This page contains the links to official documents of the European Association of Zoos and Aquaria (EAZA) and the American Association of Zoos and Aquaria (AZA) with regards to elephant management and disease control: - EEHV-monitoring of calves -EEAV-treatment protocol -EEHV-antibody monitoring -Necropsy forms -Reproduction guideline -TB-recommendations -Elephant transport protocol -Vaccination advice -How to make a blowpipe -How to make a mouth opener Best Practice Guideline EAZA EEHV EEHV monitoring calves EAZA EEHV treatment protocol EAZA EEHV antibody monitoring EAZA Necropsy form EAZA Necropsy form AZA Reproduction guidelines EAZA TB recommendations USA TB recommendations EAZA Transport protocol EAZA Vaccination advice EAZA EDV Tusk fracture guideline How to make a blow pipe syringe How to make a mouth opener Urine collection for progesterone Hematology and urinalysis manual Elephant Care Manual (FAO) Musth management and Care Hand-raising manual Documents

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

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

This page directs you to the following reproduction-related topics in elephants: -estrous cycle -normal birth process -vaginal vestibulotomy -tumors and cysts in the reproductive organs -cesarian -dystocia -fetal retention -infertility (female) -infertility (male) To dashboard Reproduction Estrous cycle Endoscopy urogenital tract Pregnancy confirmation Normal birth process Dystocia Vaginal vestibulotomy Fetotomy Tumors and cysts I need your input to write these chapters: Cesarian Infertility (female) Infertility (male)

A series of videos guides you through the aspects of a full elephant necropsy. These recordings were made for a workshop given in Myanmar in 2019 and are kindly provided by the MIchigan State University. To necropsy report index Necropsy Procedure EAZA Necropsy protocol Videos elephant necropsy These videos were prepared for workshops given to elephant veterinarians in Myanmar by Elephant Care International. http://elephantcare.org Necropsy procedure Preparation Ante/postmortem changes Sample collection Circulatory system Respiratory system Reproductive system Brain + neural system Integument Multi-systemic Musculo-skeletal Foot Tusks and molars Renal and urinary To page top

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

This case report describes a colic episode in an adult Asian elephant. Salmonella sp. was identified in a fecal sample taken during this period of colic. - colic -Salmonella To colic general information CAse report Colic and Salmonellosis in an adult Asian elephant Date: Place: Data provided by: History This adult multiparous female had been on GnRH-vaccine for over 4 years. Because of chronic joint disease, the elephant had been on phenylbutazone for over 1 year in combination with omeprazol. Sudden onset of apathy, anorexia and hardly drinking water. Normal feces. Occasionally the elephant goes into a sitting position or lateral recumbancy, showing moderate straining activities. After this labor-like behaviour, herd mates investigate the perineal area of the elephant with their trunk. Differential diagnose: Labour, colics (intestinal, uterine or urinary) Treatment The administration of phenylbutazone was discontinued No specific treatment was given on the first day. Treatment results During the night the elephant became more active and the symptoms decreased. The next morning, the animal behaved normal. Diagnostic notes Salmonella sp. was cultured from the feces on the day it showed the above mentioned symptoms To page top

