Bio 120 LE 3 Reviewer

7/17/2019 Bio 120 LE 3 Reviewer

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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

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

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 Hostile butmicroorganisms

can live

Small

Intestine

pH 4-5 Enterococci

Lactobacilli

Large

intestine

(ileum and

colon)

pH 7 Many bacteria

RESPIRATORY TRACT

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)





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 firstappear; malaise – feeling of being ill

2. Acute period – symptoms reach their

peak

3. Decline period

4. Convalescent

Microbial factors of virulence

Pathogenicity – ability of the microbe

to establish infection and cause disease

Virulence – quantitative measure of

pathogenicity & refers to the capacityof a microorganism to overcome the

host’s 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

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 (non-

pathogenic), 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

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.

1.) Cytokines – interferon, ILS, TNF if cell-

mediated immunity

Produced by activated T cells

It will destroy pathogen via inflammation

2.) Helper cells – helps B cells to activateplasma 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

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

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 flexibilityConnection between variable and constant

region is disulfide bridges

Fab is more variable; needed to detect

IgM –also with extra fragment because it forms

pentamerous configuration

-

Joined by J chain (allows flexibility of

molecules)

With extra fragment

because it binds to mastcells to produce

histamine



-

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

Initial exposure mostly IgM but a few IgG

Second exposure: Mostly IgG



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Bio 120 LE 3 Reviewer