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Gastrointestinal System > Microbiology of the Gastro-Intestinal System > Flashcards

Microbiology of the Gastro-Intestinal System Flashcards

1
Q

Normal flora of the GIT

A

The host’s normal gut flora is large
• Most of these bacteria are anaerobic
• They compete with potential pathogens for nutrients and
for places to attach to the colon wall
• The normal host flora can also produce substances toxic
to potential pathogens
• Microorganisms usually do not multiply in the esophagus
and stomach but are present in ingested food and as
transient flora
Normal flora (NF) of the GIT
• The stomach is usually sterile especially after a meal
– Gastric juices, acids, and enzymes, which help to protect
the stomach from microbial attack, are produced
– Most microorganisms are susceptible to the acid pH of the
stomach and are destroyed with exceptions of:
• Spore-forming bacterial species in their spore phase
• Cysts of parasites
• Helico bacter py lori
– Organisms that are pH-susceptible and survive are
generally protected by being enmeshed in food, and they
move to the small intestine
– Stomach acidity greatly reduces the number of organisms
that reach the small intestine
15/10/2020
2
Normal flora (NF) of the GIT
• The small intestine contains few microorganisms
– Obligate anaerobes far outnumber the facultative Gramnegative rods
• Make up more than 90% of the microbial flora of the large
intestine
– Gram-positive cocci, yeasts, and Pseudomonas
aerugi nosa are also usually present in the large
intestine
Normal flora (NF) of the GIT
• The GIT population may be altered by antibiotics
• In some cases, certain populations or organisms are
eradicated or suppressed, and other members of the
indigenous flora are able to proliferate
• This alteration can be the cause of a severe necrotizing
enterocolitis (C lostridium/Clostridioides
di fficile), diarrhea (S taphylococcus aureus), or
other superinfection

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2
Q

Microorganisms which are not susceptible to the acid pH of the stomach and are not destroyed

A

Spore forming bacterial species in their spore phase

Cysts of parasites

Helicobacter pylori

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3
Q

What can the alteration of the GIT population cause

A

Severe necrotizing enterocolitis-C./Clostridioides difficile

Diarrhoea-S. aureus

Other superinfections

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4
Q

Natural defences of the GIT

A

Gastric Acid

GUT associated lymphoid tissue(GALT)

Bowel normal flora(NF)

Bile Salts

Motility

Protection against toxins

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5
Q

Gastric acid

A

Major first defense

Decreases organisms that enter
intestine

People with less acid are
at increased risk of
infection

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6
Q

GUT Associated Lymphoid Tissue

A

Cellular: lymphocytes,
macrophages + lymphoid
tissue

Humoral: secretory- IgA

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7
Q

Bowel Normal Flora(NF)

A

Resistance to adhesion
by pathogens as receptor
site are blocked

Protection lost after
antibiotics -disturb NF
balance

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8
Q

Bile salts

A

Inhibit and may even kill
some organisms except
for enterobacteriaceae
and enterococci

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9
Q

Motility

A

Assists in clearing
pathogens

Prevent dehydration with
IV or oral rehydration

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10
Q

Protection against toxins

A

Microsomal enzymes of
hepatocytes

Detoxifies some drugs and
endotoxin

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11
Q

Gastroenteritis

A

A syndrome characterized by gastrointestinal symptoms including nausea, vomiting, diarrhoea and abdominal discomfort

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12
Q

Diarrhoea

A

Commonly defined as three or more loose stools in a 24-
hour period
– It is considered acute when the duration is 14 days or less
and persistent when the duration is 14 days or longer
– Usually resulting from disease of the small intestine and
involving increased fluid and electrolyte loss
– The most common outcome of GIT infection

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13
Q

Traveller’s diarrhoea

A

Any diarrhoeal illness associated with travelling

Enterotoxigenic Escherichia coli is the leading cause

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14
Q

Dysentery

A

Characterized by the presence of blood or mucus or both in stools

It is most often the result of inflammation of the small
bowel or colon in response to invasive bacterial infection

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15
Q

Enterocolitis

A

Inflammation involving the mucosa of both the small and large intestine

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16
Q

Cholera

A

An acute infection of the gastrointestinal tract caused by the comma shaped Gram negative bacterium, Vibrio
cholerae

