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Microbio Exam 1 > GI Bacteria Lecture Notes > Flashcards

GI Bacteria Lecture Notes Flashcards

1
Q

3 general pathogenic mechanisms for development of bacterial gastroenteritis

A
  1. ingestion of preformed toxin with rapid onset of illness
  2. Ingestion of organisms that produce toxins in vivo that cause disease; sudden or delayed onset
  3. Infection by enteroinvasive organisms with delayed onset; can be locally or systemically invasive
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2
Q

How are virtually all bacterial diarrheal diseases treated?

A

-supportive care to replace fluid and electrolytes

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3
Q

Physiology and structure of Vibrionaeceae

A
  • motile, curved gram negative rods
  • facultative anaerobes
  • growth stimulated by Na+ but no exacting nutritional requirements
  • common inhabitants of both fresh and salt water environments
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4
Q

Vibrio cholera strains that invariably produce cholera toxin and possess a pathogenicity island encoding intestinal colonization factors

A

-Vibrio cholera O1 and O139

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5
Q

Pathogenesis of Vibrio cholera: where does it colonize, is it invasive?

A
  • colonizes proximal small bowel where it secretes cholera toxin which is the cause of massive diarrhea
  • not an invasive disease
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6
Q

T/F: You need the vibrio cholera bacteria to achieve the severe diarrhea.

A

-False; purified cholera toxin is sufficient; bacterium serves as a delivery system

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7
Q

Cholera Enterotoxin (CT) structure

A

-A-B subunit toxin; 5 B to 1 A

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8
Q

B subunit of CT function; what it is encoded by?

A
  • responsible for binding holotoxin to GM1 ganglioside receptors on enterocyte
  • phage encoded
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9
Q

A subunit of CT function

A
  • enters cytoplasm where it separates into A1 and A2 peptides
  • A1 affects GTP binding protein, Gsalpha, which regulates AC
  • ADP-ribosylates Gsa causing AC to be permanently turned on resulting in increase in cAMP
  • increase in cAMP/PKA blocks Na+ absorption and causes Cl- efflux through CFTR which water follows out
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10
Q

Major channel affected by cholera enterotoxin?

A

-CFTR

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11
Q

Cholera epidemiology: how is it spread?

A

-fecal-oral route via contaminated food or water

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12
Q

Cholera extraintestinal reservoirs

A
  • environmental reservoir thought to be aquatic sources–estuarine environment
  • often in association with copepod, zooplankton, shellfish, and aquatic plants
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13
Q

Cholera epidemiology: host susceptibility/inoculum size and reasons why.

A
  • need large inoculum

- because stomach acidity is an important barrier

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14
Q

Hypochlorhydria and Cholera

A

-due to surgery, antacids, infection with H. pylori predisposes to infection by raising the pH of stomach

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15
Q

Age incidence of cholera by endemic vs. non-endemic areas

A
  • immune status is important
  • high incidence in young children in endemic areas
  • all ages affected in non-endemic areas
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16
Q

Spectrum of Cholera diarrheal illness

A
  • wide spectrum: from asymptomatic to mild, moderate, or severe (cholera gravis)
  • very rapid onset is possible
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17
Q

Clinical Characteristics of Cholera infection

A
  • voluminous watery diarrhea without abdominal cramps or fever
  • in severe purges, stool loses color and odor and flecks of floating mucus give rise to term “rice water stool”
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18
Q

What are the major symptoms of cholera due to?

A
  • depletion of water and salts from intravascular and extracellular spaces of the body by loss into gut lumen
  • death can results from dehydration and electrolyte loss leading to shock
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19
Q

Treatment of cholera (2 ways)

A
  1. replace lost water and salts (rehydration), usually by oral route, or IV in severe cases
  2. antibiotics (tetracycline, doxycycline, trimethoprim-sulfamethoxazole for children) can shorten duration but are not essential
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20
Q

Prevention of Cholera

A
  • adequate santitation (clean water/chlorination)

- adequately cooked seafood

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21
Q

Vibrio Parahaemolyticus is the leading cause of _________ and can also cause _________.

