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273 Cards in this Set
- Front
- Back
what are the three main regions of the LRT?
|
1. bronchi
2. bronchioles 3. alveoli |
|
what are the normal flora of the LRT?
|
none
|
|
what makes up 25% of the protein secreted in the nasophaynx?
|
IgA
|
|
what two options do organisms have to reach the LRT?
|
1. inhaled in small droplet nuclei
2. normal flora that is able to adhere to the LRT surfaces |
|
what is a LRT disease which is characterized by cough paroxysm consiting of short expiratory bursts followed by an inspiratory gasp which causes a distinctive sound?
|
whooping cough
|
|
whatis the causitive angent of whooping cough? (2)
|
1. Bordetella pertussis (majority of cases)
2. Bordetella parapertussis |
|
Bordetella pertussis gram + or -?
|
gram -
|
|
Bordetella pertussis structure?
|
coccobacilli
|
|
what other organism does Bordetella pertussis infect?
|
TRICK! Only a human pathogen
|
|
is Bordetella pertussis intra or extracellular?
|
extracellular
|
|
does Bordetella pertussis produce toxin?
|
yes
|
|
is Bordetella pertussis invasive?
|
no
|
|
what allows Bordetella pertussis to bind to cilia of respiratory tract and bind recepotors on PMN's that stimulate uptake?
|
Filamentous hemagglutinin (FHA)
|
|
what are the 4 toxins produced by Bordetella pertussis?
|
1. Pertussis toxin
2. Adenylate cyclase toxin 3. Dermonecrotic toxin 4. tracheal cytotoxin |
|
describe the classification of pertussis toxin?
|
A/B toxin or Type III exotoxin
|
|
what two roles does pertussis toxin function in?
|
1. adhesion
2. G-protien ribosylation resulting in increased cAMP levels |
|
what systemic indicator reveals the presence of pertussis toxin?
|
Lymphocytosis
|
|
what protective function does pertussis toxin function in for Bordetella pertussis?
|
inhibits phagocytosis and monocyte migration
|
|
what is the classification of adenylate cyclase toxin?
|
secreted A/B toxin or Type III endotoxin
|
|
what is the mode of action for adenylate cyclase toxin?
|
enters the cell and causes increased cAMP production
|
|
what are the effects of adenylate cyclase toxin on cells of the respiratory epithelium?
|
increases mucus production and damages ciliated cells
|
|
what are the effects of adenylate cyclase toxin on the immune system?
|
Inhibits leukocyte production, migration, and killing
|
|
what is the action of dermonecrotic toxin?
|
vascular smooth muscle contraction resulting in local ischemic damage
|
|
tracheal cytotoxin is said to be a by product of?
|
peptodiglycan synthesis in host cells
|
|
what two effects does tracheal cytotoxin have on tracheal epithelial cells?
|
1. interferes with DNA production
2. causes release of IL-1 which is a fever-inducing agent |
|
of all the toxins produced by Bordetella pertussis which actually is responsible for the whooping cough?
|
tracheal cytotoxin
|
|
what is the main traget of Bordetella pertussis?
|
ciliated epithelium
|
|
how does FHA bind to PMN's?
|
via CR3
|
|
which two toxins are responsible for the increased mucus production seen in patients with whooping cough?
|
Pertussis toxin and adenylate cyclase toxin
|
|
what causes the systemic manifestations (seizures, encephalopathy) related to whooping cough?
|
the cough itself causes anoxia which results in the systemic manifestations
|
|
how is whooping cough mainly transported?
|
aerosol droplets
|
|
what is the attack rate of pertussis?
|
50-100%
|
|
in unvaccinated populations, what age group is most at risk for whooping cough?
|
ages 1-5
|
|
what are the two sources of whooping cough spreading?
|
unimmunized children and adults with wanning protective immunity
|
|
what is the incubation time for whooping cough?
|
1-3 weeks
|
|
what is the enitre time frame of the Bordetella pertussis infection?
|
6-10 weeks
|
|
What is the phase (whooping cough): lookis like URT infection, lasts 1-2 weeks, nonproductive dry cough develops?
