Otitis

How long does herpangina last? The danger of herpes sore throat and the rules of complex treatment

Herpetic tonsillitis has a number of synonyms that more accurately and correctly define the pathological inflammatory process: herpes tonsillitis, herpetic tonsillitis, herpangina, enteroviral vesicular pharyngitis, ulcerous tonsillitis.

Herpes sore throat occurs as a result of an enterovirus infection. Sore throat of viral origin - tonsillitis, will be called herpetic, although it has nothing to do with the herpes virus.

It received its name due to the similarity of the rashes with herpetic lesions of the mucous membranes and the general definition of pain symptoms in case of a sore throat.

The course of herpes sore throat always has an acute form, and the development and outcome of the disease will depend on some determining factors: the strength of the immune system, the virulence of the virus and the surrounding epidemiological situation.

Pathogen and etiology of the disease

What is herpes sore throat? This is an acute viral infection that affects the mucous membrane of the mouth, throat, and pharynx, accompanied by anginal pain (as with ordinary bacterial sore throat). The lesions are herpetic in nature not in origin, but in the form of the rash.

The Coxsackie virus has about 30 varieties. Enteroviruses are quite widespread in the external environment and can cause diseases in humans. These include the Coxsackie virus serotype A, B, which is the causative agent of viral sore throat, intestinal, respiratory infections and meningitis.

The virulence (ability to cause disease) of the pathogen is due to its stability in the external environment. It is inactivated only by high temperatures (warming up to 75 - 80°C). It is preserved when frozen, for a long time - in wastewater, contaminated air (in enclosed spaces).

Children from 2 to 10 years of age are susceptible to the disease (up to a year they rarely get sick) and adults aged 30 to 40 years. This age criterion is not a determining factor in the occurrence of infection.

Children get herpes sore throat more often than adults, but the disease is more severe. Adults get sick less often due to the fact that, having been ill in childhood, they acquired specific immunity, but only to the type of one pathogen. When infected with a different serological group, new herpesvirus diseases may arise.

People with reduced resistance get sick more often. Poor nutrition, poor living conditions (unsanitary conditions, violation of microclimate conditions), bad habits, and chronic concomitant diseases contribute to infection.

Herpetic tonsillitis occurs in the form of an outbreak in the summer and autumn months (July - September). Sporadic cases of the disease are observed in winter and spring.

It is transmitted by airborne droplets (sneezing, coughing), orally - fecally and by contact. The virus enters the human body through the mucous membranes, where it settles, invades cells and actively multiplies.

Pathogenesis of herpes tonsillitis

Replication of the enterovirus occurs in the epithelial cells of the intestinal mucosa and oral cavity (lymphoid formations). The pathogen circulates in the bloodstream (viremia) and spreads throughout the body, causing intoxication and the appearance of characteristic symptoms.

The affected cells die, creating necrotic lesions. Exudate accumulates in areas of necrosis, which leads to the appearance of a papular rash. Rashes rarely merge into larger lesions, usually when the disease is complicated by a bacterial infection. The development of the disease is characterized by an increase in intoxication, the occurrence of local pain syndrome and a deterioration in the general condition of the patient.

The course of the disease is significantly influenced by:

degree of virulence of the pathogen;
body resistance;
route of transmission of the virus (method of infection);
exogenous factors (nutrition, microclimate, lifestyle);
age (children get sick more seriously).

Clinical picture of herpetic tonsillitis

The incubation period of the disease for herpetic viral sore throat is 2 - 4 days. With strained immunity, it can be 10 days. Herpes sore throat develops suddenly and acutely in adults, as in children. Over the course of one to two hours, there is a sharp increase in body temperature with the development of febrile and pyretic fever.

General symptoms of the disease:

malaise (headache, body weakness, dizziness);
loss of appetite;
sleep disturbance;
abdominal pain, nausea;
myalgia.

One to two days after the development of primary symptoms, the appearance of specific clinical signs is noted.

Herpetic tonsillitis manifests itself:

acute stabbing pain in the throat, which gradually increases;
hyperemia and swelling of the mucous membrane of the oral cavity and pharynx;
dysphagia (impaired swallowing - pain);
the appearance of a papular-vesicular rash on the mucous membranes of the mouth and pharynx;
dyspepsia and vomiting.

Throughout the entire period of the disease, viral herpes tonsillitis is accompanied by hypersalivation (increased salivation). The decompensatory function of the salivary glands in this case plays the role of a protective mechanism. Frequent and increased salivation helps to wash the affected tissues and accelerates their regeneration.

Important! It is necessary to increase fluid intake during illness (especially during febrile syndrome) to prevent dehydration and reduce intoxication.

A secondary symptom of the disease is the development of lymphadenitis (inflammation of the lymph nodes). Lymphoid formations (cervical, submandibular, parotid lymph nodes) respond to the spread and reproduction of the virus by increasing. They are observed to be sore and dense, which, if the course is favorable, disappears as they recover.

Experts consider a characteristic symptom of the disease to be the phenomenon of hyperthermia, which occurs in two stages: the first increase in body temperature is observed on the first day of illness, followed by a slight decrease, and the second one on the 3rd day of illness, which is critical or peak.

Stages of development of herpangina:

The first two days are characterized by general symptoms of a viral infection (hyperthermia, sore throat, general malaise, runny nose, nasal congestion).
On the 2-3rd day after the onset of symptoms, bright red bubbles appear on the oral mucosa, soft palate, tonsils, and back wall of the pharynx. A day later they become transparent white with serous exudate, bordered by a red corolla (size 1 - 2 mm), similar to a herpetic rash. The temperature is slightly lowered, but remains stable. Myalgia, stabbing pain in the throat, and diarrhea develop.
The third day of illness is accompanied by pyretic fever (39 - 41°C). The condition worsens, painful symptoms increase.
On the 4th day, after a few hours (from 2 - 3 hours to a day), the papules pass into the stage of vesicles, which open (the temperature decreases slightly). Very painful ulcers appear. The more complex the disease, the greater their number. On average, the number is 5 - 12 vesicles, with complications - up to 20. Sometimes the vesicles merge, forming large foci.
On the 5th - 6th day of the process, the ulcers dry out with the formation of crusts, the condition of the patient improves significantly, and the signs of intoxication of the body weaken. If bacterial microflora is involved in the process, the vesicles become ulcerated and erosions occur.
With a favorable course, on the 7th-8th day of the disease, the signs of pharyngitis (inflammation of the pharyngeal mucosa) decrease, the crusts are washed off, the mucous membrane regenerates and no traces of the previous lesion are observed.

After 10 days from the onset of the disease, the pain in the lymph nodes disappears. Their inflammation disappears by the second week (14 - 16 days of illness).

Diagnosis and prognosis of herpes tonsillitis

Viral herpes tonsillitis is fairly easy to diagnose. When making a diagnosis, the following are taken into account: the epidemiological situation at the time of the onset of the viral infection, the etiology of the disease, and clinical symptoms.

A characteristic symptom complex allows one to accurately determine the diagnosis. The need for additional laboratory tests arises with an atypical form of herpes tonsillitis. Blood samples, smears of mucous secretions of the nasopharynx, oral cavity, and intestinal contents are examined.

In this case, virological and serological research methods are used. The presence of specific antibodies, cultural and biochemical properties of the pathogen are determined. Differential diagnosis is aimed at excluding diseases in which a similar clinical picture is observed. Based on the nature of the rash, catarrhal, purulent tonsillitis, diphtheria, scarlet fever, and aphthous stomatitis are excluded.

Viral tonsillitis (herpes) in most cases has a favorable prognosis. With a strained immune system, recovery occurs in 10 to 14 days. A severe course of the disease and an unfavorable prognosis are rarely observed - with a significant decrease in immunity or illness in children before the first year of life.

Features of treatment

Specific therapy methods have not been developed. Herpetic infection (tonsillitis) as a treatment involves the use of symptomatic remedies, alleviating the general condition of the patient and reducing intoxication of the body.

Drug treatment includes the use of:

antipyretics;
antiallergic (if necessary);
vitamin and mineral preparations;
immunomodulators.

Important! When diagnosing herpes sore throat (tonsillitis), the use of antibacterial agents in the first days of the disease is not advisable. Antibiotics and antiherpetic drugs have no effect on the virus.