A
  • seafood-borne bacterial gastroenteritis**recent history of seafood consumption should make you think of this*
  • also causes wound infections (1/3 of sporadic infections) after exposure to warm seawater
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22
Q

Clinical characteristics of V. parahaemolyticus

A
  • mostly watery diarrhea

- with cramps, nausea, vomiting, sometimes fever and chills, and bloody diarrhea (rare)

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23
Q

V. parahaemolyticus: duration and treatment

A
  • self-limited, around 3 days

- rarely needs treatment: ORS (oral rehydration solution) and tetracycline

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24
Q

95% of seafood-related deaths are due to ____________.

A
  • V. vulnificus

- common inhabitant of coastal waters and shellfish but not all strains are pathogenic

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25
Q

2 distinct clinical syndromes (and their portals of entry) of V. vulnificus

A
  1. wound infection: occurs after exposure of wound to seawater during warm months
  2. Primary sepsis: in compromised hosts after eating contaminated seafood
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26
Q

Characteristics of wound infections caused by V. vulnificus

A
  • cellulitis, sometimes with vesicles or bullae followed by necrosis
  • sometimes progresses to sepsis and death
  • more severe in patients with some type of chronic disease (diabetes, cirrhosis, leukemia, etc
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27
Q

Who do we see primary sepsis from V. vulnificus in?

A
  • compromised hosts with pre-existing hepatic or other chronic diseases
  • due to eating contaminated seafood
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28
Q

Prevention method of V. vulnificus infection

A

-because of high mortality, patients at risk (cirrhosis and hemochromatosis) should avoid raw shellfish and those at risk with wounds should avoid seawater

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29
Q

Characteristics of primary sepsis

A
  • chills, fever, prostration, and hypotension
  • usually secondary skin lesions on extremities with erythematous or ecchymotic areas -vesicles or bullae- necrotic ulcers
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30
Q

Many of the opportunistic pathogens from the gut are members of the Enterobacteraceae as they have a competitive advantage ___________.

A

-when their is inflammation

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31
Q

While most E. coli are not pathogenic, some highly adapted clones have developed with specific virulence factors that are capable of causing disease in healthy individuals. These strains may cause what 3 things?

A
  • enteric/diarrheal disease
  • UTI (local spread from GI to GU)
  • sepsis/meningitis (from bacteremia)
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32
Q

Physiology and structure of E. Coli

A
  • gram-negative rods

- facultative anaerobe

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33
Q

Key tests for identifying E. Coli

A
  • negative oxidase test

- most are lactose-fermenters (pink) on MacConkey agar

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34
Q

Special test to detect E.Coli O157:H7

A

-MacConkey sorbitol agar

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35
Q

Enterotoxigenic E. Coli (ETEC) pathogenesis

A
  • aka toxigenic E. Coli
  • produce cholera-like enterotoxin
  • adhere to small bowel enterocytes and induce watery diarrhea by secretion of heat labile (LT) and/or heat-stable (ST) enterotoxins
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36
Q

What is the most common cause of travelers’ diarrhea?

A

-ETEC

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37
Q

Enteropathogenic E. Coli (EPEC) pathogenesis

A
  • adhere to small bowel enterocytes, but destroy normal microvillar architecture, inducing characteristic attaching and effacing lesion
  • cytoskeletal derangements are accompanied by an inflammatory response and diarrhea
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38
Q

3 steps of EPEC destruction/pathogenesis

A
  1. initial adhesion
  2. protein translocation by type III secretion
  3. pedestal formation
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39
Q

Enterohemorrhagic E. Coli (EHEC) pathogenesis

A
  • induce attaching and effacing lesion, like EPEC, but in colon
  • Shiga toxin
  • can cause hemolytic- uremic syndrome (HUS)
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40
Q

The distinguishing feature of EHEC is the elaboration of shiga toxin. What does this toxin do?

A
  • protein-synthesis inhibitor

- systemic absorption of which leads to potentially fatal complication following an episode of bloody diarrhea

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41
Q

Hemolytic-Uremic Syndrome: what can cause it and what is it characterized by?

