The improvements in viral find more load in treatment-experienced patients after a short period of treatment with ATC were similar to or greater than those observed with other investigational deoxycytidine analogue NRTIs, including dexelvucitabine and racivir (racemic emtricitabine) [7,8]. Dexelvucitabine (DFC; Reverset, D-d4FC, DPC-817) appears to have a similar resistance profile to ATC, also

having activity in vitro against HIV-1 with M184V and TAMs [9,10]; however, its development has been halted because of the high incidence (above 10–15%) of grade 4 hyperlipasaemia in a follow-up long-term extension study in patients who were receiving 200 mg DFC without 3TC or FTC. In a randomized, double-blind study of 42 treatment-experienced patients with the M184V mutation, there was a mean decrease in viral load of 0.4 log10 copies/mL in the 26 patients who received racivir in place of 3TC in their existing treatment for 28 days, with subset analysis showing a mean decrease in viral load of 0.7 log10 copies/mL in the 14 patients in the racivir-treated group with M184V and fewer than three TAMs [8]. Approximately 43% of patients in the current study had at least three TAMs at baseline, Doramapimod indicative of resistance to the NRTIs zidovudine and stavudine and a potentially reduced response to the NRTIs abacavir, didanosine and tenofovir [11]. The activity of the two ATC doses over the 21-day treatment period appeared to

be influenced to some degree Etoposide by the number of TAMs present at baseline, with the 600 mg bid dose being more effective in patients with fewer than three TAMs at baseline than in those with at least three TAMs, while the

800 mg bid dose was equally effective in patients with fewer than three TAMs and those with at least three TAMs at baseline. However, it is possible that there are other reasons for this observed difference, such as a slight imbalance in pretreatment viral load between the two groups and differences in prior treatment and in resistance to the other anti-HIV drugs the patients were receiving. While, in general, the activity of ATC was greatest in patients with M184V alone, patients with TAMs, including patients with four or more TAMs, achieved significant reductions in viral load with ATC treatment. Thus, the in vitro antiviral activity exhibited by ATC against HIV-1 laboratory strains and clinical isolates with NRTI resistance mutations is confirmed by the clinical data presented here. These data indicate that ATC may be useful in the treatment of HIV-1-infected patients with virus containing mutations that render it resistant to treatment with other NRTIs. Very few genotypic changes were detected over the 21-day period of functional monotherapy with ATC and no patient had developed the L74V, K65R, Y115F or V75 mutation at day 21. Previously, no resistance to ATC had been observed during a study of 10-day monotherapy with ATC in treatment-naïve HIV-1-infected patients [6].

Therefore, polysaccharide intercellular adhesin, also called the slime exopolysaccharide component, and accumulation-associated protein Selleckchem Autophagy inhibitor have been described as factors playing an essential role in biofilm formation (Cramton et al., 1999; Mack, 1999; O’Gara & Humphreys, 2001; Götz, 2002). A number of methods

are available to detect the capability of staphylococci to colonize the biomedical devices. The Congo red agar (CRA) assay described by Freeman et al. (1989) and/or the microtiter plate (MtP) test devised by Christensen et al. (1985) were most commonly used as the phenotypical methods for slime and/or biofilm production. We would like to point out that the slime-positive strain (measured by the CRA test) does not necessarily indicate the ability of this strain to form a biofilm (by the Ibrutinib nmr MtP test). Therefore, ‘slime’ and ‘biofilm’ terms cannot be used alternatively. In this study, a collection of 146 nasopharyngeal S. epidermidis strains was screened for the presence of genetical biofilm markers (icaAD and aap genes), the ability of slime secretion using the CRA test and biofilm formation by the MtP method. The aim of our work was to evaluate the relationship between these phenotypic data and the genotypic pattern of the screened strains. The collection of 146 S. epidermidis strains isolated from the nasopharynx of lung cancer patients was included

in the present study. These strains were collected during patients’ hospitalization at The Department of Thoracic Surgery of Medical University of Lublin. The patients with resectable lung cancer received a preoperative antimicrobial prophylaxis according to hospital policy (piperacillin, cefuroxime alone or in combination with amikacin). At the time of sampling, none of the patients had clinical symptoms of airway infections. The study has been

