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UF / Biology / MCB 2000 / What are the differences between natural, and semi-synthetic antibioti

What are the differences between natural, and semi-synthetic antibioti

What are the differences between natural, and semi-synthetic antibioti

Description

School: University of Florida
Department: Biology
Course: UF Microbiology
Professor: Abdolkarim asghari
Term: Spring 2016
Tags: immune system, antibiotics, Vaccines, and Environment
Cost: 50
Name: MCB2000: Exam 4 Study Guide
Description: Study guide questions for the final exam.
Uploaded: 04/21/2018
37 Pages 13 Views 22 Unlocks
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MCB2000- Exam 4 Study Guide


What are the differences between natural, and semi-synthetic antibiotics?



1. What are chemotherapeutic agents?  

• Chemotherapeutic drugs: any chemical used to treat any kind of disease;  medicine that you take  

• Antimicrobial chemotherapy: chemotherapeutics that are against  microorganisms  

• Chemotherapeutics  

o All of the chemicals you take to prevent against disease

• Chemotherapeutic agents  

o Drugs/ chemicals that treat human diseases (combat disease in the body)  ▪ Lung disease, heart disease, infectious diseases, etc.  

2. List the characteristics of an ideal antimicrobial drug?  

• Must have selective toxicity; non-toxic to the host  


What is beta-lactam ring?



o Antibiotics, antifungal, anti-protozoan  

• Microbicidal rather than microbistatic  

o Microbistatic only stops the growing; does not kill them  

o Microbicides- kills them  

• Relatively soluble; functions even when highly diluted in body fluids  o Must be absorbed in order to be used in the body  

• Remains potent long enough to act and is not broken down by the body  prematurely  

• Does not lead to development of antimicrobial resistance  

• Complements or assists the activities of the host’s defenses  

• Remains active in tissue and body fluid  

• Readily delivered to the site of infection  


What are chemotherapeutic agents?



• Reasonably priced  

• Does not disrupt the host’s health by causing allergies or predisposing the host  to other infections  If you want to learn more check out What is the meaning of sexual selection?

3. What are the differences between natural, and semi-synthetic antibiotics?  • Semisynthetic drugs: originally isolated from natural resources, but are modified  in the laboratory  

o When making Penicillin- use the natural base and slightly alter it  

o Semisynthetic penicillin is made in the lab by adding different side chains  onto the beta lactam ring made by fungus  

o Resistant to penicillinases and have broader spectrum of activity than natural  penicillin  

• Synthetic drugs: drugs produced entirely by chemical reactions; not made by any  organisms naturally  

• Antibiotics- chemicals that are produced naturally by fungi and protozoa  o Discovered this and now we make our own antibiotics  We also discuss several other topics like melanocytes are nerve cells that function in touch reception

• Natural antibiotics  

o Natural penicillin produced by penicillium are effective against gram-positive  cocci and spirochetes

4. List sites on infectious agents that could be used as a target for antimicrobial agents  • Actions of various physical and chemical agents upon the cell  

o Cell wall is one of the best targets on a microbial agent  

▪ Made of peptidogelygen  

▪ Unique to bacteria  Don't forget about the age old question of which of the following are tabular, intrusive bodies?

▪ Not all bacteria have a cell wall- if there is no cell wall these chemicals will  not affect them  

o Cell membrane  

▪ If it is disrupted the cell will immediately die  

▪ Problem- there are lot of similarities between cell wall of bacteria and  humans  

▪ Not the best target for bacteria  

▪ One of the better targets with fungi  

o look for selective toxicity  

▪ body identifies targets in the infectious agents that are absent in the  human host  

o cellular synthesis  

▪ if we can find processes/pathways that are specific to the microorganism,  we can target those pathways to stop cell synthesis  

o protein synthesis  

▪ completed in the ribosome

▪ ribosome of prokaryotes are different than the ribosome of eukaryotes  because they are different sizes  If you want to learn more check out What is the plate tectonics?

o DNA and RNA are also good targets  

▪ Target replication so the cell can’t replicate  

▪ Target transcription- cell can’t make RNA  

▪ Target translation- cell can’t make protein  

• Targets when trying to damage bacteria  

o Cell wall

o Cell membrane  

o Metabolism  

o Protein synthesis  

o Nucleic acid (DNA and RNA)  

• first target of antibiotics is the cell wall  

o Beta lectin ring- main structure of penicillin-based antibiotics  

o Penicillin G and methicillin

o Methicillin produced when they found out a lot of bacteria were resistant to  penicillin G  

o Now there is staph that is resistant to methicillin  

o Bacteria break down the ring and then the antibiotics don’t work anymore  ▪ Issue with MRSA  

o Cell wall has peptidoglycan- affected by beta lectin ring  

• Fungi have no cell wall made of peptidoglycan

o Can’t use penicillin If you want to learn more check out intermediate algebra study guide

o Azoles and polyenes affect the function and synthesis of ergosterol  (component of cell membrane of fungi)  

o We don’t have ergosterol so this is a good way to fight fungi  Don't forget about the age old question of refers to characteristics that we recognize as constant, recurring, or coherent.

o Polyenes effect function

o Azole effect synthesis  

• Viruses are obligate intracellular pathogens  

o Use the host mechanisms to multiply and grow

o Use the host for replication, transcription, translation  

o Not easy to use antibiotics- don’t work against viruses  

o Attack attachment- don’t allow virus to attach to a cell  

o Fighting HIV- prevent entry  

o Acyclovir against herpes  

o AZT prevents reverse transcriptase which converts RNA of virus into DNA  5. What is Beta-Lactam ring? Which group of antibiotics contain beta lactam ring?  • Penicillin- target cell wall synthesis  

o MRSA is resistant  

o Has beta lactam ring in structure- responsible for the way that penicillin  reacts  

o Methicillin has the same beta lactam ring structure  

▪ Semi-synthetic drug  

▪ MRSA: methicillin- resistant staph aureus  

o Amoxicillin has the structure  

o Penicillin G is the original antibiotic produced by the fungi  

o Every version of penicillin has a common structure and then something  added to it  

▪ Allows us to use the antibiotic longer and reduce resistance  

• Beta lectin ring- main structure of penicillin-based antibiotics  

• Penicillin G and methicillin

• Methicillin produced when they found out a lot of bacteria were resistant to  penicillin G  

• Now there is staph that is resistant to methicillin  

• Bacteria break down the ring and then the antibiotics don’t work anymore  o Issue with MRSA  

• Cell wall has peptidoglycan- affected by beta lectin ring  

6. Why ribosomes are excellent targets against many infectious diseases  • Target protein synthesis  

o We have different sized ribosomes than the prokaryotic ribosome (70s vs  80s)  

• protein synthesis is an important target  

o size and composition of ribosomes differs from humans to bacteria  7. Which groups of microorganisms produce antibiotics and why?  • Antibiotics: chemicals against bacteria  

o Some fungi make antibiotics to kill the competition

o Penicillin is made by the Penicillin G fungi  

• Antibiotics- chemicals that are produced naturally by fungi and protozoa  • Fungi produced antibiotics to protect their food supply (dead plant materials)  8. Describe the mechanism of action and name different antibiotics discussed in this  course  

• Mechanisms of drug resistance  

o Modify the drug  

o Prevent the drugs from getting in  

o Bypass your pathway and go to a detour  

o Goal is to not let the drug affect your body processes  

• Cromolyn, theophylline, epinephrine- mechanisms of action of some drugs used to  treat type 1 hypersensitivity  

• Mechanisms of resistance  

o May break down the drug, pump the drug out, inactivate the drug, use an  alternative pathway  

• Penicillin- target cell wall synthesis  

o MRSA is resistant  

o Has beta lactam ring in structure- responsible for the way that penicillin  reacts  

o Methicillin has the same beta lactam ring structure  

▪ Semi-synthetic drug  

▪ MRSA: methicillin- resistant staph aureus  

o Amoxicillin has the structure  

o Penicillin G is the original antibiotic produced by the fungi  

o Every version of penicillin has a common structure and then something  added to it  

▪ Allows us to use the antibiotic longer and reduce resistance  

• Cephalosporium – target cell wall synthesis  

• Basitracian- does not affect cell wall synthesis, but effects the transport of the  cell wall to the outside of the cell  

o Cell wall synthesized inside the cell and then carried over to the outside  • Streptomycin- affects protein synthesis  

• First antibiotics that was discovered was penicillin by Alexander Fleming o Penicillin notatium created by fungi  

• Tetracycline- antibiotic that targets protein synthesis  

• Vancomycin- targets cell wall synthesis  

o Different than penicillin and cephalosporium  

o Used to treat MRSA  

o Does not have the beta lactam ring structure so it can work against MRSA  • Antimetabolites  

o Man-made chemicals  

o Sulfa drugs  

o Sulfonamide- target folic acid synthesis

▪ Targets A to B part of the pathway  

o Trimetoperine- target folic acid synthesis  

▪ Targets a different place than sulfonamide  

▪ Target C to D part of the pathways

• Translation and transcription- RNA  

• Replication- DNA  

• Ceprophiloxicine- targets DNA gyrase (holds the DNA together)  

o Gyrase loses control of the DNA and cannot control it which affects  replication  