The use of antibacterial agents may be necessary to prevent complications when the pathological process worsens and the development of concomitant bacterial infection. An important point in the fight against a viral infection is to ensure that the patient remains in bed and drinks plenty of fluids.

Local treatment for sore throat:

Frequently rinse the mouth with decoctions of medicinal plants - chamomile, sage, calendula (oak bark).
For severe pain, use a 2% lidocaine solution (rinse) or Orasept spray as a local anesthetic.
Treat the affected areas with antiseptic solutions (aqueous solution of gentian violet, Chlorophyllipt, Ingalipt, Tantum Verde). The drugs do not act on the virus, but their use prevents the development of a bacterial infection. Treatment should be avoided if the throat is very sore.

Important! With this pathology, inhalations and warming of a sore throat cannot be performed. This will lead to generalization (spread) of the inflammatory process.

If the course of the disease is favorable, sufficient treatment will be to consume plenty of fluids to avoid dehydration and reduce intoxication and adherence to bed rest in combination with good nutrition.

Food should be nutritious and easy to digest. It is recommended to prepare first courses, purees, and fine-grained porridges. Eat food often, in small portions. After each dose, rinse your mouth and throat with the above products.

If severe symptoms of intoxication develop - nausea, vomiting, convulsions (especially in children), treatment of the patient at home is not allowed. Such clinical signs may indicate the development of complications (meningitis, encephalitis) and require emergency hospitalization.

Prevention of herpes tonsillitis

Prevention of herpes virus infections, including herpes tonsillitis, comes down to increasing and strengthening the body’s immune status, observing personal hygiene rules and reducing the possibility of infection.

Basic preventive measures:

Compliance with hygiene rules - mandatory hand washing before eating and after visiting public places (shops, institutions, vehicles).
If possible, avoid crowded places to prevent infection.
Increasing and strengthening the body’s nonspecific resistance (good nutrition, decent conditions and lifestyle).

Strengthening the body, frequent walks in the fresh air and an active lifestyle helps improve immunity.

The formation of active immunity for herpes sore throat (tonsillitis) is carried out on the 10th - 14th day of the disease.

The specificity of immunity lies in the body's immunity to a specific serotype of enterovirus, which excludes re-infection.

– an acute infectious disease caused by the Coxsackie virus A or B, which manifests itself as serous inflammation of the oral cavity and pharynx. Viruses of this group belong to enteroviruses, are tropic to muscle, epithelial, and nervous tissue, which in some cases causes complications associated with damage to the membranes of the brain, heart muscle, and liver. Children of preschool and primary school age are most prone to the disease, while herpangina is much more severe in children in the first year of life.

Symptoms

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The disease begins with a sharp rise in temperature. The general condition worsens, the patient refuses to eat, he is bothered by nausea and headaches, diarrhea, and pain when swallowing. In a third of all cases of the disease, muscle pain may be present, in particular abdominal pain, and in children of the first year of life - cramps. At the same time, the mucous membrane of the oropharynx becomes inflamed, swollen, and covered with a pinpoint red papular rash. Within a few hours, the papules turn into vesicles with transparent contents, the size of which ranges from 1 to 8 mm. The number of rash elements is usually up to twenty. Soon the vesicles open, and the exposed ulcers are covered with a coating of fibrin.

Fibrinous films on the mucous membrane can resemble pus, but differ in that they are fused to the underlying tissue and are difficult to remove. Each ulcer is surrounded by a hyperemic cushion. The oral cavity becomes painful, itching is possible, and salivation appears. Difficulties arise in eating any food, since the mucous membrane is easily injured and painful, becomes very sensitive even to temperatures slightly above 40°C, and swallowing is difficult. At the height of clinical manifestations on the mucous membrane of the oropharynx, regional lymph nodes enlarge and become painful. The duration of the disease is on average six days, after which complete recovery occurs. A person who has recovered from the disease may remain a carrier of the Coxsackie virus and be a source of infection.

At the age of 3-6 years, herpangina can often be combined with serous meningitis, which complements the clinical picture with meningeal symptoms (stiff neck, Kernig's sign, trismus of masticatory muscles, etc.). A week after recovery, neurological symptoms disappear, but there is a high probability of relapse of meningitis. Serous meningitis at an earlier age can be fatal. In general, the prognosis is serious.

Herpangina can be complicated by myocarditis, which also worsens the prognosis and requires clinical observation throughout the entire period of illness and during convalescence.

In the case of the development of an erased form of herpangina, changes in the mucous membrane of the oropharynx are limited to redness and swelling. In general, the disease is milder or practically asymptomatic.

Causes and pathogenesis

The Coxsackie virus is transmitted by airborne droplets, through contaminated food (fruits, vegetables, milk), and fecal-orally. The incidence often increases in the summer. The infection can cause outbreaks of epidemics that have a wave-like character. In epidemic terms, a person suffering from herpangina or serous meningitis, as well as a healthy carrier, is dangerous.

Once on the mucous membranes of the nasopharynx, the Coxsackie virus penetrates the intestines and lymph nodes, where it multiplies intensively. On the third day of illness, a critical amount of viruses appears in the blood. This greatly facilitates their access to nervous and muscle tissue, which determines the general serious condition of the patient. When examining individual muscle fibers affected by the Coxsackie virus, dystrophic changes and necrosis were revealed. Examination of the affected meninges (with concomitant serous meningitis) revealed severe swelling and hemorrhages.

Studies have shown that the same type of Coxsackie virus can cause different clinical forms. After an infection, persistent immunity to a virus of a certain type develops, which does not exclude the possibility of certain immune protection against some other viruses of this group.

Diagnostics

A preliminary diagnosis is made based on the clinical picture of the disease. The most typical localization of rashes for herpangina is the posterior wall of the pharynx, soft palate, and tonsils. If a secondary bacterial infection occurs, the appearance of the rash may change.

In the first hours, it is necessary to exclude the possibility (contact with allergens, taking medications, insect bites) of food poisoning. One of the diagnostic signs of a disease caused by the Coxsackie virus is two peaks of temperature, on the first and third day.

To identify the Coxsackie virus, the contents of the bubbles on the pharyngeal mucosa are examined. Blood serum is also examined for the presence of antibodies to the virus. Enzyme immunoassay, complement fixation reaction, and indirect hemagglutination reaction are used. Virus typing is carried out by adding diagnostic immune fluorescent sera.

Neurological examination is indicated to rule out serous meningitis. In case of special complaints or the presence of clinical symptoms, the condition of the heart, kidneys, and liver is examined.

Treatment

Bed rest, the patient is isolated until recovery. The food is liquid, semi-liquid, pureed, mushy. Drink plenty of vitamin C (rosehip decoction, natural lemonade, tea with lemon). Drinking regimen is important for the timely elimination of toxins, however, when inflammation spreads to the membranes of the brain, the amount of fluid is limited and diuretics are used. In case of meningitis or the presence of febrile convulsions, the patient is hospitalized for the entire duration of treatment; after recovery, observation by a neurologist is indicated.

Treatment of herpangina is symptomatic. Antiseptic solutions are prescribed locally to prevent secondary bacterial infections, as well as drugs that relieve irritation of the mucous membrane and reduce pain. In particular, use a 10% solution of sodium tetraborate in glycerin, a 5% solution of marborane in dimexide, Castellani liquid, methylene blue, a warm solution of soda and sage decoction for rinsing, and a 2% solution of lidocaine. As an astringent, it is good to use a decoction of oak bark for rinsing.

To reduce swelling, antihistamines are used: suprastin, diazolin, calcium gluconate.

To relieve symptoms of general malaise, non-steroidal anti-inflammatory drugs are prescribed: ibuprofen, nimesulide.

Prevention

To prevent transmission of the virus from a patient with herpangina, precautions are taken during treatment and care. At home, the patient is in a separate well-ventilated room, he has separate dishes and personal hygiene items. After recovery, the quarantine is valid for another two weeks.

In order to exclude cases of infection of children in children's institutions, doctors, health workers, teachers, nannies, kitchen and dining room workers who have had herpangina or have been in contact with the patient are suspended from work for two weeks.

There is no specific prevention.

Enterovirus infection is a group of acute diseases of the digestive tract that are caused by RNA-containing pathogens of the Enterovirus genus.

