Tuesday, February 27, 2007
Shewanella infection in decompensated liver disease: a septic case.
Shewanella infection in decompensated liver disease: a septic case.
J Gastroenterol. 2007 Jan
Otsuka T,
Noda T,
Noguchi A,
Nakamura H,
Ibaraki K,
Yamaoka K.
Department of Internal Medicine, Karatsu Red Cross Hospital, 1-5-1 Futago, Karatsu, Saga, 847-8588, Japan.
Shewanella species are an unusual cause of disease in humans. However, reports of Shewanella infections have been increasing, and hepatobiliary disease has been proposed as a predisposing factor following a critical course. We report the first Japanese septic case of decompensated liver disease in which this bacterium acted as a definite pathogen. A 67-year-old Japanese man with primary sclerosing cholangitis was admitted to our hospital complaining of fever, general fatigue, pain, and a rash on the lower left extremity. He was tentatively diagnosed with necrotizing fasciitis caused by Vibrio vulnificus because of his decompensated cirrhotic liver and history of consuming raw fish. Thereafter, the diagnosis was altered to cellulitis and Shewanella septicemia on the basis of the characteristics of his skin lesion and an arterial blood culture. He died of multiple organ failure on the eleventh day in the hospital. Since several reports have demonstrated that Shewanella can cause lethal sepsis in patients with hepatobiliary disease, we should be aware of the pathogenicity of this bacterium.
PMID: 17322999 Pub Med
RELATED:
Description of Shewanella glacialipiscicola sp. nov. and Shewanella algidipiscicola sp. nov., isolated from marine fish of the Danish Baltic Sea, and proposal that Shewanella affinis is a later heterotypic synonym of Shewanella colwelliana.
Int J Syst Evol Microbiol. 2007 Feb
Satomi M,
Vogel BF,
Venkateswaran K,
Gram L.
National Research Institute of Fisheries Science, Fisheries Research Agency, 2-12-4 Fukuura, Kanazawa-ku, Yokohama 236-8648, Japan.
Two novel species belonging to the genus Shewanella are described on the basis of a polyphasic taxonomic approach. A total of 40 strains of Gram-negative, psychrotolerant, H(2)S-producing bacteria were isolated from marine fish (cod and plaice) caught in the Baltic Sea off Denmark. Strains belonging to group 1 (seven strains) were a lactate-assimilating variant of Shewanella morhuae with a G+C content of 44 mol%. The strains of group 2 (33 strains) utilized lactate, N-acetylglucosamine and malate but did not produce DNase or ornithine decarboxylase. Their G+C content was 47 mol%. Phylogenetic analysis of the 16S rRNA gene sequence data placed the two novel species within the genus Shewanella. Group 1 showed greatest sequence similarity with S. morhuae ATCC BAA-1205(T) (99.9 %). However, gyrB gene sequence analysis and DNA-DNA hybridization differentiated these isolates from S. morhuae, with 95.6 % sequence similarity and less than 57 % DNA relatedness, respectively. Group 2 strains shared more than 99 % 16S rRNA gene sequence similarity with the type strains of Shewanella colwelliana and Shewanella affinis, but gyrB sequence similarity ( approximately 85 %) and the results of DNA hybridization ( approximately 28 %) indicated that the new isolates represented a novel species. Furthermore, when compared to each other, the type strains of S. colwelliana and S. affinis had almost identical gyrB sequences and significantly high DNA reassociation values (76-83 %), indicating that they belonged to the same species. Based on the conclusions of this study, we propose the novel species Shewanella glacialipiscicola sp. nov. (type strain T147(T)=LMG 23744(T)=NBRC 102030(T)) for group 1 strains and Shewanella algidipiscicola sp. nov. (type strain S13(T)=LMG 23746(T)=NBRC 102032(T)) for group 2 strains, and we propose that Shewanella affinis as a later heterotypic synonym of Shewanella colwelliana.
Full Text Article
J Gastroenterol. 2007 Jan
Otsuka T,
Noda T,
Noguchi A,
Nakamura H,
Ibaraki K,
Yamaoka K.
Department of Internal Medicine, Karatsu Red Cross Hospital, 1-5-1 Futago, Karatsu, Saga, 847-8588, Japan.
