సర్పి

వికీపీడియా నుండి
ఇక్కడికి గెంతు: మార్గసూచీ, వెతుకు
సర్పి
వర్గీకరణ & బయటి వనరులు
Herpes(PHIL 1573 lores).jpg
Herpes labialis of the lower lip. Note the blisters in a group marked by an arrow.
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DiseasesDB 5841 33021
m:en:eMedicine {{{m:en:eMedicineSubj}}}/{{{m:en:eMedicineTopic}}} 
MeSH {{{m:en:MeshID}}}

సర్పి (Herpes) అనేది హెర్పెస్ సింప్లెక్స్ (Herpes Simplex) అనే సూక్ష్మజీవుల వల్ల వ్యాపిస్తుంది. ఇందులో రెండు రకాలు: హెచ్.యస్.వి టైప్ 1 (HSV Type1) మరియు హెచ్.యస్.వి టైప్ 2 (HSV Type 2). సర్పి సాధారణంగా జననేంద్రియాల వద్ద, నోటి వద్ద, నుదురు పైన, కళ్ళకు, తలకు సోకుతుంది. హెచ్.యస్.వి టైప్ 2 వల్ల జననేంద్రియాలవద్ద సోకే సర్పి స్త్రీ పురుషులలో నొప్పితో కూడిన కురుపులతో ఏర్పడుతుంది. హెచ్.యస్.వి టైప్ 1 వల్ల సోకే సర్పి నుదురు పైన, కళ్ళకు, తలకు సోకుతుంది. జననేంద్రియాల ద్వారా అప్పుడే పుట్టిన పిల్లల కంటికి సోకవచ్చును. మెదడుకు సోకిన సర్పి అన్నింటికన్నా ప్రమాదమైనది. జ్వరం, కీళ్ల నొప్పులు, ఒళ్లంతా నొప్పులు, జననావయవాల్లో మంట, దురద... ఎన్ని మందులు వేసుకున్నా ఫలితం శూన్యం. తగ్గినట్టే తగ్గి మళ్లీ తిరగబెడుతుండటంతో మానసిక ఆందోళన. హెర్పిస్ బారినపడిన వారిలో కనిపించే పరిస్థితి ఇది జననాంగ సర్పి (Genital Herpes) లైంగిక సంపర్కం ద్వారా సంభవించే సుఖ వ్యాధి.

అతి సూక్ష్మమైన వైరస్ హెర్పిస్. జీవితాంతం బాధించే ఈ వైరస్‌ను హెర్పిస్ సింప్లెక్స్ వైరస్ అంటారు. ఇది రెండు రకాలు. ఒకటి హెచ్ఎస్‌వి 1, హెచ్ఎస్‌వి 2.

  1. హెచ్ఎస్‌వి 1 : ఇది నోటి దగ్గర పొక్కుల రూపంలో బయటపడుతుంది. పెదవుల చుట్టూ తెల్లని నీటి పొక్కులలాగా కనిపిస్తుంది. ఇది ముఖ్యంగా తల్లిదండ్రులు, తోటి పిల్లల నుంచి వ్యాపిస్తుంది. ఎక్కువగా పిల్లల్లో కనిపిస్తుంది. సాధారణంగా ఇవి వచ్చి పోతూ ఉంటాయి.
  2. హెచ్ఎస్‌వి 2 : జననావయవాల దగ్గర పొక్కులతో బయటపడుతుంది. దీనినే జెనిటల్ హెర్పిస్ అంటారు. చిన్న చిన్న నీటి పొక్కులలాగా వచ్చి పగిలిపోతుంటాయి. తగ్గినట్టే తగ్గి తిరిగి రావడం జరుగుతుంది. లైంగిక వ్యాధులలో నిత్యం వేధించే ఈ సమస్య దైనందిక జీవితాన్ని చిన్నాభిన్నం చేస్తుంది.

