CLOSTRIDIOSIS

General information

Clostridiosis represents a group of diseases caused by members of the Clostridium species. They occur worldwide and can affect many mammalian species, including elephants. Clostridium spp. are gram-positive, rod-shaped, anaerobic bacilli. They form spores that may persist in the soil for months or years. Some of these organisms may be found in the normal flora of the digestive tract and become pathogenic only if accessible tissue is damaged as a result of deep penetrating trauma to the muscle bundles or a compromised gastrointestinal mucosa.

Clostridial organisms produce exotoxins, with local and/or systemic effect; including hemolysis and local tissue necrosis. These toxins are produced when the organism grows in the host tissues with the exception of the toxin of Clostridium botulinum, which is formed outside the body and ingested orally by the host. Some Clostridial organisms can produce multiple toxins, each with a specific activity.

 

Clostridiosis in elephants

The following manifestations of clostridiosis have been described in elephants:

  • Tetanus (C. tetani)

  • Enterotoxemia (C. perfringens)

  • Enterocolitis (C. difficile)

  • Malignant edema (C. septicum)

  • Blackleg  (C. chauvoei, C. septicum) has been reported once, but this report could not be tracked down (Prescott, C.W. 1971. Blackleg in an elephant. Vet Rec 88:1971)

  • Botulism (C. botulinum)

Elephant care manual for mahouts and camp managers

Preecha Phuangkum Richard C. Lair and Taweepoke Angkawanith

Tetanus

 

Tetanus is caused by a long-living anaerobic bacterium that is found in the soil and in moist areas. Tetanus is usually found in elephants that have suffered deep wounds, usually in the foot and particularly through the footpad being pierced by a metal object such as an old, rusty nail. After the bacteria have entered the elephant's body they thrive and, after an incubation period of 15-20 days, neurotoxins are produced that damage the nervous system and cause typical muscular spasms.

Between about 1977 and 1992 Thailand experienced, on a massive scale, thieves cutting off elephants' tusks by stealth in order to sell them. One result was that many tuskers contracted tetanus and died.

Path of infection: Infection proceeds from stepping on a piece of metal or other contaminated object that causes a deep wound. With elephants, however, the wound might not be obvious because elephants can and do use their trunks to gather dirt (which might be contaminated) to stuff in wounds, including cut tusks. When tetanus enters a tusk's pulp cavity, it spreads very quickly because it thrives in environments where there is no oxygen.

All wounds must, of course, be carefully cleaned but be especially careful where the puncture is from nails or rusty old metal, especially in an area that has long housed many animals. After infection, the disease does not progress quickly and the elephant will appear normal for 15-20 days (sometimes even longer) before symptoms appear. Even if the elephant receives treatment, the survival rate is very low.

Clinical signs:

  • The elephant often has a temperature of over 37.8° C or 100° F, although this is not certain. The breath will be noticeably hot to feel.

  • The eyes will be very red, and the soft tissue inside the mouth and the trunk will be a dark red.

  • The elephant is listless and does not eat or drink water.

  • The nervous system is affected, and the leg muscles harden in muscular contraction; the tail has a supple, snake-like feel.

  • There are periodic spasms, particularly when the elephant is startled, as by a loud noise or bright light.

  • In following days, it becomes difficult for the elephant to walk and stand because of the contraction of the leg muscles.

  • The jaws lock tightly, making it difficult to chew food. Eating and drinking become very difficult and the elephant dies.

Treatment:

  • Consult a veterinarian immediately.

  • Even though tetanus is not contagious to other elephants, separate the elephant from other animals as it will be more peaceful.

  • Take the elephant to a shady shelter with a clean surface, such as a concrete floor (it should not be slippery) to prevent it from introducing earth or other unclean materials into the wound or the pulp cavity.

  • The area should have good ventilation.

  • In cases of an exposed pulp cavity, it is best to clean it with running tap water through a hose. Wash all wounds thoroughly with clean water then flush with an antiseptic solution such as Betadine or Povidine-iodine 1% in a 20:1 solution. Finally, apply an anti-insect powder that includes an antibiotic, such as Negasunt.

  • Hand feed the elephant with small amounts of easy to eat foods with high nutritional value, such as ripe bananas, sticky rice, ripe papayas, etc. 

  • Clean the wound every day.

Prevention: For elephants that have open wounds or exposed pulp cavities in tusks, prevent the elephant from contracting tetanus by daily cleaning of the wound and by keeping the elephant on a clean surface. Otherwise the elephant is likely to introduce dirt or other unclean material that could contain tetanus germs into the wound.

