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Chickenpox
Chickenpox is caused by the varicella-zoster virus and causes a characteristic itchy vesicular rash. It is highly contagious and spreads through respiratory droplets. The rash progresses rapidly from macules to papules to vesicles and crusts over within 4-7 days. Complications can occur in immunosuppressed individuals and include pneumonia and encephalitis. Vaccination with the live attenuated varicella vaccine provides effective protection.
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Introduction to Chickenpox, caused by varicella-zoster virus, characterized by rash and fever.
Historical milestones in understanding Chickenpox, including early research, vaccine developments.
Interesting facts on the name origin and cultural beliefs about contracting Chickenpox.
Details about the VZV, its infection mechanisms, symptoms, latency, and reactivation.
Sources of infection, infectivity periods, secondary attack rates, and transmission pathways.
Incubation period and the clinical features of Chickenpox, including stages of infection.
Rash distribution, rapid evolution through stages, and accompanying fever during rash onset.
Key differences between Chickenpox and Smallpox, including incubation, rash characteristics, and fever.
Complications associated with Chickenpox, especially in immunocompromised individuals.
General prognosis for healthy children and higher morbidity in adults and immune-compromised.
Methods for diagnosing Chickenpox and controlling outbreaks through isolation and antiviral therapy.
Preventive measures including passive and active immunization against Chickenpox.
Details on Chickenpox vaccination, its efficacy, dosage, contraindications, and side effects.
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Chickenpox
- 1. Chickenpox (varicella) Dr. Rajalekshmy.P.R Dept ofSwasthavritta Amrita School of Ayurveda 1
- 2. INTRODUCTION • Acute highlyinfectious disease caused by varicella-zoster virus. • World wide in distribution and occurs in both epidemic and endemic forms. • Chickenpox and herpes zoster are regarded as different host responses to same etiological agent. • Characterized by vesicular rash that may be accompanied by fever and malaise. 2
- 3. HISTORY • Primary varicellainfection was not reliably distinguished from smallpox until 19th century. • 1875-Steiner demonstrated that varicella was caused by an infectious agent by inoculating volunteers with vesicular fluid from a patient with acute varicella. • Clinical observations of relationship between varicella and herpes zoster were made in 1888 by Von Bokay, when children without the evidence of varicella immunity acquired varicella after contact with herpes zoster. 3
- 4. • 1954-VZV wasisolated from vesicular fluid of both chickenpox and zoster lesions in cell culture by Thomas weller. • 1970- live attenuated vaccine was developed in Japan. • March 1995- Vaccine licensed for use in US. • May 2006- the first vaccine to reduce the risk of herpes zoster was licensed. 4
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- 9. Some facts… • Howit got its name? • It has been said to be derived from chickpeas, based on resemblance of the vesicles to chickpeas or to come from the rash resembling chicken pecks. Some parents believe that it is better for children to contract chickenpox than to get the vaccine, and they deliberately expose their children to the virus, sometimes by taking them to chickenpox parties. 9
- 10. AGENT • Varicella –Zostervirus(Human (alpha)herpes virus 3). • DNA virus; member of herpes group. • VZV only affects humans, and commonly causes chickenpox in children, teens and young adults and herpes zoster (shingles) in adults and rarely in children. • Varicella-zoster virus (VZV) causes primary, latent, and recurrent infections. 10
- 11. • The primaryinfection is manifested as varicella (chickenpox) and results in establishment of a lifelong latent infection in cranial nerves sensory ganglia and spinal dorsal root ganglia. • When cellmediated immunity wanes with age or following immune suppressive therapy, virus may reactivate resulting in herpes zoster in about 10-30% persons. • Latent infection causes painful, vesicular ,pustular eruption in the distribution of one or more sensory nerve roots. • Virus can be grown in tissue culture. 11
- 12. SOURCE OF INFECTION •A case of chickenpox • Virus occurs in the oropharyngeal secretions and lesions of skin and mucosa. • Rarely, the source of infection may be a herpes zoster patient. • Virus can be isolated from the vesicular fluid during the first 3 days of illness. 12
