Ticks in Reptiles — Symptoms, Causes, Diagnosis, Treatment, Recovery, Management, Cost

Ticks in Snakes

Most Common Symptoms

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What are Ticks?

Ticks do more than just suck your snake’s blood; they can also transmit diseases such as sweating sickness, inclusion body disease (IBD), blood poisoning (which can all be fatal), and paramyxovirus, which can cause respiratory and central nervous system damage. Severe infestations can be lethal due to anemia (lack of iron in the blood) or respiratory failure. In the wild, ticks are commonly found on snakes and do not pose as big of a threat as those snakes that live in captivity. This is because in captivity, the ticks have no place to go and will set up a breeding colony in the cage or enclosure. Also, in captivity, your snake has no way to get away from the ticks as they do in the wild.

Ticks are ectoparasites that affect snakes and can cause various illnesses such as anemia (low iron), paralysis, and even death. There are two kinds of ticks that affect snakes which are soft (argasidae) and hard (ixodidae). Because ticks are rather large, you can usually see them before they start to create symptoms such as decreased appetite, behavioral changes, and lethargy. Your snake may be found spending a lot of time in the water bowl, trying to get rid of the pests. Ticks can spread many diseases such as tick-borne relapsing fever, anaplasmosis, Southern tick-associated rash illness (STARI), tick paralysis, American babesiosis, Colorado tick fever, tularemia, Lyme disease, and Rocky Mountain spotted fever.

Symptoms of Ticks in Snakes

Although you may see the ticks before your snake shows symptoms, there are signs you may notice, which are:

  • Aggravation or irritation
  • Excessive time in the water bowl
  • Lack of appetite progressing to refusal to eat
  • Weight loss
  • Abnormal behavior
  • Rubbing against objects
  • Not shedding like normal
  • Crusty or pitted scales
  • Hemorrhages (red spots on scales)
  • Anemia (excessive sleepiness, not eating, depression)


  • Hard ticks have 13 types and more than 650 species. This parasite will stick to its host for up to a month (or more) and can consume 200 to 600 times its weight.
  • Soft shell ticks have five types and over 150 species. These pests will stay on your snake for a shorter time than hard ticks (only a few minutes to several days) and can ingest about 10 times their body weight.

Causes of Ticks in Snakes

The cause of ticks commonly includes:

  • Overcrowding
  • Lack of handling and medical care
  • Unsanitary conditions
  • Transferral of ticks from owners

Diagnosis of Ticks in Snakes

Ticks are usually easy to spot so the veterinarian should have no trouble diagnosing your snake. However, the consultation will include a brief history of your pet and a physical examination, including vital signs such as heart rate, temperature, and respiration rate. Laboratory tests will also be needed to rule out transmitted diseases and infections. These usually include a complete blood count (CBC), serum biochemistry analysis, urinalysis, and fecal examination.

Treatment of Ticks in Snakes

You can remove the ticks yourself if you know the best way to do so. The proper way to remove a tick (other than letting your veterinarian do it) is to use tweezers or forceps to grab the pest by the mouth and pull slowly. Once you remove the tick, wipe the area with an alcohol pad and put the tick into alcohol to kill it. The veterinarian will likely do it for you if you ask, and will prescribe antibiotics to reduce the chance of infection due to bite wounds and transferrable pathogens from the ticks.

Treating the Snake Environment

You will need to remove your snake from the enclosure and place it somewhere safe while you disinfect the cage. The entire enclosure must be treated with a cyfluthrin product, especially in corners and crevices where the ticks can hide. Get rid of any hide boxes, logs, and other items made of wood because these are almost impossible to treat effectively. Let the cage air dry and then you can place your snake back in the cage.

Recovery of Ticks in Snakes

Your snake should be fine once your veterinarian removes the ticks and provides medicine if needed. If your snake has any complications from the tick bite, the prognosis may be different, but with prompt treatment from a veterinary professional that specializes in reptiles, chances of successful treatment are good. Keep treating the cage once a week for several months to prevent reinfestation from breeding colonies.


Mites in Reptiles

In the first issue of REPTILES magazine, I wrote an article on mites and ticks. I mentioned several suggestions for treating these ectoparasites. A young reader over interpreted one suggestion, and using the old adage that if a little is good, a lot is better, he killed his pet lizard. This was a sad situation. To make things worse, his father, an attorney, tried to sue me. Fortunately, he did not win. But he did bring it to the forefront that his son was not the brightest kid on the block.

douglas mader, DVM

This Burmese python was covered with so many snake mites that the mites were leaving the host and invading the cage.

Mites can be both a nuisance and a costly problem in any reptile collection. Once the ectoparasites have been identified, they can be treated, but it can be a challenge.

There are more than 250 different species of mites that parasitize reptiles. The three most commonly encountered are the snake mite (Ophionyssus natricis), the lizard mite (Hirstiella trombidiiformis) and the chigger mite (also known as grain mites, in the family Trombiculidae). Most adult mites are hematophagous, meaning that they suck blood, but the chigger mite is only parasitic in its larval form.

Acariasis is the term for an infestation with mites (and ticks), and is commonly associated with unsanitary cage conditions, poor husbandry practices, and recent imports or acquisitions. Mites commonly enter a collection arriving on newly acquired animals that have not been quarantined properly. Once established in a cage, mites quickly spread to other animals.

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It should be pointed out that mites are found in both captive and wild populations. However, in captivity, where the parasites are confined to a limited space, their concentrations increase dramatically. In the wild, the parasites will disperse, thus the host is not so heavily affected.

Mites are capable of causing serious problems in captive reptiles. Heavy infestations of mites can consume a large enough quantity of blood from their reptilian host to cause a potentially life-threatening anemia.

