Contributor: Arjumand Bano Syed 
Rocky Mountain spotted fever is an acute febrile illness caused by Rickettsia rickettsii. The disease received its name because it was first reported from the Rocky Mountains of Idaho and Montana during the 1890's. The disease has been reported from all states (except Maine, Alaska, and Hawaii), as well as from Canada, Mexico, Columbia, and Brazil. A number of species of ticks are infected with rickettsia rickettsii in nature, but only two are important in transmitting spotted fever to humans. These are Dermcentor andersoni, which is the principal vector in the Western USA, and Dermcentor variabilis assumes this role in Eastern USA. Amblyomma americanus and Dermcentor variabilis are the common vectors in the west South Central states. Ticks become infected by feeding on infected animals. Infected female ticks transmit the agent transovarially to at least some of their offspring.
The causative microbe, Rickettsia rickettsii is the prototype for the rickettsial group of agents. The minute organisms are purple when stained by Giemsa method or red Macchiavello technique; most of them are gram negative. These organisms often occur in pairs and possess a cell wall similar in structure and chemical composition to that of gram negative bacteria; there are cell membrane, cytoplasmic granules corresponding to ribosomes, and prokaryotic organization of nuclear material. The cell membrane is selectively permeable; the cell wall is the focus of important antigens and an endotoxin - like substance.
Rocky mountain spotted fever in humans is acquired from the bite of an infected tick. After an attached tick has fed for 6-10 hours, ricketsiae released from salivary glands are inoculated into the dermis, from where they spread through lymphatic and blood vessels to the systemic and pulmonary circulation. Rickettsiae attach to the endothelial cell membrane by a rickettsial surface protein, induce phagocytosis, escape from the phagosome presumably by phospholipase A2 activity, and replicate in the cytol by binary fission. Ricketsiae kill the heavily infected cell directly with prominent injury to the cell by increasing it's permiability. Injury has been associated with free radical - induced membrane damage, phospholipase A2 activity, and protease activity. The fever is caused by IL-1, IL-6, and TNFa. The acute phase response and the kellikrien-kinin system may be activated. Coagulation is regulated to effect deposition of hemostatic plug in foci of in foci of endothelial necrosis without triggering true disseminated intravascular coaulation. Perivascular T-cells and macrophages mediate immune destruction of intracellular richettsia by secretion of  INFγ and TNFa, which stimulates target cell synthesis of ricketsicidal nitric oxide.
The microscopic lesions are focal hemorrhages and intramural and perivascular lymphocytes and macrophages. A very small proportion of infected blood vessels contain thrombi that if present, are usually eccentric and non occlusive. Most infected foci comprise a large network of contagious, infected endothelium of the microcirculation. In the skin these foci are locate principally in the dermis. In the brain the lesion is called typhus nodules, found most frequently in the brain stem, though they are not pathognomonic. Other neuralgic lesions include microinfarcts of white matter, and a mild, mononuclear cell - rich leptomeningitis. Lungs are heavy and congested, and microscopically include mononuclear interstitial pneumonia and interstitial and alveolar edema and hemorrhages. The heart is grossly normal, except for epicardial or endocardial petechiae, but usually has a mild mononuclear interstitial myocarditis. The liver shows portal triaditis and focal hepatic necrosis. Because ricketsiae grow best at temperature of 32° - 35°C, classical vascular lesions are frequently detected in cooler parts of the body such as the testis and epididymis. Erythrophagocytosis occurs in hepatic Kupffer cells and macrophages within lymph nodes and spleen.