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Reovirus - successful treatment of small elapids

Raymond Hoser
488 Park Road
Park Orchards, Vic, 3114
Phone: (0412) 777 211
E-mail: XXX (see bottom of webpage)

Originally published in November 2003 in Crocodilian 4(3):23-27.


Recently a fluid-borne viral infection, swept through a number of Australian reptile collections causing mortalities in smaller elapids (Hoser 2003).

My own collection was the first in which the cause of death was accurately identified.

In this collection four neonate Death Adders (Acanthophis spp.) died in June 2003.

Four other neonate Death Adders survived the virus.

All other snakes in the collection, consisting of adult Death Adders or other species survived either without symptom or with lesser symptoms than the smaller snakes.

The virus was tracked to an incoming snake (another Death Adder) and by further tracking it was diagnosed as going through more than a dozen other collections.

Those which had small neonate elapids also had heavy losses, which until then had been written off as death by causes unknown.

Tests at the Victorian Institute For Animal Science (VIAS) using an Electron Microscope (EM) identified the virus as a previously unknown Reovirus.

Before that the virus had been presumptively diagnosed as the better-known Ophidioparamyxovirus (OPMV) which presents similar symptoms in affected snakes.

The cause of death in the Death Adder tested was identified by Veterinary Pathologist Malcolm Lancaster as a reovirus in the brain (Lancaster 2003).

As part of a detailed study into the virus and it's affects on captive snakes, survival statistics in affected collections and a collation of relevant keeping records, I was able to determine the optimal means to combat the effects of the virus and increase survivorship of affected snakes.

This paper lists the known signs of infection.

Then it gives the best means of treatment.

What follows is a summary only.

The treatment indicated later was successful in treating many affected snakes in my own collection, including (in particular) a neonate Death Adder (Acanthophis lancasteri/bottomi) accidentally infected in early September 2003, which if left untreated would have certainly died.

It made a full recovery.

The details of that and other recent cases of successful treatment are not given here.

This particular reovirus shows up clinically in a similar manner to the better known Ophidioparamyxovirus (OPMV) and treatment for that and other reptile viruses would perhaps be best done along similar lines to that indicated here.


In the first instance the signs of infection may be subtle and easily missed by many keepers. Sometimes one or more dead snakes are the first indicator.

Assuming that the snakes are healthy long-term captives, any decline in health in more than one snake at the same time must be taken as indicative of a viral infection.

Viral infections are most often noted by spontaneous development of respiratory ailments in snakes or rapid emaciation of specimens. These are the two most commonly identified signs of the reovirus that affected my own collection and others in the same line of infection.

These symptoms are most pronounced in elapids under 45 cm in length and as a trend, elapids over this length won't die from the reovirus unless they also have other health problems or husbandry conditions aren't optimal.

Notwithstanding the obvious signs of reovirus just noted, there are numerous other indicators, most of which that are known are listed below. If snakes display more than one of these traits, they should be watched particularly closely. Most will not show all the traits below, but they are given for completeness sake. If more than one snake in the collection display such traits, then virus should probably be assumed and any snakes in ill health or suboptimal condition treated.

Signs of reovirus infection include:

    1. Rapid emaciation.
    2. Excessive defecation and/or urination (leading to emaciation).
    3. Excessive drinking, (usually in larger snakes, with smaller snakes refusing to voluntarily drink).
    4. Loss of appetite.
    5. Unusual restlessness and/or listnessness.
    6. Failure to thermoregulate properly, usually by going to the coolest part of the cage.
    7. Abnormal postures, resting positions and/or so-called 'stargazing'.
    8. Inability to slough probably due to listnessness or emaciation.
    9. Regurgitation (usually as a result of rapid emaciation or emaciated condition, or snake too cool to digest food due to improper themoregulation - all virus related).
    10. Signs of respiratory infection in about 30-70% of affected snakes, manifesting as any of the following: failure to flick tongue, tongue sticking together, exudate from the mouth, digging to remove exudate from mouth (and/or dust on snout as residue from digging), "popping" through nostrils, blocked nostrils, head held raised and puffing of neck (the latter being the most serious sign).
    11. In neonate snakes the skin on the belly becoming more translucent than normal allowing the internal organs to be more strongly noticed.
    12. In the 24-36 hours before death, the affected snake will tend to become unusually restless and will usually die a painful death and in convulsions. Some severely emaciated snakes will not die in convulsions, but instead just die in a listless manner.
    13. Progression from first noticeable signs of infection to death can be rapid and is usually about a week in neonate snakes and longer for larger snakes, noting that larger snakes are less likely to succumb.
    14. Other signs of viral infection that occasionally crop up (usually) in larger snakes include mouthrot and panopthalmitis.

