All surfaces colonized besides blood stream and tissue.

Occupying niches that pathogens might occupy

Producing acids

Producing bacterions (chemicals that kill of competition)

1. Suspect microbe always found in diseased individual never in healthy one (exceptions - carriers of yeast infections)

2. Be able to culture microbe on artificial medium in lab (not always possible)

3. Pure cultures of microbe must be able to cause the disease in test animals

3. Reisolate same microbe from experimentally infected animal

- A disease that is spread from one host to another

- Example?

Communicable disease

Ex. HIV

- A disease that is easily spread from one host to another

- Example?

Contagious disease

Ex. Flu

- A disease that is not transmitted from one host to another

- Example?

Noncommunicable disease

Ex. Skin cancer

- A type of severity or duration of a disease in which the SYMPTOMS DEVELOP RAPIDLY (DISEASE ENDS SOON)

-Example?

Acute Disease

Ex. Flu

- A type of severity or duration of a disease in which the DISEASE DEVELOPS SLOWLY (DISEASE LAST A LONG TIME)

-Example?

Chornic disease

Ex. Arthritis

- A type of severity or duration of a disease in which the DISEASE HAS A PERIOD OF NO SYMPTOMS WHEN THE PATIENT IS INACTIVE

- Example?

Latent disease

Ex. Herpes

- Opportunisic infection after a primary (predisposing) infection

-Example?

Secondary infection

Ex. Bacterial pnemonia

- A disease with no noticeable signs or symptoms (inapparent infection, asymptomatic)

- Example?

Subclinical disease

Ex. Typhloid Mary

- A type of transmission of disease that occurs when pathogen reproduces in vector

(When someone who is sick flies acrossed America and spreads the disease)

Mucous membranes

Skin

Parenteral route

Respiratory tract

GI tract

Genitourinary tract

Conjunctiva

Most often thru broken skin

Sometimes hair follicles

Sweat ducts

Injections

Bites

Surgery

Cuts

Dry skin splitting

Adherence

Enzymes

Glycocalyx: Streptococcus mutans

Fimbriae: Escherichia coli

Coagulase: Coagulate blood

Kinases: Digest fibrin clots

Hyaluronidase: Hydrolyses hyaluronic acid

Collagenase: Hydrolyzes collagen

IgA proteases: Destry IgA antibodies

Siderophores: Take iron from host iron-binding proteins

Antigenic variation: Alter surface proteins

- Inactivated toxin used in a vaccine

Ex. Tetanus vaccine

Is this a ENDOTOXINS or EXOTOXINS:

Source: Gram (-)

Relation to microbe: Present in LPS of outer membrane

Chemistry: Lipid

Fever?: Yes

Neutralized by antitoxin?: No

LD₅₀: Relatively large

Is this ENDOTOXINS or EXOTOXIN:

Source: Mostly Gram (+)

Relation to microbe: By-products of growing cell

Chemistry: Protein

Fever?: No

Neutralized by antitoxin?: Yes

LD₅₀: Small

Making protein channels in the plasma membrane

Disrupting phospholipid bilayer

Fever

Nausea

Vomiting

Diarrhea

Shock

Death

S. aureus

Steptococcus pyogenes

Respiratory tract

Gastrointestinal tract

Genitourinary tract

Skin - lesions

Blood

Coughing

Sneezing

Feces

Saliva

Urine

Vaginal secretions

Biting arthropods

Needles

Syringes

Intact skin

Mucous membrane and their secretions

Normal microbiota

Natural killer cells and phagocytic white blood cells

Inflammation

Fever

Antimicrobial substances

Skin - keratin is a protective protein

Mucous membranes

Ciliary escalatory: microbes trapped in mucus are transported away from the lungs

Lacrimal apparatus: Washes eye

Saliva: Washes microbes off

Urine: Flows out

Vaginal secretions: Flows out

Fungistatic fatty acid in sebum

Low pH (3-5) of skin

Lysozyme in perspiration, tears, saliva, and tissue fluids

Low pH (1.2-3.0) of gastric juice

Transferrins in blood find iron

NO (Nitric oxide) inhibits ATP production

Neutrophils: Phagocytic

Basophils: Produce histamine

Eosinophils: Toxic to parasites and some phagocytic

Dendritic cells: Initiate adaptive immune response

Monocytes: Phagocytic as mature macrophages

Lymphocytes: Involved in specific immunity

Redness (erythema)

Pain

Heat

Swelling (edema)

Acute-phase proteins activated (complement, cytokine, and kinins)

Vasodilation (histamine, kinins, prostaglandins, and leukotrienes)

Margination and emigration of WBCs

Tissue repair

Histamine

Kinins

Prostaglandins

Leukotrienes

Hypothalamus normally set at 37 degrees Celsius.

Gram (-) endotoxin cause phagocytes to release interleukin-1 (IL-1).

Hypothalamus releases prostaglandins that reset the hypothalaus to a high temperature

Body increases rate of metabolism and shivering which raise temperature

When IL-1 is eliminated, body temperature falls (crisis)

Classical

Alternative

Lectin

Transferrins

Antimicrobial peptides

Antibodies

Lymphocytes

Macrophages

Increase transferrins

Increase IL-1 activity

Overall enhancement of immune function

Inhibits some pathogens

Tachycardia (Rapid heart beat)

Acidosis

Dehydration

____________ and __________ are most antigenic.

__________ and __________ are less antigenic

Proteins and polysacchrides

Lips and nucleic acid

Penicillin + Serum proteins = Antigen

Poison Ivy - Urusiol oil = Hapten; + Tissue proteins = Antigen

IgG- Structure:

Location:

Complement Fixation (Y/N):

Placental Transfer (Y/N):

