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Pulmonary > Pulmonary Microbiology > Flashcards

Pulmonary Microbiology Flashcards

1
Q

Tularemia:Francisella Tularensis
Microbiology:

A

Gram-, aerobic, non-motile, non-spore

coccobacillus

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2
Q

Tularemia: Francisella Tularensis

Mechanism of disease/Virulence Factors:

A 
Survives host’s innate immune response:
i. ↓LPS immunostimulation
ii.Capsule = complement resistance
iii.↑Survival in macrophages from iglABCD
transposon mutagenesis
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3
Q

Tularemia: Francisella Tularensis

Epidemiology

A

Not spread person-person

  • Yet, occurs in rural areas b/c infected animals
  • Incubation from hours –> weeks
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4
Q

Tularemia: Francisella Tularensis
Transmission: Modes of Infection:

A

i. Insect bites (ticks + deerflies) = ulcerogland.
ii. Exposure to sick animals (rabbits) = “””
iii. Rubbing eyes post infection = oculogland.
iv. Airborne = pneumonic
v. Contaminated Food/Water = oropharyngeal

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5
Q

Tularemia: Francisella Tularensis

- Normal outbreak vs. Bioterrorism Use

A

i. Bioterrorism outbreak has point-source outbreak
(urban, non-agricultural city)
ii.Respiratory illness in healthy persons

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6
Q

Tularemia: Francisella Tularensis

Disease Types:

A
  1. Ulceroglandular Tularemia (most common):
  2. Glandular Tularemia
  3. Oculoglandular Tularemia
  4. Oropharyngeal Tularemia
  5. Pneumonic Tularemia
  6. Typhoidal Tularemia (rare)
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7
Q

Ulceroglandular Tularemia

Presentation

A

(most common):

  • Skin ulcer at infection site (bug bit) - (“ulcero-”)
  • Swollen glands (“glandular)
  • Fever, chills, headaches, exhaustion
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8
Q

Glandular Tularemia

Presentation

A
  • Swollen glands (“glandular)

- Fever, chills, headaches, exhaustion

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9
Q

Oculoglandular Tularemia

Presentation

A
  • Swollen glands + eye pain, redness, discharge, eyelid ulcer.
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10
Q

Oropharyngeal Tularemia

Presentation

A

(eating poorly cooked infected meat)

- Fever + GI symptoms (sore throat, vomit, diarrhea)

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11
Q

Pneumonic Tularemia

Presentation

A

(in elderly and also with typhoidal tularemia)

- Pneumonia symptoms = cough, chest pain, difficulty breathing

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12
Q 
Typhoidal Tularemia (rare)
Presentation
A
  • Fever, exhaustion, vomit, diarrhea, pneumonia

- Enlarged liver + spleen

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13
Q

Tularemia: Francisella Tularensis
Diagnosis:

A
  1. Blood Culture for F. Tularensis
  2. Serology for Tularemia (blood test measuring immune response)
  3. CXR (patchy infiltrates)
  4. PCR sampling ulcer
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14
Q

Tularemia: Francisella Tularensis
Treatment:

A

Tularemia cured w/antibiotics Streptomycin and Tetracycine

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15
Q

Comparing Tularemia w/

Anthrax + Plaque CXR:

A
  1. Anthrax: dry, nonproductive cough w/
    widened mediastinum on CXR
  2. Plague: watery/bloody productive cough w/acute
    bacterial pneumonia signs on CXR
  3. Tularemia: non-productive cough w/patchy infiltrates.
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16
Q

Anthrax: Bacillus Anthrax (Ba)
Microbiology:

A
  • spore forming rod
  • Gram+, facultative anaerobe, non-motile
  • Spore (infectious form) viable 100yrs in soil
  • Spore (1-5 um) reaches lungs
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17
Q

Anthrax: Bacillus Anthrax (Ba)

Mechanism of disease/Virulence Factors:

A
  1. Ingested by pulmonary/cutan/GI macrophage
  2. Surviving spores released to hilar lymph node
  3. Spores vegetate –> acq. virulence factors:
    - Anti-phagocytic non-antigenic capsule (poly-dglutamic acid)***
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18
Q

Anthrax: Bacillus Anthrax (Ba)

- AB Toxin (Anthrax Exotoxin)?

A

i. B = Protective Antigen (binds receptor/endo)
ii.A1= Edema Factor (calmodulin activated AC)
↑cAMP –> swelling, medast. edema + ↓PMN
iii. A2= Lethal Factor (metalloprotease) xMAPKs –> no signaling –> cell death

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19
Q

Anthrax: Bacillus Anthrax (Ba)

Epidemiology/Transmission:

A

:1. Reservoir=cows; farmers safe (spores on soil)

  1. Imported wools/hides “Woolsorer’s Disease”
  2. Misdiagnosed: plague, tularemia (Category A)
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20
Q

Anthrax: Bacillus Anthrax (Ba)

Disease Types/Symptoms

A

Toxins –> SWELLING, SEPSIS, NECROSIS

  1. Cutaneous Anthrax (natural + bioterrorism)
    - Eschar (black = “Anthracis”), swelling (Edema Factor)
  2. Inhalation Anthrax: Spores (natural + bioterrorism) - TWO PHASES
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21
Q

Anthrax: Bacillus Anthrax (Ba)

Inhalation Anthrax: Spores (natural + bioterrorism) - TWO PHASES

A
  • Phase 1: Flu-like Symptoms
    i. Fever, aches etc –> SOB, chest pain
    ii. +/- non-productive cough
  • Phase 2: Hemorrhagic Mediastinitis w/Pleural Effusions
    i. NOT pneumonia b/c infection of hilar/mediastinal lymph nodes
    ii. MEDIASTINAL WIDENING
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22
Q

Anthrax: Bacillus Anthrax (Ba)
Diagnosis:

A

Culture rarely shows +Ba

  1. Differentiate from flu (phase 1 symptoms)
    - Flu won’t have SOB, nausea, vomit; Anthrax won’t have rhinorrhea
  2. Gram stain, immunofl. Ab stain CSF, blood smears for G+ boxcars
    - NO SPORES WILL BE SEEN
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23
Q

Anthrax: Bacillus Anthrax (Ba)
Treatment:

A

Incubation can be 6 weeks, leading to:

  1. 40 days ciprofloxacin/doxy IV prophylaxis + 1 other (ampicillin)
  2. Vaccine
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24
Q 
Yersinia Pestis (Plaque)
Microbiology:
A
  • Chubby Gram- rods w/bipolar inclusion bodies
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25
Q 
Yersinia Pestis (Plaque)
Mechanism of disease/Virulence Factors:
A
  • Fraction 1 (F1) paralyzes phagocytes upon
    ingestion; ↓innate + adaptive immunity
  • Yp –> skin –> macrophages –> lymph nodes
    (inguinal > axillary; “boubon”=groin) –>
    bloodstream (septicemia) –> ↑organ failure
  • Ex: subcutaneous hemorrhage (“Black death”)
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26
Q 
Yersinia Pestis (Plaque)
Epidemiology:
A
  • Bubonic plague is most common form
  • 1° Plague Pneumonia + 2° Plague Pneumonia
    (following bubonic)
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27
Q 
Yersinia Pestis (Plaque)
/Transmission:
A
  • Bubonic Transmission: flea + ground rodent
  • *New Mexico + SW USA
  • 1° Plague Pneumonia: infected person/cat
  • *Expected bioterrorism
  • *Plague pneumo (1°+2°) = contagious
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28
Q 
Yersinia Pestis (Plaque)
Disease Types:
A
  1. Bubonic: “Boubo” = swelling of lymph nodes
  2. Septicemic: severe toxemia +/- buboes
  3. Pneumonic:
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29
Q 
Yersinia Pestis (Plaque)
Symptoms Bubonic: :
A

Bubonic: “Boubo” = swelling of lymph nodes (inguinal) ~60% fatal

  • Flea (vector) bite –> 1-8 day incubation
  • Swollen, painful lymph nodes
  • +/- macular/ulcerative lesions at flea bite site
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30
Q 
Yersinia Pestis (Plaque)
Symptoms Septicemic:
A

Septicemic: severe toxemia +/- buboes

  • Rapid progression
  • Petechiae —> extreme DIC
  • Vomit + diarrhea
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31
Q 
Yersinia Pestis (Plaque)
Symptoms Pneumonic: :
A

Pneumonic: ~100% fatal if untreated

  • 2°=spreading from primary infection (bubonic flea bite)
    i. Contagious; requires isolation + prophylaxis for all exposed
    ii. Sputum production = bloody/watery > purelent
  • 1°=same symptoms as 2°, but precede septicemia
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32
Q 
Yersinia Pestis (Plaque)
Differential Bulbo presentation:
A
  • Tularemia: inoculation lesion more prominent; no septicemia
  • Strep/staph adenitis: less septic and lymph node is more plaible, less painful; purulent lesions
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33
Q 
Yersinia Pestis (Plaque)
Differential Septicemic:
A

meningococcemia, rickettsioses

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34
Q 
Yersinia Pestis (Plaque)
Differential Pneumonic presentation:
A

broad; G- rods confirm plague

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35
Q 
Yersinia Pestis (Plaque)
Diagnosis:
A
  1. +Ab for F1 antigen (Rapid Antigen Detection) OR Immunofl. for Yp
  2. history of exposure (flea/rodent) + symptoms
  3. Gram stain for Yp safety pin from bubo, SCF, blood, sputum
  4. Culture Yp on BAP/enteric media (b/c Yp = enerobacteriacae)
  5. Failure to respond to B-lactams/macrolines
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36
Q 
Yersinia Pestis (Plaque)
Staining appearance?
A

