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Infectious Disease Git
1. INFECTIOUS DISEASE
CHAPTER SIX
GASTROINTESTINAL AND
INTRAABDOMINAL INFECTIONS
Acute gastroenteritis
(mainly, infectious
diarrheas) is second only
to cardiovascular disease
as a cause of death
worldwide. In the U.S.,
acute gastroenteritis is
second only to viral
respiratory disease as a
cause of acute illness,
prompting an estimated
73 million physician
consultations each year.
3. Microscopy, Inc. antrum, where it resides
Used with in the mucous layer. H.
permission pylori damages mucous-
secreting cells and also
promotes an acute and
chronic inflammatory
response that may lead to
a sequence of events:
acute gastritis followed
by chronic superficial
gastritis, then atrophic
gastritis, intestinal
metaplasia, dysplasia, and
adenocarcinoma. The
stomach infected with H.
pylori also develops
lymphoid follicles
(lymphoid tissue is not
normally present in the
stomach), which can
evolve into a low-grade
4. malignancy known as
MALT lymphoma. Why
some persons develop
these various
manifestations of H.
pylori infections while
others do not remains
largely unclear.
H. pylori colonizes at
least one-half of the
world’s population, with
high colonization rates in
developing countries
where the infection is
usually acquired during
childhood. About 35% of
persons in the U.S. are
colonized and, as the
frequency of colonization
is about 0.5% per year,
about 50% of persons >
5. 60 years of age in the
U.S. and other developed
countries may be
infected. Fecal-oral
transmission occurs, and
lower prevalence rates
correlate with higher
standards of living and
sanitation.
H. pylori is associated
with about 70% to 90%
of duodenal ulcers, about
70% of gastric ulcers, and
with about 60% to 80%
of gastric carcinomas.
There is evidence that the
prevalence of H. pylori in
the U.S. has been
declining, and it is
suggested that this may
explain, at least in part,
6. the declining incidence of
peptic ulcer disease and
adenocarcinoma of the
stomach. However, the
incidence of reflux
esophagitis, Barrett’s
esophagus, and
adenocarcinoma of the
esophagus in the U.S. has
been increasing, leading
to the provocative
suggestion that certain
strains of H. pylori may
be protective against the
serious consequences of
gastroesophageal reflux
disease (GERD).
FOOD POISONING
Figure 2 Centralized food
10. permission multiply in the host in
order to cause disease.
Symptoms of botulism
Figure 5 are delayed because
Vibrio the toxin must be
parahaemolyticus absorbed and then
- halophilic, fixed to neural tissue.
facultative Toxin production
anerobic, rod within the patient's
bacterium that gastrointestinal tract
causes a food- following ingestion of
borne illness the organism is
known as seafood characteristic of food
poisoning. poisoning due to
Usually Bacillus cereus (long
transmitted incubation type),
through eating infant botulism,
raw or Clostridium
undercooked perfringens,
seafood such as enterotoxigenic E.
oysters. Less coli, Shiga toxin-
13. with severe disease.
Shigella species, the
classic agents of bacillary
dysentery, currently cause
< 2% of outbreaks in the
U.S., while
Campylobacter jejuni,
although responsible for
> 200,000 cases of
diarrhea each year, causes
<1% of reported food-
borne outbreaks. Shiga
toxin-producing E. coli
strains assume
importance
disproportionate to their
frequency because of the
severe complications
(discussed below).
Listeria monocytogenes
causes occasional
14. outbreaks of food-borne
illness in the United
States, which can result in
life threatening disease
especially in young
children and among the
elderly. Brucella species
cause occasional
outbreaks of disease
(brucellosis) in the U.S.
and are usually acquired
from cheese made from
unpasteurized milk, raw
milk, or raw meat.
Parasites associated with
outbreaks of food-borne
disease in the U.S. in
recent years include
Cyclospora cayetanensis
(cyclosporiasis) and
Cryptosporidium parvum
15. (cryptosporidiosis).
Listeria monocytogenes
has been associated with
outbreaks traced to dairy
products.
The syndromes of food
poisoning vary according
to the organism, the
organ(s) affected and the
time of onset after
ingestion:
Onset within 1 hour
suggests ingestion of a
chemical.
Onset between 1 and 6
hours suggests ingestion
of a preformed toxin,
usually due to food
contaminated with S.
aureus or Bacillus
16. cereus.
Onset within 8 to 16
hours raises a number of
possibilities, especially
bacteria such as
Clostridium perfringens
and enterotoxin-
producing strains of
Bacillus cereus that must
multiply in the
gastrointestinal tract
prior to causing disease.
Onset beyond 16 hours
also raises a number of
possibilities, including
various bacteria and
viruses.
Staphylococcal food
poisoning and short-
incubation B. cereus food
poisoning are
17. characterized by vomiting
and crampy abdominal
pain. Diarrhea occurs in
about one-third of cases.
A later onset of crampy
abdominal pain with
diarrhea is characteristic
of Clostridium
perfringens and long-
incubation B. cereus food
poisoning, but these same
symptoms can be caused
by many other enteric
pathogens.
