Microbiology Study Guide COMPLETED.docx

BMS 150 – Microbiology Study Guide – Issue 1 – URT Microbiome and Infections 1) Distinguish between the upper and lower respiratory tracts; distinguish between the respiratory zone and conducting zones. Upper: nostril, nasal cavity, oral cavity, pharynx Lower: Trachea, broncus, lung, diaphram 2) Des...

BMS 150 – Microbiology Study Guide – Issue 1 – URT Microbiome and Infections 1) Distinguish between the upper and lower respiratory tracts; distinguish between the respiratory zone and conducting zones. Upper: nostril, nasal cavity, oral cavity, pharynx Lower: Trachea, broncus, lung, diaphram 2) Describe the mucuociliary escalator and other mechanisms of innate immunity in the respiratory tract as you progress from the conducting zone to the respiratory zone. Conducting zone: tubes outside/inside the lungs (nose, nasal cavity, pharynx, larynx, trachea, bronchi, lungs. Function: Filter, warm, moisten air Respiratory zone: aveoli, alveolar duct/sac, respiratory bronchioles (anywhere gas exchange takes place) Changes on the path from conducting to respiratory: hyeline cartilage plates → smooth muscle. Pseudo stratified ciliated columnar epithelium → simple squamous epithelium. No more cilia. No more mucous. 3) Compare and contrast the microbiomes of the upper and lower respiratory tracts. Explain the differences between the two. Upper: Diverse! Nose: haemophilus bacteria, veillonella bacteria, diphtheroid. Nasal cavity: staphylococcus bacteria, diphtheroid Pharynx: Staphylococcus bacteria, diphtheroid, streptococcus bacteria Lower: Free of resident microbiota due to cilia, mucosa, alveolar macrophages, IgA, natural antibiotics→ defensins and lysozymes Normal Microbiome of Pharynx and nasal cavity: 5) Describe key characteristics of each of the following groups of bacteria found as normal microbiota of the upper respiratory tract: haemophilus, veillonella, staph, diphtheroids, strep Type Aerobic or anaerobic? Opportunistic? Examples Fun Fact GFs required to live (1 or both) Condition Haemophilis Gram - Aerobic or facultative anaerobic Yes Also, VERY helpful haemopholis influenzae Grow on chocolate agar, not blood agar Fastidious: picky eaters=hard to grow in labs X factor- hemin V factor NAD+ (h. Influenzae requires both) Influenza Veillonella Gram - aerobic Yes Veillonell parvula Can break down lactate → ATP (potent lactate fermenters) Can break down nitrate → nitrate oxide (potent nitrate reducers) endocarditis and osteomyelitis *systematic disease Staphylococcus Gram + Facultative anaerobic VERY Staphylococcus aureus Sepsis, pnuemonia, menegitis, toxic shock, osteomyelitis, pimples, folliculitus, scalded skin syndrom Diphtherios Gram + Aerobic Propionibacterium acnes Looks like bacteria that cause diphtheria, BUT don’t cause it (Corynebacterium cause it!) hair follicles, lowers skin pH and can cause pimples Alpha- hemolytic streptococci Gram + Facultative anaerobic S. pneumonia (alpha) Biliverdin green growth (beta) S. pyogens= most concerning Beta: completely lyse Alpha: partially lyse Gamma: No hemolysis 4) Identify the various species of bacteria associated with the URT microbiome 6) Describe the classic signs and symptoms of strep throat Painful swallowing, bad breath, fever, malaise, headache 7) Describe, in detail, the virulence factors listed in class for S. pyogenes M protein (C3b inhibitor), hyaluronic acid capsule- encapsules cell so it can’t be detected by phagocytes (coagulase), streptokinases- breaks down clots to be released, C5a peptidase chemotaxis, attracts WBC to the site of infection, pyrogenic toxins, releases MANY cytokines (causing fever and rash), streptolysin O- lysing all human blood cells (RBC, WBC, platelets) *This is why it is considered beta-hemolytic* 8) Describe the diagnosis and treatment of streptococcal pharyngitis, as well as its epidemiology Epidemilogy: <50% of pharyngitis, spread via respiratory droplets in 1.5M radius, common in crowded areas, common in winter, was deadly before antibiotics, requires serological testing 9) Describe scarlet fever and rheumatic fever 10) Describe diphtheria, including: causative agent, a definition of pseudomembrane, a mechanism of action for diphtheria toxin, mode of transmission, diagnosis and treatment Causative Agent: Corynebacterium diptheriae Pseudomembrane: FIND DESCRIPTION Mode of Transmission: It is lysogenic, so it inserts itself into the host cells genome and is copied alongside the hosts genome. Not always pathogenic, must be injected with the lysogenic phase to be pathogenic Diagnosis: Elek Test (antibody test against diphtheria toxin) and pseudomembrane presence? Treatment: Antitoxins (neutralizing