Clostridium, Actinomyces israelii, Nocardia asteroides, Aeromonas, Plesiomonas Flashcards
Describe the physical structure of Clostridium
G+ Rods, Usually Rounded Ends
Pairs/Short Chains
Sporulatin
Describe the oxygen sensitivity of Clostridium
Anerobic
Clinical presentation of Clostridium botulinum
18-24 hour incubation
Bilateral Cranial Nerve Palsies with Progressive Descending Flaccid Paralysis
How do people die of Clostridium botulinum?
Involvement with heart or diaphragm
Main sources of Clostridium botulinum infection?
Home-Canned Foods, Rarely commercial
Entry Woulds, like needles (botox, black tar heroin)
How does Clostridium botulinum manifest in children?
Rapidly colonizes gut, replaces developing flora
Floppy Baby Syndrome
Caused by spores in honey
Pathogenesis of Clostridium botulinum?
AB neurotoxin
- B binds neuron end plates, A blocks ACh release
No ACh = Flaccid Muscle Paralysis
How does Clostridium botulinum block ACh release?
Cleaving synaptobrevin
How is Clostridium botulinum controlled?
Use Antitoxin from CDC as early as possible
Clinical presentation of Clostridium tetani
Rigid Paralysis
Eventually Death from Inability to Breathe
Epidemiology of Clostridium tetani?
Spores in soil/feces
Introduces by fomites in skin
How do neonates get Clostridium tetani?
Umbilical stump infection
Pathogenesis of Clostridium tetani?
A-B neurotoxin, tetanospasmin
- Absorbed at neuromusc. junction, retrograde transport to motor neuron - Binds irreveribly to and re-uptaken by presynaptic mem. of inhib neurons - Cleaves synaptobrevin, no GABA release
How is Clostridium tetani controlled?
DTaP, Tdap
What can you do for a tetanus patient?
Tetanus Immune Globulin antitoxin avoid stimulation Early tracheostomy to prevent laryngospasm suffication Muscle Relaxants Metronidazole
Describe the presentation of Clostridium perfringens
Infected wound suppurating
Foul Discharge, Tissue Necrosis
Toxemia, Shock Death
Also – can present as food poisoning –> gut necrosis
Epidemiology of Clostridium perfringens
Traumatic Tissue Injury, Esp if anaerobic conditions
Why is Clostridium perfringens typically polymicrobial?
Other infection will produce the anoxic environemnt Clostridium perfringens requires
Pathogenesis of Clostridium perfringens?
Extracellular enzyme secretions destroy tissue, allow invasion
- alpha toxin
- hyaluronidase, collagenase
- beta-toxin
- enterotoxin
Gas from ferm. causes tissue distention, compressed vessels
What does alpha toxin do?
Its a lecithinase (phospholipase)
How is Clostridium perfringens controlled?
Prompt surgical debridement
How is Clostridium perfringens treated?
Metronidazole, Penicillin, and Clindamycin stop growth
Clinical presentation of Clostridium difficile?
Usually following antibiotics
Watery Diarrhea early
Leukocytes penetrate connective tissue of bowel
- Form pseudomembrane
Which anti-biotics are most prone to cause Clostridium difficile development?
beta-lactams, clindamycin
Development of Clostridium difficile associated diarrhea requires what two things
- presence of C diff
2. disruption of native flora
Who gets Clostridium difficile?
People on antibiotics or PPIs
Normal influence of Clostridium difficile on the colon?
Important for T-reg development
Most Clostridium difficile patients are infected where?
A Health Care Setting
Pathogenesis of Clostridium difficile?
Enterotoxin (Toxin A) – Fluid Acc
Cytotoxin (Toxin B) – Kills gut epithelial cells
How is Clostridium difficile controlled/treated?
Stop previous antibiotics if you can Replenish gut flora Vancomycin, Metronidazole Fecal transplant Fluid Replacement
Physical structure of Actinomyces israelii
G+
Branching, Fragmenting Filaments
Oxygen sensitivity of Actinomyces israelii?
Facultative anerobes
Actinomyces israelii colonies are in what shape?
Molar tooth
Clinical presentation of Actinomyces israelii?
Swollen, pyogenic abscess with draining fistulae (lumpy jaw)
“Sulfur granules” apparent in collected pus
Common in face/neck, lungs, ab, skin
How do people typically get Actinomyces israelii infection?
Tooth extraction or poor oral hygiene
Thoracic inf from aspiration
abdominal inf from perforated gut/appendix
Foot from soil bacteria
Who gets Actinomyces israelii?
IC patients
How is Actinomyces israelii treated?
Surgical drainage of abscess
Parenteral Pen G for a few weeks
Unique physical traits of Nocardia asteroides?
Actinomycete
Shorter mycolic acids, partially acid fast
aerobic, lives in soil
Clinical presentation of Nocardia asteroides?
Lobar Pneumonia in Alcoholics or IC
Lung abscesses
Can spread to brain –> meningitis, brain abscess
In foot from soil
How do people get Nocardia asteroides infection?
Opportunistic infection
Lung aspiration of vomit
How is Nocardia asteroides treated?
SxT
Physical structure of Aeromonas hydrophilia, plesiomonas shigelloides?
G- Rod
Fac. anerobe
Motile
Where are Aeromonas hydrophilia, plesiomonas shigelloides found?
Common Fish Pathogens
Aeromonas hydrophilia - Fresh
Plesiomonas shigelloides - Salt
Clinical presentation of Aeromonas hydrophilia, plesiomonas shigelloides infection?
Gastroenteritis – can be watery or blood and mucas
Cellulitis from infected wounds
Myonecrosis
How do people typically get Aeromonas hydrophilia, plesiomonas shigelloides?
Infected food, water
Tissue entry after trauma (fish-hook)
SCUBA biofilms
Pathogenesis of Aeromonas hydrophilia, plesiomonas shigelloides?
LPS, PG toxicity
ACT toxin
Pili grab onto gut epithelium
How is Aeromonas hydrophilia, plesiomonas shigelloides controlled?
Avoid undercooked seafood
How do you treat Aeromonas hydrophilia, plesiomonas shigelloides?
SxT, Tetracycline
