Herpes

Herpes Disorders Recurrence Transmission and prevention Diagnosis Epidemiology Treatment

Disorders

HSV infection causes several distinct medical disorders. Common infection of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands (herpes whitlow). More serious disorders occur when the virus infects and damages the eye (herpes keratitis), or invades the central nervous system, damaging the brain (herpes encephalitis). Patients with immature or suppressed immune systems, such as newborns, transplant recipients, or AIDS patients are prone to severe complications from HSV infections. HSV infection has also been associated with bipolar disorder, schizophrenia, and Alzheimer's disease, although this is often dependent on the genetics of the infected person .

In all cases HSV is never removed from the body by the immune system. Following a primary infection, the virus enters the nerves at the site of primary infection, migrates to the cell body of the neuron, and becomes latent in the ganglion. As a result of primary infection, the body produces antibodies to the particular type of HSV involved, preventing a subsequent infection of that type at a different site. In HSV-1 infected individuals, seroconversion after an oral infection will prevent additional HSV-1 infections such as whitlow, genital herpes, and keratitis. Prior HSV-1 seroconversion seems to ameliorate the symptoms of a later HSV-2 infection, however HSV-2 can still be contracted. Most indications are that an HSV-2 infection contracted prior to HSV-1 seroconversion will immunize that person against HSV-1 infection. This is not necessarily good, as prior HSV-1 infection has the tendency to ameliorate the effects of symptomatic HSV-2 reoccurrences.

Orofacial infection

Orofacial herpes affects the face and mouth. Infection occurs when the virus comes into contact with oral mucosa or abraded skin. Infection by the type 1 strain of herpes simplex virus (HSV-1) is the most common cause of orofacial herpes, though cases of oral infection by the type 2 strain are increasing.

Herpes infections are largely asymptomatic; when symptoms appear they will typically resolve within two weeks.The main symptom of oral infection is acute herpetic gingivostomatitis (inflammation of the mucosa of the cheek and gums), which occurs within 5–10 days of infection. Other symptoms may also develop, including painful ulcers—sometimes confused with canker sores—fever, and sore throat. Primary HSV infection in adolescents frequently manifests as severe pharyngitis with lesions developing on the cheek and gums. Some individuals develop difficulty in swallowing (dysphagia) and swollen lymph nodes (lymphadenopathy). Primary HSV infections in adults often results in pharyngitis similar to that observed in glandular fever (infectious mononucleosis), but gingivostomatitis is less likely.

Recurrent oral infection is more common with HSV-1 infections than with HSV-2. Prodromal symptoms often precede a recurrence. Symptoms typically begin with tingling (itching) and reddening of the skin around the infected site. Eventually, fluid-filled blisters form on the lip (labial) tissue and the area between the lip and skin (vermilion border). The recurrent infection is thus often called herpes simplex labialis. Rare reinfections occur inside the mouth (intraoral HSV stomatitis) affecting the gums, alveolar ridge, hard palate, and the back of the tongue, possibly accompanied by herpes labialis.

Genital infection

Following the classification HSV into two distinct categories of HSV-1 and HSV-2 in the 60s, it was established that "HSV-2 was below the waist, HSV-1 was above the waist". Although genital herpes is largely believed to be caused by HSV-2, genital HSV-1 infections are increasing and now exceed 50% in certain populations, and that rule of thumb no longer applies. HSV is believed to be asymptomatic in the majority of cases, thus aiding contagion and hindering containment. When symptomatic, the typical manifestation of a primary HSV-1 or HSV-2 genital infection is clusters of inflamed papules and vesicles on the outer surface of the genitals resembling cold sores. These usually appear 4–7 days after sexual exposure to HSV for the first time.Genital HSV-1 infection recurs at rate of about one sixth of that of genital HSV-2.

In males, the lesions occur on the shaft of the penis or other parts of the genital region, on the inner thigh, buttocks, or anus. In females, lesions appear on or near the pubis, labia, clitoris, vulva, buttocks or anus. Other common symptoms include pain, itching, and burning. Less frequent, yet still common, symptoms include discharge from the penis or vagina, fever, headache, muscle pain (myalgia), swollen and enlarged lymph nodes and malaise. Women often experience additional symptoms that include painful urination (dysuria) and cervicitis. Herpetic proctitis (inflammation of the anus and rectum) is common for individuals participating in anal intercourse. After 2–3 weeks, existing lesions progress into ulcers and then crust and heal, although lesions on mucosal surfaces may never form crusts. In rare cases, involvement of the sacral region of the spinal cord can cause acute urinary retention and one-sided symptoms and signs of myeloradiculitis (a combination of myelitis and radiculitis): pain, sensory loss, abnormal sensations (paresthesia) and rash. Historically this has been termed Elsberg syndrome, although this entity is not clearly defined.

