Anaerobes Flashcards
Clostridium perfringens
Morphology:
1) Gram Positive Bacilli (Rods)
2) Spores!
_Heat-Resistant
_Resistant to Drying (Desiccation) and Disinfectants
_Can Survive for Years in Environment as Spores
______________
Diagnosis:
1) Anaerobic Culture
2) Hemolytic on Blood Agar
3) Gas Gangrene when it grows
4) Food-Borne: Clinical
______________
Pathogenesis:
1) C. perfringens Type A is most important.
Source: @ Colon and @ Soil
2) Alpha-Toxin:
Phosopholipase, Disrupting Host Cell membranes
=> Cell Lysis!!
(Most important)
3) Theta-Toxin:
Alters Capillary Permeability.
Toxic to Heart Muscle.
_______________
Epidemiology:
1) Spores form Environment or Colonic Flora:
_Bullet Wounds, Compound Fractures, Automobile Accident
2) Delay Between Injury and Manifestations b/c Spores Need Time to Multiply
_~48 Hours later(w/ significant delay btween injury and surgery)
3) Gas Gangrene:
@ Traumatic Wounds with Muscle Damage when Contaminated.
______________
Manifestations: 1) Gas Gangrene: _Alpha-Toxin _@ Muscle (1) Severe Pain @ Site with Heaviness/Pressure (2) Rapidly Spreading Edema and Necrosis (3) Foul-Smelling Odor @ Site (4) Crepitus (5) Hemorrhagic Bullae
Systemic Absorption of Toxin: (1) Intravascular Hemolysis (Hemolytic Anemia) (2) Shock (3) Renal Failure (4) Coma, Death (Surgical Emergency)
______________
2) Food Poisoning:
_Enterotoxin
_Heat-Resistant Spores survive cooking; Multiply when food is left out.
Source: Warm Meat Dishes, e.g. Stews, Soups, Gravies.
_#3 Food-Borne in U.S.
(1) Nausea
(2) Abdominal Pain
(3) Diarrhea
**Vomiting is Rare
=> Contrast: Staph Causes Vomiting
**No Fever
_Incubation Period: 8-24 hrs
_Spontaneous Recovery: Within 24 hrs.
______________
Treatment:
1) Excise devitalized tissue!!
2) Broad-Spectrum Cephalosporins
(b/c often other bugs contaminate too)
3) Massive Doses of Penicillin
4) Hyperbaric Oxygen Chamber to slow disease spread.
5) Food-Borne: Supportive
Clostridium botulinum
Morphology:
1) Gram Positive Rods (Bacilli), Large
2) Spores:
_Resistant to Long Boiling
_Requires Moist Heat (Autoclave) to Destroy
____________
Diagnosis:
1) Only in Reference Labs: Toxins in blood, intestinal contents, or remaining food.
(require mice inoculation)
____________
Pathogenesis:
1) Botulinum Toxin
_Most potent toxin in nature.
_Binds to NMJ and Blocks Release of ACh
=> Flaccid Paralysis
(Neurotoxic Exotoxin)
2) Botox is Heat-Labile, but Resistant to GI Enzymes
=> Readily Absorbed into Blood if Unheated Toxin is Ingested.
____________
Epidemiology:
1) Spores @ Soil, Ponds, Lakes
2) Most Often:
Home-Canned Products
(Haven’t been heated to sufficient temps.)
3) Frequently seen in Infants 3 weeks - 8 months.
_ Weaning or with Dietary Supplements, especially Honey!!
(Honey is not sterile).
____________
Manifestations (in order):
First Signs:
1) Nausea, Dry Mouth
Later:
2) Cranial Nerve Signs
(Ptosis, Dysphagia, etc.)
3) Symmetric Descending Paralysis
4) Respiratory Paralysis
____________
Treatment:
1) Mechanical Ventilation
2) Horse C. botulinum Anti-Toxin
(Adults Only)
Clostridium tetani
Morphology:
1) Gram Positive Rod (Bacilli), Slim
2) Spores: Drumstick appearance
_Viable in Soil for many years
_Resistant to Boiling for several minutes.
_Resistant to Most Disinfectants.
3) Tetanus Toxin _Antigenic _Readily Neutralized by AntiToxin _Heat-Labile _Rapidly Destroyed by GI Enzymes \_\_\_\_\_\_\_\_\_\_\_\_
Pathogenesis: 1) Tetanospasmin (Tetanus Toxin) _Degrades protein required for NT Release. (Glycine and GABA) _Neurotoxic Exotoxin
2) => Thus, Inhibits Inhibitory Neurons
3) => Spastic Paralysis
____________
Epidemiology:
1) Spores @ Soils, especially Manure-Treated Soils
2) Introduced into Wounds Contaminated with Soil or Foreign Body:
_Wounds Often Small: e.g. via Splinter or Nail.
