print

Rocky Mountain spotted fever

back

Pathogenesis and Transmission

Rickettsiae are obligate intracellular bacteria. Spotted fever group rickettsiae (like R. rickettsii and R. conorii) can grow in the nucleus or in the cytoplasm of the host cell. Once inside the host, the rickettsiae multiply, resulting in damage and death of these cells.

Disease transmission

Ticks are the natural hosts of R. rickettsii, serving both as reservoirs and as vectors. The two major vectors of R. rickettsii in the United States are the American Dog tick (Dermacentor variabilis) and the Rocky Mountain Wood tick (Dermacentor andersoni).

Ticks may obtain the pathogen by feeding on small mammals such as chipmunks and squirrels functioning as reservoirs for R. rickettsii. During feeding of larval and nymphal stages on these animals, ticks are most often infected with R. rickettsii. Once infected, ticks may spread the infectious agent transstadially among their own population, or transovarially from the female tick to its offspring. The latter seems to be the primary way by which R. rickettsii propagates in nature. Dogs and humans may also function as reservoirs, but probably constitute incidental hosts and display clinical signs of disease.

Ticks transmit the rickettsiae to all vertebrates primarily through their saliva during feeding. It usually takes several (5 to 20) hours of attachment and feeding before the rickettsiae are transmitted to the host. Less commonly, infections may occur following exposure to crushed tick tissues, fluids, or tick feces.

Dissemination of Rickettsia rickettsii

R. rickettsii enters the circulation system after being inoculated into the host body during the tick bite and disseminates throughout the body. The pathogens are obligate intracellular bacteria that grow and multiply primarily within the cytoplasm and, occasionally, in the nuclei of endothelial cells lining arterioles and venules resulting in vasculitis and increased vascular permeability. This causes blood leakage into adjacent tissues leading to a rash that is traditionally associated with Rocky Mountain spotted fever (only typical in humans) and causing damage to organs and tissues. Activation of the coagulation cascade leads to thrombosis and thrombocytopenia. Plasma loss leads to increased interstitial fluid volume and oedema.

Although platelet consumption is considered as the primary cause of thrombocytopenia in clinical cases, anti-platelet antibodies have also been identified in infected dogs. A tendency towards a more fulminant disease has been reported in Springer spaniels with phosphofructokinase deficiency and in German shepherd dogs.




  

Figure 1: Transmission electron micrographs showing in vitro infection of chick embryo fibroblasts with Rickettsia rickettsii (R). Cells are infected, grown in monolayer culture and harvested at different periods for analysis. Left: Infected cell grown in culture for 92 hours. Some bacteria appear to be enclosed within host cell membranes. A prominent feature is the greatly swollen cisterna of the rough endoplasmatic reticulum (RER).
Right: Infected cell grown in culture for 117 hours. Measurement bar in both figures 3 ┬Ám.

   

Further information

Occurrence Maps

Each country has its specific occurrence of CVBDs depending on climate and endemic vectors. See the maps

Clinical Sessions

The following authentic case reports provide insights into selected CVBD cases

View all

Interesting Links

CVBD and parasito­logical relevant websites. More...

CVBD Digest Articles

Findings from the CVBD symposia. More...