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67 Cards in this Set
- Front
- Back
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NF
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Typical adults contain 10^13 self cells and about 10 times as many bacteria Generally on skin and mucous mb. Not in deep tissue |
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NF
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Wide variety of conditions and thus a wide variety of NF. Host species Host site Host Sub Site -Different organisms in different parts of the body |
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Acquisition of NF
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Rapid growth of Lactobacilli in vagina just before birth -first NF for infant Other NF comes from personal contact, breathing, eating |
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Function of the NF
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Nutritional support GI tract development Stimulation of host defense Direct defense against microbial pathogens |
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Role of NF in nutrition and GI anatomy
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Degrade food and utilize components -Derive up to 2% of our energy from this Vitamin production (K and B) -NF organisms produce these vitamins |
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Germ-Free animals
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Born and raised in a sterile environment Require vitamin supplements Suffer from malabsorption Lack Villi for absorption Smaller lymph nodes Fewer lymphocytes and phagocytes Lower Ab levels |
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Disturbances to NF
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Diarrhea Emotional stress Changes in diet Illness Ab therapy Every medication may affect the patients NF |
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NF defense against Infectious Disease
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Bacterial interference or antagonism NF colonization by pathogens -competition for nutrients -specialized adherence factors -production of inhibitory substances Disturbance of NF increases susceptibility to ID |
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NF of the Skin
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Skin is normally impermeable and is constantly being re-inoculated Dry, lower fluctuation of temperatures pH 4-6, sweat flushes, high salt concentration Stapylococcus epidermidis |
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NF of the respiratory tract
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Healthy lungs should be sterile Primary Carriage site of Staphylococcus aureus Transient carrier site for potential pathogens: -streptococcus pneumoniae -Neisseria meningitidis -Haemophilus influenzae -ear and sinus infections pneumonia, meningitis |
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NF of the Mouth
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widest variety of micro-environments in the body -Hard to soft surfaces -aerobic and anaerobic -mechanical action of chewing, drinking -enzymatic and chemical action of saliva -acts like continuous culture system |
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NF of the mouth
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NF changes during lifetime- when adult teeth come in One of 3 sites where natural flora cause disease in their natural site in immunocompetent hosts -streptococcus mutans - tooth decay -anaerobes - periodontal disease |
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NF of the GI tract
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Number varies greatly with this site Stomach have lowest number of organisms: -low pH -Second site where NF causes disease in natural site - heliobacter pylori (ulcers) Upper intestines have moderate number: -Bile salt concentrations are high -Digestive enzymes concentration is high |
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NF of the GI tract
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Colon has the largest population in all of body -10^10 bacteria per gram of feces As you descend down the GI tract: -pH increases -Digestive enzymes decrease -becomes more anaerobic -Colon is primarily anaerobes, 99% |
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NF of female genitourinary tract
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Vaginal Flora influenced by pH -changes at puberty and menopause -changes due to hormonal influence NF is sparse before puberty and after menopause -pH is slightly alkaline -NF derived from skin, colon Lactobacilli help keep organisms out during child bearing years |
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Vaginal acidity mechanism
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Estrogen>glycogen>lactic acid |
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Three types of Infectious diseases
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Non-communicable Communicable Nosocomial Infections |
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Non-communicable diseases caused by normal flora organisms
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Candida yeast infections E Coli Urinary Tract infections Heart infection with mouth bacteria after invasive dental work, caused by own NF |
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Non-communicable diseases |
Food Poisoning: -Stapyhlococcal food poisoning -botulism is adults Legionnaire's disease from HVAC Environmental Sources: -Fungal spores (valley fever) -Tetanus from bacterial endospores from soil |
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Vertical spread of communicable diseases
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Mother to child -transplacental during birth -breast milk -rubella, AIDS, herpes |
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Horizontal spread of communicable disease |
Saliva skin to skin fomite transmitted fecal-oral vector transmitted zoonoses veneral |
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Direct transmission of communicable disease
