Herpes simplex
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Herpes simplex

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    Herpes simplex Herpes simplex Presentation Transcript

    • Herpes infection Ghodiwala Tossif Ml-610
    • Herpesviridae Virus classification Group: Group I (dsDNA) Order: Herpesvirales Family: Herpesviridae
    • INTRODUCTION A. Herpesviridae - large, enveloped dougle stranded DNA viruses; morphologically alike; share a common mode of replication. B. Herpesviruses - ubiquitous and cause infections ranging from painful skin ulcers to chickenpox to encephalitis.
    • C. An outstanding property - the ability to establish latent infections, to persist indefinitely in infected hosts, and to periodically become reactivated. D. With all these viruses, immunocompromised patients, especially those with altered cellular immunity, have more frequent and severe infections, including severe disease from reactivation of the virus E. Effective antiviral drugs available to treat these infections.
    • CLASSIFICATION A. Alphaherpesviruses are fast growing, cytolytic viruses that establish latent infections in neurons. Herpes simples virus type 1 and 2 (HSV-1 and HSV- 2) and Varicella- zoster virus (VSV) are members of this subfamily. These three viruses produce vesicular rashes both in their primary infections and in reactivation.
    • B. Betaherpesviruses include the slow growing Cytomegalovirus (CMV) - so named because it causes the cells it infects to become cytomegalic – become massively enlarged. These viruses become latent in secretory glands and kidneys. This subfamily also includes the newly identified human Herpesviruses 6 and 7. • Human herpesvirus 6 causes a common childhood illness – sixth disease – roseola infantum. • Human herpesvirus 7 – is closely related to human herpesvirus 6, but is not firmly associated with human disease.
    • C. Gammaherpesviruses, exemplified by Epstein Barr virus (EBV) infect and become latent in lymphoid cells. A new herpesvirus – also called Kaposi's sarcoma associated herpesvirus has been detected in over 90% of Kaposi's sarcomas and a rare type of B cell lymphoma from AIDS patients.
    • Structure
    • Replication Cycle • 1. Virus attaches to the cell receptors (heparan sulfate moiety of cellular proteoglycans) via glycoprotein spikes. • 2. Enters the cell after pH independent fusion with the cell membrane. • 3. Tegument proteins are released, one of which shuts down cellular protein synthesis.
    • • 4. The nucleocapsid is transported along the cytoskeleton to a nuclear pore where viral DNA is released, enters the nucleus, and circularizes. • 5. Viral gene expression is tightly regulated, with three classes of mRNA's, alpha, beta, and gamma, being transcribed in an ordered sequence by cellular RNA polymerase II.
    • • 6. The virus buds through the nuclear membrane. • 7. Enveloped virions accumulate in endoplasmic reticulum and the mature virions are released by exocytosis. The length of the replication cycle varies from 18h (HSV) to over 70h (CMV).
    • Pathogenesis Entry by skin or mucous membranes viral multiplication sensory nerve lysis of cells root ganglia vesicles latency ulcers REACTIVATION COLD FEVER SURGERY UNKNOWN
    • HOW IS LATENCY MAINTAINED? Not fully understood. If interested read about HHV Latency Associated Transcript
    • HERPES SIMPLEX VIRUS DISEASE:
    • Course of the Disease • The incubation period for herpes - 2 to 7 days. • Persons with primary herpetic lesions are infectious for about 7 to 12 days. • Genital, rectal, or oral herpes recurs in 60 to 80% of persons whose primary infection was symptomatic. • These recurrent episodes of herpes are milder and of shorter duration than the initial outbreak.
    • Epidemiology • HSV-1 and 2 infections are life-long. • The virus is found in the lesions on the skin but can be present in body fluids including saliva and vaginal secretions. • As a result of poor hygiene in underdeveloped countries, HSV-1 antibodies are found in more than 90% of children.
    • Epidemiology 2 • HSV-2 is normally spread sexually and is found in the anus, rectum and upper alimentary tract as well as the genital area. • An infant can be infected at birth by a genitallyinfected mother. • The infant can also be infected in utero if the mother’s infection spreads. • Because of the infant’s underdeveloped immune system, the resulting infection can be very severe and sometimes be deadly.
