1. RUBELLA
RABIES
Dr
Kamran Afzal
Asst Prof
Microbiology

3. Rubella virus
• Family – Togaviridae
• Genus – Rubivirus
• Enveloped
• Spherical virus carrying
hemagglutinin
• Virus multiply in the
cytoplasm of infected cell
• Rapidly inactivated by
chemical agents, ultraviolet
light, low pH and heat

4. Transmission
• Adults and children
– Acquired, (i.e. not congenital)
– Transmitted via airborne droplet emission
– May also be present in the urine, feces
– The reservoir exists entirely in active human cases
– Replication in nasopharynx and regional lymph nodes
– 5-7 days Viremia, with spread to tissues
• Fetus
– Placenta and fetus infected during viremia, in a
pregnant female

5. Systemic Events

6. Clinical Features
• Malaise
• Low grade fever
• Morbilliform rash
– Rash starts on face and extremities
– Rarely lasts more than 5 days
– No features of the rash give clues to
definitive diagnosis of Rubella
First described as distinct clinical entity in German literature
– ‘German measles’

7. Clinical Features
• Incubation period 14 days
• Maculopapular rash and lymphadenopathy
occur 14 days after exposure
• The clinical events occurring in the
neonatal age are more important and
divided into two major groups
1. Post Natal Rubella (Acquired)
2. Congenital Rubella

8. Complications
Arthralgia or arthritis
adult female up to 70%
children rare
Thrombocytopenic purpura
1/3,000 cases
Encephalitis
1/6,000 cases
Neuritis rare
Orchitis rare

9. Congenital Rubella Syndrome (CRS)
• Maternal viremia with Rubella infection during
pregnancy may result in infection of placenta and fetus
• Infection may lead to fetal death or premature delivery
• Severity of damage to fetus depends on gestational age
• Up to 85% of infants affected if infected during first
trimester
• >20 weeks of pregnancy, fetal defects are uncommon
• The growth rate of fetal cells is reduced
– Leads to deranged and hypoplastic organ development
– Results in structural damage and abnormalities

10. • Microcephaly
– Deafness
– Mental retardation
• Cataracts
• Heart defects
• Bone alterations
• Liver and spleen damage

11. Classical Triad in CRS
Classical Triad
• Microcephaly / Deafness
• Cardiac abnormalities
• Cataract

12. Laboratory Diagnosis
• Positive serologic test for Rubella IgM antibody
• 4 x rise in Rubella IgG by any standard serologic assay -
- Agglutination, ICT, ELISA, HAI
• Isolation of Rubella virus from clinical specimen
– nasopharyngeal swab, urine

13. Serology

14. Interpretation of Serology

15. Isolation and Identification of virus
• Nasopharyngeal or throat swabs taken 6 days
prior or after appearance of rash are a good
source of Rubella virus
• The virus can be cultured on continuous cell
lines Rabbit kidney cells
(RK 13)
and
Vero cells
• Cell cultured antigens can be detected by IF
methods

16. Treatment and Prevention
• Rubella is a mild self limited illness
• No specific treatment or Antiviral treatment is indicated
• Clinically missed Rubella in the 1st 3-4 months of
pregnancy is associated with fetal infections
• CRS can be prevented by effective immunization of the
young children and teenage girls

17. Rubella Vaccine
• Composition Live virus (RA 27/3 strain)
• Duration of
Immunity Lifelong
• Schedule At least 1 dose
• Should be administered as MMR or MMRV
• INDICATIONS
– All infants 12 months of age and older
– Susceptible adolescents and adults without documented
evidence of Rubella immunity
– Emphasis on non-pregnant women of childbearing age

18. RABIES

19. Rabies
It is an acute infectious disease of warm-blooded
animals and humans characterized by an involvement
of the nervous system resulting in death

20. Rabies Virus
 Genus: Lyssavirus
(lyssa: the Greek goddess of madness, rage, and frenzy)
 Include members of the Rhabdoviridiae family
Rabies, Makola, Duvenhage
 Morphology:
 Enveloped bullet-shaped virus
 5 structural proteins
 SS RNA, negative sense, non-segmented, non-polar

21. Transmission of Rabies virus
 The dog is the most common cause of
Rabies transmission worldwide, cats second
 In developed countries: dogs are
immunized, other species of wild animals
are reservoirs
 Bats: always considered rabid

22. Transmission of Rabies virus
 Infected saliva enters bite wounds
 Virus migrates up peripheral nerves to the spinal cord
and reaches the brain
 Virus shed in the saliva during, before or after clinical
symptoms
 Aerosol transmission: documented from caves with
large populations of infected bats
 Organ donations: documented from early corneal
transplantation (2004)

