IntroductionEwingella americana is a gram negative rod, and the only species in the genus Ewingella. It was first identified and characterized in 1983. Ewingella is in the family Enterobacteriaceae. The organism is rarely reported as a human pathogen, though it has been isolated from a variety of clinical specimens including wound, sputum, urine, stool, blood, conjunctiva and peritoneal dialysate.[1] The bacterium is named in honor of William H. Ewing, an American biologist who contributed to modern taxonomy.
[edit] EpidemiologyRespiratory tract infections following retainment in intensive care units has been observed in several instances. Vascular bypass surgery is a reported risk factor for colonization.[2][3] Debate currently exists as to this organism's predilection for immunocompromised patients.[4]
[edit] Pathophysiology and BiochemistryE. americana is an organism with simple nutritional needs that can survive in water and citrate solution and preferentially grows at 4°C. Domestic sources of water including air conditioning units, ice baths and wound irrigation systems have been cited as sources of infection.[5]
[edit] References1.^ Nam-Hee Ryoo, Jung-Sook Ha, Dong-Seok Jeon, Jae-Ryong Kim, Hyun-Chul Kim. (2005). "A Case of Pneumonia Caused by Ewingella americana in a Patient with Chronic Renal Failure.". J Korean Med Sci 20: 143–5. doi:10.3346/jkms.2005.20.1.143. ISSN 1011-8934. PMC 2808562. PMID 15716620.
2.^ Bear, N., K. P. Klugman, L. Tobiansky, and H. J. Koornhof. (1986). "Wound colonization by Ewingella americana.". J. Clin. Microbiol. 23 (3): 650–651. PMC 268717. PMID 3958154.
3.^ Devreese, K., G. Claeys, and G. Verschraegen. (1992). "Septicemia with Ewingella americana.". J. Clin. Microbiol. 30 (10): 2746–2747. PMC 270514. PMID 1400980.
4.^ Heizmann, W. R., and R. Michel. (1991). "Isolation of Ewingella americana from a patient with conjunctivitis.". Eur. J. Clin. Microbiol. Infect. Dis. 10 (11): 957–959. PMID 1794367.
5.^ Farmer, J. J., III, B. R. Davis, F. W. Hickman-Brenner, A. Mc-Whorther, G. P. Huntley-Carter, M. A. Asbury, C. Riddle, H. J. Wathern-Grady, C. Elias, G. R. Fanning, A. G. Steigerwalt, C. M. O’Hara, G. K. Morris, P. B. Smith, and D. J. Brenner. (1985). "Biochemical identification of new species and biogroups of Enterobacteriaceae isolated from clinical specimens.". J. Clin. Microbiol. 21 (1): 46–76. PMC 271578. PMID 3881471.
Retrieved from "http://en.wikipedia.org/wiki/Ewingella_americana" Acessado em 05/08/11
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Ralstonia pickettii
Ralstonia pickettii
From MicrobeWiki, the student-edited microbiology resource
Classification
Bacteria; Proteobacteria; Beta Proteobacteria; Burkholderiales; Ralstoniaceae
Ralstonia Picketti
NCBI: Taxonomy
Ralstonia Pickettii
Synonyms: Burkholderia picketti, Burkholderia solanacearum, Alcaligenes eutrophus
Strains: 12J,12D
Description and Significance
Ralstonia pickettii is a gram-negative, rod shaped beta proteobacteria found in moist environments such as soils, river and lakes [2]. It has also been identified in biofilms in plastic water pipes [1]. It is an olgiotrophic organism, making it capable of surviving in areas with a very low concentration of nutrients [1]. Several strains have shown an ability to survive in environments highly contaminated with metals such as Copper (Cu), Nickel (Ni), Iron (Fe) and Zinc (Zn). The ability to persist in these harsh conditions makes R. picketti a unique candidate for bioremediation. In a study done by Fett et al., R. pickettii was shown to be resistant to environments with up to 1200 µg/mL of Cu, surviving by using phosphates to sequester the metal [3].
Genome Structure
There are two separate strains of Ralstonia pickettii, 12 D and 12 J of sizes 3.5 Mb and 3.0 Mb respectively [7]. While their rRNA sequence is indentical, there are significant differences in their genomic structures [7]. The 12 D strain contains two circular chromosomes 3,647,724bp and 1,323,321 bp in size; as well as three circular plasmids 389,779 bp, 273,136 bp and 51,398 bp in size [8]. The 12 J strand also consists of two circular chromosomes 3,942,557 bp and 1,302,228 bp in size; but has only one circular plasmid that is 80,934 bp in size [9].
Cell Structure and Metabolism
Ralstonia pickettii is a gram-negative rod shaped bacteria. These bacteria are culturable in the lab and often form dense dark white colonies. It is strictly an aerobe and is not capable of fermentive respiration [4]. As a chemoheterotroph it depends on an outside carbon source for cell growth, meaning that in remediation, biostimulation can result in increased results of disposing of the pollutant [1]. And, as a siderophore, R. pickettii thrives in environments containing high levels of Iron, and is capable of sollublizing Fe3+ [5]. R. pickettii can also break down several aromatic hydrocarbons or volatile organic compounds (VOC’s) such as cresol (C7H8O), phenol (C6H5OH) and toluene (C7H8). These chemical compounds are commonly found in household products including antiseptics, germicides and cleaners. They are hazardous to the environment, and often accumulate to toxic levels in soil and groundwater [1]. R. pickettii is able to exploit this resource by using the hydrocarbons as both a source of carbon and energy. This process is achieved through a series of multi-enzyme pathways, including the Tbu pathway which converts aromatic hydrocarbons to catechols [1]. Another distinguishing feature of this bacteria is that is can metabolize aromatic hydrocarbons in hypoxic environments. Unlike other toluene metabolizing bacteria, R. pickettii can break down toluene even when oxygen levels are only 25% of air-saturated water [1].
Pathogenesis
Ralstonia pickettii pathology does not follow an easy definition; although no fully healthy human has ever become ill from R. pickettii, the bacteria has seriously affected humans with poor health. Several hospitals have reported outbreaks - in particular, patients with cystic fibrosis and Crohn’s Disease have been shown to be infected R. pickettii [2]. Of the 55 reported cases of infection by R. pickettii, the majority are due to contaminated solutions such as water, saline and sterile drugs [6]. These solutions are usually contaminated when the product is manufactured, due to the fact that R. pickettii has the ability to pass through 0.45 and 0.2mm filters that are used to stearilize medicinal products [6]. As a result when given as a drip solution, intravenously, or for endotracheal suctioning these contaminated solutions often lead infection in both the blood stream and the respiratory system [6].
Ecology and Biotechnology
The ability of Ralstonia pickettii to withstand high metal concentrations led to multiple test to determine if the bacteria could be used for bioremediation. The fact that R. pickettii grows easily in so many environments and does act as a pathogen makes it a great option. In vitro tests have shown that through biostimulation, R. pickettii was capable of degrading such contaminates as TCE and aromatic hydrocarbons [1]. The PKO1 strain has a future to be a great biodegrader as it was capable of remediating several pollutants [1]. The LD1 strain showed the ability to degrade chlorinated phenolic compounds [1]. These CPC’s were frequently used, as pesticides are an extremely common contaminate [1].
References
1. Adley C, Pembroke J, Ryan M. (Feb 2007) Ralstonia pickettii in environmental biotechnology potential and applications. Journal of Applied Microbiolgy. Vol 103. pp 754-764.
2. Coenye T, De Vos P, Goris J, Vandamme P. (2003). Classification of Ralstonia pickettii-like isolates from the environment and clinical samples as Ralstonia insidiosa. International Journal of Systematic and Evolutionary Microbiology. Vol 53. 2003 pp 1075-1080
3. Fett J, Konstantinidis K, Isaacs N, Long D, Marsh T. (Feb 2003).Microbial Diversity and Resistance to Copper in Metal-Contaminated Lake Sediment. Microbial Ecology. Vol 45. Feb 2003. pp 191-202
4. Buckner D, Colona P. (Jul 1997) Nomenclature for Aerobic and Facultative Bacteria. Clinical Infectious Diseases. Vol 25. pp 1-10
5. Biebl M, Bonatti H, Eller M, Fille M, Hoeller E, Lass-Floerl C, Stelzmueller I, Weiss G. (2006) Ralstonia pickettii-innocent bystander or a potential threat?. Clinical Microbial Infect. Vol 12. pp 99-101
6. Ryan, M. P., J. T. Pembroke, and C. C. Adley. (2006) Ralstonia Pickettii: a Persistent Gram-negative Nosocomial Infectious Organism." Journal of Hospital Infection Vol 62. March 2006. pp278-84.
7. "Ralstonia Pickettii." JGI Genome Portal - Home. Web. 25 Apr. 2010..
8. "HAMAP: Ralstonia Pickettii (strain 12D) Complete Proteome." ExPASy Proteomics Server. Swiss Institute for Bioinformatics. Web. 25 Apr. 2010..
9. "HAMAP: Ralstonia Pickettii (strain 12J) Complete Proteome." ExPASy Proteomics Server. Swiss Institute for Bioinformatics. Web. 25 Apr. 2010..
Author
Page authored by Jeff Eggleston and Sarah Dionne, students of Prof. Jay Lennon at Michigan State University.
REF: http://microbewiki.kenyon.edu/index.php/Ralstonia_pickettii Acessado em 09/05/2011
From MicrobeWiki, the student-edited microbiology resource
Classification
Bacteria; Proteobacteria; Beta Proteobacteria; Burkholderiales; Ralstoniaceae
Ralstonia Picketti
NCBI: Taxonomy
Ralstonia Pickettii
Synonyms: Burkholderia picketti, Burkholderia solanacearum, Alcaligenes eutrophus
Strains: 12J,12D
Description and Significance
Ralstonia pickettii is a gram-negative, rod shaped beta proteobacteria found in moist environments such as soils, river and lakes [2]. It has also been identified in biofilms in plastic water pipes [1]. It is an olgiotrophic organism, making it capable of surviving in areas with a very low concentration of nutrients [1]. Several strains have shown an ability to survive in environments highly contaminated with metals such as Copper (Cu), Nickel (Ni), Iron (Fe) and Zinc (Zn). The ability to persist in these harsh conditions makes R. picketti a unique candidate for bioremediation. In a study done by Fett et al., R. pickettii was shown to be resistant to environments with up to 1200 µg/mL of Cu, surviving by using phosphates to sequester the metal [3].