The snake mite has been implicated as a vector for various infectious disease-causing agents in reptiles, such as Aeromonas hydrophila, Leucocytozoon and certain hematozoa. Aeromonas hydrophila is a bacteria commonly associated as a cause of pneumonia and infectious stomatitis, or mouth rot, in snakes. There has also been speculation that mites may be involved in the transmission of inclusion body disease of boid snakes.

Also worth noting, there has also been one report of the snake mite causing skin disease in humans.

Mite infestations are usually quite obvious. In the worst case scenario, the reptile will have mites visibly crawling all over the body. Mites vary in color, depending on the species and how recently it has taken a blood meal. The snake mite may be either black or tan, depending on the sex of the mite and its age. The lizard mite and the chigger are usually red to orange in color.

Mite-infested animals will usually have a dull, lackluster appearance. The mites tend to accumulate in areas of the reptile’s body that afford the most protection from the environment, including under the chin, or gular folds in snakes; the eardrums of lizards; under the scutes, the peri-ocular regions around the eyes and inside the skin folds around the cloaca.

Female mites lay eggs (up to 90 in number), off of the host, and in the cracks and crevices of the terrarium. This is why cleaning the infested animal’s environment is so important in mite control.

Treat animals severely debilitated from concurrent disease, or from a mite-related anemia with resulting weakness, first before attempting to treat the mites. If a snake is anemic and dehydrated from blood loss, it would be prudent to have a veterinarian administer fluids or perform a blood transfusion, if necessary, prior to treating the animal for mites. It is also a wise idea to start the animal on antibiotic therapy because mites can potentially carry many reptile diseases.

Mites and ticks can cause havoc in any reptile collection. The parasites are easily diagnosed and, with the right plan, can be exterminated. Given that some of the suggested treatments can be just as toxic to the patient as they can be to the pests, it is wise to get advice from someone with experience before trying to treat your animals by yourself the first time. And whatever you do, don’t sue your veterinarian if you don’t follow instructions.

Douglas R. MADER, MS, DVM, DABVP (REPTILE/AMPHIBIAN), is a graduate of the University of California, Davis. He owns the Marathon Veterinary Hospital in the Conch Republic, and is a world-renowned lecturer, author and editor. He sits on the review boards of several scientific and veterinary journals.


Parasitic Diseases of Reptiles

, BVetMed, DZooMed, DACZM, DECZM (herpetology), FRCVS, University of Georgia

Ophionyssus natricis (common snake mite).

Courtesy of Dr. Stephen Divers.

Orange Hirstiella mites located in the inguinal fold of an iguana.

Courtesy of Dr. Stephen Divers.

Embryonated ova from a black-headed Timor python characteristic of both Rhabdias and Strongyloides (100X), If viewed carefully, the larva within the egg can often be seen moving.

Courtesy of Dr. Stephen Divers.

Rhabdias/Strongyloides larvae found in fresh feces. It is virtually impossible to differentiate these two parasites except by clinical history. Rhabdias is primarily a parasite of the respiratory system, and Strongyloides a parasite of the GI tract. Fortunately, they are easily treated with the same anthelmintics.

Courtesy of Dr. Stephen Divers.

Hookworm ( Kalicephalus spp) ova from a blood python (100X).

Courtesy of Dr. Stephen Divers.

Entamoeba invadens trophozoite (left) and cyst (right) (1,000X oil immersion).

Courtesy of Dr. Stephen Divers.


A limited number of ectoparasites are seen, except on wild and newly acquired reptiles. Mites are distributed worldwide, and most reptilian species are affected. Reduced vitality and, in heavy infestations, death due to anemia may occur. Skin of affected reptiles appears coarse, and dysecdysis is frequent. The common snake mite (Ophionyssus natricis) and lizard mite (Hirstiella spp) are generally permethrin is specifically licensed for use in reptiles, and ivermectin is also frequently effective in squamates.

Ticks are common on reptiles, and heavy infestations may result in anemia. Argasid ticks may cause paralysis, with muscle degeneration at the site of the bite. The transmission of green-lizard papilloma–associated virus, several hemogregarines, and the filarid worm Macdonaldius oscheri have been associated with ticks. Ticks can transmit Ehrlichia ruminantium, the cause of heartwater, and consequently the importation of African reptiles has been controlled. Ticks can be removed manually or by using permethrin spray. Systemic antibiotics are often indicated because of systemic infections associated with multiple cutaneous bite wounds and, potentially, with transmission of pathogenic bacteria.

Leeches have been found on the legs, head, neck, and in the oral cavity of a variety of turtles and crocodilians.

Chelonians frequently have cutaneous myiasis. Bot flies (including Cuterebra sp) create a cutaneous wound in which to lay their eggs, which hatch into bots that live in cyst-like structures until mature enough to leave the wound. These lesions are characterized as a lump under the skin; on closer inspection, they have an opening often lined by a black, crusted material. Treatment consists of slightly expanding the natural opening and manually removing the bot with a forceps. The wound is then flushed with povidone-iodine , chlorhexidine, etc, and an antibiotic ointment is instilled. Systemic antibiotics are indicated in reptiles that have multiple lesions. Cutaneous myiasis also occurs secondary to existing wounds, and maggots must be manually removed and the underlying lesion treated with topical and systemic antibiotics as needed. During heavy fly season, turtles often are housed indoors or with screens over their enclosures to offer some protection.

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Ectoparasite infestations are best prevented by thorough screening and quarantine of all new animals entering a collection.


