What are the main causes of herpes encephalitis. How is herpes encephalitis diagnosed and treated. Is herpes encephalitis contagious and can it be prevented. What are the long-term effects of herpes encephalitis.

Understanding Herpes Encephalitis: An Overview

Herpes encephalitis is a rare but serious condition characterized by inflammation of the brain, typically caused by the herpes simplex virus (HSV). This severe form of encephalitis can lead to significant neurological complications if not promptly diagnosed and treated. While the condition itself is not contagious, the virus that causes it can be transmitted from person to person.

How does herpes encephalitis develop? The herpes simplex virus, which commonly causes cold sores and genital herpes, can in some cases spread to the brain, leading to encephalitis. This occurs when the virus reactivates from its dormant state in the body’s nerve cells and travels along nerve pathways to the brain.

Causes and Risk Factors of Herpes Encephalitis

The primary cause of herpes encephalitis is infection with the herpes simplex virus, particularly HSV-1 and HSV-2. HSV-1 is more commonly associated with herpes encephalitis, especially in adults. However, other factors can increase the risk of developing this condition:

• Weakened immune system due to conditions like HIV/AIDS or cancer
• Recent organ transplantation and associated immunosuppressive therapy
• Stress or physical trauma that can trigger viral reactivation
• Congenital infections in newborns during childbirth

Are certain individuals more susceptible to herpes encephalitis? While anyone can potentially develop herpes encephalitis, it is more commonly observed in individuals with compromised immune systems, newborns, and elderly adults. Additionally, people who have never been exposed to the herpes simplex virus may be at higher risk of severe infection if they contract the virus for the first time.

Recognizing the Symptoms of Herpes Encephalitis

The symptoms of herpes encephalitis can range from mild to severe and may develop rapidly. Early recognition of these symptoms is crucial for timely intervention. Common signs and symptoms include:

• High fever
• Severe headache
• Confusion and altered mental state
• Seizures
• Nausea and vomiting
• Stiff neck
• Sensitivity to light (photophobia)
• Speech and language difficulties
• Memory problems
• Hallucinations

How quickly do symptoms of herpes encephalitis progress? The onset of symptoms can be sudden and may worsen rapidly over a few hours to days. In some cases, mild flu-like symptoms may precede the more severe neurological manifestations.

Diagnosis and Testing for Herpes Encephalitis

Prompt and accurate diagnosis of herpes encephalitis is critical for effective treatment. Healthcare providers employ a combination of clinical evaluation and diagnostic tests to confirm the condition:

1. Neurological examination to assess cognitive function and motor skills
2. Magnetic Resonance Imaging (MRI) or Computed Tomography (CT) scans to visualize brain inflammation
3. Electroencephalogram (EEG) to detect abnormal brain activity
4. Lumbar puncture (spinal tap) to analyze cerebrospinal fluid for signs of infection
5. Polymerase Chain Reaction (PCR) test to detect viral DNA in cerebrospinal fluid

Why is early diagnosis of herpes encephalitis crucial? Early diagnosis allows for prompt initiation of antiviral therapy, which can significantly improve outcomes and reduce the risk of long-term neurological complications.

Treatment Approaches for Herpes Encephalitis

Treatment of herpes encephalitis typically involves a multifaceted approach, focusing on antiviral therapy and supportive care:

Antiviral Medications

The primary treatment for herpes encephalitis is intravenous administration of antiviral drugs, such as acyclovir. This medication works by inhibiting viral replication, thereby reducing brain inflammation and preventing further damage.

Supportive Care

Patients often require intensive supportive care to manage symptoms and complications:

• Intravenous fluids to prevent dehydration
• Anti-seizure medications to control convulsions
• Pain relievers and fever reducers
• Mechanical ventilation if respiratory function is compromised
• Monitoring of intracranial pressure

How long does treatment for herpes encephalitis typically last? Antiviral therapy is usually administered for 14 to 21 days, depending on the severity of the infection and the patient’s response to treatment. However, supportive care may be required for a longer period as the brain heals and neurological function improves.

Potential Complications and Long-Term Effects

While prompt treatment can significantly improve outcomes, herpes encephalitis can still lead to long-term complications in some cases:

• Memory impairment
• Personality changes
• Speech and language deficits
• Seizure disorders
• Motor skill impairments
• Cognitive difficulties
• Vision problems

Can the effects of herpes encephalitis be reversed? While some individuals may experience full recovery, others may face persistent neurological deficits. Rehabilitation therapies, including physical therapy, occupational therapy, and speech therapy, can help improve function and quality of life for those with lasting effects.

Prevention and Risk Reduction Strategies

Preventing herpes encephalitis primarily involves reducing the risk of herpes simplex virus infection and managing existing infections:

• Practice safe sex to reduce the risk of genital herpes transmission
• Avoid close contact with individuals experiencing active herpes outbreaks
• Maintain good hygiene practices, including regular handwashing
• Strengthen the immune system through a healthy lifestyle
• Consider antiviral suppression therapy for individuals with frequent herpes outbreaks

Is there a vaccine available to prevent herpes encephalitis? Currently, there is no vaccine specifically designed to prevent herpes encephalitis. However, research is ongoing to develop vaccines against herpes simplex virus infections, which could potentially reduce the risk of encephalitis as well.

Living with Herpes Encephalitis: Support and Recovery

Recovery from herpes encephalitis can be a challenging and lengthy process. Patients and their families often require ongoing support and resources:

Rehabilitation Services

Many patients benefit from a comprehensive rehabilitation program, which may include:

• Physical therapy to improve mobility and strength
• Occupational therapy to enhance daily living skills
• Speech and language therapy to address communication difficulties
• Cognitive rehabilitation to improve memory and thinking skills

Psychological Support

Coping with the aftermath of herpes encephalitis can be emotionally challenging. Psychological support services, including counseling and support groups, can be invaluable for patients and their families.

Long-Term Medical Care

Ongoing medical follow-up is essential to monitor for potential complications and manage any persistent symptoms. This may include regular neurological assessments and imaging studies.

How can families support loved ones recovering from herpes encephalitis? Family members play a crucial role in the recovery process by providing emotional support, assisting with daily activities, and advocating for appropriate medical care and rehabilitation services. Education about the condition and its potential long-term effects can help families better understand and support their loved ones’ needs.

Advances in Research and Future Perspectives

Ongoing research in the field of herpes encephalitis aims to improve diagnosis, treatment, and prevention strategies:

Diagnostic Advances

Researchers are exploring new diagnostic techniques, including advanced neuroimaging and biomarker detection, to enable earlier and more accurate diagnosis of herpes encephalitis.

Novel Therapeutic Approaches

Investigations into new antiviral drugs and immunomodulatory therapies seek to enhance treatment efficacy and reduce the risk of long-term complications.

Neuroprotective Strategies

Studies are underway to develop neuroprotective agents that could minimize brain damage during the acute phase of herpes encephalitis.

Vaccine Development

Efforts to develop an effective vaccine against herpes simplex virus continue, with potential implications for preventing herpes encephalitis.

What promising developments are on the horizon for herpes encephalitis treatment? Recent research has shown potential in using combination therapies that target both viral replication and the inflammatory response in the brain. Additionally, personalized medicine approaches based on genetic factors and immune system profiles may lead to more targeted and effective treatments in the future.

In conclusion, herpes encephalitis remains a serious neurological condition that requires prompt diagnosis and treatment. While challenges persist, ongoing research and advancements in medical care offer hope for improved outcomes and quality of life for those affected by this condition. As our understanding of the disease mechanisms deepens, we can anticipate more effective prevention strategies and therapeutic interventions in the years to come.

Encephalitis (for Teens) – Nemours KidsHealth

What Is Encephalitis?

Encephalitis is an inflammation (swelling and irritation) of the brain. In most cases, a

viruscauses this inflammation.

Encephalitis is also called acute viral encephalitis or aseptic encephalitis.

Who Gets Encephalitis?

Encephalitis (in-seh-fuh-LYE-tus) is a rare disease. Most cases happen in children, the elderly, and people with a weakened immune system (from HIV/AIDS, cancer, etc.).

Several thousand cases of encephalitis are reported to the Centers for Disease Control and Prevention (CDC) every year. But health experts think that many more cases happen that aren’t reported because symptoms vary and can be mild.

What Are the Signs & Symptoms of Encephalitis?

Symptoms in mild cases of encephalitis usually include:

• fever
• headache
• poor appetite
• loss of energy
• a general sick feeling

Serious cases of encephalitis can cause:

• a high fever
• severe headache
• nausea and vomiting
• stiff neck
• confusion
• personality changes
• convulsions (seizures)
• problems with speech or hearing
• hallucinations
• memory loss
• drowsiness
• coma

Because encephalitis can happen during or after common viral illnesses, symptoms of these illnesses can start before encephalitis happens. But often, it appears without warning.

What Causes Encephalitis?

Three groups of viruses are common causes of encephalitis:

1. Herpes viruses, such as chickenpox, EBV (Epstein-Barr virus, which causes mono), and herpes simplex (which causes cold sores).
2. Viruses and other germs transmitted by insects, like West Nile virus (spread through a mosquito bite) and the germs that cause Lyme disease and Rocky Mountain spotted fever (spread through tick bites).
3. Viruses that cause once-common childhood infections, such as measles, mumps, and German measles. Thanks to immunizations, it’s rare today for someone to develop encephalitis from these illnesses.

Less often, encephalitis can be:

• caused by an infection from
  bacteria, such as bacterial meningitis
• a complication of other infectious diseases like syphilis
• due to a parasite, like toxoplasmosis (found in infected cat feces) in people with weakened immune systems

Is Encephalitis Contagious?

Brain inflammation itself is not contagious. But the viruses that cause encephalitis can be. Of course, getting a virus does not mean that someone will develop encephalitis.

page 2

How Is Encephalitis Diagnosed?

Doctors use several tests to diagnose encephalitis, including:

• imaging tests, such as computed tomography (CT) scans or magnetic resonance imaging (MRI), to check the brain for swelling, bleeding, or other problems
• electroencephalogram (EEG), which records the electrical signals in the brain, to check for unusual brain waves
• blood tests to look for bacteria or viruses in the blood. These also can show if the body is making antibodies (specific proteins that fight infection) in response to a germ
• lumbar puncture, or spinal tap, which checks cerebrospinal fluid (the fluid that surrounds the brain and spinal cord) for signs of infection

How Is Encephalitis Treated?

Most people with encephalitis need care in a hospital, usually in an intensive care unit (ICU). Doctors will watch their blood pressure, heart rate, breathing, and body fluids to prevent further swelling of the brain.

Medicines

• Antiviral drugs can treat some forms of encephalitis, such as the type caused by the herpes simplex virus.
• Corticosteroids may be used to reduce brain swelling.
• Anticonvulsants might be given to someone having seizures.
• Over-the-counter (OTC) medicines, like acetaminophen, can help with fever and headaches.
• Antibiotics don’t work against viruses, so aren’t used to treat most forms of encephalitis.

Many people with encephalitis make a full recovery. In some cases, brain swelling can cause lasting problem like learning disabilities, speech problems, memory loss, or lack of muscle control. Speech therapy, physical therapy, or occupational therapy can help in these cases.

How Long Does Encephalitis Last?

Most of the time, the

acutephase of the illness (when symptoms are the most severe) lasts up to a week. Full recovery can take longer, often several weeks or months.

Can Encephalitis Be Prevented?

The best way to prevent encephalitis is to avoid getting infected with the viruses or other germs that can cause it. Regular hand washing will help limit the spread of some of these germs. Staying as healthy as possible by eating a balanced diet and getting plenty of rest can help keep your immune system in shape. Immunizations are also an important way to protect people from diseases like chickenpox and measles.

In areas where viruses and other germs are transmitted by insect bites, protect yourself by wearing long sleeves and pants and applying an insect repellent. Also, try to avoid unnecessary outdoor activities at dawn and dusk when mosquitoes are most likely to bite.

When Should I Call the Doctor?

Get medical care right away if you have any of these symptoms:

• a severe headache
• convulsions (seizures)
• stiff neck
• can’t look at bright lights
• double vision
• trouble walking
• problems with speech or hearing
• trouble moving an arm or leg
• loss of sensation anywhere in the body
• sudden personality changes
• problems with memory
• extreme drowsiness
• loss of consciousness (passing out)

Encephalitis – Causes & Risk Factors

What Is Encephalitis?

Encephalitis, or inflammation of the brain tissue, is rare, affecting about one in 200,000 people each year in the U. S.

When it strikes, it can be very serious, causing personality changes, seizures, weakness, and other symptoms depending on the part of the brain affected.

Children, the elderly, and those with a weak immune system are most vulnerable. The disease is usually caused by one of several viral infections, so it’s sometimes referred to as viral encephalitis.

Most people who have mild encephalitis fully recover. The most appropriate treatment and the patient’s chance of recovery depend on the virus involved and the severity of the inflammation.

In acute encephalitis, the infection directly affects the brain cells. In para-infectious encephalitis, the brain and spinal cord become inflamed within one to two weeks of contracting a viral or bacterial infection.

What Causes Encephalitis?

Viral encephalitis may develop during or after infection with any of several viral illnesses including influenza, herpes simplex, measles, mumps, rubella, rabies, chickenpox, and arbovirus infection including West Nile virus.

Herpes simplex type 1 virus is one of the more common and serious causes of viral encephalitis. Herpes-related encephalitis can erupt rapidly, and may cause seizures or mental changes and even lead to coma or death. It occurs when the herpes simplex type 1 virus travels to the brain rather than moving through the body to the surface of the skin and producing its more common symptom, a cold sore. Early recognition and treatment of herpes encephalitis can be life-saving. You are not more likely to get encephalitis if you have cold sores.

Arbovirus encephalitis is another form of viral encephalitis. It is caused by various viruses that are carried by insects (such as mosquitoes and ticks). Unlike herpes, arboviral infections are seasonal, occurring primarily in summer and early fall, and are clustered in specific regions, such as in the case of St. Louis encephalitis.

In rare instances, bacterial, fungal, parasitic, or rickettsial infections cause encephalitis. Cancer or even exposure to certain drugs or toxins may also cause encephalitis.

What Are the Symptoms of Encephalitis?

The symptoms of encephalitis are usually sudden and severe.

They include:

• Fever
• Drowsiness, lethargy, and possibly coma
• Headaches
• Personality changes, irritability, or emotional outbursts
• Confusion
• Weakness in one or more areas of the body
• Seizures
• Bulging soft spots in infants

Seek medical attention right away if you or someone else has any of these symptoms.

How Is Encephalitis Diagnosed?

Many clues as to the cause of encephalitis come from an exposure history. Because a person with encephalitis is usually disoriented, family and friends are key to getting a good history. It is important to know if the person may have come into contact with mosquitoes or ticks, infected animals, or sick people.

Your doctor may also order an MRI scan, spinal tap, or electroencephalogram (EEG).

Blood tests to check for bacteria or viruses and the immune cells produced in response to them can also be helpful.

Rarely, an analysis of a brain tissue sample (biopsy) may be necessary to confirm the diagnosis in cases where symptoms are getting worse and treatments aren’t working. It can be very important to identify the type of encephalitis in order to give the right treatment.

What Are the Treatments for Encephalitis?

Because complications from encephalitis can be serious, the condition requires hospitalization. Treatment will depend largely on your age and condition, as well as the form and cause of the disease.

If encephalitis is caused by a bacterial infection, it can be treated with intravenous antibiotics. Treatment for herpes-related encephalitis includes supportive care, as well as intravenous antiviral therapy with a drug such as acyclovir. Other treatments may be used to lower fever, provide hydration, treat seizures if they develop, and reduce any pressure in the skull.

