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157 Cards in this Set
- Front
- Back
Name the Clinical Presentation of
1. Adenovirus (2) 2. Rhinovirus 3. Coronavirus (2) 4. HPIV (2) 5. RSV |
1. Pharyngitis & Cnojunctivitis
2. Common cold 3. Common cold, SARS 4. Croup & Bronchitis 5. Croup (most common viral cause) |
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Describe the Survival time on dry inanimate surfaces
1. Adenovirus 2. Rhinovirus 3. Cornovirus 4. RSV |
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Describe the Seasonality for the following viruses
1. Rhinoviurs 2. Coronavirus 3. Adenovirus 4. HPIV-3 5. HPIV 1 & 2 6. RSV 7. Influenza 8. Group A strp |
Rhinovirus: March -October
Adenovirus: All year long HPIV-3: March-July HPIV1, 2: Aug-Nov All the rest include winter |
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Name the Size, Nucleic Acid & Baltimore class for the following
1. Rhinovirus 2. Adenovirus 3. Influenzavirus 4. RSV 5. Coronavirus 6. HPIV |
1. Group IVa
2. Group I 3. Group Vb 4. Group Va 5. Group IVb 6. Group V |
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For the following virus, name the assay
1. Influenza virus 2. RSV 3. HPIV 1-4 4. Adenovirus |
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Name the UPPER tract Disease (6)
LOWER tract diseases (4) |
1. Common cold, Croup, Ottis media, Sinsusitis, Epiglottis, Phayngitis
2. Whooping cough, Bronchitis, Bronchiolitis, Pneumonia |
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Upper Tract vs. Lower Tract
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Upper
1. Higher O2, cooler, weaker filter, biota, larger pathogens 2. Lower 02, warmer, stronger immune response, sterile, smaller pathogens |
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What causes
1. Epiglottitis 2. Whooping Cough 3. Bronchiolitis |
1. H. influezae
2. B. pertussis 3. RSV |
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What causes (2)
1. Croup (2) 2. Ottis media & Sinusitis (2) 3. Common cold (2) |
1. Parainfluenzae virus & RSV
2. S. pneumoniae & H. influenzae 3. Rhinovirus & Adenovirus |
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Name the agents that causes phayngitis
1. ++++ 2. ++ (3) 3. + (4) 4. least important (4) |
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Name the FIVE infections that cause Bronchitis
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Parainfluenzae virus, RSV, Influenzae virus, M. pneumoniae & C. pneumoniae
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What does the mucus contain (5)
What enzymes are produced in the URT (3) |
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Compare LOWER & UPPER respiratory tracts across
1. Temp 2. Area 3. Epithelium 4. Antibodies 5. Size of pathogen |
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Mucus
1. Yellow indicatres 2. Green 3. Red |
1. Staph
2. Pseudomonas 3. Blood |
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Rule of thumb of Frank vs. Secondary pathgones
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1. Profession/Frank/Overt - Viral
2. Secondary/oppurtunistic- Bacterial |
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PREDISPOSING factors for microbial pathogenesis (6)
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Damage to host EPITHELIUM
Presence of FOREIGN body Disruption of normal flora d/t ANTIBIOTIC therapy Damaged/Deffecient IMMUNE defences Drug/Radiation SUPPRESSION of immune sytem Normal Bacterial in ABNORMAL places |
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EXOGENOUS Transmission
1. Normally 2. Small droplets vs. Dried droplets |
1. Primary Pathogen
2. Small = suspended for long time Dried = EVen longer |
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Respiratory Droplet Nuclei
1. Respiratory secretions are largely 2. Describe 3. Holds 4. Tiny flake consists of (4) 5. Flake held aloft by |
1. Mucous
2. Mucin- highly glycosalated 3. 600x weight in water 4. Dried protein, Salts, IgA & Microorganisms 5. Brownian Movement |
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Endogenous infections
1. normally d/t 2 E.g. |
1. Normal Microflira
3. Enterobacteriiae or Klebseilla in RT |
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Two type of exongenous Pneumonia?
