Clinical correlations #4

Med Micro 2008

Upper Respiratory Tract Infections

Divya Ahuja, M.D.

November 2008
 Burden of URI
 Significant morbidity and
direct health care costs
 Direct costs of $ 17
billion annually
 Occasionally leads to
fatal illness
 Excessive use of
antibiotics a major issue
 The Common Cold
■ Children average 8 per year, adults 3
■ Parainfluenza isolated in 1955
■ Rhinoviruses 30 to 35%; coronaviruses about 10%,
miscellaneous known viruses about 20%, presumed
undiscovered viruses up to 35%, group A streptococci 5% to
10%
■ Seasonal variation
– Rhinovirus early fall
– Coronavirus- winter
■ Day cares are culture media
■ Sinusitis often present by CT scan; “rhinosinusitis” might be a
better term
■ Common symptoms are sore throat, runny nose,
nasal congestion, sneezing,
■ Sometimes accompanied by conjunctivitis,
myalgias, fatigue
The common cold
 Transmission of rhinoviruses
■ Direct contact is the most efficient means of
transmission: 40% to 90% recovery from
hands.
■ Infectious droplet nuclei
■ Brief exposure (e.g., handshake) transmits in
less than 10% of instances
■ Kissing does not seem to be a common mode
of transmission.
 Clinical characteristics
■ Incubation period 12-72 hours
■ Nasal obstruction, drainage, sneezing,
scratchy throat
■ Median duration 1 week but 25% can last 2
weeks
■ Pharyngeal erhema is commoner with
adenovirus
 Diagnosis and treatment
■ Main challenge is to distinguish between uncomplicated
cold and streptococcal pharyngitis or bacterial sinusitis
– Good examination
■ Marked exudate suggests
– Streptococcal infection
– Adenovirus
– Diphtheria
■ Rapid antigen tests for group A streptococcus
■ Rapid techniques for influenza, RSV, parainfluenza
■ Treat with NSAIDs and whatever else your grandmother
advises
 Acute bacterial sinusitis
■ Viral infection--> obstruction of ducts and compromise
of mucocilary blanket--> acute infection from virulent
organisms (most often S. pneumoniae and H.
influenzae)--> opportunistic pathogens
■ Nose blowing generates high intranasal pressures that
deposit bacteria into the sinus cavity
■ Complicates 0.5% of common URI
■ More common in adults than in children
Paranasal sinuses
Waters view (left); Coronal CT
 Acute sinusitis: complications
■ Maxillary: usually uncomplicated
■ Ethmoid: cavernous sinus thrombosis
(40% mortality)
■ Frontal: osteomyelitis of frontal bone;
cavernous sinus thrombosis; epidural,
subdural, or intracerebral abscess;
orbital extension
Acute sinusitis: complications (2)
 Sphenoid: Rare, but usually misdiagnosed,
with grave consequences; extension to internal
carotid artery, cavernous sinuses, pituitary,
optic nerves; common misdiagnoses include
ophthalmic migraine, aseptic meningitis,
trigeminal neuralgia, cavernous sinus
thrombosis
 Case
■ BR 59 year old white female
■ Diplopia and left temporal headache
■ Thought to have temporal arteritis
■ Started on Prednisone 100mg once daily
■ Noted to have 6th nerve palsy
■ MRI 9/03 normal
 Case
■ Persistent headaches
■ CT 10/03 normal, ESR 12 (on steroids)
■ Repeat MRI 3/04 showed (2.3/1.5cm) mass in the left
orbital apex involving the sinus
■ Developed left Ptosis, left fixed dilated pupil and left
2nd to 6th nerve palsies
■ CT head showed 1.5/2 cm hypo dense mass in the left
basal ganglia
 Chronic sinusitis
 Bacterial: Cultures show a variety of
opportunistic pathogens including
anaerobes but problem is mainly anatomic,
not microbiologic
 Fungal: suspect especially when a single
sinus is involved; syndromes associated
with nasal polyposis can have high
morbidity
 Spectrum of fungal sinusitis
 Simple colonization
 Sinus mycetoma (fungus
ball)
 Allergic fungal sinusitis
 Acute (fulminant) invasive
sinusitis (notably,
rhinocerebral mucormycosis)
 Chronic invasive fungal
sinusitis
 Otitis externa
 Acute, localized: often S. aureus or
S. pyogenes
 Acute diffuse (swimmer’s ear):
gram-negative rods, especially Ps.
