Pathological presentation:  

Rickettsiae spread via the blood stream, enter endothelial cells, proliferate within the cytoplasm and nuclei of endothelial and vascular smooth muscle cells of the microcirculation of virtually all organs, and directly injure  the foci of infected cells.

The consequence is systemic vascular damage that is the pathologic basis for the rash, interstitial pneumonia, interstitial myocarditis, meningoencephalitis, hepatic portal triaditis, and interstitial nephritis.

Microscopically, the vasculitis consists of swollen or necrotic endothelial cells, intramural and perivascular infiltration, predominantly by macrophages and T-lymphocytes with  few polymorphonuclear leukocytes, focal extravasation of erythrocytes and occasionally, usually non-occlusive, eccentric thrombi in the foci of rickettsial infection.

In the skin these foci are located principally in the dermis. Cutaneous histopathology of Rocky Mountain spotted fever is caused by endothelial damage by the rickettsial  organisms which elicit an initial lymphohistiocytic small vessel vasculitis with progression to Leukocytoclastic vasculitis. The vasculitis in Rocky Mountain spotted fever is thus considered to be a form of septic vasculitis.

In the brain the lesions assume a characteristic appearance, so-called typhus nodules, found most frequently in the  brain stem.

These  perivascular accumulations of mononuclear cells, which measure 100 to 180 micrometer in diameter, indicate a probable rickettsial infection though they are not pathognomonic.

Other neuropathologic lesions include microinfarcts of white matter and a mild mononuclear cell-rich leptomeningitis.

Lungs are congested and heavy.

Microscopic pulmonary lesions include mononuclear interstitial pneumonia and interstitial and alveolar edema and hemorrhages.

The heart is grossly normal except for epicardial petechiae, but it usually manifests a mild mononuclear interstitial myocarditis on microscopic examination.

The hepatic portal triaditis and multifocal perivascular interstitial nephritis correspond to foci of infection of hepatic portal blood vessels and the renal microcirculation near the corticomedullary junction, respectively.

Erythrophagocytosis occurs in Kupffer cells and macrophages within sinus of lymph nodes.

In fulminant Rocky Mountain spotted fever there are more thrombi and fewer intramural and perivascular leukocytes in foci of vascular injury. 

Disseminated vascular foci of rickettsial infection and microvascular injury result in leakage of intravascular fluid into the interstitial space with consequent edema and hypovoluemia.

Consumption of platelets and coagulation factors in thrombi at the sites of injury can cause thrombocytopenia and in very severe cases more severe coagulopathy.

Focal lesions in the skin are the cause of rash. Vasodilatation and petechiae are the basis of the cutaneous erythematous macules and central “spots” respectively.   

Increased vascular permeability of the infected pulmonary microcirculation may result in noncardiogenic pulmonary edema.

Myocardial injury is not a significant factor.

Central nervous system lesions are the cause of coma, seizures, multifocal, neurologic signs, and probably cardio-respiratory arrest.

Jaundice correlates with hemolysis and portal triadal inflammation.

Acute renal failure results from hypovolemic prerenal azotemia or, in more severe cases, acute tubular necrosis.

Vasculitis in the gastrointestinal tract is the apparent pathologic basis for nausea, vomiting, and abdominal pain and tenderness.