______________
Manifestations:
1) Trismus (Lock-Jaw):
_Masseter Muscles are often First Affected
2) Swallowing and Respiratory Muscles
3) Back Muscles (opisthotonos) in extreme cases.
______________
Diagnosis:
1) Clinical
______________
Treatment:
1) Human Tetanus Ig (HTIG)
_Neutralizes unbound toxin
2) Supportive
3) Benzodiazepines:
_Relax muscles
______________
Prevention:
1) Routine Active immunization with DTaP: Tetanus Toxoid combined with Diphtheria Toxoid and Pertussis Vaccine.
2) Or, Primary Immunization in Childhood and DT for Adults.
3) Prophylactic HTIG for Unimmunized ppl with Tetanus-prone Wounds ASAP. (Passive Immunity)
Clostridium difficile
Morphology:
1) Gram Positive Rod
2) Spores
Pathogenesis:
1) A Toxin: Enterotoxin
=> Diarrhea
_Causes Cell Rounding
_and Disruption of Intercellular Tight Junctions,
_Followed by Altered Membrane Permeability and Fluid Secretion.
2) B Toxin: Cytotoxin
=> Pseudomembrane composed of Fibrin, Leukocytes, Necrotic Colonic cells.
______________
Epidemiology:
1) Normal Colonic Flora in 2-5% of ppl
2) Disease Follows administration of Broad-Spectrum Antibiotics
(Due to alteration of colonic flora)
(esp. Ampicillin, Cephalosporins, Clindamycin)
______________
Manifestations: 1) Mild Diarrhea: _ Watery or Bloody _ Abdominal Cramps _ Leukocytosis _ Fever
2) Pseudomembranous Colitis (PMC):
_Severe Inflammation of colon
_Viewed on Endoscopy
_Occasionally Lethal
______________
Diagnosis:
1) Rapid Enzyme Immunoassay (EIA) of Toxins A, B @ Stool Samples.
______________
Treatment:
1) Discontinue Antibiotics if possible
2) Metronidazole or Vancomycin, (oral)
Bacteroides fragilis
Morphology:
1) Gram Negative Rods (Bacilli), Slim
2) Pale-Staining
3) Encapsulated:
Inhibit Phagocytosis
4) Surface Pili (Adhesion)
5) Produce Superoxide Dismutase
_Tolerant to Oxygen
______________
Pathogenesis:
1) Normal Colonic Flora
=> Trauma or Disease, e.g. Ruptured Diverticulitis
(Endogenous Infection)
2) **Forms Abscesses
Typically Mixed Infection with Other Anaerobes and Facultative Bacteria, e.g. E. coli
______________
Manifestations:
- *Abscess Results in:
1) Abdominal Pain
2) Low-Grade Fever
If Abscess Ruptures:
3) More Abscesses
4) Peritonitis
______________
Treatment:
1) Drainage of Abscess
2) Debride Necrotic Tissue
3) Metronidazole, Clindamycin
Anaerobes
Most Anaerobes Produce Endogenous Infections.
Growth:
1) Fail to grow in presence of 10% oxygen
2) Oxygen Tolerance Varies
3) Anaerobes lack the Cytochromes Required to Use Oxygen
4) Catalase, Superoxide Dismutase: _Neutralize Toxic Oxygen Products (Hydrogen peroxide and Superoxide _Most Anaerobes Lack these Enzymes _Many Virulent Anaerobes Have them
______________
Classification:
1) Anaerobic Gram Positive Cocci: (Form Chains)
=> Peptostreptococcus
2) Anaerobic Gram Negative Bacilli, Non-Sporing:
=> Bacteroides
=> Fusobacterium
=> Porphyromonas
______________
Epidemiology, Pathogenesis:
1) Colonize Oxygen-Deficient areas of the body
2) Most Anaerobic infections are Derived from Normal Flora
3) Typically when Displaced into Normally Sterile Tissues
4) Most Anaerobic infections are Mixed.
______________
Manifestations: 1) Necrotizing Fasciitis 2) Thrombophlebitis 3) Bacteremia 4) Foul-Smelling Pus and Crepitation (Gas in Tissues) => Signs of Anaerobic Infx.
______________
Isolation:
1) Pus/Fluid from infected site is preferred as Transport Medium
Diagnosis:
1) Gram Stain: Diagnostic b/c normal would be sterile.
______________
Treatment:
1) Drain Abscess
2) Metronidazole if *Below Diaphragm.
(Fecal Anaerobes are Resistant to many Beta-Lactams.)
3) Penicillin if Above *Diaphragm
