Microbiology Final Flashcard
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| Human Microbiota |
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| Our bodies carry 10x as many bacterial cells as human cells -bacteria that are normally found at various nonsterile body sties are called commensal organisms The consortium of colonizing microbes is called the human microbiota or microbiome -Thiese microbe populations change constantly, and vary with type of tisse and condition -they can also cause disease if they reach an abnormal location |
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| Human Microbiota- skin |
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| Skin is difficult to colonize because it is dry, salty, acidic, and contains protective oils -10^12 microbes in moist areas of skin such as the scalp, ears, armpits, genital and anal areas They are mostly gram-positive bacteria that are more resistant to salt and dryness examples: Staphylococcus epidermidis Propionibacterium acnes -degrades skin oil -inflames sebaceous glands -causes acne |
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| Human Microbiota- Nose and Mouth |
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| At first a human infant's mouth is colonized with: -Nonpathogenic Neisseria (gram-negative cocci) -Streptococcus, lactobacillus (gram-pos rods) As teeth emerge, others species grow: -Prevotella and Fusobacterium: between the gums and teeth, these anaerobic spaces allow anaerobic bacteria to grow better -Streptococcus mutans: tooth enamel The nasopharynx and oropharynx are populated by Staphylococcus auerues and S. epidermis -these bacteria are normally harmless, but they may cause disease if they enter the bloodstream |
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| Mucociliary escalator |
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| The lungs and trachea are usually sterile -cilated mucous lining of the trachea, bronchi, and bronchioles makes up the mucociliary escalator -this sweeps foreign particles up and out of the lung |
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| Stomach |
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| The stomach is highly acidic so few microbes are able to survive -Helicobacter pylori: able to survive at pH1, burrows into protective mucus, can cause gastric ulcers Hypochlorydia- this is decreased stomach acidity that is caused by malnourishment -Vibrio cholerae is the what causes Cholera, when the stomach is less acidic it is able to pass through it to reach the small intestine where it can start the infection |
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| Intestine |
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| The intestine contains 10^9 to 10^11 bacteria/gm of feces -ratio of 1,000 anaerobes: 1 facultative organism Organisms tha inhabit the intestine: Bacteroides thetaiotaomicron -anaerobe -breaks down complex carbohydrates into products that can be absorbed by the body Escherichia coli -facultative anaerobe -catabolizes gluconate, a component of secreted mucus The intestine's microbial population is complex but balanced -antibiotic therapy disrupts this balance and may lead to poor digestion or disease, ex Pseudomembranous colitis, which is caused by Clostridium difficile |
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| Probiotics |
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| these are living microes that are ingested to restore the natural microbial balance. -most commonly used genera are Bifidobacterium and Lactobacillus |
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| Urogential tract |
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| The kidneys and urinary bladder are normally sterile -the urethra contains Staphylococcus epidermidis and some members of Enterobacteriaceae -may cause urinary tract infections Composition of the vaginal microbiota changes with the menstrual cycle -acidic secretions favor Lactobacillus acidophilus -anitbacterial anitbiotic therapy allows Candid albicans to proliferate, causing a yeast infection |
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| Risks and Benefits of Microbiota |
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| Commensal microbes benefit the human host -Make vitamins and digest food -prevent colonization of pathogens by competing for nutrients pathogens need -make immunomodulin proteins -have ptoential use as vaccine delivery vehicles Opportunistic pathosgens cause disease when immune system barriers are breached, the host is said to be immunocompromised -Bacteroides fagilis: a harmless bacteria in the gut, but can invade tissues through surgical wounds, causing abscesses that persist and can lead to anaerobic gas gangrene |
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| Overview of the Immune System |
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| Nonadaptive (innate) immunity -barriers to infection -nonspecific responses to destroy all invading cells -present at birth Adaptive Immunity -Reaction to specific antigens, parts of foreign proteins, sugars, chemicals -Body reacts to antigens when exposed -Retains "memory" of those antigens which allows for a faster response if exposed for a second time |
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| White Blood Cells (WBCs) |
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| WBCs are formed by differentiation of stem cells produced in the bone marrow Types: Neutrophils (PMNs) and monocytes -engulf and destroy microbes by phagocytosis -monocytes differentiate into macrophages and dendritic cells Basophils and eosinophills -release toxins to poison microbes Lymphocytes -T cells, modulate specific immune response, develop in th Thymus -B cells, produce antibodies to bind antigens, develop in Bone marrow |
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| Lymphoid Organs |
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| Primary lymphoid organs are where lymphocytes mature and spend most of their life, they are only periodically released where they migrate from one place to another ex. Thymus Secondary lymphoid organs -this is where lymphocytes encounter the antigens, such as the spleen and lymph nodes |
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| Physical barriers to infection (Innate Host Defenses) |
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| Skin -contains keratin- hard proteins that can't be degraded by microbial enzymes, oil (sebum) also protects and is slightly acidic to help protect -Skin-associated lymphoid tissue (SALT) is a consortium of specialized cells that recognize microbes that went past the physical barrier -mostly make up of Langerhans cells, which are dendritic cells that can phagocytose microbes |
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| Mucous Membranes (innate host defenses) |
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| -Trap, destroy pathogens -mucous layers slough off, remvoed -cilia remove microbes from lungs Must be selectively permeable to exchange nutrients and export products and wastes |
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| Gut-associated Lymphoid Tissue (GALT)(innate host defense) |
