Block VIII, Week VIII
Terms
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- general pathophysiology of burn injuries
-
thermal insult -> vascular damage (release of vasoactive substances)
*subsequent inflammatory rxn, release of inflamm. mediators
*increased vascular permeability, third spacing of fluids - three features seen grossly in burn injury?
-
1. zone of coagulation (center of injury, non-viable tissue)
2. zone of stasis (marked inflammation, border zone of viability and vascular integrity)
3. zone of hyperemia (viable tissue surrounding injury) - describe 1st - 4th degree burns
-
1. 1st degree - pain, erythema, reddening of skin surface
2. 2nd - pain, skin blisters
3. 3rd - destruction and ulceration of skin, may be white, leathery, often no pain in center
4. deep injury to SQ tissue - what is the continuum of heat injury?
- heat cramps -> heat exhaustion -> heat stroke
- medications that predispose to heat injury?
-
B-Blockers
anticholinergics
lithium
diuretics
TCAs
antihistamine - why are antipyretics NOT indicated in heat stroke?
- increased temp. is not due to hypothalamic dysfunction
-
manifestations of heat stroke in:
1. muscles
2. kidneys
3. coagulation ability
4. pulmonary
5. hepatic -
1. rhabdomyolysis, elevated CPK
2. insufficiency, acute renal failure
3. DIC, hemorrhage
4. tachypnea, pulmonary edema, ARDS
5. elevated AST, ALT - treatment of heat stroke?
-
*rapid cooling (ice packs in groin, axillae, neck - NOT on limbs)
*rehydration
*O2 - 4 degrees of frostbite?
-
1st - edema, erythema, decreased sensation
2nd - clear blister formation
3rd - necrosis of skin, blood filled blisters
4th - skin and soft tissue gangrene - treatment for frostbite?
-
*rewarming ASAP
*elevation to reduce edema
*protect with sterile dressings, silver sulfadiazine ointment
*oral and topical corticosteroids to decrease release of inflammatory mediators - definition of hypothermia?
-
body temp <95 deg. F
(body heat loss exceeds production) - mild hypothermia is defined as?
- body core T 33-35 deg. C
- s/s seen in mild hypothermia?
-
*cold, shivering
*peripheral vasoconstriction
*lethargy, confusion, impairment of judgement
*decreased fine motor skills - moderate hypothermia is defined as?
- body core T 28-32 deg. C
- s/s of moderate hypothermia?
-
*increasing CNS depression, stupor
*cardiorespiratory depression (hypotension, bradycardia, bradypnea)
*peripheral vasoconstriction
*risk of atrial & ventricular arrythmias - severe hypothermia is defined as?
- core body T <29 deg.C
- s/s of severe hypothermia?
-
*loss of thermoregulatory control
*rigidity
*apnea
*pulselessness
*unresponsive, fixed pupils
*arreflexia - treatment of hypothermia?
-
rapid rewarming
bretylium for arrythmias - describe the ECG changes seen in severe hypothermia
- Osborne waves (J waves)
-
what is the difference between an:
1. exogenous infection
2. endogenous infection
3. toxin-induced skin disease -
1. MC - cuts, bites, skin disease, burns
2. skin manifestations of an underlying disease process. (systemic infections, underlying tissue)
3. toxin produced at a different site - what are some environmental factors that increase the chance of exogenous infection?
-
moisture
trauma
introduction of foreign body
pressure (ie. bedsore)
compromised blood supply (PVD, DM) - what is folliculitis?
- infection of hair follicles
- where on the body is folliculitis MC seen?
- areas of friction and sweat gland activity
- MCC of folliculitis?
- Staph aureus
- which bacteria causes "hot-tub" folliculitis?
- P. aeruginosa
- which bacteria is a major skin anaerobe that contributes to acne?
- Propionibacterium acnes
- what is furuncle?
- BOIL - small abscess in the region of a hair follicle
- MCC of furuncles?
- Staph aureus
- what leads to recurrent furunculosis?
