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120 Cards in this Set

  • Front
  • Back
Humoral Immunity
1. Immunity results from antibodies.
2. Involves B lymphocytes (B cells).
Cellular Immunity
Involves interaction of T lymphocytes (T cells)
Antigens
Cause a highly specific immune response.
Epitope (antigenic determinant)
Specific region on antigen that antibodies recognize.
Haptens
Low MW molecules that aren’t antigenic unless attached to a carrier.
Antibodies: (Immunoglobulins; Ig)
1. Globular proteins made in response to antigens.

2. Recognize and bind to the antigen they are made against.

3. Microbe may have several epitopes that different antibodies can be made against.
IgG
80% of antibodies in serum (most common in serum).

► Can enter tissue fluids.
► Can cross placenta; give immunity to fetus.
► Enhance phagocytosis; neutralize toxins, bacteria & viruses; activate compliment.
IgM
5-10% of antibodies in serum.

► Pentamer (five monomers); very large.
► Surface of B cells; can’t enter tissues.
► Agglutinates (clumps) antigens; enhance phagocytosis; neutralize bacteria; activate compliment.
► First antibodies produced in response to infection.
IgA
10-15% of antibodies in serum (monomer)

► Dimer: most common type in mucous membranes and secretions (mucus, saliva, milk).
► Most abundant in the body.
► Prevents microbial attachment to mucous membranes.
IgD
0.2% of antibodies in serum.

► Surface of B cells.
► No known function; may kill B cells that produce antibodies against host cells.
IgE
0.0002% of antibodies in serum.

► Bound to mast cells and basophils in body.
► Allergic reactions; destruction of parasitic worms.
B cell activation
► B cell surface antibodies bind to antigen.
► Antigen is taken inside and processed.
► Fragment of antigen binds with MHC class II.
Major histocompatibility complex (MHC)
membrane glycoproteins found in all mammalian nucleated cells.

► MHC class II-antigen complex displayed on membrane of B cell.

► Receptor on surface of T helper (TH) cell binds MHC II-antigen complex.

► TH cell is activated and releases cytokines.

► Cytokines activate the B cell.
Plasma cells
antibody producing cells.

► Produce antibodies to the antigen that caused B cell activation.
Memory cells
Involved in secondary response to antigen.
Agglutination
Antibodies cause antigens to clump together.

► Reduces number of antigens to deal with.
Opsonization
Coats antigen with antibodies.

► Enhances phagocytosis.
Antibody-dependent cell-mediated cytotoxicity
► Resembles opsonization; microbe not engulfed by immune cell.
Neutralization
IgG blocks attachment of viruses and toxins to host cells.
Compliment activation
inflammation, cytolysis, and phagocytosis.
Helper T Cells (CD4+ T cells)
► Recognize antigen presented on APCs by MHC II.
► Binds to the MHC II-antigen complex.
► APC secretes a stimulatory molecule.
► Initial binding and stimulatory molecule activate TH cell to produce cytokines.
► Cytokines stimulate TH cell to proliferate.
Cytotoxic T Cells (CD8+ T cells)
► Recognize antigen presented on “non-self” cells by MHC class I.
● Virus infected cells, cancer cells, etc.

► Transforms TC cells into Cytotoxic T Lymphocytes (CTLs).

► CTLs destroy cell:

● Perforins = create channels in the plasma membrane.
● Granzymes = apoptosis (cell suicide).
Cytokines
Proteins used by immune cells to communicate.
► Produced by immune cells; especially TH cells.
► Now known as interleukins.
Chemokines
cytokine that causes migration of leukocytes to site infection or tissue damage.
Tumor Necrosis Factor (TNF)
Inflammation reactions.
Antibody titer
Amount of antibody in serum.
Adaptive immunity
immunity against specific microbes and substances.
Naturally Acquired Active Immunity
1. Exposed to antigen, become ill, and recover.

