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Abstract Background Hydroxychloroquine and chloroquine have been used for hospitalized coronavirus disease 2019 patients because of their antiviral and anti-inflammatory function. However, little research has been published on the impact of the immunomodulatory effect of (hydroxy)chloroquine on humoral immunity. Case presentation We report a case of symptomatic severe acute respiratory syndrome coronavirus 2 reinfection, diagnosed 141 days after the first episode, in a 56-year-old man of Black African origin treated with hydroxychloroquine for lupus erythematosus. No anti-severe acute respiratory syndrome coronavirus 2 IgG antibodies could be detected 127 days after the initial episode of coronavirus disease 2019. Conclusions The treatment with hydroxychloroquine probably explains the decreased immune response with negative serology and subsequent reinfection in our patient. As humoral immunity is crucial to fight a severe acute respiratory syndrome coronavirus 2 infection, the use of (hydroxy)chloroquine is likely to have a detrimental effect on the spread of the virus. This case emphasizes that more needs to be learned about the role of antibodies in protecting against severe acute respiratory syndrome coronavirus 2 (re)infection and the role of (hydroxy)chloroquine on humoral immunity.

Abstract Background Carbapenemase-producing Enterobacteriaceae (CPE) are emerging pathogens that represent a major public health threat. In the University Hospital of Brussels, the incidence of new patients with CPE rose from 1 case in 2010 to 35 cases in 2015. Between January and August 2015, five patients became infected/colonized with CPE during their stay in the same room in the intensive care unit (ICU). Since the time period between those patients was relatively short and the strains belonged to different species with different antibiograms and mechanisms of resistance, the hypothesis was that the environment could be a possible source of transmission. Methods and results Environmental samples suggested that a contaminated sink was the source of the outbreak. Besides other strains, Citrobacter freundii type OXA-48 was frequently isolated from patients and sinks. To investigate the phylogenetic relationschip between those strains, pulsed-field gel electrophoresis was performed. The strains isolated from patients and the sink in the implicated room were highly related and pointed to sink-to-patient transmission. In total, 7 of 8 sinks in the isolation rooms of the ICU were found to be CPE contaminated. To control the outbreak, the sinks and their plumbings were replaced by new ones with another structure, they were flushed every morning with a glucoprotamin solution and routines regarding sink practices were improved leading to discontinuation of the outbreak. Conclusions This outbreak highlights that hospital sink drains can accumulate strains with resistance genes and become a potential source of CPE.