With proper care, most people recover from encephalitis. Infants and elderly people are at greater risk of permanent brain damage.

How Can I Prevent Encephalitis?

The elimination of smallpox and the use of vaccines against mumps, measles, and rubella have lowered cases of encephalitis, especially in children.

Vaccines have been developed for people who travel to high-risk areas as well.

Other ways to prevent it are to avoid viruses that can lead to the disease (like herpes) and to protect yourself against mosquito and tick bites.

Herpes Simplex Encephalitis: Practice Essentials, Background, Pathophysiology

Herpes simplex encephalitis – Knowledge @ AMBOSS

Last updated: August 17, 2021

Summary

Herpes simplex encephalitis (HSE) is an inflammation of the brain parenchyma, typically in the medial temporal lobe, that is caused by either herpes simplex virus 1 (HSV-1) or herpes simplex virus 2 (HSV-2). It is the most common cause of fatal sporadic encephalitis in the US. HSE has a bimodal distribution, commonly affecting patients younger than 20 years of age and older than 50 years of age. Patients with HSE typically present with a prodrome of headaches and fever, followed by sudden focal neurological deficits, altered mental status, and possible seizures. Characteristic clinical findings and brain imaging showing temporal lesions should raise suspicion for HSE. Lumbar puncture often reveals lymphocytic pleocytosis. The diagnosis is best confirmed with polymerase chain reaction (PCR) testing of cerebrospinal fluid. Because HSE has a rapidly progressive and potentially fatal course, treatment with acyclovir should begin as soon as the disease is suspected. The mortality rate is as high as 70% if left untreated, and relapse is possible but uncommon.

Epidemiology

References:^[1]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

References:^[2]

Pathophysiology

References:^[2][3][4]

Clinical features

• Duration: a few hours to days
• Nonspecific symptoms

HSE may resemble bacterial meningitis, but the combination of altered mental status, seizures, and focal neurological deficits is more common for HSE!

References:^[6]

Diagnostics

Approach

^[7][8]

• Strongly suspected HSE: Start immediate treatment prior to investigations (see “Antimicrobial treatment of herpes simplex encephalitis”).
• All patients require:
• Initial negative PCR with high clinical and/or radiological probability: Continue empiric treatment and repeat HSV PCR after 3–7 days. ^[9]
• Further testing (e.g., brain biopsy) is not routinely required; consider if there are contraindications for LP or uncertain diagnosis in treatment-refractory patients.

Empiric treatment should be initiated while awaiting the definitive diagnosis, as the progression of HSE is very rapid. ^[7][10]

Blood studies

• Prior to LP ^[7][11][12]
• Simultaneous to LP: serum glucose
• Additional testing

CSF studies

^[7][8]

• MRI head: most sensitive and specific imaging modality ^[10]
  • Indication: all patients with suspected HSE
  • Findings
• CT head with and without intravenous contrast ^[11]
  • Indications
  • Findings
    • Early stages : often no detectable abnormalities ^[12][13]
    • Later stages: unilateral or bilateral hypodense zones in the temporal lobe

Always consider HSE when imaging suggests potential meningoencephalitis and temporal lobe involvement; bilateral temporal lobe abnormality is a pathognomic sign of HSE. ^[7]

• Indication: all patients with suspected HSE encephalitis
• Findings
  • Abnormal in > 80% of patients ^[10]
  • Characteristic finding: periodic lateralized epileptiform discharges from the affected temporal lobe

Pathology

• Macroscopic: typical temporal lobe distribution with visible necrosis
• Microscopic
  • Hemorrhagic-necrotizing inflammation
  • Eosinophilic nuclear inclusions (Cowdry bodies)

References: ^[14]

Differential diagnoses

The differential diagnoses listed here are not exhaustive.

Treatment

Antimicrobial treatment for herpes simplex encephalitis

^[7][9][10]

All patients should be hospitalized and a neurology consult is highly recommended; intensive care must be readily available. ^[13]

• Antiviral treatment
  • Start immediate treatment with intravenous acyclovir without waiting for diagnostic confirmation.
  • Duration of treatment: 14–21 days ^[15]
  • Patients with acyclovir resistance and immunocompromised patients: Consult infectious diseases. ^[16][17]
• Additional treatment

Monitor for nephrotoxicity during treatment with acyclovir. Manage with adequate hydration and adjust dosages for renal function. ^[8][10]

Management of complications

Acute management checklist for herpes simplex encephalitis

• Perform a thorough neurological examination.
• Obtain IV access and draw routine laboratory studies (e.g., CBC, BMP, liver chemistries).
• Check for rapidly reversible causes of altered mental status (e.g., point of care glucose).
• Identify and treat any life-threatening complications (e.g., airway compromise, ↑ ICP, status epilepticus).
• Order monitoring (e.g., cardiac monitoring, frequent neurological checks).
• Consider CT head if suspected ↑ ICP, intracranial hemorrhage, or intracranial abscess.
• Perform lumbar puncture if no LP contraindications and send CSF analysis including HSV PCR.
• Start empiric IV acyclovir prior to LP if strong clinical suspicion.
• Consider empiric antibiotics for bacterial meningitis and corticosteroids.
• Order MRI head and EEG for stable patients.
• Consult neurology.
• Consult ICU for ICP management, refractory seizure control, or advanced airway management.
• Consult infectious disease for immunocompromised patients or acyclovir resistance.

Prognosis

• Fatal in up to 70% of cases if left untreated ^[2]
• In patients receiving treatment, the mortality rate is still as high as 20–30%. ^[3]
• Relapse may occur.
• Residual deficits may remain in some cases (e.g., paresis, cognitive deficits, psychopathological symptoms)

Prevention

• There are no known effective strategies for preventing herpes simplex encephalitis in older children (beyond the neonatal period) or adults. ^[19]
• Although the herpes simplex virus itself is highly contagious, person-to-person transmission of HSV encephalitis has not been described, and neither isolation nor chemoprophylaxis for close contacts is necessary.

References

1. Klein RS. Herpes simplex virus type 1 encephalitis. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/herpes-simplex-virus-type-1-encephalitis?source=search_result&search=herpes%20encephalitis&selectedTitle=1~41.Last updated: August 15, 2014. Accessed: November 6, 2016.
2. Anderson WE. Herpes Simplex Encephalitis. In: Singh NN, Herpes Simplex Encephalitis. New York, NY: WebMD. http://emedicine.medscape.com/article/1165183-overview#a5. Updated: June 15, 2016. Accessed: November 6, 2016.
3. Shorvon SD, Andermann F, Guerrini R. The Causes of Epilepsy: Common and Uncommon Causes in Adults and Children.
   Cambridge University Press
   ; 2011
   : p. 468
4. Anderson WE. Herpes Simplex Encephalitis. In: Singh NN, Herpes Simplex Encephalitis. New York, NY: WebMD. http://emedicine.medscape.com/article/1165183-overview#showall. Updated: June 15, 2016. Accessed: November 6, 2016.
5. Anderson WE. Herpes Simplex Encephalitis. In: Singh NN, Herpes Simplex Encephalitis. New York, NY: WebMD. http://emedicine.medscape.com/article/1165183-overview#a3. Updated: June 15, 2016. Accessed: November 2, 2016.
6. Anderson WE. Herpes Simplex Encephalitis Clinical Presentation. In: Singh NN, Herpes Simplex Encephalitis Clinical Presentation. New York, NY: WebMD. http://emedicine.medscape.com/article/1165183-clinical#showall. Updated: June 15, 2016. Accessed: November 6, 2016.

7. Tunkel AR, Glaser CA, Bloch KC, et al. The Management of Encephalitis: Clinical Practice Guidelines by the Infectious Diseases Society of America. Clinical Infectious Diseases. 2008; 47
   (3): p.303-327.
   doi: 10.1086/589747 . | Open in Read by QxMD

8. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison’s Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2).
   McGraw-Hill Education / Medical
   ; 2018

9. Stahl JP, Mailles A. Herpes simplex virus encephalitis update. Current Opinion in Infectious Diseases. 2019; 32
   (3): p.239-243.
   doi: 10.1097/qco.0000000000000554 . | Open in Read by QxMD

10. Gnann JW, Whitley RJ. Herpes Simplex Encephalitis: an Update. Current Infectious Diseases Reports. 2017; 19
    (3).
    doi: 10.1007/s11908-017-0568-7 . | Open in Read by QxMD

11. Walls R, Hockberger R, Gausche-Hill M. Rosen’s Emergency Medicine.
    Elsevier Health Sciences
    ; 2018

12. Chaudhuri A, Kennedy PGE. Diagnosis and treatment of viral encephalitis. Postgraduate Medical Journal. 2002; 78
    (924): p.575-583.
    doi: 10.1136/pmj.78.924.575 . | Open in Read by QxMD

13. Steiner I, Budka H, Chaudhuri A, et al. Viral encephalitis: a review of diagnostic methods and guidelines for management. European Journal of Neurology. 2005; 12
    (5): p.331-343.
    doi: 10.1111/j.1468-1331.2005.01126.x . | Open in Read by QxMD

14. Patel MR. Imaging in Herpes Encephalitis. In: Smirniotopoulos JG, Imaging in Herpes Encephalitis. New York, NY: WebMD. http://emedicine.medscape.com/article/341142-overview. Updated: July 14, 2015. Accessed: November 6, 2016.
15. Gilbert, DN; Chambers, HF. Sanford Guide to Antimicrobial Therapy 2020.
    Antimicrobial Therapy, Inc
    ; 2020

16. Bergmann M, Beer R, Kofler M, Helbok R, Pfausler B, Schmutzhard E. Acyclovir resistance in herpes simplex virus type I encephalitis: a case report. Journal of Neurovirology. 2016; 23
    (2): p.335-337.
    doi: 10.1007/s13365-016-0489-5 . | Open in Read by QxMD

17. Schulte EC, Sauerbrei A, Hoffmann D, Zimmer C, Hemmer B, Mühlau M. Acyclovir resistance in herpes simplex encephalitis. Annals of Neurology. 2010; 67
    (6): p.830-833.
    doi: 10.1002/ana.21979 . | Open in Read by QxMD

18. Pandey S, Rathore C, Michael BD. Antiepileptic drugs for the primary and secondary prevention of seizures in viral encephalitis. Cochrane Database of Systematic Reviews. 2016
    .
    doi: 10.1002/14651858.cd010247.pub3 . | Open in Read by QxMD

19. Venkatesan A, Geocadin RG. Diagnosis and management of acute encephalitis: A practical approach. Neurology: Clinical Practice. 2014; 4
    (3): p.206-215.
    doi: 10.1212/cpj.0000000000000036 . | Open in Read by QxMD

20. Anderson WE. Herpes Simplex Encephalitis. In: Singh NN, Herpes Simplex Encephalitis. New York, NY: WebMD. http://emedicine.medscape.com/article/1165183-overview#a6. Updated: June 15, 2016. Accessed: November 6, 2016.

21. AK AK, Mendez MD. Herpes Simplex Encephalitis. StatPearls. 2021
    .

Viral encephalitis Information | Mount Sinai

Herpes Viruses

The herpes virus family includes at least 8 distinct viruses that cause infections in humans. These viruses include the herpes simplex virus, varicella-zoster virus (the cause of chickenpox and shingles), Epstein-Barr virus (the cause of mononucleosis), cytomegalovirus, and herpes virus 6. Although any herpes virus can cause encephalitis, the herpes simplex virus (HSV) is the most common cause of encephalitis.

HSV is the second most common cause of encephalitis in the United States. Herpes simplex encephalitis (HSE) can be caused by either a new HSV infection or reactivation of a latent pre-existing herpes infection. HSE tends to be most severe when it affects young children and older people. Most adults who contract HSE are older than age 50.

There are two distinct types of the herpes simplex virus:

• Herpes simplex virus 1 (HSV-1) causes most cases of herpes encephalitis in children and adults. HSV-1 is the main cause of oral herpes infections, but it can also cause genital herpes.
• Herpes simplex virus 2 (HSV-2) causes most cases of encephalitis in newborn infants. The virus is transmitted from an infected mother during childbirth. HSV-2 is the main cause of genital herpes, but it can also cause oral herpes infections.

Herpes simplex encephalitis is the only type of viral encephalitis that is treatable. Due to its severity, treatment with acyclovir is administered promptly if suspicion for herpes simplex encephalitis is raised, even while awaiting diagnostic procedures. If left untreated, herpes simplex encephalitis can be fatal. Death may occur even with acyclovir treatment, and many survivors are left with moderate or severe neurological impairments.

Arboviruses

Arboviruses, including the West Nile virus, are transmitted by blood-sucking insects such as mosquitoes and ticks. West Nile virus initially develops in birds, which function as the reservoir of infection. Mosquitoes transmit the virus when they bite a susceptible host such as an animal or a human. (The mosquito itself remains quite healthy. ) The insects that play a role in this disease-transmission process are referred to as vectors.

Arboviruses multiply in blood-sucking vectors. In fact, the word arbovirus is an acronym for ARthropod-BOrne virus. Insects are arthropods and mosquitoes, ticks, and the other blood-sucking insects may carry such arboviruses. Mosquitoes are the most common vector for arboviruses.

In general, the virus first passes through an insect before infecting a person. These infections are not transmitted through casual contact from one person (or animal) to another. (However, a very small number of West Nile virus infections have occurred through blood transfusions, organ transplantation, and possibly breastfeeding.) Only a small percentage of people who are infected by an arbovirus develop encephalitis.

Arboviruses that cause encephalitis are primarily found among three virus families: Togaviridae, Bunyaviridae, and Flaviviridae.

In the United States, the main mosquito-borne encephalitis strains are Eastern equine, Western equine, St. Louis, La Crosse, Jamestown Canyon, and, in particular, West Nile. Equine encephalitis causes disease in both humans and, as its name implies, horses. Powassan encephalitis is caused by a less common tick-borne flavivirus that occurs primarily in the northern United States. Jamestown Canyon virus disease is caused by a bunyavirus closely related to the La Crosse encephalitis virus.

Japanese encephalitis, which is also transmitted by mosquito, is the most common form of viral encephalitis outside of the United States. It is endemic in rural areas in east, south, and southwest Asia, especially China and Korea. Venezuelan equine encephalitis is found in South and Central America. Dengue and chikungunya are arboviruses found in Central and Southern America, Africa, and Asia that may also cause inflammatory diseases of the nervous system, including encephalitis. The mosquito species that transmits dengue and chikungunya, Aedes aegypti, also carries the Zika virus. There have been a few recent reports of encephalitis associated with Zika virus infection.

Different arboviruses cause different forms of encephalitis. Although the overall disease is the same, there are subtle differences in symptoms and the type of brain damage they produce.

West Nile Virus (WNV)

Until 1999, the West Nile virus was generally restricted to Africa, the Middle East, southwestern Asia, Eastern Europe, and Australia. It emerged in the United States with the first outbreak in New York City in 1999. WNV is now found in birds and mosquitoes in every state except Alaska and Hawaii.

Human cases of West Nile encephalitis have been reported throughout the continental United States and Alaska. In 2018, states with the highest incidence of neuroinvasive WNV included North Dakota, Nebraska, South Dakota, Montana, and Iowa.

How WNV is Transmitted

WNV, discovered in Uganda in 1937, circulates primarily between birds and mosquitoes and can be carried long distances by migrating birds. In a given geographic area, the appearance of the virus among birds and mosquitoes generally precedes infection in humans. WNV has infected over 110 species of birds. It can be deadly to some types of birds such as crows and jays.

During the season when mosquitoes are prevalent, a sampling of dead birds is analyzed to determine if they died of WNV. This sampling technique is used to predict a potential outbreak of WNV in humans.