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move without help from one person to another usually requires close contact Skin to skin- papillomavirus, MRSA (athletes) Blood-borne- Hep B&C, AIDS -require inoculation of blood, blood products |
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Salivary/respiratory spread of communicable |
can be very direct or somewhat indirect with respiratory droplets usually pathogens that infect respiratory tract -mononucleosis -common cold -influenza virus -measles -chicken pox |
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Fecal-Oral spread of communicable infections |
Direct or indirect -usually intestinal pathogens -salmonella, shigella, E Coli, campylobacter Contaminated water Contaminated food |
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Indirect transmission of communicable disease
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Requires an intermediary Fomites- inanimate objects that spread disease -cold virus and influenza virus -Same for diarrheal diseases (norovirus, shigella) -Door knobs, toys, gym, keyboard, shopping cart |
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Biological vectors
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Indirect spread through arthropods -malaria, lyme disease, yellow fever, rocky mountain, spotted fever, plague Mechanical: passive transport on feet of arthropods infected human(animal)>bite of vector>human |
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Animal infections(zoonoses) and reservoirs
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diseases transmitted from animals to humans direct contact- rabies, anthrax, pasteurella indirect contact- lyme disesase, RM spotted fever Vertebrate animal>vector |
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Venereal Disease
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Spread through sexual contact -HepB, HIV, HPV -Neisseria gonorrhoeae -Syphilis -Chlamydia |
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Sporadic
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Infection that is only observed occasionally
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Endemic
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Infection that is present at low, but constant level |
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Epidemic
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Infection thats level of infection is higher than usual in a population |
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Pandemic
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Infection that is widespread (sometimes worldwide), infection with high attack rate
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Primary Infection
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Infection that causes the initial infection
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Secondary Infection
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New infection occurring due to body weakened by primary infection Spread of primary infection to another body site -secondary pneumonia from skin infection |
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Subclinical
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Person is infected without any visible signs of infection, but can still transmit -Typhoid Mary |
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Local Infection
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Contained to a particular area -abscesses, boils, pneumonia, urinary tract |
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Systematic infection
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enters blood stream and spreads to other body regions -secondary spread of urinary tract infection to blood and lungs |
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Septicemia
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Pathogens multiplying in blood -Bacteremia specific to bacterial infection in blood -Viremia specific to viruses infecting blood |
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Toxemia
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Toxins in the bloodstream
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Nosocomial Infections (hospital acquired)
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Not present on admission, acquired during hospitalization (in 5-15% of patients) Transmitted to patients by: -Health-care professionals -contaminated equipment -spread of NF High mortality rate due to high resistance -not a threat to normal, healthy people |
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Pathogenicity Terms
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Pathogen: microbe that causes infection Pathogenicity: Potential to cause disease Primary Pathogen: Disease in strong/healthy Opportunistic P'n: Disease in compromised host -old age and infants -genetic and acquired immunodifficiency -breach of protective barriers |
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Evolution of pathogenicity
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Doesn't make sense for a pathogen to kill host Mutations are random and undirected Pathogens best adapted and selected to reproduce Many pathogens lose virulence over time and become less deadly -energy costly to replicate virulence dna if it is not being used |
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Factors Influencing Virulence
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Ability to colonize host -attach to tissues, survive host defenses Ability to cause damage to host -toxins, stimulation of host defenses to cause damage Inoculum: 1 to 10^9 depending on pathogen and host. |
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Three possible outcomes of microbial invasion
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Organism removed by host defense Organism colonizes without overt disease -persistence of organism in or on host -subclinical infection Organism multiplies causing tissue damage -clinical infectious disease -steps of infectious disease |
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Entry of microbes (Step 1 of infection) |
