Bact Inf of GI Tract Flashcards

1
Q

Bacterial Gastroenteritis

A
  • Inflammation of the stomach & intestines
  • Symptoms include nausea, vomiting & abdominal cramps; diarrhea
  • Rarely life-threatening, unless dehydration
  • Pathogenic bacteria destroy cells by making cytotoxins and stimulating inflammatory mediators
  • They cause thinning of the epithelium (effacement) and increase intestinal permeability
  • Pathogenic bacteria produce toxins that stimulate the enteric nervous system=nausea, cramping, vomitting
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2
Q

Clostridium species

A

-characterized by PeritrichousFlagellae - all around
-spore formation
-

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3
Q

only two bacteria that produce endospores?

A

clostridium and bacillus

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4
Q

Clostridium botulinum causes:

A

botulism

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5
Q

Clostridium tetani causes:

A

TETANUS

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6
Q

Clostridium perfringens causes:

A

GAS GANGRENE

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7
Q

Clostridium perfringens causes

A

FOOD POISONING associated with (meats & gravy)

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8
Q

Clostridium difficile causes:

A

PSEUDOMEMBRANOUS ULCERATIVE COLITIS

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9
Q

Clostridial Food Poisoning: pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source?

A
  • Pathogen: Clostridium perfringens
  • Infectious Dose: none; toxin-based disease
  • Characteristic Disease: “Food Poisoning” intense self-limiting diarrhea due to Clostridium enterotoxin; vomiting and nausea; lasts 24-48 hours
  • Complications: dehydration, muscle strain
  • Incubation Time: ~8-12 hours
  • Infection Source: animal reservoirs; Meats; Gravy; Cream sauces
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10
Q

common cause of food poisoning?

A

Clostridium perfringens enterotoxin

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11
Q

BACTERIAL TOXIN-MEDIATED DIARRHEA

A
  • Clostridium perfringens – meats, gravy

- Enterotoxigenic E. coli – contaminated water

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12
Q

BACTERIAL TOXIN-MEDIATED VOMITING

A
  • Staphylococcus aureus – dairy, produce, meats

- Bacillus cereus – starchy foods, rice

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13
Q

Gas Gangrene: pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source?

A
  • Pathogen: Clostridium perfringens
  • Infectious Dose: endogenous microbe
  • Characteristic Disease: Anaerobic invasive disease; exotoxins cause necrosis & toxemia; proteolytic enzymes break down tissue & proteins; isobutyric, isovalenic, & propionic acid byproducts; H2S gas (ROTTEN EGG SMELL)
  • Complications: Disease is not usually fatal; amputation or other disfiguring intervention may be essential
  • Infection Source: endogenous to human mucos- alpha toxina; invades devitalized tissues where injury or cancer has created anaerobic and acidified growth conditions
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14
Q

Clostridium perfringens virulence factor?

A

-EXTRACELLULR TOXIN = ALPHA TOXIN = it acts on choline phosphoglyeride = Destroys host cell membrane!
-theta-toxin = hemolysis and necrosis
-DNAse, hyaluronidase and collagenase
ENZYMES THAT ALLOW INVASSIVENESS POTENTIAL

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15
Q

Pseudomembranous Colitis pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source?

A
  • Pathogen: Clostridium difficile
  • Infectious Dose: ~1,000 spores needed
  • Characteristic Disease: extreme diarrhea; explosive, with gas; irritable bowel syndrome; ulcerative lesions
  • Complications: chronic diarrhea and/or chronic colitis; dehydration
  • Incubation Time: ~12-72 hours
  • Infection Source: Endogenous form – clindamycin or ampicillin therapy with overgrowth; Nosocomial spread - spore-saturated healthcare environment
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16
Q

someone hospitalized and treated with antibiotics clindamycin/ampicillin, and then there is overgrowth bc other GI flora killed=explosive diarrhea? What caused?

A

Clostridium difficile

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17
Q

Clostridium difficile virulence factors?