Edema in elephants is not uncommon. The 2 most frequently seen forms are edema in the neck, head and upper parts of the front legs (EEHV-HD) and ventral edema (general edema). Figure 1. (a) A focal moderate ventral edema. Note the smooth skin structure with reduced wrinkles in the edematous region. (0.1 African elephant, 33yrs.) (b) Focal moderate ventral edema in lateral view. (0.1 African elephant, 22yrs., 2.5 months before giving birth) (c) A moderate ventral edema extending to the external genital region. (0.1 African elephant, 46yrs., advanced pregnancy >18 months). Figure 2. Ventral edema in a 7 yr-old Asian elephant bull suffering of Salmonellosis (Photo: Willem Schaftenaar). Click here to read this case report. Figure 3. A 45 yr-old female African elephant with ventral edema showing signs of irritation (left) and sloughing of skin (right, arrow). Differential diagnosis of ventral edema In the young elephant a swelling around the umbilicus can be an indication of an umbilical hernia , sometimes accompanied by local edema. A blunt trauma of the abdominal wall can result in an abdominal hernia. Intestines can be visualized using ultrasound examination. Figure 4. Asian elephant (>35yrs) with traumatic ventral hernia. Movement of the intestines and fecal balls in the subcutaneous space could be visualized during transcutaneous ultrasound examination. Photo: Willem Schaftenaar Pathogenesis In general The body always tries to maintain the balance between intravascular and interstitial fluid, driven by four different pressures acting in the capillary bed (Fig. 5). In addition, the capacity of the lymphatic system is critical for the physiologic reabsorption of interstitial fluid and its return transport into the blood circulation (Fig. 5). Beside an increased permeability of the capillary wall, any alteration in each of these five factors can cause edema. In particular an increase in the capillary hydrostatic pressure and a decrease in the plasma oncotic pressure (= osmotic pressure induced by the plasma proteins) lead to an increased shift of fluid towards the interstitial space. If this fluid load exceeds the lymphatic capacity, fluid will accumulate and edema will develop. The aforementioned parameters do vary across different body regions, leading to a locally varying susceptibility to edema development. Therefore, edema can occur both multifocal (e.g. EEHV-HD) or focal (e.g. ventral edema) with respect to the predisposition of certain body regions and the underlying cause. The latter can be systemic or focal. The localization of edema is also determined by gravity forces and species-specific anatomical characteristics. Extracellular fluid will have the tendency to migrate downwards due to gravity. Extracellular spaces that are surrounded by tightly fitting, non-elastic tissue, are not prone to show edema, even if they are at the lowest point of the body: in humans edema can easily develop in the feet, while in elephants edema has never been reported in the distal parts of the limbs. Figure 5. Four critical parameters are determining fluid shift in the capillary bed through the semipermeable capillary wall. An increase in capillary hydrostatic pressure and interstitial oncotic pressure leads to an increased fluid shift towards the interstitial space, as well as a decrease in plasma oncotic pressure and interstitial hydrostatic pressure. The lymphatic vessels are running in parallel to the blood vessels and are collecting the interstitial fluid according to their transport capacity. In elephants According to Mikota (2006), no single underlying etiology for ventral edema in elephants has been identified so far. More likely, it presents a non-specific response to a variety of physiological stressors (Mikota 2006). In our opinion these stressors or pathological alterations can be categorized based on the general pathogenesis of an edema (Fig. 5). With this approach, each condition reported to be associated with edema in elephants so far, can be ascertained to one of the four defined etiologic categories (Fig. 6). Fowler & Mikota (2006) consider the ventral distribution of an edema in elephants caused by the gravitation of fluids into this area. But if gravitation alone would present the critical parameter for the characteristic ventral occurrence of an edema in the elephant, one would expect the swelling to occur primarily in the distal limb regions. The very thigh skin surrounding the legs with minimal elasticity may prevent this pattern. Apart from this, we assume the anatomy and physiology of the lymphatic system to explain the specific distribution pattern of ventral edema in elephants (Fig. 7). Unfortunately, anatomical knowledge on the lymphatic system in elephants is limited to one incomplete description in a fetal Asian elephant (Mariappa 1986). In this individual, a peculiarity was reported with the Cisterna chyli located in the thoracic cavity (Mariappa 1986). In humans, the horse, dogs & cats the Cisterna chyli is located in the abdominal cavity (Berens von Rautenfeld 2000, Herpertz 2013, Salomon et al. 2008). We do rather question the validity of the report for the fetal Asian elephant, than expect a significant peculiarity in the anatomy of the lymphatic system in the elephant. Figure 6. Four defined etiologic categories for edema in elephants, each with examples reported in the existing literature. Note that underlying alterations may vary extremely but result in the same clinical sign of accumulated interstitial fluid. Therefore, due to the lack of solid evidence, our line of arguments is largely based on the anatomy of the lymphatic