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J Food Prot. 2002 Sep;65(9):1394-405.
Inactivation of acid-adapted and nonadapted Escherichia coli O157:H7 during drying and storage of beef jerky treated with different marinades.

Calicioglu M, Sofos JN, Samelis J, Kendall PA, Smith GC.

Center for Red Meat Safety, Department of Animal Sciences, Colorado State University, Fort Collins 80523, USA.

The inactivation of both acid-adapted and unadapted Escherichia coli O157:H7 during the processing of beef jerky was studied. Following inoculation with the pathogen, beef slices were subjected to different predrying marinade treatments, dried at 60 degrees C for 10 h, and stored at 25 degrees C for 60 d. The predrying treatments evaluated were as follows: (i) no treatment (C), (ii) traditional marinade (TM), (iii) double-strength TM modified with added 1.2% sodium lactate, 9% acetic acid, and 68% soy sauce with 5% ethanol (MM), (iv) dipping into 5% acetic acid for 10 min followed by application of TM (AATM), and (v) dipping into 1% Tween 20 for 15 min and then into 5% acetic acid for 10 min followed by TM (TWTM). Bacterial survivors were determined during drying and storage using tryptic soy agar with 0.1% pyruvate, modified eosin methylene blue agar, and sorbitol MacConkey agar. Results indicated that bacterial populations decreased during drying in the order of TWTM (4.9 to 6.7 log) > AATM > MM > C > or = TM (2.8 to 4.9 log) predrying treatments. Populations of acid-adapted E. coli O157:H7 decreased faster (P < 0.05) in AATM and TWTM than nonadapted cells during drying, whereas no significant difference was found in inactivation of acid-adapted and nonadapted inocula in C and TM samples. MM was more effective in inactivating the nonadapted than the adapted inoculum. Bacterial populations continued to decline during storage and dropped below the detection limit (-0.4 log10 CFU/cm2) as early as day 0 (after drying) or as late as day 60, depending on acid adaptation, predrying treatment, and agar medium. The results indicated that acid adaptation may not increase resistance to the hurdles involved in jerky processing and that use of additional antimicrobial chemicals or preservatives in jerky marination may improve the effectiveness of drying in inactivating E. coli O157:H7.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12233848&dopt=Abstract

J Food Prot. 2002 Sep;65(9):1417-21.
Effect of organic acids and temperature on survival of Shigella flexneri in broth at pH 4.

Zaika LL.

U.S. Department of Agriculture, Agricultural Research Service, Eastern Regional Research Center, Wyndmoor, Pennsylvania 19038, USA. lzaikrserrc.gov

The survival of bacterial pathogens in acidified foods depends not only on the hydrogen ion concentration, but also on the type of acid and the storage temperature. Shigella flexneri is a foodborne pathogen that is acid tolerant. The survival of S. flexneri 5348 in brain heart infusion broth supplemented with 0.04 M acetic, citric, lactic, malic, or tartaric acid and adjusted to pH 4 with HCI or NaOH was studied. The control medium was brain heart infusion broth adjusted to pH 4 with HCI. Stationary-phase cells were inoculated into media at initial populations of 6 to 7 log10 CFU/ml and incubated at 4, 19, 28, and 37 degrees C. A two-phase linear inactivation model was applied to plate count data to derive lag times (tL) and slopes of the curves, from which D-values and time required for a 4-log10 decrease in population (T4D) were calculated. In all cases, survival increased with decreasing temperature. For each acid, tL, the D-value, and T4D increased with decreasing temperature. All acids inhibited S. flexneri to some extent but to differing degrees as follows: lactic acid, acetic acid > citric acid, malic acid, tartaric acid > HCl. The T4D values for the control medium and for media containing acetic, citric, lactic, malic, and tartaric acids were 64, 47, 50, 34, 58, and 52 h, respectively, at 37 degrees C and 2,607, 1,498, 1,905, 1,346, 1,726, and 2,134 h, respectively, at 4 degrees C. The results of this study indicate that organic acids may aid in the inactivation of Shigella. However, these data also suggest that foods stored at or below room temperature containing low levels (< 1%) of acids could cause illness if contaminated with Shigella.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12233851&dopt=Abstract

J Rheumatol. 2002 Sep;29(9):2006-11.
Treatment of catastrophic antiphospholipid syndrome with defibrotide, a proposed vascular endothelial cell modulator.

Burcoglu-O'Ral A, Erkan D, Asherson R.

Department of Hematology and Oncology, University of Pittsburgh, Pennsylvania, USA.

