Please help us continue educating the public about herpes and cold soresMAKE A DONATION
SPEAK TO A COUNSELLOR (weekdays 9am-5pm)
TOLL FREE PHONE: 0508 11 12 13
FROM A MOBILE: 09 433 6526
MAKE A DONATION
View the NZHF genital herpes guidelines here
Produced by the Professional Advisory Board (PAB) of the Sexually Transmitted Infections Education Foundation
This document is a consensus opinion of the Professional Advisory Board (PAB) of the Sexually Transmitted Infections Education Foundation. The PAB has representation from medical and nursing disciplines involved in the management of people with genital herpes. The PAB works on a voluntary basis.
These guidelines have been produced by considering available literature, both local and international, and by basing the recommendations on the evidence in the literature or reasonable suppositions and opinions of experts.
The guidelines’ recommendations have been rated under the following evidence-based categories:
Grade A: Very strong evidence
Based on well-designed prospective randomised controlled clinical trials.
Grade B: Fairly strong evidence
Based on evidence from case-control or cohort studies, or clinical trials lacking one or more of the above features.
Grade C: Weak evidence or firmly held opinion
Based on published case reports, well-written reviews or consensus.
Primary infection: Recently acquired infection with HSV-1 or HSV-2 with an absence of antibodies to either type on serological testing.
Non-primary infection: Recently acquired infection with a virus type in the presence of antibodies to the other virus type, e.g. HSV-2 in a person with previous antibodies to HSV-1, but the absence of antibodies to HSV-2 on serological testing.
First episode: First clinical episode of genital HSV-1 or HSV-2. Maybe a primary or non-primary or first recognised clinical expression of previously acquired infection weeks, months or years before.
Recurrence: Previously acquired HSV-1 or HSV-2 infection with antibodies to the same type on serological testing.
The special authority and Hospital Medicines List restriction were removed from 1 March 2016 (Pharmac).
This is recommended first-line treatment.
Prescribe enough tablets for patients to be able to self-initiate treatment at the onset of symptoms.
Only recommended for people with HSV confirmed on testing. Given daily to prevent recurrences and reduce asymptomatic shedding. Suggest prescribing for 12 months, followed by a break of 3 months to see if recurrences are still frequent and/or bothersome.
Fact: Genital herpes is caused by both HSV-1 and HSV-2 although HSV-1 is less likely to cause recurrent symptoms.
Fact: As HSV-1 and -2 have different natural histories, it is important to ask for specific typing (so patients can be better informed).
Fact: Serological testing is not recommended as an acute diagnostic or routine screening tool. It is recommended only in limited clinical scenarios (see page 9).
Fact: HSV antibodies take several weeks and even months to develop after infection; false negatives and false positives are common.
Fact: All first episodes of genital herpes should be treated regardless of the timing of onset of symptoms (see page 10).
The purpose of this guideline is to dispel common misconceptions and hopefully improve current management of those with herpes infection.
The NZHF has a range of resources to assist patients and clinicians.
Phone: Herpes Helpline tollfree 0508 11 12 13
A diagnosis of genital herpes can have a profound effect. Patients tell us they want –
There are no vaccines currently available for HSV infection, but the pipeline is rich with candidates in various phases of development. Vaccines are currently being developed both to prevent HSV-2 infection (preventive) and to treat HSV-2 infection (therapeutic).1
Genital herpes is an infection caused by the herpes simplex virus (HSV) and, for practical purposes, encompasses lesions on the genital area and nearby areas (i.e. buttocks, anal area and thighs). Genital herpes may be due to HSV-1 (the usual cause of orolabial herpes) or HSV-2 (more commonly associated with genital lesions). It is a very common infection that is often under-recognised, as a person may be asymptomatic or have only very minor symptoms.
HSV-2 prevalence varies between countries, being higher in the USA than in Europe, Australia and New Zealand. It also varies depending on the demographics of the population being tested.2 Consistent findings between countries are that HSV-2 seroprevalence increases with:
Age: The incidence of new infections is highest amongst young adults, but an infection is lifelong, overall prevalence increases with increasing age.2Participants in the Dunedin Multidisciplinary Health and Development cohort study provided serum for HSV-2 antibody status at the ages of 21, 26, 32 and 38. By the age of 38, 26.8% of women had been positive for HSV-2 compared to 17.3% for men, confirming a higher biological susceptibility to infection for women. The infection rate for women was highest at age 21-26 compared to 26-32 for men and then declined in both genders with age, consistent with decreasing infectivity of long-term prevalent infections.3
HSV-1 seroprevalence studies cannot distinguish between oral and genital infection sites which makes it much more difficult to estimate the prevalence of genital HSV-1 infection. Clinical case data has limitations as well. That said, HSV-1 accounts for 35% of confirmed anogenital infections in Australia4 and similarly, a Waikato-wide study found 30-40% of anogenital isolates are due to HSV-1 each year.5 In that study, HSV-1 accounted for 53% of positive isolates from under-25 year olds, 30% in the 25–35 year olds, and 26% from over-35 year olds. Likewise, an Auckland Sexual Health Clinic study in 2004 found most true primary (see Glossary of terms page 3) episodes of genital herpes were HSV-1, whilst non-primary first episodes (see Glossary of terms page 3) and recurrences were mostly HSV-2.6
Like HSV-2, HSV-1 seroprevalence increases with increasing age and tends to be more common in women.7
Note: Routine typing of isolates enhances a clinician’s ability to give prognostic information and optimal clinical care. It is no longer accurate to assume that genital herpes is due to HSV-2 infection, as a substantial proportion of people will have HSV-1.8 The natural history of genital HSV-1 infection is towards significantly fewer clinically apparent recurrences and much less subclinical shedding. Also, prior HSV-1 infection does not alter the risk of acquisition of HSV-2, although it does lessen the symptoms; it is important for those diagnosed with HSV-1 genital herpes to understand that they remain at risk of HSV-2 infection.
Most infections are acquired from someone who is unaware they are infected, who may have mild or asymptomatic infection.
Herpes simplex virus enters the body, either through a break in the skin or through mucous membranes, during direct contact with infected secretions or mucosal surfaces. For genital infections, this is usually during sexual contact, with HSV-2 commonly transmitted during vaginal or anal sex and HSV-1 commonly passed on through oral-genital sex.
Transmission is most likely to occur:
Therefore, sexual contact should be avoided when active lesions are present.
Transmission may occur when a partner is shedding virus asymptomatically. Most people who acquire genital herpes get it from someone who is unaware they are infected, who may have mild or asymptomatic infection.10
It is important to remember that not all first episodes of HSV-1 or HSV-2 represent a new or recently acquired the infection. It may be a first clinically recognised episode of a previously unrecognised or asymptomatic infection acquired weeks, months or years previously.
The virus is readily inactivated at room temperature and by drying; hence, non-contact forms of spread, for example via fomites (inanimate objects) are considered unlikely. Autoinoculation resulting in spread to different anatomical sites can occur (e.g. orolabial, whitlow), although this is believed to be uncommon. Grade C
Nearly everyone, both men and women, with genital HSV-2 infection, sheds virus from time-to-time without symptoms, which is why sexual transmission can occur during asymptomatic periods. These intermittent episodes of asymptomatic viral shedding are more frequent:
The viral load threshold for transmission from an episode of asymptomatic shedding has not been established. For a given individual it is impossible to be certain when asymptomatic viral shedding occurs, but it is important not to give the impression that people are infectious all the time.
Male and female condoms do not give absolute protection for a variety of reasons: condoms do not cover all affected areas, condom breakage or slippage may occur, close genital contact or contact with infectious secretions may occur during foreplay, etc.11Nonetheless, consistent condom use offers moderate protection against HSV-2 infection in both men and women.12Grade B Data on male condoms preventing transmission to men or on the efficacy of female condoms is lacking. Condom use should be discussed with the couple and tailored to the individual circumstances.
People who do not acquire HSV-1 during childhood are at risk of HSV-1 at any site, including genital infection, during adulthood. Transmission may occur whilst receiving oral sex from someone who has oral HSV-1, even if the source partner is asymptomatic. It is estimated that up to a third of persons who are HSV-1 antibody positive do not have a clinical diagnosis of oral herpes,13 but will still shed HSV-1 virus.14 It is generally accepted that prior orolabial HSV-1 infection protects an individual against genital HSV-1. Possible exceptions may be those infected simultaneously at more than one site or those with very recent HSV-1 infection who have not yet seroconverted. Oral HSV-2 in isolation is uncommon.
Oral-genital contact should be avoided when oral lesions are present. Grade C
Aciclovir, famciclovir and valaciclovir all suppress symptomatic and asymptomatic shedding, by up to 80-95%.15 Also, it has been shown that suppressive once-daily valaciclovir results in reduced transmission to the discordant partner.16 For partners, there was a 48% reduction in acquisition of HSV infection and a 75% reduction in clinical symptomatic genital herpes. Other antivirals may be similarly effective, but this has not been proven in clinical trials.
In most studies, pre-existing HSV-1 infection does not decrease the risk of HSV-2 infection, but prior HSV-1 means HSV-2 infection is more likely to be asymptomatic.17 If HSV-2 genital infection is acquired first, then a new HSV-1 genital infection does not affect the frequency of recurrences.
Clinical diagnosis alone is insensitive and inaccurate, with a 20% false positive rate.17Suspected genital herpes must be confirmed by PCR. Recurrent lesions, which have not been previously confirmed, likewise should be tested for HSV. However, it is important not to delay appropriate therapy while awaiting confirmation.
Detection of herpes simplex virus DNA by PCR in the lesion establishes the diagnosis. Vesicles offer the best source of the virus. However, results depend on multiple factors, including the adequacy of the specimen and the time delay between the onset of symptoms and presentation, therefore a negative result may not exclude infection.
