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		<title>Annals of Clinical Microbiology and Antimicrobials - Latest articles</title>
		<link>http://www.ann-clinmicrob.com</link>
		<description>The latest articles from Annals of Clinical Microbiology and Antimicrobials (ISSN 1476-0711) published by 
				
				BioMed Central
		</description>
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				    <rdf:li rdf:resource="http://www.ann-clinmicrob.com/content/7/1/11"/>			    
            
				    <rdf:li rdf:resource="http://www.ann-clinmicrob.com/content/7/1/10"/>			    
            
				    <rdf:li rdf:resource="http://www.ann-clinmicrob.com/content/7/1/9"/>			    
            
				    <rdf:li rdf:resource="http://www.ann-clinmicrob.com/content/7/1/8"/>			    
            
				    <rdf:li rdf:resource="http://www.ann-clinmicrob.com/content/7/1/7"/>			    
            
				    <rdf:li rdf:resource="http://www.ann-clinmicrob.com/content/7/1/6"/>			    
            
				    <rdf:li rdf:resource="http://www.ann-clinmicrob.com/content/7/1/5"/>			    
            
				    <rdf:li rdf:resource="http://www.ann-clinmicrob.com/content/7/1/4"/>			    
            
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		<item rdf:about="http://www.ann-clinmicrob.com/content/7/1/11">
            
            <title>An uncommon presentation for a severe invasive infection due to methicillin-resistant Staphylococcus aureus clone USA300 in Italy: a case report </title>
			<description>Background:
Methicillin resistant Staphylococcus aureus (MRSA) has been considered for many years a typical nosocomial pathogen. Recently MRSA has emerged as a frequent cause of infections in the community. More commonly, community-acquired (CA)-MRSA is a cause of infections of the skin and soft-tissues, but life-threatening infections such as necrotizing pneumonia and sepsis can occasionally occur.Case presentationThis report describes an uncommon presentation of invasive CA-MRSA infection in an adolescent without known risk factors. The presentation was typical for bacterial meningitis, but the clinical findings also revealed necrotizing pneumonia. Following the development of deep venous thrombosis, the presence of an inherited trombophilic defect (factor V Leiden) was detected. The patient was successfully treated with an antibiotic combination including linezolid and with anticoagulant therapy. CA-MRSA was isolated from both cerebrospinal fluid and blood. The isolates were resistant to oxacillin and other beta-lactam antibiotics and susceptible to the other antibiotics tested including erythromycin. Molecular typing revealed that the strains contained the Panton-Valentine leukocidin genes and type IV SCCmec, and were ST8, spa type t008, and agr type 1. This genetic background is identical to that of the USA300 clone. 
Conclusions:
This report highlights that meningitis can be a new serious presentation of CA-MRSA infection. CA-MRSA strains with the genetic background of the USA300 clone are circulating in Italy and are able to cause severe infections. </description>
			<link>http://www.ann-clinmicrob.com/content/7/1/11</link>
			
			 	<dc:creator>Piero Valentini, Gabriella Parisi, Monica Monaco, Francesca Crea, Teresa Spanu, Orazio Ranno, Mirella Tronci and Annalisa Pantosti</dc:creator>
			
			<dc:source>Annals of Clinical Microbiology and Antimicrobials 2008, 7:11</dc:source>
			<dc:date>2008-04-30</dc:date>
			<dc:identifier>doi:10.1186/1476-0711-7-11</dc:identifier>
			
			
							
					<prism:publicationName>Annals of Clinical Microbiology and Antimicrobials</prism:publicationName>
					
			
							
					<prism:issn>1476-0711</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>11</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-04-30</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.ann-clinmicrob.com/content/7/1/10">
            
