Microbiology Exam 3

  1. parasitic relationship
    one organism benefits (parasite) one is harmed (host)
  2. Parasite
    an organism that lives at the expense of another host organism
  3. Ectoparasites
    • parasites that live on the surface 
    • ie- ticks and lice
  4. Endoparasites
    • parasites that live inside the host
    • ie hookworm
  5. Obligate parasites
    • must spend at least part of its life cycle in or on a host
    • ie malaria
  6. Facultative parasites
    • normally live on their own, but can obtain nutrients from a host 
    • ie fungi
  7. Permanent parasites
    • remain in a host
    • ie tapeworm
  8. Temporary parasites
    • feed on host and then vacate
    • ie mosquito
  9. Accidental parasites
    • feed on organisms that are not their normal host
    • ie- ticks will go for anything, not just one specific host
  10. Hyperparasitism
    • a parasite that is infected by its own parasite
    • ie- mosquitoes that carry malaria
  11. Vectors and types
    • things that transmit parasitic diseases
    • 2 types: biological vector and mechanical vector
  12. Biological vector
    • a vector that carries a parasite during a key part of the parasites life cycle
    • ie mosquito carrying malaria
  13. Mechanical Vector
    • A vector that transmits a parasite from one place to another but not during any particular part of the parasites life cycle
    • i.e. flies that spread parasitic eggs
    • mechanical vectors are often accidental, such as with the flies
  14. Types of hosts
    • definitive hosts
    • intermediate hosts
    • reservoir hosts
  15. Definitive hosts
    provide a place for the parasite to reproduce
  16. Intermediate Hosts
    • provide a "home" for the parasite during non reproductive phases of the life cycle
    • many parasites have intermediate hosts that will transfer them to another host
    • ie- snail
  17. Reservoir hosts
    • infected organisms that provide parasites that infect other organisms
    • ie- deer, domestic animals
    • ie- your dog gets a tick and brings it into your house and it bites you
  18. How do parasites evade the host immune response?
    • 1. Form cysts- they can house themselves in cysts that provide an outer protective covering so hosts can't see/detect them
    • 2. Antigenic variation- Change their surface markers faster than the host immune system can recognize them and make antibodies
    • 3. Cause the host to make antibodies that are ineffective at recognizing them
    • 4. Get within host cells where they can "hide" from the immune system
  19. Why is there no vaccine for malaria?
    • bc malaria evades the host immune system by changing its surface markers faster than the host immunes system takes to recognize them and make antibodies
    • they change the antigens and act like chameleons and your immune system has to start over every time
    • this is called antigenic variation
  20. What are 2 special ways that parasites can divide?
    • 1. Schizogony
    • 2. Hermaphroditic
  21. Schizogony
    • "multiple fission"
    • one parasite makes many copies of itself producing many offspring
  22. Hermarphroditic division
    • parasite contains both male and female reproductive systems
    • ie- proglottid (long tube filled with eggs) in tapeworms
  23. Protists
    • mostly unicellular eukaryotic cells
    • many are autotrophs
  24. Types of protists
    • plant-like protists
    • fungus-like protists
    • animal-like protists (aka protozoans)
  25. Plant like protists
    • Diatoms: toothpaste, act as a desiccant
    • Euglenoids: free living and parasitic
    • Dinoflagellates: red tides (algal bloom), produce toxins- so don't swim in red water
  26. Fungus-like Protists
    • Water molds: mildew- can cause respiratory problems
    • Slime molds: feed on decaying matter
  27. Animal-Like Protists
    • are also called Protozoans
    • Trichonympha: lives in termite gut (symbiotic relationship- breaks down cellulose in wood)
    • Trypanosoma (African sleeping sickness), Leishmania (spread by sand fleas), Giardia and Trichomonas (STD parasite): all infect humans
    • Amoeba: cause various forms of amoebic dysentery
    • Plasmodium: causes malaria- high fever, chills, hallucinations
    • Toxoplasma: causes toxoplasmosis- can be found in rodents and small birds, outdoor cats can get it and then pregnant women can get it from cleaning their litter box- causes birth defects
    • Cryptosporidium: Found in water causes go problems, very contageous
  28. Describe the steps of the malaria life cycle
    • 1. an infected mosquito bites a person, injects saliva containing parasite, which goes into person's blood stream. it is a sporozoite at this stage
    • 2. Sporozoites travel through the blood stream and entire the liver into hepatocytes and undergo schizogony division to form mature schizonts, which rupture and release merozoites
    • 3. Merozoites re enter the blood stream and enters erythrocytes (RBCs). They are then called trophozoites
    • 4. Some merozoites can develop into gametocytes that won't rupture and then these are taken up by new mosquitoes that bite you
    • 5. Once in the mosquito, they are oocytes that develop into sporozoites that will migrate to a salivary gland and the process starts again
