Due to the fact that there are many unknowns in the mechanisms of rickettsia infection, Rocky Mountain spotted fever can be difficult to treat, especially if not diagnosed for a long period of time after infection. The main drug that is used to treat Rocky Mountain spotted fever is the tetracycline antibiotic, Doxycycline (CDC). This drug is commonly known as one of the major antibiotics for treatment of malaria and various gram-negative bacterial infections. Another drug that has been used in the past to treat infection is chloramphenicol, but is not recommended due to the fact that it increases risk of fatal outcomes (CDC). The mechanism that doxycycline uses to treat Rocky Mountain spotted fever pertains to the fact that it is able to bind directly to bacteria. To treat rickettsia infections, Doxycycline binds to the 30S ribosomal subunit of the bacteria to inhibit its protein synthesis (Doxycycline). In R. rickettsii, the inhibition of protein synthesis causes for the bacteria to be unable to replicate and enter various endothelial cells. Treatment with this antibiotic should be continued until at least three days after the reduction of fever in patients, and on average total treatment ranges from approximately one to two weeks (CDC). In the past, studies have been done to see the effects of doxycycline as a treatment for rickettsia disease, but the desired results of were never quite obtained due the difficulty of dosage and side effects of the drug (Purvis and Edwards 2000). This study also alluded to that fact that one of the major side effects of the antibiotic is that it could potentially cause permanent staining of the teeth at higher doses.
While there is no current vaccine for the disease, a study done in the past year shows an attempt to create immunity using recombinant forms of OmpB (Riley et al 2015). Similar attempts at enhancing protection from infection with R. rickettsii using recombinant forms of OmpB with adhesion 2 have shown some success in a series of studies conducted on infected mice (Gong et al. 2015). While this route is very similar to the study done by Riley et al., the results of Gong et al. showed some success due to the fact that the scientists focused heavily on protective antigens already present in the host. Even though these studies produced slightly enhanced protection from the disease, the research here falls short of finding a very viable way to increase immunoprotection of the disease (Gong et al. 2015). This is due to the fact that antibody response to R. rickettsii is already present in hosts not treated with additional OmpB and the enhancement of antibody response is not enough to cause immunity.