Safety pin appearance of Yp
b/c ends of rod take up more
than center (“bipolar staining)

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37
Q 
Yersinia Pestis (Plaque)
Exam Prompt?:
A

Pt recently camping in new Mexico suddenly develops fever…

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38
Q 
Yersinia Pestis (Plaque)
Treatment:
A 
IMMEDIATE
1. Gentamicin (streptomycin)
2. Doxy/Cipro
3. Pneumonic post exposure:
doxy for 7 days
4. No vaccine
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39
Q

Brucella spp.(Brucellosis) “Brucella”:

Microbiology:

A

Brucella abortus (cows), suis (pigs)
melitensis (sheep/goats)
- Small Gram- coccobacillus

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40
Q

Brucella spp.(Brucellosis) “Brucella”:

Mechanism of disease/Virulence Factors:

A
  1. Brucella penetrates skin, lung, eye, etc.
  2. Lymph spread –> facultative intracellular
    growth of RES (liver/spleen, bone)
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41
Q

Brucella spp.(Brucellosis) “Brucella”:

Epidemiology/Transmission:

A
  • USA: wild animal (cow, sheep, pig) reservoir
  • Transmission: contact + unpasteur cheeze
    i. vet, farmer, slaughterhouse (animal handling)
    ii.Recent Mediterranean/Mexican immigrant (bad
    cheese)
  • NO Human-human transmission
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42
Q

Brucella spp.(Brucellosis) “Brucella”:

Disease/Symptoms:

A

Brucellus (UNDULANT FEVER)

  1. Slow-moving, chronic infection w/relapse fever/nightsweats (undulant)
  2. Can be acute onset w/↑fever + flu sypmtoms
  3. Infects bone (lower vertebrae), heart, liver
  4. Typical lesion = granuloma (bone/liver)
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43
Q

Brucella spp.(Brucellosis) “Brucella”:

Diagnosis:

A

In DDx with TB

  1. Serology (↑anti-Brucella)
  2. Cultured on rich medium (1 week): bone marrow > blood.
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44
Q

Brucella spp.(Brucellosis) “Brucella”:

Treatment:

A
  1. Prolonged course of antibiotics (doxycycline + aminoglycosides)
  2. Control in USA: vaccinate cattle + pasteurize milk for cheese
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45
Q 
Coxiella Burnetii (Q Fever):
Microbiology:
A 
Coxiella Burnetii (Cb)
- Gram- bacillus w/ Endospore form
(imp for inhalation mode of entry, possible
terrorism, and cause of pneumonia)
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46
Q 
Coxiella Burnetii (Q Fever):
Mechanism of disease/Virulence Factors:
A
  • Obligate intracellular parasite (requires host ATP for growth)
  • Replicates w/in phagolysosome
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47
Q 
Coxiella Burnetii (Q Fever):
Epidemiology/Transmission:
A
  • Mode of entry: inhalation of animal aerosol
  • Also, handling of animal viscera, aminotic fluid,
    placenta, drinking raw milk, ticks.
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48
Q 
Coxiella Burnetii (Q Fever):
Disease/Symptoms:
A

Q Fever Gram- bacillus

  1. 1/3 - 1/2 asymptomatic
  2. Acute febrile illness
  3. Atypical pneumonia (spore like form)
  4. Can lead to liver (granulmoatis hep) or heart (endocarditis) damage
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49
Q 
Coxiella Burnetii (Q Fever):
DDx:
A
  1. Atypical pneumonias / Pneumonic Tularemia
  2. Ehrlichioses/RMSF
  3. Mycobacterial infections
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50
Q 
Coxiella Burnetii (Q Fever):
Diagnosis:
A
  1. Serological - ↑Ab titer for Coxiella Burnetti
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51
Q 
Coxiella Burnetii (Q Fever):
Treatment:
A

Most spontaneously resolve, but doxycycline ↓chronic infn.

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52
Q 
Mycobacterium Tuberculosis (MBT):
Buzz Words:
A

HIV (↓Tcells)

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53
Q 
Mycobacterium Tuberculosis (MBT):
Additional Forms:
A
  • bovis = cows
  • avium = HIV pts
  • leprae = leprosy
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54
Q 
Mycobacterium Tuberculosis (MBT):
Microbiology:
A
  • Large, non-motile rod-shaped bacterium
  • Not gram+/-; no characteristics of either
  • Gram stain = ghost cells (weakly gram+)
  • Serpentine cord colonies (from cord factor)
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55
Q 
Mycobacterium Tuberculosis (MBT):
Mechanism of disease/Virulence Factors:
A
  • Obligate aerobe (find in apex of lung)
  • Facultative intracellular parasite (macrophage)
  • Cell Wall: peptidoglycan + 3 ↑lipid proteins:
  • MBT bind to macros mann. receptors (LAM) or
    via complement receptors/Fc receptors (bypass
    oxidative burst w/compl binding)
  • Inhibits phago-lyso fusion of macros
  • ↓Oxidative toxicity mechanism of macros
  • Antigen 85 - MTB secreted protein; may wall off
    immune system, protecting MTB
  • Slow generation can allow growth under the radar
    of the immune system.
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56
Q 
Mycobacterium Tuberculosis (MBT):
Epidemiology/Transmission:
A

Rate on the decline

  • Coughing is most common
  • 25% of exposed become infected
  • 10% of infected –> disease in lifetime (1°)
  • 10% risk for HIV+ –> disease each year (1°)
  • Most common: Reactivation TB
  • Not contagious until disease (vs. infection)
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57
Q 
Mycobacterium Tuberculosis (MBT):
*Mis-used or mis-prescribed Rx =
A

resistance*

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58
Q 
Mycobacterium Tuberculosis (MBT):
Two Types of Resistance?
A
  • Multi-Drug-Resistant TB (MDR TB)
    i. Resistant to isoniazid + rifampicin
  • Extensively-Drug-Resistant TB (XDR TB)
    i. Resistant to isoniazid + rifampicin +
    fluoroquinolone + amikacin/kanamycin/
    capreomycin
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59
Q 
Mycobacterium Tuberculosis (MBT):
***Both MDR/XDR TB common in pts who?
A

Don’t take meds as described

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60
Q 
Mycobacterium Tuberculosis (MBT):
Preventative Treatment:
A

(isoniazid 2/wk 9mos)
- Preventative therapy = secondary prevention
(stop infected –> disease)
- Screen persons at ↑risk infection–> disease

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61
Q 
Mycobacterium Tuberculosis (MBT):
Disease: Latent (exposed≠contagious) vs Disease (active=contagious)
A
  • MBT contained by lymphocytes + macrophages

- TB stages of disease (most won’t get to stage 5)

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62
Q 
Mycobacterium Tuberculosis (MBT):
Disease Stages:
A 
Stage 1
Stage 2 ~ 7-21 days post-infection
Stage 3 ~ “Cell Mediated Response” ~ 6-10 weeks
Stage 4 
Stage 5 ~ The Damage We See!
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63
Q 
Mycobacterium Tuberculosis (MBT):
Disease Stage 1:
A

Stage1

  1. Aerosolized droplet nuclei (3-5 bacilli, infective ~5um each) inhaled
  2. Ingested by alveolar macrophages (TB begins when droplet arrives)
    - Large droplets remain in nose/pharynx (URT) = no infection
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64
Q 
Mycobacterium Tuberculosis (MBT):
Disease Stage 2:
A

Stage 2 ~ 7-21 days post-infection

  1. MTB multiplies in macrophages –> other macrophages are recruited
  2. New macrophages phagocytose MTB, but cannot destroy them
  3. Some MTB spread to lymph nodes in macrophages
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65
Q 
Mycobacterium Tuberculosis (MBT):
Disease Stage 3:
A

Stage 3 ~ “Cell Mediated Response” ~ 6-10 weeks

  1. Lymphocytes (T-cells) release gamma-IFN –> activate macrophages
  2. Activated macrophages destroy MTB (this is when pt is tuberculin+)
  3. Activated macros release inflammatory/lytic molecules against MTB, leading to tissue damage and tubercles surrounded by macros
    - Tubercle = caseating granulomas
    - MBT imprisoned by macrophages (guards), instructed by T-cell (warden)
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66
Q 
Mycobacterium Tuberculosis (MBT):
Disease Stage 4:
A

Stage 4

  1. Unactivated macrophages targeted by MTB –> tubercle grows
  2. Growing tubercle invades bronchus –> pulmonary blood –> milliary TB
    * **Milliary TB = Disseminated TB = Systemic TB
    i. Exudative Lesions = ↑PMN, replication without resistance
    ii. Productive/Granulomatous Lesions = host becomes hypersensitivty.
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67
Q 
Mycobacterium Tuberculosis (MBT):
Disease Stage 5:
A

Stage 5 ~ The Damage We See!

