about the project
Medical news
For authors
Licensed books on medicine
<< Previous Next >>


The term "hepatitis" refers to diffuse inflammation of the liver tissue of various etiologies. Among hepatitis, primary (independent nosological units) and secondary (developing with other diseases) are distinguished. By etiology, primary hepatitis is more often viral, alcoholic, drug, autoimmune. Acute (up to 6 months) and chronic (over 6 months) hepatitis are distinguished with the course.

Acute hepatitis. Viral hepatitis. Viral hepatitis is one of the most difficult general medical problems, since they are widespread and have an unfavorable outcome. Often after acute infection, chronic hepatitis forms (especially often with hepatitis C); possibly the development of cirrhosis; the etiological relationship between hepatocellular carcinoma and hepatitis B and C. viruses has been proven.

Currently, 5 hepatotropic viruses are known. The viruses are named after the letters of the English alphabet from A to E. Each year, new candidates are added to this list, recently viruses F, G, TTV that cause parenteral hepatitis have been identified. In addition, there is a group of unspecified viral hepatitis in which no known viruses have yet been identified. In such cases, the term "hepatitis neither A nor B nor C" is used.

Hepatitis A and E are classified as diseases with fecal-oral (enteral) transmission mechanism, completely reversible course (Table 28.1). Carrier and chronic course, as a rule, is not formed. Vaccines are designed for viral hepatitis A and B.

Viral hepatitis A (Botkin's disease). The disease is endemic and epidemic in nature. Hepatitis A virus (HAV) belongs to the Picornaviridae family, has a diameter of 27 nm, contains one RNA chain, and has 7 genotypes. Distributed everywhere. The virus is stable in the environment. The incubation period is 15-40 days. About 80% of cases are children under the age of 15. The disease usually has a mild cyclic course, accompanied by slight jaundice and nonspecific symptoms. Hepatic tests changed. In most infected individuals, the disease proceeds in an anicteric, often subclinical form. The fulminant form occurs in 0.1% of cases. Virus replication occurs in the liver. Hepatocytes are damaged, apparently, not due to the direct cytopathic effect of the virus, but as a result of the immunopathological mechanisms triggered by it. Activation of all parts of the immune

Table 28. Comparative characteristics of viral hepatitis transmitted by fecal-oral route

HCC - hepatocellular carcinoma

Sign Viral hepatitis A Viral hepatitis E
Pathogen Viral Hepatitis A HAV Viral Hepatitis E HEV
Genome RNA RNA
Family Picornaviridae Caliciviridae
Virus size 27 nm 27–38 nm
Incubation period 15-45 days 15-50 days
Antibodies Anti-HAV IgM, Anti-HAV IgG Anti-HEV IgM, anti-HEV IgG
Chronization - -
Mortality <0.1% 0.2% (10-20% in women in the third trimester of pregnancy)
HCC development risk - -
The system leads to the rapid accumulation of antiviral antibodies, which help to stop the replication of the virus and cleanse the body with complete recovery. The diagnosis is confirmed by the detection of specific markers in the blood serum - antiviral antibodies of the IgM class (anti-HAV IgM antibodies) using enzyme-linked immunosorbent assay. Thanks to the development of molecular biological research methods, it became possible to determine specific viral nucleic acids - RNA, which also confirms the diagnosis. After the disease, lifelong immunity due to anti-HAV IgG antibodies remains.

Viral hepatitis E. The causative agent belongs to the family Caliciviridae, the diameter of the hepatitis E virus (HEV) is 27–38 nm, the genome is represented by one RNA strand. Hepatitis E is characterized by uneven distribution (outbreaks in India, Nepal, Pakistan, China, a number of countries in Africa and Latin America).

It is rare in Moscow in the form of imported cases. The disease resembles viral hepatitis A. The difference is mainly the waterway. The virus infects children, adolescents, young adults. The incubation period is 15-60 days. The disease usually proceeds in a mild form. Mortality 0.5-3.0%. The exception is pregnant women in the II — III trimester. Their disease has a fulminant course, mortality reaches 20%.

Hepatitis B, C and D have a parenteral (through blood and its products, through the secrets of the body) transmission mechanism (Table 28.2).

Comparative characteristics of parenteral viral hepatitis

Viral hepatitis B can occur in the form of mono-infection or co-infection, if there is a simultaneous infection with hepatitis B virus and delta virus.

