The additional necroses of the superficial fascia and fat produces a thin watery malodorous fluid and crepitance (usually associated with polymicrobial infections including Enterobacteriaceae and Clostridiae spp) are results in more evident signs of necrotizing infection.

Patients with SIRS can have high fever, anxiety, altered mental status, leukocitosis, shock and tachypnea. In that particular case, when severe soft tissue infections is already selleck inhibitor suspected, the usage of the LRNIC scoring system for prediction of NF are very useful for exact diagnosis [2, 20]. By the time the progression of clinical signs becomes obvious, the appearance is usually that of a late NF phase, with visible bruising, bullae and cutaneous necrosis due to the extension of the necrotizing process from the deep fascia and horizontal spread [1]. The case history click here at that moment should suggest the causative microorganisms of infection. Nevertheless, the lack of cutaneous findings early in the course of the disease makes the diagnosis more challenging, and a high suspicion is essential for each clinical sign that appears on the skin and subcutaneous tissue. The accumulation of gas formation

in the soft tissue, which is seen in half of all NF cases, is another cardinal sign of NF diagnosis. It is clearly visible on plain x-ray pictures. More useful clinical findings are visible with eFT508 concentration ultrasound, CT Org 27569 scan and MRI. We prefer an additional skin puncture with large gauge needles to mobilize gas from subcutaneous spaces. If we do not find any gas bubbles, but the clinical picture presents other relevant clinical

signs of NF, we must perform a radical surgical debridement as soon as possible, and prescribe broad-spectrum antibiotics that cover aerobic and anaerobic microbial species [15, 24]. Diagnostic imaging modalities The most important clinical signs of NF are tissue necrosis, putrid discharge, bullae, severe pain, gas formations in soft tissue, rapid spreading through fascial planes and the lack of classical tissue inflammatory signs, i.e. “”dolor, color, rubor, tumor and functio laesa”". Today, CT and MRI are superior methods compared to sonography, scintigraphy and plain radiography, which also provide useful information about the nature and the extent of necrotizing infection [1, 2, 35]. Nevertheless, physical examination and a clear understanding of the clinical picture are the most important means in establishing an early diagnosis of any type of NSTI and NF [6, 36]. Treatment Successful treatment of NSTI requires a multidisciplinary approach from the onset and coordination between general practitioners and surgeons for outpatient cases, and between the surgeons and other specialists in hospital facilities. The first and economically most important decision in treating necrotizing infections concerns the need for hospitalization.

Moreover, vimentin is selectively expressed in aggressive learn more breast cancer cell lines [3]. Elevated vimentin expression level correlates well with up-regulated migration and invasion of cancer cells [3, 4]. The transfection of the non-invasive human breast cancer cell line (MCF7) with vimentin gene led to accelerated invasiveness [5]. Other data showed that more invasive breast cancer lines expressed vimentin, suggesting its usefulness in identifying cases with poorer prognosis [6]. Vimentin reactive cells in benign and malignant breast tissue have been described by many

authors [4, 7]. The same applies to a possible association with clinically aggressive behavior of tumours [7], which may be explained by VEGFR inhibitor correlation with estrogen receptor negativity [8, 9], high Ki-67 level [9] and poor differentiation of tumours (high grade) [10, 11]. Few reports are in opposite, as they showed that vimentin expression did not inversely predict patient survival [12]. The cDNA microrray experiments enabled the identification of different subgroups of breast tumours with distinct molecular signatures [13–15]. This molecular classification delineated at least four biologically different phenotypes:

luminal phenotype (generally, estrogen receptor positive tumours), normal breast-like phenotype and estrogen receptor negative tumours, comprising the subgroups of HER2 (overexpression of ERBB2 oncogene) and basal-like phenotypes (tumours expressing genetic markers that are characteristic of the myoepithelium of the normal mammary gland, such as epidermal growth GF120918 order factor receptor, p63 and basal cytokeratins CK 5/6,

CK 14, CK17 [13–15]. It is also known that a subgroup with HER 2 overexpression and basal-like phenotype correlate with poor prognosis. Many efforts have been undertaken to reproduce this classification Fenbendazole with the use of immunohistochemistry instead of assessment of mRNA [16–18]. Some researchers suggested that immunohistochemically triple negative tumours (ER, PgR, and HER 2-negativity) could reliably be defined as basal-like tumours, making these two subgroups synonymous [19]. Others believe that equating triple negative tumours with basal-like breast cancer is misleading [20]. However, there is a common agreement that the key point of basal-like characteristics is triple negativity of tumours. On the other hand, it should be stressed that not only basal-like cancers harbour a triple negative phenotype at the mRNA level, and normal-breast like cancers also have this feature [13, 21]. It has been shown that typical features of basal-like tumours include the expression of: high molecular weight cytokeratins – CK5/6, 14, 17 (so-called basal type cytokeratins) [18, 22, 23], expression of epidermal growth factor receptor (EGFR), c-kit, P53, and vimentin [4, 16, 18, 20, 23, 24].

