Rickettsia – Rocky Mountain Spotted Fever

On the name of its discoverer H. T. Ricketts, who discovered ‘Rocky Mountain Spotted Fever’, this group of bacteria are named as Rickettsia. However, this group is also referred to as the “spotted fever” (typhus fever) group after the disease produced by the best known of these pathogens (Rickettsia prowazekii). 

Their natural distribution is by host vectors such as lice, fleas, ticks, mites etc in which they exist as harmless parasites or even symbionts. On being transferred to other animal hosts or humans by bites, scratches or inhalation, they produce very serious disease symptoms.

Morphology of Rickettsias

The Rickettsias are small rods with the fine structure typical of gram-negative eubacteria.

The genera Rickettsia and Coxiella are obligate intracellular parasites that differ in their location within the host cell. Both enter their host cells by inducing phagocytosis, even by cells that are not normally phagocytic. Within host cells, the rickettsias reproduced by binary fission.

The rickettsias are not motile as no flagella have been observed. They do not produce endospores.

Pathogenesis

The rickettsias causes several human diseases which are transmitted by arthropod vectors such as fleas, mites, lice and ticks. They are apparently not pathogenic to these arthropods but are pathogenic to man and other animals. Some diseases of man are fatal e.g. the typhus fever which is epidemic caused by R. prowazeki, transmitted to man by body lice.

Rickettsias normally enter the body through the bite and dust from hides or pelts of infected animals may contain large numbers of highly infectious spores from dried fecal material of arthropod parasites such as ticks. They are disseminated through the blood stream, enter endothelial cells by induced phagocytosis, escape from the phagosome, multiply intracellularly and eventually destroy their host cells.

A common target in rickettsial infections is the endothelial lining of the small blood vessels. The bacteria recognize, enter and multiply with in endothelial cells, causing necrosis of the vascular living. Among the immediate pathological consequences are vasculities, perivascular infiltration by inflammatory cells, vascular leakage and thrombosis. These pathogenic effects are manifested by skin rash, edema, hypotension and gangrene.