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VIRAL HEPATITES

The problem of the viral hepatites remains most actual, as these diseases according to their spread step down only to acute respiratory and acute intestinal infections. Viral hepatites is most frequent cause of chronic hepatitis and liver cirrhosis. In some patients viral hepatites may have lethal outcomes.

The problem of the viral hepatitis is present under fixed attention of many scientists of the whole world. At present time definite successes in study of etiology, epidemiology, clinic, diagnostics of this polyetiological viral disease have been possessed.

Etiology

At present time further viruses, causing viral hepatitis are known: virus of hepatitis A (VHA), virus of hepatitis  (VHB), virus of hepatitis E (VHE), virus of hepatitis D (VHD), associated with VHB, virus of hepatitis C (VHC), virus of hepatitis G, and recently new types of probable causative agents of hepatitis were discovered - Sen and TT viruses, the role of virus of hepatitis F is under discussion. Search of new viruses, causing viral hepatitis continues. In literature one may come across different names of disease, caused by these viruses: infection hepatitis, epidemic hepatitis, serum hepatitis, syringe hepatitis. Uniting all these terminis - Botkin's disease. Indicated diseases caused by different viruses, possess many in general, however highly essential clinical, epidemiological, biochemical and immunological peculiarities that have been revealed. These peculiarities demand conduction of differential diagnosis between them. As a result of the above said, group of experts of WHO recommend to differentiate further variants of viral hepatitis: viral hepatitis A (VHA); viral hepatitis  (VHB); viral hepatitis E (VHE); viral hepatitis C (VHC); viral hepatitis D (VHD), viral hepatitis G (VHG).

Virus of hepatitis A (VHA). Agent was first discovered in 1973 by Feinstone. This is RNA-containing virus. Complete viral bodies as well as empty parts (capsules) with size of 27-30 nm can be noticed under electronic microscope. On their surfaces capsomeres are seen. Nucleopeptide of VHA does not possess surface projections and covering. Core structure is not revealed in the virion. Virus contains 4 peptides (VP1-4), participating in reactions of immune precipitation. It is assumed that VP1 and VP3 are located pertly on the surface and VP2 and VP4 are present inside the virion. However, up till date, there is not authentic informations about their meaning in relation to antiqenicity and immunogenicity.

VHA is stable during pH 3.0-9.0, sensitive to formaldehyde, may remain preserved for a period of few months or even years during temperature + 4 Ñ, for weeks - during room temperature. Complete inactivation of virus takes

 

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place during 85 Ñ in a period of 5 minutes. VHA is resistant to chlorine, in comparison with other viruses of this group and may enter through barriers of water cleaning stations. Complete inactivation of virus steps on during concentration of chlorine 2.0 - 2.5 mg/L with exposition for a period of 15 minutes, of lime chloride - 10 mg/L during 15 minutes.



Virus of hepatitis A may reproduce in number of human and monkey cellular cultures, from where viral antigen is obtained. It is necessary to remark, that successful adaptation of VHA towards culture of cells is very much necessary for study of biological properties, for obtaining of source of reagents for diagnostics (antigen, antiserum), as well as for construction of vaccines (live, killed).

Virus of hepatitis  (VHB). VHB in natural condition is revealed in sick people and carriers, in forest marmots, in earth squirrels, in Peiking ducks. This DNA-containing virus is pathogenic for human and few types of primates - chimpanzee, gorillas. VHB causes acute and persistent infection, primarily damages liver.

Virus consists of nucleus and covering. Further antigenic structure of VHB is differentiated: HBsAg - surface, HBcAg - internal (core), HBeAg - reflects infectiouness of virus.

Towards these antigens in organism of patients antibodies are produced: anti-HBs, anti-HBc, anti-HBe.

Presence of HBsAg in human organism testifies the presence of acute and latent proceeding infection. It is assumed, that prolonged conservation of HbsAg in serum of the blood in sick man may testify transfer of the process into chronic form. HBsAg is revealed in majority of patients in incubation stage. HBcAg is practically not determined in blood and fixed in directly by DNA-polymerize reactions, falling positive in acute period of disease, as well as after many months and years in carriers. Soon after discovery of HBsAg in blood of patients anti-HBc appear. Most often they are observed in carriers of infection. In early stages of disease HBeAg is revealed, which is then replaced by anti-HBe. Very important diagnostic information may be obtained by using methods of determination of DNA HBV. For this purpose molecular hybridization of nucleic acids and polymerize chain reaction (PCR) is used. Genospecific viral DNA is observed in serum of blood, in bioptates of liver, in lymphocytes of peripheral blood. Mentioned method enables to discover very small quantities of viral DNA in investigated samples, which moderately increases reliability of diagnosis.

Virus of hepatitis C (VHC). Virion of virus of hepatitis C consists of nucleus and lipid external membrane. Genome is represented by single chain RNA. VHC is heavily resistant in environment, and particularly in biological fluids such as preparations of blood, sperm and others. It is sensitive to chloroform, to other desinfective solutions and high temperatures (100 Ñ and more).

Antigenic structure of VHC is less studied. It is established, that antibodies (Ig of M and G class) are produced to virus in the organism of the patient. Their discovery in blood serum of patient testifies presence of acute or chronic disease.

 

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Antibodies may stick to definite level during 6-9 months, and thereafter their titers in serum decrease upto complete disappearance.

Virus of hepatitis D (VHD). VHD represents itself as defective virus particle of size 30 - 35 nm, contains internal antigen (HDAg), made up of small circular RNA and surface covering, which is HBsAg VHB. It is considered that reproduction of virus is possible only during presence of HBsAg in organism of patient, therefore hepatitis D proceeds always as a coinfection or superinfection, joining to VHB.

Human's organism replies to VHD infection by production of antibodies of IgM class, which are used in diagnostics of the disease.

Virus of hepatitis E (VHE). Virus of hepatitis E has been isolated from feces of patients with jaundice. Spherical particles similar to virus were able to discover due to the method of immune electronic microscopy. Material for investigation was collected from volunteers, infected by material from patients with jaundice with assumed diagnosis of viral hepatitis E. It is supposed, that VHE may be caused by few strains of virus of different antigens.

At present time a test-system, giving the possibility of discovering antigens of virus in fecal matter has been elaborated. Serums of reconvalescenes are used for that.

Epidemiology

Viral hepatitis A is an antroponosis. The source of disease is sick person in prejaundice period and during 15-20 days of climax period of the disease and virus carrier. Primary localization of virus is gastrointestinal tract. Mechanism of transmission is fecal-oral. Virus is excreted from the organism of sick person with feces. Specific factors of hepatitis A virus transmission are water and blood. Character of water infection depends upon conditions of water supply and its relation with fecal contamination. Intermediate factors of transmission are flies, transferring virus with feces on products of nutrition, dishes.

