Respiratory Tract Infections 3 Flashcards

1
Q

Mumps is caused by which viral family

A

Paramyxoviridae family

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2
Q

Mumps: Biology & Epidemiology

A
• Paramyxoviridae family
• Enveloped ss(-)RNA virion
• 2 glycoproteins
• HN – mediates hemagglutination
and neuraminidase activity
• F – fusion to the host cell
• One serotype, endemic worldwide
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3
Q

Mumps transmission

A

Aerosol transmission

  • Infections are often asymptomatic/subclinical
  • Outbreaks are associated with crowded conditions (colleges, community gatherings, etc…)
  • Rising number of cases in recent years
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4
Q

Mumps Pathogenesis

A
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5
Q

Mumps Parotitis clinical presentation

A
  • 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
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6
Q

Mumps complications

A
  • 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
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7
Q

Prevention of mumps

A

MMR/MMRV Vaccine

• Vaccine is ~88% protective with 2 doses

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8
Q

How does bacterial pharyngitis present

A

• 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

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9
Q

How does viral pharyngitis present

A
  • 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
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10
Q

Bacterial causes of pharyngitis

A

Strep pyogenes
Fusobacterium necrophorum
Strep dysgalactiae

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11
Q

Viral causes of pharyngitis

A

Rhinovirus
Coronavirus
Adenovirus

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12
Q

S. pyogenes: Biology

Most common cause of pharyngitis

A

• 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

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13
Q

Clinical Presentation: Pharyngitis

A
  • 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
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14
Q

Clinical Presentation: Scarlet Fever

A
  • 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
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15
Q

Which infection presents with strawberry tongue

A

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
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16
Q

Explain the polymicrobial infection seen in Chronic Tonsillitis & Peritonsillar Abscess

A
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.

17
Q

How to manage Chronic Tonsillitis & Peritonsillar Abscess

A

Management involves broad-spectrum antibiotics, drainage and potentially surgery.

18
Q

Clinical Presentation: Peritonsillar Abscess

A
  • Fever
  • Dysphagia
  • Severe throat pain , drooling to avoid swallowing saliva
  • “Hot potato”/muffled voice
  • Trismus
19
Q

What complication can pharyngitis lead to

A

Acute rheumatic fever

20
Q

• Multisystem disease resulting from an autoimmune reaction to untreated or unresolved infection with GABHS. Typically develops ~3 weeks after infection

Which disease is this

A

Acute rheumatic fever

21
Q

What type of sensitivity is seen in rheumatic fever

A

Type II Hypersensitivity reaction

22
Q

Explain the molecular mimicry seen in acute rheumatic fever

A

• 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

23
Q

Clinical Presentation: Acute Rheumatic Fever

A
  • Fever (usually low-grade)
  • Polyarthralgia
  • Carditis
  • Murmur, irregular heart beat, CHF
  • Polyarthritis
  • Erythema marginatum
  • Subcutaneous nodules
  • Sydenham’s chorea
24
Q

How to diagnose acute rheumatic fever

A
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

25
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
26
What type of hypersensitivity is PSGN
Type III
27
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
28
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
29
How is C. diphtheriae spread
Transmitted by droplet spread, direct contact and fomites (rare) Humans are primary reservoir
30
Main virulence factor for C. diphtheriae
``` Diphtheria toxin (DT) • Genes for toxin acquired via lysogenic conversion - bacteriophage ```
31
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 ```
32
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
33
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%
34
How to prevent c diptheriae
DTaP vaccine (Td or Tdap)
35
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
36
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
37
Which tests are used to test for presence of C. diphtheriae
Elek test - show lines of precipitation after incubation PCR
38
How to prevent complications of Strep pyogenes
Penicillin treatment