Dr Sam Sweet on captive varanids and parasites
There is some very interesting information in an infrequently-cited short paper by Hubert Bosch (H. Bosch, 1999. Parasite burdens of monitors in captivity, pp. 189-192 in Horn & Boehme (eds.), Advances in Monitor Research II. Mertensiella 11). This paper reports necropsy findings on over 400 captive monitors of 26 species. Since the work was conducted between 1965 and 1985, it is likely that the vast majority of animals were WC, although they had been maintained in captivity for varying periods.
Over half (53%) of this sample had no detectable parasite burdens. Of the rest, 32% had nematodes either in the digestive tract (21%) or as filarial worms elsewhere in the body (11%). Tapeworms were found in 17%, and 12% had Entamoeba infections. Other endoparasites including coccideans, flukes, acanthocephalans and pentastomes were uncommonly found (each <4%). 21% of animals examined had two or more parasitic taxa present.
It is important to note that this survey did not consider blood parasites (such as malaria, hemogregarines or microfilariae), which can have important negative effects in wild lizard populations. However, it suggests that most gastrointestinal parasites are either uncommon or not of overriding concern in captive monitors. The only deaths ascribed to parasites in this study involved Entamoeba, but since most monitors harbor these pathogens anyway it seems that lethal infections were secondary to other causes.
A major distinction when thinking about parasites is between organisms that can directly reinfect captive monitors (protozoans, including amoebas and coccideans), and those that require at least one intermediate life history stage in some other organism. For the latter group, WC captives will have only the parasite loads with which they arrived, and most such infections will decline over time as adult parasites die off -- unless the animals are reinfected via their prey.
Parasites, bacteria, fungi and viruses also evolve, and are adapted to the physiology of particular hosts. The physiological differences between endotherms and ectotherms are quite broad, and unless an organism is already adapted to make such a transition as part of its life cycle the chances of spontaneous, novel transmission are quite small.
There are of course parasites whose life history stages begin in insects or snails, shift to frogs or lizards, and have birds or mammals as their definitive hosts. They have evolved specific tolerances to be able to do this. There are also organisms (such as Salmonella) that will live in almost any digestive tract (at that level, protein is protein, and poop is poop), and can be transmitted among very distantly related organisms. However, you appear to be asking about "emerging infectious diseases" (EIDs), things that make a jump to a novel host, rather than about things with longstanding life cycle features that involve multiple species.
There is a strong generalization in the evolutionary history of diseases and parasites that says that a well-adapted disease/parasite is one that is easily transmitted but does not kill its host. Things that kill you straightaway do not get transmitted to very many others, and so it is with things that are very hard to transmit. Success from the point of view of a disease organism or a parasite involves infecting the maximum number of hosts, and this goal is best achieved via low virulence. There is an ongoing arms race between parasite and host where each tries to outwit the other.
EIDs are examples of an initial stage in that process. Nipah, SARS, bird flu, Ebola, HIV, etc. are all recent "imports" from other endotherms into humans. Humans have not yet evolved effective resistance to these pathogens, and natural selection occurs by the mortality of that segment of the population least able to combat the toolkit of the pathogen. Notice that the known or presumed reservoirs for all of these diseases are other endotherms (mostly other mammals, particularly primates, bats and pigs) -- we haven't got "turtle flu" or "salamander rabies". Again, this is because human physiology shares a lot more with that of other mammals than of reptiles.
So, you should not worry about exterminating New York City if your sav coughs. What you should worry about are generic pathogens such as Salmonella (wash up, and do not drink monitor bath water).
What you should worry about even more is a principle of “Reptile EIDs”: just as humans can get nasty stuff for which we are unprepared from eating raw monkeys or sleeping in pig poo, your animals can get a variety of (usually unnamed and unrecognized) diseases and parasites from each other. Viruses that have low virulence in African monitors may be quite novel to Australian monitors and might kill them pronto; tegus probably have bugs that no monitor can combat and vice versa. You can’t be 100% safe (since some of the worst offenders may be asymptomatic in their normal hosts), but careful quarantine of new acquisitions and a general awareness of the need to keep it clean and to not switch furnishings around among cages will go a long ways towards preventing problems. More broadly, this is also why no one should release native species back into the wild if they have been exposed to related species from distant places.
Aside from protozoans, the gut parasites monitors get have complicated life histories involving intermediate hosts (ie a smaller animal such as an insect or mollusc picks up the parasite's eggs as it grazes and the eggs hatch into the intermediate form of the parasite in the insect/mollusc/whatever's body, then the monitor eats the host animal and the parasite transforms into its final form inside the monitor. While in the monitor it lays eggs, which are spread outside the monitor's body when it defecates. An insect/mollusc/whatever comes along and grazes where the monitor once defecated and gets infected with the parasite. And so on.
In other words, monitors can't get non-protozoan gut parasites from each other or from the eggs of other monitors. - David Kirshner