Wooden Tongue

Wooden tongue is a well-defined disease of the soft tissues of the mouth region in adult cattle. It is caused by A. lignieresii coccobacillus, part of the normal bacterial flora of the upper digestive tract. The bacteria usually invade the skin through a wound or minor trauma caused by sticks or straw or barley awns.

The disease is fairly acute, with swelling in the affected part, under the jaw and in the regional lymph nodes. The clinical symptoms are excess salivation, difficult mastication and inappetance.

The condition is seen either as an outbreak in several animals simultaneously or as an individual case in a single animal, often in association with a diet change


Parasitic gastroenteritis is associated with large numbers of nematodes in the abomasum and intestines. The nematodes in the abomasum are generally considered to be the primary pathogens, with those in the intestines playing a lesser but synergistic role. In the United Kingdom, the predominant worms in the abomasum belong to the genus Ostertagia, with Ostertagia ostertagi the most abundant. In the small intestine, Cooperia oncophora and Nematodirus helvetianus are commonest. There are two common forms of ostertagiasis, type I and type II.

Type I Ostertagia infection

This disease is most common in late summer and autumn and causes profuse watery diarrhoea in calves at grass. The faeces are usually green because of the grass diet. Developing larvae within the gastric glands of the abomasum cause the lumen of these glands to distend and stretch the cellular lining. As a result, the mature functional parietal and peptic cells are superseded by undifferential cells. As the infection progresses adjacent non-parasitized glands also become affected and their parietal cells replaced by non-functional undifferentiated cells. The pH of the abomasum increases and leakage of macromolecules and protein occurs across the damaged mucosa, resulting in hypoproteinaemia and increased concentrations of pepsinogen in the plasma. There is a rapid loss of weight, largely due to changes in grazing behaviour. In chronic cases, submandibular oedema may result.

The direct cause is the ingestion of large numbers of O. ostertagi infected larvae over a relatively short period of time. The number of infected larvae on pasture is lowest in May and June, but rises to a peak in late August and September. This pattern arises from a sequence of events which starts with calves turned out in April or May onto pasture grazed by cattle (and especially calves) during the preceding year. These calves ingest some of the infective larvae which have overwintered. It takes three weeks for these larvae to develop into adults and start laying eggs. The rate of hatching of these eggs depends on climatic conditions, reaching a peak in midsummer. The hatched larvae migrate or are washed out of faecal pats onto surrounding herbage to await ingestion by the eventual host. Wet summers produce an early peak, but numbers decrease more rapidly due to rapid depletion of numbers in faecal pats and dilution due to the more abundant grass growth. Conversely, dry summers delay the build-up, as the release of the larvae from the faecal pats is delayed until the autumn rains.

In dairy herds typical cases of type I Ostertagia infection occur in spring-born calves turned out in midsummer onto pastures grazed and contaminated in the spring and early summer by autumn-born calves. In a recent survey, it was found that 65% of farmers used the same pasture each year for calves. The disease is not usually a problem in spring-calving beef herds, as the calves are too young to consume much grass in the early part of the season. As a result, the peak of infective larvae does not develop until September or October, when most calves are weaned and housed. However, autumn-born beef calves may suffer from type I Ostertagia infection in the absence of preventative measures. In areas where climatic conditions allow autumn-born calves to be turned out in March or early April, type I Ostertagia infection may occur 4 to 6 weeks after going to grass.

Type II Ostertagia infection

Infective larvae ingested from September onwards undergo a change in their normal parasitic development, resulting in a period of delayed development at the early fourth larval stage while within the abomasal wall. The change is thought to be brought about by either cold or desiccation in their preparasitic exposure. In the late autumn, calves may harbour many thousands of such larvae. Type II ostertagiasis results when these inhibited larvae resume their development, usually from February to May, the emerging larvae causing the same lesions as those causing type I disease.

Although adult cattle acquire immunity by the age of 18 months, occasionally bulls grazing calf paddocks or cows suffering from immunosuppression due to other diseases such as fascioliasis, may suffer from type II ostertagiasis.

Nematodiriasis in calves

Nematodirus battus, mainly a parasite of sheep, has recently been found to be transmittable by cattle, both on farms where annual alternation of sheep and cattle has taken place, and even where cattle only are kept. It has caused severe outbreaks of diarrhoea in calves.


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