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CONTE
NT
 RUBELLA
 VIRAL HEMORRHAGIC FEVER
 HEPATITIS
 Rubella is a mild disease
 Common childhood infection with minimal systemic upset
 Also known as three days measles or German measles
 First isolated in tissue culture in 1962
 Serious complications are very rare
 Can affect anyone of any age
RUBELLA VIRUS
 Member of togavirus family
 Genus- Rubivirus
 Enveloped virus with a single stranded RNA-positive stranded
 Lipoprotein envelop
 Surface spikes contain hemagglutinin
 Spherical shaped
 Icosahedral nucleocapsid
 Diameter=50-70 nm
 Incubation period is 14 to 21 days.
 Multiply in the cytoplasm of infected cell
 Virus is inactivated by ether, chloroform, formaldehyde and beta propiolactone
 Destroyed at 56°C
SYMPTOMS
 Malaise
 Head ache
 Mild fever (38.9°C or lower)
 Mild conjunctivitis
 Red itchy eyes
 Rash begins on forehead and face (lasting 1-3 days)
 Enlarged lymph nodes
 Aching joints ,especially in young women's
 Infection in pregnant women can cause death of the fetus or congenital malformations
•Infection in pregnant women can cause death of the fetus or congenital malformations​
•Skin manifestations are called "Blueberry muffin lesions"​
 Virus cross the placenta and cause congenital Rubella syndrome in newly born
PATHOGENESIS
 Initial replication of virus occurs in-Nasopharynx and local lymphnodes
 From there spread to internal organs and skin via blood
 Transmission via direct or droplet contact with respiratory secretions
 Spread when an infected person coughs or sneezes​
 Spread by direct contact with infected mucus from the nose and throat​
 From pregnant women to Fetus through blood stream​
 Virus found in the blood 5 to 7 days after infection and spreads throughout the body​
 Virus contagious for about one week after the rash appearance​
IMMUNITY
 Infection leads to lifelong immunity ( Second cases of rubella do not occur)​
 Antibody cross the placenta and protects the newborn
LABORATORY DIAGNOSIS
 Hemagglutination inhibition test
 EIA (Enzyme Immuno Assay)
 Latex agglutination
 CFT
 Neutralization test
SPECIMEN
 Inoculation of tissue culture media with throat, blood or urine
TREATMENT
 Live attenuated vaccines are administered to children at 15 month of age.
 Approved during the year 1969
 Vaccine produce a long lasting immunity against virus
 MMR also given
 Gamma globulin is used for treatment (But it is not a specific treatment)
PREVENTION
VIRAL HEMORRHAGIC FEVER
 It is an infection that can cause severe, life threatening illness
 Acute systemic febrile syndrome
 Highly infectious
 Infectious during viremia stage
 It is cause by 4 different virus families
> Filoviridae
> Bunyaviridae
> Arenaviridae
> Flaviviridae
FLAVIVIRUS
 Not all members of these families cause VHF​
 All VF viruses are small, ss RNA viruses with lipid envelope membranes
 Damage the walls of tiny blood vessels, making them leak, and can hamper the blood's ability to clot
 Some hemorrhagic fever include:​
* Dengue
* Ebola
* Lassa
* Marburg
* Yellow fever
 Most commonly occur in –Tropical areas​
 There is no cure​
 Vaccines available only for few types​
 Prevention is the best approach​
 Human outbreak are sporadic and irregular​
SYMPTOMS
 Vary by disease
o Fever
o Fatigue
o Weakness
o Dizziness
o Muscle, Bone or Joint aches
