In our case report, it was the local port physician who suspected the disease in two sailors that were sent to his office by the ship’s Navitoclax solubility dmso agent. He promptly alerted the port health officer for further evaluation and preventative measures being aware that the toxins do not produce immunity but do accumulate, thus remnants of the poisonous fish might produce further disease. Confirmation of ciguatoxin in fish by appropriate laboratory diagnosis is not available as a routine test in most parts of the world.

At present, therefore, ciguatera fish poisoning diagnosis is based on the presentation of typical symptoms and time course, the history of having eaten a reef fish in a “ciguatera belt” region like the Caribbean, and the exclusion of other diagnoses that could account for the symptoms. Ciguatera fish poisoning has symptoms in common with paralytic and neurotoxic

shellfish poisonings, scombroid and pufferfish toxicity, botulism, bacteremia, and several neurologic conditions.[2] In our case the diagnosis was strongly supported by the fact that multiple seafarers from a single ship that consumed the same fish, all experienced typical signs, symptoms, and time course consistent with ciguatera fish poisoning. Ciguatoxins Quizartinib are known as highly potent natural substances that cause symptoms even in low doses. In our case study, we observed a relationship between severity of symptoms and amount of fish ingested. Owing to the preparation of food from a common source on ships, attack rates in crews are high. In a Norwegian cargo ship 85% of crew members got sick.[5] In a port in the UK, half of the crew (14 people) on a Colombian ship ate white snapper in the Caribbean; as a result,

all persons got sick with gastrointestinal symptoms and most with neurological symptoms.[7] In our case report from Hamburg, all 14 sailors that ate from the fish got sick. A varying degree of symptoms persisted for at least 2 weeks after the ciguatoxic fish meal in all but 1 affected sailors. While most authors describe the vanishing of symptoms after 1 to 4 days, others emphasize that neurological and neuropsychiatric symptoms may persist CHIR-99021 nmr for years.[1, 2, 9] On grounds of this uncertainty, the repatriation of the two most severely affected sailors was supported by the port medical officer (C. S.) for medical reasons. Published data on the case fatality rate of the disease vary between <0.1 and 7%.[1, 2, 7] Even if no fatality occurs, the disease may pose a threat to the ship’s operations and safety due to the neurological and neuropsychiatric symptoms that are associated with the intoxication. Hallucinations, giddiness, depression, or sleeping problems may potentially affect the function, vigilance, and judgment of the seafarers on duty. Costs to the ship operator may derive from diagnostic test and treatment.

, 2004; Somma et al., 2010). Variations in the produced toxin levels in the literature can be explained by differences in extraction or culturing of the isolates (Vogelgsang et al.,

2008a; Depsipeptide solubility dmso Kokkonen et al., 2010; Fanelli et al., 2012). Sequenced fragments of eight F. poae isolates were very homologous (99–100%) and showed 81% homology with the tri7 gene (E-value 1e−57) of Fusarium graminearum 88-1. Several studies have been carried out to detect natural contamination of cereals and grain-based products with mycotoxins producing species of the FHB complex using PCR assays. Lee et al. (2001) identified genetic differences between the trichothecene biosynthetic pathways of the NIV and DON chemotypes NVP-BEZ235 price and developed a rapid method for Gibberella zeae genotype identification based on PCR analysis. Ward et al. (2002) designed specific primers based on the tri12 gene sequences to identify NIV-producing F. graminearum isolates. Chandler et al. (2003) developed a number of PCR assays to amplify tri7 and tri13 sequences to characterize isolates of F. gramineraum, F. culmorum and F. cerealis in terms of their NIV and DON potential production. Quarta et al. (2005) were able to develop specific primers

targeting the tri3 and tri7 genes to identify 3A-DON, 15A-DON and NIV-F. culmorum producers based on the sequences of Fusarium graminearum described by Lee et al. (2001) and Ward et al. (2002). In our study, the PCR program was adjusted

to different annealing temperatures and the number of cycles was reduced to obtain a rapid and reliable technique. The selected primers were evaluated on genomic DNA extracted from acetylcholine 125 F. poae isolates from 13 different countries and eight different hosts, plus other Fusarium species tested (see ‘Materials and methods’ section). The F. poae isolates showed the presence of the 296-bp partial tri7 DNA fragment (Fig. 1), whereas no product was amplified from other Fusarium species. In our cereal sample analyses, Fusarium poae was the species with higher isolation frequency (15 isolates) in all seed samples analysed, followed by F. graminearum (seven), F. oxysporum (four), F. chlamydosporum (three), F. acuminatum (one), F. equiseti (one) and F. sporotrichioides (one). All of these isolates were tested with the new primer set for potential NIV-F. poae producers and only F. poae isolates amplified the expected fragment. Moreover, DNA obtained from seed samples amplified the product of 296 bp according to the size of our NIV-F. poae-specific PCR. This work was supported by FONCYT-SECYT PRH32-PICT 2008/110 and PIP 167 CONICET. “
“λ Red recombineering is a DNA cloning and engineering technique involving recombination between homologous regions. The homologous recombination is mediated by the λ Red genes consisting of redα, redβ and gam.

