Abdominal surgery for male castration, laparoscopic ligation of the ovarian pedicles, umbilical hernia and abdominal surgery to treat repeated colics are described here. To procedures Surgery Surgery in elephants usually follows the rules that are applicable to surgery in horses. Standing sedation with or without local anesthesia is required for minor procedures, while general anesthesia (in lateral or dorsal recumbancy) is required for large procedures (such as abdominal surgery) and if standing sedation poses a risk for the surgeons. See for anesthetic procedures the anesthesia page . Abdominal surgery in elephants Access to the elephant's abdomen is restricted to a relatively small area between the last ribs on the cranio-dorsal side, the hind leg on the caudal side fusing together in the ventral midline. Indications for abdominal surgery described in the literature are limited: cesarean sections have all resulted in the death of the dam. However, a dorso-lateral approach has been used for castration of male African and Asian elephants (Fowler 1973, Byron 1985, Fourner 1994). Fourteen male African elephants (12–35 years old) were anesthetized with etorphine and supported in a sling in a modified standing position, and positive pressure ventilated with oxygen (Rubio-Martinez 2014). Anesthesia was maintained with IV etorphine. Vasectomy was performed under field conditions by bilateral, open‐approach, flank laparoscopy with the abdomen insufflated with filtered ambient air. A 4‐cm segment of each ductus deferens was excised. Behavior and incision healing were recorded for 8 months postoperatively. Successful bilateral vasectomy (surgical time, 57–125 minutes) was confirmed by histologic examination of excised tissue. Recovery was uneventful without signs of abnormal behavior. Large intestine lacerations (3 elephants; 1 full and 2 partial thickness) were sutured extracorporeally. One elephant that was found dead at 6 weeks, had no prior abnormal signs. Skin incisions healed without complication. Laparoscopic ligation of the ovarian pedicles has been performed in free ranging African elephants (Stetter 2004). A specially designed 90 cm long operating laparoscope was used to reach for the ovaries. An umbilical hernia was diagnosed in a 2-wk-old Asian elephant (Elephas maximus) by physical and ultrasonographic examinations (Abou-Madi 2004). Umbilical herniorrhaphy was elected because the defect was large (approximately 7 cm long and 10 cm deep) and could potentially lead to incarceration of an intestinal loop. General anesthesia was induced with a combination of ketamine, xylazine, and diazepam and maintained with isoflurane in oxygen. The hernial sac was explored and contained fibrous tissue, fat, and an intestinal loop but no adhesions. The hernial sac was resected and the body wall closed using the technique of simple apposition. Following a superficial wound infection, the surgical site healed with no further complications. There is one anecdotal report on successfull abdominal surgery in a 14-month-old African elephant suffering of repeated colics ( click here for the case report). References Abou-Madi, N., Kollias G.V., Hackett R.P., Ducharme N.G., Gleed R.D., and Moakler J.P. 2004. Umbilical herniorrhaphy in a juvenile Asian elephant (Elephas maximus ). J. Zoo & Wildl. Med35(2): 221–225, 2004. Byron H.T., Olsen J., Schmidt M., Copeland J.F. and Byron L. 1987. Abdominal surgery in three adult male Asian elephants. J. Am. Vet. Ass. 187, 11. Foerner J.J., Houck R.I., Copeland J.F., Schmidt M.J., Byron H.T. and Olsen J.H. 1994.Surgical castration of the elephant (Elephas maximus and Loxodonta africana ). J. Zoo & Wildl. Med. 25 (3), pp 355-359. (Click here for summary) Fowler M .E., Hart R. 1973. Castration of an Asian elephant, using etorphine anesthesia. J. Am. Vet Ass 163, 6. Rubio- Martinez L.M. Hendrickson D.A., Stetter M., Zuba J.R. and Marais H.J. 2014. Laparoscopic Vasectomy in African Elephants (Loxodonta africana ). Veterinary Surgery 43 (2014) 507–514. Stetter M.D. 2004. Laparoscopic surgery in elephants. Int. Elephants Res. Symp. Fort worth, Texas. December 2-5, 2004 Non-abdominal surgery in elephants Surgical procedures not associated with open access to the abdomen are more common. Despite the enormous healing capacity of the elephant skin, wound healing often takes place per secundam, because it is hard to protect the sutured wound against negative mechanical and biological influences. However, even large wounds (like in vaginal vestibulotomy ) will heal completely per secundam, leaving at most a 2 mm fistula ( click here for wound healing in vaginal vestibulotomy). Trunk injuries are hard to repair because of the extreme mobility of this organ. Many attempts to suture large perfortaing trunk wounds have have failed or at best resulted in partial adhesion of the sutured sites. Repair of a perineal hernia has been described ( click here to read this case report).

This page directs you to the reference values of hematology and blood chemistry in Asian and African elephants, including toxicology and endocrinology. To serum chemistry Reference values (blood): - Hematology - Blood chemistry - Toxicology - Endocrinology All values (IU) All values (Conv. Un) All values (IU) All values (Conv. Un) Asian elephant African elephant One study in 10 healthy Asian elephants showed that most Asian elephant hematology and biochemistry parameters are highly individual, requiring individual normal values for accurate interpretation (Perrin, 2020).

