Medical nutrition (diet)Symptomatic treatment
Etiotropic therapy
Etiotropic therapy of acute respiratory diseases, depending on the pathogens causing them, can be:
1) antiviral (for ARVI of viral etiology);
2) antibacterial (for ARVI of bacterial, mycoplasma or chlamydial etiology);
3) complex (for viral-bacterial infections, viral infections with bacterial complications).
Antiviral therapy includes the use of biological (interferons and immunoglobulins) and chemotherapeutic agents.
The success of antiviral therapy for ARVI is inseparable from compliance with the mandatory conditions:
1) emergency use;
2) regularity of intake;
3) compliance of drugs with the etiology of ARVI.
The most universal antiviral drugs are preparations of human leukocyte interferon. Currently, the domestic medical industry produces dosage forms intended for injection (intramuscular, subcutaneous, intravenous) and instillation (intranasal and inhalation use).
Human leukocyte interferon for instillation has low antiviral activity (up to 10,000 IU) and therefore requires repeated use and is used with better results in the treatment of children than adults. It is instilled into the nasal passages, 5 drops at least 5 times a day (for 2-3 days) when the first clinical symptoms of ARVI appear.
Interferon preparations for injection have high antiviral activity (100,000, 250,000, 500,000, 1,000,000 IU) and are therefore more suitable for the treatment of ARVI in adults.
Indications for prescribing the drug are moderate to severe clinical course of viral acute respiratory infections, as well as a state of functional immunodeficiency. There are no contraindications to prescribing the drug. The drug can be used in combination with other pathogenetic and symptomatic agents. Combined use with corticosteroid hormones should be avoided! When hormones cannot be excluded, it is recommended to use them separately with an interval of up to 6 hours.
For viral acute respiratory infections, short but intensive courses of 3-6 injections (100,000-1,000,000 IU depending on the severity and age of the patient 1-2 times a day) are preferable during the first 3 days of the disease, then according to indications (severe course, development of complications, to achieve stabilization of the clinical and immunological effect) the course can be extended with a frequency of administration every other day, 1-2 injections in subsequent weeks.
Good clinical efficacy has been achieved with the inhalation use of interferon preparations in aerosols with varying degrees of particle dispersion depending on the level of damage to the respiratory system.
There are pathogenetic and pharmacokinetic justifications for this:
the drug is delivered after the pathogen to the place of its direct colonization and reproduction;
the drug directly in unaffected cells causes a state of immunity to viral infection;
the drug increases the activity of local immune factors;
interferon administered by inhalation acquires different pharmacokinetic properties;
it remains in the body longer, and its preferential distribution and deposition in the tissues of the respiratory system makes it possible to reduce its therapeutic dose.
The degree of dispersion of the inhaled aerosol depends on the level of damage to the respiratory system:
1) when the lesion is localized in the trachea and large bronchi, it is advisable to inhale aerosols of medium dispersion with aerosol particle diameter of 1-5 microns;
2) when the lesion is localized in small bronchi, bronchioles and alveoli, the introduction of fine aerosols with a particle diameter of less than 1 micron is indicated.
The frequency of inhalations depends on the day of illness. When using interferon on the first day of the disease, a single inhalation of interferon at a dose of 500,000-1,000,000 IU is sometimes sufficient. If symptoms persist, inhalations are continued daily for the first 3 days, then every other day, if necessary, reducing the degree of dispersion and dose. For pneumonia, the course can be up to 10-15 inhalations.
Immunoglobulins
The most effective is anti-influenza donor gamma globulin (immunoglobulin), which is administered intramuscularly for severe forms of influenza to adults, 3 ml (3 doses); children - 1 ml (1 dose). The indicated doses are re-prescribed after 8 hours for severe symptoms of intoxication. In the absence of anti-influenza immunoglobulin, normal human immunoglobulin is used in the same doses, which also contains, albeit in smaller quantities, antibodies against influenza viruses and other pathogens of acute respiratory infections. It is better to prescribe immunoglobulins in the early stages of the disease, since the specific effect of these drugs is noted only when they are administered in the first 3 days of the disease.
Specific antiviral drugs are used in accordance with the expected etiology of acute respiratory infections.
For influenza A, the following drugs are used:
1. Remantadine (0.05 g) is prescribed in the early stages of the disease, especially on the first day, when it gives a pronounced effect, according to the scheme:
1) 1st day of illness, 100 mg 3 times a day after meals (on the 1st day, a single dose of up to 300 mg is possible);
2) 2nd and 3rd days of illness, 100 mg 2 times a day after meals;
3) 4th day of illness 100 mg 1 time per day after meals.
It is effective against influenza caused by type A virus and only when used early - in the first hours and days from the onset of the disease.
2. More effective are arbidol and virazole (ribavirin), which act on influenza viruses of both types A and B, when taken at the onset of the disease, 0.2 g 3 times a day before meals for 3-4 days.
3. Oxolinic ointment (0.25-0.5% in tubes) is applied (lubricate the nasal passages 3-4 times a day during the first 3-5 days of the disease). It softens catarrhal symptoms and shortens their duration. Therapeutic It has an effect only in the first days of the disease.
For adenovirus infection with symptoms of conjunctivitis, keratitis, keratoconjunctivitis, the following are indicated:
1) deoxyribonuclease 0.05% solution, 1-2 drops into the conjunctival fold;
2) Poludan (powder in ampoules of 200 mcg) is used in the form of eye drops and (or) injections under the conjunctiva. Poludanum solution, intended for instillation (instillation) into the eye, is prepared by dissolving the contents of the ampoule (200 mcg of powder) in 2 ml of distilled water. When stored in the refrigerator, the prepared solution can be used for 7 days. It is instilled into the conjunctival sac of the affected eye 6-8 times a day. As the inflammatory phenomena subside, the number of instillations is reduced to 3-4 times a day.
For subconjunctival injections, the contents of the ampoule are dissolved in 1 ml of water for injection and 0.5 ml (100 mcg) is administered under the conjunctiva of the eye daily or every other day (the drug dissolved for injection cannot be stored). A course of 10-15 injections is carried out in a hospital setting under the supervision of an ophthalmologist:
1) bonaftan in the form of tablets for oral administration and 0.05% ophthalmic ointment in 10 g tubes;
2) tebrofen (0.25-0.5% eye ointment in tubes);
3) Florenal (0.25-0.5% eye ointment in tubes).
Eye ointments are placed behind the eyelids 3 times a day, towards the end of treatment - 1-2 times a day. Duration of treatment is 10-14 days.
For herpes viral acute respiratory infections, acyclovir is prescribed intravenously 5-2.5 mg/kg every 8 hours (15-37.5 mg/kg per day) or vidarabine intravenously 10-20 mg/kg per day for 7-10 days, cyclovax orally 200 mg 5 times a day for 5 days.
Sulfonamide drugs and antibiotics (tetracycline, erythromycin, penicillin, etc.) do not have any effect on the viruses that cause ARVI, they do not reduce the incidence of complications. When they are prescribed for prophylactic purposes, pneumonia occurs more often in patients with influenza than in patients who have not received these drugs. Antibacterial agents, unreasonably used for viral acute respiratory infections, have a negative impact on the state of the body’s immune system and nonspecific defense mechanisms.