  29. Fungi (mycology)
    • unicellular (yeast) or multicellular heterotrophs
    • many are saprophytes
    • can be opportunistic- move in and cause an infection if there is space
  30. saprophytes
    get nutrients from decaying matter
  31. types of fungi
    • bread molds
    • sac fungi
    • club fungi
    • ringworm
  32. bread molds
    rarely cause human disease except for Rhizomes- an opportunistic infection (often occurs in uncontrolled diabetics)
  33. Sac fungi
    • penicillium species make antibiotics and cheeses (roquefort and camembert)
    • yeast ferment to produce bread, beers and wines
    • ie- candidia albicans causes yeast infection
    • ie- aspergillus causes respiratory infections (found in moldy bread)
  34. Club Fungi
    • Amanita: produces lethal toxins- rye plant- causes red rash
    • Claviceps: causes ergot (in rye plants)
    • Cryptococcus: the cause of opportunistic respiratory infections in the immunocompromised
  35. Ringworm
    • a fungus, not a worm
    • identified as a circle ring on the skin
  36. Helminths and types
    • Worms
    • 2 types: Bilaterally symmetrical worms and parasitic worms
  37. Parasitic worms
    • flukes
    • tapeworms
    • adult roundworms
    • larval roundworms
  38. flukes
    • tissue flukes 
    • blood flukes
  39. tissue flukes
    • lung: Paragonimus westermani (intermediate host is snail and crustaceans)
    • liver: Clonorchis sinensis (3rd most prevalent- snail and fish) and Fascia hepatica
  40. Blood flukes
    Schistosoma: second in prevalence after malaria
  41. Tapeworms
    • can be found in beef, pork, dogs, fish
    • cook meat well done to avoid
  42. Adult roundworms
    • Trichinella spiralis: causes trichinosis (found in pork)
    • Enterobius vermicularis: pinworms; carried in humans, not dogs/cats. 
    • Ancylostoma duodenale: hookworms
    • Ascarids: very large worms, migrate throughout the body
    • Dracunculus: Guinea Worm- found in drinking water, can be as thick as spaghetti
  43. Larval Roundworms
    • require a mosquito host
    • Wucheria bancrofti (elephantiasis)- migrate to lymphatic system and clog it causing swelling
  44. Schistosoma
    • causes schistosomiasis
    • live in water
    • shape shifting parasite
    • changes form as it grows making it hard to treat
    • uses snail as an intermediate host
  45. Arthropods (types)
    • Arachnids
    • Insects
    • Crustaceans
  46. Arachnids
    • have 2 body regions
    • ticks carry encephalitis and borrelia burgdoferis, the causative agent of Lyme Disease, rickettsias that cause rocky mountain spotted fever and the bacterium that causes tularemia
  47. Insects
    • have 3 body regions
    • body lice can carry rickettsia too
    • fleas can carry bubonic plague
    • common house flies carry pathogens from feces to human food
    • tsetse flies carry African Sleeping sickness
    • Mosquitoes carry western equine encephalitis, malaria, west nile virus, dengue fever, yellow fever
    • reduviid bugs carry chaga's disease
  48. what type of mosquito carries malaria
  49. Crustaceans
    • can be intermediate hosts- can be hosts for pathogens transmitted to humans through the food chain
    • crayfish, crabs
  50. Pathogen
    any agent that causes disease in a host
  51. Host
    any organism that harbors another organism
  52. symbiosis and types
    • association between 2 or more species
    • types: mutualism (both organisms benefit), commensalism (one benefits, other unaffected), parasitism (one benefits, other is harmed)
  53. contamination
    microorganisms are present
  54. infection
    • multiplication of a parasitic organism in or on a host
    • mostly bacterial
  55. Infestation
    presence of larger parasites (worms and insects)
  56. Disease
    any disturbance of health where host cannot function normally
  57. Pathogenecity
    • capacity to cause disease
    • can depend on how many organisms infect the host
  58. Virulence
    • intensity of the disease produced by a pathogen
    • can vary among types of organisms
    • can very even within one species of pathogen depending on i.e. strains
    • can be increased during animal passage
    • can be decreased by attenuation (weakening) and/or transposal of virulence (pathogen is passed to new species and becomes adapted to new species and is no longer virulent to the original species)
  59. Normal Microflora
    • Resident microflora are always present in the body
    • they are present in skin, conjunctiva, mouth, nose, throat, intestine, urogenital tract, mucous membrane
    • not present in blood nervous system or stomach (except h.pylori in stomach)
  60. Transient microflora
    • only there for a certain period of time under certain conditions
    • ie skin when especially warm or moist
  61. Opportunistic infection
    • Microorganisms that do not usually cause disease but can take advantage of certain conditions
    • immunocompromised due to malnutrition, age (very old or young), radiation, immunosuppression or AIDs are at risk
    • the microbe is present at an unusual site on the host (e.coli usually found in colon can cause disease if in wound or urinary tract)
    • bacteria fills niche left open due to disturbance of normal microflora (ie abx)
