Download Microbial Diseases of the Digestive System

Chapter 25
Microbial Diseases of the Digestive system:
The Digestive System
Learning Objective
25-1 Name the structures of the digestive
system that contact food.
Figure 25.1 The human digestive system.
Oral Cavity
Parotid (salivary) gland
Tongue
Pharynx
Teeth
Esophagus
Insert Fig 25.1
Liver
Gallbladder
Stomach
Duodenum
Small intestine
Pancreas
Large intestine
Rectum
Anus
Normal Microbiota of the Digestive
System
Learning Objective
25-2 Identify parts of the gastrointestinal
tract that normally have microbiota.
Your normal flora
Millions of bacteria per mL of saliva
 Mouth, pharynx, and esophagus
 Stomach has few resident microbes
 Small and large intestine

◦ 100 trillion bacteria in the intestines (most in
the large intestine)
◦ 60% of the dry weight of feces is bacteria
Your defenses
Stomach
 Paneth cells

◦ Sense bacteria and secrete antimicrobial
proteins called “defensins”

Immune system surveillance
Vaishnava S et al. PNAS 2008;105:20858-20863
Bacterial Diseases of the Mouth
Learning Objective

25-3 Describe the events that lead to
dental caries and periodontal disease.
Figure 25.4 The stages of tooth decay.
Plaque
Decay
Enamel
Dentin
Pulp
Insert Fig 25.4
Bone
Root
Healthy tooth with
plaque
Decay in enamel
Advanced decay
Decay in dentin
Decay in pulp
Dental caries
Figure 25.5 The stages of periodontal disease.
Plaque
Tooth
Gum
(gingiva)
Insert Fig 25.5
Bone
Cementum
Periodontal
ligament
Healthy gingivae
Gingivitis
Periodontal pockets
Periodontitis
Periodontal disease
Prevention

Brushing
◦ Removal of food particles
◦ Removal of bacteria
◦ Neutralizing acid
Flossing
 Mouthwash
 Fluoride

◦ Hardens enamel
Bacterial Diseases of the Mouth
Disease
Dental caries
Periodontal disease
Acute necrotizing
gingivitis
Pathogen
Initially S. mutans,
then Gram positive
rods and filamentous
bacteria
Porphyromonas spp.
Prevotella intermedia
Diseases of Lower Digestive System
Learning Objective

25-4 List the causative agents, suspect
foods, signs and symptoms, and
treatments for staphylococcal food
poisoning, shigellosis, salmonellosis,
typhoid fever, cholera, gastroenteritis,
and peptic ulcer disease.
Diseases of Lower Digestive System

Infection: growth of a pathogen
◦ Incubation is from 12 hours to 2 weeks
◦ Fever

Intoxication: ingestion of toxin
◦ Symptoms appear 1 to 48 hours after ingestion
Gastroenteritis: diarrhea, dysentery
 Treatment: oral rehydration therapy

Diarrheal disease
Bacterial, viral, protozoan, parasitic
 Defined as passing three or more
loose or liquid stools per day
 Three varieties

◦ acute watery diarrhea – lasts several
hours or days, and includes cholera
◦ acute bloody diarrhea – also called
dysentery; and
◦ persistent diarrhea – lasts 14 days or
longer
Diarrheal disease
Second leading cause of death in children under 5
 Kills 1.5 million children per year
 2 billion cases per year
 Dehydration and electrolyte imbalance