  1. Caseous centers of tubercle/granuloma liquefy –> ↑MTB growth extracellularly
  2. Extracellular growth –> necrosis of nearby bronchi –> cavity formed
  3. Cavity (allows for spread) –> healing –> calcified fibrosis –> Gohn complex or Simon foci (metastatic foci, usually reactivated because contain viable organism)
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68
Q 
Mycobacterium Tuberculosis (MBT):
Diagnosis: non-specific, systemic + pulmonary signs/symptoms
A
  1. Symptoms: cough, fever, night sweats, weight loss, hemoptysis
  2. Signs: cachexia (↓Tcell function), consolidation signs, pyurea, mening.
  3. PPD (Purified Protein Derivative): infection (latent), not disease
    - MTB component injected, if macrophages have been activated
    - Also “Quantiferon Gold” for IFN-ɣ
  4. Radiograph
    - Primary TB = lymphadenopathy + pleural effusion any area of lung
    - Reactivation TB = upper lobe only, cavitation
    - Miliary + caseating granuloma w/multinucleated giant cells
  5. Acid Fast+ via Ziehl-Neelson Stain (cell wall lipids don’t dissolve w/ addition of red acid EtoH, holding fast to the red acid) + NAA test
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69
Q 
Mycobacterium Tuberculosis (MBT):
MTB's cell wall consists of three major components a major determinant of virulence for the bacterium?
A

i. Mycolic Acid: H2Ophobic lipid shell; ↓permeability of MBT cell = protective from
macrophage ROS defense
ii.Cord Factor: 2xmycolic acid + dissacharide. Allows parallel growth of bacterium, inhibits PMN migration,
found only in virulent stains.
iii.Wax-D: Freund’s adjuvant envelope

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70
Q 
Mycobacterium Tuberculosis (MBT):
↑Lipid in MBT Cell Wall does five things:
A
  1. Impermeable to stains
  2. Antibiotic resistance
  3. Acid/base-resistant (fast)
  4. Resistant to compl-lysis
  5. Intra-macrophage growth
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71
Q 
Mycobacterium Tuberculosis (MBT)
Treatment:
A 
Take combination therapy exactly as prescribed!
1. 6-9 months of standard:
- RIPE
=Rifambin, Isoniazide, Pyrazinamide, Ethambutol
- At least two drugs needed
- Never add a single new drug
- Directly observe therapy
- Monitor toxicity
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72
Q 
Mycobacterium Tuberculosis (MBT)
**Patients are no longer infective if they:
A
  1. Adequate multi-therapy
  2. Respond well to Rxs
  3. 3 negative cultures
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73
Q

Pertussis (Whooping Cough): Bordetella Pertussis

Microbiology:

A
  1. Gram-, aerobic, coccobacillus
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74
Q

Pertussis (Whooping Cough): Bordetella Pertussis

Mechanism of disease/Virulence Factors:

A
  1. Pertussis toxin: A-B toxin alters intracellular
    protective pathways
  2. ↑Adenylate Cyclase: taken up by PMNs, monos,
    lymphos –> ↓ROS synthesis
  3. Filamentous Hemagglutinin (FHA): pili rod that
    binds cilia (target with mAb)
  4. Tracheal Cytotoxin: paralyzes ciliated cells
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75
Q

Pertussis (Whooping Cough): Bordetella Pertussis

Epidemiology/Transmission:

A
  • 200K cases each year before vaccine
  • Nowdays, untreated “merely annoyed” patients
    become reservoirs for disease
  • Transmission: human-human
  • Infants get it from seemingly healthy carers
  • Adolescents (waining vaccination) can get it
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76
Q

Pertussis (Whooping Cough): Bordetella Pertussis

Disease/Symptoms:

A

Whooping Cough

  • Can last as annoyance for 7 weeks
  • Clinical Illness Stages: (1-6 weeks post exposure)
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77
Q

Pertussis (Whooping Cough): Bordetella Pertussis

Three Stages:

A

Catarrhal Stage ~ “Common Cold”
Paroxysmal Stage ~ “The Whooping Cough”
Convalescent Stage ~ “Cough Subsides”

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78
Q

Pertussis (Whooping Cough): Bordetella Pertussis

Catarrhal Stage ~ “Common Cold”

A
  • Common cold findings for 1-2 weeks
  • Unlike most URIs, cough increases
  • Most contagious in this stage
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79
Q

Pertussis (Whooping Cough): Bordetella Pertussis

Paroxysmal Stage ~ “The Whooping Cough”

A
  • Paroxysmal attacks w/inspiratory gasp through narrowed glottis
  • Patients become hypoxemic, cyanotic
  • Most complications arise in this stage
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80
Q

Pertussis (Whooping Cough): Bordetella Pertussis

Convalescent Stage ~ “Cough Subsides”

A
  • Cough goes away gradually; may come back with another URI
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81
Q

Pertussis (Whooping Cough): Bordetella Pertussis

Diagnosis:

A

Requires special growth medium for culture swab of throat

  • PCR based tests
  • CXR: looking for pneumonia/URI
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82
Q

Pertussis (Whooping Cough): Bordetella Pertussis

Treatment:

A

Acellular Pertussis (aP) replaced whole-cell pertussis

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83
Q

Diphtheria: Corynebacterium diphtheriae

Corynebacterium?

A

“Koryne”: club

“Bacterion”: little rod

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84
Q

Diphtheria: Corynebacterium diphtheriae
Microbiology:

A

Non-spore forming rod

  • Corynebacteria = gram+, aerobic, non-motile, rod shaped bacteria
  • Form irregular, club shape (Chinese symbol)
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85
Q

Diphtheria: Corynebacterium diphtheriae

Mechanism of Disease/Virulence Factors:

A
  • Avirulent –> toxic by lysogenic conversion
  • Diphtheria toxin (Dt) is required for virulence
  • Dt coded by tox gene on lysogenic beta-prophage
    (no phage = avirulent)
  • Follows A (toxic enzyme) + B (adhesin) model
  • B binds to heparin-binding EGF (hbEGF)
  • A (endocytosed) ADP-ribosylates EF-2 and halts
    protein synthesis.
    One molecule enough to kill one cell.
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86
Q

Diphtheria: Corynebacterium diphtheriae

Epidemiology/Transmission:

A

No cases in US; endemic if no DPT vaccine (prophylaxis)

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87
Q

Diphtheria: Corynebacterium diphtheriae
Diseases:

A
  1. Organism (A+B) colonizes in pharynx forming pseudomembrane
  2. Toxin (A) gets in blood –> organ damage (HEART + Cranial Nerves).
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88
Q

Diphtheria: Corynebacterium diphtheriae
Presentation:

A
  1. Sore throat + pseudomembrane on tonsils, throat, pharynx
  2. Neck swelling (severe disease)
  3. Skin lesions (cutaneous diphtheriae)
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89
Q

Diphtheria: Corynebacterium diphtheriae
Diagnosis:

A

If + immediately report to CDC!

  1. REQUIRED culture of Corynebacteria Diphtheriae (nose/throat swab)
  2. Any confirmation of actual exotoxin (Dt)
  3. Additional tests for affected organs (CT of neck, EKG etc)
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90
Q

Diphtheria: Corynebacterium diphtheriae
Treatment:

A
  1. Antitoxin - for symptomatic, diffuse cases
    - Neutralizes circulating Dt (not effective against bound toxin)
  2. Antibiotics (erythromycin/penicillin) - asymptomatic, localized/cutaneous cases
    - Eradicate/halt production of toxin; good for preventing transmission
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91
Q

Nocardiosis: Nocardia asteroides Complex
Microbiology:

A
  • Gram+ bacilli with branching beaded (coccobacillary) filaments (hyphae)
  • Saprophytic (soil normal flora, H2O)
  • Aerobic actinomycetes
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92
Q

Nocardiosis: Nocardia asteroides Complex

Mechanism of disease/Virulence Factors:

A
  1. Have short (40-60 C) mycolic acid chains (stain
    weakly acid-fast)
  2. Catalase + superoxide dismutase protect against
    PMN/macrophage damage
  3. Cord factor (dimycolic acid) prevents phaglysosome fusion
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93
Q

Nocardiosis: Nocardia asteroides Complex

Epidemiology/Transmission:

A
  • Inhaled
  • Cutaneous skin wound in infected soil
  • No person-person / nosocomial infections
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94
Q

Nocardiosis: Nocardia asteroides Complex

***Common in pts w/underlying debilitations:

A
  • Immunocompromised + steroid use
  • Underlying chronic lung disease
  • Diabetes, heme maligancies, AIDS
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95
Q

Nocardiosis: Nocardia asteroides Complex
Diseases:

A

(Nocardiosis) opportunistic pathogen –> pulmonary disease
General: acute inflammation –> necrosis + abscesses
1. Nocardia asteroides inhaled –> grows in lung (infected = pneumonia)
2. Leads to lung abscesses
3. Can become systemic –> infection/abscess in brain, blood, heart

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96
Q

Nocardiosis: Nocardia asteroides Complex
Presentation:

A

Immunocompromised patients

  • Pulmonary nocardiosis: hemoptysis, fever/night-sweats, chest pain
  • Cerebral nocardiosis: headache, confusion, seizures
  • Cutaneous nocardiosis: ulcers
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97
Q

Nocardiosis: Nocardia asteroides Complex
Diagnosis:

A
  1. Smear/culture on BCYE (yeast extract + activated charcoal)
  2. Gram stain
  3. Acid Fast stain to confirm
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98
Q

Nocardiosis: Nocardia asteroides Complex
Treatment:

A

Sulfas!