approved by the Ethical Committee of the Medical University of Vasopressin Receptor Lublin. Informed consent was obtained from all patients. Clumping factor detection using the Slidex Staph Kit (BioMerieux, France), a coagulase-test tube and the ID32Staph system (BioMerieux) was performed for species identification of staphylococcal isolates. Staphylococcus epidermidis strain ATCC 12228 and S. epidermidis ATCC 35984 were used in biofilm assays as a negative and a positive control, respectively. Biofilm formation in vitro was carried out as described by Christensen et al. (1985) and Mack et al. (1992), with a slight modification. All strains were grown overnight at 35 °C in Trypticase soy broth (TSB; Biocorp, Poland) as well as in a medium supplemented with 0.5% glucose and 4% NaCl. The cultures were diluted 1 : 200 in the appropriate medium (TSB as standard conditions and TSB supplemented with 0.5% glucose plus 4% NaCl as inducing conditions), and 200 μL of cell suspensions per well were used to inoculate sterile 96-well polystyrene microtitrate plates (Nunc, Denmark).

This is the first randomly selected sample of off-label and unlicensed prescribing from a major teaching hospital in Australia. No similar study has been published. Off-label Target Selective Inhibitor Library screening prescribing was higher for inpatients, compared with outpatients or emergency department patients. Patients in Australia will be exposed to drugs, doses or formulations which have not been evaluated

for licensing in that paediatric population. The current system of licensing drugs requires legislative change so that when a substantial evidence-base is available for a drug’s efficacy and safety it is incorporated with the license otherwise there will continue to be inadequate evidence of prescribing especially in paediatrics in Australia. 1. Therapeutics Goods Administration. Therapeutics Goods Administration – Product Information Search Facility, 2008 ongoing. Australia: Australian Government. (https://www.ebs.tga.gov.au/).

2. MIMS Australia. Monthly Index of Medical Specialities (eMIMS) 2008. E. Kiteterea, A. Jonesa, T. Evansa, Y. Jania,b aUCLH NHS Foundation Trust, London, UK, bUCL School of Pharmacy, London, UK Discharge summaries should include documentation of medication changes. All patients should be discharged with at least 2 weeks supply of medication. Ninety-five per cent of patients were discharged with at least 2 weeks supply of medication and 56% of discharge summaries had complete documentation of medication changes. Further work is required to ensure all discharge summaries are completed with adequate documentation and all patients are Tanespimycin cell line discharged with at least 2 weeks supply of medication. A discharge summary is the communication of clinical information from the hospital to the GP and patient. Standards of discharge summaries include documentation of any changes to the patient’s regular medication, any newly started medication and any stopped medication with documentation of reasons for these changes. At our organisation, the discharge policy states that on discharge from the hospital, patients should have at least 2 weeks

supply of their long LY294002 term medication. This supply may be from the hospital – either as a near patient dispensing (NPD) supply or to take away (TTA) supply – or from the patient’s own supply of medication (POD) – either on the ward or at home. The aim of this audit was to assess whether the standards for documentation of medication changes on discharge summaries were being met, and to assess whether patients had at least two weeks supply of regular medication on discharge, as per hospital policy. The standards were 100% of discharge summaries should include documentation of changes to medication and 100% of patients should be discharged with at least 2 weeks supply of medication. Data were collected over seven working days, from all but one of the inpatient sites at our organisation. Maternity, critical care and paediatric wards were excluded.

We are grateful to Dr Ian Toth at the Scottish Crop Research Institute

for supplying the Pa strains, to Rita Monson for providing cDNA and Nick Thomson for help with bioinformatic comparisons. T.J.E. was supported by a Collaborative Award in Science and Engineering from Leatherhead Food Research. This work was funded by the BBSRC. Fig. S1. Multiple sequence alignment of PflA. Table S1. Supplementary strains and primers used in this study. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author LDK378 concentration for the article. “
“Lipopolysaccharide is a major immunogenic structure for the pathogen Yersinia pseudotuberculosis, which contains the O-specific polysaccharide (OPS) that check details is presented on the cell surface. The OPS contains many repeats of the oligosaccharide O-unit and