- repeated self-inoculation
- a confluence of multiple furuncles becomes a ?
- carbuncle
- treatment for furuncles and folliculitis
-
most are self-resolving
(furuncles may require drainage) - treatment for chronic furunculitis?
- bacitracin, neomycin cream
- treatment for carbuncles?
- surgical drainage, Abx. tx (cloxacillin, flucloxacillin)
- what class of exogenous infections do the following belong to: impetigo, erysipelas, cellulitis?
- spreading infections
- four exotoxins of Staph aureus?
-
1. alpha toxin
2. exfoliatin
3. PTSAgs (pyrogenic toxin superantigens)
4. TSST-1 (toxic shock syndrome toxin) - which exotoxin is found in almost all S. aureus?
- alpha toxin
- function of alpha toxin of S. aureus?
-
forms pores in lipid bilayer
(causing cell lysis, death, tissue necrosis) - function of exfoliatin toxin of S. aureus?
- cleaves desmoglien, separates skin layers
- which Staph exotoxin is produced by a bacteriophage?
- exfoliatin
- two exotoxins found in Streptococcus pyogenes?
-
M protein
SPEs (streptococcal pyrogenic antigens) - which strep exotoxin is present on all strep?
- M protein (surface protein)
- significance of M protein as an exotoxin for strep?
- can determine the sequelae fo a strep infection (ie. nephrotogenicity)
- how many different SPE toxins are there?
- 9
- SPE types A and B are associated with?
- toxic shock
- SPE type C is associated with?
- scarlet fever
- what is the difference between impetigo, erysipelas, and cellulitis?
-
impetigo - confined to epidermis
erysipelas - involved dermal lymphatics
cellulitis - major focus is SQ fat layer - in general, which is the more aggressively spreading bacteria when it comes to skin infections: staph or strep?
-
strep
(opposite of endocarditis) - two MC organisms found in impetigo?
-
staph
strep - what is the characteristic clinical appearance of impetigo?
- honey colored crust
- in impetigo - what is significant about the exudates and crust?
- contain infectious bacteria (if the crust is not removed, new lesions form about the periphery)
- possible complication of impetigo caused by group A strep?
- poststreptococcal glomerulonephritis
- treatment of impetigo?
-
penicillin
bacitracin or mupirocin to limit spread
(treatment may not prevent glomerulonephritis) - strains of S. aureus with the group II bacteriophage may cause what skin infection?
- bullous impetigo
- function of group II bacteriophage in S. aureus?
- encodes for exfoliatin toxin (this cleaves desmoglein in epidermis, results in superficial flaccid bullae that are easily ruptured)
- treatment for bullous impetigo?
- anti-staph antibodies
- MCC of erysipelas?
-
Strep
(pyogenes, occasionally group B, C or D) - erysipelas are MC in which age group?
- elderly
- describe an erysipela
-
abrupt onset
fiery red swelling of face or extremities
well defined margins
rapid progression
intense pain - erysipelas can progress to?
-
lymphadenitis
septicemia
local skin necrosis - treatment for erysipelas?
-
penicillin
erythromycin - describe the borders of cellulitis compared to the borders of erysipelas
-
cellulitis - borders blend with surrounding tissues
erysipelas - distinct borders - describe the clinical presentation of cellulitis
-
localized pain
erythema
swelling
heat
can spread rapidly - what may cellulitis be accompanied by?
- lymphangitis and inflammation of draining lymph nodes
- two MCC of cellulitis?
-
Staph aureus
Strep pyogenes - which is worse - staph or strep cellulitis?
-
strep
(more rapidly spreading, diffuse, frequently associated with lymphangitis and fever) - recurrent strep cellulitis is due to what strains?
- group A, C or G strep PLUS skin lesions
- when is recurrent staph cellulitis seen?
- in immunocompromised or chronic nasal carriers
- what bacteria commonly causes cellulitis in DM and PCD?
- Strep agalactiae
- what bacteria commonly causes periorbital cellulitis in children?