No vaccine yet exists for elephants but if an elephant with a wound seems to have been exposed to tetanus, a veterinarian can inject an antitoxin to prevent infection from the bacteria.

Tetanus

 

Tetanus is a potentially fatal disease characterized by muscular spasms caused by a neurotoxin produced by the bacterium Clostridium tetani (vetmed.ucdavis.edu, 2021). These organisms, and their spores, are found in the intestinal tract of several mammalian species and are abundant in the soil, where they can survive for many years. The spores can enter open wounds, particularly puncture wounds, where they proliferate under the right anaerobic conditions. When the spores die, they release the tetanospasmin neurotoxin that is responsible for clinical signs. The size of the wound does not correlate to risk of developing tetanus. Even superficial wounds have been associated with clinical cases.

Clinical signs of tetanus in horses usually include history of a wound (typically within the preceding month) and stiffness, lameness, or colic. These signs generally progress quickly to an abnormal gait, trembling, and muscle spasm. An inability to open the mouth, known as “lockjaw”, may occur. Horses can exhibit profuse sweating, saliva accumulation in the mouth, and may aspirate feed material. Excitement, including loud sounds or bright light, often exacerbates clinical signs. Horses may become very sensitive to touch. Stiffness in the leg muscles may result in a characteristic “sawhorse” stance. Affected horses can progress to severe muscle rigidity, making it difficult to rise, urinate, or defecate. Respiratory failure can occur.

 

Tetanus in elephants

Only a few cases of clinical tetanus in elephants have been described in the literature (Goss 1947, Burke 1975, Fowler & Mikota 2006) or have been reported anecdotally for Asian elephants in Southeast Asia. Inspection of the pads and nails is imporatant for the detection of wounds. Sharp objects, like steel nails may have penetrated the pad. (Illegaly) cut off tusks may  provide an opportunity for C. tetani to infect the tusk pulpa. After an incubation period of 7-20 days, the elephant will show symptoms similar to those seen in horses. Spasms are usually aggravated when the elephant is startled. Burke reports an 8-year-old female that was unable to open her mouth:

"She was hypersensitive to noise and touch, becoming tense and raising her tail. Her body temperature was 37°C (98.6°F, normal range 36–37°C /97–99°F). An elevated body temperature can be expected when there are spasms. Although there were several cracks around the toenails, none of the wounds were thought to be anaerobic. 100,000 units of tetanus antitoxin (TAT) were administered and the next day she seemed somewhat relaxed. However, on the third day she was found in lateral recumbency and in tetanic spasms. A sedative (112 grams of chloral hydrate per rectum) was administered.

Periodic sedation was necessary to keep her relaxed. She was raised to her feet with a sling and left in the sling overnight. On the fifth day she was unable to stand without the sling. Over the previous 5 days 360,000 units of TAT were administered subcutaneously. The elephant was kept in a sling and force-fed a slurry of bran mash through a stomach tube for 29 days, at which time she began to masticate and swallow feed"(Fowler & Mikota 2006).

 

Treatment

Tetanus antitoxin should be administered at a dose of 225 units/kg body weight, half intravenously, the other half intramuscularly. Anaphylactic shock is a hazard of this therapy because tetanus antitoxin is a horse serum product. Be prepared to administer epinephrine Broad-spectrum antibiotics should be administered to kill organisms that may not be reached with wound cleansing. The elephant should be placed in a non-stimulating environment and tranquilized as appropriate.

Supportive care is crucial to success. Be prepared to sling the elephant. Water may be administered by rectal lavage. For food, the author uses a slurry of quick-cooking rolled oats. The quantity of the breakfast cereal selected is put into boiling hot water, allowed to cool, and then diluted to a consistency that may be pumped through a stomach pump. (Fowler & Mikota 2006).

 

Vaccination

In a preliminary study, measurable titers against tetanus were achieved in Asian elephants vaccinated with a 1 ml dose of monovalent equine tetanus toxoid followed by a booster at 4 weeks. The titers remained elevated for >1 year; however, the appropriate vaccination interval has not yet been determined. Annual vaccination is commonly practiced, although it is likely that the duration of immunity may be longer. In a study in which 9 Asian elephants were involved, Muir et al (2021) demonstrated that the antibody titers in these elephants remained at adequate levels with little fluctuations when 3-5 years intervals were applied. It is therefore recommended to adhere to the suggested vaccination regime for horses with booster vaccinations every 2-3 years.

