Step Children 0-4 Children 5-11 All 12 years or older

Step 1 Short Acting β-agonist Short Acting β-agonist Short Acting β-agonist
Low dose ICS Low dose ICS Low dose ICS
Step 2 or or or
Cromolyn Cromolyn, LTRA, Nedo, Theo Cromolyn, LTRA, Nedo, Theo
Low dose ICS Low Dose ICS + LAβA
Step 3 Medium dose ICS and or
LAβA, LTRA, or Theo Medium dose ICS
Medium dose ICS Medium dose ICS Medium dose ICS
Step 4 and and and
LAβA or Montelukast LAβA LAβA
High dose ICS High dose ICS High dose ICS
Step 5 and and and
LAβA or Montelukast LAβA LAβA
High dose ICS High dose ICS
High dose ICS
and and
and
Oral CS Oral CS
Step 6 LAβA or Montelukast
and and
LAβA LAβA
Consider Oral Systemic CS

Most likely diagnosis? Asthma

How would you work this up?
PFTs, bronchodilators, give him a spirometer and use bronchodilator at home to see if helped
Greater than 12% = asthma
Less than 12% - repeat in 4-6 weeks after course of oral or ICS
Better – likely asthma
No improvement – likely COPD (or CHF if old and fluid filled)
Current treatment for primary episode – SABA
Long term approach – define a treatment regimen that decreases his episodes

Streptococcus – gram + cocci in pairs or chains (not seen on sputum culture), all are CATALASE NEGATIVE
  S. pneumo – alpha hemolytics, optochin sensitive, bile soluble (RUSTY SPUTUM & MOPS)
o Lancet shape, encapsulated, Most OPtochin Sensitive, Meningitis, Otitis media, Pneum, Sinusitis
o Rusty sputum Dx: Gram stain sputum sample, Quellung reaction to detect polysaccharide capsule
o Virulence factors: colonizes oropharynx (adhesins bind epi), spread to LRT (secretory IgA protease, pneumolysin,
neuramindase), antiphagocytic mechanisms (CAPSULE)
 S. pyogenes – beta hemolytic, bacitracin sensitive, Group A, long chains
o Disease: localized suppurative dz (Strep throat, skin infxn), toxin mediated dz (scarlet fever, TSS), nonsuppurative
AI dz (RF, acute glomerulonephritis)
o Virulence factors: capsule, M protein, C5a peptidase, lipoteichoic acid and F protein (bind fibronectin), M and F
proteins mediate invasion, toxins (exotoxin, streptolysin S and O, streptokinase A and B, 4 DNases)
o Dx: antigen detection Tx: PCN, cephalosporins, ampicillin/amoxicillin, vancomycin
 S. agalactiae – beta-hemolytic, bacitracin resistant, Group B, cause pneumonia/bacteremia/meningitis
o Early onset (first wk d/t infected mom)– types 1a, 3 & 5 Late onset (exogenous source)– type 3
Adult (prego)– Types 1a & 5
o Virulence factors: Polysaccharide capsule Tx: PCN, ampicillin, vancomycin
Haemophilus influenza – small gram-negative rods
 Epi: Serotyping by capsule, types a-f (typeable), non-typeable (no capsule), 90% Hib Disease: epiglottitis,
pneumoniae, meningitis
 Virulence factors: difficult to grow (chocolate agar w/ factors X and V), capsule, endotoxin (induce inflame), pili & IgA
protease
 Prevention = vaccine (type b capsule conjugated to tetanus or diphtheria toxoid or meningococcal protein  increases
immunogenicity)
Mycoplasma pneumoniae
 Disease: Cause atypical (walking) pneumonia Epi: only humans affected Dx by antigen spec IgM
 Virulence factors: no cell wall, P1 adhesin, superantigen activity w/ massive release of TNF-alpha, IL-1 & IL-6
o Can trigger AI hemolytic anemia when pt is exposed to cold  mediated by “cold agglutinins”
Mycobacterium (M. tuberculosis & M. avium)
 Dx: PPD, gram stain sputum (acid-fast)
 GRANULOMAS, acid fast b/c lipid rich cell wall, survive in pulm macs (cord factor prevents phagolysosome fusion), CMI
Pseudomonas aeruginosa
 Gram – rod, pairs, flagellated, oxidase +, non-lactose fermenter, produce dyes, capsule  mucoid appearance
 Cause cystic fibrosis & VAP major cause of nosocomial infections
 Virulence factor: pili, capsule, biofilm formation, exotoxin A, Exoenzyme S, antibiotic resistance
Klebsiella pneumoniae – red currant jelly sputum
 Gram – rod, fast lactose fermenter, pink colonies on MacConkey agar
 Virulence factors: anti-phagocytic capsule, blood tinged sputum, ^ drug resistance, necrotic destruction of alveolar spaces
Bordetella pertussis – whooping cough = BIG INHALATION
 Very small gram-neg coccobacillus, non-motile, oxidase positive
 Prevention: vaccine DTP & DTaP (pertactin, pertussis toxin) Tx: macrolides (erythromycin)
 Virulence factors: pertactin & filamentous hemagglutinin, pertussis toxin (AB toxin)  permanently inactivates inhibitor Gi
protein = inc cAMP elevating respiratory secretions/mucus, adenylate cyclase toxin, tracheal toxin
Staphylococcus – gram + cocci growing in clusters, catalase +, S. aureus coagulase + but staph coagulase neg
 Virulence factors: capsule, protein A (binds ab to Fc to inhibit C’ fixation/opsonization/ADCC), coagulase, teichoic acid
(adhesion), clumping factor
Legionella pneumophilia **VS PSEUDOMONAS that likes to grow on all agars!  this doesn’t = very specific shape/plate
 Gram – slender rods, stain w/ silver on Buffered Charcoal Yeast Extract agar (require iron/cysteine), intracellular infection,
bacterial porin protein
 Inhalation of infected water aerosols (no human-human transmission)
Chlamydophilia psittaci
 Intracellular organism transmitted from birds
Nocardia
 Avoid intracellular killing due to expression of cord factor (mycolic acid) prevents fusion of phagosome

