Microbiology Exam 2

25 July 2022
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Are Viruses Living or Nonliving?
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They are only considered living when they are inside of a host cell, using their resources and energy. Outside of a host they are considered intert.
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When are Viruses considered to be "alive"?
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When they are inside of a host cell. When inside, their nucleic acid (ONLY RNA OR DNA) become active. *Virus replicates
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Obligatory Intracellular Parasites
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Require livinghost cell in order to multiply - Such as Viruses.
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Defining a Virus
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1) Contains 1 Nucleic Acid (DNA or RNA) 2) Protein coat surrounds the DNA or RNA 3)Multiply within host using host machinery ---because they don't have the ways of making/obtaining their own nutrients. like ATP or enzymes.
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Virus Characteristics
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*Some are enclosed by an envelope which consists of lipids, proteins, carbohydrates *some have spikes *only infect the cells of ONE host.
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Host Range
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The spectrum of host cells that a virus can infect. -invertebrates -vertebrates -plants -protist -fungi -bacteria The virus must be able to attach to a the particular host's cell. **Host range is determined b specific attachment sites on the host cell's surface
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Bacteriophages
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Bacteria that is infected by a virus
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How do Viruses attach to a host cell
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Through receptors on the host cell's surface. There must be an interaction.
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Capsid
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Protein coat that surrounds the Nucleic Acid of a virus. (not the whole virus itself. That's an envelope.) ****Made up of individualized Capsomeres**** *accounts for most of the mass of a viral cell.
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Capsomeres
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Protein subunits that make up a capsid (think of tiny balls that come together to make a huge coating around the Nucleic Acid) *capsomeres can be made up of multiple types of proteins or one single type of protein
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Envelope
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Surrounds the virus as a whole. *Synonymus to a somatic cell's Plasma Membrane. But around a virus. ***Composed of proteins, lipids and carbs. *Could be covered in spikes NOT ALL VIRUSES HAVE ENVELOPES
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Spikes
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Cover the envelope of the cell Composed of protein and carbohydrates. -Used for attachment to the host cell Spikes differ, and can be identified as different virus by the host body. That's why you can get the flu more than once a year, there's a change in spikes. -Can be used for identification for some virsus under microscope.
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Helical Capsid
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Long rods that are flexible and rigid These surround the Nucleic Acid. *Capsids are hollow cylinders surrounding the nucleic acid. *CAN OR CANNOT HAVE A ENVELOPE. Without envelope = they look like long noodles, because it's just the capsid and no sphereical shape WITH the envelope = they look like balls, but with their Nucleic acids all tangled inside.
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Polyhedrical Capsid
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These are icosahedron, and are 20 triangle shapes, with 12 corners. THEY CAN BE WITH OR WITHOUT ENVELOPE -Without envelope, you can see their individual caposomere and their many different triangular faces of the Capsid WITH envelope, they appear ordinarily spherical, and like a normal cell. (Some have spikes)
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Complex Capsid
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They have a variety of weird shapes within the one virus cell, and look just straight up weird. They can be bacteriaphages and just look mutuant
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Family names suffix for Taxonomy
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-viridae Ex. Herpesviridae
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Genus name suffix Taxonomy
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-virus Genus Simplexvirus Ex. Herpesvirus
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Viral species
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A group of viruses sharing the same genetic information and ecological niche (niche=host) Viral species are designated by descriptive common names, such as human immunodeficiency virus (HIV),
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Subspecies
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They are determined by the NUMBER that is attached to the specific genus of the family. These are viruses that can affect humans HIV-1, HIV-2
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Plaque
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Areas of clearing where the the virus has killed the bacteria
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PFU
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Plaque Forming Unit *Concentrations of viral suspensions measured by the number of plaques
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Cytopathic Effect
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CPE This is cell deterioration after a virus infects a monolayer of cells that appears to be growing just fine. The cells clump together as they deteriorate.