o Nausea and vomiting
o Diarrhea
 SYMPTOMS THAT CAN BECOME LIFE THREATENING
o Bleeding under the skin, internal organs or from mouth, eyes, or ear
o Nervous system malfunctions
o Coma
o Kidney failure
o Respiratory failure
o Liver failure
o Delirium
PATHOGENESIS
 The target organ is the vascular bed (hemorrhage)
 The replication of virus is intracellularly
 Cytokine release leads to shock and hypotension
 Affects platelet functions (thrombocytopenia)
 Affects bone marrow and clotting factors
DIAGNOSIS
 Molecular detection by RT-PCR
 Blood test
 Urine test
TREATMENT
 There is no cure for VHF
 Vaccination exist for only a few types
 Antiviral drug ribavirin (rebetol, Virazole) might shorten the course of some infections and
prevent complications in some people
 Other medications are being developed
 Hepatitis is the inflammation or necrosis of liver cells
 It may be of toxic origin or viral infection
 It may be temporary (acute) or Long term (chronic)
 Over time chronic form may progress to :
*Scarring of the liver
*Liver failure
*Liver cancer
 Viruses which damage the liver cells- Hepatitis viruses
 Various antigens are responsible for hepatitis, they are:
1. Hepatitis A virus (HAV)
2. Hepatitis B virus (HBV)
3. Hepatitis C virus (HCV)
4. Hepatitis D virus (HDV)
5. Hepatitis E virus (HEV)
1.Cytomegalovirus
2.Epstein-Barr viruses
3.Herpes simplex virus
4.Yellow fever viruses
 98% of Hepatitis caused by Hepatitis A, B, C, D and E
 Other viruses responsible for hepatitis are :
 Hepatitis A is subacute disease
 Occur mainly in children and young adults
 Caused by Hepatitis A virus
 Virus also known as Enterovirus 72
 Infectious hepatitis
 Does not cause chronic liver disease
 Picornavirus family
 Genus- Hepatovirus
 Incubation period-approximately 1 month
 Humans serve as the reservoir
HEPATITIS A VIRUS
 Naked icosahedral capsid
 Positive sense ss RNA
 Inactivated by chlorine treatment of drinking water, formalin and UV radiation
PATHOGENESIS
 Oral cavity > GI tract > Blood > Liver
 Replicates in hepatocytes
 Spread by fecal-oral route
 Person to person contact
 Through contaminated food and water
 Dirty hands
 Contaminated shellfish-clams, oysters, mussels
 Spherical virus
 Enveloped
 27 nm diameter
 Genome approximately 3.2 KB in length
 Virus stable at PH 2.4 for 6 hours
 3' end of genome is associated with a DNA polymerase molecule
 Have 4 major open reading frames (ORF)
ORF-S
ORF-P
ORF-X
ORF-C
 Hepatitis B virus is a complex structure with 3 distinct antigens​:
1.HBcAg- Hepatitis B core antigen
2.HBsAg- Hepatitis B surface antigen
3.HBeAg- An independent protein circulating in the blood
•Acute​​
•Age preference-Young adults, Babies and toddlers​​
•Lasts up to 6 months( with or without symptom)​​
•Incubation period-2-5 months​​
•Family- Hepadnaviridae Hepatitis caused by HBV is called serum hepatitis or long
incubation hepatitis or MS-2or Antigen hepatitis​
PATHOGENESIS
 Involves 3 steps:
1. Entry of virus
2. Multiplication and spread of virus
3. Liver cell damage
 Transmitted only in blood and body fluids
 Replication of virus starts in the hepatocytes
 HBsAg particles are liberated in to the blood stream
 During HBV infection, the host immune response causes both hepatocellular damage and viral clearance
 Most liver injury is caused by cytotoxic T lymphocytes.