2. Last a life-time (measles) or a few years (intestinal diseases).
Naturally Acquired Passive Immunity
1. Transfer of immunity from mother to baby through placenta or milk.

2. Temporary immunity (polio, rubella).
Artificially Acquired Active Immunity
Result of vaccination: injection of antigens into body.
Artificially Acquired Passive Immunity
Injection of antibodies from immune individual into the body.
Variolation
Inoculation with a needle tip coated in smallpox.
Vaccine
Suspension of organisms or fractions of organisms used to induce immunity
Live Attenuated vaccines
use whole, living, weakened microbes.

► Advantages: High, long-term effectiveness.

► Disadvantage: danger that microbes can mutate to a virulent form.

► Sabin polio vaccine and MMR (measles, mumps, rubella).
Inactivated Killed vaccines
use killed microbes.

► Advantages: cannot become virulent.
► Disadvantage: may not provide long-term immunity; often require booster doses.
► Rabies, Influenza, Salk polio vaccine, etc.
Subunit Vaccines
made with antigenic fragments of the microbe created in a lab.

► Advantages:
● Safer; cannot reproduce.
● No extra material; fewer side effects.

► Disadvantage: Can’t be made for all microbes
► Hepatitis B vaccine.
Toxoids
inactivated toxins.

► Advantage: directed at toxins made by pathogens.
► Disadvantage: require a series of injections for full immunity; require boosters.
► Tetanus, diphtheria.
Conjugated Vaccines
Combine poorly antigenic material from pathogen with antigenic substance.
Nucleic Acid (DNA) vaccines
NEWEST

► Plasmid DNA encoding proteins is injected into muscles.
► Muscle cells produce the proteins (antigens).
► Proteins are carried to red bone marrow and stimulate both humoral and cellular immunity.

► Advantage: not infectious; don’t require refrigeration; don’t require syringes/needles.

► Disadvantage: Doesn’t not work for polysaccharides
Chemotherapy
destruction of pathogens without harming the host.
Antibiotic
Substance produced by a microbe that inhibits another microbe.

► Easily discovered, few are of value.
► Most are toxic or we have better ones.
Selective toxicity
Toxic to pathogen, not to host.
Penicillinases (β-lactamases)
Enzymes that hydrolyze β-lactam ring of antibiotics.
Semisynthetic Penicillins
β-lactam core made by mold, side chains added chemically.

► Developed to overcome disadvantages of natural penicillins.
Drug Resistance
1. ► Enzymatic destruction/inactivation of drug (ex. Penicillinases)

2. ► Prevention of penetration of drug to target site in microbe.

3. ► Alteration of drug’s target site (ex. Streptomycin can no longer bind to ribosome).

4. ► Ejection of the Antibiotic from the cell (ex. Tetracycline)
Misuse of antibiotics
► Less developed countries: antibiotics purchased without prescriptions.

► Dose and length of treatment often incorrect.

► US: unnecessary or inappropriate prescriptions.

► Encourages survival of resistant strains.
Synergism
effectiveness of two drugs given together is greater than either alone.

► Penicillin weakens cell wall so Streptomycin can enter.
Antagonism
effectiveness of both drugs lower when used together than when used separately.
Endogenous infection
infection caused by organisms that are already part of the hosts flora.
Virulence Factor
Anything (action, substance produced, etc.) that contributes to the pathogenicity of a microbe.
Vesicles
Epidermis; small, fluid-filled lesions.
Bullae
Epidermis; fluid-filled lesion > 1 cm
Macules
Epidermis; flat, red lesions.
Papules
Dermis; raised, fluid-filled lesions.
Pustules
Dermis; raised, pus-filled lesions.
Koplik’s spots
Red patches with white centers in mouth opposite molars.

-MEASLES (Rubeola):
Meningitis
Inflammation of the meninges.
Encephalitis
Inflammation of the brain.
Buboes
Infected lymph nodes; swollen and tender.
Lymphangitis
Sign of sepsis; inflamed vessels visible as red streaks under skin from infection site.
Cutaneous (Anthrax)
Contact with materials containing spores; spore enters skin lesion.