 

References tetanus

  1. Goss, L.J. 1942. Tetanus in an elephant. Elephas maximus. Zoologica NY 27:5–6.

  2. Burke, T.J. 1975. Probable tetanus in an Asian elephant. JZ&WM, vol 6 – 1 22-24

  3. Fowler, M.E. and Mikota, S.K. 2006. Preventive health care and physical examination / Chemical Restraint and General Anesthesia in. In: Biology, Medicine, and Surgery of Elephants. 2006. Ed. Fowler & Mikota page 68-84, 147-148.

  4. Lindsay, W. A., Wiedner, E., Isaza, R., Townsend, H. G., Boleslawski, M., Lunn, D. P. 2010. Immune responses of Asian elephants (Elephas maximus) to commercial tetanus toxoid vaccine. Vet Immunol Immunopathol 133 (2-4), 287-289

  5. Transmissible Diseases Handbook. 2019. Infectious diseases Fact sheet TETANUS (Annex 4)

  6. Muir, Y.S.S., Bryant, B., Campbell-Ward, M., Higgins, D.P., 2021. Retrospective anti-tetanus antibody responses of zoo-based Asian elephants (Elephas maximus) and rhinoceros (Rhinocerotidae). Developmental & Comparative Immunology 114, 103841.. doi:10.1016/j.dci.2020.103841

  7. https://ceh.vetmed.ucdavis.edu/health-topics/tetanus

 

Enterotoxemia (C. perfringens)

Enterotoxemia is caused by the toxin of Clostridium perfringens. There are 4 subtypes of C. perfringens, all grwoing under anaerobic conditions that have been associated with elephants: type A, C, D and E. The diagnosis 'enterotoxemia' in based on culture and PCR of the toxin-associated genes in the histological lesions. 

Clinical manifestation in elephants

Although there are few reports of enterotoxemia caused by C. perfringens in elephants, it might be an underreported disease in this species (see references below). Usually the disease has an acute course, with symptoms like diarrhea, colic, lethargy, anorexia and finally collaps in lateral recumbancy. If not treated agressively in time, the elephant usually dies. C. perfringens  is an environmental bacterium which can be present in the elephant's gut without doing any harm. Under certain conditions (gastric pH decrease by nutritional overload of easily digestable carbohydrates or badly fermented silage products) it can overgrow the natural gut flora and produce large amounts of toxins that lead to the symtoms described above. Septicemia can lead to multiple abdominal organs involvement, as well as muscles.

When young elephants are affected, the disease resembles Elephant Endotheliotropic  Herpes Virus-Hemorrhagic Disease (EEHV-HD) as the symptoms in both diseases are associated with Disseminated Intravascular Coagulopathy (DIC). In some reports C.perfringens  enterotoxemia and EEHV-HD were simultaneously diagnosed in diseased elephants (Boonsri et al. 2018, Costa et al, 2022).

The prevalence of C. perfringens in European zoos was studied in 2020: in fecal samples of 86 healthy Asian elephants the presence of type A and type E was PCR-confirmed in 3 animals (2.2%). All fecal samples obtained from 50 African elephants were negative.

In an overview of necropsy reports of 226 Asian elephants and 110 African elephants kept in the European Taxon Advisory Group between 1985 and 2018, 4 Asian elephants and 1 African elephant were reported to have died from an ulcerative enteritis caused by C. perfringens (Hes 2022).

 

Few reports on enterotoxima in elephants are available in the literature. One author described the outbreak of C. perfringens in a group of African elephants kept in a European zoo (Göltenboth et al 1974): 2 days after feeding fresh grass, a young elephant developed diarrhea and was lying down more frequently. It was treated with a spasmolytic and vitamin C. The following morning it seemed much better and was returned to the group of 4 young elephants, where it deteriorated within 1 hour and died. At necropsy, severe blood staint edema and gas accumaltion was found in the subcutis of the neck, pharynx and larynx as well as a severe cathharal enteritis and gas accumulation in all internal organs, from which C. perfringens was cultured. A second case in a young elephant of the same herd occured 5 weeks later, again 2 days after feeding fresh grass. Symptoms were even more pronounced and C. perfringens was cultured form all organs (septicemia). The third elephant of the group fell ill a few days later. This animal did not develop diarrhea, but was lethargic and refused to eat and drink for 5 days. Despite of treatment with antibiotics and all kinds of supportive medications (including IV-administration of Clostridium antitoxin), it died after 10 days of illness. At necropsy more chronic lesions were found: enteritis, fatty liver degeneration, bronchopneumonia and myocardial degeneration. In this animal C. perfringens could not be detected.

