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Pathology
Lecture 43 Intestinal Infections and Inflammation
1) To be familiar with abnormal patterns of fluid/stool handling in the GI tract.
Diarrhea is stool production in excess of 250 g containing 70-95% water. Dysentery
is low-volume, painful, bloody diarrhea.
Secretory diarrhea: net intestinal fluid secretion, >500 mL isotonic fluid.
Osmotic diarrhea: high luminal osmolarity, >500 mL, abates upon fasting.
Exudative diseases: mucosal destruction leads to output of purulent bloody stools.
Deranged motility: improper gut neuromuscular function, highly variable patterns.
Malabsorption: produces voluminous, bulky stools with increased osmolarity and
combined with excess stool fat (steatorrhea).
2) To know the basic elements of GI tract protection against infection, and the
broad categories of pathogenesis in GI infection.
Protective mechanisms:
Intrinsic to GI tract: gastric acidity, native intestinal flora (competition, toxic
metabolites), bowel motility, local immune response (GALT, IgA), digestive
enzymes, and other (intestinal mucus, bile).
Behavioral/social: personal hygiene and community sanitation.
Broad categories of pathogenesis:
- Organisms specifically pathogenic for GI tract.
- Native mixed flora of GI tract become pathogenic due to decreased bowel integrity,
risk of peritonitis, septicemia.
3) For the various viral, bacterial, protozoal, and metazoal diseases of GI tract, be
able to recognize the following (in each group): common infectious agents,
clinical manifestations, at-risk population groups, pathologic features, and
special features.
Disease
Infectious agents
Viral
Rotavirus
Enteric adenovirus
Norwalk virus
Bacterial
Ingested toxin
(Staph, Vibrio
cholerae)
Toxigenic
organisms
(toxigenic E. coli)
Enteroinvasive
(Salmonella,
Shigella, Yersinia)
Clinical
manifestation
Nausea, vomiting,
watery diarrhea
Explosive diarrhea
and abdominal pain;
neurotoxin of C.
botulinum may
produce respiratory
failure.
Incubation hoursdays, Secretary and
the toxins produced
area and dehydration.
Cytotoxic
enterotoxins and
enteroinvasive
processes produce
dysentery.
At-risk pop.
Pathologic features
Special features
Infants <2
years
Older children,
adults
Locations of
poor hygiene,
developing
nations,
consuming
uncooked
foods
especially
chicken and
pork.
Micro: nonspecific;
small bowel villus
blunting or flattening:
↑mononuclear cells
Variable, typically
surface epithelial
damage (ulceration);
increased mitotic rate
(regeneration); edema,
congestion; variable
leukocyte population.
May resemble Crohn's
disease (Yersinia,
mycobacterial).
All enteroinvasive
organisms may
simulate acute
ulcerative colitis
Incubation 1-2 days
Symptomatic period 1-3
days
Salmonella: linear ulcers
localized over Peyer’s
patches
Shigella: distal colon
purulent exudate.
Yersinia: Peyer’s patches
necrotizing granulomas
Clostridium Perfringens:
necrotizing lesions
Mycobacterium
tuberculosis:
granulomatous infection
with tendency for
transmural scarring and
constriction.
Protozoal
Metazoal
Amebiasis
(Entamoeba
histolytica)
Dysentery, intestinal
pain, fever
Developing
countries
Giardiasis (Giardia
lamblia)
Acute or chronic
diarrhea; crampy
abdominal pain;
possible steatorrhea
Institutionalize
and day care
populations
commonly
affected
Hookworm,
strongyloides,
tapeworm
Usually minor GI
tract symptoms: more
likely to produce
nutritional
deficiencies and/or
anemia of blood loss
Unsanitary
conditions ,
consuming
raw or
undercooked
meat
Flasks shaped ulcer
"undermining"
produces larger areas of
ulceration
Pear-shaped binucleate,
flagellate trophozoite
resembles "ghost"
sickle-shaped forms
adherent to villus
services of epithelial
cells
Parasites attach and
small bowel, reproduce
eggs are excreted in
feces, some may invade
locally.