There are strict indications for prescribing antibacterial chemotherapy drugs and antibiotics - only for extremely severe and complicated forms of influenza and only in an infectious diseases hospital.
Antibacterial therapy is indicated for acute respiratory infections of mycoplasma, chlamydial and bacterial etiology, secondary (bacterial) complications of viral acute respiratory infections, activation of a chronic bacterial infection against the background of a viral acute respiratory infection. The choice of antibiotic depends on the expected etiology of acute respiratory infections, bacterial infection, the results of bacteriological examination of sputum and determination of the sensitivity of isolated microorganisms to antibiotics.
The basis for the success of antibacterial therapy is adherence to the following principles:
1) timeliness of appointment;
2) compliance with the sensitivity of the microorganism to the selected drug;
3) selection of the most effective and least toxic drug;
4) taking into account the pharmacokinetic characteristics of the drug;
5) dynamic monitoring of the sensitivity of the isolated microorganism to antibiotics;
6) timely drug withdrawal (prevention of toxic, allergenic and immunosuppressive effects of drugs);
7) prevention of mycoses (fungal diseases) with long-term use of antibiotics (prescription of antifungal drugs).
Pathogenetic treatment all forms of influenza and other acute respiratory infections are aimed at detoxification, restoration of impaired body functions, and prevention of complications.
Detoxification therapy
During a febrile period with mild and moderate forms of the disease, the patient is advised to drink plenty of fluids (up to 1-1.5 l/day) containing vitamins C and P (5% glucose solution with ascorbic acid, tea (preferably green), cranberry fruit juice, infusion or decoction of rose hips, compotes, fruit juices, especially grapefruit and chokeberry), mineral waters.
Pathogenetic therapy for severe forms that occur with severe intoxication is enhanced by detoxification measures - intravenous drip administration of 5% glucose solutions - 400 ml, Ringer's lactate (lactasol) - 500 ml, rheopolyglucin - 400 ml, hemodez - 250 ml ( no more than 400 ml per day for no more than 4 days), isotonic sodium chloride solution in total - up to 1.5 l / day against the background of forced diuresis using a 1% solution of Lasix or furosemide 2-4 ml to avoid pulmonary edema and brain The administration of coenzymes (cocarboxylase, pyridoxal phosphate, lipoic acid) improves tissues and helps reduce intoxication.
In case of severe symptoms of secondary toxic damage to the brain, intravenous infusion of 5 ml of a 20% solution of piracetam in 10 ml of isotonic sodium chloride solution is recommended once a day for 5-6 days, then 0.2 g of piracetam tablets 3 times a day . In case of severe toxicosis, corticosteroid drugs are prescribed - prednisolone 90-120 mg/day or equivalent doses of other glucocorticoids, oxygen therapy.
Antihemorrhagic therapy(prevention of bleeding) consists in prescribing adequate doses of ascorbic acid, calcium salts (chloride, lactate, gluconate), rutin. In severe forms, antihemorrhagic therapy is reduced to combating the developing DIC syndrome.
Improving microcirculation can be achieved both by normalizing blood dynamics in the pulmonary circulation and by normalizing systemic hemodynamics.
Normalization of hemodynamics (blood circulation) in the pulmonary circulation is achieved by prescribing the following respiratory agents:
1) camphor has a tonic effect on the cardiovascular system (strengthens the contractile function of the myocardium) and the respiratory system (released through the mucous membrane of the respiratory tract, has a bactericidal effect, causes an expectorant effect, improves alveolar ventilation). Subcutaneous administration of camphor oil 2-4 ml 3-4 times a day is recommended. When treated with camphor, the formation of infiltrates (oleoma) is possible;
2) sulfocamphocaine (10% 2 ml in ampoules) - a compound of sulfocamphoric acid and novocaine, has all the positive properties of camphor, but does not cause the formation of oleomas. It is rapidly absorbed when administered subcutaneously and intramuscularly, and can be administered intravenously. Apply 2-3 times a day;
3) cordiamine - 25% solution stimulates the respiratory and vasomotor centers, used 2-4 ml subcutaneously, intramuscularly and intravenously 3 times a day for severe arterial hypertension in patients with severe and extremely severe acute respiratory viral infections, especially complicated by pneumonia and during periods of crisis .
In case of a significant decrease in the contractility of the left ventricle (with the development of infectious-allergic myocarditis, complicating the course of severe influenza and other acute respiratory infections), it is possible to use cardiac glycosides - 0.06% solution of corglicon up to 1 ml, 0.05% solution of strophanthin up to 1 ml. You should remember the hypersensitivity of the inflamed myocardium to cardiac glycosides and use them intravenously in small doses (for example, 0.3 ml of a 0.05% solution of strophanthin).
Bronchodilators are indicated for the development of bronchospasm syndrome with bronchitis and bronchiolitis, which disrupts the ventilation function of the lungs, contributes to the development of hypoxemia (decreased blood oxygen saturation), delayed inflammatory effusion and the development of pneumonia. An arsenal of drugs used to treat bronchospastic conditions is presented below.
Symptomatic bronchodilators:
1) ipratropium (Atrovent, Treventol);
2) oxitropium;
3) salbutamol;
4) berotec (fenoterol);
5) bricanil.
Pathogenic agents:
1) theophylline;
2) aminophylline;
3) diprophylline;
4) theobiolong;
5) teopek;
6) theol.
Combination drugs
1) theophedrine (theophedrine, theobromide, caffeine, amidopyrine, phenacytin, ephedrine hydrochloride, phenobarbital, cytisine, belladonna extract) 1/2-1 tablet 2-3 times a day;
2) solutan (liquid belladonna extract, liquid datura extract, liquid primrose extract, ephedrine hydrochloride, novocaine, sodium iodide, ethyl alcohol) 10-30 drops 3-4 times a day.
Desensitizing drugs (antiallergic) are used in the complex therapy of ARVI as an antiallergic component, and the side effect of some of them helps to combat sleep disorders due to severe intoxication. In clinical practice, diphenhydramine, diprazine, diazolin, tavegil, suprastin, fenkarol, bicarfen, astemizole, pheniramine maleate, and peritol have been used for the treatment of influenza and acute respiratory infections.
Correction of the protective functions of the macroorganism consists of measures to improve the function of the local bronchopulmonary defense system and, according to indications, immunomodulatory therapy.
The local bronchopulmonary protective system includes the normal function of the ciliated epithelium, normal microcirculation, and the production of protective factors. Influenza viruses and other acute respiratory infections themselves, as well as emergency conditions that develop in severe cases, cause dysfunction of the bronchopulmonary defense system, which contributes to the introduction of an infectious pathogen into the tissue and the development of inflammation (pneumonia) in it. Improvement in the function of the bronchopulmonary protection system occurs with the use of bromhexine (in tablets of 8-16 mg 2-3 times a day), ambroxol, which stimulate the formation of surfactant - a surfactant that prevents the collapse of alveoli and is bactericidal.
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Medical nutrition (diet)Symptomatic treatment
Influenza viruses affect almost all warm-blooded animals (people, animals, birds, etc.). Influenza of genus A is more virulent and contagious than viruses of genus B and C. This is explained by the fact that in viruses of genus A, the surface antigens hemagglutinin (H) and neuraminidase (N) determine the greatest intensity of intoxication (H) and immunosuppressive effect (N).
