This page directs you to a variety of non-infectious disease conditions in elephants: -bone fractures -botulism -colic -dental problems -dermatology -esophagus obstruction/impaction -esophagus spasm -hiccup -intoxication -lameness/orthopedic problems -mesenteric hernia -ophthalmology -perineal hernia -reproduction problems -tetanus -umbilical hernia Non-infectious diseases Bone fractures 'Hiccup' Botulism Clostridiosis Colic (abdominal pain) Dentistry Intestinal impaction Intoxication Lameness/orthopedic problems Mesenteric hernia Dermatology Edema Esophagus obstruction Esophagus spasm Ophthalmology Perineal hernia Reproduction problems Tetanus Umbilical hernia Clostridiosis I need your input to write these chapters: Bloat Constipation Neonatal problems Urinary/kidney problems Clostridiosis Tetanus Enterotoxemia Clostridioides difficile Malignant edema Black leg Clostridium novyi Botulism

This chapter describes cases reports submitted by veterinarians worldwide. Case reports Dentistry Back to Top Tusk fracture in 36 months old African elephant Tusk fracture repair in 9 yr-old Asian elephant Tusk fracture repair in 4 yr-old African elephant Tusk (crack) fissure repair in 22 yr-old Asian elephant Tusk sulcus infection in adult Asian elephant T usk sulcus trauma after tusk fracture (2x) Tush loss in female Asian elephant Mandibular fracture Weight loss due to abnormal molar change Supernumerary tusk in an African elephant Dermatology Skin wounds in adult Asian elephant Wound treatment after fetotomy Wound treatment after vaginal vestibulotomy Temporal gland impaction: non-surgical treatment Temporal gland impaction: surgical treatment Back to Top Reproduction Vaginal vestibulotomy (1996) Vaginal vestibulotomy (2014) Fetotomy Back to Top Ophthalmology Bilateral corneal opacity Back to Top Orthopedic problems Partial pad and nail loss in a 54 yrs-old female Asian elephant Back to Top Infectious diseases Salmonellosis in a group of African elephants Salmonellosis in 7 yr-old Asian elephant Colic and Salmonellosis in an adult Asian elephant Salmonella septicemia in an adult Asian elephant Elephant Endotheliotropic Herpes Virus-Hemorrhagic Disease (EEHV-HD) Fasciolasis in a group of African elephants Rabies in an Asian elephant Back to Top Non-infectious diseases Clostridium botulinum in a herd of elephants Back to Top Clostridium perfringens enterotoxemia in a 6 weeks-old African elephant Intoxication Dieffenbacchia intoxication Paraquat intoxication Back to Top Gastro-intestinal problems Esophagus spasm in an adult Asian elephant Esophagus impaction in a 4.5-yrs-old African elephant Hernia mesenterialis and intestinal rupture in an Asian elephant calf (1 year old) Intestinal impaction caused by Saccharum bengalense in a captive juvenile Asian Elephant: Implications for captive management. Back to Top Miscellaneous Hiccup Asian elephant with suspected hypocalcemia Hiccup Asian elephant with polycystic nephritis Perineal hernia Colic and abdominal surgery Allonursing in an African elephant Back to Top

ElephantMedicine.info provides information about infectious and non-infectious diseases in elephants, case reports, clinical and laboratory procedures and management guidelines. -Elephant Medicine -Diseases -Treatment -Anesthesia -Dental problems -Tusk repair -Laboratory tests - Hematology -elephant disease treatment -dental problems -locomotion -diagnostic procedures -physical examination -laboratory procedures -reproduction and birth procedures -anesthesia procedure -lameness -pedicure Elephant Medicine Get started A website for veterinarians taking care of elephants Sharing your clinical experience in ELEPHANT MEDICINE with elephant clinicians worldwide This website provides information about elephant diseases, procedures and recommendations. It also includes a collection of clinical case reports, submitted by veterinarians from all over the world. You will find cases that have been successfully treated, but also cases that had a sad ending. Some basic disease information is provided as well as descriptions of clinical and laboratory procedures. The information on this website is subject to changes, as our knowledge about diseases in elephants will grow by sharing our experiences. Veterinarians involved in elephant medicine are encouraged to submit reports of their experiences. Together we can create a platform for the current and next generations of veterinarians. For the benefit of an amazing, but vulnerable species: the elephant. Disclaimer: The content of this website, such as graphics, images, text and all other materials, is provided for reference and educational purposes only. The content is not meant to be complete or exhaustive or to be applicable to any specific individual's medical condition. The information is based on scientific literature, open source information and anecdotal information provided by trusted sources. You assume full responsibility for using the information on this site, and you understand and agree that the authors are not responsible or liable for any claim, loss or damage resulting from its use by you or any user. Contact

EEHV hemorrhagic disease in elephants is often fatal as a result of DIC. Antibody assays and PCR monitoring may help to treat affected elephants in an early stage. This page describes the virus, the disease, its treatment, plasma transfusion, cross matching and standing sedation. To infectious diseases Elephant Endotheliotropic Herpes Virus-Hemorrhagic Disease (EEHV-HD) Compiled by Willem Schaftenaar History: EEHV-HD is caused by a delta-herpesvirus. The virus has evolved with the elephant species and is older than the currently living elephant species. Most (if not all) adult elephants are latently infected with EEHV. Young elephants between 1 and 9 years of age can be susceptable for an often fatal syndrom: EEHV-Hemorrhagic Disease. It is hypothesized that the long half-lifetime of maternal antibodies (EEHV maternal antibodies can circulate for up to 36 months in a calf) protects the calf against developing this syndrome. If this is true, it means that calves need to be exposed to EEHV during the phase in which antibodies are decreasing, but still protecting the calf. Fatal