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parasitic relationship
one organism benefits (parasite) one is harmed (host)
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Parasite
an organism that lives at the expense of another host organism
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Ectoparasites
- parasites that live on the surface
- ie- ticks and lice
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Endoparasites
- parasites that live inside the host
- ie hookworm
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Obligate parasites
- must spend at least part of its life cycle in or on a host
- ie malaria
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Facultative parasites
- normally live on their own, but can obtain nutrients from a host
- ie fungi
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Permanent parasites
- remain in a host
- ie tapeworm
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Temporary parasites
- feed on host and then vacate
- ie mosquito
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Accidental parasites
- feed on organisms that are not their normal host
- ie- ticks will go for anything, not just one specific host
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Hyperparasitism
- a parasite that is infected by its own parasite
- ie- mosquitoes that carry malaria
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Vectors and types
- things that transmit parasitic diseases
- 2 types: biological vector and mechanical vector
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Biological vector
- a vector that carries a parasite during a key part of the parasites life cycle
- ie mosquito carrying malaria
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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
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Types of hosts
- definitive hosts
- intermediate hosts
- reservoir hosts
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Definitive hosts
provide a place for the parasite to reproduce
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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
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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
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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
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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
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What are 2 special ways that parasites can divide?
- 1. Schizogony
- 2. Hermaphroditic
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Schizogony
- "multiple fission"
- one parasite makes many copies of itself producing many offspring
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Hermarphroditic division
- parasite contains both male and female reproductive systems
- ie- proglottid (long tube filled with eggs) in tapeworms
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Protists
- mostly unicellular eukaryotic cells
- many are autotrophs
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Types of protists
- plant-like protists
- fungus-like protists
- animal-like protists (aka protozoans)
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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
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Fungus-like Protists
- Water molds: mildew- can cause respiratory problems
- Slime molds: feed on decaying matter
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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
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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
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Fungi (mycology)
- unicellular (yeast) or multicellular heterotrophs
- many are saprophytes
- can be opportunistic- move in and cause an infection if there is space
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saprophytes
get nutrients from decaying matter
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types of fungi
- bread molds
- sac fungi
- club fungi
- ringworm
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bread molds
rarely cause human disease except for Rhizomes- an opportunistic infection (often occurs in uncontrolled diabetics)
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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)
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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
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Ringworm
- a fungus, not a worm
- identified as a circle ring on the skin
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Helminths and types
- Worms
- 2 types: Bilaterally symmetrical worms and parasitic worms
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Parasitic worms
- flukes
- tapeworms
- adult roundworms
- larval roundworms
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flukes
- tissue flukes
- blood flukes
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tissue flukes
- lung: Paragonimus westermani (intermediate host is snail and crustaceans)
- liver: Clonorchis sinensis (3rd most prevalent- snail and fish) and Fascia hepatica
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Blood flukes
Schistosoma: second in prevalence after malaria
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Tapeworms
- can be found in beef, pork, dogs, fish
- cook meat well done to avoid
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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
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Larval Roundworms
- require a mosquito host
- Wucheria bancrofti (elephantiasis)- migrate to lymphatic system and clog it causing swelling
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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
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Arthropods (types)
- Arachnids
- Insects
- Crustaceans
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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
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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
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what type of mosquito carries malaria
Anopheles
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Crustaceans
- can be intermediate hosts- can be hosts for pathogens transmitted to humans through the food chain
- crayfish, crabs
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Pathogen
any agent that causes disease in a host
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Host
any organism that harbors another organism
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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)
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contamination
microorganisms are present
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infection
- multiplication of a parasitic organism in or on a host
- mostly bacterial
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Infestation
presence of larger parasites (worms and insects)
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Disease
any disturbance of health where host cannot function normally
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Pathogenecity
- capacity to cause disease
- can depend on how many organisms infect the host
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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)
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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)
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Transient microflora
- only there for a certain period of time under certain conditions
- ie skin when especially warm or moist
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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)
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Classification of disease
- inherited
- congenital
- degenerative
- nutritional deficiency
- endocrine
- mental
- immunological
- neoplastic
- iatrogenic
- idopathic
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Inherited disease
defects in DNA passed to offspring causing disease
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Congential Disease
structural or functional defects present at birth
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Degenerative disease
- develop as aging occurs
- ie emphysema
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Nutritional Deficiency Disease
- make patient more suseptable to other disesaes
- ie anemia
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Endocrine Disease
- hormonal disturbance
- ie diabetes
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mental disease
ie creutzfeld-Jakob
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Immunological disease
- lupus, AIDS, allergies
- immune system not functioning properly
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Neoplastic disease
- abnormal cell growth
- can be induced by viruses- ie cervical cancer caused by HPV
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Iatrogenic Disease
- caused by medical treatments
- aka nosocomial infections
- these are diseases acquired at a hospital or medical setting
- ie MRSA
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Idiopathic disease
have an unknown cause
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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
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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)
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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
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Virulence factors
structural or physiological factors that help the microbe cause disease
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How do bacteria get inside the host?