INFECTIOUS
DIARRHEA:
OVERVIEW
Infectious diarrhea is the
second most common
18. cause of death worldwide
and the leading cause of
death in early childhood.
In the U.S., infectious
diarrhea causes death
mainly in older and
debilitated persons.
However, disastrous
consequences can occur
in previously healthy
persons. Pathogen-
associated complications
from infectious diarrhea
include mycotic
aneurysm of the aorta
with Salmonella species,
the hemolytic-uremic
syndrome and renal
failure with Shiga toxin-
producing strains of E.
coli, and Guillain-Barré
19. syndrome with
Campylobacter jejuni.
The clinician’s primary
task is to discern which
patients need further
investigation including
stool cultures, which need
empiric antimicrobial
therapy, and which need
only quot;tincture of timequot;.
According to various
estimates, there are > 200
million episodes of
diarrhea in the U.S. each
year (by one estimate, 1.4
episodes per person),
resulting in > 73 million
physician consultations,
28 million office visits,
1.8 million
hospitalizations, and
20. 5,000 deaths. Answers to
a series of questions
usually determine the
optimum approach to
diagnosis and therapy.
When a patient presents
with diarrhea as the chief
complaint, important
questions include the
following:
Is the problem best
classified as diarrhea?
Diarrhea is usually
defined as 3 or more
loose stools per day, 2
loose stools with
abdominal symptoms, or
> 250 grams of stool per
day for 7 days. “Loose
stools” not meeting one
21. of these criteria may be
part of another illness, or
may fall within the range
of normal bowel
functioning. However, it
is acceptable to consider
any increased frequency
or decreased
consistency of bowel
movements as
“diarrhea.”
Is the problem likely
infectious or non-
infectious?
Most cases of
community-acquired
diarrhea are probably
caused by infection.
Non-infectious causes
include drugs, primary
gastrointestinal diseases
22. such as inflammatory
bowel disease, food
allergies, endocrine
disorders (such as
thyrotoxicosis), carcinoid
syndrome, and
paraneoplastic
syndromes. Ischemic
colitis due to cocaine
should be considered in
the differential diagnosis
of abdominal pain and
bloody diarrhea in a
young or middle-aged
adult.
What is the duration of
the illness, and did it
begin suddenly or
gradually?
Sudden onset of
diarrhea can be caused
23. by a pre-formed toxin or
by a specific enteric
pathogen usually
associated with an acute
diarrheal syndrome.
Diarrhea of gradual
onset is often caused by
pathogens that tend to
cause prolonged
diarrheal illness such as
Giardia lamblia.
What is the
epidemiologic setting?
Has the patient recently
traveled to a developing
country? Has the patient
recently taken antibiotics
(raising the possibility of
C. difficile colitis)? Has
there been exposure to
persons with diarrhea, or
24. who are at high risk of
diarrhea (such as
children in day-care
centers)? Is there a
history of ingestion of
unsafe foods (such as
unpasteurized milk or
cheese, raw shellfish,
raw eggs, or raw meat)
or water (such as from
lakes or streams)? Has
there been contact with
animals or pets,
including reptiles (which
are notoriously
associated with
Salmonella species)?
How is the patient’s
general health and
immunocompetence?
Dehydration secondary
25. to acute diarrheal illness
carries increased risk of
morbidity and mortality
at the extremes of life:
infants and the elderly.
Persons who are on
immunosuppressive
medication or who have
advanced HIV disease
are at high risk of
diarrhea due to
opportunistic pathogens
including parasites.
Is the diarrhea likely to
involve mainly the
small bowel or the
large bowel?
About 90% of cases of
acute, community-
acquired infectious
diarrhea in the U.S.
26. represent “small bowel
diarrhea” characterized
by infrequent watery
stools. About 5% to 10%
of cases represent “large
bowel diarrhea” or the
dysentery syndrome,
characterized by
frequent, small-volume
stools that often contain
mucus or blood.
Frequently, however, the
pattern of diarrhea
doesn’t fit neatly into one
or the other of these
categories.
Is the diarrhea
medically important?
Diarrhea is a common
experience and usually
runs a benign course,
27. even in persons with
underlying conditions.
Most patients do not
require stool cultures
and other studies. The
character and duration of
the diarrhea, the
associated symptoms
and signs, and the
epidemiologic features
usually determine
whether further
investigation is
warranted.
SHIGA TOXIN-
PRODUCING E. COLI
(E. COLI 0157:H7 AND
OTHER SEROTYPES)
Strains of E. coli that
28. produce Shiga toxin, also
known as
enterohemorrhagic E. coli
strains, were recognized
in the U.S. in 1982 and
now cause an estimated
20,000 cases of diarrheal
disease each year.
Although uncommon in
primary care (<1% of all
cases of infectious
diarrhea), these strains
can cause severe
hemorrhagic colitis, the
hemolytic-uremic
syndrome, and
thrombotic
thrombocytopenic
purpura.