Mucous membrane is the easiest route Hair follicles or sweat glands can be portals |
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Adherence of Microbes (Step 2 of infection)
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Attachment to host cells Helps pathogen resist removal mechanisms Determines site of infection -Surface molecules on pathogen, called adhesins or ligands, bind specifically to complementary surface receptors on cells of certain host tissues |
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Surviving host defenses
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Mucosal surface defenses Invasion of host cells Evading specific immune defenses -phagocytes -antibody -complement Iron Limations |
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Evading Mucous membrane mechanisms
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Immobilization or destruction of host cilia -production of toxins that destroy cells -toxins can stop the cilia from beating Production of IgA Protease: less foreign looking -IgA traps organism in mucus for removal -Ag-binding portion binds "bugs" -Fc portion binds to mucus. IgA protease removes the Fc portion |
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Invasins
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Specialized adhesions that induce "forced phagocytosis" into cells that can't kill them |
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Advantages of host-cell invasion
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Provides nutrient rich habitat Devoid of competing NF organisms Protection from immune defense |
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Trojan Horse
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Some bacteria want to be ingested by professional phagocytes and block mechanisms that would kill them once inside. Phagocytes can move around body and carry pathogen
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Defense against Phagocytes
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Kill phagocytes by producing leucocidin toxins Prevention of phagocytosis with capsules -capsules and leukocytes are both highly negatively charged |
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Survival inside phagocytes
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Block fusion of phagolysosome Block pH drops Produce catalase and superoxide dysmutase |
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Defense against antibodies
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Antigenic Phase Variation -change non-essential parts of targeted antigens -Ab no longer recognize them -immune system has to start at step 1 IgA Proteases Release soluble Ags to bind to Abs away from the cell, a capsule |
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Defense against complement
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Capsule can mask or cover complement-activating surface components Coating with circulating IgA -Prevents binding of IgM or IgG Inactivation of complement components -halts complement activation -prevents actions of complement |
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Production of Tissue damage
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May be due to direct destruction of host tissue -Exotoxins: Generally secreted and enzymatic -Endotoxins: Part of Gram(-) mb May be due to host's immune response |
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Exotoxins
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Proteins produced inside pathogenic bacteria as part of their growth and metabolism Most commonly Gram(+), but can be Gram(-) Secreted into the surrounding medium Used to obtain host intracellular nutrients and help organism spread through tissues Disrupt normal cell f'n and destroy host tissues Good vaccination candidates by Th response and toxoids Potent in minute doses |
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Endotoxins (lipid A) |
Lipid portions of lipopolysaccharides as part of the outer mb of the cell wall of Gram(-) bacteria Liberated when the bacteria die and the cell wall breaks apart Toxicity due to immune response of host |
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Major actions of Exotoxins
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Disrupt cell f'n by enzymatic activity Down regulate cell activity (protein synthesis) Upregulate activity out of control (increased cAMP) -can lose up to 40 pounds in a day by water loss Membrane disrupting toxins -Cells lyse or lose functional ability Leukocidins kill WBCs, hemolysins lyse RBCs |
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Major actions of Exotoxins |
Break down tissues and help bacteria spread -Hyalurodase: Breaks down hyaluronic acid, which cements cells together -Collagenase: Digest fiber of connective tissue -DNAse: Digest extracellular debris Superantigens indiscriminately bind Th cells to APCs -stimulate excessive cytokine production |
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Response to low endotoxin concentrations |
Produces beneficial alarm reaction and fever due to release of IL-1 and TNFalpha Complement activation- inflammation Lymphocyte activation- enhances Ab synthesis |
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Response to high endotoxin concentrations
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Endotoxic shock - may be lethal Hypotenstion Clotting factors activated - clots formed Causes multi-organ system failure |
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Antibiotic Dates |
First Ab (Salvarasan) discovered in 1908 Ab era - 1940-1990 |
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Post-Ab Era
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Pan-resistant bacteria are increasing Pipeline of new drugs is disappearing Resistance to new drugs is rapid |
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Avoidance of the Post-Ab Era
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Slow the evolution of resistance Appropriate use of Ab Drug combinations Attack virulence factors |
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