A

EXTRACELLULAR PRODUCTS:

1) Toxin A = enterotoxin; cell death and tissue necrosis; found in ulcerative colitis stools
2) Toxin B = potent cytotoxin; responsible for apoptosis & major tissue ulceration

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18
Q

Clostridium difficile DIAGNOSIS and TREATMENT

A
  1. Endoscopy & *Gold Standard Toxin Immunoassay
  2. Remove the offending antibiotic
  3. Most C. difficile strains - susceptible to vancomycin
    * 4. Metronidazole - specifically for anaerobes; partially reduced by anaerobic metabolism & taken into DNA; inhibits DNA synthesis*
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19
Q

drug specific for anaerobic bacteria?

A

metronidazole - inh DNA synthesis (NARROW SPECTRUM ANTIBIOTIC)

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20
Q

spore formation

A
  • location: terminal, subterminal, or central spore
  • bacterial makes it when environment is threatening or not ideal = smallest form able to continue bacterial life if environment is good later on
  • calcium dipicolinate accumulates i nthe core of developing spores –> water expelled = spore w/ exosporium, spore coat, cortex, and cytoplasm with DNA
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21
Q

where do spores germinate and what else do they do in there? Name of disease?

A
  • Pseudomembranous Ulcerative Colitis

- IN intensines – secrete toxin A and B

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22
Q

Hypertoxic strain BI of Pseudomembranous Ulcerative Colitis does what?

A

eliminates neg feedback regulation for toxxin production=more severe effects

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23
Q

Botulism toxin does what?

A
  • Flaccid paralysis = inhibiton at PRESYNAPTIC JUNCTION = nerves dont fire
  • blocks the neuromuscular junction preventing contraction
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24
Q

tetanus toxin does what?

A

Spastic paralysis = inhibition of pathway so muscles cant relax (INH IN ANTERIOR HORN)

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25
Q

Infant and Wound Botulism: pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source?

A
  • Pathogen: Clostridium botulinum
  • Infectious Dose: ~100 - 1,000 spores
  • Characteristic Disease: constipation; diplopia; symmetric nerve involvement; flaccid paralysis (“floppy baby syndrome”);
  • Complications: lingering weakness, dyspnea, up to one year after primary disease
  • Treatment: anti-toxin administered by IV (CDC)
  • Infection Source: Contaminated honey from which spores can be ingested (infant form < 6 months); contamination of wounds & spore germination in tissues (adults); BoTox mishap
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26
Q

Classic Food borne Botulism: pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source?

A
  • Pathogen: Clostridium botulinum
  • Infectious Dose: ~100 - 1,000 spores
  • Characteristic Disease: vomiting and diarrhea; abdominal pain, early; later, diplopia and muscle weakness with symmetric nerve involvement (18-24 hours after ingestion); flaccid paralysis death from respiratory failure
  • Complications: lingering weakness, dyspnea, up to one year after primary disease
  • Treatment: anti-toxin administered IV (CDC)
  • Infection Source: Food contaminated with preformed toxin; usually improper home canning of vegetables
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27
Q

double vision in patient… potential suspect=

A

botulism

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28
Q

which part of LPS is heat stable?

A

o-antigen

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29
Q

which part of LPS can be detected via agglutination?

A

o-antigen

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30
Q

antigenic structire of LPS?

A

have an extra k-antigen external to o-antigen

  • k-antigens are virulence antigens
  • H-antigens = determined by the flagellin amino acid sequence= secere forms of disease
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31
Q

different strains of E. Coli

A
  • Enterohemorrhagic E. coli (EHEC) -O157:H7 causes bloody diarrhea and kidney failure
  • Enteroinvasive E. coli (EIEC) - invades the intestinal wall and causes diarrhea
  • Enteropathogenic E. coli (EPEC)-causes diarrhea outbreaks in newborn nurseries
  • Enterotoxigenic E. coli (ETEC)-toxin attacks the intestinal lining, causing Traveler’s Diarrhea
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32
Q

Enterohemorrhagic E. coli (EHEC) causes:

A
  • O157:H7 causes bloody diarrhea and kidney failure

- the strain that usually kills people

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33
Q

Enteroinvasive E. coli (EIEC) causes:

A

invades the intestinal wall and causes diarrhea

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34
Q

Enteropathogenic E. coli (EPEC) causes

A

causes diarrhea outbreaks in newborn nurseries

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35
Q

Enterotoxigenic E. coli (ETEC) causes

A

toxin attacks the intestinal lining, causing Traveler’s Diarrhea

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36
Q

Hemolytic Uremic Syndrome (EHEC): pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source; virulence factors?

