«Poliovirus. Enteroviruses. Rotaviruses. Rhabdoviruses. Hepatitis viruses.»
Families: Picornaviridae (pico, meaning small).
Genus: Enterovirus.
The genome is RNA, which surrounded by capsid. They are nonenveloped viruses.
Poliovirus cultivation in cell culture.
Antigenic properties:
Poliovirus strains have been classified into three types: 1, 2 and 3.
Type 1 is the most common and causes most epidemics (rarely type 3). Type 2 usually causes latent infection.
The source of infection: patient or carrier.
The mode of infection:
1. The virus is transmitted by the fecal-oral route through ingestion.
2. Inhalation or entry through conjunctiva of droplets of respiratory secretions may also be posible modes of entry in close contacts of patients in the early stage of the disease.
Pathogenesis.
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It then spreads to the regional lymph nodes and enters the blood stream (viremia).
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After further multiplication in the reticuloendothelial system, the virus enters the bloodsteram again and is carrier to the spinal cord and brain.
Clinical forms of poliomyelitis.
Clinical forms
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Symptoms
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Material for diagnostics
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1. Without damage of CNS.
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Inapparent infection
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Without clinical symptoms
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Feces
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Abortive infection
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Fever, intoxication, catarrh of the respiratory tract, disfunction of intestinal tract.
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Feces, wash-out from nasopharynx.
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2. With damage of CNS.
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Nonparalytic poliomyelitis
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Serous meningitis
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Feces, Liquor, wash-out from nasopharynx.
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Paralytic poliomyelitis
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Flaccid paralysis
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Laboratory diagnosis:
1. Virological method. Virus cultivation in the cell culture. Identification of virus by NT.
2. Serological method – CFT, NT.
Specific prophylaxis.
1. Active immunisation:
Live polio vaccine 1, 2, 3 types (Russian).
Inactivated vaccine from virus of poliomyelitis 1, 2, 3 types (France).
2. Passive immunisation:
Human immunoglobulin is of little value.
2. Enterovirus.
Enteroviruses of medical importance include:
1. Coxsackievirus A types 1-24.
2. Coxsackievirus B types 1-6.
3. Echovirus types 1-34 (enteric cytopathogenic human orphan).
4. Enterovirus types 68-71.
The genome is RNA which surrounded by capsid. They are nonenveloped viruses.
Cultivation:
1. Echovirus – cultivation in the cell culture.
3. Coxsackievirus B – cultivation in the cell culture.
The source of infection: patient or carrier.
The mode of infection:
1. The virus is transmitted by the ingestion (through contaminated water and food).
2. Droplet infection.
The main clinical forms:
1. Diarrhea.
2. ARVD.
3. Paralytic disease of children (infantile paralysis).
4. Serous meningitis.
5. Herptonsillitis.
6. Myocarditis, pericarditis.
Laboratory diagnosis:
1. Virological method. Material for diagnostics: feces, wash-out from nasopharynx, liqour.
2. Serological method – CFT, NT.
3. Rotaviruses.
Families: Reoviridae. The genome is RNA which surrounded by capsid. They are nonenveloped viruses.
The source of infection: patient or carrier.
The mode of infection:
Virus is transmitted by the ingestion (through contaminated food and water).
Clinical symptoms: Diarrhea (feces have yellow colour, 10-15 times), vomit, dehydration of organism.
Laboratory diagnosis.
Material for diagnosis
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Method of diagnostics
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Feces
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1) Electron microscopy
2) RPHA
3) EIA
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Serum
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Serological method: RSHA, NT, CFT.
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4. Hepatitis viruses.
The term «viral hepatitis» refers to a primary infection of the liver by any one of a heterogeneous group of «hepatitis viruses», which currently consists of types A, B, C, D, E, G and unstudied viruses F, TTV (Transfusion Transmitted Virus).
Hepatitis viruses are taxonomically unrelated. Except for type B which is a DNA virus all the others are RNA viruses. The features common to them are their hepatotropism and ability to cause a similar icteric illness, ranging in severity from the unapparent to the fulminant fatal forms.
As all types of hepatitis viruses cause a clinically indistinguishable acute illness, their differentiation is based on their serological and molecular markers.
Hepatitis virus type A.
Families: Picornaviridae.
HAV is nonenveloped RNA virus.
The source of infection: patient.
The mode of infection.
HAV transmission is by the fecal-oral route. Infection is by ingestion.
Pathogenesis:
The virus multiplies in the intestinal epithelium are reaches the liver by hematogenous spread.
Clinical forms:
1) Acute with jaundice (intoxication, Jaundice, hepatosplenomegaly).
2) Acute without jaundice.
3) Inapparent infection.
