Skip to main content

Parvo virus B19 - Pure Red Cell Anemia

Best-documented viral cause of RBC aplasia in

 

  • Chronic Hemolysis
  • Immunocompromised
  • Fetus in utero

Pathology:

Cytotoxic to marrow erythroid progenitor cells by  binding to red cell "P" antigen.

Clinical course:

Normal children: <2wk course. Anemia not present or appreciated.
            Rx: Not required

Hemolytic patient: brief cessation of erythropoiesis may precipitate Aplastic crisis  in already low lifespan RBC.
Most occurs once in life, but should should be isolated from at risk pts.
           Rx: B.T if required.

Recovery in both the cases is spontaneous, with nucleated RBC & reticulocytosis.

Immuno-compromised: severe, no spontaneous recovery, >1 blood transfusion.
          Rx: High dose IVIG.

In-Utero:  2nd, 3rd foetal wastage, hydrops fetalis.

Investigations:


Bone marrow under light m/s:
  • decreased erythroid precursors,
  • characteristic nuclear inclusions in erythroblasts
  • giant pronormoblasts
Lab:
  • PCR
  • Serum IgM & IgG titers.

Comments

Popular posts from this blog

Management of Neurocysticercosis in Children: Association of Child Neurology Consensus Guidelines

Lab tests: Routine screening of family members of children with NCC is not recommended. If at all screening is performed, fecal testing of the family for ova/cyst can be done. The use of serological tests for diagnosis and clinical decision making in children with NCC is not recommended. Radiological tests: The MRI need not be done following CT in the following situations -  The CT conclusively demonstrates the presence of a scolex within the cyst  In the absence of demonstration of scolex – If a solitary cystic/ring-enhancing lesion has all other typical sizes, shape, and location characteristics of NCC Multiple lesions in different stages are present, including some cystic or ring enhancing or calcified MRI should be considered after CT in the following situations – Atypical imaging features (conglomerate lesions, subarachnoid or intraventricular lesions) along with the absence of scolex CT features create suspicion of intraventricular, subarachnoid, or intraspinal NCC Atypical clin