CURING A SEVERE DIGESTIVE AILMENT IN AN AUSTRALIAN DEATH ADDER (ACANTHOPHIS ANTARCTICUS)

There are several means by which favorable intestinal flora may be introduced to a snake.

Death Adders (Genus Acanthophis) are unique among the family Elapidae in that their appearance and biological habits have evolved in a manner convergent with viperid snakes (Hoser, 1989). Notwithstanding these obvious differences, in terms of husbandry and feeding requirements, they fit within the normal profile of a larger elapid. This includes types of food eaten, diseases affecting the snakes and treatments for them.

On 21 March 2003, I acquired a (17 cm total length) neonate red (heterozygous) Blue Mountains female Death Adder (Acanthophis antarcticus) from Alex Stasweski. He is a keeper/breeder based in the Sydney suburb of Blacktown.

The snake had been born on 21 February the same year from an exceptionally large grey female.

In order to detail the cause and type of ailment/s this snake had and the basis for the decision to commence probiotic treatment a detailed history of the snake's prior diseases and husbandry is given.

The husbandry for the snake was typical for that given to all Hoser elapids (see Hoser 2004) and which as a rule is problem free (excluding for a single reovirus infection in 2003). The cage is a plastic tub of a size appropriate for the snake (in the main a 30 cm long X 20.5 cm wide X 10.5 cm (high) container) for the period covered by this paper (about 15 months).

One end is heated by an undertub heat mat (thermofilm) and the other end has a water container. The heat gradient is created by only part of the container floor being exposed to heat. The heat is on 24 hours (until breeding age attained, which is not applicable to this snake in the context of this paper).

Either by voluntary feeding, or if the snake wasn't voluntarily feeding, by force or assist feeding. Dietary intake varied, but was in line with that used to successfully raise other Death Adders and other venomous snakes. See also below.

This snake became infected with a reovirus in mid 2003 (see below and also refer to Hoser 2003a, 2003b). This reovirus was brought into my collection earlier on 15 February 2003 on a large Floodplain Death Adder (A. cummingi) from Stuart Bigmore, who had himself acquired the virus via a Taipan (Oxyuranus scutellatus) from the Australian Reptile Park (ARP) in October 2002.

In November 2002, when John Weigel, the park owner became aware of virus/es decimating the park's collection (on advice from a veterinary surgeon), he failed to notify all recipients of his stock of the disease, meaning that at materially relevant times, Bigmore and others downline from him were unaware of their collections having virus until notified by myself in mid 2003.

Later tests revealed 2 strains of Ophidioparamyxovirus (OPMV) and a reovirus at the ARP, the total number not necessarily reflecting adversely on the park or keepers, but rather as a result of the size of the collection, diversity of sources of stock and the fact that their stock had in fact been tested for viruses.

With aggressive treatment, the Death Adder subject of this paper managed to recover (or so it seemed). Treatment included pallative drug therapy (Baytril) for the associated respiratory infection. This was diluted and administered orally.

When injected Baytril may cause necrosis at the injection site and so this was never done to treat reovirus affected snakes with secondary respiratory infections.

Force-feeding and force-drinking was also done during the period of worst symptoms. The snake was also held in a warm room (no lower than 26 degrees Celcius) when most ill and when it was not otherwise thermoregulating properly.

While the snake appeared to recover from the reovirus, the recovery may not have been complete (see records below).

Alternatively, stresses imposed on the snake (in part by myself) may have led to a relapse of ailment.

In terms of the reovirus, it attacks certain snakes more severely than others, the general theme being small elapids are most at risk and if untreated generally die. In terms of my own collection, four out of eight most at risk Death Adders (neonates) died. Adults and larger snakes, while affected by the virus, were not as severely affected and none died save for one that was brought in infected and died very shortly after from both reovirus and a host of other ailments.

All other affected collections had proportionately higher mortalities, due mainly to failure to correctly diagnose or treat the disease and/or secondary infections.

