GI infections – Flashcards

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question
infectious agent in the stomach?
answer
Helicobacter pylori
question
infectious agents of the small intestine?
answer

Vibrio Cholerae

E. Coli (ETEC)

Salmonella Enteritidis

Salmonella typhi

Camplobacter jejuni

Yersinia enterocolitica

 

question
what are the infectious agents that live in the large intestines?
answer

Shigella dysenteriae

E. Coli (EHEC)

Vibrio parhaemolyticus

Clostridium difficile

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Infectious agents that lead to intoxication only?
answer

clostridium perfringens

Staphylococcus aureus

Clostridium botulinum

bacillus cereus

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enteric gram-negative bacilli
answer

Vibrio

Campylobacter

Helicobacter

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Heliobacter pylori
answer

Shape: slender, spirally curved rods

 

Type: Gram negative

 

Location/Habitat: human stomach mucosa (normal flora or disease)

 

Transmission: fecal-oral transmission (food or water-borne transmission)

 

Clinical manifestations: chronic gastritis and peptic ulcer dz; bacterial use flagella to invade and move below the epithelium; urease releases ammonium and protect the bacteria; colonization is most often asymptomatic, but some people develop an intense inflamm. response that leads to gastritis and peptid ulcer dz = associated with development of GASTRIC CANCER

 

Distinctive Properties: flagella (allows penetration into gastri mucus layer); CagA protein (kills cells and stimulates inflammation); adhesions

 

Exotoxins and exoenzymes: urease (neutralizes gastric acids and helps it get to base), acid-inhibitory protein, mucinase, and VacA cytotoxin (induces cell death in epithelial cells)

 

Diagnosis: gastric biopsies; serology; breath test and blood test; fecal antigen test

 

Treatment: best tx is sequential/combinational treatment with rabeprazole (proton pump inhibitor) and amoxicillin (for 5 days), THEN rabeprazole+clarithromycin+tinidazole (5 days)

 

Prevention: no vaccine

 

question
epidemiology of H. pylori
answer

by age 50, approx. 40% of Americans will be colonized.

 

A person who is colonized has a 10% chance of developing ulcers

 

*** Under-developed countries have higher colonization rates, but they have lower disease rates!

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Clinical manifestations/pathology of H. pylori
answer

after ingestion, the bacteria use their flagella to move beneath the mucin layer and attach to the gastric epithelium. --> the production of urease releases AMMONIA and protects the bacteria from the acidic pH

--> colonization is often ASYMPTOMATIC, but some individuals develop and intense inflammatory response that leads to gastritis and ulcer formation

 

vacuolating cytotoxin seems to play significant role in the inflammation

 

chronic gastritis is associated with development of gastric cancer!!

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CagA protein
answer

H. Pylori infection

 

surface complex injects THIS protein into host cells, killing the cell (needle-like structure injects this protein into host cell)

 

it is not present in all strains, but it is associated with the more VIRULENT strains

 

stimulates INFLAMMATION

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urease
answer

neutralizes gastric acids (because rxn leads to ammonia production = neutralization)

 

stimulates neutrophil and monocyte chemotaxis

 

helps H. pylori invade and tolerate the acidic environment

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VacA (vacuolating) cytotoxin
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induces vacuolation and cell death in epithelial cells


stimulates inflammation  (neutrophil migration)

question
13C-urea --> 13CO2 tests
answer

diagnosis of H. pylori

 

formerly used breath test (less sensitive0

 

now use it as a blood test


other methods of diagnosing H. Pylori:  serology (tells you past or present infection); and fecal (stool) antigens test

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what is helicobacter similar to?
answer
Campylobacter, which is still more distant taxonomically to Vibrio and E. coli
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what is Vibrio most closely related to?
answer

E. Coli and the other enterobacteriaceae

 

(campylobacter and helicobacter are more distant)

question
shape of Listeria?
answer

small gram-positive coccobacilli - short rods

 