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Virion
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Complete, fully developed, infectious viral particle composed of nucleic acid and surrounded by protein coat that protects it from the environment and is a vehicle of transmission from one host cell to another. **AKA MATURE PHAGE
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Lytic Cycle
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The cycle that bacteriophages use to multiply. WHERE THE CYCLE ENDS WITH LYIS AND DEATH OF HOST CELL.
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Lysogenic Cycle
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The cycle that bacteriophages use to multiply. Where the host cell remails alive after the cycle.
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Phage Lysozyme
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Enzyme released by the bacteriophage tails to break down bacteria cell wall so they can enter the bacteria.
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Lytic Cycle of a T-Even Bacteriophage
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1) ATTACHMENT to bacteria cell wall by tail fibers to complementary receptor sites 2) ENTRY of viron DNA inside the bacteria, and the protein capsid is left outside of the bacteria cell 3) BIOSYNTHESIS goes underway to use the host machinery to interfear with host DNA synthesis, and makes the phage DNA instead 4) MATURATION is undergone when capsids are assembled around the DNA, and the "assembly line" happens to form the virions 5) RELEASE or LYSE happens when the new virions are released to infect other cells. The host cell does not survive through this cycle.
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Prophage
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The Virus and the bacteria's DNA combined into one.
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Oncogene
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a gene that can bring about malignant transformation *Also called a cancer causing gene
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Pathology
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Scientific study of disease "Patho" disease/suffering - Logos "study of/science" =Concerned with the changes brought by the disease and change it has on the body.
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Pathogenesis
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The MANNER in which a disease DEVELOPS
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Eitology
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The study of the CAUSE of the disease
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Koch's Postulates
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1) Same pathogen must be present in EVERY CASE of the disease (aka to be consistant) 2) Pathogen must be isolated from the disease host and grown in pure culture 3)Pathogens from the pure culture must cause the disease when it is incoulated into a healthy, suspetible lab animal and then cause disease 4) The pathogen must be isolated from the inoculated animal and must be shown to be the original organism - Both organisms infecting both host must match the kind of organism that is grown and extracted.
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Koch's Postulates
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Used to determine the causative agent for bacterial diseases
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Symptom
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SUBJECTIVE A change in a body function that is felt by a patient as a result of disease. -Subjective and not measurable by empircial data: PAIN.
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Sign
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OBJECTIVE A change in a body that can be measured and obsterved -Anything empirical: Lesions, fever, swelling
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Syndrome
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A specific group of signs and symptoms that accompany a specific disease
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Communicable Disease
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Any disease that spreads from one host to another, directly or indirectly.
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Contagious disease
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A communicable Disease that is EASILY spread from one person to the next.
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Non-communicable disease
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Not spread from one host to another *the microbes exist outside the body, and only produces disease when introduced inside *TETANUS*
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Incidence of a disease
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Number of people who DEVELOP and contract this disease within a certain period of time. *Diagnosed cases of HIV in 2009 alone
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Prevalence of a disease
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Number of people EXISTING WITH the particular disease at a given time. *Known cases of HIV at the point of year 2009 TAKES INTO ACCOUNT OLD AND NEW CASES FROM YEARS BEFORE
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Sporadic Disease
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Occurs only OCCASIONALLY *Typhoid fever within the US
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Endemic disease
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A disease that is constantly present in a population *Common cold
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Epidemic Disease
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If many people in a CERTAIN AREA acquire a certain disease in a relatively SHORT PERIOD of time. *Influenza, AIDS
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Pandemic Disease
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An epidemic disease that occurs worldwide *A worldwide Influenza, and AIDS
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Acute Disease
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A disease that develops rapidly but only last for a short period of time *influenza
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Chronic Disease
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Develops slowly, and the body's reactions might be less severe, but the disease is likely to continue to recur for long periods of time.
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Subacute Disease
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Symptoms between acute and chronic diseases - in the middle *Infection and bronchitis.
