[lou_lou]

who has been on antibiotics without being given kefir/ rebuilds intestinal flora?

http://immunedisorders.homestead.com/antibiotics.html

Antibiotic Overuse & The Immune System
Immune System
Immune Stressors
Contact Us Site Map Resources Immune Products Supplements


Disease


Deficiency


Autoimmune


Immune 101


Introduction


Antibiotics


Free Radicals


Hormones


Infection


Poor Digestion


Poor Nutrition


Radiation


Stress


Toxins

Contact Us Site Map Resources Immune Products Supplements

Immune System
Antibiotic Overuse

By 1965 over 25,000 different antibiotic products had been developed. There was a fanatical enthusiasm for their use. Diseases that used to be killers became no more than an inconvenience.



Researchers and physicians felt that the area of bacterial infection and disease had been conquered. Tuberculosis is a bacterial disease. Anthrax is a bacteria. So is Strep, Staph, E. coli and Salmonella. The list is virtually endless.



According to researchers today the constant use of antibiotics with humans and livestock is a leading factor in our growing inability to eradicate disease. The overuse of these “wonder drugs” has improved the strength of our ever-evolving bacterial population.



Our efforts have pushed them to evolve. We shoot them with a big “gun”; they mutate, become stronger and elude that “gun” down the road. Then a new bigger “gun” is required.



Viruses and bacteria are extremely adaptable. Some bacteria can now live in bleach. The stronger these enemies become, the stronger, more complicated and costly antibiotics need to be to eliminate them. Some infections are now antibiotic resistant like staph and strep. Both have antibiotic resistant strains. There are others.



Joshua, a Wisconsin microbiologist, and Esther Lederberg “showed that the use of antibiotics in colonies of bacteria in which even less than 1 percent of the organisms were genetically resistant could have tragic results.



The antibiotics would kill off the 99% of the bacteria that were susceptible, leaving a vast nutrient-filled petri dish free of competitors for the surviving resistant bacteria. Like weeds that suddenly invaded an untended open field, the resistant bacteria rapidly multiplied and spread out…” The Coming Plague by Laurie Garrett



In 1997, David Dacha, Director of the Center for Disease Control (CDC) said, “In recent years antibiotics have become less effective against infectious agents, and we are concerned with the ‘post’ antibiotic era”. We are running out of “guns”.



Antibiotics Cut Off Immune Response

Dr. Peter D’Adamo says that antibiotics cut off immune response. Your body’s responsibility for fighting an infection has been taken over by medication.



He further states, “Did you know that antibiotics only reduce the level of infection? Your body’s immune system is still required to finish the battle.



When you allow your body to go to war on its own terms, without antibiotic intervention, it develops not only a memory of specific antibodies to the current infection and any similar to it, but also the ability to fight more effectively the next time it is challenged or attacked.”



As the invaders are getting stronger, our immune systems are increasingly more ill prepared.



Yeast Infections

Dr. D’Adamo continues by saying that, “continued and heavy use of antibiotics destroys not only the infection, but all of the good bacteria (healthy gut flora) in the digestive tract.



Many people experience diarrhea, and quite often women become subject to recurring and persistent yeast infections.” Candida albicans is the usual yeast offender. There are other species.



Other things that trigger candida infections, according to Elizabeth Lipski, author of Digestive Wellness are birth control pills, steroid medications, and sugar. She states that probiotics help keep candida in check.



These fungal and bacterial overgrowths initiated through use of antibiotics or other things mentioned give off endotoxins (toxins produced within the body) that suppress immune system function by knocking out commun-ication pathways between cells of the immune system.



Without these pathways in operation, immune cells don’t attack. Healthy gut flora supports immune function but does not replace those communication pathways. Reference: Dr. Jesse Stoff



When To Take Antibiotics

Antibiotics, when appropriately used, are important medical tools that save lives. If your immune system isn’t up to the task, by all means take them. Compensate for their use.



One way is by increasing the number of good immune supportive bacteria in supplement form according to Dr. Jesse Stoff. Bifidobacteria and lactobacilli (probiotics) are friendly bacteria that can add balance to the intestines.



Support immune function. “If microbes are becoming more resistant and virulent, we must increase our own resistance and strength to outsmart them. We must boost immune function so that people well be less receptive to infection.” Elizabeth Lipski, MS,CCN
Home Page

See also Immune 101





Fast Facts

Antibiotics kill bacteria however your immune system is still required to finish the battle. Any remaining bacteria not overcome can become stronger through mutation resulting in antibiotic resistance and stronger bacterial opponents.



