Otitis

Herpetic sore throat, its symptoms and photos of the throat in children and adults. Enterovirus infection Case history enterovirus infection herpangina

Every year, hundreds of Ukrainian children become infected with enterovirus infections, which manifest themselves in the form of rashes and sores on the hands, soles of the feet, mouth and throat against the background of a rise in body temperature to +38°C or more. Infection occurs most often in summer at beach resorts. Many people infected with enteroviruses experience the disease with minimal complaints or are completely asymptomatic, but can remain carriers of the viruses for several months. An infection that has entered the body usually disappears within 5-10 days on its own without any special treatment. Enterovirus infections are transmitted by airborne droplets or fecal-oral routes. Most often they affect children under the age of 10 years (children under the age of 5 are especially susceptible to these diseases).

There are typical and atypical forms of enteroviral infections. Typical forms of infection include herpangina, exanthema, epidemic myalgia and aseptic serous meningitis. Atypical - uveitis, pancreatitis, nephritis, encephalomyocarditis of newborns, mixed infections.

Symptoms of enterovirus infection

They begin to appear approximately 3-7 days after the first contact with the virus. The symptoms are quite varied: nausea, vomiting, watery stools up to 10 times a day, various rashes. Body temperature is high, sometimes up to 40 degrees. Usually 1-2 days after the end of the fever, a rash appears on the arms, legs, and mouth in the form of red spots with blisters (vesicles).

The rash on the skin may resemble chickenpox, and in the mouth - (it is important to remember that these diseases are caused by various pathogens, and the herpes virus has nothing to do with enterovirus infection, so in the latter case it is useless to lubricate the blistering rashes with acyclovir ointment). Other symptoms of this disease: loss of appetite, headache, ulcers in the mouth, tongue, and throat. Sometimes patients may have almost no symptoms of the disease, but at this time they are still a source of infection of the virus to other people.

Most often, enteroviruses cause diseases in children, as well as in patients with weakened immune systems. In both cases, patients may have a fever and sore throat, followed by mouth sores a few days later.

Complications resulting from enterovirus infection occur rarely, and the disease usually goes away on its own, but there are exceptions. Sometimes dehydration occurs and a secondary bacterial infection develops. Very rarely, meningitis, encephalitis, acute flaccid paralysis, and heart damage may develop

Treatment and prevention of enterovirus infection

There are no special medications for the treatment of enterovirus infection. There is also no vaccine against these diseases. The disease goes away on its own in 3-10 days (sometimes two weeks). It is not recommended to use antibiotics, antivirals, etc., since in this case they do not bring benefit, but, on the contrary, can even cause harm. Therefore, doctors advise that in case of enteroviral exanthemas, relieve pain, ease the patient’s well-being with the help of non-steroidal anti-inflammatory drugs and rinsing the mouth with a special solution, prevent dehydration (drink plenty of fluids), and also monitor for complications (if they appear, consult a doctor immediately). The best prevention of enterovirus infection is to avoid contact with infected people, disinfect objects that may have the virus and, of course, drink only boiled or bottled water. You should also wash your hands regularly with soap and hot water.

What is Herpetic tonsillitis (herpetic tonsillitis)

Herpangina(syn.: ulcerous tonsillitis, aphthous pharyngitis, vesicular pharyngitis) - an acute infection with a sudden rise in body temperature, dysphagia, pharyngitis, sometimes abdominal pain, nausea and vomiting.

A characteristic sign of herpetic sore throat- vesicular rashes prone to ulceration on the back of the pharynx or soft palate.

What causes herpetic sore throat (herpetic tonsillitis)

Herpetic sore throat was described by T. Zagorsky in 1920. The causative agents are Coxsackie viruses of group A, most often the lesions are caused by viruses of serovars 2-6, 8 and 10. Less commonly, herpetic sore throat is caused by Coxsackie viruses of group B or ECHO viruses.

Pathogenesis (what happens?) during Herpetic tonsillitis (herpetic tonsillitis)

Coxsackie viruses are ubiquitous. There is a characteristic seasonality of incidence with an increase in the summer-autumn months. The main routes of transmission are fecal-oral and contact (through nasopharyngeal secretions). The routes of entry and spread of the pathogen are identical to those of polioviruses. The main natural reservoir is humans, but infection is also possible from various animals, such as pigs.

Symptoms of Herpetic tonsillitis (herpetic tonsillitis)

Incubation period is 7-14 days. The disease begins with a severe flu-like syndrome; characterized by decreased appetite, malaise, irritability, fever and weakness. Later, sore throat, drooling (pain localized in the nasopharynx and pharynx) and acute rhinitis appear. Then, on the back wall of the pharynx, tonsils, soft palate, uvula, and the front part of the oral cavity, vesicles with serous contents appear, surrounded by a halo of hyperemia, reminiscent of herpetic lesions. Bilateral anterior cervical lymphadenopathy is characteristic. The elements gradually dry out with the formation of crusts, sometimes the blisters can ulcerate or fester (the addition of bacterial infections). In more severe cases, diarrhea, nausea and vomiting may occur.

Complications
When the process is generalized - meningitis, encephalitis and myocarditis.

Diagnosis of herpetic sore throat (herpetic tonsillitis)

An accurate diagnosis of herpetic sore throat is established using virological and serological studies. The material for virological research is pharyngeal swabs (during the first 5 days of illness). For a serological study (neutralization reaction) to detect an increase in antibody titer, sera collected in the first days of the disease and after 2-3 weeks are used. The most informative of the laboratory diagnostic methods is the immunofluorescence method.

Differential diagnosis is based on the age of the child, the seasonality of the disease, the type and location of the elements of the lesion in the oral cavity. With herpetic sore throat, there are no herpetic rashes on the skin of the face, bleeding of the mucous membrane and hypersalivation are not characteristic, and there is no gingivitis. Often the disease is accompanied by the symptom of “abdominal pain” resulting from myalgia of the diaphragm.

Methods for studying herpetic sore throat
1. Blood test: moderate leukocytosis

2. Identification of the pathogen
- Test material: washings and smears from the nasopharynx, intestinal contents, which infect cell cultures (for example, HeLa or monkey kidneys) and suckling mice (the latter is especially important for the identification of group A Coxsackie viruses, which exhibit a weak cytopathogenic effect in vitro)

In the presence of a cytopathic effect, the virus is typed by adding diagnostic immune sera labeled with fluorescein

Based on the nature of pathological changes in mice, the Coxsackie virus belongs to group A or B.

