The Bad Bug is Back: Acinetobacter Baumannii Bacteremia Outbreak during the COVID-19 Pandemic in an Intensive Care Unit.

Background: Epidemiology of nosocomial infections may show variability because of under-estimation of infection control measures (ICMs) in coronavirus disease 19 (COVID-19) outbreak. Aim: To investigate the Acinetobacter bacteremia outbreak developed in an intensive care unit (ICU) between March 20 to May 15, 2020, examine the risk factors, and re-evaluate ICM retrospectively. Material and Methods: A retrospective cohort analysis was conducted to determine the risk factors, pulsed field gel electrophoresis (PFGE) was performed for analysis of the outbreak, ICM practices were observed by a team, and infection control interventions were undertaken. Results: Acinetobacter bacteremia developed in 17 patients (21.5%) within 79 COVID-19 patients included in the study. The mean age of the bacteremic patients was 67.3 (SD = 14.82) years, and 82.4% of them were male; of these, 15 died, leading to 88.2% mortality. The bacteremia rate was higher compared with a 14-month period preceding the COVID-19 pandemic (17/79 versus 12/580 patients, respectively). PFGE revealed that the outbreak was polyclonal. On multi-variate analysis, the bacteremia development rate was 13.7 and 5.06 times higher with central venous catheter (CVC) use and in patients with chronic obstructive pulmonary disease (COPD), respectively. The mortality rate was higher in bacteremic patients (p = 0.0016). It was observed that ICMs were not followed completely, especially change of gloves and hand hygiene. Contamination of A. baumannii was observed in 38% of the gloves. Conclusion: COPD and CVC use were determined as risk factors for Acinetobacter bacteremia development, and failures in ICM may have led to cross-contamination of endemic A. baumannii. The outbreak could be controlled within 3 weeks of interventions.

Plasma and Breast Milk Pharmacokinetics of Tenofovir Disoproxil Fumarate in Nursing Mother with Chronic Hepatitis B-Infant Pairs.

Tenofovir use is associated with lower risk of mother-to-infant transmission of the virus, and discontinuation of the treatment is not safe. However, the safety of the drug during pregnancy and breastfeeding is not clear. In this study, we aimed to determine the tenofovir concentration in plasma of mother-infant pairs along with breast milk in chronic hepatitis B patients during the lactation period. A total of 11 mother-infant pairs were enrolled in the study. All the mothers received tenofovir disoproxil fumarate (TDF) 245 mg/day for at least 1 month because of chronic hepatitis B infection. Maternal blood, breast milk, and infant blood samples were obtained concomitantly. Tenofovir concentrations were determined by liquid chromatography-tandem mass spectrometry. The median concentrations of tenofovir in maternal plasma and breast milk samples were 88.44 (interquartile range [IQR], 62.47 to 116.17) ng/ml and 6.69 (IQR, 4.88 to 7.03) ng/ml, respectively. Tenofovir concentrations were undetectable (<4 ng/ml) in all of the infant plasma samples. The ratio of tenofovir concentration in breast milk to that in maternal plasma was 0.07. Tenofovir disoproxil fumarate passes through the breast milk in a small amount. Infants had no detectable tenofovir level in their plasma. Our study suggests that tenofovir disoproxil fumarate treatment is safe during the breastfeeding period in chronic hepatitis B patients.

Peginterferon add-on results in more HBsAg decline compared to monotherapy in HBeAg-positive chronic hepatitis B patients.