A ±4.5-yrs-old male African elephant calf had been rescued from the wild after being injured in a bush fire. While in the rescue facility, it developed episodes of “choke”, caused by impaction of the esophagus with ingested foodstuff. This resulted in regurgitation, and the inability to eat and drink without the food or liquid dribbling out of the animal’s mouth. Multiple treatment interventions under general anesthesia are described. Case report Esophagus impaction in a 4.5-yrs-old African elephant Date: 2019-2021 Place: Botswana Data provided by: Rob Jackson DVM History “Choke” symptoms can be associated with: Congenital abnormalities of the upper digestive system; symptoms usually show up when the animal is weaned and starts eating solid food. Megaesophagus, which can be congenital or acquired; Foreign bodies that get stuck in the upper digestive system; Impaction or blockage of the stomach/duodenum; Abnormal function of the cardiac sphincter which is the valve allowing food to flow into the stomach. Blockage of the upper digestive system can cause damage to the esophagus resulting in strictures and narrowing, which makes the problem worse or even necrosis and rupture of the oesophagus. Regurgitation can result in food and liquid entering the trachea and the lungs. This causes a foreign body pneumonia, which in chronic cases can result in the eventual death of the animal. A ±4.5-yrs-old male African elephant calf had been rescued from the wild after being injured in a bush fire. While in the rescue facility, it developed episodes of “choke”, caused by impaction of the esophagus with ingested foodstuff. This resulted in regurgitation, and the inability to eat and drink without the food or liquid dribbling out of the animal’s mouth. “Choke” symptoms can be associated with: Congenital abnormalities of the upper digestive system; symptoms usually show up when the animal is weaned and starts eating solid food. Megaesophagus, which can be congenital or acquired; Foreign bodies that get stuck in the upper digestive system; Impaction or blockage of the stomach/duodenum; Abnormal function of the cardiac sphincter which is the valve allowing food to flow into the stomach. Blockage of the upper digestive system can cause damage to the oesophagus resulting in strictures and narrowing, which makes the problem worse or even necrosis and rupture of the oesophagus. Regurgitation can result in food and liquid entering the trachea and the lungs. This causes a foreign body pneumonia, which in chronic cases can result in the eventual death of the animal. Treatment At first consultation, the elephant was not eating and was salivating. Under standing sedation, a stomach tube was advanced into the esophagus which immediately created passage. Painkillers, antibiotics, and Buscopan were given The cause of the blockage could not be determined. Ten weeks later, the animal showed similar symptoms, however, they were more severe and they had possibly been going for longer than the previous episode. Awaiting the arrival of the vet, the animal was given Buscopan, antibiotics and anti-inflammatories. As there was no improvement, the elephant was sedated again. This time, 4 sedations during 2 days were required before the blockage of the esophagus could be cleared. High volumes of fluids were given intravenously, tubes of different diameters were introduced (one for flushing with water and one for drainage), and foodstuff was removed mechanically. The impaction could be visualised with a three-meter endoscope as twigs and leaves jammed proximal to the cardiac sphincter. The esophagus appeared enlarged and flaccid. The wall of the stomach looked normal at endoscopic inspection. The animal was treated with a long course of antibiotics, liquid food slowly changing to solids over two months and he recovered well. Four months later the animal once again showed signs of discomfort, inappetence, regurgitation and salivation. Finally he vomited chewed bark and milk. He did not respond to the treatment with antibiotics, NSAIDs and Buscopan. He was sedated again for three hours, initially standing and then recumbent. The esophagus was blocked and passage of a tube failed. However, large volumes of chewed bark could be removed manually from the oro- and nasopharynx. The pharynx and esophagus were completely blocked with chewed bark. A large-bore tube was introduced into the proximal esephagus and a small-bore tube within it attached to a hose pipe was used to flush the esophagus and pharynx. At the same time high volumes of intravenous fluids and rectal fluids were administered. After this procedure, antibiotics and NSAIDs, steroids were given for several days. Sildanefil rectally was used to try and relax the cardiac sphincter. The following day the elephant was anesthetized and went into lateral recumbency. Medetomidine/butorphanol was used for induction of anaesthesia, which was maintained with intravenous ketamine. A cuffed endotracheal tube was inserted into the trachea. The two tubes as described above were introduced into the esophagus. Large volumes of finely chewed bark were flushed from the esephagus, through the mouth and trunk. A handful of 12 mm gravel was also recovered. Eventually the esophagus and the stomach were cleared from these materials. No abnormalities gross lesions were seen with the endoscope. The esophagus was suspected to be flaccid and dilated, with possible damage at the level of the cardiac sphincter, possibly caused by impaction with gravel. During anaesthesia high volumes of intravenous and rectal fluids were given. Grey, hard stools were being passed irregularly. A secondary impaction as a result of pain and dehydration was suspected. No discomfort was observed. Fluid, intravenous and rectal continued during several days after anaesthesia. Finadyne was given at lower dose to treat the impaction. Oral fluids were being swallowed and volumes were slowly increased. The administration of antibiotics was continued as complications in the form of a regurgitation pneumonia were anticipated. The prognosis for full recovery was guarded as recurrence was anticipated. In the following 2 months, the elephant went through several similar episodes, which luckily resolved on their own. Repeated bouts of pneumonia were expected, which need to be treated aggressively each time they occur. This follows a classic congenital abnormality/megaesephagus pattern but in this case the damage resulting in the impaction may be the result of injuries from the original fire, possibly by inhalation. However, it cannot be ruled out that this animal is just a naughty, hand-reared baby elephant eating strange objects. Treatment results Two months after the last treatment the elephant calf is recovering well, tired but improving. Showing some discomfort in one leg. Suspect an infection or damaged areas of skin with secondary infection. He showed ventral oedema which improved with a course of antibiotics. It appears that areas of skin are sloughing off. Antibiotic treatment has been instituted. The skin problems are suspected to be part of a systemic infection originating from a regurgitation pneumonia. Another theory to explain the skin necrosis is the involvement of an autoimmune circulatory component as there had been peripheral lesions on the ears at the start of treatment, which later also showed oedema. To page top