Serovars are determined by the complement fixation reaction (FFR), neutralization reaction, and indirect hemagglutination reaction (IRHA) with type-specific antisera.

Treatment of herpetic tonsillitis (herpetic tonsillitis)

Treatment of herpetic sore throat is symptomatic.

Prescribe hyposensitizing drugs (Diazolin, Suprastin, Fenkarol, Claritin, Peritol, etc.) in dosages appropriate to the child’s age, and antipyretics (Tylenol, Calpol, Efferalgan, etc.).

Due to the constant trauma to the lesions and the insignificant effectiveness of drugs in the form of ointments, the disease can last 12-14 days.

Local therapy is recommended in the form of irrigation with liquids or using aerosol antiseptics, proteolytic enzymes, antiviral drugs, painkillers and keratoplastics. For this purpose, it is recommended to irrigate the affected elements with 0.1% or 0.2% enzyme solutions (trypsin, chymotrypsin, chymopsin, etc.). Then aerosols are used (“Hexoral”, “Tantum Verde”, “Ingalipt”), which have an antiseptic, analgesic, and enveloping effect.

A good effect is achieved with frequent use of liquid antiviral agents (leukocyte interferon).

To enhance epithelialization processes, it is recommended to use ultraviolet irradiation and helium-neon laser light, aerosol preparations “Vinizol”, “Panthenol”, etc., as well as tablets for resorption in the oral cavity (sebidine, faringosept), which have an antiseptic and bactericidal effect.

After general and local treatment, it is necessary to provide for the organization of a balanced diet and the inclusion of immunomodulators (Imudon, Immunal, etc.) in therapy.

Prevention. Specific vaccine prophylaxis is carried out due to the abundance of pathogenic serotypes of the Coxsackie and ECHO viruses. Gamma globulin is indicated for children who have been in contact with patients - at the rate of 0.5 ml/kg body weight.

The prognosis is favorable: the disease ends in complete recovery.

Prevention of herpetic tonsillitis (herpetic tonsillitis)

Preventive measures in epidemic foci should be the same as for other respiratory viral infections. Isolation of the first patients, if carried out on the first day of illness, is effective, as it reduces the spread of infection in the children's group. The contagiousness of patients with enterovirus infection sharply decreases from the 7-8th day of illness, and the return of the convalescent to their group at the child care facility does not lead to a relapse of the epidemic outbreak.

Which doctors should you contact if you have herpetic tonsillitis (herpetic tonsillitis)

Infectious disease specialist
Otorhinolaryngologist

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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 lamellar 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 inflammatory process in the pharynx, tonsils and palate, with vesicular rashes, often developing into ulcerations. The disease in childhood is severe.

There is pronounced pain in the oral cavity and a rise in body temperature to significant levels. The consequences are also dangerous - pathologies of the kidneys, brain, heart.

To combat this specific disease in children, preventive measures to eliminate routes of infection are important due to the fact that effective treatment measures have not yet been found.

The disease is caused by viruses.

Extensive damage occurs:

tissues of the palatine tonsils;
pharyngeal ring.

We are talking about specific rashes. Children are characterized by a rash in the mouth and surrounding area, on the face, arms and legs. Pediatricians have defined the term “hand-foot-mouth” for such symptoms.

Herpetic sore throat. Not to be confused with the herpes virus

Do not be deceived by the designation of a pathology that has nothing to do with herpes, and even more so with classic sore throat.

The process begins with the introduction of enteroviruses Coxsackie A, B, ECHO (echoviruses). Doctors called this inflammation by this term purely because of the visual similarity of tiny formations in the form of bubbles, which contain a whitish liquid inside, with herpes rashes. Herpetic blisters cause severe pain, similar to a sore throat caused by bacteria. We emphasize that inflammation also spreads to the tissues of the tonsils.

Reference. To define the disease, there are other names - ulcerous tonsillitis, herpetic tonsillitis, etc. In medical practice, pathology is usually designated by a special term (enteroviral vesicular stomatitis).

Pediatrics deals with the prevention of ulcerous tonsillitis in children from three to ten years of age. There are rare cases of the disease at an earlier age, with a long and severe course and the development of complications.

Why is this type of sore throat almost never found in newborns?

In pediatrics, this fact is associated with the presence of so-called passive immunity in infants. Babies have a certain supply of antibodies from their mother, passed on to them while still in the womb. Additional antibodies contained in mother's milk are also supplied during breastfeeding.

Herpetic sore throat. Forms of the disease

You should know about herpetic sore throat that it occurs in the form of a separate disease or component of:

encephalitis;
meningitis;
myalgia.

The listed diseases are often accompanied by exposure to the Coxsackie virus.

Enteroviral vesicular stomatitis. The mechanism of virus penetration. Causal relationship

The development of the disease begins with the penetration of RNA-containing Coxsackie viruses and ECHO (a group of enteroviruses) into the child’s body.

Contributing factors:

general weak defense mechanism;
a series of acute respiratory diseases;
insufficient ability to protect mucous tissues (local immunity).

The disease manifests its insidiousness in the form of an unexpected epidemic spreading in children's groups (school, kindergarten, recreation centers). The three summer months and September are considered the most dangerous period. Warm air, which is favorable for the survival of viruses, increases the possibility of infection.

Three ways of distribution:

through the air (talking, coughing, sneezing);
dirty fingers - into the mouth (pacifier, baby dishes, food, household items);
tactile contacts (discharge from the nasopharynx).

Note. Doctors advise avoiding swimming in bodies of water with sewer outlets in the summer. It is believed that this is another way of contracting the virus.

Children usually become infected from each other. But these can also be pets.

Important! It is important to keep in mind that the child’s recovery does not mean that he has ceased to be a source of infection. For a month after recovery, the pathogen (disease-causing infection) continues to be released.

The pathogens first occupy the mucous membrane of the nasopharynx, then penetrate through the lymphatic pathways into the intestines and into the blood, gradually attacking all tissues and organs. The spread and reproduction of viruses is determined by the pathogen itself and the degree of “combat efficiency” of the immune system. Pathology provokes new foci of inflammation and expanding areas with dead cells.

