No data available that match "DNA, Bacterial"

*  DNA confirms identity of bacteria behind London's Great Plague in the 17th...
Pulp from inside the teeth was extracted and anaslysed for traces of bacterial DNA ( ... The DNA was sent to experts at the Max Planck Institute for the Science of Human History ... DNA analysis found traces of the bubonic plague bacteria Yersinia pestis. *It is the ... Researchers searched for DNA in the teeth of the skeletons where genetic material can be ......
*  Plasmid facts, information, pictures | articles about Plasmid
plasmid A structure in bacterial cells consisting of DNA that can exist and replicate ... Laboratory DNA Science: An Introduction to Recombinant DNA Techniques and Methods of ... plasmids can be transferred along with the bacterial DNA, and this activity is controlled ... The foreign DNA is often inserted in such a way that the expression of the foreign gene ......
*  CELLS alive! Glossary
Genophore This bacterial equivalent of a chromosome is a double stranded DNA, usually in ... Explore the Bacterial Cell Model.. Giardiasis A disease also called "beaver fever" caused ... Read more about bacterial growth phases in E. coli Divide and Multiply. ... Deoxyribonucleic Acid, DNA Self-replicating macromolecule containing the genetic code of ......
*  Draft Genome Sequence of Pseudoalteromonas sp. Strain PAB 2.2 Isolated from...
Rapid extraction of bacterial genomic DNA with guanidium thiocyanate. Lett Appl Microbiol ... The DNA was extracted using an adaptation of Pitcher's protocol (8). The genomic DNA was ... CAP3: a DNA sequence assembly program. Genome Res 9:868-877. doi:.10.1101/gr.9.9.868 [ ... of the libraries was evaluated using a 2100 Bioanalyzer and a High-Sensitivity DNA kit ( ......
*  September 2011 - Analyst Blog
A single DNA aptamer functions as a biosensor for ricin Elise A. Lamont, Lili He, Keith ... have properties that make them desirable as biosensors for bacterial contaminants in food ... A single DNA aptamer functions as a biosensor for ricin. Elise A. Lamont, Lili He, Keith ... A DNA hybridization detection based on fluorescence resonance energy transfer between dye ......
*  Safety and immunological responses to human mesenchymal stem... : AIDS
Plasma levels of bacterial DNA correlate with immune activation and the magnitude of ... chemokines and bacterial products such as lipopolysaccharides (LPS) translocated from the ......
*  Title page for ETD etd-11082004-113624
bacterial chromatin *dna bending *type ii dna binding protein *holliday junction *dna ... in the presence of four-way junction DNA, suggesting its role in DNA recombination. In a ... DrHU has no marked preference for DNA with nicks or gaps compared to perfect duplex DNA, ... DNA Binding Properties of Histone-Like Protein HU from Deinoccus radiodurans Suggest ......
*  Grant will increase genomics and biomedical research at BHSU > Black Hills...
This grant also provides critical support for the Western South Dakota DNA Core Facility ... and studying the genetic expression, processing, and evolution of bacterial enzymes known ... WestCore provides genetic services such as DNA sequencing, and genotyping to other South ......
*  Progressive genomic convergence of two Helicobacter pylori strains during mixed...
Genomic DNA was extracted using the QIAamp DNA Mini Kit (QIAGEN, Germany) according to ... Inference of bacterial microevolution using multilocus sequence data. Genetics 2007;175: ... Ten microlitres of bacterial suspension (108 CFU/mL) from each isolate was inoculated ... The peopling of the Pacific from a bacterial perspective. Science 2009;323:527-30. ......
... mutans strain NG8 chromosomal DNA or from plasmid DNA derived from NG8 chromosomal DNA. ... On the bacterial factor in the aetiology of dental caries. 42. Coffman, R. L., D. A. ... A DNA vaccine encoding a cell-surface protein antigen of Streptococcus mutans protects ... It was shown over forty years a go that the bacterial species that is the primary ......

No data available that match "DNA, Bacterial"

(1/38768) Detection of Chlamydia pneumoniae but not cytomegalovirus in occluded saphenous vein coronary artery bypass grafts.

