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Geology topics

Elliott R. Jacobson

Publications and source records attributed to Elliott R. Jacobson.

6 recordsLinked to original sources

Bilateral palpebral reduction and concurrent mycoplasmosis in a wild Agassiz's desert tortoise (Gopherus agassizii)

A wild Agassiz's desert tortoise, Gopherus agassizii , with bilateral eyelid reduction and plaques of tissue covering the superior surface of both corneas was examined in the field and subsequently submitted to the University of Florida for diagnostics. Polymerase chain reaction (PCR), from a swab of both corneas, was positive for Mycoplasma agassizii . Two months later, the tortoise was euthanatized and necropsied. There was increased bulbar exposure associated with dermal excoriation of periocular scales in both superior and inferior palpebra resulting in an increased palpebral fissure opening. Concurrently, there was bilateral conjunctivitis of the nictitating membranes and squamous metaplasia of the bulbar conjunctiva. Using PCR, Mycoplasma testudineum , another pathogen of tortoises, was identified in both nasal cavities, and the upper respiratory tract histopathological findings were consistent with those described for M . testudineum in Agassiz's desert tortoises. Although eye disease has been reported in desert and gopher ( Gopherus polyphemus ) tortoises with mycoplasmosis, widespread loss of palpebral tissue, conjunctivitis of the nictitans, and squamous metaplasia of the bulbar conjunctiva have not been reported in tortoises.

Veterinary Opthalmology

Mycoplasmosis and upper respiratory tract disease of tortoises: a review and update

Tortoise mycoplasmosis is one of the most extensively characterized infectious diseases of chelonians. A 1989 outbreak of upper respiratory tract disease (URTD) in free-ranging Agassiz's desert tortoises ( Gopherus agassizii ) brought together an investigative team of researchers, diagnosticians, pathologists, immunologists and clinicians from multiple institutions and agencies. Electron microscopic studies of affected tortoises revealed a microorganism in close association with the nasal mucosa that subsequently was identified as a new species, Mycoplasma agassizii . Over the next 24 years, a second causative agent, Mycoplasma testudineum , was discovered, the geographic distribution and host range of tortoise mycoplasmosis were expanded, diagnostic tests were developed and refined for antibody and pathogen detection, transmission studies confirmed the pathogenicity of the original M. agassizii isolate, clinical (and subclinical) disease and laboratory abnormalities were characterized, many extrinsic and predisposing factors were found to play a role in morbidity and mortality associated with mycoplasmal infection, and social behavior was implicated in disease transmission. The translation of scientific research into management decisions has sometimes led to undesirable outcomes, such as euthanasia of clinically healthy tortoises. In this article, we review and assess current research on tortoise mycoplasmosis, arguably the most important chronic infectious disease of wild and captive North American and European tortoises, and update the implications for management and conservation of tortoises in the wild.

The Veterinary Journal

Serologic and molecular evidence for testudinid herpesvirus 2 infection in wild Agassiz’s desert tortoise, Gopherus agassizii

Following field observations of wild Agassiz’s desert tortoises ( Gopherus agassizii ) with oral lesions similar to those seen in captive tortoises with herpesvirus infection, we measured the prevalence of antibodies to Testudinid herpesvirus (TeHV) 3 in wild populations of desert tortoises in California. The survey revealed 30.9% antibody prevalence. In 2009 and 2010, two wild adult male desert tortoises, with gross lesions consistent with trauma and puncture wounds, respectively, were necropsied. Tortoise 1 was from the central Mojave Desert and tortoise 2 was from the northeastern Mojave Desert. We extracted DNA from the tongue of tortoise 1 and from the tongue and nasal mucosa of tortoise 2. Sequencing of polymerase chain reaction products of the herpesviral DNA-dependent DNA polymerase gene and the UL39 gene respectively showed 100% nucleotide identity with TeHV2, which was previously detected in an ill captive desert tortoise in California. Although several cases of herpesvirus infection have been described in captive desert tortoises, our findings represent the first conclusive molecular evidence of TeHV2 infection in wild desert tortoises. The serologic findings support cross-reactivity between TeHV2 and TeHV3. Further studies to determine the ecology, prevalence, and clinical significance of this virus in tortoise populations are needed.

California;Nevada

Mycoplasma testudineum in free-ranging desert tortoises, Gopherus agassizii

We performed clinico-pathological evaluations of 11 wild Agassiz's desert tortoises (Gopherus agassizii) from a translocation project in the central Mojave Desert, California, USA. Group 1 consisted of nine tortoises that were selected primarily due to serologic status, indicating exposure to Mycoplasma testudineum (seven) or both M. agassizii and M. testudineum (two), and secondarily due to clinical signs of upper respiratory tract disease (URTD). Group 2 consisted of two tortoises that were antibody-negative for Mycoplasma and had no clinical signs of URTD, but did have other signs of illness. Of the Group 1 tortoises, M. testudineum, but not M. agassizii, was amplified by polymerase chain reaction and DNA fingerprinted from two tortoises. Using light microscopy, mild to severe pathologic changes were observed in one or more histologic sections of either one or both nasal cavities of each tortoise in Group 1. Our findings support a causal relationship between M. testudineum and URTD in desert tortoises.

California

Oxalosis in wild desert tortoises, Gopherus agassizii

We necropsied a moribund, wild adult male desert tortoise ( Gopherus agassizii ) with clinical signs of respiratory disease and elevated plasma biochemical analytes indicative of renal disease (blood urea nitrogen [415 mg/dl], uric acid [11.8 mg/dl], sodium >180 mmol/l] and chloride [139 mmol/l]). Moderate numbers of birefringent oxalate crystals, based on infrared and electron microscopy, were present within renal tubules; small numbers were seen in colloid within thyroid follicles. A retrospective analysis of 66 additional cases of wild desert tortoises was conducted to determine whether similar crystals were present in thyroid and kidney. The tortoises, from the Mojave and Sonoran deserts, were necropsied between 1992 and 2003 and included juveniles and adults. Tortoises were classified as healthy (those that died due to trauma and where no disease was identified after necropsy and evaluation by standard laboratory tests used for other tortoises) or not healthy (having one or more diseases or lesions). For all 67 necropsied tortoises, small numbers of crystals of similar appearance were present in thyroid glands from 44 of 54 cases (81%) and in kidneys from three of 65 cases (5%). Presence of oxalates did not differ significantly between healthy and unhealthy tortoises, between age classes, or between desert region, and their presence was considered an incidental finding. Small numbers of oxalate crystals seen within the kidney of two additional tortoises also were considered an incidental finding. Although the source of the calcium oxalate could not be determined, desert tortoises are herbivores, and a plant origin seems most likely. Studies are needed to evaluate the oxalate content of plants consumed by desert tortoises, and particularly those in the area where the tortoise in renal failure was found.

Journal of Wildlife Diseases