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Pulmonary Week 4 > Immunocompromised Host Pulmonary Infections > Flashcards

Immunocompromised Host Pulmonary Infections Flashcards

1
Q

what are the basic principles involved with immunocompromised patients?

A
  1. may be unable to tell you they are sick and they feel fine because their immune system isn’t strong enough to mount a response
  2. often have more extensive disease than is apparent
  3. may require longer treatment than individuals with a “normal” immune system
  4. acquire infections with organisms that usually are not pathogens, “environmentals” or “comensals”
  5. the type of organism causing the infections correlates with the type of immunodeficiency (not all immunodeficiencies are equal)
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2
Q

what are the common features of lung infections in immunocompromised individuals?

A
  1. abnormal frequency of infections

recurrent pneumonia in HIV and diabetics

  1. abnormal/severe presentation of infections

pneumococcal septic shock in splenectomized patients, disseminated histoplasmosis in HIV patients, fulminant acute pulmonary aspergillosis in stem cell transplant

  1. unusual infections
    - Pneumocystis jiroveci
    - Burkholderia cepacia
    - Nontuberculous mycobacteria
    - Aspergillus
    - Nocardia
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3
Q

35 y/o man with AML (acute myeloid leukemia) had induction chemotherapy and total body radiation in preparation for stem cell transplant. He is now on day 7 post-stem cell infusion. Absolute neutrophil count is 0. He has been on levofloxacin and fluconazole for prophylaxis.
He develops fever 102F, mild shortness of breath, pleuritic chest pain and dry cough.
Sputum Gram stain and culture is obtained, xray shows a faint right lower lobe infiltrate.
He is started on piperacillin/tazobactam and vancomycin.

Blood culture is growing a NON lactose fermenting Gram negative rod. The most likely organism causing pneumonia in this patient is:

A. Proteus

B. Legionella

C. Salmonella

D. Pseudomonas

E. Klebsiella

A

pseudomonas

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4
Q

what are the risk factors for developing pseudomonas pneumonia?

A
  1. neutropenia
  2. solid organ and stem cell transplant
  3. hospital acquired, critical care, intubated
  4. tracheostomy
  5. CF and bronchiectasis
  6. frequency COPD exacerbations, steroid use
  7. recent antibiotic use
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5
Q

what is neutropenia?

A

mild – < 1000 PMN/μl

moderate <500 PMN/μl

severe <100 PMN/μl

it matters how immunocompromised you are and for how long!

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6
Q

which antibiotics work on pseudomonas?

A
  1. quinolones = ciprofloxacin and levofloxacin
  2. penicillins = piperacillin/
    tazobactam
  3. cephalosporins = cefepime, ceftazidime, ceftolozane/tazobactame, ceftazidime/avibactam
  4. carbapenems = imipenem, meropenem, doripenem – NOT ertapenem
  5. aminoglycosides = gentamicin, tobramycin, amikacin –> these should NOT be used alone because they’re don’t have good distribution to tissues from the blood
  6. polymyxins = colistin, polymyxin B
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7
Q

what do you give to critically ill patients with pseudomas pneumonia?

A

combination therapy!! until you know what the organism is and what it’s susceptible to; then you can cut down to 1 drug

if the resistance is more than 10% in that area/hospital give 2 drugs!!

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8
Q

Our patient improves after 7 days of treatment with piperacillin tazobactam, fever resolves, and he is switched back to prophylactic antibiotics

5 days later ANC is now 20, platelets 10 and he develops a new fever. He is started again on IV piperacillin-tazobactam, but 48h later he is still febrile and his respiratory status is deteriorating. New sputum and blood cultures are obtained.

chest CT shows 2 peripheral masses. What is the next step in management?

A. add voriconazole

B. change piperacillin-tazobactam to meropenem

C. add trimethoprim sulfamethoxazole

D. obtain a lung biopsy

E. continue current antibiotics, awaiting culture

A

A. add voriconazole

there’s lots of things you can do with a patient like this so none of these are really wrong but you should recognize that this patient has 2 infiltrates and one of them has a halo around it which is specific for aspergillosis

can’t do a biopsy because his platelets are super low and he’d bleed to death

so you would add an anti-fungal and anti-staphylococcal coverage

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9
Q

where does aspergillum come from?

