HSV and VZV vs CMV and EBV
How to tell HSV and VZV and CMV and EBV apart when a board question makes them look alike.
HSV/VZV are sensory-neuron vesicle viruses; CMV is owl-eye immunosuppression/congenital disease; EBV is CD21 B-cell mono and malignancy.
Side by side
HSV causes oral/genital vesicles, encephalitis, keratitis, or neonatal disease; VZV causes chickenpox or dermatomal zoster from dorsal root ganglia reactivation.
CMV causes congenital disease, mono-like illness, retinitis, colitis, and transplant disease; EBV causes mononucleosis, B-cell transformation, and several lymphoid or epithelial cancers.
HSV and VZV establish latency in sensory neurons and reactivate along mucocutaneous or dermatomal distributions.
CMV establishes latency in monocytes and causes disease in immunosuppression; EBV infects B cells through CD21 and drives atypical lymphocytosis or proliferation.
Multinucleated giant cells, Cowdry A inclusions, temporal lobe encephalitis, or dermatomal vesicles support HSV/VZV patterns.
Owl-eye inclusions support CMV; heterophile antibodies, atypical lymphocytes, and CD21 B-cell tropism support EBV.
The trap
All are herpesviruses with latency, so latency site, syndrome, and inclusion pattern separate them.
The repair move
For herpesviruses, name the latency cell or tissue before matching the clinical syndrome.
Try a free question
CoreA 32-year-old woman has 4 days of fever, headache, and confusion progressing to a focal seizure. CSF shows lymphocytic pleocytosis with elevated red blood cells; MRI shows asymmetric hyperintensity in the right temporal lobe with patchy enhancement. Which organism is most likely?
Show answer and explanation
Answer: A. Herpes simplex virus 1. Herpes simplex virus 1 encephalitis preferentially involves the temporal lobes, producing fever, focal neurologic signs, and hemorrhagic CSF with lymphocytic pleocytosis.
Why the other choices are tempting
- B. Cytomegalovirus causes retinitis, colitis, esophagitis, and pneumonitis in immunocompromised hosts with owl-eye inclusions, not temporal lobe encephalitis in immunocompetent adults.
- C. Epstein-Barr virus causes infectious mononucleosis with heterophile antibodies and atypical lymphocytes, not necrotizing temporal lobe encephalitis.
- D. Varicella-zoster virus causes chickenpox or dermatomal zoster; it can produce a vasculopathy but is not the classic temporal lobe encephalitis pathogen.
- E. JC virus causes progressive multifocal leukoencephalopathy with subcortical demyelination in advanced HIV or natalizumab-treated patients, not acute hemorrhagic temporal lobe disease.
Flashcards
Tap a card to flip it.
Where do HSV and VZV classically establish latency?
HSV and VZV establish latency in sensory neurons.
What encephalitis pattern supports HSV?
Temporal lobe encephalitis supports HSV.
Quick answers
What is the fastest way to tell HSV and VZV from CMV and EBV?
HSV/VZV are sensory-neuron vesicle viruses; CMV is owl-eye immunosuppression/congenital disease; EBV is CD21 B-cell mono and malignancy.
What is the key clue for HSV and VZV?
HSV causes oral/genital vesicles, encephalitis, keratitis, or neonatal disease; VZV causes chickenpox or dermatomal zoster from dorsal root ganglia reactivation.
What is the key clue for CMV and EBV?
CMV causes congenital disease, mono-like illness, retinitis, colitis, and transplant disease; EBV causes mononucleosis, B-cell transformation, and several lymphoid or epithelial cancers.
What is the common trap with HSV and VZV vs CMV and EBV?
All are herpesviruses with latency, so latency site, syndrome, and inclusion pattern separate them.