-Papule, then vesicles which rupture and form a depressed ulcer with a black eschar (scab).
Gastrointestinal (Anthrax)
Vehicle; ingestion of undercooked food containing spores.

-Nausea, abdominal pain, bloody diarrhea, and ulcers in GI tract.
Inhalation (Anthrax)
Vehicle; breath in spores from surroundings.

-Mild fever, cough, chest pain, septic shock.
Edema toxin (Anthrax)
Local edema; interferes with phagocytosis by macrophages.
Lethal toxin (Anthrax)
Kills macrophages.
Epicardium
Outer layer of heart wall.
Myocardium
Middle layer of heart wall.
Endocardium
Inner layer of heart; lines the heart muscle and valves.
Endocarditis
Inflammation of the endocardium.
Gas Gangrene
Death of soft tissue resulting from loss of blood supply.
Ischemia
Wound interrupts blood supply; tissue becomes anaerobic.
Alveoli
Air sacs that make up lung tissue.
Spikes (Influenza)
Proteins embedded in envelope.
H spikes (Influenza)
Attachment to body cells.
N spikes (Influenza)
Allow virus to exit cells after replication.
Paneth cells
Granule containing cells in the small intestine (phagocytosis, defensins, and lysozyme.)
Dysentery
Severe diarrhea accompanied by blood or mucus.
Gastroenteritis
Inflammation of the stomach and intestinal mucosa.
Cholera toxin (lysogenic)
Causes secretion of water and electrolytes.
Oxazolidinones
Treatment of MRSA infections.
Impetigo of the newborn (Staphylococcal)
► Causative agents: Staphylococcus aureus; occasionally Streptococcus pyogenes.

► Transmission: direct contact through minor abrassions; fomites.

► Symptoms: vesicular rash forms, vesicles rupture, and crust over.

► Virulence factors: coagulase, exfoliative toxin, host response to infection.

► Treatment: topical antibiotics; hexachlorophene – containing skin lotions.
Scalded Skin syndrome (Staphylococcal)
underlying tissue becomes infected.

► Usually children under 2 as complication of Staphylococcal infection.

► Symptoms: macular-type lesion around nose and mouth; become bright red areas that spread.
● Within 48 hours affected skin peels off in sheets.

► Virulence factors: exfoliative toxin.

► Treatment: antibiotic therapy required.
Toxic Shock Syndrome (TSS) (Staphylococcal)
► Causative agent: Staphylococcus aureus

► Transmission: endogenous infection.

► Symptoms: fever, vomiting, sunburn-like rash, followed by shock, sometimes organ failure.

► Virulence factors: Toxic shock syndrome toxin 1 (TSST-1; superantigen exotoxin) formed at infection site, circulates in the blood.

► Results from: highly absorbent tampons, nasal surgery, surgical incisions, complications after giving birth.
Invasive Group A streptococcal infection
► Causative agent: Streptococcus pyogenes

► Transmission: direct contact.

► Bacteria attack: solid tissue (cellulitis), muscle (myositis), muscle covering (necrotizing fasciitis).

► Destroys tissues as fast as surgeon can remove it.
► 40% mortality rates.
Warts (papillomas) (Skin)
1. Causative agent: Papillomavirus species.

2. Transmission: direct contact; incubation of several weeks.

3. Symptoms: projection of cells.

4. Virulence factors: viral infection of epidermal cells causes overgrowth of cells.

5. Treatments: freezing, drying, laser removal.
Smallpox (Variola): Orthopoxvirus (Skin)
1. Causative agent: Orthopoxvirus; smallpox (variola) virus

2. Transmission: aerosol (via respiratory route)

3. Symptoms: pustules that may be nearly confluent; more concentrated on extremities

4. Middle Ages: 80% of the population was infected with small pox.

5. Treatment: none; preventative vaccine.

First disease ever eradicated
Chickenpox (Skin)
mild childhood disease; deaths due to pneumonia or encephalitis.