- 13. INFECTIVITY • Period ofcommunicability 1 to 2days before and 4 to 5 days after appearance of rash. • Infectivity ceases once the lesions are crusted. • Virus tend to die out before pustular stage. 13
- 14. SECONDARY ATTACK RATE •Chickenpox is highly communicable. • Secondary attack rate in household contact is up to 90%. 14
- 15. HOST FACTORS AGE Among childrenbelow 10 yrs of age Can occur in adults also(severe) IMMUNITY One attack confers lifelong immunity. Secondary attacks are rare. Cell mediated immunity prevents recurrence and reactivation of latent infection. IgG antibodies persist for life time and prevents from varicella. SEX Both sex equally affected 15
- 16. CONGENITAL VARICELLA SYNDROME Infectionduring first trimester • Foetus gets intra uterine infection. • Resulting in severe damage • Characterized by LBW, micro opthalmia, choroido retinitis, cataract, hypotrophic limbs with hypotonicity and zoster like lesions/scars. Infection during last trimester • No developmental defects • Mild attack with rashes(maternal antibodies) Infection during last few days before delivery • Newborn will develop chickenpox during neonatal period and it will be severe. 16
- 17. ENVIRONMENTAL FACTORS • Chickenpoxshows a seasonal trend in India, mostly occur during first six months of the year. • In temperate climates there is little evidence of seasonal trends. • Overcrowding favours transmission. 17
- 18. TRANSMISSION • Transmitted fromperson to person by droplet infection and droplet nuclei. • Portal of entry - respiratory tract. • Fomites doesn’t play a significant role in transmission. • Virus can cross the placenta and cause congenital varicella. • Chickenpox can also spread from people with shingles. 18
- 19. PATHOGENESIS Inhalation of respiratorydroplets Virus infects upper respiratory tract Viral proliferation in regional lymph nodes of the URT( 2-4 days after initial infection) Stage of primary viremia Viral replication in other organs (liver & spleen) VZV infection of cells of the malphigian layer produces both intercellular oedema and intracellular oedema, resulting in the characteristic vesicle. diffuse viral invasion of capillary endothelial cells and the epidermis. Stage of secondary viremia 19
- 20. INCUBATION PERIOD • Usually14 to 16 days • 10 to 21 days have also been reported. 20
- 21. CLINICAL FEATURES • Wideclinical spectrum. • May vary from a mild illness with only a few scattered lesions to severe febrile illness with widespread rash. • Divided into 2 stages a) Pre-eruptive stage b) Eruptive stage 21
- 22. PRE-ERUPTIVE STAGE • Onsetis sudden with mild or moderate fever, pain in back, shivering and malaise. • Very brief stage lasting for 24 hr. • In adults-more severe and last for 2-3 days before rash comes out. 22
- 23. ERUPTIVE STAGE • Inchildren the rash is often the first sign. • It comes on the day the fever starts. Characteristics • Distribution • Rapid evolution • Pleomorphism • Fever 23
- 24. DISTRIBUTION • Symmetric rashes. •Centripetal in distribution. a.First appears on the trunk (abundant) b.Then to face, arms and legs (less abundant) • Mucosal surface are generally involved. • Axilla may be affected. • Palms and soles not usually affected. • Density of eruptions diminishes centrifugally. 24
- 25. RAPID EVOLUTION Macule PapuleVesicle Pustule 25
- 26. • Rash advancesquickly through the stage of the macule, papule, vesicles and scab. • Vesicles are dew – drops like in appearance, present on the skin, containing the clean fluid superficial in site, with the easily ruptured wall and surrounded by an area of inflammation and are not umblicated. • The vesicles may form the crusts without going through the pustular stage. • Scabbing begin 4 – 7 days after the rash appearance. 26
- 27. PLEOMORPHISM • All stagesof the rash (Papule, vesicles & crusts) may be seen simultaneously at one time in same area. • This due to the rash appearing in the successive crops for the 4 – 5 days in same area. 27
- 28. FEVER • The feverdoes not run high. • Temperature rises with each fresh crop of rash. 28
- 29. smallpox chickenpox 1.Incubation period12days(7-17days) 15days(7-21days) 2.Prodromal symptoms Severe Usually mild 3.Distribution of rash • Centrifugal • Palms and soles involved. • Axilla usually free. • Predominant on extensor & bony prominence. • Centripetal • Rarely affected. • Axilla affected. • Mostly on flexor surface. 4.Characteristics of rash • Deep-seated. • Vesicles multilocular & umbilicated. • Only one stage of rash seen. • No area of inflammation around vesicle • Superficial. • Unilocular & unumbilicated. • Pleomorphic. • Area of inflammation around rash seen. 5.Evolution of rash • Slow deliberate and majestic passing through definite stage. • Scab formed in 10-14 days after rash appears. • Evolution of rashes very rapid. • Forms in 4-7days after the rash appears. 6.fever • Subsides with the appearance of rash, but may rise again in the pustular stage. • Temperature rises with each fresh crop of rash. 29