            <title>Fatal bacteremia due to immotile Vibrio cholerae serogroup O21 in Vientiane, Laos &#8211; a case report</title>
			<description>Background:
Human infections with non-O1, non-O139 V. cholerae have been described from Laos. Elsewhere, non cholera-toxin producing, non-O1, non-O139 V. cholerae have been described from blood cultures and ascitic fluid, although they are exceedingly rare isolates.Case presentationWe describe a farmer who died with Vibrio cholerae O21 bacteremia and peritonitis in Vientiane, Laos, after eating partially cooked apple snails (Pomacea canaliculata) and mussels (Ligumia species). The cultured V. cholerae were non-motile. PCR detected ompW and toxR gene regions but not the ctxA, ompU, omp K and TCP gene regions. Although the organisms lacked flagellae on scanning electron microscopy, they possessed the Vibrio flagellin flaA gene.
Conclusion:
Severe bacteremic non-O1, non-O139 V. cholerae is reported from Laos. The organisms were unusual in being non-motile. They possessed the Vibrio flagellin flaA gene. Further research to determine the reasons for the non-motility and virulence is required.</description>
			<link>http://www.ann-clinmicrob.com/content/7/1/10</link>
			
			 	<dc:creator>Rattanaphone Phetsouvanh, Masami Nakatsu, Eiji Arakawa, Viengmone Davong, Manivanh Vongsouvath, Olay Lattana, Catrin E Moore, Satoshi Nakamura and Paul N Newton</dc:creator>
			
			<dc:source>Annals of Clinical Microbiology and Antimicrobials 2008, 7:10</dc:source>
			<dc:date>2008-04-25</dc:date>
			<dc:identifier>doi:10.1186/1476-0711-7-10</dc:identifier>
			
			
							
					<prism:publicationName>Annals of Clinical Microbiology and Antimicrobials</prism:publicationName>
					
			
							
					<prism:issn>1476-0711</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>10</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-04-25</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.ann-clinmicrob.com/content/7/1/9">
            
            <title>Mycobacterium avium subspecies paratuberculosis is not associated with Type-2 Diabetes Mellitus</title>
			<description>Background:
The role of pathogenic mycobacteria in diabetes has been a focus of speculation since a decade without any meaningful insights into the mechanism of diabetes causation vis a vis mycobacterial factors. Two of our studies based on PCR identification of mycobacterial DNA and detection of antibodies specific to the recombinant antigens and whole cell lysates of the Mycobacterium avium subsp. paratuberculosis (MAP) shown a clear association of MAP with the presence of type 1 diabetes mellitus (T1DM).
Methods:
In this study, we sought to investigate if or not type 2 diabetes (T2DM) patients harbour humoral responses to MAP. Using three different MAP antigen preparations, humoral antibody profiles were estimated for 57 T2DM patients and 57 healthy controls. Statistical analysis was performed with the Chi-square test with Yates' corrections.
Results:
We observed insignificant levels of humoral antibodies against recombinant heparin binding haemagglutinin (HbHA), glycosyl transferase (Gsd) and MAP whole cell lysate in the blood of subjects with T2DM as compared to healthy controls.
Conclusion:
We found no obvious association of MAP with the incidence of T2DM in Sardinian patients.</description>
			<link>http://www.ann-clinmicrob.com/content/7/1/9</link>
			
			 	<dc:creator>Valentina Rosu, Niyaz Ahmed, Daniela Paccagnini, Adolfo Pacifico, Stefania Zanetti and Leonardo A Sechi</dc:creator>
			
			<dc:source>Annals of Clinical Microbiology and Antimicrobials 2008, 7:9</dc:source>
			<dc:date>2008-04-22</dc:date>
			<dc:identifier>doi:10.1186/1476-0711-7-9</dc:identifier>
			
			
							
					<prism:publicationName>Annals of Clinical Microbiology and Antimicrobials</prism:publicationName>
					
			
							
					<prism:issn>1476-0711</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>9</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-04-22</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
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		<item rdf:about="http://www.ann-clinmicrob.com/content/7/1/8">
            
