Mechanisms of Bacterial Pathogenesis

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Transcript Mechanisms of Bacterial Pathogenesis

Medical Microbiology
Chapter 19
Mechanisms of Bacterial
Pathogenesis
Terms
Pathology – study of disease
 Etiology – cause of disease
 Pathogenesis – manner in which a
disease develops
 Infection – invasion or colonization of
the body by pathogenic microorganisms
 Disease – change from a state of health

Diseases


How are diseases catagorized?
Spread:
– Communicable
– Contagious
– Noncommunicable

Categorization according to how often they
occur in a given location:
– endemic - constantly present
– epidemic - disease occurring in excess of normal
expectancy
– Pandemic - worldwide epidemic
Disease

Severity or duration:
– Acute
– Chronic
– Latent

Extent of infection:
– Local infection
– Systemic infection
– Bacteremia, septicemia, toxemia, viremia
Disease
Primary infection vs. secondary
infection
 Subclinical infection

Spread of Disease


Etiology or etiological agent - cause of a disease
Reservoir - continual source of pathogens
– human, animal, non-living

Mechanisms of Transmission:
– contact transmission - from one person to
another person
direct
 indirect (through a fomite)
 droplet (sneezing, coughing and talking)

Spread of Disease (cont.)
– Vehicle Transmission - transmission of disease
by a medium

water, food, air
– Vector Transmission - transmission of disease
by an insect

Nosocomial infections
Epidemiology

Epidemiology is the study of the
frequency and distribution of disease
– Examples
The CDC

The Centers for Disease Control and
Prevention (CDC) is the nation’s center
for epidemiology
– The CDC tracks some 50 infectious diseases
nationwide
– they help county and state agencies during
epidemics
– The CDC publishes a weekly newsletter
called Morbitity and Mortality Weekly
Virulence Factors

Successful pathogens have a variety of factors
that contribute to their ability to cause disease
– these are called virulence factors
Mechanisms of Pathogenesis

Successful pathogens carry out a
sequence of events:
– transmission to a susceptible host
– gain access to the host
– adherence to the target tissue
– colonization and sometimes invasion
– damage to the host
– exit from the host
– transmission to a new host
Mechanisms of Pathogenesis

Transmission
– Contact, vehicle, vector, etc.

Access – Portals of Entry
– Mucous membranes
– Skin
– Parenteral Route – through damage to the
skin or mucous membranes
– Table 19.1
Adherence and Invasion

Adherence:
– Adhesins


Many are found on fimbriae
Table 19-2
– Capsules
– Biofilms

Invasion – some pathogens can cross the
mucous membranes
Colonization

Colonization – bacteria can evade the immune
system and replicate to cause disease.
– Antiphagocytic structures:
 Capsule – extremely important virulence factor
– They are also poorly antigenic (polysaccharides)
 Cell walls (mycobacteria)
– Intracellular growth
– Antigenic variation – changing of antigens
– Inactivation of antibodies or complement
Damage

Damage:
– Enzymes
– Toxins
– Inappropriate Immune Responses
 Exaggerated inflammation (endotoxin)
 Cross-reactive antibodies - strep throat and
rheumatic fever/glomerulonephritis
Enzymes

Enzymes are released from cells and
damage host tissues
– Leukocidins - kill white blood cells
– Hemolysins - cause the lysis of RBCs


b hemolysin - complete breakdown of RBCs
a hemolysin - incomplete breakdown of RBCs
– Streptokinase/Staphylokinase - breaks down
blood clots

How could this be related to virulence?
Enzymes (cont.)
– Coagulase - causes the formation of blood
clots
almost all pathogenic strains of S. aureus
produce this enzyme
 How does this contribute to virulence?

– Collagenase - breaks down collagen

produced by the clostridia that cause gas
gangrene
– Proteases, hyaluronidase, phospholipase C,
etc.
Endotoxin

What is endotoxin?
– the lipid A portion of lipopolysaccharide
(LPS)
Fever - elevated body temperature
 Vasodilation (leading to shock)
 Inflammation
 can even result in death

Exotoxins
These are substances released from
bacteria that damage host tissues.
 Cytotoxins - cause damage to cells
– Erythrogenic toxins – (S. pyogenes)

damage cells lining capillaries and cause
blood to leak out under the skin (scarlet
fever).
Exotoxins

Enterotoxins - cause damage to the
gastrointestinal tract
– diarrhea and vomiting
– Caused by electrolyte loss (resulting in
water loss into the large intestine)
Cholera and some E. coli infections
(traveler’s diarrhea) – Figure 19-3 B
 staphylococcal food poisoning

Exotoxins (cont.)
– Some enterotoxins also kill the cells lining the
intestines causing dysentery (bloody diarrhea)
 bacterial dysentery (Shigella) and E. coli
O157:H7 infections

Neurotoxins - inhibit the normal functioning
of the nervous system
– Tetanus toxin (Clostridium tetanii) blocks
inhibitory nerve impulses that allow muscles to
relax
 Lock Jaw
Exotoxins (cont.)
– Botulinum toxin (Clostridium botulinum) inhibits
the functioning of motor neurons causing
flaccid paralysis (muscles can’t contract)
– 1mg can kill 1,000,000 guinea pigs
– Figure 19-3 C

Table 19-3
Superantigens

Superantigens - toxins that stimulate nonspecific activation of T-cells
– These then release large amount of cytokines
leading to shock
– toxic shock syndrome is caused by a
superantigen produced by Staphylococcus
aureus
– can result in death
– Figure 19-4