హెర్పిస్ వైరస్ పురుషుల నుంచి స్త్రీలకు లేదా స్త్రీల నుంచి పురుషులకు శృంగారం జరిపే సమయంలో వ్యాప్తి చెందుతుంది. కలయిక సమయంలో చర్మం చిట్లినప్పుడు పుండ్లు, గాయాల ద్వారా ఈ వైరస్ వ్యాపిస్తుంది. శరీరంలోకి ప్రవేశించిన ఈ వైరస్ కొద్ది రోజుల్లోనే ప్రభావం చూపిస్తుంది. ఈ వైరస్ వెన్నెముక చివరి భాగం శాక్రమ్ చుట్టూ ఉండే నాడుల సముదాయంలో చోటు చేసుకుని నిద్రావస్థలో ఉండిపోతుంది. ఈ నిద్రాణ స్థితిలో ఎలాంటి లక్షణాలూ చూపించకుండా అవ సరమైనప్పుడు తన ప్రతాపాన్ని చూపించి అతలాకుతలం చేస్తుంది. రోగిలోని రోగ నిరోధక వ్యవస్థ బలహీనపడినప్పుడు మానసిక ఆందోళన, శారీరక ఆందోళన ఉన్నప్పుడు, వాతావరణ పరిస్థితులు మారినప్పుడు లేదా ఏదైనా తీవ్రమైన అనారోగ్య సమస్యలు వచ్చినప్పుడు ఇది సునామీ లాగా విజృంభిస్తుంది.

కారణాలు[మార్చు]

అపరిశుభ్రమైన వాతావరణం, వ్యాధి నిరోధక శక్తి తగ్గిపోవడం, సరైన ఆహార సమతుల్యత లేకపోవడం.

లక్షణాలు[మార్చు]

మామూలుగా అయితే తొలి దశలో జననాంగాల్లో మంట, నొప్పి, మూత్రంలో మంట ఉంటుంది. ఒళ్లంతా నొప్పులు, గజ్జల్లో, చంకల్లో గడ్డలుగా ఉంటుంది. తరువాత క్రమక్రమంగా లైంగిక భాగాలపై చిన్న చిన్న నీటి పొక్కులు కనిపిస్తాయి. ఈ నీటి పొక్కులు రెండు, మూడు రోజులలో పగిలి పుండ్లలాగా తయారవుతాయి. ఈ దశలో రోగికి సమస్య వచ్చినట్లు తెలుస్తుంది. తొలిసారి లక్షణాలు కనిపించినప్పుడు సరైౖన చికిత్స తీసుకుంటే ప్రారంభ దశలోనే సత్వర నివారణ జరుగుతుంది. కానీ చాలా మందిలో వైరస్ ఉండిపోవడం వల్ల నిదానంగా ఉంటూ తిరిగి బయటపడుతూ ఉంటుంది. దీనినే హెర్పిస్ రికరెంట్ అటాక్ అంటారు.

హెర్పిస్ రికరెంట్ అటాక్స్[మార్చు]

వాతావరణ పరిస్థితుల్లో ఉన్న తీవ్రమైన తేడాలు, మానసిక ఆందోళన, విపరీతమైన శారీరక ఆందోళన వల్ల హెర్పిస్ రికరెంట్ అటాక్స్ వస్తాయి. దీనిలో లక్షణాల తీవ్రత అంతగా లేకపోయినా కొన్ని రోజుల్లో పుండ్లు మానిపోతాయి. నీటి పొక్కులు చితికి పుండ్లుగామారినప్పుడు హెర్పిస్ వైరస్ పుండు రసిలో ఉంటుంది. ఈ సమయంలో రతిలో పాల్గొంటే భాగస్వామికి అంటుకునే ప్రమాదం ఉంటుంది. ఎలాంటి పుండ్లూ, గాయాలూ లేకపోయినా అవతలి వ్యక్తికి అంటుకునే అవకాశం ఉంటుంది. స్త్రీలలో నెలసరి సమయంలో రక్తస్రావం వల్ల చిన్న చిన్న పొక్కులు ఉన్నా తెలియవు. వీరికి హెర్పిస్ ఉన్నట్లు తెలియకపోయినా, లోలోపల హెర్పిస్ ఉండే అవకాశం ఉంటుంది.

