RICKETTSIAE

MORPHOLOGY & IDENTIFICATION small (0.3-0.5 x 0.8-2.0 um) gram-negative, pleomorphic, aerobic, obligate intracellular (Energy Parasites) coccobacilli (lack flagella, non-motile) divide by binary fission that may reside in the cytoplasm or within the nucleus of the cell that they invade they metabolize host-derived glutamate via aerobic respiration and the citric acid (TCA) cycle reservoir are animals and arthropds (humans are accidentally infected with these organisms) all are transmitted by arthropod vectors (e.g., ticks, mites, lice or fleas) VECTORS WOOD TICK (Dermacentor andersoni) DOG TICK (Dermacentor variabilis) PATHOGENESIS MOT: inoculated into the dermis of the skin by a tick bite or through damaged skin from the feces of lice or fleas TARGET CELLS: spread through the bloodstream and infect the endothelial cells lining the small blood vessels. Destruction of endothelial cells results in leakage of blood and subsequent organ and tissue damage due to loss of blood into the tissue spaces VIRULENCE FACTORS Adhesins: OmpA (outer membrane protein A)

cytoplasm where they replicate. 3. The mode of exit from the host cell varies depending upon the species - R. prowazekii exits by cell lysis - R. rickettsii get extruded from the cell through local projections (filopodia). F actin in the host cell associates with R. rickettsii and the actin helps to "push" the bacteria through the filopdia - O. tsutsugamushi exits by budding through the cell membrane and remains enveloped in the host cell membrane as it infects other cells. HOST DEFENSES Humoral immunity antibody-opsonized Rickettsia are phagocytosed and killed by macrophages Cell-mediated immunity Delayed type hypersensitivity develops following rickettsial infections. THREE MAJOR GROUPS: (based on clinical characteristics of disease)

RICKETTSIAL DISEASES (1) ROCKY MOUNTAIN SPOTTED FEVER caused by Rickettsia rickettsii most severe and most frequently reported rickettsial disease in the United States first recognized in 1896 in the Snake River Valley of Idaho and was originally called "black measles" because of the characteristic rash 3-5% mortality (death may occur during the end of the second week due to kidney or heart failure) RESERVOIR: wild rodents(primary) VECTOR: Ixodid (hard) ticks INCUBATION PERIOD: 7 days (range 2-14 days) CLINICAL MANIFESTATIONS: the classic triad of findings for this disease are fever, rash, and history of tick bite severe headache, muscle pain, nausea, vomiting, abdominal pain, and cough The rash typically are painless that appears 2-5 days after onset of illness on the ankles and wrists. Initially begins as small, flat, non-itchy, faint pink 1-5 mm macules that represent a focus of vascular infection and surrounding vasodilation progress to become the characteristic red, spotted (maculopapular) rash of Rocky Mountain spotted fever on the 6th day, owing to the leakage of edema fluid from the affected blood vessels, with the development of a hemorrhage (petechia) in the center of the lesions Early (macular) rash on sole of foot Late (petechial) rash on palm and forearm (2) RICKETTSIALPOX caused by Rickettsia akari RESERVOIR: mite & wild rodents VECTOR: mouse mite INCUBATION PERIOD: 7-24 days CLINICAL SYNDROMES typically a mild disease that has two phases: first phase a papule develops at the site of the mite bite and quickly ulcerates and forms an eschar. This initial phase occurs approximately 1 week after the bite. second phase is characterized by sudden onset of fever, chills headache and myalgia and is followed 2 to 3 days later with a generalized rash. The rash is papulovesicular and crusts over in the later stages. The pox heal within 2 to 3 weeks without scarring. Fatalities are rare

RICKETTSIOSES:

1. Adhere to endothelial cells lining the small blood vessels by parasite-induced phagocytosis 2. Once in the host cell, the bacteria lyse the phagosome membrane with a phospholipase and escape into the host cell

EGBII; 8-15-11

(3)

SCRUB TYPHUS caused by Orientia (Rickettsia) tsutsugamushi occurs in Asia, Australia and the Pacific Islands RESERVOIR: mites and wild rodents VECTOR: chiggers, the larval form of a mite INCUBATION PERIOD: 1-3 weeks CLINICAL SYNDROMES characterized by sudden onset of fever, chills headache and myalgia. maculopapular rash develops 2 - 3 days later. The rash appears first on the trunk and spreads to the extremities (centrifugal spread). Mortality rate in outbreaks are variable.

disease is mild and resolves within 3 weeks even if untreated.

DIAGNOSIS Clinical diagnosis: initial diagnosis Laboratory diagnosis: Direct detection after skin punch tissue biopsy: Giemsa stain Direct/indirect fluorescent antibody test PCR Weil-Felix test (agglutinate OX strains of Proteus vulgaris; no longer recommended) TREATMENT antibiotic treatment should be initiated immediately Doxycycline Drug of choice 100 mg every 12 hours for adults or 4 mg/kg body weight per day in two divided doses for children under 45 kg for a minimum total course of 5 to 10 days Tetracyclines contraindicated in pregnant women because of risks associated with malformation of teeth and bones in unborn children Chloramphenicol is an alternative drug PREVENTION prevention of tick bites protective clothing, insect repellents, etc. tick control no vaccine is available

(4) EPIDEMIC TYPHUS/LOUSE-BORNE TYPHUS caused by Rickettsia prowazekii transmitted by human body louse occurs among people living in crowded, unsanitary conditions such as those found in wars, famine and natural disasters RESERVOIR: humans (primary), squirrel, fleas VECTOR: louse INCUBATION PERIOD: 8 days CLINICAL SYNDROMES Epidemic typhus is characterized by sudden onset of fever, chills, headache, myalgia and arthralgia. After 7 days, maculopapular (can be petechial) rash appears. In contrast to the rash seen with Rocky Mountain Spotted Fever, the rash in epidemic typhus develops on the trunk first and spreads to the extremities (centrifugal spread) Brill-Zinsser disease is recrudescent epidemic typhus. It occurs decades after the initial infection. clinical course of the disease is similar to epidemic typhus but is milder and recovery is faster. The skin rash is rarely seen. diagnosis is made on the basis of a fever with unknown origin and a history of previous exposure to epidemic typhus. (5) MURINE/ENDEMIC TYPHUS caused by Rickettsia typhi occurs worldwide RESERVOIR: rats and cat flea VECTOR: rat flea INCUBATION PERIOD: 1-2 weeks CLINICAL SYNDROMES fever, chills headache and myalgia. rash develops in many but not all cases. The rash begins on the trunk and spreads to the extremities (centrifugal spread).

EGBII; 8-15-11