BIOM 1073 Week 12 Part 1-Digestive Infections

BIOM 1073
Week 12
Part 1:
Digestive Infections
© 2018 Pearson Education, Inc.

Structures of the Digestive System
Digestive System Structures-divided into two groups:

1. Gastrointestinal Tract (GI tract)
• Muscular tube acts as a pathway from the mouth to
the anus
• Most organs are protected by the peritoneum
2. Accessory Digestive Organs
• Organs involved in grinding food or providing
digestive secretions (enzymes, bile, hormones)
which aid in chemical breakdown of food

Major and Accessory structures of the digestive
system

Teeth
Enamel: Hard calcified
• Physically fragment food tissue, Contains no living
cells, so cannot repair
damage from decay or
from wear
Dentin: Layer beneath
enamel
Pulp: The soft tissue at
the center of teeth,
contains nerves, blood
vessels and connective
tissue
Gingiva (Gums): Soft
tissues that cover and
protect tooth roots 4
Tongue-mixes food with saliva, forms a bolus (moist
ball of food) push to back of mouth, easily swallowed
Salivary glands-secrete saliva into ducts which

deliver saliva into the oral cavity
Three pairs:
1. Parotid
2. Submandibular
3. Sublingual

Copyright © 2014 John Wiley & Sons, Inc. All rights reserved.
Liver
• Digestion functions: produce bile to break down fats; many
metabolic and regulatory roles
Gallbladder
• Stores bile when food digestion is not occurring; secretes it
when fatty food enters the duodenum
Pancreas
• Produce digestive enzymes, and
sodium bicarbonate (buffers stomach
acid) also produces hormones
(endocrine system)

Peritoneum
•Largest serous
membrane in the body
•Lines the abdominal
cavity (parietal
peritoneum) and covers
the abdominal organs
(visceral peritoneum)

Copyright © 2014 John Wiley & Sons, Inc. All rights reserved.
Microbiome of the Digestive System
• Each milliliter of saliva contains millions of bacteria
• Esophagus, stomach, and duodenum
• These regions are almost free of microbes.
• Peristalsis and rapid transport of food help prevent
microbial colonization
• Tongue, teeth, jejunum, ileum, colon, and rectum
• Viridans streptococci most prevalent in this
region
• Steptococcus mutans prevalent on teeth surface

Microbiome of the Digestive System
Lower small intestine and colon
• Most bacteria are Gram-negative Bacteroides
• Also bacteria Lactobacillus, Escherichia, Enterobacter,
Proteus, Klebsiella, fungus Candida and protozoa Entamoeba
• These microbes are microbial antagonists (protective) and
produce vitamins (eg B12, K) that we use) as their wastes
• Mucous membrane prevents entry of microbes into the
bloodstream (protective)
• Oral antimicrobials can inhibit intestinal microbiota-lead to
transient or opportunistic infection (remember talking about C.
candida and C. diff.?)

Review Break
• Take a break and do questions # 1, 2, 3 of the

review activity for this chapter (found on
Blackboard) for a review of this microbiome.
10
Bacterial Diseases
of the Digestive System
11

Periodontal Disease: Dental Caries
aka cavities
Signs and symptoms
• Holes or pits in teeth; can result in tooth
loss
Pathogen
• Streptococcus mutans
• Lactobacillus spp.
12

Pathogenesis: The process of tooth decay.
1. Streptococcus mutans produces dextran (an insoluble, sticky slime) from

sucrose; dextran plus adhesion factors form plaques (a biofilm), leading to
plaque formation in pits and crevices on enamel
2. Lactobacillus spp. ferment sugars to acids (~pH5); dissolves enamel
3. Allows them to invade dentin and pulp of tooth, eventually, blood vessels,
nerves and may destroy tooth
4. Decay continues into dentin and then into:
5. Pulp of tooth, eventually, blood vessels, nerves and may destroy tooth 13
Prevention
• Healthy eating
• Good oral hygiene a dental pellicle (a protein film) forms on
enamel seconds after a tooth is cleaned or after chewing;
protects the tooth from the acids produced by
oral microorganisms after consuming carbohydrates
plaque
14

