[3] As with all rickettsial organisms, R. typhi is a zoonotic agent that causes the disease murine typhus, displaying non-specific mild symptoms of fevers, headaches, pains and rashes.

[7] R. typhi was once one of the most prevalent causes of rickettsial diseases worldwide, but has since experienced a drop in case reports with the implementation of pest control programs.

[8][9][10] The microorganism is concentrated in warmer climate and coastal ports where there is an abundance of rats and their fleas, which are the preferred hosts for the pathogen.

[13] Epidemiologist Kenneth F Maxy recognized this and began questioning and isolating the presence of another typhus within the United States aside from R. prowazekii, he detailed this in an article released in 1926.

[23][24] There is also some evidence that other domestic animals such as dogs and sheep,[25] as well as opossums,[23] could be involved in the R. typhi transmission cycle, but studies are currently limited.

[20][27] Most patients present with a fever, and many have a rash and headache,[26] although it can also lead to disseminated, multisystem disease including infections of the brain, lung, liver, kidney, and heart endothelia.

[28][29] As these signs and symptoms are similar to those produced by other diseases, including other rickettsiae, murine typhus is difficult to diagnose clinically.

[27] In addition to non-uniform and non-specific symptoms, there is a lack of diagnostic tests effective during the acute stages of the illness, leading to delayed appropriate treatment.

[21] Doxycycline is the antibiotic of choice as it is shown to shorten the course of illness,[26] although 99% of those infected will clear the disease within weeks without specific treatment.

[1] Rickettsia typhi is a small, gram-negative intracellular bacterium that establishes the murine typhus infection in mammals and fleas.

[30] Murine typhus was once one of the most prevalent rickettsial diseases in the world,[8][9][10] having isolated the R. typhi causative agent from nearly every continent around the globe except for Antarctica.

[14][11] In addition to the widespread distribution, the bacterium is particularly concentrated in regions that boast warmer climates year-round and hug the coasts.

[8][9][14] This predilection is due to these regions' favourable climatic conditions for the survival of flea and wildlife hosts, leading to their greater abundance and ability to maintain the rickettsial organism as reservoirs in the environment.

[8][14] Historically, thousands of murine typhus cases were reported in the United States every year;[8][9][10][14] however, the disease experienced a sudden decline in incidence in the 1940s with the implementation of pest control programs to remove the flea and rodent reservoirs responsible for rickettsial transmission in urban dwellings.

[8][9][10][14] It is estimated that R. typhi prevalence is actually higher than the measured value, since murine typhus is often underreported and misdiagnosed because of its non-specific and mild clinical presentation (fever, headache, generalized pain, and rashes).

[25] Cats and opossums are thought to be fairly significant reservoirs for murine typhus in urban environments due to their unpicky ectoparasites and close association with humans.

[8][14][11] Transmission through contact with arthropod feces may be through an open wound, the respiratory tract (inhalation), or the conjunctivae of the mammalian host.

[14] As with all rickettsiae species, R. typhi is a zoonotic agent with humans serving as aberrant dead-end hosts, and thus do not play an ecological role in the bacterium's transmission and lifecycle.

[16] Even when stringent physiologic conditions are met, when grown in media that mimics the environment of host cytoplasm, pathogen activity cannot survive very long.

It has been shown that utilizing indirect fluorescent antibody assays and western blot analysis together provide reliable differentiation among the species.