system in horses and extrapolated to the elephant (Berens von Rautenfeld 2000, Salomon et al. 2008; Fig. 7). Assuming that the lymphatic watersheds in the elephant are running similar to the situation in the horse, it becomes obvious that the characteristic location of a ventral edema presents the region between the major transversal and horizontal watershed (Fig. 7). In this proximal part of the lymphatic territory VII, the lymphatic vessels drain towards the deep abdominal lymphatic centers and have no connection to a relevant superficial lymphocentrum. Therefore, it seems reasonable that increased abdominal pressure (e.g. during late pregnancy) may reduce the drainage of this territory. At the same time, interstitial hydrostatic pressure in the subcutaneous tissue of this body region may be low compared to the limb or the thoracic wall where bony and muscular structures are supporting the lymphatic capacity. These factors together with gravitation can serve as an explanation for the specific distribution of ventral edema in elephants. In contrast, the limbs may rarely be affected by edema, because the relatively rigid skin in combination with the underlying musculoskeletal apparatus will result in kind of a physiologic compression bandage as reported for the horse (Aurenz 2020). Figure 7. Hypothesized lymphatic territories in the elephant. The seven distinct lymphatic territories with their specific drainage areas were extrapolated from the situation in the horse (Berens von Rautenfeld et al. 2000) and numbered accordingly. The blue lines indicate the lymphatic watersheds. Note the proximal part of area VII is lacking a connection to a relevant superficial lymphocentrum. Treatment of ventral edema Given the wide diversity of underlying causes (Fig. 6) no general treatment protocol can be defined. In the literature, hot and cold pressure bandages (du Toit 2001) and increasing protein in the diet (Fowler & Mikota 2006) have been recommended. The administration of Furosemide (1mg/kg i.m.) has been unsuccessful (Martelli 2006). Considering the different etiological pathways leading to an edema, we strongly encourage the treatment of the underlying cause. To do so, an underlying cause needs to be determined or at least a classification according to Figure 6 should be strived for. The latter seems realistic by a thorough anamnesis and clinical examination. For example in cases of heart failure, positive inotropic agents may reduce the capillary hydrostatic pressure and simultaneously support the lymphatic capacity, as shown in humans (Scallan et al. 2016). In less severe cases of assumed cardiorespiratory insufficiency, which has been observed to repeatedly cause ventral edema in geriatric Asian females during hot summer days, herbal medicine can present a helpful approach (Crataegus Dilution vet.®, DHU-Arzneimittel GmbH & Co. KG, Karlsruhe, Germany; three times a day, 6.0-8.0ml orally) (personal observation in four cases). In addition to the treatment of the underlying cause, or in cases where only a symptomatic treatment is realizable, the following methods may facilitate the reabsorption of an edema. Moderate walking will centrally activate the lymphatic flow and subsequently increase the lymphatic capacity. Hence locomotion is considered a critical part of edema therapy in horses (Aurenz 2020). A sufficient amount of satisfying recumbent rest will also support the reabsorption of interstitial fluid by reducing the negative impact of gravitation. Moderate pressure washing may have a positive effect similar to manual lymph drainage in horses (Aurenz 2020). Under the assumption of a similar anatomy of the lymphatic system, adhering to the protocols established in equine lymph drainage seems a reasonable approach (Berens von Rautenfeld 2000). Given that the selectively applied pressure for manual lymph drainage could be applied by a water jet, even treating from a safe distance might become an option. Further research is needed to base such an approach on scientific findings and formulate a detailed practical guidance. Additional note With respect to our very limited knowledge on the anatomy of the lymphatic system in elephants and the corresponding physiological pathways, a major part of this compilation is very hypothetical. Although we based these hypotheses on evidence from other mammalian species, they remain to a certain amount speculative and should be interpreted with caution. References Aurenz S (2020). Manuelle Lymphdrainage beim Pferd. Hands on 2:25-31. Berens von Rautenfeld D, Rötting A, Rothe K, Lüdemann W, Boos A, Schubert T, Hertsch B (2000). Manuelle Lymphdrainage beim Pferd zur Behandlung der Beckengliedmaße - Teil 1: Anatomische Grundlagen und Behandlungsstrategien. Pferdeheilkunde 16:30-36. Caple IW, Jainudeen MR, Buick TD, Song CY (1978). Someclinico-pathologicfindings in elephants (Elephas maximus) infectedwithFasciolajacksoni. Journal of Wildlife Diseases 14:110-115. Chandrasekharan K (2002). Specific diseases of Asian elephants. J Indian Vet Assoc Kerala 7:31-34. du Toit J (2001) Veterinary care of African elephants. South Africa, South African Veterinary Foundation and Novartis. Emanuelson K, Agnew DW (2002). Wasting syndrome in a bull African elephant (Loxodonta africana). IAAAM Joint Conf, New Orleans, Louisiana. Emanuelson K, Kinzley C (2000). Salmonellosis and subsequent abortion in two African elephants. IAAAM Joint Conference New Orleans, Louisiana. Fowler ME, Mikota SK (2006). Biology, Medicine, and Surgery of Elephants. Iowa, USA, Blackwell Publishing. Fuery A, Pursell T, Tan J, Peng R, Burbelo PD, Hayward GS, Ling PD (2020). Lethal hemorrhagic disease and clinical illness associated with the elephant EEHV1 virus are caused by primary infection: Implications for the detection of diagnostic proteins. Journal of Virology 94:1-14. Heard DJ, Kollias GV, Merritt AM, Jacobson ER (1988). Idiopathic chronic diarrhea and malabsorption in a juvenile African elephant (Loxodonta africana). The Journal of Zoo Animal Medicine 19:132-136. Herpertz U (2013). Ödeme und Lymphdrainage. Stuttgart, Schattauer Verlag. Howard L, Schaftenaar W (2019). Elephant endotheliotropic herpesvirus. Fowler´s zoo and wild animal medicine: current therapy. E. Miller, N. Lamberski and P. Calle. St. Louis, Elsevier:672-679. Jensen J (1986). Paralumbar kidney biopsy in a juvenile African elephant. Proc Amer Assoc Zoo Vet, Chicago, Illinois. Lueders I, Young D, Maree L, van der Horst G, Luther I, Botha S, Tindall B, Fosgate G, Ganswindt A, Bertschinger H (2017). Effects of GnRH vaccination in wild and captive African elephant bulls (Loxodonta africana) on reproductive organs and semen quality. PLoS ONE 12:e0178270. Mariappa D (1986). Anatomy and histology of the Indian elephant. Michigan, USA, Indira Publishing House, Michigan, USA. Martelli P (2006). Veterinary problems of geographical concern - Section III Indochina and Bangladesh. Biology, Medicine, and Surgery of Elephants. M. E. Fowler and S. K. Mikota. Ames, Iowa 50014, USA, Blackwell Publishing: p. 452. Mikota SK (2006). Chapter 18 - Integument System. Biology, Medicine, and Surgery of Elephants. M. E. Fowler and S. K. Mikota. Ames, Iowa 50014, USA, Blackwell Publishing: pp. 253-261. Morris P, Held J, Jensen J (1987). Clinical pathologic features of chronic renal failure in an African elephant (Loxodonta africana). 1st Intl Conf Zool Avian Med, Turtle Bay, Hawaii. Murray S, Bush M, Tell L (1996). Medical management of postpartum problems in an Asian elephant (Elephas maximus) cow and calf. J Zoo Wildl Med 27:255-258. Perrin KL, Kristensen AT, Bertelsen MF, Denk D (2021). Retrospective review of 27 European cases of fatal elephant endotheliotropic herpesvirus-haemorrhagic disease reveals evidence of disseminated intravascular coagulation. Scientific Reports 11(1):14173 Pinto M, Jainudeen MR, Panabokke R (1973). Tuberculosis in a domesticated Asiatic elephant (Elephas maximus). VetRec 93:662-664. Salomon F-V, Geyer H, Gille U (2008). Anatomie für die Tiermedizin. Stuttgart, Enke Verlag. Scallan J, Zawieja S, Castorena-Gonzalez J, Davis M (2016). Lymphaticpumping: mechanics, mechanisms and malfunction. J Physiol 594.20:5749-5768. Seneviratna P, Wettimuny S, Seneviratna D (1966). Fatal tuberculosis pneumonia in an elephant. Vet Med Small Anim Clin 60:129-132. Windsor RS, Scott WA (1976). Fascioliasis and salmonellosis in African elephants in captivity. British Veterinary Journal 132:313-317. Edema by Christian & Linda Schiffmann Definition A local or general swelling due to excessive accumulation of fluid in the interstitial space of tissues. This condition can be caused by various underlying alterations. Depending on the composition of the fluid (in particular the protein content), an edema can be further categorized. Relevance of edema in elephants In elephants the occurrence of the so-called ventral edema is a well-known and quite common clinical symptom (Mikota 1994) (Fig. 1 and 2). Ventral edema is defined as edematous swelling in the ventral abdominal wall and tissues surrounding the external genitalia (Mikota 2006). Although the clinical impact of ventral edema is often not visible, the underlying mechanism indicates a disturbance of the internal fluid balance. In addition, edema in the submandibular region and multifocal has been described in cases of hemorrhagic disease due to herpes virus infection (EEHV-HD) (Fuery et al. 2020, Howard & Schaftenaar 2019). Clinical signs The characteristic swelling in edema may develop immediately or over the course of several days, depending on the underlying cause. Edemas caused by a local inflammatory response may be warm and painful upon palpation. The swelling in case of ventral edema without any underlying inflammatory process may feel slightly cooler compared to other body regions. Palpation is not painful and moderate pressure with the thumb may result in a dent. Such dent may also be produced if the edema is the result of an inflammatory process, in which case the pressure will provoke a pain reaction. Compared to non-edematous areas, the skin will look smoother with reduced wrinkles (Fig. 1a). If ventral edema extends from the umbilical to the genital area (Fig. 1c), the skin may become irritated through the repeated contact with the medial hind legs while walking. In severe cases, this irritation may lead to pressure necrosis and sloughing (Mikota 2006). In cases without such complications, edema may resolve without treatment within months (Mikota 1994), although this will heavily depend on the underlying cause, which should be treated accordingly. Prevention Depending on the underlying cause, the occurrence of ventral edema in elephants can be prevented. A continuous health monitoring program with focus on individuals at peculiar risk such as geriatric elephants, pregnant females or individuals suffering from cardio-respiratory or renal insufficiency will enable early supportive and/or curative treatment. Is ventral edema bad? Although ventral edema as such may not necessarily present a serious condition in an elephant, it is often associated with serious health issues and bears the risk for complications. Therefore this symptom should be investigated thoroughly and its development monitored closely.

