Antibiotic resistance can be a result of horizontal gene transfer,[30] and also of unlinked point mutations in the pathogen genome and a rate of about 1 in 108 per chromosomal replication. The antibiotic action against the pathogen can be seen as an environmental pressure; those bacteria which have a mutation allowing them to survive will live on to reproduce. They will then pass this trait to their offspring, which will result in a fully resistant colony.

The four main mechanisms by which microorganisms exhibit resistance to antimicrobials are:

Drug inactivation or modification: e.g. enzymatic deactivation of Penicillin G in some penicillin-resistant bacteria through the production of β-lactamases.
Alteration of target site: e.g. alteration of PBP—the binding target site of penicillins—in MRSA and other penicillin-resistant bacteria.
Alteration of metabolic pathway: e.g. some sulfonamide-resistant bacteria do not require para-aminobenzoic acid (PABA), an important precursor for the synthesis of folic acid and nucleic acids in bacteria inhibited by sulfonamides. Instead, like mammalian cells, they turn to utilizing preformed folic acid.
Reduced drug accumulation: by decreasing drug permeability and/or increasing active efflux (pumping out) of the drugs across the cell surface.[31]
There are three known mechanisms of fluoroquinolone resistance. Some types of efflux pumps can act to decrease intracellular quinolone concentration. In gram-negative bacteria, plasmid-mediated resistance genes produce proteins that can bind to DNA gyrase, protecting it from the action of quinolones. Finally, mutations at key sites in DNA gyrase or Topoisomerase IV can decrease their binding affinity to quinolones, decreasing the drug's effectiveness.[32] Research has shown that the bacterial protein LexA may play a key role in the acquisition of bacterial mutations giving resistance to quinolones and rifampicin.[33]

While this does arouse the obvious argument that antibiotic use should be scaled back in all but the most necessary of cases, it also means that antibiotics, when taken, should be taken with absolute thoroughness. You see, according to theory, an incomplete dose of antibiotics would kill only the bacteria least resistant to the drug, leaving only the 'strongest' ones to remain, propagate and infect others. This process, repeated, results in a strain of bacteria more and more resistant to antibiotic treatment, one that will eventually, in theory, infect longer and spread more thoroughly than any other strain. This in turn leads to the presence of antibiotic-resistant strains that can infect the human population, but which cannot be treated effectively by medicine.

а педиатрические конторы не практикуют тесты взрослых, живущих с ребенком?

, мы пьем уже сейчас всевозможные пробиотики отдельно от а/б, вот только приживаются ли...

Т.е есть обратилась бы к холисту/гомеопату/натуропату и тд, когда инфекции нет. Поверь, бороться можно. Можно насовсем от этого избавиться.

принимаете курс антибиотика и запиваете пробиотиком?
или уже все-таки курс приема завершен

Извини, Алтей, но для меня это все шарлотанство чистой воды, не вижу ни пользы, ни смысла (как ты в антибиотиках)

нет, курс только начат. пробиотики принимаем так, чтобы интервал был не менее 3 часов.
еще кефир + йогурт с живыми, тоже конечно не с а/б.

да пож-та. Предпочитаете давать антибиотики по несколько раз в году - нет ничего проще