Kidney disease is quite common in elephants. The analysis of urine is important. This page describes the routine urinalysis and some specific features related to elephant urine. Protein detection can be done by refractometry and sulfosalicylic acid (SSA)precipitation. Comparing osmolarity in serum and urine gives an indication for the presence of kidney failure. To lab diagnosis Urinalysis The routine urinalysis is a quick and relatively inexpensive test which can be readily performed in a field laboratory. Ideally urine should always be collected at the same time as blood for hematology and clinical chemistry (if possible) and before any treatment is administered. Urine should be examined as soon as possible after collection, because artifacts will occur in the urine over time (cells lyse, crystals form in vitro). If a delay is anticipated before analysis, the urine should be refrigerated. Refrigerated urine should always be brought to room temperature before testing. A complete urinalysis consists of 1) evaluation of physical characteristics, 2) measurement of specific gravity, 3) dipstick analysis and 4) examination of sediment. Equipment and Materials Microscope Refractometer Slides Urinalysis dipsticks Urine sediment stain Physical Characteristics of Urine 1. Evaluate and record urine color Normal mammalian urine is yellow to amber. Urine volume and concentration affect the depth of the color. Some examples of various urine colors and corresponding common possible causes: 2. Evaluate and record urine turbidity Fresh urine is clear to very slightly cloudy. Urine may become more cloudy if left standing or if refrigerated. The turbidity of the urine sample is reported as: clear, slightly cloudy, cloudy, opaque, or flocculent. Excess turbidity results from the presence of suspended particles in the urine. The cause can usually be determined based on the results of the microscopic urine sediment examination. Common causes of abnormal turbidity include: increased cells (RBC, WBC) numerous crystals bacteria lipiduria (lipids often rise to the surface) mucus (especially in horses) semen fecal contamination 3. Odor Ammonia is formed from urea by bacterial action. An ammonia smell may be prominent in retained or old urine samples. An acetone small may suggest ketosis. Some drugs may impart a characteristic odor. 4. Volume Urine volume may be estimated from urine specific gravity. In general, volume and specific gravity (S.G.) are inversely related in health and in most diseases. Exceptions include: Diabetes mellitus. Polyuria and high S.G. coexist because of glucosuria. Acute and chronic renal disease. Oliguria (↓ urine volume) may be accompanied by a lack of renal concentrating ability. 5. Measure specific gravity (S.G.) Specific gravity is the ratio of the refractive index of urine compared to water. Refractometry is the easiest method to measure urine S.G.Dipsticks are not as accurate. Glucose and protein may falsely ↑ urine S.G. Knowledge of the hydration status is necessary to interpret the S.G. Urine S.G. can vary from 1.001 to 1.065 in most healthy animals but this range also includes values associated with renal abnormalities. S.G. has been inadequately studied in elephants and obtaining a baseline during health and evaluating sequential samples during illness is recommended. Isosthenuria (fixed S.G.) is the constant maintenance of urine S.G in the range of the glomerular filtrate (1.008-1.012). Isosthenuria means the kidney is neither concentrating nor diluting urine. Hyposthenuria is a S.G. < 1.008. In hyposthenuria the kidneys still have some water-balance function. 6. Perform dipstick analysis and record results. Mix the urine Dip the dipstick; remove extra urine Start timing Compare to chart on bottle in good light The dipstick method is not reliable for protein detection in elephants. Using the SSA-method is more reliable (see 6.1) 6.1 Urine protein detection. "PROT-SSA" represents the reaction observed on the sulfosalicylic acid (SSA)precipitation test. The SSA reagent is added to a small volume of urine. Acidification causes precipitation of protein in the sample (seen as increasing turbidity), which is subjectively graded as trace, 1+, 2+, 3+ or 4+. Unlike the "PROT-STIX" test, the SSA reaction will detect albumin andglobulins (although it is more sensitive to albumin). In addition, the SSA detects Bence-Jones proteins, although it often underestimates them. In alkaline urine, the SSA reaction is a more accurate measure of urine protein content than the dipstick. The most accurate measurement of urine protein output is measurement of urine protein excretion over 24-hours. False positives Contrast media Antibiotics in high concentration, e.g. penicillin and cephalosporin derivatives Uncentrifuged turbid urines can look positive. Therefore, SSA should always be performed on urine supernatant. False negatives Highly buffered alkaline urine. The urine may require acidification to a pH of 7.0 before performing the SSA test. Dilute urine Turbid urine - may mask a positive reaction. https://www.klimud.org/public/atlas/idrar/web/www.diaglab.vet.cornell.edu/clinpath/modules/ua-rout/protssa.htm 7. Urine sediment examination Centrifuge a fresh urine sample for 5 minutes at about 1500 RPM Remove supernatant Add 1-2 drops of stain to sediment Tap the bottom of the tube to mix Transfer one drop to a slide and place a coverslip Examine the entire coverslip at 10X and 40X * Low maginification (10x): casts, large crystals, debris, parasitic ova are visible * High magnification (40x): leukocytes, erythrocytes, epithelial cells, fat droplets, small crystals, sperm, debris and bacteria are visible To page top

Resting behavior and allonursing in elephants are described in this page. Resting in lateral recumbancy requires a trustful social environment. Comfortable resting is promoted by the provision of sand piles. A case of allonursing (drinking milk from a non-mother) describes this phenomenon in an African elephant that never produced offspring herself. Behavior & Training Resting behavior Behavior & Training Resting behavior Allonursing Case Report: Spontaneous Lactation and Allonursing in a Captive African Elephant (Loxodonta africana ) Date: December 2024 Place: Erfurt Zoo Data provided by: Tina Risch, DVM Introduction Allomothering, the care of an infant by an individual other than the biological mother, is a well-known behavior in social animals, including African elephants (Loxodonta africana). However, allonursing—the act of an allomother providing milk to a non-biological calf—is rare and typically observed in females with previous reproductive experience. This case report describes an unusual instance of allomothering and allonursing by a nulliparous (never pregnant) adult female African elephant in a zoo setting. Case Presentation As a neonate, a male captive African elephant calf (Banjoko) started looking for drinking opportunities from 3 adult females, including its mother. When he was 5 month-old, the 29-year-old female herd member, named Csami, admitted him unrestrictedly (figure 1). Csami, a wild-caught elephant, arrived at the zoo at the age of four and had never been pregnant. The calf's biological mother, Chupa, continued to actively nurse her offspring while at the same time Csami's involvement progressively intensified. Notably, Csami had previously shown nurturing behaviors towards Chupa's older calf, a 4-year-old female. However, Csami's maternal instincts towards the youngest calf manifested to the extent that she began producing a milk-like fluid. Figure 1. The 