Genome Structure
There are two separate strains of Ralstonia pickettii, 12 D and 12 J of sizes 3.5 Mb and 3.0 Mb respectively [7]. While their rRNA sequence is indentical, there are significant differences in their genomic structures [7]. The 12 D strain contains two circular chromosomes 3,647,724bp and 1,323,321 bp in size; as well as three circular plasmids 389,779 bp, 273,136 bp and 51,398 bp in size [8]. The 12 J strand also consists of two circular chromosomes 3,942,557 bp and 1,302,228 bp in size; but has only one circular plasmid that is 80,934 bp in size [9].
Cell Structure and Metabolism
Ralstonia pickettii is a gram-negative rod shaped bacteria. These bacteria are culturable in the lab and often form dense dark white colonies. It is strictly an aerobe and is not capable of fermentive respiration [4]. As a chemoheterotroph it depends on an outside carbon source for cell growth, meaning that in remediation, biostimulation can result in increased results of disposing of the pollutant [1]. And, as a siderophore, R. pickettii thrives in environments containing high levels of Iron, and is capable of sollublizing Fe3+ [5]. R. pickettii can also break down several aromatic hydrocarbons or volatile organic compounds (VOC’s) such as cresol (C7H8O), phenol (C6H5OH) and toluene (C7H8). These chemical compounds are commonly found in household products including antiseptics, germicides and cleaners. They are hazardous to the environment, and often accumulate to toxic levels in soil and groundwater [1]. R. pickettii is able to exploit this resource by using the hydrocarbons as both a source of carbon and energy. This process is achieved through a series of multi-enzyme pathways, including the Tbu pathway which converts aromatic hydrocarbons to catechols [1]. Another distinguishing feature of this bacteria is that is can metabolize aromatic hydrocarbons in hypoxic environments. Unlike other toluene metabolizing bacteria, R. pickettii can break down toluene even when oxygen levels are only 25% of air-saturated water [1].
Pathogenesis
Ralstonia pickettii pathology does not follow an easy definition; although no fully healthy human has ever become ill from R. pickettii, the bacteria has seriously affected humans with poor health. Several hospitals have reported outbreaks - in particular, patients with cystic fibrosis and Crohn’s Disease have been shown to be infected R. pickettii [2]. Of the 55 reported cases of infection by R. pickettii, the majority are due to contaminated solutions such as water, saline and sterile drugs [6]. These solutions are usually contaminated when the product is manufactured, due to the fact that R. pickettii has the ability to pass through 0.45 and 0.2mm filters that are used to stearilize medicinal products [6]. As a result when given as a drip solution, intravenously, or for endotracheal suctioning these contaminated solutions often lead infection in both the blood stream and the respiratory system [6].
Ecology and Biotechnology
The ability of Ralstonia pickettii to withstand high metal concentrations led to multiple test to determine if the bacteria could be used for bioremediation. The fact that R. pickettii grows easily in so many environments and does act as a pathogen makes it a great option. In vitro tests have shown that through biostimulation, R. pickettii was capable of degrading such contaminates as TCE and aromatic hydrocarbons [1]. The PKO1 strain has a future to be a great biodegrader as it was capable of remediating several pollutants [1]. The LD1 strain showed the ability to degrade chlorinated phenolic compounds [1]. These CPC’s were frequently used, as pesticides are an extremely common contaminate [1].
References
1. Adley C, Pembroke J, Ryan M. (Feb 2007) Ralstonia pickettii in environmental biotechnology potential and applications. Journal of Applied Microbiolgy. Vol 103. pp 754-764.
2. Coenye T, De Vos P, Goris J, Vandamme P. (2003). Classification of Ralstonia pickettii-like isolates from the environment and clinical samples as Ralstonia insidiosa. International Journal of Systematic and Evolutionary Microbiology. Vol 53. 2003 pp 1075-1080
3. Fett J, Konstantinidis K, Isaacs N, Long D, Marsh T. (Feb 2003).Microbial Diversity and Resistance to Copper in Metal-Contaminated Lake Sediment. Microbial Ecology. Vol 45. Feb 2003. pp 191-202
4. Buckner D, Colona P. (Jul 1997) Nomenclature for Aerobic and Facultative Bacteria. Clinical Infectious Diseases. Vol 25. pp 1-10
5. Biebl M, Bonatti H, Eller M, Fille M, Hoeller E, Lass-Floerl C, Stelzmueller I, Weiss G. (2006) Ralstonia pickettii-innocent bystander or a potential threat?. Clinical Microbial Infect. Vol 12. pp 99-101
6. Ryan, M. P., J. T. Pembroke, and C. C. Adley. (2006) Ralstonia Pickettii: a Persistent Gram-negative Nosocomial Infectious Organism." Journal of Hospital Infection Vol 62. March 2006. pp278-84.
7. "Ralstonia Pickettii." JGI Genome Portal - Home. Web. 25 Apr. 2010.
8. "HAMAP: Ralstonia Pickettii (strain 12D) Complete Proteome." ExPASy Proteomics Server. Swiss Institute for Bioinformatics. Web. 25 Apr. 2010.
9. "HAMAP: Ralstonia Pickettii (strain 12J) Complete Proteome." ExPASy Proteomics Server. Swiss Institute for Bioinformatics. Web. 25 Apr. 2010.
Author
Page authored by Jeff Eggleston and Sarah Dionne, students of Prof. Jay Lennon at Michigan State University.
REF: http://microbewiki.kenyon.edu/index.php/Ralstonia_pickettii Acessado em 09/05/2011
quarta-feira, 13 de abril de 2011
Bacterioides
Bacteroides species are anaerobic bacteria that are predominant components of the bacterial florae of mucous membranes[1] and are therefore a common cause of endogenous infections. Bacteroides infections can develop in all body sites, including the CNS, the head, the neck, the chest, the abdomen, the pelvis, the skin, and the soft tissues. Inadequate therapy against these anaerobic bacteria may lead to clinical failure.
Because of their fastidiousness, they are difficult to isolate and are often overlooked. Their isolation requires appropriate methods of collection, transportation, and cultivation of specimens.[2] Treatment is complicated by 3 factors: slow growth, increasing resistance to antimicrobial agents,[3] and the polymicrobial synergistic nature of the infection.[4]
The B fragilis group, a member of the Bacteroidaceae family, includes B fragilis (causes the most clinical infections), Bacteroides distasonis, Bacteroides ovatus, Bacteroides thetaiotaomicron, and Bacteroides vulgatus. These bacteria are resistant to penicillins, mostly through the production of beta-lactamase. They are part of the normal GI florae[1] and predominate in intra-abdominal infections and infections that originate from those florae (eg, perirectal abscesses, decubitus ulcers). Enterotoxigenic B fragilis (ETBF) is also a potential cause of diarrhea.[5]
Pigmented Prevotella, such as Prevotella melaninogenica and Prevotella intermedia (which were previously called the Bacteroides melaninogenicus group), Porphyromonas (eg, Porphyromonas asaccharolytica), and nonpigmented Prevotella (eg, Prevotella oralis, Prevotella oris) are part of the normal oral and vaginal florae and are the predominant AGNB isolated from respiratory tract infections and their complications, including aspiration pneumonia, lung abscess, chronic otitis media, chronic sinusitis, abscesses around the oral cavity, human bites, paronychia, brain abscesses, and osteomyelitis. Prevotella bivia and Prevotella disiens (previously called Bacteroides) are important in obstetric and gynecologic infections
REF: http://emedicine.medscape.com/article/233339-overview Access: 13,apr,2011
Bacteroides Infection
Author: Itzhak Brook, MD, MSc; Chief Editor: Burke A Cunha, MD
Bacteroides is a genus of Gram-negative, bacillus bacteria. Bacteroides species are non-endospore-forming, anaerobes, and may be either motile or non-motile, depending on the species.[1] The DNA base composition is 40-48% GC. Unusual in bacterial organisms, Bacteroides membranes contain sphingolipids. They also contain meso-diaminopimelic acid in their peptidoglycan layer.
Bacteroides are normally mutualistic, making up the most substantial portion of the mammalian gastrointestinal flora,[2] where they play a fundamental role in processing of complex molecules to simpler ones in the host intestine.[3][4][5] As many as 1010-1011 cells per gram of human feces have been reported.[6] They can use simple sugars when available, but the main source of energy is polysaccharides from plant sources.
One of the most important clinically is Bacteroides fragilis.
Bacteroides melaninogenicus has recently been reclassified and split into Prevotella melaninogenica and Prevotella intermedia.[7]
PathogenesisBacteroides species also benefit their host by excluding potential pathogens from colonizing the gut. Some species (B. fragilis, for example) are opportunistic human pathogens, causing infections of the peritoneal cavity, gastrointestinal surgery, and appendicitis via abscess formation, inhibiting phagocytosis, and inactivating beta-lactam antibiotics.[8] Although Bacteroides species are anaerobic, they are aerotolerant and thus can survive in the abdominal cavity.
In general, Bacteroides are resistant to a wide variety of antibiotics — β-lactams, aminoglycosides, and recently many species have acquired resistance to erythromycin and tetracycline. This high level of antibiotic resistance has prompted concerns that Bacteroides species may become a reservoir for resistance in other, more highly-pathogenic bacterial strains.[9] [10]
Microbiological ApplicationsAn alternative fecal indicator organism, Bacteroides, has been suggested because they make up a significant portion of the fecal bacterial population[11], have a high degree of host specificity that reflects differences in the digestive system of the host animal[12], and have a small potential to grow in the environment[13]. Over the past decade, real-time polymerase chain reaction (PCR) methods have been utilized to detect the presence of various microbial pathogens through the amplification of specific DNA sequences without culturing bacteria. One study has measured the amount of Bacteroides by using qPCR to quantify the 16S rRNA genetic marker that is host-specific.[14] This technique allows quantification of genetic markers that are specific to the host of the bacteria and allow detection of recent contamination. A recent report found that temperature plays a major role in the amount of time the bacteria will persist in the environment, the life span increases with colder temperatures
References1.^ Madigan M, Martinko J (editors). (2005). Brock Biology of Microorganisms (11th ed.). Prentice Hall. ISBN 0-13-144329-1.
