Also given is a history of other known virus cases in Australia and the ramifications of these diseases in terms of captive-held collections and potential escape into the wild. This paper notes the adverse consequences of failure to report infection to persons who received infected snakes.

Unlike most other reports on reovirus or OPMV that report in detail on the histopathology and microscopic properties of the viruses, this paper details the case from the perspective of reptile keepers in terms of observation of symptoms and diagnosis and in view of alerting other keepers of these indicators of infection.

This paper refutes claims that the primary means of transmission is airborne. It is not. Fluid-based transmission is demonstrated. For the first time ever, this paper explains previously noted differences between the progression of reovirus (and OPMV) in situ and in the laboratory. There are also numerous pointers as to which virus affected snakes will show symptoms and are (if untreated) most likely to die and those which may not or instead be asymptomatic carriers.

Evidence is also presented that indicates the following: This particular reovirus is particularly deadly to small-sized elapid snakes, on initial infection effectively stops growth in affected small snakes, is often carried by large snakes without apparent symptom, is probably a recent import into Australia and other new findings.

Virus infections can also be effectively tracked though collections with a high degree of certainty, even in the absence of detected symptoms, based on known cases within one or more collections, transaction histories and an appraisal of management practices within collections.

Which snakes may carry and shed virus isn't known, but it is likely all elapids (at least) fit this category.

Most respiratory infections in reptiles have been traditionally thought of as bacterial in origin. Such infections have been regarded as opportunistic explosions of (often natural) bacterial flora (including the likes of Pseudomonas, Aeromonas, etc) as a result of stress in captive reptiles, including poor husbandry, excessive handling and in particular cage temperature being too cool.

An example of this prevailing thinking was seen in Banks (1980) who at the time wrote:

Treatment of these infections, as indicated by texts such as Banks (1980), has generally been by removing the husbandry and related problems alleged to have caused the infection, such as cage temperature, other specimens, substrate, etc, as well as anti-biotic treatment to attack the bacterial infection and if possible the raising of the cage's temperature so as to enable the reptile's own immune system to work to it's full potential.

In 1976 a respiratory epizootic spread through a collection of fer-de-lance (Bothrops atrox) at a snake farm in Switzerland (Foelsch and Leloup, 1976). Although Pseudomonas and Aeromonas were isolated from the respiratory tracts of dead snakes, a virus since called the fer-de-lance virus (FDLV) with ultrastructural properties similar to the myxoviruses (ortho-, para- and meta-) was identified (Clark and Lunger, 1981). That the FDLV is a paramyxovirus was indicated by demonstrating it possessed a single-stranded RNA genome and had a sedimentation value of 50S (Jacobson, 2000).

In the past decade and in light of this new information, OPMV associated die-offs have been identified (either by virus isolation and/or characteristic histopathologic changes) in a variety of private and zoological collections in the United States (Jacobson, 2000).

Paramyxovirus has also been identified in lizards (Nichols, et. al. 1998).

Histopathological changes in reptiles suffering Paramyxovirus are now well documented in the scientific literature as is the progress of OPMV infections in snakes in the laboratory situation.

Paramyxovirus as identified in reptiles is believed to be from an undescribed genus (as of 2003).

In terms of the husbandry and conservation aspects of OPMV in lizards, the same applies as for snakes. However for the purposes of this paper, OPMV in snakes only is considered and then only in terms of similarities to the reovirus described herein.

Based on the reports of Jacobson (2000) and others, it appears that there are multiple forms of OPMV and some which appear to target particular species within a collection and leave other snakes apparently untouched and/or asymptomatic, meaning that the snakes carry the virus but don't show clinical signs of infection.

Contrary to assertions by Australian Reptile Park (ARP) owner John Weigel (personal phone communication 3 July 2003 and later e-mails and internet posts), the mere fact a snake does not show signs of OPMV (or reovirus) infection does not mean it isn't a carrier. Experiences in terms of the epidemic detailed in this paper adequately prove this point.

Jacobson (2000) wrote:

The symptoms of OPMV and reovirus in snakes varies, but in most diagnosed cases the most obvious (documented) target appears to be the respiratory tract.

This variation is between individual snakes and species. However there are some distinct trends between species known to be infected with the same virus (see later).

In captive snakes OPMV and other viral infections is often seen manifesting as a respiratory infection with the lung cavity swelling and fluid being exuded through the mouth.

It usually appears in an apparently spontaneous way and in spite of no apparent change to caging husbandry and the like. The only change being another (infected) reptile being moved into the facility, although this factor is often overlooked by keepers.

(In the absence of indicators of other illness or known husbandry defect, these symptoms and factors should be taken as indicative of a likely viral infection).

Other symptoms of OPMV and reovirus infection are known to include excessive urination (and sometimes drinking), often seen manifesting as a rapid emaciation of the snake (especially if the snake does not drink) and apparent loss of condition at abnormal speed, blood from the mouth and neurological signs. The latter manifest as a form of 'stargazing' or unnatural postures as seen in IBD in affected pythons and boas.

Rapid emaciation also manifests frequently in unexpected regurgitation of food and an inability to slough properly, as both processes do in the normal course of events severely tax the reptile's fluid balance.

Based on published reports and my own experience (see below), OPMV (and reoviruses) usually, but not always acts quickly in affected reptiles and appears to go through four stages once it appears in a live reptile. Death usually results from 5-12 days after symptoms appear.

These stages are as follows:

• Stage 1 - A loss of muscle tone, rapid emaciation and the reptile stretching out in a 'linear manner' with the head slightly raised. This stage may also manifest in "star-gazer" type behaviour, loss of vitality, unnatural poses and other more subtle cues.
• Stage 2 - Lasting one to two days - The reptile displays unusual restlessness and holding the mouth open. It will apparently wander around the cage aimlessly. Tongues are kept in the mouth and pupils dilated.
• Stage 3 - Seen from several hours to a day before death. This involves the mouth being kept open, sometimes only slightly and the snake will expel a pus-like material from the glottis.
• Stage 4 - Seen from several minutes to one hour preceding death. The mouth is kept fully opened, the pupils are dilated, and reptile will remain excessively active, including exhibiting bouts of convulsive behavior.

Other than treatment of secondary bacterial infections with relevant antibiotics, such as Baytril and other general pallative care, published literature says that there is effectively nothing that can be done to help affected snakes (see later).

At the terminal phase of OPMV or reovirus infection a snake will appear to be quite emaciated, even if it had appeared very healthy just days or a few weeks earlier. Put simply, the decline is rapid.

However it is now known based on this study that most of the emaciation observed is from dehydration, not necessarily a general loss of other body condition, although clearly this does decline as well and at an accelerated rate.

A hemagglutination-inhibition (HI) assay has been developed to measure antibody produced against OPMV (Jacobson et al., 1981), however in experiments, some snakes produced no antibodies some weeks after infection and others actually died before any antibodies appeared. Hence a negative HI assay cannot be taken to exclude the possibility an OPMV infection. It appears that in some snakes OPMV antibodies form about 8 weeks after infection.

The hemagglutination-inhibition (HI) assay may not work with other (non OPMV-type) viruses either.

Assuming similar to be the case in terms of reovirus infections, the delay in developing immunity may in part have explain the delayed cure of respiratory infection in a reovirus infected adult female Floodplain Death Adder (Acanthophis cummingi) and a case involving an infected Australian Scrub Python (Australiasis amethistina clarki) (see below).

The observed 8 week period is also important in terms of the commonly observed situation of affected snakes often regaining health after this period of showing OPMV-related (or like) symptoms.

Virus infections can therefore only be detected with certainty via electron microscopy (EM) and this is usually only on dead reptiles, due to the nature of tests required (brain and other vital organs tested).

Diagnosis of the virus (OPMV or reovirus) in situ is generally 'presumptive' (meaning educated guess) and based on the history of the reptile, and after death by gross and histological examination of tissues including of the lungs, respiratory tract and associated organs, brain and kidney.

One of the aims of this paper is to aid in preliminary and presumptive diagnosis in situ of viral infections in snakes to enable keepers to take rapid remedial action and reduce or even eliminate potential losses.

The information provided below also shows how virus infected snakes can be reliably predicted, based on known cases, movements of reptiles within and outside the collection as well as via an appraisal of husbandry methods.

Jacobson et. al. (1997) tested a vaccine for OPMV in western diamondback rattlesnakes (Crotalus atrox), but the results were disappointing, including death of vaccinated snakes and so a totally effective cure or preventative is not yet available.

Reoviruses were originally identified in the early 1950s during a search for weakened strains of polio. Reoviruses were isolated from the respiratory and intestinal tracts of apparently healthy individuals. Thus, the acronym reo (for respiratory, enteric, and orphan, the latter meaning not associated with human disease) was proposed and is now used.

It is now known that reoviruses can be particularly deadly on target species or age groups within a species. Several means of transmission are speculated in the literature, including via water droplets and oral-fecal transfer.

They are known to cause disease in a number of organisms, perhaps most significantly in young poultry.

An unclassified group had been identified as causing disease in snakes prior to this paper.

A group of Chinese Vipers shipped to a zoo in the United States were found to have died without apparent symptom. Tests revealed the presence of a Reovirus.

At least two similar cases involving reovirus have been positively identified are in the literature.

Notwithstanding this, effectively nothing has been published on reovirus in terms of known symptoms in affected captive reptiles, treatments and comparisons with other viral infections.

Anecdotal evidence suggests that reovirus infections may in fact be far more common than originally suspected, if not in Australia, then elsewhere and also that many presumptive diagnoses of OPMV may in fact be misdiagnosed cases of reovirus, although this evidence is somewhat speculative and can only be verified based on proper electron microscopy (EM) tests on affected and dead snakes.

Notwithstanding the potential misdiagnosis of the virus type infecting affected collections, the treatment and management of the disease in captive reptiles appears to be the same, hence partially negating the need to positively identify the virus type affecting the reptiles, rather merely the need to identify virus a the causative agent of disease in a collection.

Posts circulated on the internet under the header "Out-of-Session Item No: 01/2003 Consultative Committee on Emergency Animal Diseases" (Christie, 2003) in January 2003 indicated presumptive diagnosis of OPMV in Australian collections of snakes.

A presumptive diagnosis is best described as an 'educated guess'. It does not involve positive identification via EM, but is instead based on symptoms and sometimes histological examination of one or more corpses, indicating the likely cause of disease. The diagnosis is also made in conjunction with an assessment of the captive conditions of the reptiles and a process of elimination in terms of other potential causes such as poor husbandry and the like.

The post referred to above was an apparently leaked memo.

It listed infections, including presumptive diagnosis of OPMV in snakes at the Australian Reptile Park (ARP), Somersby, NSW, based on a mass die off of Death Adders (Acanthophis sp.) starting February/March 2002, then abating somewhat and then re-appearing in the spring months to November. Whilst starting with Death Adders, the infection later allegedly spread to other snakes including Tiger Snakes (Notechis), King Brown Snakes (Cannia) and a Woma (Aspidites).

The reptile park had moved snakes into quarantine as infections appeared, but this method failed to stop the spread of infection to other snakes, indicating that the either the entire collection was already infected or that the infection was not being contained within the wider collection.

Other species of snakes held at the ARP did not show signs of infection, which is in line with other viral infections in that they tend to only target certain species and leave others apparently untouched.

The report also stated that cases of OPMV had been presumptively identified in (unnamed) private collections in Queensland. My own inquiries in June 2003 showed that these latter cases were diagnosed by Clayton Knight of the Deception Bay Veterinary Clinic, just north of Brisbane.

The circular claimed OPMV was thought to be exotic to Australia and claimed the first known cases of it in Australia.

In all cases the diagnosis had been by clinical, gross and histological examinations.

Christie, 2003, via John Weigel implied that arrangements were being made to send samples to Elliott Jacobson to confirm the diagnosis of OPMV, but as of 24 June 2003 (Jacobson 2003b), this had not occurred.

The history of the leak is as follows:

Following an out-of-control epidemic and die off at the Australian Reptile Park (ARP), the staff there sought the help of outside veterinarians.

One thought OPMV was the cause of disease and sought a second opinion. This was confirmed and hence, as is required under law, the NSW Chief Veterinary Officer, Bruce Christie was notified.

As per usual protocol, the (later leaked) memo was sent by the NSW Chief Veterinary Officer, Bruce Christie to the Chief Veterinary Officers in the other Australian states.

This was meant to be 'in confidence' and merely as a warning to other state veterinary officers to be on the alert for the virus..

The leak was first by Mauricio Perez-Ruiz, a Northern Territory-based veterinary surgeon, who had received the memo. In confidence he sent it via e-mail in January 2003 to a close friend Peter Mirtschin of venom supplies.

Perez-Ruiz knew that Mirtschin dealt extensively with Weigel at the ARP and that he had received snakes from them and so wanted to tell him to 'watch out' (his words) in terms of snakes received from the reptile park.

Mirtschin had also had an uncontollable mass-die off of Death Adders some time earlier, including a all (twelve) neonates received from Rob Valentic in Victoria (while other recipients of the snakes had managed to keep theirs alive without problems).

Mirtschin then sent a copy of the leaked memo to Weigel asking him what was going on, which incorrectly led Weigel to believe that the memo had been sent widely.

In response to this memo, Weigel sent out his own e-mail response, including to myself, which effectively hosed down the idea of risk to other collections by claiming that the ARP had got it's house in order and stopped the spread of infection, including by notifying all recipients of it's stock during the relevant period.

Weigel sent his own response widely due to the fact that he had no idea where the original memo had gone. He then threatened to sue Perez-Ruiz for "defemation" if he reposted the memo, the result being that it ended up on a non-Australian internet bulletin board.

Perez-Ruiz wasn't impressed with Weigel's threats and in turn told numerous people that Weigel's own management of the disease at the ARP had been "a bloody disgrace" and "abysmal".

Perez-Ruiz also said that Weigel was in fear in that if a so-called "exotic virus" was positively identified, via EM, then the government may move in and seize and kill the entire stock holdings at Weigel's park. Hence Wrigel's over-riding concern to keep the plague under wraps.

Important in terms of this paper is that the ARP never (to at least February 2004) positively identified via EM the virus that caused death in their facility.

In early 2002, three new born and two one year old (est.) Death Adders (Acanthophis antarcticus) were obtained and housed in a room of a bungalow (the Hoser snake room). All were raised to adult size (55 cm or larger) within 12 months and excluding a severe mite infestation in mid year that was cleared up without casualty using pest strips (the now unavailable Dichlorvos based ones), the raising of the snakes was generally uneventful.

(For the record the mite infestation was completely my own fault and I was lucky that no snakes were lost as one of the Death Adders did decline sharply in condition as a result and took some time to recover).

All snakes were housed separately in plastic tubs and water-bowls in the cages were of a disposable nature and hence there was never possibility of transfer of waterborne vectors at any stage of cage cleaning.

This is usually where the snakes tend to rest.

Each cage has minimal furnishings and only enough to provide the snake's essential needs in terms of water, cover, and the like. Substrate is hardened sand forming a rock-like surface, which in turn (usually) has loose leaves on top. Typically the snakes thermoregulate by siting themselves at the appropriate point of the heat gradient.

Around Christmas 2002, a Queensland Carpet Python (adult) (Morelia macdoweli) and a NSW Diamond Snake (Juvenile) (Morelia spilota) were moved into the room and kept in identical conditions. Unlike the Death Adders, which had no cover other than leaves, they each had an upturned pot to shelter under, which they used.

Both appeared outwardly healthy at the time and remained so.

Their captive history was unremarkable.

On 15 February 2003, an adult male and adult female Top-end Death Adder (Acanthophis cummingi) were obtained from keeper Stuart Bigmore of Lara, Victoria and housed in the same room and under identical conditions. Both had been originally obtained from the wild, although they had been captive for some years.

Bigmore had held the male for 18 months and the female since at least 1997.

They both presented with numerous health problems, including parasitic (nematode), protozoan (green runny feces from amoebic dysentery), bacterial infections, including severe respiratory infections (fluids from mouth) and open lesions on the body (both snakes). The two snakes had previously been housed at opposite ends of the same room at the previous facility and the similarity of infections between the snakes, in spite of the caging arrangements went unnoticed at the time.

