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D Raoult

Publications and source records attributed to D Raoult.

At least 235 records · Page 13Linked to original sources
PubMed1998

[Splenic abscess caused by Coxiella burnetti in the absence of endocarditis].

INTRODUCTION: The most frequent clinical expression of chronic Q fever is culture-negative endocarditis. Other localizations are rare. EXEGESIS: We report a documented case of chronic Q fever that occurred in a 47-year-old immunocompetent man and was associated with spleen abscess, in the absence of detectable endocarditis. The spleen abscess was a complication of either a preexisting cyst or a calcified hematoma. Splenic infection with Coxiella burnetii was documented with cultures, polymerase chain reaction and immunohistochemistry. The outcome was favorable after splenectomy and a 21-month antibiotherapy. CONCLUSION: Chronic Q fever may develop in the absence of endocarditis, when a preexisting vascular lesion such as aortic aneurysm exists. A splenic cyst may have played a similar role for this patient.

Abscess↗
PubMed1998

[Cutaneous signs of Rickettsia and related microorganisms].

INTRODUCTION: Rickettsiosis are emerging, life-threatening infectious diseases that are world-wide distributed and have various manifestations. Most of the time, skin involvement is the prominent feature of clinical manifestations. Clinicians must therefore be well aware of these various clinical pictures. CURRENT KNOWLEDGE AND KEY POINTS: Knowledge about rickettsial infections has recently improved due to either the identification of new vectors and reservoirs, the description of new systemic and cutaneous signs and symptoms, or the amelioration of diagnosis methods. Cutaneous manifestations mainly depend on the type of microorganism and on the host characteristics. In some cases, they are so typical that their only identification would lead to the diagnosis. FUTURE PROSPECTS AND PROJECTS: As growing population movements may lead to an increase in the disease incidence, detailed knowledge of clinical, particularly cutaneous, manifestations of rickettsiosis is required in order to improve both diagnosis and treatment. When identified, cutaneous manifestations of rickettsiosis allow the clinician to confirm rapidly the diagnosis, using polymerase chain reaction or immunofluorescence and to institute prompt and specific treatment, thus reducing unfavorable disease outcome.

Diagnosis, Differential↗
PubMed1998

Survey of seroprevalence of Q fever in dogs in the southeast of France, French Guyana, Martinique, Senegal and the Ivory Coast.

A serological survey was carried out on 429 dogs belonging to the French military in France, French Guyana, Martinique, Senegal and the Ivory Coast. Serology against phase I and II antigens of Coxiella burnetii, the intracellular zoonotic bacterium was performed using indirect immunofluorescence techniques. Specific antibodies were found in dogs from France (9.8%), Senegal (11.6%), Ivory Coast (8.3%), French Guyana (5.2%) but not in those from Martinique. The seroprevalence among 77 dogs who had contact with sheep compared with 352 dogs who had had no contact, demonstrated a significantly higher seroprevalence in the former. Our results indicate that dogs, living close to sheep, may be infected by Coxiella burnetii and should be considered as possible sources of infection for humans.

Animals↗
PubMed1998

Outbreak of Rickettsia africae infections in participants of an adventure race in South Africa.

African tick-bite fever, caused by Rickettsia africae and transmitted by Amblyomma ticks, is an emerging rickettsiosis in southern Africa. Because of increased tourism to this area, several cases in tourists have been reported recently. We report 13 cases of R. africae infection diagnosed in France that occurred in competitors returning from an adventure race in South Africa and compare our data with previously reported findings. Most of our patients presented with fever, headache, multiple inoculation eschars, and regional lymphadenopathies, but only 15.4% had a cutaneous rash. Diagnosis was confirmed either by isolation of R. africae from an eschar biopsy specimen or by serological methods, including cross-adsorption between R. africae and Rickettsia conorii. The purpose of this study was to raise physicians' awareness of R. africae infections in an attempt to facilitate the rapid diagnosis and treatment of imported African tick-bite fever in developed countries.

Adult↗
PubMed1998

Q fever during pregnancy: a public health problem in southern France.

We describe five cases of Q fever in pregnant women that were diagnosed during the last 3 years in the town of Martigues in Southern France. Analysis of our cases and the 18 other published cases shows that Q fever is a significant cause of morbidity and mortality in pregnancy. The disease may present as an acute or chronic infection and can be reactivated during subsequent pregnancies, as is seen with other mammals. In Martigues, Q fever is present in at least one per 540 pregnancies and constitutes the most significant public health problem related to intrauterine infections.

Acute Disease↗
PubMed1998

Coxiella burnetii infection of aneurysms or vascular grafts: report of seven cases and review.