2.^ Dorland WAN (editor) (2003). Dorland's Illustrated Medical Dictionary (30th ed.). W.B. Saunders. ISBN 0-7216-0146-4.
3.^ Wexler, H. M. (Oct 2007). "Bacteroides: the good, the bad, and the nitty-gritty" (Free full text). Clinical microbiology reviews 20 (4): 593–621. doi:10.1128/CMR.00008-07. ISSN 0893-8512. PMC 2176045. PMID 17934076. http://cmr.asm.org/cgi/pmidlookup?view=long&pmid=17934076. edit
4.^ Xu, J.; Gordon, I. (Sep 2003). "Inaugural Article: Honor thy symbionts" (Free full text). Proceedings of the National Academy of Sciences of the United States of America 100 (18): 10452–10459. doi:10.1073/pnas.1734063100. ISSN 0027-8424. PMC 193582. PMID 12923294. http://www.pnas.org/cgi/pmidlookup?view=long&pmid=12923294. edit
5.^ Xu, J.; Mahowald, A.; Ley, E.; Lozupone, A.; Hamady, M.; Martens, C.; Henrissat, B.; Coutinho, M. et al. (Jul 2007). "Evolution of symbiotic bacteria in the distal human intestine" (Free full text). PLoS biology 5 (7): e156. doi:10.1371/journal.pbio.0050156. ISSN 1544-9173. PMC 1892571. PMID 17579514. http://dx.plos.org/10.1371/journal.pbio.0050156. edit
6.^ Finegold SM, Sutter VL, Mathisen GE (1983). Normal indigenous intestinal flora (pp. 3-31) in Human intestinal microflora in health and disease.. Academic Press. ISBN 0-12-341280-3.
7.^ "Bacteroides Infection: Overview - eMedicine". http://emedicine.medscape.com/article/233339-overview. Retrieved 2008-12-11.
8.^ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 0-8385-8529-9.
9.^ Salyers AA, Gupta A, Wang Y (2004). "Human intestinal bacteria as reservoirs for antibiotic resistance genes". Trends Microbiol 12 (9): 412–6. doi:10.1016/j.tim.2004.07.004. PMID 15337162.
10.^ Löfmark, S.; Jernberg, C.; Jansson, K.; Edlund, C. (Dec 2006). "Clindamycin-induced enrichment and long-term persistence of resistant Bacteroides spp. And resistance genes" (Free full text). The Journal of antimicrobial chemotherapy 58 (6): 1160–1167. doi:10.1093/jac/dkl420. ISSN 0305-7453. PMID 17046967. http://jac.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=17046967. edit
11.^ Madigan M, Martinko J (editors). (2005). Brock Biology of Microorganisms (11th ed.). Prentice Hall. ISBN 0-13-144329-1.
12.^ Bernhard and Field, A.E. and K.G.; Field, KG (2000). "A PCR Assay To Discriminate Human and Ruminant Feces on the Basis of Host Differences in Bacteroides-Prevotella Genes Encoding 16S rRNA". Applied and Environmental Microbiology 66 (10): 4571–4574. doi:http://water.rutgers.edu/Source_Tracking/Bacteroidetes/APCRAssayToDiscriminateHumanandRuminantFecesontheBasisofHostDifferencesinBacteroides.pdf. PMC 92346. PMID 11010920. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=92346.
13.^ Kreader, C.A. (1998). "Persistence of PCR-Detectable Bacteroides distasonis from Human Feces in River Water". Applied and Environmental Microbiology 64 (10): 4103–4105. doi:http://www.water.rutgers.edu/Source_Tracking/Bacteroidetes/PersistenceofPCR-DetectableBacteroidesdistasonisfromHumanFecesinRiverWater.pdf. PMC 106613. PMID 9758854. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=106613.
14.^ Layton, A.; McKay, L; Williams, D; Garrett, V; Gentry, R; Sayler, G (2006). "Development of Bacteroides 16S rRNA Gene TaqMan-Based Real-Time PCR Assays for Estimation of Total, Human,and Bovine Fecal Pollution in Water". Applied and Environmental Microbiology 72 (6): 4214–4224. doi:http://aem.asm.org/cgi/content/short/72/6/4214. PMC 1489674. PMID 16751534. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1489674.
15.^ Bell, Layton, McKay, Williams, Gentry, Sayler, A., A.C., L., D., R., G.S.; Layton, Alice C.; McKay, Larry; Williams, Dan; Gentry, Randy; Sayler, Gary S. (2009). "Factors Influencing the Persistance of Fecal Bacteroides in Stream Water". J. Environ. Qual. 38 (3): 1224–1232. doi:10.2134/jeq2008.0258. PMID 19398520.
REF: http://en.wikipedia.org/wiki/Bacteroides .Access: 13/apr/2011
Because of their fastidiousness, they are difficult to isolate and are often overlooked. Their isolation requires appropriate methods of collection, transportation, and cultivation of specimens.[2] Treatment is complicated by 3 factors: slow growth, increasing resistance to antimicrobial agents,[3] and the polymicrobial synergistic nature of the infection.[4]
The B fragilis group, a member of the Bacteroidaceae family, includes B fragilis (causes the most clinical infections), Bacteroides distasonis, Bacteroides ovatus, Bacteroides thetaiotaomicron, and Bacteroides vulgatus. These bacteria are resistant to penicillins, mostly through the production of beta-lactamase. They are part of the normal GI florae[1] and predominate in intra-abdominal infections and infections that originate from those florae (eg, perirectal abscesses, decubitus ulcers). Enterotoxigenic B fragilis (ETBF) is also a potential cause of diarrhea.[5]
Pigmented Prevotella, such as Prevotella melaninogenica and Prevotella intermedia (which were previously called the Bacteroides melaninogenicus group), Porphyromonas (eg, Porphyromonas asaccharolytica), and nonpigmented Prevotella (eg, Prevotella oralis, Prevotella oris) are part of the normal oral and vaginal florae and are the predominant AGNB isolated from respiratory tract infections and their complications, including aspiration pneumonia, lung abscess, chronic otitis media, chronic sinusitis, abscesses around the oral cavity, human bites, paronychia, brain abscesses, and osteomyelitis. Prevotella bivia and Prevotella disiens (previously called Bacteroides) are important in obstetric and gynecologic infections
REF: http://emedicine.medscape.com/article/233339-overview Access: 13,apr,2011
Bacteroides Infection
Author: Itzhak Brook, MD, MSc; Chief Editor: Burke A Cunha, MD
Bacteroides is a genus of Gram-negative, bacillus bacteria. Bacteroides species are non-endospore-forming, anaerobes, and may be either motile or non-motile, depending on the species.[1] The DNA base composition is 40-48% GC. Unusual in bacterial organisms, Bacteroides membranes contain sphingolipids. They also contain meso-diaminopimelic acid in their peptidoglycan layer.
Bacteroides are normally mutualistic, making up the most substantial portion of the mammalian gastrointestinal flora,[2] where they play a fundamental role in processing of complex molecules to simpler ones in the host intestine.[3][4][5] As many as 1010-1011 cells per gram of human feces have been reported.[6] They can use simple sugars when available, but the main source of energy is polysaccharides from plant sources.
One of the most important clinically is Bacteroides fragilis.
Bacteroides melaninogenicus has recently been reclassified and split into Prevotella melaninogenica and Prevotella intermedia.[7]
PathogenesisBacteroides species also benefit their host by excluding potential pathogens from colonizing the gut. Some species (B. fragilis, for example) are opportunistic human pathogens, causing infections of the peritoneal cavity, gastrointestinal surgery, and appendicitis via abscess formation, inhibiting phagocytosis, and inactivating beta-lactam antibiotics.[8] Although Bacteroides species are anaerobic, they are aerotolerant and thus can survive in the abdominal cavity.
In general, Bacteroides are resistant to a wide variety of antibiotics — β-lactams, aminoglycosides, and recently many species have acquired resistance to erythromycin and tetracycline. This high level of antibiotic resistance has prompted concerns that Bacteroides species may become a reservoir for resistance in other, more highly-pathogenic bacterial strains.[9] [10]
Microbiological ApplicationsAn alternative fecal indicator organism, Bacteroides, has been suggested because they make up a significant portion of the fecal bacterial population[11], have a high degree of host specificity that reflects differences in the digestive system of the host animal[12], and have a small potential to grow in the environment[13]. Over the past decade, real-time polymerase chain reaction (PCR) methods have been utilized to detect the presence of various microbial pathogens through the amplification of specific DNA sequences without culturing bacteria. One study has measured the amount of Bacteroides by using qPCR to quantify the 16S rRNA genetic marker that is host-specific.[14] This technique allows quantification of genetic markers that are specific to the host of the bacteria and allow detection of recent contamination. A recent report found that temperature plays a major role in the amount of time the bacteria will persist in the environment, the life span increases with colder temperatures
References1.^ Madigan M, Martinko J (editors). (2005). Brock Biology of Microorganisms (11th ed.). Prentice Hall. ISBN 0-13-144329-1.
2.^ Dorland WAN (editor) (2003). Dorland's Illustrated Medical Dictionary (30th ed.). W.B. Saunders. ISBN 0-7216-0146-4.