As above, these snakes were also housed separately and over coming weeks were given a cocktail of anti-biotic (Neosporin), anti-helminthic (Panacur) and anti-protozoan (Flagyl), usually administered in force-fed food items such as rodents.

At this stage, neither ate voluntarily. After initially appearing to recover slightly, the more emaciated male declined and died on 10 March 2003. The cause of death was believed to be linked to the systemic infection as both the dysentery and helminth problems had been removed and the snake had passed several 'good' feces based on rodent and other food. At the time of death the snake also had an apparently intractable respiratory infection.

After deciding not to autopsy the snake, the intact frozen corpse was lodged with the National Museum of Victoria on 14 March 2003 (NMV D71474).

The female lived. After six force-feedings, the surviving female ate voluntarily for the first time on 19 April 2003. She appeared to make a full recovery in terms of health and condition thereafter.

Notable points here are that the two above snakes were housed in the same bank of shelves as the other snakes, although until deemed healthy, they were handled with separate hooks and feeding implements, the most notable being the forceps used to offer food to the snake.

This quarantining ended around the end of March 2003 when it was decided that the adult female A. cummingi was in perfect health save for her reluctance to feed.

A persistent respiratory infection was noted, but overlooked as being a 'hang-over' from her previous poor health and not thought likely to be transferable to the other snakes. The basis of this decision (in hindsight erroneous) was that the respiratory infection was thought to be an opportunistic bacterial infection derived from the natural flora of the snake's respiratory tract and therefore not contagious.

On 25 Feb 2003, four newborn (born 22 Feb) Top-end Death Adders (Acanthophis cummingi), acquired from Ballarat-based keeper Roy Pails were moved into the room and housed as for the other snakes.

All were fed almost immediately and more-or-less until death (see below) grew rapidly and without incident. One of the males, was however slightly smaller than the other three and was generally more reluctant to eat in terms of 'assist feeding'. It was therefore generally force-fed (food literally pushed past the head and neck using forceps), rather than 'assist fed' whereby food is put into the mouth and the snake then finishes the feeding process.

The same in terms of general husbandry applied in terms of two newborn Death Adders (A. antarcticus) (born 21 Feb 2003), received from Sydney-based keeper Alex Stasweski that were moved into the room on 21 March 2003.

On 17 May 2003, 14 Red-bellied Black Snakes (Pseudechis porphyriacus) were placed in plastic cage boxes immediately adjacent to the other snakes in the same room. These snakes were literally in transit as part of a legal shipment from NSW-based keeper Rob Gleeson to keepers Fred Rossignolli and Scott Eipper in Victoria. The snakes remained in this position until taken away on 20 May 2003.

At the time the (evident) physical health of the P. porphyriacus ranged from good to emaciated and all had a severe mite infestation. The mites were killed off using pest-strips (dichlorvos-based) before the snakes were stored in the room and there was no evidence of transfer of live mites to the other snakes in the room.

The strong anti-mite protocol in the Hoser facility in the wake of the 2002 infestation made any mite transfer almost impossible. The anti-mite protocol includes automatic treatment of snakes periodically and in the absence of evidence of mites.

It also includes any 'in transit' snakes such those removed from properties of people upon their request.

On 19 May 2003, two newborn Barkly Death Adders (Acanthophis hawkei) (born 4 May 2003) and acquired from Brian Barnett of Ardeer, Victoria were placed in the same room in similar housing to that described above.

Both ate the next day, (the male by itself, the female by assist feeding) and like all the other young Death Adders, presented as being in perfect health.

As the history of the die-offs is related below, the other various possible causes of death are given (as mooted at the time). This is so that it becomes evident to the reader how the diagnosis of viral infection was first/finally reached and why other possible causes of death were properly discounted.

On 25 May 2003, the female A. hawkei was found outstretched and dead in it's cage.

The snake appeared outwardly healthy and the death appeared to be literally without explanation.

(The literature is riddled with cases like this, where the cause of death is later found out to be virally based).

The method of caging was questioned but discounted as the cause of death as the other snake in the identical adjacent cage remained healthy as had all other Death Adders raised in identical circumstance.

Attention was then drawn to the food given to the snake, This had been two fish.

Two logical theories were either the food being too large for the snake to digest or perhaps spines from the fish piercing the digestive wall and death resulting.

Most herpetologists told of this death, did without asking further questions advance these theories.

That they rushed to such a conclusion without a full appraisal of the facts is a matter of concern and also shows how common misdiagnosis of health problems by reptile keepers is.

Both theories were immediately discounted by myself.

Noting that by that stage over 100 fish had been fed to young Death Adders in the previous three months and without incident the anti-fish theory seemed to lack weight.

More importantly, the size and timing of the food also effectively ruled out the fish.

The fish that had been fed had been very small (as befitted the caution of a 'first feed'). The size and easy digestibility of the fish used had meant that they had passed out of the stomach in about 30 hours (based on this and other cases).

At the time the snake died it's stomach had been empty for some days.

The final conclusion at the time was that the death was via no known cause and that all other snakes should be monitored more closely.

On 20 April 2003 one of the young male A. cummingi (AC-4), the smaller one mentioned already, was found in it's cage having shed in a piecemeal manner. Noting that I'd been absent for three weeks, the snake was thought to have shed a week or so earlier.

By the stage the snake was found it had been moving around the cage for several days trying to remove the now severely encrusted skin. As a result it appeared exceptionally thin and emaciated.

The snake was soaked in luke warm water. This was initially for an hour and then several more, before it was possible to manually remove (using my hands) the remaining skin.

The cause of this skin retention wasn't known, but at the time was blamed on a combination of the substrate (hardened sand) and diet, (e.g. the previous 6 feeds totaling 14 Gambusia fish). The oily nature of the fish was blamed for this anomaly.

(In hindsight the diagnosis just given was probably wrong - see later).

Following three more (very small) non-fish feeds that snake was returned to a dominantly fish diet until it became of a size large enough to feed on small (pink) rats.

The snake did not die and apparently made a full recovery, being alive and well at the time this paper was written (in Feb 2004).

In terms of diagnosing respiratory ailment in the young Death Adders, there was a factor that effectively masked it.

When feeding wet and oily fish to small snakes (including young Death Adders), fluids commonly run out of the nostrils.

This may encrust and as a result the snake may have trouble breathing through partially blocked nostrils or have exudate around the lower mouth. In other words this may mimic a respiratory infection.

As this was the situation with most of the smaller Death Adders, it's likely that several may have had respiratory complaints and gone unnoticed.

Notwithstanding this, on 20 May 2003, the three other young A. cummingi were switched over to a diet of exclusively rodents. The fourth was likewise switched to rodents exclusively on 27 May 2003.

On 14 June 2003, it was noticed for the first time that the other young A. hawkei, a female A. cummingi and one of the young A. antarcticus (AAA-106) had respiratory infections that were clearly not a result of the fish being used as food.

The same conclusion was also made in relation to the other young A. antarcticus and another young male A. cummingi (AC-3), but both had since apparently recovered.

The basis of this 'new' discovery was a rapidly worsening condition in the A. hawkei, which as a result of the death of the other A. hawkei had not been fed fish (see above). In fact it's respiratory condition was by far the worst of the three, well and truly ruling out fish as causative of respiratory complaint.

The other snakes displayed a slightly open mouth with some crusty exudate around the lips. By contrast, the A. hawkei had this as well as still wet fluid oozing from the mouth and a puffed up neck, all of which indicated severe respiratory infection.

Furthermore, as indicated above, the period that the A. cummingi had been feeding on rodents (and not fish) indicated that the problem was respiratory and not fish related as first thought. The lack of fish in this snake's recent diet showed emphatically that the health problem was not related to the fish as mooted previously.

Assuming that it was a respiratory infection being dealt with, the caging of the snakes came under renewed scrutiny, but was again cleared as being more-or-less optimal.

Notwithstanding this, it was noticed that two of the snakes, the A. hawkei and the A. cummingi were restless and moving around their cages.

All water bowls had Baytril added to combat the respiratory infection (widened to include all snakes a week later, regardless of whether or not symptoms of infection had manifested). The snakes weren't given medicine directly as they tend to drink frequently anyway and the drug is known to be rapidly absorbed into the system once ingested.

Furthermore, while Baytril is a drug of choice against respiratory complaints in snakes, injection sites for the drug are known to become necrotic.

A continued evaluation of the husbandry regime of the snakes led to my concluding that if the respiratory infection was caused by a bacteria not normally present in the snakes then my use of the same forceps to feed and force-feed the snakes may contribute to it's spreading. Hence on 14 June 2003 my commencement of a policy of using separate feeding implements for outwardly infected and outwardly uninfected snakes.

The following morning the young A. cummingi was found dead in it's cage. The snake was in a loose circle and upturned, which incidentally was the same position that the adult male A. cummingi had been found in some months earlier.

The cause of death was presumed to be from one of two causes.

One was suffocation via the respiratory infection, even though in this snake it was very minor.

A second explanation mooted was that perhaps the snake itself had overheated.

Noting that the other two snakes remained alive, the overheating theory was thought possible, but unlikely and no changes were made.

That evening the A. hawkei was noticed to be in a tightly coiled position and fixed, as if in convulsions. Feeling that death was imminent, the snake was placed in the freezer. The snake was not observed while in this state, rather it was merely picked up and euthanazed.

In hindsight the snake should have been observed for some time as this may have also given further indicators as to cause of death.

The snake had been at the cool end of the cage and hence it was again determined that the Death Adders would not allow themselves to overheat and go to the cooler parts of the cage if necessary.

The A. antarcticus in the room remained alive and unlike the other two snakes had not been restless and so it was left unchanged.

In line with 'healthy' Death Adders this snake was effectively thermoregulating by straddling the hot part of the cage to maintain it's preferred temperature.

By this stage, certain facts became evident.

The snakes appeared to be dying of the same complaint or consequences from it.

Respiratory infection appeared to be a common denominator, with the possible exception of the first dead A. hawkei.

All snakes had been restless in the day or so before death, which is totally abnormal behavior for Death Adders. In captivity, these snakes usually just "sit", except when adult males go looking for a mate, which clearly wasn't the case here.

Other movement is literally from "A" to "B" and not usually in the genre of exploring or hunting.

Noting that the cages were literally sealed from one another, except via air, it appeared that the ailment must have been airborne, although the feeding implements had also been suspected as a potential means of transmission.

At this stage, there was no definitely known cause of death, but a virus appeared to be the likely culprit.

Another variable of note was the sloughing cycle. Both snakes to have died on 15 June 2003 were at the terminal phase of the sloughing cycle. Both snake's were in the situation where their eyes had been cloudy and cleared for more than a day and they were literally about to slough.

It seemed that this may have been a danger point for affected snakes and/or that affected snakes that slough are more likely to survive.

The A. antarcticus (AAA-106) in the same room was also heading towards a slough (estimated to be due about a week later) and therefore came under close observation, in anticipation of death immediately prior to slough.

Noting there were now three deaths that could not be satisfactorily explained and a possibility that these events could be repeated, it was decided to have the snakes examined by a pathologist.

This was arranged via a friend who had an account at a pathology lab, but the examination couldn't be done for a week.

Based on considerations of cost and the (in hindsight erroneous) assumption that no further deaths were imminent, the delay in examination was accepted.

On 15 June 2003 AAA-106 was noticed 'digging' with it's head. Based on close observation, this was seen to be a case of the snake wiping fluid and encrusted fluid from the infalabials.

As a result the six adult-sized Death Adders in the other room were inspected and three showed evidence of similar digging. One of the trio also had partially blocked nostrils as evidenced by it's breathing and popping of blockages.

On 21 June 2003 the two apparently recovered Death Adders were assist fed small mice.

On 22 June 2003 the apparently recovered A. cummingi (AC-3) regurgitated the mouse. The A. antarcticus of the same size did not regurgitate the same food (which was digested without incident).

Also (casually) noticed at this time was the newly restless nature of the A. cummingi in terms of wandering around the cage.

Five hours later this snake was assist fed a small fish. The theory being that the small fish would be more easily digested and the snake would then have a positive calorie balance and the benefits that brought.

It was (wrongly) assumed that once the snake had eaten the fish, it would do what normal snakes do and that is find a nice warm spot to sit in and digest it's meal.

The following morning the snake was again observed wandering around the cage aimlessly, but it had not regurgitated the fish. As indicated already, this was clearly abnormal behaviour as snakes that have just eaten as a matter of course find a warm place and "sit" in order to digest their food.

A few minutes later I heard rustling in the cage. I rushed to have a look.

The snake was in a loose S-shape and rolling over in the cage in a "death roll". Its mouth was being held wide open. After about ten seconds the snake stopped in an unnatural position and it's body had nervous twitches, not unlike a snake that'd been just run over.

There was no evidence of attempted regurgitation of the small fish that remained in the stomach.

The snake was then euthanazed by freezing.

This snake had sloughed three weeks earlier, thereby negating the theory that the sloughing cycle is generally indicative of the timing of death, merely making it a danger point.

Furthermore, on the evening of 23 June 2003 AAA-106 sloughed without incident.

This was expected.

The reason was because unlike the two sloughing snakes that died a week earlier, this one had not been abnormally restless in the days prior.

As per normal healthy snakes, this one simply stayed put, sloughed and then stayed put again.

Notwithstanding this, and the fact that the nostrils were totally blocked prior to sloughing, this snake retained a respiratory complaint as evidenced by 'popping' when breathing, after sloughing.

The most recent death and observations of this and the other snakes prior to death confirmed several important facts and effectively eliminated a number of possible causes of death.

This death of this latest snake was not caused be respiratory failure or blockage. Instead it appeared to be something nervous.

Bacterial cause of death (or complications thereof) was therefore unlikely, especially noting the minor nature of respiratory complaint in this snake.

In other words, for this snake a septicemia-based death, built on a systemic infection appeared extremely unlikely. Hence my looking for another cause of death.

Bearing in mind that this was the first death observed, save for similar observations in the second A. hawkei, it became likely that the other snakes may have died by similar means.

Noting this latest unexpected death (sharp decline in 48 hours), a new urgency appeared in terms of accurately diagnosing the problem before there were more losses.

Attention then turned towards airborne viruses (as thought to be the cause).

It was at the time of the death of the fourth snake that for the first time I was able to effectively piece together the pieces of the jigsaw as seen and relate it to OPMV (the best known virus to infect snakes) as documented in the literature.

Miscellaneous behavioral traits prior to death that had been noticed and yet more-or-less ignored in terms of significance or pattern, such as the wandering in the period before death, not thermoregulating in the same manner as 'normal' snakes, the neurological signs in the week or two prior to death, rapid emaciation and so on, were for the first time re-evaluated in terms of known OPMV symptoms (see Hoser, 2003a).

By way of partial explanation, in the week or two prior to death, all the snakes to have died had been seen resting in unnatural positions, such as that seen in pythons with IBD. This seemed to be a precursor for the decline to death.

Snakes that died had deteriorated within a fortnight or less from outwardly healthy, feeding and well-fed individuals to relatively emaciated.

Working back through the records, it was evident that all but one of the eight small Death Adders had shown symptoms of this virus. Three had apparently recovered or were well on the road to recovery. One snake that died, the fourth one had apparently nearly made a full recovery only to rapidly relapse and die.

Other notes of relevance included that loss appetite was one of the first steps in the rapid decline in health. This appetite loss was measured in terms of snakes that would voluntarily feed now refusing to do so.

My feeding records had masked this factor as those snakes were simply assist or force-fed.

Notwithstanding this, those declining snakes would assist feed or be force fed and digest food at all stages of the infection other than at the terminal restless phase in the day or two preceding death.

The only exception here being that exceptionally large items, normally held down would be regurgitated.
As a result, most snakes in my care tended to retain condition as the virus infection progressed. This would probably go against the trend in other collections where non-feeding snakes would probably be left unfed and presumed to have self-starved to death.

Records showed that almost any food assist or force-fed to the snakes at the terminal phase would be regurgitated, perhaps in response to the failure of the snake to literally sit still and digest it's food.

Another universal indicator of decline was the deliberate seeking of cooler parts of the cage by the ill snakes. The affected snakes did not thermoregulate as did healthy ones.

