Antibiotic Testing
Posted on May 24, 2011 by Administrator
Gibraltar Laboratories performs certification of label claim testing regarding the potency of antibiotics (antibiotic testing). Certification is necessary to conform to US FDA current good manufacturing practice regulations. Potency means that the labeled strength of the antibiotic is accurate and therefore an infection caused, for example, by gram positive bacteria can be treated successfully by bacitracin. The potency of antibiotics may be demonstrated under suitable conditions by their inhibitory effect on microorganisms.
A reduction in antimicrobial activity also will reveal subtle changes not demonstrable by chemical methods. Accordingly, microbial or biological assays remain gnerally the standard for resolving doubt with respect to possible loss of activity. The antibiotic testing performed at Gibraltar Laboratories is described in the chapter <81> ANTIBIOTICS—MICROBIAL ASSAYS of the USP. This chapter summarizes procedures for the antibiotics recognized in the USP for which microbiological assay remains the definitive method. The cylinder-plate or “plate” assay depends upon diffusion of the antibiotic from a vertical cylinder through a solidified agar layer in a Petri dish or plate to an extent such that growth of the added microorganism is prevented entirely in a circular area or “zone” around the cylinder containing a solution of the antibiotic.
The antibiotic test is a very demanding test that requires expert care in the preparation of the media and organisms used in the assay. The fundamental principle is that the potency of the antibiotic is directly proportional to area of death it caused. If the antibiotic is not effective all of the bacteria added to the agar will form a confluent lawn. However, if the antibiotic is potent it will diffuse throughout the test system causing a clear zone where bacterial growth was prevented . This zone can be precisely measured with a sophisticated analytical instrument. This clear area of growth is also referred to as a zone of inhibition. Standards are always included in the assay so that one knows that a given zone area corresponds to a known potency. A regression curve is obtained from several concentrations of the standard and the unknown’s potency is obtained from its zone area.
I would find it hard to answer eiethr way. I think multidrug resistance is a serious and potential threat, and there have been recommendations for some time that reports, such as that published by Walsh et al. in Lancet Infectious Diseases, be published and acted upon.Molecular epidemiological studies are a crucial underpinning to work on predicting antimicrobial resistance (PAR), especially when these elements are associated with, or are in the same ecological niche, as promiscuous mobile genetic elements, and arising in nosocomial environments.However, whilst the a/biotic pipeline could certainly have been considerably better stocked, the efforts of numerous small biotechs and academic researcher looking at alternatives to the rather poultry introduction of new a/biotic classes, seems to be chronically undervalued. There are valiant efforts to target bacterial virulence, the mechanisms of horizontal transfer, and to inhibit the means by which bacteria resistant antibiotics in all cases rendering more time for new drug discovery, but crucially more time in clinical therapy. Is it likely that we will be dealing with infections in the UK that are completely resistant to antibiotics within 10 years? Or is this simply a case of media hysteria? Yes, if the funding is not made available and we rely on the efforts of a (majority) disinterest of large pharmaceuticals to invest in new drug class leads, we will be dealing with increased prevalence of multidrug resistance as we already are in isolated pockets with some strains of Gram (+)ve bacterial pathogens.Media hype should be reflective, and not doomsaying. They should be pointing out the threats, but identifying the huge efforts being taken to provide alternative solutions brought about by the lack of real investment. We know so much more about bacteriology, molecular epidemioloigy and drug discovery now than we did in the heyday of a.biotic discovery. A/biotics were used for years without a full understanding of their mechanisms, nor the mechanisms of resistance. Many instances of a/biotic resistance spread could (and should) have ben predicted and prevented.Ironically, some of the systems biology, high-throughput infrastructures that have been stealing so much of the research funding pot (that could have gone into a/biotic and resistance research), could actually now be of some considerably use in speeding up the whole process of recognising new resistance determinants, tracking their spread and identifying resistance trends that can be exploited to clinical benefit.
The way I am understanding is your aisnkg why does our body become immune to some antibiotics, and thus making them stop working. My sons doctor told me it was because if you keep using the same antibiotic over and over again, that the bacteria, can start to resist it because it is used to it being present in the body. For example my 16 month ol son has MRSA, I work in a drug facility, so I am around the jailed population alot, and I guess I brought it home with me, since he is so young he often gets outbreaks, and they need to be treated with IV antibiotics, but the prolem with MRSA is that there are only 3 or 4 antibiotics that work on it, Clindamycin, vancomycin, those are the 2 they usually give my son. I would say he has had about 6 outbreaks since he was 6 months old, and its been very hard because at any time those medications can stop working, thats why his doctor tries alternating the two hoping that his body does not become immune to one of them, because then we woudl run out of options very quickly. I hope this was helpful.
Hi Alejandra,Your question is exelclent but there are many wrong assumptions. To start off antibiotics do not kill of bacteria. Antibiotics work by preventing the synthesis of bacterial wall. In other words new bacteria do not form when a patient is taking antibiotics. The bacteria that are in the body are eaten up by white blood cells called phagocytes.All bacteria can become resistant to all antibiotics including the acne bacteria . Please NOTE that ACNE IS NOT CAUSED BY A BACTERIA. This is the second assumption that is not correct.