Micro, Ass 6, Renee’s Questions

1.       What are the characteristics of the Influenza virus?
1. Enveloped, with segmented, single-stranded, negative-sense RNA genomes
2. What part of the influenza virus must fuse with the host cell membrane to transfer the virus?
2.       Envelope
3. What is the basis for emergence of new pandemic strains?
3.       segmented genome allows reassortment
4. What 3 proteins are located on the influenza envelope?
4.       Hemagglutinin, Neuraminidase, M2
5. Which proteins on the flu virus are targets for neutralizing antibodies?
5.       Hemagglutinin, Neuraminidase
6. Which protein is essential for the infectivity of the flu virus?
6.       M2
7. What is the replication scheme for the flu virus?
7.       1. Entry through receptor mediated endocytosis 2. Low pH of endosome required for infectivity 3. Replication in nucleus
8. Does the flu virus need a symport to release the virus into the host cell?
8.       No, low pH of endosome opens M2 channel and releases virus
9. Why does the flu virus have to replicate in the nucleus?
9.       mRNA spliced, requires capped mRNAs from host (cap-stealing)
10.         How can Influenza A, B, and C be distinguished ?
10.   Antigenic Differences between their nucleocapsid (NP) and Matrix (M) proteins
11.         What influenza infects Humans only?
11.   Influenza B
12.         What species can the Influenza A virus infect?
12.   humans, pigs, horses, avian species, aquatic mammals
13.         Which flu virus can infect humans and pigs?
13.   Influenza C
14.         How many distinct RNA segments does Flu A and B have?
14.   8
15.         Why does Flu C on contain 7 RNA segments?
15.   2 segments are found on the same protein
16.         Influenza A is subdivided into subtypes and designated by 5 things, whats the only part you need to know about?
16.   The antigenic description of the HA and NA molecules (EX. H3N2, H1N1)
17.         What part of the body is Influenza isolated to?
17.   Respiratory Tract, Upper and Lower
18.         How is Flu mainly spread?
18.   Aerosol droplets (coughing, sneezing)
19.         After infection of Flu virus when do virus titer peak?
19.   48 hours
20.         How long does it take for a person to stop shedding the Flu virus after infection?
20.   6-8 days
21.         What does influenza induce in the body that contributes to recovery?
21.   interferon (IFN)
22.         Where is the antibody response found in the body?
22.   Both Serum and Secretory
23.         What is the incubation period for the Flu virus?
23.   Short 24hrs, can be up to 4-5 days
24.         What are the initial symptoms of the Flu?
24.   Headache, chills, and dry cough
25.         What follows the initial symptoms of the Flu?
25.   high fever, myalgias, malaise, anorexia
26.         After the fever resolves from the flu how long can cough and weakness persist?
26.   1-2 weeks
27.         How do the symptoms of the flu differ in children and adults?
27.   Children have higher fever – can result in convulsions, higer incidence of vomiting and abdominal pain
28.         What are some complications of Influenza if the virus is not cleared?
28.   Primary viral Pneumonia, Combined viral-bacterial pneumonia, Bacterial pneumonia, Reye’s syndrome
29.         What population is at high risk of developing Primary Viral pneumonia after the flu?
29.   Elderly, Patients with cardiopulmonary disease
30.         How soon after onset of illness can influenza progress to Primary viral pneumonia?
30.   6-24 hrs
31.         If an elderly patient presents with Flu and shortly after develops tachypnea, tachycardia, cyanosis, high fever and hypotension, What are you worried about and how can you treat him?
31.   Primary viral pneumonia, Supportive treatment and Antivirals, monitor for bacterial superinfection
32.         What is a more likely complication of flu then primary viral pneumonia?
32.   Combined viral-bacterial pneumonia
33.         How is viral-bacterial pneumonia distinguished from primary viral pneumonia?
33.   onset is usually delayed in viral-bacterial pneumonia
34.         A patient develops shaking chills, pleuritic chest pain, and productive cough, 4 days after improving from the flu, what’s wrong?
