11/30 Upper/Mid Resp Tract Infections - Malhotra Flashcards
rhinopharyngitis
basics
sx
agents
transmission
pathphys
body response
treatment
common cold
communicable
sx:
- nasal discharge/obstruction, sore throat, malaise, headache/cough
- coryza (infl of mucous membranes in nose)
- minimal fever
- infants: fever, irritability, vomiting, diarrhea
responsible agents:
- RHINOVIRUS
- coronavirus
- parainfluenza virus
- RSV
- influenza, adenovirus
epidemiology:
- 3-8 colds a year NORMAL; 2x in kids
- incubation: 1-5 days
transmission:
- direct contact with virus via secretions
- aerosolization possible
- portal of entry: conjuctiva and nose (incr viral con in nasal secretions)
pathophysiology
- inoculation → epithelial cells on mucosa infected → virus spreads to resp mucosa → damage to respiratory mucosa by direct inf and chemical mediators
- submucosal edema
- mucociliary transport impairment
- poss bacterial superinfection
body’s response
- local interferon production
- secretory IgA (lines mucosa) and serum antibody (IgG, IgM) response
treatment
- symptomatic tx
- antihistamines with NSAIDS
- VitC (modest tx effect, no provent benefit for prevention)
-
for infants/children: relief of nasal obstruction is important! (saline nasal drops, nasal aspiration)
- why? nose breathers! bottle in mouth means youll cut them off
tonsillopharyngitis
basics
sx
agents
transmission
pathphys
body response
treatment
inflammatory illness of mucous membranes of throat
NO NASAL INVOLVEMENT
sx:
- nasal discharge/obstruction, sore throat, malaise, headache/cough
- coryza (infl of mucous membranes in nose)
- minimal fever
- infants: fever, irritability, vomiting, diarrhea
responsible agents: viral and bacterial
- bacterial: Group A beta-hemolytic streptococcus
- cause of 15-30% pharyngitis (50% in young children)
- severe complications if untreated
- viral: adenovirus, influenza, parainfluenza, EBV, enterovirus, cold viruses
- other: Chlamydia pneumonia, Mycoplasma, anaerobes
epidemiology:
- wintertime
- Group A strep more common in cold
- wintertime resp viruses: influenza, coronavirus
- enteroviruses in summer
transmission:
- direct contact (hands)
- airborne dissemination w/ some
- family members pass it to each other, esp when congregated (ex. holidays)
pathophysiology
-
inoculation → epithelial cells on mucosa infected → virus spreads to resp mucosa → damage to respiratory mucosa by direct inf and chemical mediators
- submucosal edema
- mucociliary transport impairment
- poss bacterial superinfection
body’s response
- local interferon production
- secretory IgA (lines mucosa) and serum antibody (IgG, IgM) response
treatment
- symptomatic tx
- antihistamines with NSAIDS
- VitC (modest tx effect, no provent benefit for prevention)
-
for infants/children: relief of nasal obstruction is important! (saline nasal drops, nasal aspiration)
- why? nose breathers! bottle in mouth means youll cut them off
Group A beta-hemolytic streptococcus
humans are ONLY hosts
disease of school-age children
pharyngeal colonization in asymptomatic individuals
pathogenesis
- person-to-person transmission
- organisms attach to resp epithelial cells via fimbriae → release toxins/enzymes
- tissue damage, which facilitates rapid spread of org
- hypersensitivity to eythrogenic toxins → rashes, fever
- presentation of reinfection? type-specific antibody against M-specific protein
clinical features
- short incubation period: 2-5d
- presents anywhere from subclinical to highly toxic
- sx: fever, sore throat, headache, abd pain
- pharyngeal infl with edema and tonsillar exudate
- swollen/tender anterior cervical nodes (bc these are the ones that drain the tonsils!)
-
scarlet fever : red, finely punctuate rash (“sandpaper rash”) due to erythrogenic toxin produced by certain strains of S. pyogenes
- red strawberry tongue, conjunctival injection
treatment
- antibiotics: penicillin
- tonsillectomy in some cases
complications
- suppurative
- peritonsillar/retropharyngeal abcesses
- cervical adenitis
- otitis
- sinusitis
- non-suppurative
- acute rheumatic fever (ARF)
- acute post-streptococcal glomerulonephritis (APSGN)
tonsillopharyngitis
Acute Rheumatic Fever
inflammatory disease of heart, joints, CNS, and subcutaneous tissues following untreated stretococcal infection (JONES criteria)
autoimmune process with antibodies and cellular immune response against cardiac antigens which are similar to streptococcal antigens (M protein)
croup:
laryngotracheitis/laryngotracheobronchitis
respiratory illness characterized by hoarse voice, dry ‘barking’ cough, inspiratory stridor and variable amt of respiratory distress resulting from upper airway obstruction
what is the upper airway?
