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ID unit 1 > enteric bacteria > Flashcards

enteric bacteria Flashcards

1
Q

list the enteric bacteria

A

Vibrionaceae: vibrio cholerae, vibrio parahemolyticus. Enterobacteriaceae: e coli, shigella, salmonella, yersinia. Campylobacter. Helicobacter pylori.

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2
Q

Which enteric bacteria are spread by environment

A

nontyphoidal salmonella, enterohemorrhagic e coli and vibrio cholera.

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3
Q

Which enteric bacteria are spread human to human

A

typhoidal salmonella, enterotoxigenic e coli, vibrio cholerae and shigella

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4
Q

sources of enteric pathogens

A

poultry, egg, milk, beef, vegetables

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5
Q

enteric bacteria gram staining

A

all are gram negative bacilli

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6
Q

Gram negative bacteria structure

A

Outer membrane contains lipopolysaccharide. LPS contains: lipid A (endotoxin), core polysaccharides (differs btw genera), O antigens (repeating oligosaccharides). They also contain H antigens (flagellar proteins in motile organisms) and K antigens ( capsular polysaccharide not found in all strains)

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7
Q

how do you detect fecal leukocytes

A

methylene blue stain

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8
Q

Which enteric bacteria are oxidase positive vs negative?

A

All enterobacteriacaea are oxidase negative, and ferment glucose. Vibrios are oxidase positive

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9
Q

importance of plasmids in enterics

A

can confer antibiotic resistance, produce enterotoxins, and confer adherence/ invasive factors

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10
Q

How do bacteriophage affect enteric bacteria

A

bacteriophage can change the phenotype of a bacterium it lysogenizes (ex. V. cholerae toxin)

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11
Q

define pathogenicity islands

A

regions of DNA found in chromosomes of pathogenic strains only which encode virulence factors such as toxins, invasion genes, etc.

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12
Q

What are type III secretion systems

A

method used by gram negative bacteria which play a role in invasion, intracellular survival and attachment

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13
Q

Describe watery diarrhea and the likely bacterial causes

A

copious, watery, no blood or pus. No tissue invasion. Small intestine. Causes: ETEC, EPEC, , cholera

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14
Q

Describe dysentery and likely causes

A

scant volume, blood pus or mucus. Tissue invasion. Large intestine. Causes: shigella, EIEC, campylobacter

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15
Q

Describe protracted diarrhea and likely causes

A

Lasts more than 14 days. Causes: EPEC

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16
Q

Describe bloody, watery diarrhea and likely causes

A

copious, some blood, pus, invasion. Ileum and colon. Causes: salmonella, campylobacter, yersiniae

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17
Q

describe hemorrhagic colitis and likely causes

A

copious, like liquid blood, no leukocytes or invasion. Large intestine. Causes: EHEC

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18
Q

What are the main mechanisms used by enteric bacteria

A

Toxigenic (vibrio cholerae, ETEC, EHEC), invasive (salmonella) or both (shigella)

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19
Q

define exotoxin, enterotoxin and endotoxin

A

Exotoxin: secreted out of cell by organism. Enterotoxin: exotoxin with specific effects on intestine. Endotoxin: LPS (lipid A + O antigen)

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20
Q

For each of the following, list the type of diarrhea produced upon infection and common organisms: small intestine, large intestine

A

small intestine: secretory diarrhea. V. cholera, ETEC, salmonella, Yersinia, campylobacter. Large intestine: inflammatory diarrhea. Shigella, EHEC

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21
Q

What determines relative infectivity

A

Organisms that are more sensitive to acid (such as vibrios) have higher infective doses and are more likely to be transmitted by food or water. Those with lower infective doses are more likely to be transmitted from person to person (such as shigella)

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22
Q

Describe cholera

A

Profuse watery diarrhea caused by an enterotoxin. Prototype for toxigenic diarrheas. No tissue invasion present - affects the small intestine

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23
Q

pathogenesis of cholera

A

Colonization of small bowel and toxin production. Bacteriophage conversion is important

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24
Q

Cholera colonization

A

Requires surface expressed adherence factor TCP pilus

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25
Q

Cholera toxin production

A

Encoded as part of a phage cholera toxin gene. This phage uses the TCP pilus as its receptor

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26
Q

Cholera toxin structure/function

A

A and B toxins- B subunit binds ganglioside GM1 of enterocytes and allows the A subunit to enter cytoplasm and constitutively activate adenylate cyclase, leading to increased cAMP then increased Cl secretion, decreased Na absorption and net secretion of fluid into gut lumen. The cholera toxin is cytotonic (does not kill the cell)

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27
Q

Cholera mode of transmission

A

fecal/oral- contaminated water> foods. Aquatic environments (shellfish). Also person to person

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28
Q

Cholera treatment

A

Restore fluid and electrolyte loss. Oral rehydrate solution (salt/sugar soln) or IV ringers lactate + KCl. Antibiotics shorten course (tetracyclines)

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29
Q

Vibrio parahemolyticus- mode of transmission, diseases it causes

A

Comes from raw or undercooke shellfish (it is a halophilic organism found in marine environments). Causes gastroenteritis, wound infections and septicemia.