exhibits a preferred modal chain length that has been shown to be crucial for cell protection in Yersinia. It is well established that the Wzz protein determines the preferred chain length of the OPS, and in its absence, the polymerization of O units by the Wzy polymerase is uncontrolled. However, for Y. pseudotuberculosis, a wzz mutation has never been described. In this study, we examine the effect of Wzz loss in Y. pseudotuberculosis serotype O:2a and compare the lipopolysaccharide chain-length profile to that of Escherichia coli serotype O111. In the absence of Wzz, the lipopolysaccharides of the two species showed significant differences in Wzy polymerization. Yersinia pseudotuberculosis O:2a exhibited only OPS with very short chain lengths, which is atypical of wzz-mutant phenotypes that have been observed for other species. We hypothesise that the Wzy

polymerase of Y. pseudotuberculosis O:2a has a unique default activity in the absence of the Wzz, revealing the requirement of Wzz to drive O-unit polymerization to greater lengths. “
“Flavodoxin (Fld) is a bacterial electron-transfer protein Selleck Sirolimus that possesses flavin mononucleotide as a prosthetic group. In the genomes of the Pseudomonas species, the mioC gene is the sole gene, annotated Fld, but its function remains unclear. In this study, phenotype microarray analysis was performed using the wild-type and mioC mutant of pathogenic Pseudomonas aeruginosa PAO1. Our results showed that the mioC mutant is very resistant to oxidative stress. Different antibiotics and metals worked differently on the sensitivity of the mutant. Other pleiotropic effects of mutation in the mioC gene, such as biofilm formation, aggregation ability, motility and colony morphology, were observed under iron stress conditions. Most of the phenotypic and physiological changes could be recovered in the wild type by complementation.

Trap samples were added directly to 5 mL volumes of Hionic-Fluor™ scintillation fluid supplemented with 100 μL 0.5 M sodium hydroxide in 20-mL HDPE vials. Vials were incubated for 1 h at room temperature before counting in a Packard Tri-Carb® 2900TR liquid scintillation analyser autocalibrated daily with 133Ba and 14C standards. Data were interpreted using the QuantaSmart™ check details package with corrections against chloroform quench-curves. Beta emissions from 40KOH contained in the trap and from 40KNO3 in NMS were corrected for with background controls using the QuantaSmart™ package. Data shown are corrected against values

from killed controls. Cell-free extracts were prepared using a French pressure cell as previously described (Boden et al., 2010) in 50 mM PIPES-HCl buffer at pH 7.2. Enzyme activities given for both enzymes were calculated by the subtraction of endogenous rates from Hg(II)-induced rates. Assays were performed in an Ultrospec 3100 Pro UV/Visible spectrophotometer (Amersham). see more Mercuric reductase activity was measured in terms of the mercury (II)-dependent oxidation of NADH or NADPH, which were quantified by measuring absorbance

at 340 nm, given millimolar extinction coefficients of 6.22 and 6.27 mM−1 cm−1, respectively, measured in 50 mM PIPES-HCl pH 7.2 containing 2 mM MgCl2, 1 mM Na2EDTA and 1 mM dithiothreitol (Gachhui et al., 1997). Solutions were preheated to 45 °C, and extracts were kept on ice until required; 700 μL volumes of buffer were placed in preheated 1-mL optical quartz cuvettes of 1 cm cAMP path length, and 100 μL of cell-free extract was added; 100 μL 2 mM NAD(P)H solution was then added and endogenous oxidation measured; 100 μL 0.3 mM HgCl2 solution was added and NAD(P)H oxidation

measured over 5 min. Negligible abiotic oxidation of NAD(P)H was observed. Mercuric reduction by cytochrome c oxidase at the expense of reduced cytochrome c was assayed in terms of the mercuric-dependent oxidation of reduced bovine cardiac cytochrome c or of ferrocyanide using a method adapted from Sugio et al. (2010). Cytochrome c550 and ferrocyanide oxidation were measured in terms of the decrease in absorbance at 550 or 420 nm, respectively, given millimolar extinction coefficients of 19.6 and 1.04 mM−1 cm−1, respectively; 50 mM PIPES buffer at pH 7.2 supplemented with 2.2 mM ascorbic acid was used; 79 μL of buffer was placed in preheated polycarbonate cuvettes of 1 cm path length and 10 μL of 10 mg mL−1 bovine cardiac cytochrome c550 or 10 μL 100 mM potassium ferrocyanide was added; 100 μL cell-free extract was added and endogenous oxidation measured; 100 μL 0.3 mM HgCl2 solution was added to initiate reactions, and cytochrome or ferrocyanide oxidation was monitored over 10 min.

