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Signs herpes outbreak is coming

These guidelines have been produced by considering available literature and by basing the recommendations on the available evidence, both local and international.
Grade A:    Very strong evidenceBased on well-designed prospective randomised controlled clinical trials.
Grade B:    Fairly strong evidenceBased 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 opinionBased on published case reports, well-written reviews or consensus. Prescribe 48 x 400mg tablets for patients to be able to self-initiate treatment at onset of symptoms. Valaciclovir (Valtrex™) 500mg daily is listed for suppressive treatment of recurrent genital herpes, subject to a Special Authority restriction, in the pharmaceutical schedule. 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).
Serological testing can be used to diagnose genital herpes in the setting of an active genital ulcer. Fact: All first episodes of genital herpes should be treated regardless of timing of onset of symptoms (see page ??). The purpose of this guideline is to dispel common misconceptions and hopefully improve current management of those with herpes infection. Genital herpes is a common infection caused by Herpes Simplex Virus Type One (HSV-1) and Herpes Simplex Virus Type Two (HSV-2) and as many as one in five adults in New Zealand have genital herpes due to HSV-2.
Laboratory confirmation of the diagnosis and typing, by HSV PCR or viral culture, is important, but should not delay treatment.
Oral antiviral treatment of the first clinical episode should always be offered regardless of the time of symptom onset.
Neonatal HSV infection is a rare but potentially fatal disease of babies, occurring within the first 4-6 weeks of life. Specialist advice on management 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 up to 6 weeks prior to delivery.
As many as one in five adults have genital herpes due to HSV-2, but most will have asymptomatic or unrecognised disease. Genital herpes due to HSV-1 (through oral to genital transmission) has also become common; HSV-1 is a frequent cause of primary genital herpes. The natural history of genital HSV-1 infection is towards significantly fewer clinically apparent recurrences and less subclinical shedding than HSV-2. Genital herpes is an infection caused by the herpes simplex virus (HSV) and, for practical purposes, encompasses lesions on the genitals and nearby areas (i.e. HSV-2 prevalence varies between countries, being higher in the USA than in Europe, Australia and New Zealand. 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. Like HSV-2, HSV-1 seroprevalence increases with increasing age and tends to be more common in women. Note: Routine typing of isolates enhances a clinician’s ability to give prognostic information and optimal clinical care. 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.
It is important to remember that not all first episodes of HSV-1 or HSV-2 represent a new or recently acquired infection. 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. 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.
The viral load threshold for transmission from an episode of asymptomatic shedding has not been established. Aciclovir, famciclovir and valaciclovir all suppress symptomatic and asymptomatic shedding by up to 80-95%.
People who do not acquire HSV-1 during childhood are at risk of HSV-1 at any site, including genital infection, during adulthood. 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. For patients with active lesions, either culture or PCR (depending on local laboratory availability), but not serology, are the recommended diagnostic methods. Clinical diagnosis alone is insensitive and inaccurate, with a 20% false positive rate.17 Suspected genital herpes must be confirmed by appropriate laboratory tests. HSV DNA detection by polymerase chain reaction (PCR) increases HSV detection rates compared with virus culture.
The person ordering serology should be able to supply appropriate pre- and post-test counselling.
The window period for antibodies developing following infection is usually 2-6 weeks, but may be longer (months). Primary infection: Recently acquired infection with HSV-1 or HSV-2 with an absence of antibodies to either type on serological testing. Recurrence: Previously acquired HSV-1 or HSV-2 infection with antibodies to the same type on serological testing. The first clinical episode of genital HSV-1 or HSV-2 may, but does not always, reflect recent infection.
Aciclovir prescriptions do not require specialist authorisation and the medication is available through any pharmacy. It is not necessary or desirable to attempt to cover all these issues at the initial clinical assessment. Similarly, a diagnosis of acute radiculitis (herpetic lumbosacral radiculoneuropathy or Elsberg syndrome) tends to be overlooked, yet may cause acute urinary retention, constipation and sacral neuralgia. Sporadic herpes simplex encephalitis is an acute necrotising viral encephalitis that is more usually caused by primary infection with HSV-1. 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. Therapy should be initiated regardless of how long the lesions have been present and before virological confirmation. Lesions may not completely heal over during the course of drug treatment; similarly, mild neurological symptoms may not yet have fully resolved. Topical aciclovir creams are not recommended because they are less effective than oral aciclovir (see page ??). It is important to ensure that patients receive accurate up-to-date information about genital herpes. Social and psychological issues should be addressed both at the first appointment and at follow-up.
Psychological impact of the disease on the patient and their relationships (particularly important in the long term).
It may be appropriate to offer the opportunity for their partner to have questions answered as well.
Practice nurses or nurses who have training in this area may also be a good source of counselling support. 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.
For those choosing episodic antiviral therapy, this is more effective when patients start therapy themselves at the first signs of a recurrence. Recommendations on counselling and follow-up are based on internationally accepted standards of practice.
There is effective oral antiviral treatment for frequent, severe or problematic genital herpes. Management of recurrent herpes depends on whether there is prior virological confirmation of infection.
Only 10-25% of persons who are HSV-2 seropositive report a diagnosis of genital herpes, which suggests that most have unrecognised symptomatic or completely asymptomatic infections.28 However, once told they are HSV-2 seropositive, more than 50% are able to identify clinically symptomatic recurrences that may have previously been thought to be due to other conditions. In straightforward cases with a prior laboratory-confirmed diagnosis, the clinical history is often the principal means of determining that the patient has a recurrent episode, but other genital conditions, e.g. The atypical or non-ulcerative presentations of genital herpes can mimic most genital diseases, hence the need to consider more than one diagnosis at any given time.
