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Herpes Simplex Virus (HSV)

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HSV-1-normally associated with orofacial infections and encephalitis and HSV-2 usually causes genital infections and can be transmitted from infected mothers to neonates.

Has a peak incidence between age 1 and 3 years.

HSV-1 is primarily transmitted by infected oral secretions or active lesions of other patients.

Common severe infections include encephalitis, meningitis, neonatal herpes, and, in immunocompromised patients, disseminated infection.

Mucocutanteous infections cause clusters of small painful vesicles on an erythematous base.

The oral lesions are clusters of vesicles, which subsequently break down rapidly to form 1- to 5-mm shallow ulcers with a yellow-gray base and an erythematous halo.

If these small lesions coalesce irregular ulcerations may appear.

Lesions may develop throughout the oral cavity mucosa, on and around the lips, along the gingivae, on the anterior of the tongue, and the hard palate.

Reactivation of the virus in the trigeminal sensory ganglion may result in herpes labialis.

Recurrent labial herpes affects about one third of the US population.

Recurrent herpes simplex labialis occurs 1 to 6 times per year.

2012 it was estimated approximally 417 million globally sexually active adults 15 to 49 years of age and had an existing prevalent HSV-2 infection.

From 1999-2010 a US survey showed a 15.7% prevalence of HV-2 among patients 14 to 49 years of age.

The diagnosis is usually clinical: typical appearance and location of the lesions.

Less commonly viral culture, Tzanck smear, direct fluorescent antibody testing, and amplification of viral DNA using PCR are used for diagnosis.

 

 

 

A Tzanck smear demonstrating multinucleate giant cells is highly suggestive of HSV infection, but culture and antibody staining results are diagnostic.

 

 

 

Tissue biopsy may also be used to obtain a definitive diagnosis.

 

Laboratory confirmation by culture, PCR, direct immunofluorescence, or serologic testing can be done.

Both types of herpes simplex virus (HSV), HSV-1 and HSV-2, can cause oral or genital infection.

Most often, HSV-1 causes gingivostomatitis, herpes labialis, and herpes keratitis.

Reactivation of the virus in the trigeminal sensory ganglion may result in herpes labialis.

Complications of herpetic gingivostomatitis include: secondary bacterial infection, viremia, Bell’s palsy, and meningoencephalitis.

 

In rare cases, HSV can cause a systemic infection, although in healthy hosts its presentation is generally limited to a mucocutaneous vesicular eruption.

HSV-2 usually causes genital lesions.

Transmission of HSV results from close contact with a person who is actively shedding virus.

Viral shedding occurs from lesions but can occur even when lesions are not apparent.

Herpetic gingivostomatitis is the most common specific clinical manifestation of primary herpes simplex virus (HSV) infection in children.

More than 90% of Herpetic gingivostomatitis cases are caused by HSV type 1.

Has a mean incubation period of 4 days.

Incubation period ranges from 2 to 12 days.

Patients may experience a prodromal sensation of burning or paresthesia at the inoculation site.

Herpetic Gingivostomatitis has a mean incubation period of 4 days.

Incubation period ranges from 2 to 12 days.

Fever, malaise, irritability, anorexia, loss of appetite, sleeplessness, and headache may be present.

Oral lesions that appear 1 to 2 days later are usually accompanied by severe pain in the mouth, fever, hypersalivation, halitosis, and refusal to eat or drink.

The oral lesions are clusters of vesicles, which subsequently break down rapidly to form 1- to 5-mm shallow ulcers with a yellow-gray base and an erythematous halo.

These ulcer lesions extremely painful and have a tendency to bleed.

Herpetic gingivostomatitis lesions heal without scarring.

The gingiva is inflamed, swollen, red, friable, and bleed easily when touched.

The cervical, submandibular, and submental lymph nodes are usually swollen and tender.

If these small lesions coalesce irregular ulcerations may appear.

Lesions may develop throughout the oral cavity mucosa, on and around the lips, along the gingivae, on the anterior of the tongue, and the hard palate.

These ulcer lesions extremely painful and have a tendency to bleed.

Herpetic gingivostomatitis lesions heal without scarring.

The gingiva is inflamed, swollen, red, friable, and bleed easily when touched.

The cervical, submandibular, and submental lymph nodes are usually swollen and tender.