Preventive medicine in elephants include several vaccinations foot care, monitoring for EEHV and tuberculosis and fecal check for parasites Preventive Medicine EEHV Monitoring Fecal check Foot care Tuberculosis γ-interferon testing Tuberculosis DPP tesing Vaccination To page top

The "Infectious diseases"pages directs you to diseases caused by viruses, bacteria, protozoa and parasites. Infectious diseases Virus infections Rabies Foot and Mouth disease Encephalomyocarditis EEHV Pox virus Bacterial infections Tuberculosis Anthrax Salmonellosis Leptospirosis Pasteurellosis Parasite infections Ectoparasites Stomach bots Nematodes Cestodes Trematodes Blood parasites Cutaneous filariasis Zoonotic diseases To page top

A variety of clinical procedures are described here: anesthesia, standing sedation, necropsy, broncho-alveolar lage, trunk wash, body condition score, serum banking, monitoring estrous cycle, pedicure, plasma transfusion, tusk repair, injection technique. Blood collection Hand-rasing Fecal quality control Foot care - curative Foot Care - regular Necropsy procedure Plasma transfusion Surgery Trunk wash procedure Tusk repair procedure Clinical Procedures Anesthesia Banking serum Body condition score Broncho-alveolar & Gastric lavage Injection techniques Monitoring estrous cycle Procedures

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