Download 11-Vibrios-Campylobacters-Helicobacter-and-Associated-Bacteria

MICROBIOLOGY LEC | VIBRIOS, CAMPYLOBACTERS, HELICOBACTER
and ASSOCIATED BACTERIA
Tutor: DR. ZARA |
Lecture Date: DEC 8, 2020 |
1ST SEM
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TOPIC OUTLINE
I. VIBRIOS
i. V. cholerae
 Morphology and Identification
 Antigenic structure and Biologic function
 Pathogenesis and Pathology
 Signs and Symptoms
 Diagnostic Laboratory Tests
 Immunology
 Treatment
 Prevention, and Control
ii. V. parahemolyticus
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Very Actively motile by means of a polar
flagellum
Non-acid fast, non-spore, non-encapsulated
Pleomorphic
iii. V. vulnificus
II. AEROMONAS
i. A. hydrophila
III. PLEISOMONAS
IV. CAMPYLOBACTER
i. Campylobacter jejuni
ii. Campylobacter coli
V. Helicobacter pylori
Vibrio, Aeromonas, Campylobacter, and
Helicobacter are Gram-negative rods that are all widely
distributed in nature. Vibrio cholerae produces an
enterotoxin that causes cholera, a profuse watery
diarrhea that can rapidly lead to dehydration and death.
Campylobacter jejuni is a common cause of enteritis in
humans. Helicobacter pylori is associated with gastritis
and duodenal ulcer disease.
I.
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VIBRIOS
Vibrios are among the most common bacteria in
marine and estuarine waters, worldwide.
Comma-shaped, curved and sometimes
facultatively anaerobic, fermentive rods
Catalase and oxidase positive
Motile: monotrichous or multitrichous polar
flagella
Can grow at 14 to 40 degree centigrade
All species require sodium chloride for growth
(Halophilic: “salt loving”)
i.
VIBRIO CHOLERAE
 MORPHOLOGY AND IDENTIFICATION
A. Typical Organisms
 Comma-shaped, curved rod 2-4 um long
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B. Culture
 Produces convex, smooth, round colonies
that are opaque and granular (very small) in
transmitted light.
 Grow well at 37°c on many kinds of media
(like EMB, MAC)
 Grows well on thiosulfate-citrate-bilesucrose (TCBS) agar (very selective media) 
produces
yellow
colonies
(sucrose
fermented) that are readily visible against
the dark-green background of the agar.
 Unlike Enterobacteriaciae (E.coli and
Klebsiella) that ferments lactose: in TSI it
turns yellow and in MAC agar turns pink
 Non-sucrose-fermenting vibrios (e.g., most
strains of V. parahaemolyticus and V.
vulnificus) produce green colonies on TCBS
agar.
 Oxidase positive, which differentiates them
from enteric gram-negative bacteria. (This
will automatically rule out E.coli or
Klebsiella)
 Oxidase Test Positive – when the paper turns
violet : meaning they are Aerobic
 ALKALOPHILES - Grow at a very high pH (8.5–
9.5 average of 9) and are rapidly killed by
acid.
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To ensure optimal recovery of vibrios, stool
specimens should be collected early on the
course of the diarrheal illness.
 If processing is delayed- mixed specimen in a
Cary-Blair transport medium and refrigerate.
 When ingesting contaminated water, the
concentration of the inoculum should be
high for it to elicit diarrhea (10 2 does not
cause diarrhea; should be higher in
concentration)
**In areas where cholera is endemic, direct
cultures of stool on selective media, such as
TCBS, and enrichment cultures in alkaline
peptone water are appropriate. However,
routine stool cultures on special media such as
TCBS generally are not necessary or cost
effective in areas where cholera is rare.
C. Growth Characteristics
 Susceptible to the compound O/129 (2, 4diamino-6,7-disopropylpteridine phosphate)
which differentiates them from Aeromonas
species, which are resistant to O/129.
 Halotolerant (Salt-loving organisms)and
NaCl (<0.5 to 4.5%) often stimulates their
growth.
 Another difference between vibrios and
aeromonads is that vibrios grow on media
containing 6% NaCl, but Aeromonas does
not.
 Another difference between vibrios and
aeromonads is that vibrios grow on media
containing 6% NaCl, but Aeromonas does
not.
 Ferments sucrose (turn it to yellow with
green background) and mannose but not
arabinose.
 Facultative anaerobe
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Halotolerance is the adaptation of living
organisms to conditions of high salinity.