నిర్ధారణ[మార్చు]

కొన్ని లక్షణాల ఆధారంగా వ్యాధిని గుర్తించవచ్చు. అపరిచిత వ్యక్తులతో లైంగికంగా కలిసిన తరువాత వారం రోజులలో నీటి పొక్కుల లాగా ఏర్పడతాయి. కొన్ని రోజులకు తగ్గినట్టే తగ్గి మళ్లీ కనిపిస్తాయి. దీనిని బట్టి హెర్పిస్‌ను గుర్తించవచ్చు. పీసీఆర్ టెస్ట్, హెచ్ఎస్‌వి 1 అండ్ 2, ఐజీజీ, ఐజీఎమ్ వంటి పరీక్షలు ఉపయోగపడతాయి. పుండ్ల దగ్గర ఉండే స్రావాలను సేకరించి కల్చర్ టెస్ట్, డీఎన్ఎ టెస్ట్, యూరిన్ టెస్ట్ వంటి పరీక్షల ద్వారా నిర్ధారించుకోవచ్చు.

దుష్ఫలితాలు[మార్చు]

గర్భిణిలకు మొదటి నెలలో హెర్పిస్ సోకితే గర్భస్రావం అయ్యే అవకాశాలు ఎక్కువగా ఉంటాయి. ప్రసవ సమయంలో గర్భిణికి హెర్పిస్ ఉంటే పిల్లలకు వచ్చే అవకాశం ఉంటుంది. దీనిని నియోనాటల్ హెర్పిస్ అంటారు. వెన్నెముకలోని నాడీ మండలానికి హెర్పిస్ వస్తే అంగ స్తంభన సమస్య ఎదురు కావచ్చు. శీఘ్ర స్ఖలనం సమస్య కూడా రావచ్చు. కొందరిలో నాడీ మండలంలో హెర్పిస్ వచ్చి మెదడులో మెనింజైటిస్‌కు కారణం కావచ్చు.

చికిత్సలు[మార్చు]

సర్పికి చాలా రకాల చికిత్సలున్నాయి. ఆయుర్వేదంలో వేప ఆకులతో చేసిన మాత్రలు వేసుకోవడం, వేపగింజల నూనె సర్పిపైన పూయడం వంటివి చేస్తుంటే సర్పి నయమవుతుంది.

నివారణ[మార్చు]

ఆహారంలో పోషక విలువల సమతుల్యత సరిగా ఉండేలా చూసుకోవాలి, ఇంటి పరిసరాలు పరిశుభ్రంగా ఉంచుకోవాలి.

erpes viruses cycle between periods of active disease—presenting as blisters containing infectious virus particles—that last 2–21 days, followed by a remission period, during which the sores disappear. Genital herpes, however, is often asymptomatic, though viral shedding may still occur. After initial infection, the viruses move to sensory nerves, where they become latent and reside life-long. Causes of recurrence are uncertain, though some potential triggers have been identified. Over time, episodes of active disease reduce in frequency and severity.

Herpes simplex is most easily transmitted by direct contact with a lesion or the body fluid of an infected individual. Transmission may also occur through skin-to-skin contact during periods of asymptomatic shedding. Barrier protection methods are the most reliable method of preventing transmission of herpes, but they merely reduce rather than eliminate risk. Oral herpes is easily diagnosed if the patient presents with visible sores or ulcers. Early stages of orofacial herpes and genital herpes are harder to diagnose; laboratory testing is usually required.

A cure for herpes has not yet been developed. Once infected, the virus remains in the body for life. However, after several years, some people will become perpetually asymptomatic and will no longer experience outbreaks, though they may still be contagious to others. Treatments with antivirals can reduce viral shedding and alleviate the severity of symptomatic episodes. Vaccines are in clinical trials but have not demonstrated effectiveness. It should not be confused with conditions caused by other viruses in the herpesviridae family such as herpes zoster, which is caused by varicella zoster virus. The differential diagnosis includes hand, foot and mouth disease due to similar lesions on the skin.