|
catarrhal phase
|
|
what is the phase (whooping cough): characterized by whooping cough which peaks at 30 episodes per day and ends in vomiting and lasts 2-6 weeks?
|
paroxysmal phase
|
|
what is the phase (whooping cough): descrease in intensity and frequency of cough?
|
convalescent phase
|
|
when should I be clinically suspicious of whooping cough?
|
when patient has cough longer than 2 weeks
|
|
what serologic findins might tip me off to a Bordetella pertussis infection?
|
high leukocytosis with predominance of lymphocytes
|
|
what is the method of choice for diagnosing a Bordetella pertussis infection?
|
direct antigen testing via PCR (good sensitivity and specificity) or flourescent antibody staining (low sensitivity)
|
|
what is the DOC for treatment of whooping cough?
|
erythromycin
|
|
what are the two types of vaccines availible for whooping cough?
|
whole cell and acellular (inactivated pertussis toxoid)
|
|
what other inactivated toxoids are included in the acellular Bordetella pertussis vaccine?
|
inactivated toxoids from diphtheria and tetanus
|
|
what infectious disorder is characterized by inflammation of tracheobronchial tree where mucous membranes are edematous and persistant cough in absense of LRT infection?
|
Acute Bronchitis
|
|
when does acute bronchitis normally occur?
|
winter months
|
|
what LRT disease is characterized by acute, viral, ilness occuring at or before 2 years of age with wheezing, hyperaeration, cough, rhinorrhea, repiratory distress?
|
bronchiolitis
|
|
what are the 3 main causes of bronchiolitis in order of their prevelance?
|
1. respiratory synctial virus (RSV) 45-75%
2. Parainfluenza virus type 1, 2, 3 15-35% 3. Human metaneumovirus |
|
what pathologic agent is the leading cause of LRT infections in children world-wide?
|
RSV
|
|
what family of viruses does RSV belong to?
|
paramyxoviridae
|
|
does RSV have a naked capsid or is it enveloped?
|
enveloped
|
|
describe the viral genome of RSV?
|
single negative sense strand RNA
|
|
what are the proteins which are integral to RSV infectivity and pathogenicity?
|
F and G glycosylated surface protiens
|
|
what is the function of the F protien of RSV?
|
F protein mediates viral penetration vi fusion and penetration with cell membranes and melds infected cells with uninfected cells
|
|
what is the function of the G protien?
|
viral attachment protien which allows virus to stay on target cells
|
|
what tests are availible for diagnosis of RSV virus?
|
1. ELISA or DFA (direct flourescent antibody???)
2. nasal wash culture which presents with syncytia |
|
in unvaccinated populations, how many children are infected with RSV by age 3?
|
virtually all
|
|
where does inoculation with RSV occur?
|
nose or eyes
|
|
what is RSV incubation period?
|
4-5 days
|
|
there is a bias towards which type of TH cell response with RSV?
|
TH2, but what is needed is TH1
|
|
what immune response is most important in the defense against RSV?
|
cell-mediated immunity
|
|
what antibodies appear most effective against RSV?
|
those that bind to F and G glycoproteins
|
|
describe the first clinical manifestations of RSV infection?
|
nasal congestion, pharyngitis, fever, cough which deepens with LRT involvement
|
|
most common presentations of RSV infections are? (2)
|
1. pneumonia
2. bronchiolitis |
|
how can you tell when LRT involvement is occuring with a RSV infection? (3)
|
1. dyspnea
2. increased respiration rate 3. intercostal retractions |
|
what is a common complication of RSV infections?
|
Otitis media
|
|
what is the primary treatment of RSV infections in otherwise healthy children?
|
supportive care
|
|
what are the 2 forms of passive immunization availble fo RSV infections?
|
1. RSVIG immunoglobulin
2. Palivizumab - monoclonal antibodie reactive with F protein of RSV |
|
what family does the parainfluenza virus belong to?
|
paramxyoviruses
|
|
describe the genome of the parainfluenza virus?
