Infectious mononucleosis - Causes, symptoms and treatment. MF.
Jun 04, 2018
Infectious mononucleosis, aka Filatova's disease, glandular fever, monocytic tonsillitis, Pfeiffer's disease. It is an acute form of Ebstein-Barr virus infection( EBVI or EBV-Epstein-Barr virus), characterized by fever, genitalized lymphadenopathy, tonsillitis, hepatosplenomegaly( enlargement of the liver and spleen), and specific changes in the hemogram.
Infectious mononucleosis was first discovered in 1885 by NF Filatov, he noticed a febrile illness accompanied by an increase in the majority of lymph nodes.1909-1929 - Burns, Taidi, Schwartz and others described the changes in the hemogram in this disease.1964 - Epstein and Barr isolated one of the causative agents of the herpesvirus family from lymphoma cells, the same virus was isolated from infectious mononucleosis.
As a result, it was concluded that this virus( Epstein-Barr virus), depending on the form of the flow, gives various diseases:
- acute or chronic mononucleosis,
- malignant tumors( Brekit's lymphoma, nasopharyngeal carcinoma, lymphogranulomatosis),
- the onset of autoimmune diseases( consider the involvement of the virus in lupus erythematosus and sarcoidosis),
- CSU( chronic fatigue syndrome).
Epstein-Barr virus - DNA containing a virus, the capsule of which is surrounded by a lipid envelope. It belongs to the group of Y-herpesviruses( human herpesvirus type 4) and has antigenic components common with other viruses from the herpesviridae family. VEB has tropism( selective damage) to B-lymphocytes, this is the peculiarity of the pathogen, because it multiplies in the cells of the immune system, causing these cells to clone their own, viral DNA, which subsequently leads to secondary immunodeficiency! Also VEB tropism is to some tissues - to the lymphoid and reticular, this explains the generalized lymphadenitis and hepatosplenomegaly( enlargement of the liver and lachrymation).It is possible that the features of the structure and the presence of tropism to the cells of the immune system cause a persistent persistence and create the risk of malignancy of the infected cells.
In the external environment it is not particularly stable, sensitive to high temperatures( more than 60 ° C) and disinfectants, but it is stored when frozen.
The prevalence is ubiquitous. The incidence of morbidity is observed more often in spring and autumn seasonality. The frequency of epidemic upsurge is recorded every 7 years.
Causes of infection with infectious mononucleosis
Age characteristics of infection: children of 1-5 years are more often ill. Up to a year do not get sick because of the presence of passive immunity, which is created by immunoglobulins, transferred from the mother transplacentally( through the placenta during pregnancy).Adults do not get sick, because 80-100% have already been immunized, ie they either had a sick childhood or were ill in an erased clinical form.
Source of infection - sick people with various clinical symptoms( even with erased), excretion can persist up to 18 months.
is airborne( due to the instability of the pathogen this pathway takes place in close contact),
- contact-household( contamination of saliva with the patient's saliva),
- parenteral( transfusion, transplantation - organ transplantation),
- transplacental( intrauterine infection, from mother to child)
Symptoms of infectious mononucleosis
The period of infection and symptoms can be divided into several periods:
1. Introduction of the causative agent = incubation period( from the momentintroducing to the first clinical manifestations) lasts for 4-7 weeks. During this period, the virus penetrates through the mucous membranes( oropharynx, salivary glands, cervix, gastrointestinal tract).After that, the virus begins to contact B-lymphocytes, infecting them, replacing their genetic information with their own, this causes further disorganization of the infected cells - they also get "cell immortality" - in fact, uncontrolled division, in addition to foreign DNA, and this is very bad, becausethey no longer perform a protective function, but simply carry the virus.
2. Lymphogenous invasion of the virus into regional lymph nodes, manifested by an increase in some groups of lymph nodes( for 2-4 days and lasts up to 3-6 weeks), near which there was a primary infection( airborne infection - cervical / submandibular and occipital lymph nodes,inguinal).Lymph nodes are enlarged 1-5 cm in diameter, painless, not soldered to each other, arranged in the form of a chain - this is especially noticeable when turning the head. Lymphadenitis is accompanied by intoxication and fever up to 39-40⁰С( appears simultaneously with an increase in lymph nodes and lasts up to 2-3 weeks).