A
  • Pathogen: Escherichia coli, O157:H7, butcan be other STEC (O26-no flagellin strain, O104:H4)
  • Infectious Dose: as few as 10 cells
  • Characteristic Disease: Bloody diarrhea; hemorrhagic colitis; RBC destruction
  • Complications: Kidney failure; death
  • Incubation Time: 24 – 72 hours
  • Infection Source: Fecal contamination of water or food
  • Virulence Factors: Only 8% of E. coli produce Shiga-like toxins (SLT-1 & SLT-2); cause >75% of severe E. coli infection==>POTENT TOXIN THAT PREVENTS PROTEIN SYNTHESIS=CELL DEATH
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37
Q

Enteroinvasive E. coli (EIEC): pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source; virulence factors?

A
  • Pathogen: Escherichia coli
  • Characteristic Disease: Bloody diarrhea (dysentery); colonizes epithelial cells of the colon; necrosis, ulceration & inflammation, stool with fecal PMN’s
  • Complications: Kidney failure; death
  • Infection Source: Fecal contamination of water or food
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38
Q

non-invasive E. Coli species and characteristics/toxins

A
  • MORE LIKE CHOLERA - CLOUDY WATER POOP = WATERY DIARRHEA
  • EPEC - associated with babies
  • ETEC -LT toxin= heat labile toxin -increases cAMP levels = release of water and ions; ST toxin=heat stable toxin-increases cGMP
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39
Q

invasive E. Coli species and characteristics/toxins

A
  • MORE LIKE DYSENTERY = BLOODY DIARRHEA
  • EIEC = nontoxigenic
  • EHEC = toxogenic - shiga-like cytotoxin = inhibits protein synthesis
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40
Q

Shiga-like toxin does what? which organism?

A

POTENT TOXIN THAT PREVENTS PROTEIN SYNTHESIS=CELL DEATH

EHEC

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41
Q

LT-toxin does what? which organism?

A

heat labile toxin -increases cAMP levels = release of water and ion

ETEC

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42
Q

ST-toxin does what? which organism?

A

ST toxin=heat stable toxin-increases cGMP

ETEC

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43
Q

Death more likely from EHEC or EIEC?

A

EHEC!

44
Q

Traveler’s Diarrhea (ETEC): pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source; virulence factors?

A

-Pathogen: Escherichia coli
-Infectious Dose: 100 x 106 – 10 billion (NEED LARGE DOSE)
-Characteristic Disease: Nausea, vomiting,diarrhea 1 -3 days
-Complications: Dehydration
-Incubation Time: 24 – 72 hours
-Infection Source: Fecal contamination of water
or food
-Virulence Factors: LT & ST (labile & stable toxins); increase cAMP (LT) & cGMP (ST)

45
Q

SLIDE 11

A

SLIDE 11

46
Q

Enteropathogenic E. coli (EPEC): pathogen; characteristic of disease; complications; infection source?

A
  • Pathogen: Escherichia coli, EPEC strains
  • Characteristic Disease: Infantile diarrhea; copious stools, watery; like cholera
  • Outbreaks associated with nurseries
  • Infection Source: Bottle-fed babies; formula made with impure water; Improperly sterilized bottles, nipples, rings
47
Q

Uropathogenic Escherichia coli:

A
  • K1 antigen E. coli and Meningitis:Capsular polysaccharide/K1 antigen marker characteristic for meningitis associated strains. (KIDNEY INFECTIONS)
  • P-pilus E. coli & Pyelonephritis: Specific trophic factors; the “P pilus” of uropathogenic E. coli binds to kidney glycolipid
48
Q

Lab Testing for Escherichia coli

A
  • Facultative anaerobe
  • Heavy lactose fermentation
  • Iridescent metal looking sheen on EMB:
  • MacConkey agar bright pink colonies
  • Indole test is DIAGNOSTIC for E. coli infection
49
Q

E. coli: Extracellular Products

A
  1. Heat-labile AB-type enterotoxin (LT) Intense water and chloride hypersecretion = gut hypermotility (CRAMPING) and watery diarrhea
  2. Heat-stable enterotoxin (ST) - activates guanylate cyclase in enteric epithelial cells = fluid hypersecretion
  3. Shiga-like toxin I & II (SLT): Associated with hemorrhagic colitis & hemolytic uremic syndrome (HUS)
50
Q

Can exotoxins be enterotoxins too? vice versa?