3.^ Wexler, H. M. (Oct 2007). "Bacteroides: the good, the bad, and the nitty-gritty" (Free full text). Clinical microbiology reviews 20 (4): 593–621. doi:10.1128/CMR.00008-07. ISSN 0893-8512. PMC 2176045. PMID 17934076. http://cmr.asm.org/cgi/pmidlookup?view=long&pmid=17934076. edit
4.^ Xu, J.; Gordon, I. (Sep 2003). "Inaugural Article: Honor thy symbionts" (Free full text). Proceedings of the National Academy of Sciences of the United States of America 100 (18): 10452–10459. doi:10.1073/pnas.1734063100. ISSN 0027-8424. PMC 193582. PMID 12923294. http://www.pnas.org/cgi/pmidlookup?view=long&pmid=12923294. edit
5.^ Xu, J.; Mahowald, A.; Ley, E.; Lozupone, A.; Hamady, M.; Martens, C.; Henrissat, B.; Coutinho, M. et al. (Jul 2007). "Evolution of symbiotic bacteria in the distal human intestine" (Free full text). PLoS biology 5 (7): e156. doi:10.1371/journal.pbio.0050156. ISSN 1544-9173. PMC 1892571. PMID 17579514. http://dx.plos.org/10.1371/journal.pbio.0050156. edit
6.^ Finegold SM, Sutter VL, Mathisen GE (1983). Normal indigenous intestinal flora (pp. 3-31) in Human intestinal microflora in health and disease.. Academic Press. ISBN 0-12-341280-3.
7.^ "Bacteroides Infection: Overview - eMedicine". http://emedicine.medscape.com/article/233339-overview. Retrieved 2008-12-11.
8.^ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 0-8385-8529-9.
9.^ Salyers AA, Gupta A, Wang Y (2004). "Human intestinal bacteria as reservoirs for antibiotic resistance genes". Trends Microbiol 12 (9): 412–6. doi:10.1016/j.tim.2004.07.004. PMID 15337162.
10.^ Löfmark, S.; Jernberg, C.; Jansson, K.; Edlund, C. (Dec 2006). "Clindamycin-induced enrichment and long-term persistence of resistant Bacteroides spp. And resistance genes" (Free full text). The Journal of antimicrobial chemotherapy 58 (6): 1160–1167. doi:10.1093/jac/dkl420. ISSN 0305-7453. PMID 17046967. http://jac.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=17046967. edit
11.^ Madigan M, Martinko J (editors). (2005). Brock Biology of Microorganisms (11th ed.). Prentice Hall. ISBN 0-13-144329-1.
12.^ Bernhard and Field, A.E. and K.G.; Field, KG (2000). "A PCR Assay To Discriminate Human and Ruminant Feces on the Basis of Host Differences in Bacteroides-Prevotella Genes Encoding 16S rRNA". Applied and Environmental Microbiology 66 (10): 4571–4574. doi:http://water.rutgers.edu/Source_Tracking/Bacteroidetes/APCRAssayToDiscriminateHumanandRuminantFecesontheBasisofHostDifferencesinBacteroides.pdf. PMC 92346. PMID 11010920. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=92346.
13.^ Kreader, C.A. (1998). "Persistence of PCR-Detectable Bacteroides distasonis from Human Feces in River Water". Applied and Environmental Microbiology 64 (10): 4103–4105. doi:http://www.water.rutgers.edu/Source_Tracking/Bacteroidetes/PersistenceofPCR-DetectableBacteroidesdistasonisfromHumanFecesinRiverWater.pdf. PMC 106613. PMID 9758854. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=106613.
14.^ Layton, A.; McKay, L; Williams, D; Garrett, V; Gentry, R; Sayler, G (2006). "Development of Bacteroides 16S rRNA Gene TaqMan-Based Real-Time PCR Assays for Estimation of Total, Human,and Bovine Fecal Pollution in Water". Applied and Environmental Microbiology 72 (6): 4214–4224. doi:http://aem.asm.org/cgi/content/short/72/6/4214. PMC 1489674. PMID 16751534. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1489674.
15.^ Bell, Layton, McKay, Williams, Gentry, Sayler, A., A.C., L., D., R., G.S.; Layton, Alice C.; McKay, Larry; Williams, Dan; Gentry, Randy; Sayler, Gary S. (2009). "Factors Influencing the Persistance of Fecal Bacteroides in Stream Water". J. Environ. Qual. 38 (3): 1224–1232. doi:10.2134/jeq2008.0258. PMID 19398520.
REF: http://en.wikipedia.org/wiki/Bacteroides .Access: 13/apr/2011
terça-feira, 29 de março de 2011
Bacterioides ovatus
Introduction
Background
This article describes infections caused by the Bacteroides fragilis group and other anaerobic gram-negative bacilli (AGNB) that were previously included in the Bacteroides genus but are now included in the Prevotella and Porphyromonas genera. Infections due to AGNB are common, yet the specific identification of AGNB in these infections is difficult.
Bacteroides species are anaerobic bacteria that are predominant components of the bacterial florae of mucous membranes1 and are therefore a common cause of endogenous infections. Bacteroides infections can develop in all body sites, including the CNS, the head, the neck, the chest, the abdomen, the pelvis, the skin, and the soft tissues. Inadequate therapy against these anaerobic bacteria may lead to clinical failure.
Because of their fastidiousness, they are difficult to isolate and are often overlooked. Their isolation requires appropriate methods of collection, transportation, and cultivation of specimens.2 Treatment is complicated by 3 factors: slow growth, increasing resistance to antimicrobial agents,3 and the polymicrobial synergistic nature of the infection.4
The B fragilis group, a member of the Bacteroidaceae family, includes B fragilis (causes the most clinical infections), Bacteroides distasonis, Bacteroides ovatus, Bacteroides thetaiotaomicron, and Bacteroides vulgatus. These bacteria are resistant to penicillins, mostly through the production of beta-lactamase. They are part of the normal GI florae1 and predominate in intra-abdominal infections and infections that originate from those florae (eg, perirectal abscesses, decubitus ulcers). Enterotoxigenic B fragilis (ETBF) is also a potential cause of diarrhea.5
Pigmented Prevotella, such as Prevotella melaninogenica and Prevotella intermedia (which were previously called the Bacteroides melaninogenicus group), Porphyromonas (eg, Porphyromonas asaccharolytica), and nonpigmented Prevotella (eg, Prevotella oralis, Prevotella oris) are part of the normal oral and vaginal florae and are the predominant AGNB isolated from respiratory tract infections and their complications, including aspiration pneumonia, lung abscess, chronic otitis media, chronic sinusitis, abscesses around the oral cavity, human bites, paronychia, brain abscesses, and osteomyelitis. Prevotella bivia and Prevotella disiens (previously called Bacteroides) are important in obstetric and gynecologic infections.
Pathophysiology
Most infections due to AGNB originate from the endogenous mucosal membrane florae. Knowledge of the common mode of distribution allows for a logical choice of antimicrobial therapy for infections in these sites.
AGNB infections are generally polymicrobial. The number of isolates can reach 5-10 organisms. The type of copathogens depends on the infection site and the circumstances of the infection. Antimicrobial therapy should be directed at all major aerobic and anaerobic pathogens. AGNB promote infection through synergy with their aerobic and anaerobic counterparts and with each other.
An indirect pathogenic role of AGNB is their ability to produce the enzyme beta-lactamase, which allows them to protect themselves and other penicillin-susceptible organisms from the activity of penicillins.
Frequency
United States
The exact frequency of AGNB infection is difficult to calculate because of inappropriate methods of collection, transportation, and cultivation of specimens. AGNB are more commonly found in chronic infections. Their rate of recovery in blood cultures is 2-5% and higher with patients who have predisposing conditions.
International
The frequency of these infections appears to be higher in developing countries, where therapy is often inadequate or delayed.
Mortality/Morbidity
The mortality rate has decreased over the past 3 decades because of early recognition and initiation of proper prophylactic and therapeutic antimicrobial therapies.
Age
AGNB infections can occur in patients of all ages; however, the frequency of head and neck infections is higher in pediatric patients than in other patients.
Clinical
History
AGNB infections occur more often in chronic infections and in association with the predisposing conditions discussed below. However, they can also cause acute infections (ie, maxillary sinusitis associated with dental infections, intra-abdominal infections following perforation).6,7
•CNS infections
◦AGNB can cause various intracranial infections, including brain abscess, subdural empyema, epidural abscess, and meningitis (usually from contiguous spread from adjacent foci of infection). Brain abscesses are commonly caused by chronic infections in the ears, the mastoids, the sinuses, the oropharynx, the teeth, or the lungs.
◦Hematogenous spread can occur after dental, oropharyngeal, pulmonary, or intra-abdominal infection. Rarely, bacteremia of another origin or endocarditis leads to such infection.8 •Head and neck infections: Anaerobes, including AGNB, are recovered from various infections, especially in their chronic form. Head and neck infections include chronic otitis media9 ; sinusitis10 ; mastoiditis; tonsillar,10 peritonsillar, and retropharyngeal abscesses; cervical lymphadenitis; all deep neck space infections; thyroiditis; odontogenic infections; and postsurgical and nonsurgical head and neck wounds and abscesses.11 ◦Sinusitis is complicated by anaerobes, including AGNB, when it becomes chronic and oxygen levels decline. Anaerobes are isolated from 10% of patients with acute maxillary sinusitis (mostly secondary to odontogenic infection), but they are found in as many as 67% of chronic infections of the maxillary, ethmoid, frontal, and sphenoid sinuses.12,10 The infection may spread via anastomosing veins or contiguously to the CNS. Complications include orbital cellulitis, meningitis, cavernous sinus thrombosis, and epidural and subdural brain abscesses.
◦Tonsillitis, whether acute or chronic, may have AGNB involvement.13,10 AGNB can also be involved with tonsillitis complications, including internal jugular vein thrombophlebitis, which often causes postanginal sepsis. Prevotella species and other anaerobes are recovered from tonsillar or retropharyngeal abscesses without any aerobic bacteria, and they are isolated in cases of Vincent angina.
•Pleuropulmonary infections: Aspiration of oropharyngeal or gastric secretions and periodontal or gingival disease are risk factors for anaerobic pleuropulmonary infection due to AGNB and to other anaerobes. The infection can progress from pneumonitis to necrotizing pneumonia and lung abscess, with or without empyema.14 •Intra-abdominal infections15 ◦Secondary peritonitis and abdominal abscesses generally occur after entry of enteric organisms into the peritoneal cavity through perforation of the intestine or other viscus as a result of obstruction, infarction, or trauma.
◦The more distal the perforation, the more numerous the types and number of organisms that gain access into the peritoneal cavity (ie, perforations in the descending colon are associated with spillage of more organisms than perforations in proximal parts of the colon).
◦Enterotoxigenic B fragilis are considered an emerging enteropathogen-causing diarrhea.
