Mycoplasmosis Symptoms
Mycoplasmosis are infectious diseases that are caused by mycoplasmas, characterized by a polymorphism of clinical manifestations with a primary lesion of respiratory organs, urogenital tract and CNS.
Etiology. Mycoplasmas are the smallest free living prokaryotes, capable of autonomous growth and reproduction, occupy an intermediate position between viruses, rickettsia, bacteria and protozoa. They belong to the family Mycoplasmatacae, which includes 2 genera - Ureaplasma and Mycoplasma. Mycoplasmas are small polymorphic gram-negative microorganisms in sizes from 0.1 to 10 microns, contain RNA and DNA, mobile.
The unique properties of mycoplasmas are the absence of a cell wall( instead of a three-layer membrane), the smallest for the prokaryotic genome size( 500-1000 MD), the presence of a minimal amount of organelles, membrane parasitism. The latter property is due to the inability of mycoplasmas to synthesize cholesterol, which forces them to use the plastic material of the host cell. Attachment to the surface of the cell occurs due to actin-like protein-adhesin. Possible penetration of mycoplasmas into cells - into alveolocytes, phagocytes, etc. Pathogens are capable of prolonged persistence in the human body. Mycoplasma isolates pathogenicity factors - hemolysin, neurotoxin and hydrogen peroxide, U. uralyticum - urease enzyme that breaks urea to ammonia. Pathogens have immunosuppressive activity, stimulate the replication of viruses in the cell( HIV, oncogenic viruses, etc.).The main target cells are the epithelium of the respiratory and urogenital tracts, the oral cavity, alveolocytes, phagocytes, endothelium of the capillaries, etc.
For the human pathogenic 16 species of mycoplasmas..pneumoniae is the causative agent of respiratory mycoplasmosis, U. urealyticum, M. hominis and M. genitalium - diseases of the urogenital tract, M. incognitis - generalized mycoplasmosis, M. orale and M. salivamm - periodontitis, pulpitis, stomatitis, osteomyelitis, M. artritidis and Mfermentas - arthritis.
Mycoplasmas are unstable in the external environment, killed by low and high temperatures, with a change in pH, ultrasound, UV, standard disinfectants, detergents. Sensitive to macrolides, tetracyclines, fluoroquinolones, resistant to penicillin and other( 3-lactams, cephalosporins, carbapenems, sulfonamides.)
Epidemiology Mycoplasmas occupy 4-6 place in the etiologic structure of acute respiratory infections, they are etiological agents 5-30% of acute respiratory infections and 6-25% of pneumonia( in the period of epidemic upsurge - 30-60%)
The source is patients with manifest and subclinical forms of mycopdasmosis.for several weeks
The transmission pathways are airborne, sexual and vertical. In view of the low resistance of mycoplasmas in the environment, the airborne droplet pathway is realized only in close contact, therefore the foci of the disease are recorded in families, closed and semi-closed groups( preschool andschools, hostels, barracks, etc.).
Respiratory mycoplasmosis is characterized by autumn-winter-spring seasonality. Epidemic ups are observed once every 4-8 years. Schoolchildren are more often ill( 11-15 years) and young people. Postinfectious immunity persists for 5-10 years, so repeated diseases are possible.
Pathogenesis. Several stages are distinguished in the pathogenesis of mycoplasmosis.
1. Introduction and multiplication in the entrance gate. Entrance gate for.pneumoniae is the mucosa of the respiratory tract, for U. urealiticum, M. hominis and M. genitalium - the mucosa of the urogenital tract, for M. orale and M. salivarum - the oral mucosa. In the place of the entrance gate there is a multiplication of pathogens on the surface of cells and inside them.
2. Dissemination. As a result of the accumulation of mycoplasma and their toxins fall into the blood. Dissemination of pathogens also occurs in infected neutrophils and macrophages. There is direct damage to various organs - the central nervous system, heart, liver, kidneys, joints, etc. In addition, the unfavorable effect exerted by mycoplasma toxins. Hemolysin damages the cells of the ciliary epithelium, causes hemolysis of red blood cells, a violation of microcirculation, the development of vasculitis and thrombosis. Neurotoxin has a toxic effect on the central nervous system and cardiovascular system, increases the permeability of the blood-brain barrier. Toxic properties are hydrogen peroxide and ammonia, which secrete mycoplasma.