Nowadays, outbreaks of enterovirus infection are increasingly observed in many countries around the world. The danger of diseases of this group is that the clinical symptoms can be very diverse. In most cases, there is a mild course, characterized by minor malaise, but serious complications can occur, including severe damage to the respiratory system and central nervous system, as well as the kidneys and digestive tract.

Pathogens and routes of their transmission

The vast majority of RNA-containing enteroviruses are pathogenic for humans.

To date, over 100 types of pathogens have been identified, including:

ECHO viruses;
Coxsackie viruses (types A and B);
pathogens (polioviruses);
unclassified enteroviruses.

The pathogens are ubiquitous. They are characterized by a high degree of stability in the external environment, tolerate freezing, as well as treatment with antiseptics such as 70% ethanol, Lysol and ether. Enteroviruses quickly die during heat treatment (they cannot tolerate heating up to 50°C), drying and exposure to formaldehyde or chlorine-containing disinfectants.

Natural reservoirs for pathogens are water bodies, soil, some food products, and the human body.

note: In feces, enteroviruses remain viable for up to six months.

In most cases, the source of the pathogen is a sick person or a virus carrier, who may completely lack clinical signs of enterovirus infection. According to medical statistics, among the population of some countries, up to 46% of people can be carriers of pathogens.

Main routes of transmission:

fecal-oral (with a low level of hygiene);
contact-household (through contaminated objects);
airborne (if the virus is present in the respiratory system);
vertical transmission (from an infected pregnant woman to a child);
water (when swimming in polluted waters and watering plants with wastewater).

note: cases of infection with enteroviruses have been recorded even through water in coolers.

This group of acute diseases is characterized by seasonal outbreaks in the warm season (summer-autumn). Human susceptibility to enteroviruses is very high, but after an infection, type-specific immunity remains for quite a long time (up to several years).

Symptoms of enterovirus infection

Enterovirus infection in adults and children can cause a number of pathologies characterized by varying degrees of severity of the inflammatory process.

The most severe pathologies include:

inflammation of the myocardium (heart muscle);
pericarditis (inflammation of the pericardial sac);
hepatitis (anicteric);
serous (damage to the soft membranes of the brain);
acute paralysis;
kidney damage;
newborns.

Less dangerous manifestations:

three-day fever (including with skin rashes);
gastroenteritis (inflammation of the digestive tract);
herpetic sore throat;
lymphadenopathy;
polyradiculoneuropathy;
inflammation of the conjunctiva;
inflammation of the choroid;
damage to the optic nerve;
vesicular pharyngitis.

note: When enterovirus D68 enters the body, bronchopulmonary obstruction often develops. A characteristic symptom is a severe cough.

Severe complications rarely develop in adult patients with good immunity. They are typical for people with reduced body resistance - children (especially young children) and people suffering from serious diseases (malignant tumors).

note: the variety of clinical manifestations is due to a certain affinity of enteroviruses for many tissues of the human body.

The most characteristic clinical signs of enterovirus infection in children and adults:

The duration of the incubation period for enteroviral infections in most cases ranges from 2 days to 1 week.

Most often, when infectious agents of this type enter the body, a person develops ARVI.

Symptoms of the catarrhal form of enterovirus infection:

runny nose;
cough (dry and rare);
increased temperature (usually within subfebrile range);
hyperemia of the mucous membrane of the throat;
digestive disorders (usually not very significant).

As a rule, a person recovers within a week from the onset of the disease.

Symptoms of enteroviral fever:

febrile reaction within 3 days from the onset of the disease;
moderate signs of general intoxication;
skin rashes (not always);
deterioration in general health (mild or moderate).

note: Enteroviral fever is also called “minor illness” because the symptoms do not last long and their severity is low. This form of pathology is relatively rarely diagnosed, since most patients do not even seek medical help.

With this form of enterovirus infection, children may experience symptoms of damage to the upper respiratory tract (catarrhal manifestations). In young children, the disease can last up to 2 weeks or more.

A sign of herpangina against the background of an enterovirus infection is the formation of red papules on the mucous membranes. They are localized in the area of the hard palate, uvula and arches. These small rashes quickly transform into vesicles, which after 2-3 open with the formation of erosions or gradually resolve. Herpangina is also characterized by enlargement and tenderness of the submandibular and cervical lymph nodes, as well as hypersalivation (salivation).

The main clinical manifestation of enteroviral exanthema is the appearance on the skin of patients of a rash in the form of spots and (or) small pink blisters. In most cases, the skin elements disappear after 2-3 days; At the site of their resolution, peeling of the skin is observed, and the upper layers come off in large fragments.

Important: exanthema can be diagnosed in parallel with meningeal symptoms.

Symptoms of serous meningitis against the background of enterovirus infection:

photophobia (photophobia);
increased sensitivity to sounds;
severe headache when bringing the chin to the chest;
lethargy;
apathy;
psycho-emotional arousal (not always);
high body temperature;
convulsions.

Oculomotor disorders, disturbances of consciousness, muscle pain and increased tendon reflexes are also possible.

Meningeal symptoms last from 2 days to one and a half weeks. The virus can be detected in the cerebrospinal fluid for 2-3 weeks.

Symptoms of enteroviral conjunctivitis:

pain (stinging) in the eyes;
tearfulness;
photophobia;
redness of the conjunctiva;
swelling of the eyelids;
copious discharge (serous or purulent).

note: with enteroviral conjunctivitis, one eye is initially affected, but soon the inflammatory process spreads to the second.

Signs of enterovirus infection in children

Children (especially children under 3 years of age) are characterized by an acute onset of the disease.

The most common clinical manifestations of enterovirus infection are:

sleep disorders;
fever;
chills;
diarrhea;
catarrhal symptoms;
myalgia;
dizziness;
weakness;
exanthema and (or) sore throat (not always).

Currently, the causative agent of enterovirus infection can be identified in one of four ways:

Changes in general blood test:

slight leukocytosis;
hyperleukocytosis (rare);
neutrophilia (early stage);
eosinophytosis and lymphocytosis (as the disease progresses).

Important:establishing the presence of a virus in the body is not indisputable evidence that it was this pathogen that provoked the disease. Asymptomatic carriage occurs quite often. The diagnostic criterion is an increase in the number of antibodies (in particular, immunoglobulins A and M) by 4 or more times!

Differential diagnosis

Herpes sore throat, which is caused by the Coxsackie virus, should be differentiated from herpes simplex and oral candidiasis (fungal). Serous meningitis caused by infection with enteroviruses should be distinguished from damage to the meninges of meningococcal etiology.

If symptoms of the gastroenteric form occur, other intestinal infections should be excluded. It is important to differentiate exanthema from rashes caused by rubella and hypersensitivity reactions (allergic).

Etiotropic (i.e., specific) treatment methods have not been developed to date.

Treatment of enterovirus infection in adults involves detoxification and symptomatic therapy. Therapeutic tactics are determined individually for each patient depending on the nature, location and severity of the pathological process. According to indications, patients are given antiemetics, painkillers and antispasmodics.

When treating enterovirus infection in children, rehydration therapy often comes to the fore, i.e. eliminating dehydration and restoring electrolyte balance. For this purpose, saline solutions and 5% glucose are either given orally or administered through intravenous infusion. Children are also given detoxification therapy and, if necessary, given antipyretics (antipyretics).

To combat viruses, intranasal administration of a solution of leukocyte interferon is indicated.

If complications occur due to the addition of a secondary bacterial infection, the patient is prescribed a course of antibiotic therapy. Lesions of the nervous system often require the use of hormonal therapy with corticosteroids.

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2017

Other specified infections characterized by damage to the skin and mucous membranes (B08.8), Enteroviral infection, unspecified (B34.1), Enteroviral exanthematous fever [Boston exanthema] (A88.0), Enteroviral vesicular stomatitis with exanthema (B08.4), Enteroviral vesicular pharyngitis (B08.5)

Short description

Approved
Joint Commission on Healthcare Quality
Ministry of Health of the Republic of Kazakhstan
dated May 12, 2017
Protocol No. 22

Enterovirus infections (Enterovirosis)- a group of anthroponotic acute infectious diseases caused by enteroviruses, characterized by fever and polymorphism of the clinical picture (with predominant damage to the central nervous system, cardiovascular system, gastrointestinal tract, muscular system, mucous membranes and skin).

