Brigham and Women's Hospitals

Infectious Disease

Updated: May 23, 2020

Diagnostics and Infection Control

  1. BWH-specific inpatient COVID-19 testing pathways and infection control guidelines can be found here
  2. Please reference the Diagnostics chapter and Infection Control sections for further details

Infectious Diseases Consultation

  1. The infectious diseases consult teams should be consulted on all inpatients who have been diagnosed with COVID-19

Biothreats

  1. COVID flag or precaution review/removal
  1. Page COVID Flag Management at p39635 (available 7 AM-10 PM; please only page after 10 PM for urgent bed flow issues that require a flag change)
  1. Bed flow questions/problems for inpatients related to COVID-19
  1. Page COVID Nurse Administrator at p39284
  1. Clinical questions about COVID-positive inpatients
  1. Page ID team following the patient
  1. All other COVID-related clinical questions on inpatients
  1. Page COVID Clinical at p39634
  1. Other Infection Control questions
  1. Page Infection Control at p11482 (available 8 AM-8 PM; please only page after 8 PM for emergencies)
  1. Brigham guidelines for inpatient COVID-19 flags, precautions, and bed flow questions
  1. Visit PikeNotes for further information
  1. Outpatient COVID-19 questions
  1. Visit covidambulatory.org or place an Infectious Diseases e-consult

COVID-19 Treatment with Antivirals

  1. A breakdown of the potential therapeutic options for COVID-19 can be found in the Therapeutics chapter.
  2. The BWH Infectious Diseases COVID-19 treatment guidelines can be used to access current BWH protocols based on enrolling clinical trials (Partners login required)

Secondary Infections

  1. Available data on secondary infections in COVID-19 are limited. To date, viral co-infection data suffers from inconsistencies.
  1. One study in San Francisco found ~20% of symptomatic COVID-19 patients were also PCR positive for another pathogen (Kim et al, JAMA, 2020)
  2. In contrast, two studies in San Francisco and Wuhan, China where hospitalized COVID-19 patients tested for influenza and RSV found that none of these patients had evidence of viral co-infection (Myers et al, JAMA, 2020; Chen et al, Lancet, 2020)
  1. The incidence of nosocomial infections are approximately 8% among hospitalized COVID-19 patients.
  1. A meta-analysis of 806 hospitalized COVID-19 patients found 8% developed bacterial and/or fungal infections during admission (Rawson et al, Clin Infect Dis, 2020).
  2. Two smaller cohort studies have reported similar nosocomial infection rates - 8% of 150 hospitalized patients (Ruan et al, Intensive Care Med, 2020) and 13.5% of 52 mechanically ventilated patients (Yang et al, Lancet Resp Med, 2020). In contrast, one study of 339 COVID-19 patients over 60 years of age with severe and critical disease found bacterial secondary infection rates of 42.8% (Wang et al, J Infect, 2020)
  3. The most common reported infections were pneumonia (32%), bacteremia (24%), and urinary tract infections (22%) (He et al, Infect Control Hosp Epidemiol, 2020)
  1. Nosocomial infections are associated with increased COVID-19 severity and death
  1. There is a strong association between nosocomial infection and mortality (He et al, Infect Control Hosp Epidemiol, 2020; Wang et al, J Infect, 2020)
  2. In a pre-print study, patients with severe COVID-19 suffered a higher rate of secondary infection compared to those with non-severe COVID-19 (Zhang et al, unpublished report)
  1. Organisms reported included those commonly seen with hospital-acquired infections
  1. Fungal pathogens such as Candida albicans, Aspergillus species, Pneumocystis jirovecii, and Mucor species have been described in a small subset of patients
  2. Bacterial pathogens include drug-resistant Pseudomonas aeruginosa, Acinetobacter species, extended spectrum beta-lactamase (ESBL) Klebsiella sp. and E.coli, and vancomycin-resistant Enterococcus sp.
  1. Risk factors for secondary bacterial and fungal infections
  1. In a single center study of 65 COVID-19 patients, invasive devices (OR 4.28, 95% CI: 2.47–8.61), diabetes (OR 3.06, 95% CI: 1.41–7.22), and the use of one or more class of antibiotic (OR 1.84, 95% CI: 1.31–4.59) were significant predictors of nosocomial infection (He et al, Infect Control Hosp Epidemiol, 2020
  2. Glucocorticoid treatment (38% in He et al, Infect Control Hosp Epidemiol, 2020) was also found to be positively associated with secondary infection
  3. There is a disproportionate high use of antibiotics despite paucity of evidence for bacterial secondary infection (He et al, Infect Control Hosp Epidemiol, 2020; Zhou et al, Infect Control Hosp Epidemiol, 2020; Rawson et al, Clin Infect Dis, 2020)
  1. Empiric antibiotic and antifungal treatment should not be standard of care
  1. 75% of patients who developed secondary bacterial or fungal infection were already receiving prophylactic antibiotics. This suggests prophylactic agents may not prevent hospital-acquired infections and risk selecting for more drug-resistant pathogens (He et al, Infect Control Hosp Epidemiol, 2020)

