Clinical Correlations #4 Med Micro 2008: Upper Respiratory Tract Infections

Clinical correlations #4 Med Micro 2008 Upper Respiratory Tract Infections Divya Ahuja, M.D. November 2008

Burden of URI 

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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 ■ ■ ■

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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

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Day cares are culture media Sinusitis often present by CT scan; “rhinosinusitis” might be a better term

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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

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Marked exudate suggests – Streptococcal infection – Adenovirus – Diphtheria

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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 ■

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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 ■ ■ ■

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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 

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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  

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Simple colonization Sinus mycetoma (fungus ball) Allergic fungal sinusitis Acute (fulminant) invasive sinusitis (notably, rhinocerebral mucormycosis) Chronic invasive fungal sinusitis

Otitis externa  

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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  

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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 

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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 ■

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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) ■ ■

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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 

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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) ■

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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 ■

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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) ■

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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