In one fatal case, acute myonecrosis was found in an 8 yr-old Asian elephant, resembling blackleg/ black quarter(C. chovoei) or malignant edema (C. septicum) (Rahman, 2009). The elephant calf showed clinical signs of sudden illness characterised by loss of appetite with high fever (39°C) and reluctance to walk. The animal was treated with an intramuscular injection of enrofloxacin, 5 mg/kg body weight. The animal did not respond to treatment and its condition deteriorated rapidly. The animal stopped taking feed and water, became recumbent and finally died within 48 h of the onset of clinical signs. At necropsy, dark, discoloured, swollen muscles with rancid odour from the affected region and intramuscular aspirates were observed. C. perfringens was cultured from these lesions and the presence of alpha-toxin genes could be demonstrated by PCR.

One case reports describes a fatal infection of Clostridium perfringens type C in an adult Asian zoo elephant (Costa et al. 2022). Evidence of involvement of EEHV4 was demonstrated by qPCR and the presence of intranuclear inclusion bodies in the endothelial cells of the intestinal blood vessels.

Treatment of C. perfringens enterotoxemia

In most cases it will be hard to make the diagnose in the living elephant. When enterotoxemia is suspected, agressive antimicrobial therapy, preferably based on an antibiogram and supportive therapy is mandatory. Depending on their bioavailability, antibiotics should be given IV or IM. Oral administration might result in low absorption from the intestines due to the enteritis. IV and rectal administration of fluids and IM NSAIDs are highly recommended.

Early treatment of enterotoxemia  is essential for the survival of the elephant. The list of recommended drugs is shown below. The clinician should not hesitate to administer all these drugs and should even sedate the sick elephant if needed for its treatment. 

Circulatory support:

Rectal fluids: Luke-warm water 10-20 ml/kg BW TID or QID, up to every 2 hours

​Crystalloids: IV as a bolus of 0.3-4 ml/kg BW

Antibiotic treatment:

Penicillins are the first choice antibiotics. Penicillin G can be given IV and will have a quick action.

Amoxicilline is a good representative as well (11 mg/kg IM q 24 h). 

 

Pain management:

Pain management (opioids, NSAIDs) is recommended if there are clear signs of pain or discomfort:

  • Butorphanol: 0.008-0.014 mg/kg IM Q 4 hrs

  • Flunixin: 0.25 to 0.5 mg/kg IM SID

  • Omiprazole: 0.7 to 1.4 mg/kg PO SID

 

Anti-inflammatory treatment:

Gluco-corticosteroid drugs are indicated in case of suspicion of DIC.

Dexamethasone: 0.05-0.1 mg/kg IV or IM SID for 1-3 days.

Prevention

Although there is no scientific data on the efficacy of preventive vaccination, several zoos do practice annual vaccination with a multivalent vaccine. Care should be taken not to use an oil-based adjuvant, as these may cause necrosis around the injection site

As a general precaution, major diet changes should always be introduced slowly. When large amounts of easily digestible carbohydrates (like fresh grass, large amount of  vegetables and silage) become available as a major food component, the diet change should be made over period of 7-10 days in order to allow the intestinal flora to adapt to the new diet.

References:

  1. Bacciarini, L.N., Pagan, O., Frey, J., Grone, A., 2001. Clostridium perfringens b2-toxin in an African elephant (Loxodonta africana) with ulcerative enteritis. Vet. Rec. 149, 618–620.

  2. Boonsri, K.,  Somgird, C., Noinafai, P.,Pringproa, K., Janyamethakul, T.,  Angkawanish, T., Brown, J.L., Tankaew, P., Srivorakul, S., and Thitaram, C. 2018. Elephant Endotheliotropic herpes Virus associated with Clostridium perfringens infection in two Asian elephants (Elephas maximus) calves. Journal of Zoo and Wildlife Medicine 49(1): 178–182, 2018.

  3. Costa T, Rocchigiani G, Zendri F, Drake G, Lopez J, Chantrey J and
    Ricci E. 2022. Elephant Endotheliotropic Herpesvirus 4 and Clostridium
    perfringens Type C
    fatal Co-infection in an adult Asian Elephant (Elephas maximus). Animals 2022, 12, 349. https://doi.org/10.3390/ani12030349.