In 2008, the New Zealand Ministry of Health supported and propagated guidelines for HIV testing in medical settings [22]. This included recommendations that all persons with a history of unprotected sexual exposure that could result in HIV transmission, specifically MSM and those seeking assessment for sexually transmitted infections, should be offered testing. It is important

that this guideline is promoted, and the impact assessed, including collecting information on HIV testing according to sexual behaviour. Moreover, the possibility of HIV infection should be considered in a wide range of clinical situations. Testing needs to be encouraged particularly among Pacific and Māori MSM, who need Akt inhibitor to be made aware of the value of HIV testing and of accessible venues where this can be undertaken. Our findings also show that testing for HIV must be considered for people of all ages if they are currently, or have been in the past, at risk. In the area of sexual health the emphasis tends Caspase inhibitor to be on young people, but age should not be a major arbiter of HIV testing. The AIDS Epidemiology Group is funded by the New Zealand Ministry of Health. The authors acknowledge the long-term commitment

from clinicians who provide information on people diagnosed with HIV infection in New Zealand. “
“The aim of the study was to assess the incidence and costs of adverse events (AEs) among patients with HIV infection treated with nonnucleoside reverse transcriptase inhibitors (NNRTIs) from the health care system perspective. US medical and pharmacy claims during 2004−2009 were examined to select adult new NNRTI users with HIV infection. The incidence of selected AEs and time to occurrence were assessed

during the first year. Episodes of care for each AE were identified using claims associated with AE management. For each AE, a propensity score model was used to match patients with an AE to those without (1:4) based on the propensity of having an AE. Mean total health care costs, AE-associated costs and incremental costs per episode, and annual total health care costs per patient were calculated. Of the 2548 NNRTI-treated patients, 29.3% experienced AEs. The incidence ranged from 0.4 episodes/1000 DOCK10 person-years for suicide/self-injury to 14.9 episodes/1000 person-years for dizziness, 49.8 episodes/1000 person-years for depression and 150.3 episodes/1000 person-years for lipid disorder. The mean AE-associated cost (duration) per episode ranged from $586 (88 days) for lipid disorder to $975 (33 days) for rash, $2760 (73 days) for sleep-related symptoms and $4434 (41 days) for nausea/vomiting. The mean incremental cost per episode ranged from $1580 for rash to $2032 for lipid disorder, $8307 for sleep-related symptoms and $12 833 for nausea/vomiting.

, 2000; Dryla et al., 2003). Two transport systems have been described as being involved in acquisition of heme in S. aureus. The first of these, the iron-regulated surface determinant (isd) system, consists of several proteins that have been shown to transfer heme in vitro (Mazmanian et al., 2003; Muryoi et al., 2008; Zhu et al., 2008). It has been proposed that these proteins form a relay system that is able to bind exogenous heme through surface-bound IsdB and IsdH proteins and then transfer it via IsdA and IsdC to membrane-associated IsdE (Mazmanian et al., 2003; Muryoi et al., 2008; Zhu et al., 2008). selleck inhibitor IsdE is the lipoprotein component of the membrane-bound IsdDEF ABC transporter

and contributes to the growth of S. aureus on hemin as a sole iron source (Grigg et al., 2007). The isdD and isdF genes are thought to encode the membrane protein and permease components, respectively, which are believed to enable import of heme into the cytoplasm of S. aureus in conjunction with isdE (Mazmanian et al., 2003; FDA-approved Drug Library Hammer & Skaar, 2011). Some components of the Isd system are

multifunctional. IsdA binds a range of protein ligands including fibrinogen, fibronectin, involucrin, loricrin, and cytokeratin K10 and also binds and inhibits lactoferrin and is required for survival on human skin (Clarke et al., 2004, 2007, 2009; Clarke & Foster, 2008). IsdB binds to platelets via the GPIIIb/IIa integrin (Miajlovic et al., 2010). So, there is evidence that Isd components have roles other than heme transfer in S. aureus. The heme transport system (hts) was first identified as a putative ABC transporter locus, which, when inactivated, results in decreased heme uptake. When htsB and htsC mutants were grown on a mixture of isotopically labeled heme and transferrin as iron sources, the ratio of heme to transferrin uptake decreased (Skaar et al., 2004). More recently, htsABC has been identified as encoding an uptake system for the siderophore, staphyloferrin A (Beasley et al., 2009). The crystal structure of HtsA, the membrane-anchored ATP-binding

