Elephant Disease Fact sheets       

Endotheliotropic Herpesvirus  (EEHV)
Elephant Care International Fact Sheet

Susan Mikota DVM

Updated December 2007

Etiology

  • a novel virus there are at least three known typesEEHV 1, 2, and 3.  EEHV 1 and 3 have two subtypes each
  • 1st observed in pulmonary nodules in African elephants in 1970s incidental finding
  • the  African elephant harbors both types  and may be a reservoir for disease in both African and Asian elephants
     

Epizootiology

  • little known
  • index case in U.S. in 1995 (National Zoo)
  • over 40 cases documented in U.S., Europe;Asia since 1983
  • mainly young elephants although adults have also succumbed
  • some cases in Asian elephants with no known  direct contact  with African elephants  
     

Transmission and Pathogenesis

  • the herpes virus found in wild African elephant pulmonary nodules is the same virus that has caused generalized fatal disease in two captive African elephants in the U.S.
  • the herpes virus found in skin papillomas and vulvar lymphoid patches on wild and captive African elephants fatal for Asian elephants
  • viremia causes endothelial cell death resulting in capillary leakage and hemorrhage
  • myocardial hemorrhage results in shock and death
     

Clinical signs in elephants

  • very sudden onset and rapid course (1-5 days)
  • lethargy, anorexia
  • edema of head, neck, trunk, thoracic limbs
  • cyanosis, ulceration of the tongue
  • decreased RBC, WBC, platelets
  • tachycardia


Diagnosis (Premortem):

  • virus has not yet been isolated
  • viremia PCR can detect viral antigen
  •   recent serological tests (2002) developed
  • contact for PCR diagnostics and serological test:

Erin Latimer, MS/ Laura K. Richman, DVM, PhD, Diplomate ACVP
            National Zoo
            3001 Connecticut Ave, NW

            Washington, DC 20008

202-633-4252 (Erin)
(301) 398-4741(Laura) 1; email:Latimere@si.edu    

RichmanL@MedImmune.com

Diagnosis (Postmortem)

  • hemorrhagic diathesis
  • petecchial hemorrhages in heart and throughout peritoneal cavity
  • pericardial effusion
  • hepatomegaly
  • cyanosis of the tongue
  • oral and intestinal ulcers
  • PCR test performed at the National Zoo,

See above for contact information

Postmortem: histopathology

  • microhemorrhages and edema throughout myocardium, tongue, liver, intestine as well as other organs
  • hepatocellular degeneration
  • intranuclear inclusion bodies in the capillary (or larger caliber vessels with EEHV3) endothelium of affected organs

 

Differential diagnosis

     diseases with sudden onset and rapid death

  • encephalomyocarditis
  • salmonellosis
  • enterotoxemia (clostridial)
  • toxicity
  • hypovitaminosis E

Management

  • prognosis poor

over 10  cases treated;  4 cases survived

  • Famciclovir + supportive
  • avoid intermingling of Asian and African elephant.
  • train neonates for exam and bleeding
  • close daily observations;  especially young elephants
  • daily oral exams

Zoonotic potential

  • host range seems limited to elephants
  • no evidence of transmission to humans

Herpesvirus References Dec  2007

Elephant Care International Bibliographic Database (www.elephantcare.org)

     1.    Wellehan J.F., Johnson A.J., Childress A.L., Harr K.E. and Isaza R. 2007. Six novel gammaherpesviruses of Afrotheria provide insight into the early divergence of the Gammaherpesvirinae.Vet Microbiol 2007 Aug 19; [Epub ahead of print].
Abstract: The Afrotheria represent an early branching of placental mammals. Only two herpesviruses from Afrotheria have been previously identified, and the genus Proboscivirus in the subfamily Betaherpesvirinae has been proposed for them. Six novel gammaherpesviruses were identified in four species in the superorder Afrotheria by detection and analysis of their DNA polymerase genes. Elephantid herpesvirus 3 (ElHV3) and Elephantid herpesvirus 4 (ElHV4) were identified from conjunctival swabs from Asian elephants (Elephas maximus). ElHV3 was also found in a vaginal swab from one elephant with vaginitis. Elephantid herpesvirus 5 (ElHV5) was identified from vaginal swabs of two Asian elephants with vaginal plaques. Elephantid herpesvirus 6 was discovered in a conjunctival swab from an African elephant (Loxodonta africana). Procavid herpesvirus 1 (PrHV1) was found in spleen and conjunctival swabs of rock hyrax (Procavia capensis). Trichechid herpesvirus 1 (TrHV1) was identified from skin and buffy coats of Florida manatees (Trichechus manatus latirostris). ElHV3 and ElHV4 form a distinct cluster, and ElHV5, ElHV6, TrHV1, and PrHV1 form a second cluster. These viruses may have codiverged with their host species. Phylogenetic analysis of these novel herpesviruses suggests that two separate groups of gammaherpesviruses may have codiverged with the Afrotheria.

     2.    Ehlers B., Dural G., Marschall M. et al. 2006. Endotheliotropic elephant herpesvirus, the first betaherpesvirus with a thymidine kinase gene.Journal of General Virology 87: 2781-2789.
Abstract:
Endotheliotropic elephant herpesvirus (elephantid herpesvirus 1; ElHV-1) is apathogenic for African elephants (Loxodonta africana), but causes fatal haemorrhagic disease in Asian
elephants (Elephas maximus). This is thought to occur through transmission from African elephants in places where both species are housed, such as zoological gardens. The virus has caused considerable losses in North American and European zoological gardens and thus severely impedes breeding of the endangered Asian elephant. Previously, the ultrastructural and genetic characterization of ElHV-1 from a male Asian elephant that died from the disease at the Berlin zoological gardens in 1998 have been reported. Here, a partial characterization of the ElHV-1 genome is presented. A 60 kbp locus, spanning 34 open reading frames, was analysed. Most of the detected genes were found to be conserved among the herpesviruses and showed an overall arrangement most similar to that of betaherpesviruses, in particular Human herpesvirus 6 and Human herpesvirus 7. Most importantly, in addition to a protein kinase gene that is homologous to the human cytomegalovirus UL97 gene, a thymidine kinase (TK) gene was found, which is generally missing in betaherpesvirus genomes. Thus, ElHV-1 is the only known betaherpesvirus to encode a TK gene. This peculiarity might contribute to the fulminant pathogenicity of ElHV-1, but also provide a crucial enzymic activity for developing an efficient antiviral therapy with currently available nucleoside analogues.

