BIOM 250: Exam 4 Study Guide
BIOM 250: Exam 4 Study Guide BIOM 250
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This 16 page Study Guide was uploaded by Davis Notetaker on Wednesday April 27, 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 21 views. For similar materials see Micro Hlth Sci: Infect Disease in Biology at Montana State University.
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Date Created: 04/27/16
Mon 4/11 Innate Host Defenses Part 1 Terminology Innate host defenses nonspecific defenses Adaptive defenses specific defenses Barriers physical ● Skin & mucous membranes ○ Skin has layers to prevent pathogen invasion ○ Mucous membranes secrete mucus to trap pathogens ○ Cilia traps pathogens ● Washing actions clear out potential pathogens ○ E.g. tears, saliva, urine, vaginal secretions ● Reflexive actions dispel pathogens ○ Cough, sneeze, vomit, diarrhea ○ Pathogens also take advantage of these for spreading to a new host Barriers chemical ● Skin salt in perspiration, acidic sebum (from glands in skin) ● Stomach gastric acid ● Body secretions lysozyme (breaks down peptidoglycan) Cellular Defenses Blood ● 60% fluid “plasma” (antibodies, proteins) ● 40% formed elements ○ Erythrocytes (RBC’s) ○ Leukocytes (WBC’s) ○ Platelets/thrombocytes (for clotting) Leukocytes Neutrophils, aka polymorphonuclear leukocytes (PMN’s) ● Phagocytic (look & act like amoeba) ● Active during initial infection ● Can enter tissues to take care of an infection there ● # of PMN’s increases during bacterial infection ● Phagocytosis kill pathogens intracellularly (kind of like ‘ingestion’) Eosinophils ● “Somewhat” phagocytic ● See increase during parasitic invasion or if allergy is present Basophils ● Release histamine (triggers inflammation + allergy symptoms) Monocytes ● Mature into macrophages (phagocytic) Lymphocytes ● Involved in adaptive immunity: B & T cells ● Numbers increase during viral infection Extracellular killing Natural killer (NK) cells type of lymphocyte ● Kill cells infected with virus ● Excretes cytotoxic proteins (toxic to living cells) WBC Differential count (“Diff count”) Diff count measures how close/far from normal an individual’s count is for each type of WBC, with a greater count in any category indicating the likely presence of a pathogen WBC mnemonic: Never Letonkeys tBananas: Neutrophils Lymphocytes Monocytes Eosinophils Basophils Wed 4/13 Disease: Leprosy disease/infection Leprosy aka Hansen’s Disease etiologic agent Mycobacterium leprae (caused by: name, type of Acidfast bacterium (cell wall made of waxy lipid layer) m/o, other characteristics) aerobic reservoir (where it is harbored naturally) mode of transmission to ● Unclear, spreads persontoperson; respiratory humans (& susceptible droplets suspected, generally transmitted from people) some kind of close contact ● Not very contagious, about 95% of people are naturally immune pathogenesis (progression of Two forms of leprosy: disease within body, virulence 1. Tuberculoid factors) a. incubation is 25 years b. “anesthetic”, i.e. loss of sensation c. nerve damage d. weakened skin pigment 2. Lepromatous a. ncubates 912 years b. granulomas form, as a result of host cellular defenses symptoms ● Changes in skin pigmentation ● Patches of skin with loss of sensation ● Lesions that do not heal after several weeks to months ● Muscle weakness ● Numbness in extremities treatment/prevention/control Diagnosis: ● Skin scraping – acid fast stain ● Can’t be grown in a lab without a host medium (armadillo or mouse foot pad), because pathogen is obligate (no genes for independent growth) Treatment: ● Longterm antibiotics (612 months) or multidrug therapy (MDT) (not drug resistant) ● Some damage may be permanent, as treatment reduces granulomas but can’t repair lost tissue ● Free MDT offered by WHO in endemic countries Prevention: ● No vaccine Inflammation ● Occurs with any tissue injury, e.g. microbial infection, wounds, burns ● Can occur in any