    • Definitions of Infection Types First Clinical Episode • Primary infection – First infection ever with either HSV-1 or HSV-2 – No antibody present when symptoms appear – Disease is more severe than recurrent disease • Non-primary infection – Newly acquired HSV-1 or HSV-2 infection in an individual previously seropositive to the other virus – Symptoms usually milder than primary infection – Antibody to new infection may take several weeks to a few months to appear 22
    • Definitions of Infection Types Recurrent symptomatic infection • Antibody present when symptoms appear • Disease usually mild and short in duration Asymptomatic infection • Serum antibody is present • No known history of clinical outbreaks 23
    • Types of Infection Infection Type Lesions/ Symptoms Type-specific antibody at time of presentation HSV-1 HSV-2 First episode, Primary (Type 1 or 2) +/Severe, bilateral - - First episode, Non-primary Type 2 +/Moderate + - First episode, Recurrence Type 2 +/Mild +/- + Symptomatic, Recurrence Type 2 +/Mild, unilateral +/- + Asymptomatic, Infection Type 2 - +/- + 24
    • Transmission a. HSV-1- usually transmitted in saliva (kissing, sharing of glasses, etc.) b. HSV-2 transmitted by • 1. sexual contact (HSV-2 can infect genitalia, anorectal tissues, or the orpharynx) • 2. autoinoculation • 3. during pregnacy and labour c. Both types can cause oral and genital lesions.
    • Special “at risk” groups: • Neonates • Immunocompromised • Physicians, nurses, dentists, etc. in contact with oral and genital secretions.
    • Immunity a. During primary infection, interferon and natural killer cells limit the progression of the infection. b. Antibody directed against envelope glycoproteins can neutralize extracellular viruses and help limit their spread. Antibody can also participate in ADCC. Viruses can escape antibody neutralization and clearance by: • (1) Direct cell-to cell spread- limiting their time spent outside the cell. • (2) Latent infections of the neurons • (3) Binding the antibody “upside down” with Fc receptors and/or inhibiting C3b c. Cell mediated immunity is essential for controlling and resolving HSV infections. Without functional cell mediated immunity, the virus may disseminate to vital organs and the brain ADCC-Antibody-dependent cellular cytotoxicity
    • Clinical Presentations • The classical presentation of HSV-1 and 2 is the lesion – a clear vesicle on an erythematous base – “the dewdrop on a rose petal”- which then progresses to pustular lesions, ulcers, and crusted lesions.
    • • Primary herpes infection may be asymptomatic or symptomatic. • In women, the primary infection is usually more severe than in men. • lymphadenopathy, as well as flu-like symptoms including fever, headache, malaise, and muscle aches during the first few weeks of infection.
    • Recurrent oral infection is more common with HSV-1 infections than with HSV-2. Symptoms typically progress in a series of eight stages • Latent (weeks to months incident-free): The remission period; After initial infection, the viruses move to sensory nerve ganglia (Trigeminal ganglion), where they reside as lifelong, latent viruses. Asymptomatic shedding of contagious virus particles can occur during this stage.
    • • Prodromal (day 0–1): Symptoms often precede a recurrence. Symptoms typically begin with tingling (itching) and reddening of the skin around the infected site. This stage can last from a few days to a few hours preceding the physical manifestation of an infection and is the best time to start treatment.
    • • Inflammation (day 1): Virus begins reproducing and infecting cells at the end of the nerve. The healthy cells react to the invasion with swelling and redness displayed as symptoms of infection.
    • • Pre-sore (day 2–3): This stage is defined by the appearance of tiny, hard, inflamed papules and vesicles that may itch and are painfully sensitive to touch. In time, these fluid-filled blisters form a cluster on the lip (labial) tissue, the area between the lip and skin (vermilion border), and can occur on the nose, chin, and cheeks.
    • • Open lesion (day 4): This is the most painful and contagious of the stages. All the tiny vesicles break open and merge to create one big, open, weeping ulcer. Fluids are slowly discharged from blood vessels and inflamed tissue. This watery discharge is teeming with active viral particles and is highly contagious. Depending on the severity, one may develop a fever and swollen lymph glands under the jaw.
    • • Crusting (day 5–8): A honey/golden crust starts to form from the syrupy exudate. This yellowish or brown crust or scab is not made of active virus but from blood serum containing useful proteins such as immunoglobulins. This appears as the healing process begins. The sore is still painful at this stage, but, more painful, however, is the constant cracking of the scab as one moves or stretches their lips, as in smiling or eating. Virusfilled fluid will still ooze out of the sore through any cracks.
