Respiratory Tract Infections 3 Flashcards
Mumps is caused by which viral family
Paramyxoviridae family
Mumps: Biology & Epidemiology
• Paramyxoviridae family • Enveloped ss(-)RNA virion • 2 glycoproteins • HN – mediates hemagglutination and neuraminidase activity • F – fusion to the host cell • One serotype, endemic worldwide
Mumps transmission
Aerosol transmission
- Infections are often asymptomatic/subclinical
- Outbreaks are associated with crowded conditions (colleges, community gatherings, etc…)
- Rising number of cases in recent years
Mumps Pathogenesis
Mumps Parotitis clinical presentation
- Low grade fever, malaise, myalgia, headache and anorexia
- Parotitis may be unilateral or bilateral
- Swelling of the parotid and tenderness
- Earache
- difficulty eating, swallowing, talking
Mumps complications
- Orchitis – most common complication after parotitis • Sterility is rare but subfertility may occur
- Oophoritis
- Meningoencephalitis• Usually self-limited
- Rare: Loss of hearing, Pancreatitis & Thyroiditis
- Most patients experience complete recovery with no long term effects
Prevention of mumps
MMR/MMRV Vaccine
• Vaccine is ~88% protective with 2 doses
How does bacterial pharyngitis present
• Acute onset
• Sore throat, fever
• Nausea, vomiting and headache often present
• Erythematous posterior pharynx and palatine
tonsils
• Tender cervical lymphadenopathy
• While or yellow exudate in tonsillar crypts
How does viral pharyngitis present
- Gradual onset
- Low-grade fever
- Less erythema and swelling of the pharynx
- Discrete ulcerative lesions
- Tonsils generally not involved
- conjunctivitis, coryza, cough may be present
Bacterial causes of pharyngitis
Strep pyogenes
Fusobacterium necrophorum
Strep dysgalactiae
Viral causes of pharyngitis
Rhinovirus
Coronavirus
Adenovirus
S. pyogenes: Biology
Most common cause of pharyngitis
• Gram positive cocci (in chains; discoid colonies)
• β-hemolytic
• Lancefield Group A
• Important for Rapid Strep test
• PYR positive
• detection of pyrolidonyl arylamidase (hydrolysis of L-pyrrolidonyl-β-naphthylamide)
• Bacitratin sensitive
*GABHS - Group A β-hemolytic streptococcus
Clinical Presentation: Pharyngitis
- Develops ~2-4 days after exposure
- Abrupt onset of fever, sore throat, malaise, headache, dysphagia
- Erythematous posterior pharynx and palatine tonsils
- Tender cervical lymphadenopathy
- Palatal petechiae
- Tonsils may have white or yellow exudate
Clinical Presentation: Scarlet Fever
- Fever, headache, sore throat, nausea, vomiting and malaise
- Diffuse, sandpaper-like rash develops, initially on trunk and groin then spreads to face
- Accentuation of the rash in flexor creases (i.e., under the arm, in the groin), termed “Pastia’s lines
Which infection presents with strawberry tongue
Scarlet fever!
- Initially a thick, white coat and swollen papillae seen on tongue (white strawberry tongue)
- White coating desquamates leading to red strawberry tongue appearance
Explain the polymicrobial infection seen in Chronic Tonsillitis & Peritonsillar Abscess
Polymicrobial Infection • Group A Strep (GABHS) 1st colonizer • Staph aureus (MRSA) 2nd colonizer • Gram-Negative Anaerobic Rods (GNAR) 3rd colonizer • Bacteroides is representative species
Endogenous flora Staph aureus establish biofilm and anaerobes GNAR establish abscess in necrotic tissue.
How to manage Chronic Tonsillitis & Peritonsillar Abscess
Management involves broad-spectrum antibiotics, drainage and potentially surgery.
