3: Resp ID 1 Handout Flashcards
Most common cause of URIs (general)
Viral
What is noteworthy re: the ideal environment for Rhinovirus replication?
Preferentially replicate at 33C (upper airways), not 37
After rhinovirus, other frequent causes of common cold (6)
parainfluenza, coronavirus, Influenza C, Coxsackie A&B, Adenoviruses
Common cold symptoms (4)
Nasal discharge/ congestion, mild sore throat, cough, afebrile (except kids may be)
Treatment of common cold. How long does it last?
Symptomatic. ~1 week or less, self-limiting.
Etiology of sinusitis
Usually bacterial infec secondary to viral URI
Presentation of sinusitis (3)
fever, purulent nasal discharge, sinus tenderness
2 most common microorganisms in sinusitis
Strep pneumoniae, Haemophilus influenzae -each ~35% of cases
Most common cause of pharyngitis in children <3 and adults
Viral
Most common cause of pharyngitis age 5-15
Strep pyogenes
Pharyngitis presentation (4)
Fever, sore throat, edema, hyperemia of tonsils and pharyngeal walls
What illnesses are collectively called croup?
Acute laryngitis, laryngotracheobronchitis (viral croup), and epiglottitis (bacterial croup)
Why is croup more concerning in young children?
Narrower airway -> obstruction with inflammation is of concern.
Croup usually resolves within ___
about a week
Rhinovirus is most likely to present as ___. How does it spread and attach?
Rhinitis. Spread by contact or aerosol. Binds ICAM-1 of URT epithelial cells
What causes tissue damage/ destruction in rhinitis?
Immune response. Virus itself does not kill its host cells.
What other problems does the immune system create for itself in rhinitis (2)
Local infection -> inc ICAM-1 expression -> facilitates viral spread. Exudate blocks airways, can -> sinusitis or otitis media
Despite downsides of the immune response, the pro is ____
IgA immunity to the serotype down the road!
What effect does parainfluenza virus have on infected cells?
Utilizes fusion (F) surface proteins. Infected cells -> multinucleate giant cells
Clinical presentation of parainfluenza virus
Children: croup and pneumonia. Adults: moderately severe rhinitis
Parainfluenza virus virulence factors allowing establishment of infection
Aerosols. Viral hemagglutinin (HA) envelop proteins interacts w sialic acid on cell surfaces -> endocytosis. Viral neuraminidase env protein cleaves HA-SA bond -> viral spread
How does parainfluenza virus -> clinical presentation of croup
Progress down tracheal and bronchial epithelium -> inflam & swelling of mucus membranes -> narrowing of lumen (insp stridor) and barking cough
How is parainfluenzavirus diagnosed?
Symptoms, possible lab hemaglutination activity in resp secretions + serology for anti-HA antibodies
Treatment of parainfluenza virus
Supportive: cool mist, O2 if severe. Corticosteroids.
Second most common causative agent of rhinitis
Coronavirus (usually indistinguishable from rhinovirus infection)
What is SARS
rapidly progressive viral pneumonia (+fever, dyspnea, cough), can -> resp failure, death
Spread of coronavirus
Inhalation through respiratory aerosols
Timing of coronavirus symptom manifestation
3 day incubation period + 6-7d of cold symptoms
Treatment for coronavirus
Supportive care
Influenza genome
A & B: 8 segments
C: 7 segments
Is influenza A or C more virulent?
A. C often -> asymptomatic infections
With which type(s) of influenza do we not see antigenic shifts? Why?
B & C. No animal reservoir.
What is happening microscopically during the initiation of influenza C infection?
Like parainfluenza: utilizes hemagglutinin (envelope) + sialic acid on host cell surface. NA cleavage -> spread.
Does influenza C kill its host cells? What is the result?
It can -> tissue damage + immune response (IL-1 & IFN-gamma)
Diagnosis of influenza C
Nasopharyngeal swab rapid antigen test. Can culture & detect HA type via RBC agglutination test.
Treatment for influenza C. Is there a vaccine?
Supportive: acetaminophen, hydration, rest. No vaccine available.
Most common infections with Coxsackie A
herpangia (mucosal epithel infec -> red vesicles, fever, sore throat) & hand-foot-and-mouth disease
Most common manifestation of Coxsackie B infection
Pleurodynia, myocarditis (50% of cases), pericarditis
Both Coxsackie A & B can cause ___ (3)
URI. Infection of anterior horn motor neurons or meninges -> aseptic meningitis or paralysis
Typical season for coxsackie virus. Transmission.
Summer and fall. Fecal to oral or aerosol.
Diagnosis of coxsackie virus
Isolate virus, serology
Treatment for coxsackie infection
Supportive. Anti-inflammatory agents for symptomatic infections.
Where is latent adenovirus often found following infection?
Tonsillar adenoids
How is it that adenovirus can be given as a live vaccine without causing infection?
Serotypes have a specific site of infection and assoc disease. Immunize away from favored site.