The stress of captivity coupled with a closed environment predisposes to heavy burdens of parasites with direct life cycles. Every effort must be taken to rid reptiles of parasite burdens and the environment of intermediate hosts.

Pathogenic trematodes infect the vascular system of turtles and infect the oral cavity, respiratory system, renal tubules, and ureters of snakes. Chemotherapeutic agents have not effectively eliminated these parasites, although praziquantel has shown some promise.

Tapeworms are found in all orders of reptiles but are rare in crocodilians. Reptiles may act as the definitive, paratenic, or intermediate hosts for a large number of species. Although most species of tapeworms are generally nonpathogenic in wild reptiles, weight loss and death have been reported. The complex life cycle of cestodes and restricted geographic range of intermediate hosts limit the number of cases in captive reptiles. When present, proglottids may be found around the cloaca, or typical cestode ova may be isolated from feces. Treatment is with praziquantel , repeated in 2 wk. Plerocercoids of the genus Spirometra may be found as soft swellings in the subcutis. These larval stages may be removed surgically.

Nematodes are found in all orders of reptiles, and several genera are important. Strongyloides spp frequently inhabit the intestinal tract of reptiles; larvae are seen in the respiratory tract and respiratory exudate. In snakes, the larvae have been seen within granulomas distributed throughout the body wall, suggesting that the larvae may be able to penetrate the skin. Overwhelming parasitism is common when poor hygiene results in highly contaminated environments. Rhabdias and related species have been found in the lungs of a variety of snakes; embryonated ova may be found in the oral cavity and in lung aspirates. Embryonated ova and free larval forms may be seen in the feces. Larvae resembling Rhabdias also have been seen in the gingiva of snakes with stomatitis. Infections often are subclinical but may be associated with secondary bacterial pneumonia. In severe cases, death may result.

Stomach worms of the genus Physaloptera are seen in lizards. Gastric ulceration may occur in severe infections. Ova are elliptical and may be embryonated. Numerous snakes are infected by Kalicephalus spp. This hookworm, capable of transcutaneous infestation, prefers the upper GI tract and causes erosive lesions at sites of attachment. Ova are similar to those of Physaloptera spp. Large granulomas caused by the above species have also caused GI obstruction in snakes.

Ascarids frequently infect reptiles. Ova are similar to those of ascarids from mammalian hosts. Severe lesions and death may be seen in infected snakes. Clinically infected snakes frequently regurgitate partially digested food or adult nematodes and are anorectic. The major lesions are large granulomatous masses in the GI tract; they may abscess and perforate the intestinal wall.

Many other nematode species may be found in reptiles. Capillarid, trichurid, and oxyurid ova may be found on fecal examination. The nonpathogenic larval and oval forms of parasites of prey items (eg, Syphacia obvelata, the mouse pinworm) may be found when infected prey is consumed. Treatment should be attempted when evidence of parasitism is present.

Some larval forms of nematodes are suspected or confirmed to penetrate the skin (eg, Strongyloides and Kalicephalus), bypassing the oral reinfection route. The subtle nature of reinfection by this route often goes unnoticed until the reptile is overwhelmed by parasites. Close attention to the immediate removal of excreta and fastidious sanitation help reduce parasite burdens in captivity.

Dermal lesions caused by the spirurid worm Dracunculus spp may be seen. Numerous species of spirurids infect the mesentery, coelomic cavity, and blood vessels. These worms require a mechanical vector, so their incidence is reduced in captive-bred reptiles or in reptiles that have been in captivity longterm. Treatment consists of increasing the environmental temperature to 95°–98°F (35°–37°C) for 24–48 hr. However, some “cool-adapted” reptiles may not tolerate this treatment.


Pentastomes are found in a wide variety of reptiles, with variable pathogenicity. Pentastomid infections are occasionally associated with pneumonic signs, but these primitive arthropods can inhabit any tissue, and symptoms will vary with their migration path and tissues responses. Pentastomes were initially found primarily in tropical poisonous snakes; however, as more necropsies on reptiles were performed, more were found. Necropsy results from 88 bearded dragons showed that 11 were infested with pentastomes. No truly effective treatment has been reported, but praziquantel at dosages of 8 mg/kg and ivermectin at 5–10 times normal dosages have been shown to reduce ova numbers being shed but have not eliminated the worms. The most novel approach has been to endoscopically locate and mechanically remove all the adult pentastomes. Recognition of pentastomal infestations is important, because these parasites are thought to present a zoonotic risk.

Protozoal Diseases

Numerous protozoans are found on reptiles; most are harmless commensals. The most serious protozoal pathogen of reptiles is Entamoeba invadens. Clinical signs are anorexia, weight loss, vomiting, mucoidal or hemorrhagic diarrhea, and death. Entamoebiasis may be epidemic in large snake collections. Herbivores appear less susceptible than carnivores; a number of reptiles that seldom become affected or die can serve as carriers, including garter snakes, northern black racers, and box turtles. Although most turtles are resistant, the giant tortoises are susceptible. Other resistant groups include eastern king snakes, crocodiles, and cobras (possibly as an adaptation that allows them to eat snakes). Most boas, colubrids, elapids, vipers, and crotalids are highly susceptible. Transmission is by direct contact with the cyst form. Hepatic abscesses containing numerous E invadens trophozoites are common in chronic cases. At necropsy, gross lesions may extend from the stomach to the cloaca. The intestine shows areas of ulceration that tend to coalesce, caseous necrosis, edema, and hemorrhage. Multifocal abscesses in a swollen, friable liver are seen in the hepatic form. Identification of trophozoites or cysts in a wet preparation of fresh feces or tissue impressions, or in histologic sections, is diagnostic. Turtles and snakes should not be housed together.

