L23 Pneumonia in immunocompromised patients

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jknell
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200947
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L23 Pneumonia in immunocompromised patients
Updated:
2013-02-16 17:30:03
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Pulmonary II
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Pneumonia, immunocompromised
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  1. Immunocompromised hosts
    General principles
    -Can get pneumonia from "normal" pathogens: CAP, atypical, aspiration, nosocomial...

    • Predisposed to severe infections with "normal":
    • -lack of Ig: encapsulated organisms
    • -complement deficiency: Neisseria species

    • Opportunistic: organisms don't usually infect people with intact immune system
    • -Disease is quicker, more severe
    • -emperic treatment often needed

    • Common immunodeficiencies:
    • -Granulocytopenia
    • -T cell dysfunction
    • -Chemotherapy and steroids
    • -Injuries to mucosal barriers
  2. Pneumonia
    agranulocytosis or Ig deficiency
    • Presentation: (acute)
    • -fever
    • -hypotension
    • -infiltrates on CxR
  3. Pneumonia
    T cell defects
    • Presentation: slower progression (over days)
    • -progressive cough
    • -fever (later)
    • -SOB (later)
    • -extrapulmonary manifestations
  4. Pneumonia
    Major pathogens in immunocompromised
    • Pneumocystis
    • Cryptococcus
    • Aspergillus
    • Viruses
  5. Pneumocystis
    History, pathophys, epidemiology
    • History:
    • -pre 1988, very few cases
    • -HIV (pre-HART): most common CAP leading to admission; "Pneumocystis carinii = PCP"
    • -P. carinii found to only infect cats; Pneumocystis jirovecii is human pathogen (still called PCP)
    • -Now, infrequent (due to antiretrovirals and prophylaxis)

    • EM:
    • -No reliable in vitro culture system
    • -Major surface gycoprotein (MSG) undergoes antigenic variation to evade host immunity
    • -MSG may also inhibit surfactant production
    • -multiple strainss exist

    • Pathogenesis:
    • -airborne transmission
    • -trophic form attaches to type 1 pneumocytes
    • -organism can lay dormant for years without causing overt disease
    • -CD4 cells play central role in host defense (macrophages and Abs play small role)
    • -Organism proliferates, fills alveolar space (foamy eosinophilic exudate)

    • Epidemiology:
    • -initially thought to be reactivation: children generally have + antibodies by age 4
    • -Reinfection also occurs
    • -AIDs infection corolates with CD4 count <200 cells/mm3

  6. Pneumocystis
    Presentation, labs, dx, Tx
    • Clinical presentation:
    • -Slowly progressive cough and fever
    • -sputum production in 30%
    • -Exam may be normal
    • -CxR: diffuse interstitial infiltrates:
    • Labs:
    • -CD4 count <200
    • -LDH elevated (high LDH is a poor prognostic sign)
    • -PO2 and PCO2 decreased

    • Dx
    • -induces sputum (or bronchoalveolar lavage - no longer needed)
    • -Sputum cytology:
    • -Bx and staining, less frequently done

    • -Lung biopsy with silver stain
    • -New tests: PCR, plasma S-adenosylmethionine

    • Tx:
    • -IV treatment for serious illness:
    • **TMP/SMP is mainstay treatment
    • -Pentamidine
    • -Clindamycin + Primaquine
    • -Steroids if pO2 <70
    • -PO tx for mild-moderate disease:
    • **TMP/Sulfa
    • -Clindamycin + primaquine

    Mortality: depends on pO2 and stage of illness
  7. Cryptococcus
    yeast
    Pathogen, epidemiology, pathogenesis
    • Pathogen:
    • -round, encapsulated yeast
    • -reproduction: simple, narrow-based budding
    • -Serotypes:
    • -C. neoformans
    • -C. gattii
    • -Can culture from blood on solid media (48-72h):
    • -produce urease
    • -Makes black pigment (melanin) on niger seed agar

    • C. neoformans: (serotypes A, D, and AD)
    • -soil rich in bird droppings (pigeons)

    • C. gattii: (serotypes B and C)
    • -eucalyptus trees

    • Epidemiolgy:
    • -normal host: usually asymptomatic
    • -most children have Ab before age 10
    • -Immunocompromised: serious, progressive and disseminated disease
    • -Dogs and cats also infected

    • Pathogenesis:
    • -Polysaccharide capsule upregulates in vivo
    • Function:
    • 1. inhibits phagocytosis
    • 2. depletes complement
    • 3. inhibits antibody formation
    • 4. dysregulated cytokines
    • 5. interferes with antigen presentation
    • -Melanin is also a virulence factor: antioxidant

