Microbial Diseases of the

Digestive System
C. 25

Microbial Diseases of the Digestive System

Pathogens/toxins enter food and water supply

from feces of infected people animals (fecal-oral cycle)

Second major cause of illness in US (which is 1st)

CDC:

US Est. ~76 M cases/year of food borne diseases (5,000

deaths)

Major problems in developing countries

Fecal-oral cycle can be broken by

proper sewage disposal

disinfection of drinking water
proper food preparation and storage
rapid and reliable diagnosis
Effective vaccines

The Digestive System

Fig. 25.1

Includes the gastrointestinal

(GI) tract and accessory
structures such as teeth,
tongue, liver, gallbladder and
pancreas
Millions of microbes/ml of
bacteria in saliva
Less abundant in stomach and
small intestine
100Bs/g in feces in large
intestine
Up to 40% of fecal mass is
microbial cell material
Assist in digestions of foods,
synthesize vitamins, etc.

Bad vs Good Microbes

What are the defending mechanisms
offered by the GI tract?
Lysozyme in saliva
High acid (HCl) content in stomach
Low pH 1-2
Antimicrobial defenses of the small
intestine e.g. defensins and lysozyme
by Paneth cells

Bacterial Diseases of the Mouth

- Dental Caries

Figs. 25.2 & 25.3

>700 spp of microbes in the oral cavity

Streptococcus mutans attachment to teeth
Breaks down sucrose into fructose and glucose
Uses glucose to make dextran
Dextran helps bacteria to adhere to teeth and offers
protection (dental plaque, a type of biofilm, >400 spp.,
streptococci and Actinomyces)
Fructose fermented to lactic acid (S. mutans and
lactic acid bacteria) leads to tooth decay

Stages of Tooth Decay

A tooth with plaque accumulation in difficult-to-clean areas

Decay initiates as enamel is attacked by acids formed by S. mutans
Decay advances through the enamel and dentin by Lactobacillus spp.
Decay enters the pulp and may form dental abscesses in the tissues
surrounding the root by mixed bacterial populations
Prevention:
minimal ingestion of sucrose, remove plaque by regular brushing,
flossing and professional cleaning, and the use of fluoride
Use of sugar alcohols (such as mannitol and sorbitol) as sugarless
Figure 25.4
sweetener

Periodontal Disease

Figure 25.5

Inflammation/degeneration of structures that support teeth

Gingivitis infection restricted to gums,
bleeding of the gums while the teeth are being brushed
Periodontitis
Destruction of bone and tissue that support teeth loss of the
teeth (Porphyromonas spp.)
Treatments:
Surgical removal of periodontal pockets or injecting a gel to
slowly release doxycycline

Bacterial Diseases of the Lower Digestive System

Symptoms include:

Diarrhea, abdominal cramps, nausea and vomiting;

gastroenteritis (stomach and intestinal mucosa); and
dysentery (severe diarrhea accompanied by blood or
mucus)

Treatment:

Fluid and electrolyte replacement (oral rehydration

therapy)

Intoxication: Ingestion of a toxin:

Symptoms appear 1 to 48 h after ingestion

Short incubation time and usually no fever

Infection: Growth of a pathogen:

Incubation period: 12 h to 2 weeks

To allow multiplication and invasion of tissue

Microbes penetrate intestinal mucosa and pass through

to infect other systemic organs
Fever is one of the bodys general responses to an
infective organism

Staphylococcal Food Poisoning

Vegetative cells (noninvasive)

Tolerates 60oC for 30 min

Resistant to drying and high osmotic pressures(salt
wont affect)

Virulence factor:

Enterotoxin - Heat stable (survives 30 min of boiling)

Toxin quickly triggers the brains vomiting reflex
center

Intoxication dose 1 M microbes/g of food

S. aureus does well in foods with higher-than-normal
osmotic pressure or low moisture level.

Outgrow most competing bacteria

High risk foods include custards, cream pies and ham

Prevention:

Adequate refrigeration (to avoid temp abuse)

and hand hygiene

Recovery: ~within 24 h and the mortality rate is

almost 0%

Diagnosis:

is based on the short incubation time.

