A pandemic within a pandemic? Admission to COVID-19 wards in hospitals is associated with increased prevalence of antimicrobial resistance in two African settings.

BACKGROUND: Patients who develop severe illness due to COVID-19 are more likely to be admitted to hospital and acquire bacterial co-infections, therefore the WHO recommends empiric treatment with antibiotics. Few reports have addressed the impact of COVID-19 management on emergence of nosocomial antimicrobial resistance (AMR) in resource constrained settings. This study aimed to ascertain whether being admitted to a COVID-19 ward (with COVID-19 infection) compared to a non-COVID-19 ward (as a COVID-19 negative patient) was associated with a change in the prevalence of bacterial hospital acquired infection (HAI) species or resistance patterns, and whether there were differences in antimicrobial stewardship (AMS) and infection prevention and control (IPC) guidelines between COVID-19 and non-COVID-19 wards. The study was conducted in Sudan and Zambia, two resource constrained settings with differing country-wide responses to COVID-19. METHODS: Patients suspected of having hospital acquired infections were recruited from COVID-19 wards and non-COVID-19 wards. Bacteria were isolated from clinical samples using culture and molecular methods and species identified. Phenotypic and genotypic resistance patterns were determined by antibiotic disc diffusion and whole genome sequencing. Infection prevention and control guidelines were analysed for COVID-19 and non-COVID-19 wards to identify potential differences. RESULTS: 109 and 66 isolates were collected from Sudan and Zambia respectively. Phenotypic testing revealed significantly more multi-drug resistant isolates on COVID-19 wards in both countries (Sudan p = 0.0087, Zambia p = 0.0154). The total number of patients with hospital acquired infections (both susceptible and resistant) increased significantly on COVID-19 wards in Sudan, but the opposite was observed in Zambia (both p = ≤ 0.0001). Genotypic analysis showed significantly more ß-lactam genes per isolate on COVID-19 wards (Sudan p = 0.0192, Zambia p = ≤ 0.0001). CONCLUSIONS: Changes in hospital acquired infections and AMR patterns were seen in COVID-19 patients on COVID-19 wards compared to COVID-19 negative patients on non-COVID-19 wards in Sudan and Zambia. These are likely due to a potentially complex combination of causes, including patient factors, but differing emphases on infection prevention and control, and antimicrobial stewardship policies on COVID-19 wards were highlighted.

Detection of carbapenemases blaOXA48-blaKPC-blaNDM-blaVIM and extended-spectrum-ß-lactamase blaOXA1-blaSHV-blaTEM genes in Gram-negative bacterial isolates from ICU burns patients.

BACKGROUND AND OBJECTIVES: Burn patients are highly susceptible to invasion by multidrug-resistant Gram-negative bacteria (MDR-GNB) through post-burn damage. The prevalence of MDR-GNB isolated from burns patients has increased dramatically in the last decade, representing a serious risk to patients admitted to burns units worldwide. The challenges of managing infected burns patients are exacerbated in poor resource settings. This study was designed to develop a pathway for the rapid diagnosis of multidrug-resistant (MDR) Gram-negative infections and identify the bacterial genes including blaOXA1, blaTEM, and blaSHV encoding ESBLs and blaOXA48, blaKPC, blaNDM, and blaVIM encoding carbapenemases from the patient of post burns infection.  METHODS: Clinical isolates were collected (August 2017 to August 2018) from Intensive care unit (ICU) of Burn Centre. Antibiotic susceptibility testing and phenotypic detection of ESBLs and carbapenemases was performed by disk diffusion, double disk synergy test (DDST), combination disk test (CDT), and Imipenem + EDTA combined disk test (IMP + EDTA CDT). Polymerase chain reaction (PCR) detection was performed for ESBLs blaOXA1-blaSHV-blaTEM and carbapenemases genes blaOXA48-blaKPC-blaNDM-blaVIM RESULTS: In total, of 170 Gram-negative isolates, 104 (61.2%) were confirmed as multidrug-resistant (MDR); Pseudomonas aeruginosa was found to be the most prevalent 43/104 (41.4%), followed by Klebsiella pneumoniae 17/104 (16.4%), Acinetobacter baumannii12/104 (11.5%), and 6/104 Proteus mirabilis (5.8%). All isolates (100%) were resistant to cefotaxime and ceftazidime, while the meropenem resistance was 58.7%. ESBL and carbapenemase genotypes were found to be associated with higher MAR index (0.65-0.88) and MIC (> 32 µg/ml) values P. aeruginosa was the major ESBL and carbapenemase producer as determined by phenotypic testing and PCR. blaTEM positive isolates among ESBLs producers were predominant 81.8% (27/33), followed by 27.3% blaOXA1 and blaSHV, respectively. blaVIM positive isolates among carbapenemase producers were predominant 47.7% (21/44), followed by 27.3% blaKPC, 20.5% blaOXA48, and 11.4% blaNDM positive isolates. CONCLUSIONS: The predominant organism causing burn infections was ESBL and carbapenemase-producing Pseudomonas aeruginosa. There are only limited effective antibiotics against such strains. blaVIM and blaTEM individually and in co-existence with blaKPC, blaOXA48, blaSHV, and blaOXA1 confer antimicrobial resistance in burns patients. Rapid detection of ESBL and carbapenemase genes will inform treatment strategies improving the outcome for post-burn patients in ICU.