  62. Classification of disease
    • inherited
    • congenital
    • degenerative
    • nutritional deficiency
    • endocrine
    • mental
    • immunological
    • neoplastic
    • iatrogenic
    • idopathic
  63. Inherited disease
    defects in DNA passed to offspring causing disease
  64. Congential Disease
    structural or functional defects present at birth
  65. Degenerative disease
    • develop as aging occurs
    • ie emphysema
  66. Nutritional Deficiency Disease
    • make patient more suseptable to other disesaes
    • ie anemia
  67. Endocrine Disease
    • hormonal disturbance
    • ie diabetes
  68. mental disease
    ie creutzfeld-Jakob
  69. Immunological disease
    • lupus, AIDS, allergies
    • immune system not functioning properly
  70. Neoplastic disease
    • abnormal cell growth
    • can be induced by viruses- ie cervical cancer caused by HPV
  71. Iatrogenic Disease
    • caused by medical treatments
    • aka nosocomial infections
    • these are diseases acquired at a hospital or medical setting
    • ie MRSA
  72. Idiopathic disease
    have an unknown cause
  73. How are diseases spread?
    • Communicable infectious diseases: spread from one host to another, ie children harbor many
    • Contageous diseases: are highly communicable (rubella, flu)
    • Noncommunicable infectious diseases: not spread from one host to another
  74. How could a noncommunicable infectious disease be caused?
    • disruptions in an individuals microflora- ie UTI from e.coli moving from colon to urinary tract
    • Ingestion of microbial toxins- food toxicity
    • Infections from the environment (ie cellulitis from insect bite)
  75. How do bacteria cause disease?
    many have virulence factors such as adhesion pili (have sticky ends that allow sticking to a host cell), enzymes that break down host defences such as WBCs, toxins
  76. Virulence factors
    structural or physiological factors that help the microbe cause disease
  77. How do bacteria get inside the host?
    Penetration of skin (through a cut), mucous membranes, sexual transmission, ingestion, inhalation, fomites
  78. fomite
    • an inanimate object that can carry pathogenic organisms
    • ie door handle, remotes, cellphone etc
  79. Adherence
    • binding of bacteria to host cell 
    • this is the essential first step of infection
    • bacteria have proteins called adhesins
  80. Adhesins
    • bacterial proteins found on attachment pilli and capsules
    • adhesins are specific for particular host membrane proteins
    • they block phagocytes (pacman immune cell) from engulfing them. therefore some adhesins can be virulence factors
  81. Colonization
    • growth of microbes on surface of epithelial cells (skin, mucous membrane, etc)
    • most microbes are invasive (can get inside host tissues)
  82. Examples of how diff bacteria colonize
    • streptococci make hyaluronidase "spreading factor" that digests hyaluronic acid, a host "glue" that helps hold tissues together. the glue is dissoved and microbe can get deeper to cause more issues and evade our immune system
    • staph aureas use coagulase to clot blood. this keeps immune cells from reaching the site of infection
    • other bacteria have streptokinase, an enzyme that dissolves clots (used in heart attacks). so now it can break free from the clot to go invade other cells
    • some bacteria enter cells (chlamydia, rickettsia) and use the cell as a safe haven to grow and divide (mycobacteria)
  83. is invasiveness the same for all microbes
    no, it varies between microbes and can differ depending on the type of host cell invaded
  84. toxin
    something that is poisonous to other organisms
  85. Types of bacterial toxins
    • exotoxins: strong soluble toxins secreted into host tissues
    • endotoxins: weak toxin unless in large quantities, part of the bacterial cell wall, released when bacteria divide or die
  86. exotoxin info
    • mostly gram + but some gram - bacteria release them
    • made of polypeptides
    • some are enzymes- ie hemolysins are exotoxins that break open RBCs
    • ie luekocydins/leukostatins
  87. leukocidins
    • destroy WBCs
    • first neutrophils (first ones on scene) then macrophages
  88. leukostatins
    stop white blood cells from engulfing bacteria
  89. Endotoxin info
    • gram negative bacteria release them 
    • treating host with antibiotics that kill these endotoxin releasing bacteria can actually lead to endotoxic shock (severe fever and possible fatal low blood pressure, tissue damage)
    • made of LPS
  90. hemolysis
    the breakdown of the membrane of the red blood cell by hemolysin
  91. Types of hemolysis
    • Alpha
    • Beta
    • Gamma
  92. Alpha hemolysis
    • partial breakdown of hemaglobin
    • leaves a greenish hue which can be seen on blood agar plate
    • characteristic of streptococcus pneumonia
  93. Beta Hemolysis
    • complete breakdown of hemoglobin in vicinity of bacteria 
    • characteristic of s. pyogenes
    • plate will be clear, maybe yellow
  94. Gama hemolysis
    • lack of hemolysis
    • blood agar plate will stay red
    • chracteristic of e. faecalis
  95. Intoxication vs infection
    • some diseases are caused by ingestion of bacterial toxin, this is called intoxication not infection
    • ie- botulism- hits within hours of ingestion, too soon for colonization with clostridium botulinum, illness due to toxin- dont buy bulging or dented cans for this reason
  96. More bacterial toxins
    • Neurotoxins
    • Enterotoxins
  97. Neurotoxins
    • act on nervous system tissues
    • botulism (used for cosmetics) releaves spasms in dystonia, tetanus toxins
    • botox may need to be diluted bc of the toxins
  98. Enterotoxins
    • act on digestive tract
    • can be antigens that activate immune cells and gives us an immune response
    • toxoids
  99. toxoids
    • toxins that have been altered so that they do not act as toxins, but still act as antigens
    • can be used as vaccines bc they will still give an immune response
  100. How do viruses cause disease
    • must attach and get inside cells in order to multiply
    • viruses cause changes in the host cell called the cytopathic effect (CPE)- make the host cells look wonky
  101. how can CPE happen
    • viruses can integrate into host genome and produce viral proteins that show up on the surface of the host cell eventually. the cell will put the proteins on the surface to try to signal to the immune system somethings wrong
    • or viruses can kill host cell outright by stopping normal cell protien synthesis or by bursting lysosomes in the cell
  102. inclusion bodies
    • dense areas of the cell that contain viral nucleic acids, proteins or clumps of new virus particles
    • can be seen in infected host cells
  103. types of viral infections
    • productive
    • abortive
    • latent
    • persistant
  104. productive viral infections
    virus invades cell and immediately multiplies
  105. abortive viral infections
    • virus invades cell but cannot make the proteins necessary to multiply
    • therefore nothing happens
  106. latent viral infections
    • virus is not active after initial infection
    • initial infection then retreats and is dormant
    • herpes virus retreats into nervous system and can be reactivated at a later time in the host
