This case report outlines an investigation into sudden death in a llama where many of the predisposing factors and gross pathology common with enterotoxaemia Type D in sheep were present. Samples were not taken to obtain laboratory confirmation of enterotoxaemia Type D due to the advanced autolysis of the carcass. A review of the literature found that the gross pathology of enterotoxaemia Type D in llamas is not well described, including the presence of glycosuria.
The llama was part of a small non-commercial sheep, llama and alpaca flock in the Narrabri NSW district. The single llama and single alpaca had been grazing separately from other animals in a 0.6-hectare paddock for two months. The investigation took place in August 2023.
The llama and alpaca were observed by farm staff three days before the visit and were normal. On the morning of the visit the llama was found dead in the paddock and the Local Lands Service District Veterinarian was requested to undertake a diagnostic investigation. The alpaca and sheep in the flock were all normal.
The llama, which had been purchased 12 months prior, was three years old. It had not been vaccinated since arrival, and its vaccination status prior to arrival was unknown.
Both the llama and alpaca had been drenched with a triple-action drench 20 days prior to the visit. A worm egg count conducted 4 days before the visit had found negligible egg numbers.
On arrival, a paddock inspection found the paddock to be covered by a thick sward of grass, mostly kikuyu (Cenchrus clandestinus), interspersed with lush green patches of winter-growing perennial rye (Lolium perenne) and some short burr medic (Medicago polymorpha) (see Figure 1). This pasture was atypical for the district and was explained by regular sprinkler irrigation. The presence of lush green patches was explained by a water trough overflow accident two weeks prior, which flooded parts of the paddock. This flood irrigation, combined with a period of unseasonably mild winter weather, had produced the patches of lush pasture.
The paddock inspection did not identify any potentially toxic plants.
The llama carcass was in lateral recumbency with severe opisthotonos. The legs had disturbed the soil, consistent with paddling (see Figure 2).
A small amount of fresh watery diarrhoea was present around the perineum and on the adjacent ground.
The upper eye was intact and as crows had been a persistent problem on the holding this finding suggested the death occurred after dusk the previous evening, approximately within the last 18 hours. Eye fluid tested negative for nitrate/nitrite.
Opening the carcass to display stage found the contents in advanced autolysis, exceeding what would be expected with a minimum night temperature of 6°C. However, the kidneys did not show significantly more advanced autolysis than other organs.
Excess clear, serous pericardial fluid was present. A 'chicken fat clot' was not observed in the pericardial fluid.
A full bladder was present, and the urine tested strongly positive for glucose using a dipstick.
No other gross pathology was observed.
Due to the advanced state of autolysis, samples were not submitted for either Clostridium perfringens toxin assay or brain histopathology.
Immediately prior to the visit, Patrick Staple's Flock and Herd paper1 was consulted for possible differentials for sudden death in New World camelids. Of the listed differentials, only enterotoxaemia Type D was consistent with the history and gross pathology observed.
The author has limited experience with New World camelids but found the similarities with the typical history and gross pathology seen in sheep enterotoxaemia Type D cases to be striking.
While a review of the literature found references indicating that enterotoxaemia Type D is a cause of mortality in llamas2,3,4, the author was unable to locate any case reports specifically addressing enterotoxaemia Type D in llamas.
A 2023 literature review of bacterial diseases of alpacas and llamas4 reported enterotoxaemia Type A is a common disease of newborn alpacas and enterotoxaemia Type C commonly affects newborn camelids. Staples1 notes that with alpacas sporadic cases of Type D enterotoxaemia have been reported in alpacas in North America and that a small number of alpaca sudden death submissions to the NSW Department of Primary Industries Animal and Plant Health Laboratories had detected epsilon toxin in ileal content.
A review of laboratory submissions from New World camelids in England and Wales (2000-11)4 reported that, of the 44 confirmed cases of clostridial disease, they were largely identified as clostridial enterotoxaemia where C. perfringens enterotoxins were present. However, the paper did not differentiate between enterotoxaemia types or New World camelid species.
Fowler6 indicates that the clinical signs of enterotoxemia Type D seen in New World camelids are similar to those in sheep, presenting with sudden death and neurological signs, including convulsions, circling, lateral recumbency with opisthotonos and paddling.
A description of the typical gross pathology associated with enterotoxaemia Type D in llamas could not be found in the literature. Fowler6 notes that the gross pathology in enterotoxaemia Type D in New World camelids has not been adequately described.
Most references indicate that diagnosis is based on history and clinical signs with confirmation by toxin identification4,5,6.
In this llama sudden death, several predisposing factors and gross pathology changes commonly described in Australia with enterotoxaemia Type D of sheep7,8,9 were present. These include an uncertain or unvaccinated status, sudden changes in diet to low fibre lush feed, sudden death, the carcass found in lateral recumbency with opisthotonos and evidence of paddling, rapid autolysis, excess pericardial fluid, and glycosuria.
In the author's experience, strong glycosuria is confirmatory of enterotoxaemia Type D in lambs when typical risk factors, clinical signs, and gross pathology are present. These include no current vaccination, grazing lush feed or on a high grain diet, opisthotonos, lateral paddling, excess pericardial fluid and unusually rapid autolysis (if post-mortem is undertaken several hours after death). Other possible causes of glycosuria are unlikely to be associated with these clinical signs and gross pathology.
Features in this case that differed from enterotoxaemia Type D in sheep were the mature age of the llama and the absence of advanced autolysis in the kidneys compared to the other abdominal organs.
Although this case lacks laboratory confirmation for enterotoxaemia Type D, the correlation with enterotoxaemia Type D in sheep—considering the history, clinical signs, gross pathology, and glycosuria—strongly suggests enterotoxaemia Type D as the cause of death.