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Didier Raoult - One of the best experts on this subject based on the ideXlab platform.
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Epidemiological serosurvey of vector-borne and zoonotic pathogens among homeless people living in shelters in Marseille: cross-sectional one-day surveys (2005–2015)
European Journal of Clinical Microbiology & Infectious Diseases, 2020Co-Authors: Tran Duc Anh Ly, Vanthuan Hoang, Meriem Louni, Sekene Badiaga, Hervé Tissot-dupont, Pierre-edouard Fournier, Philippe Brouqui, Didier Raoult, Philippe GautretAbstract:Homeless people are often exposed to unhygienic environments as well as to animals carrying arthropods which both transmit zoonotic infections and human louse-borne pathogens. We attempted to determine the prevalence of antibodies against several vector-borne and zoonotic pathogens among homeless adults living in Marseille. During the 2005–2015 period, we collected sera samples from 821 homeless adults living in shelters. Antibodies against Bartonella quintana , Bartonella henselae , Borrelia recurrentis , Coxiella burnetii , Francisella tularensis (with a cut-off of 1:100), Rickettsia akari , Rickettsia conorii , Rickettsia felis , Rickettsia prowazekii , and Rickettsia typhi (with a cut-off of 1:64) were searched by microimmunofluorescence (MIF). MIF-positive serum samples were confirmed by cross-adsorption to characterise cross-reacting antigens and immunoblotting. Positive sera by Western blot were further tested using qPCR. We evidenced a prevalence of 4.9% seroreactivity to at least one pathogen including phase II C. burnetii (2.1%), B. quintana (1.7%), R. conorii (0.4%), R. prowazekii (0.4%), R. typhi (0.1%), B. recurrentis (0.1%), and F. tularensis (0.1%). No DNA from any pathogens was detected. A comparison with studies conducted prior to the 2000–2003 period showed a decrease in the overall seroprevalence of several vector-borne and zoonotic infections.
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encodes an intracytoplasmic protein
2016Co-Authors: Zuzana Sekeyova, Veronique Roux, Didier RaoultAbstract:‘Gene D ’ is the PS120-protein-encoding gene, first described in Rickettsia conorii and Rickettsia japonica. Sequence analysis of a 3030 bp fragment of ‘gene D ’ in 24 representatives of the genus Rickettsia was carried out to complete phylogenetic analyses previously inferred by comparison of gene sequences encoding citrate synthase, 17 kDa antigen and rOmpA and rOmpB. The phylogenetic relationships between Rickettsiae were inferred from the comparison of both the gene and the derived protein sequences, using the parsimony, neighbour-joining and maximum-likelihood methods. Five distinct groups of Rickettsiae were identified. These were: the Rickettsia massiliae group, including R. massiliae, Bar 29, Rickettsia rhipicephali and Rickettsia aeschlimannii; the Rickettsia rickettsii group containing Rickettsia sibirica, ‘Rickettsia mongolotimonae ’, Rickettsia parkeri, strain S, Rickettsia africae, the R. conorii complex, Rickettsia slovaca, Rickettsia honei, R. rickettsii, R. japonica and Rickettsia montanensis; the group currently containing only Rickettsia helvetica; the Rickettsia akari group including Rickettsia australis, R. akari and the ELB agent; Rickettsia prowazekii and Rickettsia typhi clustered in the typhus group. As significant bootstrap values were obtained for most of the nodes, sequence comparison of ‘gene D ’ should be considered as a complementary approach in phylogenetic studies of Rickettsiae
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Genome Sequence of Rickettsia australis, the Agent of Queensland Tick Typhus
Journal of bacteriology, 2012Co-Authors: Xin Dong, Didier Raoult, Khalid El Karkouri, Catherine Robert, Pierre-edouard FournierAbstract:ABSTRACT Rickettsia australis strain PhillipsT was isolated in Queensland, Australia, in 1950. It is the tick-borne agent of Queensland tick typhus, a disease endemic in Australia. The 1.29-Mb genome sequence of this bacterium is highly similar to that of Rickettsia akari but contains two plasmids.
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A case of Rickettsialpox in Northern Europe.
International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases, 2012Co-Authors: Aurélie Renvoisé, Jan W Van't Wout, Jan-gerrit Van Der Schroeff, Matthias F. C. Beersma, Didier RaoultAbstract:We report the first case of Rickettsialpox caused by Rickettsia akari in the Netherlands. The diagnosis was suspected based on clinical grounds and was confirmed by Western blot analysis with cross-adsorption. Because the arthropod vector (Liponyssoides sanguineus) is ubiquitous, we suspect that the disease is under-diagnosed in non-endemic areas.
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Genome sequence of Rickettsia australis, the agent of Queensland tick typhus
2012Co-Authors: Xin Dong, Didier Raoult, Khalid El Karkouri, Catherine Robert, Pierre-edouard FournierAbstract:typhus, a disease endemic in Australia. The 1.29-Mb genome sequence of this bacterium is highly similar to that of Rickettsia akari but contains two plasmids. The genus Rickettsia is composed of small Gram-negative, obli-gate intracellular alphaproteobacteria (1) that underwent pro-gressive genomic reduction (2). However, paradoxically, recent genomic studies have suggested that genome reduction was asso-ciated with increased virulence in Rickettsiae (3). Rickettsia aust-ralis was first identified in residents of Northern Queensland, Australia, in 1950 (4). This bacterium is a spotted fever group Rickettsia and causes Queensland tick typhus (QTT). QTT is en-demic in the eastern part of Australia, where it is transmitted to humans through the bites of Ixodes holocyclus or Ixodes tasmani ticks (6). It is considered to bemostly mild and is characterized by fever, headache, and myalgia followed by the development of a maculopapular or vesicular rash, an inoculation eschar (65 % of cases), and lymphadenopathy (71%) (5)
Christopher D Paddock - One of the best experts on this subject based on the ideXlab platform.