Susceptibility to the disease is high. Mainly children and adults under 30 year fall ill.

The source of hepatitis  virus in nature is ill person with acute or chronic form, healthy carrier. Natural way of transfer is sexual. Infection may be transferred even during kisses through traumatized mucous, through milk of mother, through placenta from ill mother to fetus (vertical path of transmission). Parenteral way of the transmission includes blood and its preparations transfusion, injections, manipulations, operative interventions.

Susceptibility to the disease is high. Most often drug addicts, homosexuals, prostitutes, medical personnel (surgeons, obstetrician-gynecologists, workers of hemodialysis departments, manipulative nurses, doctors-infectionists) fall ill with hepatitis B.

Epidemiology of viral hepatitis D has been studied insufficiently. It is assumed, that source of infection is sick person, basic.path of transmission is parenteral.

 

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Persons suffering from VHB or HBsAg-carriers are more susceptible. Epidemiology of viral hepatitis E is identical to epidemiology of VHA, and hepatitis C - to hepatitis B.

Pathogenesis

Pathogenesis of viral hepatitis is still not studied completely due to big difficulties, caused by absence of accessible experimental model of the disease. At the base of existing notions about pathogenesis of acute viral hepatitis lay clinical observations, life time investigations of liver tissue and comparative study of viral hepatitis in animals.

Entrance of the agent of the disease into the organism of patient takes place perorally (VHA, VHE), by sexual way (VHB, VHC), parenterally (VHB, VHC, VHD and not excluded for VHA and VHE), vertically (not excluded for all viral hepatitis).

The agent approaches regional lymphatic glands, where its massive reproduction takes place - the second phase of pathogenetic process. The agent causes damage of cells and their death. Organism replies on this negative influence by immune reaction of reticular tissue of the lymphatic glands, executing "barrier" function. This corresponds to period of incubation. On this level infections process may stop. In insufficiency of "barrier" function the phase of generalization of infection (primary virusemia) begins.

Virus continues to enter from lymphatic glands into blood in a large quantities. Clinically this phase is manifested by signs of intoxication and beginning of the damage of liver. In this phase viruses of hepatitis are connected with thrombocytes. Due to composition of their phospholipid membrane they violate, metabolism of arachidonic acid is intensified, that leads to increase in their adhesive and aggregate activeness. Viruses of hepatitis also render action on cells of endothelium of small vessels, cause destruction of the structure of their biomembrane. As a result of such influence, highly active endoperoxides are formed from arachidonic acid (compulsory component of phospholipids of membrane), rendering powerful influence on adhesion and aggregation of thrombocytes, erythrocytes. Such influence of viruses of hepatitis on the blood cells and endothelium of vessels already in the phase of virusemia renders essential influence on coagulative and anticoagulative system of the blood causes disseminated intravascular coagulopathy. The first stage of DIC-syndrome develops. Degree of these disorders depends on massivity of virusemia and determines the disease course.

The phase of virusemia is confirmed by determination of HBsAg in the blood of the patient. Besides virusemia parenchymatous diffusion also happens. Viruses of hepatitis penetrates into the liver cells. Reproduction of virus is realized in hepatocytes. Virus also revealed in erythrocytes, thrombocytes, in the cells of pancreas, reticuloendothelial system. The inculcation of virus into hepatocytes leads to disorder of intracellular metabolic process, especially in

 

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membranes of hepatbcytes. The lesion of membranes accelerates destruction of hepatocytes.

The mechanism of the damage of hepatocytes, other cells of the organs and systems is studied insufficiently. Syndrome of cytolisis also plays the leading role in pathogenesis of viral hepatitis B. However, virus of hepatitis  doesn't possess the direct cytopathogenic action.

F.Dubleu, A. Bluger consider that immune reactions, connected with T-cells, have the leading meaning in the pathogenesis of syndrome of cytolisis. The penetration of virus into hepatocytes and reproduction in hepatocytes leads to accumulation of viruses in surface membrane. Circulation of antigens in the blood causes sensibilization of T-lymphocytes. The activation of T-lymphocytes leads to distinction and depression of the agent and to differention of subpopulation of T-lymphocytes. Effect of T-killer causes cytolisis of hepatocytes. Autoimmune reactions intensify cytolitic syndrome and necrosis of liver.

Pathogenesis of viral hepatitis  is explained from viral-immunogenetic position, because it is known that power of immune response is genetically determinated. Immune reaction may be strong (in fulminate form of hepatitis), flabby and adequate. Only adequate immune reaction promotes cyclic course and favorable outcomes of the disease.

The scientific achievements of the last years opened new points of view to pathogenesis and therapy of different forms of viral hepatitis. The study of metabolic processes on the level of cell allowed to open new aggressive components, which have negative influence on its structure and functions.

The surplus activity of the processes of free radical oxygenation renders destructive influence on cells membranes. As a result free radicals are accumulated in the cells. The process of lipids oxygenation is intensified (peroxide oxygenation of lipids - POL). It is known that lipids are the basic structural component of the cells. Antioxydant system of the organism is defending mechanism, supporting free radical oxygenation of the physiological level. Due to research of the last years it was shown that activation of the processes of peroxide oxygenation of lipids plays the essential role in the pathogenesis of viral hepatitis and leads to alteration Q{ structure and functions of membrane of hepatocytes, thrombocytes and other cells. It's worth to underline that simultaneously with activation of POL the considerable depression of antioxydantic activity of the blood serum is marked.

In case of extremely high activity of POL exhaustion of AOS takes place, which leads to disorder of activity of cellular ferments, particullary of glucolysis, glucohenolysis and to rupture of phoshorilation. As a result, cell loses energetic potential. It leads to destruction of cell. Along with this permeability of membrane of hepatocyte and its internal structural components are disturbed. Corrosion of hepatocyte takes place*, its synthetic, disintoxicative and other function are lost. Disturbance of permeability of lysosomal membranes causes exit proteolytic ferment into cytoplasm, which complete the deSth of hepatocyte.

 

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At the last years data about molecular mechanism of the damage of hepatocytes membranes were received. It is known that interferones cause depression of reproduction of viruses.

Leukocytaric and fibroblastic interferones may be produced practically by all cells. Immune gamma-interferon is produced by gamma-interferon immunocompetentive cells during immune response.