•Female genital tract infection: These infections include bacterial vaginosis; soft tissue perineal, vulvar, and Bartholin gland abscesses; endometritis; pyometra; salpingitis; tubo-ovarian abscesses; adnexal abscess; pelvic inflammatory disease, which may include pelvic cellulitis and abscess; amnionitis; septic pelvic thrombophlebitis; intrauterine device–associated infection; septic abortion; and postsurgical obstetric and gynecologic infections.
•Skin and soft tissue infections
◦Infections involving AGNB include superficial infections, such as infected cutaneous ulcers, cellulitis, secondary diaper rash, gastrostomy or tracheostomy site wounds, infected subcutaneous sebaceous or inclusion cysts, eczema, scabies or kerion infections, paronychia, hidradenitis suppurativa, and pyoderma.
◦Subcutaneous tissue infections and postsurgical wound infections that may also involve the skin include cutaneous and subcutaneous abscesses, decubitus ulcers, infected diabetic (vascular or trophic) ulcers, breast abscesses, bite wounds,16 anaerobic cellulitis and gas gangrene, bacterial synergistic gangrene, infected pilonidal cyst or sinus, Meleney ulcer, and burn wound infection.
◦Deeper anaerobic soft tissue infections include necrotizing fasciitis, necrotizing synergistic cellulitis, gas gangrene, and crepitus cellulitis. These infections can involve the fascia alone or also the muscle surrounded by the fascia, inducing myositis and myonecrosis.
◦Anaerobic infections, such as decubitus ulcers or diabetic foot ulcers, are generally polymicrobial and are often complicated by osteomyelitis or bacteremia.
◦Deep tissue infections, such as necrotizing cellulitis, fasciitis, and myositis, often involve clostridial organisms and Staphylococcus pyogenes. They may be polymicrobic; may contain gas and gray, thin, putrid pus; and are associated with bacteremia and mortality.17 •Osteomyelitis and septic arthritis: Osteomyelitis in the long bones and the cranial and facial bones is frequently polymicrobic and may be associated with anaerobes in patients with peripheral vascular disease and decubitus ulcers.18 •Bacteremia
◦The prevalence of anaerobes, including AGNB, in bacteremia was once 5-15%. However, rates declined to 2-6% in the 1990s. Increased awareness of the importance of anaerobes and enhanced recognition of the types of clinical infection caused by these organisms, along with appropriate prophylaxis and treatment, have been proposed as explanations for the decreased incidence of anaerobic bacteremia from 1974–1988.19 However, recent studies have reported a resurgence in anaerobic bacteremia. A study from the Mayo Clinic (Rochester, MN) has reported that the mean incidence of anaerobic bacteremia increased from 53 cases per year during 1993–1996 to 75 cases per year during 1997–2000 to 91 cases per year during 2001–2004 (an overall increase of 74%).20 ◦The authors concluded that the sources of anaerobic bacteremia are now more varied than they once were, especially among immunosuppressed individuals and persons with complex underlying disease.
◦Which organisms are involved depends on their portal of entry and the underlying disease. The common isolates are the B fragilis group (60-75% of isolates).8 The B fragilis group and clostridial organisms are associated with a GI source.
◦Pigmented Prevotella, Porphyromonas, and Fusobacterium are associated with the oropharynx and a pulmonary source.
◦Fusobacterium species involve the female genital tract.
◦Propionibacterium acnes is associated with a foreign body.
◦Peptostreptococcus species are associated with all sources but especially with oropharyngeal, pulmonary, and female genital tract sources.
◦Predisposing factors include neoplasms; hematologic disorders; organ transplant; intestinal obstruction; decubitus ulcers; dental extraction; diabetes mellitus; postsplenectomy; use of cytotoxic agents or corticosteroids; total-body irradiation; and recent GI, obstetric, or gynecologic surgery.
◦Features typical of anaerobic bacteremia include metastatic lesions, hyperbilirubinemia, and suppurative thrombophlebitis.
◦The risk of mortality is 15-30% and improves with early appropriate antimicrobial therapy and resolution of the primary infection.
Causes
•Conditions that predispose to AGNB infections include the exposure of sterile sites to a high inoculum of indigenous mucous membrane florae; use of antibiotics that are ineffective against AGNB; reduced blood supply; and tissue necrosis, which lowers the oxidation-reduction potential and favors the growth of anaerobes. Conditions that lower the blood supply include trauma, foreign body, malignancy, surgery, edema, shock, colitis, and vascular disease.6,7 •Infection with aerobic bacteria can make the local tissue conditions more favorable for the growth of anaerobes. The host defenses can become impaired by anaerobic conditions and anaerobic bacteria.
•Anaerobic infection often manifests as suppuration, thrombophlebitis, abscess formation, and gangrenous destruction of tissue associated with gas.
•Anaerobes, including AGNB, are common in chronic infections. Therapy with antimicrobials, such as aminoglycosides, trimethoprim-sulfamethazine, and older quinolones, frequently fails to eradicate anaerobes.
•Certain infections that often involve anaerobes include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia, lung abscesses, amnionitis, endometritis, septic abortions, pelvic inflammatory disease, tubo-ovarian abscess, peritonitis following viscus perforation, abscesses in and around the oral and rectal areas, and pus-forming necrotizing infections of soft tissue or muscle.6,7 •Some tumors, such as colonic, uterine, and bronchogenic carcinomas and necrotic tumors of the head and the neck, can become infected with anaerobes.
More on Bacteroides Infection
Overview: Bacteroides Infection
Differential Diagnoses & Workup: Bacteroides Infection
Treatment & Medication: Bacteroides Infection
Follow-up: Bacteroides Infection
REF: http://emedicine.medscape.com/article/233339-overview . Acessado em 29/03/11
Background
This article describes infections caused by the Bacteroides fragilis group and other anaerobic gram-negative bacilli (AGNB) that were previously included in the Bacteroides genus but are now included in the Prevotella and Porphyromonas genera. Infections due to AGNB are common, yet the specific identification of AGNB in these infections is difficult.
Bacteroides species are anaerobic bacteria that are predominant components of the bacterial florae of mucous membranes1 and are therefore a common cause of endogenous infections. Bacteroides infections can develop in all body sites, including the CNS, the head, the neck, the chest, the abdomen, the pelvis, the skin, and the soft tissues. Inadequate therapy against these anaerobic bacteria may lead to clinical failure.
Because of their fastidiousness, they are difficult to isolate and are often overlooked. Their isolation requires appropriate methods of collection, transportation, and cultivation of specimens.2 Treatment is complicated by 3 factors: slow growth, increasing resistance to antimicrobial agents,3 and the polymicrobial synergistic nature of the infection.4
The B fragilis group, a member of the Bacteroidaceae family, includes B fragilis (causes the most clinical infections), Bacteroides distasonis, Bacteroides ovatus, Bacteroides thetaiotaomicron, and Bacteroides vulgatus. These bacteria are resistant to penicillins, mostly through the production of beta-lactamase. They are part of the normal GI florae1 and predominate in intra-abdominal infections and infections that originate from those florae (eg, perirectal abscesses, decubitus ulcers). Enterotoxigenic B fragilis (ETBF) is also a potential cause of diarrhea.5
Pigmented Prevotella, such as Prevotella melaninogenica and Prevotella intermedia (which were previously called the Bacteroides melaninogenicus group), Porphyromonas (eg, Porphyromonas asaccharolytica), and nonpigmented Prevotella (eg, Prevotella oralis, Prevotella oris) are part of the normal oral and vaginal florae and are the predominant AGNB isolated from respiratory tract infections and their complications, including aspiration pneumonia, lung abscess, chronic otitis media, chronic sinusitis, abscesses around the oral cavity, human bites, paronychia, brain abscesses, and osteomyelitis. Prevotella bivia and Prevotella disiens (previously called Bacteroides) are important in obstetric and gynecologic infections.
Pathophysiology
Most infections due to AGNB originate from the endogenous mucosal membrane florae. Knowledge of the common mode of distribution allows for a logical choice of antimicrobial therapy for infections in these sites.
AGNB infections are generally polymicrobial. The number of isolates can reach 5-10 organisms. The type of copathogens depends on the infection site and the circumstances of the infection. Antimicrobial therapy should be directed at all major aerobic and anaerobic pathogens. AGNB promote infection through synergy with their aerobic and anaerobic counterparts and with each other.
An indirect pathogenic role of AGNB is their ability to produce the enzyme beta-lactamase, which allows them to protect themselves and other penicillin-susceptible organisms from the activity of penicillins.
Frequency
United States
The exact frequency of AGNB infection is difficult to calculate because of inappropriate methods of collection, transportation, and cultivation of specimens. AGNB are more commonly found in chronic infections. Their rate of recovery in blood cultures is 2-5% and higher with patients who have predisposing conditions.
International
The frequency of these infections appears to be higher in developing countries, where therapy is often inadequate or delayed.
Mortality/Morbidity
The mortality rate has decreased over the past 3 decades because of early recognition and initiation of proper prophylactic and therapeutic antimicrobial therapies.
Age
AGNB infections can occur in patients of all ages; however, the frequency of head and neck infections is higher in pediatric patients than in other patients.
Clinical
History
AGNB infections occur more often in chronic infections and in association with the predisposing conditions discussed below. However, they can also cause acute infections (ie, maxillary sinusitis associated with dental infections, intra-abdominal infections following perforation).6,7
•CNS infections
◦AGNB can cause various intracranial infections, including brain abscess, subdural empyema, epidural abscess, and meningitis (usually from contiguous spread from adjacent foci of infection). Brain abscesses are commonly caused by chronic infections in the ears, the mastoids, the sinuses, the oropharynx, the teeth, or the lungs.