IR (KBr), ν (cm−1): 3256 (NH), 3083 (CH aromatic), 2955, 1489, 741 (CH aliphatic), 1610 (C=N), 1503

(C–N), 679 (C–S). 1H NMR (Thiazovivin in vitro DMSO-d 6) δ (ppm): 3.87 (s, 2H, CH2), 4.12 (d, J = 5 Hz, 2H, CH2), 5.02–5.13 (dd, J = 5 Hz, J = 5 Hz, 2H, =CH2), ARRY-438162 manufacturer 5.79–5.88 (m, 1H, CH), 7.40–8.56 (m, 10H, 10ArH), 10.13 (brs, 1H, NH). 5-Aminocyclohexyl-2-[(4,5-diphenyl-4H-1,2,4-triazol-3-yl)sulfanyl]methyl-1,3,4-thiadiazole (6c) Yield: 75.6 %, mp: 172–174 °C (dec.). Analysis for C23H24N6S2 (448.61); calculated: C, 61.58; H, 5.39; N, 18.73; S, 14.30; found: C, 61.61; H, 5.37; N, 18.76; S, 14.27. IR (KBr), ν (cm−1): 3190 (NH), 3093 (CH aromatic), 2972, 1467, 749 (CH aliphatic), 1620 (C=N), 681 (C–S). 1H NMR (DMSO-d 6) δ (ppm): 1.1–1.65 (m, 10H, 5CH2 cyclohexane), 3.03 (m, 1H, CH cyclohexane), 4.22 (s, 2H, CH2), 7.33–8.06 (m, 10H, 10ArH), 10.16 (brs, 1H, NH). 5-Aminophenyl-2-[(4,5-diphenyl-4H-1,2,4-triazol-3-yl)sulfanyl]methyl-1,3,4-thiadiazole (6d) Yield: 50.9 %, mp: 192–198 °C (dec.). Analysis for C23H18N6S2

(442.60); calculated: C, 62.42; H, 4.10; N, 19.00; S, 14.49; found: C, 62.36; H, 4.09; N, 18.97; S, 14.53. IR (KBr), ν (cm−1): 3199 (NH), 3011 (CH aromatic), 2968 (CH aliphatic), 1610 (C=N), 1504 (C–N), 683 (C–S). 1H NMR (DMSO-d 6) δ (ppm): 4.02 (s, 2H, CH2), 6.98–7.54 (m, 15H, 15ArH), 4EGI-1 clinical trial 10.42 (brs, 1H, NH). [5-Amino-(4-bromophenyl)]-2-[(4,5-diphenyl-4H-1,2,4-triazol-3-yl)sulfanyl]methyl-1,3,4-thiadiazole (6e) Yield: 89.4 %, mp: 203–205 °C (dec.). Analysis for C23H17BrN6S2 (521.45); calculated: C, 52.98; H, 3.29; N, 16.12; S, 12.30; Br, 15.32; found: C, 52.73; H, 3.27; N, 16.15; S, 12.27. IR (KBr), ν (cm−1): 3167 (NH), 3110

(CH aromatic), 2954, 1441 (CH aliphatic), 1602 (C=N), 680 (C–S). 1H NMR (DMSO-d 6) δ (ppm): 4.22 (s, 2H, CH2), 6.89–7.65 (m, 14H, 14ArH), 10.23 (brs, 1H, NH). [5-Amino-(4-chlorophenyl)]-2-[(4,5-diphenyl-4H-1,2,4-triazol-3-yl)sulfanyl]methyl-1,3,4-thiadiazole (6f) Yield: 94.7 %, mp: 215–218 °C (dec.). Analysis for C23H17ClN6S2 (477.00); calculated: C, 57.91; H, 3.59; N, 17.62; S, 13.44; Celecoxib Cl, 7.43; found: C, 57.71; H, 3.60; N, 17.58; S, 13.39. IR (KBr), ν (cm−1): 3245 (NH), 3065 (CH aromatic), 2977 (CH aliphatic), 1611 (C=N), 1506 (C–N), 695 (C–S). 1H NMR (DMSO-d 6) δ (ppm): 3.89 (s, 2H, CH2), 7.39–7.64 (m, 14H, 14ArH), 10.36 (brs, 1H, NH). [5-Amino-(4-methoxyphenyl)]-2-[(4,5-diphenyl-4H-1,2,4-triazol-3-yl)sulfanyl]methyl-1,3,4-thiadiazole (6g) Yield: 53.6 %, mp: 152–154 °C (dec.).