Algorithm for the impact of Coxsackie viruses and echoviruses:

Selectively damages cells in nerve tissue, mucous membranes and muscles, including the heart.
Penetration into the depths of the oral mucosa.
Reproduction.
Swelling and cell death.
Formation of fluid and vesicles.
Bursting of bubbles and leakage of whitish liquid.

In this case, some of the pathogenic flora dies. The rest of the microflora is dealt with (when it enters the stomach) by the body’s immune system.

Note. Be careful if your child is sick with respiratory pathologies and the flu. They may be accompanied by herpes sore throat. A viral strain that was previously defeated by the child’s body is no longer dangerous, but an introduced new pathogen can cause the rapid spread of a different type of inflammatory process. Recurrence of enteroviral stomatitis is an extremely unlikely prognosis.

Herpetic sore throat. Symptoms

The latent form of the disease varies from seven to fourteen days, in some cases up to several days. This is a dangerous period, since the child is already a virus carrier, although symptoms have not yet appeared.

General picture of the disease and specific manifestations

The onset of the acute phase of the disease is similar in symptoms to influenza symptoms:

Severe malaise.
Disturbed appetite and sleep.
Raising the temperature to 40 °C for several hours.
Painful sensations on the skin.
Severe intoxication (nausea, vomiting).
Feelings of pain in the head, muscles, arms, legs, back and abdomen.
Pain syndrome when rotating the eyeballs.
Diarrhea in children under two years of age. Enteroviruses actively attack the mucous membrane of the digestive system, disrupting its functional abilities.

Specific pattern of symptoms:

Feeling of severe pain in the throat, aggravated by swallowing food. Refusal of infants from mother's milk or liquid cereals from a bottle.
Excessive salivation, irritation around the mouth.
Obstruction of the nasal passages, runny nose, frequent cough.

Analysis of the clinical picture

A characteristic feature of enteroviral vesicular stomatitis is the rapidly deteriorating condition of the mucous membrane.

Over the course of two days:

Visually noticeable redness and increase due to swelling in the volume of a number of organs (tonsils, palatine arches, posterior wall of the pharynx, tongue).
Painful reaction of the lymph nodes. Pay attention to the neck, lower jaw, area behind the ears.
Formation of small nodules in the oral cavity and on the tonsils. We are talking about reddish papules with a diameter of several millimeters. Over the course of two days, the nodules fill with liquid and lighten, becoming bubbles -

vesicles, whitish dots surrounded by inflamed red rims. These formations are very painful and unpleasant for the child in a physiological and psychological sense.

After three to four days, the vesicles begin to burst, exudate flows out of them, and white or gray ulcers with a pronounced red rim form in place of the former vesicles. An extremely painful period begins for the baby - the impossibility of adequate nutrition due to severe pain in the throat while eating food or drinking.

The severity of the disease directly depends on the abundance of rashes in the oral cavity. If the number of nodules is about ten, we are talking about moderate severity; if their number is more than twenty vesicles, the process has acquired a severe form. Often, local and extremely painful erosion forms at the site of ulcer formation. Be prepared for the child to completely refuse any food!

Five days have passed

The ulcerative formations began to heal with crusts. After a few more days, the crusts from the mucous membrane are removed without problems or traces through the process of salivation. The tonsils decrease in volume, their swelling disappears, inflammation in the pharynx “dieses down,” the lymph nodes stop hurting and gradually regain their original shape. Full recovery takes ten to fifteen days.

Hidden form. Repetition (relapse)

There is also a hidden course of the disease. In a child, severe swelling and redness of the mucous membrane can be detected, but vesicles and erosion do not form.

If the immune defense is weakened, the child may experience a recurrence of vesicles after three days. This phenomenon is necessarily accompanied by a sharp increase in body temperature with an intensification of all the symptoms characteristic of severe intoxication of the body.

Important. A weak defense mechanism of the body means the risk of the virus passing through the blood vessels to all organs and systems. It is accompanied by the development of dangerous diseases (meningitis, hemorrhagic conjunctivitis, myocarditis, pyelonephritis).

Problems of diagnosis

The characteristic course of herpetic sore throat will not raise any special questions for an otolaryngologist. The diagnosis can be made without laboratory testing.

When examined, local rashes will be found in the child’s oral cavity:

papules;
vesicles;
ulcers

Affected:

tonsils;
sky;
pharyngeal mucosa (different time periods of formation and healing).

A blood test should show a slight increase in the normal level of leukocytes - this is an indicator of the inflammatory process.

When are laboratory tests prescribed?

With symptoms similar to other pathologies.

An erased or atypical form of the disease is the basis for the following additional measures:

Accurate identification of the pathogen using microscopic examination of the fluid isolated from their vesicles (wash, swab from the nose and pharynx),
An enzyme-linked immunosorbent assay technique that allows one to identify the body’s response to enteroviruses (a fourfold increase in the quantitative index of antibodies).
Examination by a neurologist. It is necessary to exclude the risk of developing meningitis.
Cardiac examination. I prescribe it for children who feel pain in the cardiac region.
Visit to the nephrologist. Care should be taken to eliminate the risk of pyelonephritis (changes in the child’s urine).

What other diseases are ulcerous tonsillitis differentiated from?

Thrush - in infants, chicken pox, stomatitis.

Differences:

During thrush, a coating in the form of white cottage cheese forms on the tongue and gums. If you remove it, redness will remain.
Herpetic stomatitis is localization of nodules in the area of the tongue and gums. Enteroviral vesicular stomatitis - rashes on the tonsils, pharynx and palate. Herpetic stomatitis in children occurs much less frequently than herpes sore throat.
The whitish liquid should not be confused with pus. Pus forms only in the follicular and lacunar form of the disease on the tonsils, without spreading further. Herpes sore throat - the appearance of a runny nose. Purulent tonsillitis – the absence of such a symptom.
Catarrhal tonsillitis (without a runny nose) and herpes (erased appearance) are similar in symptoms and occur without rashes in the mouth. A stuffy nose and liquid discharge from it most likely indicate a viral infection.