In addition to mosquito-to-human transmission, other causes of human infection have included blood transfusions and organ transplantation. (The U.S. now uses screening tests to detect West Nile virus in all donated blood and organs.) There have also been very rare cases of mother-to-child transmission during pregnancy, and one confirmed case of transmission through breastfeeding.

Severity of WNV

About 80% of people infected with WNV will not develop symptoms. Twenty percent will develop West Nile fever (which includes fever, headache, and occasional skin rash). Less than 1% of infected people will develop neuroinvasive disease, the most severe form of WNV, which includes encephalitis and meningitis. WNV neuroinvasive disease is fatal in about 10% of cases. Survivors often experience lingering physical and mental neurological effects, which are sometimes permanent.

Neuroinvasive disease symptoms include high fever, headache, stiff neck, stupor, disorientation, coma, tremors, convulsions, muscle weakness, and paralysis. There are currently no vaccines to prevent WNV or specific antiviral drugs to treat it.

Tick-borne Encephalitis Viruses

Tick-borne encephalitis (TBE) is commonly found in many countries throughout Europe, Asia, and the former Soviet Union, but it is reported only rarely in the U.S. Powassan encephalitis is the main tick-borne encephalitis found in the United States and Canada. The first human encephalitis fatality caused by deer tick virus, which is closely related to Powassan virus, was reported in 2009. Cases of tick-borne encephalitis have also been reported in association with Rocky Mountain spotted fever, but this is a bacterial (rickettsial), not viral, infection.

Other Viral Causes of Encephalitis

Rabies

The rabies virus is transmitted from the saliva of an infected animal. The encephalitis it causes is virtually always fatal but although it is more common in Eastern Europe, it is very rare in the U.S. Only 1 or 2 cases are typically reported each year, usually from contact with raccoons, bats, or other wild animals.

Encephalitis Associated with Childhood Diseases

Vaccines have virtually eliminated encephalitis caused by common childhood infections such as measles, mumps, rubella, and chickenpox. Encephalitis can still occur in rare cases, particularly with immunocompromised children.

Adenoviruses

Adenoviruses typically cause respiratory or eye infections but, in rare cases, can cause encephalitis as well. The risk is greatest for people who have weakened immune systems.

Enteroviruses

Enteroviruses consist of a large group of viruses (including coxsackieviruses) that enter the body through the gastrointestinal tract and are often responsible for a “stomach flu.” They account for only a small percentage of viral encephalitis cases, especially in children. Polio (or poliomyielitis), a disease that has been virtually eliminated in North America through the widespread use of vaccines against the polio virus, is caused by a member of the Enterovirus family. Polio can rarely cause encephalitis, particularly in children.

Neonatal herpes simplex Symptoms & Causes

In-Depth

At Children’s Hospital Boston, we understand that you may have a lot of questions when your child is diagnosed with neonatal herpes simplex.

•           What exactly is it?

•           What are potential complications in my child’s case?

•           What are the treatments?

•           Are there any possible side effects from treatment?

•           How will it affect my child long term?

We’ve tried to provide some answers to those questions here, and when you meet with our experts, we can explain your child’s condition and treatment options fully.

Background

According to the Centers for Disease Control and Prevention (CDC), about .03% of babies born in the United States contract neonatal herpes simplex, most of them as they pass through the birth canal—in rare circumstances, it is also possible for a baby to be infected in the uterus or immediately after birth.

• Some studies indicate that delivery by Caesarean section, which avoids the birth canal, can reduce the risk of congenital herpes.  

Causes

The herpes simplex virus can be transmitted from a mother to her baby before, during or after birth.

• If you have had a history of herpes infections, make sure to let your doctor know before you give birth.

Symptoms

Some signs that your baby may have herpes are:

• irritability
• blisters anywhere on her body
• trouble breathing
  • grunting
  • blue appearance (cyanosis)
  • rapid breathing
  • short periods of no breathing
• jaundice
• bleeding easily

Herpes simplex infections can be divided into three categories:

• localized skin infection— small, fluid-filled blisters on the skin and around the eyes and mouth that burst, crust over, and heal
• encephalitis —an inflammation of the brain, which can cause problems with brain and spinal cord function, including seizures
• disseminated herpes infection— the most dangerous type of herpes infection. The herpes virus is spread throughout your child’s body and can affect multiple organs, including the liver, brain, lungs, and kidney.

A baby infected with herpes may not have all the symptoms of the disease.

• Most symptoms surface by the end of the baby’s first week, while more severe central nervous system problems will not appear until the baby’s second week.

If left untreated, encephalitis and disseminated herpes infections are potentially fatal.

Long-term outlook

Neonatal herpes simplex is a serious condition that can even be fatal if left untreated. If we begin treatment quickly, however, we can minimize the long-term effects on your child’s health.

For more information, see the Treatment and Care tab.

Questions to ask your doctor

Many parents are concerned about neonatal herpes simplex and can have lots of questions about the condition and how it can affect their baby.

You may find it helpful to jot down questions as they arise—that way, when you talk to your doctor, you can be sure that all of your concerns are addressed.

Here are some questions to get you started:

• Should I get tested for herpes?
• What can I do to prevent infection?
• I have herpes. Is there any way to prevent passing it on to my baby?
• What steps can we take if my baby does get infected?
• What’s the long-term outlook for a baby with neonatal herpes?

FAQ

Q: What is herpes simplex?
A: Herpes simplex is a virus that can be passed from mother to baby, and potentially cause a serious infection in a newborn.

Q: How common is neonatal herpes simplex?
A: About 1 out of every 3,500 babies born in the United States contracts neonatal herpes simplex.

Q: Why is neonatal herpes simplexa problem?
A: Neonatal herpes simplex is a serious condition that requires immediate treatment. If left untreated, the virus can cause brain and spinal cord function, as well as cause harm to the liver, lungs and kidneys. For more information on potential problems, see Signs & Symptoms [LINK].

Q: Is there any way to prevent infection?
A: Most babies born to mothers infected with the herpes simplex virus are completely healthy. However, a baby is at greater risk for contracting herpes if the mother’s first herpes infection occurs in the third trimester of pregnancy.

• Some studies indicate that delivery by Caesarean section, which avoids the birth canal, can reduce the risk of congenital herpes.  

Q: How can I tell if my baby has neonatal herpes simplex?
A: Signs that your baby may have herpes are:

• irritability
• blisters anywhere on her body
• trouble breathing
  • grunting
  • blue appearance (cyanosis)
  • rapid breathing
  • short periods of no breathing
• jaundice
• bleeding easily

However, some of these symptoms are also present with other conditions, so the best way to know for sure is to check with your child’s doctor.

Q: How is neonatal herpes simplex diagnosed?
A: Diagnosis is sometimes difficult because babies with neonatal herpes may not have the characteristic blisters of the disease. In addition, many symptoms of herpes resemble other diseases or disorders. However, the following tests can diagnose neonatal herpes:

• Skin culture — taking a sample of the blister by scraping or removing a piece of tissue
• Blood test
• Swab culture — taking a sample with a cotton swab from the nose, throat or rectum
• Urine test
• CT scan or MRI scan of the head

If you or your doctor suspects that your baby may have neonatal herpes simplex, we typically test both the mother and the baby for the presence of the virus.

• If you are pregnant and know that you have herpes simplex or know that you’ve recently been exposed to the virus, ask your doctor to perform a test.

Q: What are our treatment options?
A: Here at Children’s, physicians in our Fetal-Neonatal Neurology Program treat neonatal herpes simplex in infants.

• We treat babies with neonatal herpes simplex with a course of intravenous antiviral medication over a period of several weeks.
  • The most commonly used treatments for neonatal herpes are called ganciclovir and valganciclovir.

Q: What is my child’s long-term outlook?
A:Neonatal herpes simplex is a serious condition that can even be fatal if left untreated. If we begin treatment quickly, however, we can minimize the long-term effects on your child’s health.

For more information, see the Treatment and Care tab.

Q: What makes Children’s different?
A: Our physicians are expert, compassionate and committed to focusing on the whole child, not just his condition—that’s one reason we’re frequently ranked as a top pediatric hospital in the United States.

And at Children’s, we consider you and your child integral parts of the care team and not simply recipients of care. You and your care team will work together to customize a plan of care for your child.

Herpes simplex infections – health.vic

Notification requirement for herpes simplex infections

Notification is not required.

Primary school and children’s services centre exclusion for herpes simplex infections

Young children with cold sores who are unable to comply with good hygiene practices should be excluded while the lesion is weeping. Lesions should be covered by a dressing, where possible.

Infectious agent of herpes simplex infections

Human herpes simplex virus (HSV) types 1 and 2 cause disease.

Identification of herpes simplex infections

Clinical features

HSV has been isolated from nearly all visceral and mucocutaneous sites. The clinical presentation depends on portal of entry, age, immune status and type of HSV (1 or 2) infection.

Cold sores are the most common manifestation of herpetic infection, and are characterised by a perioral primary lesion, latency and a tendency to local recurrence. Anal and perianal infections are common among sexually active populations of men who have sex with men.

In children with atopic dermatitis/eczema and immunosuppressed patients, HSV may cause a generalised eruption that requires hospitalisation for antiviral therapy. Cutaneous HSV may become chronic in patients with HIV infection or other immunosuppression, with recalcitrant crusted lesions and ulceration, or the infection may disseminate to cause severe extensive disease with visceral organ involvement. Herpes simplex may be complicated by erythema multiforme or Bell’s palsy, which is often more disabling than the infection itself.

HSV types 1 and 2 generally produce distinct clinical syndromes, depending on the portal of entry.

HSV-1

The primary infection may be mild and generally occurs in early childhood before the age of 5 years. About 10 per cent of primary infections cause a more severe form of disease manifested by fever and malaise. This may last a week or more, and can be associated with vesicular lesions leading to ulcers in and around the mouth (gingivostomatitis), eye infection (keratoconjunctivitis), a generalised vesicular skin eruption complicating chronic eczema or, more rarely, encephalitis. In immunosuppressed populations, syndromes such as pneumonitis or hepatitis may occur.

Features of gingivostomatitis include ulceration of the tongue, gums, lips and anterior buccal mucosa; severe systemic toxicity; and lymphadenopathy.

Reactivation of latent viral infection in the dorsal root ganglia results in cold sores appearing as clear vesicles on an erythematous base. These usually occur on the face and lips, and crust and heal in a few days. This reactivation may be precipitated by trauma, fever, intercurrent disease, or environmental factors such as windy days or sunburn.

HSV-2

This virus is the usual cause of genital herpes, although genital herpes can also be caused by type 1 virus. Genital herpes occurs mainly in adults and is sexually transmitted. Primary and recurrent infections occur, with or without symptoms.

The principal sites of primary disease in women are the cervix and vulva. Recurrent disease generally involves the vulva, perineal skin, legs and buttocks. In men, lesions appear on the glans penis or prepuce, and in the anus or rectum of those engaging in anal sex. Other genital or perineal sites, as well as the mouth, may also be involved in either gender, depending on sexual practices.

HSV-2 infection is, rarely, associated with aseptic meningitis and radiculitis. It can be a cause of recurrent aseptic meningitis (Mollaret’s) disease and transverse myelitis.

Diagnosis

The diagnosis may be suggested by cytologic changes in tissue scrapings or biopsy. Confirmation is made by direct fluorescent antibody tests, by isolation of the virus from oral or genital lesions or other sites, or by detection of HSV DNA by nucleic acid testing of lesion fluid or cerebrospinal fluid. Techniques are also available to differentiate type 1 from type 2 antibody, if required. HSV infections are best confirmed by isolation of virus in tissue culture or lesion scrapings, with the greater yield from vesicular lesions. More than 90 per cent of the population has antibodies to HSV-1 by the fifth decade of life.

Incubation period of herpes simplex viruses

The incubation period varies from 2 to 12 days.

Public health significance and occurrence of herpes simplex infections

Asymptomatic infections with HSV-1 are common. Seventy to ninety per cent of adults have circulating antibodies to HSV-1, indicating previous infection.

HSV-1 is a common cause of meningoencephalitis. Vaginal delivery in pregnant women with active genital infection carries a high risk of disseminated visceral infection, encephalitis and death to the newborn.

HSV-2 is frequently associated with sexually transmitted infections, and 20–30 per cent of adults have antibody evidence of exposure. The prevalence is greater in socioeconomically disadvantaged groups and those with multiple sexual partners.

Reservoir of herpes simplex viruses

Humans are the reservoir.

Mode of transmission of herpes simplex viruses

Transmission of HSV infections occurs through close contact with a person shedding virus from a peripheral site, at a mucosal surface, or in genital or oral secretions. Inoculation of virus onto susceptible surfaces such as oropharynx, cervix, conjunctivae or small cracks in skin is required for infection. Contact with HSV-1 in the saliva of carriers is the most important mode of spread. Contact of healthcare workers with patients who are shedding HSV may result in an infection of the tip of the finger (herpetic whitlow). It begins with intense itching and pain, and is followed by vesicle formation and then ulceration.

Transmission of HSV-2 to nonimmune adults is usually by sexual contact.

Period of communicability of herpes simplex infections

Secretion of virus in the saliva may occur for up to 7 weeks after recovery from stomatitis.

Patients with primary genital lesions are infective for 7–10 days. Those with recurrent disease are infectious for 4–7 days with each episode.

Susceptibility and resistance to herpes simplex infections

Everyone is susceptible to infection. The disease does not usually confer protective immunity because the virus tends to become latent in dorsal root ganglia of the spine, where it may be reactivated at a later date.

Control measures for herpes simplex infections

Preventive measures

No vaccine is currently available.

Health education and personal hygiene should be directed towards minimising transfer of infectious material and reducing the risk of exposure of high-risk groups.

Emphasise personal hygiene to minimise the transfer of infectious material. Wear gloves when in direct contact with infectious lesions, and wash hands with soap and water afterwards.

Correct and consistent use of condoms during sexual intercourse decreases the risk of infection.

Control of case

Nongenital herpes

For symptomatic treatment of minor attacks, use povidone iodine 10 per cent paint applied three times daily, and/or topical antiviral therapy. Therapy should be self-initiated and commenced at the earliest sign of onset. Consult the current version of Therapeutic guidelines: antibiotic.

Sun protection is important in preventing recurrences of facial herpes simplex.

Specialist advice on systemic antiviral treatment should be sought for:

• severe primary or severe recurrent attacks
• attacks complicated by erythema multiforme
• primary or recurrent attacks in HIV-infected patients or the immunosuppressed.
• recurrent episodes of lymphocytic meningitis (Mollaret’s meningitis).

Patients with active lesions should have no contact with newborns, children with burns or eczema, or immunosuppressed patients. Consider caesarean section before the membranes rupture when primary or recurrent genital infections occur in late pregnancy, to minimise the risk of neonatal infection.

Contact isolation is required for disseminated severe infections and for infected neonates because of the risk to other neonates or pregnant women.

Anogenital herpes

Patients should be fully screened for other sexually transmissible infections, including HIV infection, on their first presentation.

For initial attack or infrequent recurrent attacks, treatment usually consists of valaciclovir, famciclovir or aciclovir. For suppression of frequent recurrent attacks, aciclovir or valaciclovir is generally used. Consult the current version of Therapeutic guidelines: antibiotic.

If there is breakthrough during prophylaxis, higher doses may be successful. Relapse may occur at the cessation of prophylaxis.

Control of contacts

Not applicable.

Control of environment

Not applicable.

Outbreak measures for herpes simplex infections

Not applicable.