Penetration of skin (through a cut), mucous membranes, sexual transmission, ingestion, inhalation, fomites
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fomite
- an inanimate object that can carry pathogenic organisms
- ie door handle, remotes, cellphone etc
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Adherence
- binding of bacteria to host cell
- this is the essential first step of infection
- bacteria have proteins called adhesins
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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
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Colonization
- growth of microbes on surface of epithelial cells (skin, mucous membrane, etc)
- most microbes are invasive (can get inside host tissues)
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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)
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is invasiveness the same for all microbes
no, it varies between microbes and can differ depending on the type of host cell invaded
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toxin
something that is poisonous to other organisms
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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
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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
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leukocidins
- destroy WBCs
- first neutrophils (first ones on scene) then macrophages
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leukostatins
stop white blood cells from engulfing bacteria
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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
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hemolysis
the breakdown of the membrane of the red blood cell by hemolysin
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Alpha hemolysis
- partial breakdown of hemaglobin
- leaves a greenish hue which can be seen on blood agar plate
- characteristic of streptococcus pneumonia
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Beta Hemolysis
- complete breakdown of hemoglobin in vicinity of bacteria
- characteristic of s. pyogenes
- plate will be clear, maybe yellow
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Gama hemolysis
- lack of hemolysis
- blood agar plate will stay red
- chracteristic of e. faecalis
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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
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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
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Enterotoxins
- act on digestive tract
- can be antigens that activate immune cells and gives us an immune response
- toxoids
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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
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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
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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
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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
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types of viral infections
- productive
- abortive
- latent
- persistant
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productive viral infections
virus invades cell and immediately multiplies
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abortive viral infections
- virus invades cell but cannot make the proteins necessary to multiply
- therefore nothing happens
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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
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Persistant viral infections
- virus invades cell and multiplies continuously for months or years
- ie hepatitis b virus
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How do eukaryotes cause disease?
fungi, protozoa and helminths are eukaryotes that cause disease
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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
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Protazoa causing disease
- plasmodium causes malaria- reproduces in RBCs
- Giardia causes giardiasis- infecte intestinal tissues
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Helminths causing disease
- worms are extracellular parasites
- can release toxic wastes and antigens that can cause allergy in host for different immune reactions
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Sign
- characteristic of a disease that can be seen by observing a patient
- swelling, redness, rash, cough, pus, fever, vomiting, etc
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Symptom
- characteristic of disease that can only be felt by the patient
- pain, shortness of breath, nausea, sore throat, general malaise
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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
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Types of infectious diseases
- acute
- subacute
- chronic
- latent
- local
- focal
- systemic
- primary
- secondary
- superinfection
- mixed
- subclinical
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acute infection
- develops rapidly
- over quickly
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subacute infection
- between accute and chronic
- ie gum disease
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chronic infection
develops slowly, hangs around
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latent infection
periods of inactivity (herpes, HIV, malaria)
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local infection
- confined to a specific area of the body
- ie cellulitis in the ankle
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focal infection
infection in a specific area but antigens and toxins can spread
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systemic infection
- affects most of the body
- usually due to microbe entering blood stream and spreading throughout host
- septicemia, bacteriemia, viremia, toxemia, sapremia
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primary infection
- initial infection of a healthy host
- ie flu
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secondary infection
- follows a primary infection, usually in a host that is immunocompromised
- ie pneumonia
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Superinfection
- secondary infection that results from the loss of normal microflora
- cdiff
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mixed infection
- caused by several species of organisms
- ie tooth cavities
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subclinical infection
- doesnt produce all signs and symptoms
- host may not know of infection and act as carrier
- typhoid mary
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Stages of infection
- 1.incubation period
- 2.prodromal period
- 3.invasive phase
- 4.decline phase
- 5.convalescence period
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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
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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
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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
-
decline phase
symptoms subside due to treatment or successful host immune response
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convalescence period
- healing, tissues are repaired
- can last a while
- flu- feeling better soon but takes a while to feel 100% better
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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
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Why study epidemiology?