-
Haemophilus influenza type b
(spread from sinusitis, otitis media, epiglottitis) - what bacteria, commonly found in aquatiums, causes cellulitis?
- Mycobacterium marinarum
- when is pseudomonas cellulitis MC seen?
- hospitalized and immunocompromised hosts
- treatment of cellulitis?
- erythromycin
- MC wound pathogen in clean surgical wounds?
- Staph aureus
- pathogen found in cat bite wounds?
- Pasteurella multocida
- MC pathogen in burn wounds?
- Pseudomonas aerunginosa
- MC pathogen in puncture wounds?
- Clostridium tetani
- MC pathogen in traumatic wounds?
- Clostridium perfringens
- describe the shape and gram staining of Pasteurella multocida
- gram negative rod
- what is characteristic about the staining of Pasteurella multoceda?
- bipolar staining
- biochemical characteristics of Multocida pasteurella?
-
nonmotile
catalase +
oxidase +
facultative anaerobe - where is Pasteurella multocida commonly found?
- normal flora in respiratory and GI tracts of animals and birds
- two virulence factors posessed by Pasteurella multoceda?
-
capsule (antiphagocytic)
endotoxin - complications of a Pasteurella multoceda infection?
-
*osteomyelitis
*septicemia, meningitis - treatment for a Pasteurella multoceda infection?
-
penicillin or tetracycline
*unless* cat bite -> then treat with ampicillin and don't suture! - 25% of burns result in?
-
pseudomonal infection
(can lead to septicemia with >50% mortality) -
regarding pseudomonas:
1. gram stain, structure
2. oxidase
3. fermenting or non-fermenting?
4. aerobe or anaerobe? -
1. gram - rod
2. oxidase +
3. non-fermenting
4. primarily aerobe - what is significant about the nutrient requirements of Pseudomonas aeruginosa?
- not many nutrients required, can grow in distilled water and many other environments
- significance of the water soluble pigments produced by pseudomonas?
-
*can flouresce under UV light
*green pus typical
*fruity odor -
function of the following virulence factors posessed by pseudomonas?
1. pili
2. flagella
3. capsule -
1. attachment
2. dissemination
3. antiphagocytic -
function of the following exotoxins produced by pseudomonas aeruginosa?
1. elastase
2. alkaline phosphatase
3. phopholipase C
4. heat stabile phospholipase -
1. tissue damage
2. proteolysis, tissue damage
3. tissue damage
4. tissue damage - treatment of burns infected with pseudomonas aeruginosa?
-
*topical application of antibacterial agents (ie. silver nitrate)
*surgical debridement - best antibiotic combination to treat pseudomonas?
-
ALWAYS TEST SENSITIVITY 1ST
-aminoglycoside + extended spectrum penicillin -
describe clostridium in the following context:
1. gram stain, shape
2. aerobe or anaerobe
3. spore or no spore? -
1. gram + rod
2. strict anaerobe
3. spore forming - MC species in clostridium cellulitis?
- C. perfringens
- what causes the crepitus felt in clostridial cellulitis?
- gas found in skin
- treatment of clostridial cellulitis?
-
debridement
penicillin - what is the difference between type I and II necrotizing fasciitis?
-
type I - seen in pts following a surgical procedure, with DM or severe PVD (caused by mixed aerobic and anaerobic bacteria)
type II - formerly streptococcal gangrene, caused by group A strep. - bacterial causes of synergistic necrotizing fasciitis?
- combination of gram - rods and strict anaerobes (ie. Bacteroides or Clostridia)
- where is necrotizing fasciitis commonly seen?
-
on or about feet
(rapid extension along fascia in to leg) - treatment for necrotizing fasciitis type I?
- ampicillin PLUS clindamycin PLUS FQ
- four types of "endogenous" skin infections?
-
abscesses
necrosis
rashes
noninfectious lesion - MCC of abscesses?
- intravascular infx (esp. staph aureus)
- two manifestations of necrosis?