Treatment measures

There is no specific treatment for the disease (elimination of the virus).

The therapy is aimed at mitigating the course of the pathology, combating intoxication, and increasing the protective functions of the child’s body, which itself copes with the infectious lesion.

A set of necessary measures:

Taking serious measures to isolate sick children.
General therapy.
Local therapy.

Drug treatment:

Drugs with antiallergic effects to reduce the negative effects of toxins, to relieve swelling and stop itching (Zodak, Erius and others).
Paracetamol, Nurofen (other analogs) to fight fever and relieve pain.
Antiseptics for mouth rinsing, designed to prevent the development of the inflammatory process (for example, furatsilin solution).
Means aimed at treating ulcerative formations.
Solutions and aerosols (only from the age of three) with bactericidal and analgesic properties.
A number of pain-relieving and tissue-healing tablets (for example, Decathylene).

Additional events

These include:

Abundant fluid absorption. The process of infection, dehydration and poisoning of the body with toxins occurs literally in hours, and in infants it is even faster. Excess water helps regulate body temperature and reduce the risk of damage from viral toxins. Precautionary measures - feed a sick child carefully and slowly, using a teaspoon, as this is a painful procedure for him. For children after three years of age, it is allowed to use straws, tubes, and special sippy cups.
Various gargling techniques. Use healing natural herbs (decoctions of chamomile, sage, etc.). Count on procedures at one-hour intervals (half-hour intervals are also possible).
Saline and soda solution. With its help, the inflammatory process is localized, pain is reduced, disinfection is carried out, and viral formations and ulcerative crusts are washed away. The procedure is applicable only for children who already know how to gargle. For the younger group, it is worth trying the method of irrigating the pharynx with a decoction using a syringe (be sure to remove the needle before the procedure). The main thing is for the baby to be convinced that the procedure is not painful and does not pose any threat. Teach him to open his mouth in time and spit out water correctly after irrigation.
Bed rest. The acute phase of the disease is in the first week - until the temperature normalizes.

Note. Herpetic sore throat in its normal course should not last more than two weeks. Its duration depends on the age of the child, the severity of the course and the ability to resist infection.

Medications, the use of which for the treatment of herpetic stomatitis is prohibited:

Antibacterial drugs. We remind you that fighting viruses with antibiotics does not make sense. Antibacterial drugs are prescribed only in the presence of a pyogenic infection. Special suspensions are approved for use for children.
Drugs for the treatment of herpes. Herpetic type viruses are not related to enteroviral vesicular stomatitis. The use of such medications is pointless and even harmful due to the risk of side effects.
A line of broad-spectrum antiviral drugs and immunomodulators. There is a possibility of acquiring undesirable side effects with extremely low chances of a positive effect on the inflammatory process.

Important. Decisively avoid procedures such as inhalations and application of compresses, which activate blood circulation at the site of the inflammatory process and provoke the movement of pathogenic flora with the blood to other organs and systems. Do not apply iodine or other “burning” agents to ulcers! Irritation of the mucous membrane causes unnecessary suffering to the child.

Problems of complications

Let us reassure parents – the disease does not cause severe complications in most children. Recovery is rapid, and the prognosis is usually favorable.

Problems may arise in children with weakened immune defenses. There is a danger of infection spreading and affecting a number of organs.

Possible complications:

The disease during the course of herpetic sore throat and after recovery (rarely) is pyelonephritis, serous meningitis.
Development of meningitis under the guise of Kernig's syndrome.
Encephalitis is a disease that affects brain tissue.
The development of myocarditis, inflammation of the heart muscle.

Important. Severe pain in the head, convulsions, loss of consciousness, disorientation in a child is a serious reason to immediately call a doctor. For an infant, the listed symptoms mean the need for a clinical form of treatment. The greatest risk of mortality from meningitis occurs before the age of three.

Disease prevention

Once the diagnosis is confirmed, quarantine is prescribed for 14 days for all sick children and those who have been in contact with them. Since there is no vaccination for this type of pathology, there remains a means for its prevention - gamma globulin.

Other measures:

Early diagnosis.
Means for strengthening general and local immune defense.
Work to reduce the risk of infection.

Note. Do not rely on detergents or chlorinated water. Enteroviruses are only afraid of harsh heat treatment (60 °C).

For parents. Remember that you are not dealing with bacteria, but with a dangerous virus, so no special treatment is provided.

Conclusion. Therapeutic measures should be aimed at significantly alleviating symptoms, reducing physiological and psychological stress, and reducing pain.

Dental surgeon

Vaccines

With the drug Pentaxim

Vaccination with Infanrix

Against hemophilus influenzae

Poliomyelitis

For measles

Chickenpox

Flu

Hepatitis A

Hepatitis B

Mumps

For rubella

Pneumococcal infection

Tick-borne encephalitis

Dear visitors of the Farmamir website. This article does not constitute medical advice and should not serve as a substitute for consultation with a physician.

According to modern concepts, the term “enterovirus infection” unites a group of diseases caused by numerous viruses of the genus Enterovirus and Parechovirus of the Picornaviridae family, characterized by an intoxication syndrome and polymorphism of clinical manifestations.

Enteroviruses (EV) and parechoviruses (PE) are ubiquitous microorganisms that are transmitted from person to person through direct and indirect contact. They cause a wide range of diseases in people of all ages, but most often in children.

Enterovirus infection (EVI) is a typical anthroponosis, the sources of infection in which are patients or virus carriers. Among healthy children, the percentage of virus shedding varies from 7.2 to 20.1%, and at the age of under 1 year it reaches 32.6%. The relative contribution of symptomatic and asymptomatic forms to maintaining viral circulation is unknown, but it is likely that all are important.

The level of natural immunity increases with age. In some areas, over 90% of children are immune to enteroviruses by the age of 5 years. Between 30 and 80% of adults have antibodies to the most common serotypes. Seropositivity of the population is higher in regions with low social and hygienic levels. Therefore, it is often considered as an indicator of the standard of living of the population and the effectiveness of anti-epidemic protection in general.

Traditional classification divides enteroviruses into five groups. Each of them contains a variable number of serotypes.