Periodontal Disease: Gingivitis
• Inflammation and infection of
tissues surrounding and
supporting the teeth (gums =
gingiva)
Signs and symptoms

• Hard deposits of tartar (hard
deposits of mineralized plaque)
• Inflammation of gums
• Anaerobic pockets (spaces)
form at base of teeth
Pathogen
• Porphyromonas gingivalis
Periodontal Disease
Pathogenesis
• P. gingivalis, anaerobic
• Colonize pockets and release
protein-digesting proteases
• These enzymes break
down the gingival tissue
• Bacteria invade bone, causing
osteomyelitis, teeth loosen
and fall out
Prevention
• Healthy eating, good oral
hygiene

Periodontal Disease: Acute Necrotizing Ulcerative
Gingivitis (ANUG)
• aka trench mouth

• Rare form of periodontal disease
Pathogen
• Do not know exact cause, but suspect anaerobes and
spirochetes eg Treponema
Signs and Symptoms
• Craterlike ulcers between teeth, extensive gum bleeding, foul
taste in mouth, grayish biofilm on gums
17

Periodontal Disease: Acute Necrotizing Ulcerative
Gingivitis (ANUG)
Epidemiology
• Reversible if caught early
• Documented as early as the 4th century B.C.
• The term “trench mouth” came into use during World War I
• Soldiers in battlefield trenches-poor oral hygiene, intense
psychological stress, poor diet developed severe
infections of the gums
18

Review Break
• Take a break and do questions # 4, 5 of the review

activity for this chapter (found on Blackboard) for a
review of periodontal diseases.
19
Peptic Ulcers
• Erosions of the linings of the stomach (gastric ulcer) or small
intestine (duodenal ulcers)
Signs and symptoms
• Abdominal pain is main symptom
• Erosion of stomach or duodenum lining
• Ulcers can lead to internal bleeding, bowel obstruction
Pathogen
• Helicobacter
pylori
20

Peptic ulcers
Pathogenesis
Virulence factors
• Flagella enable burrowing through stomach lining
• Adhesins facilitates attachment to gastric cells
• Urease neutralizes stomach acid
21

Peptic Ulcers
Epidemiology
• Fecal-oral transmission
• Stress may worsen ulcer symptoms
Treatment, and prevention
• Treated with antimicrobials and drugs that inhibit
stomach acid
• Prevented by avoiding fecal-oral transmission
22

Bacterial Gastroenteritis
• Inflammation of stomach or intestines caused by the
presence of bacteria
• Associated with contaminated food or water and poor
living conditions
General features
• Regardless of causative agent: nausea, vomiting, diarrhea,
abdominal pain, cramps
• Rare cases-spreads beyond GI tract, leading to kidney
failure or anemia
• Dysentery-severe, painful type of gastroenteritis
• Produces loose, frequent stools containing mucus and
blood
23

Bacterial Gastroenteritis
Pathogen
A number of pathogens cause particular types of
gastroenteritis
1. Shigellosis
2. Traveler's Diarrhea
3. Campylobacter Diarrhea
4. C. diff. (Antimicrobial-Associated) Diarrhea
5. Salmonellosis and Typhoid Fever
6. Cholera
24

1. Bacterial Gastroenteritis:
Shigellosis
Signs and Symptoms
•Fever, abdominal cramps, diarrhea, sometimes bloody stool
Pathogen and virulence factors
• Four species of Shigella
• Gram negative, all species produce:
• Type III secretion systems-complexes spanning membranes of
bacterial cell, insert into a host cell’s membrane, forming a channel
through which bacterial proteins can enter
• Enterotoxins-target epithelial cells lining the intestines, causing
diarrhea
Pathogenesis
• Pathogen colonizes cells of the small, then large intestine
• See next slide for details
25

