Oral lesions in patients with SARS-CoV-2 infection: could the oral cavity be a target organ?

Several viruses transmitted through saliva, such as herpes simplex virus, cytomegalovirus, and Zika virus, are capable of infecting and replicating in the oral mucosa, leading to painful oral ulcers. Few studies have described the oral manifestations of coronavirus disease 2019 (COVID-19). There is growing evidence that angiotensin-converting enzyme 2 (ACE2), the main host cell receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is highly expressed on the epithelial cells of the tongue and of the salivary glands, which may explain the development of dysgeusia in patients with COVID-19. Hence, it is important to understand if SARS-CoV-2 can infect and replicate in oral keratinocytes and fibroblasts, causing oral ulcerations and superficial necrosis. Here, we report a series of 8 cases of COVID-19 infection, with oral necrotic ulcers and aphthous-like ulcerations which developed early in the course of disease after the development of dysgeusia and affected the tongue, lips, palate, and oropharynx. A short review of the literature regarding the important role of ACE2 in SARS-CoV-2 cellular entry is also provided, bringing new insights into oral keratinocytes and minor salivary glands as potential targets.

Alternative drugs against multiresistant Gram-negative bacteria.

OBJECTIVES: Enterobacterales and other non-fermenting Gram-negative bacteria have become a threat worldwide owing to the frequency of multidrug resistance in these pathogens. On the other hand, efficacious therapeutic options are quickly diminishing. The aims of this study were to describe the susceptibility of 50 multiresistant Gram-negative bacteria, mostly pan-resistant, against old and less-used antimicrobial drugs and to investigate the presence of antimicrobial resistance genes. METHODS: A total of 50 genetically distinct isolates were included in this study, including 14 Acinetobacter baumannii (belonging to ST79, ST317, ST835 and ST836), 1 Pseudomonas aeruginosa (ST245), 8 Serratia marcescens and 27 Klebsiella pneumoniae (belonging to ST11, ST340, ST258, ST16, ST23, ST25, ST101, ST234, ST437 and ST442). The isolates were submitted to antimicrobial susceptibility testing and whole-genome sequencing to evaluate lineages and resistance genes. RESULTS: Our results showed that some strains harboured carbapenemase genes, e.g. blaKPC-2 (28/50; 56%) and blaOXA-23 (11/50; 22%), and other resistance genes encoding aminoglycoside-modifying enzymes (49/50; 98%). Susceptibility rates to tigecycline (96%) in all species (except P. aeruginosa), to minocycline (100%) and doxycycline (93%) in A. baumannii, to ceftazidime/avibactam in S. marcescens (100%) and K. pneumoniae (96%), and to fosfomycin in S. marcescens (88%) were high. Chloramphenicol and quinolones (6% susceptibility each) did not perform well, making their use in an empirical scenario unlikely. CONCLUSIONS: This study involving genetically distinct bacteria showed promising results for tigecycline for all Gram-negative bacteria (except P. aeruginosa), and there was good activity of minocycline against A. baumannii, ceftazidime/avibactam against Enterobacterales, and fosfomycin against S. marcescens.

Pseudooutbreak of rapidly growing mycobacteria due to Mycobacterium abscessus subsp bolletii in a digestive and respiratory endoscopy unit caused by the same clone as that of a countrywide outbreak.