BACKGROUND: A causal relation between atherosclerosis and chronic infection with Chlamydia pneumoniae and/or cytomegalovirus (CMV) has been suggested. Whether the unresolved problem of venous coronary artery bypass graft occlusion is related to infection with C pneumoniae and/or CMV has not been addressed. METHODS AND RESUTLS: Thirty-eight occluded coronary artery vein grafts and 20 native saphenous veins were examined. Detection of C pneumoniae DNA was performed by use of nested polymerase chain reaction (PCR). Homogenisates from the specimen were cultured for identification of viable C pneumoniae. Both conventional PCR and quantitative PCR for detection of CMV DNA were applied. Differential pathological changes (degree of inflammation, smooth muscle cell proliferation [MIB-1]) were determined and correlated to the detection of both microorganisms. C pneumoniae DNA could be detected in 25% of occluded vein grafts. Viable C pneumoniae was recovered from 16% of occluded vein grafts. Except for 1 native saphenous vein, all control vessels were negative for both C pneumoniae detection and culture. All pathological and control specimens were negative for CMV DNA detection. Pathological changes did not correlate with C pneumoniae detection. CONCLUSIONS: Occluded aorto-coronary venous grafts harbor C pneumoniae but not CMV. The detection of C pneumoniae in occluded vein grafts warrants further investigation.  (+info)

(2/38768) Acinetobacter bacteremia in Hong Kong: prospective study and review.

The epidemiological characteristics of 18 patients with acinetobacter bacteremia were analyzed. Patients (mean age, 55.5 years) developed bacteremia after an average of 14.1 days of hospitalization. Fifteen of 16 patients survived bacteremia caused by Acinetobacter baumannii. Cultures of blood from the remaining two patients yielded Acinetobacter lwoffii. Most patients (78%) resided in the general ward, while four patients (22%) were under intensive care. Genotyping by arbitrarily primed polymerase chain reaction analysis and the temporal sequence of isolation were more useful than phenotyping by antimicrobial susceptibility in the determination of the source of bacteremia, and the intravascular catheter was the leading infection source (39% of cases). The possibility of an association of glucose with the pathogenesis of acinetobacter infection was raised.  (+info)

(3/38768) Legionnaires' disease on a cruise ship linked to the water supply system: clinical and public health implications.

The occurrence of legionnaires' disease has been described previously in passengers of cruise ships, but determination of the source has been rare. A 67-year-old, male cigarette smoker with heart disease contracted legionnaires' disease during a cruise in September 1995 and died 9 days after disembarking. Legionella pneumophila serogroup 1 was isolated from the patient's sputum and the ship's water supply. Samples from the air-conditioning system were negative. L. pneumophila serogroup 1 isolates from the water supply matched the patient's isolate, by both monoclonal antibody subtyping and genomic fingerprinting. None of 116 crew members had significant antibody titers to L. pneumophila serogroup 1. One clinically suspected case of legionnaires' disease and one confirmed case were subsequently diagnosed among passengers cruising on the same ship in November 1995 and October 1996, respectively. This is the first documented evidence of the involvement of a water supply system in the transmission of legionella infection on ships. These cases were identified because of the presence of a unique international system of surveillance and collaboration between public health authorities.  (+info)

(4/38768) Classification of thermophilic streptomycetes, including the description of Streptomyces thermoalcalitolerans sp. nov.

A polyphasic taxonomic study was undertaken to clarify relationships within and between representative thermophilic alkalitolerant streptomycetes isolated from soil and appropriate marker strains. The resultant data, notably those from DNA-DNA relatedness studies, support the taxonomic integrity of the validly described species Streptomyces thermodiastaticus, Streptomyces thermoviolaceus and Streptomyces thermovulgaris. However, the genotypic and phenotypic data clearly show that Streptomyces thermonitrificans Desai and Dhala 1967 and S. thermovulgaris (Henssen 1957) Goodfellow et al. 1987 represent a single species. On the basis of priority, S. thermonitrificans is a later subjective synonym of S. thermovulgaris. Similarly, 10 out of the 11 representative thermophilic alkalitolerant isolates had a combination of properties consistent with their classification as S. thermovulgaris. The remaining thermophilic alkalitolerant isolate, Streptomyces strain TA56, merited species status. The name Streptomyces thermoalcalitolerans sp. nov. is proposed for this strain. A neutrophilic thermophilic isolate, Streptomyces strain NAR85, was identified as S. thermodiastaticus.  (+info)

(5/38768) Burkholderia cocovenenans (van Damme et al. 1960) Gillis et al. 1995 and Burkholderia vandii Urakami et al. 1994 are junior synonyms of Burkholderia gladioli (Severini 1913) Yabuuchi et al. 1993 and Burkholderia plantarii (Azegami et al. 1987) Urakami et al. 1994, respectively.