            <title>Miliary tuberculosis with no pulmonary involvement in myelodysplastic syndromes: a curable, yet rarely diagnosed, disease: case report and review of the literature</title>
			<description>Background:
Although tuberculosis is not uncommon among patients with myelodysplastic syndrome (MDS), only a few reports of such patients suffering from miliary tuberculosis (MT) exist. MT often presents as a fever of unknown origin and it is a curable disease, yet fatal if left untreated.Case presentationWe report a case of MT with no clinical or laboratory indications of pulmonary involvement in a patient with MDS, and review the relevant literature. Mycobacterium tuberculosis was isolated from the liquid culture of a bone marrow aspirate.
Conclusion:
Even if the initial diagnostic investigation for a fever of obscure etiology is negative, MT should not be excluded from the differential diagnosis list. Since it is a curable disease, persistent and vigorous diagnostic efforts are warranted. In suspected cases, mycobacterial blood cultures should be collected as soon as possible after hospital admission and early bone marrow aspirate with mycobacterial cultures is advocated.</description>
			<link>http://www.ann-clinmicrob.com/content/7/1/8</link>
			
			 	<dc:creator>Ioannis K Neonakis, Michael G Alexandrakis, Zoe Gitti, George Tsirakis, Elias Krambovitis and Demetrios A Spandidos</dc:creator>
			
			<dc:source>Annals of Clinical Microbiology and Antimicrobials 2008, 7:8</dc:source>
			<dc:date>2008-03-13</dc:date>
			<dc:identifier>doi:10.1186/1476-0711-7-8</dc:identifier>
			
			
							
					<prism:publicationName>Annals of Clinical Microbiology and Antimicrobials</prism:publicationName>
					
			
							
					<prism:issn>1476-0711</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>8</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-03-13</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.ann-clinmicrob.com/content/7/1/7">
            
            <title>Primary psoas abscess due to Streptococcus milleri</title>
			<description>Primary Psoas abscess (PPA) is an infrequent clinical entity with obscure pathogenesis and vague clinical presentation. High index of clinical suspicion is required for the diagnosis of psoas abscess. We also emphasises the importance of bacteriological confirmation of microorganism involved, although Staphylococcus aureus remains the commonest pathogen. We report an extremely rare case of PPA caused by Streptococcus milleri. Only one case has been reported in literature so far.</description>
			<link>http://www.ann-clinmicrob.com/content/7/1/7</link>
			
			 	<dc:creator>Nitin B Bagul, Abeywardana MS Abeysekara and Sabu Jacob</dc:creator>
			
			<dc:source>Annals of Clinical Microbiology and Antimicrobials 2008, 7:7</dc:source>
			<dc:date>2008-02-26</dc:date>
			<dc:identifier>doi:10.1186/1476-0711-7-7</dc:identifier>
			
			
							
					<prism:publicationName>Annals of Clinical Microbiology and Antimicrobials</prism:publicationName>
					
			
							
					<prism:issn>1476-0711</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>7</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-02-26</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.ann-clinmicrob.com/content/7/1/6">
            
            <title>Correction: Helicobacter pylori and gastroduodenal pathology: New threats of the old friend</title>
			<description>Since publication of our article (Ahmed and Sechi: Ann Clin Microbiol Antimicrob 2005, 4:1), we have noticed several errors.</description>
			<link>http://www.ann-clinmicrob.com/content/7/1/6</link>
			
			 	<dc:creator>Niyaz Ahmed and Leonardo A Sechi</dc:creator>
			
			<dc:source>Annals of Clinical Microbiology and Antimicrobials 2008, 7:6</dc:source>
			<dc:date>2008-02-20</dc:date>
			<dc:identifier>doi:10.1186/1476-0711-7-6</dc:identifier>
			
			
							
					<prism:publicationName>Annals of Clinical Microbiology and Antimicrobials</prism:publicationName>
					
			
							
					<prism:issn>1476-0711</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>6</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-02-20</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.ann-clinmicrob.com/content/7/1/5">
            
            <title>Fatal necrotizing pneumonia due to a Panton-Valentine leukocidin positive community-associated methicillin-sensitive Staphylococcus aureus and Influenza co-infection: a case report</title>
			<description>Recent studies have described a number of fatalities due to methicillin-resistant Staphylococcus aureus (MRSA) and influenza virus co-infection. MRSA isolates provide a challenge to caregivers due to inherent wide range antibiotic resistance. Many facilities have instituted screening methods, based on the presence of antibiotic resistance genes, to identify MRSA positive patients upon admission. However, the resistance profile of the pathogen does not necessarily determine the severity of disease caused by that organism.We describe a fatal case of necrotizing pneumonia in a patient co-infected with Influenza B and a community-associated, PVL-positive methicillin-susceptible Staphylococcus aureus (MSSA).</description>
			<link>http://www.ann-clinmicrob.com/content/7/1/5</link>
			