Verona integron-encoded metallo-Beta-lactamase (VIM) and Vietnam extended-spectrum Beta-lactamase (VEB) producing pseudomonas balearica from a clinical specimen.

Pseudomonas balearica, a saprophyte found in marshy and marine habitats, is not routinely differentiated from P. aeruginosa and P. stutzeri using automated systems and hence has not been reported from clinical samples. This study describes the identification of P. balearica using MALDI-TOF-MS and 16S rDNA sequence from a patient admitted to an intensive care unit (I.C.U.). The isolate was found to be Verona integron-mediated Metallo-b-lactamase (V.I.M.), and Vietnam extended-spectrum b-lactamase (V.E.B.) producer and resistant to Ceftriaxone, Imipenem, and Tobramycin. P. balearica can be a source for horizontal transfer of blaVEB and blaVIM. Its pathogenesis has yet to be understood.

A case of NDM-carbapenemase-producing hypervirulent Klebsiella pneumoniae sequence type 23 from the UK.

INTRODUCTION: Hypervirulent capsular type K1 Klebsiella pneumoniae strains of clonal complex 23 (CC23) are associated with severe community-acquired pyogenic liver abscesses, often complicated by metastatic infections and significant mortality. The majority of hypervirulent strains reported are susceptible to most antibiotics except ampicillin. To the best of our knowledge, this is the first case of New Delhi metallo-ß-lactamase (bla NDM)-producing hypervirulent K. pneumoniae from the UK. CASE PRESENTATION: We present a case of pyogenic liver abscess in a 63-year-old female of Bangladeshi origin, with a recent diagnosis of pancreatic cancer. The patient was treated with piperacillin/tazobactam and blood cultures grew a fully susceptible Escherichia coli. Despite antimicrobial therapy and drainage of the abscess, the patient continued to deteriorate and died on day seven of admission. The fluid drained from the liver abscess grew a fully susceptible E. coli and a multi-drug-resistant K. pneumoniae. Two weeks prior to admission, a rectal screening swab grew a metallo-ß-lactamase-producing K. pneumoniae. Molecular characterization revealed that both the K. pneumoniae isolates belonged to the hypervirulent K1 cluster of CC23, sequence type 23. The isolate from the rectal screen was positive for the bla NDM metallo-ß-lactamase gene. CONCLUSION: The emergence of carbapenemase-producing hypervirulent K. pneumoniae strains presents a new and significant threat to global public health. Management of these infections will be extremely challenging due to the limited treatment options available and they are likely to be associated with an even greater mortality.

Detection of carbapenemases, AmpC and ESBL genes in Acinetobacter isolates from ICUs by DNA microarray.

The accumulation of multiple inherent and acquired resistance mechanisms in Acinetobacter spp. results in emergence of "pandrug resistant" strains which is one of the major concerns in healthcare sectors worldwide. Surveillance of the carbapenemase/ extended-spectrum ß-lactamases (ESBLs) genes in A. baumannii by phenotypic methods is challenging especially in developing countries, like Pakistan. In this context, a novel microarray (CT 103XL Check-MDR) assay was used for simultaneous detection of genes encoding clinically important carbapenemases and ESBLs. The results were compared with the phenotypic methods including MHT, Rapidec Carba NP, EDTA+DDST and Rosco (KPC/MBL). The results of the microarray were also confirmed by PCR. All of the strains of A. baumannii (47) were resistant to imipenem and meropenem. Microarray and PCR results showed presence of OXA-23 in all the isolates of A. baumannii while 36.17% also harbored PER. Rosco kit test showed 100% sensitivity to detect carbapenemases but exhibited low specificity to classify them. Rapidec Carba NP test has 100% sensitivity and specificity to detect the carbapenemases when compared with microarray. Sensitivity and specificity of microarray assay were 100% for bla-genes in comparison to PCR. This reveals that Check-MDR CT103 XL assay is an accurate method for the identification of ESBLs and carbapenemase genes in A. baumannii in comparison to the other methods.

Bacteremia in a human caused by an XDR strain of Pseudomonas fulva.

This is the first report from Pakistan of a case of bacteremia in a human due to P. fulva, an opportunistic infection with increased risk of a drug resistant phenotype. P. fulva was isolated from blood of a 45 years male admitted in surgical ICU. Isolate was identified by the MALDI-TOF-MS and was extensively drug resistant (XDR) strain. Isolate was found negative for metallo ß lactamase (MBL) and extended spectrum ß lactamase (ESBL) types by phenotypic and polymerase chain reaction (PCR) assays. It was concluded that P. fulva is an emerging opportunistic pathogen.