E. coli 0157:H7 differs
from most E. coli strains
29. by its production of one
or more Shiga toxins and
by its inability to ferment
sorbitol. Other serotypes
of E. coli sometimes
produce Shiga toxins, but
these are uncommon in
the U.S. These E. coli
strains adhere tightly to
mucosal cells, especially
in the ascending and
transverse colon. The
toxin molecule damages
mucosal cells and also
enters the systemic
circulation, where it
causes vascular and
endothelial damage that
can lead to capillary leak
syndrome, thrombosis,
hemolysis, and renal
30. failure.
Most human infections
have been transmitted by
beef, and are thought to
result from fecal
contamination of meat
during slaughter.
Undercooked hamburger
meat has been famously
associated with E. coli
0157:H7 outbreaks. It has
been estimated that a
hamburger purchased at a
fast food restaurant in the
U.S. contains meat from
as many as 1000 cows.
Outbreaks have also been
associated with the
ingestion of unchlorinated
drinking water,
unpasteurized apple cider,
31. alfalfa sprouts, leaf
lettuce, mesclun lettuce,
radish sprouts, milk, and
other foods and
beverages. New standards
for food processing have
been introduced in the
U.S. with the aim of
reducing the prevalence
of this pathogen.
However, the infectious
dose is low, possibly as
low as 100 bacteria.
Therefore, prevention is
difficult and person-to-
person spread may occur.
After an incubation
period of 3 to 4 days
(range 1 to 8 days),
patients classically
present with crampy
32. abdominal pain and
bloody stools. The pain is
often severe and out of
proportion to the findings
on physical examination
of the abdomen. About
one third of patients have
fever, which
characteristically follows
the appearance of blood
in the stool. Some
persons infected with E.
coli 0157:H7 remain
asymptomatic, and others
experience crampy
abdominal pain with little
or no diarrhea. Most
patients, however, have
bloody diarrhea caused by
hemorrhagic colitis. Data
from large series suggest
33. that up to 90% of patients
experience bloody
diarrhea at some point
during the illness, with
about 60% of patients
having blood in their
stools at the time of
presentation. Severe
abdominal pain prior to
the onset of fever often
suggests acute
appendicitis, while pain
combined with bloody
stools suggests
inflammatory colitis.
SALMONELLA
SPECIES OTHER
Figure .
THAN S. TYPHI
Salmonella - rod
(SALMONELLOSIS)
prokaryote
35. gram-negative rods.
Recent studies showing
high levels of DNA
similarity among
Salmonella isolates have
led to the reclassification
of all clinically important
Salmonellae into a single
species, Salmonella
choleraesuis. There are 7
subgroups of Salmonella
choleraesuis, and more
than 2300 serovars are
recognized based on 3
major antigens (the
somatic O antigen, the
surface Vi antigen, and
the flagellar H antigens).
Most clinical laboratories
continue to report isolates
by their familiar names;
36. for example, Salmonella
typhimurium rather than
Salmonella choleraesuis
serotype typhimurium.
Although S. typhi and S.
paratyphi colonize only
humans, non-typhoidal
Salmonella strains are
widespread throughout
the animal kingdom.
Human disease is usually
associated with food
products, most commonly
poultry and eggs.
Infection of poultry flocks
is widespread. Ingestion
of uncooked or lightly
cooked eggs is therefore a
risk factor for disease.
However, outbreaks and
cases have been linked to
37. numerous foods including
tomatoes, alfalfa sprouts,
cantaloupe, and freshly
squeezed orange juice.
Some patients with
salmonellosis give a
history of keeping exotic
pets, especially reptiles,
of which up to 90%
harbor Salmonella
organisms.
Salmonella infection is
frequently asymptomatic.
There is no reliable
serologic test, and a
single negative stool
culture does not exclude
the possibility that a food
handler might be an
intermittent shedder of
Salmonella organisms.
38. Given both the wide
distribution of Salmonella
in foodstuffs and the
frequency of
asymptomatic Salmonella
carriage, it is difficult to
envision how any
restaurant might prevent
the occasional case of
Salmonella transmission
despite emphasis on
hygienic practices.
Salmonella infection is a
risk of everyday life,
especially for persons
who dine out frequently.
Salmonella infection
nearly always arises by
ingestion of the bacteria.
Gastric acidity is the first
line of host defense, since
39. Salmonella survives
poorly if at all at the
normal gastric pH (< 1.5).
On the basis of previous
data, it has been accepted
that ingestion of >105
Salmonella organisms is
necessary to cause
disease. However, more
recent data indicate that a
lower inoculum (<103
organisms) can cause
disease. Because
Salmonella survives well
at pH values of 4.0 or
higher, persons with
atrophic gastritis (which
is common among the
elderly) or who are taking
gastric pH-raising
medications (antacids,
40. H2-blockers, or proton
pump inhibitors) are at
increased risk of
salmonellosis.
