Bacterial Inf of Upper Respiratory Tract Flashcards

1
Q

Normal Flora - NOSE

A
  • Staphylococcus epidermidis and Staphylococcus aureus = G+ cocci clusters facultative anaerobes. (INC ISSUE IN HOSPITALS)
  • Corynebacterium spp. – G+ rod, pleomorphic, non spore forming
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2
Q

Normal Flora - NASOPHARYNX

A
  • Streptococcus - Gram + cocci, chains
  • Viridans group = S. mutans, S. mitis, S. milleri and S. salivarius (OPPORTUNISTIC INFECTIONS IN SOME CASES)
  • Moraxella catarrhalis – Gram neg, diploid-coccobacillus. Aerobic
  • Bacteroides (ANAEROBE! IT HIDES OTHERWISE IT CANT SURVIVE)
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3
Q

Normal NASOPHARYNX flora but primary SEASONAL disease causing pathogens:

A
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Neisseria meningitides
  • Moraxella catarrhalis
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4
Q

Pathogens - Streptococcus:

A
  • Gram positive cocci in chains
  • Catalase negative: differentiates it from Staphylococcus
  • Group A - S. pyogenes -Beta
  • Group B - S. agalactiae - Beta
  • Group D - S. bovis
  • Group D -Enterococcus faecalis
  • α-hemolytic - S. pneumoniae
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5
Q

a-hemolysis seen in a pathogen then it MOST LIKELY IS:

A

S. Pneumoniae

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6
Q

STREPTOCOCCAL PHARYNGITIS

A
  • Characterized by redness of the throat, patches of adhering pus, scattered tiny hemorrhages, fever. (STREP THROAT)
  • Streptococcus pyogenes – Differentiated by - β-hemolytic (the others have Alpha or gamma hemolysis)
  • Rapid Strep tests target the cell wall antigen
  • Catalase NEGATIVE
  • M-Protein - antipagocytic - essential for virulence - NOT CROSS PROTECTIVE = CANNOT VACCINATE AGAINST IT
  • Capsule - not in all strains, inhibits phagocytosis
  • –>Streptococcal/Pyrogenic Exotoxins
  • super antigens: nine proteins - SPE-A, SPE-B….= fever, rash, T-cell proliferation, B-cell suppression
  • scarlet fever-Only scarlet fever is usually preceded by strep throat symptoms. **
  • toxic shock
  • necrotizing fasciitis
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7
Q

Streptococcal/Pyrogenic Exotoxins

A
  • super antigens: nine proteins - SPE-A, SPE-B….= fever, rash, T-cell proliferation, B-cell suppression
  • scarlet fever-Only scarlet fever is usually preceded by strep throat symptoms. **
  • toxic shock
  • necrotizing fasciitis
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8
Q

Risks of not treating Streptococcus pyogenes :

A

—Scarlet Fever – (TOXIN RELEASE AT THE END OF INFECTION - THATS WHY WE DONT LET IT RUN COURSE) SPE release - redness of skin and a white coating on the tongue.
—Acute rheumatic fever – (DUE TO IMMUNE RESPONSE OF PATIENT THAT CROSS REACTS WITH OUR OWN TISSUE) fever, joint pain, chest pain, rash, skin nodules, uncontrollable jerky movements. Acute inflammatory process. ORGANISMS WILL BE CLEARED - INFECTION GONE BUT STILL RHEUMATIC FEVER –> MEMORY WITH STREP THROAT = MORE SEVER RXN
—Necrotizing fasciitis – (TOXIN SUPERANTIGEN RELEASE) SPE release, skin infections
—acute glomerulonephritis: (ANTIGEN ANTIBODY COMPLEX THAT GETS STUCK IN KIDNEYS WHICH RESULTS IN IMMUNE RESPONSE TO KIDNEY ISSUE) childhood that begins 1-4 weeks after streptococcal pharyngitis
3-6 weeks after skin infection; deposition of antigen-antibody complexes in the glomeruli;
edema, hypertension, hematuria, proteinuria, decreased serum complement levels

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9
Q

Streptococcus pyogenes is in what Streptococcal group?

A

GROUP A

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10
Q

DIPTHERIA organisn, toxin, and symptoms

A
  • Organism: Corynebacterium diphtheriae – is a variable shape, non-motile, non-spore forming, Gram positive rod (“Chinese letters”)
  • Diphtheria exotoxin - lysogenized by a bacteriophage (Exotoxin not a part of Diphteria genome originally - it was put there at some point)
  • Deadly - Toxin mediated disease
  • Controlled by toxoid vaccine
  • Mild sore throat, slight fever, high fatigue and malaise.
  • Neck swelling is often dramatic
  • whitish gray membrane – tonsils, throat, nasal cavity
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11
Q

Diptheria pathogenesis

A
  • Not invasive - toxin is absorbed by the bloodstream. (IT COLONIZES THE TISSUE BUT IT DOESNT MOVE TO OTHER AREAS)
  • Classic gray-white membrane - clotted blood, epithelial cells of the mucous membrane, and leukocyte infiltrate.
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12
Q

What can be confused with pharyngeal diptheria?