3. The spread of the virus through the lymphatic and blood vessels will be accompanied by generalized lymphadenopathy and hepatosplenomegaly - appearance on 3-5 days. This is due to the proliferation of infected cells, their death, and as a consequence, the release of the virus from the dead cells, followed by infection of new cells, and further infecting organs and tissues. The defeat of the lymph nodes, as well as the liver and spleen, are associated with the trophicity of the virus to these tissues. As a consequence of this, other symptoms may also join:
- jaundice of the skin and sclera,
- rashes of different nature( polymorphic exanthema),
- darkening of urine and clarification of stool.
4. The immune response: as the first defense lines are interferons, macrophages. Afterwards, they are helped by T-lymphocytes - they lyse( absorb and digest) the infected B-lymphocytes, including where they settle in the tissues, and the viruses emerging from these cells form with the antibodies of the CEC( circulating immune complexes), which are very aggressive for tissues - this explains the involvement in the formation of autoimmune reactions and the risk of lupus, diabetes, etc., the formation of secondary IDS( immunodeficiency state) - due to damage to B-lymphocytes, because they are the ancestors of IgG andM as a traceThere is no synthesis of this infection, and also due to depletion of T-lymphocytes and increased apoptosis( programmed death).
5. The development of bacterial complications is formed on the background of IDS, due to the activation of our bacterial microflora or the attachment of an alien. As a result, angina, tonsillitis, adenoiditis develop. These sympoms develop by the 7th day from the onset of intoxication.
6. The stage of recovery or in the case of severe IDS - chronic mononucleosis. After recovery, a stable immunity is formed, and in the event of a chronic course, multiple bacterial complications with concomitant asthenovegetative and catarrhal syndrome occur.
Diagnosis of infectious mononucleosis
1. Virological( excretory excretion from saliva, swallow swabs, blood and liquor), the results come in 2-3 weeks
2. Genetic - PCR( polymerase chain reaction) - DNA detection of the
virus 3. Serological: reactionheterogemagglutination( not used, because it is low-specific and little informative) and ELISA( immunoassay) is the most used, because it allows to determine specific IgG and M specifically for the Epstein-Barr virus, even with their small number(acute or chronic)
4. Immunologic examination( immunogram):
- of T-lymphocytes( CD8, CD16, IgG /M/ A) and CEC - this indicates an immune response and good compensation;
- CD3, CD4 / CD8
5. The method of leukocyte concentration allows to determine the presence of atypical mononuclears and heterophilic antibodies, which are isolated by mononuclear cells. The detection of these atypical cells can be registered in the incubation period.
6. Biochemical methods: will indicate the decompensation of organs and systems: direct bilirubin, ALT and AST, timolin assay, transaminases and alkaline phosphatase.
7. Hematologic examination( UAC): Lc, Lf, M, ESR, Nf with a shift of the formula to the left.
Treatment of infectious mononucleosis
1. Etiotropic treatment( against the pathogen): isoprinosine, arbidol, valciclovir, acyclovir
2. Patonetic( blocks the mechanism of the pathogen): immunomodulators( interferon, viferon, timolin, thymogen, IRS-19, etc.) and immunostimulants(tsikloferon) - but the appointment under the control of the immunogram, because at this disease is very high risk of developing autoimmune diseases that can be compromised by these drugs,
3. Antibiotic therapy in connection with secondary bacterial microflora, more commonly appointed broad-spectrum antibiotics from the group of cephalosporins to identify the sensitivity of the pathogen to the antibiotic, and after a narrower focus.
4. Symptomatic therapy: antipyretic, local antiseptic, etc., depending on the dominant symptomatology.
Clinical follow-up for 6 months or more with pediatrician, infectious diseases specialist, specialists in narrow areas( ENT, cardiologist, immunologist, hematologist, oncologist), using additional clinical and laboratory studies( see Diagnostics + EEG, ECG, MRIetc).Also, exemption from physical culture, protection from emotional stresses - compliance with the protection regime for about 6-7 months. It should always be on the alert, because any compromise can trigger the triggering of autoimmune reactions.
Complications of infectious mononucleosis
- Hematologic: autoimmune hemolytic anemia, thrombocytopenia, granulocytopenia;a rupture of the spleen is possible.
- Neurological: encephalitis, cranial nerve palsy, meningoencephalitis, polyneuritis. GASTROINTESTINAL TRACT: development of a diabetes of 1 type, defeat of a liver.
- Respiratory organs: pneumonia, airway obstruction.
- Heart and vessels: systemic vasculitis, pericarditis and myocarditis.
Prevention of infectious mononucleosis
Hygiene compliance. Isolation of the patient for 3-4 weeks, taking into account clinical and laboratory data. Also use of diagnostic measures before and during pregnancy. Specific prevention is not developed.
Doctor therapist Shabanova IE