INTRODUCTORY PART:

ICD-10 code(s):

ICD-10
Code	Name
A85.0	Enteroviral encephalitis, enteroviral encephalomyelitis
A87.0	Enteroviral meningitis; meningitis caused by the Coxsackie virus/meningitis caused by the ECHO virus
A88.0	Enteroviral exanthematous fever (Boston exanthema)
V08.4	Enteroviral vesicular stomatitis with exanthema, viral pemphigus of the oral cavity and extremities
B08.5	Enteroviral vesicular pharyngitis, herpangina
В08.8	Other specified infections characterized by damage to the skin and mucous membranes; enteroviral lymphonodular pharyngitis
B34.1	Enteroviral infection, unspecified; Coxsackievirus infection, NOS; ECHO virus infection, NOS

Date of development of the protocol: 2017

Abbreviations used in the protocol:

HELL	arterial pressure
ICE	disseminated intravascular coagulation
mechanical ventilation	artificial ventilation
ITS	infectious-toxic shock
ELISA	linked immunosorbent assay
CT	CT scan
MRI	Magnetic resonance imaging
ICD	international classification of diseases
UAC	general blood analysis
OAM	general urine analysis
AKI	acute kidney injury
ICU	intensive care unit
PCR	polymerase chain reaction
RNA	ribonucleic acid
RN	neutralization reaction
RNGA	indirect hemagglutination reaction
RSK	complement fixation reaction
SZP	fresh frozen plasma
CSF	cerebrospinal fluid
ESR	erythrocyte sedimentation rate
Ultrasound	ultrasonography
CNS	central nervous system
EVI	enterovirus infection
ECG	electrocardiography
EchoCG	echocardiography
EEG	electroencephalography

Protocol users: emergency doctors, paramedics, general practitioners, infectious disease specialists, therapists, neurologists, ophthalmologists, dermatovenereologists, otorhinolaryngologists, surgeons, anesthesiologists-resuscitators, healthcare organizers.

Level of evidence scale:

A	A high-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias, the results of which can be generalized to an appropriate population.
IN	High-quality (++) systematic review of cohort or case-control studies or high-quality (++) cohort or case-control studies with very low risk of bias or RCTs with low (+) risk of bias, the results of which can be generalized to the relevant population .
WITH	Cohort or case-control study or controlled trial without randomization with a low risk of bias (+), the results of which can be generalized to the relevant population or RCT with a very low or low risk of bias (++ or +), the results of which cannot be directly distributed to the relevant population.
D	Case series or uncontrolled study or expert opinion.
GPP	Best clinical practice.

Classification

Classification

Depending on the severity of clinical

And x manifestations:
· asymptomatic (preclinical);
· manifest (clinical);

Depending on the clinical form:
Typical forms:
- herpetic sore throat;
- epidemic myalgia;
- aseptic serous meningitis;
- enteroviral exanthema;
atypical forms:
- inapparent form;
- minor illness (“summer flu”);
- catarrhal (respiratory) form;
- encephalitic form;
- encephalomyocarditis of newborns;
- polio-like (spinal) form;
- epidemic hemorrhagic conjunctivitis;
- uveitis;
- jade;
- pancreatitis.
mixed forms (mixed infection):
- meningitis and myalgia;
- meningitis and herpangina;
- herpangina and exanthema;
- other.

Depending on the severity of the current:
· light;
· medium-heavy;
· heavy.

Severity criteria:
- severity of intoxication syndrome;
- severity of local changes;

Depending on the current:
· sharp smooth;
· with complications;
· recurrent.

Depending on the presence of complications:
· uncomplicated form;
· complicated form (indicating the complication):
− pneumonia;
− acute respiratory distress syndrome;
− edema-swelling of the brain;
− convulsive syndrome;
− hypovolemic shock;
− acute kidney injury;
− others.

Diagnostics

DIAGNOSTIC METHODS, APPROACHES AND PROCEDURES

Diagnostic criteria

Complaints at the time of examination and/or in the medical history:
Asymptomatic (preclinical) stage: does not actively complain.

Clinical stage (uncomplicated): complaints and clinical manifestations depend on the form of the disease. Combined symptoms of various clinical forms are often observed.

The most common clinical manifestations of EVI:
· Acute onset;
· Fever (up to 38 - 40ͦ C);
· Headache;
· Weakness, malaise;
· Dizziness;
· Nausea, vomiting;
· Hyperemia of the pharynx;
· Granularity of the posterior pharyngeal wall;
· Hyperemia of the face, neck, upper half of the body;
· Rash on the face, torso, limbs (including palms and feet);
Enanthema on the oral mucosa;
· Scleral vascular injection.

Name of clinical form	Main complaints	Clinical manifestations
Herpangina	Sore throat (moderate or absent)	The general condition is relatively satisfactory. Hyperemia of the mucous membrane of the soft palate, palatine arches, uvula, and posterior pharyngeal wall. Within 24-48 hours, from 5-6 to 20-30 small grayish-white papules with a diameter of 1-2 mm appear, which can occur in groups or separately. Further dynamics are erosion bubbles. A halo of hyperemia forms around the erosions. Erosions heal within 4-6 days without defects in the mucous membrane. The disease often recurs.
Epidemic myalgia (pleurodynia, Bornholm disease)	temperature rise to 39.0-40.5°C general weakness, nausea (often vomiting) · Strong headache pain in the pectoral muscles, epigastric and umbilical areas, back, limbs	The pain intensifies with movement and coughing, often becomes excruciating and is accompanied by profuse sweating. The duration of painful attacks ranges from 5-10 minutes to several hours (usually 15-20 minutes). The pharynx is hyperemic, granularity is often detected on the mucous membrane of the palate, and cervical lymphadenitis is characteristic. Some patients have hepatosplenomegaly. The average duration of the disease is 3-7 days. With an undulating course of the disease (2-3 exacerbations with an interval of 2-4 days), the duration of the disease increases to 1.5-2 weeks.
Serous meningitis	temperature rise to 39.0-40.5°C · severe headache of a bursting nature	General hyperesthesia (hyperacusis, photophobia, skin hyperesthesia) is characteristic. Meningeal symptoms. In some cases, psychomotor agitation and convulsions are observed. Catarrhal phenomena are possible. Flatulence often occurs, and palpation of the abdomen reveals rumbling.
Enteroviral exanthema (epidemic, or Boston, exanthema, as well as measles-like and rubella-like exanthema)	temperature rise to 39.0-40.5°C general weakness · severe headache and muscle pain · sore throat Rash on the face, trunk, limbs, particularly the hands and feet Enanthema on the oral mucosa	It is one of the mild forms of EVI. The rash is rubella-like, less commonly maculopapular, bullous, petechial, and persists for 2-4 days. There is a spotted enanthema on the mucous membrane of the oropharynx. Cervical lymphadenitis. In the acute period, pharyngitis and conjunctivitis often occur. There may be phenomena of meningism or a combination with serous meningitis. In some cases, hand-foot-oral cavity syndrome is observed. Fever lasts 1-8 days.
Minor illness (Coxsackie and ECHO fever; three-day or indeterminate fever; “summer flu”)	· temperature increase · weakness moderate headache · vomit myalgia · abdominal pain	Clinically characterized by short-term fever (no more than 3 days). Catarrhal phenomena from the upper respiratory tract occur in less than two thirds of patients. A two-wave course of the disease is possible.
Catarrhal (respiratory) form	· temperature increase · runny nose · dry cough · weakness	A common form of EVI. Characterized by rhinitis with serous-mucous discharge, dry cough, hyperemia and granularity of the mucous membrane of the pharynx. Possible manifestations of the disease in the form of pharyngitis with regional lymphadenitis and short-term low-grade fever. In uncomplicated cases, fever persists for about 3 days, catarrhal symptoms for about a week.
Enteroviral diarrhea (viral gastroenteritis, “vomiting disease”)	temperature rise to 38.0-39.0 °C loose stools · lack of appetite · repeated vomiting Catarrhal symptoms (often)	The febrile period lasts on average about a week. Simultaneously with the increase in body temperature, loose stools without pathological impurities are observed up to 2-10 times a day. Abdominal bloating is characteristic, pain on palpation is possible (more pronounced in the ileocecal region). There is no appetite, the tongue is coated. In the first days, repeated vomiting is often observed, but even with the duration of dyspeptic symptoms from 2 days to 1.5-2 weeks, significant dehydration does not occur. Hepatosplenomegaly is sometimes noted. Signs of catarrhal inflammation of the upper respiratory tract are often observed.
Paralytic form (spinal, polio-like)	· slight increase in temperature Paresis of the lower extremities (morning lameness)	It is more often registered in the warm season in the form of sporadic cases in children 1-5 years old. It occurs predominantly in the form of mild paralytic forms. Severe forms occur rarely. A third of patients experience a preparalytic period, which is characterized by symptoms characteristic of other forms of enterovirus infection (minor disease, respiratory, herpangina). More often, paresis occurs acutely, against the background of complete health. A gait disturbance occurs in the form of a limp, with the knee bending, the foot hanging down, the leg rotating outward and a decrease in muscle tone. Superficial and deep reflexes are not impaired; Hypo- or hyperreflexia is less common. Paresis passes relatively quickly, usually with complete restoration of motor functions, but in rare cases, hypotension and wasting of the affected muscles persist for several months.
Encephalitis and meningoencephalitis	temperature rise to 39.0-40.5°C · Strong headache repeated vomiting without relief	General hyperesthesia (hyperacusis, photophobia, skin hyperesthesia) is characteristic. Meningeal symptoms. In severe cases - impaired consciousness, possible convulsions, focal neurological symptoms (nystagmus, cranial nerve palsies, etc.).
Pericarditis and myocarditis	moderate increase in temperature general weakness pain in the heart area	More often, heart damage develops in older children and adults after suffering a respiratory form of enterovirus infection (after 1.5-2 weeks), less often - in isolation. On examination, expansion of the borders of the heart, dullness of tones, and pericardial friction noise are revealed. The course of the disease is benign, the prognosis is favorable.
Epidemic hemorrhagic conjunctivitis	sensation of a foreign body, “sand” in the eyes · lacrimation photophobia	The disease begins acutely with damage to one eye. In some cases, after 1-2 days the other eye is affected. On examination, swelling of the eyelids, hemorrhages in the hyperemic conjunctiva and scanty mucopurulent or serous discharge are revealed. The disease most often proceeds benignly, recovery occurs in 1.5-2 weeks.

