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GI First half > microbiology > Flashcards

microbiology Flashcards

1
Q

campylobacter jejuni

A

food borne cause of fever, abdominal pain and diarrhea; both kids and adults

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2
Q

rotavirus

A

most common cause of viral gastroenteritis in infants/children; can lose fluids and become dehydrated

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3
Q

escherichia coli

A

hemolytic-uremic syndrome in kids

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4
Q

cryptosporidiosis

A

watery diarrhea in immunocompromised adults by cryptosporidium

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5
Q

listeriosis

A

congenital infection that is present with meningitis and sepsis at birth – food or water borne

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6
Q

norwalk virus

A

common cause of diarrhea in adults

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7
Q

shigellosis

A

dysentery with bloody diarrhea

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8
Q

cholera

A

massive fluid loss

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9
Q

what is the agent that is associated with duodenal peptic ulcers?

A

H pylori

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10
Q

vibrio parahaemolyticus

A

found in raw shellfish

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11
Q

yersinia enterocolitica

A

invasive; extraintestinal infection

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12
Q

staph aureus causes food poisoning through…

A

food poisoning through elaboration of an enterotoxin that causes explosive diarrhea within 2 hrs of ingestion

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13
Q

entamoeba histolytica

A

colonic mucosal invasion with exudate and ulceration; stool with blood and mucus
self limited diarrhea with following liver abscess(via submucosal invasion –> veins –> portal system –> liver)

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14
Q

Special defenses of saliva

and organisms with a resultant tactic?

A

secretory IgA in saliva that selectively inhibits adherence of bacteria

Neisseria gonorrhœae (which causes gonorrhea), Strep pneumoniae, and Haemophilus influenzae type B all releases a protease that destroys IgA.

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15
Q

small intestine defenses

A 
peristalsis
flow of liquids
shedding of epithelium
peyers patches
igA
mucous
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16
Q

peyers patches

A

cells that are only in the ileum

– they sample antigen, initiate immune response in the mucosa, and activate T and B cells

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17
Q

body flora increase in numbers with…

A

distance from stomach

few in esophagus or stomach

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18
Q

common oral flora

A 
Many anaerobes: 
a-streptococci, 
Neisseria spp., 
diptheroids (nonpathogenic corynebacteria), 
lactobacilli, 
spirochetes (treponema denticola), 
mycoplasma
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19
Q

B-hemolytic strep groups vs a-hemolytic strep groups

A

B - complete hemolysis
—pyogenes or agalactiae
a - partial hemolysis
—pneumoniae or viridans

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20
Q

a-streptococci types that is abundant in flora of mouth? throat?

A

viridans is more common in mouth

pneumoniae is more common in the pharynx/throat

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21
Q

viridans streptococci

A

streptococci with no defined Lancefield group antigens (Lancefield classification is based on carbohydrate antigens on the bacterial surface); normal flora of the respiratory tract but can cause dental caries, bacterial endocarditis, and other disorders in immunocompromised hosts.

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22
Q

6 types of strep viridans

c,mm,sss

A
  • S. mutans = dental caries
  • S. mitis = cheek region
  • S. sanguinis, no preference of locations
  • S. salivarius = dorsal side of the tongue
  • S. salivarius ssp. thermophilus
  • S. constellatus, occasional human pathogen,
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23
Q

the strep of dental caries

A

strep mutans

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24
Q

strep of cheek region?

A

strep mitis

25
Q

strep of dorsal side of tongue?

A

strep salivarius

26
Q

lactobacilli

A

Gram-positive facultative anaerobic or microaerophilic rod-shaped bacteria. They are part of the lactic acid bacterial group, whose members convert lactose and sugars to lactic acid. In humans they are present in the vagina and the GI tract. They are typically benign, except in the mouth where they are associated with cavities/dental caries.

27
Q

Periodontitis

A

requires bacteria to occur but that alone is not sufficient –> genetics and environment also play a role

28
Q

periodontitis due to diabetes mellitus –

A

porphyromonas gingivalis

29
Q

periodontitis with cardiovascular disease –

A

Porphyromonas gingivalis
Tannerella forsythia
T. denticola

30
Q

pariodontitis with adverse pregnancy

A

porphyromonas gingivalis

31
Q

common oral pathogens

A 
B-streptococci
staph aureus
herpesvirus
coxsackievirus
HPV
candida
\+others
32
Q

B-Streptococci

A

•may present as pharyngitis (strep throat), scarlet fever (rash), impetigo (infection of the superficial layers of the skin), or cellulitis (infection of the deep layers of the skin).

Invasive, toxigenic infections can results in necrotizing fasciitis, myositis, and strep TSS. Patients may also develop immune-mediate post-strep sequelae, such as acute RF and acute glomerulonephritis

33
Q

staph aureus

A
  • Coagulase-negative Staph
  • Staph mucositis (stomatitis) in debilitate elderly patients
  • Oral mucositis – inflammation of oral mucosa resulting from chemotherapeutic agents or ionizing radiation  erythema or ulcerations
  • Stomatitis – any inflammatory condition of oral tissue, including mucosa, dentition/periapices, and periodontium; Includes mucositis
34
Q 
Others
GNR
GPR
GNC
GPC
A

o GNRs: prevotella (+ B-lactamase), fusobacteria
o GPR’s: proprionobacterium, actinomyces
o GPC’s: peptostreptococci, peptococci, gemella
o GNC’s: veillonella species

35
Q

herpesvirus

A
  • **all herpesviruses have identical morphology and cannot be distinguished under electron microscopy.
  • Linear double-stranded DNA; 150-200 kbp
  • Icosahedral capsid, 162 capsomeres
  • Infect mucousal epithelial cells and Replicate in the nucleus
  • Viral particles bud through nuclear membranes and into membrane of exocytic vesicles
  • HSV-1 typically causes oral herpes, but HSV-2 can cause oral infections if spread during oral sex
36
Q

coxsackievirus

-type types?