• Riphampacine- affects the RNA synthesis  

• Polymyxin- cell membrane drugs  

9. Which of the above antibiotics inhibit: cell wall, cell membrane, protein/DNA/RNA  synthesis  

• Cell wall  

o Penicillin  

o Amoxicillin  

o Methicillin  

o Cephalosporium  

o Basitracian (effects transport of cell wall to outside of the cell)  

o Vancomycin  

• Cell membrane  

o Polymyxin  

• Protein/DNA/RNA synthesis  

o Streptomycin (protein)  

o Tertracyclin (protein)  

o Ceprophiloxicine (DNA)  

o Riphampacine (RNA)  

• Explain the rationale behind the use of antimetabolites such as sulfa drugs and  trimethoprim in treating bacterial infections.  

o Sulfa drugs target metabolic activities  

o Sulfa drugs  

o Sulfonamide- target folic acid synthesis  

▪ Targets A to B part of the pathway  

o Trimetoperine- target folic acid synthesis  

▪ Targets a different place than sulfonamide  

o Target C to D part of the pathways

o Target folic acid synthesis- needed to create proteins, DNA and RNA  o Sulfa drugs are similar to para-aminobenzoic acid (precursor to folic acid)  o Sulfa drugs competitively bind with enzyme meant for PABA -> block folic  acid production  

• Why folic acid synthesis is a good target for antibiotics.  

o Bacteriostatic drugs- don’t harm humans

o Good target for antibiotics because humans take up folic acid in the diet, we  don’t synthesis it ourselves  

10. How UV light radiation damages bacteria? How X-ray and Gamma rays damage the  DNA  

• UV light  

o Damages the cell by forming dimers

o Fuses the two Ts together- they bond together and are no longer recognized  as two separate Ts  

o Doesn’t look like any of the base pairs and then your cells don’t know what  they should put instead  

▪ Causes mutations  

o Damage is superficial- won’t result in internal cancer  

▪ Need to go to shade every once in a while, to allow the skin to repair itself  • Gamma rays

o Break the chromosome in half and the damage is irreversible  

o Deeply penetrated into the tissue and cause cancer  

• Radiation is a physical way to damage the cell  

o UV light, X-rays and gamma rays  

o UV light causes thymine dimer- fuse two thymines together  

o Gamma rays and X-rays break chromosomes- more harmful than UV light  11. Define selective toxicity. How this is a problem with developing anti-viral and anti fungal drugs.  

• Characteristics of the ideal antimicrobial drug/ chemical  

o Must have selective toxicity- non-toxic to the host  

o identifies targets in the infectious agents that are absent in the human host  • No drugs and treatment for a lot of viruses  

o They are obligate intercellular pathogens- find host, go in host  

▪ If it goes into the body and doesn’t enter the cell it won’t cause you harm  ▪ Presence of a virus in your blood is not toxic, only when they enter a cell  o No membrane, no cell wall, no protein synthesis, no transcription  o Rely on the host- the host does everything for them  

• Antiviral drugs  

o Viruses are obligate intracellular pathogens  

o They go inside human cells and they have to use the host for their functions  ▪ Use host enzymes for transcription, translation and replication  

o Not a lot of choices when there is a virial infection

o Supportive therapy: not curing the disease, just alleviating the symptoms  o Stop the virus by preventing the penetration into the host  

o Un-coating is a good target  

o Inhibit replication of the virus

o Prevent the virus from assembling  

• Antifungal drugs

o So much toxicity- there is a lot of similarity between these cells and human  cells  

12. List the mechanisms by which bacteria develop resistance and spread the resistant  genes to other bacteria.  

• Drugs become resistant  

• Penicillin

o Beta lactamase breaks down the beta lactam ring and the drug doesn’t work  anymore  

• A drug must enter a cell to be effective  

o Microbes modify their surface molecules, so the drug cannot enter  o Change the target of the drug  

• Pump drug out so the drug does not accumulate inside the cell  

• Microbial cell changes the way it operates inside  

• Makes an alternate metabolic pathway  

o Make a detour  

• Mechanisms of drug resistance  

o Modify the drug  

o Prevent the drugs from getting in  

o Bypass your pathway and go to a detour  

o Goal is to not let the drug affect your body processes  

• Spreading resistance  

o random genetic mutations spread horizontally through conjugation or  transduction  

o Carried by plasmids or small segments of DNA (transposons) which can jump  from one DNA piece to another  

o Mutation is acquired and transmitted through normal reproduction  o Survival of the fittest -> more antibiotic resistant bacteria  

13. Give examples and mechanisms of action of anti-fungal and anti-viral drugs discussed  in lectures.  

• Agents used to treat fungal infections  

o Chitin cell wall in fungi  

▪ Can’t give penicillin  

o Cell wall has ergosterol- target of drugs  

o Macrolide polyenes and Azoles are the two classes of antifungal drugs  o Macrolide polyenes  

▪ Amphotericin B  

▪ Works against ergosterol

• Binds to the fungal membrane and makes it leaky  

o Azoles  

▪ Ketoconazole, fluconazole, miconazole, and clotrimazole  

▪ Work against ergosterol  

• Interferes with sterol synthesis in fungi

o Cells are very similar to humans in many ways which makes it hard to target  them  

▪ Similar metabolic activities, eukaryotes

▪ Most of these drugs are superficial because they should not be take  internally  

▪ Can have a lot of side effects because of the similarity these cells have to  humans  

• Actions of antiviral drugs  

o No drugs and treatment for a lot of viruses  

▪ They are obligate intercellular pathogens- find host, go in host  

• If it goes into the body and doesn’t enter the cell it won’t cause you  harm  

• Presence of a virus in your blood is not toxic, only when they enter a  cell  

▪ No membrane, no cell wall, no protein synthesis, no transcription  ▪ Rely on the host- the host does everything for them  

o Some viruses have their own enzymes for replication, but this is a unique  scenario  

o Enfuvirtide (Fuzeon)

▪ Prevents the entry of the HIV virus into the host  

o Inhibition of nucleic acid synthesis  

▪ Acyclovir are structural analogs  

▪ Mimic the structures that allow the virus to make their own DNA  ▪ Mimic A and G- purine analog  

▪ Most effective against the herpes virus  

o Ribavirin  

▪ Purine analog, used for respiratory syncytial virus (RSV) and some  hemorrhagic fever viruses  

o AZT- affects the synthesis of HIV  

▪ Affects reverse transcriptase

▪ RT inhibitor  

o Inhibition of viral assembly and release  

▪ Virus produces a large piece of protein that has to be chopped into small  pieces and must be used to assemble a new virus  

▪ Need protease in order to chop the HIV protein into small segments to be  incorporated into the viruses  

▪ Protease inhibitors can stop proteases from chopping up these proteins  o Treat HIV with a combination of RT inhibitors and PI inhibitors  

▪ HIV always is mutating so these drugs might not always work  

o We don’t have a lot of options with viruses  

14. Define sterilization, decontamination, and sanitation.  

• Sterilization  

o Refers to killing all life forms

o Removing all viable microorganisms and viruses- some organisms are killed  faster than others.  

o Some have endospores- dormant form of life  

▪ Makes it harder to kill them; most difficult to kill of all living things  o Sterilization kills all life forms (including endospores) and viruses  

o Boiling water will not kill endospores and some viruses  

• Disinfection

o Physical process of killing microorganisms and pathogens  

o Killing through the use of chemicals  

o Remove the toxins and the organisms  

o Can’t be used on the human body- usually used on inanimate objects  • Decontamination  

o Neutralization or removal of dangerous substances, radioactivity, or germs  from an area, object or person  

• Sanitation  

o Condition relating to public health (cleaning drinking water and sewage  disposal)  

15. List the microbes according to their resistance to physical and chemical agents. Know  the specifics of each group of organisms that make them more resistance to chemical  agents (slide 3).  

• Most to least resistant  

o Prions  

▪ Infectious proteins, CJD, Mad Cow disease  

▪ Example: with mad cow, the disease can live inside the meat even when it  is cooked  

▪ Acellular and hard to destroy  

o Endospores  

▪ Dormant forms of life  

▪ Produced by bacillus and clostridium  

▪ Bacillus causes anthrax  

▪ Clostridium causes CDAD, gangrene  

o Staph and pseudomonas  

▪ Organism that causes opportunistic infection  

▪ Has porins- channels that go into the organism  

▪ Makes it hard to kill pseudomonas with chemicals  

o Protozoan cysts  

▪ Cyst is a transmission form  

▪ When it gets into your body it turns into torphozoites  

▪ Harder to kill than bacteria, viruses or fungus  

o Protozoan trophozoites  

o Most gram-negative bacteria  

o Fungi and fungal spores  

o Most gram-positive bacteria  

o Enveloped viruses

▪ Easiest to kill out of all entities  

• Gram negatives are harder to kill than gram positives  

• Why gram-negative bacteria are generally more resistant to chemicals than  gram positive bacteria?  

o Gram negative are more resistant to chemicals than gram positives  ▪ They have porins- channels that prevent the chemical from entering the  bacteria (additional layer)  

16. Name a specific gram-negative bacteria that is very resistant to killing by chemicals,  and it is a major cause of opportunistic infections in hospitals.  

