Rickettsiae primarily target vascular endothelial cells, causing febrile illness and rash in the mammalian host.
Transmission is predominantly via tick bites, with certain pathogens transmitted by human body lice and mites.
Fever, headache, myalgia, and malaise are common to rickettsial, ehrlichial, and Anaplasma infections; rash is common in rickettsial disease, occasional in ehrlichial infection, and rare in anaplasmosis.
The early signs and symptoms of infection are often nonspecific and can mimic self-limited viral illnesses or other life-threatening illnesses.
Early empiric treatment with doxycycline should be considered in highly suspicious cases until rickettsial infection is definitively ruled out, as delayed treatment can lead to severe sequelae and high mortality rates.
Rickettsial diseases are curable infections that, if unrecognized, can be readily lethal. Early nonspecific symptoms can mimic benign viral illnesses and should be considered in any patient who presents with constitutional symptoms, fever, headache, and a characteristic petechial rash. The advent of modern molecular technologies, including genetic analysis, has allowed for significant taxonomic reclassification of the rickettsiae, including moving the family Bartonella (see Chap. 154) and the genus Coxiella out of the order Rickettsiales to the orders Rhizobiales (Bartonella) and Legionellales (Coxiella). “Rickettsiae” now includes a polyphyletic group of microorganisms in the class Proteobacteria, comprising species belonging to the genera Rickettsia, Orientia, Ehrlichia, Anaplasma, and Neorickettsia. Several nonrickettsial agents that were historically included in the group of infections loosely termed the rickettsioses remain incorporated in the discussion of rickettsial disease herein to reflect that precedent.1
Historically rickettsiae and Rickettsia-like organisms (eg, Coxiella burnetii) were endemic pathogens; the rise of international travel, however, has allowed for the spread of rickettsial infections to nonendemic areas.
ETIOLOGY AND PATHOGENESIS OF SPOTTED FEVER AND TYPHUS GROUPS
Rickettsiae are obligate, intracellular, Gram-negative bacteria. They are pleomorphic 0.3 to 1 µm coccobacilli composed of DNA and RNA and reproduce through binary fission. Rickettsiae are propagated by arthropod vectors that use mammals (and sometimes the arthropods themselves) as reservoirs of infection. Rickettsiae are separated into the spotted fever group and the typhus group on the basis of common genetics, immunologic patterns, and intracellular growth characteristics. The typhus group lives entirely within the cell cytoplasm, whereas the spotted fever group can reside within the cytoplasm or nucleus. Rickettsiae are differentiated by unique antigenic structures on cell surface proteins. Rickettsia rickettsii has 2 major surface proteins, outer membrane protein A (OmpA) and outer membrane protein B (OmpB), which are the main targets for serologic testing. Additionally, Sca1 and Sca2 are autotransporter proteins that play a role in actin-based mobility and induction of phagocytosis of host cells.
Infection occurs through arthropod-induced breaks in the skin allowing access of the pathogen to the blood and lymph. Spotted fever rickettsiae are injected into the host through the saliva of the feeding tick, whereas typhus group ...