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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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DISPATCHES Rickettsia parkeri Infection after Tick Bite, Virginia
2013Co-Authors: Timothy J. Whitman, Christopher D Paddock, Allen L. Richards, Cindy L. Tamminga, Patrick J. Sniezek, Ju Jiang, David K. Byers, John W. SAbstract:We describe a man with a febrile illness and an eschar that developed at the site of a tick bite. Rickettsia parkeri was detected and isolated from the eschar. This report represents the second documented case of R. parkeri rickettsiosis in a US serviceman in eastern Virginia. In the United States, 4 species of spotted fever group (SFG) rickettsiae are recognized as pathogens of humans. These include Rickettsia rickettsii, the cause of Rocky Mountain spotted fever (RMSF); R. felis, the cause of fleaborne spotted fever; R. akari, the agent of Rickettsialpox; and R. parkeri (1,2). Of these, R. rickettsii is the only pathogen definitely associated with tick bites. In 2004, Paddock et al. described the first recognized case of infection in a patient with R. parkeri (1). That patient, a US serviceman living in the Tidewater region o
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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.
James A. Comer - One of the best experts on this subject based on the ideXlab platform.
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SEROLOGIC EVIDENCE OF Rickettsialpox (RICKETTSIA AKARI) INFECTION AMONG INTRAVENOUS DRUG USERS IN INNER-CITY BALTIMORE, MARYLAND
2014Co-Authors: James A. Comer, Theodore Tzianabos, Colin Flynn, David Vlahov, E. Childs, Rickettsial Zoonoses BranchAbstract:Abstract. We tested single serum samples from 631 intravenous (IV) drug users from inner-city Baltimore, Mary-land for serologic evidence of exposure to spotted fever group rickettsiae. A total of 102 (16%) individuals had titers $ 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 IV 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 IV 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 IV drug users for any acute febrile illness of undetermined etiology. Two important spotted fever group Rickettsia species that are pathogenic to humans are endemic to the United States: R. rickettsii, the etiologic agent of Rocky Mountain spotted fever, and R. akari, the agent of Rickettsialpox.1 The epide-miology and public health importance of these two organ
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DISPATCHES Rickettsialpox in North Carolina: A
2013Co-Authors: Allan Krusell, James A. Comer, Daniel J. SextonAbstract:We report a case of Rickettsialpox from North Carolina confirmed by serologic testing. To our knowledge, this case is the first to be reported from this region of the United States. Including Rickettsialpox in the evaluation of patients with eschars or vesicular rashes is likely to extend the recognized geographic distribution of Rickettsia akari, the etiologic agent of this disease. R ickettsialpox is caused by infection with Rickettsia akari. Disease in humans was first described in 1946 in residents of apartments clustered in a three-block area in the borough of Queens, New York City (1). Subsequently, small outbreaks of Rickettsialpox were recognized in several U.S. cities
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Serologic evidence of a Rickettsia akari-like infection among wild-caught rodents in Orange County and humans in Los Angeles County, California.
Journal of vector ecology : journal of the Society for Vector Ecology, 2007Co-Authors: Stephen G. Bennett, James A. Comer, Heather M. Smith, James P. WebbAbstract:We detected antibodies reactive with Rickettsia akari, the etiologic agent of Rickettsialpox in humans and in 83 of 359 (23%) rodents belonging to several species, collected in Orange County, CA. Reciprocal antibody titers >1:16 to R. akari were detected in native mice and rats (Peromyscus maniculatus, P. eremicus, and Neotoma fuscipes) and in Old World mice and rats (Mus musculus, Rattus rattus, and R. norvegicus), representing the first time that antibodies reactive with this agent have been detected in four of these species and the first report of these antibodies in rodents and humans west of the Mississippi River. We then tested serum samples from individuals who used a free clinic in downtown Los Angeles and found that 25 of 299 (8%) of these individuals had antibody titers >1:64 to R. akari. Serologic evidence suggested that R. akari or a closely related rickettsia is prevalent among several rodent species at these localities and that infection spills over into certain segments of the human population. Isolation or molecular confirmation of the agent is needed to conclusively state that R. akari is the etiologic agent infecting these rodents.
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Rickettsialpox in a patient with HIV infection
Journal of the American Academy of Dermatology, 2003Co-Authors: Scott R. Sanders, James A. Comer, Sherif R. Zaki, Damian Di Costanzo, James Leach, Howard Levy, Krishna Srinivasan, Christopher D PaddockAbstract:We describe the first case of Rickettsialpox in a patient infected with HIV. Immunohistochemical staining of biopsied lesions showed a relatively large number of rickettsiae within the papulovesicular rash. Rickettsialpox is easily treated and may resemble more serious cutaneous eruptions in patients infected with HIV. This diagnosis should be considered in immunocompromised city-dwellers, with fever and a papulovesicular rash.
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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.
Seung Hyun Lee - One of the best experts on this subject based on the ideXlab platform.