Laboratory diagnosis:
1. EIA – for determination of IgM to HAV in the serum.
2. EIA – for determination of IgG to HAV in serum.
3. EIA – for determination of antigen (HAV) in the feces.
Specific prophylaxis.
1. Acute immunisation:
Inactivated cultural vaccine (Hep-A-in-Vac) – Russian.
2. Passive immunisation:
Normal human immunoglobulin.
Hepatitis virus type B (Dane particle).
Type B hepatitis is the most widespread and the most important type of viral hepatitis.
Families: Hepadnaviridae.
HBV is a DNA virus with outer envelope (supercapsid).
Antigens of HBV:
Hbs-Ag – surface antigen. This antigen found in the blood of patient, saliva, urine, semen, cervical secretions. Hbs-Ag is a receptor for adsorbtion virus on the hepatocytes.
Hbc-Ag – hepatitis B core antigen. It is not secreted and does not circulate in blood, but can be demonstrated in hepatocytes.
Hbe-Ag is a soluble nonparticulate nucleocapsid protein. This antigen found in the blood with Hbs-Ag – Active replication of virus.The presence of Hbe-Ag in blood provides a convenient and readily defectable marker of HBV replication and high infectivity.
Hbx-Ag – present in patient with severe chronic hepatitis and hepatocellular carcinoma.
The source of infection: patient or carrier.
The mode of infection:
1. Transfusion of carrier blood (therapeutic, diagnostic, prophylactic and even nonmedical procedures are now the main modes of infection).
2. Sexual transmission of HBV (through semen, vaginal secretions).
3. Intranatal transmission, rarely – transplacental.
4. By organ transplants.
Pathogenesis:
HBV multiply in the hepatocytes without cytopathogenic action (chronic productive infecton)
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Hepatocytes carry viral antigens and are subject to antibody dependent NK cell and cytotoxic T cell attack.
Clinical forms:
2. Chronic hepatitis.
The clinical picture of hepatitis B is similar to that of type A, but it tends to be more severe and protracted.
Laboratory diagnosis.
1. EIA – for determination of Hbs-Ag and Hbe-Ag in the blood of patient.
2. Genetic method – PCR.
3. Serological method (EIA) – for determination of IgM to Hbc-Ag.
Specific prophylaxis.
1. Active immunisation: the currently preferred vaccine is genetically engineered by cloning the S gene of HBV in bakers yeast.
2. Passive immunisation – human immunoglobulin against hepatitis B.
5. Rhabdoviruses.
Families: Rhabdoviridae.
Genus: Lyssavirus.
Rabies virus – bullet shaped, enveloped viruses with single RNA genome.
Rabies virus cultivation in the cell culture, chick embryo, animals (white mouse).
Rabies.
Rabies has been recognised from very ancient times as a disease transmitted to humans and animals by the bite of «mad dogs».
The source of infection: wild animals – fox, wolf; domastic animals – dogs, cats.
The mode of infection. Infection is transmitted through the bite of animals (with the saliva).
Pathogenesis.
The incubation period is usually from 1-3 months, though it may be as short as 7 days or as long as three years. The incubation period is usually short in persons bitten on the face or head, and long in those bitten on the legs. This may be related to the distance the virus has to travel to reach the brain.
The virus appears to multiply in the muscles, connective tissue or nerves at the site of deposition for 48-72 hours. It penetrates the nerve endings and travels in the axoplasm towards the spinal cord and brain. The movement of the virus in the axons is passive, at a speed of about 3 mm per hour. The infection spreads centripetally from the axon to the neuronal bodies and progressively up the spinal cord through the synapses of the neurons. The virus ascends rapidly to the brain where it multiplies and spreads centrifugally along the nerve trunks to various parts of the body including the salivary glands. It multiplies in the salivary glands and is shed in the saliva. The presence of the virus in the saliva and the irritability and aggression brought on by the encephalitis ensure the transmission and survival of the virus in nature. The virus ultimately reaches virtually every tissue in the body, throgh the centrifugal dissemination may be interrupted at any stage by death. The virus is almost invariably present in the cornea and the facial skin of patients because of their proximity to the brain. This provides a method for the antemortem diagnosis of human rabies. The virus may also be shed in milk and urine. Viremia is not clinically significant though it has been demonstrated under experimental conditions.
Laboratory diagnosis.
1. IFT – for determination of Ag in the films from the cornea.
2. Virological method.
After death:
1. Microscopic method – demonstration of Negri bodies in the brain.
2. IFT – for determination of Ag in the material.
3. Virological method.
Specific prophylaxis.
1. Active immunisation: antirabic cultural inactivated vaccine (Rabivac).
Contra-indication to vaccination:
Acute infection diseases, Chronic diseases.
Allergic reactions.
Pregnancy.
2. Passive immunisation:
Antirabic immunoglobulin from blood of house.
Antirabic human immunoglobulin.
