Sarah Reed

Microbiology 02

1. What are the different types of symbiosis? List and give a short definition for each.
Symbiosis is the living together of two or more species in an intimate relationship. There
are three types of symbiotic relationships: commensalism, mutualism, and parasitism. In
commensalism the symbiont benefit, while the host is unaffected. An example of com-
mensalism is barnacles attached to whales; the barnacles have a place to live and feed
and the whales are unaffected. Parasitism is a symbiotic relationship in which the host
is adversely affected. Ticks and other blood sucking insects feed, they benefit while ad-
versely effecting the host. Mutualism is the symbiotic relationship in which both the host
and the symbiont benefit. In many examples neither could survive without the other,
such as termites and the protozoa that live in their gut. The protozoa digest cellulose for
the termite, and the termite provides a ʻhomeʼ and nutrients for the protozoa.

2. What is a nosocomial infection?

A nosocomial infection is an infection that was not present or incubating at the time of
admission but was acquired as a result of treatment in a hospital, healthcare facility, or
clinical setting. The most common nosocomial infections are of the urinary and respira-
tory tracts, incision sites, and blood. Compromised patients are more susceptible to in-
fections from their normal flora or organisms introduced during invasive procedures.
The constant use of antimicrobial drugs in a hospital results in a higher concentration of
more virulent drug resistant organisms then would be found elsewhere. The infectious
agents are then passed down the chain of transmission to the patient.

3. Describe three of reservoirs of infection in humans.

The reservoir is the primary habitat from which a pathogen originates and serves as the
source from which individuals can acquire the infection. Non-living, or environmental,
reservoirs include soil, water and air harbor pathogens such Clostridium and Giardia.
Living reservoirs are either human or non-human animals that are the (often asympto-
matic) carriers; this results in the likelihood of the pathogen being permanently main-
tained in a population. Zoonotic infections are those that are passed from animals to
humans such as West Nile Virus, Influenza, or Malaria. Humans are the significant res-
ervoir in a number of communicable diseases.

4. Compare and contrast exotoxins and endotoxins with regard to their chemical nature,
source, effects on human body cells and resulting symptoms, and examples.
An exotoxin is secreted by a living bacterial cell, while an endotoxin is released (not se-
creted) after the cell is damaged or lysed.
 Endotoxin Exotoxin

Chemical Nature Lipopolysaccharide (LPS) Usually proteins

• Lipid A • Act Enzymatically
• Structural component of
outer membrane

Source Gram-negative Bacteria Gram-negative and Gram-

positive Bacteria, Fungi,
Algae, Protozoa

Effects on Body Cells Systemic, less specific action
• Elicit a variety of inflamma-
tory responses
Specific to cell type
• Block conduction of the
nerve impulse or synap-
tic transmission
• Damage cell membranes
causing cell to lyse
• Block or modify protein
synthesis
• Override the specificity of
immune response

Symptoms Fever, malaise, flu-like symp- Fever, nausea, vomiting,

toms, cough, headache and
respiratory distress, upper
respiratory infections, airway
inflammation, intravascular
coagulation, hypotension,
shock, sepsis
severe diarrhea, bloody
diarrhea, skin lesions,
rash, violent coughing,
muscle pain, hypotension,
paralysis

Examples Neisseria gonorrhoeae, Strep- Clostridium botulinum, Vi-

tococcus pyrogenes, Salmo- brio cholerae, Bacillus an-
nella, Shigella, Escherichia coli thracis, Staphylococcus
aureus

5. Humans have innate inborn resistance. What is meant by this?

Innate inborn resistance is present at birth, is non-specific, is not affected by prior con-
tact with the infectious agent, and is not mediated by lymphocytes. Innate resistance
includes first-line defenses (physical, chemical, and genetic barriers), cell communica-
tion (cytokines, surface receptors, adhesion molecules), sensor systems (toll-like recep-
tors, complement system), inflammation (and fever), interferons (response to viral infec-
tion), and phagocytes.

