L24-25: Upper Respiratory Tract Infections Flashcards
What does the upper respiratory tract consist of?
Conjuctiva, nose, larynx, nasolacrimal ducts, pharynx, epiglottis, middle ear, sinuses and nasal cavity
Where do particles of different size end up?
5-10 um: nasal turbinates, mucus
2-10 um: trachea
0.3-1 um: terminal airway and alveoli
<0.3 um: stay suspended in air
What are most respiratory system membranes composed of?
Ciliated epithelium (creates mucocililary escalator)
Which URT tissues are considered sterile?
Mastoid air cells, middle ear, sinuses, trachea, bronchi, bronchioles, and alveoli (conjuctiva normally)
Normal flora of nose
Staphylococcus epidermidis and Staphylococcus aureus (G+ cocci facultative anaerobes), Corynebacterium spp (G+ rod pleomorphic and non-spore forming)
Normal flora of the nasopharynx
Streptococcus (Viridans – S. mutans, S. mitis, S. milleri, S. salivarius), Moraxella catarrhalis (G- coccus aerobic), Bacteroides
Nasopharynx pathogens common in normal flora in cooler months
Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningtitides
Group A Strep pathogens
S. pyogenes (beta)
Group B Strep pathogens
S. agalactiae (beta)
Group D Strep (and other) pathogens
S. bovis (not hemolytic) and Enterococcus faecalis
a-hemolytic Strep pathogen
S. pneumoniae
What diseases do S. pyogenes cause?
Streptococcal pharyngitis, scarlet fever, acute rheumatic fever, streptococcal toxic shock syndrome (STSS)
What disease can occur post-streptococcal infection?
Acute glomerulonephritis (due to deposition of antigen-antibody complexes in glomeruli) – causes edema, hypertension, hematuria, proteinuria, decreased serum complement levels
Characteristics of S. pyogenes
Gram+, grows in chains, B-hemolytic, group A Strep (A antigen in cell wall differs antigenically from other Streps to identify easily)
S. pyogenes virulence factors
M protein, F protein, capsule, SPEs, streptolysin O, streptokinase, C5a peptidase
M protein
Antiphagocytic, essential for virulence (80 serotypes that are not cross protective, which is why we don’t vaccinate)
Capsule
Not in all strains, inhibits phagocytosis and aids in adherence to epithelial cells
Streptococcal pyrogenic exotoxins
Nine different super antigens (SPE-A, SPE-B, etc.) that cause scarlet fever (only one preceded by strep throat symptoms), toxic shock, and necrotizing fasciitis, along with fever, rash, T-cell proliferation and B-cell suppression
How do we treat streptococcal pharyngitis?
Most cases recover spontaneously in 7 days but confirmed cases should be treated with 10 days of penicillin or erythromycin to prevent the progression to worse diseases
How does scarlet fever occur?
SPE release causes redness of skin and a white coating on the tongue
How does acute rheumatic fever occur?
Acute inflammatory process (strong immune response) causes fever, joint pain, chest pain, rash, skin nodules, and uncontrollable jerky movements due to neurotoxicity – can be fatal – immune response kills the organism but starts attacking the body’s tissues
Important difference between scarlet fever and rheumatic fever/acute glomerulonephritis
Scarlet fever releases a toxin to damage the tissues, so once the bacteria is gone, there is no more damage being done; rheumatic fever and acute glomerulonephritis damage our bodies by the response of the immune system, therefore the microbe needs to be kicked out as soon as possible so that the immune response stops or it could be fatal (and it also keeps a memory so future infections pose a dangerous risk)
How does necrotizing fasciitis occur?
SPE release, skin infections (caused by S. pyogenes infection somewhere else)
What organism causes diphtheria?
