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Chapter 20: Infectious Diseases Affecting the
Gastrointestinal Tract
Microbiology Fundamentals: A Clinical Approach. Marjorie
Cowan, 1st ed.
Part C
Modified by JDB
Bacterial Diseases of the Mouth
Tooth and Gum Infections
Difficult to pinpoint when normal biota biofilm becomes a
pathogen biofilm
If left undisturbed, normal biota biofilm eventually contains
anaerobic bacteria that can damage the soft tissues and
bones (periodontium) surrounding the teeth
Also, the introduction of carbohydrates to the oral cavity can
result in the breakdown of hard tooth structure due to the
production of acid
Bacteria live on the teeth as well as the soft structures of
the mouth
Numerous species live in large accretions known as dental
plaque, a type of biofilm
Bacteria held in the biofilm by specific recognition molecules
Alpha-hemolytic streptococci are the first colonizers of the
tooth surface after it has been cleaned
Pellicle: mucinous glycoprotein covering on the tooth to
which streptococci attach
Other species attach specifically
to proteins or sugars on the
surface of streptococci
Microscopic view of dental plaque,
showing Gram-positive and Gramnegative bacteria.
Dental Caries (Tooth Decay)
(More)
Most common infectious disease of human beings
Involves the dissolution of solid tooth surface
due to the metabolic action of bacteria
Teeth are a hard surface and do not shed cells
Allows for the accumulation of masses of
microorganisms and their products – dental
plaque (More)
Oral bacteria convert sucrose and other
carbohydrates into lactic acid that then erodes
the tooth enamel
Symptoms not noticeable, but range from:
Minor disruption in the outer enamel surface of the tooth
Complete destruction of enamel
Destruction of deeper layers (Cavities)
Deeper lesions can result in infection to the soft tissue
inside the tooth called the pulp
Infection leads to pain known as a “toothache”
Causative agents:
Over 700 species of bacteria have been
isolated from the oral cavity
Main cause - Streptococcus mutans
S. mutans
Oral, alpha-hemolytic streptococcus
Likely caused by a mixed species consortium consisting of
other Streptococcus species and some lactobacilli
Early childhood caries may be caused by a newly
discovered species Scardovia wiggsiae
Pathogenesis and Virulence Factors
Initiation: In the presence of sucrose, S. mutans and other
streptococci produce sticky polymers of glucose called
fructans and glucans
These adhesives help bind them to the smooth enamel
surfaces
Contribute to the sticky bulk of the plaque biofilm
Advanced decay: Lactobacillus spp are important in
advancing the front of decay once it is established
If plaque is not removed from sites that readily trap
food, it can result in a carious lesion
Streptococci, Lactobacillus and other bacteria produce
acid as they ferment carbohydrates
If acid is immediately flushed and the plaque is diluted in
the mouth, it has little effect
In denser regions of plaque, acid can accumulate in direct
contact with enamel
pH lowers to below 5 and calcium phosphate in the
enamel can be dissolved
The initial lesion can remain localized in the enamel
and repaired with inert materials (fillings)
If the deterioration reaches the level of the dentin,
tooth destruction speeds up, and the tooth can be
destroyed
Transmission and Epidemiology
Bacteria that cause dental caries are transmitted to babies
and children by their close contacts
Mother or closest caregiver
Evidence for transfer of oral bacteria between children
at day care centers
Culture and Diagnosis
Dental professionals diagnose caries based on the
tooth condition
Culture of the lesion is not routinely performed
Prevention and Treatment
The best way to prevent dental caries is
through dietary restriction of sucrose and
refined carbohydrates
Regular brushing and flossing to remove plaque are also
important
Trace amounts of fluoride added to drinking water can
incorporate into tooth structure and strengthen enamel
