Locomotion problems in elephants are usually symptoms of degenerative joint diseases and lesions of the pad or nail. This chapter describes (1) the diagnosis of orthopedic problems (observationa and video recording, radiology, thermology), (2) nail issues, (3) sole/pad issues, (4) degenerative joint disease and some miscellaneous problems related to lameness. Continue Orthopedic problems This chapter consists of the following paragraphs: Normal features of the locomotion system Sole-related clinical problems Nail-related clinical problems Lameness / abnormal locomotion Prevention of orthopedic problems Radiography elephant foot Elephants do not often show signs of lameness. Nevertheless, orthopedic problems are quite common. A survey about the causes of death in the European studbooks of African and Asian elephants over 5 years of age, revealed that in 12% and 30% respectively of the cases, orthopedic problems played a major role in the cause of death (Hess 2022). The most frequently reported problems are related to the feet, joints and muscles. A special issue is the occurrence of metabolic bone disease in bottle-raised young elephants. Normal features of the locomotion system Normal featurs Anatomical features of the skeleton The elephant has some special features that distinguishes them from other mammals. The long bones are massive, lacking the typical bone marrow cavities. Instead, the long bones of elephants are completely filled with dense cancellous bone, where hemopoiesis is taking place. In the standing elephant, the angles of the joints are almost straight. The neck is relatively short. Figure 1: Asian elephant (Green Hill Valley, Myanmar). Figure 2: African elephant skeleton (Veterinary Faculty Utrecht University, the Netherlands) Foot anatomy terms Front foot = fore foot = manus Hind foot = rear foot = pes Phalanges = toes = digits Pad = sole = slipper Palmar = front pad Plantar = back pad Carpus = wrist Tarsus = ankle Nail = horn wall + nail pad horn Fat cushions Each foot of the elephant is equipped with a large subcutaneous cushions which play an important role in distributing forces during weight bearing and in storing or absorbing mechanical forces. One study about these cushions in the African elephant was published by Weissengruber in 2006 . In both the forelimb and the hindlimb a 6th ray, the prepollex or prehallux, is present. These cartilaginous rods support the metacarpal or metatarsal compartment of the cushions. None of the rays touches the ground directly. The cushions consist of sheets or strands of fibrous connective tissue forming larger metacarpal/metatarsal and digital compartments and smaller chambers which are filled with adipose tissue. The compartments are situated between tarsal, metatarsal, metacarpal bones, proximal phalanges or other structures of the locomotor apparatus covering the bones palmarly/plantarly and the thick sole skin. Within the cushions, collagen, reticulin and elastic fibres are found. In the main parts, vascular supply is good and numerous nerves course within the entire cushion. The high concentration of sensory receptors such as Vater–Pacinian corpuscles within the cushion and Meissner corpuscles in dermal papillae of the adjacent skin might rank an elephant’s foot among the most sensitive parts of its body. Together, the mechanical and sensory functions of the feet enhance the ability of elephants effectively to move through and analyse their physical environment. The micromorphology of elephant feet cushions resembles that of digital cushions in cattle or of the foot pads in humans but not that of digital cushions in horses. Copied illustration of the foot anatomy from Weissengruber et al., 2006 (doi: 10.1111/j.1469-7580.2006.00648.x Normal locomotion Elephants predominantly support on their pads (foot soles). The nails are not used to force locomotion. This is nicely demonstrated in the slow-motion video below (BBC). During walking the head of the elephant shows minimal movements. If there is any form of lameness, especially in one of the front legs, the animal might use its head to facilitate the movement of the front leg in cranial direction. In the absence of orthopedic problems, the hind feet are placed cranial to the foot step of the front foot on the same side. This is clearly demonstrated in the slow-motion video of African elephants in the Namibian desert below (BBC) and the normal-speed video of an adult Asian elephant bull in Vietnam. Elephants can't trot, canter, gallop or jump. They always walk in normal gait. When they walk slowly, their speed is approximately 4 km/h (2.5 miles/h). However, they can reach a speed of 25-60 km/h (16-25 miles/h) over a short distance. The hind foot is placed in the foor print of the front foot or even slight more cranial. Normal anatomical features of the elephant foot Usually the forefeet of the Asian elephant have 5 nails and the hind feet only 4. The African elephant has 4 nails on the forefoot and 3 on the rear one. The weight of the body is evenly distributed over the toes by means of a thick cushion , placed between the sole and the phalanges (photo African elephant foot Kruger National Park, South Africa). The digits form a ±45° angle with the sole, as shown in the radiograph below (Fowler and Mikota 2006). This photo shows the longitudinal section of the elephant foot with the sole, nail, phalangeal bones, cushion and tendons. Note the short distance between the nail and the distal phalangeal bone (Fowler and Mikota 2006) The nails are numbered medial to lateral. If there are 4 nails in front they are numbered 2,3,4,5. The bones don’t change – there are always 5 digits so digit 1 is still there but there in no associated nail. In Asian elephants there are typically 4 nails on the rear foot so they are numbered 2,3,4,5. The African elephant's toes are numbered 5,4,3,2 (front) and 5,4,3 (rear) respectively. This diagram shows the bones of the front foot and the respective phalanges of an Asian elephant (Fowler&Mikota 2006) This diagram shows the bones of the hind foot and the respective phalanges of an Asian elephant (Fowler&Mikota 2006) Radiograph of the left front foot of an Asian elephant, showing the phalangeal bones P1,P2 and P3 (Fowler&Mikota 2006) Sixth toe The elephant has unique cartilaginous structures in the feet that are thought to have a stabilizing function. In the front foot the structure is is called a prepollex. It attaches between the first carpal bone and the first metacarpal bone and extends to the sole. In the hind foot it is called a prehallux. A recent study has claimed that this structure should be considered a sixth toe because over time the tissue becomes hard like bone. The healthy sole The sole (pad or slipper) of the elephant's foot is a thick cornified but flexible integumentory structure, with a surface relief that looks almost similar to the skin. It is important to respect this surface when performing pedicure. The thick sole must protect the elephant from penetrating trauma by foreign bodies. A healthy sole is maintained by providing a dry environment. Long periods in muddy and humid circumstances can lead to sole injuries and even sole detachment. The photos show the nicely structured sole of a (dead) wild African elephant (Kruger National Park, South-Africa) and the sole of a captive Asian elephant. The sole of the elephant foot should have a minimum thickness of 2 cm. This can be measured by ultrasound examination. Its surface should be rough with a distinct relief. The growth of the sole epithelium is from 0.5 to 1.0 cm per month. If the sole does not wear sufficiently, it becomes thickened, and because the thickening is seldom uniform, defects are produced that lead to pocket formation and overgrowth, which sets the stage for infection. The healthy nail The nail consists of two parts: the wall and the sole part, which are connected at the sole side. This junction is an important area where infections can emerge if its integrity has been severed by excessive abrasion on hard floors (concrete stable, tar roads) or wrong pedicure. This connection site is comparable with the so-called 'white zone' in hoofed mammals. The white line (or white zone) structure is illustrated in the figures and photos below (Benz, 2005). The nails should be shorter than the pad, without cracks and U-shaped. The skin in between 2 nails should be clean and flexible. When there is hyperkeratosis in this area, this may cause discomfort to the elephant as the hard hyperkeratotic tissue acts as a foreign body by pinching the interdigital skin an dirt can accumulate into the interdigital space. There should be room for at least one finger between 2 nails. The thermographic images of a healthy nails shows a regular distribution of the temperature dispersed over the entire nail. Like in hoofed mammals, the nails are connected with the underlying phalanges by lamellae or horn leaflets. Benz (2005) describes the different parts of the nail: a: corial part of the horn wall: cuticle area b: lamellae (horn leaflets) c: white zone d: sole horn Cuticle and sweat glands The cuticle of the nail is the keratinized skin at the junction with the nail. They should be soft and flexible. This is a vulnerable area as microorganisms may pass this natural barrier after (micro)trauma. The elephant seems to maintain the cuticles by rubbing them gently against objects. Elephants that are kept in moist, muddy conditions, are likely to develop problems with the cuticles. They may overgrow and become hardened when they dry, resulting in cracks and infection. During pedicure, one should be well aware of the protecting function of the cuticles and never remove more than necessary. References Benz, A. 2005. The elephant’s hoof: Macroscopic and microscopic morphology of defined locations under consideration of pathological changes. Master's thesis, Veterinary Faculty of the University Zürich, Switzerland. Fowler M.E. and Mikota S.K. 2006. Biology, Medicine, and Surgery of Elephants. 271-290. Hess A. 2022. 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 Master's thesis, Department of Exotic Animal and Wildlife Medicine University of Veterinary Medicine Budapest, Hungary. Schiffmann C. 2021. Posture Abnormalities as Indicators of Musculoskeletal Disorders in 12 Zoo Elephants – a Visual Guide. Gajah 53 (2021) 20-29. Weissengruber, G.E., Egger, G.F., Hutchinson, J.R., Groenewald, H.B., Elsässer, L., Famini, D. and Forstenpointner, G. (2006), The structure of the cushions in the feet of African elephants (Loxodonta africana). Journal of Anatomy, 209: 781-792. https://doi.org/10.1111/j.1469-7580.2006.00648.x To page top

Nail issues in elephants are common and usually need treatment. Pedicure should be part of the management procedures. Untreated nail cracks can result in osteoarthritis of the phalangeal joints. Radiography procedures are described in this chapter. Back to index orthopedic problems Nail lesions The most common nail lesion is the crack , perpendicular to the ground. These cracks are often the result of overpressure on the nail tip, when the nail is longer than the sole. In that situation, each step the elephant makes results in heavy forces on the nail tip during the phase when the elephant unwinds its foot. As demonstrated clearly in the slow-motion video below, the tip of the elephant's nails hardly touches the ground. When the nail becomes too long like in the Asian elephant nail in this photo, the excessive pressure on the nail edge can cause a small crack that enlarges over time if not properly treated. Cracks in the nails of an African elephant When left untreated, these cracks will become larger and can affect deeper structures, resulting in an abscess , pododermatitis or even osteomyelitis of the phalangeal bones. If only the horn-producing tissue is involved, we usually call this a pododermatitis. When the infection is trapped in the underlying tissue, an abscess can easily develop. Onychia is an infection or trauma to the horn lamellae of the nail, which may result in complete loss of the nail. Pododermatitis in the nail of an African elephant. Note the excessive wear of the sole. Nail abscess with osteolysis in an Asian elephant. Nail abscess with complete loss of the 2 distal phalanges osteolysis in an Asian elephant. If phalanges are affected as the result of a deep nail abscess and pododermatitis, the recommended treatment of such an osteitis is the surgical removal of the affected bones. Click here to read more about this treatment. More examples of nail abscesses (photos: Susan Mikota). Treatment may take a long time, requiring multiple pedicure sessions, daily cleaning and foot soaks (click here for foot soak information) Traumatic onychia in an Asian elephant. Complete nail loss due to traumatic onychia in an Asian elephant. Diagnostic procedures nail lesions Use your eyes: check if there is any visible lameness. Describe the visible lesions. Use your hand: does the affected area feels warm? Is it painful when pressure is applied? Use your nose: if there is a wound, try to identify the smell of necrosis. Take a swab for bacterial culture. Additional diagnostic steps: If there is a deep lesion: radiographs should be taken to look at the integrety of the underlying bony structures (phalanges and phalangeal joints). Thermography may help to identify if the affected area has a higher temperature than the surrounding tissues. Radiography of the elephant's foot Radiography foot A powerful portable X-ray machine (100 kV or more) is required to visualize the bony structures in the elephant foot. Digital plates largely increase the quality of the image. It is important to work under safe conditions. Under free contact management , the fore foot can be positioned on a stand for the oblique palmar-dorsal shooting direction. The angle required for visualization of the phalangeal joints is indicated in the images below. Oblique palmar-dorsal image of the hind foot under free contact management condition (Mumby et al 2015) Positioning for the oblique dorsal-plantar image of the hind foot, this foot can be can be positioned on a stand (Mumby et al 2015). A different approach is required when working under protected contact management . The elephant needs to be trained to position its legs on a horizontal bar of the training wall. It should also be accustomed to the proximity of the X-ray-machine, the plate and the protective clothing