Infectious Disease Alert Updates
Legionella Revisited
SOURCES: Euser SM, de Jong S, Bruin JP, et al. Legionnaires’ disease associated with a car wash installation. Lancet. 2013;382:2114.
van Heijnsbergen E, et al. Confirmed and potential sources for Legionella reviewed. Environ Sci Technol 2015 April 1 (Epub ahead of print).
Environmental investigation has shown that Legionella organisms may be found throughout nature, as well as colonizing drinking water systems and other man-made water structures that either mist, bubble, or spray water. When and why these organisms become infectious to humans is not always clear. The Netherlands have been performing source investigations and environmental surveillance for Legionella organisms for many years through a National Legionella Outbreak Detection Programme, and have uncovered some surprising sources for human infection.
Recent investigation examined the case of an 81-year-old man who presented to a hospital with fever and bilateral pulmonary consolidation, subsequently confirmed to be due to L. pneumophila serogroup 1 strain based on urinary antigen testing and isolation of the organism from respiratory secretions. Following a 24-day hospital stay, he was discharged to home. The Legionella Outbreak Detection Programme investigates all potential sources for human infection and, in this case, examined 26 samples collected from four potential sources: the home taps and shower; the taps and shower at a hotel where the patient stayed; a fountain near the hotel; and a car wash where he washed his car with a hand-held power hose. All of the samples from the home, the hotel, and the fountain were negative. But two samples taken from the car wash were positive for L. anisa and a sample from the car wash hose contained L. pneumophila, which appeared identical to the patient’s isolate based on amplification fragment length polymorphism testing. The temperature of the hose was 21.5°C (70.7°F). This finding suggests the car wash was the source for the patient’s infection.
Retrospective examination revealed two patients diagnosed with Legionellosis three years earlier who reported using the same car wash. At that time, investigation of the car wash turned up only a single positive sample for L. anisa. Samples from various car wash installations taken throughout the Netherlands between 2002 and 2010 found that two of 11 were positive for non-pneumophila Legionella spp. Such car washes are used throughout the Netherlands, and could serve as a source of Legionella infection. This information could lead to regular inspection of car wash installations, recommendations for routine maintenance and disinfection, and equipment modification.
Treatment of Latent Tuberculosis
SOURCE: Goswami ND, et al. Predictors of latent tuberculosis treatment initiation and completion at a U.S. public health clinic: A prospective cohort study. BMC Public Health 2012;12:468-475.
Initiation — and completion — of self-administered treatment for latent tuberculosis (TB) infection (LTBI) remains a challenge for clinicians. Treatment for LTBI is considered optional, even for those with recent exposure and skin test conversion who may be at the highest risk for active TB (approximately 50% within two years of exposure). Public Health Guidelines “strongly recommend” treatment for such cases, somewhat more exuberant than the standard “recommended” treatment for LTBI, but hardly requisite.
These authors investigated demographic, medical, and behavioral factors associated with a willingness to initiate and continue treatment for LTBI in adults (18 years or older) attending a public health TB clinic in Raleigh, NC. Between 2008 and 2009, 496 adults met the CDC guidelines for LTBI treatment, and upon entry to the clinic, were interviewed, counseled, and provided a self-administered questionnaire which inquired as to their health, social factors, and attitude toward TB and treatment. All medications were provided free of charge through the clinic on-site pharmacy. Primary endpoints were the number of people who initiated treatment (as defined by picking up at least one month of medication), and the number who completed treatment (defined as picking up 9 months of INH medication within a 12-month period or 4 months of rifampin within a 6-month period).
Of the 496 participants, 87% were racial/ethnic minorities and 65% were foreign born. Nearly two-thirds were referred to the clinic by their employers for screening and evaluation, and 19% were identified during contact investigations. Only 130 (26%) persons started LTBI treatment, and 70 (14%) completed therapy. Half (52%) of those receiving INH completed treatment, and 61% of those receiving rifampin completed treatment. Nearly two-thirds of those receiving INH completed at least 6 months of treatment, although compliance with both regimens diminished over time. Seven of 99 (7%) persons receiving INH were switched to rifampin, and 1/31 (3%) receiving rifampin was switched to INH.