cases in Asian elephants have been reported over 20 times more than in African elephants. One of the hypotheses is that African elephant are shedding the virus much more frequent than Asian elephants, which offers a better opportunity for the calf to build up a solid immunity during the period that it is still protected by maternal antibodies. Asian elephants can carry EEHV1a, EEHV1b, EEHV4 and EEHV5, of which EEHV1a has caused the vast majority of the fatal cases. African elephants can carry EEHV2, EEHV3a, EEHV3b, EEHV6 and EEHV7. EEHV3 and EEHV6 have been associated with fatal cases, while the other African EEHV-subtypes are associated with lymphoid nodules in lungs and skin of African elephants. There is one report of a fatal case caused associated with EEHV3 in an Asian elphant. Like all herpesviruses, EEHV has a latent phase in a so far unknown tissue of the elephant body. For reasons that are not yet known, the virus can be reactivated, probably due to a (temporary) weakening of the elephant's immune system. The virus migrates to the mucous membranes of the mouth, trunk, eyes and the female genital tract. Shedding in semen or mucous membranes of the penis has not yet b een reported. Shedding has been observed in a zoo-kept herd of Asian elephants after the introduction of a bull and on a second occasion after the introduction of 2 females (Titus, 2022). In another zoo, 2 young Asian elephant calves died of EEHV1 within 2 weeks after the introduction of a breeding bull (Dublin zoo, 2024). Both calves appeared to have no antibodies against EEHV1a and EEHV1b. These findings suggest that the introduction of adult elephants in a herd can induce virus reactivation and consequently virus shedding. (Maternal) antibodies Humoral antibodies can be demonstrated by using recently developed antibody assays. A fluorescence based assay (Lips assay) has become available in the USA (Fuery, 2020) and an ELISA-based assay in the Netherlands (Hoornweg, 2021 ) . Serological studies using these assays demonstrated that maternal antibodies remain circulating for up to 36 months in elephant calves (Fuery, 2020). These maternal antibodies are transmitted in the uterus. The long period during which they are circulating at high levels in a young elephant, suggests that this species is able to absorb antibodies excreted by the dam in her milk. This is also suggested by Takehana et al 2024 , who described that the antibody level in a bottle-fed elephant calf decreased within 14 months as compared to 2 other calves in the same herd, in which antibodies remained high for more than 2 years. However, this hypothesis still needs to be proven. EEHV-subspecies and subtype-specificity has been demonstrated for these assays (Hoornweg, 2023 ) . Another finding was that antibodies against EEHV4 were not protective against fatal EEHV1a infections, while antibodies against EEHV1a seem to protect against illness caused by EEHV4 and EEHV5. Hoornweg et al. studied 23 fetal EEHV-HD cases in European zoos and found that all fatalities had low antibody levels against gH/gL of the EEHV (sub)species they succumbed to (Hoornweg, 2024) . During the first 12 months of life, maternal antibodies seem to remain stable at a high level, which seems to protect the calf from developing Hemorrhagic Disease when infected by EEHV. This may explain why clinical EEHV-cases have never been reported below the age of 1 year. This has lead to the hypothesis that young elephants need to be exposed to EEHV while they are still (partly) protected by maternal antibodies. Shedding of EEHV by herd mates is therefore essential for the calf to build up natural immunity. In an elephant that is permanently infected with EEHV, shedding takes place after reactivation of EEHV. In 2 elephant orphanages in Sri Lanka (31 and 93 elephants), all calves had high levels of EEHV-gB antibodies. These 2 institutions never lost a calf to EEHV-HD. This leads to the conclusion that the larger herd sized in these 2 orphanages (compared to zoos increases the likelihood of cantact between EEHV-shedders. Herpes viruses in general can become reactivated during a stressful situation, when the immune system of the host seems to become weaker, possibly under the influence of endogenous glucocorticosteroids. Specific stress inducers that result in EEHV-reactivation are not yet known for elephants. It is tempting to hypothesize that social stress could be one of those factors, as elephants are highly social animals. Zoos generally try to avoid stress situations for their animals, including elephants, especially when there is a young calf in the herd. In the light of the recent findings, the absence of stress might as well work against the development of acquired immunity against EEHV in young calves. The same hypothesis could be valid for elephants in wild situations: if social stress factors are absent in some of the wild situations (less contact with other herds due to habitat fragmentation, less contact with bulls in musth), reactivation frequency of EEHV may be reduced in (sub)adults, preventing calves younger than 12 months from building up immunity during the crucial time frame when they are still protected by maternal antibodies. Clinical signs and diagnosis: 10-14 days before the elephant shows clinical signs of EEHV-HD, the presence of the virus can be demonstrated in the blood by qPCR (EDTA blood sample). It is important to monitor the presence of EEHV in calves between 1 and 9 years of age on a weekly base. As soon as the presence of EEHV has been confirmed, the number of monocytes and platelets are indicative for the further development of the virus in the days to come. When monocytes and platelets are stable and the viral load remains below 5.000 Viral Genome Equivalents (VGE's)/ml, close observation is required. As soon as the viral load in the blood increases or monocytes or platelets drop, immediate treatment is required. If the initial viremia has passed unnoticed, the young elephant may display one or more of the following unspecific symptoms: lethargy, reduced appetite, lameness, abnormal sleeping pattern, soft feces. In more advanced cases petechiae are seen on the tongue, edema on the head and