Introduction to particular
bacteriology
Classification
Katalin Kristóf MD PhD
Introduction to bacteria and bacterial
diseases
Bacteria, the oldest form of life on earth, are remarkably
diverse and exist in astounding numbers
Diseases caused by bacteria include some of the most
common infections in the world, as well as some of the
most important human scourges, past, present, and
probably future
At the same time, each of us is colonized by more
bacterial cells than we have human cells in our bodies
Generally, this is a peaceful
and even productive
(symbiotic) relationship, but
occasionally even these welltolerated residents of the
human biosphere cause
disease
Human Microbiome Project study
Annu Rev Genomics Hum Gene 2012
Bacterial Taxonomy
Includes three components:
1. Classification : orderly arrangement
2.
Identification of an unknown unit
3.
Nomenclature : naming the units
Classification of bacteria
Bacteria have been classified according to phenotype, including size,
shape, staining properties, and biochemical properties, since the
beginning of microbiology
In recent years, classification has been dominated by genotype,
especially relaying on conserved molecules, such as 16S ribosomal
RNA
Although there is a considerable degree of overlap between phenotype
and genotype, as would be expected, dichotomies occur
In the future, taxonomy, understanding of pathogenesis, and
diagnostics will be increasingly based on genotype.
As bacteriology advances in its differentiation of genera and species, as
subspecies diversity is increasingly appreciated, as variation within
individual host is better understood, and as the evaluation of pathogens
is better outlined, a grounding in evolutionary biology and ecology also
will be more critical
Hierarchy
Evolutionary
relationships
Species are groups
that interbreed (have
productive sex)
How this goes
Species
Genus
Family
Order
Class
Division
Phylum
Kingdom (1969)
Domain (80’s)
The Three-Domain System
Domains are above the kingdom level.
proposed by Carl Woese based on rRNA studies of prokaryotes
domain model more clearly shows prokaryotic diversity
The Three-Domain System
Have no cell nucleus or any
other membrane organelles
within their cells.
Hot springs, home of
thermophiles
6 Kingdom System
ARCHAEBACTERIA
EUBACTERIA
PROTISTA
FUNGI
PLANTAE
ANIMALIA
Classification is always a work in progress.
The tree of life shows our most current understanding.
New discoveries can lead to changes in classification.
Until 1866: only two kingdoms,
Plantae
Animalia and Plantae
Animalia
Classification is always a work in progress.
The tree of life shows our most current understanding.
New discoveries can lead to changes in classification.
Until 1866: only two kingdoms,
Plantae
Animalia and Plantae
Animalia
– 1866: all single-celled
organisms moved to
kingdom Protista
Protista
Classification is always a work in progress.
The tree of life shows our most current understanding.
New discoveries can lead to changes in classification.
Until 1866: only two kingdoms,
Plantae
Animalia and Plantae
Animalia
– 1866: all single-celled
organisms moved to
kingdom Protista
Protista
– 1938: prokaryotes moved
to kingdom Monera
Monera
Classification is always a work in progress.
The tree of life shows our most current understanding.
New discoveries can lead to changes in classification.
Until 1866: only two kingdoms,
Plantae
Animalia and Plantae
Animalia
– 1866: all single-celled
organisms moved to
kingdom Protista
Protista
– 1938: prokaryotes moved
to kingdom Monera
– 1959: fungi moved to
own kingdom
Monera
Fungi
Classification is always a work in progress.
The tree of life shows our most current understanding.
New discoveries can lead to changes in classification.