  • Immunocompetent: at least 6 months
  • Immunocompromised: at least 12 months
  • Sulfa, ceftriaxone, and amikacin in difficult cases
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99
Q

Streptococcus Pneumoniae “Pneumococcus”

Microbiology:

A

Lancet shaped diplococcus

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100
Q

Streptococcus Pneumoniae “Pneumococcus”

Mechanism of Disease/Virulence Factors: 10

A
  1. Polysaccharide capsule
  2. Pneumolysin
  3. Hyaluronidase
  4. Neuraminidase
  5. Pili:
  6. Wall Teichoic Acid (WTA) and LipoTeichoic Acid (LTA)
  7. Choline Binding Protein (CBP)
  8. Competence Protein
  9. Autolysin (LytA)
  10. Lipoproteins
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101
Q

Streptococcus Pneumoniae “Pneumococcus”
Mechanism of Disease/Virulence Factors:
Polysaccharide capsule

A

Anti-phagocytic

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102
Q

Streptococcus Pneumoniae “Pneumococcus”
Mechanism of Disease/Virulence Factors:
Pneumolysin

A

Pore-forming toxin binds to
cholesterol in cell membranes –> cell lysis + T/B
cell + TLR4 mediated inflammation

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103
Q

Streptococcus Pneumoniae “Pneumococcus”
Mechanism of Disease/Virulence Factors:
Hyaluronidase:

A

↑spread in hyal. acid tissues

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104
Q

Streptococcus Pneumoniae “Pneumococcus”
Mechanism of Disease/Virulence Factors:
Neuraminidase:

A

xN-acetylneruaminic acid from surface GPs = damage + ↑binding sites

105
Q

Streptococcus Pneumoniae “Pneumococcus”
Mechanism of Disease/Virulence Factors:
Pili:

A

↑adhesion to epithelium.

106
Q

Streptococcus Pneumoniae “Pneumococcus”
Mechanism of Disease/Virulence Factors:
Petpidoglycan + Teichoic Acid: Wall Teichoic
Acid (WTA) and LipoTeichoic Acid (LTA)

A

Have (-) phosph groups neutralized by choline (vs. Dalanine normally)

  • TA + peptidoglycan = C Polysaccharide (CP)
  • CRP (liver inflammatory mol) binds CP
  • CRP + CP –> complement activation
  • CP + PRR –> cytokine secretion
107
Q

Streptococcus Pneumoniae “Pneumococcus”
Mechanism of Disease/Virulence Factors:
Choline Binding Protein (CBP):

A

Wall hydrolytic enzymes that bind choline on WTA/LTA and release inflammatory wall components (LytA)

  • Others bind respiratory epithelium (PsaA)
  • Others bind complement factor H (↓phago)
108
Q

Streptococcus Pneumoniae “Pneumococcus”
Mechanism of Disease/Virulence Factors:
Competence Protein:

A

Get DNA from environment for drug resistance, capsule, etc.

109
Q

Streptococcus Pneumoniae “Pneumococcus”
Mechanism of Disease/Virulence Factors:
Autolysin (LytA):

A

Disrupt cell wall –> release inflammatory contents

110
Q

Streptococcus Pneumoniae “Pneumococcus”
Mechanism of Disease/Virulence Factors:
Lipoproteins:

A

↑↑functions (ex iron uptake)

111
Q

Streptococcus Pneumoniae “Pneumococcus”

Epidemiology/Transmission:

A

↑ in midwinter

  1. S. Pneumoniae = commensal microbiota
  2. Colonizes 60% healthy children, 30% adults
    i. Can be cleared OR progress to disease
    ii. Asymptomatically carried (carriage state)
  3. Primary vector = children, then = 65+
  4. Transmitted by close contact
112
Q

Streptococcus Pneumoniae “Pneumococcus”

Diseases:

A

Colonizes nasal cavity –> disease via direct/heme spread

113
Q

Streptococcus Pneumoniae “Pneumococcus”
Community Acquired Pneumonia (Direct)
Disease:

A
  1. Bacteria avoid structural/chemical respiratory defense –> airway
  2. Replicate in alveoli –> spread of infection –> inflammation
  3. Alveolar damage –> Capillary leakage –> ↑PMNs + complement +
    RBC (iron source for bacteria)
  4. PMNs/complement can’t do anything to bacteria (capsule), but ↑inflam
    ===alveolar filling with inflammatory fluid –> suffocation
114
Q

Streptococcus Pneumoniae “Pneumococcus”
Community Acquired Pneumonia (Direct)
Symptoms:

A

Cough, fever, shaking chills/sweat, SOB, pleuritic pain

  • Crackling sounds; ↑TF
  • Rust colored sputum
  • CXR: multiple/segmental infiltrates in one lobe
115
Q

Streptococcus Pneumoniae “Pneumococcus”
Community Acquired Pneumonia (Direct)
Diagnosis:

A

Sputum Sample

  1. Little saliva (should have ↓squamous epithelium)
  2. Gram stain = gram+, lancet shaped diplococci with ↑PMNs
116
Q

Streptococcus Pneumoniae “Pneumococcus”
Community Acquired Pneumonia (Direct)
Treatment:

A
  1. Outpatient:
    - Abx 1 (no order): macrolide, doxycyclilne, amoxicillin (+/-clav), quinolone
  2. Inpatient - if in doubt hospitalize for initiation therapy
    - Abx 1: penicillin, ampicillin, ceftrixone
    - If no improvement in 48 hrs –> resistance determined
    - ↓Mortality if given B-lactam AND macrolide
117
Q

Streptococcus Pneumoniae “Pneumococcus”
Meningitis (Heme)
Disease:

A

Most common non-endemic cause of meningitis

  1. Most commonly occurs via bacteremia
  2. Evasion of phagocytosis + production of inflammation as described
118
Q

Streptococcus Pneumoniae “Pneumococcus”
Meningitis (Heme)
Symptoms:

A

Headache, stiff neck, photophobia, seizures, coma

(↑Pressure on brain), frontal bulge in infants above fontanel.

119
Q

Streptococcus Pneumoniae “Pneumococcus”
Meningitis (Heme)
Diagnosis:

A

Blood +/- CSF ar tested

120
Q

Streptococcus Pneumoniae “Pneumococcus”
Meningitis (Heme)
Treatment:

A

Abx 1: pencillin/vancomycin or ceftriaxone

121
Q

Streptococcus Pneumoniae “Pneumococcus”
Otitis Media/Sinusitis (Direct)
Disease:

A

Most common middle ear infection

  1. Nasal colonization –> Eustachian tube –> middle ear (neuroaminidase)
  2. Predisposing factors: viral mucosal congestion, pollutants/allergens
122
Q

Streptococcus Pneumoniae “Pneumococcus”
Otitis Media/Sinusitis (Direct)
Diagnosis:

A

Observe tympanic membrane

123
Q

Streptococcus Pneumoniae “Pneumococcus”
Otitis Media/Sinusitis (Direct)
Treatment:

A
  1. Antibiotic 1: Amoxicillin + clavulanic acid

2. Abx 2 (if amox fails): ceftriaxone

124
Q

Streptococcus Pneumoniae “Pneumococcus”
Sepsis (Heme)
Disease:

A
  1. Secondary from primary pneumonia/meningitis

2. Primary cases in immunocompromised pts (asplenia) / recent surgery.

125
Q

Streptococcus Pneumoniae “Pneumococcus”

Quellung Reaction shows?

