Smallest known DNA viruses. Structure Non-enveloped 18-26 nm diameter Single-stranded DNA, 5.6 kb Icosahedral Parvovirinae (vertebrates) Parvovirus Erythrovirus Dependovirus (requires helper virus, such as an adenovirus) Bocavirus Amdovirus Densovirinae (invertebrates)` B19 virus most common. Diseases Erythema infectiosum (cutaneous rash) Polyarthropathy syndrome (acute or chronic) Transient aplastic crisis (severe acute anemia) Pure red cell aplasia (chronic anemia) Hydrops fetalis (fetal anemia) Simplest animal viruses infecting humans, responsible for - childhood exanthema - erythema infectiosum (fifth disease). Smallest viruses (18–26 nm size) Non-enveloped with icosahedral symmetry Only DNA viruses - possess single-stranded DNA Depend upon the host cell enzymes for replication Transmission - Respiratory route, followed by blood transfusion and transplacental route. Infects precursors of RBCs: Parvovirus B19 has a special tropism for erythroid progenitor cells present in adult bone marrow and foetal liver as it binds to blood group P antigen as receptors; which are present on the RBC surface. This results in red cell destruction and inhibition of erythropoiesis Erythema infectiosum (or fifth disease) Transient aplastic crisis Pure red cell aplasia Non-immune hydrops fetalis Papular-purpuric gloves and socks syndrome Known to cause foetal loss through hydrops fetalis; severe anaemia, congestive heart failure, generalized oedema and foetal death No evidence of teratogenicity. Risk of foetal death highest when infection occurs during the second trimester of pregnancy (12%). Molecular methods: PCR - detects viral DNA (e.g. genes coding for VP1 and VP2) from serum, tissue or respiratory secretions. Real time PCR - used for quantification of viral load in blood, during acute infections Antibody detection: ELISA – detecting antibodies against VP1 and VP2 antigens. IgM appears early - recent infection and remains elevated for 2–3 months Antigen detection: Immunohistochemistry - detect viral antigens in fetal tissues and bone marrow. No antiviral drug is available Symptomatic treatment is given Immunoglobulins containing neutralizing antibodies to human parvovirus are available commercially No antiviral drug is available Symptomatic treatment is given Immunoglobulins containing neutralizing antibodies to human parvovirus are available commercially Measles is an acute, highly contagious childhood disease characterized by fever & respiratory symptoms, followed by typical maculopapular rash. Transmission Droplets inhalation over short distances and, less commonly, Small-particle aerosols - remain suspended especially in schools, hospitals, and enclosed public places in the air for longer period. Spread-The virus multiplies locally in the respiratory tract; then spreads to the regional lymph nodes → enter into the bloodstream in infected monocytes (primary viremia)→further multiply in reticuloendothelial system → spills over into blo

1. Parvovirus and Measles virus
DR MAYURI BHISE
AIIMS RAJKOT

2. What are parvoviruses?
 Smallest known DNA viruses.
 Structure
Non-enveloped
18-26 nm diameter
Single-stranded DNA, 5.6 kb
Icosahedral

3. Classification
Parvovirinae (vertebrates)
Parvovirus
Erythrovirus
Dependovirus (requires helper virus, such
as an adenovirus)
Bocavirus
Amdovirus
Densovirinae (invertebrates)`

4. Parvovirus infections in human
 B19 virus most common.
 Diseases
 Erythema infectiosum (cutaneous rash)
 Polyarthropathy syndrome (acute or chronic)
 Transient aplastic crisis (severe acute anemia)
 Pure red cell aplasia (chronic anemia)
 Hydrops fetalis (fetal anemia)

5. Morphology
 Simplest animal viruses infecting humans, responsible for -
childhood exanthema - erythema infectiosum (fifth disease).
 Smallest viruses (18–26 nm size)
 Non-enveloped with icosahedral symmetry
 Only DNA viruses - possess single-stranded DNA
 Depend upon the host cell enzymes for replication.

6. Pathogenesis
 Transmission - Respiratory route, followed by blood transfusion
and transplacental route.
 Infects precursors of RBCs: Parvovirus B19 has a special
tropism for erythroid progenitor cells present in adult bone marrow
and foetal liver as it binds to blood group P antigen as receptors;
which are present on the RBC surface.
 This results in red cell destruction and inhibition of erythropoiesis

7. Clinical Manifestations
 Erythema infectiosum (or fifth disease)
 Transient aplastic crisis
 Pure red cell aplasia
 Non-immune hydrops fetalis
 Papular-purpuric gloves and socks syndrome

8. Congenital Parvovirus Infection
 Known to cause foetal loss through hydrops fetalis;
severe anaemia, congestive heart failure, generalized
oedema and foetal death
 No evidence of teratogenicity.
 Risk of foetal death highest when infection occurs during
the second trimester of pregnancy (12%).

9. Laboratory diagnosis
Molecular methods:
 PCR - detects viral DNA (e.g. genes coding for VP1 and
VP2) from serum, tissue or respiratory secretions.
 Real time PCR - used for quantification of viral load in
blood, during acute infections

10. Laboratory diagnosis
 Antibody detection: ELISA – detecting antibodies
against VP1 and VP2 antigens. IgM appears early -
recent infection and remains elevated for 2–3 months
 Antigen detection: Immunohistochemistry - detect
viral antigens in fetal tissues and bone marrow.

11. Treatment
 No antiviral drug is available
 Symptomatic treatment is given
 Immunoglobulins containing neutralizing antibodies to human
parvovirus are available commercially

12. Measles
 Measles is an acute, highly contagious childhood disease
characterized by fever & respiratory symptoms, followed by
typical maculopapular rash.