Possible presentations of adenovirus infection (4)
Resp infec (rhinitis) w ability to progress to atypical pneumonia, conjunctivitis, hemorrhagic cystitis (presents w hematuria and dysuria), gastroenteritis
Virulence factor for adenovirus
Binds to cells utilizing hemagglutinin
Treatment of adenovirus
live virus vaccine of specific serotype - only used in military
Possible clinical presentations of strep pyogenes (4)
pharyngitis, impetigo, erysipelas (type of superficial cellulitis w dermal lymphatic involvement), cellulitis
Virulence factors of strep pyogenes and what they do (4)
Streptokinase (plasminogen to plasmin -> fibrinolysis), M protein resists phagocytosis, hayluronidase breaks down CT, DNase
Strep pyogenes releasing toxin can result in (2)
scarlet fever or streptococcus toxic shock syndrome
Treatment of strep pyogenes
Penicillin G (IV or IM)
What antibodies are present in someone who has had a strep pyogenes infection?
anti-streptolysin O
Top 2 causes of bacterial pneumonia in COPD
- nontypeable H flu
2. Moraxella catarrhalis
Moraxella catarrhalis virulence factors (4)
pili for attachment to mucosa, antigenic variation, endotoxin, capsule
Possible clinical presentations of moraxella catarrhalis (3)
Otitis media, sinusitis, pneumonia
Where does Moraxella catarrhalis generally colonize initially?
Nasopharynx, then spread to mucosal surfaces -> endotoxin (OM, sinusitis, pneumonia)
What are the biochemical features of Moraxella Catarrhalis that can aid in diagnosis (4)
Hydrolyzes tributyrin, produces DNase, reduces nitrite and nitrate, no ferm. of sucrose, glucose, maltose, or lactose
Treatment of moraxella catarrhalis
Amoxicillin-Clavulanate, 2 or 3 gen cephalosporins, TMP-SMX
Why is it that only lysogenic corynebacterium diphtheriae cause systemic disease?
Toxin is carried by a phage
Clinical presentation of corynebacterium diphtheriae infection
local -> pseudomembrane + airway obstruction. Systemic -> arrhythmia, myocarditis and polyneuritis - cranial and periph nerve palsy
What is the pseudomembrane of c. diphtheriae composed of? (3)
Bacterial cells, WBCs and necrotic mucosa
What is diphtheria toxin, and what does it do?
AB toxin ADP ribosylates eukaryotic elongation factor-2 (eEF2), inactivating this protein -> no translation
Characteristics of c. diphtheria allowing for identification
Gram + rod, looks like chinese letters under micro, forms black colonies on potassium tellurite
C. diphtheria treatment
Antitoxin, penicillin, or erythromycin.
1 cause of community acquired pneumonia
Strep pneumoniae
Local (2) and systemic (3) infections caused by strep pneumo
Local: lobar pneumonia, OM. Systemic: osteomyelitis, septic arthritis, endocarditis
Why are asplenic individuals at increased risk of strep pneumo infection?
Capsule, unable to clear antibody-coated organisms
What is the Quellung reaction
Combining antibody with organism with specific polysaccharide capsule antigen -> swelling and opaque
What organisms is the Quellung reaction positive for?
Strep pneumo, e. coli, h. flu, klebsiella pneumo, n. meningitides, salmonella
What patient factors might help strep pneumo establish an infection (3)
Viral infection, allergy, or smoking hinder clearance of strep
How can strep pneumo seed infection in meninges?
Pt lacks anti-capsular IgG, allowing invasive strain to enter lung lymphatics -> bloodstream -> meninges
Strep pneumo classification for ID - inc __-hemolytic, catalase, and optochin sensitivity
Gram + diplococci, alpha hemoytic, catalase neg, susceptible to optochin. Quellung +
Treatment of strep pneumo
Penicillin or cephalosporins for most but Vanco for meningitis.
What makes up the pneumovax vaccine?
Capsular polysaccharides
What type of h. flu is encapsulated and which is not? Which c olonize locally vs more invasive?
Hib: encapsulated, more invasive. Non-typeable: no capsule, colonizes locally.
Local clinical presentations of Hib (3)
epiglottitis, OM, pneumonia
Systemic presentations of Hib (3)
Meningitis, septic arthritis, cellulitis
How does Hib evade the immune response? (2)
IgA protease to evade sec IgA, capsule to avoid phagocytosis
How does Hib spread in the body?
Resp droplets -> invades submucosa -> spreads via bloodstream -> CNS, soft tissue, large joints
Hib laboratory identification
Gram neg, requires hemin (X factor) and NAD (V factor) on chocolate agar. Immunofluorescence and + Quellung
Treatment of Hib
3rd gen cephalosporin e.g. ceftriaxone
What may be given to close contacts of Hib infected individuals?
Rifampin for prophylaxis
Common clinical presentation of RSV
Children: bronchiolitis, pneumonia. Adults: rhinitis
Virulence factors of RSV
G surface protein: attachment, F surf prot: fusion of host cells.
Transmission of RSV
hand to hand or aerosol
Pathogenesis of bronchiolitis with RSV
Attaches to bronchiolar epithel w protein G -> lower resp infec -> necrosis and inflamm of bronchioles -> mucus obstrx airway -> bronchiolitis and wheezing
How does RSV cause pneumonia?
Same as bronchiolitis but in alveoli.
Treatment of RSV
Supportive. Albuterol, aerosolized ribavirin
What prevention of RSV is available? Who gets it?
Synagis, a F antigen vaccine. High risk infants: premies, lung or heart disease.
