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febrile invasive diarrhea Flashcards

1
Q

most communicable bacterial diarrheal agent

A

Shigella

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2
Q

Shigella

what color on MacConkey?

A

G- bacilli, non-motile non-lactose fermenting (non-coliform):
white on MacConkey agar

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3
Q

Shigella: extra or intracellular?

A

intracellular: can invade and multiply in colonic epi cells–>cause inflammatory dis. of large bowel

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4
Q

Shigella diarrhea or dysentery?

A

either or both

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5
Q

Shigella: four species groups

A

S. dysenteriae Group A (most sev.)
S. flexneri, Group B
S. boydii, Group C
S. sonnei, Group D (least severe)

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6
Q

in US Shigella most common affects ??

what S. spp in US??

A

kiddos (1-4yo)
all age groups are susceptible
S. sonnei (D) and S. flexneri (B)

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7
Q

Shigella reservoir

carry org how long after recovery?

A

only humans

1 mo

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8
Q

Shig: low or high inf. dose?

transmitted how?

A

low (10^2)
secondary attack rate is high

fecal-oral route, direct person-person, vehicles (food and water), and mech. vectors (flies)
-so basically anything, sneaky Shigella

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9
Q

Shigella assoc. with age/gender/season

A

kiddos 1-4

no gender or season assoc.

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10
Q

Shig risk factor

A

poor personal hygiene

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11
Q

Shigella is a biphasic descending illness:

cause bacteremia?

A

diarrhea followed by dysentery

does NOT cause bacteremia

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12
Q

after ingested, Shig orgs reach ?? where they initially multiply and ?? which does what ??

A

small bowel

release toxin which stimulates active secretion of water and e-lytes from jejunum

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13
Q

Shig proceeds to the ?? where it invades/penetrate via the ?? then moves cell-cell going on to multiply in the ??

A

colon
penetrates via follicle associated M cells
mucosal epi cells (enterocytes) (facultative IC)

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14
Q

Shigella in the enterocytes results in ??

A

inflammatory response, bleeding, sloughing of cells, formation of abscess and ulcers

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15
Q

what type of Shig can cause HUS

A

S. dysenteriae type 1

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16
Q

Shig virulence factors is dependent on ??

A

temp reg

prod. >=37 degrees

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17
Q

Shig virulence factors: enterotoxins

A

ShET1 and ShET2

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18
Q

Shig virulence factors: surface Ags

A

induce “parasite directed” endocytosis into M cells and spread btw epi cells

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19
Q

Shig virulence factors: OspE proteins:

how do they increase bac. cell-to-cell spreading and promote colonization?

A

highly conserved among EHEC, EPEC, and Salmonella
reinforce host cell adherence to basement mem by interacting with integrin-linked kinase (ILK) –>which suppresses epi detachment

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20
Q

Shig vir factors: Shiga toxins (Stx)

only what Shig species?

A

cytotoxins

only S. dysenteriae type 1

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21
Q

Shig Stx acts at level of ?? causing ??

can also ??

A

60S ribosome causing irreversible inactivation of EF-1 and INF-y
activate apoptosis in macros (think EHEC and STEC)

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22
Q

Shig presentation

triad of sev. dysentery

A

variable: mod diarrhea to sev. dysentery:

triad of cramps, tenesmus (painful straining), and frequent small volume bloody mucoid discharge

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23
Q

Shig onset?

initial symptoms ??? for this spp ???

A

incubation for 24-72 hrs (1-3 days)

fever, systemic manifestations, cramps, vomiting, diarrhea (watery) for S. sonnei (most common in US)

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24
Q

Shig dysentery after initial symptoms characterized by ??

sev. cramps most common in ??

A

blood, mucus, PMNs in stool
fever, cramps tenesmus
kiddos and oldies

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25
Q

Shig causes daily loss of ?? which can result in ??

A

serum protein (200-300 mL) in feces–>depletion of nitrogen stores–>malnutrition, growth stunting

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26
Q

complications of Shig

A

long term carrier state!
reactive arthritis
HUS
autoimmune disease

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27
Q

reactive arthritis most common in ind. with ??
presents how??
what occurs ??

A

HLA-B27
polyarthritis: mild–>severe, may last days
polyclonal B cell activation

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28
Q

HUS occurs in Shig due to ?? only produced by ??

triad??