Causative agent: Varicella-zoster virus (Herpesviridae)

Transmission: aerosol (via respiratory route).

Symptoms: infections localizes in skin in ~2 weeks.

► 3-4 day vesicular rash; vesicles fill with pus, rupture, form scabs.
► Virus becomes latent in a central nerve ganglion.
Shingles (herpes zoster) (Skin)
► Causative agent: Varicella-zoster virus reactivated by stress or lowered immune system.

► Transmission: endogenous virus from chickenpox infection.
● Virus moves along peripheral nerves to the sensory nerves of the skin.

► Symptoms: vesicles appear in localized areas.
● Limited to one side of the body, burning or stinging pain, nerve damage may occur (blindness, paralysis).
Measles (Rubeola) (Skin)
Causative agent: Rubeola virus

Transmission: aerosol (via respiratory route)

► Extremely contagious; infectious before symptoms appear.

► Possible eradication due to measles, mumps, rubella (MMR) vaccination.
● Humans are the only host.
● 5 million cases to almost zero.

Symptoms and Disease:
► Incubation of 10-12 days, then common cold symptoms appear (runny nose, cough, watery eyes).

► Macular rash appears on face, spreads to extremities; high fever.

► Diagnostic indicator: Koplik’s spots; red patches with white centers in mouth opposite molars.
Rubella (German measles) (Skin)
Causative agent: Rubella virus.

Transmission: aerosol (via respiratory route)

Symptoms and Disease:
► 2-3 week incubation.
► Macular rash and low fever; milder disease than measles, often undetected.
► Encephalitis occurs in 1 in 6000 (mostly adults).
Congenital rubella syndrome (Skin)
► Birth defects caused by infection of the mother during pregnancy.

► Deafness, heart defects, severe brain damage, death.

► 15% of babies with congenital rubella die within the first year.
Bacterial Meningitis (Bacterial Nervous System)
Causative agents:
► Viral: mostly Enteroviruses
● Probably most common type of meningitis, but tend to be mild cases.

► Bacterial: Three bacteria cause 70% of bacterial meningitis cases and deaths:
● Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis.
Transmission: aerosols (respiratory tract) or endogenous infection.

Symptoms:
► Fever, headache, stiff neck; followed by nausea, vomiting; progress to convulsions, coma.
► Death occurs quickly from shock and inflammation

Virulence factors:
► All have capsules; protect from phagocytosis and compliment = rapid reproduction in the blood.
● S. pneumoniae capsule (lysogenic phage).


5. Mortality rate: varies with pathogen; high for an infectious disease.

6. Treatment: vaccines and Cephalosporin (antibiotic).
Tetanus (Bacterial Nervous System)
Causative agent: Clostridium tetani

Transmission: puncture wound (must have anaerobic environment).

Symptoms: muscle spasms; start with jaw, moves to back, then to muscles involved in swallowing.
► Death from spasms of respiratory muscles.

Virulence factors: neurotoxin tetanospasmin (exotoxin) enters CNS; blocks muscle relaxation.

Mortality rate: 50% developing areas; 25% U.S.

Prevention/Treatment:
► Preventative toxoid vaccination (DTaP; Td).
► Temporary immunity: tetanus immune globulin (TIG).
Botulism (Bacterial Nervous System)
Causative agent: Clostridium botulinum

Transmission: foodborne.

Symptoms: nausea (no fever), double vision, general weakness, then progressive flaccid paralysis for 1-10 days.
► Death from respiratory or cardiac failure.

Virulence factors: lysogenic neurotoxin (exotoxin) enters CNS, prevents muscle contraction.

Mortality rate: depends on toxin serotype.
► Type A: 60-70% if untreated.
► Type B: 25% if untreated.
Poliomyelitis (Viral Nervous System)
Causative agent: Poliovirus

Transmission: vehicle transmission: fecal-oral route (via contaminated water).