Table 28.2 HCC - hepatocellular carcinoma
Sign Viral hepatitis b Viral hepatitis C Viral hepatitis D
Pathogen HBV hepatitis B virus HCV hepatitis C virus Hepatitis D virus HDV
Family Hepadnaviridae Togaviridae genus Flaviviridae Unclassified viruses
Virus size 42 nm 35-50 nm 40 nm
Incubation period 30-180 days 20—90 days 30-40 days
Antigens HBsAg, HBcAg, HBeAg, HBV-DNA HCAg, HCV DNA HDAg
Antibodies Lnti-HBsAg, Anti-HBcAg, Anti-HBeAg Anti-HCV IgM, Anti-HCV IgG Anti-HDV IgM, anti-HDV IgG
Chronization 5-10% 60-75% 2–70%
Mortality 0.2-1.0% 0.2-3.3% 2-20%
HCC development risk there is there is there is

Acute hepatitis B without the delta virus is caused by the hepatitis B virus (WU) of the Hepadnaviridae family, 42 nm in diameter, containing circular double-stranded DNA. The complete virion (Dane particles) contains a number of viral antigens: HbsAg - the surface ("Australian") antigen, HbcAg - the core antigen, HbeAg - the replication or infectivity antigen, HbxAg - the least studied, presumably, it causes the malignant transformation of liver cells. Only the full virion carries an infectious beginning, it is precisely its presence in the blood and body secrets that makes them contagious.

When HBV enters the body, primary viremia develops (the circulation of the virus in the blood). The virus accumulates in lymphoid tissue, Kupffer cells of the liver, germ cells, bone marrow. A primary immune response develops. In case of adequate severity, the virus is eliminated, the patient develops an anicteric form of hepatitis B (in 70%). With an insufficient immune response, a secondary generalization of the process develops. The virus tropism to hepatocytes is realized. HBV using protein molecules HbsAg is adsorbed on hepatocytes and the DNA of the virus enters the cell. The DNA strand that makes up the complete ring is destroyed, a DNA fragment is embedded in the hepatocyte genome. The synthesis of viral proteins begins, and the hepatocyte's own proteins are also used by the virus. The type of disease progression is related to the size of the integrated DNA.

If the inserted DNA fragment was close to the full ring, then the viral protein is quite genetically foreign to the body, and the cells of the immune system quickly destroy such viruses - a fulminant form of the disease develops. This may seem like an easy outcome, but it should be borne in mind that the viral protein is embedded in the cell membrane of the hepatocyte for subsequent inclusion in the viral membrane. Cells of the body's immune system, responding to a foreign protein, destroy the hepatocyte itself. Therefore, in the synthesis of a virus that is sufficiently foreign to the body, mass destruction (necrosis) of hepatocytes occurs with this protein on the surface by cells of the immune system (mainly T-lymphocytes - killers).

If the integrated viral DNA had a sufficiently large defect, then the synthesized viral protein is more similar to the proteins of the body and the reaction of the immune system is moderate. As a result, chronization of the process may occur.

In the pathogenesis of hepatocyte damage, cross-sensitization of immune system cells to hepatocyte antigens of their own can occur due to a certain similarity of hepatocyte and virus antigens, and due to the reaction of immune system cells with both a viral protein and a hepatocyte protein containing a viral protein .

All HBV antigens and antibodies formed to them are markers of the infectious process. Their various combinations characterize the stage of the course of the disease. Markers of actively ongoing infection are HbsAg, HbeAg, anti-Hbc IgM, specific viral DNA and DNA polymerase. With a completed infection in the blood, anti-Hbs and anti-Hbc IgG are determined. Long-term persistence of HbsAg and HBeAg indicates a possible development of the chronic process.

There are mutants of HBV-genetic variants that differ in the nucleotide sequences of DNA. Patients infected with a mutant HBV strain have a higher rate of disease progression, more often cirrhosis of the liver is formed, and the effect of therapy is worse.

Viral hepatitis delta is caused by a small (36 nm) spherical virus (HDV), consisting of a genome (RNA) and a protein that encodes the synthesis of a specific delta antigen. The uniqueness of HDV is that it is defective and its replication depends on the helper virus - HBV, in essence, it is a virus of the virus. The reproduction of HDV and the realization of its pathogenic properties is carried out only in the body infected with HBV. Therefore, patients with chronic hepatitis B and HbsAg carriers have an increased risk of HDV infection. An HDV molecule is created from an HBV envelope and an RNA strand. At the same time, the activity of HBV decreases, since it loses its surface components. HDV has a pronounced cytopathic effect and destroys hepatocyte.