-
purpura fulminans
ecthyma gangrenosum - what is purpura fulminans?
- skin manifestations of DIC
- when is erythmea gangrenosusm commonly seen?
-
in immunocompromised
usually with P. aeruginosa - what type of rash would be seen in meningiococcemia?
- hemorrhagic rash
- what type of rash is seen in typhoid fever, rocky mountain spotted fever?
- macular rash
- scarlet fever is caused by?
- group A strep exotoxin
- scalded skin syndrome and TSS are caused by what bacteria?
- Staph
- SSSS is most commonly seen in which age group?
- children <5yr (including neonates)
- SSSS is caused by what in particular?
-
Staph aureus group II
*toxin - exfoliatin - TSS is caused by what in particular?
- toxic shock sydrome toxin (TSST) - present in 5-25% of S. aureus
- can Strep cause a toxic shock syndrome?
-
yes
strep can produce pyrogenic exotoxins that cause streptococcal toxic shock syndrome (STSS) - skin manifestations of TSS?
-
diffuse red rash
*lasts 1-2 wks, then see peeling of skin - other clinical s/s of TSS?
-
*redness of eyes, mouth, throat
*confusion, seizures, H/A
*myalgias
*hypotension
*organ failure - mortality rate of TSS?
- 30-60%
- treatment of TSS?
-
fluid replacement
general supportive care
clindamycin
gamma globulin -
define:
1. autograft
2. syngeneic graft -
1. from one part of an individual to another part of the same individual
2. between genetically identical individuals of the same species -
define:
1. allogeneic graft (allograft)
2. xenogeneic graft (xenograft) -
1. between genetically disparate individuals of the same species
2. between individuals of different species - most grafts are of what type?
- allografts
- what are the two ways in which recipient T cells can be activated against graft antigens?
-
1. direct recognition (some transplants)
2. indirect recognition (all transplants) - describe indirect recognition of graft antigens
- host APCs activate host T cells using host MHC molecules
- describe direct recognition of graft antigens
-
donor APCs activate host T cells in host lymph node using donor MHC molecules
(donor MUST have same MHC molecules as host in order for this to occur) - compate the rejection time of a primary allograft vs a secondary (repeated) allograft
-
primary - longer time to rejection
secondary - shorter time until rejection due to immunological memory - initial graft rejections are usually due to what immune response?
-
T cell activity
(NOT antibodies) -
in relation to major and minor histocompatibility genes, discuss the:
location -
major - MHC I and II
minor - all chromosomes -
in relation to major and minor histocompatibility genes, discuss the:
# of loci -
major: 5-10
minor: 100+ -
in relation to major and minor histocompatibility genes, discuss the:
rejection speed -
major - rapid
minor - variable -
in relation to major and minor histocompatibility genes, discuss the:
generation of Ab -
major - lots of Ab generated
minor - few if any made -
in relation to major and minor histocompatibility genes, discuss the:
polymorphism -
major - high (lots of variety)
minor - low -
in relation to major and minor histocompatibility genes, discuss the:
function -
major - Ag presentation
minor - ? - in relation to major and minor histocompatibility genes, discuss the: tolerization by the host immune system
-
major - difficult
minor - easier - what is the "law of transplantation"
-
a recipient MAY reject a graft if that graft expresses histocompatibility genes (antigens) not
expressed by host genes
[recipient may reject a graft if it is foreign] - what happens to a graft that is taken from a homozygote and given to a heterozygote?
- acceptance
- what heppens to a graft that is taken from a heterozygote and goven to a homozygote?
- rejection
- what are the 3 patterns of rejection?
-
1. chronic rejection
2. acute rejection
3. hyperacute rejection - T cells mediate what kinds of rejection?
- chronic and acute rejection
- how long for graft destruction in chronic rejection?
- weeks -> months -> years
- how long for graft destruction in acute rejection?
- 10-14 days
- what is the hyperacute rejection mediated by?