A
  • Picornaviridae family
  • Enterovirus and a single stranded RNA virus – Infects host cells and cause them to lyse

Separable into 2 groups, A and B, which are based on their effects on mice
o A results in muscle injury, paralysis and death
 Cause herpangina (painful blisters in the mouth, throat, hands, feet) = hand/foot/mouth disease; children

37
Q

HPV

A

• Can infect oral and genital areas

o HPV is a major cause of squamous esophageal carcinoma!

38
Q

candida

A
  • Candida is a yeast, which is normal flora in some, but can cause infection when in the wrong location or in immunocompromised patients (HIV)
  • upper GI tract disease = candidiasis or thrush (C. albicans is most common species)
  • Candida are dimorphic – grow as ovid yeast cells or elongated pseudohyphal/hyphael cells
  • The hyphael form is the virulent form
39
Q

what form of candida is virulent?

A

hyphael

40
Q

few normal flora in esophagus because of…

A

constant swallowing

41
Q

immunocompromised patients infection….

A

 Herpes/CMV, HPV & Candida

  • HSV-1 infection of the esophagus is usually in immunocompromised
  • Immunocompromised hosts — HSV esophagitis occurs most frequently in solid organ and bone marrow transplant recipients. HSV and CMV are the most commonly identified pathogens in esophagitis patients who have undergone bone marrow transplantation.
  • HSV is a less common cause of esophagitis in patients with HIV infection than in transplant recipients. The most common cause of esophagitis in patients with advanced AIDS is candida, whereas the most common viral cause is CMV.
42
Q

two normal organisms of stomach

A

lactobacilli and fusobacterium

43
Q

main causative organism of gastritis/gastric cancer?

A

H pylori

44
Q

H, pylori

A

 Gram-negative Spiral shaped rod
 Microaerophilic; Urease-positive
 only environmental reservoir = humans and primates  in 50% of stomachs
 The only bacterium classified as a type I carcinogen by WHO
 Colonizes gastric epithelium and induces a strong inflammatory response

45
Q

h pylori gastric infection clearance?

A
  • Inflammation never clears infection – people are chronically colonized unless treated with antibiotics
  • People can get recolonized after they are treated with antibiotics if they are re-exposed
  • One consequence of acute inflammation is ulceration on gastric epithelial surfaces.
46
Q

H pylori gastric pathogenesis

A

1 - Binds to gastric mucosa; uses:Urease, mucinase, phospholipase, flagella
2 - Epithelial damage 
o Urease, VacA (vacuolating cytotoxin), CagA (cytotoxin associated gene A)
3 - Chronic superficial gastritis (superficial inflammatory infiltration) 
o Arginase, superoxide dismutase, catalase
4 - Chronic deep gastritis (deep inflammatory infiltration) 
o Arginase, superoxide dismutase, catalase
5 - Early stage of chronic atrophic gastritis (CAG) 
6 - Late stage of chronic atrophic gastritis (CAG) 
7 - Gastric carcinoma (and/or intestinal metaplasia)

47
Q

three important virulence factors of H pylori

A

urease
VacA
CagA

48
Q

urease as h pylori virulence factor

A

survive pH stress by converting urea to ammonia and CO2

o UreI is a proton gated pore; UreAB (two subunits, A and B) catalyzes reaction

49
Q

VacA

A

vacuolating cytotoxin
o Causes the formation of large, nonfunctional endosomal-lysosomal hybrids
o Induces mitochondrial membrane permeability and reduced transmembrane potential in a dose-dependent fashion
o Releases cytochrome and induce apoptosis
o Can inhibit the ability of T cell to become activated

50
Q

CagA

A

pokes into cell and injects CagA directly into cytoplasm of cell
o Encoded on pathogenicity island; Modulates numerous host cell pathways
o Oncoprotein

51
Q

three factors used in H pylori colonization?

A

urease
mucinase or phospholipase
flagella

52
Q

three factors used in H pylori direct damage to tissue?

A

urease
VacA
CagA

53
Q

h pylori defense against phagocytes?

A

SOD - superoxide dismutase
catalase
arginase

54
Q

transmission of H pylori

A

• Exact route is unknown (likely oral-oral)
• Genetic fingerprinting studies show that isolates from an individual are identical; from unrelated individuals are different; from spouses are different; children are similar to isolates from one parent
• Suggests once a strain colonized, much genetic change occurs over time
• Not due to horizontal exchange with other bacteria
o Co-infections are rare

55
Q

old gastric ulcers treatment dogma

A

caused by excessive acid, damages tissues and causes inflammation
o Bland diet, histamine, H2 receptor blockers, surgery to remove ulcers
o Success: ulcers recur if H2 blockers are discontinued
o Cost: H2 receptor-blockers cost $60-100 per month (for life)

56
Q

new gastric ulcers dogma

A

caused by H. pylori infection causes inflammation and damage to tissue
o Antibiotic regimen (1-4 weeks) of one or two antibiotics plus antacid
o Success: no recurrence after completion of therapy
o Cost: two weeks of therapy costs

57
Q

H pylori is protective against…

A

asthma
active TB
esophageal cancer

58
Q

triple therapies for H pylori infection

A

1) omeprazole, amoxicillin, and clarithromycin
2) lansoprazole, amoxicillin, and clarithromycin
3) busmuth subsalicylate, metronidazole, tetraycline and H2 blocker

59
Q

ways to detect h pylori infection

A

1) glemsa or wirthin-starry stain (histologically)
2) urease tests
3) culture

GI First half (8 decks)

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