Enterovirus infection and pregnancy[ 15-17 ] :
A newborn can become infected in utero, but more often during childbirth or immediately after it. The outcome depends on the virulence of the particular circulating serotype, the mode of transmission, and the presence or absence of passively transmitted maternal antibodies.
Coxsackie infection during pregnancy can cause congenital malformations of the cardiovascular (tetralogy of Fallot, aortic atresia, tricuspid valve atresia), genitourinary and digestive systems in the newborn. Enterovirus can cause severe infection of the central nervous system in newborns.

Epidemiological history:
· contact with a patient with fever, symptoms of intoxication, symptoms of damage to the central nervous system, gastrointestinal tract, muscles, mucous membrane, skin, during the last 2-10 days;
· contact with a virus carrier or a patient with a confirmed diagnosis of “Enterovirus infection” during the last 2-10 days;
· transmission routes - water, food, household contact, airborne droplets, transplacental;
· transmission factors - feces, conjunctival secretions, saliva, tears, nasal contents, sputum, vesicle contents (exanthema), food products (water, vegetables, less often milk), household items (toys);
· epidemiological factors:
- failure to maintain personal hygiene;
- drinking water from drinking fountains;
- failure to comply with “respiratory etiquette” (failure to use masks, handkerchiefs);
- swimming in fountains and stagnant ponds;
-staying in crowded places, in public transport;
- buying products “from hand”;
- seasonality summer-autumn;
- family and group outbreaks are characteristic.
· the disease is widespread, susceptibility is universal;
· risk groups: children (more often), young people, pregnant women, people with impaired immune systems.

Laboratory research[ 1,2,6, 13,14 ,17 ] :
Basic:
· UAC: leukopenia, leukocytosis, relative lymphocytosis, monocytosis, moderate increase in ESR.
· OAM: proteinuria, cylindruria, microhematuria (with toxic kidney damage).
· ELISA or RPGA- paired sera are used, obtained with an interval of 10-12 days (the first on the 4-5th day of illness, the second after the 14th day of illness). The diagnostic criterion is an increase in antibody titer by 4 times or more.
· PCR feces (nasopharyngeal mucus) on Enterovirus: RNA detection Enterovirus.
CSF examination (for meningitis):
- color - the cerebrospinal fluid is transparent or slightly opalescent;
- pressure - liquid flows out in a stream or frequent drops;
- lymphocytic pleocytosis;
- increase in protein to 1-4.5 g/l (the highest - with the development of meningoencephalitis);
- sugar is normal;
- reduction of chlorides.

Additional:
· immunochromatographic test of feces for enterovirus;
· test Xpert EV for enterovirus in CSF samples from patients with symptoms of meningitis (based on PCR analysis).

Instrumental diagnostic methods- carried out according to indications (if complications develop):
· ECG: signs of myocarditis;
· Chest X-ray: signs of pneumonia;
· CT and MRI of the brain: cerebral edema, signs of meningoencephalitis, dyscirculatory encephalopathy;
· Ultrasound: assessment of the size of the liver and spleen;
· EchoCG: signs of myocarditis, endocarditis, heart failure;
· EEG: signs of convulsive activity, brain death due to encephalitis.

Indications for consultation with specialists:
Indications for consultation with other specialists are determined by the form of infection:
· consultation with a surgeon - for epidemic myalgia;
· consultation with an ophthalmologist - for epidemic hemorrhagic conjunctivitis;
· consultation with a cardiologist - for pericarditis and myocarditis;
· consultation with a neurologist - for meningitis and the meningoencephalitic form of enterovirus infection;
· consultation with a pulmonologist - in case of development of pneumonia and bronchitis;
· consultation with a dermatologist - in case of damage to the skin;
· consultation with a resuscitator - to determine the indications for transfer to the ICU.

Diagnostic algorithm:(scheme)

Differential diagnosis

Differential diagnosis and rationale for additional studies[1,2,5-12,17 ]

Disease	Similar symptoms	Distinctive symptoms	Laboratory tests
Infectious mononucleosis	Lymphadenopathy, tonsillitis, hepatolienal syndrome, fever	Duration is no more than 1 month, systemic enlargement of lymph nodes predominates.	Positive Paul-Bunnell test. There are more than 10% of atypical mononuclear cells in the blood.
Rubella	Enlarged occipital lymph nodes, exanthema	Epidemiological history, short duration of symptoms, only the occipital lymph nodes are affected.	Antibodies to the rubella virus are in increasing titer.
Toxoplasmosis	Encephalitis, lymphadenopathy, hepatomegaly, jaundice, exanthema.	Epidemiological history, chorioretinitis, calcifications in the brain, visceral lesions.	Bacteriology, serology, RSK, RNIF, skin test
Acute meningoencephalitis (viral, bacterial etiology).	Meningeal, encephalic syndrome, polio-like syndrome	Epidemiological history, the clinical picture is more clearly defined, with bacterial non-meningococcal meningitis - the presence of foci of infection.	Microbiology, serology, virology, immunofluorescence diagnostic method
Adenovirus infection	Fever, nasopharyngitis, lymphadenitis	Epidemiological history, acute course, lymphadenitis of predominantly regional lymph nodes	Virology, serology with increasing antibody titer, immunofluorescence study, hemogram.
Enterovirus infection	Fever, exanthema, polyadenia, hepatolienal syndrome, encephalitis.	Herpangina, diarrhea, lymphadenitis is less pronounced.	Serology in increasing titer.
Sepsis	Fever, intoxication, multiple organ manifestations, exanthema, meningitis, otitis media, sinusitis, pneumonia.	Presence of a primary focus (skin, lungs, intestines, etc.)	Isolation of the pathogen from blood and other material, negative test for HIV-AT, hypogammaglobulinemia, normal amount of CD-4.
Chronic viral hepatitis	Decreased appetite, enlarged liver, spleen, polyadenia, jaundice.	Connection with previous viral hepatitis, symptoms are moderate, multiple organs are not typical.	GV markers (A, B, C, D) in the blood serum, decreased CD-8, normal CD-4 level.
Intestinal infection, salmonellosis (generalized form).	Diarrhea, weight loss, fever, intoxication, presence of lesions in other organs (meningitis, pneumonia)	Generalized forms develop only in children in the first months of life. The premorbid background is burdened, most often a nosocomial infection	Stool, blood cultures, serology (RPHA)
Helminthic infestations.	Decreased appetite, lethargy, weight loss, diarrhea, polyadenia.	Epidemiology, malabsorption syndrome is not typical.	Detection of helminth larvae in feces, duodenal contents, sputum, urine.
Tuberculosis	Polyadenia, intoxication, lung damage, central nervous system, fever, weight loss, weakness, hepatolienal syndrome.	Epidemiological history, presence of the primary complex in the lungs	Bacteriology - isolation of BC from sputum, Rg - examination of the lungs (foci, cavities). Tuberculin tests.
Mumps and mumps of other etiologies.	Enlargement of the parotid salivary glands.	With parotitis: occurs acutely, resolves within 10 days, other salivary glands, orchitis, pancreatitis may be involved. With a tumor, salivary stone disease, the process is one-sided.	Serological studies with increasing antibody titer (IATI). Rg - logical research methods.