tissue or organ ○ the suffix “itis” denotes inflammation in an organ, ○ ex: tonsillitis, appendicitis, dermatitis, arthritis, sinusitis, and more. Symptoms ● Heat ● Redness ● Swelling ● Pain Causes When damaged, cells release a variety of chemicals that trigger: ● Vasodilation (increased blood flow) ● Vascular permeability (fluid to tissues) ● Diapedesis occurring from the presence of: ○ Phagocytes in tissues (most commonly neutrophils) ○ Pus, which is a mixture of dead WBCs, microbes and tissue debris Benefits 1. Destroys the agent of injury (such as phagocytes) 2. Limits extent of injury (e.g. clotting) 3. Repairs damaged tissue (but may leave a scar (connective tissue)) Fri 4/15 Innate Host Defenses Part 2 Disease: Tuberculosis disease/infection Tuberculosis etiologic agent Mycobacterium tuberculosis (caused by: name, type of m/o, Acidfast bacteria other characteristics) reservoir (where it is harbored Has been in humans too long to determine a clear origin naturally) mode of transmission to Transmission: Respiratory droplets humans (& susceptible Risk groups: people) ● Those who have tested HIV + ● alcoholics ● Jailhouse inmates pathogenesis (progression of Pulmonary TB (Lungs) disease within body, virulence ● Mycobacteria replicate within macrophages factors) ● Granulomas form around bacteria these are walled off “tubercles” formed from aggregated WBC’s ● Can lead to Latent TB: mycobacteria is dormant, non infectious, many are asymptomatic ● Abnormal cell death develops ○ caseous necrosis of granulomas (interior looks like soft, white cheese) Extrapulmonary TB ● spreads beyond the lungs: bones, meningitis, urogenital, etc ● Problem in children , immunosuppressed Miliary TB ● systemic spread, usually fatal Virulence factors: Drug resistance ● Multiple Drug ResistantTB (MDRTB) resistant to top 2 drugs (rifampicin & isoniazid) ● Extreme Drug ResistanceTB (XDRTB) resistant to 3 of 6 drugs ● Total Drug ResistanceTB (TDRTB) resistant to ALL current drugs ● Lack of medication for TB has motivated a return to older, riskier drugs with dangerous side effects symptoms Many asymptomatic (latent TB) Fever Very bad cough for more than 3 weeks Pain in chest No appetite Weight loss Weakness or fatigue Eventually, coughing up blood or sputum treatment/prevention/control Control: ● Required Screening (Mantoux (tuberculin) test) ● Vaccine exists, bacillus CalmetteGuerin (BCG), but not available in US ○ commonly used in children in other parts of the world. Effectiveness varies per case per country Treatment: ● Antibiotics ● Requires months to complete Mantoux test 1. TB antigen is injected under the skin 2. If antibodies are present a reaction occurs that causes the injection site to swell, indicating the tested subject has been exposed to TB Nonspecific Defenses: Fever ● Characterized by an increase in body temp ○ This is triggered by infection or tissue damage ● The benefits of a fever include: ○ Inhibition of microorganism ○ Speeds up defensive cells Molecular Defenses Interferons ● Viral infection of a cell triggers the production of an interferon ● Interferon signals “infection” to uninfected cells, which can then make antiviral proteins to prevent the spread of infection Limits: ● Doesn’t help the cell that has already been infected ● Short term (colds & influenza) ● Used clinically has side effects in high doses (clinically active dose) Complement Pathways Complement ● Series of 20 proteins in plasma ● Act in a “cascade” (or “bucket brigade”) Triggered in two ways: 1. Classical pathway Antibodies bound to microbes 2. Alternate pathway pathogen surface interaction with complement proteins Results: ● Opsonization ○ Enhancement of phagocytosis (process by which phagocytes ‘digest’ pathogens) ○ Plays a role in inflammation ● Membrane Attack Complex (MAC) destroys microbes via cytolysis Mon 4/18 Adaptive Host Defenses Types of Immunity ● Active immunity ○ Body makes antibodies after exposure to antigens ○ Memory a