aeruginosa
 Chronic: mainly with chronic otitis
media
 Malignant: life-threatening
infection in diabetics; Pseudomonas
aeruginosa
 Malignant otitis externa
 Diabetes mellitus
 Pseudomonas
aeruginosa
 Osteomyelitis of
the temporal bone
 Involvement of
vital structures at
base of brain
 Acute otitis media
■ S. pneumoniae and H. influenzae the
leading causes in all age groups
■ Moraxella catarrhalis: ? emerging role
■ Some case may be viral (RSV, influenza,
enteroviruses)
■ Mycoplasma pneumoniae: inflammation of
the tympanic membrane (“bullous
myringitis”)
 Acute otitis media
 Critical role of
eustachian tube as
conduit between
nasopharynx, middle
ear, and mastoid air
cells
 Children have shorter,
wider eustachian tubes
than adults
 Diagnosis and treatment
■ Presence of fluid in the middle ear AND
■ Ear pain, drainage, hearing loss
■ The fluid may take weeks to resolve
■ Amoxicillin remains the drug of choice
■ Beta-lactamase producing strains of H.
influenza will need amoxicillin/clavulanic
acid or cephalosporins
Chronic otitis media and mastoiditis
■ Prolonged middle ear effusions in
patients with previous episodes of
acute otitis media. Often “skin flora” or
anaerobic organisms
■ Mastoiditis: Less common nowadays.
formerly severe complications. Often
anaerobic.
 Acute pharyngitis
■ Most cases are viral
■ Most important bacterial cause is
Streptococcus pyogenes (15-20%)
■ Presents with sore or scratchy throat
■ In severe bacterial cases there may be
odynophagia, fever, headache
Acute pharyngitis: physical exam
■ Viral:edema and hyperemia of tonsils
and pharyngeal mucosa
■ Streptococcal: exudate and hemorrhage
involving tonsils and pharyngeal walls
■ Epstein-Barr virus (infectious mono):
may also cause exudate, with
nasopharyngeal lymphoid hyperplasia
 Pharyngoconjuntival fever
■ Adenoviral pharyngitis
■ Pharyngeal erythema and exudate may
mimic streptococcal pharyngitis
■ Conjunctivitis (follicular) present in
1/3 to 1/2 of cases; commonly
unilateral but bilateral in 1/4 of cases
 Vesicular lesions
■ Herpangina
– Uncommon
– Due to coxsackieviruss
– Small, 1-2 mm vesicles on the soft palate,
uvula, and anterior tonsillar pillars which
rupture to form small white ulcers
– Occurs mainly in children
■ Herpes simplex virus
 Vincent’s angina and Quinsy
■ Vincent’s angina: anaerobic pharyngitis
(exudate; foul odor to breath)
■ Ludwig’s angina- cellulitis of dental origin
■ Quinsy: peritonsillitis/peritonsillar abscess.
