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DISCUSSIONS
• INTRODUCTION • ATEOLOGICAL AGENT • PATHOGENESIS • VARICELLA AND HERPES ZOOZTER • IMMUNOLOGY OF DISEASE • LAB DIAGNOSIS • CONTROL OF DISEASE
INTRODUCTION
• Chicken pox or varicella is an highly infectious acute illness caused by VZV
• Disease is characterised by vesicular rashes accompanied by fever and malaise
• World wide(both endemic and epidemic)
History……
There was a description of an illness similar to chicken pox more than 2,000 years ago in ancient Babylonian era. In 800’s/900's AD, Muhammad ibn Zakariya Razi, recorded some of the first known information on chicken pox and noted the differences between measles and small pox.
In 1500s, Giovanni Filippo, Italian physician give detailed description of chicken pox. In 1600s, English physician named Richard Morton gave the name chickenpox to what he thought was a milder form of smallpox. In 1767, English physician, William Heberden, show that small pox and chicken pox were different and found that once infected with the chicken pox, the person remained immune.
In 1875, Rudolf Steiner, proved that chicken pox infection is contagious. Fluid from a chicken pox blister rubbed on the skin of healthy volunteers and the volunteers got chicken pox. Von Bokay suggested the connection between shingles and chicken pox in 1909. In 1920’s/1930’s studies confirmed the connection when children inoculated with zoster vesicles (shingles virus) came down with chicken pox.
Aetiological agent
• VZV or Human alpha herpes virus 3 (HAHV3)
• dsDNA virus • Life long latentency • Reactivation
Morphology of virus
• 100 – 200 nm diameter • Icosahedra capsid with 162 capsomer • Capsid contain linear dsDNA • Lipid enveloped virus • Envelop bears peplomers • In-between capsid and envelop tegument
present • Virus multiply in nucleus of infected cell
Route of transmission
• Respiratory route • Droplet infection and by droplet nuclei • Secondary contact attack rate 90% • Unlikely from fomites. • Cross placental infection to neonates
Source of infection
• A patient with chicken pox or herpes zoster
• Virus present in oropharyngeal secretion and lesions of skin and mucosa
• Scabs are not infective
Period of infectivity
• 1 – 2 days before the appearance of rash • 4 – 5 days after the appearance of rash • Virus tends to die out before pustule
stage • when the lesions crusted – more
infective
Host factors
• Primarily among children under 10 yr old • Few persons escapes from infection • Disease is sever in adult • The virus is highly species specific • G.pig adapted VZV can produce varicella
like disease in G.pig
Environmental factors
• Show seasonal trend • Disease occurs mostly during first 6
months of year • Over crowding favours infection • In temperate climate seasonal trend is
less common
Varicella and Zoster
• Varcella ( chicken pox ) and Zoster (shingles) regarded as deferent host response to the same virus.
• Primary infection cause chicken pox. • The patient recovered naturally. • Establishment of latent infection in cranial
nerve sensory ganglia and spinal dorsal route ganglia for decades without clinical manifestation.
Conti……
• When the cell mediated immunity wanes (age or immune-suppression) The virus get reactivated resulting in herpes zoster
• This occur in 10 – 30 % individuals.
Clinical features of varicella
Illness vary from a mild with only few scattered lesions to severe febrile illness with widespread rash
Adulthood chicken pox is more sever Disease has two stages 1 Pre eruptive stage 2 Eruptive stage
Pre eruptive /prodromal stage
• Onset of illness • Mild to moderate fever • Malaise • Shivering • Lasting about 24 hrs in children • 2 - 3 days for adult
Eruptive stage
• Skin rash appears Rash advances macula -> papule -> vesicle -> scab Do not go to pustule stage Dew drops on skin Superficial Easily ruptured
• Surrounded by inflammatory area • Vesicles are non umbilicated usually • Scabbing begins 4–5 days after rash appears
Chicken pox rash
• Rash is symmetrical • First appear on trunk abundantly • Then comes on face arms and legs less abundantly • Mucosal surface, genital area, axilla are involved • Buccal and pharyngeal mucosa affected • Palms and soles not affected usually • The density of eruption diminishes centrifugally
Pleomorphism
• All stages of the rash may be seen simultaneously at a time, in same area
• Due to the appearance of 4 – 5 day successive crop
• With appearance of every crop, fever comes
Complications
• Secondary bacterial infection • Sever cardiovascular and neurological
problems in immune-defective patients • In-utero and neonatal infection • Fatal in patients with DIVC
Secondary infection
• Group A – β streptococci, S. aureus. • Cellulitis, erysipiels, epiglotitis,
osteomylitis, scarlet fever & meningitis.
