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BIOM 250: Week 11,12

by: Davis Notetaker

BIOM 250: Week 11,12 BIOM 250

Davis Notetaker
GPA 3.3

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About this Document

Notes on material covered weeks 11 and 12. Topics include: Adaptive Immunity, Immune System, Immunodeficiency Disorders Diseases: Measles, HIV/AIDS, Polio
Micro Hlth Sci: Infect Disease
Kari Cargill
Class Notes
Microbiology for Health Sciences: Infectious Diseases
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This 9 page Class Notes was uploaded by Davis Notetaker on Wednesday April 27, 2016. The Class Notes belongs to BIOM 250 at Montana State University taught by Kari Cargill in Winter 2016. Since its upload, it has received 15 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
Wed 4/20  Study showed Dyson brand hand dryers actually lead to ​ore​ potential spread of vaccines than  paper towels    News:  Zika Virus ­ emerging disease generating more concern as studies find it is easily transmissible  through mosquitoes and even person to person via sexual activity    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    Rubella aka German Measles  ● Highly contagious  ● Can be transmitted via nasal secretions  ● 1969 vaccine developed  ● Complications: congenital rubella syndrome    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 the ​one 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 th​​ymus  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 (T )  C 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)   ○ thought to have been transmitted via monkey hunting in Africa  ● 1980 AIDS first recognized as a disease   ● 1983 HIV identified as etiologic agent  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  ○ Can extend lives by years  ○ If caught early enough, daily use minimizes transmission  ○ 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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