Infection Control Today

DEC 2018

ICT delivers to infection preventionists & their colleagues in the operating room, sterile processing/central sterile, environmental services & materials management, timely & relevant news, trends & information impacting the profession & the industry

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Page 28 of 32

28 ICT December 2018 Shedding of Pathogens The following studies review the impact of pathogens shed by colonized patients. Hand Contamination for MDROs: Patients' hands are a source of microorganisms and may be contaminated with MDRO. In a study by Cao (2016), they sampled patient hands on discharge from an acute care facility and entering a post-acute care (PAC) facility and found that 24.1 percent had at least one MDRO on their hands (VRE=13.7 percent, MRSA=10.9 percent, resistant Gram-negative bacteria=2.8 percent.) Patel (2017) similarly tested the hands of patients entering a PAC facility and found hands were frequently contaminated (MRSA=10.8 percent, VRE=13.6 percent, resistant Gram-negative bacteria=5.7 percent). Patient hands and the environment were positive for the same organism in 21.9 percent of visits. Both studies demonstrate a risk of MDRO pathogens of primary concern transmitted via patients' hands. MRSA: McKinnell (2013) performed a literature review to study whether nasal testing for MRSA was adequate to detect MRSA. It was found that MRSA colonization of other body sites (including the axilla and perineum) is common and that some proportion of patients with extranasal colonization of MRSA have negative nasal swabs. In most studies, MRSA colonization was reported at 2-6 percent of the people tested. The most likely extranasal site to be positive for MRSA is the oropharynx (throat below the mouth), so saliva may also be disseminating pathogens such as MRSA. Oral care can reduce this microbial burden (Munro 2011), especially for ventilated patients. As noted above, patients may also be colonized in their feces with MRSA at high levels (Boyce 2007). VRE: Mayer (2003) found that patient continence did not impact the rate at which patient rooms tested positive for VRE. Also, the number of colonies for samples that were VRE positive was not different for patients that were continent versus incontinent. The authors also noted that several of the patients that were continent had cultures for VRE at >1x108 CFU per gram of feces, which is a high level of fecal contamination and may help explain the environmental contamination even with continent patients. Lee (2018) examined patient dissemination with VRE and environmental contamination with VRE in an ICU setting. About 5 percent of patients were VRE positive on admission and 3.6 percent of ICU patients acquired VRE while in the ICU. Sixteen percent of randomly selected environmental samples were positive for VRE. Medical equipment shared between ICUs was much more likely to be contaminated with VRE than equipment dedicated for one ICU, reinforcing the need to disinfect portable medical equipment between patients. Acinetobac ter baumannii: Thom (2011) found that 9.8 percent of environ- mental surfaces were positive for Acine- tobacter baumannii (AB) in rooms with patients with a history of AB infection or colonization or currently colonized by AB. Forty-eight percent of the patient rooms were positive in at least one sample point tested, indicating widespread sur face contamination is likely for patients colonized or infected with AB. Clostridium difficile: Crew (2018) looked at the relationship between antibiotic use and healthcare onset C diff infections. Asymptomatic carriers of C. diff by stool sample were more likely to have positive skin samples and environmental samples. Recurrent or persistent C. diff shedding and contamination of the patient environment may persist for up to six weeks after CDI treatment is complete, indicating this risk continues even after diarrhea resolves. Freedberg (2016) studied whether the previous bed patient receiving antibiotics affected the risk of Clostridium diffcile infection (CDI) for the next patient. They found that the cumulative incidence of CDI was 0.72 percent when the prior bed occupant had received antibiotics and 0.43 percent when they did not. The authors theorized that patients on antibiotics produce more C. diff, which is disseminated into the environment. While that does not affect the risk of C diff for the patient, if other patients enter an environment where there is more C. diff, this increases the risk of exposure to C. diff and subsequent infection. There is also some evidence of air contamination as a route of dissemination for C. diff. Best (2010) studied airborne dispersal of C. diff from symptomatic patients. They reported that patients with CDI can excrete 1x104 to 1x107 CFU of C. diff spores per gram of feces. After air testing patients with CDI and active diarrhea, 10 percent had air samples positive for CDI, while 2 percent of symptomatic patients without diarrhea had positive air samples. Ten percent of environmental surface samples were positive for C. diff. This suggests the environment and the air around the patient become contaminated even without diarrhea. Yui (2017) found ceiling vents as reservoirs of C. diff, with six of 19 sites (31.6 percent) positive after terminal cleaning. Sethi (2010) looked at the issue of environmental shedding of C. diff. Some patients are known to continue to shed C. diff in their stool after diarrhea resolves, but current CDC guidelines state that contact precautions can be eliminated after diarrhea resolves. In this study, the mean time to resolve diarrhea was 4.2 days and only 7 percent (2/28) of patients still had C. diff in their stool at the end of treatment, while about 30 percent of patients still had C. diff positive skin samples and roughly 15 percent had positive environmental samples. At the time of treatment, 60 percent of patients had skin contamination with C. diff. However, when tested at later times and while asymptomatic, 56 percent (15/27) had C. diff in their stool 1-4 weeks after treatment, suggesting antibiotics supress C. diff levels in stool, but after the protective effect is removed, the C. diff levels return without symptoms. Healthcare workers were estimated to contaminate their hands with C. diff 50 percent of the time during patient skin contact after resolution of diarrhea. Riggs (2007) studied the shedding of asymptomatic carriers of C. diff. They report that about two of three patients colonized with C. diff become asymptomatic carriers. In their study, 51 percent (35/68) of resident physicians were asymptomatic carriers of toxigenic C. diff strains. Twelve patients colonized with C. diff were tested 1-3 months later and 83 percent (10/12) had positive stool samples. Revolinski (2018) reviewed select literature on C. diff colonization and found that in one study, 4 percent of patients were colonized with C. diff on hospital admission and 3 percent became colonized during hospitalization. In another study, 15 percent of patients were colonized with toxigenic C. diff while another 5 percent were colonized with non-toxigenic C. diff. A study in Australia found that 8 percent of patients were colonized with C. diff. A Dutch study found that 6 percent of patients were colonized with C. diff on admission. Nine percent of these patients developed CDI while only 2 percent of those not colonized at admission developed CDI. A meta-analysis from 2015

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