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PubMed2003

Antimicrobial activity of SMAP-29 against the Bacteroides fragilis group and clostridia.

OBJECTIVES: The cathelicidin-derived peptide SMAP-29 exerts rapid and broad-spectrum antimicrobial activity against aerobic bacteria and fungi. In this study, the effects of the peptide against the Bacteroides fragilis group, including antibiotic-resistant isolates, Clostridium perfringens and Clostridium difficile reference and clinical isolates, were investigated. METHODS: The microbicidal activity of SMAP-29 against eight reference and 100 clinical anaerobic strains from a national collection was assessed using a microdilution susceptibility assay, and by determining the killing kinetics on selected strains. The killing mechanism was investigated further by means of a two-colour fluorescent permeabilization assay, and by scanning electron microscopy (SEM). RESULTS: The Bacteroides fragilis group, Clostridium reference strains and most clinical isolates were inhibited in vitro by 1-2 microM (3.2-6.4 mg/L) SMAP-29, and killed by 1.5- to 2-fold higher peptide concentrations. The anaerobic bacterial cells were 90%-100% permeabilized within 2 h of exposure to bactericidal concentrations of the peptide. The SEM images of bacteria exposed to SMAP-29 provide morphological evidence that the envelope is an important target of the bactericidal activity of this peptide. These results are consistent with earlier studies indicating that SMAP-29 kills aerobic bacteria with a membranolytic mechanism, and suggest that both aerobic and anaerobic bacteria share surface features that are targeted by this peptide. CONCLUSIONS: These studies demonstrate that the spectrum of antibacterial activity of SMAP-29 includes the B. fragilis group and Clostridium species, and encourage further investigations of the therapeutic potential of this peptide.

Anti-Bacterial Agents↗
PubMed1994

Diltiazem and superoxide dismutase modulate hepatic acute phase response in gram-negative sepsis.

This study assessed the hepatic acute phase response and cellular Ca2+ regulation in septic animals and in hepatoma cell lines in vitro. Sepsis was induced in male Sprague-Dawley rats by implanting in their abdominal cavities fecal pellets impregnated with live Escherichia coli and Bacteroides fragilis. 8 h after implantations, rats were treated with diltiazem (1.2 mg/kg) or superoxide dismutase (SOD) (5 x 10(3) units/kg). After 24 h, plasma acute phase proteins (APP) were determined by immunoelectrophoresis, and hepatic APP-mRNAs by Northern blot hybridization. Effects of diltiazem, verapamil, or SOD on hepatic cells were determined in rat Reuber H-35 and human HepG2 hepatoma cells. Sepsis induced a significant increase in plasma APP and their hepatic mRNAs. Diltiazem and SOD reduced the sepsis-induced elevations in plasma lactate, the febrile response and mortality. APP expression in H-35 and HepG2 cells, stimulated by interleukin 1 (IL-1), IL-6, and dexamethasone, was inhibited by diltiazem or verapamil but not SOD. The results suggest that a heightened hepatic APP response in septic animals accompanies systemic/metabolic derangements and a significant animal mortality. Because diltiazem was previously shown to prevent sepsis-related disturbances in hepatic cellular Ca2+ regulation, its mediation of decrease in APP, systemic/metabolic response, and mortality may be effected through modifications in cellular Ca2+ regulation. The data from hepatoma cells show an attenuation of the AAP can result from direct effects of a calcium blocker. However, whether the blocker primarily modifies cellular Ca2+ regulation and secondarily effects APP gene expression, or directly effects gene expression remains unknown.

Acute-Phase Proteins↗
PubMed1994

T-lymphocyte Ca2+ signalling and proliferative responses during sepsis.

Alterations in T-lymphocyte kinetics and/or activation have been implicated in burn and traumatic injury. This study evaluated concanavalin A (Con A) regulation of both intracellular Ca2+ (Cai2+) and proliferation in T-lymphocytes harvested from spleens of septic rats. Rats were implanted with fecal pellets containing Escherichia coli (150 colony forming units (CFU)) and Bacteroides fragilis (10(4) CFU). T-cell[Ca2+]i was measured before and after treatment of cells with ConA, using Fura-2 and microfluorophotometry. Splenic lymphocytes were cultured for 72 h with Con A to assess their proliferative response. As compared to sterile-implanted rats, the septic rat T-lymphocytes Cai2+ response to Con A significantly decreased on days 1 and 2 after implantation. A significant decrease in T-cell proliferative response to Con A, compared to sterile controls, was found in septic rats on day 2 but not on day 1. These results suggest that Con A-mediated proliferation in T-cells occurs secondarily to a decrease in cellular Ca2+ signalling. The depression in the T-cell proliferative response during sepsis could contribute to a decrease in host's resistance against sepsis.

