Macrolides and clindamycin suppress the release of Shiga-like toxins from Escherichia coli O157:H7 in vitro

Murakami, Junko; Kishi, Kenji; Hirai, Kazuyuki; Hiramatsu, Kazufumi; Yamasaki, Takahiro; Nasu, Masaru

doi:10.1016/s0924-8579(00)00126-6

Cited by 47 publications

(30 citation statements)

References 19 publications

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“…It was reported that subinhibitory concentrations of norfloxacin, classified as the new quinolones, promoted the Stxs production from EHEC O157 [6,13,23]. In contrast, × 1 and × 50 MIC of ERFX as a new quinolone suppressed the production of Stx 2e from ETEEC O139 in the present study.…”

Section: Discussioncontrasting

confidence: 63%

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Effect of Antimicrobial Agents on the Production and Release of Shiga Toxin by Enterotoxaemic <i>Escherichia coli</i> Isolates from Pigs

Uemura

Sueyoshi

Taura

et al. 2004

The Journal of Veterinary Medical Science

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ABSTRACT. Edema disease (ED) of pigs is an enterotoxaemic disease caused by enterotoxaemic Escherichia coli (ETEEC) infection. Antimicrobial therapy for pigs with ED is controversial because it may induce death of sickish piglets. In this study, we investigated the effects in vitro of 7 antimicrobial agents, ampicillin, gentamicin, colistin, bicozamycin, fosfomycin, sulfamethoxazole-trimethoprim and enrofloxacin, on the release and production of shiga toxin (Stx) 2e by ETEEC strains. We found that more Stx 2e accumulated in the bacterial cells than was released into supernatant. Associated with inhibition of cell wall synthesis, the exposure to ampicillin or fosfomycin increased the release of Stx 2e. The production levels of Stx 2e in all antimicrobial-treated cultures were equal to the level in the control or less than in the control. These results suggest that cell wall synthesis inhibitors, such as ampicillin and fosfomycin, may change for the worse in the signs in ETEEC infectious pigs. On the other hand, gentamicin, colistin, bicozamycin and enrofloxac in may be useful for the treatment of pigs with ED. KEY WORDS: antimicrobia, edema disease, enterotoxaemic Escherichia coli, shiga toxin 2e, swine.J. Vet. Med. Sci. 66(8): 899-903, 2004 Edema disease (ED) of the pig has been found throughout the world since ED was first reported in Ireland in 1938 [17]. ED has been a sporadically occurring disease found mainly in post-weaned piglets that causes systemic vascular damage as a result of intestinal infection with shiga toxinproducing Escherichia coli (STEC) [1,2,5]. The STEC is also called enterotoxaemic Escherichia coli (ETEEC) [14]. After ETEEC colonizes in the intestines, shiga toxin (Stx) 2e produced by the ETEEC is absorbed into the capillary vessels and then damages the endothelial cells [1,2,5]. The manifestations of ED include palpebral edema, neurological impairment, lateral recumbence and sudden death [1,2]. The speed of onset and severity of clinical signs and gross pathological lesions are related to the dose of the toxin. Intervals between injection and onset of the disease vary from 7 to 28 hr, the mean time to death being from 24 to 42 hr [2]. Classical ED has been seen to occur sporadically and subside spontaneously [1,2,8,11]. Recently, ED has tended to persist and spread, causing great economic damage to pig farmers [20,21,24].Antimicrobial administration has been used as one of the most common treatments for the eradication of STEC from the intestines of humans and animals [12,14,16,22]. Nevertheless, some antimicrobial agents have been reported to increase the release of Stxs from enterohemorrhagic Escherichia coli (EHEC) associated with enterohemorrhagic colitis and hemolytic uremic syndrome of humans in vitro [4,10,13,22,23]. In ED affected farms, deaths of piglets associated with antimicrobial treatment have increased in number [7,24]. Until now, however, there has been no investigation to determine the effect of antimicrobial agents on the production and release of Stx 2e by ETEEC.In ...

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Section: Discussioncontrasting

confidence: 63%

“…Nevertheless, some antimicrobial agents have been reported to increase the release of Stxs from enterohemorrhagic Escherichia coli (EHEC) associated with enterohemorrhagic colitis and hemolytic uremic syndrome of humans in vitro [4,10,13,22,23]. In ED affected farms, deaths of piglets associated with antimicrobial treatment have increased in number [7,24].…”

mentioning

confidence: 99%

Effect of Antimicrobial Agents on the Production and Release of Shiga Toxin by Enterotoxaemic <i>Escherichia coli</i> Isolates from Pigs

Uemura

Sueyoshi

Taura

et al. 2004

The Journal of Veterinary Medical Science

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“…Studies using subinhibitory concentrations of 13 antibiotics (including trimethoprim-sulfamethoxazole, azithromycin, gentamicin, penicillins, streptomycin, ciprofloxacin, fosfomycin, and expanded-spectrum cephalosporins) found that all antibiotics increased the amount of toxin in at least one of three strains studied (6). Others have suggested that macrolides do not stimulate toxin production (18,21,33). DNA gyrase inhibitors (quinolones), folate metabolism inhibitors (trimethoprim-sulfamethoxazole), and to a lesser extent, cell envelope-active agents (penicillins and cephalosporins) have all been described as inducing toxin gene expression, while drugs that interfere with translation or transcription do not induce expression (10).…”