Clinical Presentation: Peritonsillar Abscess
- Fever
- Dysphagia
- Severe throat pain , drooling to avoid swallowing saliva
- “Hot potato”/muffled voice
- Trismus
What complication can pharyngitis lead to
Acute rheumatic fever
• Multisystem disease resulting from an autoimmune reaction to untreated or unresolved infection with GABHS. Typically develops ~3 weeks after infection
Which disease is this
Acute rheumatic fever
What type of sensitivity is seen in rheumatic fever
Type II Hypersensitivity reaction
Explain the molecular mimicry seen in acute rheumatic fever
• Immune response targeted at streptococcal
antigens also recognizes human tissues
• Cross-reactive antibodies bind to endothelial cells of heart valve
• Leads to recruitment/activation of lymphocytes and lysis of endothelial cells
Clinical Presentation: Acute Rheumatic Fever
- Fever (usually low-grade)
- Polyarthralgia
- Carditis
- Murmur, irregular heart beat, CHF
- Polyarthritis
- Erythema marginatum
- Subcutaneous nodules
- Sydenham’s chorea
How to diagnose acute rheumatic fever
Evidence of preceding GABHS infection • Positive throat culture • Rapid antigen test • Recent scarlet fever • Elevated or rising ASO titer, antiDNAse B, or other streptococcal antibody titer
Jones Criteria
What disease other than Acute rheumatic fever results from pharyngitis
PST streptococcal glomerular nephritis
• Immune complex disease that develops 1-3 to weeks after a GABHS pharyngitis
What type of hypersensitivity is PSGN
Type III
What happens with PSGN
• Circulating antigen-antibody complexes deposit in glomerulus
• Leads to complement activation and consequent inflammation and injury of kidney
• Presents as an acute nephritic syndrome
• Systemic symptoms such as headache,
malaise, anorexia and flank pain may also be
present
Corynebacterium diphtheriae: Biology
- Genus: Corynebacterium
- Gram positive rods
- Non-motile, Non-spore forming
- Aerobic
- Club-shaped; Pleomorphic
- “Chinese letters” arrangement
- Non-pathogenic Corynebacteria spp. are members of normal flora in pharynx, nasopharynx and on skin.
- Only strains harboring phage-encoded toxin can cause disease
- Other medically-important species:
- C. jeikeium: associated with bacteremia, IV catheter colonization
- C. minutissimum: RTI’s, wound infections
How is C. diphtheriae spread
Transmitted by droplet spread, direct contact and fomites (rare)
Humans are primary reservoir
Main virulence factor for C. diphtheriae
Diphtheria toxin (DT) • Genes for toxin acquired via lysogenic conversion - bacteriophage
C. diphtheriae: Pathogenesis
• Binding mediated by the B subunit • Both A and B subunits enter cell in vacuole • A-subunit moves into cytosol and goes to its target, elongation factor 2 (EF-2) • A-subunit inactivates EF-2 by ADP- ribosylationàshuts off protein synthesisàcell death
Clinical Presentation: Diphtheria
- Usually manifests as pharyngitis or tonsillitis
- Malaise, sore throat and fever often occur
- Intact pseudomembrane on palate, tonsils or pharynx
- Extensive lymphadenopathy “Bull-Neck”
- Complication: Carditis, Nerve damage
Complications of C. diphtheriae
Myocarditis with cardiac arrhythmias (most common cause of death )
•Develops 2-6 weeks from start of infection; earlier onset associated higher mortality
Inflammation and damage of nerves In 1-8weeks
• paralysis of soft palate and pharynx
renal failure, thrombocytopenia ,DIC,shock
• Case fatality of 5% - 10%
How to prevent c diptheriae
DTaP vaccine (Td or Tdap)
What agar does C. diphtheriae grow on
Tinsdale agar
- contains L- cysteine and sodium thiosulfate that are H2S indicators.
- Cultivation 24 hours, 37 °C in an aerobic atmosphere
What is potassium telluride important for
Potassium tellurite is the selective agent (inhibits most of the upper respiratory tract normal flora) that turns the media brown-black as a result from the reduction of potassium tellurite to metallic tellurite
Which tests are used to test for presence of C. diphtheriae
Elek test
- show lines of precipitation after incubation
PCR
How to prevent complications of Strep pyogenes
Penicillin treatment