Containment of
Salmonella infection
depends on an intact T-
lymphocyte system
including macrophage
function. Persons at risk
of serious consequences
of Salmonella infection
include (1) persons with
impaired T-cell function
because of
lymphoproliferative
disorders, other
malignancies, HIV
disease, or
immunosuppressive
medication; and (2)
41. persons with disorders
that cause “macrophage
blockade” such as
hemoglobinopathies
(notably, sickle cell
disease), bartonellosis,
malaria, schistosomiasis,
and disseminated
histoplasmosis.
The 5 recognized
syndromes of
salmonellosis are
gastroenteritis, enteric
fever (discussed
separately, below),
bacteremia and
endovascular infection,
localized metastatic
infections, and the
asymptomatic carrier
42. state.
Gastroenteritis due to
non-typhoidal Salmonella
usually presents as
nausea, vomiting, and
diarrhea 6 to 48 hours
after the ingestion of
contaminated food or
water. A high inoculum
of Salmonella correlates
with increased severity
and duration of the
illness. The stools are
usually loose, of
moderate volume, and
without blood.
Occasionally the disease
can present as classic
“small bowel diarrhea”
with large volume, watery
stools or as classic “large
43. bowel diarrhea” with
small volume stools
accompanied by
tenesmus. Fever, chills,
nausea, vomiting, and
abdominal cramps are
common. Occasionally,
right lower quadrant pain
suggesting acute
appendicitis dominates
the clinical picture
(pseudoappendicitis).
Bacteremia is
documented, when
sought, in up to 4% of
immunocompetent
persons with Salmonella
gastroenteritis.
Unrecognized episodes of
transient bacteremia are
probably common. More
44. prolonged bacteremia
correlates with
immunosuppression.
Multiple positive blood
cultures for Salmonella
should raise the
possibility of
intravascular infection
including mycotic
aneurysm or endocarditis.
Localized metastatic
infection occurs in up to
5% to 10% of patients.
The major syndromes are
as follows:
Endocarditis occurs in
up to 0.4% (or 1 in 250)
patients with Salmonella
bacteremia, usually in
persons with pre-existing
45. heart disease.
Central nervous system
infections including
meningitis, ventriculitis,
and brain abscess are
more common in infants,
especially neonates.
Osteomyelitis and septic
arthritis are encountered
most frequently in
persons with sickle cell
disease, bone disease,
or immunosuppression.
Osteomyelitis due to
Salmonella species most
commonly affects the
femur, tibia, humerus, or
lumbar vertebrae. Septic
arthritis due to
Salmonella species most
commonly affects the
46. knee, hip, or shoulder.
Reactive arthritis
affecting multiple joints
occurs most often in
persons who have the
HLA-B27
histocompatibility
antigen.
Soft tissue infections
usually occur in the
setting or local trauma
and
immunosuppression.
Urinary tract infection
usually occurs in the
setting of ureteral or
bladder stones,
malignancy, renal
transplants, or, in some
parts of the world,
schistosomiasis.
47. Successful treatment
often requires attention
to structural
abnormalities.
Other complications
include pneumonia,
hepatobiliary infection,
splenic infection, and
genital infections.
The asymptomatic
carrier state develops in
0.2% to 0.6% of persons
with non-typhoidal
salmonellosis, and is
more common in
women and in persons
with abnormalities of
the biliary tract. The
long-term carrier state is
defined by persistence
of Salmonella in stool
48. or urine cultures for > 1
year.
SHIGELLA SPECIES
(SHIGELLOSIS)
Shigella species are the
classic agents of
dysentery and are highly
communicable.
Shigellosis remains an
important cause of
morbidity and mortality
in developing countries,
mainly in children. At
least 19,000 cases occur
in the U.S. each year.
Shigella are gram-
negative bacilli with 4
recognized serogroups:
49. group A (Shigella
dysenteriae), group B
(Shigella flexneri), group
C (Shigella boydii), group
D (Shigella sonnei).
Within these 4 serogroups
are about 40 serotypes, of
which Shigella
dysenteriae serotype 1
(also known as the Shiga
bacillus) causes the most
severe disease. Shigella
sonnei now accounts for
about 60% to 80% of
cases of shigellosis in the
U.S.
Like Salmonella, Shigella
can contaminate food and
water, causing occasional
common source
outbreaks. However,
50. person-to-person
transmission is the
dominant mode of
transmission. As few as
10 to 100 Shigella
organisms can cause
disease; therefore,
shigellosis is highly
communicable. After
exposure to a case of
shigellosis in a
household, about 40% of
persons between and 1 to
4 years of age and about
20% of persons of all
ages develop the disease.
Outbreaks of shigellosis
occur in crowded, closed
environments such as
nurseries, day care
centers, institutions, and
51. cruise ships.
Following ingestion,
Shigella organisms
multiply in the small
intestine resulting in
concentrations of 107 to
109 bacteria per mL of
intestinal fluid.
Symptoms commonly
result from small
intestinal involvement,
but the hallmark
symptoms of
shigellosis—the
dysentery syndrome—
result from mucosal
invasion and toxin
production in the colon.
Inflammation is severe
but relatively superficial,
and bacteremia is
52. therefore uncommon.
