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118 Cards in this Set
- Front
- Back
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T or F: Corynebacterium diphtheria are gram + aerobic rods
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T
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What disease is caused by C. diphtheria exotoxins?
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Diphtheria
(duh) |
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What two body systems are affected by Diphtheria?
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Respiratory tract
Skin/cutaneous (milder form) |
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T or F: Diphtheria can also present in some humans but in an asymptomatic, carrier state (aka human reservoir)
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T
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How is Diphtheria spread?
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by close contact c infectious material either from:
1)respiratory secretions via direct contact or aerosols (airborne droplet) or 2)skin lesion exudates |
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How does C. diphtheria cause disease (ie what is its mechanism)?
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C. diphth produces toxigenic strains which inhibit protein synthesis of elongation factor 2, which is a component of all protein synthesis
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How can you check to see if a pt had a previous Diphtheria infection?
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check IgG titers
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toxoid
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inactivated toxin
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T or F: Not all C. diphth. make toxins
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T
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T or F: During the 1930s and 1940s, diphtheria virtually eliminated secondary to vaccination
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T
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Production of the Diphtheria toxin depends on what?
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a bacteriophage
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What are the fxns of the B-, T-, & A-domains of C. diphth exotoxin?
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B domain: binds to cell
T domain: inserts into target cell memb. A domain: insertion of A component, catalytic activity, inactivates EF-2 (stopping cellular protein synthesis) |
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What is the basic definition of Respiratory Diphtheria?
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an upper respiratory tract illness characterized by SORE THROAT, low-grade FEVER (<101F), and an ADHERENT MEMBRANE of the tonsil(s), pharynx, and/or nasal cavity (PROBLEMS SWALLOWING)
Adherent memb: A local lesion in URT (upper respiratory tract) is produced and involves necrotic injury to epithelial cells (specifically where the aerosol attaches). Plasma leaks into the area & a fibrin network forms interlaced c C. diphth cells. This "pseudomemb" covers the site of the local lesion. It is at this site where the C. diphth produce the exotoxin that enters the blood & lymphatic system, then affects susceptible tissues (heart, NS) Incubation period of 2–5 days |
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Describe the Diptheria pseudomembrane:
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-tightly adherent to underlying tissue (resulting in bleeding with dislodgement),
- sharply demarcated, - classically gray in color -scraping causes bleeding |
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What is the clinical presentation of a pt c severe Diphtheria (aka "Bull neck"?
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- is associated with extensive "membranous pharyngitis"
- massive SWELLING of the TONSILS, UVULA, CERVICAL LYMPH NODES, submandibular region and anterior NECK - respiratory STRIDOR , respiratory insufficiency and death - SUFFOCATE after aspiration of the membrane. |
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What are 3 diagnostic approaches that can help you indicate Diphtheria?
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clinical features
throat/nasal cultures (eg on McLeod's media) detection of toxin via PCR or ELISA |
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What Tx is available for Diphtheria?
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Hospitalization & ISOLATION (b/c emergent care needed)
Airway support (prepared for possible tracheostomy) Memb removal (laryngoscopy or bronchoscopy) Antitoxin Penicillin (PCN) or erythromycin Test & Treat (c PCN or erythromycin) close contacts & observe for 1 wk Tx completed when have 2 consecutive negative cultures Prevention: serial immunization or periodic booster (toxoid [inactive toxin] vaccine); personal & environmental hygiene |
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What bacteria causes Tetanus?
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Clostridium tetani
(another duh) |
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Describe some basics of C. tetani
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rod-shaped, gram + obligate anaerobe; spore forming; present in the gut of mammals (as parasites); widely found in soil (as spores)
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T or F: C. tetani have a characteristic "tennis racket appearance"; with the racket part being the spore
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T
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T or F: C. tetani spores are very hardy (ie survive a long time)
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T
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How does a pt generally contract Tetanus?
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via a penetrating injury resulting in the inoculation of C. tetani spores along c a co-factor (since most normal healthy pts don't get tetanus c C. tetani alone)
Co factors include: -Co-infection c other bact -Devitalized tissue (as in DM pts) -foreign body -localized ischemia |
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T or F: Neonatal tetanus still causes approximately 5-7% of neonatal deaths worldwide
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T
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Describe the Tetanus pathogenesis
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After inoculation/penetration, the C. tetani produces the exotoxin tetanospasmin, which travels via retrograde axonal transport to spinal cord/brainstem, where it then binds to receptors blocking neurotransmission
Net effect: inhibition of neurons that modulate excitatory impulses from the motor cortex. Inhibition of anterior horn cells and autonomic neurons result in increased muscle tone, painful spasms, and widespread autonomic instability. |
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What is the net effect of the Tetanus pathogenesis?
