Clinical Bacteriology – Lecture 08/22/23

Host Microorganism Interactions Prelims

OUTLINE
I. Encounter between Host A.3. Animals as Microbial NOSOCOMIAL INFECTION
and Microorganism Reservoirs • Hospital acquired infection
ANIMALS AS MICROBIAL RESERVOIRS
A. The Human Host’s A.4. Insects as Vectors • Animal bite (rabies)
Perspective • Insect vectors
A.5. Environment as a • Can contaminate food and water supply
A.1. Microbial Microbial Reservoir
• Animals used for human food carry numerous bacteria
Reservoirs and
Transmission
Zoonotic – infectious disease from animals
A.2. Humans as
Microbial Reservoirs INSECTS AS VECTORS
• Common role of insects
® Malaria (mosquito)
ENCOUNTER BETWEEN HOST AND MICROORGANISM ® Arthropods (lice and scabies)

Ectoparasites

ENVIRONMENT AS A MICROBIAL RESERVOIR

• Fungal infections
® Soil and natural environmental debris
® Acquired by inhalation to soil and dust particles
• Non-Fungal infections
® Penetrating wound

Figure 1. Summary of Microbial Reservoirs,

and Modes of Transmission to Humans.

MICROBIAL RESERVOIR AND TRANSMISSION

• Reservoir
® Environment, or place of origin of the infecting agent
• Modes of Transmission
® Various means by which the human host may acquire
microbial agents
• Vectors
® Agents of transmission that bring the microorganism from the
reservoir to the host that is a living entity
• Vehicle/Fomite Figure 2.
® Gents of transmission that bring the microorganism from the
reservoir to the host that is a nonliving entity MICROORGANISM COLONIZATION OF HOST SURFACES
A. Host’s Perspective
HUMANS AS MICROBIAL RESERVOIRS
• Colonization- persistent survival of microorganisms on a surface
• Newborns first encounter microbial agents
of the human body
• Acquisition of strep throat through touching
® Skin
• Coughing and common colds
® Mucous Membrane
• Hepatitis by blood transfusion Skin and Skin Structure
• STD by sexual contact
• Physical barrier
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• First defenses
• Skin
® Salt inhibits microbes
® Lysozyme hydrolyzes peptidoglycan
® Fatty acids inhibit some pathogens

Figure 3.

Protective Characteristics of the Skin and Skin Structures

Skin Structure Protective Activity

Outer layers Physical barrier
Sloughing of outer layer Figure 4.
Provide dry, acidic and cool condition that
limit bacterial growth B. Microbial Colonization
Hair follicles, Production of acid, alcohols, and toxic lipids • Commensal
sweat glands, ® Harmless relationship between a colonizer and human host
sebaceous glands
Conjunctival Flushing action of tears removes
epithelium microorganisms
covering the eyes Tears contains lysozyme that destroy
bacterial cell wall
Skin associated Mediate specific and nonspecific protection
lymphoid tissue mechanisms against microorganisms
Table 1.
Mucous Membrane

General Protective Specific Protective Characteristics

Characteristics
Figure 5.
Mucus – major Mouth- flow of saliva
protectice GIT- low pH & proteolytic enzyme
component of URT- nasal hair MICROORGANISM ENTRY, INVASION, AND DISSEMINATION
mucus membrane Female GUT- vaginal lining & ectocervic • The Host’s Perspective
Mucus associated ® Disruption of Surface Barriers
lymphoid tissue § Loss of Acidity of the stomach
Table 2. § Dryness of skin
® Accidental
® Intentional
® Responses to Microbial Invasion of Deeper Tissues
§ Non-Specific Responses
o Biochemical (remove essential nutrients like Iron)
o Cellular (phagocytes)
- Phagocytes: PMNs and macrophages
- Inflammation
Phagocytes
• Cells that ingest and destroy bacteria and other foreign particles
• 2 TYPES:
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 ® PMNs (Polymorphonuclear leukocytes) Complement Attracts phagocytes to site of infection
® Macrophages System Helps phagocytes recognize and bind to
(coordinated bacteria
INGESTION PHASE OF PHAGOCYTOSIS group of serum Directly kills gram-negative bacteria
proteins)
Coagulation Attracts phagocytes to site of infection
System (wide Increases blood and fluid flow to site of
variety of proteins infection
and other Walls of site of infection to physically inhibit
biologically active spread of microorganisms
compounds)
Cytokines Multiple effects that enhance the activities
(proteins secreted of many different cells essential to
by macrophages nonspecific and specific defensive
Figure 6. and other cells) responses
Table 3.
• Polymorphonuclear leukocytes
® Develop in the bone marrow (short lives- a day or less) MANIFESTATION OF INFLAMMATION
® Circulating in blood and tissues • Swelling- caused by increased flow of fluid and cells to the affected
® 1st cells on the scene of bacterial invasion body sites
• Redness- result in vasodilation of blood vessel at the infection site
• Heat- results from increased temperature of affected tissue
• Pain- due to tissue damage and pressure from increased flow of
fluid cells

