Delayed Antibiotic-Induced Lysis of Escherichia coli in vitro is Correlated with Enhancement of LPS Release

Berg, C. Van Den; Neeling, Albert J. de; Schot, Corrie S.; Hustinx, W N M; Wemer, J.; Wildt, Dick J. De

doi:10.3109/00365549209054648

Cited by 53 publications

(29 citation statements)

References 19 publications

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“…The LPS release from E. coli during a 6 h growth period was 16.8 µg (inoculum size of 10 5 cfu/mL, [235]). The calculated amount of LPS in milk from infected quarters was approximately 10 5 times higher than the highest LPS value observed in blood.…”

Section: Endotoxin Clearancementioning

confidence: 99%

Severity of E. coli mastitis is mainly determined by cow factors

et al. 2003

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-Intramammary infections of dairy cows with Gram-positive bacteria such as Staphylococcus aureus (major cause of mastitis) have received a lot of attention because of their major economic impact on the dairy farm through production losses induced by an increase in somatic cell count. Management strategies, including greater awareness for efficient milking and hygienic measures, have limited the spread of Gram-positive bacteria and resulted in a significant decrease of proportion of S. aureus isolates and subclinical mastitis worldwide. Other organisms such as coliform subspecies and Streptococcus uberis, both environmental bacteria that cause clinical mastitis, have received less attention. Escherichia coli causes inflammation of the mammary gland in dairy cows around parturition and during early lactation with striking local and sometimes severe systemic clinical symptoms. This disease affects many high producing cows in dairy herds and may cause several cases of death per year in the most severe cases. It is well known that bacterial, cow and environmental factors are interdependent and influence mastitis susceptibility. Many studies, executed during the last decade, indicate that the severity of E. coli mastitis is mainly determined by cow factors rather than by E. coli pathogenicity. During E. coli mastitis, the host defense status is a cardinal factor determining the outcome of the disease. Today, we know that the neutrophil is a key factor in the cows' defense against intramammary infection with E. coli. Effective elimination of the pathogen by neutrophils is important for the resolution of infection and the outcome of E. coli mastitis. This review is a compilation of some major findings over the last 15 years concerning mainly host factors that modulate and influence neutrophil function and the mammary inflammatory reaction. The individual chapters address: virulence factors of E. coli strains, how neutrophils kill E. coli, connection between endotoxins, tumor necrosis factor-a and nitric oxide, severity classification of E. coli mastitis, lifespan of neutrophils, host factors that influence severity, tissue damage and production loss.

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Section: Endotoxin Clearancementioning

confidence: 99%

Severity of E. coli mastitis is mainly determined by cow factors

et al. 2003

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“…In meningococci, it was observed that isolates from patients had higher endotoxin-liberating activities than strains isolated from carriers (3). During normal growth, until the stationary phase, most endotoxin remains bound to the cell (4,25,65,69), and a stable ratio of bacterial counts and endotoxin concentration (total and shed) is usually observed (4,25,41,68,78).…”

Section: Endotoxinmentioning

confidence: 99%

“…During treatment of Haemophilus influenzae type b meningitis, peptidoglycans released from the bacterial cell wall into the cerebrospinal fluid (CSF) also contribute to meningeal inflammation (12). Jarisch-Herxheimer reactions that occur during treatment of secondary syphilis were proven not to be mediated by endotoxin (66 (44,79), most of the bacteria were killed within 2 h, whereas endotoxin levels still increased after 6 h. In two studies (52,78), the increase in endotoxin concentrations leveled off after 1 to 2 h, whereas bacterial counts still decreased. In two other studies (9,25), the time course of bacterial killing and endotoxin release occurred in parallel.…”

Section: Endotoxinmentioning

confidence: 99%

“…In this manner, a physical separation is made between bacterial cell-bound endotoxin (which will not pass through the filter) and non-bacterial cell-bound or free endotoxin. The reliability of this method for differentiating between free and cell-bound endotoxin has been questioned (40), and indeed, in one study (78), no differences were detected in the levels of total (unfiltered) and free (filtered) endotoxin either in untreated cultures or in cultures after exposure to antibiotics. However, a shift from cell-bound to free endotoxin was observed in four studies (25,65,67,69), and in one clinical study (4), total endotoxin levels decreased after antibiotic treatment, whereas free endotoxin levels increased.…”

Section: Endotoxinmentioning

confidence: 99%

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Clinical relevance of antibiotic-induced endotoxin release

Prins

Deventer

Kuijper

et al. 1994

Antimicrob Agents Chemother

138

101

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“…These disease processes have an associated mortality rate of c. 50%, even where appropriate antibiotics are used and intensive care management is A possible explanation for this high mortality is the release of additional endotoxin during antibiotic the rap^.^ Various in-vitro studies have reported release of significant amounts of endotoxin when bacteria are exposed to bactericidal antibiotics. 5- 9 The present study aimed to determine the amount of endotoxin released from bacteria in vitro when exposed to antibioticsduring logarithmic phase growth. The results were correlated with morphological changes in the bacteria following exposure to the antimicrobial agents.…”

Section: Introductionmentioning

confidence: 99%

Antibiotic-induced release of endotoxin from bacteria in vitro

Crosby

Bion

Penn

et al. 1994

Journal of Medical Microbiology

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Summary. The ability of cefotaxime, ciprofloxacin, piperacillin and tobramycin to cause release of endotoxin was examined in vitro with cultures of Enterobacter cloacae and Escherichia coli. Endotoxin was measured by a quantitative limulus amoebocyte lysate assay and its presence was confirmed by silver staining of the lipopolysaccharide moiety following SDS-PAGE. The morphology of the bacteria during antibiotic exposure was examined by scanning electronmicroscopy. Cefotaxime, ciprofloxacin and piperacillin caused significant endotoxin release, correlating with their ability to affect cell-wall morphology, causing filamentation, wall breakage and cell lysis. In contrast, little endotoxin was released when bacteria were exposed to tobramycin and no morphological changes were observed when bacteria were exposed to bactericidal concentrations of this aminoglycoside. Its antimicrobial spectrum and bactericidal activity make tobramycin an appropriate agent for treatment of sepsis caused by gram-negative bacteria and its lack of propensity to elicit excessive release of endotoxin may avoid exacerbation of endotoxin-related shock in sepsis.

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Delayed Antibiotic-Induced Lysis of Escherichia coli in vitro is Correlated with Enhancement of LPS Release

Cited by 53 publications

References 19 publications

Severity of E. coli mastitis is mainly determined by cow factors

Severity of E. coli mastitis is mainly determined by cow factors

Clinical relevance of antibiotic-induced endotoxin release

Antibiotic-induced release of endotoxin from bacteria in vitro

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