In our study, the nosocomial infection rate in the ICU was noted to be higher among COVID-19 patients compared to non-COVID-19 patients; however, it was not statistically significant. COVID-19 patients seem to be more predisposed to catheter-associated urinary tract infection (CAUTI) potentially due to longer duration of indwelling urinary catheter-days despite a higher proportion of non-COVID-19 patients having urinary catheters. Moreover, our study also reflected a relatively low ICU nosocomial infection (8.5%) compared to other studies [2, 3, 10, 11], which ranges from 7.2 to 46% co-infection in critically ill COVID-19 patients. Nosocomial infections in critically ill COVID-19 patients are also known to have poorer mortality, often requiring intensive care [2, 3, 10, 11]. However, our study was unable to show the rate of mortality amongst patients with secondary infection.
Additionally, on top of having invasive devices, critically ill COVID-19 patients may have increased susceptibility to nosocomial infections due to lymphopenia and reduced immune functions . Studies have observed lymphopenia present in COVID-19 patients, which was also reflected in our preliminary observations in our first few COVID-19 cases in Singapore [5, 12]. Additionally, steroids was not part of standard treatment for acute respiratory distress syndrome in our COVID-19 patients. Furthermore, the COVID-19 virus evades the immune system through the inhibition of interferon type I recognition and signalling, prevents recognition of antigen-presenting plasma and myeloid dendritic cells , and undermines lymphocytic activation , possibly increasing the hazard for COVID-19 patients to acquire nosocomial infections. However, further studies are warranted to determine if lymphopenia and paresis of other components of the immune response plays a part in nosocomial infections in COVID-19.
Furthermore, the relatively stable nosocomial infection rate in non-COVID-19 patients during the study could also be attributed to heightened infection prevention and control practices during the COVID-19 outbreak. Enhanced precautions, such as improved hand hygiene practices decreases the transmission of nosocomial infections between patients in the ICU. However, changes in care practices such as minimizing contact with suspected or confirmed COVID-19 patients and rostering of available manpower could possibly affect nosocomial infection rates, such as CAUTI in COVID-19 patients as opposed to non-COVID-19 patients. All ICUs in TTSH and NCID are also protocolled to nurse patients in the semirecumbent position unless contraindicated, which reduces the risks of PVAP infection in both patients’ group. Additionally, COVID-19 patients were placed in prone position when medically required. Thus, longer length of stay, use of invasive devices, and reduced immune functions could be potential reasons which resulted in a higher nosocomial infection rate in COVID-19 patients compared to non-COVID-19 patients [7, 14].
Our study has several limitations. First, the small number of nosocomial infections makes it difficult to analyse the risk factors for nosocomial infections and include device-days into our model. Second, we did not audit the adherence to process measures that were in place to prevent nosocomial infections. Hence, we were unable to identify the reasons for CAUTI being the main device-associated infection in COVID-19 patients.
In conclusion, although the incidence of nosocomial infection was not significantly affected by COVID-19 in our centre, continued vigilance to ensure adherence to IPC measures is needed.