1. Bacterial Gastroenteritis: Shigellosis
Pathogenesis
Shigella
Shigella invades
neighboring epithelial
cells, thus avoiding
Shigella attaches to immune defenses.
Epithelial cells
epithelial cell of colon.
An abscess forms as
epithelial cells are
killed by the infection.
Shigella triggers
endocytosis. Shigella that
enters the blood
is quickly
phagocytized
Phagocyte and destroyed.
No bacteremia.
Shigella multiplies
Treatment
in cytosol. • Supportive treatment
• antimicrobials if necessary
Traveler's Diarrhea
Pathogen
• Escherichia coli:
• Most common and important of bacteria that cause diarrhea in
travelers
• Is a coliform: lives in the colon
• Many O, H and K antigens have been used to describe
different strains of E. coli
• Many are harmless, but some have genes for virulence factors
(eg adhesins, fimbriae, toxins) causing severe foodborne
diseases
eg dangerous strain: E. coli 0157:H7
• Produce shiga-like toxins which inhibit protein synthesis, kill
cells, can cause kidney failure; Produce Type III secretion
system 27
• Primarily associated with ground beef
Traveler's Diarrhea
Pathogenesis
• Diarrhea 24-72 hours after consumption
• Shiga-like toxin adheres to neutrophils and spread
throughout body widespread host cell/tissue death
• Hemolytic uremic syndrome: massive RBC death can clog
kidneys, leading to life-threatening kidney failure and death
• More common in children, after 2-14 days of diarrhea caused
by E. coli
Diagnosis, treatment, and prevention

• Diagnosis-signs and symptoms
• Treatment-fluid and electrolyte replacement
• Antidiarrheal drugs prolong the symptoms by delaying
28
expulsion of bacteria-avoid them!
Campylobacter Diarrhea
Pathogen and virulence factors
• Campylobacter jejuni
• Gram negative; adhesins, cytotoxins, endotoxin lipid A
• C. jejuni survives in host cell after being phagocytized
Pathogenesis, epidemiology, signs and symptoms

• Most common cause of bacterial gastroenteritis (US)
• Chickens main source of human infections
• One study found C. jejuni in 81% of chickens
• Virulence factors are not completely understood, but cause
colonization/invasion of jejunum, ileum, colon, causing
bleeding lesions and inflammation
29

Campylobacter Diarrhea
• Most cases resolve without treatment
• Prevention-proper hygiene after handling raw poultry
Rare complication: Guillain-Barre Syndrome

• Triggers immune attack against nerves
• Causes muscle weakness, sometimes paralysis
• Symptoms may last for a few weeks to several years
• Most people recover fully, but some have permanent nerve
damage, some have died
• ~40% of GBS cases (US) are thought to be triggered
by Campylobacter infection
30

C. diff. Diarrhea
aka Antimicrobial-Associated Diarrhea
Signs and symptoms
• Ranges from 5-10 clear, watery, foul smelling bowel movements
per day, to pseudomembranous colitis in severe cases
• Pseudomembranous colitis
• Life-threatening, inflammation
• 10+ bloody stools per day
• Formation of pseudomembranes
• Collections of connective tissue,
dying leukocytes and dead colon cells
Pathogen
• Clostridium difficile, gram positive
31

C. diff. Diarrhea
Pathogenesis
• Normal intestinal large intestine microbe
• Antimicrobial use = overgrowth of C. difficile, can overtake
normal immune system
• Produces two toxins that mediate inflammation and
pseudomembrane formation
• Toxin A: breaks junctions of mucous membranes
• Toxin B: kills colon cells
Treatment and Prevention
• Metronidazole, vancomycin
• Eat probiotics
• Avoid unnecessary use of antimicrobials
32

C. diff. Diarrhea
Epidemiology
• Contact with C.diff or contaminated items
• C. diff. is a normal bacteria in the gut of many people
• Estimated ~20% of hospital patients carry it
• Generally noninvasive: does not leave the colon
• If it does leave can be life-threatening
• Use of microbial drugs, particularly extended use can be a
trigger; and any antimicrobial can trigger the disease
• By-product of modern medicine; was rare until widespread
use of antimicrobials
33

Bacterial Gastroenteritis:
5. Salmonellosis and Typhoid Fever
Pathogen and virulence factors *serotypes=distinct groups within
• Salmonella enterica a single species
• Serotypes* Typhi and Paratyphi in contaminated food or
water Typhoid fever
• Serotypes Enteritidis and Typhimurium in contaminated
eggs  Salmonellosis
• Salmonella tolerate acidity of stomach and pass to the
intestine; live in intestines of virtually all vertebrates
• Adhesions (attachment), type III secretion system (introduce
toxins into host cells)
• Toxins disrupt numerous cellular activities or cause apoptosis
34