7-month-old African elephant calf, Banjoko, nursing from Csani, the allomother that never produced a calf herself (Erfurt Zoo, Germany, 2024) Clinical Observations and Milk Analysis A sample of the fluid secreted by Csami was collected and analyzed for fat, protein, lactose, and pH levels. These values were compared to a milk sample obtained from Chupa. The results are summarized in Table 1. The results indicate that Csami's milk-like fluid closely resembled Chupa's milk in composition, suggesting that the fluid could adequately support the calf's nutritional needs with regard to fat, protein and lactose. Table 1. Comparative analysis of milk composition from Chupa (dam) and Csami (allomother). Discussion The phenomenon of allomothering is widely observed in species that rely on cooperative group dynamics, such as lions, seals, and elephants. While allonursing is less frequent, it has been documented in elephants, typically involving females with prior lactation experience. This case represents a rare instance of spontaneous lactation and allonursing by an elephant with no prior reproductive history. The physiological mechanism behind Csami's lactation remains unclear but is must be linked to hormonal or social factors triggered by the presence of the calf. This behavior may enhance calf survival by providing supplemental nutrition and fostering stronger social bonds within the herd. To the best of our knowledge, this case is one of only two recorded instances of allonursing by a nulliparous elephant. The first case was reported from Gangala-na-Bodio Elephant station in Congo, documented by Harald H. Roth in 1961 (figure 2). Figure 2. A 32-month-old African elephant nursing from an allomother that never produced a calf herself (Der Zoologische Garten, 1961) Conclusion This report highlights the complex social structures and nurturing behaviors of African elephants. Csami's spontaneous lactation and allonursing underscore the adaptability and cooperative nature of elephants in captivity. Reference Roth HH. Short communication. Der Zoologischen Garten 26, 1.2, pg 123. 1961. Allonursing

The most important zoonotic disease in elephants is tuberculosis. Other examples of zoonotic pathogens are cowpox, Salmonalla, Anthrax, and Pasteurella. Several microbes are opporunistic pathogens, like rabies, leptospirosis, foot and mouth disease, and organisms involved in local processes (abscess, feces, urine, exudate). Zoonoses Zoonotic diseases in elephants. Zoonotic diseases are defined as infectious disease of humans caused by a pathogen (an infectious agent, such as a bacterium, virus, parasite or prion) that can jump from a non-human (usually a vertebrate) to a human and vice versa. Some of these pathogens can be considered as opportunistic, others as primary infections. Relevant primary pathogens in elephants are : Bacterial diseases Mycobacterium tuberculosis complex (MTBC). The prevalence of MTBC in captive elephants in European zoos is relatively high. A study of the post-mortem reports between 1985 and 2024 showed that 20/301 Asian elephants and 12/196 African elephants had died of MTBC (Data from EAZA elephant TAG, WS). From 1997 through 2011, the median point of prevalence within the Asian elephant population in USA-zoos was 5.1%, with a range from 0.3% to 6.7%. In contrast, the annual point prevalence during the same time period within the African elephant population was 0. Although exact data about the prevalence of MTBC in range countries are not known, there are many reports of MTBC in captive and to (a lesser degree) wild Asian elephants. Data on MTBC in African elephants in range countries are limited. Click here to read more about tuberculosis in elephants. Non-tuberculous mycobacteriosis: Mycobacterium elephantis ; only found in humans, never in elephants. However, the strain is genetically related to Mycobacterium confluentis and M. smegmatis cultured form lung lesions in an elephant (Lacasse, 2007) . Bacillus anthrax: Click here to read more about anthrax in elephants. Pasteurella multocida: Click here to read more about Pasteurellosis in elephants. Salmonella spp .: Click here to read more about salmonellosis in elephants. Leptospira interrogans found in urine of captive elephants in Asia. This is a potential risk for humans in close contact with these elephants (Athapattu 2019). Click here to read more about leptospirosis in elephants. Viral diseases: Cowpox virus (Orthopoxvirus bovis) . Asian elephants are very sensitive to a pox virus infection, African elephants to a lesser degree. The fluid that fill the pox vesicles are full of virus. Once the fluid is exposed, humans can become infected. Click here to read more about pox virus infections in elephants. Foot and Mouth disease virus (FMD-virus): Asian elephants are very sensitive to FMD. There is only one report of FMD in an African elephant that was experimentally infected. Click here to read more about FMD in elephants. Rabies: transmission of rabies virus from elephants to humans have never been reported, but saliva of diseased rabid elephant is a potential risk for humans. Click here to read more about rabies in elephants. Opportunistic pathogens: Opportunistic pathogens can be found in the environment, but when concentrated in a pathological condition in an animal (abscess, feces, urine, exudate), they can cause disease in humans: Escherichia coli Pseudomonas Bacteroides spp. Staphylococcus aureus Streptococcus spp. Klebsiella spp. Mycobacterium avium Fungi: there are no reports on fungus infections in humans acquired through contact with elephants. Serological responses detected in elephants without evidence of causing disease: Elephants may be (temporary) silent carriers of several potentially pathogenic microbes. The historical contact is expressed by the presence of antibodies in the blood of the elephant. Examples of these conditions are: African horse sickness virus : the presence of antibodies in African elephants has been described (Barnard, 1995). Humans are usually not affected. However, severe disease has been reported in lab workers who were producing a AHSV-vaccine (van der Meyden, 1991; Reid,1991). Influenza type A : 1 serologically positive elephant reported (Schröder 1992). Eastern equine encephalitis: 1 serologically positive elephant reported (Christy, 2009) Bluetongue : antibodies were detected in 7 out of 109 serum samples of captive Asian el ephants in India (Bhat, 1998). Canine distemper: antibodies were detected in 25 out of 144 serum samples of captive Asian elephants in Thailand (Ono, 2006). Yersinia pestis (plague); In one study in wild African elephants 0.3% of the cohort animals were found seropositive for antibodies against Yersinia pestis (Gordon, 1979). No transmission of plague from elephants to humans has been reported. Toxoplasma gondii : 35% of captive elephants in a study in Thailand was serologically positive (Udonsom 2022). As the elephant is not an end-host for toxoplasmosis, transmission of toxoplasmosis from elephants to humans is unlikely to occur. Cryptosporidium spp .: found in African elephants at a European zoo (Gracena, 2002). No transmission to humans has been reported. References Athapattu TPJ, Fernando BR, Koizumi N, Gamage CD. Detection of pathogenic leptospires in the urine of domesticated elephants in Sri Lanka. Acta Trop. 2019 Jul;195:78-82. doi: 10.1016/j.actatropica.2019.04.029. Epub 2019 Apr 29. PMID: 31047864. Barnard BJH, Bengi RG, Keet DF, Dekker