6. Describe at least three physical mechanisms that are part of the first line of defense.
The physical mechanisms of the first line of defense are the barriers that separate and
shield the interior of the body from the surrounding environment. These include the skin,
mucous membranes, and normal microbiota. Intact skin provides the most difficult bar-
rier for microbes to penetrate. The outer (dead) layers are composed of the hard, water-
repelling protein keratin and are constantly being sloughed off. he cells of the mucosa
are constantly bathed in mucous and other secretions that help to wash microbes from
the surface; this process is also sometimes aided mechanically by cilia. Normal flora
provide considerable protection from pathogens. One effect is that normal flora provides
competition for binding sites and nutrients. Another is that members of our normal flora
produce compounds that are toxic to other organisms; an example is Lactobacillus pro-
ducing an acidic pH in the vagina.

8. What are macrophages? How do they function?

A macrophage is a type of leukocyte whose purpose is to ingest cellular debris and
pathogens. They exist in nearly all tissues in the body. Macrophages originate as mono-
cytes that migrate into body tissues from the blood by diapedesis where they differenti-
ate depending on the type of cytokines the cell encounters. Macrophages play a key
role in the inflammatory response, elimination of pathogens, and initiation of the immune
response acting in both non-specific and specific defenses. In addition to ingesting cell
debris and foreign material, macrophages are antigen-presenting cells. After digesting a
pathogen, the antigens will be presented on the surface of the macrophage by MHC II
proteins stimulating other immune cells (such as T Helper Cells) to respond the patho-
gen.

9. Name all of the steps in phagocytosis.

Event

Activation and Phagocytes migrate to the area of invasion by inflamma-

Chemotaxis tory mediators such as pathogen factors, complement
proteins, chemokine, and cytokines.

Adhesion Phagocytes recognize and bind to pathogen-associated

molecular patterns (PAMPs)

Engulfment The phagocyte sends pseudopods out to surround and

Phagosome Formation engulf the pathogen and places it in a vesicle called a
phagosome

Digestion and Phagoly- Inside the phagocyte, lysosomes containing digestive

sosome Formation enzymes, microbicidal chemicals, and oxidizing agents
produced by the golgi apparatus fuse with the phago-
some producing a phagolysosome

Residual Body and The phagolysosome containing the undigestible mate-

Discharge rial, now termed the residual body, is discharged from
the phagocyte via exocytosis
10. Explain how each of the following avoids being killed by phagocytes:
Avoiding Phagocytosis

Streptococcus pneumonaiae • Polysaccharide capsules resist engulfment

• Inactivates complement components
• Leukocidins which kill phagocytes

Mycobacterium tuberculosis • Survives inside phagocytes

• Survives inside phagolysosome because of waxy,
hydrophobic cell wall containing mycolic acid which
are not easily attacked by lysosomal enzymes
• Inhibit the fusion of the phagosome with the lyso-
some
• “Hide” inside non-phagocytic host cells
• Killing phagocytes after ingestion
• Reduce interleukin response

Streptococcus pyogenes • Leukocidins which kill phagocytes

• Peptidase which inhibits chemotaxis by degrading
the chemoattractant that recruits phagocytes
• Polysaccharide capsule and M protein that resists
engulfment

Shigella dysenteria • Survives inside phagocytes,

• Lyses the phagosome then replicate in their cyto-
plasm,
• induces apoptosis (programmed cell death) in
macrophages

11. Describe the cell morphology, colors, and percentage of the total white blood cell
count for each type of white blood cell that would be distinguished by a hematologist
analyzing a stained blood smear.
Leukocytes Percent Blood Smear: Appearance
(%)
>1% of Blood Volume

Basophil 0.5% 9-10 µm in diameter; a granular leukocyte; with

an irregularly shaped (bi- or tri-lobed), pale-
staining nucleus; cytoplasm contains many
coarse bluish-black granules of variable size.
 Leukocytes Percent Blood Smear: Appearance
(%)
>1% of Blood Volume

Neutrophil 55%-90% 12-15 µm in diameter; a granular leukocyte; the

dark blue nucleus is divided into 2-5 lobes; the
cytoplasm is virtually transparent containing fine
pink-purple granules.

