Herpes Simplex infection is produced by the viruses herpes simplex (HSV-1) and herpes simplex 2 (HSV-2). HSV-1 is mostly responsible for the oral infection and HSV-2 for the genital infection. Occasional cases of oral herpes simplex are produced by HSV-2. Here only the oral herpetic infection produced by HSV-1 will be presented.
Around 90% of the U.S. population is affected with this disease. Ninety-nine percent of affected individuals undergo a subclinical infection that in children may be confused with eruption gingivitis. One percent of affected individuals develop the full-blown disease. The primary infection or primary herpetic gingivostomatitis occurs mostly in children from age six months to puberty. Among HIV+ and AIDS patients also young children are most often affected. Cases in adults are also seen. Vesicles are the basic manifestations of the disease. These vesicles, initially intraepithelial in location, coalesce forming bullae which extend to the dermis thus, becoming subepithelial. Vesicles and bullae break, leaving painful ulcers. The ulcers are seen in any of the oral mucosas and the oropharynx. The gingiva is hyperplastic and characterized by marked erythema, especially of the interdental papillae. Occasional crusting over these ulcers, especially on the lip, is also seen in the late stage of the infection. There is increased body temperature, regional lymphadenopathy and incapacity to eat properly. The clinical manifestations are more severe in immunocompromised patients especially those with advanced AIDS. The primary infection lasts up to two weeks and resolves itself without leaving scars or sequelae. After the clinical and/or subclinical infection subsides the virus goes into latency in regional ganglion, such as the Gasser ganglion, and the affected patient becomes a carrier. The most frequent excitants such as: GI upsets, stress, menses, solar radiation, extreme cold, other infections, as, will reactivate the virus in around 40% of carriers. This reactivation induces migration from the ganglion to the peripheral epithelial cells where the virus replicate. This new viral load will produce recurrent lesions which are generally less severe than the primary ones.
| This 11 year old girl had a history of elevated body temperature and inability to eat properly for the last 4 days. Note the marked gingival erythema and the swollen interdental papillae. There was marked halitosis. | Note the ulcers on the lower lip of this 8 year old boy with primary herpetic infection. The ulcers are partially covered with a yellowish necrotic epithelial slough. Also note the erythematous and markedly hyperplastic gingiva. | This photo was taken from a 22 year old male with a 3 days history of increased body temperature, malaise and inability to eat. Arrow 1 points to seropurulent exudate. Arrow 2 points to the hyperplastic erythematous gingiva and arrow 3 points to several lip ulcerations. This patient was treated with antibiotics to prevent secondary infection. |
Therapeutic protocols
Primary intraoral herpetic infection is not commonly seen in patients with AIDS. When present, its severity dictates the treatment which as a rule will be intravenous medication with acyclovir or if there is acyclovir resistance, with intravenous foscarnet (Foscavir). Both these medications need to be administered and controlled by a physician.
SYSTEMIC ANTIBIOTICS can be used only to prevent secondary infection.
FOR PATIENTS ALLERGIC TO PENICILLIN:
ANALGESIC & ANTIPYRETIC
For moderate pain:
Recurrent herpetic infection
References relevant to herpes simplex (with abstracts)