Murine typhus fever probably has occurred for centuries as a sporadic or endemic disease, but only since 1931 has it been clearly distinguished from classic epidemic louse-borne typhus. During the early part of this century in the United States murine typhus was confused with Brill’s disease. However, in 1926 Maxey, after extensive investigation, concluded that the typhus occurring in the southeastern United States must have a reservoir other than man, and he mentioned mice and rats specifically. He further suggested that fleas, mites, or ticks could be the vector. Mooser, in 1928, observed a basic difference in behavior of certain strains of typhus rickettsiae in the tissues of guinea pigs. Dyer and colleagues isolated typhus rickettsiae from rat fleas in Baltimore (1931), and Mooser, Zinsser, and Ruiz Castaneda found the agent in rats in Mexico City. Mooser subsequently named the disease “murine typhus” to indicate
The etiologic agent, Rickettsia mooseri is similar to Rickettsia prowazeki in metabolic, biochemical, and staining characteristics; however, in size, R. mooseri is slightly smaller and more uniform. R. mooseri and R. prowazeki are classed together in the typhus group by virtue of the fact that they possess a common soluble antigenic moiety.
Epidemiology and Transmission.
Rats infected with murine typhus are found scattered throughout the world in circumscribed areas. In the United States reservoirs of the disease are found along the southern Atlantic seaboard and in states bordering on the Gulf of Mexico. Other known areas of infection are Mexico, South America, the Mediterranean littoral, and Manchuria. However, the disease is widespread, occurring elsewhere in such areas as Ethiopia, Malaysia, and Australia.
Murine typhus is maintained in nature as a mild infection of rats, and is transmitted from rat to rat by the rat louse or by the rat flea, Xenopsylla cheopis. A flea becomes infected while feeding on a rat during the acute phase of an infection. The rickettsiae multiply in the flea without causing any damage to the host. Once infected the flea continues to discharge rickettsiae in its feces for the remainder of its life; however, infected female fleas do not transmit R. mooseri via their eggs to the next generation of fleas.
Man usually acquires the disease when bitten by an infected flea. Rat fleas generally prefer to feed on rats, but they will attack man if rats become scarce. At the same time that an infected flea sucks blood it deposits feces that are teeming with rickettsiae. These may be rubbed into the flea bite wound or, as dried aerosol of feces and micro-organisms, they may gainaccess to the body through the mucous membranes of the conjunctivae or respiratory tract. Infection of man is an accidental occurrence and is not related to the maintenance of the disease in nature.
Information on the pathology of murine typhus is limited. It is usually assumed that the lesions are essentially the same as those in epidemic typhus.
Clinical Manifestation and Course.
The incubation period of murine typhus lasts from six to fourteen days. The symptoms are similar to those of epidemic typhus, the principal differences being that murine typhus is milder and shorter, the rash is less extensive and persists for shorter periods, there are fewer complications, and the case fatality rate is lower.
Clinical Diagnosis of Murine Typhus Fever .
The diagnosis of murine typhus may be suspected when a patient has a sustained fever of several days’ duration accompanied by headache, generalized aches and pains, and a macular or maculopapular rash appeaxing on ox day oitset offever. The rash is first noted on the trunk and later spreads to the extremities; the face, palms, and soles are not involved. Since murine typhus is present in many of the areas where Rocky Mountain spotted fever (RMSF) occurs, it is helpful to remember that the rash of RMSF first appears on the wrists and ankles, rapidly spreads up the extremities to the trunk, and regularly involves the palms and soles.
The patient with murine typhus usually gives a history of activities that have brought him into contact with place* where rats are numerous. However, there is often, no definite recollection of a flea bite.It is impossible on clinical evidence aline to distinguish an ordinary7 case of murine typhus from a case of Brill-Zinsser disease or a milH of epidemic typhus. Epidemiologic and laboratory data will almost always’ be required to arrive at a definitive diagnosis.
Both the complement-fixation and Weil-Felix tests are employed in the laboratory to confirm the clinical suspicion of a murine typhus infection. Rising antibodies to the commercially available soluble, typhus group antigen indicate either a primary epidemic typhus, Brill-Zinsser disease, or murine typhus infection. From the time of onset Brill-Zinsser disease antibodies are IgG in type. In contrast, the antibodies produced in the acute phase of murine and epidemic typhus are characteristically IgM. One may have to resort to specific washed rickettsial antigens to distinguish between epidemic and murine typhus. In murine typhus as in primary epidemic typhus 4 to 8 units of antigen are required to obtain optimal fixation of complement during the acute phase of illness.
The Weil-Felix test employing Proteus OX-19 strains is regularly positive in murine typhus. Isolation of R. mooseri from patients may be accomplished early in the course of the disease by inoculating blood into guinea pigs, mice, or chick embryos. (See Laboratory Diagnosis in Epidemic Typhus.)
Even when untreated, murine typhus is usually a mild disease with fatalities occurring only in the elderly. The use of specific therapy further reduces the duration and severity of the disease.
Treatment of murine typhus is similar to that for epidemic typhus. However, the usual mildness of murine typhus permits more leeway in a therapeutic regimen. For example, tetracycline can be used as the preferred drug, thus avoiding the greater potential toxicity of chloramphenicol.
Prevention and Control.
Measures to prevent and control murine typhus depend upon limiting the rat population. The first step is to reduce the flea population of rat colonies by dusting rat runs with DDT or its equivalent. Following this, rat populations are reduced by poisoning, trapping, eliminatiag rat harborages, and rat-proofing buildings.
A vaccine has been produced and demonstrated to be effective. However, its use is hardly justified in view of the clinical mildness and sporadic nature of the disease.