BIOM 250 Exam 2 Study Guide
BIOM 250 Exam 2 Study Guide BIOM 250
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This 20 page Study Guide was uploaded by Davis Notetaker on Saturday March 5, 2016. The Study Guide belongs to BIOM 250 at Montana State University taught by Kari Cargill in Winter 2016. Since its upload, it has received 62 views. For similar materials see Micro Hlth Sci: Infect Disease in Biology at Montana State University.
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Date Created: 03/05/16
Eukaryotic Microorganisms (part 1) Friday 2/12 Parasitology Parasite lives inside a host organism, usually at the expense of host Hosts ● Definitive/primary host where parasite reaches maturity and reproduces if possible ● Intermediate host carries parasite while parasite is in an immature stage of development Vectors (insects) ● Mechanical vector physical transmission, where the parasite has no life cycle in the vector i.e. the vector is not essential to the parasite’s life cycle ● Biological vector usually a biting insect the vector is essential in some part of the parasite’s life cycle Protozoa unicellular, eukaryotic microorganisms classified by type of motility (ability to move around) ● ciliated these protozoans possess hairlike organelles called cilia, which are used for swimming, crawling, attachment, feeding and sensation ● flagellated flagella are whiplike organelles generally used for propulsion or feeding ● amoebas alter shape by extending/retracting pseudopods (“false feet” are temporary projections of cell membranes) ● nonmotile Protozoan Diseases disease/infection Giardiasis etiologic agent Giardia lamblia (caused by: name, type of m/o, flagellated protozoan other characteristics) reservoir (where it is harbored contaminated water and infected mammals (humans are the naturally) primary host) mode of transmission to fecaloral route: contaminated water/food, direct contact humans (& susceptible (diapers, hands) people) susceptibility: 2030% in developing countries daycare center outbreaks are common (up to 70% infected) pathogenesis (progression of active form, called trophozoite: disease within body, virulence adhesive disc attaches to wall of intestine (feeds on mucus) factors) inactive, resistant,ineffective form, cyst: passed in feces (up to 14 billion per stool) & persists in water Diagnosis: fecal sample under microscope (trophs & cysts visible) string test: encapsulated string is swallowed with one end fastened outside of the mouth. Capsule dissolves and string travels to the intestine via normal mode of digestion, then extracted and tested for presence of protozoa symptoms diarrhea (large quantity, frothy) weight loss sulfurous flatulence treatment/prevention/control treatment: oral medication prevention: avoid contaminated water, hand washing, etc. control: water treatment cysts are resistant to chlorine/iodine treated water cysts are fairly large and can be filtered, or alternatively, boiled disease/infection Toxoplasmosis etiologic agent Toxoplasma gondii (caused by: name, type of m/o, non motile protozoa other characteristics) reservoir (where it is harbored domestic, outdoor cats (definitive host) naturally) other animals (intermediate hosts) mode of transmission to ingestion of cat fecal material humans (& susceptible or ingestion of undercooked meat or unwashed produce people) (most likely manner of infection in US) pathogenesis (progression of becomes ‘walled off’ by host defenses disease within body, virulence (can inhabit host for years, esp. brain) factors) first time infection can cross placenta Diagnosis: test blood for antibodies see parasites in blood or tissues symptoms many asymptomatic, otherwise mostly mild symptoms include swollen lymph nodes (2040% of US pop has been infected) Pregnant women miscarriage, birth defects (mental retardation, blindness) ~4000 cases in the US per year Immunocompromised reactivation of organism, which can lead to encephalitis (inflammation of the brain) or death treatment/prevention/control treatment: none for congenital cases medication for infected adults prevention: avoid raw meat Mon 2/15 No School Wed 2/17 Fungi Unicellular and multicellular eukaryotic microorganisms Mold risk groups: immunocompromised (eg asthma (mold allergy), lung disease, etc) Infections Opportunistic superficial infections: skin, hair, nails subcutaneous: below skin systemic: invasion of organs Fungal