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Microbio Exam 1 > GI Bacteria I and II > Flashcards

GI Bacteria I and II Flashcards

1
Q

Where is there a dramatic increase in the flora present in the GI tract? What type of organisms are they?

A
  • Large bowel

- predominantly anaerobes and E. Coli

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2
Q

3 major mechanisms that lead to Gastroenteritis

A
  1. ingestion of preformed toxin present in contaminated food
  2. infection by toxigenic organisms, which proliferate in the gut lumen and elaborate an enterotoxin
  3. infection by enteroinvasive organisms
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3
Q

Onsets of the 3 major mechanisms of gastroenteritis

A
  1. ingestion of preformed toxin has rapid onset
  2. infection by toxigenic organisms can have rapid or delayed onset of illness
  3. infection by enteroinvasive organisms have delayed onset
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4
Q

Virtually all bacterial diarrheal diseases are treated with _________. Any exceptions?

A
  • supportive care only
  • exceptions are salmonella non-typhi in certain high risk. salmonella typhi always, Clostridium difficile, cholera, shigella
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5
Q

What causes Travelers’ Diarrhea. How is it prevented and treated?

A
  • ETEC as diagnosed by referral labs
  • Drink only bottled beverages and steaming hot food when in endemic areas no ice cubes in drinks
  • Treat via oral rehydration and potentially shorten its duration with antimicrobials and antimotility agents
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6
Q

Common prescriptions given for Travelers’ Diarrhea

A
  • fluoroquinolone +/- loperamide

- Rifaximin

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7
Q

Stool culture is the primary test for detection of what bacteria?

A
  • Salmonella
  • Campylobacter
  • Shigella
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8
Q

What is a common transport medium of stools called?

A

-Cary-Blair

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9
Q

MacConkey Agar

A
  • semi-selective agar

- contains inhibitors of Gram + bacterial growth (bile salts and CV), lactose, peptone, and pH indicator

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10
Q

Role of lactose, peptone, and bile salts of MacConkey Agar

A
  • bile salts and Cv inhibit gram positive growth
  • lactose: lactose fermentors use lactose, produce acid, lower pH, and make colonies pink/red.
  • peptone: utilized by non-lactose fermenters, produce ammonia, raise pH, and make clear colonies
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11
Q

Sorbitol MacConkey helps identify ____________. How?

A
  • shiga toxin producing EHEC

- by including sorbitol, which these strains cannot utilize so they grow as white circular colonies

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12
Q

Vibrio cholerae

A
  • causes cholera
  • curved, gram negative, flagellated rod- rapidly motile
  • secretes cholera toxin
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13
Q

Where does V. cholerae colonize, what does it secrete, and what is its action?

A
  • proximal small intestine
  • secretes cholera toxin
  • CT increases intracellular cAMP in intestinal epithelial cells leading to increased secretion of chloride ions and decreases Na absorption–water flows out and causes diarrhea
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14
Q

V. cholera needs to survive harsh stomach acids to reach lumen of small intestine where it infects individuals. What can one infer about the inoculation size needed? What kinds of patients may be at higher risk?

A
  • larger inoculation

- patients on medication for reduced stomach acid production

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15
Q

V. cholera can be found in water sources. Fresh or salt water?

A

-both

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16
Q

Structure and mechanism of cholera toxin

A
  • carried by CTXphi phage
  • 2 subunit toxin with the A subunit being catalytic/pathological portion
  • toxin enters cell, retrograde transport through golgi and ER, A1 subunit acts of AC, increase cAMP, increase PKA activity which phosphorylates CFTR and get copious Cl-secretion and diarrhea
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17
Q

Transmission of cholera

A

-fecal-oral transmission via contaminated food or water

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18
Q

Subclinical infection of cholera effects

A
  • short-term excretion following mild or subclinical infection
  • majority of cases are subclinical
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19
Q

Hypochlorhydria

A
  • lower stomach acidity

- leads to increases severed and lowers infectious dose

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20
Q

Can V. Cholera survive outside of a human host? If yes, what are its reservoirs?