A

Ab to the polysaccharide capsule

126
Q

Streptococcus Pneumoniae “Pneumococcus”

Predisposing Risk Factors:

A
  1. Asplenia (↓clearance)
  2. Defects in complement/Ab
  3. Diabetes, Chronic Lung disease, CHF, Alcohol
    abuse (bad PMNs)
  4. Prior URI (influenza)
127
Q

Streptococcus Pneumoniae “Pneumococcus”

BAP Culture for S. Pneumococcus

A
  1. α-hemolytic - (partial) destroys hemoglobin (pneumolysin)
  2. Catalase negative
  3. Inhibited by optochin/ehtyl hydrocupreine (used to diff btw S. pneumo vs. S. viridans)
  4. Inhibited by bile salts (deoxycholate)
128
Q

Streptococcus Pneumoniae “Pneumococcus”

Prevention:

A
  1. Pneumovax: vaccine w/23 capsular polysaccharides from 23 common serotypes
  2. Prevnar 13: w/13 common serotypes + diptheria toxin.
129
Q

Atypical Pneumonia:
Chlamydia Pneumoniae: C. Pneumoniae
Microbiology:

A

Chlamydia ~ gram- and inhibited by ampicillin, but
no peptidoglycan wall
- Biphasic lifecycle with 2 distinct forms

130
Q

Atypical Pneumonia:
Chlamydia Pneumoniae: C. Pneumoniae
Biphasic lifecycle with 2 distinct forms

A
  1. Elementary Body (EB) endocytosed into cell –>
    inhibits phagolysosome fusion but metabolically
    inert
  2. EB –> RB (more metabotically active)
  3. RB = obligate intracellular parasite
  4. RB divides –> transforms back to mature EB
  5. Mature EB Released to infect more cells
131
Q

Atypical Pneumonia:
Chlamydia Pneumoniae: C. Pneumoniae
Mechanism of Disease/Virulence Factors

A
  1. Secretes Type Three Secretions (TTS) proteins in

cell cytosol –> inhibit pathways

132
Q

Atypical Pneumonia:
Chlamydia Pneumoniae: C. Pneumoniae
Epidemiology/Transmission:

A
  1. Psittacosis reservoir = birds; spread by
    aerosolization
  2. Pneumoniae reservoir = humans
  3. Trachomatis reservoir = humans; spread by
    contact w/eye secretions
    - Trachoma = leading/preventable cause of blind
    - C. Trachomatis is mostly silent; ↑transmission
    because infected people still have sex
133
Q

Atypical Pneumonia:
Chlamydia Pneumoniae: C. Pneumoniae
Diseases: Pneumoniae

A

Diseases: most have mild disease; some have severe disease
Pneumoniae (6-10% of community acquired pneumonia)
1. Caused by chlamydia pneumoniae (7-21 day incubation)
2. Spread via respiratory route
3. C. pneumoniae + serum lipoprotein –> immune complex –> atherosclerosis –> CAD

134
Q

Atypical Pneumonia:
Chlamydia Pneumoniae: C. Pneumoniae
Disease: Psittacosis (parrot fever)

A
  1. Caused by chlamydia psittaci found in birds

2. Inhaled from dead bird feces –> mild/severe respiratory tract infection

135
Q

Atypical Pneumonia:
Chlamydia Pneumoniae: C. Pneumoniae
Disease: Ocular, Respiratory and Gential Tract Infections

A
  1. Caused by Chlamydia trachomatis (most common STI in industrialized countries) that infect squamocolumnar cells of mucosa
136
Q

Atypical Pneumonia:
Chlamydia Pneumoniae: C. Pneumoniae
Trachoma (Immunotypes A-C)

A

Chronic conjunctivitis –> inflammation + scarring –> inward folding of eyelid –> eyelash scratches conjunctiva + cornea –> blindness.

137
Q

Atypical Pneumonia:
Chlamydia Pneumoniae: C. Pneumoniae
Trachoma Genital Tract Infections (Immunotpes D-K)

A
  • Associated with cervical squamous cell carcinoma

- Neonatal pneumonia/conjunctivitis can occur when child passes through birth canal; give erythromycin and eyedrops

138
Q

Atypical Pneumonia:
Chlamydia Pneumoniae: C. Pneumoniae
Presentation:

A

Incubation 3-4 weeks, gradual onsest

  1. Most infected are asymptomatic/mild respiratory illness
  2. Scant sputum
  3. Prominent cough even with antibiotics
  4. Ronchi, rales, Hoarseness
139
Q

Atypical Pneumonia:
Chlamydia Pneumoniae: C. Pneumoniae
Diagnosis:

A
  1. IgM titer > 1:16
  2. 4-fold IgG↑
  3. PCR testing for C.
    Pneumoniae specific DNA
140
Q

Atypical Pneumonia:
Chlamydia Pneumoniae: C. Pneumoniae
Treatment:

A

60% of cases have mixed infections with other bugs

  1. Doxycycline except in <9 y/o and pregnant women
  2. Alternate: erythromycin or new macrolides
141
Q

Atypical Pneumonia:
Legionellas pneumophilia: Legionnaires
Microbiology:

A
  1. Aerobic, gram- rods, nonencapsulated, facultative

intracellular parasite.

142
Q

Atypical Pneumonia:
Legionellas pneumophilia: Legionnaires
Mechanism of Disease/Virulence Factors:

A
  1. Inhalation –> ingested by alveolar macros
  2. Replicate and avoid phago-lysosome fusion in
    macrophages
  3. Injects bacterial proteins into host cell that alter
    host’s vesicular system –> form specialized
    vesicular system = bacterial ER
  4. Bacterial ER supports replication>
143
Q

Atypical Pneumonia:
Legionellas pneumophilia: Legionnaires
Epidemiology/Transmission:

A
  1. Legionella bacteria in water sources left in heat -
    hot water tanks, air conditioners, etc
  2. Transmission: contaminated mist/vapor
  3. No human-human spread
144
Q

Atypical Pneumonia:
Legionellas pneumophilia: Legionnaires
Diseases:

A

Legionnaires’ Disease = atypical pneumonia

  1. At risk: elderly, immunocompromised, smokers, alcoholics
  2. Males > females
  3. Incubation 2-10 days
145
Q

Atypical Pneumonia:
Legionellas pneumophilia: Legionnaires
Presentation:

A

Legionnaire’s Disease: 2-14 day incubation

  1. High fever, chills, cough, aches (flu-like sypmtoms)
  2. CXR for pneumonia
  3. Milder form: Pontiac Fever
    - Creates flu-like symptoms very acutely (2 days); clears quickly (5 days) without pneumonia
146
Q

Atypical Pneumonia:
Legionellas pneumophilia: Legionnaires
Diagnosis:

A
  1. Most will have diagnosable pneumonia (CXR) b/c replication in macros
  2. Urinary Antigen Test: finds Legionella in urine sample
  3. UAT + pneumonia = Legionnaires’ Disease
  4. Serology
147
Q

Atypical Pneumonia:
Legionellas pneumophilia: Legionnaires
Treatment:

A

Delayed treatment = ↑mortality

  1. Levofloxacin/azithromycin
  2. Newer macrolides
  3. Tracyclines < 12 years; quinolones > 18 years
148
Q

Atypical Pneumonia:
Mycoplasma pneumoniae: M. pneumoniae
Microbiology:

A
  1. Smallest free-living organisms; no cell wall

2. Nutritionally requires cholesterol

149
Q

Atypical Pneumonia:
Mycoplasma pneumoniae: M. pneumoniae
Mechanism of Disease/Virulence Factors:

A
  1. Produces polarized adhesin complex to attach
    lung epithelium
  2. Attaches to surface of respiratory epithelium
  3. Does not enter/penetrate epithelium
  4. Mycoplasma’s diacyl-lipoprotein interacts with
    TLR2 + TLR6 –> inflammation
  5. ↑Macrophage activation clears infection, but also
    causes disease symptoms.
150
Q

Atypical Pneumonia:
Mycoplasma pneumoniae: M. pneumoniae
Epidemiology/Transmission:

A
  1. Frequently found in temperate climates
  2. Late summer/early fall
  3. Frequent in closed populations
151
Q

Atypical Pneumonia:
Mycoplasma pneumoniae: M. pneumoniae
Diseases: Primary Atypical Pneumonia

A
  1. Highest rate of pneumonia 5-20 years old

2. 3 week incubation, compared to influenza (3 days)

152
Q

Atypical Pneumonia:
Mycoplasma pneumoniae: M. pneumoniae
Diseases: Nonspeecific (nongonococcal) urethritis

A
  1. Caused by Ureaplasma urealyticum
153
Q

Atypical Pneumonia:
Mycoplasma pneumoniae: M. pneumoniae
Diseases: Postpartum Fever/Pelvic Inflammatory Disease

A
  1. Caused by M. Hominis
154
Q

Atypical Pneumonia:
Mycoplasma pneumoniae: M. pneumoniae
Presentation:

A

Gradual onset; days –> weeks

  1. Persistent slowly worsening dry cough causing chest tenderness
  2. Fever, malaise, headache, chills, sore throat
155
Q

Atypical Pneumonia:
Mycoplasma pneumoniae: M. pneumoniae
Diagnosis:

A

All non-specific

156
Q

Atypical Pneumonia:
Mycoplasma pneumoniae: M. pneumoniae
Treatment:

A

Antibiotic prophylaxis for immunocompromised patients

157
Q

Atypical Pneumonia:
Mycoplasma pneumoniae: M. pneumoniae
Buzz Words:

A

***Persistent slowly worsening dry cough!

158
Q

Opportunistic Pneumonia:
Acinetobacter baumannii: A baumannii
Microbiology:

A

Opportunistic pathogen
- A. baumannii = gram-, aerobic, pleomorphic bacillus found in hospital environments
- Cultured from respiratory secretions, wounds, urine
(colonizations, not infections)
- Nosocomial b/c baumannii = water organism
colonizes in H2O (IV/irrigating solutions)

159
Q

Opportunistic Pneumonia:
Acinetobacter baumannii: A baumannii
Mechanism of disease/Virulence Factors:

A
  • A. baumannii causes apoptosis/cell death in
    laryngeal epithelium via OMP38
  • OMP38: outer membrane protein that releases
    cytochrome C + apoptosis inducing factor
  • Additional virulence factors:
    i. Acquired antibiotic resistant genes
    ii.Efflux pumps preventing antibiotics
    iii.Integrons with multiple resistant determinants
160
Q

Opportunistic Pneumonia:
Acinetobacter baumannii: A baumannii
Epidemiology/Transmission:

A

Hospital acq > Community acq
1. A baumannii in soil and water
2. Community acquired A baumannii pneumonia in
southeast Asia + Australia

161
Q

Opportunistic Pneumonia:
Acinetobacter baumannii: A baumannii
Diseases:

A

Commonly in susceptible patients (“opportunistic”); in hospital setting think “4 Ws”

  1. Pneumonia (Wind = ventilators)
  2. Blood Infection/meningitis (Wire = blood/IV)
  3. Urinary Tract Infection (Water = urinary catheter)
  4. Skin wounds (Wounds = skin infection)
162
Q

Opportunistic Pneumonia:
Acinetobacter baumannii: A baumannii
Presentation:

A
  1. Fever (bacterial infection)
  2. Inflamed (red, swollen, warm, painful) skin wounds
  3. Orange, bumpy skin lesions
  4. Cough, chest pain, dyspnea (pneumonia)
  5. Burning urination (UTI)
  6. Sleepiness, headache, stiff neck
163
Q

Opportunistic Pneumonia:
Acinetobacter baumannii: A baumannii
Diagnosis:

A

Culture blood, urine, tissue for A. Baumannii

  1. CXR - pneumonia
  2. Lumbar puncture - meningitis
164
Q

Opportunistic Pneumonia:
Acinetobacter baumannii: A baumannii
Treatment:

A

A. baumannii inherently resistant to multiple antibiotics; colonization is not treated; infection is!

165
Q

Opportunistic Pneumonia:
Acinetobacter baumannii: A baumannii
Rx that +/- work:

A
  1. Meropenem (ultra broad)
  2. Polymyxin B + E(Colistin)
  3. Amikacin (xprot translation)
  4. Rifampin (xDNA synth)
  5. Minocycline/tigecycline
166
Q

Actinomycosis: Actinomyces israelii Complex

Buzz Words

A
  • Sinus Tract
  • Painless abscess
  • Sulfur Granules
  • Dental Procedures
167
Q

Actinomycosis: Actinomyces israelii Complex
Microbiology:

A
  1. Gram+ bacilli with branching beaded (coccobacilary) filaments (hyphae)
  2. Non-spore, non acid-fast, anaerobic
  3. Normal flora of mouth + GI tract
168
Q

Actinomycosis: Actinomyces israelii Complex

Mechanism of Disease/Virulence Factors:

A
  1. Opportunistic pathogen –> chronic disease
  2. Endogenous bacterium that attacks when mucosa is disrupted (dental plaque, tonsillar crypts, infection, trauma surgery)
  3. Post-injury environment has ↓O2 = ↑growth
169
Q

Actinomycosis: Actinomyces israelii Complex

Epidemiology/Transmission:

A

Endogenous source (normal flora)

170
Q

Actinomycosis: Actinomyces israelii Complex
Diseases:

A
  • Post-injury, endogenous bacteria burrow sinus tract to skin/mucosa
  • Eroding abscesses formed after mucous membrane damage (mouth/GI)
  • Abscess = sulfur granules of solidified yellow mycelial masses
171
Q

Actinomycosis: Actinomyces israelii Complex

Types based on structural location:

A

i. Pulmonary Actinomycosis

ii. Cervico-facial (Jaw/Face) Actinomycosis (lumpy jaw)

172
Q

Actinomycosis: Actinomyces israelii Complex
Presentation:

A

Slow-infection (chronic disease)

  1. Chest pain with deep breath + SOB
  2. Sputum producing cough
  3. Lethargy, night sweats, weight loss
173
Q

Actinomycosis: Actinomyces israelii Complex
Diagnosis:

A

Aspiration material w/ sulfur granules

- Grow granules for gram stain, IF stain histopathology

174
Q

Actinomycosis: Actinomyces israelii Complex
Treatment:

A

IV penicillin (4-6 wks) –> oral penicillin (several months).

175
Q 
Fungal Respiratory Infections
Systemic Mycosees (DIMORPHIC)
A
  1. Histoplasma capsulatum:
  2. Blastomyces Dermatidis:
  3. Coccidiodes immitis:
176
Q

Fungal Respiratory Infections
Systemic Mycosees (DIMORPHIC)
Histoplasma capsulatum:
Microbiology:

A

Dimorphic w/distinct tuberculate (bumpy) conida
- Mold in soil w/bird or bat excrement in Ohio River
Valley + Central America
- Yeast targets RES system

177
Q

Fungal Respiratory Infections
Systemic Mycosees (DIMORPHIC)
Blastomyces Dermatidis:
Microbiology:

A

Like histo but does not survive in macros

  • Mid-South endemic > south east > mid-west
  • Middle age older men.
178
Q

Fungal Respiratory Infections
Systemic Mycosees (DIMORPHIC)
Coccidiodes immitis:
Microbiology:

A

Tissue form: spherule

  • Very contagious; considered bioweapon
  • Endemic to semi-erid Southwest USA
179
Q

Fungal Respiratory Infections

Opportunistic Mycosees:

A
  1. Aspergillus spp.:
  2. Zygomycetes (Mucormycosis):
  3. Pneumocystis Jerovici(Carnii):
180
Q

Fungal Respiratory Infections
Opportunistic Mycosees:
Aspergillus spp.:
Microbiology:

A

Aspergillus spp.: 45° branch septate hyphae
- Nosocomial infections (hospital air ducts) in
immunocompromised patients

181
Q

Fungal Respiratory Infections
Opportunistic Mycosees:
Zygomycetes (Mucormycosis):
Microbiology:

A

90° broad septate; ↑ post-soil disturbance (tornado)

182
Q

Fungal Respiratory Infections
Opportunistic Mycosees:
Pneumocystis Jerovici(Carnii):
Microbiology:

A

Not cultured
- fungal + protozoan traits –> thin cysts with sporozoites (no hyphae, cholesterol in membrane >
ergesterol)

183
Q

Fungal Respiratory Infections
Systemic Mycosees (DIMORPHIC)
Diseases: Damage

A

Our immune response to phago-resistant fungi

184
Q

Fungal Respiratory Infections
Systemic Mycosees (DIMORPHIC)
H. Capsulatum disease

A

Histoplasmosis

i. No symptoms > mild flu > pneumo
ii. Immunocompromised/infants have ↑Risk

185
Q

Fungal Respiratory Infections
Systemic Mycosees (DIMORPHIC)
B. Dermatitidis disease

A

Blastomycosis

iii. Acute pneumo (Brown, purulent / bloody sputum) + wart-like skin lesions > meningitis
iv. Looks like TB / Cancer b/c lung masses develop

186
Q

Fungal Respiratory Infections
Systemic Mycosees (DIMORPHIC)
C. Immitis disease

A

Coccidiodomycosis (Valley fever - San Joaquin, CA)

i. None > Flu > skin lesions > meningitis
ii. Men, dark skinned, immunocompromised ↑risk for dissemination.

187
Q

Fungal Respiratory Infections
Systemic Mycosees (DIMORPHIC)
H. Capsulatum, B. Dermatitidis, C. Immitis:
Treatment:

A

None > azole > amphotercin B

188
Q

Fungal Respiratory Infections
Opportunistic Mycosees:
Diseases: Damage

A

Our immune response to phago-resistant fungi

189
Q

Fungal Respiratory Infections
Opportunistic Mycosees:
A. spp. disease

A

Aspergillosis

i. pervious respiratory disorders; aspergilloma @ pre-existing lesion.

190
Q

Fungal Respiratory Infections
Opportunistic Mycosees:
Zygomycetes spp. diseases

A

Mucormycosis/Zygomycosis

i. Acidosis (diabetes) pts or corticosteroids pts
ii. Presents as pneumonia or rhinocerebral form (causes rapid death).