Animals↗
PubMed1984

Hepatic and systemic metabolic responses to aerobic and anaerobic intra-abdominal abscesses in a highly reproducible chronic rat model.

A single, uniform abscess was formed in 100% of the animals inoculated with a fecal pellet made of sterile rat feces, agar, and a known number and strain of bacteria. The effects of monoclonal Escherichia coli abscess (83 rats) were compared to those of sterile abscess (34 rats) and sham operation (35 rats without abscess). Bacteroides fragilis was added to the sterile pellet to study the effect of an anaerobic monoclonal abscess (16 rats) or of a biclonal abscess containing both aerobes and anaerobes (32 rats). After inoculation, a peritonitis stage with leucopenia, hypoglycemia, body weight loss, and slight fever was followed by the abscess stage with leucocytosis and a slight hyperglycemia. Mild hepatic energy charge deficiency and hepatic lactic acidosis were observed in sterile abscess rats, and slightly enhanced energy charge was seen in monoclonal E. coli abscess rats. The addition of B. fragilis to the sterile pellet, alone or together with E. coli, produced hepatic energy charge deficiency and hepatic lactic acidosis, which were significantly enhanced compared with the monoclonal E. coli abscess rats. The greatest effect was seen in the biclonal E. coli plus B. fragilis abscess, suggesting that anaerobic or combined aerobe and anaerobe abscesses may produce a greater hepatic injury than an aerobic organism abscess alone. This may account for the apparent synergic interaction between aerobic and anaerobic organisms.

Abdomen↗
PubMedDate not supplied

Development of Candida albicans and C. albicans/Escherichia coli/Bacteroides fragilis intraperitoneal abscess models with demonstration of fungus-induced bacterial translocation.

The development of models of both Candida albicans and mixed C. albicans/Escherichia coli/Bacillus fragilis peritonitis in immunologically normal mice are described, each with significant mortality and intra-abdominal abscess formation. C. albicans inoculated alone induced bacterial translocation into abscesses, and the addition of bacteria reduced the number of, but did not eliminate. C. albicans in abscesses. There was no synergy seen between fungi and bacteria in terms of either morbidity or mortality.

Abdominal Abscess↗
PubMed1998

[A case report of epidural abscess due to anaerobic bacteria, producing a mass of gas].

A 54-year-old female was admitted to our hospital on May 8, 1996, for evaluation of fever and headache. Her cerebrospinal fluid showed elevation of the cell count and total protein. The thoracic and lumbar MRIs revealed abnormal gas occupying the epidural space at the sacral level, and extended as high as 9th thoracic level. The gas spread inside the iliopsoas and paraspinal muscles. Anaerobic bacteria such as Bacteroides fragilis and Peptostreptococcus productus were cultured from the spinal fluid and Bacteroides was also detected from the epidural tissues obtained during laminectomy. The infectious source was decubitus extending around the sacral bone. The combination therapy of debridement with peroxide, catheter drainage of epidural abscess, intravenous and intrathecal antibiotics, and laminectomy presented her good outcome. This is a rare case of anaerobic bacterial spinal abscess, showing epidural and intramuscular gas as a prominent feature.

Abscess↗
PubMed2003

Adrenomedullin is increased in the portal circulation during chronic sepsis in rats.