Shewanella species are an unusual cause of disease in humans. However, reports of Shewanella infections have been increasing, and hepatobiliary disease has been proposed as a predisposing factor following a critical course. We report the first Japanese septic case of decompensated liver disease in which this bacterium acted as a definite pathogen. A 67-year-old Japanese man with primary sclerosing cholangitis was admitted to our hospital complaining of fever, general fatigue, pain, and a rash on the lower left extremity. He was tentatively diagnosed with necrotizing fasciitis caused by Vibrio vulnificus because of his decompensated cirrhotic liver and history of consuming raw fish. Thereafter, the diagnosis was altered to cellulitis and Shewanella septicemia on the basis of the characteristics of his skin lesion and an arterial blood culture. He died of multiple organ failure on the eleventh day in the hospital. Since several reports have demonstrated that Shewanella can cause lethal sepsis in patients with hepatobiliary disease, we should be aware of the pathogenicity of this bacterium.
PMID: 17322999 Pub Med
RELATED:
Description of Shewanella glacialipiscicola sp. nov. and Shewanella algidipiscicola sp. nov., isolated from marine fish of the Danish Baltic Sea, and proposal that Shewanella affinis is a later heterotypic synonym of Shewanella colwelliana.
Int J Syst Evol Microbiol. 2007 Feb
Satomi M,
Vogel BF,
Venkateswaran K,
Gram L.
National Research Institute of Fisheries Science, Fisheries Research Agency, 2-12-4 Fukuura, Kanazawa-ku, Yokohama 236-8648, Japan.
Two novel species belonging to the genus Shewanella are described on the basis of a polyphasic taxonomic approach. A total of 40 strains of Gram-negative, psychrotolerant, H(2)S-producing bacteria were isolated from marine fish (cod and plaice) caught in the Baltic Sea off Denmark. Strains belonging to group 1 (seven strains) were a lactate-assimilating variant of Shewanella morhuae with a G+C content of 44 mol%. The strains of group 2 (33 strains) utilized lactate, N-acetylglucosamine and malate but did not produce DNase or ornithine decarboxylase. Their G+C content was 47 mol%. Phylogenetic analysis of the 16S rRNA gene sequence data placed the two novel species within the genus Shewanella. Group 1 showed greatest sequence similarity with S. morhuae ATCC BAA-1205(T) (99.9 %). However, gyrB gene sequence analysis and DNA-DNA hybridization differentiated these isolates from S. morhuae, with 95.6 % sequence similarity and less than 57 % DNA relatedness, respectively. Group 2 strains shared more than 99 % 16S rRNA gene sequence similarity with the type strains of Shewanella colwelliana and Shewanella affinis, but gyrB sequence similarity ( approximately 85 %) and the results of DNA hybridization ( approximately 28 %) indicated that the new isolates represented a novel species. Furthermore, when compared to each other, the type strains of S. colwelliana and S. affinis had almost identical gyrB sequences and significantly high DNA reassociation values (76-83 %), indicating that they belonged to the same species. Based on the conclusions of this study, we propose the novel species Shewanella glacialipiscicola sp. nov. (type strain T147(T)=LMG 23744(T)=NBRC 102030(T)) for group 1 strains and Shewanella algidipiscicola sp. nov. (type strain S13(T)=LMG 23746(T)=NBRC 102032(T)) for group 2 strains, and we propose that Shewanella affinis as a later heterotypic synonym of Shewanella colwelliana.
Full Text Article
Labels: necrotizing fasciitis, Shewanella infections, Shewanella septicemia, Vibrio vulnificus
# posted by Pat O'Connor @ 9:46 AM
Tuesday, February 20, 2007
Review article: bacterial flora and pathogenesis in hepatic encephalopathy
Review article: bacterial flora and pathogenesis in hepatic encephalopathy
Aliment Pharmacol Ther. 2007 Feb
Williams R.
The UCL Institute of Hepatology, Royal Free and University College Medical School, University College London, UK.