EH, Verwoerd DW. 1995. Epidemiology of African horsesickness: antibodies in free-living elephants (Loxodonta africana) and their response to experimental infection. Onderstepoort journal of Vet. Res. 62, 1995. Bhat N, Manickam R, Arunp W.1998. Detection of bluetongue antibody and antigen in Indian elephants, spotted deer and blackbucks. Indian Journal of Animal Sciences 68 (2) : 135, February 1998 Christy L. Rettenmund CL, Terrell SP, Miller M. 2009 Eastern Equine Encephalitis Virus (EEEV) Titers in African Elephants (Loxodonta africana) At Disney’s Animal Kingdom. American association of Zoo Veterinarians Conference 2009 Feldman M, Isaza R, Prins C, Hernandez J. 2013. Point prevalence and incidence of Mycobacterium tuberculosis complex in captive elephants in the United States of America, Veterinary Quarterly, 33:1, 25-29. Gordon DH, Isaacson M, Taylor P. 1979. Plague Antibody in Large African Mammals. Infection and Immunity, Nov. 1979, p. 767-769 Gracenea M, Gómez M., Torres J, Carné E, Fernández-Morán J. 2002. Transmission dynamics of Cryptosporidium in primates and herbivores at the Barcelona zoo: a long-term study. Veterinary Parasitology, 104(1), 19–26. doi:10.1016/s0304-4017(01)00611-2. Lacasse C, Terio K, Kinsel MJ, Farina LL, Travis DA, Greenwald R, Lyashchenko MDKP, Miller M, Gamble KC. 2007. Two cases of atypical mycobacteriosis caused by Mycobacterium szulgai associated with mortality in captive african elephants (Loxodonta africana). Journal of Zoo and Wildlife Medicine 38(1): 101–107, 2007. Oni O, Wajjwalku W, Boodde O, Chumsing W. 2013. Canine distemper virus antibodies in the Asian elephant (Elephas maximus). The Veterinary Record, September 23, 2006. Reid, R, van der Meyden, CH, Erasmus, BJ, Meyer, H and Hamilton, AMP. 1991. Encephalitis and chorioretinitis associ[1]ated with neurotropic African horsesickness virus infection in laboratory workers. Part II. Ophthalmological findings. S Afr Med J 81:454–458. Schröder, H.D., Fischer, M. and Ippen, R. 1992. Contribution to the occurrence of infection of zoo mammals with influenzavirus type A. Erkrankungen der Zootiere. Verhandlungsbericht des 34. Internationalen Symposiums uber die Erkrankungen der Zoo- und Wildtiere, Santander-Spain, pp. 119–125. Udonsom R, Nishikawa Y, Fereig RM, Topisit T, Kulkaweewut N, Chanamrung S, Jirapattharasate C.2022. Exposure to Toxoplasma gondii in Asian Elephants (Elephas maximus indicus) in Thailand. Pathogens 2022, 11, 2. van der Meyden, CH, Erasmus, BJ, Swanepoel, R. and Prozesky, OW. 1991. Encephalitis and chorioretinitis associated with neurotropic African horsesickness virus infection in laboratory workers. Part I. Clinical and neurological observa[1]tions. S Afr Med J 81:451–454. Zachariah A, Pandiyan J, Madhavilatha G, Mundayoor S, Chandramohan B, Sajesh P, et al. Mycobacterium tuberculosis in Wild Asian Elephants, Southern India. Emerg Infect Dis. 2017;23(3):504-506. https://doi.org/10.3201/eid2303.161741 To page top

Molar teeth in elephants: development, age estimation, malformation, malpositioning, molar extraction and shortening of molar teeth are presented in this chapter. Back to dentistry A very informative article about the development of molar teeth and several disorders in molars and tusks has been written by D.A. Fagan, J.E.Oosterhuis, and A. Roocroft (Colyer Institute). Click here to read the entire manuscript. Molar development Written by Willem Schaftenaar Dental formula in elephants The molars in elephants differ from other mammalians. In each side of the mandible and the maxilla a single molar tooth develops at a time. This molar consists of lamellae that are compressed together to form one dental element, which slowly progresses in forward direction, pushed as it is by a new molar that is developing caudal to the functional molar. During their entire life span, an elephant develops only 6 molars on each side of the mandible and upper jaw. The lamellae are fused together with cement and at the grinding side covert with enamel. The different length of the lamellae give the molars its irregular shape at the grinding surface, which is extra supported by the difference in hardness between enamel and dentine. During the development of molar teeth, two processes are very important: Dentinogenesis: the formation of dentin. Amelogenesis: the formation of enamel. Any disturbance in these processes may result in malformation or poor quality of that molar, which is manifested as dental dysplasia. Such an abnormal molar may be weak and prone to deformity, malposition and malocclusion. This can lead to food impaction and consequently infection of the peridontal structures. The condition of the molar teeth is important for the physical condition of the elephant. The body mass of both breeding and non-breeding female zoo elephants shows a cyclic undulation with peaks separated by many years, and correlated with the total surface of the functional the molar teeth (Schiffmann 2018). Molars are important for the estimation of the age of an elephant. The numbers of the lamellae are quite specific for the sequential number of the molar. These numbers differ slightly between Asian and African elephants. So, by counting the lamellae of the presented molar, the sequential number of that particular molar tooth can be estimated. The lamellae of molars that have not yet erupted are loose. The same applies for molars in the embryonic stage. A drawing of the distinctive Occlusal Wear Patterns characteristic of Asian and African elephant molar dentition. It is this unique diamond shaped patten which provides the origin of the African elephant's scientific name Loxodonta - from the Greek word loxos - meaning oblique. (Modified from KINGDON 1971 & STERNDALE 1929) Age estimation This table shows when a new molar erupts and at which age this particular molar is replaced by a new one. When the number of lamellae has informed us about the sequential number of the molar tooth, we can simply look at this table to estimate the age of the elephant. The final molar tooth that appears is the 6th one, that erupts at the age of 40 years. When this molar is gone (usually between 60 and 80 years), no new molar develops and the elephant will have no proper molars to mastigate its food. This radiograph shows the tusks and the molar teeth in the skull of a young elephant. Each tusk has a large, distinct pulpa chamber (Courtesy: Basel Zoo). This radiograph shows you the mandibles. As indicated on the picture, each side contains a very small erupted molar on the left side, followed by another (erupted) molar in the middle and finally a large molar on the right side. (Courtesy: Basel Zoo). The erupted molar in the middle consists of 6 lamellae. This means that it is the second molar tooth that has developed in this elephant. There is still a small remnant of the first molar. The 3rd molar is at the point of eruption. The dentition of the jaw on the X-ray corresponds with the dentition of the jaw preparation. Both elephants was approximately 2,5 years old. Molar tooth disorders Molar tooth disorders are quite common in elephants, especially in the older ones. The progressive changes of the molars make them prone to malpositioning. Pathological changes during the development of the molar before it erupts, can result in a deformed or rotated tooth. Like in all animals with teeth, the quality of the food correlates with the quality of the teeth. If the speed of the abrasive wear is faster than the mineralization, the pulp