body mechanism for retaining information about (almost) every threat it has been exposed to ● Passive immunity ○ Premade antibodies are received from another source (e.g. from mother) ○ No memory but provides immediate protection Both types can be acquired naturally or artificially Active Passive Naturally ❖ Development of antibodies ❖ Antibodies transferred from Acquired after illness mother to baby via (via placenta ❖ Lasts years to a lifetime or breast milk) (memory) ❖ Only lasts as long as antibodies live (no memory): weeks to months Artificially ❖ Comes from ❖ Premade antibodies acquired by Acquired vaccination/immunization injection ❖ Won’t cause disease but still ❖ Immediate protection but provokes an immune protection is temporary (no response memory) ❖ Memory is longterm Vaccines All are made from nonvirulent antigens, but this can be done in several ways: Types of Vaccines ● Killed microorganisms, such as influenza, rabies, Salk polio ● “Attenuated” microorganisms these are live but weakened, examples include MMR, Sabin polio ● Toxoids inactivated toxins, such as tetanus, diphtheria ● Subunit vaccines only part of antigen is used, e.g. new pertussis vaccine, hep B vaccine ● DNA vaccines new, experimental method of using genetically engineered DNA to instruct cells to produce antigen Misconceptions about vaccines ● Improvement of hygiene and sanitation had already begun to suppress disease before vaccines were introduced ● The US has been virtually wiped of vaccinepreventable diseases, so there is no need for children to be vaccinated ● Children receiving multiple vaccinations for different diseases at the same time is associated with an increased risk of harmful side effects and can overload the immune system In general, vaccines have some risks associated with them, but they are much smaller than the risks associated with the diseases they prevent Wed 4/20 Disease: Measles disease/infection Measles aka Rubeola etiologic agent Measles Virus (MeV) (caused by: name, type of m/o, Probably one of most contagious diseases on earth other characteristics) reservoir (where it is harbored naturally) mode of transmission to Respiratory transmission humans (& susceptible 90% of susceptible people contract the illness if exposed people) pathogenesis (progression of Complications disease within body, virulence ● Sinusitis, pneumonia ,encephalitis factors) ● Subacute sclerosis panencephalitis (SSPE) ○ 1 in 100,000 cases ○ Caused by virus persisting in the brain ○ 68 years after illness children would exhibit mental deterioration & death ○ highest risk if infected at younger than 2 years old ○ nearly always fatal if not caught early symptoms ● Fever ● Raised, red rash ● Koplik’s spots ○ Small, white spots inside mouth treatment/prevention/control Treatment: SSPE Antiviral drugs and interferon used if it is caught early enough Mortality rate: Developed countries < 1% Developing countries 1013%, even with existence of vaccine (estimated more than 450 deaths daily worldwide) Prevention: MMR vaccine (measlesmumpsrubella) 1963 Hilleman developed the 1st vaccine 9095% of a vaccinated pop achieves herd immunity Immune System Immune System has 2 branches 1. Humoral immunity antibodies found in fluids (blood, lymph, secretions) = “humors” i. Provides resistance to bacteria, viruses & toxins outside of cells b. B cell lymphocytes i. Develop in thebone marrow (in humans) c. Plasma cells, which are mature B cell lymphocytes, who produce d. Antibodies that act against specific antigens 2. Cell mediated immunity (CMI) a. T cell lymphocytes i. Recognize antigens ii. T cells are developed in thymus b. Provides resistance to abnormal eukaryotic cells: i. Euk m/o’s e.g. fungi, protozoa, parasites ii. Intracellularlyinfected cells/phagocytes iii. New Organs transplant rejection 1. Rejection due to new organs with foreign antibodies iv. Cancer 1. overwhelms T cells Antibodies Are immunoglobulins (lg) These are protein molecules that