A

NO

Vice versa= YES

51
Q

Diagnosis of E. coli Infection

A
  1. Specimens include urine, blood, pus, spinal fluid, sputum or other material as indicated by the locale of the infection.
  2. Culture on blood & differential media; especially EMB agar or MacConkey
  3. Serotype analysis for specific strains
52
Q

Treatment for E. coli Infections

A
  1. Simple fluid and electrolyte replacement solution is sufficient for watery diarrhea: ORAL REHYDRATION SOLUTION: Glucose (13.5g/L); Sodium Chloride (2.6g/L); Potassium Chloride (1.5/L); Trisodium Citrate Dihydrate (2.9g/L)
  2. Antibiotics can shorten duration of GI infection. Sensitivity testing.
53
Q

ORAL EHYDRATION SOLUTION:

A

Glucose (13.5g/L); Sodium Chloride (2.6g/L); Potassium Chloride (1.5/L); Trisodium Citrate Dihydrate (2.9g/L)

54
Q

Proteus Species- GI issues: pathogen; characteristic of disease; complications; infection source?

A
  • Pathogen: Proteus mirabilis and Proteus vulgaris
  • Characteristic Disease: UTI (especially complicated infections); also bacteremia, pneumonia, & focal lesions in debilitated patients
  • Found frequently as commensal species (ie can be normal flora)
  • Infection Source: Nosocomial infection is important for Proteus vulgaris; often UTI; Community-acquired infection when bacteria escape GI tract (normal flora commensal)
55
Q

Proteus distinguishing characteristics/lab

A

-Distinguished by culture on Christensen’s urea agar. (Red color: urea hydrolysis & alkaline pH due to ammonia production)
-Very motile (swarming on solid agar)
-Slow lactose fermentation
____________
-DONT REALLY NEED TO DISTINGUISH THESE GUYS NOW:
-P. vulgaris is indole positive; resistant to both ampicillin & penicillin.
-P. mirabilis is indole negative;susceptible to high penicillin levels

56
Q

Klebsiella Species- GI issues: pathogen; characteristic of disease; complications; infection source?

A
  • Pathogen: Klebsiella pneumoniae
  • Characteristic Disease: respiratory infection; consolidation pneumonia
  • Complications: acute, severe pneumonia observed in middle-aged alcoholic men; ESBL strain are especially problematic
  • Infection Source: Present in the respiratory tract & feces of about 5% of “normal” individuals; Respiratory droplet transmission; susceptible patients are at risk
57
Q

first thing to notice when/if culturing proteus:

A

urease production and swarming on solid agar = very motile = will appear as concentric rings

58
Q

Klebsiella pneumoniae: ESBL - distinguishing features

A
  • Highly antibiotic resistant strains; major ESBL organism (Extended Spectrum Beta-Lactamase producers; also E. coli )
  • Generally susceptible to 3rd generation cephalosporins; dual therapy required
  • problem in india and africa
59
Q

Serratia Species: pathogen; characteristic of disease; complications; infection source; indentification?

A
  • Pathogen: Serratia marcescens
  • Characteristic Disease: pneumonia, bacteremia, especially in narcotics addicts & hospitalized patients
  • Complications: endocarditis (bacteria on heart valves)
  • Infection Source: Environmental contaminant; Opportunistic pathogen
  • Identification: Red colony pigmentation on nutrient agar; Multiple drug resistance; resistant to penicillins & aminoglycosides; Treated with 3rd-generation cephalosporins
60
Q

two organism that will pretty much grow on anyting?