of the operators. Lateral shooting position of the right front foot of an Asian elephant under protected contact. The angle of the beam depends on which phalanges need to be visualized. To avoid superposition and depending on the selected phalanges, the beam should have a more or less oblique direction. (Courtesy Rotterdam Zoo). Oblique dorsal-plantar shooting position of the left rear foot (Courtesy Rotterdam Zoo). Click here to view the radiograph. Oblique palmar-dorsal shooting postion of the right front foot of an Asian elephant under protected contact. Note that the X-ray machine is positioned upside down (use a support block to protect the electric wires)! (Courtesy Rotterdam Zoo and Emmen Zoo). Click here to view the radiograph. Lateral shooting postion of the left hind foot of an Asian elephant under protected contact (Courtesy Rotterdam Zoo). Click here to view the radiograph. Some examples of radiographs of the distal part of the right front leg of a 24 yr-old female Asian elephant at Rotterdam Zoo (the Netherlands) are shown below. The elephant is under standing sedation for an unrelated reason. Lateral shooting position of the right front leg (distal part of the radius and ulna, Courtesy Rotterdam Zoo). Click here to view the radiograph. Anterior-posterior shooting position of the right radio-carpal and ulnar carpal joint AP front leg (Courtesy Rotterdam Zoo). Click here to view the radiograph. Posterior-anterior shooting position of the right radial-carpal and ulnar-carpal joint (Courtesy Rotterdam Zoo). Click here to view the radiograph. Lateral position of the right carpal joint (Courtesy Rotterdam Zoo). Click here to view the radiograph. Lateral shooting position of the right foot (Courtesy Rotterdam Zoo). Click here to view the radiograph. Lateral shooting position of the right tarsal joint (Courtesy Rotterdam Zoo). Click here to view the radiograph. Lateral shooting position of the right tarsal joint (Courtesy Rotterdam Zoo). Click here to view the radiograph. Posterior-anterior shooting position of the right tarsal joint (Courtesy Rotterdam Zoo). Stereo radiography A technique, which is called stereo radiography can help interpreting the X-rays. Two radiographs of the same areas are made each of them taken 10 cm more lateral from the other. Digital images were converted to bitmap (BMP) format to preserve image quality. The 3D stereoradiograph images can be constructed using special software (Bentley 2021). The images can be viewed with red-cyan 3D glasses. Illustration of how 3D stereoradiograph images are produced. (a) Original radiograph that provides the ‘‘left’’ image for the 3D Anaglyph software. (b) Paired radiograph used for ‘‘right’’ image. (c) Completed stereoradiograph that has been inverted with red-cyan settings applied. (Bentley 2021) Thermography of nail lesions Thermographic imaging can be used to measure the absolute temperature and the difference in temperature between the lesion and its surrounding tissues. Below a severe case of a nail abscess-related osteomyelitis and osteolysis of Ph4 in an old Asian elephant bulls is shown. The thermografic image shows a low temperature of the skin that covers the affected are. This is suggestive for a large necro-purulent process. The thermographic image shown here demonstrates the low temperature of the skin covering the abscess, associated with deep lesions of D4 of the left front leg of an Asian elephant bull, involving a lot of necrosis and complete loss of the distal phalanx of the toe. On radiology this bone is completely missing and the distal part of the toe shows an irregular surface: Osteomyelitis and purulent arthritis of the Ph3-4 joint of D4. Treatment nail lesions Treatment of nail lesions Pedicure is usually the treatment of choice in cases of nail lesions. There are a few principles to be respected in pedicure: Use proper equipment Always remove all abnormal horn tissue (undermined, infected) and loose nail flaps. Make the transition from healthy horn to the deepest point of the lesion as smooth as possible. Directly adjacent to the lesion, the horn must be flexible and as thin as a piece of paper. Permanently check this flexibility by gently pressing the area where just cut away the horn. The most important pieces of equipment needed for pedicure are 2 hoof knives (left and right handed), a scalpel and a sharpening stone for hoof knives, preferably with round edges (see photos above). Just with hoof knives alone, most of the clinical pedicure treatment can be done. A scalpel can be useful when very small pieces of horn are to be removed adjacent to a lesion. A horse hoof rasp is a useful tool to shorten the nail and remove excessive horn from the sole. Care should be taken NOT to make the nail edges round, what is often practiced (see below). A strong nail brush is needed for cleaning the nail prior to pedicure and a smaller brush can be used to remove dirt from areas that cannot be reached by a large brush. Small wood carving knives can be used when thin layers of nail horn are to be removed (similar to the use of a scalpel). Pedicure equipment Very often the tip of the nails are made round by rasping the corners. There is no justification for doing so rather than a cosmetic one. However, one should avoid to remove tissue from the nail wall/nale sole junction (comparible to the "white line " in the horse hoof) as this junction is a very important barrier against infiltration of dirt and pathogens. So the advice is: do not file the nail corners to leave the entire white line in tact. Situation before a pedicure session of a deep nail crack Situation after a pedicure session of a deep nail crack Pedicure around a (deep) crack serves 2 main purposes: Draining of infected area Removing pressure on the wound, which enables the regeneration of destroyed horn lamellae. In order to achieve both goals, the deepest point of the crack has to be freed from covering horn. One should start making the horn wall thinner at a distance of several centimeters from the lesion and continue the pedicure towards the deepest point in a gradual way. Each nail crack should be considered as being a wound, because the crack has usually damaged the horn lamellae. When the pedicure has reached the wound area, it is of utmost importance that the edges bordering the wound are made as thin and flexible as possible. Check this by pressing your finger on the horn adjacent to the wound. Large cracks usually need to be treated in several sessions. Bleeding may occur when the lamellae are cut, which is no direct reason to worry! Pain reactions of the elephant will tell the operator when the session should be stopped and continued a few days later Cuticle lesions The cuticles form a natural barrier against dirt and pathogens. When they overgrow the nails, this protective barrier is weakened and infiltration of microoganisms may result in lesions in the horn lamellae underneath the nail (onychia). Sweat glands are embedded in the cuticles. Overgrown cuticles may become hard and crack or form interdigital callus. When abnormal horn tissue blocks the sweat glands, fluid pockets may be formed. This can be a painful process and needs to be treated. Minor cuticle lesion in a African elephant, which may be connected to a deeper lesion underneath the nail. Explorative pedicure is probably needed to find the cause (Courtesy: Barcelona Zoo) Extensive overgrown cuticles with feathering and interdigital callus formation (Fowler & Mikota 2006) Interdigital callus formation in an Asian elephant (Courtesy: Susan Mikota) Sweat glands are present in large numbers in the cuticles. When the cuticles are overgrown, they may form pockets in which the sweat-fluid may accumulate ("blisters"or "blebs"). When cutting in such a fluid-filled pocket, the contents may squirt out (see video; courtesy: Susan Mikota). Careful (!) trimming of the cuticles is only indicated when they have overgrown the nail (Courtesy: Susan Mikota) Applying oil on the cuticles will make them softer and may resolve the problem of cuticle overgrowth in most situations. Example of a pedicure procedure of a pododermatitis in conjunction with a cuticle lesion in an African elephant (courtesy Barcelona Zoo) Pododermatitis in the nail of an African elephant. Note the excessive wear of the sole and the large defect of the cuticle. Second step: follow-up the necrotic tissue and find the connection with the cuticle defect. Note that a large part of the nail was undermined, causing the cuticle defect. First step in pedicure: making the horn on each side of the lesion thinner and removing necrotic tissues. By frequently removing all necrotic tissues and keeping the edges of the wound thin, the horn lamellae can produce healthy horn again. SUCCESSFUL TREATMENT OF DIGITAL OSTEITIS BY INTRAVENOUS REGIONAL PERFUSION OF CEFTIOFUR IN AN AFRICAN ELEPHANT (Loxodonta africana ) (Dutton C.J., Delnatte P.G., Hollamby S.R., and Crawshaw G.J. Journal of Zoo and Wildlife Medicine 48(2): 554–558, 2017) A 41-yr-old African elephant (Loxodonta africana) presented with a swollen third digit of the left forelimb and a 2-cm hole in the pad. Corrective trimming, topical treatments, and an oral antibiotic resulted in apparent resolution; however, it reoccurred after 4 mo. Radiographs suggested bone lysis in the third phalanx, with the primary differential diagnosis being septic osteitis. Flushing with metronidazole solution and intravenous regional perfusion (IVRP) of the foot were commenced. A tourniquet was applied just above the carpus, an interdigital vein was identified by ultrasound, and into this vein 2 g (20 ml) of ceftiofur sodium solution, followed by 60 ml of heparinized saline, was administered. The foot was kept raised for 25 min and then the tourniquet was removed. IVRP was repeated every other day for 70 treatments over 6 mo. Healing occurred, which was confirmed radiographically. IVRP offers an excellent treatment modality in a well-trained elephant. SURGICAL REMOVAL OF INFECTED PHALANGES FROM AN ASIAN ELEPHANT (Elephas maximus ) Gage, L. Blasko D, Fowler M.E. and Pascoe J. Joint Conference AAZ/WDA/AAWV After unsuccessful antimicrobial treatment of an osteitis in a 40 yr-old Asian elephant, surgical removal of the affected phalanges resulted in the complete healing of the foot. Click here to read the report. Digital osteitis treatment Literature Bentley C.E., Cracknell J.N., Kitchener A.C., Pereira Y.M., Pizzi R. 2021. Improved diagnosis of foot osteoarthritis in elephants (Elephas maximus , Loxodonta africana ) using stereoradiography. Journal of Zoo and Wildlife Medicine 52(1): 67–74, 2021. Dutton C.J., Delnatte P.G., Hollamby S.R., and Crawshaw G.J. 2017. Successfull treatment of digital osteitis by intravenous regional prefusion of ceftiofur in an african elephant (Loxodonta africana) . Journal of Zoo and Wildlife Medicine 48(2): 554–558, 2017). Gage, L. Blasko D, Fowler M.E. and Pascoe J. 1995. Surgical removal of infected phalanges from an asian elephant (Elephas maximus ). Joint conference AAZV / WDA/ AAWV . Mumby, C., Bouts, T., Sambrook, L., Danika, S., Rees, E., Parry, A., Rendle, M., Masters, N. and Weller, R. (2013), Validation of a new radiographic protocol for Asian elephant feet and description of their radiographic anatomy. Veterinary Record, 173: 318-318. https://doi.org/10.1136/vr.101696 . Fowler M.E. and Mikota S.K. 2006. Biology, Medicine, and Surgery of Elephants. 271-290. To page top

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. 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

The morphology of elephant blood cells is described and demonstrated by photos. To hematology Hematology gallery Compiled by: Willem Schaftenaar and Fieke Molenaar On this page we give examples of normal blood cells stained with Wright-Giemsa. An excellent description of normal and abnormal white blood cells in elephants was published by Stasi et al in 2017. Click here to read that article. Morphology of blood cells, stained with Wright-Giemsa Wright-Giemsa stained blood smear of a healthy adult Asian elephant displaying normal erythrocytes, 1 heterophil, 1 bi-lobed monocyte and several thrombocytes (Courtesy: Rotterdam Zoo). Wright-Giemsa stained blood smear of a healthy adult Asian elephant displaying normal erythrocytes, 1 bi-lobed monocyte, 1 lymphocyte and several thrombocytes (Courtesy: Rotterdam Zoo). The images below were published in the Proceedings of the Zoo and Wildlife Health Conference 2020, 23-31: Molenaar F.M. 2020. Developing haematology skills to enable decision making in suspected cases of Elephant Endotheliotropic Herpesvirus hemorrhagic disease. Heterophil (H), single lobed and bi-lobed monocytes (M), lymphocyte (L). The arrows pont at platelets (Courtesy: Fieke Molenaar). Immature heterophils: bands (Courtesy: Fieke Molenaar). Eosinophil (Courtesy: Fieke Molenaar). Lymphocyte (Courtesy: Fieke Molenaar). Immature lymphocyte (Courtesy: Fieke Molenaar). Monocyte (Courtesy: Fieke Molenaar). Monocytes (Courtesy: Fieke Molenaar). Immature monocytes (Courtesy: Fieke Molenaar). Lymphocyte and 2 monocytes (Courtesy: Fieke Molenaar). Platelets (arrows) (Courtesy: Fieke Molenaar). Erythrocytes: "codocytes" (target cells with a bulls-eye appearance) occur naturally in elephants (Courtesy: Fieke Molenaar). Fragmented erythrocytes Fragments of erythrocytes (schistocytes) as can be seen in elephants suffering of Disseminated Intravascular Coagulation (e.g. EEHV-HD) (Courtesy: Fieke Molenaar). To page top

Sharing clinical cases amongst elephant veterinatians and caretakers will increase our knowledge, so we can treat elephants better. Knowledge Elephant medicine is a specialism that is usually obtained after many years of working with elephants. Compared to the amount of literature that is available for equine practicioners, the amount of literature about elephant medicine is very limited. Recognition On this website we collect clinical data from field workers in range countries and zoos. By showing these experiences on this website, we hope to help you, veterinarians and elephant care takers, when you are confronted with a clinical problem. Maybe you recognize similar symptoms and syndromes in your sick animal and learn how your case might be treated. Sharing By using the contact button, you can share your information and questions with us, so we can add new opinions to the existing case reports or add a new report. WHY THIS WEBSITE?

