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90 Cards in this Set

  • Front
  • Back
extraneous effect caused by a vaccine
adverse reaction
"side effect"
adverse reaction
any event following a vaccination
adverse event
may not be a true adverse reaction
adverse event
common with inactivated vaccines
local adverse reactions
usually mild and self-limited
local adverse reactions
systemic adverse reactions are
nonspecific
peripheral myopathy with complete body weakness; rapid or gradual associated with some vaccines
guillain-barre syndrome
very rare adverse reaction which can be minimized by screening
allergy
used to kill bacteria and prevent contamination of vaccines
thimerisol
encephalopathy following pertussis vaccine is a
permanent contraindication
severe allergy to prior dose of vaccine or component is a
permanent contraindication
severe illness; contraindication or precaution when giving live and inactivated vaccines
precaution for BOTH
dose of corticosteroids which lead to immunosuppression
> or equal to 20 mg per day or 2 mg / kg per day
when you should get a flu vaccine following tx with transplant
after 6 months and then annually
Locally Activates vascular endothelium
IL-1
Increases adhesion of macrophages
IL-1
Allows macrophages & PMNs to leave blood and
enter infected tissue
IL-1
Locally Activates lymphocytes
IL-1
Systemically promotes fever and IL-6
production
IL-1
Locally lymphocyte activation and antibody
production
IL-6
B-cell growth and differentiation
IL-6
Proliferation of thymocytes and peripheral T-cells
IL-6
Augments NK-cell activity
IL-6
Only local effects
IL-8 and IL-12
Chemotactic factor for PMNs
IL-8
Increases access of effector cells
IL-8
Activates PMNs
IL-8
Activates NK cells
IL-12
Induces the differentiation of CD4 T cells
into TH1 cells
IL-12
are critical in the control of
parasitic infections
T cells
crucial in eradicating
parasitic infection
TH1 cells and cytokines
in unicellular parasitic infections IL-12 is produced by
phagocytic cells
in unicellular parasitic infections IFN-γ is produced by __
under the induction of IL-12
NK cells and T cells
in unicellular parasitic infections Macrophages are activated by
IFN-γ
For intracellular protozoan (unicellular)
infections __ is the primary cytokine
controlling the resolution of the infection
IFN-γ
TH2 cells and cytokines driving
eosinophils, mast cells and IgE are crucial
in eradicating the infection from the GI tract
multicellular helminth infections
In Multicellular (Helminth) Infections IL-4 production is induced by
the helminth
In Multicellular (Helminth) Infections __ drives TH2 cell proliferation and
maturation of B cells and production of IgE and
IgG4
IL-4
In Multicellular (Helminth) Infections IL-5 production causes an increase in
eosinophil production
In Multicellular (Helminth) Infections IL-4, 9 and 3 cause an increase in
mast cells
In parasitic disease is a potent negative
regulator of both TH1 and TH2
IL-10
Prevents an overwhelming inflammatory
response thus preventing tissue damage and
possible death
IL-10
Down regulates IL-5 and IFN-γ
IL-10
Transforming Growth Factor β
(TGF- β) is produced by
activated macrophages and
T cells
Decrease TNF-α production and
inflammation
TGF- β
Act synergistically with IL-10 to inhibit
macrophage effector functions
TGF- β
Along with IL-10 helps maintain a
balance between protection and disease
TGF- β
Exact role not known
IgE and Eosinophils
In vitro parasite specific IgE and
eosinophils can kill certain parasites by
ADCC
Most important cell in the response to
parasitic infections
activated macrophages
is the main mechanism by
which the parasites are killed by activated macrophages
Nitric oxide
stimulate the production
of nitric oxide and IL-10 and TGF-β inhibit
nitric oxide production
TNF-α and INF-γ
– Malaria
– Toxoplamosis
– Trypanosoma
Infections in which CD8 are important
are the most effective of the
phagocytes at killing fungi
Neutrophils
are much less
potent than neutrophils or activated
macrophages at killing fungi
Inactivated macrophages
can kill fungi either directly (rare)
or indirectly after activation to produce
cytokines such as TNF-α and IFN-γ
NK cells
Released from NK cells, CD8 cells, and
CD4 TH1 cells
IFN-γ
Promotes the activation of macrophages
IFN-γ
Promotes the differentiation of naïve CD4
cells into TH1 cells
IFN-γ
Prevents the differentiation of naïve CD4
cells into TH2 cells
IFN-γ
is crucial to
the control and resolution of systemic
fungal infections
CD4 T-cell mediated immunity
cause skin, nail, and hair
infections only
Dermatophytes
topical disease only, never
systemic disease
Dermatophytes
TH1 response or delayed hypersensitivity
response is most important with
immunity to dermatophytes
with immunity to dermatophytes __ results in chronic disease and little
inflammation
TH2 response or type I hypersensitivity
with immunity to dermatophytes __ limits the disease and has a greater
inflammatory response
TH1 response or DT hypersensitivity
Bacteria with a large
quantity of __ on its surface
evade complement in
the absence of
antibodies
sialic
acids
Streptococcus pyogenes and
Staphylococcus aureus evade
complement when
Ab are not present
Have long half-lives in tissue
macrophages
Most abundant of the WBCs
pmns
Normally not present in tissues but are attracted
into infected tissue by cytokines released from
phagocytosing macrophages and chemotactic
factors released by complement activation
pmns
Become the dominant phagocytic cell at the site
of infection
pmns
initiate the inflammatory
response when infection is the cause
Macrophages
Mucosal secretions contain __ in greatest
quantity
IgA
They prevent viral replication within
infected cells and its spread into uninfected
cells
Interferon α& β in virally-infected cells
Activate NK cells to kill virus-infected cells
Interferon α& β in virally-infected cells
Increase MHC class I expression
Interferon α& β in virally-infected cells
Consist of physical barriers, complement,
acute-phase proteins, phagocytic cells, NK
cells, interferon α& β
innate response
can bind to surface
antigens on the virus preventing binding to
the host cell
Specific antibodies
can bind the viral antigen on the host cell surface,
activate complement and result is cell lysis
Ab
can bind the viral antigen on the host cell surface,
activate ADCC by activating NK cells and
result in cell death by apoptosis
Ab
Starts with activation of T-cells in draining
lymphoid tissue
acquired immune response
influence the
differentiation of CD4 cells during the
adaptive immune response
Cytokines released by cells during the
innate immune response
is produced primarily by dendritic
cells and macrophages and drive the
differentiation to TH1 cells
IL-12
IL-12 and INF-γ prevent the development of
TH2 cells
promote activation of B-cells
and the differentiation of CD4 cells into
TH2 cells
IL-4 and IL-6
IL-4 prevents the differentiation of CD4
cells into
TH1 cells
It takes days for activated effector Tcells
to emigrate to the site of infection
5-6
Major envelope glycoprotein
gp-160