  107. Persistant viral infections
    • virus invades cell and multiplies continuously for months or years
    • ie hepatitis b virus
  108. How do eukaryotes cause disease?
    fungi, protozoa and helminths are eukaryotes that cause disease
  109. fungi causing disease
    • produce reproductive spores that can be inhaled, ingested or enter host through damaged skin
    • produce enzymes that attack host cells
    • can release toxins or cause allergic reactions ie- aflotoxins can be ingested in peanut butter made from moldy peanuts, people may falsley think they have a peanut allergy
  110. Protazoa causing disease
    • plasmodium causes malaria- reproduces in RBCs
    • Giardia causes giardiasis- infecte intestinal tissues
  111. Helminths causing disease
    • worms are extracellular parasites
    • can release toxic wastes and antigens that can cause allergy in host for different immune reactions
  112. Sign
    • characteristic of a disease that can be seen by observing a patient
    • swelling, redness, rash, cough, pus, fever, vomiting, etc
  113. Symptom
    • characteristic of disease that can only be felt by the patient
    • pain, shortness of breath, nausea, sore throat, general malaise
  114. Syndrome
    • combination of signs and symptoms that occur together and are characteristic of a certain disease- helps clinicians diagnose
    • fever, malaise, swollen lymph nodes, leukocytosis (increased WBC count)
    • some diseases have classic signs and symptoms while other can present themselves differently in different people
  115. Types of infectious diseases
    • acute
    • subacute
    • chronic
    • latent
    • local
    • focal
    • systemic
    • primary
    • secondary
    • superinfection
    • mixed
    • subclinical
  116. acute infection
    • develops rapidly
    • over quickly
  117. subacute  infection
    • between accute and chronic
    • ie gum disease
  118. chronic infection
    develops slowly, hangs around
  119. latent infection
    periods of inactivity (herpes, HIV, malaria)
  120. local infection
    • confined to a specific area of the body
    • ie cellulitis in the ankle
  121. focal infection
    infection in a specific area but antigens and toxins can spread
  122. systemic infection
    • affects most of the body
    • usually due to microbe entering blood stream and spreading throughout host
    • septicemia, bacteriemia, viremia, toxemia, sapremia
  123. primary infection
    • initial infection of a healthy host
    • ie flu
  124. secondary infection
    • follows a primary infection, usually in a host that is immunocompromised
    • ie pneumonia
  125. Superinfection
    • secondary infection that results from the loss of normal microflora
    • cdiff
  126. mixed infection
    • caused by several species of organisms
    • ie tooth cavities
  127. subclinical infection
    • doesnt produce all signs and symptoms
    • host may not know of infection and act as carrier
    • typhoid mary
  128. Stages of infection
    • 1.incubation period
    • 2.prodromal period
    • 3.invasive phase
    • 4.decline phase
    • 5.convalescence period
  129. incubation period
    • time between the person becomes infected and teh appearance of signs and symptoms
    • can last hours to years depending on infection
    • chicken pox 14-21 day inc. period
  130. Prodromal period
    • onset of signs and symptoms, often vague at first (malaise, headache)
    • host is contageous, but often still going out infecting everyone bc they dont feel awful
    • can last varying amounts of time
  131. Invasive phase
    • typical signs and symptoms appear
    • the height of symptoms is called the acme
    • pathogens invade and damage tissue
    • can be fulminating (sudden and sever) or chronic (slower)
    • fever is caused by pyrogen (can be our own or the bacterias) acting on host hypothalamus- hyp resets and changes our temp to kill heat sensitive bacteria
  132. decline phase
    symptoms subside due to treatment or successful host immune response
  133. convalescence period
    • healing, tissues are repaired
    • can last a while
    • flu- feeling better soon but takes a while to feel 100% better
  134. Epidemiology
    The study of factors and mechanisms involved in the frequency and spread of diseases and other health-related problems within populations of humans, other animals, or plants