Halotolerant species tend to live in areas
such as hypersaline lakes, coastal ...
Colonies of V. cholerae growing on thiosulfate, citrate,
bile salts, and sucrose agar. The glistening yellow
colonies are 2–3 mm in diameter and are surrounded
by a diffuse yellowing of the indicator in the agar up to
1 cm in diameter. The plate is 10 cm in diameter.
 ANTIGENIC
STRUCTURE
AND
BIOLOGIC
CLASSIFICATION
 Share a single heat-labile flagellar H antigen.
 Antibodies to the H antigen are probably not
involved in the protection of susceptible hosts.
(It means even if you develop antibody against H
antigen it doesn’t mean you are Immune to
vibrio cholera)
 Has O LPS Confer serologic specificity.
 V. Cholerae strains sero groups 01 and O139
(Bengal strain) cause (epidemic and pandemic)
cholera in humans while other vibrio may cause
sepsis or enteritis.
 Antibodies to the O antigens tend to protect
laboratory animals against infections with V
cholerae.
 Occasionally, non-O1/non-O139 V cholerae
causes cholera-like disease.
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Activation of subunit A1 yields increased levels of
cAMP and results in prolonged hypersecretion of
water and electrolytes.
There is increased sodium-dependent chloride
secretion, and absorption of sodium and chloride
by the microvilli is inhibited.
Electrolyte-rich diarrhea occurs with as much as
20-30L/day, resulting in dehydration, shock,
acidosis and death.
Two biotypes of epidemic have been defined
 Classic
 El Tor.
El Tor biotype:
- produces a hemolysin
- gives positive results on the VogesProskauer test and sensitive to Polymixin B
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V cholerae O139 is very similar to V cholerae O1
El Tor biotype.
V cholerae O139 does not produce the O1 LPS
and does not have all the genes necessary to
make this antigen.
V cholerae O139 makes a PS capsule like other
non-O1 V cholerae strains, but V cholerae O1
does not make a capsule.
The V. cholerae Serogroup O1 antigen has
determinants that make possible further
subtyping; these serotypes are Ogawa, Inaba and
Hikojima. Furthermore, two biotypes of
epidemic V. cholerae have been defined, classic
and El Tor. The El Tor biotype produces a
hemolysin, gives positive results on the VogesProskauer test and is resistant to polymyxin B.
Typing is used for epidemiologic studies.
Vibrio cholera enterotoxin
 Produce a heat-labile enterotoxin, consisting of
subunits A.
 Ganglioside GM1 (receptors located in the GIT)
serves as the mucosal receptor for subunit B,
which promotes entry of subunit A into the cell.
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When you ingest a contaminated water, the
cholera toxin which is made up of Subunit A
and B, the Subunit B will be the one to bind to
the GM1 Ganglioside receptor. Once the subunit
B binds to the GM1 receptor, the subunit A
detaches ( yung color BLUE mahihiway kay
GREEN- Subunit B) hence the Subunit A will
enter the Cytoplasm where it binds to G protein
that will then activate binding to Adenylate
cyclase. This adenylate cyclase will stimulate
the increased production of cAMP now opening
the Cystic Fibrosis Transmembrane receptor so
mag o-open, mabubutas yung epithelial tissue:
THE GATE IS OPEN hence you will excrete a lot
of Na then water, and a lot of electrolytes as
well.
How much can you lose? – you can have a
diarrhea that is 20 – 30 L a day which is di mo
mapigilan 
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The genes for V cholerae enterotoxin are on the
bacterial chromosome. Cholera enterotoxin is
antigenically related to LT of Escherichia coli and
can stimulate the production of neutralizing
antibodies. However, the precise role of
antitoxic and antibacterial antibodies in
protection against cholera is not clear.
 PATHOGENESIS AND PATHOLOGY
 Pathogenic only for humans.
 Infectivity: A person with normal gastric acidity
may have to ingest as many as 1010 or more V.
cholerae  Vehicle is water
 When the vehicle is food, as few as 10 2–104 
This is also the infectious does in a person with
achlorhydria or hypochlorhydria.
 Organisms are necessary because of the
buffering capacity of food.
 V. cholerae is a noninvasive mucosal pathogen,
therefore, they do not reach the bloodstream
(does not cause bacteremia) but remain within
the intestinal tract.
 Virulent V. cholerae organisms attach to the
microvilli of the brush border of epithelial cells.
