- Werner Solbach added an answer:Detection of Genital Tuberculosis..PCR vs PAMP?
I want to know the relation of Molecular PCR testing and Pathogen Associated Molecular Pattern detection by reproductive immunology for MTB detection in Genital Tuberculosis.
There have been many conflicting view about the test. Recently I have noticed that PCR negative sample often is PAMP positive and clinicaly there is no MTB symtoms.
Is this largely possible that due to tenhnical constraints a PCR negative sample my come PAMP positive without any cilinically relevant symtpoms...?
If you suspect tuberculosis, you should aim to find the AFBs, either by microscohem, you py, culture or by PCR. If you don´t find them, you have either not got the right material or there is no tuberculosis. Fals positive PAMP tests to be expected.Following
- Gehendra Mahara added an answer:Does anyone explain me that how to do the study about PM 2.5 and tuberculosis infection?
Does anyone explain me that how to do the study about PM 2.5 and tuberculosis infection?
Thank you very much Amar Sir...Following
- Marc-Antoine Perrenoud added an answer:Does anyone know which kit is the best for large spectre PCR (identifiactions Eubacterias, mycobacterias, resistance genes TB)?
I'm starting my tests next week, I will test 4 different kits from 4 brands and I desire to know if anyone has tested FastPCR for diagnosis purpose with one of those ready-to-use pcr mixes? I Could use some guidance about which one will be the best.
- Roche Fastart PCR Master
- Takara Clontech Premix Ex Taq Hot Start Version
- Applied Biosystems AmpliTaq Gold Fast mastermix
- Kapa Biosystems Fast HotStart Readymix(2x)
The goal is simply to detect pathogens and identify them in culture or directly in samples patients. I also need to be able to analyse resistances genes. I'm trying to make my amplification method a lot faster than it's actually is (about 2:45 now)..
Thanks a lot !
I started my PCR tests 2 weeks ago and i already dropped 3 Master mix due to way too high sensibility, probably those mixs are better for use in human genomics.
(Roche Fastart PCR Master, Takara Clontech Premix Ex Taq Hot Start Version, Kapa Biosystems Fast HotStart Readymix(2x)
So I choose the Applied Biosystems AmpliTaq Gold Fast mastermix who seems to works fine for now with a high sensibility of 10^2cp/5ul for large spectre research of eubacterias, with no contaminations and a PCR time of about 45minutes my results were fine enought to continue with all my criterias (Mycobacterias, 28S panfungal, 18S panfungal, Resistance gene INHA, RPOB, KATG, and OXYR.) I'll see next week if it works for those criterias too.Following
- Is there any method to detect TB directly using Blood?
In majority of the cases sputum,body fluids correlating to symptoms TB is diagnosed but can blood samples be used directly?and/or is lysing agent required preferentially?
Can also use florescent dyes to detect CWD forms in blood.Following
- Hafid Soualhine added an answer:Can anyone help with XDR-TB treatment?I want to investigate a rather new chemotherapy with well-known medications for XDR-TB. Unfortunately, there are no facilities and safety to conduct the experiment on TB-infected cell lines here in Iran. Please help me provide the way to do this work.
Just to keep in minde, that there is no data supporting the correlation between in vitro and in vivo effect. It will be interesting to investigate but in parallel, conduct a study in vivo on patient population and compare with the treatment outcome.
As director of BSL-3 facility, you must have a permit to transfer your XDR strains to other facilities, and follow the international guidlines for IATA transportation. in other words, your strains must be transported as Category A.Following
- Muhammad Javed added an answer:How do you rate the success of diagnosis of tuberculosis from blood through PCR?
Thanks in advance for your replies.
In under developed countries the cost of PcR is very high. A positive tuberculin test in the absences of BCG helps better than pcRFollowing
- Alexandre Carvalho added an answer:Should INH prophylaxis be done in patients with long term steroid use?
45 year-old women was admitted to OPH d/t retinal vasultis. She has a plan to recieve long term and high dose steroid. But, her chest X-ray showd inactive tuberculosis and no history of treatment of TB. Should she take INH for prevention of occurence of acvtive TB ?