PCR has a low false positive rate. However, a negative test result does not necessarily exclude HSV infection since all methods are dependent on an adequate collection of the specimen. Viral typing is routinely reported.
Serology is not recommended for the following reasons:
For most partners of positive patients, education and not serology is recommended because of false positive/false negative serology results.
A positive HSV-2 serology result may cause significant psychological morbidity (see page 13).
KEY INFORMATION TO DISCUSS WITH A PATIENT WHO ASKS FOR A BLOOD TEST
Table 1: Interpreting Blood Test Results
The first clinical episode of genital HSV-1 or HSV-2 may, but does not always, reflect recent acquisition of infection. It may represent a primary HSV infection or a new non-primary infection or a first recognised clinical expression of a previously acquired infection. It is not possible to reliably distinguish between these on clinical grounds alone. Nonetheless, as the first episode genital herpes is generally more severe and/or more prolonged, treatment should always be offered regardless of time of symptom onset.
Valaciclovir prescriptions do not require specialist authorisation and the medication is available through any pharmacy. Patients are often very unwell and therapy should be initiated regardless of how long the lesions have been present and before virological confirmation. This is based on evidence that the virus is shed from the infected area for a median of 11 days, with systemic and local symptoms lasting 2-3 weeks if untreated. Oral antiviral therapy substantially reduces the duration and intensity of symptoms.18,19Grade A
Management for patients presenting with the first episode of genital herpes should encompass the following:
(a) Virus swab for PCR for diagnosis.
(b) Consider screening for other STIs if appropriate, although this may be deferred to a follow-up visit, as it is often too painful.
4. Treatment involving:
(a) Oral antiviral therapy.
(b) Symptomatic treatment.
(c) Provide patient information with written material or refer to www.herpes.org.nz
(d) Acknowledgement of the psychosocial impact of the disease.
(e) Referral to support systems – Herpes Helpline tollfree 0508 11 12 13.
5. Appropriate follow-up arrangements.
It is not necessary or desirable to attempt to cover all these issues at the initial clinical assessment. However, recognition of the psychosocial impact of the diagnosis, and the provision of adequate information and/or referral to the Herpes Helpline, is important.
It may be helpful to discuss how results will be given, e.g. in person, over the phone. If giving results over the phone, check the person is in an appropriate situation to receive the call.
Symptoms may appear 2-20 days following exposure to infection with the virus. However, initial symptoms of genital herpes may not be recognised or may not occur until months to years later. Symptom severity differs markedly with severe cases having lesions lasting up to 3 weeks.
The prodrome (if experienced) is signalled by flu-like symptoms of fever, headache and general myalgia, accompanied by local tingling, irritation and/or pruritus or pain in the genital region. Rapidly, pruritic erythematous papules appear, followed by multiple small vesicles that contain clear to a cloudy fluid. These vesicles rupture within 1-2 days to form painful, sloughy, shallow ulcers with irregular margins, which may become confluent. The area may be oedematous and can be extremely tender. Pain on urination is typical, particularly in women and spontaneous urination may be impossible. The ulcers dry to form crusts and later heal, leaving a transient red macule with minimal scarring (if any). Less commonly, lesions can pass through the blister phase quickly and blisters may not be noticed. Involvement of the cervix occurs but speculum examination may not be possible. Lesions may also appear extra-genitally, commonly on thighs and buttocks and less commonly on hands, lips, face and breasts. Local lymph nodes, i.e. inguinal nodes with genital infection, are usually enlarged and tender.
Women are more severely affected than men. Immunosuppressed people may develop a very extensive disease.
A relevant specialist should review any patient with complications.
An examination should include inspection of the genital region; speculum examination should be considered but may need to be delayed if discomfort is anticipated.
Laboratory confirmation of the diagnosis is important, but should not delay the initiation of treatment. A negative result does not necessarily exclude a diagnosis of HSV (see pages 8-9).
If there is a possibility of pregnancy, please refer to page 18. Refer immunocompromised patients, or those with herpetic proctitis, to an appropriate specialist, e.g. infectious diseases, sexual health.
The recommended treatment for first episode genital herpes:
Lesions may not completely heal over during the course of drug treatment; similarly, mild neurological symptoms may not yet have fully resolved. Nonetheless, a further course of therapy is not usually indicated unless new lesions continue to appear.
2. Intravenous antivirals
Intravenous (IV) aciclovir therapy could be considered for patients who have severe disease or complications that necessitate hospitalisation.24
3. Topical antivirals
Topical aciclovir creams are not recommended because they offer a minimal clinical benefit (see page 16).
In addition to oral antivirals, other measures to control symptoms should be suggested. Paracetamol 4-hourly is usually adequate, but stronger pain relief may be necessary. Drinking fluids hourly produce dilute urine that is less painful to void. Female patients can be advised to sit in a bath or bowl of warm water to pass urine. Advice about drying lesions with the lowest setting of a hair dryer may be helpful. Bathing in salt water (e.g. half a cup of household salt in the bath or 2 teaspoons per litre of warm water for topical application) may help relieve pain and promote healing. Adequate pain relief should be provided. Topical anaesthetic jelly such as lignocaine (Xylocaine) gel applied 5 minutes before micturition helps relieve the pain. As lignocaine is a potential skin sensitizer, patients should be warned to use it for the shortest possible time (usually 1 or 2 days maximum). Grade C
It is important to ensure that patients receive accurate up-to-date information about genital herpes. A range of printed materials can be downloaded from the NZHF website or ordered at no cost (please refer to resources listed on the inside front cover). Primary care practitioners should have access to these resources or be able to advise their patients on how to obtain them, e.g. www.herpes.org.nz. There is also a Herpes Helpline 0508 11 12 13, a telephone service which is free to all New Zealanders.
Informing the patient of the diagnosis can be a delicate matter. Health providers may find it helpful to review the 3 minute PowerPoint resource on the NZHF website www.herpes.org.nz which provides information on what patients tell us they want to know at this point in their management. Although initial counselling can be provided at the first visit, it may be preferable to wait until the initial outbreak settles to discuss chronic aspects of the infection. Written materials, such as the NZHF Myth vs Facts leaflet and The Facts booklet, should be offered to patients at the first visit with discussion and further questions encouraged at the follow-up and subsequent visits.
See Key Information for Health Professionals to Give Patients in Counselling on page 34. Grade C
Follow-up is important for those with first episode herpes. For most patients, one visit is insufficient to properly manage the impact of genital herpes. Counselling and advice often form the major part of a follow-up appointment and time should be allowed for this. The practitioner should be alert to the possibility of further psychological problems manifesting after a diagnosis of genital herpes.
At the initial visit, a follow-up appointment should be offered for 5-7 days later, to evaluate symptoms, their psychological status, complete a full STI screen if appropriate, discuss results and answer any questions they may have. It should be noted that it might take longer than 5 days for skin lesions to heal completely. Further therapy is not usually required unless new lesions continue to appear.
Anticipatory episodic therapy is recommended. Episodic antiviral therapy is more effective when patients start therapy themselves at the first signs of a recurrence. Grade A
Suppressive antiviral therapy can be considered for those with frequent and/or severe recurrences or associated psychosocial morbidity. It is suggested that either a minimum of two recurrences or approximately 3 months without suppressive therapy is required to establish the pattern.
Management of recurrent herpes depends on whether there is prior virological confirmation of infection. Management of patients presenting with recurrent herpes should encompass the following:
(a) Viral swab for PCR for diagnosis; confirmation of diagnosis at least once is strongly recommended.
(b) Consider exclusion of other STIs if appropriate.
4. Treatment involving:
(a) Either episodic therapy or suppressive therapy where appropriate.
(b) Symptomatic treatment.
(c) Education concerning transmission, epidemiology, etc; provide written material.
(d) Acknowledgement of the psychosocial impact of the disease.
(e) Referral to support systems – Herpes Helpline tollfree 0508 11 12 13 or visit www.herpes.org.nz.
5. Appropriate follow-up arrangements.
Sufficient time should be allowed to address all these aspects.
A specialist should review any patient with complications.
The aim of episodic treatment is to reduce symptoms and duration of viral shedding during recurrences, rather than reduce the frequency of recurrences. Further, early therapy may abort episodes, that is, lesions may be prevented from progressing beyond the papular stage.26,27 In situations where patients have well-recognised prodromes and/or have less frequent recurrences, some may find episodic treatment preferable to continuous suppressive therapy.
Effective episodic antiviral treatment of recurrent herpes requires initiation of therapy during the prodrome that precedes some outbreaks or within one day of lesion onset. Beyond this timeframe, there is no clear benefit, so it is important that a prescription is readily available. In consultation with the patient, sufficient quantities of medication may be prescribed with instructions to start treatment as soon as symptoms begin. Grade A
If the patient is pregnant, specialist consultation is recommended (see page 18). In cases of immunocompromised patients, refer to an appropriate specialist.
Prescribe enough tablets for patients to be able to self-initiate treatment at the onset of symptoms.
Note: Famciclovir is not subsidised or marketed in New Zealand.
Suppressive therapy is an oral antiviral taken continuously over a given period of time that effectively reduces the frequency of recurrences. Grade A
The main aims of suppressive therapy are:
Aciclovir, famciclovir and valaciclovir all suppress symptomatic and asymptomatic shedding, by up to 80-95%.15Suppressive once-daily valaciclovir has been shown to reduce transmission to an uninfected partner with a 48% reduction in acquisition of HSV infection and a 75% reduction in clinical symptomatic genital herpes.16 Other antivirals may be similarly effective, but this has not been proven in clinical trials. Patients may wish to consider this as a useful adjunct to safer sex behaviour and the use of condoms for the prevention of genital herpes transmission.
