Patients with systemic inflammatory and autoimmune diseases are at risk of vaccine-preventable illnesses.

OBJECTIVE: To evaluate vaccine coverage and humoral immunity to tetanus, diphtheria and poliomyelitis in adults followed for systemic inflammatory and/or autoimmune diseases (SIADs). METHODS: A cross-sectional study was conducted between June and August 2006 in a monocentric cohort of adults with SIAD. A standardized questionnaire was administered to collect medical, therapeutic and vaccine coverage data. Blood samples were collected in order to measure antibody titres against diphtheria, tetanus and poliomyelitis (DTP). RESULTS: One hundred and eighty-six patients, 32% males, mean (s.d.) age 51 (16) years, 79% receiving CSs and/or immunosuppressants, were included. The vaccine coverage was 29% for diphtheria, 48% for tetanus and 33% for poliomyelitis. The percentages of patients with no humoral immunity against DTP were 44, 21 and 12%, respectively, decreasing to 37.5, 10 and 0%, respectively, for those who had received a vaccine booster in the last 10 years. In a multivariate analysis, age and CS treatment were associated with the absence of humoral immunity against diphtheria and female sex, CD4(+) T cell <200/mm(3) and an absence of tetanus vaccine booster in the last 10 years with the absence of humoral immunity to tetanus. CONCLUSION: Vaccine coverage against tetanus, diphtheria and poliomyelitis is low in patients with SIAD despite the risk in this population of severe infection, especially when receiving immunosuppressants. A significant proportion of them had no humoral immunity against diphtheria or tetanus. Specific immunization schedules need to be optimized in these patients.

Clinical management of rapidly growing mycobacterial cutaneous infections in patients after mesotherapy.

BACKGROUND: Increasing numbers of patients are expressing an interest in mesotherapy as a method of reducing body fat. Cutaneous infections due to rapidly growing mycobacteria are a common complication of such procedures. METHODS: We followed up patients who had developed cutaneous infections after undergoing mesotherapy during the period October 2006-January 2007. RESULTS: Sixteen patients were infected after mesotherapy injections performed by the same physician. All patients presented with painful, erythematous, draining subcutaneous nodules at the injection sites. All patients were treated with surgical drainage. Microbiological examination was performed on specimens that were obtained before and during the surgical procedure. Direct examination of skin smears demonstrated acid-fast bacilli in 25% of the specimens that were obtained before the procedure and 37% of the specimens obtained during the procedure; culture results were positive in 75% of the patients. Mycobacterium chelonae was identified in 11 patients, and Mycobacterium frederiksbergense was identified in 2 patients. Fourteen patients were treated with antibiotics, 6 received triple therapy as first-line treatment (tigecycline, tobramycin, and clarithromycin), and 8 received dual therapy (clarithromycin and ciprofloxacin). The mean duration of treatment was 14 weeks (range, 1-24 weeks). All of the patients except 1 were fully recovered 2 years after the onset of infection, with the mean time to healing estimated at 6.2 months (range, 1-15 months). CONCLUSIONS: This series of rapidly growing mycobacterial cutaneous infections highlights the difficulties in treating such infections and suggests that in vitro susceptibility to antibiotics does not accurately predict their clinical efficacy.

Evaluation of a new test, genotype HelicoDR, for molecular detection of antibiotic resistance in Helicobacter pylori.

The eradication rate of Helicobacter pylori by standard therapy is decreasing due to antibiotic resistance, mainly to clarithromycin. Our aim was to provide a new molecular test to guide the treatment of new and relapsed cases. We first studied 126 H. pylori strains for phenotypic (MIC) and genotypic resistance to clarithromycin (rrl mutation) and levofloxacin (gyrA mutation) and then developed a DNA strip genotyping test on the basis of the correlation results and literature data. Clinical strains (n = 92) and gastric biopsy specimens containing H. pylori (n = 105) were tested blindly with the new molecular test GenoType HelicoDR. The presence of mutations or the absence of hybridization with wild-type sequences was predictive, in rrl for clarithromycin resistance in 91 cases (mostly the A2147G mutation) and in gyrA for levofloxacin resistance in 58 cases (mutations at codon 87 or 91). Genotyping revealed a mix of genotypes in 33% of the cases, reflecting a coinfection or selection for resistant mutants. The sensitivity and specificity of detecting resistance were 94% and 99% for clarithromycin and 87% and 98.5% for levofloxacin, respectively. The concordance scores were 0.96 for clarithromycin and 0.94 for levofloxacin. With global resistance rates of 46% for clarithromycin and 25% for levofloxacin, which were observed for consecutive positive biopsy specimens from 2007 and 2008, the positive and negative predictive values for detecting resistance were 99% and 94% for clarithromycin and 96% and 96% for fluoroquinolone. GenoType HelicoDR is efficient at detecting mutations predictive of antibiotic resistance in H. pylori when applied to strains or directly to gastric biopsy specimens.