Viral hepatitis C causes a virus of the family Flaviviridae, with a diameter of 50-60 nm, containing one strand of RNA. There are 6 genotypes and more than 100 subtypes of this virus. A feature of hepatitis C virus (HCV) is its genetic heterogeneity, due to the rapid substitution of nucleotides. The pathogenesis of HCV infection is not well understood. The virus enters the body in the same way as HBV, although it can penetrate intact skin. Having tropism for hepatocytes, the virus has a direct cytopathic effect on them. HCV proteins can induce hepatocyte apoptosis. Damage to hepatocytes may be associated with a specific or nonspecific immune response of the body. Due to the genetic heterogeneity of HCV, it has many antigenic variants (“quasivids”), which makes it difficult to implement an adequate immune response. The virus as it eludes the immune system, is able to persist for a long time in the human body and cause chronic hepatitis. HCV antigen - HCAg - is not detected in blood serum.

Viral hepatitis G causes hepatitis G virus (HGV), which belongs to the Flaviviridae family, contains RNA in the genome and is characterized by significantly less variability than HCV. The virus has a parenteral route of transmission, often found in combination with hepatitis B, C and D (24 - 37%), without burdening the course of the disease.

All viral hepatitis is anthroponosis. The source of parenteral viral hepatitis are carriers (HbsAg, HCAg), patients with chronic hepatitis B or C, much less often - patients with acute viral hepatitis. Infectious agents are found in almost all body fluids and secrets (blood, urine, saliva, bile, tears, feces, breast milk, vaginal secretions, semen, cerebrospinal fluid, umbilical cord blood). However, the real epidemiological danger in hepatitis B is blood, sperm and saliva, since the concentration of the virus in other fluids is low. With hepatitis C, the concentration of the virus in the blood, semen and other biological substrates is significantly lower than with hepatitis B.

HBV can be spread naturally: through sexual contact, vertically from the mother’s HbsAg (+) to the fetus or newborn. Artificial transmission routes are created during treatment and diagnostic measures, accompanied by a violation of the integrity of the skin and mucous membranes (injections, dental procedures, gynecological and gastroenterological examinations with insufficient processing of instruments); transfusions of blood and its components, if they contain hepatitis viruses; with acupuncture, tattooing, performing ritual rites, piercing the earlobe, piercing, manicure, cosmetic procedures performed by common tools.

In the recent past, the most common method of infection was post-transfusion (with blood transfusion).
In the main risk group were patients with hemophilia and other blood diseases. Among them, the proportion of infected with HBV and HCV was very high (up to 90%). Thanks to the established standards for donor screening, blood transfusion and intravenous administration of blood products have become safer. A special risk group consists of medical workers, both nursing staff and doctors. Among the medical specialties, surgeons, dentists, gynecologists and pathologists are in the first place. The epidemic of parenteral hepatitis (B and C) in Russia in recent years is due to a catastrophic increase in the number of people using intravenous drugs. This is the so-called injection route of infection. Virus transmission occurs by using a common syringe or needle. There are times when the drug itself is infected. The proportion of hepatitis C infected among drug addicts is especially high, but varies significantly in different countries. In Russia, in some regions it makes up 50%. Hepatitis B is rarely seen in people under 14 years old. The peak incidence occurs at the age of 15-20 years.

Morphological characteristics of acute viral hepatitis. Macroscopically, the liver becomes large and red. Histologically, in the liver tissue, hepatocyte necrosis is determined, which can be spotty, periportal, centrilobular, bridged, submassive and massive. Hepatocytes are in a state of hydropic and balloon dystrophy. Some hepatocytes are in a state of apoptosis with the formation of Kaunsilmen's bodies. Abundant infiltration is detected in the portal tracts and in the acini, represented mainly by lymphocytes and macrophages, mixed with a small amount of white blood cells. Hyperplasia and focal proliferation of Kupffer cells are noted. Regenerative hepatocytes are found in the third acinus zone. Cholestasis is possible.

In some cases, in the liver with viral hepatitis, submassive and massive necrosis of hepatocytes develop. This form of the disease is called fulminant, or rapidly progressive. Clinically, it is characterized by the development of acute hepatic cell failure and often leads to the death of the patient. If the patient survives, then in the future he develops post-necrotic cirrhosis of the liver.