A
  • can be due to EHEC E Coli O157

- hemolytic anemia, acute kidney failure (uremia), and low platelet count (thrombocytopenia)

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42
Q

Enteroinvasive E. coli (EIEC) pathogenesis

A
  • invades colonic epithelial cell, lysis the phagosome and moves through the cell by nucleating actin microfilaments
  • might move laterally through epithelium by direct cell-to-cell spread or might exit and reenter the basolateral PM (like Shigella)
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43
Q

Enteroaggregative E. Coli (EAEC)

A
  • adheres to small and large bowel epithelia in thick biofilm
  • elaborates secretory enterotoxins and cytotoxins
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44
Q

ETEC Epidemiology

A
  • contaminated food and water
  • major cause of childhood diarrhea in developing countries
  • leading cause of travelers’ diarrhea
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45
Q

EPEC epidemiology

A
  • person to person transmission

- leading cause of infantile diarrhea in developing countries

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46
Q

EHEC epidemiology

A
  • food, water, and person to person transmission

- major cause of bloody diarrhea in developed nations

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47
Q

EAEC epidemiology

A
  • mode of transmission unknown
  • important cause of chronic diarrhea in developing countries
  • emerging cause of acute, chronic, and travelers’ diarrhea
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48
Q

EIEC epidemiology

A
  • contaminated food

- outbreaks in developed countries

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49
Q

ETEC Clinical disease

A

-acute watery diarrhea

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50
Q

EPEC clinical disease

A

-severe acute diarrhea or dysentery and vomiting, may be persistent

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51
Q

Dysentery

A

-severe diarrhea with blood and pus

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52
Q

EHEC

A

-watery and bloody diarrhea, may be complicated by HUS

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53
Q

EAEC

A

-mucoid diarrhea, often persisent

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54
Q

EIEC

A

-watery diarrhea or dysentery

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55
Q

Shigella spps physiology and structure

A
  • facultative anaerobe
  • gram negative
  • rod-shaped
  • member of enterobacteraceae
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56
Q

Key tests for identification of Shigella spps

A
  • oxidase negative
  • non-motile
  • non-lactose fermenter on MacConkey
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57
Q

T/F: Shigella and E.coli are the same organism but continue to be differentiated for epidemiologic purposes, recognition of clinical disease, and potential treatment differences.

A

True

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58
Q

General steps of Shigella spp. pathogenesis

A

-translocation of intestinal epithelium by bacterium and development of the infectious process leading to bacillary dysentery

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59
Q

What cells does Shigella cross in the colon?

A

-cross M (microfold) cells of the follicle-associated epithelium that covers the lymphoid nodules associated with the colonic mucosal tissues

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60
Q

What does shigella do in the subepithelial location?

A
  • causes extensive apoptosis of macrophages
  • this allows escape of bacteria into tissues and efficient basolateral entry into epithelial cells, followed by cell to cell spreading, which generates sufficient intracellular colonization
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61
Q

The expansive macrophage apoptosis assoc. with shigella can also trigger ________. How else is this triggered?

A
  • inflammation through the release of IL-1B

- amplified by presence of intracellular bacteria that activate NOD1 pathway

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62
Q

How does shigella induce the NOD1 pathway of inflammation?

A

-release of peptidoglycan (PGN) which induced NF-KB activation and chemokine expression

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63
Q

Where does Shigella primarily impact? What will this tissue look like?

A
  • distal colon
  • acute mucosal inflammation and erosion and purulent exudate
  • pale, granular, inflamed mucosa with patches of coagulated exudate from a massive recruitment of PMNs inducing rupture of the epi barrier
64
Q

Although locally invasive, Shigella does not _______.

A

-cause bacteremia or disseminate

65
Q

Epidemiology of Shigella

A
  • strictly a human pathogen (no animal reservoir)
  • fecal-oral transmission
  • person-to-person spread
66
Q

What are most US cases of Shigellosis caused by?

A

-Shigella sonnei

67
Q

Where is Shigellosis most common in the US?