Until 1866: only two kingdoms,
Animalia and Plantae
Plantae
Animalia
– 1866: all single-celled
organisms moved to
kingdom Protista
Protista
– 1938: prokaryotes moved
to kingdom Monera
Archea
– 1959: fungi moved to
own kingdom
Fungi
Bacteria
– 1977: kingdom Monera
split into kingdoms Bacteria and Archaea
The History and Evolution of Bergey’s
Manual
1. Bergey’s Manual of Determinative Bacteriology (1923-1994)
9 Editions (1 volume each )-These are mainly phonetic
2. Bergey’s Manual of Systematic Bacteriology:
1s t edition (4volumes);1984-1989; Mix Phylogenetic/Phenetic5 Kingdoms
2nd Edition (5 volumes) (2001-2012);Phylogenetic-3 Domains
Bergey’s Manual of Systematic Bacteriology
First edition -Published in 4 volumes:
Volume 1 (1984) -Gram-negative Bacteria of general, medical, or industrial
importance
Volume 2 (1986) -Gram-positive Bacteria other than Actinomycetes
Volume 3 (1989) -Archaeobacteria, Cyanobacteria, and remaining Gramnegative Bacteria
Volume 4 (1989) -Actinomycetes
Second Edition-published in 5 volumes:
Volume 1-(2001) The Archaea and the deeply branching and phototrophic
Bacteria
Volume 2-(2005)-The Proteobacteria
Volume 3-(2009)- The Firmicutes
Volume 4-(2011)- The Bacteroidetes, Spirochaetes, Tenericutes (Mollicutes),
Acidobacteria, Fibrobacteres, Fusobacteria, Dictyoglomi, Gemmatimonadetes,
Lentisphaerae, Verrucomicrobia, Chlamydiae, and Planctomycetes
Volume 5-(2012)- The Actinobacteria
Bergey’s Overview Volume 2
18
Linnaeus’s System - Nomenclature
Binomial nomenclature is a two-part scientific naming
system.
– uses Latin words
– scientific names always written in italics (or underlined)
– two parts are the genus name and species descriptor
– The genus always begins with a capital letter and the
species is always lower case
Escherichia coli
Escherichia coli
Scientific Names
Scientific
Binomial
Source of Genus
Name
Source of
Specific Epithet
Klebsiella
pneumoniae
Pfiesteria
piscicida
Salmonella
typhimurium
Streptococcus
pyogenes
Penicillium
chrysogenum
Honors Edwin Klebs
The disease
Honors Lois Pfiester
Disease in fish
Honors Daniel Salmon
Stupor (typh-) in
mice (muri-)
Forms pus (pyo-)
Trypanosoma
cruzi
Corkscrew-like (trypano-, Honors Oswaldo
borer; soma-, body)
Cruz
Chains of cells (strepto-)
Tuftlike (penicill-)
Produces a yellow
(chryso-) pigment
Casual / common name – for local use, varies from country to
country e.g. “typhoid bacillus” – Salmonella typhi (scientific name)
Species Definition
Eukaryotic species:
A group of closely related organisms that breed among
themselves
Prokaryotic species:
A population of cells with similar characteristics
Clone: Population of cells derived from a single cell
Strain: Genetically different cells within a clone
Culture: grown in the lab
Viral species:
Population of viruses with similar characteristics that
occupies a particular ecological niche
Family – Genus - Species
Taxonomy
Kingdom: Bacteria;
Phylum: Firmicutes;
Class:
Bacilli;
Order:
Bacillales;
- Family: Acyclobacillaceae (genus: Acyclobacillus);
- Family: Bacillaceae (genus: Bacillus, Geobacillus);
- species: Bacillus anthracis
- Family: Paenibacillaceae (genus: Paenibacillus,
Brevibacillus);
- Family: Planococcaceae (genus: Sporosarcina).
Irregular, non-spore-forming Gram-positive
rods
Corynebacterium diphteriae
Other corynebacterium spp.
Listeria monocytogenes
Erysipelothrix rhusiopathiae
Lactobacillus spp.
Corynebacterium diphteriae - diphteria
Diphteria is an acut, (exo)toxin-mediated disease
caused by the bacterium Corynebacterium
diphteriae
Name: greek diphteria (leather hide)
C. diphteriae
aerobic, gram-positive, non-spore forming bacillus
related phylogenetically to mycobacteria and
actinomycetes (micolic acid)
History
Hippocrates provided the first clinical description of diphtheria in the 4th century B.C.
In the 17th century, murderous epidemics of diphtheria swept Europe; in Spain the disease
became known as "El garatillo" (the strangler"), in Italy and Sicily as "the gullet disease".
In the 18th century, the disease reached the American colonies where it reached epidemic
proportions about 1735. Often, whole families died of the disease in a few weeks.
Observed by Klebs in 1883, culture by Loeffler in 1884
in 1884, Loeffler concluded that C. diphtheriae produced a soluble toxin, and thereby
provided the first description of a bacterial exotoxin.
in 1888, Roux and Yersin demonstrated the presence of the toxin in the cell-free culture fluid
of C. diphtheriae which, when injected into suitable lab animals, caused the systemic
manifestation of diphtheria.
Two years later, von Behring and Kitasato succeeded in immunizing guinea pigs with a heatattenuated form of the toxin and demonstrated that the sera of immunized animals
contained an antitoxin capable of protecting other susceptible animals against the disease.