Noting the positioning of the cages and the relative sizes and robustness of the snakes affected, there was initially nothing likely that would indicate those snakes likely to be affected as opposed to those that wouldn't, at least in terms of snakes of the same general size class (as in four snakes from a litter of four month-old snakes). Nor was there any indication as to those which would survive the infection and those that wouldn't.

Having said this, there was a noticeable trend among infected snakes that did apparently determine survivorship.

Those that exhibited respiratory symptoms only appeared to survive. By contrast, those that also showed nervous disorders in terms of unnatural resting positions died (see later).

This effectively meant that in the case of these snakes, death could be predicted up to a week in advance if the first signs were detected (see later).

Another trend of note in these cases was that the snakes that were being aggressively force and assist fed tended to survive. The only possible exception to this was one of the Acanthophis cummingi although it too was left unfed for a period after it initially went off it's food.

The baby Death Adders in my collection came from three separate facilities. At those facilities and others that received the off-spring there were no die offs like experienced above.

This effectively cleared them as the source of the original infection.

Noting that the pythons in the room were apparently unaffected and had been held since 2001, it was evident that the virus was A/ Not from them and 2/ Even if infecting them, was leaving them unscathed and effectively targeting the Death Adders.

Furthermore there was no evidence of viral infection where they came from.

The eventual diagnosis of virus, (probably OPMV) by myself on the morning of 23 June 2003, arose on the basis of a process of elimination.

Significant here and of major importance for other keepers is that the diagnosis was made on the basis of clinical signs and an accurate appraisal of the housing and husbandry of the snakes only. There was no histological or microscopic examination prior to the diagnosis.

This is important as it means that diagnosis can be made earlier than previously thought and due to the highly infectious nature of the disease, potential casualties reduced.

Possible causes of the deaths in my snakes that had been mooted, including those above, also included exposure to pest-strip and a delayed reaction (dichlorvos). This failed on the basis that all young Death Adders suffered the disease at more-or-less the same time, whereas based on the idea that the pest-strips were the cause, the two A. hawkei shouldn't have got sick for some months.

Furthermore past usage of pest strips to treat mites (including preemptively for incoming snakes), indicated that the dosage levels used for these snakes was well within safe limits (small section of strip (2.5 cm square) with snake in 30 cm long container for 30-60 minutes only).

It's also worth noting that in the past I experimented with massive amounts of pest strip exposure on reptiles, including a full strip (15 cm X 9 cm) with a snake and a lizard overnight in a small container and neither showed any adverse affects.

That respiratory failure caused death in all the snakes and was the root cause was refuted by the last death.

Fluid transferred diseases were initially ruled out on the basis of the physical isolation of the snakes and the lack of mites or other means of transfer (see below).

Husbandry related ailments were comprehensively rejected on the basis of past success with the same snakes (Acanthophis) in identical conditions, including the five adults raised the previous year (raised from newborn to adult size in 12 months).

A perusal of all available literature in terms of reptile diseases in general, including the major works of Mader (1996) left no alternatives other than virus and probably OPMV as the cause of death.

Furthermore the piecing together of the known information and the observations of the snakes that died, also revealed a pattern typical of OPMV as detailed by Jacobson (2000, 2003a) and others who have published extensively on this specific ailment.

In fact that pattern of infection and death was textbook OPMV.

There simply was no other alternative other than virus.

In the morning of 23 June 2003 and with a new sense of urgency, confirmation of the diagnosis of this disease was sought. This was not as easy as expected. Being a Sunday, most of my calls were simply carried over to the next day.

On the Monday, the pathologists who were to do the inspection said that frozen corpses (as I had) were not suitable for histopathology.

This was also confirmed over the phone by veterinary surgeon Peter Cameron, who suggested euthanazing another seriously ill snake, if and when that became available.

In terms of myself, that never occurred as no more snakes died at my facility, but we did gain access to a steady stream of snakes from other collections (see later).

It was evident that by this stage, the only way to confirm diagnosis of virus in the dead snakes I held was via Electron Microscopy (EM) and so I made phone enquiries with this regard. Herpetologist Neil Davie was able to direct me to Gary Crameri of the Australian National Animal Health Laboratory (ANAHL) for these tests.

On the same day (24 June 2003) the corpse of AC-3 was forwarded to the Victorian Institute for Animal Health (VIAS), Mark Williamson and in turn from them to ANAHL in Geelong for confirmation of the diagnosis via electron-microscopy.

Several scientists identified a previously unknown reovirus in the brain as the cause of death for AC-3. A full report was submitted by Veterinary Pathologist Malcolm Lancaster 26 September 2003 confirming this diagnosis of death resulting from reovirus in the brain.

For this snake at least, virus was only found in brain tissue.

As of mid 2003 and prior to the spread of infection as connected to the cases detailed in this paper, the following appeared to be the (known) situation in Australia.

According to the records of Queensland-based reptile vet, Clayton Knight, of Deception Bay Veterinary Clinic presumptive diagnosis of OPMV (see above) has been made in Australia for 'about 8 years'.

Based on specimens he's seen and the histological examinations of them, he's noted a greater preponderance of neurological symptoms as opposed to respiratory in terms of causing death, even though respiratory disease appears in most suspected cases.

This more-or-less equated with the deaths I experienced.

His own view is that IBD is rare in Australia by comparison.

In Melbourne, veterinary surgeon Peter Cameron, of North Altona Veterinary Clinic (who has a strong reptile interest) has made presumptive diagnosis of about half a dozen cases and just one of IBD.

Cameron formed the view that OPMV was as of 2003 fairly common in Australian collections but that it is underdiagnosed due to several factors including reluctance of keepers to pay for histological examinations of reptiles that are already dead.

In his broadcast e-mail of 25 January 2003, (Weigel 2003a), John Weigel said much the same thing in an e-mail which read in part as follows

Whether or not this is so, can probably never be determined, but notwithstanding the comments (preceding) there is some strong evidence to suggest that OPMV or the reovirus subject of this paper, with which it may have been confused is in fact new here in Australia (see later).

Both vets named above said that most of their cases of suspected OPMV related to pythons, but that was expected as these are by far the more common snakes in captivity in Australia.

Notwithstanding this preponderance of cases relating to pythons, the experiences of both the Australian Reptile Park in 2002 and myself in 2003, indicates that other species such as Death Adders (Acanthophis) are far more susceptible to this particular reovirus and/or OPMV-like infections than most other reptiles. This trend is also evident in research results from the USA, which rates elapids as being more susceptible than pythons.

According to Nichols, et. al. 1998:

The fact that elapids are not rated as highly susceptible as viperids may in part relate to the lesser number that are captive in the USA and Europe rather than the real position in terms of susceptibility.

As to other reasons as to why pythons feature in suspected OPMV cases that veterinary surgeons get and not elapids, there are other important factors.

As a generalization, it is only inexperienced reptile keepers with one or two pets, who take sick reptiles to veterinary surgeons. On the basis of costs and numbers more experienced keepers with large collections tend to source drugs and treatments themselves and self-treat their reptiles.

And it's only the experienced keepers who tend to have elapids!

Working backwards, some other mass die outs of Death Adders and other elapids in various collections attributed to poor husbandry in the past may in fact have been due to undiagnosed virus.

Speaking with various keepers in the Eastern states who had experienced numerous undiagnosed deaths, it appeared at first that virus may be an underlying cause.

However in many but not all of these cases, virus was able to be eliminated as the cause as more detail became available.

Reovirus and OPMV remains little known, particularly in terms of different viruses or strains and the effects on different species.

In terms of keeping OPMV out of collections, Jacobson et. al. 1992 as paraphrased by Oros, et. al. said:

In terms of the neurological effects and likely death via these, there was no known treatment or cure until now.

This is now not necessarily so - see later this paper.

Strict quarantining of incoming reptiles, implements and the like would including separate housing of incoming specimens for at least 6 months (excluding periods of dormancy).

However the 'expiry date' of the reovirus in terms of snakes or collections that have survived infection and apparently become immune has not actually been determined.

And it is this premature introduction of an infected snake into my mainstream collection that caused my die off!

The same applies in terms of OPMV, where in at least one case detailed in the literature, snakes have been known to shed virus for at least 10 months (See Cranfield and Graczyk on pp. 392-394 of Mader 1996).

Before the publication of this paper, the most recent views on the subject were stated by Elliott Jacobson on his website at:

It read:

Until now, the general view among veterinary surgeons and private herpetologists has been that the virus is transmitted by airborne means in situ.

I can now report that for this reovirus at least this is not so (the evidence of this follows in this paper). While airborne transmission may technically be possible, it is not as a rule the case.

In practical terms transmission is by one means only: Fluids.

This includes blood, including as transmitted via snake mites, saliva, including as transferred via water bowls, shared water bowls (in which the virus can persist for some time), saliva left on food tongs and the like.

Noting that saliva and other fluids from snakes can be smeared onto a person's hands and remain moist for some time, it is even remotely possible that handling of reptiles by keepers in one another's collections may spread the virus.

Jacobson also wrote:

However for both the reovirus and OPMV's it's likely to be species of snake that can harbor the virus without ill effect (at least at one stage of their life cycle, as in when adult).

No further Death Adders died at the Hoser facility after 23 June 2003 and hence the scientists at VIAS and ANAHL never got freshly killed or euthanazed snakes to look at from the Hoser facility.

However they were given other (mainly frozen) snake corpses from other die off's for examination.

In terms of pathology, it's worth noting the following. Newly dead snakes should be placed in the fridge - not freezer - before being taken to a lab for examination. The freezing of the reptile will destroy tissues making histological examination all but impossible. EM is still possible however.

It took about a week after the death of the fourth death adder on 23 June 2003 to get a complete and clear picture in terms of the Hoser virus infection, its transmission within the collection and related issues.

Notwithstanding this, the tracing of the infection through other collections based on the accurate diagnosis of my own source was remarkably easy.

The delay of some days in terms of getting the full picture was due to a masking of things in my collection as shown shortly and due in part to the rapid movement of infected snakes between collections.

Based on the above, the incoming adult A. cummingi or the P. porphyriacus were initially suspected to have been the most likely sources of the infection.

Both Eipper and Rossignolli who received the P. porphyriacus reported that some of their snakes died from OPMV-like symptoms (as described above in terms of appetite loss and/or respiratory complaint). By end June 2003, Eipper had lost five out of six juveniles, (the sixth dying a few days later) and four adults survived (but later dying over the following months). Rossignolli lost one out of four adults, of which he later said, 'it just stopped eating and starved to death'.

(He lost two more over the next few months).

Notwithstanding this indicator that the P. porphyriacus had virus, and noting what was published about the OPMV virus being airborne it was thought possible that the virus in the P. porphyriacus may have come from my snakes, not the other way around (see later).

None of the dead P. porphyriacus were postmortemed or tested for cause of death.

(Such failures are part of the reason that diseases such as reovirus or OPMV may run rampant in the herpetological community).

The first A. hawkei death occurred within a week of obtaining it and as such is regarded as aberrant. The snake wasn't autopsied (partly on account of it's small size) and unlike the latter three snakes that died, there remains that the chance that it's death may not have been from OPMV and was from some other as yet unknown cause. The corpse was retained.

In terms of the incoming adult A. cummingi not much was known initially, other than the fact that some Taipans (Oxyuranus) that Bigmore had passed on to Rossignolli at the same time also exhibited signs of respiratory complaint when obtained. They were all large adults and apparently recovered.

Checking through my notes, in particular noting the respiratory problem in the large female A. cummingi and the death of the adult male and that AC-4 had shown signs of virus as far back as April 2003 in terms of trouble sloughing and later respiratory complaint, it was assumed that the female A. cummingi had brought the infection into my collection.

I then (erroneously) assumed that the virus was transmitted via airborne means to the P. porphyriacus.

A scenario thought too horrifying to consider was that both the A. cummingi from Bigmore and the P. porphyriacus had the same virus.

As it happened, that was to be the case!

That I had a virus infection in my collection was known.

At least from 23 June 2003!

As Scott Eipper had previously advised me in phone conversations of his dying P. porphyriacus my phone call to him on 23 June 2003 was merely to confirm a potential diagnosis of virus by myself in terms of his snakes.

What had previously been told of as cases of death by 'unknown causes' became subject of some questioning by myself.

The result was a summary of death via a process of rapid emaciation, dehydration, respiratory complaint, improper thermoregulation, wandering in cage and then being found dead for each and every snake … all of which fitted a virus.

This was particularly so noting the general hardiness of the species and the general adequacy of his caging.

In other words he had the same problem as myself.

Ditto for Rossignolli's dead P. porphyriacus although his recollections were not quite as detailed.

In terms of viruses and noting their high degree of contagion, it was imperative that myself, Stuart Bigmore, Eipper, Rossignolli and others of relevance knew the state of play.

All were phoned and then e-mailed all relevant information as taken from the internet (via the search engines and so on), including a general precis of what was known about OPMV and other viruses that affect snakes.

In other words, these people were being advised of the fact that they either had the virus or probably did and to quarantine their own snakes from all others, including each other and also including other collections.

Since receiving the infected P. porphyriacus, Eipper alone had transferred snakes to six other people! All were contacted immediately and along that line at least, the infection was stopped.

I called Bob Gleeson on Monday 24 June 2003 to tell him that P. porphyriacus sent from him and been provisionally diagnosed with a virus (then thought to probably be OPMV) and were dying.

Overlooked at the time (but for a few days only) was another transaction of significance.

In early May 2003, Fred Rossignolli shipped six one month old Tiger Snakes (Notechis scutatus) to Gleeson. Another six went to another NSW-based keeper Alex Stasweski. When picked up by myself to take from Fred's residence in Victoria to NSW the snakes had mites.

These mites were removed immediately by myself using pest strips and besides that the snakes presented as healthy.

The snakes started dying about a month after the keepers got them, so that by end June 2003, Gleeson was down to three and Stasweski was down to two.

(More died later).

Both described symptoms consistent with the virus preceding death.

Three weeks after dropping off the Tiger Snakes at Gleeson's I took the P. porphyriacus to deliver to Melbourne.

They too had mites, which were found to be ubiquitous in Gleeson's collection.

The mites were removed with pest strips in Melbourne before being passed on to Eipper and Rossignolli.

As already noted, they had virus.

For Rossignolli, this was the second time he'd brought in virus infected snakes!

For Stasweski, the problem was particularly serious as he also had a litter of baby A. antarcticus in the same room!

Unwittingly, I'd been transporting a plague of death from Victoria to NSW and back again!

In terms of the month-old Tiger Snakes, another Melbourne-based keeper (John DeBenedictine) took the balance of the litter the day after I took 12 to NSW, hence he too got the virus into his collection.

Interestingly however, Eipper obtained a pair from Rossignolli the day after they were born. (Snakes born on 27 March, taken by Eipper on 28 March).

At the time, they were mite free and as of end June 2003 were evidently virus free and doing well.

And so in terms of the virus infection in my collection and that to which I had a role, the above summed up the state of play preceding the diagnosis of infection.

It seemed like a pretty shocking record, but I think is actually far better than it could have been.

In my case it was merely days after the first death that I was onto the cause and alerting relevant people of the state of play.

Weigel and the ARP took 8 months.

Now if that seems bad, it's worth noting that no other keepers in these chains (running to Weigel) and beyond, or to myself, previous and beyond, even got to the point of diagnosing the virus and therefore never advised of the virus to people they'd passed snakes onto (until either myself or Weigel (allegedly) sent the message out).

The point I make is simple: Reptile keepers have until now been too casual about how they deal with death and disease in their collections and the consequences as seen here can be dire!

There was another issue of note. That was from where the Bigmore infection came from.

As I had no idea where his collection of about twenty snakes came from I could only guess and so in the first instance didn't pursue this line of inquiry.

He possessed foreign (exotic) snakes as in Boa Constrictors (Boa constrictor), Burmese Pythons (Python molurus) and Retics (Python reticulatus).

I initially assumed that the infection may have come in via these snakes, but was unhappy with this theory on the basis that those snakes had been held for some years and the evidence all indicated that the virus was recent to Bigmore's collection.

