Study Guide #4 (chapters 14-18).pdf

Exam #4 Microbiology Lecture Study Guide Chapters 14-18 Chapter 14: Biomedical, Applications: Vaccines, Diagnostics, Therapeutics, and Molecular Methods. Section 14.1: A Brief History of Vaccines 1. What was the Chinese proc...

Exam #4 Microbiology Lecture Study Guide Chapters 14-18 Chapter 14: Biomedical, Applications: Vaccines, Diagnostics, Therapeutics, and Molecular Methods. Section 14.1: A Brief History of Vaccines 1. What was the Chinese procedure called variolocation? What pathogen were the practitioners trying to gain protection from? The practitioner blew a powder made from dried scabs of smallpox lesions into a health individual’s nose; the resulting smallpox infections tended to be milder. o Done to gain protection from smallpox. 2. What was Edward Jenner’s contribution to science? What pathogen was involved? He created a new method of purposely infecting people with pathogens to spur immunity. o Cowpox 3. What was Louis Pasteur’s contribution to vaccine development? Developed an early version of the rabies vaccine to protect humans, as well as a vaccine to protect cattle against anthrax. 4. In the 20th century, smallpox was eradicated. What is the next disease targeted for eradication? Why might this be difLicult to achieve? Polio o May be difLicult to eradicate because it may be a struggle to maintain consistent vaccination access, especially in war-torn areas. 5. Describe the 1998 study that was published in The Lancet that harmed vaccination effort. What is the vaccination in question and what happened to the study and lead author? The paper described a study of just 12 patients and claimed a correlation between the measles, mumps, and rubella (MMR) vaccine and the development of autism. o The vaccine in question was the MMR vaccine. The study was retracted as bad science. The lead author lost his medical license amid charges of fraud and malpractice. 6. What disease is showing the strongest reemergence in the US and UK due to declining vaccination rates? Measles Section 14.2: Overview of Vaccines 1. Vaccines induce which type of immunity? (REVIEW the information in Chapter 12 explaining that humoral immunity is naturally or artiLicially acquired, and is either active or passive, to refresh your memory) Exam #4 Microbiology Lecture Study Guide Chapters 14-18 ArtiLicially acquired active immunity 2. What must be stimulated for a vaccine to be considered effective? (NOTE: Typically, the more closely the vaccination agent resembles the pathogen encountered in nature, the more likely it is to elicit a strong adaptive immune response and produce immunological memory [Memory B and T cells]). Immunological memory must be stimulated, without causing the disease they are trying to prevent. 3. What is herd immunity? Provided that a sufLicient percentage of the rest of the population is vaccinated, nonvaccinated individuals still reap the protective beneLits of immunization. o The fewer disease-susceptible people in a community, the harder it is for a pathogen to be transmitted to a susceptible host who could then spread the disease. 4. What two vulnerable populations are protected by herd immunity? Babies who have not yet been fully vaccinated Immune-compromised people 5. Your textbook contains the following statement, “Shingles as a sequela to chickenpox is discussed at length in Chapter 17.” Look up the deLinitions of “sequela, or sequela.” Knowing the deLinition, explain what the statement, “shingles is a sequela to chickenpox”. HINT: A sequel to a Lilm or book means that events occur after the initial Lilm or book events happened. The word sequel is in the word sequela. Sequela: a pathological condition which is the consequence of a previous disease or injury. o Shingles is a consequence that occurs after having chickenpox. 6. What are live attenuated vaccines? Vaccines that contain pathogens that have been altered so that they do not cause disease (are not pathogenic) but are still infectious. 7. What is the beneLit of live attenuated vaccines? What are 3 drawbacks of live attenuated vaccines? BeneLits: o They are the closest to the pathogen encountered in nature and therefore tend to stimulate potent immunological responses that are accompanied by long lived memory. o Broader Protection Drawbacks: o The agent in them could cause disease in an immune-compromised host. o Sporadically, the live attenuated pathogen can mutate to an infectious form and cause disease. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 o Can potentially transmit other infectious agents, such as other viruses, if the tissue culture is contaminated. 8. What are inactivated vaccines? Vaccines that consist of whole inactivated pathogens, such as killed bacteria or inactivated viruses, or parts of pathogens. 9. What are two advantages that inactivated vaccines have over live attenuated vaccines? What is one disadvantage? Advantages: o Stable at room temperature, which makes them easy to ship and store o Their noninfectious nature means they are safe for immune-compromised patients. Disadvantage: o Their lack of infectivity means they are quickly cleared from the body, which limits exposure to the antigens and necessitates booster doses to achieve full immunity. 10. What is the difference between inactivated whole-agent and inactivate subunit vaccines? What is one advantage that whole-agent vaccines have over subunit vaccines? Inactivated whole-agent vaccines: contain the entire pathogen, which has been rendered inactive by heat, chemicals, or radiation. o The beneLit of whole-agent vaccines is that the agent is essentially the same as what would be encountered in nature but can’t cause disease in a weak host or mutate to cause disease. Subunit vaccines: do not include the whole pathogens; instead, they consist of puriLied parts of the pathogen (antigens from the actual pathogen) or antigens produced by genetic engineering (NOT directly puriLied from the pathogen). 11. What is an adjuvant? A pharmacological additive that enhances the body’s natural immune response to an antigen. 12. What is a recombinant subunit vaccine? Vaccines that are puriLied from a genetically engineered expression system. 13. What is a toxoid vaccine? Give two examples of vaccines that have toxoid components? A type of subunit vaccine that are made with naturally occurring bacterial toxins that have been puriLied and inactivated. o DTaP o Tdap § They have tetanus and diphtheria components. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 14. What are conjugate vaccines? What two molecules are usually conjugated? Why must this be done? Vaccines created by linking polysaccharides to a protein antigen to stimulate an immune response in a vaccinated patient. 15. What are mRNA vaccines? (You may want to review the process of proteins synthesis that we learned about in Chapter 5.) These vaccines rely on delivering mRNA – the genetic instructions for assembling a protein – to host cells, whereupon the host cells translate the mRNA to build an antigenic protein that triggers an immune response. NOTE: The Moderna and PLizer COVID-19 vaccines are mRNA vaccines. The mRNA sequence of the SARS-CoV-2 spike protein is encapsulated by lipid nanoparticles. The lipid nanoparticles stabilize the mRNA and facilitate the delivery of the mRNA sequences into the cells by passing through the cell’s lipid bilayer. Without the lipid nanoparticles, mRNA would not be able to cross the cell’s plasma membrane, and it would be degraded quickly by the body. Once the mRNA sequence is in the cell, it will be translated into the spike protein. Once the spike protein is released by the cell, antigen processing cells will present various epitopes of the spike protein on its surface. Immune cells will see these as “foreign” and elicit T and B cell responses. The primary exposure (1st shot) produces a spike of IgM antibodies, then a small amount of IgG. The second exposure (2nd shot) will result in isotope switching and IgG will predominate. Booster shots (3rd shot) have been recommended. PLizer and Moderna have produced “bivalent” vaccines. “Bi” means two, so the bivalent vaccine contains mRNA sequences that code for spike proteins from two different SARS-CoV-2 variants (the original COVID-19 virus strain and the Omicron BA. 1 subvariant). Unfortunately, no vaccine is 100% effective. Data shows that if you have been vaccinated, your chances of dying from COVID-19 is reduced. You may still get infected (this is called a “break-through case”), but the infection should not be as severe as experienced in most non-vaccinated individuals. Remember, mRNA CANNOT cause you to contract the disease and it does not change your DNA. mRNA is only a set of instructions used to create a protein. (FYI – this is testable material). 16. What are recombinant vector vaccines? Immunization method where genes from a pathogen are packed inside a harmless virus or bacterium. The engineered vector is then puriLied and introduced into the body. 17. What are DNA vaccines? Currently the majority of DNA vaccines being developed focus which two disease/injections? Relatively new vaccines that use a pathogen’s DNA to stimulate an immune response. o HIV o Cancer Section 14.3: Immunological Diagnostic Testing Exam #4 Microbiology Lecture Study Guide Chapters 14-18 1. DeLine serology. The study of what is in a patient’s serum. 