Classification[మార్చు]

Herpes simplex is divided into two types: HSV type 1 and HSV type 2.[1] HSV1 primarily causes mouth, throat, face, eye, and central nervous system infections, while HSV2 primarily causes anogenital infections.[1] However, each may cause infections in all areas.[1]

Signs and symptoms[మార్చు]

HSV infection causes several distinct medical disorders. Common infection of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands (herpes whitlow). More serious disorders occur when the virus infects and damages the eye (herpes keratitis), or invades the central nervous system, damaging the brain (herpes encephalitis). Patients with immature or suppressed immune systems, such as newborns, transplant recipients, or AIDS patients are prone to severe complications from HSV infections. HSV infection has also been associated with cognitive deficits of bipolar disorder,[2] and Alzheimer's disease,[3] although this is often dependent on the genetics of the infected person.

In all cases HSV is never removed from the body by the immune system. Following a primary infection, the virus enters the nerves at the site of primary infection, migrates to the cell body of the neuron, and becomes latent in the ganglion.[4] As a result of primary infection, the body produces antibodies to the particular type of HSV involved, preventing a subsequent infection of that type at a different site. In HSV-1 infected individuals, seroconversion after an oral infection will prevent additional HSV-1 infections such as whitlow, genital herpes, and keratitis. Prior HSV-1 seroconversion seems to reduce the symptoms of a later HSV-2 infection, although HSV-2 can still be contracted. Most indications are that an HSV-2 infection contracted prior to HSV-1 seroconversion will also immunize that person against HSV-1 infection.[citation needed]

Many people infected with HSV-2 display no physical symptoms—individuals with no symptoms are described as asymptomatic or as having subclinical herpes.[5]

Condition Description Illustration
Herpetic gingivostomatitis Herpetic gingivostomatitis is often the initial presentation during the first herpes infection. It is of greater severity than herpes labialis which is often the subsequent presentations. Around 90% of the U.S. population is affected with this disease.[6]
Herpesgingiva.JPG
Herpes labialis Infection occurs when the virus comes into contact with oral mucosa or abraded skin.
Cold sore.jpg
Herpes genitalis When symptomatic, the typical manifestation of a primary HSV-1 or HSV-2 genital infection is clusters of inflamed papules and vesicles on the outer surface of the genitals resembling cold sores.
SOA-Herpes-genitalis-female.jpg
Herpetic whitlow Herpes whitlow is a painful infection that typically affects the fingers or thumbs. Occasionally infection occurs on the toes or on the nail cuticle.
Herpetic whitlow in young child.jpg
Herpes gladiatorum Individuals that participate in contact sports such as wrestling, rugby, and soccer sometimes acquire a condition caused by HSV-1 known as herpes gladiatorum, scrumpox, wrestler’s herpes, or mat herpes, which presents as skin ulceration on the face, ears, and neck. Symptoms include fever, headache, sore throat and swollen glands. It occasionally affects the eyes or eyelids.
Herpetic keratoconjunctivitis Primary infection typically presents as swelling of the conjunctiva and eyelids (blepharoconjunctivitis), accompanied by small white itchy lesions on the surface of the cornea.
Herpesviral encephalitis A herpetic infection of the brain that is thought to be caused by the retrograde transmission of virus from a peripheral site on the face following HSV-1 reactivation, along the trigeminal nerve axon, to the brain. HSV is the most common cause of viral encephalitis. When infecting the brain, the virus shows a preference for the temporal lobe.[7].
Hsv encephalitis.jpg
Herpesviral meningitis HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral meningitis.
Neonatal herpes simplex Neonatal HSV infection is a rare but serious condition, usually caused by vertical transmission of HSV (type 1 or 2) from mother to newborn.
During immunodeficiency In patients with a weakened immune system, herpes simplex can cause unusual lesions in the skin. One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut.[8]
Herpetic sycosis Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicle.[9]:369
Eczema herpeticum Infection with herpesvirus in patients with chronic atopic dermatitis may result in spread of herpes simples throughout the eczematous areas.[9]:373
Herpes esophagitis Symptoms may include painful swallowing (odynophagia) and difficulty swallowing (dysphagia). It is often associated with impaired immune function (e.g. HIV/AIDS, immunosuppression in solid organ transplants).
Herpes esophagitis.JPG

Pathophysiology[మార్చు]

Herpes is contracted through direct contact with an active lesion or body fluid of an infected person.[10] Herpes transmission occurs between discordant partners; a person with a history of infection (HSV seropositive) can pass the virus to an HSV seronegative person. The only way to contract Herpes simplex virus 2 is through direct skin-to-skin contact with an infected individual.[citation needed] To infect a new individual, HSV travels through tiny breaks in the skin or mucous membranes in the mouth or genital areas. Even microscopic abrasions on mucous membranes are sufficient to allow viral entry.