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Detection of Rickettsia rickettsii, Rickettsia parkeri, and Rickettsia akari in Skin Biopsy Specimens Using a Multiplex Real-time Polymerase Chain
2016Co-Authors: Reaction Assay, William L. Nicholson, Amy M. Denison, Bijal D. Amin, Christopher D PaddockAbstract:Background. Rickettsia rickettsii, Rickettsia parkeri, and Rickettsia akari are the most common causes of spotted fever group rickettsioses indigenous to the United States. Infected patients characteristically present with a maculo-papular rash, often accompanied by an inoculation eschar. Skin biopsy specimens are often obtained from these lesions for diagnostic evaluation. However, a species-specific diagnosis is achieved infrequently from pathologic specimens because immunohistochemical stains do not differentiate among the causative agents of spotted fever group Rickettsiae, and existing polymerase chain reaction (PCR) assays generally target large gene segments that may be difficult or impossible to obtain from formalin-fixed tissues. Methods. This work describes the development and evaluation of a multiplex real-time PCR assay for the de-tection of these 3 Rickettsia species from formalin-fixed, paraffin-embedded (FFPE) skin biopsy specimens. Results. The multiplex PCR assay was specific at discriminating each species from FFPE controls of unrelated bacterial, viral, protozoan, and fungal pathogens that cause skin lesions, as well as other closely related spotted fever group Rickettsia species. Conclusions. This multiplex real-time PCR demonstrates greater sensitivity than nested PCR assays in FFPE tissues and provides an effective method to specifically identify cases of Rocky Mountain spotted fever, Rickettsialpox, and R. parkeri rickettsiosis by using skin biopsy specimens
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Detection of Rickettsia rickettsii, Rickettsia parkeri, and Rickettsia akari in Skin Biopsy Specimens Using a Multiplex Real-time Polymerase Chain Reaction Assay
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 2014Co-Authors: Amy M. Denison, William L. Nicholson, Bijal D. Amin, Christopher D PaddockAbstract:Spotted fever group Rickettsia (SFGR) species are a large and diverse assemblage of obligately intracellular, Gram-negative bacteria that reside in fleas, ticks, and mites. At least 9 named SFGR species are endemic to the United States, including several known pathogens. However, most indigenous spotted fever group (SFG) rickettsioses are caused by Rickettsia rickettsii, Rickettsia akari, or Rickettsia parkeri, the etiologic agents of Rocky Mountain spotted fever (RMSF), Rickettsialpox, and R. parkeri rickettsiosis, respectively [1]. Each of these infections is characterized by fever and a generalized exanthem, and skin biopsy specimens are often obtained to establish a presumptive diagnosis. Rickettsia rickettsii is transmitted by several tick species, including Dermacentor variabilis, Dermacentor andersoni, and Rhipicephalus sanguineus. Several hundred to several thousand cases of RMSF are reported annually in the United States, predominantly from the central and southeastern states [2]. RMSF is the most severe SFG rickettsiosis; the case-fatality rate of untreated infections can be >20%. A maculopapular or petechial rash is identified on most patients, but an inoculation eschar is rarely described [3–5]. Rickettsia akari is transmitted to humans from the bite of the house mouse mite (Liponyssoides sanguineus) [6]. Rickettsialpox is milder than RMSF and is typically associated with an inoculation eschar and a maculopapular rash that may be vesicular. In the United States, Rickettsialpox exists as an urban zoonosis, and almost every documented US case has originated from a large metropolitan center [7]. The intentional release of Bacillus anthracis as a weapon of bioterrorism in 2001 elevated physician awareness of eschar-associated illnesses, including Rickettsialpox [8]. Rickettsia parkeri was first identified as a cause of disease in humans in 2004 [9]. The Gulf Coast tick (Amblyomma maculatum) is the vector of R. parkeri and is distributed throughout much of the southeastern and mid-Atlantic United States [10]. This moderately severe illness shares features with RMSF and Rickettsialpox, namely, the occurrence of 1 or more inoculation eschars, and a maculopapular rash, occasionally with vesicular or petechial components [9]. The sympatric distribution of the tick vectors and Rickettsia species, and the clinical and histological similarities of 1 or more of the cutaneous manifestations of RMSF, R. parkeri rickettsiosis and Rickettsialpox (Figures 1 and and2),2), necessitate the use of advanced methods to confirm and distinguish these infections. In addition, various other viral, bacterial, fungal, or protozoan pathogens may cause eschar or rash lesions that are clinically or histologically similar to those caused by SFGR [10, 11]. Immunohistochemical staining techniques are useful to confirm SFG rickettsioses; however, these assays are not species specific [7,9]. Species-specific identification of the diseases is achieved infrequently from formalin-fixed, paraffin-embedded (FFPE) specimens [12], because relatively large segments of particular gene targets are used conventionally to establish a molecular diagnosis from blood or fresh tissues [13]. Species-specific confirmation from FFPE skin biopsy specimens is particularly challenging because formalin causes nucleic acid fragmentation that characteristically limits the size of successful polymerase chain reaction (PCR) amplicons [12], and skin biopsies typically provide relatively small amounts of pathogen DNA for molecular analysis. This work was initiated to develop a reliable real-time PCR assay to amplify small but specific DNA fragments of 3 of the most frequently encountered pathogenic SFGR in the United States from FFPE skin biopsy specimens. Figure 1 Clinical and histological resemblance between the inoculation eschar of Rickettsia parkeri rickettsiosis (A and C) and Rickettsialpox (B and D). Clinically, both lesions are characterized by a 0.5- to 1.5-cm necrotic crust surrounded by an erythematous ... Figure 2 Clinical and histological similarities among rashes of Rocky Mountain spotted fever (A and D), Rickettsia parkeri rickettsiosis (B and E), and Rickettsialpox (C and F). Each infection may exhibit an erythematous maculopapular rash (A–C). The histological ...