NO SPORES

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organisms that live in soil-plant environments
answer

Listeria

Bacillus

Clostridium

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Listeria monocytogenes
answer

Shape: small coccobacilli, short rods

 

Type: Gram positive

 

Location/Habitat: widespread in nature; soil-plant environments; considered normal flora in domestic animals; in animal feces

 

Transmission: contaminated commercially-prepared food (remember: they are facultative anaerobes and are psychrophilic); humans must ingest; often spread through animal feces, so may be considered zoonotic; transplacental transmission from mother to fetus

 

Clinical manifestations: 1) Ingestion of L. monocytogenes in food 2) replication in intestinal epithelial cells with invasion into submcosa

3) replication in macrophages in submucosa

4) asymptomatic to flu-like symptoms, nausea, vomiting 5) bloodstream invasion with spread to meninges (immunocompromised or very young) (replication in macrophages)

6) Transplacental spread to developing fetus with septicemia and meningitis (replication in macrophages)

 

Distinctive Properties:  beta-hemolysis due to listeriolysin (lyses phagosome membrane so that organism can get into macrophage cytoplasm and replicate); ActA (actin polymerization on one end of bacterium; intracell. movement)

 

Diagnosis: 1) monocytosis in peripheral blood and CSF (remember: elevation in MONOCYTES and not neutrophils)

2) Gram stain of CSF

3) Culture of CSF, blood = definitive (blood agar)

4) early detection is rare, esp. when you have asymptomatic individuals

 

Treatment: ampicillin, TMP-SMX, high-dose penicillion, erythromycin (in immunocomp., elderly, neonates)

 

it is CEPHALOSPORIN resistant!!!!

 

Prevention: 1) no vaccine 2) limit those types of foods in pregnant women and the immunocompromised

3) strict adherence to standard pathogen control programs in food industry

4) new products to kill the Listeria in the food (i.e. bacteriophage Intralytix that kills only the listeria)

question
listeriolysin
answer

Listeria Monocytogenes

 

this enzyme couses β-hemolysis in blood agar

 

it lyses the phagosomal membrane and allows the pathogen to escape the phagosome and enter cytoplasm of macrophages

 

Remember: L. monocytogenes doesn't like to kill the macrophage, it just wants to get into the cytoplasm so it can replicate

question
ActA
answer

found in Listeria monocytogenes


leads to actin polymerization ON ONE END of the bacterium = intracellular movement



similar process in Shigella, but Shigella is in epithelial cells


spreads from cell to cell without ever exiting into the extracellular environment

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Epidemiology of Listeria monocytogenes
answer

major concern in the food industry


outbreaks associated with: milk, cheeses, hot dogs, luncheon meats, fresh vegetables, smoked fish products


READY TO EAT FOODS


significant increase in hospilitization rates


disease depends on dose, age, and immune status

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Listeria disease in Healthy adults
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usually asumptomatic or mild flu-like diarrheal illness

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incubation period = 1-2 days - appears to be shorter with invasive disease

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symptoms associated with eating a large dose of Listeria

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most common form of disease, but the least recognized

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referred to as listeria gastroenteritis (b/c intestinal manifestation part of presentation

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*** fever, headache, nausea, vomiting

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rarely diagnosed without multiple cases

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Listeria disease in immunocompromised, elderly adults, and neonates
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severe invasive disease

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incubation period typically 2-3 weeks and from eating a SMALL dose

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may be preceded by flu-like GI symptoms

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blood stream invasion = septicemia, encephalitis, meningitis

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AIDS patients are 300x more likely to get invasive listeriosis

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Listeriosis in pregnant women and the fetus
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mild to severe invasive disease

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pregnant women have 20x higher risk of infection

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similar flu-like disease as other healthy adults

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bloodstream invasion (non systemic symptoms in mother)

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TRANSPLACENTAL TRANSMISSION TO FETUS

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*** rarely a problem for the mother, but serious problem for the fetus:

1) first trimester spontaneous abortions

2) stillbirth or seriously ill newborn

3) third trimester - may cause premature delivery

question
bacteria transmitted transplacentally and cause infection in utero
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Listeria monocytogenes - listeriosis

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Treponema pallidum - congenital syphilis

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Borrelia burgdorferi - Lyme disease

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Listeriosis in Neonates
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*** Severe invasive disease - meningitis

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1) Early onset (;2days postpartum) = acquired transplacentally; septicemia, pneumonia, meningitis; granulomas; 80% mortality rate

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2) Late onset (1-2 weeks postpartum) = acquired at or soon after birth (not sure from where: birth canal or transmission from other babies); blood stream invasion = meningitis; good evidence for hosptial acquired infections

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What antibiotic is Listeria resistant to?
answer
cephalosporin
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spore forming bacteria?
answer

anaerobic: Clostridium


aerobic: Bacillus

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Clostridium perfringens
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Shape: spore forming rods; large non-motile with square, "box-car" ends

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Spores: subterminal spores; do not form spores in clinical specimens (in vitro or in tissue); they do sporulate in the intestines and in some foods

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Type: anaerobic Gram-positive

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Location/Habitat: soil; intestinal tract of humans and animals; isolated from intestinal tract and female genital tract

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Transmission:

1) Traumatic infections:

a) exogenous: contamination with dirt/dust

b) endogenous: escape of intestinal bacteria (stabbing and gunshot wounds)

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2) non-traumatic infections: ENDOGENOUS, simultaneous or idiopathic; spreads from intestinal tract WITHOUT OBVIOUS TRAUMA

;

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Clinical manifestations: 1) Anaerobic cellulitis - traumatic or non-traumatic;

Remember: ***localized to dead tissue, with little invasion of healthy tissue

*** lots of gas production

*** little alpha-toxin production

* common in patients with diabetes and/or poor circulation

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2) Myonecrosis - gas gangrene; traumatic or simultaneous

*** major alpha-toxin production; necrotizing invasion of healhty muscle

*** gas formation

*** may progress to bloodstream invasion, septicemia, intravascular hemolysis - fatal

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;

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Distinctive Properties: moderate anaerobes (more aerotolerant than C. tetani, for example); common in soil, intestinal tract of humans and animals; large nonmotile rod with square, "box-car" ends; subterminal spores (sporulate in intestines and in some foods); large amounts of gas production during growth

(CO2 + H2 plus foul smelling volatile amines such as putrescine and cadaverine); produces several lethal toxins (but only a few have definitive roles in disease); C. perfringens in 80-90% of clostridial infections

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Toxins: responsible for serious disease in humans and animals; strain typing based on toxinc profiles for ;,;,;,;-toxins

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Diagnosis:; rapid diagnosis is crucial; Lab: Anaerobic culture (24 hrs) - Look for beta-hemolysis (double zone: alpha-toxin and theta-toxin); gram stain

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Treatment:; debridement of necrotic tissue; ancillary measure - high doeses of penicillin; hyperbaric oxygen (alos effective against MRSA and invasive asperillgus); wound dressing with charcol for bad smell

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;Prevention: no vaccine; treat wounds to preven infection

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Enterotoxin:; 3rd most common cause of food poisoning (but these strains are uncommon); requires ingestion of contaminated food (esp. gravy, stews, and meat products) - they contain mixture of the organism and the preformed enterotoxin - -; LEADS to DIARRHEA and fever (look at another slide)

;

question
different exotoxins lead to different diseases. What are they?
answer

neurotoxic:

1) botulism (C. botulinum) 2) tetanus (C. tetani)

;

histotoxic:

1) gas gangrene (C. perfringens, novyi, C. septicum, C. histolyticum, others)

2) pseudomembranous colitis (C. difficile)

;

enterotoxic:

food poisoning (C. perfringens)

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;-toxin (alpha toxin)
answer

C. perfringens


=phospholipase C (lecithinase) - most important toxin in humans!!