◦Hematogenous spread can occur after dental, oropharyngeal, pulmonary, or intra-abdominal infection. Rarely, bacteremia of another origin or endocarditis leads to such infection.8 •Head and neck infections: Anaerobes, including AGNB, are recovered from various infections, especially in their chronic form. Head and neck infections include chronic otitis media9 ; sinusitis10 ; mastoiditis; tonsillar,10 peritonsillar, and retropharyngeal abscesses; cervical lymphadenitis; all deep neck space infections; thyroiditis; odontogenic infections; and postsurgical and nonsurgical head and neck wounds and abscesses.11 ◦Sinusitis is complicated by anaerobes, including AGNB, when it becomes chronic and oxygen levels decline. Anaerobes are isolated from 10% of patients with acute maxillary sinusitis (mostly secondary to odontogenic infection), but they are found in as many as 67% of chronic infections of the maxillary, ethmoid, frontal, and sphenoid sinuses.12,10 The infection may spread via anastomosing veins or contiguously to the CNS. Complications include orbital cellulitis, meningitis, cavernous sinus thrombosis, and epidural and subdural brain abscesses.
◦Tonsillitis, whether acute or chronic, may have AGNB involvement.13,10 AGNB can also be involved with tonsillitis complications, including internal jugular vein thrombophlebitis, which often causes postanginal sepsis. Prevotella species and other anaerobes are recovered from tonsillar or retropharyngeal abscesses without any aerobic bacteria, and they are isolated in cases of Vincent angina.
•Pleuropulmonary infections: Aspiration of oropharyngeal or gastric secretions and periodontal or gingival disease are risk factors for anaerobic pleuropulmonary infection due to AGNB and to other anaerobes. The infection can progress from pneumonitis to necrotizing pneumonia and lung abscess, with or without empyema.14 •Intra-abdominal infections15 ◦Secondary peritonitis and abdominal abscesses generally occur after entry of enteric organisms into the peritoneal cavity through perforation of the intestine or other viscus as a result of obstruction, infarction, or trauma.
◦The more distal the perforation, the more numerous the types and number of organisms that gain access into the peritoneal cavity (ie, perforations in the descending colon are associated with spillage of more organisms than perforations in proximal parts of the colon).
◦Enterotoxigenic B fragilis are considered an emerging enteropathogen-causing diarrhea.
•Female genital tract infection: These infections include bacterial vaginosis; soft tissue perineal, vulvar, and Bartholin gland abscesses; endometritis; pyometra; salpingitis; tubo-ovarian abscesses; adnexal abscess; pelvic inflammatory disease, which may include pelvic cellulitis and abscess; amnionitis; septic pelvic thrombophlebitis; intrauterine device–associated infection; septic abortion; and postsurgical obstetric and gynecologic infections.
•Skin and soft tissue infections
◦Infections involving AGNB include superficial infections, such as infected cutaneous ulcers, cellulitis, secondary diaper rash, gastrostomy or tracheostomy site wounds, infected subcutaneous sebaceous or inclusion cysts, eczema, scabies or kerion infections, paronychia, hidradenitis suppurativa, and pyoderma.
◦Subcutaneous tissue infections and postsurgical wound infections that may also involve the skin include cutaneous and subcutaneous abscesses, decubitus ulcers, infected diabetic (vascular or trophic) ulcers, breast abscesses, bite wounds,16 anaerobic cellulitis and gas gangrene, bacterial synergistic gangrene, infected pilonidal cyst or sinus, Meleney ulcer, and burn wound infection.
◦Deeper anaerobic soft tissue infections include necrotizing fasciitis, necrotizing synergistic cellulitis, gas gangrene, and crepitus cellulitis. These infections can involve the fascia alone or also the muscle surrounded by the fascia, inducing myositis and myonecrosis.
◦Anaerobic infections, such as decubitus ulcers or diabetic foot ulcers, are generally polymicrobial and are often complicated by osteomyelitis or bacteremia.
◦Deep tissue infections, such as necrotizing cellulitis, fasciitis, and myositis, often involve clostridial organisms and Staphylococcus pyogenes. They may be polymicrobic; may contain gas and gray, thin, putrid pus; and are associated with bacteremia and mortality.17 •Osteomyelitis and septic arthritis: Osteomyelitis in the long bones and the cranial and facial bones is frequently polymicrobic and may be associated with anaerobes in patients with peripheral vascular disease and decubitus ulcers.18 •Bacteremia
◦The prevalence of anaerobes, including AGNB, in bacteremia was once 5-15%. However, rates declined to 2-6% in the 1990s. Increased awareness of the importance of anaerobes and enhanced recognition of the types of clinical infection caused by these organisms, along with appropriate prophylaxis and treatment, have been proposed as explanations for the decreased incidence of anaerobic bacteremia from 1974–1988.19 However, recent studies have reported a resurgence in anaerobic bacteremia. A study from the Mayo Clinic (Rochester, MN) has reported that the mean incidence of anaerobic bacteremia increased from 53 cases per year during 1993–1996 to 75 cases per year during 1997–2000 to 91 cases per year during 2001–2004 (an overall increase of 74%).20 ◦The authors concluded that the sources of anaerobic bacteremia are now more varied than they once were, especially among immunosuppressed individuals and persons with complex underlying disease.
◦Which organisms are involved depends on their portal of entry and the underlying disease. The common isolates are the B fragilis group (60-75% of isolates).8 The B fragilis group and clostridial organisms are associated with a GI source.
◦Pigmented Prevotella, Porphyromonas, and Fusobacterium are associated with the oropharynx and a pulmonary source.
◦Fusobacterium species involve the female genital tract.
◦Propionibacterium acnes is associated with a foreign body.
◦Peptostreptococcus species are associated with all sources but especially with oropharyngeal, pulmonary, and female genital tract sources.
◦Predisposing factors include neoplasms; hematologic disorders; organ transplant; intestinal obstruction; decubitus ulcers; dental extraction; diabetes mellitus; postsplenectomy; use of cytotoxic agents or corticosteroids; total-body irradiation; and recent GI, obstetric, or gynecologic surgery.
◦Features typical of anaerobic bacteremia include metastatic lesions, hyperbilirubinemia, and suppurative thrombophlebitis.
◦The risk of mortality is 15-30% and improves with early appropriate antimicrobial therapy and resolution of the primary infection.
Causes
•Conditions that predispose to AGNB infections include the exposure of sterile sites to a high inoculum of indigenous mucous membrane florae; use of antibiotics that are ineffective against AGNB; reduced blood supply; and tissue necrosis, which lowers the oxidation-reduction potential and favors the growth of anaerobes. Conditions that lower the blood supply include trauma, foreign body, malignancy, surgery, edema, shock, colitis, and vascular disease.6,7 •Infection with aerobic bacteria can make the local tissue conditions more favorable for the growth of anaerobes. The host defenses can become impaired by anaerobic conditions and anaerobic bacteria.
•Anaerobic infection often manifests as suppuration, thrombophlebitis, abscess formation, and gangrenous destruction of tissue associated with gas.
•Anaerobes, including AGNB, are common in chronic infections. Therapy with antimicrobials, such as aminoglycosides, trimethoprim-sulfamethazine, and older quinolones, frequently fails to eradicate anaerobes.
•Certain infections that often involve anaerobes include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia, lung abscesses, amnionitis, endometritis, septic abortions, pelvic inflammatory disease, tubo-ovarian abscess, peritonitis following viscus perforation, abscesses in and around the oral and rectal areas, and pus-forming necrotizing infections of soft tissue or muscle.6,7 •Some tumors, such as colonic, uterine, and bronchogenic carcinomas and necrotic tumors of the head and the neck, can become infected with anaerobes.
More on Bacteroides Infection
Overview: Bacteroides Infection
Differential Diagnoses & Workup: Bacteroides Infection
Treatment & Medication: Bacteroides Infection
Follow-up: Bacteroides Infection
REF: http://emedicine.medscape.com/article/233339-overview . Acessado em 29/03/11
quinta-feira, 27 de janeiro de 2011
Comamonas testosteroni
Comamonas testosteroni, formerly known as Pseudomonastestosteroni, is a non-fermenting, gram(-), oxidase(+) bacterium with a wide geographic distribution in water and soil, and a little apparent capacity of causing human infections. We present two cases of Com. testosteroni bacteraemia, occurred to our hospital within a month's period.
ref: http://www.blackwellpublishing.com/eccmid15/abstract.asp?id=37695 . Acessado em 27/01/11
ref: http://www.blackwellpublishing.com/eccmid15/abstract.asp?id=37695 . Acessado em 27/01/11
Aeromonas veronii
Aeromonas veronii is a gram-negative, rod-shaped bacterium found in fresh water and in association with animals. It can be a pathogen of humans and a beneficial symbiont of leeches. In humans A. veronii can cause diseases ranging from wound infections and diarrhea to septicemia in immunocompromised patients. In leeches, this bacterium is thought to function in the digestion of blood, provision of nutrients or preventing other bacteria from growing.