front legs and finally cyanosis (purple tongue). Sometimes the severe symptoms are the first ones to be discovered. Photo: courtesy of Florence Ollivet-Courtois The most relevant tools needed for the diagnosis of EEHV-HD are: qPCR and total WBC, platelet count and blood smear (manual count of monocyte and heterophyls). The monocyte/heterophil (M/H) ratio is an important prognostic indicator for EEHV-HD. A ratio below 1 is reason for great concern and immediate treatment should be started. Blood smears are essential for manual differentiation of the white blood cells and recognition of the morphology. Note that the presence band-heterophils in young elephants is a bad sign! Lactate is an important serum parameter to monitor in a EEHV-HD case. Normal values are between 0--0.11 mmol/L (0-1 mg/dL). Values >0.44 mmol/L (4 mg/dL) are indicative for perfusion problems due to DIC (see below). EEHV-HD patients often have lactate value > 0.22 mmol/L (2 mg/dL) (Wiedner, pers. comm. 2022). Reports from Thailand suggest that a (primary?) infection with EEHV4 is generally associated with intestinal problems (Kittisirikul, 2025). At rectal examination, edema of the rectal mucosa can be diagnosed. This finding is supported by histopathological findings in fatal EEHV-HD cases ( Sripiboon, 2013) . Disseminated Intravascular Coagulopathy (DIC) One of the main reasons an EEHV infection can lead to severe illness or death is the development of DIC in young calves that are not adequately protected by (maternal) antibodies. DIC results from a severe, dysregulated immune response triggered when endothelial cells are damaged by the virus (endothelial glycocalyx degradation). Two independent studies have clearly demonstrated the occurrence of DIC in fatal cases of EEHV-HD (Guntawang, 2021; Perrin, 2021). In the treatment protocol for EEHV-HD, addressing DIC is a top priority. Cytokine Storm? In recent years, researchers have questioned whether a cytokine storm—described in human hemorrhagic fevers such as Ebola and Dengue—also plays a role in the development of EEHV-related DIC in elephants. A recent study reported a significant increase in interleukin-6 (IL-6) and interleukin-10 (IL-10) levels in the tissues and blood of six elephants suffering from clinical EEHV1a-HD (Hoornweg, 2025). Moreover, 2 elephants with clinical EEHV1a-HD that were treated with glucocorticosteroids, had lower serum levels of IL6 and IL10 than those that were not treated and even lower than the assumed reference level. Both elephants survived the clinical EEHV-HD infection. Elevated levels of these two interleukins are commonly associated with cytokine storms, suggesting that this phenomenon may also occur in EEHV-HD. These findings support the theory that the administration of glucocorticosteroids are indicated in the early phase of the hemorrhagic disease. Photo: courtesy African Lion Safari Park Photo: courtesy Amersfoort Zoo Pathological findings at necropsy The most prominent signs of EEHV-HD at necropsy are those that resulted from DIC: hemorrhages in most of the organs, joints and muscles, ranging from petechiae to large hematomas. There may also be a hydro-or hemopericardium. Hemorrhages in the heart, intestines, brain and liver of a yound elephant that died of EEHV1a-HD. Photos by Arun Zacharia Click here for the EAZA elephant TAG EEHV treatment protocol Treatment of EEHV-HD Early treatment of EEHV-HD 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. Repetitive sedations have been given to sick calves without negative effects. If butorphanol is used to obtain sedation, it should not be antagonized as it will help to relieve the pain in the patient. Circulatory support: Rectal fluids: Luke-warm water 10-20 ml/kg BW TID or QID, up to every 2 hours NB: As repeated rectal fluid administrations may be needed, the anus of the elephant may become sensitive to these procedures. Rx: mix 15 ml lidocaine 2% with some lubricant and carefully apply on the anus. Wait for 10 minutes before placing the tube in the rectum for the administration of fluids. Repeated rectal exploration may be cause painful irritation of the anal sphincter and perianal skin. Adding lidocain to the lubricant may facilitate the exploration. Crystalloids: IV as a bolus of 0.3-4 ml/kg BW When blood or plasma is available, the administration of those products has preference over crystolloids. Whole blood transfusion: Indicated in case of anemia or severely delayed coagulation. The advantage of whole blood administration lays in the rapid availability: no waiting time for preparing plasma. A practical strategy is to collect sufficient blood from a donor elephant to make it available for whole blood (1-2 L) and save the rest to prepare it for plasma transfusions. Dosage whole blood transfusion: 1-2 L. Cross matching needs to be done prior to the transfusion. Plasma transfusion: IV bolus of 0.5-2 ml/kg BW (after minor cross matching of donor and recipient blood) For plasma transfusion in elephants see: Emergency care for elephants clinically ill from Elephant Endotheliotropic Herpes Virus–hemorrhagic disease (EEHV-HD, EAZA Elephant TAG, compiled by Fieke Molenaar (ZSL-Whipsnade zoo), Mads Bertelsen and Kathryn Perrin (Copenhagen zoo), Imke Lueders (GEOLifes), Lauren Howard (Houston zoo), Willem Schaftenaar (vet adv. EAZA Elephant TAG, 9 February 2021) Plasma is currently considered one of the best supportive therapies to provide, as platelets, clotting factors and potentially protective antibodies can thus be provided. Note that the freezing process activates platelets, which may render them useless at the time of transfusion. Therefore - where possible - freshly collected plasma is preferred. The following should be considered for plasma transfusions: If frozen plasma is available, this can be given in an early stage of the disease to save time (despite the activated and spent platelets). Blood collection from an adult elephant (plasma donor) should be initiated to provide fresh plasma as soon as possible. Cross-matching the donor animals with the recipients, especially if one donor will be used on multiple occasions. For more information about plasma transfusion: click here Anti-inflammatory treatment : Gluco-corticosteroid drugs are indicated in case of suspicion of DIC. Recent research could demonstrate an increase of interleukin 6 (IL6) and interleukin 10 (IL10) in tissues of elephants that succumbed to EEHV-HD and below-normal levels in blood of 2 survivors that were treated with glucocorticosteroids (Hoornweg, 2025). Dexamethasone: Used in 2 EEHV1a-HD survivor cases: Case 1: started with 0.2 mg/kg (200 mg) IV and continued daily for 12 days (final dose 0.007 mg/kg = 7 mg). Case 2: 2 mg/kg iv SID for 5 days, followed by 1 mg/kg iv SID for 2 days Triamcinolon : 0.067 mg/kg IV SID for 1-3 days (used in 1 EEHV1a-HD survivor case). Methylprednisolone sodium succinate: 0.5 mg/kg IV or IM; much higher doses are used for treatment of shock in horses: 10 - 20 mg/kg IV. Please note that in human medicine DIC (e.g. in Covid-19 cases) is treated with Dexamethasone 0.1mg/kg SID for 7-10 days ( https://www.who.int/news-room/q-a-detail/coronavirus-disease-covid-19-dexamethasone#:~:text=Recommendation%201%3AWHO%20strongly,medication%20for%20another%20condition .) Antiviral treatment: Several antiviral drugs are routinely used, although none of these have proven to be effective; preliminary studies are suggesting that the TK-gene of EEHV does not make the virus sensitive for the group of “ciclovirs” that is currently used. Famciclovir has been used most frequently, followed by ganciclovir. In the absence of the former antivirals, aciclovir has been given in several cases. Famciclovir: 15 mg/kg orally or rectally, TID Aciclovir: 15 mg/kg BID orally, rectally or IV (Ganciclovir: 5 mg/kg BW BID 5 mg/kg IV, BID, each dose given slowly diluted in 1 liter of NaCl. NB Ganciclovir is not preferred, as it is considered a potential human carcinogen, teratogen, and mutagen) Antibiotic treatment: A broad-spectrum antibiotic is recommended as the integrity of the intestinal wall may be disrupted and gut bacteria may leak into the abdominal cavity. Pain management: Pain management (opioids, NSAIDs) is recommended if there are clear signs of pain or discomfort Butorphanol (first choice): 0.008-0.014 mg/kg IM Q 4 hrs Flunixin: 0.25 to 0.5 mg/kg IM SID Omeprazole: 0.7 to 1.4 mg/kg PO SID Immunostimulating drugs: Immunostimulants have been used in one case of EEHV1a-HD: Interferon alpha 2a or 2b (25 mIU/2.5 ml Intron A, Merck or 4.5 mIU/0.5 ml Roferon A, Roche) were administered at 27–33 mIU intramuscularly once a day on days 1–12 then every 48 hours to day 20, administered by dart on days with no treatment session, incomplete delivery on days 8 and 14. Bacterial plasmid DNA in a liposome carrier (Zelnate DNA immunostimulant, Bayer HealthCare LLC) was given to the same elephant (2 ml intramuscularly on days 0, 4, 7 and 12). It should be noted that the same elephant was also given anti-inflammatory treatment (dexamethasone). WS personal note: It should also be noted that interferon levels are expected to be elevated in case of a cytokine storm. As there is no scientific proof of the benefits of interferon treatment in EEHV-HD, care must be taken to use any interferon-containing drug formulation! Adjunctive drugs: Oxygen should always be standby and administered as soon as signs of hypoxemia are seen. Furosemide (1 mg/kg IM ) has been given occasionally. Vitamin C, routine used in Asia (dos age depends on product; use equine dose). Vitamin E (dosage depends on product; use equine dose). Monitoring the course of the disease: The serum lactate level gives an indication of the organ perfusion. In EEHV-HD patients, the lactate level is often higher than 2 mmol/L (normal value: 0-1 mmol/L). Rehydration by the fluid administrations will help to decrease an elevated lactate. Platelet counts during the treatment course are helpfull in evaluating the success of the treatment. The administration of whole blood and plasma will compensate partly the loss of platelets and also provide antibodies if the donor is an adult elephant. It is advisable to make sure that the donor does have antibodies. Blood pressure : in severe EEHV-case, the blood pressure may decrease or decrease. Fluid administration may help to stabilize the blood pressure. When the patient has a vascular shock, the blood pressure may be low. A fast administered bolus of rectal fluids (0.5-5 ml/kg BW) within 15-30 minutes may help to increase the blood pressure. To standing sedation Treatment of EEHV-HD Cross-matching procedure Based on design elaborated by Houston Zoo, Inc. Step one: Prepare a 3-5% red cell suspension. 1. Collect blood from both donor and recipient in EDTA. 2. Centrifuge the tube and separate the plasma from the red cells. Save both. 3. Place 1 drop of recipient red cells into a small (2-5 ml) clean test tube. 4. Add approx. 1-2 ml of normal saline to the tube with the red cells (or 1 drop RBC to 40 drops saline) 5. Centrifuge at 2500 RPM for 20 seconds. 6. Remove the supernatant, leaving the red cell button on the bottom. 7. Repeat steps 4-6 three times (for a total of 4 washes). 8. Add 1 drop of newly washed recipient red cells to a new test tube. 9. Add approximately 20-40 drops of saline and mix to suspend the red cells. This should be an approximate 3-5% cell suspension to work with. Step two: Minor cross-match (for plasma transfusion). 1. Add 1 drop of the recipient’s 3-5% red cell suspension to a labeled test tube. Add 1 drop of the recipient’s 3-5% red cell suspension to another labeled test tube to be used as a control. 2. Add 2 drops of donor plasma or serum to the test tube. 3. Add 2 drops of saline to the control tube. 4. Incubate these tubes at 37oC for 15 minutes. 5. Centrifuge the tubes for 20 seconds at 2500 RPM. 6. Observe the supernatant for signs of haemolysis. If present in the cross-match tube and not the control tube, the match is not compatible. If present in both, start again with a new cell suspension. 7. If no haemolysis, then gently rock the test tube back and forth to re-suspend the cell button. Observe the cell button while rocking the tube and grade for the presence of agglutination. Grade on a 0-4 scale where 0 is no agglutination and 4 is heavy clumping. Record your results. Step three: Major cross-match (for whole blood transfusion). 