Eosinophil 1%-3% 12-15 µm in diameter; a granular leukocyte; gen-

erally bi-lobed nucleus; cytoplasm contains large,
coarse red-orange granules

Monocyte 3%-7% 16-20 µm in diameter (largest of the WBCs); an

agranular irregularly shaped leukocyte; large,
(Macrophages, Den-
kidney or horseshoe shaped, wrinkled nucleus;
dritic Cells)
blue-grey cytoplasm that contains many vacu-
oles

Lymphocyte 20%-35% 8-10 µm in diameter; an agranular leukocyte;

large, smooth, rounded, dark blue nucleus; pale-
(Natural Killer Cells,
blue to clear cytoplasm (NKCs, B-Cells, and T-
T-Cells, B-Cells)
Cells are indistinguishable in a blood smear)

12. List all components of the third line of defense and how they function.
The key cells of the third line of defense are T and B lymphocytes. T-cells respond to
MHC molecules. Helper T Cells bind to MHC Class II molecules whereas Cytotoxic T
Cells bind to MHC I molecules on antigen presenting cells. One fragment of any patho-
gen antigen will be presented by MHC molecules to our T cells, generating an immune
response. B-cells produce antibodies that recognize and respond to particular microbes
and antigens. Interaction between lymphocytes and antigens produce effector cells
(short lived, combat the antigen) and memory cells (long-lived). Immunological memory,
the ability to generate a secondary immune response, is an important component of the
third line of defense. The ability to recognize self verses non-self is the immune systems
ability to not attack their own body cells.

13. List the steps of APC MHC II presentation of foreign antigens.

Major Histocompatibility Complex
(MHC) II Presentation

The pathogen is phagocytized The antigen presenting cell engulfs the patho-
gen

The pathogen is digested A phagolysosome is formed and the antigen is

digested into fragments
 Major Histocompatibility Complex
(MHC) II Presentation

MHC picks up antigenic fragments The endoplasmic reticulum produces Class II

MHC proteins which bind to the antigenic
fragments inside of the phagolysosome

Displayed on Plasma membrane The vesicle containing the antigenic fragment

and MHC proteins moves through the golgi
apparatus to the plasma membrane and the
complex is displayed at the cell surface where
they interact with T helper cells

14. List the steps of MHC I presentation of foreign antigens.

Major Histocompatibility
Complex
(MHC) I Presentation

Viral/Bacterial Infection The antigen presenting cell is infected by a patho-

gen

MHC picks up abnormal The bacterial/viral peptides are transported to the

peptides endoplasmic reticulum where they are incorporated
to the MHC protein

Displayed on Plasma mem- The vesicle containing the abnormal peptides and
brane MHC proteins moves through the golgi apparatus to
the plasma membrane and the complex is dis-
played at the cell surface for the cytotoxic T cells

15. Discuss the basic structure of the antibody molecule.

All antibodies are large glycoproteins that have a similar structure consisting of two
heavy chains (high molecular weight polypeptide chains) and two light chains (lower
molecular weight polypeptide chains) joined by disulfide bonds creating a Y-shaped
molecule. Each chain consists of a variable region (the antigen binding sites) connected
to a constant region (binding site for cells) at hinge regions.