Influenza B viruses are characterized by a smaller number of mutations and antigenic drift, therefore epidemics are defined once every 3-4 years. Influenza type C does not mutate and is not epidemic.
The problem with influenza infection is that the human influenza A virus is capable of exchanging genetic information with avian and animal influenza viruses to form mutants that have new pathological features and virulence.
The ideal model for genetic shuffling (drift) of viral RNA segments is the pig. Several strains of influenza viruses can be registered in her body at the same time. Pigs are particularly sensitive to human and avian influenza viruses.
Today, up to 170 combinations of potential influenza A subtypes are known. This explains why influenza remains an uncontrolled and poorly controlled infection to this day. The formation of the antigenic shift of the influenza A virus is still unpredictable. The lack of immunity in the population to the virus, which has undergone rapid mutation (shift), and its high virulence are the main factors in the formation of the pandemic (WHO, ERS, 2009-2016).
The first influenza A pandemic in 1918 made history by killing 50 million people. The most severe pandemic of our time was caused by the 2009 Californian influenza A (H1N1), which resembled the Spanish flu.
However, it is quite difficult to assess the damage caused by influenza infection. For example, it is known that the mortality rate for viral bacterial pneumonia (VbP) reaches 10% (in our practice, all deaths in 2009-2016 are associated with influenza A/California, H1N1).
However, statistics do not take into account other infectious and non-infectious complications of influenza infection. The death of the columnar epithelium of the tracheobronchial tree due to apoptosis of the affected cells, the immunosuppressive effect of the influenza virus allows the breakthrough of a bacterial infection, often opportunistic flora of the oral cavity, bronchial tree, into the systems and organs of the body, forming infectious complications of influenza.
The release of mature viruses is accompanied by massive cell death, tracheobronchitis and toxemia. Due to the destruction of the natural protective barrier of the mucous membrane of the trachea and bronchi, viruses enter the bloodstream and other organs and systems. Translocation of the influenza virus is accompanied by the formation of distant viral-bacterial lesions.
Influenza is characterized by a significant intoxication syndrome, which develops due to the massive death of cells affected by the virus. The first cycle of viral replication in the superficial cells of the tracheobronchial tree lasts about 4-6 hours, the progeny reaches 103 IU/ml.
An increase in the virus content to 106-1010 IU/ml triggers the programmed death of the affected cells. This determines the further escalation of the infectious process, which consists of viremia and generalization of the viral infection. The formation of the disease occurs in the next 24 hours, when the concentration of viruses reaches 1023 IU/ml. This explains why influenza is an extremely dynamic process.
In general, we observed the following infectious viral-bacterial complications of ARI, influenza: VbP, pleurisy, infectious exacerbation of COPD and bronchial asthma, acute purulent tracheobronchitis, acute bacterial rhinosinusitis, tonsillopharyngitis, otitis media, heart damage (myocarditis, pericarditis), brain (arachnoiditis , encephalitis, meningitis, Guillain-Barre syndrome), pyelonephritis, sepsis, toxic hemorrhagic pulmonary edema, invasive pulmonary aspergillosis, relapse of erysipelas and exacerbation of chronic infections, incl. viral
On the other hand, as a result of intoxication, characteristic damage to the vascular system develops - hemorrhagic capillary toxicosis, which underlies non-infectious complications of influenza. The development of non-infectious complications is associated not so much with the cytopathic effect of viruses, but with pathoimmune mechanisms.
Among the non-infectious complications of ARI and influenza, the following were observed: acute tubulointerstitial nephritis, acute renal failure, intestinal paresis, acute pancreatitis, manifestation of diabetes mellitus, cardiovascular complications (transient ischemic attack, acute cerebrovascular accident, myocardial infarction, venous and arterial thrombosis), radiculitis , neuralgia, polyneuropathy, myositis, exacerbation/manifestation of idiopathic fibrosing alveolitis.
It is not possible to clinically differentiate the etiology of ARI and influenza. Therefore, taking into account the possible severe consequences of influenza, all cases, especially during the epidemic period, should be considered as influenza. Let us note that the greatest epidemic danger is represented by patients with a mild course of influenza infection, who continue to lead an active lifestyle and infect a large number of others.
Verification of ARI, influenza A and B is possible after a virological study. A smear should be taken at the first sign of a cold, maximum in the first 2-3 days. Nasopharyngeal swabs for polymerase chain reaction (PCR) are taken from the inferior turbinate of each nostril with deep insertion, turning the stick in a circular motion. The sample can be stored at temperatures up to +4 °C for no more than 24 hours.
To understand the etiology, we try to carry out PCR diagnostics of influenza in all possible cases of first contact and always in severe cases, complications, sepsis, early ALI or ARDS, etc. Practice shows that in the next infected person, the influenza infection can acquire a complicated or fatal course.
Treatment of ARI and influenza is started without waiting for the result of PCR diagnostics. A negative result for influenza A, B does not exclude the presence of another viral infection and should not be a reason for not prescribing antiviral therapy.
To verify the infectious complication of ARI and influenza, bacteriological studies are indicated. For example, a nasopharyngeal smear, sputum analysis, Eram staining of sputum samples, microbiological culture to determine sensitivity to antibiotics. If bacteremia is suspected, blood culture, preferably before prescribing antibiotics, and microbiological examination are necessary.
Control indicators include: blood tests, biochemical studies, blood gases, radiography, spiral CT or MRI of relevant organs and other studies as indicated.
Treatment of patients with influenza should be etiotropic and pathogenetically justified. Etiotropic antiviral drugs (EPDs) are used to prevent the development of severe forms of the disease, complications and deaths. EPP administration begins no later than 36-48 hours from the onset of the first symptoms of the disease. This standard of use of EPP ensures maximum clinical effectiveness.
In the formation of complications, the importance of the fact that the absolute majority of patients (95%) with the manifestation of ARI or influenza does not take EPP is obvious. As before, 82% of patients are admitted to the hospital 5-7 or even 10-14 days after the onset of clinical manifestations of ARI and influenza.
In all cases of ARI and influenza, EPP is prescribed at the first visit. Most often Ingavirin, because it effectively suppresses the reproduction and cytopathic effect of influenza A and B viruses and adenoviruses, parainfluenza. We cannot agree with the opinion that antiviral therapy is not indicated for mild to moderate influenza infections.
The manifestation of clinical manifestations indicates an active course of a viral infection, this is always clear. However, we do not know how the virus will behave in a particular person, whether there will be infectious or non-infectious complications or how the infectious process will resolve (cases ranging from mild tracheobronchitis to a fulminant course with the formation of fatal hemorrhagic pneumonia within 24 hours have been observed).
Particular attention is paid to persons at risk for severe ARI, influenza, and the formation of complications: obesity (BMI > 32 kg/m2), diabetes mellitus, COPD, bronchial asthma, cardiovascular pathology, chronic kidney disease, anemia, secondary immunodeficiency (for example , alcoholism, drug addiction, cachexia, liver cirrhosis, taking immunosuppressants, oncopathology), lobar or bilateral VbP, constant use of acetylsalicylic acid; pregnant women.