Most large snakes do not show signs of infection, but they may still carry the virus and affect other snakes. Snakes in this group include large Red-bellied Black Snakes (Pseudechis porphyriacus) and Taipans (Oxyuranus spp.)

Hence if one snake in a collection is assumed to be affected, all in a collection should be assumed to be infected.


Most collections that had highest losses did so because the keepers failed to realise the importance of acting quickly to treat the virus, or alternatively didn't regard the signs of respiratory or other complaint as being too serious until it became too late.

In other words, to avoid losses, the central theme is to act fast and act proactively.

Notwithstanding the preceding comment about infections of collections, part of the proactive treatment is to assume all snakes are not infected and isolate all from one another by using separate feeding and cleaning implements for each cage.

This may also cut potential losses.

Sterilization is best by use of continually boiling water for ten minutes if implements need to be shared.

In other words, metal feeding tongs only.

In case I haven't made it clear, I should note that all evidence shows that in situ this virus is transmitted via fluids only. That is via shared water bowls, shared cloths to clean water bowls, snake mites and saliva left on feeding tongs and forceps.

In other words your keeping regimen should as much as is practicable exclude potential virus spreads via these means.

There is no evidence (yet) to suggest that as a matter of course this reovirus is airborne.

If you believe you have a virus infecting any of your snakes you must as a matter of decency not knowingly trade infected stock and/or warn appropriately and also notify all other persons whom you have moved or traded reptiles with in the recent past, at least including the previous 12 months. Failure to do so may allow other keepers to either have avoidable losses or themselves unknowingly trade on infected stock.

Most importantly remember that snakes that do not show signs of infection are not necessarily virus free. They may be carriers (but not showing symptom). In fact that seems to be the most common state for most elapids. In terms of this particular reovirus, pythons seem particularly resistant, but that does not mean they too may not be carriers. At the moment whether or not pythons will carry and shed the virus is unknown.


The two most serious signs of infection are:

    • Respiratory infection
    • Failure to thermoregulate properly

If snakes show signs of either, then proactive treatment is mandatory.

Use all methods indicated below as necessary for the snake.

Snakes thought to be infected should be assumed to have respiratory infection and/or likely to have one and be watched very closely. If no respiratory infection is detected, treatment should be via Baytril in the water bowl at a ratio of .5 ml per 200 ml.

If respiratory infection manifests in any observable way, Baytril should be diluted at a rate of .2 ml per 10 ml and fed orally to the snake at an appropriate rate (e.g. .2 ml to a 15 cm (total length) Death Adder) daily until symptoms disappear, whereupon Baytril remains in the water bowl at the indicated rate.

Larger snakes that are affected will drink much greater amounts of water and this is indicative of infection. They will not tend to emaciate and do not need force-drinking, even when force-fed (see below).

Affected smaller snakes will stop voluntarily drinking and will emaciate rapidly and must be force-drank daily until they are seen (or detected) drinking voluntarily again. This may not be for anything between a day and a month. Force-drinking young snakes is a major plank of success in terms of saving these snakes and will help avert death via neurological symptoms, seizures and the like.

All affected snakes must be moved to a warm room with the coolest part of the cage no cooler than 25-26 degrees celcius. This will enable the snake's immune system to work at it's best and also allow for digestion of food.

Force-feeding of affected neonate snakes is also essential for treatment success. This recommendation applies to all snakes except otherwise very well-fed and healthy adults, which will generally be able to ride though an infection without major problem.

Affected snakes should be force-fed regularly and items that are small enough to be digested easily. Badly affected snakes will regurgitate rodents. Freshwater fish such as Gambusia or carp are preferred for the most ill snakes.

Snakes not quite as ill can be fed skinks, but these should have their bodies cut along their length with scissors to aid digestion. The difference between a skink without regular cuts along the body and one without is stark and digestion time (in and out of stomach) can be halved by slitting the skink.

