Identification of vancomycin-resistant enterococci clones and inter-hospital spread during an outbreak in Taiwan.

BACKGROUND: In 2003, nosocomial infections caused by vancomycin-resistant enterococci (VRE) occurred rarely in Taiwan. Between 2003 and 2010, however, the average prevalence of vancomycin resistance among enterococci spp. increased from 2% to 16% in community hospitals and from 3% to 21% in medical centers of Taiwan. We used molecular methods to investigate the epidemiology of VRE in a tertiary teaching hospital in Taiwan. METHODS: Between February 2009 and February 2011, rectal samples and infection site specimens were collected from all inpatients in the nephrology ward after patient consent was obtained. VRE strain types were determined by pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST). RESULTS: A total of 59 vanA gene-containing VRE isolates (1 per patient) were obtained; 24 originated from rectal sample surveillance of patients who exhibited no symptoms (22 Enterococcus faecium and 2 Enterococcus faecalis), and 35 had developed infections over 3 days after admission (32 E. faecium, 2 E. faecalis, and 1 Enterococcus durans). The 59 VRE isolates demonstrated vancomycin minimum inhibitory concentrations (MICs) of ≥256 µg/m. The MIC range for linezolid, tigecycline, and daptomycin was 0.25-1.5 µg/mL, 0.032-0.25 and 1-4 µg/mL, respectively. For 56 isolates, the MIC for teicoplanin was >8 µg/mL. The predominant types in the nephrology ward were MLST types 414, 78, and18 as well as PFGE types A, C, and D. CONCLUSION: VREs are endemic in nephrology wards. MLST 414 is the most predominant strain. The increase VRE prevalence is due to cross-transmission of VRE clones ST 414,78,18 by undetected VRE carriers. Because similar VRE STs had been reported in a different hospital of Taiwan, this finding may indicate inter-hospital VRE spread in Taiwan. Active surveillance and effective infection control policies are important controlling the spread of VRE in high risk hospital zones. All endemic VRE strains are resistant to teicoplanin but are sensitive to daptomycin, linezolid, and tigecycline.

Nasopharyngeal microbial profiles associated with the risk of airway allergies in early childhood.

BACKGROUND: Airway microbiota may play an important role in regulating the immune response related to allergic respiratory diseases. A molecular-based approach was used to analyze the association between nasopharyngeal microbiota, serum immunoglobin (Ig)E levels, and childhood respiratory allergies. METHODS: Nasopharyngeal swabs were collected from children aged 36 months with three phenotypes, including allergic respiratory diseases plus atopy, atopy alone, and healthy controls for microbiome analysis using Illumina-based 16S rRNA gene sequencing. RESULTS: In total, 87 children were enrolled, including 36 with allergic respiratory diseases plus atopy, 21 with atopy alone, and 30 healthy controls. Proteobacteria (45.7%), Firmicutes (29.3%), and Actinobacteria (15.3%) were the most prevalent phyla in the study population. Compared with healthy controls, a lower Chao1 index was found in children with allergies (P < 0.035), indicating that bacterial richness was inversely associated with airway allergies. Additionally, in comparison with healthy controls, the genera Acinetobacter, Moraxella, Asaia, and Rhodococcus were more abundant and positively correlated with total serum IgE levels in children with allergies (P < 0.01), whereas the genera Enterococcus and Rickettsia were inversely correlated with total IgE levels, and also appeared to be negatively associated with airway allergies (P < 0.01). CONCLUSIONS: The composition of the nasopharyngeal microbiota alteration may have an influence on childhood respiratory allergies. The inverse association between bacterial richness and allergies postulated that children living in a microbially hygienic environment may increase their risk of developing respiratory allergies.

Community-Associated Methicillin-Resistant Staphylococcus Aureus Colonization in a Birth Cohort of Early Childhood: The Role of Maternal Carriage.

Background: Methicillin-resistant Staphylococcus aureus (MRSA) colonization in infants may pose a risk for subsequent infection in children. The study aimed to determine S. aureus colonization patterns in infancy, and strain relatedness between maternal and infant colonization. Methods: A prospective cohort study was conducted for nasopharyngeal S. aureus detection in neonates at delivery; in children at 1, 6, 12, 24, 36, and 60 months of age; and from mothers immediately after the delivery of their baby and when their child is 1 month old. A questionnaire for infants and mothers was administered at each planned visit. Results: In total, 521 and 135 infant-mother dyads underwent nasopharyngeal swab collection at 1 month and immediately after delivery, respectively. Among the 521 dyads at 1 month of age, concordant S. aureus colonization was found in 95 dyads, including MRSA in 48.4% (46/95). No concordant MRSA carriage was present among the 135 dyads at delivery. The genetic relatedness of concurrent MRSA-colonized dyads showed that more than two-thirds (32/46 [69.6%]) had identical genotypes, mainly ST 59/PVL-negative/SCCmec IV. Infants aged 1 month had the highest incidence of S. aureus, and the trend declined to a nadir at the age of 12 months. Carrier mothers who smoked cigarettes may increase the risk of infant Staphylococcus colonization (odds ratio, 2.12; 95% confidence interval, 1.23-3.66; p < 0.01). Conclusions: Maternal-infant horizontal transmission may be the primary source of MRSA acquisition in early infancy. The avoidance of passive smoking could be recommended for the prevention of S. aureus carriage.

Longitudinal investigation of nasopharyngeal pneumococcal carriage in early childhood: The PATCH birth cohort study.