Staphylococcal Food Poisoning
Pathogen
Symptoms
Staphylococcus aureus
Nausea, vomiting, and
diarrhea
Intoxication/Infection
Intoxication
Enterotoxin
(superantigen)
None
Treatment
Figure 25.6 The sequence of events in a typical outbreak of staphylococcal food poisoning.
Food containing protein is cooked (bacteria usually killed).
Then food is contaminated by worker with staphylococci on
hands (competing bacteria have been eliminated).
Food is left at room temperature. Organisms incubate in food
(temperature abuse)
long
Insert
Figenough
25.6 to form and release toxins.
(Reheating will eliminate staphylococci but not the toxins.)
Food containing toxins is eaten.
In 1–6 hours, staphylococcal intoxication occurs.
Figure 25.7 Invasion of intestinal wall by Shigella bacterium.
M cell on
epithelia
wall
Shigella
bacterium
Insert Fig 25.7
Figure 25.8 Shigellosis.
Shigella
M cell
Epithelial cell lining
intestinal tract
Membrane ruffle (see Figure 25.7)
Shigella enters an epithelial cell.
Insert Fig 25.8
Shigella multiplies inside the cell.
Shigella invades neighboring epithelial cells,
thus avoiding immune defenses.
Mucosal abscess
An abscess forms as epithelial cells are
killed by the infection.The bacteria rarely
spread in the bloodstream.
Shigellosis (Bacillary Dysentery)
Pathogen
Symptoms
Shigella spp.
20 BM/day, diarrhea is
often bloody, cramps, fever
Intoxication/Infection
Infection
Endotoxin and Shiga
exotoxin
Isolation of bacteria
Oral rehydration,
Fluoroquinolones
Diagnosis
Treatment
Figure 1 Risk of shigellosis per 100?000 travelers to different regions of the world.
Karl Ekdahl , Yvonne Andersson
The epidemiology of travel-associated shigellosis?regional risks, seasonality and serogroups
Journal of Infection Volume 51, Issue 3 2005 222 - 229
http://dx.doi.org/10.1016/j.jinf.2005.02.002
Figure 25.9 Salmonellosis.
Salmonella
M cell
Epithelial cell lining
intestinal tract
Membrane ruffle
Salmonella enters an epithelial cell.
Insert Fig 25.9
Salmonella multiplies within vesicle
inside the cell.
Salmonella multiplies in mucosal cells; there
the inflammatory response results in
diarrhea. Occasionally, the bacteria cross the
epithelial cell membrane and enter the
lymphatic system and bloodstream.
Lymph node
Bloodstream
Typhoid Fever
Caused by Salmonella typhi
 No animal reservoir
 Bacteria spread throughout body in
phagocytes
 1–3% of recovered patients become
chronic carriers
 5-20 liters of liquid stool passed daily

Mary Mallon (aka Typhoid Mary)
Disease
Salmonellosis
Typhoid Fever
Pathogen
Salmonella
enterica
Nausea and
diarrhea
S. typhi
Symptoms
Intoxication/
Infection
Infection
Endotoxin
High fever,
headache,
significant
mortality
Infection
Endotoxin
Diagnosis
Isolation of
bacteria;
serotyping
Isolation of
bacteria;
serotyping
Treatment
Oral rehydration
Quinolones;
cephalosporins
Salmonellosis vs. typhiod fever
30
25
Reported cases per 100,000 population
Salmonellosis
20
Typhoid fever
15
Insert Fig 25.10
10
5
0
’34
’40
’46
’52
’58
’64
’70
Year
’76
’82
’88
’94
’00
’06
Vibrios

Cholera
◦ Vibrio cholerae serotypes that produce cholera toxin
◦ Toxin causes host cells to secrete Cl−, HCO−, and
water

Noncholera vibrios
◦
◦
◦
◦
Usually from contaminated crustaceans or mollusks
V. cholerae serotypes other than O:1, O:139, El Tor
V. parahaemolyticus
V. vulnificus
Figure 25.11 Vibrio cholerae, the cause of cholera.
Vibrio cholerae
Insert Fig 25.11
Disease
Pathogen
Symptoms
Cholera
Vibrio
cholerae O:1
and O:139
Diarrhea
with large
water loss
Noncholera Vibrios
V. parahaemolyticus V. vulnificus
Cholera-like
diarrhea, but
generally milder
Intoxication/ Cholera
Infection
toxin
(exotoxin)
Infection,
enterotoxin
Rapidly
spreading
tissue
destruction
Infection,
siderophores
Diagnosis
Isolation of
bacteria
Isolation of
bacteria
Isolation of
bacteria
Treatment
Rehydration; Rehydration;
doxycycline antibiotics
Antibiotics
Figure 25.12 Pedestal formation by Enterohemorrhagic E. coli (EHEC) O157:H7.
Insert Fig 25.12
Escherichia coli Gastroenteritis
EPEC
Stimulate host-cell actin to form
pedestals beneath attachment site
EIEC
Access intestinal submucosa through
M cells
EAEC
Not invasive; enterotoxin causing a
watery diarrhea
EHEC
(STEC)
Phage-encoded Shiga toxin
Escherichia coli Gastroenteritis
Intoxication/Infection: infection;
endotoxin
 Diagnosis: PFGE of sorbitol-negative E.
coli
 Treatment: oral rehydration