2. What is agglutination? What two molecules are required for positive agglutination reactions? A reaction in which antibodies bind antigens into a clump. o Cells that display multiple antigens on their surface. o Cells with tiny synthetic beads coated with antigens. 3. What type of serological test is used for blood typing and conLirming a syphilis diagnosis? Treponema Pallidum particle agglutination assay (TPPA) test 4. Use the information in FIGURE 14.8 Plaque reduction neutralization test (PRNT) to describe the steps of plaque reduction neutralization tests (PRNT). What is the testing detecting? (1) Draw patient’s blood and isolate serum. (2) Virus is added to a series of serum dilutions. If antibodies against the virus are present, they coat the virus and limit its infectivity. (3) Virus/serum mixture is added to cultured cells and incubated. Antibody- coated virus can’t infect cells. (4) Observe incubated plate Detects patient antibodies against a speciLic virus. 5. What is a plaque? Areas that develop in a lawn of cultured cells as the cells are infected and lysed by a virus. NOTE: For questions 6-8, carefully read the ELISA section of the textbook and use the images in FIGURE 14.9 Direct, Indirect, and Sandwich ELISA to visualize each step of the process. 6. What does the direct ELISA detect in a patient’s serum? What does a positive reaction look like? What does a positive reaction indicate? (NOTE: use the information for the direct ELISA, NOT the modiLied direct ELISA). Detects speciLic antigens in the patient’ serum. A positive reaction looks like changes in color or emits light in the wells of the microplate. A positive reaction indicates that the speciLic antigen is present. 7. What does the indirect ELISA detect in a patient’s serum? What does a positive reaction look like? What does a positive reaction indicate? Detects speciLic antibodies in the patient’s serum. A positive reaction looks like changes in color in the wells of the microplate. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 A positive reaction indicates that the patient has antibodies speciLic to the antigen being tested. (NOTE: The above ELISA names make sense. In a direct ELISA, you are directly looking for the pathogen in a patient’s serum that is causing a current, active infection. An indirect ELISA detects antibodies made against an antigen. Antibodies that last in the circulation long after the pathogen has been cleared from the body, so you are indirectly detecting exposure to a pathogen by detecting antibodies produced against a pathogen. The presence of antibodies indicates that either the infection has been cleared, or that a persistent infection is occurring. You can still have low numbers of antigen in circulation even when antibody is present, but in general direct ELISAs detect current infections, and indirect ELISAs are used to detect if you have been exposed to an antigen and have elicited an immune response). 8. What does a sandwich ELISA detect in a patient’s serum? What does a positive reaction look like? What does a positive reaction indicate? (NOTE: Use the description for the simplest form of sandwich ELISA. You don’t need to know the difference between indirect and direct sandwich ELISAs). Detects a speciLic antigen in a patient’s serum, but it is more sensitive and overcomes the downside of the direct ELISA. A positive reaction looks like a color change in the wells of the microplate. A positive reaction indicates that the speciLic antigen is present. 9. What is immunoJluorescence microscopy? What molecule is Lluorescent tagged? What is the tagged molecule detecting? A protocol where Lluorescent-tagged antibodies that recognize a speciLic antigen are incubated with tissue or cell samples, followed by observing the sample with a specialized UV light microscope. o Antibodies o A speciLic antigen 10. What is Jlow cytometry? What special piece of equipment is required for Llow cytometry? A process by which cells can be sorted using a Llow cytometer and is useful for enumerating speciLic cells. o Fluorescence-activated cell sorter (FACS) 11. What are IGRAs? What is the assay mainly used for in the USA? What is this assay detecting? Interferon Gamma Release Assays (IGRAs) is a test that measures how a patient’s T cells respond to Mycobacterium tuberculosis antigens. o Mainly used to detect tuberculosis (TB) in the early stages in vaccinated populations. o Detects T cells that release a certain amount of interferon gamma, which indicates that the patient has a latent or active tuberculosis. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 12. What molecules do western blots detect? How is a western blot performed? Detect speciLic proteins in a sample and reveal the size of the protein being detected. o Separate proteins by size using an electrophoresis, load samples onto polymer gel, and run an electrical current to the gel. Section 14.4: Selected Genetic Applications in Medicine What does the abbreviation PCR stand for? What does this application do? Polymerase Chain Reaction o Made to detect viruses in donated blood. PCR methods create billions of copies of a target gene in just a few hours. Even at their earliest stage – PCR is sensitive enough to detect even a single viral particle in a sample. What is Taq polymerase? Why is it used in PCR? An enzyme from the hot spring’s bacterium Thermus aquaticus. o Used as a heat resistant DNA polymerase. What is a thermocycler? When performing PCR, three different temperatures are cycled. What occurs during each temperature range? Machine used to perform polymerase chain reaction (PCR); controls the heat of the reaction, cycling between the different temperatures of different steps in PCR. o High temperature (95*C): separates double-stranded DNA into single strands that can be copied. o Lower temperature (between 50*C and 65*C): allows the primers to anneal (or pair) with the template DNA to serve as a start point for the DNA polymerase to copy the template. o Extension Period (between 65*C and 75*C): allows DNA polymerase to copy the target DNA. What is gel electrophoresis used for? Method used to separate molecules (especially nucleic acids and proteins) based on their size. What is real-time PCR (also called quantitative PCR or qPCR)? A modiLied PCR method that uses Lluorescence imaging to visualize DNA copies as they are made – making the data “real time,” or immediate. What is RT-PCR? What does it detect? Reverse Transcription PCR (RT-PCR) is another form of PCR that is useful for detecting RNA in a sample – such as the genome of an RNA virus like SARS-CoV- 2 NOTE: Do not confuse real time PCR with RT-PCR – they are different. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 In addition to Taq polymerase, what additional enzyme is used when performing RT-PCR? What is the function of this enzyme? Reverse transcriptase o Used in conjunction with primers to build DNA that is complementary to RNA molecules in a sample. NOTE: SARS-CoV-2 is a positive-sense, single-stranded RNA virus. Remember that positive sense RNA viruses have RNA that is directly used as an mRNA template which is translated into viral proteins using the host cell’s molecular machinery. The current diagnostic method to detect an active COVID-19 infection is RT-PCR. Reverse transcriptase (RT) makes a DNA copy of the SARS-CoV-2 RNA. A certain region of this DNA that is speciLic for the viral strain is then ampliLied using standard PCR techniques. (FYI – this is testable material). Why was the Genetic Information Nondiscrimination Act of 2008 (GINA) passed? To protect patients from discrimination based on genetic information. What does the term recombinant DNA (rDNA) refer to? Refers to DNA that is generated or engineered by combining DNA from different organism. What are restriction enzymes? Enzymes that are used to generate compatible or sticky ends of complementary base pairs between the copied DNA and the plasmid to construct recombinant DNA. What is transformation? Is a process by which cells take up DNA from their environment. What type of tool is CRISPR-Cas9? Gene-editing tool What does the CRISPR part of CRISPR-Cas9 do? Includes a guide RNA that acts like a molecular GPS for Linding the desired genetic sequence that is to be cut out – the guide RNA nucleotide sequence is complementary to the target DNA nucleotide sequence. What does the Cas9 part of CRISPR-Cas9 do? Serves as the scalpel that cuts the targeted DNA sequence; enzyme cuts both strands of the targeted DNA, generating a double strand break. What is gene therapy? The process of introducing genetic material that is not a human cell as a treatment. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 In general, what do microarray assays investigate? The differences between healthy cells and diseased ones, such as cancer cells. Chapter 15: Antimicrobial Drugs Section 15.1: Introduction to Antimicrobial Drugs 1. DeLine antimicrobial drugs. Therapeutic compounds that kill microbes or inhibit their growth. 