A 
shiga toxin (Stx)
S. dysenteriae, type 1
triad: microangiopathic hemolytic anemia, thrombocytopenia, acute renal failure
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29
Q

Shig immunity

A

spp. specific

can turn off host prod. of anti-bacterial peptides

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30
Q

Shig dx
pres?
in feces?

A

bloody, mucoid stools and fever

fecal leukocytes, PMNs, and RBCs

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31
Q

Shig dx
Cx?
serology?

A

need selective media (MacConkey-white)

done to ID spp

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32
Q

Shig dx: ??? can be useful in ddx bacillary dysentery from amoebic dysentery

A

sigmoidoscopic examination

bacillary: diffuse ulcer pattern
amoebic: focal ulcers

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33
Q

Shig ddx

A

Salmonella, yersinia, EIEC, campylobacteria, amoebia
less common: EHEC and C. diff
basically all other agents of febrile diarrhea

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34
Q

Shig ddx EIEC: how similar?

A

sim. pathogenesis, virulence factors, disease manifestations

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35
Q

Shig vs. amebic dysentery: see ??? but no ??? with amebic

A

RBCs and trophozites but few if any PMNs

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36
Q

Shig tx
consider abx for it will ?? and ??

BUT

A

fluid replacement
reduce disease duration from 5-7 days to 3 days
AND eliminate carrier state
BUT abx resistants (plasmid-mediated) is a problem

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37
Q

Shig prevention

A

wash yo hands!
community recognition, participation, education on hand washing, esp for kiddos
vaccine in development

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38
Q

commonalities of Campy, Yersi, Salmonella

A

G- (only Campy ox +)
zoonosis
all invasive and can cause a bacteremia: Salm>Yersi>Campy(worst!)

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39
Q

virulence factor for invasiveness of Campy, Yersi, Salmonella

A

outer membrane component

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40
Q

Campy, Yersi, Salmonella are all

A

facultative IC pathogens in macrophages

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41
Q

dx Campy, Yersi, Salmonella via

if fever??

A

Cx and micro.examination of feces for fecal leukocytes

if fever, blood cx

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42
Q

Campy, Yersi, Salmonella tx

A

supportive unless substantive fever–>means extra intestinal disease (systemic?) so give abx

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43
Q

complications of Campy, Yersi, Salmonella ??

A

reactive polyarthritis assoc. w. HLA B27 and pseudoappendicitis Yersi>Campy>Salm (like Shig!)

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44
Q

Campylobacter jejuni

A

G- ox positive curved motile rod

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45
Q

Campy found in

A

chickens, other birds, dogs, livestock, etc

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46
Q

Campy infection causes

temp specificities?

A

diarrhea, dysentery or both
also assoc. with jejunal lesions and extra intestinal infections (bacteremia-it’s invasive!)
grows well at 42 deg. C under reduced O2 tension (microaerophilic) w. selective abx

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47
Q

?? used to be the leading cause of bacterial diarrheal disease ww, passed up by Salmonella

A

Campy

2 mil/yr in US

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48
Q

Campy reservoir

low or high infectious dose??

transmitted how?

risks

A

GIT of birds, domestic fowl, swine, cattle, sheep, dogs, etc

low infectious dose (800)

NOT usually person-person but via transmission from food sources, contaminated water
raw mild and undercooked chicken OR fecal contaminated foods

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49
Q

Campy age/gender/season assoc.

A

no age/gender

peaks in summer

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50
Q

Campy injures both the ???
lesions show an ??
isolates produce ??
–>resulting in ??

A

sm and large intestine
acute exudative and hemorrhagic inflammation
an enterotoxin and/or a cytotoxin (Stx)
diarrhea and/or dysentery

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51
Q

Campy virulence factors

A

enterotoxin: heat-labile (like LT of ETEC or CT of cholera)-seen in some strains from ppl w. acute secretory diarrhea
cytotoxin: Stx–>ulceration of mucosa

invasion factor

cytolethal distending toxin (CDT)

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52
Q

Campy invasion factor:??? proteins which are secreted through ?? upon contact with eukaryotic cell

A

Cia (Campy invasion Ags) secreted thru flagella filament

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53
Q

Campy invasion factor mechanism

A

disrupts epi cell tight junctions
allows cells to replicated IC in macros and induce apoptosis
triggers activation of NF-kB and MAPK signaling pathways

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54
Q

Campy Cytolethal distending toxin

mechanism?

