Smallpox was a deadly disease that killed millions each year until its eradication in 1980 through a global vaccination campaign led by the WHO. It was caused by the variola virus and spread through respiratory droplets. Symptoms included a distinctive pustular rash that progressed through several stages. There was no treatment, so prevention through vaccination was critical. Edward Jenner's discovery of the cowpox vaccine in 1798 laid the foundation for eventually eliminating the disease worldwide over the following centuries through expanded vaccination efforts.

1. EPIDEMIOLOGY OF SMALL POX
Mrs. NAMITA BATRA GUIN
ASSOCIATE PROFESSOR
COMMUNITY HEALTH NURSING

2. INTRODUCTION
• Smallpox is a serious, contagious and sometimes fatal
disease
• At its height, 10-15 million cases a year, with 2 million
deaths
• There is no specific treatment for smallpox, and the
only prevention is vaccination.
• The name smallpox is derived from the Latin word
“spotted” and refers to the raised bumps that appear on
the face and body of an infected person.
• It is caused by variola virus, Orthopoxvirus genus

3. HISTORY
• Mummified remains of Ramses. (1157 B.C.)

4. HISTORY
• Smallpox was likely carried from Egyptian traders to
India
• By 1967 it became a major killer in not less than 33
countries
• Those who survive became immune
• As a result, physicians intentionally infected healthy
persons with smallpox organisms

5. VARIOLATION
• It is the act of taking samples (pus from pustules
or ground scabs) from patients whose disease had
been benign, and introducing it into others through
the nose or skin

6. EDWARD JENNER

7. EDWARD JENNER’S CONTRIBUTION
• He found that, the cowpox would protect the patient
from smallpox
• He proposed it in 1798
• In England vaccination with cowpox became
compulsory in 1853
• Jenner was honoured for his technique, and ‘Vaccine’
became the universally used term to indicate introducing
material under the skin to produce a protection against
disease

8. EPIDEMIOLOGY
• Smallpox is no more, due to aggressive vaccination campaign
by WHO.
• It is believed that the virus began in rodents, and as prehistoric
man killed and ate the rodents, the virus was passed on to
humans. Once humans became the new host, there was no
stopping the deadly viruses spread of devastation.
• This was due to the fact that around 9000 BC humans began to
cultivate crops and settle into much larger communities. With
larger groups, the virus could move from person to person
without exhausting its supply of hosts.

9. VARIOLA VIRUS

10. CAUSATIVE AGENT
• Smallpox is caused by 2 variations of the virus variola.
• The deadliest form is Variola Major.
• This is the largest animal virus visible with light microscope
appear as smooth rounded rectangles.
• It is the only virus that do not need a cell’s nucleus to replicate
and are larger than some bacteria.
• Variola Minor can leave large scars and can possibly cause
blindness.
• Smallpox is a highly contagious disease with a long incubation
period, usually between 12-14 days.

11. PATHOGENESIS
• Portal of entry: respiratory tract or inoculation on skin
• Source of infection: Excretions from the mouth and
nose, rather than scabs
• During incubation the virus proceeds through infection,
replication, and liberation (usually accompanied by cell
necrosis) first at the site of inoculation and then to the
regional lymph nodes, then deeper lymph nodes and
bloodstream

12. PATHOGENESIS
• 4 orthopoxviruses are known to infect humans: variola,
vaccinia, cowpox, and monkeypox
• Variola major is severe and the most common form
with more extensive rash and higher fever with a death
rate of 30%
• Variola minor has less common presentation and
much less severe with death rate of 1%

13. PATHOGENESIS
• Variola Major has 3 clinical presentations based on the
nature and evolution of the lesions:
– Ordinary: most frequent, corresponds to classical description
– Modified: milder and may occur in previously vaccinated
people; rarely fatal
– Flat and Hemorrhagic: very severe but uncommon

15. PATHOGENESIS
• The multiplication cycle starts by the virus binding to a host
cycle.
• Once in the host cell, it will un coat the exterior enveloped
virion, and then un coats the inner enveloped virion.
• Now that the inner enveloped virion is uncoated, the DNA
uncoils along with multiple viral enzymes.
• This process starts the replication of the genome that occurs in
the cytoplasm.
• This also makes smallpox unique in that replication usually
takes place in the nucleus, not the cytoplasm, since viruses
generally don’t have cytoplasm.
• Once the DNA replicates to make a virion, the virion then
passes through the cell membrane and is enveloped
simultaneously and is then released to repeat the process.