- 30. VARITIES OF CHECKENPOX • Varicella bulla: characterized by formation of bullous eruptions. • Varicella ganrenosa: It is seen in ill-nourished children and there are dark crusts are formed in the eruptions which on separation leave behind ulcers. • Varicella haemorrhagica: Uncommon virulent form of varicella . Hemorrhages occur into the vesicles and bleeding may take place from the mucous membrane. 30
- 31. COMPLICATIONS • Chickenpox ismild and self limiting disease. • In uncomplicated cases mortality less than 1%. • Severe complication occur in immunosuppressed patients and may also occur in normal children and adults. • Varicella pneumonia is rare in healthy children but is the most common complication in neonates, adults and immuno-compromised patients. • Other complications-haemorrhages, pneumonia, encephalitis, acute cerebellar ataxia and Reye’s syndrome. 31
- 32. • Maternal varicelladuring pregnancy causes foetal wastage and birth defects – cutaneous scars, atrophied limbs, microcephaly, LBW, cataract, micropthalmia, chorio- retinitis, deafness, cerebro-cortical atrophy. • If varicella develops within 5 days afer delivery, newborn is at risk of disseminated disease and should receive varicella zoster immunoglobulin. 32
- 33. • Associated withacute retinal necrosis and progressive outer retinal necrosis, both of which occur with increased frequency among AIDS patients. • Cellulitis, erysipelas, osteomyelitis, scarlet fever and rarely meningitis are observed. • Immuno compromised patients are at increased risk of complications of varicella, including those with malignancies, organ transplants or HIV infection and those receiving high doses of corticosteroids. 33
- 34. PROGNOSIS • Chickenpox thataffects a healthy child is usually a self-limiting disease. • Increased morbidity occurs in adult and immune compromised populations. 34
- 35. LABORATORY DIAGNOSIS • Rarelyrequired as clinical signs are clear-cut. • Examination of the vesicle fluid in electronic microscope shows round particles(brick shaped in smallpox). • Scrapings of vesicle floors shows multinucleated giant cells coloured by Geimsa stain(not in smallpox). • Serology is used for epidemiological surveys. 35
- 36. CONTROL Notification Isolation of casesfor 6 days after onset of rash Disinfection of articles soiled by nose and throat discharge • Anti viral therapy against varicella – Acyclovir, Valacylovir, Famiciclovir and foscarnet. • Acyclovir can prevent development of systemic disease in varicella infected immune suppressed patients and halt progress of zoster in adults. • Acyclovir does not prevent post herpetic neuralgia. 36
- 37. PREVENTION •Passive- Varicella zosterimmunoglobulin •Active- Vaccine 37
- 38. VARICELLA ZOSTER IG •Given within 72 hrs of exposure particularly in immune suppressed person. includes: •Susceptible person receiving immunosuppressive therapy •Congenital cellular immunodeficiency. •Acquired immunodeficiency. •Susceptible and exposed persons eg. In pregnant women •New-borns, premature infant with low birth weight. • VZIG has no therapeutic effect. •IM injection; Dose: 12.5unit/kg body weight, maximum of 625 units.38
- 39. VACCINATION • Live attenuatedfreeze dried varicella vaccine(varivax) • Developed by using Oka strain of virus in Japan, grown on human diploid cells. • Recommended for children between 12 months and 12 years. • Dose-0.5ml subcutaneously • 90% efficacy • Immunity lasts for 10 to 15 yrs. • For primary immunization in adults, 2 doses are recommended with 4 to 8 weeks interval. 39
- 40. CONTRAINDICATIONS • Should notbe given to immune compromised individuals including HIV +ve children and adults or pregnant women. ADVERSE REACTIONS • Occurs 4-6 weeks after vaccination. • 25%-tenderness and erythema • 10-15%- fever • 5%- localized maculopapular or vesicular rash 40
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Editor's Notes
- #33 Disseminated disease refers to a diffuse disease-process, generally either infectious or neoplastic. The term may sometimes also characterize connective tissue disease. A disseminated infection, for example, has extended beyond its origin or nidus and involved the bloodstream to "seed" other areas of the body.
- #34 an acute, sometimes recurrent disease caused by a bacterial infection, characterized by large raised red patches on the skin.
- #41 Contraindicated to persons allergic with neomycin. Salicylates should be avoided for 6 weeks(to prevent Reye’s syndrome).