It is unknown whether peginterferon (PEG-IFN) add-on to entecavir (ETV) leads to more HBsAg decline compared to PEG-IFN monotherapy or combination therapy, and whether ETV therapy may prevent HBsAg increase after PEG-IFN cessation. We performed a post hoc analysis of 396 HBeAg-positive patients treated for 72 weeks with ETV + 24 weeks PEG-IFN add-on from week 24 to 48 (add-on, n = 85), 72 weeks with ETV monotherapy (n = 90), 52 weeks with PEG-IFN monotherapy (n = 111) and 52 weeks PEG-IFN + lamivudine (combination, n = 110) within 2 randomized trials. HBsAg decline was assessed at the end of PEG-IFN (EOP) and 6 months after PEG-IFN (EOF) discontinuation. Differences in baseline characteristics were accounted for using inversed probability of treatment weights. At EOP, a HBsAg reduction of ≥1log10 IU/mL was more frequently achieved for patients in the add-on or combination therapy arms (both 36%), compared to PEG-IFN mono (20%) or ETV (8%) (add-on vs PEG-IFN mono P = 0.050). At EOF, the HBsAg reduction ≥1log10 IU/mL was only sustained in patients treated with ETV consolidation (add-on vs combination and PEG-IFN mono: 40% vs 23% and 18%, P = 0.029 and P = 0.003, respectively). For add-on, combination, PEG-IFN mono and ETV, the mean HBsAg-level change at EOF was -0.84, -0.81, -0.68 and -0.33 log10 IU/mL, respectively (P > 0.05 for PEG-IFN arms). HBeAg loss at EOF was 36%, 31%, 33% and 20%, respectively (P > 0.05). PEG-IFN add-on for 24 weeks results in more on-treatment HBsAg decline than does 52 weeks of PEG-IFN monotherapy. ETV therapy may maintain the HBsAg reduction achieved with PEG-IFN.

Alisporivir with peginterferon/ribavirin in patients with chronic hepatitis C genotype 1 infection who failed to respond to or relapsed after prior interferon-based therapy: FUNDAMENTAL, a Phase II trial.

Alisporivir (ALV) is an oral, investigational host-targeting agent, with pangenotypic activity against hepatitis C virus (HCV). This randomized, double-blind, placebo-controlled, Phase II study explored the efficacy and safety of ALV with peginterferon-α2a/ribavirin (PR) in patients with chronic HCV genotype 1 infection in whom prior PR had failed (43% relapsers, 34% null responders and 23% partial responders). Four-hundred-and-fifty-nine patients were randomized (1:1:1:1) to ALV 600 mg once daily (QD), ALV 800 mg QD, ALV 400 twice daily (BID) or placebo plus PR for 48 weeks. When the global ALV trial programme was put on clinical hold, all patients in this study had received ≥31 weeks of randomized treatment; patients completed 48 weeks on PR alone. All ALV groups demonstrated superior rates of complete early virologic response (cEVR; primary endpoint) vs PR alone (P ≤ 0.0131), with highest cEVR rate seen with ALV 400 mg BID (74% vs 36% with PR alone; P < 0.0001). Respective SVR12 rates (key secondary endpoint) were 65% vs 26% in prior relapsers, 63% vs 5% in partial responders and 68% vs 3% in null responders. In patients who received >40 weeks of randomized treatment, the SVR12 rate was 89% for ALV 400 mg BID vs 30% for PR alone (P = 0.0053). Rates of viral breakthrough and relapse were lowest with ALV 400 mg BID. One case of pancreatitis (fully recovered) occurred with ALV/PR. Common AEs were headache, fatigue, anaemia, neutropenia and nausea. Hypertension was infrequent, but more common with ALV. ALV merits further investigation in interferon-free regimens in combination with direct-acting antiviral agents.

Comparison of community-onset healthcare-associated and hospital-acquired urinary infections caused by extended-spectrum beta-lactamase-producing Escherichia coli and antimicrobial activities.

OBJECTIVE: We aimed to compare community-onset healthcare-associated (CO-HCA) and hospital-acquired (HA) urinary tract infections (UTIs) caused by extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli in terms of epidemiology, clinical outcomes and antimicrobial activities. METHODS: Patients from both groups with ESBL-producing E. coli detected by urine culture between January 2009 and January 2011 were included in this retrospective study. Relevant demographical, microbiologic and clinical data were obtained from case records. RESULTS: A total of 173 patients (mean age of 58 years, 74% female) were included, of whom 75 (43.4%) had a CO-HCA UTI and 98 (56.6%) had an HA UTI. Eighty (46.2%) patients had more than one comorbid disease, of whom 57 (32.5%) had urological problems. The most common clinical manifestations were pyelonephritis (43.9%) and urosepsis (16.2%). An age of > 65 years (p = 0.005) in addition to urinary catheterisation (p = 0.001), urosepsis (p = 0.001) and mortality (p = 0.001) were significantly more common in the HA UTI group. Acute cystitis (p = 0.027), complicated cystitis (p = 0.001) and non-urologic neoplasm (p = 0.032) were significantly more common in the CO-HCA UTI group. No isolate was resistant to carbapenems or fosfomycin. Sensitivities to nitrofurantoin, amikacin, trimethoprim sulfamethoxazole-trimoxazole and quinolones were 97.6%, 89%, 29.4% and 17.9% respectively. Both groups showed similar rates of antibiotic resistance. CONCLUSION: ESBL-producing E. coli should be taken into consideration in patients with a CO HCA UTI, not only in hospital settings but also in outpatient settings. We suggest ertapenem as a first-line empirical treatment for patients with an upper UTI and fosfomycin and nitrofurantoin for those with a lower UTI when ESBL-producing E. coli is suspected.