Necropsy index Necropsy procedure (videos) Necropsy protocol forms

This page describes the technique of blood collection and hematology with special attention to white blood cell counts in elephants (because of different monocytes, manual counting is required in elephants). Hematology Blood collection Hematology Blood chemistry Reference values blood Blood collection There are 3 anatomical sites on the elephants body where blood can be collected: One of the ear veins (or arteries for arterial blood sample) One of the branches of the saphenous veins (hindlegs) Cephalic vein (front legs) How to collect a blood sample: Most elephants can be trained for this procedure using positive reinforcement training. If not trained, standing sedation (or general anesthesia) in case of free ranging elephants) will be required. When alpha-2 agonists are used , vasoconstriction may hinder the access to the ear veins, especially in young calves. Combining alpha-2 agonists with butorphanol may help to increase the filling of these veins. When the environmental temperature is low, the ear veins may collapse. Flushing the inner side of the ear with large amounts of warm water (or packing the area with heated bean or rice bags) can increase the filling of these veins. The collection site should be clean and dry before blood is collected. Ear veins : press firmly on the site where you can see the shape of the vein. Press until you see the vein becoming larger in diameter. Use a small butterfly needle and collect the blood in a vacuum blood tube. If not available, you can use a small needle (23G) and a syringe and empty the syringe in the blood collection tube after removing the needle. To avoid damaging the blood cells (hemolysis), the tube should be filled slowly while flushing the blood carefully against the wall of the tube, that is slightly tilted. Saphenous and cephalic veins : these veins are larger in diameter than the ear veins, but covered by a thicker skin. A 19G or 21G needle (preferably connected to a vacuum tube) can be used and should be inserted perpendicular to the skin. Indication of the blood collection sites on the front leg (left photo, Vena cephalica) and the inner side of the hind leg (middle and right photo, Vena saphena). Blood collection from the inner side of the ear using a butterfly needle and vaccum tube. Blood cellection from the inner side of the hind leg of a well-trained adult Asian elephant bull using a vacuum bottle for collecting large amounts. Courtesy: Rotterdam Zoo Hematology This chapter includes a lab manual that was developed for a Healthcare and Welfare Workshop for elephant veterinarians given in Myanmar in 2018, organized by Elephant Care Asia (an initiative or elephant Care International - http://elephantcare.org/ . Get PDF of the manual PLEASE NOTE: white blood cell differentiation in elephants must always be done by MANUAL DIFFERENTIATION Erythrocytes: Erythrocytes in elephant whole blood EDTA samples can best be counted on an automated blood cell analyzer. Such an analyzer automatically measures the hematocrit . After centrifugation of the blood sample, a plasma evaluation should always be performed. The morphology of the erythocytes should be examined microscopically in a (preferably fresh) blood smear , stained with Wright-Giemsa. If no automated cell counter is available, manual erythrocyte count is a second option. Total white Blood count (WBC): Automated analyzers have limited value in elephant hematology. However, they can be used to measure the total amount of white blood cell. Automated cell counters come in several forms. Those used for other mammalians can only be used for total WBC in elephants. Manual WBC count can be done using a Hemocytometer Counting Chamber . Differential White Blood Cell (WBC) count: Automated analyzers cannot be used to differentiate the white blood cells of elephants. This should ALWAYS be done by manual counting the different cell types on blood smears , stained with Wright-Giemsa. See also the Manual Differential WBC Count . Platelets: Estimating the platelet count is best done by calculating the average of platelets counts in 10 fields x 15,000, which gives the Estimated platelet count/µL . See also: Manual platelet count (Cornell University) . Reference values: The table below shows the normal hematology values for Asian and African elephants (Wiedner, E. 2015). References Perryn K.L. et al. 2020. Biological variation of hematology and biochemistry parameters for Asian elephant (Elephas maximus), and applicability of population-derived reference intervals. Journal of Zoo and Wildlife Medicine 51(3): 643–651 Steyrer C, Miller M, Hewlett J, Buss P and Hooijberg EH (2021) Reference Intervals for Hematology and Clinical Chemistry for the African Elephant (Loxodonta africana). Front. Vet. Sci. 8:599387 Weisbrod T.C., Isaza R., Cray C., Adler L., and Stacy N.I. 2021. The importance of manual white blood cell differential counts and platelet estimates in elephant hematology: blood film review is essential. Veterinary Quarterly, 41:1, 30-35, DOI: 10.1080/01652176.2020.1867329. (Click here for the complete text). Wiedner E. 2015. Proboscidea. In: Fowler's Zoo and Wild animal Medicine 8. Species 360 - ZIMS 2023. Reference values To hematology gallery Back to Top To lab diagnosis Hematology Blood collection

An adult Asian elephant suffered form a severe infection of Salmonellosis (S. saintpaul). It went down and was unresponsive. Hematology and treatment results are discussed. To Salmonellosis Next case Next case Case Report Next case Salomonella saintpaul septicemia in an adult Asian elephant Next case Date: 2021 Location: Italy (zoo) Submitted by: Fieke Molenaar DVM and Pasqualino Silvestre DVM History Three months after the move to another zoo, a 37 year-old female Asian elephant (Elephas maximus) presented mild lethargy and a reduction of food and water intake. Mild colics were suspected and the elephant was treated with non-steroidal anti-inflammatories (NSAID, meloxicam i.m. ~ 0.2 mg/kg) and spasmolytics (metamizole and butylscopolamine bromide i.m., ~ 80 and 5mg/kg). As no improvement was noticed on Day 2, a standing sedation was carried out (detomidine i.m., ~ 0.018 mg/kg, and butorphanol (i.m., ~ 0.017 mg/kg). Rectal fluids (20 L of hand-warm tap water) and i.v. fluids (4 L of 0.9% saline solution) were administered, as well as i.m. injections with amoxicillin (~ 15 mg/kg), vitamin B-complex and vitamin E/selenium. Flunixin meglumine was given in the auricular vein. Sedation was reversed using atipamezole (i.m., ~ 0.05 mg/kg). Blood was collected during this procedure. Unfortunately, the elephant collapsed 9 hours later in lateral recumbency. The animal was unresponsive and could be approached while it kept its eyes wide open (see videos). The araol mucosa was very pale. After 25 minutes it managed to stand up without any assistance but remained lethargic. Respiration was shallow. During the night the elephant went down in lateral recumbency again. During the following 5 days, the elephant was sedated every day for treatment and blood collection. Next case Collapsed Asian elephant due to septicemia caused by Salmonella saintpaul . Note the pale oral mucosa. The state of paralysis very much looks like the paralysis seen in botulism ( see case report ). Laboratory results: Hematology: Leucopenia was evident on the first blood smear that was made, with a clear increase of bands and a reduction of matured heterophils. An interesting finding was the presence of immature granulocytes (myelocytes) that could not be identified exactly. The platelet count was low and schistocytes (fragments of erythrocytes) were observed in each view. The presence of schistocytes is suggestive for the presences of a coagulopathy. In conclusion: based on the hemogram, a diffuse intravascular coagulopathy (DIC) was suspected, most likely associated with septicemia caused by a bacterial infection or a toxicosis. Interestingly, EEHV 3/4 was detected by a combined PCR test for subtype 3 and 4 in a blood sample and in trunk swabs. The elephant had been tested PCR positive for EEHV4 previously. A trunk swab taken from the conspecific that shared the enclosure was PCR-negative. For photos of elephant heterophils, bands, platelets and schitsocytes: click here . Human myelocyte, containing both primary (azurophilic) and secondary/specific (pink or lilac) cytoplasmic granules. The proportion of secondary granules increases as the cell matures. The nucleus is round and lacks a nucleolus. Courtesy: ASH Image Bank Myelocyte of the Asian elephant in this case report. The quality of this photo is poor as it was taken with a cell-phone through the ocular lens of the microscope. Urinalysis: Daily urine samples were taken and analyzed using a dipstick and refractometer from Day 3 onwards. Initially a high specific gravity with a low pH was determined, suggestive for severe dehydration and metabolic acidosis. Fecal culture and treatment: A fecal sample collected on Day 3 was submitted for bacteriology. The treatment plan focused on the suspected septicemia. Treatment with NSAID was continued and the antimicrobial treatment was switched to enrofloxacin (per rectum, ~ 2.5 mg/kg) and metronidazole (per rectum, ~ 11 mg/kg). Administration of vitamin B-complex and E/selenium was repeated on day 4 and day 5. Preventive measures In an attempt to find the causative agent of the suspected septicemia, stored hay was inspected for mould and other conditions that favor (an)aerobic growth of toxin producing bacteria, more specifically Clostridium spp. All sand in the enclosure was replaced; drains and surfaces were disinfected with 5% sodium hypochlorite before new sand was brought in. Treatment (continuation) On Day 9 Salmonella saintpaul sensitive for enrofloxacin was isolated from the feces. Until Day 6, dehydration was getting worse, based on hematological findings (increased Ht) and urinalysis (increased specific gravity). On Day 7 no feces were produced (probably caused by the anorexia and repeated administration of detomidine) and diphteric necrotic tissue was observed during the administration of rectal fluids. In the mean time, hematology results started to show evidence of recovery from the septicemia: bands had dropped from 36% (Day 5) to 11%, while platelets increased from 320 (Day 2) to 437 x109/L. WBCs increased from 3.3 (Day3) to 10.5 x 106/L. Interestingly, the number of myelocytes increased to 35% on Day 7, but sharply dropped to 5% on Day 8 and they totally disappeared after that day. All hematological parameters were normal when checked again on Day 48 and 55. In order to stimulate the appetite and the intake of fibrous food, daily sedations were discontinued as from Day 8, and the focus of treatment moved to provide gastro-protection and stimulation of the duodenal motility by the administration of ranitidine (oral, ~ 0.25 mg/kg) twice daily. Water soaked bran and hay ad lib, bamboo browse and banana tree-trunks were offered as much as possible. Sugar-containing food items were restricted to treats for compliance to vocal commands by the keepers in order to get cooperation from the elephant for the necessary treatment procedures. The animal regained its strength and body condition over the 3 month-period following this clinical episode. The presence of EEHV3/4 in the blood and trunk swab can be explained by a virus reactivation due to the sudden deficiency of the immune system as a result of the septicemia and DIC. No clinical impact is to be expected from this finding, as the animal known to be a carrier of EEHV4. References 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 . To page top