All these examples serve to underpin the importance of taking a detailed history and thorough physical examination of the whole skin, including oral mucosa. All genital lesions not previously diagnosed should have a viral swab taken with an explanation to the patient why this has been done. An option is to instruct patients how to take a swab themselves and deliver direct to the laboratory. Herpes recurrent lesions can occur on the hands, arms, shoulders and other areas of the body, commonly around the buttocks; the diagnosis is often overlooked.
Lumbar sacral radiculopathy can recur, but usually with less severe symptoms than in primary infection. People with genital herpes may become anxious or depressed and this may unmask or amplify disorders such as phobias or obsessive-compulsive disorder. Recommendations on education and counselling and follow-up are based on internationally accepted standards of practice. Effective episodic treatment of recurrent herpes requires prompt initiation of therapy during the prodrome or within one day of symptom onset.
Standard therapy in New Zealand for suppression of herpes recurrences is oral aciclovir 400mg twice daily. Withdrawal of therapy should be for a sufficient length of time to establish whether the pattern of recurrence has changed, for example, a minimum of two recurrences or for 3 months.
Valaciclovir (Valtrex™) is available for suppressive treatment of recurrent genital herpes, subject to a Special Authority restriction, for those with recurrences not responding to aciclovir. The aim of episodic treatment is to reduce symptoms and duration of viral shedding during recurrences, rather than reduce the frequency of recurrences. 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.29 30 Beyond this timeframe, there is no clear benefit, so it is important that a prescription is readily available. With long-term suppressive therapy it is strongly advisable to have virological confirmation of the diagnosis before commencing treatment.
The duration of therapy should be negotiated between the patient and the clinician; however, a treatment period of a year is recommended with periodic reassessment. Suppressive therapy does not alter the natural history of recurrences long term and it is common to have a recurrence soon after withdrawal of therapy. The use of intermittent suppressive therapy is also considered a point for negotiation with the patient.
Topical aciclovir creams are less effective than oral aciclovir.38 Hence, use of topical treatment is not recommended. Evidence for other therapies (oral L-lysine, aspirin, liquorice root cream, lemon balm, aloe vera cream, etc.) is limited. 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. Neonatal HSV infection is a rare, but potentially fatal, disease of babies, occurring within the first 4-6 weeks of life.
Most neonatal HSV infections are acquired at birth, generally from mothers with an unrecognised genital herpes infection acquired during pregnancy. All women should be asked by their primary caregiver at their first antenatal visit if they or their partner have ever had genital herpes and given information on the potential risks of transmission in pregnancy; this includes the risk of genital HSV-1 from oral-genital contact.
Concerns around herpes infection during pregnancy tend to relate to the risk of neonatal infection. Neonatal herpes is a rare but potentially serious infection, which may be associated with significant morbidity and mortality. Primary maternal infection before the 20th week of pregnancy may be associated with miscarriage,42 and in the second and third trimesters may be associated with preterm delivery. 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.46,47 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. Although reactivation of HSV-1 is less than common than that of HSV-2, there is evidence that the reactivated HSV-1 may be more readily transmitted to the neonate. Of infants with proven HSV infection, 80% have no documented history of herpes infection in either the mother or her partner. There are no randomised controlled trials to guide optimal delivery management for pregnant women with genital herpes.
However caesarean section is not completely protective, as transmission of infection has occurred occasionally in the presence of intact membranes.
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.
In the case of recurrent genital herpes, maternal antibodies are protective and it has been argued that the benefits of caesarean section are low in this group of women, even if lesions are present at the time of delivery.
However, there are theoretical concerns that maternal aciclovir therapy may suppress the production of neutralising antibodies to the immunogen, glycoprotein D, thus having an effect on passive immunity to the fetus, and may suppress rather than treat newborn infections, thus leading to a delay in presentation of neonatal disease. Management of the woman should be in keeping with her clinical condition, using aciclovir in standard doses as indicated (see page ??). Provided delivery does not ensue, the pregnancy should be managed expectantly and vaginal delivery anticipated. For further management advice, see Management of Pregnant Women with Recurrent Genital Herpes, page ??. Note: The first clinical episode may not be due to a primary infection, as previous infection may not have been recognised. Delivery should be by caesarean section, particularly in those women infected within 6 weeks of delivery because of high rates of asymptomatic shedding of HSV and insufficient time for a complete antibody response between infection and delivery.
If vaginal delivery is unavoidable, consider treatment of mother with aciclovir and request an urgent referral to a paediatrician experienced in HSV infection (see Neonatal HSV Infection, page ??).
A retrospective study of the clinical presentation and outcome of herpes zoster in a tertiary dermatology outpatient referral clinic. Herpes zoster ophthalmicus in patients at risk for the acquired immune deficiency syndrome (AIDS). Natural history of herpes zoster ophthalmicus: predictors of postherpetic neuralgia and ocular involvement. Varicella zoster virus retrobulbar optic neuritis preceding retinitis in patients with acquired immune deficiency syndrome.
Valaciclovir compared with acyclovir for improved therapy for herpes zoster in immunocompetent adults. Comparison of the efficacy and safety of valaciclovir and acyclovir for the treatment of herpes zoster ophthalmicus.
This is a viral infection of the lips and mouth which is caused by the herpes simplex virus a€“ termed HSV.