Campylobacter Gastroenteritis
Pathogen
Symptoms
Intoxication/Infection
Diagnosis
Reservoir
Campylobacter jejuni
Fever, abdominal pain,
diarrhea
Infection
Isolation of bacteria
Chickens, cows
Traveler’s Diarrhea
ETEC
 EAEC
 Salmonella
 Shigella
 Campylobacter

Figure 25.13 Helicobacter pylori infection, leading to ulceration of the stomach wall.
Mucus layer protects
stomach from activity of
gastric acids (HCl)
Helicobacter pylori
Mucus layer
Urease, a bacterial enzyme, produces highly
alkaline ammonia by activity on urea. The
ammonia neutralizes hydrochloric acids of
stomach. (NH3 + HCl
NH4Cl)
Hydrochloric acid
Insert Fig 25.13
Mucus-secreting
epithelial cells
lining stomach
Connective tissue
Submucosal cell
Blood capillary
Lymphocyte
(cross section)
Neutrophil
Plasma cell
Helicobacter Peptic Ulcer Disease
Pathogen
Symptoms
Helicobacter pylori
Peptic ulcers
Intoxication/Infection
Diagnosis
Infection
Urea breath, bacterial
culture
Antimicrobial drugs
Treatment
Yersinia Gastroenteritis
Pathogen
Symptoms
Intoxication/Infection
Diagnosis
Transmitted
Y. enterocolitica,
Y. pseudotuberculosis
Abdominal pain and
diarrhea, usually mild; may
be confused with
appendicitis
Infection
Endotoxin
Bacterial culture; serotyping
Meat, milk
Clostridium and Bacillus Gastroenteritis
Pathogen
Symptoms
C. perfringens C. difficile
Diarrhea
Diarrhea to
colitis
B. cereus
Nausea and
vomiting;
diarrhea
Intoxication/ Infection
Infection
Exotoxin
Infection
Exotoxin
Intoxication
Diagnosis
Cytotoxin
assay
Isolation of
bacteria
Isolation of
bacteria
Clostridium and Bacillus Gastroenteritis
Pathogen
Treatment
C. perfringens C. difficile
B. cereus
Oral
Metronidazole; None
rehydration
discontinue
other antibiotic
therapy
Source of
Infection
Meats
Elimination of
normal
microbiota
Rice
dishes
Clostridium dificile (C dif.)
Growing threat in hospitals
 Common following a long course of
antibiotics
 Uncommon in people who haven’t been
on antibiotics
 Treatments:

◦ Antibiotics
◦ Surgery
◦ Fecal transplantation
Viral Diseases of the Digestive System
Disease
Mumps
Pathogen
Mumps virus
Symptoms
Swollen
parotid
glands
Incubation
16–18 days
Diagnosis
Symptoms
Treatment
Preventive
vaccine
Figure 25.14 A case of mumps.
Insert Fig 25.14
Hepatitis
An inflammation of the liver
 May result from drug or chemical toxicity, EB
virus, CMV, or the hepatitis viruses

