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Folio edition · Set in Instrument Serif & Archivo

Paeds Vivasallergy-and-immunology

Paeds Vivas · allergy-and-immunology

Secondary immunodeficiency — branching viva

Branching viva on secondary immunodeficiency in children: recognising that acquired immune failure is commoner than primary, sorting the cause into the six mechanism-based categories, linking cause to immune arm to organism to prophylaxis, applying the five-step management ladder, and deciding when immunoglobulin replacement is and is not indicated.

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Target exams

RACP DCEMRCPCH ClinicalRCPSC Pediatrics

Target exams

RACP DCEMRCPCH ClinicalRCPSC Pediatrics
Prompt
Oncology ward: a seven-year-old on induction chemotherapy for acute lymphoblastic leukaemia presents with fever and an absolute neutrophil count of 0.2 × 10⁹ per litre. The examiner asks: what is your framework, what is the immediate threat, how will you manage it now, and what prophylaxis belongs in his long-term plan — then branches to a child on long-term high-dose steroids presenting with dry cough and hypoxia and asks you to predict the organism and the defence, and finally to a rituximab-treated child with low IgG and asks you to justify why you would NOT automatically start immunoglobulin.

Opening question

Take me through your framework when a child presents with infection that you suspect is due to secondary immunodeficiency. Why does the mechanism matter more than the label "immunocompromised"? [1] [2]

Branch 1 — the immediate threat (febrile neutropenia)

The child is febrile and profoundly neutropenic on chemotherapy. What is the immediate threat, what empirical management is required within the hour, and why is this treated as sepsis rather than observed? [1] [4]

Branch 2 — predict the organism (the steroid case)

Now picture a child on high-dose corticosteroids for four weeks presenting with dry cough and hypoxia. Which organism do you predict, which prophylaxis should already have been in place, and at what dose-duration threshold? [4] [1]

Branch 3 — the trap (rituximab and low IgG)

A child treated with rituximab for nephrotic syndrome now has a low IgG. Why would you NOT automatically start immunoglobulin, what decides whether replacement is indicated, and what is the expected natural history of the B-cell depletion? [3] [2]

Closing — the general rule

In one sentence, what is the single rule that decides whether a child with secondary hypogammaglobulinaemia receives immunoglobulin replacement, and why does over-treatment matter as much as under-treatment? [3] [1]

References

  1. [1]Chinen J, Shearer WT. Secondary immunodeficiencies, including HIV infection. J Allergy Clin Immunol, 2010.PMID 20042227
  2. [2]Tuano KS, Seth N, Chinen J. Secondary immunodeficiencies: An overview. Ann Allergy Asthma Immunol, 2021.PMID 34481993
  3. [3]Otani IM, Lehman HK, Jongco AM, et al. Practical guidance for the diagnosis and management of secondary hypogammaglobulinemia: A Work Group Report. J Allergy Clin Immunol, 2022.PMID 35176351
  4. [4]Maertens J, Cesaro S, Maschmeyer G, et al. ECIL guidelines for preventing Pneumocystis jirovecii pneumonia in haematological malignancies and stem cell transplant recipients. J Antimicrob Chemother, 2016.PMID 27550992