Many veterinarians have little to no experience dealing with uncommon species. It can also be hard to find resources, especially Australian-based resources, for species such as camels. This case shows that much of what is known from commonly-dealt-with species is also applicable to other species, and species-specific information can be sought from experts in the field.
In January 2018 a producer north of Albury, who had 12 camels, called, as he had two young camels die suddenly. One had been noticed drinking from a near-empty dam that the camels had been using as a mud wallow. It died shortly thereafter, without signs of struggle. The producer was concerned about blue-green algae toxicity, although no algae was visible. The dead camels were noticed scouring two weeks previously and had been drenched with an oral abamectin, oxfendazole and levamisole drench which seemed to resolve the issue.
The second camel had been noticed to be ‘off colour’ by the owner the night before and had been treated with long-acting penicillin as well as abamectin, oxfendazole and levamisole drench and a vitamin A, D & E injection. It survived the night but died the following morning. Approximately an hour before death the animal started twitching and then became disorientated and started circling. After it died froth was observed coming from the mouth of the carcase.
The producer was also concerned about phalaris toxicity as a short green pick had just grown after some rain.
On the 11th of January the two dead camels were post mortemed after performing two immunochromatographic test (ICT), a rapid, in-field test for anthrax, which were negative. Although the ICT kit is not validated for use in camels, the negative results and the fact that anthrax was not a likely differential were enough assurance to proceed with the post mortem.
The post mortems revealed dense, fluid-filled lungs. The intestines contained a lot of gas, as did the stomach. Some blood was found in the pericardial fluid on one and the other had some small haemorrhages on the heart. The spleen looked normal. The liver was light brown in colour and the heart was thought to be quite large for the size of the animal, however the apex was pointed, not round, so it was assumed to be normal for camels. In both cases the kidneys appeared to be decomposing faster than the rest of the organs. It was unknown if this finding was significant as it was an extremely hot day and the post mortem had been conducted in the afternoon, more than seven hours after death. However, the resemblance of the carcases to that of a sheep that died of pulpy kidney was noted.
Differentials included clostridial infection, salmonella infection, blue-green algae toxicity, pneumonia, phalaris toxicity and anthrax.
While examination with Polychrome Methylene Blue was inconclusive for anthrax it was ruled out in both cases by PCR.
Routine culture of the lung found a mixed moderate growth from one animal and a profuse predominant growth of Escherichia coli (non-haemolytic) from the other, which was thought to be insignificant.
A sample of water from the dam was tested and found to be negative for blue-green algae.
Selective enrichment culture for Salmonella was negative.
Marked autolysis was found in all the tissues examined, with reduction in tissue architecture. Most changes to tissue architecture were interpreted as post mortem autolytic change. There were also large rod-shaped bacteria found that were thought to be post mortem overgrowth. In the lung, blood vessels were diffusely, moderately congested. Multifocally, alveoli were filled with eosinophilic proteinaceous fluid, a sign of pulmonary oedema. There was mild to moderate multifocal congestion of blood vessels found in the kidney.
The brain was also examined, and some autolysis was present. Blood vessels were moderately congested and there were minimal multifocal areas of extravasated erythrocytes (haemorrhage). Vacuolation of the neuropil was noted in the cerebrum, brainstem and mesencephalon but it was difficult to distinguish from autolysis. Some neurons were eosinophilic and rounded with reduced cellular staining definition.
At this point it was thought that the diagnosis of Clostridium perfringens type A was quite likely, and the lab was consulted to see if there was any way of confirming the diagnosis. They suggested sending the intestinal contents to the Vetnostics lab where a foal faecal PCR was run. The results were:
|Clostridium difficile Toxin A RNA||Not Detected|
|Clostridium difficile Toxin B RNA||Not Detected|
|Clostridium perfringens Toxin A RNA||Detected|
|Clostridium perfringens CPE Toxin RNA||Not Detected|
|Clostridium perfringens cpb2 Toxin RNA||Not Detected|
|Clostridium perfringens netF Toxin RNA||Not Detected|
|Equine Coronavirus RNA||Not Detected|
|Rotavirus RNA||Not Detected|
|Salmonella spp. DNA||Not Detected|
|Cryptosporidium spp. DNA||Not Detected|
It was found that Clostridium perfringens type A toxin DNA and RNA were identified in the sample reflecting transcription of this toxin gene. It is unknown how likely it is for alpha toxin to be an incidental finding in the intestines of camels.
Searching for information about clostridial infections in camels proved difficult. A paper found online suggested that Clostridium perfringens type A is the most common clostridial infection in camels1. Another suggested that Salmonella infection or other predisposing factors contribute to enterotoxemia in camels caused by Clostridium perfringens type A2.
Australian specific information and advice was sought from Natalie Rourke, a veterinarian working at the Werribee Open Range Zoo. She confirmed that Clostridium perfringens type A is documented in juvenile camels. Upon consultation of the Sydney Post-Graduate Foundation series C no. 2 Camels a compendium, she described recorded signs including petechiae in the thoracic musculature, cerebellum and brainstem, pharyngeal mucosa, surface of the lung and epicardium and abomasum. Kidneys may be enlarged, darkened and capsule adherent. These signs are largely consistent with what was found.
Dr Rourke also said that the prevention section listed a vaccine she was unfamiliar with and recommended use in the late pregnant cow plus the vaccination of calves in the first few months of life. Most outbreaks of enterotoxaemia are associated with concurrent disease or suboptimal feeding and husbandry practices.
To see if there would be any potential benefit from using the Ultravac 5-in-1 vaccine to vaccinate camels, Lee Taylor from Zoetis was contacted. This vaccine was listed as containing Clostridium perfringens type D toxoid. The aim was to see if this was likely to have any cross protection against Clostridium perfringens type A.
Clostridium perfringens type D can produce both the alpha and epsilon toxins while Clostridium perfringens type A only produces alpha toxin3. In principle this difference means that there could be some protection against alpha toxin produced by Clostridium perfringens type A from this vaccine.
While the cause of death in this situation could not be absolutely confirmed it was thought likely that the cause of death in these camels was due to infection with Clostridium perfringens type A. While currently unknown if Ultravac 5-in-1 would be able to offer any protection against Clostridium perfringens type A in camels there is a possibility that it could.
This report would not have been possible without the expertise of Natalie Rourke, veterinarian at the Werribee Open Range Zoo, Lee Taylor from Zoetis and Leah Manning from EMAI.