Rocky Mountain spotted fever is an infection caused by the bacterium Rickettsia ricketsii. Since the 1920’s, it has led to over 20,000 US cases per year. This potentially fatal illness uses ticks as a vector to transmit the disease. It is known to be the most common fatal tick-borne disease. Its difficulty to diagnose is what makes the disease so dangerous. The symptoms it produces are common amongst many other illnesses such as fever, rash, nausea, abdominal pain, and other infections. By the time a correct diagnosis is made, the effects of the disease may have already taken its toll on the infected (CDC 2013).
It is important to be made aware of the structural and functional characteristics of the bacterium in order to know how to properly avoid and prevent the transmission of RMSF.
R. rickettsii is an aerobic gram-negative bacterium. This means that the cell wall of the bacterium contains about 2-3 layers of interconnected peptidoglycan proteins that are surrounding by an outer membrane. The peptidoglycan proteins prevent the osmotic lysis of the bacteria when in a hypotonic environment (CCBCMD, 2014). Being aerobic in nature means that the bacterium can undergo respiration in the presence of oxygen. This process occurs in the mitochondria of the bacterium. The Rickettsia bacterium can use the oxygen molecules as terminal electron acceptors. In this respiration process, organic substrates are oxidized to create and generate energy molecules called ATP and other simpler organic compounds (NCBI, 2015).
It is also an obligate intracellular bacteria. Rickettsia bacteria are in the phylum of alpha-protobacteria which means that they are able to survive even with low amounts of nutrients and therefore have a longer generation time in comparison to other gram-negative bacteria (CDC 2013).
The R. rickettsii bacteria uses ticks as its mode of transmission. The most common ticks that carry the disease are the American Dog Tick which is known as Dermacentor variabilis as well as the Rocky Mountain Wood tick which is also known as Dermacentor andersoni. These ticks serve as both the hosts of the bacteria as well as reservoirs (Bayer, 2015). Ticks obtain the R. rickettsii bacteria from feasting on small mammals during the nymphal or larval stages of the infected animals. Once a singular tick is infected, it disseminates the bacteria amongst its own nearby population which is known as transmitting the infectious agent transstadially. If the tick is female it can spread the infection transovarially meaning that the tick has the capability of passing the bacteria to its offspring (Bayer, 2015). The ticks then transmit the infection through their saliva when feeding on vertebrates. However, the disease can also be contracted by coming into contact with the tick feces or other tick tissues and fluids (CDC, 2013).
Once the tick vector attaches to a host for approximately 5-20 hours, R. rickettsii enters the circulatory and lymphatic systems. It disseminates using these organs. R. rickettsii have an affinity for the endothelial cells which line the blood vessels throughout the body. This ensures a quicker passage and circulation of the bacteria. Due to this tropism for blood vessels, the R. rickettsii bacteria has a quicker transmission when compared to other Rickettsia bacteria (Bayer, 2015).
Uniquely, the R. rickettsii bacteria has a commensal relationship with its tick vectors but it causes severe disease in vertebrates and especially humans. The basis of this drastic change in relationship upon transmission of the R. rickettsii bacteria from its arthropod vector to a human host lies in the differing environmental conditions from host to host. The human endothelial cells allow the multiplication of R. rickettsii bacteria at 34*C and then proceed to undergo cell lysis which further disseminates the pathogen. This differs from the tick cell lines which allow little to no division and do not undergo any lysis. Tick cells are able to tolerate the burdens of the bacteria where human endothelial cells cannot. This is what causes the commensal relationship in tick vectors compared to the parasitic and harmful relationship the bacteria have with human hosts (Policastro, 1997).
The bacteria attach to the outer membrane of endothelial cells through the OmpA protein. This protein specializes in the induction of the bacteria’s engulfment and is one of two major outer membrane proteins the bacteria possess, the other protein being OmpB. In addition to induction, the proteins function in being conformational epitopes (Cuhna, 2016). After evading the body’s natural defense system in the form of phagocytes, the bacteria replicate through binary fission. Being obligate intracellular bacteria, R. rickettsii quickly and primarily divide in the cytosol of the endothelial cells. Once replication occurs and the bacteria is spread from cell to cell, they are propelled by polar polymerization of the host’s actin proteins which allows propulsion without cell lysis (Bayer, 2015). This process causes vasculitis in the endothelial cells due to the localization of the bacteria. This leads to greatly increased vascular permeability which then results in characteristic symptoms of RMSF such as edema, hypovolemia, hypotension, and hypoalbuminemia (Cuhna, 2016). These symptoms manifest as the characteristic rash that comes with an infection with RMSF. This etiology is what makes RMSF and the R. rickettsii bacteria dangerous as it can lead to very fatal side effects.
The further distribution of R. rickettsii throughout the blood vessels leads to the subsequent development of even more vascular injury. These injuries include interstitial pneumonia, interstitial myocarditis, glial nodules in the perivascular tissue of the central nervous system (Cuhna, 2016). Lesions also occur on the skin, in the GI tract, liver, pancreas, kidneys, and the skeletal muscles. This extensive vascular damage activates the release of platelets and the generation of thrombin in order to activate the body’s immunodefense system and physiologic response to the bacteria. This response eventually leads to vascular necrosis and thrombosis due to the proliferation of the R. rickettsii bacteria with necrosis and myocarditis being the usual cause of death in very severe cases (Cuhna, 2016).
As previously mentioned, the diagnosis for RMSF is difficult as it mimics symptoms from many other diseases. In humans, classic clinical signs for the infection include fever, rash, and the presence of a tick bite. Once the disease has been accurately diagnosed, it is recommended that the patient undergoes appropriate antibiotic treatment. Some antibiotic treatments when engaged within days of proper diagnoses reduce the risk of death exponentially. Bacterial antibiotic medications would most likely be prescribed when diagnosed. These antibiotics include Doxycycline, Vibramycin, and tetracycline (Bayer, 2015).
Despite the severity of symptoms, RMSF and the contraction of R. rickettsii can be managed. Mortality rates by the disease vary with the time it takes for a proper diagnosis, the delay in treatment, as well as age and strength of one’s immune system. When untreated, the mortality rate is approximately 25% but when adequately treated it decreases to less than 5% (Cuhna, 2016). One should also take many safety precautions when travelling to areas with a tick population. Preventative measures greatly decrease the risk of disease transmission. Some of these measures include wearing long clothing which cover the skin to ensure no skin is exposed, using insect and tick repellants, as well as regularly checking for tick bites. If a tick is discovered, it is best to handle the removal of the tick with care as to avoid spreading its feces or tissues into the skin which is one of the ways RMSF is transmitted. Following these safety precautions, RMSF can be adequately managed.