GI Pathogens
Mechanisms:
1) Toxin production invitro/in vivo
2) Adhesive/aggregative- occupy microvilli
3) Invasive- inflammation
Transmission: 7 Fs: feces, food, fluids, fingers, fomites, fornication, flies; depends on # CFUs required to cause disease
Defenses:
1) Stomach- low pH
2) Small Intestine: large volume; proteases, bile, IgA
3) Large Intestine: large # flora produces inhibitory substances and occupies adhesive sites
Bug
V. Chorlea
V. parahemolyticus
General characteristics
- net loss of water
Dehyration: rice water stool
- Not invasive
- Acid Sensitive
- halophilic, can grow in absence
- caused by serotype O1/O139
Epidemiology
- Gulf coast/ Africa
- Warm months
- requires salt
V. Vulnificus
Enterobacteriaceae
E. coli
ETEC
Transmission
- Human pathogen
- Consumption of
contaminated
water/food
- No person to
person transmision
Virulence Factors
Cholera toxin: encoded
phage
- Bind to cells
- ADP-ribosylating enzyme
(↑ cAMP)
-turns off Na absorption
- increase Cl secretion
- Gastroenteritis year
round
- Septicemia and wound
infections in warm months
- severe wound infections
and sepsis
- Esp. affects ICH: cirrhosis,
renal fail
- consumption of
improperly cooked
seafood or raw
oysters
- Eating raw oysters
(sepsis)
See V. Chorlea
- exposure can induce
mucosal immunity (IgA)
- asymptomatic carrier
states
- High infectious dose
- Contaminated
food/water (no
person to person)
- Labile toxin similar to
cholera toxin; activates
adenylate cyclase ↑ cAMP
- Stable toxin: ↑ cGMP,
Treatment
Abs can shorten
duration of toxin
secretion and
decrease spread
Support with IV
fluids
See V. Chorlea
- Protein capsule protects
against phagocytosis and
complement
Gram negative rods
Motile
Lactose fermenter
Commensals, or acquired virulence
Weanling diarrhea (ST)
Traveler’s diarrhea
- Watery diarrhea
Antibiotics decrease
duration/severity of
diarrhea
EPEC
EHEC
Shigella
Salmonella
typhi
(S.
typhimurium
is most
common in
US)
Infant diarrhea, no WBC;
sometimes vomiting
- Effacing microvilli and attaching
cell membrane leads to activation
of signal transduction
- Mortality 25-50%
- O157:H7 assoc w/ HUS, causes
bloody diarrhea (4-10 days), also
fever, cramps (1st)
- Hus: hemolytic anemia, oliguric
RF, thrombocytopenia
- Hemorrhage and edema of
transverse and ascending colon
“thumbprinting”
- invasive enteric pathogen
-watery diarrhea to Dysentery- freq
stools of small vol, w/ pus and
blood
- nonmotile, lactose nonfermenting
- Typhoid fever
- High daily fevers 4-8 weeks
- invased gallbladder (carrier),
kidney, and reinvasion of gut
mucosa (causes inflammation and
can lead to diarrhea)
- doesn’t adhere to endothelium
- Motile, lactose nonfermenter
- age extremes, esp kids
<10 yrs
- s. dysenteriae: developing
contries (most severe, only
1 w/ shiga toxin)
- s. sonnei: most common
US, mildest
- s. flexneri/ boydii
The rest have cytotoxins
- 70% of kids <15
Endemic in homosexual
males
Epidemics in DCC, jails
- Incubation: 14-50
hrs
- Oral/fecal, hands,
foods, tabletops
- Reservoir:
asymptomatic kids/
adults
stimulates CL secretion,
inhibits NaCl abs.
- Reservoir: animals
- contaminated beef,
lamb, pultry, apple
jice, salami,
mayonnaise, radish
sprouts
- Person to person
too
- Low infectious dose
- human only
- low infectious dose
- direct contact, sex,
food and water
- attach Gb3R to renal
epithelium and damages
glomeruli
- Host-human
- Person to person
- Low ID, more
common in PPI and
antacid use
- invades intestinal
epithelium (inflammatory
leukocytes in LP)
- Release inflamm mediators
results in blood in lumen
- Invade colonic mucosa,
multiply intracellular and
spread from cell to cell, leads
to focal mucosal ulcers and
inflammation
- Shiga toxin inactivates 60S
ribosomal subunit stops
protein synthesis
- invades across mucosa and
hids in mononuclear cells in
lymph nodes
- Multiples and causes
bacteremia that spreads to
liver and spleen
- Multiplys in macrophages in
liver and spleen (not killed
intracellularly)
Prevent: bismuth
subsalicylate 4x/day
Diagnosis:
phenotypic culture
HeLa cells; genotype
PCR
Rehydrate and Abs
Diagnosis: culture
stool on SMAC,
detect non 0157:H7
by PCR or DNA
probes
Do not give
antimotility drugs or
AB (makes it worse)
Fecal sample:
leukocyte +
Diagnose w/ DNA
probe/PCR
Treat: Abs reduce
duration of illness
and period of
infectivity, AB
resistance is
common
- Isolate org from
blood, stool, or
urine
- Amp, cefriaxone,
bactrim
For carriers use
amp+ probenecid or
Salmonella
choleraesuis
- focal infection: vascular
endothelium endocarditis or
vascular infections
- Diarrhea
- adheres well
- conditions impairing
phagocytosis are
susceptible to bacteremia
(HbSS, AIDS, leukemia)
Salmonella
enteritides
- Osteomyelitis (in HbSS) and
diarrhea
- adheres well can cause I.E.,
intravascular infections
See above
Yersinia
enterocolitica
Yersinia
pseudotuberculosis
H. pylori
- Diarrhea, fever, ab pain for 2 wks
- Chronic disease can develop
- Affects mainly terminal ileum, if
mesenteric lymph nodes involved
(can mimic appendicitis)
- nonmotile, lactose nonfermenter
- common in Scandinavian
and Europe
- spiral, gram neg rod w/ corkscrew
motility
- Gastritis, peptic ulcers, gastric
carcinoma, MALT associated
lymphoma
- highest colonization due
to poor sanitation
- colonization in US ↑ w/
age (protects against
esophageal reflux)
- Host: pigs
- more common in
PPI and antacid use
- get from food,
water, zoonosis
(turtles and chickens)
- Host: humans/
animals (2000+)
- more common in
PPI and antacid use
- get from food,
water, zoonosis
- Zoonotic infections
in contaminated
foods like milk, meat,
water (Belgian
chocolates)
- Blood transfusion
- Incub: 1-10 days
- human primary
source
- fecal-oral trans
- Increases then released and
causes continuous bactermia
w/ high fevers
- Multiplies in LP
- induce fluid secretion by ↑
cAMP and prostaglandins
- Enters BS (rapid kill by
phagocytes)
Bactrim x6 wks
See above
- no AB, due to ↑
shedding duration
- Plasmids w/ virulence genes
- Resist phagocytosis
- Plasmids w/ virulence genes
- Resist phagocytosis
- can grow at 4C
- Urease + (neutralizes
stomach acid)
- pass through gastric mucosa
cause epithelial damage
- Stimulates inflame response
(ulcers)
- nonlactose
fermenter and
biochem properities
- Treat ICH and
bacteremia w/ AB
Treat w/ Cipro, 3rd
gen cephalopsporin,
bactrim
Diagnose: IgM, IgG,
IgA antibody ELISA
- Titer no correlate
w/ severe
- warthin-starry
silver stain
- Biopsy specimen:
urease+
- urease breath test
Treat: PPI+ tetra+
metronidazole+
bismuth or amox,
clarithro