191
Q

Fungal Respiratory Infections
Opportunistic Mycosees:
P. Jerovici (Carinii) disease

A 
Pneumocystis pneumonia (PcP)
i. Looks like diffuse interstitial pneumonia; death from asphyxia
192
Q

Fungal Respiratory Infections
Opportunistic Mycosees:
A. spp., Zygomycetes spp., P. Jerovici (Carinii):
Treatment:

A
  1. Asp./Zyg. = amphotercin B + excision

2. Pneumocystosis = O2 + trimethorpim-sulfa-methoxazole

193
Q

Influenza Viruses

Microbiology:

A
  1. Enveloped, segmented ss-negative RNA
  2. Three types (A, B, C); A based on hemagglutinin
    (HA) and nueraminidase (NA)
194
Q

Influenza Viruses
Mechanism of Disease/Virulence Factors:
Surface proteins:

A
  • HA: virion attachment/entry; antigenic domain +
    receptor binding sites; ↑AA substitution
  • NA: virion release; inhibit NA to prevent spread
  • M2 (influenza A only): ion channel involved in
    uncoating virus; target of aman-/rimantadine
  • NS1: IFN antagonist; ↓host mRNA processing
195
Q

Influenza Viruses
Mechanism of Disease/Virulence Factors:
Genome:

A
  • A/B have 8 segments (C=7, no NA gene)
  • Ressortment of genes btw co-infected human and
    animal influenza –> new strain
196
Q

Influenza Viruses

Epidemiology/Transmission:

A
  1. Transmission: human airborne droplets
    (coughing, sneezing, talking + on surfaces)
  2. Influenza A Reservoir = avian, human, swine
    - Avian: virus grows in resp/GI; found in feces
    - Avian reservoir important b/c allows ressortment
    and extra-human reservoir
  3. B/C reservoir = mainly human
  4. ↑Antigenic Drift: minor point mutations in HA +
    NA during viral replication from ↑immunity
  5. ↑Antigenic Shift: major changes in HA/NA during
    ressortment –> pandemic b/c new strain from
    ressortment = ZERO IMMUNITY
  6. Seasonality (Influenza A + B): winter/spring
197
Q

Influenza Viruses

Diseases:

A 
The Flu (contagious respiratory illness caused by influenza)
Lower respiratory complications cause most deaths.
198
Q

Influenza Viruses

Complications:

A
  1. Pneumonia:
    i. Primary Viral: abrupt onset, deterioration in 1-4 days
    ii. Secondary Bacterial (superfinection): bacterial infection during viral recovery (viral-bacterial pneumo) or after recovery (post-influenza bacterial pneumo)x
  2. Pregnancy: cause fetal loss + congenital malformation (2-3rd trimester)
  3. ↑Time for shedding in elderly and immunocompromised
  4. Children are at risk (↓immunity) for pneumo, meningitis, encephalitis
    * **Acetaminophen for fever in children; aspirin –> Reye’s (head/liver)
199
Q

Influenza Viruses

Presentation:

A

Upper and lower respiratory tracts infected

  1. Flu like symptoms: fever, chills, headache, fatigue, myalgia, runny nose, sore throat, and dry cough
  2. Short incubation (2 days) - rapid onset
  3. Systemic symptoms (fever, etc) go away, but respiratory persist
  4. If pneumonia arises, hemoptysis and SOB
200
Q

Influenza Viruses

Diagnosis:

A
  1. Swab nasopharynx for rapid antigen detection (immunoassay)
    - Titers peak at 48 hours (before symptoms, bad for spread of virus)
    - No ↑Neutrophils or peripheral white cells = VIRAL
  2. RT PCR
    * **Rule out bacterial cause; bacteria will have productive cough with ↑neutrophils and positive pneumococcal culture
201
Q

Influenza Viruses

Treatment:

A

Vaccination is most important to ↓morbidity/mortality

  1. Amantadine/Rimantidine: inhibit M2 ion channel (effective in Infl. A)
  2. Zanamivir/Oseltamivir: NA inhibitors; prevent viral release/spread (A/B)
202
Q

Influenza Viruses

Structure: HA

A

Binds host sialic acid, also on RBC so causes agglutination; Sialic acid receptors in respiratory tract allow viral entry.

203
Q

Influenza Viruses

Structure: NA

A

Cleaves neuraminic acid (mucin barrier) exposing sialic acid for HA binding; on release it cleaves HA-sialic acid

204
Q

Influenza Viruses

Structure: M2

A

Channel allows H+ into endosome; ↓pH = dissociation of viral protein.

205
Q

Hantavirus Pulmonary Syndrome (HPS)

Microbiology:

A

Hantavirus (Bunyviridae Family)
Spherical, lipid-enveloped particles
Trisegmented, -RNA genome

206
Q

Hantavirus Pulmonary Syndrome (HPS)

Mechanism of Disease/Virulence Factors:

A
  • Segment: nucleocapsid protein
  • Segment: RNA-dep RNA polymerase
  • Segment: G1/G2 envelope proteins
207
Q

Hantavirus Pulmonary Syndrome (HPS)

Epidemiology/Transmission:

A

“Airborne Infectious Disease”
1. infection from breathing air containing aerosolized rodent saliva, urine, feces.
2. Rural USA (farms, fields, forests)
3. Several hantaviruses can cause HPS; each virus
is carried by specific rodent
- Ex: Si Nombre in Deer Mouse only
4. No human-human

208
Q

Hantavirus Pulmonary Syndrome (HPS)

Diseases:

A

HPS = severe, sometimes fatal respiratory disease

  1. Inhaled rodent saliva/urine/feces
  2. Viral load recruits lymphoblasts + macros to pulmonary tissue
  3. Activated immune cells –> ↑cytokine release
  4. Endothelium is activated
  5. ↑Capillary permeability –> pulmonary edema
209
Q

Hantavirus Pulmonary Syndrome (HPS)

Presentation:

A

Flu like symptoms –> life-threatening pneumonia
Two Stages of Disease:
1. Rapid Onset of Pulmonary Edema
- ↑Viremia at onset of disease
- Flu-like symptoms
2. Respiratory Failure + Cardiogenic Shock
- Cough, SOB, fluid accumulation, ↓BP, cardiogenic shock

210
Q

Hantavirus Pulmonary Syndrome (HPS)

Diagnosis:

A

Early phase is often confused with influenza virus
Rural rodent exposure is key + tetrad
1. Thrombocytopenia
2. Leukocytosis (left shift)
3. Abnormal lymphoblasts
4. ↑HCT b/c of ultrafiltration into lungs
5. Serological testing (IgM + IgG) or RT-PCR will work

211
Q

Hantavirus Pulmonary Syndrome (HPS)

Treatment:

A

No treatment, cure, vaccine; supportive care

  1. Even though hypotensive, no additional volume!
  2. ↑B1-adrenergic cardiostimulation for ↑BP
212
Q

Respiratory Syncytial Virus (RSV),
Human Metapneumovirus (hMPV), and
Human Parainfluenzaviruses 1-4 (hPIVs)
Disease:

A

Viral pathogens of young children&raquo_space; elderly/immunocompromised

213
Q

Respiratory Syncytial Virus (RSV),
Human Metapneumovirus (hMPV), and
Human Parainfluenzaviruses 1-4 (hPIVs)
Microbiology: (for all three)

A
  1. Enveloped, non-segmented (no ressortment),
    negative-RNA
  2. Tropism restricts entry to ↑/↓resp tract cells, thus
    no systemic infections
214
Q

Respiratory Syncytial Virus (RSV),
Human Metapneumovirus (hMPV), and
Human Parainfluenzaviruses 1-4 (hPIVs)
Virulence Factors:

A
  1. Fusion Protein(F): viral entry/fusion to adjacent
    cells –> syncytia
  2. G: unknown gp where RSV binds; RSV can also
    bind nuclein
  3. HN (HA-NA): hMNV + hPIV bind here
215
Q

Respiratory Syncytial Virus (RSV),
Human Metapneumovirus (hMPV), and
Human Parainfluenzaviruses 1-4 (hPIVs)
Mechanism of Disease

A
  • Virus infect airway epithelium in ↑resp tract –> ↓resp tract via dendritic cells
  • Cause airway inflammation, necrosis, sloughing of
    epithelium, excessive mucin production, and interstitial lung infiltrates
216
Q

Respiratory Syncytial Virus (RSV),
Human Metapneumovirus (hMPV), and
Human Parainfluenzaviruses 1-4 (hPIVs)
Epidemiology/Transmission:

A
  1. RSV: #1 cause of ↓RT illness/pneumo in kids
  2. hMPV: #2 cause of ↓resp tract illness in kids
  3. hPIV3: #2 cause of pneumonia in kids
    - hPIV common in elderly/immunocompromised
  4. All transmit person-person via large droplets
    - Very seasonal: fall/spring****
    - Community emergence; not widespread (flu)
217
Q

Respiratory Syncytial Virus (RSV)

Diseases:

A

RSV #1 cause of bronchiolotis + pneumonia < 1 y/o infant

  1. RSV infects Nasopharnx –> LRT
  2. LRT infection can be permanent (chronic lung disease or asthma)
  3. Predisposing factors: Prematurity, early infection (<3 month old), lung/heart disease, SCID, ↓Oxygen supply
    * **RSV infections in adults are also common, just known for infants
218
Q

Respiratory Syncytial Virus (RSV)

Presentation:

A

Begins with URT symptoms –> LRT symptoms in 2 days

219
Q

Respiratory Syncytial Virus (RSV)

Diagnosis:

A

Culture from URT, ELISA for antigen, RT-PCR

220
Q

Respiratory Syncytial Virus (RSV)

Treatment:

A

No vaccine, care is supportive (↑FiO2, fluids, bronchodilator)

  1. Palvizumab: Ab for RSV (↓viral load ≠ severity)
  2. Ribavirin: nucleoside analog interferes w/viral replication
221
Q 
Human Metapneumovirus (hMPV)
Diseases:
A

Bronchiolitis +/- pneumonia in infants/elderly

222
Q 
Human Metapneumovirus (hMPV)
Presentation:
A

Similar to RSV, may also see myalgia

223
Q 
Human Metapneumovirus (hMPV)
Diagnosis:
A

RT-PCR is best (serological is bad- most children are + by 10)