Tails are not as easily cut (like slitting the body) or as easily digested as cut bodies and should be avoided in the most debilitated snakes.

As a rule, affected neonate snakes should be force-fed items that pass through the stomach (not the whole digestive tract) within 30-50 hours and should be force-fed every three to four days while affected by virus.

Force-feeding should be continued until the snake is well and truly free of all symptoms and on a trajectory to rapid growth and good health.

Force-feeding and force-drinking is often best done at the same time.

Most snakes will tolerate this without a problem and if held vertically, at the time of forcing, gravity alone will prevent reflux until the snake is put back in the cage, whereupon (assuming it's done properly) the snake will hold and push further down the food and drink.

Under no circumstance should a neonate elapid be allowed to lose condition to make it more vulnerable to virus or other infection, and this includes if it appears uninfected but others in the collection are infected.

While the minimum cage temperature should be 25-26 degrees, it should still have a basking spot around 30 degrees or slightly higher to enable it the right to actively thermoregulate. The cage minimum temperature is essentially as a safeguard to ensure that food will digest no matter where the snake rests.

Provided treatment is proactive and well before the snake reaches the restless stage that precedes death (36-24 hours beforehand), you should be able to prevent the snake ever reaching that stage and hence death will be averted.

Experience shows that it takes from 2-6 weeks for snakes to develop immunity to the virus in terms of it's body's defences overcoming it and hence that is how long pro-active treatment may be needed.

Furthermore, the virus does tend to relapse and to date it has no known 'use-by-date'. However snakes known to be infected in June 2003 were still infected and showing symptoms (in relapse) in October 2003, giving a minimum shelf-life of four months.

Shedding time is a very high-risk period for affected small snakes.

Due to emaciation, some snakes will also have difficulty shedding. A proactive approach is required here. Shedding in snakes commences with the lifting of scales from the snout about 1-4 days after the eyes clear. If the snake has not completely sloughed within 60 minutes of the first lifting of scales from the snout, the skin should be manually removed immediately.

If this is not possible (most likely) then the snake should be soaked in luke warm (30 degree) water for as long as it takes to make it more easily removed and removable. In most cases this will be less than 60 minutes and in the worst cases within 12 hours.

In this situation, it will be far less stressful on the already debilitated snake for you to remove the skin than to chance it and let the snake try to do it by itself.

Nothing emaciates a snake more quickly than it being restless and unable to properly slough.

As already inferred, any other ailments or disorders that a snake may have, even if not directly virus related, should be aggressively treated. Snakes with one or more ailments, including pre-existing ones such as parasitic worm burdens will take much harder hits from the virus and hence be at greater risk.

Hence in summary the four keys to success in treating affected snakes are:

    • Treat for respiratory ailment and aggressively even if the infection only appears minor.
    • Put snake in room with minimum temperature of 25-26 Degrees Celsius and keep heat gradient in cage (going higher)
    • Force-feed regularly (especially for smaller snakes)
    • Force-drink if the snake if it emaciates rapidly (including at time of feeding)

The fifth important step is manual shedding if necessary.


As a result of my general dissemination of information about this virus in Sydney in 2003 (see Hoser 2003), a case of virus infection in nine neonate Death Adders was diagnosed in a Sydney collection in October 2003. At this stage there is no known direct connection between this infection and the line of infection that attacked my own and other collections, even though the virus appears to be the same.

Some of the five dead specimens are now being tested at the Elizabeth Macarthur Institute in Sydney.

The importance here is that the virus may attack almost any collection and from almost any possible source. No keeper can guarantee that they may not get affected by this or another virus at some time in future, hence the importance of knowing the best methods to treat the virus.

The method given here has worked and so far is the best known.


The many fellow keepers who have assisted in collating known information on the reovirus and related issues. Also acknowledged are several scientists at VIAS (Victoria), ANAHL (Victoria) and the Elizabeth Macarthur Institute (NSW), who have or are performing tests on various snake corpses.


Hoser, R. T. 2003. OPMV in Australian Reptile Collections. Macarthur Herpetological Society Newsletter, June 2003. 38:2-8.

Lancaster, M. 2003. Snake Necropsy, AC-3. 26 September: 2pp.

Herpetology papers index.

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