Modern EPPs for influenza A and B viruses are: oseltamivir, zanamivir, imidazolyl ethanamide (Ingavirin). The first two are antineuraminidase by their mechanism of action, the third is antinucleoprotein.
Oseltamivir is prescribed 75 mg (in severe cases of influenza, pneumonia and pregnant women - 150 mg) 2 times a day for 5 days, in severe cases - up to 7-10 days. Zanamivir is used at a dose of 10 mg 2 times a day for 5 days (the drug of choice for pregnant women; control of possible bronchospasm is necessary). A feature of the influenza A/California (H1N1) virus is its initial resistance to adamantane drugs - rimantadine. In addition, rimantadine is ineffective against influenza B and other acute respiratory infections.
Imidazolylethanamide (Ingavirin) is a low-molecular pseudopeptide that is an analogue of natural peptidoamine isolated from the nervous tissue of a marine mollusk Aplysia californica. Ingavirin specifically affects influenza viruses types A and B, as well as other “cold” viruses.
The mechanism of the antiviral effect of the drug is to disrupt conformational maturation and delay the migration of the synthesized nucleocapsid protein of the influenza virus from the cytoplasm to the nucleus, which is a necessary condition for the implementation of the infectious process in cells infected with the influenza virus. Therefore, by suppressing virus reproduction at the nuclear phase, according to the mechanism of action, Ingavirin is an antinucleoprotein drug.
When studying interferon (IFN) status, it was found that after a single dose of Ingavirin at a dose of 90 mg/day, the drug has a modulating effect on the functional activity of the IFN system, causing an increase in its content in the blood within the upper limits of the physiological norm (8-16 U/ml) after 24-48 hours, increases and normalizes the reduced ability of blood leukocytes to produce IFN-a, IFN-y.
The anti-inflammatory effect is due to the suppression of the production of key anti-inflammatory cytokines. Thus, Ingavirin not only has an inhibitory effect on the reproduction of influenza viruses, but also has immunomodulatory and anti-inflammatory activity.
The positive effect of Ingavirin in most cases becomes obvious approximately 48 hours from the start of treatment (or after taking the 2nd capsule), when patients notice an improvement in their well-being and a decrease in the severity of the main symptoms, which coincides with the dynamics of the average values of maximum body temperature.
For example, in double-blind, randomized, placebo-controlled, multicenter studies in adults and children (2010-2015), it was shown that in the Ingavirin group, fever lasted 1.5 ± 0.2 days, headache lasted 2.1 ± 0, 2 days, dizziness - 1.7 ± 0.2 days, weakness - 3.3 ± 0.2 days, and in the placebo group - 3.0 ± 0.3 days, 3.1 ± 0.3 days, 2. 4 ± 0.2 days and 4.9 ± 0.2 days, respectively.
Manifestations of cough in the Ingavirin group disappeared within 4 days in 77% of patients, rhinitis in 78%, tracheitis in 57%, and in the placebo group over the same period in 52, 65 and 31%, respectively. Similar dynamics of flu symptoms were observed in the group of children aged 7-12 years.
In adults and children, the use of Ingavirin significantly reduced the duration of the febrile period, intoxication syndrome and catarrhal symptoms. Secondary complications of influenza (VfP, acute tonsillopharyngitis) were diagnosed only in patients in the placebo group (8%).
The effectiveness of Ingavirin was confirmed by virological studies: after 24 hours of treatment, the isolation of influenza virus from nasal swabs stopped in 36% of patients (observation period - 5 days). Elimination of the virus within the same time frame occurred in only 13% of patients receiving placebo.
It is important that taking Ingavirin was not accompanied by side effects on the gastrointestinal tract, central nervous and cardiovascular systems, and no allergic reactions were recorded. It is known that the LD50 of the drug exceeds the therapeutic dose by more than 3000 times. Our 5-year experience of using Ingavirin confirms the absence of any side effects.
In an open comparative study of the clinical effectiveness of Ingavirin and oseltamivir, it was found that in most patients the temperature returned to normal in the first 24-36 hours from the start of treatment. After 36 hours of treatment, body temperature was consistently normal in patients of both groups.
Ingavirin is prescribed for adults at 90 mg/day (in severe cases 180 mg/day), for children over 7 years old - 60 mg/day, for 5-7 days. It can be noted that imidazolylethanamide affects not only influenza viruses, but also other viruses that initiate ARI. In severe, complicated cases of influenza, positive results have been established from the simultaneous administration of Ingavirin 180 mg/day and oseltamivir 300 mg/day for 5-10 days. Indicated for emergency prophylaxis of contact persons.
It should be noted that in real conditions, in the vast majority of cases, patients for some reason take symptomatic drugs, immunomodulators, and IFN inducers. 5% of patients take EPP at the prehospital stage. In this regard, we are holding an explanatory conversation about the need to take EPP as a priority.
Among the anti-cold medications, we also discuss symptomatic medications that can be prescribed for ARI and influenza, not instead of, but together with EPP. For example, antipyretics (paracetamol, ibuprofen) for hyperthermia (at > 38 ° C, in cases of hypoxemia, fever is contraindicated, since it determines a further drop in saturation), severe cerebral and cardiovascular disorders.
Symptomatic therapy for ARI and influenza may include the following drugs: fenspiride (almost all patients with ARI have symptoms of tracheobronchitis), various forms of IFN (viruses are always immunosuppressive), IFN modulators (tilorone), acetylcysteine (erdostein), antioxidant (thiotriazoline), lactobacilli , diclofenac, low molecular weight heparin, immunoglobulins for intravenous administration, colony-stimulating factor (filgrastim), prostacyclin analogue (iloprost) and others according to indications.
Glucocorticosteroids and acetylsalicylic acid are not indicated. Antibiotics are possible only with the development of viral and bacterial complications. Prescribed under the supervision of microbiological studies, taking into account leukocytosis, levels of procalcitonin and CRP. In our practice, for ARI and influenza, we combine the use of antibiotics with the prescription of EPP, for example, Ingavirin.
For the first contact doctor, it is difficult to resolve the issue of hospitalization. Modern principles of medical triage of patients with ARI and influenza will help with this, which distinguish the following group for hospitalization: saturation< 92 % (у беременных < 94 %), частота дыхания >30 in 1 min, heart rate > 130 in 1 min, peak expiratory volumetric flow rate< 33 %; артериальное давление < 90/60 мм рт.ст., нарушение сознания, гипертермия >38.5 °C, age > 65 years, hemoptysis, organ failure.
In severe cases of influenza, there is a high risk of developing ALI with early acute respiratory failure (ARF), which, in the absence of treatment effect, progresses to the development of ARDS. ALI syndrome is manifested by gas exchange disturbances and deterioration in the elasticity of the lungs, which leads to a high “cost” of breathing.
The schematic diagram of respiratory support includes the following sequential stages: in cases of decreased saturation< 92 %, респираторного индекса (РИ) 200- 300 мм рт.ст. на старте проводилась интенсивная оксигенотерапия под контролем пульсоксиметрии, скорость потока 10-15 л/мин, в течение 15 минут (64 % больных).