CAMPYLOBACTER
SPECIES
Figure
Campylobacter Diarrhea caused by
jejuni is an Campylobacter jejuni is
enteric, curved- one of the most common
rod prokaryote infectious diseases
(bacterium). It is worldwide. More than 1
the bacterium that million cases occur each
causes year in the U.S., where
campylobacterios Campylobacter is isolated
is, one of the from stool cultures more
most common frequently than either
bacterial causes Salmonella or Shigella
of diarrheal species. Campylobacter
illness in the jejuni is therefore an
United States. It important pathogen in
is a relatively primary care.
fragile bacterium Campylobacter fetus is
54. predominantly food-borne
but can result from direct
contact with animals,
including household pets
(notably, puppies or
kittens with diarrhea).
Fecal-oral transmission
occurs, and men who
have sex with men are at
increased risk. However,
transmission from food
handlers appears to be
uncommon. Some studies
suggest that disease can
result from ingestion of as
few as 500 bacilli. Like
Salmonella,
Campylobacter is
inhibited by hydrochloric
acid in the stomach and
might therefore occur
55. more commonly when
gastric pH is raised
because of gastritis or
medications.
Campylobacter species
invade the intestinal
mucosa and also elaborate
various extracellular
toxins with cytopathic
activities.
Campylobacter jejuni
causes disease throughout
the year in the U.S., but
sharp peaks of
Campylobacter disease
occur during the summer
and early fall. The disease
especially affects children
< 1 year of age and
persons between 15 and
29 years of age. This
56. pattern in the U.S.
contrasts sharply with the
pattern in developing
countries, where
Campylobacter affects
persons of all ages and
especially during the first
5 years of life.
Mishandling of raw
poultry and consumption
of undercooked poultry
are now considered to be
the major risk factors to
Campylobacter infection.
The incubation period of
Campylobacter jejuni
gastroenteritis is usually
between 1 and 7 days
(average, 2 to 4 days). In
about two thirds of cases,
the disease begins with
57. abdominal pain and/or
diarrhea. The remaining
patients have a prodrome
that suggests a flu-like
illness (see below). Pain
is often severe and can be
the predominant
symptom. In other
patients, fever is the
predominant
manifestation of the
disease. The diarrhea can
consist of frequent loose
stools, massive watery
stools, or grossly bloody
stools. Most patients (at
least 50% in one study)
have 10 or more bowel
movements on the worst
day of the illness. Gross
blood is commonly
58. present in bowel
movement during the
second and third days of
the illness. Mild
leukocytosis is often
present.
CLOSTRIDUM
DIFFICILE AND
ANTIBIOTIC-
ASSOCIATED
COLITIS
Diarrhea is a relatively
common complication of
antimicrobial therapy and
is associated with
Clostridium difficile in
about 10% to 30% of
cases.
Pseudomembranous
59. colitis due to C. difficile,
the most severe form of
antibiotic-associated
diarrhea, occurs in about
1 in 10,000 courses of
antibiotic therapy in
ambulatory patients. C.
difficile elaborates two
large toxin molecules, an
enterotoxin known as
toxin A and a cytotoxin
known as toxin B. About
60% of adults in the U.S.
have serum antibodies to
C. difficile, suggesting
that asymptomatic
colonization is relatively
common. Prevalence
surveys indicate
colonization of the colon
by C. difficile in about
60. 3% or less of healthy
adults, 2% to 8% of
elderly persons in nursing
homes, and up to 20% of
persons who are
hospitalized. Person-to-
person transmission of C.
difficile occurs, and can
be reduced by
handwashing before and
after patient encounters
and by use of disposable
gloves (followed by
handwashing) during
direct contact with
patients.
Symptoms typically begin
5 to 10 days after a course
of antimicrobial therapy,
but can start as early as
the first day of treatment
61. and as late as 10 weeks
after treatment has been
discontinued. A common
presentation consists of
acute onset of watery
diarrhea with low-grade
fever and abdominal pain.
The disease ranges in
severity from mild to
fulminant. Overall, about
30% to 50% of patients
have fever and 20% to
33% have abdominal
pain. Despite prominent
involvement of the
rectosigmoid area in most
cases, gross blood is
seldom present in the
stool.
63. one-third of all diarrhea-
related hospitalizations
worldwide, with about
800,000 deaths each year.
Nearly all children are
infected by age 3 years.
In the U.S., diarrhea due
to rotaviruses accounts
for an estimated 500,000
physician visits, 50,000
hospitalizations, and 20 to
40 deaths, at an annual
cost > $1 billion.
Of the 3 recognized
groups of rotaviruses (A,
B, and C) are recognized,
group A accounts for
most outbreaks. The
disease is presumably
spread mainly by fecal-
oral transmission, which
64. explains in part its high
frequency in childcare
centers. Rotaviruses
infect villous epithelial
cells in the jejunum and
ileum. Children with
rotavirus infection
typically present with
fever, vomiting, and
diarrhea. Dehydration can
be significant. Adults
remain susceptible to
rotavirus infection, but
serious morbidity and
mortality is rare except
among the elderly.