, 2008). Kawai et al. (2011) recently suggested that LCP proteins transfer WTAs and other anionic polymers from the lipid carrier to the cell wall AZD2281 datasheet peptidoglycan in B. subtilis. Comparative growth of LCP mutants on bacitracin gradient plates showed that the LCP triple mutant was highly susceptible (Fig. 3a). The bacitracin MIC of the triple mutant was 4 μg mL−1 compared to 32 μg mL−1 for wild type and all LCP single

and double mutants. The hyper susceptibility of the LCP triple mutant to bacitracin could therefore be due to an additional shortage of the lipid carriers caused by the lack of the putative WTA ligase function of LCP proteins. In line with the proposed function of LCP proteins, previous studies showed a decrease in the WTA content of LCP mutants in different species (Hübscher et al., 2008; Kawai et al., 2011). Therefore, we analysed the WTA content of LCP single mutants and the triple mutant in S. aureus, via detection of the cell wall phosphorus BMS-907351 mouse content (Ames & Dubin, 1960). The previously described decrease in the WTA content of the ΔmrsR mutant (Hübscher et al., 2009) could be confirmed here, and the WTA contents of the Δsa0908 and Δsa2103 mutants were decreased to 62% and 95% of the wild type level, respectively (Fig. 3b). An almost complete depletion of

WTA was observed in the triple LCP mutant, with cell wall phosphorus content down to 2% of the wild type. Re-introduction of single LCP genes into the triple mutant restored WTA levels to 94%, 81% and 69% of wild type levels for sa2103, msrR and sa0908, respectively. The capacity of all LCP proteins to restore the WTA content to

a certain degree confirmed a partial functional redundancy that has been shown for other phenotypes such as growth defects, beta-lactam resistance, biofilm formation and self-agglutination (Over et al., 2011). The very low WTA content of the LCP triple mutant confirmed that LCP proteins in S. aureus have an essential function in WTA loading of the cell wall. The three LCP genes in B. subitlis are conditionally essential, meaning that an LCP triple mutant in B. subtilis is only viable when tagO (tarO) is also deleted, thereby preventing the flux of precursors into the WTA synthesis pathway (Kawai et al. 2011). The effect of TarO (TagO) inhibition on the LCP triple mutant was tested to Dichloromethane dehalogenase detect a possible connection between LCP proteins with WTA synthesis or assembly in S. aureus, as found for B. subtilis (Kawai et al., 2011). Subinhibitory concentrations of tunicamycin, which are known to inhibit TarO (TagO; Campbell et al., 2011), could partially complement the growth defect of the LCP triple mutant (Fig. 4a). The minimal doubling time of the triple mutant decreased from 49 ± 2 to 34 ± 2 min upon tunicamycin treatment. Inhibition of TarO in the wild type did not significantly affect the minimal doubling time of 25 ± 0.

However, the protective efficacy of the http://www.selleckchem.com/products/gsk1120212-jtp-74057.html protein remained to be evaluated. SS2 strain ZYS was isolated from the brain of a diseased piglet and expressed muramidase-released protein, extracellular protein factor and suilysin (Tang et al., 2006). All the field strains used in this study were derived from samples of different tissues (lung, brain, joint, heart and blood) of diseased pigs with pneumonia and systemic infection (meningitis, arthritis, endocarditis or septicaemia) from 16 provinces (municipalities) of China. All S. suis strains were maintained on tripticase soy agar (Difco Laboratories, Detroit, MI)

plus 10% bovine serum or cultured in Todd–Hewitt broth medium (THB) (Oxoid, Wesel, Germany) plus 10% bovine serum to mid-log phase (OD600 nm of 0.4) at 37 °C under aerobic conditions. Laboratory Escherichia coli strains DH5α and BL21 were used as nonadherent and noninvasive recipients of recombinant protein-containing plasmids pET-28a (+). The purified recombinant HP0272 (accession no. YP_001197640) was performed as described previously (Zhang et al., 2008) and then was resolved on a 10% v/v polyacrylamide vertical slab gel with a 4% v/v stacking gel. After electrophoresis, the gel was visualized by being stained with CBB R-250 and the band of interest was picked, digested with trypsin and then subjected to matrix-assisted laser desorption/ionization-time