16. TRANSMISSION
• Humans are the only natural host of smallpox (no
animal reservoir)
• Transmission generally occurs from direct and fairly
prolonged face-to-face contact, usually within a distance
of 6 feet (1.8 m).
• Infected aerosols and air droplets spread in face-to-face
contact
• The virus can cross the placenta, but the incidence of
congenital smallpox is relatively low.

17. STAGES OF SMALL POX
• Incubation Period – 12-14 days, person is not contagious
• Prodrome Phase
– Begins abruptly with fever, malaise, headache, head and
body aches, prostration, and often nausea and vomiting
– Body temperature rises to at least 101 F and is often higher
• When the first visible lesions appear the fever may start to go
down - most contagious period
• Rash emerges as small red spots on tongue and in mouth (about
24 hours before the appearance of rash on the skin)
• Lesions in the mouth and pharynx enlarge and ulcerate quickly,
releasing large amount of virus into the saliva

18. STAGES OF SMALL POX
• Rash Phase
• Centrifugal distribution
• Palms and soles are involved
• lesions are all in the same
stage of development on that
part of the body
(unlike chickenpox)

21. PATHOLOGIC FEATURES
Skin: Capillaries in the papillary dermis dilate, cells enlarge, vacuolate,
and degenerate. Affected cells contain round or oval inclusion bodies,
called Guarnieri's bodies, that measure 2 to 8 µm, and compose of viral
particles and proteins; each body is the locus of viral replication and
assembly. Later, viral inclusions occupy large portions of cytoplasm. Cells
may lose normal orientation, condense, and detach. Cellular degeneration
spreads in the middle layer of the epidermis.
Respiratory and Digestive Tracts: Smallpox can affect the epithelium
of the tongue, throat, trachea, gullet, and appendix Necrosis begins in
superficial cells, and then penetrates to form ulcers. The trachea may have
sharply defects 1 to 2 mm in diameter.

22. PATHOLOGIC FEATURES
Lungs: Alveolar cells are swollen, mitotic, or degenerating with
accompanying bacterial growth.
Heart: Cardiac involvement in smallpox is not often but can
include hyperemia and small hemorrhages.
Liver: Endothelial cells become swollen and necrotic.
Spleen: The spleen is enlarged and engorged with blood, and
there are small hemorrhages in the red and white pulp.
Kidney: Pathologic changes in the kidney are most
prominent in the center (medulla). Tubular epithelial cells are
swollen, degenerated, or mitotic.

23. OUTCOME OF INFECTION
• Those who survive usually have scars
• In eye involvement, blindness could occur
• Recovery results in long lasting immunity
• No evidence of chronic or recurrent infection

24. VACCINATION
• Live vaccine virus
• Administered using a bifurcated
needle, not an injection
• Bifurcated needle is dipped into the vaccine and then
used to prick the skin 15 times in about 3 seconds in a
5mm radius area
• Administered into the superficial layer of the skin

26. COURSE OF VACCINATION
• If vaccination is successful a red, itchy bump develops
at the vaccine site in 3-4 days; a papule surrounded by
erythema
• In the first week the bump becomes a blister, fills with
pus, and begins to drain
• During the second week the blister begins to dry and a
scab forms; the scab then falls off leaving a scar
• It is given on the right side universally

27. CONTROL
• Only after WWI most of Europe become smallpox free,
and only after WWII transmission stopped throughout
Europe and North America
• In developing countries smallpox continued largely
unabated until middle of 20th century
• 1958: Soviet Union proposed to the WHO that a global
smallpox eradication program be undertaken

28. CONTROL
• The campaign was based on a two fold strategy
– 1. Mass vaccination campaigns in each country
using a vaccine of ensured potency and stability that
would reach at least 80% of the population
– 2. Surveillance-Containment - isolation of patients
and the vaccination of family members and other
contacts in the immediate vicinity

29. CONTROL
• Ring vaccination: The strategy involves the
following steps:
– Rapid identification and isolation of all smallpox cases
– Identification and vaccination of contacts of smallpox
cases
– Monitoring contacts for development of fever and
isolating them if fever occurs
– Vaccination of household members of contacts if no
contraindications to vaccination exist

