Anaerobic Pathogens Flashcards
clostridium sp.
*OBLIGATE ANAEROBIC
*gram POSITIVE rods
*FORM ENDOSPORES
*part of the normal flora
clostridium difficile (C diff) - overview
*gram POS anaerobic rod that freely forms spores
*oxygen is toxic
*infection limited to large intestine
*disease is toxin-mediated (not invasive)
clostridium difficile - virulence factors
- Toxin A (enterotoxin) - causes cell death of intestinal mucosa
- Toxin B (cytotoxin) - causes actin depolymerization
C diff - toxin A (enterotoxin)
*chemotactic for neutrophils; stimulates infiltration of PMNs
*cytopathic effect: disruption of tight cell-to-cell junction
*increased permeability of intestinal wall and subsequent diarrhea
C diff - Toxin B (cytotoxin)
*causes actin to depolymerize, with resultant destruction of cellular cytoskeleton
3 required events to get C diff infection:
hospitalization (usually), followed by:
1) change in normal GI flora (ANTIBIOTICS)
2) acquire C diff spore (usually from environment or another person)
3) inadequate IgG response to toxins A and B
what is the name of the disease caused by C diff infection
pseudomembranous colitis
risk factors for C diff
**recent antibiotic exposure
*hospitalization
*recent GI surgery
*recent chemotherapy
*proton pump inhibitors
what is the highly virulent strain of C diff in North America
BI/NAP1
*more likely to cause death
C diff - clinical manifestation
*acute onset of severe, watery diarrhea
*fever, toxicity, high WBC count
**COMPLICATION = TOXIC MEGACOLON
C diff - treatments
*oral vancomycin (recurrences can occur)
*stool transplant is highly effective for recurrent infections
C diff - diagnosis
*demonstration of Toxin A and B in the stool by ELISA
clostridium perfringens - overview
*gram positive rod
obligate anaerobe
**beta (DOUBLE RING) hemolysis
what is the pathogen characterized by beta double ring hemolysis
clostridium perfringes
clostridium perfringens - virulence factors
*alpha toxin - lyses erythrocytes and other cells; mediates massive hemolysis
*beta toxin - causes intestinal stasis and necrotic lesions
*enterotoxin - alters membrane permeability and causes diarrhea
clostridium perfringens - clinical presentation (in soft tissues)
*GAS GANGRENE (characterized by gas formation)
*cellulitis, fasciitis, myositis with myonecrosis
*often follows trauma
*infection leads to muscle necrosis and septic shock
*can cause death within 24 hours
clostridium perfringens - clinical presentation (food poisoning)
*only in intestine and only making enterotoxin
*causes watery diarrhea, abdominal cramps
*transmitted by poultry
clostridium perfringens - diagnosis
*gram stain (gram + rods)
*anaerobic culture
clostridium perfringens - treatment
high dose penicillin & surgical debridement
clostridium tetani - overview
*anaerobic spore-forming
*gram positive rod
*classic “stepping on a rusty nail”
clostridium tetani - virulence factors
*tetanus toxin (tetanospasmin)
*taken up by motor neurons (by pinocytosis)
*INHIBITS the INHIBITORY NEURON
*irreversible lack of inhibition of motor neuron produces tetanus (motor neuron is constantly active)
primary host defense against clostridium tetani
antibodies against the tetanus toxin (this is why we get the vaccine)
3 clinical entities of tetanus disease
1) generalized tetanus
2) localized tetanus
3) neonatal tetanus
generalized tetanus
generalized musculature spasms involving the whole body
localized tetanus
musculature spasms restricted to localized area of primary infection
neonatal tetanus
neonatal infection primarily involving the umbilical stump; very high mortality
PREVENTION = vaccinate mom before delivery
clostridium tetani - diagnosis
*clinical presentation (spasmatic paralysis)
*demonstration of seronegative state (no tetanus antibodies)
clostridium tetani - treatment
*tetanus immunoglobulin (TIG) from CDC
*benzos (relax muscles)
*penicillin (decrease organism number - slowly)
clostridium botulinum - virulence factor & its effect
*produces botulinum toxin - cleaves SNARE proteins, preventing Ach release at the neuromuscular junction
*causes FLACCID paralysis
clostridium botulinum - primary host defense
antibody against the toxin (but we do not immunize against it)
foodborne botulism
*initially - blurred vision, dry mouth, constipation, abdominal pain
*progression to bilateral descending weakness of peripheral muscles with flaccid paralysis
other forms of clinical botulism
*infant botulism
*wound botulism
*inhalation botulism
clostridium botulinum - diagnosis
*clinical presentation
*finding the suspected food source
clostridium botulinum - treatment
*botulinum antitoxin (from CDC)
anaerobic colonic gram NEGATIVE rods
*NON-spore forming
*LPS is a major virulence factor
*part of the normal flora
*obligate anaerobes
*there are a lot of these
actinomyces sp.
*BRANCHING gram POSITIVE rods, obligate anaerobes
*DENTATE appearing colonies on agar
*normal PERIODONTAL flora
*active infections tend to produce and “SPIT OUT” “SULFUR GRANULES” in pus
*tend to cross tissue planes
*often associated with dental caries/extraction and other maxillofacial trauma; treat with PENICILLIN