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Latent Disease
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Causative agents are inactive for long periods of time, then becomes active to produce symptoms *any latent viruses of the Herpesvirus family. Such as shingles or chicken pox that lay on the nerve cells.
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Herd Immunity
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When many immune people are present in a community When the number of people vaccinated goes UP, The chance of the risk to encounter the disease goes DOWN.
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Local infection
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Invading pathogens are limited to a small area of the body. *Boils and absecesses
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Systematic (generalized) infection
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Spread THROUGHOUT the body bu blood or lymph *measles
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Focal Infection
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Systematic infection that BEGAN as a local infection *Local infections can enter blood or lymphatic vessels and can spread to other specific parts of the body *can arise in areas such as teeth, tonsils, or sinuses
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Sepsis
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Toxic inflammatory condition arising from the spread of microbes from a focus of infection
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Septicemia
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Blood poisoning *multiplication of pathogens within the blood
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Bacteremia
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Bacteria in the blood
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Toxemia
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Presence of toxins within the blood
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Viremia
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Presence of virus in the blood
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Primary Infection
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Acute infection that causes an initial illness
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Secondary Infection
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Caused by opportunistic pathogen after immune system weakened by primary infection. Pneumonia is a consequence of AIDS, and is a secondary infection.
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Predisposing Factors
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Makes the body more suspectible to diease and may alter the course of disease. *gender (females have higher incidence of UTIs *genetic background ( inherited genes from parents like sickle cell anemia) *Lifestyle/Occupation *Climate/Weather Stress/Fatigue
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Subclinical Disease
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An infection that doesn't cause any noticiable illness Poliovirus and hepatitis A. You can carry it but you never contract it.
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Reservoirs of infection
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Can be human, animal, or nonliving
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carriers
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Those who carry the pathogens and transmit them to others without exhibiting any sign of illness
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Zoonoses
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Diseases that occur in wild and domestic animals and can be transmitted to humans *rabies *Lyme disease
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Noliving Reservoirs of Infection
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Soil AND Water. Bacteria strands can be found within them and contaminate them and then they can infect humans
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3 means of disease transmission
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1) Contact (by means of direct contact, indirect contact, or droplet transmission) 2) Vehicle (Transmission via a medium like food, water air, blood, bodily fluids, air) 3) Vectors (animals that carry pathogens to host)
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3 types of CONTACT transmission
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1) Direct Contact - Kissing touching hugging 2) Indirect Contact-Fomite(something normal infected) 3) Droplet transmission - microbes spread by coughing, sneezing, laughing, talking
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Pathogenicity
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The ability to cause disease by overcoming the dfense of the host
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Mechanical transmission
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Passive transport (fly landing on burger)
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Virulence
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The extent oe degree of pathogenicity AKA DANGER
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Biological Transport
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Active process. Mosquito biting an individual, giving malaria.
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Portals of Entry
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1) Mucous Membranes 2) Skin 3) Direct deposition beneith the skin or membranes - (the parenteral route)
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Epidemiology
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The study of when/where disease occurs and how disease is transmitted in populations **there is always an epidemiologist at each large hospital to prevent nosocomial diseases and keep them under control.
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Portal of Entry - Mucos Membrane
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Lining of GI Respiratory tract Genitoruitary tract, Conjunctiva (eyeball and the lining of it) Most common way is GI and Respiratory tract.
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Case Reporting
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Health care workers must report specified disease to local, state, and national offices -by doing this, (by law) this documentation raises awareness so the nation can prevent epidemics or a pandemic from occuring. *examples: AIDS, measles, gonorrhea tetanus, typhoid fever. CAN LEAD TO EDUCATION ABOUT ILLNESSES.
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ID(subscript)50
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ID= Infectious Dose Infectious dose for 50% of population ***How many endospores that are necessary to infect 50% of the population.
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Nationally Notifiable Diseases
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Diseases in which physicians are required by law to report.