34.   Influenza followed by bacterial pneumonia
35.         What are the most common culprits of bacterial pneumonia after the Flu?
35.   S. pneumonia, S. Aureus, H. influenza
36.         What are some atypical causes of bacterial pneumonia?
36.   M. pneumonia, Chlamydia pneumonia
37.         What syndrome is characteristic of noninflammatory cerebral edema and fatty infiltration of the liver?
37.   Reye’s syndrome
38.         What does Reye’s syndrome result in, how is this tested?
38.   severe hepatic dysfunction, elevated serum transaminase and ammonia levels
39.         What type of Antigenic variation results from minor point mutations in a single HA gene?
39.   Antigenic drift
40.         How does antigenic shift change the Influenza virus?
40.   major antigenic changes that result from replacement of either the HA or NA gene segment (Ex. H1 aH3)
41.         What type of antigenic variation is responsible for most of the major influenza pandemics?
41.   Antigenic Shift
42.         What is the definition of a pandemic strain?
42.   New subtype with no existing human immunity, highly pathogenic, transmitted easily between humans
43.         What type of tests are available to detect influenza A and B?
43.   immunoassay-based nasopharyngeal swabs
44.         How are inactivated vaccines made and how are they administered?
44.   purified virus grown in eggs, whole virus or subvirion, inactivated with formalin or ?-propiolactone, Administered IM
45.         T/F The inactivated vaccine protects against influenza infection.
45.   F – Does not protect against infection but induces resistance to illness
46.         Who is approved for the Live vaccine FluMist?
46.   Healthy kids 2-17, Health Adults 18-49
47.         This year who does the CDC recommend get the Flu vaccine?
47.   EVERYONE – Universal Influenza Vaccination
48.         Who is the influenza vaccine recommended for?
48.   Pregnant women in 2nd-3rd trimester during flu season, Healthy kids 6mo-5yrs, People 50+yrs, Any age with Chronic medical conditions, Nursing home residents and providers, People who care for those at high risk, Children/Teens with long-term aspirin therapy
49.         How do Amantadine and Rimantadine work as antiviral agents?
49.   Inhibits the M2 ion channel of influenza A
50.         Who are amantadine and Rimantadine used for?
50.   individuals at high risk, people with egg allergies that can’t receive flu vaccine
51.         T/F Resistance to Aniviral Agents can develop.
51.   T – results from single amino acid substitutions in the transmembrane domain of the M2 channel; H3N2 and H1N1 are resistant