A
  • day care centers

- areas with crowded living conditions such as urban centers or residential institutions

68
Q

Clinical disease of Shigella

A
  • locally invasive organisms that causes an inflammatory type diarrhea
  • affects mainly lower GI
  • high fever, abdominal cramps, and bloody, mucoid diarrhea (dysentery)
69
Q

What is the method of choice to diagnose Shigella?

A

-culture via differential and selective media

70
Q

Treatment of Shigella

A
  • most episodes are self-limited but severe disease (dysentery) or disease in compromised people will benefit from antibiotic treatment
  • Fluoroquinolone due to low resistance
71
Q

Salmonella spps physiology and structure

A
  • facultative anaerobe
  • gram negative
  • rod shaped
  • member of enterobacteraceae
72
Q

Key tests to identify salmonella

A
  • oxidase-negative
  • motile
  • non-lactose fermenters on MaConkey agar
73
Q

Pathogenesis of Salmonella: how does it cross the epithelial barrier and where does it occur?

A

-cross M cells of follicle associated epithelium mainly in Peyer’s patches of ileal portion of small intestine but also in colon

74
Q

What does salmonella do in the subepithelial space?

A
  • might cause macrophage apoptosis via effector protein injection (Type 3 secretion system) encoded by Spi1
  • can also switch to Spi2 expression which allows injection of effector proteins that allow bacteria to modify vacuole to support growth and multiplication
75
Q

2 types of Salmonella

A
  • Typhi

- non-typhoidal

76
Q

Epidemiology of Non-typhoidal Salmonella

A
  • principle reservoirs are birds, mammals, reptiles, and amphibians THINK PETS
  • one of the most common agents of bacterial gastroenteritis in US
  • fecal oral transmission and…
  • contaminated food (poultry, eggs, and milk products)
77
Q

Top 3 bacterial enteropathogens

A
  • Shigella
  • Salmonella Nontyphi
  • Campylobacter
78
Q

Epidemiology of typhoidal salmonella

A
  • primarily colonize humans
  • consumption of fecally contaminated food or water
  • cause systemic illness (typhoid or enteric fever) usually with little or no diarrhea
79
Q

Clinical disease of Salmonella Typhi

A
  • highly endemic in poor countries
  • abdominal pain, fever, chills, and constitutional symptoms
  • acute phase: fever and bacteremia, followed by abdominal pain and rash (rose spots), then there may be hepatosplenomegaly, intestinal bleeding and perforation, may occur with secondary bacteremia and peritonitis
80
Q

What may cause the hepatosplenomegaly, intestinal bleeding and perforation in Typhoid fever?

A

-related to ileocecal lymphatic hyperplasia of peyer’s patches

81
Q

Clinical disease of Salmonella non-typhi: How is it acquired?

A
  • usually results from improperly handled food that has been contaminated by animal or human fecal material
  • can also be acquired from fecal-oral route from other humans or farm/pet animals
82
Q

Clinical symptoms of Salmonella Gastroenteritis

A
  • nausea, vomiting, fever, diarrhea (may be bloody), and cramping
  • usually within 1-3 days of ingesting contamination
  • higher the ingested dose, worse the symptoms and longer the duration
  • self-limited usually
83
Q

Salmonella and the immunocompromised

A

-especially at risk to have bactermic infection like osteomyelitis in patients with sickle cell disease

84
Q

Why may enteric fever (Salmonella Typhi) be hard to diagnose from culture of fecal matter?

A

-organism is often absent from stool when diagnosis is considered

85
Q

Treatment of Salmonella (Typhi and enteritidis)

A
  • Enteritidis: usually not needing antimicrobial unless severe (high fever, severe diarrhea, immunosupressed) and may prolong shedding
  • Typhi: always treat enteric fever with antibiotics
86
Q

Prevention methods of Salmonella

A

-2 licensed TYPHOID vaccines that offer incomplete protection and should be considered for travelers to endemic regions

87
Q

Campylobacter jejuni structure and physiology

A
  • gram negative, seagull, “s” shaped rods,
  • special growth conditions: microaerobic atmosphere, 42 celcius
  • flagellated**important virulence factor
  • extensive genetic variation
88
Q

Important tests distinguishing C. jejuni

A
  • oxidase positive, catalase positive

- differentiated from other species by ability to hydrolyze sodium hippurate

89
Q

The essential lesion in campylobacter jejuni enteritis is an acute inflammatory enteritis, which commonly extends down the intestine to affect the ________.

