Rickettsia have the structural features of typical prokaryotic cells. They are small, rodlike or coccobacillary shaped (Figure 1), and have a typical double-layered, gram-negative cell wall. However, they stain poorly and, because of their usual occurrence inside host cells, are best visualized under the light microscope with one of the polychrome stains, such as Giemsa or Macchiavello.

Fig1. Electron micrograph of Rickettsia prowazekii in experimentally infected tick tissue.

A. Physiology

The obligate requirement for an intracellular environment for rickettsial replication is not fully understood, but its plasma membrane is leaky and, therefore, easily permeable to host cell nutrients and coenzymes. These intracellular parasites employ host-derived car bon sources, amino acids, and nucleosides for their own metabolism. They lack a glycolytic pathway but retain the enzymes necessary for the Krebs cycle. This genus is closely related to the ancestor of mitochondria, found within eukaryotic cells. The rickettsial electron transport chain and adenosine triphosphate–generating machinery closely resemble those found in current-day mitochondria. Rickettsia contain a number of antigens that convey both group and species specificity.

 B. Pathogenesis

Rickettsia are transmitted to humans by arthropods, such as fleas, ticks, mites, and lice. Depending on the rickettsial species, rodents, humans, or arthropods can serve as reservoirs of infectious organ isms. Rickettsia species have an affinity for endothelial cells located throughout the circulatory system. Following a bite by an infected arthropod, the organisms are taken into cells by a process similar to phagocytosis. The organisms degrade the phagosome membrane by production of a phospholipase C. The Rickettsia in the spotted fever group multiply in both the nucleus and cytoplasm of host cells. They appear to mobilize host cell actin fibrils that facilitate their exit into adjacent cells in a manner similar to that of the genera Listeria and Shigella. The Rickettsia within the typhus group are not capable of actin-based motility; cannot escape the cell via cytoplasmic extensions; and, therefore, are limited to growth within the cytoplasm until the host cell eventually dies, releasing the bacteria. In both cases, the rickettsiae spread throughout the body via the blood stream or lymphatics. Focal thrombi are formed in various organs including the skin (Figure 2), and a variety of small hemorrhages and hemodynamic disturbances create the symptoms of illness.

Fig2. Child’s right hand and wrist displaying the characteristic spotted rash with raised or palpable purpura, which is pathognomonic of vasiculitis (the fundamental lesion of Rocky Mountain spotted fever).

C. Clinical significance—spotted fever group

 1. Rocky Mountain spotted fever: Rocky Mountain spotted fever is a potentially lethal, but usually curable tickborne disease, and is the most common rickettsial infection in the United States. The disease is caused by Rickettsia rickettsii. Human infection is initiated by the bite of an infected wood or dog tick. Ticks can transmit the organism transovarially to their progeny and, thereby, the organism can be maintained without mammalian hosts in specific geo graphic regions for many years. Currently in the United States, such infected tick populations are prevalent in south-central states and along the mid-Atlantic coast. The disease usually occurs with highest frequency during the warmer months when tick activity is greatest. Symptoms begin to develop an average of 7 days after infection. The disease is characterized by high fever and malaise, followed by a prominent rash that is initially macular but may become petechial or frankly hemorrhagic (see Figure 2). The rash typically begins on the extremities, involving the palms and soles, and develops rapidly to cover the body. In untreated cases, vascular disturbances leading to tissue infarction and maryocardial or renal failure may ensue. Two thirds of cases of Rocky Mountain spotted fever occur in children younger than age 15 years, with the peak incidence occurring between ages 5 and 9 years. A potential diagnostic problem occurs in those infected patients (approximately 10 percent) in whom a rash does not occur. These cases of “spotless” Rocky Mountain spotted fever may be severe and end fatally.

2. Other spotted fevers: Tickborne spotted fevers similar to Rocky Mountain spotted fever are found in several regions of the world. They vary in severity and are caused by organisms such as Rickettsia conorii, Rickettsia canadensis, and Rickettsia sibirica. A clinically different disease, rickettsialpox, is caused by Rickettsia akari. It has been reported in the United States and the former Soviet Union. The vector for R. akari is a mite, and its reservoir is the common house mouse or similar small rodents. Rickettsialpox is characterized by scattered papulovesicles that are preceded by an eschar at the site of the mite bite and with mild constitutional symptoms of a few days’ duration. Figure 3 illustrates the spot ted fevers caused by rickettsial organisms.