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Wide Dispersal and Possible Multiple Origins of Low-Copy-Number Plasmids in Rickettsia Species Associated with Blood-Feeding Arthropods
Applied and environmental microbiology, 2010Co-Authors: Gerald D. Baldridge, Christopher D Paddock, Nicole Y. Burkhardt, Marcelo B. Labruna, Richard C. Pacheco, Philip C. Williamson, Peggy M. Billingsley, Roderick F. Felsheim, Timothy J. Kurtti, Ulrike G. MunderlohAbstract:Plasmids are mobile genetic elements of bacteria that can impart important adaptive traits, such as increased virulence or antibiotic resistance. We report the existence of plasmids in Rickettsia (Rickettsiales; Rickettsiaceae) species, including Rickettsia akari, "Candidatus Rickettsia amblyommii," R. bellii, R. rhipicephali, and REIS, the Rickettsial endosymbiont of Ixodes scapularis. All of the Rickettsiae were isolated from humans or North and South American ticks. R. parkeri isolates from both continents did not possess plasmids. We have now demonstrated plasmids in nearly all Rickettsia species that we have surveyed from three continents, which represent three of the four major proposed phylogenetic groups associated with blood-feeding arthropods. Gel-based evidence consistent with the existence of multiple plasmids in some species was confirmed by cloning plasmids with very different sequences from each of two "Ca. Rickettsia amblyommii" isolates. Phylogenetic analysis of Rickettsial ParA plasmid partitioning proteins indicated multiple parA gene origins and plasmid incompatibility groups, consistent with possible multiple plasmid origins. Phylogenetic analysis of potentially host-adaptive Rickettsial small heat shock proteins showed that hsp2 genes were plasmid specific and that hsp1 genes, found only on plasmids of "Ca. Rickettsia amblyommii," R. felis, R. monacensis, and R. peacockii, were probably acquired independently of the hsp2 genes. Plasmid copy numbers in seven Rickettsia species ranged from 2.4 to 9.2 per chromosomal equivalent, as determined by real-time quantitative PCR. Plasmids may be of significance in Rickettsial evolution and epidemiology by conferring genetic plasticity and host-adaptive traits via horizontal gene transfer that counteracts the reductive genome evolution typical of obligate intracellular bacteria.
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Isolation of Rickettsia akari from eschars of patients with Rickettsialpox.
The American journal of tropical medicine and hygiene, 2006Co-Authors: Christopher D Paddock, Tamara Koss, Marina E. Eremeeva, Gregory A. Dasch, Sherif R. Zaki, John W. SumnerAbstract:Rickettsialpox is a cosmopolitan, mite-borne, spotted fever rickettsiosis caused by Rickettsia akari. The disease is characterized by a primary eschar, fever, and a papulovesicular rash. Rickettsialpox was first identified in New York City in 1946 and the preponderance of recognized cases in the United States continues to originate from this large metropolitan center. The most recently isolated U.S. strain of R. akari was obtained more than a half century ago. We describe the culture and initial characterization of five contemporaneous isolates of R. akari obtained from eschar biopsy specimens from New York City patients with Rickettsialpox. This work emphasizes the importance and utility of culture-and molecular-based methods for the diagnosis of Rickettsialpox and other eschar-associated illnesses.
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Increased detection of Rickettsialpox in a New York City hospital following the anthrax outbreak of 2001: use of immunohistochemistry for the rapid confirmation of cases in an era of bioterrorism.
Archives of dermatology, 2003Co-Authors: Tamara Koss, Sherif R. Zaki, Eric L. Carter, Marc E. Grossman, David N. Silvers, Asher D. Rabinowitz, Joseph Singleton, Christopher D PaddockAbstract:Background Rickettsialpox is a self-limited febrile illness with skin lesions that may be mistaken for signs of potentially more serious diseases, such as cutaneous anthrax or chickenpox. The cluster of cutaneous anthrax cases from bioterrorism in October 2001 likely heightened awareness of and concern for cutaneous eschars. Objectives To apply an immunohistochemical technique on paraffin-embedded skin biopsy specimens for diagnosing Rickettsialpox, and to compare the reported incidence of Rickettsialpox before, during, and after the cluster of cutaneous anthrax cases. Design Case series. Setting Dermatology department in a large tertiary care hospital in New York City. Patients Eighteen consecutive patients with the clinical diagnosis of Rickettsialpox from February 23, 2001, through October 31, 2002. Main Outcome Measures Results of immunohistochemical testing of skin biopsy specimens and of serological testing. Results Immunohistochemical testing revealed spotted fever group Rickettsiae in all 16 eschars and in 5 of the 9 papulovesicles tested. A 4-fold or greater increase in IgG antibody titers reactive with Rickettsia akari was observed in all 9 patients for whom acute and convalescent phase samples were available; 6 patients had single titers indicative of Rickettsialpox infection (≥1:64). Of the 18 patients, 9 (50%) presented in the 5 months following the bioterrorism attacks. Conclusions Rickettsialpox remains endemic in New York City, and the bioterrorism attacks of October 2001 may have led to increased awareness and detection of this disease. Because Rickettsialpox may be confused with more serious diseases, such as cutaneous anthrax or chickenpox, clinicians should be familiar with its clinical presentation and diagnostic features. Immunohistochemical staining of skin biopsy specimens, particularly from eschars, is a sensitive technique for confirming the clinical diagnosis.