2. Who discovered penicillin? Alexander Fleming 3. What is the difference between broad-spectrum to narrow-spectrum drugs? Broad-spectrum drugs: effective against both gram-negative and gram-positive bacterial cells. Narrow-spectrum drugs: target a limited range of bacteria. o Preferred because they present less disruption to the normal microbiota than do broad-spectrum drugs. 4. What is empiric therapy? A standard, accepted, or typical treatment based on clinical presentation in the absence of deLinitive or complete clinical data. NOTE: When someone seriously ill comes to the ER with a bacterial infection, the doctor may not know the exact bacterium that is causing the issue. To be safe, they may begin treatment with a broad-spectrum antibiotic to protect the patient from a wide variety of Gram-positive and Gram-negative bacteria until the speciLic organism is identiLied. Broad- spectrum antibiotics are only used for a short period of time, so that minimal damage is done to the normal microbiota. Many times, this will occur if a patient is admitted in serious condition and the doctor doesn’t have a clear idea of what bacteria is causing the issue. This way, there is a greater chance of initially helping the patient until they determine the causative agent. 5. Prolonged treatment with broad-spectrum antimicrobial drugs can disrupt our normal microbiota. What infection are hospitalized patients at risk for due to prolonged use of broad-spectrum antimicrobial drugs? Clostridioides difJicile infection 6. What is the difference between bacteriostatic and bactericidal antimicrobial drugs? (NOTE: the sufLix “-cide” means “to kill”. I.e. Homicide means killing of a human, so bacterial means killing bacteria). Bacteriostatic antimicrobial drugs: prevent bacteria from growing. Bactericidal antimicrobial drugs: actively killing bacteria. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 7. What is a serious drawback that can occur when using a bacterial drug for an endotoxin-producing Gram-negative bacterial infection? It could trigger a dangerous surge in LPS levels in the patient. 8. What are the differences between antibiotics, synthetic antimicrobials, and semisynthetic? Antibiotics: naturally occurring antimicrobial compounds. Synthetic Antimicrobials: wholly manufactured by chemical processes. Semisynthetic Antimicrobials: naturally occurring antibiotics that can be chemically modiLied to improve their pharmacological actions and/or stability. 9. Drugs that have been modiLied from their core molecule are denoted by “generations”. Which of the following would be oldest generation drug? Which would be the newest generation drug? Which would have the most expanded capabilities over the predecessors? [possible answers: 1st generation, 2nd generation, 3rd generation, 4th generation]. Oldest Generation Drug – 1st generation Newest Generation Drug – 4th generation Most capabilities over the predecessors – drugs in later generations have expanded capabilities over their predecessors. 10. DeLine the selective toxicity of a drug. Meaning that it inhibits or kills the targeted microbe without damaging host cells. 11. What is the therapeutic index of a drug. The ratio of the maximum tolerated or safe dose to the minimum effective or therapeutic dose. 12. TRUE or FALSE. IF the statement is False, correct it: A drug with a high therapeutic index is safer than a drug with a narrow therapeutic index. True 13. Because the kidneys and liver are key organs that metabolize and eliminate drugs, they may be particularly susceptible to damage by certain drugs. What is the general name for a drug that is toxic to the kidneys? What is the general name for a drug that is toxic to the liver? Toxic to kidneys – nephrotoxic Toxic to liver - hepatotoxic 14. When talking about drugs, what is half-life? The time it takes for half of a dose to be eliminated or deactivated by the body. Section 15.2: Survey of Antibacterial Drugs NOTE: You read this earlier in the chapter, but it is worth repeating: Most antibiotics that inhibit protein synthesis or block metabolic pathways are considered bacteriostatic, Exam #4 Microbiology Lecture Study Guide Chapters 14-18 whereas most drugs that target the bacterial cell wall, cell membrane, or nucleic acids (DNA or RNA) act as bactericidal drugs. NOTE: FIGURE 15.4 Key antibacterial drug targets is a helpful synopsis of this subject. Each of the names given in this image are drug family names. Unless I speciLically ask a question in this study guide about an example of a drug in a speciLic drug family, we will talk about drug families. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 TABLE 15.1 Summary of Key Antibacterial Drug Families. This table will help you answer many questions in the study guide. 1. What super family of drugs work by blocking cell wall synthesis? What molecule do most bacterial cell walls consist of? Beta-lactam antimicrobials o peptidoglycan 2. What is the function of beta-lactamases? Enzymes that inactivate beta-lactam drugs 3. How do beta-lactamase inhibitors such as clavulanate work? Beta-lactamase inhibitors have a beta-lactam ring structure and bind strongly to beta-lactamase enzymes. This binding blocks beta-lactamase from deactivating the administered antimicrobial. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 4. Which generation of cephalosporin is used to combat MRSA/ORSA strains? Fifth generation 5. What drug family is effective against a variety of multidrug-resistant (MDR) bacterial strains, so they are often reserved to Light strains that are healthcare- acquired? Carbapenems 6. What does the abbreviation CRE stand for? Carbapenem-resistant Enterobacterales (CRE) 7. What does the abbreviation CRA stand for? Carbapenem-resistant Acinetobacter (CRA) 8. What drug family is not a beta-lactam, but inhibits cell wall synthesis? Glycopeptides 9. What is the name of the glycopeptide drug used to treat MRSA and Clostridiodes difJicile infections? vancomycin 10. What antibiotic is the Staphylococcus aureus strain VRSA resistant to? (HINT: what does the “V” stand for?) vancomycin 11. What does the drug isoniazid target? Tuberculosis o Interferes with mycolic acid construction in cell walls of acid-fast bacteria. 12. What molecule is targeted by quinolones and rifamycin? Quinolones – DNA replication enzymes, namely DNA gyrase and topoisomerases. Rifamycin – RNA polymerase 13. What drug family targets folic acid synthesis? Sulfa drugs (or sulfonamides) 14. Why are human cells not affected by sulfonamide drugs? Mammals do not make their own folic acid and therefore do not have the enzyme these drugs target. 15. What is drug synergism? The combined effectiveness of two drugs that is greater than the sum of their effectiveness when used alone. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 Section 15.3: Drugs for Viral and Eukaryotic Infections 1. Why is it more difLicult to develop drugs that target viruses and eukaryotes? This is difLicult to do without inLlicting collateral damage on our own cells. 2. What category of antiviral drugs stimulate an immune response to viruses? interferons NOTE: We already learned about Live categories of antiviral drugs that inhibit speciLic steps viral activity in Chapter 6, so we won’t be covering them in this chapter. 3. When are antiviral drugs most effective? When viruses are actively replicating. 4. Name two structures that most antifungal drugs target? (1) Fungal cell walls (2) Fungal plasma membranes 5. Azoles, allylamines, and polyenes target fungal plasma membranes. What molecule are they speciLically targeting? ergosterol 6. What type of microbe causes athlete’s foot and ringworm? Fungus 7. What do antifungal echinocandin drugs target? An enzyme that makes beta-glucan, a component of the fungal cell wall. 8. What two processes does the antifungal drug Jlucytosine target? (1) DNA replication (2) Blocks transcription 9. Name the two groups of antiprotozoan drugs. (1) Antimalarial drugs (2) Nonmalarial antiprotozoan drugs 10. What challenge are physicians facing with many antimalarial drugs, such as chloroquine and hydroxychloroquine? It is increasingly common for malarial pathogen resistance to these drugs. o As seen with chloroquine, malarial protozoans are increasingly able to resist quinine and quinine derivatives such as meLloquine. 11. What does the antiprotozoan drug, metronidazole (Flagyl) target? Nucleic acids Exam #4 Microbiology Lecture Study Guide Chapters 14-18 o Effective against Toxoplasma gondii (toxoplasmosis), Trichomonas vaginalis (trichomoniasis), and the intestinal protozoans Giardia lamblia (giardiasis) and Entamoeba histolytica (amoebiasis). 12. How does the anthelminthic drug praziquantel work? It essentially paralyzes these parasites. Paralyzed intestinal worms and Llukes release their attachment to the intestinal wall and are then expelled in the feces. Section 15.4: Assessing Sensitivity to Antimicrobial Drugs 1. Why are antimicrobial susceptibility tests performed? To assess if the pathogen is likely to be treatable with a particular antimicrobial drug. 2. What is the Kirby-Bauer test? This test is used to determine a bacterium’s susceptibility to antimicrobial drugs. 