Microbio

• Normal Flora.
• Mucas Membranes.
• Cilia.
• Macrophages.

Streptococcus pyogenes.

Corynebacterium diphtheriae

• Rhinoviruses.
• Coronaviruses.

• Streptococcus pneumoniae.
• Streptococcus pyogenes.
• Haemophilus influnzae.

• Staphylococcus aureus.
• Pseudomonas aeruginosa.

Bordatella pertussis.

• Streptococcus pneumoniae.
• Staphylococcus aureus.
• Klebsiela pnemoniae.
• Haemophilus influenzae.
• Pseudomonas aeruginosa.
• gram positive cocci.
• gram negative bacilli.

Mycoplasma pneumoniae.

Legionnella pneumophila.

Mycobacterium tuberculosis.

Bacillus anthracis.

• coronavirus. CoV
• common cold type virus (not influenza type virus).

• Pneumocystis jiroveci (Pneumocystis carinii)
• (a fungus)

• 2 polypeptide chain toxin
• fragment A inhibits protein synthesis leading to cell death.
• fragment B target mammalian heart and nervous system cells.

• hemagglutinin.
• Exotoxin.
• Endotoxin.
• Pertussis toxin.

LPS (lipopolysaccharide).

Antigen that helps Bordatella to attach to cilia.

paralyzes cilia on respiratory cells.

• produces cardiovascular shock.
• septicemia w/n hours of infection.
• Death 2-3 days.

• tender tonsils with pus-filled lesions.
• high fever.
• acute throat soreness.
• chills.
• headache.

pseudomembrane.

• excessive mucus secretion.
• sneezing.
• inflammation of mucous membranes.
• sore throat.
• headache.
• cough.

• fever.
• sneezing.
• vomiting.
• mild dry persistent cough.

• Mucus.
• masses of bacteria fill the airway.
• strong violent cough (whoops sound 50%).
• cyanosis (blue skin lack of oxygen).
• difficulty keeping airway open.

• Secondary infection common at this stage.
• Mild cough last for months.

Inflammaiton and damage to the glomeruli of the kidneys.

• Immune complexes damage the heart valve in cross-reaction.
• Fever.
• Chorea.
• Malaise.
• Arthritis.
• 2-5% mortality.

• Presence of organisms elicit inflammatory response, fluid accumulation.
• Cough.
• Fever.
• Chest pain.
• Shortness of breath.
• Rapid breathing.
• Production of sputum w/Cough

• No respiratory signs.
• Fever.
• Malaise.
• 3-10% contract Mild pneumonia w/ insidious onset.

• Organisms colonize near alveoli.
• Organisms prevent fusion of phagosomes and lysosomes so survives w/n macrophage.
• Symptoms similar to classic pneumonia.
• Milder form = Pontiac Fever.

• Bad cough.
• Pain in chest.
• Cough up blood or sputum.
• weakness or fatigue.
• weight loss.
• no appetite.
• chills.
• Fever/night sweats.

• No symptoms.
• Does not feel sick.
• cannot spread tb to others.
• test positive on skin test.
• has normal chest xray and sputnum test.

• Chills.
• Fever.
• Headache.
• Severe sweats usually self limiting.
• similar to primary atypical pneumonia.
• chronic infection - endocarditis.

• Cardiovascular shock.
• Septicemia w/n hours of infection.
• Death w/n 2-3 days.

• High fever.
• Dry cough.
• shortness of breath.
• Difficulty breathing.
• X-rays indicating pneumonia.

• Cough.
• Fever.
• Shallow respiration.
• cyanosis.

a prophage produces exotoxin.

• clotted blood.
• cells.
• leukocytes killed by the exotoxin.

200 viruses cause the common cold.

pharyngeal organisms pass into the Eustation tube and cause infection.

As children age, eustachian tube grows and angle changes.

• Catarrhal stage.
• Paroxysmal stage.
• Convalescent stage.

• normal flora.
• High dose of organism inhaled.
• endogenous or direct contact of respiratory secreations from carrier.

Organism prevent fusion of phagosome and lysosome so survives w/n the macrophage.

• Air conditioners.
• Ornamental fountains.
• Produce sprayers.

Mycolic acid (acid fast postive stain).

• phagocytized by macrophage by grow w/n the macrophage.
• grow replicate, lyse macrophage and infect new cells.

• Contain live organisms and macrophages.
• walled off by fibroblasts, lymphocytes and neutrophils.
• may become calcified.

• due to cell mediated immune response.
• neutrophil inflitration and fluid accumulation in alveoli.

• Coxiella burnettii.
• a rickettsia organism (must have some life cycle w/n another cell).

• Phagocytized by host cells.
• Replicated w/n the phagolysosomes and eventually rupturing the cell.
• ruptured cell releases new pathogenic organisms.

large cell variant may have a type of endospore at one end thereby giving resistance uncharacteristic of other rickettsia.