There they multiply and liberate cholera toxin
and perhaps mucinases and endotoxin.
 Any medication or condition that decreases
stomach acidity makes a person more
susceptible to infection with V cholera.
 SIGNS AND SYMPTOMS
 The spectrum of disease due to V. cholerae ranges
from asymptomatic intestinal colonization to mild,
moderate, or severe diarrhea. About 50% of infections
with classic V. cholerae are asymptomatic, as are about
75% of infections with the El Tor biotype.
 The incubation period after ingestion of a sufficiently
high infectious dose of V. cholerae is 12 hours to 3 days
for persons who develop symptoms, depending largely
on the size of the inoculum ingested.
 Profuse diarrhea sometimes called “rice water
stools” - contain mucus, epithelial cells, and large
numbers of vibrios. (Commonly asked in board
exams: Rice Water Stool is Very typical of V.
cholerae)
 Sudden onset of nausea and vomiting
 Abdominal pain
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Leg cramps (because you lose a lot of electrolyte
particularly your Potassium)
Sunken eyes ( because of severe dehydration)
SHOCK – because of severe fluid losses
Hypovolemic Shock - Low blood pressure
 DIAGNOSTIC LABORATORY TESTS
A. Specimens
 Mucus flecks from stools
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Collected early in the course of the diarrheal
illnessand inoculated within 2-4 hours of
collection
B. Smears
 Not distinctive
 Dark-field or phase contrast microscopy 
Show the rapidly motile vibrios (because of
their polar flagella)
C. Culture
 TCBS agar
 pH near 9 - Alkalophile
 18 hours
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Growth is rapid in alkaline peptone broth or
water, containing NaCl with a ph of 8.5 or on
TCBS.
D. Specific Tests
 Slide agglutination tests using anti-O group 1
or group 139 antisera (results in
Agglutination – Positive result)
 Immunochromatographic dipstick test
 IMMUNITY
 Gastric acid
 An attack of cholera is followed by immunity to
reinfection, but the duration and degree of
immunity are not known
 TREATMENT
 Fluids and electrolytes-most important part of
treating cholera patients to correct the severe
dehydration and salt depletion
(because what kills the px is not the toxin but
severe dehydration)
 Antimicrobial agents are effective against V.
cholerae, but these play a secondary role in px
management. Appropriate antimicrobial therapy
can also reduce the duration and amount of
shedding og Vibrio organism in the stool.
 Oral tetracycline and doxycycline
 Resistance: carried by transmissible plasmids.
 In children and pregnant women, alternatives to
the tetracycline (cannot give to children; also
causes yellow discoloration of teeth) include
erythromycin (because we cannot give
Doxycycline to pregnant women because of its
teratogenic effect) and furazolidine
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GALISTE | GAOYEN | IBARRA | LAMORIN | LAYDA|LESCAIN |MANZANO | NGALNGALO
 EPIDEMIOLOGY, PREVENTION AND CONTROL
 Most likely by V. cholerae O1 of the classic
biotype and largely originating in Asia, usually
the Indian subcontinent.
 Cholera is endemic in India and Southeast Asia.
 Vibrios survive in water for up to 3 weeks
 Cholera is a disease that is spread by contact
involving individuals with mild or early illness by
water, food, and flies.
 V. cholerae lives in aquatic environments.
 Lives attached to algae, copepods, and
crustacean shells. It can survive for years and
grow, but when conditions are not suitable for
growth, it can become dormant (they’re still
present but they don’t replicate)
 Control rests on education and on improvement
of sanitation, particularly of food and water.
Patients should be isolated, their excreta
disinfected, and contacts followed up.
Chemoprophylaxis with antimicrobial drugs may
have a place.
Repeated injection of a vaccine containing either
lipopolysaccharides extracted from vibrios or
dense Vibrio suspensions can confer limited
protection to heavily exposed persons (eg, family
contacts) but is not effective as an epidemic
control measure.
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VIBRIO PARAHEMOLYTICUS
Halophilic
Causes acute gastroenteritis after ingestion of
Contaminated seafood such as raw fish or
shellfish.
IP:
12–24 hours, nausea and vomiting,
abdominal cramps, fever, and watery to bloody
diarrhea occur (due to its characteristic
invasiveness) - Fecal leukocytes
No enterotoxin
Facultative anaerobe
Does not grow well on some of the differential
media used to grow Salmonellae and Shigellae,
but it does grow well on blood agar.
Grows well on TCBS, where it yields green
colonies (does not ferment sucrose).
