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Chapter 30
Pathogenicity of Microorganisms
Symbiosis
the “living together” of two organisms in a variety of
relationships
Host-Parasitecommensalism
Relationships
mutualism
parasitism
Saprophytic organisms
obtain nutrients from dead or decaying organic matter
some are pathogenic but most are considered scavengers
Parasites
Parasites are organisms that live on or within a host organism
and are metabolically dependent on the host
types of parasites
ectoparasite
lives on surface of host
endoparasite
lives within host
Types of Hosts
Final host
host on (or in) which parasite either gains sexual maturity or
reproduces
Intermediate host
serves as temporary but essential environment for some stage of
parasite’s development
Transfer host
is not necessary for development but serves as vehicle for reaching
final host
Reservoir host
nonhuman organism infected with a parasite that can also infect
humans
Parasitism and Disease
Infection
growth and multiplication of parasite on or within host
Infectious disease
disease resulting from infection
Pathogen
any parasitic organism that causes infectious disease
Primary (frank) pathogen – causes disease by direct interaction with
healthy host
Opportunistic pathogen – part of normal flora and causes disease when
it has gained access to other tissue sites or host is
immunocompromised
Pathogenicity
ability of parasite to cause disease
Factors Impacting Outcome of
Host-Parasite Relationships
Factors:
number of organisms present
the degree of virulence of pathogen
virulence factors
e.g., capsules, pili, toxins
host’s defenses or degree of resistance
Table 30.1
Figure 30.1 Mathematical Expression of Infection
Virulence
Virulence:
degree or intensity of pathogenicity
determined by three characteristics of the pathogen
invasiveness
ability to spread to adjacent tissues
infectivity
ability to establish focal point of infection
pathogenic potential
degree to which pathogen can cause damage to host
Aspects of Pathogenic Potential
Toxigenicity
ability to produce toxins
Immunopathology
ability to trigger exaggerated immune responses
Measuring Virulence
Lethal dose 50 (LD50)
number of pathogens that will kill 50% of an experimental
group of hosts in a specified time
Infectious dose 50 (ID50)
number of pathogens that will infect 50% of an experimental
group of hosts in a specified time
Figure 30.2:Determination of LD 50
Strain A LD is 30, B LD is 50 hence, A is more virulent.
Pathogenesis of Viral Diseases
Fundamental process of Viral infection in a host cell:
maintain reservoir –a place to live and multiply before
infection
enter host
contact and enter susceptible cells
replicate within cells
release from host (immediate or delayed)
…Viral infection
spread to adjacent cells
Evade host immune response
be cleared from body of host, establish persistent
infection, or kill host
be shed back into environment
Maintaining a Reservoir
most common reservoir of human viruses are humans
and other animals
some viruses are acquired early in host’s life and cause
disease later
most often, viruses are transmitted from one host to
another host and cause infection in a short time frame
Viral Entry
Occurs at a variety of sites:
via body surface
via sexual contact, needle sticks, blood
transfusions, and organ transplants
via insect vectors
organisms that transmit pathogen from one
host to another
Adsorption
Adsorption
attachment to the cell surface
results from binding of viral protein to host cell
receptors
binding of virus to receptor results in cell penetration
or delivery of viral nucleic acid to host cell cytoplasm
Entry of Human Virus Nucleic Acids
into Host Cell
Direct entry of nucleic acid
e.g., polio virus- enters the host cell and deliver viral nucleic acid into the cytoplasm
of cell
It enters through the human gastrointestinal tract but produces diseases in the
central nervous system. endocytosis and release of nucleic acid from capsid
(uncoating)
e.g., pox viruses- causes small pox
