'Slapped cheek' facial rash followed by lacy reticular truncal rash in school-age children; risks include aplastic crisis in hemolytic anemias and hydrops fetalis in pregnancy.
Also known as: fifth disease, 5th disease, parvovirus B19, slapped cheek syndrome, erythema infectiosum
Overview
Common childhood viral exanthem caused by parvovirus B19, a single-stranded DNA virus that targets erythroid progenitors via the P antigen (globoside) receptor. The classic 'slapped cheek' rash heralds resolving viremia; arthropathy is common in adults.
Epidemiology
Worldwide; outbreaks in late winter and spring in school-age children. By age 15, ~50% are seropositive. Transmission via respiratory droplets and blood products. Infectious BEFORE the rash appears — patients are no longer contagious by the time the rash is recognized.
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Question 1Infectious DiseaseMedium
A 9-year-old boy with homozygous sickle cell disease is brought to the emergency department with 3 days of fatigue, pallor, and shortness of breath. He attends a public elementary school, has a 4-year-old sibling who recently had a cold, and received his annual inactivated influenza vaccine 2 weeks ago. On exam he is pale and tachycardic. Hemoglobin is 4.2 g/dL (baseline 8.5 g/dL) with a markedly low absolute reticulocyte count, and parvovirus B19 IgM is positive. Which of the following is the strongest risk factor for this patient developing transient aplastic crisis?
AAttendance at a public grade school
BUnderlying chronic hemolytic anemia
CAbsence of prior parvovirus B19 immunity
DHousehold contact with a recent illness
EFunctional asplenia from autosplenectomy
Reveal answer & full explanation
Correct answer: B — Underlying chronic hemolytic anemia
AAttendance at a public grade school
BUnderlying chronic hemolytic anemia✓
CAbsence of prior parvovirus B19 immunity
DHousehold contact with a recent illness
EFunctional asplenia from autosplenectomy
Why Underlying chronic hemolytic anemia is correct
Parvovirus B19 binds the P antigen (globoside) on erythroid progenitors and halts erythropoiesis, producing transient reticulocytopenia.
In a healthy child this brief shutdown is silent because the normal red cell lifespan is ~120 days. In sickle cell disease (or other chronic hemolytic anemias such as hereditary spherocytosis or thalassemia), red cell survival is drastically shortened, so even a few days of arrested erythropoiesis cause the abrupt hemoglobin drop with a low reticulocyte count seen here, the defining feature of transient aplastic crisis.
This underlying hemolytic state, not the exposure route, is what converts a benign childhood exanthem into a life-threatening event, making it by far the strongest risk factor.
Why the others are wrong
Attendance at a public grade school — School and daycare exposure raises the chance of acquiring parvovirus B19, but it explains how the infection was caught, not why the marrow failed; most exposed children have mild illness or none.
Household contact with a recent illness — A sibling with coryza is a plausible droplet source, but acquiring the virus is not what determines severity; the host's marrow reserve is.
Absence of prior parvovirus B19 immunity — Being seronegative makes infection possible but, like the other exposure factors, governs susceptibility to infection rather than the catastrophic anemia, which depends on the shortened red cell lifespan of hemolytic disease.
Functional asplenia from autosplenectomy — functional asplenia is the classic infection risk in sickle cell disease, but it predisposes to overwhelming sepsis from encapsulated bacteria such as Streptococcus pneumoniae; transient aplastic crisis comes from parvovirus arrest of erythropoiesis against a red cell lifespan already shortened by sickling, which stays short whether or not the spleen still functions.
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Immunocompromise (pure red cell aplasia and chronic anemia)
Pathophysiology
Virus binds the P antigen (globoside) on erythroid progenitors, halting erythropoiesis and producing transient reticulocytopenia. The classic exanthem is immune-complex-mediated and appears as viremia resolves, explaining lack of contagiousness when the rash is visible.
Clinical presentation
Symptoms
Mild prodrome with low-grade fever, headache, coryza 5-7 days earlier (often missed)
Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA or PAEA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants; End of Rotation™ is a program of the Physician Assistant Education Association.