UTI - Urinary Tract Infection
Pathogenic / virilent strains of certain bacteria cause Urinary Tract Infections (UTIs)
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)
A UTI occurs when E. Coli "families" take up residence in the
urinary tract wall
~80-90% of UTIs are caused by the bacterium
E. Coli
E. Coli E. Coli does not belong in the urinary tract.
To colonize and cause
an infection, E. Coli
(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).
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
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 environmentAfter 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 waterNeeds just a little
moisture. Air provides enoughFeeds 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
mirabili s (grows more slowly than
E. Coli
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 Chlamydia and Mycoplasma may
be sexually transmitted 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.