This page describes eye problems in elephants and how to treat them. Blepharitis, conjunctivitis, cornea edema, keratitis, vitamin A deficiency, corneal ulcer, cataract, hypopion, uveitis, synechia, iris prolaps, and panopthalmitis. Ophthalmology Compiled by Dr. Khyne U Mar, DVM and Willem Schaftenaar, DVM Eye problems are common in elephants. They are often the result of trauma and present as superficial or deep cornea lesions and ulcers. Cataracts are also regularly seen in elephants. If the vision in one eye is reduced, the animal should be approached with care from that side. In a study in 1478 captive elephants (2956 eyes) in Thailand, 17.83% of the examined eyes from 369 elephants (24.97% of the total number of elephants) had anterior ocular abnormalities. The most common lesions in these examined eyes were frothy ocular discharge (5.85%), corneal edema (5.31%), and conjunctivitis (5.18%). In addition, epiphora, phthisis bulbi, other corneal abnormalities, anterior uveitis, and lens abnormalities were noted. Almost all lesions increased in frequency with age (Kraiwong, 2015). Regular ophthalmic examination in elephants should be included in their annual health check program. Early detection and treatment of any ocular abnormality may avoid the development of subsequent irreversible ocular pathology. Clinical examination overview and diagnostic techniques The clinical examination of the eye starts with the anamnesis (history) and observation of the animal. The eyelashes should be long in order to protect dirt and objects from touching the surface of the eye. They are located mostly superior to the eye and can be as long as 11 cm. The inferior eyelid has less and smaller (2 cm) lashes. A unique feature of the elephant eye is the lack of a lacrimal apparatus (lacrimal glands as well as nasolacrimal duct) and eye brows. Tear films simply flow towards the medial canthus and exit along a groove in the skin onto the face in Asian elephants (Wong et al. 2012). The area around the eyes is therefore often wet. A Schirmer tear test can be performed in elephants. In a research cohort of 80 healthy Asian elephants the mean value was 34.3+/- 1.7 mm/min with older elephants (>40 years) having higher values than younger ones (<20 years). The cornea should be clear, without any irregularities. The iris of an elephant varies in color from tan, yellow, brown or the combinations. Blepharospasm is a strong indication for ocular disease. Conjunctiva cultures can be taken, though the strong palpebrae can make sampling for culture a challenge. Ophthalmic anesthetics can be used safely in elephants and may facilitate clinical examination and allow ophthalmoscopic examination of the deeper ocular structures. The pupillary light response can be performed if the elephant trusts the clinician enough to approach the animal with a proper light source at the required short distance. This test should be performed in subdued light. The menace response can be performed if the animal allows the clinician at short distance by moving fingers towards the elephant's eye without causing air movement. The numerous hairs on the skin of the palpebrae are not true cilia or true eyelashes as they are not associated with the margins of the palpebrae (Wong et al 2012, J. Zoo and Wildlife Med., 43(4), pp 793-801). The lower eyelid is more developed and ascends to a greater degree than the upper lid descends (Suedmeyer, 2006). (Photo KUMar) The iris of an elephant can have several colors: tan, yellow, brown or a combination. (Photo: W.Schaftenaar) A white, circumferential ring, similar to the arcus senilis in man is noticed in 40+ yr Asian elephant (fat deposit or aging?). (Photo: KUMar) Fluorescein staining of the cornea may be difficult as the elephant will close its eye immediately when approached. A fluorescein strip can be placed in a 10 ml syringe with sterile water or saline; this solution can then be sprayed over the eye in a constant flow using a blunt small gauge needle. This should be sprayed on the eye from the medial or lateral side. It helps when at the same time a steady water stream is directed at the periocular skin, which may result in relaxation of the animal. After fluorescein has been sprayed on the cornea, the eye should be flushed with sterile saline to remove excessive fluorescin. If present, cornea defects will stain green under blacklight and even under regular light. Cataracts which appear as a white central spot and keratitis (diffuse, superficial cloudiness of cornea) are frequently seen in elephants. Vision can be checked by passing the light of a flashlight (or cell phone) from the ear over the eye to observe for a blinking reflex. Ophthalmoscopy in the untrained elephant can be quite a challenge, as the animal will usually not allow this kind of close examination that moreover uses a light source. However, the animal can be trained to allow ophthalmoscopy. The third eyelid or nictitating membrane is located at the ventro-medial aspect of the orbit. Inside the nictitating membrane, an oblong, flanged-shaped piece of hyaline cartilage supports the anterior palpebral aspect of the nictitating membrane. The harderian gland that is located here, plays a role in the lubrication of the cornea. Zeis's glands (modified sebaceous glands) are located in the margins of the lid. They produce an oily substance that helps lubricate the cornea. Blinking reflex The nictitating membrane in an Asian elephant (arrow).(Photo: KUMar) Blinking reflex using a smartphone's flash light in an Asian elephant with chronic keratitis. (Video: W.Schaftenaar) Ultrasonographic examination The clinical examination of the elephant's eye can benefit from transcutaneous ultrasonographic examination. The anterior eye chamber, the lens end the posterior eye chamber can be visualized using a 4-7 MHz convex probe (Bapodra et al. 2010). Following are descriptions of the anatomical components of the eye and the medical condition that may occur Eyelids Blepharitis is an inflammation of the eyelids than can be caused by trauma (rubbing), parasite infection or as part of a localized dermatitis. The accompanying symptoms are blepharospasm, epiphora (tearing that appears as wet skin area below the eye) and often photophobia. Sometimes lice (Haematomyzus elephantis ) or ticks (Amblyomma tholloni) can be found on the eyelids causing local skin lesions. Blepharitis in an Asian elephant. (Photo: KUMar) Small skin lesion caused by ticks (Amblyomma tholloni) (Photo: KUMar) Conjunctiva The conjunctiva is the tissue that lines the inside of the eyelids and covers the sclera (the white part of the eye ). It is composed of unkeratinized, stratified squamous epithelium with goblet cells , and stratified columnar epithelium . The conjunctiva is highly vascularized, with many microvessels . Conjunctivitis is an inflammation of the conjunctiva and is a common finding in elephants. In some cases small nodules and vesicles may be observed (lymphoid tissue on histology), possibly associated with chronic irritation. A conjunctivitis is often the result of trauma (hard object, dust, irritating liquid or smoke). Conjunctivitis is also seen in poxvirus infections. Conjunctivitis in an Asian elephant (From: Elephant care manual for mahouts and camp managers, FAO 2005 , Conjuctivitis and keratitis in an Asian elephant. Note the swollen mucosa. (Photo: KUMar) The conjunctival sac is a connection between the palpebral and bulbar conjunctiva. Under certain conditions (hypoproteinemia, trauma, insect bites or allergic reactions), a prolapse of this part of the cornea can develop, which protrudes like a mucosal sac between the eye and the lower eyelid. Prolapse of the conjuncitival sac in an Asian elephant. (Photo: KUMar) Cornea The cornea is transparent because it lacks cells and blood vessels and has no pigment. The cornea should always be wet thanks to a pre-corneal film tear. Oxygen and nutrients are available from the aqueous cornea tear film, the limbal capillary plexus and the palpebral conjunctival capillaries. Several disorders of the elephant cornea have been reported. Most of the corneal lesions seem to have a traumatic cause: trauma by rubbing, allergy by environmental irritants such as exposure to direct sunlight or continued exposure to dryness or small particles, e.g. dust, smoke, grass seed etc. that damage the corneal epithelium. Hypovitaminosis-A has also been suggested as a cause of cornea disorder as well as hypoproteinemia. Acanthamoebae Spp. has been identified in corneal swabs. It's presence has been associated with corneal ulcers (Dangolla, 2005). However, the protozoa was also found in swabs taken from healthy elephant eyes (Wijesekara, 2007). Corneal edema Corneal edema, also called corneal swelling, is a buildup of fluid in the cornea. It is caused by dysfunction of the endothelial membrane on the inner side of the cornea, that normally pumps fluid out of the cornea in order to keep it transparent and clear. This can happen after a blow to the eye or a puncture of the cornea (e.g. by small branches), or by contact with toxic substances. Cornea edema in an Asian elephant. (Photo: KUMar) Cornea edema in an Asian elephant. (Photo: KUMar) Cornea opacities - keratitis Opacities in the cornea are called keratitis and are very common in elephants. They present as whitish, "cloudy" areas usually in the central part of the cornea. It has been suggested that they are caused by trauma (thorns, heat, dust, and chemicals), direct sunlight or chronic dehydration. The cornea must be checked for foreign bodies. In severe keratitis, the entire cornea turns white. This reduces the vision of the animal to only being able to distinguish just between light and dark. This can be tested with the blinking reflex . In some cases, keratitis can be painful: the elephant shows blepharospasm and the third eyelid may be protruded (partly) over the eyeball. In that case involvement of the iris should be considered. It is recommended to perform cytology, aerobic bacterial culture, and sometimes fungal culture. When opacities are only found in the superficial epithelium, and dispersed over the entire cornea surface, it might be the result of hypovitaminosis-A (vitamin A is essential for the normal functioning of the corneal epithelium, including the production of the tear film). This condition is called "xerophthalmia". As fluid makes its way into the cornea it can accumulate and cause the formation of small bullae or "blisters." This is called bullous keratopathy. If the blisters break or rupture, a corneal ulcer will result. Mild, superficial opacity in the central area of the cornea in an Asian elephant (keratitis). (Photo: KUMar) To page top Diffuse, superficial opacities spread over the entire cornea of an Asian elephant, possibly caused by hypovitaminosis-A (xerophthalmia). (Photo: KUMar) Mild keratitis in an Asian elephant. (Photo: KUMar) Severe keratitis involving the entire cornea of an Asian elephant. (Photo: KUMar) Severe keratitis with protrusion of the third eyelid in an Asian elephant. This could be an expression of pain, in which case iris involvement should be considered. (Photo: KUMar) Corneal ulcer A cornea ulcer is an open sore on the cornea. The epithelial outer layer and the middle layer of the cornea (stroma) are disrupted. This condition is also called a melting corneal ulcer. Usually the primary cause is trauma of the cornea. This traumatic lesion can become infected by bacteria (Pseudomonas, Neisseria spp, fungi and other microbes. This condition is very painful a nd blepharospasm is often seen. The elephant may be rubbing the area around the affected eye against an object. There may be protrusion of the third eyelid. An ulcer is usually the result of trauma. Treatment of keratitis with NSAID's or glucocorticosteroids increases the risk of ulceration. As a reaction to the ulcer and to repair the lesion, blood vessels will grow into the stroma of the cornea, visible as small red lines, sometimes forming a network of small vessels. This process takes several weeks. When the cornea surface has been repaired, the remnants of these blood vessels will be visible as white connective tissue strands. The major risk in an ulcerated cornea is perforation of the entire cornea, which will result in loss of the ocular fluids and complete loss of the eye. When blood vessels fail to grow towards the ulcer, the ulcer remains in an unchanged form as an indolent corneal ulcer, needing a special treatment. Two manifestations of a severe keratitis and cornea ulcer with a prolapse of the iris in an Asian elephant. (Photo: KUMar) Hypopyon Hypopyon keratitis is an accumulation of pus (heterophils and fibrin) in the anterior eye chamber (between cornea and lens). It is accompanied by profuse discharge and signs of ocular pain. Ultrasonographic examination may be helpful for diagnosing pus in the anterior chamber. One case report describes the treatment of hypopyon in an Asian bull elephant. Hypopyon and uveitis have been described in a case of leptospirosis (Fowler. 