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46 Cards in this Set
- Front
- Back
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What are the 2 opposing mechanisms involved in pathogenesis? |
Innate immunity/antigen-specific immunity protecting against pathogens and tumors and Microbial virulence mechanisms (mediated by virulence factors) that allow the pathogen to evade immunity, survive in the host, and spread to others. |
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What is notable about disease symptoms? |
They generally result from inflammation caused by host response, can be caused by toxins of pathogen designed to damage host and/or chronic infections (result in erosion/destruction of host tissue/organs). Host inflammation can cause morbidity and mortality. |
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Where did antibiotics originate and what do they do? |
They were originally natural products (penicillin and streptomycin) and they block essential microbial-specific function. |
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What will future antibiotics exploit? |
New targets identified by studies of microbial pathogenesis. |
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What is the difference between opportunistic and normal flora? |
opportunistic: cause disease in immune compromised (elderly, infants, sick, immune deficient, AIDS) Normal flora: commensal or symbiotic, cause no symptoms. |
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What are disease producing microbes maintained by? Do they always cause disease? |
colonization: occasionally cause disease Infection: always cause disease. |
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True/False: Normal Flora are often beneficial. |
True. They can exclude pathogens by occupying available niches, and they can produce some vitamins (especially vitamin K) |
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Where do normal flora reside? |
Gut (large intestine), oral cavity, upper airways, genital tract, urinary tract, skin, eye surface. |
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What is the typical life cycle of a pathogenic microbe? |
Acquisition by host, exploitation of a host niche environment (usually in sterile tissue), evasion of host defenses (usually partial), multiplication in the host, produce disease symptoms, transmission to others. |
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How is the evolutionary success of a pathogen measured? |
By its ability to infect or colonize additional hosts, not in its ability to kill its host. |
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True/False: Pathogens must be transmitted efficiently. |
False, although it helps, some (such as HIV and TB) just remain in a host long enough to maximize their chance to be passed to others. |
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How can some bacteria survive if they kill their host quickly? (e.g. anthrax or cholera) |
They produce enough bacteria in a watery diarrhea (or spores on the savanna) to guarantee their transmission. |
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What situations favor emerging pathogens? |
Poverty, malnutrition, poor air quality, overpopulation pushing humans into new environments/new pathogens, high human density teaches pathogens to transmit more efficiently in man, close association with billios of domestic animals, high mobility of humans. |
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What are the major host defenses? |
Mechanical barriers, chemicals, phagocytes, pattern recognition receptors (TLR, mannose-binding lectin), complement, cytokines (IL-1, IL-2, etc) antibodies, T-cells, and NK-cells. |
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How do phagocytes (PMN and macrophages) defend against microbial infections? |
They ingest and destroy microbes. Finding them by chance encounters and chemotaxis (cell-wall breakdown products, complement fragments, leukotriene from stimulated lymphocytes). They recognize microbes w/ specific receptors for molecules on their surface (C3b, Antibody (Fc), and repeating structures on microbe surfaces |
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How do antibodies work differently alone and in conjunction with complement? |
Alone: blocks adherence, toxin activity, and enzymatic activity. With complement: aggregates and opsonizes toxins/microbes, lyses host cells bearing bacterial or viral antigens and lyses some gram - bacteria. |
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What does it me to opsonize? |
To increase the chance of phagocytosis and digestion by phagocytes. |
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What is complement's role in opsonophagocytosis? |
C3 is activated by classical pathway, lectin pathway, or alternative pathway, then interacts to create surface deposition mediates. C5a: chemotaxis C3b, iC3b: opsonization C5b, C6, C7, C8, C9: Lysis through membrane attack complex. |
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What is the purpose of NK cells? |
They lyse host cells identified by IgG (ADCC, cells infected with virus and bacteria) or tumor antigens (from tumor surveillance) They also are a significant producer of gamma-interferon: cell mediated immunity against intracellular bacteria and viruses. |
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What do cytokines do? |
Provide communications b/t immune cells Activate (or inactivate) immune cells Can stimulate inflammation&protection against infections. Can restore tissue to a non-inflammatory state Mediates many of the inflammatory symptoms of infectious disease. |
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What is the purpose of interferons? |
To interfere with viral replication and to enhance innate and cell-mediated immunity (by activating monocytes and lymphocytes) |
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What are PRRs? |
Pattern Recognition Receptors: family of TLR (toll-like receptors), C-reactive protein, Mannose-binding lectin, etc. |