Fig. 25.6

Bacillus cereus Gastroenteritis

Large, Gram +ve, endospore-forming, common
in soil and vegetation
Spores are heat resistant
Heating eliminates competing bacteria in food
Most common in grains and cereals e.g. rice
Ingestion of bacterial exotoxin produces
symptoms (intoxication)
Almost entirely diarrhea in nature (8-16 h
after ingestion)

Cholera
Vibrio cholera: slightly curved, Gram(-) rod,
single polar flagellum (noninvasive)
Grows in small intestine and produce cholera
exotoxin

Toxin causes host cells to secrete water and

electrolytes, esp K+
Watery stools 12 to 20 L of fluids lost in a day
(leads to shock, collapse and often death)
Usually no fever
Blood may become so viscous that it affects proper
function of vital organs
Untreated cases may have 50% mortality rate (<1%
today)

Treatment: Antibiotics i.e. doxycycline and

intravenous replacement of the lost fluids and
electrolytes
Oral vaccines: Provide short period protection
(moderate effectiveness)
Not common in yet in North America (has arrived in
Haiti)

Figure 25.11

http://textbookofbacteriolo
gy.net/staph.html

Clostridium Infections
Clostridium perfringens gastroenteritis
Gram positive, endospore-forming, obligatory anaerobic
Grow in intestinal tract, producing exotoxin (abdominal pain & diarrhea)
Usually associated with improper cooling of foods

C. difficileassociated diarrhea
Grows following prolonged antibiotic therapy
Discontinuation of the antibiotic and oral rehydration therapy needed
Associated with hospitalized patients and nursing home residents (often
due to poor hand hygiene of health care workers)

http://textbookofbacteriology.net/staph.html

Escherichia coli Gastroenteritis

As traveler's diarrhea, foodborne illness
outbreaks & epidemic diarrhea in nurseries
Enteroaggregative E. coli
Noninvasive but produces enterotoxin
Produces a watery diarrhea, cause a stacked-brick
configuration

Enteroinvasive E. coli

Invades the intestinal wall, produces

inflammation, fever & Shigella-like dysentery

Diarrhea usually self-limiting,

Best treatment: oral rehydration or

antimicrobial drugs

Biocell v.30 n.2 Mendoza mayo/ag

o. 2006

Preventive measures:

Proper food handling, safe water supply, proper

sewage disposal & for travelling, may use
prescribed antibiotics

Gossney et al. 1999, Emerg Infect Dis. 5:216.

Enterohemorrhagic E. coli (EHEC)

Destroy microvilli and form
pedestal-like projections
(noninvasive)
E. coli O157:H7

(O=cell wall antigen and H=flagella antigen)

Virulence factors: Shiga-toxin

(STEC)

Ability to adhere to the intestinal mucosa

Causes causes self-limiting diarrhea

Cattle are the main reservoir

(unaffected by the bacteria)
In US, 2-3% of domestic cattle
carry STEC which contaminate the
carcass at slaughter
Other potential sources:
Contaminated leafy vegs, raw alfalfa
sprouts and tomatoes, farm visits or
petting zoos

Small infective dose: ~ <100

Hemolytic uremic syndrome

(HUS)

Dangerous complication blood

in the urine, kidney failure
5% mortality for small children
Treatments: iv rehydration and
careful monitoring of serum
electrolyte
May require kidney dialysis or
even transplants

Shigellosis

Shigella sonnei

causes a relatively mild dysentery. Most

common spp. in North America (NA)

S. dysenteriae

causes a severe dysentery and prostration. Less

common in NA but causes 20% death rate in
tropical areas

Virulence factors:

Shiga toxin (which causes inflammation and

bleeding), invasive to M cells, able to spread to
other cells, resistant to phagocyte-mediated killing

Infections:

Long incubation periods (12 h to 2 weeks)

Infective dose is small

Shigella spp.

attach to M cells, induce membrane ruffles and

result in the uptake of bacteria into the cells

Spread from person to person

Treatments: fluoroquinolones and oral
rehydration

Figs. 25.7, 25.8

Salmonellosis
Salmonella:
>2,000 serotypes, invasive

Invasive (multiply in mucosa cell )

