Mononucleosis Symptoms
Infectious mononucleosis is a common systemic lymphoproliferative disease, most commonly caused by the Epstein-Barr virus. Toxoplasma gondii and other viruses( CMV, human immunodeficiency virus and human herpesvirus type 6, recognized as the cause of sudden exanthema) can cause clinically similar diseases. These same etiological agents are presumably capable of causing the development of chronic fatigue syndrome.
Epstein-Barr virus infection( EBVI) is an infectious disease of the viral etiology characterized by a variety of clinical manifestations and takes the form of acute and chronic infectious mononucleosis, malignant tumors( Burkitt's lymphoma, nasopharyngeal carcinoma, etc.), autoimmune diseases, chronic fatigue syndrome.
Etiology. The virus was discovered in 1964.A. Epstein and Y. M. Barr. The Epstein-Barr virus( EBV) belongs to the group of gamma-herpesviruses( herpesvirus type 4).The virion contains DNA, has a spherical shape, its diameter is 120-200 nm. Taking into account the ability of VEB to transform B-lymphocytes, two strains of the virus - type 1( A) and type 2( B) are isolated. The virion contains a capsid and a shell formed from the host cell material. During the replication of the virus, the capsid antigen( VCA), the early antigen( EA) and the nuclear antigen( EBNA) are sequentially expressed, which is used in the serological diagnosis of stages of the infectious process.
The main target cells for EBV are B-lymphocytes, which have a specific CD21 receptor on the membrane to this virus. Infected B-lymphocytes acquire the ability to unlimited proliferation( "cellular immortality", immortalization) and the synthesis of heterophilic antibodies( polyclonal activation).In addition, VEB affects the epithelium of the oropharynx, ducts of the salivary glands, cervix, gastrointestinal tract, vascular endothelium and immunocompetent cells - T-lymphocytes( CD3), natural killer cells( CD16), neutrophils, macrophages. The defeat of cells of the immune system leads to the development of IDS.The virus is an inducer of autoimmune reactions.
VEB has the capacity for prolonged persistence in target cells. As a result of an unproductive infection, EBV-infected cells are transformed into malignant cells.
VEB is unstable in the external environment, sensitive to high temperatures( over 60 ° C), to standard disinfectants, stored when frozen and dried.
Disease usually affects children, adolescents and young adults and is especially common among engaged students in early autumn and spring. Once the virus enters the body, it multiplies in lymphocytes( white blood cells).Typical symptoms( sore throat, fever and debilitating fatigue) usually appear after the incubation period, approximately 10 days in children and after 30-50 days in adults. Acute symptoms usually disappear after 6-10 days, although some residual weakness may persist for another two to three months. Mononucleosis is most often not a serious illness;complications such as a brain or heart infection or spleen rupture are very rare.
Epidemiology. EBVI is one of the most common human infectious diseases. Antibodies to EBV are found in 60% of children in the first two years of life and in 80-100% of adults. The source is the patients with manifest and asymptomatic forms of EBVI.It was found that patients with acute EBVI secrete the virus within 1 to 18 months.
Transmission routes - airborne, contact-household, parenteral, sexual, vertical. The air-drop path is the main one, however, because of low volatility and instability, EBV is realized only with close contact. With the contact-household way, the transmission factor is saliva( "kissing disease").Infection is facilitated by crowding, non-compliance with personal hygiene rules, the use of common utensils, toys, household items, etc. It is possible to transfer blood and its drugs, sex and mother to the fetus.
Theis widely distributed. The acute form is characterized by spring and autumn seasonality, epidemic upsurge once every 6-7 years. Infants are rarely ill, which is associated with transplacental transmission of maternal antibodies. In developed countries and observing the rules of personal hygiene, EBV infection often occurs after adulthood. So, in the USA, 50% of students are not infected with EBV, which leads to outbreaks of acute EBVE in this contingent( "student illness").In developing countries, with a low sanitary culture of the population, the majority of children become infected by the age of 3, and practically the entire population by the age of majority. In our country, acute EBVI is more often registered in the age group between 1 and 5 years of age( 45%).
Causes of
• Mononucleosis is often transmitted through saliva, hence its second name, "Kiss Disease".It can also be transmitted through a mouth-hand-mouth contact or through a common towel or dishes.
• Infection can be transmitted through blood transfusion.
Symptoms of
• Headaches.
• Weakness and fatigue.