A
  • Yes
  • copepods, shellfish, algae, water hyacinths
  • needs estuarine environments where there’s mixing of salt and fresh water
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21
Q

Symptoms of severe dehydration due to V. Cholera infection

A
  • sunked eyeballs
  • wrinkled fingers
  • loss of skin turgor (sign of severe dehydration)-aka skin tenting
  • rice water stools: straw like color and flecks of intestinal mucus
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22
Q

How does one treat cholera?

A
  • by replenishing fluids and electrolytes that are lost in the stool
  • WHO formula oral rehydration salts
  • addition of glucose to stimulate Na uptake
  • Ringer’s lactate via IV
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23
Q

Tetracycline treatment can shorten duration of diarrhea in V. cholera infections, but why is this not the first line of defense?

A
  • patients may die from dehydration before antibiotics can work
  • rehydration is the most important therapy
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24
Q

What is the leading bacterial cause of seafood-associated gastroenteritis in the US?

A
  • Vibrio parahaemolyticus

- multiple outbreaks in coastal states associated with crabs, oysters, shrimp

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25
Q

Symptoms of Vibrio parahaemolyticus infection

A
  • watery, self-limited diarrhea with cramps, nausea, vomiting, sometimes bloody diarrhea
  • wound infection after exposure to warm seawater are also seen
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26
Q

When do vibrio parahaemolyticus infections peak?

A
  • summer

- when seafood becomes more regular

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27
Q

2 methods of acquiring Vibrio vulnificus infection

A
  1. ingesting raw seafood

2. wound infection after exposure to seawater during warm months

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28
Q

Vibrio vulnificus wound infection: symptoms and progression

A
  1. cellulitis, sometimes with vesicles or bullae follwed by necrosis
  2. sometimes progresses to bactermemia and death, particularly in those with liver disease
  3. often after exposure of wound to seawater during warm months
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29
Q

Vibrio vulnificus “primary sepsis”: how does one get it? symptoms?

A
  • infected by eating raw seafood
  • organism invades bloodstream from the intestine causing a syndrome characterized by fever, chills, prostration, and hypotension
  • usually have secondary skin lesions on the extremities, with erythematous or ecchymotic areas-vesicles or bullae- necrotic ulcers
  • high death rate -50-60%
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30
Q

Who is most at risk for primary sepsis from Vibrio vulnificus?

A
  • people with pre-existing hepatic or other chronic disease
  • Cirrhosis, AIDS, malignancy, hemochromatosis, immunosuppressive meds
  • estrogen can be protective, so more than 90% of cases in males
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31
Q

Enterobacteriaceae is a large family of what kind of bacteria?

A

-gram negative rods found mostly, but not exclusively, in the gut lumen where they live as facultative anaerobes

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32
Q

True/False: all strains of E.coli cause diarrhea.

A

false; have extraintestinal and diarrheagenic strains

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33
Q

ETEC features

A
  • important in developing countries: children, travelers
  • watery diarrhea
  • short duration
  • fecal-oral route
  • plasmic virulence factors
34
Q

2 plasmid virulence factors of ETEC

A
  1. Heat-labile enterotoxin: same mechanism of cholera toxin; raise cAMP, resulting in intense and prolonged hypersecretion of Cl and Water, while also inhibiting Na absorption
  2. Heat-stable enterotoxin:
    strain with both toxins associated with more severe disease
35
Q

How is ETEC transmitted?

A

-fecal-oral route

36
Q

EPEC is usually seen in what patient population?

A

-infants in developing countries

37
Q

Signs and symptoms of EPEC infection

A
  • watery diarrhea and vomiting (fever sometimes)
  • usually short duration, but can be protracted and deadly
  • atypical strains emerging in developed countries with chronic diarrhea
38
Q

Transmission of EPEC

A
  • person to person

- why it can occasionally cause outbreaks in infant daycares in US

39
Q

EHEC (enterohemorrhagic E. Coli) reservoir and how/where people can acquire it?

