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By Peter Teska, Jim Gauthier and Carol Calabrese
In healthcare facilities, the patient environment includes patient-care equipment and environmental surfaces and is well established as contaminated with pathogens that can cause infection. Patients with active infections with antibiotic-resistant organisms, coughs, purulent wounds, diarrhea, or vomiting are recognized as a source of pathogens and the use of transmission-based precautions (as recommended by the CDC) is central to preventing dissemination of pathogens that can ultimately result in an infection for other patients.
Colonized patients also represent a risk of pathogen dissemination but since the rate of is generally believed to be lower for colonized patients than infected patients, most of the attention in preventing pathogen dissemination is related to infected patients. However, since the number of colonized patients and the rate at which they disseminate pathogens into the environment is generally less well understood, the overall burden may be much more significant than is currently recognized.
Consistent and correct use of standard and transmission-based precautions is generally relied on to protect healthcare workers and help control pathogen cross transmission for colonized (i.e., asymptomatic) patients. However, it is far from clear that the typical compliance levels with hand hygiene, environmental surface cleaning and use of barriers are adequate to manage this risk. As a result, interest has grown to better understand the role of colonized patients.
Where do potential pathogens come from in colonized hosts?
Colonization is referred to as the presence of microorganisms in or on a host, with growth and multiplication but without tissue invasion or cellular injury (PHAC 2013). A colonized person shows no obvious signs of disease yet can spread microorganisms into the environment through normal day-to-day activities. While most of the microorganisms shed are non-pathogenic to the colonized host, there may be bacteria that is pathogenic to other people, depending on the portal of entry or the immune system strength of the susceptible host. The potential for pathogen dissemination from an asymptomatic person is high as the average human body contains ~0.3 percent bacteria by weight (or about half a pound for the average person) (Sender, 2016).
Three common sources of bacteria shed by people include, feces, saliva and skin cells.
• Feces: Kelly (1994) notes that the colon contains more than 500 species of bacteria and that healthy feces may contain more than 1x1012 colony forming units (CFU)/gram of feces. Sender more recently estimated that the intestines may contain from 1x108 to 1x1011 bacteria per milliliter. One study (Stephen, 1980) demonstrated that bacteria were 54.7 percent of the total mass of solid feces in a healthy individual, although other estimates have put the number as low as 30 percent. Both estimates demonstrate that billions of bacteria are released from the body. Ray (2002) found a mean of 7.5 log10 VRE per gram of stool. Boyce (2007) found some patients with diarrhea who were excreting MRSA in quantities between 107 â 109 CFU/gram of stool.
Using a toilet puts high numbers of bacteria into the toilet bowl, where they can become aerosolized during flushing. Even flushing an empty toilet bowl can aerosolize bacteria from inside the bowl (Knowlton, 2018). Thus, a focus on toilets as a prime vector of bacterial dissemination seems justified.
• Saliva: Saliva is colonized with many bacteria. Lamont (2010) estimated that there are 1x108 bacteria per milliliter of saliva and Sender estimated 1x109 bacteria per milliliter. Droplets of saliva are spread into the environment by talking, breathing, coughing, sneezing, singing and other activities. These activities occur within and outside healthcare facilities, so this risk is not unique to healthcare. Any oral suctioning is an additional risk for contamination of the environment.
• Skin: Skin is the body’s largest organ at ~1.8m2 and provides a diverse environment for bacteria, including warm damp areas, cooler dryer areas, hair, no hair and openings into the body (ears, nose, mouth, anus, etc.). Estimates of skin shedding calculate that of the 19 million skin cells on our body, 30,000 to 40,000 skin cells are shed daily (American Academy of Dermatology Association, 2018). Meadow (2015) reports that humans shed 1x106 particles of >0.5 micrometers per hour, many of which contain bacteria, although the exact percentage is difficult to determine. However, there are up to 1x1011 bacteria per m2 on skin, so skin cell shedding involves disseminating significant numbers of bacteria. Patients with burns, autoimmune diseases, morbid obesity or eczema would likely have higher rates of shedding.
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.