1. Add 1 drop of the donor’s 3-5% red cell suspension to a labeled test tube. Add 1 drop of the donor’s 3-5% red cell suspension to another labeled test tube to be used as a control. 2. Add 2 drops of recipient’s plasma or serum to the test tube. 3. Add 2 drops of saline to the control tube. 4. Incubate these tubes at 35-37oC for 15 minutes. 5. Centrifuge the tubes for 20 seconds at 2500 RPM. 6. Observe the supernatant for signs of haemolysis. If present in the cross-match tube and not the control tube, the match is not compatible. If present in both, start again with a new cell suspension. 7. If no haemolysis, then gently rock the test tube back and forth to re-suspend the cell button. Observe the cell button while rocking the tube and grade for the presence of agglutination. Grade on a 0-4 scale where 0 is no agglutination and 4 is heavy clumping. Record your results. Anchor 1 References: Fuery, A, Pursell,T., Tan, J, Peng, R, Burbelo, P.D., Hayward, G.S., Ling, P.D.2020. Lethal Hemorrhagic Disease and Clinical Illness Associatedcwith Elephant Endotheliotropic Herpesvirus 1 Are Caused by Primary Infection: Implications for the Detection of Diagnostic Proteins. J. Vir. Volume 94 Issue 3. Guntawang T, Sittisak T, Kochagul V. ,Srivorakul S., Photichai K., Boonsri K., Janyamethakul T., Boonprasert K., Langkaphin W.5, Chatchote Thitaram C. and Pringproa K. 2021. Pathogenesis of hemorrhagic disease caused by elephant endotheliotropic herpesvirus (EEHV) in Asian elephants (Elephas maximus ). Scientific Reports (2021). 11:12998. https://doi.org/10.1038/s41598-021-92393-8 Hoornweg TE, Schaftenaar W, Maurer G, van der Doel PB, Molenaar F, Chamour-Galante A, Vercammen F, Rutten V and de Haan CAM. 2021. Elephant Endotheliotropic Herpes Virus is omnipresent in elephants in European zoos and an Asian elephant range country. Viruses 2021, 13, 283. https://doi.org/10.3390/v13020283. Hoornweg TE, Perere VP, Karunarathne NS, Schaftenaar W, Mahakapuge AN, Kalupahana AN, Rutten VPMG, de Haan CAM. 2022 . Young elephants in a large herd maintain high levels of elephant endotheliotropic herpesvirus-specific antibodies and do not succumb to fatal haemorrhagic disease. Transboundery and Emerging Diseases 69-5 . https://doi.org/10.1111/tbed.14644. Hoornweg TE, Schaftenaar W, Rutten VPMG, de Haan CAM. 2024. Low gH/gL (Sub)Species-Specific Antibody Levels Indicate Elephants at Risk of Fatal Elephant Endotheliotropic Herpesvirus Hemorrhagic Disease. Viruses. 2024; 16(2):268. https://doi.org/10.3390/v16020268. Hoornweg TE, Schaftenaar W, IJzer J, Mulder MMP, Lugtenburg M, van Beest A, de Haan CAM and Rutten VPMG (2025) Elevated IL-6, IL-10, and IFN-g levels in fatal elephant endotheliotropic herpesvirus – hemorrhagic disease cases suggest an excessive proinflammatory cytokine response contributes to pathogenesis. Front. Immunol. 16:1645752. doi: 10.3389/fimmu.2025.1645752 Howard L.L. & Schaftenaar W. 2017. Elephant Endotheliotropic Herpes Virus. In: Fowler’s Zoo and Wild Animal Medicine Current Therapy, Volume 9. Kittisirikul N, Angkawanish T, Langkaphin W, Chaopong O, Thaitam B and Sripiboon S. 2025 Challenging management of clinical EEHV4 infection in an adult Asian elephant. 21st International Elephant Conservation and Research Symposium. Fort Worth IEF, December 5-8. Luz S & Howard L.L. 2017. Elephant Endotheliotropic Herpesvirus (EEHV) in Asia. Recommendations from the 1st Asian EEHV Strategy Meeting (On behalf of the Asian EEHV Working Group), second edition. 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 (2021) 11:14173, https://doi.org/10.1038/s41598-021-93478-0. Sripiboon S, Tankaew P, Lungka G and Thitaram C. 2013. The occurrence of Elephant Endotheliotropic Herpes Virus in captive Asian elephants (Elephas maximus ): first case of EEHV4 in Asia. Journal of Zoo and Wildlife Medicine 44(1): 100–104, 2013. Takehana K, Hoornweg TE, Schaftenaar W), Rutten VPMG, de Haan CAM, Matsuno K. 2024. Elephant endotheliotropic herpesvirus gB-specific antibody levels in sera of Asian elephants (Elephas maximus) in Japanese zoos. J Vet Med Sci 86(12): 1279–1283, 2024 doi: 10.1292/jvms.23-0503. Titus SE, Patterson S, Prince-Wright J, Dastjerdi A, Molenaar FM. 2022. Effects of between and within Herd Moves on Elephant Endotheliotropic Herpesvirus (EEHV) Recrudescence and Shedding in Captive Asian Elephants (Elephas maximus ). Viruses, 14(2) 2022. doi:10.3390/v14020229. Wissink N. et al. 2018.Using in-house hematology to direct decisionmaking in the successful treatment and monitoring of a clinical and subsequently subclinical case of Elephant Endotheliotropic Her Vitus 1B. J. of Zoo and Wildlife Med., 50(2): 498-502 For more information see: http://eehvinfo.org/ To page top

Pasteurellosis I'm a title. Click here to edit me.

My Items I'm a title. Click here to edit me.

CASE REPORT Dentistry

Bone fractures are not uncommon in elephants. Radiography is needed for a proper diagnosis. A case of mandibular fracture is described in this chapter. To non-infectious diseases Bone fractures Mandibular fracture Mandibular fracture Mandibular fracture Mandibular fracture Mandibular fracture Mandibular fracture Bone fractures Mandibular fracture

Dirt, foreign bodies, a short tusk remnant after a tusk fracture and parasites (Cobboldia sp) can cause a purulent sulcus infection in elephants. To parasitology To dentistry case report Tusk sulcus infection Place: Dak Lak elephant Conservation Center Vietnam Date: 2017 Data provided by: Van Thinh Pham, DVM History Purulent discharge from the dental sulcus in an adult Asian elephant bull since a few days. The area around the sulcus was itching, demonstrated by the bull by frequent rubbing the tusk base against trees. Diagnosis Frequent blowing sand in the sulcus area may also be the cause of this problem. in this case, no sand or dirt was present in the sulcus. An infection with larvae of the stomach bot ( Cobboldia sp. ) was suspected. Treatment The dental sulcus area was cleaned with cotton wool and flushed with Betadine and the bull was treated with ivermectin SQ, 0,2 mg/kg BW Treatment results The sulcus lesion healed completely within 7 days. Cobboldia (stomach bot) larvae 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.

