Microbial Diseases of the

Cardiovascular
and Lymphatic Systems
Chapter 23

Objectives
Know some infectious
diseases of the
cardiovascular &
lymphatic systems
Bacteria
Protozoan
Viral

The Cardiovascular System and Lymphatics System

Heart:
Pump blood to the rest of the body

Blood and blood vessels

Transports nutrients to and wastes from cells
Many of the bodys innate defensive systems are
found in blood & lymph

WBCs:
Defend against infection

Lymphatics:
Transport interstitial fluid to blood

Lymph nodes:
Contain fixed macrophages to clear pathogens & T
and B lymphocytes

Lymphoid organs:
Tonsils, appendix, spleen & thymus

Sepsis and Septic Shock

Sepsis (septicemia):
Whole-body inflammatory state (systemic) due to
bacteria growing in the blood
Accompanied by fever, chills, rapid heart and
respiratory rates (release mediators of inflammation)
High count of white blood cells
Often accompanied by lymphangitis (inflamed lymph
vessels), red streaks under the skin, along the arm or
leg

Severe sepsis:
Drop in blood pressure, failure of a body organ

Septic shock (final stage):

Low blood pressure cannot be controlled in spite of
adequate fluid resuscitation

Figure 23.3

Sepsis
Gram-negative sepsis

Endotoxins cause blood pressure to decrease

Antibiotics can worsen condition by killing bacteria (Why?)
Treatment involves attempts to neutralize the LPS components and
inflammation causing cytokines (drugs to reduce clotting)

Gram-positive sepsis

Nosocomial infections due to invasive procedures & intro of Gm+ m/os

Exotoxins, cell wall, or even bacterial DNA

Staphylococcus aureus,Streptococcus pyogenes & Group B streptococcus

Enterococcus faecium and E. faecalis (important group; inhabitants of colon;
cause infections of wounds & urinary tract )
Why is antibiotic (Peni) resistant enterococci of major concern?
(Vancomycin resistant)

Puerperal fever (childbirth fever)

Streptococcus pyogenes (Group A -hemolytic)

Transmitted to mother during childbirth by attending physicians and
midwives (infections from uterus to abdominal cavity & sepsis)
Antibiotics and modern hygienic practices prevent such infection

Bacterial Infections of the Heart

Endocarditis:

Inflammation of the endocardium

Inner layer of the heart
Lines the heart valves and muscle

Subacute bacterial endocarditis:

Major cause: -hemolytic streptococci from mouth

Enterococci and staphylococci may also be involved
Arises from infection elsewhere in the body, i.e. teeth, tonsils, body piercing
Pathogens will clear except people with abnormal heart valves
Fever, general weakness & heart murmur

Acute bacterial endocarditis:

More rapidly progressive type
Major cause: Staphylococcus aureus from mouth
Leads to rapid destruction of heart valves

Pericarditis:

(fluid enclosed sac surrounding the heart)

Also caused by streptococci

Rheumatic Fever

Autoimmune complication of Streptococcus pyogenes

infections; aged 4-18
Often follows a strep throat; short period of arthritis and
fever; produces subcutaneous nodules at joints
Inflammation of heart valves for ~50% of patients,
probably from a misdirected immune Rx against
streptococcal M protein
Renewed immunological damage with repeated sore throats
Leading cause of heart disease in the young in
underdeveloped world

Figure 23.5

Tularemia
Francisella tularensis
Gram-negative rod, BSL-3 m/o
Bacteria reproduce inside phagocytes
transmitted from rabbits and squirrels by deer
flies or ticks; respiratory infection by dust
contaminated with urine or feces of infected
animals
Treatment: tetracycline for 10-15 days

Example of zoonotic disease

Characteristic clinical syndromes:
ulceroglandular (common type ~ 75% of all
forms).
complicated by pneumonia, meningitis, or
peritonitis
Referred to as rabbit fever or deer fly fever
Figure 23.6

Anthrax
Caused by Bacillus anthracis

Gram-positive, endospore-forming, large aerobic rod, found in soil

Infected cattle

Fulminating (sudden appearance) and fatal sepsis

Cattle are routinely vaccinated

Humans also infected

Cutaneous anthrax

(20% mortality)

90% of naturally occurring cases (preferred entry point)

