Canine Rocky Mountain Spotted fever: a retrospective study of 30 cases

Rocky Mountain spotted fever (RMSF) was diagnosed in 30 dogs examined at North Carolina State University, Veterinary Teaching Hospital between 1984 and 1997. Historical, physical examination, and laboratory abnormalities were reviewed. Diagnostic criteria included a four-fold rise in antibody titer to Rickettsia rickettsii (R. rickettsii) (n=15) or a single R. rickettsii antibody titer of 1:1,024 or greater (n=15; when this initial titer was determined one week or more after the onset of clinical signs). Fifteen (50%) dogs were greater than seven years of age, and 13 (43%) dogs were between two and seven years of age. There was no sex predilection. Only five (17%) dogs had a history of known tick exposure. Presumably due to delayed diagnosis, dogs with antibody titers of 1:1,024 or greater at the time of presentation had a higher incidence of more severe neurological dysfunction (e.g., ataxia, hyperesthesia, vestibular disease, and seizures) and cutaneous lesions (e.g., hyperemia, edema, petechiae, ecchymoses, and necrosis). Laboratory findings included anemia, leukocytosis accompanied by toxic granulation of neutrophils, hypoalbuminemia, and coagulation abnormalities; signs were generally more severe in the 15 dogs with R. rickettsii antibody titers of 1:1,024 or greater at the time of presentation. Twelve (40%) dogs in this study were severely thrombocytopenic (less than 75 x10(3) platelets/microl; reference range, 200 to 450 x 10(3)/microl), without clinical evidence of fulminant disseminated intravascular coagulation. In this study, the survival rate following R. rickettsii infection was 100%.     

Seroprevalence of Coxiella burnetii antibodies in wild deer populations in eastern Australia

Coxiella burnetii causes significant reproduction losses in livestock and the disease Q fever in humans. Transmission of C. burnetii is facilitated by the stability of the bacterium in the environment and the susceptibility of a variety of host species to infection. Consequently, inter-species transmission occurs frequently through either direct or indirect contact. Wildlife may represent reservoirs of C. burnetii and could therefore be a source of infection for domestic animals. Understanding the prevalence of C. burnetii infections at the wildlife-livestock interface is important for disease control. This study aimed to investigate the extent of C. burnetii exposure in wild deer in eastern Australia. Serum samples were obtained from 413 wild deer from seven regions in four eastern Australian states from 2017 to 2020. Antibodies were detected using a commercial Q fever antibody kit validated for ruminants. Seroprevalence of C. burnetii antibodies in deer was determined and true prevalence estimated, for each region. The overall seroprevalence of C. burnetii antibodies in wild deer was 3.4% (14 seropositive of 413 deer sampled) with true prevalence estimated to be 4.3% (95% credible interval: 0.6%, 10.9%). Seropositive deer were identified only in Queensland (7/108 seropositive) and northern New South Wales (7/120 seropositive). This geospatial distribution is consistent with seropositivity in other animal species and indicative of the level of C. burnetii in the environment. The low seroprevalence suggests that wild deer are unlikely to be a major reservoir species for C. burnetii in eastern Australia but may still be implicated in inter-species transmission cycles.