Pathogenic / virilent strains of certain bacteria cause UTIs

A UTI is usually caused by an over-proliferation of certain bacteria within the urinary tract

-   These bacteria should not be in the urinary tract in large numbers.   These misplaced bacteria damage and inflame the mucus membranes and walls of the urinary tract, resulting in typical UTI symptoms.

-   Pathogenic bacteria typically enter the bladder via the urethra.   However, infection may also occur via the blood or lymph. it is well established that colonization of the vaginal mucosa with bacteria from the GI tract precedes the presence of bacteria in womens' urine.

-  Most recurrent UTIs are caused by reintroduction of bacteria from faeces. (Schaeffer, 1979)  

~80-90% of UTIs are caused by the bacterium E. Coli

E. Coli normally lives in the colon, where it enjoys a symbiotic relationship with us, helping to break down our waste.   E. Coli does not belong in the urinary tract.

A UTI occurs when E. Coli "families" take up residence in the urinary tract wall

To colonize and cause an infection, E. Coli have little “velcro-like” projections that adhere to the bladder (or other UT) wall linings to prevent their removal.    Hair-like projections (called pili) on the cell surface of E. Coli bacteria contain glue-like lectin glycoprotein molecules, that adhere to uroepithelial cells lining the bladder or urinary tract walls to  form multicellular communities, called a biofilm.  Once the E. Coli is adhered, it is protected from being flushed out by urine. How they adhere is not definitely known, but Ofek et al suggests thats sugar residues on the surface of uroepithelial cells may serve as receptors for the binding of some E. coli strains  (Ofek, 1978). 

 D-mannose supplementation can release their hold

In vitro tests using uroepithelial cells from premenopausal women with no UTI history showed that adherence is maximal at pH 4 to 5 and at bacterial-to-epithelial-cell ratios of 5,000 or more, suggesting that there are a limited number of receptors on the epithelial cell surface; adherence tended to be higher during the early (estrogen-dependent) phase of the menstrual cycle and diminished shortly after the time of expected ovulation; the same E. coli strain which adhered avidly to uroepithelial cells from some individuals barely adhered to cells from other women;  (Schaeffer, 1979)

Getting to know E. Coli

This E. Coli is not the same as its mutant species associated with unsanitary food processing.   The mutant species has hospitalized and killed people.

E. Coli thrives in an acid environment

•   E. Coli even thrives in acidic urine conditions with a pH as low as 2.    It is capable of synthesizing its nutritional requirements from the surrounding acids in its environment

•  After arrival, the typical E. Coli activity cycle in your urine is that you increase urine acidity:

(1) By becoming dehydrated

or

(2) By drinking/eating acid-containing or acid-forming foods or drinks that have a predominantly acid effect (E.g, cranberry juice, soda, lots of sugar).

•   E. Coli  (and other gram-negative bacteria) have a burst of growth until they use up all the acid.   At that point their alkaline waste and endotoxins, which they are living in, drastically slows their multiplication rates and they become semi-dormant

Acid/Alkaline Balance

•   Less acidity after menopause reduces infection risk.   Lactobacilli (beneficial organisms) increase the acidic environment in the female urinary tract. Reductions in their number (E.g. occurs with estrogen loss after menopause) increase pH and therefore the risk of infection

E. Coli is a hardy critter and is hard to kill.  Here are some of its virulence factors:

•  Multiplies fast.   Can double its colony in 20 minutes

•  Not fussy about where it lives.   Thrives on medical equipment, catheters, hands, mouth, nose, any mucous membrane, in hair, bladder, on a towel, door handles, toilet seats, in tap water

•  Needs just a little moisture.   Air provides enough

•   Feeds on almost anything.   Can synthesize its own amino acids, purines and pyrimidines using the nitrogen donor molecule, glutamine (Berks, 2002)

•  Can grow aerobically and anaerobically

•   Lives in human temperatures (a mesophile).  Optimum growth occurs at 25 - 40 °C, but can also survive freezing and boiling temperature (Abigail F. Weliver, Heat as a Microbial Agent)

•  Can quickly mutate to resist antibiotics.   Can actually live on soap!

•  Can produce a capsule (outer protective layer) to resist phagocytosis (engulfment) by immune system

•  Produces Type II toxins that damage host cell membranes

•  Produces cell wall components that trigger damaging inflammatory response - E.g. Lipopolysaccharides (LPS), also called endotoxins

The other 10-20% of UTIs are mainly caused by:

•   Staphylococcus.   S. saprophyticus accounts for ~5-10% of UTIs, mostly in younger women;

•   Klebsiella (gram-negative, another acid-lover), Enterococci, and Proteus mirabilis (grows more slowly than E. Coli in acid pH; produces uric acid (urea) as waste product; this bacteria WOULD be slowed down by increasing urine acidity with such as cranberry juice).   Generally, cause UTI's in older women;

•  MORE RARELY.   Chlamydia trachomatis (obligate, intracellular bacteria i.e.only reproduces inside human cells), Mycoplasma hominis (bacteria lacks cell wall, therefore unaffected by common antibiotics), Neisseria gonorrheae  (may cause UTIs in both men and women, but these infections tend to remain limited to the urethra and reproductive system). Since Chlamydia and Mycoplasma may be sexually transmitted, infections require treatment of both partners. These bacteria cannot be treated with d-mannose.

References

ANTHONY J. SCHAEFFER,* SUSAN K. AMUNDSEN, AND LAWRENCE N. SCHMIDT (Jun 1979) Adherence of Escherichia coli to Human Urinary Tract Epithelial Cells, INFECTION AND IMMUNITY: pgs 753-759 PDF

Ofek, I., E. H. Beachey, and N. Sharon. (1978) Surface sugars of animal cells as determinants of recognition in bacterial adherence. Trends Biochem. Sci. 3:159-160.

Ofek, I., D. Mirelman, and N. Sharon. (1977) Adherence of Escherichia coli to human mucosal cells mediated by mannose receptors. Nature (London) 265:623-625.

Wellens A, Garofalo C, Nguyen H, Van Gerven N, Slättegård R, Hernalsteens JP, Wyns L, Oscarson S, De Greve H, Hultgren S, Bouckaert J. (Apr 30, 2008) Intervening with urinary tract infections using anti-adhesives based on the crystal structure of the FimH-oligomannose-3 complex. PLoS One. 3(6): e2040.