Suzana Radulovic - One of the best experts on this subject based on the ideXlab platform.
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CLINICAL ARTICLES Isolation of Rickettsia akari from a Patient in a Region Where Mediterranean Spotted Fever Is Endemic
2016Co-Authors: Suzana Radulovic, Hui-min Feng, Miro Morovic, Boris Djelalija, Vsevolod Popov, Patricia Crocquet-valdes, David H. WalkerAbstract:Rickettsia akari was isolated from blood collected from a patient in Croatia in 1991. We believe this is the first human isolate of R. akari to be reported in more than 40 years and the first ever from southern Europe. The Croatian isolate was antigenically and genetically indistinguishable from the prototype American strain and a Ukrainian strain. In all probability, Rickettsialpox would be diagnosed more frequently and over a wider geographic area if physicians gave greater consider-ation to the diagnosis and if laboratory diagnostic methods were better able to distinguish among spotted fever group rickettsioses. Rickettsialpox is a self-limited illness caused by Rickettsia akari, transmitted to humans by the bite of Liponyssoides san-guineus, a mite ectoparasite of the domestic mouse [1-11]. The distribution of transovarially infected mites determines the epidemiology of the disease. Aside from hundreds of cases in the cities of the northeastern United States during the late 1940s and the 1950s [4- 6, 9, 12-16], Rickettsialpox has bee
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Involvement of TLR2 and TLR4 in cell responses to Rickettsia akari
Journal of Leukocyte Biology, 2010Co-Authors: Marco A. Quevedo-diaz, Suzana Radulovic, Chang Song, Yanbao Xiong, Haiyan Chen, Larry M. Wahl, Andrei E. MedvedevAbstract:A better understanding of the pathogenesis of Rickettsial disease requires elucidation of mechanisms governing host defense during infection. TLRs are primary sensors of microbial pathogens that activate innate immune cells, as well as initiate and orchestrate adaptive immune responses. However, the role of TLRs in Rickettsia recognition and cell activation remains poorly understood. In this study, we examined the involvement of TLR2 and TLR4 in recognition of Rickettsia akari, a causative agent of Rickettsialpox. Transfection-based complementation of TLR2/4-negative HEK293T cells with human TLR2 or TLR4 coexpressed with CD14 and MD-2 enabled IκB-α degradation, NF-κB reporter activation, and IL-8 expression in response to heat-killed (HK) R. akari. The presence of the R753Q TLR2 or D299G TLR4 polymorphisms significantly impaired the capacities of the respective TLRs to signal HK R. akari-mediated NF-κB reporter activation in HEK293T transfectants. Blocking Ab against TLR2 or TLR4 markedly inhibited TNF-α release from human monocytes stimulated with HK R. akari, and TNF-α secretion elicited by infection with live R. akari was reduced significantly only upon blocking of TLR2 and TLR4. Live and HK R. akari exerted phosphorylation of IRAK1 and p38 MAPK in 293/TLR4/MD-2 or 293/TLR2 stable cell lines, whereas only live bacteria elicited responses in TLR2/4-negative HEK293T cells. These data demonstrate that HK R. akari triggers cell activation via TLR2 or TLR4 and suggest use of additional TLRs and/or NLRs by live R. akari.