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LD(subscript)50
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LD=Lethal Dose Lethal Dose (OF A TOXIN) for 50% of population.
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Morbidity Rate
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How many people are affected by disease
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Adhesin
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Also called a ligand that helps the pathogen adhere to the host cell in order to invade it *Located on the pathogen.
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Mortality Rate
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How many people have died resulting from this disease
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M Protein
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Surface Protein in Cell wall component of bacteria that helps with bacterial attachment to an epithelia cell Resists phagocytosis of WBC ***INcreases Virulence of the bacteria
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Microbial antagonism
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Competition for nutrients ****When normal microbiota can prevent pathogens from causing an infection
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Mycolic Acid (Waxy Lipid)
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A cell wall component that can prevent phagocytosis It can even multiply within the phagocyte
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Coagulases
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Form blog clots within the blood. An enzyme that a pathogen uses to clot the blood to prevent phagocytosis What causes Staph to be so deadly and prevent blood from flowing to parts of the body
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Collagenase
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Enzyme produced by bacteria. It breaks down the protein collagen and breaks down the connectrive tissue of muscles and other body organs and tissue.
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IgA Proteases
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Enzymes that the bacterial cell can give off to Destroy antibodies
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Antigenic Variation
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Antigens line the ouside of a bacterial cell for the attachment to the host cell. The body makes antibodies to attach to these antigens to destroy them and prevent their wrongdoing However, when pathogens alter their surface antigens, making the antibody that the body made unusable. THIS SNEAKY SNAKE MOVE IS ANTIGENIC VARIATION. By the time the immune response reaches a pathogen, the pathogen has already alters its antigens and is unaffected by antibodies. ***The flu does this
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Siderophores
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The iron sealing protein that bacteria use to attach to the iron tigher than the iron within the host cell's
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Toxic
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Substance that contributes to pathogenicity - creates disease *Poisonous substatnces that are produced by certain microorganisms ---They are transported through the body by blood, or lympth. CAUSE *Fever *Cardiovascular disturbances *diarrhea *Shock
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Toxigenicity
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Ability to produce a toxin
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Toxemia
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Presence of toxic in the host's blood
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Antitoxins
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Antibodies made within the host cell (humans) that can resist the presence of exotoxin (the proteins that are expelled from the gram positive cell)
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Toxoid
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A type of inactive toxin (that is changed by heat, or other chemicals) that a person can take that will up their production of antitoxins within the body) *Ex. are the Diptherioa and tetanus shots that can be used to avoid toxicity in the body.
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Exotoxins
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Causes damage to cell host A type of protein made inside of the pathogen. These exotoxins are then secreted into the surrounding metium, and then the cell dies. =Toxins made within the cell and EXO the cell, leading to its death First way that bacteria cells make toxins for the spreading of disease. GRAM POSITIVE
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Endotoxin
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Causes damage to host cell The LIPID portions of the outer membrane of cell wall. The exotoxins are liberated when the bacteria cell die and the cell walls break apart This is the second way that toxins are produced from bacteria cells GRAM NEGATIVE
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Membrane Disrupting toxins
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A type of toxin released from the pathogen that causes lysis of the cell by: 1) forcing the formation of protein channels in the plasma membrane, 2)DIsrupting the phospholipid bilayer of the host cell.
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Superantigens
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Causes an intense immune response due to release of cytokines from host cell. Such as: -Fever -Nausea -Vomiting -Shock -Diarrhea -Shock -Death An intense response could be that of Toxic shock syndrome or food poisoning.
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Endotoxins
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When a bacterial cell dies (from the presence of antibiotics) the cell membrane (since it is GRAM NEGATIVE, THE OUTTER PORTION AROUND THE PEPTOGLYCIAN) is destroyed, and sends out toxins during its death. These toxins are sourced from the LIPID portion of the membrane. Causes symptoms of a sickness to get worse, but they will soon get better after the toxins are eliminated. They can induce a miscarriage.
