Diarrheal diseases are major causes of morbidity, with attack rates ranging from two to 12 or more illnesses per person per year in developed and developing countries. In addition, diarrheal illnesses account for an estimated 12,600 deaths each day in children in Asia, Africa, and Latin America. The causes of diarrhea include a wide array of viruses, bacteria, and parasites, many of which have been recognized only in the last decade or two. While enterotoxigenic Escherichia coli and rotaviruses predominate in developing areas, Norwalk-like viruses, Campylobacterjejuni, and cytotoxigenic Clostridium difficile are seen with increasing frequency in developed areas; and Shigella, Salmonella, Cryptosporidium species, and Giardia lamblia are found throughout the world. The rational management of infectious diarrhea requires the highly selective use of laboratory tests for these varied etiologic agents, depending on the clinical and epidemiologic setting. The purpose of this review is to provide an overview of the magnitude, special settings, and etiologies of diarrhea endemic to developed and developing countries. This information permits a practical approach to the diagnosis and management of common diarrheal illnesses in different settings.Tremendous advances have been made during the past 15-20 years in the recognition of a wide variety of viral, bacterial, and parasitic enteric pathogens that are important causes of diarrhea throughout the world. Indeed, most of the leading etiologies of diarrhea in developed and developing countries include viruses (rotaviruses, Norwalk-like viruses, and enteric adenoviruses), bacteria (enterotoxigenic Escherichia coli, Campy/obacter species, and cytotoxigenic C/ostridium difficile), and parasites (Cryptosporidium species) that have been recognized only since 1970. A review of the relative importance of the various microbial etiologies of diarrhea in these areas requires consideration of the setting in which the illnesses occur. We must first recognize that prospective, community-based studies reveal that acute gastrointestinal (OJ) illnesses are extremely common, ranging from one to three illnesses per person per year in developed countries to five to 18illnesses per person per year in children living in impoverished
Enteropathogenic Escherichia coli (EPEC) causes diarrhoea in children in developing countries. Many EPEC genes involved in virulence are contained within the locus of enterocyte effacement (LEE), a large pathogenicity island. One of the genes at the far righthand end of the LEE encodes EspF, an EPEC secreted protein of unknown function. EspF, like the other Esps, is a substrate for secretion by the type III secretory system. Previous studies found that an espF mutant behaved as wild type in assays of adherence, invasion, actin condensation and tyrosine phosphorylation. As EPEC can kill host cells, we tested esp gene mutants for host cell killing ability. The espF mutant was deficient in host cell killing despite having normal adherence. The addition of purified EspF to tissue culture medium did not cause any damage to host cells, but expression of espF in COS or HeLa cells caused cell death. The mode of cell death in cells transfected with espF appeared to be pure apoptosis. EspF appears to be an effector of host cell death in epithelial cells; its proline‐rich structure suggests that it may act by binding to SH3 domains or EVH1 domains of host cell signalling proteins.
Enteropathogenic Escherichia coli (EPEC) causes severe, watery diarrhea in children. We investigated ATP release during EPEC-mediated killing of human cell lines and whether released adenine nucleotides function as secretory mediators. EPEC triggered a release of ATP from all human cell lines tested: HeLa, COS-7, and T84 (colon cells) as measured using a luciferase kit. Accumulation of ATP in the supernatant medium was enhanced if an inhibitor of 5'-ectonucleotidase was included and was further enhanced if an ATP-regenerating system was added. In the presence of the inhibitor/regenerator, ATP concentrations in the supernatant medium reached 1.5-2 microM 4 h after infection with wild-type EPEC strains. In the absence of the inhibitor/regenerator system, extracellular ATP was rapidly broken down to ADP, AMP, and adenosine. Conditioned medium from EPEC-infected cells triggered a brisk chloride secretory response in intestinal tissues studied in the Ussing chamber (rabbit distal colon and T84 cell monolayers), whereas conditioned medium from uninfected cells and sterile filtrates of EPEC bacteria did not. The short-circuit current response to EPEC-conditioned medium was completely reversed by adenosine receptor blockers, such as 8-(p-sulfophenyl)-theophylline and MRS1754. EPEC killing of host cells releases ATP, which is broken down to adenosine, which in turn stimulates secretion via apical adenosine A2b receptors. These findings provide new insight into how EPEC causes watery diarrhea.
c Orthopedic surgeons at our institution have noticed an increase in the number of infections due to Propionibacterium acnes, especially following operations on the shoulder. We collected P. acnes isolates from our hospital microbiology laboratory for 1 year and performed antimicrobial susceptibility testing on 28 strains from the shoulder. Antibiotics with the lowest MIC values against P. acnes (MIC 50 and MIC 90 ) included penicillin G (0.006, 0.125), cephalothin (0.047 and 0.094), and ceftriaxone (0.016, 0.045), while others also showed activity. Strains resistant to clindamycin were noted. Propionibacterium acnes has been recognized as a significant and emerging pathogen in orthopedic surgery over the last 10 years, especially after operations on the shoulder and especially following shoulder arthroplasty with prosthetic material (1-3). At our institution, the number of recognized cases of P. acnes has increased noticeably over the last few years. Formulating treatment recommendations for patients with P. acnes orthopedic infections can be difficult, however, given the paucity of data on antibiotic susceptibility patterns. Many of the early reports on P. acnes antibiotic susceptibilities are from patients with facial acne who were attending dermatology clinics. Other studies are now decades old (4, 5) or originate from countries in which antibiotic usage patterns are much different from those in North America (6, 7), leading us to question whether we can rely on those reports.We performed testing on 33 strains of P. acnes collected between November 2010 and December 2012, 28 of which were from orthopedic surgeries on the shoulder and 5 of which were isolates from bloodstream or other deep infections. P. acnes was identified using the MicroScan rapid anaerobe identification method (Siemens Healthcare, W. Sacramento, CA). We tested this strain collection against a panel of 10 antibiotics, with an emphasis on antibiotics that might actually be used to treat postoperative orthopedic infections. We used the Etest method (bioMérieux, Durham, NC) on anaerobic brucella blood agar. Two previous studies indicated that MICs obtained by Etest correlated well with results obtained using the agar dilution method (8, 9), and other experts consider the Etest an accepted method (10). Etest results obtained using anaerobic brucella blood agar were compared to those obtained using CDC anaerobe blood agar on a subset of 6 strains. Inocula were prepared to a 0.5 McFarland standard from 48 h of growth on anaerobic blood agar. Blood agars were from Anaerobe Systems (Morgan Hill, CA). We tested only a single isolate from each patient, although most patients had more than one positive culture. P. acnes was cultured anaerobically at 37°C for 48 to 72 h using the GasPak EZ anaerobe container system (BD Corp., Franklin Lakes, NJ).The results of our study are reported in Table 1. MICs measured on brucella blood agar were the same as those measured using CDC anaerobe agar. The penicillins (penicillin G and amoxicillin) and cephalosporins...
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