If ineffective (for example, PaCO2 > 50 mm Hg, pH< 7,35 ед., РаО2< 60 мм рт.ст., отсутствие прироста PaО2/FiО2) - перевод на неинвазивную вентиляцию легких (НИВЛ, СиПАП-терапия (Continuous Positive Airway Pressure - СРАР).
With the development of ARDS, PSV and BiPAP (Pressure Support Ventilation - PSV, Ventilogik LS, Ventimotion 2 devices) modes are more preferable than CPAP. During the first day of stay in the intensive care unit, NIBL is performed continuously, with short breaks, lasting 10-20 minutes, expiratory pressure from 4 to 20 cm water column. (WHO, ERS, 2009-2016).
If NIBL is contraindicated (for example, facial trauma) or is ineffective after starting within 1 hour, ARDS develops: persistence of acute respiratory failure (ARF) with 100% oxygen supply, saturation< 85 %, ЧД >40/1 min, heart rate > 120/1 min, blood pressure< 100/60 мм рт.ст., РаСО2 >60 mmHg, pH< 7,2 ед., РаО2< 60 мм рт.ст., PaО2/FiО2 < 200 мм рт.ст.; нестабильная гемодинамика, признаки нарушения сознания; показан перевод на искусственную вентиляцию легких (ИВЛ) (11 % больных).
If a decision is made to start mechanical ventilation, then the “protective ventilation” mode is used; the main task is to ensure an adequate minute volume of ventilation with minimal risk of voluto- and barotrauma of the lungs. We use volume (VC) and pressure (PC) control modes, auxiliary mode (SIMV + vol.contr., Servo-i device). Sedation and adaptation to mechanical ventilation are carried out with an infusion of dexmedetomidine 0.25-3 mcg/kg/h.
Regardless of the ventilation mode, we set the following parameters: if possible, FiO2 0.8-0.6-0.4; tidal volume 6-8 ml/kg of proper body weight, minute volume 8-10 l/min; hardware frequency 20-25 per minute; PEEP is 5-20 cm water column, plateau pressure is up to 25-30 cm water column, i.e. We comply with the principles of the baby lung concept.
If possible, we lower the oxygen concentration, but with control of saturation > 90-92%. Against this background, we carry out sanitation of the bronchial tree every two hours, daily sanitation using a fiber-optic bronchoscope.
In severe ARDS (PaO2/FiO2< 150 мм рт.ст.) возможны рекрутмент-маневр (открытие альвеол) путем создания СРАР 40 см вод.ст. в течение 40 с, назначение проно-позиции (WHO, ERS, 2009-2016).
In terms of subsequent prevention of influenza infection and complications, we recommend seasonal vaccination against influenza for all convalescents of ARI and influenza; have a package of EPP at home to start taking an effective antiviral drug in the first hours of the onset of a viral infection.
Over the years of observation (2009-2016), we did not note any cases of hospitalization, complications or deaths in persons vaccinated with the influenza vaccine.
Mavrodiy V.M., Artemenko V.Yu.
They belong to the orthomyxovirus family. There are influenza viruses types A, B and C.
The influenza virus has a spherical shape, with a diameter of 80-120 nm. The nucleocapsid has helical symmetry and is a ribonucleoprotein strand (NP protein), arranged in the form of a double helix, which makes up the core of the virion. RNA polymerase and endonucleases are associated with it. The core is surrounded by a membrane consisting of the M protein, which connects the ribonucleoprotein strand to the lipid bilayer of the outer shell. Among the proteins of the supercapsid shell, two are of great importance:
1) neuraminidase – a receptor protein that ensures the penetration of the virus into the cell;
2) hemagglutinin. Performs a receptor function, has an affinity for glycoproteins of receptors in cells of the mucous membrane of the respiratory tract.
The genome of the virus is represented by a minus-strand fragmented RNA molecule. Replication of orthomyxoviruses primarily occurs in the cytoplasm of the infected cell. Viral RNA synthesis occurs in the nucleus. The host cells provide the virus with new RNA transcripts, the 5 ends of which are used to cap the 5 ends of the viral messenger RNA.
Influenza viruses A, B and C differ from each other in the type-specific antigen associated with the M and NP proteins. The narrower specificity of type A virus is determined by hemagglutinin (H-antigen). There is high antigenic variability within the genus.
The variability of the H-antigen determines:
1) antigenic drift - changes in the H-antigen caused by point mutations in the gene that controls its formation;
2) antigenic shift - a complete replacement of a gene, which is based on recombination between two genes.
Initially, the pathogen replicates in the epithelium of the upper respiratory tract, causing the death of infected cells. The virus enters the bloodstream through damaged epithelial barriers. Viremia is accompanied by multiple lesions of the capillary endothelium with an increase in their permeability. In severe cases, extensive hemorrhages are observed in the lungs, myocardium and various parenchymal organs.
The main symptoms include a rapid increase in body temperature with accompanying myalgia, runny nose, cough, and headaches.
The pathogen is widespread, with an increase in incidence observed in the cold months. The main route of transmission of the pathogen is airborne. Children and the elderly are most susceptible.
Laboratory diagnostics:
1) express diagnostics - determination of virus antigens in the cytoplasm of the epithelium of the nose and nasopharynx in fingerprint smears using the ELISA method;
2) infection of cell cultures or chicken embryos with nasal discharge, sputum or nasopharyngeal washings (obtained in the first days of the disease);
3) serodiagnosis (RSK, RTGA, enzyme activity inhibition reaction).
Specific prevention:
1) for passive immunization – human influenza immunoglobulin;
2) for active immunization - live and inactivated vaccines.
Treatment: amantadine derivatives (rimantadine).
2. Parainfluenza. PC viruses
Parainfluenza virus and RS virus belong to the family Paramyxoviridae.
These are spherical viruses with a spiral type of symmetry. The average virion size is 100–800 nm. They have a supercapsid shell with spinous processes. The genome is represented by a linear, non-segmented RNA molecule. The RNA is associated with a major protein (NP).
The shell contains three glycoproteins:
1) HN, which has hemagglutinating and neuraminidase activity;
2) F, responsible for fusion and exhibiting hemolytic and cytotoxic activity;
3) M protein, which forms the inner layer of the viral shell.
Virus replication is completely realized in the cytoplasm of host cells. The human parainfluenza virus belongs to the genus Paramyxovirus. Viruses are characterized by the presence of their own RNA-dependent RNA polymerase (transcriptase).
Based on the differences in the antigenic structure of the HN, F and NP proteins of human parainfluenza viruses, four main serotypes are distinguished. Types 1, 2 and 3 are antigenically related and cross-react with mumps virus antigen. Type 4 viruses do not have a clear antigenic relationship.
The pathogen reproduces in the epithelium of the upper respiratory tract, from where it enters the bloodstream, causing viremia.
Clinical manifestations in adults most often occur in the form of catarrh of the upper respiratory tract. In children, the clinical picture is more severe, often with symptoms of intoxication. The disease is most severe in young children.
The main route of transmission of the parainfluenza virus is airborne. The source of infection is the patient (or the virus carrier).
Laboratory diagnostics:
1) rapid diagnostics - detection of antigens in the cells of the nasal passages using ELISA;
2) isolation of the pathogen in monolayers of human or monkey embryonic kidney cultures;
3) serodiagnosis (RSC, RN, RTGA with paired sera of sick people).