Characterized by severe watery non bloody diarrhea-rice watery stools

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17
Q

Food poisoning

A

Food-borne outbreak

GIT and/or neurological symptoms

Two or more persons
– Exceptions: Botulism, chemical poisoning = 1 case

Within 72 hours

Common meal (same occasion)

NOTIFIABLE medical condition

Most common causes: Salmonella species,
Staphylococcus aureus, C. botulinum, C. perfringens

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18
Q

Bacteria, viruses & parasites causing GIT
infections:

Inflammatory Diarrhoea

A

Bacteria:

Shigella
EHEC
Salmonella enteritidis
Campylobacter jejuni
Vibrio parahaemolyticus
Clostridium/ Clostridioides difficile

Viruses: None

Parasites:

Entamoeba histolytica

Infection is in the colon

Leucocytes and
sometimes blood = Dysentery

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19
Q

Bacteria, viruses & parasites causing GIT
infections:

Non inflammatory diarrhoea

A

Bacteria:

ETEC
EAEC
Vibrio cholerae
Clostridium perfringens
Bacillus cereus
Staphylococcus aureus

Viruses:

Rota, Noro, Adeno &
Astrovirus

Parasites:

Giardia lamblia
Cryptosporidium parvum
Cyclospora cayetanensis
Microsporidia

Acute watery diarrhoea
Proximal small bowel
Seldom leucocytes

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20
Q

Bacteria, viruses & parasites causing GIT
infections
GIT and Systemic infection

A

Bacteria:

Salmonella enterica
serovar Typhi
Salmonella spp. (NTS)
Yersinia enterocolitica
Campylobacter spp.

Viruses:

Polio
Enteroviruses

Parasites:
Entamoeba histolytica
Echinococcus
granulosis
Strongyloides stercoralis

Generally involves
small bowel
Few leucocytes

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21
Q

The types of Diarrhoeal diseases

A

Enterotoxin-mediated

Invasive:
-Invasion of the Bowel mucosal surface

-Invasion of Full-Bowel thickness with lymphatic spread

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22
Q

Enterotoxin-mediated

A

Bacteria associated with enterotoxin production do not
invade the gut wall

The toxin does not elicit an inflammatory response

Patients usually do not have a fever

The pre-formed toxin is already present in the ingested
food- because toxin can act proximally in the bowel (the small intestine), the incubation period is relatively short, usually less than 12 hours

Rapid onset of symptoms following food ingestion

When patients present to a physician, they usually report an illness that started the day of or the day before presentation

They typically have a large number of non- bloody, watery stools and frequently have vomiting and abdominal cramping, particularly during defecation

Examples include:

-Enterotoxigenic Escherichia coli - accounts for the
largest percentage of cases of diarrhea in travelers to
underdeveloped areas
-Vibrio cholerae
-Staphy lococcus aureus
-Clostridium perfringens, and
-Bacillus cereus

I

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23
Q

Invasion of the Bowel Mucosal Surface

A

Organisms cause an inflammatory response

Characterized by the presence of fecal leukocytes, fever and leukocytosis

Organisms must first replicate in the colon, and then
invade the mucosal surface

Incubation period is usually longer than the enterotoxin -mediated diarrhea

Infections only involve the superficial mucosal surface of the bowel

Bacteremia or metastatic infection is infrequent

Patients may present with dysentery, characterized by
gross blood and pus in the stool

Examples:

  • Salmonella spp.
  • Campylobacter spp.
  • Shigella spp.,
  • Enterohaemorrhagic E. coli strains, and
  • Entamoeba histolytica
24
Q

Invasion of Full-Bowel Thickness with Lymphatic Spread

A

These organisms can invade the bowel wall, causing
bacteremia, and mesenteric lymphadenitis

Can be mistaken for appendicitis

Diarrhea may be absent at the onset of the disease

Red blood cells and fecal leukocytes are often present in the stool

Gross blood in the stool can occur in about 25% of
patients with Y. enterocolitica infection

Patients with Salmonella enterica ser Typhi infection may become chronic carriers and unknowingly spread the infection to others

Examples:

  • Salmonella enterica ser Typhi and
  • Yersinia enterocolitica
25
Q

Specimen Collection and Handling

A

Stool specimens: transported to the laboratory shortly after
collection
– Preservatives (polyvinyl alcohol or formalin) must be
avoided if bacterial cultures are ordered
Microscopy, Culture and Sensitivity performed on same
specimen therefore, normal specimen container used
– If rectal swabs are to be processed, Cary- Blair or a similar
transport medium should be used

