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      A Clean, Well-Lighted Place1

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          Abstract

          Edward Hopper (1882–1967) Drug Store (1927) Oil on canvas (73.6 cm × 101.9 cm) The Museum of Fine Arts, Boston, Massachusetts, USA Bequest of John T. Spaulding, 48.564 “The man’s the work. Something doesn’t come out of nothing,” Edward Hopper once said. This private and introspective man, known for his dry wit and “monumental silences” and for expressing himself “tersely but with weighted exactness in a slow reluctant monotone,” was offering a glimpse into the creative process as it applied to him. Much was made of the sense of isolation and despair in his work and their connection with modern life. But “The loneliness thing is overdone,” he noted. “My aim in painting is always, using nature as the medium, to try to project upon canvas my most intimate reaction to the subject as it appears when I like it most; when the facts are given unity by my interest and prejudices.” “Hudson River Dutch” is how Hopper described his ancestry in Nyack, New York. The son of a dry goods merchant, he was not discouraged in his artistic ambitions, though his family did steer him toward commercial illustration for its earning potential. The skill stood him in good stead during the lean years. He attended the New York School of Art and studied under Robert Henri, one of the fathers of American Realism, “the most influential teacher I had.” He visited Europe several times. “Paris had no great or immediate impact on me.” But when he returned to the United States, his work reflected what he had seen abroad. “It took me ten years to get over Europe.” Hopper settled in New York, where he would make his primary residence. He moved into a 74-step, cold-water walk-up with a sky-lit studio in Greenwich Village. He had to haul coal for the furnace up four flights of stairs, but the space suited his self-sufficient and frugal nature. He painted many major works there and, despite a reasonable measure of success during his lifetime, never pursued more plush quarters. During a career that spanned 60 years and saw the heyday of abstract expressionism, as well as a resurgence of realism in the United States, he made a unique contribution. In a 1932 exhibition at the Museum of Modern Art, his work was described as “part of a new international progressive trend emerging within modernism, represented by a balance between ‘form’ and ‘content’ in its work.” Hopper’s approach, which appealed to his colleagues from all factions, explored natural and artificial light on surfaces, particularly on the vernacular architecture of American cities: motels, gas stations, storefronts, diners, apartments. “What I wanted to do was to paint sunlight on the side of a house.” His work employed classical elements and formal discipline in the dispassionate presentation of everyday scenes. Hopper captured what he called “our native architecture with its hideous beauty, its fantastic rooms, pseudo-gothic, French Mansard, Colonial, mongrel or what not, with eye searing color or delicate harmonies of faded paint, shouldering one another along interminable streets that taper off into swamps or dump heaps,” and by capturing it, he defined it. His images, often described as theatrical or cinematic, went on to inspire the cinema and its greats, among them John Huston, Elia Kazan, John Cassavetes. Alfred Hitchcock credited Hopper for influencing his films Rear Window and Psycho. “The whole answer is there on the canvas,” Hopper said in lieu of explaining his paintings. “I hope it will not tell any obvious anecdotes since none are intended.” Just like the content of his paintings, the form was stripped of extraneous details. He sought perfection in perspective, geometric structures, and two-dimensional space, as well as in the use of color and light. “As a child I felt that the light on the upper part of a home was different from that on the lower part. There is a sort of elation about sunlight on the upper part of a house.” He described his style as “an amalgam of many races” and refused to belong to any school. “Hopper is always on the verge of telling a story,” observed novelist and art critic John Updike, referring to scenes whose very stillness suggests that something is about to happen. A room seems either recently vacated or soon to be occupied. If inhabited, it is always sparsely, and that also goes for public places―theaters, restaurants, offices. Any occupant has either just arrived or is ready to leave, psychologically absent, or lost in thought. Human presence is not required, although the viewer is always allowed in, either through an open window or some other vista. And the night is just as paintable as the day, or even more so because of its mysterious, even ominous, contrasts