No data available that match "Genes, Bacterial"

*  Escherichia coli Stress Response as a Tool for Detection of Toxicity -...
Bacterial Biosensors for Detection of Toxicity. *. Global Gene Expression Profiling of the BarA- ......
*  Large-scale chromatin structure of inducible genes: transcription on a...
This bacterial selectable marker was replaced by a kan/neo prokaryotic/eukaryotic selectable marker ... DHFR gene induced) and after heat shock (Hsp70 genes induced), Zn addition (MT genes induced), or ... Clustering of multiple specific genes and gene-rich R-bands around SC-35 domains: evidence for ... Human chromosome mapping of single copy genes. In FISH: A practical approach. B. Beatty, S. Mai, J. ......
*  Irruption of genomics in the search for disease related genes | Gut
... bacterial artificial chromosomes or BACs10). About 3000 YACs and 30 000 BACs are sufficient to ... For a given gene, the sequence present in the common ancestor is called the root of the gene for ... The number of genes was not known with certainty, and it was believed to be around 100 000 or more ... Gene expression profiling predicts clinical outcome of breast cancer. Nature2002;415:530-6. ......
*  Getting The Mooney Treatment - The Loom
An ancestral set of body-axis genes (called Hox genes), for example, was passed down to different ... Case 2: The bacterial flagellum. Many species of bacteria such as E. coli use spinning tails to ... An ancestral set of body-axis genes (called Hox genes), for example, was passed down to different ... the axis of a developing fly's body is controlled by genes from the same family of genes that ......
*  Bananas and genetic engineering: Past, present and future - latimes
In the case of the black sigatoka field trial, bananas were engineered with rice genes that carry ... Bananas genetically modified to fight bacterial wilt make two proteins from sweet pepper. One of ... What is a "resistance gene" anyway? How does a plant ward off pests? ... bacterial wilt and a mold called Panama disease, as well as higher levels of vitamin A and iron, ......
*  Gene links to anorexia found by Children's Hospital of Philadelphia r... ( ...
Gene,links,to,anorexia,found,by,Children's,Hospital,of,Philadelphia,researchers,biological,biology ... I family of interferons that activate Th1-type innate immune responses against viral and bacterial ... "We did not detect other obvious candidate genes, but we did generate a list of other genes that we ... or SNPscommon gene variants that typically act as pointers to a gene region with a small effect on ......
*  Critical hearing gene helps send auditory messages to brain ( By studying a...
The researchers found that mice lacking the gene otoferlin are profoun... Study of the genes ... gene,helps,send,auditory,messages,to,brain,biological,biology news articles,biology news today, ... By studying a gene earlier linked to deafness in humans researchers n... ... I family of interferons that activate Th1-type innate immune responses against viral and bacterial ......
*  veterans - Page 3.14
The first observation of a bacterial gene called MCR-1 in the United States has scientists worried ... Scientists use a 'gene gun' to insert a gene from a flowering plant called rockcress into… ......
*  Fluorescent Protein Vectors for Cloning and Bacterial Expression, Living Colors
Gene Expression Profiling * ExpressHyb Hybridization Solution * Glass Microarray Hybridization ... Fluorescent Protein Vectors for Cloning & Bacterial Expression. These bacterial expression vectors ... Bacterial expression. Additional Information. Please see the product's Certificate of Analysis for ... Electroporation of Cas9-sgRNA ribonucleoproteins (RNPs) for gene editing in diverse cell types ......
*  The seeds of genetic modification |
But inserting the bacterial gene in the soybean seed made the plants resistant to RoundUp. Hoogheen ... "We have scientists that figured out that gene that the bacteria moved? [We] take that gene out and ... we put a gene into the bacteria that we'd like to have moved, and the bacteria move the gene for us ... Genetic modification, gene transformation and genetic engineering, even biotechnology in an ......

No data available that match "Genes, Bacterial"

(1/25659) Chemokine mRNA expression in gastric mucosa is associated with Helicobacter pylori cagA positivity and severity of gastritis.