A

-colon and rectum

90
Q

What does histology of C. jejuni show?

A

-acute inflammation of the mucosa with edema, infilitration by PMNs and crypt abscess formation

91
Q

For infection to become established, Campylobacters must first survive ______. Therefore, what facilitates these infections?

A
  • gastric acidity to colonize the jejunum and ileum

- lowering gastric acidity facilitates infections

92
Q

Abdominal pain in Campylobacter enteritis may be intense, continous, and radiate where? What is this called? What causes this pain?

A
  • right iliac fossa
  • Pseudo-appendicitis
  • this pain is caused by terminal ileitis and mesenteric adenitis
93
Q

Campylobacter has reservoirs in ______ and ______. It is commensal in the ____________ and a pathogen in the ___________.

A
  • water and animals
  • Avian GI tract
  • Human GI tract
94
Q

What is the main vehicle of transmission of campylobacter?

A

-improperly cooked poultry

95
Q

Clinical disease of campylobacter jejuni enteritis

A
  • incubation period of 1-3 days
  • fever, abdominal cramping which may be severe, diarrhea that is watery or bloody lasting several days to 1 week
  • usually self-limited and does not need antimicrobials; can be treated with antibiotics if caught early
96
Q

One of the rare complications following campylbacter infections is ________. What is this?

A
  • Guillain-Barre Syndrome (GBS)

- acute, self-limited, immune mediated attack on the peripheral nervous system resulting in ascending motor paralysis

97
Q

Why is C. jejuni infection thought to lead to GBS?

A
  • C. jejuni produces a ganglioside-like structure in its outer core of the lipooligosaccharide and the immune response to these ganglioside mimics cross-reacts with relevant ganglioside target in PNS
  • leads to demyelination or axonal degeneration of peripheral nerves
98
Q

Laboratory diagnosis of C. jejuni

A
  • stool culture using selective media designed specifically for isolation of campylbacter species
  • gram-stain of stool in acute disease may be helpful in rapid diagnosis
99
Q

Genetic variation of Campylobacter

A
  • intra and intergenomic recombination

- variable LOS, variable capsule, flagellin modifications

100
Q

Frequency of GBS after C. jejuni infection

A

1/100,000

-most common cause of acute neuromuscular paralysis

101
Q

Clostridium difficile structure and physiology

A
  • gram positive bacillus
  • obligate spore forming anaerobe
  • common inhabitant of gut in low numbers
102
Q

Clostridium difficile usually follows after patients have done what?

A

-treated with a broad spectrum antibiotic, which disrupt the intestinal flora and allow the organism (in colonized patients) to increase and express its toxins and other virulent factors leading to disease

103
Q

C. difficile produces 2 major toxins: what do they do?

A
  • TcdA (toxin A)
  • TcdB (toxin B)
  • they are glucosyltransferases that inactivate Rho, Rac, and Cdc42 in target cells
104
Q

How do toxin A and toxin B of C. difficle enter cells?

A

-enterotoxins enter cell through receptor mediated endocytosis and require an acidified endosome for translocation

105
Q

Toxin A and toxin B effects

A
  • both cause cytopathic effects, with toxin B having more potent effects on cells
  • A: increases permeability of colonic epithelial layers and may effect expression of chemokines in human intestinal epithelial cells
  • Both: disrupt tight junctions of epi barriers and enhance migration of neutrophils into the intestines
106
Q

Epidemiology of Clostridium difficile

A
  • most common cause of antibiotic associated diarrhea

- hospital and community acquired

107
Q

Patient related factors for acquiring C. difficle

A
  • age (increased risk in elderly)
  • surgery
  • chemotherapy
  • laxatives
  • defects in humoral immunity
108
Q

C. difficile spectrum of illness

A

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

109
Q

________________ indicates severe disease.

A

-endoscopic evidence of pseudomembrane formation in colon

110
Q

A significant proportion of patients treated with _________ have a C. diff relapse.