Herpetic gingivostomatitis typically resolves in 10 to 14 days.

The infection may spread to other parts of the body by autoinoculation: perioral lesions, herpetic esophagitis, herpetic keratitis, and eczema herpeticum.

Reactivation of the virus in the trigeminal sensory ganglion may result in herpes labialis.

The diagnosis is usually clinical: typical appearance and location of the lesions.

Less commonly viral culture, Tzanck smear, direct fluorescent antibody testing, and amplification of viral DNA using PCR are used for diagnosis.

Treatment is mainly symptomatic

The use of NSAIDs, and hydration are typical.

 

 

 

Chlorhexidine gluconate mouthwash can be used to decrease mucosal pain and to prevent secondary infection.

Systemic acyclovir is considered for severe herpetic cases and, should be initiated within 3 days of the onset of symptoms.

The use of NSAIDs, and hydration are typical.

It can occur in adolescents and adults but most commonly affects children aged 6 months to 5 years.

After the initial infection, HSV remains dormant in nerve ganglia, from which it can periodically emerge, causing symptoms. Recurrent herpetic eruptions are precipitated by

Overexposure to sunlight

Febrile illnesses

Physical or emotional stress

Immunosuppression

Unknown stimuli

Generally, recurrent eruptions are less severe and occur less frequently over time.

HSV usually causes mucocutaneous infection but sometimes causes keratitis, and serious CNS infection can occur in neonates and in adults.

After initial infection, HSV remains dormant in nerve ganglia, from which it can periodically emerge, causing symptoms.

Diagnose mucocutaneous infections clinically, but do viral culture, PCR, or antigen detection if patients are neonates, immunocompromised, or pregnant or have a CNS infection or severe disease.

 

A Tzanck smear demonstrating multinucleate giant cells is highly suggestive of HSV infection, but culture and antibody staining results are diagnostic.

 

Tissue biopsy may also be used to obtain a definitive diagnosis.

 

Thymidine kinase inhibitors are the most commonly used antivirals to treat HSV infections: acyclovir, valacyclovir, and famciclovir.

 

Treatment is symptomatic; antiviral therapy with acyclovir, valacyclovir, or famciclovir is helpful for severe infections and, if begun early, for recurrent or primary infections.

Give IV acyclovir to patients with serious infections.

For mucocutaneous infections, consider oral acyclovir, valacyclovir, or famciclovir; for herpes labialis, an alternative is topical penciclovir or docosanol.

Sun-Saharan Africa has 80% of sexually active women and up to 50% of sexually active men infected with HSV-2, the most severely infected area in the world.

Recurrent herpes simplex labialis appears at the vermillion border of the lip and 90% of cases.

Recurrent herpes simplex labialis occurs in the palate in 5% of cases, and rarely may involve the chin or the oral mucosa.

Recurrent herpes simplex labialis presents as papules on an erythematous base and becomes vesicular within hours.

Recurrent herpes simplex labialis eventually progresses through ulceration, crusting and healing within 72-96 hours.

Herpes simplex virus type 2  (HSV-2)  is one of the most common sexually transmitted infections worldwide.

Herpes simplex virus type 2  (HSV-2)  Is a primary cause of genital and neonatal herpes and genital ulcer disease.

HSV-2 infection increases the risk for HIV infection by at least two fold.

HSV-2  infection is a lifelong one.

The prevalence  of HSV-2  among individuals aged 14-49 years participating in the NHANES  2005-2008  was 16.2% overall, with the highest seroprevalence highest among women, 20.9%, and  blacks, 39.2%.

Preventing HSV-2  infection includes minimizing the number of sexual partners, avoiding concurrent sexual partnerships and using condoms.

All patients with HSV-2 infection  should  be tested for HIV infection.

Recurrent herpes simplex labialis associated in 60% of patients with prodromal symptoms of tingling, itching and burning before skin lesions appear (Cernik C et al).

Recurrent herpes simplex labialis treated usually with acyclovir, valacyclovir, and famciclovir.

Herpes simplex virus 2 is the most common cause of genital ulcers worldwide.

Herpes simplex virus 2 is one of the most frequent sexually transmitted infections worldwide with estimated 536 million infected persons and an annual incidence of 23.6 million cases among people 15-49 years.

In the US 16% of adults are HSV2 seropositive.