The published literature on Reoviruses and OPMV has indicated certain inalienable facts.

• They are viruses.
• In the laboratory infected snakes progress in a more-or-less linear manner, until death, or if they survive, tend to develop symptoms within a well-defined time frame.
• Contrary to the above, in reptile collections, virus outbreaks may or may not occur simultaneously.
• In the laboratory symptoms usually occur shortly after infection and death is typical within 3 weeks.
• In the laboratory it took up to 6-8 weeks for affected snakes to produce detectable antibodies to OPMV. No similar test results are known for reoviruses.
• Anecdotal reports, including in the scientific literature implicate snake mites as being a vector for virus outbreaks.

In terms of my own virus infection and determining it's spread (retrospectively) I had the benefit of detailed records and hence was able to make a number of previously unreported findings.

But the questions of note tended to stem from the erroneous assumption that the infection was airborne.

They also arose on the basis of the established fact that my own cases of virus infection could have their infection dates determined on the basis of first signs of symptoms and death. In other words the deaths were within 8 weeks of infection and before the development of antibodies and recovery.

These known facts also explained why the large female A. cummingi took several weeks to recover from the apparently intractable respiratory infection.

The initially asked questions included:

• Assuming that the virus came into my collection on the adult A. cummingi, why did it take so long for an airborne infection to affect the rest of the collection?
• Was it possible that there was another non-airborne means of infection and if so what?
• If the virus is airborne, why are mites implicated with it's spread by some authors. Surely airborne viruses don't need mites as a vector?
• The baby A. cummingi were in cages in a line marked 1, 2, 3, 4. and, based on symptoms and/or deaths were infected in the following order 4, 1, 3, with 2 being missed. Why?
• Noted by myself, Alex Stasweski and Rob Gleeson was that virus infected snakes stopped growing. In my case this was reflected in the growth records of all affected snakes as in those who died and those who recovered. Noting that one of the young female A. cummingi didn't show any symptoms or stop growing, it was assumed (perhaps erroneously - see later) it hadn't been infected. The question again is why? This is especially as the snakes on either side were.
• Was there a way to determine which snakes would live and which would die?
• What is the 'use-by date' in the virus in an infected snake that has recovered?

All the above questions, except the last, can in fact be easily answered based on my own records.

Furthermore the answers to go to the heart of dealing with viruses in infected collections.

That this reovirus at least is not usually airborne is proven by the fact that the large A. cummingi failed to transmit the infection to any other snakes until after the same feeding implements were used for this and the other snakes.

Noting that water bowls in cages were separate and not cleaned with a shared cloth, the only means of transmission was the feeding forceps.

In my case these were about 30 cm long and were used to hold mice and the like in front of feeding snakes.

In the case of my snakes, the infected adult A. cummingi obviously bit the forceps (actually many times) and the saliva left behind was the infected fluid that was then wiped onto other rodents which were eaten by other snakes.

In terms of the smaller assist-fed snakes, the ends of the forceps were then wiped inside the mouths of uninfected snakes.

This also explained why the allegedly airborne virus was unable to jump from the cages of the infected young A. cummingi into the uninfected cage.

Thus to stop the spread of the virus all that I needed to do was to stop using infected forceps.

All other aspects of my husbandry acted to prevent the natural spread of this virus in my collection.

A lack of mites in my collection also prevented spread of virus from one snake to another.

That the virus is in the normal course of events spread via fluids and not air, was further demonstrated in the case of Rossignolli.

Newborn Tiger Snakes (Notechis) that had been placed into a new cage separate from the rest of Rossignolli's collection were in the first instance unaffected.

Noting that he had the virus in other snakes in the same room, transfer would have been a given if it were airborne. Instead it was only after mites had made the move into the cage that infection took place.

The transfer at Gleeson's facility from Tiger to Black snakes was also a function of the mite infection.

As of end June 2003, Alex Stasweski had no mites in his collection and was using separate caging and implements for his Tiger Snakes. Four of six died, but so far there was no evidence of cross-infection of immediately adjacent cages with young and highly susceptible Death Adders.

Then there are some other assumptions that could be tested on the basis of my own records and those other cases connected to this reovirus outbreak.

Assuming for a moment that this reovirus had been in Australian collections for some years (see below), a logical question facing myself was why I never had such an infection over many years of maintaining a huge collection in the 1970's and 1980's.

The only answer I could think of is that because almost all my reptiles had been caught by myself in the wild or were progeny of them, as opposed to being from other collections, there was no route of infection into my collection.

By contrast, none of the snakes mentioned in this paper were caught in the wild by myself.

Notwithstanding the above, the general view of most herpetologists, veterinary surgeons and the like is that this reovirus and/or OPMV is a recent import into Australia and thus it was not present in the past.

Trying to go back into the past to test the assumption is quite difficult, but I can say with confidence that I have never come across anything like what's documented above and believe that it may well be a recent import.

There is also one sizeable piece of evidence in favor of this contention.

In the early 1990's Fred Rossignolli amassed a sizeable collection of venomous snakes for his snake-show business. These came from keepers all over Australia, including many who routinely trade in reptiles.

He has on and off continued to acquire new snakes to 2003, albeit on a reduced basis and as recently as September 2002 'borrowed' snakes from several prominent keepers to add to his large snake show that he did in an open pit at the Royal Melbourne Show. He'd done the same thing for some previous year's shows as well.

The snakes are allowed to free-roam in the pit, intermingle and drink from a single water bowl for several days. Snakes are not removed at night. Mites are ubiquitous on Fred's snakes and that was the case in the 2002 show, which I assisted with.

In other words, if there was a contagious reovirus in Victorian collections as of September 2003, it'd be odds-on that Fred would have had it.

Noting the generally free trade between collectors in all Australian states, it's also likely that if the reovirus or OPMV were in collections in other states it'd have shown up in Victoria as well and including in Rossignolli's collection.

In 8 November 2002, Fred Rossignolli gave me on short-term loan an adult Female Death Adder (Acanthophis antarcticus). It was infested with mites and these were immediately removed via pest strip.

It was then placed for some days with two males in my collection in a single cage to allow them to mate.

As it happens, the males apparantly ignored the female and one (AAA-102) tried to mount the other (AAA-101).

They shared drinking water and any viruses would have transmitted between the snakes.

There was no transfer of reovirus, OPMV or anything like it.

Feeding, growth and other records confirm this.

After sloughing and voluntarily feeding on 8 rodents in several feedings, the female snake was returned to Rossignolli on 10 January 2002.

In other words, we have established that as of November 2002, Rossignolli's collection did not have reovirus or OPMV.

We also know that the virus was not in his collection the previous May. Then Rossignolli bred Tiger Snakes and these were distributed to various keepers, including DeBenedictine.

These were all raised without incident.

DeBenedictine received infected Tiger Snakes from Rossignolli in 2003 and in spite of identical keeping methods, they died in the same way as other infected snakes.

The infection into Rossignolli's collection must therefore have come from the Taipans he got from Bigmore on 15 February 2003.

There is no other potential source!

Stuart Bigmore of Lara Victoria, works for Ford Motor Company and in early 2003 took up an 18 month position at Hiroshima in Japan. As a result his reptile collection was distributed to several other keepers to look after during his time of absence. This was in February 2003. All took the reptiles on an 'all care no responsibility' basis as a favor for him.

As a result several other keepers received infected snakes and infected their collections. Included among these was Haydn McPhie who took Bigmore's Scrub Pythons (Australiasis amethistina) and another keeper who took his King Brown Snakes (Cannia australis).

'Downline' from them in the following months there was little infection of other collections due to the limited number of snake transfers between collections.

However in February 2003, it was known by myself and Rossignolli that the snakes we personally received from him had presented in ill-health at the time, which is not normal for Bigmore in terms of his husbandry.

The room his reptiles are kept in is large and spotlessly clean. The building alone cost $40,000 to build in 2002 and is the envy of most other reptile keepers.

In terms of the spread of the virus infection in Bigmore's collection, that was easy to work out.

Water bowls in each cage were cleaned using the same cloth. Whatever cleansing agent he used didn't work to kill the virus. That was known from as far back as February, when two Death Adders from separate cages in opposite sides of the room presented with the same dysentery infection. This is typical of shared water.

Based on the above it was simple to assume that the virus I'd got, was present in all other snakes in his care, even if they did not all show symptoms.

The above is not an attack on Bigmore's husbandry practices, but does show how even in the best looked after collections one simple oversight or procedural anomaly can lead to invasion by a well-placed infectious agent. A similar accusation could be leveled against myself in terms of the typical use of the same forceps to feed all snakes in my collection.

Taking charge of Bigmore's affairs in terms of his reptiles in his absence was Neil Davie, who incidentally was pivotal in organizing the EM on my dead A. cummingi.

Davie also partially confirmed my claim that the virus had come from Bigmore's collection when he noted that my claim explained the previously unexplainable fact that at Bigmore's facility an adult Scrub Python (Australiasis amethistina) had an intractable respiratory infection for some months that hadn't responded to Baytril (as they usually do) and that an Inland Taipan (Oxyuranus microlepidotus) had died.

Following the e-mailing to Davie of what I'd gained from the internet on OPMV, he phoned me to advise the following:

Bigmore received a Taipan (Oxyuranus) from Weigel in October 2002 and at no time before, during or since, had Bigmore been advised of an OPMV epidemic at Weigel's Australian Reptile Park.

I was shocked to hear this (as it contradicted Weigel's broadcast e-mail of early 2003) and sought confirmation only to be told the same by both Bigmore and Davie (Bigmore 2003).

On 27 June 2003, Bigmore wrote:

The October date fitted well within the known parameters of how this reovirus and OPMV in general works in collections and explained it's relatively recent appearance in Bigmore's collection. In other words my suspicion that the virus source was not the long-term captive exotics was effectively vindicated.

The Taipan was further indicted by the following facts:

The ARP arranged a swap for a large Taipan of Bigmore's for a smaller one (the infected one). The ARP was to use Bigmore's for breeding with the pay-off that he'd get half the young.

Bigmore had not received any other new snakes or other reptiles in the 18-month period preceding February 2003.

This meant that the Taipan was indicted even in the absence of knowledge of an OPMV epidemic at the ARP!

There was no other suspect!

The significance of this new information was completely staggering.

For Weigel not to have advised Bigmore of 'OPMV' in October 2002 was totally understandable. The snake sent out was outwardly healthy and to that stage Weigel did not know the cause of his own die off, which by his own e-mail admission was literally out of control and spreading among snakes that previously seemed outwardly unaffected.

Weigel's e-mail makes it clear that quarantining of outwardly infected snakes failed to stop the spread of OPMV in his collection due to other outwardly unaffected snakes being carriers of the virus.

However when Weigel became aware of the virus and it's consequences in November 2003 he had an obligation to notify all persons likely to be affected and this included Bigmore, as Weigel himself indicated in his e-mail (quoted above).

Noting that Bigmore's collection wasn't distributed until February 2003, all virus cases derived from Bigmore's stock could have been avoided if Weigel had at any stage in the intervening three months advised Bigmore.

As to why Bigmore was not properly notified I can only guess (see below), but the toll of Weigel's known negligence and recklessness is huge and may have ramifications for many years to come.

It's notable that the first general knowledge of the Weigel/Australian Reptile Park outbreak was via a leaked e-mail that Weigel didn't approve of.

If Weigel had in fact alerted all recipients of his stock of the risks of 'OPMV', then perhaps his outrage at the e-mail may have been justified. But noting that at least one recipient of his stock didn't know of the 'OPMV' epidemic, it's perhaps a travesty that the leaked e-mail didn't get a wider circulation.

In terms of myself, instead of archiving the e-mail, if I'd forwarded it to those on my own e-mail list, including Bigmore, then perhaps the whole fiasco involving his snakes would have been avoided.

In a phone conversation on 3 July 2003, Weigel denied that his Taipan was the source of Bigmore's infection. Initially he denied sending Bigmore the snake. This later changed to him getting the collection manager at the ARP to call the courier, thereby somehow absolving him of blame.

He later said "See, I never sent the snake, Craig Adams is the blame".

Weigel then said that as the snake showed no symptoms of 'OPMV' at the time it was shipped, it could not have been the source of Bigmore's outbreak.

Weigel said that as the snake showed no signs of 'OPMV' it wasn't necessary for him to advise Bigmore of 'OPMV'.

That contradicted the contents of his broadcast e-mail which made it clear that all recipients of ARP stock had been notified.

The fact that the Taipan sent by Weigel ( and his keeper Adams) appeared outwardly healthy merely meant that the Taipan from the ARP was a carrier, nothing less.

In broadcast e-mails and a webposting at:

Weigel's claim that no symptoms equals no infection is wrong, but in fairness to him, and assuming his view to be genuine, then he is not the first keeper (or probably the last) to have fallen into this trap.

Put simply, no symptoms does not mean not infected.

Weigel also wrote:

The statement was not true.

Bigmore's collection was broken up on 15 February 2003 which was before he went to Japan, not after. There had been no 'wheeling and dealing' as asserted by Weigel and furthermore we know Bigmore's collection was the source of infection based on the lines of infection direct from Bigmore's snakes.

No amount of claims by Weigel amounted to anything resembling proper a rebuttal of the likelihood that the ARP's Taipan had been the source of the Bigmore infection.

As noted and based on the spread of the reovirus in both Bigmore's and Rossignolli's collections we now know that Taipans (Oxyuranus scutellatus) generally survive these infections without complication. In other words they can be asymptomatic carriers

The whole basis of the phone call from Weigel to me on 3 July 2003 was to demand and force a retraction of the idea that the ARP's Taipan was the source of the Bigmore OPMV infection.

However, Weigel provided nothing to rebut the already irrefutable evidence from both what we knew about Bigmore's collection, the spread of the virus from there and the details of Weigel's own broadcast e-mail, all of which proved with much certainty that it was the Taipan from the ARP that was the source of the Bigmore infection.

Weigel's phone call merely presented a possible explanation s to why he didn't notify Bigmore of the 'OPMV' infected Taipan (that he didn't think it was infected).

It also meant that either the phone comments to that effect or the e-mail from him were untrue.

As to which, I can only guess.

So what exactly was the death toll directly caused by Weigel's negligence in terms of failing to alert Bigmore of the 'OPMV' in the Taipan?

That's a question that cannot be answered in full because as of February 2004, most of those people affected are only just starting to count the losses of their snakes and/or other new infections also apparently linked to the Australian Reptile Park's transactions are only starting to manifest. In June 2003 it was a situation of casualties mounting on an almost daily basis.

This eased off somewhat after this, but as of February 2004 there were still losses and relapses in affected collections.

In terms of keepers downline from Fred Rossignolli alone, we had more than a dozen deaths!

In terms of dead snakes, we have dozens, with probably dozens more likely to die and perhaps hundreds infected with this reovirus and what's more, perhaps indefinitely.

If I hadn't put out the alarm at end June 2003, the death toll would have gone far higher!

In other words, there is absolutely no doubt at all that it was the ARP Taipan that was the source of Bigmore's OPMV infection. The only element of doubt now is what Weigel's state of mind was at the time the snake was sent, again after the OPMV infection was detected at the ARP and again at the time he sent out the broadcast e-mail claiming to have notified affected collectors.

However based on what's now known about Weigel's own outbreak the fact remains that Bigmore should have been warned of the possibility of infection from Weigel and he wasn't.

Even if as Weigel were to (unreasonably) contend, that it was not his Taipan that was the source of the Bigmore 'OPMV' outbreak, the fact remains that if Bigmore had been warned by Weigel, the infection would not have progressed past his collection.

Interestingly and following the publication of a paper detailing the spread of this virus, then thought to be OPMV, Craig Adams, Assistant Manager, Australian Reptile Park sent out a spam e-mail taking blame for the non-notification by the ARP of the Bigmore infection.

In the e-mail dated 25 Jul 2003 he wrote:

The only remaining question now being how many other recipients of ARP stock were missed?

As of early 2004, it has become evident that at least two other keepers who traded stock with Weigel's reptile park in the relevant period were not advised of the virus risk once it became apparent.

Both collections have in turn had heavy losses of stock and/or inadvertently passed on the problem with infected to stock to other collections, causing losses in those collections and/or yet more.

