Murine typhus is an uncommon flea-borne infectious disease caused by Rickettsia typhi. The illness is less commonly diagnosed in the United States than in the developing world because of improvements in hygiene and rat control efforts. However, Texas has experienced an increasing number of cases since 2004 and currently diagnoses between 500 and 700 cases per year. California has confirmed between 150 and 200 cases per year during the same time period.
Rickettsia typhi is a gram-negative, obligate, intracellular bacillus. It is primarily transmitted by the Oriental rat flea, Xenopsylla cheopis. Additional vectors include the cat flea, Ctenocephalides felis and the mouse flea, Leptopsyllia segnis. Fleas become infected when they bite infected animals, such as rats, cats, or opossums. One infected, fleas remain permanently infected for the remainder of their lives. People who have close contact with feral cats and rodents are at greatest risk of contracting murine typhus.
When an infected flea bites a person, the bite punctures the skin. Fleas deposit their feces in the wound while feeding, leading to infection. People can also become infected by inhaling infected flea feces or by rubbing it into their eyes. Murine typhus does not spread from person to person.
The incubation period from exposure to onset of symptoms is usually between 5 and15 days. Murine typhus is typically a mild illness. Signs and symptoms are generally nonspecific. The most common symptoms are fever, headache, malaise, chills, myalgias, cough, nausea, and vomiting. About half of patients develop a rash near the end of the first week of illness. The rash typically begins as a maculopapular eruption on the trunk and spreads peripherally, sparing the palms and soles. However, the pattern of rash development is too variable to be diagnostic. The classic triad of fever, headache and rash is present in about one third of patients. Patients with glucose-6-phosphate dehydrogenase deficiency (G6PD) and advanced age are more likely to develop neurologic and cardiac complications. G6PD associated hemolysis is thought to potentiate rickettsia-induced vasculitis.
Common laboratory findings include elevations of creatine kinase (CK), ALT, AST, and LDH. Other laboratory abnormalities include hypoalbuminemia, hyponatremia, and thrombocytopenia. White blood cell count is usually normal.
The best diagnostic test is an indirect immunofluorescence assay for IgG antibodies to Rickettsia typhi. A single titer of 128 or higher can be consistent with recent infection. Titers of 1:16 to 1:64 can be seen in recent or past infection. A fourfold increase in antibody titer between acute and convalescent specimens collected 2 to 4 weeks apart is consistent with recent infection.
Treatment with doxycycline decreases the average length of febrile illness from approximately 2 weeks to less than 4 days. Treatment should be continued for 3 days after resolution of symptoms. Ciprofloxacin is also effective and should be used for patients in whom doxycycline is contraindicated.
Specimen requirement is serum. Blood should be collected in a red top tube.
References
Stern RM et al. A headache of a diagnosis. N Engl J Med 2018;379:475-79.
Lara GP et al. Murine Typhus, Comb med (Cali). 2012;43(2):175-180.
Blanton LS, Murine Typhus: A Review of a Reemerging Flea-Borne Rickettsiosis with Potential for Neurologic Manifestations and Sequalae. Infect Dis Rep. 2023;15(6):700-716.