52.         How do Neuraminidase inhibitors work as antiviral agents?
52.   inhibit virus release, limiting spread
53.         What are 2 types of Neuraminidase inhibitors?
53.   Relenza (zanamivir), Tamiflu (oseltamivir phosphate)
54.         When do Neuraminidase inhibitors need to be administered to be most effective?
54.   within 48 hrs of symptoms developing
55.         What is different about the Paramyxoviruses compared to the Influenza viruses?
55.   Paramyxoviruses are nonsegmented
56.         What are the characteristics of a paramyovirus?
56.   Consist of 2 Subfamilies, containing 5 genera, Enveloped, Nonsegmented, negative stranded RNAviruses
57.         Where do paramyxoviruses replicate?
57.   Cytoplasm
58.         What is an important characteristic of paramyxoviruses that can cause syncytia formation?
58.   They fuse at the cell surface
59.         What respiratory pathogen is important in infants and children?
59.   Human parainfluenza viruses (hPIV)
60.         What are the major causes of croup?
60.   hPIV 1, 2, and 3
61.         What are the major causes of pneumonia and bronchiolitis?
61.   hPIV3
62.         What is hPIV4 linked to?
62.   mild upper respiratory illnesses
63.         Where do PIVs initially infect?
63.   mucous membranes of nose and throat
64.         What can severe hPIV3 infections result in?
64.   bronchopneumonia, bronchiolitis, bronchitis
65.         What are the typical symptoms of hPIV infection in children?
65.   cough, hoarseness and fever
66.         If a childs cough becomes brassy, “seal-like” or barking and stridor ensues, what has developed?
66.   Croup
67.         What other viral infection can cause the same hPIV Croup symptoms?
67.   Influenza A
68.         Chlamydia trachomatis can cause similar symptoms to what virus?
68.   hPIVs
69.         What pathogens can cause bronchitis similar to hPIVs?
69.   Streptococcus pneumonia, Mycoplasma pneumonia
70.         Can symptoms of adenovirus, rhinovirus, or coronavirus be distinguished from mild cases of hPIV infection?
70.   No
71.         When are hPIV 1 and 2 infections most common?
71.   Fall
72.         If croup develops in the winter months what is usually the culprit?
72.   influenza or RSV
73.         How are hPIVs transmitted?
73.   direct contact, large droplet spread
74.         T/F Reinfection with the same serotype of PIV is uncommon.
74.   F – common and can occur relatively quickly
75.         T/F There are no vaccines or antivirals used for hPIVs.
75.   T
76.         What is responsible for many lower respiratory tract infections in children?
76.   Human metapneumovirus (hMPV)
77.         What is the MOST important cause of viral lower respiratory tract disease in infants and children worldwide?
77.   Respiratory Syncytial Virus (RSV)
78.         Where does RSV initially infect?
78.   nasopharynx
79.         If RSV spreads to the lower respiratory tract, how long does it take and what are the symptoms?
79.   1-3 days, cough and low-grade fever develop
80.         T/F RSV can cause permanent lung damage and the development of asthma.
80.   T
81.         Where can RSV antigens be found?
81.   both epithelium and in exfoliated epithelia cells plugging the airways
82.         T/F RSV is uncommon in adults.
82.   F – common in normal adults; symptoms – rhinorrhea, cough, headache, fatigue, fever
83.         What patients are at high risk for RSV
83.   premature infants, children with chronic lung disease, Premature infants ;1yr at start of RSV season
84.         How is RSV spread?
84.   Large droplet or Fomite contamination
85.         What the heck is a Fomite?
85.   any inanimate object or substance capable of carrying infectious organisms (ex. bedding, cloth, stethoscope)
86.         What is the treatment for RSV infection?
86.   mostly supportive, ensure adequate oxygenation, hydration, and nutrition
87.         What is Synagis (palivizumab) and who is it use for?
87.   recombinant monoclonal antibody that neutralizes RSV, used for high risk infants