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Spotted Fever Group and Typhus Group Rickettsioses in Humans, South Korea
2013Co-Authors: Yeon Joo Choi, Won Jong Jang, Jonghyun Kim, Ji Sun Ryu, Seung Hyun LeeAbstract:The presence of the nucleic acid of the spotted fever group (SPG) and typhus group (TG) rickettsiae was investigated in 200 serum specimens seropositive for SFG rickettsiae by multiplex-nested polymerase chain reaction with primers derived from the rickettsial outer membrane protein B gene. The DNA of SFG, TG, or both rickettsiae was amplified in the 24 serum specimens, and sequence analysis showed Rickettsia conorii, R. japonica, and R. felis in the specimens. R. conorii and R. typhi were found in 7 serum specimens, which indicated the possibility of dual infection in these patients. These findings suggest that several kinds of rickettsial diseases, including boutonneuse fever, Rickettsialpox, R. felis infection, and Japanese spotted fever, as well as scrub typhus and murine typhus, are occurring in Korea. Human rickettsioses, known to occur in Korea, include mainly scrub typhus, murine typhus, and epidemic typhus. Scrub typhus, caused by Orientia tsutsugamushi, a major rickettsial disease in Korea, is transmitted through the bites of mite larvae. An earlier study by Choi and colleagues reported that 34.3 % of febrile hospital patients in autumn were seropositive for the disease (1). Rickettsia typhi, transmitted by the fleas of various rodents, causes murine typhus, which is a milder form of typhus than human typhus (2). The first patient with murine typhus in Korea was reported in 1959. Two cases of murine typhus confirmed by culture were reported since 1988 (3,4), and now>200 cases of murine typhus are presumed to occur annually in South Korea. Epidemic typhus is caused by R
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Diagnosis of scrub typhus by immunohistochemical staining of Orientia tsutsugamushi in cutaneous lesions.
American journal of clinical pathology, 2008Co-Authors: Dong-min Kim, Won Jong Jang, Kyunghee Park, Chol-jin Park, Sung-chul Lim, Seung Hyun LeeAbstract:We assessed the clinical usefulness of immunohistochemical staining on skin biopsy specimens for the diagnosis of scrub typhus compared with indirect immunofluorescent antibody assay (IFA), the definitive diagnostic method for scrub typhus, in a prospective study of 125 patients with possible scrub typhus in 2005 and 2006. Skin biopsy specimens were obtained from 63 patients. To minimize the effects caused by antibiotics on immunohistochemical results, 46 patients were assessed before antibiotic administration (4 patients received antibiotic therapy before admission; 13 underwent skin biopsy after antibiotic administration at our hospital). Compared with IFA results, immunohistochemical results on maculopapular skin lesions demonstrated a sensitivity of 0.65 and a specificity of 1. Immunohistochemical results on eschars demonstrated a sensitivity of 1 and a specificity of 1. For immunohistochemical staining performed on skin lesions within 3 or 4 days of administration of antibiotics that are effective for Rickettsia, the antibiotics did not greatly influence diagnostic sensitivity. Immunohistochemical staining of skin biopsy specimens, particularly that of eschars, is sensitive and specific, and this technique can be reliable for confirming the diagnosis of scrub typhus. Scrub typhus is an acute febrile disease characterized by high fever, headache, and rash; these symptoms are caused by the intracellular gram-negative bacteria Orientia tsutsugamushi. It is a major febrile disease in Korea, Japan, China, Thailand, etc. The reservoir of O tsutsugamushi is wild rats, and chiggers are the vector. Bacterial infection happens when chiggers bearing O tsutsugamushi bite human beings and aspirate human tissue fluid. Eschars are formed on the sites bitten by the chiggers; fever, maculopapular rash, muscle ache, headache, anorexia, lymph node enlargement, and other signs and symptoms appear at the time of the formation of eschar. The presence of eschar has been reported to be an important finding for the diagnosis of Rickettsialpox or scrub typhus. 1
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spotted fever group and typhus group rickettsioses in humans south korea
Emerging Infectious Diseases, 2005Co-Authors: Yeon Joo Choi, Won Jong Jang, Jonghyun Kim, Ji Sun Ryu, Seung Hyun Lee, Kyunghee Park, Hyung Suk Paik, Youngsang Koh, Myung Sik Choi, Ik Sang KimAbstract:The presence of the nucleic acid of the spotted fever group (SPG) and typhus group (TG) rickettsiae was investigated in 200 serum specimens seropositive for SFG rickettsiae by multiplex-nested polymerase chain reaction with primers derived from the rickettsial outer membrane protein B gene. The DNA of SFG, TG, or both rickettsiae was amplified in the 24 serum specimens, and sequence analysis showed Rickettsia conorii, R. japonica, and R. felis in the specimens. R. conorii and R. typhi were found in 7 serum specimens, which indicated the possibility of dual infection in these patients. These findings suggest that several kinds of rickettsial diseases, including boutonneuse fever, Rickettsialpox, R. felis infection, and Japanese spotted fever, as well as scrub typhus and murine typhus, are occurring in Korea.
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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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.
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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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.