• Staph and pseudomonas  

o Organism that causes opportunistic infection  

o Has porins- channels that go into the organism  

o Makes it hard to kill pseudomonas with chemicals  

17. List the physical, chemical and mechanical methods of control of microbial growth?  What are the differences between disinfectants and antiseptics?  

• Physical  

o Dry heat- oven  

o Radiation- ionizing radiation that is deep and penetrating or non-ionizing o Wet heat- autoclave or boiling water  

o Need a much higher temperature for dry heat to do the same thing as moist  heat  

o Moist heat penetrates the microbes much better  

• Mechanical  

o Filtration- put water through the filter; water passes through, but microbes  are stuck in it  

o .45-micron measurement would trap bacteria  

o .22-micron measurement would trap viruses and bacteria  

• Chemical  

o Gas or liquid  

o Harsh chemicals and mild chemicals  

• Disinfection

o Physical process of killing microorganisms and pathogens  

o Killing through the use of chemicals  

o Remove the toxins and the organisms  

o Can’t be used on the human body- usually used on inanimate objects  • Antiseptics  

o Can achieve a lot of the same things as a disinfectant  

o Milder chemicals that can be used on human skin and living tissues  18. Define terms described in table 10.2 (slide 13)  

• Chemotherapeutic drugs: any chemical used to treat any kind of disease;  medicine that you take  

o Any chemical used in the treatment, relief or prophylaxis of a disease  • Prophylaxis: prevents the disease from happening in the beginning

o Use of a drug to prevent imminent infection of a person at risk  

• Antimicrobial chemotherapy: chemotherapeutics that are against  microorganisms  

o The use of chemotherapeutic drugs to control infection  

• Antimicrobials: all-inclusive term for any antimicrobial drug, regardless of its  origin  

• Antibiotics: chemicals against bacteria  

o Substances produced by the natural metabolic process of some

microorganism that can inhibit or destroy other microorganisms  

o Some fungi make antibiotics to kill the competition  

o Penicillin is made by the Penicillin G fungi  

• Semisynthetic drugs: originally isolated from natural resources, but are modified  in the laboratory  

o Drugs that are chemically modified in the laboratory after being isolated  from natural sources  

o When making Penicillin- use the natural base and slightly alter it  

• Synthetic drugs: drugs produced entirely by chemical reactions; not made my  any organisms naturally  

• Narrow-spectrum (limited spectrum): only killing a specific group of organisms  o Antimicrobials effective against a limited array of microbial types  o Ex: A drug effective mainly against gram=positive bacteria  

• Broad- spectrum (extended spectrum): kills a large population of bacteria  o Antimicrobials effective against a wide variety of microbial types  

o A drug effective against both gram-positive and gram-negative bacteria  o Also kills your normal flora/ microbiome  

o Doctors usually prescribe these because they are easier and require less  testing  

19. List and describe mode of action antiviral drugs discussed in the lectures (selective  drugs listed in table 10.4- slide 17-18)  

• Actions of antiviral drugs  

o No drugs and treatment for a lot of viruses  

▪ They are obligate intercellular pathogens- find host, go in host  

• If it goes into the body and doesn’t enter the cell it won’t cause you  harm  

• Presence of a virus in your blood is not toxic, only when they enter a  cell  

▪ No membrane, no cell wall, no protein synthesis, no transcription  ▪ Rely on the host- the host does everything for them  

o Some viruses have their own enzymes for replication, but this is a unique  scenario  

o Enfuvirtide (Fuzeon)

▪ Prevents the entry of the HIV virus into the host  

o Inhibition of nucleic acid synthesis

▪ Acyclovir are structural analogs  

▪ Mimic the structures that allow the virus to make their own DNA  ▪ Mimic A and G- purine analog  

▪ Most effective against the herpes virus  

o Ribavirin  

▪ Purine analog, used for respiratory syncytial virus (RSV) and some  hemorrhagic fever viruses  

o AZT- affects the synthesis of HIV  

▪ Affects reverse transcriptase

▪ RT inhibitor  

o Inhibition of viral assembly and release  

▪ Virus produces a large piece of protein that has to be chopped into small  pieces and must be used to assemble a new virus  

▪ Need protease in order to chop the HIV protein into small segments to be  incorporated into the viruses  

▪ Protease inhibitors can stop proteases from chopping up these proteins  o Treat HIV with a combination of RT inhibitors and PI inhibitors  

▪ HIV always is mutating so these drugs might not always work  

o We don’t have a lot of options with viruses  

• Target cell wall

o Penicillins

o Cephalosporins  

o Carbapenems  

• Target protein synthesis  

o Aminoglycosides  

o Tetracyclines  

o glycylcyclines  

o macrolides  

• target folic acid synthesis  

o sulfonamides  

• target DNA or RNA  

o fluoroquinolones

• target cytoplasmic or cell membrane  

o polymyxins  

20. How anti-HIV drugs work? How drugs against flu work?  

• HIV  

o Enfuvirtide (Fuzeon)

▪ Prevents the entry of the HIV virus into the host  

o AZT- affects the synthesis of HIV  

▪ Affects reverse transcriptase

▪ RT inhibitor  

o Treat HIV with a combination of RT inhibitors and PI inhibitors  

▪ HIV always is mutating so these drugs might not always work

• HIV  

o An RNA virus that must be converted to DNA and then it gets into the host  chromosome  

o Reverse transcriptase changes the RNA to DNA  

o Reverse transcriptase inhibitors to prevent this change and stop the virus  o Protease inhibitor  

▪ Second drug against HIV  

▪ Usually given in combination with Reverse transcriptase inhibitors  ▪ Protease packages and processes the protein

• Flu  

o Tamiflu and Relenza  

▪ Block the entry of the virus by interfering with the fusion of the virus with  the cell membrane  

▪ Stop the release of the virus- prevent the spread of the virus  

▪ Won’t stop you from getting sick but stops the virus from spreading shorten the duration the sickness  

▪ Can be given to the people around you as a prophylactic drug- preventing  the infection  

21. List and describe the antibacterial actions of skin, mucous membrane?  • Skin  

o Low PH, sweat, high salt, lysozymes (kill cell wall of bacteria), normal flora  o Saliva and tears have lysozymes  

• Mucous membrane  

o Layer of insulation that covers respiratory tract and other parts of the body  • First line of defense: normal flora, saliva, skin, mucous membrane  • Physical barriers- skin, mucous membranes  

22. Name the elements involved in nonspecific immunity, give examples for each.  • Innate immunity

o Nonspecific- doesn’t care what infection you have

▪ Protects you regardless  

▪ Divided into first and second line of defense  

▪ Born with this type of immunity- you are protected right away  

▪ Responds the same way regardless of the infection  

▪ Fever, inflammation  

▪ First line of defense  

• Physical barriers- skin, mucus membranes  

• Surface protection  

• Molecules and enzymes that protect you  

▪ Second line of defense  

• Phagocytic cells which engulf and remove the infection from the body  • Inflammation- swelling, redness, pain, warmth  

o Results in tissue repair  

• Fever

o Bacteria enters the body and the temperature rises  

o Slows down the viruses and activates the immune system  

o Molecules work faster to fight against infection

o Too high of a fever will damage the brain tissue  

• Complement proteins  

• First and second line of defense is innate  

o Nonspecific  

o No memory  

23. Where all blood components are originated from?  

• Components of the blood come from the stem cells in the bone marrow  • Stem cells can be shaped into anything you want; red blood cells, white blood  cells, platelets  

24. What are MHC proteins? What is their significance? Which cells contain MHCI and/or  MHCII  

• Every cell in the body has MHC molecules on the surface- help them to distinguish  self from non-self  

o Bind to antigens derived from pathogens and display them on the cell surface  for recognition by the T cells  

• Reaction to graft  

o MHC1- every cell in the body has this except red blood cells  

▪ Unique to you; nobody has the same one  

o MHC1 is different from in a graft

▪ Macrophages try to fight the cells in the graft  

• The stem cells recognize different MHC  

• MHC matching database for MHC1 and MHC2  

• MHCI: beta 2 subunits that can be recognized by CD8 co-receptors  • MHCII: beta 1 and beta 2 subunits that can be recognized by CD4 co-receptors.  o Control which lymphocytes can bind to a certain antigen (different  lymphocytes express different T-cell receptor co-receptors)  