Acinetobacter baumannii: Thom (2011) found that 9.8 percent of environmental surfaces were positive for Acinetobacter 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 surface 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 difficile 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 found 8.1 percent of patients were colonized and that 22 percent of patients colonized at admission developed C. diff while only 3 percent of non-colonized patients developed CDI. These studies suggest low but consistent levels of patients are colonized with C. diff when entering healthcare facilities.
ESBL-Producing bacteria: Cochard (2014) studied ESBL producing Enterobacteriaceae rates in French nursing homes. Surveillance of residents found the colonization rate was 9.9 percent. Fifteen percent of residents had been recently hospitalized and 35.4 percent had recently received antibiotics. Staff compliance with infection prevention protocols were low. Hand hygiene compliance was 25.7 percent, glove use was 45.9 percent, PPE use was 13.3 percent and waste management compliance was 46.7 percent. Homes with the highest compliance rates had the lowest ESBL colonization rates and those with the lowest compliance rates had the highest ESBL carriage rates.
To minimize the risk of environmental contamination by colonized patients, additional practices may be appropriate.
• Patient hand hygiene: Hand sanitizer readily available for patients to use prior to meals, entering or leaving their room, after toileting, etc. would be beneficial. The use of disposable alcohol-based hand wipes can reduce the number of organisms on the patient’s hands.
• Disinfection of surfaces at the point of care: Reducing the bio-burden in the patient care environment can be improved by coaching staff to be actively engaged in keeping the high-touch surfaces of the patient environment clean. All disciplines need to be educated to disinfect the environment before and after certain activities and/or procedures that may contaminate the near-patient environment. This can be accomplished by providing a safe disinfectant at point of care. This can also help ensure that mobile patient care equipment is disinfected between patients.
• Decolonization: Some facilities have implemented daily bathing with chlorhexidine gluconate (CHG) for any patient with a “line” (central line or Foley). Patients undergoing certain surgical procedures, or being admitted to an ICU, could also be screened for MRSA and if positive, treated with mupirocin. Pre-op skin cleansing the night before and morning of surgery with CHG may also reduce shedding of potentially pathogenic organisms. Some facilities more broadly decolonize patient nares for all surgical procedures involving implants or if the patient is deemed a high risk.
• Cleaning validation: Ensuring all surfaces have had contact with cleaner/disinfectants will keep bioburden low. Regular audits are recommended by the CDC (Guh 2010).
Humans continuously shed bacteria into their environment. All people colonized with certain pathogens discussed above can shed bacteria that can potentially cause infections in others. Colonization is an underappreciated source of pathogen dissemination that contributes to widespread environmental contamination as many studies showed. Dissemination of pathogens that result in hand or surface contamination is an important step in ultimately causing a healthcare acquired infection and needs to be studied further. Healthcare facilities should assess current policies and procedures to determine the implications of patient colonization within their facility.
Peter Teska is a Diversey infection prevention application expert; Jim Gauthier is a Diversey senior clinical advisor, and Carol Calabrese is a Diversey senior clinical advisor.
Public Health Agency of Canada (PHAC). Routine practices and additional precautions for preventing the transmission of infection in health care. Ottawa, ON: Her Majesty the Queen in Right of Canada; 2012. Available from: http://publications.gc.ca/collections/collection_2013/aspc-phac/HP40-83-2013-eng.pdf
Sender R, Fuchs S, Milo R. Revised Estimates for the Number of Human and Bacteria Cells in the Body. PLoS Biol, 2016;14(8):e1002533. doi:10.1371/journal.pbio.1002533.
Kelly CP, et. al. Clostridium difficile colitis. N Engl J Med, 1994; 330 (4): 257-262.
Stephen AM. The microbial contribution to human fecal mass. J Med Microbiol, 1980; 13(1): 45-56.
Ray AJ, et al. Nosocomial transmission of vancomycin-resistant enterococci from surfaces. JAMA 2002; 287:1400-1401.
Revolinski SL, et. al. Clostridium difficile exposures, colonization, and the microbiome: implications for prevention. 2018; 39(5): 596-602.