Reference strains of Burkholderia cocovenenans and Burkholderia vandii were compared with strains of other Burkholderia species using SDS-PAGE of whole-cell proteins, DNA-DNA hybridization and extensive biochemical characterization. Burkholderia gladioli and B. cocovenenans were indistinguishable in the chemotaxonomic and biochemical analyses. Burkholderia plantarii and B. vandii had indistinguishable whole-cell protein patterns but the B. vandii type strain differed from B. plantarii strains in several biochemical tests. The DNA-DNA binding levels (higher than 70%) indicated that (i) B. gladioli and B. cocovenenans, and (ii) B. plantarii and B. vandii each represent a single species. It is concluded that B. cocovenenans and B. vandii are junior synonyms of B. gladioli and B. plantarii, respectively.  (+info)

(6/38768) Taxonomic relationships of the [Pasteurella] haemolytica complex as evaluated by DNA-DNA hybridizations and 16S rRNA sequencing with proposal of Mannheimia haemolytica gen. nov., comb. nov., Mannheimia granulomatis comb. nov., Mannheimia glucosida sp. nov., Mannheimia ruminalis sp. nov. and Mannheimia varigena sp. nov.

The present paper presents the conclusions of a polyphasic investigation of the taxonomy of the trehalose-negative [Pasteurella] haemolytica complex. Clusters previously identified by ribotyping and multilocus enzyme electrophoresis (MEE) have been evaluated by 16S rRNA sequencing and DNA-DNA hybridizations. Results obtained by the different techniques were highly related and indicated that the [P.] haemolytica complex contains distinct genetic and phenotypic groups. At least seven species were outlined, five of which were named. We refrained in formal naming of more groups until additional strains are characterized. Five 16S rRNA clusters were identified corresponding to distinct lineages previously outlined by MEE. Within 16S rRNA cluster I two distinct genotypic groups have been outlined in addition to [P.] haemolytica sensu stricto (biogroup 1). Each of the clusters II, III, IV and V represent at least one new species. The investigations underline that [P.] haemolytica sensu stricto only contains strains that do not ferment L-arabinose even though they are referred to as 'biotype A' of [P.] haemolytica. The five 16S rRNA clusters identified had a common root relative to the other species within the family Pasteurellaceae, and the overall sequence similarity among these five clusters was higher than what is observed within the existing genera of the family. The allocation of the trehalose-negative [P.] haemolytica complex to a new genus seems to be indicated. Based on the polyphasic investigation performed a new genus Mannheimia is proposed for the trehalose-negative [P.] haemolytica complex. At the present stage two previously named species are transferred to this new genus and three new species are described. [P.] haemolytica is reclassified as Mannheimia haemolytica comb. nov., whereas Pasteurella granulomatis, Bisgaard taxon 20 and [P.] haemolytica biovar 3J are reclassified and combined in the species Mannheimia granulomatis comb. nov. Mannheimia glucosida sp. nov. corresponds to [P.] haemolytica biogroups 3A-3H and the beta-glucosidase and meso-inositol-positive strains of [P.] haemolytica biogroup 9. All typable strains within M. glucosida belong to serotype 11. Mannheimia ruminalis sp. nov. consists of strains previously classified as Bisgaard taxon 18 and [P.] haemolytica biogroup 8D. Finally, Mannheimia varigena sp. nov. includes [P.] haemolytica biogroup 6 as well as Bisgaard taxon 15 and Bisgaard taxon 36. The type strains are NCTC 9380T (M. haemolytica), ATCC 49244T (M. granulomatis), CCUG 38457T = P925T (M. glucosida), CCUG 38470T = HPA92T (M. ruminalis) and CCUG 38462T = 177T (M. varigena).  (+info)

(7/38768) Phylogenetic structures of the genus Acinetobacter based on gyrB sequences: comparison with the grouping by DNA-DNA hybridization.

