The Experts below are selected from a list of 2022 Experts worldwide ranked by ideXlab platform
Jaime Fergie - One of the best experts on this subject based on the ideXlab platform.
-
Murine Typhus in south texas children an 18 year review
Pediatric Infectious Disease Journal, 2018Co-Authors: Ashley Howard, Jaime FergieAbstract:Background Murine Typhus is a zoonotic infection caused by Rickettsia typhi that remains endemic in South Texas. In 2003, only 9 Texas counties reported Murine Typhus compared with 41 counties in 2013. Methods A retrospective study of children discharged with a confirmed diagnosis of Murine Typhus from Driscoll Children's Hospital between January 1998 and September 2016. Results Two hundred thirteen children (113 female) 3 months through 19 years of age (mean, 11.2 ± 4.5 years) were identified. Cases occurred throughout the year. Children were admitted after a mean of 7.7 ± 5.3 days of fever. The most common symptoms were fever (100%), poor appetite (71.9%), malaise/fatigue (69.0%) and headache (67.6%). The most common laboratory abnormalities were elevated C-reactive protein, hypoalbuminemia, elevated erythrocyte sedimentation rate, elevated transaminases and elevated band count with normal total white blood cell count. Children defervesced in a mean of 31.87 ± 21.36 hours after initiation of doxycycline. Hospitalization lasted for a mean of 2.7 ± 1.8 days when children were administered doxycycline within 24 hours of admission compared with, 4.1 ± 1.8 days, P ≤ 0.0001 when started later. Eleven patients (5.1%) were admitted to the pediatric intensive care unit and were older, P = 0.0009. No children died. Conclusions Murine Typhus is endemic in South Texas. Children who were treated earlier with doxycycline had a shorter hospitalization than were those who began therapy later. Recognition of Murine Typhus is important to prevent delay in treatment and development of complications.
-
Murine Typhus in children, South Texas.
Emerging infectious diseases, 2007Co-Authors: Kevin Purcell, Jaime Fergie, Kevin Richman, Lisa RochaAbstract:Children from South Texas were evaluated for immunoglobulin G to Rickettsia typhi, the causative agent of Murine Typhus. Of 513 children, 8.6% of those 1-5 years of age, 13.3% of those 6-11 years of age, and 13.8% of those 12-17 years of age had positive results.
-
Spontaneous splenic rupture in a child with Murine Typhus.
The Pediatric infectious disease journal, 2004Co-Authors: Jaime Fergie, Kevin PurcellAbstract:A 10-year-old boy hospitalized with Murine Typhus infection had splenic rupture as a complication. Surgical intervention was not required. He recovered and was discharged a week after admission. This is the first reported case of spontaneous splenic rupture in a child with Murine Typhus.
-
Murine Typhus in South Texas children.
The Pediatric infectious disease journal, 2000Co-Authors: Jaime Fergie, Kevin Purcell, Diane M WanatAbstract:BACKGROUND Murine Typhus is a zoonotic infection caused by Rickettsia typhi. This illness used to be endemic in the southeastern and gulf coast of the United States and is now only rarely reported in South Texas and Southern California. Murine Typhus causes a febrile illness with headache and rash that has been well-described in adults. OBJECTIVE To define the epidemiologic and clinical characteristics, laboratory findings, hospital course and response to therapy of children discharged from our hospital with a diagnosis of Murine Typhus. METHODS Retrospective chart review of all children discharged from Driscoll Children's Hospital, Corpus Christi, TX, from January 1, 1990, to June 30, 1998, with a diagnosis of Murine Typhus. Patients. Thirty children (17 females) ages 2 to 17 years (mean, 10 +/- 4 years). RESULTS Eighty percent of the children were admitted between May and November, and 67% had a history of contact with or exposure to a potential animal reservoir. Children were admitted after a mean of 7 +/- 4 days. The most common clinical features were fever 100%, rash 80% and headache 77%. Laboratory abnormalities included elevated erythrocyte sedimentation rate (75%), elevated serum transaminases (67%), hyponatremia (66%) and increased immature leukocytes without leukocytosis (63%). Only one child had leukocytosis and 40% had leukopenia. Defervescence occurred a mean of 35 +/- 19 h after initiation of appropriate antibiotics. Hospitalization lasted for a mean of 7 +/- 3 days. There were no readmissions and no patients died as a result of the infection. CONCLUSIONS Despite being rarely reported in this country now, Murine Typhus continues to be an important cause of fever and hospitalization for children in South Texas. Children with Murine Typhus develop an illness similar to that reported in adults with fever, rash and headache. Children respond quickly to therapy with doxycycline or tetracycline and recover completely from their illness.
Didier Raoult - One of the best experts on this subject based on the ideXlab platform.