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Rickettsialpox in turkey
Emerging Infectious Diseases, 2003Co-Authors: Mustafa Ozturk, Tamer Gunes, Mehmet Kose, Christopher Coker, Suzana RadulovicAbstract:To the Editor: Rickettsialpox is often described as a chickenpox-like disease and is caused by Rickettsia akari, a spotted fever group Rickettsia that is transmitted to humans by the bite of mites (Liponyssoides sanguineus). Although the mite host (typically a mouse) is widely distributed in cities, the disease is infrequently diagnosed. It is typically characterized in patients by the appearance of a primary eschar at the site of a mite bite followed by fever, headache, and development of a papulovesicular rash. Symptoms normally appear 9–14 days after the mite bite and are often unnoticed by the affected person. In documented Rickettsialpox cases, the presence of a papule that ulcerates and becomes a scar approximately 0.5–3.0 cm in diameter is reported (1–3). Three to 7 days later, symptoms are more pronounced, with patients experiencing the sudden onset of chills, fever, and headache followed by myalgia and the appearence of generalized vesicular skin rashes. Less frequently, photophobia, conjunctival injection, cough, generalized lymphadenopathy, and vomiting are reported. The first well-described clinical case of Rickettsialpox was documented in New York City in 1946 (1). Historically, most documented Rickettsialpox cases have occurred in large metropolitan areas of the United States (2), where the causative agent, R. akari, circulates primarily between the house mouse (Mus musculus) and its mite (Liponyssoides sanguineus). Recently, Rickettsialpox cases have been reported from Croatia, Ukraine, South Africa, Korea, and North Carolina (3,4). R. akari was isolated from the blood of a patient suspected of having Mediterranean spotted fever rather than Rickettsialpox; this was the first human isolate of R. akari reported in >40 years (4). Recent reports of a Rickettsialpox case in North Carolina (3), R. akari seropositivity found in HIV-positive intravenous drug users in the inner city of Baltimore, Maryland (5), and in Central and East Harlem, New York City (6), as well as Rickettsialpox cutaneous eruption in an HIV patient in New York (7), indicate that R. akari rickettsiosis is more common than previously thought and presents the risk of sporadic outbreaks worldwide. We describe the clinical presentation of Rickettsialpox in a 9-year-old boy from Nevpehir, located in the middle region of Turkey. Previously, a report from the Antalya area of Turkey described the prevalence of serum immunoglobulin (Ig) G antibodies in humans directed against R. conorii (spotted fever group Rickettsia) (8); however, Rickettsialpox was not reported in Turkey. This report of what we believe to be the first described Rickettsialpox case from Turkey further extends the recognized geographic distribution of R. akari. A 9-year-old boy was admitted to the Kayseri hospital with fever >39°C and generalized papulovesicular exanthema. One week before admission, fever, profuse sweating, headache, and dysuria were present. On admission, physical examination indicated generalized vesicular, bullouse, and papular exanthema involving the lips and oral cavity. Notable pathologic findings at admission included a black eschar on the boy’s penis, bilateral prominent conjunctival ejection, and bilateral lower pulmonary rales. The leukocyte count was 13,300/mm3, hemoglobin was 14.49 mg/dL, and the platelet count was 544,000/mm3. Serum electrolytes and blood urea nitrogen levels and results of coagulation study and urine analysis were normal. Routine blood cultures taken 24 hours postadmission were sterile. Specific antibodies (IgG; IgM) against Varicella were not detected in serum samples (Duzen Laboratories, Ankara, Turkey). Additionally, the patient reported mice on the family’s farm. A diagnosis of Rickettsialpox was made and doxycycline treatment (200 mg/kg) was initiated. The patient serum sample was tested by indirect immunofluorescence assay (IFA) for IgG and IgM antibodies reactive with R. akari (Kaplan strain), R. typhi (Wilmington), R. rickettsii (Sheila Smith), and R. conorii (Malish 7). Serum IgG titers of 1/1280 and IgM of 1/40 to R. akari were detected and confirmed through cross-adsorption with Rickettsial antigens (R. rickettsii, R. conorii) (9,10). Higher reciprocal titers were obtained against R. akari antigens than against R. rickettsii and R. conorii antigens (reciprocol titers of 1,024 vs. 512 and 512, respectively). We observed a difference in reduction in antibody titers against R. akari after adsorption with R. akari (Kaplan) (<16), R. rickettsii (256), and R. conorii (256). Antibodies against R. typhi were not detected. The IFA result confirmed the clinical diagnosis of R. akari infection. After 2 days of doxycycline treatment, the patient was afebrile, and the Rickettsialpox infection resolved without scars or complications. In summary, we present a case in which the presence of an eschar on the patient’s penis, the failure of lesions to appear in crops, the sparsity of lesions, and mice on the family’s farm led to a diagnosis of Rickettsialpox, which was confirmed by cross-adsorption serologic findings. This case indicates that Rickettsialpox is an emerging infectious disease in Turkey. We recommend further studies to define the prevalence of R. akari and the worldwide distribution of Rickettsialpox.
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Rickettsialpox in Turkey.
Emerging infectious diseases, 2003Co-Authors: Mustafa Ozturk, Tamer Gunes, Mehmet Kose, Christopher Coker, Suzana RadulovicAbstract:To the Editor: Rickettsialpox is often described as a chickenpox-like disease and is caused by Rickettsia akari, a spotted fever group Rickettsia that is transmitted to humans by the bite of mites (Liponyssoides sanguineus). Although the mite host (typically a mouse) is widely distributed in cities, the disease is infrequently diagnosed. It is typically characterized in patients by the appearance of a primary eschar at the site of a mite bite followed by fever, headache, and development of a papulovesicular rash. Symptoms normally appear 9–14 days after the mite bite and are often unnoticed by the affected person. In documented Rickettsialpox cases, the presence of a papule that ulcerates and becomes a scar approximately 0.5–3.0 cm in diameter is reported (1–3). Three to 7 days later, symptoms are more pronounced, with patients experiencing the sudden onset of chills, fever, and headache followed by myalgia and the appearence of generalized vesicular skin rashes. Less frequently, photophobia, conjunctival injection, cough, generalized lymphadenopathy, and vomiting are reported. The first well-described clinical case of Rickettsialpox was documented in New York City in 1946 (1). Historically, most documented Rickettsialpox cases have occurred in large metropolitan areas of the United States (2), where the causative agent, R. akari, circulates primarily between the house mouse (Mus musculus) and its mite (Liponyssoides sanguineus). Recently, Rickettsialpox cases have been