AIM: To investigate the association between the quantity of gastric chemokine mRNA expression, severity of gastritis, and cagA positivity in Helicobacter pylori associated gastritis. METHODS: In 83 dyspeptic patients, antral and corpus biopsies were taken for semiquantitative reverse transcription polymerase chain reaction (RT-PCR) and histological grading of gastritis. Gastritis was evaluated by visual analogue scales. Quantities of chemokine (IL-8, GRO alpha, ENA-78, RANTES, MCP-1) RT-PCR products were compared with G3PDH products. Each sample was also evaluated for the presence of cagA and ureA mRNA by RT-PCR. RESULTS: mRNA expression of all five chemokines was significantly greater in H pylori positive than in H pylori negative mucosa. In H pylori positive patients, in the antrum C-X-C chemokine mRNA expression was significantly greater in cagA positive patients than in cagA negative patients, but there were no significant differences in C-C chemokine mRNA expression. In H pylori positive patients, chemokine mRNA expression in the corpus was less than in the antrum. In contrast to the antrum, only GRO alpha mRNA expression was significantly greater in cagA positive infection. Polymorphonuclear cell infiltration was correlated with C-X-C chemokine mRNA expression. Significant correlations were also found between bacterial density and C-X-C chemokine mRNA expression. CONCLUSIONS: In H pylori infection, C-X-C chemokines may play a primary role in active gastritis. Infection with cagA positive H pylori induces greater gastric chemokine mRNA expression in the antral mucosa, which may be relevant to the increased mucosal damage associated with cagA positive H pylori infection.  (+info)

(2/25659) Evolutionary relationships of pathogenic clones of Vibrio cholerae by sequence analysis of four housekeeping genes.

Studies of the Vibrio cholerae population, using molecular typing techniques, have shown the existence of several pathogenic clones, mainly sixth-pandemic, seventh-pandemic, and U.S. Gulf Coast clones. However, the relationship of the pathogenic clones to environmental V. cholerae isolates remains unclear. A previous study to determine the phylogeny of V. cholerae by sequencing the asd (aspartate semialdehyde dehydrogenase) gene of V. cholerae showed that the sixth-pandemic, seventh-pandemic, and U.S. Gulf Coast clones had very different asd sequences which fell into separate lineages in the V. cholerae population. As gene trees drawn from a single gene may not reflect the true topology of the population, we sequenced the mdh (malate dehydrogenase) and hlyA (hemolysin A) genes from representatives of environmental and clinical isolates of V. cholerae and found that the mdh and hlyA sequences from the three pathogenic clones were identical, except for the previously reported 11-bp deletion in hlyA in the sixth-pandemic clone. Identical sequences were obtained, despite average nucleotide differences in the mdh and hlyA genes of 1.52 and 3.25%, respectively, among all the isolates, suggesting that the three pathogenic clones are closely related. To extend these observations, segments of the recA and dnaE genes were sequenced from a selection of the pathogenic isolates, where the sequences were either identical or substantially different between the clones. The results show that the three pathogenic clones are very closely related and that there has been a high level of recombination in their evolution.  (+info)

(3/25659) A 55-kilodalton immunodominant antigen of Porphyromonas gingivalis W50 has arisen via horizontal gene transfer.

A 55-kDa outer membrane protein of Porphyromonas gingivalis W50 is a significant target of the serum immunoglobulin G antibody response of periodontal disease patients and hence may play an important role in host-bacterium interactions in periodontal disease. The gene encoding the 55-kDa antigen (ragB, for receptor antigen B) was isolated on a 9.5-kb partial Sau3AI fragment of P. gingivalis W50 chromosomal DNA in pUC18 by immunoscreening with a monoclonal antibody to this antigen. The 1.6-kb open reading frame (ORF) encoding RagB was located via subcloning and nested-deletion analysis. Sequence analysis demonstrated the presence of an upstream 3.1-kb ORF (ragA) which is cotranscribed with ragB. A number of genetic characteristics suggest that the ragAB locus was acquired by a horizontal gene transfer event. These include a significantly reduced G+C content relative to that of the P. gingivalis chromosome (42 versus 48%) and the presence of mobility elements flanking this locus in P. gingivalis W50. Furthermore, Southern blotting and PCR analyses showed a restricted distribution of this locus in laboratory and clinical isolates of this bacterium. The association of ragAB+ P. gingivalis with clinical status was examined by PCR analysis of subgingival samples. ragAB+ was not detected in P. gingivalis-positive shallow pockets from periodontal disease patients but was present in 36% of the P. gingivalis-positive samples from deep pockets. These data suggest that the ragAB locus was acquired by certain P. gingivalis strains via horizontal gene transfer and that the acquisition of this locus may facilitate the survival of these strains at sites of periodontal destruction.  (+info)