With long-term suppressive therapy, it is strongly advisable to have virological confirmation of the diagnosis before commencing treatment. Patients who have suggestive symptoms but do not have virological confirmation of recurrences, or who have complications or ongoing issues relating to their herpes, should see a specialist.
If the patient is pregnant, specialist consultation is recommended (see page 18).
In cases of immunocompromised patients, refer to appropriate specialist.
Recommended treatment regimens for suppressive therapy include:
Suggest prescribing for 12 months, followed by a break of 3 months to see if recurrences are still frequent. Grade C
20-25% of patients may experience recurrent episodes whilst on suppressive therapy. Other genital conditions may mimic and/or coexist and, even if symptoms are suggestive of breakthrough recurrences, such patients are advised to see a specialist. The usual recommended dose of valaciclovir may need to be altered if breakthrough episodes are confirmed; suppressive therapy does not alter the natural history of recurrences long term and it is common to have a recurrence soon after the withdrawal of therapy. It is helpful to anticipate this and to provide sufficient medication to allow prompt self-initiated treatment of any early recurrences. It is suggested that either a minimum of two recurrences or approximately 3 months without suppressive therapy is necessary to establish a new pattern.
Some patients may need to be on suppressive therapy for years. Valaciclovir is well tolerated and safety and efficacy data are supportive of longer-term use.33 Neurotoxicity (lethargy, confusion, hallucinations and involuntary movements) has been reported in those with renal impairment.
Topical aciclovir creams are less effective than oral aciclovir.34 Hence, the use of topical treatment is not recommended. Topical antiviral creams are available over the counter but are no longer subsidised on the pharmaceutical schedule.
Newer topical agents such as immune modulators are currently in clinical trials.
Evidence for other therapies (oral L-lysine, aspirin, liquorice root cream, lemon balm, aloe vera cream, etc.) is absent.
Although rare in immunocompetent individuals, clinically refractory (large, severe and sometimes atypical) lesions due to genital HSV may occur in patients with severe immunodeficiency, including late-stage HIV disease. Immunocompromised individuals need a referral to specialist care.
Neonatal herpes is a rare but potentially serious infection, which may be associated with significant morbidity and mortality. Infection may be acquired antenatally, at the time of delivery or post-partum:
Primary maternal infection in early pregnancy may be associated with miscarriage,36 and in the second and third trimesters may be associated with preterm delivery. Rarely, primary maternal infection may result in disseminated infection of the fetus with skin lesions, chorioretinitis or microcephaly or hydrocephalus at birth.37 The long-term outlook for these infants is very poor. A minority with late intrauterine HSV infection will present at delivery with skin or eye lesions. The prognosis for successful anti-viral therapy in these infants is far better than that for newborns with more long-standing intrauterine infection.38
Antenatal recurrent disease, where HSV is not shed at delivery, is rarely associated with adverse neonatal outcomes. The risk of intrauterine fetal infection from recurrent maternal HSV infection is extremely low:39
Several factors influence the risk of a newborn acquiring HSV infection at the time of delivery, the most important of which is whether the mother has newly acquired vs recurrent genital disease. The greatest risk of perinatal transmission is when a previously seronegative woman has a primary first episode of genital herpes near or at the time of delivery. Under such circumstances the risk of neonatal HSV infection is 50%.
Although reactivation of HSV-1 is less common than that of HSV-2, there is evidence that reactivated HSV-1 may be more readily transmitted to the neonate. The same strategies are required for prevention of both HSV-1 and HSV-2.44
Transmission rates are lowest for women who acquire herpes before pregnancy, with the risk being about 0.05% for such women who have no signs or symptoms of an outbreak at delivery. Maternal antibodies cross the placenta and are protective.If lesions are present at delivery, there is a small risk of transmission of 0.25-3%.43 Specifically, the risk for transmission of reactivated HSV-2 infection appears to be less than 1%.46
Women with HIV and HSV-2 co-infection have a greater risk of transmitting HSV-2, as HSV-2 shedding is increased in HIV co-infected women.47
Of infants with proven HSV infection, 80% have no documented history of herpes infection in either the mother or her partner. The decreasing prevalence of HSV-1 in childhood increases the susceptibility of young adults to genital HSV-1 including women of reproductive age and hence increases the risk of neonatal HSV.48
Aciclovir has been used widely in pregnancy. There is less experience with valaciclovir but it is expected that valaciclovir as a prodrug of aciclovir should be safe. In the majority of situations, the benefits of antiviral therapy outweigh possible risks.
Antiviral therapy is indicated for treatment of primary and recurrent episodes as in non-pregnant women and for prophylaxis to reduce the risk of recurrence at the time of delivery. An increased frequency of dose is indicated in late pregnancy because of an increased plasma volume.
The following is a summary of the available evidence on the use of antivirals in pregnancy:
There are no established protocols for the use of antiviral medications in pregnancy, but the following regimens are frequently used:
Valaciclovir 1g bd for 7/7
There are no randomised controlled trials to guide optimal delivery management for pregnant women with genital herpes.
Caesarean section has been demonstrated to significantly reduce vertical transmission in women with primary infection in late pregnancy or at the time of delivery.
Because the risk of vertical transmission in recurrent disease is low there has been debate about the benefit of delivery by caesarean section in women who have recurrent episodes at the time of labour. In the US delivery by caesarean section in this situation is recommended but in the Netherlands there has been a policy of offering vaginal delivery for recurrent genital herpes at the time of delivery since 1987 without an apparent increase in neonatal herpes infection.
It has been shown that the presence of symptoms at delivery correlates relatively poorly with the detection of HSV from genital sites or lesions by HSV PCR. Assessment of viral shedding is based on clinical assessment.56
Caesarean section is not completely protective, as transmission of infection has occurred occasionally in the presence of intact membranes. Prolonged contact with infected secretions may further reduce the benefits of abdominal delivery.57
No definitive studies have been carried out on the relationship between the duration of rupture of membranes in the presence of clinical lesions and the transmission of HSV to the fetus. Previously, 4 hours has been suggested as a cut-off time beyond which caesarean section may be no longer beneficial. However, there is no evidence that there is a duration of premature rupture of membranes beyond which the fetus does not benefit from caesarean delivery.58
Because the risk of maternal-fetal transmission is high when primary infection is acquired within 6 weeks of delivery, maternal and neonatal aciclovir therapy should be considered if there has been membrane rupture for more than 4 hours or where a vaginal delivery is unavoidable.59
In a large prospective cohort study of women who had herpes cultures taken in labour, HSV was isolated in 202 women and, overall, neonatal transmission occurred in 10 (5%).43 Caesarean delivery significantly reduced the HSV transmission rate in women from whom HSV was isolated (1 of 85 [1.2%] caesarean vs 9 of 117 [7.7%] vaginal). Risk factors for neonatal HSV infection included:
• First-episode infection
– Of 26 first episode cases, transmission occurred in 8.
• HSV-1 vs HSV-2 isolation at the time of labour
– None of the 140 women with viral shedding due to HSV-2 reactivation infected their babies.
– HSV-1 reactivation in 2/11 women resulted in neonatal infection.
• The use of invasive monitoring.
• Premature delivery.
• Young maternal age.
There was a high caesarean section rate in those noted to have genital lesions in labour. The data from this study was pooled with two other cohorts (from the USA and Sweden) and provided further evidence that during reactivation HSV-1 may be more readily transmissible to the neonate than HSV-2. This pooled cohort study also showed that maternal HSV-1 antibody does not offer significant protection against HSV-2.60
In the Netherlands since 1987 it has been the policy not to offer women caesarean section in the presence of a recurrence at term and there has not been a resultant increase in the incidence of neonatal herpes.
In other countries, guidelines recommend that women who have signs or symptoms of a recurrent infection in labour should be offered caesarean section, but as a relative, rather than absolute, indication for abdominal delivery.58
In summary, there is a lack of robust evidence to guide management in the case of recurrent lesions at the onset of labour. Traditionally delivery by cesarean section has been offered and ideally discussion about the relative risks should occur antenatally in the event of this scenario. Because the risk of transmission is low (1-3%) some women may opt for a vaginal delivery. Factors such as prematurity, HSV-1 rather than HSV-2 and an expected long labour which may all predispose to maternal fetal transmission should be considered.
Disseminated infection from genital or oro-labial infection is rare, but may be life-threatening. Viraemia in the mother during primary infection may result in neonatal multi-organ involvement with significant mortality. The diagnosis may be delayed if vesicular skin lesions are absent or sparse.
Hospital admission and the use of intravenous aciclovir are required for severe disease in pregnancy. The diagnosis of disseminated disease should be considered in any woman presenting with systemic disease in pregnancy.
Little data is available on the management of preterm prelabour rupture of membranes in association with primary herpes simplex infection. Multidisciplinary discussion is required taking into consideration the gestation reached. Treatment with aciclovir 5mg/kg 8 hourly should be administered pending delivery. Caesarean section is considered to be beneficial despite prolonged rupture of membranes. Corticosteroids are not contraindicated.58
One study has shown that expectant management of 29 women with preterm premature rupture of membranes at 65 The mean duration of membrane rupture was 13.2 days (range 1-35 days), 45% were delivered by caesarean section and 8% received antiviral therapy for control of symptoms.
All women should be asked at the first antenatal visit if they or their partner have had genital herpes. A study of 3192 pregnant women and their partners identified that 22% of women were at risk of HSV-1 or HSV-2.56 Of 582 women susceptible to HSV-1, 14 women or 2.5% (3.5% adjusted for length of gestation) acquired HSV-1; the only independent risk factor was a history of a partner with oral herpes. Of 125 women susceptible to HSV-2 infection, 17 or 14% (20% adjusted for length of gestation) acquired HSV-2 infection. Also, the risk of becoming infected was eight times greater in relationships of a year or less, than for those in longer duration relationships. Most newly acquired infections were subclinical.
