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187 Cards in this Set
- Front
- Back
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Immunity |
Ability to recognize and protect against nonself |
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Antigen |
Any substance that can be recognized by your immune system |
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Epitope |
The part of the antigen that is recognized by the immune system |
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Inflammation |
A vascular response to protect and heal tissues Attempts to isolate invaders |
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Premunition |
Presence of a parasite induces immune response that conveys resistance to further infection; parasite remains alive but it's reproduction and other activities are restrained |
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Concomitant Immunity |
Presence of parasite induces immune response that conveys resistance to further infection; parasite eliciting response is unaffected |
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Acquired Immunity |
-Specific to particular non-self material -Requires prior exposure -Requires time for development during 1st exposure -Occurs more rapidly and vigorously on 2nd exposure |
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Humoral Immune Response |
Involves B-cells & T-cells, and antibodies |
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Cell Mediated Immune Response |
Involves T-cells, no antibodies |
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Cytokines |
Substances released by cells of the immune system to communicate with other cells of the immune system |
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Interleukins |
Activate macrophages and lymphocytes |
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Tumor Necrosis Factor (TNF) |
Mediates inflammation; fever |
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Interferons |
Activates cells of the immune system Activates endothelial cells to allow lymphocytes and phagocytes to pass through wall of vessel |
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Innate Immunity |
-Not specific for one particular pathogen -Does not require prior exposure -Occurs rapidly and vigorously with each exposure -Dramatically influenced and strengthened as a consequence of acquired immune response |
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Phagocytes |
Can recognize nonself: abundant expression of Toll-like receptors Carry out phagocytosis Bind with antigens using receptors to identify self from nonself |
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Lysosomes |
What do phagocytes produce? |
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Cytotoxic Compounds |
Cell killer |
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H2O2 O OH Radicals |
What are the reactive oxygen intermediates? |
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Nitric oxide Nitrite Nitrate |
What are the nitrogen reactive intermediates? |
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Mononuclear Phagocyte System |
Fixed phagocytes Develop from monocytes that arise from cells in bone marrow Can produce cytokines |
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Macrophages |
What are monocytes called when they're in lymph nodes, spleen, and lung? |
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Kupffer |
What are monocytes called when they're in the liver? |
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Microglial Cells |
What are monocytes called when they're in the CNS? |
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Polymorphonuclear Leukocytes (Granulocytes) |
Circulating phagocytes in blood |
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Neutrophils |
Most abundant white blood cell First like if defense |
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Eosinophils |
Antiparasitic white blood cells |
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Basophils |
White blood cell thay appears in inflammatory responses Contains anticoagulant, which prevents blood from clotting too quickly |
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B Cells |
Mature in bone marrow Produce antibodies and release into bloodstream Have antibody Receptor on cell surface Can recognize nonself Only cells that produce antibodies |
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Plasma Cells |
Produce large amounts of specific antibody, then die |
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Memory B Cells |
Long lived Produce specific antibody rapidly upon second exposure |
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T Cells |
Mature in Thymus gland Have T-cell receptors that can recognize nonself Produce cytokines that activate transcription factors in target cells |
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T-Helper Cells |
Have coreceptor protein CD4 and CD28 |
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CD4 and CD28 |
What are the two costimulatory molecules? |
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Cell-mediated Immunity |
In which kind of immunity are T-helper 1 cells involved in? |
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Humoral Immunity |
In which kind of immunity are T-helper 2 cells involved in? |
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Cytotoxic T Lymphocytes |
Have coreceptor protein CD8 Bind with target cell and secrete protein that causes pores in membrane Can cause apoptosis within target cell (lysis) |
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T-Memory bells |
Long lived Activated during 2nd exposure |
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Mast Cells |