If tuberculosis reactivation is a concern, we can not rely only on X-ray to decide. It is necessary to determine the existence of latent tuberculosis with tuberculin test and, if not definite, with IGRA.
I believe long term corticotherapy is not an indication for INH prophylaxis, though.Following
- Himanshu Taneja added an answer:Can someone recommend a Tuberculosis disease dataset?I am looking for a dataset regarding Tuberculosis disease. Does anyone know a dataset or how to find a free dataset?
I would like to design a new hybrid clustering or classification to detect anomaly regarding Tuberculosis disease from big dataset.
Did you get any dataset? I am also looking for the same. Please respond if you found one.Following
- Alfonso J. Rodriguez-Morales added an answer:Wont Mycobacteria isolated from stool specimen confer TB infection?
Does isolate from a stool sample prove a person is infected with TB?
Yes. Diagnosis in stool has very low sensitivity, but is specific. If positive is TB and should be treated.Following
- Demba Jammeh added an answer:Which DNA extraction kit do you use for sputum sample stored with Ethanol 90%?
I have TB sputum samples stored with ethanol 90%. We tried the Genolyse kit but with low DNA yield.
Maybe boom extraction method is more recommended?
I advice you to use Qiagene Kit. you will get better DNAFollowing
- How should I treat a patient with recurrent meningeal TB who is seven months pregnant?
She got TB a long time ago and she had taken complete medication, but now she is at the 7th month of pregnancy and she has got TB again, but this time to brain. So what is the best way to treat her?
All the drugs of TB are teratogenic.
Is there any anti-tubercular drug without teratogenicity? If there is please suggest it here.
The following antituberculosis drugs are contraindicated in pregnant women:
Other than that every other Anti-TB drug is fair game. In medicine we weigh the benefits against the potential risks of using drugs. Also, who ever told you that all anti- tubercular drugs where teratogenic? Show me the proof that Ethambutal is teratogenic. You cannot. All anti-tubercular drugs should be used during pregnancy only if the benefit justifies the potential risk to the fetus. In the case that you are describing, the conclusion to this is a no-brainer. Either you give the drugs other than mentioned above or the patient and her fetus die.Following
- Peter J Didier added an answer:Histopathology shows Granulomatous endometritis but PCR is negative. What can be the reason?
Two tissue sections are sent to lab for detection of mycobacteium tuberculosis in endometrium, histopathology report shows Granulomatous endometritis and PCR shows negative for mycobacterium tuberculosis what are the possibilities in this issue and is this situation common or uncommon. primers specific to IS6110 were used, Dear researchers can any one provide your suggestions and information in this regard
I'm going to presume that the patient has a positive skin test for TB and special stains for mycobacteria and fungi are negative which explains why TB PCR was requested. If that's not the case then you should look at a nice review by Almoujahed et al (AM j Clin PAth 2002:117, 771-775) Many of these granulomatous lesions are focal and a reaction to a previous surgery (foreign bodies) or hemorrhage (necrobiosis, endometrial ablation). Systemic conditions like sarcoidosis and Crohn's disease should be ruled out but tuberculosis is the most common systemic etiology. In rare cases, cytomegalovirus infection has been implicated.
PCR is not flawless. The IS6110 primers test for Mtb complex organisms with about 85-95% sensitivity in some studies but only 30-75% sensitivity in other studies depending on extraction methods. The specificity runs about 75% so false positives are possible including positive tests for distantly related organisms like M. simiae. It will not detect other mycobacteria like M. avium/intacellulare complex, M. xenopi, M. gordonae, M. fortuitum, M. kansasii. In reality positive tests by this method should be confirmed by another method and negative tests do not rule out involvement of other mycobacteria.Following
- Hafid Soualhine added an answer:Does anyone have the experience of amplification of 2.5 kb plus gene of Mycobacterium tuberculosis??
I am trying to amplify a 3 kb gene of Mycobacterium tuberculosis which is of high GC rich..
