Enteric Bacterial Infections (Inflammatory): Cross, Ryan

Question 1

90% of infectious diarrheas are caused by bacteria, parasites, or viruses?

Answer 1

Viruses

Question 2

Persistent diarrhea (>2 weeks) is likely caused by:

Answer 2

Parasite

Question 3

When treating chronic diarrhea, start considering the possibility that the pt has:

Answer 3

HIV

or is infected with CMV, M. avium intracellulare

Question 4

Bloody diarrhea =
You will see these cells in the stool:
Small or large volume?
Colon or SB affected, commonly?

Answer 4

inflammatory diarrhea aka dysentery
WBCs and RBCs
Small volume
Colon commonly affected

Question 5

Watery diarrhea =
Colon or SB affected commonly?
Small or large volume
Colon or SB affected, commonly?

Answer 5

non-inflammatory diarrhea
No cells
Large volume
SB usually affected

Question 6

7 pathogens causing inflammatory diarrhea:

Answer 6

Shigella
EHEC
EIEC
Salmonella
C. jejuni
C. difficile
Yersinia enterocolitica

Question 7

List characteristics Salmonella, Shigella, and E. coli have in common.

Answer 7

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

Question 8

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?

Answer 8

C/S America- S. dysenteriae
U.S.- S. sonnei
Fecal oral route of infection or contaminated food/water
Low infectious dose

Question 9

Discuss the pathogenesis of Shigella.

Answer 9

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.

Question 10

Describe the clinical course of Shigella infection.

How do you treat it?

Answer 10

Self-limiting, lasts ~1 week.
50% become bloody diarrhea
Complications: reactive arthritis, urethritis, conjunctivitis (Reiter’s Syndrome)

Tx: Ceftriaxone, ciprofloxacin, azithromycin

Question 11

List the 5 major strains of E. coli that cause diarrhea.

Answer 11

EHEC- enterohemorrhagic
EAEC- enteroaggregative
ETEC- enterotoxigenic
EIEC- enteroinvasive
EPEC- enteropathogenic

Question 12

How do you get EHEC?

Answer 12

undercooked meat, contaminated veggies/milk. Human-human as well

Question 13

Describe the pathogenesis of EHEC.

Answer 13

Has a pathogenicity associated island (PAI)
T3SS- injects PAI carrying receptor transcript into host cell
Pedestal forms and allows for bacterial attachment
—> Diarrhea

Question 14

Describe the clinical course of EHEC.

Which strain is most likely to cause widespread outbreaks, HUS, and ischemic colitis?

Answer 14

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

Question 15

EHEC produces this toxin:

What does this toxin do?

Answer 15

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

Question 16

Hemolytic Uremic Syndrome. What’s going on?

Answer 16

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

Question 17

Describe the Dx of EHEC and specifically, O157:H7 strains.

How do you ID presence of shiga-toxin?

Answer 17

Sorbitol-MacConkey agar
O157:H7 will be white colony
EHEC and other E. coli will grow pink
PCR for shiga-toxin

Question 18

Tx for EHEC?

Answer 18

Supportive care w/ monitoring for complications
Avoid antidiarrheals
Abx not helpful and may induce more shiga-toxin release

Question 19

Why is EIEC called enteroinvasive?

Answer 19

It enters intestinal cells and multiplies—> invades adjacent cells. Similarly to Shigella

Question 20

This species of Salmonella causes typhoid fever:

Does it cause gastroenteritis?

Answer 20

S. enterica.

Does NOT cause gastroenteritis. Whereas non-typhoid Salmonella enteritidis does (food poisoning).

Question 21

Describe vectors for Salmonellosis.

Main species to know?

Answer 21

S. enteritidis main species. 
Dairy
Meat
Poultry, eggs
Pet reptiles
Human-human

Question 22

Describe the pathogenesis of Salmonellosis.

Answer 22

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.

Question 23

Describe the clinical presentation of Salmonellosis.
How do you Dx it?
Tx?

Answer 23

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.

Question 24

Causative agent of Typhoid (Enteric) Fever:
Reservoir?
Transmission?
Young or old pts?
Causes in the U.S.?

Answer 24

Salmonella enterica serotype typhi
Humans only reservoir
Transmitted human-human via fecal-oral, contaminated food/water
Typically younger pts
Foodborne in the U.S.

Question 25

Outline the pathogenesis of typhoid fever.

Answer 25

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.

Question 26

Outline the clinical course of Typhoid fever.

Answer 26

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.

Question 27

How do you Dx and Tx Typhoid fever?

Any preventative measures?

Answer 27

Dx: culture, can take time, may need to wait for incubation period

Tx: Ceftriaxone, ciprofloxacin, azithromycin

Prevention: vaccine

Question 28

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?

Answer 28

Campylobacter jejuni
Thin, spiral shaped gram (-) rods
Farm animals
Low infectious dose- highly transmissible

Question 29

Describe the clinical presentation of C. jejuni.
Clinical course?
Dx?
Tx?

Answer 29

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)

Question 30

Tell me about complications of C. jejuni infection.

Also, you look nice today.

Answer 30

::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::

Question 31

Yersinia enterocolitica:
Micro morphology and gram stain?
Sources?
Infxn involves what part of GI tract?

Answer 31

Gram (-) coccobacillus w/ bipolar staining
Sources: pork, raw milk, contaminated water, pet feces
Infx preferentially involves ileum, appendix, rt colon. Thus, can mimic appendicitis.

Question 32

Yersinia enterocolitica:
Clinical presentation?
Dx?
Tx?

Answer 32

Abd. pain- main feature
n/v/f/d
Pharyngitis, arthralgia, erythema nodosum

Dx: stool culture

Tx: most cases do not warrant tx

Question 33

This bug is the MCC of nosocomial diarrhea and abx-assoc. diarrhea.
Micro morph and gram stain?
Who carries it?
Transmission?

Answer 33

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

Question 34

Pathogenesis of C. diff, please.

Answer 34

::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

Question 35

Describe the 4 clinical presentations of C. diff.

Answer 35

:: 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.

Question 36

Risk factors for C diff infxn?
Dx:
Tx?

Answer 36

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.