Herpetic encephalitis – Kiev Association of Anesthesiologists

WHAT IS ENCEPHALITIS CAUSED BY THE SIMPLE HERPES VIRUS

Herpeptic encephalitis is a severe viral infection of the central nervous system, usually located in the temporal and frontal lobes in adults. It usually causes a flu-like illness with headache, hyperthermia, followed by seizures, cognitive abnormalities, behavioral disorders, and local neurological symptoms.

WHY THE DIAGNOSIS IS FREQUENTLY REMAINED

The clinical picture of herpes simplex virus encephalitis varies from patient to patient. Prodromal syndrome may be absent; cognitive impairment may be mild; local neurological symptoms can be misinterpreted as manifestations of a stroke; seizures can be assessed as symptoms of epilepsy, cognitive abnormalities – nonspecific delirium, behavioral disorders – psychiatric illness.The clinician may reject the idea of ​​invasive testing to a more distinctly matured version of viral encephalitis. A recent analysis of 16 published cases in the time frame 1993–2005. revealed some period of delay in performing CSF examination. Even when performing a study in the early stages of the development of the disease, the results can be falsely negative: CSF cytosis is within the normal range in 5-10% of cases, especially in children; computed tomography during the first week of the disease reveals normal data in a third of patients; nuclear magnetic resonance within normal limits in 10% of cases; Initially, the results of the polymerase chain reaction (PCR) of the cerebrospinal fluid may give a negative result.

VALUE

Encephalitis caused by the herpes simplex virus is not common, but if acyclovir is absent in the treatment or if it is prescribed with a delay in time, it is accompanied by high mortality and a large number of complications. Acyclovir suppresses viral replication and prevents the progression of the disease within the brain, reduces mortality from 70% or more in untreated patients to 19%. The most significant consequences of delayed treatment are neuropsychiatric disorders and amnesia due to local involvement of the limbic system.

HERPETIC ENCEPHALITIS IS COMMON

Herpes simplex is the most commonly identified cause of infectious encephalitis in UK studies. It is responsible for 5-10% of all encephalitis cases in the world. The annual incidence of herpes simplex virus encephalitis in the general population is 0.2–0.4 / 100,000. It affects all people, regardless of age. There are no seasonal fluctuations.It occurs in all age groups, but most often in children and the elderly: approximately 33% of all patients are in people under the age of 20, 50% are over 50. Of the two types of herpes simplex virus (HSV-1, HSV-2), HSV-1 encephalitis is more common in adults, HSV-2 in newborns and infants. Other viruses that cause encephalitis are varicella-zoster virus, Epstein-Barr virus, cytomegalovirus, human herpes viruses 6 and 7.

HOW HERPETIC ENCEPHALITIS IS DIAGNOSED

CLINIC

Usually there is a prodromal period, during which malaise, hyperthermia (90%), headache (81%), nausea and vomiting (46%) develop.It lasts for several days. Symptoms suggestive of encephalitis:

– progressive behavioral disorder (71%),

– signs of local epilepsy (71%), such as olfactory hallucinations, periodic disturbances of consciousness,

– local neurological symptoms (33%) such as unilateral paralysis,

– cognitive problems (24%), such as difficulty finding the necessary words, memory impairment, confusion.

RESEARCH

If encephalitis caused by herpes simplex virus is suspected, it is necessary to perform brain imaging methods (if possible, nuclear magnetic resonance, if not possible – computed tomography) and analysis of cerebrospinal fluid (in the absence of contraindications, such as the effect of plus tissue or coagulopathy).Research should be performed as an emergency. Nuclear magnetic resonance is a method of visualization of choice, violations are recorded in 90% of cases. Imaging of the brain helps to substantiate the diagnosis of herpetic encephalitis and to exclude contraindications for lumbar puncture. In this case, one-sided or asymmetric amplified signals are usually detected in the temporal lobes, the insular region of the cortex, and the orbital surface of the frontal lobes. These abnormalities are nonspecific for herpes. Differential diagnosis includes other causes of limbic encephalitis (such as paraneoplastic, autoimmune limbic encephalitis), cerebral gliomatosis (a rare brain tumor), middle cerebral artery ischemia, and status epilepticus consequences.

When analyzing the cerebrospinal fluid, an increased number of lymphocytes is usually detected (10 – 500 * 10 ⁶ / l, on average 100 * 10 ⁶ / l), sometimes in erythrocytes with or without xanthochromia, reflecting the hemorrhagic nature of encephalitis, a moderately increased amount of protein , normal or moderately reduced glucose concentration. The diagnosis of herpes simplex virus encephalitis is confirmed by the detection of viral nucleic acids in the cerebrospinal fluid using PCR. The method has a sensitivity of 96–98%, a specificity of 95–98%, eliminating the need for a brain biopsy.The minimum remains positive for 5-7 days after the start of antiviral therapy. In the early stages of the disease, the DNA of the virus may not be detected; in such cases, repeated use of PCR of the cerebrospinal fluid after 3–7 days makes it possible to establish the diagnosis.

Electroencephalography in the diagnosis of herpetic encephalitis has a high sensitivity (84%), but low specificity (32%). But it can be helpful in identifying non-convulsive seizure activity when the beneficial effects of anticonvulsant therapy can be obtained.

TREATMENT OF HERPETIC ENCEPHALITIS

Without waiting for confirmation of the diagnosis of herpes simplex encephalitis, in all cases of suspected encephalitis, empiric therapy with acyclovir at a dose of 10 mg / kg should be prescribed as an intravenous infusion for one hour with repeated administration every 8 hours for 14-21 days, provided normal kidney function. Increasing the dose is recommended for immunosuppressed patients. If bacterial meningitis is possible, adequate antibiotic therapy should be prescribed.In cases of seizures, anticonvulsants are prescribed in accordance with generally accepted standards. With an increase in intracranial pressure, appropriate treatment is necessary. The role of additional glucocorticoid administration has not been determined.

BASIC POSITIONS

1. Encephalitis caused by the herpes simplex virus, a potentially curable disease, but in the absence of appropriate treatment can cause death or severe neuropsychiatric disorders.

2. The diagnosis is suggested for acute or subacute occurrence of: behavioral abnormalities, local or generalized seizures, local neurological symptoms, cognitive impairment, usually hyperthermia and headache.

3. If suspected, urgent visualization of the brain (mainly nuclear magnetic resonance), analysis of cerebrospinal fluid – microscopy and DNA are required (in the absence of contraindications for lumbar puncture). It should be remembered that in the early stages, they may be within the normal range.

4. If the diagnosis is suspected, intravenous acyclovir should be administered immediately.

According to Sabah M., James M., Zeman A. Herpes simplex encephalitis // BMJ.-2012. – V.344: e3166.

Prof. Belyaev A.V.

90,000 To recover from encephalitis twice: Martha’s case

Martha’s first symptoms of viral encephalitis appeared in April 2016.Against the background of complete health, a 12-year-old girl developed 90,097 speech disorders of unknown nature . Within a few days, her condition worsened rapidly: a fever appeared and the girl stopped speaking. She was admitted to the intensive care unit of her community hospital near Orihuela, Alicante, where she received treatment for 90,097 herpes simplex encephalitis.

Despite the fact that this disease can cause irreversible damage, in Martha’s case they were not severe, and at the end of the treatment she was discharged.“The doctors told us she was cured, , but I noticed that something was happening to my daughter ,” says Fuensanta, the patient’s mother who has been a nurse for 25 years.

A few weeks after returning to normal life Martha had an anxiety attack and again speech disorders, but in this case they were complicated by a violation of gait and a change in behavior. The patient was re-admitted to the intensive care unit of the local hospital ; her condition worsened every day.Marta’s mother recalls that at the beginning of the treatment there was an apparent improvement, but it was not enough:

My daughter seemed to have turned into a 12-year-old baby: she could not speak, walk and eat on her own.

By chance, Marta’s relatives had an acquaintance whose daughter suffered from encephalitis, and she recommended that they contact the Hospital Sant João de Deu Barcelona clinic. “In June 2016, I contacted Josep Dalmau, and he referred me to Thaís Armangué.” “I knew from the first minute that they would cure my daughter,” says Fuensanta.

March again fell ill with encephalitis , but this time it was caused by its own defense mechanisms, which, as a result of excessive activation in response to a viral infection, which she suffered a few weeks earlier, provoked an immunological attack of the brain. Several years ago, staff working in the Neuroimmunology Program of the Clinical Hospital of Barcelona and the Hospital Sant Joan de Deu Hospital of Barcelona discovered the existence of such a connection. This allowed Martha to diagnose and start immunosuppressive therapy.

Treatment of anti-NMDA receptor encephalitis

The neuroimmunology department of the Hospital Sant Joan de Deu Barcelona was investigated and a repeat antibody test was recommended in the laboratories of IDIBAPS at the Clinical Hospital Barcelona. Thus, it was found that a significant part of 90,097 cognitive and behavioral disorders in Marta was due to persistent inflammatory process associated with 90,097 encephalitis, which was caused by antibodies to NMDA receptors.

After confirming the diagnosis, Dr. Armange prescribed a different type of immunotherapy from the one used up to this point. “The decision was made to transfer treatment to the most aggressive type of immunotherapy ,” says the neuroimmunologist. This treatment, which was planned in Barcelona, ​​was delivered to the patient at the residence of by medical professionals from Alicante in conjunction with colleagues from Barcelona . The multidisciplinary follow-up was subsequently carried out at the Hospital Sant Joan de Deu Barcelona.

From the very first session of immunotherapy, impressive changes were noted.

This is how Fuensanta describes how her daughter reacted to a therapy that had already been completed and resulted in significant improvement. Marta still visits our hospital from time to time to have specialists monitor her physical, psychological and cognitive development. However, the girl already does not need any treatment.

“She draws again – she always liked it,” says her pleased mother.Fuensanta assures that when Martha is fully recovered, they plan to travel to London again, and to create a blog to communicate with other families with the goal (in her words) “We need to give social support to those who are going through critical moments; we want to help children like our daughter. ”

Clinical analysis. Herpetic meningoencephalitis in a patient over 20 years old.

Of the total number of viral encephalitis, herpetic encephalitis accounts for an average of 10-20%. According to WHO materials, mortality from herpes infection ranks second after influenza in the structure of mortality from viral infections.Diagnostics of viral neuroinfections is difficult, requires material and technological costs, highly qualified medical personnel. The percentage of deciphering viral neuroinfections in leading clinics in the world rarely exceeds 40-50%.
A clinical case of a favorable outcome of herpetic meningoencephalitis in a patient on the background of conservative therapy is described.
Key words: viral meningitis, herpetic meningoencephalitis, herpetic neuroinfection, CSF filtration.

Authors: prof.d.m.s. Shmyrev V.I., prof. d.m.s. Devyatkin A.V., Ph.D. Kalenova I.E., Gavrilov D.Yu., Sharinova I.A., Litvinov N.I.

Introduction
Herpes simplex meningoencephalitis can be caused by herpes simplex virus type 2 (HSV-2) and varicella-zoster and herpes zoster viruses. Mortality in this pathology is 15-20%, and without antiviral therapy 70%. Surviving patients often have persistent neurological deficits.
The most common forms of herpetic lesions of the central nervous system are encephalitis, which can occur both against the background of other organ lesions (generalized skin-visceral form) and isolated.
Herpetic encephalitis (HE) occurs with a frequency of 2-4 per million population per year. Children account for about a third of all cases.
PGs have dermatoneurotropism. This means that they primarily affect the skin, mucous membranes with stratified epithelium, eyes and central nervous system. In the latter case, the most severe, life-threatening pathological processes develop in the form of encephalitis, meningoencephalitis, meningoencephalomyelitis, etc.
HE can develop in connection with both reactivation of an infection latently existing in the brain (according to modern concepts, in about 2/3 of patients), and with exogenous infection with a highly virulent virus strain (in 1/3 of patients).
HSVs are able to enter the central nervous system by a hematogenous route or along the nerve trunks (mainly along the branches of the trigeminal nerve and the olfactory tract). It is already considered proven that they spread mainly by the neural pathway. From the Gasser’s node, the virus enters the subcortical nuclei, trunk nuclei, thalamus and reaches the cerebral cortex. When the virus spreads through the olfactory tract, the hippocampus, temporal gyrus, islet and cingulate gyrus (i.e., the limbic system) are affected, and then, in most cases, the midbrain, trunk and cerebral hemispheres are captured.
In terms of clinical manifestations, HE is a classic example of encephalitis. It is characterized by four main syndromes: syndrome of impaired consciousness, hyperthermic syndrome, convulsive syndrome, and focal disorder syndrome.
Herpetic encephalitis begins acutely (usually after 1-5 days of the ARI clinic) with a sudden increase in temperature (usually more than 39 ° C), which decreases poorly even while taking antipyretic drugs. Consciousness is impaired: at first there may be short-term (within several hours) excitement, which is replaced by lethargy, drowsiness, lethargy.Subsequently, the oppression of consciousness progresses to its complete loss. More often, against the background of high fever, impairment of consciousness manifests itself in the form of a pronounced, deep, persistent oppression of it (coma of varying degrees). Consciousness returns gradually, and after its stable recovery, signs of focal disorders syndrome remain. In this case, the frontal lobes of the brain are often affected, which is clinically manifested by mnestic-intellectual disorders. The syndrome of focal disorders can also include dysfunctions of any cranial nerves with the development of the corresponding clinic.Possible paresis of the type of hemiplegia, asymmetry and loss of reflexes, the appearance of pathological reflexes. Another feature of HE is persistent convulsive syndrome. Convulsions are more often generalized in nature. Hyperthermic syndrome is also a characteristic feature of HE, but sometimes so-called “cold” HE is encountered.
Mortality in HE before the appearance of acyclovir was 70-74%. Today, with timely initiated adequate etiotropic therapy, it has decreased to 5-6%. Nevertheless, as already noted, herpetic lesion of the brain is a necrotic process, therefore, after HP, the likelihood of neurological consequences is high.They can be both temporary and permanent. However, against the background of modern antiviral therapy, not only mortality has decreased, but also the outcomes of HE in surviving patients have improved.
Meningitis with herpetic lesions of the central nervous system usually develops against the background of encephalitis, i.e. proceeds as meningoencephalitis (GME). Moreover, the inflammation of the meninges is serous in nature.
Isolated lesions of the meninges of HSV are rare. It is impossible to diagnose herpetic meningitis on clinical grounds alone.Special methods of laboratory examination are required. However, with prolonged or recurrent serous meningitis, HSV tests are needed along with other studies.
Case description
A 28-year-old woman with a diagnosis of “Acute herpetic meningoencephalitis. Cerebral edema. Right-sided hemiparesis.Exacerbation of chronic right-sided sinusitis. Diffuse bilateral endobronchitis. Endoscopic surgery on the right maxillary sinus from 17.04.10: submucosal vasotomy of the inferior turbinates. Tracheostomy from 28.04.10. ”
Medical history.
In late November – early December 2009, the patient was observed on an outpatient basis with trigeminal neuralgia.
At the end of March 2010, the patient traveled to Cuba.
The patient noted a deterioration in her condition on April 5, 2010, when nasal congestion appeared.On 12.04.10, a pronounced headache occurred. On April 15, 2010, the headache worsened, dizziness, disorientation, nausea, vomiting, hyperthermia (body temperature 38.8 C) appeared. Hospitalized in KB No. 1 in the ENT department with a diagnosis of acute purulent sinusitis.
The course of the disease.
A 28-year-old patient was admitted to the ENT department on 17.04.10 due to right-sided sinusitis.
CT scan of the paranasal sinuses from 17.04.10: CT picture of right-sided sinusitis. Slight thickening of the mucous membrane in the left frontal sinus.Hypertrophy of the inferior turbinates. Curvature of the nasal septum.
An emergency operation was performed: submucosal vasotomy of the inferior turbinates.
Biopsy of the contents of the right maxillary sinus: Areas of edematous and sharply inflamed polyposis-altered mucous membrane, bordered by respiratory epithelium with signs of hypersecretion, were sent.
Microbiological examination from 20.04.2010 of swabs from the throat and nose revealed: Acinetobacter spp.-abundant growth, sensitive to moxifloxacin, vancomycin.
On the day of admission, cerebral symptoms increased, disorientation appeared, the patient was consulted by a neurologist. Neurological status on admission: Stunned. Dysphoric, disoriented in place, time and property. personality. Rigidity of the occipital muscles 3 p, Kernig’s m from 2 sides, Pupils D = S, vivid photoreactions, nystagmus in extreme leads. Tendon reflexes are lively and symmetrical. There are no pathological foot marks. PUP and PEP perform with intention from 2 sides, more on the right.
An analysis of the cerebrospinal fluid was taken, serous meningitis was diagnosed (in the cerebrospinal fluid: cytosis more than 800/3 with a predominance of lymphocytes of more than 50%, with a slight increase in protein, Pandy’s reaction is negative).
Microbiological examination of the cerebrospinal fluid microflora was not isolated.
In the KLA upon admission: HB- 116g / l, erythrocytes-3.69×1012, platelets-223, leukocytes-12.4×109, p / i-14%, s / i-76%, eo-1%, base-0% , lymph-7%, mon-2%, ESR-36mm / h.
In the biochemical analysis of blood and coagulogram, general analysis of urine on admission, no changes were found.
CT of the brain upon admission: no pathological changes in the brain were revealed.
From 18.04 in the intensive care unit for serous meningitis. Detoxification and anti-edema therapy was carried out, despite the treatment being carried out, the patient’s condition with negative dynamics. Focal neurological symptoms (right-sided deep hemiparesis, pathological foot signs), depression of consciousness to coma, several episodes of tonic-clonic seizures appeared.
On April 19, 2010, a repeat MRI scan of the brain was performed from. (see Figure 1): In the basal parts of the temporal lobe there is an encephalitic focus with dimensions 57 * 39 * 50 mm. Perifocal edema is not pronounced. The median structures are not changed.
Conclusion: the picture of the revealed changes in the left hemisphere in the temporal region most likely corresponds to inflammatory changes (encephalitis). Differentiate with ischemic changes.
On April 19, 2010, an analysis of the cerebrospinal fluid was taken for PCR diagnostics of pathogens of viral neuroinfections, microbiological research.A decrease in cytosis to 610/3 was noted.
20.04.10 Respiratory disorders appeared, the patient was transferred to mechanical ventilation. From 28.04 a tracheostomy was applied.
In the study of the cerebrospinal fluid from 19.04, the DNA of the virus of 1 and 2 types was detected. In connection with the herpetic etiology of the process, antiviral therapy was started.
On April 27, 2010, CT scan of the brain was repeated: CT scan of inflammatory changes (encephalitis) of both hemispheres – negative dynamics, with the presence of zones of cerebral edema in the lesions.
The patient was consulted by an infectious disease specialist, a neurosurgeon; translation was refused due to the absence of an epidemiological danger to others, the severity of the patient’s condition.
Against the background of the therapy, positive dynamics: an increase in the level of wakefulness to stunning, trying to execute elementary commands. In control studies of cerebrospinal fluid – a decrease in cytosis to 147/3 from 04/26/2010, lymphocytes about 70%. Analysis of cerebrospinal fluid in the dynamics of Table 1
The level of respiratory support is gradually reduced, 03.05.10 the patient was transferred to spontaneous breathing.
A consultation was held with the participation of infectionists, neurologists, resuscitators to decide on the need to transfer the patient to an infectious diseases hospital.
Conclusion: Acute meningoencephalitis caused by herpes simplex virus types 1 and 2 (HSV DNA in the cerebrospinal fluid) with foci of cerebromalacia. Taking into account the endogenous nature of the infection, it does not need isolation. The transfer of the patient to the neuroinfection department of the Clinical Infectious Diseases Hospital No. 1 of the mountains is shown.Moscow.
The patient was transferred to CIB # 1.
In the neurological status at the time of transfer, consciousness is at the level of stunning, follows simple instructions, rapid exhaustion persists, right-sided hemiparesis is more pronounced in the leg, the impression of sensorimotor aphasia.