A
  1. holy water sprinkler
  2. vacuum cleaner (aerosolizes dust)
  3. mulching
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10
Q

what are the risk factors for aspergillosis?

A
  1. severe* and prolonged* neutropenia
  2. receipt of high doses of glucocorticoids
  3. other drugs or conditions that lead to chronically impaired cellular immune responses like immunosuppressive regimens administered to treat autoimmune diseases and to prevent organ rejection, AIDS
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11
Q

what do you see in aspergillosis microscopy?

A

thin septated hyphae that are the same thickness everywhere without bumps

narrow angle branching

looks like coral on microscopy and dandelions on cultures

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12
Q

what is the radiographic appearance of aspergillosis?

A

CXR are nonspecific and can even be normal in immunocompromised patients so do a CT

  1. nodular lesions, can be peripheral, close to pleura
  2. halo sign
  3. crescent sign
  4. frequently involves both lung and brain so get brain MRI
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13
Q

what is an aspergilloma?

A

something previous has caused a cavity in the lungs and now asperillus has formed a ball-shaped colony in the cavity that isn’t invading into the lung tissue

usually pretty benign; can resect surgically but ONLY if there’s symptoms

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14
Q

what is chronic pulmonary aspergillosis?

A

go look at the CT

chronic invasive asperigillosis

really hard to treat; give 2 months of anti-fungals

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15
Q

how do you diagnose aspergillosis?

A

risk factors + clinical picture + radiology + tissue dx!! put it all together because sometimes someone can have positive cultures but they’re fine

can be difficult – can colonize respiratory tract; BC never positive…

tissue diagnosis is the gold standard!! but with someone who is immunocompromised it’s hard to get a piece of lung

aspergillus galactomannan (from BAL more sensitive than from blood) and beta-D glucan can be suggestive but are not specific

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16
Q

what are zygomycetes?

A

a mold that under microscopy looks like broad, ribbon-like nonseptated right angle branching that’s bumpy coral

often seen in diabetics or transplants

they invade lung and sinuses and get to the brain and can kill people in days

treat with mphotericin B, newer azoles (posa-, isavuconazole) and surgical excision

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17
Q

how do you treat aspergillosis?

A

empirical and as soon as suspected in high risk pts

  1. aoriconazole, IV then PO
  2. posaconazole
  3. isavuconazole
  4. liposomal Amphotericin B
  5. echinocandins (caspofungin, micafungin, anidulafungin) – not first line; more of a salvage therapy

combination therapy is frequently used

give prophylaxis in pts with high risk hematologic malignancies

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18
Q

what is nocardiosis?

A

like aspergillosis, it can affect skin, lung, brain.

it’s an agent of mycetoma in immunocompetent host; you can have chronic foot infections that lead to sinus tract infections

can disseminate; blood cultures can be positive

often seen in solid organ transplant, chronic steroids, ETOH, DM, CGD, anti-TNF, less common AIDS

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19
Q

how do you treat nocardiosis?

A

treat with Bactrim, carbapenems (imipenem), aminoglycosides (amikacin) in COMBINATION

penems are needed when there’s brain involvement

you have to know the species before you give specific treatment

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20
Q

what does the nocardia gram stain look like?

A

gram stain shows weakly acid fast positive bacteira

looks like really thin tangled weeds

aerobic

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21
Q

what does a nocardia pneumonia CT look like?

A

you’ll have lung and brain involvement; looks a lot like aspergillosis

you’d have to get blood cultures and with nocardia you’re more likely to get positive blood cultures than in aspergillosis

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22
Q

what are the 4 B’s of nocardiosis?

A

beaded

branching

brain

bactrim

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23
Q

40 year old man with a history of splenectomy is brought in by family to ED with fever for 2 days, productive cough – greenish sputum with blood streaks, confusion. In ER hypotensive, altered, requires intubation, fluids and pressors.