The final organism identification is achieved by
the use of various standard biochemical tests.
Usually no specific treatment other than
rehydration is required since the gastroenteritis
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is self-limited. However, antimicrobial therapy
could be considered for patients in whom the
diarrheal illness does not resolve within 5 days;
doxycycline and/or fluoroquinolones are
appropriate choice for antibiotic therapy and
would shorten the duration of the illness.
V. Parahaemolyticus is usually oxidase-positive
Spontaneously resolved in 1–4 days with no
treatment other than restoration of water and
electrolyte balance.
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VIBRIO VULNIFICUS
Severe wound infections, bacteremia, and
probably gastroenteritis.
is a free-living bacterium and part of the normal
marine microbiota in association with bivalves
and crustaceans
Oysters (commonly asked in board exams) and
shellfish
Alcoholism or liver disease.
Wounds may become infected in normal or ICH
Bullous skin lesions, cellulitis, and myositis with
necrosis.
TCBS
Teracycline; Ciprofloxacin
Wound infections may be mild but often proceed
rapidly (over a few hours), with development of
bullous skin lesions, cellulitis, and myositis with
necrosis
The two most common clinical presentations of
V. vulnificus infection are rapidly progressive
wound infections due to skin/soft tissue injuries
following exposure to contaminated seawater
and primary bacteremia/sepsis following the
consumption of contaminated raw oysters.
V. vulnificus can invade the bloodstream without
causing gastrointestinal symptoms
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Vibrio spp. ( Family Vibrionaceae) Associated with Human Disease
i. Aeromonas hydrophila
II.
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AEROMONAS
Ubiquitous inhabitants of fresh and brackish
water
Aeromonads are Gram-negative, facultative
anaerobic rods that ferment carbohydrates and
may resemble morphologically members of the
family of Enterobacteriaceae
1–4 μm long and are motile.
Colony morphology large zones of hemolysis (bhemolytic) on blood agar.
Cultured from stool
(+) oxidase reaction
Aeromonas species are differentiated from
vibrios by showing resistance to the compound
O/129 and lack of growth on media containing
6% NaCl. (Most differentiating characteristics –
please remember)
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Most common spp of Aeromonas
Predominantly Not associated with diarrhea
Contaminated Fresh water
Swelling of Lower Extremities (yung dinaanan ng
tubig – Exposed Extremities)
Releases cytotoxin (in the cytoplasm) and
Hemolysins that hemolyzes RBC
Wound infections from trauma that occurs in a
water environment and are caused primarily by
a hydrophila. Most commonly associated with
human infection: A. hydrophila, A. caviae, A.
veronii.
Tetracyclines, aminoglycosides, and thirdgeneration cephalosporins (Ceftriaxone).
Aeromonas species are also associated with
extraintestinal infections such as bacteremia and
wound infections
Most commonly, uncomplicated cellulitis
develops within 48 hours of the injury, but
systemic symptoms may also develop. In
addition to antimicrobial therapy, the
suppurative necrosis surrounding the wound
may require surgical debridement
Produce hemolysins.
Cytotoxins
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III.
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Plesiomonas shigelloides is an oxidase (+)
It is a water and soil organism and has been isolated
from freshwater fish and many animals.
Plesiomonas grows on the differential media used to
isolate Salmonella and Shigella from stool specimens
Cross-reactions with Shigella antisera occur.
Plesiomonas can be distinguished from shigellae in
diarrheal stools by the oxidase test:
o Plesiomonas is oxidase positive, and shigellae
are not.
Positive for dnase
Most isolates from humans have been from stool
cultures of patients with diarrhea
IV.
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PLESIOMONAS
CAMPYLOBACTER JEJUNI &
CAMPYLOBACTER COLI
C. jejuni and C. coli have emerged as common human
pathogens
Causes:
o Enteritis
o Occasionally systemic infection
i. CAMPYLOBACTER
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Cause both diarrheal and systemic diseases
H. pylori – Causes gastric infection
C. jejuni – Prototype organism in the group and is a
very common cause of diarrhea in humans.
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MORPHOLOGY AND IDENTIFICATION
A. Typical Organisms
 C. jejuni and the other campylobacters are gram (-)
rods with comma, S, or “gull wing” shapes.