Herpes doesna€™t always develop symptoms a€“ it does not always cause any outward, visible signs. Kissing or touching and any sexual contact with the area that is infected spreads oral herpes. Many individuals have symptoms of itching, burning, and tingling proceeding the outbreak of blisters or sores.
The most concentrated pain from these sores occurs at the onset and can make drinking or eating hard. If a child with cold sores is less than 6 weeks old, the babya€™s physician needs to be notified if oral blisters or sores appear. Individuals with weakened immunity systems should also notify their primary care physician if sores or blisters appear. A physician will make a tentative diagnosis on data provided by the patient and on the physician exam. Topical anesthetic such as lidocaine (xylocaine, Nervocaine, Dilocaine, Zilactin-L) can be approved for pain relieve of oral blisters and lesions. Oral or IV drugs exist for HSV but only for individuals with weakened immune systems, infants younger than 6 weeks or those with severe disease. Topical Denavir (penciclovir) creams can shorten attacks of recurrent HSV-if it is applied early, normally before lesions develop. These medications may stop viral reproduction in the skin but do not eradicate HSV from the body or stop later outbreaks. This website is for informational purposes only and Is not a substitute for medical advice, diagnosis or treatment.
Herpes zoster infection (shingles) results from the reactivation of varicella zoster virus infection. While varicella virus infection mostly affects the young, shingles and its complications mainly affect older persons. The initial stage of shingles precedes the active stage with a conundrum of symptoms that last several days or weeks before the shingle rash appears. The rash develops from maculopapular lesions forming a beltlike pattern on the patient's trunk, but the band of rash may appear anywhere on the body including the eyes. The main symptom associated with postherpetic neuralgia is pain, which persists for a long period beyond the resolution of the shingles rash. The lidocaine 5% patch has been shown to be easy to use, safe, tolerable, and efficacious in the management of PHN pain. Gabapentin prevents allodynia and hyperalgesia associated with PHN pain as well as the associated sleep disorder.


Anticonvulsants have been shown to be equally efficacious; however, drug selection may involve trial and error. Approvals valid for 12 months where the patient has genital herpes with two or more breakthrough episodes in any 6 month period while treated with aciclovir 400mg twice daily.
Approvals valid for 12 months where the treatment remains appropriate and the patient is benefiting from treatment.
Minor lesions are common; any recurring localised genital symptoms or lesions should be investigated as possible genital herpes. 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. It may be a first clinically recognised episode of a previously unrecognised or asymptomatic infection acquired weeks, months or years previously. 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. Transmission may occur whilst receiving oral sex from someone who has oral HSV-1, even if the source partner is asymptomatic. Other antivirals may be similarly effective, but this has not been proven in clinical trials.
Specificity of culture is virtually 100%, but sensitivity is highly dependent on the stage of the clinical lesions, with an isolation rate of over 90% from vesicular or pustular lesions, 70% from ulcerative lesions, but only 27% at the crusting stage.18 Delayed transport of the specimen to the laboratory may further reduce yield.
This is largely because it avoids problems that may affect culture results such as inadequate quantity of specimen, bacterial contamination, and inadvertent inactivation of virus by sub-optimal handling and sample transport delays. However, a negative test result does not necessarily exclude HSV infection since all methods are dependent on adequate collection of the specimen and, for culture in particular, on correct specimen handling and prompt transportation to the laboratory.
The aim is to collect any vesicular fluid that may be present and to collect virus-infected cells from the base of the lesion. If not, you may need to specify “for herpes simplex DNA” and offer clinical explanation as to why this is the preferred test over culture, e.g.
A positive HSV-2 serology result may cause significant psychological morbidity (see page ??-??).
If the blood test being done only tests for HSV-2 antibodies, a negative test does not rule out the possibility of the person having genital herpes caused by type 1. Because false negatives and false positives occur, the results have to be weighed together with the clinical presentation and patient’s history.
HSV-1 is a common infection, usually acquired in childhood, and may be shed from the oropharynx by asymptomatic individuals. HSV-2 in a person with previous antibodies to HSV-1, but absence of antibodies to HSV-2 on serological testing. May be a primary or non-primary or first recognised clinical expression of a previously acquired infection weeks, months or years before.
It may represent a primary HSV infection or a new non-primary infection or a recurrence of a previously asymptomatic infection (see Table 2 on page ??). Patients are often very unwell and therapy should be initiated regardless of how long the lesions have been present and before virological confirmation. However, initial symptoms of genital herpes may not be recognised or may not occur until months to years later.
Rapidly, pruritic erythematous plaques appear followed by a cluster of small vesicles that contain clear to cloudy fluid. Acute, generally benign, lymphocytic meningitis may occur; HSV-2 is associated with aseptic meningitis in up to 36% of adult women and 13% of men with primary HSV-2 infection. Referred pain can affect the saddle area distribution, S3 and 4, of the sacral nerve and the bladder detrusor muscle.
Early treatment with oral steroids is effective;24 the use of antiviral agents is less clear, but is still commonly recommended. Clinical features are often nonspecific, as is common with all forms of encephalitis, and include headache, signs of meningeal irritation, altered mental status, and seizures.
Mild forms of this condition are common and present with mildly itchy, pink-red blotches, starting on the extremities. In most cases of disseminated infection, lesions are confined to the skin, but hepatitis, pneumonitis and other organ involvement may occur, with or without vesicular skin lesions. Clinical diagnosis is insensitive, for example, ulceration may be due to aphthous ulcers, Stevens Johnson syndrome, fixed drug eruption, self-inflicted (sometimes unknowingly) trauma and autoimmune blistering disease (rare). Refer immunocompromised patients, or those with herpetic proctitis, to an appropriate specialist, e.g. Valaciclovir and famciclovir are not subsidised, although this may change as and when generic formulations become available. Nonetheless, a further course of therapy is not usually indicated unless new lesions continue to appear.