More significantly however, is not that the ARP finally admitted fault in terms of shipping an infected Taipan and then failing to notify Bigmore of the risk, but rather that the infection that caused the die off at the ARP was almost certainly the same reovirus that affected collections downline from them, including Bigmore, myself, Rossignolli, Gleeson, Eipper, DeBenedictine, Stasweski and others and not an OPMV as first thought.

Fortunately the OMPV-like reovirus is now becoming well-known here in Australia as a result of a series of progressive reports published in herpetological journals here and posts by myself and others on internet forums.

General knowledge of the virus has flushed out other cases not covered in this paper (for reasons of space and to avoid repetition of detail), so far all of which can be traced and linked to the Australian Reptile Park.

I'll repeat the salient parts (as above). It commenced thus:

Why Weigel wanted to keep the outbreak under wraps was uncertain, however other parts of the e-mail indicated that the outbreak was now under control and that:

Based on the Bigmore situation, we know that part of the e-mail to be factually incorrect.

The urgency of the situation is perhaps better summed up in the report that apparently generated the Weigel e-mail.

The statement appears to corroborate evidence to the effect that 'OPMV' (in this case being this reovirus) is a new and deadly arrival in terms of Australian reptiles.

Now obviously John Weigel at the ARP did not generate the disease in his lab and deliberately unleash it onto the Australian herpetological community, so the logical question then becomes from where did this virus come from?

Weigel's first e-mail alleged the infection came from multiple sources based on his educated opinion. This view was later amended (in June 2003) to three likely sources, whom he said all denied any possibility of being the source.

If that is in fact so, then the three keepers probably need to be censured as wholesale denying the possibility of a snake from a large collection being a potential vector of 'OPMV' or other virus and without relevant tests is at best conjecture and at worst reckless.

Weigel's censure of those keepers is in my view justified.

However his own hypocrisy is evident when in spite of overwhelming evidence he then denies the possibility that a snake the ARP sent was a vector for the virus.

In other words, Weigel has condemned people for doing what he himself has done … denied any possibility that his collection was a source of infection.

(He was alone among the people named in this paper in terms of denying the fact that his collection had the virus).

Notwithstanding this, the Weigel e-mails point to 'OPMV' being derived from other Australian collections.

Weigel also points to recent imports of exotic non-native reptiles in anticipation of an amnesty as being the potential original source of 'OPMV' in Australia.

Here he may be close to the mark.

However there is another side to this that is also worth exploring.

The 'OPMV' (in actual fact reovirus) that has devastated the above collections, including the ARP has essentially targeted elapids and while usually only moderately adverse to large snakes, is generally deadly to smaller ones and juveniles.

Most exotic snakes brought into Australia have not been elapids and assuming them to be more-or-less immune to 'OPMV' or at least less likely to be carriers than elapids, the most obvious source would probably be an elapid.

Hence my own view that the relatively small number of imported elapids are of greatest interest.

Oddly enough it was the ARP itself that recently acquired some large King Cobras (Ophiophagus hannah), which by virtue of their size would be likely to mask an 'OPMV' (Reovirus) infection, but still infect other reptiles.

We know this by noting how well larger elapids have coped with the reovirus infections, including most of Rossignolli's 50-odd large elapids.

Suspicion in this direction was added by the fact that the ARP was the first place that 'OPMV' appears to have surfaced (excluding the suspected, but unidentified cases listed above). Also the ARP's own internal quarantine failed to stop the spread of the infection until identified at least 8 months after it first manifested, indicating that the 'OPMV' may have spread through their entire collection and merely been masked by many snakes failing to show detectable symptoms.

Thus it is entirely possible that the ARP itself may have brought in 'OPMV' as shown by the lack of 'OPMV' in collections such as Rossignolli's as late as November 2002, and as a result of the failure to notify Bigmore and others of the infection, the ARP may have in effect foisted this virus into the Australian herpetological community, and perhaps ultimately into the wild here.

My theory (above) in terms of the source of the ARP's 'OPMV' outbreak may be erroneous. But the situation is far too serious to be left in doubt.

All suspected vectors and dead snakes at the ARP could have (I assume) been examined, including electron micrographed in order to help ascertain the true source of the infection.

The potential seriousness of this reovirus, misidentified at first as 'OPMV' means that such investigation should be done sooner, rather than later … that is if the pathway hasn't been left for too long already to be obscured in total.

In fairness to Weigel, he said in his post that the imported King Cobras were tested for OPMV and showed negative.

He has not however produced reports to show that. However there are some points of note there.

• One is that a negative result doesn't mean the snake does not carry a virus (see Jacobson's statement above), especially if the inspection was merely a physical examination of a live snake in terms of outward condition.
• The second is that the alleged test cited (whatever it was) may not have been able to detect the said reovirus known to have infected the various collections. Elliott Jacobsen's papers make it clear that a negative result with the correct test, still cannot be taken as definitive that the snake is not infected as either virus or antibody may not be in the tissue sample tested.
• Weigel has not produced any evidence to suggest that the actual reovirus was ever looked for via Electron Microscopy in either the King Cobras or any other snakes he held.

Notwithstanding these salient facts, unlike for the Taipan sent to Bigmore from the ARP which in it's case is an only suspect, Weigel has himself claimed at least three suspected sources of infection into his own facility and at this late stage and due to the muddying of the picture at their end by Weigel himself, it'd probably be nearly impossible to now determine the incoming source of infection to the ARP some two years earlier. The King cobras are merely one identified suspect, not the only 'smoking gun'.

'OPMV' cases presented to veterinary surgeons to date have generally come from zoological collections and large private facilities. Means of infection was generally not detected, but rather assumed.

The microscopic or sub-microscopic size of virus particles has led to the assumption that transmission was by air, probably via droplets expelled via the nostrils of affected snakes. This theory has had several factors supporting it. These include the obvious 'popping' of nostrils in affected snakes as air is expelled and the fact that snakes in separate cages in collections become affected.

Fluid borne transmission of infections in collections is usually done by mites (or so it's been generally believed and written) and yet 'OPMV' has spread in mite-free collections.

The air-borne transmission theory was also thought to be attributable to the Hoser infection in the first instance. However a close appraisal of infection records tended to work against this theory. This was especially after it became clear that three Death Adders (Acanthophis) that had showed no symptoms were in fact unaffected as deduced by their continued appetite, growth and lack of respiratory complaint. One of the trio, a young A. cummingi was obviously not affected as the other three from the litter showed all the most severe symptoms of the disease, save for one, which merely lacked neurological signs and recovered.

However in the first instance the main reason the airborne infection theory was questioned was because the original vector a large A. cummingi was kept in a cage immediately adjacent to other unaffected snakes for two months, with direct straight-line air contact of less than 6 cm and yet there was no transfer of infection.

Transfer from this affected snake then effected more or less simultaneously over an apparently random selection of snakes some months later.

Hence the investigation of a new variable, any new variable that led to this new transmission.

The only change was the dropping of individual feeding and handling implements for the carrier snakes.

As it had been noticed that all snakes tended to bite the forceps when feeding on held rodents, it became obvious that here was a fluid transfer means.

In another similar example, the four young A. cummingi were housed in cages in a linear manner, numbered 1, 2, 3, 4 and yet the infection progress was 4, 1, 3 with 2 being missed.

Holes connecting the cages gave a potential nostril to nostril distance of less than 4 cm. Furthermore, noting the rectangular shape of the containers and the propensity of all snakes to sit more or less parallel and 'in line' in response to the positioning of the heat mat running along the underneath of the cages, these snakes would have spent some weeks more or less permanently within 20 cm of one another. In spite of this, it was evident that airborne particles from cages 1 and 3 failed to infect cage 2.

A similar situation existed in terms of the two uninfected adult A. antarcticus which sat literally within 6 cm of infected adults including via direct line of nostril contact via cage air holes for some weeks without becoming infected and were left in this position after the reovirus was detected (firstly on the probably incorrect assumption that they were infected and not showing symptoms and then on the more likely assumption that there was no serious risk of them being infected, even though they were unaffected, due to the newly commenced practice of not sharing feeding implements).

In all other virus infections sourced down from Bigmore a fluid-based means of transmission was identified.

When none was found, there was no apparent virus transfer. This appeared to be the case in the mite free newborn Tiger Snakes (Notechis) that Eipper received in March 2003 from Rossignolli and again in terms of the failure of the virus to jump from later infected Notechis held by Stasweski to uninfected Acanthophis immediately adjacent.

Further evidence of the fluid-based transfer of the virus came in the general infections of the Gleeson and Rossignolli collections that both had mites throughout. Likewise for the transfer in the Bigmore collection which had a wet cloth as a transfer medium.

This also reconciles a correlation noted by previous authors in relation to OPMV, that being that snake mites are a vector.

If this reovirus and/or 'OPMV' was in fact airborne in transfer, then mites would seem to be a particularly inefficient means of transfer and effectively a non-issue.

We know this isn't so.

The fluid borne means of transfer also explains differential rates of infection in collections in terms of it reflecting cleaning water bowls with a given cloth as they get soiled and not as a block.

This also reconciles with statements by Jacobson that indicate that the virus does not last long in dry environments and yet persists for some time in water (liquid environments).

It also reconciles with the need to physically infect snakes with fluid based medium in the laboratory situation if one intends infecting snakes.

A remaining question then becomes when do infected snakes shed virus (become infective)?

In the laboratory situation infected snakes become increasingly infective as the virus replicates. Based on the progress of the infection through the various collections, in particular that of Gleeson, it's fair to assume that snakes can become infective carriers of this reovirus within three weeks of first becoming infected.

The real time may in fact be far shorter.

By end June 2003 and after contacting the various people who had received virus infected snakes, the nature of this reovirus in terms of Australian collections had become generally known to me.

In the 6 months since then, I have been able to receive and treat infected snakes of several species and treatment methods have been refined greatly so that if and when vulnerable and infected snakes are identified and properly managed, death should be rare, not routine.

John DeBenedictine, who'd received 7 infected neonate Tiger Snakes (Notechis scutatus) from Fred Rossignolli, was first contacted by myself on 1 July 2003.

This was well after most other virus affected keepers had been spoken to.

Prior to then I had not been in contact with him.

Before allowing John Debendictine to tell about his snakes, I was able to inform him that he had received virus infected snakes and that most if not all had died.

I was also able to tell him that the pre-death symptoms included loss of appetite, stunted or no growth and that he probably found the snakes dead in a belly-up position.

On all counts I was correct.

Debendictine received the snakes from Rossignolli in early May 2003, the day after I took the infected snakes from the same litter to two Sydney-based keepers.

Debendictine had lost six out of seven snakes. He at that stage had no idea as to cause of death.

All had appeared normal at first and ate and grew apparently normally for a few weeks before the snakes manifested symptoms and started declining. His most recent death had been a week prior (around 24 June).

All six had not been seen dying, but had been found belly-up in their cages. There was no evidence seen of respiratory infection.

These were the same things observed by Stasweski and Gleeson with their neonate Tiger Snakes.

In other words the effects of reovirus on these snakes was the same in every case and therefore tended to be predictable for the species.

Notable is that a year earlier Debendictine had received some other mite-infested neonate Tiger Snakes from Rossignolli a month after they'd been born, had treated the snakes for mites and had raised every one without problem.

Once again, the relatively new reovirus was indicated as the cause of death for his 2003 born Tiger Snakes as all other factors were the same.

Debendictine's observations again drew attention to a previously neglected trend in snakes that had died from reovirus, at least in terms of previously published accounts. In the case of the Death Adders that actually died in my custody (as opposed to being euthanazed before death), namely one A. hawkei, one small A. cummingi and Bigmore's original male A. cummingi, all were found dead in a belly-up position.

In other words such could (in combination with other signs) could be treated as indicative of reovirus.

Notable however was that in Eipper's Red-bellied Black Snakes (Pseudechis porphyriacus), there was no belly-up position at death. Also unlike the Tiger Snakes, all the Red-bellied Black Snakes showed some sign of respiratory complaint before death.

Hence the use of belly-up death (or lack of it) or respiratory infection or lack of it, to definitively indicate reovirus should not be relied upon as certain, even if the species trend is known.

By way of example a later 'unexplained' death of another neonate Red-bellied Black Snake from another litter at Eipper's facility in August 2003 was in a belly-up position.

The snake showed classic signs of reovirus and was submitted for tests.

Eipper's fear was that the snake was cross-infected before the alert was raised by me in June 2003.

That later appeared to be the case and Eipper considered taking legal action against Weigel for negligence as a result.

Notwithstanding the assertions in Weigel's posts that he believed 'OPMV' derived from private collections outside of the ARP's, the fact remained that as of October 2003, no hard evidence has been provided by Weigel or others to support this contention, even though clearly it was a possibility.

In an e-mail dated 26 June 2003, Weigel (Weigel 2003b) had refused to answer questions put to him in this regard via an earlier e-mail from myself.

We have no names, details of snakes allegedly received and identified as potential infection sources, or the like.

Assuming all transactions to be legal, there should be no impediment on this information being generally and publicly made known.

One can only ask why Weigel refused to have his e-mail assertions of 25 January 2003 tested for veracity.

As this paper relies only on hard evidence to support contentions, the source of the ARP's 'OPMV' outbreak cannot be pursued beyond what is already related.

In other words it remains unknown.

Mauricio Perez-Ruiz said that Weigel didn't want any positive virus identification in the ARP's collection as it could then be used as a basis for the NSW Agriculture Department to come in and kill all their reptile holdings. The fear was real as this had been done already for poultry and birds found to be infected with exotic viruses such as Newcastle Disease.

Mauricio Perez-Ruiz justified all the ARP's tactics as being directed to avoiding that possibility.

To allay that fear, I sought and got an indemnity from the wildlife authorities that if I were to identify infected collections, reptiles would NOT be seized.

The Weigel transfer to Bigmore had also been done without correct paperwork (in other words it was illegal) and in order to protect Weigel's interests, I sought and got an indemnity from the Victorian Wildlife authority not to prosecute him over the matter.

This was important as had he been prosecuted for the offence, his reptile park may have been closed down and Weigel himself lost a multi-million dollar asset.

These undertakings were given in July 2003 and allowed for a more co-operative approach to be taken in terms of investigating the virus.

Affected keepers were no longer in fear of being raided and having stock seized and destroyed.

There are some key facts that should however be related in terms of the apparent newness of the reovirus here in Australia.

As recently as August/September 2002, Fred Rossignolli borrowed snakes from several prominent reptile keepers to place in a large pit as part of a two-week snake display at the Royal Melbourne Show. Due to the ever-present mites that almost immediately infested all snakes and the sharing of a single water bowl, any infections such as reovirus or OPMV would have transmitted then.

As already noted, as recently as November 2002 Rossignolli did not have the reovirus, nor did he have it in early 2002 when that year's mite-infested neonate Tiger Snakes were distributed by his friend Simon Watharow to several Melbourne keepers including Debendictine. Working backwards, and looking at from whom Rossignolli borrowed snakes in August/September 2002, one of those collections from whom he borrowed snakes was Bigmore's, meaning that at the same time he too did not have the reovirus, further and independently pinpointing the October 2002 date of infection.

Bigmore raised the possibility that another snake, namely the male Floodplain Death Adder (Acanthophis cummingi) later passed on to myself, may have been the source of the infection.

The basis of this possibility was that the snake was a 'poor-doer' ever since being acquired.

That came from Andrew Geddy.

The snake was ruled out as the vector to Bigmore's collection on the basis of it being acquired 18 months earlier in 2001.

If it had carried the reovirus, then Rossignolli's collection would have had it in September/November 2002 and we know for a fact that he didn't. Ditto for my own collection.

Furthermore Geddy had directly supplied Rossignolli with snakes in the period preceding November 2002 and yet we know emphatically that Rossignolli's collection had not got the virus. Hence that snake and Geddy's collection in total was ruled out as a potential source for the virus.

Also noted was that Geddy's own cleaning regimen (same cloth, all cages) wouldn't have stopped the reovirus from attacking his entire collection if just one snake there had been infected.