-
Ab
(Abs are usually against MHC class I) - two situations in which hyperacute rejection occurs?
-
1. recipient is repeatedly exposed to graft antigens
2. naturally occuring Ab exists - how fast is the graft destroyed in a hyperacute rejection?
- within a few days
- why is there little cellular infiltrate seen in a hyperacute rejection compared to the other rejection types?
-
no time for vasculature to get established - therefore no way for inflammatory cells to get there
(other graft types have time for vasculature to get established) - incompatibilities with minor histocompatiblity genes generally results in what type of rejection?
- chronic
- incompatibilities with major histocompatiblity genes generally results in what type of rejection?
- acute
- which type of organ transplant is hyperacute rejection commonly seen in?
- renal
- what are some factors affecting graft rejection?
-
1. presensitixation
2. degree of genetic mismatch
3. lymphatic drainage
4. tissue typ einvolved
5. graft size
6. immune response genes - describe lymphatic drainage issues in relation to graft rejection
- decrease lymphatic drainage, increase chance of survival (less way for APCs and T cells to drain to lymph nodes)
- describe graft size in relation for graft rejection
- increased graft size sometimes increases survivability "overwhelmed immune system"
- what is significant about liver transplants and rejection?
-
liver transplants seen to be viable across genetic barriers (HLA mismatch)
(many surgeons believe that HLA matching has no relevance to survival of liver transplants) - what is a unique type of rejection seen in bone marrow transplants?
- graft-vs-host (GVH)
- how can acute GVH be prevented?
- deplete marrow of mature T cells before transplanting
- does MHC matching need to be performed for bone marrow transplants?
-
yes - some needs to be done
(necessary for positive and negative selection to operate) - why do T cells not respond well to xenografts?
- MHC I and II molecules on those cells re too different to fil well with host TCRs
- 3 mechanisms of hyperacute rejection seen in xenografts?
-
1. pre-existing antibodies to carbohydrate structures
2. compliment
3. MK cell mediated killing of donor cells lacking appropriate MHC I molecules - what happens when pig cells are transfected with human DAF, CD59 genes, etc?
- pig cells are now able to INACTIVATE HUMAN COMPLIMENT components binding to their surface
- what happens when pig cells are transfected with human MHC I genes?
- pig cells now have MHC I molecules to bind inhibitory receptors on human NK cells and prevent attack
- how can a general immune deficiency be induced in order to minimize/prevent reaction to a graft?
-
1. radiation
2. Ab against T cell markers
3. drugs cytotoxic for rapidly dividing cells
4. drugs with narrow specificity for proliferating T cells (cyclosporin) -
Cutaneous manifestations of:
1. papillomavirus
2. parvovirus B19
3. herpesviruses - HSV and VZV
4. herpesviruses - EBV and HHV-6
5. herpesviruses - CMV
6. smallpox -
1. papules
2. macules, papules
3. vesicles
4. macules
5. macules, papules
6. vesicles, pustules -
cutaneous manifestations of
1. coxsackie
2. measles
3. rubella -
1. vesicles
2. macules, papules
3. macules - following the primary infection - where does VZV establish latent infection?
-
dorsal root ganglia
-or-
extramedullary cranial nerve ganglia - in what type of patients does VZV cause serious morbidity and mortality?
- immunosuppressed patients
- recurrent VZV disease is called?
- Zoster or shingles
- most cases of VZV occur in what population?
- children <15yrs
- seasonality to VZV?
- winter and early spring
- incidence of Zoster in pts that have had varicella?
- 20%
- reactivation of VZV is associated with what conditions?
-
aging
immunosuppression - seasonality for zoster?
- NONE
- manifestations of zoster in the immunocompromised?
-
may disseminate
(causing skin lesions, CNS, pulmonary, hepatic involvement) - transmission of VZV?