23. Rabies virus attacks the Central
Nervous System
Watch as the rabies
virus from an exposure
on the leg spreads up
the spinal cord to the
brain and throughout
the rest of the body
Rabies virus entering
the body

24. Incubation Period
 Averages 3-8 weeks
 Can be as short as 1 week or up to 1 year
 Bite location and viral load are the two most important
factors in incubation of the virus

25. Pathogenesis
 Budding from the plasma membrane of muscle cells
into unmyelinated nerve endings
 Retrograde axoplasmic flow to the CNS
 Virus replication in dorsal root ganglia (DRG) and
anterior horn cells
 Prophylaxis at this stage cannot prevent death

27.  Eventually, the virus spreads centrifugally from the
CNS to the heart, skin, salivary and serous glands in
the tongue
 All major organs may contain the virus (except blood)
 Organs from patients with unexplained neurologic
disease may transmit rabies by transplantation

28. Clinical features in Humans
 General weakness, discomfort, fever or headache
 Prickling or itching sensation at the site of bite
 Cerebral dysfunction
 Anxiety, confusion, agitation, delirium
 Abnormal behavior
 Hallucinations, and insomnia
 Hydrophobia
 The acute period of disease ends after 2 to 10 days
 Once clinical signs of rabies appear, the disease is
nearly always fatal

29. Laboratory Diagnosis
 Serology
 Virus cultivation
 The Direct Fluorescent Antibody test (DFA)
 Histopathology

30.  Serology
 Circulating antibodies appear slowly but they are
usually present by the time of onset of clinical
symptoms
 Virus cultivation
 The most definitive means of diagnosis is by virus
cultivation from saliva and infected tissue
 Virus cultivation can be done using cell cultures or
the specimen is inoculated intra-cerebrally into mice

31.  Direct Fluorescent Antibody
The Direct Fluorescent Antibody test (DFA) is done on
corneal impressions or neck skin biopsy

32.  Histopathology of Brain
 Negri bodies are diagnostic of Rabies

33. SPECIFIC GUIDELINES AND
PROCEDURES
Management of Potential Rabies
Exposure

34. Management and Prevention
Pre-exposure prophylaxis
 Inactivated rabies vaccine is given to persons at
increased risk of rabies e.g. vets, animal
handlers, laboratory workers etc
Post-exposure prophylaxis
 In cases of bites, suspected dogs and cats should be
held for 10 days for observation
 If signs develop, they should be killed and their
tissues examined

35. Post-exposure Prophylaxis
 Wound treatment - surgical debridement
 Passive immunization - human rabies
immunoglobulin is given around the area of the wound
and an I/M dose
 Active immunization - The human diploid cell vaccine
(HDCV) is administered I/M, 5 doses are given on days
1,3,7,14 and 28
 Combined treatment with passive and active
immunization is much more effective than active
immunization alone

36. Recommended Post-exposure Prophylaxis
Category of exposure to suspect rabid Post-exposure measures
animal
Category I – touching or feeding None
animals, licks on intact skin (i.e. no
exposure)
Category II – nibbling of uncovered skin, Immediate vaccination and local
minor scratches or abrasions without treatment of the wound
bleeding
Category III – single or multiple Immediate vaccination and
transdermal bites or scratches, licks on administration of rabies
broken skin; contamination of mucous immunoglobulin; local treatment of the
membrane with saliva from licks, wound
exposures to bats.

37. Rabies Vaccines
The vaccines which are available for humans are
inactivated whole virus vaccines
 Nervous Tissue Preparation
 Duck Embryo Vaccine
 Human Diploid Cell Vaccine (HDCV) - this is
currently the best vaccine available with an
efficacy rate of nearly 100% and rarely any
severe reactions, however it is very expensive

38. Treatment
POST-EXPOSURE TREATMENT (PET)
 LOCAL WOUND TREATMENT
- Wash with soap/detergent and water preferably for
10 min
- Apply alcohol or povidone iodine antiseptic
- Anti-Tetanus toxoid I/M
- Avoid suturing and wound dressing

39. Antimicrobials
- Co-amoxiclav
- Cloxacillin
- Cefuroxime

40. Special Conditions
 Babies born of rabid mothers should be given ARV as
early after birth as possible
 Pregnancy and infancy are not C/I to treatment
 Bites of rodents, rabbits, guinea pig- NO PET
 Dogs, cats, livestock, wild animals- Give PET

41. Prevention and Control
 Canine rabies accounts for more than 99% of all
human rabies
 Control measures include
 Stray dog control
 Vaccination of dogs
 Quarantine of imported animals

42. Oral Rabies Vaccination for animals

43. A raccoon consuming a bait laden with ORV

44. What kind of animals get rabies?
 The rabies virus can
infect all mammals

45.  Animals less likely to get rabies

46. Animals that don’t carry rabies
 Frogs, turtles, birds, bees and snakes