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(mostly) Gastrointestinal Flashcards

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1
Q

What are some common features of Enterobacteriaceae organisms?

A

G-
facultatively anaerobic
type III secretions
all have capsules

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2
Q

What biochemical tests are used for Enterobacteriaceae

A

IMViC

MacConkey’s Agar (lactose fermentation)

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3
Q

What are the 4 most common causes of food-borne outbreaks?

A

Salmonella
Campylobacter
Shigella
E. coli

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4
Q

How is Escherichia coli identified in culture?

A

Lac+

green metallic sheen on EMB agar from acid production

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5
Q

What are the three general clinical presentations of E. coli?

A

diarrhea
UTI
sepsis/meningitis

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6
Q

What is the most common cause of UTIs?

A

Uropathogenic E. coli (UPEC)

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7
Q

What types of E. coli cause diarrhea? (5 of them)

A 
enteropathogenic (EPEC)
enterohaemorrhagic (EHEC)
enterotoxigenic (ETEC)
enteroaggregative (EAEC)
enteroinvasive (EIEC)
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8
Q

Clinical presentation of EPEC, pathogenic mechanism, and epidemiology?

A

watery, self-limiting diarrhea

intimin attachment protein binds to small intestine microvilli and inhibits water uptake

common in young children (esp. in nurseries/day care)

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9
Q

Clinical presentation of ETEC and pathogenic mechanism?

A

Travelers’ diarrhea: watery diarrhea, increased gut motility, abdominal cramps, lasts about 4 days

CFA adhesion pili for brush-border membrane
produces 4 toxins (2 LT and 2 ST) which, respectively, increase cAMP and activate production of cGMP (which causes water secretion)

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10
Q

Clinical presentation and treatment of EHEC?

A

diarrhea starts off watery then turns bloody WITHOUT fever.
Can progress to hemolytic-uremic syndrome (uremia and organ failure due to damage of flomerular endothelium by systemic toxin)

NO antibiotics (they induce toxin gene)

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11
Q

Mechanism and epidemiology of EHEC?

A

shiga-like toxin (AB toxin that inhibits protein synthesis); can become systemic even though bacteria isn’t invasive

O157:H7 strain causes community epidemics from ground beef, water, or vegetable produce (esp sprouts)

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12
Q

Clinical presentation of EIEC?

A

watery diarrhea with fever and cramps, my progress to bloody diarrhea (indistinguishable from Shigella dysenteriae type 1)

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13
Q

Clinical presentation and mechanism of EAEC?

A

infant diarrhea in developing countries
#2 cause of travelers’ diarrhea in most countries
persistent watery diarrhea with vomiting

aggregative pili; forms biofilms

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14
Q

What is the breakdown of watery vs. bloody diarrhea for E. coli?

A

Watery: EPEC, ETEC, EAEC
Bloody: EHEC, EIEC

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15
Q

What is the virulence factor of E. coli causing neonatal meningitis?

A

K1 capsule (mimics host NCAM receptors making it a bad antibody target)

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16
Q

What are the treatment options for GI presentations of E. coli?

A

watery diarrhea- don’t treat (or only supportive care)

bloody diarrhea- NO ANTIBIOTICS for EHEC
EIEC- SxT, fluoroquinolones, or azithromycin ?

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17
Q

How is Salmonella enterica identified in culture?

A

Lac-
H2S+ (S-S agar)
grows in selective media with bile salts (deoxycholate)

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18
Q

What subspecies of S. enterica cause Typhoid fever?

A

S. Typhi and S. Paratyphi

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19
Q

What is the pathogenesis of Typhoid fever?

A
  • bugs penetrate intestinal epithelium (invasive)
  • S. Typhi enters blood from intestinal mucosa
  • disseminates via macrophages to liver, spleen, gall bladder
  • death from intestinal hemorrhage
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20
Q

What is the clinical presentation of Salmonella enterica Cholerasuis?

A

Bacteremia/septicemia

mainly in immunocompromised

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21
Q

What is the clinical presentation of S. enterica Enteriditis?

A

gastroenteritis/enterocolitis

nausea, vomiting, profuse diarrhea, fever
self-limiting within 2-5 days
can colonize gall bladder and shed for weeks

especially transmitted in eggs and poultry

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22
Q

Epidemiology of Salmonella?

A

all are spread fecal-oral (through water, eggs/poultry, fertilized crops, pets)

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23
Q

Pathogenesis of S. enterica?