Loss of intrahepatic HBsAg expression predicts sustained response to peginterferon and is reflected by pronounced serum HBsAg decline.

There is a lack of knowledge regarding the effect of peginterferon (PEG-IFN) on the expression of intrahepatic hepatitis B core and surface antigen (HBcAg and HBsAg) in chronic hepatitis B (CHB) and its relation with response to therapy. Fifty-two HBeAg-positive and 67 HBeAg-negative CHB patients with paired liver biopsies taken at baseline and after 1 year of PEG-IFN therapy were studied. After PEG-IFN therapy, HBeAg-negative patients showed a significant reduction in both intrahepatic HBcAg (P = 0.04) and HBsAg expression (P < 0.001). In contrast, a reduction in intrahepatic HBcAg expression was not observed in HBeAg-positive patients, while a trend in reduction of intrahepatic HBsAg staining was found (P = 0.09). Post-treatment, 7 (13%) HBeAg-positive and 9 (14%) HBeAg-negative patients had no expression of intrahepatic HBsAg. Patients without any intrahepatic HBsAg expression post-treatment were more likely to achieve a combined response (HBeAg loss with hepatitis B virus (HBV) DNA <2000 IU/mL for HBeAg -positive and HBV DNA <2000 IU/mL and normal alanine aminotransferase for HBeAg-negative CHB): 71% vs 5% for HBeAg-positive (P < 0.001) and 60% vs 16% for HBeAg-negative patients (P = 0.004), respectively. Moreover, a more profound decline of serum HBsAg was observed in patients with absence of intrahepatic HBsAg staining (3.1 vs 0.4 log IU/mL, P < 0.001 and 1.7 vs 0.4 log IU/mL, P = 0.005 for HBeAg-positive and HBeAg-negative CHB, respectively). In conclusion, PEG-IFN reduces expression of intrahepatic HBsAg. Loss of HBsAg as assessed by immunohistochemistry from the liver predicts a sustained response and is reflected in a pronounced serum HBsAg decline.

Chronic hepatitis C responds poorly to combination therapy in chronic hepatis B carriers.

BACKGROUND: The effect of conventional interferon-based therapy of hepatitis B virus (HBV) and hepatitis C virus (HCV) dual infection is controversial. Yet, no studies have been carried out into pegylated interferon treatment for chronic HBV/HCV coinfection. We aimed to evaluate the response rate and side effects of conventional or pegylated interferon combined with ribavirin on chronic HBV/HCV coinfection therapy. METHODS: The study included 36 chronic hepatitis patients (M/F: 28/8, mean age 47+/-12 years) who were positive for HBsAg and anti-HCV. They were tested for the presence of HBV-DNA by hybridisation assay, and the samples giving negative results were retested by polymerase chain reaction (PCR). All patients were tested for HCV-RNA using PCR, and the HCV genotype was determined. RESULTS: Nineteen patients were given standard interferon either alone or in combination with ribavirin, whereas 17 were given pegylated interferon and ribavirin combination therapy. None of the patients had HBV-DNA positivity; however, all had HCV-RNA detectable by PCR. All the patients had HCV genotype 1b. The mean alanine aminotransferase and aspartate aminotransferase levels were 118+/-65 U/l and 90+/-95 U/l respectively. Five patients in each group discontinued the treatment due to side effects. Only two patients (one from each group) reached sustained virological response. CONCLUSION: Neither pegylated nor conventional interferon based regimes were effective for HBV/HCV coinfection, in which the dominant virus was HCV. Pegylated interferon and ribavirin therapy was not superior to conventional interferon based regimes in the treatment of HBV/HCV coinfection.