2006. Infectious diseases. In: Fowler and Mikota, 2006, 403). Hypopyon Iris and uvea The iris is a diaphragm that regulates the influx of light. It is a very vulnerable structure that consists of two layers: the outer (anterior) pigmented fibrovascular layer (known as stroma, which lacks an epithelial layer) and the inner (posterior) surface covered by a heavily pigmented epithelial layer that is two cells thick (the iris pigment epithelium). This anterior surface projects as the dilator muscles. The high pigment content of the iris blocks light from passing through to the retina, restricting it to the pupil. The outer edge of the iris, known as the root, is attached to the sclera and the anterior ciliary body . The iris and ciliary body together are known as the anterior uvea . Uveitis Any lesions in the anterior part of the eye can result in damage to the iris. Parts of the affected iris may come into contact with the inner layer of the cornea (anterior synechia) or the lens (posterior synechia). If there is also a corneal ulcer, the iris may prolapse through the ulcer (iris prolapse). Iris lesions are considered to be very painful in all animal species. These conditions need immediate veterinary attention. Lesions of the iris and uvea are called uveitis . If only the anterior part is involved, we call it iritis . In reality it will be hard to distinguish these conditions in elephant ophthalmology, unless proper ophthalmoscopy can be performed under sedation or general anesthesia. Lens The lens is a transparent biconvex structure in the eyes that, along with the cornea , helps to refract light to be focused on the retina . Any lesions of the lens will result in white discoloration and loss of transparency (cataract). This is seen as a white area in the central pupillary space. Young cataracts will appear as cloudy structures. A mature cataract appears as a completely white pupil. A complete, mature cataract will reduce the vision of the elephant which may finally result in complete blindness of the affected eye. When an elephant is approached on the side of the blind eye, the clinician should be aware of the compensating behavior of the elephant, when it tries to keep its functional eye on the investigator. Cataracts are quite common in Asian elephants in range countries. One paper notes that 6-8% of the elephants kept in Sri Lanka suffer from this condition (Kuruwita, 1991). Several causes of cataracts are known in other animal species: trauma, overexposure to sun light, deficiency of vitamin A, C, E or riboflavin, diabetes and dehydration. Often the cause of a cataract in elephants cannot be determined. Early stage of a cataract in an Asian elephant. (Photo: KUMar) Advanced stage of a cataract in an Asian elephant. (Photo: KUMar) Advanced stage of a cataract in an Asian elephant. (Photo: KUMar) Panopthalmitis and phthisis bulbi Panophthalmitis is inflammation of all layers of the eye including the intraocular structures. It has been documented in nine eyes postmortem during a field study of eye lesions in African elephants ( McCullagh, 1969). Phthisis bulbi is a shrunken, non-functional eye. It may result from severe eye disease, inflammation or injury. Phthisis bulbi after chronically infected cornea ulcer. (Photo: KUMar) Subdermal injection of Plancentrex (0.1 mg/ml) in an Asian elephant with uveitis. (Photo: KUMar) Summary of the most frequently used drugs in ophthalmology Standard frequency of treatment applications: 3-5 per day Antibiotic treatment should be based on sensitivity test Flushing with 0.9% NaCl solution is recommended before every topical drug application The elephant's eye can be flushed using a long, small diameter tube place on a syringe. (Photo: KUMar) Treatment options in elephant ophthalmology Blepharitis: Treatments of blepharitis in elephants have not been described in the literature. A similar approach as in other mammals is recommended: elimination of the cause (parasites, dermatitis) and flushing the eye (see photo below) with saline solution, 3-5 times a day. Conjunctivitis, prolapse of the conjunctival sac : elimination of the cause and flushing the eye with saline solution, 3-5 times a day and antibiotic ointment, 3-5 times a day. Corneal edema: flushing with a hypertonic saline solution, 3-5 times a day. Keratitis in early stage: flushing with saline solution, 3-5 times a day, antibiotic ointment, 3-5 times a day. If there is no ulceration, topical application of 0.1% dexamethasone eye drops may be used; be aware that corticosteroids will stop the regeneration of the epithelial cells. Chronic keratitis: treatment will have no effect. Xerophthalmia: oral vitamin A supplementation. Corneal ulcer: flushing with saline solution, and topical application of antibiotic eye ointment 3-5 times a day. Topical application of Diclofenac sodium 1% eye solution may help reducing the pain. Promising results of the use of autologous serum have been reported (Janyamethakul, 2015), applied twice daily. Preparation of autologous serum: Five 10 ml. syringes were used to collect a total of 50 ml. Then, the blood was allowed to clot for 2 hours at room temperature before being centrifuged at 3,000 rpm for 15 minutes. The separated serum was collected (about 20-25 ml.) into a sterile container to which 1 mg. of gentamicin was added. The autologous serum was then aliquoted into sterile tubes, each containing 3 ml. Additionally, the serum was stored at 4°C and used within 7 days. Topical treatment with acetylcysteine (0.02%) was used in case of a corneal abscess along with gentamycin and atropine (Pipitwanichtham, 2023). Other treatments attempts that have been tried: Indolent (non-healing) corneal ulc ers are hard to treat. Debridement of necrotic corneal stro ma should be considered. This can be done by using a cotton tip, or in more severe cases the abnormal cornea tissue can be scraped using a corneal spatula. Theoretically, after the debridement, the cornea should be protected by a contact lens as used in horses. This has been repo rted once in a 44 yrs-old Asian elephant, in which case the lens was lost soon after application. In elephants flushing the eye and applying antibiotic eye ointment and autologous serum is probably the only possible post-debridement treatment. Stem cell application: pr omising results were seen at the Elephant Conservation Center Lampang (Thailand). Although never reported in elephants, the application of a few droplets of cyano-acrylate might be an alternative for a contact lens in elephants. Hypopyon: pain relief (NSAID), systemic antibiotics (DDX: leptospirosis!). Uveitis and Synechia: Atropine sulfate eye ointment (1%), 4-6 times a day, is a commonly used mydriatic drug in horses. It may stabilize the blood-aqueous barrier, reducing vascular protein leakage, minimizing pain from ciliary muscle spasm, and reducing the chance of synechia formation by causing pupillary dilatation. Pupil dilation is an indicator for the drug to be effective on the ciliary muscles. In horses even topical atropine has been shown to prolong intestinal transit time, reduce and abolish intestinal sounds, and diminish the normal myoelectric patterns in the small intestine and large colon of horses. Whether this also applies to elephants is unknown. Subdermal injection of placental extract (Placentrex®) is a common treatment for uveitis, hypopyon and corneal opacities in elephants in Asia (Suedmeyer, 2006). See also photo below. Iris prolapse: systemic NSAID, flushing with saline solution, 3-5 times a day. As the cornea is perforated by the prolapsed iris, the elephant should be treated systemically with antibiotics. Cataract: only 2 cases of (mature) cataract removal by phaecoemulsification have been reported (cataract surgery-UK and cataract surgery-USA). However, artificial lenses to replace the removed lens contents are not available. The significant lens instability (first noted following the initial stages of surgery in the USA-case, i.e., during creation of the anterior capsulorhexis) prevented implantation of an intraocular lens implant. See for more detailed information the references below (Cerrata, 2019 and Manchip 2020). Panophthalmitis: Enucleation is the only treatment indicated for this condition. However, there are no published data on the treatment of panophthalmitis. Placentrex Flushing References and further reading: Bapodra P, Bouts T, Mahoney P, Turner S, Silva-Fletcher A, and Waters M. 2010. Ultrasonographic examination of the Asian elephant (Elephas maximus) eye. Journal of Zoo and Wildlife Medicine , Vol. 41, No. 3, 409–417. Cerreta, A.J., McMullen Jr R.J., Scott, H.E., Ringenberg, J.R., Hempstead, J.E., DeVoe, R.S., Loomis, M.R., and Minter, L.J.. 2020. Bilateral Phacoemulsification in an African Elephant (Loxodonta africana). Hindawi Case Reports in Veterinary Medicine Volume 2019, Article ID 2506263, https://doi.org/10.1155/2019/2506263 or click here to download the manuscript. Dangolla A, JS Edirisinghe and ID Silva (2005). Association of Acanthamoeba with a corneal ulcer in a captive elephant (Elephas maximum maximus). Proceedings of 57th Annual Convention and Scientific Sessions of the Sri Lanka Veterinary Association. 33pp Fowler M. 2006. Infectious diseases. In: Biology, Medicine and Surgery of Elephants, Ed. Fowler and Mikota, 148. Janyamethakul T, Moleechat P, Gohain R, Somgird C, Pongsopavijit P, and Wititkornkul B. 2015. Efficacy of Autologous Serum as An Adjunct Treatment for A Melting Corneal Ulcer in A Captive Asian Elephant. Thai Journal of Veterinary Medicine: Vol. 45: 2, Article 18. Kraiwong, N., P. Sanyathitiseree, K. Boonprasert, P. Diskul, P. Charoenphan, W. Pintawong and A. Thayananuphat (2016). "Anterior ocular abnormalities of captive Asian elephants (Elephas maximus indicus) in Thailand." Vet Ophthalmol 19(4): 269-274. Kuruwita VY and Abeysinghe AB. 1991. Surgical correction of blindness due to mature cataract in a domesticated Asian elephant. International Seminar on Veterinary Medicine in Wild & Captive Animals, Bangalore, India, November 8 to 10, 1991; 23 Manchip, K.E.L., Sayers, G., Lewis, J.C.M., and Carter, J.W. 2019. Unilateral phacoemulsification in a captive African elephant (Loxodonta africana). Open Veterinary Journal, (2019), Vol. 9(4): 294–300. ISSN: 2218-6050 (Online) DOI: http://dx.doi.org/10.4314/ovj.v9i4.3 . or click here to download the manuscript. McCullagh, K.G. and Gresham, G.A. 1969. Eye lesions in the African elephant (Loxodonta africana). Res Vet Sci 10(6): 587–589. Pipitwanichtham S, Dittawong P, Meetipkit P, Sitdhibutr R, Pattanapon N, Kasornsri M, Phetudomsinsuk K, Thongtip N, Sripiboon S. Case report: Corneal stromal abscess in a captive Asian elephant: diagnosis and treatment regimes. Veterinary Integrative Sciences 2023; 21(3): 693 - 703 DOI; 10.12982/VIS.2023.050 . Suedmeyer Wm. K. 2006. Special senses. In: Biology, Medicine and Surgery of Elephants, Ed. Fowler and Mikota, 399-403. Use of a contact lens for horses in an Asian elephant (PDF) Wijesekara PNK, Bandara KAPA, Dangolla A, Silva ID and Edirisinghe JS. 2007. Incidence of Acanthamoebae Spp . in the eyes of a group of captive elephants in Sri Lanka. Conference: International Elephant Conservation & Research Symposium Florida USA At: Orlando, Florida USA, November 2007. Wong MA, Isaza R, Cuthbert JK, Brooks DE and Samuelson DA. 2012. Periocular anterior adnexal anatomy and clinical adnexal examinaton of the adult Asian elephant (Elephas maximus) . Journal of Zoo and Wildlife Medicine , Vol. 43, No. 4, pp. 793-80. To page top