Outbreaks of rotavirus
diarrhea can occur in
nursing homes,
sometimes with
dehydration and death.
65. NOROVIRUSES AND
OTHER
CALICIVIRUSES
Caliciviruses, so-named
because of cup-life
indentations on their
Figure . surfaces (calix is Latin for
Norwalk virus from “cup” or “goblet”) cause
stool sample from vomiting, diarrhea, or
an individual with both. Noroviruses
gastroenteritis. (previously called the
F.P. Williams, U.S. Norwalk agent, after an
Environmental outbreak in Norwalk,
Protection Agency Ohio, led to the first
isolation) and similar
agents cause more than
one-third of outbreaks of
nonbacterial
gastroenteritis in the U.S.,
66. affecting persons of all
age groups. Some studies
suggest that up to 90% of
persons are eventually
infected. Like rotaviruses,
caliciviruses are spread
mainly by fecal-oral
transmission and infect
villous cells in the small
intestine, causing diarrhea
as a result of
malabsorption. Onset of
illness can be gradual or
abrupt, with crampy
abdominal pain being the
usual first symptom. Most
patients develop both
vomiting and diarrhea,
but either of these
symptoms can
predominate. Some
67. patients experience only
mild watery diarrhea,
while others have a more
severe illness with
vomiting, headache, and
constitutional symptoms.
Caliciviruses have been
difficult to isolate by
culture. No convenient
diagnostic test is
available, although
numerous tests are in
various stages of
development. Treatment
is supportive, and rapid
recovery within 48 to 72
hours is the rule.
Astroviruses and
other agents of viral
68. gastroenteritis
Astroviruses and enteric
(group F) adenoviruses
have been firmly
established as causes of
diarrhea. Astroviruses
cause diarrhea primarily
in young children.
Serologic studies indicate
that the majority of
children are infected by 6
years of age. Illness is
usually manifested by
headache, malaise, and
diarrhea, with nausea
being less common. The
illness tends to be milder
than rotavirus diarrhea,
although occasional
patients require
hospitalization.
69. Secondary cases in adult
contacts are less common,
and experimental studies
indicate that astroviruses
usually do not produce
symptoms in adults. Both
astroviruses and enteric
adenoviruses have been
isolated by culture. A
commercially available
test is available for
detection of enteric
adenoviruses, which also
cause diarrheal disease in
children.
Other viruses that may
sometimes cause diarrhea
but in which the etiologic
or causal relationship has
not yet been firmly
established include
70. coronaviruses,
echoviruses, coxsackie A
and B viruses, non-group
F adenoviruses,
picobirnaviruses,
picotrirnaviruses,
pestiviruses, and
toroviruses.
E. COLI OTHER THAN
SHIGA TOXIN-
PRODUCING
STRAINS
Escherichia coli, a major
component of the normal
intestinal flora and the
most carefully studied of
all living organisms,
causes diarrhea by at least
6 mechanisms, identified
71. by the adjectives used to
describe the respective
strains:
Shiga-toxin producing
strains (STEC; also
called
enterohemorrhagic E.
coli or EHEC), discussed
above.
Enterotoxigenic strains
(ETEC), the usual cause
of traveler’s diarrhea.
Enteroinvasive strains
(EIEC), which cause
dysentery with high fever
and bloody diarrhea that
contains
polymorphonuclear
leukocytes. These
strains belong to certain
serogroups (such as
72. 028, 052, and 0112),
which are rare in the
U.S.
Enteropathogenic
strains (EPEC) cause
disease by adhering
tightly to epithelial cells
and effacing their brush
borders. These strains,
also called
“enteroaggresive,” have
been associated with
nursery outbreaks and
with persistent diarrhea
in young children.
Enteroaggregative
strains (EAEC, also
known as EaggED)
adhere to cells and
seem to cause diarrhea
by several mechanisms
73. including both
stimulation of the
guanylate cyclase
system and also
cytotoxicity. These
strains have been
associated with diarrhea
mainly in developing
countries, but also cause
persistent diarrhea in
persons with advanced
HIV disease.
Diffusely adherent E.
coli (DAEC) may cause
disease by massive
attachment to the gut
mucosa, thereby
diminishing the
absorptive surface.
Diagnosis of E. coli as the
cause of diarrhea in one
74. of the latter syndromes is
usually not accomplished
by most clinical
laboratories. Therefore,
consultation with a state
health department may be
advisable when an
outbreak of severe
diarrhea occurs and
cultures for the usual
pathogens are
unrevealing.
CHOLERA AND NON-
CHOLERA VIBRIOS
Figure .