Erythema nodosum: an evaluation of 100 cases.

OBJECTIVES: In this study, we investigated the clinical features, etiology, and also predictive factors of secondary erythema nodosum (EN) in patients with EN. METHODS: A total of 100 patients (mean age: 37 years) diagnosed with EN between 1993 and 2004 in our clinic were included in the study prospectively. A skin biopsy was performed in 46 of the patients. Patients were considered to have secondary EN when an underlying condition was found, and to have primary EN when no such condition was found. For the diagnosis of the underlying diseases, the pertinent diagnostic criteria and/or diagnostic methods were used. Categorical and continuous variables were compared by using chi-square and Mann-Whitney U tests respectively. Multiple regression analysis was applied to the significantly different variables. RESULTS: The majority of the patients were female (female/male: 6/1) and nearly half (47%) of the cases had a determined etiology. The leading etiology was poststreptococcal (11%), followed in decreasing order by primary tuberculosis (10%), sarcoidosis (10%), Behçet's syndrome (BS) (6%), drugs (5%), inflammatory bowel diseases (IBD) (3%), and pregnancy (2%). Fifteen (15%) patients complained of cough; the diagnosis was primary tuberculosis in eight cases and sarcoidosis in seven. Four patients with arthritis were diagnosed as having BS (in 3) and Crohn's disease (in 1). All the patients were followed for a mean duration of 4.5 years. The nodosities relapsed annually in 62% (33/53) of idiopathic EN patients but in only one (BS) in the secondary EN group. The histology was consistent with EN in all biopsied patients. Our study revealed that fever, leukocytosis, elevated CRP level, accelerated ESR, presence of cough, sore throat, diarrhea, arthritis, and pulmonary pathology were predictors of secondary EN. Recurrence in EN significantly predicted primary EN. All of the patients had bed rest and the majority was given an anti-inflammatory agent (naproxen sodium). The outcomes were usually favorable within 7 days. The patients with an underlying disease were given the specific treatment. CONCLUSION: EN has been associated with numerous diseases. In order to reduce cost and duration of diagnosis, every centre should determine its own most frequent etiologic factors. Predictive variables for secondary EN should also be determined and an optimum management for such patients should be clarified. Our study revealed streptococcal pharyngitis, primary tuberculosis, sarcoidosis, IBD, and BS as the main etiologies of EN.

Hepatitis B core-related antigen levels are associated with response to entecavir and peginterferon add-on therapy in hepatitis B e antigen-positive chronic hepatitis B patients.

Hepatitis B core-related antigen (HBcrAg), a new serum marker, may be useful in monitoring chronic hepatitis B infection. HBcrAg was measured in 175 hepatitis B e antigen-positive patients treated with entecavir (ETV) with or without peginterferon (PEG-IFN) add-on therapy. Decline in HBcrAg was stronger in patients with vs. without combined response (ETV: -3.22 vs. -1.71 log U/mL, p <0.001; PEG-IFN add-on: -3.16 vs. -1.83 IU/mL, p <0.001) and in patients with vs. without hepatitis B surface antigen (HBsAg) response (ETV: -2.60 vs. -1.74 log U/mL, p <0.001; PEG-IFN add-on: -2.38 vs. -2.15 log U/mL, p = 0.31). HBcrAg was associated with combined response (adjusted odds ratio 0.3, 95% confidence interval 0.2-0.5, p <0.001), but was not superior to quantitative HBsAg (qHBsAg).

Predictors of response to tenofovir disoproxil fumarate plus peginterferon alfa-2a combination therapy for chronic hepatitis B.

