Organism Disease Geography Transmission Distinctive Features

R. prowazekii Epidemic typhus Brill-

Zinsser disease

Worldwide (war, famine) Louse feces Endothelial infection; centrifugal rash; reactivation with mild

disease

R. typhi Murine typhus Worldwide (rat related) Rat flea feces Similar to epidemic typhus, but mortality is lower

Spotted Fever Group

Organism Disease Geography Transmission Distinctive Features

R. rickettsii Rocky Mountain spotted

fever

North and South America Tick bite Endothelia and vascular smooth muscle infected; centripetal rash,

eschar rare

R. conorii Boutonneuse fever Africa, Southern Europe, India Tick bite Prominent eschar, tache noire

R. africae Africa tick fever Africa, Caribbean Tick bite Multiple eschars

R. sibirica North Asia tick typhus Eurasia Tick bite Typical spotted fever with eschar

R. japonica Japanese spotted fever Japan Tick bite Typical spotted fever with eschar

R. australis Queensland tick typhus Eastern Australia Tick bite Typical spotted fever with eschar

R. akari Rickettsialpox United States, Ukraine, Korea,

Croatia

Mite bite Mild spotted fever with eschar

R. felis Similar to murine typhus United States Opossum flea Similar to murine typhus

Orientia tsutsugamushi Scrub typhus Eastern Asia and Western

Pacific region

Chigger bite Eschar common, insects present in scrub vegetation

Ehrlichiosis Group

Organism Disease Geography Transmission Distinctive Features

Ehrlichia chaffeensis Monocytic ehrlichiosis United States, Europe Tick bite Fever, lymphadenopathy, no eschar, rash in 40%

Anaplasma

phagocytophilum and E.

ewingii

Granulocytic ehrlichiosis United States, Europe Tick bite Fever, lymphadenopathy, no eschar or rash

The innate immune response to rickettsial infection is mounted by natural killer cells, which produce g-interferon, reducing bacterial proliferation. Cytotoxic T-lymphocyte responses are

critical for elimination of rickettsial infections. IFN-g and TNF, from activated natural killer cells, CD4+, and CD8+ T lymphocytes, stimulate the production of bactericidal nitric oxide.

Cytotoxic T lymphocytes lyse infected cells, reducing bacterial proliferation. Rickettsial infections are diagnosed by immunostaining of organisms or by detection of antirickettsial

antibodies in the serum.

Morphology

Typhus Fever.

In mild cases, the gross changes are limited to a rash and small hemorrhages due to the vascular lesions. In more severe cases, there may be areas of necrosis of the skin with gangrene of

the tips of the fingers, nose, earlobes, scrotum, penis, and vulva. In such cases, irregular ecchymotic hemorrhages may be found internally, principally in the brain, heart muscle, testes,

serosal membrane, lungs, and kidneys.

The most prominent microscopic changes are the small-vessel lesions that underlie the rash and the focal areas of hemorrhage and inflammation in the various organs and tissues affected.

Endothelial swelling in the capillaries, arterioles, and venules may narrow the lumina of these vessels. A cuff of mononuclear inflammatory cells usually surrounds the affected vessel. The

vascular lumina are sometimes thrombosed, but necrosis of the vessel wall is unusual in typhus compared with RMSF. Vascular thromboses lead to the gangrenous necroses of the skin and

other structures in a minority of cases. In the brain, characteristic typhus nodules are composed of focal microglial proliferations with an infiltrate of mixed T lymphocytes and

macrophages ( Fig. 8-45 ).

Scrub typhus, or mite-borne infection, is usually a milder version of typhus fever. The rash is usually transitory or might not appear. Vascular necrosis or thrombosis is rare, but there may

be a prominent inflammatory lymphadenopathy.

Date: 2016-04-22; view: 684