3. What is a zone of inhibition? A clear zone that forms around a disk infused with a test drug. 4. When performing the Kirby-Bauer test, how is it determined if bacteria are susceptible, resistant, or exhibit an intermediate response to an antibiotic? The diameter of the zone of inhibition that may develop around a drug infused disk is measured and compared to a standard table to ascertain if the bacterium is susceptible, resistant, or intermediate in its response to the tested drug. NOTE: FIGURE 15.14 Kirby-Bauer test (disk diffusion test) is a good visual representation of what a zone of inhibition looks like and how to determine the antibiotics effectiveness against a certain strain of bacteria. 5. What is minimal inhibitory concentration (MIC)? The lowest concentration of the antimicrobial drug that inhibits the microbe’s growth. 6. DeLine minimum bactericidal concentration (MBC). The minimum concentration of the drug that kills at least 99.9% of the bacteria present. Section 15.5: Drugs Resistance and Proper Antimicrobial Drug Stewardship 1. DeLine antimicrobial resistance. A situation in which a microbe, which could be a bacterium, virus, fungus, protozoan, or helminth, is not affected by a drug therapy that is intended to inhibit or eliminate the pathogen. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 2. What are superbugs? Resistant microbes 3. DeLine intrinsic resistance. Built-in qualities that help some bacteria naturally resist antimicrobial drugs. 4. DeLine acquired resistance. A form of antimicrobial drug resistance that develops due to genetic mutations. 5. List three main ways that microbes evade antimicrobial drugs. Altering the drug’s target Inactivating the drug Reducing drug concentrations inside the cell by blocking drug entry or by pumping the drug out of the cell. 6. What do plasmids carry? How are they transferred? Plasmids commonly carry genes that encode drug-inactivation tools. They are spread by horizontal gene transfer. 7. What are two key factors that have accelerated drug resistant pathogens? Noncompliance with prescribed dosing parameters Antimicrobial misuse 8. List Live microbes that are on the CDCs urgent threat list. C. difJicile Drug-resistant Neisseria gonorrhoeae Drug-resistant Candida auris (a type of fungus) Carbapenem-resistant Enterobacterales (or CRE) Carbapenem-resistant Acinetobacter (CRA) Chapter 16: Respiratory Infections Section 16.1: Overview of the Respiratory System 1. What is the most common microbial portal of entry? Respiratory route 2. What is the function of mucus in the upper respiratory system? Warms and humidiLies inhaled air and traps microbes and debris. 3. What is the function of cilia? Sweep the debris-laden mucus toward the nose and mouth. 4. DeLine sinusitis. NOTE: recall that the sufLix “it is” means “inLlammation of”. InLlammation and swelling of the sinus membranes. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 5. DeLine pharyngitis. What is the common term for pharyngitis? InLlammation of the pharynx (throat); mainly caused by bacteria, viruses, or allergens. a. Commonly called a “sore throat” 6. DeLine epiglottitis. Why is the condition dangerous? InLlammation and swelling of the epiglottis, which can block the airway. NOTE: We learned about the mucociliary escalator in Chapter 11. Review the mucociliary escalator information and FIGURE 16.3 Mucociliary escalator. 7. DeLine laryngitis, tracheitis, and bronchitis. Laryngitis: inLlammation of the larynx. Tracheitis: InLlammation and swelling of the trachea. Bronchitis: InLlammation of the bronchi and/or bronchioles. 8. What is the medical term for croup? What respiratory structures are inLlamed when an individual has croup? Laryngotracheobronchitis a. InLlammation of the larynx, trachea, bronchi, and bronchioles. 9. What is stridor? What condition is associated with stridor? Wheezing or loud breathing associated with airway obstruction. a. Associated with croup. 10. DeLine pneumonia. What is the function of alveoli? InLlammation of the lung tissue, especially of the alveoli. a. Alveoli – specialized regions of the lungs where gas exchange occurs. 11. DeLine systemic infection. Infections that affect the whole body. 12. DeLine dyspnea. Shortness of breath Section 16.2: Viral Infections of the Respiratory System 1. What type of microbe causes the most common respiratory infection called the common cold? Viruses 2. DeLine serovar. Genetically distinct variants of the same species that are distinguished according to their different surface antigens. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 3. Which two viruses and their serovars are estimated to cause 60-80% of all colds? Rhinoviruses and coronaviruses 4. Why is it unlikely that a vaccine to the common cold will likely never be developed? There are so many different viruses that cause colds. 5. What virus is the leading cause of acute lower respiratory tract infections in children under Live years of age world-wide? Respiratory Syncytial virus (RSV) 6. List three more serious illnesses that human parainJluenza virus (HPIV) infections can cause in children and the elderly. (You are required to know the full virus name and its abbreviation). Croup (Laryngotracheobronchitis) Bronchitis Pneumonia 7. Adenoviruses are responsible for up to 10% of respiratory illnesses in children. What are three non-respiratory illnesses that certain adenoviruses cause? Conjunctivitis (pink eye) Gastroenteritis (diarrhea) Bladder infections (cystitis) 8. What are two important glycoproteins virulence factors located on the surface of the inLluenza virus? (You need to know the name and the abbreviation of each, and that both are spike proteins). Hemagglutinin (HA) Neuraminidase (NA) NOTE: We learned about these factors in Chapter 6. Review the information about these factors. 9. The Spanish inJluenza outbreak of 1918 killed millions of people worldwide. What was the reason there was so much death? (HINT: What caused the death?). The population had a strong immune response and experienced what is called a cytokine storm. NOTE: When reading Training: Tomorrow’s Health Team, How to Fight the Flu, did you notice that all four antiviral drugs ended with “vir”? Most, if not all, antiviral drugs end with “vir” – you can remember this since the word virus has “vir” in the spelling. 10. Why is it recommended that individuals get an inLluenza vaccine every year? The viral candidates usually change from year to year. NOTE: We learned about antigenic drift and antigenic shift in Chapter 6. Review the information about these processes. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 11. Why can individuals who were vaccinated for the Llu still contract the Llu? Vaccine formulation is based on an educated guess regarding which strains will be circulating during the season; sometimes a strain begins circulating widely that wasn’t included in that year’s vaccination, reducing the vaccine’s efLicacy. 12. Severe acute respiratory syndrome 1 and 2 (SARS-CoV-1 and SARS-CoV-2) and middle eastern respiratory syndrome (MERS-CoV) are caused by which type of virus? (HINT: What does the abbreviation “CoV” stand for?). coronavirus 13. What host cell receptor does the SARS-CoV-2 spike protein bind to? Angiotensin-converting enzyme 2 (ACE2) on host cells 14. List Live tissues that express ACE2. Can you now understand why there are many different types of complications seen when people contraction SARS-CoV-2? kidneys heart blood vessels neurons lungs 15. Acute respiratory distress syndrome (ARDS) can be observed in severe cases of COVID-19. What occurs in the body if a patient developed ARDS? Rapidly progressing form of an inLlammatory lung injury that leads to a sudden and marked reduction in blood oxygenation. 16. What is the difference between a viral variant and a viral strain? (NOTE: Even though we refer to different strains of SARS-CoV-2 as “variants”, they are in actuality “viral strains”.) Viral Variant: an isolate of a virus that has at least one mutation that makes it genetically distinct from the original form of the virus. Viral Strain: A term used to refer to viral variants that have mutations with physiological consequences. 17. What is hanta pulmonary syndrome (HPS) and how is it contracted? An acute and potentially fatal respiratory illness that humans can acquire when they inhale airborne dust particles that contain hantavirus particles (also called sin nombre virus) shed in rodent urine or feces. 18. DeLine pulmonary edema. Fluid accumulation in the lungs Section 16.3: Bacterial Infections of the Respiratory System 1. DeLine otitis media. Why are children especially susceptible to otitis media? Exam #4 Microbiology Lecture Study Guide Chapters 14-18 Middle ear infection a. Their eustachian tubes are shorter, narrower, and oriented such that draining into the pharynx is less efLicient. 2. What bacterium is the primary cause of strep throat? (Be speciLic- include group.) Group A streptococcus (GAS), S. pyogenes 3. Besides culturing the pathogen, what test is used to conLirm the diagnosis of streptococcal pharyngitis? Rapid strep test for bacterial antigens 4. What important virulence factor is produced by Streptococcus pyogenes which helps it invade host tissues? The M protein of the S. Pyogenes 5. What is the etiological agent of scarlet fever? Erythrogenic toxin from Streptococcus pyogenes. 