Polioviruses - serotypes 1-3.
Coxsackie viruses group A - serotypes 1-22, 24.
Coxsackie viruses group B - serotypes 1-6.
Echoviruses (ECHO) - serotypes 1-9, 11-21, 2427, 29-33.
Enteroviruses - serotypes 68-71, 73-91, 93102, 104-107, 109-111, 113, 114, 116.

The number of new enterovirus serotypes continues to grow.

ECHO viruses 22 and 23, previously classified as enteroviruses, were isolated in 1999 into the independent genus Parechovirus and received the designations HPEV1 and HPEV2. Parechoviruses share biological, clinical and epidemiological characteristics with enteroviruses, but differ significantly from them in their genomic sequence. Currently, 11 serotypes of parechoviruses have been described.

According to the latest classification of viruses (2003), based on genomic characteristics, non-polio human enteroviruses are represented by 4 species (A, B, C, D).

Enteroviruses are RNA viruses. They are stable in the external environment, but are inactivated at temperatures above 50°C (at 60°C in 6-8 minutes, at 100°C instantly). At a temperature of 37°C they can be stored for 50-65 days. Viruses survive for a long time in water (in tap water - 18 days, in river water - 33 days, in sewage water - 65 days). They die under the influence of ultraviolet irradiation and when dried. Solutions of iodine, 0.3% formaldehyde, 0.1 N HCl or chlorine at a concentration of 0.3-0.5 mg/l quickly destroy viruses.

Epidemiology

Enteroviruses exist in nature thanks to two reservoirs: natural (soil, water, food) and the human body, in which they can accumulate and through which, accordingly, spread.

The main epidemiological feature of the infection is the ability to form the so-called in humans. “healthy virus carrier” with long-term, up to several weeks, release of the pathogen into the external environment. This factor contributes to the survival of the virus in the human population, despite the high level of immune individuals. For the same reason, enteroviruses, along with influenza viruses, are the most common cause of nosocomial viral infections.

Infection with enteroviruses and parechoviruses occurs throughout the year, but a significant increase in the incidence of EVI in the northern hemisphere occurs in the summer and autumn months. In warm regions, this periodicity is absent; in the tropics, the infection is recorded all year round.

EVI occurs in all age groups. However, its incidence is inversely proportional to age. Approximately 75% of EVIs recorded annually by WHO occur in children under 15 years of age. Children under 1 year old get sick several times more often than older children and adults. For unknown reasons, males are at greater risk of developing EVI.

The main mechanism of infection transmission is fecal-oral, carried out through food, water and household contact. Less commonly, the infection is transmitted by airborne droplets and transplacentally (from mother to fetus). Apparently, droplet introduction of the virus into the respiratory tract is accompanied by subsequent evacuation of the pathogen into the oropharynx, where, after ingestion, it enters its ecological niche - the intestines, followed by the traditional development of the infectious process.

Direct contact with infected feces occurs when swaddling infants. Therefore, infants are the most “effective” transmitters of infection. Indirect transmission occurs in poor sanitation conditions through contaminated water, food and household items.

An important route of spread is through contact with contaminated objects and the hands of another person, followed by inoculation of the virus through the mouth, nose or eyes. Cases of infection have been described when swimming in sea water contaminated by sewage. Studies show that secondary infections occur in 50% of family contacts. Infected individuals are most contagious during the first week of illness.

Every 3-4 years there are epidemic outbreaks of the disease caused by various serotypes of viruses. The serotypes that infect humans change significantly every year. The reasons why specific virus serotypes appear and disappear are not known. It has been suggested that the accumulation of a "critical mass" of susceptible young children may be necessary to maintain the epidemic process.

Examples of previously unknown serotypes that have emerged to cause disease outbreaks include:

Coxsackie A6, which has caused outbreaks of an atypical form of enteroviral exanthema in children in several countries in Europe, the Far East and North America.
Enterovirus D68, which has been responsible for an increase in respiratory illnesses in the United States and other countries since 2008, and most recently in Missouri, Illinois, and several other states in the late summer/early fall of 2014. Rare cases of polymyelitis-like illness associated with enterovirus D68 also occurred in New Hampshire in 2011 and in California in 2012–13.

During outbreaks, the number of cases of EVI can increase several times. The world often experiences almost global epidemics. For example, the epidemic caused by ECHO 9 in the late 50s or the pandemic of acute hemorrhagic conjunctivitis caused by enterovirus 70 in 1969 and ECHO 11 in 1979-80. Enterovirus 71 has caused local outbreaks of EVI involving a small number of patients over several years and regional epidemics in the Far East involving hundreds of people.

Pathogenesis and pathomorphology

The entry points for infection are the mucous membranes of the oral cavity, intestines and upper respiratory tract. Enteroviruses, which do not have an outer protein shell, freely pass the “gastric barrier” and settle on the cells of the small intestinal mucosa. It is this natural feature of the infection that served as the reason for the single taxonomic name “enterovirus” for this large and quite different group of viruses in their characteristics (by the way, contrary to the popular belief about their frequent and almost obligatory participation in the development of viral diarrhea!).

Subsequently, the pathogen replicates in the lymphoid tissue and epithelial cells of the intestine and mesenteric lymph nodes. Once in the blood, the virus causes primary viremia, which corresponds to approximately the third day of illness.

Enteroviruses exhibit the greatest tropism for cells of the central nervous system and muscle tissue. However, other organs are also involved in the process: heart, liver, pancreas, lungs, kidneys, intestines; blood vessels of the eyes.

Clinical manifestations, the nature of the course, and the outcome of the disease depend on the biological properties of the virus, its predominant tropism, and the state of cellular and humoral immunity. In particular, Coxsackie A viruses experimentally cause muscle damage and flaccid paralysis in newborn mice, and Coxsackie B viruses cause central paralysis without muscle pathology.

At the same time, the same serotype of enterovirus can cause different clinical forms of the disease. But there is also a certain organotropy of some enterovirus serotypes, which is confirmed by the uniformity of clinical manifestations during epidemic outbreaks (with a predominance of myalgia, for example, serous meningitis, heart and eye lesions). In all affected organs, swelling, foci of inflammation and necrosis are detected.

Persons who have undergone EVI develop type-specific immunity that lasts for many years, possibly for life.