HSV asymptomatic shedding occurs at some time in most individuals infected with herpes. It can occur more than a week before or after a symptomatic recurrence in 50% of cases.[11] Virus enters into susceptible cells via entry receptors[12] such as nectin-1, HVEM and 3-O sulfated heparan sulfate.[13] Infected people that show no visible symptoms may still shed and transmit virus through their skin; asymptomatic shedding may represent the most common form of HSV-2 transmission.[11] Asymptomatic shedding is more frequent within the first 12 months of acquiring HSV. Concurrent infection with HIV increases the frequency and duration of asymptomatic shedding.[14] There are indications that some individuals may have much lower patterns of shedding, but evidence supporting this is not fully verified; no significant differences are seen in the frequency of asymptomatic shedding when comparing persons with one to twelve annual recurrences to those who have no recurrences.[11]

Antibodies that develop following an initial infection with a type of HSV prevents reinfection with the same virus type—a person with a history of orofacial infection caused by HSV-1 cannot contract herpes whitlow or a genital infection caused by HSV-1. In a monogamous couple, a seronegative female runs a greater than 30% per year risk of contracting an HSV infection from a seropositive male partner.[15] If an oral HSV-1 infection is contracted first, seroconversion will have occurred after 6 weeks to provide protective antibodies against a future genital HSV-1 infection.

Diagnosis[మార్చు]

Primary orofacial herpes is readily identified by clinical examination of persons with no previous history of lesions and contact with an individual with known HSV-1 infection. The appearance and distribution of sores in these individuals typically presents as multiple, round, superficial oral ulcers, accompanied by acute gingivitis.[16] Adults with non-typical presentation are more difficult to diagnose. Prodromal symptoms that occur before the appearance of herpetic lesions help differentiate HSV symptoms from the similar symptoms of other disorders, such as allergic stomatitis. When lesions do not appear inside the mouth, primary orofacial herpes is sometimes mistaken for impetigo, a bacterial infection. Common mouth ulcers (aphthous ulcer) also resemble intraoral herpes, but do not present a vesicular stage.[16]

Genital herpes can be more difficult to diagnose than oral herpes since most HSV-2-infected persons have no classical symptoms.[16] Further confusing diagnosis, several other conditions resemble genital herpes, including fungal infection, lichen planus, atopic dermatitis, and urethritis.[16] Laboratory testing is often used to confirm a diagnosis of genital herpes. Laboratory tests include: culture of the virus, direct fluorescent antibody (DFA) studies to detect virus, skin biopsy, and polymerase chain reaction (PCR) to test for presence of viral DNA. Although these procedures produce highly sensitive and specific diagnoses, their high costs and time constraints discourage their regular use in clinical practice.[16]

Until recently, serological tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice[16]. The older IgM serologic assay could not differentiate between antibodies generated in response to HSV-1 or HSV-2 infection. However, the new Immunodot glycoprotein G-specific (IgG) HSV test is more that 98% specific at discriminating HSV-1 from HSV-2. [17] It is the opinion of some modern medical professionals that the new IgG test should always be clinically preferred to the old IgM test, however not all doctors appear to be informed of the availability of the newer, reliable IgG tests. [18]

Prevention[మార్చు]

Barrier protection, such as a condom, can reduce the risk of herpes transmission.