A

bind to brush border and invade epithelium, enter bloodstream

typhoid toxin (A2B5)

  • A1 ADP-ribosylates G proteins
  • A2 damages DNA and halts cell replication
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24
Q

How is Shigella identified in culture?

A

Lac-

H2S-

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25
What are the relevant species of Shigella?
S. dysenteriae (S. flexneri in 3rd world) (S. sonnei in US)
26
Clinical presentation of Shigella?
only a GI pathogen acute onset watery diarrhea and fever followed by blood and mucus in stool subsides in <1 week, but dehydration is a problem
27
What is the epidemiology of Shigella?
fecal-oral | 4 Fs: food, fingers, feces, flies
28
Pathogenesis of Shigella?
phagocytosed by M cells in intestinal mucosa (invasion factors Ipas secreted by TIIISS) engulfed by macrophages, lyse the phagolysosome, and replicate in cytoplasm, spread via actin tails Shiga enterotoxin (intracellular toxin) disrupts protein synthesis
29
How does Yersinia stain?
bipolar staining (Wright-Giemsa, Wayson's)
30
Virulence factors of Yersinia?
YadA adhesin T3SS (yops)- inhibit MAP kinase pathway, prevent phagocytosis, inhibit platelet aggregation V and W antigens allow intracellular growth
31
What is the mode of transmission of Y. pestis?
zoonosis (NOT GI)
32
Clinical presentation of Y. pestis?
Bubonic plague 1-8 day incubation malaise, headache, vomiting, painful buboes on groin and other lymph nodes Septicemic (primary or secondary to bubonic): purpura, DIC, necrosis Pneumonic (can be primary or secondary to bubonic or sepsis): cough with blood-tinged sputum, bilateral alveolar involvement, nearly 100% fatality within 24hours
33
Epidemiology of Y. pestis?
zoonotic: spread by rat fleas | main reservoirs in US are deermice and Prairie dogs
34
Control and treatment of Y. pestis?
insecticide to kill fleas before rats vaccine (formalin-killed) for people with repeated exposure oral tetracycline (doxycycline) for exposed but asymptomatic. Intramuscular streptomycin once symptoms develop. Pneumonic plague treatment rarely successful
35
Mode of transmission of Y. enterocolitica and pseudotuberculosis?
GI- spread in feces, contaminated water, or milk cattle and hogs are reservoirs
36
Clinical presentation and control of Y. enterocolitica and pseudotuberculosis?
enterocolitis with intestinal abscesses- severe bloody diarrhea with abdominal cramps and fever (up to 2 wks) mesenteric adenitis (mimics appendicitis) controlled by ampicillin (can also use 3rd gen cephalosporin or SxT)
37
Mode of transmission and virulence factors for Klebsiella pneumonia (and K. oxytoca)
Aerosol transmission large capsule
38
Clinical presentation of K. pneumonia and K. oxytoca?
hemorrhagic and necrotizing pneumonia (50-100% fatal)
39
Mode of transmission and clinical presentation of Klebsiella granulomatis?
STD Granuloma inguinale- painless anal or genital sores, lesions gradually progressive (look like syphilis ulcers, but they are soft whereas syphilis is hard)
40
Mode of transmission and clinical presentation of Proteus mirabilis and P. vulgaris?
contact transmission (lots of flagella cause swarming motility) ``` cause UTI (#2 most common) urease production causes alkaline urine and bladder stones ```
41
Mode of transmission and clinical presentation of Serratia marcescens?
contact transmission: opportunistic nosocomial infections causes pneumonia, bacteremia, endocarditis in immunocompromised
42
What is the general control/treatment for Enterobacteriaeceae?
isolate source, serotype for positive diagnosis, control flies/rodents ampicillin, 3rd gen cephalosporins, quinolones, sulfa, streptomycin all effective, but must test susceptibility of particular strain UTI: SxT is first choice, then Fosfomycin (don't use fluoroquinolones for uncomplicated UTI because of resistance)
43
What are the common prophylaxis for traveler's diarrhea?
rifaximin for ETEC | azithromycin for travel to Southeast Asia (campylobacter)
44
What do Vibrios look like in culture?
G- | "comma" shaped rod with polar flagellum and 2 circular chromosomes
45
Where do vibrios live, and what characteristics allow them to live there?
Live in the ocean alkalophilic (pH9, sensitive to acid pH<6 so antacid allows colonization) halotolerant to halophilic (like high salt concentration)
46
Clinical presentation of V. cholerae?