The phylogenetic relationships of 49 Acinetobacter strains, 46 of which have previously been classified into 18 genomic species by DNA-DNA hybridization studies, were investigated using the nucleotide sequence of gyrB, the structural gene for the DNA gyrase B subunit. The phylogenetic tree showed linkages between genomic species 1 (Acinetobacter calcoaceticus), 2 (Acinetobacter baumannii), 3 and TU13; genomic species 6, BJ15, BJ16 and BJ17; genomic species 5, BJ13 (synonym of TU14) and BJ14; genomic species 7 (Acinetobacter johnsonii), 10 and 11; and genomic species 8 and 9. The phylogenetic grouping of Acinetobacter strains based on gyrB genes was almost congruent with that based on DNA-DNA hybridization studies. Consequently, gyrB sequence comparison can be used to resolve the taxonomic positions of bacterial strains at the level of genomic species. However, minor discrepancies existed in the grouping of strains of genomic species 8, 9 and BJ17. The phylogenetic tree for these strains was reconstructed from the sequence of rpoD, the structural gene for the RNA polymerase sigma 70 factor. The latter tree was 100% congruent with the grouping based on DNA-DNA hybridization. The reliability of DNA-DNA hybridization may be superior to that of sequence comparison of a single protein-encoding gene in resolving closely related organisms since the former method measures the homologies between the nucleotide sequences of total genomic DNAs. Three strains that have not been characterized previously by DNA-DNA hybridization seem to belong to two new genomic species, one including strain ATCC 33308 and the other including strains ATCC 31012 and MBIC 1332.  (+info)

(8/38768) Roseovarius tolerans gen. nov., sp. nov., a budding bacterium with variable bacteriochlorophyll a production from hypersaline Ekho Lake.

Eight Gram-negative, aerobic, pointed and budding bacteria were isolated from various depths of the hypersaline, heliothermal and meromictic Ekho Lake (Vestfold Hills, East Antarctica). The cells contained storage granules and daughter cells could be motile. Bacteriochlorophyll a was sometimes produced, but production was repressed by constant dim light. The strains tolerated a wide range of temperature, pH, concentrations of artificial seawater and NaCl, but had an absolute requirement for sodium ions. Glutamate was metabolized with and without an additional source of combined nitrogen. The dominant fatty acid was C18:1; other characteristic fatty acids were C18:2, C12:0 2-OH, C12:1 3-OH, C16:1, C16:0 and C18:0. The main polar lipids were diphosphatidylglycerol, phosphatidylethanolamine, phosphatidylglycerol and phosphatidylcholine. The DNA G+C base composition was 62-64 mol%. 16S rRNA gene sequence comparisons showed that the isolates were phylogenetically close to the genera Antarctobacter, 'Marinosulfonomonas', Octadecabacter, Sagittula, Sulfitobacter and Roseobacter. Morphological, physiological and genotypic differences to these previously described and distinct genera support the description of a new genus and a new species, Roseovarius tolerans gen. nov., sp. nov. The type strain is EL-172T (= DSM 11457T).  (+info)

The principal problem with inserting an unmodified mammalian gene into the bacterial chromosome, and then gett?

The principal problem with inserting an unmodified mammalian gene into the bacterial chromosome, and then getting that gene expressed, is that      
A)prokaryotes use a different genetic code from that of eukaryotes.      B)bacteria translate polycistronic messages only.      
C)bacteria cannot remove eukaryotic introns.     
D)bacterial RNA polymerase cannot make RNA complementary to mammalian DNA.      
E)bacterial DNA is not found in a membrane-enclosed nucleus and is therefore incompatible with mammalian DNA.

The correct answer is C. Eukaryotic genes have "introns", large regions that need to be removed from the RNA before translation. Bacterial genes do not have introns, and the transcribed mRNA will therefore encode an enzyme that is way to big. It has no way to remove the introns from the RNA.

What is the difference between bacterial infection and yeast infection?

I have bacterial  infection could I use monostat 3 for that?

A bacterial infection is caused by a bacteria and needs antibiotics. A yeast infection is caused by an overgrowth of yeast  and you use an anti fungal such as monostat for that. They are not the same thing. If you have been diagnosed with a bacterial infection a doctor would have had to do that so where is your prescription. If you are self diagnosing, bad idea.

how do you get rid of a bacterial infection of the skin from tanning booths?

bacterial infection
the bacteria isnt like MRSA its more like white blochs on my skin that dnt get any color like dry patches?

Tinea Versicolor is what you probably have. They can be white, brown, or a red color. It is not due to the tanning bed. It is from bacteria that is naturally on everyone's skin. Most people can not see it until they develop a tan simply because these spots do not tan. Heat can help them develop but will not cause the bacteria. Dandruff shampoo can help if the bacteria hasn't developed much.

Tinea versicolor is cause by a yeast type of skin fungus, which is present on normal skin. If the skin is oily enough, warm enough and moist enough, it starts to grow into small "colonies" on the surface of the skin. In these colonies the yeast grows like crazy and leaks out an acidic bleach. This changes the skin color. The patches are lightly reddish brown on very pale skin but they don't tan. Because of lack of any tanning, they look like white spots on darker or tanned skin. This is most often seen on the neck, upper chest, upper arms and back. There may be a fine, dry scale on it.