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

This page describes the normal birth process in elephants, including progesterone and ultrasound monitoring, preparation, list of requirements for veterinary assistance, transrectal massage to induce the Ferguson reflex and post-partem care. To reproduction Normal birth process This chapter is based on the EAZA Guidelines for the reproduction-related management of female elephants . Taken care at the birth process means that the pregnancy has been confirmed. More detailed information is provided in the chapter: pregnancy confirmation. After a pregnancy period of 87- 95 weeks (610- 670 days, 20-22 months), parturition is sometimes announced by subtile changes in the behaviour of the elephant. Twentyfour hours observation including the use of a (time-lapse) video recorder starting in week 85 may add to information about relevant events prior to parturition: night pacing, kneeling down, climbing, short periods of separation from the group, beating the vulva with the tail, frequent production of small-sized feces and small quantities of urine, loss of mucous plug, playing with mucous plug, rupture of the allantois sac, labour waves. Preceding any recommendation in this chapter, the following remarks need to be made: It is a myth to think that a multiparous elephant does not need to be monitored and assisted during parturition according to this protocol. Too many calves have been born dead or very weak because of the fact that parturition had started unnoticed and stopped unnoticed. In our view, this protocol should be followed in ALL cases of elephant parturition as much as the elephant management allows. It is a also myth that oxytocin is a harmless drug to be used in elephant parturitions. In at least 3 cases the administration of oxytocin has been associated with the occurrence of an uterus rupture because of insufficient cervix dilatation. It should never be used without ultrasonographic examination of the cervix uteri. The visible presence of the allantois sac as a subcutaneous bulging mass under the tail is not a guarantee for a sufficiently dilated cervix. Many elephants, including very experienced multiparous elephants may just stop the parturition process, often unnoticed. Hypocalcemia is one of the main causes for this phenomenon to happen.This will compromise the health of the calf. Don’t relay only on what you see from the outside! For a proper judgment about the presence of labor activities or the progress of parturition, your professional judgment should be based on the results of progesterone tests and ultrasonographic examinations. If you do not believe in the above mentioned statements, you may find yourself confronted with a dead elephant calf or a dead elephant mother or both. So, discuss this item with your staff and make your decision before you start breeding your elephants. If the management of elephants in your zoo does not allow blood sampling or ultrasonographic examinations, you must be aware of the risks associated with a silently interrupted birth process, no matter the reproductive experience of the animal involved. Safety for the personnel should never be challenged by unacceptable risks. Predicting the time of parturition, measures and observations: Daily blood sampling from week 89: every other a day progesterone assay, until week 91 (637 days). From week 91 (637 days): daily assays and as soon as progesterone starts to decrease: sample twice daily. Daily monitoring of progesterone is only possible if you have a nearby facility that runs these assays on a daily basis. Find out from your nearby hospital in the early stage of pregnancy! Many veterinary labs do not have tests that are sensitive for levels of progesterone (P4) in elephants 1-3 days prior to delivery. Also check the availability during the weekend. NOTE: a decrease of progesterone to baseline level is not always occurring. A 23-yrs-old Asian elephant at the Rotterdam zoo (with a baseline progesterone level < 0.6 nmol/l) delivered a healthy calf while her progesterone remained above 0.65 nmol/l. Progesterone plasma concentration during pregnancy. After a gradual decrease in the last months of gestation, progesterone drops to baseline level a few days before parturition. Note that the absolute height of the progesterone concentration depends on the assay used! Different assays measure different metabolites = different levels! Signs of an approaching parturition may include: ·Loss of mucous plug (not seen in many facilities) ·Pre-and post-parturition ventral edema may be noticed. ·Group members may react differently (vocalizations, restlessness) ·In most cases (75%) rupture of allantois sac and loss of allantois fluid (looks like urine) is seen within 2 hours prior to birth. ·The size of fecal balls may get smaller towards the end of pregnancy. ·Frequency of urination may increase around parturition, resulting in more “watery” consistency of the urine, resembling more like allantois fluid . ·Development of mammary gland and production of milk shortly before birth is often seen, however this may also occur in a much earlier stage of pregnancy . Milk accumulation can be visualized using transcutaneous ultrasonography several hours prior to parturition. ·Softening of the pelvic ligaments (due to estrogen surge) may result in slightly abnormal locomotion of the hind legs. Parturition/Preparations for calving: ·Training and/or desensitizing of the pregnant elephant for veterinary intervention, like blood sampling, injections, IV-infusions, milking and rectal manipulations ·If possible, store some colostrum (freezer) or store plasma obtained from the dam in weeks prior to parturition. ·Have artificial milk available (Salvana GmbH, Germany; hand raising has been done at Emmen Zoo and Berlin Zoo) ·Check restraint chains and fixation points for the legs and one extra fixation point between the hind legs for pulling devices. Soft ropes for pulling the calf away if needed should be available. The use of a calf harness has been described. ·Check the stable and place bars where a calf could possibly escape. Block all possible escaping routes for the calf (not for staff!!). ·Take out all obstacles. ·Be prepared for closing the elephant house for the public (sign post, etc.) ·Make sure there is a good stock of commercial cat litter or saw dust to be used on a concrete floor as soon as the calf is born. This will absorb much of the allantois fluids and prevent the animals from slipping on the wet floor. ·2 or 3 pairs of keeper-gloves (soccer) to get a better grip on the wet, slippery calf when needed ·Plastic hose pipe (with pump, if necessary) for rectal cleaning with lukewarm water ·3 birth-chains with proper handles (2 for the legs, 1 for trunk or tail); find a way to avoid back sliding when manual extraction (vaginal vestibulotomy) is required. ·Drugs to be kept in store: ·Ca-borogluconate for I.V. infusion ·Estradiol gel (EstroGel® 0.06%) ·Oxytocin ·Lidocain ·Xylazine, detomidine or medetomidine ·Butorphanol ·Azaperone ·Atipamezole ·Doxapram ·Oxygen ·(Betadine®-)iodine solution for navel disinfection (umbilical infection is a major cause of perinatal complications) ·Lubricant (many liters). J-lube®, a concentrated lubrication powder, has proven to be very useful. The normal calving process should take place within 2 hours after rupture of membranes (release of fetal fluids). If the plasma progesterone level decreases to below base line concentration, this is a signal that calving should take place within 48 hours. Prolonged intervals have been reported (as long as 14 days) still resulting in the birth of a living calf, but it is very likely that this is due to a disturbance of the normal birth process that should be corrected