Inclusion body disease

Inclusion Body Disease (IBD) in the boid family of snakes, particularly Boa constrictor, has been recognized since the mid-1970s. It is so named because of the characteristic intracytoplasmic inclusions which are observed in clinical examinations in epidermal cells, oral mucosal epithelial cells, visceral epithelial cells, and neurons. In the 1970s and 1980s the disease was most commonly observed in Burmese pythons, Python molurus bivittatus. From the 1980s till the present day, it has been most commonly observed in boa constrictors, Boa constrictor from S. America.

All boid snakes should be considered susceptible to the disease. Many zoos quarantine boas specifically as a result of this high risk before introducing them into their permanent collections and (breeding) programs. While the disease has not been identified in non-boid snakes, it is yet unknown whether non-boid snakes harbour the virus. The primary host of this virus has not yet been identified but mites are thought to be primary hosts or at least a contributory factor.

Its distribution is worldwide, specifically in captive boid snakes. Its occurrence in the wild is unknown. Strangely enough, the disease has only been identified in adult and sub-adult specimens. Even so, all age groups are considered susceptible. There are also anecdotal reports of the infection in neonates. A retro-like virus infection was suspected as the causative agent of IBD, but identification of highly divergent arenavirus sequences from Boa constrictors with IBD (Stenglein et al., 2012; Bodewes et al., 2013) suggested arenaviruses to be the etiological agent of IBD. Cell culture isolation of several arenaviruses from boid snakes with IBD further solidified, but did not yet confirm, the etiological relationship between IBD and arenaviruses (Hetzel et al., 2013).

Clinical signs

Clinical signs may vary, regurgitation and neurological symptoms being the most prominent in the early and later stages of its progression.

In boa constrictors, the first signs may include off and on regurgitation, and some develop head tremors. Dysecdysis (abnormal shedding) may occur. Some develop chronic regurgitation and anorexia [lack of appetite or refusal to feed]. However, not all infected snakes may regurgitate. Boas lose weight and may develop clogged nares (nostrils), stomatitis or secondary pneumonia. The disease can rapidly progress to produce nervous system disorders, such as disorientation, corkscrewing of the head and neck, holding the head in abnormal and unnatural positions, rolling onto the back or stargazing. Stomatitis, pneumonia, undifferentiated cutaneous sarcomas, lymphoproliferative disorders, and leukemia have all been observed in affected specimens. Burmese pythons generally show signs of central nervous system disease without manifestation of other clinical signs and regurgitation is not seen in Burmese pythons, only in boas. These are symptoms similar to those seen in specimens infected by Chlamydia–specifically Chlamydophila psittaci, the so-called parrot's disease.

Several snakes have been seen with proliferative pneumonia, while inclusions are commonly seen in the liver, kidney, and pancreas. Cases have also been observed where there are only very few inclusions. In a few snakes with signs of central nervous system disease, and with a severe encephalitis, no inclusions have been seen in any cells. While the presence of characteristic inclusions is diagnostic for the disease, the absence of such inclusions does not necessarily indicate that the snake is not diseased or is free from the IBD virus. While cells having inclusions may show mild degenerative changes, inflammation is rarely seen in visceral tissues. In the brain, mild to severe encephalitis occurs, with lymphocytic perivascular cuffing. Several snakes with lymphoproliferative disorders have been identified with lymphoid infiltrates in multiple organs.

Laboratory diagnosis

The disease can be diagnosed in live snakes through blood tests. For hematologic and plasma biochemical determinations performed in affected specimens, 0.6 ml of blood was placed in each of three microtainer tubes containing lithium heparin. All samples were submitted for hematological and plasma biochemical determinations within 30 min after collection. This is essential. Whole blood examination included RBC, WBC, differential WBC, and determination of PCV, and Hb concentrations. Plasma biochemical analyses also included determination of concentrations of sodium, potassium, chloride, carbon dioxide, urea nitrogen (BUN), creatinine, calcium, glucose, phosphorus, total bilirubin, cholesterol, uric acid, total protein, albumin, globulin, alkaline phosphatase, SGOT, SGPT. For comparative purposes, clinically affected boa constrictors were arbitrarily categorized as either acutely affected (<2 months following onset of signs) or chronically affected (>2 months following onset. Acutely affected snakes exhibit leukocytosis, relative lymphocytosis, lower total protein and globulin values, and significantly higher SGOT values than do chronically affected snakes [Schumacher, Juergen, Elliott R. Jacobson, Bruce L. Homer, Jack M. Gaskin – 1994].

Primary route of transmission

The primary route of transmission has not yet been identified. This is most probably by direct contact but may also be a result of its transmission to developing embryos in viviparous species and eggs in oviparous species. Venereal transmission is also indicated as a possibility. The snake mite, Ophionyssus natricis has been implicated as a possible vector for the virus since mite infestations are commonly seen in epizootics of IBD and in captive specimens of these snakes. There is still much to be learned about the pathology caused by these mites. Mites are sometimes very difficult to eradicate due to their resistance to certain toxins used to eliminate them.

Permethrin and Laxazol [both of which contain the active agent permethrin] are known to be effective against mite infestations, but should be used with great caution and only in small quantities due to their toxic nature. There are also several non-chemical substances that may be just as effective. These biological agents are sprayed onto the infested animal and desiccate the mites, rendering them unable to lay their eggs or consume blood beneath the scales of their host [the infested snake or other reptile]. The incubation period for mite eggs is thought to be about 10–14 days, so the treatment should be repeated after 10 days to ensure that any eggs that hatch or larvae that develop into nymphs are also quickly eliminated from the host before reaching sexual maturity and able to repeat their reproduction cycle.

Prognosis and treatment

To date, there is no known treatment of the disease IBD. Snakes diagnosed with IBD or suspected of having the disease should be euthanized since there is no known cure and because progression and transmission of the virus is both very rapid and destructive. All newly acquired snakes should therefore be quarantined for at least 3–6 months [preferably 6 months] before being introduced into established collections. The recommended period of quarantine for any wild caught boa or python is at least 4–6 months.

Note

Because mites are considered as a primary risk [host] in the transmission of the disease [and other diseases in reptiles], the control and elimination of mite infestations in all reptile enclosures is crucial. Wooden cages (e.g. plywood) should not be used to house boids or should be discarded, unless sealed with urethane or some other reliable sealeant in order to prevent the migration of mites from one enclosure to the next. Fiberglass cages of infected snakes should be cleaned with bleach and left to dry properly before being used to house other snakes.

References

External links

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