     3.    Hildebrandt T.B., Hermes R., Ratanakorn P. et al. 2006. Ultrasonographic assessment and ultrasound-guided biopsy of the retropharyngeal lymph nodes in elephants.   2006 Proceedings American Association of Zoo Veterinarians, pp. 117-118.
Abstract: So far there are no valid diagnostic tools available for identifying latent carriers of endotheliotropic elephant herpes virus (EEHV).  For this reason, the lateral retropharyngeal lymph node complex (LARELYNOC) of elephants, identified during postmortem studies as target organ for EEHV and suitable for transcutaneous biopsy, was grossly described. Transcutaneous ultrasound (3.5 MHz) was applied behind the ear region to identify the LARELYNOC containing up to four single lymph nodes on each side. The lymph node tissue is situated 20-50 mm below the skin surface. An ultrasonographic assessment of the LARELYNOC and two biopsies were performed on 39 healthy Asian elephants (Elephas maximus). Samples were tested for EEHV via PCR. Whole blood samples were also collected and tested for active EEHV infection. Lymph nodes were ultrasonographically classified as active (calculated mean volume=17.4 6.9 cm3, P>0.001), inactive (calculated mean volume=3.1 0.6 cm3, P<0.001), or chronic active (calculated mean volume=10.6 1.0 cm3, P<0.05). Histology confirmed not only the presence of lymph tissue but also the ultrasonographically diagnosed reactivity status of the lymph node biospies.  Although all samples including whole blood were found to be negative for the EEHV DNA particles, the successful development of this procedure in elephants could prove beneficial for the screening of not only latent EEHV infections but might also be a less dangerous alternative method for the diagnosis of zoonotic infections such as tuberculosis.

     4.    Reid C.E., Hildebrandt T.B., Marx N. et al. 2006. Endotheliotropic elephant herpes virus (EEHV) infection. The first PCR-confirmed fatal case in Asia.Vet Q 28: 61-64.
Abstract: Since 1995, 4 suspected cases of Endotheliotropic Elephant Herpes Virus (EEHV) infection, i.e. based on clinical presentation, have occurred in Asia without resulting in epidemic outbreaks as expected. In order to confirm the presence of EEHV on the continent of Asia, viral DNA particles from liver samples of a wild-caught 3-year-old elephant found dead at a Cambodian elephant sanctuary and clinically diagnosed with EEHV, were PCR processed using known EEHV strain primers. The presence of EEHV viral nucleic acids was confirmed and the nucleic acids had a 99% sequence similarity to the U.S.A strain (gene bank locus: AF117265) and 97% sequence similarity to the European strain (gene bank locus: AF354746) assigning this case to the EEHV-1 cluster. More than the confirmation of EEHV on the continent of Asia, is the phylogenic relationship to the USA and European strains with no corresponding contact or transport of USA or European elephants to Asia. Thus, this brings many of the traditional theories into question. Although almost forgotten, this disease is still ramped in captive elephant populations worldwide and continues to devastate particularly the neonatal and weaning-age population. Special attention and continued research are needed specifically in the area of basic virology and epidemiology.

     5.    Wellehan J.F.X., Johnson A.J. and Isaza R. 2006. Identification of two novel herpesviruses associated with ocular inflammation in Asian elephants (Elephas maximus). 
2006 Proceedings American Association of Zoo Veterinarians, p. 173.
Abstract: Disease caused by a herpesvirus (EEHV) is a serious concern in Asian elephant (Elephas maximus) calves.  Herpesviruses are known for latency and life-long infections, with periodic shedding from mild inflammatory lesions in adapted adult hosts, and ocular disease has been seen with other herpesviruses in other species.  Ocular inflammation is not uncommonly seen in Asian elephants. Degenerate PCR primers targeting a conserved region of herpesvirus DNA-dependent DNA polymerase were used to amplify products from eye swabs of eight Asian elephants with epiphora, blepharitis, and conjunctivitis.  Nucleotide sequencing of the PCR products showed two novel herpesviruses distinct from EEHV.  Comparative sequence analysis shows that these viruses are probable members of the subfamily Gammaherpesvirinae. The sequence phylogeny of these viruses has implications for both viral and host evolution.  Further understanding and characterization of these viruses is needed to understand their role in elephant health.

