intracellular bacteria – Flashcards
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| what are portals of entry for intracellular bacteria? |
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| natural or aquired openings leading to internal organs |
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| how do bacteria colonize? where do they often enter? how do they resist the body's defenses? what happens once the bacterial population stabilizes? |
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| bacteria enter through mucosal surfaces or sites of injury and resist cilia/mucus clearance mechanisms by invading and infecting the respiratory mechanisms or resident macrophages. once the bacterial population stabilizes, they can start dividing and often take control of cells. the cells controlled often die and the bacteria spill out, able to infect the body more systemically. |
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| what is tissue trophism? |
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| bacteria target specific tissues that have nutrients they require, (rickesia likes endothelial cells, for O2 and nutrients from the bloodstream) |
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| what is an obligate intracellular pathogen? what does invasion of particular cells depend on? |
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| a type of bacteria that needs to invade out cells for nutrients/ATP. invasion of particular cells depends on the eukaryotic cell and the specific needs of that bacteria |
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| what is the endocytic response in terms of intracellular bacteria? |
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| molecules, (protein-protein, protein-proteoglycan, etc), on the bacterial surface link up to corresponding ones on the cell surface, and it is engulfed. |
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| how do cells normally deal with forgein organisms they engulf? |
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| cells usually engulf foreign organisms and take them in as phagosomes to be fused with lysosomes |
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| how do bacteria like chlamydia invade cells and avoid destruction? |
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| chlamydia directs the cell's phagosomes away from lysosomes, and are able to connect to the vacuole's surface and monitor the cell's environment and take in what they need. |
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| how does listeria infect intracellularly? by what mechanism does it attach? how does it affect the cytoskeleton? can it leave the vacuole? what implication does this have for the immune system's function? |
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| listeria has InlA and InlB which bind to E cadherins on the surface cells of the intestine, after doing which, it is taken into the cell. once inside it activates the cell's enzymes to de-polymerize actin, allowing the cells to more fluidly phagocytize the bacteria. once the listeria have been phagocytized, they can leave the vacuole and re-polymerize the actin, and use it as a tail to move from cell to cell, thus evading the immune system. |
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| what is a type III secretion system? |
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| a method bacteria use to gain entrance to host cells, by which they initially use pili to make contact with the host cell membrane and then form a pore by which proteins can be injected into the host cell/nutrients can be extracted from the host cell. |
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| what kinds of things can be transferred into the host cell by a pathogen via the type III secretion system? |
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| transcription factors, to allow the host cell control via the invading pathogen |
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| how do intracellular bacteria spread in the host via circulating fluids such as blood and lymph? what particular mechanisms might they need to shut down in this regard? |
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| intracellular organisms can spread via infection of WBCs, monocytes in particular, but also neutrophils and lymphocytes can be affected. these pathogens are also able in some instances to turn off the apoptotic response of infected WBCs. this can lead quickly to systemic infections. |
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| how does direct spread of infection via intracellular bacteria occur? |
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| at an open orifice or along skin, (esp mucosal surfaces), pathogens can utilize enzymative mechanisms such as secretion of hyaluronidase, proteases, collagenases, (MMPs), lipases, and nucleases to help the pathogen migrate through tissues to new cells |
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| what is a major risk for pregnant mothers infected with listeria? another major risk for anyone infected? |
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| listeria in the intestine can bind actin, and use it as a tail to get to and infect other cells such as monocytes/macrophages in the extracellular/submucosal area. these infected WBCs can then travel around the body, including the placenta, and possibly kill the fetus or cause meningitis in anyone infected |
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| what toxins can intracellular bacteria produce? |
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| toxins such as endotoxins (LPS), and exotoxins as well as fermentation end products and O2 consumption |
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| what are some mechanisms intracellular bacteria employ in resistance of host immune response? |
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| resistance to lysozyme and basic proteins, (eg. defensins). resistance to endocytosis and phagocytosis, (eg. capsule), and resistance to intracellular destruction, a key component of which is prohibition of lysosomal killing for intracellular bacteria |
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| does gene expression in intracellular bacteria change with transitioning acute into chronic infections? does this change the bacteria? |
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| yes. the bacteria can downregulate genes for host cell entry, and start to take on a "persistent forms" that can be less metabolically active |
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| how can chronic infections change over time? what might kick off a change? |
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| someone can be infected while young, and the bacteria simply enters a persistent form with a low enough activity level that the immune system doesn't respond. however when the host ages, and the internal environment changes, this can cause the infection to become more active and cause disease |
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| what are some host responses/factors that can contribute to pathology? |
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| acute inflammation, chronic inflammation, (residual scarring |
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| what are some specific host responses/factors that can contribute to pathology? |
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| mechanical changes, chemical changes, (pH changes, fatty acids that act as detergents), cellular response via phagocytes, (macrophages, monocytes, neutrophils), and lymphocytes, or a humoral response via antibodies |
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| what are type 1 pathogens? what immune system response do they elict? |
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| viruses and intracellular bacteria induce a TH1 immune response, mediated by CD4 and CD8 effector cells, a mixed response where the body is trying any method to rid itself of the infection |
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| can intracellular bacteria increase the life of cells they infect? |
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| yes, monocytes usually live about a day in the body, but those infected can live for months in vitro |