cassette protein of this transporter, bound to ferric staphyloferrin A has been described, confirming the specificity of this system for the siderophore (Grigg et al., 2010). However, the possibility of an additional Avelestat (AZD9668) role for HtsABC in heme acquisition has been suggested (Grigg et al., 2010; Hammer & Skaar, 2011). The importance of these systems during infection was recently addressed using a ΔhtsAΔisdE mutant strain, which was used to infect mice in a staphylococcal pneumonia model and a systemic infection model. A difference in bacterial load during infection was only observed in the systemic infection model, with significantly lower numbers of bacteria recovered from the lungs, heart, and kidneys of ΔhtsAΔisdE-infected mice than from animals infected with wild-type S. aureus.

We identified 17 unique subclones, four resistant to amoxicillin, eight to d-cycloserine, two to kanamycin, and three to tetracycline (Table 1). All four resistance genes of the amoxicillin-resistant subclones (pAC1 to pAC4) encoded β-lactamases. The resistance genes of pAC2 and pAC3 were nearly identical to ARGs recently identified from human gut microbiota using functional metagenomics

(Sommer et al., 2009). The pAC4 subclone harbored a new resistance gene, encoding a protein with only 53% identity to a β-lactamase from the newly sequenced pathogen Riemerella anatipestifer RA-GD (Yuan et al., 2011). All eight resistance genes in the d-cycloserine-resistant subclones (pCY1 to pCY8) encoded d-alanine-d-alanine ligases. Except for the resistance genes in check details pCY3 and pCY6, all other resistance genes were new, with identities ranging from 73% to 81% to known d-alanine-d-alanine ligases. Two kanamycin-resistant

subclones (pKM1 and pKM2) were obtained. In pKM1, the resistance gene encoded a protein identical to the first reported bifunctional antibiotic-resistance Protein Tyrosine Kinase inhibitor enzyme 6′-aminoglycoside acetyltransferase-2″-aminoglycoside phosphotransferase from Enterococcus faecalis (Ferretti et al., 1986). In pKM2, a new fused resistance gene was identified, encoding a protein (designated KM2) of 274 amino acids. The N-terminus of KM2 (amino acids 1–189) exhibited 42% identity to a previously dipyridamole characterized AAC(6′) from Enterococcus hirae (Del Campo et al., 2005). The C-terminus (amino acids 190–274) was 35% identical to a hypothetical protein (GenBank accession number: CBL37632) from Clostridiales sp. SSC/2. Three different clades were reported previously in AAC(6′) enzymes and the

N-terminus of KM2 was assigned to clade B with other proteins from this family (Fig. 1; Salipante & Hall, 2003; Mulvey et al., 2004; Riesenfeld et al., 2004; Donato et al., 2010; Partridge et al., 2011). Three tetracycline-resistant subclones (pTE1–pTE3) were obtained. All harbored known ribosomal protection-type resistance genes, including tet(O), tet(W), and tet(32). The tetracycline efflux gene tet(40) was also found in pTE1. 6′-aminoglycoside acetyltransferase-2″-aminoglycoside phosphotransferase (YP_004149647) 6′-aminoglycoside acetyltransferase (CAE50925) To determine whether both domains of KM2 identified in this study were involved in kanamycin resistance, sequences encoding the two domains and the full-length protein were individually cloned and the MIC values of the three different recombinant strains were determined. The results showed that the N-terminal domain conferred kanamycin resistance, with the same MIC value as the full-length protein (256 μg mL−1), whereas the MIC value of the C-terminal domain was the same as the vector control strain (2 μg mL−1). These results indicated that only the N-terminal domain of the novel protein conferred kanamycin resistance.

055). When restricting the analysis to the subgroup of patients who were on the most common current regimens (i.e. boosted