In terms of the Hoser collection, a successful treatment regime was developed and used to prevent any deaths beyond the fourth snake on 22 June 2003, and this included numerous snakes brought into the facility that had been infected with the virus and/or were infected at the Hoser facility (usually deliberately for management ease) or in one case accidentally in a neonate Northern Hill Death Adder (Acanthophis bottomi).

Rather than giving a verbal appraisal of events leading to the need to engage in probiotic therapy, the relevant snake's entire feeding and other records are reproduced below.

It's file number was AAA-106.

Note: Heads and limbs are removed from (dead) mice for feeding to smaller snakes.

While readers may question the dietary intake of the above snake (fish and the like), there have been no long-term adverse effects on numerous other Death Adders and other elapids raised similarly. Excluding the effects stemming from the reovirus, force and assist-fed elapids self-feed within a fairly short period. Other raised Death Adders in the collection, including the other three surviving "at risk" neonate Death Adders, fed on similar diets remain in good health and self-feeding. Other neonate Death Adders acquired in 2003 and deliberately quarantined from the virus affected snakes were also raised without incident on varied diets, including rodents and fish.

The above is mentioned so that readers do not suspect that the dietary intake is the likely cause of the digestive problem.

While the cause of the digestive problem in this Death Adder isn't known, it is most likely a result of the continued anti-biotic therapy as this has been indicated as causative of similar disorders in humans.

However of note is that this is the only reptile in the Hoser facility to have had the gut impaction with undigested bone material and later inability to digest food. To that extent this snake was unique. Noting that other Death Adders (and other snakes) were at times given similar housing, treatments (for reovirus related ailments), feeding regimes and so on, there is no good explanation as to why this was the only snake to develop a condition whereby it was unable to digest food.

The snake was apparently recovered from the reovirus and in good health before the more recent decline in health. The first signs of decline manifested in the form of regurgitation of food and was at attributed to incorrect climate regime in the cage (see the notes).

The first major sign of trouble was the lower gut impaction caused by the failure to digest bone material.

No doubt the severe constipation caused other problems including a general decline of the snake.

One manifestation was that the snake failed to thermoregulate properly, in that it stayed away from the heated area of the cage.

The continuation of the snake's suboptimal temperature probably worsened it's condition as evidenced by a decline in it's ability to digest food and the passing of food in a progressively more undigested state.

The snake also took on a severely ragged and emaciated appearance that was totally at variance to all other snakes at the facility.

The intestinal blockage was manually massaged out over some weeks and by at the same time feeding food that even if impacted would pass through the snake easily. While this did in fact eventually lead to a clearing of the blockage (impacted bones), it allowed the underlying problem of failure to digest food to become more evident.

Food fed to the snake (chopped) would be passed undigested and without any smell of digestion or feces within a day or two.

It was at this point that it was clear that the snake wasn't digesting food and that if left untreated, it's condition was terminal.

Consultation with veterinary surgeons and prominent herpetologists in Australia failed to find a precedent to this condition. No other people reported reptiles passing food totally undigested.

Hence there was no treatment that could be prescribed or indicated.

No one came up with any suggestions and it was at this point I literally started to clutch at straws or ideas for inspiration, knowing that doing nothing would result in a dead snake.

It was at this point (23 May 2004) that probiotic treatment was trailled.

The basis of the decision was:

The snake was moved into a warm room, meaning that while one end of the cage remained heated via a heat mat, the rest of the cage had a floor of 26 Degrees Celcius, meaning that even if it chose to avoid heat, it would remain warm enough to properly digest food.

The treatment was as follows:

An acidophilus tablet was placed in lukewarm water and crushed. It was partially dissolved into the water (as best as could be done) and then sucked up into a syringe barrel. Three mls of the solution was then pumped into the esophagus and then massaged into the stomach. At the same time the snake was force-fed offal from a mouse. The choice of food was deliberate as it was about as "easy to digest" as possible, without being in a slurry form.