16. What are the steps involved in B cell activation.

Humoral Immunity

Antigen Binding B cell receptor binds to a specific antigen

antigen. Once a B cell encounters its specific
antigen it engulfs it
 Humoral Immunity

Antigen Presentation MCH Class II complexes move the engulfed an-

tigen to the surface of the B-cell

B-Cell Cooperation/Recognition T-helper cells that bear receptors for the antigen
from the same microbe interacts and binds with
the b-cell

Activation T-cells give off signals (interleukins and b-cell

growth factors) that activate the b-cell

Clonal Expansion The activated b-cell divides producing plasma

cells and memory cells (long-term cells that can
react to the same antigen in the future)

Antibody Synthesis Plasma cells are short lived cells that synthesize
and release antibodies

17. Describe the mechanisms of action of antibodies.

The mechanisms of action of antibodies are activation of complement, neutralization,
agglutination and precipitation, opsonization, and direct killing. The binding of an anti-
body to an antigen can trigger the the classical pathway of the complement cascade. In
neutralization, antibodies bind to the surface receptors on a virus or active site on bacte-
ria which prevents them from binding to host cells. Agglutination is the cross-linking of
bacterial cells by antibodies which renders them immobile and easier to phagocytize.
Precipitation is the rounding up of dispersed antigens for phagocytes. The process in
which pathogens are coated with specific antibodies so they will be easily recognized
and bound to phagocytes is called opsonization. In direct killing, when antibodies bind to
a pathogen it becomes a target for destruction by Natural Killer cells that attach to the
antibody and release compounds directly to the pathogen, killing it.

18. Describe the production of antibodies using the clonal selection theory.
The clonal selection theory describes an immunological process that determines which
anti-body producing cells (B and T lymphocytes) will be produced. Each lymphocyte has
a unique antibody on its surface which will connects to a specific antigen forming an
antigen-antibody complex. When an antigen is introduced a chemical change is trig-
gered and only the cells that make the appropriate antibody can bind with the antigen
activating the lymphocyte. Once the lymphocyte is activated, it rapidly multiplies creat-
ing effector cells (T and B cells) and memory cells.

19. A person has antibodies the measles virus. Identify three ways in which these anti
bodies could be acquired.
Three ways in which a person could acquire antibodies to the measles virus are passive
naturally acquired immunity, active naturally acquired immunity, and active induced im-
munity. An example or passive natural immunity is the transfer of a mother IgG measles
antibodies across the placenta, these antibodies offer the infant protection for the first
few months of its life. Active natural immunity is the result of an immune response upon
exposure to an antigen, contracting the actual measles infection. Deliberate exposure to
antigens that induce an immune response, as with the measles vaccine, is active in-
duced immunity.

20. If a splinter of wood were to enter the skin and introduce microorganisms to that
site, what specific early and late events of inflammation would respond to that newly in-
fected site? Describe the sequence of signs and symptoms, vascular and tissue events,
and cells and mediators involved.
Inflammation is initiated in response to invading microbes or tissue damage which
leads to a cascade of events that include vasoconstriction, vasodilation, edema, and the
migration of leukocytes into the area. This process is identifiable by a series of signs
and symptoms characterized by rubor (redness), calor (warmth), tumor (swelling), dalor
(pain), and loss of function. Immediately following the injury, chemical mediators are re-
leased that stimulate leukocytes and cause vasoconstriction. Vasoconstriction only lasts
a short period of time and is quickly followed by vasodilation which also causes blood
vessels to become permeable. By the action of chemotaxis, leukocytes (following cyto-
kines) begin to migrate out of the blood vessels into the interstitial space via diapedesis.
Mast cells in the connective tissue as well as basophils, neutrophils, macrophages, and
platelets leave the blood to combat pathogenic invaders. Fluid also leaks into the injury
site and caused edema. Pus, composed mainly of leukocytes and debris generated by
phagocytosis, accumulates at the site. The actual wound healing begins late in the in-
flammation process after sufficient cleansing of the area has taken place. Proliferation
phase can last up to four weeks. The affected area may be composed of a mixture be-
tween specific tissue cells and other tissue known as granulation tissue. If this granula-
tion tissue is not removed it will remain and form scar tissue. The final stage occurs
when new cells mould into their surroundings to once again produce a functioning tis-
sue.