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ID Week 5 > ICL 2.21: Helicobacter, Campylobacter & Vibrio > Flashcards

ICL 2.21: Helicobacter, Campylobacter & Vibrio Flashcards

1
Q

what is the causitive agent of gastric ulcers?

A

helicobacter pylori

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2
Q

what did people used to think caused gastric ulcers?

A

Excess acid, smoking, stress, spicy foods

these are now recognized as AGGRAVATING, not causal, factors

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3
Q

what is the microbiology of helicobacter pylori?

A

gram (-) helical rods

microaerophilic = tiny little bit of oxygen

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4
Q

are helicobacter pylori motile??

A

yes

tufts of several polar flagella (4-7)

highly motile!!

corkscrew motility like spirochetes but different mechanism

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5
Q

how is helicobacter pylori transmitted?

A

fecal-oral and oral-oral

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6
Q

is carriage with helicobacter pylori common?

A

incidence of carraige in developing countries is high

it’s lower in developed countries

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7
Q

how does H. pylori enter into the acidic stomach?

A

the stomach lumen is really acidic so it’s a pretty hostile environment so H. pylori overcomes this by:

  1. production of urease which converts urea to NH3 + CO2

NH3 raises the pH in the immediate vicinity of the bacteria and acts a buffer

  1. flagella

H. pylori is highly motile, can quickly reach the mucin layer

the mucin layer is mostly negatively-charged sulfated polysaccharides, acts as buffer to protect gastric epithelial cells – it has a neutral pH 7

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8
Q

what mechanisms does H. pylor use to reach the gastric epithelium from the lumen of the stomach?

A

so the problem is that the mucus in the mucin layer of the stomach is really thick and viscous and hard to get through so to overcome this H. pylori:

  1. has flagella which confer corkscrew motility on the helical cells
  2. express mucinase and phospholipases to liquify the mucus
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9
Q

how does H. pylori colonize the gastric epithelium?

A

so the problem is that stomach contents flow through the GI system so H. pylori colonizes the gastric epithelium by:

  1. expression of adhesins like:

BabA which binds Lewis b Ag

SabA which binds sialyl Lewis X

HpaA which binds neuraminyl-lactose

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10
Q

how does H. pylori evade the immune system?

A
  1. catalase, arginase and superoxide dismutase detoxify ROS produced by immune cells
  2. H. pylori LPS not very toxic or immuno-genic, looks like “self” (carbohydrates identical to Lewis antigens x and y)
  3. H. pylori flagellin is poorly recognized by TLR5
  4. VacA protein inhibits T cell proliferation, interferes with B-cell Ag presentation.
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11
Q

how does H. pylori cause damage?

A
  1. ammonia produced by urease damages host cells
  2. cytotoxin VacA causes influx of cations in vacuoles – gastric cells swell and die; also loosens junctions between epithelial cells
  3. colonization itself may elicit inflammatory response, with infiltration of submucosal tissues by immune cells
  4. NAP (neutrophil activation protein) activates immune cells to produce ROI
  5. CagA phosphorylates host proteins, promoting activation of NF-kB and production of IL-8 (crucial determinants of chronic inflammation)
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12
Q

what serious illness is H. pylori linked to?

A

gastric cancer

H. pylori has mutagenic properties that trigger DNA ds-breaks and DNA damage which leads to cancer!

CagA (+) strains are particularly associated with cancer risk

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13
Q

how does H. pylori cause gastric cancer?

A
  1. colonization of stomach by H. pylori
  2. after a few weeks/months the bacteria causes chronic superficial gastritis
  3. then you can get either:
    - chronic atrophic gastritis –> gastric adenocarcinoma –> proliferation in the prescence of ROS and RNS results in DNA damage and mutation
  • lympoproliferative disease –> B cell MALT lymphoma
  • peptic ulcer disease
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14
Q

how do you diagnose H. pylori?

A
  1. silver stain of gastric epithelial cells = small curved rods associated with the surface of gastric epithelial cells
  2. urease test/staining/culture of biopsy = invasive
  3. serologic test, urea breath test = non-invasive
  4. culture/PCR
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15
Q

how do you culture H. pylori?

A

3 days for isolated colonies to appear, under reduced O2 / increased CO2 @ 37oC on BAP (blood agar plate)

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16
Q

how do you treat H. pylori?

A

NIH recommends that all patients with gastric or duodenal ulcers caused by H. pylori be treated with antimicrobials

but with the antibiotics you need to include a proton-pump inhibitor!!!

this is because PPIs don’t work well at low pH aka the stomach

but if someone has an asymptomatic H. pylori infection you actually shouldn’t treat them because it appears to offer protection from gastroesophageal reflux disease and adenocarcinomas of the lower esophagus and gastric cardia

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17
Q

what are the key virulence factors of H. pylori?