  135. Why study epidemiology?
    • To help understand the cause of a disease
    • to plan and evaluate intervention and prevention strategies more effectively
  136. What must epidemiologists be able to do
    describe and analyze the distribution and the determinants in person, place and time
  137. Distribution
    where does it happen
  138. Determinants in person, place and time
    • number of cases of the disease
    • what segmant of the population is affected
    • how long does the disease last in the population
  139. Three factors that interact to cause disease
    • agent: microbe/chemical
    • host: who
    • environment: where
  140. Etiology
    study of causes and origins of diseases- where they originate from
  141. Incidence
    number of new cases of a disease for a specified time period
  142. Prevalence
    total number of people infected in a population at any one time by a disease
  143. Morbidity rate
    number of individuals affected by a disease during a set period of time
  144. Mortality rate
    number of deaths of individuals due to a disease during a set period of time
  145. Is incidence or prevalence higher when a disease breaks out
    they begin at nearly the same but prevalence is higher than incidence since incidence is only new cases at a specific time
  146. Endemic
    • a disease that is constantly present in a specific population over a relatively short period of time
    • native to that area
  147. Epidemic
    when an endemic increases its morbidity and/or mortality rate suddenly causing a public health problem/concern
  148. pandemic
    epidemic spread world wide
  149. Sporadic Disease
    random and unpredictable manner involving isolated cases that pose no great threat to the population as a whole
  150. Ways that disease spreads
    • Common-source outbreak
    • Propagated endemic
  151. common-source outbreak
    • due to contact with a contaminated substance
    • many people become ill suddenly but outbreak can be controlled quickly once the contaminant is identified
    • ie 500 people eat salmonella contaminated chicken at a wedding. Many people sick, but controlled fast
  152. Propagated epidemic
    • arises from different person-to-person contact
    • number of cases rises more slowly than common source but can take longer to be controlled
    • has to travel from person to person and with incubation times this makes it take longer
  153. Portals of entry
    • mucous membranes (most important one)
    • ear
    • eye
    • nose
    • mouth
    • mammary glands
    • urethra
    • vagina
    • anus
    • placenta
    • broken skin
  154. Portals of exit and how
    • eyes: tears
    • ears: earwax
    • nose: secretions
    • mouth: saliva, sputum
    • broken skin: blood
    • skin: flakes
    • mammary glands: milk, secretions
    • vagina: secretions, blood
    • seminal vesicle: semen, lubricating secretions
    • urethra: urine
    • anus: feces
  155. Modes of transmission
    • Contact transmission
    • Vehicle transmission
    • Vector transmission
  156. Contact transmission
    • Direct contact: touching a person or animal, ie a bite
    • Indirect contact by fomites: touching an inanimate object with the disease, ie stepping on a nail
    • Droplets: disease transmitted by droplets from infected persons nose or mouth
  157. Direct contact diseases
    • rabies
    • rat bite fever
    • syphilis
    • gonnorhea
    • herpes
    • staph infections
    • cutaneous anthrax
    • genital warts
  158. Indirect contact by fomites diseases
    • tetanus (step on nail)
    • common cold
    • enterovirus
    • ringworm
  159. Droplet diseases
    • common cold
    • influenza
    • measles
    • Q fever
    • pneumonia
    • whooping cough
  160. Types of vehicle transmission
    • Waterborne
    • Airborne, including dust particles
    • foodbourne
  161. Waterborne diseases
    • cholera
    • shigellosis
    • leptospirosis
    • campylobacter infections
  162. Airborne diseases
    • chickenpox
    • tuberculosis
    • coccidiodoycosis
    • histoplasmosis
    • influenza
    • measles
  163. Foodborne diseases
    • intoxication with alfatoxins and botulinum toxin
    • paralytic shellfish poisoning
    • staph food poisoning
    • typhoid fever
    • salmonellosis
    • listeriosis
    • toxoplasmosis
    • tapeworms
    • hepatitis A
  164. Types of vector transmission
    • mechanical: on insect bodies, ie a fly carrying parasitic eggs on its leg lands on your sandwich
    • biological: vector has/carries the disease ie tick or flea
  165. mechanically transmitted vector disease
    • e.coli diarrhea
    • salmonellosis
    • trachoma
  166. types of biological vector diseases
    • malaria
    • plague
    • yellow fever
    • typhus fever
    • rocky mountain spotted fever
    • chagas disease
    • lyme disease
  167. Nosocomial infections- how common and why
    • contacted when someone is being treated at a medical center
    • acquired at a hospital or other medical facility
    • occur in 10% of patients admitted to US hospitals
    • often due to certain medical treatments- IV, urinary catheters
  168. What are the most common types of nosocomial disease
    • e.coli (UTI)
    • staphylococcus aureus
    • streptococcus
  169. What are the two types of nosocomial infections
    • Exogenous
    • Endogenous
  170. Exogenous nosocomial infections
    caused by organisms that enter patient from the environment, other patients, staff, visitors, insects, or fomites (ie a catheter is inserted that has pathogenic bacteria)
  171. Endogenous nosocomial infections
    • Caused by opportunistic infection by patients own microflora
    • due to immunocompromised host, reduction of microflora due to antibiotic treatment, or a mechanical device (such as a catheter introducing colon e coli into the urethra)
  172. What ways can you limit nosocomial infection
    • WULMP
    • Wash hands
    • Use gloves
    • Limit prophylactic antibiotic use
    • Maintain sterility
    • Prevent insect infestations
  173. Innate immune system
    • nonspecific host defenses
    • this part of our immune system responds in a generic way to any threat
    • the acquired immune system is specific
  174. Specific defenses
    • against a particular agent
    • requires lymphocytes (a specific type of white blood cell) to recognize antigens from a virus or bacterial cell
    • the lymphocytes will make antibodies specific for those antigens
  175. nonspecific defenses
    • act against ANY type of invading agent
    • the first line of defense against pathogens
    • AKA innate immunity (respond in a generic way)