-
Murine Typhus in returned travelers a report of thirty two cases
American Journal of Tropical Medicine and Hygiene, 2012Co-Authors: Gaelle Walter, Elisabeth Botelhonevers, Cristina Socolovschi, Didier Raoult, Philippe ParolaAbstract:Murine Typhus, caused by Rickettsia typhi and transmitted mainly by the rat fleas, Xenopsylla cheopis, has emerged in the field of travel medicine. We analyzed retrospectively the epidemiological, clinical, and biological characteristics of the 32 Murine Typhus cases that were diagnosed during the past 3 years at the World Health Organization Collaborative Center for Rickettsial diseases, Marseille, France. All of the cases occurred in travelers and most of them had returned from Africa (N = 13 of 32) and South-east Asia (N = 12 of 32). Exposure to rats was reported only in a few (N = 2 of 32) patients. Almost half of the cases were diagnosed in August and September. Only four patients presented the classic triad: fever, rash, and headache. Moreover, we report the first known cases of a hemophagocytic syndrome associated with this disease. Murine Typhus must be considered as an etiologic agent of febrile illness in returning travelers, particularly in those with unspecific symptoms.
-
Murine Typhus in the homeless
Comparative immunology microbiology and infectious diseases, 2011Co-Authors: Sékéné Badiaga, Didier Raoult, Samir Benkouiten, Hind Hajji, Philippe BrouquiAbstract:Abstract Homeless populations are particularly exposed to many vector-borne diseases because of their poor living conditions. We tested sera from 299 homeless people recruited in 2010 and 2011 in Marseilles, France for antibodies to Rickettsia typhi by microimmunofluorescence using a titer of 1:25 as a cut-off titer, and we confirmed the results by Western blot and cross-adsorption studies. Sixty-three persons (22%) had antibodies against R. typhi. The Murine Typhus seroprevalence rates have significantly increased in homeless populations between the 2000–2003 and 2010–2011 periods. These findings indicate that the homeless are increasingly exposed to flea-borne Murine Typhus in Marseilles. One might suggest that multiple strikes of sanitation workers resulting in the increase of waste and construction sites combined with the poor living conditions of the homeless expose this population to rodents and their fleas. Further annual studies are necessary to follow rodent-associated diseases among homeless people in Marseille.
-
Murine Typhus as a cause of fever in travelers from tunisia and mediterranean areas
Journal of Travel Medicine, 2010Co-Authors: E Angelakis, Cristina Socolovschi, Philippe Parola, Elizabeth Botelho, Chantal Roure Sobas, Christophe Piketty, Didier RaoultAbstract:Background. Travelers are exposed to a variety of health risks in unfamiliar environments and fever is a common problem in patients returning from travel abroad. Rickettsial diseases are increasingly frequently being reported among international travelers. Here we present cases of Rickettsia typhi infection, the agent of Murine Typhus, that were identified in our laboratory the last year, in travelers from Tunisia. Methods. For each patient we tested an acute-phase serum sample and for one patient we tested a convalescent-phase serum sample. IgG and IgM antibody titers were estimated with use of the microimmunofluorescence (MIF) assay. Western blot (WB) assay was performed for all the patients. Results. We identified three cases of Murine Typhus after a travel in Tunisia. All cases were observed during late summer and early autumn and patients were suffering by persistent fever. None of them presented rash or inoculation eschar. MIF was positive for Rickettsia sp. in the acute-phase serum samples of two patients. In one patient, two acute-phase serum samples were Rickettsia sp. negative whereas a third convalescent-phase serum sample that was obtained 2 weeks after was Rickettsia sp. positive. By WB assay we identified infection by R typhi. A treatment was immediately started and patients became apyretic. Conclusions. In the countries of North Europe, although autochthones cases of Murine Typhus have not been described, sporadic cases of R typhi infection are identified in travelers who visited Murine Typhus endemic areas. Murine Typhus should be considered in the diagnosis of febrile illness without rash in travelers returning from disease endemic areas, like the south Mediterranean area.