|
ssRNA that is negative sense
|
|
what distinguishes the parainfluenza virus from other paramxyoviruses?
|
envelope glycoprotien neuraminidase and presence of hemagglutinating properties
|
|
what does the hemagglutinin-neurominidase protein complex do?
|
allows virus to bind to sailic acid receptors
|
|
what allows for fusion and infection of target cells by the parainfluenza virus?
|
F protien like that found in RSV
|
|
what is the gold standared laboratory test for parainfluenza virus diagnosis?
|
cell culture from NS wash or respiratory secretions
|
|
what can be used for rapid diagnosis of the parainfluenza virus?
|
DFA
|
|
what can be added to tubes containing the virus to determine if it has hemadsorptive properties?
|
guinea pig RBC's
|
|
the parainfluenza virus is the leading cause of ___ in the US?
|
laryngitis
|
|
describe laryngitis
|
erythema and swelling of lateral walls of the trachea just below vocal cords
|
|
what is the most common presentation of parainfluenza virus infections?
|
common cold (URT infection)
|
|
where is the initial site of infection for the parainfluenza virus?
|
mucous membranes of nose and throat
|
|
how does the parainfluenza virus get to the LRT?
|
it spreads down respiratory tract just like RSV
|
|
how long does a croup cough (laryngitis) usually last?
|
3-4 days
|
|
what is the suggested therapy?
|
supportive therapy with corticosteroids
|
|
what vaccines are availible to treat children with parainfluenza virus infections?
|
none
|
|
what is a recently discovered virus (2001) that closely resembles RSV and has a high infection rate in children?
|
Human metapneumovirus (HMPV)
|
|
what is the most practical method of testing for HMPV?
|
PCR
|
|
what is a disorder characterized by infection of lung parenchyma involving the alveoli or interstitium?
|
Pneumonia
|
|
describe the prevelance of acute pneumonia in the US?
|
6th leading cause of death
|
|
what is the leading cause of community aquired pneumonia?
|
Streptococcus pneumoniae
|
|
is Streptococcus pneumoniae gram + or -?
|
gram +
|
|
what is structure of Streptococcus pneumoniae?
|
cocci
|
|
are Streptococcus pneumoniae catalase positive or negative?
|
negative
|
|
why do Streptococcus pneumoniae sometimes appear gram negative?
|
the contain autolysin which destroys the bacteria and releases the gram + stain
|
|
what usually allows Streptococcus pneumoniae to get to LRT positions?
|
aspiration of URT secretions
|
|
what are the two main virulence factors which Streptococcus pneumoniae uses?
|
1. Capsul for protection
2. Causes inflammation |
|
how does the capsul help Streptococcus pneumoniae avoid recognition by phagocytes?
|
more than 80 different serotypes so it is constantly changing to avoid detection
|
|
what function does the capsul play in preventing opsonization of Streptococcus pneumoniae?
|
it bind protein H which degrades C3b
|
|
what is the function of pneumolysin?
|
decreases oxidative bust which reduces effectiveness of PMNs
|
|
what does Streptococcus pneumoniae production of DNAse's allow for?
|
lysing of neutrophil NETs (cell traps)
|
|
how does Streptococcus pneumoniae cause massive inflammation of lung tissue?
|
it contains autolysin which destroys the bacteria, but releases teichoic acid which binds to TLR receptors causing the release of inflammatory cytokines
|
|
what does pneumolysin do that increases inflammation?
|
it activates compliment by binding near Fc regions on immunoglobulins
|
|
what plays a crucial role in eliminating Streptococcus pneumoniae from circulation?
|
the spleen
|
|
how does Streptococcus pneumoniae cause bacterial meningitis?
|
it can bind to blood brain barrier epithelium and damage it which allows bacteria in
|
|
what are the 3 major risk factors for Streptococcus pneumoniae infection?
|
1. loss of splenic function
2. decreased responsiveness to polysaccharide antigens 3. increased rat of decline in serum antibody cocentrations |
|
what is the site of early IgM response to Streptococcus pneumoniae infection?