Only a handful of fetotomies have been performed in elephants. The case described here is the only one in which the dam survived. Wound healing is similar to the vaginal vestibulotomy, however, wound infection may occur due to the heavy manipulations during the long procedure and the passage of sharp bony fragments of the fetus through the created opening. To Reproduction To dermatology Case report Fetotomy and wound treatment Date: 2008 Place: Rotterdam Zoo Data provided by: Willem Schaftenaar History A 37 years old matriarch Asian elephant failed to deliver her 5th calf. At 13 months from the failed parturition, a herd mate of this animal delivered a healthy full-term calf. The calf tried to nurse from the matriarch and this elephant actively encouraged the calf to do so. Within 6 hours of this behavior, the matriarch displayed intense labor. After 24 hr, the hind legs of the retained calf could be palpated transrectally in the vagina, and several sharp fetal bone fragments (dorsal spines, fractured ribs) were palpated as they almost penetrated the vaginal wall. At that time, the animal was completely exhausted and contractions had ceased. With a failed attempt to extract the fetal carcass through the intact birth canal using two Krey-Schöttler fetotomy hooks, a decision was made to perform a vagino-vestibulotomy. Onset of labor 6 hours after the birth of a calf in the herd Six hours after the birth of a calf in the herd, labour in the matriach started, 13 months after the first signs of labour had come to a stop. Treatment The animal was chained on one front leg and the opposite hind leg. 150 mg xylazine was slowly hand-injected intravenously. During the entitre procedure (11 hours) extra doses of 75 mg xylazine were given intravenously every 50-60 minutes. Four 4 local depositions of 20 ml Lidocain 2% (with adrenaline) were injected in the midline below the anus. Epidural anesthesia was not used, however new insides have proven that this is an important method to reduce movement of the tail and decreases pain perception in the perineal region. The animal remained standing throughout the entire procedure. A 15cm skin incision was made in the midline. A rubber (cattle) stomach tube with a 10x60mm window at the tip was inserted in the vestibulum vaginae and advanced till the tip reached the dorsal edge of the incision. The vestibulum vaginae was incised over the window of the tube. The legs of the calf could be visualized in the horizontal part of the vagina. At least 4 fractured ribs were found, probably fractured by the natural contractions of the uterus duting the past 24 hours. The fractured ends had penetrated the wall of the vestibulum on the left caudo-ventral side, but not completely perforated, resulting in several tears of the mucosa (20cm long). The roof of the vestibulum vaginae had some mucosa tears too, also not perforating the wall totally. The carcass was cut into more then 100 large pieces; many ribs were removed one by one to avoid damage to the wall of the vestibulum vaginae. A complete fetotomy was performed using a Thygesen fetotome (Utrecht model). Finger knifes, Krey Schüttler hooks, saw directors and calf delivery chaines were used to cut the carcass in smaller lieces and pull them out. Large pieces were pulled out with extra support by a calving-pully for cattle. A long blunt "eye-hook" (used to grab a dead cattle or horse fetus in the orbit) was modified at the spot making it a prolonged knife (like a "finger knife" for fetotomy). Muscles were split from their bone attachment using this knife and blunt fingers. Lumbs of the carcass that were too big to pass through the fetotomy opening, were removed via the normal birth canal. After 3 hours 40 ml Duphaspasmin (11.58 mg isoxsuprinelactate per ml, Fort Dodge NL8514) ws injected i.m. followed 30 minutes later by another 40 ml Duphaspasmin i.m. as well as 100 ml Amoxicilline 20% (200 mg amoxicilline trihydrate/ml, NL 2795) i.m. After 9 ¾ hours the entire carcass of the fetus was removed. 5 ml Oxytocin (oxytocine 10 IU/ml, NL3852) was given intravenously. The uterus was flushed with large amonts of luke-warm water using a plastic hoose pipe. The water was drained as much as possible. Ten liters of 0.09% NaCl was brought into the uterus using a cattle stomach tube and a funnel. Thirty minutes after the previous injection, another 5 ml Oxytocin (oxytocine 10 IU/ml) was given i.v. The uterus started to show moderate contraction on the ventral side. The rest of the uterus was still filled with air. A custom-made balloon (100 ml volume) catheter was advanced into the urinary bladder. The mucosa of the vestibulum vaginae was sutered with 2/0 PDS, continuous Cushing stitches. The overlying muscular tissue and connective tissue was sutured in 2 layers using) Vicryl, continuous stitches. Only the dorsal 5 cm of the skin was sutured intradermally using 1 Vicryl, single stitches. The mucosa of the vulva and the distal part of the vaginal vestibule had been severed by the passage of large lumps of the carcass with sharp bony edges. A 84 kg female calf carcass was removed in more than 100 pieces. The carpal joints were in flexed position and could not be bent unless the flexor tendons were cut thorught. This condition is known as arthrogryposis. Whether this had caused the initial dystocia remains inclear. Antibiotic treatment (150 ml amoxicilline 20%, i.m. SID) was given for 9 days. The balloon catheter came out one day after the fetotomy. During the following weeks the vulva and vaginal vestibule became heavily infected and large pieces of necrotic tissues were lost. After 5 days transrectal ultrasonographic examination demonstrated that there was still a lot of detritus in the uterus. Five ml. of oxytocine (10 IU/ml) was given i.m. Surprisingly the uterus was still responsive to oxytocine, as aftre a few hours a lot of fluid was discharged through the vulva. When this was repeated 2 days later, no reaction of the uterus was observed. Making an incision in the vaginal vestibule guided by a plastic tube (with a window cut out) advanced in the vaginal vestibule. The Thygesen fetotome is advanced into the horizontal birth canal. Most parts of the fetus were removed through the vulva, which allowed a relatively small incision of the vaginal vestibule Krey-Schüttler hook Thygesen Fetotome Giggli saw director Custom-made balloon catheter Finger knife Pieces of the carcass were put together to check whether bones were missing. One femoral condyl was missing. It was found the following day. Note the arthrogryposis in the right carpal joint. The left carpal joint is stretchted after cutting through the flexor tendons. Treatment results All sutures came off after 14 days, which facilitated the daily treatment of the distal part of the birth canal: flushing with 50-100 liters of 0.09% saline solution through the surgical wound. This treatment was continued for several weeks. Six weeks after the fetotomy, the elephant was sedated again with xylazine, and the necrotic area of the surgery wound was debrided. In the following weeks, the surgery wound and the wounds in the distal part of the birth canal started to heal nicely. Ten weeks after the fetotomy the surgery wound had reduced in size from 15cm to 10 cm. Flushing with saline water was discontinued. At 14 weeks the surgery wound was 5.7 cm long. At 5 months the skin and mucosa of the vaginal vestibule had fused completely, leaving a 4 cm opening. The elephant was sedated again with xylazine and the skin-mucosa fusion was surgically disconnected. Over a circular area of 4 cm around the opening, the skin was seprated from the vaginal vestibule. The vaginal vestibulum was closed in 2 layers using 2/0 Moncryl; first layer: Schmieden suture; second layer: Lambert suture. The skin was left open. All sutures came off after 5 days. It was decided to allow the wound to heal per secundam. The wound was flushed with saline solution on a daily base. Two months later, the wound diameter was 4 cm and the epithelization between skin and mucosa was complete again. One year after the fetotomy the opening was still 4 cm. Standing sedation was performed using xylazine. The tissues around the fistula were injected with a total amount of 17 ml Lidocain 2% (with adrenaline). A small strip of the epithelium layer that formed the edges of the fistula was cut off and the subcutis was incised, separating the vestibulo-vaginal wall from the skin over 2-3 cm. The vestibulo-vaginal wall was closed using Vicryl 1, continous Utrecht-uterus suture. Antiseptic, silver impregnated gauze was inserted in the subcutaneous space. The gauze was sutured to the ventral edge of the wound using Vicryl 1 to facilitate later removal. The skin was closed using a continuous intracutaneous suture (Vicryl 1). Three extra single matrass sutures (Vicryl 6) and 1 single suture were applied as an extra support for the intracutaneous sutures. The ventral part of the fistula was left open to allow later removal of the gauze. 9 days after wound dressing: all sutures came off. The vaginal wound is retracting in the subcutaneous space (thus enlarging the wound surface). Diameter of skin wound: 6 cm. 15 months after fetotomy:wound almost closed, leaving a permanent opening of 3 mm, Wound healing Severely swollen vulva 3 days after the fetotomy. Two months after the fetotomy, the wound starts healing nicely. Necrotic tissue protruding through the vulva, 12 days after fetotomy. Five months after the fetotomy, epithelization of the edges of the skin and mucosa has interrupted wound healing Five months after the fetotomy, wound dressing is performed. The vaginal vestibule is closed. Photo taken before closing the skin. Five days after the surgical wound correction, all sutures came off. One year after the fetotomy, a second wound dressing is performed. One week later, the wound opened and the subcutaneous drain came off. Eighteen months after the fetotomy, the wound was closed, leaving only a 3 mm opening (black structure above the pink connective tissue area. Conclusion of the author: the skin should not be sutured after a vestibulotomy or a fetotomy in elephants, as it delays the healing process. Closing the vaginal vestibule is also questionable, as the mucosa around the surgical wound is heavily contaminated by the strong manipulations needed for the procedure, resulting in wound infection. Healing per secundam of the entire wound is recommended, no matter how hard it is for a vet to leave such a big wound open! To page top

