. Ostertagia infective larvae overwinter successfully on pasture and can persist until midsummer. Typical egg production patterns in calves involve a prepatent period, after introduction to pasture in mid to late May, of approximately 3 weeks. Peak egg production occurs at about 6–8 weeks and is followed by a gradual decline in egg counts into the fall. Hypobiosis is very apparent in this region and is most pronounced in late fall (October–November). Most of the winter population of Ostertagia in cattle are hypobiotic fourth stage larvae and there appears to be a gradual resumption of development in the spring. Type II ostertagiasis is rare. Infective larvae build up on pasture over the summer and there can be significant numbers available to calves in the fall. These larvae can cause pathologic damage in the abomasum as reflected by marked increases in plasma pepsinogen levels in these calves.