Section: Discussionmentioning

confidence: 99%

Rifaximin Does Not Induce Toxin Production or Phage-Mediated Lysis of Shiga Toxin-Producing Escherichia coli

Ochoa

Chen

Walker

et al. 2007

Antimicrob Agents Chemother

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Diarrhea in children is often caused by enteropathogen infections that might benefit from early empirical antibiotic therapy. However, when the definition of the pathogen requires sophisticated laboratory studies, the etiology of enteritis is not known early in illness. Empirical therapy may be dangerous if the child is infected with a Shiga toxin-producing Escherichia coli (STEC) strain because antimicrobials may increase Shiga toxin (Stx) release, resulting in increased risk of microangiopathic hemolytic anemia with acute renal failure (hemolytic-uremic syndrome [HUS]) and death. There is a need for antimicrobials that would be effective against multiple bacterial enteropathogens yet not induce Stx release or increase the risk of HUS. Rifaximin has been evaluated in adults for treatment of bacterial enteritis and has a good record for safety and efficacy, but it has not been evaluated extensively in children with gastroenteritis. We therefore evaluated rifaximin's potential for phage induction, drug-induced bacteriolysis, and toxin release in 57 STEC strains (26 O157 and 31 non-O157 strains). Growth in ciprofloxacin, a known Stx phage inducer, caused bacteriolysis and release of toxin in 25/26 (96%) O157 strains and 15/31 (48%) non-O157 strains. In contrast, rifaximin did not induce phage replication or lysis in any strain. Toxin release in the presence of rifaximin was not different from release in the absence of antibiotic. Rifaximin, unlike many antibiotics used to treat pediatric gastroenteritis, does not induce phage-mediated bacteriolysis and Stx release.Bacterial enteropathogens represent important pediatric pathogens worldwide. Many of the agents causing gastroenteritis are known or predicted to respond to antibiotic therapy (e.g., Shigella,

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“…Some studies report antibiotic treatment of patients with STEC infection to be beneficial and others do not (reviewed in reference 23). Similarly, studies examining the ability of antibiotics to promote Stx production in vitro have given mixed results (9,13,18,21,25,37). In several studies Stx expression was assessed by enzyme-linked immunosorbent assay (ELISA), Western blotting, or mRNA levels, and these indirect assays may not accurately reflect levels of biologically active Stx, since not all subunits may be part of assembled functional AB 5 complexes.…”

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confidence: 99%

Different Classes of Antibiotics Differentially Influence Shiga Toxin Production

McGannon

Fuller

Weiss

2010

Antimicrob Agents Chemother

163

128

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Shiga toxin (Stx) in Escherichia coli O157:H7 is encoded as a late gene product by temperate bacteriophage integrated into the chromosome. Phage late genes, including stx, are silent in the lysogenic state. However, stress signals, including some induced by antibiotics, trigger the phage to enter the lytic cycle, and phage replication and Stx production occur concurrently. In addition to the Stx produced by O157:H7, phage produced by O157:H7 can infect harmless intestinal E. coli and recruit them to produce Shiga toxin. To understand how antibiotics influence Stx production, Stx lysogens were treated with different classes of antibiotics in the presence or absence of phage-sensitive E. coli, and Stx-mediated inhibition of protein synthesis was monitored using luciferase-expressing Vero cells. Growth-inhibitory levels of antibiotics suppressed Stx production. Subinhibitory levels of antibiotics that target DNA synthesis, including ciprofloxacin (CIP) and trimethoprim-sulfamethoxazole, increased Stx production, while antibiotics that target the cell wall, transcription, or translation did not. More Stx was produced when E. coli O157:H7 was incubated in the presence of phage-sensitive E. coli than when grown as a pure culture. Remarkably, very high levels of Stx were detected even when growth of O157:H7 was completely suppressed by CIP. In contrast, azithromycin significantly reduced Stx levels even when O157:H7 viability remained high.

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Macrolides and clindamycin suppress the release of Shiga-like toxins from Escherichia coli O157:H7 in vitro

Cited by 47 publications

References 19 publications

Effect of Antimicrobial Agents on the Production and Release of Shiga Toxin by Enterotoxaemic <i>Escherichia coli</i> Isolates from Pigs

Effect of Antimicrobial Agents on the Production and Release of Shiga Toxin by Enterotoxaemic <i>Escherichia coli</i> Isolates from Pigs

Rifaximin Does Not Induce Toxin Production or Phage-Mediated Lysis of Shiga Toxin-Producing Escherichia coli

Different Classes of Antibiotics Differentially Influence Shiga Toxin Production

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