(4/25659) Cloning and expression of the dnaK gene of Campylobacter jejuni and antigenicity of heat shock protein 70.

Campylobacter jejuni is a leading cause of infectious diarrhea throughout the world. In addition, there is growing evidence that Guillain-Barre syndrome, an inflammatory demyelinating disease of the peripheral nervous system, is frequently preceded by C. jejuni infection. In the present study, the hrcA-grpE-dnaK gene cluster of C. jejuni was cloned and sequenced. The dnaK gene consists of an open reading frame of 1,869 bp and encodes a protein with a high degree of homology to other bacterial 70-kDa heat shock proteins (HSPs). The overall percentages of identity to the HSP70 proteins of Helicobacter pylori, Borrelia burgdorferi, Chlamydia trachomatis, and Bacillus subtilis were calculated to be 78.1, 60.5, 57.2, and 53. 8%, respectively. Regions similar to the Escherichia coli sigma70 promoter consensus sequence and to a cis-acting regulatory element (CIRCE) are located upstream of the hrcA gene. Following heat shock, a rapid increase of dnaK mRNA was detectable, which reached its maximum after 20 to 30 min. A 6-His-tagged recombinant DnaK protein (rCjDnaK-His) was generated in E. coli, after cloning of the dnaK coding region into pET-22b(+), and purified by affinity and gel filtration chromatography. Antibody responses to rCjDnaK-His were significantly elevated, compared to those of healthy individuals, in about one-third of the serum specimens obtained from C. jejuni enteritis patients.  (+info)

(5/25659) Yops of Yersinia enterocolitica inhibit receptor-dependent superoxide anion production by human granulocytes.

The virulence plasmid-borne genes encoding Yersinia adhesin A (YadA) and several Yersinia secreted proteins (Yops) are involved in the inhibition of phagocytosis and killing of Yersinia enterocolitica by human granulocytes. One of these Yops, YopH, dephosphorylates multiple tyrosine-phosphorylated proteins in eukaryotic cells and is involved in the inhibition of phagocytosis of Y. enterocolitica by human granulocytes. We investigated whether antibody- and complement-opsonized plasmid-bearing (pYV+) Y. enterocolitica inhibits O2- production by human granulocytes in response to various stimuli and whether YopH is involved. Granulocytes were preincubated with mutant strains unable to express YadA or to secrete Yops or YopH. O2- production by granulocytes during stimulation was assessed by measuring the reduction of ferricytochrome c. PYV+ Y. enterocolitica inhibited O2- production by granulocytes incubated with opsonized Y. enterocolitica or N-formyl-Met-Leu-Phe (f-MLP). This inhibitory effect mediated by pYV did not affect receptor-independent O2- production by granulocytes in response to phorbol myristate acetate, indicating that NADPH activity remained unaffected after activation of protein kinase C. The inhibition of f-MLP-induced O2- production by granulocytes depends on the secretion of Yops and not on the expression of YadA. Insertional inactivation of the yopH gene abrogated the inhibition of phagocytosis of antibody- and complement-opsonized Y. enterocolitica by human granulocytes but not of the f-MLP-induced O2- production by granulocytes or tyrosine phosphorylation of granulocyte proteins. These findings suggest that the specific targets for YopH are not present in f-MLP receptor-linked signal transduction and that other Yop-mediated mechanisms are involved.  (+info)

(6/25659) Complete nucleotide sequence of the 27-kilobase virulence related locus (vrl) of Dichelobacter nodosus: evidence for extrachromosomal origin.