    • • Healing (day 9–14): New skin begins to form underneath the scab as the virus retreats into latency. A series of scabs will form over the sore (called Meier Complex), each one smaller than the last. During this phase irritation, itching, and some pain are common. • Post-scab (12–14 days): A reddish area may linger at the site of viral infection as the destroyed cells are regenerated. Virus shedding can still occur during this stage.
    • HSV-1 • • • • • • • Oral Herpes – Herpetic Gingivostomatitis Herpes labialis (fever blisters or cold sores) Herpetic whitlow Eczema herpeticum Keratoconjunctivitis Encephalitis Disseminated infections
    • HSV-2 • Genital herpes • Neonatal herpes • Aseptic meningitis
    • Herpes labialis (fever blisters or cold sores) • a milder, recurrent form of infection characterized by crops of vesicles, usually at the mucocutanous junction of the lips or nose. Reoccurs frequently at the same site usually with less severe symptoms.
    • Oral Herpes : Herpetic Gingivostomatitis • an infection of the oral mucosa characterized by redness of oral tissues, formation of multiple vesicles, painful ulcers and fever. Occurs primarily in children characterized by fever, irritability and vesicular mouth lesions. Primary disease is more severe and lasts longer than recurrences. Lesions heal spontaneously in 2-3 weeks. Many children have asymptomatic primary disease and produce neutralizing antibody.
    • Symptoms The symptoms can be mild or severe and may include: • Not able to chew or swallow • Sores on the inside of the cheeks or gums • Fever • General discomfort, uneasiness, or ill feeling • Very sore mouth with no desire to eat • Halitosis (bad breath)
    • Herpetic whitlow • A herpetic whitlow is a lesion (whitlow) on a finger or thumb caused by the herpes simplex virus. • 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.
    • 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, which presents as skin ulceration on the face, ears, and neck. • Symptoms include fever, headache, sore throat and swollen glands. It occasionally affects the eyes or eyelids.
    • Eczema herpeticum • Eczema herpeticum is a rare but severe disseminated infection that generally occurs at sites of skin damage produced by, for example, atopic dermatitis, burns, long term usage of topical steroids or eczema. • It is also known as Kaposi varicelliform eruption, Pustulosis varioliformis acute and KaposiJuliusberg dermatitis. • This infection affects multiple organs, including the eyes, brain, lung, and liver, and can be fatal.
    • Keratoconjunctivitis
    • • Keratoconjunctivitis is inflammation of the cornea and conjunctiva. • Primary infection typically presents as swelling of the conjunctiva and eyelids (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.
    • Herpes esophagitis • Herpes esophagitis is a viral infection of the esophagus caused by Herpes simplex virus. • While the disease most often occurs in immunocompromised patients, including post-chemotherapy, immunosuppression with organ transplants and in AIDS.
    • • Patients with herpes esophagitis experience odynophagia, or painful swallowing and dysphagia. • Other symptoms can include food impaction, hiccups, weight loss, fever and on rare occasions upper gastrointestinal bleeding and tracheoesophageal fistula.
    • Herpesviral encephalitis • Herpes simplex encephalitis (HSE) is a rare, but severe viral infection of the human central nervous system. It is estimated to affect at least 1 in 500,000 individuals per year. • The majority of cases of herpes encephalitis are caused by herpes simplex virus-1 (HSV-1) • About 10% of cases of herpes encephalitis are due to HSV-2, which is typically spread through sexual contact.
    • • 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.
    • Pathophysiology • 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.
    • • HSE results in rapid death in approximately 70% of cases. • survivors suffer severe neurological damage. • Only a small population of survivors (2.5%) regain completely normal brain function. • Earlier treatment (within 48 hours of symptom onset) improves the chances of a good recovery.
    • Genital Herpes • painful vesicular lesions of the male and female genitals and anal area. • Lesions more severe and protracted in primary disease than in recurrence. • Asymptomatic infections occur in both men and women. • Many infections are asymptomatic – many people have antibody to HSV-2 but have no history of disease.
    • How common is genital herpes? • CDC estimates that, annually, 776,000 people in the United States get new herpes infections. • Nationwide, 16%, or about one out of six, people aged 14 to 49 years have genital HSV-2 infection. • Over the past decade, the percentage of persons with genital herpes infection in the United States has remained stable.