A

-oral vancomycin

111
Q

2 ways to detect C. diff infection

A
    1. TcdA detection from stool immunoassay; same with TcdB

2. ELISA to detect glutamate dehydrogenase; if positive, then PCR for tcda and tcdb genes

112
Q

C. difficile infection is commonly treated how? what is severely ill?

A
  • discontinue treatment with offending microbial agents
  • if severe illness of infection, oral therapy with vancomycin or metronidazole is instituted
  • fecal implants, anion-exchange resins absorption of toxin, pulse-dosing with vancomycin
113
Q

3 groups of etiologic agents of the gut NOT causing acute gastroenteritis

A
  • Anaerobes
  • Helicobacter pylori
  • Enterococcal spps
114
Q

What are the major sites for anaerobes?

A
  • oral cavity
  • GI tract (colon)
  • female genital tract
115
Q

Pathogenesis of anaerobic infection

A

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

116
Q

Strict anaerobes will only thrive at sites that are ____________.

A

-poorly vascularized and not exposed to air

117
Q

Because there are many specific of anaerobes, most anaerobic infections are ___________.

A

-polymicrobial

118
Q

Anaerobic characteristics

A
  • organisms that fail to grow in air including microaerophilic conditions (10%CO2)
  • foul odor, gas production
  • vary in tolerance to air depending on levels of superoxide dismutase, which removes toxin superoxide and catalase, which removes hydrogen peroxide
119
Q

Pathogenic anaerobes tend to be more __________.

A

-aerotolerant

120
Q

Physiology and structure of Bacteroides fragilis

A
  • gram negative rod

- grows in presence of bile-esculin

121
Q

Natural history of C. difficile infection

A
  • spores ubiquitous in environment and are ingested
  • spores are quiescent in colon
  • perturbation of gut flora, increased nutrient for spores, germination of spores, toxin production, diarrhea
122
Q

Infection caused by B. fragilis

A
  • typically occurs as an abscess
  • breaching of gut wall allows escape of microbes. These cause peritonitis when they get into the peritoneal cavity
  • early in this process the enterobactereacae may predominant and often times these infections cause discrete areas where anaerobes take over
123
Q

Why is B.fragilis thought to be able to form an abscess?

A
  • capsular polysaccharide resists phagocytosis
  • CD4+ Th17 reaction to its capsule that may induce abscesses
  • its LPS endotoxin induced minimal inflammation
124
Q

Why are anaerobes often underdiagnosed and underappreciated as causative agents of infection?

A

-successful culture often requires maintaining oxygen-free environment with special transport medium and handling procedures

125
Q

Treatment of choice for B. fragilis. Is this the same for all anaerobes?

A
  • Metronidazole (flagyl)
  • penicillin has good coverage, but B fragilis is typically resistant due to beta-lactamase expression
  • therapy should consider polymicrobial etiology
  • surgical debridement/drainage of necrotic tissue
126
Q

Helicobacter pylori physiology and structure

A
  • gram negative, curved rod
  • highly motile (flagella)
  • urease positive
127
Q

Clinical disease caused by B.fragilis

A

-infection typically occurs as an abscess in normally sterile spaces where there has been exposure to contents of the gut lumen

128
Q

Helicobacter pylori niche and why it is necessary?

A
  • resides in thick lining of stomach
  • specialized to colonize stomach and duodenum
  • usual niche provides partial protection from acid, competitors, and host immune responses
129
Q

Why is urease important for H. pylori?

A

-produces bases (ammonia) from urea to neutralize acid in its local environment in the stomach

130
Q

H. pylori strains expressing _________ are 60-70% more likely to cause disease.

A

-CagA, cytotoxin

131
Q

CagA secretion and function

A
  • cytotoxin
  • secreted into host cells by type 4 secretion apparatus
  • inhibits clearance by altering host cells signaling through its tyrosine phosphorylation activity
132
Q

2 cytotoxins H. pylori may express

A
  • CagA

- VacA

133
Q

Induction of chemokines like IL8 via CagA attracts neutrophils, and result in what 3 things?

