The surge in wildlife farming enterprises over the last decade has certainly exposed wildlife veterinarians to a host of different disease-related challenges, many of which were new, and in the bulk of cases were a direct result of intensification of game farming. As with all biological systems, disease problems arise when population numbers increase beyond the natural carrying capacity of the system. However, even though problems with disease increases in frequency under these conditions, knowledge and effective management thereof can limit losses to such an extent that population numbers will still exceed production levels achievable under natural conditions. Even though this is a controversial subject, this is the principle on which successful farming is based.

In an attempt to remain practical, the conditions that will be discussed in the next six issues are not a summary of what is known to occur in the literature. Most of the conditions described in the literature do not account for prevalence and simply discuss what has occurred, even if it happened only once or very rarely. In these articles, I will discuss diseases and conditions that may threaten successful keeping and / or farming with specific South African wild ruminant species. In addition to discussing the underlying causes and factors involved in precipitating these diseases, advice in the appropriate context will be provided.

In this article, relevant toxic conditions are discussed, considering the circumstances leading to susceptibility and precipitation of intoxication.

Toxic plants (phytotoxicosis)

Various plant toxins exist, most of which have evolved as a protective mechanism against being defoliated, i.e. eaten by animals. The most commonly utilised, protective toxic principle used by many different plants is tannins (refer to Part 1 of this series for the discussion on the effects of tannin ingestion).

Compared to domestic ruminants, wild ruminants are significantly less susceptible to plant intoxications for multiple reasons. Firstly, wild ruminants show much stronger instinctive avoidance behaviour that is likely to have a genetic basis with a strong learned component from older herd members. Secondly, most wildlife species are selective feeders, especially browser species like impala, nyala and kudu. These species can optimally utilise valuable pasture where other animals like cattle and sheep would die. Lastly, as a function of their diet, browser species have evolved the ability to ingest and detoxify plant toxins such as tannins much more effectively than domestic ruminants. This results in a much higher tolerance to ingested toxic plants, meaning that the lethal dose of certain plants is much higher for these species. This also implies that within the wild ruminant group, grazing animals will show a greater susceptibility to plant intoxication and that the most susceptible of the grazing species would be the bulk grazers such as buffalo, wildebeest and eland. These attributes of wildlife regarding plant intoxication help explain the sporadic pattern of intoxication if and when it does manifest in these animals. In my experience, plant intoxications occur in individual animals and very rarely result in mass mortality, which is often the case with domestic ruminants.

Circumstances under which plant intoxications does occur in wildlife, include the following scenarios:

  • Intensification resulting in overgrazed conditions leaves very little vegetation options other than unutilised toxic plants, precipitating forced ingestion of toxic plants.
  • Bulk grazers like buffalo and wildebeest can unintentionally consume toxic plants hidden in grass pastures.
  • Toxic plants can contaminate harvested and baled roughage like lucerne or other hay. When these contaminated bales are milled and mixed into a ration, a larger number of animals are likely to become affected compared to the previous two scenarios.
  • Lastly, burning of natural veld often results in a flush of toxic plants since many of these are pioneer plant species. Too frequent and unjustified burning of natural grazing would thus increase the number of toxic plants on a property, thereby also increasing the potential risk of intoxication.

The following plant intoxications have been seen in various wildlife species over the years:

Tannins

Plant tannins should be regarded as the most significant intoxication, resulting in malnutrition in wildlife. For detailed discussion about tannins, refer to Part 1 of this series.

Poison leaf / Gifblaar (Dichapetalumcymosum)

Poison leaf is a well-known toxic plant that occurs in the northern regions of the country, often accompanying wild seringa (Burkea africana) trees. This plant is often incorrectly blamed for unexplained mortalities in these regions. It is highly toxic and ingestion of only a few leaves can be lethal. Affected animals die suddenly without clinical signs, most often in early spring, as it is the first green vegetation available after the winter. Browser species avoid the consumption of poison leaf, even if it is the only vegetation available. Bulk grazing species like buffalo are the most commonly affected and farmers are advised to rather keep browsing-type species in poison leaf camps.