88.         What family is Rhinovirus part of?
88.   Picornaviridae
89.         How many serotypes do Rhinoviruses have?
89.   ;100
90.         What characteristics does the Rhinoviruses have?
90.   Small, non-enveloped, positive-strand RNA virus
91.         What is the distinguishing feature of the mRNA of Rhinovirus?
91.   5’VPg
92.         What differentiates Rhinoviruses from other picornaviruses?
92.   Inactivated by pH 6.0 or lower
93.         Why is Rhinovirus difficult to grow in culture?
93.   requires reduced temperature (33C) for optimal growth
94.         What does Rhinovirus bind to get into the host cell?
94.   iCAM-1
95.         How does Rhinovirus exploit the host cell?
95.   IFN and TNF-? upregulate iCAMs, Rhinovirus binds iCAMs
96.         Once the Rhinovirus enters the cell what is the first event that takes place?
96.   Translation of a polyprotein
97.         How are Rhinovirus viral proteins released from the polyprotein?
97.   following specific cleavage events by the virally encoded proteases
98.         How is translation of picornavirus genomes initiated?
98.   cap-independent mechanism
99.         What is the IRES (internal ribosome entry site)?
99.   Sequence near the 5’ end of picornavirus genome that initiates translation
100.      How is translation of picornavirus genomes linked to host cell translation?
100.           Linked to mechanism by which host cell translation is inhibited.
101.      What are the characteristics of a Coronavirus?
101.           Large, Enveloped, positive-stranded RNA virus, Genome capped at 5’ end, has 3’poly A+ tail
102.      What RNA virus has the largest Genome?
102.           Coronavirus
103.      How is the polymerase polyprotein of the coronavirus translated?
103.           1. cis-cleavage of viral polymerase which synthesizes a (-)sense antigenome, 2. antigenome is template for synthesis of sub-genomic mRNA
104.      What is unique about the coronavirus mRNA synthesis mechanism?
104.           “leader-primed” – results in nested set of overlapping mRNAs with common 3’ end
105.      What allows for a high frequency of recombination in the coronavirus?
105.           “Leader-primed” – polymerase “hopping”
106.      What percentage of Upper respiratory infections does coronavirus cause in humans?
106.           15-20%
107.      What “severe atypical pneumonia” was caused by a coronavirus in 2003?
107.           SARS
108.      T/F coronaviruses cause a significant amount of GI problems?
108.           T
109.      What do Rhinovirus and coronavirus infections do to the nasal mucosa?
109.           Cause shedding of the ciliated epithelium
110.      Why are conventional vaccinations not feasible for coronaviruses and rhinoviruses?
110.           Large # of serotypes for rhinoviruses, high frequency of recombination for coronaviruses
111.      What is Structure of Adenovirus?
111.           Linear, double-stranded DNA genome, 36 kilobase pairs, No envelope
112.      What does Adenovirus cause infection in?
112.           Respiratory, Eye, GI
113.      What is Adenovirus stable against?
113.           detergents, low pH
114.      How many serotypes of Adenoviruse are known to infect humans?
114.           49
115.      Where does replication and assembly of Adenovirus occur?
115.           Nucleus
116.      How is adenovirus spread?
116.           Respiratory or fecal-oral route
117.      What Bug is associated with pharyngoconjunctival fever in children?
117.           Adenovirus
118.      Conjunctivitis that feels like “sand in the eye” is caused by what bug?
118.           Adenovirus
119.      What is the main pathogenic species of Pseudomonads?
119.           P. aeruginosa
120.      What bug is widely distributed in nature and is highly resistant to antibiotics and can rapidly evolveresistance?
120.           Pseudomonads
121.      What characteristics do Pseudomonas have?
121.           Gram Negative, motile, aerobic rods, Produce Soluble Pigments
122.      What allows pseudomonas to grow just about anywhere?
122.           Obligate aerobes – can us CO2, atmospheric ammonia, nitrogen sources
123.      An organism that grows at 42C is diagnostic for what bug?
123.           Pseudomonas
124.      What do cultures of Pseudomonas smell like?
124.           Grapes
125.      What type of pigmented siderophores do pseudomonas produce and what color are they?
125.           Pyocyanin – Blue, Pyoverdin – fluorescent yellow pigment
126.      What do some strains of pseudomonads produce that is induced in the CF lung?
126.           Alginate
127.      What does an overproduction of alginate result in?
127.           mucoid phenotype
128.      Who do pseudomonads cause a problem for?
128.           immune suppressed people
129.      What type of toxin do pseudomonads produce?
129.           Exotoxin A
130.      How does Exotoxin A effect the cell?
130.           causes necrosis by blocking protein synthesis
131.      What 2 toxins have an identical mechanism of blocking protein synthesis, but are produced by different bugs?
131.           Exotoxin A and diphtheria
132.      What bug is associated with Swimmers ear frequently?
132.           Pseudomonas
133.      What type of rash can you get if you are on a medical conference and you shave your legs before going into a hot tub that doesn’t have enough chemicals? what bug caused it?