infraglottic tissues, larynx, trachea, +/- lungs
etiologic agents
- most commonly VIRAL
- parainfluenza 1 (most common), other parainfluenzas
- influenza
- RSV
- adenovirus
- rhinovirus
- bacteria: staphylococcus, streptococcus, C. diphtheriae
- atypicals: Mycoplasma
epidemiology
- 15% of LRT disease in peds (6mo-5y, with highest rate in 7-36mo)
- late fall/eary winter illness
- boys > girls
- transmitted by close contact, droplet nuclei, hand contact
pathophysiology
- inf in nasopharynx → travels to resp epi of larynx/trachea/beyond
- difuse tracheal infl with erythema and edema → airway narrowing, inhibition of ciliary fx, tracheal epithelial cell destruction
- obstruction of tracheal lumen
- impairment of vocal cords
- histo shows: marked edema and cellular inflictration with histiocytes, lymphocytes, plasma cells, PMNs
clinical features
- URI sx, low grade fever
- barking cough (“seal bark”), hoarseness and insp stridor indicating upper airway obstruction
- incr resp distress
- asphyxial death might follow
diagnosis
- clinical dx based on signs/sx
- imaging: lateral neck xray (looking for narrowed airway = “steeple sign”)
- consider foreign body aspiration in ddx
treatment
- mist therapy
- hydration
- oxygen postetially useful
- steroids
- racemic epinephrine in severe cases
- ANTIBODIES RARELY USED (bc usually viral)
sinusitis
purulent infection of mucosal linigs of one or more of paranasal sinuses
- acute vs chronic
- usually followed URI
etiology
- bacterial (Haemophilus sp, Pneumococcus, mixed inf)
- viral (rhinovirus, influeza, parainfluenza)
- fungal
- allergic
clinical presentation
- fever, cough, rhinorrhea, facial pain/pressure, headache, nasal obst
- posterior pharyngeal pus (dropping from sinuses)
- purulent nasal discharge
- sinus tenderness
- facial swelling (Potts puffy tumor = pus collection under periosteum of frontal bone)
diagnosis
- history, exam
- bloodwork: CBC, ESR
- transillumination of sinuses
- radiological imaging: CT scan looking at air/fluid levels
complications
- intracranial: meningitis, brain abcess (epidural, subdural), cavernous sinus/cortical vein thrombosis
- orbital: esp in kids, cellulitis/abcess, subperiosteal abcess
- respiratory: sinopulmonary disease (esp chronic cases)
treatment
- antibiotic tx
- beta lactams
- TMP/SMZ
- quinolones
- severe disease: hospital admit, IV antibiotics (cefuroxime, ceftriaxone)
- consider vancomycin for resistant strains
- surgical intervention
influenza
acute respiratory infection caused by orthomyxoviridae
ssRNA virus
-
RNA genome surrounded by nucleocapsid (protein) surrounded by matrix (protein) with two glycoprotein structures radiating out from matrix surface
- hemagglutinin (HA)
- neuraminidase (N)
3 major antigenic types:
- influenza A
- infects humans/mammals
- infects birds (avian flu)
- influenza B
- humans only
- influenza C
- infects humans and swine
each type has mutiple antigenic subtypes
transmission
- droplet spread with inhalatino of large airborne particles
- incubation pd: 1-7d (avg 2-3d)
- max viral shedding = most severe illness
epidemiology
- outbreaks can happen on local, national, global level
- marked seasonality: exclusive wintertime activity
- type A assoc with most severe and widespread disease
pathogenesis/immunity
- affects resp epithelium (larynx, trachea, bronchi)
- major site of inf: ciliated columnar epithelial cells
- cell necrosis seen early → local edema and cell inflitration follow
- infection of peripheral blood mononuclear cells: PMNs/lymphocytes/monocytes fx impaired, which then contributes to overall pathogenicity
- repair begins in 3-5d with systemic/mucosal/cellular immune responses
- pre-existing antibody req for protection
clinical presentation (look at slides)
diagnosis
- clinical dx
- rapid antigen testing: DFA or IFA with rapid turnaround time
treatment
- supportive
- avoid aspirin in children (bc viral)
- antivirals are available
- neuraminidase inhibitors (zanamivir, oseltamivir)
complications
- bacterial secondary inf (pneumonia - Staph aureus, H influenza, S pneumoniae; otitis media, sinusitis)
- acute myositis
- Reye’s syndrome
influenza prevention: vaccines, chemoprophylaxis (neuraminidase inhibitors)f
influenza glycoprotein structures
- hemagglutinin (HA)
- required for attachment to cells
- HA inhibiting antibodies neutralize virus capabilty in infect → key index of immunity
- neuraminidase (N)
- required for release of virus from infected cell
- N-antibody correlates with viral shedding/illness severity
*subclassification of influenza A is based on glycoproteins HA and N
- infA has 3 HA proteins and 2 N proteins known to circulate in humans
- variation in HA and N is the basis for antigenic drift and antigenic shift
antigenic drift
antigenic shift
antigenic drift
- minor changes in HA and/or N structures (usually point muts)
- occurs in influenza A, B, C
antigenic shift
- extensive changes in HA and/or N structures → new subtypes of influenza A (only)
- new subtype = no immunity to it = phenomenon responsible for PANDEMICS