 Motile, with a single polar flagellum, and do not
form spores
B. Culture
 Selective media – blood free, charcoal-based
selective medium agar (CSM) for isolation of C.
jejuni
 Incubation must be in an atmosphere with reduced
O2 (5% O2) with added CO2 (10% CO2)
 Incubation at 42°C
 Although C. jejuni grows well at 36 to 37°C,
incubation at 42°C prevents growth of most of the
other bacteria present in feces, thus simplifying the
identification of C. jejuni.
 Skirrow’s medium contains:
o Vancomycin
o Polymyxin
o Trimethoprim to inhibit growth of other
bacteria
o Colonies tend to be colorless or gray, watery
and spreading or round and convex and bot
colony types may appear on one agar plate.
o May be less sensitive than other
commercial products that contain charcoal,
other inhibitory compounds and
cephalosporin antibiotics.
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a. No change with alpha-napthylamine and sulfanilic acid
means nitrite absent.
b. Turns red with alpha-napthylamine and sulfanilic acid
means nitrite present, positive nitrate reduction test
c. No change with zinc means positive nitrate reduction
test
d. Turns red with zinc means negative nitrate reduction
test
C. Characteristics
 C. jejuni and the other campylobacters pathogenic
for humans are oxidase and catalase (+).
 Do NOT ferment carbohydrates.
 Nitrate reduction, hydrogen sulfide production,
hippurate tests, and antimicrobial susceptibilities
can be used for further identification of species.
NITRATE REDUCTION
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Inoculate with loop
Incubate
Additional solutions
o Sulfanilic acid (A)
o Naphthylamine (B)
(+) = Red
o Nitrate to nitrite
No color, add Zinc
o (+) = Not red
o (-) = Red
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GALISTE | GAOYEN | IBARRA | LAMORIN | LAYDA|LESCAIN |MANZANO | NGALNGALO
ANTIGENIC STRUCTURE and TOXINS
When you ingested contaminated poultry products
o LPS with endotoxic activity.
o Cytopathic extracellular toxins and enterotoxins
PATHOGENESIS and PATHOLOGY
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Oral route
Poultry products
C. jejuni is susceptible to gastric acid
104  Infection
Multiply in the small intestine  Invade the
epithelium and produce inflammation 
Appearance of red and white blood cells in the
stools.
Bloodstream is invaded and a clinical picture of
enteric fever develops.
Localized tissue invasion coupled with the toxic
activity appears to be responsible for the enteritis.
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Campylobacter fetus subspecies venerealis is a rare
cause of human disease.
CLINICAL FINDINGS
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Most affected are immunocompromised host
especially HIV positive patients.
Acute onset of crampy abdominal pain because of
toxins, profuse diarrhea that may be grossly bloody
since it is invasive, headache, malaise and fever.
Self-limited means not necessary to treat with
antibiotics to a period of 5 to 8 days if you are
immunocompetent means no DM and kidney
disease just ingested contaminated poultry products.
But if you are immunocompromised treat with
antibiotics, you can give your tetracycline or
ciprofloxacin.
Erythromycin and therapy shortens the duration of
fecal shedding of bacteria.
Certain serotypes of C. jejuni have been associated
with postdiarrheal Guillain-Barré syndrome - is an
ascending muscle paralysis, paralyzes first your
lower extremities and ascends to your diaphragm,
which leads to difficulty in breathing. Then the
patient is place in ICU with mechanical ventilator.
Reactive arthritis - joint pain and Reiter’s syndrome
may also follow acute campylobacter diarrhea.
ii. Campylobacter fetus
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Opportunistic pathogen that causes systemic
infections in immunocompromised patients.
Oral route (POE)
Causes bacteremia and systemic infection.
Capsule-like structure on the surface of the
organism.
V.
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Helicobacter pylori
This bacterium is a common question in revalida! 
MORPHOLOGY and IDENTIFICATION
A. Typical Organisms
 Has multiple flagella at one pole and is actively
motile. (unlike Vibrio in which there is only one
flagella on its pole)
B. Culture
 Grows well in 3–6 days when incubated at 37°C in a
microaerophilic environment, as for C jejuni. (Most
of them are incubated at 37 to 42°C)
 The media for primary isolation include Skirrow’s
medium (same with Campylobacter) with
vancomycin polymyxin B, and trimethoprim (these
are the antibiotics contained in the Skirrow’s, which
inhibit the growth of gram-positive organisms),
chocolate medium, and other selective media with
antibiotics (e.g., vancomycin, nalidixic acid,
amphotericin).
