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85 Cards in this Set

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Type of Vaccine
Type of Vaccine
Live attenuated
Type of Vaccine
Toxoid, Acellular Pertusis
Type of Vaccine
Haemophilus Influenza (meningitis)
Type of Vaccine
Streptococcus pneumoniae (23 serotypes)
Type of Vaccine
No protein
Pneumococcal Polysaccharide Vaccine.

Contains 23 serotypes of Strept bacteria.
Type of Vaccine
Killed, Whole inactive
(United States)
Type of Vaccine
Live Attenuated = Sabin
(herd immunity)
Type of Vaccine
Killed, Whole inactive
Type of Vaccine
Live Attenuated

Live vaccines are generally required for enveloped viruses!
Paramyxo and Togaviruses are enveloped.
Type of Vaccine
Live Attenuated

Herpes are enveloped. Enveloped tend to require live vaccines.
Type of Vaccine
Killed, Whole inactive

Killed vaccines are sufficient for naked viruses.
Type of Vaccine
Type of Vaccine
Subunit, Recombination
Type of Vaccine
Subunit, Recombination
Coomb's Test
Used for Rho-antibody; antibody binding cells; crossmatch blood transfusion donors
Direct Fluorescent Antibody - detects antigen on tissue.

Indirect Fluorescent Antibody - detects pathogen-specific antibodies on tissue.
Class I compatibility testing, as it relates to Organ Transplantation
Lymphos are mixed with antisera. If antibodies recognize their specific epitope on the cells, they will be bound there and addition of complement will result in cell lysis. A dye is used to show leaky cells.
Monoclonal Antibodies (mAbs)
Hemocyte antibodies to target cell antigens; HER2; Campath (CD52)
IgE, Mast Cells, Eosinophils, Histamine, Leukotrienes, SRSA, IL-4, IL-5, Eotaxin, C3a, C5a
Type I
Antibodies (IgG)
Attacking cells, tissues (must be particulate)
Type II
Goodpasteur’s Syndrome
Grave’s Disease
Myasthenia gravis
Autoimmune Anemia
Autoimmune hemolytic anemia
Abs bind to rbc and lyse (Type II) rbc is a cell
Rheumatic Fever
Detect Abs cross-reacting with Streptococcus pyogenes and cardiomyocytes (Type II)
Grave’s Disease
Abs that activate the TSH receptors (Hyperthyroidism) (Type II)
Masthenia gravis
Abs bind to Acetylcholine Receptors (Type II)
Multiorgan, Immune Complex, Anti-DNA Abs
Type III Classic!
type I
Juvenile, T cells destroy Beta cells in Islets of Pancreas, Usually Th1 T cells; Delayed hypersensitivity (IV)
Autoimmune destruction of myelin in CNS, T-cell mediated and Ab involved (Type II, IV). Organ specific autoimmune disease, involves loss of tolerance. T-cells recognize myelin antigen.
Multiple Sclerosis
Hypothyroidism; Destruction by antibodies and T cells specific for thyroid antigens.
Hashimoto’s Thyroiditis
AIRE deficiency involved in Central Tolerance. These patients develop several severe autoimmune diseases
No T or B (common receptor for the cytokines IL-2, IL-4, IL-7, IL-9 IL-15)
IL-7 is the important cytokine. Girls can inherit this from carrier parents.
X-Linked SCID
(Boys) detected early by Pediatricians.
Adenosine Deaminase (ADA), PNP, Jak3, RAG1/RAG2
Pathology: Class I, TAP No CD8
Class II no CD4 T cells
Bare Lymphocyte Syndrome
Hypoplasia or aplasia of thyroid; Associated with tetany; Cardiac problems
DeGeorge Syndrome
X-Linked Lymphoproliferative Disease
SAP (Slam-Associated Protein)
Abnormal response to EBV.
Uncontrolled CD8 and B Cells.
X-linked Agammaglobulinemia
Pre-B cell receptor signaling. Will do heavy chain gene arrangement, but not light.
Decreased IgG
Absence of germinal centers
Absence of plasma cells
Therapy is passive immunization with IVIG (ISG). Immune Serum Globulin.
BTK Deficiency.
Malignancies, Rash, Eczema, Thrombocytopenia
Cytoskeletal Remodeling
Defect in lymph activation and trafficking to inflammation.
Progressive decrease in T-Cells
Inability to produce Ab in response to T-cell independent polysaccharide antigens.
Vaccines that are polysacc based will not make antibody for.
Wiscott-Aldrich Syndrome
Ataxia Telengectasia
Autosomal Recessive
Defect in DNA repair for maintaining genome stability.
Decreased T-cells
Decrease in IgA, IgG2
Normal B-cells
Prone to Infections and Malignancies, Balance problems (cerebellum)
Many Autoimmune Diseases, Central Tolerance; AIRE
Dysregulated T cell proliferation, T cells don’t die through FAS/FASL
Autoimmune Lymphoproliferative Disease (ALPS)
Treg cells are not present to regulate other cells. (Peripheral Tolerance). Patients develop Th1-mediated autoimmune diseases
Neutrophil killing defective (prone to Aspergillis, Staph, Strep)
Chronic Granulomatous Disease (CGD)
Adhesion defect, migrate out of blood vessels, APC-T interaction; Leukocytosis in blood (they can’t migrate out of the blood-no homing)
Leukocyte Adhesion Deficiency
Big Granules. Lysosome defect, and the neutrophils can’t kill
Chediak Higashi
Neisseria infections
MAC (C5b-C9)
Paroxysmal Nocturnal Hemaglobineuria (PNA)
DAF Deficiency
Take a couple weeks (immune response). First phase rejection, followed by a second phase rejection (memory)
