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Host-Microbe Interactions
Chapter 19
19.1 Anatomical Barriers As
Ecosystems
Some bacteria have symbiotic relationships with
their hosts
Mutualism - both benefit (K and B vitamins)
Commensalism - bacteria benefit with no harm
to the host
Parasitism - microbe grows at the expense of
the host
19.2 Normal Flora
The normal flora are those bacteria that are
commonly found on/in the body of a healthy
host
Many play critical protective roles for the host
Staphylococcus aureus and scalded skin
syndrome
Clostridium difficile and aggressive antibiotic
therapy
19.3 Principles of Infectious Disease
Infection - usually parasitic colonization by a
microbe
Clinical manifestations
Subclinical (apathogenic) - none apparent
Clinical (pathogenic) - symptoms of disease
Course of infection
Primary - disease caused by the initial infection
Secondary - because of the initial infection,
another microbe can establish an infection
Example: Influenza virus infection can be followed
by Klebsiella pneumoniae pneumonia
19.3 Principles of Infectious Disease
Pathogenicity
The capacity for a microbe to cause disease
Some microbes are primary pathogens and
usually cause disease after colonization
Others are opportunistic pathogens and cause
disease only in conjunction with some other
unusual event
Immunocompromised status
Compromised normal flora
19.3 Principles of Infectious Disease
Characteristics of infectious disease
Communicable or contagious diseases are readily
transmitted person to person (e.g., influenza, measles,
pertussis
Other diseases are not contagious (including West Nile
virus, anthrax) since they are not transmitted person to
person
Infection is also a function of quantity of microbes
The infectious dose is expressed as ID50
The ID50 for a microbe is the number of bacteria or viruses
needed to infect 50 of 100 people given the dose
This number varies among pathogens (anthrax = 10,000)
Incubation period - no symptoms
19.3
Principles
of
Infectious
Disease
Illness - phase of disease
Convalescence - recovery from disease
Some people can be carriers for some infectious
agents (”Typhoid Mary”)
Duration of Symptoms
Acute - rapid onset, short duration
Chronic - slow onset, long duration
Latent - agent is never eliminated
Recrudescence is the recurrence of a latent viral infection
19.3 Principles of Infectious Disease
Distribution of the pathogen
Most are localized to a specific tissue
Others can be systemic
Some localized infections can become
systemic; often a poor prognostic indicator
Microbes and their products in the blood
Bacteremia - bacteria in blood
Viremia - virus in the blood
Toxemia - toxins in the blood
Septicemia - life-threatening; bacteria
replicating in the blood
19.4 Establishing the Cause of
Infectious Disease
Koch’s postulates of infectious disease
etiology
The microbe must be present in every
instance of the disease
The microbe must be isolated and cultured
from a diseased animal
Introduction of the microbe into a
susceptible animal must result in the
disease
The microbe must be reisolated from the
animal
19.4 Establishing the Cause of
Infectious Disease
Molecular postulates of infectious disease
etiology
The virulence factor or gene(s) must be
detected in pathogenic members of a species,
but not nonpathogenic members
Introduction of the gene(s) that encodes the
virulence factor into a nonpathogen must
convert the microbe into a pathogenic strain
The gene(s) must be expressed when
introduced into a susceptible animal
Antibodies or immune cells (e.g., Tc cells) must
protect the animal from the disease
19.4 Establishing the Cause of
Infectious Disease
The mechanisms of disease
Production of exotoxins that are ingested
Colonization of the host surface (skin or
mucosa), followed by exotoxin production
Invasion of host tissues
Invasion of host tissues, followed by
exotoxin production
19.5 Establishment of Infection
Adherence
Mediated by glycoproteins termed adhesins
Typically have specificity for host cell surface proteins
Colonization
Replication of bacteria at the site of adherence
Secretion of factors that impair the host response, such as IgA
proteases (enzymes that digest IgA dimers)
Expression of iron-binding molecules, termed siderophores
Delivery of effector molecules into host cells
Often virulence factors that damage the host cell
19.6 Invasion - Breaching the
Anatomical Barriers
Penetration of the skin
Cuts, abrasions, or burns
Vector (flea, mosquito)
Penetration of the mucous membranes
Directed uptake by cells
Exploitation of antigen sampling by immune cells
Dendritic cells
Macrophages
19.7 Avoiding the Host Defenses
Hiding within a host cell avoids antibodies
Avoiding killing by complement system proteins
Neisseria gonorrhoeae inactivates the C3b complement
protein
Avoiding destruction by phagocytes
Bacillus anthracis kills macrophages
Streptococcus pyogenes produces streptolysin O that
damages phagocytic cell membranes
Polysaccharide capsules are resistant to phagocytosis
Strep pyogenes (protein G) and Staph aureus (protein
A)secrete proteins that bind to Fc portions of antibodies,
thus neutralizing them
19.8 Damage to the Host
Exotoxins
Proteins secreted by various pathogenic bacteria
Can be local or systemic
Fatal in small amounts
1 gram of botulinum toxin is sufficient to kill the Earth’s
human population
Potent antigens, but exert their effect before antibodies
can be synthesized
A-B toxins - two parts; A is toxic, B dictates target
Membrane-damaging toxins - hemolysin disrupts RBC
membranes
Superantigens “trick” large numbers of helper T cells
into producing inflammatory cytokines
19.8 Damage to the Host
Endotoxins
Endotoxins are lipopolysaccharides (LPS)
Lipid A (toxic)
Polysaccharide
Normally found as outer cell membrane
component of Gram- bacteria
Bind to Toll-like receptors on phagocytic cells,
which results in the release of tumor necrosis
factor from the cells
TNF causes capillary leakage and inflammation
This can lead to hypotension and disseminated
intravascular coagulation - aka, septic shock
19.9 Mechanisms of Viral
Pathogenesis
Viruses do not encode toxins
Their principal cause of damage is death of the cell
In some viral infections, the immune response is so
aggressive that it causes immunopathology
Many viruses encode immune-modulating proteins
that subvert the immune response
Shut down MHC class I processing and presentation
Impair the interferon pathway
Viral cytokines
Interference with apoptosis (death signals from T and NK cells)