 Blood transfusion​​
 Sexual transmission​​
 Neonates gets infection from mothers​​
 Through contaminated syringes and needles
TREATMENT
 Interferon
 Lamivudinae
 Adefovir
 Entecavir
PREVENTION
 Lead a healthy lifestyle
 Use sterile syringe
 Avoid stress
 Follow the rules of personal hygiene
 Observe the rules of anti-epidemic
regime
 Belongs to family- flaviviridae
 Genus-Hepacivirus
 Chronic
 More common in adults
HEPATITIS C VIRUS
 Spherical
 30-60 nm diameter
 Enveloped virus
 Have 2 viral envelope glycoproteins – E1 & E2
 Glycoproteins surrounded by lipid envelope
 Genome has ss RNA
 RNA have 10,000nucleotides
 Genome have single large open reading frame
PATHOGENESIS
 Virus replicates in the hepatocytes
 HCV cause acute and chronic hepatitis
 Acute state followed by chronic hepatitis
 Chronic hepatitis leads to cirrhosis and hepatocellular carcinoma
 Transmission through the transfusion of blood
 Sexual transmission
 Mother to child
TREATMENT
 There is no prophylactic vaccine or specific immunoglobulin against hepatitis C
 There is effective antiviral treatment
 Acute
 Infects any age
 Co infects with Hepatitis B
 Found only in hepatitis B-infected persons
 HDV use HBsAg for assembly
 Similar to several plant viroids
 It has Delta antigen
 Family- Deltaviridae
 Genus - Hepacivirus
HEPATITIS D VIRUS
 HDV is spherical
 36 nm particle
 Outer coat composed of HBV surface antigen
 Have circular ss RNA
 HDV has 1679 nucleotides
 RNA replication is mediated by host RNA polymerase Ⅱ
 Closest relative of HDV is a satellite virus of plants
TRANSMISSION
PATHOGENESIS
 Replication of virus takes place within hepatocytes-results in the cytotoxicity and direct liver damage​
 Hepatitis E is also known as enterically transmitted hepatitis
 Incidence of this disease is high in pregnant women, but low in others
 Family- Hepeviridae
 Genus-Orthohepevirus
 Incubation period-2 to 9 weeks
 Enters the liver through intestine and blood
 Spherical
 Non enveloped
 Linear ss RNA
PATHOGENESIS
 The virus get in to the host through the oral route into the gastrointestinal tract
 The virus then reaches the liver through the portal vein
 Then replicates and enter in to the bile and blood stream
 Infectious viral particles present in the bile, feces and blood during the late incubation phase(32 days)
 Anti HEV antibodies of IgA, IgG and IgM types appear in the blood during the course of the disease
TRANSMISSION
DIAGNOSIS
 Examination of serum under an electron microscope for virus particles
 Nucleic acid detection by RT-PCR
 Detection of HEV antibodies (IgM and IgG) in the serum by ELISA
Rubella,VHF,Hep.pptx
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Rubella,VHF,Hep.pptx

  • 1. CONTE NT  RUBELLA  VIRAL HEMORRHAGIC FEVER  HEPATITIS
  • 2.
  • 3.  Rubella is a mild disease  Common childhood infection with minimal systemic upset  Also known as three days measles or German measles  First isolated in tissue culture in 1962  Serious complications are very rare  Can affect anyone of any age RUBELLA VIRUS  Member of togavirus family  Genus- Rubivirus  Enveloped virus with a single stranded RNA-positive stranded  Lipoprotein envelop  Surface spikes contain hemagglutinin  Spherical shaped  Icosahedral nucleocapsid  Diameter=50-70 nm  Incubation period is 14 to 21 days.  Multiply in the cytoplasm of infected cell  Virus is inactivated by ether, chloroform, formaldehyde and beta propiolactone  Destroyed at 56°C
  • 5.  Malaise  Head ache  Mild fever (38.9°C or lower)  Mild conjunctivitis  Red itchy eyes  Rash begins on forehead and face (lasting 1-3 days)  Enlarged lymph nodes  Aching joints ,especially in young women's  Infection in pregnant women can cause death of the fetus or congenital malformations
  • 6. •Infection in pregnant women can cause death of the fetus or congenital malformations​ •Skin manifestations are called "Blueberry muffin lesions"​
  • 7.  Virus cross the placenta and cause congenital Rubella syndrome in newly born
  • 8. PATHOGENESIS  Initial replication of virus occurs in-Nasopharynx and local lymphnodes  From there spread to internal organs and skin via blood