A
  • group A streptococcal pharyngitis and infectious mononucleosis
  • NEED TO CHECK IF THE WHITE COVERING IS PUS OR IF IT IS THE OUTER MUCOSAL COVERING OF DIPTHERIA
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13
Q

Diphtheria toxin mechanism

A
  • released inactive.
  • A and B subunit: B – binds to host receptor; A - inactivation of elongation factor-2 (EF-2), stop protein synthesis and induce cell death. True enzyme (enzyme will continue to work on other cells after killing one)
  • Disease survival - severe damage to the heart, kidneys and nerve cells - B subunit receptor
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14
Q

A-B toxins

A

two components: active and binding
-released in inactive form –> B-subunit binds cell = uptaken by cell –> actve portion lyses itself off and becomes active –> inactivates elogation factor 2 –> prevents protein synthesis by ribosome = CELL DEATH

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15
Q

Pinkeye – conjunctivitis- Bacterial - CAUSATIVE AGENTS:

A

COMMON - (NORMAL FLORA IN CONJUNCTIVA THAT CAUSED INFECTION FOR SOME REASON)

  • Haemophilus influenzae (also causes miningitidis – Gram negative rod
  • Streptococcus pneumoniae – pneumococcus

LESS COMMON:

  • Moraxella lacunata,
  • enterobacteria
  • Neisseria gonorrhoeae
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16
Q

Pinkeye – conjunctivitis- Bacterial - PREVENTION AND TREATMENT:

A
  • Removed from school or daycare settings
  • Hand washing, rubbing eyes, common towels.
  • Gentamicin or ciprofloxacin eye drops.
  • Resistant Haemophilus influenza, and Streptococcus pneumoniae exist locally
17
Q

OTITIS MEDIA/SINUSITIS - causative agents

A
  • Haemophilus influenzae
  • Streptococcus pneumoniae -Hemolysis ALPHA
  • Moraxella catarrhalis
18
Q

Streptococcus pneumonia hemolysis?

A

alpha - hemolysis

19
Q

diference bw bacterial to viral pink eye?

A

-more swelling, more puss, inflammation WITH BACTERIA

20
Q

what is alpha hemolysis

A

-the organism that is spread onto a blood agar plate only partially kills blood cells = greenish color - Incomplete killing

21
Q

what is beta hemolysis

A

-the organism on blood agar plate completely kills the cells = white patch on plate

22
Q

Streptococcus pneumoniae

A
  • normal flora
  • in some cases, especially compromised immune systems-
  • paranasal sinusitis,
  • middle ear infections (otitis media)
  • lobar pneumonia
  • meningitis
23
Q

CHLAMYDIA

A
  • Taxonomy - family Chlamydiaceae
  • Chlamydia trachomatis
  • Chlamydophila psittaci
  • Chlamydophila Pneumoniae
  • Chlamydophila – very small- obligate intracellular parasites
  • HAVE TO BE INSIDE THE CELL
  • elementary bodies (EB) - metabolically inactive, infectious
  • reticulate bodies (RB) -metabolically active noninfectious forms
24
Q

elementary bodies (EB)

A

metabolically inactive, infectious

25
-reticulate bodies (RB)
metabolically active noninfectious forms
26
Chlamydia trachomatis
- trachoma, adult inclusion conjunctivitis, neonatal conjunctivitis, infant pneumonia. - Pathogenesis: direct destruction of host cells during replication the host inflammatory response. - The organisms gain access to cells by minute abrasions or lacerations – granuloma formation in conjunctiva - NO immunity - no clearin - How serious is this disease? VERY - can cause blindness - Follicular conjunctivitis - diffuse inflammation. - conjunctiva scarring, eyelids turn inward. - The turned in eyelids abrade the cornea
27
Adult inclusion conjunctivitis
Acute follicular conjunctivitis- same serovars associated with genital infections – occurs in sexually active adults. Mucopurulent discharge, keratitis, corneal infiltrates and some vascularization.
28
Neonatal conjunctivitis
- Infants exposed to C. trachomatis at birth. 5-12 days after birth, eyelids swell. Untreated may last 12 months - conjunctival scarring and corneal vascularization occur. - Infants who are untreated or are treated topically only are at risk for developing C. trachomatis pneumonia.
29
Infant pneumonia
-Onset 2-3 weeks after birth. Bronchitis with a dry cough, afebrile.
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Chlamydophila pneumoniae
- Most severe infections involve only one lung lobe. - Cannot be readily differentiated from -Mycoplasma pneumoniae, Legionella pneumophila and respiratory viruses. - C. pneumoniae infection may be involved many cases of atherosclerosis.
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Chlamydophila psittaci
- related to birds! - Infection by respiratory tract - bacteria spread to the reticuloendothelial cells - liver and spleen. - multiply in these sites producing focal necrosis - seeded due to hematogenous spread. - lymphocytic inflammatory response on the alveolar and interstitial spaces.
32
most people have serologic evidence of:
Chlamydophila pneumoniae