E invadens is best treated with metronidazole . Tetracycline and paromomycin have been used but are considered ineffective against the hepatic form. Strict sanitation and hygiene measures should be observed.

Flagellates, especially Hexamita spp, have been reported to cause urinary tract disease in chelonians and intestinal disease in snakes. The “Giardia” seen in some cases of enteritis in snakes may actually be Hexamita or one of the relatively nonpathogenic flagellates that inhabit the intestinal tract of snakes. Differentiation between the species requires expertise, and special preservatives and stains are required to identify most of these organisms. Metronidazole has been used to treat flagellates. Indigo snakes, king snakes, and uracoan rattlers should be treated at the low end of this dosage range. Early studies with benzimidazoles are very encouraging and should also be considered as a viable therapy.

Several coccidial organisms have been reported: Klossiella from the kidney, Isospora from the gallbladder and intestine, and Eimeria from the gallbladder. The severity of disease varies with the coccidia and affected species. Because of their direct life cycle, these parasites can increase to tremendous numbers, especially in immunosuppressed reptiles. Oocysts are not fragile and can survive for weeks in a dessicated condition. Fastidious, daily cleanings are necessary to remove all feces and feces-contaminated food and water. Insects and other food items must be removed on a daily basis, because they are another source of contamination (eg, crickets may eat the oocysts while gathering fluid from the feces). Persistent treatment using sulfadimethoxine is required until infection is resolved, often taking 2–4 wk; success should be measured by serial fecal samples.

Trimethoprim -sulfa is another useful drug to treat coccidia. Care should be taken when using sulfa in reptiles with dehydration or renal compromise. If in doubt, a balanced electrolyte solution should be administered PO at appropriate dosages. Even under the best conditions, treatment will eliminate coccidia in only 50% of cases. Treatment resulting in a reduction of coccidia is still important, and coccidial numbers should be periodically monitored.

Plasmodial (malarial) organisms, as well as other intracellular blood protozoans, have been reported in reptiles. Their significance is unknown, and treatment is not considered necessary.

Cryptosporidiosis is frequently reported in association with postprandial regurgitation (snakes, Cryptosporidium serpentes), diarrhea (lizards, Cryptosporidium saurophilum), marked weight loss, and chronic debilitation. The organism affects the GI mucosa, resulting in marked thickening of the gastric rugae and loss of segmented motility. A mass in the gastric region is often, but not always, palpable in snakes, and contrast radiographs or endoscopic examination reveals rugal thickening. Many lizards, including Old World chameleons and savannah monitors, are affected primarily in the intestine. Mucosal thickening develops as a result of invasion by numerous cryptosporidial organisms. Diagnosis can be made using acid-fast stains on fresh feces or on the coating from regurgitated items or endoscopic gastric biopsies, which will identify the tiny oocysts. Although several treatments have been suggested, none (except for hyperimmune bovine colostrum) have been consistently effective. Intensive supportive care will often stabilize and help prolong the life of the affected reptile. Euthanasia is a valid option for infected reptiles. Cryptosporidiosis was previously considered a zoonotic disease; however, it now appears that the species commonly found in reptiles do not affect mammals.


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Figure 21.2 Ecdysis in a corn snake ( Pantherophis guttatus guttatus ).

When the separation fails to occur, whether in part or totally, the condition is known as dysecdysis.

Dysecdysis is when ecdysis fails. It occurs in snakes, and to a lesser extent, lizards.

The causes of dysecdysis are many and varied, but can include any condition which can cause dehydration so reducing lymphatic fluid available to separate the skin layers. If the reptile is malnourished, dysecdysis may occur due to a lack of proteolytic enzymes. Alternatively old scars, a lack of an abrasive surface in the vivarium upon which to start the process or severe ectoparasitism may also cause dysecdysis.

Scale rot is a colloquial term for a range of conditions affecting the reptile skin which result in severe infections.

Septicaemic cutaneous ulcerative disease

Septicaemic cutaneous ulcerative disease (SCUD) is seen in aquatic chelonians. Citrobacter freundii has been implicated which, once it has gained access to the bloodstream, produces ulcers in the skin and loosening of scales with debilitation and, in many cases, death. Other bacteria such as Pseudomonas and Aeromonas are also involved (Figure 21.3).

Figure 21.3 SCUD in a red-eared terrapin, Trachemys scripta elegans .

This is a form of scale rot seen in semi-aquatic species such as garter or water snakes. It can, however, occur in any species which is exposed to a persistently damp substrate. The outer layer of skin develops blisters of a clear fluid which become secondarily infected with environmental bacteria such as Aeromonas spp., Serratia spp., or Pseudomonas spp. These can progress to septicaemia. Occasionally these conditions may involve a fungus such as Aspergillus spp.

Reptile abscesses have recently been quoted as being more accurately termed fibriscesses (Huchzermeyer & Cooper, 2001). Instead of liquid pus, reptiles and birds form solid, caseous, dried pus surrounded by a thick shell of fibrous tissue. This is due to the lack of lysozymes and the secretion of huge amounts of fibrin into the abscess (Figure 21.4). These may form anywhere, but a common site in chelonians is the middle ear, causing a bulging of the ear drum (Figure 21.5). The pathogens involved are frequently Gram-negative species, although the presence of fungi has been well recorded.

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Figure 21.4 Dysecdysis in a green iguana ( Iguana iguana ).

Figure 21.5 Aural abscess in a spur-thighed tortoise ( Testudo graeca ).

Erythema, petechiae and ecchymoses

These three conditions may all be present at the same time or may appear individually.