  176. What are the nonspecific defenses?
    • 1. Physical barriers
    • 2. Chemical barriers
    • 3. Cellular Defenses
    • 4. Inflammation
    • 5. Fever
    • 6. Molecular defenses
  177. Physical barriers
    • skin and mucous membranes
    • mucous membranes are easiest way for microbes to get in bc they line the orfices to the outside world
  178. chemical barriers
    • antimicrobial activity in body fluids
    • enzymes in saliva and tears
    • defensins on our hands act as natural purell
    • stomach acid
  179. Cellular defenses
    phagocytes- brought to needed area by chemotaxis. find, bind, ingest and digest the microbe
  180. inflammation
    • a sign the immune system is working
    • longterm inflammation can cause damage to tissue
    • rubor, tumor, calor, dolor (redness, swelling, heat, pain)
  181. Fever
    • can kill microbes or inactivate toxins
    • fever with vaccinations yeild a better immune response
    • hypothalamus resets body temp to attack
  182. Molecular defenses
    interferons and complement
  183. Why do we have physical barriers
    • function to keep out infectious agents
    • also secrete chemicals
  184. how does your skin become vulnerable to infection
    • heat
    • cold
    • abraisions
    • insect and animal bites
    • burns
  185. Preventing infection from mucous membranes
    • cover organs that are exposed to the outside world
    • flushing of these membranes helps to keep them free of microbes- runny nose, coughing, sneezing, vomiting, diarrhea, urinating are ways of flushing
  186. When do we need our cellular defenses
    • when the skin or mucous membranes have been compromised by pathogens
    • when other defenses such as bleeding, blood clotting, constriction of blood vessels, cannot contain infection and pathogens reach the bloodstream
  187. Whats in your blood
    • plasma: fluid protien
    • formed elements: cells
  188. formed elements
    • all are derived from pluripotent stem cells in bone marrow
    • red blood cells: carry oxygen
    • platelets: are essential for blood clotting
    • granulocytes: show granules when stained, lobed nuclei (all are myeloid cells)
    • agranulocytes: do not show granules when stained, round nuclei
  189. granulocyte types
    • basophils: release histamine to signal inflammation
    • mast cells: release histamine in allergies
    • eosinophils: involved in allergies and helminth infections
    • neutrophils: guard skin and mucous membranes, report whats been found
  190. Agranulocyte types
    • Monocytes: myeloid cells, develop into macrophages in tissue
    • Lymphocytes: lymphoid cells; B cells and T cells involved in specific defenses
  191. Phagocytes
    • pacmen
    • circulate through the body and "eat" up or "engulf" other cells or foreign particles
    • two types: neutrophils and monocytes
  192. Neutrophils
    • the very first cells to encounter infectious agents at site of entry
    • cannot divide and live only 1-2 days
    • high numbers
    • seen in pus
  193. Monocytes
    • circulate in blood and can invade tissues
    • develop into macrophages
    • can reside in one tissue or wander through the blood stream
    • can live for months to years
    • play an important role in specific defenses as well (present antigens to T cells)
  194. How does phagocytosis happen
    • 1. find foreign agent (by chemotaxis)
