Margaret Price

St. Luke School of Medicine, Houston, Texas, United States

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Publications (6)17.78 Total impact

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    ABSTRACT: Background: CDI is the leading, definable cause of healthcare-associated diarrhea. Molecular PCR assays for toxigenic genes are increasingly being utilized for CDI detection. Objective: To evaluate the prevalence of asymptomatic and symptomatic CDI at a university hospital using a realtime PCR assay. Methods: All adult patients present in a large, university hospital in Houston, Texas during 4 days were screened for enrollment. Subjects provided stool specimens or rectal swabs and completed a questionnaire. Fecal specimens were tested by realtime PCR for toxin A and B genes and ELISA for toxins A and B (Wampole). Confirmation of realtime PCR results by selective, anaerobic (CCFA) culture and conventional PCR for toxin genes for morphologically consistent isolates was performed. Results: 199 (53%) of 375 patients were enrolled from January 8-11, 2013. 103 (52%) of 199 study participants provided a stool sample or rectal swab. Overall, 12% of subjects reported diarrhea at enrollment. CD was detected by PCR in 18 (17%) of 103 subjects who provided a fecal sample, including 4 symptomatic and 14 asymptomatic subjects. Among CD-positive subjects, the one symptomatic (CDI) patient tested was positive versus 3/13 (23%) asymptomatic CDI (AsCDI) patients positive by ELISA. Previous hospitalization or residence in a healthcare facility, antibiotic or antacid receipt, or history of previous CDI was not associated with development of CDI or AsCDI. Considering detection of AsCDI as a false positive, the positive predictive value of the realtime PCR assay is 22%. Conclusion: The mean monthly CD detection rate at this university hospital increased significantly from 13.4 per 10,000 patient days (95% CI, 11.6 to 15.1) to 27.0 per 10,000 patient days (95% CI, 23.9 to 30.1; p<0.001) after changing from cell cytoxocity assay to realtime PCR for CDI diagnosis. However, in the setting of low diarrhea prevalence (12%), relatively frequent asymptomatic CDI (14%), and infrequent symptomatic CDI (4%), the positive predictive value of the PCR assay is poor and may be contributing to significant asymptomatic CDI detection at this hospital. An adjunct test to realtime PCR such as an ELISA for toxin production or a fecal test for inflammation may be necessary to confirm that CD is causing symptomatic disease.
    IDWeek 2013 Meeting of the Infectious Diseases Society of America; 10/2013
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    ABSTRACT: Background: Clostridium difficile(CD) infection (CDI) is the most important definable cause of healthcare-associated diarrhea. CD has been recovered from food animals and retail meats. Objective:To evaluate whether CD contamination of food, including meat and non-meat products, served to hospital patients may represent a route of CDI transmission. Methods: ~15 grams of each food item served over 80 days were collected from a single university hospital in Houston, Texas. One gram of each food was added to two 10-mL tubes with BHI supplemented with 0.1% taurocholate. One tube was heat-shocked at 80οC for 10 min. Both tubes were incubated anaerobically at 37οC for 72 h. 100 µL of BHI media was subcultured on a selective toxigenic CD culture plate, which was incubated anaerobically for 72h at 37οC. Food CD were screened by characteristic odor, morphology, and toxin production. Results: (Insert Table). 26 (28%) of 98 collected food samples were positive for CD. All food items were cooked except for some vegetables and fruits. 17/59 (29%) meats were contaminated including 4/8 (50%) turkey, 4/12 (33%) seafood, 2/17 (12%) beef, 1/8 (13%) pork, and 6/14 (43%) chicken or egg products. 6/27 (22%) vegetables or fruits, 0/2 grains, and 3/5 (60%) desserts were also positive for CD. All food CD strains were toxigenic. Comparison of food and patient CD strain types is planned. Conclusion: Significant C. difficile contamination of food items prepared for hospital patients was detected. Contaminated food may represent an important route of transmission for CDI in hospitals. Current cooking temperatures may be inadequate to eradicate CD contamination. Future studies are needed to evaluate the role of contaminated food in CDI transmission in healthcare settings and to determine if changes in food preparation or item selection are warranted. Table. Food Tested for Clostridium difficile Food Type No. Sample Tested No. Samples Positive for CD (%) Average Temperature of Food at Collection (οC) Turkey 8 4 (50) 33 Seafood 12 4 (33) 54 Beef 17 2 (12) 51 Pork 8 1 (13) 40 Chicken/eggs 14 6 (43) 53 Vegetable/Fruit 27 6 (22) 44 Grain 2 0 37 Dessert 5 3 (60) 17 Total 93 26 (28)
    IDWeek 2012 Meeting of the Infectious Diseases Society of America; 10/2012