1 month after transfer to CIB # 1, she was re-hospitalized at Clinical Hospital # 1 of the Presidential Administration of the Russian Federation. The patient was examined by neurologists, in neurological status: Conscious. Emotionally labile, disinhibited, criticism is reduced.No speech disorders were found. Moderately expressed mnestic-intellectual decrease (21 points on the MMSE scale). There are no meningeal signs. ChMN side: no pathology. There are no paresis, sensory disturbances, or pathological foot signs.
Treatment:
1.complex etiotropic therapy – zovirax 1500 mg / day from 20.04.10, for 12 days, ceftriaxone 4 g / day i.v., from 30.04 zovirax i.v. cap 1000 mg / day, additionally cycloferon 250 mg i.v. Meronem 3 -4 g / day, tavanic 500 mg / day IV.
2. Upon admission, the procedure of extracorporeal filtration of cerebrospinal fluid was performed using a single-puncture “pendulum” method, against the background of which general cerebral symptoms (headache, nausea, disorientation) decreased; 586), up to 202/3 (neutrophils 89, lymphocytes 113). The patient had no complications after the procedure.
3. Also, anti-edema, neuroprotective, metabolic, anticonvulsant, immunostimulating therapy was carried out.
Conclusion.
A clinical case of the course of herpetic meningoencephalitis against the background of conservative therapy, CSF filtration procedure with a favorable outcome is described.
References.
1. Yushchuk N.D., Klimova E.A., Dekonenko E.P., Fedoseenko G.I. // Herpetic neuroinfections-2003. Moscow GOU VUNMTs MH RF.-p. 4-32.
2. Lobzin Yu.V., Pilipenko VV, Gromyko Yu.N. // Meningitis and encephalitis. – 2006 Folio. St. Petersburg.- p. 65-70
3. Protas II // Herpetic encephalitis. -2000. Minsk: LLC “Met” .- p. 12-126
4. Sorokina M.N., Bezukhikh S.M. // Defeat of the nervous system in herpes infection-1996. SPb .: SPbNIIDI.-p.5-30
5. Gintsburg A.L., Romanova Yu.M. // Polymerase chain reaction in the diagnosis and control of treatment of infectious diseases. – 1998. – No. 2. – P. 35 39.
6. Nesterenko V.G., Bekhalo V.A., Lovenetsky A.N.// Clinic, treatment and laboratory diagnosis of human herpesvirus diseases: A guide for doctors /.- M., 1998 .– 46 p.
7. Rakhmanova A.G., Prigozhin V.K., Neverov V.A. et al // Infectious Diseases: A Guide for General Practitioners /. – M.-SPb, 1995. – 304 p.
8. Isakov V.A., Borisova V.V. Laboratory diagnosis of herpesvirus infections // Unknown epidemic: herpes. – Smolensk, 1997 .– S. 20-31.
9. Sorokina MN, Bezukh SM // Damage to the nervous system in herpes infection. – SPb, 1996 .– 35 s
10. Weber B. // Biology of herpes virus infections and tagers of anti viral therapies Int.Meet. Skin Therapy Update-1994- – EADV, EADV Board. – 1994. – P.46

Article added on April 17, 2013

description of the disease, symptoms, treatment recommendations

Reference information: Herpetic encephalitis – a class of human diseases, a brief description, possible causes of diseases, modern and popular recommendations of doctors for the treatment of the disease

Disease Class:

Viral infections characterized by lesions of the skin and mucous membranes

Description

Herpetic encephalitis is an acute brain damage caused by the herpes simplex virus, more often type 1 (HSV-1), less often type 2 (HSV-2).Most researchers view it as a complication of herpes infection. Seasonal fluctuations are not characteristic of herpetic encephalitis. Two peaks in incidence occur at 5-30 years of age and over 50 years of age. In more than 95% of cases, the herpes simplex virus type 1 is the causative agent of herpes encephalitis. The pathogenesis of herpes encephalitis disease is heterogeneous. In children and young people, primary herpes can occur in the form of encephalitis. In this case, the herpes encephalitis virus, apparently, enters the central nervous system from the nasal mucosa, being transported along the axons of the olfactory neurons to the olfactory bulb.However, most adult patients with herpes simplex encephalitis either have a history of herpes or are seropositive for herpes simplex virus type 1. Approximately 25% of patients with herpes simplex encephalitis have different strains of the virus in the oropharyngeal mucosa and brain tissue. In these cases, encephalitis is caused by re-infection with another strain of herpes simplex virus type 1 with the penetration of the pathogen into the central nervous system. Clinic. The disease occurs after a prodromal period, which proceeds as an acute respiratory viral infection with herpetic eruptions on the mucous membranes.Symptoms of damage to the nervous system develop sharply. They are accompanied by a moderate meningeal syndrome, the severity of which is rapidly increasing. Loss of consciousness, coma may occur. Typical violations of the higher cortical functions: aphasia, amnesia, behavioral changes, hallucinations, partial and generalized seizures. The course of the disease is unfavorable. In the absence of treatment, 80% of patients quickly develop coma and die. It is also possible a lightning-fast course of the disease with the rapid development of cerebral edema and the subsequent development of intervening with respiratory arrest.In patients who survived, symptoms reverse with persistent residual effects. Diagnostics. For the diagnosis, it is important to combine the acute onset of the disease and typical clinical signs that have arisen against the background of herpesvirus infection with herpetic eruptions. A study of the cerebrospinal fluid is mandatory. It flows out under increased pressure, lymphocytic or mixed (lymphocytic-neutrophilic) pleocytosis, a moderate increase in the amount of protein are determined in it.The glucose content does not often change. In 50% of cases of herpetic encephalitis, erythrocytes are detected as a manifestation of the hemorrhagic nature of the lesion. Changes on CT and MRI do not appear immediately. A few days after the onset of the disease, it is possible to detect abnormalities (hypointense foci on CT and hyperintense in T2-weighted images on MRI) in the frontotemporal lobe of the brain, cingulate gyrus and in the islet area.Confirm the nature of the lesion of the central nervous system using PCR …It allows detecting the DNA of the herpes virus in the cerebrospinal fluid. Treatment. Although the course of herpetic encephalitis is extremely severe, it is one of the few variants of encephalitis for which there is specific therapy.

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How herpesvirus disguises itself and enters the brain – a study by scientists

On the topic

COVID-19 spread across continents last year – research

An international team of scientists has discovered a molecular mechanism that helps the herpes simplex virus (HSV-1) enter the brain.In this they were helped by experiments on cultures of mouse brain cells. The study was published in the Journal of Experimental Medicine, reports “LIGA.News”.

This infection first appears on mucosal surfaces: the virus infects epithelial cells and then spreads from peripheral nerves to the central nervous system. As a result, it can infect the brain and cause herpes encephalitis, a rare disease with a high mortality rate.

The protection of neurons is somewhat different from the immunity of cells of other organs that this virus infects, and usually it successfully prevents the penetration of the pathogen, but not always.People with AIDS and other severely immunocompromised patients are at risk.

Researchers cut out certain genes from the genome of the virus and then infected the neurons of mice with these strains. It turned out that the most suitable candidate for the role of activator of the “masking” process is the viral gene VP1-2 and the protein encoded by it with the same name.

When virus particles enter the brain, this protein cuts ubiquitin from STING (one of the main immunity proteins that triggers the body’s cascade response to infection) – part of the amino acid structure of the protein.STING then becomes ineffective in binding the pathogen.

When VP1-2 was excised from the genome of the virus, the microglial immunity “saw” the infection.

If it is possible to create drugs that block such a specific “skill” of the herpes simplex virus type 1, it will be possible to increase the chances of a successful treatment for herpes encephalitis.

It is noted that although the study is focused on herpevirus, there are parallels to the coronavirus.

“Our results provide hope that if we can prevent the virus from blocking the STING protein, we can stop it from replicating.This could open up new principles for the treatment of herpes, flu, and coronavirus, “- said in the message.

As a reminder, scientists investigated whether the coronavirus could become more infectious.

Read on

Herpes simplex

Herpes simplex (ancient Greek ἕρπης, lat. Herpes simplex) – a creeping, spreading skin disease) is a viral disease with a characteristic rash of grouped vesicles on the skin and mucous membranes.It is caused by two types of herpes viruses: HSV-1 and HSV-2. The most common form of infection is labial (labial). The visible symptoms of the labial form are often referred to as a “cold”, such as a cold on the lips ^[3] (this should not be confused with a cold as an acute respiratory viral infection). In second place in terms of frequency of occurrence is genital herpes, which mainly affects the genital area. HSV-1 usually causes infections of the mouth, neck, face, eyes, and central nervous system, while HSV-2 is characterized by anogenital lesions.However, both types of the virus can cause lesions in both sites, for example, after infection with orogenital forms of sexual intercourse. Some types of herpes viruses affect a wide variety of sites.

There are also other forms of viral lesions: herpetic felon, lat. herpes gladiatorum, which occurs in wrestling athletes, ocular herpes (keratitis), forms of herpetic encephalitis, meningitis, neonatal herpes, and Bell’s palsy is also thought to be caused by this virus.

It should be noted that other members of the family Herpesviridae , such as shingles caused by the varicella-zoster virus, cause similar symptoms. In addition, differential diagnosis also involves consideration of other diseases of the hands, feet, mucous membranes of the mouth, characterized by similar injuries.

There is currently no cure for herpes. Available drugs only suppress the multiplication of the virus, but do not remove fragments of viral DNA from neurocytes.Therefore, there is always the possibility of relapse, especially with immunodeficiencies (for example, with HIV infection, tumors or after organ transplantation). After a few years, relapses begin to be asymptomatic, although the person is contagious to others. Treatment with antiviral drugs can suppress the activity of the virus and relieve symptoms. Vaccines under development have not been proven effective in clinical trials.

Transmission routes

Herpes simplex virus is most easily transmitted by direct contact with damaged tissues or body fluids of the host.Transmission can also occur transcutaneously (through the skin) during periods of asymptomatic virus carriage. Barrier methods are the most reliable and nevertheless, they only reduce the likelihood of transmission, not excluding it. Oral herpes is easily diagnosed only if there are external manifestations – wounds or ulcers. In the early stages, there are no symptoms of the disease and herpes can only be diagnosed by laboratory methods.

In the external environment at room temperature and normal humidity, the herpes simplex virus persists for a day, at a temperature of 50-52 ° C it decomposes in 30 minutes, and at low temperatures (-70 ° C) the virus is able to remain viable for 5 days.On metal surfaces (coins, doorknobs, water taps), the virus survives for 2 hours, on wet sterile medical cotton and gauze – during the entire drying time (up to 6 hours) ^[4] .

Symptoms

Herpes simplex virus (HSV) causes several identical medical disorders. Infection of the skin, mucous membranes can cause lesions on the face and mouth (labial herpes), genitals, or hands (herpetic felon). More serious disorders occur when a virus infects the eyes (herpetic keratitis) or invades the central nervous system, damaging the brain (herpetic encephalitis).Patients are people with an unformed immune system (newborns) or immunodeficiencies, such as organ transplant recipients with AIDS. Cognitive deficits that occur in patients with bipolar disorder and Alzheimer’s disease have also been associated with the virus, although this is primarily determined by the patient’s heredity.

After the initial infection, the herpes virus is permanently incorporated into the genome of the host cell and will never be removed by the immune system.It enters the nerve endings in the skin and travels along them to a sensitive neuron located in the ganglion ^[5] , where it goes into a latent stage.