Diagnosis	Rationale for differential diagnosis	Surveys	Diagnosis exclusion criteria
Serous meningitis and meningoencephalitic form of enterovirus infection	Mumps infection Tuberculous meningitis Meningococcal infection Pneumococcal meningitis Hib meningitis	Mumps, pancreatitis, orchitis Bacterial examination of blood, cerebrospinal fluid, sputum for TBC, Bacterial examination of a throat smear, cerebrospinal fluid, blood for meningococcus, pneumococcus, hemophilus influenzae	-ELISA (IgM) -PCR of feces
Epidemic myalgia	Acute surgical pathology Pleurisy Angina pectoris	Surgeon consultation X-ray of the lungs ECG	-PCR of blood, cerebrospinal fluid
Poliomyelitis-like form of enterovirus infection	Polio	Virological examination of blood and stool	-RN, RSC, RTGA and precipitation reaction in gel with enteroviral antigen -PCR of blood, cerebrospinal fluid -virological examination of nasopharyngeal mucus, CSF, feces, blood
Enteroviral exanthema	Scarlet fever Measles Rubella Allergy	Stages of rashes, nature and localization of exanthema	-RN, RSC, RTGA and precipitation reaction in gel with enteroviral antigen -PCR of blood, cerebrospinal fluid -virological examination of nasopharyngeal mucus, CSF, feces, blood
Herpangina	Aphthous stomatitis		-RN, RSC, RTGA and precipitation reaction in gel with enteroviral antigen -PCR of blood, cerebrospinal fluid -virological examination of nasopharyngeal mucus, CSF, feces, blood
Enteroviral diarrhea	Acute diarrheal infections	Bacterial examination of feces for pathogenic flora	-RN, RSC, RTGA and precipitation reaction in gel with enteroviral antigen -PCR of blood, cerebrospinal fluid -virological examination of nasopharyngeal mucus, CSF, feces, blood

Algorithm for the differential diagnosis of serous meningitis:

Symptoms	Enteroviral meningitis	Mumps meningitis	Tuberculous meningitis
Age		Preschool and school age	Any
Epidemiological background	Summer autumn	Winter spring	Social factors or contact with a patient, history of pulmonary or extrapulmonary tuberculosis, HIV infection
Onset of the disease	Acute	Acute	Gradual, progressive
Clinic	Headache, sharp, short-lived, repeated vomiting, fever up to 38.5-39ºС, two-wave fever with intervals between waves of 1-5 days	At the height of the disease, after inflammation of the salivary glands, but sometimes before the development of mumps, severe headache, vomiting, and hyperthermia appear	Moderate headache, fever up to 37-39ºС
Organ damage	Enteritis, exanthema, herpangina, myalgia, hepatolienal syndrome	Damage to the salivary glands (mumps, submaxillitis, sublinguitis), orchitis, pancreatitis	Specific damage to various organs, tuberculosis of lymph nodes with hematogenous dissemination
Meningeal symptoms	From the 1st-2nd day of illness, mild, short-term, absent in 20% of cases	Positive meningeal symptoms	Moderately expressed, in dynamics with increasing
General blood analysis		Normal, sometimes slight leukocytosis or leukopenia, neutrophilia, moderate increase in ESR	Minor changes in leukogram parameters, moderate increase in ESR
Color, transparency of cerebrospinal fluid	Colorless, transparent	Colorless, transparent	Transparent, when standing for 72 hours, a delicate film of fibrin falls out
Pleocytosis (cells/µl)	At the beginning mixed, then lymphocytic from several hundreds to 2000	Lymphocytic from several hundreds to 500	Mixed from 30 to several hundreds
Protein content in liquor (g/l)	Normal or reduced	Normal or increased to 1.0	1,0-10,0
Glucose content in liquor	Moderately increased	Normal or moderately increased	Significantly reduced
Chloride content (mmol/l)	Moderately increased	Moderately increased	Significantly reduced

Differential diagnosis of diseases accompanied by exanthema:

Symptoms	Meningococcemia	Measles	Scarlet fever	Pseudotuberculosis	Enteroviral exanthema
Onset of the disease	Acute, often violent, with an increase in body temperature, a violation of the general condition	Catarrhal symptoms and intoxication, increasing over 2-4 days	Acute, fever, sore throat, vomiting	Acute, with a gradual increase in symptoms, fever, abdominal pain	Acute, with an increase in body temperature, a violation of the general condition
Temperature response	Rapid rise to high numbers in the first hours of the disease	Up to 38-390C, two-wave (during the catarrhal period and during the period of rashes)	High, up to 38-39C0 for 2-3 days	High, prolonged fever, which may be wavy	from subfebrile to febrile numbers of various duration (from 1 to 7-10 days)
Intoxication	Expressed	Expressed within 5-7 days	Expressed	Pronounced, long-lasting	Moderately expressed
Qatar of the upper respiratory tract	Phenomena of nasopharyngitis	Severe: barking cough, rhinitis, conjunctivitis	Absent	Absent	Herpetic rashes on the palatine arches, soft palate, signs of pharyngitis
Time of appearance of the rash	1st day of illness, first hours of illness	On the 3-4th day of illness	1-2 days of illness	3-8th day of illness	1st-3rd day of illness
Order of rashes	Simultaneously	Stages of rashes, starting from the face, over 3 days	Simultaneously	Simultaneously	Simultaneously
Mophrology of the rash	Hemorrhagic, stellate, irregularly shaped, with necrosis in the center	Maculopapular, irregular in shape, prone to merging on an unchanged skin background	Finely punctate, abundant, hyperemic no skin background	Polymorphic (small dotted, finely spotted) on a constant skin background	Punctate or small maculopapular, sometimes hemorrhagic
Rash size	From petechiae to extensive hemorrhages	Medium and large	Small	Small	Small
Localization of the rash	Buttocks, thighs, less often - arms and face	Depending on the day of the rash (1st day - on the face, 2nd day - on the face and torso, 3rd day - on the face, torso and limbs)	Throughout the body (except for the nasolabial triangle), mainly on the flexor surfaces, symmetrical thickening in natural folds	On the flexor surfaces of the limbs, around the joints, like “socks”, “gloves”, “hood”	On the face, torso and limbs
Reversal of the rash	Necrosis and scars at the site of extensive hemorrhages	It turns into pigmentation in the same order in which it appeared	Disappears without a trace after 3-5 days	Disappears without a trace	The rash persists for several hours or a day and disappears without leaving a trace of pigmentation.
Peeling	Absent	Small pityriasis	Large-lamellar, at 2-3 weeks of illness	Small pityriasis on the body and large-plate on the palms and feet on the 5-6th day	Absent
Changes in the oropharynx	Hyperemia, hyperplasia of lymphoid follicles of the posterior pharyngeal wall	Diffuse hyperemia of the mucous membrane, Belsky-Filatov-Koplik spots, enanthema on the soft palate	Limited hyperemia of the pharynx, the phenomenon of purulent sore throat, crimson tongue	Raspberry tongue	On the mucous membrane of the palatine arches and soft palate there are papules, which dynamically turn into vesicles. After 1-2 days, the vesicles ulcerate and become covered with white detritus.
Changes in other organs and systems	May be associated with meningitis	Conjunctivitis, laryngitis, pneumonia	Absent	Damage to the intestines, liver, spleen, joints	May be combined with meningitis, herpangina
General blood analysis	Hyperleukocytosis, neutrophilia, increased ESR	Leukopenia, neutropenia, in case of complications - increased ESR	Leukocytosis, neutrophilia, accelerated ESR	High leukocytosis and neutrophilia, significant increase in ESR	Moderate leukocytosis with neutrophilia, ESR within normal limits or moderately elevated

