Microbio of GIT

Clinical history
-Type of illness: duration, fever, pain, blood, vomiting, pattern of diarrhea, weight
loss
-Travel
-contaminated food/water exposure
-Sick contacts
-Antibiotic use (within last 2 weeks)
-Immune status
Infectious diarrhoea clinical syndromes
-Acute water diarrhoea
-Diarrhoea with blood
-Persistent diahoerra with sign of mal-absorption
Clinical features of acute diarrhoea
Few voluminous stools small bowel origin
Passage of many small volume stools large bowel
Dysentery, fecal urgency Colitis
Predominance of vomiting gastro
Predominance of fever mucosal invasion: systemic inflammatory response
Enteric pathogens: viral (most common about 50-70%), bacterial, parasitic, others
VIRUSES (copy the table from his slide): notovirus, rotavirus, adenovirus, CMV
BACTERIA:
Most common: campylobacter, salmonella non-typhi, shigella spp. EHEC
Travel related: enteric fever, shigella dysenterioe, vilbrio spp. Plesimonoas, other E
coli
Food poisoning: S aureas, Bacilla cereus, clostridum spp.
Antibiolet c associated: C difficile
Others: Yersina enterocolitica (same genesis as plague, can replicate at 4C!),
gelicobacter and arcobacter, aeromonas
Viruses:
Sporadic Diarrhoea: rotavirus,
Oubreak: Calcivirus (?), Astrovirus, rotavirus, adenovirus
Diarrhoea in immunocompromised hosts
Food borne diseases
-Intoxication: intoxication due to ingestion of preformed toxins
-Infections: infection due to ingestion of microorganisms
-Toxicoinfection: or it can be a result of both
There are some that can form toxin AND cause disease at the same time
Intoxications
-Disease as a result of ingestion of toxins in the food

-Large no of organism are initially required in food

-Toxin is produced by the pathogen while growing in the food
The toxin can be either heat labile or heat stable
-Symptoms generally come quickly
Infections: different organisms have a different number from which they can cause
disease e.g. shigella is only 10-100 (v contagious), but for salmonella you need
10^5.
-Cells penetrate through membranes multiply and produce toxins
-Symptoms can be local (enteric) or distant (Listeria moncytogenes can cause
sepsis in preg women? Vibrio vulnificus caused by shellfish or liver cirrhosis, EHEC)
SI infections
LI infections copy
Foodborne infections incubation times
-Short incubation within 1 day usually: emetic syndrome or diarrhoeal syndrome: S
aures, B cereus, C perfringens
-Intermediate incubations
-Long incubaton
-V Long incubation: Hep A (can be 2 weeks!), or mainly parasitic, bacteria or viral
Lab Exam (some can examine up to 12 microorganisms at once!)
-Stools: gross exam, microscopic (RBC and WBC), culture, multiplex PCR
-Blood cultures for septicaemia
-Serological tests
-Toxin assays
-Histopathological exam
-Breath test H pylori
Treatment of infectious diarrhea
-Supportive therapy
-Anti secretory drugs: racecadotroil enkephalinase inhibitor
-Antimicrobial chemo
-Probiotics: for rotavirus disease; fecal microbiota transplantations for C difficile
diseases, w/ risk of bowel perforation (?)
-Vaccinations: Rotavirus, hep A
Antibiotic therapy: Most acute diarrhea is VIRTAL and does not require antibiotics
-Antibiotics are not required for many bacterial cases
-Antibiotics may be used to reduce duration and severity of infection; prevent
serious extra intestinal complication spread of infection
-Antibiotics can cause neg effects: increase toxin release in EHEC leading to HUS
-Prolonged excretion of pathogenic organisms
-??
Hepatic infection (separate from enteric infections)
Acute Hep
Infectious: Epstein Barr, Yellow fever, Q fever