• MHCI: expressed when cells have been infected with a virus  

o Cytotoxic T cells to destroy infected cells  

• MHCII: only expressed by professional antigen presenting cells. ( ex;  macrophages)  

25. What are the differences between different forms of B cells, differences between B  cells and T cells  

• B cells have antibodies on their surface  

• T cells have TCR on the surface  

• T cells need APC to see the antigen  

• B cells can directly see the antigen  

• T cells: CMI  

• B cells: AMI  

• CMI and AMI are forms of acquired immunity  

• B cells and T cells (acquired immunity)

• B cells and T cells see the infection (stem cells from bone marrow)  • B cells- activated and move to other parts of the body  

• T cells- have to mature in the thymus before they can be activated  • APC- see the antigen, recognize the antigen, process the antigen, present it to  the T cells  

• APCs- B cells, macrophages, dendritic cells  

• T cells can’t see the infection directly  

• T cells are activated -> activate other cells  

• Antigens are seen by B cells -> become activated, become plasma cells that  produced antibodies to fight the infection  

• Some cells become memory cells- partially activated  

o Remember infection for the future  

o Some B cells and T cells  

o If the infection comes back, they bind to it much faster than before  o Memory cells can last a lifetime (chicken pox)

o Can last for months, years or a lifetime  

• B cells and T cells see the infection (stem cells from bone marrow)  • B cells- activated and move to other parts of the body  

• T cells- have to mature in the thymus before they can be activated  • APC- see the antigen, recognize the antigen, process the antigen, present it to  the T cells  

• APCs- B cells, macrophages, dendritic cells  

• T cells can’t see the infection directly  

• T cells are activated -> activate other cells  

• Antigens are seen by B cells -> become activated, become plasma cells that  produced antibodies to fight the infection  

• Some cells become memory cells- partially activated  

o Remember infection for the future  

o Some B cells and T cells  

o If the infection comes back, they bind to it much faster than before  o Memory cells can last a lifetime (chicken pox)

o Can last for months, years or a lifetime  

26. What are cytokines? Interferon? Give examples  

• Cytokines  

o General class of molecules to which chemokines, interferons, and  interleukins  

o cytokines are proteins produced by the immune system cells  

o used to attack bacteria, communication, activating each other  

o two cells communicate and produced cytokines -> trigger other cell to start  multiplying or doing something to fight infection  

o result of body producing inflammatory compound  

• interferons

o infected cell releases interferons causing nearby cells to heighten their anti viral defenses  

o important against viruses  

o tumor necrosis factor: important for cancer cells  

▪ destroy and kill other cells

o Natural antivirus compounds  

o Protect cells against viral infection  

o fight against viruses  

o one cell is infected with the virus -> produced interferons -> alerts other cells  -> other cells are protected because they produced interferon inside ->  interferon fights incoming viruses  

o interferes with RNA -> blocks replication so the virus can’t cause damage  o don’t directly kill viral infections; but immune system response  

27. What are the complement proteins? What are their functions?  

• complement proteins  

o group of proteins always present in the blood  

o inactive form -> infection enters the body and they are activated  

o complement fixation when they are activated  

o activation: complement protein starts to break down  

o bacteria comes in-> complement protein binds to the surface of the bacteria  and becomes activated  

o once it is activated the pieces of the protein start to accumulate on the  surface of the bacteria  

o results in the formation of membrane attack complex (MAC)

o formation of MAC pokes a hole in the membrane of the bacteria  

▪ cell dies from leaks in the membrane- lysis of the cells  

o other complements bind and coat the bacteria- opsonization  

▪ labeling bacteria  

▪ helps with phagocytosis- the phagocytes are more attracted to the  bacteria  

o kill infection, coat infection, attract phagocytic cells  

• part of second line of defense  

28. Define: lymphocytes, leukocytes, and erythrocytes  

• Lymphocytes  

o T cells, B cells and NK cells  

o main cells in lymph  

• leukocytes  

o White blood cells = leukocytes  

o Counteract foreign substance and disease  

o Lymphocytes are a subcategory  

• Erythrocytes  

o Erythrocytes are red blood cells- no role in the immune system  

29. Difference between active and passive immunization.  

• Actively develop immunity

o Making your own B cells, T cells and antibodies

o Naturally developed by getting sick- viral/ bacterial exposure  

o Receiving vaccine- artificially (develop your own B, T and antibodies)  • Passively develop immunity

o Receive antibodies from someone else  

o Made in somebody else’s body (person or animal)  

o Mother from placenta to fetus -> IgG  

o When baby is born and breast feeding the baby gets antibodies  

▪ No B cells, no T cells, just antibodies  

▪ Naturally acquired passive immunity  

o Receive antibody from somebody else through injection  

▪ Immunoglobin therapy- form of passive immunity  

• Artificial because you receive it from somebody else  

▪ Already formed antibodies; no B cells, no T cells  

▪ Snake bite and receive antivenom- develop immunity that protects you  • Artificial passive acquired immunity  

30. What are some practical uses of ELISA test?

• ELISA test  

o Based on antigen and antibody principle  

o Make a plate with 96 wells on it – put different amounts of antigen/antibody in  each well  

o Antigens and antibodies interact -> add substrate to it and color develops  o Colorimetric test- color develops due to enzyme reactions  

o More color -> more enzyme -> more antibody present  

o Detect presence of infectious agent  

o Direct technique to detect the presence of pathogen  

o Used to detect presence of antibody produced by the patient against infection  (indirect)

o Use this to measure titer amount- how much virus?  

o Quantitative and qualitative  

o Can detect exposure, amount of virus, directly and indirectly detecting virus  o Use labels to test the presence of the disease  

o Harmless and easy to do  

o Enzyme linked immunosorbent assay  

31. Distinguish between natural acquired immunity and artificial acquired immunity. Give  examples

• Naturally acquired  

o When baby is born and breast feeding the baby gets antibodies  

▪ No B cells, no T cells, just antibodies  

▪ Naturally acquired passive immunity  

o Naturally developed by getting sick- viral/ bacterial exposure

• Artificially acquired  

o Immunoglobin therapy- form of passive immunity  

▪ Artificial because you receive it from somebody else  

o Receiving vaccine- artificially (develop your own B, T and antibodies

o Snake bite and receive antivenom- develop immunity that protects you  ▪ Artificial passive acquired immunity

32. Define cell-mediated immunity? Humoral immunity? List the major components/cells  involved  

• cell mediated immunity  

o does not involved antibodies  

o involved activation of phagocytes, antigen-specific cytoxic T-lymphocytes and  release of cytokines  

o protective function is the cells  

o T helper cells: provide protection against pathogens  

o Mature T cells become effector T cells after encountering an APC  

o APCs (macrophages, dendritic cells, and B cells) put antigenic peptides on the  receptor T cells  

o Activated effector T cells  

▪ Cytotoxic T cells: kill infected cells by apoptosis  

▪ TH1 cells: activate macrophages  

▪ TH2 cells: stimulate B cells and producing antibodies  

o Directed at microbes that survive phagocytes  

o Most effective in removing viral infections  

• Humoral Immunity  

o Mediated by macromolecules found in extracellular fluids  

o Secreted antibodies, complement proteins and antimicrobial peptides  o Involves substances found in body fluid  

o Aspects involving antibodies = AMI  

o Cytokine production, memory cell generation,

o Effector functions of antibodies- pathogen and toxic neutralization,  complement activation, opsonin promotion of phagocytosis and pathogen  elimination  

33. Know different components of an antibody structure. Which part of antibody binds to  antigen?  

• Antibodies  

o Proteins produced by the plasma cells  

o Recognize the antigen  

o Antibody for every antigen  

o Plasma cells produce the antibody to recognize the infection  

o Immune complex formation: interaction between antibody and antigen  o Antigen and antibody relationship is very specific  

o Opsonization: coat the bacteria with the antibodies  

o If a virus or toxin enters the body -> antibody can neutralize this and prevent  them from binding to their target  

o Antibody binds to the toxin before it reaches the cell it is trying to destroy  o Agglutination  

▪ Aggregation  

• Trap the bacteria in the web of antibodies

• Become immobilized  

• Prevent them from moving around- slow them down so the immune  system can take care of them much faster  

o Lysing of the bacteria  

▪ Complement fixation  

▪ Complement proteins recognize the bacteria  

o Enhances the activity of phagocytic cells  

o Neutralization of toxins and viruses  

• Antibodies are proteins made and secreted by activated B cells called plasma  cells  

• Each B cell produced one type of antibody  

• Antibodies are soluble- don’t last very long  

• Every antibody is made of two heavy chains and two light chains  

• FAB binds to the antigen  

• FAB- antigen binding fragment  

• FC- constant fragment

• Every antibody can bind to two antigens at the same time  

• Every antibody is different in their FAB portion- what makes the antibody specific  • Classes of antibody- Igg, IgM, IgA, IgE  

