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Gut microbiota modulation: Probiotics, antibiotics or fecal microbiota

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Intern Emerg Med (2014) 9:365–373
DOI 10.1007/s11739-014-1069-4
IM - REVIEW
Gut microbiota modulation: probiotics, antibiotics or fecal
microbiota transplantation?
Giovanni Cammarota • Gianluca Ianiro •
Stefano Bibbò • Antonio Gasbarrini
Received: 25 February 2014 / Accepted: 10 March 2014 / Published online: 25 March 2014
Ó SIMI 2014
Abstract Gut microbiota is known to have a relevant role
in our health, and is also related to both gastrointestinal and
extradigestive diseases. Therefore, restoring the alteration
of gut microbiota represents an outstanding clinical target
for the treatment of gut microbiota-related diseases. The
modulation of gut microbiota is perhaps an ancestral, innate
concept for human beings. At this time, the restoration of
gut microbiota impairment is a well-established concept in
mainstream medicine, and several therapeutic approaches
have been developed in this regard. Antibiotics, prebiotics
and probiotics are the best known and commercially
available options to overcome gastrointestinal dysbiosis.
Fecal microbiota transplantation is an old procedure that has
recently become popular again. It has shown a clear effec-
tiveness in the treatment of C. difficile infection, and now
represents a cutting-edge option for the restoration of gut
microbiota. Nevertheless, such weapons should be used
with caution. Antibiotics can indeed harm and alter gut
microbiota composition. Probiotics, instead, are not at all
the same thing, and thinking in terms of different strains is
probably the only way to improve clinical outcomes.
G. Cammarota
G. Ianiro
S. Bibbò
A. Gasbarrini
School of Medicine and Surgery, Catholic University,
Rome, Italy
G. Cammarota
G. Ianiro
S. Bibbò
A. Gasbarrini
Division of Internal Medicine and Gastroenterology,
Department of Medical Sciences, A. Gemelli University
Hospital, Rome, Italy
G. Cammarota (&)
A. Gemelli University Hospital,
Largo A. Gemelli 8, 00168 Rome, Italy
e-mail: gcammarota@rm.unicatt.it
Moreover, fecal microbiota transplantation has shown
promising results, but stronger proofs are needed. Consid-
erable efforts are needed to increase our knowledge in the
field of gut microbiota, especially with regard to the future
use in its modulation for therapeutic purposes.
Keywords Gut microbiota
Gut microbiota modulation