The investigation of Geddy and his collection was done as a matter of procedural fairness to ensure that any and all suspected snakes, and not just the ARP's Taipan were checked and either indicted or cleared as being potential vectors of the virus.

Rossignolli borrowed snakes in 2002 from more than six other keepers. Those keepers in turn had derived stock from over 30 in the previous 12 months alone including most of Australia's better known private keepers, many of whom also supplied the Australian Reptile Park after the mid 2000 fire killed most of their own stock.

Based on the results already provided, there was no reovirus in those collections.

Hence overwhelming support for the contention that the reovirus now seen is 'new' to Australia.

Weigel has not provided any details of the alleged source/s of the ARP outbreak, so his claims cannot yet be independently checked.

Weigel has a well earned reputation for making public statements that even with a cursory check turn out to be false. Included were some claims he once made on the "australianherps" list server in terms of Australian pythons that were patently false, or another bizarre claim that he made in 2001 stating that the holotype for "Pseudechis australis" was in fact a Pailsus. The many divided subcaudals in the former snake specimen clearly excluded the possibility, meaning that either Weigel hadn't even looked at the holotype or if he had was merely telling a deliberate lie.

As a result of Weigel's actions to date and his prior form, we have a serious deficiency in terms of identifying the true source of the reovirus infection now being seen in Australia.

Hence most existing evidence points to the ARP as being the original source of the Australian infection, or perhaps an original outside source, which either recently acquired an infected animal from overseas and/or had little if any contact with other prominent reptile keepers, other than the ARP being the direct conduit for the infection into Australia.

Most importantly however is strong evidence that this strain of reovirus at least is new to Australia.

As the reovirus becomes more thoroughly studied and known, both here in Australia, and outside Australia, if it is identified elsewhere, then there is a possibility that the original source may be found.

It took some years for the source of the Chytrid fungus adversely affecting temperate zone frogs to be traced back to equatorial Africa, so it remains possible that the geographic source and original species host/s of this reovirus may eventually be located.

In terms of the cases detailed here, there was little if any coordinated plan of dealing with the infection until well after much of the damage had been done.

This in the main stemmed from total ignorance by the keepers in terms of the causes of the disease and deaths at the time they were occurring.

Excluding myself, the other relevant keepers by and large regarded all the deaths as unfortunate but not from treatable or avoidable conditions.

In hindsight this was completely wrong.

All deaths in reptile collections should be treated as avoidable unless proven otherwise (regardless of cause).

One exception to this was Bigmore who attacked the respiratory infections with Baytril, the drug of choice for such infections. Rossignolli also treated snakes with respiratory infections the same way, but snakes that lost appetite were merely allowed to starve and die.

Had Rossignolli taken a far more proactive approach, most, if not all his losses could have been avoided, mainly due to the fact that in his case it was larger and mainly adult elapids being affected.

This (and earlier) statements are not intended to be attacks on Rossignolli, Weigel or anyone else, but are statements of the facts as they are and in my case here, written with the full benefit of hindsight and a far greater body of knowledge acquired in the period since the deaths occurred.

In the case of most of the rest, the virus infections manifested in young snakes at great speed and death resulted so fast that treatment of any form simply wasn't considered.

Again with hindsight a more proactive (and relevant) approach may have saved many snakes.

In the case of the Red-bellied Black Snakes, Eipper noted that they declined in condition rapidly and then died, appearing emaciated. Respiratory infection was noted merely as an afterthought and not as being a root cause of death in Eipper's view.

In terms of the Tiger Snakes, both Stasweski and Gleeson failed to note evidence of respiratory infection at all, even after being questioned about it. They merely reported that the snakes would decline rapidly and die.

I was able to observe a Tiger Snake dying from the reovirus at Gleeson's facility on 4 July 2003 and failed to see any signs of respiratory disease.

The snake did however exhibit other traits of the reovirus infection in terms of lack of growth as compared to healthy snakes, emaciation, unnatural resting positions, failure to thermoregulate and at the terminal phase seizures and convulsions.

In terms of myself, at the first instance the respiratory infections were overlooked and only dealt with when it became plain that at least one snake, the male A. hawkei, was in terminal decline.

It was also the only snake I had die that appeared to be debilitated by the respiratory infection. For the others it appeared as being 'present', but also merely an inconvenience as opposed to life threatening.

In hindsight that may not have been the best approach.

Aggressive treatment for respiratory infection is therefore indicated for virus infected snakes.

Baytril is the drug of choice for affected reptiles. It's properties include necrosis at the site of injection and rapid absorption into the system, even if ingested orally.

Based on these salient facts and the small size of the affected snakes (most under 30 cm), I initially chose to administer the drug into the water in the cage as had been done with success for young poultry that were at similar risk from respiratory complaint.

In terms of water bowls the following should be noted.

The liquid is fairly tasteless, even when concentrated and when diluted at a few drops per 50 ml (in line with the treatment indicated for poultry), the water's taste remains effectively unchanged. The snakes will still drink the water.

In the first instance Baytril was added to the water of the young female A. antarcticus and after a week of no ill effect, the Baytril treatment was widened to include all Death Adders in the collection, including those visibly unaffected.

This was later upped to a dosage of .3 ml per 200 ml for obviously affected snakes.

Notwithstanding this, in a severe September/October 2003 case I orally administered high doses of Baytril by so-called 'force-drinking'.

The method was later refined for later cases and in terms of snakes inherited by myself that were clearly infected, all recovered, save for a pair of Red-bellied Black Snakes that died within 48 hours of receipt.

I later chose to administer doses of Baytril orally diluted at raw to 5 parts water.

The dose rate was .1 ml raw Baytril (.5 ml water) per 50 grams of snake once and then every 48 hours as needed until no signs of respiratory or related ailment was present.

Most snakes showed signs of dramatic recovery within 12 hours after the first dose.

(Force-drinking involves inserting a syringe barrel down the throat of the snake as far as the barrel will go. The liquid is then slowly expelled and then massaged down the snake's belly by gentle rubbing of the ventral surface with a finger. While this is being done, the snake is held with the anterior end facing up and the tail down, hence allowing gravity to assist in holding down the fluid. The snake is then placed back into it's cage and as a matter of course it would raise it's head and neck and hold the fluid down).

In terms of the neonate Tiger Snakes held by Stasweski and Gleeson, there were other factors worth noting.

Part of the general trend in virus infected snakes is a loss of appetite, even at the early stages of active infection. This much appears to be a general trend.

Stasweski tended to offer food to the snakes and generally if they refused to eat, they were left alone. His death rate at 4 out of 6 by end June was higher than Gleeson's 3 out of 6 (with a fourth death on 4 July).

This figure is particularly notable, given that Gleeson's also at one stage had to contend with mites, which is certainly no mean feat in small elapids.

Gleeson by contrast to Stasweski had followed earlier advice from me and force-fed the snakes. He said one of the three deaths was due to error on his part by him force-feeding too large an item to the snake and it dying there and then.

Assuming Gleeson's diagnosis to be correct, this meant that only two (later three) of his snakes actually died as a result of the virus. Noting the survivorship trends in my own Death Adders this again tended to indicate that there was benefit in force-feeding virus affected snakes that would otherwise not eat.

While there are general benefits in maintaining a positive calorie balance in ailing snakes, the exact reason for the apparent benefits of force-feeding in virus affected snakes isn't known. But the trend was clearly evident.

(Force-fed snakes may have had a stronger propensity to drink and hence rehydrate themselves).

Further proof of this trend was seen in Gleeson's housing of the neonate Tiger Snakes.

As late as 4 July 2003 all were still being housed in a shared cage. Due to the shared water, it was obvious that all must have been in contact with the virus here as well as previously and therefore become infected.

Two of the snakes remained outwardly healthy and had been force/assist fed throughout. They had apparently recovered from infection and were by that stage on a strong growth trajectory.

This mirrored the situation in my own recovered neonate A. cummingi (AC-4) and the two neonate A. antarcticus.

It's now known that perhaps even more important is the need to force-drink small snakes affected by the reovirus (see Hoser 2003b).

Large snakes will tend to drink more to counter their rapid emaciation due to the virus. As a result, they tend to stay hydrated and ultimately survive.

Small and neonate snakes tend to emaciate rapidly and in fact will not even drink. Hence their condition worsens most rapidly.

Over dehydration appears to be a major factor contributing to the neurological factors seen that ultimately lead to death in snakes.

As a result, later cases I managed (either at other people's facilities or in terms of affected snakes I brought in to treat) involved force-drinking of small (evidently) not drinking snakes. Baytril was administered liberally as well and the result of this (added) treatment was no losses of snakes managed by myself (excluding a pair of Red-bellied Black snakes that died within 48 hours of receipt).

This paper has concentrated on affected snakes. However it is those which appear to unaffected which have tended to cause the greatest problems.

This has been because they've been moved from collection to collection on the misguided belief that they are virus free.

In terms of this reovirus the affects tend to be predictable for given species and age classes and this is important in terms of large collections with asymptomatic snakes.

In my own collection, the larger Adult-sized Death Adders came down with minor respiratory complaints, improper thermoregulation and loss of appetite at more or less the same time as the small neonate snakes.

They did as a group tend to show signs of infection later than the smaller snakes, perhaps in response to their lower metabolic rates.

However the symptoms of disease were relatively minor and save for the addition of Baytril in their water bowls at a fairly late stage, they all recovered without treatment of any form.

All were allowed to starve and due to their obese condition, looked no worse after the symptoms subsided, whereupon they recommenced feeding.

Evidence of respiratory infection was only diagnosed after each snake was checked for abnormal digging and dust on their snouts.

Had the snakes been kept in cages with a paper substrate, this would not have been detected.

What this means is that not only are signs of reovirus likely to differ from snake to snake, but signs observed will also depend on the housing methods employed.

The unaffected Carpet Snake and Diamond Python were later fed rodents that had been bitten by infected Death Adders. Neither snake declined in any way.

Hence the snakes either got the virus and showed no symptoms or simply didn't get the virus.

As there is no simply means to test the adult snakes, other than by trying to cross infect them with another uninfected snake via drinking water, the (cautious) assumption at this stage is the former.

However the reovirus did manifest quite severely in two larger Death Adders.

One, an adult sized (63 cm long) female was fed a dead rat on 1 July 2003.

On 19 July 2003, and after an absence from home for the intervening period, it was seen to have a severe case of mouth-rot on the front of the lower jaw.

Noting that the snake had never eaten a live food item in it's life, it was obvious that the infection was not caused by known injury or attack.

The presumption therefore was that the infection resulted from the snake's wiping exudate from the mouth.

The infection apparently worsened for a few days and then self-stabilized.

Not withstanding this, on 26 July the infected area was cleaned of adhered dirt and debris and cleaned out with a few cotton wool buds dipped in luke-warm water. Betadine was then applied as a disinfectant. The lesion appeared to be concentrated in a hole near the front of one side of the lower jaw, near the anterior end and no further.

Prior to then, the reluctance to treat the snake had been due to the snake approaching a slough.

Even with this cleaning and handling, unshed scales were inadvertently removed by hand from part of the snake's head.

Four days later the snake shed in three pieces and more importantly it did not pass any feces.

For a Death Adder not to pass feces when sloughing (+ or - at least two days) as in this case is significant and further indicates something amiss with the snake.

Notwithstanding this, the mouthrot apparently healed without incident and the snake's health recovered. On 17 August 2003, it ate again, voluntarily.

However on 13 October 2003, the mouthrot was seen to have relapsed. Once again this infection appeared to be linked to the sloughing cycle.

Hence my conclusion that adverse effects of the virus and secondary infections are exacerbated by stress factors such as pre-slough.

Two days later the skin was shed in one piece and the mouthrot appeared improved, but it had not healed completely.

The indicator of note was whether or not the wound was weeping. If it was weeping the view would be that it is ongoing and getting worse. A scabbed and dry wound would be interpreted as stabilized and healing.

Three days later the snake was seen luring (with her tail), which is a sign of hunger for these snakes and she was offered and ate a half-grown rat.

On 26 October the snake was inspected and the mouthrot appeared to be worsening and weeping.

A close examination of the mouth showed it to be worse than first suspected.

Bone of lower law on one side had come loose and was held on by dead skin. It was facing off mouth and literally fell off.

The mouth was in general was full of red lesions, but mainly around the single infected area and there was also noticeable white crusty exudate (only a little) in the back of the throat either from the mouth wounds or perhaps the respiratory canal.

Put bluntly, the picture was not good.

When handled, the snake did a slightly runny feces (again not indicative of good health).

The mouthrot wound and mouth were cleaned with cotton wool buds and then (undiluted) betadine was applied.

The snake was subsequently dosed with .2 ml of Baytril with 5 ml of water and then .5 ml of flagyl with another 5 ml of water via two 5 ml syringes. As the snake bit the syringes it drew some blood from itself. It also passed a slightly runny feces that would probably have passed as OK, but was not a "perfect 10".

The mouth improved slowly and on 20 November 2003 the snake was seen for the first time in some weeks sitting in a classic horse-shoe position indicating it was hungry. (This is the position these snakes sit with head near tail).

The snake was therefore offered a mouse and took it and apprantly recovered completely.

Where the law part of the jaw was missing, whitish flesh formed a cover, leaving part of the upper jaw exposed due to the environment.

However the snake's health remained unaffected in the long term with it behaving otherwise normally.

Excluding the above case, there is a case of mouthrot associated with viral infection in the literature.

Noting how rare this ailment is in elapids, it'd be reasonable to infer that the weakened immunity of the snake in terms of the reovirus assumed to infect the snake was a causative factor of the mouthrot.

This case is noted here in that spontaneous mouthrots seen in long-term and otherwise healthy captives (as above), may in fact have a viral cause.

Viruses as a trend tend to attack weak, old, young, and otherwise impaired snakes. In fact the same applies for most other animals.

Hence in terms of this reovirus, larger and healthy elapids tend not to show sign of infection, even if carrying it. Hence the general immunity shown by larger elapids such as Taipans.

In the case of Death Adders, neonates are very vulnerable and as size increases, so too does immunity.

In the captive situation, it seems that a Death Adder of 39 cm (15 inch) or longer, will usually be able to ride through a reovirus infection without major problem.

However there was a case in September/October this year that showed that size alone is not always an indicator of success.

On 15 August 2003, I acquired a 45 cm (18 inch) subadult (approximately 18 month old) female Death Adder (A. antarcticus) and inadvertently cross-infected it with the reovirus.

The time of cross-infection wasn't determined, but on 22 September 2003, the snake showed signs of severe infection, including severe respiratory infection, wandering excessively, emaciation, improper postures and so on.

This condition declined over the following week and in spite of the snake being moved to a 'warm room' it regurgitated a small force-fed 1/4 grown mouse on 28 September 2003.

The same thing happened with a very small fish that was force-fed, indicating the snake's condition was in sharp decline.

Regurgitation of a small fish is regarded as very bad news as these are the most easily digested solid food items being far more readily digested than things such as lizards or the more difficult to digest rodents.

Noting also on 1 October 2003 that the snake's feces was also somewhat runny, the snake was force-fed a water solution containing Baytril for the respiratory infection and then another containing flagyl to attack any harmful protozoa.

Baytril was also put in the snake's water bowl.

The snake's condition improved somewhat and on 5 October 2003 the snake was force-fed a small fish which it held down and digested, the same process being repeated on 9 October and on 11 October a 1/3 grown mouse was force-fed and held down in spite of the snake's remaining in the coolest part of the cage (about 26 degrees Celsius).

The food items also had Baytril injected into them as well as in one case a dose of Panacur and another case a dose of Droncit (drugs to treat nematodes and cestodes).

The snake's recovery continued and a large number of parasitic worms were passed in the feces.

In other words, this snake appeared to have taken a particularly hard hit from the reovirus due to other pre-existing health problems.

The parasites on their own would not have been life threatening and nor would the reovirus have been.

However in combination they were a potentially fatal mix!

A disturbing trend seen in infected snakes was an apparently spontaneous relapse of ailment in snakes that had otherwise appeared to recover from symptoms.

In September, all three smaller Death Adders that had recovered (see earlier) apparently relapsed.

All regurgitated food, lost appetite, showed signs of rapid emaciation and showed signs of respiratory infection.

Treatment was immediate and pro-active.