|
spleen
|
|
what is the DOC for treating Streptococcus pneumoniae infections?
|
penicillin, but decreased PBP affinity for penicillin has made Streptococcus pneumoniae resistant
|
|
what are alternative antibiotics for Streptococcus pneumoniae infection which are still very effective? (3)
|
1. vancymycin
2. quinilones 3. 3rd generation cephalosporins |
|
what is very important to ensure before taking a culture of Streptococcus pneumoniae?
|
no antibiotics have been given yet
|
|
what distinguishes Streptococcus pneumoniae from other alpha-hemolytic strep?
|
solubility in bile caused by autolysin and sensitivity to optochin
|
|
are there vaccines availble for Streptococcus pneumoniae?
|
yes, consist of more than 23 different inactivated capsuls which represent 85% pf pneumonia infections
|
|
what is the new Streptococcus pneumoniae vaccine which is approved for young children?
|
Prevnar
|
|
what is the problem with vaccines against Pneumococcal agents?
|
the less common pathogenic types are taking over the place occupied by the ones being suppressed via vaccines
|
|
is Haemophilus influenza gram + or -?
|
gram -
|
|
what is the structure of Haemophilus influenza?
|
coccibacilli
|
|
what allow Haemophilus influenza to adhere to the mucosal epithelial cells?
|
fimbriae
|
|
what helps Haemophilus influenza avoid binding to IgA?
|
IgA proteases
|
|
as with most gram negative bacteria what antigenic component exists in the outer-membrane?
|
LPS
|
|
what is the key survival mechanism of Haemophilus influenza?
|
its ability to form a capsul
|
|
what is the capsul in Haemophilus influenzacomposed of?
|
PRP (polyribitol phosphate polysaccharide)
|
|
what is the most effective capsul type?
|
Type B -> invasive infections
|
|
what does the Hib vaccine help to make antibodies against?
|
Type B capsuls of the Haemophilus influenza
|
|
what are some of the localized disease that the unencapsulated Haemophilus influenza can produce?
|
otitis media, sinusitis, bronchitis
|
|
how does the spread of Haemophilus influenza occur?
|
airborne droplets or direct contagion with secretions
|
|
invasive infections with Haemophilus influenza usually occur in what age range?
|
3 months to 6 years
|
|
what does Haemophilus aegypticus cause?
|
pink eye (purulent conjunctivitis
|
|
what are some presentations of encapsulated Haemophilus influenza?
|
1. Pneumonia
2. Epiglottitis 3. Meningitis 4. Lesser presentation -Cellulitis -Septic Arthritis |
|
what is the DOC for Haemophilus influenza and why?
|
Cephalosporin because Haemophilus influenza produces beta-lactamase
|
|
what is the special agar that must be used to culture Haemophilus influenza?
|
chocolate agar - heated blood agar
|
|
antibody specific to ___ is protective?
|
PRP (polyribosylribitol polysaccharide)
|
|
what is the vaccine that is currently used for ages 2 months and up?
|
conjugated PRP vaccine
|
|
is Klebsiella pneumoniae gram + or -?
|
gram -
|
|
what is the structure of Klebsiella pneumoniae?
|
bacilli
|
|
is Klebsiella pneumoniae extracellular or intracellular?
|
extracellular
|
|
where is Klebsiella pneumoniae part of the bodies normal flora?
|
the human GI tract
|
|
what is a large difference between most Enterobacteriaciae and Klebsiella pneumoniae?
|
it has a thick polysaccharide capsul
|
|
what does Klebsiella pneumoniae cause when untreated in the respiratory tract?
|
sever pyognic pneumonia
|
|
who is most at risk for respiratory infections with Klebsiella pneumoniae?
|
compromised hosts such as alcoholics, diabetics, and COPD patients
|
|
what is a major concern with Klebsiella pneumoniae infections in regards to treatment?
|
increasing antibiotic resistance that has left Klebsiella pneumoniae nearly resistant to all antibiotics
|
|
what is a free-living ubiquitous bacteria that is an important nosocomial opportunistic pathogen in multiple settings?