Foot and sole or pad lesions are common in elephants and should be treated. Abnormal wear of the pad can be the result of joint disease. Sole lesions can result in fistulas. Pedicure must be part of the management. Foot and mouth disease and cowpox virus can cause complete slaughing of the pad. Back to index orthopedic problems Foot problems Foot problems in elephants under human care are frequently seen. Several anatomical structures can be involved in foot problems: the sole (pad or slipper), the nails, the joint ligaments, the tendons, the distal phalanges and the joints. Many of the problems are management-related. Abnormal wear, inappropriate substrate, stereotypic repetitive movements and lack of space to move around are some of the major causes of orthopedic problems in elephant feet. A separate chapter on regular foot care in elephants under human care can be found here . An elephant suffering of foot problems will often demonstrate one or more of the following symptoms: Swelling, pain Lameness, reluctance to move Black tracts on or beneath nails Discharge / bad odor Nail cracks Overgrowth / over-wear (nails and/or sole) Dry or overgrown cuticles Examination of the foot If the animal is well trained, it should lift its legs to allow inspection of the nails and pad of each foot. Alternatively the feet can be examined with the elephant in lateral recumbency. Check the nail cuticles. Remember that elephants have sweat glands in their cuticles. Cuticles should not be too short as this may facilitate the invasion of microorganisms. However, they should also not be too long. Elephants seem to care for their nails by rubbing them along hard objects or their own legs. Overgrown cuticles may result in accumulation of sweat: when trimmed or when pressure is exerted on the cuticles, watery fluid may be discharged ( see video ). The nails and the sole are interconnected by a structure that is an equivalent of the white area in horses and cattle. It forms a delicate connection, where microbes can penetrate into deeper layers to cause an infection (pododermatitis) ultimately resulting in osteitis and arthritis of the interphalangeal joints. The nails should never be longer than the pad, as they should not bear weigth when the elephant is standing still nor during walking (see video) . Long nails can easily develop a tear, giving access to microbes. The pad of the sole must be thick and have a distinct pattern of grooves. When wear is insufficient, the grooves may become too deep and form an easy entrance for stones, dirt and microbes, which may result in a sole abscess. Too much wear results in a smooth surface and a thin pad, vulnerable for deeper sole lesions. African elephant walking in Namibian desert (slow motion). Note how the pad and the nails form one supporting surface. The nails are not used for support. (Footage of BBC documentary) Sole lesions Sole lesions Normal sole of an Asian elephant kept in a zoo Normal sole of an Asian elephant semi-free ranging in the forest. Normal sole preparation of a free-ranging African elephant (Kruger National Park, South Africa) In order to maintain a healthy sole and nails, there should be a balance between wear and (re)growth of sole and nail tissues. The main factors that determine the wear are the type of substrate, activity of the elephant and the humidity. Best Practice Guidelines The EAZA Best Practice Guidelines for Elephants recommend: Indoor and outdoor substrates should: 1. Provide choice to the elephant, allowing elephants to explore and investigate a range of substrates within their enclosure. This can provide increased activity and the cognitive benefits of decision-making. 2. Provide a degree of flexibility and accommodate the vast body mass of an elephant. Flexible ‘soft substrate’ works to absorb impact, easing the pressure on the joints and feet. 3. Provide good drainage which is beneficial for respiratory, skin and foot health. Soft substrate (such as sand) can act as a “bio floor”, allowing drainage of urine and ensuring animals are not standing in their own quite aggressive urine or lying on wet/cold floors. 4. Provide opportunities for enrichment, such as digging/hiding food which can improve musculature. 5. Allow dust bathing which provides enrichment and is beneficial for skin health. Hard floors Should be used only in places where long standing of elephants is not expected to occur and the elephant’s time in these areas should be minimised where possible. Concrete or rubber floors should have a non-abrasive but not smooth finish. Solid floors should be cleaned regularly and disinfected where appropriate and should provide appropriate drainage to avoid pooling of urine where elephants stand. Sand floors If used, type of sand should be considered. It should not be dusty, should drain well and not be able to compact (in the enclosure or gut). Sand that includes fine sand, silt or clay grades is likely to result in a dusty enclosure and compact into a solid floor. Sand grains need to be of a single size to reduce compaction. A grain with a round, rather than angular, shape will reduce compaction and will not be over wearing on the feet. Sand depth should be of 0,8 m minimum depth, but 1,5 m is recommended. Daily maintenance of sand includes daily watering to prevent excessive dust. Sand must be regularly turned to prevent compaction and build-up of bacteria that can grow in anoxic conditions. Sand floors need to be easily accessed by specially designed heavy machinery (such as truck loaders), and purposely built concrete ramps are a must. Where sand is retro fitted into enclosures, drains should be protected with permeable membranes and sand depths maximised where possible. Door runners should be subject to increased maintenance procedures to mitigate sand ingress. Alteration of door runners can be considered in preference to removal of substrates. Benefits of sand include the ability to build up pillows or mounds which may be used by older animals to sleep against or aid older/arthritic elephants when getting up. Animals also can benefit from rolling/ playing in or on mounds and they can act as visual barrier. The drainage provided is beneficial to aid calves in standing up quickly post birth. Sand can be used in outdoor areas, in all weather, and can withstand extreme cold or wet weather (with appropriate drainage). Grass If possible (i.e. space available will not be significantly compromised with paddock rotation technique), allow grazing access for elephants, which prolongs foraging times. Under improper environmental conditions the following sole lesions can develop: Figure 1. Excessive wear: too much wear results in a smooth surface and a thin pad, vulnerable for deeper sole lesions.The sole of an adult elephant should be at least 20 mm thick. Figure 2. Insufficient wear: the grooves may become too deep and form pockets, which are an easy entrance site for stones, dirt and microbes and can lead to a sole abscess. Figure 3. Crack/tear Figure 4. Sole fistula/ulcer/abscess Figure 5. Sole detachment (partial or complete) Result from primary infection (cowpox and Foot-and-mouth disease) Secondary infection after trauma, moisture, weight overload, dirt: Figure 1. The sole of this zoo-kept African elephant is too thin and health a smooth surface, making it vulnerable to cracks, perforations and nail lesions. Note the small cracks in the nails. Figure 2. Overgrown pad and nails. See also: International Elephant Foundation. Figure 3. Crack in sole of African elephant kept on a concrete floor Figure 4. Fistula/ulcer/abscess in the sole of an Asian elephant spending most of the time on the streets in Laos. Figure 5. Partial sole detachment in an Asian elephant orphan at the Dak Lak Elephant Conservation Center (Vietnam), caused by keeping him on a wet floor (rainy season). Injuries to the sole of the foot are particularly difficult to manage because it is hard to keep them clean and prevent infection. Careful pedicure of the sole may reveal bruces in the soft horn tissue, that resulted from abnormal local pressure on the sole. (Courtesy: Susan Mikota). These bleedings are blood lines in the horn lamellae (not to be confused with sole bruses) that may be seen when abnormal forces have been excerted on the nail (e.g. too long nail) (Courtesy: Susan Mikota). Perforated, infected sole lesions due to trauma (Courtesy: Susan Mikota) Partial pad and nail loss in a 54-yrs-old female Asian elephant. Click here to read the case report. Foreign body pad perforation One case report describes the treatment of a pad abscess resulting from the penetration of a wire through the pad in a 19-yr-old female Asian elephant (Elephas maximus ) housed at the Paris Zoo (Ollivet-Courtois 2003). The cow presented with acute right forelimb lameness and swelling that persisted despite 4 days of anti-inflammatory therapy. Under anesthesia, a 10 x 0.5 x 0.5 cm wire was extracted from the sole of the right foot. There was a 2-cm-deep, 7-cm-diameter abscess pocket that was subsequently debrided. Regional digital i.v. perfusion was performed and repeated 15 days later, using cefoxitin and gentamicin on both occasions. Between treatments, the cow received trimethoprim–sulfamethoxazole and phenylbutazone orally. Within 2 days of administering anesthesia and the first perfusion treatment, the lameness improved dramatically. When phenylbutazone was discontinued 1 wk after the first treatment, the lameness had completely resolved. At the second treatment, there was no evidence of further soft tissue infection, and the abscess pocket had resolved. A 10 x 0.5 x 0.5 cm piece of curved wire was found penetrating the right front foot of a female Asian elephant. A rope tourniquet was placed above the right carpus, and venous access was obtained using a 21-gauge, 0.8 mm butterfly catheter in a palmar superficial vein of the right foot to perform regional interdigital perfusion. Complete sole detachment can be caused by: Foot-and-Mouth disease (FMD) Generalized Cowpox infection. Foot and Mouth disease Both elephant species are susceptible to FMD. However, severe disease has been reported (anecdotically) more in Asian elephants than in African elephants. A description of FMD in African elephants after experimental (!) infection is found here (Howell, 1973). In range countries it is important to avoid direct and indirect contact between cattle and elephants, especially during FMD-outbreaks in the cattle population. Vaccination of cattle is important to reduce the risk of FMD to elephants living in the same area as cattle. For vaccination data, see also: The use of Vaccination of FMD in zoo animals (Schaftenaar, 2002) Complete sole detachment in an African elephant after experimental infection with FMD-virus. Cowpox Both elephant species are susceptible to cowpox infections, though more severe clinical impact is seen in Asian elephants. Symptoms can range between external pox lesions on the skin to complete sole detachment, as well as internal pox lesions in various organs. Vaccination is practiced in European zoos (for vaccine information, click here ). NB: Cowpox disease is a zoonotic disease! To reduce the pressure on a thin or perforated sole, a rubber sole can be glued on the thin sole. This material can last for 2-6 weeks when properly glued to the sole. Avenir Light is a clean and stylish font favored by designers. It's easy on the eyes and a great go-to font for titles, paragraphs & more. A more frequently used tool to reduce the pressure on the sole, is a sandal or boot made locally, fitting the foot of the elephant. This shoe should be removed daily to inspect and treat the injury. Custom-made sandal, Fowler & Mikota 2006 Custom-made boots, Singapore zoo 2007 Another example of custom-made sandals to protect an injured sole (Myanmar. Courtesy Susan Mikota) These sandals were made by commercial companies Teva and Nike (Courtesy Susan Mikota) Edges of the sole bordering the sole defect were thinned (Dak Lak Elephant