Your intestines are loaded with bacteria. Balanced bacteria (both “good” & “bad”) in the intestines supports immune function. An overgrowth of “bad” bacteria can occur after antibiotic use because antibiotics can’t tell the difference and kill “good” bacterial as well. This suppresses immune function; releases toxins. Others things like alcohol can also disturb bacterial balance.



A bacterial imbalance can result in yeast overgrowth. The immune system is partly responsible for keeping yeast at bay.

"Immune System Solutions - Products & Principles"


Everything you need to know about taking care of your immune system naturally.
Taking care of your immune system can mean understanding the downside to antibiotics and what you can do.

[lou_lou]

http://jac.oxfordjournals.org/cgi/content/full/49/1/25

Journal of Antimicrobial Chemotherapy (2002) 49, 25-30
© 2002 The British Society for Antimicrobial Chemotherapy

--------------------------------------------------------------------------------

The 2000 Garrod Lecture


Factors impacting on the problem of antibiotic resistance
Stuart B. Levy,*

Center for Adaptation Genetics and Drug Resistance, Tufts University School of Medicine, Boston, MA 02111, USA

Abstract

Antibiotic resistance has become a major clinical and public health problem within the lifetime of most people living today. Confronted by increasing amounts of antibiotics over the past 60 years, bacteria have responded to the deluge with the propagation of progeny no longer susceptible to them. While it is clear that antibiotics are pivotal in the selection of bacterial resistance, the spread of resistance genes and of resistant bacteria also contributes to the problem. Selection of resistant forms can occur during or after antimicrobial treatment; antibiotic residues can be found in the environment for long periods of time after treatment. Besides antibiotics, there is the mounting use of other agents aimed at destroying bacteria, namely the surface antibacterials now available in many household products. These too enter the environment. The stage is thus set for an altered microbial ecology, not only in terms of resistant versus susceptible bacteria, but also in terms of the kinds of microorganisms surviving in the treated environment. We currently face multiresistant infectious disease organisms that are difficult and, sometimes, impossible to treat successfully. In order to curb the resistance problem, we must encourage the return of the susceptible commensal flora. They are our best allies in reversing antibiotic resistance.

Today we can list a number of organisms in both hospitals and the community that thwart treatment because they are resistant to not one, but to many different antibiotics (Table).1 The term multidrug resistance (MDR), which initially described resistant mammalian tumour cells, and later strains of Mycobacterium tuberculosis, now describes multidrug resistance in any microorganism—bacterium, fungus or parasite. The emergence of MDR is clearly related to the quantity of antibiotics and how they are being used.2,3 It may reflect acquisition of different resistance determinants on the same DNA molecule, or single determinants, such as multidrug pumps, that specify efflux activity against different antibacterials.4 Besides the known pathogens, the relatively recent appearance of opportunistic organisms, intrinsically resistant to many drugs, is now complicating the advances that we have made in medical technologies. With a larger number of immunocompromised patients and longer time periods spent in an immunocompromised state, these organisms have become ‘specialized’ pathogens—typically attacking only the most vulnerable patients. Among these opportunistic pathogens are the enterococci, the coagulase-negative staphylococci, Pseudomonas aeruginosa and Acinetobacter baumanii. Those physicians attending medical school 20–30 years ago probably did not even discuss these organisms as important pathogens, though today they cause prominent, even potentially lethal, problems in hospitals worldwide

[lou_lou]

http://home.caregroup.org/clinical/a...otic_Intes.htm

chemistry/function:

The intestinal flora is made up of many kinds of living bacteria that have a symbiotic relationship with the rest of the body. At least 400 friendly species exist; L. acidophilus and B.bifidus are principal species that have been linked with successful rebuilding of friendly gut flora and which are available in supplement form. L. acidophilus and B. bifidus may produce B vitamins including niacin, folic acid, biotin, and B6, as well as vitamin K
In addition to providing the body with useful nutrients, probiotics inhibit pathogenic bacteria in the gut in multiple ways:

• They secrete various substances, such as lactic and acetic acids, to decrease the pH of the gastrointestinal tract and vagina, rendering them less hospitable to pathogenic bacteria.