Erythema is the reddening of skin tissues due to vascular congestion beneath. It can be seen in reptiles as a pink hue to the areas between scutes in the case of chelonians (Figure 21.3) and crocodilians, or the more generalised reddening of the skin seen in snakes. Erythema is often suggestive of septicaemia.

Petechiae are pin-point subepithelial haemorrhages. They can be seen in the mouth, where they are often associated with oral infection such as ‘mouth rot’. They may be seen over the body suggesting septicaemia. Other conditions producing petechiae include clotting deficiencies, for example, consumption of rodent prey which has itself consumed a warfarin-type poison.

Ecchymoses are larger areas of haemorrhage, and may be caused by severe local infection disseminated intravascular coagulation (DIC) or conditions mentioned above.

Overgrown beaks and claws

Overgrown beaks are common in chelonians, and are often due to a lack of abrasive foodstuffs or abrasive surfaces from which to eat them.

However, it should be noted that some species have perfectly normal apparently ‘long’ claws. An example is the male red-eared terrapin, which uses its claws as a display aid to attract and mate the female.

An example of a physiologically normal colour change is seen in the Chamaeleonidae which will often darken in colour as they become stressed. Green iguanas often become yellow brown in colour as they become stressed or unwell, bearded dragons often become dark coloured and many of these species will exhibit darkening at the site of an injection. Areas of previous trauma may become whitened.

The snake mite, Ophionyssus natricis appears as red to dark-coloured pin-head mites hiding under the overlapping edges of scales. They may be seen in water dishes in which the reptile has been bathing. They can cause severe irritation, pruritus and self-trauma, as well as causing anaemia and dysecdysis. In addition, they can transmit Aeromonas spp. bacteria, which may cause septicaemia and viruses, for example, inclusion body disease (IBD). Other mites include the cloacal mites of aquatic turtles of the family Cloacarus spp. In addition, there is of course the non-parasitic harvest mite or Neotrombicula autumnalis , which may be brought in on straw and hay bedding material. The adult itself is not an irritant but the six–legged larval stage is and may cause the reptile to traumatise itself.

In the United Kingdom, Ixodes ricinus (the sheep or deer tick) and Ixodes hexagonous (the hedgehog tick) are seen. In tortoises, these are naturally the areas around the neck inlet and in front of the hind legs. They may cause local damage and can transmit pathogens. These include bacteria ( Staphylococcus aureus , the cause of tick pyaemia and Borrelia burgdorferi , the cause of Lyme’s disease) as well as haemoparasites and viruses. Some of the soft-bodied ticks ( Amblyomma marmoreum and A. sparsum ) have been implicated in the transmission of Cowdria ruminantium the cause of heart water disease in mammals. These ticks are common on wild-caught imported reptiles.

Myiasis is a problem for any reptile kept in insanitary conditions or those with diarrhoea. Members of the blue bottle, black bottle and green bottle families are all capable of laying eggs on a tortoise. In peak conditions these can hatch into larvae or maggots within 1–2 hours. These then burrow away from the light, into the body of the tortoise causing severe trauma, infections, shock and ultimately death.

Leeches tend not to be such a problem in the United Kingdom, but can affect aquatic species all over the world. The family Annelidae are the most dangerous, and cause large wounds which continue to bleed after the leech has detached. These may then become secondarily infected. They can also transmit haemoparasites, bacteria and viruses.

Traumatic and spontaneous damage

Traumatic damage can be due to attacks by predators or other reptiles, for example, males fighting over a female. In some species, for example, green iguanas, the male mounting the female during mating bites the shoulder area vigorously, causing open wounds. Dog attacks are common in tortoises (Figure 21.6). In the United Kingdom, it is unlawful to feed live vertebrate prey to any animal; but invertebrate live prey can be offered and these can still cause trauma to a sick or anorectic reptile. Unprotected heat sources frequently cause severe burns.

Figure 21.6 Dog bite wounds are common in juvenile tortoises.

In some chelonians, scutes may be seen to lift off, often weeping clear fluid beneath them. This is frequently associated with underlying renal disease.

Iatrogenic causes of skin damage are also seen in some reptiles such as chelonians. This can occur after over-administration of vitamin A, which can cause sloughing of the epidermal layer on the head, neck and limbs, exposing the underlying dermis.

Fibrosarcomas and squamous cell carcinomas of the head are seen in lizards and snakes. Melanomas are also seen in pigmented species such as the bearded dragon ( Pogona vitticeps ). Viral-induced fibropapillomas are frequently seen in green turtles ( Chelonia mydas ), where herpesviruses have been implicated. Another herpesvirus is a common cause of ‘grey-patch disease’ in this species, where circumscribed papular grey lesions appear over the whole body. In addition, papillomata have been regularly reported in Lacertidae (sand, wall and emerald lizards), occurring over the dorsum of the individual lizard.

Bacteria associated with skin problems

Gram-negative bacteria can cause skin abscesses, septicaemia and areas of skin sloughing. Others such as Mycobacteria spp . may be seen associated with the appearance of classical tuberculous lesions. The mycobacteria found are more commonly environmental ones, for example, Mycobacterium marinum (Girling & Fraser, 2007) and Mycobacterium chelonae , rather than the human or cattle TB organisms.

Dermatophilus congolensis has been associated with skin disease in a number of lizards and snakes and D. chelonia e has been isolated from captive chelonians (Masters et al. , 1995).

Dermabacter spp. related bacteria have been associated with a proliferative cheilitis syndrome in Agamid lizards (Koplos et al. , 2000). This has also been seen to cause proliferative lesions around the cloaca and over the legs (Pasmans et al. , 2010) and is now thought to be due to the bacterium Devriesea agamarum. Gram-negative bacterial infections of the hind feet of Savannah monitor lizards seems to be another common condition and is associated with an overly abrasive and damp substrate leading to foot abrasion and secondary infection (Stahl, 2003).