3. Development of serous inflammation. Adhesion of mycoplasmas to target cells leads to a violation of tissue architectonics, intercellular contacts, cellular metabolism and the structure of cell membranes. As a result, dystrophy, metaplasia, death and desquamation of epithelial cells, microcirculation disorders, increased exudation, necrosis, in infants - hyaline membranes. In the genesis of cell damage in the early stages of the infectious process, a direct role is played by the direct cytodestructive effect of mycoplasmas. Further, the immune component of inflammation associated with the deposition of immune complexes and the infiltration of tissues by cells participating in the immune response is attached. Peribronchial, perivascular and interstitial infiltration of affected tissues with lymphocytes, plasma cells, histiocytes, macrophages, monocytes and single neutrophils is formed. In addition, close contact of mycoplasmas with the cell membrane is important, under the conditions that the response protective reactions inevitably lead to cell damage. From the 5th-6th week of the disease, the autoimmune mechanism of inflammation comes to the fore, which plays a particularly important role in the chronic form of mycoplasmosis.
4. Development of the immune response, induction of IDS and autoimmune reactions. Factors of congenital resistance( mucociliary clearance, neutrophils, macrophages, complement, interferons) and immune response by cellular( CE) 8-lymphocytes) and humoral types( antibodies of classes IgM, IgA, IgG) participate in antimycoplasmic protection. Mycoplasma effectively counteracts the protective reactions of the macroorganism. They paralyze the movement of the cilia of the ciliated epithelium. Close association with cells and antigenic mimicry lead to a violation of mycoplasma recognition by macrophages. Pathogens infect neutrophils and macrophages, thus inducing unfinished phagocytosis. In addition, this leads to a disruption of the cooperation of cells participating in the immune response by cellular and humoral types. The development of secondary IDS promotes the formation of a mixed infection involving chlamydia, bacteria, viruses, fungi and protozoa. In recent years, the direct activating effect of mycoplasmas on the replication of HIV, oncogenic viruses, etc. has been proved. It has now been established that mycoplasmas cause the polyclonal activation of T and B lymphocytes, which in combination with the presence of cross antigens with tissues of the lungs, brain, liver, pancreasgland, smooth muscle, lymphocytes and erythrocytes leads to the development of autoimmune reactions.
5. Outcomes. The outcomes of the primary infection, taking into account the state of the immune system, are recovery, transition to a chronic or latent form. In the normal state of the immune status, the organism is sanitized from mycoplasmas. Patients with IDS develop a latent form of mycoplasmosis, in which pathogens persist in the body for a long time. There is a deactivation of the gene that codes for the synthesis of the P protein( adgezina), which allows mycoplasmas to elude the immune response. In conditions of immunosuppression, the pathogen again begins to multiply. With deep IDS, mycoplasmosis acquires a chronic course with localization of inflammation at the site of the entrance gates and / or with the formation of a wide range of diseases - rheumatoid arthritis, bronchial asthma, chronic interstitial pulmonary fibrosis, immune cytopenias, etc.
Classification. A.P.Kazantsev( 1997) identifies the following clinical forms of mycoplasmosis:
The duration of the incubation period is 3-11 days.
Clinical forms are rhinitis, pharyngitis, laryngotracheitis, bronchitis, otitis media, myringitis, eustachitis, sinusitis. The most common mycoplasmal pharyngitis. The disease begins acutely or gradually. Body temperature is normal, subfebrile or febrile.
Symptoms of intoxication are moderately expressed. Typical are complaints of dryness, perspiration and sore throat, dry cough, nasal congestion. Less common are the common cold, conjunctivitis, scleritis, hyperemia of the face. With pharyngoscopy, there is diffuse hyperemia and granularity of the posterior pharyngeal wall. The course of the disease is favorable. Fever is stopped, usually in 3-5 days, but the subfebrile condition can persist for 1-2 weeks. Catarrhal symptoms disappear after 7-10 days. The most common complication is otitis, less common are myringitis, eustachitis, and sinusitis.