REf: . Acessado em 25/jan/2011
Classification
Higher order taxa
Bacteria; Proteobacteria; Gammaproteobacteria; Aeromonadales; Aeromonadaceae; Aeromonas
Species
Aeromonas veronii
NCBI:[1]
Description and significance
A. veronii is a rod shaped, motile, gram negative, facultative anaerobe. The bacteria are usually not found in groups or pairs but as individual cells.[5] A. veronii is commonly found in soil and various water systems all over the world. It is most often associated with the leech. The blood digested by the bacteria in the leech has been found to contain various antimicrobial properties. It is capable of lowering high concentrations of bacteria through the activatons of the membrane attack complex. This complex creates permeable membranes in a foreign bacteria, essentially inactivating the bacteria. The A. veronii seem to be unsusceptible to this complex, allowing it to proliferate while other bacteria can not. This leads to a very limited number of microbial flora in the digestive tract of the leech, which is extremely uncommon.[4] The population of Aeromonas veronii is greatly effected by the consumption of blood. Tests have shown that dramatic changes occur during this time, the majority of A. veronii bacteria are found not in the epithelial tissue but in the IntraLuminal Fluid (ILF).[5]
Genome structure
The bacteria is made up of 2758 bp of linear DNA. Studies have found that certain genes ( Ast, Alt, and Act) may play a significant role in infection of host organisms. The aeroslysin-hemolysin genes were found to cause diarrhea in some patients who had A. veronii in their digestive system. [2]
Cell structure and metabolism
The bacterial cell contains a cytoplasm membrane , a thin layer of peptidoglycan and an outer layer composed of lipopolysaccharides (LPS). The catalase gene is important for the degradation of toxic hydrogen peroxide to much more useful molecules, water and oxygen. The expression of the catalase gen is influenced by introduction to extremely low levels of H2O2 during growth and the stationery phases.It has been suggested that H2O2 is used as an antimicrobial by the host cell to damage the DNA, RNA, proteins of invading pathogens. Only those microbes that are able to metabolize hydrogen peroxide would be able to survive in a host cell. [6]
Ecology
The A. veronii bacteria can be found in a number of habitats, including humans, mosquitos and leeches. It is primarily found in the digestive tract of the leech where it maintains a symbiotic relationship with its host. The medicinal leech, Hirudo medicinalis is capable of consuming six times its own body weight. The crop is the area of the digestive tract colonized by A. veronii. It is also the area where blood is stored after ingestion, and where water and salt are absorbed from the blood. . Blood is stored in the crop of the digestive tract. Studies have suggested that one of the reasons A. veronii is one of the two predominant microbial flora of the digestive tract is due to the antimicrobial properties of ingested blood.[4] A. veronii provides a number of contributions to the symbiotic relationship it share with the leech. It appears the bacteria helps maintain the flora of the digestive tract, helps in digestion of blood and it also provides necessary nutrients, such as vitamin B complex, not found in abundance in blood.[5][12]
Pathology
Medicinal leeches are used after reconstructive or plastic surgery due to their anticoagulating properties and relative inexpense. Studies have shown that without prior antibiotic treatment, up to 20% of patients receiving leech treatment become infected with Aeromonas.[4] Aeromonas species have been shown to have pathogenic properties in a human host. The problem arises if other more pathogenic bacteria are transmitted by leech therapy. Studies looked at whether other bacteria could proliferate or or persist inside the digestive tract for an extended period of time.[4] Virulence is caused by a number of factors such as the pili, flagella and S-layer though non e have been shown to be the sole cause of symptoms during infection.[2]
Current Research
Currently, studies are being conducted on the medicinal leech, Hirudo medicinalis due to its popularity as an anticoagulant after plastic and reconstructive surgery. These studies focus on the flora of the digestive tract, primarily to determine how effective they are against bacteria that may be pathogenic to humans. The studies look at the whether or not A. veronii is able to contain growth of other bacteria and remain the dominating flora.[4] Current research is also studying the role of A. veronii in a human host. Without antibiotic treatment prior to leech therapy, patients are highly susceptible to infections caused by the bacteria. Though leech therapy is a cost effective treatment with many benefits, it can pose harm to humans.[8] Continual studies of the H. medicinalis and its microial flora are essential to learning more about the complexity of communities withing a host organism. The simple community within the H. medicinalis makes it a perfect model for future studies.[8] Research has been done on the catalase gene of the A. veronii and the role it plays in the symbiotic realtionship between symbiont and host. This is a great model for studying other symbiotic relationships and how their environment may effect growth.[6]
References
1. Abdullah, A.I., Hart, C.A., and Winstanley, C. 2003. Molecular characterization and distribution of virulence-associated genes amongst Aeromonas isolates from Libya. Journal of Applied Microbiology, v. 95, p. 1001-1007.
2. Aguilera-Arreola, M.G. Hernandez-Rodriguez, C., Zuniga, G., Figueras, M.J., Garduno, R. A., and Castro-Escarpulli, G. 2007. Virulence potential and genetic diversity of Aeromonas caviae, Aeromonas veronii, and Aeromonas hydrophilia clinical isolates from Mexico and Spain: a comparative study. Canadian Journal of Microbiology, v. 53, p. 877-887.
3. Han, H., Taki, T., Kondo, H., Hirono, I., and Aoki, T. 2008. Pathogenic potential of a collagenase gene from Aeromonas veronii. Canadian Journal of Microbiology, v. 54, p. 1-10.
4. Indergand, S., and Graf, J. 2000. Ingested blood contributes to the specificity of the symbiosis of Aeromonas veronii biovar sobria and Hirudo medicinalis, the medicinal leech. Applied and Environmental Microbiology, v. 66, p. 4735-4741.
5. Kikuchi, Y., and Graf J. 2007. Spatial and temporal population dynamics of a naturally occurring two-species microbial c ]ommunity inside the digestive tract of the medicinal leech. Applied and Environmental Microbiology, v. 73, p. 1984-1991.
6. Rio, R.V.M., Anderegg, M., and Graf, J. 2007. Characterization of a catalase gene from Aeromonas veronii, the digestive-tract symbiont of the medicinal leech. Microbiology, v. 153, p. 1897-1906.
7. Sen, K., and Lye, D. 2007. Importance of flagella and enterotoxins for Aeromonas virulence in a mouse model. Canadian journal of Microbiology, v. 53, p. 261-269.
8. Silver, A.C., Rabinowitz, N.M., Kuffer, S., and Graf, J. 2007. Identification of Aeromonas veronii genes required for colonization of the medicinal leech, Hirudo verbena. Journal of Bacteriology, v. 189, p. 6763-6772.
9. Thomsen, R.N., and Kristiansen, M.M. 2001. Three cases of bacteraemia caused by Aeromonas veronii biovar sobria. Scandinavian Journal of Infectious Diseases, v.33, p.718-719.
10. Vazquez-Juarez, R.C., Romero, M.J., and Ascencio, F. 2004. Adhesive properties of a LamB-like outer membrane protein and its contribution to Aeromonas veronii adhesion.
11. Vila , J., Ruiz, J., Gallardo, F., Vargas, M., Soler, L., Figueras, M.J., and Gascon J. 2003. Aeromonas spp. and traveler’s diarrhea: clinical features and antimicrobial resistance. Emerging Infectious Diseases, v. 9, p. 552-555.
12. Worthen, P.L., Gode, C.J., and Graf J. 2006. Culture-independent characterization of the digestive-tract microbiota of the medicinal leech reveals a tripartite symbiosis. Applied and Environmental Microbiology, v. 72, p. 4775-4781.
REF.: http://microbewiki.kenyon.edu/index.php/Aeromonas_veronii . Acessado em 25/jan/2011
REf: . Acessado em 25/jan/2011
Classification
Higher order taxa
Bacteria; Proteobacteria; Gammaproteobacteria; Aeromonadales; Aeromonadaceae; Aeromonas
Species
Aeromonas veronii
NCBI:[1]
Description and significance
A. veronii is a rod shaped, motile, gram negative, facultative anaerobe. The bacteria are usually not found in groups or pairs but as individual cells.[5] A. veronii is commonly found in soil and various water systems all over the world. It is most often associated with the leech. The blood digested by the bacteria in the leech has been found to contain various antimicrobial properties. It is capable of lowering high concentrations of bacteria through the activatons of the membrane attack complex. This complex creates permeable membranes in a foreign bacteria, essentially inactivating the bacteria. The A. veronii seem to be unsusceptible to this complex, allowing it to proliferate while other bacteria can not. This leads to a very limited number of microbial flora in the digestive tract of the leech, which is extremely uncommon.[4] The population of Aeromonas veronii is greatly effected by the consumption of blood. Tests have shown that dramatic changes occur during this time, the majority of A. veronii bacteria are found not in the epithelial tissue but in the IntraLuminal Fluid (ILF).[5]
Genome structure
The bacteria is made up of 2758 bp of linear DNA. Studies have found that certain genes ( Ast, Alt, and Act) may play a significant role in infection of host organisms. The aeroslysin-hemolysin genes were found to cause diarrhea in some patients who had A. veronii in their digestive system. [2]
Cell structure and metabolism
The bacterial cell contains a cytoplasm membrane , a thin layer of peptidoglycan and an outer layer composed of lipopolysaccharides (LPS). The catalase gene is important for the degradation of toxic hydrogen peroxide to much more useful molecules, water and oxygen. The expression of the catalase gen is influenced by introduction to extremely low levels of H2O2 during growth and the stationery phases.It has been suggested that H2O2 is used as an antimicrobial by the host cell to damage the DNA, RNA, proteins of invading pathogens. Only those microbes that are able to metabolize hydrogen peroxide would be able to survive in a host cell. [6]
Ecology
The A. veronii bacteria can be found in a number of habitats, including humans, mosquitos and leeches. It is primarily found in the digestive tract of the leech where it maintains a symbiotic relationship with its host. The medicinal leech, Hirudo medicinalis is capable of consuming six times its own body weight. The crop is the area of the digestive tract colonized by A. veronii. It is also the area where blood is stored after ingestion, and where water and salt are absorbed from the blood. . Blood is stored in the crop of the digestive tract. Studies have suggested that one of the reasons A. veronii is one of the two predominant microbial flora of the digestive tract is due to the antimicrobial properties of ingested blood.[4] A. veronii provides a number of contributions to the symbiotic relationship it share with the leech. It appears the bacteria helps maintain the flora of the digestive tract, helps in digestion of blood and it also provides necessary nutrients, such as vitamin B complex, not found in abundance in blood.[5][12]
Pathology
Medicinal leeches are used after reconstructive or plastic surgery due to their anticoagulating properties and relative inexpense. Studies have shown that without prior antibiotic treatment, up to 20% of patients receiving leech treatment become infected with Aeromonas.[4] Aeromonas species have been shown to have pathogenic properties in a human host. The problem arises if other more pathogenic bacteria are transmitted by leech therapy. Studies looked at whether other bacteria could proliferate or or persist inside the digestive tract for an extended period of time.[4] Virulence is caused by a number of factors such as the pili, flagella and S-layer though non e have been shown to be the sole cause of symptoms during infection.[2]
Current Research
Currently, studies are being conducted on the medicinal leech, Hirudo medicinalis due to its popularity as an anticoagulant after plastic and reconstructive surgery. These studies focus on the flora of the digestive tract, primarily to determine how effective they are against bacteria that may be pathogenic to humans. The studies look at the whether or not A. veronii is able to contain growth of other bacteria and remain the dominating flora.[4] Current research is also studying the role of A. veronii in a human host. Without antibiotic treatment prior to leech therapy, patients are highly susceptible to infections caused by the bacteria. Though leech therapy is a cost effective treatment with many benefits, it can pose harm to humans.[8] Continual studies of the H. medicinalis and its microial flora are essential to learning more about the complexity of communities withing a host organism. The simple community within the H. medicinalis makes it a perfect model for future studies.[8] Research has been done on the catalase gene of the A. veronii and the role it plays in the symbiotic realtionship between symbiont and host. This is a great model for studying other symbiotic relationships and how their environment may effect growth.[6]
References
1. Abdullah, A.I., Hart, C.A., and Winstanley, C. 2003. Molecular characterization and distribution of virulence-associated genes amongst Aeromonas isolates from Libya. Journal of Applied Microbiology, v. 95, p. 1001-1007.