Treatment abroad

Herpetic sore throat is an acute infectious inflammation that involves the tissue of the posterior wall of the pharynx, tonsils, and palate with the appearance of vesicular rashes on them, prone to ulceration. In children, especially under 3 years of age, the course is often severe, with pronounced soreness of the oral cavity and high fever. Herpes sore throat is dangerous due to the development of severe complications of the kidneys, brain and heart. There is no specific treatment for the disease, which is why prevention and knowledge of the routes of infection are so important.

What is herpes sore throat in children

Herpetic sore throat is an acute, virally caused inflammatory lesion of the tissue of the palatine tonsils, pharyngeal ring, palate in the form of rashes. In children, the rash often covers not only the epithelium of the oral cavity, but also the skin around the mouth, hands and feet. In international pediatrics, this symptom is called “hand-foot-mouth.”

Despite the name, this disease is not caused by the herpes virus, and it has nothing to do with herpes or true sore throat. The pathological condition is caused by enteroviruses Coxsackie A, B or ECHO (echoviruses). And the name of the disease is associated with the similarity of visually observed vesicles (small vesicular formations filled with whitish contents) on the mucous membrane of the tonsils and pharynx with herpetic vesicles. The mention of “sore throat” emphasizes the acute sore throat characteristic of the bacterial form of tonsillitis and emphasizes that the inflammation affects the tissue of the tonsils.

Synonyms for herpetic tonsillitis are ulcerous tonsillitis, herpetic tonsillitis, Zagorsky's disease, vesicular pharyngitis, herpangina. The scientifically approved name of the disease in medicine is enteroviral vesicular stomatitis.

In pediatrics, herpes sore throat is more common in children aged 3 to 10 years. The most severe course of the disease and the development of complications are observed in children under 3 years of age, although at this stage the disease is rare.

In newborns and infants, vesicular stomatitis develops much less frequently, which is associated, as pediatricians believe, with the acquisition of certain antibodies from the mother through the placenta in the prenatal period and later - during the period of newborns and breastfeeding - along with breast milk (so-called passive immunity).

Herpetic sore throat can occur both as a separate disease and as a concomitant or preceding pathology with encephalitis, meningitis, myalgia, which are also provoked by exposure to the Coxsackie virus.

Rashes in a child around the mouth, on the arms and legs are a sign of herpetic sore throat

Causes of development and mechanisms of infection

The cause of the development of enteroviral vesicular stomatitis is the RNA-containing Coxsackie and ECHO viruses, which belong to the group of enteroviruses. Provoking factors:

low resistance of the child's body;
frequent ARVI;
weak local protection function of mucous membranes.

Enteroviral stomatitis in childhood is often observed in the form of an epidemic outbreak among children. The peak prevalence of sore throat in children's groups (schools, kindergartens and camps) and families occurs from June to September. In warm air, enteroviruses spread much more actively. The disease is highly contagious.

Pathogenic viruses can be transmitted through three routes:

airborne (communication, coughing, sneezing);
fecal-oral (through infant nipples and dishes, food, toys, dirty fingers that children put in their mouths);
contact (saliva, nasopharyngeal secretions).

There is an assumption that infection with the Coxsackie virus is possible through water when swimming in rivers near sewer discharge points.

The main source of infection is a sick child who is a carrier, and sometimes a pet. Recovering children can also spread the infection, since the pathogen is released within a month after the patient’s condition returns to normal. The pathogens invade the cells of the mucous membrane of the nasopharynx, penetrate through the lymphatic tract into the intestines, multiply rapidly and penetrate the blood, spreading throughout all tissues and organs. The degree of spread and reproduction depends on the type of pathogen and the strength of the immune defense. Lingering in tissues, viruses provoke the development of inflammation and necrosis (areas with dead cells).

Both Coxsackie viruses and echoviruses specifically and selectively infect tissue cells of nerves, mucous membranes and muscles (including the heart). Having penetrated the thickness of the oral mucosa, the virus actively multiplies, causing swelling of cells and their death. In the area of necrosis, fluid accumulates and vesicles form. After the bubbles burst, their contents flow out. Some pathogens die, others are eliminated in the stomach by the body’s immune complexes.

Often, herpes sore throat in childhood begins when the child is ill with influenza or ARVI. If the baby has been ill, the body develops a stable protective reaction of the immune system to the viral strain that caused the disease. But when a pathogen of another type is introduced into the body, there is a possibility of a new infection. However, repeated enteroviral stomatitis in pediatrics is quite rare.

Doctor Komarovsky talks about enteroviruses - video

Symptoms of enteroviral vesicular stomatitis

In children, the latent (incubation) period usually lasts from 7 to 14 days. It happens that it is shortened to 2–5 days. At this time, the child is a carrier of the virus, but does not feel any symptoms of the disease.

General and specific signs

The onset of infection resembles the symptoms of influenza:

Malaise, severe weakness.
Disorders of appetite, sleep.
Fever up to 39–40 °C (acute onset, temperature rises within 2–4 hours);
Skin soreness.
Nausea, attacks of vomiting (the younger the child, the stronger the severity of intoxication).
Pain in the head, back and abdominal muscles, limbs.
Pain when moving the eyeballs or light pressure on them.
Diarrhea is possible, especially often in children under 2 years of age. This occurs due to the influence of enteroviruses, which actively affect the mucous membranes of the digestive organs, causing dysfunction.

Specific symptoms accompany general ones. This:

severe pain in the throat, acute - when trying to swallow, contact of the affected areas with pieces of food and water; newborns and infants usually refuse the mother's breast and bottle;
increased salivation, irritation in the corners of the mouth;
runny nose, nasal congestion;
cough.

Clinical picture of herpetic sore throat

With enteroviral vesicular stomatitis, a rapid change in the condition of the mucous membrane occurs. In the first 24–48 hours the following is observed:

severe redness and swelling of the tonsils, palatine arches, back of the pharynx, tongue;
painful enlargement of the lymph nodes under the neck, jaw, behind the ears - on both sides;
the appearance in the mouth and on the tonsils of small, up to 2–3 mm in diameter, papules (nodules) of a reddish color, which after 2 days lighten, turning into water-filled bubbles - vesicles, surrounded by an inflamed red rim. Their peculiarity is a high degree of pain.

Swelling, hyperemia, red dotted rashes - signs of herpetic sore throat

After 48–72 hours, the blisters burst with their contents flowing out and the formation of white-gray ulcers with pronounced redness along the contour. At this stage, the child cannot swallow food due to a very severe sore throat.

The more severe the course of the disease, the more abundant the rash in the oral cavity. In typical cases, the number of vesicles does not exceed 10–12; in severe cases, 20 or more are found. Often, ulcers merge into painful erosions (so a child of any age refuses to eat).

By the end of 4–5 days of illness, the ulcers are covered with crusts. On days 6–8 after the appearance of ulcerations on the mucous membrane, the crusts that appear in their place are easily washed away along with saliva, leaving no traces. Swelling of the tonsils and inflammation in the pharynx are reduced. On days 8–10, the soreness of the lymph nodes disappears. Inflammation of the lymph nodes and their reduction in size occurs by 10–15 days.

Many children have erased signs of herpetic sore throat, manifested by severe swelling and redness of the mucous membrane, but without vesicles and erosion. If the child is weakened, vesicular rashes often recur after 2–3 days. This is accompanied by a jump in body temperature and an increase in all symptoms associated with intoxication of the body.