antibodies), antibiotics (erythromycin) and vaccination (DTaP) 11) Describe the signs and symptoms of the common cold. Sneezing, congestion, sore throat, malaise, “hacking” cough, rhinorrhea (runny nose) Symptoms usually last a week, although the cough can persist 12) Define rhinovirus and relate rhinoviruses to picornaviruses and enteroviruses. Rhinoviruses (enteroviruse that infect the nose): +ssRNA, non-enveloped Rhinovirus is a member of the picornavirus family **13) Define ICAM-1 and relate to the attachment and entry of a typical rhinovirus. What is the significance of the optimal receptor binding temperature? *** ICAM-1 is a ligand for integrin that rhinovirus binds to, in order to enter the cell via endocytosis Binding between ICAM-1 and Rhino virus is optimal at 33 degrees Celsius (temperature unique to nose and URT) **14) Describe the manner in which rhinoviruses bind to ICAM-1, including an explanation of why this makes rhinoviruses less immunogenic. *** The proteins of Rhino virus are deep within the capsid, and have a deep canyon for binding, making it difficult to recognize 15) Briefly describe the mechanism by which rhinoviruses replicate and exit within the endosome of the host cell. Rhinoviruses first starts replication by being endocytosed after binding to ICAM-1. The low pH within the endosome dissolves the capsid and releases viral nucleic acid into the cytoplasm. It is then translated, and replicated. At the same time, the viral RNA is used to create structural proteins. The viruses are then assembled. Once assembled, then exocytosed. *** Is both lytic and non lytic? * 16) Describe the relationship between HRV infections and secondary bacterial infections. The severity of infection is related to the type of Serotype HRV-B: Less severe and less frequent HRV-A/C: More severe, effects vary from country to country HRV infections increase one’s susceptibility to bacteria (secondary infections) Specifically, HRV’s disrupt tight junctions by acting on their associated proteins (ZO-1), increasing the release of IL-6 and IL-8 (which increases expression of ICAM-1, allowing for greater endocytosis), increasing NFK-b which induces PAFR expression (allowing for greater adherence of S. pneumoniae, and reducing levels of TNF-a and IL-8, which reduce the body’s response to infection. 17) Describe adenoviruses and compare with the rhinoviruses. Adenoviruses (cocksackie viruses): ssDNA, Non-enveloped, icosahedral. People are susceptible at any age. Can cause infection in any part of the body (due to receptor presence on various cell types throughout the body). Uses lysis. Uses endocytosis. INHIBIT DNA/mRNA/protein synthesis Rhino: ssRNA, enveloped. Can only cause infection in URT. Uses lysis? Uses endocytosis. Uses RNA/protein synthesis to proliferate. 18) Briefly describe the pathogenesis of adenoviruses Adenoviruses attach and enter via endocytosis Bind to CAR receptors NOT ICAM-1. 19) Describe the structure and genome of a typical coronavirus Coronavirus: +ssRNA, enveloped, has spike glycoprotein trimers on membrane. 20) Describe the mechanism for attachment and entry of coronaviruses *** Coronavirus’s S1/S2 complex binds to ACE2 Receptor S complex is cleaved via TMPRSS2 protease on the target cell membrane. S1 is cleaved, and so is S2’ S2 is activated and the viral membrane fuses with the host membrane 21) Distinguish between HHV-1 and HHV-2 HHV-1: cold sores, blisters, close contact, face/mouth, pharyngitis HHV-2: genital, sexual intercourse 22) Describe mononucleosis to include: causative agent, initial signs/symptoms, relationship to mucosal epithelia and underlying B cells, oral hairy leukoplakia, burkitt’s lymphoma, chronic fatigue, nasopharyngeal caner, and infectious mononucleosis. Causative agent: HHV-4- epstein-Barr Virus EBV: enveloped, ds DNA, icosahedral capsid, infects B lymphocytes, can become latent, prevents apoptosis in infected cells Symptoms: sore throat, fever, extreme fatigue Pathogenesis: initiates in respiratory epithelial mucosal cell → tonsil/tongue rich in lymphocytes → site for shedding → underlying B-cells become infected → lytin in E.C → lysogenic in B-cells (incorporated into host cell DNA) → circulate FOREVER (but won’t cause another infection, but can migrate out of E.C and shed into mucous through respiratory tract → saliva → spread Oral hairy leukoplakia (curable): elderly, immune system is lacking, Burkitt’s lymphoma, chronic fatigue, nasopharyngeal cancer: malnutrition, poor immune system Infectious mononucleus: teens with vigorous immune system Asymtpomatic: Child whose immune system is normal 23) Briefly describe the treatment and prevention of mononucleosis: Rest and don’t share saliva