Typhus Group Rickettsiosis, Germany, 2010-20171

Abstract

Typhus group rickettsiosis is caused by the vectorborne bacteria Rickettsia typhi and R. prowazekii. R. typhi, which causes murine typhus, the less severe endemic form of typhus, is transmitted by fleas; R. prowazekii, which causes the severe epidemic form of typhus, is transmitted by body lice. To examine the immunology of human infection with typhus group rickettsiae, we retrospectively reviewed clinical signs and symptoms, laboratory changes, and travel destinations of 28 patients who had typhus group rickettsiosis diagnosed by the German Reference Center for Tropical Pathogens, Hamburg, Germany, during 2010-2017. Immunofluorescence assays of follow-up serum samples indicated simultaneous seroconversion of IgM, IgA, and IgG or concurrence in the first serum sample. Cytokine levels peaked during the second week of infection, coinciding with organ dysfunction and seroconversion. For 3 patients, R. typhi was detected by species-specific nested quantitative PCR. For all 28 patients, R. typhi was the most likely causative pathogen.

Keywords: PCR; Rickettsia prowazekii; Rickettsia typhi; bacteria; cytokines; epidemic typhus; murine typhus; serology; travel; vector-borne infections; zoonoses.

Figure 1

Countries and US states in which 27 of 28 patients acquired typhus group rickettsiosis diagnosed in Germany, 2010–2017. For 1 of the 28 patients, no information was available. Most infections were acquired in Southeast Asia, although 3 autochthonous cases were found in Germany. Each dot symbolizes 1 patient.

Figure 2

Typical exanthema in a typhus patient after travel to Thailand. The rash is maculopapular and nonpruritic.

Figure 3

Cytokine and chemokine levels in serum from patients with imported and autochthonous typhus group rickettsiosis and controls, Germany, 2010–2017. Using a bead-based LEGENDplex assay (BioLegend, Fell, Germany), we analyzed 16 serum samples from healthy persons without rickettsial disease and 26 samples from 21 patients with typhus group rickettsiosis in parallel. We assigned 17 serum samples to the acute phase of illness (7 on days 0–7 and 10 on days 8–14), 4 to the prolonged phase, and 5 to the convalescent phase. Most serum cytokine levels started to increase in the first week of illness, peaked in the second week, and then started to decline again, except for IL-21 and IL-22, which reached their highest levels in the third week after symptom onset. Data are expressed as mean ± SD. Statistical analyses were performed by using the Kruskal-Wallis test and subsequently the Dunn multiple comparisons test. IFN, interferon; IL, interleukin; IP, interferon γ–induced protein; MIP, macrophage inflammatory protein; VEGF, vascular endothelial growth factor. Asterisks indicate statistically significant differences: *p<0.05; **p<0.01; ***p<0.001.