I have easily amplified a 3 kb fragments using a two-steps amplification PCR. You have to design your own primers that must be GC rich at the 3' end, and high Tm and choose an amplification program without the annealing step, A programm containing denaturation and élongation steps. In this case you can set up the denaturation step at 95C for 30s and annealing/élongation step at 72 C for 90s to 120 s for 35 - 40 cycles. This is particularly interesting if you have a non specific bands less than 3kb with others methods.
You can try this using the simple AmpliTaq. that is less expensive.
Alternatively, you can use Phusion (as previously recommanded by other colleagues) and add DMSO,
Another way is to use a mix of 2 Taq polymerases, we have amplified a fragments more than 15 Kb in lenght. or you can use a mix of two polymerase like Advantage GC 2 Polymerase Mix & PCR Kit (Clontech).Following
- Farida Iskakova added an answer:A 37 year old female remains sputum positive for AFB in the eastern part of India since 1990 despite treatment. What is the probable explanation?A 37 year old female at the age of 15 years in the year 1990 was first diagnosed to have sputum positive tuberculosis. She had been treated many times with first line and 2nd line ATDs. She symptomatically improved but her sputum positivity remains the same. In 2004 she was diagnosed as a case of total drug resistance as per DST report and again at present her DST shows sensitivity to pyrazinamide, ethionamide, PAS and capreomycin. Still she is sputum positive for AFB though there is no symptoms and she is leading a totally normal life.
What could be the possible explanation for such a scenario?
Any explanation will be greatly appreciated.
It needs to genotype for the estimation of MBT strains. Are they M.tuberculosis or another types. Might be right, it is the combination of TB and MOTT.Following
- Alfonso J. Rodriguez-Morales added an answer:Are there any studies about the impact of climate change and variability on the epidemiology of the Tuberculosis?
In Vector-Borne diseases, but also in some respiratory infectious diseases including influenza, studies have demonstrated relationships and influences of climate change and variability on disease epidemiology, but what about tuberculosis?
Thanks, but not specificly addressing TB.Following
- Majid Avijgan added an answer:Where can I test and confirm Anti-tuberculosis and Anti-HIV activity for Plant extract samples?
Hi friends, I wish to do Antituberculosis and Anti HIV activity for Plant samples. Do you people know about any one doing out sourcing these experiments. I am ready to pay for this work. Or I will give authorship This work is my own interest on natural drug discovery.
I have several studies on the echinophora platyloba as an anti fungal herb. I have experience of what you are looking for. It is easy and simple, just invite from one of the pharmaceutic for co-operation. I have one co-worker in my paper as Dr Mohadese Mahboubi. Her email is as email@example.comFollowing
- Marco Tovar added an answer:Should MDR TB contacts be given chemoprophylaxis or kept under observation ?
As cases of MDR TB have increased in the last few years, do we need to treat PPD or IGRA convertors with chemoprophylaxis, or should we observe for active disease?
In reality, there is not enough evidence to recommend preventive therapy for household contacts of MDR TB patients. (http://www.ecdc.europa.eu/en/publications/Publications/201203-Guidance-MDR-TB-contacts.pdf)
But, there is some experience reporting effectivity of preventive therapy in children. (http://pediatrics.aappublications.org/content/109/5/765.short).Following
- Dragica Pesut added an answer:What is the incidence of Tuberculosis in medical Residents?I have recently noted an upsurge in the incidence of tuberculosis (both pulmonary and extrapulmonary) in medical Residents. What precautions/ measures can prove effective in curtailing such an occurrence?
I fully agree that the measures of TB infection control should be in place at health care facilities. They usually are in place at TB departments. It is considered that health care providers working at triage are more exposed to TB. In 2013, a cross-sectional study from Japan involved HCWs from a hospital without TB-specific wards. The screening for latent tuberculosis infection (LTBI) has been performed by interferon gamma release assay (Quantiferon TB Gold in tube). LTBI prevalence rate was 11% and questionnaire revealed previous close contact of the staff with TB patients. Please find attached the paper.Following
- Jan van Ooyen added an answer:Is there any mycobacterial protein which is non toxic when over expressed in M.tuberculosis but toxic when over expressed in M.smegmatis?