• Classes of antibody- Igg, IgM, IgA, IgE  

• IgG is most abundant in the blood  

• IgA is in secretion: body fluids, saliva  

o Mucosal immunity- protect you from incoming infection  

o Prevent virus or bacteria from attaching and entering  

• IgG passes through the placenta and protects the fetus from infection  • IgM shows up after first infection  

o Made of five antibodies that work together  

• IgE is involved in allergies and recognizes allergens  

• Primary response  

o First exposure to an infection  

o Main antibody that shows up is IgM

▪ Slow to develop and doesn’t last very long  

▪ Low level response  

o Not a lot of IgG  

34. Define Opsonization. What is the effect of opsonization? Name two opsonin molecules • Opsonization: coat the bacteria with the antibodies  

• Opsonization

o Cover bacteria with proteins with antibodies

o When you coat them with the molecules it facilitates phagocytosis more easily  o Facilitation of phagocytosis  

o Neutralization- prevent attaching to their targets  

▪ Inactivate toxins  

▪ Exotoxins are proteins with a target- go to the target and damage it

• If an antibody reaches them before they reach the target they can’t cause  damage  

▪ Diphtheria vaccine  

• Produce antibodies against diphtheria toxin so you won’t get sick if you  got the actual disease  

• Opsonin molecules  

o Molecules that promote phagocytosis by binding to a microbe  

▪ C-reactive protein, mannose binding lectin, C3b  

▪ Antibodies  

35. What is meant by hypersensitivity? List, give examples and briefly describe each type.  • Hypersensitivity- develop exaggerated response  

o Body overreacts to something the body should not over react to  

o Could be a result of genetic issues or something else  

o Immediate type (type 1)  

▪ IgE that you have had before leads to allergic reactions  

▪ Immediately respond and begin to produce histamines  

▪ May result in diarrhea, asthma, anaphylactic shock  

▪ Systemic- rashes across the body  

o Action of antibody mediated- IgG mediated (type 2)  

▪ If you need a blood transfusion  

• RH factors (+ and -), A, B, O  

• You can only receive blood from the people who have the same markers  on their blood  

• If you are positive you can receive a negative, but not the other way  around  

▪ If you receive the wrong blood your body produced antibodies against the  blood and kills the blood cells  

▪ RH factor- plays a role in developing a baby that the mother’s blood tried to  attack the blood cells of the baby  

• If the mother is RH negative and the baby is RH positive -> mother  

develops antibodies against RH and attacks red blood cells  

o Immunocomplex mediated- formation issues between antigen and antibody  (type 3)  

▪ Results in neutralization, agglutination, opsonization, complement fixation ▪ Inflammatory- causes inflammation when immunocomplex is trapped in the  body  

▪ Lupus- body attacks its own tissue, general pain (autoimmune disease)  ▪ Serum sickness

▪ Entrapment of immunocomplex throughout the body  

o Delayed type (type 4)  

▪ CMI- cell mediated immunity  

▪ See the infection the next day

▪ Has to go through T cells and CMI  

▪ Ex: poison Ivy; takes time for it to be processed in the body  

▪ Ex: TB skin test

• Immunodeficiency  

o Missing components of the immune system  

o Can be genetic (primary) or acquire them later in life (secondary)  • Autoimmunity  

o Difficulties with the immune system  

• Hypersensitivity  

• Body reacts to something in a way that it shouldn’t  

• Type 1

o Immediate type hypersensitivity  

o Pet dandruff, pollen, etc. (allergies)  

o IgE mediated  

o Anaphylaxis, allergies, hay fever, asthma  

o Allergic reactions to penicillin, dust mites, pollen  

o Allergy test- give you a small amount of allergen under your skin and look for  a reaction

▪ See which one you are positive for and which ones you are negative to  ▪ Give it to you over time to desensitize you  

• Change your IgE to IgG  

• IgG does the same thing as IgE, but it does not contribute to  

degranulation and does not lead to allergies  

• Degranulation of mast cells and basophils- produce histamines  (inflammatory; causes water eyes, itchy throat, excessive fluid  

production)

• IgE goes down and IgG goes up- desensitization  

o Stop mast cells and basophils from degranulation  

▪ Involves calcium and AMP

▪ Cromolyn, theophylline, epinephrine- mechanisms of action of some  drugs used to treat type 1 hypersensitivity  

▪ Cortisone- reduces the immune system reaction and lowers the histamine  levels  

o Autoimmune disease- give drugs to lower the immune system (produce less  B cells, and T cells)  

▪ Protection against diseases goes down to- > more prone to diseases  ▪ Autoimmune disease is less severe  

• Type 2  

o React to receiving blood from someone else  

o IgG mediated  

o Blood group incompatibility, pernicious anemia, myasthenia gravis  (autoimmune disease- produce antibodies against your own thyroid gland)  o Blue baby syndrome (erythroblastosis fetalis)  

▪ Mother is negative RH and the fetus is positive RH  

▪ Red blood cells of the baby have another molecule on top of it  

▪ Mother does not have this molecule- recognize this as an antigen  ▪ First baby is fine- it takes the mother until the baby is born to realize the  different RH factors

▪ Second baby is in danger because of memory B cells and T cells  

▪ Destruction of the red blood cells of the second baby by the mother’s  immune system  

▪ Rohgam is the drug used to save the baby  

• Type 3  

o Immune complexes develop a deposit

o Inflammation- results in other immune system issues  

o Destroying tissue of your own when there is continued inflammatory issues  o Lupus  

o Antigen/antibody complex mediated  

o Systemic lupus erythematosus, rheumatoid arthritis, serum sickness  (antibodies produced in horse blood -> allergic reaction to serum content  from the horse), rheumatic fever (streptococcal infection- can lead to having  a weak heart for the rest of your life)  

o Arthus reaction- skin reaction  

o Antigen and antibody complex deposits under the skin and causes this  reaction  

• Type 4  

o Delayed type  

o Takes time to develop  

o TB test or poison ivy  

o T cell mediated  

o Infection reactions, contact dermatitis, graft rejection, allergic reaction to  jewelry  

o TB test- inject proteins from microbacteria (cousin of TB)  

▪ The body develops CMI-takes 48 to 78 hours to develop

▪ Results in bumps that must be measured  

• If it is big enough it is TB, if it is small there is no TB  

36. Define primary and secondary (acquired) immunodeficiency? Give examples and  indicate the target tissue in each case  

• Immunodeficiency  

o Missing B cells, T cells, phagocytic cells, complement proteins  

o Results in less than perfect immune system  

o B cell deficiency

▪ Agammaglobulinemia  

• Don’t have B cells  

• Causes primary immunodeficiency- congenital, born with it

o T cell deficiency  

▪ DiGeorge syndrome- missing T cells (primary)  

o Secondary development  

▪ Stress, malnutrition, HIV (destroy white blood cells)  

o Immunosuppressive drugs lower the immune system  

▪ Given with radiation, severe burns  

▪ Taking steroids  

o Removing the spleen can lead to secondary immunodeficiency

o Primary can happen to bone marrow, thyroid, etc.

• Immunodeficiency  

o Missing components of the immune system  

o Can be genetic (primary) or acquire them later in life (secondary)  

37. List and describe different forms of vaccine. (page 495-502)  

• Live attenuated vaccines  

o Created by reducing virulence of a pathogen  

o Alters infectious agent so it becomes less virulent  

o Live bacteria or virus, but weakened form- attenuated  

o Cause very mild form of the disease  

o Live vaccine can grow and provide a long-lasting immunity  

o Requires fewer doses  

o CMI- cell mediated immunity  

o Dead cells can’t divide so immunization with live cells is much more effective  ▪ Need to get multiple shots  

• Inactivated killed vaccines  

o Contains virus partials, bacteria or pathogens  

o Killed by heat or formaldehyde  

o Virus is killed but it still has capsid molecules

o Even though the virus is dead the stuff from the virus stimulates B cell and T cells  • Subunit vaccines  

o Subunit vaccine  

▪ Take bacteria or virus DNA or protein- take components of these and  synthesis pieces of bacteria in the laboratory  

▪ Take toxins and inactivate them -> toxoids  

▪ Make diphtheria toxin a toxoid and inject it into people to get a primary  response  

• Conjugated vaccines  

o Attach a poor antigen to a strong antigen  

o Creates a stronger immunological response to the poor antigen  

• Nucleic acid (DNA) vaccines  

o Take the DNA that codes for a protein or antigen and extract it from the  pathogen  

▪ Take a gene from the pathogen  

▪ Put the gene into a plasmid -> put it into another bacteria and amplify it ->  inject it into people  

▪ Injecting them with just the DNA  

▪ Incorporate the DNA into the cells in the body  

▪ We begin to develop B cells, T cells and antibodies against this bacterial DNA  ▪ The person is never injected with a live vaccine