before the health of the calf is jeopardized. There is one report of a parturition taking place without a complete drop to base line level. The calving process is a natural process. Elephants should give birth in their own social environment, excluding any external disturbing factors (e.g. noisy building in the neighborhood, visits of unknown individuals, etc.). With a well trained animal, blood sampling and ultrasonographic examinations can be done while the animal is temporarily separated from the group. Immediately afterwards, the animal should return to its group. All efforts should be made to make sure that the calf is born in the group while the mother is NOT chained! This will stimulate the acceptance of the calf by the mother and group members and is an investment for future breeding successes for the entire elephant group. To determine the right moment when calving starts, 2 parameters are essential: - The progesterone blood level - The relaxation of the cervix, monitored by ultrasonographic examination. Progesterone: the sensitivity of the equipment and the time needed to run the assay are the bottleneck for using the progesterone concentration as a reliable tool. Today many human hospitals use advanced equipment with a very low detection level that can provide results in less than 2 hours. Make sure that you have made arrangements with a lab long before you expect the parturition. Ultrasonography: to use this technique as a reliable tool, it is indispensable for the veterinarian to gain experience long before the elephant birth is expected. This will enable the veterinarian to distinguish a normal cervix from the relaxed cervix (figure 4a + b) from the normal cervix. Preferably a 3.5 MHz probe should be used transrectally. Longitudinal, transrectal ultrasonographic image of the vagina and the closed cervix of a pregnant e lephant. The same image as with the vagina and cervix indicated with white lines. Transversal, transrectal ultrasonographic vagina and cervix of a pregnant elephant. Allantois sac with cloudy fetal fluid in the (partly) dilated cervix of an Asian elephant 12 hours prior to delivery (transverse section, white arrows: allantois sac, open arrow: pelvic bone) The same image with the vagina and the closed cervix indicated by white lines. Note the folds in the cervix uteri. Allantois sac with cloudy fetal fluid in the (partly) dilated cervix of an Asian elephant 12 hours prior to delivery (longitudinal section, white arrows: allantois sac, open arrow: pelvic bone) During the last 2 weeks of gestation, the mucous that is present in the vagina during gestation will be discharged gradually. This is a clear indication for a pending parturition. Recognizable onset of parturition occurs normally within 24-48 hours after progesterone has dropped to below base-line level. In these guidelines the absence of visible signs of parturition in the same time frame is considered an abnormal condition; this status requires veterinary intervention. At this point 2 situations may occur: the parturition process has started but has been interrupted without or with spontaneous rupturing of the allantois sac. Interpretation of findings and action to be taken 1. No rupture of allantois sac noticed If the calf is not born by natural way 24 hours after blood progesterone has dropped to baseline level, rectal palpation and ultrasonographic examination of the cervix is highly recommended. This will demonstrate the rate of relaxation of the cervix, the presence of the allantois sac or parts of the fetus in the cervix or vagina and should be repeated at least every 8 hours. A blood sample should be taken to measure the calcium level. If below 2.5 Mmol/l, calcium should be administered as an IV-infusion (NB: when given in an ear vein, it should be given strictly IV in order to avoid damage to the vein) or orally (suggestion: calcium syrup concentrate for human use, enveloped in the carton core of toilet paper, covered and sealed with fresh tamarind paste has worked well; most elephants will eat it, including the carton material). The effect of the calcium administration should be confirmed by rectal palpation (increase of contractibility of the uterus) and determination of the blood calcium level. Store an EDTA and heparine sample for herpes virus diagnostic purpose (both cells and plasma in freezer after separation). Transrectal ultrasonographic examination at 48 hours: A. No relaxation of the cervix at 48 hours: search for calf movements and nail position of the fetus (palpation and ultrasound) and blood flow in fetal vessels (ultrasound). Transcutaneous ultrasonographic examination (both flanks have a small ”window” where visualization of fetal movements may be seen) may help to determine the status of the fetus. Apply estrogens rectally. Good results have been obtained by the rectal and transdermal (perineum) application of an estradiol containing estrogen gel (Estrogel 0,06%, total dose 700-800 mg estradiol). The effect on the cervix dilatation should be monitored closely by transrectal ultrasonography! At this time, at least 1 hour after the local application of estradiol, rectal massage should be applied to test and stimulate the contractibility of the uterus. Technique: remove feces from rectum, flush out the rectum, use abundant lubrification, keep both gloved hands (NB: the rectal mucosa is vulnerable due to estrogens) with the fists joined in a firm grip and press with the wrists or the dorsal sides of the hands against the pelvic ring to stimulate the pelvic receptors until strong labor waves appear or at least 10 minutes. When labor waves occur, continue this massage for 3 hours (if needed change operator). Check regularly by means of ultrasound the condition of the cervix. If there is still no cervix relaxation, continue monitoring the viability of the calf. If no fetal parts can be detected, consider the presence of pseudopregnancy (ovarian tumor, dysfunction of the pituitary gland, etc.). The application of estradiol gel (total dose: 400-500 mg 17-β-estradiol) as described above may be repeated 3-4 hours after the first treatment if the cervix dilatation is still incomplete. B. Partial or complete relaxation of the cervix at 48 hours or later as a result of the situation described under 1A: Apply rectal massage to test contractibility of the uterus. If limited or no reaction, the administration of oxytocin is contra-indicated. In this case, the administration of calcium is recommended (even when blood calcium level is within normal ranges). After 2 hours the use of estradiol as described under 1.A is recommended. Only if uterus contraction can be provoked by the rectal massage, the use of oxytocin may be considered using the following dosage: 25-50 IU oxytocin s.c. or i.m. (if needed use a blow dart). Oxytocin should be used with care, as it may dramatically exhaust the contractibility of the uterus muscles as well as the general condition of the female. There might also be the risk of reduced blood circulation in the umbilical chord, due to the spasms in the myometrium. Prostaglandine E (dinoproston) has been used on a few occasions for cervix dilatation (after the administration of estradiol) and to stimulate uterus contractions. As there is still limited knowledge of its efficacy after transrectal administration and the risk of stormy uterus contractions, it should only be used when any obstructions or abnormalities of the calf can be ruled out. Depending on the progress obtained, rectal massage and the administration of oxytocin are the 2 major treatments to follow from this point. In between these treatment events, the animal should be exercised to relieve the pain and stimulate position changes of the calf and preferably it should be kept