and shadows. Drug Store, on this month’s cover, is one of Hopper’s nocturnal works. During one of his visits to Europe, he saw Rembrandt’s Night Watch, “The most wonderful thing…. It almost amounts to deception.” In his own work, he came to view the night as an opportunity to scrub a scene from the hustle and bustle. In the darkness, it seems, he could focus on the unexceptional and familiar elements of the uninhabited streets and capture the essence of places. In Drug Store, drama resides strictly on the weight of darkness in back of the setting against the brightly lit establishment forward. The lamp above the entrance lights the window, which with the awning pulled up all the way, is unabashedly exposed. Emotion is rendered in place and time, not human terms. In painting this street icon, Hopper as always, sought the “most exact transcription possible.” But what might have been a most sterile, even disturbing, presentation is rendered here with softness and calm. The storefront glows against the surroundings, its curtains and colorful vessels inviting and homelike but for the commercial signage. The wedgelike positioning foreshadows another one of Hopper’s famous corner establishments, Nighthawks. Silbers Pharmacy was typical of the profession in the early part of the 20th century. The move away from artisan plasters, powders, and carbonated waters saw increasingly flamboyant advertising of medications based on better understanding of disease etiology and the mechanisms of drug action. These new drugs were a mixed bag of cure and trouble, just like today’s offerings. In this journal issue alone, countless examples underline unintended consequences in the use of otherwise effective medications, among them antimicrobial drugs. Commonly used to treat infections, these drugs also may change intestinal microflora and make patients vulnerable to other infections, as with Clostridium difficile. In addition to increased C. difficile–associated disease, severity is also increasing from a new strain. And while clinical illness used to occur almost exclusively among the elderly in healthcare facilities, it is now seen in the community, among the young, and apart from antimicrobial drug treatment. Some retail meats contain the pathogen, though its role there is unknown. Changes in disease setting alter who is at risk and what the risk factors are. The clean, well-lighted healthcare setting where antimicrobial drug use leads to pseudomembranous colitis does not describe the risk for or characteristics of community-acquired infections with C. difficile. “I was never able to paint what I set out to paint,” Hopper said. During the unpredictable course of the creative process, inspiration injects itself unawares, the miscellaneous and extraneous intercede, color dictates, or thought transforms the initial intention to an unrecognizable final result. The artist’s discerning eye must complete the process by honing in on the essential. Public health scientists at work to stay ahead of pathogens also come up against unpredictability in the creative process. Much like Hopper, they must have an eye for the setting. One is not like another, and light makes all the difference. And while the whole answer may indeed be there on the canvas, for Hopper the essence was found in the light, whereas for the scientist trying to capture and define risk factors for infection, the essence may still be lurking in the shadows.

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          Clostridium difficile Infections among Hospitalized Children, United States, 1997–2006

          The epidemiology of Clostridium difficile infection (CDI) has been shifting over the past decade. Since 2000, the molecular evolution of the hypervirulent toxigenic bacterial strain BI/NAP1/027, which causes severe disease in massive outbreak settings, has been well documented ( 1 – 4 ). Furthermore, the increasing detection of this strain in the United States and other countries coincides with reports of increasing hospitalizations either resulting from or complicated by CDI and associated with increased case-fatality rates ( 5 – 7 ). Although in the past it was not thought to affect pediatric populations substantially, CDI has more recently been implicated as an increasingly prevalent diarrheal pathogen in children ( 8 – 10 ). Moreover, evidence suggests that a large proportion of pediatric CDI cases are community-acquired infections and that many of these infections lack the traditional risk factor of exposure to antimicrobial drugs ( 11 – 13 ). These changes in the epidemiology of pediatric CDI, although not definitively caused by the BI/NAP1/027 strain, are likely related to this strain because at least 2 reports suggest a high prevalence (10%–38%) of this strain in pediatric CDI populations and a 4× increase in complication rates associated