Basophil-like cells Not phagocytic Releases histamines, serotonin, etc Involved in inflammation response and allergies |
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Natural Killer Cells |
Lymphocyte-like cells Kill infected cells (lysis) |
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Lymphocyte activated killer cells |
NK cells that respond to cytokines |
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Complement Proteins |
Series of proteins activated in a sequence in response to invading pathogen |
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Classical Pathway |
Depends upon antibodies bound to surface of pathogen Causes lysis and stimulates phagocytosis |
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Alternative Pathway |
Depends upon polysaccharides on outer surface of pathogen Causes lysis and stimulates phagocytosis |
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Regulatory proteins inactivate the first component of complement when it binds to host cells |
What are host cells not lysed in the complement? |
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Major Histocompatibility Complex |
Group of genes that code for proteins embedded in cell surfaces |
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Class I MHC Proteins |
Found on surface of virtually all cells |
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Class II MHC Proteins |
Found primarily on macrophages and lymphocytes |
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Antibodies |
Immunoglobulins 10^11 types Labels |
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They rearrange gene segments during development |
How do RAG 1 and 2 genes account for the variability in antibodies? |
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Antigen binding fragment Variable Region |
What is the Fab region? |
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Phagocytosis/Opsonization |
What happens if the Fc region is recognized by a macrophage? |
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Opsonization |
Antibody dependent phagocytosis (IgG) |
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Antibody dependent Phagocytosis |
What does the antibody IgG signal? |
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Neutrophils Eosinophils |
Which phagocytes have receptors for Fc regions of bound antibodies? |
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Natural Killer Cells |
Which mast cells have receptors for Fc regions of bound antibodies? |
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Antibody Dependent, Cell-mediated Cytotoxicity (ADCC) |
Phagocytize and or adhere to pathogen and release cytotoxic compounds |
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T-Cell Receptors |
Has a variable region and a constant region Occur in the surface of T-cells (constant region is transmembrane) Have coreceptors (transmembrane) |
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Bind to antigen (epitope) Coreceptor binds with MHC class II Transmit signals into T cells and produce cytokines |
How do T-Cell receptors work? |
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Delayed Type Hypersensitivity (DTH) |
Type of cell mediated immunity Depends on activated macrophages Requires at least 24 hours from antigen introduction to response |
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It is deposited at the site if inflammation in an attempt to keep invader isolated in one place |
What is fibrin used for during inflammation? |
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Fibrosis |
The accumulation of modules of inflammatory tissue (granulomas) |
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Immediate Hypersensitivity |
Involves mast cells with receptors for Fc region of IgE antibodies Causes release of histamine, etc |
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Dialation of local blood vessels and increased permeability Blood plasma escapes, causing swelling and redness Neutrophils move out and attack first, followed by macrophages |
What does the release of histamine, etc by IgE cause? |
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Anaphylaxis |
First exposure causes over production of IgE Second exposure causes massive mast cell response Systemic |
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Cornified Skin / Sclerotized |
The process by which the outer most layer of skin becomes hardened and tough |
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Skin Mucous Layers |
What are the two physical barriers of the body? |
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Shift Surface Antigen |
Changes the antigen on the surface of their cell |
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Shed Surface Antigen |
Antigens fall off |
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Absorb Host Antigens |
Parasite coats itself in host antigens |
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Inhibit Binding of Fc Region |
Attaches protein to Fc region of host antibody to prevent binding |
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Cleave off Fc Region |
Cleaves off Fc region of bound antibodies so host immune cells can't bind |
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Migrate around Host |
How can parasites outrun the host immune system? |
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Shift Shed Absorb Inhibit Fc Cleave Fc Migrate |
What are all the ways parasites can circumvent the hosts antibodies? |
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Inhibit IL-1 and IL-2 Cause non specific proliferation of B cells (exhausts immune system) Produce antioxidants |
What are the ways in which parasites can circumvent the hosts cytokines? |