30. MANAGEMENT OF AN OUTBREAK
• Surveillance is easier because of the distinctive rash
• Containment involves efficient detection of cases and
identification and vaccination of contacts
• Patients diagnosed with smallpox should be physically
isolated
• All specimen collectors, care givers and attendants
coming into close contact with patients should be
vaccinated
• Medical care givers, attendants, and mortuary workers
should wear gloves, caps, gowns, and surgical masks

31. MANAGEMENT OF AN OUTBREAK
• Contaminated clothing and bedding, if not incinerated,
should be autoclaved or washed in hot water containing
bleach
• Fumigation of premises with formaldehyde
• Airborne and Contact Precautions in addition to
Standard Precautions should be implemented for patients
with suspected smallpox

32. ERADICATION
• In India : Last case reported on 17th May 1975 in
Bihar
• In April 1977 declared free from smallpox
• 26th October 1977 the last naturally occurring case
of smallpox was recorded in Somalia
• In 1978 two cases were reported. These were both
from people working in labs with smallpox in
England
• 8th May 1980, WHO declared that smallpox has
been eradicated

33. FACTORS THAT LED TO ERADICATION
• Epidemiological factors:
– No known animal reservoir
– No long-term carrier of the virus
– Life-long immunity after recovery from the disease
– Detection of cases, the rash was so characteristic
– Sub-clinical infection did not transmit the disease
– Vaccine highly effective
– International co-operation

34. EPIDEMIOLOGY OF CHICKEN POX

35. INTRODUCTION
• Acute, highly infectious disease caused by Varicella-
Zoster (V–Z) virus
• Chicken pecked skin appearance, chickpea appearance
• World-wide in distribution and occurs in endemic and
epidemic forms
• Chickenpox and Herpes zoster as different host
responses to the same etiological agent
• In India, approx. 28,000 cases per year

36. EPIDEMIOLOGICAL DETERMINANTS: AGENT
• Agent: Human (alpha) herpes virus
– Primary infection causes chicken pox
– Recovery followed by latent infection
– Reactivation results in zoster- a painful, vesicular,
pustular eruption in distribution of one or more sensory
nerve roots
– Can be grown in tissue culture
• Incubation period: 14-16 days (7-21 days)

37. EPIDEMIOLOGICAL DETERMINANTS:AGENT
• Source of infection
• Usually a case of chicken pox
• Virus present in oropharyngeal secretions and lesions
of skin and mucosa
• Rarely may be a patient with herpes zoster
• It can be isolated from the vesicular fluid during the
first 3 days of illness

38. EPIDEMIOLOGICAL DETERMINANTS: HOST
•Age
– Children under 10 years of age
– Few escape until adulthood but can be severe in adults
• Immunity – One attack give durable immunity
– Maternal antibody protects the infant for few
months
– No age is exempt in the absence of immunity
– IgG antibodies persist for life and correlate with
protection
– Cell mediated immunity is important in recovery
• Pregnancy: Risk for fetus and neonate

39. EPIDEMIOLOGICAL DETERMINANTS:
ENVIRONMENTAL
•It shows a seasonal trend, occurring mostly during the
first six months of the year
• Overcrowding
• In temperate climates, there is little evidence of
seasonal trend

40. TRANSMISSION
•Droplet infection and droplet nuclei
• ‘Face to face’ (personal) contact
• Portal of entry: respiratory tract
• Virus is extremely labile, so fomites unlikely to
transmit
• Contact infection plays a significant role when an
individual with herpes is an index case
• Congenital varicella - it crosses the placental barrier
and infects the foetus

41. CLINICAL FEATURES
•Clinical spectrum
– Mild illness with few scattered lesions
– Severe febrile illness with widespread rash
• Pre-eruptive stage
– Sudden onset with mild to moderate fever
– Pain in the back, shivering and malaise
– Duration about 24 hours
– In adults, prodromal illness is usually more severe and
may last for 2-3 days before the rash

42. CLINICAL FEATURES
• Eruptive stage: in children the rash comes on day the fever
starts and first sign
• The distinctive features of rash are
– Rash is symmetrical
– Appears on the trunk and then comes to face, arms ,legs
– Mucosal surfaces (buccal, pharyngeal) are involved
– Axilla affected. Palms and soles usually not involved
– The density of eruption diminishes centrifugally
– Pleomorphism
- All stages of rash (papules, vesicles and crusts) may be seen
simultaneously in the same area