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Exotoxin
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Source - Gram + Relation to microbe - by products of growing cell Chemistry - Protein molecule Fever? No Neutralized by antitoxin? Yes LD(subscript) 50- Small amounts to make reaction
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Endotoxin
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Source: Gram - Relation to Microbe - Outer membrane Chemistry - Lipid A Fever? Yes Neutralized by Antitoxin? No (causes blood clotting) LD(subscript) 50? Relatively large, not as potent
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Cytopathic Effects
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Visible effects of viral infection (the visible effects are within the cell) 1) Stops mitosis 2)Inclusion bodies
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Inclusion bodies
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Granules found in cytoplasm or nucleus of some infected cells. These granuels make up the assembled parts of a viron
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Cytocidal Effects
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Kills host cell
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Non-Cytocidal Effects
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Doesn't kill the host cell, but does greatly damage it "Cyto" = Cell "Cidal" = Kill
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Ergot Toxin
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Comes from a Fungi Creates hallucinations and affects blow circulation similar to LSD
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Aflatoxin
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Toxin of a Fungi that grows on plants Found on peanut plants Can be found in peanut butter IS CARCINOGENIC
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Dingoflagellates
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A type of algae that is RED and is what shellfish eat. Whenever we eat shellfish, we can become sick from it because it ate the dingoflagellates that we get sick from. This domino effect produces SAXITOXIN.
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Saxitoxin
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A type of nerurotoxin that lead to people getting very sick from eating shellfish that have injested dingoflagellates
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Immunity
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The ability to ward off disease caused by microbes and to protect from environmental agents such as pollen, drugs, foods, chemicals, and animal dander Also called resistance
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Susceptibility
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Vulnerability or lack of immunity
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Three lines of defense
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1)Skin and mucous membranes 2)Defensive cells, inflammation, fever, and antimicrobial substances (WBC) 3)Specalized lymphocytes like T and B cells and antibodies
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Innate immunity
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Defenses against ANY pathogen *Present at birth *Will always have our whole lives Involves both FIRST (prevent entry) and SECOND (eliminate pathogens) line of defense
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Adaptive Immunity
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Immunity/Resistance to a CERTAIN pathogen *Uses the THIRD line of defense
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Lacrimal apparatus of Mucus Membrane
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First line of defense, as a mucus membrane Washes the eye (lacrimal is the tear component of eye) *washes eye to wash microbes from settling on your eye
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Mucus of Mucus Membrane
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First line of defense Trapes microbes in the respritory and GI tract by the gobulet cells that secrete and the pathogens that it catches by its sticky substance
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Hairs of Mucus Membranes
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First line of defence Hairs in ear and nose trap microbes and pollen and pollutents
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Saliva of Mucous Membrane
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First line of defense Washes off microbes from teeth and mouth
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Toxins NOT broken down by gastric juices
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Clostridum Staph
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Formed Elements
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Part of the Second line of defense: BLOOD The formed particles within the blood that's susupended in the plasma. 1)WBC (leukocytes) 2)RBC (Erythrocytes) 3)Platelets
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Granulated White Blood Cell
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1) Neutrophils - Function - Phagocytosis. -They are mobile, so they can reach the site of infec. -They are active in the initial site of the infection 2) Basophiles - Function - Produce histamine (Important for inflammation and allergic reactions) 3) Eosinophils - Function - Kills (mostly helminths) by producing toxic proteins. -They cannot injest the bad guy, so they surround it and kill it with its killey molecules
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Agranulated White Blood Cells
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1)Monocytes (Macrophages when mature) - *Function is phagocytosis *swelling of lymph nodes because the monocytes leave the blood and enter the tissues. 2) Dendritic Cells - Have long extentions to assist in phagocytosis 3)Natural Killer Cells - Destroy target cells (tumor cells)
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Neutrophils
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WBC Phagocytes.a Mobile. Leave blood to treat infection
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Basophiles
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WBC Produce Histamine for allergic reaction and inflammation
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Eosinophails
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WBC Kills parasites by surrounding the parasite and releasing toxins to kill it.
