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BIOM 250: Week 10,11 Notes

by: Davis Notetaker

BIOM 250: Week 10,11 Notes BIOM 250

Marketplace > Montana State University > Biology > BIOM 250 > BIOM 250 Week 10 11 Notes
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About this Document

These notes cover lecture topics from weeks 10 & 11 following the last exam: Innate Host Defenses Adaptive Host Defenses Vaccines Diseases: TB
Micro Hlth Sci: Infect Disease
Kari Cargill
Class Notes
Microbiology, Infectious Diseases
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This 9 page Class Notes was uploaded by Davis Notetaker on Friday April 22, 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 10 views. For similar materials see Micro Hlth Sci: Infect Disease in Biology at Montana State University.


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Date Created: 04/22/16
Mon 4/11  Innate Host Defenses ­ Part 1  Terminology  Innate host defenses ­ nonspecific defenses  Adaptive defenses ­ specific defenses  Host Defenses Overview  The body has many types of mechanisms for defense.  Host defense types include:  Physical, chemical, cellular, inflammation, fever, molecular    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”)   Below shows normal levels of WBC presence, a Diff count measures how close/far from normal  an individual’s count is, with a greater count indicating the presence of a pathogen  ● Neutrophils 40­75%  ● Lymphocytes 20­45%  ● Monocytes 2­10%  ● Eosinophils 1­6%  ● Basophils 0­1%     WBC mnemonic:  Never Let​o​nkeys​​ tBananas:  Neutrophils  Lymphocytes  M​onocytes  Eosinophils   B​asophils      Fri 4/15  Innate Host Defenses ­ Part 2  Disease: Tuberculosis  TB is an ancient disease (tubercular decay has been found in remains of Egyptian mummies)  Historically has gone by other names: “consumption”, “white plague”  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   Tuberculosis Impact  ● ⅓ people are infected worldwide (9 million new cases/year)  ● TB is the leading killer of those afflicted with HIV   ● Historically TB was a major killer in US & Europe:   ○ ~10,000 new cases in US in 2013  TB Politics  Continued TB problem in US is often more of a political problem than a problem of insufficient  resources  Political policies cut down TB funds   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    Misconception  Fact  Improvement of hygiene and sanitation had  Diseases only disappeared after the use of  already begun to suppress disease before  vaccines  vaccines were introduced  The US has been virtually wiped of  This threatens herd immunity, and does not  vaccine­preventable diseases, so there is no  protect against disease exposure from  need for children to be vaccinated  traveling, immigration, emerging diseases  and other diseases that still circulate the US   Children receiving multiple vaccinations for  Vaccinations do have an associated risk, but  different diseases at the same time is  risks of vaccination have to be considered  associated with an increased risk of harmful  against the risk of disease. See Risk from  side effects and can overload the immune  Disease vs Risk from Vaccines below  system    Risk from Disease vs Risk from Vaccines  Risk from Vaccine  Risk from Disease  MMR  Measles  ● Can cause encephalitis or severe  ● Pneumonia occurs in 6/100 cases  allergic reactions in 1/1,000,000  ● Encephalitis occurs in 1/1,000 cases  cases  ● Death occurs in 2/1,000 cases  Rubella  ● Congenital Rubella Syndrome: 1/4  cases  DTaP  Diphtheria  ● Continuous crying, followed by full  ● Death occurs 1/20 cases  recovery occurs 1/1,000 cases  Tetanus  ● Convulsions or shock, followed by full  ● Death occurs 2/10 cases  recovery occurs 1/14,000 cases  Pertussis  ● Pneumonia occurs 1/8 cases  ● Acute encephalopathy occurs 0­10.5 /  ● Encephalitis occurs 1/20 cases  1,000,000 cases  ● Death occurs 1/200 cases    Vaccine ­> Autism “Hoax”  ● 1998 paper by Wakefield was published linking MMR vaccine & autism in 12 UK children  ● His experiments were not reproducible, and 10/12 co­authors retracted the published  findings  ● 2004 Wakefield was under investigation, and the investigation found that the paper was  likely motivated by a conflict of interest, to support a patented single measles vaccine  ● 2010 Wakefield was banned from medical practice in UK  ● The paper was declared fraudulent in Feb 2011  Consequences  ● Roughly 95% vaccination coverage is required to achieve herd immunity  ● In 1988, up to 92% of UK pop had the MMR vaccination and measles was  declared “under control”, with 56 measles cases each year   ● After the paper, less than 80% of the population was receiving MMR vaccination  ● Then in 2008 a measles endemic broke out with 1348 cases each year and  resulting in 2 deaths    Thimerosal Concern   “Thimerosal is a mercury­based preservative that has been used for decades in the United  States in multi­dose vials (vials containing more than one dose) of medicines and vaccines.  There is no evidence of harm caused by the low doses of thimerosal in vaccines, except for  minor reactions like redness and swelling at the injection site. However, in July 1999, the  Public Health Service agencies, the American Academy of Pediatrics, and vaccine  manufacturers agreed that thimerosal should be reduced or eliminated in vaccines as a  precautionary measure.”  CDC ​[1]    Just a ‘nod’ to significant achievement:  Maurice Hilleman (1919­2005): Accredited with major contributions to a safer society   ● Behind the development/improvement of more than 40 vaccines: measles,  mumps, rubella, hep A, hep B, chickenpox, meningitis, pneumonia, influenza,  Marek’s disease (in chickens)  ● Discovered the viruses hep A and rhinoviruses  ● Discovered antigenic shift and drift in influenza     [1] “Thimerosal in Vaccines Thimerosal | Concerns | Vaccine Safety | CDC.” [Online].  Available​ [Accessed:  18­Apr­2016]. 


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