May spread to liver
producing amoebic liver
abscess.
Agammaglobulinemic
patients at risk for severe
disease
4) To understand the microbiologic basis for different types of pathogenesis within
the area of bacterial enterocolitis. Differences among bacterial pathogens with
regards to adhesion/replication, enterotoxins, and invasion produce different types of
pathogenesis.
5) For “Other Inflammatory Processes,” to be familiar with at-risk patient groups,
the pathophysiology of the process, range of clinical disease, preferred anatomic
sites of involvement, and pathologic features. See number 6.
6) To know, in detail, the information under #5 (above) for common causes of GI
tract inflammation such as diverticulitis and appendicitis.
Disease
At-risk groups
Pathophysiology
Clinical disease
Anatomic sites
Pathologic features
Necrotizing
enterocolitis of
newborn
1st 3 months, premature,
low-birth-weight,
formula fed
Ischemia, pathogenic
organisms, high protein
concentration, GI tract
immaturity.
Anabiotic-associated
(pseudomembranous)
colitis
Patients finishing a full
course of broadspectrum antibiotics
Proliferation of toxinforming organisms
(Clostridium difficile)
Diverticulitis
Appendicitis
50% of Patients >60 yr
in developed nations
Adolescents and young
adults
Outpouching (<1 cm
diameter) along taeniae
coli due to weak wall
and increased pressure
Abdominal distention,
tenderness, paralytic
ileus, bloody diarrhea.
Severe cases perforation, septicemia,
and shock.
Terminal ileum and
ascending colon
Mucosal ulceration to
full-thickness necrosis of
bowel wall
Acute, chronic diarrhea;
usually no history of
prior GI disease.
Usually asymptomatic
(80%); may have
cramping, vague
abdominal discomfort,
constipation, and
distention
Sigmoid colon
Obstruction of appendix
lumen (fecalith),
↑ pressure, compressed
veins, ischemic injury,
bacteria proliferate =
acute inflammation
Periumbilical pain
localizing to RLQ,
nausea and vomiting,
guarding, rebound
tenderness, low-grade
fever, elevated WBC's
Appendix
Obstruction and/or
perforation of
diverticulum produces
inflammation, with
granulation tissue and
fibrosis
Gross: edema, injected
serosal vessels, exudates
micro: mucosal
ulceration, neutrophils
through wall, fibrinopurulent exudate
Colon
Denuding of surface
epithelium;
mucopurulent exudate
merging to form
"pseudomembrane"
7) To recognize patients in special risk categories for GI tract
infection/inflammation, as covered in “Special circumstances for GI
inflammation/infection.”
HIV-infected patients: wide array of opportunistic infections; possible entity of
primary AIDS associated enteropathy.
Bone marrow transplantation: direct GI injury due to pre-transplant therapy
(radiation, chemotherapy); opportunistic infections; graft-versus-host disease.
Granulocytopenia: peripheral WBC count <1000/cubic mm carries high risk of
infection, normal gut flora are a potential source of gram-negative sepsis.
Acute typhilitis (cecitis): necrotizing colitis, preferentially localized to cecum; cancer
patients were neutropenia; 70% incidence gram-negative or Clostridial species.
8) To understand the concept of peritonitis, its causes, pathologic findings and
outcomes.
Peritonitis is localized or generalized inflammation of the peritoneal cavity.
Causes: may be infectious due to bacteria escaping through the GI wall or
spontaneous growth of natural flora (due to proteinaceous effusion - ascites). May be
non-infectious due to bile, pancreatic enzymes, or foreign body.
Pathologic findings: edema, vascular congestion (injected appearance) of small blood
vessels; fibrinopurulent exudate on peritoneal surface (pus appearance).
Outcomes: resolution; walled off abscesses; organization of exudate as fibrous
adhesions.
9) To be responsible for all material covered in Lecture Notes for “Intestinal
Infections and Inflammation.” Review notes.