A

(CDT): tripartite AB toxin where dtA and CdtC comprise the binding components and CdtB is the active subunit

CdtB is transported to the nucleus–>induces double stranded breaks in DNA and arrests the cell in G2 phase
-may play a role in malignancy

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55
Q

Campy immunity

A

Ab mediated

56
Q

Campy disease often has a ??

A

prodrome:

fever (12-24 hrs before diarrhea) ha, myalgia, malaise

57
Q

Campy onset??

most common presentation??

A

1-7 days
enteritis with diarrhea: loose, may be watery, may have dysentery
malaise, fever, abdominal pain (cramping)

58
Q

is Campy self-limiting?

A

yes, improvement in several days

59
Q

may also see ?? in Campy

which persists for ??

A

acute colitis: fever, tenesmus, sev. dysentery, sev. abd. cramps
1 wk

60
Q

may also see ?? which can get bad enough to mimic ??

caused by ??

A

mesenteric LAD–>severe acute LRQ pain, can mimic appendicitis
Yersi>Campy>Salmy
caused by org getting to LN and causing sev. inflammation

61
Q

Campy can also have extra intestinal manifests:

A

bacteremia

reactive arthritis in HLA-B27 peeps

62
Q

Autoimmune manifests of Campy

what else can cause it?

A

Guillain-Barre: acute polyradiculoneuritis; AI attack on peripheral nerve myelin
Campy chief instigator–>sev. axonal form
also CMV, EBV, HIV and vaccinia virus
Pen 19, O:19, Lior 11, Lau 19 and 3/25

63
Q

how Campy causes Guillain-Barre

A

LPS antigenic ally resembles human gangliosides Gm1 and GD1a
anti-Gm1 Abs–>cause symptoms

64
Q

Campy jejuni assoc. with this malignancy

A

immunoproliferative small intestine disease (IPSID), a form of MALT lymphoma

responds to abx

65
Q

recurrent acute Campy triggers

A

IBD

66
Q

may carry/excrete Campy after recovery for ??

life-long??

A

2-3 wks

life-long in animals,

67
Q

dx Campy: unique pres. features and labs

A

prodrome and fever
motile curved rods in feces and sea-gull shapes
+fecal leuks and RBCs
Cx feces at 42d C under microaerophilic conditions

68
Q

Campy ddx

A

all febrile diarrhea/dysentery orgs

69
Q

Campy tx

A

Erythromycin or other macrolide abx
and aminoglycosides
both are protein-synthesis inhibitors

70
Q

Yersinia enterocolitica

A

G- non-coliform (white on MacConkey), motile, bipolar staining (safety pin) coccobacillus
>50 serotypes, 5 biotypes

71
Q

Yersi is ?? so can multiply in ??

A

facultative IC, can multiply in epi cells and macros

72
Q

Yersi causes ??

important cause of ??

A

diarrhea, mesenteric LAD, systemic disease with local abscesses
pseudoappendicitis

73
Q

Yersi temp range

A

optimal: 22-29 C, can grow from 0-42

74
Q

Yersi found in …

A

GIT of wild and domestic animals

agent of sporadic outbreaks

75
Q

Yersi: low or high infectious dose ??

transmitted how??

A

high: 10^9
BUT person-person still happens
most common vehicles: milk, milk products, canned meat, meat products, blood transfusions

76
Q

Yersi age/gender/season

A

kiddos
no gender pref.
WINTER! (think Swedes?)

77
Q

Yersi virulence: orgs invade via the ???

and establish residence in ??

may extend to ??

A

M cells of Peyer’s patch

reticuloendothelial tissue, in LP, and muscular is mucosa

mesenteric LNs–>flamed and ulcerated nodes

78
Q

complication of Yersi invasion

A

bacteremia, intestinal perf and peritonitis

79
Q

Yersi virulence expression controlled by 2 feedback loops

A

temp and Ca2+

80
Q

Step 1. Yersi org enters body in food/drink only produces ?? and ??

A

invasin: adhesion which binds to B1 integrin and induces endocytosis
ST-like enterotoxin (ETEC-guanylate cyclase)

81
Q

Step 2. at 37d C synthesis of ??? stops and

synthesis of ?? begins

A

invasion and ST-like toxin

proteins which mediate resistance to complement-mediated killing

82
Q

Step 2.2. ?? are also synthesized but only when low levels of ??

mechanism ??

other activity ??