with this strain compared with other strains ( 14 , 15 ). Current age-specific epidemiology of CDI among children remains poorly studied. Literature predating the emergence of the epidemic strain suggests that although up to 67% of all neonates (i.e., 1 data source potentially indicates a higher chance of accuracy. In addition, the format in which we analyzed 1 of the databases (Kids’ Inpatient Database [KID]) did not enable separating newborn discharges (defined as those hospitalizations during which the child was born) from those of other children 55 years on a maternal record, and mixed neonatal and maternal records), i.e., no chart reviews are undertaken by the agency. For the current study, all data were derived in aggregate from the publicly available HCUPNet website ( 18 ). Because the years for which data were available were 1997, 2000, 2003, and 2006, our observations were limited to these periods. We examined the annual incidence of CDI-related hospitalizations on the basis of the International Classification of Diseases, 9th revision, clinical modification (ICD-9-CM), code 008.45 (intestinal infection with C. difficile) as a proportion of all hospitalizations. We additionally determined the time trends for CDI as the principal discharge diagnosis in this population. Finally, to understand better the context of increasing CDI-related hospitalizations, we examined trends in hospitalizations related to other diarrheal diseases, specifically Salmonella (ICD-9-CM 00.30), rotavirus (ICD-9-CM 008.61), viral enteritis (ICD-9-CM 008.8), and other infectious enteritides (ICD-9-CM codes 009.0–009.3, 487.8). The second analysis was a cross-sectional characterization of all CDI hospitalizations for patients 80% of all hospitalized children <1 year of age in the HCUP and KID databases. We could not determine whether the relatively high rate of CDI-related hospitalizations among non-newborn infants represents predominantly true disease or colonization. Although more specific than recovery of a toxin-producing strain from culture, even the detection of free toxins A, B, or both in the stool of a symptomatic infant does not ensure a pathogenic role for C. difficile, especially if another cause for diarrhea can be identified. Rates of hospitalizations for rotavirus infections have exhibited a similar increase as those with CDI between 1997 and 2006. Although 2 recent analyses of discharge data for adults suggest that non-CDI causes of diarrhea are not likely leading to a reporting bias as the explanation for the observed increase in CDI rates ( 22 , 23 ), the situation may be different for children in whom rotavirus is a serious pathogen and related hospitalizations are clearly increasing. Although Kim et al. did not report an increase in the frequency of testing for C. difficile in their study, our findings implicate this finding as a distinct possibility that needs to be investigated further ( 9 ). Our study has several limitations. First, case identification was based on administrative coding, thus predisposing to misclassification. However, the degree of misclassification may not be substantial because multiple studies have shown the ICD-9-CM code 008.45 to be a relatively accurate way to identify CDI ( 24 – 26 ). Second, because we had no clinical data available, we could not distinguish stool colonization from CDI infection. Third, we were unable to distinguish community-acquired from healthcare-associated disease. However, our study has several strengths. Because we explored 2 databases and discovered results that are highly consistent not only with each other but with those of previous recent investigations, we have augmented the accuracy of estimates of pediatric CDI incidence ( 9 ). In addition, our data are generalizable to most US-based institutions that care for the pediatric populations. This generalizability sets our results apart from those reported previously because they were limited to the highly specialized setting of children’s hospitals ( 8 , 9 , 11 ). In summary, the incidence of CDI in the pediatric population appears to be increasing in US hospitals. A reporting bias for diarrheal diseases may play a role in this trend given the concomitant increase in rotavirus-related hospitalizations we identified. Future data may clarify this finding because widespread immunization with available rotavirus vaccines may soon lead to reduced incidence of related hospitalizations. The low incidence of CDI-related hospitalizations among newborns reflects current recommendations against routine testing and may support the concept that C. difficile does not cause disease among neonates. In contrast, the relatively high rate of CDI-related hospitalizations among non-newborn infants indicates an urgent need for studies to determine how often C. difficile causes true disease in this population.