Diseases in Focus 25.3 Characteristics of Viral Hepatitis
Insert healthy liver photo from
Diseases in Focus 25.3, p. 731.
If possible on this slide, include title:
Viral Hepatitis
Diseases in Focus 25.3 Characteristics of Viral Hepatitis
Insert damaged liver photo from
Diseases in Focus 25.3, p. 731.
If possible on this slide, include title:
Viral Hepatitis
Hepatitis Viruses
Disease
Transmission
Pathogen
Chronic
Liver
Vaccine?
Disease?
Hepatitis
A
Fecal-oral
Picornaviridae
No
Hepatitis
B
Parenteral, STI Hepadnaviridae Yes
Recombinant
Hepatitis
C
Parenteral
Filoviridae
Yes
None
Hepatitis
D
Parenteral,
HBV
coinfection
Deltaviridae
Yes
HBV vaccine
Hepatitis
E
Fecal-oral
Caliciviridae
No
HAV vaccine
Inactivated
virus
Applications of Microbiology:
A Safe Blood Supply

Nucleic acid testing (NAT) is used to test
donated blood and plasma:
◦ HCV
◦ HIV
◦ West Nile virus

Virus inactivation is used on plasma
Viral Gastroenteritis
Pathogen
Rotavirus
Norovirus
Symptoms
Vomiting, diarrhea;
1 week
Vomiting, diarrhea;
2–3 days
Incubation period
1–3 days
18–48 hours
Diagnostic test
EIA
PCR
Treatment
Oral rehydration
Figure 25.16 Rotavirus.
Insert Fig 25.16
Diseases in Focus 25.4 Viral Diseases of the Digestive System
Insert photo from
Diseases in Focus 25.4, p. 736.
If possible on this slide, include title:
Norovirus
Norovirus
Figure 25.17 The trophozoite form of Giardia lamblia, the flagellated protozoan that causes giardiasis.
Insert Fig 25.17
Mark left by
ventral sucker
Giardiasis
Pathogen
Giardia lamblia
Symptoms
Protozoan adheres to
intestinal wall, leading to
diarrhea
Reservoir
Water or mammals
Diagnosis
FA test
Treatment
Metronidazole; quinacrine
Figure 25.18 Cryptosporidiosis.
Intestinal
mucosa
Oocyst
Insert Fig 25.18
Cryptosporidiosis
Pathogen
Cryptosporidium hominis
Symptoms
Self-limiting diarrhea; may
be life-threatening in
immunosuppressed people
Reservoir
Cattle; water
Diagnosis
Acid-fast stain; FA; ELISA
Treatment
Oral rehydration
Number of reported cases
Chapter 12, unnumbered figure B, page 357.
Insert Figure B from
Clinical Focus on p. 357.
If possible on this slide, include title:
Cryptosporidium hominis in the U.S.
[Note C. hominis must be italicized]
Year
Cryptosporidium hominis in the U.S.
Figure 12.19b Amebae.
Red blood cells
Insert Fig 12.19(b)
Nucleus
Entamoeba histolytica
Figure 25.19 Section of intestinal wall showing a typical flask-shaped ulcer caused by Entamoeba
histolytica.
Normal mucosa
Ulcer
Insert Fig 25.19
Amebic Dysentery
Pathogen
Entamoeba histolytica
Symptoms
Abscesses; significant
mortality rate
Reservoir
Humans
Diagnosis
Microscopy; serology
Treatment
Metronidazole
Helminthic Diseases of the
Digestive System
Learning Objective