Clinic

Incubation period with EVI it lasts from 2 to 35 days (usually 2-3 days). A unique feature of enteroviruses is their ability to cause “unpredictable variants” of the disease. The same type of virus can cause both very mild, erased forms of the disease affecting, for example, the respiratory tract or intestines, and extremely severe variants affecting the nervous and cardiovascular systems.

One type of virus can cause both large epidemics and isolated diseases. At the same time, enteroviruses of different serotypes can cause the same clinical syndromes.

Some syndromes are more common in certain age groups: for example, aseptic meningitis is usually observed in infants, and myalgia and myopericarditis - in adolescents and young adults; herpetic sore throat - in children aged 3 months to 16 years, acute hemorrhagic conjunctivitis - in patients aged 20 to 50 years.

The vast majority of cases of EVI (more than 80%) are asymptomatic, about 13% of cases are mild febrile illnesses, and only 2-3% of cases develop a severe form of the disease, mainly in young children and people with impaired immune systems.

Main clinical forms of acquired enterovirus infection

Herpangina(vesicular stomatitis, Zagorsky disease) is most often caused by Coxsackie viruses A and B, less often by ECHO viruses. This form of EVI is mainly registered in children 3-10 years old. Occurs both in the form of sporadic cases and epidemic outbreaks; can occur in an isolated form, but is often combined with meningitis, myalgia, and exanthemas.

The onset of the disease is acute. The intoxication syndrome is moderately expressed, characterized by decreased appetite, headache, weakness, and lethargy. Body temperature rises to febrile levels and persists for 1-3 days.

Local changes are characterized by hyperemia of the mucous membrane of the soft palate, palatine arches and tonsils, uvula and the appearance of small papules 1-2 mm in size with a red rim, transforming into vesicles. They persist for 24-48 hours, then open and form erosions with a gray-white coating. The number of vesicles usually correlates with the severity of the disease. Pathological changes in the pharynx disappear after 6-7 days. There is an increase in tonsillar and submandibular lymph nodes.

Herpetic sore throat should be differentiated from herpetic stomatitis caused by the herpes simplex virus (HHV types 1 and 2). The symptoms of these processes are very similar, but stomatitis is characterized by the predominant location of the enanthema on the mucous membrane of the hard palate, cheeks, tongue and gums. Since EVI is more common in children than herpes simplex, herpangina should be considered as a more likely disease in such cases.

Epidemic myalgia(pleurodynia, Bornholm's disease, "devil's disease"). Myalgia is most often caused by Coxsackie B viruses (serotypes 1-6), less commonly by Coxsackie A viruses. This form is in most cases observed in adolescents and young adults and, in essence, is a viral myositis.

Palpation of the affected muscle is always painful, the muscle is swollen. The pain is usually localized around the costal margin. About half of patients experience pain in the lower pectoral muscles on one or both sides, while the other half experience pain in the upper abdominal muscles. In children, the pain can be localized lower, simulating the clinical picture of an “acute abdomen.”

Characterized by the sudden onset of severe spastic pain in the muscles, which intensifies with a change in body position or inhalation. The attack of spasm ends the same way it begins - suddenly. Damage to the muscles of the limbs is often observed. The attack lasts from 30-40 seconds to 15-30 minutes, rarely - 1 hour. After an attack of pain, body temperature may rise to high levels and myoglobinuria may appear.

The duration of the disease is short, from 1 to 6 days, the course is wavy, after 1-3 days there may be a repeated rise in body temperature.

Serous meningitis. Aseptic meningitis caused by enteroviruses is the most common form of central nervous system (CNS) damage associated with this infection. Parechovirus (PeV3) should be considered the second most common viral cause of meningitis in young children.

It is characterized by an acute onset, body temperature rises to 38-39°C and is constant. A sharp headache, vomiting, and sometimes impaired consciousness and convulsions appear. Positive meningeal symptoms are noted. Fever and meningeal symptoms usually persist for 3-7 days, and a two-wave temperature curve is possible.

The diagnosis is confirmed by examining cerebrospinal fluid. The liquor flows out under pressure, transparent or slightly opalescent. Cytosis of up to 100-500 cells in 1 μl is typical. In the first days of the disease, cytosis can be neutrophilic, later - lymphocytic. The amount of protein is normal or increased. The content of sugar and chlorides is within normal limits. Normalization of the composition of the cerebrospinal fluid usually occurs by the end of the 3rd week.

In infants, severe intoxication syndrome, cerebral symptoms, and pathological changes in the cerebrospinal fluid can be observed in the absence of positive meningeal signs (“asymptomatic liquor-positive meningitis”). This form is extremely difficult for clinical diagnosis.

In practice, aseptic meningitis is often diagnosed by lumbar puncture in children with fever without a visible source of infection. The presence of genetic material of the virus in the cerebrospinal fluid (positive PCR result) reliably confirms the etiology of the disease.

Encephalic form(stem, cerebellar). The disease begins acutely. Body temperature rises to 39-40°C, chills and vomiting are noted. Then changes in consciousness, convulsions, focal symptoms appear, and there may be brainstem disorders (swallowing, breathing and cardiovascular disorders).

In the cerebrospinal fluid there is slight cytosis, high protein content. Severe cases of damage to the nervous system were observed during infection caused by enterovirus type 71 (outbreaks in Transbaikalia and China). Clinical symptoms were described as rhombencephalitis (lesions in the area of the bottom of the 4th ventricle) involving all centers located in this area: severe bulbar syndrome with impaired swallowing, phonation and respiratory disorders.

The outcome is often favorable with recovery within 2-4 weeks, usually without residual effects. However, mono- or hemiparesis may persist. Residual effects are observed mainly in young children.

Characterizing this type of pathology, it is necessary to point out the predominantly demyelinating type of changes in the structures of the central nervous system according to the type of acute disseminated encephalomyelitis (encephalitis, ADEM), which actually explains many points in the development of the disease: features of symptoms, prognosis, connection with a possible severe progressive process like multiple sclerosis or panencephalitis.

Paralytic form(spinal) can be caused by various serotypes of enteroviruses, the most important of which is enterovirus 71, the only serotype associated with outbreaks of paralytic diseases. Large outbreaks involving hundreds of cases, mostly in children over the age of six, have been reported in eastern Europe, Russia, Taiwan and Thailand.