 The colonies are translucent and 1–2 mm in
diameter. (Larger colonies (mm) than Vibrio which
are micrometer in size)
C. Growth Characteristics
 Oxidase positive and catalase positive.
 Motile, and is a strong producer of urease (an
enzyme that converts Urea into Ammonia and CO2
creating a positive color PINK). (Urease positive is a
very typical characteristic of Helicobacter; and this is
the one commonly asked in the revalida)
PATHOGENESIS and PATHOLOGY
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Compared with the polysaccharide capsules of
pathogens such as Neisseria meningitidis and
Streptococcus pneumoniae). In a mouse model of C.
fetus infection, the presence of the S protein as a
surface capsule correlated with the ability of the
bacteria to cause bacteremia after oral challenge and
cause death in a high percentage of the animals.
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GALISTE | GAOYEN | IBARRA | LAMORIN | LAYDA|LESCAIN |MANZANO | NGALNGALO
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H. pylori is the most common organism that causes
duodenal ulcer & gastric ulcer.
H. pylori also produces a protease that modifies the
gastric mucus and further reduces the ability of acid
to diffuse through the mucus.
H. pylori produces potent urease activity, which
yields production of ammonia and further buffering
of acid.
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H. pylori is quite motile, even in mucus, and is able to
find its way to the epithelial surface.
H. pylori overlies gastric-type but not intestinal-type
epithelial cells.
Toxins and lipopolysaccharide may damage the
mucosal cells, and the ammonia produced by the
urease activity may directly damage the cells.
In Acute H. pylori infection, the patient will experience
abdominal pain  if left untreated; it will lead to chronic
H. pylori infection  Chronic H. pylori infection will lead
to three complications 
(1) Antral predominant gastritis,
(2) Nonatrophic pangastritis,
(3) Corpus-Predominant Atrophic Gastritis
(CPAG)
Once H. pylori enters the host it will invade the GIT  it
will release urease (survival)  Ammonia production
which further buffer the acid  pH becomes less acidic
 which in turn signal your parietal cells to secrete more
acid  ulcer
 In CPAG, corpus part of the stomach will undergo
atrophy then it will lead to Intestinal metaplasia (change
of lining epithelium)  then Dysplasia  Gastric cancer
The Chronic H. pylori complication that leads to duodenal
ulcer is the Antral Predominant Gastritis.
CLINICAL FINDINGS
It also has flagella (motility)  travels to intestinal
epithelial cells  it will adhere to the cells  from where
it attaches it releases also toxins (damage the host) 
they go to epithelial cell cytoplasm  intracellular
replication  while undergoing replication they will try
to destroy the mucosa and they create crater/ ulcer
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Acute infection: Upper gastrointestinal illness with
nausea and pain, vomiting and fever may also be
present.
The acute symptoms may last for less than 1 week
or as long as 2 weeks.
After colonization, the H pylori infection persists for
years and perhaps decades or even a lifetime.
About 90% of patients with duodenal ulcers and 50–
80% of those with gastric ulcers have H pylori
infection.
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[So if you are asked which one is more common
ulcer (by H. pylori) the answer is DUODENAL ULCER
(90%)]
Before you get to be diagnosed with Ulcer, you have
to undergo Endoscopy  Endoscope inserted to
your mouth going down to your GIT and they will try
to visualize (through video) if there’s ulcer in your
stomach or duodenum (Endoscopy or gastroscopy)
 if there’s ulcer, the Doctor will take a tissue
sample from that ulcer  Tissue sample will be
examined by the Pathologist (biopsy)  and if
there’s dysplastic or malignant changes seen  you
will be diagnosed with gastric cancer.
G. Diagnosis urea breath tests
DIAGNOSTIC LABORATORY TESTS
A. Specimens Gastric Biopsy
o Stool samples may be collected for H. pylori
antigen detection.
B. Smears
o A gastroscopy procedure with biopsy is required.
o Spiral-shaped organisms.
C. Culture
D. Antibodies
o The serum antibodies persist even if the H. pylori
infection is eradicated, and the role of antibody
tests in diagnosing active infection or after
therapy is therefore limited.
The presence of H. pylori will result in an increase in the
ratio of 13CO2 to 12CO2 in expired breath. (Breath smells
like urine).
E. Rapid tests to detect urease activity.
F. Gastric biopsy with a color indicator.
o If H pylori is present, the urease rapidly splits the
urea (1–2 hours), and the resulting shift in pH
yields a color change in the medium. In vivo tests
for urease activity can be done also.
