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Transcript
Characteristics of Bacteria

Virulence- the degree of pathogenicity; depends on the presence of certain cell
structures and on bacterial exo and endotoxins.

Flagella- protein filaments that extend like long tail from the cell membranes of
some bacteria. The flagella can facilitate movement toward or away from a
chemical concentration gradient in a process called chemotaxis.

Pili- straight filaments arising from the bacterial cell wall. They are shorter than
flagella and do not move. They can serve as adherence factors (adhesins), which
may enhance the bacteria’s ability to cause disease.

Capsules- protective walls that surround the cell membranes of some bacteria.
They are typically composed of simple sugar residues. The bacteria secrete the
sugar substances, which then coat the inner cell wall. Capsules “protect” the
bacteria from phagocytization by macrophages and neutrophils.
o
Tests used to visualize capsules
 India ink stain- the stain is not taken up by the capsule and thus
appears as a transparent halo around the cell.





Quellung reaction- bacteria are mixed with antibodies that bind to
the capsule. When the antibodies bind, the capsule swells to an
observable size.
Endospores- formed only by two genera: aerobic Bacillus and anaerobic
Clostridium.
Endospores are metabolically dormant forms of bacteria that are resistant to heat,
cold, drying, and chemical agents. They are formed when there is a shortage of
needed nutrients; they can lie dormant for years.
Biofilm- extracellular polysaccharide network that forms a “bandage” around
bacteria. The biofilm allows bacteria to bind to medical devices (like IV
catheters), and it protects them from attack by antibodies and the immune system.
Ex. Staphylococcus epidermidis tends to form biofilms on IV catheters and can
cause sepsis.
Exotoxins- proteins released by both Gram + and Gram – bacteria.
o Neurotoxins- exotoxins that act on the nerves or motor endplates to cause
paralysis. Examples: tetanus and botulinum toxins
o Enterotoxins- exotoxins that act on the GI tract to cause diarrhea.
Enterotoxins inhibit sodium chloride resorption, activate NaCl secretion,
or kill intestinal epithelial cells. The end result is the osmotic pull of fluid
into the intestines.

Effects of enterotoxins
 Infectious diarrhea- bacteria colonize and bind to the GI
tract. The diarrhea will continue until the bacteria are
destroyed by the immune system or antibiotics. Examples
include Vibrio cholera, Escherichia coli, Campylobacter
jejuni, and Shigella dysenteriae.

Food poisoning- bacteria grow in food and release
enterotoxins in the food. The diarrhea and vomiting is
usually short-lived (<24 hours). Examples include Bacillus
cereus and Staphylococcus aureus.
o Pyrogenic exotoxins- stimulate the release of cytokines and can cause
rash, fever, and toxic shock syndrome. Examples include S. aureus and
Streptococcus pyogenes.
o Tissue invasive exotoxins- allow bacteria to destroy and tunnel through
tissues. This includes enzymes that destroy DNA, collagen, fibrin, NAD,
red blood cells, and white blood cells.

Endotoxins
An endotoxin is lipid A, which is a piece of the outer membrane
lipopolysaccharide of Gram – bacteria. Lipid A/endotoxin is very toxic and is
released when the bacterial cell undergoes lysis. Endotoxins are also shed in small
amounts from living bacteria.
o Administering antibiotics to a patient with a Gram – infection may worsen
the person’s condition because all of the bacteria will be lysed, releasing
large quantities of endotoxin.
o Unlike exotoxin, endotoxin is a normal part of the outer portion of the
bacteria that sheds off.

Septic shock- a common and deadly response to both Gram- and
Gram + bacterial infections. Septic shock is a leading cause of
death in ICU units.

Bacteremia- by definition, bacteria in the bloodstream. The
bacteria can be detected by isolating the bacteria in blood cultures.
Brushing your teeth causes bacteremia with few effects. However,
bacteremia can progress to sepsis.

Sepsis- bacteremia that causes a systemic immune response to the
infection. Symptoms may include a fever, elevated white blood
cell county, and rapid heart rate.

Septic shock- sepsis that results in dangerous drops in blood
pressure and organ dysfunction. Bacteremia from a localized
infection may release toxins that circulate in the bloodstream and
stimulate immune cells. The immune cells release proteins, such as
tumor necrosis factor (TNF).

Septic shock can be fatal (>40%). Mortality rises with
every organ system that fails.
The table below lists the possible effects of septic shock on various organ systems.
System
Vascular
Effect
Vasodilation
Result
Decreased blood pressure
Heart
Myocardial depression
Kidneys
Acute renal failure
Liver
Hepatic failure
Brain
Coagulation system
Encephalopathy
Disseminated intravascular
coagulation
Decreased cardiac output,
decreased blood pressure
Decreased urine output,
accumulation of toxins
Accumulation of metabolic
toxins; hepatic
encephalopathy
Alteration in mental status
Clotting, bleeding
Effects of specific toxins
Clostridium tetanus produces the tetanus toxin, which causes uncontrolled muscle
contractions with lockjaw and tetanic paralysis of respiratory muscles.
C botulinum produces botulinum toxin, which causes paralysis with respiratory muscle
paralysis. Botulinum toxin is the most potent exotoxin.
Streptococcus pyogenes produces pyrogenic toxin, which activates the mediators of
sepsis and can result in scarlet fever.
Staphylococcus aureus- toxic shock syndrome toxin. May produce symptoms such as
fever, rash, diarrhea, and shock.