In multi-variate analysis, factors independently associated with treatment initiation included close contact with a TB case, a non-employment reason for screening, lower education level, and having a regular physician. Persons with underlying medical conditions, who were considered a greater risk for TB reactivation, were more likely to complete treatment than those at lower risk (45% vs 17%, P < .01). While income/geographic factors did not appear to influence a willingness to start treatment, persons living in higher income areas were more likely to complete their treatment than those in lower income areas (81% vs 42%, P = .08).
Other studies have demonstrated higher rates of treatment initiation than this. And yet, I can vouch for the difficulty in convincing people about the benefits of LTBI treatment — even those at greater risk for reactivation — but especially those who are younger, healthy, born outside the United States, and have unremarkable chest radiographs. Even when we know it’s the right thing to do — and the patient is at higher risk for reactivation — there are just no teeth to the current Public Health recommendations. How are clinicians supposed to encourage people to accept treatment for LTBI when there is no imperative to do so?
Transmission of Clostridium difficile from Asymptomatic Carriers
SOURCE: Curry SR, et al. Use of multilocus variable number of tandem repeats analysis genotyping to determine the role of asymptomatic carriers in Clostridium difficile transmission. Clin Infect Dis 2013;57(8):1094-1102.
Active surveillance and expedited infection control contact precautions have been shown to reduce the risk of nosocomial transmission of MRSA and other hospital-acquired organisms. While newer molecular screening techniques using PCR allow for more rapid screening for C. difficile colonization, questions remain about whether such surveillance is of sufficient value to justify the expense and the burden to the microbiology laboratory.
These experts examined both stool and environmental C. difficile isolates from hospital patients screened for clinical purposes, as well as C. difficile isolates detected from peri-rectal swab samples, initially collected for the purposes of screening patients for vancomycin-resistant Enterococcus (VRE). Multilocus variable number of tandem repeats analysis (MLVA) was employed to examine the genetic relationship between the isolates, and to craft a minimum spanning tree, looking for temporal associations between genetically similar isolates.
For the first portion of the study, clinical stool specimens from 158 patients were positive for C. difficile toxin; isolates were obtained from 92% of these cases for analysis. Of these 158 patients, 56 (43%) were considered hospital-onset (HO-CDI), while 57 (46%) were considered acquired at another institution or relapsors, 34 (22%) were considered carriers; and 13 (10%) were consider community-acquired.
In addition, screening tests performed on 4979 specimens from 3006 patients were positive for toxigenic C. difficile strains in 422 specimens, yielding 417 C. difficile isolates. Not surprisingly, the presence of C. difficile in a sample was strongly associated with the presence of VRE. Of the 314 patients with toxigenic C. difficile strains, 38% also had VRE. In addition to these, environmental isolates were collected.
In all, 739 isolates were examined by MLVA, yielding 524 unique genotypes. Of these, 230 formed 78 complexes of highly related isolates; carrier strains were important to the creation of 5 of these complexes. The 027-genotype 1 strain made of 41% of the isolates— these were broken into 170 genotypes and 26 complexes for analysis.
Of the 56 cases of HO-CD, nearly one–third (30%) were associated with other cases ofC. difficile infection, and another third (29%) were related to carriers identified during surveillance screening. Of those cases related to colonized subjects, 9 of the cases were classified as non-ward transmissions, 2 as ward-transmissions, 2 as environmental transmissions (from a prior bed occupant); and 2 were indeterminate. This study also demonstrated that colonized individuals can serve as an important source for environmental contamination, perhaps weeks before transmission occurred. In addition, the incubation period for active C. difficile infection may be greater than 1 week prior to the onset of symptoms. One patient’s screening tests were positive 35 days prior to collection of a positive clinical specimen for symptoms, and was the presumed source for one other HO case. Seven symptomatic patients tested positive on screening surveillance samples 8 to 28 days prior to their diagnosis.
Through sophisticated genetic analysis and modeling of a huge number of clinical, surveillance, and environmental C. difficile isolates, this study demonstrates that asymptomatic colonization and/or colonization prior to the onset of symptoms was an important source for 59% of the cases of HO-CDI at their facility. Even the best infection control program cannot capture asymptomatic colonization with C. difficile without benefit of a surveillance program.
Legionella Revisited; Treatment of Latent Tuberculosis; Transmission of Clostridium difficile from Asymptomatic Carriers
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