Describe clinical presentation |
1. CAPS( community acquired pneumonia)
-Acute -Subacute/Chronic 2. Nocosomia -Acute |
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What is SPUTUM (3)
Important for diagnosis of (1) |
1. From lung, thick & contains mucus
2. LOWER RT infections |
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Growth media for
1. Bordetella pertussis 2. C. diptheria |
1. Bordet-Gengou
2. Tinsdale agar |
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Match the virus with the Associated ATTACHMENT protein
1. Class IV Fiber protein 2. Fusion Factor 3. Spike Protein (peplomer) 4. F factor 5. G protien 5. HA (Hemgglutinin) |
1. Adenovirus
2. HPIV 3. Coronoavirus 4. HPIV 5. RSV 6. Influenza virus |
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Transmission via
0. Aerosol (6) 1. Formites 2. Fecal-Oral 3. Swimming Pool 4. Self-Innoculation (2) |
0. Adenovirus, Rhinovirus, Cornovirus, RSV, HPIV & Influenzae
1. Adenovirus 2. Coronavirus 3. Adenovirus 4. Adenovirus, RSV |
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Name the VIRUS, that replicates at the following SITES
1. Mucoepithelial (lytic) 2. Lamina Propria (UPPER RT) 3. Ciliated Nasal Epithelium 4. Nasalpharyngeal Epithelium 5. I 6. Adenoids (latent) |
1. Adenovirus
2. Rhinovirus 3. Coronavirus 4. RSV 5. influneze 6. Adenovirus |
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Adenoviridae
1. Clinical Syndromes (2) 2. Family 3. Genus 4. NA 5. Class 6.. Capsisd |
1. Pharyngitis & Conjunctivitis
2. Adenoviridae 3. Mastadenoviridae 4. LINEAR ds DNA 5. Class I 6. Icosahedral |
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ADENOVIRUS:Name the serotypes & Hemagglutination Group for
1. A 2. C Which is the longest & has the greatest capability to agglutinate |
1. Group C
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Main types of Viral entrance into the cell (2)
Main THREE Viral exits from |
1. Membrane fusion & Receptor Mediated
2. Budding (influenza), Cytolysis (adenovirus) & Synctia w/ CPE (measles) |
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Which Adenovirus Capsid is responsible for
1. Attachment & Hemagglutination 2. Made of |
1. Capsid Protien IV
2. Fiber |
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Name the function of the following ADENOVIRIDAE proteinst
1. E1A (4) 2. E1B (3) 3. E3 4. E4 5. VA RNA |
1. Activated viral gene TRANSCRIPTION, Binds supressor, p105Rb promotes transformation, deregulates cell growth, & inhibits IFN
2. Binds supressor, p53 promotes transformation & Blocks apoptosis 3. Prevents TNF 4. Limits CPE 5. Inhibits IFN response |
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ADENOVIRUS
1. Fiber protien role 2. Serotypes 2 & 5 have what receptor 3. Describe 4. Belonging to what family Penton Base 5. Activity 6. Roles (3) |
1. Enables ATTACHMENT
2. CAR 3. Cell surface glycoprotien 4. IgG superfamily 5. TOXIC 6. Inhibition of mRNA synthesis, Cell Rounding & Tissue Damage |
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ADENOVIRUS Illness in
1. INFANTS & Young Children (3) 2. Chidren 3. Military recruits (2) 4. Adults 5. immunocmpromised |
1. Ferbile undifferntiated infection, Pertussis-LIKE syndrome & Pneumonia
2. Pharyngoconjunctival Fever 3. ARDs & Pneumoniae 4. Phaynconjunctival fever 5. Pneumoniae |
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Adenovirus
1. Most infections occur in 2. Associated w/ what other systsems (3) 3. Lytic outcome 4. Latent outcome |
1. Children <14 yrs old
2. Ocular, Respiratory & GI systems 3. Mucoepithelial Cells 4. Adenoid Cells |
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Adenovirus
1. Survival Time 2. Transmission (4) |
1. 7 days - 3months
2. Aerosols, Formtis, Swimming Pools & Fingers |
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Rhinovirus
1. Clincal Syndrome 2. Virus fFamily 3. Medically significant viruses (2) 4. Envelope 5. Capsid 6. NA 7. Class |
1. Common COLD
2. Picornaviridae 3. Enteroviruses & Polioviruses 4. Naked 5. Icoasahedral 6. (+) ss RNA 7. Group IVa |
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FOR Rhinovirus, explain what feature allows it tobe:
1. transmissable 2. Less sesnitive to alcohol/disinfectants 3. Upper RT infection 4. High number of viral serotypes |
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Rhinovirus
1. Cell Recepteor 2. Enters via surface? On? 3. Spread 4. THREEoutcomes |
1. ICAM-1
2. Cleft/Canyon on Lamina Propria 3. Cell to Cell 4. Cell damage, Cillia immobilized & Viral Shedding |
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RHINOVIRUS
1. Reservoir 2. Symptoms most sever in 3. Seasonality 4. Antigenicity |
1. Humans
2. Young children 3. Summer months 4 115 sereotypes |
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RSV
1. Most likely route 2. Possible replication (2) |
1. Lacrimal & Nasolacrimal → Nose → Trachea → Lungs
2a. Independnat manner, propelled by cilliary cells, lining lacrima & respiratory mucosa b. w/ Reinfection in adjoining cells by Snyctal contact or short range diffusion |
