Rubella is a mild viral infection that can cause serious birth defects if contracted during pregnancy. It is caused by the rubella virus, which is an enveloped RNA virus. Common symptoms include rash, fever, and joint pain. While usually mild, infection during pregnancy can lead to miscarriage or congenital rubella syndrome in infants. Vaccination has largely controlled rubella outbreaks. Viral hemorrhagic fevers are severe illnesses caused by RNA viruses that damage blood vessels and can cause bleeding. Hepatitis refers to liver inflammation, which can be caused by several viruses like hepatitis A, B, C, D, and E viruses through blood or fecal-oral transmission.

1. CONTE
NT
 RUBELLA
 VIRAL HEMORRHAGIC FEVER
 HEPATITIS

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

4. SYMPTOMS

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

11. VIRAL HEMORRHAGIC FEVER

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

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 :

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

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

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​

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

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

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

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

38. TREATMENT
 There is no prophylactic vaccine or specific immunoglobulin against hepatitis C
 There is effective antiviral treatment

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

43. TRANSMISSION
PATHOGENESIS
 Replication of virus takes place within hepatocytes-results in the cytotoxicity and direct liver damage​

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

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

50. TRANSMISSION

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