BACKGROUND: The nontuberculous mycobacteria (NTM) are widely spread. In Brazil, 2,520 cases of rapidly growing mycobacteria (RGM) infections after medical procedures were reported, with 5.4% of cases related to nonsurgical invasive procedures and with an occurrence of 1 clone (BRA100) of Mycobacterium abscessus subsp bolletii. OBJECTIVE: To describe a pseudooutbreak of M abscessus subsp bolletii in an endoscopy and bronchoscopy unit. METHODS: The alert for a pseudooutbreak was given when 3 patients, in the same week, had a positive bronchoalveolar lavage culture for M abscessus subsp bolletii. The patients had no symptoms/signs of mycobacterial infection; thus, contamination of bronchoscopes was suspected. Samples for culturing were collected from bronchoscopes, digestive endoscopes, automated disinfection machines, and the water supply. Clinical samples were identified by polymerase chain reaction restriction-enzyme analysis (PRA) of the hsp65 gene and their pulsed-field gel electrophoresis pattern was compared with environmental samples. RESULTS: The investigation demonstrated a contamination of bronchoscopes, digestive endoscopes, and disinfection machines. Molecular typing demonstrated that all strains belonged to the same clone (MAB01), identical to clone BRA100. DISCUSSION: Cross-transmission due to poor disinfection as well as resistance to glutaraldehyde may play roles in the spread of MAB01 M abscessus subsp bolletii, which may have a unique resistance to the environment and adaption to human hosts. However the water supply may have played a role. Attention is needed to ensure the quality of water used to rinse disinfected equipment.

Virulence and resistance pattern of a novel sequence type of linezolid-resistant Enterococcus faecium identified by whole-genome sequencing.

Empirical use of linezolid has been advocated in neutropenic febrile patients colonised by vancomycin-resistant enterococci (VRE) because of the risk of bloodstream infection (BSI). This study aimed to genetically describe a vancomycin-resistant Enterococcus faecium (VREfm) BSI isolate resistant to linezolid (VRLRE) in a patient previously colonised by VREfm and to determine the incidence of colonisation and infection by VREfm in a bone marrow transplant unit over a 10-year period. Data for VREfm colonisation and infection were evaluated. PCR for the vanA and vanB genes, pulsed-field gel electrophoresis (PFGE) and microdilution antimicrobial susceptibility testing (vancomycin, teicoplanin, linezolid and aminoglycosides) were performed. Three isolates, including the VRLRE, were selected for whole-genome sequencing by Ion Torrent™, with E. faecium CP006620-Aus0085 used as a reference. Eighty-seven VREfm were analysed; all were linezolid-susceptible and harboured vanA, except for one blood isolate from a febrile neutropenic patient colonised by VREfm who received linezolid for 12 days and developed a BSI by VRLRE (linezolid MIC≥8µg/mL). Linezolid resistance was associated with a G2576T mutation in the 23SrRNA gene. PFGE analysis demonstrated that the 87 isolates belonged to four major clusters; however, the VRLRE presented only 50% similarity. Three sequence types (STs) were identified: ST412 (the predominant clone, which was more virulent compared with the other isolates); ST478 (linezolid-susceptible VREfm); and a novel ST named ST987 (VRLRE). SNP analysis showed a higher similarity between linezolid-susceptible VREfm and the predominant clone compared with VRLRE. VRLRE presented a G2576T mutation and belonged to a novel ST (ST987).

Polyclonal outbreak of bloodstream infections caused by Burkholderia cepacia complex in hematology and bone marrow transplant outpatient units.

AIM: The objective was to describe an outbreak of bloodstream infections by Burkholderia cepacia complex (Bcc) in bone marrow transplant and hematology outpatients. METHODS: On February 15, 2008 a Bcc outbreak was suspected. 24 cases were identified. Demographic and clinical data were evaluated. Environment and healthcare workers' (HCW) hands were cultured. Species were determined and typed. Reinforcement of hand hygiene, central venous catheter (CVC) care, infusion therapy, and maintenance of laminar flow cabinet were undertaken. 16 different HCWs had cared for the CVCs. Multi-dose heparin and saline were prepared on counter common to both units. FINDINGS: 14 patients had B. multivorans (one patient had also B. cenopacia), six non-multivorans Bcc and one did not belong to Bcc. Clone A B. multivorans occurred in 12 patients (from Hematology); in 10 their CVC had been used on February 11/12. Environmental and HCW cultures were negative. All patients were treated with meropenem, and ceftazidime lock-therapy. Eight patients (30%) were hospitalized. No deaths occurred. After control measures (multidose vial for single patient; CVC lock with ceftazidime; cleaning of laminar flow cabinet; hand hygiene improvement; use of cabinet to store prepared medication), no new cases occurred. CONCLUSIONS: This polyclonal outbreak may be explained by a common source containing multiple species of Bcc, maybe the laminar flow cabinet common to both units. There may have been contamination by B. multivorans (clone A) of multi-dose vials.