Interferon may influence on complex of defensive reaction (phagocytosis, inflammation, antigen expression). Interferon is the most important factor of nonspecific resistance. However, interferon has influence on differentiation and activation of effector cells of immune system. The activation of monocytes (macrophages), increased generation of peroxide radicals, increased phagocytes activity are observed under influence of interferon. Thus, at the present time interferon is considered not only as antiviral remedy, but also as important regulator of interaction between cells. Due to investigations of the last time it was established that antiviral effect of interferon is not connected with direct interaction with viruses. Antiviral effect is connected with change of metabolic processes in the cells.

It is established that there is decreased produce of interferon in the patients with viral hepatitis B, especially in patient with severe course of the disease. In fulminate course of acute viral hepatitis  interferon is not revealed in the blood serum.

Anatomic pathology

Morphological changes in liver take place in all tissual components -parenchyma, connective tissue, reticuloendothelium, in lesser degree in bile pathway, diffuse damage of the organs occurs. Degree of damage fluctuates from insignificant dystrophic and single necrotic changes of epithelial tissue of lobules of liver during mild forms till massive and submassive necroses of liver parenchyma. Three variants of acute form of the disease are differentiated: acute cyclic, cholestatic and massive necrosis of liver.

During acute cyclic form diffuse damage of epithelial and mesenchymial elements is observed. Decompensation of beam structure with orderly placement of hepatocytes with their considerable polymorphism is noted.

Along with the dystrophic changes, expressed processes of regeneration with figures of mitosis and abundance of double nuclear cells are determined. Characteristics are presence of scattered necrosis hepatocyties in all lobules. Changes of mesenchymial elements inside the lobules are expressed in proliferation of Kupffer's cells with their change into macrophages. Cytoplasm of these cells are basophilic, contains bile pigment. Capillaries in the center of lobules are dilated. Proliferation of lymphohistocytary elements with admixtures of plasmatic cells eosinophils and neutrophils are marked in the portal tract. Along with this, reticular hyperplasia of spleen and portal lymphatic vessels is observed. Clinical manifestations of the disease correspond to the severity of destructive changes in parenchyma of liver.

During cholestatic variant of viral hepatitis majority of morphological changes are observed in intrahepatic bile passages with picture of cholangitis and pericholangitis.

 

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Clinical manifestations

Clinical picture of all viral hepatites is very much similar and differs in percent relation by severity of the course of the disease and its outcomes. Viral hepatitis A and E are characterized by cyclic benign course with complete reconvalescence. In hepatitis Â, Ñ and D medium serious and serious course, lingering and chronic forms of disease and lethal consequences are inrarely observed.

Depending upon the expressiveness of clinical manifestations of the disease and degree of functional disorders of liver, established by biochemical tests, light, medium serious, serious and malignant (fulminate) forms of viral hepatitis are differentiated. All atypical cases of the disease (non-jaundice, obliterated, subclinical) are concerned to mild forms, because as clinical manifestations and functional changes are weakly expressed in such patients.

During evaluation of severity of the disease, expressiveness of intoxication and jaundice is taken into attention along with enlargement of sizes of liver and spleen, loss in weight, level of bilirubin in blood serum.

High intoxication, polyarthralgia, expressed dyspeptic symptomocomplex are typical for fulminate and serious forms of viral hepatitis. Prolonged intensive jaundice, hypotonia, bradycardia, changing into tachycardia, slackness, subfebrile temperature, decrease in diuresis, testifies about serious or even malignant course of viral hepatitis with indefinite prognosis.

Laboratory tests are used for evaluation of severity of disease: tests of concentration of general bilirubin in blood serum of patients, the prothrombin index.

Viral hepatitis have principally cyclic course. Incubation period is different. In hepatitis A it is in average 15-30 days, during viral hepatitis B 30-180 days. The disease begins with signs of general intoxication - so called pre-jaundice period. There are the next variants of prejaundice period:

1) Dyspeptic variant - patients complain of appetite absence, nausea, sometimes vomiting. Temperature is subfebrile. Duration of period is 3-7 days.

2) Astenovegetative variant - patients complain of weakness, headache, malaise, decrease of appetite. Body temperature is subfebrile or 37-38 Ñ;

3) Influenza-like variant - patients complain of headache, weakness; muscular pain, decrease of appetite. Body temperature is 37.5-39 Ñ, and in separate cases 39-40 Ñ. Duration of 2nd and 3rd variant of prejudice period is of 5-7 days;

4) Polyarthralgic variant - it is observed mainly during hepatitis B and C. Patients complain of pain in joints, sometimes muscular pain, weakness, decrease of appetite. During this, subfebrile temperature is in majority of the patients. Duration of this period is 7-14 days;

5) Mixed type - all above mentioned signs of intoxication in various degree of manifestation.

The next period of the disease is climax period. The state of the majority of the patient becomes better. The temperature is normalized, urine becomes dark, colorness stool. Scleras are icteric, jaundice grows gradually (Fig. 11). The further course of the disease depends on degree of liver damage by the virus, which determines

 

 

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the severity of the "disease. During light course of viral hepatitis jaundice grows in a period of 3-5 days. It is present on one level during one week. Disappearance of jaundice is observed on 15-16 day. Urine becomes more light at the end of the first-second week of the jaundice period, it is of yellow or orange color.

During medium serious and serious course of the disease yellowish coloring of scleras and skin is more intensive, jaundice period is prolonged (20-45 days). In majority of the patients the signs of cardiovascular system disorder are observed. There are hypotonia, bradycardia, muffled hearts sounds. In 80-90 % of the patients liver is enlarged, its surface is smooth, borders are curved, moderately painful. In 30-40 % of patients spleen is palpated. During serious course of viral hepatitis in some patients meteorism of abdomen, caused by disorders of digestion (signs of damage of pancreas, secretory glands of stomach and disorders of biocenosis of gastro-intestinal tract) is observed. In some patients skin itch is observed - the so called cholestatic variant of the course of the disease.

Different changes are observed in central nervous system. Already during mild course of viral hepatitis adynamia, slackness, disorders of sleep may be present.

In serious cases clear cerebral disorders caused by considerable dystrophic changes in the liver, endogenic intoxication and increase of the activity of the processes of POL are observed.

In the period of reconvalescence reverse development of symptomatic of disease, normalization of biochemical indices is marked.

Outcomes of the disease. Viral hepatitis most often ends with complete reconvalescence. In some patients may be cholecystitis, cholangitis, pancreatitis, dyskinesia of bile excreting pathways after an acute hepatitis. In 5-10 % of patients lingering course with periodical aggravations, caused by prolonged persistence of virus is observed. In such cases chronic hepatitis develops. This variant of the course of the disease is typical for viral hepatitis  and C; chronic hepatitis may end up by liver cirrhosis.

