Reptile & Amphibian Forums

I had one of the many snakes that died, sent to Texas Veterinary Medical Diagnostic Laboratory System, located at College Station, Texas. If you are interested please e-mail me and I will e-mail you the completed necrospy report. This will give you some vague idea what this dreadful disease is all about. As a matter of information, only one of the 9 animals that sucumbed to this disease, showed any real physical decline, namely a large female rhino viper ( Bitis Nasicornis ), none of the others showed any signs of a disease at all, good weight, color, just immediately prior to death, a listlesness, and loss of appetite week or so prior to death.
cressm3@comcast.net I have already sent a copy to Mr. hoser

Yes, please send to me direct at adder@smuggled.com. I note that you said you already sent me a copy, but it was wiped along with about 200 other incoming e-mails due to incoming virus (how appropriate?). So please send again.
Thanks again.

Adress: schilperoordp@wellant.nl

Thanks in advance

Cheers,
Peter

My address is tang91766@yahoo.com

I would like to learn about this dreadful disease and also get a feel for how reports of this nature are put together: ie what is done in a necropsy.

I am sure by reading the report, I can learn a lot and get a feel for the scope of usefulness of necropsies.

cheers.
-----
Longtang. I like snakes and rats.

Hey Barry,
Do you know what snake brought the illness to your collection? Was it an import or an animal that has already been establish for a while or was it a captive born snake???? Mail me the report..... I would like to look it over..... niceynice27@yahoo.com

The summary of the disease from Mader's book is below:
Also posted temporarily at:
http://www.smuggled.com/OPMV15.htm
Pages 392-394 from Mader (ed.)

47

OPHIDIAN PARAMYXOVIRUS

MICHAEL R. CRANFIELD and THADDEUS K. GRACZYK

Ophidian paramyxovirus (OPMV) was first isolated in 1973 from a Fer-de-lance (Bothrops oojeni) after an outbreak in a Switzerland Serpentarium, which killed 25% of 431 specimens.' Since then, there have been at least 10 documented outbreaks of paramyxovirus in private and zoological collections. Two major outbreaks were documented to be associated with importations from southeast Asia and Costa Rica. Paramyxovirus has been isolated from all major snake families: Elapids, Boids, Colubrids, and Viperids. Pit vipers appear to be the most susceptible ' yet during a die-off involving predominantly Mojave rattlesnakes, copperheads housed adjacent showed no signs of illness.

Paramyxovirus is an RNA virus 120 to 150 nm in diameter and reproduces by budding from cell membranes. Multiple strains, perhaps genera of paramyxovirus, may eXiSt 2

CLINICAL SIGNS

There are no pathognomonic signs for the diagnosis of paramyxovirus infection. The disease presents with a tremendous variation of signs, which makes diagnosis difficult for the clinician. The symptoms are divided into three categories .3

1. Acute and Peracute

a. Minimal to nonetent promontory signs, anorexia,

and regurgitation occasionally seen. Animals often just found dead.

b. Acute respiratory compromise and/or neurologic involvement (head tremors and stargazing) are commonly seen.

c. The time from exposure to death can range from 6 to more than 10 weeks.

d. The infection may overwhelm the immune system with death occurring prior to a detectable antibody response.

c. Improper husbandry and environmental conditions may play a critical role in immunologic incompe tence, particularly the absence of a thermal gradient.

2. Chronic "Poor Doer"

a. Anorexia, hypophagia, and regurgitation are the earliest signs and have been seen up to 7 months prior to any other signs of disease.

b. Animals exhibit other general signs of debilitation such as reluctance to move, increased use of heat plates, emaciation, and poor muscle tone.

c. Various organ systems may be affected to different

degrees: Respiratory-variable degrees of stridor and dyspnea, developing into secondary bacterial pneurnonia. Gastrointestinal-gascous bowei distention, rnucoid diarrhea, malodorous stools, and protozoal overgrowth.

d. Specimens demonstrate high titers (up to 1:320).

Antibody presence does not prevent viral shedding, as demonstrated by animals able to infect or induce seroconversion in cagernates.

c. Animals eventually succumb to the disease but actively shed virus and pose the greatest threat to the collection.

f. Antiprotozoal (Flagyl, Scone) and antibacterial (Amielyde-V, Aveco and Cc, Fort Dodge, IA) treatment increase survival times.

3. Clinically Healthy Animals

a. Viral shedding persists in the face of high antibody titers based on the ability to seroconvert and/or infect cagemates.

b. Specimens remain asymptomatic for up to 10 months.

c. Sustained high titers may be indicative of a chronic carrier state and not necessarily immunity.

d. Most of the individuals eventually become chronic

"poor doers."

c. Some specimens have been documented as overcoming a viral encounter and surviving.