Non-infectious: drug induced, ischaemic, autoimmune, etc (the effects can mimick
that of actual Hep)
Hep A: single stranded RNA, v small, affects liver
Diagnosis: simple serology: look at IgM, IgG, test with total antibody
Hep B: d stranded DNA, genome complicated, can have a lot of errors in its
replication, a lot of different serology markers, and different can indicate different
stages of infections; we can never really get rid of it can reactivate
Course of chronic Hep B infection
-Immune tolerant time; immune clearance, immune control (longest, nothing is
really happening), immune escape (marked carcinoma or sclerosis)
NEED 3 SEROLOGY MARKERS:
-HBsAb
We need all three (what>) to see if past infection, current, or vaccination
Hep C: there is a window period between infection and when antibody comes up (70
days)
Other infections syndromes
-Oesophagitis: Candida sp, herpes simplex virus
-Gastritis: helicobacter pylori
-Colitis (in immunocompromised host): cytomegalovirus, adenovirus,
mycobacterium TB, mycobacterium ovium complex, dimorphic fungi
-Proctitis (STDs): chlamydia trachomatis, Neisseria gonorrhea, cyphilius, treponema
pallidum
*Hemactocrit indicates dehydration.
Campylobacter jejuni most common bac infection, ab pain, diarrhoea common in
this
Vivrio and Campyloobacter spp are slightly curved Gram neb bacteria
Vibrio cause a toxin mediated secretory diarrhoea (few WBC)
Campylobacter cause an invasive diarrhoea
Complication of Campylobacter jejuni can be Guille Barr syndrome
We cant see viruses in microscopy
Most common parasite is Giardia Iambilia infection: malabosprtive diarrhoea
characterized by frothy, foul selling stools, 1 to 2 hrs after meals
Very common pathogen in immigrants (poor water sanitations), spread on hands
Fecal oral: cyst form swallowed initiating infection
-Metronidazole or Tinidazole: can get a secondary lactose intolerance in the weeks
to months after infection
Bacterial dysentery caused by invasive bac pathogens: typically have grossly bloody
stools, fever and appear ill

Major agents; Shigella, Campylobacter, Salmonella and EHEC

*Shigella is v contagious so may want to give an antibiotic to keep the household
from getting it, but usually self-limiting DONT HAVE TO GIVE ANTIBIOTIC just
because it is a bacterial infection
Giving antibody to child may promote antibody resistance
Rotavirus: prominent in winter; there is no specific antiviral therapy
Norovirus viral gastro; rapid onset: nausea, vomiting, diarrhoea, important cause
of outbreaks we can keep getting reinfected as opposed to rotavirus so there is no
long last immunity, survives in environmental and common disinfectants, but killed
by bleach; v horrible feeling
Enough to shut a ward down
<exam> C difficile toxins A and B: stimulation of proinflammatory cytokines
resulting in colitis; increased permeability, cell death, loos of tight junction
diarrhoea
Has wide spe
We have an emergence of hypervirulent strain
Treatment failures: re-infectiona nd relapses
Most important: stop concurrent Abx therapy, if possible
Treatments: oral metronidazole, oral vancomycin (if the former doesn't work) and iv
metronidazole
Or fecal transplant
Fever from Africa: malaria, Hep A, typhoid fever (Salmonella Typhi), Dengue,
Entamoeba histolytica (?) Ulcer in GIT (the effect away from the problem):
E coli = most common gram neg bacteria; reptiles, chicken and and salmonella
(gram neg) go together
Salmonella:
V sensitive to acid acidity of stomach will kill majority of organism ingested- those
are on proton pump inhibitors will have a lower threshold for getting salmonella
Salmonella can occur in people with ab aortic aneurysm
EHEC/ Eoli: enterohaemorrhagic/shiga-toxin producing E coli, isolates unable to
ferment sorbital are unusual among e cli
Typical clinical course for STEC: begins with water diarrhoea, increasingly bloody,
and severe and pain is a sign
HBV: surface antigen position, core IgM positive: blood or sexual acquisition;
majority of people clear HBV naturally; HBeAg is a marker for active viral replication;
vaccination important in prevention
We need to know when we immunize people for HBV

For ruling out malaria, do thick and thin films, do blood cultures for typhoid
Hep secondary to acute Hep A infection; spread by fecal oral route, hep is almost
always acute, but self limited, vacc!