The vrl locus is preferentially associated with virulent isolates of the ovine footrot pathogen, Dichelobacter nodosus. The complete nucleotide sequence of this 27.1-kb region has now been determined. The data reveal that the locus has a G+C content much higher than the rest of the D. nodosus chromosome and contains 22 open reading frames (ORFs) encoding products including a putative adenine-specific methylase, two potential DEAH ATP-dependent helicases, and two products with sequence similarity to a bacteriophage resistance system. These ORFs are all in the same orientation, and most are either overlapping or separated by only a few nucleotides, suggesting that they comprise an operon and are translationally coupled. Expression vector studies have led to the identification of proteins that correspond to many of these ORFs. These data, in combination with evidence of insertion of vrl into the 3' end of an ssrA gene, are consistent with the hypothesis that the vrl locus was derived from the insertion of a bacteriophage or plasmid into the D. nodosus genome.  (+info)

(7/25659) Genetic characterization of a new type IV-A pilus gene cluster found in both classical and El Tor biotypes of Vibrio cholerae.

The Vibrio cholerae genome contains a 5.4-kb pil gene cluster that resembles the Aeromonas hydrophila tap gene cluster and other type IV-A pilus assembly operons. The region consists of five complete open reading frames designated pilABCD and yacE, based on the nomenclature of related genes from Pseudomonas aeruginosa and Escherichia coli K-12. This cluster is present in both classical and El Tor biotypes, and the pilA and pilD genes are 100% conserved. The pilA gene encodes a putative type IV pilus subunit. However, deletion of pilA had no effect on either colonization of infant mice or adherence to HEp-2 cells, demonstrating that pilA does not encode the primary subunit of a pilus essential for these processes. The pilD gene product is similar to other type IV prepilin peptidases, proteins that process type IV signal sequences. Mutational analysis of the pilD gene showed that pilD is essential for secretion of cholera toxin and hemagglutinin-protease, mannose-sensitive hemagglutination (MSHA), production of toxin-coregulated pili, and colonization of infant mice. Defects in these functions are likely due to the lack of processing of N termini of four Eps secretion proteins, four proteins of the MSHA cluster, and TcpB, all of which contain type IV-A leader sequences. Some pilD mutants also showed reduced adherence to HEp-2 cells, but this defect could not be complemented in trans, indicating that the defect may not be directly due to a loss of pilD. Taken together, these data demonstrate the effectiveness of the V. cholerae genome project for rapid identification and characterization of potential virulence factors.  (+info)

(8/25659) Characterization of Moraxella (Branhamella) catarrhalis lbpB, lbpA, and lactoferrin receptor orf3 isogenic mutants.

Pathogenic members of the family Neisseriaceae produce specific receptors to acquire iron from their host's lactoferrin and transferrin. Recently, putative Moraxella catarrhalis lactoferrin receptor genes and a third open reading frame (lbpB, lbpA, and orf3) were cloned and sequenced. We describe the preliminary characterization of isogenic mutants deficient in LbpB, LbpA, or Orf3 protein.  (+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.

How do the genes on chromosome 17 relate to cancer?

How do the genes on chromosome 17 (Death Chromosome)  relate to cancer?

Changes in chromosome 17 have been identified in several types of human cancer. These genetic changes are somatic, which means they are acquired during a person's lifetime and are present only in certain cells. A particular chromosomal abnormality called an isochromosome 17q occurs frequently in some cancers. This abnormal version of chromosome 17 has two long (q) arms instead of one long arm and one short (p) arm. As a result, the chromosome has an extra copy of some genes and is missing copies of other genes.

An isochromosome 17q is commonly found in a cancer of blood-forming tissue called chronic myeloid leukemia (CML). It also has been identified in certain solid tumors, including a type of brain tumor called a medulloblastoma and tumors of the brain and spinal cord known as primitive neuroectodermal tumors. Although an isochromosome 17q probably plays a role in both the development and progression of these cancers, the specific genetic changes related to cancer growth are unknown.

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.