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Coronavirus
1. Clinical symptoms (2) 2. Structure & Envelope (SE) 3. Family 4. NA 5. Baltimore Class 6. Characteristic |
1. Common Cold & SARS
2. HELICAL & Enveloped 3. Coronaviridae 4. +ss linear RNA 5. Class IVb 6. Fringe (spike proteins) |
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Coronavirus S protein
1. other names (2) 2. THREE roles |
1. peplomer or spike protein
2. Tissue tropism, Attachment (to carbs) & Neutralizing antibodies (via antigenic epitopes) |
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Coronavirus EPI
1. Isolation is 2. Isolated from (2) 3. Neutralizing Antibodies are? Thus? 4. Transmission via (2) 5. Survival Time |
1. DIFFICUTL
2. Humans & Animals 3. Shot-lived, thus Re-infection possible 4. Droplets & Fecal-Oral route 5. 3 hours |
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Coronavirus
1. Replication at temp? 2. Where? 3. Related disease |
1. 33-34°C
2. Ciliated Nasal Epithelium 3. SARS Coronavirus |
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Paramyxoviridae
1. Name 2 familes 2. 2 viruses |
1. Paramyxoviridae
HPIV 2. Pneomovirinae RSV |
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HPIV
1. Name Famile 2.Subfamily 3. Genera for 1 & 3 4. Genera for 2 & 4 5. Envelope 6. NA 7. Baltimore |
1. Paramyxoviridae
2. Paramyxovirinae 3. Respirovirus 4. Rubulavirus 5. Envelope 6. (-)ss RNA 7.Class Va |
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HPIV
1. Clinical Syndrome (2) 2. Name the proteins |
1. Croup & Bronchitis
2. HN, Fusion Factor & V protein |
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HPIV
1. Role of Fusion Factor (2) 2. HN (2) V protein (fusion protein) 3. Role 4. Fxns (3) |
1. Viral Entry & Neutralizes ABs
2. H enters, N leaves 3. EVASION 4a.Prevent APOPTOSIS b. ALTER cell cycle c. Inhibit ds RNA signalling d. Preven IFN biosynthesis |
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Name the PEAK incidence & syndrome most commonly related to
0. Which is MEDICAL emergency 1. HPIV-3 2. HPIV-1 3. HPIV-1 & -3 |
HPIV-1 Croup
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RSV
1. Family 2. Subfamily 3. Genus 4. S & E 5. NA 6. Baltimore Class |
1. Paramyxoviridae
2. Pneumovirinae 3. Pneumovirus 4. HELICAL (other is coronal) & Envelope 5. (-)ss RNA 6. Class IVa 7. |
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RSV
1. Name Surface Proteins (2) 3. Difference vs. HPIV (2) |
1. Fusion factor (peplomer)
2. G glycoprtoein 3. NO HN & HELICAL |
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RSV
1. Number 1 viral cause of 2. DO NOT |
1. Croup
2. VACCINATE |
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Croup
1. Causes (3) 2. Usually in (2) 3. Involves 4. Distinctive |
1. RSV, HPIC, Pneumovirus
2. Infants & Young Children 3. Swelling & Narrowing of the Airway 4. Cough "barking like a seal" |
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RSV Pathogenesis
1. Entry via 2. F & G protein meidate 3. F mediates 4. 1⁰ site of replication? Where in cell? 5. CPE 6. Can spread to? Time? |
1. Epithelia of Nose & eye
2. ATTACHMENT 3. Membrane fusion 4. NASOPHARYNGEAL epithelium in Cytoplasm 5. Loss of Fxn 6. Lower RT in 2-5 days |
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RSV
0. ER 1, Affect in <1 yr old 2. Children 3. Older Children & Adults |
0. Bronchiolits & Pneumoniae
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RSSV
1. Clinical Outcome essentially 2. Mediated bt |
1. EXCESSIVE immune response
2. CD8+ T cells |
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Influenzae
1. Resevori 2. Transmitted 3. Virus survives 4. Course 5. Epidemics duration |
1. Humans
2. Respiratory droplets 3. +/- 24 hrs 4. Self Limiting 5. 4-6 weeks |
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Compare Symptoms of Flu & Cold across
1.Fever 2. Headache 3. General Malaise 4. Nasal Discharge 5. Sore Throat 6. Vomiting/Diarrhea |
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Influenzae =
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Flu
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Adult Symptoms of Flu/ Descrbe each phase
1. Incubation perida 2. Sudden (2) 3. Abrupt (5) 4. Recovery 5. Patient is contangious 6. When is the Highest Risk of 2ary Infection |
1.1-4 days, followed by Rapid onset
2. Malaise & Headache for a flew HOURS 3. Rise of FEVER, CHILLS & MYLAGIA. Loss of APPETITE & DRY cough. 3-8 days 4. 7-10days 5. Day 1 (before symptoms appear) to 12 6. 6-12 days AFTER infection |
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Child Flu like symptoms
1. Same as 2. PLUS (3) 3. Often, but not always 4. In children <3yrs |
1. Adult
2. HIGH fever, Vomiting, Ottis Media 3. CROUP 4. FERBILE convulsions |
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FLU complications
1. Virus Related 2. Bacteria related 3. Organ 4. Neuro symptoms |
1. 1⁰ Viral Pneumoniae
