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Bacterial Infections in Stool- what to do?
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Bacterial Infections in Stool- what to do?

I have 6 strains of moderate to abundant bacterial infections in my stomach: Staphylococcus spp.(moderate), Staphylococcus aureus(moderate), Enterococcus species (abundant), Alpha Hemolytic Streptococcus(abundant), Gamma Hemolytic Streptococcus(abundant), and Cornybacterium species(moderate).

Has anyone else ever had these results? What sort of medications were you put on?

All my doctor told me was to increase my 8 billion + live culture acidophilus to 3 times per day.
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I haven't had the exact situation like you're talking about but I would think *normally* a GI specialist would put you on a powerful antibiotic that's not absorbed easily into the bloodstream like Flagyl for example.  That's usually used for infections in stool, colon but each bug has it's own special antibiotic that is more effective than others.  If you have ALL those (holy smokes..poor thing i'm sorry) then maybe a typical standard dose of Flagyl for so many days followed by the antibiotic.  If you want a 2nd opinion it costs money on this site but you could ask the GI specialist for his advice on what he would do (I forget how much it $15 I think..)

Probiotics is a good idea though, usually the best are the most expensive (like VSL 3 I think..that's a good one) but yeah normally you want to kill the bacteria first then probiotics...sounds like your doctor wants you to ride it out - which I've heard most bacteria strains eventually all die out anyway but it makes for a long drawn out process..I've heard some strains last weeks to months but not totally sure :( so...yeah good luck!  
Thanks for the advice!! I will have to see what my doctor says about that medicine. I would rather go ahead and knock the viruses out instead of "waiting out!" bc that's not fun! Thanks again!
hi victoria listen i am going threw alot with the same thing,but the problem with me is that they have no clue what they are treating, they just keep guessing, and when they do that they don't know if they are using the meds to kill it so in a month or so here i am back in the hospital or doctors office on  diffrent meds my suggestion to you is to research on the bacteria in your stool. there are alot more medications to choose from so please be aware of the bacteria.There are diffrent gram positives and gram negitives. i have been fighting mine for 5 years now and it is very sad that they have not gave me the right meds for it,I had to do my own research to figure it out on my own,and if you go in to the doctors knowing more then them, they get angry right away. and don't want to here about it the real problem we have is that the doctors are making a killer kick back from all of these meds the perscribe if they cured us they would go broke, honestly
victoria another thing look up bactericidal antibiotics and bacteriostatic antibiotics.bactericidals kill bacteria directly where bacteriostatics pervent them from dividing.

Enterococci are part of the normal intestinal flora of humans and animals but are also important pathogens responsible for serious infections. The genus Enterococcus includes more than 17 species, but only a few cause clinical infections in humans. With increasing antibiotic resistance, enterococci are recognized as feared nosocomial pathogens that can be challenging to treat.

Enterococcus species are hardy, facultative anaerobic organisms that can survive and grow in many environments. In the laboratory, enterococci are distinguished by their morphologic appearance on Gram stain and culture (gram-positive cocci that grow in chains) and their ability to (1) hydrolyze esculin in the presence of bile, (2) grow in 6.5% sodium chloride, (3) demonstrate pyrrolidonyl arylamidase and leucine aminopeptidase, and (4) react with group D antiserum. Before they were assigned their own genus, they were known as group D streptococci.

Enterococcus faecalis and Enterococcus faecium are the most prevalent species cultured from humans, accounting for more than 90% of clinical isolates. Other enterococcal species known to cause human infection include Enterococcus avium, Enterococcus gallinarum, Enterococcus casseliflavus, Enterococcus durans, Enterococcus raffinosus and Enterococcus mundtii.[1] E faecium represents most vancomycin-resistant enterococci (VRE).

Isolation of enterococci resistant to multiple antibiotics has become increasingly common in the hospital setting.[2] According to National Nosocomial Infections Surveillance (NNIS) data from January 2003 through December 2003, more than 28% of enterococcal isolates in ICUs of the more than 300 participating hospitals were vancomycin-resistant. Clonal spread is the dominant factor in the dissemination of multidrug-resistant enterococci in North America and Europe.[3] Virulence and pathogenicity factors have been described using molecular techniques. Several genes isolated from resistant enterococci (agg, gelE, ace, cylLLS, esp, cpd, fsrB) encode virulence factors such as the production of gelatinase and hemolysin, adherence to caco-2 and hep-2 cells, and capacity for biofilm formation.[4, 3]

Enterococci have both an intrinsic and acquired resistance to antibiotics, making them important nosocomial pathogens. Intrinsically, enterococci tolerate or resist beta-lactam antibiotics because they contain penicillin-binding proteins (PBPs); therefore, they are still able to synthesize some cell-wall components. They are intrinsically resistant to penicillinase-susceptible penicillin (low level), penicillinase-resistant penicillins, cephalosporins, nalidixic acid, aztreonam, macrolides, and low levels of clindamycin and aminoglycosides. They use already-formed folic acid, which allows them to bypass the inhibition of folate synthesis, resulting in resistance to trimethoprim-sulfamethoxazole.