In the authors experience with a paramyxovirus outbreak, the animals with a regular appetite became anorectic, developing respirato compromise. They became severely lethargic and died within 1 week of the onset of signs. A few specimens developed horizontal head tremors that var ied from subtle to broad-swinging movements frequently accompanied with stargazing behavior. One specimen, a bushmaster (Lactesis mutus), did not show any clinical signs despite maintaining a scropositive status for 9 months. A Northern copperhead (Aghistrodon contortrix) placed in an adjacent aquarium did not develop a titer or lesions after 8 weeks of exposure to the bushmaster .4

DIAGNOSIS

Antemortem diagnostics consist of monitoring changes in scrum antibody titers by hemagglutination inhibition. Animals are considered to be positive with a titer of @ 1:20. Titers only reflect exposure, and a rising titer is necessary for diagnosis of active disease. The virus is dife cult to isolate and to date has not been isolated from a live specimen. There are no commercial laboratories offering viral isolation or serologic testing for paramyxovirus.

The laboratory of Dr. Elliottjacobson, (College of Veterinary Medicine, University of F71orida, Gainesville, FL) is currently performing hemagglutination inhibition (HI) serologic testing for titers to OPMV Ideally, enough blood should be collected so that 0.5 cc of plasma can be obtained. Blood should be pieced in either lithiurn-heparin rnicrotainer tubes or sodium-heparin glass tubes, centrifuged, plasma removed and placed in separate tubes (ideally cryotubes), and frozen for shipment on dry ice. Plasma should be stored frozen (ideally in an ultrafreezer at - 70'C or at normal refrigerator freezer temperature) until shipped. Scrologic testing is limited to 1 week per month.

Presumptive diagnosis of paramyxovirus infection may be based on a history of exposure and clinical signs. 111 animals should be closely monitored. A thorough clinical examination should be performed including pulmonary auscultation and a fecal examination. If OPMV is suspected, serum should be assayed for the presence of antibody by HI. If abnormal lung sounds are detected, transtracheal washes for cytolo and bacterial culture should be per formed. Definitive diagnosis of OPMV infection requires isolation of the virus from tissues thus far, this has only been achieved with tissue samples harvested at postmortem examination.

Postmortem diagnosis consists of typical gross, light, and electron microscopic changes in pulmonary tissue (Fig. 47-1).

1. Gross pathologic lesions range from no visible lesions to clear mucus in the oral cavity, slight pulmonary conges lien, and a frothy serous exudate in the air sacs. Severe cases may exhibit cascous exudative pneumonia.

2. Histologic lesions in the respiratory system include squamous metaplasia with mild proliferation of epithelial cells; thickening of the respiratory interstitium with macrophages, mononuclear cells, and minimal fibrosis; moderate amounts of cellular debris, bacterial colonies and exudate filling the primary bronchus and air spaces. Epithelial cells may contain cosinophilic cytoplasmic inclusions. The brain often has multifocal areas of gliosis and minimal perivascufar cuffing. Moderate ballooning of axon fibers may occur in the brain stem and proximal spinal cord.'

In many snakes with param oviral lesions in the lung, there is also hepatic pathology consisting of diffuse hepatic necrosis and/or multifocal pyogranulomatous inflammation. Pancreatic duct hyperplasia and hyperplasia of acinar cells with cystic dilation have been observed.'

Electron microscopy of cytoplasmic inclusions from an Ottoman viper showed them to be tubular, 12 to 18 nm diameter particles, which had "the regular periodicity of ribonucleoprotein helices of paramyxoviruses.""

NECROPSY PROTOCOL

Athorough necropsy should be performed as soon as possible. Blood should be collected, centrifuged, and serum frozen pending histologic findings. It is recommended that three sets of tissue be collected the first may be preserved in 10% neutral buffered formalin for conventional staining and microscopic examination; the second should be placed in formalin for 48 hours, then removed and placed into 70% ethanol. This will i prove the likelihood of finding lesions utilizing special staining techniques.' A third set of tissues should be frozen and kept for virus isolation, should this be indicated by histopathologic findings. Special attention should be given to include lung, liver, kidney, and splenopancreatic tissue in all sets of tissue saved.

PREVENTION AND CONTROL

Strict quarantine policies should be followed for all incoming snakes, particularly those that ar more susceptible or snakes from questionable origin. The following applies mainly for zoological situations but can be modified to suit other scenarios.

Recommended general quarantine protocol

1. Quarantine all new animals for a minimum of 60 to 90 days.

2. Obtain a minimum of two "clean" fecal specimens.

3. House quarantine animals individually to monitor

food consumption and fecal output.