2. 2⁰ Bacterial Pneumonia (BAD) 3. Myocardial inflammaiton 4. Guillain Barre, Encephalitis & Reye's syndrome (exasperated by Aspirin) |
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Influenzae B
1. Two lineages 2. Which is covered by TRIVALENT vaccine 3. Inf. B may lead to (2) 4. Responsible for what % of PEDIATRIC influenzae cases 5. Often Co infection w/ |
1. Vicotria & Yamagata
2. Victoria 3. Fulimant Disease, Reye's Syndrome 4. 38 5. S. aureus |
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Compare INFLUENZAES across Subtypes, Hosts, Human Epidemics, Morbidity & Mortality for the following:
1. Type A 2. Type B 3. Type C |
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Describe the Zoonotic Life cycle of Type A Influenzae
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Name the Important N & H for Inluenza A
Most common |
N1,2 & H1,2,3 & 5
MC: H1N1 |
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Influenzae A HEMAGGLUTININ
0. Description (3) 1. Shape 2. % of Viral Protein 3. Main Site for 4. KEY 5. 4 subtypes 6. Role of Cellular Proteases (3) |
0. Low pH induced, Comformationallu controlled trigger for MEMBRANE FUSION
1. Rod 2. 25% 3. Neutralizing ABs 4. Highly VARIABLE 5. HA 1-3 & 5 6. Found in RT, Responsible for Cell TROPISM & Cleaves HA →Active Form |
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Influenzae
1. Enters CELL via 2. Enters VESICLE 3. Leaves via |
1. Receptor mediated endocytosis
2. Membrane Fusion 3. Budding |
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Neuroamindase
0.Other name 1. Human Subtypes 2. Action (3) 3. Leads to (3) 4. Function (2) 5. No Stimulation to Neutralizing ABs |
0. SIALIDASE enzyme
1. N1 & N2 2. Cleaving Receptor: Removes terminal SIALIC Acid residues from glycoproteins/lipids 3. Viral UNCLUMPING/RELEASe & subsequent INFECTION 4. RELEASE of BUDDING irus & helps MOVE virus through MUCIN layer 5. N is IN CELL |
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Influenzae Pathogenesis
0. Antibodies only triggered AFTER 1. 4 main steps 2. 3 immune responses 3. 3 less frequent outcomes |
0. First round of replication
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Influenzae Pathogenesis
0. Antibodies only triggered AFTER 1. 4 main steps 2. 3 immune responses 3. 3 less frequent outcomes |
0. First round of replication
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Compare Influenza A, B & C across
1. Severity 2. Animal Resevoir 3. Pandemics 4. Epidemics 5. Drift 6. Shift |
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Compare Drift vs. Shift across
1. Speed of Alteration 2. Location 3. Type of CHANGE 4. Seen in |
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Influenza
1. Diagnosis (3) 2. Retrospective diagnosis (4) 3. Thus |
1. Symptoms + Time of Year + Knowledge of Epidemic
2. Growth on eggs, Detection of antigens (CF, EIA & HAI), Antibody titer, RT-PCR 3. Needs to be treated immedeately |
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Anti-Flu Drugs
1. Vs. Influenza A (Amantadine & Rimatidine) 2. Vs. Influenza A & B (Zanamivir & Oseltamvir (tamiflu)) |
1. Inhibits uncoating by attacking M2 protien
2. Inhibits NA → Forms Useless clumps → Blocking release |
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Issue with Amantadine & Rimatidine)
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1. resitance
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FDA flu TRIVALENT vaccine (USA 2011-2012) will include (3)
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1. H1N1, H3N2 & B (victoria strain)
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Inactivated Vaccine
1. Administration 2. >6months dose 3. >65 yrs old dose Live Attenuated 4. Administration 5. Patients (3) |
1. INTRAMUSCULAR
2. Standard 3. HIGH 4. INTRANASAL 5. Healthy, NON-pregnant between 2-49 yrs old |
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Name EIGHT possible BACTERIAL respiratory infections
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Match the Bacteria with the following symptoms
1. Pharyngitis 2. Severe Pharyngitis 3. SINUSITIS, Pneumonia & Otitis Media 4. EPIGLOTTITIS, Pneumonia & Otitis Media 5. Otitis Externa 6. Chonic Bronchitis 7. Bronchopneumoniae & Lung Abscesses 8 Necroitizing Bronchial Pneumonia 9. Pneumoniae & Pontiac Fever 10 .Tuberculosis |
1. Strep. pyogenes (strep throat)
2. Coryne. diptherium (diptherium) 3. Strep pneumoniae 4. H. influenzae (does NOT cause Inlfuenzae) 5. Pseudomonas (swimmer's ear) 6. Bordetella pertussis (whooping cough) 7. Klebsiella pneumoniae 8. Pseudomonas in Cystic Fibrosis 9. Leigonella pneumophila (legionnaire's disease) 10 .M. tuberculosis . |
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Streptococci
1. Stain 2. Shape 3. Motile 4. Spore Forming 5. Catalase 6. Metabolism |
1. Positive Blue
2. Cocci in Chains 3. No 4. No 5. No 6. Lactose Fermenter |
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Transmission
1. Droplets 2. Endogenous 3. Fresh water |
1. Strep pneumoniae, L. pneumonophilia
2. S. pneumoniae 3. Psuedomonas |