Enterococci also have acquired resistance, which includes resistance to penicillin by beta-lactamases, chloramphenicol, tetracyclines, rifampin, fluoroquinolones, aminoglycosides (high levels), and vancomycin. The genes that encode intrinsic or acquired vancomycin resistance result in a peptide to which vancomycin cannot bind; therefore, cell-wall synthesis is still possible.

Unlike streptococcal species, enterococci are relatively resistant to penicillin, with minimum inhibitory concentrations (MICs) that generally range from 1-8 mcg/mL for E faecalis and 16-64 mcg/mL for E faecium. Therefore, exposure to these antibiotic agents inhibits but does not kill these species. Combining a cell wall–active agent such as ampicillin or vancomycin with an aminoglycoside may result in synergistic bactericidal activity against enterococci.

The acquisition of vancomycin resistance by enterococci has seriously affected the treatment and infection control of these organisms. VRE, particularly E faecium strains, are frequently resistant to all antibiotics that are effective treatment for vancomycin-susceptible enterococci, which leaves clinicians treating VRE infections with limited therapeutic options.

Newer antibiotics (eg, quinupristin-dalfopristin, linezolid, daptomycin, tigecycline) with activity against many VRE strains have improved this situation, but resistance to these agents has already been described. A mutation (G2576U) in the domain V of the 23S rRNA is responsible for linezolid resistance,[3] whereas resistance to quinupristin-dalfopristin may be the result of several mechanisms: modification of enzymes, active efflux, and target modification. Resistance of E faecalis and E faecium to daptomycin, a newer cyclic lipopeptide antibiotic that acts on the bacterial cell membrane, has also been reported.[5]

Six phenotypes of vancomycin resistance, termed VanA, VanB, VanC, VanD, VanE, and VanG, have been described. The VanA and VanB phenotypes are clinically significant and mediated by 1-2 acquired transferable operons that consist of 7 genes in 2 clusters termed VANA and VANB operons. In 1988, these gene clusters first were reported in enterococcal strains. VanA is carried on a transposon Tn1546 that is almost always plasmid-mediated.

In the United States and Europe, the 3 major phenotypes include VanA, VanB, and VanD. VanA is the most common, and enterococcal isolates exhibit high-level resistance to both vancomycin and teicoplanin, while VanB isolates have variable resistance to vancomycin and remain susceptible to teicoplanin. The VanC phenotype is mediated by the chromosomal VANC1 and VANC2 genes, which are constitutively present in E gallinarum (VANC1) and E casseliflavus (VANC2). These genes confer relatively low resistance levels to vancomycin and are not transferable. To date, the VanD, VanE, and VanG phenotypes have been described in only a few strains of enterococci.

Three patients infected with vancomycin-resistant Staphylococcus aureus (VRSA) have been reported in the United States.[6, 7] The in vivo conjugative transfer potential of the vanA resistance gene from vancomycin-resistant E faecalis to methicillin-resistant S aureus (MRSA) was confirmed in the first of these cases. This poses an emerging threat to patient safety. E faecium isolates with a complex-17 lineage have also emerged in hospital and community settings in 5 continents over just the past 2 decades. This continued global spread of resistant organisms and the creation of new, highly virulent pathogens from transfer of resistance genes underscore the importance of infection control and prevention, active surveillance, and use of appropriate antibiotics.
just trying to give you a little information before you go to the doctors good luck!!!!

Corynebacteria (from the Greek words koryne, meaning club, and bacterion, meaning little rod) are gram-positive, catalase-positive, aerobic or facultatively anaerobic, generally nonmotile rods. The genus contains the species Corynebacterium diphtheriae and the nondiphtherial corynebacteria, collectively referred to as diphtheroids. Nondiphtherial corynebacteria, originally thought to be mainly contaminants, have recently been recognized as pathogenic, especially in immunocompromised hosts.