Endospores enter through minor cut

If the m/os enter the blood stream, 20% mortality but <1% w antibiotic therapy

Gastrointestinal anthrax

(>50% mortality)
Ingestion of undercooked food contaminated food (a rare form of anthrax)
Symptoms: nausea, abdominal pain & bloody diarrhea, lesions in GI tract

Inhalational (pulmonary) anthrax

(100% mortality)

Inhalation of endospores
High probability to enter the bloodstream
Illness progresses in 2 or 3d and kills patient 24-36 h

Anthrax
Virulence factors

Endospores
Survive and multiply in macrophages
Edema toxin (causes local edema & swelling, interferes
phagocytosis by macrophages)
Lethal toxin (targets and kills macrophages)
Capsule (not polysaccharide but amino acid residues, does not
stimulate an immune response)
Bacteria proliferate in the blood w/o any effective inhibition;
these toxin-secreting bacteria ultimately kill the host

Treatment

Antibiotics such as ciprofloxacin or deoxycycline, long period

that up to 60 days
Live, a single dose of attenuated vaccine for cattle
Inactivated form of toxin to vaccinate humans, 6X injections
in 18 months, followed by annual booster

Gangrene

Ischemia: Loss of blood supply to tissue

Necrosis: Death of tissue
Gangrene: Death of soft tissue
Gas gangrene: Death of muscle tissue with gas production

Clostridium perfringens, gram-positive, endospore-forming anaerobic rod,

grows in necrotic tissue with gas production
Toxin to kill cells & produce necrotic tissue; enzymes to degrad collagen &
proteinaceous tissue for spreading
Improperly performed abortions due to the invasion of uterine wall
Treatment includes surgical removal of necrotic tissue; hyperbaric
chamber; penicillin

 Yersinia pestis

Plague

Gram-negative rod
Bacteria can survive and grow in phagocytes

Reservoir: Rats, ground squirrels, and prairie dogs

Vector: rat fleas (Xenopsylla cheopsis)
Bubonic plague: Bacterial growth in blood and lymph;
most common form (80-95% of cases today); 50-75%
mortality rate
Septicemic plague: Septic shock

Pneumonic plague:
mortality rate

Bacteria in the lungs; 100%

Easily spread by aerosol droplets

Virulence factors: capsule, ability to survive and grow in

phagocytic cells, ability to sense temp (37oC or 25oC) and
Ca2+ (high or low) to turn on or off virulence factors
Treatment: streptomycin & tetracycline
Diagnostic: Look for capsular Ag
Vaccine: available for field and lab workers

Brucellosis (Undulant Fever)

Brucellosis is the most common bacterial

zoonotic disease, endemic in Middle East
Brucella
Gram-negative coccoid rods that grow in phagocytes

B. abortus (elk, bison, cows)

B. suis (swine)
B. melitensis (goats, sheep, camels)

Undulating fever

Gibraltar fever, Malta fever, Mediterranean fever

Fever spikes to 40C each evening

Transmitted via milk from infected animals or

contact with infected animals

Typhus
Epidemic typhus

Rickettsia prowazekii
Gram-negative cocci; obligate intracellular
parasites of eukaryotes
Reservoir:
Rodents

Vector:

Body louse Pediculus humanus corporis

Transmitted when louse feces rubbed into bite wound

Treatments: tetracycline & chloramphenicol

Endemic murine typhus:

Rickettsia typhi
Reservoir:
Rodents

Vector: rat flea (Xenopsylla cheopsis)

Spotted Fevers
(Rocky Mountain Spotted Fever)
Rickettsia rickettsii

Can be passed from one generation of

ticks to another through eggs
Best-known rickettsial disease in US
Measles-like rash except that the rash
appears on palms and soles (mistaken for
measles)
Mortality (20%) if treatment is not
prompt
Tetracycline and chloramphenicol are
effective

Figure 23.18

Human Herpesvirus 4 Infections

Epstein-Barr virus (EB)
Infectious Mononucleosis

Childhood infections are

asymptomatic
Intense immunological response in
young adulthood
Transmitted via saliva (kissing)
Characterized by proliferation of
monocytes (unusual lobed nuclei)
Diagnostic: IgM detection using
fluorescent technique

Burkitts lymphoma

Nasopharyngeal carcinoma
Causes cancer in immunosuppressed individuals and malaria
and AIDS patients
Common childhood cancer in Africa