Structure: Monomer

Location: Majority of serum antibodies

Complement Fixation: Yes, Fix complement

Placental Transfer: Yes, cross placenta

IgM - Structure:

Complement Fixation (Y/N):

Known Function:

Structure: Pentamer

Complement Fixation: Yes, Fix complement

Known Functions: Aggultinates microbes; first Ab produced in response to infection

IgA- Structure:

Location:

Known Function:

Structure: Dimers

Location: In secretions

Known Function: Mucosal protection

IgD- Structure:

Location:

Known Function:

Structure: Monomer

Location: In blood, lymph, and on B cells

Known Function: On B cells, initiate immune response

IgE- Structure:

Locations (3):

Known Functions (2):

Structure: Monomer

Location: On mast cells, basophils, and in blood

Known Functions: Allergic reactions; lysis of parasitic worms

Neutralization

Antitoxin & Antivenin

Agglutination

Precipitation

Opsonization

Complement fixation

Complement cascade

- Exposure to antigen stimulates B cell proliferation and differentiation into plasma cells + memory cells

- Plasma cells produce ABs in quantity

- Memory cells produce Abs next time antigen present

B cells (specific)

Dendritic cells (general)

Macrophages (general)

How long does it take humoral immunity to work:

1° (primary) respsone

2° (secondary) response

1° (primary) respsone - typically 7-10 days, IgMs first then IgG

2° (secondary) response - typically 1-3 days, mostly IgG from memory cells

Regulatory T Cells (T_R):

Supress __________________

Shuts down _______________

Maintain __________________

Supress other T cells

Shuts down T-cell mediated immune response

Maintain immunological tolerance--supres autoreactive T-cells

Cells which don't express MHC 1.

Ex. Fluke

Natural- Infection

Artificial- Vaccine/Toxoid

Natural - mother to fetus across placenta; colostrum

Artificial - antibodies produced in another animals (ex. horse), purified

- Over-reaction of immune system resulting in host tissue damage or death

Examples (3)?

Hypersensitivity

Ex. Allergies, Transplant rejection, Autoimmunity

Itching

Edema (increased capillary permeability)

Vascular dilation (erythema)

Smooth muscle contraction (Ex. bronchial constriction -- not asthma)

Exposure to Anitgen

Triggering peripheral blood vessel dilation throughout entire body

Lower blood pressure

Shock

Edema

Respiratory constriction

Death

1st exposure to allergen = SENSITIZING DOSE, NO ALLERGINIC RESPONSE

2nd exposure = SHOCKING DOSE, SIGNIFICANT MASSIVE ALLERGIC RESPONSE

Induce formation of IgG's to allergen

IgG's do not induce mast cell degranulation

IgG's compete with IgE's for binding antigen = blocking

If allergens bound to IgG's, they can't bind to IgE mast cells

IgG or IgM antibodies

Complement

Target cell lysis is mediated by Ab's (IgG, IgM)

Complement

Kiler cells

Incompatible blood transfusions

Hemolytic disease of newborns

An-Ab complexes get deposited on membranes in various tissues (ex. kidney, joints, lungs)

Inflammation and complement activation

Local destruction of host tissue (Ex. Glomerulonephritis)

Respone in a Type IV (Cell-mediated) Reaction?

24-48 hours:

1st exposure:

2nd exposure:

24-48 hours after contact with antigen most common = Contact dermatitis

1st Exposure = Sensitizing dose

2nd Exposure = Immune response

Type I

Type II

Type III

Type I - Anitbodies against pathogens

Type II - Antibodies react with cell-surface antigens

Type III (Immune Complex) - IgM, IgG, complement immune complexes deposit in tissues

Type IV - Mediated by T cells

Type V (Stimulatory) - Similar to Type II, but antibodies bind specifically to cell surface receptors

Example: Grave's Disease

Target Tissue: Thyroid->Stimulation

Example: Lupus

Target Tissue: Systemic, Abs against cell components, kidneys

Example: Insulin-Dependent Diabetes

Target Tissue: Insulin secreting cell of pancreas

T cells

Macrophages

Complement-fixing antibodies

Brain

Region of Cornea

Testes

Heart Valves

Achilles Tendon [After freezing]

Fetus

- A type of graft that USES AN IDENTICAL TWIN'S TISSUE

Ex. Kidney

- A type of graft that USES NON-HUMAN TISSUE

Ex. Pig health valves

Reverse transcriptase - (aDNA polymerease) copies RNA -> DNA

Integrase - (an andonuclease) inserts HIV DNA into host chromosomes

Protease - cleaves viral core protein

LRT infection

Rod

Obligate aerobe

Slow grower

Doesn't gram stain, but is acid fast

Resists drying and most antimicrbials

Immunity is cell mediated- macrophages and T-cells

1. Tubercle bacilli inhaled

2. Tb travels to alveoli, usually phagocytized by macrophages

3. Sometimes Tb survives inside macrophages --> dormant

4. Dormancy = Latent infection, can remain dormant > 80 years

5. Accumulation of macrophages and other cells around infected macrophage-> formation of tubercle

6. Host induced inflammation damages lung tissue

7. Over tie tubercle may heal becoming calcified (seen in X-rays)

8. If does not heal, lesion enlarges, Tbs multiply-> active infection -> highly contagious

9. Dormant Tb can be reactiated

There is resistance due to Random Chance Mutation.

In any population of bacteria there is the probability of finding at least one organism that is already resistant.

-10 % of people infected with TB, develop active TB

-90% of people infected with TB, TB is dormant

As the rate of HIV increases, TB increases.

Dormant TB becomes reactivated in a person when s/he becomes infected with HIV and develop AIDS.

Immigration

Lack of isolation

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