Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
30 Cards in this Set
- Front
- Back
|
What are the 6 host-microbe ecosystems?
|
1. Normal flora (microbiota): associated with healthy tissue
2. Commensalism: microbe +, host not +/- 3. Mutualism: both microbe and host + 4. Parasitism: microbe +, host - 5. Infection: growth within host 6. Disease: injury to host |
|
|
Where are most normal flora found in the body and how much of the body does that surface comprise?
|
1. Skin: 2m2
2. Mucous membrane: 400m2 |
|
|
What are the three importances of normal flora in the body?
|
1. Physiologically important commensal organisms
2. remove or out-compete microbes that become harmful 3. keep harmful microbes out |
|
|
What are mucous membranes and where are they found?
|
Single layer epithelial cells in direct contact with external environment; covered by protective mucous layer; major site of infection; found in areas with direct contact to external environment
|
|
|
How do microbes interact with mucous membranes?
|
bind through ligand on microbe surface to receptors on epithelial cells
|
|
|
What is a biofilm and what is their significance?
|
microbial colony attached to a surface (often external like catheters)and encased in a polysaccharaide material; contains different kinds of microbes; causes 2/3 of human bacterial infections; provide protective environment to microbes shielding against immune system and antibiotics
|
|
|
Why does the mouth make a perfect microbial niche?
|
moist with tons of nutrients and a good pH; 10^6 microbes per 1mL saliva, mostly bacteria with some fungi; microbes can adhere to teeth fighting silivary flow
|
|
|
How do microbes colonize the mouth from birth?
|
sterile at birth, acquire aerobes, teeth growth, acquire anaerobes; form a pellicle, a film of salivary glycoproteins, on tooth surface; streptococci are first to colonize, followed by fusobacteria, then actinomyces, forming biofilm on tooth surface (dental plaque)
|
|
|
Discuss dental caries
|
1. Etiological agent: stept mutans et al
2. Virulence factor: sugar polymer dextran and pili allow biofilm formation on tooth 3. Susceptibility: high sugar diet, sugar broken down by s. mutans into fructose and glucose for food for microbes 4. Prevention: brush and floss, floridated toothpaste and water |
|
|
Discuss normal flora of the GI tract and the effect of oral antibiotics on them
|
Most sterile towards the upper tract; bacteriodes exist in large intestine; composition changes during early development; oral antibiotics kill all normal flora allowing resistant species to overgrow (opportunistic pathogens), normal flors regrow once AB stop
|
|
|
What contributions do intestinal micorbes provide?
|
Vitamin synthesis, gas production, odor production, organic acid production, glycosidase reactions, and steroid metabolism; probiotics are said to displace harmful microbes
|
|
|
Discuss normal flora of the skin and how their number and type are affected
|
susceptible to change, mostly gram + bacteria and fungi (propionibacterium causes acne), most having to do with sweat glands; type and # affected by age, weather and personal hygiene
|
|
|
What are the main normal flora of the respiratory tract?
|
Staphylococcus, streptococcus, candida; lower tract usually devoid because of constant clearing by antibodies and ciliary action
|
|
|
Discuss normal flora of UG tract and how they change
|
upper regions normally sterile, urethra have facultative gram - (e. coli adn proteus mirabilis); lactobacilius exist in the female; typpes in vagina change with age/development
|
|
|
What is a pathogen and what are the two different kinds?
|
an organism that causes disease;
1. primary: affects health host 2. opportunistic: affects compromised host |
|
|
What is the difference between pathogenicity and virulence?
|
ability to cause disease versus the degree at which it diseases
|
|
|
What are virulence factors?
|
traits connected with pathogenicity, often carries on plasmids or regions of chromosome called pathogenicity islands; pathogens usually contain multiple VFs
|
|
|
What are the major problems with Koch's postulates?