All snakes were moved into a warm room (now of 25-27 degrees Celsius minimum), given Baytril orally and then force-fed fish, which in all cases were held down.

All three apparently recovered without incident, being switched back to rodents as soon as they appeared to have stabilized and seemed likely to hold them down (which they did).

That snakes can recover and then relapse in terms of this virus is a disturbing fact. It implies that snakes may in fact shed virus long after they are visibly 'cured' and adds to the uncertainty as to the 'use-by date' of the virus in snakes, if there is in fact one at all!

It also throws into question how snakes develop antibodies to the virus and how long they work effectively against the virus.

An unknown factor is how the virus is able to relapse in snakes that have previously 'beaten' it.

In the case of humans, viruses such as herpes may spontaneously relapse and manifest in infected individuals either at random or at times of stress.

The same may be the case in terms of this reovirus in snakes, but put simply, the real story isn't known.

On 17 August 2003, I obtained a pair of neonate Northern Hill Death Adders (Acanthophis lancasteri) from Drew Williams of Bendigo (born 12 July 2003).

The name 'lancasteri' appears to be a nomen nudem, making the correct designation for these snakes A. bottomi (see Storr, Smith and Johnstone 2002).

The male had not been feeding voluntarily, but the female had been a good feeder.

In terms of my own keeping methods, this was effectively meaningless as the snakes tend to be force-fed or assist-fed at that age as a matter of convenience. As snakes get older, their feeding response improves, negating the need to continue force or assist feeding, the cessation being timed to coincide with the snake attaining a degree of robustness commensurate with increased size as well as a slight drop in food intake so as to spur on the normal hunger response.

Such a feeding regimen allows for rapid gains in condition and seems to have no known adverse effects on the long term.

Snakes are switched to assist and voluntary feeding as they mature, which is usually within about 4 months.

These above-mentioned Northern Hill Death Adders were small, both being about 17 cm long when obtained.

On 3 September 2003, I accidentally force-fed the female with a set of virus infected tongs.

I realized this within minutes of doing so, but then knew that decline was imminent.

The snake rapidly declined so that within a week it's condition appeared emaciated and it regurgitated food.

The snake sought out the coolest part of the cage (not thermoregulating properly) and adopted the incorrect (stargazing) posture.

On 11 September 2003, the snake was attempting to slough and had removed the skin from the top of it's head.

Four hours later it had not moved or got any more skin off.

This was then forcibly removed by myself by first soaking the snake for an hour and then removing the skin carefully by hand.

The snake was then force-drank water, due to it's emaciation and evidence that it had no intention of voluntarily drinking.

The snake was also force-fed tiny fish (Gambusia) which in turn had Baytril injected in them and were 'washed down' with more water via a syringe to aid digestion.

Notwithstanding this aggressive treatment, the snake's condition continued to worsen so that by 19 September 2003, the snake was very emaciated and had a severe respiratory infection that didn't appear to responding well to Baytril.

The dosage was increased as a result and administered via a 1 ml syringe (only about 1/4 filled), as had been done already to force drink the snake.

This was done by holding the snake vertically and force injecting water into the throat. Gravity alone would force it down.

Once placed back into the cage, the snake would raise it's head and would tend to lap up the water previously injected into the snake's throat.

There was never any attempt to regurgitate the water in this or other snakes similarly treated, however of note is that not too much water should be given at a time using this method.

Also noticed as of 19 September 2003 was that if the snake was held upside down, the internal organs all showed up very clearly through the ventral scales. This is not normally the case in young Death Adders and was further evidence of severe illness.

Over the following week the snake's condition appeared to improve markedly and the snake also passed a normal feces.

On 4 October 2003 the snake was observed itself drinking from the water bowl in the cage, for the first time in a long time and improvement was further evidenced on the following day when for the fist time in many weeks the snake did not stay in the coolest part of the cage, but instead thermoregulated by straddling the heated section to find the optimal temperature.

From then on recovery in this snake continued in a linear manner.

As of 11 October 2003, this snake was 8 cm shorter and considerably lighter in weight than the unaffected male. The male had been the same length and thinner when acquired on 17 August 2003, less than two months earlier.

By end January 2004 this snake's growth trajectory had been restored and it was 33 cm in total length and in continued good health.

The significance of this case is as follows.

A snake known to be infected and showing severe neurological signs was able to be treated aggressively and made a recovery.

Without this treatment, death would have been a certainty.

Noting that this was a newborn Death Adder and these snakes appear to be most vulnerable to the reovirus (with the possible exception of Red-bellied Black Snakes), it seems that with correct procedure, most, if not all deaths in captivity from the reovirus may be avoidable.

The keys to success are speed and correct procedure in terms of sick, or likely to get sick snakes.

Two more lines of infection besides that outlined in this paper have been identified in the period late 2003, early 2004. Both lines have direct connections with the Australian Reptile Park. However, unlike the Bigmore line of infection, the known source collections have themselves had many sources of potential incoming vectors, thereby making the ARP just one of a number of potential sources.

Significant here isn't whether or not the ARP has traded more affected snakes at any time, but rather that the virus appears to have become more widespread in Australia in the period at end 2003 and due to the fact that many unaffected but carrier snakes appear to be still being traded, the virus will become more ubiquitous in coming years.

Put another way, it's likely that any person in Australia who trades in elapid snakes regularly to and from other collections, is likely to sooner or later have their collection exposed to this virus. Hence the need to be vigilant in terms of trying to stop it's spread in collections and/or deal with it should it make an appearance.

Based on the ARP's experiences with the virus outbreak, it appeared that Death Adders (genus Acanthophis) were the most susceptible to the virus.

Because of the limited scope of my collection at the relevant time (Death Adders and pythons only), my own corroborating experiences while supporting the contention that Death Adders were the most susceptible snakes, didn't really advance the idea further.

However based on mortality in collections of other species known to be affected, including Copperheads (Austrelaps), Tiger Snakes and Red-bellied Blacks, it seemed that the Red-bellied Black snakes actually had a higher mortality rate.

13 of 14 of the Red-bellied Black Snakes shipped by Gleeson in mid 2003 died. The only survivor was a 180 cm (very large) adult male that Rossignolli received.

Initially I attributed the higher than expected mortality rate to the keeping practices of both Rossignolli and Eipper, (the inference being that maybe they weren't quite up to scratch), but the theory took a hiding in early 2004 when I received a shipment of seven more infected Red-bellied Black Snakes.

The two largest were feeding, appeared in visibly good health and shipped on to Rossignolli immediately. They were however carriers of the virus, but in terms of Rossignolli and his collection (also known to be infected), this was not in itself an issue.

For the record, he'd already ordered the snakes from the keeper with full knowledge that they had the virus.

Of the five retained, all were showing signs of virus infection. Two died within 48 hours of receipt.

In terms of those snakes, they were very thin and emaciated and while the speed of their deaths was a surprise, the fact that they died wasn't.

Put another way, they seemed OK the day before they were found dead in their cage.

Of the three remaining, they were in marginally better condition and aggressive treatment enabled all to survive.

This included force-feeding and force-drinking, first including including Baytril and then various worming treatments including Panacur and Droncit, as well as Flagyl.

Included in this treatment was a feeding regimen that commenced with small fish and was shortly upgraded to rodents and then strips of meat, which as a high-protein feed actually enables snakes to gain condition more quickly than a pure rodent diet.

Notable here however is that these evidently ill and non-feeding emaciated snakes were large (all a metre or more in length), which as a size class would be out of the danger zone for most Death Adders.

In other words the Red-bellied Black snakes appeared to be suffering more severely when infected by the virus than the Death Adders.

Of the three surviving Red-bellied Black Snakes, all three sloughed about 5 weeks after being acquired and at a time when they were on an obvious upswing in terms of body mass and condition.

Notwithstanding this, none were able to slough, all having to be bathed in water and then manually sloughed (me doing it by hand).

This emaciation was attributed to the secondary effects of the virus and again indicated that the species is particularly vulnerable to the virus.

In my situation I was alive to the virus and shedding issues and did not allow unshed skin to remain on the snakes more than a few hours after the first head shields had been removed as part of the sloughing process.

However had such snakes been in a facility where the manager was unaware of the virus and the need for snakes to slough properly and not to retain skin, then the health of the snakes could well have been fatally compromised.

Bearing in mind that to date only a limited number of species have been known to be exposed to the reovirus, which other elapid species are likely to suffer greatly from infection, isn't completely known.

The full extent of the reovirus infection from Bigmore's collection is not yet established. However it's likely that as a result of the alarm being put out by myself in June 2003, the spread of the virus along that line of infection will be checked.

Moving up the line and down again to other recipients of Weigel's snakes is not known.

He has not disclosed who these people are, so their management of potentially infected snakes, results and so on are totally unknown.

Giving Weigel the benefit of any doubts and assuming that he did in fact notify other recipients of infected snakes as alleged in his e-mail of 25 January 2003, we get to the next problem which is the source of Weigel's infection.

Weigel claimed that he thought the infection came from at least three other keepers all of whom he alleges denied giving him stock that is in any way tainted.

If those keepers, (whoever they are) have made such denials, they should be questioned further due to what's known about the transmission of the reovirus and how easily it can be masked within a collection, including via asymptomatic carriers.

The reovirus in Australia may well predate Weigel's own actions in dispersing the virus, even though in the case of Victoria and parts of NSW at least, Weigel appears to have given the virus it's first major beachhead.

Based on known reovirus attributed mortalities in the collections of myself, Eipper, Bigmore, Rossignolli, Gleeson, Stasweski, DeBenedictine and others there are certain facts that have become known.

The central theme of this paper is failure. My own collection quarantine, I thought of as being 'best practice'. It failed to stop an unknown and undetected virus infection, even if it was only by something as small and insignificant as a pair of forceps! Most, if not all other collections mentioned had similar failings, as in they allowed virus into their facilities and without effective barrier.

Furthermore my own view is that these included some of Australia's best-managed collections and hence comments adverse to them in this paper should not be taken as attacks on them, but rather a warning to everyone else.

As a corollary to this, I spoke with managers of most of Australia's largest public and private reptile collections in June 2003 and found without exception that every single one of them was effectively unable to stop and deal with an unannounced virus infection via newly acquired reptiles, such as a single infected and asymptomatic snake!

Noting that reovirus and other viruses are likely to become a more relevant issue for reptile keepers in Australia and elsewhere in future, the above lessons are salient to all.

Noting the likelihood of an increase of viruses in collections in coming years, reptile keepers can best manage viruses by asking themselves the following simple question:

If a reptile that presents as healthy is obtained and yet unknowingly carries a virus, may it infect the rest of your collection?

If the answer is either a maybe or a yes, then keeping protocols need to be altered to remove that possibility.

Noting that the histological and EM aspects of diagnosis of viruses are time consuming, usually done after death of at least one reptile and often not conclusive in themselves (in terms of histological diagnosis), diagnosis of viruses will tend to be presumptive (educated guesses) in most cases.

Notwithstanding this shortcoming in terms of diagnosis, because viruses can be such a serious problem and because they can be so devastating in large collections and those with large numbers of small snakes, especially elapids, management of viruses in situ is required and preferably before deaths start to mount.

If a virus is suspected in a collection, all possible steps should be taken to ascertain the following:

• Likely source of infection
• Means of transmission in a collection
• Reptiles likely to be most affected.
• Plan of treatment for all reptiles likely to be affected and means to isolate those believed unaffected.

Much of what's required has already been outlined, however some points are worth noting here.

• If in doubt, the worst should be expected and in large collections this can become a logistical nightmare. As a matter of procedure all cages, feeding implements and the like should be isolated from one another so that there is no further transfer of pathogens.
• Other sources of transfer such as shared cloths, mites or forceps must be eliminated.
• If there is a shortage of implements such as forceps (likely), then these must be sterilized between uses with different reptiles.
• The best means to do this is via immersion in continually boiling water for at least ten minutes (hence metal implements only).
• Baytril or similar anti-respiratory treatment should be added to water bowls of likely to be affected snakes preemptively to prevent these infections. If respiratory infection appears, even if mild, it should be treated aggressively and with larger doses of baytril diluted in water and force-drank. A 200 gram snake can take up to .3 ml diluted in 10 ml of water orally without obvious ill effect. Undiluted Baytril will harm the snake if force-drank.
• As a matter of course, all reptiles should be maintained in optimal condition and be kept well-fed, especially smaller and growing snakes.
• Force/assist feeding of neonate and small snakes that don't voluntarily feed is recommended.
• Force drinking of small and emaciated snakes is advised if it is obvious that they are either not voluntarily drinking or not drinking enough. For larger snakes this isn't generally necessary except to administer medicines. You will notice larger snakes that are infected will voluntarily drink more to cover for their increased urination.
• In terms of clearing snakes and cages as being 'no longer infectious', this part of virus management is not yet known.

However the following is known.

Viruses do not survive long in dry waterless environments and a cage that has been completely dried out, de-mited and left empty for more than two months can be presumed virus free.

In terms of virus affected reptiles, this is harder to ascertain. Noting my own failure in this regard and other people's findings, viruses such as reoviruses and OPMV must be regarded as being in infected reptiles indefinitely, unless and until it is proven otherwise.

Claims by Weigel of a so-called 'two-month test' are not applicable in terms of this reovirus.

The theory of the test is that if no snakes in a collection show signs of virus symptom for two months it is declared 'clean'.

In terms of this reovirus, snakes have been known to be affected for at least ten months and to relapse symptoms over this period.

If a virus carrying reptile is found to be gravid, it should be allowed to produce eggs or young in a dry mite free cage and eggs or young should be removed immediately. Based on what happened in terms of Rossignolli's Tiger Snakes (above), this should allow for virus-free young.

Notwithstanding this, these snakes should be quarantined for at least six months for signs of virus after being born or hatching.

Management of virus affected snakes has already been covered in this paper.

A method for doing this is postulated below. I have not myself yet done it, but do regard it as feasible.

(If considering such experimentation in Australia, it's probably wise to seek regulatory approval).

A snake formerly infected with a virus but suspected as being virus-free based on it's renewed good health for at least six months, should be placed in a new cage and without water for at least a week, or if this period is deemed too long, then for as many days as possible without compromising the snake's good health.

The snake can then have a water bowl with fresh clean water added to the cage.

The idea here is that viruses are known to persist in water for some time and assuming that the snake itself has developed antibodies to fight the virus, any residual virus in the snake or picked up when drinking should be eliminated by the snake itself.

After another week or so in the cage and when it has become evident that the snake has taken drinks from the water bowl this snake can be removed and another virus free snake added.

This second snake should be of a type known to be very susceptible to the virus. Examples include newborn Death Adders (Acanthophis), newborn Red-bellied Blacks (Pseudechis) and newborn Tiger Snakes (Notechis).

Assuming the snake does not develop the virus, it is then reasonable to infer that the original snake was also probably virus free.

However as some snakes, even of susceptible species and age do for unknown reasons seem to escape adverse effect from the virus (as seen in two of Gleeson's Tiger Snakes), more than one snake should be tested before it is definitively concluded that the tested snake does not have virus.

On 22-23 June 2003, when speaking to several people about the reovirus in my collection, some advised me against widely publicizing the fact. The advice centered on an assumption that some people may 'shun' or 'vilify' me as a result.

Weigel claimed he got the same advice and cited it as his reason for trying to keep his own infection under wraps.

Among those people who proffered this advice to me was a respected veterinary surgeon, which again mirrored the claims of Weigel in terms of his infection. Whilst the advice given to me was candid and with a view to looking after my best interests, this was ultimately rejected.

Part of this rejection was based on the obvious consequences of the attempts by Weigel to keep his own virus infection generally unknown.

In fairness to Weigel, I by that stage had hindsight knowledge that he hadn't been privy to at the time he made his decision.

The beginning of Weigel's broadcast e-mail dated 25 January 2003 condemned the person (Maurico Perez-Ruiz) who leaked out the details of the Australian Reptile Park's infection.

While other parts of Weigel's e-mail generally ran on the theme that the virus outbreak was under control and that all relevant people had been notified, we know that not to be true. Bigmore at least wasn't and the list of others may be extensive.