Fluoride also encourages the remineralization of teeth
that have begun the demineralization process
Fluoride is also added to toothpastes and mouth rinses
Treatment of a carious lesion
Removal of the affected part of the tooth or whole
tooth in advanced caries
Restoration of the tooth structure with an artificial
material
Dental Caries
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Disease Table 20.4 Dental Caries
Causative
Organism(s)
Streptococcus mutans,
Scardovia wiggsiae, others
Most Common
Modes of
Transmission
Direct contact
Virulence Factors
Adhesion, acid production
Culture/Diagnosis
–
Prevention
Oral hygiene, fluoride
supplementation
Treatment
Removal of diseased tooth
material
Periodontal Disease
(More)
97% - 100% of the population has some manifestation by age 45
Most are due to bacterial colonization and varying degrees
of inflammation
Periodontitis
(More)
Initial stage is called gingivitis - swelling, loss of normal
contour, patches of redness, and increased bleeding of
the gingivae (gums), pockets or spaces develop between
the tooth and gum
If this condition persists, periodontitis develops:
The natural extension of gingivitis into the periodontal
membrane and cementum results in damage by an
inflammatory response
This increases the size of pockets between the tooth
and the gingival and can cause bone resorption
enough to loosen and possible lose the tooth
Many different bacteria including members of
Porphyromonas are found in these infections
Causative Agent
Periodontal disease is mediated by communities of
microorganisms rather than a single organism
Polymicrobial biofilms containing the right combination
of bacteria begin the periodontal destruction process
Tannerella, Aggregatibacter, Porphryomonas, and
perhaps Fusobacterium
Common predisposing factor: when the plaque
becomes mineralized
Produces a calculus above and below the gingival
margin that can induce varying degrees of
periodontal damage
Presence of a calculus leads to
a series of inflammatory
events that allow the
bacteria to cause disease
Treatment
Removal of calculus and plaque - maintenance of
good oral hygiene
Surgery to reduce the depth of periodontal pockets
may be required
Antibiotic therapy, either systemic or in periodontal
packings may be utilized
Acute Necrotizing Ulcerative Gingivitis
(More)
The most destructive periodontal diseases
These diseases are synergistic infections involving Prevotella
intermedia, Treponema vincentii, and Fusobacterium
species
Together they produce several invasive factors that
cause rapid advancement into the periodontal tissues
The condition is associated with severe pain, bleeding,
pseudomembrane formation, and necrosis
Periodontitis
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Disease Table 20.5 Periodontitis
Disease
Periodontitis
Causative
Organism(s)
Polymicrobial community
including some or all of
Tannerella forsythia, Aggregatibacter
actinomycetemcomitans,
Porphyromonas gingivalis, others
Most Common
Modes of
Transmission
–
Virulence
Factors
Induction of inflammation,
enzymatic destruction of tissues
Culture/
Diagnosis
–
Prevention
Oral hygiene
Treatment
Removal of plaque and calculus,
gum reconstruction, tetracycline,
possibly anti-inflammatory
treatments
Mumps (More) – Paramyxovirus - Paramyxovirvividae
A self-limited mildly epidemic illness associated
with painful swelling at the angle of the jaw
Incubation period of 2 to 3 weeks
Signs and Symptoms
Initial symptoms: fever, nasal discharge, muscle pain, and
malaise
May be followed by inflammation of the salivary glands,
producing gopher-like swelling of the cheeks
(parotitis)
Multiplication in the salivary glands followed by invasion
of other organs, especially testes, ovaries, thyroid
gland, pancreas, meninges, heart, and kidneys
Symptoms: cramping, nausea, vomiting, and diarrhea
Toxin triggers brain vomiting reflex center
Rapid recovery- usually within 24 hours
Parotitis - Swelling of the parotid salivary gland
Can cause considerable discomfort