Specific prophylaxis is not used.
PC virus is the main causative agent of lower respiratory tract diseases in newborns and young children. Belongs to the genus Pneumovirus.
It is characterized by low stability, virions are prone to self-disintegration, and in purified form they exhibit pronounced polymorphism. There are three small types of PC virus, the antigenic differences between which are determined by a specific surface antigen.
The pathogen replicates in the epithelium of the airways, causing the death of infected cells, and exhibits pronounced immunosuppressive properties, which explains the high frequency of secondary bacterial infections.
PC virus causes annual epidemic respiratory tract infections in newborns and young children; Adults can be infected, but their infection is mild or asymptomatic.
Laboratory diagnostics:
1) express diagnostics - determination of virus antigens in nasal discharge using ELISA;
2) specific antigens are detected in RSC and RN.
Causal therapy has not been developed.
3. Adenoviruses
The family Adenoviridae includes two genera – Mastadenovirus (mammalian viruses) and Aviadenovirus (avian viruses); the first includes about 80 species (serovar), the second - 14.
The family includes viruses with a naked capsid (no outer shell) and cubic type of symmetry. The virion size is 60–90 nm. The genome is represented by a linear double-stranded DNA molecule.
The mature virus consists of 252 capsomeres, including:
1) hexons containing type-specific antigenic determinants that act upon the release of hexons in the virion, responsible for the manifestation of the toxic effect;
2) pentons containing small virus antigens and a reactive soluble antigen of the family, which determine the hemagglutinating properties of viruses.
Antigenic structure:
1) surface antigens of structural proteins (species- and type-specific);
2) hexon antigens (group-specific);
3) complement-fixing antigen (identical for different serotypes).
The main transmission routes are airborne and contact.
The symptoms of lesions are caused by the reproduction of the pathogen in sensitive tissues. Based on the type of damage to sensitive cells, three types of infections are distinguished:
1) productive (lytic). Accompanied by cell death after the exit of the daughter population;
2) persistent. It is observed when the rate of reproduction slows, which allows tissues to replenish the loss of infected cells through the normal division of uninfected cells;
3) transformative. In tissue culture, cells transform into tumor cells.
The main clinical manifestations of adenoviral infections.
1. Most often - ARVI, which occurs as influenza-like lesions. The peak incidence occurs in the cold season. Outbreaks are possible throughout the year.
2. Pharyngoconjunctivitis (pharyngoconjunctival fever). The peak incidence occurs in the summer months; The main source of infection is the water of swimming pools and natural reservoirs.
3. Epidemic keratoconjunctivitis. The lesions are caused by infection of the cornea due to injury or medical procedures. Erosion of the cornea up to loss of vision is possible.
4. Infections of the lower respiratory tract.
Laboratory diagnostics:
1) isolation of the pathogen by inoculation into cultures of human epithelial cells; the material being examined is nasal discharge, pharynx, conjunctiva, feces;
2) detection of viral antigens in cells by immunofluorescence microscopy;
3) RSC, RTGA and RN of cytopathic effect in cell culture.
Treatment: There are no specific drug therapies.
Specific prevention: live vaccines, including weakened viruses of the dominant serotypes.
4. Rhinoviruses
They belong to the Picornaviridae family.
Virions have a spherical shape and cubic type of symmetry. Size 20–30 nm. The genome is formed by a positive-sense RNA molecule that is not segmented. The size of the molecule is small. An RNA molecule is linked to one protein molecule. The capsid shell consists of 32 capsomers and 3 large polypeptides. There is no supercapsid shell.
Virus replication occurs in the cytoplasm. Assembly of host cells and filling of the capsid also occur in the cytoplasm; virus release is accompanied by cell lysis.
Viruses lose their infectious properties in an acidic environment. They are well preserved at low temperatures. The temperature required for replication is 33 °C; increasing it above 37 °C blocks the last stage of reproduction.
Rhinoviruses are divided into two large groups based on their ability to reproduce in cells:
1) viruses of group H. They multiply and cause cytopathic changes in a limited group of diploid cells, the human embryo and a special line (K) of HeLa cells;
2) group M viruses. They multiply and cause cytopathic changes in the kidney cells of monkeys, human embryos and various continuous cell lines of human cells.
Under optimal cultivation conditions, a cytopathic effect is manifested.
Antigenic structure:
1) based on the structure of a single type-specific antigen, 113 immunologically heterogeneous groups are distinguished; there is no group-specific antigen;
2) in humans, rhinovirus infection causes the production of neutralizing antigens and a state of immunity.
The main route of transmission is airborne droplets, the reservoir is a sick person (the pathogen is released within 1–2 days before the onset of symptoms and 2–3 days after the onset of the disease).
Rhinoviruses are localized in the epithelial cells of the nasal mucosa with copious secretions, and in children - the bronchial mucosa, causing a runny nose, bronchitis, and bronchopneumonia.
After the illness, a short-term immunity remains, which is effective only against the homologous strain. It is determined by secretory immunoglobulins of the IgA type.
Laboratory diagnostics:
1) isolation of viruses from cell cultures infected with nasal discharge;
2) rapid diagnostics - immunofluorescent method; allows detection of viral antigen in the cytoplasm of epithelial cells of the mucous membrane.
Treatment: there are no specific antiviral therapy, treatment is symptomatic.
Specific prevention: immunoprophylaxis is not carried out due to the large number of serological variants of the pathogen.
5. Reoviruses. PC viruses
Reoviruses belong to the family Reoviridae.
Virions are spherical in shape, diameter 60–80 nm. The capsid is built according to icosahedral symmetry. Double-stranded RNA consists of ten fragments. The inner and outer capsids contain eight separate proteins. One of the outer capsid proteins is responsible for binding to specific cellular receptors; with the help of another, the virus penetrates the host cell.
Viral replication occurs in the cytoplasm of host cells.
Reoviruses are cultivated in various cell cultures. The cytopathic effect appears late and resembles nonspecific degeneration of the cell monolayer.
There are three serotypes of reoviruses. They have a common complement-fixing antigen and type-specific antigens (outer capsid protein). Viruses have hemagglutinating activity.
The main route of transmission is airborne droplets.
Reoviruses are primarily reproduced in the epithelial cells of the mucous membrane of the mouth, pharynx, small intestine, and regional lymph nodes, from where they enter the lymph and blood. Viruses are able to pass through the placenta and have an embryopathic effect.
Laboratory diagnostics:
1) isolation of the virus in cell culture and in newborn mice;
2) identification of the virus - in the neutralization reaction and RTGA;
3) serodiagnosis (RTGA).
Specific prevention and etiotropic therapy have not been developed.
PC virus. Belongs to the family Paramyxoviridae, genus Pneumovirus.
The family includes “dressed” viruses with helical symmetry, the genome of which is formed by a linear non-segmented RNA molecule associated with a major (NP) protein; the average virion size is 100–800 nm.
The shell contains:
1) HN-glycoprotein. Has hemagglutinating and neuraminidase activity;
2) F-glycoprotein. Responsible for the merger. Exhibits hemolytic and cytotoxic activity;
3) M protein. Forms the inner layer of the viral shell.
Virus replication is completely realized in the cytoplasm of host cells.