     6.    Zuba J.R., Oosterhuis J.E. and Pessier A.P. 2006. The toenail "abscess" in elephants: treatment options including cryotherapy and pathologic similarities with equine proliferative pododermatitis (canker).   2006 Proceedings American Association of Zoo Veterinarians, pp. 187-190.
Abstract: Foot problems potentially represent the single most important clinical disease of captive elephants.  Predisposing factors include obesity, lack of exercise, nail or sole overgrowth, improper foot care, poor hygiene, inappropriate enclosure surfaces, poor conformation, malnutrition and secondary skeletal disorders such as degenerative joint disease.  Furthermore, factors such as elephant management philosophy, disposition of elephants, facilities and competency of staff in caring for elephant feet will contribute significantly to the foot health of captive animals.  It is important to note that these conditions are rarely reported in free-ranging elephants. The elephant toenail abscess is characterized grossly by proliferative outgrowth of "crab meat-like" tissue that may acutely rupture through the surface of the nail wall and/or adjacent cuticle or sole. True abscess formation with localized collections of suppurative material is not a consistent clinical feature.  In most cases, the inciting cause of these lesions are typically not found and are likely due to one or more of the predisposing factors listed above.  Once established, these frustrating lesions require extensive, intensive and prolonged medical attention.  If not cared for properly, these wounds may progress to phalangeal osteomyelitis and the need for surgical intervention.  Sole abscesses are equally frustrating and difficult to manage with proposed etiologies similar to toenail lesions. There are no reports in the literature describing the pathology of the classic proliferative abscess tissue of the elephant nail abscess.  Although variously interpreted as fibrous or granulation tissue, the authors are unaware of previous histologic descriptions of this tissue.  Biopsy samples of toenail abscess tissue from two Asian elephants (Elephas maximus) at the San Diego Wild Animal Park (SDWAP) consisted of stratified squamous epithelium arranged in columns resembling horn tubules.  The predominant histologic finding was marked, near diffuse, hydropic degeneration of keratinocytes.  There were multifocal areas of suppurative inflammation with admixed bacterial colonies.  Inflammatory foci comprised only a small portion of the lesion and were interpreted as the external surfaces of the biopsy with likely secondary bacterial colonization. Because descriptions of the normal histology of the elephant toenail could not be located, a grossly normal toenail from a different Asian elephant was obtained to compare histologic features with those of the toenail abscesses.  Sections demonstrated formation of the toenail in a manner similar to that of the hoof of the horse and cattle with tubular, intertubular and laminar horn.  Primary and secondary epidermal laminae were identified.  Proliferative lesions of horn-producing epithelium associated with ballooning degeneration and inadequate keratinization of keratinocytes, have been described in horses as equine "canker" and coronary band dystrophy.  Equine canker is most commonly observed in the hind feet of draft horses and begins in the frog sometimes with extension to the sole and hoof wall.  Grossly, lesions are characterized by soft white papillary to "cauliflower-like" tissue associated with a foul odor. Similar to what is noted in elephant foot problems, predisposing factors for the development of equine canker include poor hygiene or wet environmental conditions. There is a lack of gross and histologic description of the normal nail and sole tissue of the elephant and further investigations are warranted.  A review of the anatomy and histology of the normal equine hoof may provide a basic understanding of the elephant nail until more specific and detailed elephant information is available.  From our investigation, the authors offer that a more accurate description of the elephant toenail abscess would be proliferative pododermatitis, the term synonymous with equine canker.  A more colloquial term such as "elephant canker" may be appropriate, as well. Canker in the horse is an uncommon but difficult to treat disease of the hoof.  Historically, treatment options for elephant toenail abscesses include corrective trimming, superficial debridement and application of topical disinfectants or antibiotics. Others have constructed innovative sandals to treat and protect the affected sole or nail with success. The use of regional intravenous perfusion of the affected limb with antibiotics has also been successful. Since the elephant nail abscess now appears to be histologically and clinically comparable to equine canker, this novel characterization of an old disease may offer unique insight for treatment.  In the least, it has provided our practice with a new list of treatment options and experienced equine clinicians for consultation who have been managing patients with a similar disease for many years. One of the Asian elephants at the SDWAP has had chronic toenail abscesses for over 2 yr. Radiographs of the affected digits, as reported by others to assess degree of involvement, have fortunately been negative for evidence of osteomyelitis.  Several bacterial and fungal cultures of deep tissue biopsies and swabs of affected lesions have resulted in a mixture of organisms with no consistent single etiologic agent.  Biopsies were found negative for presence of viral DNA (elephant papillomavirus and herpesvirus) by PCR.  Typical elephant foot care at the SDWAP includes trimming and debriding with hoof knives, foot soaks and topical antibiotics.  Although difficult, attempts are made in keeping the affected foot clean and dry.  Following recommendations for the treatment of equine canker, we recently implemented the routine use of cryotherapy in all elephants with proliferative pododermatitis with improved success in the control and recession of exuberant nail lesions. The proliferative tissue of the nail is first cleaned then disinfected, debrided, trimmed with hoof knives and allowed to dry. Modified brass branding tools with contact surfaces of variable size (2-5 cm diameter) and shape (round or ovoid) are placed into liquid nitrogen (-196 C) for several minutes and then placed directly on the cankerous tissue for 30-60 sec.  This process is then repeated 4-5 min later, following a complete thaw of tissue.  Within 24 hr, the cryoburned tissue becomes macerated and necrotic and is readily removed with gentle scrubbing.  Cryotherapy offers the advantage of destroying tissue to a deeper level than trimming alone and provides hemostasis, as well.  Because of decreased sensation at the cryotherapy treatment site, a memorable painful event is avoided and the elephant patient is more routinely accepting of this technique. With the use of hoof knives, we typically remove 2-3 mm of proliferative tissue before the patient refuses further treatment, presumably due to discomfort.  With cryotherapy, we are able to remove an additional 3-5 mm of tissue by cell freezing and necrosis.  The result is quicker resolution of cankerous lesions without the need for aggressive, and potentially painful, interventions. In conclusion, it appears that elephant nail abscesses can best be described as proliferative pododermatitis, or canker, as is seen in other species.  Further gross and microscopic descriptions of normal and pathologic nail or sole lesions are necessary.  Routine cryotherapy has shown promise in the treatment of these chronic, frustrating and potentially devastating lesions of our captive elephants.

     7.    Hildebrandt T.B., Hermes R., Ratanakorn P. et al. 2005. Ultrasonographic assessment and ultrasound-guided biopsy of the retropharyngeal lymph nodes in Asian elephants (Elephas maximus).Vet Rec 157: 544-548.
Abstract: Endotheliotropic herpesvirus causes a fatal disease in young Asian elephants,but there are no methods for identifying latent carriers of the virus. During the postmortem study of one female African elephant and three male and two female Asian elephants, a lymph node located bilaterally caudoventral to the parotid gland, approximately 1.5 to 5 cm below the skin, was identified as  suitable for transcutaneous ultrasound-guided biopsy. An ultrasonographic assessment and two biopsies were performed on 39 Asian elephants, and these lymph nodes were classified ultrasonographically as active, inactive or chronically active. The calculated mean (se) volume of 10 active lymph nodes was 17.4 (6.9) cm(3), and that of three chronically active lymph nodes was 10.6 (1.0) cm(3), whereas the mean volume of 17 inactive lymph nodes was 3.1 (0.6) cm(3). The presence of lymph node tissue in samples obtained by ultrasound-guided biopsy from three animals that were maintained under conditions that allowed for additional sampling was confirmed histologically. The dna extracted from the lymphoid tissue and the whole blood of all the elephants was negative for endotheliotropic herpesvirus by PCR.

     8.    Fickel J., Liekfeldt D., Richman L.K. et al. 2003. Comparison of glycoprotein B (gB) variants of the elephant endotheliotropic herpesvirus (EEHV) isolated from Asian elephants (Elephas maximus).Vet Microbiol 91: 11-21.
Abstract: The recently described elephant endotheliotropic herpesviruses (EEHV) have been associated with the deaths of numerous captive elephants. A proposed tool for the detection of EEHV infection in elephants is the PCR-based screening for EEHV-DNA in whole blood samples. Unfortunately, this detection method has only been successful in post-mortem analyses or in animals already displaying clinical signs of EEHV disease, thus rendering this method unsuitable for identification of carrier elephants. Here, we focus on glycoprotein B (gB) for serologic assay development, since gB is an envelope protein known to induce a neutralising antibody response in other herpesvirus infections. We sequenced the entire gB gene from five Asian elephants with EEHV, representing four different gB variants. Computer-aided methods were used to predict functionally important regions within EEHVgB. An extra-cytoplasmic region of 153 amino acids was predicted to be under positive selection and may potentially contain antigenic determinants that will be useful for future serologic assay development.

