Salmonella!!! MICROM442 Deck 20 Enteric Pathogens Flashcards
1
Q
salmonella is gram what?
A
GM-
2
Q
salmonella produces
A
H2S
3
Q
salmonella are motile or non-motile?
A
motile
4
Q
do salmonella ferment lactose
A
NO
5
Q
what type of anaerobe is salmonella?
A
facultative
6
Q
6 subspecies of salmonella enterica, which infects?
A
warm blooded hosts
7
Q
are there many or very few serovars of enterica subspecies?
A
MANY, ~1454
8
Q
what type of host range is enterica serovar typhimurium?
A
broad host range
9
Q
enterica serovar typhimurium =
A
NTS or non-typhodial salmonella
10
Q
NTS
A
- significant animal carriage, cause gastroenteritis in humans
- bacteremia in immunocompromised hosts
11
Q
serovar typhi and parathypi A are both
A
human adapted ie NO animals
12
Q
Sx of serovar typhi and parathypi A?
A
- enteric fever [typhoid and paratyphoid]
- accumulation of pseudogenes is likely related
to host restriction
13
Q
5 other Salmonella enterica subspecies
infect?
A
cold blooded hosts
14
Q
5 other Salmonella enterica subspecies
infect are causative agents of?
A
gastroenteritis in humans following reptile exposure
15
Q
5 other Salmonella enterica subspecies
A
- relatively acid labile;
- resists desiccation;
- not readily killed by freezing >:(
- facultatively intracellular pathogens
16
Q
Type III secretion systems [T3SS]
A
associated with salmonella
17
Q
peyers patches=
A
clusters of subepithelial, lymphoid follicles found in the intestine
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
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
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
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
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
NTS Sx
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
NTS history
consuming undercooked poultry, eggs, dairy, and outbreaks
from foods containing contaminated ingredients; exposure to
reptiles
27
becuase NTS causes bactermeia the patient is usually
presumed immunocompromised until proven otherwise
28
NTS related outcomes
- 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
Typhoid fever
greek word typhus=smoky, describing delirium in patients
30
typhoid fever introduced as disease after
pierre louis found infected abdominal lymoh nodes in autoposies in patients with gastric fever
31
Who identified salmonella enterica (tyohoid fever)?
Karl Ebert
32
what is the only known resevoir for typhi?
humans
33
is typhi rare/common in us?
rare
34
symptoms of typhi are flu-like so
-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
salmonella typhi infection cycle starts in the
small intestine
36
3 possible outcomes
-diarrhea, hemorrhage perforation
-cholecystitis, CARRIER state
-fever kidney and other organs infected
37
diarrhea, hemorrhage perforation symptoms of typhi stem from
small intestine-> inflammation and ulceration of PEYER patches
38
cholecystitis, CARRIER state
-fever kidney and other symptoms of typhi stem from
ingestion-> small intestine -> lymph nodes -> trasnient bactermia -> multuplication in macrophages in liver/spleen/bone marrow -> bile -> GALLBLADDER
39
fever kidney and other organs infected symptoms of typhi stem from
ingestion-> small intestine -> lymph nodes -> trasnient bactermia -> multiplication in macrophages in liver/spleen/bone marrow -> SEPTICEMIA
40
incubation of typhi lasts until
multiplication in macrophages in liver/spleen/bone marrow and then symptoms emerge
41
typhi chronic carrier state
-bacterial persistence in gallbladder without
overt signs of infection
excrete bacteria in urine or stool for greater than 12 months after acute infx
42
typhi chronic carriers are typically
female or has gall stones, tyhoid mary (mary mallon)
43
typical complications of typhi
GI hemmorrhage, intestinal perforation, encephalopathy and relapse
44
Dx of NTS
stool culture; blood culture when indicated by presence of symptoms and immune deficit[s]
45
Dx of typhoid
-stool culture [30-40% +]
- Blood cultures [40-80%+];
- Bone marrow culture [90% +] often remain positive even after initiation of Abx
46
Dx NTS and typhi (?)
H2S produces BLACK colonies on Hektoen agar
47
Prevention ncludes
-sanitation & pet care
-proper food handling
-adequate cookine
-avoiding unpeeled fruits/veggies in endemic regions
48
prevention con.
typhoid vax; 6 yrs and older = attenuated oral Ty21a: 4 doses, effective but short lived and requires a booster every 5 years
49
typhoid vax con.
2 yrs and older, Vi antigen: a single i.m. injection; boosters needed every 2 yrs
50
Rx NTS
- 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
Rx NTS
- 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
Rx Typhoid
drug of choice is fluoroquinole
53
Rx tyohoid
- 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
