Rash Illness
Paige Jordan RN, BSN
Region II
Epidemiologist
Objectives





Describe the public health action required to
respond to a suspected case of smallpox
Describe the epidemiology, mode of transmission
and presenting symptoms of papulovesicular
rashes
Describe the differential diagnosis of
papulovasicular rashes and other diseases of
public health significance
Describe how to use the Diagnostic Algorithm for
evaluation of rash illness
Describe the laboratory diagnosis of
papulovasicular rashes
Public Health Significance




Smallpox eradicated in 1970’s. Heightened
concern that the variola virus might be used as
an agent of bioterrorism.
Ruling out rash illnesses facilitates the
diagnosis/confirmation of smallpox
Many rash illnesses of public health significance
require ruling out other differential diagnosis
A good understanding of rash illnesses allows for
early identification, diagnosis, treatment, control
and prevention of disease.
Public Health Action

Identify personnel to respond to a suspected case of
smallpox.
Personnel must have:
 Documented immunity to smallpox
 Unvaccinated personnel : - Fit tested N 95 mask
- No contraindication to
smallpox vaccination
 Documented immunity to measles, rubella and varicella
 Completed training in smallpox investigation & response
Public Health Action

Educate providers to immediately isolate undiagnosed
hospital patients with acute, generalized vesicular or
pustular rash illness, to include:



Airborne precautions
Contact precautions
Notification of the ICP
Public Health Action
Educate providers to recognize major and minor
smallpox diagnostic criteria , as follows
Major Criteria
Febrile prodrome: occurring 1-4 days before rash onset:
fever >101°F and at least one of the following: prostration,
headache, backache, chills, vomiting or severe abdominal
pain.
 Classic smallpox lesions: deep-seated, firm/hard,
round, well-circumscribed vesicles or pustules; may be
umbilicated or confluent.
 Lesions in the same stage of development: on any one
part of the body (e.g., the face, or arm) all the lesions are in the
same stage of development (i.e. all are vesicles, or all are
pustules).

Public Health Action
Minor Criteria





Centrifugal distribution: greatest concentration of
lesions on face and distal extremities
First lesions on the oral mucosa/palate, face,
forearms
Patient appears toxic or moribund
Slow evolution: lesions evolve from macules to
papules  pustules over days (each stage lasts 1-2
days)
Lesions on the palms and soles (majority of cases)
Public Health Action
Educate hospitals to report immediately cases of :

Acute febrile pustular or vesicular rash illness immediately

Educate hospitals to report hospitalized cases of varicella
immediately
Public Health Action
Triage reports of pustular/ vesicular rash illness
according to CDC criteria, as follows:
 High risk




Moderate risk



Febrile prodrome AND
Classic smallpox lesions AND
Lesions in same stage of development
Febrile prodrome AND
1 major OR >=4 minor criteria
Low risk


No/mild febrile prodrome
Febrile prodrome and < 4 minor criteria
Rash Illness Algorithm
Goal


Evaluation of cases
Classification of cases into risk categories according
to major & minor criteria
Assumptions / Limitations
- Will miss the first case of smallpox until
day 4-5 (by excluding maculo-papular
rashes)
- Will miss an atypical case of smallpox
(hemorrhagic, flat/velvety or highly
modified) if it is the first case.
Patient with
Acute, Generalized
Vesicular or Pustular Rash Illness
Institute Airborne & Contact Precautions
Alert Infection Control on Admission
Low Risk for Smallpox
Moderate Risk of Smallpox
High Risk for Smallpox
(see criteria below)
(see criteria below)
(see criteria below)
ID and/or Derm Consultation
VZV +/- Other Lab Testing
as indicated
ID and/or Derm Consultation
Alert Infx Control &
Local and State Health Depts
History and Exam
Highly Suggestive
of Varicella
Diagnosis
Uncertain
Varicella Testing
Optional
Test for VZV
and Other Conditions
as Indicated
Non-Smallpox
Diagnosis Confirmed
Report Results to Infx Control
Evaluating Patients for
Smallpox
No Diagnosis Made
Ensure Adequacy of Specimen
ID or Derm Consultant
Re-Evaluates Patient
Smallpox Response Team
Collects Specimens and
Advises on Management
Cannot R/O Smallpox
Contact Local/State Health Dept
Testing at CDC
NOT Smallpox
Further Testing
SMALLPOX
Public Health Action
High Risk of Smallpox  Report
Immediately

Contact IDEP emergently to arrange smallpox testing
through CDC

Consider infectious disease and/or dermatology
consultation

Consider testing for chickenpox, if appropriate

Clinical and epidemiological data may be collected using
the vesicular rash illness form

If a specific disease is diagnosed, use the investigation
form for that disease.

