(Dr. Lasaca)
Complement System:
1. Opsonization-C3b enhancement
2. Cytolysis- inv. of c5-c9
3. Inflammation- release of histamine
Vascular permeability
Bacterial Non-Granulomatous
# Of invading organisms
Portals of entry
Inoculation
Decisive Period
(Int. Defense Mechanism)
=Mucous membranes
-Resp.tract
-GIT
-GU
-Conjunctiva
=Skin
=Parenteral rout
-Penetration/invasion
of host defenses
-Capsules
-Cell wall comp.
-enzymes
-siderophores
-Antigen variation
-cytoskeleton
- damage
to host cells/
cytopathic
effect
-direct
Adherence
Organism destroyed
Latent/smoldering
Infection
(char. Lesions
can t be seen)
(+) Rep
Overt
Infection
(vis ible)
Offending organis m
Engulfed by macrophages
Ingestion
Phagososme
Phagolysosome
Residual bodies
Release of materials
STAPHYLOCOCCUS
- Normal flora: Nasopharynx and skin
- Infective only following large dose inoculation
- Most often form SUPPURATIVE lesion with walled off
abscesses or spreading cellulitis
- Mild regional lymphandenitis
- S. Aureus Sepsis!FATAL! Emergency!
Furuncles (Boil)
Focal SUPERFICIAL suppurative inflammation of skin
beginning in a single hair follicle
Carbuncle:
deeper SUBCUTANEOUS suppurative spreading
laterally, generally involving skin of UPPER BACK or
NECK
Impetigo
Superficial infection, mostly in children, COLORED
CRUST, both by staph and strep
if strep Lymphangitic spread (Red Streaks)
Pneumonia
Generally destructive bronchopneumoniamay rupture
into pleura EMPYEMA
Endocarditis
Left or right sided
Most frequently destructive vegetative endocarditis
TOXIN RELATED DISEASES
1. Staph Food Poisoning
toxin in contaminated food
acute, self- limited, onset 1-6 hours after consumption
2. Toxic Shock Syndrome
sporadic
Related to infected tampons , intractable shock,
sometimes fatal
3. SSS
-
BACI LLUS:
Anthrax
B. Anthracis
Exotoxin hemorrhage, inflammation
Predominantly, a disease of sheep
In humans, forms a malignant pustule at entry site
(blisters, necrosis, edema, inflammation)
Pustular Lesion
CLOSTRI DIUM
soil
invade underconditions:
1.
Low Oxygen tension
2.
Previous tissue damage
3.
Poor phagocytosis
-poor immune system of patient
Clostridium tetani
Tetanospasmin Neurotoxin bloodstream binds to
peripheral nerve endings ascends to cell body in CNS,
all without causing no harm when it passes into the
pre-synaptic terminals of inhibitor spinal interneurons
production sympathetic manifestations
Clostridium Botulinum
Spores resist boiling
ingestion of toxin blood attaches to synaptic
vesicles of cholinergic nerves blocks release of
acetylcholine
descending paralysis
Found in:
1.
2.
3.
4.
Home-canned food
Less oxygen tension
Pickles
Sauerkraut
STREPTOCOCCUS:
2 Disease Patterns:
-Suppurative Inflammation
-Hypersensitivity disease
-Rheumatic Fever
-Glumerulonephritis
-Erythema Nodosum
1. Scarlet Fever
auto strep PHARYNGITIS + Rash caused by
Erythrogenic toxin
3-15 years old
Ras pberry/Strawberry tongue
Notorious ly associated with post streptococcal sequelae
2. Impetigo
3. Bronchopneumonia
Strep Pneumoniae
Most cases of Lobar Pneumonia (Polysaccharide
Caps ule)
bacterial meningitis
GRAM (+) BACILLI
1.
2.
3.
Bacillus
Clostridium
Corynebacterium
Clostridium Perfringes
Invasive infections:
Necrotizing cellulitis
Myonecrosis (gas gangrene)
produces gas bubbles in tissues (crepitations)
extensive necrosis of muscles
toxins induce active hemolysis
Clostridium difficili:
Ps eudomembranous colitis
(+) inflammatory exudates spewing out from crypts
seen: Clindamycin, Lincomycin, Cephalosporins
Antibiotic therapy
E.Coli
-