• Sore throat and enlarged tonsils.
• Swollen lymph nodes in the neck, under the armpits and in the groin.
• Fever( with a temperature fluctuation that reaches a maximum of 38.5-39 ° C in the evening).
• Loss of appetite.
• Bound or inflamed muscles.
• Temporary yellowing due to moderate reversible liver damage.
Pathogenesis. The entrance gates for VEB are the mucosa of the upper respiratory tract. There are several stages of the pathogenesis of the disease.
1. Invasion of EBV through epithelial cells into lymphoid tissue. Penetrating through epithelial cells, the virus enters the lymphoid tissue and infects B-lymphocytes.
2. Defeat of B-lymphocytes. The virus binds to the CD21 receptor of B-lymphocytes, penetrates the cell and integrates its DNA into its genome. B cells begin to multiply rapidly, their death by apoptosis decreases. Polyclonal activation of B-lymphocytes is developing, which is accompanied by the production of heterophilic antibodies to erythrocytes of ram, horse, bull, aminopenicillin and others.
3. Dissemination of VEB.Viralemia does not play a leading role in the dissemination of the pathogen. The spread of EBV occurs by hematogenous and lymphogenous pathways in the composition of infected B cells. First of all, the virus affects the lymphoid organs( palatine and pharyngeal tonsils, lymph nodes, liver, spleen), in which reticular hyperplasia and infiltration with mononuclears - benign lymphoreticulosis develops. In severe cases, foci of necrosis and dystrophy form in the lymphoid tissue.
4. Development of the immune response, the formation of secondary IDS and autoimmune reactions. The first line of defense of the body from EBV include the system of interferon, macrophages and natural killer cells( CD16).The next step is the immune response by cellular and humoral types. A clone of sensitized cytotoxic CDS cells is formed, carrying out the lysis of EBV-infected B lymphocytes. Simultaneously with the immune response, secondary SDI formation and induction of autoimmune processes occur. The extracellular virus binds to specific anti-EBV antibodies to form immune complexes that circulate in the blood for a long time and cause the development of autoimmune reactions. There are violations of the factors of congenital resistance - reduced production of interferon, the functional activity of neutrophils, macrophages and natural killer cells, there are changes in the cytokine status. Violation of the immune response by humoral type is associated with polyclonal activation of B lymphocytes, as a result of which the production of specific antibodies is reduced, there is no switching of immunoglobulin synthesis from IgM class to IgG, secretory IgA formation is reduced. VEB depresses the immune response by cellular type - induces apoptosis T-lymphocytes( CD95), T-helpers( CD4), memory cells( CD45RO), disrupts the function of cytotoxic T-lymphocytes( CD8).
5. Development of bacterial complications. The consequence of IDS is the activation of opportunistic microflora. The most striking manifestation is tonsillitis, which is the result of a viral-bacterial association.
6. Outcomes. Depending on the state of the immune system, the genetic predisposition, the influence of various external factors( stress, concomitant infections, surgeries, environmental problems, etc.), the following outcomes of the disease are possible: latent infection, chronic EBVI, IDS, oncological diseases( Burkitt's lymphoma, nasopharyngeal carcinoma,lymphogranulomatosis, leukoplakia of the tongue and oral mucosa, cancer of the stomach, intestines, salivary glands, uterus), autoimmune diseases( systemic lupus erythematosus, rheumatoid arthritis, Indra Sjogren, lymphoid interstitial pneumonitis, chronic hepatitis, uveitis, etc.), chronic fatigue syndrome.
Acute EBVI occurs in the form of acute infectious mononucleosis, which was first described by NF Filatov( 1885) and E. Pfeifer( 1889).
The incubation period is from 4 to 7 weeks.
| period | occurrence Form | Gravity | course | phase Complications | |
| Congenital. Acquired | Typical( infectious mononucleosis).Atypical( erased, asymptomatic, visceral) | Light. Medium-heavy. Heavy | Acute. Tightening. Chronic | Active. Inactive | Hepatitis, splenic rupture, Reye's syndrome, renal and hepatic insufficiency, serous meningitis, encephalitis, polyradiculoneuropathy, myocarditis, interstitial pneumonia, hemolytic anemia, thrombocytopenia, etc. |
The acute EBVI clinic is represented by acute mononucleosis-like syndrome. According to Simovanyan E. N., Bovtalo LF, 2004, the syndromal model of acute infectious mononucleosis caused by EBV includes the following symptoms( %):
