Microbes benefit without harming or benefiting the host
Microbes and their host benefit
Microbes benefit at the expense of harming the host
Abnormal proteins that cause slowly progressive neurodegenerative diseases like Creutzfeldt-Jakob and kuru.
Replication is dependent on the host cell's DNA-dependent RNA polymerase.
Positive strand RNA virus
Similar in structure to host cell mRNA, and able to be directly translated by host cell ribosomes without any involvement of RNA polymerase
Negative strand RNA virus
Requires RNA-dependent RNA polymerase to create a positive strand for translation by host cell ribosomes
A positive strand virus that requires reverse transcriptase, integrase, and protease for successful replication
Bacterial sexual reproduction involving transfer of genetic material via a transfer factor, i.e. pilus
Bacterial sexual reproduction involving uptake of free-floating genetic material after the death of another bacteria
Bacterial sexual reproduction that involves transfer of genetic material by bacteriophages
Obligate intracellular prokaryotes with a small genome and no cell wall, impervious to cell-wall-synthesis inhibiting antibiotics.
Intracellular bacteria with a cell wall, that are transmitted by arthropod vectors, e.g. Rocky Mountain Spotted Fever
Intracellular bacteria with a cell wall, that are transmitted by direct contact between hosts
Intracellular bacteria transmitted by ticks, that specifically target and multiply within monocytes and neutrophils
Gram negative intracellular bacteria found in cattle, sheep, and goats, that can be transmitted to humans through direct contact with infected animals
Class of fungi that exist as molds at one temperature, and yeasts at another, e.g. blastomycosis, histoplasmosis, and coccidiomycosis
The result of sexual reproduction between fungi
Sporangiospores aka conidia
The result of asexual reproduction of fungi
The vector and intermediate host where sexual reproduction of malaria gametocytes occurs
The immature form of malaria that is injected into a human host via the saliva of the female anopheles mosquito, then enters and matures into schizonts within liver cells
The mature form of malaria release from liver cells, that go on to infect and destroy the host's RBCs
Transmission is fecal-oral. Ova penetrate the GI epithelium, migrate to the respiratory tract, clime the trachea, and enter the esophagus and GI tract as a mature worm
Transmission is via larval penetration of skin. Larvae migrate to the respiratory system and enter the GI tract
A pneumonia-like presentation with c/c of cough, caused by helminth infection and migration of worms up the trachea to reach the esophagus
Infect external body surfaces, causing local tissue damage, and sometimes acting as vectors, e.g. scabies, chiggers, lice, and fleas.
The number of new cases of infectious disease within a defined population over a given period of time.
The number of active cases at any given time.
An area with a stable incidence and prevalence of a given disease
An abrupt increase in the incidence of an illness
Spread of a disease beyond continental boundaries or from an endemic region to a non-endemic region
Proteins released from bacteria during growth that modify or inactivate host cell components leading to cell death or dysfunction
Bacterial products that cause diarrhea, vomiting, and a toxic shock like syndrome, e.g. shiga toxin
A component of gram negative bacterias' outer membranes that are released during bacterial cell death causing gram negative shock
Components of pathogens that allow them to bind to host cells, e.g. ligands, adhesins, pilli
Components of pathogens that discourage phagocytosis, e.g. capsule, slime/mucous layers
Enzymes produced by pathogens that allow them to penetrate host tissue, e.g. phospholipase, elastase, collagenases, hyaluronidase, and protease
Macrophages found in connective tissue
Classic complement pathway
Requires antigen-antibody complex activation, part of adaptive or specific immunity
Alternative complement pathway
Direct activation of the complement system by some gram negative bacteria independent of antigen-antibody complex activation, part of innate or non-specific immunity.
Natural killer cells
Granular lymphocytes that arise from bone marrow and directly kill tumor cells and cells infected with intracellular pathogens by perforation of cell membranes
B lymphocyte mediated, attacks extracellular pathogens and toxins
T lymphocyte mediated, attacks intracellular pathogens, e.g. viruses, rickettsiae
Macromolecules (proteins or polysaccharides) on the surface of pathogens that are recognized as foreign and stimulate an immune response.
An active site on an antigen (antigenic determinant). One antigen can have one or many of these.
Small substances that can't produce an immune response on their own, but can when bound to a carrier protein, e.g. penicillin
A protein complex found in all cells of the body, capable of binding to intracellular viral proteins, these stimulate CD8+ T lymphocytes (cytotoxic T cells) to destroy the infected cells
Protein complex found only in antigen presenting cells. These cells engulf pathogens, break them down, and present products to stimulate CD4+ T lymphocytes (helper T cells).
TH 1 cells
A differentiated form of activated CD4+ T cells that stimulates cytotoxic T cells, i.e. cellular immunity
A differentiated form of activated CD4+ T cell that activates B lymphocytes to become immunoglobulin producing plasma cells, i.e. humoral immunity
MHC Class 1 HLA types
HLA-A, HLA-B, HLA-C
MHC Class 2 HLA types
HLA-DR, HLA-DP, HLA-DQ
The trunk portion of the Y-shaped immunoglobulins
The arms of the Y-shaped immunoglobulins
Antigen binding sites
Variable regions at the tips of the FAB fragments of immunoglobulins
The most abundant immunoglobulin type. Long-lived and able to cross the placenta, these do not indicated active infection, unless levels increase 4-fold
Immunoglobulin present in body secretions, and responsible for protecting vulnerable mucous membranes
A large, pentamer immunoglobulin that is short-lived and unable to cross the placenta. A spike in serum IgM is an indicator of acute infection
An immunoglobulin bound to the surface of B lymphocytes. When bound, can trigger T-cell dependent or T-cell independent antibody production, depending on pathogen type
Immunoglobulin that binds to mast cells and basophils, triggering release of histamine. Involved in parasitic and hypersensitivity reactions
CD4+ T cells
Helper T cells, stimulated by antigen-bound MHC II on APCs, triggering clone formation, and activation of cellular and humoral immunity depending on pathogen type (intracelluar v. extracellular)
CD8+ T cells
Cytotoxic T cells, directly kill cells infected by intracellular pathogens via cytolytic enzymes, cytokines, and perforins.