In infected cell cultures, two antigens are isolated:
1) antigen A is resistant to treatment with ether, induces the synthesis of neutralizing and complement-fixing antigens;
2) antigen B induces the synthesis of complement-fixing antigens.
RS virus is the main causative agent of lower respiratory tract diseases in newborns and young children. The pathogen replicates in the epithelium of the airways, causing the death of infected cells.
The PC virus is characterized by low stability, virions are prone to self-disintegration, and in purified form they exhibit pronounced polymorphism, taking several forms.
After recovery, unstable immunity is formed.
The main route of transmission is airborne droplets.
Laboratory diagnostics:
1) isolation of the PC virus on human cell lines;
2) rapid diagnostics - determination of the virus antigen in nasal discharge and mucosal cells using ELISA;
3) release of specific antigens in RSC and RN.
Treatment: there is no etiotropic therapy. Treatment is symptomatic.
There is no specific prevention.
45. Pathogens of ARVI
Parainfluenza virus and RS virus belong to the family Paramyxoviridae.
These are spherical viruses with a spiral type of symmetry. The average virion size is 100–800 nm. They have a supercapsid shell with spinous processes. The genome is represented by a linear, non-segmented RNA molecule. The RNA is associated with a major protein (NP).
The shell contains three glycoproteins:
1) HN, which has hemagglutinating and neuraminidase activity;
2) F, responsible for fusion and exhibiting hemolytic and cytotoxic activity;
3) M protein.
Virus replication is completely realized in the cytoplasm of host cells. The human parainfluenza virus belongs to the genus Paramyxovirus. Viruses are characterized by the presence of their own RNA-dependent RNA polymerase (transcriptase).
Based on the differences in the antigenic structure of the HN, F and NP proteins of human parainfluenza viruses, four main serotypes are distinguished.
The pathogen reproduces in the epithelium of the upper respiratory tract, from where it enters the bloodstream.
Clinical manifestations in adults most often occur in the form of catarrh of the upper respiratory tract. In children, the clinical picture is more severe.
The main route of transmission of the parainfluenza virus is airborne. The source of infection is the patient (or virus carrier).
Laboratory diagnostics:
1) rapid diagnostics (ELISA);
2) isolation of the pathogen in monolayers of human or monkey embryonic kidney cultures;
3) serodiagnosis (RSK, RN, RTGA with paired sera).
PC virus is the main causative agent of lower respiratory tract diseases in newborns and young children. Belongs to the genus Pneumovirus.
Characterized by low stability, virions are prone to self-disintegration.
The pathogen replicates in the epithelium of the airways, causing the death of infected cells, and exhibits pronounced immunosuppressive properties.
PC virus causes annual epidemic respiratory tract infections in newborns and young children; Adults can be infected, but their infection is mild or asymptomatic. The main route of transmission is airborne droplets.
After recovery, unstable immunity is formed.
Laboratory diagnostics:
1) express diagnostics - determination of virus antigens in nasal discharge using ELISA;
2) specific antigens are detected in RSC and RN.
Causal therapy has not been developed.
From the book Microbiology: lecture notes author Tkachenko Ksenia Viktorovna3. Infectious agents and their properties Among bacteria, according to their ability to cause disease, there are: 1) pathogenic; 2) opportunistic; 3) saprophytic. Pathogenic species are potentially capable of causing an infectious disease. Pathogenicity is the ability
From the book Microbiology author Tkachenko Ksenia ViktorovnaLECTURE No. 15. Causative agents of intestinal infections - the Enterobacteriaceae family 1. Characteristics of the Enterobacteriaceae family The Enterobakteriaceae family includes numerous representatives that have a common habitat - the intestines. Enterobacteriaceae are divided into: 1) pathogenic
From the book Biology [Complete reference book for preparing for the Unified State Exam] author Lerner Georgy Isaakovich1. General characteristics and pathogens of PTI Foodborne toxic infections (PTI) are a large group of acute intestinal infections that develop after eating foods contaminated with pathogens and their toxins. Clinically, these diseases are characterized by sudden
From the author's bookLECTURE No. 17. Causative agents of zooanthroponotic infections 1. Plague The causative agent of plague belongs to the genus Yersinia, species Y. pestis. These are gram-negative polymorphic small rods with rounded ends. They are motionless. There is no dispute. In the patient’s body and during reproduction on nutrients
From the author's bookLECTURE No. 19. Gram-negative bacteria - causative agents of purulent-inflammatory diseases 1. Haemophilus influenzae Family Pasterellaceae, genus Haemophilus, species H. influenza. These are small or medium-sized straight rods, non-spore-forming, immobile, gram-negative, aerobes. IN
From the author's bookLECTURE No. 23. Pathogens of ARVI 1. Influenza viruses Belong to the orthomyxovirus family. There are influenza viruses of types A, B and C. The influenza virus has a spherical shape, with a diameter of 80-120 nm. The nucleocapsid has helical symmetry and is a ribonucleoprotein strand (NP protein),
From the author's bookLECTURE No. 24. Causative agents of viral airborne infections 1. Measles and mumps viruses The mumps virus and the measles virus belong to the Paramixoviridae family. Virions are spherical in shape with a diameter of 150–200 nm. In the center of the virion there is a nucleocapsid with a helical
From the author's bookLECTURE No. 28. Causative agents of viral hepatitis 1. Hepatitis A virus Hepatitis A virus belongs to the picornavirus family, the genus of enteroviruses. The hepatitis A virus is morphologically similar to other representatives of the enterovirus genus. The genome is formed by a single-stranded molecule + RNA; He
From the author's book3. Other causative agents of viral hepatitis Hepatitis C virus is an RNA virus. Its taxonomic position is currently not precisely determined; it is close to the flavivirus family. It is a spherical particle consisting of a nucleocapsid surrounded
From the author's book13. Infectious agents and their properties Among bacteria, according to their ability to cause disease, they distinguish: 1) pathogenic species are potentially capable of causing an infectious disease; Pathogenicity is the ability of microorganisms, upon entering the body, to cause and
From the author's book46. Pathogens of ARVI (Adenoviruses) The Adenoviridae family includes two genera - Mastadenovirus (mammalian viruses) and Aviadenovirus (avian viruses); the first includes about 80 species (serovars), the second – 14. The family unites viruses with a naked capsid (there is no external
From the author's book47. Pathogens of ARVI (Rhinoviruses. Reoviruses) Rhinoviruses belong to the family Picornaviridae. Virions have a spherical shape and a cubic type of symmetry. Size 20–30 nm. The genome is formed by a positive-sense RNA molecule that is not segmented. The capsid shell consists of 32
From the author's book55. Other causative agents of viral hepatitis Hepatitis C virus is an RNA virus. Its taxonomic position is currently not precisely determined; it is close to the flavivirus family. It is a spherical particle consisting of a nucleocapsid surrounded
ARVI– various acute infectious diseases resulting from damage to the epithelium of the respiratory tract by RNA and DNA containing viruses. Usually accompanied by fever, runny nose, cough, sore throat, lacrimation, symptoms of intoxication; may be complicated by tracheitis, bronchitis, pneumonia. Diagnosis of ARVI is based on clinical and epidemiological data confirmed by the results of virological and serological tests. Etiotropic treatment of ARVI includes taking antiviral drugs, symptomatic - the use of antipyretics, expectorants, gargling, instillation of vasoconstrictor drops into the nose, etc.