Liver x receptor modulates diabetic retinopathy outcome in a mouse model of streptozotocin-induced diabetes. Diabetes. 2012;61:3270–9.PubMedCentralPubMedCrossRef 23. Guilford BL, Ryals JM, Wright

DE. Phenotypic changes in diabetic neuropathy induced by a high-fat diet in diabetic C57BL/6 mice. Exp Diabetes Res. 2011;2011:848307.PubMedCentralPubMedCrossRef 24. Zeng XY, Wang selleck chemical YP, Cantley J, Iseli TJ, Molero JC, Hegarty BD, Kraegen EW, Ye Y, Ye JM. Oleanolic acid reduces hyperglycemia beyond treatment period with Akt/FoxO1-induced suppression of hepatic gluconeogenesis in type-2 diabetic mice. PLoS One. 2012;7:e42115.PubMedCentralPubMedCrossRef 25. Moitra J, Mason MM, Olive M, Krylov D, Gavrilova O, Marcus-Samuels B, Feigenbaum L, Lee E, Aoyama T, Eckhaus M, Reitman ML, Vinson C. Life without white fat: a transgenic mouse. Genes

Dev. 1998;12:3168–81.PubMedCentralPubMedCrossRef 26. Kim JK, Gavrilova O, Chen Y, Reitman ML, Shulman GI. Mechanism of insulin resistance in A-ZIP/F-1 fatless mice. J Biol Chem. 2000;275:8456–60.PubMedCrossRef 27. Suganami T, Mukoyama M, Mori K, Yokoi H, Koshikawa M, Sawai K, Hidaka S, Ebihara K, Tanaka T, Sugawara A, Kawachi H, Vinson C, Ogawa Y, Nakao K. Prevention and reversal of renal injury by leptin in a new mouse model of diabetic nephropathy. FASEB J. 2005;19:127–9.PubMed 28. Keren P, George J, Keren G, Harats D. Non-obese diabetic (NOD) mice exhibit an increased cellular immune response to glycated-LDL but are resistant to high selleck chemicals llc fat diet induced atherosclerosis. Atherosclerosis. 2001;157:285–92.PubMedCrossRef 29. Fox TE, Bewley MC, Unrath KA, Pedersen MM, Anderson RE, Jung DY, Jefferson LS, Kim JK, Bronson SK, Flanagan JM, Kester M. Circulating sphingolipid biomarkers in models of type 1 diabetes. J Lipid Res. 2011;52:509–17.PubMedCentralPubMedCrossRef 30. Colombo C, Haluzik M, Cutson JJ, Dietz KR, Marcus-Samuels B, Vinson C, Gavrilova O, Reitman ML. Opposite http://www.selleck.co.jp/products/CHIR-99021.html effects of background genotype on muscle and liver insulin sensitivity of lipoatrophic mice. Role of triglyceride clearance. J Biol Chem.

2005;278:3992–9.CrossRef 31. check details Breyer MD, Bottinger E, Brosius FC 3rd, Coffman TM, Harris RC, Heilig CW, Sharma K. Mouse models of diabetic nephropathy. J Am Soc Nephrol. 2005;16:27–45.PubMedCrossRef 32. Brosius FC 3rd, Alpers CE, Bottinger EP, Breyer MD, Coffman TM, Gurley SB, Harris RC, Kakoki M, Kretzler M, Leiter EH, Levi M, McIndoe RA, Sharma K, Smithies O, Susztak K, Takahashi N, Takahashi T. Mouse models of diabetic nephropathy. J Am Soc Nephrol. 2009;20:2503–12.PubMedCentralPubMedCrossRef 33. Qi Z, Fujita H, Jin J, Davis LS, Wang Y, Fogo AB, Breyer MD. Characterization of susceptibility of inbred mouse strains to diabetic nephropathy. Diabetes. 2005;54:2628–37.PubMedCrossRef 34. Agellon LB, Walsh A, Hayek T, Moulin P, Jiang XC, Shelanski SA, Breslow JL, Tall AR.