Only 10-25% of patients with HSV-2 infections have recognized genital herpes.

Most cases of HSV-2 are acquired without a clinical history of genital herpes.

Risk of sexual transmission of HSV-2 does not correlate with recognition of clinical signs and symptoms but more likely correlates with viral mucosal shedding.

HSV encoded proteins bind HIV in co-infected cells and directly promote transcription of HIV.

Patients infected with both HIV and HSV-2, reactivation of HSV-2 has been associated with increased HIV levels in the blood and genital tract.

Clinical manifestations of HSV-2 range from insignificant or mild genital symptoms in most persons with HIV infection to severe genital ulcer disease in patients with advanced HIV.

Shedding of herpes simplex virus occurs from the genitals in patients with HIV infection often when they have no symptoms or observable lesions.

Most patients with HSV2 intermittently shed virus on the genital skin or mucosa

HSV- 2 may increase the infectiousness of HIV.

The risk of transmission of HIV-1 to sexual partners is 4 fold among HIV patients with a symptomatic genital ulcer, compared with HIV patients without a genital ulcer: the majority of genital ulcers are related to HSV-2 infection (Gray RH).

HSV encoded proteins bind HIV in co-infected cells and directly promote transcription of HIV.

Patients infected with both HIV and HSV-2, reactivation of HSV-2 has been associated with increased HIV levels in the blood and genital tract.

Clinical trials reveal that daily treatment for HSV-2 for 8-12 weeks can reduce plasma HIV-1 levels by 0.25 to 0.50 log10 copies per mL.

Daily acyclovir does not reduce risk of transmission of HIV-1 despite reductions in plasma HIV-1 levels and a 73% reduction in the occurrence of HSV-2 genital ulcers (Partners in Prevention HSV/HIV Transmission Study Team).

Most patients with infections are asymptomatic or have minimal signs and symptoms.

Suppressive therapy with antiviral treatment prevents recurrence of localized diseasein people with genital, ot orolabial HSV infections.

Signs include blisters or sores on the lips, mouth, nose, face genitals, and buttocks.

Infections are very contagious and are spread by direct contact with the skin lesions.

Herpes labialis is a common cause of mouth area infection with HSV-1.

Most patients wit an HSV-1 infection will be infected by age 20 year.

Herpes Simplex encephalitis is the most frequent recognized form of sporadic encephalitis in the U.S.

Neuroimaging and electroencephalography usually indicate the presence of involvement of the temporal lobes in Herpes simplex encephalitis.

The basal ganglia and cerebellum are rarely involved in herpes simplex encephalitis.

In encephalitis nucleic acid amplification test for herpes simplex virus type 1 in the cerebrospinal fluid is highly sensitive and specific for the diagnosis.

Use of condoms, in a pooled analysis, moderately protects against HSV-2 acquisition: consistent use of condoms reduced risk of acquiring HSV-2 by 30% compared to persons who reported no condom use(Martin EY).

Rarely this virus can cause life-threatening hepatitis in pregnant women, usually in the third trimester, and in the absence of mucocutaneous lesions.

22% of pregnant women are seropositive for herpes simplex virus, and 2% of susceptible pregnant women acquire a primary herpes simplex virus infection (Xu F et al, Brown ZA et al).

Approximately 15,000 fetuses per year are potentially exposed to acyclovir and other similar drugs.

In the Danish study 1804 patients were exposed to acyclovir, valacyclovir and famciclovir during the first trimester of pregnancy: major birth defects were detected in 2.2% of infants exposed to these antiviral drugs and 2.4% of the unexposed infants (Pasternak B, Hviid A).

Neonatal HSV outcome depends on extent of disease, with approximately 30% of infants with disseminated disease dying and 20% have neurologic sequelae (Kimberlin DW et al).

Only 6% of neonates with HSV CNS disease die, while 70% have permanent neurological damage.

Neonatal HSV with skin, eye and mouth disease is usually only rarely associated with neurologic impairment a not with death.

HSV in sensory ganglia have latent periodic reactivation of localized disease.

Whether CNS HSV subclinically reactivates is not known.

Infants with neonatal HSV and surviving with CNS involvement have improved neurodevelopment outcomes with oral acyclovir therapy for 6 months (Kimberlin DW et al).

 

 

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