Can pass thru mucosa and enter lymphatic and
cardiovascular systems and eventually spread to organs

Replicates inside macrophages

Incubation: 12 to 36 h
Mortality:
Low (<1%, infants and seniors; due to septic shock caused
by endotoxin

Poultry contamination:

Salmonella enterica (S. enteritidis & S. typhimurium) is

well adapted to commercial chicken production. Can
survive in albumin (resistant to lysozyme)

Treatment:
Antibiotics not necessary;
Self-limiting; oral rehydration therapy

Fig. 25.9

 Typhoid fever

Typhoid Fever

Associates with poor sanitation, wars and

natural disasters

Symptoms:

high fever (40oC) and continual headache,

diarrhea (2nd or 3rd week), ulceration of the
intestinal wall (severe cases)

Salmonella typhi

16 M cases and 0.6 M death worldwide every

year
US: 350-500 annual cases, 70% due to
foreign travels
Pathogen in feces of humans

Incubation period: longer (2-3 weeks)

Salmonellosis (12-36 h)

Treatment:

With antibiotics e.g. quinolones, mortality

rate is decreased from 20% to 1%

Vaccines: killed or live orally ingested

Recovered patients (1 to 3%) become carriers

harbor Salmonella in gallbladders

http://en.wikipedia.org/wiki

Typhoid Mary
Mary Mallon (1869-1938), also known as
Typhoid Mary, was the first person in the
United States to be identified as a healthy
carrier of typhoid fever. Over the course of
her career as a cook, she infected 47 people,
three of whom died from the disease. Her
notoriety is in part due to her vehement denial
of her own role in spreading the disease,
together with her refusal to cease working as a
cook. She was forcibly quarantined twice by
public health authorities and died in quarantine.
It was also possible that she was born with the
disease, as her mother had typhoid fever during
her pregnancy.
What rights do these people have?
As a health care worker, how will you serve this
group of people?

http://en.wikipedia.org/wiki

Helicobacter Peptic Ulcer Disease

A spiral-shaped, microaerophilic bacterium

H. pylori causes stomach cancer
30 to 50% of the population in the developed
world become infected
~15% of those infected develop ulcers
3% may develop gastric cancer
H. pylori can grow in the highly acidic environment
of the stomach. They produce urease to convert
urea to ammonia. This results in a local high pH
for bacterial growth
Treatment: use of antibiotics would lead to the
disappearance of peptic ulcers
Detection: urea breath test ingestion of
radioactively labeled urea and detect for heavy
CO2 in about 30 min; look for antigens of H. pylori
in stools or blood
Fig. 25.13

Hepatitis
Hepatitis

Transmission

Causative agent

Fecal-oral

Picornaviridae

Chronic
liver
disease?
No

Vaccine?

Parenteral,
STD

Hepadnaviridae

Yes

Recombinant

Parenteral

Filoviridae

Yes

No

Pareteral, HBV
coinfection

Deltaviridae

Yes

HBV vaccine

Fecal-oral

Caliciviridae

No

No

Inactivated
virus

Urinary Tract and Reproductive

Systems Infections
Chapter 26

Urinary and Reproductive Systems

Urinary system
Composed of organs to regulate chemical composition and
volume of the blood
Secrete mostly N waste products and water
Prone to infections from external contacts
Mucosal membranes are ideal for bacterial growth

Reproductive system
Shares organs of the urinary system
Produce gametes for reproduction; female provide support
and nourishment for embryo and fetus
Sexual contact promote exchange of m/os

Urinary Organs
Two kidneys, 2 ureters, 1 urinary
bladder and 1 urethra
In male, urethra is for both urine
and seminal fluid
Physiological valves prevent the
backflow of urine to kidneys to
avoid LUT infections
Acidity of urine has antimicrobial
properties
Flushing action of urine to remove
the microbes
Normal urine is sterile but pick up
m/os through the urethra
Figures 26.1