Whether or not Weigel's failure to communicate to Bigmore was due to a deliberate intent on Weigel's part or simply oversight isn't known, even though Craig Adams has since claimed oversight. Furthermore, Weigel's habit of making obviously false and untrue statements in e-mails (at least) is well-known (for example see his e-mail of 3 Feb 2001 re Pailsus weigeli) or those he posted to the same list about Indonesian Pythons and therefore any explanation from him in this regard must be regarded as questionable. For that matter it also casts some doubt in terms of his e-mail dated January 2003 re 'OPMV' which has more-or-less been accepted here as accurate.

The results of Weigel's failure to properly and/or widely advise of his own virus outbreak have in hindsight been devastating.

All collections down from Bigmore's could have avoided the virus outbreaks had Weigel widely disclosed his epidemic so that Bigmore knew that his own collection was at risk, and/or if Weigel had notified Bigmore direct.

Consequently, in the case of myself I chose the opposite tack and that was to notify all relevant parties of my infection.

As no reptiles had left my collection, that may sound simple, but due to my role as courier in the P. porphyriacus and Notechis transfers between NSW and Victoria I felt obliged to notify all relevant parties.

Notable is that there was no ill-feeling displayed towards me, even though I'd literally been the courier of death for those people's collections.

The same protocol was adopted by Bigmore, Rossgnolli, Eipper and other persons in the chains below Bigmore.

The result being that as of the last week of June 2003, this leg of the virus epidemic was hopefully stopped in it's tracks.

If a fellow keeper is small-minded enough to condemn myself or the others in the chain of infection for having virus in their collection, or allowing it in, then so be it.

I am not perfect and freely admit that my quarantine system as of early 2003 failed to allow the virus in. But more importantly, if disclosing my own imperfections helps stop others from making the same procedural errors in the light of this relatively newfound threat, I'll put up with any condemnation.

Thus the advice must be:

A question that nagged others and myself in terms of this reovirus outbreak and other alleged OPMV cases in the late 1990's and since is why has 'OPMV' or this reovirus not surfaced earlier as a problem in Australian collections. Two possibilities are that it (or other virus) was either present in collections for many years and simply undiagnosed, or perhaps it had been brought in, perhaps with non-native reptiles, which appears to be the thinking of many people in Australia (see previous).

This is a question that should be answered sooner rather than later and may take some government expenditure to do so.

If the reovirus is non-native it may at some stage in future pose a serious threat to native reptiles in a similar manner to which the Chytrid fungus has annihilated many native frogs. In other words, virus infected reptiles must never be let loose.

Based on this worst case scenario and further noting the means of transmission of reovirus (fluid borne), it is essential and urgent that strictly controlled tests be done on the effects of reovirus if released into the wild.

Notwithstanding this risk, my own educated guess is that the reovirus (or variants thereof) would not pose a serious threat to most wild reptiles.

The disease is to an extent limiting in that infected animals die and by and large reptiles do not regularly interact. A counter to this would be reovirus infecting a common water source or similar causing a die-off in a single location.

In the captive situation, even when there are mass die off's it's usual for some to survive (for reasons not always clear). Assuming the same to be the case in the wild, this would mean the worst case scenario in the bush would probably be a population crash, which in most (but not all) cases would rectify itself after a period of time.

Based on the known fecundity of most snakes, this crash and rebound would probably run it's course in less than 20 years in a given location.

A related issue is that of so-called snake controllers. These are the people who release reptiles into the bush after they have removed them from suburban houses and the like.

Hoser (1995) talks extensively about the potential perils of releasing wildlife back into the wild.

Virus infection can be added to the list.

The Victorian wildlife authority is currently reviewing it's procedures in terms of releasing snakes into the wild.

It may well be safer to simply prohibit the re-release of most snakes.

Another issue facing licenced snake catchers is the potential passing on of disease from captive snakes to wild snakes in transit.

In my own case, as a licenced snake removalist in Victoria some snakes removed from private properties have at times been held in the room with the Death Adders 'in transit'. These specimens have included snakes caught locally, late at night and brought to the house by members of the public.

These snakes must be kept well apart from captive snakes.

In hindsight, the anti-mite treatment of all incoming reptiles, including those 'in transit' will not necessarily be enough to guard against virus infections if they are held in proximity to the permanent collection unless other isolating mechanisms are used, including never using the same handling implements, water containers and the like.

In terms of what pet shops and private dealers can do in terms of potential virus infections, well, that's a major headache for which simple answers are simply not available. As it stands, a sizeable portion of reptile-dealing pet shops in Victoria at least are struggling to cope with simple issues like mite plagues and other basic husbandry issues (although there are some notable exceptions).

The speed at which reovirus, OPMV (and perhaps similar) infections can cause mass die outs in captive collections is further reason to split captive breeding colonies of rare and endangered species.

Noting that in most states there is only one or two major public zoos, concentration of populations of Australia's endangered species in such a handful of facilities would border on the reckless.

Sound conservation, especially of reptiles, must therefore incorporate more facilities, which must therefore include private keepers.

In terms of Australia, I have therefore recommended a conference between relevant stakeholders to work out a protocol to deal with the key research issues indicated above and proper conservation and legal issues that may arise from the scientific findings that emerge.

Similar conferences should be held outside Australia, where the same issues are likely to emerge.

My own view is that it should be a criminal offence for a person to knowingly trade in virus infected reptiles and/or failure to notify a recipient if and when a suspected infection occurs.

Movement permits for reptiles have long been a bone of contention for reptile keepers in Australia. They are generally regarded as being a waste of time and paperwork and I have also peddled this idea in the past.

Notwithstanding this, the prospect of reovirus, OPMV and similar infections spreading in Australian collections means that accurate tracking of movements is essential to stop them.

While permits themselves may be unnecessary it is recommended by myself that there is a system in force whereby a central register is kept of all wildlife movements in captivity so that infections can be tracked as needed.

If the system is free of charge, including for interstate transfers (as in Victoria at the moment, but not in NSW or Queensland), then compliance will probably be higher.

Outside Australia the whole issue becomes more difficult to deal with given the far freer trade in wildlife, including across international boundaries.

This question is beyond the scope of this paper. However assuming for a moment that this newly identified reovirus came into Australia via the illegal trade, that in effect would support the contention that open legal, and quarantined imports are preferred to the current 'ban' which has driven trade underground.

It's also notable that a respected institution as in the ARP, against which no allegations of illegality are made (save for the Taipan swap with Bigmore, which didn't have paperwork and for which an indemnity has now been given) and who have access to the best available veterinary surgeons, vast amounts of money and funds, has evidently provided the source of a much wider virus outbreak.

That they were the source of the infection as known is more a case of bad luck than bad management, as indicated by the fact that others in the line of infection also unwittingly traded infected snakes.

Hence, my own view that one set of rules should be enforced against all reptile holders regardless of their status in terms of public, private or whatever.

My view is that a total ban on any exotic reptiles anywhere in Australia is preferable, to letting them in to be traded legally. However for a ban to be effective, there must be NO EXCEPTIONS.

The no exceptions should include major public zoos and significant private holdings as well.

Backed by immediate euthanazia of all exotics if located by officials - no exceptions and heavy fines for all caught with them (no exceptions), exotic reptiles could be effectively kept out of Australia indefinitely given Australia's huge law enforcement bureaucracy which rivals that of the former communist countries in Eastern Europe in terms of size.

The recent glut of exotic reptiles in Australia has been fuelled by several factors, including the fact that there is a general perception that they will soon be legalized (see the Weigel e-mails) and the fact that penalties for holding them illegally (if caught) are minimal.

In 2001, keepers Chris Hay and Rob Valentic were caught with a stash of illegal exotic reptiles, including highly venomous species, a hydroponic drug crop, stealing power from the supplier and illegal firearms.

The magistrate Alan Spillane gave them a good behavior bond (no effective fine, penalty or conviction). This was upheld in spite of an appeal to a higher court by the local wildlife officials. The precedent is currently the foundation for the continued illegal importation of exotic reptiles, in part fuelled by the larger zoos and the like who have shared in the proceeds, including from the Valentic/Hay bust (see Hoser 2003c).

Hence (for example) a case in June 2003 where another Victorian keeper charged with possession of illegal exotics was fined a few hundred dollars only, in spite of the reptiles he held being valued at many thousands of dollars.

In yet another case a Victorian woman with Corn Snakes (Elaphe guttata) received a mere good behaviour bond (no conviction).

Noting that this reovirus presents in an identical manner to the better known OPMV, it is likely that some of the findings in relation to this reovirus apply to OPMV infections. In the absence of information to the contrary, my advice is that this should be assumed.

These findings are as follows:

• In situ transmission is generally via fluids, not air. This means, blood, saliva, water bowls, bowl washers and mites. Most common means between cages is shared washing cloths for water bowls or transfer by mites. Less common is via saliva or fluids left on feeding tongs or forceps.
• This reovirus effectively stops growth in young snakes for the duration of infection and is another hitherto unrecognized indicator of the virus.
• Feeding of otherwise non-feeding snakes by assist or force-feeding may be beneficial in terms of nursing ill snakes. Reovirus affected snakes will generally hold down and digest food without problem at all stages of the infection except at the terminal (restless phase), even if they do not voluntarily take food. Their ability to hold down and digest large or relatively hard to digest items (as in small hairy mice) is reduced. Digestion is (often) also dependent on the coldest part of the cage being sufficiently warm to enable it to take place.
• Force-drinking small and emaciated snakes is a major weapon in the defence armory, especially when combined with anti-respiratory infection drugs such as Baytril.
• All things being equal, snakes with neurological symptoms early on are more likely to die, regardless of care, while those exhibiting only respiratory symptoms have a much greater chance of survival. However aggressive treatment of even the worst affected snakes, by incorporating all known methods of treatment and care can mean success
• Failure to properly thermoregulate is another factor indicative of reovirus infection, and is commonly the first sign in otherwise healthy long-term captives.
• Progression of reovirus infections in snakes in laboratories AND in the captive situation is highly predictable based on identifying time of infection. Infection time can also be deduced by working backwards from when symptoms are detected if these parameters are known for the species.
• Within a given species, size (or lack thereof) directly indicates likelihood of surviving a reovirus infection as does other factors in terms of general health and the presence or absence of other ailments.
• Published reports on OPMV question whether or not it affects neonate snakes. This reovirus is far more deadly in small snakes than large and in the absence of proper tests for the kind of virus causing disease, the age class of snakes most affected may be an indicator of virus type infecting the snakes.
• Contrary to previously published reports that snakes that are 'poor doers' are indicative of virus infection while non-poor doers are not, in terms of a single collection, the evidence here suggests that all snakes in a collection may have virus, but many will fail to show signs and be erroneously cleared as healthy when carrying virus. In other words, the poor do-ers with other pre-existing problems are much more likely to succumb to reovirus (as seen in the case of the two large A. cummingi received by Hoser on 15 Feb 2003 and the later case involving the 45 cm A. antarcticus).
• Reovirus related deaths in snakes may be indicated by a snake's body being found in a loosely curled 'belly-up' position. For the species in the genera Notechis and Acanthophis at least, this is almost a general trend.
• Reovirus infections in different collections can be easily and accurately predicted based on snakes known to be infected, movements between collections, an appraisal of cage cleaning, water sources, mites and feeding methods. This includes accurate identification of snakes carrying the virus but showing no symptoms.
• Snakes that exhibit sloughing problems due to apparent emaciation and drying of skin onto the body may be showing indications of virus infection. This is particularly if the snake is one that has not previously had sloughing problems or is of a species not prone to shedding problems. Snakes that do not slough within an hour of removing the front of the head's scales off should be soaked in luke warm (30 degree Celsius) water for an hour or as long as necessary to enable the skin to be manually removed. This should be done as indicated as delays in skin removal will stress the snake immensely and at best cause rapid decline and at worst death.

In June 2003 I published a paper detailing what was then known about the virus infection, then presumptively diagnosed as OPMV (Hoser 2003a).

Hence the alert was out in terms of the Australian herpetological community in terms of this virus.

On 10 October 2003, I received a phone call from a distressed snake keeper (Jamie) in Sydney.

He'd received 9 neonate Northern Hill Death Adders (A. lancasteri) from Drew Williams in August 2003 (from the litter born on 12 July 2003) and 5 had already died from what appeared to be the same reovirus that had affected myself and the others listed in this paper.

The snakes showed identical symptoms and another two of the remaining four were in a state of terminal decline.

The keeper was advised to treat as indicated in this paper.

To that point he had not been treating the affected snakes in any proper way and so the deaths were somewhat predictable.

The keeper was experienced with Death Adders having raised them previously without incident and all indicators were that a viral infection was to blame for the deaths.

The corpses had been retained for testing by myself and the scientists at VIAS, but those tests were ongoing at the time this paper was written.

In terms of ascertaining the source of infection, this was an obvious question I had, but to find the original source of infection may not be easy as it could have been on a carrier snake (no symptoms) and from a collection without obvious sign of infection.

The keeper initially thought that the snakes were infected at the time they arrived from Drew Williams. While this is not impossible, all others from the same litter in other collections remained in good health (excluding mine of course, of which one was infected by myself and by that stage recovering).

In other words, the Williams collection seemed not to be the source.

Furthermore, when I saw the Williams collection in August 2003 there was no evidence of viral infection and according to Williams (and Eipper as well), that remained the case at his facility as recently as 10 October 2003, December 2003 and later.

By the way, I visited Williams on return from Adelaide and had not been in contact with my own snakes for a fortnight and hence there had been no possibility of viral transfer from my collection to his.

Hence the investigation of other possible sources of infection.

This may never be determined, but there was another interesting possibility.

This keeper had received a Taipan from a Sydney-based breeder who had also supplied the Australian Reptile Park with Taipans after the fire that burnt down the snake holding building in mid 2000 and before the virus outbreak there in 2002.

The keeper had not however noticed any evidence of viral infection or unexplained deaths in his collection.

Noting that Taipans seem to be asymptomatic in terms of this reovirus, that wouldn't be unusual, even if all the snakes carried the virus.

Were the Taipans he held and bred the carriers of the infection?

Or were they the original source of the ARP's infection?

These questions may never be answered.

However ignoring the speculation above, of significance is that this new infection had no known links to the ARP/Bigmore line of infection.

Once again it underlines the fact that a virus infection can attack a reptile collection without warning, with great speed, from almost any transaction and even from the most reputable of sources.

Had the keeper been more proactive, his losses may well have stopped before he lost five snakes, but in fairness to him, the speed of infection and deaths may have taken him by surprise.

Outside Australia the same situation could occur.

Hence the central theme of this paper is for keepers to be alert to the threat caused by viruses and know what to do if a viral infection attacks the collection.

Also if in doubt as to the health of snakes, it is better to act sooner rather than later.

Various keepers, veterinary surgeons and others who freely shared what they knew about this reovirus, OPMV, their own thoughts, experiences and the like.

Included among these people are: Craig Adams, Brian Barnett, Peter Cameron, Brendan Carmel, Gary Crameri, Neil Davie, John DeBenedictine, Scott Eipper, Robert Gleeson, Elliott Jacobson, Clayton Knight, Malcolm Lancaster, Haydn McPhie, Debra Middleton, Roy Pails, Mauricio Perez-Ruiz, Mick and Mip Pugh, Fred Rossignolli, Alex Stasweski, John Weigel, Judy and Peter Whybrow, Mark Williamson, Paul and Sarah Woolf.

All reptiles mentioned in the paper above were held and/or moved under various permits as issued by the relevant state wildlife authorities and/or those movements not covered by movement permits were indemnified in July 2003 in order to facilitate a frank and open discussion of the issue and for this indemnity the relevant wildlife authorities are thanked for their cooperation in this matter.

To this extent, the relevant officials with the wildlife authorities in Australia have chosen to be part of the solution to the problem, rather than to aggravate the problem and for this they are thanked.

Comments about husbandry practices of various keepers are made here in as frank and accurate a manner as possible and not to personally attack these people. For the purposes of this paper it has been essential to mention all relevant facts including such things as cage cleaning methods, mite infestations and so on.

This paper highlights failures (which to some extent have been emphasized) as well as successes so as to assist others to avoid failures in future.

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