Although there is no clear evidence to support guidelines in the situation of the partner with a history of previous herpes infection, the following are recommended on theoretical grounds: Grade C
Although routine serological screening in pregnancy has been recommended by some authors, universal screening is not likely to be cost effective because of the high number needed to treat to prevent a single case of neonatal herpes.66
Note: All women with a history of genital herpes infection should be given information on postnatal neonatal surveillance. No interventions are completely protective against maternal fetal transmission.
(in consultation with a specialist)
For further management advice, see Management of Pregnant Women with Recurrent Genital Herpes, page 23.
Note: The first clinical episode may not be due to a primary infection, as previous infection may not have been recognised. Type PCR and serological testing in conjunction with clinical evaluation will help identify primary HSV in pregnancy. All results should be discussed with an expert knowledgeable in interpreting these results and who is aware of the sensitivity and specificity of available testing methods.
– It is common practice to deliver by caesarean section because of the small risk of infection in the neonate.
– However, because the fetal risk is low, this must be set against the risks to the mother of caesarean section and this is therefore regarded as a relative rather than absolute indication for caesarean section.38 Grade C
– Ideally, this scenario should be discussed with the woman early in pregnancy by the primary caregiver in conjunction with specialist advice.
– The risk of maternal fetal transmission is higher with shedding of HSV-1 than with HSV-2.
Investigation and surveillance in the neonate
See Management of Neonatal HSV Infection, page 27.
(in consultation with a specialist)
Neonatal HSV infection rates vary from country to country, with national surveys reporting a wide range in annual incidence. The number of cases per 100,000 live births in Western Europe (France 1.15, United Kingdom 1.65, and the Netherlands 3.2)70-72 is lower than reported for Scandinavia (Sweden 6.5)73 and North America (USA 9.6 and Canada 5.9). Marked differences in incidence can also exist within countries.46
- Neonatal HSV infection is a rare, but potentially fatal, disease of babies, occurring within the first 4-6 weeks of life. Symptoms are non-specific and a high index of suspicion is required.
- Most neonatal HSV infections are acquired at birth, generally from mothers with an unrecognised genital herpes infection acquired during pregnancy.
- Any baby developing skin vesicles or atypical bullous, pustular skin lesions, particularly on the scalp or face (vaginal deliveries) or over the buttocks (breech presentation) must be referred immediately to a paediatrician.
- Specialist obstetric and paediatric advice on management and anticipatory guidance should be sought for a woman with a history of genital herpes and active lesions at term and especially in the high-risk situation of a first episode within 6 weeks of delivery.
The differences in reported rates are likely multifactorial, including differences in case definition and study design as well as differences in rates of HSV acquisition amongst maternal populations. Reliable New Zealand data are lacking but a prospective national active surveillance in Australia from 1997 to 2011 found an incidence of 3.7 per 100,000 live births. This incidence was stable over this time period but noted a significant increase in the cases of HSV-1 infections compared to HSV-2 (OR, 1.10 95% CI, 1.00-1.21). This study also found a decrease in mortality in the latter part of the study. Prospective longitudinal data of this nature are helpful in providing accurate incidence and epidemiological data to help guide effective education and prevention strategies.78
Primary Transmission to the Fetus and NewbornHSV-1 and HSV-2 can be transmitted to the fetus or newborn infant at one of three times: intrauterine, perinatally and postnatally.46 However, the majority of cases of neonatal HSV result from women who acquire genital HSV-1 or HSV-2 infection at or near term.
Intrauterine infectionThe intrauterine infection causes approximately 5% of neonatal HSV infection. It results from either transplacental HSV transmission or an ascending HSV infection from the cervix.
Perinatal infectionThe main risk of transmission to the neonate is at delivery, where contact with HSV-infected secretions in the birth canal accounts for most neonatal HSV infection.46 The site of entry is usually the eye, nasopharynx or an abrasion secondary to scalp electrodes or forceps. Roughly 60-80% of infants with neonatal HSV disease are born to women with unrecognised infection.
Several factors influence the risk of the newborn acquiring HSV infection, the most important of which is whether the mother has newly acquired or recurrent genital disease. The risk is greatest when a previously seronegative woman acquires genital herpes (HSV-1 or HSV-2) near the time of delivery. Under such circumstances, the risk of neonatal HSV infection is 50%, while vertical transmission rates of 25% are found in those with a non-primary first episode (infection with one virus type, e.g. HSV-2, in the presence of antibodies to the other virus type e.g. HSV-1).
In contrast, the transmission rates are lowest for women who acquire herpes before pregnancy, with the risk being about 0.05% for such women who have no signs or symptoms of an outbreak at delivery. If lesions are present at delivery, there is a small but still significant risk of transmission of 0.25-3%.43 High maternal titres of a type-specific neutralising antibody are associated with substantially lower risk and severity of neonatal infection; risk factors include invasive obstetric procedures, such as fetal scalp electrodes, a method of delivery, and prolonged rupture of membranes.43 Recent studies report an increasing proportion of genital and neonatal herpes infection from HSV-1 strains.
Postnatal infection accounts for approximately 10% of cases. Sources of postnatal HSV infection include maternal breast milk, skin and oral lesions, and HSV lesions on caregivers, other family members and medical staff, having close contact with the newborn.
Intrauterine HSV infectionThis is rare and usually occurs after primary herpes infection in pregnancy. Transplacental transmission before the 20th week of pregnancy may cause spontaneous abortion in as many as 25% of cases. In contrast to neonatal herpes infection, the signs of intrauterine HSV infection are present at delivery and may include intrauterine growth retardation, hydranencephaly, chorioretinitis and skin scarring. The long-term outlook for these infants is very poor. A minority with intrauterine HSV infection will present at delivery with skin or eye lesions. There is frequently a history of prolonged rupture of membranes, often as long as 2 weeks. The prognosis for successful anti-viral therapy in these infants is better than that for newborns with more long-standing intrauterine infection and complications such as hydranencephaly, but a small group will have severe, disseminated disease or fatal pneumonitis.38
Neonatal HSV infectionThere is no clear pattern of signs and symptoms that identify babies with neonatal HSV disease, meaning a high index of suspicion is required.
Presenting symptoms of neonatal HSV infection include fever, lethargy, seizures and respiratory distress. Vesicles may be present in only 40%at presentations and some infants will have no vesicles at any time during the course of their illness. Fever may be absent initially.79 Mortality is highest in those with an altered conscious state, seizures, disseminated intravascular coagulation, and prematurity.
The usual age for onset of symptoms in neonatal HSV infection is between5 and 21 days of life, but there may be a delay in presentation if the significance of the symptoms is not initially recognised. Physicians caring for sick infants in the first 6 weeks of life should always be aware that neonatal HSV infection remains a possibility, even when no parental history of herpes infection is given.74
The presentation is divided into three categories (Table 2), each of which has different clinical symptoms and outcomes. There is overlap within these categories and patients can progress from one category to another if not treated early.
Table 2: Classification of Neonatal HSV Infection46
Skin, eyes and/or mouth (SEM) infection79
SEM = Skin, Eyes and/or Mouth; CNS = Central Nervous System; DIS = Disseminated
Nearly half of neonates with HSV infection will present with lesions confined to the skin, eyes or mucous membranes. This is the most readily recognised form of the disease, with most babies having vesicular skin lesions at sites of trauma, such as over the presenting body part, fetal scalp electrode sites and eyelid margins. Lesions usually appear between one and two weeks of age but are sometimes evident shortly after birth when prolonged rupture of membranes has been present. Typically, vesicles overlie an erythematous base and contain clear or slightly cloudy fluid. Need to look carefully for eye involvement as this can initially be asymptomatic with an early ophthalmologic review if symptoms appear.
Although rarely fatal if lesions are confined to the skin and mucosal sites, without antiviral treatment many neonates progress to either the disseminated or CNS forms of the disease. In addition, more than one-third of those with untreated localised SEM lesions develop signs of major neurological impairment such as microcephaly, spastic quadriplegia or sensory loss by 12 months of age. A study of infants with presumed SEM disease reported that 24% had HSV DNA detected in their CSF by PCR testing, suggesting that HSV can infect the CNS without overt neurological symptoms.83
There are data to suggest that three or more recurrences of cutaneous vesicles in the first 6 months of life are predictive of poor neurological outcome.84 Specifically, the likelihood of developing normally is nearly 100% when there are fewer than three recurrences within the first 6 months of life compared with only 79% when three or more recurrences occur during this period. At the time of such episodes, PCR detection of HSV-DNA in the CSF may explain the emergence of new neurological deficits.85
Almost one-third of neonates with HSV infection will have the only encephalitis. Infants usually present between 10 days and 4 weeks of age with symptoms of fever or temperature instability, lethargy, poor feeding and irritability, followed by seizures, bulging fontanelle and focal neurological signs. Cerebrospinal fluid (CSF) findings typically include 50-100 white blood cells x 106 per litre, predominantly mononuclear cells, normal to low glucose and elevated protein concentrations, both of which increase over the first few days. At present, many are devoid of skin lesions but overall 60-70% will have skin vesicles at some point during the disease course.79
Untreated, the mortality rate approaches 50% with most survivors suffering severe neurological impairment. Morbidity is higher among infants with HSV-2 infection than among those with HSV-1 infection.46 Even with the use of high dose aciclovir, morbidity has shown little improvement. Relapses may occur.
The disseminated disease develops in about one-quarter of neonates with HSV infection. It is more common in preterm infants and carries the worst prognosis. Symptoms generally develop in the first 14 days of life. Clinical findings include a sepsis-like presentation with respiratory distress, haemodynamic instability, jaundice, hepatomegaly, elevated liver enzymes, bleeding with associated coagulopathy, and seizures with signs of meningitis, encephalitis or respiratory failure. Vesicular skin lesions may not be present in up to 50% of cases. Mortality in untreated patients is approximately 90% and even with antiviral therapy, may still be as high as 20-30%.