Vibrio cholerae - Vibrio cholerae causes a
Gram-negative, life-threatening secretory
facultatively diarrhea by stimulating
anaerobic, curved the adenylate cyclase
(vibrio-shaped), rod system of the
76. with the ingestion of
inadequately cooked
seafood or food that has
been contaminated with
seawater. Raw oysters are
incriminated in about
one-half of cases in the
Gulf Coast states, where
the disease is most
common in the U.S., but
outbreaks are associated
with other types of
shellfish. Between 1973
and 1998, 40 outbreaks of
V. parahemolyticus
infection were to the
CDC, accounted for >
1000 illness. Explosive
watery diarrhea is usually
the first symptom and is
often accompanied by
77. crampy abdominal pain.
The organism can be
isolated on TCBS agar.
The disease is usually
mild and self-limited, but
occasional deaths occur in
young children, elderly
persons, or persons who
are severely debilitated.
ENTERIC FEVER
(TYPHOID AND
Figure
Rose spots on the PARATYPHOID
chest of a patient FEVERS)
with typhoid The elimination of
fever due to the typhoid as a major public
bacterium health problem in the
Salmonella typhi. U.S. was due largely to
Symptoms of improved sanitation
typhoid fever rather than to antibiotics
78. may include a or to the vaccine, which is
sustained fever as only partially effective.
high as 103° to Occasional outbreaks of
104° F (39° to typhoid fever still occur,
40° C), weakness, but about three-fourths of
stomach pains, cases are acquired abroad,
headache, loss of and especially from
appetite. In some Mexico, the Philippines,
cases, patients and India. The risk of
have a rash of typhoid among U.S.
flat, rose-colored travelers is greatest
spots. among those who visit the
CDC/Armed Indian subcontinent.
Forces Institute Paratyphoid fever is an
of Pathology, enteric fever syndrome
Charles N. due to Salmonella species
other than S. typhi.
Farmer
Typhoid fever is caused
by Salmonella
choleraesuis subspecies
choleraesuis serotype
79. typhi, commonly known
as S. typhi. A similar
illness is caused by
Salmonella paratyphi A,
Salmonella schottmuelleri
(formerly S. paratyphi B),
and S. hirschfeldii
(formerly S. paratyphi C),
and occasionally by other
Salmonella species.
Enteric fever is a
“penetrating” intestinal
infection in the sense that
the bacteria penetrate the
small bowel mucosa,
where the multiply in
intestinal lymphoid tissue
and especially in the large
aggregates of
lymphocytes in the ileum
known as Peyer’s
80. patches.
Lymphohematogenous
dissemination results in
high fever and other
disease manifestations.
The organisms grow
within reticuloendothelial
cells, and satisfactory
host defenses require
intact cell-mediated (T-
lymphocyte) immunity.
Typhoid fever usually
affects persons < 30 years
of age (children,
adolescents, and young
adults). After an
incubation period of 5 to
21 days, patients present
with abdominal pain,
fever, chills, and
constitutional symptoms.
81. Diarrhea is seldom the
presenting complaint, and
about 30% of patients,
especially adults,
experience constipation
rather than diarrhea. The
illness characteristically
evolves over several
weeks:
First week: stepwise
fever that becomes
sustained (that is, the
temperature does not
return to the baseline),
often with relative
bradycardia and usually
with positive blood
cultures.
Second week:
abdominal pain, often
(but < 50% of cases)
82. with a rash consisting of
faint salmon-colored
macules on the trunk
and abdomen (rose
spots).
Third week:
hepatosplenomegaly
with, in severe cases,
intestinal bleeding and/or
perforation caused by
erosions of Peyer’s
patches. Complications
include shock, stupor,
delirium, seizures,
psychosis, myelitis, and
pneumonia.
Diagnosis is most
conveniently made by
blood cultures, which are
positive in 40% to 80% of
83. patients.
BILIARY TRACT
INFECTIONS
Cholecystitis and
cholangitis are relatively
common causes of acute,
recurrent, and chronic
abdominal pain.
Occasional complications
of biliary tract disease
include acute pancreatitis
caused by gallstones and
liver abscess.
Cholecystitis usually
results from obstruction
of the cystic duct with
subsequent bacterial
invasion of the
84. gallbladder. In the U.S.,
cholelithiasis is the cause
of cystic duct obstruction
in > 90% of cases, and
women are affected twice
as frequently as men.
Cholecystitis can be acute
or chronic. More often
than not, both types of
inflammation are present,
as evidence of chronic
inflammation including
fibrosis is found in about
95% of gallbladders
removed for presumed
acute cholecystitis.
Acute cholecystitis, with
or without gallstones,
typically presents with
pain in the right upper
quadrant of the abdomen,
85. fever, nausea, and
vomiting. Common
pathogens in biliary
infections include aerobic
gram-negative bacilli
(e.g., E. coli, Klebsiella
species, Enterobacter
species, Proteus species,
and Pseudomonas
aeruginosa), aerobic
gram-positive cocci
(enterococci, streptococci,
and staphylococci), and
anaerobic bacteria (e.g.,
Bacteroides species,
Clostridium species,
Fusobacterium species,
and peptostreptococci).
Acute ascending
cholangitis (also called
toxic or suppurative
86. cholangitis) occurs in the
setting of common bile
duct obstruction, most
commonly from
gallstones
(choledocholithiasis).