This modified toxin was suitable for immunizing animals to obtain antitoxin, but it was found
to cause severe local reactions in humans and could not be used as a vaccine.
in 1909, Theobald Smith, in the U.S., demonstrated that diphtheria toxin that had been
neutralized by antitoxin (forming a Toxin-Anti-Toxin complex, TAT) remained
immunogenic and eliminated local reactions seen in the modified toxin. For some years,
beginning about 1910, TAT was used for active immunization against diphtheria. TAT had
two undesirable characteristics as a vaccine. First, the toxin used was highly toxic, and the
quantity injected could result in a fatal toxemia unless the toxin was fully neutralized by
antitoxin. Second, the antitoxin mixture was horse serum, the components of which tended
to be allergenic and to sensitize individuals to the serum.
in 1913, Schick designed a skin test as a means of determining susceptibility
or immunity to diphtheria in humans. Diphtheria toxin will cause an
inflammatory reaction when very small amounts are injected intracutaneously. The
Schick Test involves injecting a very small dose of the toxin under the skin of the
forearm and evaluating the injection site after 48 hours. A positive test
(inflammatory reaction) indicates susceptibility (nonimmunity). A negative test (no
reaction) indicates immunity (antibody neutralizes toxin).
in 1929, Ramon demonstrated the conversion of diphtheria toxin to its nontoxic,
but antigenic, equivalent (toxoid) by treating with formaldehyde. He provided
humanity with one of the safest and surest vaccines of all time, the diphtheria
toxoid.
in 1951, Freeman made the remarkable discovery that pathogenic (toxigenic)
strains of C. diphtheriae are lysogenic, (i.e., are infected by a temperate Beta
phage), while non lysogenized strains are avirulent. Subsequently, it was shown
that the gene for toxin production is located on the DNA of the Beta phage.
in the early 1960s, Pappenheimer and his group at Harvard conducted
experiments on the mechanism of a action of the diphtheria toxin. They studied the
effects of the toxin in HeLa cell cultures and in cell-free systems, and concluded
that the toxin inhibited protein synthesis by blocking the transfer of amino acids
from tRNA to the growing polypeptide chain on the ribosome. They found that this
action of the toxin could be neutralized by prior treatment with diphtheria antitoxin.
Subsequently, the exact mechanism of action of the toxin was shown, and the
toxin has become a classic model of an ADP-ribosylating bacterial exotoxin.
Pathogenesis
Susceptible person may aquire toxigenic diphteria bacilli in
the nasopharynx
The organism produces a toxin that inhibits cellular protein
synthesis and is responsible for local tissue destruction
and membrane formation
The toxin produced at the site of the membrane is
absorbed into the bloodstream and then distributed to the
tissues of the body
The toxin is responsible for the major complication of
myocarditis and neuritis and can also cause low platelet
counts and protein in the urine
Pathogenesis
Toxin mediated disease!
Acquisition of phage
leads to toxigenicity
(lysogenic conversion )
Exotoxin ( polypeptid )
A fragment: toxic
function
B fragment: transport
and binding function
The toxic function
A fragment: toxic function
after binding to the receptor (particularly on the surface of
heart & nerve cells, epithelial cells) this is released in the
cytoplasm
catalyses adenosine diphosphate-ribosylation of
elongation factor 2 (EF-2) / this factor is required for the
movement of nascent peptide chains on ribosomes/
inactivation of all of the host cell EF-2 molecules causes
death of the cell=complete termination of protein
synthesis
cell death
Clinical features
Reservoir – only humans
Transmission route
from human to human by respiratory droplets
breathing aerosolized secretions of infected
individuals (rarely)
by direct physical contact (rarely)
Communicability
Up to several weeks without antibiotics
Incubation period
2-5 days (range:1-10 days)
Clinical features
(Disease can involve almost any mucous membrane)
Localized damage as the results of exotoxin
production
exudative pharyngitis ( tonsils, pharynx, larynx )
the exudate evolves into a thick pseudomembrane
(blood plasma leaks into the area and a fibrin network forms
which is interlaced with rapidly-growing C. diphtheriae cells. )
difficult to dislodge without making the underlying tissue bleed
– typical symptom!