Lecture 12: Infectious Agents of Respiratory Tract II (M. THOMAS/JOHNSON)

Rhinovirus - Picornaviridae – positive sense ssRNA, naked
  Virulence factors: troposim determined by viral polypeptides VP 1-4  >100 serotypes, ICAM-1 (host receptor), restricted
virus growth >33 degrees C (so mostly URT)
Coronavirus – positive sense ssRNA, enveloped
 Surface glycoproteins = crown like appearance, viral spike (S or E2) protein
 Disease: SARS & MERS (URT can progress to LRT bc have different proteins) along w/ conventional coronavirus
Adenovirus –dsDNA, non-enveloped
 Virulence factors: fiber proteins binds to CAR receptor, many serotypes
 Epi: different serotypes cause different disease (resp, GI, conjunctivitis), aerosol & fecal oral transmission, resistance to
detergents (chlorine in pools)
Measles or Rubeola- Koplik spots, exanthema w/ CCC & P
 Paramyxoviridae – negative sense ssRNA genome, enveloped
 Attachment protein (hemagglutinin that binds sialic acid on target cell), fusion protein (binds CD46 and CD150), pneumonia
is complication of infection, giant cell pneumoniae w/out rash
 Prevention: MMR (live attenuated vaccine)
Mumps – paramyxoviridae –negative sense ssRNA genome, enveloped
 Hemagglutinin (H) & Fusion (F) protein, viremia in parotid glands, principal sx = parotid gland swelling
Parainfluenza virus - paramyxoviridae –negative sense ssRNA genome, enveloped
 Bark like a seal  croup  inflammation of epiglottis and trachea
 Hemagglutinin neuraminidase (HN) protein & fusion (F) protein Steeple sign on imaging
Respiratory Syncytial Virus (RSV) – paramyxoviridae  negative sense ssRNA, enveloped
 Fusion protein F mediates virus to host cell, lacks hemagglutinin and neuraminidase activity
 Epi: peak age of hospitalization 2-3 mos, significant m&m in elderly
 Disease: primarily causes URT infection  severe = bronchiolitis, assoc w/ development of childhood asthma, predisposes
for 2ndry pneum and otitis media
 Virulence factors: age of infection, syncytia formation (escapes Ab), impairs ciliary beat
 Prevention: Synagis (at-risk pts)
Influenza Virus 1 – Orthomyxoviridae – negative sense ssRNA genome w/ 8 segments, enveloped
 Genome is replicated in cell nucleus
 Virulence factors: Hemagglutinin (HA), Neuraminidase (NA), M2 protein
 Ab responses are strain specific
 Disease: predisposes to 2nd bac infection, type I IFNs control spread but cause flu-like sx
 Tx: NA (influenza A/B) & M2 (A) are targets for drugs
 Genetic drift (point mutations) vs genetic shift (A)  segmented genome, HA protein binds different sialic acid residues
 Influenza A – zoonosis, not influenza B or C
Hanta virus – Bunyaviridae – negative sense ssRNA segmented genome, enveloped
 Infection by contact w/ rodents & excreta cause HPS (hantavirus pulm syndrome) & HHF (hantavirus hemorrhagic fever)

FUNGI
Pneumocystis jiroveci (carinii)
 Cup shaped organism, “flying saucer”, virulence factor = cyst formation, common in AIDS pts
 Dx: ground glass appearance on X-ray, Gomori silver stained tissue
Aspergillus fumigatus “BLACK MOLD”
 Filamentous mold w/ septated & branched hyphae
 Virulence factors: spore formation, opportunistic growth in pre-existing lung cavity, tissue invasion (immunocompromised)
 Disease: fungus ball, hypersensitivity pneumonitis
Histoplasma capsulatum – “spaghetti and meatballs appearance”
 Virulence factors: intracellular survival (inside macs), granulomas Epi: Midwestern USA, bird & bat droppings
Coccidiodes immitis – box chains, endospore-containing
 Epi: Desert areas of Southwestern USA (San Joaquin Valley fever) Dz: self-limiting flu-like illness
Dx: skin test for Ags (like PPD)
Blastomcyes dermatitidis – Rotting wood & beaver dams
 Dimorphic broad-based buddying yeast (dumbbell shape)
 Epi: Endemic in Midwestern USA (Mississippi River Valley) **no bird or bat droppings
Cryptococcus neoformans –thick capsule
 Virulence factors: Anti-phagocytic capsule, spread via bloodstream
 Epi: Pigeon droppings Dx: india ink Dz: solitary pulmonary nodules (often asx), but commonly
meningitis
 Tx: amphotericin B (amphoterrible)