Fig3. Spotted fevers caused by Rickettsia.

C. Clinical significance—typhus group

1. Louseborne (epidemic) typhus: Louseborne typhus is caused by Rickettsia prowazekii. [Note: Epidemic typhus is a different dis ease from salmonella-induced typhoid fever. Both were originally thought to be variations of the same disease, which was called “typhus” after the Greek word meaning “stupor.” When the two diseases were determined to be caused by different organisms, the salmonella-induced disease was named “typhoid,” meaning “typhuslike.”] R. prowazekii is transmitted from person to person by an infected human body louse that excretes organisms in its feces. Scratching louse bites facilitates the intro duction of the pathogen from louse feces into a bite wound. Infected lice are themselves eventually killed by the infecting bacterium. Thus, this disease is not maintained in the louse population, but, rather, lice serve as vectors, transmitting the organism between humans.

 a. Typhus epidemics: Typhus occurs most typically in large epidemics under conditions of displacement of people, crowding, and poor sanitation. Currently a major focus of such outbreaks is found in northeast Africa. The epidemic form of typhus has not occurred in the United States since early in the 20th century. However, sporadic cases of typhus have occurred in the eastern half of the United States, where the reservoir appears to be flying squirrels. The pathogen is probably transmitted from flying squirrels to humans via the bite of ectoparasites. Clinical symptoms of typhus develop an average of 8 days after infection and include high fever; chills; severe headache; and, often, a considerable degree of prostration and stupor. Although rash may be observed, unlike the rash associated with Rocky Mountain spotted fever, the epidemic typhus rash spreads centrifugally from trunk to extremities. The disease lasts 2 weeks or longer, and tends to be more severe in older individuals. Complications of epidemic typhus may include central nervous system dysfunction, myocarditis, and death.

b. Brill-Zinsser disease (recrudescent typhus): This is a usually milder form of typhus that occurs in persons who previously recovered from primary infections (10 to 40 years earlier). Latent infection is thought to be maintained in the reticuloendothelial system and probably serves as a reservoir for the organism in interepidemic periods.

 2. Other forms of typhuslike fever: Murine (endemic) typhus, caused by Rickettsia typhi, is a clinically similar but usually milder disease than that caused by R. prowazekii. Human infections are initiated by the bites of infected rat fleas, and a worldwide reservoir for R. typhi exists in urban rodents. Murine typhus was endemic in rat infested areas, particularly in the southeastern United States and in the Gulf of Mexico region. However, with improving rodent control, it has become rare in this country. [Note: The cat flea, which also resides on skunks, opossums, and raccoons, is still a significant vector of murine typhus in the United States.]

D. Laboratory identification

A variety of serologic procedures have been developed, most of which rely on the demonstration of a rickettsia-specific antibody response during the course of infection. Suspensions or soluble extracts of rickettsia are used to demonstrate group- and species-specific antibodies by indirect immunofluorescence. Alternatively, although not widely available, infected cells can be detected by immunofluorescence or histochemical procedures on some clinical samples such as punch biopsies from areas of rash. Polymerase chain reaction (PCR) amplification can also be employed for the specific diagnosis of rickettsial diseases.

 E. Treatment

Doxycycline is the drug of choice for the treatment of Rocky Mountain spotted fever in both adults and children, except for pregnant women who should be treated with chloramphenicol (Figure 4). The risk of dental staining with doxycycline is minimal if a short course is administered. The decision to treat must be made on clinical grounds, together with a history or suspicion of contact with an appropriate arthropod vector, before the seroconversion data are available. Early therapy for Rocky Mountain spotted fever is important, because delay beyond the 5th day of illness is associated with an increased mortality rate.

Fig4. Summary of Richettsia disease. 1 Indicates first-line drug; 2 indicates alternative drug.

F. Prevention of infection

Prevention depends on vector control, for example, delousing, rodent-proofing buildings, or clearing brush in tick- or mite-infested areas as appropriate. Personal protection should include wearing clothes that cover exposed skin, use of tick repellents, and frequent inspection of the body and removal of attached ticks. It is of interest that infected ticks do not transmit the infection until several hours of feeding have elapsed. Prophylactic therapy with doxycycline or another tetracycline is not recommended following tick exposure because less than 1 percent of ticks in endemic areas is infected with R. rickettsii. Patients who experience tick bites should seek treatment if any systemic symptoms, especially fever and headache, occur in the following 14 days. Vaccines are not currently licensed for use in the United States.

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