Viral multiplication in the salivary glands is followed by
invasion of other organs
Testes, ovaries, thyroid gland, pancreas, meninges,
heart, and kidney
Despite invasion of multiple organs, prognosis of most
infections is complete, uncomplicated recovery with
permanent immunity
Complications in Mumps
In 20 – 30% of young adult males, mumps infection
localizes in the epididymis and testes, usually on
one side only
Orchitis and epididymitis can be painful
No permanent damage usually occurs
Transmission and Epidemiology of Mumps Virus
Humans are exclusive natural hosts
Communicated primarily through salivary
and respiratory secretions
Most cases occur in children under the
age of 15, and most are subclinical
Lasting immunity follows any form of mumps infection
No long-term carrier reservoir exists in the population
Prevention and Treatment
Symptomatic treatment to relieve fever, dehydration, and pain
Vaccine recommendations
MMR at 12 and 15 months, booster at 4 – 6 years
Healthcare workers and college students who haven’t
had both doses are advised to do so
Mumps
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Disease Table 20.6 Mumps
Causative
Organism(s)
Mumps virus (genus
Paramyxovirus)
Most Common
Modes of
Transmission
Droplet contact
Virulence FactorsS
Spike-induced syncytium
formation
Culture/Diagnosis
Clinical, fluorescent Ag tests,
ELISA for Ab
Prevention
MMR live attenuated vaccine
Treatment
Supportive
Gastritis and Gastric Ulcers (More) - Helicobacter pylori
Helicobacter pylori thrives in the acidic
environment of the stomach and has been
linked to a variety of gastrointestinal ailments
Long-term infection with H. pylori might be
a contributing factor to stomach cancer
Gastritis: sharp or burning pain emanating from the abdomen
Gastric ulcers (AKA peptic ulcer) are actual lesions in the
mucosa of the stomach
Duodenal ulcer: lesion in uppermost
portion of the small intestine
Signs and Symptoms
Severe ulcers can be accompanied
by bloody stools, vomiting
Symptoms are often worse at night,
after eating, or under conditions of
psychological stress
Benign Gastric Ulcer
Causative Agent
Helicobacter pylori - Gram-negative,
microaerophilic, curved rods
Closely related to Campylobacter
Pathogenesis and Virulence Factors
H. pylori bores through the outermost mucus
layer that lines the stomach epithelium to
avoid low pH of stomach
Attaches to specific binding sites on the cells
and entrenches itself
Produces large amounts of urease – converts
urea to ammonia – creates local high pH
in the area of growth
Dozens of the curved
bacteria fill the lumen of a
gastric foveola (pit).
Ammonia and other products (proteases) are toxic to
the epithelial cells
Before the bacterium was discovered, spicy
food, high-sugar diets, and psychological
stress were considered to be the causes of
gastritis age
These factors merely aggravate the
underlying infection
Transmission and Epidemiology a
Mode of transmission remains a mystery
Studies have revealed that the pathogen is present in
a large portion of the population
Occurs in the stomachs of 25% of healthy, middle-aged
adults and 60% of adults over 60 years of age
H. pylori is probably transmitted from person to person
by the oral-oral or fecal-oral route
Seems to be acquired early in life and carried
asymptomatically until its activities begin to damage
the digestive mucosa
Other animals are susceptible to H. pylori and develop
gastric ulcers
It has been proposed that it is a zoonosis transmitted
from an animal reservoir
Bacterium also found in water sources
Prevention and Treatment
The only preventative approaches currently are those that
diminish some of the aggravating factors
Over-the counter remedies offer symptom relief
Most of them neutralize stomach acid
Best treatment is a course of
antibiotics augmented by
acid suppressors
Gastritis and Gastric Ulcers
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Disease Table 20.7 Gastritis and
Gastric Ulcers
Causative Organism(s)
Helicobacter pylori
Most Common Modes
of Transmission
?