Urinary & Reproductive Organs

Refer to the text book on the structure of reproductive systems
Microbes usually enter reproductive system through
the vagina (in females) or urethra (in males)

Figures 26.2 26.3

Normal Microbiota
Urinary bladder and upper urinary tract are
sterile (acidic urine and flushing action)
Anterior urethra

May be inhabited by Staphylococcus epidermidis,

Enterococcus faecalis and some alpha-hemolytic streptococci
Occasionally some enteric bacteria (e.g. E. coli, Proteus) and
Corynebacteria, (from the skin, vulva or rectum)
Lactobacillus sp
Male urethra is usually sterile
in association

Vagina:

Lactobacillus acidophilus predominant during child bearing

age
Keeps vaginal pH low (3.8-4.5) & produce hydrogen peroxide
prevents establishment of potential pathogens
Estrogens (sex hormones) promote the growth of lactobacilli
by enhancing the production of glycogen. Break down to
glucose eventually lactic acid
Other m/os include streptococci, various anaerobes, some
Gram ve, and Candida albicans, etc.
Pregnancy & menopause decrease estrogen levels and
increase infection

with vaginal
epithelial cell

Cystitis
Inflammation of bladder

More common in women (8X; why?)

Female urethra is <2 long; closer to the anal opening
Symptoms include dysuria (difficult, painful, urgent urination) & pyuria (urine
contains pus)

Usually caused by coliforms (why?)

E. coli (~85%), and Staphylococcus saprophyticus (coagulase ve)

May also be caused by Proteus, Klebsiella, Enterococcus, Pseudomonas species
(characteristics?)
>100 CFU/ml of potential pathogens in female urine sample is significant

Diagnostic:

Urine test for leukocyte esterase (LE), an enzyme produced by neutrophils

Contributing factors:

careless personal hygiene and sexual intercourse

Treatment: Antibiotics

Antibiotic-sensitivity tests may be required (why?)

Trimethoprim-sulfamethoxazole, fluoroquinolone antibiotics or ampicillin

Urethritis
Inflammation of urethra
Symptoms dysuria, painful or difficult
urination

Pyelonephritis
Inflammation of the kidneys (one or both)
25% of untreated cystitis progress to pyelonephritis
Usually a complication of lower urinary infection
Can be due to systemic infections (why?)
E. coli responsible for about 75%
>10,000 CFU/ml and a positive LE test
If the infection becomes chronic, scar tissues will be
formed and impaired the function of kidneys
Treatment broad-spectrum antibiotics, e.g. second or
third generation cephalosporin

A 20-year-old woman feels a stinging

sensation when urinating and feels an urgent
need to urinate, even if very little urine is
excreted. Lactose-fermenting, gram-ve rods
are culture from her urine. What is the
name of the organism?

 Bacterial vaginosis (BV)

Most common cause of vaginal infections
Due to changing condition within vagina. Rise
in pH, light discharge (fishy smell)
Gardnerella vaginalis, Mobiluncus sp,
Peptostreptococcus sp, and Mycoplasma
hominis

Vaginitis

Clue cell

Gram stain of urethral smear

G. vaginalis, Mobiluncus sp

Vaginal tissue infections characterized by

redness, swelling and tenderness

Candidiasis (Candida albicans)

Trichomoniasis (STI)
Trichomonas vaginalis (protozoan)
Gram stain of urethral smear
C. albicans

Candidiasis
Candida albicans (yeast)
By the age of 25, 50% women may
encounter at least 1 yeast infection (8590% due to this m/o)
Grows on mucosa of mouth, intestinal
tract, and genitourinary tract; an
opportunistic pathogen
Causes nongonococcal urethritis (NGU)
in males
Causes vulvovaginal candidiasis in
females
Diagnosis is by microscopic identification
and culture of yeast
Diabetes and antibiotic therapy are the
predisposing factors
Treatment: topical fungicides such as
clotrimazole or miconazole; or a single
dose of oral fluconazole

Trichomoniasis

Trichomonas vaginalis, an anaerobic

protozoan
Found in semen or urine of male carriers
(STI) and vagina of women
Often accompanied by coinfection with
gonorrhea
Vaginal infection causes irritation and
profuse discharge (frothy, yellow-green
discharge with a strong odor); no
symptoms for men
Incidence is higher than that of
gonorrhea and chlamydia but is
considered relatively benign (associated
with low birth weight)
Diagnosis is by microscopic identification
of protozoan
Treatment: antiprotozoan such as
metronidazole
Figure 26.15

Common Types of Vaginal Infections

These are epithelial (clue) cells from a
vaginal swab. These cells are infected
with what organism?