Antibiotics
Probiotics
Fecal microbiota transplantation
Gut microbiota in health and disease
An enormous number of microbes colonize our body, both
inside and out. They number from 10 trillion to 100 trillion
cells, outnumbering human eukaryotic cells at least by
tenfold. Most of them reside in our intestine, forming the
so-called ‘‘human gut microbiota’’ [1]. Gut microbiota and
its whole genome (called microbiome) provides humans
with genetic and metabolic features that they did not
develop by themselves. Gut microbiota and host act,
therefore, in a symbiotic manner, constituting essentially a
complex ‘‘super-organism’’ [2].
Most microbes, especially anaerobes, cannot be cultured
through standard microbiological tools. Such technical
limitations have encumbered our understanding of gut
microbiota. The development of new, culture-independent
techniques for the study of intestinal microbes, such as
high-throughput DNA sequencing and other metagenomics
technologies, has enhanced our knowledge in the field of
gut microbiota [3]. Many initiatives have been established,
and are still ongoing, both in the United States (Human
Microbiome Project) [2] and in Europe (MetaHIT Con-
sortium) [4], which attempt to characterize microbes of our
body and their genomes, and to assess their role in human
health and disease.
123
366
Nevertheless, gut microbiota composition is not yet
completely defined. Bacteria are certainly the most repre-
sented micro-organisms, reaching more than 1 kg of
weight and more than 1,100 species. Bacteroidetes and
Firmicutes usually are the predominant phyla in adult
people, whereas Actinobacteria, or Proteobacteria are less
common [4, 5]. The human microbiota also contains ar-
chaea, viruses (mainly bacteriophage), fungi and other
Eukarya (as Blastocystis and Amoebozoa), [5].
Three main enterotypes, with different metabolic traits,
have been recently identified [6]. They are distinguished by
their relative abundance of one of the following three
genera: Bacteroides (prevalent in enterotype 1); Prevotella
(more represented in enterotype 2); Ruminococcus (more
abundant in enterotype 3). The presence of a specific en-
terotype may depend on a particular long-term dietary
pattern: animal-based diets, rich in fat and protein, support
the development of enterotypes 1 and 3, while a high
carbohydrate diet favors the growth of enterotype 2 [7].
Moreover, short-term dietary modifications have been
proven to alter the human gut microbiota [8]. The rapidity
of our microbiota in switching between different functional
profiles may be an evolutionary trick that humans have
acquired over time.
At birth, the human gut is sterile, and is rapidly colo-
nized by the maternal microbiota; both route of delivery
and type of feeding influencing its composition [9]. Both
environmental and genetic factors [10] contribute to the
development of a ‘‘core native microbiome,’’ which
achieves stability during early life, and is maintained over
time in the absence of major alterations [11].
In health, gut microbiota plays a relevant role within our
body, being involved in many functional processes essen-
tial for our homeostasis, such as the control of several
metabolic pathways, the metabolism of nutrients, and is
also xenobiotic, the production of vitamins and micronu-
trients, the development and maturation of mucosal and
systemic immunity, the regulation of gastrointestinal
motility, and the maintenance of intestinal epithelium
barrier integrity [12].
Qualitative or quantitative impairment of gut microbiota
composition causes the loss of such a homeostasis, leading
to the development of a disease state.
Several illnesses are known to be influenced by the
imbalance of gut microbiota. They include: inflammatory
bowel disease (IBD,) [13], irritable bowel syndrome (IBS,)
and other functional diseases of the gastrointestinal tract
[14], gastroenteric infections [15], colorectal cancer [16],
liver diseases [17, 18], and also non gastrointestinal dis-
eases such as obesity and the metabolic syndrome [19, 20],
autism [21], and allergic diseases [22]. However, just as the
impairment of gut microbiota can lead to a pathological
condition, so its manipulation can restore the prior state of
123
Intern Emerg Med (2014) 9:365–373
homeostasis. Healing the alteration of gut microbiota,
therefore, represents an outstanding clinical target for the
treatment of gut microbiota-related diseases.
Available possibility to modulate gut microbiota
The modulation of gut microbiota is perhaps an ancestral,
innate concept for human individuals. As recently descri-
bed by Leach [23], the Hadzabe people, a hunter-gatherer
tribe of Tanzania, often eat the raw intestines of hunted
preys, and also use the animal’s stomach, full of its
microbial matter, as hand cleanser; such a behavior helps to
increase the diversity of gut microbes among tribe mem-
bers. Since a decreased bacterial diversity has been found
in several diseases, including IBD [24], IBS [25], obesity
and metabolic diseases [26, 27] and asthma [28], such a
custom by the Hadzabe tribe can be considered a primitive
kind of therapeutic modulation of gut microbiota.
Antibiotics
Antibiotics are the cornerstone of the treatment of infec-
tious disease [29]. However, bacterial resistance to antibi-
otics has increased over time, and keeps on rising [30]. The
quintessence of this phenomenon is represented by the
growing difficulty in eradicating H. pylori infection [31]
because of the rise in antibiotic resistance.
The improvement in our knowledge of gut microbiota
reveals that antibiotics behave in a two-edged manner
toward our intestinal microbes [32]; simultaneously, anti-
biotics demolish both pathogenic bacteria and healthy ones.
Moreover, absorbable antibiotics, even if administered for
an extra-intestinal disease, attack the microbial flora any-
way, because of their widespread, systemic diffusion
within our body. Such a phenomenon leads to the impair-
ment of gut microbiota with a consequent increase in
susceptibility to its associated diseases. This pathophysio-
logical mechanism is well recognized as being the trigger