Herpes whitlow

Herpes whitlow (herpetic whitlow) is a painful infection that typically affects the fingers or thumbs. Occasionally infection occurs on the toes or on the nail cuticle. Herpes whitlow can be caused by infection by HSV-1 or HSV-2.HSV-1 whitlow is often contracted by health care workers that come in contact with the virus; it is most commonly contracted by dental workers and medical workers exposed to oral secretions. It is also often observed in thumb-sucking children with primary HSV-1 oral infection (autoinoculation) prior to seroconversion, and in adults aged 20 to 30 following contact with HSV-2-infected genitals.

Symptoms of herpetic whitlow include swelling, reddening and tenderness of the skin of infected finger. This may be accompanied by fever and swollen lymph nodes. Small, clear vesicles initially form individually, then merge and become cloudy. Associated pain often seems large relative to the physical symptoms. The herpes whitlow lesion usually heals in two to three weeks.

Herpes gladiatorum

Individuals that participate in contact sports such as wrestling, rugby, and soccer sometimes acquire a condition caused by HSV-1 known as herpes gladiatorum, scrumpox, wrestler’s herpes, or mat herpes. Abraded skin provides an area of entry for HSV-1. Symptoms present within 2 weeks of direct skin-to-skin contact with an infected person. They include skin ulceration on the face, ears, and neck, fever, headache, sore throat and swollen glands. It occasionally affects the eyes or eyelids. In one of the largest outbreaks ever among high-school wrestlers at a four week intensive training camp, HSV was identified in 60 of 175 wrestlers. Lesions were on the head in 73 percent of the wrestlers, the extremities in 42%, and the trunk in 28%. Physical symptoms sometimes recur in the skin. Previous adolescent HSV-1 seroconversion would preclude most herpes gladiatorum, but being that stress and trauma are recognized triggers, such a person would be likely to infect others.

Ocular herpes

Ocular herpes is a special case of facial herpes infection, known as herpes keratitis. Ocular herpes is generally caused by HSV-1. It begins with infection of epithelial cells on the surface of the eye and retrograde infection of nerves serving the cornea. Primary infection typically presents as swelling of the conjunctiva and eye-lids (blepharoconjunctivitis), accompanied by small white itchy lesions on the surface of the cornea. The effect of the lesions varies, from minor damage to the epithelium (superficial punctate keratitis), to formation of dendritic ulcers. Infection is unilateral, affecting one eye at a time. Additional symptoms include dull pain deep inside the eye, mild to acute dryness, and sinusitis. Most primary infections resolve spontaneously in a few weeks. Healing can be aided by the use of oral and topical antivirals.

Subsequent recurrences may be more severe, with infected epithelial cells showing larger dendritic ulceration, and lesions forming white plaques. The epithelial layer is sloughed off as the dendritic ulcer grows, and mild inflammation (iritis) may occur in the underlying stroma of iris. Sensation loss occurs in lesional areas, producing generalised corneal anaesthesia with repeated recurrences. Recurrence can be accompanied by chronic dry eye, low grade intermittent conjunctivitis, or chronic unexplained sinusitis. Following persistent infection the concentration of viral DNA reaches a critical limit. Antibody responses against the viral antigen expression in the stroma can trigger a massive autoimmune response in the eye. The response may result in the destruction of the corneal stroma, resulting in loss of vision due to opacification of the cornea. This is known as immune-mediated stromal keratitis.

Herpes simplex encephalitis

Herpes simplex encephalitis (HSE) is one of the most severe viral infections of the human central nervous system. It is estimated to affect at least 1 in 500,000 individuals per year. About 1 in 3 cases of HSE result from primary HSV-1 infection, predominantly occurring in individuals under the age of 18; 2 in 3 cases occur in seropositive persons, few of whom have history of recurrent orofacial herpes. Approximately 50% of individuals that develop HSE are over 50 years of age.

HSE is thought to be caused by the retrograde transmission of virus from a peripheral site on the face following HSV-1 reactivation, along a nerve axon, to the brain. The virus lies dormant in the ganglion of the trigeminal cranial nerve, but the reason for reactivation, and its pathway to gain access to the brain, remains unclear. The olfactory nerve may also be involved in HSE. For unknown reasons the virus seems to target the temporal lobes of the brain.

Most individuals with HSE show a decrease in their level of consciousness and an altered mental state presenting as confusion, and changes in personality. Increased numbers of white blood cells can be found in patient's cerebrospinal fluid, without the presence of pathogenic bacteria and fungi. Patients typically have a fever. and may have seizures. The electrical activity of the brain changes as the disease progresses, first showing abnormalities in one temporal lobe of the brain, which spread to the other temporal lobe 7–10 days later.

Without treatment, HSE results in rapid death in approximately 70% of cases. HSE is fatal in around 20% of cases treated, and causes serious long-term neurological damage in over half of survivors. Only a small population of survivors (2.5%) regain completely normal brain function.