A

E. Coli or Serratia marcescens

61
Q

opportunistic pathogens:

A

pseudomonas, klebsiella, liegionella, serratia

62
Q

The Enteric “Exclusive Pathogens”

A
  • Gram - bacilli, (slender rods); No spores.
  • NOT normally found as commensals:
  • Salmonella sp - enterobacteriae
  • Shigella sp-enterobacteriae
  • Vibrio sp-vibrionaceae
  • Campylobacter jejuni - campylobacterales
  • Helicobacter pylori - campylobacterales
  • Listeria monocytogenes
63
Q

Salmonellosis: pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source; virulence factors?

A
  • Pathogen: NOT TYPHI - Salmonella enterica serotypes (Typhimurium; Enteritidis; Saintpaul; Bredeney)
  • Infectious Dose: 1 x 106 cells
  • Complications: Dehydration
  • Characteristic Disease: Non-bloody diarrhea (Loose stool) ;nausea; vomiting; pain X 1-2 weeks; rash
  • Incubation Time: 8 – 48 hours
  • Infection Source: Zoonotic; poultry; eggs; contaminated meat; Inadequately pasteurized contaminated mil; Infected reptiles; Infected humans
64
Q

Typhoid Fever: pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source; virulence factors?

A
  • Pathogen: Salmonella enterica serotypes Typhi and Paratyphi
  • Infectious Dose: 10,000 cells
  • Complications: Intestinal perforation; peritonitis; Kidney failure; Internal bleeding; death
  • Characteristic Disease: High fever; headache; muscle pain; stomach ache; malaise; rose spots
  • Incubation Time: 10 – 24 days (per dose)
  • Infection Source: Fecal contamination of water; Fecal – oral transmission
  • localized to gallbladder if carrier state and extreted in feces
65
Q

Hallmarks of Typhoid Fever:

A
  • Lymphoid hyperplasia
  • Focal liver necrosis
  • Gall bladder inflammation (carrier state)
  • Patch inflammation (Lung - pneumonia; Bone marrow - osteomyelitis)
  • Intestinal hemorrhage: necrotic ulceration of Peyer’s patches
66
Q

Typhoid Fever course of infection:

A

Ingestion—>Bacteremia–>Septicemia—> Clearing & Localization (Liver; Gall Bladder)—> Shedding in feces

67
Q

Salmonella diagnosis

A
  • Culture on Maconkey agar: growth but NO fermentation
  • secondary culture on S/S agar; H2S gas (black deposits)
  • Slide agglutination based on O, H & Vi Ag’s (capsule); NAAT (PCR)
68
Q

salmonella treatment

A
  • Management of symptoms;quinolones for GI disease
  • Cephalosporins for septicemia
  • Cholecystectomy to abolish carrier state-REMOVE GALLBLADDER
  • Surgical drainage of focal abscesses
69
Q

endothelial & endocardial infection associated with which salmonella?

A

S. enterica serotype Choleraesuis

70
Q

who is predisposed illness by Salmoella

A

-Elderly patients are predisposed: plaques, artificial valves, prostheses, frail health, comorbid disease

71
Q

Sickle cell disease predisposes to

A

osteomyelitis caused by Salmonella species

72
Q

Shigella organism details and the disease caused?

A
  • Non-motile,
  • non-lactose fermenting;
  • No H2S
  • Disease is bacillary dysentery
73
Q

bacillary dysentery cased by what pathogen and what are some factors?

A

-Shigella

  • it is a Human disease
  • Seasonal pattern
  • Climate & socioeconomic conditions
  • Institutional epidemics
74
Q

young person with mental retardation, in a daycare and epidemic among people in the daycare? Incontinence? What may be the cause?

A

Shigella

75
Q

Shigella species designations determined by?

A

-the o-antigen present on LPS

76
Q

Shigella groups

A
  • **MOST PATHOGENIC -Group A - S. dysenteriae (most pathogenic)
  • Group B - S. flexneri (recently assoc. with outbreaks among MSM population)
  • Group C - S. boydii (endemic in India)
  • **MOST PROMINENT AND MILD=-Group D - S. sonnei (most common in United States; mildest course)
77
Q

shigella genome analysis:

A

Shigella evolved from E. coli due to virulence plasmid acquisition

78
Q

Shigellosis: pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source?