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| what is the key goal for intracellular bacteria, and those cells they invade? |
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| intracellular bacteria want to avoid lysosomal contact, and the host cells want the pathogen-containing vacuoles to interact with lysosomes |
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| can intracellular bacteria extrude themselves from cells they infect by taking their vacuole to the plasma membrane and being released? |
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| yes |
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| what are some extracellular mechanisms employed by intracellular bacteria in and around macrophages? why would they want to do this? |
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| prevention of chemotaxis/cytokine release, (via type 3 secretion), and phagocytosis resistance, (via capsules in extracellular bacteria). doing this protects the cell from macrophagic destruction or opens up the macrophage for invasion |
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| are there certain receptors intracellular bacteria specifically choose to bind and others they purposefully ignore? |
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| yes, intracellular bacteria bind to complement receptors on the host cell, because if they bind to the IgG or Fc receptors, an oxidative burst is triggered |
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| how does legionella evade host cell defense? |
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| legionella avoids triggering an oxidative burst as well as diverts the phagosome to another pathway to resist phagolysomal function, (sent to the golgi or ER instead) |
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| how does M. tuberculosis evade host cell defense? |
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| M. tuberculosis modifies or aborts normal route of phagosome maturation. in this, the pathogen controls the vacuole to keep it from binding to the lysosome, by changing the pH, (lower pH is more likely to bind to a lysosome), or by changing protein/sugar molecule expressions on the vacuole membrane, (mannose6P is one recognized by the lysosome) |
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| how does chlamydia evade host cell defenses? |
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| chlamydia diverts the phagosome to another pathway to resist phagolysomal function, (sent to the golgi or ER instead) |
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| how do coxiella burnetii and salmonella evade host cell defenses? |
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| these resist degradation by inhibiting degradation enzymes, however they cannot survive in an activated macrophage, (tolerance) |
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| how do listeria, shigellae, and rickettsae evade host cell defenses? |
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| these can escape from the phagosome, however they are now subjected to MHC class I pathway of antigen processng and presentation, (escape) |
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| what are the 3 basic ways that bacteria use to escape lysosomal killing? |
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| escape, tolerance, and avoidance |
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| what bacteria is responsible for rocky mtn spotted fever? what carries it? what is its virulence? what cells does it like to infect? |
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| rickettsia rickettssii, which is carried by ticks or lice. its virulence factor is its intracellular invasion of endothelial cells, (creating a very severe vasculitis) |
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| what does rickettsia prowazekii cause? what is its vector? where does it invade and what can it cause? |
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| rickettsia prowazekii causes louse-borne typhus, and the vector is the human body louse. it replicates in endothelial cells, and can therefore cause vasculitis. |
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| what organism causes scrub typhus? what is its vector? where does it invade and what can it cause? |
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| rickettsia tsutsugamushi. the vector is mites, (chiggers, red mites). it replicates in endothelial cells, and can therefore cause vasculitis. |
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| can rickettsia escap vacuoles? |
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| yes |
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| can 2 different invading intracellular bacteria exist in the same vacuole? |
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| yes |
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| what intracellular bacteria causes Q fever, (acute+chronic)? how is it transmitted to humans? what is its virulence, symptoms? |
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| coxiella burnetii, (member of rickettsiaeae). it is inhaled from livestock and pets, its virulence is intracellular replication, resistance of lysosomal degradation & formation of immune complexes in chronic disease. acute symptoms include 20d incubation, sudden onset of headache, chills, mild respir, 50% have hepatosplenomelagy. chronic symptoms include months to years incubation with subacute endocarditis, insidous with poor prognosis. |
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| what causes human monocytic ehrlichiosis? what is its vector? what are the symptoms like? |
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| ehrlichia chaffeensis, which is spread via the lone star tick. its virulence factor is intracellular replication, with the ability to sequester or destroy infected circulating cells. the symptoms are like those of rocky mtn spotted fever, ~12d after tick bite = high fever, headache, malaise, myalgia, and leukopenia/thrombopenia, (what differentiates it from rocky mtn spotted fever) |
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| what does chlamydia trachomatis cause? how is it transferred? what are its symptoms? |
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| trachoma, urogenital infections, and reiter's disease. it is transferred sexually, at birth, or via breaks in skin or mucous membranes. its virulence factors are intracellular replication and prevention of phagolysosomal fusion. symptoms include inflammation of the urogenital tract w/ mucopurulent discharge. with trachoma, inflammation around the eye, and with reiter's syndrome -urethritis, conjunctivities, polyarthritis, and mucocutaneous lesions |
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| what does chlamydia pneumoniae cause? how is it is transmitted? what is its virulence? symptoms? |
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| bronchitis, pneumonai, sinusitis, and potentially atherosclerosis, alzheimers disease and MS. it is transmitted by respiratory secretions. its virulence factors are intracellular replication and prevention of phagolysosomal fusion. the symptoms are often asymptomatic, persistent cough and malaise |
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| what does chlamydia psittaci cause? how is it is transmitted? what is its virulence? symptoms? |
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| psittacosis, (parrot fever), severe pneumonia. its transmission is from infected birds' resp. tract. its virulence is replication in vacuoles and prevention of phagolysosomal fusion. symptoms include pulmonary non-productive cough, rales, consolidation |
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| what are key factors for bacterial survival? |
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| recognition of environmental conditions and rapid response, (eg. iron stores or depletion), ability to alter gene response under new conditions - favors adaptation and ultimately survival, growth phase of of organism, (most chronic intracellular organisms change gene and protein expression in the stationary growth phase to enhance survival) |
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| is disease the primary objective of the organism? |
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| no |