Complications

The most threatening outcome of viral hepatitis is acute or subacute massive necrosis of liver, during which picture of acute or subacute hepatic encephalopathy is observed. An acute hepatic encephalopathy (AHE) is typical for acute hepatitis.

The term "acute hepatic encephalopathy" denotes unconscious condition of the patient with violation of reflex activity, convulsions, disorder of life vital functions as,a result of deep brake of action of cerebral cortex with its spread on to subcortex and below laying parts of central nervous system. This sharp brake action of nervous-psychic activity is characterized by disorder of movements, sensibility, reflexes and by absence of reactions on different irritators.

Hepatic coma is an endogenic coma, caused by endogenic intoxication as a result of loss of function and breakdown of liver.

There are the next stage of AHE - precoma I, precoma II and properly coma.

 

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Precoma I is characterized by non constant disorder of consciousness, unsuitability of mood, depression, lowered capability towards orientation, tremors, inversion of sleep. Patients are irritated, sometimes - euphoric. They are troubled by paroxysms of depression, doom, presentiment of death. Fainting, short time unconsciousness, giddiness, hiccup, nausea, vomiting may be observed. Jaundice grows. Bradycardia is changed by tachycardia. Tendon reflexes are raised. Such condition prolongs from few hours to 1-2 days with moving into second stage.

In the second stage of precoma consciousness is more hampered, losses in memory is a characteristic feature, alternated with attacks of tachymotor and sensory exciment till delirium. During awakening orientation in time, space and action is absent. Tendon reflexes are high. Jaundice raises sharply. Muffed heart sounds, tachycardia, hypotonia are revealed.

Rhythm of respiration is disturbed. Liver begins to decrease in size. Hepatic insufficiency is inrarely accompanied with hemorrhagic syndrome due to development DIC-syndrome. In 1 /3 of patients nasal hemorrhages, gastrointestinal hemorrhages, uterine bleeding and hemorrhages of other localization are observed. Diuresis decreases. Abdomen is inflated, peristaltic of intestine is decreased. Such condition continues for 12 hours - 2 days.

During the third stage properly coma complete loss of consciousness and disappearance of reflexes is marked. Pathological reflexes may be too. Rigidity of muscles of extremities, hyperkineses, convulsive syndrome, and thereafter complete areflexia are observed. Expressed tachycardia, hypotonia, disorder of rhythm of respiration are revealed. Diuresis decreased considerably till anuria. The death of the patients is through 6-24 hours. The patients perish from massive hemorrhages or in development of severe metabolic acidosis.

Diagnosis

Preliminary diagnosis of viral hepatitis is based on epidemiological anamnesis, finding of the development of the disease, clinical picture with account of peculiarities oi the ways of the transmission, duration of incubation period, presence of prejaundice period, presence of typical subjective and objective signs with account of the patients age.

Diagnosis is confirmed by routine and specific laboratory tests. In routine blood test of the patients with viral hepatitis lymphocytosis is observed with moderately expressed course and in serious course of the disease - anemia and leucopenia. ESR is slightly decreased. In urine urobilin and bile pigments are observed. During climax period, particularly during medium serious and serious forms, there are no stercobilin in stool.

Increased content of general bilirubin, primarily on account of its direct fraction is observed in blood serum during all jaundice period. Ratio of direct and indirect fraction composes 3:1. In all patients already in pre-jaundice period of the disease, during all jaundice period and in the period of early reconvalescence increased activity of ALT, AST is observed, testifying about the presence of cytolytic processes in liver.

 

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Specific antigens (HBsAg) and antibodies to antigens of all known at present time viruses of hepatitis are revealed in the blood of patients with help of these methods. Discovery of antibodies of class of IgM testifies about acute disease. Discovery of other classes of immunoglobulins antibodies testifies about lingering or chronic course of viral hepatitis or about earlier infectious process or about disease in the past.

Differential diagnosis

Differential diagnosis of viral hepatites is necessary to perform with diseases like leptospirosis, yersiniosis, mononucleosis, malaria, mechanic and hemolytic jaundice, toxic hepatoses.

Leptospirosis is characterized by acute beginning of the disease, often with chill, continuation of fever during of climax of the disease and jaundice, pain in muscles, especially in calfs, hemorrhagic syndrome. In blood leucocytosis with neuthrophillosis and shift in the formula to the left, accelerated ESR are observed. Activity of ALT and AST is moderately raised or normal relation of direct and indirect bilirubin 1:1. In blood serum concentration of urea and residual nitrogen increases. Stool is colored. In urine erythrocytes, leukocytes, like wax cylinders are marked in large quantity. Diuresis decreased till anuria.

In generalized forms of yersiniosis jaundice may be also observed, however it is accompanied by fever, metastatic focuses in other organs and tissues, leucocytosis with nuetrophilosis, accelerated ESR, aggravations and relapses. Diagnosis is confirmed by serological methods with specific yersiniotic antigen.

In malaria there are clear alternation of attacks fever with chills, replaced by heat and sweat and periods of apyrexia. Often painful, increased in size spleen is marked. In blood hemolytic anemia, in fat drop blood and smear different forms of malarial plasmodia are reveled. In blood serum indirect fraction of bilirubin predominates.

In mechanic jaundice stones in gall bladder and bile passages, enlargement of head of pancreas and other signs are revealed with help of ultrasound investigation. In majority of the patients moderate increase of activity of ALT, AST, leukocytosis, accelerated ESR are marked. Hemolitic jaundice is characterized by anemia, accelerated ESR, increase of indirect fraction of bilirubin. Stercobilin is always present in stool.

Differential diagnosis of viral hepatites with hepatoses is complicated and demands from doctor thoughtful and painstaking work. During this essential significance possesses correctly taken anamnesis.

Treatment

Treatment is used in complex and depends on the clinical form and gravity of disease course. At mild course of a viral hepatitis in the acute period it is possible to prescribe only semi-bed regime, diet ¹ 5, polyvitamines and desensitizing preparations: calcium gluconate, diazolin, diprazin or tavegil. In

 

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case of meteorism, feeling of gravity in epigastrium area after the meal, unstable feces - festal, pancurmen, allochol, cholenzym are indicated.