The aetiology of hepatic encephalopathy has not been conclusively established, but it is widely agreed that ammonia derived primarily from enteric bacterial flora plays a central role. Recent research on the pathogenesis of hepatic encephalopathy reinforces previous findings, supporting an integral role of bacteria-derived ammonia and reveals other potential mechanisms by which bacterial flora and pathogens may be pathophysiologically important. This review discusses this research and considers its implications for the therapeutic management of hepatic encephalopathy. Besides producing ammonia, the enteric flora generates other neurotoxic products, such as phenols and mercaptans, that may potentiate the effects of ammonia. Bacteria may also constitute a primary source of the benzodiazepine-like compounds implicated in neuropsychiatric symptoms in patients with liver disease. New evidence suggests that acute bacterial infections, long recognized as important precipitants of hepatic encephalopathy, may mediate clinical worsening through effects on systemic inflammatory responses. Considered together, these data suggest wide-ranging pathophysiological contributions of bacteria to hepatic encephalopathy and underline the potential for an integral role of antibiotics and other bactericidal agents in its management.
PMID: 17295848 [PubMed - in process]
RELATED:
Review article: the current pharmacological therapies for hepatic encephalopathy.
Aliment Pharmacol Ther. 2007 Feb
Bass NM.
University of California, San Francisco, CA, USA.
Effective treatment options for hepatic encephalopathy are limited. Based on the principle that intestinal-derived ammonia contributes to the pathogenesis of hepatic encephalopathy, current therapeutic approaches are directed at reducing bacterial production of ammonia and enhancing its elimination. Non-absorbable disaccharides are first-line therapy for hepatic encephalopathy, but published clinical studies evaluating their safety and efficacy are limited. Alternative therapies such as benzodiazepine receptor antagonists, branched-chain amino acids, and l-ornithine-l-aspartate also have limited clinical data supporting their use. Studies of antibiotics indicate that they are effective in the treatment of hepatic encephalopathy, but adverse effects and concerns about long-term safety have limited the widespread use of most. Rifaximin is a minimally absorbed antibiotic that concentrates in the gastrointestinal tract and is excreted mostly unchanged in faeces. It has been studied extensively in the treatment of hepatic encephalopathy and appears to confer therapeutic benefits greater than those of placebo and non-absorbable disaccharides and at least comparable with those of systemic antibiotics. Rifaximin was also well tolerated in patients with hepatic encephalopathy and is not associated with clinical drug interactions or clinically relevant bacterial antibiotic resistance. In conclusion, non-absorbed antibiotics such as rifaximin offer a favourable benefit-risk ratio in the treatment of hepatic encephalopathy and may help to improve patient outcomes.
PMID: 17295849 [PubMed - in process]
Aliment Pharmacol Ther. 2007 Feb
Williams R.
The UCL Institute of Hepatology, Royal Free and University College Medical School, University College London, UK.
The aetiology of hepatic encephalopathy has not been conclusively established, but it is widely agreed that ammonia derived primarily from enteric bacterial flora plays a central role. Recent research on the pathogenesis of hepatic encephalopathy reinforces previous findings, supporting an integral role of bacteria-derived ammonia and reveals other potential mechanisms by which bacterial flora and pathogens may be pathophysiologically important. This review discusses this research and considers its implications for the therapeutic management of hepatic encephalopathy. Besides producing ammonia, the enteric flora generates other neurotoxic products, such as phenols and mercaptans, that may potentiate the effects of ammonia. Bacteria may also constitute a primary source of the benzodiazepine-like compounds implicated in neuropsychiatric symptoms in patients with liver disease. New evidence suggests that acute bacterial infections, long recognized as important precipitants of hepatic encephalopathy, may mediate clinical worsening through effects on systemic inflammatory responses. Considered together, these data suggest wide-ranging pathophysiological contributions of bacteria to hepatic encephalopathy and underline the potential for an integral role of antibiotics and other bactericidal agents in its management.
PMID: 17295848 [PubMed - in process]
RELATED:
Review article: the current pharmacological therapies for hepatic encephalopathy.
Aliment Pharmacol Ther. 2007 Feb
Bass NM.
University of California, San Francisco, CA, USA.
