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INTRODUCTION

Rickettsial infections are caused by pleomorphic gram-negative organisms that contain both DNA and RNA. They are obligate intracellular parasites, have typical bacterial cell walls and cytoplasmic membranes, and divide by binary fission. The order Rickettsiales includes only 2 families, the Anaplasmataceae and the Rickettsiaceae. Ehrlichia and Anaplasma species are from the family Anaplasmataceae, whereas spotted fever and the typhus group, as well as the causative agent of scrub typhus (Orientia tsutsugamushi), are from the family Rickettsiaceae. All of these diseases are commonly referred to as rickettsial diseases.

PATHOGENESIS

Rickettsial infections have many features in common, including multiplication of the organism in an arthropod host; geographic and seasonal occurrences that are related to the arthropod life cycle, activity, and distribution; zoonotic illnesses with humans as incidental hosts (except for louse-borne typhus); and fever, rash (except some cases of ehrlichiosis and anaplasmosis), headache, myalgias, and respiratory tract symptoms. Ticks become infected by feeding on the blood of infected animals, through fertilization, or by transovarial passage. Once attached, the infected tick is able to transmit the disease to humans during feeding. After attachment to humans has occurred (6–24 hours), rickettsiae are released from the salivary glands and multiply in the endothelial cells lining the small blood vessels, resulting in cell damage. These organisms produce a vasculitis following replication within the endothelial lining and smooth muscle cells of blood vessels, leading to generalized capillary and small-vessel endothelial damage, increased vascular permeability, thrombus formations, and tissue necrosis. This process consumes platelets and results in the characteristic thrombocytopenia. Many of the other initial symptoms and signs are referable to this pathogenesis, which can affect any organ system. Although the thrombus-mediated vascular occlusion that occurs may play a role in severe rickettsial infections, disseminated intravascular coagulation (DIC) occurs rarely. Hyponatremia, which is another laboratory hallmark of many rickettsial infections, is the result of initial active secretion of salt into renal tubules. Subsequently, the syndrome of inappropriate production of antidiuretic hormone (SIADH) can further aggravate the hyponatremic state. Organisms from the typhus (except scrub typhus) and spotted fever groups contain endotoxins, and most will survive only briefly outside of a host (reservoir or vector).

The epidemiology, clinical manifestations, and outcomes of each rickettsial disease are discussed below. Because diagnostic methods and treatment are similar for most rickettsial disorders, these are discussed at the end of the chapter.

ROCKY MOUNTAIN SPOTTED FEVER

EPIDEMIOLOGY

According to the Centers for Disease Control and Prevention, from 2006 to 2013, the median number of cases per year for spotted fever rickettsiosis (formerly reported as Rocky Mountain spotted fever [RMSF] until 2010) in the United States was 2426 (range 1815–4470). Of these cases, approximately 76% occurred between April and October, and 8.5% of the cases were in children less than 15 years of age. Although the disease is rare in infants, RMSF has ...

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