reported from Croatia, Ukraine, South Africa, Korea, and North Carolina (3,4). R. akari was isolated from the blood of a patient suspected of having Mediterranean spotted fever rather than Rickettsialpox; this was the first human isolate of R. akari reported in >40 years (4). Recent reports of a Rickettsialpox case in North Carolina (3), R. akari seropositivity found in HIV-positive intravenous drug users in the inner city of Baltimore, Maryland (5), and in Central and East Harlem, New York City (6), as well as Rickettsialpox cutaneous eruption in an HIV patient in New York (7), indicate that R. akari rickettsiosis is more common than previously thought and presents the risk of sporadic outbreaks worldwide. We describe the clinical presentation of Rickettsialpox in a 9-year-old boy from Nevpehir, located in the middle region of Turkey. Previously, a report from the Antalya area of Turkey described the prevalence of serum immunoglobulin (Ig) G antibodies in humans directed against R. conorii (spotted fever group Rickettsia) (8); however, Rickettsialpox was not reported in Turkey. This report of what we believe to be the first described Rickettsialpox case from Turkey further extends the recognized geographic distribution of R. akari. A 9-year-old boy was admitted to the Kayseri hospital with fever >39°C and generalized papulovesicular exanthema. One week before admission, fever, profuse sweating, headache, and dysuria were present. On admission, physical examination indicated generalized vesicular, bullouse, and papular exanthema involving the lips and oral cavity. Notable pathologic findings at admission included a black eschar on the boy’s penis, bilateral prominent conjunctival ejection, and bilateral lower pulmonary rales. The leukocyte count was 13,300/mm3, hemoglobin was 14.49 mg/dL, and the platelet count was 544,000/mm3. Serum electrolytes and blood urea nitrogen levels and results of coagulation study and urine analysis were normal. Routine blood cultures taken 24 hours postadmission were sterile. Specific antibodies (IgG; IgM) against Varicella were not detected in serum samples (Duzen Laboratories, Ankara, Turkey). Additionally, the patient reported mice on the family’s farm. A diagnosis of Rickettsialpox was made and doxycycline treatment (200 mg/kg) was initiated. The patient serum sample was tested by indirect immunofluorescence assay (IFA) for IgG and IgM antibodies reactive with R. akari (Kaplan strain), R. typhi (Wilmington), R. rickettsii (Sheila Smith), and R. conorii (Malish 7). Serum IgG titers of 1/1280 and IgM of 1/40 to R. akari were detected and confirmed through cross-adsorption with Rickettsial antigens (R. rickettsii, R. conorii) (9,10). Higher reciprocal titers were obtained against R. akari antigens than against R. rickettsii and R. conorii antigens (reciprocol titers of 1,024 vs. 512 and 512, respectively). We observed a difference in reduction in antibody titers against R. akari after adsorption with R. akari (Kaplan) (
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Rickettsia-Macrophage Interactions: Host Cell Responses to Rickettsia akari and Rickettsia typhi
Infection and immunity, 2002Co-Authors: Suzana Radulovic, P. W. Price, Magda S. Beier, Jariyanart Gaywee, J. A. Macaluso, Abdu F. AzadAbstract:The existence of intracellular Rickettsiae requires entry, survival, and replication in the eukaryotic host cells and exit to initiate new infection. While endothelial cells are the preferred target cells for most pathogenic Rickettsiae, infection of monocytes/macrophages may also contribute to the establishment of Rickettsial infection and resulting pathogenesis. We initiated studies to characterize macrophage-Rickettsia akari and -Rickettsia typhi interactions and to determine how Rickettsiae survive within phagocytic cells. Flow cytometry, microscopic analysis, and LDH release demonstrated that R. akari and R. typhi caused negligible cytotoxicity in mouse peritoneal macrophages as well as in macrophage-like cell line, P388D1. Host cells responded to Rickettsial infection with increased secretion of proinflammatory cytokines such as interleukin-1β (IL-1β) and IL-6. Furthermore, macrophage infection with R. akari and R. typhi resulted in differential synthesis and expression of IL-β and IL-6, which may correlate with the existence of biological differences among these two closely related bacteria. In contrast, levels of gamma interferon (IFN-γ), IL-10, and IL-12 in supernatants of infected P388D1 cells and mouse peritoneal macrophages did not change significantly during the course of infection and remained below the enzyme-linked immunosorbent assay cytokine detection limits. In addition, differential expression of cytokines was observed between R. akari- and R. typhi-infected macrophages, which may correlate with the biological differences among these closely related bacteria.
James E. Childs - One of the best experts on this subject based on the ideXlab platform.
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Rickettsialpox in New York City
Annals of the New York Academy of Sciences, 2003Co-Authors: Christopher D Paddock, James A. Comer, Tamara Koss, Marina E. Eremeeva, Gregory A. Dasch, Sherif R. Zaki, John W. Sumner, Joseph Singleton, Bryan Cherry, James E. ChildsAbstract:Rickettsialpox, a spotted fever rickettsiosis, was first identified in New York City (NYC) in 1946. During the next five years, approximately 540 additional cases were identified in NYC. However, during the subsequent five decades, Rickettsialpox received relatively little attention from clinicians and public health professionals, and reporting of the disease diminished markedly. During February 2001 through August 2002, 34 cases of Rickettsialpox in NYC were confirmed at CDC from cutaneous biopsy specimens tested by using immunohistochemical (IHC) staining, PCR analysis, and isolation of Rickettsia akari in cell culture, as well as an indirect immunofluorescence assay of serum specimens. Samples were collected from patients with febrile illnesses accompanied by an eschar, a papulovesicular rash, or both. Patients originated predominantly from two boroughs (Manhattan and the Bronx). Only 8 (24%) of the cases were identified prior to the reports of bioterrorism-associated anthrax in the United States during October 2001, and lesions of several patients evaluated during and subsequent to this episode were suspected initially to be cutaneous anthrax. IHC staining of biopsy specimens of eschars and papular lesions were positive for spotted fever group Rickettsiae for 32 patients. Of the eleven patients for whom paired serum samples were obtained, all demonstrated fourfold or greater increases in antibody titers reactive with R. akari. The 17-kDa protein gene sequence of R. akari was amplified from eschars of five patients. Four isolates of R. akari were obtained from cutaneous lesions. Possible factors responsible for the increase in clinical samples evaluated for Rickettsialpox during this interval include renewed clinical interest in the disease, improved diagnostic methods, epizootiological influences, and factors associated with the recent specter of bioterrorism.