-
Murine Typhus algeria
Emerging Infectious Diseases, 2008Co-Authors: Nadjet Mouffok, Philippe Parola, Didier RaoultAbstract:To the Editor: Rickettsioses, or typhoid diseases, are caused by obligate intracellular bacteria of the order Rickettsiales. The ubiquitous Murine Typhus is caused by Rickettsia typhi. Although cat fleas and opposums have been suggested as vectors in some places in the United States, the main vector of Murine Typhus is the rat flea (Xenopspylla cheopis), which maintains R. typhi in rodent reservoirs (1). Most persons become infected when flea feces containing R. typhi contaminate broken skin or are inhaled, although infections may also result from flea bites (1). Murine Typhus is often unrecognized in Africa; however, from northern Africa, 7 cases in Tunisia were documented in 2005 (2). We conducted a prospective studyin Algeria which included all patients who had clinical signs leading to suspicion of rickettsioses (high fever, skin rash, headache, myalgia, arthralgia, eschar, or reported contact with ticks, fleas, or lice) who visited the Oran Teaching Hospital in 2004–2005 for an infectious diseases consultation. Clinical and epidemiologic data as well as acute-phase (day of admission) and convalescent-phase (2–4 weeks later) serum samples were collected. Serum samples were sent to the World Health Organization Collaborative Center for Rickettsial Diseases in Marseille, France. They were tested by immunofluoresence assay (IFA), by using spotted fever group (SFG) rickettsial antigens (R. conorii conorii, R. conorii israelensis, R. sibirica mongolitimonae, R. aeschlimmanii, R. massiliae, R. helvetica, R. slovaca, and R. felis) and R. typhi and R. prowazekii as previously reported (3). When cross-reactions were noted between several rickettsial antigens, Western blot (WB) assays and cross-absorption studies were performed as previously described (4). A total of 277 patients were included. We report 2 confirmed cases of R. typhi infection in patients from Algeria. The first patient, a 42-year-old male pharmacist who reported contact with cats and dogs parasitized by ticks, consulted with our clinic for a 10-day history of high fever, sweating, headache, arthralgia, myalgia, cough, and a 6-kg weight loss. He had not received any antimicrobial drugs before admission. No rash, eschar, or specific signs were found. Standard laboratory findings were within normal limits. No acute-phase serum sample was sent for testing. However, IFAs on convalescent-phase serum were negative for SFG antigens (except R. felis: immunoglobulin [Ig] G 64, IgM 128), but they showed raised antibodies against R. typhi and R. prowazekii (IgG 2,048, IgM 1,024). The second patient, a 25-year-old farmer, was hospitalized for a 5-day history of fever, headache, diarrhea, and lack of response to treatment with amoxicillin and acetaminophen. He reported contact with cats and cattle. A discrete macular rash and pharyngitis were observed. Standard laboratory findings were within normal limits, except neutrophil count was elevated at 11.2/μL (normal levels 3–7/μL). Acute-phase serum was negative for rickettsial antigens. Convalescent-phase serum obtained 2 weeks later was positive for several SFG antigens (IgM only; the highest level was 256 for R. conorii), and higher levels of antibodies were obtained against R. typhi and R. prowazekii (IgG 256, IgM 256). WB and cross-absorption studies confirmed R. typhi infection (Figure). Both patients recovered after a 3-day oral doxycycline regimen and have remained well. (A single 200-mg dose of oral doxycycline usually leads to defervescence within 48–72 hours [1]). Figure Western blot assay and cross-adsorption studies of an immunofluoresence assay–positive serum sample from a patient with rickettsiosis in Algeria. Antibodies were detected at the highest titer (immunoglobulin [Ig] G 256, IgM 256) for both Rickettsia ... Murine Typhus is a mild disease with nonspecific signs. Less than half of patients report exposure to fleas or flea hosts. Diagnosis may be missed because the rash, the hallmark for rickettsial diseases, is present in <50% of patients and is often transient or difficult to observe. Arthralgia, myalgia, or respiratory and gastrointestinal symptoms, as reported here, are frequent; neurologic signs may also occur (5). As a consequence, the clinical picture can mimic other diseases. A review has reported 22 different diagnoses that were proposed for 80 patients with Murine Typhus in the United States (6). Serologic tests are the most frequently used and widely available methods for diagnosis of rickettsioses (7). IFA is the reference method (7). However, R. typhi may cross-react with other rickettsial antigens, including SFG rickettsiae, but especially with the other Typhus group rickettsia, R. prowazekii, the agent of epidemic Typhus (8). Epidemic Typhus is transmitted by body lice and occurs more frequently in cool areas, where clothes are infrequently changed, and particularly during human conflicts. It is still prevalent in Algeria (9). This cross-reactivity led to some difficulties in interpreting serologic results (10). However, WB and cross-adsorption studies can be used when cross-reactions occur between rickettsial antigens. They are useful for identifying the infecting rickettsia to the species level and for providing new data about the emergence or reemergence of rickettsioses, as reported here. These assays are, however, time-consuming and only available in specialized reference laboratories. Clinicians need to be aware of the presence Murine Typhus in Algeria, especially among patients with unspecific signs and fever of unknown origin. Tetracyclines remain the treatment of choice.
