IDENTIFICATION OF HELODERMATID ADENOVIRUS 2 IN A CAPTIVE CENTRAL BEARDED DRAGON (POGONA VITTICEPS), WILD GILA MONSTERS (HELODERMA SUSPECTUM), AND A DEATH ADDER (ACANTHOPHIS ANTARCTICUS).

Adenoviruses are medium-sized DNA viruses with very high host fidelity. The phylogenetic relationships of the adenoviruses strongly resemble that of their hosts, consistent with evolutionary codivergence. The genus Atadenovirus appears to have evolved in squamate hosts. Perhaps the best known of the squamate adenoviruses is Agamid adenovirus 1 (AgAdV1), found most commonly in central bearded dragons (Pogona vitticeps), where it is a prevalent cause of hepatitis/enteritis, especially in young animals. All previous reports of adenoviruses in bearded dragons were AgAdV1. Helodermatid adenovirus 2 (HeAdV2) was first seen in Mexican beaded lizards (Heloderma horridus). Subsequently, partial adenoviral polymerase gene sequence from a western bearded dragon (Pogona minor) in Australia was found to share 99% nucleotide homology with HeAdV2. This article reports the discovery of a virus identical to HeAdV2 in a captive central bearded dragon in Florida and wild Gila monsters (Heloderma suspectum) in Arizona. Additionally, a partial adenoviral polymerase gene sharing 98% homology with this HeAdV2 was discovered in a death adder (Acanthophis antarcticus) in Australia. These findings call into question the provenance of HeAdV2. Further studies of atadenoviral host range, diversity of adenoviruses in captive animals, and characterization of adenoviruses from wild squamates are indicated.

A PRELIMINARY ANALYSIS OF PROLONGED ABSORPTION RATE OF PONAZURIL IN RED-FOOTED TORTOISES, CHELONOIDIS CARBONARIA.

Coccidial disease is significant in tortoises; Testudines intranuclear coccidiosis (TINC), caused by an unnamed coccidia, causes high mortality in diverse tortoise species. There is a lack of information on anticoccidial drugs in tortoises. The drug ponazuril has demonstrated efficacy in treating mammals infected with similar coccidial disease. Previous empirical use of ponazuril in TINC cases suggests that it may be an effective treatment. In this study, 20 mg/kg of ponazuril was orally administered to tortoises with the goal of achieving blood concentrations known to be effective for anticoccidial therapy in mammals. Ponazuril was measured in tortoise plasma, and noncompartmental analyses of pharmacokinetic parameters were attempted. Ponazuril in these tortoises did not achieve the desired concentrations known to be effective for anticoccidial treatment in mammals. Tortoises showed prolonged oral absorption, and despite sampling for 168 hr (1 wk), a terminal elimination rate constant and half-life were not able to be determined. Additional studies are needed to fully characterize ponazuril pharmacokinetics in red-footed tortoises. The optimal dose for treating TINC remains to be determined.

A possible role for inflammation in mediating apoptosis of oligodendrocytes as induced by the Lyme disease spirochete Borrelia burgdorferi.

BACKGROUND: Inflammation caused by the Lyme disease spirochete B. burgdorferi is an important factor in the pathogenesis of Lyme neuroborreliosis. Our central hypothesis is that B. burgdorferi can cause disease via the induction of inflammatory mediators such as cytokines and chemokines in glial and neuronal cells. Earlier we demonstrated that interaction of B. burgdorferi with brain parenchyma induces inflammatory mediators in glial cells as well as glial (oligodendrocyte) and neuronal apoptosis using ex vivo and in vivo models of experimentation. METHODS: In this study we evaluated the ability of live B. burgdorferi to elicit inflammation in vitro in differentiated human MO3.13 oligodendrocytes and in differentiated primary human oligodendrocytes, by measuring the concentration of immune mediators in culture supernatants using Multiplex ELISA assays. Concomitant apoptosis was quantified in these cultures by the in situ terminal deoxynucleotidyl transferase mediated UTP nick end labeling (TUNEL) assay and by quantifying active caspase-3 by flow cytometry. The above phenomena were also evaluated after 48 h of stimulation with B. burgdorferi in the presence and absence of various concentrations of the anti-inflammatory drug dexamethasone. RESULTS: B. burgdorferi induced enhanced levels of the cytokine IL-6 and the chemokines IL-8 and CCL2 in MO3.13 cells as compared to basal levels, and IL-8 and CCL2 in primary human oligodendrocytes, in a dose-dependent manner. These cultures also showed significantly elevated levels of apoptosis when compared with medium controls. Dexamethasone reduced both the levels of immune mediators and apoptosis, also in a manner that was dose dependent. CONCLUSIONS: This finding supports our hypothesis that the inflammatory response elicited by the Lyme disease spirochete in glial cells contributes to neural cell damage. As oligodendrocytes are vital for the functioning and survival of neurons, the inflammation and subsequent apoptosis of oligodendrocytes induced by B. burgdorferi could contribute to the pathogenesis of Lyme neuroborreliosis.