Symptoms: headache, sore throat, fever, nausea, sometimes paralysis and death.

Virulence factors:
► Initial multiplication in throat & small intestine = sore throat and nausea.
► Invades tonsils and lymph nodes then blood (viremia).
► Some cases: virus enters CNS, infects nerve cells, cells die = paralysis; death from respiratory failure.

Mortality rate: decreased to zero with vaccines; four cases in 2005 of unvaccinated children.
Rabies (Viral Nervous System)
Causative agent: rabies virus (Lyssavirus).

Transmission: animal bite; (saliva on skin).

Symptoms:
► Initially: mild, varied symptoms; resemble other common infections.
► Periods of agitation and calm; mouth spasms or hydrophobia.
► Extensive damage to cells of CNS.

Virulence factors:
►Enters and replicates in PNS, moves to the CNS where it destroys nerve cells.
● Variant in US that can replicate in human epidermal cells and then enter PNS.

► Immune system response: death caused by encephalitis


Mortality rate: 100% with no treatment.
Haemophilus influenzae (Bacterial Meningitis)
► Common normal flora of the throat.

► Occurrence: mostly children under 4, especially around 6 months old.
● Was 45% of all cases before vaccine.

► Symptoms: general meningitis symptoms.

► Mortality rate: 6%
Neisseria meningitidis (Meningococcal meningitis)
► Normal flora in nose and throat of carriers.

► Occurrence: mostly children under 2; college students.

► Symptoms: sore throat leading to bacteremia, then meningitis symptoms.
● Distinguishing feature: rash, doesn’t fade when pressed.
● Symptoms are mostly caused by endotoxin.
● Can cause death hours after onset of fever.

► Symptoms caused by endotoxin; produced quickly.

► Mortality rate: 80% without antibiotics; 9-12% with treatment.
Meningitis caused by Streptococcus pneumoniae
► Normal flora of nose and throat of carriers; most common cause of bacterial meningitis.

► Occurrence: mostly children 1 month - 4 years.

► Symptoms: general meningitis symptoms.

► Mortality rate: 30% children, 80% elderly.
What is the Connection between blood plasma and lymph?
► Some plasma leaves blood vessels, enters interstitial spaces (spaces between tissue cells).
● Referred to as interstitial fluid.

► Interstitial fluid moves around tissue cells, picked up by lymph capillaries.
● Fluid is referred to as lymph.
Lymph capillaries
Microscopic lymphatic vessels surround tissue cells.
Septic shock
Drastic drop in blood pressure.
Sepsis & Septic Shock (Bacterial disease)
► First stage: sepsis.
● Cytokine release results in: increase in blood vessel permeability, fever, chills, accelerated breathing and heart rate.

► Second stage: severe sepsis.

● Septic shock: drastic drop in blood pressure.
● Low blood pressure, insufficient blood flow to organs.

► Third stage: organ failure.

● Death: low blood pressure no longer controlled with fluids.
Capsule
Composed of amino acid residues; not detected by the immune system.
Plague (Vector-Transmitted)
Causative agent: Yesinia pestis
► Disease of rats, squirrels, rodents.

Transmission: vector (fleas) or inhalation.
► Also: scratches, bites of domestic cats.

Symptoms:
► Buboes in groin and armpits, fever, septic shock.

Virulence factors:
► Ability to survive and grow inside phagocytes.
► Gram (-) endotoxin.

Disease:

► Bacteria enter blood and are phagocytized; grow inside phagocytes in blood and lymph.
► Large number of organisms emerge, massive infection, large amounts of endotoxin released.
Hantavirus Pulmonary Syndrome (Viral Hemorrhagic Fever)
1. Causative agent: Sin nombre hantavirus
► Natural reservoir: small rodents.

2. Transmission: Inhalation of virus in dried urine and feces of rodents.

3. Symptoms: fever, headache, muscle aches, chills, lungs fill with fluids; fatal pulmonary infection.

4. Virulence factors: viral replication.

5. Treatment: none
Subacute bacterial endocarditis
develops slowly (weeks to months).

► Causative agent: mostly Streptococci sp.

