KC ID Flashcards
(245 cards)
*Compare and contrast staph vs. strep TSS
STAPH
- 15-30y
- women > men
- pain is rare
- erythroderma rash
- mortality <3%
STREP
- 20-50y
- either sex
- ++pain
- tissue necrosis
- mortality 30-70%
BOTH
- hypotension
- renal failure
- thrombocytopenia
*Treatment for TSS
- Fluid
- O2
- Source removed
- Pressors PRN
- Clindamycin 600-900 mg IV q8 + Tazo/Vanco
- Consider IVIG if poor response
*2 ways to test for botulism
- Detection of botulinum toxin in blood
- Detection of botulinum toxin or C. botulinum in gastric contents, stool, wound, or in the suspected food source
*Name of bacteria causing botulism
clostridium botulinum
*Differential diagnosis botulism
MG
GBS
Pontine infarct
Tick paralysis
Eaton-Lambert syndrome
Paralytic shellfish poisoning
*4 types of botulism. Which is the most common?
Infantile
Wound
Iatrogenic/ Inadvertent
Unclassified
Food borne
*infant is most common per Rosens
*List 2 specific treatments for botulism
Equine antitoxin
BabyBIG
What bacteria is responsible for pertussis
Bordetella pertussis
Explain the clinical progression of pertussis
Catarrhal: 1-2 weeks of URTI sx, cough, indistinguishable from other URTIs
Paroxysmal: 1-2 weeks of increasing cough with whoop +/- post tussive emesis
Convalescent: 1-6mo of a waning cough
Infants may present with apnea instead of the whooping cough
How is pertussis treated
Why do we treat it?
Azithromycin 500mg PO on day one and 250 mg PO day 2-5. Treatment does not reduce the severity of the illness but does help to reduce infectivity
Treat it because it decreases transmission from 3 weeks to 5 days
What pathogen causes tetanus
Toxin produced by Clostridium Tetani
What is the pathophysiology of tetanus
Neurotoxin binds to the motor nerve ending and irreversible blocks the presynaptic release of inhibitory GABA neurons. Without inhibition the motor neurons undergo sustained excitatory discharge, resulting in muscle spasm
What is the major cause of death in tetanus
Autonomic dysfunction: tachycardia, hypertension, hyperpyrexia, cardiac dysrhythmias, diaphoresis
List 3 complications of tetanus
Forceful tetanic muscle spasm can cause vertebral subluxation, fractures, joint dislocation, rhabdomyolysis, laryngospasms, airway edema, dysrhythmias
Think about ortho, rhabdo, dysrrhtymia
How is tetanus diagnosed? What is one clinical test?
Clinically; would cultures are of little value and positive only 30% of the time
Spatula test: touching the oropharynx with a tongue blade. +Ve test if this produces a reflex masseter muscle spasm and the patient bites down on the spatula
Spatula 94% sensitive 100 % specific
What is one differential for tetanus
Strychnine poisoning
What are the main principles of tetanus management
- Supportive care - benzos for spasm, labetalol for autonomic dysfunction, avoid unnecessary stimulation. Intubation and muscle paralysis if necessary
- Tetanus immunoglobulin 500 units IM OPPOSITE from wound to eliminate unbound and circulating toxins
- Prevention of further toxin production - Metronidazole 500mg IV Q6H5
- Vaccination - Tetanus toxoid 0.5mL IM at presentation, 6 weeks, and 6 months
When is tetanus prophylaxis indicated?
Fully vaccinated within 10 years: no vaccination or toxin
Partially or unknown vaccination with minor wound: vaccination only
Partially or unknown vaccination with minor wound: Tetanus toxoid 250mg IM + vaccination series
High risk wound: >6 hr old, >1 cm deep, contaminate, denervated, ischemic, infected
What is the difference between Tdap and DAPT? When are each used
DTP: Diphtheria, tetanus, activated pertussis. Used less now
TdAP: tetanus, diphtheria, acellular pertussis
Used in younger children and as a booster
Those younger than 7 years old should receive diphtheria-tetanus
or DTaP. Patients 7 years old or older should receive Tdap.
What are the 5 types of botulism
Food borne, baby botulism, wound botulism, unclassified botulism, inadvertent (ex. iatrogenic from cosmetic use)
What is the mechanism of paralysis in botulism
Neurotoxins bins to the presynaptic nerve membrane and inhibit the release of acetylcholine causing paralysis
What is the clinical presentation of botulism
Cranial nerve palsies: diplopia, blurred vision, dysphonia, dysphagia, ptosis, vertigo
Descending symmetric paralysis(proximal muscles are weaker than distal muscles)
Anticholinergic toxidrome (constipation, urinary retention, dry skin) and nausea, vomiting, abdominal cramps
No sensory or pain deficits. Reflexes are normal or diminished. Mental status is preserved
How is botulism diagnosed
Clinical diagnosis, confirmed with botulism toxin found in blood or wound (may need to send to special lab)
How is botulism differentiated from Guillain Barre, tick paralysis, or myasthenia gravis
Guillain Barre - ascending weakness with paraesthesia
tick paralysis - ascending weakness with limited bulbar involvement
Myasthenia gravis - pupillary response is preserved and no autonomic symptoms are present; improvement with ice or edrophonium