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Monocytes
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(Macrophages when mature) -WBC *Function is phagocytosis *swelling of lymph nodes because the monocytes leave the blood and enter the tissues.
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Dendritic Cells
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WBC - Have long extentions to assist in phagocytosis -Found in the epidermis to weed out the pathogens
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Natural Killer Cells
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WBC -Found in blood and bone marrow - Destroy target cells (tumor cells)
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Lymphocytes
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1. Natural Killer Cells 2. T Cells 3. B Cells
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Phagocytes in blood
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1) Macrophages-dominate in LATER phages 2) Dendritic Cells 3) Neutrophils -Dominate in INITIAL process of pathogen elimination
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Pseudopods
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Hairlike extentions that draw the bacteria closer to the phagocyte (like a macrophage) so it can engulf it
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Cytokines
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These are released once the phagocyte has attached to the bactieral cell. *these compounds are used to signal more phagocytes to come and help the digestion of these invaders
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Phagosome
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The enclosed, membranous wrapped and engulfed bacteria. It is then brought back INTO the phagocyte cell
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Pathogen Mechanisms to evade phagocytosis
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1) Capsules - inhibit attachment 2) Toxins - prevent injestion of bacteria 3) Biofilm formation - too high of population 4) Survival inside of the phagocyte - An enzyme is secreted to prevent formation of the phagolysosome, so, it stays alive within the phagosome
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Second like of defense
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1) Phagocytosis 2) Inflammation 3) Fever 4) Antimicrobial Substances
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Signs of inflammation
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1) Redness 2) Heat 3) Pain 4) Swelling (edema) 5) Loss of function (this is only in severely rare cases, depending on the site/size of infection
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Edema
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Swelling
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Abscess
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Inflammation of tissue due to pathogenic cells and other human cells in the site to prevent infection
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Chemical Substances released in site of injury
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Histamines and Kinins
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Fever
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Cytokines are sent to the brain to alert brain to release hormine molecules to "reset" body temperature via the HYPOTHALAMUS Fever; body increases its rate of metabolism, temperature rises, shivering occurs to try to increase the body temperature.
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Compliment Proteins
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Produced in the liver, they help/compliment both: *Innate immune system *adaptive immune system *******These proteins are potent so they must be activated for them to be effective.
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Cascade
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A series of steps that triggers the next protein to be activated from it's inactivated C protein state.
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C3
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Compliment Protein 3 Once activated, it helps with: -Inflammation -Phagocytosis -Cytolysis
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Inactive Compliment Proteins
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Any "C" protein witha number following Ex. C3, C4
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Active Compliment Protein
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The number and letter proteins must be split into two smaller fragments to be activated. Any "C" protein with a number and a subscript (smaller) number following it. C3a + C3b = C3
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C3b
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Attach to the outside of the cell, to be a kind of magnet to show the phagocyte where exactly to go to break down the bacteria. - This assists the process of phagocytosis. Breaks down C5
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C5a and C3a
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cause mast cells to release histamine, resulting in ENHANCED INFLAMMATION
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C5b, C6, C7, C8
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All bind together to make the the receptor (They come together to act like a magnet) to attract C9 to come to the cell to form the membrane attack complex, resulting in lysis of the cell.