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;

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beta hemolytic rxn in blood agar

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Nagler rxn on egg yolk agar

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Widespread tissue destruction

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;-toxin (theta toxin)
answer

C. perfringens


produced by most strains (human and animal)


beta-hemolysis - blood agar

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oxygen-labile hemolysin called perfringolysin O-in humans

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similar to tetanolysin (C. tetani) and streptolysin O (S. pyogenes)

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kills and lyses phagocytic cells

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Enterotoxin
answer

C. perfringens

;

may be produced by all toxin-type strains


FOOD POISONING


Fluid secretion, diarrhea

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(1-5% of all type A strains produce this toxin)

question
Transmission of C. perfringens
answer

1) Traumatic infections:

a) exogenous: most common as contamination of a wound with dirt/dust from environment

b) endogenous: escape of intestinal bacteria to other body sites following trauma (stabbing and gunshot wounds)

;

2) non-traumatic infections: ENDOGENOUS, simultaneous or idiopathic; spreads from intestinal tract to tissue, peritoneal cavity, and bloodstream WITHOUT OBVIOUS TRAUMA

question
Epidemiology of C. perfringens
answer

1) traumatic infections: typical trauma includes surgery, compound fractures, motor vehicle crashes, pressure sores, thermal or electrical burns, frostbite, injection of illicit drugs

;

(studies of war wounds show that 90% of contaminated wounds contain clostridial organisms, but only 2% develop disease)

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2) Non-traumatic infections: associated with over or occult malignancy (colorectal or hematologic);

***frequently mixed infections with C. perfringens, C. septicum, C. novyi

*mortality rates approaching 100%

question
Compare and contrast anaerobic cellulitis and myonecrosis
answer
[image]
question
enterotoxin in C. perfringens
answer

3rd most common cause of food poisoning (but these strains are uncommon);

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requires ingestion of contaminated food (esp. gravy, stews, and meat products) - they contain mixture of the organism and the preformed enterotoxin - -; LEADS to DIARRHEA

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Can also be formed in SMALL BOWEL; noninvasive

- incubation period is wide: 8-16 hours

- shorter period: if large amount of toxin is ingested

- longer period: if bacteria is ingested and toxin is produced in intestines

;

Diarrhea with fever, rare vomiting - SHORT DURATION

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Clostridium difficile
answer

Shape: longer and thinner rods

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Type: Gram positive; spore forming

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Spores: sporulate well in INTESTINES

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Location/Habitat: normal flora, but can be acquired during hospitalization; found in soil, water, and intestines of various animals

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Transmission: 1) Classical Dz: overgrowth of normal flora, but may be recent acquisition (from another person or the environement); induced by antibiotic treatment; person-environment-person transmission (rectal thermometers)

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2) Severe dz: new anti-biotic resistance - person-to-person (via fecal contamination containing cells or spores); person-environment-person transmission (rectal thermometers)

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Clinical manifestations: adherence to mucosa, growth, and toxin production IN COLON; mild to severe diarrhea; severe inflammation with destruction of colonic epithelial cells; ***yellow pseudomembrane in colon; ulceration of colon

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Distinctive Properties: Toxin A and Toxin B - lead to fluid secretion, inflammation, and cell death.; New NAP1 severe strains produce 20x more of these toxins; non-toxigenic C. diff (used prophetically); binary toxin (highly associated with NAP1 strains that cause more severe disease)

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Diagnosis: clinical presentation of diarrhea; yellow pseudomembrane on colonoscopy; C. diff antigen detection in stool sample (includes antigen detection of toxins A;B and glutamate dehydrogenase (GDH); Xpert C difficile PCR

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Treatment: metronidazole, vancomycin, fidaxomicin; re-establish normal flora via probiotics and fecal transplantation and non-toxigenic C. diff

