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MICRO 442 > Salmonella!!! MICROM442 Deck 20 Enteric Pathogens > Flashcards

Salmonella!!! MICROM442 Deck 20 Enteric Pathogens Flashcards

1
Q

salmonella is gram what?

A

GM-

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2
Q

salmonella produces

A

H2S

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3
Q

salmonella are motile or non-motile?

A

motile

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4
Q

do salmonella ferment lactose

A

NO

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5
Q

what type of anaerobe is salmonella?

A

facultative

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6
Q

6 subspecies of salmonella enterica, which infects?

A

warm blooded hosts

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7
Q

are there many or very few serovars of enterica subspecies?

A

MANY, ~1454

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8
Q

what type of host range is enterica serovar typhimurium?

A

broad host range

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9
Q

enterica serovar typhimurium =

A

NTS or non-typhodial salmonella

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10
Q

NTS

A
  • significant animal carriage, cause gastroenteritis in humans
  • bacteremia in immunocompromised hosts
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11
Q

serovar typhi and parathypi A are both

A

human adapted ie NO animals

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12
Q

Sx of serovar typhi and parathypi A?

A
  • enteric fever [typhoid and paratyphoid]
  • accumulation of pseudogenes is likely related
    to host restriction
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13
Q

5 other Salmonella enterica subspecies
infect?

A

cold blooded hosts

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14
Q

5 other Salmonella enterica subspecies
infect are causative agents of?

A

gastroenteritis in humans following reptile exposure

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15
Q

5 other Salmonella enterica subspecies

A
  • relatively acid labile;
  • resists desiccation;
  • not readily killed by freezing >:(
  • facultatively intracellular pathogens
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16
Q

Type III secretion systems [T3SS]

A

associated with salmonella

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17
Q

peyers patches=

A

clusters of subepithelial, lymphoid follicles found in the intestine

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18
Q

SPI-1 con.

A
  • triggers pyroptosis [inflammatory cell death]
    Greek roots ‘pyro’ meaning fire;
    ‘ptosis’ [p is silent!] meaning to fall [die]
  • inflammation results in diarrhea and attracts macrophages
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19
Q

SPI-1 [Salmonella pathogenecity island-1; there at least 7!]

A
  • nano-scale needle complex injects bacterial
    effectors into host cell
  • invasion of GI mucosa via entering M cells
  • spreads to Peyer’s patches
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20
Q

SPI-2 [Salmonella pathogenicity island-2]

A
  • survival in macrophage
    [mutants that cannot survive in macrophages are avirulent]
  • phagolysosomal modification: spacious phagosomes
  • prevents phagosome maturation
  • blocks accumulation of toxic oxidative
    products in phagosome
  • From Peyer’s patches dissemination via blood and lymph
  • dissemination inside macrophages;
  • survival in target organs inside macrophages
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21
Q

SPI-2 Con. VIRULENCE

A

-flagella: organ of motility; important for colonization and environmental fitness [chemotaxis]

-Recognized by adaptive immune systems:
- B cells
- T cells

-Recognized by innate immune system:
- TLR5 in GI mucosa
- NLRC4-mediated pyroptosis

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22
Q

SPI-2 host defenses con.

A
  • Pyroptosis: key host defense mechanism
  • production and release of IL-1b [endogenous pyrogen]
    promotes inflammatory state
  • releases intracellular Salmonella
  • taken up and destroyed by PMNs;
  • cell death itself is inflammatory
  • [release of intracellular contents]
  • release of HMGB-1 [high-mobility group box 1], normally in
    nucleus by virtue of weak binding to DNA, activates
    macrophages and other immune cells
23
Q

Capsule: polysaccharide Vi antigen

A
  • expressed by S. enterica serovar Typhi
  • Vi-antigen negative strains less infectious and less virulent
  • limits immune recognition
  • increases intracellular survival
  • reciprocal regulation with flagellar expression
24
Q

NTS causes

A

gastroenteritis and enterocolitis

25
Q

NTS Sx

A

diarrhea [can be bloody], fever, stomach cramps
- may have nausea, vomiting, headache
- incubation period of 6 hrs to 6 days; symptoms for 4 -7d
- most recover without need of Abx and should not take
antibiotics [prolongs illness!]