A
  • reservoir is cattle
  • contaminated food: ground beef, produce, juice
  • water: drinking, swimming
  • petting zoos
  • person-to-person transmission
40
Q

Does EHEC need a low or high inoculum?

A

-low

41
Q

EHEC pathogenesis

A
  • Shiga toxin that injured intestinal cell walls and blood vessels leading to bleeding
  • once in blood stream the toxin damages other vessels, especially those in the kidney leading to kidney failure
  • diarrhea is this main issue, it is the damage to other organs
42
Q

Shiga toxin encoding and structure

A
  • encoded by lambda-like bacteriophages

- 5 identical B, 1 A subunit

43
Q

Mechanism and action of shiga toxin

A
  • B subunits bind GB3 which is present on many cell types
  • transported retrograde to ER
  • A subunit is an N-glycosidase
  • depurinates 28S ribosomal subunit
  • PROTEIN SYNTHESIS CEASES
44
Q

What is the most common cause of renal failure in children?

A

-Hemolytic-uremic syndrome

45
Q

Hemolytic-Uremic Syndrome can follow what infection? what is it?

A
  • thrombotic microangiopathy: blocking small blood vessels due to parts of destroyed RBCs
  • can affect any organ
46
Q

Risk factors of hemolytic-uremic syndrome

A
  • age
  • WBC count
  • vomiting
  • anti-motility agents
  • antibiotics
47
Q

Enteroaggregative E.Coli (EAEC) epidemiology

A
  • childhood diarrhea in developing countries: can be persistant, associated with growth retardation
  • travelers
  • Emerging pathogen in developed countries
  • HIV
48
Q

Clinical features of EAEC

A
  • watery diarrhea
  • mucous with/without blood
  • intestinal colic
  • growth retardation
49
Q

Describe Shigella species bacterium

A
  • Gram-negative rods
  • facultative anaerobe
  • enterobacteraceae
  • oxidase-negative, non-motile, appears as non-lactose fermenter on MacConkey agar
50
Q

How many species of Shigella? Which is most common in the US?

A
  • 4
  • S. dysenteriae Serogroup A
  • S. flexneri serogroup B
  • S. boydii Serogroup C
  • S. sonnei Serogroup D** most common in US
51
Q

Symptoms of Shigella species and how infectious is it?

A
  • HIGHLY infection: ~10 organisms

- locally invasive organism, fever, abdominal cramps, bloody/mucoid diarrhea

52
Q

Is Shigella found outside of humans?

A

no

53
Q

Describe Shigella enterocolitis

A
  • acute inflammation
  • pale, granular and inflamed mucosa with patches of coagulated exudate
  • massive recruitments of PMNs inducing rupture of epithelial barrier
54
Q

Cellular pathogenesis of Shigella. How does it cross the epithelial barrier? What happens once inside?

A
  • translocation by the bacteriun of the intestinal epithelium and development of the infectious process leads to bacillary dysenteru
  • cross M cells as well
  • taken up by macrophages in which they induce apoptosis which produced proinflammatory cytokines and PMN recruitment
  • enter enterocytes basolaterally
55
Q

T/F: Shigella is invasive, and therefore, causes bacteremia.

A

False; no bacteremia

56
Q

Salmonella description

A
  • gram-negative rod
  • enterobacteraceae
  • motile
  • oxidase negative
  • non-lactose fermenter on MacConkey agar
57
Q

2 types of salmonella to watch out for

A

Salmonella enteritidis

Salmonella Typhi

58
Q

Transmission of salmonella

A
  • fecal-oral pathogen

- leading foodborne pathogen

59
Q

Reservoirs and infectious dose of salmonella

A
  • many host reservoirs (birds, mammals, reptiles, amphibians)
  • infectious dose is large
60
Q

Symptoms of salmonella typhi

A
  • bacteremia, fever, systemic dissemination constitute typhoid fever
  • may result in chronic infection of biliary tree, joints, bones, meninges
61
Q

Salmonella pathogenesis mechanism

A

-enter GI by ingestion of contaminated food
-attach to M cells or pass between cells
-cause influx of immune cells (can survive inside macrophages or kill them)
-

62
Q

Ultimate control of salmonella infection requires _________.