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Inhibition of neurons that modulate excitatory impulses from the motor cortex. Inhibition of anterior horn cells and autonomic neurons result in increased muscle tone, painful spasms, and widespread autonomic instability.
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T or F: Since C. tetani is anaerobic, it manifests in very deep tissue to avoid any O2 contact
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T
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What is the incubation period of Tetanus?
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days to months, but avg is 7 days
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What are some common clinical manifestations of Tetanus?
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Opisthotonus (Stiff hyperextension)
Risus sardonicus (presence of Sardonic smile) Autonomic System Sx: -Rigid abdomen -Periods of apnea -Profuse sweating -Cardiac arrhythmias -Labile hypertension or hypotension -Fever |
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Describe Sx of Neonatal tetanus
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Sx appear from 4-14 days after birth; onset is typically more rapid
Sx include: rigidity, spasms, trismus (lockjaw), inability to suck, & seizures Occurs in infants who have not acquired passive immunity because the mother has never been immunized. Usually due to poor aseptic technique when cutting umbilical cord of unimmunized moms |
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What causes neonatal tetanus?
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Poor aseptic technique to umbilical cord of unimmunized moms (usually IgG transmits from mom to kid)
or The application of unconventional substances to the umbilical stump (eg, ghee, or clarified butter, juices, and cow dung) |
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What are the Tx options for Tetanus?
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-stabilize pt, debride wound
-To control spasms: minimize stimuli, sedation, neuromuscular blockade -bind up free toxin: immune globin -use abx like PCN or metronidazole -IMMUNIZE (no immunity c natural disease/natural disease does not produce immunity) |
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How long is the recovery from Tetanus infection?
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4-6 wks since Tx kills most axon terminals and pt needs to regrow these terminals
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T or F: Clostridium botulinum is a gram + rod c spores
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T
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Describe C. botulinum
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-obligate anaerobe, spore forming, ubiquitous
-a potential bioterrorism agent |
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What are the clinical forms of Botulism?
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-food-borne (ingestion of preformed toxin)
-infant (colonization of immature GI tract) -wound (infection c in vivo toxin production) -inhalational |
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Which is the most common clinical form of Botulism?
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infant botulism (colonization of immature GI tract)
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How many types of botulisms are there?
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8 diff kinds
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Describe the pathogenesis of botulism:
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once inside the body, the exotoxin disperses widely via the vascular system & binds to a specific receptor (synaptotagmin 2) on the PRESYNAPTIC sides of peripheral cholingeric synpases & enters cell. After gaining entrance to cell's cytoplasm, the exotoxin produces an irreversible disruption in stimulation-induced Ach release by that presynaptic nerve terminal
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What receptor does C. botulinum exotoxin bind to?
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synaptotagmin 2
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What is the recovery period for Botulism?
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6 months b/c requires new synapse for recovery
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C. tetani & C. botulinum toxins MOA:
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effects on nerve-muscle (tetanus - continuous stimulation; botulinum (botox) - blocks stimulation by blocking ACH, thus paralyzing)
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What is probably the most potent known poison?
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Botulinum toxin
FYI: estimated that one gram of aerosolized botulism toxin could kill at least 1.5 million people MLD (minimum lethal dose in experimental mice) is 0.0003 mcg/kg (MLD for sodium cyanide 10,000 mcg/kg) |
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T or F: Botulinum toxin has no smell or taste
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T
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T or F: Botulinum is resistant to degradation by gastric acidity and human alimentary enzymes, BUT denatured by heating above 80C
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T
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Describe Botulism epidemiology
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110 cases annually in US
70% infant botulism: honey and environmental dust 25% food borne: home canned foods, fermented fish from Alaska 5% wound: “black tar” heroin injection |
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Describe infant botulism
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Median age 3-4 months
Constipation, weakness, feeding difficulties, descending or global hypotonia, drooling, anorexia, irritability, and weak cry Diagnosis: clinical presentation, confirmed by isolation of C. botulinum spores or toxin from stool |
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What is the clinical presentation of botulism?