-
Aerosolized droplets
Direct contact
*very contagious* - describe the pathogenesis of a primary VZV infection
-
* virus spreads to lymphatics, then to blood
*viremia causes seeding of liver and spleen
*secondary viremia occurs about 14 days post infection - manifests as infection of skin and mucosal surfaces - describe Ig levels after a VZV infection
-
IgM and IgA decrease after 1yr
IgG declines but persists at a low level - what type of immunity plays a role in host defense against recurrent VZV infection?
-
cellular immunity
CTLs
NK cells
ADCC - paitents that are deficient in cell mediated immunity are at risk of?
- severe disease caused by VZV
- incubation period of VZV?
-
14-17 days
(shorter in immunocompromised pts) - in which patient group are prodromal symptoms of VZV absent?
- young children
- prodromal symptoms seen in older pts?
-
fever (1-6 days)
H/A
backache
sore throat - describe the appearance and character of the varicella rash
-
crops of vesicles appear every 2-4 days
*rash appears on trunk first, then spreads to limbs - in what stage of the rash is moderate to severe pruritis present?
- vesicular stage
- evolution of the vesicles in a chickenpox rash
-
1. thin walled vessicle with clear fluid ->
2. vesicle becomes cloudy and depressed in center with irregular border ->
3. crust forms in center and eventually replaces remaining portion of vesicle at periphery - when is the vesicle no longer infectious?
- when it crusts
- describe the skin lesions seen in shingles
-
*crops of varicella like lesions
*involves a single dermatome
*pain, parasthesias
*never cross midline - MC reactivation of VZV occurs at which spinal levels?
- trunk (T3-L2)
- DDx of zoster that involves trigeminal nerve?
- HSV
- MC complication of VZV in children?
- bacterial infection
- other complications of VZV?
-
encephalitis
hepatitis
pneumonia - when is hemorrhagic chickenpox seen?
-
immunocompromised pts
(50% mortality rate) - a bacterial infection of chickenpox can result in?
- bullous impetigo
- treatment of VZv if needed?
-
acyclovir
sorivudine
famcyclovir
valacyclovir
foscarnet - what type of VZV vaccine is available?
-
live, attenuated
(doesn't prevent shingles) - what can be given to provide passive immunization to chickenpox?
-
VZIG
(varicella zoster immunoglobulin)
*effective when administered up to 3 days after exposure - major use for VZIG?
-
immunocompromised children
newborn infants whose mothers have active varicella at the time of delivery - HHV-6 causes what childhood disease?
- roseola infantum (exanthema subitum - "sudden rash")
- characterize the onset of roseola infantum?
-
fever as high as 105
lasts 3-4 days - in roseola infantum - what occurs after the rash?
-
lymphadenopathy
(fever is prodromal) - where does HHV-6 primarily infect and replicate?
- CD4+ T cells
- describe the rash and prognosis of roseola infantum (exanthema subitum)
-
faint macular rash
mild self-limiting disease - hand-foot-and mout disease (HFMD) is primarily caused by?
-
coxsackie viruses A9, A16
enterovirus 71 - what is the classic sign of HFMD?
-
exanthema on buccal mucosa
(also found on dorsum of hands and margin of heels) - HFMD primarily occurs in which population?
- children <4 yrs of age
- herpangina is primarily caused by?
- coxsackie A viruses
- describe the s/s of herpangina
-
abrupt onset
fever, sore throat, excessive salivation
*grouped, grey vesicles in mouth - course of herpangina?
-
*self limiting*
fever lasts 1-4 days
disease lasts 4-5 days - how many serotypes of measles are there?
-
one
(reason for effectiveness of vaccine) - function of H and F protien located on viral envleope of the measles virus?
-
H protien - promotes attachment to cell receptors
F protien - promotes viral-cell and cell-cell fusion - transmission of measles?
-
respiratory droplets
-or-
direct contact with nasal or throat secretions - how long after the rash appears is transmission of measles possible?
- 4-5 days
- what is a characteristic histologic feature of measles infection?
-
multinucleated giant cells
(with eosinophilic and intranuclear inclusion bodies) - how does measles cause immunosuppression?