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            Hypervirulent Clostridium difficile Strains in Hospitalized Patients, Canada1

            Clostridium difficile infections (CDIs) have increased in incidence and severity within the past decade in North America and Europe ( 1 ), in large part because of the emergence of the hypervirulent North American pulsed-field type 1 (NAP1/027/III) strains ( 2 – 5 ). Recently, interest has increased in the ribotype 078 strain. A 2007 North American study showed that ribotype 078 strains predominated in swine and cattle (83%–94% prevalence), but were rare in a group of hospitalized persons (4% prevalence) ( 6 ). However, in studies from Europe and the United States, 078/V strains were found at a prevalence ranging from 3% to 11% ( 7 – 9 ). In a subsequent study by the US group, analysis of the toxinotype V strains from humans and food animals showed that 83% of strains were either NAP7 or NAP8 ( 10 ). A Dutch group has recently shown that 078/V strains increased from 3% to 13% during February 2005–2008 and can be considered hypervirulent ( 11 ). Our study aimed to determine the incidence rate of infections attributed to hypervirulent NAP7/078/V and NAP8/078/V strains of C. difficile in hospitals in Canada. The Study The Canadian Nosocomial Infection Surveillance Program is a collaborative effort between the Canadian Hospital Epidemiology Committee, a subcommittee of the Association of Medical Microbiology and Infectious Disease Canada, the Centre for Infectious Disease Prevention and Control, and the National Microbiology Laboratory of the Public Health Agency of Canada. The Canadian Nosocomial Infection Surveillance Program conducted prospective surveillance including collection of stool specimens from patients showing the presence of CDI during November 2004–April 2005 and during March and April in 2007 and 2008. An infection was considered healthcare-associated CDI if the patient’s symptoms occurred at least 72 hours after hospital admission or if the symptoms resulted in readmission of a patient who had been hospitalized within the 2 months before the symptom onset date and who was not a resident in a long-term care facility or nursing home ( 12 ). An infection was considered community-onset CDI if the healthcare-associated definition was not met. Outcomes 30 days postinfection were recorded to capture severe cases, which were defined as infections in patients admitted to an intensive care unit, in patients who had undergone colectomy, or in patients who had died ( 12 ). Deaths were assessed by the Canadian Hospital Epidemiology Committee member and categorized into 3 groups: 1) death directly attributable to CDI, 2) death indirectly related to CDI by exacerbation of an existing disease condition, or 3) death not a result of CDI. The assessment was made from information obtained from medical charts, nurse logs, laboratory reports, and consultation with nursing and medical staff. All stool specimens were cultured for C. difficile, and isolates were analyzed by PCR and pulsed-field gel electrophoresis (PFGE) at the National Microbiology Laboratory. PFGE, ribotyping, and toxinotyping were performed as described ( 10 , 11 ). MICs were determined by agar dilution or Etest. The primers used for PCR and sequencing are listed in Table 