Lantana camara

Very few cases of clinical disease have been reported. Contrary to poison leaf, Lantana is commonly utilised by browsing species and in moderation does not seem to cause toxicity. However, sudden high intake of Lantana can be toxic and only browser species like impala have been affected. Cases only occur when newly introduced animals are exposed to large quantities of Lantana.

Tulip / Tulp (Homeria / Moraea spp)

Tulip is a pioneer weed occurring in significant concentrations in the Highveld regions. The plant most commonly occurs in low-lying wetland areas, especially on the fringes of the receding zone. Bulk grazing species like buffalo and wildebeest accidentally consume these plants when grazing in wetland areas, especially during early spring in summer rainfall areas. The toxin is cardiotoxic and thus results in heart failure. Clinical signs can range from acute death to ill-thrift associated with diarrhoea.

Less commonly reported cases of intoxication have occurred in wildlife with rooibessie (Solanum tettense), ragwort (Senecio spp) and inkberry (Cestrum spp).

More reports of other/new sporadic plant intoxications are expected to occur in wildlife in the future, but these are unlikely to have a significant impact on wild ruminant populations. As pointed out earlier, it is important to note that the sporadic nature of plant intoxications in wild ruminants makes them the ideal option to utilise regions or camps on a property known to cause intoxication in domestic ruminants.

Mycotoxicosis

Mycotoxins are produced by fungal organisms (mould) while growing on carbohydrate substrates. Typically, significant mould growth will occur on damaged grain or hay in the presence of moisture. Wet bailed lucerne or concentrates with high moisture content (e.g. bags of game pellets that got wet) are classic examples of circumstances conducive to mould growth and mycotoxin production. There are numerous different types of harmful mycotoxins, with aflatoxin and ochratoxin being among the most common. The deleterious effects of these toxins are multiple and can range from acute to chronic liver and kidney failure respectively. It has been shown that mycotoxins in even small subclinical quantities may result in production-related deficits like abortions, weak offspring, poor conceptions, ill-thrift / loss of condition and immunosuppression, and long-term exposure may be carcinogenic. This concept is important to understand since many farmers will utilise mouldy feed (often bought very cheaply) by diluting it into a mixed ration. The risk of production loss with this practice is high and should be avoided. In recent times, mycotoxin binder chemicals have been developed as feed additives in an attempt to reduce the harmful effects of trace amounts of mycotoxins. However, this does not remove the risk or justify the use of mouldy feed.

Salt intoxication / Water deprivation

Water deprivation (salt toxicity) is a serious, common and probably under-diagnosed condition affecting wildlife, especially recently translocated animals. Certain species have evolved mechanisms of conserving water and some also have a high tolerance to intake of water with a high salinity (i.e. brackish water). These species include the desert-adapted animals like oryx. However, even these species can become salt-intoxicated. Direct ingestion of toxic salt levels is unusual, as salt content of feed or water would in fact restrict intake thereof. Salt is often added to feed, especially licks, as a method to restrict intake. It is thus not direct intake of salt that is dangerous (i.e. salt licks are safe) but rather the lack of water intake, i.e. water deprivation that results in toxic salt accumulation in the animal’s body, especially the brain. A period of water deprivation, followed by sudden ingestion of water, results in osmotic swelling of the brain that can be fatal.

In wildlife, the most common scenario resulting in water deprivation is lack of water intake following a relocation event. Stressed animals will invariably pace up and down a boundary fence in an attempt to return from where they were captured. The specific boundary fence can often be predicted since the animals will normally pace along the fence in the direction of where they were captured. If no water source is provided close to this area of the camp and/or a nearby water source is out of reach outside the camp, a high risk of water deprivation exists and death can ensue within three to five days after relocation. The risk for this condition also increases when the only water source is a single artificial watering point. Make sure that a temporary water source is available along the boundary fence. The risk of water deprivation is also greatly reduced if resident animals of the same species are present, since joining such a herd will provide the introduced animals with the location of water in a camp.