Clinically, it resembles the spinal form of poliomyelitis with the development of asymmetric flaccid paralysis without sensory disorders. The disease is typical for young children. Often the disease begins with symptoms characteristic of other forms of EVI (respiratory, intestinal, etc.).

However, more often paresis develops acutely; in the midst of complete health, gait disturbance (limping), recurvation in the knee joint, rotation of the foot, and muscle hypotonia appear. Reflexes on the affected side are preserved or even increased. The disease progresses favorably and ends with the restoration of all functions. In rare cases, residual effects may persist.

Transverse myelitis- damage to the spinal cord: spastic paresis and paralysis of the arms (less often) and legs (more often) with dysfunction of the pelvic organs (retention or incontinence of urine and stool).

Possible damage to the nervous system in the form of Guillain-Barre syndrome. It is characterized by an acute onset, severe intoxication, an increase in body temperature to febrile levels, and the rapid development of muscle paralysis, mainly of the lower extremities, neck, and intercostal muscles. Breathing, swallowing and speech are quickly impaired. Death in some cases occurs on the 2-4th day from the onset of the disease.

Enteroviral fever(“minor illness”, three-day fever, summer flu) The disease is caused by all serotypes of Coxsackie viruses A and B, less commonly ECHO. The onset is usually acute, moderate intoxication is possible, body temperature rises to 38.5-40°C and often has a biphasic character.

Abdominal pain, myalgia, conjunctivitis, and enlarged cervical lymph nodes are possible. In some cases, fever is the only symptom of the disease. The duration of the disease is often 3-4 days.

Along with the catarrhal form, it also occurs quite often and forms a symptom complex of a mild disease with a three-day fever, clinically reminiscent of the flu (“dry catarrh”, absence of pronounced respiratory manifestations). It occurs mainly in the summer, and is often recorded as one of the forms of the disease during an outbreak in children's groups.

Enteroviral exanthema(epidemic exanthema, Boston exanthema, Berlin exanthema) is caused by the ECHO, Coxsackie A and B viruses. It is most common among children in the first years of life. The main symptom of the disease is maculopapular exanthema, moderate intoxication, and increased body temperature.

The rash appears simultaneously on an unchanged skin background, can be quite varied in morphology (spotty, maculopapular, pinpoint, hemorrhagic), persists for 1-2 days and disappears without a trace.

One of the most common variants of enteroviral exanthema is a disease that occurs with damage to the skin of the hands and feet, and the mucous membrane of the oral cavity (hand, foot and mouth disease - HFMD, translated as hand-foot-mouth syndrome), caused by Coxsackie A viruses (5th, 10th, 16th serotypes). In domestic practice, until recently it was called foot-and-mouth disease-like syndrome.

This disease, pathognomonic for enterovirus infection, is characterized by moderate intoxication and increased body temperature. At the same time, a rash appears on the fingers and toes - spots, papules and vesicles with a diameter of 1-3 mm, surrounded by a halo of hyperemia.

The elements are located in the interphalangeal folds, both on the palmar and on the back of the hands. The arrangement of elements on the feet is similar. Vesicular rashes are possible on the mucous membrane of the tongue and oral cavity (usually on the mucous membrane of the cheeks and palatine arches), quickly turning into small erosions (herpangina). Vesicular rashes are often located on the skin of the nasolabial triangle (a fairly typical symptom) and the gluteal region. Proximal separation of the nail plate from the nail bed has also been associated with HFMD.

The very fact of the appearance of symptoms of stomatitis and exanthema directly indicates that herpangina, Boston exanthema, and hand-foot-mouth syndrome are, in fact, variants of the infectious process with the dominance of one or another topic of the lesion. We should not forget that the described form can be combined with more severe damage to the brain and heart.

Intestinal form(enteroviral diarrhea, gastroenteritis) is usually caused by Coxsackie B viruses (serotypes 1-6), Coxsackie A (2nd, 9th serotypes), and some serotypes of ECHO viruses. Mostly young children are affected. Sporadic diseases and local outbreaks are often recorded, mainly in the spring and summer.

The onset is acute, with an increase in body temperature to 38-39°C. Intoxication is not expressed, the condition is slightly disturbed. Vomiting is a common symptom, often repeated (2-3 times), abdominal pain and flatulence are possible; stool becomes more frequent up to 6-8 times a day and is enteritic in nature (thin, watery).

Respiratory form(catarrhal). During the interepidemic period for influenza, this form of EVI accounts for 2.5 to 11% of respiratory infections in children. Young children are more often affected. The onset is acute, intoxication syndrome is characteristic (weakness, headache, malaise), chills are possible against the background of increased body temperature.

Catarrhal syndrome is manifested by rhinitis with serous-mucous discharge, dry cough, hyperemia and granularity of the posterior pharyngeal wall. Quite rarely, the bronchi and lung tissue are involved in the process. Fever lasts 3-5 days, catarrhal symptoms last about a week. Young children may develop laryngeal stenosis caused by the ECHO11 virus. The lack of specific signs that fundamentally distinguish this form from other respiratory viral infections makes its identification difficult.

Enterovirus infections of the heart(EVIS). The most common are myocarditis and encephalomyocarditis of newborns - an extremely severe variant of Coxsackie B infection (serotypes 1-5). The sources of infection are postpartum women or medical staff. Routes of transmission: transplacental and household contact.

The onset of the disease is acute or gradual, body temperature rises to febrile levels and may have a two-wave character. Cardiac syndrome is pronounced: general cyanosis of the skin, acrocyanosis progresses, the boundaries of the heart expand, dullness of heart sounds appears, systolic murmur occurs, and edema is possible.

Damage to the central nervous system is observed: the child refuses to breastfeed, becomes lethargic, drowsy, does not respond to people around him, tonic-clonic convulsions occur, and the large fontanel bulges. Coma may develop. Most patients have an enlarged liver, and possible disruption of its functions.

Death can occur in the first hours from the onset of the disease or on the 2-3rd day from cardiovascular failure. The tropism of the virus to the cells of striated muscle, as was shown in the example of pleurodynia, indicates that damage to the heart muscle may be more frequent than is commonly believed. And the process does not always end fatally. Myocarditis is “visible”, and forms without pronounced manifestations of heart failure are not diagnosed in a timely manner.

