Microbio Exam 3

What are the two different types of immunity?

innate and adaptive

Innate System

-front line (already in our body)
-Non specific mechanisms:
1. First Line: Anatomical barriers (skin, mucous membranes), Secretory Chemicals (Lysozyme in saliva, tear, and earwax, Interferon Complement pro)

2. Second Line: cellular mechanisms (white blood cells-N E B M NK cell)

Anatomical barriers examples

Skin, mucous membranes, lacrimal glands (has lysozyme that only affects gram positive bacteria), saliva, ciliary escalator

Adaptive system

-delayed immunity
-T cells: cell mediated immunity
1. TH= T helper
2. TC= T cytotoxic

-B cell: Hummoral Immunity
1. B cell---> plasma cell ----> antibody

white blood cells are also called what?

leukocytes

B cells are leukocytes but specifically what?

lymphocyte

Leukocycte examples

-Neutrophils
-Monocytes
-Basophils
-Eosinophils

Lymphocytes examples

-NK cell
-B cell
-T cell

Neutrophils

-1st white blood cell to come to infection
-highly phagocytic
-leave blood, enter infected tissue, destroy microbes
-nucleus is polymorphonuclear leukocytes

Monocytes

phagocytic function

Phagocytosis

engulfing and destruction of particulate matter by phagocytes

Order of phagocytosis

1. Chemotaxis: attraction of WBC to location of a injury

2. Adherence (Attachment): Attachment to surface of microbe
-Opsonins (Antibody & complement protein)
-Opsonization: facilitate or enhance phagocytosis

3. Ingestion: bring inside
-phagosome
-w/ low pH, enzyme activated

4. Digestion: Digest
-Phagolysosome

5. Exocytosis: Undigested materials exit cell

Basophils

dilate blood vessels when histamine releases

Eosinophils

-cause allergic reaction
-fight helminths
-fight viral infections

Natural Killer cells

-kill infected cell
-produce holes into membranes: perforins

Secretory Chemicals

1) Lysozyme
2) Interferon: produced by virally infected cell
3) Complement

Inflammation

4 cardinal signs:
1. redness
2. heat
3. swelling (edema)
4. pain

Inflammation Mediators

-Histamine
-Prostaglandins
-Kinins
-Leukotrienes
-Complement

Steps in inflammation

vasodilation, chemotaxis and diapedesis as WBC migrate into area, tissue repair

Fever

-reduce iron availability
-phagocytic cells more active

Complement System

Functions:
1. Membrane Attack Complex (MAC)
-make holes into microorganisms & lysis it

2. Opsonize

3. Inflammatory Response

Specific Immunity: Adaptive Immunity

-cellular immunity: attacks antigens found inside cells
*viruses, some fungi, & parasites

-hummoral immunity: fights invaders outside cells
*bacteria & toxins

Antigens

stimulate immune system
-molecule on organism or cell
-Exogenous Antigen: toxins, secretions, cell wall, flagella
-Endogenous Antigen: protozoa, fungi, bacteria
-Epitopes: antigen composed of this

Hapten

too small on its own, but can be combined w/ larger molecule

Antibodies: IgG

-pass through the placenta
-most prevalent
-80% of circulating Abs
-old infection= IgG high, IgM low

Antibodies: IgM

-1st to appear
-10 antigen binding sites
-pentamer
-new infection: IgM high, IgG low

Antibodies: IgA

-local antibody
-mucous membrane: mucus, saliva, tears, breastmilk

Antibodies: IgD

-expressed on B-cell

Antibodies: IgE

-attached to surface of mast cells & basophils
-cause release of histamine
-causes allergic reaction

Antibody Function

Agglutination: Ag binding sites can bind to 2 separate foreign Ag
-causes clumping easier to phagocytize

Neutralization: block binding of pathogen to host cell

Antibody-dependent cell-mediated cytotoxicity
-Antibodies attached to target cell
-Cause destruction by macrophages, eosinophils, & NK cells

Opsonization:
-Coat Ag w/ Ab
-It's phagocytosis is enhanced---> antibody mediated cytotoxicity

Complement & Activation

Lymphocytes

B cells:
-activation form of plasma cell
-memory cell

T cells:
-T helper (Th cells: CD4 cells)
-T cytotoxic (Tc cells: CD8 cells)

Natural killer cells

Major Histocompatibility Complex (MHC)

MHC 1: on membrane of nucleated animal cells
-all cells accept RBC
-recognized by T cytoplasmic (Tc) or CD8 cell

MHC 2: on the surface of antigen: presenting cells (APC's)
-B cells
-Macrophages
-Dendritic cells
-recognize ThCD4 cell

Cells involved in Humoral Immunity

-Macrophages
-T-helper cells (CD4)
-B cells

Cells involved in cellular memory

-Macrophages
-T-helper
-T cytotoxic cell (CD8)

Antibody titer

measuring the titer of a specific antibody against a specific antigen

Monoclonal antibodies

-producing a clone of antibodies against a particular antigen in lab
-test for hepatitis

Primary response

first time infected

Secondary response

most recent infection

Vaccines

1. Attenuated (live) vaccine:
-Ex: MMR (Measles, Mumps, Rubella)

2. Inactivated (killed) vaccine
-Ex: Hepatitis, Influenza

3. Toxoids: toxic (inactive toxins)
-Ex: tetanus

Allergies are what?

immune response to non-pathogenic agent

Allergies: Anaphylactic (type I)

-less than 30 min
-IgE attach to mast cell & basophil, release histamine

Allergies: Cytotoxic (type II)