The incidence of fungal infections in reptiles has been quoted between 0.4% (Austwick & Keymer, 1981) and 4% (Jacobson, 1980). These include: Aspergillus spp. (Austwick & Keymer, 1981; Tappe et al. , 1984; Girling, 2002; Girling & Fraser, 2009); Mucor spp. (Lappin & Dunstan, 1992; Heatley et al. , 2001); Paecilomyces spp. (Heard et al. , 1986; Schumacher, 2003; Diaz-Figueroa et al. , 2008); Candida albicans (Austwick & Keymer, 1981; Migaki et al. , 1984); Fusarium spp. and Chrysosporium spp. (Austwick & Keymer 1981; Schumacher 2003); Sporothrix schenckii, Pestalotia pezizoides and Geotrichum candidum (Cheatwood et al. , 2003); Beauveria bassiana (Gonzalez Cabo et al. , 1995); Penicillium griseofulvum (Oros et al. , 1996); Alternaria spp. (Rossi & Rossi, 2000); Cryptococcus spp. (Hough, 1998); Scolecobasidium humicola (Weitzman et al. , 1985) and the primary fungal pathogen the Chrysosporium anamorph of Nannizziopsis vriesii (CANV) in bearded dragons, brown tree snakes and chameleons (Pare et al. , 1997; Nichols et al. , 1999; Bowman et al. , 2007; Abarca et al. , 2009). CANV produces the so-called ‘yellow skin disease’ of bearded dragons and may be fatal to a wide range of reptiles (Figure 21.7).

Figure 21.7 CANV fungal infection in a Boa constrictor is frequently fatal.

Many of these fungal infections appear to enter the reptilian body via the skin (Austwick & Keymer, 1981). With increasing use of antibiotic therapy in pet reptiles and the discovery of new fungal species associated with disease (e.g., CANV), the incidence of fungal disease appears to be on the increase (Fraser & Girling, 2004).

There are more and more cases of viral associated disease being diagnosed in reptiles each day. Herpesviruses causing grey patch disease have been found in turtles, papilloma viruses in lizards, and pox viruses in caimans (a member of the family Crocodylia).

Many species exhibit scale and skin abnormalities. These vary from cleft palates, to failure of scales to develop at all. In addition, many colour variations have been specifically bred for.

This has been diagnosed in green iguanas and corn snakes, although it is rare. It is associated with an increased turnover of skin and so an increase in ecdysis. It may also be associated with loss of dorsal spines in iguanas, tachycardia, increased aggression, polyphagia and weight loss overall (Hernandez-Divers et al. , 2001). Normal thyroid reference ranges are difficult to find, but 0.21–6.78 nmol/L have been reported for Calotes and Sceloporus lizards.

This has been reported in giant chelonia (Frye, 1991). It may also be due to the presence of goitrogens in the diet such as brassicas. Myxoedema and heart failure are the most commonly seen clinical signs.

Reptiles can sense pain but do not appear to respond to thermal pain in the way that birds and mammals do; that is, they do not remove themselves from the heat source even when it is resulting in severe burns. Unprotected heat lamps which allow reptiles close contact are dangerous, as are so-called ‘hot-rocks’ when the thermostat breaks. Full skin thickness burns and even death of the reptile are not uncommon (Figure 21.8).

Figure 21.8 Full skin thickness burns can be seen where heat lamps are left unprotected as in this monitor lizard.

This is mainly seen in aquatic chelonians and chameleons. The presenting signs include ocular oedema, xerophthalmia, middle ear abscessation, hyperkeratosis, lethargy and anorexia. It is preferable that vitamin A supplements should be given orally to minimise toxicity. Values of 200 IU/30 g bodyweight have been quoted dosed twice, 7 days apart (Harkewicz, 2001).

This can occur if parenteral vitamin A is given in doses exceeding 10,000 IU/kg. Initially it presents as dry skin, but may progress to whole skin sloughing. Management is as for thermal burns.

This has been reported by Frye (1991) as resulting in spontaneous splitting of the skin in anorexic/cachexic pythons and may be associated with a collagen defect. Injections of 10–20 mg/kg vitamin C per day are advised.

This has been reported in caimans and other reptiles which eat marine fish. The presence of free radicals in oily frozen marine fish can result in a relative vitamin E deficiency which can lead to steatites, skin sloughing, and necrosis of fat and secondary infections. Dietary supplementation with vitamin E at 1 IU/kg until resolution of signs is recommended.

This may be seen in reptiles which consume large amounts of eggs, such as some snakes and monitor lizards. Unfertilised eggs contain avidin, an anti-vitamin to biotin which may lead to a relative deficiency. The main signs are neurological, but fracturing and splitting of keratin structures such as scales and claws and beaks along with abnormal sloughing may be seen. Removal of eggs from the diet results in a cure in most cases.

This can result in shell deformities in chelonians. See the section on musculoskeletal diseases for further information. In addition, calcinosis cutis and circumscripta have been reported in reptiles with multifocal crusting and thickened skin which can then ulcerate. These two conditions are often related to calcium imbalances – more often hypercalcaemia, but also to areas of skin damage.

‘Mouth rot’ is the colloquial term for stomatitis, commonly seen in many reptiles particularly in snakes and chelonians.

The causes are many and varied. It can be caused by secondary infections with Gram-negative bacteria. The initial cause of the damage can be rubbing of the snout on vivarium glass, particularly in snakes. The use of opaque tape stuck to the outside of the glass helps the snake to ‘see it’, preventing this injury.