Boyce JM, et al. Widespread environmental contamination associated with patients with diarrhea and methicillin-resistant Staphylococcus aureus colonization of the gastrointestinal tract. Infect Cont Hosp Epidemiol, 2007; 28 (10):1142-1147.
Knowlton SD, et al. Bioaerosol concentrations generated from toilet flushing in a hospital-based patient care setting. Antimicrob Resist Infect Infect Control, 2018; 7:16. DOI 10.1186/s13756-018-0301-9
Lamont RJ, et. al. Oral microbiology at a glance. 2010, Wiley -Blackwell. West Sussex UK.
American Academy of Dermatology Association, “How skin grows”, 2018. Retrieved from: https://www.aad.org/public/kids/skin/how-skin-grows.
Meadow JF, Altrichter AE, Bateman AC, et al. “Humans differ in their personal microbial cloud.” Souza V, ed. PeerJ. 2015; 3:e1258. doi:10.7717/peerj.1258.
Cao J, et. al. Multi-drug resistant organisms on patients’ hands: A missed opportunity. JAMA Intern Med, 2016; 176 (5): 705-706.
Patel PK, et. al. “Patient hand colonization with MRDOs is associated with environmental contamination in post-acute care. Infect Cont Hosp Epidemiol, 2017; 38 (9): 1110-1113.
McKinnell JA, et. al. Quantifying the impact of extranasal testing of body sites for Methicillin-Resistant Staphylococcus aureus colonization at the time of hospital or intensive care unit admission. Infect Cont Hosp Epidemiol, 2013; 34 (2): 161-170.
Munro N, et al. Ventilator-associated pneumonia bundle. AACN Adv Crit Care, 2014; 25(2): 163-175
Mayer RA, et. al. Role of fecal incontinence in contamination of the environment with vancomycin-resistant Enterococci. Am J Infect Cont, 2003; 31 (4): 221-225.
Lee AS, et. al. Defining the role of the environment in the emergence and persistence of vanA Vancomycin-Resistant Enterococcus (VRE) in an intensive care unit: A molecular epidemiological study. Infect Cont Hosp Epidemiol, 2018; 39(6): 668-675.
Thom KA, et. al. “Environmental contamination because of multi-drug resistant Acinetobacter baumannii surrounding colonized or infected patients”. Am J Infect Cont, 2011; 39 (9): 711-715.
Crew PE, et. al. “Correlation between hospital-level antibiotic consumption and incident health care facility-onset Clostridium difficile infection”, Am J Infect Cont, 2018; 46: 270-275.
Freedberg DE, et. al. “Receipt of antibiotics in hospitalized patients and risk for Clostridium difficile infection in subsequent patients who occupy the same bed”. JAMA Intern Med, 2016; 176 (12): 1801-1808.
Best EL, et. al. “The potential for airborne dispersal of Clostridium difficile from symptomatic patients”. Clin Infect Dis, 2010; 50 (1): 1450-1457.
Yui S, et al. “Identification of Clostridium difficile reservoirs in the patient environment and efficacy of aerial hydrogen peroxide decontamination”. Infect Cont Hosp Epidemiol, 2017; 38 (12):1487-1492.
Sethi AK, et. al. “Persistence of skin contamination and environmental shedding of Clostridium difficile during and after treatment of C. difficile Infection”, Infect Cont Hosp Epidemiol, 2010; 31 (1): 21-27.
Riggs MM, et. al. “Asymptomatic carriers are a potential source for transmission of epidemic and nonepidemic Clostridium difficile strains among long-term care facility residents”, Clin Infect Dis, 2007; 45: 992-998.
Cochard H, et. al. “Extended-Spectrum Î²-lactamaseâproducing Enterobacteriaceae in French nursing homes: an association between high carriage rate among residents, environmental contamination, poor conformity with good hygiene practice, and putative resident-to-resident transmission”, Infect Cont Hosp Epidemiol, 2014; 35 (4): 384-389.
Guh A, et al. Options for evaluating environmental cleaning”. Centers for Disease Control and Prevention 2010. Available at: www.cdc.gov/hai/pdfs/toolkits/Environ-Cleaning-Eval-Toolkit12-2-2010.pdf