Host-Parasite Relationship

Normal Human Microflora

Microbes that populate the human body in
mutualistic or commensalistic relationships.

Resident flora constant group of

microbes that survives and grows in &
on the body
Transient flora inhabits the body for
short periods of time
o For a few days/weeks; most are
harmless but few are
opportunistic
o Opportunistic pathogens- under
an immunocompromised
situation, the pathogen
proliferates

Staphylococcus aureus found

on the skin

TEETH
Gingival membrane and
periodontal membrane
Gingivitis caused by Gingiva
Periodontitis periodontal membrane
caused by Fusobacterium via cytolysis

Plaques formed by synthesis

of dextrin produced by
Streptococcus mutans

GASTROINTESTINAL TRACT
Stomach

pH 2

Small
Intestine
Large
intestine
(ileum and
colon)

pH 4-5
pH 7

Hostile but
microorganisms
can live
Enterococci
Lactobacilli
Many bacteria

RESPIRATORY TRACT
Process of Pathogenicity
a. Loose association
b. Adhesion glycocalyx (made of
polysaccharides) adhere
c. Association enzymes are needed to
lyse the cells so that pathogens can
enter
eg. Cysteine protease
SKIN
Apocrine sweat glands
contaminated by
microorganisms when puberty
is reached causing body odor
Before puberty: sterile apocrine glands

Upper respiratory tract is more prone to

infection because it is more proximal to
external environment
URINARY TRACT
Lactobacillus acidophilus (hehe) found in
vagina
Before puberty: alkaline pH
After puberty: acidic pH because of L.
acidophilus; feminine wash maintains pH
(Acidic pH prevents the thriving of Candida
albicans which can cause vaginitis)

Microorgansims can compete antagonistically

Some indigenous microbes provide the
host with protection against potentially
pathogenic microorganisms through
mechanism known as antagonism
Antagonism is the result of competition
for nutrients, alteration of the
environment (oxygen tension or pH) or
the release of products that inhibit the
microbes

Eg. Candida albicans vaginitis

Clostridium difficile inflammation of colon
called pseudomembrane colitis (PCM)
Staphylococcus aureus acute staphylococcal
encephalitis

Doctor will prescribe antibiotics that

will target Gram-negative but the Grampositive will proliferate due to
elimination of its competitor

Microorganisms can grow synergistically

SYNERGISM - some strains or species of
microorganisms grow better in
combination than alone
Cross-feeding/Syntropism
o 2 populations supply each
others nutritional needs
e.g Enterococcus faecalis requires folic acid &
Lactobacillus arabinosus requires
phenylalanine
General concepts of host-parasite relationships
Infection refers to the growth of
microbes in the tissue of a host
Infectious disease cause damage to
host
Infectious microorganisms persist in reservoirs
Microbes generally live and multiply
without damaging their reservoirs
INANIMATE RESERVOIR soil, water, food
e.g. Anthrax caused by B. anthracis

Mastitis (disease of mammary glands in

cows when they touch the soild during
grazing) caused by Streptococcus
agalactiae
Fecal coliforms in contaminated water
ANIMATE RESERVOIR
E.g. Neisseria gonorrheae gonorrhea
Treponema pallidum syphilis

CARRIERS -Human beings may harbor

an infectious microbe in their bodies in
the absence of disease and spread it to
the other susceptible individuals
o Healthy carriers no visible
signs of disease at any time
o Incubatory carrier in initial
stages of disease before clinical
symptoms appear
o Convalescent carrier
recovered from the disease, no
longer have symptoms but still
carry the disease (MOST
DELIKS)
CARRIER STATES
Temporary present for a brief period
Intermittent periodic shedding of
microbe
Permanent continuous carriage and
shedding of infectious agent
ZOONOSES animal diseases transmissible to
humans
e.g Brucellosis (cattle, sheep, pig)
Anthrax (cattle, sheep)
Salmonellosis (chicken, turkey, rodents)
Diseases can be transmitted directly or
indirectly
To cause a disease, an infectious agent
must first be transmitted from the
reservoir to a susceptible host.
Transmission may occur directly from
the reservoir to host or indirectly via an
intermediate between the host and
reservoir.