for C. difficile infection [33], but is also involved in the
pathogenesis of other enteric infections [34] or in the
intestinal outgrowth of fungi. [35] Moreover, it appears to
also influence the development of other diseases, such as
obesity [36].
In addition, gut microbiota disruption caused by anti-
biotic therapy may lead to the development of antibiotic
resistance [37]. Antibiotics have indeed been shown to
provoke the enrichment of phage-encoded genes that con-
fer resistance via disparate mechanisms both to the
administered antimicrobial, as well as to other unrelated
antibiotics [38]. Therefore, the relationship between anti-
biotics and gut microbiota is truly complex, and should be
investigated carefully to identify the correct application of
Intern Emerg Med (2014) 9:365–373
antibiotics for gut microbiota-related diseases, and to
improve disease outcomes.
Probiotics and prebiotics
According to the 2001 FAO/WHO definition, probiotics
are ‘‘live micro-organisms, which when administered in
adequate amounts confer a health benefit on the host’’ [39].
The rationale for the use of probiotics for the treatment of
gut microbiota-related disease is the restoration of intesti-
nal homeostasis by beneficial microbes. Most probiotics
consist of Lactobacilli and Bifidobacteria, but also yeasts
such as Saccharomyces boulardii have been used with
good outcomes [40]. Suggested mechanisms of action
include the inhibition of microbial adherence and translo-
cation, the establishment of a restrictive luminal environ-
ment (e.g., through, modification of the luminal pH), the
production of peptides with antibacterial properties (such
as bacteriocins), or the induction of an host immune
response (such as expression of human defensins) [41]. In
clinical practice, probiotics have been used for the treat-
ment of many diseases, even without solid evidence. [42].
Assessing the effectiveness of probiotics in a specific dis-
ease can be difficult, mainly because of the large hetero-
geneity among different studies in terms of administered
strains, dosage, length of treatment, and administration
methods [43].
In addition, considering all probiotics the same thing,
without taking into account strain specificity, impairs an
adequate understanding of their real therapeutic potential.
Several lines of evidence, both in vitro models as well as
in vivo human studies, support the variability in actions
and outcomes among different strains [44, 45]. Further
trials should, therefore, involve probiotics not as such, but
with a strain-specific approach [46].
Prebiotics were defined for the first time in 1995 by
Gibson and Roberfroid [47] as ‘‘non-digestible food
ingredients that beneficially affect the host by selectively
stimulating the growth or activity of one of a limited
number of bacterial species already present in the colon,
thus improving host health.’’ To include other fields that
may profit by prebiotic action [48], this definition has been
renewed by Roberfroid in 2007: ‘‘A prebiotic is a selec-
tively fermented ingredient that allows specific changes,
both in the composition or activity in the gastrointestinal
microflora that confer benefits upon host well-being and
health’’ [49, 50]. To be classified as a prebiotic, a food
ingredient needs to fulfill the following criteria: resistance
to gastric acid secretion and to hydrolysis by digestive
enzymes; absorption in the upper gastrointestinal tract and
fermentation by the intestinal gut microbiota; and stimu-
lation of the growth or activity of beneficial microbes. At
present, only inulin and trans-galacto-oligosaccharides
367
completely meet such a definition [48]. Two bacterial
genera, respectively, Lactobacilli and Bifidobacteria, are
the main target of prebiotics [50], even if other strains have
also been proven to benefit of prebiotic properties [51].
Proposed mechanisms of the action of prebiotics include
an increase in the production of short-chain fatty acids
(SCFA) or a decrease of intestinal pH [52]. To date, defi-
nite evidence of the effectiveness of prebiotics for the
treatment of gut microbiota-related diseases is lacking, and
adequate trials have not yet been performed.
Fecal microbiota transplantation (FMT)
FMT, also known as ‘‘fecal infusion’’ or ‘‘fecal bacterio-
therapy’’, refers to the introduction of a liquid filtrate of
stools from a healthy donor into the gastrointestinal tract of
a patient for the treatment of specific diseases. The
administration of feces for therapeutic purposes was first
described more than 1,500 years ago by Ge Hong [53].
Afterward, in the sixteenth century, Li Shizhen treated
several gastrointestinal symptoms, such as diarrhea, con-
stipation, vomiting or pain, by fecal products. The trans-
plantation of enteric bacteria (later called transfaunation)
was applied also in veterinary science, for the cure of
animals unable to ruminate, as described by the Italian
anatomist Fabricius Acquapendente in the seventeenth
century [54]. The consumption of camel stools has been
described both by German soldiers during World War II, as
well as by Bedouins as a treatment for dysentery [55].
FMT came to the attention of mainstream medical sci-
ence only in the late 50’s: in 1958, Eiseman, a surgeon
from Colorado, successfully treated four patients with
pseudomembranous colitis using fecal enemas [56]. The
efficacy of FMT against C. difficile infection was later also
confirmed. Early attempts, however, even if almost always
successful, were described in occasional case series and
anecdotally carried out in a totally empirical way.
Both the rising epidemic of C. difficile infection and the
growing scientific interest toward the gut microbiota have
recently led to the renewal of FMT. Recently, a profound
change in the epidemiology of C. difficile infection has
occurred, with a rise in its frequency, severity, and mor-
tality [57]. Both the refractoriness of the infection to
standard therapy as well as its probability of recurrence
have also increased [58], representing an important clinical
issue. Positive results shown by FMT in the eradication of
recurrent C. difficile infections have encouraged the use of