Effective treatment options for hepatic encephalopathy are limited. Based on the principle that intestinal-derived ammonia contributes to the pathogenesis of hepatic encephalopathy, current therapeutic approaches are directed at reducing bacterial production of ammonia and enhancing its elimination. Non-absorbable disaccharides are first-line therapy for hepatic encephalopathy, but published clinical studies evaluating their safety and efficacy are limited. Alternative therapies such as benzodiazepine receptor antagonists, branched-chain amino acids, and l-ornithine-l-aspartate also have limited clinical data supporting their use. Studies of antibiotics indicate that they are effective in the treatment of hepatic encephalopathy, but adverse effects and concerns about long-term safety have limited the widespread use of most. Rifaximin is a minimally absorbed antibiotic that concentrates in the gastrointestinal tract and is excreted mostly unchanged in faeces. It has been studied extensively in the treatment of hepatic encephalopathy and appears to confer therapeutic benefits greater than those of placebo and non-absorbable disaccharides and at least comparable with those of systemic antibiotics. Rifaximin was also well tolerated in patients with hepatic encephalopathy and is not associated with clinical drug interactions or clinically relevant bacterial antibiotic resistance. In conclusion, non-absorbed antibiotics such as rifaximin offer a favourable benefit-risk ratio in the treatment of hepatic encephalopathy and may help to improve patient outcomes.
PMID: 17295849 [PubMed - in process]
Labels: bacterial flora, Hepatic encephalopathy, Non-absorbable disaccharides, pharmacological therapies, Rifaximin
# posted by Pat O'Connor @ 5:15 AM
Wednesday, February 14, 2007
Review article: bacterial flora and pathogenesis in hepatic encephalopathy.
Review article: bacterial flora and pathogenesis in hepatic encephalopathy.
Aliment Pharmacol Ther. 2007 Feb;25
Williams R.
The UCL Institute of Hepatology, Royal Free and University College Medical School, University College London, UK.
The aetiology of hepatic encephalopathy has not been conclusively established, but it is widely agreed that ammonia derived primarily from enteric bacterial flora plays a central role. Recent research on the pathogenesis of hepatic encephalopathy reinforces previous findings, supporting an integral role of bacteria-derived ammonia and reveals other potential mechanisms by which bacterial flora and pathogens may be pathophysiologically important. This review discusses this research and considers its implications for the therapeutic management of hepatic encephalopathy. Besides producing ammonia, the enteric flora generates other neurotoxic products, such as phenols and mercaptans, that may potentiate the effects of ammonia. Bacteria may also constitute a primary source of the benzodiazepine-like compounds implicated in neuropsychiatric symptoms in patients with liver disease. New evidence suggests that acute bacterial infections, long recognized as important precipitants of hepatic encephalopathy, may mediate clinical worsening through effects on systemic inflammatory responses. Considered together, these data suggest wide-ranging pathophysiological contributions of bacteria to hepatic encephalopathy and underline the potential for an integral role of antibiotics and other bactericidal agents in its management.
PMID: 17295848 [PubMed - in process]
***** RELATED ARTICLES *****
Management of hepatic encephalopathy in patients with cirrhosis.
Best Pract Res Clin Gastroenterol. 2007
Wright G,
Jalan R.
Liver Failure Group, The UCL Institute of Hepatology, Division of Medicine, University College London, 69-75 Chenies Mews, London WC1E 6HX, UK.
The term hepatic encephalopathy encompasses a spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction. Distinct syndromes are identified in acute liver failure and cirrhosis. Rapid deterioration in consciousness level and increased intracranial pressure that may result in brain herniation and death are a feature of acute liver failure whereas manifestations of hepatic encephalopathy in cirrhosis include psychomotor dysfunction, impaired memory, increased reaction time, sensory abnormalities, poor concentration and in severe forms, coma. In patients with acute-on-chronic liver failure the pathophysiology remains undefined. Ammonia has been considered central to its pathogenesis. In the brain, the astrocyte is the main site for ammonia detoxification, during the conversion of glutamate to glutamine. An increased ammonia level raises the amount of glutamine within astrocytes, causing an osmotic imbalance resulting in cell swelling and ultimately brain oedema. Recent studies suggest that inflammation and it modulators may play a synergistic role with ammonia in the pathogenesis of hepatic encephalopathy. Therapy of hepatic encephalopathy is directed primarily at reducing ammonia generation and increasing its detoxification. The currently accepted regimens to treat hepatic encephalopathy such as lactulose and protein restricted diets need further clinical trials and therefore placebo controlled clinical trials in hepatic encephalopathy are justified. In liver failure, ammonia metabolism involves multiple organs and therefore ammonia reduction will require simultaneous targeting of these organs. The present review describes the pathophysiological basis of hepatic encephalopathy and evaluates the available therapies.