Other causes of common
bile duct obstruction
include benign or
malignant strictures,
extrinsic compression,
and parasitic infestation
(usually Ascaris
lumbricodes in the U.S.).
Patients with acute
ascending cholangitis
often have evidence of
severe sepsis, and about
50% to 60% of patients
manifest “Charcot’s
triad” of fever, jaundice,
87. and right upper quadrant
abdominal pain.
ACUTE
APPENDICITIS AND
MESENTERIC
LYMPHADENITIS
(PSEUDOAPPENDICI
TIS SYNDROME)
Acute appendicitis should be
considered in all patients
with fever, right lower
quadrant abdominal pain,
anorexia, and vomiting.
However, these finding are
nonspecific and the clinical
presentation of acute
appendicitis can be atypical.
Several diseases closely
mimic acute appendicitis
88. including mesenteric
lymphadenitis. Studies
suggest that 8% of all
persons and up to 20% of
admitted to the hospital for
suspected acute
appendicitis may have
mesenteric lymphadenitis
instead.
Acute appendicitis is
usually caused by
obstruction of the organ’s
narrow lumen by fecaliths,
foreign bodies, enlarged
lymphatic follicles, or
tumors. The mucosa and
wall become ischemic,
promoting bacterial invasion.
Unchecked, the
inflammatory process
89. progresses to gangrene
(infarction) and then
perforation, allowing aerobic
and anaerobic bacteria to
enter the peritoneal cavity.
Peritonitis can be localized
as a right lower quadrant
mass or abscess, or can be
generalized. In either case,
patients usually become
septic.
Mesenteric
lymphadenitis
(pseudoappendicitis) is
most commonly caused
by Yersinia enterocolitica
and Yersinia
pseudotuberculosis. Non-
typhoid Salmonella
species and
Campylobacter jejuni
90. have also been associated
with this syndrome.
Streptococci were not
infrequently associated
with this syndrome in the
preantibiotic era. Unusual
etiologies reported in
recent years include
infectious mononucleosis
(Epstein-Barr virus) and
intestinal anthrax.
ACUTE
DIVERTICULITIS
Acute diverticulitis is a
common problem in
primary care because of
the high prevalence in our
society of diverticulosis
of the colon. Acute
91. diverticulosis is often
self-limited, but can lead
to serious complications
including sepsis,
intraabdominal abscess
formation, and death.
Acute diverticulitis is actually
a “peridiverticulitis” in that
the inflammatory reaction is
almost entirely extrinsic to
the colon. Microperforations
of diverticula cause
contamination of the
peritoneal cavity by the
aerobic and anaerobic flora
resident to the normal colon
(notably, Bacteroides
species, E. coli, and
enterococci). The result is
often a small abscess within
the pericolonic fat (Stage 1)
92. that, if not contained, may
expand and spread (Stage
2) and then rupture, causing
generalized suppurative
peritonitis (Stage 3). If the
bowel lumen communicates
with the inflammatory
process, more colonic
contents enter the peritoneal
cavity leading to extensive
fecal contamination of the
peritoneal cavity and
intraabdominal abscesses
(Stage 4).
PERITONITIS
Intraabdominal infections
can be confined to the
peritoneal cavity, to one
or another organ, or, more
93. commonly involve both.
Infectious peritonitis can
be diffuse or localized.
Examples of localized
peritonitis secondary to
acute cholecystitis, acute
appendicitis, and acute
diverticulitis have already
been discussed. Diffuse
(generalized) peritonitis
and intraabdominal
abscess nearly always
mandate admission to the
hospital.
Primary peritonitis
(spontaneous bacterial
peritonitis) occurs in up
to 10% of patients with
alcoholic cirrhosis) and
occurs rarely in patients
with ascites caused by
94. congestive heart failure,
nephritic syndrome,
metastatic tumors,
systemic lupus
erythematosus, or other
disorders. E. coli is the
most common infecting
bacterium. Anaerobic
bacteria are rare in
primary peritonitis.
Peritonitis can also be
caused by tuberculosis,
Neisseria gonorrhoeae
and Chlamydia
trachomatis infections.
Secondary peritonitis
usually results form
spillage of bacteria from
the gastrointestinal tract,
as occurs in acute
appendicitis with rupture,
95. acute diverticulitis,
ischemic bowel disease,
intestinal obstruction due
to neoplasm, and
penetrating injuries. Other
causes of secondary
peritonitis include acute
suppurative cholecystitis
(see above), chronic
ambulatory peritoneal
dialysis, complicated
genitourinary tract
infections, and ruptured
abscess from an
intraabdominal organ
such as the liver,
pancreas, kidney, or
fallopian tube. Secondary
peritonitis typically
involves both aerobic and
anaerobic bacteria.
96. Intraabdominal
abscesses arise from one
of several mechanisms:
(1) local spread of
infection within the
peritoneal cavity; (2)
hematogenous seeding of
an organ; and (3) necrosis
of an organ followed by
bacterial colonization and
superinfection.