of the molar tooth can become exposed. Insufficient abrasive wear (for example if the diet contains insufficient branches) will result in the opposite: long molar teeth, which often often are rotated. A loose piece of an old molar in this 40 yrs-old Asian elephant caused pain, which became manifest by the animal's reluctance to eat hard food items. Video: Willem Schaftenaar Sometimes, especially when there is a certain degree of molar mal-positioning, the peridontal area can become infected. This is a painful condition which may lead to reduced appatite or selective food consumption, avoiding hard items. An example of mal-formation and rotation of the molar tooth in an Asian elephant. Click here to read a case report about this condition. Courtesy: Christian Schiffmann Excessive abrasive wear of the molar teeth in this elephant had opened the pulp cavity of the anterior lamella of this lower molar tooth af an African elephant. Courtesy Peter Kertesz. Insufficient abrasive wear or disturbed pre-eruption molar development has resulted in excessively long molar teeth in this 60 yrs-old female Asian elephant. As a result the animal could not masticate her food properly, which was expressed by the poorly digested, long fibers present in the feces. The photo in the middle was taken a few years after the first one. Molar extraction and shortening The extraction of a molar tooth in an elephant is quite challenging. The indication for an extraction is usually mal-positioning and abnormal abrasive wear of the tooth, which has a negative impact on the elephant's well being. Click here to watch the video about the extraction of the mal-positioned molar tooth in a female Asian elephant. This photo shows the extracted molar tooth. The cut in this tooth was made to get sufficient grip on the tooth for the extraction. Note the abnormal abrasive wear on the anterior side of the molar I n another adult Asian elephant the lower molar had been worn down insufficiently and this obstructed t he normal chewing action. By using a special pneumatic oscillating saw and chisel the length of the molar was reduced sufficiently to restore the normal chewing activities. The photos show stills from a video ; note the special designed gingiva protector, a high potent vacuum cleaner and the oscillating saw in use. The short video fragment shows the end result of the shortened molar tooth. References Biology, Medicine, and Surgery of Elephants. Fowler & Mikota, 271-290. Fagan DA, Oosterhuis JE, and Roocroft A. Captivity Disorders in Elephants: Impacted Molars and Broken Tusks. Colyer Institute, San Diego (Ca) USA. Kertesz P. 1993. A colour atlas of Veterinary dentistry and oral surgery. Wolfe Publishing. ISBN 0 7234 1542 0. Schiffmann C, Hatt J-M, Hoby S, Codron D, Clauss M. 2018. Elephant body mass cyclicity suggests effect of molar progression on chewing efficienc y . Mammalian Biology, Volume 96, May 2019, Pages 81-8. Treatment insufficient molar wear Lucha the elephant visits the dentist (youtube.com) To page top Molar issues Molar development Age estimation Molar tooth disorders Molar tooth extraction Molar development Age estimation Molar disorders Molar extraction

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Salmonellosis is a zoonotic disease that affects many vertebrate species. It has been described for the first time as a pathogen in elephants in 1940 (Matzek 1940). The symptoms of salmonellosis can range from mild depression, colic, diarrhea, ventral edema, weight loss, cachexia to death. To infectious diseases Salmonellosis General information General information Salmonellosis is a zoonotic disease that affects many vertebrate species. It has been described for the first time as a pathogen in elephants in 1940 (Matzek 1940). The symptoms of salmonellosis can range from mild depression, colic, diarrhea, ventral edema, weight loss, cachexia to death. A fatal Salmonella hadar infection in an 18-year-old African elephant has been described, including necrosis and sloughing of the region above the toes (Scott 1984). Subclinical infections do also occur (Scharling 2021). One case of abortion in an African elephant has been described (Emanuelson 2000). Salmonellosis can manifest itself as an acute illness as well as a chronic disease. Different serotypes have been associated with intestinal disease and death (S. typhimurium , S. blockley ) (Matzke 1940, Windsor 1972 and 1976, Chooi 1988). S. saintpaul was associated with septicemia in an adult Asian elephant (Molenaar 2021). The source of the infection is not always found, but can be contaminated food, infected conspecifics, care takers and other species sharing the exhibit with the elephant. Diagnosis of salmonellosis Detection of Salmonella spp. in feces is by culture or PCR the most common way to demonstrate the presence in an elephant. However, shedding of the pathogen is intermittent, which means that multiple fecal samples taken in a period of at least 3 days are required. Salmonella spp. are more likely to be detected in elephants with abnormal feces. Selective media like selenite cystine broth and MacConkey agar are part of the routine culture method for Salmonella spp . (FAO 1992). To detect Salmonella in food samples in general, molecular testing in addition to conventional culture-based methods can be used. Multiplex quantitative PCR (qPCR) has proven to be a fast, easy to perform, and sensitive molecular technique for the detection of Salmonella species and various Salmonella serovars (Heymans 2018). Treatment of salmonellosis The decision to treat an elephant for salmonellosis depends on the clinical situation. Subclinical infections may be hard to clear. If attempted, treatment should be based on an antibiogram. In humans, common first-line oral antibiotics for susceptible Salmonella infections are fluoroquinolones (for adults) and azithromycin (for children). Ceftriaxone is an alternative first-line treatment agent (CDC 2018). In order to reduce the risk of antibiotic resistance to these antibiotics, their use in elephants should be considered only after the antibiogram has demonstrated that other antibiotics (e.g. sulfonamides) are not effective. Information on dosage and administration of antibiotics can be found on: https://www.elephantcare.org/formulary References: Chooi K.F., and Z. Z. Zahari. 1988. Salmonellosis in a Captive Asian Elephant. The Journal of Zoo Animal Medicine, Vol. 19, No. 1/2 (1988), pp. 48-50 Matzke, M. 1940. Salmonella typhimurium Infection in Elephants. Tierarztliche Rundschau 1940 Vol.46 pp.521-522 Emanuelson K.A., Kinzley C.E. 2000. Salmonellosis and subsequent abortion in two African Elephants ( Loxodonta africana ). IAAAM 2000. Heymans R, Vila A, van Heerwaarden C.A.M., Jansen C.C.C., Castelijn G.A.A.,van der Voort, Biesta-Peters E.G. (2018). Rapid detection and differentiation of Salmonella species, Salmonella Typhimurium and Salmonella Enteritidis by multiplex quantitative PCR. PLOS ONE 13(10) Molenaar, F.M and Silvestre S. 2021. Clinical approach to colic and collapse in an Asian elephant (Elephas maximus ) with Salmonella saintpaul septicaemia and subsequent ileus. Vet Rec Case Rep. 2021;e214. https://doi.org/10.1002/vrc2.214. Scharling F.S., Bertelsen M.F., Sós E., Bojesen A.M. 2021. Prevalence of Salmonella species, and Clostridium difficile in feces of healthy elephants (Loxodonta africana and Elephas maximus ). Journal of Zoo and Wildlife Medicine 51(4), 752-760. Scott W.A. 1984. Salmonellosis in an African elephant. Vet. Rec. October 13, 391. Windsor R.S. and Ashford W.A. 1972. Salmonella infection in the African elephant and the black rhinoceros. Tropical Animal Health and Production volume 4, pp 214–219. Windsor R.S. and W. A. Scott. 1976. Fascioliasis and Salmonellosis in African elephants in captivity. Br. vet., 132, 313 Websites: http://www.fao.org/3/T0610E/T0610E.pdf https://www.cdc.gov/salmonella/infantis-10-18/advice.html https://www.elephantcare.org/formulary Salmonellosis Case reports Abdominal pain and salmonellosis Salmonellosis in 7 yr-old Asian elephant Salmonella septicemia in adult Asian elephant