recognize & bind to antigens Each antibody is specific to one antigen: Yshaped molecule w/ 2 antigenbinding sites that are specific to the antigen Classes of antibodies lgG (8085%) Majority of circulating ab lgG come from mothers: cross the placenta to protect the fetus IgM (510%) Pentamer 1st to appear w/ new antigen, but short lived Next exposure to the same antigen is generally responded to with mostly lgG IgA (15%) Secretory antibody found in secretions (e.g. saliva, sweat, colostrum, mucous membranes, breast milk) IgD (2%) not much is known about it IgE (.002%) responsible for allergic reactions Antigenantibody interactions ● Neutralize toxins (by blocking off the active site) ● Inactivate viruses & bacteria by preventing these from binding to host cells ● Agglutination (agab complex) can enhance phagocytosis by coating antigens ● Start complement actions (cause cell lysis) Friday 4/22 Active T Cells 1. Helper T cells (T H a. Stimulates other T&B cells to react to an antigen b. Mainly where HIV infections found 2. Cytotoxic T cells (TC) a. Kills abnormal euk. Cells 3. Delayed hypersensitivity T cells (T D a. Attracts macrophages to specific location of concern b. Also triggers delayed allergic reactions Examples: Mantoux test Inject TB ag under skin If abs present reaction occurs Allergic contact dermatitis, eg latex, jewelry allergies Clonal Selection Theory ● Presence of a foreign antigen stimulates a specific response “selection” of counterspecific cell occurs ● Maturation of selected stem cells ● During presence of a foreign antigen, relevant cells become active B&T lymphocytes and “clones” of these are produced en mass SelfTolerance ● Elimination or inactivation of “antiself” B & T cell lines ● Occurs during fetal development ● If not: possibly leads to autoimmune disorders Monoclonal antibodies (mabs) Abs are very specific/unique, and this makes them a good tool for infection identification Ex: Hybridoma B cells interacting with tumor cells leads to production of hybridoma These generate antibodies commonly used for diagnosis (or therapy) Diagnostic Uses: rapid chlamydia test Uses antichlamydia abs Interacts with chlamydia ags (if present) and test indicates + Therapeutic uses: Humanized mabs (through a process of genetic engineering) ● Immune system suppressant: ○ Prevents transplant rejection ○ Can be used to treat allergic asthma, and in some cancer treatments Immunodeficiency Disorders Primary disorders genetic defects Secondary disorders infectious agents, leukemias, meds, radiation HIV/AIDS Acquired Immunodeficiency Syndrome (AIDS) Human Immunodeficiency Virus (HIV) ● Origin ~1908 in Central Africa: SIV trans to humans ○ Simian Immunodeficiency Virus (SIV) HIV 2 types of HIV: ● HIV1 most common worldwide ● HIV2 mostly occurs in West Africa (less virulent) Subtypes HIV1 has 11 subtypes ● 90% of US cases are HIV1, clade B HIV Structure ● Ss RNA genome ● Reverse transcriptase enzyme “Retrovirus” ● Helical capsid ● Enveloped ● Spikes gp120 “glycoprotein” Retrovirus ● Reverse transcription ○ generation of complementary DNA (cDNA) from RNA ○ This is then incorporated into the host cell’s DNA Life Cycle 1. Attachment a. Susceptible cells are CD4 cells b. Virus gp120 spike “fits” the cell’s CD4 antigens and CXCR4 (or CCR5) coreceptor i. Individuals without this coreceptor can be exposed multiple times without contracting the disease 2. Penetration a. Virus envelope fuses with the cell membrane 3. Reverse transcription a. Provirus b. Latent at this point c. Reverse transcription process has a very high mutation rate: i. A person may have more than 1 million variants during the asymptomatic stage, and 100 million variants during the symptomatic stage 4. Biosynthesis a. Synthesis of proteins & RNA 5. Maturation 6. Release: via budding Disease Progression Group 1: HIV infection In the first few weeks an exposed person experiences: ● High viremia (highest level of virus in blood at this stage, an exposed