BACKGROUND: In patients with chronic hepatitis B, tenofovir disoproxil fumarate (TDF) plus pegylated interferon (PEG-IFN) for 48-weeks results in higher rates of hepatitis B surface antigen (HBsAg) loss than either monotherapy. AIM: To identify baseline and on-treatment factors associated with HBsAg loss at Week 72 and provide a model for predicting HBsAg loss in patients receiving combination therapy for 48 weeks. METHODS: A secondary analysis of data from an open-label study where patients were randomised to TDF (300 mg/day, oral) plus PEG-IFN (PI, 180 µg/week, subcutaneous) for 48 weeks (TDF/PI-48w); TDF plus PEG-IFN for 16 weeks, TDF for 32 weeks (TDF/PI-16w+TDF-32w); TDF for 120 weeks (TDF-120w) or PEG-IFN for 48 weeks (PI-48w). Logistic regression methods were used to identify models that best predicted HBsAg loss at Week 72. RESULTS: Rates of HBsAg loss at Week 72 were significantly higher in the TDF/PI-48w group (6.5%) than in the TDF/PI-16w+TDF-32w (0.5%), TDF-120w (0%) and PI-48w (2.2%) groups (P = 0.09). The only baseline factor associated with response was genotype A. HBsAg decline at Week 12 or 24 of treatment was associated with HBsAg loss at Week 72 (P < 0.001). HBsAg decline >3.5 log10 IU/mL at Week 24 in the TDF/PI-48w group resulted in a positive predictive value of 85% and a negative predictive value of 99% for HBsAg loss at Week 72. CONCLUSIONS: HBsAg decline at Week 24 of TDF plus PEG-IFN combination therapy may identify patients who, after completing 48 weeks of treatment, have a better chance of achieving HBsAg loss at Week 72.

Fibrinolytic activity and d-dimer levels in Behçet's syndrome.

OBJECTIVE: Thrombophlebitis occurs in a third of patients with Behçet's syndrome (BS). The thrombotic tendency in BS has been studied with inconclusive results perhaps due to the inadequate numbers of patients studied during the acute phase of the thrombosis as well as the lack of appropriate diseased controls. We have studied tissue-type plasminogen activator (t-PA) and its inhibitor (PAI-1), and d-dimer levels in BS patients with and without thrombosis both in the acute and chronic phases along with suitable diseased and healthy controls. METHODS: t-PA and PAI-1 were studied by ELISA and d-dimer by semiquantitative latex agglutination slide test in 30 BS patients without deep vein thrombosis (DVT), 10 BS with acute DVT (ADVT), 25 BS with chronic DVT, 27 with ankylosing spondylitis, 26 diffuse systemic sclerosis, 15 patients with ADVT due to other causes, 10 patients with sepsis, and 23 healthy controls. RESULTS: The t-PA levels in BS with ADVT were significantly lower than those in patients with ADVT due to other causes (7.4 +/- 6.2 vs. 13.4 +/- 6.3, P = 0.027) while PAI-1 levels did not show significant differences between the groups (P = 0.60). The numbers of patients with d-dimer levels of > or = 0.5 microg/ml in BS with ADVT were similar to those found in patients with ADVT due to other causes (9/10 vs. 14/14). CONCLUSION: The relatively low t-PA levels point to a defect in fibrinolysis in BS. d-dimer levels are increased in the acute phase of thrombosis in BS.

Fever of unknown origin: a review of 20 patients with adult-onset Still's disease.

In this study we aimed to investigate the findings in patients with adult-onset Still's disease (AOSD) admitted with fever of unknown origin (FUO) during the last 18 years in our unit, in order to discover the ratio of such patients to all patients with FUO during the same period, and to determine the clinical features of AOSD in FUO. The number and the aetiologies of the patients with FUO diagnosed between 1984 and 2001, and the clinical features of those with AOSD, were taken from the patient files. The diagnosis of AOSD was reanalysed according to the diagnostic criteria of Cush et al. [11]. The presumed diagnoses before a diagnosis of AOSD was established were also noted. The chi(2) and Fisher's exact tests were used for statistical analysis. We studied 130 patients with a diagnosis of FUO, 36 (28%) of whom had collagen vascular diseases. Of these 36 patients, 20 (56%, 12 female, 8 male, mean age 34 years, range 16-65) had AOSD. Clinical and laboratory findings were as follows: fever (100%), arthralgia (90%), rash (85%), sore throat (75%), arthritis (65%), myalgia (60%), splenomegaly (40%), hepatomegaly (25%), lymphadenopathy (15%), anaemia (65%), neutrophilic leukocytosis (90%), increased erythrocyte sedimentation rate (100%), elevated transaminase levels (65%), a negative RF (100%), and a negative FANA (80%). Antibiotics had been prescribed in 18 (90%) of cases. The presumed infectious diagnoses were streptococcal tonsillitis/pharyngitis (50%), infective endocarditis (four patients), sepsis (two patients) and acute bacterial meningitis (two patients). The presumed non-infectious diagnoses were acute rheumatic fever (three patients), seronegative rheumatoid arthritis (two patients) and polymyositis (two patients). Sixteen patients were followed for a mean duration of 30 months (range 2-59). A remission was obtained with indomethacin in three cases (19%), and with prednisolone in the remainder. Relapse was detected in three cases (19%). AOSD is one of the most frequent aetiologies of FUO. During the diagnostic course of a patient with FUO, a maculopapular rash and/or arthralgia and/or sore throat should raise the suspicion of AOSD. Because the disease has heterogeneous clinical findings, certain bacterial infections (e.g. streptococcal pharyngitis and sepsis) are generally considered and the prescribing of antibiotics is common.