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| this is an innate mucosal immune system in the gastrointestinal system. -includes tonsils and Peyer's patches -M cells are found through out the intestinal surface and wedged between epithelial cells. Thes fixed cells take up microbes from the intestine and release them on the other side to be taken up by macrophages Macrophages engulf and try to kill the organism. |
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| Chemical barriers to infection (innate host defense) |
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| Defensins -small, antimicrobial, cationic peptides -destroy invader's cell membrane -produced by many human cells -two classes of vertebrate defensins: Alpha defensins: stored in cytoplasmic granules Beta defensins: Not stored in granules |
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| The Acute inflammatory Response |
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| Infection releases microbes to tissue -Resident macrophages phagocytose bacteria and release vasoactive factors that increase bloow volume and capillary permeability to help deliver WBC's. Capillary cells express selectins, which slow down macrophage movement to allow them to move into the endothelium to attack the bacteria Additional macrophages extravasate or squeeze btw capillary cells and leave them to attack bacteria |
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| Bradykinin (an acute inflammatory response) |
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| Damaged tissue cells in the area of inflammation will release bradykinin, which loosen tight junctions btw endothelial cells to promote extravasation -They also bind to mast cells in the area and cause them to degranulate, which releases histamine which stimulates vessels to open further so blood plasma and platelets can be released into the area Prostaglandin is an enzyme that is also released which stimulates nerve endings and stimulate itching and pain |
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| Chronic Inflammation |
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| Results from the persistent presence of a foreign object, which causes permanent tissue damage Causes: Pathogens that resis host defenses (Mycobacterium tuberculosis) -Nonliving irritant material (wood splinters, asbestos) -autoimmunity (Crohn's disease) The body "walls off" site in granuloma -deposits fibroconnective tissue around lesion, which causes tissue hardening known as fibrosis |
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| Phagocytosis |
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| Phagocytes must avoid attacking host cells -host cell glycoprotein CD47 prevents attack Phagocytes are enhanced by opsonization, which is a process where antibodies surrounding the macrophages bind the bacteria and the fc portion of the antibodies bind to the macrophage surface, allowing them to engulf the invader |
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| Oxygen-independent killing pathways (phagocytosis) |
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| Once the phagosome and lysosome fuse it can either result in oxygen-dependent of independent killing pathways. Oxygen-independent mechanisms include enzymes like lysozyme to destroy the cell wall,compounds like lactoferrin to sequester iron away from the microbe, and defensins which are small cationic antimicrobial peptides |
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| Oxygen-dependent killing pathways of phagocytosis |
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| These kill thru production of various oxygen radicals. NADPH oxidase yields superoxide anion, hydrogen peroxide, and eventually hydroxyl radicals. Macrophages, mastcells, and neutrophils also generate reacive nitrogen intermediates such as Nitric oxide (NO), nitrite (NO2), and nitrate (NO3) All of these reactive oxygen species attack bacterial membranes and proteins. These mechanisms cause the large increase in oxygen consumption during phagocytosis known ans the oxidative burst. |
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| Natural Killer Cells |
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| Destroy infected and cancerous host cells Healthy cells make surface MHC class I antigens 0cancderous and infected cells stop making MHC I MHC proteins are important for recognizing self and for presenting foreign antigens to the adaptive immune system When natural killer cells encounters a cell lacking these markers, it secretes perforins protein into the target cell -which creates membrane pores to lyse the cell |
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| Toll-Like receptors |
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| Microbes posses unique structures that immediately tag them as foreign -these pathogen-associated molecular patterns (PAMPs) ar recognized by Toll-like receptors prsent on various host cell types Once bound to their ligands, the TLRs trigger an intracellular regulatroy cascade -cause host cell to release proteins called cytokines which bind to various immunce cells, and direct them to engage the invader |
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| Complement pathway |
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| is a mechnism that enhances or complements the killing effect of antibodies on bacteria. The system consists of about 20 proteins which activate each other via proteolytic cleavage. The alternative complement pathway begins with complement factor C3 C3 normally made and degraded quickly -it is stabilized by Gram negative LPS -it inserts into bacterial outer membrane -once inserted it reacts with other components (factor B, factor D, properdin -cleaves C5 to C5b, which then binds C6, C7 -these form a prepore complex in the target cell membrane, which then forms a membrane attack complex (MAC) that lyses the target membrane |
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| Opsonin |
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| is any factor that can promote phagocytosis of an organism, such as factor C3b, which binds to bacterial cell surface, tagging it, making it easier for PMNs (neutrophils) to grap and engulf the organism |
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| Anaphylatoxins |
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| These proteins trigger degranulations of vasoactice factors like histamine from endothelial cells, msat cells, or phagocytes. They can also stimulate chemotaxis of immune cells Examples are C5a and C3a |
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| Fever |
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| Healthy body temperature is btw 36-38 degrees C. They hypothalamus acts as the body's thermostat -Pyrogens are substances that cause fever Exogenous pyrogens (which originate from outside the body, usually a bacterial toxin) induces the release of endogenous pyrogens (which are made inside the body, like IFN, TNF, IL-6) -they stimulate the production of prostaglandins -cross the blood-brain barrier, and changes the responsiveness of the thermosensitive neurons that make up the thermoregulatory center, i.e. it turns up the thermostat Turning up the temperature causes microbes to grow slower since they are not at their optimal temperature and may also reduce iron availability to bacteria, causing them to grow slower and allows the body to subdue the infection before it grows too much |