    • -Grows well at body temp; inhibited growth at higher temps
    • -Macrophages and CMI important in limiting growth
    • -Pathology variable (depending on host): absense of inflammatory rxn --> intense granulomatous inflammation
  8. Cryptococcus
    Presentation, dx, Tx
    • Presentation:
    • -ranges from asymptomatic to severe cough, SOB and chest pain
    • -not much fever
    • -Nl host: nodular infiltrates, nodules later calcify
    • -Mass like lesions, hilar adenopathy, cavitation
    • -Disseminates to CNS, bond, skin, prostate, eye

    • CxR:
    • Dx:
    • -Stains (India Ink, H&E, GMS)
    • -Culture from sputum or BAL
    • -Serology: Cryptococcal antigen

    • Tx:
    • -Isolated pulmonary infection: fluconazole
    • -CNS: Amphotericin + 5FC
  9. Invasive mold infections
    • -Common in pts with AML, BMT
    • -Severe neutropenia present in 96% of cases before onset

    • Aspergillus is most common; others
    • -Scedosporium
    • -Mucorales (zygomycetes) - diabetes pts
    • -Dematiaceous fungi
    • -Fusarium

    • Epidemiology:
    • -Incidence varies by location, 1-13% per year
    • Risk factors:
    • -Iron overload, multiple blood transfusions (Macrophages busy consuming iron)
    • -CMV infection
    • -Graft vs Host disease

    • Immune response: need both to contain infection
    • -Macrophages (and polys) - steroids inhibit macrophages
    • -Th1 cells

    • Pathology:
    • -Tissue invasion, vessels... leading to infarct
    • -Hematogenous spread
  10. Invasive mold infections
    presentation, Dx, Tx
    • Clinical presentation:
    • -progressive dry cough
    • -dyspnea
    • -pleuritic chest pain
    • -fever (despite broad coverage with Abx)
    • -pulmonary infiltrates:

    • Dx:
    • -Biopsy and culture, but biopsy often difficult
    • -Galactomannan testing for Aspergillus from serum (sensitivity 71%, specificity89%) or BAL (sensitivity 58%, specificity 96%)
    • -1,3‐beta‐D‐glucan is common in cell wall of many molds, but not specific
    • CT: suggestive of IMI, but should be confirmed with CT guided biopsy
    • -Nodules 1 cm or greater
    • -Halo sign (aspergillus) (top) or reverse halo sign (mucorales)
    • -Air crescent sign (bottom)
    • -Cavities

    • Tx:
    • -Mortality high
    • -Prophylaxis now standard

    • Etiologic diagnosis important:
    • –Aspergillus:  Voriconazole,  Amphotericin, Echinocandins
    • –Mucorales:  Amphotericin, Posaconazole
    • –Scedosporium:  Voriconazole for apiospermum, prolificans resistant to all
  11. Aspergillus
    • -Causes allergic reaction in the airways (Allergic Bronchopulmonary Aspergillosis - ABPA)
    • -Causes cavitary and disseminated disease
    • -Most infectious is A. fumigatus
    • -Septate hyphae with branching at acute angles, distinguished by their "fruiting heads":
  12. Cytomegalovirus 
    CMV
    • -Often present in immunosuppressed (but not always causing disease)
    • -30-50% of adults have CMV antibody; CMV persists in latent state
    • -In HIV, can be recovered from lung, not usually alone: Tx not indicated
    • -Transplant: CMV has predilection for the organ transplanted
  13. CMV Pneumonitis
    • lung transplant patients:
    • -disease in first 3 months after transplant (if not on prophylaxis); or 3 months following cessation of prophylaxis
    • -may mimic rejection
    • -increases the risk for rejection

    • Primary: seronegative recipient given seropositive donor
    • -disease from primary is worse than reactivation
    • -involves multi organ systems

    • Radiograph: patchy or diffuse ground glass opacities, patchy consolidations, small nodular opacities
    • -less common: thickened bronchovascular bundles, tree-in-bud airway pattern, reticular opacities, small pleural effusions

    • Dx: tests detect viral replication/antigens
    • -Viral load assay of blood or BAL
    • -CMV pp65 antigenemia
    • -Shell-vial cultures

    • Histopathology is the gold standard:

    • Tx:
    • -IV ganciclovir
    • -Oral valganciclovir
    • -Foscarnet for ganciclovir resistance

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