Fusion of viral envelope
e.g. influenza –fusion of viral envelope with cell membrane of host
Primary Replication
Primary replication
some replicate at site of entry, cause disease at
same site, and do not spread throughout body
others spread to distant sites and then replicate
e.g., polio viruses enter through gastrointestinal tract
but produce disease in central nervous system
Evasion of Host Defenses
begins when the virus first infects the host
for the virus to cause a successful infection, it
must be able to avoid host immunity so it can
spread to a sufficient number of host cells to
amplify the number of virions
Viral Spread and Cell Tropism
Viral spread vary but most common is by
bloodstream and lymphatic system
Viremia- presence of virus in blood
Spread by way of nerves e.g rabies
Tropisms
Viruses exhibit cell, tissue, and organ specificities
Virus-Host Interactions
Cytopathic viruses
local necrosis with ultimate host death
alternatively, can trigger apoptosis (programmed cell death)
i.e host cell dies, often before viral replication can occur
Noncytopathic viruses
cause latent or persistent infections
…Non-Cytopathic Viruses
Do not immediately cause cell death
cause latent or persistent infections
productive non-cytopathic viruses
produce persistent infection with the release of only a few new
particles at a time
nonproductive non-cytopathic viruses
do not actively make virus at detectable levels for a period of
time (latent infection)
these viruses may become productive by environmental
stressors or other factors
Other Outcomes of Virus-Host
Interaction
Clinical illness
some tissues can be quickly repaired after viral damage
e.g., intestinal epithelium
others cannot be easily repaired
e.g., tissues of central nervous system
Integration of viral DNA
may result in transformation of host cells into cancerous cells due
to viral DNA interference with host DNA growth cycle regulation
…Virus Shedding
last step in infectious process is shedding of the
virus in the environment
needed for maintenance of viral source in a host
population
often occurs at same body surface used for
entry of the virus
at this stage host is very
contagious/infectious/stay far…..can spread
in some infections, host is dead (end of host)
and no shedding occurs-e.g Rabies
Maintain a reservoir
Like viral infection Bacteria too need a place to live
Pathogenesis
of
Bacterial
before and after causing infection
Diseases
initial transport
to/entry into host
adhere to, colonize, and/or invade host
…Bacterial infection
initially evade host defenses
multiply or complete life cycles
on or in host
damage host
Maintaining a Reservoir of the
Bacterial Pathogen
For human pathogens, most common reservoirs
are:
other humans
animals
environment
Transport of the Bacterial
Pathogen to the Host
Direct contact
e.g., coughing, sneezing, body contact
Indirect contact
vehicles (e.g., soil, water, food)
arthropod vectors
fomites – inanimate objects that harbor and
transmit pathogens
Attachment and Colonization by the
Bacterial Pathogen
Adherence structures:
Structures such as such as pili and fimbriae and specialized
adhesion molecules on bacterium’s cell surface bind to
complementary receptor sites on host cell surface
Colonization:
Colonization is the establishment of a site of microbial
reproduction on or within host
does not necessarily result in tissue invasion or damage
Evasion of Host Defenses by
Bacteria
Successful pathogens can evade destruction by
host :
by:
Formation of capsule- Neisseria gonorrhoeae
production of leukocidins- substance that destroy
phagocytes before phagocytosis can occur –
Streptoccocus pneumoniae, Staphyloccocus
Endotoxins
Table 30.4-Bacterium polymerised host actin into long tail and
for propulsion from one cell to another and out of the host.
Bacterial Invasiveness
Varies among pathogens
e.g., Clostridium tetani (tetanus) produces a
number of virulence factors (e.g toxin and
proteolytic enzymes ) but is non-invasive i.e it
does not spread from one tissue to another.