NZHF resources are available to assist patients and clinicians with education and counselling.
For most patients, one visit is insufficient to properly manage the impact of genital herpes.
It should be noted that it might take longer than 5 days for skin lesions to heal completely. It is suggested that either a minimum of two recurrences or approximately 3 months without suppressive therapy is required to establish the pattern. Shared management is important for the patient to feel a measure of control; the clinician should aim to be the facilitator of education and treatment options.
For example, lichen sclerosus results in increased skin fragility; because this condition is usually itchy, secondary scratching may cause superficial erosions and haemorrhagic bullae are not uncommon. Atypical presentation is not unusual and HSV should be considered in any recurrent intermittent inflammatory genital lesions regardless of appearances.
Other causes of recurrent genital lesions should be considered, but in the event of continuing recurrent lesions and viral culture swabs remaining negative, PCR testing of lesions or type-specific herpes serology testing may aid diagnosis. Recurrent, benign, aseptic meningitis, known as Mollaret’s meningitis, may occur with HSV-2. Sufficient quantities of medication should be prescribed with instructions to start treatment as soon as symptoms begin.
The recommended period of treatment is 12 months, which may be repeated year-by-year, if necessary.
In consultation with the patient, sufficient quantities of medication may be prescribed with instructions to start treatment as soon as symptoms begin. 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. Patients who do not have virological confirmation of recurrences or who have complications or severe problems relating to their herpes should see a specialist. Patients should be given a reasonable break from therapy to reassess their pattern of recurrence to determine whether it has reduced with time. The usual recommended dose of aciclovir may need to be altered if breakthrough episodes are confirmed; aciclovir has poor oral bioavailability and some patients require multiple doses throughout the day.
It is helpful to anticipate this and to provide sufficient medication to allow prompt self-initiated treatment of any early recurrences.
Aciclovir is well tolerated and safety and efficacy data are supportive of longer-term use.37 Neurotoxicity (lethargy, confusion, hallucinations and involuntary movements) has been reported in those with renal impairment.
Practitioners should be aware that this type of therapy is an option, particularly for patients who are keen to avoid a recurrence during a specified period, e.g.
Topical antiviral creams are available over the counter, but are no longer subsidised on the pharmaceutical schedule. Disseminated maternal herpes in pregnancy (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. About 90% of neonatal herpes infections are acquired during labour through direct contact with infected genital secretions. Rarely, primary maternal infection may result in disseminated infection of the fetus with skin lesions, chorioretinitis or microcephaly or hydrocephalus at birth.43 The long-term outlook for these infants is very poor. Under such circumstances the risk of neonatal HSV infection is 57%, while vertical transmission rates of 25% are found in those with a non-primary first episode (infection with one virus type in the presence of antibodies to the other virus type) near or at the time of delivery. Risk factors for neonatal HSV infection included first-episode infection, HSV-1 vs HSV-2 isolation at the time of labour, the use of invasive monitoring, premature delivery and young maternal age.
Previously, 4 hours has been suggested as a cut-off time beyond which caesarean section may be no longer beneficial.
In the absence of definitive data, it is recommended that prophylactic aciclovir from 36 weeks should be used selectively, rather than routinely offered, for women with a history of recurrent genital herpes, e.g.
A small study of plasma levels of aciclovir at delivery in women on suppressive aciclovir at a dosage of 400mg tds from 36 weeks showed that levels were often suboptimal despite good adherence.
Continuous aciclovir in the last 4 weeks of pregnancy reduces the risk of both a clinical recurrence at term and delivery by caesarean section.
Type specific culture or PCR and serological testing in conjunction with clinical evaluation will help identify primary HSV in pregnancy. It is a member of the same family (Herpesviridae) as herpes simplex virus, Epstein-Barr virus, and cytomegalovirus.
Because the nasociliary branch innervates the globe, the most serious ocular involvement develops if this branch is affected. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference.
In excess of 60% of people older than 60 years, especially those with diminished immunity due to diabetes and cancers, are afflicted by herpes zoster. Patients with early signs of shingles complain of headaches, hypersensitivity to light, flulike symptoms without fever, itching, tingling, and burning or pain around the affected area. The features of PHN pain vary from mild to excruciating in severity, can be constant or intermittent, or triggered by trivial stimuli. Prednisone use in conjunction with acyclovir resulted in the reduction of the pain associated with acute herpes zoster. The application of capsaicin to the skin produces a burning sensation, which triggers the release of substance P, a neuropeptide, from pain fibers. Lidocaine is an amide-type local anesthetic agent that stabilizes neuronal membranes by inhibiting the ionic fluxes required for the initiation and conduction of impulses. Pharmacologically, this action may potentiate or prolong neuronal activity since reuptake of these biogenic amines is important physiologically in terminating transmitting activity. It binds with high affinity to the alpha2-delta site (an auxiliary subunit of voltage-gated calcium channels) in central nervous system tissues to produce antinociceptive effects. If there is inadequate response to one anticonvulsant agent, another agent should be tried. Opioid analgesics in combination with acetaminophen or nonsteroidal anti-inflammatory drugs may be useful as a last resort in patients with severe PHN pain unrelieved by other drugs. Nerve blocks provide periods of dramatic pain relief, which promotes the desensitization of sensory pathways. The outcome of treatment of shingles is often unsatisfactory, although the antiviral medications reduce the duration of pain during the acute phase but do not prevent PHN complications and pain.