Medial displacement of the tonsil; often
spread of infection to carotid sheath
■Diphtheria
■fibrous pseudomembrane with necrotic epithelium and leukocytes
 Diphtheria
■ Classic diphtheria (Corynebacterium
diphtheriae): slow onset, then marked toxicity
■ Arcanobacterium hemolyticum (formerly
Cornyebacterium hemolyticum): exudative
pharyngitis in adolescents and young adults
with diffuse, sometimes pruritic maculopapular
rash on trunk and extremities
Miscellaneous causes of pharyngitis
■ Primary HIV infection
■ Gonococcal infection
■ Diphtheria
■ Yersinia entercolitica (can have
fulminant course)
■ Mycoplasma pneumoniae
■ Chlamydia pneumoniae
 Treatment
■ Symptomatic
■ Penicillin for Strep throat
■ Macrolides for pen allergic patients
■ Add an antianaerobic agent for Vincent’s
and Ludwig’s angina
Acute laryngotracheobronchitis (croup)
■ Children, most often in 2nd year
■ Parainfluenza virus type 1 most often in U.S.A. but other
agents are Mycoplasma pneumoniae, H. influenza
■ Involvement of larynx and trachea: stridor, hoarseness,
cough
■ Subglottic involvement: high-pitched vibratory sounds
■ Can lead to respiratory failure (2% get hospitalized)
 Croup
■ Rhinorrhea, sore throat, mild cough, fever
■ Parainfluenzae and influenza can be identified by
nasopharyngeal swab
■ Rapid tests are available
■ Treat with vaporizers, nebulized adrenaline
■ Systemic or nebulized corticosteroids in the severely
sick
 Acute epiglottitis
 A life-threatening
cellulitis of the epiglottis
and adjacent structures
 Onset usually sudden (as
opposed to gradual onset
of croup); drooling,
dysphagia, sore throat
 H. influenzae the usual
pathogen both in children
(the usual patients) and
adults
 Acute suppurative
parotitis
■ Uncommon, but high
morbidity and mortality
■ Usually associated with
some combination of
dehydration, old age,
malnutrition, and/or
postoperative state
■ S. aureus the usual
pathogen
Deep fascial space infections of
the head and neck
■ Several syndromes according to anatomic
planes
■ Can complicate odontogenic or
oropharyngeal infection
■ Ludwig’s angina: bilateral involvement of
submandibular and sublingual spaces
(brawny cellulitis at floor of mouth)
 Deep fascial space infections of
the head and neck (2)
■ Lemierre syndrome: suppurative thrombophlebitis
of internal jugular vein (Fusobacterium
necrophorum)
■ Retropharyngeal space infection: contiguous
spread from lateral pharyngeal space or infected
retropharyngeal lymph node; complications
include rupture into airway, septic thrombosis of
internal jugular vein
 Severe acute respiratory
distress syndrome (SARS)
■ Caused by a previously unrecognized
coronavirus—genome has now been
sequenced.
■ Clinical manifestations are similar to
those of other acute respiratory
illnesses—notably, influenza
■ Cases in U.S.—associated mainly
with travel or as secondary contacts
 SARS: CDC case definition (2003)
■ Respiratory illness of unknown etiology AND
■ Measured temperature > 100.4 degrees F (38
degrees C) AND
■ One or more clinical findings of respiratory illness
AND
■ Travel within 10 days of onset of symptoms to an
area with documented or suspected cases OR close
contact with a case
 SARS: Case definition (2)
■ Clinical findings of respiratory illness:
cough, SOB, dyspnea, hypoxia, or
radiographic findings of either pneumonia
or ARDS
■ Travel includes certain areas (mainland
China, Hong Kong, Hanoi, Singapore) and
also airports with documented or suspected
community transmission
 SARS: Radiographic findings
■ Early: a peripheral/pleural-based
opacity (ground-glass or
consolidative) may be the only
abnormality. Look especially at
retrocardiac area.
■ Advanced: widespread
opacification (ground-glass or
consolidative) tending to affect the
lower zones and often bilateral.
■ Pleural effusions,
lymphadenopathy, and cavitation
are not seen.
Dr. Carlo Urbani (1956-2003)
■ 2/28/03: Recognized
SARS while examining a
patient in Hanoi.
■ Identified outbreak and
raises the alarm.
■ Stayed caring patients
despite multiple illnesses
in staff—sent wife and
three children back to Italy
■ 3/29/03: Died of SARS