this procedure worldwide, especially in Western Countries.
Well-designed studies, both large case series [59] and
randomized controlled trials [60], have been conducted to
assess its effectiveness.
In addition, the recent advancement in our understand-
ing of gut microbiota has given a solid pathophysiological
123
368
background to FMT. Accounting our microbial flora as a
bodily organ [61] let the interpretation of FMT change
from being considered a mere injection of feces to
becoming a true organ transplantation. Such a conceptual
transition has led FMT to being used in the treatment of
several diseases associated with the disruption of gut
microbiota, such as inflammatory bowel disease (IBD) [62]
and the metabolic syndrome [63].
FMT may be more effective than probiotics in the res-
toration of altered gut microbiota, since a fecal infusion
overcomes the intrinsic quantitative gap of probiotics (oral
probiotic doses are usually more than three orders of
magnitude lower than the 100 trillion native micro-organ-
isms of the large bowel). In addition, the administration of
fecal flora establishes a durable alteration of the recipient’s
gut microbiota [64], while probiotics are able to colonize
the gut lumen only for a temporary period [65].
FMT can be performed through various routes: naso-
gastric or nasojejunal tube, upper endoscopy, retention
enema, as well as colonoscopy [66]. In early usage,
retention enemas were the preferred mode of delivery [67].
In a recent systematic review of studies using FMT for the
treatment of recurrente C. difficile infection, Cammarota
et al. [68] report that the lower gastrointestinal route
(colonoscopy, enema) leads to the achievement of higher
eradication rates than upper delivery (gastroscopy, naso-
gastric or nasojejunal tube) (81–86 versus 84–93 %,
respectively).
In theory, among different lower gastrointestinal routes,
colonoscopy appears to be a more reliable route than
retention enemata for the treatment of C. difficile infection,
since it can reach the whole colon (while enemas only
ascend to the left colon), and colonoscopy can also assess
the features of the disease: such as its extent and severity
[69, 70].
Nevertheless, low invasiveness and costs of the retention
enema approach and its proven efficacy even when self-
administered, [71] make it extremely competitive for a
routine use.
Probably the optimal route of administration does not
exist absolutely, and any of the therapeutic routes should
be chosen depending on the features and the location of the
disease, as shown by the successful results obtained in the
treatment of metabolic diseases by duodenal administration
of feces [62].
Further discoveries of the therapeutic chances of FMT,
and its systematic application to several gut microbiota-
associated diseases will make the specific administration
route an important issue. The growth of many beneficial
bacteria is indeed influenced by their specific transfer
through the gastrointestinal tract. Many spore-forming
Firmicutes require transit through the upper gastrointestinal
tract to work effectively. Bacteroidetes can be injured by
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Intern Emerg Med (2014) 9:365–373
gastric acid secretion, and a lower route may be preferable
[72, 73]. A combined approach of delivery has not yet been
attempted [74], and may perhaps become an option in the
future.
Donor selection is certainly easier for FMT than for
other organ transplants, since there is no need of immu-
nological matching of donor and recipient. Nevertheless,
an accurate evaluation is necessary to avoid disease
transmission to the recipient, and unfortunately, the trans-
fer of unknown pathogens is not completely avoidable [75].
Usually, to overcome the repulsion of the patient toward
receiving an infusion of feces (the so-called yuck factor,)
donors are usually friends or family members, both related
and unrelated. The administration of feces derived from
related donors appears to achieve slightly higher resolution
rates than stools from unrelated ones (respectively, 93
versus 84 % resolution rates) for the treatment of C. diffi-
cile infection, as observed through systematic review by
Gough et al.. Donor gender, instead, does not influence
eradication rates [76].
Initially, the medical history of potential donors is col-
lected, usually by clinical questionnaire. The following
clinical characteristics have been proposed: [67] as abso-
lute contraindications to the donation of feces for the
treatment of C. difficile infection: known human immu-
nodeficiency virus (HIV), hepatitis B or C infections;
known exposure to HIV or viral hepatitis (within the pre-
vious 12 months); high-risk sexual behaviors; use of illicit
drugs; tattoos or body piercing performed within 6 months;
incarceration or history of incarceration; known current
communicable disease (e.g., upper respiratory tract infec-
tion); risk factors for variant Creutzfeldt–Jakob disease;
travel (within the last 6 months) to areas of the world
where diarrheal illnesses are endemic or with high risk of
traveler’s diarrhea; history of IBD, IBS and other func-
tional diseases; history of gastrointestinal malignancy or
known polyposis; use of antibiotics within the preceding
3 months, immunosuppressant, chemotherapeutic drugs;
and recent consumption of a potential allergen for the
recipient. The following features are deemed as relative
contraindications: history of major gastrointestinal surgery;
the metabolic syndrome, autoimmune diseases, atopic
diseases, and chronic pain syndromes [67].
After completion of the questionnaire, potential donors
undergo serum and stool testing. Donor serum testing
includes screening for HIV, Hepatitis A Virus, Hepatitis B
Virus, Hepatitis C Virus and syphilis, while donor stool
testing consists of stool culture for common enteric
pathogens, C. difficile toxin, Giardia antigens, Cryptospo-
ridium antigens, Helicobacter pylori antigens, helminths,
ova and parasites.
This protocol has been applied with success for donor
selection in the management of C. difficile infection by
Intern Emerg Med (2014) 9:365–373 369