    • 2. Bind to foreign agent
    • 3. Ingest foreign agent
    • 4. Digest foreign agent
  195. What is the signal that something is wrong?
    • 1. infectious agents AND infected tissues release chemical substances
    • 2. some granulocytes release histamine (mast cells and basophils)
    • 3. Phagogytes already at the site release cytokines
    • All of these combine to attaract the phagocytes by chemotaxis- find surface markers of bacteria, recognize and move towards it
  196. Cytokines
    • immune chemicals that work on one another
    • how immune cells talk to eachother
  197. Adherence
    in order to ingest a foreign agent, the phagocyte must first stick to it
  198. How can bacteria resist phagocytic adherence
    • some bacteria can resist adherence by having a thick antiphagocytic slime capsule
    • but your immune system can fight back
  199. How can the immune system fight back against the antiphagocytic slime capsule
    • by opsonizing- coating a bacterial cell with antibodies or complement
    • complement will bind to the phagocyte as well and the phagocyte will have receptors for the antibodies
  200. ingestion
    a quick process where the pseudopodia (temporary protrusions) of phagocytes move to surround the offending bacterial cell and fuse to form a phagosome
  201. Digestion and 2 ways
    • intracellular killing
    • 2 ways of digestion: Lysosomes and reactive oxygen
  202. Lysosomes
    • contain digestive enzymes that break down microbes 
    • fuses with phagosome to form phagolysosome (lysosome, phagocyte and bacteria particle fused)
  203. phagolysosome image
    Image Upload 1
  204. Reactive oxygen
    hydrogen peroxide, nitric oxide, superoxide ions, and hypochlorite ions damage cell microbial membranes
  205. 3 ways bacteria resist host digestion
    • 1. contain capsules that are not able to be digested: yersinia pestis
    • 2. Block phagolysosomal fusion (can grow and divide): mycobacterium tuberculosis, leishmania
    • 3. Release toxins that kill phagocytes: staph- leucocidin; strep- streptolysin
  206. leucocidin
    • destroys white blood cells
    • secreted by staphlyococcus
  207. streptolysin
    • stops white blood cells from engulfing bacteria
    • released by streptococcus
  208. MBP
    • Major basic protein 
    • released by eosinophils
    • punches holes in helminth body to break it up so it can be taken up by phagocytes
  209. Extracellular killing
    • phagocytes cannot engulf large infectous agents such as worms
    • Eosinophils therefore release MBP that punches holes in the helminth's body, allowing it to then be phagocytosed bc it is chopped up into smaller pieces that can be engulfed
    • NK cells can kill extracellularly too
  210. explain how natural killer cells can kill a suffering cell
    • If a cell is infected with a virus it puts the viral proteins on cell surface to show the immune system it is infected
    • nk cells recognize specific proteins on the surface of virus-infected cells and cancer cells and secrete perforin and granzyme to poke holes in the cell and initiate apoptosis
  211. How are cancer cells recognized by nk cells
    they have mutated receptors that are recognized as "weird" that NK cells will notice and act on
  212. 2 ways NK cells kill
    • perforin: blows holes in cell
    • granzyme: initiates apoptosis

    NKs secrete both of these proteins
  213. Functions of the lymphatic system
    • 1. collects excess fluid from spaces between cells (reduces swelling)
    • 2. Transports digested fats to the circulatory system
    • 3. Its the route of circulation for your immune cells
  214. explain how the lymphatic system is the route of circulation for immune cells
    • phagocytes gather in the lymph and help filter out bad stuff
    • lymphatic vessels allow flow of fluid (lymph) and cells through your lymph nodes
    • eventually drains into your blood stream via subclavian veins
  215. relationship between lymphatic system and circulatory system
    • lymphatic system parallels circulatory system 
    • runs through the same places
  216. What are the lymphatic organs
    • lymph nodes
    • thymus
    • spleen
    • peyer's patches
    • appendix
    • tonsils/adenoids
  217. Lymph nodes
    • lymph filters foreign agents through nodes throughout your body containing T cells, B cells and phagocytes
    • these can become inflammed when youre reacting to an infection
    • doctor will feel these for inflammation
  218. Thymus
    • t cells originate in the bone marrow but mature here
    • this is also where t cells undergo training
  219. Spleen
    • largest lymphatic organ (engulfs worn out blood cells)
    • both B and T cells migrate to the spleen as well as phagocytes
    • phagocytes present antigens to B and T cells
  220. Are phagocytes part of innate or acquired immune system?
    part of innate systme but helps with specific acquired system by presenting antigens
  221. Peyer's patches
    in small intestine
  222. Appendix
    • helps with immunity
    • previously thought to have no function
  223. Tonsils/Adenoids
    • usually the first parts of the lymphatic system to become inflamed
    • first things that a lot of germs run into when trying to enter our system- this is why many have them removed if they are getting too many infections
  224. Anatomy of a lymph node
    • There are more afferent (ways in) vessels than efferent (ways out) to trap fluid
    • bc you want to keep lymph in the node as long as possible to give phagocytes and WBCs time to survey and find anything that shouldnt be there
  225. What are the signs of inflammation?
    • the below are signs that your immune system is working, but if its too much or lasting too long you may need medical treatment
    • latin: rubor, tumor calor, dolor
    • english: redness, swelling, heat, pain
  226. Acute Inflammation
    a host defense
  227. Histamine
    a chemical that acts as a flare gun to say all hands on deck to cause inflammation
  228. Describe what happens during accute inflammation
    • histamine is released by basophils and mast cells in injured tissue
    • massive release of histamine  can cause anaphylactic shock (epinepherine causes constriction)
    • histamine causes vasodilation for increased blood flow causing heat
  229. Effects of histamine
    • increased vasodilation (causes increased blood flow to cause heat and redness)
    • increased permeability- fluid leaves blood (brings antibodies and nutrients) builds up around injured cells to cause edema- helps to wall off area to prevent infection from spreading
    • release of bradykinin and prostaglandins at site of injury- (cause blood vessels to dilate) results in pain
    • phagocytes leave blood stream and arrive at site of injury by diapedesis
  230. diapedesis
    • the squeezing out of phagocytes through leaks in blood vessels
    • blood vessels start to get leaky which allows this
  231. pus
    WBCs (usually neutrophils) killed in the line of duty plus dead microbes and other cellular debris
  232. 11 Steps of skin infection
    • 1. cut allows bacteria under skin
    • 2. damaged cells release histamine and bradykinn
    • 3. Capillaries become dilate bringing more blood to tissue
    • 4. capillaries increase permeability allowing fluids to accumulate
    • 5. blood clotting- scab forms
    • 6. Bacteria multiply in cut
    • 7. phagocytes enter tissue by diapediesis
    • 8. phagocytic cells find bacteria and tissue debris by chemotaxis and engulf them
    • 9. larger blood vessels dilate increasing more blood to tissue
    • 10. As dead cell and debris are removed, epithelial cells multiply and grow under scab