Spontaneous pneumothorax: a rare complication of miliary tuberculosis.

Pneumothorax is a rare complication of miliary tuberculosis. In this report, a 25-year old patient developing pneumothorax while on the treatment for miliary tuberculosis treatment is presented and the related literature has been reviewed. Pneumothorax, although rare, should be considered when a patient with miliary tuberculosis develops a sudden, severe pain on either side of the chest with breathlessness. The treatment should be tailored according to the size of pneumothorax either pleural drainage through chest tube or needle aspiration. Meanwhile, antituberculous treatment should be continued without interruption.

Tuberculous lymphadenopathy in adults: a review of 35 cases.

We retrospectively reviewed clinical, diagnostic, therapeutic and prognostic features of 35 patients (25 female, 10 male, mean age: 33 years, range: 16-70) with tuberculous lymphadenopathy (TB LAP) which had been followed since 1980. The diagnosis was established by tissue sampling in 32 cases (caseating granulomatous adenitis in 89%) or presence of acid-fast bacilli (AFB) in the aspirate in 2 cases and in the drainage in 1 case. Paraffin-embedded granulomatous tissues were stained by Ehrlich-Ziehl-Neelsen (EZN) and also Mycobacterium tuberculosis DNA was studied by polymerase chain reaction (PCR) (n = 21). The patients were admitted with enlarging LAP (34%), draining LAP (9%), and both systemic complaints and enlarging LAP (57%). Cervical lymph nodes were the most frequently involved site (77%). Pathologic findings on chest X-ray were seen in 23%. Erythrocyte sedimentation rate (ESR) was higher than 100 mm/hour in 25% and associated with systemic complaints. Tuberculin skin test was positive in 91%. AFB could not be seen in any granulomatous tissue (n: 21), but PCR study was positive in 33% (7/21). All patients were given anti-TB treatment (INH,RMP,EMB and/or PZA). Surgical excision of draining LAP with surrounding inflammatory tissues in addition to the medical treatment was needed in 2 cases. Clinical improvement was obtained within 3 months of the treatment and ESR returned to normal within 5 months. After completion of the treatment, 22 patients were followed-up; mean duration was 3 years, and none relapsed. In conclusion, a patient with TB LAP generally presents with a few small, painless, cervical lymph nodes, which are slowly enlarging. For exact diagnosis, excisional biopsy for histologic and microbiologic studies is essential. Use of anti-TB drugs is the main therapeutic option.

A rare complication of miliary tuberculosis: intestinal perforation.

Small bowel perforation is a rare complication of miliary tuberculosis. We report the case of a 21-year old patient who developed a small bowel perforation 70 days after the initiation of adequate tuberculosis treatment. We also present a review of the literature.

Polymorphisms of HLA-DP are associated with response to peginterferon in Caucasian patients with chronic hepatitis B.