  • 9.  Transmission via direct or droplet contact with respiratory secretions  Spread when an infected person coughs or sneezes​  Spread by direct contact with infected mucus from the nose and throat​  From pregnant women to Fetus through blood stream​  Virus found in the blood 5 to 7 days after infection and spreads throughout the body​  Virus contagious for about one week after the rash appearance​ IMMUNITY  Infection leads to lifelong immunity ( Second cases of rubella do not occur)​  Antibody cross the placenta and protects the newborn LABORATORY DIAGNOSIS  Hemagglutination inhibition test  EIA (Enzyme Immuno Assay)  Latex agglutination  CFT  Neutralization test SPECIMEN  Inoculation of tissue culture media with throat, blood or urine
  • 10. TREATMENT  Live attenuated vaccines are administered to children at 15 month of age.  Approved during the year 1969  Vaccine produce a long lasting immunity against virus  MMR also given  Gamma globulin is used for treatment (But it is not a specific treatment) PREVENTION
  • 12.  It is an infection that can cause severe, life threatening illness  Acute systemic febrile syndrome  Highly infectious  Infectious during viremia stage  It is cause by 4 different virus families > Filoviridae > Bunyaviridae > Arenaviridae > Flaviviridae FLAVIVIRUS
  • 13.  Not all members of these families cause VHF​  All VF viruses are small, ss RNA viruses with lipid envelope membranes  Damage the walls of tiny blood vessels, making them leak, and can hamper the blood's ability to clot  Some hemorrhagic fever include:​ * Dengue * Ebola * Lassa * Marburg * Yellow fever  Most commonly occur in –Tropical areas​  There is no cure​  Vaccines available only for few types​  Prevention is the best approach​  Human outbreak are sporadic and irregular​
  • 14. SYMPTOMS  Vary by disease o Fever o Fatigue o Weakness o Dizziness o Muscle, Bone or Joint aches o Nausea and vomiting o Diarrhea  SYMPTOMS THAT CAN BECOME LIFE THREATENING o Bleeding under the skin, internal organs or from mouth, eyes, or ear o Nervous system malfunctions o Coma o Kidney failure o Respiratory failure o Liver failure o Delirium
  • 15. PATHOGENESIS  The target organ is the vascular bed (hemorrhage)  The replication of virus is intracellularly  Cytokine release leads to shock and hypotension  Affects platelet functions (thrombocytopenia)  Affects bone marrow and clotting factors DIAGNOSIS  Molecular detection by RT-PCR  Blood test  Urine test TREATMENT  There is no cure for VHF  Vaccination exist for only a few types  Antiviral drug ribavirin (rebetol, Virazole) might shorten the course of some infections and prevent complications in some people  Other medications are being developed
  • 16.
  • 17.  Hepatitis is the inflammation or necrosis of liver cells  It may be of toxic origin or viral infection  It may be temporary (acute) or Long term (chronic)  Over time chronic form may progress to : *Scarring of the liver *Liver failure *Liver cancer  Viruses which damage the liver cells- Hepatitis viruses  Various antigens are responsible for hepatitis, they are: 1. Hepatitis A virus (HAV) 2. Hepatitis B virus (HBV) 3. Hepatitis C virus (HCV) 4. Hepatitis D virus (HDV) 5. Hepatitis E virus (HEV)
  • 18. 1.Cytomegalovirus 2.Epstein-Barr viruses 3.Herpes simplex virus 4.Yellow fever viruses  98% of Hepatitis caused by Hepatitis A, B, C, D and E  Other viruses responsible for hepatitis are :
  • 19.
  • 20.
  • 21.  Hepatitis A is subacute disease  Occur mainly in children and young adults  Caused by Hepatitis A virus  Virus also known as Enterovirus 72  Infectious hepatitis  Does not cause chronic liver disease  Picornavirus family  Genus- Hepatovirus  Incubation period-approximately 1 month  Humans serve as the reservoir HEPATITIS A VIRUS  Naked icosahedral capsid  Positive sense ss RNA  Inactivated by chlorine treatment of drinking water, formalin and UV radiation
  • 22.
  • 23. PATHOGENESIS  Oral cavity > GI tract > Blood > Liver  Replicates in hepatocytes  Spread by fecal-oral route  Person to person contact  Through contaminated food and water  Dirty hands  Contaminated shellfish-clams, oysters, mussels
  • 24.
  • 25.
  • 26.
  • 27.