1. Macrorestriction patterns were analyzed with BioNumerics V4.5 (Applied Maths, Sint-Martens-Latem, Belgium). Table 1 Primers used in study of hospitalized patients with Clostridium difficile infection, Canada, 2004–2008 Primer Sequence (5′ → 3′) Specificity tcd3 TGCAATTATAAAAACATCTTTAAAC tcdC PaLoc negative regulator tcd4 TATATCTAATAAAAGGGAGATTG cdtB-F1 TGGACAGGAAGAATAATTCCTTC cdtB binary toxin subunit B cdtB-R1 TGCAACTAACGGATCTCTTGC E5 CTCAAAACTTTTTAACGAGTG ermB erythromycin/clindamycin resistance E6 CCTCCCGTTAAATAATAGATA GyrAF TTGAAATAGCGGAAGAAATGA gyrA DNA gyrase subunit A GyrAR TTGCAGCTGTAGGGAAATC GyrBF GAAGGTCAAACTAAAACAAA gyrB DNA gyrase subunit B GyrBR GGGCTCCATCTACATCG Fifteen NAP7 and 4 NAP8 patterns were identified from isolates obtained from 2,794 patients (overall prevalence 0.68%). Table 2 lists the patients and epidemiologic information, and the Figure shows the corresponding genomic fingerprint patterns. During the study period, the incidence rate increased as follows: 8/1,785 (0.5%) in 2004–2005; 5/638 (0.8%) in 2007; and 6/371 (1.6%) in 2008. Of the 19 patients identified, 14 were men with an average age of 70.8 years (not including 1 pediatric case), and 4 were women with an average age of 52.2 years; the overall average age was 61.5 years (Table 2). CDI was considered as community onset in 7 (37%) of 19 cases, and severe CDI was manifested in 3 (15.8%) case-patients (1 was healthcare-associated CDI and 2 were community-onset CDI). At 30 days postinfection for CDI, 26.3% of all patients had died, 1 death a direct result of CDI (5.3%), and 1 indirectly related; 10.6% of total deaths were attributable to CDI. Table 2 Epidemiologic information from hospitalized patients with Clostridium difficile infection, Canada, 2004–2008* Year and patient ID Province Age, y/sex Source Severe CDI† Outcome‡ 2004–2005 O1-0059 Ontario 62/M Healthcare-associated No Discharged O2-0053 Ontario 35/M Community-onset No Died-not attrib O3-0042 Ontario 64/F Community-onset No Discharged Q1-0028 Quebec 66/M Healthcare-associated Yes Died-attrib H1-0040 Nova Scotia 70/M Healthcare-associated No Discharged S1-0054 Saskatchewan 72/M Community-onset No Discharged S1-0063 Saskatchewan 82/M Community-onset Yes Discharged O7-0121 Ontario 74/M Healthcare-associated No Survived-hosp 2007 O1-7-0011 Ontario 87/M Community-onset No Survived-hosp O4-7-0011 Ontario 82/M Community-onset Yes Died-contrib Q1-7-0017 Quebec 40/F Healthcare-associated No Discharged O8B-7-0002 Ontario 65/M Healthcare-associated No Died-not attrib Q5-7-0013 Quebec 71/M Healthcare-associated No Discharged 2008 B1-8-0052 British Columbia 44/F Healthcare-associated No Discharged B1-8-0059 British Columbia 73/M Healthcare-associated No Discharged A3-8-0022 Alberta 38/F Community-onset No Discharged O2B-8-0015 Ontario 75/F Community-onset No Survived-hosp Q1-8-0008 Quebec 81/M Healthcare-associated No Died-not attrib O5-8-0001 Ontario 2/M Healthcare-associated No Discharged *ID, identification; CDI, Clostridium difficile infection; Died-not attrib, death not attributable to CDI; Died-attrib, death directly attributable to CDI; Survived-hosp, patient survived but was still in a hospital at endpoint; Died-contrib, CDI indirectly contributed to death.
†Required admission to intensive care unit due to CDI, received a colectomy, or died.