Table 1 Fully published reports on FMT treatment

First author Year Indication Study design No. of patients

Eiseman 1958 Pseudomembranous colitis Case series 4

Cutolo 1959 Pseudomembranous colitis Case report 1
Collins 1960 Pseudomembranous colitis Case series 4
Fenton 1974 Pseudomembranous colitis Case report 1
Bowden 1981 Pseudomembranous colitis Case series 16
Schwan 1984 C. difficile infection Case report 1
Tvede 1989 C. difficile infection Case series 6
Bennet 1989 IBD Case report 1
Borody 1989 IBS and IBD Case series 55
Flotterod 1991 C. difficile infection Case report 1
Andrews 1992 Chronic constipation Case report 1
Paterson 1994 C. difficile infection Case series 7
Harkonen 1996 Pseudomembranous colitis Case report 1
Lund- Tønnesen 1998 C. difficile infection Case series 18
Gustafsson 1998 C. difficile infection Case series 9
Persky 2000 C. difficile infection Case report 1
Aas 2003 C. difficile infectiona Case series 18
Borody 2003 IBD Case series 6
Jorup-Ronstrom 2006 C. difficile infection Case series 5
Nieuwdrop 2008 C. difficile infection Case series 7
You 2008 C. difficile infection Case report 1
Hellermans 2009 C. difficile infection Case report 1
MacConnachie 2009 C. difficile infection Case series 15
Garborg 2010 C. difficile infection Case series 40
Grehan 2010 C. difficile infectiona Open-label trial 10
Khoruts 2010 C. difficile infection Case report 1
Rohlke 2010 C. difficile infection Case series 19
Russell 2010 C. difficile infection Case report 1
Silverman 2010 C. difficile infection Case series 7
Yoon 2010 C. difficile infection Case series 12
Kelly 2011 C. difficile infection Case series 26
Polak 2011 C. difficile infection Case series 15
Brandt 2012 C. difficile infection Multicenter long-term follow-up study 77
Hamilton 2012 C. difficile infection Open-label trial 43
Jorup-Ronstrom 2012 C. difficile infection Case series 32
Kahn 2012 C. difficile infection Case report 1
Mattila 2012 C. difficile infection Case series 70
Nagy 2012 C. difficile infection Case report 1
Neeman 2012 C. difficile infection Case report 1
Rubin 2012 C. difficile infection Case series 74
Trubiano 2012 C. difficile infection Case report 1
Vrieze 2012 Metabolic syndrome Randomized controlled trial 18
Zainah 2012 C. difficile infectiona Case report 1
Angelberger 2013 IBD Open-label trial 5
Broecker 2013 C. difficile infection Case report 1
De Leon 2013 C. difficile infectiona Case report 1
Emanuelsson 2013 C. difficile infection Case series 31
Kleger 2013 C. difficile infection Case report 1