Salmonellosis and
Typhoid Fever
Pathogenesis: contaminated food or
water is ingested, Salmonella travels
from stomach to intestines, then
Epidemiology
• Not normal part of microbiota in
humans but can live in the
intestines; eliminated in feces
• Infections travels via bloodstream to
spread to liver, spleen, bone marrow
and gallbladder; can remain there
(particularly gallbladder) and
establish a semi-permanent infection
• Person is now a carrier
35

Salmonellosis and Typhoid Fever
• Salmonellosis is usually self-limiting~ 1 week
• Typhoid fever can be treated with antimicrobial drugs
• Prevented with proper hygiene:
• “Boil it, cook it, peel it, or leave it’
36

6. Bacterial Gastroenteritis: Cholera
Pathogen, pathogenesis and virulence factors
• Vibrio cholerae, gram negative
• Only species that can survive in both saltwater and freshwater
• Recent research  environment within the human body
activates some Vibrio genes, making it more virulent than
when in water
• May explain rapid nature of cholera pandemics (seven
since 1817)
• Most important virulence factor-production of cholera toxin
(an A-B toxin): leads to the severe fluid and electrolyte loss
(due to profuse diarrhea)
37

6. Bacterial Gastroenteritis: Cholera
Signs and symptoms
• Profuse watery diarrhea
• “rice-water stools”
• Looks like water rice was boiled in
• watery, greyish, cloudy, with flecks of
mucus, and non offensive fish-like odour
• Dehydration, hypokalemia (low potassium, K),
hypovolemic shock (low blood volume); may lead to
muscle cramping, irregular heartbeat, kidney failure, coma,
death
• Presence of "rice-water" stool
• Treated with supportive care
• Available vaccine provides only short-lived immunity
• Prevented with proper hygiene
38

Common Forms of Bacterial Gastroenteritis-Overview
1.
2.
2.
3.
39

Common Forms of Bacterial Gastroenteritis (2 of 2)
4.
5.
5.
6.
40

Review Break
• Take a break and do questions # 6 of the review

review of bacterial gastroenteritis.
41
Bacterial Food Poisoning (intoxication)
aka Staphylococcal intoxication*
Signs and symptoms
• Depend on toxin
• General symptoms: nausea, vomiting,
diarrhea, and cramping, possible dehydration
Pathogen
• Staphylococcus aureus
• Most cases are self-limiting: ~ 24 hours
• Release 5 heat-stable enterotoxins (remain functional at
100ºC for up to 30 minutes, not inactivated by warming or
reheating food)
* an intoxication disorder because the food poisoning is
caused by the toxins of the bacteria
42

Bacterial Food Poisoning (intoxication*)
Pathogenesis
Epidemiology
• Outbreaks associated with
social functions
• Poor food prep hygiene
(2), unrefrigerated food for
long periods (3)

• Treated with fluid and
electrolyte replacement
• Proper hygiene can reduce
incidence
43

Review Break

review of peptic ulcers and bacterial food poisoning.
44
Viral Diseases
45

Mumps
Signs and symptoms
• Parotitis (swelling of parotid salivary
gland), face pain, fever, headache,
sore throat
• May be asymptomatic
• Upper respiratory tract, may spread to
other systems
Pathogen
• Mumps virus (Rubulavirus)
Yes, that’s Crosby,

during an NHL mumps
outbreak, 2014 46

Mumps
Pathogenesis and epidemiology
• Airborne virus
• Transmission: breathing in droplets of contaminated
saliva; sharing contaminated utensils
• Humans the only natural host
• Once very common childhood disease; with immunization,
now nearly nonexistent (developed countries)
• If virus spreads, may cause inflammation of testes (causing
sterility), meninges, pancreas; can cause deafness (rare)

• No specific treatment for mumps, comfort care only
• MMR vaccine
• Infected individuals develop lifelong immunity
47