Distal effect
Degenerative changes in these tissues, which include heart,
muscle, peripheral nerves, adrenals, kidneys, liver and spleen,
result in the systemic pathology of the disease
Pharyngeal, tonsillar
and laryngeal diphteria
Early symptoms: sore throat, anorexia, lowgrade fever
Bluish-white membrane (varying in size) =>
greyish-green, or black if bleeding has occured
Pharynx of a 39-year-old woman with bacteriologically confirmed diphtheria.
The photograph was taken 4 days after the onset of fever, malaise, and sore
throat. Hemorrhage caused by removal of the membrane by swabbing
appears as a dark area on the left.
Pharyngeal, tonsillar and laryngeal diphteria
The patient may recover at this
point
Extensive membrane formation
may result in respiratory
obstruction
If enough toxin is absorbed,
develop severe prostation,
striking pallor, rapid pulse,
stupor, and coma, and may even
die within 6 to 10 days
Severe disease:
marked edema of the
submandibular areas
and the anterior neck
Other localisation
Nose : anterior nasal diphteria
Wound
Skin : cutaneous diphteria
Eye
vulva
Complications
The most frequent:
myocarditis
Abnormal cardiac rhytms
Can occur early in the course of illness (often fatal) or
weeks later
Can lead to hearth failure
Neuritis
Affects motor nerves and usually resolves completely
Paralysis of the soft palate (3.week)
Paralysis of eye muscles, limbs, and diaphragm (5.week)
The overall case-fatality rate: 5-10 % (<5 y; >40 y)
Diagnosis
Specific treatment must never be delayed for
laboratory reports if the clinical picture is
strongly suggestive of diphteria !!!
Smears, cultivation ( from nose, throat or
other suspected lesions before
antimicrobial drugs are admitted )
Testing the virulence = toxin producing
Corynebacterium diphteriae
Gram staining: Gram-positive, (rather irregular)
Some rods are club-shaped, others are slightly
curved
Cells arranged in a manner like Chinese characters
they have the characteristic of forming irregular,
club-shaped or V-shaped arrangements in normal
growth.
Special staining=> Neisser
Neisser staining
Aim → to show metachromatic or volutin granula (polyphosphate polymers) at the ends of Corynebacteria
Stain fixed smear of cultured Corynebacteria with a
freshly prepared 2:1 mixture of Neisser I and Neisser II
dyes for 10 minutes
Rinse the slide with water
Strain the smear with crysoidine dye for 2 minutes
Do not discard dye
Dry the slide with the help of blotting paper
Rods with club ends the body of which strains yellow and end stain,
metachromatically purple (volutin granula = poli-phosphate)
Cells arranged in a manner like Chinese characters
Cultivation
Blood agar: 1-3mm, small grey colonies,
small zone of haemolysis
Clauberg medium (K-tellurit
medium)
Selective differential medium for the
isolation of C. diphteriae
Contains: potassium-tellurite and
blood glycerinate
Organisms which grow on this
medium reduce the potassium
tellurite to tellurium; resulting in
black to greyish colonies
three biotypes: gravis, mitis,
intermedium,
Loeffler’s medium ( Loeffler’s serum
+ garlic smell
medium/slope )
Selective differential medium for the
isolation of C. diphteriae
Contains: clotted serum
-Three strains of Corynebacterium diphtheriae
are recognized, gravis, intermedius and mitis.
- They are listed here by falling order of the severity
of the disease that they produce in humans.
- All strains produce the identical toxin and are
capable of colonizing the throat.
- The differences in virulence between the three
strains can be explained by their differing abilities to
produce the toxin in rate and quantity, and by their
differing growth rates
After cultivation => species
identification
Biochemical reaction
Testing the sugar break-down
Pathogenic versus apathogenic
corynebacterium strains
Molecular methods
MALDI-TOF MS
After identification =>Testing the
virulence = toxin producing
In vivo – „Römer probe”:
a culture from Loeffler medium is emulsified in water and
4 ml is injected into each of two guinea pigs, one of
which has received antitoxin previously.
Testing the virulence = toxin producing
In vitro test – „Elek plate „
A strip of filter paper soaked in antitoxin is
submerged in the medium and cultures streaked
at right angles. The toxin diffuses from the
culture streak and the antitoxin diffuses from the
filter paper. A line of precipitation is formed
where they meet in optimal concentrations.
With PCR: the tox gene
Tissue culture test
ELEK-PROBE
A strip of filter paper soaked in antitoxin is submerged in the medium
and cultures streaked at right angles. The toxin diffuses from the
culture streak and the antitoxin diffuses from the filter paper. A line of
precipitation is formed where they meet in optimal concentrations.