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Parasitism |
A symbiosis between two species in which the parasite is: - Smaller than the host - dependent on the host - has a higher reproductive rate than the host - potentially harmful to the host |
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Ectoparasite |
Lives on the outside surface of the host |
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Endoparasite |
Lives inside the host |
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Parasitoid |
Insects that lays it's eggs inside the body of another insect, whose larvae feed on the body of the host |
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Hyperparasitism |
When a parasite is the host for another parasite |
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Host |
An animal that harbors a parasite |
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Definitive Host |
Host in which parasite reaches sexual maturity; harbors adult parasite |
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Intermediate Host |
Harbors developmental (immature) stages of parasite |
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Vector |
Animal that transmits a parasite to a host; is necessary for development of parasite; may be either the definite or intermediate host |
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Paratenic Host |
Parasite resides in host and is physiologically dependent on host, but no development occurs (accidental) |
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Phoretic Host |
Mechanical transmission of a parasite (phoresis); parasite is in mouth parts or body of phoretic host, but is not physiologically dependent on host (no development in host) |
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Reservoir Host |
Non-human animal that naturally harbors a parasite that is infective to humans |
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Commensalism |
Symbiosis in which one participant benefits, whereas the other is neutrally affected |
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Phoresis |
Mechanical transmission of a parasite Parasite is on the mouth parts or body of host |
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Zoonosis |
Disease in humans caused by a parasite that normally infects non-human animals |
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Epidemiology |
Study of factors affecting transmission and distribution of a disease agent |
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Helminth |
Greek word for worm |
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Parasitic Load |
Number of parasites harbored by a host |
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Nagana |
What disease does Trypanosoma brucei brucei cause? |
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Nagana |
Causes: Anemia Fever Brain lesions Lack of coordination Paralysis Death within 15 days to months Affects: Livestock |
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Chronic African Sleeping Sickness |
What disease does Trypanosoma brucei gambiense cause? |
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Acute African Sleeping Sickness |
What disease does Trypanosoma brucei rhodesiense cause? |
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Gambiense |
Which Trypanosoma brucei sub species invades the brain? |
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Variant specific surface glycoproteins |
What is the protein coat of trypanosomas made of? |
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1000 |
How many VSG genes does T. Brucei have? |
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1 |
How many VSG genes are expressed at one time? |
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New VSG gene is copied, moved to active telomeric site Placed downstream from a promoter region Replaces resident VSG gene |
Describe how a VSG gene is replaced |
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Silent telomeric VSG gene duplicated and transposed to 2nd telomeric site where it is expressed |
Describe how a VSG is activated via duplication |
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Silent telomeric VSG becomes expressed |
Describe how a VSG gene is activated without being duplicated |
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Slender Trypomastigote |
Trypanosoma: Slender and elongated Mitochondrion undeveloped |
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Intermediate Trypomastigote |
Trypanosoma: Begins to shorten Mitochondrion developing |
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Stumpy Trypomastigote |
Trypanosoma: Short, flagellum and undulating membrane reduced Mitochondrion well developed and functional Only stage infective to vector |
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Midgut Trypomastigote |
Slender and elongated Mitochondrion developed No protein coat |
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Epimastigote |
Begins to shorten Mitochondrion less developed No protein coat |
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Metacyclic Trypomastigote |
Short, flagellum and undulating membrane reduced Mitochondrion undeveloped Protein coat present Only stage infective to mammal |
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When the parasite sheds it's protein coat, it's former antigens bind to red blood cells, causing the hosts immune system to attack it's own red blood cells |
Why does trypanosoma brucei cause anemia? |
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Found in: - Blood - Lymph nodes - Brain - nearly all organs of body Causes: - anemia - fever Symptoms: - Apathy - Sleepiness - Coma * Characterized by repeated waves of infection |