Viral Gastroenteritis
Signs and symptoms
• Similar to bacterial gastroenteritis except less severe and
vomiting is less common
• Symptoms within 24 hours of consuming contaminated food,
usually resolve within 12-60 hours
• Cramping, diarrhea, nausea, vomiting; dehydration is a
common complications
• Vomiting, bloody stool, life-threatening diarrhea and
dysentery may occur
Pathogens, pathogenesis and epidemiology

• Caliciviruses (norovirus-90%), astroviruses, rotaviruses
(infants)
• Infect cells lining the intestinal tract
• More cases occur in winter
48
• Transmission: Oral-fecal route
Viral Gastroenteritis
• Treatment is based on fluid and electrolyte
replacement
• Prevention-proper treatment of water and sewage,
good hygiene practices
• Vaccine for rotavirus exists
49

Review Break

review of mumps and viral gastroenteritis.
50
Viral Hepatitis
• Inflammation of liver, produced by autoimmune disease,
alcohol/drug abuse, genetic disorders, viral infection
Pathogen
• Five different viruses
• Hepatitis A virus (HAV)-typically mild, 99% recover
• Hepatitis B virus (HBV)
• Hepatitis C virus (HCV)
• Hepatitis Delta virus (HDV)
• Hepatitis E virus (HEV)
Pathogenesis
• Liver damage and symptoms due mostly to host immune
response to virus
• See slide 54 for more detail
51

Viral Hepatitis
Signs and symptoms
• All types: jaundice, fatigue, weight
loss, abdominal pain, vomiting
• Additional Symptoms:
• Hep A = fever
• Hep B = vomiting and joint pain
Jaundice=yellowing of the
• Hep C = dark urine
skin and eyes
• Hep D = vomiting and dark urine
• Hep E = vomiting and dark urine
• Symptoms may occur years after initial infection
52

Viral Hepatitis
Signs and symptoms cont’d
• Complications from chronic hepatitis infection: cirrhosis
liver failure liver cancer
53

Type Hep A Hep B Hep C Hep D Hep E
Pathogen
Hepatovirus Orthohepadnavirus Hepacivirus Deltavirus Hepevirus
Can survive Virus Many strains Only spread Unexplained

Pathogenesis outside cells replicates in develop during from cells co- high mortality
for days liver cells replication infected with
Hep B
Parenteral Parenteral Parenteral

Transmission Fecal-oral (needles, sex, (needles, sex) (needles, sex) Fecal-oral
blood, fluid)
No, is cleared Yes, if infected Yes, chronic in Yes, only if No, is cleared
Chronic? by immune young (90% of 75-85% of body can’t by immune
response cases) cases clear virus response
Can be transferred Can be transferred Requires Hep B co- Usually mild,
Other vertically (placenta, vertically (placenta, infection; together
Mild, 99% during birth) from during birth) from high severity (10- though high in
recover mother to baby) mother to baby) 20%) pregnant
women
Disease None Hepatic cancer Hepatic cancer Cirrhosis None

associations
Treatment/ Vaccine Vaccine Direct action HBV vaccine None

Prevention antivirals
Review Break

review of hepatitis.
55
Protozoan Diseases
56

Giardiasis
Signs and symptoms
• Often asymptomatic
• Greasy/frothy/fatty diarrhea (foul rotten egg smell)
• Associated symptoms can last up to four weeks
Pathogen
• Giardia intestinalis
• G. intestinalis cysts-resistant to
chlorine, heat, drying, stomach
acid
aka ‘beaver fever’-outbreak in which
hikers at Banff National Park
became ill from drinking stream
water contaminated with Giardia from beavers 57

Giardiasis
Pathogenesis

Giardiasis
Pathogenesis cont’d

Giardiasis
Epidemiology
• Occurs in developed and developing countries
• Very common in US
• Individuals ingest cysts from contaminated water,
food, or hands
• Treated with antimicrobials
• Oral rehydration therapy
• Prevention-good hygiene, filtering water
60

Amebiasis
Amoebas-protozoa found throughout world
Signs and symptoms
• Three types, based on health of host and virulence of strain
1. Luminal amebiasis-asymptomatic, affects otherwise healthy
people; most common
2. Invasive amebic dysentery-causes severe diarrhea, colitis,
appendicitis, ulcers, bloody-mucus containing stools, pain
3. Invasive extraintestinal amebiasis-causes necrotic lesions
in liver, lungs, spleen, kidneys
61