Approximately 20 years ago, taxonomic changes were made to diverse genera previously included within the coryneform groups. The reclassification is based on the degree of homology of RNA oligonucleotides between groups. Based on this reclassification, for example, Corynebacterium haemolyticum became Arcanobacterium haemolyticum and the JK group became Corynebacterium jeikeium.[1] More recently, Van den Velde and colleagues have suggested that species of corynebacteria would be more correctly identified based on their cellular fatty acid profiles (ie, for the C14 to C20 fatty acids).[2]

Advances in molecular biology and genome analysis now also allow for detailed descriptions of DNA-binding transcription factors and transcriptional regulatory networks. This was first described for Corynebacterium glutamicun. Web-based resources are available online at CoryneRegNet[3] and CoryneCenter.[4]

Prior to the 1990s, the incidence of diphtheria had been declining. However, an epidemic of diphtheria in the former Soviet Union was first noticed in the Russian republic in 1990 and then spread to the other newly independent states, peaking in the mid-1990s. In some endemic locations, such as India, 44% of throat and nasal swabs tested positive for C diphtheriae and Corynebacterium pseudodiphtheriticum.[5] Today, the more common scenario is nondiphtherial corynebacterial bacteremia associated with device infections (venous access catheters, heart valves, neurosurgical shunts, peritoneal catheters), as well as meningitis, septic arthritis, and urinary tract infections.

For more information about C diphtheriae infections, please see Diphtheria.

Nondiphtherial corynebacteria also cause chronic and subclinical diseases in domestic animals and can lead to significant economic losses for farmers. Examples of widespread and difficult-to-control infections include Corynebacterium pseudotuberculosis caseous lymphadenitis in sheep, goats, and alpacas; C pseudotuberculosis ulcerative dermatitis in cattle; and urinary tract infections and mastitis (affecting milk production) in cattle due to infection with Corynebacterium renale, Corynebacterium cystidis, Corynebacterium pilosum, and Corynebacterium bovis.[6, 7]

Alpha-Hemolytic Streptococci
Alpha hemolysis means the red blood cells are intact, but the hemoglobin is converted to biliverdin. This causes a greening of the blood agar plate around the colonies.

- Pneumococci (e.g. S. pneumoniae)
- Viridans and Others (e.g. S. mutans, S. viridans, Streptococcus salivarius, S. salivarius subsp. thermophilus)

Beta-Hemolytic Streptococci
Beta hemolysis is a true hemolysis of erythrocyte by the enzyme hemolysin. Clear zones will appear around the colonies on the blood agar plate.
Beta-Hemolytic streptococci are subdivided into serological groups by antibodies that recognize surface carbohydrate antigens (e.g. group A,B,C,D).
- Group A (e.g. S. pyogenes, S. dysgalactiae subsp. equisimilis, S. anginosus strains)
- Group B (e.g. S. agalactiae)
- Group C (e.g. S. equi, S. zooepidemicus:)
- Group D (Enterococci: S. bovis and S. suis)

Non-Hemolytic or Gamma-Hemolytic Streptococci
Gamma hemolysis is a misnomer, there is actually no hemolysis. Non-hemolytic or gamma-hemolytic streptococci rarely cause disease.

Find a doctor who utilizes Diagnos-Techs Labs in Tukwila, WA  (425) 251-0596.  They can send you a kit for a 3-day stool test which will determine which bacteria are present as well as which are beneficial and which need to be treated.  They can also consult with your doctor as to which antibiotics are preferable, if necessary, though your M.D. will probably know which to use.  The bacterial stool test is GP3 but I recommend the entire GI-1 which is a complete look at the GI tract... parasites, fungus/yeast, allergy, pH, blood, etc.

I have just received my stool test back from Genova diagnostic and it states:

Lactobacillus species 1+
Escherichia coli 4+
Bifidobacterium 4+

gamma haemolytic Streptococcus NP 4+
alpha haemolytic Streptococcus NP 2+
Bacillus species NP 3+

My nutritionist says I am low on Lactobacillus and this needs to be increased but also I am too high on gamma strep and also on alpha strep and bacillus.
I am going to have a 6 weeks programme to get rid off the bacillus and streps and after that increase my lactobacillus intake.

Do you have any ideas how does the gamma & alpha strep gets into your stool? Is is from food? How dangerous is it? I have been having body chills, body aches for weeks (on and off) and I wonder if these would be symptoms of the streps and bacillus?

Many thanks,

I would be interested in this too.

I have had ongoing problems for months and a second recent stool test has identified as follows:

Bacteroides 4+
Bifidobacterium 2+
Escherichia Coli 4+
Lactobacillius 1+
Enterococcus 1+
Clostridium 4+

My additional bacteria is as follows:

gamma haemolytic Streptococcus NP 1+
alpha haemolytic Streptococcus NP 3+

I have no dysbiotic flora although I did have a mould (Mucor) which I have managed to remove - was not present on my latest stool test.

I have been told that the Strep is not "bad" as such but when there is an imbalance of good to other bacteria, it can cause issues.

I am taking probiotics to increase both my Lacto and Bifidum but nothing to "remove" the strep as, as mentioned, I have been told that this will settle itself as and when there is a correct balance of beneficial to other flora.

Are you attempting to remove the strep? If so how? And what are your symptoms?
Can you share what your NP put you on to combat Alpha Strep?
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