Antibodies generated by HSV-1 virus infection seem to relieve symptoms of subsequent HSV-2 infection, but even an asymptomatic patient is still infectious. Many have noted that pre-immunization with HSV-2 virus also relieves symptoms in people infected with HSV-1 virus.Infection with the HSV-2 virus is often asymptomatic, although transmission may persist for a long time. See pathogenesis for details.

Bell’s palsy

Although the exact etiology of Bell’s palsy as a form of facial nerve palsy is currently unknown, there is a theory that the paralysis may be caused by reactivation of the HSV-1 virus. At the moment, this theory is disputed, since viruses of the HSV group are found in many people who do not have paralysis. In addition, patients with paralysis did not show a significant increase in the level of antibodies to HSV, and antiviral drugs do not improve the condition of such patients.

Alzheimer’s disease

HSV-1 appears to be one of the risk factors for Alzheimer’s disease. The nervous system of people with a certain genotype (carriers of the epsilon4 allele of apolipoprotein-E) is more susceptible to the pathogenic action of the virus, which increases the risk of developing Alzheimer’s disease. The virus interacts with components and receptors of lipoproteins. In the absence of this gene allele, the HSV-1 virus does not cause disease.

Viral DNA is localized in β-amyloid plaques, which is characteristic of Alzheimer’s syndrome.This suggests that the virus is the cause of their occurrence and, therefore, a significant etiological factor for the development of this disease.

However, a later study with a sample of several thousand people in 2008 showed a high correlation between HSV seropositivity and Alzheimer’s disease, without directly affecting this risk of the APOE-epsilon4 allele. ^[9]

Pathogenesis

The herpes virus is unable to penetrate through the intact stratum corneum of the skin, due to the absence of specific receptors on it.Herpes is transmitted by direct contact of damaged integuments with affected areas of the skin or with the biological fluids of an infected person. Transmission occurs between discordant partners: a person who has been ill (HSV-seropositive) can transmit the virus to a seronegative healthy person. The HSV-2 type virus is transmitted exclusively transcutaneously (through the skin).

After contact with the source of infection, viral particles that have got on the epithelium move with short interruptions through the skin or mucous membranes of the mouth or genitals.The virus enters cells through receptors such as nectin-1, HVEM, and 3-O sulfated heparan sulfate. The outer envelope of the virus fuses with the cell membrane. Further, the viral nucleocapsid is in the neuroplasm, where the release of viral DNA occurs. Then it is transported along the dendrites of nerve endings into the body of a sensitive neuron, located in the sensory ganglion, where they are embedded in its genetic apparatus forever. After the penetration of the virus, the process of its active reproduction in the cell begins – persistence.With labial lesions, the persistence of the virus in the neurocytes of the sensitive ganglia of the trigeminal nerve is characteristic, and with genital lesions, the lumbar.

In most people, the reproduction and shedding of the virus immediately after infection is asymptomatic. This can happen more than a week before or after the first symptoms appear in 50% of cases. The causative agent multiplies intensively in it, launching a lytic, productive type of infection. Focal degeneration of the epithelium occurs: the cells increase in size, then die, forming foci of necrosis.

Herpes viruses have cyclical periods of activity (bubbles containing viral particles form within 2–21 days) and periods of remission, during which the sores disappear. Genital herpes (HSV-2) is more often asymptomatic, although the virus multiplies and can be transmitted to other people. This is most common with the HSV-2 virus. Recurrences of the disease are not determined in time, although some triggers of the disease have been identified. Such factors include the effects of immunosuppressants (see.below). With relapse, the virus, which is in the latent stage, is activated, resulting in the formation of many infectious particles moving along the processes of the neuron, from which they subsequently pass into the epithelium of the skin and mucous membranes. Vesicles often reappear, accompanied by necrotic damage to the epithelium. The virus reproduction cycle is 10 hours. Over time, the body develops antiviral immunity and the frequency and severity of relapses decreases.

Carriage most often continues during the first 12 months after infection.The duration of such carriage with immunodeficiencies (for example, with HIV infection) is longer. There is information that some people may have a shortened carrier, but there is no reliable information to confirm this. There is no visible significant difference in the number of asymptomatic carriers when comparing individuals with one to twelve annual relapses with those who did not.

After infection, the body begins to synthesize antibodies against a specific HSV-type virus, preventing the spread of the infection.In the case of infection with the HSV-1 virus, this seroconversion (production of antibodies) will protect the body from other infectious processes caused by this virus, such as genital herpes, herpetic keratitis and felon.

Antibodies that are produced after the initial herpes infection prevent infection with the same type of virus: people who have had HSV-1 orofacial herpes do not have panaritium or genital herpes caused by HSV-1. ^{[ source unspecified 903 days ]}

In a monogamous marriage, a seronegative woman has a risk of infection from a seropositive man above 30% per year.During the first oral infection, the production of protective antibodies will take 6 weeks, after which humoral immunity will be able to protect the body from repeated genital infection.

Diagnostics

Primary orofacial herpes is easily diagnosed in people who have not previously been sick and have not had contact with HSV-1 virus carriers. Such people usually develop several round, superficial papules in the corner of the mouth, accompanied by acute gingivitis. Adults with atypical symptoms are more difficult to diagnose.Prodromal symptoms, which appear even before the appearance of visible herpetic lesions, will make it possible to differentially diagnose symptoms of HSV-type virus infection from, for example, allergic stomatitis. If the disease does not manifest inside the mouth, primary orofacial herpes may be mistaken for impetigo or bacterial contamination. In addition, mouth ulcers (aphthae) can also look like oral herpes, but no blisters appear.

Genital herpes is more difficult to diagnose, as most HSV-2 infected people do not have the “classic” symptoms.In addition, mycoses, atopic dermatitis, urethritis have similar symptoms, which complicates its diagnosis. Laboratory tests include: virological studies, RIF, PCR. Although these procedures are highly specific and provide high precision, they are too complex and expensive for ongoing clinical use.

Serological method. IgM serology does not discriminate between antibodies to HSV-1 and HSV-2 types of viruses. However, the new immuno-point glycoprotein G-specific HSV test gives more than 98% specificity and thus allows distinguishing between HSV-1 and HSV-2 types of herpes.Some foreign clinicians believe that the IgM test will soon be superseded by a new one.

Cytological method. In the scraping of the affected area of ​​the epithelium, stained according to Romanovsky – Giemsa, multinucleated cells with intracellular inclusions are found.

Virological method. Infect cell cultures and detect cytopathological action (CPE) in the form of giant multinucleated cells with inclusions that are destroyed. Identification is carried out in the reaction of neutralization of CPP, RIF with monoclonal antibodies.White plaques form on the chorionallantoic membrane of chicken embryos after 2-3 days.

Biological method. When viral material is applied to scarification of the cornea of ​​a rabbit, keratitis occurs, and encephalitis occurs in the brain of newborn mice.

Prevention of genital herpes

As with most STDs, women are more susceptible to herpes than men. In general, in a year without using antiviral drugs or condoms, the risk of HSV-2 transmission from man to woman is 8-11%.It is believed that this is due to the increased vulnerability of the mucous membranes at the points of contact. The risk of transmission from an infected woman to a man is 4–5%. Suppressive antiviral therapy reduces the risk by up to 50%. In addition, the use of antiviral drugs can prevent symptoms after infection in 50% of seropositive people. Condom use significantly reduces the risk of infection, and the risk is lower for women. The combined approach reduces risk by 75%.

It should be noted that the figures above are derived from clinical studies in subjects with frequent recurrent genital herpes (more than six cases per year).Individuals without symptoms or with a low relapse rate were excluded from these studies. Previous exposure to HSV-1 herpes reduces the risk of HSV-2 infection in women by a factor of three.

Asymptomatic carriers are unaware of the course of the disease and can infect others.

In October 2011, it was reported that the anti-HIV drug Tenofovir, when applied topically as a vaginal gel, also prevents the transmission of the herpes virus.

Barrier method

Condom use reduces the risk of transmission by 30%.

Condoms provide moderate protection against HSV-2 for both men and women. The virus does not pass through the barrier made of synthetic material and, with regular use, the risk of infection is reduced by 30%. The female condom provides more complete protection, since, unlike the male, it prevents the male body from contacting the woman’s labia. However, in this case, free contact of the scrotum, anus, buttocks and thighs is possible – areas that can come into contact with ulcers or body fluids during coitus.Thus, an increase in the level of mechanical protection is advisable only up to a certain limit, beyond which sex ends.

Condoms and rubber dams (latex cunnilingus plates) are also effective for oral sex.

Parallel use of antiviral drugs provides additional protection.

Vaccine

Currently ^{[ when? ]} vaccines are undergoing clinical trials. After successful clinical testing, they can be used to prevent transmission, prevent and treat herpes infections.

Antiviral drugs

Antiviral drugs can reduce acute virus shedding. It is believed that in treated patients, the viral particle shedding phase takes 10% of the days a year, while in untreated patients it takes 20%.

Pregnancy

The risk of mother-to-child transmission is highest if the mother becomes infected immediately before childbirth (30 to 60%). If the infection is recurrent, the risk drops to 3%. In the absence of ulcers, the risk is less than 1%.

To prevent neonatal infections, pregnant women are advised to avoid unprotected orogenital contact with an HSV-1 seropositive partner during the last trimester of pregnancy. Seronegative mothers infected with HSV have a 57% risk of transmission due to the incomplete formation of the immune response – the synthesis of antibodies that are transmitted to the child even before birth and protect him for some time after. Therefore, a woman who is positive for HSV-1 and HSV-2 will transmit the infection with a 1-3% probability.Women who are seropositive for only one of the types of the virus are half as likely to be transmitted as those who are seronegative.

Mothers infected with HSV should avoid traumatic delivery procedures (eg forceps, vacuum extractors). If there is a high risk of infection, it may be advisable to use a caesarean section.

Treatment with antiviral drugs (starting at week 36), such as acyclovir, reduces the likelihood of transmission, and therefore the need for a caesarean section.The safety of using other antiviral drugs during pregnancy is still being tested.

Treatment

There is currently no method to remove the virus from the body. Antiviral drugs only reduce the frequency, duration, and severity of relapses. Analgesics such as ibuprofen and paracetamol only reduce pain and fever. Local anesthetics such as prilocaine, lidocaine, benzocaine, or tetracaine also relieve itching and pain.

Treatment with antiviral drugs

Effective against herpes infections: acyclovir, valacyclovir, famciclovir, penciclovir.Acyclovir was discovered first, there are many generics of it.

It has been proven that acyclovir and valacyclovir are effective in the treatment of facial herpes (lips), including in cancer patients. There is no evidence to support the use of acyclovir in the treatment of primary herpetic gingivostomatitis.

Local application

When applied topically for the treatment of facial herpes, acyclovir, penciclovir, docosanol are effective. These drugs are approved for sale without a doctor’s prescription.

Gene therapy

Encouraging results have been demonstrated in the treatment of human Vero cells and animals against herpesviruses type 1 (herpes simplex virus, HSV-1), type 4 (Epstein-Barr virus, EBV) and type 5 (human cytomegalovirus, HCMV) by CRISPR / Cas9. For some regions of their DNA, guide RNA molecules were created, thanks to which Cas9 nucleases are able to recognize them in the host genome and cut them. Experiments have shown that a cut in one section of viral DNA reduces the number of infected cells by about half, and two cuts lead to almost complete removal of viruses ^{[10] [11]} .

Alternative treatments

Alternative methods act indirectly, having only a tonic, anti-inflammatory effect. Lysine, being an essential amino acid, is a plastic material for tissue regeneration. Zinc ointments, when applied to the skin, have an anti-inflammatory, antiseptic and drying effect, preventing the penetration of the virus and accelerating the healing of ulcers. This also includes aloe vera extract, fir, sea buckthorn oil and propolis as natural anti-inflammatory agents.

Immunity

During primary infection, IgM antibodies are formed, with relapses – IgG and IgA. Due to the persistence of the virus in infected people, the immunity is non-sterile and temporary – with a decrease in immunity, especially with a deficiency of natural killer cells (NK), a relapse occurs. In addition, the herpes virus itself is capable of inducing immunodeficiency, one of the mechanisms of which is the stimulation of the synthesis of “ineffective” IgG antibodies, which suppress immunity and suppress NK.In people resistant to infection, immunity is carried out by the interferon system, natural killer and T-killer cells, as well as sIgA antibodies. 80-90% of adults have IgG antibodies to HSV-1. The level of immunity significantly affects the number and severity of relapses.

Forecast

After the stage of active infection, the virus remains latently persistent in the sensitive ganglia and ganglia of the autonomic nervous system. The double-stranded strand of viral DNA is embedded in the cell genome, located in the nucleus of the neurocyte.No viral particles are produced in this phase. This is controlled by viral DNA, which contains two LAT transcripts. – transcripts associated with latency), which are contained in the set. ^[12] The gene encoding them partially overlaps with the super-early genes encoding proteins of the ICP0 type, but its transcription is carried out from the complementary DNA strand. With the deletion of this region of the genome, the resulting mutant viruses go into a latent state and their ability to reactivate is reduced.Thus, LAT transcripts are used to maintain the latency state rather than to enter it. The mechanisms of transitions themselves have not been sufficiently studied at the moment, respectively, drugs capable of controlling the activity of viruses have not yet been created.

Many infected people relapse within the first year after the initial infection. ^[5] The relapse is preceded by a prodromal period, which includes such symptoms as: tingling (paresthesia), itching, pain in the area of ​​sensitive innervation of the lumbosacral nerve skin.The prodromal period can take from several hours to several days. Antiviral therapy started in the prodromal period reduces the severity and duration of symptoms. In any case, relapses pass much easier and stop within 5-10 days, even without special therapy. ^[5] Subsequent outbreaks are usually episodic, occurring on average 4-5 times a year when no specific therapy is provided.

As mentioned, the reasons for reactivation (relapse) are not known, but some triggers are documented.Recent studies (2009) have shown that the vmw65 protein plays a key role in the reactivation of the virus. ^[13] Changes in the immune system before menses can also stimulate HSV-1 activation ^{[14] [15]} .

Concurrent infections such as SARS and others that cause fever can also lead to relapses. Probably, it is because of this that the concept of “cold on the lips” arose.

Other indicated triggers include localized facial injuries to the lips, eyes, or mouth, trauma, surgery, effects of radiation therapy, wind, UV exposure, or sunlight. ^{[16] [17] [18] [19] [20]}

The frequency and severity of outbreaks varies widely from person to person. Some develop ulcers that do not heal for weeks, while others show only slight itching and burning for several days. There is some evidence that heredity affects the rate of relapse. In the region of chromosome 21, there is a zone that includes 6 genes, which is associated with the frequency of flares.