-
Murine Typhus, Algeria
Emerging infectious diseases, 2008Co-Authors: Nadjet Mouffok, Philippe Parola, Didier RaoultAbstract:To the Editor: Rickettsioses, or typhoid diseases, are caused by obligate intracellular bacteria of the order Rickettsiales. The ubiquitous Murine Typhus is caused by Rickettsia typhi. Although cat fleas and opposums have been suggested as vectors in some places in the United States, the main vector of Murine Typhus is the rat flea (Xenopspylla cheopis), which maintains R. typhi in rodent reservoirs (1). Most persons become infected when flea feces containing R. typhi contaminate broken skin or are inhaled, although infections may also result from flea bites (1). Murine Typhus is often unrecognized in Africa; however, from northern Africa, 7 cases in Tunisia were documented in 2005 (2). We conducted a prospective studyin Algeria which included all patients who had clinical signs leading to suspicion of rickettsioses (high fever, skin rash, headache, myalgia, arthralgia, eschar, or reported contact with ticks, fleas, or lice) who visited the Oran Teaching Hospital in 2004–2005 for an infectious diseases consultation. Clinical and epidemiologic data as well as acute-phase (day of admission) and convalescent-phase (2–4 weeks later) serum samples were collected. Serum samples were sent to the World Health Organization Collaborative Center for Rickettsial Diseases in Marseille, France. They were tested by immunofluoresence assay (IFA), by using spotted fever group (SFG) rickettsial antigens (R. conorii conorii, R. conorii israelensis, R. sibirica mongolitimonae, R. aeschlimmanii, R. massiliae, R. helvetica, R. slovaca, and R. felis) and R. typhi and R. prowazekii as previously reported (3). When cross-reactions were noted between several rickettsial antigens, Western blot (WB) assays and cross-absorption studies were performed as previously described (4). A total of 277 patients were included. We report 2 confirmed cases of R. typhi infection in patients from Algeria. The first patient, a 42-year-old male pharmacist who reported contact with cats and dogs parasitized by ticks, consulted with our clinic for a 10-day history of high fever, sweating, headache, arthralgia, myalgia, cough, and a 6-kg weight loss. He had not received any antimicrobial drugs before admission. No rash, eschar, or specific signs were found. Standard laboratory findings were within normal limits. No acute-phase serum sample was sent for testing. However, IFAs on convalescent-phase serum were negative for SFG antigens (except R. felis: immunoglobulin [Ig] G 64, IgM 128), but they showed raised antibodies against R. typhi and R. prowazekii (IgG 2,048, IgM 1,024). The second patient, a 25-year-old farmer, was hospitalized for a 5-day history of fever, headache, diarrhea, and lack of response to treatment with amoxicillin and acetaminophen. He reported contact with cats and cattle. A discrete macular rash and pharyngitis were observed. Standard laboratory findings were within normal limits, except neutrophil count was elevated at 11.2/μL (normal levels 3–7/μL). Acute-phase serum was negative for rickettsial antigens. Convalescent-phase serum obtained 2 weeks later was positive for several SFG antigens (IgM only; the highest level was 256 for R. conorii), and higher levels of antibodies were obtained against R. typhi and R. prowazekii (IgG 256, IgM 256). WB and cross-absorption studies confirmed R. typhi infection (Figure). Both patients recovered after a 3-day oral doxycycline regimen and have remained well. (A single 200-mg dose of oral doxycycline usually leads to defervescence within 48–72 hours [1]). Figure Western blot assay and cross-adsorption studies of an immunofluoresence assay–positive serum sample from a patient with rickettsiosis in Algeria. Antibodies were detected at the highest titer (immunoglobulin [Ig] G 256, IgM 256) for both Rickettsia ... Murine Typhus is a mild disease with nonspecific signs. Less than half of patients report exposure to fleas or flea hosts. Diagnosis may be missed because the rash, the hallmark for rickettsial diseases, is present in
Tsuneo Uchiyama - One of the best experts on this subject based on the ideXlab platform.
-
Murine Typhus from vietnam imported into japan
Emerging Infectious Diseases, 2006Co-Authors: Momoyo Azuma, Saburo Sone, Yasuhiko Nishioka, Motohiko Ogawa, Tomohiko Takasaki, Tsuneo UchiyamaAbstract:To the Editor: In Vietnam, many febrile diseases such as malaria, dengue fever, Japanese encephalitis, scrub Typhus, and more recently, severe acute respiratory syndrome (SARS) and avian influenza have been reported. Murine Typhus cases were also reported during and before the 1960s but not thereafter (1–5). On May 3, 2003, a 54-year-old male resident of Tokushima, Japan, had onset of fever in the suburban town of Cu Chi, ≈60 km northwest of Ho Chi Minh City, Vietnam. Exanthema appeared on his trunk and limbs on May 7. He returned to Japan on May 9 and was admitted to Tokushima University Hospital on May 10. His body temperature was 39.0°C, and serum, C-reactive protein level was high (17.06 mg/dL) on admission (day 8 of illness). Unfortunately, the blood sample taken on that day was discarded. We then collected blood