person is most infectious at this stage) ● May have flulike symptoms Immune Response: ● Abs made (over a few weeks) ● Test will indicate HIV + at this stage ● Most virus already cleared from blood Group 2: Asymptomatic ● Provirus ● Still test HIV+ & can infect others Group 3: Symptomatic Early symptoms: ● Swollen lymph nodes, rashes, mouth ulcers ● Cd4 cell count decreases ● These symptoms occur after years Advanced symptoms: more severe ● Fever, diarrhea, weight loss ● Infections: thrush (yeast), shingles ● Precancerous lesions (rarely) Group 4: AIDS ● Avg ~ 10 years after initial exposure without treatment ● AIDS indicator conditions AIDS victims often have indicator diseases and/or conditions that show up due to weakened immune system ● In fact, most AIDS deaths are due to opportunistic infections Fri 4/22 HIV Propagation ● 100 billion HIV’s made daily ● Each virus only lives 6 hours ● Most of these are produced by CD4 T cells ● These T cells survive for only 2 days (they normally live years) ○ This has critical impact in the health of the host ● Every day, 2 billion CD4 T cells are made to compensate ● Net loss of 20 million cells each day HIV Testing 1. Antibody tests a. An infected individual may not have produced antibodies early in the infection, which will affect the accuracy/results of these tests i. Rapid blood test (does not require extensive lab time) ii. “Home” test card to hold blood drop is mailed iii. Oral saliva test iv. Urine test (less accurate) b. 20% of HIV infected people are unaware of being HIV+ 2. Viral tests a. Cost more money and requires more time HIV Transmission Via body fluids: ● Blood ● Semen ● Vaginal fluid ● Breast milk ● NOT: saliva, urine, sweat, tears ● NOT: insect vectors, casual contact, fomites (except intravenous needles) ○ HIV very fragile outside of host body ● Congenital transmission infants of HIV+ mothers ○ 2025% of the time transmission occurs ○ Infected infants have less than 18 months to live ○ Drug therapy minimizes transmission Prevention & Treatment ● Minimize transmission ● Antiviral drugs ○ Various modes of action: ■ Inhibition of reverse transcription ■ Protease inhibitors ■ Block CD4 antigens ○ Issues with antiviral drugs: ■ Expensive ■ Toxic ■ do not cure patients, who are still infectious ■ some HIV strains are drugresistant ● HIV vaccine ○ Difficult to develop due to: ■ Too many virus variants ■ Uncertainty of how to deal with provirus ■ Ethical issues with testing ● Found vaccines lead to higher risk for contracting the disease ● Determined there were too many unknown factors about the virus to safely continue testing ■ Too many unknown factors ● Therapy ○ Complications or symptoms are treated ○ There is no cure Mon 4/25 & Wed 4/27 Movie: A Paralyzing Fear: The Story of Polio in America Under course reserves at MSU Library Disease: Polio disease/infection Poliomyelitis etiologic agent Poliovirus (caused by: name, type of m/o, S.s. RNA other characteristics) Enterovirus capsid reservoir where it is harbored humans naturally) mode of transmission to Fecaloral route humans (& susceptible people) pathogenesis (progression of ● Incubation ~335 days disease within body, virulence ● Poliovirus binds to CD155 receptor factors) ● This leads to viremia (virus in bloodstream) ● Virus circulates to other tissues and muscles, referred to as secondary viremia Complications: Virus enters CNS & replicates in motor neurons, causing temporary or permanent paralysis symptoms Viremia asymptomatic Secondary viremia Fever, headache, sore throat Paralysis, < 1% of cases Very rarely: respiratory arrest and death treatment/prevention/control Prevention: Vaccine several types ● Attenuated virus (first vaccine developed) ● Killed virus ● Live virus taken orally, generally used in developing countries due to ease of administering the vaccine Treatment: No cure, therapies focus on relieving symptoms Fri 4/29 Exam 4 Option
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