A

YOPS: yersi outer membrane proteins
low levels of Ca2+

YOPS inhib. phago, INF-y activity, and macro. respiratory burst

have tyrosine phosphatase activity, mediate contact-dependent cytotoxic activity that depolymerizes actin microfilament network of target cell

83
Q

Yersi onset?

presentation ??

A

4-7 days

fever, abd pain, vomiting, diarrhea

84
Q

sev. Yersi presentations (age groups?)

A

fever, acute ileitis, leukocytosis (older children, adolescents)

enterocolitis (kiddos

85
Q

Yersi post-inf. complications

A

reactive arthritis in HLA-B27’s, erythema nodosum

extraintestinal infections: high serum iron–>poor px

86
Q

Yersi carriage/shedding for how long ??

A

weeks

87
Q

Yersi Cx

A

requires special medium and cold enrichment

88
Q

Yersi ddx

A

febrile diarrhea/dysentery agents

89
Q

Yersi tx

A

maintain fluid/e-lyte balance

aminoglycosides, TMP-SMX

90
Q

Salmonella serotypes highly adapted to humans

A

S. typhi (prototype-typhoid fever)
S. paratyphi
S. sendai
-no known reservoir outside humans

91
Q

Salmonella highly adapted to specific non-human hosts

A

S. cholerasuis (pigs)

-can cause inf. in humans but uncommon

92
Q

Salmo w. broad host range

A

most in this category, cause most human and nonhuman disease: S. enteritidis, S. typhimurium- “Enteritidis” Group

93
Q

Salmonella is a ??

A

G- rod,
non-lactose fermenting (non-coliform- white on MacConkey)
facultative anaerobe, non-fastidious, non-spore forming

94
Q

Salmonella is a ?? which can multiply in ??

A

facultative IC pathogen, multiply in macros and intestinal epi cells

95
Q

is Salmo motile or non-motile?

A

motile, has H Ag (flagella)

>2000 serotypes based on O and H Ags

96
Q

Salmonella peaks in what age groups

A

6 mos to 5 yrs

97
Q

Salmo reservoir??

high or low infectious dose??

transmitted how??

A

fowl (eggs), swine, cattle, dogs, sheep, cats, turtles, rodents (NOT S. typhi)

high infectious dose: 10^5-10^9 orgs

typically ingestion of food/water
human-human has happened: closed pops, daycare, oral-anal

98
Q

Salmonella may be carried for how long??

infants may shed for how long ??

A

5 wks

5-12 mos

99
Q

Salmonella seasonality

A

summer/fall

100
Q

Salmonella risk factors

why in industrialized countries?

other risk factors ?? may present w/ ??

A

use of PPIs
institutionalization

industrialized countries: bulk food processing, feed additives, food packaging/preservation, infection of chicken oviducts

Ca, AIDs, raw milk, DM, abx therapy–>may present with bacteremia

101
Q

diarrhea induced in Salmonella as org ??

what virulence factor involved ??

A

travels thru small and large intestine via activation of adenyl cyclase–>inc. cAMP

enterotoxin, like LT toxin

102
Q

Salmonella colonizes the ??? and invades the ?? (via inducing phagocytosis); invades both ?? and ??

virulence factor involved?? mechanism ?

A

ileum and cecum, mucosa
M cells and epi cells

Surface adhesion proteins: Type III secret. system (TTSSs) injects effector proteins into host cells

3 pathogenicity islands? result in cell apoptosis, necrosis, and excretion of IL-8

103
Q

Salmonella causes ?? via what virulence factor ??

induces ??

A

acute inflammation via IC multiplication/prod. of Stx

release of inflamm. cytokines that cause intestinal damage (in addition to cytotoxin)–>see RBC and PMNs/macros in feces
cytokines also elicit systemic symptoms of fever, chills, and. pain

(this inflammation also contribute to diarrhea/dysentery)

104
Q

orgs that have Stx (Shiga toxin)

A

Shigella dysenteriae (no shit)
EHEC, STEC, EIEC, EAEC
Campy
Salmonella

105
Q

Salmonella causes systemic disease via this virulence factor ??
how does it spread ??

can cause??

A

LPS

spreads to mesenteric LNs–>then circulation–>bacteremia/endotoxic shock–>into macros (facult. IC)

causes pseudoappendicitis

106
Q

what is required for Salmonella immunity/control??