on days 10, 11, 12, 14, 17, and 24 of illness for diagnosis. Minocycline was administered on day 8 and resulted in a gradual decrease in fever and rash. Weil-Felix tests on day 12 showed the serum to be positive for Proteus vulgaris OX19 (titer 160); tests for P. vulgaris OX2 and OXK were negative (titer of 10 for both). We examined blood samples for possible diseases such as malaria, dengue fever, SARS, and rickettsioses. Giemsa-stained peripheral blood samples obtained on day 11 showed no malarial parasites. Results of immunoglobulin M (IgM)-capture ELISA of serum on days 10, 11, and 17 of illness were negative for dengue antibodies. Reverse transcription (RT)–PCR of the serum on day 11 was also negative. RT-PCRs of a pharyngeal swab and urine collected on day 11 were both negative for the SARS coronavirus. These specimens were also injected into Vero cells, and no cytopathic effects were generated. RT-PCR of these cultures was also negative for SARS coronavirus. Moreover, SARS antibodies were not found in serum samples on days 11 and 14 of illness. Serum was also tested for Orientia tsutsugamushi and Coxiella burnttii on day 12 to exclude scrub Typhus and Q fever as diagnoses. Indirect immunofluorescence tests for etiologic agents of spotted fever, Murine Typhus, and epidemic Typhus were then performed with serum samples collected on days 10, 14, and 24. We used Rickettsia typhi and R. prowazekii as Typhus group (TG) rickettsial antigens and R. japonica and R. conorii as spotted fever group (SFG) rickettsiae. IgM antibody was detected for these antigens, indicating that the disease was a primary infection of rickettsiae (Table). When TG and SFG rickettsioses were compared, TG rickettsiae represented markedly higher elevated titers than SFG rickettsiae, which excluded a diagnosis of SFG rickettsiosis. PCR for the TG rickettsial genome in the convalescent-phase serum on day 10 was negative. Table IFA titers of the patient sera and the cross-absorption test* To demonstrate more detailed antigenic reactivity, Western immunoblotting was performed with serum on day 14 (6). The serum reacted similarly to the ladderlike lipopolysaccharide (LPS) of R. typhi and R. prowazekii. As expected from the group-specific nature of rickettsial LPS, no reaction was demonstrated to LPS of SFG rickettsiae, R. japonica and R. conorii, although weak reactivity, mainly to the major outer member protein of SFG rickettiae, rOmpB, and molecules of smaller sizes was shown (6,7). As described previously, rOmpB has cross-reactive antigenicity between TG and SFG rickettsiae (6). Compared with the trace reaction to rOmpB of SFG rickettsiae, an extremely high level of reaction was demonstrated to rOmpB of TG rickettsiae. These results confirmed the disease to be a TG rickettsiosis. To elucidate whether the disease was Murine Typhus or epidemic Typhus, we conducted cross-absorption tests as described previously (8,9). Serum absorbed by R. typhi showed complete absorption, demonstrating no reaction to R. typhi or R. prowazekii (Table). However, the serum absorbed by R. prowazekii resulted in incomplete absorption, demonstrating no reactivity to R. prowazekii but some reactivity to R. typhi, which was left unabsorbed. Western immunoblotting with the serum absorbed by R. prowazekii showed reactivity only to the rOmpB of R. typhi but not to that of R. prowazekii. These results confirmed the diagnosis of Murine Typhus. This is the first serodiagnosis of Murine Typhus in Vietnam since the 1960s (1–5). Since rats inhabit the area where the patient acquired the illness, Murine Typhus seems to have occurred sporadically or endemically but to have been undiagnosed since the 1960s, maybe because it was thought to have been eradicated and thus widely forgotten. This case was the first imported into Japan since the 1940s, when many Japanese soldiers and residents who returned from abroad had the disease.
-
reemerging Murine Typhus japan
Emerging Infectious Diseases, 2004Co-Authors: Satoshi Sakaguchi, Ichiki Sato, Hiroaki Muguruma, Hiroaki Kawano, Yoshito Kusuhara, Seiji Yano, Saburo Sone, Tsuneo UchiyamaAbstract:To the Editor: Murine Typhus is an arthropod-borne infectious disease caused by Rickettsia typhi, which is distributed widely around the world (1–4). In Japan, tsutsugamushi disease occurs most frequently in persons infected with rickettsioses (5). Spotted fever caused by R. japonica also occurs in the southwestern part of Japan (6,7). In the 1940s and 1950s, many Murine Typhus cases were reported in Japan. These diagnoses were made according to the clinical features of the illness and the reactivity of the serum samples to OX19 in Weil-Felix tests. A few cases were diagnosed on the basis of symptoms exhibited by animals infected with isolated rickettsiae and complement fixation tests, in addition to results of the Weil-Felix tests. The Weil-Felix test is useful for preliminary screening of rickettsiosis; however, the reaction could indicate epidemic Typhus or spotted fever in some cases. Since 1958, only three Murine Typhus cases have been reported in Japan (8). In these cases, no serologic tests for epidemic Typhus were conducted. Serum sample from patients with epidemic Typhus and Murine Typhus