Enteric Bacterial Infections (Inflammatory): Cross, Ryan Flashcards
90% of infectious diarrheas are caused by bacteria, parasites, or viruses?
Viruses
Persistent diarrhea (>2 weeks) is likely caused by:
Parasite
When treating chronic diarrhea, start considering the possibility that the pt has:
HIV
or is infected with CMV, M. avium intracellulare
Bloody diarrhea =
You will see these cells in the stool:
Small or large volume?
Colon or SB affected, commonly?
inflammatory diarrhea aka dysentery
WBCs and RBCs
Small volume
Colon commonly affected
Watery diarrhea =
Colon or SB affected commonly?
Small or large volume
Colon or SB affected, commonly?
non-inflammatory diarrhea
No cells
Large volume
SB usually affected
7 pathogens causing inflammatory diarrhea:
Shigella EHEC EIEC Salmonella C. jejuni C. difficile Yersinia enterocolitica
List characteristics Salmonella, Shigella, and E. coli have in common.
Gram (-) facultative rods
- Ferment glucose–> acid
- oxidase neg.
- reduce nitrates to nitrite
- motile, except Shigella
Antigenic structures used in serotyping (eg. O157:H7):
H- flagellar antigens
O- side chain of LPS
3 species of Shigella. Which is most common in Central/South America?
How about the U.S.?
How is it transmitted? Low or high infectious dose?
C/S America- S. dysenteriae
U.S.- S. sonnei
Fecal oral route of infection or contaminated food/water
Low infectious dose
Discuss the pathogenesis of Shigella.
Resistant to acid of stomach.
Taken up by M cells, proliferate—> lyse cell and are taken up by macrophages—> induce apoptosis—> immune response that damages mucosa, allows for further invasion.
Moves from one cell to another by using F actin (formin) to rocket into adjacent cell.
Describe the clinical course of Shigella infection.
How do you treat it?
Self-limiting, lasts ~1 week.
50% become bloody diarrhea
Complications: reactive arthritis, urethritis, conjunctivitis (Reiter’s Syndrome)
Tx: Ceftriaxone, ciprofloxacin, azithromycin
List the 5 major strains of E. coli that cause diarrhea.
EHEC- enterohemorrhagic EAEC- enteroaggregative ETEC- enterotoxigenic EIEC- enteroinvasive EPEC- enteropathogenic
How do you get EHEC?
undercooked meat, contaminated veggies/milk. Human-human as well
Describe the pathogenesis of EHEC.
Has a pathogenicity associated island (PAI)
T3SS- injects PAI carrying receptor transcript into host cell
Pedestal forms and allows for bacterial attachment
—> Diarrhea
Describe the clinical course of EHEC.
Which strain is most likely to cause widespread outbreaks, HUS, and ischemic colitis?
Little fever, acute onset abd. cramps and watery diarrhea.
Watery diarrhea—> bloody diarrhea within 24 hrs and lasts 8 days.
O157:H7 MCC of E. coli assoc. outbreaks and HUS, ischemic colitis
EHEC produces this toxin:
What does this toxin do?
Shiga-like toxin
It is an AB toxin:
B subunit- binds toxin to receptor on cells
A subunit- enters cell and halts protein synthesis, causing cell death
Hemolytic Uremic Syndrome. What’s going on?
Feared complication of EHEC.
One of main causes of AKI in kids >3yo
Shiga-like toxin gets into blood stream where it alters endothelial cell function—> platelet aggregation
–> hemolytic anemia, thrombocytopenia
–> AKI w/ dialysis req’d in 1/2 pts (most regain KF)
–> seizures, somnolence in 25%
–> 5% die
Describe the Dx of EHEC and specifically, O157:H7 strains.
How do you ID presence of shiga-toxin?
Sorbitol-MacConkey agar
O157:H7 will be white colony
EHEC and other E. coli will grow pink
PCR for shiga-toxin
Tx for EHEC?
Supportive care w/ monitoring for complications
Avoid antidiarrheals
Abx not helpful and may induce more shiga-toxin release
Why is EIEC called enteroinvasive?
It enters intestinal cells and multiplies—> invades adjacent cells. Similarly to Shigella
This species of Salmonella causes typhoid fever:
Does it cause gastroenteritis?
S. enterica.
Does NOT cause gastroenteritis. Whereas non-typhoid Salmonella enteritidis does (food poisoning).
Describe vectors for Salmonellosis.
Main species to know?
S. enteritidis main species. Dairy Meat Poultry, eggs Pet reptiles Human-human
Describe the pathogenesis of Salmonellosis.
Attach to M cells and are endocytosed:
T3SS injects proteins that trigger endocytosis.
Leaves enterocyte and is phagocytosed by macrophages in LP–> apoptosis of MP triggers inflammatory response.
Describe the clinical presentation of Salmonellosis.
How do you Dx it?
Tx?
Incubation period 1-3 days
n/v/d, abdominal cramping, (may be bloody diarrhea. Gastroenteritis!