 CLOtest (Positive= RED by Urease)
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SAMPLEX
Identification:
1. Responsible for the motility of V. cholerae.
2. It is the adaptation of living organisms to
conditions of high salinity.
3. 2 strains of V. cholerae that causes cholera in
humans.
4. Toxins released by A. hydrophila.
5. Identify the shape of C. jejuni in gram staining.
6. Identify the selective medium for C. jejuni.
7. Identification. What is the motility of
Campylobacter jejuni?
8. Identification. Best specimen for H. pylori
9. What is the appearance of Vibrio on TBCS
media?
True or False
1. Antibodies to the H antigen are highly involved
in the protection of susceptible hosts against V.
cholerae toxin.
2. V. paraheolyticus grows well on TCBS, where it
yields yellow colonies.
3. Even a 102 concentration of V. cholerae can
induce diarrhea.
4. Plesiomonas can be distinguished from shigellae
in diarrheal stools by the oxidase test with a
positive result.
5. Campylobacter jejuni atmosphere and temp is,
microaerophilic and 42°C
6. Campylobacters can form spores as part of their
virulence factor.
7. Gastric ulcer is the most common ulcer found in
patients with H. pylori infection.
8. Serum antibodies do not persist if the H. pylori
infection is eradicated.
Multiple choice
1. Among the three complications of Chronic H.
pylori infection, which one will lead to duodenal
ulcer?
a. Corpus-predominant atrophic gastritis
b. Nonatrophic pangastritis
c. Antral predominant gastritis
2. Which of the following means positive in H.
pylori? (Choose the correct answer/s)
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a. Color yellow in CLOtest
b. Increase in the ratio of 13CO2 to 12CO2
in expired breath
c. Dysplastic cells seen during biopsy
d. Pink reaction in Urease Test
3. An enzyme produced by the H. pylori, which
modifies the gastric mucus and further reduces
the ability of acid to diffuse through mucus.
a. Urease
b. Nuclease
c. Protease
d. Pepsin
4. What antibiotics are used in the primary
isolation of H. pylori, which inhibit the growth of
gram-positive organisms?
a. Vancomycin polymyxin B
b. Trimethoprim
c. Clarithromycin
d. A and B
e. A and C
5. Which of the following/s is/are true about H.
pylori?
a. It has flagellum at one pole and is
actively motile
b. Grows well in 3-6days when incubated
at 39°C in microaerophilic environment
c. Oxidase positive and catalase negative
d. Colonies are translucent and 1-2mm in
diameter
e. All of the above are true
6. Which of the following statement/s is/are true
about the clinical findings of H. pylori infection?
a. Acute illness includes nonspecific
symptoms such as nausea and vomiting,
abdominal pain and sometimes fever
b. Acute symptoms may last for less than 1
week or as long as 4 weeks.
c. About 90% of the patient with gastric
ulcers have H. pylori infection
d. H. pylori is not considered as a risk
factor for the development of gastric
carcinoma
e. None of the above are true
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7. A stool specimen from 5 years old child is
cultured in selective media having high pH
concentration. After the incubation, colonies
appear smooth and round and identified as a
comma-shaped, gram-negative, motile bacteria.
Name the bacteria isolated?
a. Aeromonas spp
b. Pseudomonas aeruginosa
c. Streptococcus pyogenes
d. Vibrio cholerae
8. Vibrio cholerae causes Cholera and mostly
occurs in developing countries, symptoms
include diarrhea and vomiting within 2-3 days
after the ingestion of contaminated water or
food. Name the type of diarrhea caused by V.
cholerae?
a. Acute watery diarrhea with blood
b. Acute watery diarrhea resembling rice
water
c. Mild watery diarrhea resembling rice
water
d. Acute watery diarrhea with no blood
9. What is the most common food that causes
foodborne
gastro-enteritis
by Vibrio
parahaemolyticus?
a. Chicken
b. Fish
c. Oysters
d. Rice
10. Which of the following statements is/are not
correct about Aeromonas spp and Plesiomonas
spp?
a. Both are oxidase positive
b. They can be found in freshwater and soil
c. They are gram-negative rods
d. Grow well on TCBS.
