Pathophysiology of Shingles (dev and sharvin)

Shingles – also known as Herpes Zoster

Causative agent – Varicella Zoster Virus (VZV) which is a double stranded DNA virus.

An initial infection by the VZV leads to chickenpox, usually at childhood in most cases. Subsequent elimination of the virus by the immune puts an end to chickenpox. However, the VZV is often able to evade elimination by the immune system and remains latent in the dorsal root ganglion or the ganglion semilunare in the base of the skull.

Shingles can only appear in people who have had chickenpox before as the first infection by the VZV always leads to chickenpox. Shingles can appear in people of any age group due to the reactivation of the virus in a single sensory ganglion, although it usually appears in people above the age of 50. The ability of the virus to evade elimination by the immune system and remain dormant is still poorly understood. The location and structure of the DNA of the virus is unknown either. Furthermore, the “true latency” of the virus has not been proven as it continues to synthesize virus specific protein in the dormant phase, meaning that it could even be a chronic low level infection. The VZV has only been detected in autopsies of nervous tissue but never in the ganglia of living people.

It’s rare for people who have had shingles to be infected again unless they have a compromised immune system. In fact, shingles usually appears in people with an impaired immune system due to factors such as aging, immunosuppressive therapies, psychological stress, malnourishment, etc. Upon reactivation, the virus replicates in the nerve cells, and virions are shed from the cells and carried down the axons to the area of skin served by that ganglion. In the skin, the virus causes local inflammation and blisters. The short- and long-term pain caused by herpes zoster comes from the widespread growth of the virus in the infected nerves, which causes inflammation. If motor nerve roots are also involved, weakness can develop in addition to sensory changes. Leptomeningeal involvement is rare but may develop when the ophthalmic branch of the trigeminal nerve is involved.

The symptoms of herpes zoster cannot be transmitted to another person. However, during the blister phase, direct contact with the rash can spread VZV to a person who has no immunity to the virus. This newly-infected individual may then develop chickenpox, but will not immediately develop shingles. Until the rash has developed crusts, a person is extremely contagious. A person is also not infectious before blisters appear, or during postherpetic neuralgia (pain after the rash is gone). The person is no longer contagious after the rash has disappeared.