Murine Typhus

Murine typhus, also known as endemic typhus or Mexican typhus, is caused by infection with the rickettsial organism Rickettsia typhi (formerly R. mooseri). Although this zoonosis is typically maintained in commensal rats by flea transmission, humans occasionally are infected. Murine typhus is one of the most prevalent rickettsial diseases of humans, even though it is underdiagnosed and its importance is generally unappreciated. R. typhi is a small, obligate, intracellular bacterium that can cause mild febrile infection in humans. It usually is transmitted via infected flea feces. When the bite site of an infected flea is scratched, rickettsiae gain access to the host through abraded skin. Under experimental conditions, however, some fleas also can transmit this pathogen via their bite. Reviews on the ecology and epidemiology of murine typhus have been provided by Traub et al. (1978), Azad (1990), Rawlings and Clark (1994), Azad et al. (1997), and Goddard (1998).

The geographical distribution of murine typhus is almost global. Although it occurs on ail continents except Antarctica, its importance as a human pathogen has diminished in recent years. Significant foci persist, however, especially in Indonesia, the People's Republic of China, Thailand, North Africa, and Central America. In the United States, the annual number of human cases has decreased from more than 5000 in 1945 and 1946 to 20— 80 per year from 1958 to the present. This zoonosis was formerly widespread throughout the southern and southwestern United States. Currently in the United States it is principally recorded in Texas, where 200 human cases were diagnosed in the 5-year period 1980—1984. Several cases are usually reported annually from California and Hawaii.

Murine typhus is maintained primarily in a cycle that involves commensal rodents of the genus Rattus and their ectoparasites, especially fleas of the genus Xenopsylla. Humans are typically infected when feeding fleas void infectious feces on their skin. The black rat (Rattus rattus) and Norway rat (R. norvegicus) are the principal reservoirs of Rickettsia typhi. Infections also have been recorded in many other mammals, including other commensal rats (Rattus spp.) worldwide, bandicoot rats (Bandicota spp.) on the Indian subcontinent, house mice (Mus musculus) worldwide, the oldfield mouse (Peromyscus polionotus) in the southern United States, the giant pouched rat (Cricetomys gambianus) in Africa, the house shrew (Suncus murinus) in the Old World, domestic cats worldwide, and the Virginia opossum (Didelphis virginiana) in North America. Within the last 20 years, peridomestic mammals such as opossums and feral cats and dogs have become more frequendy recorded reservoirs of murine typhus in Texas and southern California. Field infection rates in commensal rats of up to 46% have been reported in Burma (Myanmar), Egypt, and Ethiopia, and rates of up to 94% have been reported in some cities in Texas. New World strains of R. typhi are much less virulent (ca. 2% mortality rate in humans) than Old World strains (up to ca. 70% mortality rate).

Commensal rats almost invariably are the most important reservoirs and amplifying hosts of R. typhi. Infection in these rats is not fatal; instead, they display a persistent transient rickettsemia. This is important in extending the period during which ectoparasites, especially fleas, can feed on infective hosts. Because seropositive Virginia opossums have been associated with human cases in some regions of the United States, it appears that opossums also can be important reservoir hosts.

At least 11 species of fleas belonging to 9 different genera have been found to be infected with R. typhi in nature. X. cheopis is the most important vector. Other vectors are X. astia, X. bantorum, X. brasiliensis, Ctenocephalides felts, Pulex irritans, L. segnis, and N. fasciatus. Except for C. felis and P. irritans, all of these fleas are common ectoparasites of commensal rodents. Human cases of murine typhus usually coincide with population peaks of X. cheopis on rats. The number of cases generally declines or disappears after this flea has been controlled by chemical applications or rodent removal. Infection rates of field-collected X. cheopis in hyperendemic regions typically are 50-70%.

Infection of a flea occurs when rickettsiae are ingested while the flea is feeding on a host that has R. typhi circulating in its blood. The ingested rickettsiae then invade the midgut epithelial cells of the flea and start to replicate by transverse binary fission. Progressive rickettsial infection spreads rapidly until most or all of the midgut cells are infected after 7—10 days. Ultimately, infectious rickettsiae are released from these cells and liberated into the gut lumen, from which they are excreted in the feces. X. cheopis fleas are typically infective about 10 days after an infectious blood meal. Infective fleas can transmit the pathogen for at least another 40 days, during which time the rickettsial titer in the fleas remains at a stable, high level. Infected fleas survive with a persistent R. typhi infection and demonstrate no obvious pathological effects. This contrasts with the related pathogen, R. prowazekii, which causes a fatal infection in its louse vector. Because X. cheopis can maintain and transmit R. typhi transovar-ially, this flea may be both a reservoir and a vector of murine typhus rickettsiae.

Although modes of R. typhi transmission other than via infected flea feces are known, their significance in nature remains unclear. Because X. cheopis has been shown to transmit R. typhi by bite in the laboratory, other fleas also may be capable of transmitting R. typhi by bite. The possibility of aerosol transmission from infective flea feces has been suggested, involving inhalation of the aerosolized pathogen by susceptible mammals.

R. typhi has been detected in ectoparasites other than fleas. Because most of these arthropods do not bite humans, their presumed role is in transmitting R. typhi en-zootically among commensal rats. Ectoparasites in this category include the sucking lice Hoplopleura pacifica and Polyplax spinulosa, the mesostigmatid mites Laelaps echid-ninus and Ornithonyssus bacoti, and the chigger Ascoshoen-gastia indica. Although the human body louse (Pediculus humanus humanus) is an experimental vector of R. typhi, it apparently is not involved in natural transmission cycles.

The diagnosis of human infection usually involves the demonstration of seroconversion against R. typhi or isolation of the bacterium. Recent advances in R. typhi detection in fleas include the development of an enzyme-linked immunosorbent assay and of a technique to demonstrate a 434—base pair nucleotide sequence of the R. typhi genome using a PCR assay. These techniques are useful in patient diagnosis and in screening potential reservoir hosts.

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