38. Know different forms of vaccine. Compare killed vaccine vs. live attenuated vaccine?  What is meant by subunit vaccine? Define adjuvant, toxoid, and conjugate vaccine  • Vaccines  

o Develop form of artificial immunity  

o Makes you produce your own B cells, T cells and antibodies

o Virus is killed but it still has capsid molecules

o Even though the virus is dead the stuff from the virus stimulates B cell and T cells  o Live bacteria or virus, but weakened form- attenuated  

▪ Cause very mild form of the disease  

▪ Can divide and provide good protection  

o Dead cells can’t divide so immunization with live cells is much more effective  ▪ Need to get multiple shots  

o Live vaccine can grow and provide a long-lasting immunity  

▪ Requires fewer doses  

▪ CMI- cell mediated immunity  

▪ Herd immunity- if a certain number of people in the population are  

vaccinated, everyone else is protected  

• 70% have the vaccine, other 30% are protected- the disease is not  

spreading as much  

• Not everyone needs to have the vaccine, just 70% or above  

• Give a live vaccine to one person, it may be passed on to other people  o Subunit vaccine  

▪ Take bacteria or virus DNA or protein- take components of these and  synthesis pieces of bacteria in the laboratory  

▪ Take toxins and inactivate them -> toxoids  

▪ Make diphtheria toxin a toxoid and inject it into people to get a primary  response  

• Adjuvant  

o Modifies the effect of other agents  

o Can be added to a vaccine to boost the number of antibodies and provide longer  protection  

o Minimize the amount of material that needs to be injected  

o Can modify the immune response to immune system cells  

• Toxoid  

o Chemically modified toxin from pathogenic microbe  

o No longer toxic but still antigenic  

o Can be used for vaccine  

• Conjugate vaccine  

o Attach a poor antigen to a strong antigen  

o Creates a stronger immunological response to the poor antigen  

39. Define passive, active, artificial and natural immunity produced against infectious  agents/ give examples of each as discussed in class. Name the primary and secondary  lymphoid organs. What is the job of the lymphoid tissues, MALT, BALT, GALT and  SALT.  

• Passively develop immunity

o Receive antibodies from someone else  

o Made in somebody else’s body (person or animal)  

o Mother from placenta to fetus -> IgG  

o When baby is born and breast feeding the baby gets antibodies  

▪ No B cells, no T cells, just antibodies

▪ Naturally acquired passive immunity  

o Receive antibody from somebody else through injection  

▪ Immunoglobin therapy- form of passive immunity  

• Artificial because you receive it from somebody else  

▪ Already formed antibodies; no B cells, no T cells  

▪ Snake bite and receive antivenum- develop immunity that protects you  • Artificial passive acquired immunity  

• Actively develop immunity  

o Making your own B cells, T cells and antibodies

o Naturally developed by getting sick- viral/ bacterial exposure  

o Receiving vaccine- artificially (develop your own B, T and antibodies)  • Primary organs: Thymus, bone marrow  

• Secondary organs: Spleen, lymph nodes, lymphatic tissues, tonsils  • Mucosal associated lymphoid tissue (MALT)  

o give protection at surfaces by making IgA and IgM  

o in mucosal surfaces for defense  

• Gut associated lymphoid tissue (GALT)  

o Lymphocytes and plasma cells in small and large intestine  

• Bronchus associated lymphoid tissue (BALT)  

o Found in the lungs  

o Efferent lymphatics drain regional nodes  

• Skin-associated lymphoid tissues (SALT)  

40. What are the characteristics of primary and secondary immune response to infection.  • Primary response  

o First exposure to an infection  

o Main antibody that shows up is IgM

▪ Slow to develop and doesn’t last very long  

▪ Low level response  

o Not a lot of IgG  

o IgM is the main antibody in the primary response  

o Titer in primary is low- low amount of antibody production  

o Slow to develop- takes time (lag time)  

o Wears off quickly  

• Secondary response  

o Any exposure after the first time  

o Develops fast  

o Higher response- higher titer  

o IgG is higher

o Lasts longer  

o Much better than primary response- quickly reacts to the infection  o Vaccines- weak form of disease to mimic the primary response  

o IgG is the main antibody in the secondary response  

o Titer is secondary response is high- high amount of antibody production  o Quick to develop

o Lasts longer  

o Memory cells- produced as a result of primary response  

▪ B memory cells, T memory cells  

▪ Remember the infection next time it comes around  

▪ Partially activated, don’t produce antibodies, don’t produce molecules ▪ When the infection comes again they become fully activated  

o Only fully activated B cells (plasma cells) produced antibodies  

▪ Last for a short time  

o Vaccines mimic the primary response- tell body we have been exposed to an  infection and we need to act against it  

▪ Real disease comes again, and we are prepared for it  

• Primary infection  

o Getting infection for the first time  

o Lower response  

o igM  

o slow to develop  

o fades away quickly  

• Secondary infection  

o igG  

o High response  

o Quick to develop  

o Lasts longer  

o Memory cells (B cells and T cells)

41. What are the elements of first, second and third line of defense  • First line of defense  

o Physical barriers- skin, mucus membranes  

o Surface protection  

o Molecules and enzymes that protect you  

o normal flora, saliva, skin, mucous membrane

• Second line of defense  

o Phagocytic cells which engulf and remove the infection from the body  o Inflammation- swelling, redness, pain, warmth  

▪ Results in tissue repair  

o Fever

▪ Bacteria enters the body and the temperature rises  

▪ Slows down the viruses and activates the immune system  

▪ Molecules work faster to fight against infection

▪ Too high of a fever will damage the brain tissue  

o Complement proteins  

o fever, inflammation, phagocytic cells, complement proteins

• Third line of defense  

o Cells and supporting molecules  

o B cells and T cells are the main players  

o Always need the third line to come and finish the job

42. Name several phagocytic cells. Which phagocytic cells are also antigen presenting  cells?  

• Phagocytic cells  

o Has organelles inside called a lysozyme  

o Inside lysozyme is hydrolytic enzyme  

▪ Kill bacteria: lipase, protease, lysozyme, nuclease  

▪ Harsh chemicals- oxidizing agents (peroxides and superoxide)  

o Bacteria comes in the body and phagocytic cells are attracted to it  o Bind to the bacteria and bring it inside  

o Phagosome fuses with the lysosome  

o the fusion results in kills the bacteria  

o expose bacteria to chemicals- kills bacteria  

o the bacteria is destroyed and the waste is spit out  

o can be used to remove human dead cells, bacteria, viruses, fungi  

• Phagocytic cells- macrophages, monocytes

• recruitment of phagocytic cells- by releasing inflammatory compound phagocytic  cells are attracted to the area  

• antibodies enhance the activity of phagocytic cells  

• antigen presenting phagocytic cells  

o some phagocytes move engulfed material to the surface of the cell to  present them to other cells of the immune system  

o macrophages and dendritic cells  

43. Define and list characteristics of antigen, which molecule is the most antigenic.  • antigen  

o something the body responds to  

o phagocytic cell recognizes bacteria as a foreign invader  

o body recognizes bacteria by molecules on the surface  

o bacteria with pili, flagella, capsule, fimbria  

o antigen triggers and activated the immune system  

o bacteria comes in the body and the body responses to the antigens  o example: kidney transplant- every cell on the kidney has a molecule that is  not the same as the molecules in your body which is why you reject it  o antigen must be big enough for the immune system to see it

o proteins are the most antigenic  

o Body reacts to proteins better than any other thing  

o Vaccines are made of proteins (antigens)  

o Food particles, pollen, pet dander, dust mites are antigenic  

o Polypeptides are good antigens  

• Recognizing antigens and pathogens  

o B cells and T cells (acquired immunity)  

o Find and fight the infection  

o Antigen process

o B cells and T cells see the infection (stem cells from bone marrow)

o B cells- activated and move to other parts of the body  

o T cells- have to mature in the thymus before they can be activated  o APC- see the antigen, recognize the antigen, process the antigen, present it  to the T cells  

o APCs- B cells, macrophages, dendritic cells  

o T cells can’t see the infection directly  

o T cells are activated -> activate other cells  

o Antigens are seen by B cells -> become activated, become plasma cells that  produced antibodies to fight the infection  

o Some cells become memory cells- partially activated  

▪ Remember infection for the future  

▪ Some B cells and T cells  

▪ If the infection comes back they bind to it much faster than before  ▪ Memory cells can last a lifetime (chicken pox)

▪ Can last for months, years or a lifetime  

44. Define lysosomes, phagosome, and explain what happens as the two fuse together.  • Phagocytic cells  

o Has organelles inside called a lysosomes  

o Inside lysosome is hydrolytic enzyme  

▪ Kill bacteria: lipase, protease, lysozyme, nuclease  

▪ Harsh chemicals- oxidizing agents (peroxides and superoxide)  

o Bacteria comes in the body and phagocytic cells are attracted to it  o Bind to the bacteria and bring it inside  

o Phagosome fuses with the lysosome  

o the fusion results in kills the bacteria  

o expose bacteria to chemicals- kills bacteria  

o the bacteria is destroyed and the waste is spit out  

o can be used to remove human dead cells, bacteria, viruses, fungi  45. What does the term de-granulation refer to? Which cells are capable of  degranulation? Name an example of granules produced by these cells. • Type 1 hypersensitivity  

o Allergy test- give you a small amount of allergen under your skin and look for a  reaction