Disease disease/infection Ringworm (misnomer) etiologic agent dermatophytes (skin fungus) w/ many species: (caused by: name, type of m/o, tinea capiti on scalp other characteristics) tinea unguium in nails tinea cruri groin “jock itch” tinea pedi feet “athlete’s foot” tinea barbae beard “barber’s itch” reservoir (where it is harbored animals (commonly pets) naturally) infected individuals mode of transmission to fomites (direct contact with contaminated objects, for humans (& susceptible example nail clippers used by someone with nail fungus) people) pathogenesis (progression of minor scrapes contaminated with fungi (superficial) disease within body, virulence factors) symptoms not severe and vary depending on species: red, scaly, itchy patches, bald spots, thick nails treatment/prevention/control Treatment: Antifungal topical ointment Oral medication (for widespread conditions or nail infections where topical ointment won’t reach) Diagnosis: 1. skin appearance 2. skin sample examined under microscope Prevention: avoid objects that are likely contaminated (e.g. nail clippers) Eukaryotic Microorganisms (Part 2) Helminths (parasitic worms) multicellular Two parasitic groups of helminths: 1. Flatworms ex: flukes: leafshaped ex: tapeworms: parasites of small intestine 2. Roundworms (nematodes) Flatworms Many are freeliving, i.e. part of the ecosystem Not all are parasitic: parasitic types have suckers/hooks/etc for attachment Flukes (trematodes) In humans: lung, liver and blood flukes Have complex life cycles that involve multiple hosts Disease: Blood Fluke aka Schistosomiasis Life cycle: ● Adults live in blood vessels of human liver (420 years), where they mate and lay eggs ● Eggs travel to intestine, exit with feces and end up in fresh water ● In water: egg hatches as miracidium larva ● Larva penetrates freshwater snail where it grows into a sporocyst (larvae do not survive if no snail host is found) ● Sporocyst further develops into a form called cercaria, which leaves the snail host and swims freely until coming into contact with human skin, which it penetrates. Note that this is the only form of the blood fluke that is infectious disease/infection Schistosomiasis aka Bilharzia etiologic agent Schistosoma “split body” female lives inside the male body (caused by: name, type of m/o, other characteristics) reservoir (where it is harbored intermediate host: freshwater snails (definitive host: naturally) humans, but snail considered reservoir) mode of transmission to Cercaria contaminated water contact with skin humans (& susceptible people) pathogenesis (progression of Penetrates skin, then travels through bloodstream until disease within body, virulence arriving at the liver (where male/female mate and lay eggs) factors) eggs travel to intestine, and exit with feces Occasionally eggs lodge in tissue symptoms Initial entry usually not noticeable, but site of infection may be itchy after the fact often subclinical (asymptomatic/ minor symptoms) other symptoms can include: anemia, diarrhea, malnutrition, fever, skin itch Eggs lodged in tissue can cause chronic tissue damage: inflammation/tissue damage as the immune system responds treatment/prevention/control Diagnosis: skin lesions, presence of eggs in feces or urine, blood tests Treatment: Oral medication (for 12 days) Prevention: avoid contaminated water Control: sanitation (keep waste separate from fresh water) eliminate snail host (could be dangerous for the ecosystem) Disease: Swimmer’s itch Caused by flukes in North American lakes Definitive host is waterfowl; in humans, cercaria cause an allergic immune response (itchy rash) but ultimately don’t survive and skin conditions resolve on their own Fri 2/19, Mon 2/22 Tapeworms (cestodes) adults inhabit the small intestine of animals Tapeworm anatomy Scolex “head” end, includes suckers or hooklike parts for attachment Proglottis body segments Hermaphroditic (selffertilizing) Mature body segments are full of eggs Once mature, these segments drop off and exit with feces disease/infection Beef Tapeworm etiologic agent Tenia saginata (caused by: name, type of m/o, other characteristics) reservoir (where it is harbored Definitive host: humans naturally) Intermediate host: cattle mode of transmission to Ingestion: undercooked, infected beef aka “measly beef” humans (& susceptible people) pathogenesis (progression of cysticercus (larva) is ingested, then attaches itself