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Prevention: no vaccine; non-toxigenic C. diff; WASH YOUR HANDS (gels don't work as well)

question
Toxin A and Toxin B
answer

Clostridium difficile

 

A= enterotoxin; B= cytotoxin

 

mechanism of action on intestinal epithelial cells

 

Covalent glycosylation of RhoGTPase = interferes with intracellular signaling:

  • inhibition of actin polymerization
  • disruption of tight junction
  • increased permeability = fluid loss
  • apoptosis
  • leads to fluid accumulation, cell death, and inflammation

Toxin B is 100x more cytotoxic than A (but can be avirulent)

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NAP1
answer

Clostridium difficile

 

SEVERE STRAINS produce 20x more of A and B toxins

 

This is a hypertoxin

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NTCD
answer

non-toxigenic C. difficile

 

isolated from diarrhea along with toxigenic C difficile

 

it is just normal flora

 

now use it prophylactically

question
Binary toxin
answer

C. difficile

 

highly associated with NAP1 strains that cause more severe disease

 

has 2 components

 

actin-specific ADP ribosyltransferase toxin

 

question
C. diff transmission induced by antibiotic treatment very commonly related to . . .?
answer

1) Very commonly related:

 

clindamycin, ampicillin/amoxicillin, cephalosporins, fluroquinolones

 

(especially new severe NAP1 strains)

question
C. diff transmission is less commonly related to . . .?
answer

2) other penicillins, TMP-SMX, cotrimoxazol, macrolides

 

3) uncommonly related to: vancomycin, metronidazole (these are the two often used for treatment)

question
Classical C diff disease
answer

Nosocomial diarrhea to severe, fatal, diarrhea, and colitis

 

Susceptible populations:

1) recent antimicrobial use (look at transmission)

2) length of stay (in healthcare facility)

3) Increasing age (primarily older people - ave. 60 yr)

4) serious underlying illness

 

Primarily in hospitalized patients, undergoing antibiotic theraby (antibiotic-associated)

question
Severe C diff disease
answer

new-antibiotic resistant - nocosmial or community-acquired diarrhea

 

increased cases with:

1) increased severity (higher mortality)

2) fluroquinolone resistance

3) higher amounts of A and B toxin production

4) new toxin not found in classical strains

 

2003 increased cases in Quebec hospitals

 

isolated outbreaks in US and around the world with this new increased severity (high toxin producers), antibiotic resistance patterns (single epidemic strain -B1/NAP/027)

 

Community associated cases now observed (20% of total, half with no prior antibiotic use and in younger populations

 

another risk factor: proton pump inhibitors (omeprazole and esomeprazole)

question
Human members of the reovirus family
answer
Genus orthoreovirus

Genus rotavirus

Genus coltivirus
question
Orthoreovirus genus?
answer
respiratory- enteric- orphan virus

Three antigenic serotypes transmitted by respiratory and fecal- oral routes

Infections are asymptomatic and not important for disease

(also called orphan - - without disease)
question
Coltivirus genus
answer

named for Colorodo tick fever virus

 

arbovirus transmitted by ticks

question
Rotavirus
answer

2 shells: Naked outer icosahedral and inner icosahedral capsid

 

Segmented, double stranded RNA genome = this segmented genome allows for reassortment

 

Associated with viral RNA dependent RNA polymerase

 

Multiple genotypes/serotypes

 

Transmitted by the fecal oral route (which is most important), but also transmitted by vomit

question
what is the importance of the segmented genome of Rotavirus??
answer

segmented genomes allow for "genome reassortment" within cells infected with 2 distinct strains

 

Repeated infections = greater immunity

 

also allows for production of "live"-oral reassortant vaccines based upon naturally-attenuated animal rotavirus and important human serotypes of rotavirus

question
what age groups are most affected by rotavirus? but norovirus?
answer

R= little children, especially those under 5 years of age

 