    • • Transmission from an infected male to his female partner is more likely than from an infected female to her male partner. • Because of this, genital HSV-2 infection is more common in women (approximately one out of five women aged 14 to 49 years) than in men (about one out of nine men aged 14 to 49 years).
    • symptoms of genital herpes • Most individuals infected with HSV-1 or HSV-2 experience either no symptoms or have very mild symptoms that go unnoticed or are mistaken for another skin condition. Because of this, most people infected with HSV-2 are not aware of their infection. When symptoms do occur, they typically appear as one or more blisters on or around the genitals, rectum or mouth. The blisters break and leave painful sores that may take two to four weeks to heal.
    • • Itching or burning feeling in the genital or anal area • Flu-like symptoms, including fever • Swollen glands • Pain in the legs, buttocks, or genital area • Vaginal discharge
    • Clinical Manifestations Genital Herpes: Primary Lesions Source: Cincinnati STD/HIV Prevention Training Center 72
    • Clinical Manifestations Genital Herpes: Multiple Ulcers Source: Cincinnati STD/HIV Prevention Training Center 73
    • Clinical Manifestations Genital Herpes: Recurrent Ulcer Source: Cincinnati STD/HIV Prevention Training Center 74
    • Clinical Manifestations Genital Herpes: Periurethal Lesions Source: Cincinnati STD/HIV Prevention Training Center 75
    • Clinical Manifestations Genital Herpes: Cervicitis Source: Cincinnati STD/HIV Prevention Training Center 76
    • Clinical Manifestations Herpes on the Buttock Source: Cincinnati STD/HIV Prevention Training Center 77
    • Neonatal herpes simplex • Neonatal herpes simplex is a rare but serious condition, usually caused by vertical transmission of herpes simplex virus from mother to newborn.
    • Transmission • The majority of cases (85%) occur during birth when the baby comes in contact with infected genital secretions in the birth canal, most common with mothers that have newly been exposed to the virus, • an estimated 5% are infected in utero, and approximately 10% of cases are acquired postnatally. Detection and prevention is difficult because transmission is asymptomatic in 60% 98% of cases.
    • FACTORS INFLUENCING TRANSMISSION • • • • • Type of maternal infection (primary/recurrent) Maternal antibody status Duration of rupture of membranes Integrity of mucocutaneous barriers Mode of delivery (C-section/vaginal)
    • INCIDENCE OF NEONATAL DISEASE • 2/1000 mothers are HSV culture + at delivery asymptomatic • 50-70% affected infants born to women asymptomatic at the time of delivery • Antepartum cultures are not useful in assessing risk of neonatal infection • Increased risk w/ primary vs recurrent infection • Incidence from 1/2000 to 1/5000 live births and increasing
    • RISK OF NEONATAL HSV INFECTION • 50% risk: Infants born to women w/ primary infection near the time of delivery • 30% risk: Infants born to mothers with first episode, non-primary infection (antibody to type 1, new acquisition type 2 and vice versa) • 1 to 3% of infants born to mothers w/ recurrent infection • Passive immunity protects against infection , but has little effect on the severity of disease
    • TIMES OF TRANSMISSION • HSV of the newborn is acquired during one of three distinct time intervals: 1. Intrauterine (in utero 5%) 2. Peripartum (perinatal 85%) 3. Psotpartum (postnatal 10%)
    • DISEASE CLASSIFICATION • Disease localized to the skin, eyes and mouth SEM disease accounting for 45% of cases • Encephalitis w/ or w/out CNS involvement accounting for 30% • Disseminated infection including CNC, lungs, etc. accounting for 25% • This classification is predictive of morbidity and mortality
    • DIAGNOSTIC TESTS • Cultures from skin lesions, mouth, nasopharynx, conjunctiva, urine, stool/anorectum and CSF. • Positive cultures at more than 48 hrs are consistent w/ viral replication as opposed to colonization • Serologic tests should not be relied on • PCR testing for CSF HSV DNA is the diagnostic method of choice for HSV encephalitis
    • TREATMENT AND FOLLOW UP • • • • Acyclovir is the treatment of choice SEM 14 days of treatments CNS and disseminated disease 21 days Oral acyclovir contraindicated in neonates for HSV treatment • Ocular involvement requires trifluridine
    • Diagnosis HSV Diagnosis • Clinical diagnosis is insensitive and nonspecific • Clinical diagnosis should be confirmed by laboratory testing: – Virologic tests – Type-specific serologic tests 90