Two days later the snake passed another feces that was largely undigested, but unlike the previous one, this one did have a slight smell of feces (a poo smell), indicating a slight improvement in condition.

Notwithstanding this, the snake also showed signs of respiratory infection and so on this date a repeat of the treatment from 2 days earlier was done, but this time with Baytril as well to counter the respiratory infection.

The same treatment, minus the Baytril was repeated every two to four days for several times (see records above), with the snake showing a general improvement in condition.

On one occasion, Yakult (see below) was also given to the snake.

Noting that the snake had not been able to digest bone material for some time prior and the condition of the snake indicating bone disease or decline (as part of the general emaciation) a calcium supplement (tablet) was crushed and added to the food (in solution) on 3 June 2004. The next day the snake passed a relatively "normal" feces.

The treatment continued along the lines of force-feeding soft meaty material (mouse offal, pieces of finely chopped or minced meat), along with calcium and acidophilus, with the snake making a linear improvement to good health.

As the snake recovered, it commenced thermoregulating properly by early June 2004. This meant that it sat on or straddled the heat mat (even in the warm room).

The snake's appearance also improved to the point it again looked perfectly healthy.

Acidophilus tablets may include a range of different probiotics. The tablets used here were a generic brand from an Australian chemist that contained the following in each tablet: Lactobacillus acidophilus 750 million organisms, Lactobacillus rhamnosus 125 million organisms and Bifobacterium bifidus 125 million organisms. These totals would not have been given to the snake on each application as about half of the tablet mass was either undissolved in the water and/or not sucked into the syringe barrel used to administer to the snake. In each application, the snake may have passed up (regurgitated) small amounts of fluid, but this was not great at any stage (most being retained upon administering).

The fluid and force-feeding was done with the aid of gravity in that the snake was held head up and tail down and material massaged down the throat region after being placed in the snake's neck (the liquid) or mouth and throat (solid food material).

The Calcium supplement used was "Caltrate" a trademarked name. Each tablet contained 600 mg of Calcium Carbonate (equalling 600 mg of elemental calcium). Being administered the same way as the acidophilus tablets, it is likely that each dose only gave the snake about half the single tablet amount and that a substantial part of this actually emerged in the feces observed shortly thereafter.

Subsequent to the successful treatment of the Death Adder, a Geelong-based lizard breeder Mip Pugh said she had tested Yakult. Yakult is a fermented probiotic milk drink that contains a very high concentration of a bacterium called Lactobacillus casei (Shirota strain). She had used it on Bearded Dragons (Pogona vitticeps) that had regurgitated food without known reason.

She was uncertain if the product had helped the lizards, but it certainly had no side effects or adverse effects. The same probiotic was used once for the Death Adder (above), but not repeated on the basis that the snake's conditions seemed to be improving anyway.

Again no adverse effects were reported.

Following the successful rehabilitation of the Death Adder and conversations with other herpetologists about the problem solved, attention turned to other means to achieve the same result and the original problem.

While it is unlikely that the snake's original problem had been a die-off of it's beneficial gut flora, this was clearly the end problem and that likely to have caused it's death if left untreated.

In other words in terms of disease or diagnosis, this snake's problem had been a lack of gut flora. The treatment (that worked) was pallative care, including soft easy to digest food, controlled cool spots in the cage (warmer than otherwise allowed) IN COMBINATION with aggressive use of probiotics, the latter being essential.

It was also suggested that another way to administer probiotics to a snake affected like the Death Adder was, would be to force-feed the snake feces from a healthy snake.

This has not been trialled, but would also presumably work. The underlying question would be, which is the more effective method.

The major drawback of the fecal/oral route is the potential transmission of unwanted organisms and/or parasites.

Without sounding like a "new age" vegetarian pusher, the fact is that probiotic treatment may have wider applications in terms of reptile care than has been envisaged to date.