The presence of the virus in the cell can be detected using the following markers: a) immunohistochemical (when reacting with specific antibodies); b) histochemical (orcein according to Shikat) - HbsAg is detected in the cytoplasm of infected hepatocytes; c) morphological (hematoxylin and eosin) - a matte vitreous cytoplasm of hepatocytes upon accumulation of excess HbsAg in the smooth endoplasmic reticulum, sand nuclei of hepatocytes - in the presence of HbcAg, vacuoles with small eosinophilic inclusions are detected in the nuclei.

All viral hepatitis have four phases of the disease: 1) the incubation period, varies from 2 to 26 weeks; 2) the preicteric (prodromal) period, characterized by nonspecific symptoms; 3) icteric period, developed clinical manifestations; 4) the period of convalescence.

There are several clinical and morphological forms of acute viral hepatitis: 1) cyclic icteric, a classic manifestation of hepatitis A; 2) anicteric, 80% hepatitis C and 70% hepatitis B; 3) subclinical (inapparent); 4) fulminant, or fulminant, with massive progressive necrosis of hepatocytes;

4) cholestatic, involving small bile ducts in the process.

With simultaneous infection with HBV and HDV, co-infection develops, the disease is more severe than mono-infection, mainly in moderate form (Table 28.3). An essential feature is the two-phase course of the disease with clinical-enzymatic exacerbation. Cytolytic syndrome is expressed. The convalescence period is longer. 90% of patients recover, 10% develop chronic hepatitis.

Comparative characteristics of the combination of viral hepatitis B and D

Acute delta virus infection in a virus carrier or a hepatitis B patient is called superinfection. Persons who have antibodies to HbsAg as a result of an illness or vaccination do not develop delta hepatitis. With superinfection, the most severe and prognostically unfavorable hepatitis develops. Edematous ascites syndrome, hepatosplenomegaly, impaired protein-synthetic function of the liver,

Table 28.3
Co-infection (simultaneous infection) Superinfection (sequential infection)
3-4% 90% Seldom 7-20% 10-15% 70-80%
Malignant course Immune Recovery Chronic HBV / HDV Hepatitis Malignant course Severe acute hepatitis Chronic HBV / HDV Hepatitis
Death - Cirrhosis of the liver Death Recovery Cirrhosis of the liver

the multiwave nature of the course of the disease with repeated exacerbations, early signs of chronicity, which is observed in 70–80% of cases, in 20% the disease has a fulminant course.

Options for the course of HBV infection and outcomes of acute viral hepatitis B

Variants of the course of HBV infection and outcomes of acute viral hepatitis B (Table 28.4). Hepatitis B flows chronically in 5-10% of patients, mainly men. Hepatitis C is most prone to chronicity, which occurs in approximately 50–70% of patients, mainly women (Table 28.5). In both diseases, there is a risk of developing cirrhosis of the liver and hepatocellular carcinoma. In the USA annually

Table 28.4 HCC - hepatocellular carcinoma
Flow option Frequency Outcomes
Carriage (husband: wives = 6: 1) 5-10% Повышен риск ГЦК
Безжелтушная форма 60% выздоровлениехронизацияносительство
Острый вирусный гепатит 20—25% выздоровлениехронизация (4%)
Фульминантная форма <1% цирроз печенисмерть
Таблица 28.Варианты течения HCV-инфекции и исходы острого вирусного гепатита С
Вариант течения Frequency Исходы
Носительство (преобладают женщины) 5,6% Повышен риск ГЦК
Латентное течение 14,8%
Вялотекущий острый гепатит 55,6%
Острый гепатит тяжелого течения 15,7% цирроз печениГЦК
Острый гепатит тяжелого течения с внепеченочными проявлениями 9,3% цирроз печениГЦК

регистрируют около 1200 случаев индуцированной гепатитом В гепатоцеллюлярной карциномы. Факторами высокого риска хронизации острого вирусного гепатита считаются: легкое течение заболевания, высокая репликативная способность вируса (HBV-ДНК в высоком титре, HbeAg), низкий иммунный ответ (СD4+/CD8+<3).