Immunity to the virus is permanent.The severity and frequency of outbreaks decreases over time. After a few years, some people will not have any symptoms at all, although the virus will be secreted and able to be transmitted to others. In immunocompromised individuals, outbreaks will be more severe, longer, and more frequent; they are shown antiviral therapy. ^[21] Outbreaks can occur in former locations or in close proximity to nerve endings of infected ganglia. In the case of genital herpes, the rash appears in the same place or at the base of the spine, buttocks, or back of the thighs.Individuals infected with HSV-2 are at greater risk of contracting HIV through unprotected sex with an HIV-positive partner, ^[22] especially during HSV reactivation. ^[23]

Epidemiology

The worldwide prevalence of herpes simplex viruses ranges between 65% and 90%. ^[24] HSV-1 is more common than HSV-2, the frequency of which increases significantly with age. ^[24] The prevalence and incidence of infection is determined by the presence of virus-specific antibodies in susceptible organisms. ^[25]

For example, in the USA 57.7% of people are infected with HSV-1-type virus ^[26] and 16.2% are infected with HSV-2. Among all HSV-2 seropositive people, only 18.9% are aware of their illness. ^[27]

The source of infection is a person with active herpes. The virus can be transmitted even if there are no visible symptoms. Routes of transmission – contact-household, airborne, sexual, transplacental (from mother to fetus). The main path is the contact one. The virus is found in saliva and body fluids.Infection occurs through kisses, dishes, towels, toys. Studies for the presence of specific antibodies confirm that HSV-1 infection usually occurs at an early age, and HSV-2 infection after the onset of sexual activity. The contact pathway can be realized iatrogenically using non-sterile medical instruments (in dentistry and ophthalmology). With airborne transmission, herpes infection occurs in the form of ARVI. Children from 6 months to 3 years old are more likely to be infected by contact and airborne droplets.There is a genetic predisposition to herpes infection, some people are resistant. The disease is often family in nature (parents-children). Moreover, the mother can be resistant, and the children are infected from the father.

History

Herpes has been known for over 2000 years. It is said that Emperor Tiberius banned kissing in Rome for some time due to the large number of infected people. Herpetic bubbles are also mentioned in the work of the 16th century Romeo and Juliet .In the 18th century, the disease was so widespread among prostitutes that it was called the “occupational disease of women.” ^[28]

The term herpes simplex (Herpes Simplex) appeared in the book by Richard Bolton. in 1713, where other terms related to the topic appeared.

The herpes virus could not be found until 1940. ^[28]

The beginning of antiherpetic therapy dates back to 1960, when drugs that interfere with the replication of viral DNA were first used.Treatment of fatal or disabling diseases such as encephalitis ^[29] keratitis ^[30] has been performed in immunocompromised patients (transplant recipients) ^[31] or herpes zoster (herpes zoster). ^[32] The original preparations included: 5-iodine-2′-deoxyridine (idoxuridine), IUdR, or (IDU), as well as 1-β-D-arabinofuranosylcytosine or ara-C, ^[33] later trade names “cytosar” or “cytorabine”.Later they were used for local treatment of herpes simplex, ^[34] zoster, and chickenpox. ^[35] Different drug combinations led to different results ^[29] Administration of 9-β-D-arabinofuranozzinadenine (ara-A) or vidarabine (vidarabine) is significantly less toxic than Ara-C. Since the mid-1970s, it has been regularly used for neonatal antiviral therapy. Vidarabine was the first drug whose therapeutic dose for the treatment of life-threatening HSV was lower than the toxic one.Intravenous vidarabine was licensed by the Food and Drug Administration (FDA) in 1977. Other experimental antivirals: heparin, ^[36] trifluorothymidine (TFT), ^[37] Ribivarin, ^[38] interferon, ^[39] Virazole, ^[40] and 5-methoxymethyl-2′-deoxyuridine (MMUdR) ^[41] . The introduction of 9- (2-hydroxyethoxymethyl) guanidine (acyclovir), at the end of 1970, ^[42] was a significant achievement.In the 1980s, special studies were conducted to compare the effectiveness of acyclovir versus vidarabine. ^[43] Because of the lower toxicity and ease of control, acyclovir became the drug of choice and was licensed by the FDA in 1998. ^[44] using vidarabine. ^[44] On the other hand, acyclovir can inhibit the synthesis of antibodies and when it is used more than when using vidarabine, the growth of the antibody titer is slowed down.

Scientific research

Researchers at the University of Florida have synthesized a hammerhead-type ribozyme that specifically cleaves the mRNA of the main HSV-1 genes. Hammerhead, which attacks mRNA of the UL20 gene, significantly reduces the level of ocular HSV-1-associated infections in rabbits and reduces the release of viral particles in vivo. ^[45] This approach uses specially synthesized RNA enzymes that suppress herpes simplex virus strains. The enzyme turns off a gene responsible for the synthesis of a protein involved in the maturation and release of viral particles from an infected cell.This technique has been shown to be effective in mice and rabbits, but more research is needed before humans can use it. ^[46]

Duke University is also developing a treatment for this virus. In the normal course of the pathological process, some of the viruses are always in a latent state inside the nerve cells. Researchers are trying to figure out how to simultaneously bring all host viruses into the active stage so that the entire population can be killed at once with conventional antiviral drugs.

A class of drugs called antagomir can serve this purpose. These are artificially synthesized oligonucleotides or short RNA segments that are complementary to herpes mRNA. They can be designed in such a way that when attached to the mRNA, they will silence it, making the virus unable to remain latent. ^[47] Professor Cullen believes that a drug could be developed that can block the mRNA responsible for keeping the virus latent. ^[48]

There is also a Herpevac vaccine against HSV-2, currently in Phase III clinical trials at the US National Institutes of Health. ^[49] In 2010, it was announced that after 8 years of study, more than 8000 women in the US and Canada, despite early favorable interim reports ^[49] , had no positive results in the treatment of genital herpes. ^[50]

The dl5-29 (now known as ACAM-529) was developed in the laboratory of Harvard Medical School.replication-defective mutant virus, which has been shown to be successful in preventing HSV-2 / HSV-1 infections and in fighting the virus in infected animals.

The replication damage vaccine has been shown to induce a strong HSV-2-specific antibody and T-cell immune response; protects against infection with the wild HSV-2 virus; significantly reduces the likelihood of relapses; protects against HSV-1, and prevents the virus from returning to a virulent or latent stage. ^[51] The vaccine is currently being researched and developed by Accambis (acquired by Sanofi Pasteur in September 2008), which was due to introduce a new experimental drug in 2009. ^[52] However, the post-acquisition status of ACAM-529 is not entirely clear. According to Jim Tartaglia of Sanofi Pasteur, ACAM-529 is still under development, with clinical trials starting in 2012 at ^[53] . At the moment (2020) the drug is undergoing phase I-II studies (December 2019 – May 2023) ^[54]

The private company “BioVex” in March 2010 began the first phase of clinical trials of the ImmunoVEX vaccine. ^[55] The HSV-2 ICP0 live vaccine of attenuated HSV-2 viruses uses a fundamentally new approach explored by Dr. William Helford at Southern Illinois Medical University. ^[56]

See also

Notes

1. ↑ Disease ontology database (English) – 2016.
2. ↑ ^{1 2} Monarch Disease Ontology release 2018-06-29sonu – 2018-06-29 – 2018.
3. ↑ Herpes simplex virus (Russian). www.who.int. Date of treatment: July 27, 2019.
4. ↑ http://www.rusmg.ru/php/content.php?id=8515&pr=print (inaccessible link) Genital herpes: modern problems and solutions
5. ↑ ^{1 2 3} Gupta R., Warren T., Wald A. Genital herpes // The Lancet. – Elsevier, 2007.- December (vol. 370, no. 9605). – P. 2127-2137. – doi: 10.1016 / S0140-6736 (07) 61908-4. – PMID 18156035.
6. ↑ Mahesh R. Patel, MD. James G. Smirniotopoulos: Herpes Encephalitis: eMedicine Radiology (unspecified) (link inaccessible). Medscape .25 May 2011. Retrieved 5 May 2019. Archived March 19, 2012.
7. ↑ Jocelyn A. Lieb, Stacey Brisman, Sara Herman, Jennifer MacGregor, Marc E. Grossman. Linear erosive Herpes Simplex Virus infection in immunocompromised patients: the “Knife-Cut Sign” // Clinical Infectious Diseases (English) Russian. : journal. – 2008. – Vol. 47, no. 11. – P. 1440-1441. – doi: 10.1086 / 592976. – PMID 18937574.
8. ↑ ^{1 2} James, William D .; Berger, Timothy G. Andrews’ Diseases of the Skin: clinical Dermatology. – Saunders Elsevier, 2006 .– ISBN 0-7216-2921-0.
9. ↑ Letenneur, L; Pérès, K., Fleury, H., Garrigue, I., Barberger-Gateau, P., Helmer, C., Orgogozo, J.M., Gauthier, S., Dartigues, J.F. Seropositivity to herpes simplex virus antibodies and risk of Alzheimer’s disease: a population-based cohort study (English) // PLoS ONE: journal. – 2008. – Vol. 3, no. 11. – P. e3637. – doi: 10.1371 / journal.pone.0003637. – PMID 18982063.
10. ↑ van Diemen F. R., Kruse E. M., Hooykaas M. J., Bruggeling C. E., Schürch A. C., van Ham P. M., Imhof S. M., Nijhuis M., Wiertz E. J., Lebbink R. J. CRISPR / Cas9-Mediated Genome Editing of Herpesviruses Limits Productive and Latent Infections. (English) // PLoS pathogens. – 2016. – Vol. 12, no. 6. – P. e1005701. – doi: 10.1371 / journal.ppat.1005701. – PMID 27362483.
11. ↑ Roman Fishman. Biologists have learned how to cleanse cells from herpes viruses (Russian). nplus1.ru (July 1, 2016). Retrieved 4 July 2016.
12. ↑ Stumpf M.P., Laidlaw Z., Jansen V.A. Herpes viruses hedge their bets // Proceedings of the National Academy of Sciences of the United States of America. – 2002. – Vol. 99, no. 23. – P. 15234-15237. – doi: 10.1073 / pnas.232546899. – PMID 12409612.
13. ↑ Laura Sanders. How Herpes Re-rears Its Ugly Head (unspecified) . Science News (26 March 2009). Retrieved 5 May 2019. Archived March 19, 2012.
14. ↑ Myśliwska J., Trzonkowski P., Bryl E., Lukaszuk K., Myśliwski A. Lower interleukin-2 and higher serum tumor necrosis factor-a levels are associated with perimenstrual, recurrent, facial Herpes simplex infection in young women (eng.) // Eur. Cytokine Netw. : journal. – 2000. – Vol. 11, no. 3. – P. 397-406. – PMID 11022124.
15. ↑ Segal A.L., Katcher A.H., Brightman V.J., Miller M.F. Recurrent herpes labialis, recurrent aphthous ulcers, and the menstrual cycle // Journal of Dental Research.) Russian. : journal. – 1974. – Vol. 53, no. 4. – P. 797-803. – doi: 10.1177 / 00220345740530040501. – PMID 4526372.
16. ↑ Chambers A., Perry M. Salivary mediated autoinoculation of herpes simplex virus on the face in the absence of “cold sores,” after trauma (English) // Journal of Oral and Maxillofacial Surgery (English) Russian. : journal. – 2008. – Vol. 66, no. 1. – P. 136-138. – doi: 10.1016 / j.joms.2006.07.019. – PMID 18083428.
17. ↑ Perna J.J., Mannix M.L., Rooney J.F., Notkins A.L., Straus S.E. Reactivation of latent herpes simplex virus infection by ultraviolet light: a human model // Journal of the American Academy of Dermatology (English) Russian. : journal. – 1987. – Vol. 17, no. 3. – P. 473-478. – doi: 10.1016 / S0190-9622 (87) 70232-1. – PMID 2821086.
18. ↑ Rooney JF; Straus SE; Mannix ML; Wohlenberg, CR; Banks, S; Jagannath, S; Brauer, JE; Notkins, A.L. UV light-induced reactivation of herpes simplex virus type 2 and prevention by acyclovir) // The Journal of Infectious Diseases: journal. – 1992. – Vol. 166, no. 3. – P. 500-506. – doi: 10.1093 / infdis / 166.3.500. – PMID 1323616.
19. ↑ Oakley C., Epstein J.B., Sherlock C.H. Reactivation of oral herpes simplex virus: implications for clinical management of herpes simplex virus recurrence during radiotherapy (English) // Oral Surg Oral Med Oral Pathol Oral Radiol Endod: journal. – 1997. – Vol. 84, no. 3. – P. 272-278. – doi: 10.1016 / S1079-2104 (97) -5. – PMID 9377190.
20. ↑ Ichihashi M., Nagai H., Matsunaga K. Sunlight is an important causative factor of recurrent herpes simplex // Cutis: journal. – 2004. – Vol. 74, no. 5 Suppl. – P. 14-8. – PMID 15603217.
21. ↑ Martinez V., Caumes E., Chosidow O. Treatment to prevent recurrent genital herpes: [English] // Current Opinion in Infectious Diseases. – 2008. – Vol. 21, no. 1. – P. 42-48. – doi: 10.1097 / QCO.0b013e3282f3d9d3. – PMID 18192785.
22. ↑ Sobngwi ‐ Tambekou J; Taljaard D; Lissouba P; Zarca, Kevin; Puren, Adrian; Lagarde, Emmanuel; Auvert, Bertran. Effect of HSV-2 serostatus on acquisition of HIV by young men: results of a longitudinal study in Orange Farm, South Africa: [English] // The Journal of Infectious Diseases: j. – 2009. – Vol. 199, no. 7. – P. 958-964. – doi: 10.1086 / 597208. – PMID 19220143 .– PMC 2868899.
23. ↑ Koelle, D. M. Herpes Simplex: Insights on Pathogenesis and Possible Vaccines: [English] / D. M. Koelle, L. Corey // Annual Reviews: j. – 2008. – Vol. 59. – P. 381-395. – doi: 10.1146 / annurev.med. 59.061606.095540. – PMID 18186706.
24. ↑ ^{1 2} Chayavichitsilp, P. Herpes simplex: [English] / P. Chayavichitsilp, J. V. Buckwalter, A. C. Krakowski… Review [. – 2009. – Vol. 30, no. 4 (April). – P. 119-129. – doi: 10.1542 / pir.30-4-119. – PMID 19339385.
25. ↑ Smith J.S., Robinson N.J. Age-specific prevalence of infection with herpes simplex virus types 2 and 1: a global review.) // The Journal of Infectious Diseases: journal. – 2002. – Vol. 186 Suppl 1. – P. S3-28. – doi: 10.1086 / 343739. – PMID 12353183.
26. ↑ Xu, Fujie. Trends in Herpes Simplex Virus Type 1 and Type 2 Seroprevalence in the United States: [English] / Fujie Xu, Maya R. Sternberg, Benny J. Kottiri… [] // Journal of American Medical Association. – 2006. – Vol. 296, no. 8 (October). – S. 964-973. – doi: 10.1001 / jama.296.8.964. – PMID 16926356.
27. ↑ Xu. Seroprevalence of Herpes Simplex Virus Type 2 Among Persons Aged 14-49 Years – United States, 2005-2008 (eng.) // Morbidity and Mortality Weekly Report (MMWR): j. – 2010. – April (vol. 59). – P. 456-459.
28. ↑ ^{1 2} John Leo. The New Scarlet Letter (unspecified) . Time .2 Aug 1982.
29. ↑ ^{1 2} Chow, A. W. Cytosine Arabinoside Therapy for Herpes Simplex Encephalitis — Clinical Experience with Six Patients: [eng.] / A. W. Chow, A. Roland, M. Fiala … [] // Antimicrobial Agents and Chemotherapy: j. – 1973. – Vol. 3, no. 3 (March). – P. 412-417. – PMID 47 ^{.– PMC 444424.}
30. ↑ Kaufman H. E., Howard G. M. Therapy of experimental herpes simplex keratitis (eng.) // Investigative Ophthalmology & Visual Science. – 1962 .– August (vol. 1). – P. 561-564. – PMID 14454441. (inaccessible link)
31. ↑ Ch’ien L. T., Whitley R. J., Alford C. A., Galasso G. J. Adenine arabinoside for therapy of herpes zoster in immunosuppressed patients: preliminary results of a collaborative study (eng.) // The Journal of Infectious Diseases: journal. – 1976. – June (vol. 133 Suppl). – P. A184-91. – PMID 180198.
32. ↑ McKelvey E. M., Kwaan H. C. Cytosine arabinoside therapy for disseminated herpes zoster in a patient with IgG pyroglobulinemia // Blood. : journal. – American Society of Hematology, 1969. – November (vol. 34, no. 5). – P. 706-711. – PMID 5352659.
33. ↑ Fiala M., Chow A., Guze L. B. Susceptibility of Herpesviruses to Cytosine Arabinoside: Standardization of Susceptibility Test Procedure and Relative Resistance of Herpes Simplex Type 2 Strains: [eng.] // Antimicrobial Agents and Chemotherapy: j. – 1972. – Vol. 1, no. 4 (April). – P. 354-357. – PMID 4364937 .– PMC 444221.
34. ↑ Allen LB; Hintz OJ; Wolf SM; Huffman, JH; Simon, LN; Robins, RK; Sidwell, R.W. Effect of 9-beta-D-arabinofuranosylhypoxanthine 5′-monophosphate on genital lesions and encephalitis induced by Herpesvirus hominis type 2 in female mice // The Journal of Infectious Diseases: journal. – 1976. – June (vol. 133 Suppl). – P. A178-83. – PMID 6598.
35. ↑ Juel-Jensen B.E. Varicella and cytosine arabinoside: [English] // The Lancet. – Elsevier, 1970. – Vol. 1, no. 7646 (March). – P. 572.- doi: 10.1016 / S0140-6736 (70) -9. – PMID 41.
36. ↑ Nahmias, A. J. Inhibitory effect of heparin on herpes simplex virus: [German] / A. J. Nahmias, S. Kibrick // Journal of Bacteriology: mag. – 1964. – Vol. 87, no. 5 (Mai). – P. 1060-1066. – PMID 4289440. – PMC 277146.
37. ↑ Allen, L.B. Target-Organ Treatment of Neurotropic Virus Diseases: Efficacy as a Chemotherapy Tool and Comparison of Activity of Adenine Arabinoside, Cytosine Arabinoside, Idoxuridine, and Trifluorothymidine: [English] / LB Allen, RW Sidwell // Antimicrobial Agents and Chemotherapymotherapy j. – 1972. – Vol. 2, no. 3 (September). – S. 229-233. – PMID 47 .– PMC 444296.
38. ↑ Allen L.B., Wolf S.M., Hintz C.J., Huffman J.H., Sidwell R.W. Effect of ribavirin on Type 2 Herpesvirus hominis (HVH / 2) in vitro and in vivo: [eng.] // Annals of the New York Academy of Sciences: journal. – 1977 .– T. 284 (March). – P. 247-253. – doi: 10.1111 / j.1749-6632.1977.tb21957.x. – PMID 212976.
39. ↑ Allen, L. B. Target-Organ Treatment of Neurotropic Virus Disease with Interferon Inducers: L. B. Allen, K. W. Cochran // Infection and Immunity: j. – 1972. – Vol. 6, no. 5 (November). – P. 819-823. – PMID 4404669 .– PMC 422616.
40. ↑ Sidwell, R. W. Broad-spectrum antiviral activity of Virazole: 1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide / R.W. Sidwell, J.H. Huffman, G. P. Khare … [] // Science. – 1972. – Vol. 177, no. 4050 (August). – P. 705–706. – doi: 10.1126 / science.177.4050.705. – PMID 4340949.
41. ↑ Babiuk L.A., Meldrum B., Gupta V.S., Rouse B.T. Comparison of the Antiviral Effects of 5-Methoxymethyl-deoxyuridine with 5-Iododeoxyuridine, Cytosine Arabinoside, and Adenine Arabinoside: [English] // Antimicrobial Agents and Chemotherapy: j. – 1975. – Vol. 8, no. 6 (December). – P. 643-650. – PMID 1239978.- PMC 429441.
42. ↑ O’Meara A., Deasy P.F., Hillary I.B., Bridgen W.D. Acyclovir for treatment of mucocutaneous herpes infection in a child with leukaemia // The Lancet: journal. – Elsevier, 1979 .– December (vol. 2, no. 8153). – P. 1196.- doi: 10.1016 / S0140-6736 (79) 92428-0. – PMID 91931.
43. ↑ Whitley R; Arvin A; Prober C; Burchett, Sandra; Corey, Lawrence; Powell, Dwight; Plotkin, Stanley; Starr, Stuart; Alford, Charles. A controlled trial comparing vidarabine with acyclovir in neonatal herpes simplex virus infection.Infectious Diseases Collaborative Antiviral Study Group (English) // The New England Journal of Medicine: journal. – 1991. – February (vol. 324, no. 7). – P. 444-449. – doi: 10.1056 / NEJM1943240703. – PMID 1988829.
44. ↑ ^{1 2} Kimberlin DW; Lin CY; Jacobs RF; Powell, D. A .; Corey, L .; Gruber, W. C .; Rathore, M .; Bradley, J. S .; Diaz, P. S. Safety and efficacy of high-dose intravenous acyclovir in the management of neonatal herpes simplex virus infections.) // Pediatrics (English) Russian. : journal. – American Academy of Pediatrics, 2001. – August (vol. 108, no. 2). – P. 230-238. – doi: 10.1542 / peds.108.2.230. – PMID 11483782.
45. ↑ Molecular Therapy. Molecular Therapy – Abstract of article: 801. RNA Gene Therapy Targeting Herpes Simplex Virus (unspecified) . Nature.com (May 1, 2006). Retrieved April 12, 2011. Archived March 19, 2012.
46. ↑ University of Florida News – Potential new herpes therapy studied (unopr.) (inaccessible link). News.ufl.edu (February 3, 2009). Retrieved April 12, 2011. Archived March 19, 2012.
47. ↑ Fox, Maggie . New approach offers chance to finally kill herpes, Reuters. 2 July 2008. Retrieved April 12, 2011.
48. ↑ Kingsbury, Kathleen A Cure for Cold Sores? (unspecified) . Time .2 July 2008. Retrieved 4 May 2010.
49. ↑ ^{1 2} Herpevac Trial for Women (unopr.) . Date of treatment: March 4, 2008. Archived October 20, 2007.
50. ↑ Jon Cohen. aPainful Failure of Promising Genital Herpes Vaccine // Science: journal. 2010.15 October (vol. 330, no. 6002). – P. 304. – doi: 10.1126 / science.330.6002.304.
51. ↑ http://www.acambis.com/default.asp-id=2052.htm (inaccessible link)
52. ↑ Liza Green. Herpes Vaccine Developed at HMS Licensed for Preclinical Trials (unspecified.) (inaccessible link). FOCUS (March 7, 2008). Retrieved 5 May 2019. Archived March 19, 2012.
53. ↑ Harvard Medical School: from Herpes Vaccines (inaccessible link) , 15. April 2011
54. ↑ Dropulic, Lesia K (2019-09-15). “A Randomized, Double-Blinded, Placebo-Controlled, Phase 1 Study of a Replication-Defective Herpes Simplex Virus (HSV) Type 2 Vaccine, HSV529, in Adults With or Without HSV Infection”. The Journal of Infectious Diseases . 220 (6): 990-1000. Doi: 10.1093 / infdis / jiz225. PMID 31058977.
55. ↑ BioVex commences dosing in Phase 1 study of ImmunoVEX live attenuated genital herpes vaccine. See also: Your partner has herpes – now the good news from New Scientist .
56. ↑ Halford WP, ​​Püschel R., Gershburg E., Wilber A., ​​Gershburg S., Rakowski B. A live-attenuated HSV-2 ICP0 virus elicits 10 to 100 times greater protection against genital herpes than a glycoprotein D subunit vaccine) // PLoS ONE: journal. – 2011. – Vol. 6, no. 3. – P. e17748. – doi: 10.1371 / journal.pone.0017748. – PMID 21412438.