|
Pseudomonas aeruginosa
|
|
where can Pseudomonas aeruginosa be found naturally?
|
decaying organic matter, water, vegetation
|
|
is Pseudomonas aeruginosa gram + or gram -?
|
gram -
|
|
describe the oxygen requirements of Pseudomonas aeruginosa?
|
strict aerobe
|
|
what special characteristic of Pseudomonas aeruginosa shows up in pus at effected sites?
|
Pseudomonas aeruginosa is a pigment producer that makes pyocyanin and flourescein (gives pus a green color)
|
|
what makes infections with Pseudomonas aeruginosa hard to treat?
|
they are very antibiotic resistant
|
|
why do most healthy people not get infected with Pseudomonas aeruginosa?
|
the have a high number of functioning PMNs which is the most important defense against Pseudomonas aeruginosa
|
|
what must be lost from epithelial cells during disease, damage, or infection for Pseudomonas aeruginosa to adhere?
|
fibronectin
|
|
describe the "slime coat" that Pseudomonas aeruginosa produces
|
extracellular mucopolysaccharide termed alginate
|
|
what regulates the gene for alginate production in Pseudomonas aeruginosa?
|
Quorum sensing
|
|
in addition to quorum sensing, how can alginate production become stuck on?
|
during attack with H2)2 or activated PMNs
|
|
which patients have a high rate of alginate gene mutation causing its constituetive production?
|
CF patients
|
|
what is the benefit of having a slim layer for Pseudomonas aeruginosa?
|
it is both antiphagocytic and helps in antibiotic resistance
|
|
what pigment do Pseudomonas aeruginosa produce?
|
Pyocyanin
|
|
what does pyocyanin function as?
|
forms toxic radicals (tissue damage) and stimulates the release of IL-8 (neutrophil attractant)
|
|
is Pseudomonas aeruginosa noninvassive or invasive?
|
invasive
|
|
what exotoxin does Pseudomonas aeruginosa produce?
|
exotoxin A, but it is less potent than the form produced by diphtheria
|
|
what is critical for Ps. aeruginosa role in causing septic shock?
|
endotoxin
|
|
describe the defenses against antibody that Ps. aeruginosa displays?
|
contains beta lactamases and porin protien mutations which allow resistance to almost all antibiotics
|
|
which patient type is most likely to have antibiotic resistant Ps. aeruginosa?
|
CF patients
|
|
what is absolutely essentiat for the removal of Ps. aeruginosa from host?
|
functioning neutophils
|
|
where can Ps. aeruginosa be found?
|
just about anywhere water is present
|
|
what protects hosts from the exotoxin effect of Ps. aeruginosa in a immunocompetent individual?
|
antibody against exotoxin A
|
|
what is the LRT infection caused by Ps. aeruginosa?
|
pnuemonia
|
|
in addition to pnuemonia what other manifestations do Ps. aeruginosa infections take on? (4)
|
1. bateremia
2. meningitis 3. swimmers ear (otitis externa) 4 UTI |
|
what are the beta lactams which might be effective in treating Ps. aeruginosa?
|
1. broad spectrum penicillins like piperacillin
2. 3rd and 4th generation cephalosporins (ceftazidime, cefepime) 3. Imipenem 4. Aztreonam |
|
In addition to the penicillin based antibiotics, what other antibiotic can be used against Ps. aeruginosa?
|
Aminoglycosides
|
|
Atypical Pneumonia:
Describe characteristics upon culturing? |
organisms don't grow on standared lab bacteriology media in 1-2 days
|
|
Atypical Pneumonia:
Describe host PMN response? |
host usually has fewer PMNs than typical agents of typical pneumonia
|
|
Atypical Pneumonia:
describe antibiotic resistance? |
resistant to all beta lactams unlike typical agent of pneumonia that respond to some, broad spectrum beta lactams
|
|
Atypical Pneumonia:
what are the 3 main causitive agents of atypical pneumonia? |
1. Mycoplasma
2. Chlamydophila 3. Legionella |
|
what is the smallest free-living organism that is able to pass through filters that stop normal bacteria?
