I have an immunocompetent patient who acquired herpes simplex esophagitis, likely through oral sex. What is the natural history of herpes simplex virus (HSV) in immunocompetent individuals and what is the likely recurrence rate? Also, if the patient continues a sexual relationship with his current partner (who appears to be an asymptomatic shedder of HSV), does he need to take precautions to prevent genital lesions?
Response from David R. Haburchak, MD, FACP
I am surprised that you do not mention significant oral herpes along with the esophagitis. It would also be useful to know the age of the patient. I assume that if this is truly primary herpes esophagitis in an immunocompetent man, acquired through oral sex, that the patient had a first-time exposure to HSV-2. I also have to surmise that this was a relatively young patient who never had previous exposure to HSV-1 or HSV-2.
This would therefore be a primary HSV exposure and produce symptoms significant enough to bring him to medical attention, endoscopy, and either histologic or viral diagnosis. If the partner did transmit this infection through asymptomatic shed (and attendant low titer of virus), the patient must have been quite susceptible (lacked previous exposure, antibody, cell-mediated immunity, etc)
Assuming, therefore, that this is a primary oral HSV-2 infection, what are the risks of recurrence in this patient? Thanks to the work of Drs. Benedetti and Corey in Seattle, Washington, there actually are fairly decent data to address this situation. A prospective study reported in 1987 (in non-AIDS patients) demonstrated that the relapse rates of the HSV-1 and HSV-2 viruses are very dependent upon the location of the primary infection. In fact, the reason the 2 viruses segregate by location is probably because they relapse in the oral region in HSV-1 and in the genital region in HSV-2. Oral-labial recurrences developed in 5/12 patients with HSV-1 and only 1/27 patients with HSV-2 (P < .001). On the other hand, genital recurrences developed in 24/27 patients with HSV-2 and only 3/12 with HSV-1 (P < .01). The mean monthly rate of genital HSV-2 recurrences was .33, oral-labial HSV-1 .12, genital HSV-1 .020, and oral HSV-2 .001 (P < .01 for each comparison). Another study showed that when HSV-2 does have extragenital reactivation, it usually occurs on the legs or buttocks, probably due to nerves infected through autoinoculation at the time of the primary infection.
Based on the above data, I would not use antiviral prophylaxis to prevent recurrence of the oral/esophageal infection in this patient. Of course, if he did relapse, an evaluation of immunity is needed, and prophylaxis with acyclovir or a similar agent should be given. In the normal host, recurrences are most likely in the first few months, and taper with time.
I suspect the patient is now partially immune and probably will not acquire symptomatic genital herpes from the same partner if the partner is having minor shedding. If the partner is obviously having a reactivation, the viral load is higher and might be sufficient to cause genital disease. Therefore, I would recommend abstinence if the partner has symptomatic recurrence. Alternatively, the partner might be considered for long-term acyclovir prophylaxis, but I am not aware of any study addressing the cost/benefit of such partner therapy. The cost would also be significant.
Medscape Internal Medicine. 2002;4(2) © 2002 Medscape
Cite this: David R Haburchak. Herpes Simplex Esophagitis in an Immunocompetent Male - Medscape - Sep 16, 2002.