6. “Strawberry tongue” and sandpaper rash are clinical signs of which condition? Scarlet fever 7. Which S. pyogenes virulence factor causes autoimmune complications to the heart? What is this autoimmune complication of the heart called? M proteins a. Rheumatic heart disease 8. Which bacterium causes diphtheria? What is a bull neck that is observed in acute diphtheria infections? Gram-positive rod Corynebacterium diphtheriae a. The bull neck is swelling in the neck region. 9. If a patient is left untreated after exposure to diphtheria A-B exotoxin, a thickened, leathery structure can form on the throat. What is it called? pseudomembrane 10. What three infections does the DTaP vaccine protect against? diphtheria tetanus toxoids acellular pertussis 11. What is the etiological agent of pertussis? What is the common name for this infection? Gram-negative bacterium Bordetella pertussis a. Commonly called whooping cough Exam #4 Microbiology Lecture Study Guide Chapters 14-18 12. DeLine paroxysms. What infection is associated with paroxysms? A sudden or violent attack (severe coughing) a. Pertussis (whooping cough) 13. Why is it important to get the Tdap booster? (HINT: how long does DTaP immunity last?)? The DTaP vaccine is not long lived and the Tdap booster is needed to renew immunity to pertussis. 14. What disease was historically known as consumption? Tuberculosis (TB) 15. In current times, what is the main pathogen that causes tuberculosis (TB)? Mycobacterium tuberculosis; acid-fast, Gram-positive bacteria 16. Use the information in FIGURE 16.13 Latent tuberculosis (TB) progression to active infection, to answer the following: a. What is a granuloma? a. A small area of inLlammation due to tissue injury; tiny cluster of tissue that stores infected macrophages to limit spread of infection. b. During which stage of a TB infection do granulomas form? b. Latent tuberculosis stage c. How does latent TB progress to an active TB infection? c. Occasionally the center of the granuloma liqueLies, and the walls break down, leading to an active infection that can transmit the bacterium to others. 17. Are US citizens typically vaccinated against TB? What is the name of the tuberculin skin test regularly used to screen health workers in the US? People in the United States are not routinely vaccinated. a. Skin test – the Mantoux tuberculin test is performed by an intradermal injection of tuberculin puriLied protein derivative (PPD). 18. 48-72 hours after a tuberculin skin test is administered, the injection site is checked for induration. What is induration? Development of a hardened area at the injection site caused by inLlammation. 19. According to the CDC, what disease caused by an infective agent is among the leading causes of death in the US? pneumonia 20. DeLine dyspnea. Shortness of breath 21. What is ventilator-associate pneumonia (VAP)? Exam #4 Microbiology Lecture Study Guide Chapters 14-18 A form of pneumonia that occurs more than 48 hours after a hospitalized patient is put on a mechanical ventilator. 22. What is consolidation? What does it look like on a chest x-ray? (Use the information in the Clinical Vocabulary section to answer this question.) A term that refers to the apparent merging of the lung air sacs (alveoli) when Lluid accumulates in the lungs. a. Appears as a white or hazy opaque region on a chest x-ray. 23. Use the information in TABLE 16.2 Clinical Presentation of Pneumonia, to answer the following question: What is a productive cough? Coughing with sputum 24. What is the most common form of bacterial pneumonia? What bacterium causes it? Pneumococcal Pneumonia a. Caused by streptococcus pneumoniae 25. What is the commercial name of two vaccines that protect against pneumococcal pneumonia. PCV-13 (Prevnar 13) PPSV-23 (Pneumovax) 26. What is the etiological agent of Hib pneumonia? Gram negative Haemophilus inJluenzae bacterium 27. TRUE or FALSE? If the statement is False, correct it. Haemophilus inJluenzae is the etiological agent of inLluenza. False a. It causes pneumonia. 28. There are six main bacterial pathogens that cause atypical pneumonia, in which three are zoonotic. Name the three pathogens that are zoonotic and state the name of the illness each cause. Coxielle burnetti – Q fever Chlamydia psittaci – psittacosis Francisella tularensis – tularemia 29. What pathogen causes the most common atypical, community acquired pneumonia? Mycoplasma pneumoniae a. Walking pneumonia 30. Which genus of bacteria that causes atypical pneumonia was incorrectly categorized as a virus due to possessing virus-like characteristics? Mycoplasma Pneumonia Exam #4 Microbiology Lecture Study Guide Chapters 14-18 31. What is the etiological agent of Chlamydophila pneumonia? Chlamydophila pneumoniae 32. What pathogen causes Legionnaire’s disease and Pontiac fever? Legionella pneumophila 33. What is the etiological agent of an atypical pneumonia called psittacosis (also called ornithosis)? Birds in which animal family are especially likely to be carriers? (HINT: the root word ‘ornith’ means bird. For example, ornithology is the study of birds. This is why this disease is also referred to as ornithosis.) Chlamydophila psittaci a. Pigeons and birds in the parrot family (psittacine) such as parakeets, macaws, and cockatiels. 34. What is the etiological agent of an atypical pneumonia called Q-fever? How does someone contract this illness? Coxielle brunetti a. If someone inhales dust or aerosols from feces, urine, or birth products, or consuming unpasteurized milk products. 35. What is the etiological agent of an atypical pneumonia called tularemia? Why is this pathogen considered a potential bioweapon? Francisella tularensis a. It is an extremely infectious zoonotic disease. Section 16.4: Fungal Respiratory System Infections 1. DeLine mycosis. Fungal infection 2. What is the etiological agent of blastomycosis in the USA? What is its common name (HINT: the one named after a US City)? Blastomyces dermatitidis a. Commonly called Chicago Disease 3. What does it mean if a fungus is dimorphic? It’s able to exist in two distinct forms. 4. DeLine saprophyte. A mold form that thrives on decomposing plant matter in moist soil. 5. What are the two etiological agents of coccidioidomycosis? Which fungal species causes Valley fever? Coccidioides immitis Coccidioides posadasii Exam #4 Microbiology Lecture Study Guide Chapters 14-18 a. Valley Fever is caused by Coccidioides immitis. 6. What is the etiological agent of histoplasmosis? Dimorphic fungus Histoplasma capsulatum 7. Opportunistic fungal pathogens cause most ubiquitous mycoses. What group of individuals is most likely to contract these pathogens? Immune-compromised patients 8. What is the main fungal genus isolated from patients with invasive aspergillosis? Aspergillus fumigatus 9. What is the etiological agent of mucormycosis? Rhizopus arrhizus 10. What is the etiological agent of pneumocystis pneumonia (PCP)? Pneumocystis jirovecii Chapter 17: Skin and Eye Infections Section 17.1: Overview of the Skin Structure, Defenses, and Afalictions NOTE: As we discussed in Chapter 11, the skin is a Lirst-line innate defense. It acts as a physical barrier to prevent bacteria from entering the body. 1. What is the function of the epidermis? Remember, the preLix “epi” means “on top of” or “above”. The root word “derm” means “skin”. Defend the body a. Outermost, waterproof barrier that protects the inner basal level of cells from intruders. 2. What cells comprise most of the epidermis? What protein is a main component of these cells? What is the protein’s function? Keratinocytes a. Keratin (a waterprooLing protein) 3. What layer of skin is located below the epidermis? dermis 4. What layer associated with the skin is located below the dermis? Subcutaneous layer 5. What is melanin? What is its function? The brown pigment in our skin. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 a. Has antimicrobial properties and protects against ultraviolet radiation that depletes the skin of folic acid and causes skin damage. 6. What enzyme is found in perspiration? What is its function? Lysozyme a. Breaks down the peptidoglycan found in bacterial cell walls. 7. What is sebum? An oily or waxy substance produced by the skin’s sebaceous glands (oil glands) and is a combination of low-pH lipids and proteins that moisturize and further protect the skin. 8. DeLine dermatoses. Infections and noninfectious skin diseases. 9. DeLine lesion. What is the difference between a primary and secondary lesion? HINT: use the Clinical Vocabulary section. Clinical term for any observable abnormality of the skin. a. Primary lesions: lesions that are directly associated with a disease and are considered key features for diagnosing a variety of infections. b. Secondary lesions: lesions that are less strictly deLined and that have diverse origins; may evolve from primary lesions, or from external forces like trauma or scratching. NOTE: You should be familiar with the different types of primary and secondary lesions explained in TABLE 17.1 Primary Lesions and Table 17.2 Secondary Lesions. You will read these terms throughout this chapter. Sections 17.2 Viral Skin Infections 1. What is the etiological agent of chickenpox? How is it typically spread? Herpesviridae family virus varicella-zoster a. Typically spread through respiratory droplets and occasionally from direct contact with pox lesions. 