Further analysis of the locus was undertaken for 7 of these strains distributed in 5 clusters. Amplification obtained with primers designed on the basis of the L. sakei 23 K genome outside of sigH suggested that the genetic context is conserved in all these strains (see position of primers AML50 and AML58 in Figure 1). Polymorphism analysis of the sigH sequences brought additional information. As shown in Figure 3, 29 polymorphic sites were identified in the sigH CDS, of which only 9 were involved in 7 aa changes,

mostly conservative. Thus, SigH function selleck and coding gene location appear to be conserved in the L. sakei species. Figure 3 Polymorphic nucleotide sites of sigH sequences in L. sakei. The entire CDS sequence (561 nt) was analyzed with MEGA software http://​www.​megasoftware.​net/​. Only nucleotide residues different from the upper line sequence are written. The site numbers at the top are in vertical format. Letter-code genetic cluster according to Chaillou et al. [20] is indicated for each strain and reported subspecies are shaded differently. Polymorphic deduced aa are indicated under the sequence. L. Selleckchem BTK inhibitor lactis subspecies lactis and cremoris exhibit two comX allelic

types whose nucleotide divergence is at most 27.5% [21]. In contrast, sigH divergence (4.5% maximum divergence) was incongruent with the previously reported genotypic classification of L. sakei strains [20], DMXAA chemical structure and its two proposed subspecies (Figure 3). This discrepancy may be explained either by a particular evolutionary history of that gene in L. sakei or by the possibility PJ34 HCl that the classification based on the flexible gene pool does not reflect the phylogenetic relationships between strains which remain to be established. High nucleotide divergence between species, contrasted with generally higher conservation within species, was also observed for sigH loci in the genus Staphylococcus [22]. The reason for such high inter-species polymorphism

is unknown. However, rapid evolution after species divergence rather than lateral gene transfer may be responsible, as the phylogeny of sigH genes was reported to be concordant with species phylogeny in staphylococci [22]. As reported in this paper, functional studies were further conducted on RV2002, a derivative of L. sakei strain 23 K, for which genome data is available, and in which the endogenous β-galactosidase encoding gene is inactivated, thus enabling the use of a lacZ reporter gene [23]. Temporal transcription of sigH In B. subtilis, sigH Bsu transcription increases from mid-exponential to stationary phase [24]. We used quantitative PCR (qPCR) following reverse transcription to determine if sigH Lsa expression in L. sakei is also temporally regulated. L. sakei was cultivated in chemically defined medium (MCD) at 30°C and total RNA was extracted from cells 2 h after inoculation and every hour from 4 to 8 h.

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apples using a multiparametric fluorescence sensor. J Sci Food Agric 92:1855–1864 Beutler M, Wiltshire KH, Meyer B, Moldaenke C, Lüring C, Meyerhöfer M, Hansen U-P, Dau H (2002) A fluorometric method for the differentiation of algal populations in vivo and in situ. Photosynth Res 72:39–53PubMed Bilger W, Björkman O (1990) Role of the xanthophylls cycle in photoprotection elucidated by measurements of light-induced absorbance changes, fluorescence and photosynthesis in leaves of Hedera canariensis. Photosynth Res 25:173–185PubMed Bilger W, Björkman O (1991) Temperature dependence of violaxanthin de-epoxidation and non-photochemical fluorescence quenching in intact leaves of Gossypium hirsutum L. and

Malva parviflora L. Planta 184:226–234PubMed Bilger W, Schreiber U (1986) Energy-dependent Pictilisib research buy quenching of dark-level chlorophyll fluorescence in intact leaves. Photosynth Res 10:303–308PubMed Bilger W, Veit M, Schreiber L, Schreiber U (1997) Measurement of leaf epidermal transmittance of UV radiation by chlorophyll fluorescence. Physiol Plant 101:754–763 Björkman O, Demmig B (1987) Photon yield of O2 evolution and chlorophyll fluorescence characteristics at 77 K among vascular plants of diverse origins. Planta 170:489–504PubMed Boisvert S, Joly D, Carpentier R (2006) Quantitative analysis of the experimental O–J–I–P chlorophyll fluorescence induction