Mycoplasma laryngitis is manifested by barking cough, hoarseness of voice, sometimes inspiratory dyspnea is attached. A characteristic symptom of tracheobronchitis is a dry, compulsive paroxysmal cough without recapitulation, which is accompanied by pains in the chest and stomach, sometimes ending with vomiting. Cough can persist for several weeks and even months. Sometimes bronchitis patients develop bronchoobstructive syndrome.
Mycoplasma pneumonia, along with chlamydia and pneumocystis, belongs to the group of atypical pneumonia, which is characterized by the absence of severe fever and clear physical data, paroxysmal cough, the presence of interstitial foci on the roentgenogram.
Mycoplasma etiology of pneumonia occurs in 9-22% of children and in 6% of adults. The disease often develops in children older than 7 years of life. The incubation period is 8-40 days. Mycoplasma pneumonia begins more often gradually( in 75% of patients), less often - acutely. The initial period lasts from 2 to 12 days. Symptoms of upper respiratory tract infection( pharyngitis, conjunctivitis, rhinitis) appear. Body temperature is subfebrile, rarely normal or febrile, the symptoms of intoxication are poorly expressed.
Deterioration of the condition is noted on the 3rd-4th day of illness in acute course or on the 7th-12th day with the gradual onset of the disease. The body temperature rises to 39-40 ° C.Symptoms of intoxication are moderate, do not correspond to fever, but can be pronounced( anorexia, headaches, myalgia, repeated vomiting, lethargy).Febrile fever persists for 2-12 days, then passes into a long subfebrile condition( up to 1-7 weeks).Characterized by a dry obsessive paroxysmal cough without a reprise, there may be pain in the chest. In the future, cough becomes productive, accompanied by the separation of viscous sputum. It can persist for a long time, for 6-8 weeks, even after the disappearance of the physical changes. Respiratory failure is most often absent. Physical data are scant - on a background of hard or weak breathing dry and wet rattles are heard, dullness of pulmonary sound is noted. In 10-20% of patients, especially in adolescents, "mute pneumonia" occurs. Physical data can persist for 30-50 days. As a result of the development of secondary CID, a mixed infection with chlamydia, bacteria, respiratory viruses, herpesviruses, fungi often occurs.
In a general blood test, leukocytosis, neutrophilia with a leftward shift, an increase in ESR are detected. Radiologic examination reveals interstitial changes: strengthening of vascular and bronchopulmonary pattern, small infiltrates of linear or loopy nature, interstitial edema, atelectasis. In children of early age, pneumonia is bilateral, in adolescents it is more often one-sided( right-sided).A third of patients are diagnosed with focal, segmental and lobar pneumonia. Perhaps involvement in the pathological process of the pleura.
Evidence of a systemic nature of the disease is extrasorrhagic symptoms. Half of patients have hepatomegaly, 25% have splenomegaly, 15% have polymorphic exanthema( small-spot, rose-oole, spotted or spotted-papular).The extraspiratory manifestations include lymphadenopathy( often anterior anterior lymph nodes), liver pathology( hepatitis, focal necrosis), heart( myocarditis, focal necrosis, pericarditis), joints( arthritis, polyarthritis), kidneys( nephritis), blood( hemolytic anemia,thrombocytopenia), the nervous system( meningitis, meningoencephalitis, polyradic loneuropathy), pancreas( pancreatitis), eye( uveitis), changes on the skin( erythema nodosum, polymorphic erythema, Stevens-Johnson syndrome), dyspeptic syndrome( nausea, vomiting, pain inIvoti, diarrhea), Reiter's syndrome.
The pathology of the nervous system is rare. Symptoms of serous meningitis or meningoencephalitis appear simultaneously with the defeat of the respiratory organs or precede it. Mycoplasma can cause myelopathy and polyradiculoneuropathy.
Mycoplasmas cause urethritis, prostatitis, vulvovaginitis, colpitis, cervicitis, metroendometritis, salpingoophoritis, epididymitis, cystitis and pyelonephritis. The pathology of the urogenital tract often occurs in sexually active adolescents.
