Maintenance of its genome is carried out through vertical gene transfer where specialization of the bacterium allows it to shuttle host sugars directly into its TCA cycle.

A capsule encircling the bacterium allows for attachment to host cells and additionally acts as a defense mechanism for resisting phagocytosis.

[7] The pathogenic agent has been found on every continent, except Antarctica; however, Rocky Mountain Spotted Fever occurs mostly in North, Central, and South America.

[9] Headache, high fever, and spotted rash are some effects of the disease with more severe cases resulting in organ damage and coma.

[10][11][12] Antibiotics, such as doxycycline, target the ribosome of R. rickettsii in order to inhibit protein synthesis of the bacteria, providing a form of treatment for the disease.

[14] Energy is primarily obtained through a combination of oxidative phosphorylation of imported host carbon sources and direct harvesting of ATP via a ATP/ADP transmembrane pump.

The primary carbon source of R. rickettsii is pyruvate, though many other amino acids and TCA cycle intermediates such as glutamine, glutamate,and malate can be used.

[16] For lipid metabolism, a complete map of fatty acid synthesis enzymes have been found, allowing R. rickettsii to construct a viable cell membrane made up of lipopolysaccharides (LPS).

[14] Pathways for producing critical small molecules such as riboflavin (B2), nicotinamide (B3), pantothenate (B5), pyridoxine (B6), and biotin (B7) are all missing key enzymes, forcing R. rickettsii to rely solely on transmembrane transport proteins.

These bacteria import many of the intermediates, cofactors, and byproducts from the host cells' metabolic pathways to use for their own synthesis of necessary structures and energy for survival.

These two proteins are believed to be associated with pathogenicity of this microbe and serve as specific points that antibodies can bind to in order to prevent the bacteria from interacting with host cells.

R. rickettsii invades vascular endothelial cells that line both small and medium sized the blood vessels in the host's body.

Nitric oxide has the ability to inhibit the pathogen by negatively effecting attachment, intracellular growth, and subversion of the host cell.

It is suggested that the Sca2 gene, which is an actin-polymerizing determinant, is a distinguishing factor for the Rickettsia family, as R. rickettsii mutants with a Sca2 transposon the bacteria can avoid autophagic processes by host phagocytic cells.

RARP2 mediates the fragmentation of TGN, or the trans-Golgi network, causing attenuation of vesicular transport and glycosylation defects in infected host cells.

MHC-I is an important protein for defending against pathogens as it functions as an antigen presenting complex signaling its infection status to lyphocytes.

This small genome size allows the bacteria to maintain an intracellular lifestyle with increased pathogenicity from gene reduction.

This small genome size allows the bacteria to maintain an intracellular lifestyle with increased pathogenicity from gene reduction.

[24] A key feature allowing for differentiation is the rickettsial outer membrane protein, rOmpA and rOmpB [4] which contributes to the identification of R. rickettsii strains as virulent.

The American dog tick (Dermacentor variabilis), mainly found in the eastern United States, is the most common vector for R. rickettsii.

[33] Notably, R. rickettsii is inefficient at infecting the ovaries of adult female ticks, resulting in a lowered rate of vertical transmission.

[30] As a result of these limitations, long-term maintenance of R. rickettsii in populations of ticks relies mainly on horizontal transmission through the exchange of bacteria during feedings of infected hosts.

[38] The Centers for Disease Control and Prevention states that the diagnosis of Rocky Mountain Spotted Fever (RMSF) must be made based on the clinical signs and symptoms of the patient and then later be confirmed using specialized laboratory tests.

The majority of infections from R. rickettsii occur during the warmer months between April and September due to its most common method of transmission being via tick bite.

Additionally, rare symptoms include vision impairment and arthritis that may exist as chronic sequelae, lasting anywhere from 10 days to 4 years.

Other chronic sequelae include some cases of neurological challenges, such as impaired speech, dysphagia, ataxia, memory loss, cortical blindness, and decreased attention span.

The more severe symptoms occur later in response to thrombosis (blood clotting) caused by R. rickettsii targeting endothelial cells in vascular tissue.

[47] Prevention of Rocky Mountain Spotted Fever begins with identifying and avoiding vectors that cause exposure including ticks, lice, mites, and fleas.

[49] The first documented case of Rocky Mountain Spotted Fever (RMSF) presented in the Boise, Idaho in 1896 after being recognized by Major Marshall H.

Ricketts was the first to identify the pathogen responsible for RMSF as a gram negative bacillus, and confirm a route of transmission from infected ticks in a guinea pig model.