At medioserious and serious current of the acute form of hepatitis a bed regime is provided together with the specific treatment. Desintoxication therapy consists of plentiful drink; 5 % solution of glucose, saline solutions, ringer's solution, threesault,quartasault,20 % solution of sorbit (sorbitoli),donor Albumin (given in vein), one of enterosorbents - SKN, carbaphosfer, carbosilan, sillard P, enterosgel, polyphepan. The quantity of drunk liquid should be balanced with daily urine. Polarizing admixture: 3.7 gm potassium of Sody chlorid and 12 units of insulin on 1 liter of 5 % solution of glucose is recommended. The preparations improving metabolism in hepatocytes are indicated: ascorbinic acid, thiamin chlorid, pyridoxine hydrochloride, cocarboxylase, potassy orotat, riboxin, cytochrom C, lipamid, calcii pangamat. Last two preparations are indicated mainly in case of accompanying hepatoses with fatty infiltration of liver (alcoholism, diabetes, thyrotoxicosis, obesity). For acidosis decreasing 2 % solution of sodium of a hydrocarbonate 25-50 mL per os 3-4 times per day or on 150-200 mL intravenously should be infused.

Among etiotropic agents human recombinative a-2-interferon has moderate medical effect at acute virus hepatitis - reaferone, intron A, Realdironi or analogue laferone in powder, in amp. 1,000,000 IU: from 1st to 5-10th day of the icteric period. Next days their efficiency falls. At acute hepatitis  laferon is infused 1,000, 000 IU 2 times per day during 5-6 days, then 1,000,000 IU 1 time per day during 5 days. If medical effect is insufficient, there should be continued infusing 1 million UN 2 times per week during 2 weeks. It is worthy to use leicinferone as the basic component which is the admixture of natural á-interferons of donor leucocytes, the factor of necrosis of tumours and interleikin-1. However many clinicians challenge expediency of indication of interferon for treatment of hepatitis in acute period. More physiologic is the stimulation of endogenic interferonogenesis with the help of such inductores, as mefanam acid, prodigiosan, pyrogenal, nifluril, cycloferon.

At threat of hepatonecrosis - glucocorticoids 150-200 mg are prescribed. The dose of prednisolon per day must be reduced after the patient gets out of extremely serious condition. The volume of infusion solutions is enlarged up to 30-50 mL/kg per day. Ornithin (ornicetyl) promotes a linkage and removing out of organism nitrous bonds and improves a metabolism.

A lactulose reduces an adsorption of ammonia from intestine in blood, especially in combination with neomycin. With the aim of oppression of processes of an autolysis there should be used inhibitors of proteolytic enzymes contrical or gordox each 8 hours (I V) intravenous dropping, at improvement of a condition synthetic inhibitors. At retention of liquid in organism it is required to use spironolacton (veroshpiron), kaliumsaving diuretics, or saluretics - furosemid, etacrinic acid. Psychomotor exaltation is stopped by sodii hydroxybutyrate in combination with sibazon (seduxen), haloperidol. At increasing of hepatic failure antilymphocytic gamaglobulin is used during 1-5 days with the control of quantity

 

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of lymphocytes in a periphery blood,apparatus methods of patients blood clearing, hyperbaric oxygenation.

At cholestatic form of a virus hepatitis the are effective preparations which form complexes inside intestine with cholic acids which can not be soaked up, cholestiramin and bilignin. Fenobarbital is used which is the inductor of synthesis of glucouroniltransferas. This enzym is necessary for conjugation of bilirubin with glucuronic acid, and stimulating its egestion with bile. Fenobarbital is indicated with combination of cyanocobalamin. Simultaneously for intensifying secretion of bile nospan and cholenzym are indicated. After the termination of an acholia duodenal tubages 5-10 % solution of magnesy sulfat (1/4 - 1/2 glasses), sorbit or xilit (20 gm on 100 mL of hot water) 1 hour before breakfast are applied.

Bioflavonoids - convaflavin, carsili, legalone, silibor, quercetin are indicated in case of the alonged reconvalescence. At hyperaminotransferasaemia - aevit or tocopherol acetas,thymalin, T-activin,dipiridamol (curantyl),isoprinosin (has also antiviral property) - give positive effects. Saparal, methyluracil ( methacil), natry nucleinic,thymalin in a combination with dipiridamol,hofitol are also used. Cholagogue agents - broths of flowers of immortele, hips, thyme, mints peppery in dose of 1 dining spoon of a herb or a mixture to 1 glass of water are indicated for convalescents. Fenobarbital with cyanocobalamin are applied during 10 days in case of hyperbilirubinemia with prevalence of untied fraction of pigment; preparations of choice can be cordiamin or sibazone (seduxen) which also stimulate glucoruniltransferase of hepatocytes. At hyperbilirubinemia mainly at the expence of connected fraction stimulate a bile secretion using oxygen cocktails with cholagogue herbs and honey. Vitohepat or cobamamid stimulate neogenesis and hemopoes, accelerate regenerative processes in liver, course of treatment lasts 15-20 days. At asthenia and hypoproteinemia, and also for elimination of catabolitic influences of glucocorticoids which were used at the acute period, anabolic hormones: such as methandrostenolon (nerobol), phenobolin (nerobolil) or retabolil are indicated. For elimination of the asthenic phenomena, there are used novopasit, tinctura of Valeriana root (20 gm: 200 mL), herbs of neetle, thyme, bromidums, and in rather serious cases - chlozepid (elenium), sibazon ( seduxen), relanium, barbiturates.

At the dyspeptic phenomena caused by oppression of secretory function of digestion organs, also allochol, liobily, cholenzym, festal, panzynorm forte, pancurmen, pancreatin, pancitratit, vobensym are widely used.

At posthepatitic hepatomegalias without signs of cytolisis it is reasonable to prescribe lydase - promoting a resorption of a fibrous tissue, 10 injections every two days. It can be infused only after exclusion of inflammatory process in hepatobiliar ways (control duodenal intubation is necessary).

Chemotherapeutic preparations are indicated in case of the bacterial cholecystitis. At mild course of disease it is possible to use only a fortnight course of nicodin, in case of serious disorders antibiotics or nitrofurans preparations are indicated.

 

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It is possible to define sensitivity of microorganisms, isolated from the bile, to antibiotics. For such definition mediums are used, which content bile of the patient as it influences on essentially activity of antibiotics. Use ampicillin, carbenicilin dinatry salt, erythromicin, cefazolin, furazolidone, furagin, at Candida infection sody salt of levorin. Chemiopreparations are prescribed in average therapeutic doses during 7-8 days.