Elsevier
--------------
Management of hepatic encephalopathy: role of rifaximin.
Zeneroli ML,
Avallone R,
Corsi L,
Venturini I,
Baraldi C,
Baraldi M.
Department of Medicine and Medical Specialities, University of Modena and Reggio Emilia, Modena, Italy. zeneroli.marialuisa@unimore.it
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome, which develops in patients with acute or chronic liver failure. It is widely accepted to be due to impairment of hepatic clearance of toxic products from the gut such as ammonia. Accumulation of ammonia induces a glutamate neurotoxicity leading to an increased tone of the gamma-aminobutyric acid A (GABA-A) receptor system in the brain which results in HE. Factors either increasing the ammonia levels (protein load, constipation, sepsis, or gastrointestinal bleeding) or potentiating the functional activity of the GABAergic system [natural benzodiazepine-like compounds (NBZDs) or exogenous benzodiazepines] may act as precipitating factors of HE. NBZDs are present in trace amounts in the blood of normal subjects and have been found to be increased in the blood of patients with liver cirrhosis, with or without HE. These compounds may derive either from the diet since they have been found in plants, vegetables and animals or from gut bacteria. The observation that intestinal bacterial flora is involved in the production of both primary agent of HE (ammonia) and precipitating factors (NBZDs) suggests that the use of nonabsorbable antibiotics such as rifaximin may be useful in preventing episodes of HE in patients with liver cirrhosis. Copyright (c) 2005 S. Karger AG, Basel.
Kargar
Aliment Pharmacol Ther. 2007 Feb;25
Williams R.
The UCL Institute of Hepatology, Royal Free and University College Medical School, University College London, UK.
The aetiology of hepatic encephalopathy has not been conclusively established, but it is widely agreed that ammonia derived primarily from enteric bacterial flora plays a central role. Recent research on the pathogenesis of hepatic encephalopathy reinforces previous findings, supporting an integral role of bacteria-derived ammonia and reveals other potential mechanisms by which bacterial flora and pathogens may be pathophysiologically important. This review discusses this research and considers its implications for the therapeutic management of hepatic encephalopathy. Besides producing ammonia, the enteric flora generates other neurotoxic products, such as phenols and mercaptans, that may potentiate the effects of ammonia. Bacteria may also constitute a primary source of the benzodiazepine-like compounds implicated in neuropsychiatric symptoms in patients with liver disease. New evidence suggests that acute bacterial infections, long recognized as important precipitants of hepatic encephalopathy, may mediate clinical worsening through effects on systemic inflammatory responses. Considered together, these data suggest wide-ranging pathophysiological contributions of bacteria to hepatic encephalopathy and underline the potential for an integral role of antibiotics and other bactericidal agents in its management.
PMID: 17295848 [PubMed - in process]
***** RELATED ARTICLES *****
Management of hepatic encephalopathy in patients with cirrhosis.
Best Pract Res Clin Gastroenterol. 2007
Wright G,
Jalan R.
Liver Failure Group, The UCL Institute of Hepatology, Division of Medicine, University College London, 69-75 Chenies Mews, London WC1E 6HX, UK.
The term hepatic encephalopathy encompasses a spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction. Distinct syndromes are identified in acute liver failure and cirrhosis. Rapid deterioration in consciousness level and increased intracranial pressure that may result in brain herniation and death are a feature of acute liver failure whereas manifestations of hepatic encephalopathy in cirrhosis include psychomotor dysfunction, impaired memory, increased reaction time, sensory abnormalities, poor concentration and in severe forms, coma. In patients with acute-on-chronic liver failure the pathophysiology remains undefined. Ammonia has been considered central to its pathogenesis. In the brain, the astrocyte is the main site for ammonia detoxification, during the conversion of glutamate to glutamine. An increased ammonia level raises the amount of glutamine within astrocytes, causing an osmotic imbalance resulting in cell swelling and ultimately brain oedema. Recent studies suggest that inflammation and it modulators may play a synergistic role with ammonia in the pathogenesis of hepatic encephalopathy. Therapy of hepatic encephalopathy is directed primarily at reducing ammonia generation and increasing its detoxification. The currently accepted regimens to treat hepatic encephalopathy such as lactulose and protein restricted diets need further clinical trials and therefore placebo controlled clinical trials in hepatic encephalopathy are justified. In liver failure, ammonia metabolism involves multiple organs and therefore ammonia reduction will require simultaneous targeting of these organs. The present review describes the pathophysiological basis of hepatic encephalopathy and evaluates the available therapies.