Bacterial pathogens responsible for neonatal sepsis, sometimes with skin lesions that may be mistaken for disseminated or CNS HSV infection, include group B streptococcus, Listeria monocytogenes and gram-negative bacilli. Cutaneous infections resulting in vesicular lesions similar to neonatal HSV are bullous impetigo, varicella zoster, enteroviruses and disseminated CMV infection. Other infectious agents that might be considered are toxoplasmosis, rubella and syphilis. Finally, non-infectious cutaneous disorders that could be confused with neonatal HSV infection include erythema toxicum, neonatal pustular melanosis, acropustulosis and incontinentia pigmenti.
The poor prognosis associated with untreated neonatal HSV infection means that every effort should be made to obtain a diagnosis as early as possible. This includes prompt communication with the mother’s lead maternity caregiver. Many cases present with a sepsis-like clinical picture without identifiable risk factors; many with disseminated or CNS disease will initially lack skin lesions to assist in a timely diagnosis. A high level of suspicion is required.
Successful management relies on a high index of suspicion of HSV infection and early institution of therapy. Only about 40% of affected neonates will initially have skin lesions and most lack a parental history of genital herpes.
Consequently, physicians should consider neonatal HSV infection when confronted with an infant younger than 6 weeks of age who has vesicular or atypical bullous, pustular skin lesions or a progressive febrile illness without a bacterial cause. Particular alerting symptoms are a progressive febrile illness without a confirmed bacterial cause, which is unresponsive to antibiotics and associated with one or more of the following: skin vesicles, hepatomegaly, liver dysfunction, pneumonitis, thrombocytopenia, coagulopathy, or seizures. Other factors recently suggested being of diagnostic importance in a neonate without a rash are a maternal fever, respiratory distress requiring mechanical ventilation and CSF pleocytosis.80
Skin and oral lesions must be carefully looked for on a daily basis, particularly on the scalp and face (vaginal deliveries) or over the buttocks (breech presentation) as these may develop later in the course of disseminated and CNS disease. The index of suspicion is heightened by progressive abnormalities of liver function, particularly during the first week of life. When neonatal HSV infection is considered likely, undertake diagnostic tests and administer aciclovir immediately, before the results of definitive investigations are available.86Grade AAciclovir should be considered for an unwell infant without clinical improvement and negative bacterial cultures at 48-72 hours.87
In the presence of vesicular lesions, the base of the lesion should be scraped and sent for PCR; it requires operator expertise in obtaining an adequate specimen and a negative result should be interpreted with caution.
As neonatal HSV infection may occur in the absence of skin lesions, other diagnostic specimens are required. In addition to testing any cutaneous lesions, swabs of the nasopharynx/mouth, conjunctiva, umbilicus, rectum plus urine should be performed. Swabs are best deferred until >24 hours of age. This delay is to avoid possible contamination by maternal cervicovaginal secretions, positive results after 24 hours should reflect viral replication.
CSF should be taken for HSV PCR testing as well as usual parameters of cell count, protein and glucose. Whole blood PCR should also be performed to assist with the diagnosis of neonatal HSV infection.
PCR is a rapid, highly sensitive and specific technique, which detects minute quantities of viral DNA. It is more reliable than viral culture for CNS infections. However, although the presence of a positive PCR is highly predictive of infection, a negative result does not eliminate the possibility of disease.88A negative CSF PCR should be evaluated in conjunction with the entire clinical picture including other diagnostic modalities, and should not be used on its own to exclude CNS herpes disease. Grade A
Liver function tests, including serum transaminases, may indicate HSV hepatitis and a CXR may diagnose pneumonitis. These tests are performed on all infants suspected of neonatal HSV infection. Grade A
Neurological imaging – CT or MRI brain scan and EEG should all be considered as an important adjunct to diagnosis. MRI and CT scan can be normal early in the disease course and do not rule out HSV CNS disease.
An ophthalmology consultation should be sought in suspected or confirmed cases of neonatal HSV infection, to help identify and monitor ocular complications that may arise during the illness. Grade C
In addition, a sexual history from the parents is taken. The mother’s lead maternity caregiver is asked to obtain HSV PCR of maternal genital secretions and to perform type-specific HSV serology. This is important, even when the presentation is weeks after the delivery.
Intravenous aciclovir (20mg/kg every 8 hours) decreases the mortality and morbidity of neonatal HSV infections (see Table 2on page 26). Early therapy improves neurological outcome. The treatment duration is 14 days for SEM disease and a minimum of 21 days for CNS and disseminated infections.90 The recommendation for the longer course of aciclovir also includes those infants with SEM disease with abnormal CSF parameters, including HSV DNA detected by PCR. Grade A & B
For neonates with ocular involvement, topical therapy may be required and an ophthalmologist should be consulted. For pre-emptive therapy in high-risk asymptomatic infants without laboratory confirmation, 10 days therapy with aciclovir is recommended.
All infants with HSV CNS involvement should have a lumbar puncture at the end of aciclovir therapy to determine if the CSF is PCR negative for HSV. For those neonates when the end of treatment CSF is still PCR positive the American Academy of Pediatrics recommends repeating CSF a week later and if still positive a further week later and if persistently positive discuss with an infectious disease specialist.93 Others have suggested that neonates with PCR positive should continue receiving intravenous aciclovir until viral DNA in the CSF is no longer detected. Grade BAciclovir-resistant neonatal HSV remains rare.
A double-blind placebo-controlled study found that infants surviving neonatal HSV disease with CNS involvement had improved neurodevelopmental outcomes when they received suppressive therapy with oral aciclovir, 300mg/m2/dose administered 3 times daily for 6 months.92 Use of oral aciclovir suppressive therapy also reduced skin recurrences in infants. Regular monitoring of neutrophil count needs to occur while on suppressive aciclovir therapy, with 20-25% of study patients developing neutropenia while receiving aciclovir.94 Oral valaciclovir has not been evaluated for use as suppressive therapy. Grade A
Suppressive therapy can be considered in infants with recurrent SEM disease, but it has not been shown to alter the neurological outcome.92
A monocytic leukocytosis in the CSF is suspicious of CNS HSV infection.95 Treatment with aciclovir should be instituted before HSV PCR results are available. Aciclovir can be discontinued if an alternative diagnosis has been established or the clinical course is no longer compatible with HSV CNS disease, viral PCR testing is negative and a CT or MRI head scan is normal or does not suggest HSV encephalitis. Be aware, however, that a negative initial HSV PCR result does not exclude CNS disease. It is well established that neonatal HSV CNS infection may occur despite the findings of normal CSF counts and biochemistry, and that a negative CSF HSV PCR result may occur, especially if the lumbar puncture was performed early in the course of the illness. Consequently, repeat lumbar puncture is recommended when laboratory tests are negative but clinical suspicion remains high. Grade B & C
Empirical treatment with aciclovir is recommended if, an infant remains critically ill despite antibiotic therapy and disseminated HSV cannot be excluded, if bacterial cultures are negative, or there are signs of progressive liver dysfunction with coagulopathy.97Grade C
In addition to the administration of aciclovir, other important aspects of the infant’s management include:
Infants with neonatal HSV disease should be managed by contact precautions throughout the course of their illness.98Grade C
Long-term follow-up in survivors is instituted to monitor for sequelae and should include assessment of hearing, vision and neurodevelopment. Grade C
When a cutaneous recurrence occurs full clinical examination should be performed. If any evidence of systemic involvement is present, e.g. fever and especially irritability, a CSF examination, including HSV DNA PCR, should be performed. A low level of suspicion should be used to initiate parenteral aciclovir therapy. The abnormal result should lead to a further course of intravenous aciclovir being administered, followed by suppressive oral aciclovir until at least 6 months of age. Grade C
Neonatal HSV infection causes considerable stress within the family. The experience of many is that most couples eventually separate.99 This is because of concern over a critically ill infant, exacerbated by guilt over transmission of the virus and the demands of the long term care of an often severely impaired child. Because of this, expert education and counselling is required.Grade C
Being comfortable with discussing the diagnosis (what, why, how, etc.) is critical to the parents’ ability to understand and come to terms with what has happened. The following points are additional to Key Information for Health Professionals to Give Patients in Counselling (see page 35).
See page 34 for Key Information for Health Professionals to Give Patients in Counselling and consider referring to the Herpes Helpline tollfree 0508 11 12 13.
