Virus hepatitis A

Virus hepatitis A - acute cyclic disease with mainly fecal-oral mechanism of the transfer, characterised by a lesion of a liver and showing an intoxication syndrome, augmentation of a liver and quite often icterus.

Aetiology

The originator - a virus of hepatitis A - an enterovirus of a type 72, concerns sort Enterovirus of family Picornaviridae, diameter of 28 nanometers.

The virus genome is presented one-filamentous RNA. Existence of two serotypes and several variants and virus strains Is supposed.

The virus of hepatitis A is steady in environment: at a room temperature some weeks or can remain months, and at 4 C° - some months or years. The virus is inactivated at temperature 100 C° within 5 minutes, at 85 C° - in flow of 1 minutes Is sensitive to formalin and an ultra-violet irradiating, is rather steady against chlorine, is not inactivated by Chloroformium and an Aether.

Epidemiology

Infection contamination source are patients from an anicteric, subclinical infection contamination or patients in the incubation, prodromal seasons and an initial phase of the season of height of disease in which excrements the virus of hepatitis A or antigens of a virus of hepatitis A are found. Patients with the erased and anicteric forms of hepatitis A which quantity can exceed at 2-10 time number sick of icteric forms have the greatest epidemiological value, and revealing demands application of the complex virologic and immunologic methods few accessible in wide practice.

The leading mechanism of infestation by hepatitis A - fecal-oral, realised through water, alimentary and is contact-household pathes of transfer.

The special value gets the waterway of a transmission of infection providing occurrence of epidemic flashes of hepatitis A. The "blood-contact" mechanism of transfer of a virus of hepatitis A in cases of disturbance of rules of an asepsis is possible at carrying out of parenteral manipulations in a virusemia at sick of hepatitis A. Presence of an air-drop path of transfer precisely is not established.

Sensibility to hepatitis A the overall. Most often disease is registered at children is more senior 1 year (especially at the age of 3-12 years) and at young faces.

And seasonal rising of a case rate in the aestivo-autumnal season is peculiar to a hepatitis. It becomes perceptible as well cyclic rising of a case rate in 3-5, 7-20 years that is bound to change of immune structure of population of masters of a virus. Recurrent diseases of hepatitis A meet is rare and bound, possibly, with infestation by other serological type of a virus.

Pathogenesis

Hepatitis A - the acute cyclic infection contamination characterised by accurate change of the seasons.

After infestation by a virus of hepatitis A from an intestine inpours into blood, there is a virusemia causing development of a toxic syndrome in an initial stage of disease, with the subsequent entering in a liver. As a result of introduction and replication the virus has direct cytolytic an effect on hepatocytes, inflammatory and necrobiotic processes mainly in periportal region hepatic lobes and portal tracts educe.

Owing to complex immune mechanisms the virus replication stops, and it is deduced from a human body. Chronic forms of an infection contamination including a carriage of virus at hepatitis A educe was rarely.

Clinical picture

Hepatitis A is characterised by polymorphism of clinical implications. Distinguish following forms of a degree of manifestation of clinical implications: subclinical, erased, anicteric, icteric. On duration of flow: acute and fixing. On disease severity level: easy, moderately severe, serious.

Complications: relapses, exacerbations, lesions of bile-excreting pathes.

Outcomes: convalescences without the residual phenomena, with the residual phenomena - posthepatic a syndrome, a fixing reconvalescence, lesions of bile-excreting pathes (a dyskinesia, a cholecystitis).

In icteric cases of disease excrete following seasons: incubation, preicteric (prodromal), icteric and reconvalescences.

The incubation interval of hepatitis A averages 21-28 days (from 7 till 50 days). The Prodromal stage, lasting average 5-7 days (from 1-2 to 14-21 days), is characterised by prevalence of a toxic syndrome which can educe in various variants. The variant for which are characteristic the acute beginning with a fervescence to 38-40C° within 1-3 days, the catarral phenomena, a headache, appetite dropping, a nausea sense of discomfort in epigastric range is most often observed "feverishly-dyspepsic". Later 2-4 days become perceptible changes of a coloration of the urine getting colour of beer or tea, decolouration of the excrements sometimes having a liquid consistence. In this season the augmentation of a liver and sometimes (at 10-20 % of patients) the liens which palpation is rather sensitive becomes perceptible. At biochemical inspection tap rising of activity the AlAT. Then there comes the season of height of the disease, 2-3 weeks proceeding on the average (with fluctuations from 1 week. To 1-2 months). As a rule, icterus occurrence is accompanied by dropping of a body temperature to normal or subfebrile level, reduction of a headache and other toxic implications that serves as the important differentsialno-diagnostic character of hepatitis A.