More than 50% of the people who live to be 85 years old will develop shingles, and 80% to 85% of PHN complication occurs in patients older than 50 years. I know of crippled walking, ambulation problems with Post-herpetic neuralgia more than a year after the acute infection.
Most neonatal HSV infections are acquired at birth, generally from mothers with an unrecognised first genital herpes infection acquired during pregnancy.
Genital herpes may be due to HSV-1 (the usual cause of orolabial herpes) or HSV-2 (more commonly associated with genital lesions). That said, HSV-1 accounts for 35% of confirmed anogenital infections in Australia5 and similarly a Waikato-wide study found 30-40% of anogenital isolates are due to HSV-1 each year.6 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.
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. Increasingly, PCR is being implemented as the preferred diagnostic method for genital herpes, particularly since the advent of commercially available real-time assays.
It is important to be aware of locally available tests, as these may vary, so an appropriate sample is taken. Infection with HSV-1 does not necessarily imply sexual exposure, but genital infection with HSV-1 is increasingly common. Probable genital HSV-2 infection because oral and other non-genital site infections are uncommon. 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.
If giving results over the phone, check the person is in an appropriate situation to receive the call. These vesicles rupture within 1-2 days to form painful, sloughy, shallow ulcers with irregular margins, which may become confluent. Erectile dysfunction, dull or severe burning pain in the anogential region, loss of sensation and hypersensitivity can occur down the thighs and the lower legs.
Because prompt treatment of HSV encephalitis may minimise residual neurologic damage and prevent death, early consideration of this diagnosis is important. Some of the skin patches take on the classical ‘target lesion’ appearance, with a pink-red ring around a pale centre. Patients can be advised to bathe herpetic lesions in salt water, and women advised to urinate in a warm bath or shower to help reduce pain. A range of printed materials can be downloaded from the NZHF website, or ordered (please refer to resources listed on inside front cover). Counselling and advice often form the major part of a follow-up appointment and time should be allowed for this. At all times this process should be one of negotiation with the patient, as the pattern and severity of recurrent episodes is unpredictable.
For example, recurrent ulceration may be due to aphthous ulcers, erytheme multiforme, fixed drug eruption, self-inflicted (sometimes unknowingly) trauma and autoimmune blistering disease (rare). Eczema and less commonly psoriasis complicated by scratching may cause superficial erosions. Any recurring lesion of 1-2mm in size, occurring in the same genital area, is strongly suggestive of HSV-2 infection.
There is a significant false-negative rate in the laboratory tests for HSV, although this is less for PCR. Patients should be offered long-term suppressive antiviral management, which may need to be continued indefinitely. A range of printed materials can be downloaded from the NZHF website or ordered – please refer to resources listed on inside front cover – primary care practitioners should have access to these resources or be able to advise their patients on how to obtain them. In general, assisting the patient to take responsibility for, and control of, their disease and its treatment will help the patient overcome some of the psychological difficulties. It is suggested that either a minimum of two recurrences or approximately 3 months without suppressive therapy is necessary to establish the new pattern. A minority with late intrauterine HSV infection will present at delivery with skin or eye lesions. 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. Most patients with herpes zoster ophthalmicus present with a periorbital vesicular rash distributed according to the affected dermatome.
Reactivation of the latent virus in neurosensory ganglia produces the characteristic manifestations of herpes zoster, commonly known as shingles.
Classically, involvement of the tip of the nose (Hutchinson's sign) has been thought to be a clinical predictor of ocular involvement. This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP.
This reactivation and the accompanying inflammation lead to central nervous system dysfunction, which is manifested as debilitating pain. Initially, the host is able to produce varicella zoster virus—specific, cell-mediated immunity during the infection. The affected nerves are usually found on the trunk of the body but may sometimes be distributed on the face, neck, arm, leg, or abdomen. Keratitis occurs in approximately two-thirds of patients with HZO, often causing corneal ulceration.
Patients complain of pain in response to nonnoxious stimuli such as pressure from clothing, bed sheets, or the wind. The second objective is to treat the associated pain in the acute phase and in PHN, and the third objective is to prevent the occurrence of PHN and other complications. It has been postulated that the mechanism of the steroid effect is due to decrease in the degree of neuritis caused by the active infection, decreasing the resulting damage to affected nerves.
The depletion of substance P in the nerve fibers from repeated exposure to capsaicin results in analgesia. In patients with PHN, the lidocaine 5% patch has demonstrated relief of pain and tactile allodynia with a minimal risk of systemic adverse effects or drug—drug interactions.
The side effects to be concerned about, especially in the elderly, include nystagmus, ataxia, skin eruptions, hematological complications, and gingival hyperplasia. Carbamazepine is chemically unrelated to other anticonvulsants or other drugs used to control PHN pain.
Opioid analgesic side effects include nausea, vomiting, constipation, dizziness, headache, and respiratory depression. High-frequency TENS activates delta-opioid receptors both in the spinal cord and supraspinally (in the medulla), while low-frequency TENS activates mu-opioid receptors both in the spinal cord and supraspinally. In this technique, local anesthetics, steroids, and opioid medications are injected around the affected nerve to relieve pain. Thus, early management of shingles is essential to prevent the many complications, especially the chronic, debilitating, difficult-to-treat PHN pain that often results from the condition. For those choosing episodic antiviral therapy, it is more effective when patients start therapy themselves at the first signs of a recurrence; this requires anticipatory prescribing.