in the group. Only when the animal cannot be separated whenever required, the cow should be kept separated from the group, but with as much physical contact as possible. Oxytocin should be given in intervals of at least 2 hours for a maximum of 12-24 hours under the guidance of ultrasound to evaluate tAhe progress. Continue this approach of treatment until parts of the calf have entered the pelvic cavity. If the efforts remain unrewarded and no access to fetal parts is possible, not much can be done. Continue monitoring the viability of the calf. If the calf has died, while the membranes are still intact, the risk of intoxication is limited, but immunosuppresion could be a complication for the cow. To date, no proper data are available. The dosage of oxytocin may only be increased to 100 I.U. after parts of the calf have entered the pelvic area and progress is clearly observed. At this time, a bulge containing parts of the body under the tail of the dam should be visible. Progress of parturition must be monitored strictly at this stage. If this increased dose of oxytocin does not result in parturition a vaginal vestibulotomy should be performed soon to get better access to the calf. See next chapter. Expulsion of the calf should follow soon after the bulge appears under the tail of the dam. The allantois sac usually ruptures during the (induced) passage through the pelvic canal. One complication described at this stage, is reduced passage space as a result of edema in the urogenital canal resulting in a “catching effect” of the head and/or shoulder of the calf inside the soft part of the distal (vertical part) genital tract. Suffocation of the calf is a realistic complication. This condition has been observed several times in primiparous elephants of more advanced age. Elephants in this category should be prepared by the local application of J-Lube in the distal part of the vaginal vestibulum and massage of oestrogel/creme in the skin between anus and vulva. If this condition occurs, quick intervention is required by applying firm manual pressure from the outside on the calf in the sliding direction of the calf. Be aware of the risk of kicking by the mother. 2. Ruptured allantois sac A significant event in the parturition process is the rupturing of the allantois sac, which – when intact - acts as a hydraulic dilatator for the cervix, a natural lubrication for the dam and a pressure protection for the calf. NB: The amniotic sac that covers the body directly, usually remains intact during the expulsion of the calf and ruptures during the final passage through the birth canal and is actively removed by the dam. NB: a chained dam, may not be in the position to remove these membranes, possibly resulting in suffocation of the calf. Differentiation between urine and fetal fluids is extremely difficult; smell, creatinin test strips and possibly protein concentration could be helpful. If no progress in parturition is observed, major complications should be considered, like a dead calf, malposition of the calf (which is often dead), oversized calf, malformation and twin pregnancy. Because of the urgency of this situation, the calf should be born within 2 hours after rupture of the allantois sac and loss of allantois fluid. If not so, veterinary intervention has to take place. Two situations may occur: No fetal parts positioned in the pelvic area: treatment should aim on the urgent relaxation of the cervix. Calcium status should be determined and treated accordingly (see above). The further approach is according to 1A, however the situation is more critical for both the dam and the calf. Fetal parts have entered the pelvic area: Calcium status should be determined and treated accordingly (see above). Ultrasound is essential to determine which fetal parts have entered the birth canal, determine the position of the calf (visualization of the nails, posterior or anterior position, number of nails, trunk) and viability. Malposition (e.g. only one leg in birth canal, no head while in anterior position) is an indication for vaginal vestibulotomy or fetotomy. If no abnormalities are found during ultrasound, 50-100 I.U. of oxytocin should be given i.v. or i.m. and rectal massage should be practiced. Birth should be completed within 1 hour. Other drugs used Uterine laxants have been used in elephants on rare occasions. There are some anecdotal reports about the use of denaverinehydrochloride (Sensiblex®, Veyx) at a dose of 0,04 – 0,05 mg/kg BW (i.m.). Isoxsuprinelactate (Duphaspasmin. Fort Dodge Animal Health, 6290AA Vaals, The Netherlands) was used in a fetotomy case at 0,15 mg/kg BM (i.m.). Carbetocine (Depotocin®, Veyx), a long acting oxytocine has been used in 3 occasions dosage (0,09 µg/kg BW) i.m. Presentation of the calf A study in 46 elephants demonstrated that the overall ratio between anterior and posterior presentation was 12:34. In dystochia cases the situation was quite different: 6:3. In normal birth procedures the ratio was 6: 29. Anterior presentation has a higher risk of dystochia than posterior presentation of the calf. (Ilic D. et al. 2021. The incidence of anterior and posterior presentation at birth in Asian (Elephas maximus ) and African elephants (Loxodonta africana ): A Review Study. Indian Journal of Animal Research.DOI: 10.18805/IJAR.B-1319) It has been observed that the calf may rotate during the final phase of the expulsion, similar to what happens in horses and cattle (see video). This may be important in case of a dystocia, if the calf has remained in complete 'horizontal position' and a vaginal vestibulotomy is indicated. Note that the calf has rotated during the final phase of the expulsion. Transrectal massage: Transrectal massage is a very effective method to stimulate uterine contractions if the uterus is prepared for it . Certain conditions (especially hypocalcemia) may impair the contractions. This should be solved first. Stimulation of the pelvic wall by rectal massage is known as the Ferguson reflex . Transrectal massage of the pelvic wall is best performed by firmly pressing the closed fost against the roof and sides of the pelvic cavity and on the dorsal side of the vagina making the movements as shown in this video. Post-partum care Disinfection of the navel with Betadine® iodine is strongly recommended (if the mother allows its application). The afterbirth usually comes off within 12 hours. There are a few reports on retained (parts of) placenta for several weeks, without major complications for the dam. Hygienic measures should be applied to reduce the infectious burden for the calf. Be aware of the fact that a second calf can still be present in the dam. There are reports that second calves were born between several hours up to 3 months (the prevalence of twins in elephants is 1:3000). The calf should drink (colostrum) as soon as possible, at least within 24 hours. If not, or when the calf makes a weak impression, the banked serum (or freshly taken serum) should be given to it orally. Try to find out the reason why the calf is not drinking successfully: e.g. too small, weak, painful mammary glands, malbehaviour of the dam. If for any reason the mother is rejecting the calf, lactating herd member can take care of the calf. There is evidence that the mother takes over from this surrogate mother during the first 72 hours. If no lactating elephant is present in the herd, training for bottle feeding should start after 12 hours and continued for 72 hours. If the mother still rejects her calf, the best option for the calf is to move it to another herd with a lactating elephant. If introduction to this herd fails too, bottle feeding is the last option. To date very few bottle-raised elephants have reached the age of puberty. To page top