BACKGROUND: Polymorphisms of the HLA-DP gene are associated with the natural clearance of the hepatitis B virus in Asian patients. AIM: To investigate the association of HLA-DP polymorphisms with response to peginterferon (PEG-IFN) in Caucasian chronic hepatitis B (CHB) patients. METHODS: We studied 262 Caucasian chronic hepatitis B patients infected with HBV genotype A or D, treated with PEG-IFN for 1 year in two randomised controlled trials (HBV 99-01 and PARC study). Response was defined as an HBV DNA <2000 IU/mL at 6 months post-treatment. Variations at HLA-DPA1 and HLA-DPB1 were genotyped. RESULTS: Of the 262 patients, 58% was HBeAg-positive and HBV genotype A and D was observed in 32% and 68%, respectively. At 6 months post-treatment, 57 (22%) patients had achieved an HBV DNA <2000 IU/mL. HLA-DPB1 was independently associated with virological response [adjusted odds ratio (OR) 1.8, 95% confidence interval (CI):1.1-3.0, P = 0.025], and with an undetectable HBV DNA (adjusted OR 2.4 95% CI: 1.2-4.7, P = 0.015) when adjusted for HBeAg status and other known response modifiers. In HBeAg-positive patients, combined HBeAg seroconversion with HBV DNA <2000 IU/mL was increasingly observed with each addition of an HLA-DPB1 G-allele (adjusted OR 2.7, 95% CI: 1.2-5.9, P = 0.012). Furthermore, HLA-DPA1 and HLA-DPB1 haplotype block GG showed comparable results for virological and combined response. CONCLUSION: In this large cohort of Caucasian chronic hepatitis B patients infected with HBV genotypes A or D, polymorphisms of HLA-DP are independently associated with both virological and serological response to PEG-IFN therapy at 6 months post-treatment.

Pelvic and retroperitoneal hydatid cysts superinfected with Brucella sp. and review of infected hydatid cysts.

Hydatid disease is a zoonotic infection resulting from the tissue infestation of the larval stage of the parasite Echinococcus granulosus. Hydatid cysts superinfected with pyogenic organisms have been reported previously. Brucellosis is more prevalent in people with close contact to animals and those consuming fresh milk or fresh milk products. Although these two disorders have some similar epidemiological features, we did not encounter any hydatid cyst cases superinfected with Brucella species (sp.) in a search of medical literature (Pubmed). Here, we present a case of hydatid cyst disease superinfected with Brucella and review the literature on other hydatid cyst cases superinfected with pyogenic organisms. We conclude that in regions where brucellosis and hydatid cysts are endemic, cysts may be infected with Brucella sp.

Coexistence of blaOXA-48 and aac(6')-Ib-cr genes in Klebsiella pneumoniae isolates from Istanbul, Turkey.

This study evaluated the presence of carbapenem hydrolysing ß-lactamase genes and plasmid-mediated quinolone resistance (PMQR) determinants in 22 Klebsiella pneumoniae isolates collected from the Istanbul Medical Faculty, Turkey, which reduced the susceptibility or resistance to carbapenem. The VITEK(®) 2 system and E-tests were used to determine the minimum inhibitory concentrations needed to inhibit bacterial growth. Genes were screened by polymerase chain reaction, and gene transferability was evaluated by transconjugation. Strain clonality was investigated by pulsed-field gel electrophoresis (PFGE). All strains were OXA-48 ß-lactamase producers and three (13.6%) were also positive for the aac(6')-Ib-cr gene. Most of the strains harboured other ß-lactamase (bla) genes such as bla(TEM), bla(SHV), bla(CTX-M) and bla(VEB-1). The transconjugants mostly harboured bla(OXA-48) and other ß-lactamases separately. PFGE revealed eight pulsotypes among the isolates. The coexistence of bla(OXA-48) and PMQR in K. pneumoniae isolates may present a significant threat to health, especially in the nosocomial setting.

MEMS-based high speed scanning probe microscopy.

The high speed performance of a scanning probe microscope (SPM) is improved if a microelectromechanical systems (MEMS) device is employed for the out-of-plane scanning motion. We have carried out experiments with MEMS high-speed z-scanners (189 kHz fundamental resonance frequency) in both atomic force microscope and scanning tunneling microscope modes. The experiments show that with the current MEMS z-scanner, lateral tip speeds of 5 mm/s can be achieved with full feedback on surfaces with significant roughness. The improvement in scan speed, obtained with MEMS scanners, increases the possibilities for SPM observations of dynamic processes. Even higher speed MEMS scanners with fundamental resonance frequencies in excess of a megahertz are currently under development.