Smallpox: What the Dermatologist Should Know

Phyllis I. Spuls, MD; Jan D. Bos, MD, PhD; Donald Rudikoff, MD


Skinmed. 2004;3(4) 

In This Article

Immunology of Eczema Vaccinatum

The occurrence of eczema vaccinatum may relate to barrier disruption but also likely results from immunologic alterations that allow unbridled replication of vaccinia virus in the skin. Delayed-type hypersensitivity to recall antigens is diminished in the skin of patients suffering from atopic eczema. Effector memory T-cells are not able to perform normally in patients with active skin lesions, whereas treatment of atopic eczema tends to be associated with restitution of normal delayed hypersensitivity and normal recall antigen responses.[54] Thus, there is no intrinsic abnormality in effector immunity. One explanation of diminished effector memory T-cell function is that involved skin is overloaded with disease-related T-cells, preventing influx and normal function of other T-cell dependent immune responses.

The clinical knowledge that lesions of eczema vaccinatum develop concurrently with the primary vaccination site lesion of vaccinia indicate that innate immunity is affected in these patients. Spread of the lesions in previously unvaccinated individuals cannot be halted by acquired and specific immunity because it has not yet developed, thus innate immunity mechanisms are responsible for the course of the disease.

A recent report indicated a deficiency in the expression of the antimicrobial peptides cathelicidin and ß-defensin in both acute and chronic lesions of atopic dermatitis.[55] These keratinocytederived peptides have antifungal, antibacterial, and antiviral properties and form an essential, only recently recognized axis of innate immuni-ty.[56] This deficiency could explain the spread of a microbial agent like poxvirus in these patients, hence the development of the complication known as eczema vaccinatum.


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