13. Pathogenesis
 Transmission
 Droplets inhalation over short distances and, less commonly,
 Small-particle aerosols - remain suspended especially in
schools, hospitals, and enclosed public places in the air for
longer period.

14. Pathogenesis
 Spread-The virus multiplies locally in the respiratory tract;
then spreads to the regional lymph nodes → enter into the
bloodstream in infected monocytes (primary viremia)→further
multiply in reticuloendothelial system → spills over into blood
(secondary viremia)→disseminate to various sites.
 The virus is predominantly seeded in the epithelial surfaces
of the body, including the skin, respiratory tract, and
conjunctiva.

15. Clinical Manifestations
 Incubation period -10days which may be shorter in infants and
longer (up to 3 weeks) in adults
 Disease can be divided into three stages:
 1. Prodromal Stage
 2. Eruptive Stage
 3. Post-measles Stage

16. 1. Prodromal Stage
 Lasts for four days (i.e. from 10th to 14th day of infection)
 Fever
 Koplik’s spots
 Non-specific symptoms

17. 2. Eruptive Stage
 Maculopapular dusky red rashes
 Rashes typically appear first behind the ears → then spread
to face, arm, trunk and legs → then fade in the same order
after four days of onset
 Fever (10th day) → Koplik’s spot (12th day) → rash(14th day)

18. 3. Post-measles Stage
 Characterized by weight loss and weakness.
 There may be failure to recover and gradual deterioration into
chronic illness.

19. Complications - Secondary
Bacterial Infections
 Otitis media and bronchopneumonia are most common
 Recurrence of fever or failure of fever to subside with
the rash
 Worsening of underlying tuberculosis with a false
positive Mantoux test

20. Complications - Complications
Due to Measles Virus Itself
 Giant-cell pneumonitis in immunocompromised children, and
HIV infected people
 Acute laryngotracheobronchitis (croup)
 Diarrhoea, leads to malnutrition including vitamin A deficiency

21. Complications - Central Nervous
System Complications
 Post-measles encephalomyelitis
 Measles inclusion body encephalitis
 Subacute sclerosing panencephalitis (SSPE)

22. Laboratory diagnosis of Measles
 Specimen: Nasopharyngeal swab
 Antigen detection: By using anti-nucleoprotein antibodies
 Virus isolation: By inoculation of specimen into monkey or
human kidney cell line, produces CPE as multinucleated
giant cells (Warthin-Finkeldey cells)

23. Cont…
Antibody detection in serum: Against nucleoprotein
antigen by ELISA
Reverse-transcription PCR: detects viral RNA.

24. Treatment of Measles
 There is no specific antiviral therapy available for measles
 Treatment is symptomatic and consists of general supportive
measures
 Vitamin A - effective in reducing the morbidity and mortality
due to measles.

25. General Preventive Measures
 Airborne precaution - isolation in negative pressure
room.
 Use of PPEs - N95 mask, etc. must be followed
while handling measles cases

26. Measles Vaccine
 Live attenuated vaccine is available for measles.
 Strains: The following vaccine strains are used currently
 Schwartz strain
 Edmonston-Zagreb strain
 Moraten strain.
 Vaccine is prepared in chick embryo cell line

27. Cont…
 Reconstitution - Available in lyophilized form - has to be
reconstituted with distilled water - used within 4 hours.
 Vaccine is thermolabile - stored at -200C.
 One dose (0.5ml) containing >1000 infective viral units is
administered subcutaneously.

28. Cont..
 Combined vaccines: Measles vaccine combined form with rubella
(MR vaccine), with mumps and rubella vaccine (MMR vaccine) and
with varicella (MMR-V vaccine)
 Indication: Measles-rubella (MR) vaccine is given at 9 completed
months to 12 months along with vitamin A supplements and
second dose of MR vaccine at 16–24 months

29. Cont…
 Side effects include - Mild measles like illness, toxic shock syndrome
 Contacts - Susceptible contacts over 9-12months may be protected
against measles if the measles vaccine is given within 3 days of
exposure.
 Measles immunoglobulin - given within 3 days - 0.25mg/kg of body
weight.
 Both should not be given together. At least 8-12 weeks of gap must be
maintained.

30. Epidemiology
 Source - Cases. Carriers - not known to occur. Inapparent or
sub-clinical infections - rare.
 Reservoir - Humans - no animal reservoir.
 Infective material - Virus - shed in the secretions of nose,
throat and respiratory tract of cases of measles - during the
prodromal stage and early stage of rash.

31. Cont…
 Period of communicability - Patients are infectious from
four days before to four days after the onset of rash. Isolation
- recommended from the onset of prodromal stage until third
day of rash.
 Secondary attack rate is very high (>90%)
 Age - Measles is a childhood disease

32. Cont…
 Immunity- No age is immune if there is no previous immunity.
 There is single serotype hence one attack (vaccine or infection)
gives lifelong immunity.
 Infants are protected up to 6 months due to pre-existing
maternal antibodies.

33. Measles elimination
 WHO has introduced ‘The Strategic Plan for
achieving and maintaining Measles and Rubella
elimination in WHO South- East Asia Region:
2020–2024

34. Measles elimination
 The following objectives are set to achieve this target:
 (1) ≥ 95% coverage with two doses against measles and
rubella
 (2) Develop and sustain a case-based surveillance system
 (3) Develop and maintain an accredited measles and
rubella laboratory network
 (4) Strengthen support and linkages to achieve the above
three strategic objectives