2. Reactivation of which dormant pathogen causes shingles? Where in the body does the pathogen remain dormant until reactivation? Varicella-zoster virus a. Remains dormant in the peripheral nerves. 3. What is postherpetic neuralgia (PHN). What infection is it associated with? A chronic pain condition that results from shingles. 4. What is the etiological agent of smallpox? Before eradication, why was smallpox one of the most feared diseases? (Hint: mortality rate and transmissibility.) Exam #4 Microbiology Lecture Study Guide Chapters 14-18 Variola major virus a. It had a mortality rate of 30% and was highly contagious. 5. What is the etiological agent of oral herpes? How does oral herpes present? Remember, we learned in chapter 6 that human herpes viruses (HHV) are also called herpes simplex viruses (HSV). Both are correct. In this chapter, I will use the designation HSV to correspond with the textbook. Human Herpes virus 1 (HSV-1) a. Presents as painful, itchy, vesicular lesions that may develop on the lips about a week after infection. Initial infection may also be accompanied by a sore throat or Llu-like symptoms. b. Most infected individuals are asymptomatic, or symptoms are very minor. 6. Does HSV-1 cause a latent infection? If so, where does the pathogen lie dormant before reactivation? It can be latent and may cause Llare-ups in about 2/3rds of patients. a. Lies dormant in the trigeminal nerve. 7. TRUE or FALSE. If the statement is false, correct it. There is no cure or vaccine available for HSV-1 infections. True 8. What is the etiological agent of the measles? NOTE: the textbook isn’t clear that the measles virus is also called the rubeola virus. Another name for measles is rubeola. I will use rubeola virus when asking exam questions. Rubeola (measles) virus 9. Why is measles making a comeback? Parents have chosen not to vaccinate their children. 10. Use the information in FIGURE 17.6 Measles rash to answer the following: a. What are Koplik’s spots? Where are they found? What disease are they associated with? i. Koplik’s spots: red spots with white dots in the center. ii. Found on the tongue and in the mouth. iii. Associated with measles (rubeola). b. What is the mode of transmission for measles? iv. Respiratory route 11. What infections does the MMR vaccine protect against? Measles, mumps, and rubella 12. What is the etiological agent of German measles? What is another name for German measles? Rubella virus Exam #4 Microbiology Lecture Study Guide Chapters 14-18 German measles - Rubella 13. What causes congenital rubella syndrome (CRS)? What are three possible outcomes of CRS? HINT: DON’T use the outcomes in the Clinical Vocabulary section. Use the three general outcomes in the text. Rubella infections in pregnant women, especially during the Lirst trimester. a. Possible outcomes include stillbirth, miscarriage, or a variety of birth defects, including blindness, deafness, heart defects, and growth or mental disabilities. 14. What is the etiological agent of Jifth disease? Why is it referred to as “slapped cheek syndrome”? Parvovirus B19 a. The red facial rash makes the patient look as if they have been slapped on the cheeks. 15. Use the information in Training Tomorrow’s Health Team: MMR Vaccine Timing to answer the following question. Why isn’t the MMR and Var vaccines administered to infants until they are one year of age or older? They include live attenuated (weakened) viruses and should not be given before the immune system has time to develop. 16. What is the etiological agent of roseola? Human herpes viruses 6 & 7. 17. What are the two etiological agents of hand, foot, and mouth disease (HFMD)? Coxsackievirus A16 Enterovirus 71 18. What are the etiological agents that cause warts? papillomaviruses Section 17.3 Bacterial Infection of the Skin 1. Which bacterium plays a major role in certain types of acne? Propionibacterium acnes bacteria 2. “Staph infections” are mainly caused by which bacterium? Staphylococcus aureus bacteria 3. The textbook states that most strains of Staphylococcus aureus are mannitol fermenters and beta hemolytic. What growth media are used to determine these characteristics? Are they general growth, selective, differential, or selective and differential media? IF APPLICABLE, what does the media select for? What does it differentiate? Refer to chapter 7 to refresh your memory. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 Growth media: blood agar and Mannitol salt agar (MSA) Blood agar is a general growth media and differential media. a. Blood agar supports the growth of a wide variety of organisms. b. Blood agar can differentiate between bacteria that make hemolysins from bacteria that don’t make hemolysins. MSA is a selective and differential media. a. MSA is selective for growth of bacteria that can tolerate high salt levels. b. MSA is differential for organisms based on their ability to ferment a sugar called mannitol. 4. What two factors protect Staphylococcus aureus from phagocytosis? A protective polysaccharide capsule Protein A on its cell surface 5. What etiological agent can cause impetigo, erysipelas, cellulitis, and folliculitis? Staphylococcus aureus 6. What is cellulitis? A deeper Staphylococcus aureus infection of the lower dermal and subcutaneous fat. 7. What does the acronym MRSA stand for? What does VRSA stand for? MRSA – Methicillin-resistant Staphylococcus aureus VRSA – Vancomycin-resistant Staphylococcus aureus 8. What is the etiological agent of scalded skin syndrome? What virulence factor causes the skin to peel in sheets? Staphylococcus aureus a. Exfoliative toxins made by some strains of S. aureus NOTE: It is very important to note that certain infections caused by Staphylococcus aureus can also be caused by Streptococcus pyogenes. I have included TABLE 17.3 Select Staphylococcus aureus and Streptococcus pyogenes Virulence Factors in the Study Guide as reference and to help answer questions. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 9. Using the information in TABLE 17.3, Staphylococcus aureus can be differentiated from Streptococcus pyogenes by which two biochemical tests? Hint: S. aureus is positive for these two enzymes, while S. pyogenes is negative. Coagulase test Catalase test 10. TRUE or FALSE. If the statement is False, correct it: Streptococcus pyogenes is coagulase and catalase positive. FALSE Exam #4 Microbiology Lecture Study Guide Chapters 14-18 a. Streptococcus pyogenes is coagulase and catalase negative. 11. TRUE or FALSE. If the statement is False, correct it. Both S. aureus and S. pyogenes cause impetigo and cellulitis. True 12. What are Streptococcus pyogenes strains clinically referred to as? Group A streptococci 13. What is the function of S. pyogenes’ hyaluronic acid capsule? CamouLlage the bacteria from host and M protein on the surface that serves a binding site plasminogen to trigger a degradation cascade. 14. What is the etiological agent of necrotizing fasciitis and streptococcal toxic shock syndrome? What is necrotizing fasciitis referred to as? Streptococcal pyogenes a. Necrotizing fasciitis – “Llesh-eating disease” 15. TRUE or FALSE. If the statement is False, correct it. Pseudomonas aeruginosa is a common cause of HAIs. It is an opportunistic pathogen that readily establishes infections in people with weak immune systems, damaged skin, or other underlying health conditions. True 16. Infection with which bacterium develops in 2/3rds of burn patients? P. aeruginosa bacteria 17. What is pyocyanin? What bacterium produces it? A greenish-blue pigment that generates reactive forms of oxygen to further damage tissue. a. P. aeruginosa bacteria 18. What is the etiological agent of otitis externa? What is otitis externa? P. aeruginosa a. Otitis externa: swimmer’s ear; outer ear canal is infected 19. DeLine necrosis. Tissue death due to loss of blood Llow 20. What is the etiological agent of gas gangrene? Clostridium perfringens 21. What is the etiological agent of cutaneous anthrax? Bacillus anthracis Exam #4 Microbiology Lecture Study Guide Chapters 14-18 Section 17.4 Fungal Skin Infections 1. What are cutaneous mycoses? What are subcutaneous mycoses? Which, if either, are more serious infections? Cutaneous mycoses: fungal skin infections Subcutaneous mycoses: deeper dermal or muscle fungal infections that can be more serious than cutaneous mycoses. a. Subcutaneous mycoses are more serious infections. 2. DeLine dermatophyte. Hint: use the Clinical Vocabulary deLinition. A collection of fungal organisms that cause conditions of the skin, hair, or nails. 3. What is the etiological agent that causes many cutaneous mycoses, such a diaper rash? Candida albicans 4. What type of organism causes ringworm? Tinea (fungus) 5. What type of organism causes jock itch and athlete’s foot? Jock itch – tinea cruris Athlete’s foot – tinea pedis 6. List the main three fungal genera that cause most tinea infections. (FYI: “genera” is the plural form of “genus”; The word ‘tinea” is NOT a genus of fungi. It denotes a dermatophyte infection.) Trichophyton species Microsporum species Epidermophyton species Section 17.5 Parasitic Skin Infections 1. What is the etiological agent of the neglected tropical disease called leishmaniasis? What type of microbe is it? How is it transmitted? Leishmania species a. Microbe – protozoan b. Transmitted by the bite of infected sand Llies. 