A
  1. flagella

motility, immune evasion because not seen by TLR5

  1. urease

resistance to acidic environment of the stomach

  1. LPS

low toxicity and immunogenicity

  1. adhesins

allow retention on gastric mucosa

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18
Q

what’s the microbiology of campylobacter?

A

gram (-) spiral shaped rods

urease negative

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19
Q

what disease state does campylobacter jejuni cause?

A

1 (or #2) cause of bacterial gastroenteritis in US

it’s either this or salmonella depending on who you ask

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20
Q

what are the symptoms of a campylobacter jejuni infection?

A
  1. fever
  2. abdominal pain that can mimic appendicitis
  3. diarrhea (often bloody)

symptoms are self-limiting; only last a week

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21
Q

how is campylobacter jejuni transmitted?

A

transmission via contaminated food, milk, water

especially chicken

person-person spread is rare

22
Q

what is the pathogenesis of campylobacter jejuni?

A

damages mucosal surfaces of the jejunum and colon

mucosal surface appears ulcerated and bloody

there’s also cryptic abcesses in epithelial glands and infiltration of lamina propria with neutrophils, monocytes and eosinophils

however the virulence factors are poorly defined

23
Q

what toxin is associated with C. jejuni?

A

cytolethal distending toxin (CDT)

it delivers DNAse (CdtB) to host cell, blocking mitosis and in some cells triggering apoptosis

it has DNAse activity

it induces cell cycle arrest and death in intestinal and T-cells

induces production of IL8

24
Q

what are the important virulence factors of C. jejuni?

A
  1. capsule = immune vasion
  2. invasion factors = immune evasion, tissue damage
  3. adhesins = adherence to mucus and gastric cells
  4. toxin = CDT
  5. flagellum = motility, poorly recognized by TLR5
  6. LOS
25
Q

what is Guillain-Barre syndrome and which bacteria is it associated with?

A

C. jejuni

can be triggered by other bacteria as well (Haemophilus influenzae, Mycoplasma pneumoniae) and some viruses

causes paralysis which can last for several weeks

this is due to demylination of nerves because of autoimmune syndrome

this autoimmune response happens because the C. jejuni LOS looks identical to myelin gangliosides to out antibodies start attacking our nerves

26
Q

how do you treat Guillain-Barre syndrome?

A

plasma exchange

respirator if necessary

corticosteroids

27
Q

how do you diagnose C. jejuni infection?

A
  1. gram stain = thin, spiral shaped pink rods
  2. ELISA for campylocater common antigen
  3. culture from stool sample
28
Q

in what conditions is C. jejuni cultured?

A

takes 2-3 days for isolated colonies to appear

they need reduced O2 and increased CO2

42 C on selective medium –> 42 C is the body temperature of a chicken

29
Q

how do you differentiate H. pylori vs. C. jejuni?

A

H. pylori = urease (+), has several flagella and grows at 37 C

C. jejuni = urease (-), 1 flagella, grows at 42 C

30
Q

FLASHCARD: C. jejuni

A

1/2 cause of bacterial gastroenteritis

small, gram (-) curved rod

fastidious, microaerophilic

resembles h. pylori BUT only has 0-1 flagella, grows at 42 C, and is urease negative

zoonosis = contaminated food, unpasteurized milk, contaminated water

can cause the autoimmune disease Guillain-Barré Syndrome = paralysis because C. jejuni LOS resembles carbohydrates on surface of nerve cells

virulence factors are not well characterized –> produces a DNase toxin (CDT)

31
Q

what pathogen caused this?

overall good health presents with abdominal discomfort and diarrhea

for preceding 2d, intermittent, crampy periumbilical abdominal pain

For preceding week, mild abdominal discomfort and 3 loose bowel movements/day

Denied: drinking well water, having fever, blood in stool, recent antibiotic use, relation of pain to meals, dysuria or hematuria

remembered eating chicken at a banquet over a week earlier

stool sample contained white blood cells

A

C. jejuni

32
Q

what pathogen caused this?

kid brought to ED in Haitii because 10 h vomiting and diarrhea

Admitted; shared a cot with a pediatric patient who had similar symptoms

BP and temp were not obtained (lack of equipment), but did not feel warm

Skin recoil was less than 1 second but not instantaneous = dehydrated
mild abdominal tenderness

Stool sample was translucent fluid with small flecks of mucus = “rice water” appearance –> no feces, no blood, no WBCs

Culture of stool sample yielded Gram-negative, comma-shaped bacteria after 24 h growth (result obtained 1 wk later)

Patient fully recovered after 4 d rehydration therapy – also treated with azithromycin to reduce risk of spread

A

vibrio cholerae

33
Q

what’s the microbiology of vibrio cholerae?