N= everyone else

question
lab analysis of Rotavirus??
answer

antigen-capture ELISA of a FECAL specimen

 

usually done on infants who present to the ER with severe dehydration during the virus' peak time

question
speculated pathogenesis of Rotavirus?
answer

virus infects cells at the villus tip and then spreads quickly --> viral particles get released into lumen --> infected cells are damaged and lost and immature cells have reduced absorptive capacity = fluid accumulation in lumen = DIARRHEA


another theory: non structural protein 4 is an enterotoxin that affect Ca2+ homeostasis

question
Rotavirus vaccines!!!
answer

reassortant virus isolate containing 10 bovine virus dsRNA segments plus 1 human virus segment

 

encodes for either the major outer capsid protein : G1,G2, G3, G4 or for one major P protein serotype

 

bovine vaccine is safe; rhesus rotavirus vaccine was associated with greater rates of intussusception

question
RotaTeq®
answer

pentavalent "live" vaccine for rota virus

 

3 doses

 

perviously licensed rheusus-human tetravalent reassortant vaccine was removed after rare intussusception complications

question
Rotarix®
answer

live attenuated vaccine, containing a single attenuated human rotavirus with the major G1 serotype

 

2 doses (admission)

question
other causes of viral gastroenteritis
answer

noroviruses - no evidence of compound immunity - genus is caliciviridae; it is major cause of viral fastroeneritis in older children and adults


astroviruses - less severe dz in infants and young children (less severe than rota)


adenoviruses: serotypes 40,41, and 31 - replicate in GI tract (but minor cause of dz in infants)


enteroviruses (ex: polio) - members of genus Picornaviridae - rarely symptomatic because of lytic infection in small intestine, but can cause some symptoms in infants (they replicate in the GI, but usually asymptomatic)

question
norovirus
answer

major infectious cause of FOODBORNE ILLNESS OUTBREAKS, but associated with less mortality and morbidity


it is environmentally stable - virons are resistant to inactivation by chlorine and heating compared to other naked icoshedral viruses


multiple genotypes/serotypes with lack of long lasting immunity


typical incubation period = 24-48 hrs


predominant symptom : acute onset EMISIS


other symptoms: watery, non-bloody diarrhea

 

occurs ALL YEAR LONG

 

tx: replace fluids (no specific antiviral)

 

no routine lab assays/diagnosis, but use RT-PCR for ID in epidemilogical studies or use electron microscopy

 

NO LISCENCED VACCINE

question
general features of the enterobacteriaceae
answer

enteric gram-negative bacilli; gram-negative rods

 

found widely distributed on plants, in soil, and in the intestines of animals and humans

 

rapid growth under both aerobic and anaerobic conditions

 

differentiation based on fermentation of various carbohydrates (ALL SPECIES FERMENT GLUCOSE)


can be motile (flagella) or nonmotile


associated with many different types of human infections, including: intestinal, urinary, respiratory, wound, bloodstream, and meningeal infections


They are the major cause of NOSOCOMIAL INFECTIONS

question
all enterobac. ferment what??
answer
GLUCOSE
question
enterobact. pathogens
answer

major pathogens: Escherichia, Shigella, Salmonella

 

Opportunistic pathogens: Klebsiella, Proteus, Enterobacter, Serratia, Providencia, others

question
bacteria that are rapid lactose fermenters?
answer
Escherichia, others (coliforms)
question
lactose non-fermenters
answer

Shigella

 

salmonella

question
antigenic analysis (serotyping)
answer

O-antigen: somatic antigen (carbohydrate repeat of LPS)

 

H-antigen: flagella (if present)

 

K-antigen: polysaccharide capsule (if present)

 

fimbriae (may have more than one type - not for serotyping)

 

(these are virulence factors, but they are also used for serotyping)

question
Escherichia coli
answer

 

Shape: bacilli, rods

 

 

Type: Gram negative

 

 

Location/Habitat:

 

Transmission:

 

Clinical manifestations:

 

Distinctive Properties: 

 

Diagnosis:

 

Treatment:

 

Prevention:

 

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