In icterus development distinguish phases of increase, the maximum development and fading. First of all gets an icteric staining a mouth mucosa (a bridle, the firm sky) and scleras, further - a skin, thus usually yellowness degree corresponds to gravity of disease and reaches a "saffron" shade at serious forms of disease.

At inspection of patients in this season, along with an icterus, the tendency to a bradycardia and a hypotension, dullness of warm tints, the liver augmentation which edge is rounded off and painful at a palpation becomes perceptible austenization patients. In 1/3 cases the small augmentation of a lien becomes perceptible. In this season are most expressed darkening of urine and acholic a feces. Laboratory inspection taps characteristic signs of syndromes of cytolysis, a cholestasia and is mesenchymal-inflammatory, antibodies to a virus of hepatitis A of immunoglobulins of a class of M. are naturally defined

The easy form of disease is characterised by an ill-defined intoxication, an easy icterus (bilirubin no more than 80 mkmol/l. The moderately severe form is accompanied by a moderate intoxication, a hyperbilirubinemia within 90-200 mkmol/l. For the serious form the expressed intoxication, signs of involving a CNS (neurologic symptoms) are characteristic.

The phase of fading of an icterus proceeds usually more slowly, than the increase phase, and is characterised by an obsolescence of signs of disease. With icterus disappearance there comes the reconvalescence season, in ot1-2 to 8-12 months) At this time at patients is normalised appetite, die away astenovegetative disturbances, the dimensions of a liver, a lien are recovered. At 5-10 % of patients the fixing form of disease in about several months educes. As a rule, fixing forms come to an end with recover of patients.

In fading of symptoms at separate patients the disease exacerbations, showing deterioration of clinical and laboratory indicators educe. Relapses arise in a reconvalescence in 1-3 months After clinical recover. Patients with fixing forms of hepatitis A, exacerbations and palindromias demand careful laboratory-morphological inspection for an exception of the possible combined infection contamination and in this connection transition in the chronic form.

Besides the specified complications, at a number of patients signs of a lesion of bile-excreting pathes can be defined.

Outcome of hepatitis A usually congenial. Full recover becomes perceptible at 90 % of patients, in other cases the residual phenomena become perceptible. At separate patients it is observed Gilbert's syndrome, characterised by rising in blood serum of level of free bilirubin and an invariance of other indicators. Development of chronic hepatitis A authentically is not established, observed was rarely, contacts influence of accessory factors. The lethality does not exceed 0,04 %.

The diagnosis

It is established taking into account a complex of epidemiological data (a course of a disease after contact to sick hepatitis A or stay in unsuccessful district in the season corresponding to an incubation of hepatitis A), clinical indicators and results of laboratory researches.

The differential diagnosis of hepatitis A is spent in a prodromal stage with a flu and others an ARD, an enterovirus infection contamination. Unlike hepatitis A at a flu typically prevalence of catarral and toxic syndromes, changes of functional hepatic tests and a hepatomegalia are not characteristic. At an adenoviral, enterovirus infection contamination accompanied the liver augmentation usually expresses catarral processes of the top respiratory tracts, to a myalgia.

Treatment

Therapeutic actions in most cases confine appointment of a sparing diet with addition of carbohydrates and reduction of quantity of Adepses (a table №5), a confinement to bed in height of disease, alkaline drink and symptomatic agents. At the serious form of disease prescribe infusional therapy (Ringer's solutions, glucoses, Haemodesum). In a reconvalescence prescribe cholagogue preparations and, under indications, spasmolyticses. Convalescents of hepatitis A are subject to the dispensary clinico-laboratory inspection which duration fluctuates from 3-6 to 12 months and more in the presence of the residual phenomena.

Preventive maintenance

The complex of sanitary-and-hygienic and antiepidemic actions, same as is spent at other intestinal infection contaminations. Potable water and foodstuff, free from a virus of hepatitis A - pledge of depression of a case rate. Quality check of water water on virus contamination is necessary. Contact persons are observed and surveyed within 50 days. In the locuses disinfection chlorine is spent by keeping preparations.

Immunoprophylaxis of hepatitis A of a specific immunoglobulin on 0,05 ml/kg of mass of a body.

The active immunoprophylaxis of hepatitis A is not developed.