of flight MS analysis as described (Fountoulakis & Langen, 1997; Kussmann et al., 1997). Peptide Idelalisib clinical trial masses were searched against Urease the NCBI database using the mascot program (http://www.matrixscience.com). All experimental protocols were approved by the Laboratory Animal Monitoring Committee of Hubei Province and were performed accordingly. Thirty-two 4–6-week-old female BALB/c mice were randomly assigned to four groups of eight each. The purified recombinant HP0272 (100 μg) was emulsified with Marcol 52 (ESSO)-based adjuvant and then applied to immunized mice in group 1 intraperitoneally.

Subsequent booster injections were given on the 14th day with the same antigen. Mice in group 2 immunized with commercially SS2-inactive vaccine (China) served as positive controls. Mice in group 3 were inoculated with phosphate-buffered saline (PBS) emulsified in the same adjuvant served as negative controls, and mice in group 4 were inoculated with PBS alone as blank controls. On the 10th day after the booster immunization, sera were obtained from each group by tail vein bleeding. All mice were then challenged with a lethal dose of 2 × 109 CFU of log-phase SS2 ZYS in 0.5 mL PBS. All mice were observed for 10 days for morbidity and mortality. Microtitre plates were coated overnight at 4 °C with 200 ng 100 μL−1 of purified recombinant HP0272 diluted in sodium carbonate buffer (pH 9.6). Having been treated with washing buffer (PBS, pH 7.2, containing 0.

, 2003; Broser Belnacasan chemical structure et al.,

2008b). In addition, increased axonal innervation can be observed in the dysgranular zone (medial column of axons seen on the right side of Fig. 4B), a region immediately surrounding the S1 barrel field proper. The axons within S1 probably mediate the rapid spread of sensory information across the barrel map; this may be of importance during normal whisker sensation, when sensory input from different whiskers must be integrated to build up a representation of the external world. Another region with high axonal density across all layers is observed ∼1 mm lateral of the C2 barrel column, corresponding to the location of S2 (Fig. 4A–C; White & DeAmicis, 1977; Welker et al., 1988; Fabri & Burton, 1991; Hoffer et al., 2003; Chakrabarti & Alloway, 2006). The high density of axonal innervation in S2, originating from S1, and the spatial proximity of S2 and S1 probably underlie the extremely rapid sensory signals that are observed in these regions with voltage-sensitive dye imaging. Indeed, the signal in S2 is only resolved with voltage-sensitive Pifithrin-�� supplier dye imaging as a separately activated region when the more medially represented E2 whisker is deflected (Fig. 2B and C). Furthermore,

S1 and S2 regions are reciprocally connected, as revealed by retrograde labelling with FG (Fig. 4D) and AAV6-cre in floxed-LacZ cre-reporter mice (Fig. 4E). Approximately 8 ms after the initial sensory response in S1, a second localized region of depolarization is found in the primary motor cortex. This sensory response in M1 depends upon activity in S1, and the simplest signalling

pathway would therefore be through direct monosynaptic excitatory connections from S1 to M1 (White & DeAmicis, 1977; Porter & White, 1983; Miyashita et al., 1994; Izraeli & Porter, 1995; Farkas et al., 1999; Hoffer et al., 2003; Alloway et al., 2004; C59 cell line Ferezou et al., 2007; Chakrabarti et al., 2008). Injection into the mouse C2 barrel column of either BDA (Fig. 5A and B) or Lenti-GFP (Fig. 5C and D; Ferezou et al., 2007) results in an intense labelling of a column of axons terminating in a primary motor cortex region located ∼1 mm lateral from Bregma and spanning ∼0.5–1.5 mm anterior of Bregma. This region corresponds to the whisker primary motor cortex and it colocalizes with the secondary hotspot of depolarization imaged with voltage-sensitive dye, on average located at 1.4 mm anterior and 1.1 mm lateral to Bregma (Ferezou et al., 2007). There are interesting differences in the axonal projections from S1 to M1, when comparing the pattern of axonal output from superficial layers 2/3 pyramidal neurons to the pattern of axonal output from deep layers 5/6 pyramidal neurons. Supragranular S1 layers 2/3 pyramidal neurons showed the densest innervation of deeper layers 5/6 in M1 and stopped short of the outer layer 1 (Fig.