  4. Das A, Mazumder Y, Dutta B.K., Shome B.R., Bujarbaruah K.M. and Sharma G.D. 2008. Clostridium perfringens type A beta2 toxin in elephant (Elephas maximus indicus) and pygmy hog (Sus salvanius) with haemorrhagic enteritis in Assam, India. Afr. J. of Microb. Res. Vol.(2) pp. 196-201 2008.

  5. Goltenboth, R. and Klos, H.-G. 1974. On several diseases and causes of death in elephants in the Berlin Zoo (Zu einigen erkrankungen und todesfallen bei elefanten des Zoologischen Gartens Berlin. XVI Verhandlungsbericht Internationalen Symposiums Erkrankungen Zoo und Wildtiere, Berlin, Akademie Verlag, pp. 175–179. 

  6. Hes. A 2022.Thesis: Lesions found in the post-mortem reports of the Asian (Elephas maximus) and African (Loxodonta africana) elephants of the European Association of Zoos and Aquaria. University of Veterinary Medicine BudapestBudapest, 2022.

  7. Rahman H., Chakraborty A., Rahman T., Sharma R., Shome B.R. and Shakuntala I. 2009. Clostridial myonecrosis clinically resembling black quarter in an Indianelephant (Elephas maximus) Rev. sci. tech. Off. int. Epiz., 2009, 28 (3), 1069-1075, 2009.  

 

Clostridioides difficile

(previous name: Clostridium difficile)

Another potential pathogenic Clostridioides sp. is C. difficile. Clostridia are commonly encountered in the intestinal tract without being associated with disease, as soil and feedstuffs seem to be natural habitats for these organisms. However at rare occasions C.difficile can cause a severe, fatal enterocolitis.

 

As in entertoxemia, the disease can have a fast fatal outcome within 2-3 days. A more chronic course of enteritis was associated with the same strain of C.difficile that had killed 2 adult Asian elephants in the same herd a few days before. This elephant recovered over a period of 5 weeks of severe illness with diarrhea. It was speculated that the feeding of large quantities of broccoli, a rich source of sulforaphane, which has been shown to inhibit the growth of many intestinal microorganisms might have triggered a subsequent overgrowth by C. difficile (Bojesen et al. 2006).

The diagnose of C.difficile associated disease is based on aerobic and anaerobic culture and PCR, including the demonstration of toxins. Special culture media have been developed to grow C. difficile.

Treatment

Metronidazole and vancomycin are used to address clinical disease caused by C.difficile. The sensitivity to these drugs was studied in 6 isolates of C.difficili obtained from feces of clinically healthy Asian elephants (Sthitmatee et al. 2013). There was no evidence of resistance of these isolates to metronidazole and vancomycin. However, sensitivity may vary per country, depending on the antimicrobial policy followed. 

References

Bojesen A.M., Olsen K.E.P. and Bertelsen M.F. 2006. Fatal enterocolitis in Asian elephants (Elephas maximus) caused by Clostridium difficile. Veterinary Microbiology 116 (329–335), 2006.

Sthitmatee N.,  Warinrak T. and Wongkalasin W. 2013. Susceptibility of Clostridium difficile Isolated from Healthy Captive Asian Elephants to Metronidazole and Vancomycin. Thai J Vet Med. 43(2): 313-316.

 
 

Malignant edema (Clostridium septicum)

There is one  report on malignant edema in an adult Asian elephant that lived in a European zoo (Goltenboth et al, 1974). The elephant died within 48 hours after the onset of the symptoms, that consisted of lethargy and general malaise. Severe edema was found in the entire intestinal tract.

Black leg (Clostridium chauvoei, C. septicum)

 

There is one report of black leg in a 50 yr-old Asian elephant kept in Australia (Prescott, 1971). The animal was on a diet of fresh grass (grazing), eucalyptus and lucerne hay. Two days before it died, the elephant had been off food and fell against a round timber pallisade, hurting its right shoulder. The following day it was depressed and fell down again and was unable to stand up. It died 52 hours after the first signs of illness. At necropsy the right foreleg was swollen from carpus to shoulder. On incision of the swollen muscles, sero-sanguineous fluid and gas bubbled from the emphysematous tissues. Clostridium septicum was cultured from this fluid. The wall of the stomach and large parts of the intestines was thickened, edematous and inflamed, while the spleen was very distended.

References

1. Goltenboth, R. and Klos, H.-G. 1974. On several diseases and causes of death in elephants in the Berlin Zoo (Zu einigen erkrankungen und todesfallen bei elefanten des Zoologischen Gartens Berlin. XVI Verhandlungsbericht Internationalen Symposiums Erkrankungen Zoo und Wildtiere, Berlin, Akademie Verlag, pp. 175–179.