1. Acute onset of the disease is 80.
2. Fever 93,9-100.
3. Generalized lymphadenopathy is 100.
4. Acute tonsillitis is 80-99.5.
5. Adenoiditis - 87.9.
6. Hepatomegaly - 85,5-98,1.
7. Splenomegaly - 59,2-93,5.
8. Exanthema - 3-18.
9. Hematologic changes( leukocytosis, lymphocytosis, monocytosis, atypical mononuclears) - 86-100.
In 80% of patients, the disease begins acutely with an increase in body temperature, the appearance of symptoms of intoxication, systemic enlargement of lymph nodes, sore throat when swallowing, obstructed nasal breathing.20% of children have a gradual onset. Within a few days they complain of malaise, weakness, lethargy, loss of appetite. Body temperature is subfebrile or normal.
Body temperature gradually increases and reaches 2-4 days of the disease at 39-40 ° C.Fever persists for two to three weeks or more.
Generalized lymphadenopathy appears from the first days of illness. There are systemic lesions of five or six groups of lymph nodes, but mainly anterior and posterior groups are predominantly enlarged. Lymph nodes reach 1-5 cm in diameter, slightly painful on palpation, are not welded to each other and surrounding tissues, are arranged in the form of a "chain", "package", are clearly visible from the front when turning the head and behind( "scalloped neck").Moderate puffiness of subcutaneous tissue around the lymph nodes is possible. Part of the patients have enlarged bronchial and mesenteric lymph nodes. Generalized lymphadenopathy persists for three to six weeks or more.
Tonsillitis refers to the early symptoms of the disease. With pharyngoscopy, hyperemia of the mucous membrane of the oropharynx, hyperplasia of lymphoid follicles, half of patients - nonspecific enanthem and petechiae on the mucous palate. Tonsils enlarged to II-III degree, lacunar pattern is emphasized due to tissue infiltration or, conversely, is smoothed due to lymphostasis. On the 2nd-4th day of the disease, yellowish-white or dirty-gray raids appear in the form of islets or strips. They come from lacunae, have a rough surface( reminiscent of lace), easily removed without bleeding, rubbed, do not sink in the water. In some children, the raids spread beyond the tonsils, dense, hard to remove, do not rub and drown in the water( false-filmy tonsillitis), which dictates the need for a differential diagnosis with oropharyngeal diphtheria. In some patients, tonsillitis has a catarrhal or necrotic character. The raids disappear, as a rule, in 5-10 days.
Adenoiditis is manifested by nasal congestion, difficulty in nasal breathing in the absence of discharge from the nose, snoring breathing, especially in sleep. The patient's face acquires an "adenoid" appearance( puffiness of the face, eyelid pastosity, nose bridge, breath through the open mouth, dry lips).With rhinopharyngoscopy, the increase and raids on the pharyngeal tonsil, edema of the inferior nasal concha and mucous nasopharynx are determined. Symptoms of adenoiditis usually persist for 5-10 days.
Hepatomegaly can be detected from the first days of the disease, but reaches its maximum development by 4-10 days. The edge of the liver is acute or rounded, a tight-elastic consistency, sometimes moderately painful. Reduction of liver size occurs in one to six months. In 5-18% of patients, hepatitis develops as a complication, the pathological substrate of which is the formation of biliary thrombi, the deposition of bilirubin in hepatocytes, edema, dystrophy and necrosis of liver cells. There are darkening of the urine, icterus of the skin and mucous membranes, an increase in the bilirubin content due to the direct fraction, the activity of transaminases and thymol assay. In 20-50% of patients in the absence of jaundice and hyperbilirubinemia, an isolated increase in the activity of transaminases is recorded.
Splenomegaly refers to late symptoms. The maximum degree of enlargement of the spleen reaches 4-10 days. Disappears, usually within one to three weeks.
A part of patients on the 3rd to 14th day of the disease develop polymorphic exanthema without clear localization. Elements are spotted, papular, spotty-papular, rose-oole, small-pointed or petechial in nature, itchy skin is possible. Exanthema persists for 4-10 days, sometimes leaves pigmentation. In children receiving ampicillin or amoxicillin, the rash appears more often( 90-100%), more intense and bright. It is associated with the formation of heterophil antibodies to antibiotics, so when these drugs are given again after 1-17 months, rashes do not occur.