Corynebacterium diphtheriae
Characteristics of Corynebacterium diphtheriae
Gram+ rod, non-motile, non-spore forming, looks like Chinese letters under the microscope, causes disease with toxin
Pathogenesis of diphtheria
Not an invasive bacteria – instead toxin is absorbed by bloodstream; causes gray-white membrane made up of clotted blood, epithelial cells of mucus membrane, and leukocyte infiltrate (uvula is key); severe neck swelling
Diphtheria toxin
Powerful exotoxin that is inactive when released (true enzyme); has A and B subunit; causes disease only when strain has been lysogenized by bacteriophage
A (active) subunit of diphtheria
Causes inactivation of elongation factor 2 (EF-2) to stop protein synthesis and induce cell death
B (binding) subunit of diphtheria
Binds to host receptor (severe damage is done to heart, kidneys, and nerve cells, so this is where the B subunit receptors are)
Process of infection by A-B toxins
B portion is endocytosed, A is cleaved, stops protein synthesis and kills the cell
Causative agents of conjunctivitis
Haemophilus influenzae (Gram- rod), Streptococcus pneumoniae – also Moraxella lacunata, enterobacteria, N. gonorrhoeae
How can you distinguish bacterial conjunctivitis from viral?
Bacterial infections often have more pus and discharge
Prevention of conjunctivitis
Must remove from public, wash hands frequently, keep from rubbing eyes and using common towels
Treatment of conjunctivitis
Gentamicin or ciprofloxacin eye drops – some strains may be resistant and sometimes certain treatments work better in certain regions
Causative agents of otitis media/sinusitis
Haemophilus influenzae and Streptococcus pneumoniae – also Moraxella catarrhalis (same as conjunctivitis)
What pathogen has decreased in incidence since a vaccine was begun in the early 90’s?
Haemophilus influenzae type b
Difference between alpha and beta hemolysis
Beta hemolysis is complete lysis of the blood cell while alpha is incomplete and looks green on plate
Characteristics of Streptococcus pneumoniae
Exists as normal flora but in some cases can cause paranasal sinusitis, otitis media, lobar pneumonia, and meningitis
Branches of the Chlamydiaceae family
Chlamydia genus = Chlamydia trachomatis; Chlamydophila genus = Chlamydia psittaci, Chlamydia pneumoniae
Characteristics of Chlamydophila
Very small, obligate intracellular parasitic bacteria
Elementary bodies (EB)
Metabolically inactive but infectious forms of Chlamydia
Reticulate bodies (RB)
Metabolically active noninfectious forms of Chlamydia
Diseases caused by Chlamydia trachomatis
Trachoma, adult inclusion conjunctivitis, neonatal conjunctivitis, infant pneumonia
Pathogenesis of Chlamydia trachomatis
Directly destroys host cells during replication and solicits a host inflammatory response that causes damage; organisms gain access to the cells by minute abrasions or lacerations and cause granuloma formation; immunity is not complete – severity varies
How can Chlamydia trachomatis cause blindness?
Follicular conjunctivitis –> conjunctiva scarring –> eyelids turn inward –> abrasions to the cornea
Adult inclusion conjunctivitis (Chlamydia)
Acute follicular conjunctivitis caused by same serovar associated with genital infections; cause mucopurulent discharge, keratitis, corneal infiltrates and some vascularization
Neonatal conjunctivitis (Chlamydia)
Same serovar as genital infection occurring in infants exposed at birth; 5-12 days after birth and can last 12 months; cause conjunctival scarring and corneal vascularization
Infant pneumonia (Chlamydia)
Onset 2-3 weeks after birth, bronchitis with dry cough, afebrile
Chlamydophila pneumoniae
TWAR pathogen (Taiwan acute respiratory agent); causes pneumonia, bronchitis, and sinusitis; most severe infections involve only one lung lobe
Chlamydophila psittaci
Causes psittacosis, an infection by respiratory tract, due to bacteria spread to reticuloendothelial cells in the liver and the spleen and multiply there to produce focal necrosis – comes from birds (parrots) – treated with macrolides