Update on fluoroquinolone resistance in Helicobacter pylori: new mutations leading to resistance and first description of a gyrA polymorphism associated with hypersusceptibility.

Helicobacter pylori eradication by standard therapy is decreasing due to clarithromycin and metronidazole resistance. Fluoroquinolones are valuable drugs for alternative therapy, but their activity needs to be updated. We determined minimum inhibitory concentrations (MICs) of the newly marketed fluoroquinolones (levofloxacin, moxifloxacin and gatifloxacin) and assessed the prevalence of resistance in 128 H. pylori strains isolated in 2004-2005. The quinolone resistance-determining region (QRDR) of gyrA was sequenced for all strains. Gatifloxacin MICs (MIC(50) = 0.25 mg/L) were two- to four-fold lower than those of the other fluoroquinolones. The prevalence of resistance (ciprofloxacin MIC > 1 mg/L) was 17.2% (22 strains). All resistant strains harboured one gyrA mutation at codons 86, 87 or 91, including three new mutations (Asp86Asn, Thr87Ile and Asn87Tyr). Ciprofloxacin-susceptible strains were devoid of such gyrA mutations, but harboured a polymorphism at codon 87 that distinguished 18 isolates (17%) with a Thr87 like the reference strain J99 from 88 strains with Asn87 like the reference strain 26695. Strains with Thr87 were four-fold more susceptible to nalidixic acid, pefloxacin, ciprofloxacin and levofloxacin and were equally susceptible to moxifloxacin and gatifloxacin. The high rate of quinolone resistance in H. pylori requires the use/implication of a 'test and treat' strategy that can confidently rely on QRDR gyrA sequencing.

Psoas abscess: An unusual manifestation of Q fever.

Q fever may lead to serious complications in chronically infected patients. We report two cases of psoas abscess due to Coxiella burnetii associated with lumbar osteomyelitis secondary to an aortic aneurysmal infection. Diagnosis was based on serology, and PCR detected C. burnetii DNA in an abscess sample.

Routine use of real-time PCR for detection of Helicobacter pylori and of clarithromycin resistance mutations.

OBJECTIVES: We previously showed that real-time PCR was a reliable technique for coupled detection of Helicobacter pylori and clarithromycin resistance mutations directly from biopsies. After one year of use, we compared its performances to those of histology, which remains the most employed method for H. pylori detection from gastric biopsies. MATERIALS AND METHODS: 518 subjects underwent endoscopy during the year 2003 with biopsies taken for H. pylori detection by histology, PCR, and in case of discrepancy between the two techniques, by culture. RESULTS: The prevalence of infection, defined as positive PCR and histology, and in case of discrepancy as a positive culture, was 30% (163/518). The percentage of concordance between the two tests was 87.8% (455/518). The sensitivity, specificity, positive and negative predictive values of PCR were 98.2%, 97.5%, 94.7%, and 99.1%, respectively. The corresponding performances of histology were 87.7%, 91.3%, 82.2%, and 94.2%, respectively (p<0.001). The prevalence of clarithromycin resistance was 30%. CONCLUSIONS: PCR is more accurate in routine than histology and permits easy determination of clarithromycin resistance, which is useful in countries like France where the prevalence of resistance is high.

Mycobacterium szulgai infection in a captive population of African clawed frogs (Xenopus tropicalis).

A colony of captive Xenopus tropicalis became infected with Mycobacterium szulgai. Clinical signs, when observed, were lethargy, weight loss, and emaciation. Visceral granulomas were common findings at laparoscopy and necropsy. The diagnosis of mycobacteriosis was based on histologic appearance and Ziehl-Neelsen staining of tissues. The identification of M. szulgai organisms was based on comparison of the 16S rRNA gene sequence with several GenBank databases. There have been no reports of this mycobacterial species as the causative agent of naturally occurring disease in amphibians.

Rescue therapy with bismuth-containing quadruple therapy in patients infected with metronidazole-resistant Helicobacter pylori strains.

BACKGROUND: The emergence of H. pylori strains that are resistant to clarithromycin, metronidazole and fluoroquinolone requires the evaluation of new and effective salvage therapies. AIMS: To test the efficacy of a new formulation of a bismuth-containing quadruple therapy as a rescue therapy in patients who were infected with a H. pylori strain resistant to metronidazole, clarithromycin and fluoroquinolone or who failed multiple lines of treatment using these three antibiotics. METHODS: A total of 103 patients with confirmed H. pylori infection with a resistance profile described above were treated with Pylera(®) (3-in-1 capsules containing bismuth subcitrate potassium 140mg, metronidazole 125mg and tetracycline 125mg) 3 capsules four times a day plus omeprazole 20mg two times a day for 10 days in a named patient program. Eradication was confirmed using a urea breath test at least 28 days after the end of treatment. Efficacy and safety were studied. RESULTS: A total of 103 patients were prospectively included from June 2010 to October 2011. The eradication rate for the intent-to-treat analysis was 83% (CI95%[75-89%]); an 87% eradication rate (CI95%[80-94%]) was found for the per-protocol analysis and 81% (CI95%[80-82%]) for the intent-to-treat analysis in patients with proven resistance to metronidazole. Nine patients discontinued treatment, all due to adverse events. Two serious adverse events (AEs) were reported (memory disorders of unknown significance). Fifty-six (54%) patients reported at least one AE. CONCLUSION: This bismuth-containing quadruple therapy achieved a remarkable eradication rate as a salvage therapy in patients infected with metronidazole-resistant H. pylori strain, despite the frequent occurrence of mild-to-moderate adverse events.