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floppiness
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Describe food-borne botulism
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usually begins w/in 12 to 36 hours after ingestion of the preformed toxin
-Early stage (Prodromal) symptoms: N&V, abd pain, diarrhea, and dry mouth with sore throat -Symptomatic illness: *Cranial nerve involvement (blurred vision -secondary to fixed pupillary dilation and palsies of cranial nerves III, IV, and VI, diplopia, nystagmus, ptosis, dysphagia, dysarthria, and facial weakness) *Descending muscle weakness usually progresses to the trunk and upper extremities, followed by the lower extremities *Urinary retention and constipation *Respiratory difficulties (eg, dyspnea) requiring intubation and mechanical ventilation |
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How can you Dx for botulism?
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serum toxin assay
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Tx for Botulism?
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Stabilize patient
Remove free toxin: antitoxin or immune globulin Antibiotics for NON-GI botulism: PCN or metronidazole |
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T or F: Don't give children <1yo raw honey b/c may have botulinum spores
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T
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About how many diff mosquitoes are known to infect humans in the US
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~40
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When are the peak infection times of ticks?
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spring & summer, which is the NYMPH portion of the tick's 2yr life cycle
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What are the stages of a tick's life cycle?
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larvae-->nymph-->adult
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T or F: Nymphs are responsible for 90% of all tick infections
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T
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T or F: Ticks are the leading cause of vector-borne infections in North America (2nd is mosquitoes)
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T
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What is the most effective way to combat tick-borne diseases?
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focus on measures to prevent them from attaching to the body
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What are the 3 types of ticks?
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Ixodes scapularis (Deer Tick or Blacklegged tick)
Amblyomma americanum (Lone Star Tick) Dermacentor variabilis (Dog tick) |
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What are 7 tick-borne diseases?
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Definately know these 4:
-Lyme Disease -Rocky Mountain Spotted Fever -Babesiosis -Ehrlichiosis -Tularemia -Colorado Tick Fever -Relapsing Fever |
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What bact causes Lyme Disease?
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Borrelia burgdorferi (a gram - spirochete)
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T or F: B/c there are many subtypes of Borrelia, different borrelia may be responsible for Lyme disease in Europe and Asia
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T
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T or F: Ticks that spread Borrelia spread Lyme Disease
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T
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Which type of tick is responsible for spreading Lyme Disease in Eastern North Central, and Southern US?
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Ixodes scapularis (deer tick)
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T or F: Syphillis (Treponmea pallidum) is also a spirochete
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T; just in case you really wanted to know
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What is the regional spread of lyme disease?
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North of Maryland & Michigan & Wisconsin
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Where does the Borrelia burgdorferi live in the tick?
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in its midgut, and disseminates to salivary glands when eating
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It takes 24hrs for blood meal to reach midgut of tick, & at least 24hrs more for dissemination of bact into tick saliva. So, the tick needs to be attached to a host for how long before it can actually infect host?
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48hrs
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What are the 3 stages of clinical manifestations of Lyme Disease?
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Stage 1-Early localized
Stage 2-Early disseminated Stage 3-Late or Chronic disease |
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What is the early localized clinical manifestation of Lyme disease?
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erythema migrans
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What is some basic info on erythema migrans?
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Typically near axilla, inguinal region, behind knees, belt line
Usually asymptomatic Expansion with central clearing “bulls eye” 10% have multiple skin lesions: due to spirochetemia |
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T or F: An enlarged nymph after blood meal is ~3x bigger than normally was
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T
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What are the early disseminated clinical manifestations of Lyme disease?
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Erythema migrans ("bull's eye" rash), at sites other than original tick bite
Fatigue Malaise Head-ache or neck pain Myalgias, arthralgias Adenopathy |
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When do the early disseminated clinical manifestations of Lyme disease occur?
