IgM and IgG are usually both detected 7 to 15 days after disease onset.20 The diagnosis of recent murine typhus can be established by demonstrating a four-fold or greater rise in titer of antibody in properly collected acute and convalescent serum samples.21 In Tunisia, rickettsioses have been described since the beginning of the 20th century, but cases are poorly documented and few records are available in the literature.22 In 1995, Omezzine-Letaief and colleagues23 tested 500 sera from blood donors in Tunisia and identified that 3.6% had antibodies to R typhi.

The same year, in a prospective study among 300 patients hospitalized with fever, infectious diseases were confirmed or suspected

in 220 cases—in this group, when serology of rickettsial infections were performed systematically, MG-132 order 6% of patients had acute rickettsioses, and seroprevalence of R conorii and R typhi were 22.6 and 15.6%.24 In 2005, seven cases of murine typhus were reported in Tunisia.25 Sudden onset of fever and headache were reported in all cases, whereas a rash was noted in four patients. The rash began around the fifth day of the onset and was maculopapular and nonconfluent. Recently, nine consecutive patients with serologically confirmed murine typhus were reported.26 These patients were examined for the ocular involvement that is frequently check details observed in acute murine typhus.26 The typical cycle of R typhi involves the roof and Norway rats (Rattus rattus and Rattus norvegicus, respectively) and the rat flea (Xenopsylla cheopis). The rat reservoir not only serves as a host for the flea vector but also makes rickettsiae available in the blood for fleas, which transmit rickettsiae back to a rat host during subsequent feeding.27 Most of the reported human cases of murine typhus have been associated in sites with large rat populations. Human infection is associated with the presence of rats and their fleas living in indoor urban environments. Fleas propagate most

successfully in hot, dry environments. There is a Oxymatrine seasonal incidence which appears to be correlated with the abundance of the vector fleas, which is in late summer and early autumn when X cheopis fleas are most abundant.28 All our cases of murine typhus occurred in late summer and early autumn. Cases of murine typhus have been identified in the countries around the Mediterranean area (Figure 1). Recently in Algeria two cases of R typhi infection were confirmed in patients with fever.29 In Israel cases of murine typhus are frequently reported and Bishara and colleagues30 published 406 cases of murine typhus in Jews and Arabs. Shalev and colleagues31 identified that murine typhus is an important cause of febrile illnesses among Bedouin children as the 13.8% among 549 children with fever had serologically confirmed murine typhus.