Other methods
Epidemiological investigation
Rybotyping
PFGE
Schick probe
Skin test for check of immunity
Immunserology
Antitoxin level in patient serum
(haemagglutination)
Treatment and prevention
Treatment
Antitoxin – immediately!
Antimicrobial drugs – penicillin, erythromycin
Prevention
Toxoid (DPT, DT, boosters)
DPT=diphteria toxoid – 2,4,6,15 to 18 months,
and at 4 to 6 years
! Regular boosters are particularly important for
adults who travel to developing countries (every
10 years!)
Once quite common, diphtheria has largely been
eradicated in developed nations through wide-spread use
of the DPT vaccine
Diphtheria is a serious disease, with fatality rates
between 5% and 10%. In children under 5 years and
adults over 40 years, the fatality rate may be as much as
20%.
Outbreaks, although very rare, still occur worldwide, even
in developed nations.
Following the breakup of the former Soviet Union in the
late 1980s, vaccination rates in the constituent countries
fell so low that there was a surge in diphtheria cases.
In 1991 there were 2,000 cases of diphtheria in the USSR.
By 1998, according to Red Cross estimates, there were as many
as 200,000 cases in the Commonwealth of Independent States,
with 5,000 deaths.
Other corynebacteria
C. jeikeium
Opportunistic pathogen (especially for patient with
haematological disorders, with intravascular catheters)
with high antibioticum resistance
C. urealyticum
Opportunistic pathogen
Urinary tract infection: strong urease – producer =
formation of struvit or renal stones
C. ulcerans
Similar to clinical diphteria
C. minutissimum
Superficial infection of axillary and pubic skin
(erythrasma)
Listeria monocytogenes
Morphology
small Gram positive rod , motile ( 22ºC!)
Culture :
agar, blood-agar: characteristic small zone of
beta-haemolysis around and under colonies;
! isolation can be enhanced in 4 ºC (“coldenrichment”)
Anton-probe:purulens conjunctivitis in a rabbit
Resistant: cold, high-salt concentration
Serologic classification (slide/latexagglutination): Ia, Ib, IVb (> 90% of human
disease)
The bacterium Listeria monocytogenes was named in
honor of Joseph Lister (1827-1912), an English surgeon,
who introduced modern antiseptic surgery.
Listeria monocytogenes EM
Flagella are produced at
room temperature but not at
37°C
A particular property of L
monocytogenes is the ability
to multiply at low
temperatures
Bacteria therefore can
accumulate in contaminated
food stored in the
refrigerator.
Pathogenesis : facultative intracellular
pathogen
- The bacteria are then taken up by
induced phagocytosis, analogous
to the situation in Shigella.
- An 80 kDa membrane protein
called internalin probably
mediates invasion.
- Hemolysins listeriolysin O (LLO)
- protein that mediates actindirected motility (Act-A);
direct cell-to-cell spread of Listeria in
an infected tissue may occur without an
extracellular stage
Pathogenesis, clinical findings
soil, water, vegetation, birds, fish, variety of
mammals, insects
spreading way:
consumption of contaminated milk, soft cheese,
undercooked meat, unwashed, raw vegetables;
transplacentar
Dangerous for neonates, elderly, impaired cellmediated immunity
( pregnancy, AIDS, lymphoma…)
Infections
Intrauterin infection: - abortion or granulomatosis
infantiseptica (disseminated abscesses and
granulomas in multiple organs) early-onset sepsis
Perinatal infection: - late-onset syndrome:
meningitis, meningoencephalitis, sepsis
Immunocompromised patients : meningitis,
encephalitis, and/or sepsis
Disease in healthy adults: influenza-like illness +/gastroenteritis
Perinatal
listeriosis
- Listeriosis also may be transmitted congenitally across the placenta.
- The immunocompetent mother suffers at worst a brief, flu-like febrile illness,
but the fetus, whose defense system is still immature, becomes seriously ill.
- Depending on the stage of gestation, the fetus is either stillborn or born with
signs of congenital infection.
- Typically, multiple pyogenic foci are found in several organs (granulomatosis
infantiseptica).
- The onset of listeriosis is delayed (i.e., a few days after birth) when infection
is acquired during labor by bacteria colonizing the genital tract of the mother.