    • Diagnosis Virologic Tests • Viral culture (gold standard) – – – – – • Preferred test if genital ulcers or other mucocutaneous lesions are present Highly specific (>99%) Sensitivity depends on stage of lesion; declines rapidly as lesions begin to heal Positive more often in primary infection (80%–90%) than with recurrences (30%) Cultures should be typed Polymerase Chain Reaction (PCR) – – More sensitive than viral culture; has been used instead of culture in some settings; however PCR tests are not FDA-cleared or widely available Preferred test for detecting HSV in spinal fluid 91
    • Diagnosis Virologic Tests (continued) • Antigen detection (DFA or EIA) – Fairly sensitive (>85%) in symptomatic shedders – Rapid (2-12 hours) – May be better than culture for detecting HSV in healing lesions • Cytology (Tzanck or Pap) – Insensitive and nonspecific and should not be relied on for HSV diagnosis 92
    • Diagnosis Type-specific Serologic Tests • Type-specific and nonspecific antibodies to HSV develop during the first several weeks to few months following infection and persist indefinitely • Presence of HSV-2 antibody indicates anogenital infection • Presence of HSV-1 does not distinguish anogenital from orolabial infection 93
    • Diagnosis Uses of Type-specific Serologic Tests • Type-specific serologic assays might be useful in the following scenarios: – Recurrent or atypical genital symptoms with negative HSV cultures – A clinical diagnosis of genital herpes without laboratory confirmation – A sex partner with herpes – As part of a comprehensive evaluation for STDs among persons with multiple sex partners, HIV infection, and among MSM at increased risk for HIV acquisition 94
    • Diagnosis Evaluation of Genital Ulcer • All patients with genital ulcers should be evaluated with a serologic test for syphilis and a diagnostic evaluation for genital herpes • In settings where chancroid is prevalent, a test for Haemophilus ducreyi should also be performed 95
    • Management • There is no method to eradicate herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. • Analgesics such as ibuprofen and acetaminophen can reduce pain and fever. • Topical anesthetic treatments such as prilocaine, lidocaine, benzocaine or tetracaine can also relieve itching and pain
    • Antiviral There are several antivirals that are effective for treating herpes including: • aciclovir (acyclovir), • valaciclovir (valacyclovir), • famciclovir, • and penciclovir.
    • Management CDC-Recommended Regimens for First Clinical Episode • Acyclovir 400 mg orally 3 times a day for 7-10 days, or • Acyclovir 200 mg orally 5 times a day for 7-10 days, or • Famciclovir 250 mg orally 3 times a day for 7-10 days, or • Valacyclovir 1 g orally twice a day for 7-10 days 98
    • Management CDC-Recommended Regimens for Suppressive Therapy • • • • Acyclovir 400 mg orally twice a day, or Famciclovir 250 mg orally twice a day, or Valacyclovir 500 mg orally once a day, or Valacyclovir 1 g orally once a day 99
    • Management CDC-Recommended Regimens for Episodic Therapy • Acyclovir 400 mg orally 3 times a day for 5 days, or • Acyclovir 800 mg orally twice a day for 5 days, or • Acyclovir 800 mg orally 3 times a day for 2 days, or • Famciclovir 125 mg orally twice a day for 5 days, or • Famciclovir 1000 mg orally twice a day for 1 day, or • Valacyclovir 500 mg orally twice a day for 3 days, or • Valacyclovir 1 g orally once a day for 5 days 100
    • Management Severe Disease • IV acyclovir should be provided for patients with severe disease or complications requiring hospitalization • CDC-Recommended Regimen: – Acyclovir 5-10 mg/kg IV every 8 hours for 2-7 days or until clinical improvement – Follow with oral antiviral therapy to complete at least 10 days total therapy 101
    • Management Allergy, Intolerance, and Adverse Reactions • Allergic and other adverse reactions to acyclovir, valacyclovir, and famciclovir are rare • Desensitization to acyclovir is described by Henry RE, et al., Successful oral acyclovir desensitization. Ann Allergy 1993; 70:386-8 102
    • Management Herpes in HIV-Infected Persons • HIV-infected persons may have prolonged, severe, or atypical episodes of genital, perianal, or oral herpes • HSV shedding is increased in HIV-infected persons 103
    • Management CDC-Recommended Regimens for Daily Suppressive Therapy in HIV-Infected Persons • Acyclovir 400-800 mg orally twice a day or three times a day, or • Famciclovir 500 mg orally twice a day, or • Valacyclovir 500 mg orally twice a day 104