Enteroviral eye infection(uveitis, hemorrhagic conjunctivitis, Apollo disease). The disease affects children in the first year of life with a burdened premorbid background, and often develops as a nosocomial infection. Has a short incubation period - 3-48 hours.

The disease begins acutely. Manifestations of intoxication are pronounced: fever up to 38-39°C, anxiety, sleep inversion, loss of appetite, regurgitation or vomiting. Catarrhal syndrome is often observed. Possible enlargement of the lymph nodes and liver, the appearance of exanthema.

On the 3-4th day, inflammation of the vascular tract of the eyes develops with injection of the eyeball, serous or serous-fibrinous effusion into the anterior chamber, pupil area or retina.

On examination: severe photophobia, lacrimation, sensation of a foreign body in the eye, swollen eyelids, mucous and mucopurulent discharge. The conjunctiva is sharply hyperemic, infiltrated, and small follicles are often visible. The color of the iris becomes darker than on the healthy side, the pupil narrows. Both eyes are almost always affected (77.2-90.8% with an interval of 4-24 hours).

The infection clears up within 10 days without complications. In severe cases, keratitis can persist for several weeks, but usually does not lead to irreversible changes. Outbreaks of this disease, caused by enterovirus 70 and Coxsackie A24, occur mainly in tropical coastal countries.

Immunodeficient patients tolerate EVI with difficulty. Severe paralytic forms of the disease develop in HIV-infected people and in patients with a deficiency of the humoral immune system. Children with X-linked agammaglobulinemia often develop chronic meningoencephalitis. At the same time, immune T-lymphocytes can be responsible for a number of severe, destructive changes in tissues (damage to myocardiocytes in EVIS, myelin sheaths in NS lesions).

In addition to acquired forms of the disease, it is also possible to develop a congenital form of Coxsackie and ESNO infection with symptoms of severe myocarditis and (or) fulminant hepatitis, often in combination with encephalitis. Infants aged 1 week to 3 months may develop a syndrome that is difficult to distinguish from a severe bacterial infection with multiple organ failure (“viral sepsis”). The most common viruses isolated from such children are Coxsackie B, ECHO 11 and parechovirus serotype 3 (PeV 3).

The role of enteroviruses in the occurrence of kidney pathology, the development of appendicitis, hepatitis, cholecystitis, pancreatitis, endocarditis, and juvenile rheumatoid arthritis has been proven. There is a connection between EVI and the development of diabetes, Reye's syndrome and chronic fatigue.

The prognosis for most forms of enterivirus infection is favorable. However, CNS infections can lead to the development of neurological complications, and myopericarditis in newborns and chronic meningoencephalitis in immunocompromised patients are often fatal. Myocarditis in adults can also have serious complications.

Diagnostics

In the presence of a typical clinic, diagnosing EVI is not difficult, but in the Russian Federation mandatory laboratory confirmation of the diagnosis is required.

Laboratory diagnosis of EVI is carried out by isolating and identifying the virus in cell culture (virological method), by identifying enterovirus RNA using polymerase chain reaction (PCR).

Each method has its own advantages and disadvantages. Problems with the specificity of a positive result should be taken into account due to the high prevalence of virus carriage in certain areas. This point almost completely eliminates the use of serological tests.

The following are selected for the study: cerebrospinal fluid, conjunctival discharge, smear of discharged vesicles, blood, organ biopsies (sterile types of clinical material); smear (wash) from the oropharynx/nasopharynx, smear of herpangina ulcer discharge, fecal samples, autopsy material (non-sterile types of clinical material). Taking a certain type of material for laboratory research is carried out taking into account the clinical picture of the disease.

Laboratory confirmation of the diagnosis of EVI is:

detection of enteroviruses or their RNA in sterile types of clinical material;
detection of enteroviruses or their RNA in non-sterile types of clinical material in the presence of an etiologically deciphered outbreak of EVI and if the patient has a clinical picture of the disease characteristic of this outbreak;
detection of enteroviruses or their RNA in non-sterile types of clinical material in the absence of an outbreak and their sero- or genotype matching the specific clinical picture of the disease (HFMD, herpangina, acute hemorrhagic conjunctivitis, uveitis and others);
detection of enteroviruses or their RNA in two samples of non-sterile clinical materials of different types.

In case of registration of an outbreak or group incidence, the diagnosis of “enteroviral infection” can be established on the basis of clinical and epidemiological data.

The features of clinical forms also require special laboratory diagnostics that clarify the topic and nature of the lesion: for lesions of the nervous system - the results of lumbar puncture and neuroimaging studies of the process (MRI, CT), for lesions of muscle tissue - increased activity of “muscle” enzymes (CPK, LDH, BNP, urine myoglobin).

Treatment

There is currently no etiotropic treatment for EVI. The drug Pleconaril, developed abroad and considered promising, has not received wide recognition and is not registered in Russia.

Treatment of patients is reduced to pathogenetic and symptomatic therapy, depending on the form and severity of the disease. Painkillers and antipyretics include paracetamol and ibuprofen.

Patients with pleurodynia are advised to apply dry heat to the affected muscles. For severe pain, the use of non-opioid analgesics (diclofenac, ketoprofen, ketorolac, lornoxicam, etc.) may be required.

Immunoglobulin preparations are used as a means of preventing the disease in newborns and persons with agammaglobulinemia. Considering the extremely unfavorable prognosis, they are indicated as a therapeutic agent in newborns and patients with myocarditis (2 g/kg), although their effectiveness has not been proven.

Patients with myopericarditis are prescribed long-term bed rest, relief of heart failure and arrhythmia.

Antibiotics for EVI are used only when bacterial complications occur.

Prevention

Active immunoprophylaxis against EVI has not been developed (with the exception of poliomyelitis). Preventive measures come down to compliance with sanitary and hygienic standards.

In foci of infection, medical observation of contact persons is established: 10 days - when registering mild forms of EVI (in the absence of obvious signs of damage to the nervous system): enteroviral fever, epidemic myalgia, herpetic sore throat and others; 20 days - when registering forms of EVI with damage to the nervous system.

V.A. Anokhin, A.M. Sabitova, I.E. Kravchenko, T.M. Martynova

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