• They also secrete bacteriocins, natural antibiotics that kill undesirable bacteria.

For example, bacteria inhibited by L. acidophilus include: Bacillus subtilis, B. cereus, B. stearothermophilus, Candida albicans, Clostridium perfringens, Escheria coli, Klebsiella pneumoniae, L.bulgaricus, L. fermenti, L. helveticus, L. lactis, L. leichmannii, L. plantarum, Proteus vulgaricus, Pseudomonas aeruginosa, P. fluorescens, Salmonella typhosa, S. schottmuelleri, Shigella dysenteriae, S. paradysenteriae, S. paradysenteriae, Sarcina lutea, Serratia marcescens, Staphylococcus aureus, Streptococcus faecalis, S. lactis, Vibrio comma.

dietary sources:
Primarily found in fermented food such as yogurt, cheese, miso and tempeh. However, most fermented foods are made with L. bulgaricus or Streptococcus thermophilus. While these are friendly, beneficial microorganisms, they do not perform long-term colonization of the gut; therefore, they are not as effective as probiotic supplements at re-establishing populations of friendly bacteria.

deficiency:
A poor diet and/or antibiotic therapy are associated with a probiotic deficiency. Diarrhea, poor digestion and flatulence are frequent symptoms of deficiency.

known or potential therapeutic uses:

Allergies, candidiasis, colon cancer prevention, constipation, diarrhea, food sensitivities, intestinal dysbiosis, intestinal flora imbalance, irritable bowel syndrome, lactose intolerance, lowered immune function, urinary tract infections, vaginal yeast infections.

maintenance dose: Optimal levels of intake have not been established. A gastrointestinal tract that has a balanced, established flora, supported by a healthy diet, does not normally require supplementation. However, the presence of antibiotics in meats and other parts of the food supply may suggest a need for intermittent replenishment of viable enteric cultures. Large-scale replenishment after use of antibiotics will reduce the risk of opportunistic overgrowth of candida albicans and associated pathogens.

therapeutic dose: A supplemental dosage of at least one billion organisms per day is necessary to achieve the critical mass of bacterial restoration and successfully reinvigorate healthy intestinal ecology.

there is a huge amount of clinical information located on one page
therefore you can locate it and see that many clinical studies have shown this information to be absolutely true...

http://home.caregroup.org/clinical/a...otic_Intes.htm

a few studies examples :

References

Akaza H. New strategy of biochemoprevention on recurrence of superficial bladder cancer based on a hypothesis of the mechanism of recurrence. Gan To Kagaku Ryoho 1997;24 Suppl 1:253-256.

Aso, Y, Akazan H. Prophylactic effect of a Lactobacillus casei preparation on the recurrence of superficial bladder cancer. BLP Study Group. Urol Int 1992;49:125-129.

Aso, Y, Akaza H, Kotake T, et al. Preventive effect of a Lactobacillus casei preparation on the recurrence of superficial bladder cancer in a double-blind trial. The BLP Study Group. Eur Urol 1995;27:104-109.

Bengmark S. Ecological control of the gastrointestinal tract. The role of probiotic flora. Gut 1998 Jan;42(1):2-7. (Review)

Bennet JD, Brinkman M. Lancet. 1989 Jan 21;1(8630):164. (Letter)
Abstract: JDB had continuously active, severe UC for 7 years confirmed endoscopically and histologically. The condition was refractory to standard management including steroids and sulphasalazine and every time daily prednisone dosage was reduced below 30mg severe symptoms (bloody diarrhea, cramping tenesmus, skin lesions and arthritis recurred. For the past 4 years symptoms had been controlled with 4.2gms of alpha tocopherylquinone and a low fat diet. When the tocopheryl was discontinued or reduced, symptoms returned within 1-2 days. With a protocol developed to sterilize the bowel before surgery, his flora was greatly reduced. The donor flora was introduced by large volume retention enemas. 1 wk later tocopheryls were discontinued without any recurrence of symptoms. It has now been 6 months since this implantation of normal flora and patient has been symptom free for the first time in 11 years without any medications. 3 months after the implantation, colonic biopsy revealed chronic inflammatory cells but no active inflammation.

Berg, R, Bernasconi, P, Fowler, D, Gautreaux, M. Inhibition of Candida albicans translocation from the gastrointestinal tract of mice by oral administration of Saccharomyces boulardii. J Infect Dis 1993;168:1314-1318.