A
  • Pathogen: Shigella dysenteriae
  • Infectious Dose: ~ 200 cells
  • Characteristic Disease: Bloody stools with mucous (bacillary dysentery); cramps & rectal pain; fever, nausea, vomiting; lasts 2 – 3 days
  • Complications: Severe dehydration; febrile seizures; neurological complications in children
  • Incubation Time: 1 – 7 days
  • Infection Source: Unwashed hands; fecal contamination; Person-to-person transmission
  • MAY BE ASSOCIATED WITH OVER PACKED PUBLIC POOLS WHERE THERE ISNT ENOUGH CHLORINE TO HANDLE ALL THE DIAPERS BABIES ARE WEARING
79
Q

Shigella clinical info stuff:

A
  • Dysentery syndrome; GI tract localization
  • Virulence factors: type III secretion (includes shiga toxin and mech to transmit to humans –> like injection); intracellular growth pattern
  • Local ulceration due to Shiga toxin activity (ADP-ribosylation of 60S ribosomal unit)
  • Pseudomembrane formation compromises colon function: diarrhea
  • Susceptible to stool acidity; must be cultured immediately for successful identification
80
Q

special covert way that shigella species can move from cell to cell?

A

actin mobilization –> uses cell actin to push it through memranes into another cell (never has to leave the cell - so immune system cant see it)

81
Q

Shigellosis Diagnosis & Treatment

A
  • —DIAGNOSIS
  • Stool samples cultured on MAC or EMB: colorless colonies
  • S-S agar growth positive; No gas.
  • Serology
  • —TREATMENT
  • Electrolyte & fluid replacement
  • MDR plasmids; DOC: quinolones & SMX-TMP (sulfo-trimethoprim thing…)
82
Q

shigella vs salmonella on agar?

A

salmonella has black deposits

83
Q

2 motif for GI infections:

A
  • tissue infection and dysentry–BLOODY = EIEC, EHEC, shigella dysenteriae and shigella flexnari
  • take up into macrophages and getting into certain tissues = salmonella enterica and typhi
84
Q

SLIDE 21

A

SLIDE 21 36:00 minutes

85
Q

Vibrio cholerae organism details:

A
  • “Comma-shaped” Gram - ; motile (single polar flagellum)
  • Human disease; no animal reservoir
  • Achlorhydria from antacids & decreased gut motility may predispose
  • Slow lactose fermentation; carbohydrate fermentation with acid but no gas.
  • Oxidase positive
86
Q

Cholera: pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source; virulence factors?

A
  • Pathogen: Vibrio cholerae
  • Infectious Dose: ~ 106 – 108 cells
  • Complications: Severe dehydration; within 48 hours, 25 – 50% mortality rate if untreated
  • Characteristic Disease: Watery, colorless, “ricewater” stools; lasts 2 – 3 days; may lose up to 1 liter fluid per day
  • Incubation Time: 6 hours – 5 days
  • Infection Source: Fecal contamination of food, water; Highly contagious; huge epidemic potential; Seasonal flooding in areas with
87
Q

CHOLERA- how they make people sick?

A
  • Vibrios attach to the mature epithelium at the tips of intestinal villi via Tcp pili (toxin co-regulated pili)
  • Toxin-coregulated pili: Pathogenicity island - genetic regulation “senses” environmental pH, low osmolality, and temperature to turn on pili and choleragen production; noninflammatory
  • Cholera toxin acts at level of crypts to disrupt electrolytes;– only produced if organism finds the perfect environemnt
88
Q

Vibrio parahaemolyticus causes what and where most likely?

A
  • sudden diarrhea, abd cramping, and fever

- coastal states - esp Gulf coast with warm salty watter

89
Q

V. vulnificus associated with what food?

A

raw oysters, bacteremia, liver or iron-overload disease

90
Q

treatment for ALL bibrios?

A

tetracyclines + aminoglycosides; fluid replacement

91
Q

Campylobacter jejuni associated with what and who is at most risk?

A
  • contaminated foods, and food prep surfaces

- young adult males=high risk group bc they dont know how too cook and clean up right

92
Q

Campylobacter diarrhea: pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source; virulence factors?