|
Mycoplasma pneumonia
|
|
what is particulary unique about the structural makeup of Mycoplasma pneumonia?
|
it genetically lacks a cell wall
|
|
why does the disease incubation in Mycoplasma pneumonia tend to be longer than other respiratory infections?
|
it has a slower growth rate
|
|
what are the oxygen requirements of Mycoplasma pneumonia?
|
strictly aerobic
|
|
describe the prevelance of Mycoplasma pneumonia infections worldwide?
|
very common
|
|
what age group is most at risk for Mycoplasma pneumonia infection?
|
school age children and young adults
|
|
is Mycoplasma pneumonia invasive?
|
mostly not
|
|
where does Mycoplasma pneumonia adhere to its host cell and what facilitates this binding?
|
at the base of cilia on respirtory epithelium with the aid of tip protein (P1)
|
|
describe the direct damage to epithelial cells Mycoplasma pneumonia is responsible for?
|
produces H2)2 and causes ciliastasis
|
|
what are the two indirect damages that Mycoplasma pneumonia can cause to repiratory epithelium?
|
1. components of Mycoplasma pneumonia act as superantigens
2. Mycoplasma pneumonia stimulates antibodies cross-reactive with normal tissue antigens |
|
would repeat infections with Mycoplasma pneumonia produce a worse or more controlled effect?
|
worst effect because this would stimulate production of more cross-reactive antibodies
|
|
what is the most common presentation of Mycoplasma pneumonia infections?
|
pharyngitis/rhinitis characterized by low grade fever, mailaze, headache and nonproductive cough for 2 or more weeks
|
|
what are two secondary respiratory manifestations of Mycoplasma pneumonia?
|
1. tracheobronchitis
2. pneumonia |
|
when tracheobronchitis is associated with a prolonged nonproductive cough what might be the suspected pathogen at work?
|
pertussis
|
|
the type of pneumonia associated with Mycoplasma pneumonia infections is known as?
|
"walking pneumonia"
|
|
what percentage of community aquired pneumonia is atributed to Mycoplasma pneumonia infections?
|
~25%
|
|
recovery from Mycoplasma pneumonia infections are due mainly to what?
|
production of local IgG and IgA - enhances phagocytosis
|
|
what are the 3 choices diagnosign testing Mycoplasma pneumonia infections?
|
culture, cold agglutinin detection, and specific serology
|
|
which is the diagnostic test of choice for Mycoplasma pneumonia infections?
|
specific serology which tests for IgM or IgG titer rises
|
|
what are the three antibiotics used on all atypical pneumonia infections?
|
1. tetracycline
2. macrolide 3. quinolone |
|
Describe Chlamydophila pneumoniae?
|
basically everything is the same with disease statust, diagnosis, and treatment as compared to Mycoplasma pneumonia
|
|
what is the biggest difference between Mycoplasma pneumonia and Chlamydophila pneumoniae?
|
Mycoplasma pneumonia is free living and Chlamydophila pneumoniae is not
|
|
describe the location (intracellular, extraceullular, or faculatative intracellular) of Legionella pneumophila
|
Legionella pneumophila is a facultative intracellular pathogen
|
|
is Legionella pneumophila gram + or gram -?
|
gram -
|
|
what is the structure of Legionella pneumophila?
|
bacillus
|
|
what is the required diagnostic test of Legionella pneumophila?
|
direct detection done with DFA or BETTER, a urine antigen test
|
|
describe the oxygen requirements of Legionella pneumophila?
|
areobic
|
|
what is required to grow Legionella pneumophila in culture?
|
a plate containing L-cystein, iron, and charcoal (to neutrolize toxins produced by growing bacteria)
|
|
why is the it important to recognize Legionella pneumophila infections in the clinical setting?
|
they are not routinely tested for in normal cultures and must be specifically asked for
|
|
what is an important consideration to make when suspected Legionella pneumophila tests come back negative?
|
they usually only test for the serotype 1 and there are 14 other serotypes it could be
|
|
how is Legionella pneumophila transmitted?
