Persistence of Respiratory Disease in Tortoise Populations Subclinical Disease, Transmission, and a Possible Dilution-Effect


Meeting Abstract

19-3  Thursday, Jan. 5 11:00 – 11:15  Persistence of Respiratory Disease in Tortoise Populations: Subclinical Disease, Transmission, and a Possible Dilution-Effect SANDMEIER, FC*; MALONEY, NK; TRACY, CR; HUNTER, K; DUPRE, S; Colorado State University-Pueblo; Vanderbilt Univesity; University of Nevada, Reno; University of Nevada, Reno; University of Nevada, Reno franziska.sandmeier@csupueblo.edu

We re-analyzed data from a transmission experiment, conducted on 277 Mojave desert tortoises (Gopherus agassizii) in semi-natural enclosures from 2003-2005. New evidence has emerged that Mycoplasma agassizii, a pathogen that causes upper respiratory tract disease (URTD), exists in a subclinical state in many tortoise populations in the Mojave Desert. Tortoises without signs of disease were selected and assigned to three categories: antibody-negative (“negative”, but not naïve), antibody-positive (“positive”), and originally “negative”, but artificially infected with M. agassizii (“infected”). Groups were then paired in enclosures for two years and monitored for signs of disease monthly and antibody levels seasonally. “Negative” groups did not have higher rates of URTD when housed with “positive” or “infected” groups compared to when they were housed with other “negative” groups. However, exposure to recently seroconverting animals or animals with nasal exudate, did lead to greater instances of URTD. Therefore, both the persistence of subclinical disease and transmission from animals with active nasal discharge appear to be important in the maintenance of disease in tortoise populations. “Infected” groups paired with a “negative” group had lower rates of disease than those paired with “positive” group. This would be the first observation of a dilution effect in tortoise populations with URTD. Finally, we found no evidence of immunological memory in tortoises, nor any evidence that antibodies are protective against M. agassizii.

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