A 14-year-old girl presented with tiredness for few weeks. Upon examination there is no lymphadenopathy or hepatosplenomegaly. Her blood investigations reveled WBC – 4.5 x 109/L, Hb – 5.6 g/dl, Platelets – 135 x 103/dl A. Aplastic Anemia B. Folate deficiency C. Pernicious anemia D. Parvovirus B19 infection E. Vitamin B12 deficiency
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The textbook evidence is clear. Here is the full explanation:
Answer: D. Parvovirus B19 infection
Breaking Down the Clinical Picture
| Parameter | Value | Interpretation |
|---|---|---|
| WBC | 4.5 x 10⁹/L | Normal |
| Hb | 5.6 g/dL | Severely low |
| Platelets | 135 x 10³/dL | Normal/near-normal |
| Lymphadenopathy | Absent | Against lymphoma/EBV |
| Hepatosplenomegaly | Absent | Against aplastic anemia |
The key finding here is isolated severe anemia with a preserved white cell count and platelet count - a pattern called pure red cell aplasia (PRCA). Only the red cell line is affected.
Why Parvovirus B19?
Parvovirus B19 preferentially infects and destroys erythroid progenitors (cells expressing the P antigen/globoside receptor). It does not attack myeloid or megakaryocytic precursors, which is why WBC and platelets remain normal.
As Robbins & Kumar explains:
"A special form of red cell aplasia occurs in individuals infected with parvovirus B19, which preferentially infects and destroys red cell progenitors. Normal individuals clear parvovirus infections within 1 to 2 weeks; as a result, the aplasia is transient..." - Robbins & Kumar Basic Pathology
In a healthy immunocompetent child, parvovirus B19 causes a transient aplastic crisis - a brief but potentially severe drop in hemoglobin due to cessation of erythropoiesis. The bone marrow normally compensates by ramping up RBC production rapidly, but when B19 destroys those progenitors, a sudden severe anemia results.
In children with underlying hemolytic anemias (e.g., sickle cell, hereditary spherocytosis), this becomes especially dangerous because RBC lifespan is already short.
Why the Other Options Are Wrong
A. Aplastic Anemia - Aplastic anemia causes pancytopenia (low WBC + low Hb + low platelets) because it destroys multipotent myeloid stem cells. This girl has only anemia with normal WBC and normal platelets. Aplastic anemia also does not cause splenomegaly - but pancytopenia is the hallmark. - Robbins & Kumar Basic Pathology
B. Folate Deficiency - Folate deficiency causes macrocytic anemia with hypersegmented neutrophils. It can cause pancytopenia in severe cases, but the MCV would be elevated and there would be megaloblastic changes. The WBC is normal here, not low.
C. Pernicious Anemia - This is autoimmune destruction of gastric parietal cells (intrinsic factor deficiency) leading to vitamin B12 deficiency. It is rare in a 14-year-old (typically affects adults >50 years), causes macrocytic megaloblastic anemia, leukopenia with hypersegmented granulocytes, and neurological findings. WBC would be affected, not just RBCs.
E. Vitamin B12 Deficiency - Like folate deficiency, this produces macrocytic (megaloblastic) anemia with elevated MCV and multi-lobed neutrophils. It affects all cell lines in severe cases and would not present as isolated anemia with normal WBC and platelets. Additionally, B12 deficiency in a 14-year-old would require a specific cause (strict vegan diet, malabsorption, pernicious anemia).
Key Teaching Point
The distinguishing feature of Parvovirus B19 infection is that it causes selective red cell aplasia - not pancytopenia - because its receptor (the P antigen/globoside) is expressed only on erythroid progenitor cells (proerythroblasts), leaving myeloid and platelet precursors unharmed. The result is anemia in isolation, which is exactly what this case shows.
"Parvovirus B19 infection: causes transient severe red cell aplasia in individuals with hemolytic anemia and chronic red cell aplasia in individuals who cannot clear the infection." - Robbins, Cotran & Kumar Pathologic Basis of Disease
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