Several keepers and veterinarians have reported calcareous deposits, gut impactions and other problems, sometimes causing death in reptiles (mainly snakes).

These conditions have been blamed on various factors including ingesting substrates, poor choice of food and other reasons. However there has been little factual data to directly link one to the other, even if the substance being deposited reflects either the food or the substrate in terms of composition.

In my own situation, substrate has been of little importance in terms of reptile husbandry and in terms of food or substrate, what is unsuitable for digestion merely passes through or is regurgitated.

In terms of the Death Adder (above), it came close to death due to impaction from rodent bones. However the conclusion that rodents or their bones are unsuitable for the snakes would be patently false. Normally such material digests and dissolves in the gut of the snake (including all other Death Adders at the Hoser facility), making the failure to digest this material an issue for the snake itself and not as a result of a problem with the food per se.

(For the record, Tiger Snakes (Notechis) at the Hoser facility have been fed dog bones (sold as lamb riblets), which digest and dissolve completely in their guts).

Assuming probiotics can be used to restore proper digestive function to a Death Adder otherwise unable to digest bones, one would assume that probiotics could also be used to avert life-threatening gut impactions and accumulations in other reptiles.

Unfortunately such life-threatening conditions only appear in reptiles occasionally and often are only diagnosed after the reptile's death, when a post-mortem is undertaken.

However if and when such conditions as gut impactions, inability to digest "normal" foods, otherwise undiagnosable regurgitation problems, passing undigested food in feces, occur, then probiotic treatment should perhaps be trialled as a means to aid in effecting a recovery in the reptile. This is especially if there is no clear diagnosis of a problem and/or effective alternative treatments are lacking.

However as seen in the case above, probiotic treatment will rarely be of much use on it's own. Instead it must be a used as a part of a wider palliative regime, including a favorable temperature regime, feeding appropriately and supplementing if and when needed with vitamins, fluids and other material including perhaps treatment of some other underlying problem.

This is used for dogs, especially large breeds and it is questionable how wide it's application could be for reptiles.

Excluding those species that need sunlight for calcium metabolism, there are those reptiles that are generally fed whole food in order to get their requirements. That is, for example snakes eating whole mice and the like.

Lumps of raw meat (as in steaks) are high in protein and as a part of a snake's diet often has advantages over rodents if fed on some occasions as part of a 'balanced diet'.

It's high in protein per gram of weight and snakes gain condition far quicker on a diet of meat (if taken) than on an equivalent rodent diet. Hence it is exceptionally useful for fast growing reptiles or those which are failing to gain sufficient muscle tone and condition.

The downside of this is the lack of bone and calcium and hence the need to also retain whole food (rodents or similar) as part of the diet. Failure to do so may result in improper bone development and related health issues.

Calcium tablets are cheap, obtainable from chemists and supermarkets and may form an aid in terms of snakes fed diets high in meat but not bone. Another alternative is dog bones in the form of lamb riblets, which are also inexpensive and sold as offcuts by butchers and meat wholesalers.

Snakes here at the Hoser facility (Tiger (Notechis), Red-bellied Black (Pseudechis)) have been fed diets high in meat, with occasional riblets, calcium tablets and rodents and maintained for indefinite periods in immaculate condition on this diet. In terms of cost, this has worked out substantially cheaper than all rodent diets, which until now has been the preferred diet for most keepers.

Mip Pugh, Pete Whybrow, other Australian herpetologists and several veterinary surgeons who freely shared their ideas in terms of probiotic treatment of snakes and lizards.

Hoser, R. T. 1989. Australian Reptiles and Frogs. Pierson and Co. 238 pp.

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

Hoser, R. T. 2003b. Reovirus - Successful treatment of small elapids. Crocodilian 4(3):23-27.

Hoser, R. T. 2004. The husbandry and breeding of Death Adders. Reptiles. September.