Pasteurellosis or hemorrhagic septicemia is an often fatal disease in Asian elephants, caused by Pasteurella multocida and Mannheimia hemolictica. If diagnosed in its early stage , antimicrobial and supportive treatment should be started immediately. Elephants in certain range countries are vaccinated twice a year with commercial vaccines used in cattle. In 2020 a mass die-off of free ranging African elephants occured in Zimbabwe and Botswana, caused by Pasteurella Bisgaard taxon 45 (multocida). To infectious diseases Pasteurellosis Pasteurellosis or hemorrhagic septicemia in Asian elephants has been report in several countries in Asia, where it is a common disease in water buffalo and other ruminants. In elephants it can cause a severe generalized disease, which is often fatal. The causative pathogens are Pasteurella multocida and Mannheimia (Pasteurella) haemolytica. They are nonmotile, facultative anaerobic and may exhibit bipolar staining with Giemsa or Wright’s stain. Transmission of the pathogen can be through direct or and indirect contact and possibly through biting insects and wound contamination. It is generally assumed that Pasteurella spp. are secondary pathogens that may strike when the immune system is challenged by a primary disease or stressful condition. Higher magnification of lung impression smear showed bipolar characteristic Pasteurella sp. ( Harish, 2009) Inapparent infections have not been reported, though vaccination-induced antibodies against P. multocida can be detected using an indirect ELISA (Tankaew, 2017). This indirect ELISA was more sensitive in elephants than the indirect hemagglutination assays (IHA), which is the WHO recommended diagnostic test in farm animals. The epidemiology of hemorrhagic septicemia is not fully known. However, multiple cases were reported following periods of consecutive droughts from 2010 to 2012 and sudden heavy monsoon rains in India in 2013 (Chandranaik, 2016). Clinical symptoms Clinical symptoms may vary, ranging from its presence in foot abscess to an acute fatal disease. The FAO manual for elephant managers describes the following signs, which might be associated with hemorrhagic septicemia: There is a high fever. Take the elephant's temperature. (See page 71.) If it is over 37.8° C or 100° F, that is a sign of danger. The breath exhaled from the mouth and trunk is very hot. There is a bright red at the eyes, mouth, the end of the trunk, and other soft tissue. Swelling (edema) is found in body parts such as the throat, the shoulders, the base of the tail, the anal flap, on the belly under the legs. The elephant is listless, the trunk rests on the ground, and the ears do not flap. The elephant does not eat. The elephant frequently opens its mouth to "yawn". The body trembles and has spasms because breathing is difficult. The urine is cloudy and richly coloured. In fatal cases pneumonia, hemorrhagic tracheitis, haemorrhages on the heart, and/or lesions of acute septicemia in all other vital organs have been described (Harish, 2009; Srivastav, 2017). Pasteurellosis presents in varies forms, so many other diseases must be considered in a differential diagnosis, including anthrax, trauma, foreign-body reactions, staphylococcosis, salmonellosis, and pneumonia caused by various agents. Diagnosis Isolation and identification of Pasteurella spp. or Mannheimia haemolyticum combined with a disease presence leads to the diagnosis of hemorrhagic septicemia. If diagnosed, one should always consider that there might be involvement of another primary disease process! Confirmation of the diagnosis by PCR may lead to the source of the infection if other elephants of other animal species are involved. Treatment Immediate treatment is required when hemorrhagic septicemia is suspected. Pasteurella sp. are usually susceptible to amoxycillin, trimethoprim+sulfa an fluoroquinolones (like enrofloxacin). Antimicrobial therapy can be initiated using one of the above mentioned drugs, however samples should be taken for culture and as soon as the sensitivity of the pathogens have been determined, the therapy should be adjusted according to the antibiogram results. Supportive therapy consists of administration of fluids (rectally and/or intravenously). NSAIDs should be given if the general condition or pain reactions indicate their use. For dosages go to: https://elephantcare.org/resources/formulary/drug-index/ . Make sure that no mahouts or other people who have been in contact with the ill elephant have any contact with the healthy ele phants. The healthy elephants should be taken to a place where they have no contact with dung, urine, or uneaten food of the infected elephant. Feed the elephant with items of high nutritional value, such as bananas, unhusked rice, sugarcane, and high quality browse . When an elephant dies of hemorrhagic septicemia, the carcass must be buried or burned. The carcass should not be butchered for meat or to remove the tusks to sell because this can spread the disease to other elephants and to other animals. The FAO has elaborated an action plan for additional measures in case of hemorrhagic septicemia in elephants ( see Elephant Care Manual for Mahouts and Camp Managers ): Immediately separate the infected elephant and keep it as far away as possible from other animals. Take the infected elephant to a clean, quiet and shady spot that is easily cleaned and where run-off water and waste, such as dung and uneaten food, do not contaminate other areas. Most importantly, ensure that the water source for sick animals and healthy animals is separate. If there is only one source of drinking water, it is likely contaminated. If so, try to get the healthy animals to a new source of water. You might even have to truck water in, but you must ensure your animals are drinking pure water free of infection. Prevention In several Asian range countries elephants are vaccinated with the vaccines available for cattle, like an inactivated aluminium-precipitated vaccine used in (non-pregnant) elephants over 6 months that used to work in the timber industry in Myanmar (5ml, subcutaneous, twice a year).