Usually the infection produces few symptoms, but some people get itching, especially when sweating. The warmer the weather, the worse this condition gets. Tanning booths are warm places, so avoid them. The reasons why some get this problem and others do not are not known.

A dermatologist can easily recognize this infection, but occasionally it can be mistaken for other skin conditions. If there is any doubt a 'KOH prep', a test done quickly in the office, will confirm the diagnosis.

The infection is treated with either topical or oral medications. In very mild cases, non-prescription antifungal creams (Lotrimin-AF, Micatin) will work. Prescription antifungal lotions and sprays (Oxistat lotion, Lamisil spray) may work better. The most economical effective treatment is to apply an antifungal shampoo (Nizoral, Excel) to the body as if it were soap, but leave it on for some minutes before rinsing.

For severe, extensive or recurrent cases, a few tablets of Nizoral pills will clear things up. A newer pill, Sporonox, may replace Nizoral for this problem. These will eliminate the fungus and relive any itch and scale. The uneven color of the skin will remain several months, perhaps until one gets a tan again in the next summer.

Remember, since we all have some of this fungus, no treatment can prevent one from picking it up again forever. In many people, the rash reappears for the next few years. To prevent recurrence, preventative re-treatment with the same medication may be advised. This condition is not seen beyond mid-life, so rest assured it won't keep coming back forever

I. Definition:

Tinea versicolor is a chronic skin condition caused by a yeast living on normal skin of all people. In most people, the presence of this yeast on the skin is not visible. In some people, for unknown reasons, the yeast grows more actively and causes an itchy scaling rash. 

II. Causes: 

Tinea versicolor is caused by a yeast called Pityrosporon orbiculare. 
People who have tinea versicolor are genetically predisposed to developing a rash when this germ is present on the skin. 
When the yeast grows on untanned skin, the rash is pink to brown. When the yeast grows on tanned skin, the rash looks white because the yeast blocks out the sunlight and the skin where the yeast is growing does not tan. When growing on Asian or African-American skin, the rash can look darker or lighter than the surrounding skin depending on the patient 

III. Treatment: 

There is no permanent cure for tinea versicolor. 
Selenium sulfide 2.5 percent should be applied to the skin, between the neck and the knees, before bed every night for 2 nights and washed off the following morning. After this, use the selenium sulfide once a week to once a month in the above manner to keep the condition under control. MY NOTE: Selenium sulfide is the active ingredient in Selsun Blue

Resistant cases can be treated with an antifungal cream applied directly to the skin. 
Some doctors use pills to treat this condition. We do not do this because the pills have side effects and offer no permanent solution. 
The uneven pigmentation that can develop from this condition can be improved with daily alpha hydroxyacid lotion application to the involved areas for several months.

Tinea Versicolor
What is tinea versicolor? How is it treated? 

Tinea versicolor is a mild, superficial fungal infection, somewhat similar to ringworm (true ringworm can also result in white patches). Since the affected skin doesn't change color well with sun exposure, it usually becomes apparent as white patches during the summer months. In the winter it may seem to disappear, or even seem to become slightly darkened patches as the surrounding skin gets paler (this is where the name versicolor comes from). 

Tinea versicolor is most common in adolescents and young adults 15 to 30 years old (although it can certainly happen at any age)

How to have sex with bacterial vaginosis during pregnancy? Does my husband need to wear condoms on?

I had bacterial vaginosis on my third trimester of pregnancy though I haven't had sexual contact with my husband for several months since he's working abroad and didn't even masturbate since I lost my sex drive. My husband will arrive tomorrow and i don't know if he should wear a condom since I have this disease. Please help me. :(

Bacterial Vaginosis is a bacterial infection. You can get antibiotics for that or take a homeopathic treatment from your local drug store. 
And definately have my empathy for the long distance situation, but I don't think you're supposed to have sex until the infection clears. 

If you're going to anyway I do suggest a condom. It will make it more comfortable for both of you.

What's the difference between Viral, bacterial and fungal meningitis?

I know that they're all different types obviously, bacterial being the most severe. But what's the difference? How does it affect the meninges different and body systems etc? meningitis just caused frm typical bacteria that just gets spread through the blood into the spinal fluid?
For example makes bacterial so much worse than viral and how can viral disappear on it's own where bacterial, treatment is necessary.
The MAIN thing I need to know is WHY bacterial is so much more harmful than viral. Like, if both affect the meninges, why is viral so much less serious?