2. Aguilera-Arreola, M.G. Hernandez-Rodriguez, C., Zuniga, G., Figueras, M.J., Garduno, R. A., and Castro-Escarpulli, G. 2007. Virulence potential and genetic diversity of Aeromonas caviae, Aeromonas veronii, and Aeromonas hydrophilia clinical isolates from Mexico and Spain: a comparative study. Canadian Journal of Microbiology, v. 53, p. 877-887.
3. Han, H., Taki, T., Kondo, H., Hirono, I., and Aoki, T. 2008. Pathogenic potential of a collagenase gene from Aeromonas veronii. Canadian Journal of Microbiology, v. 54, p. 1-10.
4. Indergand, S., and Graf, J. 2000. Ingested blood contributes to the specificity of the symbiosis of Aeromonas veronii biovar sobria and Hirudo medicinalis, the medicinal leech. Applied and Environmental Microbiology, v. 66, p. 4735-4741.
5. Kikuchi, Y., and Graf J. 2007. Spatial and temporal population dynamics of a naturally occurring two-species microbial c ]ommunity inside the digestive tract of the medicinal leech. Applied and Environmental Microbiology, v. 73, p. 1984-1991.
6. Rio, R.V.M., Anderegg, M., and Graf, J. 2007. Characterization of a catalase gene from Aeromonas veronii, the digestive-tract symbiont of the medicinal leech. Microbiology, v. 153, p. 1897-1906.
7. Sen, K., and Lye, D. 2007. Importance of flagella and enterotoxins for Aeromonas virulence in a mouse model. Canadian journal of Microbiology, v. 53, p. 261-269.
8. Silver, A.C., Rabinowitz, N.M., Kuffer, S., and Graf, J. 2007. Identification of Aeromonas veronii genes required for colonization of the medicinal leech, Hirudo verbena. Journal of Bacteriology, v. 189, p. 6763-6772.
9. Thomsen, R.N., and Kristiansen, M.M. 2001. Three cases of bacteraemia caused by Aeromonas veronii biovar sobria. Scandinavian Journal of Infectious Diseases, v.33, p.718-719.
10. Vazquez-Juarez, R.C., Romero, M.J., and Ascencio, F. 2004. Adhesive properties of a LamB-like outer membrane protein and its contribution to Aeromonas veronii adhesion.
11. Vila , J., Ruiz, J., Gallardo, F., Vargas, M., Soler, L., Figueras, M.J., and Gascon J. 2003. Aeromonas spp. and traveler’s diarrhea: clinical features and antimicrobial resistance. Emerging Infectious Diseases, v. 9, p. 552-555.
12. Worthen, P.L., Gode, C.J., and Graf J. 2006. Culture-independent characterization of the digestive-tract microbiota of the medicinal leech reveals a tripartite symbiosis. Applied and Environmental Microbiology, v. 72, p. 4775-4781.
REF.: http://microbewiki.kenyon.edu/index.php/Aeromonas_veronii . Acessado em 25/jan/2011
domingo, 10 de outubro de 2010
Stenotrophomonas maltophilia
Stenotrophomonas maltophilia is an aerobic, nonfermentative, Gram-negative bacterium. It is an uncommon bacterium and human infection is difficult to treat.[1] Initially classified as Pseudomonas maltophilia, S. maltophilia was also grouped in the genus Xanthomonas before eventually becoming the type species of the genus Stenotrophomonas in 1993.
S. maltophilia are slightly smaller (0.7–1.8 × 0.4–0.7 micrometers) than other members of the genus. They are motile due to polar flagella and grow well on MacConkey agar producing pigmented colonies. S. maltophilia are catalase-positive, oxidase-negative (which distinguishes them from most other members of the genus) and have a positive reaction for extracellular DNase.
S. maltophilia is ubiquitous in aqueous environments, soil and plants, including water, urine, or respiratory secretions; it has also been used in biotechnology applications.[4] In immunocompromised patients, S. maltophilia can lead to nosocomial infections.
S. maltophilia is naturally resistant to many broad-spectrum antibiotics (including all carbapenems) and is thus often difficult to eradicate. Many strains of S. maltophilia are sensitive to co-trimoxazole and ticarcillin, though resistance has been increasing.[7] It is not usually sensitive to piperacillin, and sensitivity to ceftazidime is variable.
ref:http://en.wikipedia.org/wiki/Stenotrophomonas_maltophilia
Stenotrophomonas maltophilia is a Gram negative bacterium that is commonly found in the environment. It is intrinsically multi-drug resistant and occasionally causes bacteraemic and organ-specific infections in humans.
ref:http://www.sanger.ac.uk/resources/downloads/bacteria/stenotrophomonas-maltophilia.html
S. maltophilia are slightly smaller (0.7–1.8 × 0.4–0.7 micrometers) than other members of the genus. They are motile due to polar flagella and grow well on MacConkey agar producing pigmented colonies. S. maltophilia are catalase-positive, oxidase-negative (which distinguishes them from most other members of the genus) and have a positive reaction for extracellular DNase.
S. maltophilia is ubiquitous in aqueous environments, soil and plants, including water, urine, or respiratory secretions; it has also been used in biotechnology applications.[4] In immunocompromised patients, S. maltophilia can lead to nosocomial infections.
S. maltophilia is naturally resistant to many broad-spectrum antibiotics (including all carbapenems) and is thus often difficult to eradicate. Many strains of S. maltophilia are sensitive to co-trimoxazole and ticarcillin, though resistance has been increasing.[7] It is not usually sensitive to piperacillin, and sensitivity to ceftazidime is variable.
ref:http://en.wikipedia.org/wiki/Stenotrophomonas_maltophilia
Stenotrophomonas maltophilia is a Gram negative bacterium that is commonly found in the environment. It is intrinsically multi-drug resistant and occasionally causes bacteraemic and organ-specific infections in humans.
ref:http://www.sanger.ac.uk/resources/downloads/bacteria/stenotrophomonas-maltophilia.html
domingo, 4 de julho de 2010
Ochrobactrum antropi
Ochrobactrum anthropi is a non-fastidious, non-fermenting, Gram-negative cocco-bacillus.It is an emerging nosocomial pathogen, which has been found in environmental and hospital water sources.It has been reported to cause bacteraemias in immunocompromised patients, particularly oncology patients with indwelling catheters.Occasionally, probably because of its ability to survive in water supplies, epidemic outbreaks occur.
Ochrobactrum anthropi is resistant to most cephalosporins and penicillins due, at least in part, to the inducible expression of a single ß-lactamase.
http://jac.oxfordjournals.org/cgi/content/full/47/6/745
This organism is widely distributed in the environment, in soil, plants, and water sources including normal saline and antiseptic solutions, dialysis liquids, swimming pools, etc..
http://www.nih.go.jp/JJID/59/264.pdf
Ochrobactrum anthropi is resistant to most cephalosporins and penicillins due, at least in part, to the inducible expression of a single ß-lactamase.
http://jac.oxfordjournals.org/cgi/content/full/47/6/745
This organism is widely distributed in the environment, in soil, plants, and water sources including normal saline and antiseptic solutions, dialysis liquids, swimming pools, etc..
http://www.nih.go.jp/JJID/59/264.pdf
terça-feira, 29 de junho de 2010
Aeromonas veronii
Aeromonas veronii is a gram-negative, rod-shaped bacterium found in fresh water and in association with animals. It can be a pathogen of humans and a beneficial symbiont of leeches. In humans A. veronii can cause diseases ranging from wound infections and diarrhea to septicemia in immunocompromised patients. In leeches, this bacterium is thought to function in the digestion of blood, provision of nutrients or preventing other bacteria from growing.
http://en.wikipedia.org/wiki/Aeromonas_veronii
http://en.wikipedia.org/wiki/Aeromonas_veronii
domingo, 27 de junho de 2010
Comamonas testosteroni
Comamonas testosteroni is an a aerobic, motile, non-spore-forming, medium-to-long gram negative bacillus which occurs singly or in pairs and is known to use testosterone. It´s an a environmental microrganism of worldwide distribution that is found in water, soil, and on plants.
It´s not been recognized to be a component of the endogenous human microflora.
Ref: Comamonas testosteroni Bacteremia: A Case Report and Review of Literature, Abraha, JoEllyn M. MD.; Simon, Gary L. MD., PhD. Infectious Diseases in Clinical Practice, July 2007 - Volume 15, Issue 4 -pp 272-273. doi 10. 1097/IPC.0b13e31802ce475
http://journals.lww.com/infectdis/Fulltext/2007/07000/Comamonas_testosteroni_Bacteremia__A_Case_Report.15.aspx
It´s not been recognized to be a component of the endogenous human microflora.
Ref: Comamonas testosteroni Bacteremia: A Case Report and Review of Literature, Abraha, JoEllyn M. MD.; Simon, Gary L. MD., PhD. Infectious Diseases in Clinical Practice, July 2007 - Volume 15, Issue 4 -pp 272-273. doi 10. 1097/IPC.0b13e31802ce475
http://journals.lww.com/infectdis/Fulltext/2007/07000/Comamonas_testosteroni_Bacteremia__A_Case_Report.15.aspx
domingo, 20 de junho de 2010
Pseudomonas fluorescens
Pseudomonas fluorescens são bacilos Gram negativos em forma de bastão, possuem motilidade e multiplos flagelos.
São encontrados principalmente em solos e água (1)
Ref:
1 - htt://en.wikipedia.org/wiki/Pseudomonas_fluorescens Acessado em 27/01/11
São encontrados principalmente em solos e água (1)
Ref:
1 - htt://en.wikipedia.org/wiki/Pseudomonas_fluorescens Acessado em 27/01/11
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