Blood cultures are drawn and he is started on broad spectrum antibiotics

What test should be used to confirm the suspected etiology of this pneumonia, given that blood cultures may take several days to grow?

A. Lung biopsy

B. urine antigen

C. PCR from blood

D. procalcitonin

E. sputum gram stain and culture

A

B. urine antigen

AND

E. sputum gram stain and culture

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24
Q

what is invasive pneumococcal disease?

A

an infection in the lungs causing pneumonia and meningitis too - sometimes you can also have endocarditis

can present post-influenza

25
Q

how do you prevent invasive pneumococcal disease?

A

PCV13/PPSV23 vaccines is crucial

26
Q

what are the risk factors for invasive pneumococcal disease?

A
  1. hyposplenism and splenectomy
  2. B cell defects: multiple myeloma, SLE, transplant (HSCT with GVHD
  3. HIV
27
Q

how do you diagnose invasive pneumococcal disease?

A
  1. sputum gram stain and culture

rate of pathogen detection varies from 10-80%

  1. pneumococcus urine antigen (70% sensitive, 90% specific)
  2. blood cultures are indicated for the patients that require admission to the ICU; the sicker the patient , the higher the likelihood of positive blood cultures

low sensitivity in milder infections

28
Q

what is asplenia?

A

no spleen

congenital absence is very rare; most asplenics had it surgically removed

29
Q

what are the indications for a splenectomy?

A
  1. trauma
  2. idiopathic thrombocytopenia purport (ITP)
  3. spherocytosis, thalassemia major, hairy cell leukemia
  4. malignancies involving the spleen like Hodkigns and non-Hodgkin’s lymphoma
  5. abscess
30
Q

what are examples of functional hyposplenism?

A

so they have a spleen but it just doesn’t work well

  1. Graves
  2. SLE
  3. Sjogren
  4. vasculitis
  5. neoplasia = Hodgkin’s, CML, Sezary
  6. amyloidosis, sarcoidosis
  7. alcoholism
  8. sickle cell disease
  9. malaria
  10. elderly, neonates, prematures
31
Q

what do you see in a blood smear of someone without a spleen?

A
  1. Howell Jolly bodies (nuclear remnants) and “pocked” or “pitted” RBCs (hemoglobin containing vacuoles in senescent RBCs) due to poor clearance of RBCs
  2. target cells
  3. thrombocytosis
  4. lymphocytosis (loss of sequestration
32
Q

in asplenic patients, which populations have higher risk of infection?

A

30% of infections occur in the 1st year after splenectomy, 50% within 2 yrs, but can occur even after 20 yrs

they’re at risk for anything encapsulated!!

  1. thalassemia is the highest risk
  2. Hodgkin’s
  3. spherocytosis
  4. ITP
  5. trauma
33
Q

which bacteria are likely in asplenic patients?

A
  1. S. pneumoniae
  2. Haemophilus
  3. salmonella
  4. neisseria
  5. capnocytophaga
34
Q

which parasites are likely in asplenic patients?

A
  1. bebesia

2. ehrlichia

35
Q

which viruses are likely in asplenic patients?

A

CMV

36
Q

how do you prevent infection in asplenic patients?

A
  1. vaccination

conjugated pneumococcal vaccine, 23 valent unconjugated pneumococcal polysaccharide, Haemophilus influenzae, meningococcal

  1. prophylactic antibiotics

this is the current recommendation for sickle cell children

37
Q

40 y/o Hispanic woman from Texas was diagnosed with rheumatoid arthritis andstarted on adalimumab (Humira®) injections. Her joint disease is responding well now. Six months later she experienced generalized weakness, cough, and shortness of breath, which she attributed to the biologic and stopped taking it.

Two months later she went to visit family in Virginia where she was hospitalized with complaints of cough, shortness of breath, fatigue, chills, headaches, persistent fever, and a 16 pound weight loss. An xray shows an upper lobe infiltrate. A tuberculin skin test was placed and interpreted as negative.