The most frequent clinical presentation of chronic Q fever is endocarditis, although infections of aneurysms and vascular prostheses have also been described. We report seven new cases of Coxiella burnetii infection of aneurysms or vascular grafts. We also review the literature and compare our cases with the six previously reported cases. This study demonstrated the lack of specific symptoms associated with this disease. Moreover, prospectively, in an attempt to reevaluate the incidence of Q fever-associated vascular infection, we systematically searched for C. burnetii infections in 163 patients with aortic aneurysms or vascular grafts who underwent vascular surgery. Microbiological testing included standard culture, Q fever serology, cell culture, and polymerase chain reaction amplification of C. burnetii DNA from biopsy specimens of aneurysms or vascular grafts. A microorganism was isolated from 25 patients, including C. burnetii in two cases; both of these patients had serological titers consistent with chronic Q fever. Both patients had nonspecific clinical features, and thus their infections would have probably remained undiagnosed without our systematic testing. Therefore, since the incidence of C. burnetii vascular infection is probably underestimated, we suggest that C. burnetii serology be routinely carried out in cases of unexplained febrile illness, pain, or weight loss in patients with a history of underlying vascular disease.

Adult↗
PubMed1998

A guinea pig model for Q fever endocarditis.

A new model of experimental endocarditis, using electrocoagulation of native aortic valves, was used for the study of Q fever endocarditis. In the 20 guinea pigs electrocoagulated and inoculated with Coxiella burnetii Nine Mile phase I strain, 10 presented with infective endocarditis. Of these, 7 died spontaneously. All guinea pigs with endocarditis presented with blood cultures positive for C. burnetii, and C. burnetii antigen was found in their cardiac valves. Positive blood cultures or valvular immunopositive cells were not identified in either nonelectrocoagulated or noninoculated controls. This experimental model demonstrates that Q fever in an animal with previously damaged valves results in endocarditis. It could provide a new tool for the investigation of pathophysiology and antibiotic therapy for Q fever endocarditis.

Animals↗
PubMed1998

Killing kinetics of intracellular Afipia felis treated with amikacin.

Afipia felis is a facultative intracellular bacterium which multiplies in macrophages following inhibition of phagosome-lysosome (P-L) fusion. When A. felis-infected cells are incubated for 72 h with various antibiotics, only aminoglycosides are found to be bactericidal. We therefore studied the killing of intracellular A. felis by amikacin, and its relationship with the restoration of P-L fusion. Amikacin reduced the number of A. felis from 8.5 x 10(5) to 3.5 x 102 cfu/mL within 94 h. P-L fusion was restored after 30-40 h of incubation with amikacin. Both mechanisms may participate in the intracellular killing of bacteria.

Amikacin↗
PubMed1998

Ehrlichial DNA amplified from Ixodes ricinus (Acari: Ixodidae) in France.

Granulocytic ehrlichia 16S rDNA was amplified for the 1st time from an Ixodes ricinus (Linne) tick collected in Europe. Sequence analysis of polymerase chain reaction products from the 16S rRNA gene demonstrated the organism from which it originated to be closely related to the agent of human granulocytic ehrlichiosis, an emerging disease that was recently described in the United States; Ehrlichia phagocytophila, the agent of tick-borne fever of ruminants in Europe; and Ehrlichia equi. the agent of the worldwide equine granulocytic ehrlichiosis. These granulocytic ehrlichiae have been associated with Ixodes spp. ticks that may act as vectors. It remains to be determined if each of these granulocytic ehrlichiae, that may constitute variants of the same species, is responsible for a specific disease in animals and in humans.

Animals↗
PubMed1998

Phylogenetic analysis of spotted fever group rickettsiae by study of the outer surface protein rOmpA.

Rickettsiae are classified in the order Rickettsiales and have been included in the alpha subclass of the class Proteobacteria on the basis of 16S rRNA gene sequence comparison. To estimate the evolutionary forces that have shaped the members of the spotted fever group (SFG) rickettsiae, the ompA gene (apart from the tandem repeat units), encoding an antigenic high-molecular-mass membrane protein specific for the group, was amplified and sequenced from 21 isolates. The phylogenetic relationship between SFG rickettsiae were inferred from the comparison of both the gene and derived protein sequences, using the parsimony, neighbor-joining and maximum-likelihood methods. Three strongly supported phylogenetic sub-groups were distinguished: first, the Rickettsia conorii complex (R. conorii Malish, R. conorii M1, R. conorii Moroccan, R. conorii Indian tick typhus, Astrakhan fever rickettsia and Israeli tick typhus rickettsia); second, a cluster including Rickettsia africae, strain S, Rickettsia parkeri, Rickettsia sibirica and 'Rickettsia mongolotimonae'; and, third, a cluster including Rickettsia aeschlimannii, Rickettsia rhipicephali, Rickettsia massiliae, Bar 29 and Rickettsia montanensis. Rickettsia rickettsii, Rickettsia japonica, Rickettsia slovaca and Thai tick typhus rickettsia did not cluster with any other Rickettsia species. To test whether positive selection was responsible for sequences diversity, rates of synonymous and nonsynonymous nucleotide substitutions were compared for Rickettsia ompA alleles and indicated that this gene is undergoing neutral evolution.