Antibiotics

Choice of agent

  1. Clinical reports indicate that rates of bacterial superinfection with COVID-19 are low (see section above), but when present, increase mortality risk. Anecdotal reports suggest less MRSA superinfection than is often seen with influenza. Unnecessary antibiotics carry risks of fluid overload and drug-resistance, as well as the possibility that antibiotics may become a limited resource. (Zhou et al, Lancet, 2020; Yang et al, Lancet Respir Med, 2020; Lippi and Plebani, Clin Chim Acta, 2020; WHO, COVID-19 Interim guidance, March 2020).
  2. If antibiotics are to be used, they should reflect IDSA guidelines based on presumed source and MDRO risk factors
  1. For empiric coverage for a presumed pulmonary source of infection:
  1. In patients without risk factors for MRSA or Pseudomonas (i.e., living in community, no prior MDROs), start with ceftriaxone and azithromycin
  2. In patients with risk factors for MRSA or Pseudomonas (i.e., chronic hospitalization, prior MDR infections), start with cefepime and vancomycin and consider ciprofloxacin if high concern for Pseudomonas
  1. For coverage of potential coinfections:
  1. If concurrent influenza, treat with oseltamivir
  2. Given prevalence of lymphopenia in clinical presentation of COVID-19, consider Pneumocystis jirovecii and treat accordingly
  1. See special dispensations for oncology patients in “Oncology”

Formulation

  1. Give oral antibiotics (azithromycin, levofloxacin, ciprofloxacin, etc.) when possible to reduce volume load, unless concerns for poor oral absorption

Discontinuation

  1. Unnecessary antibiotics should be discontinued as soon as possible (ideally, within 48 hours). Clinical judgement should prevail over any specific lab value, but we suggest discontinuing when the following criteria are met:
  1. Clinical status is not deteriorating
  2. Cultures do not reveal pathogens at 48 hours and/or procalcitonin and WBC are relatively stable from 0 to 48 hours

Outpatient Management

  1. This section is in development

HIV-Positive Patients

  1. Literature on patients with HIV and SARS-CoV-2 coinfection is limited to very few case reports (Zhu et al, Journal of Medical Virology, 2020; Aydin et al, Journal of Medical Virology, 2020)
  2. It is not clear that people living with HIV (PLHIV) were at a disproportionate risk from MERS and SARS, though they are clearly at increased risk from other respiratory pathogens including influenza, pneumococcal pneumonia, and tuberculosis (Benito et al, Eur Respir J, 2012)
  3. Per WHO and CDC criteria, PLHIV, in particular those with low CD4 counts and those who are not on antiretroviral therapy, should be considered high risk for complications from COVID-19
  4. There is speculation that PLHIV may have protection against COVID-19. No data currently exist to support this idea however
  1. Antiretrovirals used to treat HIV, specifically lopinavir/ritonavir, are being investigated as potential treatments for COVID-19 (discussed in more detail in the Therapeutics chapter). ART may thus be protective against COVID-19 for PLHIV (Joob and Wiwanitkit, Journal of Medical Virology, 2020)
  2. Lymphopenia in PLHIV may potentially protect from the hyperinflammatory state thought to contribute to severe COVID-19 disease (Mascolo et al, Journal of Medical Virology, 2020)