1) Gram positive, diplococcus with capsule.
-5 to 25% of healthy persons are carriers and virulence is based on carrier resistance
2) Over 90 strains based on antibodies to capsule. Capsule is virulence mechanism
3) Cause of 60-80% of bacterial pneumonia. Impairment of cilia is major factor into getting pneumonia.
4) Seeing increasing antibiotic resistance.
5) Capsular and conjugated vaccine developed from the capsules of 23 of the most common strains
1) Gram negative rod. Capsule and endotoxin are virulence factors. Respiratory spread, can be normal flora.
2) Many strains resistant to antibiotics (KP carbapenamase). Majority of resistance factors are spread via transposons.
1) Mycoplasma pneumoniae- have no cell wall and very small. No capsule
2) long incubation period- 2-3 weeks. Slow growing.
3) Most common in people 5-25 yrs old.
4) Primary atypical pneumonia or walking pneumonia
-low-grade fever, cough, and headache. Can last 3 wks or more.
5) Spread by close contact or closed population in schools, military and families.
6) Do not respond to antibotics that interfere with cell wall structure
-No B- lactam. No vaccine. Recurrent infections common.
1) Bordtella pertussis- small gram negative aerobic rod.
2) Virulence is due to capsule, fimbriae and production of 2 major toxins
3) Toxin aids in bacterial binding to epithelial cells and causes mucous output, decreased ability of phagocytes and NK cells
-binding to B subunit aids in colonization
-fragment is cleaved and enters the cell upon attachment
Tracheal cytotoxin of pertussis
1) Breakdown component of Bordetella's peptidoglycan
2) causes death of ciliated epithelial cells and secretion of IL-1
Signs and symptoms of whooping cough
1) Catarrhal stage
-colonization of ciliated epithelium (nasopharynx, trachea, bronchi, bronchioles)
-fever, malaise and coughing--increased for 10 days
-toxins cause death of epithelial cells and build up of mucous
-bacteria can be cultured at this time and antibiotics can reduce severity of disease
2) Paroxysmal stage
-loss of ciliated epithelium cause mucous to accumulate and the infected person has prolonged and paroxysmal coughing that often ends in characeristic inspiratory gasp (whoop)
-bacteria no longer present
-may last as long as 6 wks
3) brain damage from severity of coughing in infants
4) adults have milder form that resembles bronchitis
5) component of the TDap/DTap vaccine
-after childhood booster needed every 10 yrs
-adult onset can appear as chest cold/common cold
1) Myobacterium tuberculosis- obligate aerobic bacilli, slow generation time
2) unusual cell wall, waxy lipids
-cell wall does not decolorize when treated with acid-alcohol (acid fast)
Stage one of tuberculosis
-not obligate intracellular, but can reproduce and hide from macrophages
1) breathe in organism from respiratory droplet
2) bacteria are taken up and replicate in macrophages, chemotaxic response calls other phagocytes, form tubercle/granuloma in lung tissue, also can spread to lymph nodes and other body tissues
3) caseous center is formed, may be calcified. Bacteria don't grow, remain dormant for yrs.
4) 9/10 people- immune system keeps infection controlled.
-infection can be latent.
Stage two of tuberculosis
1) 10% of those infected go on to stage 2
2) aging, stress, malnutrition and HIV can allow disease to progress
3) liquefaction occurs and caseous center enlarges and forms air-filled cavity where bacteria reproduce outside of macrophages
4) tubercle ruptures, releases bacilli into bronchiole/system
5) cough results in aerosol of respiratory droplets containing organisms. INFECTIOUS
6) chronic infections often result in gradual spread of lesions in lungs
Test and treatment of TB
1) TB skin test- delayed type hypersensitivity reaction, cell mediated response
2) antibiotic therapy is not always effective
- require at least two antibiotics due to slowness of reproduction allowing organism to become resistant
-therapy lasts months, DOTS therapy effective
-antibiotic resistant TB (MDR-TB, XDR-TB, TCR-TB)