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Membrane Attack Complex
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Formed by Compliment Protein 9, it "pokes a hole" in the transmembrane of the bacteria, and then causes the cell to lyse with the opening in it. They result in Cytolysis
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Cytolysis
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What happens (the cell lysing) after the Membrane Attack Complex (MAC) has penetrated the bacterial cell
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Serological tests
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A test to determine what kind of virus it is based on its reaction with antibodies
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B Cell
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Lympocyte that matures in the Bone Marrow *Recognizes the different antigens and makes specific antibodies against the bad antigens. *Connected to Humoral Adaptive Immunity *has antibodies ON ITS SURFACE
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T Cells
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Lymphocytes that are mature under influence of thymus *They secrete cytokines instead of antibodies. Cytokines are chemical messengers hat give instructions to other cells to preform certain functions *Connected to Cell mediated Adaptive immunity
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Antigens
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1) Proteins 2) Polysaccharides When Nucleoproteins or lipoproteins combine with the proteins or polysaccharides,t hey can act as though they are antigens ANTIGENS ARE COMPONENTS OF THE CELL WALL, AND IT IS THE "MARKER"
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Antibodies
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A PROTEIN made in RESPONSE to an antigen. The "Y" like projections that are the missing puzzle piece for the antigen and fit together.
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Lymphocytes
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B and T cells Both are found in the lymph nodes. They might be differentiated in different places (bones and thymus) but, they are still going to be released from your lymph nodes (that's why they swell when you're sick, they're sending out these B and T cells)
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Variable (V)
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Found on the distal "Y" end of the antibody, their stucture reflects the nature/structure of the antigen for which they are specific for - they are specific to the two antigen binding sites found on each antibody monomer
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IgM
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*Antibody (Ig) *"M" to describe "macro" which means large in size. *It is a pentamer, so 5 monomers joined together at J chain *It is large, so it cannot easily move around. It is simply in the blood, and found in the circulatory system since it cannot move so quickly into tissues. *First molecule to be found after an antigen exposure, so it's the first antibody to be available to react to this foreign antigen. *most effective antibody to use aggulation and to promote phagocytosis. *It is a great clumping agent - perfect for agglutination.
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IgG
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Gamma=Deep penetrating=Galloping horse=QUICK *Most common found in serum - 80% *They pass through the walls of blood vessels to enter tissue fluids in cases of inflammation. Meaning they are the ones that cross the placental layer from mother to fetus by using passive immunity *They move rather quickly *They appear after the IgM (because they're moving to more places than just within the cardiovascular system) *IgGs are found to enhance phagocytosis by opsonization
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Opsonization
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Bacteria is coated with the antibodies, which enhances the ingestion and lysis through phagocytosis. Hammock like cradling effect where the antigens are bonded to antibodies within the phagocyte, cradling it so it is suspended within the phagocyte. Found in IgGs
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IgAs
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Antibody - DIMER STRUCTURE *Found in secretions (saliva, tears, mucus, breast milk) *They are responsible for newborn protection against GI pathogens by colostrum *Neutralizes the entry of pathogens through the mucous membrane (because they're secreting stuff all the time) Breast feeding = A = Awesome = IgA
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Agglutination
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Antibodies are used to clump antigens together, therefore bonding them seperate bacterial cells together. By having them in a clump, they are easier to be consumed by phagocytosis. Antibodies IgM are used to do this because of numerous binding sites, they are more active at clumping.
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Compliment system
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IgG or IgM antiobodies can trigger this *Causes lysis of the cell
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Neutralization
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IgG antibodies inactivate inactive microbes by blocking their attachment to host cells. Prevents toxins, bacteria, and viruses from attaching.
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Serology
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The study of reactions between antibodies and antigens What is happening in the serum, so called Serology
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Antiserum
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Serum=antiserum Antiserum contains antibodies Not like antitoxins and toxins, where they are opposites of one another
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Gamma Globulin
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Contains most of the antibodoes, and is often used to transfer passive immunity (passing of antibodies from mother to infant)
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Immunoglobins
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Antibodies that are involved in the immune response AKA ANTIBODIES
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T-Cell DEpendent activation
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There are extracelllular antigens that are chilling out in the middle of no where. They are going to be taken inside the B cell, and then the antigen combines with the Major histocompatiblity complex (MHC) They are combined, the put back on the surface of the B cell, to be displayed on the surface. Because this is displayed on the outside of the B cell, it attracts the Thelper cells and then the antigen fragment (of the antigen and the MHC) is binded to the T(h) cell. By the Thelper cell and the B cell being combined, the B cell is activated. The T cell releases cytokines, which is what ACTUALLY activates the B cell. By the B cell being activated, it forms the CLONAL EXPANSION. This then produces the plasma cell which produces antibodies. Boom. ***The first antibody that is produced is IgM, followed by IgG. This is the process of T Dependent antigens.