It is a very common infection that is often under-recognised, as a person may be asymptomatic or have only very minor symptoms. 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. However, results depend on multiple factors, including the adequacy of the specimen, and a negative result may not exclude infection. However, stringent quality control is necessary because of potential contamination by ‘carryover’ DNA from other biological samples19 and local validation is recommended.
Type specific tests are used in population surveys, but their diagnostic reliability in individual patients is still debated.
The condition is usually self-limiting and tends to resolve in 1-2 weeks; in the meantime, supportive cares should be offered. Primary care practitioners should have access to these resources or be able to advise their patients on how to obtain them, e.g.
Written materials, such as the NZHF Myth vs Fact leaflet and The Facts book, should be offered to patients at the first visit with discussion and further questions encouraged at the follow-up and subsequent visits.
The practitioner may also choose to refer patients on to professional counselling, if this is available.
The practitioner should be alert to the possibility of further psychological problems manifesting after a diagnosis of genital herpes. It is also helpful to give anticipatory advice over future management options including oral antiviral therapy; recurrent HSV episodes are usually milder than the initial episode and can be treated with either intermittent therapy (treating each episode) or suppressive therapy (treating continuously over a period of months to prevent episodes).
Herpes lesions may become secondarily infected with Staphylococcus aureus and will give the appearance of a folliculitis, similar to mild forms of hydradenitis suppurativa, primary folliculitis, or scabetic nodules. The best method of obtaining confirmation during a recurrence is to take a swab for culture or PCR within 24 hours of symptoms developing.
Written materials, such as the NZHF Myth vs Fact leaflet and The Facts book, should be offered to patients with discussion and further questions encouraged at subsequent visits. The prognosis for successful anti-viral therapy in these infants is far better than that for newborns with more long-standing intrauterine infection.44 Antenatal recurrent disease, where HSV is not shed at delivery, does not have an adverse affect on neonatal outcome and the risk of intrauterine fetal infection from recurrent maternal HSV infection appears to be very low. This may be updated when more information on the effects of aciclovir on the neonate is available.
If onset of labour or need for delivery is less than 6 weeks after first clinical episode, deliver by caesarean section.4. A minority of patients may also develop conjunctivitis, keratitis, uveitis, and ocular cranial-nerve palsies. Normal aging, poor nutrition, and immunocompromised status correlate with outbreaks of herpes zoster, and certain factors such as physical or emotional stress and fatigue may precipitate an episode.Herpes zoster ophthalmicus occurs when reactivation of the latent virus in the trigeminal ganglia involves the ophthalmic division of the nerve. Treatment includes topical capsaicin cream, over-the-counter analgesics, tricyclic antidepressants, and anticonvulsants.18Cranial nerve palsies involving the third (most common), fourth, and sixth nerves may occur rarely (Figure 5).
Low levels of immune globulin have been shown to predispose patients to recurring herpes zoster infection. These vesicles become crusted within 7 to 10 days and are shed, leaving scarring and pigmented changes on the skin.
Other complications include conjunctivitis, uveitis, episcleritis and scleritis, retinitis, choroiditis, optic neuritis, lid retraction, ptosis, and glaucoma.
To achieve these objectives, antiviral agents, oral corticosteroids, and pain management are utilized. The main disadvantages when acyclovir is administered orally are low bioavailability and the 5-hour dosing frequency.
Despite the usefulness of prednisone in managing the associated pain with herpes zoster infection, it has not been shown to decrease or prevent the incidence of PHN.
Capsaicin cream must be applied three to five times daily to achieve substance P depletion from the pain fiber and analgesia.
TCA therapy should be initiated with low doses to improve tolerability and be administered at bedtime. The drawback to using carbamazepine is the serious and sometimes fatal dermatologic reactions, including toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome.
Further, high-frequency TENS reduces excitation of central neurons that transmit nociceptive information, reduces release of excitatory neurotransmitters (glutamate), increases the release of inhibitory neurotransmitters (GABA) in the spinal cord, and activates muscarinic receptors centrally to produce analgesia by temporarily blocking the pain gate. This type uses a device that measures muscle tension while the patient practices a relaxation technique such as meditation, progressive muscle relaxation, or visualization. I believe it is a neurologic condition and that it should be aggressively treated with some kind of physiologic treatments by a neurologist.
If direct HSV tests are repeatedly negative and the symptoms are recurring, the patient should be advised to have type-specific herpes serology. False negative and false positive results are common in low prevalence populations and there is no confirmatory serology testing available in New Zealand.
Symptoms may sometimes persist for weeks and rarely severe intractable pain may require opiate analgesia.
Stevens-Johnson syndrome (erythema multiforme major) is a related, much less common, but much more serious condition. Confidentiality and sensitivity are paramount; patients need to agree to a third party becoming involved. Valaciclovir (Valtrex TM) 500mg daily is available for suppressive treatment of recurrent genital herpes subject to a Special Authority restriction. For first or second trimester acquisition, suppressive aciclovir therapy may be used from 36 weeks to reduce recurrences at term and hence the need for caesarean section.
Permanent sequelae of ophthalmic zoster infection may include chronic ocular inflammation, loss of vision, and debilitating pain. Postherpetic neuralgia is very resistant to treatment and results in decreased quality of life. Periodically, endogenous and exogenous boosting of the immunity against varicella results in the virus remaining dormant for decades. Pain is the primary complaint with active-stage shingles and the symptom for which patients seek medical care. The pain, which is characterized as burning and lancinating, is chronic, intractable, and distressing.