-5 to 12 hours
-IgG or IgM
-blood group imcompatibility

Allergies: Immune complex (type III)

-3 to 8 hours
-Ag- Ab
-deposited in joints and kidneys
-damage to glomeruli
-strep throat

Allergies: Delayed Type Hypersensitivity (Type IV)

-24 to 48 hours
-cell mediated T-cell
-poison ivy
-TB test

What disease affects T helper cells (CD4)

HIV (causes less than 200 cells)

Epidemiology

study of the occurrence, transmission, avoidance & treatment (cure) of disease
-where & when
-treat & prevention
-how transmitted

Pathogen

infectious agent

pathogenesis

how particular disease change the body

Etiology

study of the cause of disease

compromised

person is weakened

immunocompromised

weak immune system

immunocompetent

good immune system

opportunistic infection

caused by a pathogen that does not normally produce an illness in healthy humans but infect weakened immune systems

Virulence

-the measure of how a certain organism cause disease
-more virulence= more able to cause disease
-Ex: capsule

Virulence Factors

characteristics that allow bacteria to be virulent

Normal Flora (microbiota)

Microbes that colonize but do not cause disease
-compete against harmful bacteria
-affect pH & oxygen availability

Normal flora varies by what?

nutrition, stress, geography

Symbiosis means what?

live together

Symbiosis: Mutualism

both bacteria & host benefit
-ex: E. coli produces nutrients

Symbiosis: Commensalism

one benefits, other unaffected
-ex: bacteria on the skin

Symbiosis: Parasitism

one benefits while other is harmed

what opportunistic pathogen is seen in burn patients?

pseudomonas aeruginosa
-causes green color

what opportunistic pathogen causes a UTI?

E. coli

what opportunistic pathogen is found in AIDS patients?

pneumocystis

Examples of portals of entry

Parenteral route
-via punctures, injections, surgery

Mucous membranes
-respiratory tract
-gastrointestinal tract
-genito-urinary tract

Skin

Symptoms

not apparent to observer

Signs

something we can measure
-Leukopenia: decrease in WBC
-Leukocytosis: increase in WBC

Syndrome

specific group of sign & symptoms accompany a particular disease
-ex: AIDS, congenital rubella syndrome

Sequela

complication, an after effect of a disease
-sign & symptoms that occur sometime later after a disease
Ex: Strep throat ----> Glomerulonephritis----> Kidney disease later
Guillian Barre Syndrome comes from (sequela for) Campylobacter

Infectious Dose

amount of bacteria that cause disease
-lower ID= more contagious

virulence factors

fimbrae, slime layers, spike proteins, capsules, M- proteins, Mycolic Acid (protect against phagocytosis)

Pathogenic mechanisms: Fc receptors

different binding

Pathogenic mechanisms: Enzymes

-coagulase: causes blood to clot
-hyaluronidase: breaks down hyaluronic acid
-collagenase: breaks down collagen
-Kinases: dissolves blood clot
-IgA protease: destroys antibodies produced by body to prevent pathogens from adhering to mucosal surfaces (Virulance factor for neisseria gonorrhoeae)

Antigen variation

every pathogen expresses on its surface a variety of proteins
-ex: Trypanosoma: African Sleeping sickness

Endotoxins

-gram negative cell wall (outer layer)
-Lipid A (makes endotoxin): lipid portion of LPS
-causes endotoxic shock
-occurs when bacteria dies

Exotoxins

produced by both gram + and gram negative

Lethal Dose

dose that causes death: less dose means more dangerous

Diphtheria toxin

make pseudo membranes, cause obstruction of airway
-Corynebacterium diptheria

Erythrogenic toxin

caused by streptococcus pyogenes (cause strep throat)
-makes red skin rash: scarlet fever
-Beta hemolytic

Botulinum toxin

causes flaccid paralysis: muscle cannot contract
-Clostridium botulinum

Exterotoxin

E. coli & Vibrio cholera

Tetanus toxin

Clostridium tetani

Exfoliatin

-staphylococcus aureus
-causes scalded skin syndrome

Vaccines: Toxoids

-toxic inactivated: no longer toxic to stimulate immune response
-Ex: tetanus toxin

Vaccines: Anti-toxins

Antibodies against toxin

Disease stages

1. Incubation period: no sign or symptoms
2. Prodromal period: vague sign & symptoms
3. Illness: severe sign & symptoms
4. Decline: sign & symptoms go down
5. Convalescence: completely recovered

Secondary infection

Separate bacteria added to infection already there (primary infection)

Modes of transmission: Contact

1. Direct: person to person
2. Indirect: Non-living object (fomite)
3. Droplet: coughing

Modes of transmission: vehicle

1. Water: Giardiasis
2. Air (further than 1 meter): Tuberculosis
3. Food: hepatitis A

Modes of transmission: Vector

1. Mechanical: vector not itself infected
-Ex: a each carrying microbes on its legs

2. Biological: vector is infected with pathogen
-Ex: Mosquito—-> plasmodium vivax——> malaria

Communicable disease

Spreads from one host to another
-Contagious: measles, influenza

Non communicable disease

Spread from one host to another
-Clostridium tetani: only produces disease when introduced into body via wounds

Acute

Rapid development, rapid recovery

Chronic

Slow development, hepatitis

Latent

Reactivation after initial infection

subclinical (in apparent) infection

When someone doesn't know they have it

Sepsis

Bacteria in blood multiply fast

Reservoirs of infection

Permanent place to reside, where the pathogen originates from
-human, animal, water, soil

Incidence

New cases

Prevalence

Total number of cases