Bernet, MF, Brassart, D, Neeser, JR, Servin, AL. Lactobacillus acidophilus LA 1 binds to human intestinal lines and inhibits cell attachment and cell invasion by enterovirulent bacteria. Gut 1994;35:483-489.

Bleichner, G, Blehaut, H, Meutec, H, Moyse, D. Saccharomyces boulardii prevents diarrhea in critically ill tube-fed patients. A multicenter, randomized, double-blind placebo-controlled trial. Intensive Care Med 1997;23:517-523.

Blomberg, L, Henriiksson, A, Conway, PL. Inhibition of adhesion of Escherichia coli K88 to piglet ileal mucus by lactobacilli species. Appl Environ Microbiol 1993;59:34-39.

Boddy, AV, Elmer, GW, McFarland, LV, Levy, RH. Influence of antibiotics on the recovery and kinetics of Saccharomyces boulardii in rats. Pharm Res 1991;8:796-800.

Buts, JP, Bernasconi, P, Van Craynest, MP, et al. Response of human and rat small intestinal mucosa to oral administration of Saccharomyces boulardii. Pediatr Res 1986;20:192-196.

Buts, JP, Bernasconi, P, Vaerman, JP, Dive, C. Stimulation of secretory IgA and secretory component of immunoglobulins in small intestine of rats treated with Saccharomyces boulardii. Dig Dis Sci 1990;35:251-256.

Caetano, JA, Parames, MT, Babo, MJ, et al. Immunopharmacological effects of Saccharomyces boulardii in healthy human volunteers. Int J Immunopharmacol 1986;8:245-259.

Charteris WP, Kelly PM, Morelli L, Collins JK. Antibiotic susceptibility of potentially probiotic Bifidobacterium isolates from the human gastrointestinal tract. Lett Appl Microbiol. 1998 May;26(5):333-337.
Sixteen Bifidobacterium isolates from the human gastrointestinal tract were assayed for susceptibility to 44 antibiotics by soft agar overlay disc diffusion on TPY agar. Five isolates (3/7 B. bifidum and 2/3 B. breve) exhibited atypical antibiotic susceptibility profiles. Poor growth in the agar overlay accounted for susceptibility of B. bifidum but not B. breve isolates. All other isolates were resistant to cefoxitin (30 micrograms), aztreonam (30 micrograms), vancomycin (30 micrograms), amikacin (30 micrograms), gentamicin (10 micrograms), kanamycin (30 micrograms), streptomycin (10 micrograms), fusidic acid (10 micrograms), trimethoprim (5 micrograms), norfloxacin (10 micrograms), nalidixic acid (30 micrograms), metronidazole (5 micrograms), polymyxin B (300 micrograms) and colistin sulphate (10 micrograms), and they were susceptible to the six penicillins studied, cephalothin (30 micrograms), cefuroxime (30 micrograms), cefaclor (30 micrograms), ceftizoxime (30 micrograms), cefotaxime (30 micrograms), bacitracin (10 micrograms), chloramphenicol (30 micrograms), erythromycin (15 micrograms), clindamycin (2 micrograms), rifampicin (5 micrograms) and nitrofurantoin (300 micrograms). In addition, they varied in their susceptibility to cephradine (30 micrograms), cephazolin (30 micrograms), cefoperazone (75 micrograms), ceftriaxone (30 micrograms), ofloxacin (5 micrograms) and furazolidone (15 micrograms). They were resistant, or only marginally moderately susceptible, to ceftazidime (30 micrograms), netilmicin (10 micrograms), sulphamethoxazole (100 micrograms), cotrimoxazole (25 micrograms) and ciprofloxacin (5 micrograms), and susceptible or marginally moderately susceptible to tetracycline (30 micrograms). All B. bifidum isolates were susceptible to cefixime (5 micrograms). Four microorganism-drug combinations were evaluated for beta-lactamase activity but its absence suggested that cell wall impermeability was responsible for cephalosporin resistance among bifidobacteria. The antibiotic susceptibility of B. animalis 25527T was similar to that of the human isolates.

Clements, ML, Levine, MM, Black, RE, et al. Lactobacillus prophylaxis for diarrhea due to enterotoxigenic Escherichia coli. Antimicrob Agents Chemother 1981;20:104-108.