Specific therapy of chronic virus hepatitises is carried out by preparations of a-interferon (intron A, roferon, realdiron, reaferon, laferon). They are effective in case of low replicative activity of the virus determined in blood virus DNA (HBeAg) at a hepatitis  and virus RNA at hepatitis C. The additional indication is high activity of serum alanineaminotransferase. One of the specified preparations inject (IM) or subcuteneous 3-5 million IU per day 3 times per week during 6 months. Treatment should be stopped, if positive results were not observed after 3 months. The positive effect is observed at 40-50 % of patients with hepatit  and at 20-30 % of patients with hepatit C. At chronic hepatit D less than 10 % of patients are released from viruses even if treatment lasts 1 year. In some cases the success of immunotherapy of virus hepatites may be increased if preliminary short course of glucocorticoids treatment (about 6 weeks) is prescribed. Combined usage of interferon and thymalin, essentiale, lamivudin, chenodesoxycholyc acids has been proved.

The side-effects of a-interferon are noticed at half of patients right after injection, among them are headache, fever, myalgia, arthralgia, general weakness. They can be prevented by means of analgetics. Among the remote side-effects are: nausea, diarrhea, depression, irritability, leuco- and thrombocytopenia. Decreasing of a dose of preparation allows to weak these disorders. There are serious complications (sepsis, psychosis, autoimmune diseases), that demand an immediate cancellation of interferonotherapy.

At chronic hepatitis  in a phase of replication peroral preparation lamivudin (zeffix) is prescribed. It provides the same level of seroconversion, as standard course of treatment by interferon.

At chronic hepatitis with low replicative activity of a virus preference is given to pathogenetic agents improving metabolic and reparative processes in liver, such as: silibor, carsil, liv-52, hepatofalk, planta, hepabenne, antral, tocopherol acetat etc.

Prophylaxis

If the patient is hospitalized, he should be placed in a private room with separate toilet facilities. The major reason for such isolation is to prevent the spread of type A hepatitis. Even with lax precautions, such spread is very rare; most patients with type A hepatitis are no longer excreting virus once they have become symptomatic. Nevertheless, there are exceptions, and isolation is prudent. Secretions and blood products should be handled with care gowns, masks, and

 

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influenza etiological structure. In 1940 T. Frensis and T. Magil isolated a virus which was quite different from the ones isolated earlier. It was suggested to name the first virus - influenza type A virus, and the virus isolated by T. Frensis - type B. In 1947 R. Tailor isolated and described a new type of influenza virus which was later named type C.

The influenza pathogen belongs to the group of orthomyxoviruses. Virions have a ball form and a diameter of 100-120 nm, they have a core of a tightly turned spiral of ribonucleic acid in the case of protein molecules.

On the external capsule there are glycoproteids in the form of a fence of pins: hemagglutinins (HA) and neuraminidase (NA) causing the development of a specific immunity after the disease.

The influenza virus quickly dies at drying,high temperature,it is resistant to low temperatures, extremely sensitive to ultraviolet rays and many disinfectants.

A characteristic feature of influenza type A virus is the changeability of its antigenic structure, changing under the influence of the population immunology.

Influenza  virus has a more stable antigenic structure and doesn't change so often. It has one neuraminidose but different hemagglutinins.

The most stable in relation to antigens is virus C. It causes only sporadic diseases and small outbreaks. It is spread mostly in Ukraine, Moldova and other southern regions.

Epidemiology

Influenza remains the most spread mass disease nowadays, which does not recognize any borders and affects great masses of the population (up to 50 % and more) at short periods of time. The influenza contagious character was noticed even in 1735 by Gexgame during the epidemic in Scotland, he called the disease "epidemicus".

A sick person is the only source of the disease. The epidemiological role of virus carriers has not been studied well. The virus quickly multiplies in the epithelial tissue of the respiratory tract mucous membrane of a sick person and in 24-48 hours there is an aerosol cloud with a great concentration of influenza virus around a patient at sneezing and coughing. As the immunity of a specific type forms very quickly,the virus disappears from the organism of a sick person on the fifth day of the disease.

Influenza infection is spread with the help of small particle aerosol dispersion. The mechanism of virus spreading is based on the condition that the virus is in the air for a long time, it has an ability to keep its infectious force under unfavorable conditions of the environment and the ability of virus particles to move with air at long distances and penetrate different parts of respiratory tracts infecting a person.

The influenza virus of full value can live and be infectious in the air for 2-3 hours. It can live for 1-2 days on the furniture and other surfaces. The ultraviolet

 

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rays, humidity decre'ase and temperature increase and other factors shorten the virus life time. The virus lives within the limits of 1-3 meters. The speed of influenza spreading depends on the speed of people moving on the territory. The considerable increase of transportation, the movement of great numbers of people within separate countries, between countries and continents ensures a constant possibility of the virus spreading at considerable distances and the ability to infect people in any part of the globe.

There are small local epidemics and pandemics. The epidemics last 10-14 weeks.

The majority of people are naturally susceptible to influenza. The sick rate depends on many factors. First of all, on the level of the population specific immunity and on the circulation of the influenza virus serotypes.

The number of the influenza cases among adults has considerably decreased during the last years, as for the children aged 7-14 the number of influenza cases is growing slowly but steadily.

The influenza  sick rate tends to grow in all the age groups.

Pathogenesis

After penetrating the respiratory tracts, the virus sticks to the epithelial cells which have receptors - things of the lipid and carbohydratic nature. When the virus fixes on the cell surface receptors some complex enzymatic processes begin to occur, they ensure its penetration a cell in which it reproduces. This complex multistage process results in the cell death, and new virions born in the cells occupy new areas of the mucous membranes. The virus multiplication cycle lasts 7-Þ hours. Every virion which penetrated a cell gives birth to 1,000 virions and there will be 1027 of them in a day. That's why the influenza incubation period is so short.

If there were no obstacles for reproduction, the entire tissue of the respiratory tract would be affected in 1-2 days and it would result in a lethal outcome. It happens in rare cases - "quick influenza" develops and a patient dies in 2 days. But it doesn't usually happen so, because a cell, in which virus reproduces, produces and secretes interferon. This interferon gets into the neighboring cells and after that they are not defenseless against the virus invasion. Interferon prevents virus protein from synthesis. The further development of virus infection depends on the struggle of these two forces - virus genome and cell interferon: either it stops at the very beginning or the disease lasts a short time and a patient gets well or the infection spreads in the lungs and fatal pneumonia develops.

The cells affected by a virus are rejected and the products of their decomposition are absorbed, causing a general feverish disease. At the same time in the submucous membrane there develop inflammatory processes with distinctive circulatory disorders, that clinically manifests by hemorrhage syndrome.

When the process spreads in the lung tissue, in severe cases with the development of influenza pneumonia, there are signs of general edema with scattered or confluent foci of hemorrhage.

 

 

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Under these conditions the influenza virus easily penetrates the blood and virusemia develops. However, virusemia at influenza doesn't last long, as the virus quickly dies under the influence of nonspecific immunity factors interferon, complement, properdin, (3-lysines, (3-inhibitors, histones, leukins, etc.