30
Q

Vibrio vulnificus- mode of transmission and Sx

A

Ingestino of contaminated seafood (oysters). Causes gastroenteritis and can proceed to extraintestinal infections in immunocompromised

31
Q

Compare ETEC, EPEC and EHEC: type of diarrhea, and virulence factors

A

Enterotoxigenic: travelers diarrhea,heat labile and heat stable toxins. Enteropathogenic: watery persistent diarrhea, Attaches and effaces. Enterohemorrhagic: bloody dysentery, attaches and effaces and produces shiga like cytotoxin

32
Q

For ETEC: Sx, treatment

A

Watery diarrhea, no blood or pus. Rare low grade fever. Abd cramps, vomiting. Treatment: supportive (fluids, salt), Abx not recommended, but if necessary fluoroquinolones. Pepto relieves Sx.

33
Q

ETEC pathogenesis

A

NO tissue invasion. Heat labile enterotoxin (same mechanism as cholera) and heat stable enterotoxin (activates guanylate cyclase raising cGMP and increasing fluid secretion). Colonizes small intestine by fimbrial adhesions to overcome peristalsis

34
Q

EPEC - population, Sx, treatment

A

infants (daycare centers). Sx: watery stools, no blood or mucus. Vomiting, low grade fever. Treatment: hydration, antibiotics.

35
Q

EPEC pathogenesis

A

NO tissue invasion. Adhere to enterocyte surface. Type III secretion of translocated-intimin receptor initiates attaching and effacing lesion (microvilli destruction, pedestal formation). This interferes with absorption leading to diarrhea

36
Q

EHEC - source,serotype, Sx

A

Food/water outbreaks. O157:H7 is major serotype. Sx: initially watery then bloody diarrhea and hemorrhagic colitis leading to hemolytic uremic syndrome. Fecal leukocytes uncommon (diagnostic feature)

37
Q

EHEC - treatment and pathogenesis

A

Treatment: supportive. Abx have no benefit. Pathogenesis: Form attaching-effacing lesions, also produce shiga-like cytotoxins which bind to Gb3 sphingolipids of enteroctes and renal endothelial cells then inhibit protein synthesis and cause tissue damage

38
Q

what are M cells

A

antigen sampling cells that overly the lymphoid follicles of the gut

39
Q

Invasive pathogens Sx and pathogenesis

A

Bacteria invade the intestine via M cells and cause structural damage to the intestine. This produces an inflammatory diarrhea- frequent low volume mucoid and/or bloody stools with tenesmus, fever or abd pain. Stools have many leukocytes

40
Q

List the invasive enteric bacteria

A

Shigella, salmonella and S. Typhi, EIEC, yersinia, campylobacter

41
Q

List the noninvasive enteric bacteria

A

virbrio cholera, ETEC, EPEC, EHEC

42
Q

Shigella classifications

A

group A: S. dysenteriae. Group B: S. flexneri. Seen primarily in male homosexuals. Group C: S. boydii primarily in India. Group D: S. Sonnei, mildest disease, most common in US

43
Q

Shigella pathogenesis

A

Enterotoxins cause watery diarrhea. Type III secretion of effector proteins. Entry via M cells, uptake by macrophages. Induces apoptosis and released bacteria invade basal side of epithelial cells. Shigella lyse the vacuole, grow in the cytoplasm and spread to neighbors. Inflammatory response increases spread but enables clearance of infection.