A

CMI

107
Q

Salmonella onset??
presentation??
duration ??
may affect who more severely?

A

12-48 hr incubation, abrupt onset
fever, chills abd. cramps, diarrhea, ha, vomiting
2-3 days normally
infants, oldies, impaired CMI

108
Q

Salmonella complications

A

reactive arthritis in HLA-B27s, bacteremia,

pseudoappendicitis

109
Q

reactive arthritis (HLA-B27s) is a complication in these infections

A 
STEC, etc
Shigella
Campy
Yersi
Salmonella
110
Q

Salmonella dx microscopic

A

fecal leuks and macrophages more than PMNs

FAT (fluorescent Ab test)

111
Q

Salmonella dx Cx

A

do: feces, water, food, blood (if fever)
enhancement, selective and ddx media
serological confirmation and typing reportable

112
Q

Salmonella dx

A

agents of febrile diarrhea/dysentery

113
Q

Salmonella tx

A

maintain fluid/e-lyte balance

abx NOT recommended for uncomp. gastroenteritis

114
Q

how to prev. salmonella

A

cook foods containing eggs all the way

115
Q

febrile invasive food-borne agents

A

Vibrio parahaemolyticus, V. vulnificus

Balantidiasis coli

116
Q

Vibrio parahaem. and V. vulnificus

A

ox +, halophilic curved rods (sim to V. cholera)

117
Q

V. para normally inhabits ??

US outbreaks relate to ???

high or low dose ??

season ??

2 major outbreaks occurred where ??

A

marine waters- animals

eating seafood shrimp

high infectious dose 10^5-10^7

summer mos

on cruise ships

118
Q

V. para can be ?? and cause ??

via what virulence factor ??

A

invasive and cause systemic disease

LT-like toxin

119
Q

V. para onset ??
presentation ??

what typ. observed ??

A

> 14 hrs
diarrhea and/or dysentery, cramps, N/V and 1/3rd are bacteremic

leukocytosis

120
Q

V. para dx: microscopy

A

direc microscopic examination of diarrheic stool:

curved rods, feca. leuks, RBCs

121
Q

V. para dx: Cx

A

isolate feces/vomit org on high NaCl media

virulent strains are Kanagawa positive and produce beta hemolysis on human blood agar

122
Q

V. para dx

A

any febrile diarrhea/dysentery agent assoc. with contact with marine environ.

123
Q

V. para tx

A

rehydration

amipicillin and other abx for sev. diarrhea/fever

124
Q

how to prev. V. para

A

don’t eat raw seafood, don’t contaminate cooked seafood

125
Q

V. vulnificus

A

like V. para in appearance and habitat

is highly invasive

126
Q

3 syndromes caused by V. vulnificus

leading cause of ??

A

wound infections (45%)
primary septicemia (43%)
gastroenteritis (5%)
leading cause of seafood assoc. fatalities in US

127
Q

V. vulnificus sev. progession

A

necrotic, rapidly progressing lesions–>fulminant sepsis w. 75-90% mortality in at risk individuals (25% normal hosts w. tx)

128
Q

those at risk for sev. V. vuln disease

A

DMs, etOHs, liver dysfunctions, hemochromatosis (Fe-overload)
don’t eat raw seafood!

129
Q

Balantidium coli

A

ciliated protozoan
largest to infect humans
causes diarrhea/dysentery

130
Q

Balantidium coli reservoir

A

pigs!

131
Q

B. coli is ingested as ?? and migrates to ?? where it develops into ?? which do what ??

A

cysts, migrate to large intestine, cecum, terminal ileum

trophozoites which replicate via binary fission and conjugation while consuming bacteria

132
Q

B. coli trophozoites reside primarily within the ?? but may ???

A

intestinal lumen

may penetrate the mucosa and cause ulcers

133
Q

B. coli presentation in immunocompetents

otherwise presentation

A

typ. asymptomatic

bloody, mucoid diarrhea, N/V, abd. pain, anorexia, wl, fever, colitis, dehydration

134
Q

B. coli dx

A

wet Sm of stool specimen; see trophozoites: LARGE, ciliary covering, spiraling motility

135
Q

Balantidium coli tx

A

volume/e-lyte replacement

tetracyclin or metronidazole

Micro (61 decks)

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