As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men.[19] On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is approximately 8-10%.[15][20] This is believed to be due to the increased exposure of mucosal tissue to potential infection sites. Transmission risk from infected female to male is approximately 4-5% annually.[20] Suppressive antiviral therapy reduces these risks by 50%.[21] Antivirals also help prevent the development of symptomatic HSV in infection scenarios—meaning the infected partner will be seropositive but symptom free—by about 50%. Condom use also reduces the transmission risk by 50%.[22][23][24] Condom use is much more effective at preventing male to female transmission than vice-versa.[22] The effects of combining antiviral and condom use is roughly additive, thus resulting in approximately a 75% combined reduction in annual transmission risk.[citation needed] These figures reflect experiences with subjects having frequently recurring genital herpes (>6 recurrences per year). Subjects with low recurrence rates and those with no clinical manifestations were excluded from these studies.[citation needed]

However, asymptomatic carriers of the HSV-2 virus are still contagious. In many infections, the first symptom a person will have of their own infection is the horizontal transmission to a sexual partner or the vertical transmission of neonatal herpes to a newborn at term. Since most asymptomatic individuals are unaware of their infection, they are considered at high risk for spreading HSV.[citation needed]

Barrier methods[మార్చు]

Condoms offer moderate protection against HSV-2 in both men and women, with consistent condom users having a 30% lower risk of HSV-2 acquisition compared with those who never use condoms[25] The virus cannot pass through a latex condom, but a condom's effectiveness is limited because it does not prevent skin contact or bodily fluid contact with the scrotum, anus, buttocks, upper thighs or area immediately surrounding the penis, all of which are susceptible to infection with and transmission of the virus. Preventing contact with these areas during sex, in addition to wearing a condom, should theoretically provide enhanced protection against herpes. Wearing clothing or undergarments such as boxer shorts that cover these susceptible areas but still allow access to the genitals through a small opening (such as a fly) should help prevent transmission and infection.

The use of condoms or dental dams also limits the transmission of herpes from the genitals of one partner to the mouth of the other (or vice versa) during oral sex. When one partner has a herpes simplex infection and the other does not, the use of antiviral medication, such as valaciclovir, in conjunction with a condom, further decreases the chances of transmission to the uninfected partner.[4] Topical microbicides which contain chemicals that directly inactivate the virus and block viral entry are being investigated.[4]

Antivirals[మార్చు]

Antivirals may reduce asymptomatic shedding; it is believed asymptomatic genital HSV-2 viral shedding occurs on 20% of days per year in patients not undergoing antiviral treatment, versus 10% of days while on antiviral therapy.[11]

Pregnancy[మార్చు]

The risk of transmission from mother to baby is highest if the mother becomes infected at around the time of delivery (30% to 60%),[26][27] but the risk falls to 3% if it is a recurrent infection, and is less than 1% if there are no visible lesions.[28] To prevent neonatal infections, seronegative women are recommended to avoid unprotected oral-genital contact with an HSV-1 seropositive partner and conventional sex with a partner having a genital infection during the last trimester of pregnancy. A seronegative mother that contracts HSV at this time has up to a 57% chance of conveying the infection to her baby during childbirth, since insufficient time will have occurred for the generation and transfer of protective maternal antibodies before the birth of the child, whereas a woman seropositive for both HSV-1 and HSV-2 has around a 1-3% chance of transmitting infection to her infant.[29][30] Women that are seropositive for only one type of HSV are only half as likely to transmit HSV as infected seronegative mothers. Mothers infected with HSV are advised to avoid procedures that would cause trauma to the infant during birth (e.g., fetal scalp electrodes, forceps, and vacuum extractors) and, should lesions be present, to elect caesarean section to reduce exposure of the child to infected secretions in the birth canal.[4] The use of antiviral treatments, such as acyclovir, given from the 36th week of pregnancy, limits HSV recurrence and shedding during childbirth, thereby reducing the need for caesarean section.[4]

Acyclovir is the recommended antiviral for herpes suppressive therapy during the last months of pregnancy. The use of valaciclovir and famciclovir, while potentially improving compliance have less well determined safety in pregnancy.