(pers. Comm. Khyne U Mar, 2023). Contact with susceptible farm animals, especially water-buffaloes and cattle should be avoided. Outbreak of Pasteurellosis in free ranging African elephants During a period of 4 months in 2020 a total of 35 African elephants were found dead in north-western Zimbabwe. The estimated age of the dead elephants ranged from 18 months–30 years. Elephants of both sexes were found dead (16 males, 9 females). The carcasses were in average body condition with hepatomegaly and splenomegaly as the most prominent gross pathological findings, with variable hemorrhages across the epicardium, liver, lungs, intestinal serosae, hepatic and splenic lymph nodes, and in one case, the diaphragm. Histopathological lesions in elephants were similar and consisted of acute multifocal heterophilic and necrotizing inflammation in liver, spleen, and lymph node, with presence of intralesional Gram-negative bacterial colonies of coccobacillary morphology. Specifically, one elephant displayed necrotizing lesions in spleen and liver, with the additional presence of fibrinocellular and bacterial emboli in the pulmonary vasculature. Presence of Gram-negative bacterial colonies without associated morphological changes was observed in veins and capillaries, prominently in the encephalon. Acute multifocal heterophilic and necrotizing lymphadenitis, hepatitis and splenitis with intralesional Gram-negative coccobacilli was observed in one. Most blood smears (n = 13/15) stained with Giemsa contained small to moderate numbers of bacteria with a bipolar, short-rod, or coccobacilli morphology (0.5–2 µm), and intracellular bacteria were observed. Of 15 sampled elephants, six showed molecular evidence of septicemic infection by Bisgaard taxon 45. There was no evidence of toxins, including those from cyanobacteria, or for any viral infection. The failure to identify Bisgaard taxon 45 in samples from all 15 elephants is likely due sample quality and delays in testing. The authors propose that stress from a combination of heat, drought, and population density were likely contributing factors in this outbreak. Food and water resources normally wane as temperatures rise during the dry season, and elephants must travel increasing distances between water points and foraging areas. The source of infection and route of transmission remain unknown in this outbreak. For more details about this mass die-off, click here . References Chandranaik BM., Shivashankar BP., Giridhar P., and Nagaraju DN. 2016. Molecular characterisation and serotyping of Pasteurella multocida isolates from Asiatic elephants (Elephas maximus ). Eur J Wildl Res (2016) 62:681–685 FAO: Elephant Care Manual for Mahouts and Camp Managers. Foggin, C.M., Rosen, L.E., Henton, M.M. et al. Pasteurella sp. associated with fatal septicaemia in six African elephants. Nat Commun 14, 6398 (2023). https://doi.org/10.1038/s41467-023-41987-z Harish, B.R., B.M. Shivaraj, B.M. Chandranaik, M.D. Venkatesh & C. Renukaprasad. 2009. Hemorrhagic Septicemia in Asian Elephants (Elephas maximus ) in Karnataka state, India. Journal of Threatened Taxa 1(3): 194- 195 . Preecha Phuangkum P., Lair RC., and Angkawanith T. 2002. Elephant Care Manual for Mahouts and Camp Managers. FAO. ISBN: 974-7946-71-8. Shrivastav AB., Rokde A., Agarwal S., and Shrivastav G. 2017. Pasturollesis: Complication of Metastatic Supporative Pneumonia Severe Stress in Asian Elephant (Elephas maximus ). Indian Journal of Veterinary Sciences & Bio technology (2017) Volume 12, Issue 4, 93-94. Tankaew P., Singh-La T., Titaram C., Punyapornwittaya V., Vongchan P., Sawada T., Sthitmatee N. 2017. Evaluation of an In-house indirect ELISA for detection of antibody against haemorrhagic septicemia in Asian elephants Journal of Microbiological Methods. Vol.134, pp30-34. Weston P. 2023. It took years to solve the mystery elephant deaths. Now, the threat is spreading. The Guardian, 2023 10 23.

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) Botulism (C. botulinum) 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) Clostridium novyi 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. To page top 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. Serum transfusion with serum from a vaccinated elephant should be considered (after cross-matching). 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 Goss, L.J. 1942. Tetanus in an elephant. Elephas maximus. Zoologica NY 27:5–6. Burke, T.J. 1975. Probable tetanus in an Asian elephant. JZ&WM, vol 6 – 1 22-24 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. 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 Transmissible Diseases Handbook. 2019. Infectious diseases Fact sheet TETANUS (Annex 4) 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 https://ceh.vetmed.ucdavis.edu/health-topics/tetanus 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: I V 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: 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. 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. 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. 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. 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. 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. Rahman H., Chakraborty A., Rahman T., Sharma R., Shome B.R. and Shakuntala I. 2009. Clostridial myonecrosis clinically resembling black quarter in an Indian elephant ( Elephas maximus ) Rev. sci. tech. Off. int. Epiz., 2009, 28 (3), 1069-1075, 2009. To page top Enterotoxemia 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. To page top Clostridium difficile Malignant edema 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. Clostridium novyi Report by Dr. Arun Zachariah et al. (Kerala Forests and Wildlife Department, Kerala, India) 19th International Elephant Conservation and Research Symposium, 2023 Chiangmai - International Elephant Foundation Since 2014, unusual mortality was observed in Asian elephants in Kerala state of South India.26 per acute mortalities were observed in a wild elephant population within a span of two years. Whereas two captive elephants were found dead with similar lesions but sporadic in nature. These animal deaths were per acute with quick autolytic changes and discharge of serosanguineous fluids from external orifices mainly anus. Possibility for Anthrax was ruled. Detailed autopsies were conducted in all the animals. Gross pathological lesions were identified as, petechial to echymotic hemorrhages in major organs, liver was friable with accumulation of gas in the parenchyma, blackening of the sub-cutaneous muscles and accumulation of serosanguineous fluid in the abdominal and pericardial cavity. Gram-positive spore bearing bacteria were seen in blood smear examination. Histologically, there was coagulative necrosis surrounded by inflammatory cells and large numbers of gram-positive rods were observed. High throughput sequencing of conserved 16S ribosomal gene revealed abundance of C.novyi in various tissue samples. Further, liver samples tested by PCR were positive for C. novyi type B flagellin and alpha toxin genes, but negative for other pathologic clostridia. Clostridium novyi type B causes infectious necrotic hepatitis in sheep and less frequently in other species. However reports of C.novyi infections in wild animals were scanty except for few species like Bighorn sheep and farmed Reindeer but not in outbreak proportions. This is the first report of C. novyi infection and mortality in Asian elephants in a large scale. Clostridium novyi Black leg 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. To page top To page top 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. Click here to see for a full description of the histological lesions in the case report described here . 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 Andrés Gamazo PJ, Pavón E, Stumpel J, Bouts T, Schaftenaar W, Kik M, de los Ángeles Jiménez Martínez M. 2023. Botulism outbreak in Asian elephants: histopathological findings at necropsy. Poster at ESVP-ECVP Congress, August 2023, Lisbon. 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 Botulism

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