Conservation Center, Vietnam) Treatment of sole lesions Excessive wear: the thin and smooth horn layer has to regrow. This means that wear has to be reduced. This can be achieved by reducing the time spent by the animal on a hard floor, changing the floor surface and substituting it by softer materials; i.e. concrete floors can be covered by an epoxy layer or deep sand. A concrete sleeping area should be replaced by a sand floor (see EAZA Best Practice Guidelines for Elephants) . The thickness of the pad can be measured by ultrasound examination. Overgrown sole: horn can be trimmed away using a hoof knife. Usually the nails will also need trimming. The use of a drawknife is not recommended, as it easily removes too much from the sole. Make sure that the nails are always shorter than the sole! Crack/tear: as these are usually the result of a too thin sole, measures to increase the sole thickness should always be taken. If the crack hasn't perforated the sole completely, the edges of the crack can be cut away using a hoof knife with the aim to prevent accumulation of dirt and to reduce the pressure on the thinnest part of the crack. A sandal should be considered is there is a risk of sole perforation. Sole fistula/ulcer/abscess: if the sole is perforated, microbes will have entered the underlying tissue. Frequent pedicure will be required in order to drain the affected tissues. The edges of the fistula need to be made as thin as possible with a smooth transition to the thicker part of the sole. This will reduce the pressure on the infected area. The fistula/ulcer/abscess must be flushed daily with saline solution and a mild disinfectant. Soaking the foot in a foot bath should be considered (see images below). Several solutions have been used in elephants (see table below). Epsom salt is probably superior to the other solutions, while copper sulfate might be too caustic for this type of injury. As long as the effluent is sufficiently drained with the help of frequent trimming, the use of systematic antibiotics is not indicated. List of foot bath solutions as described in Fowler & Mikota 2006 Simple foot soaking bath by a well trained Asian elephant, Dak Lak Elephant Conservation Center (Vietnam) Custom-made foot soaking bath, Laos (courtesy Dionne Slagter) Partial sole detachment: this condition can be the result of long exposure of the sole to water and dirt. Standing on a hard floor will predispose for this lesion. P arts of the sole that are detached from the underlying tissue must be entirely trimmed away using a hoof knife. Leaving a sole flap - even a small one - will result in extension of the infected area. The edges of the sole bordering the defect, must be made thin and smooth in order to avoid pressure of the remaining sole on the fragile exposed tissues. Regular trimming of the edges of the sole around the defect and daily flushing and foot bath are required. In some cases the use of a sandal or boot may be needed. Foot bath Complete sole detachement: this condition is usually the result of trauma or a viral infection : Foot and Mouth Disease and Cowpox have been associated with complete sole detachment, always accompanied by other severe symptoms caused by these viruses. As there are no specific treatment options for these viral diseases, only symptomatic treatment can be given. Bandaging the affected legs has been practiced, but one should not be optimistic about the results. In some cases, humane euthanasia will be the only option to prevent the animal from suffering. Traumatic sole detachment can be expected if the elephant has been trapped in a snare. Cleaning, disinfection (mild solution soaking foot bath) and sometimes bandaging of the affected foot will be necessary until the wound has closed. In some cases, the regenerated tissue that covers the wound is strong enough to withstand the pressure of the body weight. If that is not the case, a prosthesis will be needed to provide sufficient protection. References: Cowpox infection in elephants. 1996. Proceedings of the annual conference of the European Association of Zoo and Wildlife Veterinarians. Fowler ME 2006. Foot disorders. In: Biology, Medicine, and Surgery of Elephants. Fowler & Mikota, 271-290. Howell P.G. , Young E , Hedger R.S . 1973. Foot-and-mouth disease in the African elephant (Loxodonta africana ). Onderstepoort J Vet Res. 1973 Jun;40(2):41-52. Johnson G., Smith J., Peddie J., Peddie L., DeMarco J., Wiedner E. 2018. Use of glue-on shoes to improve conformational abnormalities in two Asian elephants ( Elephas maximus ). J. Zoo&Wildl Med. 49(1): 183–188, 2018. Ollivet-Courtois, F., Lécu, A., Yates R.A., Spelman L.H. 2003. Treatment of a sole abscess in an Asian elephant (Elephas maximus ) using regional digital intravenous perfusion. Journal of Zoo and Wildlife Medicine 34(3): 292–295, 2003 Schaftenaar W. 2002. Use of vaccination against foot and mouth disease in zoo animals, endangered species and exceptionally valuable animals. Rev. sci. tech. Off. int. Epiz., 2002, 21 (3), 613-623. To page top

A 1 yr-old Asian elephant suffered of colics as a result of a (traumatic) hernia mesenterialis. A torsio of the small intestines was incarcerated in the hernia. Consequently the intestine ruptured. The calf died due to acute peritonitis. To non-infectious diseases Case report Hernia mesenterialis and intestinal rupture Date: 2002 Place: Rotterdam Zoo Data provided by: Willem Schaftenaar History Species: Asian elephant Accommodation: Zoo, free contact Age, gender: 1 year, male Five years before this episode, a 3 yrs-old calf at the same zoo had died of EEHV1a . The calf (300 kg estimated BW) was heavily hit on its abdomen by a herd mate. Two days later (Day 1) it became very lethargic and stopped drinking from its mother. Day 1 08:30: Very lethargic, not eating. Laying flat on the ground, while kicking with his hind legs ( colic ). Sometimes standing with the mouth widely opened. Conjunctivae: slightly congested. Tongue: normal color. No edema on head or shoulders. Defense musculaire: normal. Rectal temperature: 36.8°C A standing sedation using xylazine (0.1 mg/kg BW IM for the calf, 0.08mg/kg BW for the dam) was performed in both the affected calf and its mother. As soon as sedation started, the calf was brought to its mothers mammary glands and it started drinking from the mother. EDTA and full blood samples were taken and rectal fluids were given during the sedation. Rectal palpation: only one handfull of soft feces in distal part of the rectum. The rectal wall is very dry. Urine sample: all values (dipstick) within normal ranges. Blood sample collected. Hematology and blood chemistry results were all within normal ranges. EDTA whole blood sample submitted for PCR on EEHV. Results: PCR-positive EEHV1a. Rx: 6 ml Finadyne (flunixinemeglumine 50 mg/ml, NL1726) i.m. 15 ml Baytril 10% (enrofloxacin 100 mg/ml, NL3489) i.m. 3000 mg famciclovir mixed with 15 ml utrasound gel per rectum. Calf during standing sedation and suckling from its mother. Note the penis relaxation, typical for alpha-2-agonist sedation. 16:30: No change. Not eating, laying. Less signs of colics. Rx: 1500 mg famciclovir mixed with 10 ml ultrasound gel per rectum. 23:00: Animal is lethargic. Laying down most of the time. Rx: 1500 mg famciclovir mixed with 10 ml ultrasound gel per rectum. Day 2 Slightly alerter than before. Treatment was continued similar to day 1. Day 3 08:30 Alerter, but no attempts to nurse from its mother. Rx: 15 ml Baytril 10% (enrofloxacin 100 mg/ml, NL3489) i.m. 1500 mg famciclovir mixed with 10 ml ultrasound gel per rectum. 16:00 Agian very lethargic. Has not eaten or nursed at all. No feces nor urine produced. Standing sedation (calf and dam, see day 1). Again the calf was drinking well during the sedation. Also defecating and urinating. Firm feces. Rx: 1500 mg famciclovir per rectum dissolved in 20 ml water. 600 ml Amynin (per ml: 50 mg glucose anhydrate, electrolytes, aminoacids and B-vitamins, NL 4137) per rectum. Blood and urine samples collected. All values within normal ranges. EDTA: EEHV-PCR signal much lower than day 1. Day 4 08:00 Alerter, has not been laying excessively long during the night. Rx: 1500 mg famciclovir per rectum (dissolved in 20 ml water). During the morning the animal has been drinking spontaneously from his mother. Treatment similar today 2. Day 5 09:00 Leaning against the poles. Rx: 1500 mg famciclovir per rectum (dissolved in 20 ml water). Keepers think his behaviour is about the same. Is drinking water from the hosepipe. Some normal feces manually removed from the rectum. 16:00 Still leaning against the poles but sometimes giving a more alert impression by moving his tail. Rx: 1500 mg famciclovir per rectum (dissolved in 20 ml water). Standing sedation (xylazin 0.1 mg/kg IM). Drinking from his mother. Day 5 08:00: Very lethargic; did not drink during the night. Tympanic, bilateral; intestinal obstruction suspected. Some dry feces were collected from the rectum. Rx: 1500 mg famciclovir per rectum (dissolved in 20 ml water). 6 ml Finadyne (flunixinemeglumine 50 mg/ml, NL1726) i.m. 15 ml Baytril 10% (enrofloxacin 100 mg/ml, NL3489) i.m. During the day the condition of the animal deteriorated. 14:00: sedated with xylazine (0.1 mg kg IM). Blood sample collected - heparin and EDTA and fluride. Rectal palpation: balloon-like intestines. The calf suddenly regurgitated and threw up stomach content. Rectal fluids were given. At 15:00 the animal died. Necropsy Necropsy hernia mesenterialis 1) Cause of death: * Rupture of the ileum resulting in peracute peritonitis. * Mesenteric hernia. * Intestinal mesentery, small intestine (jejunum), ileum: Venous infarction, acute, marked, with venous and lymphatic thrombosis, fibrinoid arterial necrosis, and interstitial haemorrhage and necrosis. * Intestinal mesentery, small intestine, hepatic capsule, pancreas: Peritonitis, fibrino-purulent, diffuse, peracute, moderate, associated with bacterial infection. 2) Significant diagnoses: * Liver: pericholangitis, eosinophilic, diffuse, chronic, severe, with bile duct hyperplasia and portal fibrosis. * Liver: hepatitis, granulomatous, eosinophilic, multifocal, chronic, moderate. 3) Incidental diagnoses: * Heart: haemorrhage, subendocardial, epicardial, multifocal, acute, mild. * Lung: pulmonary oedema, diffuse, acute, mild. * Adrenal cortex: adrenocortical necrosis, multifocal, acute. Cyanosis of the tongue and epicardial hemorrhages that are seen in EEHV-HD were also present in this case. They are the result of circulatory shock and are not pathognomitic for EEHV-HD. The intestinal contents was found freely in the abdomen. The hernia and the torio of the mesenterium is well demonstrated on the last photo. Conclusion Initially, when the PCR-result was positive for EEHV, EEHV was considered the cause of the disease and anti-EEHV treatment was started. Based on previous findings, the mother of the calf was assumed to be a carrier of EEHV1. However, the normal hemogram was not in line with what was seen in other EEHV-HD cases. At necropsy, multiple hemorrhages were seen in almost all organs, which is also seen in EEHV-HD. However, the predominant pathological conditions (hernia mesenterials, volvulus, torsio and rupture of the ileum were the cause of death. The presence of EEHV1a can only be explained as a virus reactivation due to a heavy stress respons of the calf in relation to the intestinal problems. Peritonitis in elephants has only been mentioned in a paper describing the presence of unrelated dermoid cysts in an Asian elephant (Wayn, 1991). References Wayne I., Anderson & Danny W. Scott. 1991. Epidermoid Cysts in the Skin of an Asian Elephant (Elephas maximus). Vererinary Dermarology. Vol. 2, No. 3/4, pp. 171-172. To page top