flexneri infections (Fasano et al., 1995). The ShET-2 toxin is encoded by the sen gene located on the 140-MDa invasiveness plasmid PLX3397 datasheet (Fasano et al., 1995). This toxin has been reported in different species of Shigella causing traveller’s diarrhoea (Vargas et al., 1999) and increases transepithelial conductance in an

in vitro model, although the relevance of the toxin in clinical disease is unknown (Nataro et al., 1995). The enteroaggregative heat stable toxin 1 (EAST-1) toxin is encoded by the astA gene (Savarino et al., 1996). This toxin is thought to play a role in EAEC pathogenicity. Epidemiological studies have associated this gene with E. coli pathotypes other than EAEC such as ETEC and EHEC and with other bacterial genera including Salmonella (Vargas et al., 1999; Paiva de Sousa & Dubreuil, 2001). EAST-1 is a 38 amino-acid peptide, and the astA gene is detected in commensal and diarrheic E. coli strains (Kaper et al., 2004). EAST-1 induces the production of CH5424802 concentration high levels of cGMP in the cell, inhibiting the Na/Cl

cotransport system and reducing the absorption of electrolytes and water from the intestine at villus tips (Dreyfus & Robertson, 1984), resulting in an elevated secretion of Cl− and water in crypt cells. However, the role of this toxin in the development of diarrhoea has yet to be defined. AggR is a transcriptional factor encoded by the aggR gene, which controls expression of not only adherence factors (AAFI and AAFII) but also chromosomal genes (Nataro et al., 1994). Relationships between susceptibility to several antimicrobial agents and virulence have been demonstrated. Thus, exposure to subinhibitory concentrations

of quinolones Etoposide molecular weight induces a loss of VFs contained within PAIs (Soto et al., 2006). The transference of VFs contained in PAIs and other mobile genetic elements among different species plays an important role in bacterial pathogenicity, and thus the aim of this study was to determine the presence and spread of the genes encoding the ShET-1, ShET-2 and EAST-1 toxins and AggR factor in E. coli strains causing bacteraemia and their possible relationship with both clinical and microbiological characteristics in order to elucidate whether these enterotoxins could play a role in the pathogenicity of these infectious diseases. A total of 174 E. coli blood isolates collected from patients with bacteraemia in the Hospital Clinic of Barcelona during 2002 were included. The uropathogenic E. coli (UPEC) clinical strain HC91255 was used as a control for biofilm assay.

We also demonstrated that H-NS is involved in the expression of T3SS1 genes as a suppressive factor. This suppressive effect of H-NS on the production of T3SS1

proteins was mediated by repression of ExsA expression, suggesting that ExsA is a master regulator of T3SS1 gene expression. As far as we are aware, this is the first report of an association between the H-NS and ExsACDE regulatory systems. The ExsACDE regulatory system is a highly sophisticated transcriptional regulatory system that induces T3SS gene expression when a bacterium establishes contact with host cells E7080 mouse (Yahr & Wolfgang, 2006). Expression of genes affected by H-NS is typically induced by environmental stimuli such as temperature (Falconi et al., 1998; Prosseda et al., 1998). Therefore, the combination of learn more these two regulatory mechanisms appears to constitute the gene expression system that exerts lethality

in the murine infection model that we recently used as an in vivo phenotype characteristic of T3SS1 (Hiyoshi et al., 2010). Taken together, our findings contribute to the knowledge on how V. parahaemolyticus causes wound septicemia. This work was supported by Grants-in-Aid for Young Scientists and Scientific Research on Priority Areas Applied Genomics and Matrix of Infection Phenomena from the Ministry of Education, Culture, Sports, Science and Technology of Japan. “
“Lancefield group C Streptococcus dysgalactiae is an emerging fish pathogen, which was first isolated in 2002 in Japan. Streptococcus dysgalactiae isolates collected from diseased fish in Japan (n=12), Taiwan (n=12), China (n=2), Malaysia (n=3), and Indonesia (n=1) were characterized using biased sinusoidal field gel electrophoresis (BSFGE), sodA gene sequence analysis, and antimicrobial susceptibility. These isolates exhibited high phenotypic homogeneity irrespective of the countries