- To help understand the cause of a disease
- to plan and evaluate intervention and prevention strategies more effectively
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What must epidemiologists be able to do
describe and analyze the distribution and the determinants in person, place and time
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Distribution
where does it happen
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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
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Three factors that interact to cause disease
- agent: microbe/chemical
- host: who
- environment: where
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Etiology
study of causes and origins of diseases- where they originate from
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Incidence
number of new cases of a disease for a specified time period
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Prevalence
total number of people infected in a population at any one time by a disease
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Morbidity rate
number of individuals affected by a disease during a set period of time
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Mortality rate
number of deaths of individuals due to a disease during a set period of time
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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
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Endemic
- a disease that is constantly present in a specific population over a relatively short period of time
- native to that area
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Epidemic
when an endemic increases its morbidity and/or mortality rate suddenly causing a public health problem/concern
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pandemic
epidemic spread world wide
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Sporadic Disease
random and unpredictable manner involving isolated cases that pose no great threat to the population as a whole
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Ways that disease spreads
- Common-source outbreak
- Propagated endemic
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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
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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
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Portals of entry
- mucous membranes (most important one)
- ear
- eye
- nose
- mouth
- mammary glands
- urethra
- vagina
- anus
- placenta
- broken skin
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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
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Modes of transmission
- Contact transmission
- Vehicle transmission
- Vector transmission
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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
-
Direct contact diseases
- rabies
- rat bite fever
- syphilis
- gonnorhea
- herpes
- staph infections
- cutaneous anthrax
- genital warts
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Indirect contact by fomites diseases
- tetanus (step on nail)
- common cold
- enterovirus
- ringworm
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Droplet diseases
- common cold
- influenza
- measles
- Q fever
- pneumonia
- whooping cough
-
Types of vehicle transmission
- Waterborne
- Airborne, including dust particles
- foodbourne
-
Waterborne diseases
- cholera
- shigellosis
- leptospirosis
- campylobacter infections
-
Airborne diseases
- chickenpox
- tuberculosis
- coccidiodoycosis
- histoplasmosis
- influenza
- measles
-
Foodborne diseases
- intoxication with alfatoxins and botulinum toxin
- paralytic shellfish poisoning
- staph food poisoning
- typhoid fever
- salmonellosis
- listeriosis
- toxoplasmosis
- tapeworms
- hepatitis A
-
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
-
mechanically transmitted vector disease
- e.coli diarrhea
- salmonellosis
- trachoma
-
types of biological vector diseases
- malaria
- plague
- yellow fever
- typhus fever
- rocky mountain spotted fever
- chagas disease
- lyme disease
-
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
-
What are the most common types of nosocomial disease
- e.coli (UTI)
- staphylococcus aureus
- streptococcus
-
What are the two types of nosocomial infections
-
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)
-
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)
-
What ways can you limit nosocomial infection
- WULMP
- Wash hands
- Use gloves
- Limit prophylactic antibiotic use
- Maintain sterility
- Prevent insect infestations
-
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
-
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
-
nonspecific defenses
- act against ANY type of invading agent
- the first line of defense against pathogens
- AKA innate immunity (respond in a generic way)
-
What are the nonspecific defenses?