1-4 day incubation followed by nausea, vomiting, and 1-2 loose stools acute onset of profuse watery diarrhea, "rice water stool" >20L/day, contains mucus dehydration and electrolyte loss causes circulatory collapse and death usually no fever, no pain, no blood in stool
47
What is the epidemiology of V. cholerae?
in water, carried on plankton humans are only natural host, can carry bacteria for 3-4 weeks, rarely chronic carriers O1 El Tor Ogawa (no capsule) responsible for recent outbreaks; O139 El Tor local epidemic in Calcutta
48
What is the pathogenesis of V. cholerae?
fimbriae bind gut epithelium AB5 toxin: ADP-ribolylates a G protein, activates adenyl cyclase, high cAMP causes ion secretion into gut lumen, water follows (toxin has a temperature-sensitive switch)
49
What is the treatment/control of V. cholerae?
rehydration and electrolyte replacement brings mortality from 50% to 1% doxycycline can limit # of vibrios shed, but can't stop diarrhea vaccines exist but aren't effective (~6 months), only used for serious outbreaks
50
What is the clinical presentation and pathogenesis of V. parahemolyticus?
12-24 hr incubation nausea, vomiting, watery to bloody diarrhea (with or without gastroenteritis) forms biofilms, T3SS and T6SS inject hemolytic/cytotoxic enterotoxin
51
How is V. parahemolyticus spread, and how is it treated?
distributed worldwide in oceans, obtained from consuming raw seafood (mainly oysters); #1 cause of food poisoning in Japan Control: rehydration and electrolyte replacement, doxycycline if necessary
52
What is the clinical presentation and treatment for V. vulnificus?
infected wound from handling contaminated seafood (esp shellfish), bacteremia from eating raw oysters. Causes VERY rapid hemorrhagic cellulitis and necrosis with eventual liver damage (50% fatality) treatment is doxycycline RIGHT AWAY (cipro if pregnant). Culture takes 18 hrs (too late) so start abx as soon as it's on dDx
53
What is the pathogenesis of V. vulnificus?
antiphagocytic capsule | necrotizing cytotoxin
54
What does Campylobacter look like in culture?
G- curved, helical, or gull-winged polar (sometimes bipolar) flagella microaerophile
55
How can a culture differentiate C. jejuni from C. fetus?
C. jejuni grows at 42 C | C. fetus grows at 25 C
56
Clinical presentation and treatment of C. jejuni?
gastroenteritis with cramps, fever, VERY bloody diarrhea. Usually self-limits within a week May invade bloodstream and cause enteric fever in immunocompromised Guillain-Barre (demyelinating autoimmune) can develop 1-4 weeks later Treated with rehydration tetracycline, quinolones, or clarithromycin for systemic infections
57
Epidemiology and pathogenesis of C. jejuni?
zoonosis (50-100% of chickens and turkey infected in US) acquired fecal-oral route, or consumption of contaminated milk or poultry (peaks in summer because of grilling) pathogenesis: inflammatory enterotoxin (released in large intestines)
58
Clinical presentation and treatment of C. fetus?
systemic infections, septecemia (rarely diarrhea), spontaneous abortions in cattle elderly, ill, and immunosuppressed are susceptible treated with tetracyclines, macrolides, and quinolones
59
Epidemiology and pathogenesis of C. fetus?
zoonosis (cattle); humans acquire from eating contaminated undercooked beef S-layer protein inhibits complement fixation
60
Describe the Helicobacter pylori organism
``` G- spirillum motile at 37 C oxidase+ catalase+ microaerophile acid sensitive (pH4) produce LOTS of urease (urease test positive in minutes) ```
61
Clinical presentation and treatment of H. pylori?
considered a chronic infection; no acute symptoms; non-invasive associated with gastric/duodenal ulcers (1-10%) and gastric adenocarcinoma (1-3%) can cause gastritis in GERD patients on long-term treatment with PPI - treat ulcer with bismuth subsalicylate - treat infection with tetracycline or macrolide + metronidazole - treat acid with PPI
62
How is H. pylori transmitted, and how is it detected?
may be transmitted person-to-person and/or common source infection (food, water, etc) serologic test gram stain and culture of gastric biopsy urea breath test to detect urease activity in stomach
63
What is the pathogenesis of H. pylori?
bind to base of gastric mucosal cells and to Lewis antigen (O bloodgroup) urease buffers pH by forming NH3 VacA toxin causes vacuolation of epithelial cells and release of urea CagA is secreted by T4SS and induces apoptosis, causes ulcers, may be oncogenic

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