kinetics: apparent activation energy and origin of each step. FEBS J 273:4770–4777PubMed Bonente G, Passarini F, Cazzaniga S, Mancone C, Buia MC, Tripodi M, Bassi R, Caffarri S (2008) selleck screening library The occurrence of the psbS gene product in Chlamydomonas reinhardtii and in other photosynthetic organisms and its correlation with energy quenching. Photochem Photobiol 84:1359–1370PubMed Bonora A, Pancaldi S, Gualandri R, Fasulo MP (2000) LY2874455 in vitro Carotenoid and ultrastructure variations in plastids of Arum italicum Miller fruit during maturation and ripening. J Exp Bot 51:873–884PubMed Bota J, Medrano H, Flexas J (2004) Is photosynthesis limited by decreased Rubisco activity and RuBP content under progressive water stress? New Phytol 162:671–681 Bradbury M, Baker NR (1981) Analysis of the slow phases of the in vivo chlorophyll fluorescence induction curve. Changes in the redox state of photosystem II electron acceptors and fluorescence emission from photosystems I and II.

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These results suggested that a putative transcription factor of the phtD operon is present in P. syringae pv. phaseolicola NPS3121 MCC950 clinical trial during growth at both temperatures. The putative transcription factor of the phtD operon is encoded outside of the Pht cluster In general, genes that participate in the synthesis of phytotoxins are grouped together in a particular chromosomal region, within which are encoded both structural genes and regulatory proteins involved in the process [24]. However, in the case of P. syringae

pv. phaseolicola it is unknown whether all genes necessary for the synthesis and regulation of phaseolotoxin are found within the Pht cluster. We performed a bioinformatic analysis for each of the predicted ORFs of the Pht cluster, in a search for DNA binding motifs using the Pfam database (http://​pfam.​sanger.​ac.​uk/​) [25]. According S3I-201 to this analysis, no DNA binding motif was found in the Pht gene cluster (data not shown). In order to assess

whether the putative transcription factor of the phtD operon as revealed through the mobility shift analysis was encoded outside or within the Pht region, gel-shift assays were performed using crudes extracts from P. syringae pv. phaseolicola strain CLY233, a non-toxigenic strain lacking the Pht cluster and P. KPT-8602 chemical structure syringae pv. tomato DC3000 (non phaseolotoxin-producer) grown at 18°C and 28°C in M9 minimal medium. Incubation

of the radiolabeled P phtD fragment with crude protein extracts of the above mentioned strains demonstrated the presence check of a retarded mobility complex similar to that obtained with protein extracts of P. syringae pv. phaseolicola NPS3121 (Figure 2). Mobility shift competition assays with specific and non-specific probes indicated that the observed DNA-protein binding was specific for the P phtD region (data not shown). These results indicated that the putative transcription factor binding upstream of phtD was encoded by a gene located outside of Pht region that is shared with other pathovars and thus is not specific for phaseolotoxin synthesis, and also that its presence is independent of temperature. Therefore, these results suggest that upon transfer of the Pht cluster horizontally, the regulation of phaseolotoxin synthesis adapted to pre-existing regulatory mechanisms of P. syringae pv. phaseolicola NPS3121. Figure 2 Gel shift assays with crude extracts of different pathovars of P. syringae. Radiolabeled P phtD fragment was incubated with protein extracts of P. syringae pv. phaseolicola strains NPS3121and CLY233, and P. syringae pv. tomato DC3000, grown at 18°C and 28°C in M9 minimal medium. Gel shift assays were carried out under conditions similiar to those used with crude extracts of the wild-type strain. The arrow indicates the DNA-protein complex.

acetobutylicum[81], also found in a number of Thermoanaerobacter species, these oxidoreductases may also be capable of converting pyruvate into acetyl-CoA. Formate production was consistent with the presence of PFL (Cthe_0505). While a number of studies have reported formate production [3–5, 35, 55], others have not [50, 68, 82]. These discrepancies may be a result of the use of different see more detection methods (gas chromatography

vs high pressure liquid chromatography), fermentation conditions (batch with no pH control vs bioreactor with pH control), or media composition (complex vs minimal). Expression levels of PFL were lower than that of POR Cthe_2390-2393, in agreement with end-product accumulation rates and previously reported enzyme activities [4]. Of the four putative PFL-activating enzymes (Cthe_0506, Cthe_0647, Cthe_1167, Cthe_1578) required for glycyl radical formation on the C-terminal portion of PFL [83, 84], only Cthe_0506 was detected. While this agreed with high mRNA levels in cellobiose [22] and

