Clinical signs, when present, may include lethargy, diarrhoea, pyrexia, anorexia and deer will often seek seclusion or ‘hide up’. Diarrhoea is usually watery faeces which can, occasionally, contain blood and mucous. In many cases, there are no overt clinical signs and animals die within hours of being affected; if they have hidden, then sometimes fatalities are not found before decomposition precludes testing for clostridial diseases through postmortem examination (PME).

Diagnosis prior to death can be challenging. The main diagnostic method is through observing compatible gross PME findings and examination of gut content (sampling >5 ml of the distal small intestine) for C. perfringens toxins (usually by polymerase chain reaction [PCR]). The toxins can degrade within hours of death; therefore, failure to detect them does not necessarily rule out the disease.

Tissue samples can be taken from the intestines, liver, spleen, kidney and mesenteric lymph nodes for histology (Niu et al. 2015) although tissues may be very autolysed and histopathology may not enable a definitive diagnosis.

Catarrhal enteritis with mucosal haemorrhages has been observed in conjunction with large number of C. perfringens organisms in the abomasum and small intestine during PME of sika deer (Sato and Matsuura 1998).

Clostridial enterotoxaemia is often associated with sudden changes in the environment, such as heavy rainfall, temperature fluctuations or drastic changes in the diet that upset the intestinal gut flora. Dietary changes should always be made slowly to prevent derangements in gut flora that may allow C. perfringens to multiply and secrete toxins that are then able to leave the gut and reach other organs where pathological effects are mediated through vascular changes, necrosis and haemorrhage, with associated inflammation.

The suspected early-stage infection could be treated with antibiotics although deer, as other species, usually have a short, fulminant course and are diagnosed at PME. Differential diagnoses may include anthrax, yersiniosis and death from herpes infection as malignant catarrhal fever (MCF).

Spores of the causative organism are found in both soil and the gut (and faeces) of healthy animals living in areas where the disease is common; they can remain dormant for many years in the soil. Disturbances of the contaminated soil, years down the line, can result in animals being exposed to a large number of spores, resulting in the ingestion of large numbers of bacteria. To avoid this, it is best practice to remove all carcases of all livestock found dead for incineration. Similarly, the abdominal viscera (gralloch) of culled animals should incinerated where this is practical.

Vaccinating deer against C. perfringens is highly advisable given that deer are sensitive to several types of clostridial infection/intoxication; vaccines with polyvalent clostridial toxoids are recommended.

Vaccination is common practice in zoological collections of deer and is often a pre-import requirement. Red deer make serological responses to such vaccines, although it is not known if such immune responses are actually protective because no challenge studies have been undertaken (Scala et al. 2016). The data sheet for sheep clostridial vaccines may be followed, given that there are no licensed vaccines for deer, with the inclusion of antigens for pasteurellosis if this is also a concern for the herd/holding. At weaning, deer calves are initially vaccinated and then, four weeks later, a second dose is administered. Hinds may be dosed/boosted annually and, ideally, in late pregnancy although handling may be risky at this point in gestation.