Риккетсия раккеттсии: переносчики, хозяева и механизмы передачи.

Species of bacterium

Rickettsia rickettsii is a Gram negative, intracellular, coccobacillus bacterium that was first discovered in 1902. R. rickettsii is the causative agent of Rocky Mountain Spotted Fever and is transferred to its host via a tick bite. It is one of the most pathogenic Rickettsia species and affects a large majority of the Western Hemisphere, most commonly the Americas. The pathogenic agent has been found on every continent, except Antarctica; however, Rocky Mountain Spotted Fever occurs mostly in North, Central, and South America. Ticks that carry R. rickettsii fall into the family of Ixodidae ticks, also known as "hard bodied" ticks. Ticks are vectors, reservoirs, and amplifiers of this bacteria. Ticks can contract R. rickettsii by many means. First, an uninfected tick can become infected when feeding on the blood of an infected vertebrate host; such as a rabbit, during the larval or nymph stages, this mode of transmission is called transstadial transmission. Once a tick becomes infected with this pathogen, they are infected for life. Both the American Dog Tick and the Rocky Mountain Wood Tick serve as long term reservoirs for Rickettsia rickettsii, in which the organism resides in the tick posterior diverticula of the midgut, the small intestine, and the ovaries. Notably, R. rickettsii is inefficient at infecting the ovaries of adult female ticks, resulting in a lowered rate of vertical transmission. Rickettsial colonization of the ovaries sees higher success when ticks obtain the pathogen as a larva or nymph. Reduced fecundity is also observed in ticks infected with R. rickettsii. 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. The duration of tick attachment, bacterial loads in tick saliva, and the transmission efficiency of Rickettsia are important factors underlying transmission from ticks to humans.

In addition to having vectors in the United States, R. rickettsii commonly infect certain ticks in South America. The cayenne tick (Amblyomma cajennense) and the brown dog tick (Rhipicephalus sanguineus) are both common vectors found in South America. The yellow dog tick (Amblyomma aureolatum) is another vector that infects specific parts of Brazil. Infecting horses and capybaras, the cayenne tick turns vertebrate hosts into amplifier hosts of the bacteria. Other small rodent species serve as amplifier hosts in the United States and South America. Specific requirements must be fulfilled when looking at vertebrate hosts to become amplifiers for R. rickettsii. First, there should be a large population of said host in the endemic area. Then, the vertebrate must be a primary host for the vector, so it can carry out its life cycle. Furthermore, it must be prone to infection from R. rickettsii, and once inside, the bacteria must infect the host to a great enough degree that its blood will infect other vectors that attach to the host. Finally, the host should be part of a prolific species, so that the species has a continuous supply of nonimmune amplifiers. Another way of contraction is by the bite of an infected tick. After getting bitten by an infected tick, R. rickettsiae are transmitted to the bloodstream by tick salivary secretions.

R. rickettsii are obligate intracellular bacteria, meaning they need a host cell in order to replicate and survive. This is due to the pathogen having many metabolic deficiencies and having to borrow metabolites from the host cell. R. rickettsii is unable to utilize glycolysis and the pentose phosphate pathway due to a reduced genome, and since these pathways are unusable, the bacterium must use the tricarboxylic acid cycle (TCA) as an alternative pathway. However, this can only be done through the use of the host cell's metabolites. This is possible because cell envelope glycoconjugates are synthesized using three particular sugars found in host cells, along with the other metabolites that are acquired from the host cell that will fuel the TCA Cycle. One of the metabolites that R. rickettsii uses from its host cell in order to synthesize peptidoglycan and lipopolysaccharides is a sugar called UDP N acetyl α d glucosamine. Other metabolites that are needed for this cell to survive within the host cell are imported glutamine, glutamate, and malate. These are used to regulate the flow of acetyl CoA, which is synthesized from pyruvate that the bacteria also takes from the host cell. Overall, R. rickettsii has a genome that does not encode many of the enzymes and proteins that are required for several pathways besides the TCA cycle. These bacteria import many of the intermediates, cofactors, and byproducts from the host cells' metabolic pathways to use for their own benefit and synthesis of necessary structures and energy for survival. R. rickettsii also has an outer layer or a "microcapsule", which acts similarly to the S layer or slime layer of other bacteria. This slime layer consists mostly of polysaccharides, and the "microcapsule" contributes to mechanisms involving anti phagocytosis and attachment to host cells.