Elsevier
--------------
Management of hepatic encephalopathy: role of rifaximin.
Zeneroli ML,
Avallone R,
Corsi L,
Venturini I,
Baraldi C,
Baraldi M.
Department of Medicine and Medical Specialities, University of Modena and Reggio Emilia, Modena, Italy. zeneroli.marialuisa@unimore.it
Hepatic encephalopathy (HE) is a neuropsychiatric syndrome, which develops in patients with acute or chronic liver failure. It is widely accepted to be due to impairment of hepatic clearance of toxic products from the gut such as ammonia. Accumulation of ammonia induces a glutamate neurotoxicity leading to an increased tone of the gamma-aminobutyric acid A (GABA-A) receptor system in the brain which results in HE. Factors either increasing the ammonia levels (protein load, constipation, sepsis, or gastrointestinal bleeding) or potentiating the functional activity of the GABAergic system [natural benzodiazepine-like compounds (NBZDs) or exogenous benzodiazepines] may act as precipitating factors of HE. NBZDs are present in trace amounts in the blood of normal subjects and have been found to be increased in the blood of patients with liver cirrhosis, with or without HE. These compounds may derive either from the diet since they have been found in plants, vegetables and animals or from gut bacteria. The observation that intestinal bacterial flora is involved in the production of both primary agent of HE (ammonia) and precipitating factors (NBZDs) suggests that the use of nonabsorbable antibiotics such as rifaximin may be useful in preventing episodes of HE in patients with liver cirrhosis. Copyright (c) 2005 S. Karger AG, Basel.
Kargar
Labels: Ammonia, bacterial flora, Benzodiazepines, endogenous, Hepatic encephalopathy, Liver cirrhosis, neuropsychiatric syndrome, Rifaximin
# posted by Pat O'Connor @ 7:57 AM
Friday, February 09, 2007
A case of prostatitis due to Burkholderia pseudomallei.
A case of prostatitis due to Burkholderia pseudomallei.
Nat Clin Pract Urol. 2007 Feb
Arzola JM,
Hawley JS,
Oakman C,
Mora RV.
Wilford Hall Medical Center, Urology, 8423 Feather Trail, Helotes, TX 78023, USA. jorge.arzola@lackland.af.mil
Burkholderia fungorum. From DOE Joint Genome Institute
BACKGROUND: A 67-year-old male, with a history of stable lower urinary tract symptoms, diabetes mellitus, benign prostatic hyperplasia, gonococcal urethritis, and excessive alcohol consumption, presented to the emergency room with sepsis and acute bacterial prostatitis. He had recently returned from a visit to Indonesia, where he had been a first-hand witness to the 2004 tsunami.
INVESTIGATIONS: Complete blood cell count, urine analysis, blood, urine, and prostatic abscess cultures, chest X-ray, contrasted CT of the abdomen and pelvis, and (18)F-fluorodeoxyglucose PET.
DIAGNOSIS: Melioidosis.
MANAGEMENT: Broad-spectrum empiric antibiotics were administered initially; therapy was then changed to intravenous imipenem plus cilastatin with slow initial clinical improvement. (18)F-fluorodeoxyglucose PET localized the prostate as the only nidus of infection. Ultrasound-guided fine needle aspiration of a small fluid collection of the prostate also grew Burkholderia pseudomallei. The patient improved clinically and was discharged to complete a 2-week course of intravenous imipenem plus cilastatin followed by a 3-month course of oral trimethoprim plus sulfamethoxazole. This medication was switched to co-amoxiclav and doxycycline to complete the 3-month course. The patient was well at his last follow-up, 3 months following hospital discharge.