What should be done next?

A. Restart treatment with adalimumab; the abrupt stop in treatment probably caused the symptoms

B. admit patient to an airborne isolation room and evaluate for active TB disease

C. discharge patient with contact information for the local health department

D. Send her back to Texas for TB evaluation

E. Send a Quantiferon TB blood test.

A

E. send back to texas for TB evaluation

she’s on a TNF-alpha inhibitor so her immune system isn’t working as well so you can’t rely on the test results

38
Q

what are biologics?

A

two types:
1. monoclonal antibodies (infliximab, adalimumab, certolizumab, golimumab)

  1. soluble receptor fusion proteins (etanercept)

used in RA, psoriasis, ankylosing spondylitis, IBD / Crohn disease

39
Q

what are the cons of biologics?

A

increased risk for:

  1. TB and non-tuberculous mycobacteria
  2. bacterial infections - septic arthritis, Legionella, listeriosis
  3. viral infections - hep B reactivation, hep C progression, zoster
  4. fungal infections – histoplasma, coccidioidomycosis, blastomycosis
    pneumocystis
40
Q

how are TNF-alpha inhibitors associated with tuberculosis?

A

patients on TNF-alpha inhibitors are at increased risk fo TB infection

they should be screened for latent tuberculosis by quantiferon TB, T-SPOT or PPD before they’re started on the TNF-alpha inhibitors

opinions differ in regards to sensitivity and specificity of these tests; some data suggests T-SPOT would be the most specific and sensitive in ICHpatients

treatment for LTBI should be at least started before initiating TNF inhibitors or JAK1/3 inhibitor tofacitinib; upon completion of 1 mo of treatment, can start biologic

annual screening if has risk factors for exposure to TB

41
Q

what is latent tuberculosis?

A

patients are not infectious and have no symptoms!!

there’s an average avg 5-10% risk of reactivation/lifetime

42
Q

who should be tested for latent tuberculosis?

A
  1. individuals with known exposure to TB
  2. migrants from a high incidence country (Latin America, the Caribbean, Africa, Asia, Eastern Europe, and Russia)
  3. people who live or work in high-risk settings (correctional facilities, long-term care facilities or nursing homes, and homeless shelters)
  4. health-care workers who care for patients at increased risk for TB disease
  5. infants, children and adolescents exposed to adults who are at increased risk for latent tuberculosis infection or TB disease
43
Q

which tests

A

both IGRA (interferon gamma release assays) and TST (tuberculin skin test) can be falsely negative in active disease

active disease diagnosis is made based on symptoms, risk factors, xray/CT and sputum smear/culture, NOT quantiferon

44
Q

what are the symptoms of active TB?

A
  1. weight loss
  2. low grade fever, night sweats,
  3. cough, hemoptysis.

immigrants can rarely reactivate TB as extrapulmonary disease (renal, joints, brain etc)

45
Q

how and when you would treat latent TB?

A

treat based on risk factors, exposure and +IGRA/TST

possible regimens:
1. 6-9 months daily INH + vitamin B6

  1. INH + rifapentine weekly x 12 weeks (+B6)
  2. INH + rifampin x 3 months (+B6)
  3. rifampin daily x 4 months

IGRA and TST tests DO NOT normalize after treatment; so once you have a positive TB test you’ll always have a positive test unless you immune system isn’t working

46
Q

31 y/o man received a matched unrelated donor allogeneic stem cell transplant for refractory Hodgkin lymphoma. On day 35 after transplantation he developed shortness of breath and O2 saturation drops to 85% on room air. WBC 2 days ago was 1000, 70% segs.

CXR shows diffuse bilateral infiltrates

A bronchoscopy specimen shows white cells on gram stain, but no bacteria, silver stain shows no organisms

What is the most likely etiology of this patient’s lung findings?