This category involves a subgroup of infants born to mothers with their first episode of genital herpes during late pregnancy, that is, those women infected near or at term. A paediatrician experienced in identifying the signs of neonatal HSV infection should examine these newborn infants. Grade C
Women with first episode genital HSV infection associated with either genital lesions or subclinical shedding at delivery have a 25-57% chance of transmitting HSV to their babies if they deliver by the vaginal route.42 Although not completely protective against neonatal HSV disease, elective caesarean section significantly reduces the risk of transmission and is recommended for pregnant women who have a known or presumed the first episode of genital herpes within 6 weeks of delivery, even if receiving suppressive anti-viral therapy.42Grade B
Because of the high risk of infection, an asymptomatic infant inadvertently delivered vaginally from a woman with active first episode genital lesions should be managed as for suspected neonatal HSV infection. This means the immediate collection of specimens, including CSF, for cell count, chemistry and PCR testing, HSV blood PCR, full blood count, liver function tests and surface HSV PCR swabs, ideally at 24 hours but earlier if clinically indicated. Anticipatory aciclovir therapy should be initiated. Duration of aciclovir will depend on surface HSV PCR and CSF results. Also check the mother’s total and type-specific HSV serological status, to confirm that this is a first episode of genital herpes and not a recurrence. Grade C
Similarly, when the woman has active first episode genital lesions and is febrile, or has ruptured membranes for more than 4 hours, or when fetal scalp electrodes or forceps have been used, irrespective of the mode of delivery, the infant should be managed as for suspected neonatal HSV infection. Grade C
Anticipatory aciclovir therapy can be discontinued if the neonate remains well, HSV PCR and molecular diagnostic testing have not identified HSV, and the CSF studies including PCR results are normal. If the HSV PCR of surface swabs only is positive and the neonate remains clinically well aciclovir treatment should continue for 10 days.100 Treatment is continued for 14 days when HSV is identified but CSF results are normal, and for 21 days if there is an abnormal CSF finding.101Grade B & C
Within this category are most infants born to mothers with their first episode of genital herpes during pregnancy and those with recurrent genital lesions at the time of delivery. A paediatrician experienced in identifying the signs of neonatal HSV infection should examine these newborn infants. Grade C
Anticipatory guidance including surveillance HSV PCR testing, but no empiric aciclovir, is reserved for well-appearing infants without skin or mucosal lesions at birth and born to mothers within the following categories: Grade B & C
1. First episode genital herpes more than 6 weeks before delivery.
2. First episode genital herpes within 6 weeks of delivery where the mother has delivered by elective caesarean section.
3. Active recurrent genital herpes at delivery.
4. History of recurrent genital herpes during this pregnancy.
The examining paediatrician should undertake the following:
Advise caregivers about hand washing. For mothers with vesicular breast lesions, caution those not to breastfeed while vesicles are present. Particular care when handling the baby must be taken by those with recently acquired or reactivated oral or other skin lesions. In addition to hand washing, this includes covering skin sites and, for herpes labialis or stomatitis, wearing a surgical mask and not kissing the baby until the lesions have crusted and dried.
The American Academy of Pediatrics has approved the use of aciclovir for treating first episode or recurrent genital herpes in breastfeeding mothers. Although concentrations are high in breast milk and the baby, toxicity is low.55Grade B
Genital herpes infection may present in pre-adolescent children. When it does it is important to explore carefully in the history the aetiology of the herpes infection. Possible sources of transmission include an orolabial lesion or a herpetic whitlow in another family member and autoinoculation. For example, genital herpes in a child under one year of age may result from kissing ‘all over’ by a pre-school aged sibling with orolabial herpes.
If an obvious source of the infection cannot be identified, then sexual transmission should be considered. The diagnosis must be confirmed by HSV PCR testing with typing of the herpes virus. The presence of HSV-1 does not rule out the sexual transmission, but a non-sexual route of transmission should be carefully sought, especially if there are no other pointers to suggest sexual abuse. The presence of HSV-2 in the genital area does not automatically imply sexual contact but does mean that sexual abuse, as a cause of the infection, must be seriously considered. In a recent local review of 2,162 children who had an examination in the context of allegations of sexual abuse, eight of the 1,909 children who underwent laboratory screening for sexually transmitted infections were positive for HSV and a sexual transmission was thought likely for six of these children.103
Because of these very difficult issues in diagnosis, all children with suspected genital herpes infection should be referred to a paediatrician for assessment and treatment. The paediatrician may, in turn, seek advice from a local Sexual Abuse Assessment and Treatment Service (SAATS) with special training in the area of recognition of child sexual abuse.
For the purposes of these guidelines, sexually active adolescents should be managed as adults. Adolescents who have never been sexually active should be managed as per the pre-adolescent children section above.
The above is based upon on internationally accepted standards of practice. Grade C
Genital herpes is a common and, medically speaking, usually a relatively minor condition in people who are sexually active. However, conditioning and social values contribute to individuals having a range of emotional responses when given a diagnosis of genital herpes.104-107
Successful psychosocial management of genital herpes is time-intensive. The impact of the diagnosis is influenced by the person’s coping strategies, level of social support and underlying beliefs about sexuality and sexual health. A diagnosis of herpes can also trigger worries about:
Reassure patients that they are not alone in having genital herpes. The NZ Herpes Foundation www.herpes.org.nz or Helpline tollfree 0508 11 12 13 provide specialist support, education and counselling, or refer for specialist counselling at the local sexual health clinic. Advise about reputable internet resources and stress that the online ‘cure’ claims are not scientifically supported.
The above section on counselling is based on internationally accepted standards of practice. Grade C
The following information contributes significantly to people being able to normalise the meaning of a viral STI. The challenge for health professionals is to convey that they understand that a relatively innocuous infection in medical terms may, however, be experienced as life-changing for the person. The following points are most likely to be effective when they are incorporated into the acknowledgement of the above psychosocial points:
Herpes is common, manageable and treatable.
1. Johnston C, Gottlieb SL, et al. Status of vaccine research and development of vaccines for herpes simplex virus. Vaccine, 2016;34(26):2948-52.
2. Looker KJ, Garnett GP, et al. An estimate of the global prevalence and incidence of herpes simplex virus type 2 infection. Bull World Health Org, 2008;86:805-12A.
3. Dickson N, Righarts A, et al. HSV-2 incidence by sex over four age periods to age 38 in a birth cohort. Sexually Transm Infect, 2014;90:243-5.
4. Haddow L. Increase in rates of herpes simplex virus type 1 as a cause of anogenital herpes in western Sydney, Australia, between 1979 and 2003. Sexually Transm Infect, 2006 Jun 1;82(3):255-9.
5. Gray E, Morgan J, et al. Herpes simplex type 1 versus herpes simplex type 2 in anogenital herpes; a 10 year study from the Waikato region of New Zealand. NZ Med J, 2008 Apr 4;121(1271):43-50.
6. Perkins N. Personal communication. In; 2006.
7. Gorfinkel S. Seroprevalence of HSV-1 and HSV-2 antibodies in Canadian women screened for enrolment in a herpes simplex vaccine trial. Int J STD AIDS, 2013 May;24(5):345-9.
8. Nguyen N, Burkhart CN, et al. Review: Identifying potential pitfalls in conventional herpes simplex virus management. Int J Dermatol, 2010;49(9):987-93.
9. Corey L, McCutchan A, Ronald AR, et al. Evaluation of new anti-infective drugs for the treatment of genital infections due to herpes simplex virus. Clin Infect Dis, 1992;15(Suppl.1):S99-S107.
10. Wald A. Herpes simplex virus type 2 transmission: risk factors and virus shedding. Herpes, 2004 Aug;11 Suppl 3:130A-7A.
11. Langenberg A. Interrupting herpes simplex virus type 2 transmission: the role of condoms and microbicides. In: Herpes; 2004:147A-54A.
12. Wald A, Langenberg AG, et al. The relationship between condom use and herpes simplex virus acquisition. Ann Intern Med, 2005 Nov 15;143(10):707-13.
13. Cowan FM, Johnson AM, et al. Relationship between antibodies to herpes simplex virus (HSV) and symptoms of HSV infection. J Infect Dis, 1996 Sep;174(3):470-5.
14. da Silva LM, Guimaraes AL, et al. Herpes simplex virus type 1 shedding in the oral cavity of seropositive patients. Oral Dis, 2005 Jan;11(1):13-6.
15. Wald A, Corey L, et al. Frequent genital herpes simplex virus 2 shedding in immunocompetent women. Effect of acyclovir treatment. J Clin Invest, 1997 Mar 1;99(5):1092-7.
16. Corey L, Wald A, et al. Once-daily valacyclovir to reduce the risk of transmission of genital herpes. N Engl J Med, 2004 Jan 1;350(1):11-20.
17. Langenberg AGM, Corey L, et al. A prospective study of new infections with herpes simplex virus type 1 and type 2. N Engl J Med, 1999 November 4, 1999;341(19):1432-8.
18. Bryson Y, Dillon M, et al. Treatment of first episodes of genital herpes simplex virus infection with oral acyclovir. A randomized double-blind controlled trial in normal subjects. N Engl J Med, 1983 April 21, 1983;308(16):916-21.
19. Mertz GJ, Critchlow CW, et al. Double-blind placebo-controlled trial of oral acyclovir in first-episode genital herpes simplex virus infection. JAMA, 1984 Sep 1;252(9):1147-51.
20. Berger JR, Houff S. Neurological complications of herpes simplex virus type 2 infection. Arch Neurol, 2008 May;65(5):596-600.
21. Corey L, Adams HG, et al. Genital herpes simplex virus infections: clinical manifestations, course, and complications. Ann Intern Med, 1983 Jun;98(6):958-72.
22. Engstrom M, Berg T, et al. Prednisolone and valaciclovir in Bell's palsy: a randomised, double-blind, placebo-controlled, multicentre trial. Lancet Neurol, 2008 Nov;7(11):993-1000.
23. Sullivan F, Daly F, et al. Antiviral Agents Added to Corticosteroids for Early Treatment of Adults With Acute Idiopathic Facial Nerve Paralysis (Bells Palsy). JAMA, 2016 Aug 23;316(8):874-5.
24. Beauman JG. Genital herpes: a review. American Family Physician, 2005 Oct 15;72(8):1527-34.
25. Wald A, Zeh J, et al. Reactivation of genital herpes simplex virus type 2 infection in asymptomatic seropositive persons. N Engl J Med, 2000 Mar 23;342(12):844-50.
26. Tyring SK, Douglas JM, et al. A randomized, placebo-controlled comparison of oral valacyclovir and acyclovir in immunocompetent patients with recurrent genital herpes infections. The Valaciclovir International Study Group. Arch Dermatol, 1998 Feb 1;134(2):185-91.
27. Aoki FY, Tyring S, et al. Single-day, patient-initiated famciclovir therapy for recurrent genital herpes: a randomized, double-blind, placebo-controlled trial. Clin Infect Dis, 2006 Jan 1;42(1):8-13.