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Class switching
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Also called isotype switching. This is the later types of antibodies being made from the plasma cell of the B cell
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Clonal Expansion
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More B cells being made and producing more antibodies
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Clonal Selection
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Selecting whether the B cell should be a memory cell or a plasma cell.
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Activation of B cells occurs...
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Within the lymph tissue. That's where the antigens are and all the immunity components are held.
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Memory Cells
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Have to be stimulated to make antibodies, when plasma cells are making them continiously.
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Primary response to infection
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Slow reacting. Primary, meaning this is the first time it's been encountered or interacted with. It is slow reacting because it needs to undergo clonal expansion = make plasma cells = make antibodies to this particular antigen that it is encountering for the first time.
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Secondary Response to infection
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Is faster. Since it is the second contact with the same antigen, it has the memory component, so it can react and defend itself faster than if it was the firs time approaching it.
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T INdependent activation
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The bacterial cell has a capsule, that has polysaccharides and fatty lipids on the outside of its capsule. This leads to less specificity of binding sites from the epitopes on the bacterial cell wall to the B cell receptor sites. this means that there's no need for a T-Cell to help. There is no memory cell formed, and INdependent is a weaker immune response than a T DEpendent activation
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What do T Cells do?
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T Cells are responsible for fighting pathogens that are within the host cell and cannot be easily accessed by the B cell antibodies (plasma or memory cells). *Responsible for having an organ reject because they identify the cells and the tissues as "foreign" ---also getting rid of tumor cells
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T cell maturation
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They first develop from stem cells WITHIN the bone marrow, and then they lead to the thymus for maturity. They are weeded out, and then the completely mature T cells are sent to the lymphatic tissue where they will most likely see antigens.
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Difference in receptors on surfaces
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B cells = antibodies on their surface. T Cells - T Cell receptors on surface
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How are T cells activated?
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Antigen presenting cells (APC) ^^ help in binding T cells to to antigen
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How are T Cells activated?
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Similar to how a B cell ingests the antigen to convert it into an MHC (major histocompatibility complex) on the surface of the cell for the T cell, this also happens. But instead, an APC (Antigen Presenting Cell), such as a macrophage or a dendrytic Cell will bind the antigens within. The MHC (Major Histocompatibility Complex) will bind with the antigen. This joint of MHC and antigen is present on the outside of the APC and will be joined by a T(h) cell to join it to the T helper cell.
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Payer's Patch
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Located on the intestinal wall of the gut. *it is a specalized type of lymphoid tissue that *Under the M cells
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M cells
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Take up antigens from intestinal tract. Located above the Payer's Patch They then transfer the antigens to the APC's (antigen presenting cells of T-Cell activation) and lymphocytes.
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Cytotoxic T Lymphocyte (CTL(
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A type of (ACTIVATED) lymphocyte that is in charge of killing tumor cells, and transplanted tissue. They lyse only a cell that is known to have a virus or a tumor or something in it like that. "foreign things" They are involved in attacking a "target cell" which might be a tumor or one that is virally infected 1) Releases perforin that causes pores in the target cell. This is similar to the compliment system in which the C9 makes a hole in the target cell, causing lysis 2)The cell undergoes apoptosis - death of a cell - because it is lysed
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Natural Killer Cells
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They are involved with Antibody-dependent Cell-Mediated Cytotoxicity, and they attack the large pathogenic cell on the OUTSIDE to engulf it.