    • 11. scar tissue replaces cells that cant replace themselves
  233. When does inflammation become chronic?
    • when the host can't win the battle against infectious agents
    • when this happens it will form walls, called granulomas to block off the area to prevent spread of infection
  234. Granulomas and example
    • form to wall off the infection
    • many layers of cells
    • ie: tubercles characteristic of tuberculosis- cyst from parasites can build them- consist of necrotic center surrounded by immune cells and fibrous tissue
  235. What is a fever
    • oral temperature above 37.8C (100.5F)
    • induced when the hypothalamus is "reset" to a higher temperature to burn heat sensitive bacteria and to increase the speed of your immune system
  236. What causes a fever
    exotoxins and endotoxins of bacteria that act as pyrogens, which are substances that induce fever
  237. Endogenous pyrogens
    • IL-1- interleukin 1: an immune chemcial released by macrophages to communicate to other cells to raise the temp
    • released by macrophages
    • chemical released immune response
  238. Why do we get chills?
    bc fefer causes hypothalamus to turn up temp but your outer skin hasnt warmed up yet, so you feel cold so your muscles will move to warm up causing shivering
  239. Why would you want a fever?
    • 1. slows growth of pathogens- can affect heat sensitive pathogens
    • 2. Can inactivate microbial enzymes and toxins
    • 3. Increases rate of reactions of host immune system- increases metabolism to feed your immune system
    • 4. forces host torest
  240. Why do we not want a fever to get too high
    • it can denature your proteins as well as the microbes'
    • this can cause seizures and other problems
  241. Interferon
    • interferes with viral infections
    • naturally occuring immune molecules
    • 2 main types
  242. Types of interferon
    • type I: includes alpha and beta
    • type II: gamma
  243. Type I Interferon
    • secreted by our cells that have been infected by a virus
    • acts on neighboring cells, basically knocks on their door and tells them "im a goner but save yourself" causing them to make antiviral proteins
  244. antiviral proteins
    • produced by cells that have been warned by interferon I
    • blocks viral infection and stops virus from replicating
    • interfere with viral mRNA; aka attack at the transcriptional level
  245. Type II Interferon
    • secreted by uninfected lymphocytes and NK cells
    • like caffeine that activates and jacks up macrophages
    • can induce antiviral proteins
  246. Recombinant interferon (rIFN)
    • helps WBCs work better
    • boosts immune system
    • decreases metastaisis (spreading) of cancer
    • useful for viral infections you cant do anything about (ie genital warts, hep C)
  247. Downsides of therapeutic interferon
    • unstable, breaks down quickly
    • side effects
  248. side effects of therapeutic interferon
    • fatigue
    • nausea
    • headache
    • vomitting
    • nervous system disorders
    • fever
    • liver and kidney toxicity
  249. Complement system
    • made up of 20 proteins that circulate in the plasma and can do a variety of things
    • 13 proteins participate in complement action directly
    • assists immune system
  250. Functions of complement (5)
    • can attract phagocytes to the scene 
    • enhances phagocytosis by opsonization
    • can help poke holes in membranes of bacteria to kill it (called membrane attack complex)
    • can bind to surface of non infected cells to tell them to get ready to fight
    • regulate inflammation and other immune responses
  251. opsonization
    • process where complement helps phagocytes by marking the pathogen with a tag for ingestion- coat and flag surface 
    • makes it easier for phagocyte to recognize pathogen and bind
    • antibodies (opsonins) coat surface of pathogen
    • C1 binds to antibody
    • C3b binds to microbe and activates complement receptors on phagocytes making them ready to be eaten
  252. Effects of Compliment
    • Opsonization
    • Inflammation
    • Membrane attack complex
  253. Inflammation
    C3a, C4a, C5a increase chemotaxis of phagocytes and increase release of histamine, therefore increasing inflammation
  254. Membrane attack complex
    • C3b induces the attack complex
    • this complex pokes holes in the bacterial cell walls, causing contents to leak out and they die
    • C9 pokes the holes
    • doesnt affect host membranes
  255. Acute phase response
    • cytokines produced by WBCs in response to injury and inflammation cause the liver to produce acute phase proteins
    • Interluekin 6 travels to liver and induces production of accute phase proteins, which mark things and activate complement- the increase in liver enzyme levels can mean infection, so the doctor will check this if youre sick
  256. Acute phase reactants
    bind and opsonize infectious agents and activate complement
  257. What 2 proteins are acute phase reactants?
    • C-reactive protein: secreted by liver; increases in response to inflammation and activates complement system
    • Mannose-binding protein: binds to mannose, a sugar in many bacterial and fungal cell membranes, and marks them for target
Card Set
Microbiology Exam 3
Test of 7/26/18