- 1. Physical barriers
- 2. Chemical barriers
- 3. Cellular Defenses
- 4. Inflammation
- 5. Fever
- 6. Molecular defenses
-
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
-
chemical barriers
- antimicrobial activity in body fluids
- enzymes in saliva and tears
- defensins on our hands act as natural purell
- stomach acid
-
Cellular defenses
phagocytes- brought to needed area by chemotaxis. find, bind, ingest and digest the microbe
-
inflammation
- a sign the immune system is working
- longterm inflammation can cause damage to tissue
- rubor, tumor, calor, dolor (redness, swelling, heat, pain)
-
Fever
- can kill microbes or inactivate toxins
- fever with vaccinations yeild a better immune response
- hypothalamus resets body temp to attack
-
Molecular defenses
interferons and complement
-
Why do we have physical barriers
- function to keep out infectious agents
- also secrete chemicals
-
how does your skin become vulnerable to infection
- heat
- cold
- abraisions
- insect and animal bites
- burns
-
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
-
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
-
Whats in your blood
- plasma: fluid protien
- formed elements: cells
-
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
-
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
-
Agranulocyte types
- Monocytes: myeloid cells, develop into macrophages in tissue
- Lymphocytes: lymphoid cells; B cells and T cells involved in specific defenses
-
Phagocytes
- pacmen
- circulate through the body and "eat" up or "engulf" other cells or foreign particles
- two types: neutrophils and monocytes
-
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
-
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)
-
How does phagocytosis happen
- 1. find foreign agent (by chemotaxis)
- 2. Bind to foreign agent
- 3. Ingest foreign agent
- 4. Digest foreign agent
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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
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Cytokines
- immune chemicals that work on one another
- how immune cells talk to eachother
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Adherence
in order to ingest a foreign agent, the phagocyte must first stick to it
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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
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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
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ingestion
a quick process where the pseudopodia (temporary protrusions) of phagocytes move to surround the offending bacterial cell and fuse to form a phagosome
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Digestion and 2 ways
- intracellular killing
- 2 ways of digestion: Lysosomes and reactive oxygen
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Lysosomes
- contain digestive enzymes that break down microbes
- fuses with phagosome to form phagolysosome (lysosome, phagocyte and bacteria particle fused)
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Reactive oxygen
hydrogen peroxide, nitric oxide, superoxide ions, and hypochlorite ions damage cell microbial membranes
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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
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leucocidin
- destroys white blood cells
- secreted by staphlyococcus
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streptolysin
- stops white blood cells from engulfing bacteria
- released by streptococcus
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MBP
- Major basic protein
- released by eosinophils
- punches holes in helminth body to break it up so it can be taken up by phagocytes
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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
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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
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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
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2 ways NK cells kill
- perforin: blows holes in cell
- granzyme: initiates apoptosis
NKs secrete both of these proteins
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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
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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
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relationship between lymphatic system and circulatory system
- lymphatic system parallels circulatory system
- runs through the same places
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What are the lymphatic organs
- lymph nodes
- thymus
- spleen
- peyer's patches
- appendix
- tonsils/adenoids
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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
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Thymus
- t cells originate in the bone marrow but mature here
- this is also where t cells undergo training
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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
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Are phagocytes part of innate or acquired immune system?
part of innate systme but helps with specific acquired system by presenting antigens
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Peyer's patches
in small intestine
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Appendix
- helps with immunity
- previously thought to have no function
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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
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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
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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
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Acute Inflammation
a host defense
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Histamine
a chemical that acts as a flare gun to say all hands on deck to cause inflammation
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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
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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
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diapedesis
- the squeezing out of phagocytes through leaks in blood vessels
- blood vessels start to get leaky which allows this
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pus
WBCs (usually neutrophils) killed in the line of duty plus dead microbes and other cellular debris
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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
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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
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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
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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
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What causes a fever
exotoxins and endotoxins of bacteria that act as pyrogens, which are substances that induce fever
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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
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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
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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
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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
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Interferon
- interferes with viral infections
- naturally occuring immune molecules
- 2 main types
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Types of interferon
- type I: includes alpha and beta
- type II: gamma
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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
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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
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Type II Interferon
- secreted by uninfected lymphocytes and NK cells
- like caffeine that activates and jacks up macrophages
- can induce antiviral proteins
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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)
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Downsides of therapeutic interferon
- unstable, breaks down quickly
- side effects
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side effects of therapeutic interferon
- fatigue
- nausea
- headache
- vomitting
- nervous system disorders
- fever
- liver and kidney toxicity
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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
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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
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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
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Effects of Compliment
- Opsonization
- Inflammation
- Membrane attack complex
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Inflammation
C3a, C4a, C5a increase chemotaxis of phagocytes and increase release of histamine, therefore increasing inflammation
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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
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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
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Acute phase reactants
bind and opsonize infectious agents and activate complement
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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
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