25-10
List the causative agents,
modes of transmission,
symptoms, and
treatments for tapeworms,
hydatid disease, pinworms,
hookworms, whipworms,
ascariasis, and trichinellosis.
Figure 25.20 The woldwide prevalence of human infections with selected intestinal helminths.
Percentage of world population infected
Trichinella
Flukes (liver, lung)
Tapeworms
1.0%
1.5%
3.0%
Schistosomes
6.0%
Enterobius
Insert Fig 25.20
10%
Hookworms
21%
Ascaris
30%
1
2
3
4
5
6
7
8
Number of people infected (100 millions)
9
10
11
Figure 12.27 General anatomy of an adult tapeworm.
Scolex
Hooks
Sucker
Neck
Insert Fig 12.27
Sucker
Genital pore
Ovary
Mature proglottid
will disintegrate and
release eggs
Figure 25.21 Ophthalmic cysticercosis.
Fluid-filled bladder
Scolex
Insert Fig 25.21
Figure 12.28 The life cycle of the tapeworm, Echinococcus, spp.
1
6
Adult tapeworm
releases eggs.
Intermediate
host
Scoleces from cyst
attach to intestine and
grow into adults.
2
Human intermediate host
ingests eggs. Dead end.
Egg (30–38 mm)
Adult
tapeworm
Intermediate
host
Scolex
SexualInsert Fig 12.28 Asexual
reproduction
reproduction
Definitive
host
5
Definitive host eats
intermediate host,
ingesting cysts.
2
Larva
3
Hydatid
cyst
Brood capsule
Scolex
Intermediate host
ingests eggs.
4
Larvae develop
into hydatid cysts.
Eggs hatch, and larvae
migrate to liver or lungs.
Figure 25.22 A hydatid cyst formed by Echinococcus granulosus.
Cyst
Brain
Insert Fig 25.22Left orbit
(eye socket)
Tapeworms and Hydatid Disease
Disease
Tapeworm
Hydatid Disease
Pathogen
Taenia saginata,
T. solium,
Diphyllobothrium
latum
Echinococcus
granulosus
Symptoms
Neurocysticercosis Tissue damage
Intermediate
Host
Cattle, pigs, fish
Humans
Definitive
Host
Humans
Dogs
Tapeworms and Hydatid Disease
Disease
Tapeworm
Hydatid Disease
Diagnosis
Microscopic exam Praziquantel;
of feces
albendazole
Treatment
Serology; X-ray
exam
Surgical removal;
albendazole
Figure 12.29 The pinworm Enterobius vermicularis.
Mouth
Intestine
Mouth
Ovary
Genital
pore
Anus
Intestine
Testis
Insert Fig 12.29
Genital
pore
Spicules
Anus
Adult
pinworm
Female
(8–13 mm
long)
Male
(2–5 mm long)
Egg
(55 μm
long)
Larva
Pinworm egg
Pinworms
Pathogen
Enterobius vermicularis
Symptoms
Itching around anus
Intermediate host
Humans
Definitive host
Humans
Diagnosis
Microscopy
Treatment
Pyrantel pamoate
Figure 25.23 An Ancylostoma hookworm attached to intestinal mucosa.
Hookworm
Insert Fig 25.23
Intestinal
mucosa
Figure 25.24 Ascaris lumbricoides, the cause of ascariasis.
Insert Fig 25.24
Ascaris lumbricoides
Figure 25.26 The life cycle of Trichinella spiralis, the causative agent of trichinellosis.
Ingested cysts develop into
Trichinella spiralis adults in the
pig’s intestinal wall.
Adult worms produce larvae that
encyst in the pig’s muscles.
Garbage, including
undercooked or raw pork
Capsule
Meanwhile,
other animals
eat infected
meat that has
been dumped.
Insert Fig 25.26
Human eats
undercooked pork
containing cysts that
are infective to
humans or animals
that ingest it.
Trichinellosis in humans;
ingested cysts develop into T.
spiralis adults. Adults produce
larvae that encyst in muscles. T. spiralis adult
Section of
encysted T.
spiralis
Roundworms
Disease
Hookworm
Pathogen
Necator
Ascaris
americanus,
lumbricoides
Ancyclostoma
duodenale
Trichuris
trichiura
Trichinella
spiralis
Symptoms
Anemia
Few
Abdominal
pain,
diarrhea
Few
Intermediate Larvae in soil
Host
Humans
Humans
Mammals
Definitive
Host
Humans
Humans
Humans
Humans
Ascariasis
Whipworm Trichinellosis
Roundworms
Disease
Hookworm
Ascariasis
Whipworm
Trichinellosis
Diagnosis Microscopy
Microscopy
Microscopy
Biopsy; ELISA
Treatment Mebendazole Mebendazole Mebendazole; Mebendazole;
corticosteroids corticosteroids