Хронические гепатиты. Новая классификация хронического гепатита рекомендована Международным конгрессом гастроэнтерологов в Лос-Анджелесе (1994 г.) и учитывает три категории оценки: этиологию, степень активности процесса и стадию заболевания (табл. 28.6). Руководствуясь этиологическим фактором, выделяют вирусный, аутоиммунный, лекарственный и криптогенный (неустановленной этиологии) хронический гепатит. По мнению российских патологоанатомов, перечень этиологических факторов должен быть расширен. К хроническому гепатиту следует отнести также алкогольный гепатит (эта точка зрения разделяется не всеми патологоанатомами), наследственный (при недостаточности альфа 1-антитрипсина и болезни Вильсона) и гепатит смешанной этиологии. Этиологический критерий оценки и систематизации хронического гепатита дополняется двумя клинико-морфологическими — степенью активности процесса и стадией заболевания, определенными методом полуколичественного анализа. Все хронические гепатиты считаются активными. Степень активности процесса оценивается с помощью индекса гистологической активности (ИГА) (индекса Knodell). В биоптате печени морфологом оцениваются перипортальные и мостовидные некрозы (0—10 баллов), внутридольковые фокальные некрозы и дистрофия гепатоцитов (0—4 балла), воспалительный инфильтрат в портальных трактах (0—4 балла), фиброз (0—4 балла). ИГА от 1 до 3 баллов соответствует хроническому гепатиту с минимальной активностью. При нарастании активности (ИГА 4—8 баллов) говорят о мягком течении хронического гепатита. ИГА 9—12 баллов соответствует хроническому гепатиту умеренной активности, а 13—18 баллов — тяжелому хроническому гепатиту.

При определении степени активности процесса следует учитывать проявления гепатита за пределами печени, особенно при вирусном и аутоиммунном гепатите. Внепеченочные (системные) проявления хронического гепатита, отражающие активность болезни, обусловлены как иммунокомплексными реакциями, так и сочетанием их с реакциями гиперчувствительности замедленного типа. У больных описаны узелковый периартериит, гломерулонефрит, артралгии, экзантема типа крапивницы, макулопапулезная сыпь. Порой такая разнообразная клиническая картина маскирует патологию печени.

Таблица 28.6 Классификация хронического гепатита (1994)

Категория оценки Формы хронического гепатита
I. Этиология вирусныйаутоиммунныйлекарственныйкриптогенныйалкогольныйнаследственныйсмешанный
II. Степень активности процесса — Индекс гистологической активности (ИГА) (по RGKnodell et al., 1981) 1—3 балла — минимальная активность 4—8 баллов — мягкое течение 9—12 баллов — умеренная активность 13—18 баллов — тяжелое течение
Ш.Стадия хронического гепатита — степень фиброза (по VJDesmet, 1994) — фиброз отсутствует— слабый фиброз— умеренный фиброз— тяжелый фиброз— цирроз печени
Стадия хронического гепатита определяется полуколичественной оценкой выраженности фиброза печени. Цирроз печени рассматривается как необратимая стадия хронического гепатита. Следует также оценивать критерий активности цирроза (см. ниже).

Гистологически хронический гепатит В характеризуется сочетанием следующих признаков: гидропическая и баллонная дистрофия гепатоцитов, апоптозные тельца (тельца Каунсильмена), некрозы гепатоцитов, лимфо-макрофагальная инфильтрация как в паренхиме, так и в портальных трактах, гиперплазия и пролиферация купферовских клеток, а также выраженные в разной степени склероз (фиброз) портальных трактов. Характерны также прямые маркеры HBV-инфекции (матовостекловидные гепатоциты и песочные ядра гепатоцитов).

Гистологически хронический гепатит С характеризуется сочетанием следующих признаков: жировая дистрофия гепатоцитов, наряду с гидропической и баллонной, апоптозные тельца, выраженная гетерогенность (полиморфизм — разные размеры и форма) гепатоцитов; при этом некрозы гепатоцитов выражены слабо, преобладают перипортальные, лимфоидные агрегаты и фолликулы в портальных трактах и внутри долек, гиперплазия и пролиферация купферовских клеток, расположение лимфоцитов в виде цепочек в синусоидах, поражение желчных протоков с их деструкцией и пролиферацией дуктул.

Аутоиммунный гепатит имеет хроническое течение. Этиология не установлена. Развивается преимущественно (70%) у молодых женщин. Наряду с поражением печени в сыворотке крови определяется широкий спектр аутоантител {антинуклеарные, к микросомальному антигену печени и почек, специфическому печеночному протеину (LSP), гладкой мускулатуре}, повышение IgG. Серологические маркеры вирусных гепатитов отрицательные. Более чем у половины больных выявляется HLA-B8 в сыворотке крови. Приблизительно в 10% случаев заболевание начинается как острый гепатит, у остальных пациентов начало заболевания стертое, течение постепенное. У 10—20% больных к моменту первичной диагностики имеются признаки декомпенсированного цирроза печени.

