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Type I Ostertagiasis in Yearling Steers

BR Watt, District Veterinarian, Tablelands Livestock Health and Pest Authority and J Eppleston, Project Officer, Tablelands Livestock and Pest Authority

Posted Flock & Herd August 2009


Type 1 ostertagiasis typically occurs in the winter and spring in 13-18 month old beef weaners. On the central tablelands where most calves are weaned in the autumn, unless preventative measures are taken, infective larvae become increasingly available on winter and spring pastures. This can lead to mature worm populations of 0.5 million, worm egg counts from 100 to 1000 epg and diarrhoea, weight loss and some deaths in affected cattle (Anderson et al., 1983).


A part-time cattle producer from near Hampton on the central tablelands of NSW called in early December 2008 because, over the previous two months, six of a mob of 41 young cattle became weak and died and most of the remainder showed evidence of diarrhoea and failure to thrive. The cattle, run as one mob, consisted mainly of 15 month old homebred Angus and Angus cross steers although 14 Herefords of a similar age, purchased one year previously, were included, as were a few older cows.

The homebred portion of the steers, born in spring 2007, were self-weaned and had never been drenched. The owner had also not drenched the bought in mob. The owner had never treated them to control liver fluke and had not supplemented them with selenium. The mob had been set stocked for several months on a short green mixed ryegrass, native grass, and clover pasture.

Clinical findings

Five affected steers were physically examined and the remainder of the mob was inspected. The steers that were examined were estimated to weigh between 150 and 220kg. All were in thin body condition with a rough hair coat. All had evidence of watery diarrhoea. The calf identified with a green tag was noticeably weak and listless. It also had pale mucous membranes and had profuse watery diarrhoea. The calf identified with tag numbered 21 also had crusty skin around the nose and dry skin along the back. This was presumed to be due to some exposure to St Johns wart through a fence. None were febrile and none had oral erosions.

On inspection of the remainder of the mob, most of the cattle of similar age were affected. Some showed evidence of sub-mandibular oedema. The few mature cows in the mob were in good body condition with smooth coats.

Image of emaciated weaner cattle

Five steers affected by Type 1 ostertagiasis


Sample PP PCV FWEC Pepsin GSHPx Vit B12 PACE Fluke Fluke
Units g/L % epg 0-5.0 40-300 130-500 epg ELISA S/P
Normals 70-85 30-40 u/L U/gHb pmol/L
21 47 19 660 23.5 12 288 negative 0 <30
10 49 29 260 47.3 10 166 negative 0 <30
13 67 35 660 22.3 13 184 negative 0 38
18 44 32 920 80.5 14 571 negative 0 <30
green tag 34 10 880 16.9 25 213 negative 0 <30
mean 48.2 25 676 38.1 14.8 284.4 0

Total plasma protein and in 3/5 cases the PCV, were depressed. The faecal worm egg counts were also high averaging 676 epg. Pepsin levels were markedly elevated. Glutathione peroxidise levels were low, consistent with selenium deficiency. Pestivirus, fascioliasis and cobalt deficiency all encountered on the central tablelands were ruled out based on laboratory findings.


In our experience, sub-clinical ostertagiasis is widespread (ubiquitous) on the central tablelands. Even in well managed herds with a parasite control program involving a drench at weaning and 2-3 times subsequently, we found that at least in 2008, parasitism and presumably mostly ostertagiasis cost producers about 30 kg of liveweight per head. Our limited surveys have shown that the most producers drench young cattle at weaning and one to three times subsequently so this producer is unusual in having never drenched his cattle at any stage. Smeal (1981), who investigated the cost of internal parasites in cattle on the tablelands, found that undrenched cattle were 20-30 kg lighter than cattle suppression drenched. This herd demonstrates that this loss can sometimes be substantially higher. This producer has no facilities to weigh cattle but the affected cattle weighed roughly 200 kg whereas in our experience yearling cattle at this age commonly weigh in the order of 400kg. Six cattle also died.

As Anderson et al. (1983) observed, "the diagnosis of parasitic gastroenteritis is difficult, because of the lack of specificity in clinical signs, the generally poor correlation between faecal egg counts worm counts and the impracticality of conducting other tests". On the NSW central tablelands, several other diseases can cause similar symptoms. Selenium deficiency, liver fluke and pestivirus are widespread (Watt 2007), while cobalt deficiency has been diagnosed.

These cattle were also selenium deficient. Selenium deficiency has been incriminated in ill thrift in calves and may exacerbate infectious and presumably parasitic diseases (Radostits et al. 2007). However, we frequently encounter young cattle on the tablelands with single digit GSHPx levels that appear healthy. In one production response trial, we saw no weight improvement with selenium supplementation (Eppleston and Watt, unpublished). The clinical signs, history of complete absence of anthelmintics treatments, elevated pepsin levels, depressed plasma protein levels and elevated worm egg counts lead us to conclude that the major problem was Type 1 ostertagiasis.

These calves were negative for pestivirus and showed evidence of minimal exposure to liver fluke. Vitamin B12 levels were also within the normal range.

The value of pepsin levels in diagnosing parasitism in cattle has sometimes been questioned. In this case, pepsin levels were markedly elevated. In our experience pepsin levels rarely rise above 7 u/L in cattle in which parasites are suppressed whereas in cattle exposed to parasites, pepsin levels are usually above this figure.


  1. Anderson N, Donald AD and Waller PJ. (1983) Epidemiology and Control of Parasitic Gastroenteritis of Cattle in the Temperate Climatic Zone
  2. In The Epidemiology and Control of Parasitic Gastroenteritis of Cattle in Australia Edited by N Anderson and PJ Waller, pp 47-63
  3. Radostits OM, Gay CC, Hinchcliff KW and Constable PD. (2007). Veterinary Medicine, 10th Edition, pp 1740-1741
  4. Smeal, M. Nicholls, P. Webb, R. Hotson, I. Doughty, F. and Harding, W (1981). The effect of anthelmintic treatments on growth of beef cattle in NSW. AJAR. 32: 813-23
  5. Watt BR. A Serological and Trace Mineral survey of Beef Heifers in Central NSW. Australian Cattle Veterinarian's Conference, Townsville, 2007


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