90,000 Herpes sore throat in children: causes, symptoms and prevention

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Herpes sore throat in children: causes, symptoms and prevention

Herpes sore throat in children: causes, symptoms and prevention – RIA Novosti, 18.12.2020

Herpes sore throat in children: causes, symptoms and prevention

Herpetic (herpes) sore throat is an acute inflammatory disease that is more common in children.On symptoms and prevention – in the material RIA Novosti. RIA Novosti, 18.12.2020

2020-12-18T20: 52

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MOSCOW, Dec 18 – RIA Novosti. Herpetic (herpes) sore throat is an acute inflammatory disease that is more common in children.On symptoms and prevention – in the material RIA Novosti. Symptoms of sore throat Herpes sore throat usually affects children from 3 to 10 years old, although it can develop in adults. The disease is highly contagious and is most often transmitted by contact and airborne droplets, less often through the mouth with water and food, through dirty hands and household items. The main symptom is a sore throat, which worsens when swallowing, and an elevated body temperature of 38-40 degrees. Also, herpetic sore throat is accompanied by inflammation that covers almost the entire oral cavity – the back of the pharynx, uvula, soft palate, palatine arches and tonsils.As a result, reddish blisters form there, which burst and leave small sores. As otolaryngologist Lyubov Kondratova told RIA Novosti, a rash can be in the nose and nasopharynx, and with a more severe course of the disease, it can also occur on the body. In addition, there are other symptoms of angina in children: headache, excessive salivation, body aches, weakness, diarrhea, abdominal pain, nausea, vomiting, and because of difficulty swallowing, in some cases, patients refuse to eat. Also, children have enlarged lymph nodes.With a mild course, the patient recovers, as a rule, after a week, and the fever disappears within 4-5 days. After the sores are opened, they heal in 5-6 days. Only a specialist is able to diagnose the disease, because its symptoms are similar to ARVI, influenza. It can be confused with other types of tonsillitis – catarrhal, lacunar or purulent. Due to the high contagiousness, the patient should be isolated or limited to contact with other family members. Causes and causative agents of sore throat The causative agents of this type of sore throat are Coxsackie enteroviruses of group A, less often of group B and echoviruses (ECHO).When they enter the lymph nodes, and then into the blood, the disease progresses rapidly. Angina is seasonal in nature and occurs mainly in the summer or early autumn, when children go to kindergartens and schools. Infection can occur even if the child just walked past the sick person. Also at risk are allergy sufferers, hypotrophies and those with weakened immunity. Complications of angina If a child’s angina is severe, the infection can spread throughout the body and lead to complications.Among them, serous meningitis is an inflammation of the brain, which causes symptoms such as severe headache, vomiting, lethargy, high fever, muscle stiffness. In addition, herpes sore throat in a child can lead to myocarditis, arrhythmias, pain in the heart, if the virus gets to him. Another complication is encephalitis, inflammation of the brain tissue, although with timely treatment, herpes sore throat in children goes away without serious consequences. Prevention of angina While a specific vaccine has not been developed that protects against the development of this disease, as well as measures of guaranteed prevention, because angina is highly contagious.However, you can reduce the likelihood of infection by observing some rules. First, personal hygiene should not be neglected – you should wash your hands regularly. Secondly, during seasonal epidemics, it is better to isolate a child from large groups. Thirdly, children should not touch their face with their hands and refrain from touching other people’s personal hygiene items. You should also carry out general strengthening measures, for example, hardening, and follow a balanced diet to increase immunity.A child needs to treat a sore throat on the recommendation of a doctor, while self-medication is strictly prohibited. Therapy usually consists of medication and bed rest, drinking plenty of water and gargling thoroughly. Due to the fact that this is a viral disease, the main burden falls on the immune system, which helps to fight it. The doctor may prescribe the following medications: antihistamines, antipyretics, and topical antiseptics and rinses. An antibiotic for angina can be prescribed to a child in the event of bacterial complications.During the illness, compresses and inhalations are contraindicated, and if its form is severe, then the child is hospitalized.

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MOSCOW, December 18 – RIA Novosti. Herpetic (herpes) sore throat is an acute inflammatory disease that is more common in children. On symptoms and prevention – in the material RIA Novosti.

Symptoms of sore throat

Herpes sore throat usually affects children from 3 to 10 years old, although it can develop in adults. The disease is highly contagious and is most often transmitted by contact and airborne droplets, less often through the mouth with water and food, through dirty hands and household items. The main symptom is a sore throat, which worsens when swallowing, and an elevated body temperature of 38-40 degrees.Also, herpetic sore throat is accompanied by inflammation that covers almost the entire oral cavity – the back of the pharynx, uvula, soft palate, palatine arches and tonsils. As a result, reddish blisters form there, which burst and leave small sores. As otolaryngologist Lyubov Kondratova told RIA Novosti, a rash can be in the nose and nasopharynx, and with a more severe course of the disease, it can also occur on the body.

In addition, there are other symptoms of angina in children: headache, excessive salivation, body aches, weakness, diarrhea, abdominal pain, nausea, vomiting, and due to difficulty swallowing in some cases, patients refuse to eat.Also, children have enlarged lymph nodes.

With a mild course, the patient recovers, as a rule, in a week, and the fever disappears already on the 4th-5th day. After the sores are opened, they heal in 5-6 days. Only a specialist is able to diagnose the disease, because its symptoms are similar to ARVI, influenza. It can be confused with other types of tonsillitis – catarrhal, lacunar or purulent. Due to the high contagiousness, the patient should be isolated or limited to contact with other family members.

Causes and causative agents of angina

The causative agents of this type of angina are group A Coxsackie enteroviruses, less often group B and echoviruses (ECHO). When they enter the lymph nodes, and then into the blood, the disease progresses rapidly. Angina is seasonal in nature and occurs mainly in the summer or early autumn, when children go to kindergartens and schools. Infection can occur even if the child just walked past the sick person. Also at risk are allergy sufferers, hypotrophies and those with weakened immunity.

“Those babies who are still fed with breast milk are less likely to get sick, because immunity from their mother is passed on to them. Until the age of three, the disease is very rare, ”the expert emphasized.

Complications with angina

If a child’s angina is severe, the infection can spread throughout the body and lead to complications. Among them, serous meningitis is an inflammation of the brain, which causes symptoms such as severe headache, vomiting, lethargy, high fever, muscle stiffness.In addition, herpes sore throat in a child can lead to myocarditis, arrhythmias, pain in the heart, if the virus gets to him.

Another complication is encephalitis, inflammation of the brain tissue, although with timely treatment, herpes sore throat in children disappears without serious consequences.

“Complications can be, as with other types of this disease. The heart, kidneys, joints suffer, and paratonsillar abscesses can occur in the oral cavity, in which a purulent process occurs in the peri-mucous tissue, ”said Lyubov Kondratova.

Prevention of angina

A specific vaccine has not yet been developed that protects against the development of this disease, as well as guaranteed prevention measures, because angina is highly contagious. However, you can reduce the likelihood of infection by observing some rules. First, personal hygiene should not be neglected – you should wash your hands regularly. Secondly, during seasonal epidemics, it is better to isolate a child from large groups. Thirdly, children should not touch their face with their hands and refrain from touching other people’s personal hygiene items.You should also carry out general strengthening measures, for example, hardening, and follow a balanced diet to increase immunity.

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A child needs to treat angina on the recommendation of a doctor, while self-medication is strictly prohibited. Therapy usually consists of medication and bed rest, drinking plenty of water and gargling thoroughly. Due to the fact that this is a viral disease, the main burden falls on the immune system, which helps to fight it.The doctor may prescribe the following medications: antihistamines, antipyretics, and topical antiseptics and rinses.

“Solutions are prescribed with chamomile, sage, calendula, and furacilin is also used. If the temperature rises more than 38.5 degrees, then ibuprofen and similar drugs are used. During illness, it is important to follow a diet, you need to exclude spicy, sour, salty, hot, solid and in general all foods that irritate the mucous membrane.