Chronic disease in the Mojave desert tortoise: Host physiology and recrudescence obscure patterns of pathogen transmission

Abstract

A seminatural, factorial‐design experiment was used to quantify dynamics of the pathogen Mycoplasma agassizii and upper respiratory tract disease in the Mojave desert tortoise (Gopherus agassizii) over 2 years. Groups of initially healthy animals were separated into serologically positive (seropositive), seronegative, and artificially infected groups and paired into 23 pens. We found no evidence of long‐term immune protection to M. agassizii or of immunological memory. Initially seronegative, healthy tortoises experienced an equal amount of disease when paired with other seronegative groups as when paired with seropositive and artificially infected groups—suggesting that recrudescence is as significant as transmission in introducing disease in individuals in this host–pathogen system. Artificially infected groups of tortoises showed reduced levels of morbidity when paired with initially seronegative animals—suggesting either a dilution effect or a strong effect of pathogen load in this system. Physiological dynamics within the host appear to be instrumental in producing morbidity, recrudescence, and infectiousness, and thus of population‐level dynamics. We suggest new avenues for studying diseases in long‐lived ectothermic vertebrates and a shift in modeling such diseases.

An ecoimmunological approach to disease in tortoises reveals the importance of lymphocytes

“…, Sandmeier et al. ). In addition, even healthy animals show a large degree of individual variation in both differential white blood cell counts and BKA under controlled laboratory conditions (Sandmeier et al.…”

“…, Sandmeier et al. ). We suggest that induced antibodies, produced by B‐2 cells and known to be recognized by macrophages, prolong inflammatory responses, causing the immunopathology witnessed in some, but not all, tortoises exposed to M. agassizii (reviewed in Sandmeier et al.…”

“…, Sandmeier et al. , ), it is unlikely that the sole function of lymphocytes is the production of induced antibodies. We hypothesize that B‐1 lymphocytes form a large portion of the lymphocytes quantified in these tortoises and that they function both in the production of natural antibodies and phagocytosis.…”

“…In part, this can be explained by the intermittent nature of signs of URTD and the slow immunological response of desert tortoises (Sandmeier et al. , ). Importantly, mean levels of M. agassizii and URTD were explained by different variables (Table ).…”

“…, Hurtado , Sandmeier et al. ). Therefore, tortoises may use multiple mechanisms to keep M. agassizii at levels low enough not to cause visible signs of inflammation referred to as URTD.…”