Figure 7.

• Macrophages
® Also develop in the bone marrow but first to go through
cellular phase when they are called monocytes
® Reside in specific organs (spleen, lymph nodes, liver or lungs) Figure 8. Purposes of Inflammation.
® Live for days or several weeks awaiting encounters with
invading bacteria § Specific Responses- The Immune System
® Important role in mediating immune system defenses o Immune System
- Provide human host with the ability to mount
CELLULAR ELEMENTS OF HUMAN BLOOD specific protective response to the presence of
Inflammation microorganism
• Role: - Has ‘memory’ so that if microorganism is
encountered a second or third time, an immune
® Reinforcement mechanism
mediated defensive response is immediately
® Proliferation in tissues and organs
available
• Components of Inflammation o Components of the Immune System
® Complement System - Antibody: central molecule, also referred as
® Phagocyte immunoglobulin, circulate in the serum portion of
® Coagulation System the host’s blood, present in secretion (saliva)
® Cytokines - 2 active sites: Antigen binding site and
Phagocyte binding site
Component Functions - 5 different classes of Antibody: IgG, IgA, IgM,
Phagocytes Ingest and destroy microorganisms IgD, IgE
(PMNs and o Two Arms of the Immune System
Macrophages) - Antibody-mediated immunity (humoral immunity)
- Cell-mediated immunity (cellular immunity)
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 ® Mast cells, basophils, in blood
® Half-life = 2 days
• IgG
® The class that only crosses the placenta
® 80% of serum antibodies
® Maternal IgG antibodies that cross the placenta help protect
the newborn during its first months of life
® Long lived, persisting for the life of individual
® Half-life = 23 days
• IgM
® First antibodies formed in the primaryresponse to antigens
(including pathogens)
® Short lived, remaining in the blood stream for only a few
Figure 9. 2 Major Arms of Immune System. months
® Provides protection in the earliest stages of infection
® Bactericidal to Gram (-) bacteria
® 5-10% of serum antibodies
® Agglutinates microbes; first Ab produced in response to
infection
® Half-life = 5 days

Figure 10. Lines of Defense.

Antibodies protect the host in the number of ways:

• Helping phagocyte ingest and kill microorganisms
• Neutralize microbial toxins
• Promoting bacterial clumping (agglutination)
• Inhibiting bacterial motility
• Combining with microorganisms to activate the complement
system and inflammatory response
Figure 11. Basic Structure of a Monomeric Immunoglobulin Molecule.