Streptococcus pneumoniae is a common cause of infectious diseases such as pneumonia and sepsis. Its colonization is thought to be the first step in the development of invasive pneumococcal diseases. This study aimed to investigate pneumococcal colonization patterns in early childhood. A longitudinal birth cohort study was conducted for investigating nasopharyngeal colonized pneumococci at 1, 6, 12, 18, 24, and 36 months of age, particularly focusing on the serotype distribution and antimicrobial susceptibilities. Pneumococcal conjugate vaccine (PCV) effect on nasopharyngeal colonization was also assessed. During 2013-2017, 855 infants were enrolled and a total of 107 isolates were recovered from 95 infants during the first three years of life. In this period, the prevalence of pneumococcal colonization increased, with values ranging from 0.2% (2/834) at 1 month of age to 5.9% (19/323) at 36 months of age. The investigation of serotype revealed that 81.1% (73/90) belonged to the non-PCV13 serotypes-23A, 15A, 15C, and 15B. Moreover, PCV13 serotypes significantly decreased during 2014-2015, when routine PCV13 vaccination was initiated in Taiwan. PCV13 introduction may lead to the reduction in the rates of pneumococcal isolates resistant (R) to penicillin. Under conditional PCV13 vaccination, pneumococcal isolates primarily belonged to non-PCV13 serotypes. This non-PCV13 serotype replacement exhibited lower rates of penicillin R isolates, suggesting that PCV13 administration may reduce the antibiotic-nonsusceptible pneumococcal disease burden and antibiotic use.

Risk factors of mortality and comparative in-vitro efficacy of anidulafungin, caspofungin, and micafungin for candidemia.

BACKGROUND: Although echinocandins have high in vitro antifungal efficacy according to prior reports, comparative studies on the clinical cure rates of anidulafungin, caspofungin, and micafungin in systemic candida infections have not yet been reported. METHODS: Interpretation of clinical and microbiological responses to anidulafungin, caspofungin, and micafungin in 109 cases of candidemia was done according to the published criteria. The clinical cure rates between patients treated with echinocandins and patients treated with fluconazole were also compared. The minimal inhibitory concentrations (MICs) of anidulafungin, caspofungin, micafungin, and fluconazole for these 109 blood isolates of candida were determined with the Clinical and Laboratory Standards Institute M27-A reference microdilution method. Logistic regression with forward selection was used to determine the important factors of prognosis with variables such as age, underlying diseases, acute physiology and chronic health evaluation (APACHE) III score, persistent candidemia, and antimicrobial therapy. RESULTS: Among the 109 cases of candidemia, 70 were treated with echinocandins, azoles, or amphotericin B for ≥7 days. The clinical cure rate of cases treated with antifungal agents adequately (≥7 days) and inadequately (<7 days) were 44/70 (62.9%) and 4/39 (10.2%), respectively, with significant difference (p < 0.0001). Clinical cure rates of anidulafungin, caspofungin, micafungin, and fluconazole were 18/30 (60.0%), 8/9 (88.9%), 5/7 (71.4%), and 9/18 (50%), respectively. The difference in APACHE III score between treatment success and failure cases was significant. The MIC50/MIC90 of anidulafungin, caspofungin, and micafungin for all Candida spp. were 0.03/1 µg/mL, 0.06/0.5 µg/mL, and 0.008/1 µg/mL, respectively. CONCLUSION: Adequate antifungal therapy and APACHE III score are both independent factors affecting the clinical outcome. The clinical cure rate of the echinocandins group was higher than that of the fluconazole group without significant difference. Although caspofungin had the best clinical cure rate in this study, there was no significant difference between the clinical cure rates among these three echinocandins. All Candida spp. were susceptible in vitro to these three echinocandins.

Clinical features and risk factors of mortality for bacteremia due to community-onset healthcare-associated methicillin-resistant S. aureus.

Studies comparing adult community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and community-onset healthcare-associated MRSA (COHCA MRSA bacteremia have not been available. From 1 January 2010 through 30 October 2010, a prospective observational program was conducted among all patients aged >16 years with positive Staphylococcus aureus blood cultures within 48 h after their arrival at the emergency department of our hospital. Clinical course of infection and infection foci of bacteremia were evaluated. Resistance to oxacillin was confirmed with the presence of mecA gene examined by polymerase chain reaction. Presence of TSST-1, PVL gene, SCCmec elements (I-V), mecA gene, and multilocus sequence typing were identified through methods described elsewhere. Univariate and multivariate analysis revealed that chronic renal failure was significantly more common in COHCA-MRSA than in CA-MRSA. In addition, APACHE III score was significantly higher in COHCA-MRSA than in CA-MRSA. Both the 7-day and 30-day mortality rates in COHCA-MRSA, 14.6% (7/48) and 29.2% (14/48), respectively, were higher than those in CA-MRSA without a significant difference. SCCmec II was more common in COHCA-MRSA, but SCCmecVT was more common in CA-MRSA. The majority of MRSA isolates belonged to ST59, ST239, and ST5. ST59 was significantly more common in CA-MRSA, while ST239 was nearly equally common in both CA-MRSA and COHCA-MRSA. SCCmec III and II isolates were the first and second most resistant to the antibiotics commonly used for S. aureus, whereas SCCmecVT isolates were the most susceptible to these antibiotics. We conclude that, although both CA-MRSA and COHCA-MRSA bacteremia had community onset, these 2 MRSA infections were different in underlying diseases, risk of mortality, SCCmec types, sequence types, and antimicrobial susceptibility. It is more appropriate to understand the MRSA pathogen and clinical features based on etiology and ST types than based on the location of disease onset. CA-MRSA and HCA-MRSA should be differentiated also based on etiology and ST types, in addition to location of acquisition.