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Stomatitis may also be due to the overzealous force-feeding of anorectic reptiles, to other disease or stresses leading to reduced immune system function. Uric acid crystals deposited around the base of the teeth, due to visceral gout and renal failure can allow infections to occur. Herpesvirus and iridovirus infections in terrestrial tortoises are also a cause with oral ulceration and diphtherisis. Lytic agent X – a suspected virus – has also been associated with upper digestive tract lesions in chelonia. Devriesea agamarum, a bacterium, has been reported in agamid lizards as a cause of proliferative cheilitis, pericloacal disease and dermatitis.

Diagnosis is made on impression smears and bacterial swabs of samples. A polymerase chain reaction (PCR) for diagnosing chelonian herpesvirus has been produced at the RVC London, and reptile cell lines are available through the AHVLA Weybridge to attempt virus isolation.

Alternatively, electron microscopy of samples may aid the diagnosis.

Herpesvirus may also affect the central nervous system and organs such as the liver, kidneys and gonads. Depression and neurological signs are possible.

This is particularly common in Agamidae and Chameleonidae which possess acrodont teeth. These teeth are not replaced when lost during the course of the lizard’s life. This is as opposed to pleurodont teeth (e.g., the Iguanidae) where the teeth are continually replaced. If inappropriate food is provided, such as soft fruit, which adheres readily to the teeth and rots, periodontal disease will develop. As the species with acrodont teeth cannot shed and replace the teeth, infection, often with osteomyelitis ensues.

Vomiting and regurgitation

In snakes, regurgitation may simply occur due to rough handling, particularly soon after the snake has eaten. Snakes will also regurgitate if fed, or force-fed and then kept at sub-optimal environmental temperatures. Lizards and chelonia rarely vomit.

Parasitic causes of vomiting and regurgitation

In snakes, one of the most important stomach diseases is cryptosporidiosis due to a single-celled parasite, Cryptosporidia serpentes , which invades the outer membrane of cells lining the stomach. With time, it causes a thickening of the stomach, narrowing the lumen and so reducing its elasticity and digestive powers and causing vomiting. In lizards, cryptosporidiosis mainly affects the intestines, making vomiting less likely. Cryptosporidiosis was implicated in an outbreak of vomiting in juvenile Hermann’s tortoises (McArthur et al. , 2004). It is therefore currently thought that there is a lizard-, snake- and chelonian-specific form of Cryptosporidia spp.

Diagnosis is made on clinical signs and demonstrating oocysts shed in the faeces or recovered from a stomach wash, or biopsy of the stomach wall. In snakes, the course of the disease can vary from 4 days in severe cases to 2 years in chronic ones. Externally, the snake often shows signs of a mid-body swelling, due to the thickening of the stomach wall. The parasite is passed directly from one snake’s faeces or regurgitated fluids to another. The condition is difficult to treat and frequently results in the death of the snake (Figure 21.9).

Figure 21.9 Cryptosporidiosis is a common cause of swellings in the stomach of snakes.

Other forms of parasitism may cause vomiting or regurgitation in snakes. For example, Kalicephalus spp. (the snake hookworm), which may cause extensive ulceration of the digestive system; ascarids; and in the python family, the tapeworm Bothridium spp., have been reported.

Bacterial and fungal causes of vomiting and regurgitation

Bacterial and fungal infections, granulomas and abscesses may also cause damage to the stomach, or pressure on it, and so lead to regurgitation or vomiting.

Viral causes of vomiting and regurgitation

Inclusion body disease, a retrovirus, has been associated with chronic regurgitation in boids although there are usually other clinical signs such as respiratory disease and neurological disease.

Stomach tumours, for example, gastric adenomas and adenocarcinomas, have been reported and may cause swelling.

Parasitic causes of intestinal disease

Species involved include the hookworm Kalicephalus spp.; ascarids; strongyles such as Strongyloides spp.; and tapeworms such as Bothridium spp. in pythons; and Ophiotaenia spp. in garter and water snakes.

Entamoebiasis caused by the single-celled parasite Entamoeba invadens can cause diarrhoea in snakes. Its life cycle is direct; that is, spread directly from one reptile to another. After incubating in the lining of the small intestine, each infective cyst produces eight uninucleate amoebae which invade cells lining the large intestine of the same snake. The amoebae may also penetrate into the blood stream and so end up in the liver, causing necrotising hepatitis. Diagnosis is by finding the small amoebae or cysts in the faeces (× 400 magnification is required).

Other single-celled parasites of snakes include the flagellate family, (e.g., Trichomonas spp.). Symptoms again include large bowel distension with fluid and gas, diarrhoea and increased thirst.

The ascarid family, for example, Angusticaecum spp. (10–20 cm in length!) is most significant. Oxyurid pinworms may be asymptomatic, but some may be large enough to debilitate a tortoise, particularly prior to and subsequent to hibernation. Roundworms are passed directly from chelonian to chelonian in the faeces in the infectious egg form, and may be diagnosed by the detection of these eggs in a faecal smear.

The most important group of intestinal parasites of Chelonia is the flagellate family. These include Trichomonas and Hexamita spp. The symptoms produced are rapid in onset and include anorexia, occasionally diarrhoea and frequently, the passage of undigested food in the faeces. There is often polydipsia, due partly to the inability of the damaged intestines to absorb water, and partly, in the case of Hexamita parva , due to kidney damage, as this organism migrates up the ureters from the cloaca into the kidneys. Diagnosis is made by viewing the very fast-moving organisms microscopically using × 400 magnification, although a fresh faecal specimen is required. Transmission is faeco-oral. The prognosis may be extremely poor for any chelonian severely parasitised by this organism, due to its ability to cause irreparable damage to the intestinal mucosa.