‡At 30 days after diagnosis of CDI. Figure Dendrogram analysis of macrorestriction patterns (SmaI) of the NAP7 and NAP8 Clostridium difficile strains isolated from the patients listed in Table 2. C. difficile N07-00380 is a ribotype 078 control strain. C. difficile NAP7-CDC and NAP8-CDC control strains are toxinotype V. Isolates exhibiting high-level clindamycin resistance (>256 μg/mL) and harboring ermB are indicated. The amino acid change found in the gyrA protein is shown for the moxifloxacin-resistant strain antimicrobial drug–resistance mechanisms. Sequence analysis of the tcdC gene showed that all strains carried a C184T transition that introduces a stop codon leading to a presumptive truncated protein of 61 residues, and a 39-bp deletion located downstream of the alternative stop codon. This tcdC variant has been previously described for toxinotype V strains ( 13 ). Sixteen of the isolates were ribotype 078 and 3 isolates had unknown ribotypes. All 2004/2005 and 2007 isolates were toxinotype V. The 2008 isolates were not toxinotyped. All 19 strains were susceptible to metronidazole and vancomycin. Seven isolates were susceptible to clindamycin (MIC 256). Only the 4 latter strains carried ermB and all were NAP8. Fourteen isolates that were susceptible to moxifloxacin (MIC 8 μg/mL) had no mutations in the gyrB QRDR but each had 1 mutation in the gyrA QRDR. One with MIC = 8 had an Asp71Val mutation; 3 with MIC = 16 and 1 with MIC >32 had a Thr82Ile mutation. These mutations have been previously described in moxifloxacin-resistant C. difficile ( 14 ). Conclusions C. difficile NAP7 and NAP8/078/V strains are relatively rare in hospitalized patients with CDI in Canada, in contrast to their prevalence in Europe and the United States ( 7 – 11 ). However, incidence rates have tripled from 0.5% in 2004 to 1.6% in 2008 (p = 0.22). There was a high association with a community onset, although dataset was too small to statistically confirm that increased cases were more likely to be community onset; 2 (40%) of 5 deaths were attributable to CDI. Although the number of strains studied here was small, data are consistent with other studies that indicate a community association for NAP7 and NAP8/078/V strains ( 9 – 11 ). The prevalence of these strains in Canada may be higher than suggested here if they are a common cause of community-associated CDI, as studies have indicated ( 10 , 11 ). The role of animals in acquisition of NAP7 and NAP8/078/V strains was not evaluated because animal and food contact data were not available. Molecular typing of C. difficile is typically performed by using ribotyping in Europe and PFGE/macrorestriction analysis in North America; both groups may use toxinotyping, which strictly looks at PaLoc variation. We showed a high correlation between NAP7, NAP8, ribotype 078, and toxinotype V strains by the 3 typing methods, which enabled results of separate studies to be compared. Furthermore, tcdC analysis provides an additional diagnostic tool for these strains because the gene has a 39-bp deletion and a C184T-transition in all isolates we studied. Continued surveillance is warranted in humans, animals, and retail meat to determine whether NAP7 and 8/078/V strains will continue to emerge in patients hospitalized in Canada and to determine whether the sources of these infections are related to animals or food. Surveillance is especially important given that these strains appear to be hypervirulent as has been reported for NAP1/027/III strains ( 11 ).
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              Fluoroquinolone Resistance and Clostridium difficile, Germany

              We characterized 670 Clostridium difficile isolates collected from patients in 84 hospitals in Germany in 2008. PCR ribotyping showed high prevalence of ribotype 001 and restricted dissemination of ribotype 027 strains. Fluoroquinolone resistance and associated gyrase mutations were frequent in various ribotypes, but no resistance to metronidazole or vancomycin was noted.
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                Author and article information

                Journal
                Emerg Infect Dis
                Emerging Infect. Dis
                EID
                Emerging Infectious Diseases
                Centers for Disease Control and Prevention
                1080-6040
                1080-6059
                April 2010
                : 16
                : 4
                : 751-752
                Affiliations
                [1]Centers for Disease Control and Prevention, Atlanta, Georgia, USA
                Author notes
                Address for correspondence: Polyxeni Potter, EID Journal, Centers for Disease Control and Prevention, 1600 Clifton Rd NE, Mailstop D61, Atlanta, GA 30333, USA; email: PMP1@ 123456cdc.gov
                Article
                AC-1604
                10.3201/eid1604.AC1604
                3321976
                73b6a8ad-9c00-4404-996f-8238ff4b18f0
                History
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                About the Cover
                About the Cover

                Infectious disease & Microbiology
                art and medicine,about the cover,architecture,edward hopper,drug store,drugs,clostridium difficile,art science connection,emerging infectious diseases

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