Cross: Inflamamtory Diarrhea Flashcards
Causes of inflammatory D
****SEESSCCY**** Shigella EHEC EIEC Salmonella enterica Salmonella enteritidis** C. jejuni C. difficile Yersinia enterocolitica
90% of infectious D=
viral etiology
D lasting longer than 10-14 days=
likely from a parasite
acute diarrhea
3 or more loose stools per day lasting less than 2 weeks
chronic diarrhea
more than 4 weeks-consider HIV status
bugs that cause D in HIV patients
MAI
CMV
define inflammatory D
- small volume
- often bloody (dysentery)
- WBC/RBC’s in stool
- fever is COMMON
- most often affects colon
define non-inflammatory D
- large volume
- watery
- non-bloody
- no cells in stool
- afebrile
- SMALL INTESTINE USUALLY AFFECTED
general characters for Shigella, E. coli, Salmonella
>Gram Negative >glucose fermenting with acid production? >Oxidase negative >reduce nitrates to nitrites ALL MOTILE EXCEPT SHIGELLA
flagellar antigens
H antigen
polysaccharide side chain on LPS
O antigen
Gram negative, NON-motile, NON-lactose fermenting, DOES Not PRODUCE H2S
Shigella
Strain of Shigella most commonly affecting US-school aged/day care children
Shigella sonnei-70% cases
DAYCARE CENTERS migrant workers, nursing homes, traveler to developing countries,
most common shigella strains worldwide
- Shigella dysenteriae
2. Shigella flexneri
how is shigella transmitted
fecal oral route-very low ID
shigella pathogenesis
EIEC has a similar mechanism
> taken up by M cells (resistant to gastric acid)
escape into LP-taken up by macs-> cause apoptosis
HOST INFLAMMATORY RESPONSE KILLE THE CELL IN WHICH IT IS MUTLIPLYING-ALLOWING IT TO ESCAPE
SPREADS FROM CELL TO CELL VIA MEMBRANE BOUND PROTRUSIONS -FORMINS-DEPENDENT ON HOST CELLULAR ACTIN POLYMERIZATION-LYSES MEMBRANES THAT SURROUNDS IT AND NOW IS FREE IN ADJACENT CELL
complications from Shigellosis
- reiter’s syndrome
2. HUS- from shiga toxin (AB toxin) more common with S. dysenteriae
TX for Shigellosis
Ceftriaxone
Ciprofloxacin
Azithromycin
*shortens course and reduces duration of organism shedding in tools
this bug can cause inflammatory and non-inflammatory diarrhea
E. coli
5 strains we are discussing here
how does shiga toxin work>
cleaves a base on the 28s of 60S subunit in Ribosomal subunit thus inhibiting protein synthesis
shiga toxin seen in
Shigella dysenteria
EHEC (Shiga toxigenic e coli) which include O157:H7
and O104: H4
*these are really “SHIGA-TOXIN-LIKE”
cannot ferment sorbitol-colonies white on culture
DISTINGUISHING FEATURE
EHEC-aka STEC
SOURCE OF EHEC
INADEQUATELY COOKED MEAT (HAMBURGERS)-CONTAM VEGGIES AND MIK-ALSO HUMAN-TO HUMAN
CAUSES HEMORRHAGIC COLITIS- HOSPITAL STAY IN 50%-SHIG TOXIUN LIKE S. DYSENTERIAE
EHEC
ehec Is grouped into
O157:H7-like and
non O157: H7
locus of enterocyte effacement (LEE)
PAI within EHEC that contains a TYPE III secretion system-aids in attachment and effacement of the bug onto colonic mucosa via a pedestal formation and delivery of the e coli receptor to the host cell
responsible for the diarrhea in EHEC
LEE pathogenicity island
little fever, acute onset cramps and WATERY D-becomes bloody (hemorrhagic colitis) within 24 hours-lasts up to 8 days
EHEC
EHEC strain more likely to cause outbreaks, dysentery, HUS, ischemic colitis
O157:H7
which bugs use LEE for entry
EHEC and EPEC
feared complication of EHEC and Shigellosis (less common)
5-10 days after diarrhea
HUS from SHIGA TOXIN IN BLOOD STREAM 90% of cases in children but only complicated 9% of EHEC cases 5% mortality rate 50% require dialysis-most regain function
main cause of AKI in children
HUS following EHEC infection
clinical features of HUS
microangiopathic hemolytic anemia and thombocytopenia AKI requiring dialysis in half 5-10 days after D SHISTOCYTES ON PBSMEAR neuro symptoms-seizure/somnolence
Dx of EHEC
- Sorbitol MacCOnkey agar-white colonies
2. Elisa for Shiga toxin A and B
Tx for EHEC
SUPPORTIVE care and monitoring
>ab’s are contraindicated-would spread toxin through lysis of cells-increased risk of HUS
>anti-diarrheals are contraindicated
e. coli strain similar to Shigella sonnei causing a similar disease
EIEC
food-water
person-person
transmission
movement from one cell to another for EIEC-
moves similar to Shigella sonnei-with actin polymers
replicates intracellularly and extends into adjacent intestinal cells
“formins”–not sure if it is exactlyt the same but cross lumped these two together by their means of pathogensis
doe EIEC mae toxins
no-in this way it is not like S. dystenteria
h2S producing
non-lactose-fermenting
gram negative BACillUS
salmonella
causative agents of TYPHOID fever
> Salmonella enterica subtype Typhimurium
>salmonella parathypi
causative agent of salmonellosis
NONTYPHOID salmonella
Salmonella enteritidis
*common cause fo food poisoning
does S enterica or paratyphi cause gastroenteritis?