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Culture
1. Blood Agar (sensitive to Bacitracin & CLEAR hemolysis) 2. Blood Agar (sensitive to optochin & GREEN hemolysis) 3. Percipitin line on ELEK test 4. Chocolate Agar 5. Charcoal Agar + Cephalosporin 6. Green & Yellow on Colorless media 7. Tuberculin Test |
1. S. pyogenes
2. S. pneumoniae 3. C. diptheriae 4. H. influenzae 5. B. pertussis (bordet-gengou) 6. Pseudomonas 7. M. tuberculosis |
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Strep. pyogenes
0. Clinical Syndrome 1. Type of Strep 2. What enduced pus formation 3. Type of KAntigen 4. Proteins 5. Enzymes (3) 6. Exotoxin |
0. Strep throat (Pharyngitis)
1. Group A β Hemolytic 2 LEUKOCIDIN 3. Hyaluranic Acid 4. M protein 5. Hyaluronidase, Streptokinase & Streptolysisn 6. Pyrgoenic Exotoxin |
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Strep. pneumoniae
0. Clinical Symptoms (3) 1. Type of Strep 2. Sensitive 3. Vs. S. pyogenes, missing what virulence Factors (2) |
0. SINUSITIS, Pneumonia & Otitis Media
1. α Hemolyitc 2. Taxas P sensitive 3. NO Leukocidin or Pyrogenic Exotoxins |
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Epi of Strep. pneumoniae
1. Most Common causse of 2. Flora 3. Reservoir 4. Seasonality 5. Transmission |
1. COMMUNITY acquired Pneumoniae
2. Nasopharyngeal 3. NO animal or Environmental 4. Winter & Early Spring 5. Exogenous Droplets & Endogenous |
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S. pneumoaiae
1. Major disease (3 facts from path) 2. Virulence Factors used (4) |
1. Pneumococcal pneumoniae (whole lobe, Ghon, IMMUNOCOMPETENT)
2. Capsule, IgA protease, Autolysin & Pneumolysin |
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Describe the FOUR Properties of Pneumolysin
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Strep pneumonia
1. Vaccine 2. Immunises vs. 3. High Risk individuals indicated for Vaccination (5) 4. Resistance |
1. Polyvalenc capsular pls vaccine
2. 23 MOST common serotypes 3. Chronic Disease, HIV, Alcoholics, YOUNG & ELDERLY 4. INCREASED |
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What do you expect to see on S. pyogenes Blood Agar
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What do you expect to see on a S. pneumoniae Blood Agar
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Corynebacterium diptheriae
1. Clinical Symptoms 2. Type of Bacteria 3. Arrangement on Agar |
1. Severe phayngitis (diptheriae)
2. Gram +ve Rod 3. Chinese Letters |
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Corynebacterium Pneumonic
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PS. ABCDEFG
PSeudomembrane ADP-Ribolysation Beta-Prophage Corynebacterium Diptheria EF-2 Granules |
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Corynebacterium
1. Name OTHER significant Corynebacterium & their roles (2 & 2) |
1. C. jeikuim -Baceteraemia, IV catheter colonizastion
2. C. minutissimum: RTI's & Wound Infection |
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C. diptheriae Epi
1. Vaccine 2. Endemic in (3) |
1. Diptheria Toxoid
2. Subtropical, Tropical & Break down in infastructure |
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C. diptheria PATHOGENESIS
1. Describe Organism MoA 2. Main VF 3. Genes for VF acquired via (1) 4. VF causes (3) 5. Death d/t |
1. NON-INVASIVE & does NOT enter blood stream
2. Diptheria Toxin 3. Lyosgenic Conversion 4. Inflammation, Formation of Pseudomembrane & Damage to Organs 5. Severe Pharygitis block airway -> Suffocation |
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Corynebacterium diptheria Diagnoses
1. Sample used 2. Screening vua 3. Diagnosis & Investigation via 4. Black colonies present divide into (2) 5. 3 test to be done |
Picture
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Corynebacterium diptheria
1. Why is the elek test important 2. Describe the ELEK test ? When is it toxic? |
1. NO TOXIN to VIRULENCE
Picture |
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Most common cause of CROUP
1. Viral 2. Bacterial |
1. RSV
2. H. influenzae |
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H. inlfuenzae
1. Misnomrer |
1. DOES NOT CAUSE INFLUENZAE
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Haemophilus inlfuenzae
1. Clinical Symptoms (3) 2. Bacteria Type 3. Most common causes of (2) 4. Daignosis |
1. EPIGLOTTITIS, Ottis Media & Pneumoniae
2. Gram -ve Rod, Pleomorphic & Facultative Anaerobe 3. Bacterial Croup & Epiglottitis 4. Chocolate Agar |
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H. inlfuenzae Pneumonic
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HaEMOPhilus
Epiglottitis (cherry red in children) Meningitis Ottis Media Pneumoniae |
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H. inlfuenzae
1. Most Invasive Serotype 2. Carried vy 3. name Virulence factors (5) |
1. Type B
2. 2-4% of Population 3. LPS, PRP Capsule, IgA prteases, Pili & Non-Pili adhesins |
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H. inlfuenzae Pathogenesis