11. Campylobacter jejuni is one of the most common
causes of food poisoning, which also has been
associated with post diarrheal syndrome, the
syndrome is called ________?
a. Toxic shock syndrome
b. Guillain-Barre syndrome
c. Short bowel syndrome
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d. Rett syndrome
12. Campylobacter jejuni is a microaerophilic
bacterium, which of the following statement is
true for the culture of this bacterium.
a. An atmosphere increased O2 (10%) with
added CO2 (5%)
b. An atmosphere of reduced O2 (5%) with
added CO2 (10%)
c. An atmosphere of reduced CO2 (5%) with
added CO2 (10%)
d. An atmosphere of increased CO2 (10%)
with added O2 (5%)
13. What is/are not the growth characteristics
of Campylobacter spp? Select from all the
options given below.
a. Oxidase and catalase positive
b. Produce H2S
c. Ferment carbohydrates
d. Have darting motility
14. Helicobacter pylori is associated with all of the
following, EXCEPT?
a. Malt lymphoma
b. Gastric carcinoma
c. Peptic ulcer
d. Burkitt’s lymphoma
15. Which one of the following virulence factors may
be associated with the pathogenesis of infection
caused by Helicobacter pylori?
a. Flagella
b. Lipopolysaccharide
c. Exotoxins
d. Endotoxins
16. Which one of these is not the common
laboratory tests for the identification of
Helicobacter pylori?
a. Biopsy test
b. Urease breath test
c. Stool antigen test
d. Urine test
17. Which of the following biotypes of Vibrio
cholerae is prevalent in developing countries?
a. EL Tor
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b. Classic
c. Biotype O139
d. Biotype O1
18. Aeromonas hydrophila mostly causes infections
to fish and amphibians and less pathogenic to
humans, one of the most common infection in
human is gastroenteritis. What is the other
common human disease caused by bacteria?
a. Peptic ulcer
b. Cellulitis
c. Asthma
d. Gastritis
19. Helicobacter pylori infection is most prevalent in
developing countries, in what age people the
chances of infection is the highest?
a. 10 to 30
b. 30 to 50
c. 60 and above
d. Infant
20. Vibrio vulnificus and V. parahaemolyticus both
gram-negative, motile bacteria are mostly found
in warm coastal areas. What is/are the common
source through which these bacteria can be
transferred to human and cause infections?
a. Water
b. Oysters
c. Shellfish
d. All of the above
21. ________ is less likely to cause gastroenteritis or
diarrheal disease in humans.
a. Vibrio spp
b. Salmonella spp
c. Plesiomonas spp
d. Campylobacter spp
b. A medium containing vancomycin,
polymyxin B, and trimethoprim
incubated at 42°C.
c. MacConkey agar medium incubated at
37°C.
d. Thiosulfate-citrate-bile-sucrose medium
incubated at 42°C.
23. The V. cholerae factor responsible for diarrhea is
a toxin that
a. Blocks EF-2
b. Yields increased intracellular levels of
cAMP
c. Cleaves SNARE
d. Blocks EF-1-dependent binding of
amino-acyl-tRNA to ribosomes
24. A patient presents to the emergency department
with non-bloody diarrhea for 12 hours. The
patient lives in Washington, DC, and has not
recently traveled out of the area. Which one of
the following is unlikely to be the cause of your
patient’s diarrhea?
a. Aeromonas spp
b. C. jejuni
c. H. pylori
d. V. cholera
25. This BIOTYPE that produces a hemolysin gives
positive results on the Voges-Proskauer test and
sensitive to Polymixin B
a. El Tor
b. Classic
c. Inaba
d. Ogawa
22. A 45-year-old man develops a gastric ulcer that
can be visualized on a contrast mediumenhanced radiograph of his stomach. A biopsy
specimen is taken from the gastric mucosa at the
site of the ulcer. A presumptive diagnosis can be
reached most rapidly by inoculating part of the
specimen on which of the following?
a. A medium used to detect urease
incubated at 37°C.
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Answers:
Identification
1. Polar flagella
2. Halotolerance
3. V. Cholerae strains sero groups 01 and O139
(Bengal strain)
4. Cytotoxin and hemolysin
5. Comma/ S/ Gull Wing shape, Small curved rods
6. Skirrow’s Medium
7. Darting motility
8. Breath and stool
9. V. cholerae appears yellow (ferment sucrose),
other spp are blue-green (non-sucrose
fermenters)
21.
22.
23.
24.
C
A
B
D
True or false
1.
2.
3.
4.
5.
6.
7.
8.
False – not really involved
False – green colonies
False – needs large concentration
True
True
False
False
False
Multiple choice
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
C
B, C, D
C
D
D
A
D
B
C
D
B
B
C
D
D
D
A
B
C
D
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