Amebiasis
Pathogen, pathogenesis
• Entamoeba histolytica
• Trophozoites cause symptoms
• Virulent strains produce adhesions, toxic proteins proteases
• Severity-result of virulence factors released
Pathogenesis, epidemiology
• Transmission: consumption of contaminated food/water, from
contaminated hands, or by oral-anal intercourse
• Ingest cyst; pass through acid of stomach to small intestine;
release trophozoites, migrate to large intestine, multiply; cause
symptoms in 1-4 weeks
• If trophozoites leave intestines and invade peritoneal cavity
and bloodstream = Invasive amebic dysentery or invasive
extraintestinal amebiasis
• Human carriers help maintain transmission 62

Amebiasis
• Treated with oral rehydration therapy, antibacterial
and antiamebic drugs
• Prevent with proper hygiene and safe sex practices
• Individuals in endemic areas should drink bottled
water and avoid uncooked vegetables or unpeeled
fruits
63

Review Break
• Take a break and do questions # 10, 11 of the

review activity for this chapter (found on
Blackboard) for a review of protozoan infections.
64
Helminthic Infestations
of the Intestinal Tract
65

Tapeworm Infestations
Signs and symptoms
• Usually asymptomatic
• Nausea, abdominal pain, weight loss, and diarrhea may
occur
Pathogens
• Taenia saginata: beef tapeworm
• Taenia solium: pork tapeworm
66

Tapeworms-an anatomy reminder
• Tapeworm-common
name for a cestode, a
flat, segmented,
parasitic helminth
• Intestinal parasites that
lack their own digestive
system
67

Neck=where proglottids are

produced
Proglottids=body segments Cuticle=where nutrients are
68

absorbed
• Scolex-attachment organ; hooks and suckers
• Proglottids-grow continually; mature as they push away from
scolex producing both male and female reproductive organs
• After fertilization, proglottids furthest from scolex breaks off
and exits in feces, or releases eggs into feces
69
Strobila=chain of proglottids
Pathogenesis
eg Taenia solium.
1. Proglottids shed
2. Ingested by a pig
3. Larva migrate to muscle
4. Develop into cysticercus
5. Human ingests cysticerci
6. Excyst and mature into adult
tapeworms
70

Epidemiology
• Taenia species live worldwide
• Raw or undercooked infected meat is ingested
• Regions of inadequate sewage treatment
• Regions where humans live in close contact with
livestock
• Treated with praziquantel or surgery
• Prevention relies on thorough cooking of meats
71

Tapeworm Infestations: Hydatid disease
Signs and symptoms

• Stomach upset, diarrhea, unexplained weight loss, swollen
abdomen, anemia
• Blood or the fluid from a ruptured cyst – may be coughed
up
• Jaundice – pressure from an enlarging cyst may cause
jaundice
Pathogen
• Echinococcus granulosus
• Carried by dogs in their bowel, without any symptoms of
infection; zoonosis
72

Pathogenesis and epidemiology
• Human becomes infected by ingesting eggs of the
parasite
• Accidental hand-to-mouth transfer of eggs in dog feces
eg when handling dogs or objects (including food and
water) soiled with dog feces
• Person-to-person transmission does not occur
73

Pathogenesis
74

Pathogenesis
• Eggs mature and form slowly enlarging fluid-filled cysts
hydatid cyst, may become very large
• Cysts occur most commonly in the liver or lungs, but may
occur in any organ, including the heart, brain and bones;
resemble bunches of grapes
• Cysts often do not cause symptoms unless they become
very large or break
• Cyst fluid contains parasite antigen that can sensitize the
host
• Urgent anaphylactic reaction takes place if a cyst ruptures
spontaneously or during surgical procedures
75

Treatment
• Surgical removal of the cysts
• Anti-parasitic drug therapy eg albendazole to kill
cysts
76

Pinworm Infestations
• Pinworms are nematodes
• Long, thin, unsegmented, cylindrical helminth
Signs and symptoms
• Perianal itching, irritability, sleep disturbance,
decreased appetite
• 1/3 cases are asymptomatic
77