1. Ligand 2. Receptor 3. Impairs Cilliary function 4. Antiphagocytic Activity 5. Inhibit Antibody |
1. P-2 Outer Membrane Protein
2. SIALIC acid-containing Mucin Oligosaccharides 3. LPS 4. Capsule made of PRP 5. IgA proteases |
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H. inlfuenzae
1. Positive for ______ase 2. Negative for ______ase 3. Culture 4. Which component is Hemin 5. Nicotineamide adenin dinucleotide (NAD) 6. Only Haemophilus species that requires |
1.Catalase
2. Coaglase 3. Chocolate Agar (blood enriched) 4. X-Factor 5. V-Factor 6. BOTH |
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H. inlfuenzae
1. Vaccine 2. Given 3. Incidenc <5yers old |
1. Typ B toxoid vs. Capsule
2. 2-18 months 3. DECREASED |
|
Bordetella Pertussis
1. Clinical Symptoms 2. Bacteria 3. Patients 4. Important Resevoir 5. Transmission |
1. Whooping Cough (Chronic Bronchitis)
2. Small, Gram -ve, Coccobacillus 3. UNVACINATED children 4. Adults 5. Highly Communicable |
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B. pertussis. Virulence Factors associated with:
1. Adhesion (3) 2. Growth & Toxin Release (3) 3. Local & Systemic Pathology (4) |
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B. pertussis Whooping cough. Describe the time course for
q. Incubation b. Cattarhal d. Paroxysmal e. Convalescence |
a. 0-1 Wk
b. 1-2.5 Wks d. 2- 4 Wks e. $ - 8 Wks |
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B. pertussis. Culture & Identification
1. Most severe in 2. Sample 3. Wny no Cotton/Throat swab 4. Agar |
1. CHILDREN
2. Nasopharyngeal swab/secretions 3. Susceptibe to DRYING 4. Bordet-Gengou (Charcoal Blood agar + Cephalosporin) |
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B. pertussis PREVENTION
1. Vaccine 2. Types (2) 3. Immunity |
1. DaPT
2. Inactivated, whole cell (side effects) & Fragments of Cell (Acellular components:Fha & PT) 3. ↓ Over time |
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B. pertussis
1. More severe in Children/Adults? 2. Why Vaccine given to adults? 3. Required Vaccination level to see ↓ in Casses? Graph 4. After immunisation, cases? 5. Then started increasing because? |
1. Sever->Infant; Mild->Adult
2. Stop TRANSMISSION 3. 70% 4. ↓ Cases 5. People stopped being Vaccination |
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Klebsiella pneumoniae
0. Key Symptoms 1. Clinical symptoms (2) 2. Group of Bacteria 3. Type of Bacteria (2) 4. Normally 4. FOUR virulence factors |
0. Putrid breath,w wth "RED CURRENT JELLY" sputum
1. (LIFE THREATENING) Necrotizing Bronchopneumoniae & Lung abscess 2. Enterobacteriaeceae 3. Gram -ve, Bacillus 4. 5% of health individuls 5. Aerobactin, Enterochelin, Capsule (mucoid appearance) & LPS |
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K. pneumoniae
1. Role of Capusle (mucoid appearance) 2. LPS 3. Aerobactin & Enterochelin |
1. Anti-Phagocytic
2. Necrotization of Lung Tissue 3. HIGH AFFINITY IRON uptake |
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K. pneumoniae .Necrotizing pneumonia
1. consists of (2) 2. Necrotizing if 3. Large % of cases are 4. Other bacteria involced could include (3) 5. Typical Patients (3) |
1. Lung Abcsesses/Aspiration Pneuomoniae
2.>1 are Parenxhyma replaced by DEBRIS 3. Polymicrobial 4. S. aueres, Anaerobes & Microaerophiles from Mouth Flora 2. Alcholics/People incubated inproperly/IV drug user 3. |
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Leigonella pneuomophila
0. Targets 1. TWO clinical syndromes 2. Bacteria (4) 3. May be associated with 4. >80% d/t what Serogroup 5. STAIN |
0. Aveolar Macrophages
1. Leigonnaire's Diseas (SEVERE PNEUMONIAE & FEVER)e & Pontiac Fever 2. Gram -ve rod, Motile & NON-spore forming 3. Epidemics 4. Serogroup 1 5. Silver |
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L. pneuomophila Pneumonic
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French LEGIONNAIRE w/ SILVER hemet, sitting around a CAMPFIRE w/ his IRON dagger- he is no CYSSY
Silver Stain Charcoal Yeast Culture w/ IRON & CYSTEINCE |
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L. pneuomophila
1.TRANMISSION 2. Survives 3. Type of Pathogen 4. Evasion Mechanism 5. Damage d/t |
1. Contaminated WATER SOURCe
2. ~50°C >30 mints 3. Facultative Anaerobe (in aveolar macrophage) 4. Prevent fusion of Phagosome-Lysosome 5. HOST inflammatory response |
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Psuedomonas aeruginosa
Pneumonic (2) |
PSEUDOmonas AERuginiso
Pneumoniae (cystic fibrosis) Sepsis (black lesions on skin) External otitis (swimmer's ear) UTI Drug use Diabetic Osteomyletis AER- Aeroibic Water Connection & BURN victims |
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P. aeruginosa
1. Found 2. Most Common infection of 3. Most Common Problem in 4. Immunocompromised target |
1. Fresh water sources
2. Swimmer's Ear (Otitis Externa) 3. BURN VICTIMS 4. CYSTIC FIBROSIS |
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P. aeruginosa
0. General Characterestic 1. Bacteria type (5) 2. Flagella |