Hi, I am characterizing the transcriptional regulator of Mycobacteirum tuberculosis .
Because we don't have facility for M.tuberculosis culture, I am trying to over express (using PVV16 which has Hsp60 promoter) it in M.smegmatis. but I never got colonies though the clone and vector back bone are fine. So I thought over expression might be toxic to M.smegmatis. so to check its toxicity I did frame shift mutations and found its over expression is not lethal.
However for the same protein Chip-seq data available in MTB Network Portal. By going through their publication in NAR, I realised they over expressed corresponding transcription factors in M.tuberculosis using Tet-inducible system and did Chip-seq analysis.
My question is, is over expression of my protein not toxic to M.tuberculosis but toxic to M.smegmatis or am I simply doing something wrong?
How can I get a over expression strain of M.smegmatis?
For expression and characterization of Mycobacterial genes or proteins respectively, especialy cell envelope enzymes we often use Corynabacterium glutamicum, as it ís a fast growing, gras organism reaching high cell densities. This makes it simpler to recover low yield proteins. furthermore expression vectors for tet or iptg exist.Following
- Guillermo R. Labadie added an answer:How long can a compound be stable in DMSO for?
I am slightly concerned about my overexpression studies where one of my BCG strains should confer resistance to my control compound, but it seems like either the compound cannot enter the cell or either it is not functional. Could also multiple freeze-thawing cycles affect its stability? Should I prepare fresh solutions from powder?
The stabolity problem should be by oxidation or hydrolysis.
To avoid oxidation you can buble your DMSO stock solution with Nitrogen, to eliminate the air and store in vials that close really well, using also parafilm arounf the cap.
To know if your compound is working, first you have to assay your strains with fresh prepared solution. Then you can start using your stock solution and check if after a cycle of freeze-thawing keep providing the same result.
Additionally, you cam check if it is stable running a TLC or HPLC or GC( depending the polarity and the MW of the compound)Following
- Alberto Matteelli added an answer:Between Quantiferon-Gold-In tube or T-Spot.TB, which is the best test in your opinion?
I am interested in your opinion regarding the use of these tests in the field.
I agree with all the comments above. The question should provide more details on the context and scope, to provide a more appropriate answer. There is consensus that:
1. Both tests have no value for the diagnosis of active disease (with a caveat for childhood TB)
2. They are both sub-optimal, but still adequate for the diagnosis of latent infection
3. There is no demonstrated difference between them and compared to the tuberculin skin test, in sensitivity/specificity for the diagnosis of latent infection, including immunocompromised patients
4. Operational crieria (see response from Belinda) are useful to make a choice if your intent is to organize the activities of your diagnostic laboratoryFollowing
- Ronan O'Toole added an answer:Does anyone have information about the color change during Anti-TB test by Alamar Blue Dye method?
I have done the Anti-TB test of some synthesized compounds. I would like to know the color change in details. Does it happen due to drug & strain interaction?
How & why does color change from pink to blue?
Some details are give below:
Anti-TB activity using Alamar Blue Dye
1) The anti mycobacterial activity of compounds were assessed against M. tuberculosis using microplate Alamar Blue assay (MABA).
2) This methodology is non-toxic, uses a thermally stable reagent and shows good correlation with proportional and BACTEC radiometric method.
3) Briefly, 200µl of sterile deionized water was added to all outer perimeter wells of sterile 96 wells plate to minimize evaporation of medium in the test wells during incubation.
4) The 96 wells plate received 100 µl of the Middlebrook 7H9 broth and serial dilution of compounds were made directly on plate.
5) The final drug concentrations tested were 100 to 0.2 µg/ml.
6) Plates were covered and sealed with parafilm and incubated at 37ºC for five days.
7) After this time, 25µl of freshly prepared 1:1 mixture of Alamar Blue reagent and 10% tween 80 was added to the plate and incubated for 24 hrs.