44
Q

Which shigella produce shiga toxin

A

Only S. dysenteriae type 1

45
Q

Shigella Sx

A

Incubation period of 1-4 days. Fever, malaise, vomiting, watery diarrhea, frank dysentery, blood and mucus, cramps and tenesmus. Hemolytic uremic syndrome

46
Q

Shigella infectivity

A

Very acid resistant so low infectious dose (10-100)

47
Q

Shigella transmission

A

Four F’s: food, fingers, feces, flies

48
Q

Shigella treatment

A

supportive, fluid balance. Antibiotics shorten duration of sx and shedding of bacteria- ciprofloxacin

49
Q

Salmonella transmission

A

Fecal oral route. Typhoid: only transmitted by humans. Non-typhoid: poultry, eggs, contaminated produce

50
Q

salmonella virulence factors

A

attachment, invasion (pathogenicity island 1) and survival inmacrophages (pathogenicity island 2)

51
Q

Salmonella pathogenesis

A

Invasion of M cells, transient bacteremia. Uptake by mononuclear phagocytes where salmonella multiply.

52
Q

Salmonella Sx

A

Gastroenteritis: 24-48 hrs after ingestion nausea, vomiting, headache, fever, cramps and watery diarrhea. Septicemia: prolonged fever. Typhoid fever: incubation of few days to few weeks. Constipation or inflammatory diarrhea followed by fever. Continues for 6-8 weeks untreated

53
Q

Salmonella treatment

A

Gastroenteritis is self limiting. Typhoid requires antibiotics- ciprofloxacin and ceftriaxone.

54
Q

Salmonella immunity

A

There are so many diff serovars that there is not good immunity. Typhoid vaccine effective in children > 2yrs

55
Q

List the Yersinia species and which are enteric pathogens.

A

Pestis, enterocolitica and pseudotuberculosis. The last two are enteric

56
Q

Yersinia transmission

A

domestic animals and sometimes blood transfusions (grow at low temps). Often associated with undercooked pork and dairy

57
Q

Yersinia pathogenesis and Sx

A

Infects terminal ileum producing RLQ pain. Low grade fever, watery diarrhea, some blood, fecal leukocytes. Complications include reactive arthritis (Reiters syndrome) in HLA-B27 positive pts.

58
Q

Yersinia treatment

A

Antibiotics - do not show major impact on outcome but still used

59
Q

What is the most common cause of gastroenteritis in Western worls

A

campylobacter- food borne

60
Q

List the campylobacters

A

c. jejuni and c. Coli

61
Q

Campylobacter structure and growth

A

small curved gram negative rods. Catalase and oxidase positive. Prefer microaerophilic and increased temperature for culture. Grows best on enriched media with antimicrobials that inhibit other intestinal bacteria

62
Q

Campylobacter Sx

A

diarrhea, fever, abd cramping, bloody stools, vomiting. Fecal leukocytes may be present. Complication- Guillain Barre (demyelinating dz) and Reiters syndrome (autoimmune reactive arthropathy)

63
Q

Campylobacter pathogenesis

A

Invasive, enterotoxin production and cytotoxin production. Invasion of terminal ileum and proximal colon. Motility and chemotaxis are important in colonization of gut.

64
Q

Campylobacter transmission

A

contaminated milk or water. Young pets with diarrhea, raw poulty. Highest in infants then young adult males.

65
Q

Campylobacter treatment

A

supportive fluid replacement. Antibiotics in severe cases (erythromycin or quinolones but fluoroquinolone resistance is emerging due to antibiotic usage in poultry)

66
Q

H pylori pathogenesis

A

colonizes mucus layer of stomach, does NOT invade epithelium. Causes inflammation, epithelial cell damage and neutrophil infiltration. Reduction in acid secretion leads to gastric atrophy which can progess to gastric carcinoma

67
Q

H pylori structure and culture/isolation

A

curved, motile, microaerophilic gram negative rods. Strong urease activity. Isolated on campy agar wihtout antibiotics

68
Q

H pylori Sx

A

Casues nearly all duodenal ulcers and 70% of gastric ulcers

69
Q

H pylori virulence factors

A

High motility- rapid penetration of mucus to reach less acidic epithelium. Urease- produces ammonia to raise pH. Pathogenicity islands- encode virulence genes. Toxins- vacuolating cytotoxin causes epithelial damage

70
Q

H pylori transmission

A

acquired in childhood. Life long without treatment. Fecal-oral transmission, with oral-oral and gastric-oral routes possible. Prevalence increases with overcrowding and lower socioeconomic status

71
Q

H pylori diagnosis

A

Histology of biopsy is gold standard. Rapid urease test on biopsy. Urea breath tests. ELISA for IgG

72
Q

H pylori treatment

A

Only treat those with peptic ulcers to prevent antibiotic resistance. Treatment: PPI + bismuth + tetracycline for 14 days (amoxicillin, metronidazole, clarithromycin)

ID unit 1 (12 decks)

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