General Pathology of T. b. gambiense |
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Found in: - Blood - Lymph nodes - Nearly all organs - Not brain Causes: - Anemia - Fever Symptoms: - progresses rapidly * Characterized by repeated waves of infection |
General Pathology of T. b. rhodesiense |
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Treat with Suramin, DFMO Control tsetse fly -DDT -Clear cut brush -Eliminate wildlife |
What is the treatment and control for T. b. gambiense and rhodesiense? |
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Phoresis. No vector |
How is Trypanosoma evansi transmitted? |
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Sura Transmitted by Tabanus ( Biting Horsefly) |
What disease is caused by T. evansi in Africa and what phoretic host transmits it? |
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Murrina Transmitted by vampire bats |
What disease is cause by T. evansi in south America and what is the phoretic host? |
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Dourine STD |
What disease does T. equiperdum cause and how is it transmitted? |
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Hindgut Transmitted through feces |
Where does T. cruzi develop in the vector and how is it transmitted? |
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Intracellular part |
What part of T. cruzi life cycle is in the human host? |
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Rhodnius Triatoma (Hemiptera) |
Who are the vectors or T. cruzi? |
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Dogs Cats Rats |
Who are the reservoir hosts of T. cruzi? |
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Chagas Disease Central and South America US |
What disease does T. cruzi cause and where? |
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Rupture of psuedocysts causes inflammatory response that destroys nerve cells in vicinity |
General Pathology of T. cruzi |
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Most often in children Heart muscle invaded (up to 80% of ganglion cells lost Lose of muscle tone (heart failure) Anemia, nervous disorders |
What is the acute phase or T. cruzi pathology? |
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Chagas Disease |
Caused by T. cruzi that results in a lose of muscle tone and destruction of ganglion cells in the vicinity |
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Most often in adults Heart damage Destroys autonomic ganglia of esophagus and colon Lose muscle tone Disrupts peristalsis Inability to swallow or defecate Transplacental transmission |
What is the chronic phase of Trypanosoma cruzi pathology? |
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Megaesophagus and Megacolon |
A result of chagas disease in which the muscle of the esophagus and colon lose tone and ganglion cells |
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Cell mediated |
Which type of immune response happens in the acute phase of T. cruzi pathology? |
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Humoral Classical Complement pathway |
Which type of immune response happens in the chronic phase of Trypanosoma cruzi pathology? |
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Infects cells of the immune system Sheds antigens (Not antigenic shift, no repeated waves of infection) Binds Fc region of free Ab Cleave Fc region of bound Ab |
How does T. cruzi evade the host immune system? |
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Suppresses IL-2 production Polyclonal lymphocyte activation Exhaustion |
How does T. cruzi suppress the hosts immune system? |
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Inflammatory response to ruptured psuedocysts Cell lysis and fibrosis Shed antigens absorbed by cardiac cells |
What is the immunopathology of T. cruzi? |
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No effective treatment for intracellular stages Control vectors |
What is the treatment and control for T. cruzi? |
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Phlebotomus Lutzomyia (Sand flies) |
What are the vectors for Leishmania? |
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Leishmaniasis |
What disease does Leishmania cause? |
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Promastigote |
What stage of Leishmania's life cycle is infective to the host? |
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Amastigotes |
What stage of Leishmania's life cycle is infective to the vector? |
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Africa Middle East India |
Where are L. tropica and L. major found? |
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Phlebotomus |
What is the vector for L. tropica and L. major? |
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Dogs Rodents |
What are the reservoir hosts for L. tropica and L. major? |
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Old World Cutaneous Leishmaniasis |
What disease does L. tropica cause? |
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Visceral Leishmaniasis (Dum Dum fever) (Kala azar) |
What disease does L. donovani cause? |
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Worldwide |
Where is L. donovani found? |
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Phlebotomus |
What is the vector for L. donovani? |
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Canids |
What is the reservoir host for L. donovani? |
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Visceral Leishmaniasis |
Disease caused by L. donovani that results in an enlarged spleen and causes anemia |
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The spleen and bone marrow over compensate for lost macrophages at the cost of RBC production |