|
assumes virulence is independednt of host, not all organisms can be cultured, some are not virulent alone (bioflims), cultivation can lead to loss of virulence, cannot test in humans
|
|
|
Explain portals of entry
|
pathogens must gain access to the host to cause disease, either through natural opening in the body or parenteral means like needles or surgery
|
|
|
Discuss adherence factors (adhesins) as virulence factors
|
ligands that bind to host cell receptors and can determine specificity of infection for pathogen (certain pathogens affect certain cells); glycocalyx, capsule, slime layer bind to surfaces, adherence proteins bind to receptors (M and Opa protein), lipoteichoic acid binds to receptors, fimbriae, pili bind to surfaces
|
|
|
Discuss extracellular enzymes as virulence factors
|
secreted by pathogen to dissolve structural chemicals of host cells to maintain infection, invade and spread, and avoid host defenses; hyaluronidase (degrades hyaluronic acid in extracellular matrix); collagenase (degrades collagen); coagulase forms blood clots for protection, kinases digest clots and release microbes (occurs near or in blood vessels)
|
|
|
Discuss toxins as virulence factors
|
chemicals or proteins produced by pathogen to harm tissue or trigger host immune responses that cause damage to hose
|
|
|
Disuss exotoxins as virulence factors
|
proteins released by growing pathogen that cause damage in distal areas of host (cytotoxin, neurotoxin, enterotoxin); can be cytolytic by putting pores in cell membrane, or A-B toxins, two subunits, A is enzyme, B is adherent, act on intracellular targets
-Botulinium: blocks release of acetocholine, preventing muscle contraction causing flaccid paralysis -Tetanus: blocks release of contractile inhibitors causing rigi paralysis and respiratory failure (tetanus vaccine and antitoxin both inhibit tetanus toxin) -Enterotoxin: act on small intestine by causing massive water secretion into lumen; cholera is A-B toxin (1A, 5B), A activates adenylate cyclase which makes cAMP, which stimulates secretion of Na and Cl leadig to water loss in cells |
|
|
Discuss endotoxins as virulence factors
|
lipid A portion of LPS on Gram - is released into circulation when bacteria lyses, activates complement which leads to inflammation, high [] of cytokines activates immune system and leads to septic shock (antitoxins inhibit action, toxoids inactivate by heat or chemical treatment and are used as vaccines)
|
|
|
What are superantigens and what are two examples?
|
toxins that over-stimulate immune system leading to cell damage and toxic shock; staph aureus is toxic shock syndrome toxin and causes fever and TSS; strept pyogenic exotoxin causes TSS like symptoms and fever
|
|
|
Discuss antiphagocytic factors as virulence factors
|
used to elude macrophages; two ways:
- bacterial and fungal capsules: made of polysaccharides common in the body so not seen as foreign, slippery making engulfment difficult -antiphagocytic chemicals: some prevent phagolysosome fusion, some resist phagocytosis, some make leukocidins that destroy phagoctyic WBC |
|
|
What are T cells, where are they produced, and how do they work?
|
they are a kind of lymphocyte that are produced in red bone marrow, mature in the thymus, and circulate in the blood and lymph to the lymph nodes, spleen, and Peyer's patches; they are a cell-mediated immune response and do not secrete antibodies, the act directly on endogenous invaders, cells that have intracellular pathogens, abdormal host cells with abdornal surface proteins
|
|
|
What are the three types of T cells?
|
1.cytotoxic: contain hundreds of T cell receptors, have CD8 glycoprotein on cell surface, directly kill virus/pathogen-infected cells and abdormal cells
2. helper type 1: CD4 glycoprotein, assist Tc, express cytokine receptor CCR, secrete cytokines that determine which immune response to activate 3. helper type 2: CD4 glycoprotein, activate B cells to make and secrete ABs, have cytokine receptors CCR3 and CCR4, secrete cytokines that determine which immune response to activate |
|
|
What are cytokines and which types are found in the immune system?
|
-soluble regulatory polypeptides that act as intercellular signals to leukocytes when released in immune system
-interleukins: signal to leukocytes (27 found) -interferons: antiviral proteins that may act as cytokines -GF: stimulate stem cells to divide maintaining supply of leukocytes -tumore necrosis factors: secreted by macrophages and T cells to kill tumor cells and regulate immune responses and inflammation -chemokines: signal leukocytes to inflammation or infection sites and stimulate other leukocytes |
|
|
What is the MHC?
|
major histocompatibility complex: anitgens of glycoproteins found in membranes of most cells; first IDed in graft patients, important in determining the compatibility of tissues in successful grafting; function in presenting antigenic determinants to T cells; antigens bind in antigen-binding groove of MHC molecules; two classes:
-class I: found on all cell membranes but RBC -class II: only found on B cells and antigen-presenting cells like macrophages, leukocytes, and monocytes |