General information
ARVI is an airborne infection caused by viral pathogens that mainly affect the respiratory system. ARVIs are the most common diseases, especially in children. During periods of peak incidence, ARVI is diagnosed in 30% of the world's population; respiratory viral infections are many times higher in incidence than other infectious diseases. The highest incidence is typical for children aged 3 to 14 years. An increase in incidence is observed in the cold season. The prevalence of infection is widespread.
ARVIs are classified according to severity: mild, moderate and severe forms are distinguished. The severity of the course is determined based on the severity of catarrhal symptoms, temperature reaction and intoxication.
Causes of ARVI
ARVIs are caused by a variety of viruses belonging to different genera and families. They are united by a pronounced affinity for the epithelial cells lining the respiratory tract. ARVI can be caused by various types of influenza viruses, parainfluenza, adenoviruses, rhinoviruses, 2 RSV serovars, and reoviruses. The overwhelming majority (with the exception of adenoviruses) are RNA viruses. Almost all pathogens (except for reo- and adenoviruses) are unstable in the environment and quickly die when dried, exposed to ultraviolet light, and disinfectants. Sometimes ARVI can be caused by Coxsackie and ECHO viruses.
The source of ARVI is a sick person. Patients in the first week of clinical manifestations are most at risk. Viruses are transmitted via the aerosol mechanism in most cases by airborne droplets; in rare cases, the implementation of a contact-household route of infection is possible. The natural susceptibility of people to respiratory viruses is high, especially in childhood. Immunity after an infection is unstable, short-term and type-specific.
Due to the large number and diversity of types and serovars of the pathogen, multiple incidences of ARVI in one person per season are possible. Approximately every 2-3 years, influenza pandemics are recorded, associated with the emergence of a new strain of the virus. ARVI of non-influenza etiology often provokes outbreaks in children's groups. Pathological changes in the epithelium of the respiratory system affected by viruses contribute to a decrease in its protective properties, which can lead to bacterial infection and the development of complications.
ARVI symptoms
Common features of ARVI: relatively short-term (about a week) incubation period, acute onset, fever, intoxication and catarrhal symptoms.
Adenovirus infection
The incubation period for infection with adenovirus can range from two to twelve days. Like any respiratory infection, it begins acutely, with a rise in temperature, runny nose and cough. Fever can persist for up to 6 days, sometimes lasting for two weeks. Symptoms of intoxication are moderate. Adenoviruses are characterized by the severity of catarrhal symptoms: profuse rhinorrhea, swelling of the nasal mucosa, pharynx, tonsils (often moderately hyperemic, with fibrinous plaque). The cough is wet, the sputum is clear and liquid.
There may be enlargement and tenderness of the lymph nodes of the head and neck, and in rare cases, lymph node syndrome. The height of the disease is characterized by clinical symptoms of bronchitis, laryngitis, tracheitis. A common sign of adenoviral infection is catarrhal, follicular or membranous conjunctivitis, initially, usually unilateral, predominantly of the lower eyelid. After a day or two, the conjunctiva of the second eye may become inflamed. Children under two years of age may experience abdominal symptoms: diarrhea, abdominal pain (mesenteric lymphopathy).
The course is long, often wave-like, due to the spread of the virus and the formation of new foci. Sometimes (especially when affected by adenoviruses 1, 2 and 5 serovars), long-term carriage is formed (adenoviruses remain latent in the tonsils).
Respiratory syncytial infection
The incubation period, as a rule, takes from 2 to 7 days; adults and children of the older age group are characterized by a mild course such as catarrh or acute bronchitis. A runny nose and pain when swallowing (pharyngitis) may occur. Fever and intoxication are not typical for respiratory syncytyl infection; low-grade fever may occur.
The disease in young children (especially infants) is characterized by a more severe course and deep penetration of the virus (bronchiolitis with a tendency to obstruction). The onset of the disease is gradual, the first manifestation is usually rhinitis with scanty viscous discharge, hyperemia of the pharynx and palatine arches, pharyngitis. The temperature either does not rise or does not exceed subfebrile levels. Soon a dry, obsessive cough appears, similar to that of whooping cough. At the end of the coughing attack, thick, transparent or whitish, viscous sputum is released.
As the disease progresses, the infection penetrates into smaller bronchi and bronchioles, tidal volume decreases, and respiratory failure gradually increases. Dyspnea is mainly expiratory (difficulty in exhaling), breathing is noisy, and there may be short-term episodes of apnea. On examination, increasing cyanosis is noted, auscultation reveals scattered small and medium bubbling rales. The disease usually lasts about 10-12 days; in severe cases, the duration may increase and recur.
Rhinovirus infection
Treatment of ARVI
ARVI is treated at home; patients are sent to the hospital only in cases of severe disease or the development of dangerous complications. The set of therapeutic measures depends on the course and severity of symptoms. Bed rest is recommended for patients with fever until body temperature normalizes. It is advisable to follow a nutritious diet rich in protein and vitamins and drink plenty of fluids.
Medicines are mainly prescribed depending on the predominance of one or another symptom: antipyretics (paracetamol and complex preparations containing it), expectorants (bromhexine, ambroxol, marshmallow root extract, etc.), antihistamines for desensitization of the body (chloropyramine). Currently, there are a lot of complex preparations that include the active substances of all these groups, as well as vitamin C, which helps increase the body’s natural defenses.
Vasoconstrictors are prescribed locally for rhinitis: naphazoline, xylometazoline, etc. For conjunctivitis, ointments with bromonaphthoquinone and fluorenonylglyoxal are placed in the affected eye. Antibiotic therapy is prescribed only if an associated bacterial infection is detected. Etiotropic treatment of ARVI can be effective only in the early stages of the disease. It involves the administration of human interferon, anti-influenza gammaglobulin, as well as synthetic drugs: rimantadine, oxolinic ointment, ribavirin.
Among the physiotherapeutic methods of treating ARVI, mustard bath, cupping massage and inhalations are widely used. Persons who have had an acute respiratory viral infection are recommended maintenance vitamin therapy, herbal immunostimulants, and adaptogens.
Forecast and prevention of ARVI
The prognosis for ARVI is generally favorable. The prognosis worsens when complications occur; a more severe course often develops when the body is weakened, in children of the first year of life, and in the elderly. Some complications (pulmonary edema, encephalopathy, false croup) can be fatal.
Specific prevention consists of the use of interferons in the epidemic focus, vaccination using the most common strains of influenza during seasonal pandemics. For personal protection, it is advisable to use gauze bandages covering the nose and mouth when in contact with patients. Individually, it is also recommended to increase the body’s protective properties (rational nutrition, hardening, vitamin therapy and the use of adaptogens) as a preventive measure for viral infections.
Currently, specific prevention of ARVI is not effective enough. Therefore, it is necessary to pay attention to general measures for the prevention of respiratory infectious diseases, especially in children's groups and medical institutions. General prevention measures include: measures aimed at monitoring compliance with sanitary and hygienic standards, timely identification and isolation of patients, limiting population overcrowding during periods of epidemics and quarantine measures in outbreaks.
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