4. Weigh animals as they enter and exit quarantine.

5. Animals must be feeding on a regular basis and

otherwise appear healthy before leaving quarantine. 6. Monitor animals closely for abnormal behavior and/ or posturing.

7. Euthanize all "poor doers."

8. Necropsy all quarantined animals that die or are

cuthanized.

9. Save tissues on all necropsied specimens according to previous recommendations.

10. Use footbaths when entering or departing the isolation area. Bleach is recommended.

11. Disinfect or destroy all cage materials after removal of animals from quarantine.

12. The quarantine room should have a separate set of husbandry tools. These should be disinfected after each use.

13. There should be no exchange in the air duct systems of the quarantine or isolation room and the main collection.

14. As soon as commercially available, scrologic monitoring of susceptible species should be employed on entrance and exit from quarantine.

The main mode of virus transmission is considered to be airborne with contaminated utensils and cage furniture playing a possible role. Medical management of clinical cases should include treatment with metronidazole, area-kacin, and fluids, if no ded. OPMV, like other paramyxoviruses, may cause immune incompetence and unless carefully treated, secondary bacterial infections may result in mortality.' Good husbandry practices, particularly the provision of an appropriate thermal gradient, should be integrated into the treatment if not already existing.

Cagemates of seropositive animals and those showing clinical signs should be isolated from the collection for at least 3 months from the time of diagnosis or onset of clinical signs. Necessary husbandry for that isolated group should be performed by a separate caretaker or by the same caretaker but at the end of the day after the healthy (non-affected) animals have been handled. If 90 days after the last death the remaining animals appear healthy and are seronegative by HI, they can be considered a low threat to the collection. Various stressors such as shipment and ambient temperature fluctuations may result in latent infections becoming active. Chronic carriers that are potential shedders of paramyxovirus should be identified and eliminated from the collection.

Vaccine trials have shown that snakes can develop antibody titers to inactivated vaccines but responses are variable and transient. No challenges against the vaccine have been tried. , A preliminary trial with a modified live vaccine resulted in the death of one animal and severe illness with full recovery in the other.' Further work is being completed on vaccines and the development of an ELISA test at the time of publication,

REFERENCES

1. To Isch D.W, Leloup P: Fatale endemische infection in cineum per

pentorium. Tieraeyzth 4:527, 1976,

2. Jacobson E.R.Paramyxo-like vims infection in a rock ratilesnake, j

Am Vet Mod Assoc 177(9):796, 1980

3. Lloyd M.L, FlanaganjP: Recent Developments in Ophidian Paramyxo@rus Research and Recommendations on Cntrol. Proceedings of the American Association of Zoo VeterinanaDs, Surth Padre Island, TX, 1990, pp 151 156@

4. Granfield MR, tale to DM, O'Donnell D: Ophidi n Paiainyxovirtis.

Proceedings of Avian/Exotic Symposium, Davis, L, 1991, pp 175 181,

5. Jacobson E.R, Gaskin JM, Wells 5, et al: Epi.ootic of ophidian para-

myxovirus in a zoological collection pathological, microbi logical and s rological Endings. J Zoo Wildl Mod 23(3) 318, 1992, 6. Patgicter LND, Sigler RE, Russel RG: Pneumonia in ttoman vipers

associated with a parainfluenza two-like @rus. j Wildl Dis 23(3):355, 1987@

7. jacobson ER: Personal so municatiod. 8 jac@hson ER, Gaskiii JM, Page D, et al: 111Dess associated with paramyxo like virus infection in zoological collection f snakes. j Am Vet Mod Assoc 179(1l):J227, 1981.

9. jacobson ER, Gaskin JM, Flanagan JP, et a]: Antibody reap rises of

western diamondback rattlesnakes (Grotalus atrox) to inactivated ophiad paramyxo@drus vaccin s. j Zoo Wildl Mad 22(2):]84, 1991.

10. Flanagan JP: Personal communication.

FROM: REPTILE MEDICINE AND SURGERY BY DOUGLAS R. MADER, M.S., D.VM.

Diplomate, American Board of Veterinary Practitioners (Companion Animal)

Long Beach Animal Hospital, Long Beach, California

Associate Clinical Professor, Department of Medicine and Epidemiology,

School of Vetchnary Medicine, University of California at Davis, Davis, California

Staff Veterinarian, Santa Ana Zoo, Santa Ana, California

Attending Veterinarian, Allergan Pharmaceuticals, Inc., Irvine, California

Illustrations by Geoff Stein, DVM

Note: Corrections from OCR process not made.
Also posted temporarily at:
http://www.smuggled.com/OPMV15.htm
OPMV Summary from Mader's book