28. Kaplowitz LG, Baker D, et al. Prolonged continuous acyclovir treatment of normal adults with frequently recurring genital herpes simplex virus infection. The Acyclovir Study Group. JAMA, 1991 Feb 1;265(6):747-51.
29. Mertz GJ, Jones CC, et al. Long-term acyclovir suppression of frequently recurring genital herpes simplex virus infection. A multicenter double-blind trial. JAMA, 1988 July 8, 1988;260(2):201-6.
30. Patel R, Tyring S, et al. Impact of suppressive antiviral therapy on the health related quality of life of patients with recurrent genital herpes infection. Sex Transm Infect, 1999 Dec 1;75(6):398-402.
31. Romanowski B, Marina RB, et al. Patients' preference of valacyclovir once-daily suppressive therapy versus twice-daily episodic therapy for recurrent genital herpes: a randomized study. Sex Transm Dis, 2003 Mar 1;30(3):226-31.
32. Tyring SK, Diaz-Mitoma F, et al. Oral famciclovir for the suppression of recurrent genital herpes: the combined data from two randomized controlled trials. J Cutan Med Surg, 2003 Nov-Dec;7(6):449-54.
33. Tyring SK, Baker D, et al. Valacyclovir for herpes simplex virus infection: long-term safety and sustained efficacy after 20 years' experience with acyclovir. J Infect Dis, 2002 Oct 15;186 Suppl 1:S40-6.
34. Trottet L, Owen H, et al. Are all aciclovir cream formulations bioequivalent? Int J Pharm, 2005 Nov 4;304(1-2):63-71.
35. Anzivino E, Fioriti D, et al. Herpes simplex virus infection in pregnancy and in neonate: status of art of epidemiology, diagnosis, therapy and prevention. Virology Journal, 2009;6:40.
36. Brown Z, Selke S. The acquisition of herpes simplex virus during pregnancy. N Engl J Med, 1997 Aug 21;337(8):509-16.
37. Corey L, Wald, A. Sexually Transmitted Diseases. 3rd ed: McGraw-Hill; 1999.
38. Ed., Remington JS, Klein JO, et al. Infectious diseases of the fetus and newborn infant. 6th ed. Philadelphia, PA: Elsevier Saunders; 2006.
39. Baldwin S, Whitley RJ. Intrauterine herpes simplex virus infection. Teratology, 1989;39(1):1-10.
40. Eskild A, Jeansson S, et al. Herpes simplex virus type-2 infection in pregnancy: no risk of fetal death: results from a nested case-control study within 35,940 women. BJOG, 2002 Sep;109(9):1030-5.
41. Li D-K, Raebel MA, et al. Genital Herpes and its Treatment in Relation to Preterm Delivery. American Journal of Epidemiology, 2014;180(11):1109-17.
42. Brown ZA, Selke S, et al. The acquisition of herpes simplex virus during pregnancy. N Engl J Med, 1997 August 21, 1997;337(8):509-16.
43. Brown ZA, Wald A, et al. Effect of serologic status and cesarean delivery on transmission rates of herpes simplex virus from mother to infant. JAMA, 2003 Jan 8;289(2):203-9.
44. Gardella C, Brown Z. Prevention of neonatal herpes. BJOG, 2011;118(2):187-92.
45. Randolph AG, Washington AE, et al. Cesarean delivery for women presenting with genital herpes lesions. Efficacy, risks, and costs. JAMA, 1993 July 7, 1993;270(1):77-82.
46. Corey L, Wald A. Maternal and neonatal herpes simplex virus infections. N Engl J Med, 2009;361(14):1376-85.
47. Ozouaki F, Ndjoyi-Mbiguino A, et al. Genital shedding of herpes simplex virus type 2 in childbearing-aged and pregnant women living in Gabon. Int J STD AIDS, 2006 Feb 1;17(2):124-7.
48. Woestenberg PJ, Tjhie JHT, et al. Herpes simplex virus type 1 and type 2 in the Netherlands: seroprevalence, risk factors and changes during a 12-year period. BMC Infectious Diseases, 2016;16(1).
49. Wald A. Genital herpes. Clin Evid, 2002 Dec(8):1608-19.
50. Scott LL, Sanchez PJ, et al. Acyclovir suppression to prevent cesarean delivery after first-episode genital herpes. Obstet Gynecol, 1996 Jan 1;87(1):69-73.
51. Brocklehurst P, Kinghorn G, et al. A randomised placebo controlled trial of suppressive acyclovir in late pregnancy in women with recurrent genital herpes infection. Br J Obstet Gynaecol, 1998 Mar 1;105(3):275-80.
52. Watts DH, Brown ZA, et al. A double-blind, randomized, placebo-controlled trial of acyclovir in late pregnancy for the reduction of herpes simplex virus shedding and cesarean delivery. Am J Obstet Gynecol, 2003 Mar 1;188(3):835-43.
53. Sheffield JS, Hollier LM, et al. Acyclovir prophylaxis to prevent herpes simplex virus recurrence at delivery: a systematic review. Obstet Gynecol, 2003 Dec 1;102(6):1396-403.
54. Ramsey P, Andrews W. Antiviral suppression to prevent recurrence of herpes simplex virus (HSV) infections in pregnancy: a meta analysis. Am J Obstet Gynecol, 2003;189(6):S98.
55. Sheffield JS, Fish DN, et al. Acyclovir concentrations in human breast milk after valaciclovir administration. Am J Obstet Gynecol, 2002 Jan 1;186(1):100-2.
56. Gardella C, Brown Z, et al. Risk factors for herpes simplex virus transmission to pregnant women: a couples study. Am J Obstet Gynecol, 2005 Dec 1;193(6):1891-9.
57. Brown ZA, Gardella C, et al. Genital Herpes Complicating Pregnancy. Obstetrics & Gynecology, 2005;106(4):845-56.
58. Management of genital herpes in pregnancy [Internet]. British Association for Sexual Health & HIV (BASHH) and the Royal College of Obstetricians & Gynaecologists (RCOG), 2014. (Accessed at www.rcog.org.uk/globalassets/documents/guidelines/management-genital-herpes.pdf.)
59. Smith JR, Cowan FM, et al. The management of herpes simplex virus infection in pregnancy. Br J Obstet Gynaecol, 1998 Mar;105(3):255-60.
60. Brown EL, Gardella C, et al. Effect of maternal herpes simplex virus (HSV) serostatus and HSV type on risk of neonatal herpes. Acta obstetricia et gynecologica Scandinavica, 2007;86(5):523 - 9.
61. Hemelaar SJ, et al. Neonatal herpes infections in The Netherlands in the period 2006-2011. J Matern Fetal Neonatal Med, 2014 Jul;11:1-5.
62. Hemelaar SJ, Poeran J, et al. Neonatal herpes infections in The Netherlands in the period 2006–2011. The Journal of Maternal-Fetal & Neonatal Medicine, 2014;28(8):905-9.
63. Frederick DM, Bland D, et al. Fatal disseminated herpes simplex virus infection in a previously healthy pregnant woman. A case report. J Reprod Med, 2002 Jul;47(7):591-6.
64. Thurman RH, Kõnig K, et al. Fulminant herpes simplex virus hepatic failure in pregnancy requiring liver transplantation. Aus & NZ J Obstet & Gynaecol, 2010;50(5):492-4.
65. Major CA, Towers CV, et al. Expectant management of preterm premature rupture of membranes complicated by active recurrent genital herpes. Am J Obstet Gynecol, 2003 Jun 1;188(6):1551-4; discussion 4-5.
66. Cleary KL, Pare E, et al. Type-specific screening for asymptomatic herpes infection in pregnancy: a decision analysis. BJOG, 2005 Jun 1;112(6):731-6.
67. Arvin A, Hensleigh P, et al. Failure of antepartum maternal cultures to predict the infant's risk of exposure to herpes simplex virus at delivery. N Engl J Med, 1986 September 25, 1986;315(13):796-800.
68. Kimberlin DW, Lin CY, et al. Natural history of neonatal herpes simplex virus infections in the acyclovir era. Pediatrics, 2001 Aug 1;108(2):223-9.
69. Sauerbrei A, Wutzler P. Herpes simplex and varicella-zoster virus infections during pregnancy: current concepts of prevention, diagnosis and therapy. Part 1: herpes simplex virus infections. Med Microbiol Immunol, 2007 Jun 1;196(2):89-94.
70. Braig S, Chanzy B. Management of genital herpes during pregnancy: the French experience. Herpes, 2004 Aug;11(2):45-7.
71. Tookey P, Peckham CS. Neonatal herpes simplex virus infection in the British Isles. Paediatr Perinat Epidemiol, 1996 Oct;10(4):432-42.
72. Poeran J, Wildschut H, et al. The incidence of neonatal herpes in The Netherlands. J Clin Virol, 2008 Aug 1;42(4):321-5.
73. Malm G, Berg U, et al. Neonatal herpes simplex: clinical findings and outcome in relation to type of maternal infection. Acta Paediatr, 1995 Mar 1;84(3):256-60.
74. Kropp RY, Wong T, et al. Neonatal herpes simplex virus infections in Canada: results of a 3-year national prospective study. Pediatrics, 2006 Jun;117(6):1955-62.
75. Flagg EW, Weinstock H. Incidence of neonatal herpes simplex virus infections in the United States, 2006. Pediatrics, 2011 January 1, 2011;127(1):e1-e8.
76. Jones CA, Raynes-Greenow C, et al. Population-Based Surveillance of Neonatal Herpes Simplex Virus Infection in Australia, 1997-2011. Clinical Infectious Diseases, 2014;59(4):525-31.