Another family of motile protozoa afflicting Chelonia are ciliates such as Balantidium coli and Paramecium spp. They may be seen normally in the stool of healthy animals, but they may be present in such large numbers as to cause weight loss and intestinal damage.

Entamoeba invadens has caused large intestinal and hepatic disease in herbivorous chelonians. However, this condition is less common than in snakes.

As mentioned, Cryptosporidia spp. can affect the small intestine and stomach of chelonia, and has been implicated in pancreatitis as well.

Oxyurid nematodes are common. Due to the direct life cycle of these parasites, levels may become very high enough to produce intestinal damage and debilitation. Diagnosis is by finding the eggs in the faeces (Figure 21.10).

Figure 21.10 Oxyurid nematode infections are common in reptiles and may be diagnosed by finding these classical eggs in the faeces.

The coccidian family are also important parasites in lizards, particularly geckos and chameleons. Clinical signs include anorexia, weight loss, diarrhoea, dysentery and general debilitation. Isospora amphiboluri is a cause of stunting and runting in bearded dragon neonates. Diagnosis is by finding the typically isosporean oocysts in the faeces, and disease spread is direct.

Intestinal cryptosporidiosis is a problem in geckos. Symptoms include weight loss, diarrhoea and anorexia and typically affect young hatchlings that basically fail to thrive. The pathology has been described above.

Entamoeba invadens may also be seen in carnivorous lizards, producing colic and progressive weight loss with diarrhoea.

Bacterial causes of intestinal disease

In all species, but particularly snakes and chelonians, members of the zoonotic family Salmonellae are commonly recovered. Current advice is that providing they are not causing clinical disease, no antibiotics should be given. This is to prevent antibiotic resistance, and on a practical basis no one has satisfactorily proven that such treatment can clear a reptile permanently of the bacterium.

Salmonella spp. may be carried by perfectly healthy individuals, but during other disease processes, such as parasitism, or during periods of stress, they can become opportunistic pathogens. Other bacteria found in the normal digestive system of reptiles can act as opportunistic pathogens, including many members of the E. coli family, Pseudomonas spp., Campylobacter spp., Clostridia spp., and Aeromonas spp.

Fungal causes of intestinal disease

Published reports of gastrointestinal fungal disease are rare, but fungal overgrowth appears to be a relatively common finding. Documented cases of intestinal fungal overgrowth include Penicillium, Basidiobolus ranarum and Paecilomyces .

Physical causes of intestinal disease

Foreign bodies are not uncommon in chelonians and lizards, which may consume stones, sand, soil or any other substrate present. Surgery may be required to remove some foreign bodies, although many may be passed with the aid of oral liquid paraffin and fluid therapy.

Other physical obstructions include tumours within the intestines. These are not uncommon, particularly in snakes, and may present as a swelling, or produce symptoms such as vomiting, diarrhoea, constipation or anorexia.

This has been reported in chelonian such as common snapping turtles ( Chelydra serpentina ) and spur-thighed tortoises ( Testudo graeca ). Clinical signs included ileus, anaemia, lethargy and renal failure. Radiography will highlight larger lead particles.

Possible causes of liver damage in snakes ( Entamoeba invadens ) have already been mentioned above.

Other parasitic causes include some forms of the coccidian family which gain access to the liver from the small intestine via the bile ducts.

A herpesvirus and an adenovirus have been isolated from damaged snake livers.

The protozoan Hexamita parva has been associated with intestinal, renal and hepatic disease in Chelonia.

Hepatic lipidosis is common in tortoises fed inappropriate high-fat diets. Fat becomes deposited within the liver cells themselves, enlarging the liver and, more importantly, severely affecting its function. This can lead to jaundice, anorexia and death.

Post-hibernation jaundice is often a temporary finding in tortoises however it may persist, indicating liver damage due to any one of the above or due to hepatitis from bacteria such as Salmonella spp. and Aeromonas hydrophila . In addition some forms of herpesviruses and iridoviruses have been isolated from damaged tortoise and other chelonian livers.

The liver may become calcified due to over-supplementation of the diet with calcium and vitamin D 3 .

Bacterial hepatitis due to Salmonella spp . , Aeromonas spp . or Pseudomonas spp . has all been recorded. These may or may not be associated with heavy worm burdens, many of which may migrate through or to the liver, often carrying bacteria with them.

Viral hepatitis has been reported due to adenoviruses in bearded dragons ( Pogona spp.). It is generally seen in young animals and often associated with coccidiosis resulting in poor thriving young. Serological tests are available for detection of this disease as is a PCR test. Herpesviruses have been associated with hepatitis as well as pneumonia in iguanids and agamids. Yellow-green urates may be seen in both snakes and lizards associated with hepatic dysfunction due to the presence of increased levels of biliverdin.

Hepatic lipidosis, or fatty liver syndrome, has been well documented in lizards, particularly monitors and bearded dragons. This is frequently seen when fed inappropriate high-fat diets. In bearded dragons, the feeding of excessive amounts of insects to adults (which are supposed to become more herbivorous once they reach maturity) has also been implicated (Figure 21.11). In lizards with pre-ovulatory stasis, lipidosis occurs due to the high levels of circulating yolk lipids. Lipidosis can lead to jaundice, anorexia and death. The liver may become calcified due to over-supplementation of the diet with calcium and vitamin D 3 .

Figure 21.11 Hepatic lipidosis is common in species such as the bearded dragon ( Pogona spp.). Note the tan coloured liver and fat deposits.


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