5 DIFFERENT CLASSES OF ANTIBODY

• IgA
® Predominant immunoglobulin class (saliva, tears, seminal
fluid, colostrum, breast milk, and mucous secretions of the
nose, lungs, and gastrointestinal tract)
® 10-15% of serum antibodies
® Secretions
® Mucosal protection
® Half-life = 6 days
• IgD
® Found in large quantities on the surface of B cells and lymph
® Function: unknown
Figure 12. Antibodies recognize and react with antigenic determinants or epitopes.
® 0.2% of serum antibodies
® On B cells, initiate immune response Microbial Strategies for Surviving Inflammation
® Half-life: 3 days
• IgE Avoid Killing by Phagocytes Avoid Effects of the
® Produced in response to allergens; lysis of parasitic worms (Polymorphonuclear Complement System
® Plays a major role in allergic responses Lymphocytes)
® 0.002% of serum antibodies
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 Inhibit ability of phagocyte to Use capsule to hide surface Being resistant to destructive Produce substances that
ingest by producing capsule mlecules that would agents (lysozyme destroy specific
Avoid phagocyte-mediated killing otherwise activate the ) released by lysoosmes complement proteins
by: complement system Actively and rapidly multiplying
Inhibiting phagosome-lysosome Produce substances that within phagocyte
fusion inhibit the processes Releasing toxins and enzymes
Being resistant to destructive involved in complement that damage or kill phagocyte
agents (lysozyme activation Table 5.
) released by lysoosmes Produce substances that
Actively and rapidly multiplying destroy specific • Survival Against the Immune System
within phagocyte complement proteins Microbial Strategies for Surviving the Immune System
Releasing toxins and enzymes • Pathogen multiplies and invades so quickly that damage to
that damage or kill phagocyte host is complete before immune response can be fully
Table 4. activated, or organism’s virulence is so great that the immune
response is insufficient
THE MICROORGANISM’S PERSPECTIVE • Pathogen invades and destroys cells involved in the immune
COLONIZATION AND INFECTION response
• Pathogen survives, unrecognized, in host cells and avoids
• Infection
detection by immune system
® Multiplication of microorganisms that result in damage to the
• Pathogen covers its antigens with a capsule so that an
host
immune response is not activated
• Disease
• Pathogen changes antigens so that immune system is
® Result when infection produces notable changes in human constantly fighting a primary encounter (the memory of the
physiology that are often associated to one or more of the immune system is neutralized)
body’s organ system
• Pathogen produces enzymes (proteases) that directly destroy
or inactivate antibodies
PATHOGEN AND VIRULENCE Table 6.
• Pathogen
® Microorganisms that cause infections and/or disease and the • Microbial Toxins
characteristics that enable them to cause disease are ® Toxins – biochemically active substances that are released
referred to as virulence factors by microorganisms and have a particular effect on host cells
• Opportunistic pathogens ® Intoxications – ingestion of performed bacterial toxins
® Organisms that only cause infections when one or more of
the host’s defense mechanisms are disrupted or malfunction

MICROBIAL VIRULENCE FACTORS

• Attachment
® First step of infection and disease development
(pathogenesis)
• Invasion
® Trauma
® Inhalation
® Implantation of medical devices
® Other diseases (malignancies, diabetes)
® Childbirth
® Overuse of antibiotics

• Survival Against Inflammation

Avoid Killing by Phagocytes
(Polymorphonuclear
Lymphocytes)
Inhibit ability of phagocyte to
ingest by producing capsule
Avoid phagocyte-mediated killing
by:
Inhibiting phagosome-lysosome
fusion
Clinical Bacteriology – Lecture
Avoid Effects of the
Complement System
Use capsule to hide surface
mlecules that would
otherwise activate the
complement system
Produce substances that
inhibit the processes
involved in complement
activation
Host Microorganism Interactions
Figure 13. Two General Types of Bacterial Toxins.
GENETICS OF VIRULENCE: PATHOGENICITY ISLANDS
• Pathogenicity Islands (PAIs)
® Mobile genetic elements that contribute to the change and
spread of virulence factors among bacterial populations of a
variety of species
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 ® Virulence associated genes Example: elevated blood Subjective
® “Mobility” genes – integrases and transposases pressure, abnormal heart sounds,
abnormal pulse rate, abnormal
Outcome and Prevention of Infectious Diseases laboratory results
1. Acute infection – infectious process that develop quickly Example: aches or pains,
2. Chronic infection – develop and progress slowly ringing in the ears, blurred
3. Latent infection – silent phase (viruses); without noticeable vision, nausea, dizziness,
effects on the host etc.
§ Latent Infections Table 7.
o Infectious diseases that go from being symptomatic
to asymptomatic, and then, later, go back to being
symptomatic
o Examples: Syphilis and herpes virus infections such
as cold sores, genital herpes, shingles

Figure 16.

Figure 14.

Figure 17.

IMMUNIZATION
• Active
® Modified antigens from pathogenic microorganisms are
introduced into body and cause immune response
• Passive
® Antibodies against a particular pathogen have been in one
host and transferred to a second host
Figure 15. ® Example: maternal antibodies

EPIDEMIOLOGY
Signs Symptoms • Science that characterizes these aspects of infectious diseases
Defined as some type of objective Defined as some evidence and monitor the effect diseases have on a public health
evidence of a disease of a disease that is
experienced by the
patient
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