It is quite possible that the affection of the visceral organs at influenza is connected with virusemia. However, the great majority of authors doubt the specificity of such affections, as there are no specific receptors in all the other organs, and they think that in the pathogenesis of affections the leading role doesn't belong to the cytopathogenic phenomena, it belongs to the organism reaction to toxic products or other substances, which appear at the influenza virus reproduction process.

Besides, it is a fact that even in the mild cases of the disease there are signs of the organism hemopoietic and immune system considerable depression. The number of leukocytes in blood decreases and their functions are suppressed. Macrophages become less active. Due to it bacteria and viruses become more active and the accompanying diseases take an acute form. So influenza infection is mostly a combined virus-bacterial or virus-virus infection.

In conclusion it is necessary to note that interferon production is very important for the disease outcome in the struggle between viruses and the organism protective forces. Antibodies of class IgM appear only at the end of the first week of the disease when the organism wins the first main battle, and antibodies of class IgG in two weeks.

Anatomic pathology

There are three main groups of pathoanatomic changes at influenza: the first one - primary changes, caused by the virus itself; the second ones - secondary changes, caused by influenza virus in combination with cocci and bacterial flora; the third ones - late changes in patients who had influenza and died of complications or worsening of other diseases.

The most important morphological signs of the first group are dystrophic changes of the respiratory epithelium and lungs with distinctive disorders of microcirculation; sharp plethora, edema and pericellular infiltration of submucous membrane and thickening of basal membrane.

The interalveolar septum of lung tissue are considerably thickened due to plethora and edema with leukocytic-lymphoid infiltration. The walls of small vessels and capillaries are thickened, in some vessels there are fibrous and leukocyte thromboses. The cells of alveolar epithelium became partially hyperplastic, in some places - died, there is a small microphagic exudate in the alveoli lumens.

In the second group there remain signs of pure influenza infection, but more or less they are prevailed by the purulent affections of the respiratory system and serious blood circulation disorders in the lungs. Pyo-hemorrhagic and pyo-

 

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necrotic tracheitis with a destruction of epithelium is developed in trachea. The lung tissue is low-pneumatic, the surface of the incision is motley, with alternation of large dark-red and gray foci. During microscopy massive foci of pyo-hemorrhagic pneumonia are found.

In the third group there are different kinds of pneumonia with various inflammatory exudate: purulent, pyo-hemorrhagic and abscess, plethora, edema and in some places hemorrhages into parenchymal organs, and also changes, which are characteristic of the accompanying chronic diseases.

 

Clinical manifestations

The incubation period at influenza is short - from several hours to 2-3 days. Its duration depends on the dose and toxic characteristics of the virus. The incubation period is short if the dose is big and the virulence is considerable. Thus, its duration has a prognostic meaning for a doctor.

There have been different opinions about the preliminary symptoms of the disease. It should be admitted that there is a prodromal period, which is characterized by elevated temperature for a short period of time (2-3 hours), slight malaise, chilliness, myalgias. These symptoms don't last long and are usually ignored by both a patient and a doctor. The disease begins to develop on the next day. In some patients the disease develops so fast that a practically healthy person becomes seriously ill in several minutes or hours.

The first symptoms are chilliness (always clear or poor manifested), high temperature, headaches, dizziness, a syncope condition, fever, malaise, pain in different parts of the body i.e. the symptoms of general intoxication. The headache is located in the forehead, temples and over the brows, it can be of different intensity. There is an early distinctive symptom - pain in the eye pupils especially intense at the eye movement or pressing, hyperemia of conjunctivas and sometimes scleras. Dizziness and syncope conditions are characteristic of teenagers and old people. The fever which is one of the main symptoms of influenza does not last long - 1-4 days (in 86 % patients). The "two-humped" character of the temperature is connected with the condition when the chronic infection takes an acute form or a secondary flora joins. Such symptoms as unconsciousness, delirium, convulsions and meningeal manifestations are characteristic of children at intense toxicosis.

Such symptoms as malaise, pain in the limbs and muscles, bones or in the whole body appear during the first hours of the disease and disappear when fever and other signs of toxicosis decrease. Adynamia, malaise can be considerable and are manifested from the first day of the disease. The skin on the face is hyperemic during the first 2-3 days, in severe cases they become pale with cyanotic shade. It is often a bad prognostic sign. Sweating is a characteristic feature. Intoxication is a characteristic feature of influenza, its degree and frequency vary in case of different microbes. In different epidemics there is hemorrhage syndrome,in 10-20 % cases, its symptoms are nasal bleeding, sometimes recipro-

 

 

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cal, hemorrhage in the fauces, metrorrhagia, short hemoptysis and gum bleeding sickness. Cough appears during the first days of the disease, dry, excruciating, heart-rending which is accompanied by the feeling of tickling, scratching behind the breast bone. Almost all the patients have a catarrhal syndrome which has such symptoms as rhinitis, pharyngitis, tracheitis. There are often such combined affections of the mucous membrane as rhinopharyngitis, laryngotracheitis, tracheobronchitis, etc. They usually appear in the first days of the disease. Such symptoms as herpetic rash is quite frequent, but appears on the 3rd-4th day. Photophobia and lacrimation are finite rare.

There are no specific changes on the skin. Different kinds of rash which were described result from other reasons (taking drugs, accompanying diseases). As it has been mentioned before,quite often there is herpetic rash,theoretically there is a possibility of petechiae, hemorrhages, if we take into consideration the affection of vessels and their hyperpermeability. There can be random rash.

A natural manifestation of the influenza infection is the affection of the respiratory organs, as different pathological processes take place in them, they are located on a certain level, but sometimes affect the entire area. The affection of the upper respiratory tracts is accompanied with hyperemia and swelling of mucous membrane, sometimes with slight hemorrhages. There is nasal obstruction, rough breathing, and discharge of different nature and consistence: mucous, mucopurulent, and sttaguinolent - in severe cases. During rhinoscopy swelling and hyperemia of mucous membrane can be seen, especially at the middle turbinate bone. At the same time accessory nasal sinus can be affected (maxillary sinusitis, frontal sinusitis, eustachitis with the development of otitis) with different nature of affection - from catarrhal to purulent.