BACKGROUND: A clinical hallmark of sepsis is an early, hyperdynamic cardiac phase (increased cardiac output) that degrades to a hypodynamic phase, which results in poor gut perfusion and subsequent gastrointestinal (GI) hypoxemia, tissue ischemia, necrosis and loss of gut barrier function. Studies in rat cecal-ligation and puncture suggest that the potent vasodilator adrenomedullin (AM) might initiate or maintain the hypodynamic phase. We hypothesize that AM expression is increased in acute Escherichia coli bacteremia and chronic E coli-Bacteroides fragilis sepsis. METHODS: Acute bacteremia: male Sprague-Dawley rats were anesthetized (urethane/alpha-chloralose), tracheotomized, and cannulated for monitoring blood pressure (MABP) and heart rate (HR) and for infusion of E coli (10(9) colony-forming units [CFU] E coli per 1 mL normal saline) and blood sampling. Arterial blood was withdrawn for arterial blood gas (ABG) measurements every 60 minutes. After 6 hours, we harvested lung, liver, kidney, spleen, and small intestine tissue samples and drew arterial and portal blood for AM enzyme-linked immunosorbent assay (ELISA). Chronic sepsis: a sterile gauze pad was implanted and animals recovered for 5 days. Twenty-four hours (10(9) CFU E coli and 10(9) CFU B fragilis per 1 mL normal saline; 1 injection) or 72 hours (2 injections) after the inoculation of the back sponge, rats were anesthetized, intubated, and cannulated as above. MABP, HR, and ABG were measured for 1 hour before tissue and serum harvest for AM ELISA. RESULTS: Sepsis increased HR and MABP in all groups. Acute sepsis caused a respiratory alkalosis and pH was also elevated in chronic sepsis. Serum AM levels were increased in all groups compared with baseline and remained elevated at every time point, but were not different between saline controls and septic animals at any time point, except for the portal serum from the 72-hour chronic sepsis, which was elevated. CONCLUSIONS: These data suggest that surgical manipulation alone is sufficient to stimulate AM secretion, most probably from endothelial cells. While the AM levels were decreasing at 72 hours compared with 6 hours or 24 hours in the arterial blood and the saline control portal blood, it remained elevated in the septic portal samples, suggesting that the sepsis-induced increase of AM was derived from the gut by a different mechanism than that which elevated arterial serum levels.

Acute Disease↗
PubMed2006

Etiology and epidemiology of diarrhea in children in Hanoi, Vietnam.

OBJECTIVES: This paper provides a preliminary picture of diarrhea with regards to etiology, clinical symptoms, and some related epidemiologic factors in children less than five years of age living in Hanoi, Vietnam. METHODS: The study population included 587 children with diarrhea and 249 age-matched healthy controls. The identification of pathogens was carried out by the conventional methods in combination with ELISA, immunoseparation, and PCR. The antibiotic susceptibility was determined by MIC following the NCCLS recommendations. RESULTS: Of those with diarrhea, 40.9% were less than one year old and 71.0% were less than two years old. A potential pathogen was identified in 67.3% of children with diarrhea. They were group A rotavirus, diarrheagenic Escherichia coli, Shigella spp, and enterotoxigenic Bacteroides fragilis, with prevalences of 46.7%, 22.5%, 4.7%, and 7.3%, respectively. No Salmonella spp or Vibrio cholerae were isolated. Rotavirus and diarrheagenic E. coli were predominant in children less than two years of age, while Shigella spp, and enterotoxigenic B. fragilis were mostly seen in the older children. Diarrheagenic E. coli and Shigella spp showed high prevalence of resistance to ampicillin, chloramphenicol, and to trimethoprim/sulfamethoxazole. Children attending the hospitals had fever (43.6%), vomiting (53.8%), and dehydration (82.6%). Watery stool was predominant with a prevalence of 66.4%, followed by mucous stool (21.0%). The mean episodes of stools per day was seven, ranging from two to 23 episodes. Before attending hospitals, 162/587 (27.6%) children had been given antibiotics. Overall, more children got diarrhea in (i) poor families; (ii) families where piped water and a latrine were lacking; (iii) families where mothers washed their hands less often before feeding the children; (iv) families where mothers had a low level of education; (v) families where information on health and sanitation less often reached their households. CONCLUSIONS: Group A rotavirus, diarrheagenic Escherichia coli, Shigella spp, and enterotoxigenic Bacteroides fragilis play an important role in causing diarrhea in children in Hanoi, Vietnam. Epidemiological factors such as lack of fresh water supply, unhygienic septic tank, low family income, lack of health information, and low educational level of parents could contribute to the morbidity of diarrhea in children.

Bacteroides Infections↗
PubMed1991

Pathogenesis of intraabdominal abscess formation: abscess-potentiating agents and inhibition of complement-dependent opsonization of abscess-inducing bacteria.