POLYCLONAL OUTBREAK OF BLOODSTREAM INFECTIONS CAUSED BY Burkholderia cepacia COMPLEX IN HEMATOLOGY AND BONE MARROW TRANSPLANT OUTPATIENT UNITS / Surto policlonal de infecção de corrente sanguínea causada pelo complexo Burkholderia cepacia em unidades de hospital-dia de hematologia e transplante de medula óssea

Aim: The objective was to describe an outbreak of bloodstream infections by Burkholderia cepacia complex (Bcc) in bone marrow transplant and hematology outpatients. Methods: On February 15, 2008 a Bcc outbreak was suspected. 24 cases were identified. Demographic and clinical data were evaluated. Environment and healthcare workers' (HCW) hands were cultured. Species were determined and typed. Reinforcement of hand hygiene, central venous catheter (CVC) care, infusion therapy, and maintenance of laminar flow cabinet were undertaken. 16 different HCWs had cared for the CVCs. Multi-dose heparin and saline were prepared on counter common to both units. Findings: 14 patients had B. multivorans (one patient had also B. cenopacia), six non-multivorans Bcc and one did not belong to Bcc. Clone A B. multivorans occurred in 12 patients (from Hematology); in 10 their CVC had been used on February 11/12. Environmental and HCW cultures were negative. All patients were treated with meropenem, and ceftazidime lock-therapy. Eight patients (30%) were hospitalized. No deaths occurred. After control measures (multidose vial for single patient; CVC lock with ceftazidime; cleaning of laminar flow cabinet; hand hygiene improvement; use of cabinet to store prepared medication), no new cases occurred. Conclusions: This polyclonal outbreak may be explained by a common source containing multiple species of Bcc, maybe the laminar flow cabinet common to both units. There may have been contamination by B. multivorans (clone A) of multi-dose vials.

O objetivo foi descrever um surto de infecções da corrente sanguínea por complexo B. cepacia (Bcc) nos ambulatórios de hematologia e transplante de medula óssea. Métodos: Em 15/02/2008, um surto de Bcc foi suspeitado. 24 casos foram identificados. Os dados demográficos e clínicos foram avaliados. Mãos de profissionais da saúde e ambiente foram cultivadas. Espécies foram determinadas e tipadas. Reforço da higiene das mãos, cuidados com cateteres, terapia de infusão e manutenção da câmara de fluxo laminar foram realizadas. 16 profissionais de saúde (PS) diferentes manipularam os cateteres. Heparina multidoses e soro eram preparadas em um balcão comum a ambas as unidades. Resultados: 14 pacientes tiveram B. multivorans (um paciente teve também B. cenopacia), 6 Bcc não-multivorans e um teve um agente não pertencente a Bcc. Clone A de B. multivorans ocorreu em 12 pacientes (da Hematologia), em 10 o cateter havia sido utilizado nos dias 11 ou 12 de fevereiro. Culturas ambientais e de PS foram negativos. Todos os pacientes foram tratados com meropenem e selo de ceftazidima. Oito pacientes (30%) foram hospitalizados. Não ocorreram mortes. Após as medidas de controle, nenhum novo caso ocorreu. Conclusões: Este surto policlonal pode ser explicado por uma fonte comum contendo várias espécies de Bcc, talvez a câmara de fluxo laminar comum a ambas as unidades. Pode ter havido contaminação por B. multivorans (clone A) de frascos multi-dose.