Normal infection are the research tool for the

Normal microbiota can benefit the host by preventing the
overgrowth of harmful microorganisms. 
This phenomenon is called microbial antagonism, or competitive
exclusion. (Gerard, Funke, & Case, 2016) Fecal Transplants
are widely used for treatment for persistent infections.  Humans with a current Clostridium difficile
infection are the research tool for the experiments.  There are changes in the recipient’s biology
due to the attribution of multiple bacterial cells in the donor feces (Bojanova & Bordenstein, 2016).  There are other compositions that the colon can
benefit from fecal transplants.  Some of
those components include colonocytes, archaea, viruses, fungi, protists, and
metabolites.  Pediatric Fecal microbiota
transplantation is also done to manipulate the gut microbiota in children that
have to take long term antibiotics. (Mir, Kellermayer, & Gulati, 2014).  Antibiotics cause diarrhea because they alter
the normal intestinal flora and decreases colonic bacteria resulting in
malabsorption of carbohydrates and osmotic diarrhea. Antibiotics leads to
colonization and toxin production by Clostridium difficile, which may cause
diarrhea and pseudomembranous enterocolitis. 
Fecal transplantation procedure is performed at the same time when an
enema is done.

Clostridium Difficile

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Clostridium difficile, also known as c-diff, is an infective
diarrhea. Clostridium difficile has been around for a while, the first known
case was in 1978. C-diff is a toxin producing bacteria that causes antibiotic
associated colitis. It is one of the leading causes of nosocomial infections in
hospitalized patients. C-diff has increased the morbidity and mortality in
hospitalized patients. The symptoms of C-diff are watery diarrhea possibly with
pus or blood, abdominal pain and cramping, dehydration, loss of appetite,
nausea, and possibly fever. (Khanna, 2012) The risk factors for older adults
are frequent interactions with health care systems and the changes that come
with age such as the gut microbiome. 
There are other therapies that include fidaxomicin, and fecal
bacteriotherapy, which has an excellent outcome.  (Jump, 2013)  Ingestion of infectious organisms are the
cause of diarrhea.  Organisms attack the
intestines in many ways.  Clostridium
difficile impairs the absorption by destroying cells and creating inflammation
of the colon.  A person is influenced by
genetic susceptibility to pathogenic organisms. 
A healthy colon contains short chain of fatty acids and bacteria such as
E. coli that aid in the fermentation and prevent pathogenic bacteria from
growing. (Medical Surgical Nursing, pg. 1007) Stomach acid is the first line of
defense against ingested pathogens and some medications are designed to
decrease stomach acid giving the increase of susceptibility to infection.

Difficile in the Pediatric Population


Antibiotics are not the Only Main Cause1

Some Antibiotics kill the normal
flora and expose the digestive system to infection.  Patients that receive broad-spectrum
antibiotics such as clindamycin, cephalosporins and fluoroquinolones are
susceptible to pathogenic strains of C. difficile because those medications
produce inflammation and destroy cells in the colon. (Medical Surgical Nursing,
1007).  There have been studies done
suggesting other consistent causes for Clostridium Difficile. The causes can be
severe underlying illnesses, non-surgical gastrointestinal procedures,
anti-ulcer medications, nasogastric tube and, duration of hospital stay.  (Bignardi, 1998). 
Antidiarrheal medications are contraindicated in the treatment of
infectious diarrhea because it could stretch the time to the exposure of the

Fecal Transplant

Fecal transplants involve transplanting fecal matter to the
intestines via enema, gastroscope, or nasojejunal tube.  The FDA recently relaxed the restriction on
this procedure.  Before 2012, the FDA was
not supportive of fecal transplants due to the risk of contracting diseases such
as Hepatitis A. Stool transplantation involves taking a stool specimen from a
member of the patient’s household, diluting it in normal saline, and
administering it as an enema. (Lewis, Dirksen, Heitkemper, Bucher, & Camera, 2012).  By introducing healthy bacteria by this procedure,
it re-establishes the colonization of the good bacteria to prevent clostridium
difficile infection.  Fecal
transplantation is also known as fecal bacteriotherapy or intestinal microbiota
transplantation.  The FDA has already
recommended Fecal microbiota transplantation as a form of treatment for
patients with C. Diff after a round of vancomycin regiment.  Fecal microbiota transplantation has shown to
have remarkable therapeutic results with inflammatory bowel diseases, irritable
bowel syndrome, metabolic diseases, neuropsychiatric conditions, autoimmune
diseases, allergic disorder, and chronic fatigue syndrome.  (Brandt, 2012)  There
still ongoing studies with fecal microbiota transplant in a form of a
pill.  The FDA still unsure on regulating
fecal transplants pills due to not agreeing about infectious diseases entering
the body through the first gastrointestinal barrier, so the FDA decided to
label the pill as an experimental drug. 
The FDA is also concerned that patients could contract HIV, hepatitis
and other parasites from fecal matter. (News/AP, 2014).  Dr. Thomas Louie, an infectious disease
specialist from Canada, at the University of Calgary, has developed a triple
layer gel capsule that delivers the microbiota. The triple layer prevents the
breakdown in the stomach.  Dr. Thomas has
been treating his patients with C. Diff successfully.


Fecal Transplant

When conducting Fecal Microbiota Transplant in children, it is
recommended to start by administering or placing a temporary nasal gastric
tube.  (Russell, Kaplan, Ferraro, & Michelow, 2010) FMT has become
popular within pediatric practitioner, patients, and parents. Fecal microbiota transplant
is popular with parents because it helps reduce large amounts of prescribed
medication the children must take due to Clostridium difficile infection or an
inflammatory bowel disease and gives the option to decrease the long use of those
medications.  According the World Journal
Gastroenterology, only 45 pediatric patients have been treated for recurrent Clostridium
difficile infection, and 27 patients with pediatric Inflammatory Bowel Disease.  FMT trials are still in process and currently
recruiting pediatric patients.  (Wang, Popov, & Pai, 2016)

Benefits of Fecal Transplant in the Obese Population

            Obesity is the result of
imbalance between components taken by the body and the lack of energy use.  Obesity is associated with the decrease of
intestinal barrier function and developing gut inflammation and metabolic
endotoxemia that can lead to systemic oxidative stress and chronic low-grade
inflammation.  Mice and humans have a
similar gut metagenome, mice are tested by inducing obesity and use the mice as
a model for human studies.  Commensal
bacteria, the gut epithelial, and lymphoid tissue gives essential and adaptive
immune defenses to pathogens, antigens, and enables fermentation of
carbohydrates.  Obese-prone rats have a
gut microbiota that is different from an obese resistant rat.  The obese rat microbiome has a greater
capacity to harvest energy. One study showed, Fecal transplant conducted on a
lean rat with the obese rat’s feces, increased of body fat percentage in the
lean rat’s body.  Also, fecal transplant
conducted in the obese rat with the lean rat’s feces, showed a decrease in the obese
rat’s body fat percentage. (Kulecka, et al., 2016)

of the gut microbiota is an active contributor for the development of obesity
and insulin resistance.  The regular, long
term consumption of low dose, low calorie sweeteners is known to influence the
microbiota that may predispose susceptible individuals to insulin resistance. (Nettleton, Reimer, & Shearer, 2016) Sucralose, aspartame
and saccharin, are used to reduce energy content in foods and beverages to
encourage weight loss, but has been shown to disrupt the balance and diversity
of gut microbiota. (Nettleton, Reimer, & Shearer, 2016)