133.           Hot Tub Folliculitis, Pseudomonas
134.      How are pseudomonas infections treated?
134.           Combined therapy to limit resistance
135.      What are the characteristics of Acinetobacter?
135.           Ubiquitous aerobic gram negative coccobacillus
136.      How does Acinetobacter infect?
136.           compromised patients – low pathogenic potential
137.      What strain of Acinetobacter is most common?
137.           A. baumanii
138.      What bug has recently been a major problem in the Burn Wards of Memphis?
138.           A. baumanii
139.      What pathogen is A. baumanii easily mistaken for?
139.           N. meningiditis
140.      How is A. baumanii differentiated from Neisseria?
140.           oxidase negative
141.      Why is antimicrobial testing necessary to guide therapy of Actinobyces?
141.           Extremely resistant to antibiotics
142.      What bug shows biopolar metachromic granules?
142.           B. pertussis
143.      What bug is a small gram negative coccobacillus that looks like H. influenza?
143.           B. pertussis
144.      Why do you have to let the lab know before you culture someone you suspect as having whooping cough?
144.           requires an enriched and selective medium for primary isolation – Bordet-Gengou medium
145.      How is B. pertussis transmitted?
145.           droplet inoculation
146.      What does B. pertussis produce a lot of that causes irritation, inflammation, and cough?
146.           AB exotoxins
147.      Does B. pertussis invade the ciliated epithelium?
147.           No, multiples on epithelia without invasion
148.      What controls the virulence gene expression of B. pertussis?
148.           bvgA/bvgS two component regulatory system
149.      What is the enzymatic action that is specific for the Pertussis toxin?
149.           Interfere with PMN, monocyt, and macrophage function, Lymphocytosis, Sensitization to histamine, Hypoglycemia
150.      How does the BvgS/A system regulate virulence factors?
150.           BvgS senses a stimulus, phosphate from a donor transferred to BvgS eventually goes to BvgA which Activates transcription of several genes.
151.      How Does Pertussis A toxin interfere with normal function?
151.           Conversion of ATP to cAMP cannot be stopped because the Gi protein that normally inhibits adenylate cyclase is inhibited by A toxin.
152.      How long is the incubation period for B. Pertussis?
152.           1-2 weeks
153.      When are patients most infections with B. Pertussis?
153.           Catarrhal stage
154.      How is the paroxysmal stage of B. pertussis characterized?
154.           coughing fits – with whoop inhalation, lasts about 2 weeks, high white blood cell count
155.      How is B. pertussis diagnosed?
155.           primary by clinical features, Nasopharyngeal swap
156.      Whats the drug of choice for B. pertussis?
156.           Erythromycin
157.      How is B. pertussis prevented?
157.           DTap immunization
158.      What bug is a Gram positive Rod that appear in clumps resembling Chinese letters?
158.           C. diphtheriae
159.      Where is C. diphtheriae found?
159.           Human reservoir – not found anywhere else in nature
160.      T/F Production of diphtheria toxin only occurs in cells that have been transduced with a phage that carries the toxin genes.
160.           T
161.      What is the expression of the Diphtheria toxin dependent on?
161.           iron – Low concentrations increase toxin production, High concentrations repress production
162.      What type of toxin is the Diphtheria toxin?
162.           AB toxin (like pseudomonas)
163.      What tissues are most affected by Diphtheria toxin?
163.           myocardium and peripheral nerves
164.      What does the A subunit of Diphtheria toxin inhibit?
164.           polypeptide elongation in the presence of NAd by inactivation of EF-2
165.      What is the characteristic pathology of Diptheria toxin?
165.           pseudomembrane over tonsils, pharynx, and larynx
166.      What bug can cause the characteristic “bull neck”?
166.           C. Diptheria
167.      What is the mainstay of therapy for Diphtheria?
167.           Antitoxin – immediately
168.      What is the characteristic stain of Mycobacteria?
168.           Acid fast stain positive
169.      What is unique about the M. Tuberculosis envelope?
169.           Mycolic Acid, Cord Factor, Wax-D
170.      What properties are associated with the high concentrations of lipids in the cell wall of M. tuberculosis?
170.           Impermeability to stains and dyes, Resistance to antibiotics, acidic and alkaline compounds, osmotic lysis, lethal oxidations, desiccation