8) A blue color in the well was interpreted as no bacterial growth, and pink color was scored as growth.
9) The MIC was defined as lowest drug concentration which prevented the color change from blue to pink.
The substrate in Alamar Blue is Resazurin. It changes to a pink-coloured and fluorescent compound Resorufin when reduced. It is useful for quantifying the bactericidal as well as bacteriostatic activity of compounds towards mycobacteria. Other papers describing its use in mycobacterial inhibition assays include:
Bassett IM, Lun S, Bishai WR, Guo H, Kirman JR, Altaf M, O’Toole RF (2013). Detection of inhibitors of phenotypically drug-tolerant Mycobacterium tuberculosis using an in vitro bactericidal screen. Journal of Microbiology 51(5): 651-658.
Taneja NK, Tyagi JS (2007). Resazurin reduction assays for screening of anti-tubercular compounds against dormant and actively growing Mycobacterium tuberculosis, Mycobacterium bovis BCG and Mycobacterium smegmatis. Journal of Antimicrobial Chemotherapy 60(2): 288-293.Following
- Francesc Codony added an answer:Is anyone familiar with real time PCR of m tuberculosis.?
I am getting false positive results after 35 cycles, when my positive samples come at around the 20th cycle. How can I optimize these kinds of problems?
Simply add one additional fluorescence reading step of 5s at 3ºC over the melting temperature of your PCR product in negative samples. It will minimize the fluorescence of primer dimer.
- Do you really think vitamin C added to existing TB drugs could shorten TB therapy?
"Do you really think vitamin C added to existing TB drugs could shorten TB therapy?"
Absolutely. And its nothing new.
Actually the antiseptic and bacterial qualities of ascorbic acid have long been known and mycobacteria such as TB are heavily influenced by them. Moreover there began to appear laboratory proof that TB itself depleted Vitamin C levels badly and could in itself cause subclinical scurvy.
According to Irwin Stone, who really was one of the pioneers of Vitamin C use:
"The bacteria causing tuberculosis (Mycobacteria tuberculosis) is particularly sensitive to the lethal action of ascorbic acid".
Two decades before its discovery and isolation, said Stone, ascorbic acid's effect on mycobacteria such as tuberculosis began to seep into the literature empirically. As early as 1933, McConkey and Smith took guinea pigs fed tuberculous sputum daily and split them into two groups. The first group was subjected to a Vitamin C deficient diet, while the second group, fed two teaspoonfuls of Vitamin C rich tomato juice, completed the study. McConkey's idea came from his clinical observation that patients hospitalized with the intestinal form of the tubercular disease, some of which were hemorrhaging, improved when tomato juice was added to their menu. In the Vitamin C deficient cohort group 26 of the animals died from intestinal ulcerations, while only 2 succumbed while taking tomato juice ― despite the small amounts (2mg) daily. This is what Stone meant when he said that TB was “particularly sensitive” to the lethal action of ascorbic acid.
McConkey’s work was confirmed by de Savitch ― with orange juice as the Vitamin’s source (deSavitsch et al.1934) and Birkhaug in 193811 ― both studies using what Stone felt were woefully inadequate amounts of C. But Birkhaug was on to something quite important. Not only did Vitamin C protect against “the initial invasive onslaught of”Ibid progressive tubercular disease ― but the disease itself was depleting Vitamin C levels in the body.
Actually, such linkage of TB to scurvy, historically, was also nothing new. No later than in 1689 did Richard Morton, one of the earliest writers on scurvy, mention in Phthisiologia, a book which gained him almost a century of fame, say:
“Scurvy is wont [accustomed] to occasion a consumption [tuberculosis] of the lungs.”
Birkhagh though, was essentially saying that tubercular disease caused subclinical scurvy, mentioning:
“Our study has shown that by compensating for the inevitable state of hypovitaminosis [too little] C which occurs in progressive tuberculosis, we render the animal organism more resistant against the inflammatory-necrotizing effect of tuberculosis and the initial invasive onslaught of virulent tubercle bacilli.” (Birkhaug, 1938). But what Birkhaug was not picking up, according to Erwin Stone, was that that Vitamin C was drop-dead lethal to tuberculosis.