Virulence Factors
Adhesins, urease
Culture/Diagnosis
Endoscopy, urea breath
test, stool antigen test
Prevention
None
Treatment
Antibiotics plus acid
suppressors (clarithromycin
or metronidazole plus
omeprazole or bismuth
subsalicylate)
Hepatitis
(More)
Inflammatory disease marked by necrosis of hepatocytes and a
mononuclear response that swells and disrupts the liver
architecture
Pathologic changes interfere with the liver’s excretion of
bile pigments such as bilirubin into the intestine
May result from autoimmune disease, drug, alcohol, or chemical
toxicity, EB virus, CMV, or the hepatitis viruses A - E
Causes jaundice when bilirubin accumulates in the blood and
tissues
Hepatitis A (HAV) and Hepatitis E Virus (HEV) (More)
Viruses are considered together because:
In general, far milder and self-limiting
hepatitis than the other forms
Single-stranded, nonenveloped ssRNA viruses
Transmitted through the fecal-oral route
HAV – Picornaviridae
- Picornavirus
HEV infects pregnant women - disease is more
often severe and is associated with a clinical
syndrome called fulminant hepatic failure –
15 - 25% mortality
HEV - Hepeviridae Hepevirus
Signs and Symptoms
Subclinical or accompanied by vague, flulike symptoms malaise, anorexia, abdominal pain, arthralgia, and fever
Overt cases
Jaundice
Swollen liver
Darkened urine often seen
Viruses are not oncogenic
In most everyone besides pregnant women, complete,
uncomplicated recovery results
Transmission and Epidemiology
Associated with deficient personal hygiene and lack of
public health measures
In countries with inadequate sewage control, outbreaks are
associated with fecally contaminated water and food
Most infections result from
Unhygienic food handling
Eating shellfish
Sexual transmission
Travel to other countries
Hepatitis A can occasionally be spread by blood or blood
products
Exception rather than the rule
In developing countries, children are the most common
victims because exposure occurs early in life
The virus is not carried chronically
Principal reservoirs are asymptomatic, short-term
carriers (often children) or people with clinical
disease
Prevention and Treatment
Prevention of hepatitis A is based primarily on immunization
Inactivated viral vaccine (Havrix) has been in use since
the 1990s
Administration after exposure can prevent symptoms
Short-term protection can be conferred by
passive immune globulin
Useful for people who have come into
contact with HAV-infected people
Also used when people have eaten at a restaurant
that was the source of a recent outbreak
Combined hepatitis A/hepatitis B vaccine (Twinrix)
Recommended for people with chronic liver dysfunction,
intravenous drug users, anyone engaging in anal-oral
intercourse
Travelers to areas with high rates of both diseases
should obtain vaccine coverage
No specific medicine is available for hepatitis A or
hepatitis E
Drinking lots of fluids and avoiding liver irritants such as
aspirin or alcohol will speed recovery
Hepatitis B Virus (HBV) (More) - Hepadnaviridae
Enveloped DNA virus - genome is partly double-stranded
and partly single-stranded
Intact viruses are called Dane particles
Surface (S) antigen is an antigen of clinical
and immunologic significance
Signs and Symptoms
Direct damage to liver cells
Fever, chills, malaise, anorexia, abdominal discomfort,
diarrhea, and nausea
Rashes may appear and arthritis may occur
HBV infection can be serious, even life-threatening
A small number of patients develop
glomerulonephritis and arterial
inflammation
Complete liver regeneration and restored function occur in
most patients
A small number of patients develop chronic liver
disease in the form of cirrhosis or necrosis
In some cases, chronic HBV infection can lead to liver
cancer
Patients who become infected as children have significantly
higher risks of long-term infection and disease
90% of neonates infected at birth develop chronic
infection
30% of children infected between ages 1 and 5 also
develop chronic infection
Only 6% of persons infected after age 5 develop
chronic infection
This finding is one of the justifications of routine
vaccination of children
Pathogenesis and Virulence Factors
Hepatitis B virus enters the body through a break in the skin,
mucous membrane, or by injection into the bloodstream
Eventually reaches liver cells (hepatocytes) where it
multiplies and releases viruses into the blood
Incubation period 4 – 24 weeks (7 weeks average)
The majority of those infected exhibit few overt symptoms
and eventually develop an immunity to HBV
Multiplies exclusively in the liver and continuously seeds
the blood with viruses
Electron microscopy studies have shown up to 107
virions per milliliter of infected blood
Even a minute amount of blood can transmit infection