Human herpesvirus 5 Infections

Cytomegalovirus (CMV), a very large herpes-virus

Infected cells swell (cyto-, mega-)
Latent in white blood cells, replicating very slow
Carriers shed the virus in saliva, semen & breast milk
May be asymptomatic or mild in adults
Transmitted across the placenta; may cause mental
retardation up to 40-50% if infection during pregnancy
Transmitted sexually, by blood, or by transplanted
tissue

Viral Hemorrhagic Fevers

Yellow fever
Dengue

Pathogen

Portal of entry

Reservoir

Arbovirus

Skin

Monkeys

Method of
transmission
Mosquito

Humans

(Aedes aegypti)
Mosqioto

Arbovirus

Skin

(Aedes aegypti;
Marburg, Ebola,
Lassa

Filovirus,
arenavirus

Mucous
membranes

Hantavirus
pulmonary
syndrome

Bunyavirus

Respiratory
tract

Probably
fruit bats;
other
mammals
Field mice

A. Albopictus)
Contact with blood

Inhalation

Protozoans
Note the following about each disease:

Organism involved
Reservoirs: hosts (definitive and intermediate)
Mode of transmission
Disease symptoms

Trypanosomiasis
Toxoplasmosis
Malaria
Schistosomiasis

Lyme Disease
In 1976 a group of children in Lyme
Connecticut, thought to have at first
juvenile rheumatoid arthritis, were
suspected rather to have a ticktransmitted multisystem disease.
In 1981 Willy Burgdorfer and
colleagues found an unidentified
spirochetal bacterium, Borrelia
burgdorferi, in a nymphal Ixodes
scapularis tick.
B. burgdorferi is a vigorously motile
spirochete with its cytoplasmic
membrane surrounded by
peptidoglycan and flagella.

Enzootic Life Cycle of Borrelia burgdorferi

Transmitted by Ixodes
scapularis in eastern and
central North America
Transmitted by Ixodes
pacificus in western N.A.
The small animals that
larvae feed on can be
squirrels, chipmunks, other
rodents, and birds.
Most human infections of
B. burgdorferi are
transmitted by the tiny
nymphal stage (1mm) in the
spring summer of the 2nd
year who feed agressively.

Distribution in North America

Do these ticks get turned back at the Canada-U.S border?

In B.C. areas where people have been infected: Vancouver Island, the
Lower Mainland especially the Harrison-Hope area, Okanagan, and
Kootenay area

Figure 1. Geographic extent of suitable temperature conditions for Ixodes scapularis in eastern and central Canada

B.C. and Future Projections

Initial Infection

http://www.youtube.com/watch?
v=aJHjUMZVRKA&feature=related

Upon receiving a tick bite the

characteristic bulls eye rash
called erythema migrans
(EM) develops in 3 32 days
in 70 80% of people.
This is accompanied by flulike symptoms including,
fever, fatique, malaise,
headache, slight muscle and
joint pain.
A six-week regime of
antibiotics such as biaxin,
flagyll, or high levels of
amoxicillin, can eradicate the
disease at this point

Immune Response to B. burgdorferi

The first line of host defense is

complement-mediated lysis of
the spirochete.
Histological examination of the
EM skin lesions reveals
lymphocytes, macrophages and
plasma cells.
Patients develop IgG and IgM
antibodies against many
components of the organism
By changing or minimizing
antigenic expression (hiding in
tissues) B. burgdorferi can
evade the hosts immune
responses.

Second Phase and Chronic Lyme Disease

(Third Phase)

In the second phase the infection

disseminates widely with many possible
expressions:
Acute lymphocytic menigitis, cranial neuropathy,
atrioventricular nodal block, musculoskeletal
pain in joints, bursae, tendon, muscle, bone
and eye manifestations
Patients have major sleep disturbances,
concentration and memory blocks, panic,
anxiety, depression, hearing loss, shortness
of breath, persistent headache or pressure.
Chronic Lyme Disease Expressed as one
of two conditions: autoimmune with
debilitating joint pain (wheelchair) or
neuroborreliosis.
Because of the very slow division of the
spirochete 10-14 days of antibiotics for other
bacteria would take 1 years. Controversy
over treating with antibiotics for years.