|
in aerosols of water (remember hot tub steam on cruise ships)
|
|
what harbors the Legionella pneumophila as they live in water?
|
free-living Amoeba
|
|
what persons are most at risk for Legionella pneumophila?
|
those with impaired mucociliary clearance and increased risk of aspiration of oral/pharyngeal flora
|
|
how does Legionella pneumophila enter macrophages and monocytes?
|
after compliment C3b binds to bacteria, CR3 receptors on macrophage cause it to be phagocytized
|
|
how does Legionella pneumophila avoid degredation in the phagosome?
|
it block the binding to the phagozome with lysosomes
|
|
how does Legionella pneumophila kill the cell which it has infected?
|
produces proteolytic enzymes which trigger apoptosis
|
|
what is the most important immune response against Legionella pneumophila infections of macrophages?
|
CMI because of the intracellular location of Legionella pneumophila
|
|
what patients are most at risk for sever infections with Legionella pneumophila?
|
those that are immunosuppressed with chronic disease, age, or smoking
|
|
what is the name of the acute pneumonia caused by Legionella pneumophila?
|
Legionnaire's disease
|
|
what is the avg. incubation time for Legionnaire's disease?
|
5 days
|
|
describe symptoms of Legionnaire's disease (3)
|
1. fever/chills
2. dry nonproductive cough initially 3. multilobar consolidation |
|
describe the severity of Legionnaire's disease?
|
most deadly for of pneumonia with a 5-20% mortality rate
|
|
what is the mild, self-limiting form of Legionella pneumophila infection?
|
Pontiac Fever
|
|
what is the incubation time for pontiac fever?
|
1-2 days
|
|
what is the attack rate of Legionella pneumophila?
|
over 90%
|
|
describe symtpoms of pontiac fever?(3)
|
1. fever
2. myalgia 3. non-productive cough |
|
what is the recovery time for pontiac fever?
|
2-5 days
|
|
where can Legionella pneumophila be found in nature?
|
biofilms in water associated areas
|
|
describe its tolerance to extreme conditions?
|
chlorine tolerant and heat tolerant (needs to be exposed to temps over 140 before it dies)
|
|
besides there capability to grow as free-living organisms, what other place can they live?
|
protozoan host cells
|
|
how is Legionella pneumophila spread?
|
NOT person to person, but instead from exposure to contaminated water
|
|
what is the prevention against Legionella pneumophila infections?
|
destroy the population in whatever water resevoir they are living in
|
|
what is the preferred diagnostic test for Legionella pneumophila?
|
urinary antigen ELISA
|
|
what are the antibiotics used to treat Legionella pneumophila?
|
same as all the other atypical pneumonia cauing agents: macrolide or quinilone family and tetracylcine
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what is orthomyxoviridae family of viruses commonly know associated with?
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influenza virus
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how many types of influenza are there?
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3, Type A-C
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which Type(s) are the most important pathogens in influenza?
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Type A and B
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what are the 5 key structural elements of the influenza virus?
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1. hemagglutinin (H) surface glycoprotien
2. Neuraminidase (N) surface glycoprotien 3. Matrix (M1) and Membrane (M2) proteins 4. Nucleocapsid 5. NS (nonstructural) proteins |
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what is the role of hemagglutinin glycoprotiens on the viral envelope?
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allows binding of capsid to host sailic acids and promotes fusion of viral envelope to host cell membrane
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is the H glycoprotein antigenic?
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yes
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what do antibodies to H cause to happen?
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prevent infection from occuring
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what is the role of nuerominidase (N) surface glycoprotien?
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cleaves sailic acid from host cell surface to prevent clumping of viral particles when they are released
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what does antibody to N glycoprotein cause to happen?
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does not stop infection, but it does stop spread
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is N glycoprotein antigenic?
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yes
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what are matrix (M1) proteins?
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major structural proteins
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what is the role of M1 proteins?
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promotes viral assembly
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what are membrane (M2) proteins?
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ion channel proteins
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what is the function of M2?