A
  • functioning T/B cells, liver, and spleen
  • salmonella lives within macrophages (doesn’t leave them like shigella) and traffics with macrophages to lymphatic sites
63
Q

Salmonella injects efforts via what system and what is their effect?

A
  • by type III secretion system

- rearrange actin cytoskeleton

64
Q

Typhoidal vs. Non-typhoidal (Typhimurium) Salmonella invasive disease

A

S.typhi bacteremic spread in immunocompetent hosts (enteric fever)
S. non-typhi bacteremic spread in immunocompromised hosts with greater immune activation (neutrophila and septic shock)

65
Q

Symptoms of Salmonella enteriditis

A

-gastroenteritis, enteric fever, endovascular infections, focal metastatic infections (osteo, abscess), asymptomatic

66
Q

Campylobacter

A
  • curved, gram negative (sea gull shaped)
  • microaerophilic
  • flagellated (motility important for colonization and virulence)
  • extensive genetic variation
67
Q

Extensive genetic variation of Campylobacter

A
  • intra and extragenomic recombination

- variable LOS, variable capsule, flagellin modifications

68
Q

Campylobacter reservoirs

A
  • water and animals
  • commensal in avian GI tract and pathogen in human GI tract
  • huge foodborne pathogen via poultry
69
Q

Campylobacter jejuni enteritis treatment and OTHER diseases

A
  • can be managed with antibiotics if caught early
  • oral replacement with fluids and electrolytes
  • can cause Guillain-Barre syndrome
70
Q

Symptoms of C. jejuni

A

-may have fever, no abdominal pain, diarrhea

71
Q

Guillain-Barre Syndrome

A
  • ascending paralysis
  • can be acquired from C. jejuni by virtue of cross-reacting surface antigens
  • most common cause of acute neuromuscular paralysis
  • some LOS structures trigger antibodies that cross-react with gangliosides
72
Q

When do GBS appear?

A
  • about 1-3 weeks after infection with C. jejuni

- 1/100,000

73
Q

Clostrodium difficile

A
  • gram-positive bacillus

- obligate spore forming, anaerobe

74
Q

When does one usually see a Clostrodium difficile break out? What locations can this happen in?

A
  • after antibiotic treatment
  • antibiotic associated diarrhea, pseudomembranous colitis
  • can cause community and hospital acquired infections
75
Q

Spectrum of illness for Clostrodium difficile

A

-mild to severe diarrhea, fever, abdominal cramping, leukocytosis

76
Q

Natural history of C.difficile transmission

A
  • spores ubiquitous in environment, and are ingested
  • spores quiscent in colon
  • perturbation of gut flora means increased nutrients for spores
  • germination of spores and toxin production
  • diarrhea
77
Q

What causes the diarrhea and inflammation in CDI (C. difficile infection)

A

-Toxin A and B

78
Q

CDI diagnosis

A
  • not readily cultures bc present in low numbers

- detect via toxins presence: ELISA to see if glutamate Dh is present, and if it is, PCR for genes for toxins

79
Q

CDI and treatment

A
  • mild disease needs no treatment
  • moderate disease may require some therapy (bloody stool, but not severe CDI)
  • Severe disease uses Vancomyocin (oral, not IV) or Metronidazole
80
Q

Major sites for anaerobes

A
  • oral cavity
  • GI tract
  • female genital tract
  • spore-formers may be in gut, but more common in “soil”
81
Q

Pathogenesis of anerobic infection

A

-generally results from disruption of mucosal surface followed by infiltration of resident flora into a sterile site

82
Q

There are many species of anaerobes. Thus, most anaerobic infections are ________.

A

-polymicrobial

Microbio Exam 1 (13 decks)

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