     9.    Isaza R., Hunter R.P., Richman L.K. et al. 2003. Famciclovir pharmacokinetics in young Asian elephants (Elephas maximus).  Proc. American Assoc. of Zoo Veterinarians, pp. 82-83.
Abstract: Asian elephants (Elephas maximus) are susceptible to a unique infection caused by elephant endotheliotropic herpesvirus (EEHV).3,4 Worldwide, between the years 1983 and 2000, there have been 26 confirmed deaths from this virus in Asian elephants.2 Although most cases have been fatal, treatment with famciclovir (Famvir, SmithKline Beecham Pharmaceuticals, Philadelphia,PA 19101 USA) has been associated with survival in three cases of six cases of EEHV infection proven by PCR.2,5,6 Dose selections for surviving elephants (5.5 - 8.0 mg/kg, p.o. every 8 hr) were made without the benefit of elephant pharmacokinetics and were a direct extrapolation from recommended human dosages (7 mg/kg, p.o. every 8 hr).5,6  In this study, famciclovir was administered both orally and rectally in healthy young Asian elephants. The doses tested in this study were 5 mg/kg orally, 5 mg/kg rectally, and 15 mg/kg rectally. Blood samples were analyzed for famciclovir and penciclovir using a validated LC/MS assay. Famciclovir was absorbed well by both routes and underwent rapid biotransformation to the active compound penciclovir. None of the plasma samples had detectable famciclovir. Pharmacokinetic parameters for penciclovir were determined using non-compartmental analysis. After a single oral dose of 5 mg/kg the Cmax was 1.3 g/mL with a Tmax at 1.1 h. After a rectal dose of 5 mg/kg the Cmax  was 1.2 g/mL with a Tmax at 0.34 hr. After a rectal dose of 15 mg the t was 2.6 h, with a Cmax of 3.6 g/mL at Tmax 0.66 h. These results were similar to those reported in humans where an oral dose of 500 mg (7 mg/kg) had a t of about 2 h with a Cmax of 3.3 g/mL. A dose range of 8 -15 mg/kg given orally or rectally every 8 hours should produce penciclovir concentrations in Asian elephants that are considered therapeutic in humans.

LITERATURE CITED
1. Hardman, J.G., L.E. Limbird and A.G. Gilman. 2001. In: Goodman and Gilman's The pharmacological basis of therapeutics, Tenth edition. McGraw-Hill Co. New York, New York. USA. Pp. 1322-1324.
2. Montali, R.J., Richman, L.K., Mikots,S.K., Schmitt,D.L., Larsen, R.S., Hildebrandt,T.B., Isaza,R., Lindsay,W.A. Management Aspects of Herpesvirus Infections and Tuberculosis in Elephants. International Elephant and  Rhino Research Symposium, Vienna, June 7-11, 2001.
3. Richman, L.K., R.J. Montali, R.L. Garber, M.A. Kennedy, J. Lehnhardt, T. Hildebrandt, D. Schmitt, D. Hardy, D.J. Alcendor, G.S. Hayward. 1999a. Novel endotheliotropic herpesvirus fatal for Asian and African elephants. Science. 283:1171-1176.
4. Richman, L.K., R.J. Montali, R.C. Cambre, D. Schmitt, D. Hardy, T. Hildebrandt, F.M. Hamzeh, A. Shahkolahi, G.S. Hayward. 2000.  Clinical and pathological findings of a newly recognized disease of elephants caused by endotheliotrophic herpesvirus.  J. Wild. Dis. 36:1-12.
5. Schaftenaar, W., J.M.C.H. Mensink, A.M. de Boer, T.B. Hildebrandt, and J. Fickel. 2001. Successful treatment of a subadult Asian elephant bull (Elephas maximus) infected with the endotheliotropic elephant herpes virus. Verhber. Erkrg. Zootiere. P. 40.
6. Schmitt, D., D.A. Hardy, R.J. Montali, LK Richman, Lindsay WA, R. Isaza, G. West. 2000. Use of famciclovir for the treatment of endotheliotropic herpesvirus infections in Asian elephants (Elephas maximus). J. Zoo Wild. Med. 31:518-522.

   10.    Burkhardt S., Goltz M., Bergmann V. et al. 2001. Genetic and ultrastructural characterization of a European isolate of the fatal endotheliotropic elephant herpesvirus.Journal of General Virology 82: 475-482.
Abstract: A male Asian elephant (Elephas maximus) died at the Berlin zoological gardens in August 1998 of systemic infection with the novel endotheliotropic elephant herpesvirus (EIHV-1). This virus causes a fatal haemorrhagic disease in Asian elephants, the so-called endothelial inclusion body disease, as reported from North American zoological gardens. In the present work, EIHV-1 was visualized ultrastructurally in affected organ material. Furthermore, a gene block comprising the complete glycoprotein B (gB) and DNA polymerase (DPOL) genes as well as two partial genes was amplified by PCR-based genome walking and sequenced. The gene content and arrangement were similar to those of members of the Betaherpesvirinae. However, phylogenetic analysis with gB and DPOL consistently revealed a very distant relationship to the betaherpesviruses. Therefore, EIHV-1 may be a member of a new genus or even a new herpesvirus subfamily. The sequence information generated was used to set up a nested-PCR assay for diagnosis of suspected cases of endothelial inclusion body disease. Furthermore, it will aid in the development of antibody-based detection methods and of vaccination strategies against this fatal herpesvirus infection in the endangered Asian elephant.

   11.    Ehlers B., Burkhardt S., Goltz M. et al. 2001. Genetic and ultrastructural characterization of a European isolate of the fatal endotheliotropic elephant herpesvirus.J Gen Virol 82 (Pt 3): 475-482.
Abstract: A male Asian elephant (Elephas maximus) died at the Berlin zoological gardens in August 1998 of systemic infection with the novel endotheliotropic elephant herpesvirus (ElHV-1). This virus causes a fatal haemorrhagic disease in Asian elephants, the so-called endothelial inclusion body disease, as reported from North American zoological gardens. In the present work, ElHV-1 was visualized ultrastructurally in affected organ material. Furthermore, a gene block comprising the complete glycoprotein B (gB) and DNA polymerase (DPOL) genes as well as two partial genes was amplified by PCR-based genome walking and sequenced. The gene content and arrangement were similar to those of members of the Betaherpesvirinae. However, phylogenetic analysis with gB and DPOL consistently revealed a very distant relationship to the betaherpesviruses.Therefore, ElHV-1 may be a member of a new genus or even a new herpesvirus subfamily. The sequence information generated was used to set up a nested-PCR assay for diagnosis of suspected cases of endothelial inclusion body disease. Furthermore, it will aid in the development of antibody-based detection methods and of vaccination strategies against this fatal herpesvirus infection in the endangered Asian elephant.