Inorganic and chemical intoxications

A number of chemicals exist in a farming enterprise that poses certain risks to wildlife. With most of these chemicals, the circumstances for exposure are of such a nature that the risk is negligible. Knowledge of these and the associated risks can be very useful in decisions affecting the use and management thereof.

Urea

Urea is non-protein, nitrogenous compound used as fertiliser or as an additive to ruminant feed/licks where it adds significant value by optimising rumen microbial health. Due to its toxicity, urea levels are restricted in ruminant feeds. In exposed licks containing urea, the danger exists that the urea may dissolve from the lick and may accumulate in rainwater. Animals that drink from this water may become acutely intoxicated. However, the advantages of urea at the correct concentration in the feed/lick far outweigh this danger, which can easily be managed by preventing rainwater accumulation around the lick. Significant production increases can be expected with the judicial use of urea in wild ruminant feed/licks.

NO3

As with urea, nitrates are commonly used in fertilisers. The danger exists that nitrate fertiliser can accidentally be mixed into feed or, more commonly, contaminate the water source. Caution should be exercised when using the same equipment for mixing feed and fertiliser.

Acaricides (tick-dipping agents)

Many acaricide dipping agents are used for the control of ticks on game farms. The formulation of some of these compounds may necessitate application according to weight, since systemic absorption and toxicity can result from overexposure. Residual compounds containing amitraz and organophosphates should be used with caution and never be applied using a method where overexposure is possible, e.g. step-on dips.

Anthelmintics (worm remedies)

Like acaricides, certain worm remedies also necessitate dosing according to weight, as some formulations (especially Closantel-containing drugs) have very narrow safety margins. High endoparasitic loads in captive wildlife may drive desperate farmers to use these formulations in feed or water. As a result of ineffective control of feed or water intake in a herd and multi-species camp systems, some animals may receive toxic doses and die.

Mineral supplementations

In Part 1 of this series, specific reference was made to the importance of mineral supplementation, as specific mineral deficiencies are one of the major problems facing wildlife populations, especially in captivity. However, caution must be exercised in the supplementation of certain minerals because excessive amounts can result in toxicity. Supplementation of copper and, to a lesser degree, selenium, carries the highest intoxication risk. Copper can be supplemented in the feed and water or injectable formulations can be used. The supplementation method with the lowest risk of intoxication is through feed in consultation with a ruminant nutritionist. Registered multimineral formulations for safe use in feed are readily available. Copper sulphate is a product used by some to control algal growth (algaecide) and snails (molluscicide) in water troughs. This is a very dangerous practice since high enough doses can result in copper toxicity in animals. All injectable formulations of minerals have been developed for use in domestic livestock. Although these are empirically used in wildlife, differences in species’ susceptibility to potential toxic effects can have unpredictable results. In addition, as the therapeutic dose is weight-dependent, toxicity can result from overestimation of weight.

Toxicity resulting from other elements like lead, manganese, iron and fluoride has been observed but is rare and could potentially result from natural, mineral-rich soils or contaminated water sources, especially in the vicinity of mining activities.

Growth promoters

Certain domestic ruminant feeds (especially feedlot and dairy concentrates) contain ionophore growth promoters that improve ruminal digestion and optimise concentrate feed utilisation by ruminal microbes. Although it is unlikely that these compounds at the recommended concentrations will be harmful to wild ruminants, there is a safety risk and susceptibility to the effects of ionophores may vary considerably between species. Ionophores should not be used in rhinoceros feed and should therefore be avoided in multispecies reserves.

Herbicides

Most herbicides (e.g. glyphosate) used in farming operations pose no reported health or toxicity threat. However, herbicides containing paraquat are extremely toxic and caution should be exercised when using it in the vicinity of any animal as well as humans.