A

-chronic inflammation, elevated gastrin secretion, and increased gastric acid levels

134
Q

What does VacA encode and its function

A
  • vacuolating cytotoxin

- secreted protein toxin that is responsible for the gastric epithelial erosion observes in infected hosts

135
Q

H. pylori strains that express VacA are more common among patients with _____________ than among infected patients with superficial gastritis alone.

A

-peptic ulcer disease and distal gastric cancer

136
Q

Chronic superficial gastritis due to H. pylori may lead to what 3 long-term complications?

A
  • peptic ulcer disease
  • atrophic gastritis (loss of epithelial glands)
  • gastric adenocarcinoma (gastric MALT B cell lymphoma)
137
Q

How is H. pylori transmitted?

A
  • person to person transmission esp. within families

- oral-fecal transmission is most likely

138
Q

H. pylori’s primary reservoir

A

-human

139
Q

H. pylori infections correlate to what?

A

-SES and age

140
Q

What decreases H pylori risk?

A

-improved hygiene

141
Q

Clinical diseases assoc with H. pylori

A
  • gastritis, peptic ulcers, gastric adenocarcinoma (upper GI tract complications)
  • duodenal ulcers due to hypersecretion of acid in early gastritis
142
Q

What causes the clinical diseases assoc. with H. pylori?

A

-it is the host response to infection via inflammation and hypersecretion of acid

143
Q

3 ways to diagnose H pylori

A
  • microscopy from biopsy
  • urease biochemical test
  • detection of host antibodies (good for screening, not for determining outcome of treatment)
  • doesnt grow well in culture
144
Q

Treatment of H. pylori infection

A
  • monotherapy is ineffective due to resistance
  • combination therapy required to raise gastric pH to render antibiotics more effective
  • Clarithryomycin (macrolide) and amoxicillin plus proton pump inhibitor (omeprazole)
145
Q

Enterococcus is a ________ pathogen.

A
  • nosocomial

- 2nd most common cause

146
Q

Enterococcus physiology and structure

A
  • gram positive cocci in singles, pair, and chains (looks like strep)
  • facultative anaerobe
  • major habitat is GI tract of humans and other animals
  • also found in nursing homes and hospitals
147
Q

2 major species of enteroccus; which is more common?

A
  1. E. faecalis
  2. E. faecium
    - E. faecalis is more common but E. faecium accounts for more multi-resistant strains
148
Q

Enterococcus is spread within hospital settings (hospital personnel is important reservoir) rather than from …

A

-endogenous pre-hospitalization flora source

149
Q

Pathogenesis of Enterococcus

A
  • gut colonization precedes disease in susceptible hosts
  • host factors (debilitation) rather than virulence of organism is primary determinant of pathogenesis
  • ability to exist as biofilm important for catheter related infections
150
Q

4 types of disease that Enterococcus can produce

A
  1. UTI
  2. Bacteremia/septicemia (esp. catheter associated)
  3. endocarditis
  4. intra-abdominal/pelvic infections
151
Q

Resistance to enterococcus makes its treatment difficult. Why is resistance so common in this strain?

A

-are adept at conjugative transfer of plasmids and transposons

152
Q

What is the drug of choice for enterococcus?

A
  • ampicillin for sensitive strains

- VRE and acquiring resistance to cephalosporins

153
Q

Laboratory diagnosis of Enterococcus/ hemolysis

A

-alpha or nonhemolytic on blood agar

154
Q

What is the most problematic issue of enterococcus?

A

-multi drug resistance

155
Q

How did VRE acquire its resistance?

A

-mobile genetic element that allows the organism to detect effect of glycopeptide antibiotics like vancomycin and express an altered stem peptide that still allows for cross linking, but reduced affinity for vancomycin

156
Q

Overuse of vancomysin and cephalosporins selected for VRE. Where did it acquire its cephalosporin resistance?

A

-it is intrinsic

157
Q

risk factors for acquiring VRE

A
  • prior broad spectrum antibiotic use (cephalosporins and vancomycin)
  • prolonged hospitalization
  • immunocompromised host
  • neutropenia
  • admission to ICU
  • renal failure needing dialysis

Microbio Exam 1 (13 decks)

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