in a bachelor herd of elephants
Data provided by:
A group of 6 juvenile Asian elephants had been kept under mediterraneal climate conditions for several years without major disease issues. During springtime, 5 out of these 6 elephants fell ill within 1 week and died days after showing first signs of illness. The major clinical signs consisted of gradually increasing general weakness, shivvering, mild salivation, inability to stand and proper use of the trunk. The affected elephants died within 3 days after onset of clinical signs.
The animals were fed reygrass salige, grass and pellets. Clean drinking water was available, but the animals had also access to pools with water of questionable quality.
The only unaffected elephant was the subordinate animal in the group, having less access to favorite food items.
Blood parameters were within normal ranges.
Several zebras that were kept in another part of the zoo showed neurological symptoms (shivering, shaking, paresis, inability to stand) and some of them had died too.
Paralytic Asian elephant in lateral recumbancy, unable to bring food items into its mouth after feeding on reygrass silage contaminated with Clostridium botulinum
Zebra at the same zoo with ataxia, trembling and paresis after feeding on reygrass silage contaminated with Clostridium botulinum.
Symptomatic treatment was given in the form antibiotic s, IV infusions and rectal water administration.
The diagnose was made several days after necropsy, as the toxicology samples had to be sent abroad.
Two elephants were humanely euthanized when the were unable to stand up.
Multifocal hemorrhages, edema in the heart. No evidence of virus infection. No pathogenic bacteria found.
Toxicological examination of the silage revealed the presence of vomitoxin and zearalenor (see below).
Sulphite reducing Clostridium: 800 cfu/gr
Zearalenor: low pos.
Toxin T2: neg
Stomach and intestinal content:
Clostridium botulinum toxin found in stomach contents of elephants and zebras and silage (mouse bio-assay)
Subtyping of the strain was not performed.
Botulism is caused by the toxin of Clostridium botulinum. Clostridial organisms are strict anaerobes, meaning they do not grow in the presence of oxygen or in healthy, well-oxygenated tissues. Clostridium botulinum produces seven different neurotoxins, each of which is distinct and different enough from the others that antibodies against one type do not protect an animal against botulism from another type. Botulinum toxin is one of the most potent biotoxins known. Sometimes the onset of clostridial disease is so rapid that no clinical signs are ever manifested; animals are simply found dead.
There are no scientific or anecdotal earlier reports of botulism in elephants. Botulism has been reported in horses that were exposed to botulism toxin in the feed, usually involving type C toxin. Toxin might be present as a contaminant in feed, or if there are droppings or carcasses of small rodents in the feed bunk or water tub. One problem occurs when rodents or other animals die in a field of forage, and a carcass is incorporated into a bale during baling. Contaminated hay cubes have been responsible for at least one large outbreak of botulism in horses. Even if a carcass has undergone dessication (it’s dried out) or is unrecognizable in a flake of hay, enough spores can remain to kill a horse.
Toxicoinfectious botulism is the secondmost common form of botulism in horses, and this arises when the bacterium itself is ingested from soil and colonizes the gastrointestinal tract. As it grows inside the body, it produces the toxin, and signs of disease become apparent as toxin is absorbed into the bloodstream from the intestinal tract. Clostridium botulinum type B has been associated with this form of botulism.
Signs of Botulism
The first signs that owners typically notice are the horse’s inability to eat, drooling or profuse green nasal discharge, and recumbency (inability to rise). Recumbency is also a common early sign of botulism. An affected horse might be unable to get up, or he might lie down for longer periods than usual. Closer observation reveals fine muscle fasciculations (involuntary contractions) or trembling and shaking, particularly in the shoulder and flank muscles.
Kim A. Sprayberry. 2007. Botulisme, a perfect killer: Horses are highly susceptible to botulism toxins; vaccination and feed/water management are key to prevention. December 2007 The Horse