Hematologic changes include leukocytosis, neutropenia with a stab-shift left, an increase in the number of mononuclear cells( lymphocytes, monocytes, atypical mononuclear cells), an increase in ESR.Atypical mononuclear cells are found in 85% of patients. These are single-nucleated cells with a wide cytoplasm( wide-plasma lymphocytes, lymphomonocytes).They are considered transformed T-lymphocytes, but the final origin of these cells is not established. The number of atypical mononuclear cells reaches 10-50%.They appear at the end of the first week of the disease and persist for one to three weeks, sometimes up to three to six months. Atypical mononuclear cells can occur in small numbers in other infectious diseases-CMVI, infection caused by the virus of type 6 herpes, rubella, measles, viral hepatitis, adenovirus infection, toxoplasmosis, etc.
In children of the first three years of life, the disease occurs with less distinctclinical symptomatology than in older age. There is a decrease in the duration of fever, tonsillitis( often has a catarrhal character), lymphadenopathy, hepatosplenomegaly, rapid disappearance of atypical mononuclears from the blood. On the other hand, adenoiditis, exanthema are more common, there may be catarrhal symptoms and diarrhea.
The congenital form of EBVI is described, which is associated with the vertical transmission of EBV in the ante- and intranatal periods. The clinic can resemble an innocent CMV.
Chronic EBVI. The outcomes of acute EBVI are latent infection and chronic EBVI, which develops in 20% of individuals after the acute phase of the infectious process. In adult patients, the clinic of chronic EBVI is characterized by long-term symptoms of intoxication, lymphadenopathy, hepatosplenomegaly, tonsillitis, adenoiditis, in some patients - interstitial pneumonia, uveitis, hepatitis, CNS pathology.
According to Simovanyan E.N., Sarychev AM, 2004, the syndromal model of chronic EBVI in all children includes lymphoproliferative( generalized lymphadenopathy, chronic tonsillitis, adenoiditis, hepato- and splenomegaly), infectious-inflammatory( recurrent acute respiratory infections) and intoxication syndrome, which in 75% of patients are combined with asthenovegetative syndrome, in 62.5% - with cardiac syndrome, in 36.3% of patients - with arthralgic syndrome. Chronic EBVI is characterized by a long wave-like course, periods of reactivation and remission, and therefore, according to clinical and laboratory data, it is possible to single out the stages of typical reactivation, atypical reactivation and incomplete remission.
VEB-associated tumors. Burkitt's lymphoma is more common in children aged 3 to 7 years living in Central Africa. The disease is characterized by a sharp onset, an increase in body temperature, the appearance of a tumor node in the upper jaw area, which rapidly increases in size, infiltrates soft tissues, destroys bone tissue and metastasizes into bones.
Nasopharyngeal carcinoma is recorded predominantly in the southern provinces of China. The patient is concerned about the difficulty of nasal breathing, the mucopurulent discharge from the nose. With a rhinoscope on the mucosa, a tuberous tumor is detected, which is characterized by rapid growth, destroys the bone tissue and metastasizes to the submandibular lymph nodes.
Syndrome of chronic fatigue. Etiological agents, in addition to VEB, are human herpesviruses of the 6th and 7th types, predisposing factors - dysfunction of the limbic structures of the brain, IDS, chronic stress, adverse environmental factors. The clinic includes a prolonged rise in body temperature to subfebrile digits, catarrhal symptoms, generalized lymphadenopathy, mental disorders( depression, anxiety, depression, sleep disturbance), night sweats, severe weakness, fatigue, morning breakdown, which make patients lose their ability to work.
Diagnosis
• The disease is suspected in those who have a physical examination revealing a combination of sore throat, swollen lymph glands and fever. The spleen can also be enlarged.
• Increased white blood cell count and the presence of atypical lymphocytes in the blood.
• A positive antibody test result( a blood test that shows the presence of certain antibodies against the virus) confirms the diagnosis.
• An analysis of liver function can be made.
The diagnosis of EBVI is based on the consideration of risk groups, leading clinical syndromes and laboratory examination data.
1. The virological method is based on the allocation of EBV from saliva, smears from the oropharynx, blood and liquor. The method is rather laborious, the results are obtained in 2-3 weeks, so it is rarely used at present.