			 	<dc:creator>Jill C Roberts, Sam P Gulino, K Kealy Peak, Vicki A Luna and Roger Sanderson</dc:creator>
			
			<dc:source>Annals of Clinical Microbiology and Antimicrobials 2008, 7:5</dc:source>
			<dc:date>2008-02-19</dc:date>
			<dc:identifier>doi:10.1186/1476-0711-7-5</dc:identifier>
			
			
							
					<prism:publicationName>Annals of Clinical Microbiology and Antimicrobials</prism:publicationName>
					
			
							
					<prism:issn>1476-0711</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>5</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-02-19</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.ann-clinmicrob.com/content/7/1/4">
            
            <title>In vitro activity of tigecycline and comparators against carbapenem-susceptible and resistant Acinetobacter baumannii clinical isolates in Italy</title>
			<description>Background:
In a recent multi-centre Italian survey (2003&#8211;2004), conducted in 45 laboratories throughout Italy with the aim of monitoring microorganisms responsible for severe infections and their antibiotic resistance, Acinetobacter baumannii was isolated from various wards of 9 hospitals as one of the most frequent pathogens. One hundred and seven clinically significant strains of A. baumannii isolates were included in this study to determine the in vitro activity of tigecycline and comparator agents.
Methods:
Tests for the susceptibility to antibiotics were performed by the broth microdilution method as recommended by CLSI guidelines. The following antibiotics were tested: aztreonam, piperacillin/tazobactam, ampicillin/sulbactam, ceftazidime, cefepime, imipenem, meropenem tetracycline, doxycycline, tigecycline, gentamicin, amikacin, ciprofloxacin, colistin, and trimethoprim/sulphametoxazole. The PCR assay was used to determine the presence of OXA, VIM, or IMP genes in the carbapenem resistant strains.
Results:
A. baumannii showed widespread resistance to ceftazidime, ciprofloxacin and aztreonam in more than 90% of the strains; resistance to imipenem and meropenem was 50 and 59% respectively, amikacin and gentamicin were both active against about 30% of the strains and colistin about 99%, with only one strain resistant. By comparison with tetracyclines, tigecycline and doxycycline showed a higher activity. In particular, tigecycline showed a MIC90 value of 2 mg/L and our strains displayed a unimodal distribution of susceptibility being indistinctly active against carbapenem-susceptible and resistant strains, these latter possessed OXA-type variant enzymes.
Conclusion:
In conclusion, tigecycline had a good activity against the MDR A. baumannii strains while maintaining the same MIC90 of 2 mg/L against the carbapenem-resistant strains.</description>
			<link>http://www.ann-clinmicrob.com/content/7/1/4</link>
			
			 	<dc:creator>Maria Lina Mezzatesta, Giusi Trovato, Floriana Gona, Vito Mar Nicolosi, Daria Nicolosi, Alessandra Carattoli, Giovanni Fadda, Giuseppe Nicoletti and Stefania Stefani</dc:creator>
			
			<dc:source>Annals of Clinical Microbiology and Antimicrobials 2008, 7:4</dc:source>
			<dc:date>2008-02-08</dc:date>
			<dc:identifier>doi:10.1186/1476-0711-7-4</dc:identifier>
			
			
							
					<prism:publicationName>Annals of Clinical Microbiology and Antimicrobials</prism:publicationName>
					
			
							
					<prism:issn>1476-0711</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>4</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-02-08</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.ann-clinmicrob.com/content/7/1/3">
            