frequently possess serologic cross-reactivity to R. typhi and R. prowazekii, respectively (9). Thus, the possibility of epidemic Typhus could not be excluded definitively in these cases. On May 4, 2003, a 56-year-old man living in Tokushima, Japan, sought medical care; he had a temperature of 39.1°C and exanthema on the trunk and the upper limbs. No surface lymph nodes were palpable. He was treated with lincomycin and cefditoren pivoxil with no improvement. On day 3, the patient informed caregivers that he had been in a bamboo grove on days 1 and 11 before the onset of symptoms. C-reactive protein of the serum sample collected on day 3 was positive (= 7.6 mg/dL). From this finding, spotted fever was suspected; the disease is endemic in Tokushima. On day 4, the exanthema had spread systemically, and treatment with minocycline was started, which led to a gradual decrease in fever and rashes. The patient was admitted to the Tokushima University Hospital on day 6 of the illness for diagnosis and further treatment. Serum samples were collected from the patient on days 5, 6, 9, 20, and 34. Indirect immunoperoxidase tests on the serum samples for tsutsugamushi disease, spotted fever, Murine Typhus, and Q fever on day 5 of the illness were negative for immunoglobulin (Ig) G and IgM antibodies (<1:40). Weil-Felix tests on the serum samples on days 5 and 9 of the illness were negative for OX2, OX19, and OXK. Indirect immunofluorescence of the serum samples on days 6, 9, 20, and 34 of the illness was conducted by using strains 18 and Wilmington of R. typhi, and the strain Breinl of R. prowazekii as Typhus group rickettsiae; and the strain YH of R. japonica, the strain Malish 7 of R. conorii, and the strain Tick of R. montanensis as the spotted fever group rickettsiae. All serum samples tested for the rickettsiae showed an IgM titer of 1:200. On the other hand, the IgM titers of these serum samples, to the Orientia tsutsugamushi were <1:20. For the IgG antibodies of these serum, spotted fever group rickettsiae were negative (<1:20). However, the Typhus group rickettsiae were positive for IgG antibodies. Among the Typhus group rickettsiae, strain 18 of R. typhi had the highest elevated titers. The titers to the sera on days 6, 9, 20, and 34 of illness were 1:80, 1:160, 1:160, and 1:80, respectively. Another strain of R. typhi, the strain Wilmington, had lower titers of 1:40, 1:80, 1:80, and 1:40, on days 6, 9, 20, and 34 of the illness, respectively. This could have occurred because strain 18 may be a closer antigenic relation of the causative agent than is the strain Wilmington. R. prowazekii demonstrated the lowest IgG titers among Typhus group rickettsiae for these serum samples, <1:20, 1:20, 1:40, and 1:20, on days 6, 9, 20, and 34 of the illness, respectively. These results suggested that the disease was Murine Typhus. To demonstrate more detailed antigenic reactivity, Western immunoblotting of rickettsiae was conducted by using a serum specimen from day 20. All of the rickettsiae were reactive to the serum to various extents. The serum reacted to the ladderlike lipopolysaccharide of R. typhi and R. prowazekii; the antigenicity of rickettsial lipopolysaccharide is group-specific. As expected from the immunofluorescence data, no reaction was demonstrated to the lipopolysaccharide of spotted fever group rickettsiae, R. japonica and R. montanensis, although trace cross-reactivity, mainly to rOmpB, was shown. Thus, Typhus group rickettsiosis was suspected for this case on the basis of these data. Compared to the trace reaction of spotted fever group rickettsiae to rOmpB, a stronger, but still weak, reaction was detected to the heat-labile state of rOmpB of R. prowazekii, and an extremely strong reaction was demonstrated to the heat-labile and heat-stable states of rOmpB of R. typhi. These results strongly suggested that the disease was Murine Typhus. To confirm this diagnosis, we conducted absorption tests as described previously (10). The patient serum collected on day 20 showed complete absorption by the homologous antigen, the purified R. typhi strain 18, demonstrating no reaction to R. typhi or to R. prowazekii by immunofluorescence. However, the serum showed incomplete absorption by the heterologous antigen, the purified R. prowazekii, demonstrating no reactivity to R. prowazekii but some reactivity to R. typhi. These tests confirmed the diagnosis of Murine Typhus. Murine Typhus has never been reported in Japan after the 1950s, except for the three suspected cases and this case. Although other undiagnosed cases may have occurred, they appear to be few; many febrile cases of exanthema have been examined for various rickettsioses, especially after spotted fever was diagnosed in Japan in 1984. Murine Typhus may have reemerged because of the recent increase of black rats, Rattus rattus, in Japan. This patient mentioned that he had captured a rat and disposed of the carcass about a week before the onset of symptoms. Infection could have resulted at that time from contamination with feces of infected fleas such as the oriental rat flea, Xenopsylla cheopis. Historical review indicates that this is the first complete serologic diagnosis of a Murine Typhus case in Japan.