The incidence of urogenital mycoplasmosis in women of childbearing age is 13.3%, in the presence of chronic urogenital pathology - 23.6-37.9%.During pregnancy, infection with mycoplasmas increases by a factor of 1.5-2( 40-50%).The risk of vertical transmission, according to various authors, varies from 3.5 to 96%.Intrauterine mycoplasmosis is diagnosed in 5.5-23% of newborns. The most frequent etiologic agent is M. hominis.
Infection can occur in the ante- and intranatal periods. Antenatal infection is realized by hematogenous, ascending, descending, transplacental pathways, with aspiration of infected amniotic fluid. In addition to direct damaging effects, mycoplasma causes chromosomal aberrations in the fetal cells. They induce the production of prostaglandins, leading to uterine contraction and termination of pregnancy. In addition, an adverse role is caused by mycoplasma spasm of the umbilical cord, the impact of harmful metabolic products and hyperthermia, leading to intrauterine hypoxia and delayed fetal development. Intranatal infection occurs as a result of contact of the mucous membranes of the child with the mother's birth canal and aspiration of amniotic fluid.
Due to the absence of pathognomonic symptoms, the analysis of maternal gynecological history data - the presence of colpitis, vulvovaginitis, cervicitis, metroendometritis, salpingo-oophoritis, urethritis, cystitis, pyelonephritis, infertility, habitual miscarriage, placental anomaly, premature placental abruption - is important for timely diagnosis., threats of abortion, late gestosis, polyhydramnios, chorioniaminitis, premature passage of amniotic fluid, prematures birth, postpartum endometritis, sepsis.
When infected in the antenatal period, clinical symptoms occur at birth - congenital mycoplasmosis develops. Infection in the first two weeks of pregnancy leads to blastopathy - death of the fetus or the formation of a systemic pathology similar to genetic diseases. When infection occurs at the gestational age of 15-75 days, embryopathy arises - true malformations at the organ or cell level, at the gestation period of 76-180 days - early fetopathy( false developmental anomalies associated with cystic-sclerotic deformities of the organs).A peculiarity of congenital mycoplasmosis is a rather high incidence of malformations of various organs( CNS, cardiovascular, respiratory, urinary systems, musculoskeletal system, etc.), which are registered in 63.4% of children.
Infection with a gestation period of more than 180 days leads to the development of a generalized form of congenital mycoplasmosis. Quite often there are prematurity, intrauterine growth retardation, hypoxic-traumatic CNS involvement, asphyxia. Symptoms occur at birth or appear within the next few hours after delivery. A clinic of the defeat of the respiratory system, cardiovascular system, central nervous system, hemorrhagic and lymphoproliferative syndromes. There are shortness of breath with accessory muscles, pale gray skin color, cyanosis, half of the children - foamy bloody discharge from the mouth. At auscultation, small bubbling wet rales and crepitations are heard. The roentgenogram reveals the expansion of the roots of the lungs, pneumonic foci, atelectasis, emphysema. Cardiovascular insufficiency develops, more often on the right ventricle type, edematic syndrome, sclera. Symptoms of mycoplasma meningitis and meningoencephalitis are a reduction in motor activity, tremor, convulsions, head tilt, hyporeflexia. One of the first manifestations may be acute hydrocephalus, which occurs already in the first week of life. Later, half of the children after the meningoencephalitis transferred have residual effects - lag in psychomotor development, focal signs, blindness, brain abscess, etc. In 20% of children with a generalized form of congenital mycoplasmosis, the liver is enlarged, in 10% - the spleen. Some patients have jaundice and hemorrhagic syndrome - bleeding, hemorrhages in the skin, subcutaneous tissue, internal organs( more often in the lungs and the liver), cephalohematomas.
Intranatal infection most often develops pneumonia, especially in premature babies, in whom it is characterized by a severe course and can result in death. In addition, there may be the appearance of conjunctivitis, vulvovaginitis, CNS pathology( meningitis, meningoencephalitis), carditis, abscesses and skin necrosis.