   12.    Fickel J., Richman L.K., Montali R. et al. 2001. A variant of the endotheliotropic herpesvirus in Asian elephants (Elephas maximus) in European zoos.Veterinary Microbiology 82: 103-109.
Abstract: Newly discovered, lethal elephant endotheliotropic herpesviruses (EEHV) have been identified in both Asian (Elephas maximus) and African (Loxodonta africana) elephants. Carried by otherwise healthy African elephants, they can be fatal, mainly for young Asian elephants. Since zoos often harbour both elephant species, we conducted a survey on the presence of EEHV in elephants (Asian elephants, n=57; African elephants, n=17) from 12 zoos and 3 circuses in Europe (Germany, Switzerland and the Netherlands), and 1 zoo in Israel [date not given]. Six of the 57 Asian elephants were positive for EEHV. Five elephants died of the infection, while one survived. EEHV was not detected in any of the 17 African elephants. All EEHV that affected the Asian elephants belonged to the EEHV1 group. We described the detection and the partial sequencing of an endotheliotropic herpesvirus variant (named EEHV1b) in Asian elephants, being either an EEHV endogenous to Asian elephants or indicating different sources (African elephants) of infection.

   13.    Hildebrandt T.B., Fickel J., Goritz F. et al. 2001. Survey on presence of the endotheliotropic elephant herpesvirus (EEHV) in Thai camp elephants. In: Kirk Baer C and Wilmette MW (eds), Proceedings American Association of Zoo Veterinarians, American Association of Wildlife Veterinarians, Association of Reptilian and Amphibian Veterinarians and the National Association of Zoo and Wildlife Veterinarians Joint Conference  2001, September 18, 2001-September 23, 2001, pp. 183-184. American Association of Zoo Veterinarians.

   14.    Montali R.J., Richman L.K., Mikota S.K. et al. 2001. Management Aspects of Herpesvirus Infections and Tuberculosis in Elephants.  A Research Update on Elephants and Rhinos; Proceedings of the International Elephant and Rhino Research Symposium, Vienna, June 7-11, 2001, 2001, pp. 87-95. Schuling Verlag, Vienna, Austria.
Abstract: Elephant endotheliotropic herpesvirus (EEHV) infections and tuberculosis have emerged as causes of illness and mortality in captive elephants. Twenty-six confirmed EEHV cases are documented. Since 1995, 7 have occurred in North America, 10 in Europe and 2 in Asia. A PCR test was used to detect the virus in symptomatic animals; a serological test to identify carrier elephants is under development. The African elephant is a potential source of the EEHV that is lethal for Asian elephants. Fatal infections have also occurred in Asian elephants without African elephant contacts. Three of 6 elephants recovered after treatment with antiviral famciclovir; however, more research is needed to improve the usefulness of this drug. Asian elephants that are less than 10-years old and have been moved to another facility and/or have had contact with African elephants are at increased risk for contracting EEHV. Animals traveling between facilities with a history of EEHV cases may be at greater risk. All young elephants should be monitored daily for anorexia, lethargy, body swellings and blue discoloration (bruising) of the tongue, and be trained for blood sampling and potential oral and rectal treatment with famciclovir.
Since 1996, Mycobacterium tuberculosis has affected about 3% of Asian elephants in North America. Most were from 5 U.S. States with some contacts between private herds. Mandatory annual testing for tuberculosis by trunk wash cultures was established in 1998, and 22 culture-positive M. tuberculosis elephants were identified between 1996-2001. Fifteen were treated with anti-tuberculosis drugs and 7 that died or were euthanized were proven to have tuberculosis at necropsy. Antemortem sera was available from 4/7 4 (75%) were strongly ELISA positive. Tuberculosis is uncommon in African elephants but was recently associated with M. bovis in the U.S. and M. tuberculosis in Germany. Conversely, M. bovis tuberculosis, apparently unrecognized in Asian elephants, recently occurred in Germany. Management issues of elephant tuberculosis will be discussed relative to its complex epidemiology and clinical-pathological correlations.

   15.    Ratanakorn P. 2001. Elephant Health Problems and Management in Cambodia, Lao and Thailand.  A Research Update on Elephants and Rhinos; Proceedings of the International Elephant and Rhino Research Symposium, Vienna, June 7-11, 2001, 2001, pp. 111-114. Schuling Verlag, Vienna, Austria.

   16.    Richman L.K. and Montali R.J. 2001. Elephant herpesvirus infections. In: Williams ES and Barker IK (eds), Infectious Diseases of Wild Mammals, 3rd edition pp. 170-178. Iowa State University Press, Ames, Iowa, USA.

   17.    Ryan S.J. and Thompson S.D. 2001. Disease risk and inter-institutional transfer of specimens in cooperative breeding programs: Herpes and the elephant species survival plans.Zoo Biology 20: 89-101.
Abstract: Managers of cooperative breeding programs and re-introduction projects are increasingly concerned with the risk of disease transmission when specimens are transferred among facilities or between facilities and the natural environment. We used data maintained in North American studbooks to estimate the potential risks of disease transmission by direct and indirect contact of specimens in the American Zoo and Aquarium Association's Elephant Species Survival Plan. Histological evidence for a novel herpesvirus disease transmitted between and within elephant species housed in North American facilities prompted an examination of the scope of possible transmission routes within the captive population. We found that, compared with other species managed through Species Survival Plans, elephants experience relatively few transfers between zoos. Nevertheless, the number of direct contacts with other elephants born during the study period of 1983-1996 (excluding stillbirths) was much higher than we had anticipated (&mgr; = 25 +/- 27; N = 59) and the number of potential indirect contacts was surprisingly large (&mgr; = 143 +/- 92; N = 59). Although these high rates of potential contacts complicate exact identification of infection pathways for herpesvirus, we were able to propose potential routes of transmission for the histologically identified cases. Furthermore, the extraction of data from studbooks allowed us to readily identify other specimens that did not succumb to the disease despite similar exposure. Moreover, we were able to identify other possible cases to recommend for histological examination. Herein we reveal the possibilities of multiple disease transmission pathways and demonstrate how complex the patterns of transmission can be, confounded by the unknown latency of this novel herpesvirus. This emphasizes the need for zoo veterinarians and cooperative breeding programs to consider the full potential for disease transmission associated with each and every inter-zoo transfer of specimens.

   18.    Schaftenaar W., Mensink J.M.C.H., Deboer A.M., Hildebrandt T.B. and Fickel J. 2001. Successful treatment of a subadult Asian elephant bull (Elephas maximus) infected with elephant herpes virus.  Proc. of the  International Symposium for diseases of Zoo and Wildlife Animals (Rotterdam), pp. 141-146.