Simple practices such as sharing a toothbrush
or a razor can transmit the infection
HBV has been detected in semen and vaginal
secretions, and can be transmitted by these
Cirrhosis
Virus is spread by close contact in families or institutions
Vertical transmission is possible
Predisposes the child to development of the carrier
state and increased risk of liver cancer
Also known as serum hepatitis
One of the major infectious concerns for healthcare
workers
Needlesticks can easily transmit the virus
Healthcare workers are required to have the full
HBV vaccination series
HBV remains infective for days in dried blood, for months
when stored in serum at room temperature, and for
decades when frozen
HVB Not inactivated after 4 hours of exposure to 60°C
Boiling for the same time period can destroy it
Disinfectants containing chlorine, iodine, and glutaraldehyde
show potent anti-hepatitis B activity
Prevention and Treatment
Primary prevention for HBV is vaccination
Vaccination is a must for medical and dental workers and
students, patients receiving multiple transfusions,
immunodeficient patients, and cancer patients
Vaccine now strongly recommended for newborns as
part of a routine immunization schedule
Passive immunization with hepatitis B immune
globulin (HBIG)
Gives significant immediate protection to people who
have been exposed to the virus through needle
puncture, broken blood containers, or skin or
mucosal contact with blood
Also recommended for neonates born
to infected mothers
Mild cases of HBV are managed with symptomatic
treatment and supportive care care
Chronic HBV infection can be controlled with recombinant
human interferon and other drugs
All of these can help stop virus
multiplication in many but not
all patients
None of the drugs are considered curative
Hepatitis D Virus (HDV) (More) - Deltavirus
Hepatitis D virus considered to be a subviral
satellite because it can propagate only in
the presence of HBV (cannot produce
infection on it’s own)
Transmission of HDV can occur either via simultaneous
infection with HBV (coinfection) or via infection of an
individual previously infected with HBV (superinfection))
Results in more severe complications compared to infection
with HBV alone
A greater likelihood of experiencing liver failure in acute
infections and a rapid progression to liver cirrhosis
Increased chance of developing liver cancer in chronic
infections
20% mortality rate (highest of the Hepatitis viruses)
Transmission: Parenteral (intravenous drug use)
Hepatitis C Virus (HCV) (More) - Flaviviridae
ssRNA virus
“silent epidemic” – one of the most common
reasons for liver transplants
4 million Americans are infected with the virus
Takes many years to cause noticeable symptoms
Signs and Symptoms
People have widely varying experiences with this infection
Shares many characteristics with HBV
More likely to become chronic
Of those infected, 75 – 80% will remain infected
indefinitely
Possible to have severe infections without permanent
liver damage
More common to have chronic liver disease even without
overt symptoms
Cancer may result from chronic HCV infection
Worldwide, HBV infection
is the most common
cause of liver cancer
In the U.S., liver cancer is
more likely caused by
HCV
Metastatic Hepatic Carcinoma
Transmission and Epidemiology
Virus is acquired in ways similar to HBV
More commonly transmitted through blood contact
Blood transfusions
Injecting drug users
Vertical transfer is also possible
Frequently transmitted through blood transfusions before
a blood test was available
Frequently transmitted through blood transfusions
before a blood test was available
Hemophiliacs who were treated with clotting factor
before 1985 were infected with HCV at a high rate
Once blood began to be tested for HIV and screened
for “non-A, non-B” hepatitis, the risk of
contracting HCV was reduced
Prevention and Treatment
Currently no vaccine for hepatitis C
Current treatment regimens are not curative, but prevent
or lessen damage to the liver
Hepatitis
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Disease Table 20.8 Hepatitis
Causative Organism(s)
Hepatitis A or E virus
Hepatitis B virus
Hepatitis C virus
Most Common Modes
of Transmission
Fecal-oral, vehicle
Parenteral (blood contact), direct
contact (especially sexual), vertical
Parenteral (blood contact),
vertical
Virulence Factors
–
Latency
Core protein suppresses immune
function
Culture/Diagnosis
IgM serology
Serology (ELISA,
radioimmunoassay)
Serology
Prevention
Hepatitis A vaccine or combined
HAV/HBV vaccine
HBV recombinant vaccine
–
Treatment
Hep A: hepatitis A vaccine or immune
globulin; hep E: immune globulin
Interferon, nucleoside analogs
(Pegylated) interferon, with or
without ribavirin
Incubation Period
2–7 weeks
1–6 months
2–8 weeks