Pain therapy may involve the use of multiple agents including topical analgesics, tricyclic antidepressants, anticonvulsants, narcotics, and intervention therapy (TABLE 2). The need for regular application of capsaicin must be emphasized to patients to maintain pain relief.
The dose can be titrated every 2 to 4 weeks until maximum tolerated dose to achieve results. Tramadol, a centrally active synthetic opioid analgesic, is a useful alternative because it lacks the abuse potential associated with other opioids. The cells, virus seeds, virus bulks, and bovine serum used in the manufacturing are all tested to provide assurance that the final product is free of adventitious agents.
Sero conversion following initial infection is usually 2-6 weeks, but may be longer (months). The ulcers then dry to form crusts and later heal, leaving a transient red macule with minimal scarring (if any). Clinically, this may be indistinguishable from toxic epidermal necrolysis and hospitalisation for supportive cares is indicated. There is also a Herpes Helpline 0508 11 12 13, a telephone service which is free to all New Zealanders.
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. The available data on the effect on the neonate is reassuring, although study numbers have been small.5. Antiviral medications such as acyclovir, valacyclovir, and famciclovir remain the mainstay of therapy and are most effective in preventing ocular involvement when begun within 72 hours after the onset of the rash.
Direct ocular involvement is not specifically correlated with age, gender, or severity of disease.
Optic neuritis has been noted in about one in 400 cases and may precede retinal disease or follow acute herpes zoster ophthalmicus infection (Figure 6).17,19,20The rightsholder did not grant rights to reproduce this item in electronic media.
Oral acyclovir may be beneficial as an adjunct to topical antivirals and topical steroids in severe cases of zoster keratouveitis.
Eventually, reactivation of the virus occurs as a result of decline in virus-specific, cell-mediated immunity. It can disrupt sleep, mood, work, and activities of daily living, adversely impacting the quality of life and leading to social withdrawal and depression. The parenteral route is available for patients who are unable to utilize the oral dosing route.
Additionally, patients must understand that the pain may initially increase within the first week of initiating the therapy because it initially acts as an irritant by stimulating the nerve endings before desensitizing afferent C-fibers.
Lidocaine-containing patches significantly reduce pain intensity throughout the dosing interval for up to 12 hours.
TCAs act slowly and may require up to 3 months before achieving adequate response in patients. The side effects that are associated with anticonvulsants include sedations memory disturbance, electrolyte abnormalities, liver toxicities, and thrombocytopenia.
The CDC Advisory Committee on Immunization Practices recommends routine vaccination of all persons age >60 years with one dose of zoster vaccine. Also, some do not sero convert and reversal from sero positive to sero negative status may occur if there is minimal antigenic stimulation. Less commonly, lesions can pass through the blister phase quickly and blisters may not be noticed.
Clinically, this may be indistinguishable from toxic epidermal necrolysis and hospitalisation for supportive care is indicated. Timely diagnosis and management of herpes zoster ophthalmicus, with referral to an ophthalmologist when ophthalmic involvement is present, are critical in limiting visual morbidity. Normal age-related decline and diseases such as malignancies and HIV impact the reduction in cell-mediated immunity and the reactivation of dormant varicella virus.
Occasionally, zoster can cause motor weakness in noncranial nerve distributions, calledzoster paresis. The pain is stipulated to be due to persistent C-fiber nociceptor activity in the nerve cells, although studies have shown chronic neural loss and scarring in nerves affected by herpes zoster injury. It is important to educate patients on the need for thorough hand washing after each application of capsaicin. Lidocaine patches were superior to both no treatment and vehicle patches in averaged category pain relief scores. Combining TCAs with antiviral drugs during herpes zoster infection has been shown to decrease the intensity of PHN pain but does not prevent it.
These side effects can be minimized by initiating therapy with low doses and slowly titrating doses upward over several weeks. Patients can decrease their pain by increasing their body temperature through visualization or guided imagery. It is a useful test in some clinical situations, but routine screening of asymptomatic individuals is currently not recommended.
Lesions may also appear extra-genitally, commonly on thighs and buttocks and less commonly on hands, lips, face and breasts.
The reactivated virus travels down the sensory nerve, causing pain and skin lesions (FIGURE 1).
One specific risk for patients who are immunocompromised is dissemination of the zoster rash. The weakness develops abruptly within 2 to 3 weeks after onset of the rash and can involve upper or lower extremities.
Another advantage of valacyclovir compared to acyclovir is better bioavailability, producing comparable blood levels to parenteral acyclovir.
The main side effects expected from TCA therapy are sedation, dry mouth, postural hypotension, blurred vision, and urinary retention. Zoster vaccination is not indicated to treat acute zoster, to prevent persons with acute zoster from developing PHN, or to treat ongoing PHN. Topical anaesthetic jelly such as lignocaine (Xylocaine) gel applied 5 minutes before micturition helps relieve the pain. Patients may develop blepharitis and present with ptosis secondary to edema and inflammation.
Cutaneous dissemination generally occurs only among immunocompromised patients, occurring in up to 37% of zoster cases in the absence of antiviral treatment.
Valacyclovir appears to be more efficacious in decreasing the severity of pain associated with acute herpes zoster and the duration of the PHN when compared to acyclovir.