77. Morris A, Ridley GF, et al. Australian Paediatric Surveillance Unit: progress report. J Paediatr Child Health, 2002 Feb;38(1):8-15.
78. Gardella C, Handsfield HH, et al. Neonatal herpes – the forgotten perinatal infection. Sexually Transm Dis, 2008 Jan 1;35(1):22-4.
79. Kimberlin DW. Herpes Simplex Virus Infections of the Newborn. Seminars in Perinatology, 2007 Jan 1;31(1):19-25.
80. Caviness AC, Demmler GJ, et al. Clinical and laboratory features of neonatal herpes simplex virus infection: a case-control study. Pediatr Infect Dis J, 2008 May 1;27(5):425-30.
81. Elder DE, Minutillo C, et al. Neonatal herpes simplex infection: keys to early diagnosis. J Paediatr Child Health, 1995 Aug;31(4):307-11.
82. Whitley RJ. Neonatal herpes simplex virus infections. J Med Virol, 1993;Suppl 1:13-21.
83. Kimberlin DW, Lakeman FD, et al. Application of the polymerase chain reaction to the diagnosis and management of neonatal herpes simplex virus disease. National Institute of Allergy and Infectious Diseases Collaborative Antiviral Study Group. J Infect Dis, 1996 Dec;174(6):1162-7.
84. Whitley R, Arvin A, et al. Predictors of morbidity and mortality in neonates with herpes simplex virus infections. The National Institute of Allergy and Infectious Diseases Collaborative Antiviral Study Group. N Engl J Med, 1991 Feb 14;324(7):450-4.
85. Kimberlin D, Powell D, et al. Administration of oral acyclovir suppressive therapy after neonatal herpes simplex virus disease limited to the skin, eyes and mouth: results of a phase I/II trial. Pediatr Infect Dis J, 1996 Mar 1;15(3):247-54.
86. Whitley R, Arvin A, et al. A controlled trial comparing vidarabine with acyclovir in neonatal herpes simplex virus infection. Infectious Diseases Collaborative Antiviral Study Group. N Engl J Med, 1991 Feb 14;324(7):444-9.
87. Caviness AC, Demmler GJ, et al. The prevalence of neonatal herpes simplex virus infection compared with serious bacterial illness in hospitalized neonates. J Pediatr, 2008 Aug 1;153(2):164-9.
88. Kimberlin DW. Neonatal herpes simplex infection. Clin Microbiol Rev, 2004 Jan 1.
89. Diamond C, Mohan K, et al. Viremia in neonatal herpes simplex virus infections. Pediatr Infect Dis J, 1999 Jun 1;18(6):487-9.
90. Kimberlin DW, Lin CY, et al. Safety and efficacy of high-dose intravenous acyclovir in the management of neonatal herpes simplex virus infections. Pediatrics, 2001 Aug 1;108(2):230-8.
91. Ed., Palasanthiran P, Starr M, et al. Management of perinatal infections; 2014.
92. Kimberlin DW, Whitley RJ, et al. Oral aciclovir suppression and neurodevelopment after neonatal herpes. N Engl J Med, 2011;365:1284-92.
93. Kimberlin DW, Brady MT, et al. Herpes Simplex. In: Red Book® 2015 Report of the Committee on Infectious Diseases. American Academy of Pediatrics, 2015:432-45.
94. Gutierrez K, Arvin AM. Long term antiviral suppression after treatment for neonatal herpes infection. Pediatr Infect Dis J, 2003 Apr;22(4):371-2.
95. Arvin AM, Whitley, R J, Gutierrez, K M. Herpes simplex infections. In: Remington JS KJ, Wilson CB, Baker CJ, ed. Infectious diseases of the fetus and newborn infant. 6th ed. Philadelphia: Elsevier Saunders; 2006:845-66.
96. De Tiege X, Heron B, et al. Limits of early diagnosis of herpes simplex encephalitis in children: a retrospective study of 38 cases. Clin Infect Dis, 2003 May 15;36(10):1335-9.
97. Scott LL. Perinatal herpes: current status and obstetric management strategies. Pediatr Infect Dis J, 1995 Oct 1;14(10):827-32; discussion 32-5.
98. Sakaoka H, Saheki Y, et al. Two outbreaks of herpes simplex virus type 1 nosocomial infection among newborns. J Clin Microbiol, 1986 Jul;24(1):36-40.
99. Kimberlin DW. Neonatal HSV infections: the global picture. Herpes, 2004 Aug;11(2):31-2.
100. Kimberlin DW, Baley J, et al. Management of asymptomatic neonates born to women with active genital herpes lesions. Pediatrics, 2013;131:e635-46.
101. Jones C. Vertical transmission of genital herpes: prevention and treatment options. Drugs, 2009;69:421-34.
102. Huppert JS, Gerber MA, et al. Vulvar ulcers in young females: a manifestation of aphthosis. J Pediatr Adolesc Gynecol, 2006 Jun;19(3):195-204.
103. Kelly P, Koh J. Sexually transmitted infections in alleged sexual abuse of children and adolescents. J Paediatr Child Health, 2006 Jul-Aug;42(7-8):434-40.
104. Fortenberry JD, McFarlane M, et al. Relationships of stigma and shame to gonorrhea and HIV screening. Am J Public Health, 2002 March 1, 2002;92(3):378-81.
105. Fortenberry JD. The effects of stigma on genital herpes care-seeking behaviours. Herpes, 2004 Apr;11(1):8-11.
106. Green J, Ferrier S, et al. Determinants of disclosure of genital herpes to partners. Sexually Transm Infect, 2003 Feb 1;79(1):42-4.
107. Patel R. Supporting the patient with genital HSV infection. Herpes, 2004;11(3):87-92.
108. Barnack-Tavlaris JL, Reddy DM, et al. Psychological adjustment among women living with genital herpes. J Health Psych, 2011 January 1, 2011;16(1):12-21.
109. Cook C. 'Nice girls don't': Women and the condom conundrum. J Clin Nurs, 2014 Sept;23(17-18):2691.
110. Romanowski B, Zdanowicz YM, et al. In search of optimal genital herpes management and standard of care (INSIGHTS): doctors and patients perceptions of genital herpes. Sexually Transm Infect, 2008 February 1, 2008;84(1):51-6.
111. Carney O, Ross E, et al. A prospective study of the psychological impact on patients with a first episode of genital herpes. Sex Transm Infect, 1994 February 1, 1994;70(1):40-5.
112. Cook C. 'About as comfortable as a stranger putting their finger up your nose': Speculation about the (extra)ordinary in gynaecological examinations. Culture, Health & Sexuality, 2011 Aug;13(7):767-80.
113. Gott M, Galena E, et al. Opening a can of worms: GP and practice nurse barriers to talking about sexual health in primary care. Family Practice, 2004 October 1, 2004;21(5):528-36.
Sexual Health Physicians
Dr Min Lo (Editor in Chief, HPV Guidelines)
Dr Edward Coughlan
Dr Heather Young
Infectious Disease and Sexual Health Physician
Dr Massimo Giola
NZ Dermatological Society
Dr Darion Rowan
NZ Committee of the Royal Australian and New Zealand
College of Obstetrics and Gynaecology
Dr Anne Robertson
Paediatric Society of New Zealand
Dr Lesley Voss
NZ College of General Practitioners
Dr Phil Jacobs
NZ Society of Otolaryngology, Head and Neck Surgery
Dr Julian White
Dr Christine Roke
Immunisation Advisory Centre (IMAC)
Dr Helen Petousis-Harris
Georgina McPherson (NZ HPV Project)
Hayley Samuel, PO Box 2437, Shortland Street, Auckland 1140
Tel: 09 433 6526 Email: [email protected]
Additional Peer Review provided by:*
Sexual Health Physician
Dr Jeannie Oliphant
Dr Arlo Upton
Dr Andrew Miller
Infectious Disease Pharmacist
* Members of the Joint Sexually Transmitted Infections Education Foundation and New Zealand Sexual Health Society Professional Advisory Group (PAG) 2017
Sexually Transmitted Infections Education Foundation
PO Box 2437, Shortland Street, Auckland 1140, New Zealand
Phone: 09 433 6526
Email: [email protected]
The Ministry of Health supports the use of these clinical guidelines,
developed by clinical experts and professional associations to guide clinical care.
Supported by an educational grant from New Zealand District Health Boards
© 2017 Sexually Transmitted Infections Education Foundation
12th Edition: Version 1 – September 2017
You can also access our guides online. Most are able to be downloaded in pdf form:
If you would like to get a print copy of the information booklets, fill out the form on the health professionals' request for printed materials
This website is brought to you by the Sexually Transmitted Infections Education Foundation (STIEF) - an initiative funded by the Ministry of Health through collective District Health Boards (20) to educate New Zealanders about STIs. District Health Boards (DHBs) are responsible for providing or funding the provision of health services in their district.
The medical information in this website is based on the STIEF Guidelines for the Management of Genital Herpes in New Zealand. The New Zealand Ministry of Health supports the use of these clinical guidelines, developed by clinical experts and professional associations to guide clinical care in New Zealand.
The Guidelines are a consensus opinion of the STIEF Professional Advisory Group (PAG). The PAG has representation from nationwide medical, nursing and allied disciplines involved in the management of STIs. The Guidelines are produced by considering available literature, both New Zealand wide and international, and by basing the medical recommendations on the evidence in the literature or reasonable supposition and opinions of medical experts.
Toll Free Phone: 0508 11 12 13
From a Mobile: 09 433 6526
Email: [email protected]
NZ Herpes Foundation
C/- Sexually Transmitted Infections Education Foundation (STIEF)
CPO Box 2437, Shortland Street, Auckland 1140
© Copyright 2023 New Zealand Herpes Foundation. All rights reserved. Disclaimer / Security / Privacy