PI- or NNRTI-based ART: 11 701 DCVL episodes and 269 rebound events), the adjusted RR for each 10% higher drug coverage was 0.94 (95% CI 0.88–1.00; P=0.037). This study shows that, among individuals who have already achieved VL suppression for at least 6 months, adherence as measured by drug coverage according to prescription refill data independently predicts the risk of viral rebound, and thus clinicians could benefit from routinely having such information available when seeing patients. In addition, our study shows that, among patients with Transferase inhibitor VL suppression, some have low to modest adherence and, while the risk of rebound is higher in such patients than in those with high adherence, the risk of rebound is still relatively low. Several studies have demonstrated the ability of adherence

to predict viral rebound in a suppressed population by means of self-report [45], MEMS [18], and pharmacy refill-based measures [36,39,46]. The main issue is that, among objective adherence measures, MEMS and therapeutic monitoring of plasma drug concentrations are very expensive and therefore not able to be implemented in clinical practice, in particular in low-income settings, where the prevalence of HIV is higher and adherence is a big issue. Therefore, the most widespread ART adherence measure used is self-report adherence, but it is known MAPK Inhibitor Library that this measure is subjective, tends Teicoplanin to overestimate adherence and is vulnerable to social desirability bias. This is why we attempted to assess whether adherence, based on drug prescription coverage, could be used to predict VL rebound. This measure is objective and cheap, and can be easily collected in most clinical settings, even in low-income settings. The only

difficulty is that this measure is able to be implemented only in a closed health system, where patients have a single source of medication. Among the studies that have demonstrated that an adherence measure is a useful tool for the prediction of VL rebound, the most similar to ours was the study conducted by Gross et al. [39], in that the period of adherence assessment was comparable, the two adjoining refills considered corresponded more or less to 6 months, and the time to the endpoint VL was around 3 months. Differently from our study, VL suppression was defined as two consecutive VLs <500 copies/mL and viral rebound as the second of two consecutive VL values >1000 copies/mL, and the ART adherence measure was based on drug pick-up (pharmacy refill) as opposed to the issue of prescriptions. Our study has several limitations. The first concerns drug coverage as a measure of adherence. The main advantage of this measure is that it is simple and easy to calculate and apply.

We present data from a phylogenetic and molecular clock analysis of heterocystous cyanobacteria within the family Rivulariaceae, including the genera Calothrix, Rivularia, Gloeotrichia and Tolypothrix. CH5424802 in vivo The strains were isolated from distant geographic regions including fresh and brackish water bodies, microbial mats from beach rock, microbialites, pebble beaches, plus PCC strains 7103 and 7504. Phylogenetic inferences (distance, likelihood and Bayesian) suggested the monophyly of genera

Calothrix and Rivularia. Molecular clock estimates indicate that Calothrix and Rivularia originated ∼1500 million years ago (MYA) ago and species date back to 400–300 MYA while Tolypothrix and Gloeotrichia are younger genera (600–400 MYA).

Cyanobacteria have evolved to become one of the most diverse groups of bacteria (Waterbury, 1991; Whitton & Potts, 2000; Castenholz, 2001). They contribute significantly to global primary production via photosynthesis and some contribute considerably to the nitrogen cycle via dinitrogen (N2) fixation. Genome-scale analyses suggest that oxygenic photosynthesis evolved early in the cyanobacterial radiation (Swingley et al., 2008). The capacity to use water as an electron donor in oxygenic photosynthesis, with its consequent generation of molecular oxygen, most likely appeared by 2700 million years ago (MYA) or earlier (Falcón et al., 2010). Nitrogen MK-2206 order fixation is restricted to Bacteria and Archaea, and is present throughout the cyanobacteria (albeit not in all species), that are among the ecologically most important nitrogen Baf-A1 manufacturer fixers (Capone et al., 1997; Raymond et al., 2004). In contrast to photosynthesis, the capacity to fix nitrogen is a paraphyletic event within the cyanobacterial radiation (Swingley et al., 2008). The ‘patchy’ distribution of nitrogen fixation

in cyanobacteria has been inferred to be a result of lateral gene transfer and/or gene duplication (Swingley et al., 2008). The origin of nitrogen fixation among cyanobacteria is dated at 3000–2500 MYA (Shi & Falkowski, 2008; Falcón et al., 2010), and probably appeared three times independently (Swingley et al., 2008). Taxonomic classification has divided Cyanobacteria in five subsections/groups: (1) Order Chroococcales includes unicellular cells with binary reproduction; (2) Order Pleurocapsales includes unicellular cells with reproduction by multiple bipartition; (3) Order Oscillatoriales includes filamentous colonies without heterocysts and cell division in one plane; (4) Order Nostocales includes filamentous colonies that divide in one plane and include heterocysts; (5) Order Stigonematales includes filamentous colonies with heterocysts that divide in more than one plane (Rippka et al., 1979; Waterbury, 1991; Castenholz, 2001).