Organic intoxications

Botulism

Arguably, the most common organic intoxication in all ruminants is botulism. Botulinum toxin is produced by the bacterium Clostridium botulinum and clinically results in paralysis. This organism is invariably present and proliferates during the decomposition process of any organic matter, especially in vertebrate animals that died. Under intensive conditions, small vertebrate animals like snakes and tortoises can be killed in electric fences, providing a source of potentially toxic skeletal remains. Botulinum toxin can accumulate in the skeletal remains, rendering the bones potentially toxic for a very long time after decomposition. Animals that consume or chew on these bones can ingest lethal doses of the toxin. The drive to consume skeletal remains (osteophagia) by ruminants is high in phosphate-deficient regions of the country, with animals attempting to supplement their diet with the phosphate-rich bone. This implies that supplementation of phosphate in the feed or lick can significantly decrease the botulism risk associated with osteophagia.

Another important scenario responsible for mass botulism outbreaks is associated with the decomposition process occurring in the water source. This commonly results from any vertebrate animal drowning in the water supply, especially in header tanks. In domestic ruminants, chicken litter, which may contain skeletal remains of dead chickens, is often fed as a lick. Apart from medicaments like ionophores that carry a health risk, botulism is an important risk to consider with this practice. In my experience, chicken litter is not a regularly used supplement on game ranches. Apart from phosphate supplementation to decrease the risk, vaccination against botulism is also possible and is advocated as part of the basic vaccination programme of any ruminant.

Blue-green algae (Microcystis aeruginosa)

Blue green algae are a cyanobacterial species that can produce potent toxins (i.e. microcystin) under specific environmental conditions in water sources. As with all photosynthesising organisms, nutrient-rich water (especially phosphate and nitrogen originating from organic wastes e.g. faeces) and increased water temperatures are required to precipitate a cyanobacterial bloom. These conditions can easily occur under intensive farming conditions. The toxin microcystin is indiscriminate and highly toxic to mammals, resulting in liver failure. This results in outbreaks that typically manifest with large numbers of mortalities (often multispecies), often still in the vicinity of the toxic water source. Practical ways to limit cyanobacterial growth include avoidance of soil dams under high-density, intensive systems (artificial water supply using raised water troughs is recommended) and ensuring that the water level in a soil dam remains high/full.

Envenomation

Envenomation, with reference to toxic bites from invertebrates like spiders or vertebrates like snakes, is always possible and an unavoidable risk in nature. However, similar to a wild animal’s instinctive behaviour to avoid consuming toxic plants, there is a strong instinctive drive supported by acute environmental awareness and physical abilities to avoid potentially dangerous animals like snakes. These characteristics are much weaker in domestic animals. Snake bite certainly is one of the most overdiagnosed conditions and should rather be reserved following a thorough investigation into other causes of illness or death.

References

Basson, P. 1987. Poisoning of wildlife in southern Africa. Journal of the South African  Veterinary Association, 58, 219–228.

Gallo, A., Giuberti, G., Frisvad, J. C., Bertuzzi, T. & Nielsen, K. F. 2015. Review on Mycotoxin Issues in Ruminants: Occurrence in Forages, Effects of Mycotoxin Ingestion on Health Status and Animal Performance and Practical Strategies to Counteract Their Negative Effects. Toxins, 7, 3057–3111.

Kellerman, T., Coetzer, J., Naudé, T. & Botha, C. 2005. Plant poisonings and mycotoxicoses of livestock in Southern Africa, Oxford University Press Southern Africa.

Oberholster, P. J., Myburgh, J. G., Govender, D., Bengis, R. & Botha, A.M. 2009. Identification of toxigenic Microcystis strains after incidents of wild animal mortalities in the Kruger National Park, South Africa. Ecotoxicology and Environmental Safety, 72, 1177–1182.

Osweiler, G., Carr, T., Sanderson, T., Carson, T. & Kinker, J. 1995. Water deprivation-sodium ion toxicosis in cattle. Journal of Veterinary Diagnostic Investigation, 7, 583–585.

Todd, J. R. 1969. Chronic copper toxicity of ruminants. Proceedings of the Nutrition Society, 28, 189–198.

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