2. Polymerase chain reaction allows you to determine the DNA of a virus in saliva, smears from the oropharynx, blood and cerebrospinal fluid. The sensitivity of PCR in EBV is lower( 70%) than in other herpesviral infections( 95-100%), as in the blood and other biological fluids EBV appears only when the infected B-lymphocytes are destroyed as a result of the development of the immune response. The real-time PCR method allows to determine the virus titer in biological fluids, cells, biopsy samples.
3. Serological methods include heteroagglutination reactions and enzyme immunoassay( ELISA).
• Heterogemagglutination reactions( Paul-Bunnel, Lovrik, Goff-Bauer, Li-Davidson, etc.) are based on the determination of heterophilic antibodies to erythrocytes of ram, horse, bull, which appear as a result of polyclonal activation of B-lim-
follicles and persist infor 3-12 months. The disadvantage of the method is low sensitivity( 50% in children, 70-80% in adults).In addition, heterophilic antibodies can be found in other infectious diseases - CMVI, acute respiratory viral infection, viral hepatitis, iersiniosis, toxoplasmosis, etc. In chronic EBV and VEB-associated tumors, there are no heterophilic antibodies.
• Immunoenzyme assay( ELISA) allows separate detection of IgG class antibodies to capsid antigen( VCA), IgG to early antigen( EA) and IgG to nuclear antigen( EBNA), which appear at various times, which allows to diagnose disease stages( Table.7.4).Serological markers of the active phase of EBVI are antibodies of IgM class to VCA and antibodies of class IgG to EA, markers of inactive phase - antibodies of class IgG to EBNA.
Serological markers Epstein-Barr virus infection
| Period of the disease | VCA-IgM | EA-IgG | EBNA-IgG |
| Incubation period or absence of infection | - | - | - |
| Very early primary infection | + | - | - |
| Early primary infection | + | + | + |
| Late primary infection | ± | + | ±( OP <0.5) * |
| Atypical primary infection | + | - | +( ASO, 5) |
| Early past infection | - | + | + |
| Late paste infection | - | - | + |
| Chronic infection | + | + | - |
| Reactivation | + | + | +( OD & gt; 0,5) |
| Atypical reactivation | + | - | + |
* OD - optical density.
Immunological examination in patients with EBVI reveals indicators that characterize the intensity of the immune response and immune dysfunction. The activation of the immune system is indicated by the increase in cytotoxic T-lymphocytes( CD8), natural killer cells( CD16), IgA, IgM, IgG, about the development of secondary IDS-decrease in T-lymphocytes( CD3), T-helpers( CD4), immunoregulatory indexCD4 / CD8, antibody production in response to antigenic stimulation, a decrease in the functional activity of neutrophils, macrophages, interferon production, an increase in the CEC.
Treatment of
• There is no specific treatment for infectious mononucleosis;most people recover themselves in four to six weeks. With acute symptoms, you need to rest in bed. The normal schedule of activity can be gradually renewed as the symptoms ease.
• Take non-prescription pain medications to reduce fever and headaches, body aches and sore throat.(Children should be given acetaminophen instead of aspirin.)
• Drink water and fruit juice to relieve fever and prevent dehydration.
• Use a rinse, prepared from half a teaspoon of salt, diluted in a glass of warm water, several times a day to reduce sore throat.
• In rare cases, corticosteroids may be prescribed to reduce the inflammation of the tonsils, so that they do not increase so much as to impede breathing.
• Approximately 20 percent of patients with infectious mononucleosis are also infected with streptococcal pharyngitis, which requires treatment with an antibiotic for at least 10 days.
• In rare cases, mononucleosis causes a rupture of the spleen, which requires immediate surgery.
In hospitalization young children from at-risk groups, patients with severe and complicated forms of the disease, need it. Bed rest is prescribed for an acute period, especially with splenomegaly because of the threat of rupture of the spleen. In the acute period, mechanically, thermally and chemically sparing food is recommended with the exception of obligate allergens, fried and spicy dishes, extractives. When hepatitis shows diet number 5. Particular attention is paid to caring for the oral mucosa and skin.
Etiotropic therapy involves the appointment of several groups of drugs that are used in the clinical form of the disease.