26
Q

NTS history

A

consuming undercooked poultry, eggs, dairy, and outbreaks
from foods containing contaminated ingredients; exposure to
reptiles

27
Q

becuase NTS causes bactermeia the patient is usually

A

presumed immunocompromised until proven otherwise

28
Q

NTS related outcomes

A
  • malignancy, chronic steroid use, organ transplantation,
    HIV, malaria
  • evidence of human-to-human spread in Africa during height of
    AIDS crisis
  • osteomyelitis in patients with Sickle Cell Disease
29
Q

Typhoid fever

A

greek word typhus=smoky, describing delirium in patients

30
Q

typhoid fever introduced as disease after

A

pierre louis found infected abdominal lymoh nodes in autoposies in patients with gastric fever

31
Q

Who identified salmonella enterica (tyohoid fever)?

A

Karl Ebert

32
Q

what is the only known resevoir for typhi?

A

humans

33
Q

is typhi rare/common in us?

A

rare

34
Q

symptoms of typhi are flu-like so

A

-gradually rising fever and headache, malaise, lethargy [flu like]
- abdominal pain always present as disease progresses; occasionally
‘pea soup’ diarrhea or constipation
- hepatosplenomegaly is a common finding, maculopapular rash
known as ‘rose spots’ on chest/abdomen
- systemic spread can lead to severe cases
- bacteremia, sepsis, shock, mentals status changes, and
meningitis

35
Q

salmonella typhi infection cycle starts in the

A

small intestine

36
Q

3 possible outcomes

A

-diarrhea, hemorrhage perforation
-cholecystitis, CARRIER state
-fever kidney and other organs infected

37
Q

diarrhea, hemorrhage perforation symptoms of typhi stem from

A

small intestine-> inflammation and ulceration of PEYER patches

38
Q

cholecystitis, CARRIER state
-fever kidney and other symptoms of typhi stem from

A

ingestion-> small intestine -> lymph nodes -> trasnient bactermia -> multuplication in macrophages in liver/spleen/bone marrow -> bile -> GALLBLADDER

39
Q

fever kidney and other organs infected symptoms of typhi stem from

A

ingestion-> small intestine -> lymph nodes -> trasnient bactermia -> multiplication in macrophages in liver/spleen/bone marrow -> SEPTICEMIA

40
Q

incubation of typhi lasts until

A

multiplication in macrophages in liver/spleen/bone marrow and then symptoms emerge

41
Q

typhi chronic carrier state

A

-bacterial persistence in gallbladder without
overt signs of infection
excrete bacteria in urine or stool for greater than 12 months after acute infx

42
Q

typhi chronic carriers are typically

A

female or has gall stones, tyhoid mary (mary mallon)

43
Q

typical complications of typhi

A

GI hemmorrhage, intestinal perforation, encephalopathy and relapse

44
Q

Dx of NTS

A

stool culture; blood culture when indicated by presence of symptoms and immune deficit[s]

45
Q

Dx of typhoid

A

-stool culture [30-40% +]
- Blood cultures [40-80%+];
- Bone marrow culture [90% +] often remain positive even after initiation of Abx

46
Q

Dx NTS and typhi (?)

A

H2S produces BLACK colonies on Hektoen agar

47
Q

Prevention ncludes

A

-sanitation & pet care
-proper food handling
-adequate cookine
-avoiding unpeeled fruits/veggies in endemic regions

48
Q

prevention con.

A

typhoid vax; 6 yrs and older = attenuated oral Ty21a: 4 doses, effective but short lived and requires a booster every 5 years

49
Q

typhoid vax con.

A

2 yrs and older, Vi antigen: a single i.m. injection; boosters needed every 2 yrs

50
Q

Rx NTS

A
  • Correct dehydration and electrolyte imbalances; supportive care
  • No Abx [!] for uncomplicated NTS localized gastroenteritis [without
    signs of sepsis]
  • uncomplicated NTS resolves in 4-7 days
  • exceptions: <3 mos old or immunocompromised, who can often
    have prolonged illness
51
Q

Rx NTS

A
  • obtain blood cultures for diagnosed cases to evaluate systemic spread
  • bacteremia or disseminated disease: third generation
    cephalosporin for 7-10 days
  • modify to other antibiotics [azithromycin or fluoroquinolone]
    based on resistance testing
  • extended therapy required [4 wks or more] for meningitis or
    osteomyelitis
52
Q

Rx Typhoid

A

drug of choice is fluoroquinole

53
Q

Rx tyohoid

A
  • emergence of elevated resistance detected by laboratory testing often
    necessitates use of third generation cephalosporin or azithromycin
  • normal course 10-14 days; full recovery with early detection and
    appropriate treatment
  • severe cases with delirium or shock warrant use of corticosteroids,
    which increase survival
  • chronic carries need 4 wks of Abx
  • more common in elderly and those with gallbladder disease
  • rare occurrence in children
  • cholecystectomy is an option for treatment failures

MICRO 442 (25 decks)

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