Pathogen and infestation
• Enterobius vermicularis
• Eggs ingested, hatch in small Intestine, mature in colon
• Females migrate, deposit eggs in the perianal region at night
• Eggs can be dislodged and spread the disease
Epidemiology
• Transmission-person to person through clothing or bedding
• Infections common in children
• Enterobius - most common parasitic worm in
the United States
78

Pathogenesis
79

• Diagnosis-identification of eggs or adult pinworms
• Tape test
• Treat with vermox (mebendazole)
• Prevention requires strict personal hygiene
80

Review Break

review of helminthic infections, and the remaining
questions for an overview of the lecture.
81
Lecture Overview
Digestive Tract Digestiv
e,
Urinary,
• Components of the digestive tract and accessory organs Reproductiv
tract In e
• Digestion – where it begins….how does it end
fections
• Location of normal microbiota

• Bacterial D. – dental caries, periodontal disease,
peptic ulcers, gastroenteritis (7), food poisoning
• Viral D. – mumps, gastroenteritis, hepatitis
• Protozoan D. – giardiasis, amebiasis
• Helminthic D. – tapeworm, pinworm
For each Disease: pathogen, pathogenesis, transmission,

treatment if discussed
82

Recommended Review Questions
Ch 23
Multiple Choice 1, 2, 3, 4, 5, 8, 9, 10, 12, 14, 16

Fill in the Blank None
Short Answer 23, 24
Critical Thinking None
Textbook Supporting Website:

https://openstax.org/books/microbiology/pages/24-introduction

Which statement is NOT accurate with regard to the
normal microbiota of the mouth?
A. There are over 700 species of bacteria in

the mouth.
B. Certain bacteria grow only on the teeth.
C. Viridans streptococci are the most prevalent bacteria
in the mouth.
D. There are no fungi in the mouth.

Which of the following types of microbes are NOT
normally found in the colon of a healthy individual?
A. helminths
B. bacteria
C. fungi
D. yeast

What is the causative agent of most peptic ulcers?
A. viridans streptococci
B. Helicobacter pylori
C. Escherichia coli
D. Campylobacter jejuni

What viral disease is characterized by inflammation
of the salivary glands?
A. rubella
B. mumps
C. cytomegalovirus
D. rabies

Which virus is strongly associated with liver cancer?
SELECT ALL THAT APPLY
A. HAV
B. HBV
C. HCV
D. HDV
E. HEV

What is the name of the motile feeding form of
Giardia?
A. trophozoite
B. sporozoite
C. oocyst
D. apicomplexan

How is infection by tapeworm prevented?
A. avoiding ingestion of contaminated water

B. thoroughly cooking meat
C. avoiding infected individuals
D. avoiding uncooked egg products

What type of helminth is the tapeworm?
A. gematode
B. nematode
C. trematode
D. cestode

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BIOM 1073

© 2018 Pearson Education, Inc.

Digestive System Structures-divided into two groups:

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© 2018 Pearson Education, Inc.

Salivary glands-secrete saliva into ducts which

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

• Take a break and do questions # 1, 2, 3 of the

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© 2018 Pearson Education, Inc.

1. Streptococcus mutans produces dextran (an insoluble, sticky slime) from

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Signs and symptoms

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• aka trench mouth

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

• Take a break and do questions # 4, 5 of the review

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

Diagnosis, treatment, and prevention

Pathogenesis, epidemiology, signs and symptoms

© 2018 Pearson Education, Inc.

Rare complication: Guillain-Barre Syndrome

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

• Take a break and do questions # 6 of the review

© 2018 Pearson Education, Inc.

Treatment, and prevention

© 2018 Pearson Education, Inc.

• Take a break and do questions # 7 of the review

© 2018 Pearson Education, Inc.

Yes, that’s Crosby,

© 2018 Pearson Education, Inc.

Treatment, and prevention

© 2018 Pearson Education, Inc.

Pathogens, pathogenesis and epidemiology

© 2018 Pearson Education, Inc.

• Take a break and do questions # 8 of the review

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

© 2018 Pearson Education, Inc.

Can survive Virus Many strains Only spread Unexplained

Parenteral Parenteral Parenteral

Disease None Hepatic cancer Hepatic cancer Cirrhosis None