-
*infects lymphocytes, monocytes, macrophages
*inhibits lymphocyte proliferation - how long can clinically significant immunosuppression last post-infection?
- up to 1 yr
- how long do antibodies to measles persist?
- for life
- what immune response is responsible for most symptoms seen in measles?
- cellular immune response
- how does measles differ in a CMI deficient patient?
- no rash
- describe the prodromal phase of measles. when does it begin?
-
*low grade fever, malaise
*coryza, sore throat, H/A
*conjunctivitis
*sneezing and cough
begins 8-12 days after infection - what are Koplicks spots and when do they appear in relation to the measles rash?
- red patches with central white specks that appear on buccal mucosa 2-3 days prior to onset of measles rash
- describe the rash seen in measles. where does it begin and spread?
-
maculopapular
begins at hairline - rapidly progresses to the face, neck trunck and extremities - complications fo a measles infection?
-
inner ear infx
bronchopneumonia
acute postinfectious encephalitis - death in a measles infection in children <2yrs is MC due to what complication?
- pneumonia
- treatment for measles?
-
supportive
(no antivirals) - what type of vaccine is the measles?
- live, attenuated
- measles vaccine is contraindicated in?
-
pregnancy
allergy to eggs, neomycin
comprised immunity - what is unique about the replication of the smallpox virus?
-
replicates entirely in the cytoplasm of the cell
(large dsDNA genome, doesn't need nucleus to replicate) - transmission of smallpox?
- respiratory route
- what is characteristic about the smallpox lesions?
-
*all lesions are in the same stage of development
*centrifugal (distal) rash distribution
*lesions on palms and soles
(firm, round, deep seated pustules) - describe the prodrome seen in smallpox
-
fever >101
prostration, H/A, backache, chills, vomiting, abd. pain - where do the first lesions in smallpox appear?
- oral mucosa, face or forearms
- the other diseases caused by poxviruses?
-
1. molluscum contagiosum
2. ORF
3. cowpox - what is the signifance of cowpox in relation to smallpox?
- provides immunity to smallpox
- does pseudocowpox provide immunity to smallpox?
- NO
- most vaccine responses are due to which immune response (innate or adaptive)
-
adaptive
(specificity, memory) - what are the three pathogen repication sites in the body (therefore the 3 points of focus for the immune response)?
-
1. vesicular
2. cystosolic
3. extracellular - where do most pathogenic bacteria replicate?
- vesicles
- where do most viruses live?
- cytosol
- which type of immune response activates macrophages to kill intravesicular pathogens?
- Th1 response
- whic type if immune response activates B cells to make antibodies and occurs extracellularly?
- Th2
- influenza vaccine has been "associated with"?
- Guillan Barre syndrome
- HBV vaccine has been "associated with"
- MS
- MMR vaccine has been "associated with"
-
autism
IBS - aluminum containing vaccines have been "associated with"?
-
MMF
(macrophagic myofaciitis) - what is a first generation vaccine?
-
live or attenuated
dead or inactivated - what is a second generation vaccine?
-
recombinant
extracts (proteins, peptides)
conjugated - what is a third generation vaccine?
-
DNA
(currently in clinical trials) - 2 risks of an attenuated vaccine?
-
1. necessary epitopes not present
2. wild-type reversion - give an example of a dead or inactivated vaccine
- IPV
- give an example of an extract vaccine
- diptheria and tetanus toxins
- give an example of a conjugated vaccine
-
Hib
(direceted against Haemophilus protein, LPS protein used for immunogenesis) - what is a conjugated vaccine?
- desired pathogenic epitope is combined with an immune stimulatory molecule (ie. LPS)
- DNA vaccines are currently experimental for?
-
pathogens
allergies
cancer
autoimmunity - how is an adjuvant useful in enhancing the efficacy of a vaccine?
- enhances the immunogenicity by acting on APCs
- risks of using an adjuvant in a vaccine?
- induction of inflammatory diseases (SLE, MS)