DIRECT TRANSMISSION contact between

host and reservoir
Eg. STIs like gonorrhea, non-gonococcal
urethritis, syphilis
Viral diseases like common colds,
influenza and mumps
INDIRECT TRANSMISSION via contact
with fomites (nonliving) or vectors
(biological like mosquitoes)
e.g. Conjuctivitis communal usage of
towels infected with Chlamydia
trachomatitis
Plasmodium aedes for dengue virus
Plasmodium anopheles
Symptoms appear during clinical illness
1. Prodromal period- when symptoms first
appear; malaise feeling of being ill
2. Acute period symptoms reach their
peak
3. Decline period
4. Convalescent

Microbial enzymes aid in invasion by damaging

tissue/dissolving materials.
Hemolysins enzymes that destroy
erythrocytes
e.g Streptococcus pyogenes produces
streptolysin O and streptolysin S
culture in blood agar, clearing zones
indicate its lysing
Cystein proteinases
Lysis: degrades protein
Found in pathogenic species of
Entamoeba, Trichomonas, Giardia
In Entamoeba dispar (nonpathogenic), only difference is that it
has lower levels of cysteine
proteinase
Microbes produce 2 types of toxins
1) Endotoxins produced by Gram-negative in
lipid A
2.) Exotoxins produced by Gram-positive

Microbial factors of virulence

Pathogenicity ability of the microbe
to establish infection and cause disease
Virulence quantitative measure of
pathogenicity & refers to the capacity
of a microorganism to overcome the
hosts body defenses
Organotropic -microorganisms may
have a preference for particular host
tissues organs
e.g Neisseria urogenital
Mycoplasma upper respiratory tract

Many bacteria have surface

macromolecules that promote
adherence to solid surfaces
Glycocalyx adhesive polysaccharide
matrix that extends from the surface of
many bacteria serving as a virulence
factor
e.g. adherence of Streptococcus mutans to
teeth
Eukaryotic organisms: lectins

If you want to produce vaccine: attenuate the

virulence factor.
Easier to produce virulence factor for viruses
because they are smaller and fewer virulence
factors are present.

Antigenci variation surface of

microorganisms change so they cannot be
detected by antibodies.

INNATE IMMUNE RESPONSE

Lysozyme in tears & other secretions dissolves cell wall

Reduces microbial growth
Normal flora compete with pathogens
Skin is a physical barrier, produces antimicrobial fatty acids, and its normal flora inhibits pathogen
colonization
Rapid pH change in intestine inhibits microbial growth
Flushing of urinary tract prevents colonization

CONCEPTS OF IMMUNOLOGY
Bone marrow stem cell
Pleuropotent (can differentiate into different forms of cells) & hematopoietic

Origin of immune cells

Only plasma cell can produce antibodies NOT MEMORY CELLS

Spleen high concentration of antibodies
PROCESS (See figure below)
Antigen-presenting cells (APC)
Phagocytes antigen & process inside cell then
presented to the T cell
MHC major histocompatibility complex; found
at surface of APC

MHC I binds to CD8+ cytotoxic

MHC II binds to CD4+ helper
(helps produce antibodies)

Recognized by two types of T cells (CD4+ and

CD8+)
Different peptides and diff. MHC recognized by
a certain T-cell.

self-reactive cells are destroed

during development of the immune
response
2. Memory: Immune response to a specific
antigen is faster and stronger upon subsequent
exposure because the initial atigen-exposure
induced growth & division of antigen-reactive
cells, resulting in multiple copies of antigen
reactive cells
3. Specificity: immune cells recognize & react
with individual molecules (antigens) via direct
molecular interactions (lock & key association)

There are many antigenic determinant

(AD) in one protein due to a different
sequence of amino acid. AD is
synonymous to epitope

1.) Cytokines interferon, ILS, TNF if cellmediated immunity

Produced by activated T cells
It will destroy pathogen via inflammation
2.) Helper cells helps B cells to activate
plasma cells then antibody
B cells plasma cells antibody
This is called antibody mediated or humoral
pathway
Complement oponization lysing by antibodies
of antigen

Immune cells are specific for nonself

antigens
Autoimmune disease

Characteristics:
1. Tolerance: immune cells are not able to react
with self-antigen

IgG, IgD, IgA

V- Variable C-Constant H-Heavy L-light
IgA used as a marker for gastroenteral
disease
IgG produced by vaccines

Hinge region confers flexibility

Connection between variable and constant
region is disulfide bridges
Fab is more variable; needed to detect

With extra fragment

because it binds to mast
cells to produce
histamine
IgM also with extra fragment because it forms
pentamerous configuration

Joined by J chain (allows flexibility of

molecules)

Initial exposure mostly IgM but a few IgG

Second exposure: Mostly IgG

MONOCLONAL ANTIBODY PRODUCTION:

Homogenous mixture of same antibody reacting to a specific epitope
Polyclonal mixture of different antibodies reacting to an epitope
Better to use monoclonal!
How to produce monoclonal?
Antigen Balb/C mouse (will produce antibodies) from ascetic fluid obtain antibody producing B
cells then isolate it Fuse cells to make hybridomas (antibody producing + cloned in vitro)
Fusing agent PEG polyethylene glycol
We need to fuse B-cells with myelomas (cancer cell line so immortal)
Then, place in HAT (Hypoxanthine aminopterin thymine) medium
Why? Myeloma is HGPRT- (hypoxanthine guanine phosphoribosyl transferase) but spleen cells
are HGPRT+, so we need to incorporate the hypoxanthine to culture hybridoma in vitro