26
Q

Biopsy specimens of mucosa

A 
Rectal mucosa : scrapings,
biopsies – parasites/ova  excreted 
more direct specimens,
e.g. schistosome ova; Ent.
histolytica (trophozoites)
27
Q

Gastric biopsies:

A

Helicobacter pylori take
specimens from edge of
ulcer, inflammationers to

28
Q

Intestinal fluids

A

E.g. giardiasis, strongyloides
– Not readily detected in stools
– Duodenal aspirates/biopsies
required

29
Q

Gastric Aspirates

A

TB esp. in children and
debilitated adults

Acute food poisoning-
toxins

30
Q

Other: Blood cultures

A

NB in pts with fever e.g. Salmonella infections –

invasive infection

31
Q

Direct Microscopic Examination

A

Stained or unstained slides, wet mount preparations
– Microscopic examination of the stool may reveal white blood
cells in cases of inflammatory diarrhea (e.g. Salmonella, Shigella, Y ersinia, Campy lobacter, EIEC, and various
Vibrio spp.)
– Red blood cells may be present because of intestinal wall
bleeding
– The bacteria may be visible on direct microscopic examination of
the stool
–

32
Q

Culture

A

Selective and differential culture media are commonly
used to identify bacterial pathogens in stool
– Selective media contain antimicrobials or chemicals, which
limit the growth of normal bacterial flora and enhance thegrowth of pathogenic bacteria
– The differential aspect of the medium often allows
differentiation of bacterial species based on colony
morphology
• Differences in colony appearance are usually a result of
different biochemical characteristics of the organisms

33
Q

Specific tests:

A

Antigen detection
Molecular methods

Antimicrobial susceptibility testing

34
Q

Antibiotic associated/induced diarrhoea:

Etiology:

A

Antibiotic associated diarrhoea(AAD) refers to diarrhea
following antimicrobial administration

Clostridium difficile is the most common identifiable cause

Responsible for approximately 30% of cases

Although Clostridium/Clostridioides difficile Infection (CDI)is endogenous in most cases, hospital outbreaks have clearly established that the environment can be the source as well

Generation of spores from excretions promotes person-to person spread

35
Q

Antibiotic associated/induced diarrhoea:

Pathogenesis:

A

When C. difficile becomes established in the colon of
individuals with normal gut microbiota, its numbers are
dwarfed by the other flora

Introduction of antibiotics reduces the number of
normal gut flora allowing growth of C. difficile

This is in particular: ampicillin, cephalosporins, and
clindamycin

Most strains produce both toxins, the TcdA and TcdB

Hypervirulent clones produce higher levels of both toxins and also secrete the C. difficile transferase (CDT)

Responsible for more cases and more deaths

36
Q

In Pseudo membranous colitis (PMC):

A

Colonic mucosa is studded with inflammatory plaques

These may coalesce into an overlying “pseudomembrane”composed of fibrin, leukocytes, and necrotic colonic cells

37
Q

Antibiotic Associated/Induced Diarrhoea

A

Selective media used
– However, direct detection of toxins in the stool has largely
replaced culture for diagnostic purposes
• Detection of its toxin has become routine
– Immunoassays are used to demonstrate toxin TcdA and/or
TcdB in stool
– Nucleic acid-based test have also been developed

38
Q

Antibiotic associated/induced diarrhoea:

Treatment and prevention:

A

In AAD discontinuing the implicated antimicrobial often
results in the resolution of clinical symptoms
– Antibiotics for treatment: Metronidazole/vancomycin
/Fidaxomicin
• Fidaxomicin, achieves high levels in the bowel with results
comparable to vancomycin
– Fecal transplant
– With all regimens relapses are common presumably due to
the survival of the inert spores following a treatment course

39
Q

Peptic ulcers

• Etiology:

A

– Helicobacter pylori is the etiologic agent
– The organism is found in the stomachs of 30% to 50% of
adults
– The exact mode of transmission is not known, but is
presumed to be person to person
• Fecal–oral route
• Contact with gastric secretions in some way
– Colonization increases progressively with age
– A declining prevalence in developed countries may be due
to decreased transmission because of
• Less crowding and frequent exposure to antimicrobial agents