OBJECTIVE: To define at the molecular level the vascular endothelial cell (VEC) injury characteristics of catastrophic antiphospholipid syndrome (CAPS) and to report successful therapeutic use of a VEC modulator, defibrotide. METHODS: We describe a 55-year-old man with primary APS with an intractable prothrombotic state (CAPS) resistant to combined therapy with heparin, warfarin, aspirin, and dipyridamole. Treatment with defibrotide was conducted in the context of an investigational phase II protocol where the dose was regulated and individualized by disease/patient-specific molecular and clinical markers. RESULTS: The patient entered complete remission with defibrotide treatment. During treatment, dose dependent pharmacological actions of defibrotide and key stress markers for VEC injury were identified. Evidence of defibrotide's polypharmacology included downregulation of cytokines, notably tumor necrosis factor-alpha, as the earliest effect, cellular differentiation of VEC, possibly with direct regulatory effect over cellular genes, and the reversal of platelet consumption and prothrombotic state. Von Willebrand antigen levels were used as the sole marker to guide therapy. CONCLUSION: This case demonstrates effective remission of CAPS with defibrotide treatment. In contrast to theories that CAPS is triggered by ischemic and thrombotic tissue damage, these data present VEC injury as the primary and representative lesion of CAPS. The pathogenesis may involve concurrent impairment of different VEC functions. Achieving remission may require a polypharmacologic approach, represented here by use of defibrotide.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12233899&dopt=Abstract

Traffic. 2003 Jan;4(1):36-48.
SopD2 is a novel type III secreted effector of Salmonella typhimurium that targets late endocytic compartments upon delivery into host cells.

Brumell JH, Kujat-Choy S, Brown NF, Vallance BA, Knodler LA, Finlay BB.

Biotechnology Laboratory and Departments of Biochemistry and Molecular Biology, Microbiology and Immunology, University of British Columbia, Vancouver, BC, V6T-1Z3, Canada.

Salmonella typhimuriumis a facultative intracellular pathogen that utilizes two type III secretion systems to deliver virulence proteins into host cells. These proteins, termed effectors, alter host cell function to allow invasion into and intracellular survival/replication within a vacuolar compartment. Here we describe SopD2, a novel member of the Salmonella translocated effector (STE) family, which share a conserved N-terminal type III secretion signal. Disruption of the sopD2 gene prolonged the survival of mice infected with a lethal dose of Salmonella typhimurium, demonstrating a significant role for this effector in pathogenesis. Expression of sopD2 was induced inside host cells and was dependent on functional ssrA/B and phoP/Q, two component regulatory systems. HA-tagged SopD2 was delivered into HeLa cells in a SPI-2-dependent manner and associated with both the Salmonella-containing vacuole and with swollen endosomes elsewhere in the cell. Subcellular fractionation confirmed that SopD2 was membrane associated in host cells, while the closely related effector SopD was localized to the cytosol. A SopD2 fusion to GFP associated with small tubular structures and large vesicles containing late endocytic markers, including Rab7. Surprisingly, expression of N-terminal amino acids 1-150 of SopD2 fused to GFP was sufficient to mediate both binding to late endosomes/lysosomes and swelling of these compartments. These findings demonstrate that the N-terminus of SopD2 is a bifunctional domain required for both type III secretion out of Salmonella as well as late endosome/lysosome targeting following translocation into host cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12535274&dopt=Abstract

Med Educ. 2002 Dec;36(12):1201-8.
A trading-card game teaching about host defence.

Steinman RA, Blastos MT.

University of Pittsburgh School of Medicine, PA 15213, USA. steinmaitt.edu

OBJECTIVES: To heighten the understanding of host-disease interactions by adolescents and young adults, using a trading card game format. DESIGN: A trading card game was developed in which paired students attack one another with pathogens or parry those attacks with appropriate defences. Twenty-five infectious pathogens or cancers, 30 defence agents and 6 health status modifying conditions were included. SETTING: A middle school, upper school and medical school in the United States. SUBJECTS: 8th grade, 10th grade and first year medical students. RESULTS: The game was tested using pre-test/post-test evaluations in 8th graders, 10th graders and medical students. Factual information, pathogen-organ specificity, and general concepts were tested. There was a significant increase in test scores, from 39% to 58% correct in the 8th graders (P < 0.0001), from 47% to 59% among 10th graders (P = 0.0007), and from 80% to 88% (P = 0.049) among the medical students. Responses to control questions unrelated to the game did not improve. CONCLUSION: An interactive trading card format is a useful method for conveying information about host defence.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12472757&dopt=Abstract

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