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Evidence of rodent-associated Bartonella and Rickettsia infections among intravenous drug users from Central and East Harlem, New York City
The American journal of tropical medicine and hygiene, 2001Co-Authors: James A. Comer, David Vlahov, Theresa Diaz, Edgar Monterroso, James E. ChildsAbstract:We tested serum samples collected in 1997 and 1998 from a cohort of 204 injection drug users (IDUs) recruited from Central and East Harlem, New York City, New York, for antibodies reactive with seven Rickettsial or Bartonella spp. antigens. Rodent-associated Bartonella elizabethae and Rickettsia akari were the primary etiologic agents of interest. The testing panel also included Bartonella henselae, Bartonella quintana, Rickettsia prowazekii, Rickettsia rickettsii, and Rickettsia typhi. The highest prevalence of seroreactive serum samples (46%) was found with B. elizabethae antigens; 10% of the samples reacted with B. henselae antigens, while 2% reacted with B. quintana antigens. Reactivity to the latter two antigens was likely due to cross-reactivity with B. elizabethae antigens in most instances. Among the spotted fever group Rickettsiae, 18 (9%) samples reacted with R. akari, including 10 samples (5%) that also reacted with R. rickettsii. Cross-adsorption studies demonstrated that most of the spotted fever group Rickettsiae antibodies were due to R. akari infections. Among the typhus group Rickettsiae, 5 samples reacted weakly to R. prowazekii antigens, and no samples reacted with R. typhi antigens. These findings suggest that Harlem IDUs are commonly exposed to two rodent-associated zoonotic agents. Further study of IDU populations may help elucidate transmission cycles of these agents in inner cities where higher levels of transmission occur.
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Serologic evidence of Rickettsia akari infection among dogs in a metropolitan city.
Journal of the American Veterinary Medical Association, 2001Co-Authors: James A. Comer, M C Vargas, I Poshni, James E. ChildsAbstract:Objective To determine whether dogs in New York, NY are naturally infected with Rickettsia akari, the causative agent of Rickettsialpox in humans. Design Serologic survey. Animals 311 dogs. Procedure Serum samples were obtained from dogs as a part of a study on Rocky Mountain spotted fever and borreliosis or when dogs were examined at area veterinary clinics for routine care. Dog owners were asked to complete a questionnaire inquiring about possible risk factors at the time serum samples were obtained. Samples were tested for reactivity to spotted fever group Rickettsiae by use of an enzyme immunoassay (EIA). Twenty-two samples for which results were positive were tested by use of an indirect immunofluorescence antibody (IFA) assay followed by confirmatory cross-absorption testing. Results Results of the EIA were positive for 24 (7.7%) dogs. A history of tick infestation and increasing age were significantly associated with whether dogs were seropositive. Distribution of seropositive dogs was focal. Seventeen of the 22 samples submitted for IFA testing had titers to R rickettsii and R akari; for 11 of these, titers to R akari were higher than titers to R rickettsii. Cross-absorption testing indicated that in 6 of 7 samples, infection was caused by R akari. Conclusions and clinical relevance Results suggest that dogs can be naturally infected with R akari. Further studies are needed to determine the incidence of R akari infection in dogs, whether infection is associated with clinical illness, and whether dogs can serve as sentinels for human disease.
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SEROLOGIC EVIDENCE OF RickettsiaLPOX ( Rickettsia akari ) INFECTION AMONG INTRAVENOUS DRUG USERS IN INNER-CITY BALTIMORE, MARYLAND
The American journal of tropical medicine and hygiene, 1999Co-Authors: James A. Comer, Theodore Tzianabos, Colin Flynn, David Vlahov, James E. ChildsAbstract:We tested single serum samples from 631 intravenous (i.v.) drug users from inner-city Baltimore, Maryland for serologic evidence of exposure to spotted fever group Rickettsiae. A total of 102 (16%) individuals had titers > or = 64 to Rickettsia rickettsii by an indirect immunofluorescence assay. Confirmation that infection was caused by R. akari was obtained by cross-adsorption studies on a subset of serum samples that consistently resulted in higher titers to R. akari than to R. rickettsii. Current i.v. drug use, increased frequency of injection, and shooting gallery use were significant risk factors for presence of group-specific antibodies reactive with R. rickettsii. There was a significant inverse association with the presence of antibodies reactive to R. rickettsii and antibodies reactive to the human immunodeficiency virus. This study suggests that i.v. drug users are at an increased risk for R. akari infections. Clinicians should be aware of Rickettsialpox, as well as other zoonotic diseases of the urban environment, when treating i.v. drug users for any acute febrile illness of undetermined etiology.
David H. Walker - One of the best experts on this subject based on the ideXlab platform.
