STOOL PATHOGENS:

INTERPRETATION & TREATMENT

Dysbiosis: A state of disordered microbial ecology, where harmful microbes have had been
allowed to overgrow, together with reduced beneficial flora. (Damaging effect of pathogens on the
host depends primarily on the virulence factor of the microorganism and immune defenses.)

Consequences of dysbiosis:
Depletion of vitamin b12 & some amino acids, in addition, iron and other essential nutrient
deficiencies.
Short circuit digestive enzymes.
Convert essential fatty acids into damaging fats.
Increase the potential of GI infection.
Encourage GI inflammatory diseases.
Interfere with the breakdown of bile acids and estrogen creating a fertile environment for
cancer. (LCA & DCA)
Reduced beneficial flora is associated with many digestive, metabolic and immune disorders.

Causes of dysbiosis:
Poor diet (western diet) reduced immunity
Chronic stresses poor digestion
Antibiotic usage inflammation
infection exposure to toxins

Harmful effects of poor food choices on the gut ecology:

 Unhealthy fats, poisoned meats (spiked with hormones & antibiotics), low fiber diet 
putrefactive Dysbiosis.
(Overgrowth of bacteroides  toxic by product ammonia  too alkaline gut ecology 
decreased production of n-butyrates.  less gut fuel, nutrition deficiencies, increased
secondary bile acids & estrogen formation  high-risk breast & colorectal cancer, GIT and
systemic diseases  vicious cycle of self-perpetuating.

IMMUNITY IS THE FIRST LINE OF DEFENCE AGAINST DYSBIOSIS AND PLAYS

A MAJOR ROLE IN REGULATING GUT ECOLOGY.
Diagnosis of Dysbiosis:
1- Careful patient history.
2- Comprehensive diagnostic stool analysis.
3- Organic acid comprehensive profile.
4- Testing for yeast, bacteria &/or parasites.

 GIT infection can be clinical or subclinical with GI symptoms or general vague symptoms.

I. Parasitic pathogens:
Parasitic infections are common and the incidence of infection is greatly increasing.
 Common parasitic infection include:
o Cryptosporidium parvum, B.hominis, Giardia lamblia, Ascaris, E.histolytica & D.fragilis.
Risk factors:

o Foreign country travelling.

o Poor hygiene.
o Salad bars and dining out a lot.
o Past infection
o Household partner with a parasitic infection.
o Food poisoning.
o Lowered immune defences
o Drinking tap water
Damaging effect:
o Can wreak havoc in GIT, liver and many other organs.
o Emit toxic byproducts that is the most destructive and disruptive to the digestive
activity.
Parasitic detection:
o They have intricate life cycle and mostly shed at irregular intervals.
(Parasite maybe active for one or two days then is not typically active or detectable &
may migrate to the liver  undetectable in feces.)
o Therefore two or three samples every other day with a minimum of 48 hours apart.
o It is necessary to have one of the samples done as purge inducing diarrheal episode.
o WBCs (eosinophils >3 & monocytes >7)
o Antibody testing IgG & IgM.
o Serum culture.
o IgM: it is elevated in early stages of infection, the parasite may dominate the GIT or the
immune system eradicate the pathogen. (retest after 2-3 months)
o IgG: chronic or past infection (check symptoms)
o sIgA:
 If the patient travelled to an area where the disease is endemic  recent
infection.
 If the patient is native to an area where the parasite is endemic  possible past
infection
o Sequence of events: first event  production of sIgA in saliva against parasite
 Second event occurs only in cases of impaired epithelial tissue integrity 
production of IgM, IgG, and IgG in the blood against the parasite.
 Initially all these antibodies develop against the parasitic antigen, but due to
colonic epithelial cell damage caused by proteases produced by the parasites,
lectin like receptors or due to molecular mimicry  AUTOIMMUNITY.
 Simultaneous testing for IgA, IgM and IgG in blood & sIgA in saliva against both
parasitic and target tissue antigens. (to distinguish between pathogenic vs
protective antibodies)
 Impaired immunity  reduced levels of sIgA, therefore, giving false negative.
(Highly recommended to test for total sIgA to parasitic antigens)

II. Bacteria:
 Antibody testing.
  Comprehensive Organic acid profile.
 Comprehensive diagnostic stool analysis.

III. Candida/fungal pathogens:

- Often accompany parasitic infections (The energy drain on the system by the parasite tends
to provide an opportunity for the candida + parasites feed on normal flora)
- Researches have shown definite relationship between the higher level of fungal spores &
decreased levels of desirable bacteria competition for the adhesion receptors and nutrition
- Can cause wide range of symptoms both GIT and systemic signs and symptoms (invasive
candida)
- Can migrate to other tissues (Mercury and pH alterations aids in candida migration)
affecting any organ particularly to the reproductive system in females.
- Low candida levels  no treatment (unless a parasite is present as E.histolytica  rapid
worsening and fungal overgrowth)
- Considered a factor in ADD & Autism, by formation of abnormal neurotoxic organic acid.
- TESTING:
 D-Arabinotol (DA): a metabolite of most pathogenic candida species including:
C.albicans, C.trpicalis, C.parapsilosis, C.pseudotropicalis, C.kefyr, C.Lusitaniae &
C.Guillier mondii.
(Positive DA results have had been obtained several days to weeks before +ve
candida blood cultures) normalize with treatment.
Possible to assess whether the patient has invasive candidiasis
o Serum:
 1.0 – 5.0 umol/L no evidence of invasive candida.
 5.1 – 9.0 umol/L  candida problem by not invasive.
 >9.0 umol/L  presumptive evidence of invasive candida.
o Saliva:
 3.0 – 9.0 umol/L  no evidence of invasive candida.
 9.0 – 15.0 umol/L  candida problem by not invasive.
 >15.0 umol/L  presumptive evidence of invasive candida.
 Anti-candida antibody testing:
 Candida immune complexes contain IgG candida antibodies, candida antigen
& fragments of complements.
 IgA  local mucosal infection.
 IgM & IgG  increased levels in chronic candidiasis.

Polymerase chain reaction:

 PCR has led to the development of DNA & RNA based technologies, enabling the
detection of single genome of an infection in any body fluid with improved accuracy.
 Advantages:
Ability to detect non-viable organisms that are not retrievable by culture
based methods.
Ability to detect & identity organisms that cannot or very difficult to be
cultured.
More rapid detection of organisms that grow slowly (capable of copying a
single DNA sequence of a viable or non-viable cell over a billion times
within 3-5 hours)
 Ability to detect previously unknown organisms directly in specimen by
using broad range primers.
Ability to quantify infectious organism burden in patient specimens for
better clinical responsiveness.

Functional treatment:
- Lab testing: prescriptive & natural agents based on microbial sensitivity profiling, which is
designed to target specific organism.
- Preparing for treatment: enhanced nutrition and strengthening of weakened system.
- Treatment:
 Eradicate pathogens
 Die off: killing pathogens at a pace quicker than the eliminative organ.
 Avoiding reinfection: treating partners or household members.
 Avoiding overgrowth: enhance growth of beneficial bacteria and immune function.