Bacterial infection of the DI tract II Flashcards
MacConkey Agar
culture- lactose fermentation and application of salt where
positive = red and the bacteria is E. coli (there is growth)
Negative= white (no growth because salts kill bacteria) = Salmonella, shigella and others
Indole Test
tests for indole production:
positive = red color change- Escherichia coli, Vibrio spp. and others
negative= no color change- salmonella
how do you distinguish between salmonella and shigella?
check hydrogen sulfite production:
Use gram neg enteric pathogens and look for black precipitate which is hydrogen sulfite production
- if salmonella- produces black precipitate (hydrogen sulfite)
-if shigella- no precipitate
Enteropathogenic E. coli (EPEC) characteristics: where? disease epidemiology
ePec= pediatric
characteristics: gram neg, facultative anaerobe, moderately invasive
where? Small intestine
Disease- watery diarrhea (destroy microvilli)
Epidemiology- infantile diarrhea in developing count.
pathogenesis of EPEC
-uses (BfpA- bundle forming pilus) to utilize type III secretion system (uses needle to insert pilus) onto host cell and T3SS injects Tir protein effectors that attach and efface themselves so that they stay forming a lesion
How is EPEC diagnosed and treated
-culture and biochemical test
- red (positive) on MacConkeys Agar
-Indole pos
but mostly-
PCR** (b/c others are found in asyptomatic pt too)
treatment- supportive
ETEC- enterotoxigenic E. coli kind of bacteria where is it found symptoms what organ does it act on?
- eTec = travel -travelers diarrhea
- gram neg, facultative anaerobe, non-invasive
- small intestine
- associated with travel to developing countries and consumption of contaminated water or ice
- watery diarrhea
- leading bacterial cause of diarrhea in kids in developing world
how does enterotoxigenic E. coli work (ETEC)
- has fimbriae (pili) that adhere to the epithelial cells of the small intestine and produces two different types of toxins
1) LT heat (liable toxins) with AB toxin that increases cAMP and causes massive efflux of water and electrolytes out of the intestines
2) ST heat (stable toxin) that is a no AB toxin that does not enter the cell but increases cGMP that has same effect
how do you diagnose and treat ETEC
- diagnosis- clinical hx, DNA probes to detect LT or ST encoding genes in cultures
- treatment- supportive
salmonella typhi type epidemiology how to get it inflammatory what body part
-gram neg, facultative anaerobe with flagella and H antigen
-acid tolerant
-highly adapted to humans
get it via eating contaminated food/water from infected person
-inflammatory- yes
-body part- small intestine
Incubation period for typhoid
symptoms
what comprises a sustained bacteremia
inc per- 13 days
symptoms- headache and fever
sustained- rising fever over 3 days, typhoid fever with prolonged fever of 4 wks followed by GI symptoms
-chronic colonization of gall bladder with typhoid and reinfection into the intestines.
how does s. Typhi infect
-adheres to M cells and enterocytes
-M cells- sample and present intestinal contents to immune cells like peyer’s patches that become accustomed to things that we eat
-well, s. Typhi enters M cells via type 3 secretion system mediated uptake
- and injects Ssps (salmonella secreted invasion proteins) and cause membrane ruffling around it to be released into the cytosol
and injects self into macrophage where it is then lead to lymph nodes
-escape from macrophage and cause bacteremia (fever and septicemia)
how is s. typhi diagnosed? treated?
- culture of stool and blood samps
- treat: antibiotic therapy based on susceptibility profile
Prevention
-avoid potential sources of infection- drink bottled water and thoroughly cooked food and avoid raw fruits and vegis in devel countries
-vaccination Ty21A capsule by mouth, 4 doses
ViCPS- injection, 1 dose
nontyphoidal salmonella inflammatory? body part? characteristics? source of infection difference between typhoid and nontyphoidal salmonella
inflammatory? yes
body part? small intestine
characteristics? gram neg, facultative anaerobe
source of infection- contaminated food (poultry, eggs, dairy pdts)- human to human is unlikely
difference between typhoid and nontyphoidal salmonella- there are more reservoirs than just humans in nontyphoidal
symptoms of nontyphoidal salmonella
- occur between 6-48 h post ingestion
- nausea, vomiting with ab cramps ad watery diarrhea for 3-4 days
- 50% fever
- severe dysentery like diarrhea
Nontyphoidal salmonella mechanism
- like typhi except once in macrophage it can
1) rapid kill of macrophage via multiple mechanisms- causes a massive inflammatory response that confines the infection and eliminated via active fluid secretion (diarrhea)
2) Carriage in macrophages (in immunocompromised pt) - get systemic dissemination, bacteremia - get focal infections- arthritis, osteomyelitis and endocarditis etc
Diagnosis nontyphoidal salmonella
- diagnosis- serology: detection of anti-Vi antigen antibodies
- culture that will reveal negative MacConkeys and be pos for black precipitate in hydrogen sulfite test
treatment of nontyphoidal salmonella
- Treatment
- S. gastroenteritis - electrolyte replace but Antibiotic NOT recommended (enhances carrier state)- use only when chance of septicemia
- salmonella systemic infection- antibiotic therapy depending on resistance profile
- NO vaccine
Campylobacter jejuni characteristics? body part? inflammatory? incubation time
Charcteristics -gram neg, CURVED or SEA-GULL shaped
-microaerophillic
-has many animal reservoirs (camp- has lots of animals)
body part? illium. jujunum and colon
inflammatory? yes
incubation time - 2-11 days
what does campylocater jejuni do to the body?
- it causes an ulceration and acute enteritis
- watery -> diarrhea
- causes sepsis
- sequellae cause Gillian barr syndrome (after camping, you wanna go to the bar)
Guillian Barr syndrome
- acute mediated polyneuropathy
- symmetric and aggressive muscle weakness with absent or depressed deep tendon reflexes
- could have difficulty walking to nearly complete paralysis
- 30-40% attributed to campylobacter
- weakness is due to the fact that there is something on campy that is acting like myelin that causes demyelination
diagnosis and treatment of campylobacter jejuni
- diagnosis via culture
- treatment- supportive/ antibiotic used ONLY for invasive disease based on susceptibility profile (MACROLIDE)