Like Birkhaugh, Andosca and Foley realized that tuberculosis itself created Vitamin C deficiency. Andosca: “Most authors maintain that there is a deficiency of vitamin C in tuberculous patients.” Faulkner and Taylor14, for example, disclosed an increased demand for Vitamin C with infection. Patients with tuberculosis required more than 200 mg. of ascorbic acid a day to keep the plasma level normal.
Subclinical Scurvy from TB
Bauer and Vorwerk found vitamin C deficiencies of from 1 to 4 grams in the tubercular, finding a direct parallel between the activity of tuberculosis and the extent of vitamin C deficiency. Borsalino reported a study of 140 tuberculosis patients, in which administration of vitamin C rapidly increased capillary resistance and stopped hemoptysis ― the spitting up of blood or blood-tinged sputum. However such blood loss reappeared when treatment was discontinued. By 1946, in a survey of nutrition among the northern Manitoba Indians, Moore et al reported a very high mortality rate from tuberculosis and pneumonia among these Canadian Indians ― which they attributed to a diet extremely low in Vitamin C.
As Irwin Stone pointed out, "There were many more reports in this sickening mass of continued repetition of ineffectual clinical tests where the investigators were correcting a nutritional deficiency instead of using ascorbic acid to actually combat the disease." In the meantime, the extent of Vitamin C deficiency or hypovitaminosis documented by Birkhaug with mycobacterial disease was soon realized to be equivalent in cancer, still another similarity in the two wasting diseases, ((Carneron & Pauling, 1979)
Further positive animal studies that Vitamin C was a potent anti-tubercular were run separately by Kleimenhagen, Steinbach, and Boyden.18,19,20 culminating with Getz’s study21 of over 1000 men which intimated that were there were adequate Vitamin C blood levels ― there was no Mycobacteria tuberculosis. Still, persisted Stone: "The dogma of the vitamin theory kept these clinicians from thinking of ascorbic acid as an antibiotic and using it in the necessary antibiotic dosages. Ibid
That was until Charpy's 1948 study, in which a truly massive l5 Grams or 15,000 milligrams a day were given to terminal consumptive patients. These tubercular patients were so gone that one of them died before the study got underway, but the others survived and improved strikingly despite the fact that they seemed in Charpy's words: "unaware of the enormous tuberculosis lesions they harbored", a situation apparently found analogous in studies of Vitamin C and cancer. Charpy does not go into possible toxicity of such high Vitamin C, nor the kidney stones that could result. Vitorero and Doyle, on the other hand, found excellent results in the treatment of intestinal TB merely by injecting 500 to 600 milligrams of ascorbic acid a day initially, which was reduced to 400 milligrams as improvement was shown, and then further reduced to 200 milligrams a day. Vitorero and Doyle were quite positive about the benefits of this treatment in their few cases and recommended its use for intestinal tuberculosis.
Fast-forward to 2013, In an apparently "unexpected" discovery, researchers at Albert Einstein College of Medicine determined that Vitamin C, all by itself, killed both TB and drug resistant TB on culture plates. The finding suggested that Vitamin C, added to existing TB drugs could enhance and possibly shorten TB therapy. The study was published in the online journal Nature Communications.
The molecular mechanism by which vitamin C exerted its lethal effect was that Vitamin C induced what is known as a Fenton reaction, causing iron to react with other molecules to create reactive oxygen species (ROS) that kill the TB (Mtb) mycobacteria.
What Irwin Stone had so long ago said and predicted ― that TB was “particularly sensitive” to Vitamin C ― was now fully realized scientific reality.Following
- Sandeep Moudgil added an answer:What is the provisional diagnosis?
A 27 year-old married woman was admitted due to pain in lower abdomen for 7 days. USG revealed a multilobbed and multiloculated cyst in the left lower quadrant. During laparotomy, the parietal peritoneum was found thick. It was opened. A cystic lesion containing straw colored fluid was found. loculi were broken. Biopsy was taken. She had amenorrhoea for last one year.