Treatment[మార్చు]

There is no method to eradicate herpes virus from the body, but antiviral medications can reduce the frequency, duration, and severity of outbreaks. Analgesics such as ibuprofen and acetaminophen can reduce pain and fever. Topical anesthetic treatments such as prilocaine, lidocaine, benzocaine or tetracaine can also relieve itching and pain.[31][32][33]

Antiviral[మార్చు]

The antiviral medication acyclovir

There are several antivirals that are effective for treating herpes including: aciclovir (acyclovir), valaciclovir (valacyclovir), famciclovir, and penciclovir. Aciclovir was the first discovered and is now available in generic.

Evidence supports the use of aciclovir and valaciclovir in the treatment of herpes labialis[34] as well as herpes infections in people with cancer.[35] The evidence to support the use of acyclovir in primary herpetic gingivostomatitis is less strong.[36]

Topical[మార్చు]

A number of topical antivirals are effective for herpes labialis including acyclovir, penciclovir, and docosanol.[34][37] Docosanol can be purchased over the counter in Canada and the USA.

Alternative medicine[మార్చు]

Certain dietary supplements and alternative remedies are claimed to be beneficial in the treatment of herpes. There is however insufficient evidence to support use of many of these compounds including echinacea, eleuthero, L-lysine, zinc, bee products and aloe vera.[38]

A single study indicates possible benefit from laser treatment.[39]

Prognosis[మార్చు]

Following active infection, herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the nucleus of a nerve's cell body. HSV latency is static—no virus is produced—and is controlled by a number of viral genes, including Latency Associated Transcript (LAT).[40]

Many HSV-infected people experience recurrence within the first year of infection.[4] Prodrome precedes development of lesions. Prodromal symptoms include tingling (paresthesia), itching, and pain where lumbosacral nerves innervate the skin. Prodrome may occur as long as several days or as short as a few hours before lesions develop. Beginning antiviral treatment when prodrome is experienced can reduce the appearance and duration of lesions in some individuals. During recurrence, fewer lesions are likely to develop, lesions are less painful and heal faster (within 5–10 days without antiviral treatment) than those occurring during the primary infection.[4] Subsequent outbreaks tend to be periodic or episodic, occurring on average four to five times a year when not using antiviral therapy.

The causes of reactivation are uncertain, but several potential triggers have been documented. A recent study (2009) showed that a protein VP16 plays a key role in reactivation of the dormant virus.[41] Changes in the immune system during menstruation may play a role in HSV-1 reactivation.[42][43] Concurrent infections, such as viral upper respiratory tract infection or other febrile diseases, can cause outbreaks. Reactivation due to infection is the likely source of the historic terms cold sore and fever blister.

Other identified triggers include: local injury to the face, lips, eyes, or mouth, trauma, surgery, radiotherapy, and exposure to wind, ultraviolet light, or sunlight.[44][45][46][47][48]

The frequency and severity of recurrent outbreaks vary greatly between patients. Some individuals' outbreaks can be quite debilitating with large, painful lesions persisting for several weeks, while others will experience only minor itching or burning for a few days. There is some evidence that genetics plays a role in the frequency of cold sore outbreaks. An area of human chromosome 21 that includes 6 genes has been linked to frequent oral herpes outbreaks. An immunity to the virus is built over time. Most infected individuals will experience fewer outbreaks and outbreak symptoms will often become less severe. After several years, some people will become perpetually asymptomatic and will no longer experience outbreaks, though they may still be contagious to others. Immuno-compromised individuals may experience episodes that are longer, more frequent, and more severe. Antiviral medication has been proven to shorten the frequency and duration of outbreaks.[49] Outbreaks may occur at the original site of the infection or in proximity to nerve endings that reach out from the infected ganglia. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs. HSV-2 infected individuals are at higher risk for acquiring HIV when practicing unprotected sex with HIV-positive persons,[50] particularly during an outbreak with active lesions.[51]

Epidemiology[మార్చు]

Worldwide rates of HSV infection are between 65% and 90%.[1] HSV1 is more common than HSV2 with rates of both increasing as people age.[1] Rates of infection are determined by the presence of antibodies against either viral species.[52]

In the US 17.2% of the population is HSV-2 seropositive with only 14.5% of the seropositive population aware that they are infected.[53]

History[మార్చు]

Herpes has been known for at least 2,000 years. It is said that Emperor Tiberius banned kissing in Rome for a time due to so many people having cold sores. In the 16th century Romeo and Juliet, it is mentioned that there are blisters "o'er ladies' lips." In 18th century it was so common among prostitutes that it was called "a vocational disease of women."[54]

The term Herpes Simplex appeared in Richard Boulton's A System of Rational and Practical Chirurgery in 1713, where the terms Herpes miliaris and Herpes exedens also appeared.