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promotes uncoating and viral release
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what are the antibiotics which target N glycoproteins? (2)
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1. zanamivir
2. oseltamivir |
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what are the antibiotic which target M2 proteins of influenza A? (2)
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1. amantadine
2. rimantadine |
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what is special about the influenza capsid that allows it a unique evasion capability?
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it is composed of 8 ssRNA segments which can be assembled randomly
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what is the result of the random assembly of the influenza virus capsid?
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many rearrangements produce non-active viruses, but the upside is that the ones which are active are highly variable and thus highly pathogenic
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when is the highest variability present in ssRNA reassortment during production of influenza virus in host cells?
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when host cell is infected by more than one strain which can swap ssRNA with each other
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what are the 3 functions of NS proteins of the influenza virus?
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1. RNA splicing
2. Suppression of IFN production 3. stimulates release of inflammatory cytokines |
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what actually causes the symptoms of influenza?
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the release of inflammatory cytokines caused by NS proteins
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describe the naming of influenza viruses (nomenclature organization)?
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type/place of original isolation/strain/year of original isolation,H and N antigens
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what is the term refering to the relatively minor changes to RNA H or N glyocproteins within an influenza subtype?
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antigenic drift
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why do strains which result from antigenic drift become more prevelant than previous strains?
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they are less susceptible to the current antibiotics
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what is major change in which in H and/or N glycoproteins which results in a new strain which almost no one in the population is immune to?
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antigenic shift
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antigenic shift only occurs in which influenza type?
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Type A
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what is the most likely host for the generation of these antigenic shifts that have lead to influenza pandemics in the past?
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swine
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how often does antigenic shift result in a pandemic?
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in the 20th century about once every 30 years
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what are the most severe antigenic shifts?
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when both H and N glycoproteins change
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what is the H and N makeup of avian influenza?
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H5N1
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what keeps the avian influenza from binding to human nonciliated epithelium?
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its sialic acid has alpha-2,6 linkages rather than the 2,3 linkages for sialic acid in birds
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why can humans still get infected with avian influenza?
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because we do have alpha-2,3 linkages on a small number of sialic acids in our respiratory epithelium
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what is the time frame for an epidemic?
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outbreak confined to s a specific region peak within 2-3 weeks and end withing 6 weeks
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when do influenza outbreaks almost exclusively occure>
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winter months
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what is the primary means of spread of the influenza virus?
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person to person via transfer of respiratory droplets
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what is the incubation period for the influenza virus?
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18-72 hours
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what allows influenza virus to get through mucous to underlying respiratory epithelial cells?
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N glycoprotein cleaves sailic acids of mucin allowing passage through it
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how do cells infected with influenza viruses trigger the innate immune response?
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activate TLR recoptors on macrophages
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describe the damage done to the respiratory epithelium with a severe pneumonia?
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desquamates respiratory epithelium down to one cell layer (basement membrane)making colonization by bacteria much more prevelant
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when does the shedding of viruses peak with an influenza virus infection?
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24-48 hours
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what time frame after infection are viral levels undetectable by?
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5-10 days
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what is the illness caused by infleunza primarily due to?
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cytokine release and local cell damage
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what is the key immune response to removing influenza virus from the body?
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production of cytotoxic T cells (CMI)
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what prevent reinfection with influenza viruses?
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antibodies to H and N glycoproteins
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describe uncomplicated influenza?
1. Incubation 2. Symptoms 3. Resolution Time Frame |
1. 1-4 days incubation
2. high fever/chills, dry cough, extreme malaise for several days 3. ~3 days of symptoms, completely cleared up by 7-10 days |
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describe onset of complicated, primary influenza viral pneumonia?
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rapid progression of
1. fever 2. cough 3. dyspnea 4. cyanosis |
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who is most commonly affected by primary influenza viral pneumonia?
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people with cardiovascular disease, pregnant women, and other chronic disorders
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who are secondary bacterial pneumonias most common in?
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elderly poeple with underlying lung or debilitating disease
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what are the most common secondary bacterial pneumonias?
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1. Strep pneumoniae
2. Haemophilus influenza 3. Staph aureus |