0. Ubiquitous
1. Gram -ve Rods, Aerobic, highly motile w/ multiple flagella & versatile metabolism 2. Lophotrichous |
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P. aeruginosa
1. Conventional agar 2. Colorless media 3. Smells like |
1. Mucoid colonies
2. Pyocyanin & Flurescein (green) 3. Grapes |
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CYSTIC FIBROSIS
1. Most common genetic disorder among 2. Produce 3. Leads to 4. Life Expectancy 5. Sweat test |
1. Caucasian
2. Abdnormal Mucus 3. Obstructs Airway -> Chronic Lung Infections 4. 35 years 5. <60 |
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P. aeruginosa & Cystic Fibrosis
1. Clinical syndrome 2. Abnormal CF mucus 3. Chronic inflammation causes 4. infections (2) 5. Course |
1. Necrotizing Bronchial Pneumonia
2. Ready made Biofilm 3. Accumulation of WBC 4. Permenant & Highly Drug Resistant 5. FATAL |
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Mycobacetium tuberculosis
1. Clinical Vignette (4) |
1. Immigrant, Weight Loss, Fever & Cour
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Ranks where in Top 10 dieases of low income countries
# 1, 2 & 3 |
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M. tuberculosis Cell
0. Resistant to? Sensitive to? 1. key component in cell wall 2. Cell wall also includes (3) |
0. R- Heat & S- Drying
1. Mycolic Acid |
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M. tuberculosis
1. Growth 2. Type of bacteria (4) 3. Lab growth 4. Found in (4) |
1. Long Parallel Chains "Cords"
2. Gram +ve, Aerobic, Non-Spore forming & Resists drying 3. 2-8 Weeks 4. IV users, AIDS patients, Prisons & Immigrants |
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M. tuberculosis & AIDS
1. Resistance to TB dependent on, which is absence in AIDs? Which produce? 2. vs. non-AIDS patients develop? 3. in 10% complication |
1. CD4+ T Cell
2.50-70% Extra pulmonary infection 3. CNS invasion |
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M. tuberculosis PATHOGENESIS
1. INTRACELLULAR survival in AVEOLAR macrophages 1. (2 & 1) 2. (2 & 3) 3. (2 & 2) 4. (1 & 1) |
1. Prevent Oxidative Burst & Phagosome-lysosome fusion (Sulfolipids)
2. Resist Lysosomal enzymes & ROS (Cell wall lipids, LAM & SOD) 3. Escape Phagosome, Persist in in Tissue (LAM & Mycolic Acid) 4. Grab IRON via High Affinity Sidephores (Exochelins) |
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M. tuberculosis. DESCRIBE the following categories of Resistance
1. MDR-TB: (2) 2. XDR-TB (4) 3. TDR-TB: XDR-TB |
1. Isoniazid & Rifampin (first line)
2. Fluoroquinlone (2nd line) & ONE of: Amikacin, Capreomycin & Kanamycin 3. Resistant to ALL tested drugs |
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Subacutre Lower RT infections. Name
1. Prokaryotes (3) 2. Eukaryotes (4) |
1. Mycoplasma sp., Chlamydia sp & Legionella sp.
2. Histoplasma sp, Blastomyces sp, Coccididoides sp. & Candida sp. |
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Mycoplasma sp.
1. Symptoms (4) 2. Most common in 3. When do outbreaks occur 4. Diagnosis 5. Clears up by |
1. Walking Pneumonia (Cough, Fever, Headache & Malaise)
2. Children >5 yrs old - Young adults 3.Crowded institution 4. Nothing cheap, quick & simple 5. Day 18 |
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Chlamydophilia pneumoniae
1. Symptoms 2. Most common in (2) 3. Diagnosis |
1. Walking pneumoniae
2. Children between 5-10 yrs & 50% occurs in adults 3. Nothing cheap, simple or quic |
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Name the Primary Pathogens involved in Fungal Respiratory Infections (4)
Oppurtunistic Pathogens (3) |
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All the Respirartory Fungal infections, which are
1. Primary are 2. Oppurtunistci |
1. Dimorphic
2. Monomorphic |
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What RESPIRATORY fungal infection is related to the following regions:
1. Tropical Africa 2. California desert 3. Eastern US & Latin America 4. Middle & Eastern N. america 5. Southwestern US (not California), Northern Mexico, Central & South America |
1. H. capsulatum var duboisii
2. Coccidiodes immitis 3. H. capsulatum var capsultum 4. Blastomyces dermatitidis 5. Coccidiodes psadasii |
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What RESPIRATORY fungal infection is related to the following:
1. Bat poop 2. Pigeon dropings |
1, H. capsulatum
2. Crytptococcus neoformans |
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What RESPIRATORY fungal infection is related to the following seasons
1. Late Summer/Early Fall |
1. Cocciodes
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Primary Fungal RESPIRATORY infections
1. Acquired via 2. In immmunocompromised/ competent associated w/? 3. All are? Which means |
1. INHALATION
2. Systemic mycoses 3. Dimoprhic. Enviroment→ Moulds & Tissues → Yeast |
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Primary Fungal RESPIRATORY infections Symptoms