Bacteroides fragilis and Escherichia coli are synergistic in the production of intraabdominal abscesses. However, these bacteria initiate abscess formation only when inoculated with an agent such as autoclaved colonic contents (ACC) or bran (a fiber analogue). The mechanism of action of the abscess-potentiating agent was studied. Opsonins in normal mouse serum were determined for phagocytic killing by murine neutrophils of B. fragilis and E. coli. Opsonization required fixation of complement by the alternative pathway. ACC (0.2 mg/ml) and bran (1.0 mg/ml) inhibited phagocytic killing of Proteus mirabilis in the presence of normal but not immune serum. Assay of the alternative pathway of complement activation indicated that both bacterial components and abscess-potentiating agents in an abscess-inducing mixture activated complement. These findings suggest that abscess-potentiating agents inhibit opsonization and therefore the subsequent phagocytic killing of bacteria in the nonimmune host.

Abscess↗
PubMed1997

The effect of the bacterial product, succinic acid, on neutrophil bactericidal activity.

We investigated the effect of succinic acid on neutrophil bactericidal activity in a model of intra-abdominal abscess induced in mice by the peritoneal inoculation of 5 x 10(6) cfu ml-1 E. coli and 5 x 10(8) cfu ml-1 B. fragilis plus 1 mg of bran as faecal fibre analogue. The mean pH of the induced abscesses at week 1 was 6.7, higher than the pH associated with succinic acid inhibitory activity. We therefore determined the effect of succinic acid (0-100 mM) at pH 6.7 on the bactericidal activity of mouse bone marrow-derived neutrophils. Phagocytic killing of Proteus mirabilis by neutrophils was significantly inhibited by 30-100 mM succinic acid at pH 6.7 but there was no significant effect of succinic acid on engulfment of bacteria at this pH. However, significant inhibition of intracellular killing (assayed by adding succinic acid to suspensions of neutrophils which had engulfed bacteria in low serum concentrations but in the absence of succinic acid) was noted at 70 and 100 mM. These results indicate that succinic acid inhibits neutrophil bactericidal activity at a physiological pH, principally through inhibition of intracellular killing mechanisms and therefore contributing to bacterial persistence in this model of abscess formation.

Abdominal Abscess↗
PubMed2003

T-cell proliferative responses following sepsis in neonatal rats.

Both experimental and clinical evidence suggest a suppression of T-cell function in burn and sepsis. The objective of the present study was to evaluate splenocyte and purified T-cell proliferative response and IL-2 production in septic neonatal rats. We also examined if alterations in T-cell proliferation and IL-2 production in neonatal sepsis is due to elevation in PGE2. PGE2 is known to play a significant role in T-cell suppression during sepsis in adults. Sepsis was induced in 15-day-old neonatal Sprague-Dawley rats by implanting 0.1 cm3 of fecal pellet impregnated with Escherichia coli (50 CFU) and Bacteroides fragilis (10(3) CFU). Animals receiving fecal pellets without the bacteria were designated as sterile. A group of septic and sterile rats were treated with PGE2 synthesis inhibitors, NS398 and resveratrol. These treatments of animals allowed us to evaluate the role of PGE2 in T-cell suppression during neonatal sepsis. Splenocytes as well as purified T cells were prepared and then proliferative response and IL-2 productive capacities were measured. A significant suppression of splenocyte proliferation and IL-2 production was noticed in both sterile and septic animals compared to the T cells from unoperated control rats. In contrast, the proliferation and IL-2 production by nylon wool purified T cells in sterile rats was not significantly different from control rats, whereas, a significant suppression in Con A-mediated T-cell proliferation and IL-2 production noticed in septic rat T cells compared to the sterile and control rat T cells. Such decrease in T-cell proliferation and IL-2 production was accompanied with 20-25% deaths in neonates implanted with septic pellets. No mortality was noted in sterile-implanted neonates. Treatment of animals with COX-1 inhibitor had no effect on T-cell proliferation response in both septic and sterile groups, whereas COX-2 inhibitor abrogated the decrease in T-cell proliferative response in the septic group. The treatment of animals with COX-2 inhibitor also significantly prevented the sepsis-associated mortality in neonates. In conclusion, the present study demonstrated T-cell suppression during neonatal sepsis is accompanied by a decrease in IL-2 production. Such suppressions were ameliorated with COX-2 inhibitor suggesting a role for PGE2 in the suppressed T-cell-mediated immune function in neonatal sepsis.

Animals↗