Viral immune response
APC secretes IL-12, which converts CD4+ T cells to TH1 cells. TH1 cells release IL-2 and interferon-gamma, which activates CD8+ cells.
Parasitic and allergic immune response
APC secretes IL-4 that converts CD4+ T cells into TH2 cells. TH2 cells release IL-4 and IL-5 that convert B cells into IgE producing plasma cells. IgE binds mast cells and basophils triggering release of histamine
T-cell independent antibody production
Bacteria binds IgD, directly triggering conversion of B cell to IgM and IgG producing plasma cells.
T-cell dependent antibody production
Bacteria binds IgD, B cell acts as APC and activates CD4+ T cells, which are converted into TH2 cells. TH2 cells convert B cells into IgM and IgG producing plasma cells
IL-1, IL-6, TNF, INF-alpha, and INF-beta
Cytokines of the innate or non-specific immune response
IL-2, IL-4, IL-5, and INF-gamma
Cytokines of the adaptive or speicific immune response
CSF, IL-3, IL-7, and IL-11
Cytokines that stimulate bone marrow to increase production of WBCs
Lectin-mediated complement pathway
Involves mannose binding protein, does not rely on antigen-antibody complex for activation, part of the innate or non-specific immune response
Membrane Attack Complex (MAC)
Combination of complement factors C5-C9 that functions by 4 mechanisms: direct cell perforation and lysis, opsonization, activation of leukocytes, and production of anaphylatoxin which causes activation of mast cells and basophils
Specific immunodeficiency disorders
Stem from problems with B-cell, T-cells, or both.
Non-specific immunodeficiency disorders
Stem from problems of the complement system, or of phagocytosis
Manifestations include recurrent pyogenic bacterial infections, e.g. Streptococcus pneumoniae, H. influenzae type B, Staph aureus, and gram negative bacterial infections
Transient hypogammaglobulinemia of infancy
A deficiency of IgG with normal IgA, IgM, and B cell levels, caused by failure of CD4+ cells to produce cytokines that convert B cells to IgG producing plasma cells. Manifests as recurrent URIs and otitis media, that typically resolves spontaneously by age 2-4 years.
X-linked agammaglobulinemia (Burton's)
An X-linked recessive disorder where differentiation of pre-B cells is blocked resulting in complete absence of mature B cells and undetectable levels of all serum immunoglobulin types. Manifests as meningitis and recurrent otitis media.
Common variable immunodeficiency
A disorder where terminal differentiation of mature B cells is blocked, resulting in a normal B cell level with reduced immunoglobulin levels affecting one or more immunoglobulin types. Manifests as recurrent otitis media and pulmonary infections.
Selective IgA deficiency
The most common type of humoral immunodeficiency, caused by blocked differentiation of B cells into IgA producing plasma cells. Normal levels of B cells and all other immunoglobulins are present.
Immunoglobulin G subclass deficiency
Humoral immunodeficiency with a normal number of B cells and IgA, IgM, IgD, and IgE, and a normal or increased level of total IgG, but one or more IgG subtypes is deficient.
Secondary humoral immunodeficiency
Caused by loss of immunoglobulins from the GI or GU tracts, e.g. nephrotic syndrome
Di George Syndrome
An embryonic developmental defect with partial or complete failure of the thymus to develop, resulting in T-cell immunodeficiency with recurrent and/or chronic infections. Congenital defects of the parathyroid glands, head, neck, and heart are also present.
X-linked immunodeficiency with hyper IgM
An X-linked cell-mediated immunodeficiency disorder with failure of CD4+ cells to signal plasma cell isotype switching from IgM to IgG and IgA, resulting in an overproduction of IgM. Manifests as recurrent pyogenic infections.
Causes of secondary cell-mediated immunodeficiency
Viral infections, (measles, CMV), Hodgkin's disease and other lymphomas, HIV infection
Combined T and B cell immunodeficiency disorders
X-linked SCIDS, ataxia-telangiectasia, and Wiskott-Aldrich syndrome
Hereditary angioneurotic edema
Complement system disorder with lack of C1 inhibitor causing excessive function of the classic complement pathway and elevated c-kinin (activated C1) levels leading to vasodilation and edema.
Primary disorders of phagocytosis
Chronic granulomatous diseases
Type 1 hypersensitivity reaction
An IgE mediated immediate hypersensitivity disorder
Type 2 hypersensitivity reaction
Antibody mediated hypersensitivity disorder
Type 3 hypersensitivity reaction
Antigen-antibody complex mediated hypersensitivity
Type 4 hypersensitivity reaction
Delayed, T-cell mediated hypersensitivity disorder
Removal of self-reactive T and B cells from the central lymphoid organs (bone marrow for B cells and thymus for T cells)
Removal or inactivation of self-reactive T and B cells from the peripheral body systems
A B-cell mediated autoimmune disorder with autoantibodies against TSH receptors causing excessive production of thyroid hormones (hyperthyroidism)
A B-cell mediated autoimmune disorder with autoantibodies against TSH receptors causing failure to produce thyroid hormones (hypothyroidism).
Exotoxins that lead to inappropriate direct stimulation of CD4+ cells, e.g. staphylococcal and streptococcal exotoxins. These do not require processing and presentation by APCs.