            <title>Osteomalacia in an HIV-infected man receiving rifabutin, a cytochrome P450 enzyme inducer: a case report</title>
			<description>IntroductionPeople infected with human immunodeficiency virus are frequently treated with medications that can induce or inhibit cytochrome P450 enzymes.Case presentationA 59 year old man treated with zidovudine, lamivudine, indinavir, and ritonavir for infection with human immunodeficiency virus volunteered to take part in a study of bone loss. He was found to have vitamin D insufficiency with secondary hyperparathyroidism and received vitamin D and calcium supplementation. He suffered a recurrence of infection with Mycobacterium avium intracellulare for which he received treatment with ciprofloxacin, rifabutin, and ethambutol. Subsequently, he developed worsening vitamin D deficiency with hypocalcaemia, secondary hyperparathyroidism and elevated markers of bone turnover culminating in an osteomalacic vertebral fracture. Correction of the vitamin D deficiency required 100,000 IU of cholecalciferol monthly.Rifabutin is a cytochrome P450 inducer, and vitamin D and its metabolites are catabolised by cytochrome P450 enzymes. We therefore propose that treatment with rifabutin led to the induction of cytochrome P450 enzymes catabolising vitamin D, thereby causing vitamin D deficiency and osteomalacia. This process might be mediated through the steroid and xenobiotic receptor (SXR).
Conclusion:
Treatment with rifabutin induces the cytochrome P450 enzymes that metabolise vitamin D and patients treated with rifabutin might be at increased risk of vitamin D deficiency. In complex medication regimens involving agents that induce or inhibit cytochrome P450 enzmyes, consultation with a clinical pharmacist or pharmacologist may be helpful in predicting and/or preventing potentially harmful interactions.</description>
			<link>http://www.ann-clinmicrob.com/content/7/1/3</link>
			
			 	<dc:creator>Mark J Bolland, Andrew Grey, Anne M Horne and Mark G Thomas</dc:creator>
			
			<dc:source>Annals of Clinical Microbiology and Antimicrobials 2008, 7:3</dc:source>
			<dc:date>2008-01-28</dc:date>
			<dc:identifier>doi:10.1186/1476-0711-7-3</dc:identifier>
			
			
							
					<prism:publicationName>Annals of Clinical Microbiology and Antimicrobials</prism:publicationName>
					
			
							
					<prism:issn>1476-0711</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>3</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-01-28</prism:publicationDate>
					

            <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/"/>
        </item>
	
		<item rdf:about="http://www.ann-clinmicrob.com/content/7/1/2">
            
            <title>Comprehensive bactericidal activity of an ethanol-based hand gel in 15 seconds</title>
			<description>Background:
Some studies indicate that the commonly recommended 30 s application time for the post contamination treatment of hands may not be necessary as the same effect may be achieved with some formulations in a shorter application time such as 15 s.MethodWe evaluated the bactericidal activity of an ethanol-based hand gel (Sterillium&#174; Comfort Gel) within 15 s in a time-kill-test against 11 Gram-positive, 16 Gram-negative bacteria and 11 emerging bacterial pathogens. Each strain was evaluated in quadruplicate.
Results:
The hand gel (85% ethanol, w/w) was found to reduce all 11 Gram-positive and all 16 Gram-negative bacteria by more than 5 log10 steps within 15 s, not only against the ATCC test strains but also against corresponding clinical isolates. In addition, a log10 reduction > 5 was observed against all tested emerging bacterial pathogens.
Conclusion:
The ethanol-based hand gel was found to have a broad spectrum of bactericidal activity in only 15 s which includes the most common species causing nosocomial infections and the relevant emerging pathogens. Future research will hopefully help to find out if a shorter application time for the post contamination treatment of hands provides more benefits or more risks.</description>
			<link>http://www.ann-clinmicrob.com/content/7/1/2</link>
			
			 	<dc:creator>G&#252;nter Kampf and Angela Hollingsworth</dc:creator>
			
			<dc:source>Annals of Clinical Microbiology and Antimicrobials 2008, 7:2</dc:source>
			<dc:date>2008-01-22</dc:date>
			<dc:identifier>doi:10.1186/1476-0711-7-2</dc:identifier>
			
			
							
					<prism:publicationName>Annals of Clinical Microbiology and Antimicrobials</prism:publicationName>
					
			
							
					<prism:issn>1476-0711</prism:issn>
					
			
							
					<prism:volume>7</prism:volume>
					
			
							
					<prism:startingPage>2</prism:startingPage>
					
			
							
					<prism:publicationDate>2008-01-22</prism:publicationDate>
					

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