HELL NAW
sources of Salmonella
chicken, eggs, dairy
turtles lizards other reptiles
human-human
taken up by M cells-TYPE III secretion system-bacterial prots allow for growth withing ENDOSOMES-invade LP-host response kills macrophages as well
Salmonella enteriditis
5% will develop invasive disease: bacteremia, endovascular infections, endocarditis, osteomyelitis. Predilection for aortic plaques, bone prostheses
salmonellosis
S. enteriditis
reactive arthritis seen with which bugs
Salmonella enteriditis
Shigellosis
Dx of salmonella
stool culture
tx of salmonella
not required for healthy ppl-RESISTANCE IS AN ISSUE
> only tx those at risk for disseinated infection
KNOWN OR SUSPECTED ATHEROSCLEROTIC PLAQUES
IMMUNOCOMPROMISED-HIV SICKLE CELL
TX OF SALMONELLA WHEN INDICATED
FLOROQUINOLONES
TYPHOID FEVER CAUSED BY____AND PATHOGENSESIS
resides in submucosa-peyer’s patch hyperplasia
SALMONELLA-ENTERICA SUBTYPE THPHIMURIUM
-taken up by M cells-gets in RES and LN’s-spreads to blood (sepsis can occur)-HYPERTROPHY OF PEYERS PATCHES–necrosis follows-occasionally perforation
clinical presentation of typhoid fever
1st week-fever chills bactermia
2nd week-abdominal pain and rose spots
3rd week- hepatosplenomegaly (mainly spleen)-GI bleed, perforation-2ndary bactermia
Tx of typhoid fever-Salmonella enterica typhimurium
Ceftriaxone, Azithromycin, or cipro
(Possibly resistance to florquinolone)
VACCINE AVAILABLE
most common bacterial pathogen in the developed world
Campylobacter jejuni
thin spiral shaped GNR
c. jejuni
most important cause of traveller’s diarrhea
C. jejuni
-ETEC is important too
Unpast milk, improper chicken, contam. water
c jejuni
reservoir for c jejuni
sheep cattle chicken wild birds dogs
tx of c jejuni
only for those w/ severe or at risk of severe dz
-Azithromycin or Cipro
(floro resistance on the rise)
clinical course of C jejuni
1 week incubation 3-7 day course 10 bm's per day fever watery/bloody in 15% dx=stool culture
MOA for GBS
Guillain Barre Syndrome
-molec mimicry, antibodies to LPS cross-react with peripheral and central gangliosides
complications for c jejuni
> GBS
Reactive arthritis (along with shigella and salmonella enteriditis, yersinia)
Erythema nodosa
gram negative coccobacillus with bi-polar staining
Yersinia enterocolitica
pork, water raw milk, contaminated water, pet feces
yersinia enterocolitica
Yersinia clinical course
MIMICS APPENDICITIS
-involves illeum, appendix, right colon
-multiplies in lymph tissue=Peyer’s patch hyperplasia and LN hyperplasia
N/V/F/D-EN, Pharyngitis, arthralgia
right sided abdominal pain
yersinia enterocolitica
how to tell yersinia infection form appendicitis
look for
pharyngitis
arthralgia
erythema nodosum
Tx/DX of yersinia
stool culture
most cases dont need tx
anaerobic spore forming GPR (transmitted via fecal oral route)
Clostridium difficile
important intermediaries of C diff
hospital workers hands
most common cause of AB associated dirrhea
c diff
ab’s associated with c diff diarrhea
peniccillin, cephalosporins, tetracycline, ampicillin
most common nosocomial infection, and cause of nosocomial diarrhea
c difficile
C diff pathogenesis
EXOTOXINS A AND B
THIS IS NOT AN A/B TOXIN!!!!!
ENTEROTOXIN-TOXIN A
CYTOTOXIN- TOXIN B
- EACH WITH DIFFERENT FUNCTIONS
- NOT AN A/B TOXIN
C DIFF PATHOGENESIS
ENTEROTOXIN A
ENTEROTOXIN (TOXIN A)–> DISRUPTS COLONIC MUCOSAL CELL ADHERENCE TO BASEMENT MEMBRANE-DAMAGES VILLIOUS TIPS-LEADS TO FLUID SECRETION
C DIFF PATHOGENESIS
CYTOTOXIN -TOXIN B
CAUSES DEOLYMERIZATION OF ACTIN -LOSS OF CYTOSKELETAL INTEGRITY-APOPTOSIS AND DEATH OF ENTEROCYTES
TOXIN A AND B (A>B) BOTH DO WHAT
STIMULATE MONOCYTES AND MAC -RELEASE IL8-> TISSUE INFILTRATIN WITH PMN’S
-BOTH DISRUPT TIGHT JUNCTIONS OF EPITHELIA
SECRETION-DAMAGE TO VLIIOUS TIPS-BASEMENT MEMBRANE DETTACHMENT
ENTEROTOXIN-TOXIN A
DEPOLYMERIZATION OF ACTIN-APOPTOSIS AND DEATH OF ENTEROCYTES
CYTOTOXIN-TOXIN B
CLINICAL FEATURE OF C DIFF
“CDAD w/ colitis”
- *WATERY DIRRHEA (10-15/DAY)-MAINLY
- -PSEUDOMEMBRANOUS COLITIS-
- fulminant colitisSEVERE (pain distention, fever hypovolemia)
- toxic megacolon (>7cm dilated with severe systemic toxicity)
name the hypervirulent strain of Cdiffand the treatment
NAP-1/027
fidaxomicin
gold standard for dx of c diff
cell culture cytotoxicity assay
stool + monolayer of cultured cells-if cytotoxic