2. What are the differences between cutaneous, mucocutaneous, and visceral leishmaniasis? Cutaneous leishmaniasis: skin ulcers, which are usually painless, form at bite sites and can persist for months or even years. Mucocutaneous leishmaniasis: the lesions develop in mucous membranes of the nose or mouth. It can lead to severe and permanent disLigurement as the protozoan destroys these structures. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 Visceral Leishmaniasis: the protozoan spreads throughout the body. Section 17.6 Structure, Defenses, and Infections of the Eye 1. What is the cornea of the eye? What is the conjunctiva? A transparent layer at the front of the eye that covers the iris. The conjunctiva is the epithelial membrane that covers the eyeball and lines the eyelids. It does not cover the cornea but surrounds it. 2. Besides oils, mucus, sugars, what two protective factors are contained in tears? We learned about one of these that is contained in perspiration (sweat) earlier in this chapter. What is the function of lactoferrin? Lysozyme and lactoferrin a. Lactoferrin: binds up free iron. 3. What is conjunctivitis? What is it commonly known as? InLlammation of the conjunctiva or epithelial membrane over and around the eye. a. Commonly known as “pink eye” 4. What clinical features can distinguish bacterial vs. viral conjunctivitis? The nature of the Lluid discharge from the eye. a. Bacterial: puslike discharge (often green or yellow). b. Viral: watery (but not thick) discharge. 5. What microbe causes most viral eye infections? adenoviruses 6. How can neonatal HSV eye infections be contracted? Following transmission from the mother to the infant as the baby passes through the birth canal. 7. Which two bacteria cause neonatal bacterial conjunctivitis? How is it acquired? Neisseria gonorrhoeae Chlamydia trachomatis a. It is acquired by vertical transmission at birth. 8. Why are antibiotic drops administered to baby’s eyes after delivery? To prevent infection; neonatal bacterial conjunctivitis can lead to serious eye damage if not treated. 9. What is the leading cause of bacterial blindness in the United States? What is the etiological agent of this infection? Trachoma a. Chlamydia trachomatis Exam #4 Microbiology Lecture Study Guide Chapters 14-18 10. What is keratitis? Severe inLlammation of the cornea. 11. What is the etiological agent of most herpetic keratitis infections? What nerve does this microbe lay dormant in? Herpes simplex 1 virus a. Lays dormant in the trigeminal nerve and reactivates in the ophthalmic nerve. 12. What is the leading cause of infectious blindness in the United States? Why? Herpes keratitis 13. What two organisms are the most common cause of bacterial keratitis? Pseudomonas aeruginosa Staphylococcus aureus 14. Which individuals are at highest risk for fungal keratitis? Individuals that have suffered eye trauma or have had eye surgery (including radial keratotomy to correct nearsightedness. 15. What is the etiological agent of protozoan keratitis? Acanthamoeba 16. What is the etiological agent of helminthic keratitis? What is the medical name and the common name for this infection? Onchocerca volvulus a. Medical name: Ocular Onchocerciasis b. Common name: river blindness 17. How is helminthic keratitis introduced into humans? What nerve and/or eye structure is damaged by this pathogen? An infected blackLly bites someone and introduces the larvae to the skin. a. Damages the optic nerve and/or cornea Chapter 18: Nervous System Infections Section 18.1: Overview of Nervous System Structure and Defenses 1. What is the name of specialized cells in the central and peripheral nervous system that function to transfer signals throughout the body? neurons 2. What are neurotransmitters? What is their function? Chemical messengers a. Function: cause changes in neighboring cells. Exam #4 Microbiology Lecture Study Guide Chapters 14-18 3. What is myelin and what is its function? NOTE: the presence of myelin allows the action potential to quickly travel to the end of the axon. Later in the chapter, we will be learning about demyelinating diseases, which occur when myelin is destroyed. Due to this, the electrical signal doesn’t travel as fast or is severely hindered so that it affects nerve function. A fatty layer that helps electrical impulses travel quickly 4. TRUE or FALSE. If the statement is False, correct it. The nervous system contains a rich diversity of normal microbiota that functions to compete with infecting pathogens. False a. The nervous system contains no resident microbiota (normal Llora) to compete with infectious agents that manage to invade this body system. NOTE: Due to the absence of normal microbiota (=normal Llora), the brain, spinal cord, and nerves are considered “privileged sites”. 5. What is the gut-brain axis? The complex, back-and-forth communication that occurs between the endocrine, immune, and nervous systems and the gastrointestinal tract. 6. Which nervous system tissues support and care for the CNS by supplying nutrients, removing waste, and protecting the CNS from physical shocks? Meninges a. Dura mater, arachnoid mater, and pia mater. 7. What is the function of cerebrospinal Jluid (CSF) and where is it located? Cushions and nourishes the central nervous system. a. Within brain structures 8. Use the information in Training Tomorrow’s Health Team: Diagnosing Infections Using Lumbar Puncture to answer the following: What infection is a lumbar puncture used to diagnose? Meningitis 9. DeLine meningitis, encephalitis, and meningoencephalitis. Meningitis: inLlammation of any of the meninges. Encephalitis: inLlammation of the brain. Meningoencephalitis: inLlammation of the meninges occurring along with inLlammation of the brain. Section 18.2: Viral Nervous System Infections 1. What are the two main viruses that cause meningitis? coxsackieviruses poliovirus Exam #4 Microbiology Lecture Study Guide Chapters 14-18 2. What is poliomyelitis? What is the etiological agent of poliomyelitis? NOTE: Remember, any word that ends with the sufLix “-itis” means inJlammation of. In this case poliomyelitis is inLlammation of the myelin sheath. InLlammation of the myelin sheath. a. poliovirus 3. What structural feature protects poliovirus against stomach acid? The tough protein coat 4. What is Jlaccid paralysis? A form of paralysis that develops when muscles cannot contract. 5. What is the difference between symmetric and asymmetric paralysis? Symmetric paralysis: paralysis that affects both sides of the body. Asymmetric paralysis: paralysis that affects one side of the body more than another. 6. There are two polio vaccines available called the Salk (IPV) and Sabin (OPV) vaccines. What type of vaccine formulation are each of these? What is the drawback of the Sabin vaccine? Salk: inactivated polio vaccine (IPV) Sabin: live attenuated poliovirus/ oral polio vaccine (OPV) a. Immunocompromised individuals can develop illness from the attenuated virus. In rare circumstances, patients who receive the OPV can also develop paralytic polio. 7. What diagnostic tool is used to diagnose polio? Reverse transcriptase polymerase chain reaction (RT-PCR) 8. What is the most common domesticated animal reservoir for rabies? dogs 9. What is the diagnostic sign of rabies? What are these “bodies”? The formation of Negri bodies a. Small clusters of viruses inside the neurons. 10. If a person has been bitten by a suspected rabid animal, rabies post-exposure prophylaxis is administered. What two medical treatments are included in rabies post-exposure prophylaxis? Injection with both antirabies antibodies and the inactivated vaccine for rabies. 11. What type of immunity is derived from each of these treatments? (If you need help, refer to Chapter 12.4, heading “Humoral immunity is acquired naturally or artiLicially, and is either active or passive”) Exam #4 Microbiology Lecture Study Guide Chapters 14-18 Antirabies antibodies – artiLicially acquired passive immunity Inactivated rabies vaccine – artiLicially acquired active immunity 12. How were arboviruses named? NOTE: arthropods represent a very large, diverse group of organisms that includes insects. Arboviruses are transmitted to their host mainly by insects. They are enveloped, single-stranded RNA viruses and are transmitted by arthropods such as mosquitoes or ticks. Arthropod borne 13. How is West Nile virus contracted? Through an infected mosquito bite. a. Mosquitoes become infected with the virus upon taking a blood meal from an infected reservoir, usually an infected bird. When infected mosquitoes feed on animals, some of the viruses already in their stomachs gets regurgitated into the bite of the latest victim. This passes the virus from one animal to another. 