PMID: 17287872 [PubMed - in process]
Related Article:
Burkholderia
Classification
Higher order taxa:
Bacteria; Proteobacteria; Betaproteobacteria; Burkholderiales; Burkholderiaceae
Species:
Burkholderia andropogonis; Burkholderia brasilensis; Burkholderia caledonica; Burkholderia caribensis; Burkholderia caryophylli; Burkholderia fungorum; Burkholderia gladioli; Burkholderia glathei; Burkholderia glumae; Burkholderia graminis; Burkholderia hospita; Burkholderia kururiensis; Burkholderia mallei; Burkholderia phenazinium; Burkholderia phymatum; Burkholderia phytofirmans; Burkholderia plantarii; Burkholderia sacchari; Burkholderia singaporensis; Burkholderia sordidicola; Burkholderia symbiont of Asellus aquaticus; Burkholderia terricola; Burkholderia tropica; Burkholderia tuberum; Burkholderia ubonensis; Burkholderia unamae; Burkholderia xenovorans; Burkholderia sp.; Burkholderia cepacia complex: Burkholderia ambifaria; Burkholderia anthina; Burkholderia cenocepacia; Burkholderia cepacia; Burkholderia dolosa; Burkholderia multivorans; Burkholderia pyrrocinia; Burkholderia stabilis; Burkholderia vietnamiensis
Description and Significance
Burkholderia bacteria are both human and plant pathogens as well as environmentally important bacteria. Burkholderia fungorum strain LB400 and other closely related Burkhoderia strains are good biodegraders of polychlorinated biphenyls (PCBs) with "unparalleled ability to destroy environmentally important PCB congeners" (DOE). Conversely, Burkholderia pseudomallei is the causative agent of melioidosis, as disease that harms both humans and animals, as well as septicemia and pneumonia in susceptible individuals (Godoy et al. 2003).
Genome Structure
Burkholderia fungorum is presently being sequenced by the DOE Joint Genome Institute. It has three large replicons (chromosomes) and a megaplasmid with a total of 8.1 Mb. Apparently, the large size of genomic material, which is among the larges of the soil bacteria known, may contribute to its "ecological success." Because this and related PCB-degrading bacteria have such important ecological and commerical potential for bioremediation technologies, sequencing this genome will be extremely important in shedding light on the mechanisms and organization responsible for the group's metabolic and environmental versatility. This knowledge will allow new development of "novel environmental remediation technologies and products for plant growth promotion" (DOE).
Cell Structure and Metabolism
Burkholderia bacteria are rod-shaped, motile, Gram-negative bacteria that are capable of both pathogenic characteristics and degrading PCBs. The bacteria are also generally obligately aerobic. Of the bacterial isolates found in the Arctic that are able to degrade PCBs, none used compounds such as 2-chlorobiphenyl, 3-chlorobiphenyl, camphor, citronellol, cymene, dehydroabietic acid, limonene, methanol, n-hexadecane, pentachlorophenol, phenol, or pinene as primary growth substrates (Master and Mohn 1998).
Ecology
Burkholderia bacteria are commonly found in the soil and in groundwater worldwide. Burkholderia and related bacteria have been found at soils of all tempuratures including Arctic soil of 7oC.
Pathology
Burkholderia pseudomallei is generally considered a saprophyte (grows on and uses dead or decaying organic matter as an energy source), it also causes the infectious disease melioidosis that is mostly restricted to Southeast Asia, northern Australia, and some other tropical and subtropical regions. It also occasionally causes serious invasive diseases like septicemia and pneumonia in susceptible individuals. Although the epidemiology of melioidosis is not yet fully understood, it is thought that infections are contracted by contact with the organism from contaminated ground water ("for example, in rice paddies") through puncture wounds, cuts, or abrasions in the skin (Godoy et al. 2003). Burkholderia mallei, which is very closely related to B. pseudomallei, causes glanders in horses and other equines and occasionally in humans and other animals. This disease is generally found in parts of Africa, Asia, the Middle East, and Central and South America. The human B. mallei infection is very close to an infection of B. pseudomallei (Godoy et al. 2003). In horses, the bacterial acute infection causes the development of "rapidly spreading ulcers in skin and nasal mucosa" as well as "death within a few days from septicaemia" (VEIN). The chronic disease caused by B. mallei, which is more common, results in lesions and pulmonary involvement. It can manifest in nasal form, skin form, or both nasal and skin form at the same time. Both of B. mallei and B. pseudomallei are considered potential agents of biological warfare or bioterrorism -- CDC lists them in category B of the list of bioterrorism agents (Godoy et al. 2003) . In addition to all this, Burkholderia cepacia is a pathogen associated with chronic lung disease in cystic fibrosis patients (Kiska et al. 1995).