A
  • Pathogen: Campylobacter jejuni
  • Infectious Dose: ~ 500 cells
  • Complications: Sepsis; arthritis; Guillain-Barré syndrome (acute paralysis, with chronic deficits) may be a sequela; hemorrhagic necrosis of jejunum/ileum can cause fatality
  • Characteristic Disease: > 10 bowel movements per day for 2 – 5 days; stool may be bloody
  • Incubation Time: 2 – 5 days
  • Infection Source: Zoonotic; cats, dogs, etc.; Ingestion of contaminated food, water; Person-to-person risk of spread
93
Q

Campylobacter jejuni - organism facts and treatments:

A
  • Very common as agent of gastroenteritis in the U.S.
  • Motile (flagella implicated in pathogenesis), oxidase-positive, fastidious, requires high CO2 growth condition
  • Disease is self-limiting; supportive therapy to relieve symptoms
  • Relapse rate ~20% without antibiotics
  • DOC: tetracyclines, macrolides, quinolones (but, rising resistant to quinolones)
94
Q

Helicobacter & Peptic Ulcers: pathogen; infectious dose; characteristic of disease; complications; incubation time; infection source; virulence factors?

A
  • Pathogen: Helicobacter pylori
  • Infectious Dose: unknown
  • Complications: Stomach or duodenal ulcers; erosion of stomach or small intestine lining; stomach cancer; death if ulcer perforates
  • Characteristic Disease: abdominal pain; chronic gastritis; belching; dyspepsia
  • Incubation Time: widely variable; not all infected develop ulcers
  • Infection Source: Fecal – oral contamination; Human or cat feces on hands; well water; fomite transmission
95
Q

organism extremely likely to be associated with ulcers and SOMETIMES cancer?

A

helicobacter

96
Q

Helicobacter pylori diagnosis and treatment

A
  • —–DIAGNOSIS:
  • Biopsy specimens from gastric mucosa are cultured & examined histologically (“gold standard” of diagnosis)
  • Serological ID is ~80-95% accurate
  • 13C-urea breath test, sensitive (98%); Rapid urease test
  • —-Treatment: bismuth salts (Peptobismol), H+ inhibitor, metronidazole & tetracycline/macrolide
97
Q

helicobacter pylori disease progression more common in people with w aht two factors?

A
  • o-blood type
  • smoking
  • increased pH and decreased ascorbic acid
98
Q

Listeria monocytogenes organsim details:

A
  • Gram-positive Rod
  • Facultative anaerobe
  • No spores
  • V- or L-shapes similarto Corynebacterium palisades
  • At-risk population includes pregnant women, neonates & immuno-compromised
  • Meningitis and Sepsis
  • USES ACTIN MOTILITY
99
Q

monocytogenes: in the elderly?

A

Meningitis & septicemia

100
Q

prego woman who eats soft serve or deli meats and gets GI syndrome? Disease?

A

Listeria monocytogenes

101
Q

Listeria monocytogenes: DISEASE

A
  • Range is conjunctivitis to septicemia
  • Meningitis & septicemia in the elderly
  • Granulomatosis Infantisepticum in infants - devastating, massive infection; transplacental & vaginal transmission
102
Q

Listeria Classification

A
  • Listeriosis is associated with ingestion of contaminated foods
  • Facultative psychrophile (loves the cold)
  • Narrow β-hemolysis zone on blood agar: listerolysin, pore-forming toxin
  • Internalin: adherence protein
103
Q

Listeria Diagnosis

A
  • Culture: BAP with beta-hemolysis
  • Culture: Tellurite agar - inhibits normal flora
  • Listeria produce gray to black colonies on Tellurite
  • Gram-positive rods in “pallisades”
  • Motility – actin-tail motility can be detected using traditional methods
104
Q

Listeria monocytogenes treatment and prevention:

A
  • –TREATMENT:
  • Ampicillin + an aminoglycoside; also SMX-TMP prophylaxis (current 2008)
  • For perinatal disease, treat mother locally in vaginal tract and systemically
  • –PREVENTION: People in at-risk groups should avoid eating deli meats, lunch meats, soft cheeses
105
Q

Illness due to preformed toxin organisms?

A
  • staphaureus - eggs/ creams/ dairy
  • bacillus - rice and grains
  • claustridium - meats and gravies
106
Q

which virus binds sialic acid moieties?

A

influenza