1. Virocidal preparations. Isoprinosine( inosine pranobec) suppresses the replication of RNA and DNA-containing viruses and has the properties of an immunomodulator. For light and moderate forms of acute
, the drug is prescribed in a dose of 50-100 mg / kg in 4 divided doses for 5-8 days, in severe and complicated forms - at a dose of 100 mg / kg in 4 divided doses up to 15 days. In chronic EBVI, isoprinosine is taken at a dose of 50-100 mg / kg in 4 divided doses for 7-10 days, then another 2 courses are given for 7-10 days at intervals of 10 days. Arbidol for the treatment of acute VEB mononucleosis is used for 7 days, then, if necessary, a single dose is taken 2 times a week for 4 weeks. Abnormal nucleosides( valaciclovir, famciclovir, acyclovir) suppress the replication of herpes simplex viruses of the 1 st and 2 nd types, to a lesser extent - VVZ, CMV, VEB.Valaciclovir( valtrex) for children over 12 years of age is prescribed in a dose of 1000 mg in 3 divided doses for 5-10 days, famciclovir for adolescents over 17 years and adults 500 mg 3 times a day for 7-10 days. Acyclovir is prescribed to children under 2 years of 200 mg 4 times a day, from 2 to 6 years - 400 mg 4 times a day, over 6 years - 800 mg 4 times a day, adolescents and adults - 800 mg 5 times a dayday inside for 7-10 days. In severe and complicated forms, acyclovir is administered intravenously dropwise to infants at 10 mg / kg, children between the ages of 3 months and 12 years - 250-500 mg / m2, children over 12 years-5-10 mg / kg 3 times a dayfor 7-10 days with the subsequent transition to oral administration.
2. Interferons. As a starting viferonotherapy for acute and chronic EBVI, children under 1 year of age are prescribed viferon-1, from 1 to 7 years - viferon-2, from 7 to 14 years - viferon-3, over 14 years - viferon-4 1 candle 2 timesper day for 10 days with the subsequent transition to maintenance therapy. With acute EBV, the drug is prescribed 1 candle 2 times a day 3 times a week - 2 weeks, then 1 candle 2 times a day 2 times a week - 2 weeks, then 1 candle at night 2 times a week - 2 weeks,then 1 candle at night once a week - 2 weeks. Supportive therapy for chronic EBVI consists in the appointment of viferon 1 candle 2 times a day 3 times a week for 3-12 months under the control of clinical and laboratory indicators. A single dose of genferon light in the form of rectal suppositories in children younger than 7 years is 125 thousand ME, over 7 years - 250 thousand ME.Start therapy - 1 candle 2 times a day for 10 days, supporting treatment - 1 candle per night every other day for 1-3 months. Reaferon-EU-lipint for children 2-3 years old is prescribed in severe form of acute and chronic EBVI for 250 thousand units, over 3 years - 500 thousand units 2 times per day inside for 10-20 days with the subsequent transition to maintenance therapyviferon or genferon light. Interferons for intramuscular administration( reaferon, realiron, roferon A, intron A) for children over 2 years of age are prescribed for severe and complicated forms of acute and chronic EBVI in a dose of 0.5-2 million IU once a day for 10-14 days. In the future, taking into account clinical and laboratory indicators, the patient is transferred to maintenance therapy with the use of viferon, geneferon light or intramuscular injection of interferons for 500,000-2 million ED intramuscularly 3 times a week for 3-6 months under the control of clinical and laboratory indicators.
3. Interferon inducers( neovir, cycloferon, amixin, kagocel, anaferon) as initial therapy are prescribed for mild and moderate forms of acute and chronic EBVI, as a supporting therapy - after a course of virocidal preparations and interferons. Apply a prolonged schedule of prescribing.
4. Immunoglobulins for intravenous administration( immunovinin, pentaglobin, intraglobin, intratect, octagam, octag, sandoglobulin, etc.) are prescribed for severe and complicated forms of acute and chronic EBVI.
5. Antibiotics are used in the presence of purulent overlays on the tonsils and bacterial complications. The drugs of choice are cephalosporins( cefazolin, cephalexin, cefotaxime, ceftriaxone, cefixime, etc.) and modern macrolides( azithromycin, roxithromycin, spiramycin, clarithromycin, josamycin).Use of aminopenicillin is contraindicated!