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days to months after tick bite
FYI: In some cases, this stage is 1st s preceding early localized erythema migrans |
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Name 2 more major Sx of Early disseminated Lyme disease
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Carditis
-Heart block of any degree (disease in the electrical system of the heart) -Pericarditis Neurologic-->Banwarth's Syndrome Triad -Lymphocytic Meningitis (Lumbar puncture=100WBC, lymphocytes, elevated protein, normal glucose) -Cranial Nerve Palsies (can affect both sides; usually facial like Bell's) -Peripheral Neuropathy |
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Late persistent/chronic Lyme disease
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-occurs months to yrs after initial infection, c no Tx
Musculoskeletal: -arthralgias -arthritis that affects one large joint (monoarthritis=knee) Tertiary Neuroborreliosis; -Encephalopathy -Neurocognitive dysfxn (usually subtle in US, more prevalent in Europe) -Peripheral neuropathy |
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Lyme Disease: Dx
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Early Localized disease: Erythema migrans, usually seroNEGATIVE
Early Disseminated: Facial palsy, lymphocytic meningitis, carditis, serology is POSITIVE but should never Dx by serology alone |
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Describe Lyme disease serology
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DO NOT test unless pretest probability suggest Dx, DO NOT test if erythema migrans present (you will Tx them anyway)
Test is a 2-step approach: 1)ELISA or IFA: good screening test, sensitivity is high, but high incidence of false + b/c low specificity. This is due to cross-reacting anitbodies c other Borrelia, Syphilis, Leptospirosis, Viruses, Lupus, RA, Gram negative bacteria, Malaria (5 percent of normal population) In laymen's terms for those of us who aren't Dr. Akhter: If get Neg ELISA = pt DOESN"T have Lyme disease IF get Pos ELISA = can't specifically say it's Lyme disease 2) Western Blot: to detect antibodies c higher specificity |
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If Lyme disease Sx present for <4 weeks, test for which 2 antibodies?
If >4 weeks, test for which single antibody? |
both IgM and IgG
IgG alone |
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What is the Western Blot criteria for Lyme disease?
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<4 weeks: Two of Three- IgM ospC(24), 39, 41
>4 weeks: Five of Ten- IgG 18, 21, 28, 30, 39, 41, 4, 58, 66, 93 |
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T or F: Early abx may prevent seroconversion
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T
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Describe Lyme Disease Tx if:
Tick found on body? Early Localized? Early Disseminated? |
Tick found on body (engorged nymph, endemic area): Doxycyline (a tetracycline) one dose (200mg)
Early Localized: Doxycyline (10-21 days) (treats ehrlichiosis as well); Amoxicillin, Cefuroxime (14-21 days); Remember no doxy in children (b/c discolors teeth), pregnancy or lactation (b/c results in fetal bone problems) Early Disseminated: -Facial Nerve Palsy: oral Tx as for localized -Meningitis: IV Ceftriaxone, Cefotaxime (14-28days) -Carditis: IV Ceftriaxone, Cefotaxime, Penicillin G (14-21 days) |
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What are IV Ceftriaxone & Cefotaxime
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3rd generation cephalosporins
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What bacterial infection leads to Rocky Mountain Spotted Fever (RMSF)?
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Rickettsia rickettsii
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Rickettsia rickettsii
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an obligate intracellular bact (pleomorphic Gram-negative coccobacillus)
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T or F: RMSF is the most common rickettsial disease in USA & is potentially fatal even in previously healthy young ppl
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T
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T or F: RMSF affects the contiguous 48 US states, except for Vermont & Maine
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T
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During which seasons is RMSF most prevalent?
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spring & summer
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About how many cases of RMSF are usually reported annually?
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250-1200 (BUT in 2004-2006 there were ~2000 cases)
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What populations are usually most affected by RMSF?
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children <10 yrs
adults 40-64yo men whites |
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What is the primary vector of RMSF in most of the USA?
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American dog tick (Dermacentor variabilis)
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T or F: The Rocky Mountain wood tick (Dermacentor anderson) is a major vector in the Rocky Mountain region and Canada
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T
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Describe the INITIAL clinical manifestations of RMSF
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Tick is attached for 4-6hrs
Mean incubation period is 7 days In first 3 days, 3% of pts feel the classic clinical triad (FEVER, HEADACHE, & RASH) Initially, sudden onset of fever, significant malaise, & sever headache (usually describe by pt as worst ever felt); usually accompanied by myalgia, anorexia, N&V, abd pain, & photophobia |
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Describe the LATER clinical manifestations of RMSF
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2 wks after tick bite, 60-70% of pts feel the classic clinical triad (FEVER, HEADACHE, RASH)
A rash appears typically 2-5 days after onset of fever that is small (1-5mm in diameter), blanching erythematous macules initially on wrists & ankles, c subsequent centrifugal progression to the palms & soles; spreads centripetally from wrists & ankles to arms, legs, & trunk HOWEVER, 9-12% of pts don't break out in a rash |
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What is the classic clinical triad of RMSF?