14. West Nile and La Crosse viruses are neuroinvasive. If they cause a system-wide infection (= systemic infection), what two conditions can result? Meningitis Encephalitis 15. What are the two neuroinvasive arboviruses that are most seen in the United States? NOTES: Neuroinvasive arbovirus diseases include meningitis, encephalitis, and meningoencephalitis. West Nile virus La Crosse virus Section 18.3: Bacterial Nervous System Infections 1. Which is more dangerous- bacterial or viral meningitis? Bacterial meningitis 2. There are two tests that can differentiate between viral and bacterial meningitis. What are they? Make sure that you understand why the CSF glucose test results show what they do. Measure CSF glucose levels and compare them to blood glucose levels. a. Viral meningitis does not affect glucose levels in the CSF. But bacteria in the CSF lower the usual glucose amount because they use it for energy and as a carbon source. Bacterial meningitis can also be determined by growing the bacterium from a CSF sample or Gram staining such samples. 3. How is neonatal meningitis contracted? Exam #4 Microbiology Lecture Study Guide Chapters 14-18 Bacteria are passed to a neonate from their mother during delivery. 4. What bacteria and serotype causes Haemophilus meningitis? What is the vaccine administered in the United States to protect against Haemophilus meningitis called? You don’t have to know the brand names, just the general name. Haemophilus inLluenzae type b a. Hib vaccine 5. What is the etiological agent of meningococcal meningitis? Is it Gram positive or Gram negative? Is it encapsulated or non-encapsulated? NOTE: The word meningococcal has the word “-coccal” in it. This bacterium is round—so coccus. The organism grows as diplococci. What does that mean? Neisseria meningitidis a. Gram-negative b. Encapsulated c. Diplococci – pair of/two cocci 6. What is the etiological agent of pneumococcal meningitis? Is it Gram positive or Gram negative? Is it encapsulated or non-encapsulated (Review Disease Snapshot Pneumococcal Meningitis). Streptococcus pneumoniae a. Gram-positive b. Encapsulated c. Diplococci – pair of/two cocci NOTE: Just like meningococcal, the word pneumococcal has the word “-coccal” in it. The bacteria are cocci. This organism also grows as diplococci. Both organisms are encapsulated. How do you tell meningococcal meningitis from pneumococcal meningitis? You can tell the difference between the two by their Gram staining results. Neisseria meningitidis grow as Gram negative diplococci while Streptococcus pneumoniae grow as Gram positive diplococci. Also, the word pneumococcal has the root word “pneumo-“in it. The etiological agent of pneumococcal meningitis is Streptococcus pneumoniae. 7. Which bacteria cause most cases of meningitis in the United States? Streptococcus pneumoniae 8. What is the danger of S. pneumoniae exotoxin? The exotoxin stimulates severe inLlammation and provokes host tissue damage as immune cells release oxygen radicals and enzyme-destroying proteins in response to the toxin. 9. What is the etiological agent of Listeria meningitis? How are the bacteria transmitted to humans? Listeria monocytogenes Exam #4 Microbiology Lecture Study Guide Chapters 14-18 a. Transmitted as a foodborne illness through tainted cheese, lunchmeats, or even mangos can carry the pathogen. 10. What is the advantage of Listeria monocytogenes’ intracellular lifestyle? How can the bacteria remain intracellular but still infect neighboring cells? The bacteria can grow, and divide hidden from antibody-mediated immune responses. a. L. monocytogenes doesn’t even have to enter the intercellular space to spread the infection. It forces a protein called actin in the cytoskeleton of the eukaryotic cell it’s infecting to form a “tail” and propel it like a rocket into an adjacent cell. 11. What is the etiological agent of Hansen’s disease? NOTE: Remember that Mycobacterium species are acid-fast organisms. What is the molecule that is detected when performing acid-fast staining? Mycobacterium leprae a. Mycolic acid 12. What animal is the natural carrier of Mycobacterium leprae? Why? Armadillos a. Due to their cooler body temperature (30-35*C), which is necessary for M. leprae’s growth. 13. What is the difference between the tuberculoid and lepromatous forms of Hansen’s disease? Tuberculoid: paucibacillary Lepromatous: multibacillary 14. What is the etiological agent of botulism? Where is it normally found? Clostridium botulinum a. Globally found in soils; also found in canned vegetables such as beets, carrots, and spinach. NOTE: This toxin is puriLied and used for cosmetic and medical procedures. You may be familiar with Botox. The moniker “Botox” comes from “botulism toxin”. 15. C. botulinum can form endospores. What is the danger of this to humans? HINT: improperly canned vegetables accounted for 38 percent of the 116 cases of foodborne botulism from 1996–2008 in the United States. Endospores are highly resistant bacterial structures that can survive harsh conditions, including cooking. 16. Botulism toxin causes what type of paralysis? Flaccid (relaxed) paralysis Exam #4 Microbiology Lecture Study Guide Chapters 14-18 17. What is the etiological agent of tetanus? Where is it normally found? What type of wounds are mainly associated with tetanus infections? Clostridium tetani a. Found in soils all over the world. b. Associated with wounds from rusty objects like a nail 18. What is the common name for tetanus? What is the name of the powerful toxin produced by the etiological agent of tetanus? What does the toxin do to the body— ie: what does it cause? “lock jaw” Tetanospasmin toxin a. Leads to spastic paralysis, which is an inability to relax muscles. Section 18.4: Other Nervous System Infections 1. What is the etiological agent of cryptococcosis? What type of organism is it? How is it contracted? Cryptococcus neoformans a. Fungus b. Contracted by inhaling stirred up pathogens from soil or bird droppings. 2. Infection with which fungal organism is the leading cause of death in HIV/AIDS patients? Cryptococcus neoformans 3. What is the etiological agent of African sleeping sickness? What type of organism is it? Trypanosoma brucei a. protozoan 4. How does a person contract African sleeping sickness? A bite from an infected blood-sucking tsetse Lly. 5. What is the etiological agent of primary amoebic meningoencephalitis (PAM)? How is a person typically infected with the pathogen? What is the pathogen often called due to the severity of the damage to the central nervous system it causes? Amoeba Naegleria fowleri a. Infected by swimming in warm, stagnant water. b. “the brain-eating amoeba” 6. What is the etiological agent of toxoplasmosis? What animal acts as the deLinitive host for the pathogen? Toxoplasma gondii a. Cats Exam #4 Microbiology Lecture Study Guide Chapters 14-18 7. Why shouldn’t pregnant women clean cat litter boxes? Cats shed the protozoans in their feces, and it could transmit from mother to fetus; the protozoan can cross the placenta and infect the fetus. There it invades nervous tissue and can cause convulsions, deafness, or neurological disabilities. Sometimes, a fetal toxoplasmosis infection can cause miscarriage or stillbirth. 8. What molecule is a prion? What is the name of the disease (in general) that prions cause? Infectious proteins a. Cause transmissible spongiform encephalopathy (TSE) 9. Name the two scientists that won the Nobel Peace Prizes for their work deducing that prions were the cause of certain spongiform diseases. NOTE: Daniel Gajdusek won the Nobel Prize in 1976 for deducing that an infectious protein was the cause of a disease called kuru. Stanley Prusiner won the Nobel Prize in 1997 discovering that an infectious protein caused by protein misfolding was the cause of bovine spongiform encephalitis (also known as “mad cow disease”) and the human equivalent called Creutzfeldt–Jakob disease. He coined the term “prion”. Daniel Carleton Gajdusek Stanley Prusiner 10. What is scrapie? What is BSE? A disease named for the way that affected sheep rub their skin raw on fences. Bovine spongiform encephalopathy (BSE) = mad cow disease 11. In 1996, people mainly from England died from variant Creutzfeldt-Jakob disease. How did they contract the disease? Eating beef contaminated with BSE prions 12. What is chronic wasting disease? A concern for public health ofLicials in the United States. a. Deer and elk in certain northern areas of the United States have the species- speciLic prion disease CWD. Given the cases of cross-speciLic infection through consumption of contaminated meat, there are fears that venison forms these areas could cause a new outbreak. 13. What are most human prion cases due to? What population is most likely to develop this disease? Non-variant Creutzfeldt-Jakob disease (CJD) a. The elderly are most likely to develop the disease. 14. How is a normal prion protein (denoted as PrPc) changed to the infectious form (denoted as PrPsc)? What does the “sc” stand for in PrPsc? Exam #4 Microbiology Lecture Study Guide Chapters 14-18 When the normal prion protein encounters an abnormally shaped version of itself, PrP^SC (scrapie-like prion protein), the normal prion’s shape is changed, and it becomes an infectious PrP^SC. a. The “sc” stands for scrapie.