Sexually Transmitted Infections (STIs)

Most infections of the reproductive system are
sexually transmitted infections
The 10 most common diseases are:
Bacteria (treated with antibiotics)
Chlamydia, Gonorrhea, Syphilis, Chancroid,

Viral (some antiviral drugs available)

Genital herpes, Genital warts, Hepatitis, HIV-AIDS

Arthropods (treated with insecticides)

Pubic lice, scabies

Gonorrhea
Common reportable or notifiable disease
Females may be asymptomatic
Males have painful urination and pus discharge
Virulence factors: fimbriae (attach to mucosal cells), Opa (prevents
activation of lymphocytes and turns off proliferation. This will block adaptive
immunity to gonorrhea), antigenic variation
If left untreated, may result in a serious systemic infection
Complications can involve the joints (arthritis), heart (endocarditis), meningitis, eyes
(neonatal gonorrheal ophthalmia)
Can cause PID (pelvic inflammatory disease) in women and lead to sterility
Pregnant women can infect infants during child birth and result in blindness; for preventive
measure, antibiotics are placed in the eyes of newborn

Treated with antibiotics:

e.g. cephalosporins or fluoroquinolones

Neisseria gonorrhoeae

Figure 26.7

Intracellular, diplococcus, Gram (-)

Organism attaches to oral or
urogenital mucosa by fimbriae

Chlamydia trachomatis
Most common STI in Canada and
USA (& worldwide)

Obligate intracellular pathogen

Gram-indeterminate but structurally a Gram -ve organism.

Symptoms
Men: painful urination, whitish discharge from penis
Women: itching, burning in genitals, greenish vaginal
discharge, dull pelvic pain
Both sexes can display nongononcoccoal urethritis
(NGU), trachoma, infertility and lymphogranuloma
venereum
Prostatitis and epididymitis in men, symptoms are
mild
In women (5x than men) it causes pelvic
inflammatory disease (PID), cervicitis, ectopic
pregnancy, eye infections
In infants: neonatal conjunctivitis, infant pneumonia

Chlamydia trachomatis
inclusion bodies (brown)
in a McCoy cell culture.
C. trachomatis infection
can be effectively cured
with antibiotics- e.g.
Erythromycin

Syphilis

Treponema pallidum (spirochete)

Transmitted by direct contact through skin breaks or can invades intact mucosa membrane
Can describe primary, secondary and tertiary stages cans be treated with penicillin
Congenital: Can cross placenta and infect developing fetus.

Treatment: Especially for 1o and 2o stages

body for ~ 2 weeks); doxycycline or azithromycin

1o

Benzathine pencillin (remains effective in the

2o

Figure 26.10

Viral Infections

Genital Herpes
Herpes simplex virus 2 (human herpesvirus 2, HSV-2)

Viral characteristics: ______________________

HSV-1 is primary responsible for cold sores or fever blisters
but can also cause genital herpes

Produces lesions and vesicles

Neonatal herpes transmitted to fetus or newborns,
~40% survival rate
Recurrences from viruses latent in nerve cells (similar
to cold sores & chickenpox-shingles): ~90% for HSV-2
and 50% for HSV-1
Unlike love, herpes is forever

Suppression rather than cure: Acyclovir or

valacyclovir
No vaccine is available

Genital Warts
Human papillomaviruses
Viral characteristics _______________
Treatment: Imiquimod to stimulate
interferon
HPV 16 (serotype) causes cervical cancer
and cancer of the penis

DNA test is needed to detect cancer-causing

strains

Vaccination against HPV strains