Морфологическая картина аутоиммунного гепатита соответствует тяжелому хроническому гепатиту. Характерно наличие лимфомакрофагальных инфильтратов с примесью большого количества плазматических клеток, а также появление в портальных трактах лимфоидных фолликулов, рядом с которыми могут формироваться макрофагальные гранулемы. Инфильтрат из портальных трактов может выходить в первую зону ацинуса, разрушая пограничную пластинку, образуя перипортальные или ступенчатые некрозы. Активное течение АИГ приводит к развитию мелкоузлового цирроза печени.

<< Previous Next >> = Skip to textbook content =


  1. Question 14 Viral hepatitis
    - inflammation of the liver tissue caused by viruses. Hepatitis viruses belong to different taxa and differ in biochemical and molecular characteristics, but all these viruses are united by the fact that they cause hepatitis in humans. Chronic liver diseases, including viral hepatitis B and C, are among the ten leading causes of death in the world. Currently, a large number of viruses are known.
  2. Hepatitis
    Hepatitis is an inflammation of the liver caused by an infection, chemicals, or virus. See the LIVER (PROBLEMS) article. If it is an infectious or epidemic hepatitis, see also the metaphysical explanation of the EPIDEMIC at the beginning
  3. Hepatitis
    Acute hepatitis Acute hepatitis can be caused by a viral infection, the effects of drugs and hepatotoxic substances. The disease is an acute injury to the hepatocytes. Clinical manifestations depend on the severity of the inflammatory reaction and, more importantly, on the volume of necrotic liver parenchyma. Mild inflammatory processes can occur as
  4. Hepatitis
    The term "hepatitis" means any inflammatory disease of the liver. However, in practice it is not used in relation to such focal inflammatory processes as an abscess or tuberculous focus. The concept of “hepatitis” refers only to diffuse lesions of the liver, in which the etiological spectrum is very small. Acute viral hepatitis. This acute infection is characterized by diffuse liver damage with
  5. Neonatal hepatitis
    SYNONYMS Congenital hepatitis, fetal hepatitis. DEFINITION Neonatal hepatitis is a pathology of the liver of an infectious nature in the perinatal and postnatal period of life. CODE ICD-P35.3 - congenital viral hepatitis; K77.0 - cytomegalovirus hepatitis, toxoplasma hepatitis; K75.0 - other inflammatory diseases of the liver; K75.8 - other specified inflammatory liver diseases. PREVENTION TO ALL
    - inflammatory liver disease of any etiology, continuing without improvement for at least 6 months, potentially goes into cirrhosis. The main clinical manifestations of pain, a feeling of heaviness in the right hypochondrium, dyspeptic symptoms (loss of appetite, impaired stool), weight loss, irritability, sometimes jaundice, cutaneous changes (pink lips, raspberry tongue, xanthomas, erythema
  7. Chronic hepatitis
    SKYR ?? ICHE. HEPATITIS (CGep) is a diffuse polyetiological-Ewspalitel ™ process in the liver, lasting more than 6 months. n ™ 5? ° logically CGep is characterized by degeneration or necrosis of the liver-I ™ ™ S1STOK (° T single to massive), liver tissue infiltration by immunocompetent cells and polymorphic nuclear leukocyte- 336 jQi expansion of portal tracts due to inflammatory infiltration in
  8. Hepatitis G (GG)
    The virus has not yet been classified. The main risk groups for infection were the same as in HB and HS. This suggests that hepatitis G belongs to the group of parenteral infections. General preventive measures for this group of infections should be effective even in
    It is a common disease - 50% of all diseases. It was isolated from cirrhosis of the liver when a new research method appeared - laparoscopy and intravital targeted biopsy. This is an inflammatory-dystrophic disease. For more than 6 months, progression to various degrees. The criterion for the diagnosis is the undisturbed lobular structure of the liver. Этиология I. В 50% - острый
    Вирусный гепатит утят (лат. — Hepatits viriosa anaticularum; англ. — Duck virus hepatitis; инфекционный гепатит утят, гепатит утят, ВГУ) — остро протекающая болезнь утят, характеризующаяся поражением печени и высокой смертностью, протекающая у взрослых уток без симптомов. Historical background, distribution, hazard and damage. В 1949 г. в США среди выведенных утят пекинской породы
Medical portal "MedguideBook" © 2014-2019