171.      When do Tubercles form with tuberculosis infection?
171.           Primary Disease
172.      What are calcified tubercles seen called?
172.           Ghon complexes
173.      In the absence of CMI, how can TB progress?
173.           Miliary TB
174.      What test for TB indicates infection but does not indicate disease?
174.           PPD
175.      How long do cultures of TB need to be kept to rule out disease?
175.           1-2 months
176.      What is the treatment plan for TB?
176.           Combined therapy – Isoniazid, Rigampin, pyrazinamide, and ethambutol or streptomycin, 6-9 months, patients are non-infectious within 2 weeks but not cured
177.      What is Cord Factor for?
177.           virulence factor that functions to inhibit PMN migration
178.      What are the characteristics of Actinomyces?
178.           Club-shaped, gram + rods that form Branched filaments.
179.      What do the microcolonies of actinomyces in pus look like?
179.           sulfur granules
180.      What is the reservoir of Actinomyces?
180.           Human oral and GI
181.      What is Actinomyces israelii nearly always associated with?
181.           Trauma and compromised immunity (surgery, tooth extraction, IUDs)
182.      What Disease is characterized by “lumpy jaw”?
182.           Cervicofacial actinomycosis
183.      What is the treatment for Actinomyces?
183.           Prolonged Penicillin
184.      Where is Nocardia found?
184.           Soil
185.      What does Nocardia resemble?
185.           Aerobic weakly gram positive branching rods that look like fungi
186.      What kind of acid stain do Nocardia have?
186.           weakly acid fast
187.      T/F Nocardiosis are Penicillian resistant.
187.           T – use Trimethylprim-sulfamethoxazole
188.      Does Atypical Pneumonia always include fever?
188.           No – may or may not, radiological evidence may distinguish
189.      How does growth of Chylamydia occur?
189.           biphasic developmental cycle
190.      What is a significant cause of community acquired pneumonia?
190.           Chlamydia pneumonia
191.      What are the characteristics of Chlamydia?
191.           Gram-negative spherical bacteria that are obligate intracellular parasites
192.      What is the developmental cycle of Chlamydiae?
192.           Elementary Bodies attach and enter cell, Primary Differentiation, Cell division, Rapid multiplication, Effector secretions, Secondary differentiation, EB released and Reinfect
193.      What bug is associated with chronic atherosclerotic disease?
193.           Chlamydia Pneumoniae
194.      What are the 3 predominant bacterial causes of Atypical Pneumonia?
194.           Chlamydia, Mycoplasma, Legionella
195.      What is the smallest free-living organism?
195.           Mycoplasma
196.      T/F Mycoplasma lack a cell wall.
196.           T
197.      What are the symptoms of Mycoplasma pneumoniae, and who do they typically occur in?
197.           Mild respiratory infection, sore throat and pharyngitis, occur in 1-5 YO
198.      How does mycoplasma activate inflammatory cytokines?
198.           lipoproteins interact with alveolar macrophage Toll-like receptors
199.      T/F Mycoplasma will not show up in a blood test.
199.           F – Positive blood test after 10 days of infection
200.      What is used to Treat M. pneumonia?
200.           2nd Generation – Macrolides, Tetracyclines, Fluoroquinolones
201.      What are the characteristics of Legionella?
201.           Aerobic Gram Negative Rod, facultative intracellular bacteria
202.      What is Legionnaires Disease?
202.           more severe pneumonia form of L. pneumophila infection
203.      What temperatures are Legionella dormant, have ideal growth, and survive but don’t multiple?
203.           Dormant ;20C, Ideal Growth Rate 20-50C, Survive but don’t multiple ;50C
204.      Where does L. pneumophila replicate?
204.           alveolar macrophages after inhalation
205.      How does L. pneumophila avoid phagosome-lysosome fusion?
205.           creating a specialized vacuole that resembles the endoplasmic reticulum of the host
206.      Who does L. pneumophila most often infect?
206.           middle age to older patients, smokers, chronic lung disease patients and immunocompromised
207.      How is L. pneumophila treated?
207.           Macrolides, fluoroquinolones

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