Listeriosis: a
resurgent
foodborne infection
Clinical Microbiology and Infection
Volume 16, Issue 1, pages 16-23, 10 DEC 2009 DOI: 10.1111/j.1469-0691.2009.03109.x
http://onlinelibrary.wiley.com/doi/10.1111/j.1469-0691.2009.03109.x/full#f1
Case report
In 2002, a multistate
outbreak of L. monocytogenes
infections with 46 culture
-confirmed cases,
seven deaths, and
three stillbirths or miscarriages in eight states was linked to
eating sliced turkey deli meat.
One intact food product and 25 environmental samples from
a poultry processing plant yielded L. monocytogenes.
Two environmental isolates from floor drains were
indistinguishable from that of outbreak patient isolates,
suggesting that the plant might be the source of the
outbreak.
Treatment
ampicillin (+ gentamicin), erythromycin
Natural resistance to cephalosporins!
Immunity
Cell-mediated
Prevention
Do not eat hot dogs and luncheon meats unless they are reheated until
steaming hot.
Avoid cross-contaminating other foods, utensils, and food preparation surfaces
with fluid from hot dog packages, and wash hands after handling hot dogs.
Do not eat soft cheeses such as feta, brie and camembert cheeses, blueveined cheeses, and Mexican-style cheeses such as "queso blanco fresco."
Cheeses that may be eaten include hard cheeses; semi-soft cheeses such as
mozzarella; pasteurized processed cheeses such as slices and spreads;
cream cheese; and cottage cheese.
Do not eat refrigerated pâtés or meat spreads. Canned or shelf-stable pâtés
and meat spreads may be eaten.
Do not eat refrigerated smoked seafood, unless it is contained in a cooked
dish, such as a casserole. Canned or shelf-stable smoked seafood may be
eaten.
Do not drink raw (unpasteurized) milk or eat foods that contain unpasteurized
milk.
Erysipelothrix rhusiopathiae
Morphology:
Gram positive rod ( some rods are curved
and a few are in chains )
Cultivation on blood-agar: small,
transparent glistening colonies
Erysipelothrix rhusiopathiae (Gram-positive rod)
Erysipelothrix rhusiopathiae on blood agar
Epidemiology
it is distributed an land and sea
animals worldwide
it causes erysipelas in swine
people obtain infection by direct
inoculation from animals or animal
products ( fishermen, butchers,…)
» erysipeloid
after 2-7 days incubation :
pain, the lesion is raised,
violaceus , pus is usually not
present!
(rarely septicemic disease)
Laboratory diagnosis:
full-thickness biopsy specimens or deep
aspirates from the margin of the lesion
Treatment
Self-limited in 3-4 weeks or more rapidly
with penicillin
Prevention
vaccination in swine
use of gloves
Lactobacillus spp.
Morphology:
Gram positive rod (20% anaerobic), pleomorphic
Cultivation:
Rogosa medium ( low pH, yeast extract,
peptone, …)- anaerobic conditions
1-2 mm, shiny, whit, raised with the smell of
yoghurt
Blood, tomato-juice, …
Lactobacillus sp. - Gram staining
Epidemiology
They are members of the normal flora of
human oral cavity
Gut
vagina
Clinical pictures
role in the pathogenesis of caries
rarely endocarditis
opportunistic septicaemia in an
immunocompromised patient
Treatment:
antibiotics based on the
susceptibility tests
(vancomycin resistant)
Probiotics
products designed to deliver potentially beneficial bacterial cells to the
microbiotic ecosystem of humans and other animals.
Strains of lactic acid bacteria are the most common microbes
employed as probiotics, especially Lactobacillus and Bifidobacterium
species, but lactococci, some enterococci and some streptococci are
also included as probiotics
Lactobacillus acidophilus
Bifidobacterium bifidum
the indigenous bacteria of humans serve a wide range of functions,
which include manufacture of some B vitamins and vitamin K,
synthesis of some digestive enzymes (e.g. lactase), competition with
pathogens for colonization sites, production of antibacterial and
antifungal substances that protect against harmful organisms,
production of chemicals that have been shown to be anticarcinogenic, and stimulation of the development and activity of the
immune system.
The natural balance of the body’s bacteria can be upset by several
factors such as certain medicines, antibiotics and steroids, increased
acidity in the digestive system caused by stress, lack of sleep and
poor diet, constipation or diarrhea, yeast overgrowth, fatigue, IBS and
other intestinal conditions.
Thank you for your attention