-
Reemerging Murine Typhus, Japan
Emerging infectious diseases, 2004Co-Authors: Satoshi Sakaguchi, Ichiki Sato, Hiroaki Muguruma, Hiroaki Kawano, Yoshito Kusuhara, Seiji Yano, Saburo Sone, Tsuneo UchiyamaAbstract:To the Editor: Murine Typhus is an arthropod-borne infectious disease caused by Rickettsia typhi, which is distributed widely around the world (1–4). In Japan, tsutsugamushi disease occurs most frequently in persons infected with rickettsioses (5). Spotted fever caused by R. japonica also occurs in the southwestern part of Japan (6,7). In the 1940s and 1950s, many Murine Typhus cases were reported in Japan. These diagnoses were made according to the clinical features of the illness and the reactivity of the serum samples to OX19 in Weil-Felix tests. A few cases were diagnosed on the basis of symptoms exhibited by animals infected with isolated rickettsiae and complement fixation tests, in addition to results of the Weil-Felix tests. The Weil-Felix test is useful for preliminary screening of rickettsiosis; however, the reaction could indicate epidemic Typhus or spotted fever in some cases. Since 1958, only three Murine Typhus cases have been reported in Japan (8). In these cases, no serologic tests for epidemic Typhus were conducted. Serum sample from patients with epidemic Typhus and Murine Typhus frequently possess serologic cross-reactivity to R. typhi and R. prowazekii, respectively (9). Thus, the possibility of epidemic Typhus could not be excluded definitively in these cases. On May 4, 2003, a 56-year-old man living in Tokushima, Japan, sought medical care; he had a temperature of 39.1°C and exanthema on the trunk and the upper limbs. No surface lymph nodes were palpable. He was treated with lincomycin and cefditoren pivoxil with no improvement. On day 3, the patient informed caregivers that he had been in a bamboo grove on days 1 and 11 before the onset of symptoms. C-reactive protein of the serum sample collected on day 3 was positive (= 7.6 mg/dL). From this finding, spotted fever was suspected; the disease is endemic in Tokushima. On day 4, the exanthema had spread systemically, and treatment with minocycline was started, which led to a gradual decrease in fever and rashes. The patient was admitted to the Tokushima University Hospital on day 6 of the illness for diagnosis and further treatment. Serum samples were collected from the patient on days 5, 6, 9, 20, and 34. Indirect immunoperoxidase tests on the serum samples for tsutsugamushi disease, spotted fever, Murine Typhus, and Q fever on day 5 of the illness were negative for immunoglobulin (Ig) G and IgM antibodies (
Lucas S. Blanton - One of the best experts on this subject based on the ideXlab platform.
-
Case Report: Renal Failure due to Focal Segmental Glomerulosclerosis in a Patient with Murine Typhus.
The American journal of tropical medicine and hygiene, 2020Co-Authors: Lucas S. Blanton, Megan A. Berman, Marjan AfrouzianAbstract:Murine Typhus is a flea-borne rickettsiosis caused by Rickettsia typhi. When severe, endothelial dysfunction can lead to acute kidney injury secondary to prerenal azotemia or acute tubular necrosis. Here, we describe an unusual cause of kidney injury during the course of Murine Typhus-focal segmental glomerulosclerosis.
-
Rise in Murine Typhus in Galveston County, Texas, USA, 2018.
Emerging infectious diseases, 2020Co-Authors: Karla Ruiz, Randy Valcin, Philip Keiser, Lucas S. BlantonAbstract:Murine Typhus, an undifferentiated febrile illness caused by Rickettsia typhi, is increasing in prevalence and distribution throughout Texas. In 2018, a total of 40 cases of Murine Typhus were reported in Galveston County. This increase, unprecedented since the 1940s, highlights the importance of awareness by physicians and public health officials.
-
2128. Murine Typhus and Pregnancy: Case Series and Literature Review
Open Forum Infectious Diseases, 2019Co-Authors: Melinda B. Tanabe, Lucas S. Blanton, Mauricio La Rosa De Los Rios, Camille Webb CamminatiAbstract:Abstract Background Murine Typhus is an arthropod borne disease of worldwide distribution with recent reemergence in the United States of America. There is limited data about the presentation, treatment and outcomes in the pregnant population. We report two cases of Murine Typhus in pregnancy, as well as a case series based in literature published between 1990 and 2019. Methods A comprehensive search in Pubmed database using words Murine Typhus, pregnancy, R. typhi and endemic Typhus was done. Exclusion criteria were asymptomatic Murine Typhus in pregnancy and undiagnosed febrile illness in pregnancy. Results Six articles met the criteria of symptomatic pregnant Murine Typhus infection. Four case reports plus our own 2 case reports, and 2 observational population studies. A total of 35 pregnancy patients were identified. Distribution was worldwide. Gestational age at presentation varied. Patients frequently presented with prolonged duration of fevers prior to presentation, headache, rash, thrombocytopenia and elevated hepatic transaminases. Diagnosis was mainly based on serology. Treatment varied and 8 cases did not receive any treatment at all. Overall pregnancy outcome was favorable, except in an Asian cohort reporting 6 patients with poor pregnancy outcomes. Conclusion The lack of data about Murine Typhus in pregnancy is of serious concern. Increase awareness of different presentations is needed in this population. Murine Typhus infection can mimic other pregnancy-related pathologies that have very different treatments and outcomes. More data are needed about effective treatment and safety of doxycycline use during pregnancy. Disclosures All authors: No reported disclosures.
-
Analysis of Health-Care Charges in Murine Typhus: Need for Improved Clinical Recognition and Diagnostics for Acute Disease.