    • Management CDC-Recommended Regimens for Episodic Infection in HIV-Infected Persons • Acyclovir 400 mg orally 3 times a day for 5-10 days, or • Famciclovir 500 mg orally twice a day for 5-10 days, or • Valacyclovir 1 g orally twice a day for 5-10 days 105
    • Management Genital Herpes in Pregnancy • Majority of mothers of infants who acquire neonatal herpes lack histories of clinically evident genital herpes • Risk for transmission to neonate is high (30%-50%) among women who acquire genital herpes near the time of delivery • Risk is low (<1%) in women with histories of recurrent herpes at term or who acquire genital HSV during the first half of pregnancy 106
    • Management Genital Herpes in Pregnancy (continued) • Prevention of neonatal herpes depends on: ✓ avoiding acquisition of HSV during late pregnancy ✓ avoiding exposure of the infant to herpetic lesions during delivery • All pregnant women should be asked whether they have a history of genital herpes 107
    • Management Genital Herpes in Pregnancy (continued) • At the onset of labor: – All women should be questioned carefully about symptoms of genital herpes, including prodromal – All women should be examined carefully for herpetic lesions • Women without symptoms or signs of genital herpes or its prodrome can deliver vaginally 108
    • Management Genital Herpes in Pregnancy (continued) • Safety of acyclovir, valacyclovir, famciclovir in pregnancy not definitively established, but no clear evidence for increased birth defects • Oral acyclovir may be given for first-episode or severe recurrent herpes; IV acyclovir should be used for severe infection • Suppressive acyclovir late in pregnancy reduces frequency of cesarean sections in women with recurrent genital herpes; many specialists recommend it 109
    • Prevention 110
    • Prevention Patient Counseling and Education • Goals – Help patients cope with the infection – Prevent sexual and perinatal transmission • Counsel initially at first visit • Education on chronic aspects may be beneficial after acute illness subsides • HSV-infected persons may express anxiety about genital herpes that does not reflect the actual clinical severity of their disease 111
    • Prevention Patient Counseling and Education • Counseling should include: – – – – Natural history of the infection Treatment options Transmission and prevention issues Neonatal HSV prevention issues • Emphasize potential for recurrent episodes, asymptomatic viral shedding, and sexual transmission 112
    • Prevention Counseling: Natural History • Recurrent episodes likely following a first episode; with HSV-2 more than HSV-1 – – – • Frequency of outbreaks may decrease over time Stressful events may trigger recurrences Prodromal symptoms may precede outbreaks Asymptomatic viral shedding is common and HSV transmission can occur during asymptomatic periods 113
    • Prevention Counseling: Treatment • Suppressive therapy available and effective in preventing symptomatic recurrences • Episodic therapy sometimes useful in shortening duration of recurrent episodes • When and how to take antiviral medications • Recognition of prodromal symptoms to know when to begin episodic therapy 114
    • Prevention Counseling: Transmission and Prevention • Inform current and future sex partners about genital herpes diagnosis • Abstain from sexual activity with uninfected partners when lesions or prodrome present • Correct and consistent use of latex condoms might reduce the risk of HSV transmission • Valacyclovir suppressive therapy decreases HSV-2 transmission in heterosexual couples in which source partner has recurrent herpes 115
    • Prevention Counseling: Neonatal Herpes Prevention • Risk of neonatal HSV infection should be explained to all patients, including men • Pregnant women should inform their prenatal/perinatal providers that they have genital herpes • Pregnant women without HSV-2 infection should avoid intercourse during third trimester with men who have genital herpes • Pregnant women without HSV-1 infection should avoid oral sex from a partner with oral herpes 116
    • Prevention Counseling for Asymptomatic Persons • Give asymptomatic persons diagnosed with HSV-2 infection the same counseling messages as symptomatic persons • Teach the common manifestations of genital herpes, as many patients will become aware of them with time 117
    • Prevention Partner Management • Symptomatic sex partners – Evaluate and treat in the same manner as patients who have genital lesions • Asymptomatic sex partners – Ask about history of genital lesions – Educate to recognize symptoms of herpes – Offer type-specific serologic testing 118