40
Q

Peptic ulcers

• Pathogenesis:

A
  1. Adherence to gastric mucosa

Multiple outer membrane proteins which bind to the surface
of gastric epithelial cells and certain erythrocyte antigens

  1. Motility

Flagella to swim to less acidic locale beneath the gastric mucus

  1. Persistence in the hostile environment of the stomach and
    survival of the acid stomach: Urease

Protease damage the mucosa
– 70–80% of gastric ulcers – 90% of duodenal ulcers – Gastric carcinomas, intestinal lymphomas

41
Q

Peptic ulcers:

Diagnosis

A

Specimen - Gastric mucosa biopsy

The most sensitive means of diagnosis is culture of the
gastric mucosa

Most sensitive indicator of cure following therapy

The H. pylori urease activity in biopsies

Noninvasive methods include serology and a urea breath test

For the breath test, the patient ingests 13C- or 14C-labeled urea, from which the urease in the stomach produces products that appear as labeled CO2
in the breath

Detection of antibody directed against H. pylori

Because IgG or IgA remains elevated as long as the infection persists, these tests are valuable both for screening and for evaluation of therapy
–

42
Q

Peptic ulcer:

Treatment and prevention

A

Bismuth salts (e.g, Pepto-Bismol) has antimicrobial activity

Cure rates approaching 90% have been achieved with
various combinations of bismuth salts and/or a protein pump inhibitor plus two antibiotics

Clarithromycin plus either amoxicillin or metronidazole and metronidazole plus tetracycline have been effective

Relapse rates are low, particularly when acid secretion is also controlled with the use of a proton pump inhibitor

Prevention of H. pylori disease awaits further
understanding of transmission and immune mechanisms

Prophylactic treatment of asymptomatic persons colonized with H. pylori is not yet recommended

43
Q

Diarrhoegenic E. coli:

Treatment

A

Most E. coli diarrhea are mild and self-limiting
– Rehydration and supportive measures are the mainstays
of therapy
– EHEC with hemorrhagic colitis and HUS- supportive
measures required, antimicrobials contraindicated
– TMP-SMX or fluoroquinolones reduces the duration of
diarrhea in ETEC, EIEC, and EPEC infection
– Antimotility agents are not helpful and are contraindicated
when EIEC or EHEC could be the etiologic agent

44
Q

Diarrhoegenic E. coli

• Prevention:

A

Traveler’s diarrhea incidence can be greatly reduced by

  • eating only cooked foods and peeled fruits
  • drinking hot or carbonated beverages

Avoiding uncertain water, ice, salads, and raw vegetables is a wise precaution when traveling in developing countries
•
GIT infections caused by Campyl

45
Q

GIT infections caused by Campylobacter

A

C. jejuni is by far the most common
– Primary reservoir is in animals
– Bacteria are transmitted to humans by ingestion of
contaminated food or by direct contact with pets • Mostly undercooked poultry, but outbreaks have been caused by
contaminated rural water supplies and unpasteurized milk

46
Q

GIT infections caused by Campylobacter:

Pathogenesis

A 
– Oral ingestion
– Colonization of the
intestinal mucosa
– Adherence to
enterocytes is facilitated
by action of the flagellum
– Entrance into cells in
endocytotic vacuoles
• Once inside, they move
in association with the
cell’s microtubule
structure
– Injury mechanisms include
the
• Cytotoxic cytolethal
distending toxin (CDT)
• Action of lipooligosaccharides (LOS)
released in outer
membrane vesicles
– The intestinal pathology is
that of an invasive pathogen
with acute inflammation,
crypt abscesses, and
occasional seeding of the
bloodstream
GIT infections caused by Campylobacter
• Diagnosis:
– Stool samples
– Buffered glycerol saline,
is toxic to enteric
campylobacters and
should therefore be
avoided
– Incubate at 420C- C.
fetus @ 370C
• Enteric
Campy  lobacter
require a microaerophilic
and capnophilic
environment
47
Q

GIT infections caused by Campylobacter

• Diagnosis:

A 
– Stool samples
– Buffered glycerol saline,
is toxic to enteric
campylobacters and
should therefore be
avoided
– Incubate at 420C- C.
fetus @ 370C
• Enteric
Campy  lobacter
require a microaerophilic
and capnophilic
environment
Diagnosis – Microscopic Morphology
• Campy  lobacter spp.
are motile, curved,
non  spore-forming,
oxidase positive Gramnegative rods
• May appear as long
spirals or   S’ or seagullwing shapes
• On Gram-stained smears,
these organisms stain
poorly
• They exhibit a
characteristic   darting  motility
– Colony Morphology
• Moist, runny looking,
and spreading
• Usually nonhemolytic
• Some are round and
raised and others may
be flat • C.    fetus subsp.
f  etus produces
smooth, convex,
translucent colonies
• Most do not produce
pigment
48
Q

GIT infections caused by Campylobacter

• Treatment

A

– Antimicrobial susceptibility testing not routinely performed
– Most patients recover without antimicrobial intervention
– Drugs of choice for treating intestinal campylobacteriosis
are azithromycin and erythromycin
– Ciprofloxacin and other quinolones can also be used

49
Q

GIT infections caused by Clostridium

perfringens

A 
• Outbreaks usually involve
rich meat dishes such as
stews, soups, or gravies
that have been kept warm
for a number of hours
before consumption
Two types of food poisoning
– Type A-relatively mild and
self-limited GI illness
– Type C- more serious but
rarely seen disease
• Follows the ingestion of
enterotoxin-producing
strains
• Spores of some strains are
heat-resistant and can
convert to the vegetative
form and multiply when food
is not refrigerated or is
rewarmed
• After ingestion, the
enterotoxin is released into
the upper GIT, causing a
fluid outpouring in which the
ileum is most severely
involved
50
Q

GIT infections caused by Clostridium
perfringes:

Type A

A 
caused by
enterotoxin linked to
sporulation
• After an 8- to 30-hour
incubation period, the
patient experiences
diarrhea and cramping
abdominal pain for about
24 hours
• Other than fluid
replacement, therapy is
usually unnecessary
51
Q

GIT infections caused by Clostridium
perfringes:

Type C

A 
Type C -   enteritis
necroticans  is
associated with strains
that produce β-toxin
– less comonly, α-toxin
• After at least 5 to 6 hours,
symptoms begin as acute
onset of severe abdominal
pain and diarrhea, which is
often bloody, and may be
accompanied by vomiting
• Necrotic
inflammation>>bowel
perforation
• Fatal, treatment is required
52
Q

GIT infections caused by Bacillus cereus

A

• Gram-positive bacilli
• They are aerobic or
facultative anaerobic
bacilli that form
endospores
• Catalase positive
• B. cereus food poisoning
2 forms:
– Emetic (vomiting)
– Diarrhoeal
GIT infections caused by Bacillus cereus
• Culture of suspected food or stools may be done to
quantify and isolate B. cereus
• More than 105 cereus cells per gram of
food/stools with absence of other pathogens confirms
the diagnosis
• Most food poisoning cases caused by B. cereus
do not require antimicrobial treatment • B. cereus is resistant to penicillin and all of the other βlactam antibiotics except for the carbapenems

53
Q

Clinical Syndrome caused by B. cereus:

Type:

  • Incubation Period
  • Diarrhoea
  • Vomiting
  • Duration of illness
  • Foods implicated
A 
Diarrheal:
8-16hrs
Very common
Ocassional
12-24 hrs
Meat products
Emetic:
1-5hrs
Fairly common
Very common
6-24hrs
Fried or boiled rice
54
Q

GIT infections caused by Staphylococcus

aureus

A 
Staphylococcal food
poisoning is one of the
most common foodborne
illnesses in the world
– Short incubation period
– Characteristically, the food
is moist and rich (e.g, red
meat, poultry, creamy
dishes)
– Contaminated by a
preparer who is a carrier
– If the food is left
unrefrigerated for hours
between preparation and
serving, the
staphylococci are able to
multiply and produce
enterotoxin in the food
– S. aureus enterotoxins
stimulate gastrointestinal
symptoms (primarily
vomiting)
– Once formed, these
toxins are quite stable
• They retain activity
even after boiling or
exposure to gastric and
jejunal enzymes
•
55
Q 
GIT infections caused by Staphylococcus
aureus
Dx
Tx
Px
A

Patients symptoms will guide

Supportive

Hand washing during, after and before eating

Gastrointestinal System (14 decks)

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