from where the strains were collected. Seventeen isolates were found to be resistant to oxytetracycline and carried the tet(M) gene, except for the strains collected in Taiwan and the PP1564 strain Fenbendazole collected in China. The sodA gene sequence analysis revealed that 23 isolates were identical, except for one Japanese isolate (KNH07902), in which a single nucleotide differed from that of the other isolates. Based on BSFGE typing by ApaI macrorestriction, the isolates – including the Japanese, Taiwanese, and Chinese isolates – could be grouped into one main cluster at a 70% similarity level. However, the macrorestriction genotypes of some isolates were apparently distinct from those of the main cluster. It has been reported that Streptococcus dysgalactiae belonging to Lancefield group C streptococci (GCS) (Vieira et al., 1998) was responsible for mastitis, subcutaneous cellulitis, and toxic shock-like syndrome in bovine (Aarestrup & Jensen, 1996; Chénier et al., 2008) and other animal infections (Scott, 2000; Lacasta et al., 2008).

The expression level of the housekeeping gene was used to normalize the expression data of the genes of interest. The qRT-PCR method employed here was adapted from a previous study (Lee et al., 2011). It was performed using a SYBR Green master mix (Applied Biosystems, Foster City) and an ABI StepOne Real-Time PCR system (Applied Biosystems) with two independent Obeticholic Acid cost cultures. To identify the antibiofilm compounds against S. aureus (ATCC 25923), the supernatants of 28 bacterial species were screened. The bacterial supernatants

were used at 1% (v/v) to minimize the growth reduction in S. aureus cells. While most supernatants showed no significant inhibitory effect on S. aureus biofilm formation, the supernatants of three strains did: P. aeruginosa PA14, P. aeruginosa PAO1, and S. epidermidis (Table 1). It has been recently reported that the presence of serine protease in S. epidermidis culture inhibited S. aureus biofilm formation (Iwase et al., 2010). The supernatant of P. aeruginosa PA14 also decreased the cell growth of S. aureus (Table 1), probably owing to the presence of antistaphylococcal substances produced by P. aeruginosa (Hoffman et al., 2006). The supernatant of P. aeruginosa PAO1 clearly and dose dependently inhibited the biofilm formation of two S. aureus strains (ATCC 25923

and ATCC 6538; Fig. 1a and d). However, the supernatant (1%, v/v) of P. aeruginosa PAO1 did not significantly decrease the cell growth of S. aureus, either under a static condition (Table 1) or a shaking condition (Fig. 1b and e). INK 128 supplier As the dispersion of established biofilms is important in biofilm control, the biofilm dispersal ability was investigated. As the control treatment of proteinase K, the culture supernatant of P. aeruginosa PAO1 was shown to markedly and dose dependently disassemble the pre-existing biofilm of two S. aureus strains (Fig. 1c and f). Specifically, the supernatant of P. aeruginosa PAO1 at 0.1% (v/v) detached more than 80% of the established S. aureus biofilms for 17 h. Similarly, the use of a shorter dispersion time (7 h rather than 17 h)

after the addition of the supernatant of P. aeruginosa PAO1 showed almost the Oxalosuccinic acid same result for biofilm dispersion (Fig. S1). Therefore, the supernatants of P. aeruginosa PAO1 inhibited and dispersed S. aureus biofilms. To identify the inhibitory factors, the protease activity in the supernatants of all bacterial species was measured using milk agar plates as protease activity plays an important role in the disassembly of S. aureus biofilms (Boles & Horswill, 2011). As expected, two P. aeruginosa strains showed a high protease activity (defined as a clear circle zone by degrading milk proteins) as a positive control, proteinase K, showed a high protease activity while other strains did not show significant protease activity on the milk agar plates (Fig. 2a). The amount of protease in the supernatants of P. aeruginosa corresponds to approximately 0.1 mg mL−1 of proteinase K (Fig. 2a) that inhibits S.

The possible help of interpreters may not necessarily make such conversations

more valid. An explorer, keen to find evidence of horrible stories heard elsewhere, will be only too quick to confirm the alleged habits of the little fish. In addition, it is very hard to know what fish the “natives” and the white “experts” referred to, given that the culprit is not only a very small and fragile creature but also one of many in this genus. The validity of translations of original Latin, German, Spanish, Portuguese, and French reports needs to be revisited. Updated cross-translations without a sensationalized agenda could ensure that crucial nuances are interpreted correctly and so the blurred line between embellishment and fact is captured precisely. For