Not really a rejection, just a dead organ. May be drug-related or bad surgery. Complement, B cells, T cells. Lots of dead cells
Type IV. T cells from graft are attacking the recipient’s tissues. Want to kill the mature T cells from the bone marrow donor (the graft) before transplantation.
Only in a Bone-Marrow Transplant into an Immunocompromised recipient
Antigenic Variation due to a Shuffling of Exons
Capsule, Antigenic Variation
Streptococcus (23)
Neisseria capsule and serotype, too
Toxic Shock Syndrome
Binds Beta-chain outside peptide groove.
20% of T-Cells will be activated by superantigen.
(T cells gone wild)
Has 23 different serotypes, Capsular
Streptococcus (23)
Protein A Binds IgG (the Fc portion) to inhibit phagocytosis.
Staphylococcus aureus
Contains LPS, O-side chains inhibit complement (MAC)
E. Coli, Neisseria
Gram-negative organisms
Complicated Life Cycle, Latency?, Hides in rbcs
Binds to CD21/CR2 on B cells, Persists inside B cells in latent form; Viral IL-10 competes with body's IL-10.
Epstein-Barr Virus
Antigenic Drift and Antigenic Shift
Has an IgA Protease that cleaves IgA
Neisseria (Gram -)
S. pneumoniae
Latency and reactivation causes Shingles
Varicella zoster
Intracellular in phagocytes, Granuloma formation, hard to access, avoids lysosomal killing inside macrophage
Mycobacterium tuberculosis,
Uses antigen variation, Infects CD4, macrophages, and dendritic cells. Latent infection; Downregulates MHC I expression; Destruction of mucosal CD4+ permits bacterial entry.
Defective maturation of T, B, and myeloid cells.
Defect at hematopoietic stem cell level.
Marked decrease in T and B cell numbers.
Autosomal recessive.
Associated with pancytopenia.
Reticular Dysgenesis
Genetic SAP adaptor protein defect.
Prone to abnormal EPV response, which binds CD21 of B-cells causing lymphoma.
Uncontrolled CD8 T cell proliferation and B cell proliferation. Uncontrolled hemophagocytosis.
X-linked Lymphoproliferative Disease (Purtilo’s or Duncan’s)
Similar pathogenesis as X-linked Purtilo’s or Duncan’s
Inappropriate and ineffective CD8 T Cell activation
Perforin gene mutation (can’t kill target cell)
G-protein regulation of granule exocytosis
NK cell cytotoxicty will also be affected
Familial Hemophagocytic Syndrome
No granule fusion or enzyme deficient
Neutrophils, macrophages, dendritic, NK Cells
Defective granules of NK Cells
Defect in adherence and killing
Pyogenic bacterial reinfection
Melanosomes (hair or skin pigmentation)
Chediak-Higashi Syndrome
Autoimmune Polyendocrinopathy Candidiasis Ectodermal Dystrophy
Autoimmune Polyglandular Syndrome type-1
AIRE gene mutation
Central Tolerance defect
Increase incidence of Autoimmune Disorders
Immune Dysregulation
X-linked syndrome
FOXP3 mutation
TF for development of Treg Cells CD4+ CD225+
25% of all SCID disorders
↓ B-Cells (progressive)
↓ T-Cells (progressive)
T-Cells respond poorly
↓ IgG
Purine degradation salvage pathway
Accumulation of deoxyadenosine and dATP
toxic purine metabolites
inhibits DNA synthesis
lymphocytes particularly sensitive!
SCID (adenosine deaminase deficiency)
↓ IgG
↓ IgA
Normal B-Cell numbers
Delayed T-Cell maturation
Resolves around 1.5 – 2 years of age
Transient Hypogammaglobulinemia of Infancy
E. coli and its flagellum bind to macrophage via ?
Toll-Like Receptor (TLR) on the macrophage.
...have a thin peptidoglycan with a layer of Lipids, and Polysaccharides collectively known as Lipopolysaccharide (LPS). LPS contains side chains that radiate off called O-antigens.
Gram - bacteria
is the biologically active component and causes the toxicity of LPS.
Lipid A
The ____ of LPS prevent Complement C3b binding to the cell surface and MAC forming. This is an immune evasion mechanism of Gram-ve bacteria
O side chains
Skin Abscesses
Food poisoning
Toxic Shock Syndrome
Staphylococcus a major component of the Staphylococcus aureus cell wall. It binds to the Fc domain of IgG molecules.
Protein A
Strep Throat
Scarlet Fever
Rheumatic Fever
Causes sore throat and skin infections. Secretes Exotoxin A-C that acts as a superantigen to cause fever, rash and inhibit liver clearance of endotoxin.
Streptococcus pyogenes (Group A)
The conjugate meningococcal vaccine (MCV4) was introduced in the U.S. in 2005.
Neisseria meningitis
The characteristic skin rash of meningococcal septicemia, caused by ...
Neisseria meningitidis:
Gram (-) diplococci
Polysaccharide capsule prevents phagocytosis (most important virulence factor)
Also has IgA protease.
LPS endotoxin is overproduced, causing abrupt signs.
Both meningococcus and gonococcus produce ..
an IgA protease that cleaves IgA.
Antibody & Complement opsonize yeast and activation of macrophages by Th1 cells help kill ...
Variable Surface Glycoprotein (VSG) of Trypanosoma cruzi undergoes ...
programmed antigen variation.
IFN, TNF, IL-12, NK, Th1, CTLs
Immune Control of Viruses
...binds to CD21 on B cells and transforms B cells to become malignant.