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What are PAMPs? |
Pathogen associated molecular patterns such as: cell walls of bacteria, LPS of bacteria, Flagella of bacteria, microbial DNA and RNA, etc. |
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What is TLR4? |
It is a PRR that recognizes LPS which is found on all gram negative bacteria. Y. pestis (black plague) has a variety of them. (TLR4 not important for test) |
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What is the purpose of CD4 T cells? |
They activate B cells to make antibody and mediate cell-mediated immunity (1. enhance production of cytotoxic T cells. 2. Activate macrophages to kill intracellular bacteria and destroy infected host tissue.) |
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What mediates inflammation? |
Microbial products (LPS, cell wall fragments, some toxins) Antibody and complement Cell mediated immunity (CD4 T-cells) |
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Why would a host sequester free iron? |
To protect against tissue damage by free radicals and against extracellular growth of bacteria. |
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How does a host sequester iron? |
1. Transferrin - transports and sequesters iron for host use. 2. Lactoferrin - sequesters iron from pathogens and host. 3. Fever - decreases availability of iron for bacteria during infection. |
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What must extracellular and intracellular pathogenic bacteria avoid? |
Extracellular: phagocytes or complement. Intracellular: inside phagocytes by antibacterial properties of lysosomes. |
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What is host resistance against extracellular bacteria mediated by? |
Antibody, complement, phagocytes, PRRs. |
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What is host resistance against intracellular bacteria mediated by? |
TH1 cells, macrophages, CD8 T cells, NK cells (probably), and PRRs. |
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What is host resistance against viruses mediated by? |
Antibody (blocks extracellular spread) Interferons (blocks intracellular growth) NK and CK8 cells (kills virus producing cells) |
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What are virulence factors? |
Special properties that allow pathogens to survive, spread, and cause disease. |
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What are some virulence properties? |
Exploiting a niche, adherence to host tissues, partial (or complete) escape from host immunity, means of acquiring nutrients, mechanism for transmission to next host. |
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How could a pathogen escape the host immunity? |
Protecting itself from Ab and C attack, invasion into cells and avoidance of degradation in lysosomes, interference with host and/or adaptive immunity, living in protected tissue sites. |
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Where do Streptococcus pneumoniae, streptococcus mutans, helicobacter pylori, listeria and salmonella live? |
S. pneumoniae: upper airways, cavities (lung, ear, spinal fluid, eye, etc.) S. mutans: glucan layer on teeth. H. pylori: mucus lining of stomach Listeria and salmonella: in phagocytes |
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Where do salmonella (typhoid), E.coli, Group B streptococci, Mycobacterium tuberculosis, and HIV live? |
(typhoid): bile, liver, spleen E. coli: colonize gut, bladder, ureter. Group B strep: asymptomatic in gut, can infect and kill newborns. tuberculosis: grows slowly to minimize elicitation of host immunity. HIV: grows in and kills CD4 T-cells, eliminating host anti-viral response. |
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Why is adherence by many pathogens important? |
1. Prevents them from being cleared by mucus flow. 2. Necessary to subsequent tissue and cellular invasion. 3. Presence on the mucosa is frequently critical for transmission. |
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What are exo and endotoxins? |
Exotoxins: secreted molecules that can kill, damage, or alter host cells (diphtheria toxin, cholera toxin, tetanus toxin, etc) Endotoxins: LPS in outer membrane of gram negative bacteria (only toxin b/c host makes protective inflammation against it. |
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True/False: Toxic shock toxin is a superantigen. |
True. |
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How do bacteria get iron? |
Siderophores (secreted molecules that bind iron ions) Transport of iron-binding transferrin, lactoferrin, or heme Growing intracellularly (where iron is more readily available. |
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What are some structures that aid in the evasion of phagocytosis? |
Polysaccharides, capsules, M-protein, PspA, PspC, antigenic variation (Pilin, PII, LOS) |
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How does TB, rickettsiae, and salmonella evade intracellular killing? |
TB: glycolipid cell wall resists non-activated macrophages, rickettsiae: escapes to cytoplasm Salmonella: prevents lysosome-phagosome fusion. |
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What are some things that aid in the regulation of virulence factors in response to host conditions? |
Temp, carbon source, concentration of Iron, manganese, or calcium, osmolarity, pH, stress. |
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How do vaccines work? |
By using killed pathogen or pathogen molecules to elicit immunity. Elicitation of protective immune response without an infection (antibodies and cell-mediated immunity.) |
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What are the 2 vaccine approaches? How do they work? |
Antibody: immunize with toxins (cholera, diphtheria, tetanus), adhesions (flu), or unique surface components (pneumococcus) Cell Mediated Immunity: Best elicited with live vaccines (attenuated live intracellular bacteria or viruses) |