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    ABSTRACT: Previous studies have shown that failure to produce serum antibodies to C. difficile (CD) toxin A is associated with more severe and recurrent C. difficile-associated diarrhea (CDAD); and that presence of AA genotype in the interleukin (IL)-8 gene promoter -251 position is associated with increased susceptibility to CDAD. This study examined the relationship between serum immunoglobulin G antibodies to CD toxin A and the presence of IL-8 AA genotype in hospitalized patients with CDAD. At enrollment, blood for host IL-8 genotype, serum for CD anti-toxin A antibody, and stool for IL-8 by enzyme-linked immunosorbent assay were obtained in CDAD patients and in CD-toxin-negative asymptomatic controls. Nine of 24 (37.5%) CDAD and 3 of 20 (15%) controls were CD anti-toxin A positive (P = .095). Eleven of 24 (45.8%) CDAD subjects were positive for AA genotype compared with 5 of 20 (25.0%) controls (P = .0019). One of 11 (9.1%) CDAD with AA genotype were positive for anti-toxin A antibodies compared with 8 of 13 (61.5%) non-AA genotype CDAD (P < .0001). Fecal IL-8 concentration for the single antibody-positive CDAD subject with AA genotype was lower than the median level of 822 microg/mL seen in 10 anti-toxin A antibody-negative subjects with CDAD. This study provided evidence that host susceptibility to C. difficile diarrhea is related both to a defective humoral immune response to CD toxin A and host IL-8 AA genotype.
    Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 09/2007; 5(8):964-8. · 5.64 Impact Factor
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    ABSTRACT: To assess the prevalence of diarrhea at a university-affiliated medical center and the presence of modifiable risk factors. A point prevalence survey was conducted. All patients hospitalized for more than 24 hours were asked if they were experiencing diarrhea. Stools of patients not previously tested were assessed for Clostridium difficile (CD) toxins A and B. Univariate analysis and multivariate logistic regression analyses were used to identify modifiable variables associated with diarrhea (significance defined as p < 0.05). Four hundred eighty-five hospitalized patients were interviewed, of whom 60 (12.4%) reported 2 or more loose, unformed stools in the last 24 hours. Six of 81 (7.4%) patients tested positive for CD toxin. Three (50%) of the CD toxin-positive patients had not previously been tested during the current admission. Patients with diarrhea were more likely to have tested CD toxin-positive (OR 10.6; p = 0.01), received antibiotics (OR 1.79; p = 0.04), or been hospitalized for a longer period of time (p = 0.04). Diarrhea was prevalent in 12.4% of hospitalized patients at a large university hospital at one point in time. Patients with diarrhea were more likely to have CD infection, receive antibiotics, or experience a longer hospitalization. Half of the CD diarrhea cases occurring in the hospital had been previously unidentified. Hospitalized patients should be evaluated for diarrhea on an ongoing basis with appropriate interventions instituted.
    Annals of Pharmacotherapy 07/2006; 40(6):1030-4. · 2.92 Impact Factor
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    ABSTRACT: Mucosal interleukin 8 (IL-8) and neutrophil recruitment are central to the pathogenesis of Clostridium difficile (CD) toxin-induced diarrhea (CDD). We hypothesized that like other inflammatory mucosal infections, susceptibility to CDD would relate to genetically determined variations in the production of IL-8. Fecal IL-8 production and single nucleotide polymorphism (SNP) frequency in the -251 region of the IL-8 gene were determined in hospitalized patients: 42 with CDD, 42 with CD-negative diarrhea, and 41 without diarrhea. Cases and controls were matched by age, length of hospital stay, comorbidity, and receipt of antibiotics. An association was found between the IL-8 -251 A/A allele and occurrence of CDD, 39%versus 16% (OR = 3.26, 95% CI 1.09-9.17) and 17% (OR = 5.50, 95% CI 1.22-24.8) for the two control groups. Comparing results by IL-8 genotype for the CDD cases, median and mean fecal IL-8 levels were significantly higher for the -251 A/A genotype (p = 0.03 for median and 0.001 for mean). These studies indicate a common SNP in the IL-8 gene is associated with increased susceptibility to CDD and with increased fecal IL-8 in diarrheal stools.
    The American Journal of Gastroenterology 06/2006; 101(5):1112-6. · 9.21 Impact Factor
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    ABSTRACT: Intestinal inflammation secondary to release of toxins A & B is an essential part of the pathogenesis of C. difficile diarrhea (CDD) & colitis. Physicians often initiate empiric treatment of nosocomial diarrhea with anti-C. difficile treatment in the absence of an etiologic diagnosis yet only 1 in 5-10 of such cases prove to have CDD. We compared the sensitivity & specificity of the fecal leukocytes test (microscopic presence of leukocytes in fecal smears) and a rapid commercial test for lactoferrin in the diagnosis of CDD using the tissue culture assay for cytotoxin B. The study was conducted in a large university affiliated hospital in Houston, TX among 30 C. difficile-toxin B positive and 43 C. difficile toxin B negative diarrhea controls. The sensitivity and specificity of fecal lactoferrin assay in CDD were 77% (2330) and 67% (2842) respectively. For fecal leukocytes, the sensitivity and specificity were 43% (13/30) and 88% (38/43), respectively. The agreement between fecal lactoferrin and fecal leukocytes and C difficile toxin B assays were not statistically significant (McNemer’s test). Both inflammation markers showed good concordance with the toxin B assay (p>0.05). A trend toward greater sensitivity for toxin B than for the fecal white cell test was seen (p=0.07). Fecal lactoferrin appears to be a useful and rapid laboratory method for preliminary diagnosis of C. difficile associated intestinal disease in hospitalized patients and may provide further evidence of colitis vs. C. difficile colonization.
    Infectious Diseases Society of America 2005 Annual Meeting; 10/2005