   19.    Fickel J., Richman L.K., Reinsch A. et al. 2000. Survey on the occurrence of the endotheliotropic elephant herpesvirus (EEHV) in Asian (Elephas maximus) and African (Loxodonta africana) elephants in Europen zoos.  European Association of Zoo and Wildlife Veterinarians Third Scientific Meeting, Paris, France, May 31-June 4, 2000..

   20.    Richman L.K., Montali R.J. and Hayward G.S. 2000. Review of a newly recognized disease of elephants caused by endotheliotropic herpesviruses.Zoo Biology 19: 383-392.
Abstract: There are two newly recognized herpesviruses that cause a fatal disease syndrome in elephants. They are known as the elephant endotheliotropic herpesviruses, of which one is fatal for Asian elephants (Elephas maximus) and the other for African elephants (Loxodonta africana) The disease syndrome affects predominantly young elephants and has been described in North America, Europe, and Israel. The predominant clinical signs for both species include lethargy, oedematous swellings of the head, neck, and thoracic limbs, oral ulceration, cyanosis of the tongue, and death of most elephants in 1-7 days. Three affected young Asian elephants recovered after a 3-4-week course of therapy with the anti-herpesvirus drug famciclovir. Additional reported herpesvirus-associated lesions in otherwise healthy elephants include localized skin papillomas in African elephants, proliferative vulval lymphoid patches in African elephants, and pulmonary nodules in African elephants. Recent findings suggest that these localized herpesvirus-associated lesions in healthy African elephants may be one source of the herpesvirus that causes disseminated disease and death in the Asian species and the African species. These findings have implications for management practices in facilities keeping both African and Asian elephants and in protecting natural elephant habitats from virulent forms of the virus.

   21.    Richman L.K., Montali R.J., Cambre R.C. et al. 2000. Clinical and pathological findings of a newly recognized disease of elephants caused by endotheliotropic herpesviruses.Journal of Wildlife Diseases 36: 1-12.
Abstract: The unique clinical and pathological findings in nine Asian elephants (Elephas maximus) and two African elephants (Loxodonta africana) from North American Zoos with a highly fatal disease caused by novel endotheliotropic herpesviruses are described. Consensus primer polymerase chain reaction combined with sequencing yielded molecular evidence that confirmed the presence of 2 novel but related herpesviruses associated with the disease, one in Asian elephants and the other in African elephants. Disease onset was acute, with lethargy, edema of the head and thoracic limbs, oral ulceration and cyanosis of the tongue followed by death of most animals in 1 to 7 days. Pertinent laboratory findings in 2 of 3 clinically evaluated animals included lymphocytopenia and thrombocytopenia. Two affected young Asian elephants recovered after a 3- to 4-week course of therapy with famciclovir. PM examination in the fatal cases revealed pericardial effusion and extensive petechial hemorrhages in the heart and throughout the peritoneal cavity, hepatomegaly, cyanosis of the tongue, intestinal hemorrhage and ulceration. Histologically, there were extensive microhemorrhages and edema throughout the myocardium and mild, subacute myocarditis. Similar hemorrhagic lesions with inflammation were evident in the tongue, liver and large intestine. Lesions in these target organs were accompanied by amphophilic to basophilic intranuclear viral inclusion bodies in capillary endothelial cells. Transmission electron microscopy of the endothelial inclusion bodies revealed 80 to 92 nm diameter viral capsids consistent with herpesvirus morphology. The short course of the herpesvirus infections, with sudden deaths in all but the 2 surviving elephants, was ascribed to acute cardiac failure attributed to herpesvirus-induced capillary injury with extensive myocardial hemorrhage and edema.

   22.    Schmitt D.L., Hardy D.A., Montali R.J. et al. 2000. Use of famciclovir for the treatment of endotheliotrophic herpesvirus infections in Asian elephants (Elephas maximus).Journal of Zoo and Wildlife Medicine 31: 518-522.
Abstract: Two juvenile Asian elephants (E. maximus) presented with an acute onset of facial oedema and lethargy. Examination of the oral cavity of each animal revealed cyanosis of the tip and distal margins of the tongue suggestive of endothelial inclusion body disease (EIBD) of elephants. Whole-blood samples were obtained, and polymerase chain reaction tests confirmed the presence of elephant herpesvirus. The animals were administered famciclovir (Flamvir; 500 mg/70 kg body weight, with a loading dose of 1000 mg/70 kg body weight) a potent human anti-herpesvirus drug, in the course of their disease, and recovery followed a treatment regime of 3-4 wk. These are the first known cases of elephants surviving EIBD.

   23.    Burkhardt S., Hentschke J., Weiler H. et al. 1999. Elephant herpes virus - a problem for breeding and housing of elephants.Berliner und Munchener Tierarztliche Wochenschrift. 112: 174-179.
Abstract: Herpesvirus infections which take a fatal turn on African elephants as well as on Asian elephants seem to occur increasingly not only in the USA but also in European stocks. The endotheliotropic herpesvirus causes a rapidly progressing and severe disease which makes any therapeutical effort unsuccessful and finally results in death of the animal, especially in young Asian elephants. As all attempts to culture the virus failed up to now, molecular biological procedures have to be used more often for diagnostic purpose together with the common methods of pathology, virology, and electronmicroscopical evaluation. This is a report on the case of 'KIBA', an eleven year old male elephant at the Zoological Garden Berlin, infected with the endotheliotropic elephants herpesvirus. 'KIBA' was born at the Zoo in Houston, Texas, and raised within his herd. Upon arriving in Berlin in November 1997 he adapted to the new premises and climate and new social circumstances without any problems. In June 1998 he already serviced three females of his new herd several times. In August 1998 he died after passing a peracute progression of the disease after residenting in Berlin for only 9 months. The dissection of the animal revealed some evidence on an agent damaging the endothelium. Major signs indicating this agent were bleedings in several serous membranes, mucosa and on the right atrium, as well as other parts of the myocardium. Furthermore there have been ulcerations at various localizations of the whole digestive tract. Slightly basophilic intranuclear inclusion bodies have been found histologically in endothelial cells of different organ samples. An examination of altered organ-material by electronmicroscopy made some herpesvirus-like particles visible. A virological investigation first revealed evidence of giant cell formations with solitary basophilic intranuclear inclusion bodies in different cell cultures, however, without any distinct cytopathogenic effect. Supported by molecular biological procedures the infection of 'KIBA' could be verified as the elephants herpesvirus. By means of PCR and subsequent sequence analysis a DNA-sequence typical for the elephants herpesvirus could be obtained which showed an identity of 97% with the terminase sequence of the elephant herpesvirus described by American authors. The deduced amino acid-sequences were 100% identical. To the terminase of the human cytomegalovirus, the elephant sequence had an identity of 53% (similarity: 74%). Based on the cooperation of ILAT, Institute of Veterinary-Pathology/Free University Berlin, Robert-Koch-Institut Berlin, and Zoological Garden Berlin, the cause of 'KIBA's' death could be discovered immediately. Possible implications of this case especially on breeding and keeping elephants are discussed briefly.