▪ See which one you are positive for and which ones you are negative to  ▪ Give it to you over time to desensitize you  

• Change your IgE to IgG  

• IgG does the same thing as IgE, but it does not contribute to  

degranulation and does not lead to allergies  

• Degranulation of mast cells and basophils- produce histamines  

(inflammatory; causes water eyes, itchy throat, excessive fluid  

production)

• IgE goes down and IgG goes up- desensitization  

o Stop mast cells and basophils from degranulation  

▪ Involves calcium and AMP

▪ Cromolyn, theophylline, epinephrine- mechanisms of action of some drugs  used to treat type 1 hypersensitivity  

▪ Cortisone- reduces the immune system reaction and lowers the histamine  levels  

o Autoimmune disease- give drugs to lower the immune system (produce less B  cells, and T cells)  

▪ Protection against diseases goes down to- > more prone to diseases  

▪ Autoimmune disease is less severe  

46. Which cells are transplanted during bone marrow transplant?  

• Bone marrow transplant  

o Bone marrow has stem cells (can turn into B cells and T cells)  

o The stem cells recognize different MHC  

o Destroy their white blood cells and repopulate them with the bone marrow from  another person -> these can come back and destroy your own tissue if it is not a  good match  

o Graft vs host complications  

▪ The donor material attacks the recipient  

▪ Only happens with bone marrow transplants  

o MHC matching database for MHC1 and MHC2  

• In need of a transplant they put you in the system to try to find you a match that will  work for you  

47. Compare different classes of antibodies. IgG, IgM, IgA, IgE  

• Classes of antibody- Igg, IgM, IgA, IgE  

• IgG is most abundant in the blood  

• IgA is in secretion: body fluids, saliva  

o Mucosal immunity- protect you from incoming infection  

o Prevent virus or bacteria from attaching and entering  

• IgG passes through the placenta and protects the fetus from infection  • IgM shows up after first infection  

o Made of five antibodies that work together  

• IgE is involved in allergies and recognizes allergens  

48. What is the job of eosinophil, NK, and T helper cells  

• Eosinophil  

o White blood cell containing granules

o Combat multicellular parasites  

o Control mechanisms associated with allergies and asthma  

o Develop in bone marrow and migrate to the blood  

• NK cells  

o Lymphocytes that bind to tumor cells and infected cells that don’t stimulate  antigens  

o Kill invader by inserting granules that contain perforin  

• T helper cells  

o Release T cell cytokines which suppress immune responses

o Activate growth of cytotoxic T cells and maximize bactericidal activity of  macrophages  

49. What are the differences between plasma cells and memory B cells  • Plasma

o Plasma cells produce the antibody to recognize the infection

o Only fully activated B cells (plasma cells) produced antibodies  

o Antigens are seen by B cells -> become activated, become plasma cells that  produced antibodies to fight the infection  

o Antibodies are proteins made and secreted by activated B cells called plasma  cells

• Memory B cells  

o Some cells become memory cells- partially activated  

▪ Remember infection for the future  

▪ Some B cells and T cells  

▪ If the infection comes back, they bind to it much faster than before  ▪ Memory cells can last a lifetime (chicken pox)

▪ Can last for months, years or a lifetime

o produced as a result of primary response  

▪ B memory cells, T memory cells  

▪ Remember the infection next time it comes around  

▪ Partially activated, don’t produce antibodies, don’t produce molecules ▪ When the infection comes again they become fully activated  

50. What is the relationship between Rh factor and hemolytic disease?  • If you need a blood transfusion  

o RH factors (+ and -), A, B, O  

o You can only receive blood from the people who have the same markers on their  blood  

o If you are positive you can receive a negative, but not the other way around  • If you receive the wrong blood your body produced antibodies against the blood and  kills the blood cells  

• RH factor- plays a role in developing a baby that the mother’s blood tried to attack  the blood cells of the baby  

o If the mother is RH negative and the baby is RH positive -> mother develops  antibodies against RH and attacks red blood cells  

• Blue baby syndrome (erythroblastosis fetalis)  

o Mother is negative RH and the fetus is positive RH  

o Red blood cells of the baby have another molecule on top of it  

o Mother does not have this molecule- recognize this as an antigen  

o First baby is fine- it takes the mother until the baby is born to realize the  different RH factors  

o Second baby is in danger because of memory B cells and T cells  

o Destruction of the red blood cells of the second baby by the mother’s immune  system  

o Rhogam is the drug used to save the baby  

51. Describe how blood cell count results may be interpreted?

• Agglutination

o Blood testing- give you a strip with antibodies in it (anti A, anti B, RH)  o Take blood and put a drop on each well of the strip  

o If you have A type, proteins in the red blood cells attach to the antibody and  allow the red blood cells to clump  

o If the blood is smooth it is negative for the test  

o If it clumps it is positive for the test  

o If all the blood tests are smooth (no agglutination) then you are O

o Clumping on all three tests would be AB+  

• Flow cytometry- measures number of cells  

o Take different cells and attach antibodies to them  

o Run them through the machine, separate them and measure how many cells  there are  

52. What is meant by antigen processing? APC. Which cells are involved in the process?  List APC’s  

• APC  

o Dendritic cells

o B cells  

o Macrophages  

o See the infection, process the infection  

o Dendritic and macrophages are phagocytic cells  

o APC presents the antigen to T helper cells  

o Once the TH is activated it releases cytokines -> activate other cells  o Send a message to everybody- APC sees the infection and tells the T helper  cells  

o T cells then activate the components of the immune system

• APC- see the antigen, recognize the antigen, process the antigen, present it to  the T cells  

• APCs- B cells, macrophages, dendritic cells  

• T cells need APC to see the antigen  

53. Define inflammation and list its major characteristics. Define diapedesis.  • Inflammation

o swelling, redness, pain, warmth  

o Results in tissue repair  

o Second line of defense  

o Innate immunity  

o cytokines are proteins produced by the immune system cells  

o used to attack bacteria, communication, activating each other  

o two cells communicate and produced cytokines -> trigger other cell to start  multiplying or doing something to fight infection  

o result of body producing inflammatory compound  

▪ redness, swelling, heat, pain  

o acute  

▪ quick to develop and heals quickly

▪ beneficial  

o chronic  

▪ slow to develop  

▪ damaging  

▪ lasts a long time  

o non-specific event: part of innate immunity  

o recruitment of phagocytic cells- by releasing inflammatory compound  phagocytic cells are attracted to the area  

o vasodilation- lots of blood comes to the area, lots of fluid leading to redness  and swelling  

• diapedesis  

o passage of blood cells through intact walls of capillaries  

o occurs with inflammation  

54. Compare host vs. graft and graft vs. host hypersensitivity reactions.  • Host vs graft complications  

o Recipient rejects the donor tissue  

• Graft vs host complications  

o The donor material attacks the recipient  

o Only happens with bone marrow transplants  

55. How fever is produced? Which molecules may induce fever? What are they called?  • Fever  

o Bacteria enters the body and the temperature rises  

o Slows down the viruses and activates the immune system  

o Molecules work faster to fight against infection

o Too high of a fever will damage the brain tissue  

• Endogenous pyrogens- cytokines  

o Produced by immune cells and cause increased thermoregulatory set point in  the hypothalamus  

56. Which antibody is involved in allergic reaction? Define and give examples of allergens.  What is meant by desensitization (as described in the lecture)?  