224
Q 
Human Metapneumovirus (hMPV)
Treatment:
A

No vaccine, supportive care

225
Q

Respiratory Syncytial Virus (RSV),
Human Metapneumovirus (hMPV), and
Human Parainfluenzaviruses 1-4 (hPIVs)
Take Home Messages:

A

These viruses are ID by:
AGE OF PATIENT (kids)
SEASONALITY (late fall/early spring)

226
Q

Human Parainfluenzaviruses 1-4 (hPIVs)

Diseases:

A

hPIV3 #2 cause of pneumonia + bronchiolitis in children

227
Q

Human Parainfluenzaviruses 1-4 (hPIVs)

Presentation:

A

Croup, hoarseness, systemic symptoms

228
Q

Human Parainfluenzaviruses 1-4 (hPIVs)

Diagnosis:

A

Culture, RT-PCR, ELISA OR ↑IgG/IgM

229
Q

Human Parainfluenzaviruses 1-4 (hPIVs)

Treatment:

A

No vaccine, supportive care

230
Q

Adenovirus (AdV)

Microbiology:

A
  1. DS-linear-DNA in icosahedral capsid w/out an
    envelope (nake nucleocapsid)
  2. Viral genome/particles assembled in nuclei
  3. Naked = stable against detergents, GI tract (↓pH),
    and alcohol; survive outside body
231
Q

Adenovirus (AdV)

Mechanism of Disease/Virulence Factors:

A
  1. Serotype defined by capsid penton protein
    - Attachment proteins
    - Resposnible for toxic effect
    - Penton-specific Abs = life long immunity against
    that serotype
  2. AdV hexon proteins (capsid) stimulate
    complement-fixing Abs
    - Do not confer immunity, but useful testing
232
Q

Adenovirus (AdV)

Epidemiology/Transmission:

A
  1. Transmission: inhalation of water droplets
    - Fecal oral route or direct inoculation
  2. Common in Kids = respiratory infections
  3. Military recruits = ARD
  4. Eye infections = swimming pools
  5. Endemic infections = late winter/early spring
233
Q

Adenovirus (AdV)

Diseases:

A

AdV leads to several disease from pharynx, conjunctiva, GI in children!

  • May have link to obesity?
    1. AdV replicates in oropharynx, conjunctivae, or intestine
    2. AdV induces immune response –> Cell necrosis + inflammation (acute phase)
    3. AdV may persist, spread (viremia), or become latent in tonsils, ADENOids, or Peyer’s Patches (shedding 6-18 months)
234
Q

Adenovirus (AdV)

Subsequent infections are serotype specific:

A
  • Serotypes 4 + 7 = ARD (military recruits)
  • Serotypes 40-41 = GI tract infections in kids
  • Serotypes 36+37 = obesity?
235
Q

Adenovirus (AdV)

Presentation:

A
  1. Respiratory (pharynx): cough, fever, sore throat
  2. Ocular: “sand in eye” , runny nose
  3. GI: diarrhea, vomiting
236
Q

Adenovirus (AdV)

Diagnosis:

A
  1. Culture form throat/eye/excrement for cytopathic effect in culture
  2. Penton-specific Abs
  3. Hemagglutination inhibition assays (HIA) b/c Abs to penton block penton’s ability to clump RBCs
  4. Hexon Abs confirm presence of AdV but not serotype
  5. B/c AdV persists, presence does not mean it is responsible for current symptoms; need 4x higher titer in convalescent
237
Q

Adenovirus (AdV)

Treatment:

A

No virus specific therapy

  1. Military receives attenuated, live vaccine where AdV-associated acute respiratory disease (serotype 4+7) occurs
  2. Encapsulated serotypes 4+7 are released enterically for minor infection to develop immunity
238
Q

Coranovirus

Microbiology:

A
  1. Enveloped, ss RNA+ genome virus
  2. RNA+ are like post-transcriptional eukaryotic
    mRNA (5’-methyl cap, polyA 3‘tail)
  3. No polymerase; uses host
239
Q

Coranovirus
Mechanism of Disease/Virulence Factors:
1. S (Spike protein):

A

Allows binding of CoV and fusion of viral membrane with host for entry

240
Q

Coranovirus
Mechanism of Disease/Virulence Factors:
2. HE (Hemagg-esterase):

A

Virus entry/exit

241
Q

Coranovirus
Mechanism of Disease/Virulence Factors:
3. E (Envelope protein):

A

Integral protein in viral membrane involved in morphogenesis, assembly, budding + ion channel activity used in viral replication

242
Q

Coranovirus
Mechanism of Disease/Virulence Factors:
4. M (Membrane protein):

A

Budding/envelope

243
Q

Coranovirus
Mechanism of Disease/Virulence Factors:
5. N (Nucleocapsid):

A

Binds viral genome + M protein for virion assembly and budding

244
Q

Coranovirus
Mechanism of Disease/Virulence Factors:
6. RdRp

A

(RNA-dep-RNA polymerase)

245
Q

Coranovirus
Mechanism of Disease/Virulence Factors:
7. PLprox + 3CLpro:

A

Cleave polyprotein virus

246
Q

Coranovirus

Epidemiology/Transmission:

A
  1. Transmission: HCoVs spread amongst pple
    - via airborne droplets w/cough, talk, or sneeze
    - Direct contact w/contaminated surfaces
    - SARS-CoV = mutated virus from bats that crossed
    species to humans
  2. Epidemiology
    - Children/winter infections w/HCoV common
247
Q

Coranovirus

Diseases:

A

Harmless “common cold” CoV becomes SARS!
Common Cold: CoV cause mild URI
Croup: CoV causes croup in young children
Pneumonia: uncommonly CoV can infect lower lung in elderly/children

248
Q

Coranovirus

SARS:

A

Severe lower resp infections –> pneumonia

  1. SARS-CoV infects Type II Pneumocytes –> diffuse alveolar damage
  2. Alveolar damage –> respiratory failure –> ARDS
249
Q

Coranovirus
SARS
Presentation:

A
  1. Cold symptoms > GI symptoms&raquo_space;> Neurosymptoms (rare)

2. SARS: 2-10 incubation –> fever –> flu-like symptoms –> respiratory symptoms + GI symptoms –> respiratory failure

250
Q

Coranovirus
SARS
Diagnosis:

A
  1. Common Cold: undiagnosed / self-limiting; RT-PCR for viral genome
  2. SARS: recent travel to China, Taiwan
251
Q

Coranovirus

Treatment:

A

No treatment of HCoVs
SARS:
1. Ventilatory support +/- anti-microbials for secondary infections

252
Q

Coranovirus

Replication:

A
  1. Virus enters and uncoats
  2. +RNA genome is translated –> RdRp (further genome replication)
  3. -RNA strands synthesized
  4. -RNA strands serve as template for more +RNA progeny genome and mRNAs for translation
  5. mRNAs translated –> nonreplication machinery polyproteins
  6. RdRp does not proofread = variety of CoV genomes
253
Q

Rhinovirus

Microbiology:

A
  1. Non-enveloped, +RNA virus
  2. No envelope = survive on surfaces outside body
    on surfaces
  3. But, Cannot survive outside nasopharynx b/c
    ↑ temp in lower resp/GI and ↓ pH in stomach
254
Q

Rhinovirus

Mechanism of Disease/Virulence Factors:

A
  1. RV serotypes based on receptor specificity:
    - ICAM-1
    - LDL-R
    - Sialoprotein Receptors
  2. 100 serotypes = no developed immunity
  3. Has Viral Protease that cleaves cap-binding
    complex of euk cells = shut off protein synthesis
  4. But, can still replicate using host machinery via
    IRES (internal ribosomal entry site) allowing
    selective translation of viral proteins
255
Q

Rhinovirus

Diseases:

A

RV most frequent cause of common cold (acute respiratory tract infection)

256
Q

Rhinovirus

Presentation:

A
  1. Infection by RV in nose –> 12-72 hr incubation while viral protease promotes viral protein synthesis in nasal cells –> viral inflammation
  2. Local nasal inflammatory response to virus responsible for symptoms:
    - Nasal discharge
    - Sneezing
    - Obstruction
    - Throat infection
  3. Other complaints: loss of smell and taste, cough, hoarse voice
  4. Even with sore throat, no sign of pharyngitis (exudate, erythema)
257
Q

Rhinovirus

Diagnosis:

A

Based upon symptoms

  • **If fever / systemic symptoms are present –> alternative bug!
  • **If erythema, edema, exudate appears in pharynx –> other bug!
  • **Conjunctivitis/nasal polyps –> adenovirus
258
Q

Rhinovirus

Treatment:

A
  1. Self-limiting; treat symptoms and limit contact

2. B/c of 100+ serotypes = no vaccine happening

259
Q

Rhinovirus

Epidemiology/Transmission:

A
  1. ↑ incidence in fall and spring
  2. Independent of exposure to cold, Δtemp, etc
  3. Transmission: exposure to infected respiratory secretions via inhaled particle
    - Direct contact w/doors etc
  4. Other viruses cause common cold, but w/
    ↑ nasopharyngitis and ↑ serious lung infection

Pulmonary (9 decks)

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