44M from Maine w/ myelodysplastic syndrome s/p BMT 6 weeks ago has fevers. He is on voriconazole, moxifloxacin, atovaquone, & valacyclovir. He is taking topical steroids for the past 25 days due to mild skin graft versus host disease.
2/
T 38.2C, HR 101, BP 115/80, RR 16, O2 98% on RA. Labs notable for WBC 1000 (neutrophil count 200), hemoglobin 6.1, platelets 3,000. Which of the following puts the patient at increased risk for developing invasive aspergillosis?
1/10
Answer: Neutropenia. Prolonged neutropenia is one of the biggest RF for aspergillosis. A CD4 count <100 and systemic corticosteroids are additional risk factors for invasive pulmonary aspergillosis (IPA)
For additional RF, please see the following table
2/ Neutrophils play an important role in aspergillus control
💥They entrap and kill hyphae!
3/ Is this clinically important?
A case control study looked at 15 pathology proven IPA vs 35 controls. Neutropenia was strongly associated w/ IPA
Early in neutropenia, rate of IPA development was 1%/day
IPA is almost exclusively seen in immunocompromised. In people w/ NORMAL immune system, aspergillus can cause:
🚙chronic aspergillosis (esp in those w/ prior lung injury)
🚗allergic bronchopulmonary aspergillosis
In order to use tests to our advantage, we need to know disease prevalence to calculate PPV/NPV
⭐️Disease prevalence, as well as clinical presentation, drives pretest probability, which influences post-test likelihood of disease
8/ Since we know that IPA is almost exclusively found in immunocompromised hosts, we should use that in our risk assessment to determine the disease prevalence
🌝Then we can review the clinical presentation to see if it fits with pulmonary aspergillosis (imaging, etc)
9/ So, we should ask ourselves 2 Qs:
1- What’s the pre-test prob of IPA based on prevalence (immunocompromised) and the clinical signs/symptoms of this patient?
2- What are the PPV/NPV of the test in this case (how would the result impact the decision to treat or not)?
10/ This figure is helpful for using BDG/GM for IPA
50F w/ EtOH cirrhosis & DM presents to ED w/ AMS & decreased UOP. She is febrile & hypotensive
She is started on vasopressors & CVVHD via central lines in the ICU
Due to concern for SBP, she is started on ceftriaxone
2/ Initial blood & ascites cultures show no growth. She remains critically ill for 7 days and still having fevers
In addition to blood cultures, which of the following is the next best test to order?
1/13
Answer: Serum BDG
You have suspicion for invasive candidiasis given the RF of cirrhosis, critical illness in ICU w/ central lines, dialysis, & broad-spectrum antibiotics (see other RF in table)
60M w/ asthma from China presents w/ SOB secondary to an asthma exacerbation. He has never smoked cigarettes. A CT chest shows a 7mm right upper lobe nodule
Which of the following tests should be ordered for further evaluation of the nodule?
1/14
Answer: AFB sputum culture
Without knowing much about the patient, other than age, geographic risk, smoking status, & normal immune status, most common infectious cause of a solitary pulmonary nodule (SPN) is TB.
2/ It’s possible that the SPN may be latent TB, but we need to rule out active TB first (AFB sputum cultures x3) before considering latent TB
Fungal causes are less likely. If we want to work it up, it would be pathogen specific (e.g., Cocci Ab) & not broad antigen testing (BDG)
75F w/ lupus, HTN, recent diagnosis of HIV (viral load 30,000, CD4- 57), presents to ED in winter w/ 4 weeks of shortness of breath & cough. T 38.5C, HR 105, BP 105/80, RR 20, O2 94% on 3L. Exam is notable for crackles & rhonchi in both lungs
2/ Labs: WBC 2,600, Hb 7.5 g/dL, platelet 70,000. CXR shows diffuse opacities. You have suspicion for Pneumocystis jirovecii pneumonia
Which of the following is the best non-invasive test to order to help confirm the diagnosis?
1/11
Answer: Serum BDG
⭐️LDH elevation is nonspecific and can be elevated in many diffuse pulm processes
Serum GM is not helpful in diagnosing PJP since its cell wall does not contain GM
BDG is a cell wall polysaccharide present in many pathogenic fungi including P. jirovecii