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Reports conflict on how HIV infection influences the clinical course of COVID-19. The New York City (NYC) public hospital system provides care for over 14,000 people with HIV, was central in responding to the COVID-19 pandemic, and is therefore in a unique position to evaluate the intersection of these concurrent infections. Retrospective chart review of patients presenting to NYC Health and Hospitals (NYC H+H) diagnosed with COVID-19 infection from March 1, 2020, through April 28, 2020, compared people living with HIV (PLWH) and a propensity-matched (PM) control group of patients without HIV to evaluate associations between HIV status and COVID-19 outcomes. Two hundred thirty-four PLWH presented for COVID-19 testing and 110 (47%) were diagnosed with COVID-19. Among 17,413 patients with COVID-19 and without HIV, 1:n nearest neighbor propensity score matching identified 194 patients matched on age, sex, race, and any comorbidity. In the sample with COVID-19 (N = 304), PLWH (9.1%) had lower rates of mortality than controls [19.1%; PM odds ratio (PM-OR): 0.41, 95% confidence interval (CI): 0.19–0.86]. Among hospitalized COVID-19 patients (N = 179), HIV infection was associated with lower rates of mechanical ventilation (PM-OR: 0.31, 95% CI: 0.11–0.84) and mortality (PM-OR: 0.40, 95% CI: 0. 17–0.95). In the extended pandemic period through April 2021, aggregate data by HIV status suggested elevated hospitalization and mortality rates in PLWH versus people without HIV. These results suggest that the direct biological impacts of the HIV virus do not negatively influence COVID-19-related outcomes when controlling for comorbidity and demographic variables. [ABSTRACT FROM AUTHOR]

Objectives: The study objective was to examine the epidemiological trends of KPC-producing Klebsiella pneumoniae in New York City medical centres.Patients and Methods: Single patient isolates of K. pneumoniae were collected from nine medical centres in New York City during a 3 month period from 2013 to 2014. Isolates were tested for the presence of blaKPC. Results were compared with similar surveillance studies conducted in 2006 and 2009. Infection control data, including utilization of medical devices, were analysed at a subset of hospitals.Results: There was a progressive decline in the percentage of K. pneumoniae harbouring blaKPC from 2006 to 2013-14. For the nine hospitals that participated in all three surveillance studies, the percentages of isolates with blaKPC fell from 36% in 2006 to 25% in 2009 to 13% in 2013-14. Seven of the nine hospitals had marked declines in isolates with blaKPC, while two hospitals continued to struggle with this pathogen. These two hospitals were smaller and had longer lengths of patient stay. Device utilization rates were obtained from two hospitals that successfully controlled the spread of KPC-producing K. pneumoniae; both had ∼20%-25% reduction in the usage of urinary catheters. Changes in antibiotic usage at one hospital could not explain the decline in these pathogens.Conclusions: Over the past decade there has been a steady decline in KPC-producing K. pneumoniae in most New York City hospitals. The reason for the decline is probably multifactorial, involving a reduction in device (catheter) utilization and possibly an improvement in infection control practices. [ABSTRACT FROM AUTHOR]

A carbapenem-resistant isolate of Escherichia coli was identified that possessed a 23-kb plasmid encoding Klebsiella pneumoniae carbapenemase type 2 (KPC-2). A subsequent surveillance study involving hospitals in Brooklyn, New York, revealed that, among 1417 E. coli isolates, 7 isolates (from 3 hospitals) possessed blaKPC-2. E. coli possessing KPC-2 is emerging in our region, and improved methods for detection are urgently needed. [ABSTRACT FROM AUTHOR]

Nineteen isolates of carbapenem-resistant Klebsiella species were recovered from 7 hospitals in New York City. Most K. pneumoniae belonged to a single ribotype. Nucleotide sequencing identified KPC-2, a carbapenem- hydrolyzing β-lactamase. In 3 strains, TEM-30, an inhibitor-resistant β-lactamase, was detected. Carbapenem- resistant Klebsiella species possessing KPC-2 are endemic in New York City. This study documents the identification of an inhibitor-resistant TEM β-lactamase in the United States. [ABSTRACT FROM AUTHOR]

Studies the molecular epidemiology and mechanisms of carbapenem resistance in the bacteria acinetobacter baumannii endemic in New York City, New York. Analysis of the bacterial strains using genetic fingerprinting; Variation in expression of penicillin-binding proteins in strains

Examines the resistance rates and epidemiology of Streptococcus pneumoniae in Brooklyn, New York City. Rates of antibiotic susceptibility of Streptococcus pneumoniae isolates; Percentage of isolates susceptible to penicillin; Examination of penicillin-susceptibility rates in Brooklyn neighborhoods.

Objectives Nosocomial isolates of Klebsiella pneumoniae resistant to all commonly used antimicrobial agents have emerged in many regions of the world. It is unknown if efflux systems contribute to the multidrug resistance phenotype. Methods The expression of genes encoding the efflux pump AcrAB and the global regulators MarA, SoxS and RamA were examined and correlated with antimicrobial resistance. Results Twenty isolates belonged to the two important clones representing KPC-possessing strains endemic to our region. Virtually all of these isolates had negligible or absent expression of the genes, and resistance to fluoroquinolones and aminoglycosides could be explained by alternative mechanisms. All of these isolates were susceptible to tigecycline. A group of 14 heterogeneous isolates was also examined. There was a correlation between expression of marA with expression of soxS. Only expression of soxS was significantly correlated with expression of acrB. With a background substitution in GyrA, increased expression of acrB and marA appeared to contribute to fluoroquinolone resistance in some isolates. A correlation was noted between expression of soxS and ramA (but not marA and acrB) and tigecycline MICs. Following in vitro exposure to tigecycline, resistance occurred in association with a marked increase in marA and acrB expression in isolates lacking expression of soxS and ramA. Conclusions While laboratory-derived tigecycline resistance was associated with increased acrB expression, the variation in tigecycline MICs in clinical isolates was associated only with selected regulator genes. It appears that other mechanisms beyond activation of the acrAB system mediate tigecycline resistance. [ABSTRACT FROM AUTHOR]