• Type 1

o Immediate type hypersensitivity  

o Pet dandruff, pollen, etc. (allergies)  

o IgE mediated  

o Anaphylaxis, allergies, hay fever, asthma  

o Allergic reactions to penicillin, dust mites, pollen  

o Allergy test- give you a small amount of allergen under your skin and look for a  reaction

▪ See which one you are positive for and which ones you are negative to  ▪ Give it to you over time to desensitize you  

• Change your IgE to IgG  

• IgG does the same thing as IgE, but it does not contribute to  

degranulation and does not lead to allergies

• Degranulation of mast cells and basophils- produce histamines  

(inflammatory; causes water eyes, itchy throat, excessive fluid  

production)

• IgE goes down and IgG goes up- desensitization  

o Stop mast cells and basophils from degranulation  

▪ Involves calcium and AMP

▪ Cromolyn, theophylline, epinephrine- mechanisms of action of some drugs  used to treat type 1 hypersensitivity  

▪ Cortisone- reduces the immune system reaction and lowers the histamine  levels  

o Autoimmune disease- give drugs to lower the immune system (produce less B  cells, and T cells)  

▪ Protection against diseases goes down to- > more prone to diseases  ▪ Autoimmune disease is less severe  

57. What are the immunosuppressive drugs? Their use?  

• Immunosuppressive drugs lower the immune system  

o Given with radiation, severe burns  

o Taking steroids  

58. Describe systemic anaphylaxis reaction  

• Reaction between IgE antibodies bound to mast cells and allergens that cause  release of immunological mediators  

• Happens in the skin, respiratory system, cardiovascular system and  gastrointestinal systems  

59. What is the role of neutralization in preventing viral infections?  • Neutralization- prevent attaching to their targets  

o Inactivate toxins  

o Exotoxins are proteins with a target- go to the target and damage it  ▪ If an antibody reaches them before they reach the target they can’t cause  damage  

o Diphtheria vaccine  

▪ Produce antibodies against diphtheria toxin so you won’t get sick if you got  the actual disease  

60. Define autoimmunity. Give examples of autoimmune diseases and their targets.  • Autoimmunity  

o Difficulties with the immune system  

• Autoimmune disease- give drugs to lower the immune system (produce less B cells,  and T cells)  

o Protection against diseases goes down to- > more prone to diseases  o Autoimmune disease is less severe  

• myasthenia gravis (autoimmune disease- produce antibodies against your own  thyroid gland)  

• Autoimmune disease  

o Develops later in life  

o Affects women more than men  

o Shows up with no predisposition

o Clonal anergy- destroy B cells and T cells that are against you early in life  ▪ Fetus is developing and you inactive the B and T cells that are against you  before you are born so you can be fine  

▪ Can be triggered by infection and drugs and you could develop an  

autoimmune disease again  

o Lupus  

▪ Producing antibodies against your own DNA  

▪ Body aches all over because there is inflammation all over the body

o Rheumatoid arthritis  

▪ Destroy your own joints; antibodies against your own fluids  

o Graves’ disease  

▪ Against thyroid stimulating hormone receptors  

o Myasthenia grave  

▪ Antibodies against the acetylcholine receptors on the nerve-muscle junction  alter function  

▪ Results in weak muscles  

▪ Neurotransmitters are blocked by antibodies, so signals do not reach the  muscles  

o Type 1 diabetes  

▪ Produce antibodies against your own pancreas  

o Multiple sclerosis  

▪ Destroy the myelin of the neurons  

▪ HSV-8 (a version of the herpes simplex virus) may contribute to MS  

61. What are the greenhouse gases? How they contribute to the global warming.  • CO2 and CH4 are greenhouse gases  

o Contribute to the absorption of infrared  

o UV light comes from the sun, affects the ozone layer  

o Compounds that destroy the ozone layer increase the UV light  

o CO2 and CH4 are in balance to keep the temperature stable  

62. What is the role of microbes in C, N, O and S cycle  

• Describe the role of microorganisms in recycling carbon and nitrogen  compounds. (converting CO2/CH4 to organic compounds or converting organic  compounds back to CO2 and CH4 gas)  

o Carbon cycle  

▪ Bacteria can break organic compounds into methane gas or CO2 gas  ▪ Can take CO2 and convert it to methane or vice versa  

▪ Can convert CO2 and methane to organic compounds  

• Explain the significance of this in level of greenhouse gases and global  warming.  

o Nature recycles- play a major role in C, N, O and S cycles  

o Affect the balance of CO2 and CH4 (greenhouse gases)  

▪ Phototrophs- sunlight  

▪ Autotrophs- fix CO2  

▪ Methanogens- produce methane gas  

▪ Methanotrophs- use methane gas

▪ Sunlight has inferred or UV light  

• Part of it passes through but most is absorbed by ozone layer

• Ratio between CO2 and methane is what causes global warming  

• Microbes maintain the levels of CO2 and methane which can help keep  the ozone layer safe  

• Relationship between CO2 and methane: higher levels in the air -> higher  temperature  

o Microbes can fix the CO2 or absorb methane  

• Describe the role of microorganism in nitrogen cycle (Nitrogen fixation vs. De nitrification)  

o Fix nitrogen gas into usable forms  

• 80% of air is nitrogen- microbes can fix nitrogen  

• Nitrogen fixation -> convert gas into something soluble

o Once it is fixed to something soluble it can be absorbed by plants and animals  o Nitrogen is fixed through lightening -> creates natural fertilizer through the  rain  

• Denitrification

o Removes the nitrogen from the soil (not good for farmers)  

• Nitrogen cycle  

o Denitrification- converting soluble nitrogen into gas  

o Nitrogen fixation- converting nitrogen gas into a useable form (nitrate or  nitrite)  

o Ammonification- converting organics into ammonia

63. Define; biosensors, xenobiotics, and microbial leaching.  

• biosensors  

o Sense the presence of toxins and chemicals in the soil  

o Biological weapons- spray things with microbes to show which areas are  contaminated and which are not  

• Xenobiotics

o Manmade chemicals- don’t exist naturally  

• Microbial leaching  

o Extracting metals from ore in mining  

o Extract copper, magnesium, iron, etc.  

64. Describe the role of microbes in treatment of raw sewage. What does reducing the  BOD mean?  

• Microbes involved in the sewage treatment system  

o Mixture of organic and inorganic  

o Remove organics and inorganics before releasing water back into the  environment  

o Microbes are involved in removing the organic part of the sewage  

o Primary treatment  

▪ Separation of solids from liquids- microbes are not involved

o Secondary treatment

▪ Organics are removed- microbes are involved

▪ Solid goes to the sludge digester- a lot of organic matter  

• In the big tanks microbes digest the organics and produce methane gas  (archaea)  

• Archaea are methanogens- produce methane gas that can be used as fuel  (use this to run the plant)  

• Eventually add chlorine to kill some of the microbes before releasing  them  

o Tertiary treatment  

▪ Inorganics are removed- microbes are not involved  

o Septic tank- more like a primary treatment  

• Water treatment system  

o Primary stage, secondary stage (microbes are involved), tertiary stage  o Secondary stage  

▪ Organics are removed from liquid portion of sewage  

▪ Associated with the biological oxygen demand  

• Higher the organic -> higher the BOD  

• Oxygen is affected by the presence of organic  

• Higher the organic -> less oxygen available  

• Treat raw sewage in the presence of the water to reduce BOD

• More BOD in the water -> less oxygen available to the marine life  • Reduce the BOD so it won’t affect the water  

▪ Microbes remove organic from the sewage  

▪ Aerobic  

o Solid goes to the anaerobic slug digester (microbes are also used)  ▪ After primary stage separates liquid from solid  

▪ Microbes convert organic into methane gas  

▪ Methane gas is used as fuel  

o Tertiary treatment

▪ Phosphates and other materials are removed  

▪ Nothing to do with microbes  

• Septic tank  

o A method of primary sewage treatment  

o Liquid flows to the drainage field  

o Solid collects in a tank and is pumped out every few years  

65. What is the product of anaerobic digestion that is used as fuel?  

• Solid waste goes to the anaerobic slug digester (microbes are also used)  o After primary stage separates liquid from solid  

o Microbes convert organic into methane gas  

o Methane gas is used as fuel  

o Archaea are methanogens- produce methane gas that can be used as fuel (use this to run the plant)  

66. List different forms of extremophiles. What are the black smokers? Define halophiles?  • Extremophiles  

o Microbes that thrive in extreme conditions

o Temperature extremes, pH extremes, atmospheric pressure extremes  o Black smokers  

▪ Found on the deep-sea floor

▪ Underwater volcanic vents- super concentrated compound  

▪ No oxygen, no organic compounds, lots of pressure, no light  ▪ Bacteria growing on these rocks- generate life using these minerals  ▪ Turn the minerals into biomass  

o Hot springs and boiling sulfur  

▪ Yellowstone- microbes growing in the water  

▪ Can withstand extreme salinity and high temperatures  

o Psychrophiles- cold loving  

o Acidophiles- pH <5  

o Alkaliphiles- pH>10  

o Alkaliphiles- high salt  

o Thermophiles/hyperthermophiles: heat loving microbes  

67. Define the following terms: phototrophs, autotrophs, methanotrophs, and  methanogens  

• Phototrophs- energy from sunlight  

• Autotrophs- fix CO2  

• Methanogens- produce methane gas  

• Methanotrophs- use methane gas as energy

68. What is the role of activated charcoal in treating drinking water?  • Processing of drinking water

o Taste color, odor; chemicals that have to be removed  

o Alum- removes particles  

o Activated charcoal- removes chemicals  

o Ozone, ultraviolet light, and chlorine - kill microbes

▪ Ozone needed to kill cysts  

• Drinking water  

o Alum removes suspensions  

o Activated charcoal removes the organics  

▪ Smell taste, color, odor are removed  

o Use chlorine, UV light and ozone to remove microbes  

o Chlorine important in removing cysts of protozoa from the water

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