Herpes was not found to be a virus until the 1940s.[54]

Herpes antiviral therapy began in the early 1960s with the experimental use of medication that interfered with viral replication called deoxyribonucleic acid (DNA) inhibitors. The original use was against normally fatal or disabilitating illness such as adult encephalitis,[55] keratitis,[56] in immunocompromised (transplant) patients,[57] or disseminated herpes zoster.[58] The original compounds used were 5-iodo-2'-deoxyuridine, AKA idoxuridine, IUdR, or(IDU) and 1-β-D-arabinofuranosylcytosine or ara-C,[59] later marketed under the name cytosar or cytorabine. The usage expanded to include topical treatment of herpes simplex,[60] zoster, and varicella.[61] Some trials combined different antivirals with differing results.[55] The introduction of 9-β-D-arabinofuranosyladenine, AKA ara-A or vidarabine, considerably less toxic than Ara-C, in the mid 1970s, heralded the way for the beginning of regular neonatal antiviral treatment. Vidarabine was the first systemically administered antiviral medication with activity against HSV for which therapeutic efficacy outweighed toxicity for the management of life-threatening HSV disease. Intravenous vidarabine was licensed for use by the U.S. Food and Drug Administration (FDA) in 1977. Other experimental antivirals of that period included: Heparin [62], trifluorothymidine (TFT)[63], Ribivarin,[64] interferon,[65] Virazole,[66] and 5-methoxymethyl-2'-deoxyuridine (MMUdR).[67] The introduction of 9-(2-hydroxyethoxymethyl)guanine, AKA acyclovir, in the late 1970s[68] raised antiviral treatment another notch and led to vidarabine vs. acyclovir trials in the late 1980s.[69] The lower toxicity and ease of administration over vidarabine has led to acyclovir becoming the drug of choice for herpes treatment after it was licensed by the FDA in 1998.[70] Another advantage in the treatment of neonatal herpes included greater reductions in mortality and morbidity with increased dosages, something that did not occur when compared with increased dosages of vidarabine.[70] On the other side of the equation, acyclovir seems to inhibit antibody response and newborns on acyclovir antiviral treatment experienced a slower rise in antibody titer than those on vidarabine.[70]

Society and culture[మార్చు]

Some people experience negative feelings related to the condition following diagnosis, particularly if they have acquired the genital form of the disease. Feelings can include depression, fear of rejection, feelings of isolation, fear of being found out, self-destructive feelings, and fear of masturbation.[71] These feelings usually lessen over time. Much of the hysteria and stigma surrounding herpes stems from a media campaign beginning in the late 1970s and peaking in the early 1980s. There were multiple articles worded in fear-mongering and anxiety-provoking terminology, such as the now ubiquitous "attacks," "outbreaks," "victims," and "sufferers." At one point the term "herpetic" even entered the popular lexicon. The articles were published by Reader's Digest, U.S. News, and Time magazine, among others. A made-for-TV movie was named Intimate Agony. The peak was when Time magazine had 'Herpes: The New Scarlet Letter' on the cover in August 1982, forever stigmatizing the word in the public mind.[54] The scientific reality is that most people are asymptomatic, the virus causes no real health problems for a vast majority of people, and a vast majority (around 90%) of the Earth's population carries HSV-1, 2, or both.[72][73] Herpes support groups have been formed in the United States and the UK, providing information about herpes and running message forums and dating websites for "sufferers."[74] People with the herpes virus are often hesitant to divulge to other people, including friends and family, that they are infected. This is especially true of new or potential sexual partners whom they consider casual.[75]

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