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Brown, M. B., Schumacher, I. M., Klein, P. A., Harris, K., Correll, T., & Jacobson, E. R. (1994). Mycoplasma agassizii causes upper respiratory tract disease in the desert tortoise. Infection and Immunity, 62(10), 4580–4586. 
Added by: Sarina Wunderlich (01 Jan 2009 23:10:29 UTC)   Last edited by: Beate Pfau (29 Dec 2009 08:56:58 UTC)
Resource type: Journal Article
BibTeX citation key: Brown1994b
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Categories: General
Keywords: Gopherus, Gopherus agassizii, Schildkröten = turtles + tortoises, Stress = stress, Testudinidae, Veterinärmedizin = veterinary medicine, Viren = viruses
Creators: Brown, Correll, Harris, Jacobson, Klein, Schumacher
Collection: Infection and Immunity
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Abstract     
Testudinidae Gopherus agassizii
The desert tortoise is listed by the United States government as a threatened species in part of its range. A major contributing factor in the decline of this animal has been the presence of an upper respiratory tract disease (URTD) which is characterized by a chronic disease which eventually leads to severe occlusion of the nares with viscous exudate and destruction of the respiratory epithelium. Electron microscopy of infected tissues demonstrated the presence of a mycoplasma-like organism attached to the respiratory surfaces. The mycoplasma was isolated and designated as a new species, with the proposed name Mycoplasma agassizii. The current study was designed to fulfill Koch's postulates and determine if M. agassizii was the etiologic agent of URTD. Clinically healthy animals with known antibody status were infused intranasally with pooled exudate (n = 8) from ill donor animals, with M. agassizii alone (n = 9) or in combination with Pasteurella testudinis (n = 8), with P. testudinis alone (n = 9), or with sterile broth (n = 12). The pooled exudate was culture positive for M. agassizii. Tortoises which received exudate or M. agassizii alone or in conjunction with P. testudinis were significantly more likely to develop clinical disease (P < 0.0004) than animals which received P. testudinis alone or the broth controls. Tortoises demonstrated a strong immune response to M. agassizii, and seroconversion was seen in all groups with clinical disease. M. agassizii was isolated from the upper respiratory tracts of clinically ill animals up to 6 months postinfection. On the basis of the results of these transmission studies, we conclude that M. agassizii is an etiologic agent of URTD in the desert tortoise.
Added by: Sarina Wunderlich  Last edited by: Beate Pfau
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