Lecture 20 Flashcards
Bacterial Infections of the Resp. Tract
Prefer upper/lower resp. tract
Upper are less severe then lower
lower present as pneumonia
Droplet/airborne
- hard to control
- efficient in confined spaced
Resp. Tract
Streptococcus pyogenes (“Group A Strep”)
upper resp tract infection
-Streptococcal “pharyngitis” (a.k.a. Strep throat)
Gram positive bacteria with large capsule ( >80 different strains/capsular polysaccharide)
30% of pharyngitis in kids and up to 15% in adults (rest are viral) (ages 5-15)
Human reservoir
Droplet transmission(active or 2 week carrier)
Disease is self Limiting
no Immunity to re-infection
Streptococcus pyogenes (“Group A Strep”)
Pathogenesis 3
- Strep enter upper resp. tract (throat) attaches to epithelial cells
- Multiplies in throat, uses capsule to avoid phagocytosis, secrete hemolysin and exotoxins (does not penetrate tissue)
- Symptoms appear
- Inflammation, soreness, exudate, swollen lymph nodes
Treat with antibiotics (prevent becoming asymptomatic carrier)
Throat swab to blood agar media to look for hemolytic colonies
Complication after untreated strep 3
Scarlet fever
- Scarlet fever (rare)
- strep + rash
- caused by erythrogenic exotoxin
- dmgs small blood vessels (high fever, red rash, strawberry inflamed tongue)
Complication after untreated strep 3
Glomerulonephritis
immune complexes (strep antigen + anti-strep antibodies) build up in glomeruli (blood vessels) of kidney -fever, blood in urine
occurs in recovery stage of untreated strep
Complication after untreated strep 3
Rheumatic Fever
Autoimmune disease -> antibodies formed against strep proteins react with antigens found in heart and joint tissues
- fever, inflamm of joints and heart valves
- scarring of heart tissue = heart failure
-3-4 weeks after self-limited strep infection
“Necrotizing Fasciitis” and Strep pyogenes
Flesh eating disease
- produce enzymes that degrade connective tissue
- tissue necrosis, high fever, rapid inflamm
- only by entry into skin via cuts
Resp. Tract
- Mycobacterium tuberculosis
- slow growing acid fast bacteria (mycolic acid surface)
- Lower resp. tract infection
- human only know reservoir
- lacks most virulence factors (symptoms due to immune response)
Two forms of TB: i. Primary Tuberculosis (First time infection)
5% cases (kids Immunocompromised)
- cell response fails (no t helper)
- spreads to other organs
- tissue dmg (blood sputum, coughing, necrotic cavities)
95% cases Tubercles heal by fibrosis and calcification and can be seen in chest x ray (may contain live tb)
no symptoms, latent tb, no free bacteria
- enters lungs by airborne/droplet
- m.tb in lungs ingested by phagocytes but survive and multiply inside phagocytic cells (die and release)
- 3 weeks later helper T cell activate and help phagocytes
- aggressive phagocyte kill m.tb directly or create tubercle that stop spread
Can survive in dormant state
ii. Secondary Tuberculosis
Reactivation of dormant tb in tubercles
-tubercles rupture, tb released into lungs
memory cells activate in delayed hypersensitivity
-night sweats, fever, weight loss (cytokine increase)
Happen years later depending on overall health
Diagnosis of TB
Direct test (look for tb specimens in sputum)3
- Acid-fast staining + microscopy
2. Grow M.tb on laboratory culture media
3. Nucleic acid amplification (PCR) test
Diagnosis of TB
Indirect tests - detect exposure to tb bacteria 2
- Tuberculin skin test Mantoux
- Interferon gamma release assay (IGRA)
- A blood test that detects carrying helper T-cells activated due to an exposure to M.tb
- can replace Mantoux test
Treatment of TB
Pre 1950 = Long term care in sanatorium (strengthen immune system, support care)
Today: Antibiotics
- Isoniazid, Rifampin, Ethambutol, Pyrazinamide
(usually iso + Rif)
26-30 weeks of daily treat
Directly observe therapy
Occurrence of TB
Natives have it lots
Why Tb significant heal concern
Latent
-leading cause of death due to single species
-vaccine not effective
highly infectious with 10 bacterial cells