   24.    Ferber D. 1999. Virus suspect identified in elephant deaths.Science 283: 1093-1094.

   25.    Mikota S.K. 1999. Diseases of the Elephant: A Review.Verh.ber.Erkrg.Zootiere 39: 1-15.

   26.    Richman L.K., Montali R.J., Garber R.L. et al. 1999. Novel endotheliotropic herpesviruses fatal for Asian and African elephants.Science 283: 1171-1176.
Abstract: A highly fatal haemorrhagic disease was identified in 10 young Asian (Elephas maximus) and African (Loxodonta africana) elephants at zoos in the USA between 1983 and 1997. In the affected animals there was ultrastructural evidence for herpesvirus-like particles in endothelial cells of the heart, liver, and tongue. Consensus primer polymerase chain reaction combined with sequencing yielded molecular evidence that confirmed the presence of 2 novel but related herpesviruses associated with the disease, one in Asian elephants and another in African elephants. Otherwise healthy African elephants with external herpetic lesions yielded herpesvirus sequences identical to that found in Asian elephants with endothelial disease. It is suggested that the Asian elephant deaths were caused by cross-species infection with a herpesvirus that is naturally latent in, but normally not lethal to, African elephants. A reciprocal relationship may exist for the African elephant disease.

   27.    Richman L.K., Montali R.J., Hildebrandt T. et al. 1999. Status of a new, fatal herpesvirus disease in elephants in North America and Europe.  Verhandlangsbericht des 39 International Symposium uben Erkrankungen der Zoo und Wildtiere, Wien. 39:17-21.  Verh.ber Erkrg. Zootiere 39, pp. 17-21.

   28.    Richman L.K., Montali R.J., Cambre R.C., Schmitt D. and Hardy D. 1999. Clinical and pathologic aspects of a fatal herpesvirus disease in Asian (Elephas maximus) and African (Loxodonta africana) elephants.  Proceedings of the American Association of Zoo Veterinarians, October 9, 1999, pp. 263-266.

   29.    Schmitt D.L. and Hardy D.A. 1998. Use of famciclovir for the treatment of herpesvirus in an Asian elephant.Journal of the Elephant Managers' Association 9: 103-104.

   30.    Barnard B.J.H. 1997. Antibodies against some viruses of domestic animals in southern African wild animals.Onderstepoort Journal of Veterinary Research 64: 95-110.
Abstract: Twenty-four species of South African wild animals were tested for the presence of antibodies to the viruses of 16 common diseases of domestic animals around 1993-5. Positive results were obtained for African horse sickness, equine encephalomyelitis virus, equine herpesvirus-1, bovine herpesvirus-1, Allerton disease (Herpes mammillitis; bovine herpesvirus 2), lumpy skin disease, parainfluenza, encephalomyocarditis, bluetongue, Wesselsbron disease, bovine ephemeral fever, and Akabane disease complex. No antibodies could be demonstrated against the viruses of equine influenza, equine infectious anaemia, equine viral arteritis or Rift Valley fever. The negative results support observations that the latter diseases, with the exception of equine viral arteritis, are absent in South Africa. The number of animal species found positive for a specific virus, ranged from 0-16. No antibodies were found in crocodiles or warthogs, whereas antibodies against Wesselsbron and bovine herpesvirus-1 were present in 16 species. Antibodies against viruses of horses were found almost exclusively in zebras and, although elephants reacted to African horse sickness, no neutralizing antibodies against it could be demonstrated in their sera. Zebras were also found to be positive for Wesselsbron and Akabane, which are usually regarded as viruses of ruminants. Antibodies against most viruses were encountered in all vegetation zones in South Africa, but most viruses were more prevalent in the high-rainfall zone in KwaZulu-Natal.

   31.    Bhat M.N., Manickam R. and Kumanan K. 1997. Serological evidence of bovine herpesviruses 1 and 2 in Asian elephants.Journal of Wildlife Diseases 33: 919-920.
Abstract: Antibodies were detected against bovine herpesviruses 1 (BHV 1) and 2 (BHV 2) in Asian elephants (Elephas maximus) using the passive haemagglutination (PHA) test. The study was conducted during May to December 1994 using sera collected from zoos and national parks in India. Four (4%) of 109 elephant sera had PHA titres ranging from 1:8 to 1:32 against BHV 1. 25 (23%) of the 109 elephant sera had PHA titres ranging from 1:8 to 1:64 against BHV 2. It is concluded that Asian elephants appear to be better reservoirs for herpesviruses which are serologically related to BHV 2.

   32.    Cambre R.C. and Buick W.W. 1996. Special challenges of maintaining wild animals in captivity in North America.Rev Sci Tech 15: 251-266.
Abstract: The maintenance of wild animals in captivity in North America is regulated by a number of different laws and government agencies in each country. Member institutions of zoo and aquarium associations in Canada, the United States of America and Mexico experience an extra tier of regulation in the form of industry standards, which are sometimes stricter than those imposed by government. Climate, natural disasters and harmful pest species all contribute to the challenge of keeping animals in certain locales. Vigilance against zoonotic disease transmission is maintained through industry and government-mandated sanitation standards, which are fortified by reporting regulations of local, regional and Federal health agencies. Current controversies in the keeping of particular taxa in North America include the threat to non-human primate breeding programmes precipitated by strict new import regulations, the fear of herpesvirus B infection, and commercial airline transport bans. Successive human fatalities among elephant handlers have prompted the industry and governments to re-examine the manner in which these potentially dangerous creatures are maintained in captivity.

   33.    Richman L.K., Montali R.J., Cambre R.C. et al. 1996. Endothelial inclusion body disease:  a newly recognized fatal herpes-like infection in Asian elephants.  Proceedings American Association of Zoo Veterinarians, pp. 483-486.