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CLINICAL ARTICLES Isolation of Rickettsia akari from a Patient in a Region Where Mediterranean Spotted Fever Is Endemic
2016Co-Authors: Suzana Radulovic, Hui-min Feng, Miro Morovic, Boris Djelalija, Vsevolod Popov, Patricia Crocquet-valdes, David H. WalkerAbstract:Rickettsia akari was isolated from blood collected from a patient in Croatia in 1991. We believe this is the first human isolate of R. akari to be reported in more than 40 years and the first ever from southern Europe. The Croatian isolate was antigenically and genetically indistinguishable from the prototype American strain and a Ukrainian strain. In all probability, Rickettsialpox would be diagnosed more frequently and over a wider geographic area if physicians gave greater consider-ation to the diagnosis and if laboratory diagnostic methods were better able to distinguish among spotted fever group rickettsioses. Rickettsialpox is a self-limited illness caused by Rickettsia akari, transmitted to humans by the bite of Liponyssoides san-guineus, a mite ectoparasite of the domestic mouse [1-11]. The distribution of transovarially infected mites determines the epidemiology of the disease. Aside from hundreds of cases in the cities of the northeastern United States during the late 1940s and the 1950s [4- 6, 9, 12-16], Rickettsialpox has bee
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TRANSCRIPTION OF THE Rickettsia FELIS OMPA GENE IN NATURALLY INFECTED FLEAS
The American journal of tropical medicine and hygiene, 2005Co-Authors: Jorge E. Zavala-castro, Jorge E. Zavala-velázquez, Melissa A. Small, Colette Keng, Donald H. Bouyer, David H. WalkerAbstract:Rickettsia felis is maintained transovarially in Ctenocephalides felis fleas in a widespread geographic distribution and is transmitted to humans and animals, including opossums. This Rickettsia is phylogenetically a member of the spotted fever group, most closely related to Rickettsia akari and R. australis. An unusual feature of this Rickettsia is that the gene for the outer membrane protein A (OmpA) is interrupted by stop codons. To determine if this putatively dying gene is expressed, mRNA was extracted from laboratory-maintained, R. felis-infected cat fleas. Reverse transcriptase-polymerase chain reaction amplification of three segments of the ompA gene indicated that mRNA of ompA is actively transcribed in fleas. The cDNA sequences expressed represented mRNA of the first 1860-basepair segment of ompA, which includes domains I and II, part of domain III, the region from site 1836 to site 2180, despite the presence of several stop codons, and the open reading frame from site 2788 to site 3837. The detected sequences showed several differences in the amino acid composition when compared with the previously reported sequence.
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Monoclonal antibody-based immunohistochemical diagnosis of Rickettsialpox: the macrophage is the principal target.
Modern pathology : an official journal of the United States and Canadian Academy of Pathology Inc, 1999Co-Authors: David H. Walker, Hui-min FengAbstract:Cutaneous biopsies of five eschars and two rash lesions from five patients from New York City with documented Rickettsialpox were examined by immunohistochemical methods with a monoclonal antibody directed against spotted fever group Rickettsial lipopolysaccharide for the presence and cellular location of Rickettsia akari Rickettsiae were identified in all of the five patients, with good concordance of results for the same biopsy tissues with previously reported results by the direct immunofluorescence method. In contrast with immunofluorescence, which did not reveal the location of the organisms, immunohistochemical examination demonstrated R. akari to be in perivascular cells, morphologically resembling macrophages. Evaluation with double staining for Rickettsiae and either CD68 or Factor VIII-related antigen revealed that the predominant infected cell type was CD68-positive macrophages, and only a rare Rickettsia was detected in vascular endothelium, the major target cell for other rickettsioses. These results provide a diagnostic method for Rickettsialpox and other spotted fever group rickettsioses and indicate that the elucidation of the pathogenesis of Rickettsialpox must take into account that its target cell differs from that of Rocky Mountain spotted fever, boutonneuse fever, louse-borne typhus fever, and murine typhus.
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Isolation of Rickettsia akari from a Patient in a Region Where Mediterranean Spotted Fever Is Endemic
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 1996Co-Authors: Suzana Radulovic, Hui-min Feng, Miro Morovic, Boris Djelalija, Patricia Crocquet-valdes, Vsevolod L. Popov, David H. WalkerAbstract:Rickettsia akari was isolated from blood collected from a patient in Croatia in 1991. We believe this is the first human isolate of R. akari to be reported in more than 40 years and the first ever from southern Europe. The Croatian isolate was antigenically and genetically indistinguishable from the prototype American strain and a Ukrainian strain. In all probability, Rickettsialpox would be diagnosed more frequently and over a wider geographic area if physicians gave greater consideration to the diagnosis and if laboratory diagnostic methods were better able to distinguish among spotted fever group rickettsioses.
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Emerging and reemerging Rickettsial diseases.
The New England journal of medicine, 1994Co-Authors: David H. Walker, J. S. DumlerAbstract:The article by Kass et al.1 in this issue of the Journal is an appropriate reminder that Rickettsialpox, like Rickettsial diseases in general, is still with us. The Rickettsialpox diagnosed in 13 patients at one hospital in New York City undoubtedly represents only a fraction of the actual cases of this endemic disease. Rickettsia akari is maintained in a zoonotic cycle involving house mice and mites, passing Rickettsiae transovarially from one generation of mites to the next. Such firmly established, highly evolved ecologic niches are unlikely to disappear, nor are humans likely to avoid encountering the bacteria that flourish in . . .