Nice case. In such cases its important to evaluate the whole abdomen on imaging USG or CT whichever modality is being used. And a radiologist should evaluate the patient first without history and then in the light of history/clinicals of the patient. Many a times the diagnosis missed or not considered in differentials because of being too focused on one disease/organ/subspecialityFollowing
- Timothy Mark Doherty added an answer:What is the common method to rapidly screen immunogenic subunit TB antigen?
Would the method of using human/mice PBMC and interact it with the subunit TB antigen be plausible? Afterward, the immune response i.e IFN-y and IL-2/4 will be quantified where subunit TB antigen that induce the most IFN-y production would be considered as the most immunogenic antigen.
It's true that IFN-gamma levels tell you little about protection against TB. I've never seen a study which demosntrated protection without induction of IFN-gamma, but there is no correlation between IFN-gamma levels and protection, in either animal studies or human clinical trials. It appears that IFN-gamma is necessary, but not, by itself, sufficient for protection. In populations from TB-endemic regions, IFN-gamma has not proven a good indictator of infection/risk by itself.
But with regard to BCG, there is very strong evidence (from large controlled clinical trials: see Sjogren et al. for an excellent study in vaccination of military recruits) that BCG protects against disease in adults, and also that it protects against pulmonary disease in infants (see for example, the recent very interesting study from Favorov et al. or the large meta-analysis from Colditz).
I know that it is frequently said that BCG does not protect against infection, but this assertion is not really supported by evidence. There is increasing evidence that aside from preventing disease, BCG vaccination also prevents infection with M. tuberculosis, though with a lower effectiveness. See for example, the recent study from Greenland (PMID: 24969643), or Lalvani and colleagues' recent meta-analysis. (PMID: 25097193). It's interesting that the specific study and the metanalysis of 50 years data agree almost precisely on the degree of efficacy.
However, there are two important points to remember.
1) there is general agreement that BCG vaccination is not effective in individuals already sensitised to mycobacteria - it has only proven effective in trials in TST-negative adults, and trials including both TST+ and TST- adults have shown clear differences between the two groups.
2) In addition, almost every study indicates that protection from BCG vaccination wanes with time, and there is little protection remaining 15 years after vaccination. Thus vaccinating infants protects them in childhood, but it has no appreciable effect on disease in exposed adults. Unfortunately BCG cannot be effectively used as a booster vaccine ( for the reason, see point #1).
So it is true that vaccinating infants does not protect adults from TB (the same is true for many vaccines - pertussis for example). But it is not true that the BCG vaccine does not work in adults.Following
- Utpal Sengupta added an answer:Is decontamination mandatory for all samples (blood, sputum, endometrial tissue, csf) in the case of DNA extraction for TB diagnosis by RT-PCR?We are not getting reproducible results.
Decontamination is not essential because the primers are specific for species.Following
- Olga Novikova added an answer:What is the power of dN/dS method to be used for prediction of resistant-associated mutations in M. tuberculosis strains?
Genomics, DNA Sequencing, molecular genetics, and virology
I believe it is strongly depends on context to which dN/dS method is applied. Method itself tells nothing about mutations be resistant-associated or not, but in a right context and with support from other data sources it is the good place to look.Following
- Utpal Sengupta added an answer:What are the recent Immunological markers for multidrug resistant TB cases?
What are the recent Immunological markers for multidrug resistant TB cases?
The markers mentioned above are genetic markers and not immunological markers. No immunological marker has yet been identified for drug resistant TB.Following
- Milind Panchbhai added an answer:Does anyone know about Mycobacterium tuberculosis CMC 102 H37 RV ?
Does Mycobacterium tuberculosis CMC 102 H37Rv is the same to Mycobacterium tuberculosis H37Rv if anyone know please for urgent.
sorry , I dont knowFollowing
Any of the infectious diseases of man and other animals caused by species of MYCOBACTERIUM.