example, “I buy JQ1 know of three cases” may be understood as “I know three cases,” which some may interpret as knowing three cases Epacadostat personally, ie, having seen them as patients. Suddenly, a story becomes a confirmed report. Also, historical handwritten German accounts will most likely be written in Kurrent script; some of its letters, eg, “g,” “p,” or “q,” can easily confuse a translator. Spotte’s two chapters “Culmination of Evils” and “Urinary Misconduct”[18] are particularly helpful as they also provide some original language excerpts. Finally, there may be particular reasons why locals told white visitors about the candiru. Were they kind and concerned Ponatinib order about the explorers’ well-being? Were they exaggerating a very rare occurrence to keep intruders out? To conclude this section, it should be fascinating to see what the great explorers of the time wrote about the fish. It has been said that Alexander von Humboldt, Henry Walter Bates, and Alfred Russel Wallace, despite their long years in the area, did not mention the candiru at all.[18] Bates’ classic work[24] reports on the locals’ frequent bathing, fishing, hunting, and cooling down in the river (he calls them “almost amphibious people”),

suggesting an absence of the dreaded fish. His book is devoid of any reference to genitals; this may have influenced his selection of reported information. Von den Steinen, on the other hand, switched for such passages to Latin,[11] presumably to avoid leading young readers’ minds astray. However, Regan[25] mentions Wallace’s loss of about 200 preserved fish on his journey home and cites a short unreferenced note by the explorer about the peculiar habits of the candiru, a note confirmed by sighting the original document[26] and a modern reproduction.[27] Therefore, until further confirmation, it may be premature to suggest that neither von Humboldt nor Bates ever mentioned the candiru. Admittedly, many native people have not been aware of the fish either.

3±0.2 or 1070.9±37.8 nmol methane cm−3 day−1,

respectively). The AOM rates were lower with nitrate (881.3±0.7 nmol methane cm−3 day−1) or with 2 mM sulfate (479.0±6.4 0.0 nmol methane cm−3 day−1). The original Zeebrugge sediment contained 16S rRNA gene copy numbers of 2.6 × 109 copies cm−3 for Bacteria and 3.1 × 108 copies cm−3 for Archaea (Fig. S1 in Appendix S1). Compared with the sediment used as an inoculum, a significant increase of the methanogenic (Methanosarcina mcrA) and the methanotrophic (ANME-1 and -2 mcrA) populations was observed in microcosms selleck products with ferrihydrite and hexadecane (Fig. 5). With sulfate and methane, only the number of ANME-2 copies increased. The growth of Geobacteraceae– EPZ5676 cell line although present in significant numbers – was not initiated by the addition of hexadecane or electron acceptors compared with the inoculum (Fig. 5). In contrast, the addition of sulfate and/or ferrihydrite stimulated the growth of the sulfate-reducing community in the microcosms. Experiments with ethylbenzene, naphthalene, nitrate or manganese were not monitored by real-time PCR. 16S rRNA gene clone libraries of Bacteria (n=82) and Archaea (n=93) of the Zeebrugge sediment

revealed a broad microbial diversity (Figs S2–S4 in Appendix S1). Among Bacteria, Alpha-, Gamma- and Deltaproteobacteria 16S rRNA gene sequences were recovered as well as sequences associated with Campylobacterales, Erastin manufacturer Planctomycetes, Clostridia, Actinobacteria and Chloroflexi. 16S rRNA gene sequences associated with potential pathogens, such as Neisseria and Coxiella, were also found as well as sequences associated with Geobacteraceae. Seven potential aerobic iron oxidizers of the family Acidithiobacillaceae and another seven of the Acidimicrobinea could be identified. Some clones were closely related to sequences recovered in other potentially hydrocarbon influenced environments such as the Victoria Harbour in Hong Kong, China (Zhang et al., 2008), the Belgian coast off Zeebrugge (Gillan & Pernet, 2007), the Milano mud volcano (Heijs et al., 2005) as well as the Gullfaks and Tommeliten

oil fields of the North Sea (Wegener et al., 2008; Fig. S2 in Appendix S1). The phylogenetic diversity of Archaea comprised Crenarchaeota and Euryarchaeota. In the latter, members of the Methanosarcina prevailed. Electron acceptors may accelerate hydrocarbon degradation, thus providing an increased substrate supply for methanogenesis. In this work, we evaluate the hypothesis that the addition of electron acceptors leads to accelerated hydrocarbon-dependent methanogenesis. This process may be useful to stimulate the recovery of oil-related carbon as methane from reservoirs or for bioremediation of contaminated sites. Our aim was to stimulate the initial steps in hydrocarbon degradation and thus the formation of methanogenic substrates such as acetate, CO2 and H2.