► Transmission: from focal infection (teeth, tonsils, body piercings).

► Symptoms: Fever, general weakness, heart murmur; damage to heart valves.

► Virulence factors: damage from growth, fibrin-platelet vegetations protect bacteria.

► Bacteria lodge in preexisting lesions from congenital defect, rheumatic fever.

► Form blood clots; break off and lodge in vessels.
Acute bacterial endocarditis
develops rapidly.

► Causative agent: Staphylococcus aureus.

► Transmission: from focal infection.

► Symptoms: Fever, general weakness, heart murmur; rapid damage to heart valves.

► Virulence factors: toxins and enzymes.

► Move from infection site to heart valves, rapid destruction; often fatal in days or weeks.
Diphtheria (Upper RT)
Causative agent: Corynebacterium diphtheriae.

Transmission: direct contact or airborne.

Virulence Factors:

► Exotoxin (lysogenic phage).
● Interferes with protein synthesis.
● Enters tissue cells; damages heart, kidneys, nerves.

► Membrane in throat.

Symptoms: sore throat, low fever, malaise, swelling of the neck, grayish membrane in throat, tissue damage.

● Myelin sheath deterioration in central and peripheral nervous system; loss of motor control and sensation.
Rhinitis (common cold) (Upper RT)
Causative agent: Over 200 different viruses (especially Rhinoviruses and Coronaviruses).

Transmission: fomites? airborne?

Virulence Factors: replication of virus in cells lining the nasal passages.

Symptoms: coughing, sneezing, congestion, runny nose.
Pertussis (Whooping Cough) (Lower RT)
Causative agent: Bordetella pertussis

Transmission: airborne.

Virulence Factors: capsule, destruction of ciliated cells in the trachea, toxins:

► Tracheal cytotoxin: damages ciliated cells.

► Pertussis toxin: systemic symptoms of disease.

Symptoms: accumulation of mucus, intense coughing to clear mucus, gasping for air between coughs (whooping).

► Small children: break ribs coughing.
► Infants: brain damage from lack of oxygen.
Catarrhal stage (Pertussis progression)
Common cold symptoms.
Paroxysmal stage (Pertussis progression)
Mucus accumulates, spasms of coughing (1-6 weeks).
Convalescence stage (Pertussis progression)
May take months.
Pneumonia (Lower RT)
Causative agents:

► Bacterial: Streptococcus pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Legionella species, Chlamydia pneumoniae.

► Fungi: Pneumocystis and Histoplasma capsulatium

Transmission: endogenous, airborne.


Virulence Factors: capsule.

Symptoms: involve the bronchi and alveoli.
Typical Pneumonia
► Caused by Streptococcus pneumoniae.
► Two-thirds of all cases of pneumonia.
Atypical Pneumonia
► Caused by fungi, protozoa, viruses, and other bacteria.
► Slower onset of symptoms, lower fever and less chest pain.
Cholera (Digestive System)
Causative agent: Vibrio cholera

Virulence factors: growth in small intestine, cholera exotoxin (infection & intoxication).

Symptoms: watery stools containing intestinal mucus and epithelial cells (“rice water stools”), vomiting, (no fever), shock, death.
► 12-20 liters (3-5 gallons) of fluid a day.

Mortality rate: untreated = 50%

Treatment: antibiotics, replacement of fluids and electrolytes.
Orchitis (Mumps)
Inflammation of testes; sterility possible.
Mumps
Causative agent: mumps virus (Paramyxoviridae)

Virulence factors: replication of virus in parotid glands (salivary glands).

Transmission: contact (saliva)

Disease progression:
► Virus multiplies in respiratory tract and neck lymph nodes.
► Viremia; reach salivary glands via the blood.

Symptoms: fever, pain when swallowing, inflammation and swelling of parotid glands.