Diagnosis of mycoplasmosis is based on taking into account the data of an epidemic history, clinical symptoms and laboratory examination, which includes the following methods.
With respiratory mycoplasmosis, the leading clinical syndrome is "Prolonged paroxysmal cough".Differential diagnosis is performed with infectious diseases - with whooping cough, paracutosis, chlamydia and chlamydophileosis, CMVI, tuberculous bronchoadenitis;with non-infectious diseases - with a foreign body, cystic fibrosis, a mediastinal tumor, bronchial asthma. Differential diagnosis is based on a comprehensive analysis of the history, clinical, laboratory and instrumental examination.
Mycoplasmosis treatment is complex and includes methods of etiotropic, pathogenetic and symptomatic therapy under the control of clinical and laboratory indicators. Recommended mode, taking into account the severity of the disease and therapeutic nutrition, enriched with vitamins and trace elements.
Etiotropic therapy consists in the appointment of macrolides and tetracyclines. The most effective and safe drugs of choice in children are modern macrolides - azithromycin, clarithromycin, roxithromycin, spiramycin and josamycin. In children older than 8 years of life, tetracyclines( doxycycline, monocycline) can be used. With mycoplasmosis of the upper respiratory tract drugs prescribed for 5-10 days, with pneumonia - 2-3 weeks. When lesions of the central nervous system use levomitsetin, including endolyumbalno. The complex of therapy includes interferons( viferon, viferon-suppositories, gel, geneferon light-candle, kipferon, reaferon-EC lipint, reaferon, realiron, roferon A, intron A, etc.) and interferon inducers( amixin, anaferon, neovir,kagocel, cycloferon).In severe and complicated forms, immunoglobulins for intravenous administration are prescribed: immunovin, intraglobin, pentaglobin, intrathect, octagam, gabriglobin, etc.
Pathogenetic therapy consists of the use of cytokines( leukinferon, roncoleukin, etc.) and immunomodulators( thymalin, tactivin, thymogen,imunofan, polyoxidonium, lycopide, imunoriks, derinat, sodium nucleate, immunomax, etc.) under the control of the immunogram. Disintoxication therapy for mild and moderate forms includes copious drinking, with severe and complicated forms - infusion of glucose-saline solutions. Recommended multivitamins, vitamin-mineral complexes, antioxidants, probiotics( bifi-forms, linex, probiophore, bifidumbacterin-forte, etc.), according to indications - preparations of metabolic therapy( riboxin, cocarboxylase, cytochrome, elcar, etc.), glucocorticoids, antihistaminespreparations, inhibitors of proteases( countercrasal, trasilol, gordoks), vasoactive drugs( cavinton, actovegin, cinnarizine, pentoxifylline, etc.).In case of dry paroxysmal cough, antitussive drugs( sinecode, glauvent, tusuprex, paxeladin, libexin, stopptissin, etc.) are used, with mucolytics( bromhexine, ambroxol, carbocysteine, acetylcysteine, etc.) and moistening cough, and traditional expectorants( terpinhydrate, mucaltin,glycyrs, bronchicum, piles, koldrex, licorin, tussin, etc.).Apply methods of physiotherapy( electrophoresis with heparin, ozocerite boots), massage, exercise therapy.
Symptomatic therapy includes prescription according to the indications of antipyretic drugs and cardiac glycosides.
Reconvalvesent of mycoplasmal pneumonia 1 and 2 months after recovery recommend inspection of the pediatrician and pulmonologist, determination of mycoplasmosis markers by ELISA and PCR according to indications - examination of the immune status. Prescribe a protective regime, vitamin-mineral complexes and plant adaptogens courses for 1 month for 3 months, immunomodulators under the control of immunograms, exercise therapy, massage, physiotherapy, sanatorium treatment.
Live and killed vaccines are under development, so non-specific measures play a major role in prevention. Patients with mycoplasmosis of the upper respiratory tract are isolated for 5-7 days, patients with pneumonia - for 2-3 weeks. Prevention of congenital mycoplasmosis consists in the moral education of adolescents, the use of condoms, the timely examination and treatment of women of childbearing age and pregnant women.