A

comma-shaped gram (-) rod

facultative anaerobe

34
Q

is vibrio cholerae motile?

A

yes

single-long polar flagellum

35
Q

how do you acquire a vibrio cholerae infection?

A

ingestion of contaminated water, food or improperly cooked seafood (shellfish)

John Snow did the well experiment and realized it was coming from a specific well = contaminated water

36
Q

what is the clinical presentation of vibrio cholera?

A

abrupt onset of watery diarrhea and vomiting –> 1L/hr!!!!

stools are rice water and loaded with mucus

severe dehydration; skin loses plasticity

metabolic acidosis

hypokalemia = loss of K+

hypovolemic shock

cardiac arrhythmia, kidney failure

37
Q

what is the mortality rate of V. cholerae?

A

60% if not treated within HOURS

<1% if treated though

38
Q

does V. cholerae cause disease via immune response or toxins?

A

it’s a toxin-mediated disease!!!

the toxin is specified by ctxAB genes –> if there isn’t this gene to code for the toxin then there’s no diarrhea!

ctxAB genes are expressed by the O1 and O139 serotypes

39
Q

what type of toxin does V. cholerae have? how does it work?

A

Ctx is a A-B type exotoxin

B binds to ganglioside GM1 on surface of intestinal cells

then A is internalized and ADP-ribosylates Gsα protein

normally Gsα is a GTP-hydrolyzing protein that regulates host adenylate cyclase and therefore cAMP levels

but ADP-ribosylation of Gsα by Ctx locks it in the “ON” phase, so host adenylate cyclase always produces cAMP

this leads to hypersecretion of water and electrolytes (Cl-, Na+, HCO3-)

40
Q

what are the steps in the patholgenesis of V. cholerae?

A
  1. ingestion
  2. goes through stomach rapidly using its flagellum
  3. adheres to and colonizes small intestine using several adhesins
  4. production of toxins = Ctx, Zot, Ace
  5. extensive fluid and ion loss from tissues leading to hypotension, electrolyte imbalance and death
41
Q

what is the size of the inoculum required to get a V. cholera infection?

A

ID50 is really big….

size of inoculum is crucial because bacterium is acid-sensitive

42
Q

how do you treat V. cholerae infections?

A

rehydration and electrolytes are essential and urgently needed

antibiotics are often used to shorten the course of the disease and reduce spread, but are not required

43
Q

what kind of diarrhea is associated with vibrio cholerae?

A

secretory diarrhea = copious watery stool

no blood or WBCs

44
Q

what kind of diarrhea is associated with campylobacter?

A

dysentery = low volume, blood mucus +/- WBCs

45
Q

what are the clinical symptoms of Ctx+ V. cholerae?

A

abrupt onset of watery diarrhea, can progress to severe dehydration, metabolic acidosis, hypokalemia, hypovolemic shock

46
Q

what are the clinical symptoms of Ctx- V. cholerae?

A

Gastroenteritis, milder form of watery diarrhea

47
Q

what are the symptoms of V. parahaemolyticus?

A

1 US cause of seafood-associated gastroenteritis = raw oysters!

Explosive onset of watery diarrhea within 24 h of exposure (not as high volume as cholera)

Nausea, vomiting

Abdominal cramps

Headache and low grade fever

self limiting = 3 days

treatment = rehydration

48
Q

what are the virulence factors for V. paraheomolyticus?

A
  1. hemolysin
  2. flagellum
  3. capsule
  4. other exotoxins
49
Q

what are the symptoms of a V. vulnificus infection?

A

1 cause of seafood-related US deaths

symptoms after ingestion in otherwise-healthy patients:

  1. diarrhea
  2. nausea
  3. vomiting
  4. abdominal cramps

in immunocompromised patients:

  1. bacteremia
  2. fever/chills
  3. low BP = shock
  4. blistering skin lesions (vulnificus!)

in BOTH healthy and immunocompromised patients it’ll cause necrotizing fasciitis if it enters a wound

50
Q

what are the virulence factors of V. vulnificus?

A
  1. capsule = antiphaogcytic, complement resistance
  2. cytolysin/hemolysin = tissue damage
  3. metalloprotease
  4. siderophores
  5. RtxA toxin
  6. flagellum
  7. pilus
51
Q

what are the 3 main vibrio species that cause gastroenteritis?

A
  1. V. parahaemolyticus
  2. V. volnificus
  3. V. cholerae

O1 and O139 serotypes are Ctx+ and cause cholera – other serotypes are Ctx– and cause gastroenteritis

52
Q

are vibrio infections toxin or immune mediated diseases?

A

toxins are mainly responsible for clinical manifestations

ID Week 5 (13 decks)

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