Viral meningitis can be caused by many different viruses, including common intestinal viruses and viruses associated with mumps and herpes infection. In some cases, people can get viral meningitis from drinking polluted water.

The viruses that cause meningitis are contagious, but most people who become infected don't actually develop meningitis. Viral meningitis is usually mild and often clears up within one to two weeks.

Bacterial meningitis is a serious and frequently fatal illness. Even treated early, it can result in brain damage, hearing loss or learning disabilities. Some forms of bacterial meningitis such as meningococcal meningitis are highly contagious. The bacteria are spread though coughing, sneezing, kissing or sharing items such as eating utensils or toothbrushes with an infected person. Bacteria commonly identified as causing meningitis are Neisseria meningitidis, Haemophilus influenza, group B streptococcus (in newborns) and Streptococcus pneumoniae. Other less common bacteria include tuberculosis, Listeria, Staphlococcus and Salmonella. 

Fungal and parasitic meningitis are relatively uncommon. Fungal meningitis is more common in people with a weakened immune system. 

Viral meningitis usually doesn't require treatment, although certain types of viral meningitis such as herpes meningitis (HSV1) must be treated with antiviral agents to prevent complications or even death. Doctors often recommend bed rest, fluids and over-the-counter medications to relieve fever and headache. Most people completely recover on their own.

Bacterial meningitis needs to be treated immediately to prevent serious complications and death. A number of antibiotics can be used to treat bacterial meningitis, depending on the organism causing the infection. Other medications may also be used to treat symptoms and prevent permanent damage from the disease.

When looking at the symptoms of a disease, how can a doctor determine whether it is bacterial or viral?

In other words, what is the difference between how viral infections and bacterial infections affect the body?  How are the symptoms between the two types of diseases different?  After a doctor learns what symptoms a patient has, what further tests or examinations would he/she run to determine whether the disease is bacterial or viral?

In some cases it can be tough.  But there are several ways to try & sort it out.  First, what is going around?  If a virus is spreading through the area, epidemiology suggests it is a virus.  Furthermore, viral infections tend to cause a wide range of symptoms due to the way the virus attacks the body--fever, muscle aches, headache, rash, joint aches, etc all at once highly suggest a virus.  Bacterial infections tend to be more localized--pneumonia causes respiratory symptoms primarily--not joint pain too.  A bacterial infection that has spread so much to cause a lot of symptoms (called "sepsis") has the person very very ill.  Viruses are also much more common than bacterial infections.  Often time its a educated guess (that's why MDs spend so much time in school--you have to know alot about everything to discard causative agents to make an educated guess).  They can do more tests (a Complete blood count, or CBC, will show more lymphs in a viral infection & more ploys in a bacterial).  There are also antibody tests to specific causes.  However, many times, its too expensive & not worth all the time & effort to make a definitive diagnosis.  If you are going to get better anyway in 5-7 days, most people would not want to spend $500 or more to find out EXACTLY what they had.  That's why you are told to return if not better in x days or suddenly get worse.  Then the testing can be better utilized to find a source.  Some tests would be xrays (chest etc); a spinal fluid exam, blood tests like the CBC or antibody tests, blood, urine, sputum cultures for bacteria, viral cultures, bronchial washings of the airways for tests, TB testing, there are many tests and as they become negative, more exotic & rare things are tested for.  You always start with the most obvious & proceed to the rare.

What is a good brand of folic acid for the cure of bacterial vaginosis?

I am a young teenager and I think I suffer from bacterial vaginosis, even though I've never been checked out. I was looking on the internet and came upon a cure for B.V (folic acid). I want to give it a try but I just dont know which brand to pick. Could someone help me with this?

don't believe everything you read on the web, folic acid will not cure bacterial vaginosis.  You need to see a doctor and get tested and treated appropriately.

What is the difference between a uti and bacterial vaginosis?

can bacterial vaginosis be detected from a urine sample?

A UTI is a urinary tract infection, its in the urethra or bladder. Bacterial vaginosis is actually in the vagina.
They usually diagnose a UTI with a clean catch urine sample which if done correctly should not get anything except urine since it involves cleaning the area around it first. If it is not done correctly it may be contaminated by bacteria from around the labia.
BV is usually diagnosed with a visual exam and swabs of fluid from inside the vagina.