Why does visceral leishmaniasis cause anemia? |
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New World mucocutaneous leishmaniasis |
What disease does L. brazilliensis cause? |
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Central and South America |
Where is L. brazilliensis found? |
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Lutzomyia |
What is the vector for L. brazilliensis? |
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Cats Dogs Rats |
What are the reservoir hosts for L. brazilliensis? |
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Control Vectors |
What is the treatment and control for L. tropica, major, and brazilliensis? |
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Genes Scl-1 and 2 |
What controls resistance to L. tropica and major? |
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Yes |
Can hosts resistant to L. tropica and major develop complete immunity? |
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No. Hosts may develop premunition The parasite is harmed and lays dormant |
Can hosts susceptible to L. tropica and major develop complete immunity? |
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Humoral |
In hosts susceptible to L. tropica and major, which immune response is most active? |
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Cell-mediated DTH |
In hosts resistant to L. tropica and major, which immune response is most active? |
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Lsh gene |
What controls the resistance to L. donovani? |
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Cell mediated |
In hosts susceptible to L. donovani which immune response is suppressed? |
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Humoral response |
In hosts resistant to L. donovani, which immune response is most active? |
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Tissue destruction via immunopathology |
How does L. brazilliensis cause harm to the body? |
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Trichomonas tenax |
Commensal in human mouth |
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Trichomonas vaginalis |
Infects reproductive tract of men and women; STD Men often asymtomatic In women, alters pH or vagina; becomes more basic |
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Metronidazole |
How do you treat Trichomonas vaginalis |
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Trichomonas foetus |
STD of cattle Causes abortion and sterility |
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Histomonas meleagridis |
What causes blackheads in turkeys? |
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Chickens |
What is the reservoir host for Histomonas meleagridis? |
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No. It requires the presence of a gut parasite |
Can Histomonas meleagridis cause blackhead alone? |
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Causes necrotic ulcers in liver and caecum Yellowish diarrhea Ruffled, droopy feathers Skin on head turns back |
What does Histomonas meleagridis cause in turkeys? |
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Spread through fecal contamination |
How is Giardia duodenalis spread? |
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Dogs Beavers |
What are the reservoir hosts for Giardia duodenalis? |
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Entamoeba histolytica |
What amoeba causes dysentery in humans? |
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Histomonas meleagridis Entamoeba histolytica |
Which two parasites require the presence of gut bacteria to cause disease? |
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Diarrhea Cramps Vomiting Slow development |
What are the symptoms of chronic amoebic dysentery? |
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Severe cramps Dysentery Headache Fever 15-20 bloody stools/day May lose up to 17 L of fluid/day |
What are the symptoms of acute amoebic dysentery? |
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In the gut where it causes dysentery Can penetrate the gut |
Where are the primary lesions found in the host that Entamoeba histolytica resides and what does it cause? |
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Liver and lungs Causes ectopic cysts |
Where are the secondary lesions found in the host that Entamoeba histolytica resides and what does it cause? |
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Hepatic amebiasis |
What are the cysts of Entamoeba histolytica called when they're in the liver? |
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Pulmonary amebiasis |
What are the cysts of Entamoeba histolytica called when they're in the lungs? |
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Metronidazole Control: - Sanitation - Drying - Hold feces in storage for 2 weeks |
How do you treat and control Entamoeba histolytica? |
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4 |
How many nuclei per cyst does Entamoeba histolytica have? |
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8 |
How many nuclei per cyst does Entamoeba coli have? |
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Entamoeba coli |
Commensal in human gut |
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Entamoeba gingivalis |
Commensal in human mouth No cyst |
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Iodamoeba buetschlii |
Amoeba found in human gut Forms cysts Fecal contamination |
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Naegleria fowleri |
What is the amoeba that causes Primary amoebic meningoencephalitis (PAM)? |
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Primary Amoebic Meningoencephalitis |
Brain eating disease |