The American journal of tropical medicine and hygiene, 2018Co-Authors: Rahat F. Vohra, David H. Walker, Lucas S. BlantonAbstract:Murine Typhus, caused by Rickettsia typhi, is an undifferentiated febrile illness with no available rapid and sensitive diagnostic assay for use during early disease. We aimed to compare the health-care charges in those diagnosed with Murine Typhus to those with influenza, a febrile illness with an available rapid diagnostic test. A comparison of health-care-associated charges at the University of Texas Medical Branch at Galveston demonstrated a median of $817 for influenza versus $16,760 for Murine Typhus (P < 0.0001). Median laboratory ($184 versus $3,254 [P < 0.0001]) and imaging charges ($0 versus $514 [P < 0.0001]) were also higher in those with Murine Typhus. Those receiving at least one imaging study during their illness were greater in the Murine Typhus group (91.3% versus 20.3%) (P < 0.0001). The median time needed to establish a confirmed or presumptive diagnosis was 2 days for influenza compared with 9 days for Murine Typhus (P < 0.0001). The median number of health-care encounters was greater for those with Murine Typhus (2 versus 1) (P < 0.0001). Eleven patients (15.9%) with influenza were hospitalized as a result of their illness compared with 16 (69.6%) with Murine Typhus (P < 0.0001). The estimated mortality based on disease severity at presentation by Acute Physiology and Chronic Health Evaluation II scoring was similar in the two groups-both had a median 4% mortality risk (P = 0.0893). These results highlight the need for improved clinical recognition and diagnostics for acute rickettsioses such as Murine Typhus.
-
An Unusual Cutaneous Manifestation in a Patient with Murine Typhus.
The American journal of tropical medicine and hygiene, 2015Co-Authors: Lucas S. Blanton, Alfred Lea, Brent Kelly, David H. WalkerAbstract:Abstract Murine Typhus is a flea-borne febrile illness caused by Rickettsia typhi. Although often accompanied by rash, an inoculation lesion has not been observed as it is with many tick- and mite-transmitted rickettsioses. We describe a patient with Murine Typhus and an unusual cutaneous manifestation at the site of rickettsial inoculation.
Kevin Purcell - One of the best experts on this subject based on the ideXlab platform.
-
Murine Typhus in children, South Texas.
Emerging infectious diseases, 2007Co-Authors: Kevin Purcell, Jaime Fergie, Kevin Richman, Lisa RochaAbstract:Children from South Texas were evaluated for immunoglobulin G to Rickettsia typhi, the causative agent of Murine Typhus. Of 513 children, 8.6% of those 1-5 years of age, 13.3% of those 6-11 years of age, and 13.8% of those 12-17 years of age had positive results.
-
Spontaneous splenic rupture in a child with Murine Typhus.
The Pediatric infectious disease journal, 2004Co-Authors: Jaime Fergie, Kevin PurcellAbstract:A 10-year-old boy hospitalized with Murine Typhus infection had splenic rupture as a complication. Surgical intervention was not required. He recovered and was discharged a week after admission. This is the first reported case of spontaneous splenic rupture in a child with Murine Typhus.
-
Murine Typhus in South Texas children.
The Pediatric infectious disease journal, 2000Co-Authors: Jaime Fergie, Kevin Purcell, Diane M WanatAbstract:BACKGROUND Murine Typhus is a zoonotic infection caused by Rickettsia typhi. This illness used to be endemic in the southeastern and gulf coast of the United States and is now only rarely reported in South Texas and Southern California. Murine Typhus causes a febrile illness with headache and rash that has been well-described in adults. OBJECTIVE To define the epidemiologic and clinical characteristics, laboratory findings, hospital course and response to therapy of children discharged from our hospital with a diagnosis of Murine Typhus. METHODS Retrospective chart review of all children discharged from Driscoll Children's Hospital, Corpus Christi, TX, from January 1, 1990, to June 30, 1998, with a diagnosis of Murine Typhus. Patients. Thirty children (17 females) ages 2 to 17 years (mean, 10 +/- 4 years). RESULTS Eighty percent of the children were admitted between May and November, and 67% had a history of contact with or exposure to a potential animal reservoir. Children were admitted after a mean of 7 +/- 4 days. The most common clinical features were fever 100%, rash 80% and headache 77%. Laboratory abnormalities included elevated erythrocyte sedimentation rate (75%), elevated serum transaminases (67%), hyponatremia (66%) and increased immature leukocytes without leukocytosis (63%). Only one child had leukocytosis and 40% had leukopenia. Defervescence occurred a mean of 35 +/- 19 h after initiation of appropriate antibiotics. Hospitalization lasted for a mean of 7 +/- 3 days. There were no readmissions and no patients died as a result of the infection. CONCLUSIONS Despite being rarely reported in this country now, Murine Typhus continues to be an important cause of fever and hospitalization for children in South Texas. Children with Murine Typhus develop an illness similar to that reported in adults with fever, rash and headache. Children respond quickly to therapy with doxycycline or tetracycline and recover completely from their illness.