to the disease within body, virulence small intestine, where it grows, absorbing nutrients, and factors) matures (up to 1020 m long) can survive for up to 25 years in a host, and host can carry more than one tapeworm (less common) symptoms usually asymptomatic other symptoms include: malnutrition, and more serious conditions if proglottids migrate to other parts of the body treatment/prevention/control Diagnosis: eggs or proglottids in feces Treatment: oral medication Prevention: cook beef thoroughly Control: sanitation irrigation provide clean water for cattle use of fecesfree fertilizer Roundworms (nematodes) Two types of human infections 1. Egg is infective ex: pinworm, ascaris 2. Larva is infective ex: hookworms (penetrate skin, usually feet), trichinellosis (from ingesting undercooked pork), filariasis (from mosquitoes) Pinworm Lifecycle: ● eggs are ingested & hatch in the duodenum (first part of small intestine) ● pinworm larvae grow rapidly (up to ½ inch long) and migrate towards the colon, maturing to adulthood in the process ● pinworms mate in ileum (last part of small intestine), males usually die and exit with feces ● eggladen females travel to anus, where eggs deposited (up to 15,000 eggs) and mature (w/ in 46 hours). Eggs are sticky and proximity items easily become contaminated, repeating the cycle Diagnosis: “Pinworm Paddle” collection vial with sticky adhesive on paddle end used for collection Disease: Ascariasis Life cycle: ● ingested eggs hatch in intestines ● larva burrows into gut wall ● travel through bloodstream to the lungs and through the trachea, where they are coughed up and swallowed ● swallowed larvae travel through digestive track back to intestine where they mature to adulthood, laying eggs that pass through feces disease/infection Ascariasis etiologic agent Ascaris lumbricoides (caused by: name, type of m/o, other characteristics) reservoir where it is harbored eggs in human feces naturally) mode of transmission to ingestion of contaminated food or water humans ( & susceptible Children are especially susceptible people) pathogenesis (progression of larvae in lungs can cause damage (inflammation) disease within body, virulence factors) adults in intestine can cause malnutrition or bowel blockage migrating adults can emerge from openings (e.g. nose, navel) symptoms Most asymptomatic (85% of cases) other symptoms include malnutrition shortness of breath and fever early on abdominal pain and swelling diarrhea treatment/prevention/control treatment: oral medication prevention/control: sanitation (proper disposal of feces) Disease: Filariasis Life cycle: ● mosquito bites infected person, ingesting microfilariae (early form of parasite present in blood) ● mature to larvae in mosquito ● mosquito passes larvae to next person ● larvae travel through bloodstream to lymph gland where they mature to adulthood ● females produce microfilariae disease/infection Filariasis etiologic agent Wuchereria bancrofti (caused by: name, type of m/o, other characteristics) reservoir (where it is harbored infected humans naturally) mode of transmission to mosquitoes humans (& susceptible people) pathogenesis (progression of adult worms block lymph vessels, causing fluid disease within body, virulence accumulation factors) symptoms elephantiasis (swollen limbs, scrotum) treatment/prevention/control Diagnosis: blood smear (shows microfilariae) Treatment: medication, swollen limbs wrapped in pressure bandages Prevention: mosquito control Control: get treatment for all infected persons Wed 2/24, Fri 2/26 Malaria Movie (The following items are movie questions from the D2L Quiz) 1. From the film on malaria, what was sold through "socially marketing" programs to assist the villagers with the problem of malaria? ANS: bed nets 2. T/F: Malaria can be contracted in the U.S. today. ANS: True 3. Which does NOT work to prevent new cases of malaria? ANS: vaccination (no vaccines for any eukaryotic microorganisms exist) 4. From the film on malaria, what did the Florida public health authorities do about the homeless people who might harbor the malaria parasite? ANS: Passed out mosquito repellent and educational flyers 5. What causes malaria? ANS: protozoa 6. What role do mosquitoes play in malaria? ANS: They are the biologicavectors that transmit the disease 7. T/F: From the film, the clinical vaccine trials were 100% effective at preventing malaria in volunteers in London. ANS: False disease/infection Malaria etiologic agent plasmodium species (caused by: name, type of m/o, protozoan other characteristics) 4 species infect humans reservoir (where it is harbored infected humans naturally) mode of transmission to Anopheles mosquito humans (& susceptible people) Risk groups: pregnant women & children pathogenesis (progression of sporozoites form: blood infection disease within body, virulence factors) merozoite stage: travels to liver where it replicates and is released as the liver becomes full trophozoite stage: red blood cells (RBC’s) (few minutes) replicates, cyclical rupturing of RBC’s symptoms “fever & ague” (historical descriptions); fever, shaking chills, aches (head & muscle), fatigue, nausea treatment/prevention/control Treatment: can be completely cured depending on form of parasite (and then no longer a reservoir) Prevention ● mosquito control ● bed nets ● treatment of carriers ● variety of drugs Non example: no vaccine, in fact there are no vaccines for anydisease caused by eukaryotic parasites Immunity Immunity occurs inconsistently in individuals, and ultimately immunity is unclear, but species of parasite may be a factor. P. falciparum most serious form causes 95% of malaria deaths agglutinates RBC’s ‘blackwater fever’; dark urine due to buildup of hemoglobin (HgB) in urine (sign of kidney failure) P. vivax, P. ovale relapsing fevers reemergence from liver fever every 3 days (48 hour cycle) P. mariae can stay in blood for decades, “chronic” malaria refers to this condition symptoms last ~1020 days most survive Treatment variety of drugs: Quinine found in bark of trees growing wild in certain regions first use by Peruvian natives chloroquine developed in lab to mimic quinine (but more sustainable than harvesting tree bark) Tonic Water derived from adding sweetener to bitter quinine medicine modern tonic water contains 83ppm (83 mg/liter) of quinine concentration ~2100 mg/day treats an infected adult This means ~25 liters (~7 gallons) of tonic water would need to be consumed to be an effective treatment! Artemisia Artemisia argyi , aka mugwort used in traditional Chinese medicine Artemisinin, made from Artemisia, is one of the most rapid acting drugs developed to treat malaria ACT – Artemisiabased combo therapy: prevents parasitic resistance Wed 3/02 Helminthic Therapy Experimental use of helminth m/o’s to treat autoimmune disorders/diseases “promising results” ex: whipworm hookworm schistosomes Bacteria (prokaryotes) Bacterial Growth replicate via binary fission (asexually) Replication/generation time time for binary fission to occur varies: 20 min 20 hr depending on type of bacteria (exponential growth) Bacterial Shapes used to help identify bacterial infection (suffixes) ● coccus (pl. cocci) round shaped ● bacillus (pl. bacilli) rod shaped ● Several types of “spiral” shaped bacteria: ○ vibrio (comma shaped) ○ spirillum ○ spirochete ● coccobacillus oval shaped ● pleomorphic variable shape/size Bacterial Cell Arrangements can also help identify bacterial contaminant (prefixes) ● diplo “double” ex: diplococcus ● strepto prefix indication linked/chain formation ex: streptococcus streptobacillus (common in soil) ● staphylo clustering species ex: staphylococcus ● tetrad clusters of four Prokaryotic Cell Structure All cells have an outer membrane, many have cell walls many bacteria have cell walls, made from peptidoglycan (meshlike layer) Cell wall structure of bacteria can also help describe bacteria 1. grampositive (staining characteristic) these cell walls have a thick peptidoglycan layer (up to 40 layers) retains stains 2. gramnegative thin peptid. layer also has an outer membrane does not retain stains as well 3. acidfast bacteria less peptid. lipid layer (waxy, nearly impermeable & highly resistant) grow slowly colorfast (require a special staining technique) ex: tuberculosis, leprosy 4. no cell wall ex: Mycoplasma , which causes “walking pneumonia” (less severe than other types of pneumonia) Gram stain over 100 years old “differential stain”: use of 2 or more dyes helps to disting diff cell components, i.e. differentiate bacterial components Methods of bacterial control damage bacterial cell wall penicillin inhibits peptidoglycan synthesis lysozyme enzyme found in body fluids which digests peptidoglycan What about both gram+ and gram? gramvariable Other cell structures cell (or plasma) membrane internal: cytoplasm (mainly water) ribosomes (protein synthesis) nuclear region/nucleoid (bacterial DNA/chromosome) plasmids (small extra pieces of DNA that contain nonessential genes, for ex: drug resistance) Fri 3/04 Other Cell structures internal structure vegetative cells metabolically active cells (actively growing) endospores (in some bacteria) contains DNA dormant stage, form within veg. cell survive after veg cell dies steam/heat/pressure & green dye used to stain endospores (usually not color fast) very resistant to: drying, heat, radiation, chemicals (all things that can usually kill bacteria) endospores are very hard to kill (steam, heat and pressure) often found in soil ex: tetanus, botulism (bäCHәˌ lizәm/, anthrax iClicker: tetanus transmitted through infected wound botulism foodborne anthrax foodborne, waterborne, respiratory infection Bacteria life cycle (sporulation and vegetative cycles) Sporulation endospores forms within the veg cell germination veg cell forms from endospore Bacterial endospores vs Fungal spores bacterial endospores part of resistant structure 1 veg cell = 1 endospore fungal spores method of reproduction 1 mold produces many spores disease/infection Anthrax etiologic agent bacillus anthracis (caused by: name, type of m/o, gram positive other characteristics) reservoir (where it is harbored soil, disease of cattle (germinate in cows) naturally) mode of transmission to Zoonotic form of anthrax humans (& susceptible risk group: occupational exposure people) animal contact wool, hides, meat not human to human Geographic Risk Groups endemic in central america, some countries in South America, mid Africa, South Asia (including South China) pathogenesis (progression of bacteria produces exotoxins disease within body, virulence causes edema (swelling), tissue destruction & factors) bleeding kills macrophages (phagocytic WBC’s) symptoms 3 forms of Anthrax 1. cutaneous a. spores enter skin wound and germinates Symptoms localized black scab (anthrax = “coal” gr) mortality rate of 1020% 2. respiratory a. spores are inhaled and bacteria enters the bloodstream (septicemia) Symptoms early: fever, cough (treatment possible if caught early) 23 days septicemia (100% mortality rate) 3. intestinal a. spores are ingested from contaminated meat, this damages intestinal cells Symptoms nausea, bloody diarrhea ulcerative lesions along astrointestinatract 50% mortality rate septicemia nearly always fatal, regardless of initial site of infection treatment/prevention/control Treatment antibiotics, only effective if treated early Prevention vaccine exists for high risk groups 6 injections over 18 months, with annual boosters vaccine for livestock antibiotics, if exposure is suspected ex: military vaccinated Bozeman 2008 Flying D Ranch at Spanish Creek (aka Ted Turner’s ranch) >250 dead bison from anthrax infection Anthrax as bioweapon 20012008 anthrax mail mystery anthrax endospores sent through mail as ‘white powder’ to targeted individuals contaminated other mail items, and more widespread infection caused public panic/anxiety External structure flagella pili (singular: pilus) aka fimbriae not for motility, usually used for attaching conjugation pili used to join bacteria together to transfer DNA (nonessential) ex: plasmids glycocalyx external to cell wall, polysaccharides two forms: ● slim layer (thinner) ● capsule (thicker and sticky) capsule advantages: attachment ex: plaque attaches to teeth prevents drying out protects bacterium from host defenses (WBC”s have difficulty attacking) disease/infection Pneumonia etiologic agent varies: many m/o’s including several bacteria (caused by: name, type of m/o, our focus: pneumococcal pneumonia other characteristics) streptococcus pneumoniae aka pneumococcus grampositive diplococcus capsule cell wall reservoir (where it is harbored healthy human carriers (normal respiratory flora) naturally) mode of transmission to respiratory droplets humans (& susceptible elderly, infants,... people) pathogenesis (progression of bacteria evade phagocytes (because of capsule) disease within body, virulence factors) symptoms early: mild resp symptoms leading on to high fever & chills chest pain, cough, bloody sputum treatment/prevention/control treatment: antibiotics (currently seeing increase in drug resistance) untreated has 25% mortality rate prevention: vaccine (for elderly) “pneumovax”
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