References
General:
DOE Joint Genome Institute: Burkholderia fungorum
Godoy, Daniel, Gaynor Randle, Andrew J. Simpson, David M. Aanensen, Tyrone L. Pitt, Reimi Kinoshita, and Brian G. Spratt. 2003. "Multilocus sequence typing and evolutionary relationships among the causative agents of melioidosis and glanders, Burkholderia pseudomallei and Burkholderia mallei." Journal of Clinical Microbiology, vol. 41, no. 5. American Society for Microbiology. (2068-2079)
Master, Emma R. and William W. Mohn. 1998. "Psychrotolerant bacteria isolated from Arctic soil that degrade polychlorinated biphenyls at low tempuratures." Applied and Environmental Microbiology, vol. 64, no. 12. American Society for Microbiology. (4823-4829)
Pathology
Veterinary Education and Information Network: Exotic Diseases: Dermatolotical Diseases: Glanders
Microbe Wiki
Labels: Bacteria; Proteobacteria; Betaproteobacteria; Burkholderiales; Burkholderiaceae
# posted by Pat O'Connor @ 8:18 AM
Tuesday, February 06, 2007
Bacterial isolates from severe infections and their antibiotic susceptibility patterns in Italy: a nationwide study in the hospital setting.
Bacterial isolates from severe infections and their antibiotic susceptibility patterns in Italy: a nationwide study in the hospital setting.
J Chemother. 2006 Dec;18
Nicoletti G,
Schito G,
Fadda G,
Boros S,
Nicolosi D,
Marchese A,
Spanu T,
Pantosti A,
Monaco M,
Rezza G,
Cassone A,
Garaci E,
Gruppo Cooperativo Infezioni Gravi Ed Antibiotico Resistenza FT.
The most frequent agents of severe bacterial infections and their antibiotic susceptibility patterns were determined in patients admitted to 45 Italian hospitals over the years 2002-2003. The most common diagnoses were: sepsis (33.8%), pneumonia (9.4%), intravascular catheter-associated infections (9.3%) and ventilator-associated pneumonia (8.1%). Overall, 5115 bacterial isolates were identified from 4228 patients. Three bacterial species, Staphylococcus aureus, Pseudomonas aeruginosa and Escherichia coli, accounted for more than 50% of the isolates. Other prevalent bacterial isolates were Staphylococcus epidermidis and Enterococcus faecalis, while Acinetobacter baumanii ranked third among all Intensive Care Unit (ICU) isolates. 7% of S. aureus had intermediate resistance to vancomycin. Although E.faecalis displayed no vancomycin resistance, 34% of vancomycin-resistant isolates were found among Enterococcus faecium, one of the highest rates found to date, emphasizing the difference between these two enterococcal species. All the Gram-positive pathogens were susceptible to linezolid, with the exception of approximately 2% of the enterococcal isolates that were intermediate with a minimum inhibitory concentration (MIC)=4 microg/ml. Almost 10% of Escherichia coli, 14% of Klebsiella pneumoniae, 22% of Serratia marcescens and 50% of Enterobacter cloacae were non-susceptible to cefotaxime. Amikacin was the most active antibiotic against P. aeruginosa that showed lack of susceptibility to ceftazidime, gentamicin, piperacillin and ciprofloxacin ranging from 20 to 35%. Finally, Acinetobacter baumanii showed a high level of resistance to all the antibiotics tested including imipenem (58%). The results obtained in this study, the first of its kind in Italy, offer indications for guiding empirical therapy and implementing specific interventions to fight antibiotic-resistant bacterial infections and their transmission in the hospital setting in Italy.
PMID: 17267336 [PubMed - in process]
Labels: acinetobacter, cefotaxime, ciprofloxan, enterococcus, escherichia coli, gentamicin, klebsiella pneumoniae, p.aeruginosa, piperacillan, staphylococcus epidermidis, vancomycin
# posted by Pat O'Connor @ 5:22 AM