Psoas abscess and chronic Q fever: a contiguous or hematogenous complication? A case report and literature review.

Few cases of psoas abscesses (PA) during chronic Q fever have been reported, and the route of transmission remains unknown. Here, we report a new case and have performed a systematic literature review to determinate the spreading route of this complication. Medline, EMBASE and Web of Science were searched. Local spreading was supported by endocarditis exclusion, evidence of vascular infection and absence of distantly infected sites. Among 275 retrieved references, 179 were initially rejected, and 85 additional references were rejected after full-text review. A total of 11 studies, reporting 13 cases, were included. Additionally, we reported one new case. A total of 14/14 cases reached Q fever vascular infection diagnostic criteria, and 7/14 provided adequate evidence supporting a causal relationship between Q fever vascular infection and PA. All patients presented aorta defects. In conclusion, Q fever PA results from the spreading of a local infection and occurs specifically in patients presenting a vascular graft or an abdominal aortic aneurysm.

Gastroduodenal ulcer and erosions are related to portal hypertensive gastropathy and recent alcohol intake in cirrhotic patients.

Gastroduodenal ulcers and gastroduodenal erosions are particularly frequent in cirrhotic patients, but their precise cause is unclear. The aim of this study was to identify pathogenic factors associated with ulcers and erosions in patients with cirrhosis. We studied 64 consecutive patients with cirrhosis referred for gastroscopy. The severity of portal hypertensive gastropathy was graded with an endoscopic score. H. pylori status was determined by histological examination of gastric biopsy samples or by the [13C] urea breath test. The daily alcohol intake within the preceding week was recorded. The Child-Pugh score was determined. Fifteen patients had gastroduodenal ulcer and 20 had gastroduodenal erosions. Cirrhosis was related to alcohol in 44 patients and hepatitis B or C virus in 14 patients. The portal hypertensive gastropathy was graded as severe in 12 patients and mild in 25 patients. H. pylori infection, found in 37 patients, was not related to the gastroduodenal lesions. Univariate and multivariate analysis showed the links between gastroduodenal erosions and hypertensive gastropathy and recent heavy drinking. Gastroduodenal ulcer was independently associated only with the severity of the gastropathy. In conclusion, in these patients with cirrhosis, the presence of gastroduodenal ulcer was significantly related to hypertensive gastropathy but not to H. pylori infection. Recent alcohol intake favored the occurrence of gastroduodenal erosions.

Fast and accurate quantitative detection of Helicobacter pylori and identification of clarithromycin resistance mutations in H. pylori isolates from gastric biopsy specimens by real-time PCR.

Rapid identification of patients infected with clarithromycin-resistant Helicobacter pylori without the need for culture can help to avoid useless prescriptions of clarithromycin. We developed and tested a routine real-time quantitative PCR assay dedicated to that purpose. One hundred ninety-six consecutive gastric biopsy specimens were examined by culture, histology performed by a trained physician, and rapid PCR with the LightCycler apparatus. Infection was defined as (i) positivity of culture, (ii) positivity of histology, or (iii) positivity of PCR if confirmed by positivity of a concomitant indirect test (serology or urea breath test). Susceptibility to clarithromycin was tested by E-test and PCR. The prevalence of infection was 33.7% (66 of 196 samples). The sensitivities of culture, histology, and PCR were 90.9% (60 of 66 samples), 87.9% (58 of 66 samples), and 97.0% (64 of 66 samples), respectively. The specificity of PCR was 94.6% (123 of 130 samples). The linearity of the PCR results was achieved over a 6-log range of input DNA, and we were able to accurately quantify as few as 300 bacteria and to qualitatively detect as few as 30 bacteria per DNA sample. For clarithromycin susceptibility testing, there was 98.2% (55 of 56 samples) concordance between E-test and PCR. Forty-eight strains were clarithromycin susceptible, and 9 strains were clarithromycin resistant. The single discrepancy concerned a culture which was a mixture of mutant and wild type, with a susceptible-to-resistant ratio of 11.5: the resistant population was detected by E-test but not by PCR. Our PCR assay is accurate for fast detection of H. pylori as well as of clarithromycin resistance and is also able to objectively determine bacterial density.