A. Tuberculosis reactivation

B. CMV pneumonia

C. Toxoplasmosis

D. Pneumocystis

E. mucormycosis

A

B. CMV pneumonia

based on timing and CXR

47
Q

what is cytomegalovirus?

A

CMV is a B-herpesvirus

most adults are infected so infection is usually reactivation

congenital birth defects

major cause of solid organ rejection (renal)

frequent cause of pneumonia/pneumonitis in lung and bone barrow recipients

thought to play a role in the critically ill patient with bacterial infections

blood pcr is suggestive

48
Q

how do you diagnose CMV?

A

CMV PCR from blood – quantitative – suggestive but not diagnostic of end organ involvement

shell vial culture (modified rapid culture)

histology (inclusion bodies “owl’s eye” cells and immunohistochemistry)

serology: mainly useful for pretransplant evaluation, but not diagnostic of reactivation

49
Q

which infections are common solid organ recipients immediately after transplant?

A
  1. bacterial = pneumonia, c. diff
  2. viral = HSV reactivation
  3. fungal = candida and aspergillum
50
Q

which infections are common solid organ recipients 30 days after transplant?

A

opportunistic infections:
1. pneumocystis

  1. fungi
  2. toxoplasma
  3. nocardia
  4. CMV
51
Q

which infections are common solid organ recipients 6+ months after transplant?

A
  1. reactivation of chronic
    viral infections
  2. fungal infections
    (cryptococcus, histoplasma)
  3. lymphomas and
    lymphoproliferative
    syndromes related to EBV (>1yr)
52
Q

which infections are common stem cell transplant recipients pre-transplant?

A
  1. gram negatives
  2. UTIs
  3. pneumonia
  4. sepsis
53
Q

what prophylaxis do you do for CMV?

A

SOLID ORGAN TRANPLANT
1. risk D+/R- > D+/R+ > D-/R-

highest benefit in first 3-12Mo after transplant inseronegative recipients of CMV positive organs – valganciclovir (+/- CMV immune globulin for lung transplant)

universal vs preemptive prophylaxis (guided by CMV PCR)

renal usually receive 3-6 mo depending on risk

lung transplant 12 mo or more

BM TRANPLANT
1. risk : Allogeneic > autologous; D-/R+ > D+R+ > D-/R-

most centers use preemptive approach due to toxicity

54
Q 
28 y/o man who has sex with men presents to ER with progressive shortness of breath for a month, dry cough with no sputum, intermittent subjective fevers. No chest pain. He lives in Ohio. Has no past medical history, does not travel and has no pets.
An HIV test is positive. He was never tested before. WBC 1.8k, 70% neutrophils. CD4 and viral load are pending
CXR shows bilateral ground class opacities

What is the most likely diagnosis?

A. Streptococcus pneumoniae

B. Legionella

C. Listeria

D. Pneumocystis

E. Mycobacterium avium

A

D. Pneumocystis

they have no T cells

55
Q

what are the risk factors for pneumocystis?

A
  1. cancer
  2. stem cell transplant
  3. solid transplant
  4. rheumatologic diseases on immunosuppressives (steroids)
  5. HIV
56
Q

what are the clinical, lab and CXR findings for pneumocystis?

A
  1. fever and progressive SOB
  2. hypoxia, exacerbated by minimal effort because they have no lung reserve
  3. cough with no sputum
  4. respiratory failure
  5. high LDH (not specific)
  6. CXR can be normal, CT is always abnormal
  7. sensitivity of silver stain: biopsy > BAL&raquo_space; Sputum
  8. PCR is very sensitive
57
Q

how do you treat pneumocystis pneumonia?

A
  1. bactrim = trimethoprim/sulfamethoxazole (high dose)
  2. clindamycin/primaquine
  3. atovaquone (not as effective)
  4. IV pentamidine (for severe disease only, lots of side effects)
58
Q

what is the prophylaxis for pneumocystis pneumonia?

A
  1. bactrim = TMP/SMX (low dose)
  2. dapsone
  3. atovaquone
  4. inhaled pentamidine

Pulmonary Week 4 (6 decks)

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