44. CLINICAL FEATURES
• Evolution of rashes
– The rash advances quickly through the stages of-
macule, papule, vesicle, scab
– Vesicles filled with clear fluid resembling ‘dew-drops’
– Superficial in site, with easily ruptured walls and
surrounded by an area of inflammation
– Vesicles may form crusts directly. Many lesions may
abort
– Scabbing begins 4-7 days after the rash appears
• Fever not high but exacerbations with fresh crop

46. COMPLICATIONS
• It’s a mild, self-limiting disease
• Patients at risk of complications are
– Immunosuppressive patients
– Cancer patients
– Recipients of organ transplants
– Chemo, radio, steroid therapy recipients
– HIV infected
– Children with leukemia

47. COMPLICATIONS
• Haemorrhages (varicella haemorrhagic)
• Pneumonia
• Encephalitis
• Acute cerebellar ataxia
• Reye’s syndrome
• Maternal varicella may cause foetal wastage & birth
defects
• Acute retinal necrosis
• Secondary bacterial infections (Cellulitis, erysipelas,
epiglottitis, osteomyelitis, scarlet fever and meningitis)
• Pitted scars

48. CONGENITAL DEFECTS IN BABIES
• Damage to brain: encephalitis, microcephaly,
hydrocephaly, aplasia of brain
• Damage to the eye: microphthalmia, cataracts,
chorioretinitis, optic atrophy
• Other neurological disorder: damage to cervical and
lumbosacral spinal cord, motor/sensory deficits, absent
deep tendon reflexes, anisocoria/Horner's syndrome
• Damage to body: hypoplasia of upper/lower
extremities, anal and bladder sphincter dysfunction
• Skin disorders: (cicatricial) skin lesions, hypo
pigmentation

49. LABORATORY DIAGNOSIS
• Most rapid and sensitive
 Examination of vesicle fluid under electron
microscope.
 Round particles which may be used for cultivation.
 Scrapings of floor of vesicles show multinucleated
giant cells coloured by Giemsa Stain.
 Serology for epidemiological surveys.

50. CONTROL
• No specific treatment for chickenpox
 Notification.
 Isolation of cases for about 6 days after onset of rash.
 Disinfection of articles soiled by nose and throat
discharges.
 Antiviral drugs provide effective therapy for varicella
(acyclovir, valaciclovir, famiciclovir and foscarnet)

51. PREVENTION
 Varicella zoster immunoglobulin (VZIG)
 VZIG givenwithin 72 hours of
exposure has been recommended for prevention
 Dosage:1.25-5ml intramuscularly
 Used for immunosuppressed contacts of acute
cases or newborn contacts
 Provide improvement in high risk children with
varicella

52. VACCINE
 Monovalent vaccine
 Oneor two dose schedule (0.5 mlsubcutaneous
injection)
 For children between 12-18months
 Twodose schedule for persons aged>13years
 Minimum interval between doses6weeks
 Combination vaccines(MMRV) for children9 months to
12years
 Duration of immunity probably 10years

53. DIFFERENCE BETWEEN SMALL POX AND
CHICKEN POX

54. DIFFERENCE BETWEEN SMALL POX AND
CHICKEN POX
Small pox Chickenpox
Incubation 12 days(7-17) 15 days(7-21)
Prodromal Severe Mild
Distribution ofrash Centrifugal Centripetal
Palmsand soles involved Not involved
Axilla free Axilla affected
Extensor surfaces Flexor surfaces
Characteristics of
rash
Deep seated Superficial
Multilocular, umbilicated Unilocular, dew drop
Onestageat atime Pleomorphic
No inflammation around
the vesicles
Inflammation seen

55. DIFFERENCE BETWEEN SMALL POX AND
CHICKEN POX
Small pox Chickenpox
Evolution of rash Slowand majestic,
passing through
definite stagesof
macule, papule,
vesicle and pustule
Very rapid
Scabs10-14days Scabsin 4-7days
Fever Subsideswith
appearance of rash,
may rise again at the
pustular stage
Feverappears with
eachfresh crop of rash