Pathogenetic therapy includes the appointment of immunomodulators( thymalin, tactivin, timogen, imunofan, polyoxidonium, lycopide, imunorix, derinat, sodium nucleate, IRS-19, ribomunil, bronchomunal, immunomax, etc.) and cytokine preparations( leukinferon, ronkolei-kin, etc..) under the control of the immunogram. Disintoxication therapy is carried out: for mild and moderate forms, an abundant drink is prescribed, with severe and complicated forms - intravenous drip infusions of glucose-salt solutions. Glucocorticoids in a dose of 2-3 mg / kg for prednisolone for 2-7 days are used only for severe disease, upper respiratory tract obstruction, hematologic and neurological complications, abundant rashes. Assign multivitamins, vitamin-mineral complexes, drugs of metabolic therapy( riboksin, kokarboksilaza, cytochrome, elkar, etc.), probiotics( bifiform, linex, bifidum-bacterin-forte, etc.), enterosorbents( smecta, filterum, polyphepan, enterosgel andother).According to the indications, antihistamines, protease inhibitors( contrikal, trasilol, gordoks), vasoactive drugs( cavinton, actovegin, cinnarizine, pentoxifylline, etc.), hepatoprotectors, oxygen therapy are used. Treatment of individual nosological forms( hepatitis, encephalitis, etc.) is carried out according to general principles.
Symptomatic therapy includes the appointment of vasoconstrictive drops in the nose( nasivin, adrianol, naphthysine, galazoline, etc.), irrigation of the oropharynx with solutions of antiseptics( furacilin, 2% solution of soda), infusions of medicinal plants( chamomile, sage, St. John's Wort, etc.), the use of local antiseptics( hexoral, stopangin, bioparox, strepsils, yox, lysobact, etc.) and bacterial lysates( imudon).According to the indications, antipyretic drugs and cardiac glycosides are used.
Rehabilitation
Clinical examination is conducted by the district doctor and infectious disease specialist. The duration of follow-up in acute EBV is 6 months, with chronic EBVI - up to 6 months after the disappearance of clinical and laboratory indicators of the activity of the infectious process. Multiplicity of inspections 1 time per month. According to the indications, experts are appointed( hematologist, ENT doctor, immunologist, oncologist, etc.).Laboratory and instrumental examination includes a general blood test for acute EBVI during the first month 1 time in 10 days, then 1 time in 3 months;with chronic EBVI - once a month for 3 months, then 1 time in 3 months. Markers of EBVI using the ELISA and PCR methods are examined once in 3 months, the immune status - once in 3-6 months. According to the indications, a biochemical blood test( bilirubin, ALT, ACT, thymol test, total protein, protein fractions, sialic acids, C-reactive protein, etc.) and instrumental methods of examination - ultrasound of the abdominal cavity organs, neurosonography, Doppler, EEG, REG, RKT, MRI, etc.
Rehabilitation therapy includes a curative regime - in acute EBVI, physical activity is limited for 2 months, release from physical training for 3-6 months. With chronic EBVI, the regime is selected individually. For all forms, prolonged exposure to the sun is contraindicated. When hepatitis recommend limiting fried and spicy dishes, extractives for 3-6 months. Interferon preparations and interferon inducers are treated according to the schemes of maintenance therapy. In the presence of clinical laboratory indicators of EBVI activity, virocidal preparations( inosine pranobex, anomalous nucleosides) are prescribed. Under the control of the immunogram, immunocorrective therapy is carried out, multivitamins, vitamin-mineral complexes, enterosorbents, probiotics, plant adaptogens, metabolic therapy drugs are prescribed, according to indications - hepatoprotectors.
Prevention
Specific prevention of EBV was not developed. Nonspecific prevention is carried out taking into account the ways of transmission of EBV.To prevent the transmission of the virus by airborne and contact-household routes, isolation of the patient with acute EBV is carried out for 3-4 weeks, clinical and laboratory examination of convalescents of acute and chronic EBVI, monitoring of contact and their examination according to indications. In order to prevent the transmission of EBV by parenteral route, a donor survey, reduction of indications for blood transfusions, sexual intercourse - a survey of the sexual partner and its treatment when clinical and laboratory indicators of the activity of the infection process are detected, condom use. Prevention of vertical transmission of the virus is facilitated by the timely diagnosis of EBVI in women of fertile age and pregnant women, treatment with viferon in the presence of clinical and laboratory indicators of EBVE activity during pregnancy.
• Avoid mouth-to-mouth or hand-mouth contact, or use shared towels or dishes with people infected with mononucleosis.
• If you experience any of the signs of an infectious mononucleosis, consult your doctor.
• Attention! If you are diagnosed with infectious mononucleosis and you feel a sudden sharp pain in the upper left side of your abdomen, seek professional medical attention immediately. This may be a sign of rupture of the spleen.