e.g., Bacillus anthracis (anthrax) and Yersinia
pestis (plague) also produce many virulence
Growth and Multiplication of the
Bacterial Pathogen
occurs when pathogen finds
appropriate environment within host
some pathogens actively grow in
blood plasma
bacteremia – presence of viable
bacteria in blood
Bacteria that are able to grow and multiply in various
cells of a host
Facultative intracellular pathogens
Intracellular
Pathogens
can live within host cells or in the environment
e.g., Brucella abortus can grow independently as well as in
macrophages, neutrophils and trophoblast cells
Obligate intracellular pathogens
incapable of growth and multiplication outside of a host
eg., viruses and rickettsia
Leaving the Host
must occur if microbe is to be
perpetuated
most bacteria leave by passive
mechanisms
in feces, urine, droplets, saliva
Regulation of Bacterial Virulence
Factor Expression
Often environmental factors control
expression of virulence genes
e.g., Corynebacterium diphtheriae
gene for diphtheria toxin regulated by iron
e.g., Bordetella pertussis
expression of virulence genes increased at body
temperature
e.g., Vibrio cholerae
Pathogenicity Islands
Pathogenicity Islands- large segments of
DNA that carry virulence genes
acquired during evolution of pathogen by
horizontal gene transfer
e.g., genes for type III secretion system
(TTSS)
enables gram-negative bacteria to secrete and
Toxigenicity
Intoxications
diseases that result from entry of a specific preformed
toxin into host
Toxin
specific substance that damages host
two main categories in bacteria
exotoxins
endotoxins
Exotoxins - soluble, heat-labile, proteins and usually released
into the surroundings as bacterial pathogen grows
humans exposed to exotoxins in three main ways
Exotoxins
ingestion of preformed exotoxin
bacterial colonization of a mucosal surface followed by exotoxin
production
colonization of a wound or abscess followed by local exotoxin production
most exotoxin producers are gram-positive
often travel from site of infection to other tissues or cells
where they exert their effects
Types of Exotoxins
AB exotoxins- composed of two
subunits
A subunit – responsible for toxic effect
once inside the host cell
B subunit – binds to target cell od host
specific host site exotoxins-e.g
AB Exotoxins
Composed of two subunits
A subunit – responsible for toxic effect
once inside the host cell
B subunit – binds to target cell
Specific Host Site Exotoxins
can be AB toxins
neurotoxins
target nerve tissue
e.g., botulinum toxin
enterotoxins
target intestinal mucosa
e.g., cholera toxin
cytotoxins
target general tissues
e.g., nephrotoxin
Membrane-Disrupting Exotoxins
do not have separable A and B subunits
two types
pore-forming exotoxins
Phospholipases-lyses the plasma membrane e.gClostridium perfringens-gas gagresn
Some Pore-Forming Exotoxins
Bacterial Toxins that forms pores in the
membranes:
Leukocidins –membrane-disrupting toxins
kill phagocytic leukocytes- pneumococci.
Strepto, staphyloccus
Hemolysins- other toxin that form pores in
membranes of blood cells
Hemolytic Reactions
beta-hemolysis
complete lysis
observed as zone of clearing around
colony on blood agar
alpha-hemolysis
partial lysis
Phospholipase Enzymes
Phospholipase Enzymes a second
subtype of membrane-disrupting
toxins
remove charged head group from
lipid part of phospholipids in hostcell plasma membranes
Endotoxins
Lipopolysaccharide (LPS) in gram-negative
outer membrane can be toxic to specific
hosts
called endotoxin because it is bound to
bacterium and released when organism lyses
and some is also released during
multiplication
Polymicrobial Diseases
Polymicrobial Diseases -many
infectious diseases involve the
interactions of more than one
infectious agent
these diseases can be polyviral,
polybacterial, combined viral-bacterial,
or polymycotic or protozoan
Dental Infections
Dental Infections -caused by various
odontopathogens
Formation of dental plaque creates
environment for pathogens that
produce acids and other virulence
factors
Figure 30.9: Plaque Development Process
Figure 30.11-Microscopic Appearance of Plaque
Periodontal Disease…
Periodontitis
initial inflammatory response to plaque bacteria and tissue
destruction
leads to swelling of tissue and formation of periodontal
pockets
Periodontosis
bone destruction caused by colonization of periodontal
pockets
Periodontal Disease…
Gingivitis
inflammation of gingiva caused by colonization of
periodontal pockets
Treatment, prevention, and control
oral surgery and antibiotic therapy in some cases
plaque removal and good dental hygiene
Bibliography
• Lecture PowerPoints Prescott’s Principles
of Microbiology-Mc Graw Hill Co.
• http://en.wikipedia.org/wiki/Scientific_
method
• https://files.kennesaw.edu/faculty/jhend
rix/bio3340/home.html