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370 Intern Emerg Med (2014) 9:365–373

Table 1 continued
First author Year Indication Study design No. of patients

Kump 2013 IBD Open-label trial 6

Kunde 2013 IBD Open-label trial 10
Gutman 2013 C. difficile infection Case series 2
Lofland 2013 C. difficile infection Case report 1
Quera 2013 C. difficile infectiona Case report 1
Schwartz 2013 C. difficile infection Case series 2
Song 2013 C. difficile infection Open-label trial 14
van Nood 2013 C. difficile infection Randomized controlled trial 42
Weingarden 2013 C. difficile infection Open-label trial 16
Weingarden 2013 C. difficile infection Case series 4
Zhang 2013 IBD Case report 1
IBD inflammatory bowel disease, IBS irritable bowel syndrome
a
Including also patients with IBD and C. difficile superinfection

FMT [77]. However, such an approach seems to be inad-
equate when dealing with other gut microbiota-related
diseases, such as IBD, where the composition of the
donor’s gut microbiota may influence clinical outcomes
[74]. New tools for the investigation of gut microbiota
composition, such as metagenomics and target gene
sequencing will probably aid in our understanding in this
field, and their application for the selection of donors is an
interesting future prospect.
After donation, stools are processed for being infused.
Most data about the stool preparation protocol comes from
studies applying FMT for the treatment of recurrent C. dif-
ficile infection, as reviewed by Gough and colleagues [76].
Even if there is no standardization about the required amount
of feces, using less than 50 g has been correlated with
C. difficile relapse rates [76]. Feces are then suspended in a
diluent, generally saline or water; the use of water appears to
get higher eradication rates than saline (98.5 versus 86 %),
but also higher relapse rates. Other diluents, including milk
or yoghurt, achieve resolution rates of 94 %. The suspension
is then passed through gauzes or sieve, to eliminate gross
materials. The filtrate volume is largely heterogeneous
among studies, ranging between 200 ml or less and 500 ml
or more. The use of larger volumes ([500 ml) is positively
associated (although in a nonsignificant manner) with higher
resolution rates [76].
In most cases, the transplantation is performed within
6–8 h after the donation [78, 79]. Frozen stools have,
however, shown a comparable efficacy to fresh ones for the
treatment of recurrent C. difficile infection [80]. Usually,
patients undergo a bowel preparation the day before the
infusion. Many physicians advocate using a PPI if the
upper route is chosen [74].
In trials dealing with C. difficile infection, a single
infusion of feces has usually been administered, with
excellent results [68]. Nevertheless, the future application
of FMT to chronic diseases (such as IBD, IBS, obesity)
may perhaps require several infusions to achieve success.
FMT is a theoretically promising option for several
diseases, differing from each other by pathophysiology and
clinical features. Probably, a unique protocol of stool
preparation is, therefore, an outdated idea, and in the future
every clinical indication will correspond to a different
protocol. An up-to-date overview of fully published reports
on FMT treatment for both gastrointestinal and extra-
intestinal diseases is described in Table 1.
Conclusions
The role of gut microbiota in health and disease was first
hypothesized in 1907 by Metchnikoff and Mitchell [81].
More than one century after, our knowledge of gut mic-
robiota has enormously grown, and our consideration of
gut microbiota has changed from an amalgam of microbes
to another organ of our body, forming a ‘‘super-organism’’
with us. Moreover, we have discovered a deep relationship
between gut microbiota and both gastrointestinal and ex-
tradigestive diseases. New technologies such as metage-
nomics have increased our understanding of gut microbiota
composition in health and disease.
Such gain in knowledge can potentially change our
therapeutic perspectives: gut modulation can become a
therapeutic option. Some tools, such as antibiotics or pro-
biotics, are well known, and other, such as FMT, represent
an intriguing, cutting-edge weapon. However, in the recent
past scientific community learned that ‘‘all that glitters is
no gold.’’ Antibiotics can indeed harm and alter gut mic-
robiota composition. Probiotics, instead, are not all the
same, and thinking in terms of different strains is probably

123
Intern Emerg Med (2014) 9:365–373
the only way to improve clinical outcomes. Finally, FMT,
although promising, is not yet a standardized procedure.
Considerable efforts are needed to increase our knowledge
in the field of gut microbiota, especially in regard to future
modulations for therapeutic purposes.
Conflict of interest None.
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