  • 28.  Spherical virus  Enveloped  27 nm diameter  Genome approximately 3.2 KB in length  Virus stable at PH 2.4 for 6 hours  3' end of genome is associated with a DNA polymerase molecule  Have 4 major open reading frames (ORF) ORF-S ORF-P ORF-X ORF-C  Hepatitis B virus is a complex structure with 3 distinct antigens​: 1.HBcAg- Hepatitis B core antigen 2.HBsAg- Hepatitis B surface antigen 3.HBeAg- An independent protein circulating in the blood •Acute​​ •Age preference-Young adults, Babies and toddlers​​ •Lasts up to 6 months( with or without symptom)​​ •Incubation period-2-5 months​​ •Family- Hepadnaviridae Hepatitis caused by HBV is called serum hepatitis or long incubation hepatitis or MS-2or Antigen hepatitis​
  • 29.
  • 30. PATHOGENESIS  Involves 3 steps: 1. Entry of virus 2. Multiplication and spread of virus 3. Liver cell damage  Transmitted only in blood and body fluids  Replication of virus starts in the hepatocytes  HBsAg particles are liberated in to the blood stream  During HBV infection, the host immune response causes both hepatocellular damage and viral clearance  Most liver injury is caused by cytotoxic T lymphocytes.  Blood transfusion​​  Sexual transmission​​  Neonates gets infection from mothers​​  Through contaminated syringes and needles
  • 31.
  • 32. TREATMENT  Interferon  Lamivudinae  Adefovir  Entecavir PREVENTION  Lead a healthy lifestyle  Use sterile syringe  Avoid stress  Follow the rules of personal hygiene  Observe the rules of anti-epidemic regime
  • 33.
  • 34.  Belongs to family- flaviviridae  Genus-Hepacivirus  Chronic  More common in adults HEPATITIS C VIRUS  Spherical  30-60 nm diameter  Enveloped virus  Have 2 viral envelope glycoproteins – E1 & E2  Glycoproteins surrounded by lipid envelope  Genome has ss RNA  RNA have 10,000nucleotides  Genome have single large open reading frame
  • 35.
  • 36. PATHOGENESIS  Virus replicates in the hepatocytes  HCV cause acute and chronic hepatitis  Acute state followed by chronic hepatitis  Chronic hepatitis leads to cirrhosis and hepatocellular carcinoma  Transmission through the transfusion of blood  Sexual transmission  Mother to child
  • 37.
  • 38. TREATMENT  There is no prophylactic vaccine or specific immunoglobulin against hepatitis C  There is effective antiviral treatment
  • 39.
  • 40.  Acute  Infects any age  Co infects with Hepatitis B  Found only in hepatitis B-infected persons  HDV use HBsAg for assembly  Similar to several plant viroids  It has Delta antigen  Family- Deltaviridae  Genus - Hepacivirus HEPATITIS D VIRUS  HDV is spherical  36 nm particle  Outer coat composed of HBV surface antigen  Have circular ss RNA  HDV has 1679 nucleotides  RNA replication is mediated by host RNA polymerase Ⅱ  Closest relative of HDV is a satellite virus of plants
  • 41.
  • 42.
  • 43. TRANSMISSION PATHOGENESIS  Replication of virus takes place within hepatocytes-results in the cytotoxicity and direct liver damage​
  • 44.
  • 45.
  • 46.
  • 47.  Hepatitis E is also known as enterically transmitted hepatitis  Incidence of this disease is high in pregnant women, but low in others  Family- Hepeviridae  Genus-Orthohepevirus  Incubation period-2 to 9 weeks  Enters the liver through intestine and blood  Spherical  Non enveloped  Linear ss RNA
  • 48.
  • 49. PATHOGENESIS  The virus get in to the host through the oral route into the gastrointestinal tract  The virus then reaches the liver through the portal vein  Then replicates and enter in to the bile and blood stream  Infectious viral particles present in the bile, feces and blood during the late incubation phase(32 days)  Anti HEV antibodies of IgA, IgG and IgM types appear in the blood during the course of the disease
  • 51. DIAGNOSIS  Examination of serum under an electron microscope for virus particles  Nucleic acid detection by RT-PCR  Detection of HEV antibodies (IgM and IgG) in the serum by ELISA