Fever in 50%
Illness lasts 3-4 days
5% will develop invasive dz that could lead to bacteremia, endovascular infxns, endocarditis, osteomyelitis, reactive arthritis. Predeliction for aortic plaques, bone prostheses.
Dx w/ stool culture.
Tx: age 2-50, supportive care
Fluoroquinolones for: HIV, immunocompromised, those at risk for disseminated, invasive dz, sickle cell dz, CVD, any prosthetic devices.
Causative agent of Typhoid (Enteric) Fever: Reservoir? Transmission? Young or old pts? Causes in the U.S.?
Salmonella enterica serotype typhi Humans only reservoir Transmitted human-human via fecal-oral, contaminated food/water Typically younger pts Foodborne in the U.S.
Outline the pathogenesis of typhoid fever.
Bugs taken up by/invade M cells–> MPs–> lymphatics–> blood (sepsis may occur)
Presence in submucosa leads to hypertrophy of Peyer’s patches–> necrosis of submucosa–> possible perforation of bowel wall.
Chronic carriage in biliary tract.
Outline the clinical course of Typhoid fever.
incubate 5-21 days
Week 1- rising fever/chills, pts bacteremic
Week 2- abd. pain, rose spots on abd/trunk
Week 3- hepatosplenomegaly, GI bleeding, perforation, secondary bacteremia.
If pt does not die, symptoms resolve over weeks-months.
How do you Dx and Tx Typhoid fever?
Any preventative measures?
Dx: culture, can take time, may need to wait for incubation period
Tx: Ceftriaxone, ciprofloxacin, azithromycin
Prevention: vaccine
What is the most common bacterial enteric pathogen in developed countries?
Describe the microscopic morphology and gram stain of this organism.
Reservoirs?
Highly transmissible or nah?
Campylobacter jejuni
Thin, spiral shaped gram (-) rods
Farm animals
Low infectious dose- highly transmissible
Describe the clinical presentation of C. jejuni.
Clinical course?
Dx?
Tx?
Incubate 1 week
Watery diarrhea (bloody in 15% of adults and 50% of kids)
Fever
Crampy abd. pain
Clinical course: self limited. 3-7 days
Dx: stool culture
Tx: Azithromycin, ciprofloxacin to treat severe cases (bloody stools, worsening symptoms, high fever)
Tell me about complications of C. jejuni infection.
Also, you look nice today.
::Guillain Barre Syndrome (GBS)::
abs to LPS cross-react to gangliosides in PNS and CNS–> ascending paralysis. Symptoms start 1-2 weeks after GI infection.
::Erythema nodosum::
::Reiter’s Syndrome::
Yersinia enterocolitica:
Micro morphology and gram stain?
Sources?
Infxn involves what part of GI tract?
Gram (-) coccobacillus w/ bipolar staining
Sources: pork, raw milk, contaminated water, pet feces
Infx preferentially involves ileum, appendix, rt colon. Thus, can mimic appendicitis.
Yersinia enterocolitica:
Clinical presentation?
Dx?
Tx?
Abd. pain- main feature
n/v/f/d
Pharyngitis, arthralgia, erythema nodosum
Dx: stool culture
Tx: most cases do not warrant tx
This bug is the MCC of nosocomial diarrhea and abx-assoc. diarrhea.
Micro morph and gram stain?
Who carries it?
Transmission?
Clostridium difficile
Anaerobic, spore forming, gram (+) rod
Normal flora in GI tract of 3% of gen. pop. and 30% of hospitalized pts.
Fecal-oral route- via hands of hospital personnel
Pathogenesis of C. diff, please.
::Exotoxins A and B cause glycosylation of small GTPases involved in cytoskeleton structure and signal transduction.
::Toxin A (enterotoxin)- cells break off from basement membrane, inflamm.—> fluid secretion.
::Toxin B (cytotoxin)- depolymerization of actin–> loss of cell membrane integrity–> apoptosis of enterocytes
::Both toxins: disruption of tight junctions–> more loss of fluids
Describe the 4 clinical presentations of C. diff.
:: C diff associated diarrhea (CDAD) w/ colitis- watery diarrhea, mild lower abd. pain/cramping, low grade fever, leukocytosis.
:: Pseudomembranous colitis- presents similarly to CDAD. Colonoscopy shows pseudomembranes.
:: Fulminant colitis- severe disease (severe abd. pain, distension, fever, hypovolemia)
:: Toxic megacolon- Colonic dilation > 7cm w/ severe systemic tox.
Risk factors for C diff infxn?
Dx:
Tx?
RFs: Advancing age, abx, hospitalization
Dx: PCR for toxins, cell culture cytotox. assay (gold standard, labor/time intensive).
Tx: 1st line- Metronidazole (Flagyl), although this is also a cause of C diff to begin with… Severe dz: PO Vanc, fecal transplants, Fidaxomycin may be better than Vanc.