While humans are hosts for R. rickettsii, they do not contribute to rickettsial transmission. Rather, the pathogen is maintained through its vector: ticks. R. rickettsii's survival in immune system cells increases the pathogen's virulence in mammalian hosts. Actin Based Motility (ABM) is a virulence factor that allows for the pathogen to evade the host's immune cells and spread to neighboring cells. 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. This leads to an increase in disease manifestation for the host.

R. rickettsii is an obligate intracellular alpha proteobacterium that belongs to the Rickettsiacea family. which is smaller compared to most other bacteria. This small genome size allows the bacteria to maintain an intracellular lifestyle with increased pathogenicity from gene reduction. It is maintained in its tick host by transovarial transmission. A key feature allowing for differentiation is the rickettsial outer membrane protein, rOmpA and rOmpB ]]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. However, the diagnosis of Rocky Mountain Spotted Fever is often misdiagnosed due to its non specific onset. The majority of infections from R. rickettsii occur during the warmer months between April and September. Symptoms can take 1–2 days to 2 weeks to present themselves within the host. The diagnosis of RMSF is easier when there is a known history of a tick bite or if the rash is already apparent in the affected individual. If not treated properly, the illness may become serious, leading to hospitalization and possible fatality.

During the initial stages of the disease, the infected person may experience headaches, muscle aches, chills, and high fever. Other early symptoms may include nausea, vomiting, loss of appetite, and conjunctival injection (red eyes). Most people infected by R. rickettsii develop a spotted rash, that begins to appear 2 to 4 days after the individual develops a fever. If left untreated, more severe symptoms may develop; these symptoms may include insomnia, compromised mental ability, coma, and damage to the heart, kidneys, liver, lungs, or additional organs. In rarer cases, patients may present with chest pain due to myocarditis. 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. Necrosis of skin is another rare case of sequelae.

Patients with severe infections may require hospitalization. The more severe symptoms occur later in response to thrombosis (blood clotting) caused by R. rickettsii targeting endothelial cells in vascular tissue. They may become hyponatremic, experience elevated liver enzymes, and other more pronounced symptoms. It is not uncommon for severe cases to involve respiratory system, central nervous system, gastrointestinal system, or renal system complications. In the case of meningoencephalitis, R. rickettsii causes cellular damage to brain tissue, resulting in inflammation. Additionally, acute respiratory distress syndrome and Coagulopathy occur in cases that advance to severe stages of RMSF. This disease is worst for elderly patients, males, African Americans, alcoholics, and patients with G6PD deficiency. The mortality rate for RMSF is 3 to 5 percent in treated cases, but 13 to 25 in untreated cases. The most common and effective treatment for Rocky mountain spotted fever is the anti microbial agent doxycycline. This antibiotic acts as a bacteriostatic drug by inhibiting protein synthesis via blockage of the 30S ribosomal subunit. Other treatments with chloramphenicol, fluoroquinolones, and macrolides have been explored. However, treatment with only chloramphenicol compared to other treatments (tetracycline class drugs only, both chloramphenicol and tetracycline class drugs, and neither drug) was associated with a case fatality rate three times higher.

Rocky Mountain Spotted Fever (RMSF) first emerged in the Idaho Valley in 1896 after being recognized by Major Marshall H. Wood. At the time of discovery, not much information was known about the disease. It was originally called "Black Measles" due to the infected area turning black during the late stages of the disease. The first clinical description of Rocky Mountain Spotted Fever was reported in Snake River Valley in 1899 by Edward E. Maxey. At the time, 69% of individuals diagnosed with RMSF died. Treatment recommendations changed in the 1990s to support primary therapeutic use of tetracycline class drugs. This coincided with a decrease in annual case fatality rates (CFRs) from the 1980s on to the early 1990s.