   34.    Metzler A.E., Ossent P., Guscetti F., Rubel A. and Lang E.M. 1990. Serological evidence of herpesvirus infection in captive Asian elephants (Elephas maximus).Journal of Wildlife Diseases 26: 41-49.
Abstract: In mid 1988 a 3-yr-old Asian elephant (Elephas maximus) from a circus in Switzerland died following generalized manifestation of a herpesvirus infection. In an effort to determine prevalence of infection with the herpesvirus, and due to lack of a corresponding virus isolate, it was decided to evaluate contact animals and elephants from a second herd for antibody to bovine herpesvirus 1 (BHV1) and bovine herpesvirus 2 (BHV2). Of 15 sera tested four displayed low neutralizing antibody titers to BHV2. None of the sera neutralized BHV1. However, as evidenced by protein A-mediated immunoprecipitation of metabolically radio- labeled virus-infected and mock-infected cell antigens, followed by separation of precipitation products in SDS-polyacrylamide gels, the 15 sera precipitated multiple antigens from both viruses. Similar results were obtained when using BHV4 antigens. The extent of reaction was most distinct with respect to BHV2 antigens, less prominent with BHV1 antigens, and least with BHV4 antigens. The respective protein patterns, although less marked, matched well with those obtained with bovine reference sera. Additional evaluation of sera from six elephants from two zoos in the Federal Republic of Germany gave essentially identical results. It was concluded that at least one herpesvirus, immunologically related to BHV2, may be widely distributed among captive Asian elephants, and that this virus apparently does not cause overt disease in the majority of animals

   35.    Ossent P., Guscetti F., Metzler A.E. et al. 1990. Acute and fatal herpesvirus infection in a young Asian elephant (Elephas maximus).Vet.Pathol. 27: 131-133.
Abstract: Infections with herpesvirus may cause papillomatous lesions in the Asian and African elephant.  In both species, the virus has been reported to localize only in the skin.  Disseminated nodules of epithelial cells were found in the lungs of a high percentage of wild African elephants.  In these cases, the proliferated cells contained intranuclear inclusion bodies in which herpesvirus particles were observed by electron microscopy.  The virus in those cases caused no illness.  This report documents the necropsy findings of a juvenile Asian elephant dying peracutely from massive generalized hemorrhage due to lesisons in the endothelial cells of the capillaries.  The cell nuclei frequently contained inclusion bodies in which herpesvirus particles were demonstrated.  This has not been described in elephants before.

   36.    Pilaski J., Hentscheke J., Sinn D. et al. 1988. Two virus diseases of different aetiology in Asian elephant (Elephas maximus) in samll traveling circus.Erkrankungen der Zootiere 30: 263-269.

   37.    Pilaski J., Rosenbruch M., Gelderblom H., Olberding P. and Hagenbeck C. 1987. Herpes virus infectionin an Asian elephant (Elephas maximus).Erkrankungen der Zootiere 29: 179-184.

   38.    Jacobson E.R., Sundberg J.P., Gaskin J.M., Kollias G.V. and O'Banion M.K. 1986. Cutaneous papillomas associated with a herpesvirus-like infection in a herd of captive African elephants.Journal of the American Veterinary Medical Association 189: 1075-1078.
Abstract: Proliferative cutaneous lesions developed in a herd of captive African elephants (33 from an animal importer in Texas, and 63 young elephants collected in Zimbabwe). Group-1 elephants were purchased 8 months before the arrival of the group-2 elephants. On arrival, 7 group-1 elephants had raised nodular fibrous growths, located predominantly on their trunks. Lesions were not observed in the group-2 elephants until approximately 3 months after they were acquired. Lesions on group-2 elephants began as small focal proliferative growths that regressed or that progressed into large nodular fibrous growths that were similar in appearance to those seen in the group-1 elephants. Lesions at various stages of development were biopsied and examined. Histologically, early lesions were inverted papillomas, with hyperplastic and hypertrophic epithelial cells containing amphoteric intranuclear inclusions in the lesion center. Older, large, nodular fibrous growths were ulcerated and were composed predominantly of a thickened dermis containing fibroblasts, collagen, and a mixed inflammatory cell infiltrate; inclusions were not observed in adjacent epidermal cells. Using a peroxidase- antiperoxidase technique, we did not detect group-specific papillomavirus antigens. Southern blot hybridization analysis of DNA from lesion specimens did not indicate papillomavirus- specific genomes. Electron-microscopically, inclusions consisted of aggregates of virus particles. The particles had electron- dense and electron-lucent cores and were 95 to 103 nm in diameter. Virions developed envelopes from nuclear membranes. Mature particles were seen within the cytoplasm and filled the intercellular spaces. On the basis of size, location, conformation, and envelopment, the particles most closely resembled those of herpesviruses.

   39.    Plowright W. 1981. Herpesvirus of wild ungulates, including malignant catarrhal fever virus. In: Davis JW, Karstad LH and Trainer DO (eds), Infectious diseases of wild mammals Iowa State University Press, Ames, Iowa.

   40.    Basson P.A., McCully R.M., de Vos V., Young E. and Kruger S.P. 1971. Some parasitic and other natural diseases of the African elephant in the Kruger National Park.Onderstepoort Journal of Veterinary Research 38: 239-254.

   41.    Erasmus, B. J., McCully, R. M., Pienaar, J. G., Young, E., Pieterse, L. M., and Els, H. J. The isolation of a herpes virus from the African elephant [Loxodonta africana (Blumenbach, 1797)]. Journal of General Virology . 1971.
Ref Type: Unpublished Work
Abstract: Same case as McCully, 1969, 1971;  Some references cite this article as  J. Gen. Virol. "in press" 1971, however the article was apparently never actually published.

   42.    McCully R.M., Basson P.A., Pienaar J.G., Erasmus B.J. and Young E. 1971. Herpes nodules in the lung of the African elephant [Loxodonta africana (Blumenbach, 1797)].Onderstepoort Journal of Veterinary Research 38: 225-236.
Abstract: Lymphoid nodules associated with Cowdry Type A intranuclear inclusions in epithelial and syncytial cells were found in the lungs of 74% of 50 African elephants in the Kruger National Park.  Subsequent studies proved these were caused by a herpes virus (Erasmus,McCully,Pienaar,Young, Pieterse & Els, 1971).  The disease appears to be subclinical or latent.  This virus, in common with other herpes viruses, might be more pathogenic in some other host.  The pathogenesis of the lymphoid nodules and the various stages of their formation are given and the detailed characteristics are illustrated.

   43.    McCully R.M., Basson P.A., Pienaar J.G. et al. 1969. Herpes nodules in elephants.Journal of the South African Veterinary Medical Association 40: 422.
Abstract: Full text:  The lungs of the majority of 50 elephants examined recently in the Kruger National Park had several lymphoid nodules varying in size from 3 to 30 mm (Fig. 1 arrow).  The alveolar lining cells within these nodules were metaplastic and contained Type A intranuclear inclusions (Fig. 2).  Electronmicroscopy revealed the presence of a virus in the epithelial cells.  It was subsequently successfully isolated in tissue culture and characterized as a herpes virus.

 


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