If the body's resistance is low, there is a danger of the virus spreading through the bloodstream and developing dangerous and serious diseases: meningitis, hemorrhagic conjunctivitis, myocarditis or pyelonephritis.

Diagnostics

If the course of herpetic sore throat occurs in a typical form, the otolaryngologist is able to clarify the diagnosis without laboratory tests or instrumental examination. Examination of a child's oral cavity reveals a typical arrangement of rashes in the form of papules, vesicles, ulcers on the tonsils, palate, and pharyngeal mucosa at various stages of maturation and healing. A blood test shows a slight increase in the number of white blood cells, which indicates inflammation.

The use of laboratory techniques is necessary if the complex of symptoms is similar to signs of diseases of another origin. In case of erased or atypical course of herpes sore throat, the following are prescribed:

PCR (polymer chain reaction) method. To study a washout and a smear taken from a child’s nasopharynx - it allows you to accurately determine the pathogen with a microscopic amount of fluid from the vesicles.
ELISA method (enzyme-linked immunosorbent assay). Detects a fourfold increase in the number of antibodies (immune system reaction) to enteroviruses.
Consultation with a neurologist. To exclude the development of serous meningitis when the virus spreads throughout the body and penetrates the meninges.
Examination by a cardiologist. To prevent or begin treatment of possible myocardial pathologies if a child complains of pain in the heart area.
Consultation with a nephrologist. To exclude or confirm the diagnosis of pyelonephritis if changes in urine are observed.

Herpetic sore throat is differentiated from other pathologies - thrush (in infants and newborns), chickenpox, herpetic stomatitis:

Thrush is characterized by a white, cheesy coating on the tongue, gums, and inner surface of the cheeks, which, after removal, leaves an inflamed and reddened area.
With herpetic stomatitis, the blisters are localized mainly on the child’s tongue and gums, and with enteroviral vesicular stomatitis, the rashes cover the tonsils, pharynx and palate. Practice shows that up to 3–4 years of age, herpes sore throat affects children much more often than herpetic stomatitis.
When a child suffers from bacterial tonsillitis, whitish vesicles are often mistaken for pus. But purulent formations in follicular, lacunar tonsillitis form only on the tonsils, without extending beyond them to the pharynx area. In addition, a runny nose, common with herpes sore throat, is not a typical symptom for purulent sore throat.
Catarrhal tonsillitis may resemble an erased form of herpetic tonsillitis, which occurs without a rash in the oral cavity. However, with the catarrhal form there is rarely a runny nose. If nasal congestion and discharge occurs, the baby is more likely to develop a viral infection.

Vesicles surrounded by a red border cover the upper palate with herpes sore throat

Treatment

Specific treatment for herpangina aimed at destroying the virus has not yet been developed. Therapy involves mitigating the symptoms and manifestations of intoxication while the child’s immune system independently copes with the viral infection. Comprehensive treatment includes:

first of all - isolation of children sick with enteroviral vesicular stomatitis;
carrying out general and local therapy.

Essential medications:

Antiallergic drugs (Dezal, Zodak, Diazolin, Claritin, Erius), which reduce the effect of viral toxins, relieve swelling and itching.
Drugs that relieve fever and pain - children's forms of Paracetamol, Efferalgan, Ibuprofen, Nimesulide, Nurofen.
Oral antiseptics to prevent the development of bacterial infections: furatsilin in a rinse solution, Chlorhexidine.
Means for the treatment and pain relief of ulcers - a solution of sodium tetrobarate in glycerin 10%, a solution of marborane in dimexide 5%.
Bactericidal and painkillers - Ingalipt, Tantum-Verde, Orasept, Theraflu Lar, lidocaine solution 2%, Hexoral tabs, Panavir. The use of aerosols in children under 3 years of age is unacceptable - they can provoke laryngospasm.
Absorbable tablets for pain relief and ulcer healing - Lizobact, Decathylene.

Medications in the photo

Sodium tetrobarate is used for pain relief and healing of vesicles and mouth ulcers
Efferalgan baby suppositories are used from 6 months for fever, inflammation and pain Nurofen in the form of a suspension - a children's remedy for relieving fever and pain Tantum Verde will help with pain and inflammation in the oral cavity

In addition to pharmacological treatment, the following measures are necessary:

Excessive feeding of the child. Infection, dehydration and poisoning of a child's body with toxins occurs very quickly, especially in infancy. The more fluids a child takes, the easier it is for the body to regulate temperature and reduce poisoning from viral toxins. Since it is painful for the baby to drink, you should drink it slowly, one teaspoon at a time. An older baby may be interested in drinking through a straw or a fun new sippy cup.
Active gargling. The procedure is carried out every half hour or hour with decoctions of medicinal herbs (popular folk remedies such as chamomile, calendula, sage), saline and soda solutions reduce inflammation, relieve pain, disinfect, wash away viral agents and crusts from ulcers. But this method is only available to children who already know how to do it. For a child who has not yet learned to gargle, you can try irrigating the throat with warm infusions from a syringe without a needle, if you promise something pleasant. Realizing that it is not painful and not scary, he gets used to it and opens his mouth himself, spitting out water.
Bed rest is necessary for the child during the acute period of illness (the first 3–5 days) until the temperature returns to normal.

Normally, herpetic sore throat in childhood lasts from 8 to 15 days, depending on the age group, the severity of stomatitis, and the stability of the immune system.

It is useless to try to treat herpetic sore throat with medications such as:

Antibiotics. The disease is caused by viruses, and the use of antibiotics will have no effect. Antibacterial treatment is carried out if a pyogenic infection is associated with viral stomatitis. In such cases, Amoxiclav and Sumamed in the form of children's suspensions are used for children.
Antiherpetic medications. Herpetic viruses have no effect on the development of enteroviral vesicular stomatitis. Therefore, the use of Acyclovir, Zovirax and its analogues for herpes sore throat is useless, but the likelihood of side effects remains.
Broad-spectrum antiviral drugs and immunomodulators. The effectiveness of these pharmacological agents for herpetic sore throat has not been confirmed, however, the side effects of these drugs in childhood can be pronounced.

carrying out any inhalations and using compresses - heating activates blood circulation at the site of inflammation and helps the movement of pathogens through the bloodstream to all organs;
smear ulcers and blisters with Lugol's solution, iodine, brilliant green and other agents that burn the mucous membrane and cause additional acute pain to the child.

Possible consequences and complications

Basically, herpetic sore throat in children ends with complete recovery, without consequences. The prognosis for any age is usually favorable. However, without treatment in children with weak immune systems, the virus can spread through the blood and cause damage to many organs - generalization of the infection occurs.

It is possible to develop such severe complications as:

Pyelonephritis is inflammation of the renal pelvis.
Serous meningitis. There are known cases of the disease after healing from herpes sore throat.
Kernig's syndrome is irritation of the meninges during the development of meningitis.
Encephalitis is inflammation of brain tissue.
Myocarditis is an inflammatory process in the heart muscle.

If there are any strange signs - severe pain in the head, convulsions, loss of consciousness or the appearance of disorientation in the baby, calling an ambulance and contacting a neurologist should be done immediately. If the child is less than a year old, urgent hospitalization is required.

With the development of meningitis, the death of young patients is most often recorded from the neonatal period to three years.

Disease prevention

For children with herpetic sore throat and other children who come into contact with them, a two-week quarantine is established. There is no vaccine against the disease. But it is possible to administer specific gamma globulin to children who have interacted with a sick child. Other preventive measures are aimed at early detection of signs of enteroviral vesicular stomatitis in children and strengthening the body’s immune system.

You can reduce the likelihood of infection:

strengthening the child’s immunity through good nutrition, sleep patterns, and hardening;
isolating the baby from communication with sick or recovering children.

Enteroviruses have exceptional resistance to detergents, high acidity, and chlorinated water. They can only be destroyed by heat treatment at a temperature not lower than 50–60 °C.

With vesicular enteroviral stomatitis, parents of sick children should remember that the disease is not of bacterial origin, but of viral origin, and special treatment has not been developed for this type of inflammation. The goal of therapy is to alleviate the symptoms that cause distress and pain to the child. The main thing is not to miss the moment when bacterial inflammation joins a viral infection and the spread of pyogenic bacteria through the blood in order to prevent the development of severe complications and quickly begin treatment without wasting time.