• Treatment : antibiotics
In immune deficient's
• varicella haemorrhagical. • Pneumonia. • Encephalitis. • Acute ceribellar ataxia. • Raye’s syndrome. • Acute retinal necrosis and progressive
outer necrosis.
In pregnency
• Infection in utero – Congenital malformation. – Circulatory skin lesions. – Microcephali, Limb hypoplasia. – Low birth weight. – Cataract, microphthalmia, chorio-retinitis,
deafness. – Ceribro cortical atrophy
Herpes zoster or Shingles
• Comes in individuals who had a past chicken pox • The HSV remain latent in sensory ganglia • Virus held in check by residual immunity • When immunity fallen to infective level (aging or
immune suppression) virus reactivated • This leads to inflammation of nerves. • Nuritic pain often sever and last for weeks to months • Characteristic rashes confined to the area supplied
by nerve.
Herpes zoster cont….
• Thoracic nerve commonly affected
• Ophthalmic branch of trigeminal nerve – ophthalmic zoster
• In immuno-compromised- disseminated HZ occurs
Herpes zoster cont….
Ramsay hunt syndrome
Zoster affecting the facial nerve Facial muscles not function properly, lead to facial palsy
Rashes on tympanic –membrane and external auditory canal
Immunity
• One attack give lifelong immunity • Ab-s fail to eliminate virus from sensory
nerve ganglia • Zoster occurs in patients who have
history of past infection
Lab diagnosis
• The disease can diagnosed easily by physician from symptoms
Importance of lab diagnosis chicken pox resemble mild small pox, for differential
diagnosis Methods Direct microscopy Viral culture PCR, Sero-diagnosis
Direct microscopy
Light microscopy • Toludine blue or giemsa stained smear of basal cells
of vesicle • Multinucleated giant cells and Cowdry type A intra
nuclear inclusions. Not seen in smallpox Electron microscopy • Vesicle fluid is examined • Revels rounded particle. Brick shape particle in smallpox
Culture
• Vesicle fluid can use Cell lines
– Human fibroblast cells, Vero cells – Human amnion cells, HeLa cells.
Cytopathic effect Multinucleated ballooned cells/giant cells Cowdry type A intra nuclear inclusion VZ Ag demonstration in nuclear inclusion by IF using MC Ab.
Sero-diagnosis
• VZV specific IgM Ab in patient serum can be detected by
ELISA CFT Neutralisation test IF Why IgM ? Not IgG ?
Prevention
• Identification and isolation of infected individuals.
• Varicella zoster immunoglobulin.(VZIG)
• Vaccines.
Varicella zozster immunoglobulin
• Given within 72 hours of exposure • Given to suspicious individuals. Immuno - compromised Pregnant. Newborn. Premeture infant with weight loss DOSE 12.5 units/kg bodyweight upto 625 units max Repeat dose 1 – 3 weeks
Vaccine
• Live attenuated vaccine (oka strain) • Developed by Japanese workers by serial
passage in tissue culture • Injected subcutaneously • Give protection for several years
Vaccine….
Disadvg… Vaccine is very labile and need freeze storage Modified lyophilised form is available which can
store under 20 – 80 C Dose 1 –12 yr –single dose 12 yrs above –two doses of 6 weeks intervals
Precaution
Do not give both vaccine and VZIG at a time.. Why?
Vaccination in pregnant women should be avoided.
Do not give salicylates (chance of ray’s syndrome)
Summery Varicella and zoster are caused bye same virus called VZV. During illness, fever and characteristic rashes appear which help for clinical diagnosis.
Once infected – get life long natural immunity, when this immunity falls shingles comes
Lab diagnosis is an aid for differential diagnosis
Effective preventive measures are available like vaccination and VZIG
doubts????????
Readings
1 Text book of microbiology. Baveja
2 preventive and social medicine. K. Park 3 Open resources