2. Prescott C.W> 1971. Black leg in an elephant. Veterinary Record  83, pp 598-599.

Botulism

Botulism is caused by the toxin of Clostridium botulinum (FAO). 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.

The toxin is formed by the organisms outside the elephant under certain circumstances, characterized by an anaerobic environment (pH ± 4) and an environmental temperature between 10 and 50°C (FAO). Examples of these sources are poor-quality silage or poor-quality drinking water (anaerobic conditions in a pond without streaming water).

 

Botulism in elephants

Botulism was first reported in Asian elephants in a German zoo (Elze 1962). One adult elephant became paralyzed and died within one day. A cause of this sudden death could not be determined. Four days later an adult herd mate started to show the first signs of paralysis. Initially the animal remained standing with the neck stretched in forward direction, mouth opened, salivating and teeth grinding. The elephant only ate some fruits and was extremely weak in all its legs and the trunk. Pulse frequency was 68/minute. The animal went down sleeping several times, but with great strength it managed to get up by itself. On the second day a Botulism-antitoxin serum (Sachsisches Serumwerken A.G. Dresden, DDR) is administered (3x50 ml s.c.). On the next the animal is given 37 x 50 ml of this antitoxin serum, partly s.c., partly intramuscular in 50-100 ml portions in a time span of 2.5 hours. The total dose given was 20-40 times the dose given to humans. No adverse reactions were observed. During the first 8 hours after the administration of the antitoxin, the elephant went down and was almost unresponsive, until it managed to stand up again with the help of human manpower. In the following hours it started eating some fruits and hay. In the following week the animal recovered completely. The diagnosis ‘Botulism’ was made based on the symptoms and the positive reaction on the administration of the Botulism antitoxine. Other drugs that were given throughout the disease episode were caffeine, metamizole, calciumgluconate, Methiovert® (?), Algopyrin®, papaverine and streptomysine-penicilline.

A second case of botulism in elephants was reported by Gart et.al (1977). Unfortunately, no details of that report could be retrieved.

In 2017 a severe outbreak was reported in a captive bachelor herd of 6 Asian elephant bulls in Spain, which resulted in the death of 5 of the elephants. For the case report Botulism in elephants”, click here.

 

Botulism has been reported in horses that were exposed to botulism toxin in the feed, usually involving type B and 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.

Toxico-infectious botulism is the second most 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.

Symptoms of botulism in elephants

The typical symptoms include flaccid muscle paralysis. The major clinical signs consisted of gradually increasing general weakness, shivering, muscle fasciculations (involuntary contractions) or trembling and shaking, particularly in the shoulder and flank muscles, mild to heavy salivation, inability to swallow and stand and properly use the trunk and dilated pupils that respond poorly on light. Death can occur within a few days as a result of respiratory distress.

Treatment, diagnosis and prevention

Treatment of botulism is very challenging: when treatment is started in the early phase of the disease, the administration of specific antitoxins might be helpful, as suggested in the 1962 case. In horses respiratory support is important, however challenging in elephants. Soft bedding should be provided. Eye protection with an eye ointment is important when the elephant has gone into lateral recumbency. During the phase of complete paralysis, the administration of oxygen through the trunk will probably support the oxygen exchange in the elephant’s lungs.

A definitive diagnosis of botulism can only be made by performing a mouse bioassay test.

Prevention: there is no commercially available vaccine against botulism, except for type B (AAEP)

 

References

  • Elze, K. 1962. Botulism in an elephant (Über Eine Unter dem klinischen bild des botulismus verlaufend Erkrankung beim elephanten). 4th Verhandlungsbericht Internationalen Symposiums Erkrankungen Zoo und Wildtiere, Berlin, Akademie Verlag, pp. 259–271.

  • Fowler M.E. 2006. Infectious diseases. In: Biology, Medicine and Surgery of Elephants, Ed. Fowler and Mikota, Chapter 11, Infectious diseases

  • Garlt, C., Kiupel, H. and Ehrentraut, W. 1977. Botulism in elephants (Ein beitrag zum Botulismus bei elefanten). 21st Verhandlungsbericht Internationalen Symposiums ErkrankungenZoo und Wildtiere, Berlin, Akademie Verlag, pp. 207–211.

Websites:

FAO: https://www.fao.org/3/t0756e/T0756E03.htm

American Association of Equine Practicioners (AAEP): https://aaep.org/guidelines/vaccination-guidelines/risk-based-vaccination-guidelines/botulism