Gastrointestinal Infections I (20) Flashcards

1
Q

What are the normal functions of the GI tract?

A

digestion
absorption
protection

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2
Q

What are the antibacterial substances of the mouth?

A

lysozyme and IgA

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3
Q

What are the immune defenses of the GI tract?

A

mouth - antibacterial substances, flow of saliva
stomach - low pH, varies among species and meals
intestinal mucus - physical barrier, antimicrobial enzymes
mucosal cells
GALT

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4
Q

The GI tract is _____ at birth

A

sterile
microbes acquired from environment shortly after birth

majority are anaerobes in all species
diet affects composition of flora

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5
Q

Milk-fed animals have what kind of GI flora?

A

lactobacilli

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6
Q

What is of little diagnostic value when diagnosing GI conditions?

A

fecal cultures and gram’s staining of fecal material are of little diagnostic value

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7
Q

What is present in large numbers in the GI tract?

A

e. coli
requires additional testing for interpretation

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8
Q

What is the role of normal microflora?

A

maintain normal intestinal function
prevent pathogenic bacterial growth

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9
Q

What disrupts normal microflora?

A

antimicrobials
stress
drugs that alter GI motility
sudden diet changes

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10
Q

What is gastroenteritis?

A

syndrome characterized by GI symptoms including nausea, vomiting, diarrhea, and abdominal discomfort

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11
Q

What is dystentery?

A

an inflammatory disorder of the GI tract often associated with blood and pus in the feces and accompanied by symptoms of pain, fever, abdominal cramps, usually resulting from disease of the large intestine

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12
Q

What is enterocolitis?

A

inflammation involving the mucosa of both the small and large intestine

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13
Q

What are characteristics of E. coli?

A

gram-negative rod
facultative anaerobe - can grow with or without O2
extracellular bacteria

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14
Q

What are the E. coli pathotypes?

A

enterotoxigenic E. coli (ETEC)
enteropathogenic E. coli (EPEC)
shigatoxigenic E. coli (STEC)
enteroinvasive E. coli (EIEC)

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15
Q

E. coli classification is based on what?

A

serology
pathology

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16
Q

What are the parts of E. coli based on serology?

A

cell wall O antigen
flagella H antigen
pili/fimbriae ‘F’ antigen
capsule K antigen

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17
Q

T/F: Regarding E. coli, you can predict pathogenicity based on O, H, and K antigen types

A

FALSE - these are markers to separate E. coli into groups/types

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18
Q

What confirms pathogenicity of ETEC?

A

fimbrial antigens

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19
Q

What is ETEC?

A

enterotoxigenic escheria coli

20
Q

What are the properties of ETEC?

A

normal flora of MOST animals
ubiquitous in farm environment - sheds in feces and contaminates environment

can persist on skin and mucous membranes

21
Q

How does ETEC enter the body?

A

shortly after birth via fecal-oral route

then colonize small intestine (distal jejunum and ileum)

22
Q

ETEC is an interplay between ______

A
  1. pathogen factors
  2. environment
  3. host
23
Q

What are the pathogen factors of ETEC?

A

fimbriae
enterotoxin production

24
Q

What is fimbriae (pili) regarding ETEC?

A

encoded on plasmids
proteins that extend from the cell wall
required for bacterial adhesion to CHO receptors on epithelial cells

binding is HOST-specific
F5: lambs
F4: pigs

25
Q

What is enterotoxin production?

A
  1. encoded on plasmids
  2. two toxins: heat labile (LT) and heat stable (ST) enterotoxins
    STa (calves) and STb (piglets)
26
Q

What are environmental and host factors of E. coli contamination?

A

high inoculum dose
age - intestinal receptors present ONLY in neonates
immune status

27
Q

What does immune status regarding E. coli have?

A

failure of passive transfer: colostrum deprivation leading to deficiency of antibodies
can not block binding of fimbriae

28
Q

ETEC pathogenicity is mediated by both ______

A

fimbriae & enterotoxins

binding (mediated by fimbriae) results in large numbers of bacteria in direct contact with epithelial cells

29
Q

What are the effects of E. coli enterotoxin?

A

hypersecretory (watery) diarrhea
calf scours

30
Q

What is the mechanism of damage: normal GI physiology of ETEC?

A

villus cells
crypt cells
NET effect of crypts and villi
enterotoxins

31
Q

What are vilous cells for E. coli?

A

absorb Na+ and Cl- into the cell
absorb substrates into cells via sodium co-transporters
effect: ABSORPTION

32
Q

What are crypt cells for normal GI physiology of ETEC?

A

Na+ is recycled
secretes Cl- out into lumen
effect: SECRETION

33
Q

What are NET effect of crypts and villi cells for normal GI physiology of ETEC?

A

ABSORPTION

34
Q

What are enterotoxins for normal GI physiology of ETEC?

A

stimulate adenylate cyclase
inhibit Na+ and Cl- uptake in villous cells
increased Cl- secretion in crypt cells

HYPERSECRETION

35
Q

What is important to note about ETEC and enterotoxins?

A

bound to the intestinal epithelium there is NO direct damage to the intestinal epithelium

36
Q

What are clinical signs of ETEC?

A

watery diarrhea
yellowish or white scours
no invasion, inflammation, or cell damage

37
Q

What is diagnosis of ETEC diarrhea?

A

history and management factors - incidence mainly confined to young animals
sampling - FRESH & before antibiotics
latex agglutination test
multiplex-PCR for virulence factors

NOT foul-smelling, not hemorrhagic

38
Q

T/F: In diagnosing ETEC diarrhea, fecal cultures alone are of no value

A

TRUE

39
Q

What is latex agglutination test regarding ETEC?

A

detects fimbrial antigens
- F5 and F41 in calves and lambs
F4 in pigs

40
Q

What is the method of choice for diagnosing ETEC diarrhea?

A

Multiplex-PCR for virulence factors

41
Q

What is treatment for ETEC?

A

important to correct dehydration and electrolytes
antibiotics
immunoglobulins

42
Q

How do you prevent ETEC?

A

sanitation!
disinfection
reduce overcrowding (move calves to individual calf pens)
reduce inoculum size
optimize passive transfer

43
Q

ETEC is also called _______

A

hypersecretory diarrhea

44
Q

What is EPEC or attaching and effacing E. coli (AEEC)?

A

CELL DAMAGE
hyper secretion and MALABSORPTION
usually DO NOT produce toxins
pili, intimin (eae)

45
Q

What is STEC?

A

similar to EPEC
attaching an effacing (A/E) lesions
hyper secretion and MALABSORPTION
usually produce toxins (Shiga toxins)

46
Q

What is edema disease in piglets?

A

STEC
usually occurs 1-2 wks post-weaning
produce fimbirae and toxins (Stx2e)
- binds to receptors to vascular endothelium in CNS, stomach, forehead, eyelids, and other sites

increased vascular permeability and edema
no cell damage

47
Q

What is enteroinvasive E. coli (EIEC)?

A

invades the cells, and then into the deeper portions of the intestine

only known to produce disease in humans