Amino Acid Sequence↗
PubMed1998

Rickettsia honei sp. nov., the aetiological agent of Flinders Island spotted fever in Australia.

The name Rickettsia honei, strain RBT, has been proposed for a unique spotted fever group (SFG) agent which is pathogenic for humans. This agent has previously been compared to the other SFG agents and was shown to be distinct in protein structure by SDS-PAGE and by immunoblotting. Genetic comparisons of the 16S rRNA, rompA, gltA and the 17 kDa antigen genes with the other SFG rickettsiae confirmed the phylogenetic distance between R. honei and the previously described species. Genetically, Rickettsia honei is more closely related to the Thai tick typhus (TT-118) rickettsia than to any other member of the SFG. Indeed, it is proposed that TT-118 is a strain of R. honei which was previously isolated in Thailand. These results elucidate the presence of a unique SFG rickettsial species in Australasia.

Antigens, Bacterial↗
PubMed1998

Rickettsia slovaca sp. nov., a member of the spotted fever group rickettsiae.

The name Rickettsia slovaca sp. nov. (type strain is strain B) is proposed for a member of the spotted fever group (SFG) rickettsiae which was isolated from Dermacentor marginatus ticks in Slovakia in 1968, and was recently implicated in human febrile illness. This rickettsia can be phenotypically distinguished from other SFG rickettsiae by microimmunofluorescence serotyping, SDS-PAGE, Western blotting and mAbs. Genotypic differences between R. slovaca and the other SFG representatives can be demonstrated by PCR-RFLP analysis, pulsed-field gel electrophoresis and sequencing of 16S rRNA, gltA and ompA genes.

Animals↗
PubMed1998

Ambulatory treatment of multidrug-resistant Staphylococcus-infected orthopedic implants with high-dose oral co-trimoxazole (trimethoprim-sulfamethoxazole).

We examined the effectiveness and safety of high-dose oral co-trimoxazole (trimethoprim-sulfamethoxazole) for the treatment of orthopedic implants infected with multidrug-resistant Staphylococcus species. The prospective study was conducted between 1989 and 1997 in a university medical center with ambulatory-care services. Patients eligible for the study consisted of those from whom multidrug-resistant Staphylococcus spp. organisms susceptible only to glycopeptides and co-trimoxazole were isolated from their orthopedic implants and for whom there was no contraindication to the treatment. All patients were treated orally with high-dose co-trimoxazole (trimethoprim, 20 mg/kg of body weight/day; sulfamethoxazole, 100 mg/kg/day). Patients with prosthetic hip infections were treated for 6 months, with removal of any unstable prosthesis after 5 months of treatment; patients with prosthetic knee infections were treated for 9 months, with removal of any unstable prosthesis after 6 months of treatment; and patients with infected osteosynthetic devices were treated for 6 months, with removal of the device after 3 months of treatment, if necessary. Monthly clinical evaluations were conducted until the completion of the treatment, and follow-up examinations were conducted regularly for up to 6 years. The overall treatment success rate was 66.7% (26 of 39 patients), with success rates of 62.5% for patients with prosthetic knee infections, 50% for those with prosthetic hip infections, and 78.9% for those with other device infections. Seventeen of the 28 (60.7%) patients who did not have any orthopedic material removed were cured. Eight patients stopped the treatment because of side effects, and one patient was not compliant. In three patients treatment failed because of the appearance of a resistant bacterium. Long-term oral ambulatory treatment with co-trimoxazole appears to be an effective alternative to the conventional medicosurgical treatment of chronic multidrug-resistant Staphylococcus-infected orthopedic implants which includes long-term intravenous antibiotic therapy combined with surgical debridement and removal of foreign material or its subsequent one- or two-stage replacement.

Administration, Oral↗
PubMed1998

In vitro susceptibilities of 27 rickettsiae to 13 antimicrobials.

