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The incidence of spotted fever group (SFG) rickettsioses in the United States has tripled since 2010. Rocky Mountain spotted fever, the most severe SFG rickettsiosis, is caused by Rickettsia rickettsii. The lack of species-specific confirmatory testing obfuscates the relative contribution of R. rickettsii and other SFG Rickettsia to this increase. We report a newly recognized rickettsial pathogen, Rickettsia sp. CA6269, as the cause of severe Rocky Mountain spotted fever-like illness in 2 case-patients residing in northern California. Multilocus sequence typing supported the recognition of this pathogen as a novel Rickettsia genotype most closely related to R. rickettsii. Cross-reactivity observed for an established molecular diagnostic test indicated that Rickettsia sp. CA6269 might be misidentified as R. rickettsii. We developed a Rickettsia sp. CA6269-specific real-time PCR to help resolve this diagnostic challenge and better characterize the spectrum of clinical disease and ecologic epidemiology of this pathogen.

Rocky Mountain spotted fever (RMSF) is a severe tickborne disease that can reach epidemic proportions in communities with certain social and ecologic risk factors. In some areas, the case-fatality rate of brown dog tick-associated RMSF is up to 50%. Because of the spread of brown dog tick-associated RMSF in the southwestern United States and northern Mexico, the disease has the potential to emerge and become endemic in other communities that have large populations of free-roaming dogs, brown dog ticks, limited resources, and low provider awareness of the disease. By using a One Health approach, interdisciplinary teams can identify communities at risk and prevent severe or fatal RMSF in humans before cases occur. We have developed a conceptual framework for RMSF prevention to enable communities to identify their RMSF risk level and implement prevention and control strategies.

Rocky mountain spotted fever (RMSF) causes significant illness and death in children. Although historically rare in California, USA, RMSF is endemic in areas of northern Mexico that border California. We describe 7 children with RMSF who were hospitalized at a tertiary pediatric referral center in California during 2017-2023. Five children had recent travel to Mexico with presumptive exposure, but 2 children did not report any travel outside of California. In all 7 patients, Rickettsia rickettsii DNA was detected by plasma microbial cell-free next-generation sequencing, which may be a useful diagnostic modality for RMSF, especially early in the course of illness, when standard diagnostic tests for RMSF are of limited sensitivity. A high index of suspicion and awareness of local epidemiologic trends remain most critical to recognizing the clinical syndrome of RMSF and initiating appropriate antimicrobial therapy in a timely fashion.

We report a case-series study of 5 patients with Japanese spotted fever from the Three Gorges Area in China, including 1 fatal case. Seroprevalence of Rickettsia japonica was ≈21% among the local population. Our report highlights the emerging potential threat to human health of Japanese spotted fever in the area.

Rocky Mountain spotted fever, a tick-borne zoonosis caused by Rickettsia rickettsii, is among the most lethal of all infectious diseases in the Americas. In Mexico, the disease was first described during the early 1940s by scientists who carefully documented specific environmental determinants responsible for devastating outbreaks in several communities in the states of Sinaloa, Sonora, Durango, and Coahuila. These investigators also described the pivotal roles of domesticated dogs and Rhipicephalus sanguineus sensu lato (brown dog ticks) as drivers of epidemic levels of Rocky Mountain spotted fever. After several decades of quiescence, the disease re-emerged in Sonora and Baja California during the early 21st century, driven by the same environmental circumstances that perpetuated outbreaks in Mexico during the 1940s. This Review explores the history of Rocky Mountain spotted fever in Mexico, current epidemiology, and the multiple clinical, economic, and social challenges that must be considered in the control and prevention of this life-threatening illness.

Testing for spotted fever group rickettsioses (SFGR) and the criteria for identifying suspected patients are not routinely used in Kazakhstan. In 2019, we performed a cross-sectional study in 6 sentinel hospitals in the Pavlodar region. We tested 105 hospitalized patients with SFGR-like symptoms by using PCR or indirect immunofluorescence antibody assay and identified 62 cases of SFGR. Most (78%) cases of disease were caused by Rickettsia sibirica and R. raoultii. Cutaneous signs (eschar or rash) were found in 87% of SFGR patients; 79% had a rash, 48% had an eschar, and 13% had neither. Testing of suspected rickettsia cases resulted in a 27% increase in laboratory-detected SFGR over the mean of the previous 3 years (62 vs. 49). Broadening the case definition by including fever, headache, or myalgia and expanding routine testing for suspected cases of SFGR could contribute to improved case detection and earlier treatment.