1. Mostly 2. More severe (4) 3. Accompanied with 4. Extreme cases 5. Uncontrolled |
1. Mild fever & cough
2. Chils, malaise, fever & chest pain 3. Sputum production 4. Weight loses 5. Granulomatous lesions on skin |
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mary Fungal RESPIRATORY infections Pathogenesis
1. Reach aveoli 2. Convert to 3. At respiratory mucoso |
1. Fungal spores (myceal form)
2. Yeast form 3. Colonize |
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Primary Fungal RESPIRATORY infections
1. Describe virulence of P. brasilensis 2. How can H. capsulatum grow in phagosome |
1. α-(1,3) glucagon in Cell Wall
2. ↑ Phagolysomal pH & interfere w/ enzyme activity & antigen processing |
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Primary Fungal RESPIRATORY infections
1. Best sample 2. Best technique 3. Stain |
1. SPUTUM
2. Direct microscopy 3. Giemasa & indirect FA stain |
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For coccidiomycosis
1. Type of test 2. What TWO phase antigens will be seen? |
1. Coccidiomycosis
2. Coccidiodin (mycelial phase) & Spherulin |
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What is the basis of the Exoantigen test
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1. Look for presence of SPECIFIC cell FREE ANTIGENS produced by the MYCELIAL phase
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Histoplasma capsulatum
1. Symptoms 2. Compare H.c var capsulatum vs. H. c. var duboissi across: Symptoms, Region & Size |
1. var capsulatum
-Pulmonary & disseminated infections Eastern US (Mississippi) & Latin America -Thinner Cell walls & Smaller Size (2-4um) var duboisii -Skin & Bone lesions -Subsaharan africa Thicker walled & larger yeasts (8-15) |
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Histoplasma capsulatum Epidemiology
1. Natural habitat? enriched with 2.Outbreaks associated w? 3. What is aerolized & onhaled |
1. Soil w/ HIGH NITROGEN, enriched by BAT or BIRD poop
2. Cave, bird roost, old buildings 3. Microconidia & Hpyhae |
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Histoplasma capsulatum Cinical Presentation
1. Dependent on (2) 2. Low intensity exposure leads to 3. High intensity leads to (3) |
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Blastomyces dermatidis
1. Symptom 2. Found in 3. Outbreaks associated w. 4. region (2) 5. TWO presentation 6. similar to |
1. Blastomycosis
2. DECAYING ORGANIC matter 3. CONTACT w/ SOIL 4. Middle & Easter N. america 5. Pumonary & Extrapumonary disseminated 6. Histoplasmosis |
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Coccidiodes sp.
1. Clinical Syndrome 2. Disseminated symptom 3. Inhalation of 4. Seasonality 5. C. immitis geography? 6. C. posadasii (4) |
1. Coccidiodomycosis
2. Red tender nodules on shin & right arm 3. ARTRHOCONIDIA from SOIL 4. SUMMER/Early Fall (dusty) 5. California desert 6. Desert in Southwestern USA, Northern Mexico, Central & South Americal |
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Coccidiodes
1, Is the most 2. Inhalation of a few conidia → 3. 60% 4. 40% (3) |
1. VIRULENT of the human MYCOTIC pathogens
2. Primary Coccidiomycosis 3. Asymptomatic 4. Self limited flu →Secondary from or Disseminate |
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Name the associated Major RESPIRATORY oppurtunitic pathogen
1. Chemotherapy (2) 2. Assisted venitalation 3. Malnutrition (2) 4. HIV 5. Neutropenia (WBC < 500) |
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Cryptococcus neofrmans
1. clinical Syndrome 2. Morphological features 3. Grows in? enriched by? 4. Transmission via 5. MOST COMMON fungal infection seen in |
1. Cryptococcosis
2. ENCAPSULATED yeast 3. Soil, Pigeon Poop 4. Inhalation of UNECAPSULATED yeast 5. AIDS patients |
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Cryptococcus neofrmans Pathognenesis
1. Inhaltion triggers 2. Crytococci strong affinity for 3. Capsule detectable in (2) 4. Can oxidise 5. Prevents phagocyte |
1. Production of GXM capsule
2. CNS 3. Blood & Fluid (down regulates immune response) 4. Exogenous catecholamines → melanin 5. Prevents phagocytic oxidative damage. |
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Pneumocystosis jirovecii
1. Clinical syndrome 2. MOST Common 3. Unusual characterestics (2) |
1. Pneumocystosis
2. Lacks ergosterol & difficult to grown in culture 3. SERIOUS OPPURTUNISTIC fungal illness in HIV infiltrated disease |
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Aspergillus
1. Name THREE different species 2. Found in (3) 3. Outcome dependent on 4. On stain see |
1. fumigatus, flavus & niger
2. DEACYING matter, air & soil 3. Host Factors |
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ASPERGILLOSIS
1. Primary form is 2. Secondary from is Secondary Form 3. Key characerestic 4. Can cause? in? 5. Symmptoms (3) |
1. Allergic
2. Invasive:hyphae invade tissue 3. Fungal ball (aspergilloma) 4. Acute pneumoniae in Neutropenic patients 5. Deadly, invasive pneumoniae, Hemoptysis (coughing blood) & high mortality |