No clinically significant systemic adverse effects were noted, including when used long-term or in an elderly population. Before routine administration of zoster vaccine, it is not necessary to ask patients about their history of varicella (chickenpox) or to conduct serologic testing for varicella immunity. As lignocaine is a potential skin sensitizer, patients should be warned to stop application if increasing discomfort occurs after application. A vast majority of patients will have vesicular lesions on the eyelids that resolve with minimal scarring.Conjunctivitis is one of the most common complications of herpes zoster ophthalmicus.
While cutaneous dissemination is not life-threatening, it is a marker for potential virus seeding of the lungs, liver, gut, and brain and can cause pneumonia, hepatitis, encephalitis, and disseminated intravascular coagulopathy in 10% to 50% of episodes. Rarely, patients will experience acute focal neurologic deficits weeks to months after resolution of the zoster rash, involving the trigeminal distribution contralateral to the initial rash. If catheterisation is unavoidable, a suprapubic catheter should be used to reduce the risk of ascending infection and is a less painful option. The conjunctiva appears injected and edematous, often with petechial hemorrhages.9 The findings usually resolve within one week.
Famciclovir has the advantage of having longer intracellular half-life compared with acyclovir and a superior biovailability compared to both acyclovir and valacyclovir. Cardiac conduction impairment or liver toxicity may develop in some patients, especially in elderly patients or those at high risk. When antiviral therapy starts within 72 hours of the onset of herpes zoster, acyclovir, valacyclovir, and famciclovir have been shown to significantly shorten the periods of acute pain, virus shedding, rash, and acute and late-onset complications.
The clinical features of corneal disease include direct viral infection, antigen-antibody reactions, delayed cell-mediated hypersensitivity reactions, and neurotrophic damage.7 Patients with corneal disease present with varying degrees of decreased vision, pain, and light sensitivity. Other rare neurologic complications of herpes zoster include myelitis, aseptic meningitis, and meningoencephalitis.
Both valacyclovir and famciclovir have been shown to lessen the incidence and severity of PHN. Corneal complications occur in approximately 65 percent of cases of herpes zoster ophthalmicus.7Epithelial Keratitis.
The risk for neurologic zoster complications is generally increased in immunocompromised persons.
The earliest corneal finding is punctate epithelial keratitis.10 On slit lamp examination, this appears as multiple, focal, swollen lesions that stain with rose bengal or fluorescein dye.
These lesions probably contain live virus and may either resolve or progress to dendrite formation. Punctate epithelial keratitis may present as early as one or two days after the initial skin rash, while dendrites often present at four to six days but can appear many weeks later.11Herpes zoster virus dendrites appear as elevated plaques and consist of swollen epithelial cells.
Dendrites also stain with rose bengal and fluorescein dye ( Figure 2, part b) and can be viewed by Wood's lamp or slit lamp examination. The earliest finding of corneal stromal involvement presents during the second week of disease, occurring in 25 to 30 percent of patients with herpes zoster ophthalmicus.13 The condition, known as anterior stromal keratitis or nummular keratitis, is characterized by multiple fine granular infiltrates in the anterior corneal stroma below the epithelial layer (Figure 3). Most of the infiltrates lie directly beneath pre-existing dendrites or areas of punctate epithelial keratitis. This later stage of stromal keratitis is relatively uncommon and typically develops three to four months after the initial acute episode, but development can range from one month to many years later.7 It is usually central and preceded by anterior stromal keratitis.
The keratitis may present as a lesion consisting of a localized area of inflammation affecting all levels of the stroma, or as peripheral infiltrates that may have a surrounding immune ring. Corneal edema may be a prominent feature at this stage, usually with associated anterior chamber inflammation. A chronic relapsing course is not unusual, especially without timely and adequate treatment. Corneal neovascularization and lipid infiltrates may occur in patients with uncontrolled chronic disease.
The pathogenesis of stromal disease probably involves a delayed cell-mediated hypersensitivity reaction.Neurotrophic Keratopathy. Neurotrophic keratitis is the end result of decreased corneal sensation from herpes zoster virus-mediated destruction, including susceptibility to mechanical trauma, decreased lacrimation, and delayed epithelial healing.7 Corneal thinning is a serious complication that may lead to corneal perforation.
Using preservative-free lubricating drops and ointment can prevent the development of epithelial defects.UVEITISAnterior uveitis, which is diagnosed by slit lamp examination, refers to inflammation of the iris and ciliary body and occurs frequently with herpes zoster ophthalmicus. The inflammation is generally mild and transient, but it frequently causes a mild elevation in intraocular pressure. As with stromal keratitis, the course of disease may be prolonged, especially without timely, adequate treatment.
Chronic inflammation can lead to endothelial cell injury, resulting in corneal edema.EPISCLERITIS AND SCLERITISFindings of episcleritis include localized or diffuse redness, as well as pain and swelling of the conjunctiva and episclera. Both conditions may be accompanied by localized stromal keratitis.ACUTE RETINAL NECROSIS AND PROGRESSIVE OUTER RETINAL NECROSIS SYNDROMESHerpes zoster virus is considered the offending agent in most cases of acute retinal necrosis and progressive outer retinal necrosis syndromes. Acute retinal necrosis is characterized by peripheral patches of retinal necrosis that rapidly coalesce (Figure 4), occlusive vasculitis, and vitreous inflammation.
Conversely, immunocompromised patients with progressive outer retinal necrosis are unable to mount a vitreous inflammatory response, leading to rapid involvement of the macula.



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Comments
  1. Simpson 05.04.2016 at 22:50:22
    Begin a few hours or a day studies on lysine and herpes, however a research from 1984 says.
  2. Turgut 05.04.2016 at 15:48:13
    It's advisable to treat it to cut back.