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FEVER
HEADACHE RASH |
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Describe the FINAL clinical manifestations of RMSF
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ACUTE RENAL FAILURE in severe cases
Various neurological manifestations: -lethargy, photphobia, meningismus, amnesia, bizarre behavior suggestive of psychiatric illness, or transient deafness Fatal in 5% (treated) & 20% (untreated) |
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RMSF Dx
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PE & Epidemiology:
-WBC can be low, normal, or high -Progressive thrombocytopenia -Elevated BUN & Cr, transaminitis -Lumbar Puncture=WBC<100 lymphocytic or polynuclear, normal glucose, elevated protein -Skin Bx: direct immunofluorescence -Serologic testing: acute 7-10 days after onset, convalescent 14-21 days after onset |
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RMSF Tx
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DON'T WAIT for Dx testing/serology!!! Start Tx as soon as you suspect
Give dioxycycline to all children & nonpregnant adults; Give chloramphenicol to pregnant women (fatal side effect is aplastic anemia) Usual length of Tx=7 days |
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What are 2 impt erythrocyte pathogens?
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Babesiosis (Babesia)
Malaria |
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T or F: Babesiosis causes hemolysis
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T
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T or F: Babesia microti in US and babesia divergens in Europe
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T
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What is the vector of Babesiosis?
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Ixodes scapularis (Deer tick)
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When does Babesiosis mostly occur?
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spring & summer
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Where does Babesiosis (Babesia microti) occurr?
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northeastern & northwestern US:
Long Island, New York, and Nantucket and Martha's Vineyard, Massachusetts (seropositivity in 4-7%) Surveys in Rhode Island and Connecticut suggest that as many as 9 to 21 percent of children and adults in highly endemic areas have been infected |
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T or F: In endemic areas, Babesiosis may also be transmitted by blood transfusion, transplacental
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T
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T or F: Most pts of Babesiosis have asymptomatic infection. More sever disease found in pts >50yo, depressed cellular immunity, underlying malignancy, ASPLENIC (post-splenectomy, sickle cell disease) indvls
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T
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Why is ASLPENIC bad?
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b/c spleen fxns to remove bad RBCs
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T or F: ASPLENIC pts have a very high risk for Babesiosis
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T
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Babesiosis is often misDxed as what?
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Malaria
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What are the clinical manifestations of Babesiosis?
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Incubation period: 1-3 weeks
Asymptomatic infection Sx: flu-like symptoms of fever, chills, sweats, myalgia, arthralgia, N&V or fatigue Severe hemolytic anemia c multisystem organ failure -Jaundice, hyperbilirubinemia -Hemoglobinuria -Renal Failure -Death |
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What is the Dx of Babesiosis?
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Anemia, Thrombocytopenia, lymphocytosis, transaminitis
Blood Smear: intraerythrocytic parasites but exoerythrocytic parasites possible (distinguish from plasmodium falciparum) Maltese Cross in cell(THIS IS A LANDMARK) PCR, Serology |
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Babesiosis Tx?
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usually combination; for 7-10 days (6wks for immunocompromised pt)
-Clindamycin and Quinine (tinnitus and GI issues) -Atovoquone and Azithromycin Sometimes exchange transfusion required (RBC replacment) |
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Describe some basics of Ehrlichiosis
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obligate intracellular bact
kills WBCs |
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What are the 2 forms of Ehrlichiosis infection in humans?
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human monocytic ehrlichiosis (HME)--Ehrlichia chaffeensis
human granulocytic anasplasmosis (HGA)--Anaplasma phagocytophilum |
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What is the vector for HME?
HGA? |
HME-Lone star tick (Amblyomma americanum)
HGA-Ixodes scapularis |
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What are the Ehrlichiosis clinical manifestations?
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Incubation period- 7 days
Clinical Manifestations: “Spotless Fever” Fever, persistant Malaise, myalgia, headache Rash: macular, nonspecific (30 %) Neurologic Sx: MS changes, stiff neck, clonus Mortalitiy: estimated 2-5% |
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T or F: 15% of Ixodes scapularis will have all 3 diseases (Lyme, Babesia, Ehrlichiosis)
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T
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Ehrlichiosis Dx?
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leukopenia (40-90%, often accompanied c left shift)
thrombocytopenia elevated plasma levels of aminotransferases (transaminases), lactate dehydrogenase, and alkaline phosphatase anemia & elevated plasma Cr concentration also may be seen Serology (>90% sensitive if paired) Examination of peripheral blood- intraleukocytic morulae (60-80% sensitive with HGA and <20% with HME) PCR for HME and HGA (50-70% sensitive) Immunochemical staining of ehrlichial or anaplasmal antigens in tissue. |
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Ehrlichiosis Tx?
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Will most often give doxycycline (Doxycycline efficacy reported in case reports)
Chloramphenicol???? Doesn’t work in vitro No clinical trials looking at efficacy 10 days total or 3-5 days after defervescence |