cellulose grown batch cultures [37], Raman et al. also reported high expression levels of Cthe_0647 during fermentation. While PFL and PFL-activating enzyme Cthe_0506 are encoded next to each other, the 3-fold difference in expression levels suggests that they are either transcribed independently as in Streptococcus bovis[85], or have different protein Staurosporine ic50 stabilities. While LDH was expressed,

albeit at lower levels than detected PORs and PFL, lactate production was not detected under the conditions tested. In C. thermocellum mafosfamide LDH has been shown to be allosterically activated by fructose-1,6-bisphosphate (FDP), [20] while in Caldicellulosiruptor saccharolyticus, a close relative to C. thermocellum, LDH is activated by FDP and ATP, and inhibited by NAD+ and PPi[21]. While lactate production in C. thermocellum was observed in batch cultures under carbon excess [3] and low culture pH (Rydzak et al. unpublished), this may be due to high intracellular FDP, concentrations, high NADH/NAD+ ratios, and/or high ATP/PPi ratios during transition to stationary phase [21], which may have not been reached under our growth conditions. Acetyl-CoA/ethanol/acetate branchpoint Catabolism of selleck chemical acetyl-CoA into ethanol and acetate plays an important role in NADH reoxidation and energy conservation, respectively. Acetyl-CoA can be converted into ethanol directly using a bi-functional acetaldehyde/alcohol dehydrogenase (Cthe_0423; adhE), or indirectly via an NADH-dependant aldehyde dehydrogenase (Cthe_2238; aldH) and a number of iron containing alcohol dehydrogenases (Cthe_0101, Cthe_0394, Cthe_2579; adh). Expression of Cthe_2238 (aldH), Cthe_0394 (adhY), and Cthe_2579 (adhZ) has been confirmed by real-time PCR [35]. Of these ADHs, AdhE was the most abundant ADH detected (Figure  3b).

We observed no selleck chemicals llc evidence, but can not exclude, the possibility that clinical isolates may have acquired specific pathogenicity factors beyond T3SS on plasmids or other mobile elements, as has been reported for phytopathogenic

strains [44,45]. The T3SS discovered in some strains, however, was found to be more closely related to that in biocontrolPseudomonasspp. indicating a non-pathogenic function [57]. Furthermore, only one clinical isolate had a T3SS gene compared to six environmental isolates. Comparison between the completed genome of biocontrol strain C9-1 and the in progress genome sequencing of the clinical type strain ofP. agglomeransLMG 1286T(T.H.M. Smits, B. Duffy et al., unpublished data) indicates that several features including CHIR-99021 mouse antibiotic production (revealed OSI-027 cell line by the presence ofpaaABCgenes [58]), and nectar sugar utilization as a sole carbon source are generally associated with antagonistic activity. Our results demonstrate, however, that while many biocontrol strains have such traits, not all do and thus these are not universal features of biocontrol potential. Also, we have demonstrated

for the first time the presence of the antibiotic biosynthetic genespaaABCin clinical strains, indicating that these may not be unique signatures of biocontrol isolates. What if any role pantocin may contribute to animal associations remains to be determined. There was no difference in growth at 37°C Celastrol between clinical and biocontrol isolates, with both types of strains growing poorly at this temperature compared to growth at 27°C, and reinforcing the weakness of this criteria to determine pathogenicity. Returning to the fundamental problem of insufficient confidence in identification procedures, we have shown that specific gene sequences (such asgyrBrather than 16S rDNA) are more robust than biochemical identification regardingP. agglomerans. The several reports ofP. agglomeransfrom clinical

literature upon which biosafety decisions have been based all lack a clear establishment of this species as a primary and singular cause of disease. With rare exception such isolates are not available for precise taxonomic confirmation and detailed clinical histories are typically absent for individual strains. We conducted a small survey of three clinical diagnostic laboratories in Switzerland and found thatP. agglomeransis infrequently recovered.P. agglomeranswas identified, predominantly as a polymicrobial co-isolate in patients, 21 times in the last four years at the ICM in Bellinzona (M. Tonolla, personal communication) and six times in the last three years at the Kantonsspital Lucerne (M. Hombach, personal communication).