The MICs of 13 antibiotics (doxycycline, thiamphenicol, rifampin, amoxicillin, gentamicin, co-trimoxazole, ciprofloxacin, pefloxacin, ofloxacin, erythromycin, josamycin, clarithromycin, and pristinamycin) were determined for 27 available rickettsial species or strains. We used two in vitro cell culture methods described previously: the plaque assay and the microplaque colorimetric assay. Our results confirm the susceptibilities of rickettsiae to doxycycline, thiamphenicol, and fluoroquinolones. Beta-lactams, aminoglycosides, and cotrimoxazole were not active. Typhus group rickettsiae were susceptible to all macrolides tested, whereas the spotted fever group rickettsiae, R. bellii, and R. canada were more resistant, with josamycin, a safe alternative for the treatment of Mediterranean spotted fever, being the most effective compound. Strain Bar 29, R. massiliae, R. montana, R. aeschlimannii, and R. rhipicephali, which are members of the same phylogenetic subgroup, were more resistant to rifampin than the other rickettsiae tested. Heterogeneity in susceptibility to rifampin, which we report for the first time, may explain in vivo discrepancies in the effectiveness of this antibiotic for the treatment of rickettsial diseases. We hypothesize that rifampin resistance and erythromycin susceptibility may reflect a divergence during the evolution of rickettsiae.

Animals↗
PubMed1998

Increases in the levels of Coxiella burnetii-specific immunoglobulin G1 and G3 antibodies in acute Q fever and chronic Q fever.

A detailed analysis of the humoral response to Coxiella burnetii may provide insight into the pathogenesis of Q fever, a zoonosis caused by C. burnetii. The subclasses of C. burnetii-specific antibodies were determined by immunofluorescence in 20 patients with acute Q fever and 20 patients with chronic Q fever. Although immunoglobulin G1 (IgG1) and IgG3 antibodies were found in acute and chronic Q fever, neither IgG2 nor IgG4 was detected. The detection of IgG1 and IgG3 antibodies was not due to an increase of the IgG1 and IgG3 subclasses. Moreover, IgG1 and IgG3 antibodies were not correlated, suggesting that they may play different roles in Q fever.

Acute Disease↗
PubMed1998

Coxiella burnetii induces reorganization of the actin cytoskeleton in human monocytes.

Coxiella burnetii, an obligate intracellular bacterium which survives in myeloid cells, causes Q fever in humans. We previously demonstrated that virulent C. burnetii organisms are poorly internalized by monocytes compared to avirulent variants. We hypothesized that a differential mobilization of the actin cytoskeleton may account for this distinct phagocytic behavior. Scanning electron microscopy demonstrated that virulent C. burnetii stimulated profound and polymorphic changes in the morphology of THP-1 monocytes, consisting of membrane protrusions and polarized projections. These changes were transient, requiring 5 min to reach their maximum extent and vanishing after 60 min of incubation. In contrast, avirulent variants of C. burnetii did not induce any significant changes in cell morphology. The distribution of filamentous actin (F-actin) was then studied with a specific probe, bodipy phallacidin. Virulent C. burnetii induced a profound and transient reorganization of F-actin, accompanied by an increase in the F-actin content of THP-1 cells. F-actin was colocalized with myosin in cell protrusions, suggesting that actin polymerization and the tension of actin-myosin filaments play a role in C. burnetii-induced morphological changes. In addition, contact between the cell and the bacterium seems to be necessary to induce cytoskeleton reorganization. Bacterial supernatants did not stimulate actin remodeling, and virulent C. burnetii organisms were found in close apposition with F-actin protrusions. The manipulation of the actin cytoskeleton by C. burnetii may therefore play a critical role in the internalization strategy of this bacterium.

Actins↗
PubMed1998

Massilia timonae gen. nov., sp. nov., isolated from blood of an immunocompromised patient with cerebellar lesions.

A fastidious, slowly growing, strictly aerobic, gram-negative bacterium was isolated from a culture of blood from a 25-year-old man with common variable immunodeficiency. The man had been admitted to hospital with febrile progressive cerebellar ataxia. The use of standard phenotypic schemes did not lead to identification, but sequence analysis demonstrated that the 16S rRNA gene of the isolate was most similar to those of the environmental bacteria Duganella zoogloeoides (formerly Zoogloea ramigera 115) and Telluria mixta. Further characterization of the bacterium by biochemical analysis, electron microscopy, G+C content estimation, and fatty acid analysis demonstrated significant differences between the bacterium and D. zoogloeoides and Telluria species; thus, we propose it as a new taxon with the name Massilia timonae gen. nov., sp. nov.

Adult↗