 

During fauces examination the hyperemia of tonsils, uvula palatina and posterior wall of the throat could be found. Sometimes there are granules with vascular injection and hemorrhages on the soft palate. The development of influenza laryngitis and false croup is extremely dangerous, especially in children. Patients become pale, cyanosis develops, they often breathe with the help of additional musculature, the voice remains. Lethal outcomes are not rare, because not only larynx is affected, but trachea and bronchi as well, they are full with croupous superposition. The swelling of the mucous membrane of trachea and bronchi results in their permeability and leads to the deterioration of lung ventilation. Depending on the severity of the disease the degree of manifestations is different - from the hidden forms, which can be found with the help of pharmacological tests (aerosolic injection of eusporinum) to the severe forms accompanied with dyspnea and cyanosis.

 

Complications

 

The most common and dangerous complication of influenza is pneumonia. It is necessary to mention, that even during the first days of the disease there are roentgenologic strengthening of the vessel picture in the inferiomedial parts, that

 

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looks like indistinct infiltrate, and hurried breathing, shortening of the percussion sound and appearance of so called "conductive" rhonchi, resemble pneumonia. But they often disappear without any traces in 2 - 3 days. It may not be pneumonia, but some circulatory disorders. Not everything is clear in the problem of pneumonia origin. After the detection of pathogen it was considered that during the first three days pneumonia is of virus etiology, on the 3-5 day - virus-bacterial, later -bacterial etiology. There is a picture of the so called "big motley lung" on the section. Hemorrhage pneumonia foci of different sizes can be seen along the whole length, they are small and large and separated by some parts of unaffected tissue. The foci of festering appear quite early. The rough beginning with severe toxicosis, catarrhal syndrome, significant and diverse changes in the lungs, are characteristic of influenza infection, which is complicated with pneumonia.

Diverse changes in the cardiovascular system have been described. The vascular system is usually affected, and sometimes considerably, it is probably connected with a toxic action of influenza virus on capillary vessels. Dilation of capillaries, turbid background, sometimes formation of the arterial aneurysms, are seen at the capillaroscopy. Arterial and venous pressure decreases, especially in case of pneumonia, the speed of blood flow slows down. The pulse corresponds the fever very often, there is sometimes tachycardia, especially at the beginning of the disease, in some cases there is bradycardia. The heart sounds are muffled, heart borders are widened, slight systolic murmur and sometimes extrasystoles appear. All these manifestations disappear when the general condition of the patient becomes better. There is elongation of the PQ interval, decreasing and notching, and sometimes inversion of the wave T at different abductions on the ECG. These disorders are interpreted as toxic and dystrophic. They are unstable and disappear in 1-2 weeks. The myocarditis described at influenza is disputed by other authors. More severe and diverse disorders are found in patients with chronic affections of the cardiovascular system (coronary atherosclerosis, rheumatic heart diseases, etc.). These disorders are not pathognomonic for influenza, and arise because of the aggravation of the main disease under the influence of influenza infection.

There are various affections of the nervous system during the influenza infection. The functional disorders of the vegetative nervous system are distinctively manifested. We have already got acquainted with such symptoms as sweating, changes of the pulse rate, dizziness etc. However, all these changes quickly disappear. At the same time serious affections of the central and peripheral nervous systems are observed, they are manifested as meningitis, meningoencephalitis, radiculitis, neuritis, etc. The rate of these complications is different in different epidemic outbreak. The pathogenesis of these diseases is still a difficult question. Side by side with the theories of the toxic and parainfectious factors in their development, it is possible, that the virus invasion plays a significant role.

The complications in the digestive system are less frequent, and there are evidently no specific disorders, although fur, dryness in the mouth, decreased

 

 

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appetite, and heaviness in the epigastrium are observed. These symptoms are characteristic not only of influenza, but of any disease with fever. And now such forms of influenza as gastrointestinal, intestinal and abdominal which were the results of diagnostic mistakes are mentioned in conversations but not in literature.

The changes in the urinary tracts are manifested as pyelitis, pyelocystitis and sometimes nephritis, which result from metabolic-dystrophic manifestations of fever and bacterial superinfection.

The described affections of the endocrine system (adrenal gland, thyroid and pancreas glands) are very rare and it is not possible to completely exclude the influence of influenza virus in these cases.

Diagnosis

Besides careful clinical and epidemiological findings, modern methods of lab diagnostics are used for influenza diagnosis and differential diagnosis of other diseases.

Diagnosis does not seem to be difficult during epidemic outbreaks. However, at the same time besides influenza there 30-60 % patients with the respiratory tracts affection syndrome are registered, they are not of the influenza etiology, and clinical diagnosis is even more difficult during a non-epidemic period. As we see, influenza doesn't have specific symptoms which are characteristic of it only, but there are 3 strongly pronounced symptoms: abrupt onset with chilliness, general intoxication and the affection of the upper respiratory tracts. But they also accompany other acute respiratory diseases, and that is why there are many cases when patients with the diagnosis "influenza" are taken to hospital, but they have different other infectious and non-infectious diseases. That is why it is always important first of all to take into account the epidemic situation in the region.

A short incubation period is characteristic of influenza that is why the contacts with sick people, especially in the foci 1-3 days before the disease should be taken into account. If it is possible it is advisable to make up a general conception of the disease clinical picture in the people the patient contacted.

A careful and detailed physical examination of the patients, analysis and a comparative evaluation of the revealed changes with the consideration of the time past from the disease onset is also of great importance. It is important to remember that the preceding therapy can have a considerable influence on the natural disease course, sometimes changing or allaying some symptoms, and in other cases, on the contrary, resulting in the development of the new symptoms which are not typical of influenza. These can be various manifestations of the medication disease: skin rash, lymphoadenopathy, the toxic affection of the liver, hemogenic system, development of asthmatic syndrome, etc. Only a careful analysis of all the clinical symptoms can reveal the main syndromes, the peculiar mosaic of which is characteristic of one or another nosological form.

There is not any typical temperature curve. A relatively short febrile temperature reaction (5-6 days) with a quick rise and maximum values during

 

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the first 2-3 days an'd shortened lysis should be considered to be more or less typical if the fever lasts longer than this period, it is always necessary to think of a possibility of another disease or joining of a complication. The usage of antibiotics, analgetics, sulfanilamides and glucocorticoides can considerably change a natural course of the temperature curve.

The changes in the hemogram are manifested as leukopenia or normocytosis. If there are no complications and accompanying diseases, there is absence or decrease of the eosinophils, neutropenia and relative lymphocytosis in the hemogram at influenza (the percentage of lymphocytes increases whereas their absolute number is the same). ESR is normal or insignificantly increased. The connection of the bacterial complications is accompanied with leukocytosis and neutrophilia. It is important to take into account the absolute number of elements of white blood in the dynamic of the disease.

The infection of the chicken embryos is universal method of the primary isolation and cultivation of influenza virus. This method is more accessible and sensitive than the infection of the labora


Date: 2014-12-21; view: 188


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