We found serologic evidence of spotted fever group Rickettsia in humans and dogs and typhus group Rickettsia in dogs in Reynosa, Mexico. Our investigation revealed serologic samples reactive to spotted fever group Rickettsia in 5 community members, which highlights a potential rickettsial transmission scenario in this region.

In a multicenter, nationwide, retrospective study of patients hospitalized with spotted fever group rickettsiosis in Israel during 2010-2019, we identified 42 cases, of which 36 were autochthonous. The most prevalent species was the Rickettsia conorii Israeli tick typhus strain (n = 33, 79%); infection with this species necessitated intensive care for 52% of patients and was associated with a 30% fatality rate. A history of tick bite was rare, found for only 5% of patients; eschar was found in 12%; and leukocytosis was more common than leukopenia. Most (72%) patients resided along the Mediterranean shoreline. For 3 patients, a new Rickettsia variant was identified and had been acquired in eastern, mountainous parts of Israel. One patient had prolonged fever before admission and clinical signs resembling tickborne lymphadenopathy. Our findings suggest that a broad range of Rickettsia species cause spotted fever group rickettsiosis in Israel.

In 2020, a novel spotted fever group Rickettsia was described in 3 clinically ill dogs in the United States. Using naturally infected canine blood, the novel Rickettsia sp. was isolated in epithelial (Vero E6) and mononuclear (DH82 and 030D) cell lines. The sequenced whole genome revealed a 1.27 Mb circular chromosome with 96.87% identity to Rickettsia raoultii on the basis of average nucleotide identity analysis. A maximum-likelihood phylogeny tree placed the novel Rickettsia in its own branch within the spotted fever group. Immunofluorescence revealed single rods localized along the membrane in epithelial cells and randomly distributed in the cytoplasm of mononuclear cells. We propose the name Rickettsia finnyi sp. nov., strain 2024-CO-Wats, which is available from national and international Rickettsial isolate reference collections. Fever and thrombocytopenia were among abnormalities in the 17 naturally infected dogs we describe, underscoring the pathogenic importance of R. finnyi sp. nov. and its potential public health relevance.

Background Brazilian spotted fever is a tick-borne disease caused by the bacterium Rickettsia rickettsii , whose main vector in Brazil is the tick Amblyomma sculptum . Amplifying hosts are essential for the perpetuation of this bacterium in the tick population as they can be sources of infection during bacteremic periods. Recent studies demonstrated the ability of suids ( Sus scrofa ) to sustain populations of A. sculptum , one of the main tick species found parasitizing wild boars in the midwestern and southeastern regions of Brazil. In this study, wild boars were experimentally infected with R. rickettsii by tick infestation and were evaluated for their ability to transmit the infection to A. sculptum ticks, under laboratory conditions. Methods Four wild boars were infected with R. rickettsii through infestation with R. rickettsii -infected A. sculptum adults (infected group); a fifth wild boar was infested with uninfected A. sculptum adults (control group). Simultaneously, the animals were infested with uninfected larvae and nymphs of A. sculptum . The wild boars were monitored for 28 days by clinical examination and hematological tests, real-time quantitative PCR (qPCR) of blood for the detection of Rickettsia and inoculation of blood in guinea pigs. IgG antibody titers were followed until the end of the experiment. Unfed nymphs and adults, molted from engorged larvae and nymphs that fed on wild boars, were used to infest susceptible guinea pigs and rabbits; some of these unfed ticks were tested by qPCR for rickettsial detection. Results The wild boars showed no clinical or hematological alterations, and bacteremia was not detected by qPCR or inoculation of wild boar blood into guinea pigs. Furthermore, wild boars showed a moderate humoral response, with anti- R. rickettsii endpoint titers up to 256 or 512. Rickettsial DNA was not detected in molted ticks after acquisition feeding on wild boars. Moreover, no disease or seroconversion was observed in guinea pigs and rabbits that were infested with ticks originated from wild boar acquisition feeding. Conclusions Wild boars seroconverted to Rickettsia spp. after being infested with R. rickettsii -infected A. sculptum ; however, they did not develop bacteremia and did not act as competent amplifying hosts of R. rickettsii for A. sculptum ticks. Graphical Abstract