Consider active surveillance for vesicular/pustular rash
illness in hospitals and emergency rooms.
Public Health Action
Moderate Risk of Smallpox  Urgent
Evaluation





Consider dermatology and/or infectious disease consultation
Consider testing for chickenpox (DFA)
Clinical and epidemiological data may be collected using the
vesicular rash illness form
If a specific disease is diagnosed, use the investigation form
for that disease
Recommend additional testing, if indicated
Public Health Action
Low Risk of Smallpox Manage as
Clinically Indicated



Consider testing for chickenpox (DFA), if appropriate.
Contact IDEP to arrange
Clinical and epidemiological data may be collected using the
vesicular rash illness form
If a specific disease is diagnosed, use the investigation form
for that disease
Public Health Action
Assure collection of appropriate clinical samples for
testing
Smallpox
Chickenpox
Measles
Herpes simples
Monkeypox
Rickettsialpox
On confirmation of a specific diagnosis, refer to disease
specific protocol for public health action.
Investigating Tool
IDEP’s case investigation worksheet
for investigation of febrile vesicular or
pustular rash illnesses
SMALLPOX
Single confirmed case is an
international public health emergency
Etiology
Variola Virus (Orthopoxvirus)
 Infects only Humans
 May remain viable in crusts for years at
room
temperature
 Rapidly inactivated by UV light, chemical
disinfectants

Epidemiology
All ages and genders affected
 Incubation

12 days (range 10-14 days)

Spread
Person-to-person transmission:
Droplets > Contact with contaminated clothing
and bedding > Aerosol

Infectious Period:
From the time the rash appears - particularly
in the first week of illness - until the scabs fall
off.
Smallpox Signs & Symptoms
Signs & symptoms



Fever, malaise, headache, abdominal pain,
delirium
Rash, pustules, toxemia, secondary bacterial
infections, death 5-6 days after rash
Survivors usually have deeply scarred face.
Clinical Features
Three stages of disease

Incubation
Asymptomatic

Prodromal
Nonspecific febrile illness, flu-like (may be
misdiagnosed or ignored)

Eruptive
Characteristic rash
Clinical Features

Incubation Stage
(From time of infection to onset of symptoms)
 Average 12 days (range 10-14 days)
 Problem for epidemiological investigation and
control
(e.g., quarantine) of carriers & exposed

No symptoms

Considered non-infectious during this stage
Clinical Features

Prodromal Stage
Occurs 1-4 days before rash onset
End of stage marked by mucosal (mouth) lesions
Mucosal lesions indicate onset of infectiousness



Common symptoms
Abrupt onset of fever > = 101 F
 Weakness, headache, backache

Occasional symptoms

Nausea, vomiting, abdominal pain, delirium
Clinical Features

Eruptive Stage (Rash)
“Centrifugal” (in order of appearance
& severity)

Initially oral mucosa

Occurs 1-4 days before rash onset
Face, head
Forearms, hands, palms
Legs, soles, (sometimes less so on trunk)



Clinical Features
Rash Description
 Enanthem (mucous membrane lesions)





Appears approx. 24 hours before skin rash
Minute red spots on the tongue and
oral/pharyngeal mucosa
Lesions enlarge and ulcerate quickly
May result in complaint of sore throat
Virus titers in saliva are highest during first
week of exanthem
Clinical Features
Rash Description
 Exanthem (skin rash)



Appears 2-4 days after onset of fever
First appears as macules, usually on the face
Lesions appear on proximal extremities, spread to
distal extremities and trunk.
Clinical Features
Rash Description
 Classic Smallpox Lesions





Vesicles often have a central depression (“umbilication”)
Pustules raised, round, firm to touch, deeply embedded in
the skin
Lesions in same stage of development
Most dense on face and distal extremities (centrifugal
distribution)
Lesions on palms and soles (>=50% cases)
Smallpox Clinical Course
Smallpox Rash Evolution
Stage
Days after Rash
onset
Macules
Papules
Vesicles
Pustules
Crusts
All crusts separated
0-1
2-3
3-5
6-12
13-20
21-28
Understanding the terms
(Illustration by Electronic Illustrators Group.)
http://www.hendrickhealth.org/healthy/001267.htm
Rash Evolution
World Health Organization (WHO)
SMALLPOX - RASH PROGRESSION
Day 1
Day 2
Day 3
Few raised spots
(papules)
More papules
appear
Rash more distinct
fluid accum. to
form vesicles
World Health Organization (WHO)
SMALLPOX - RASH PROGRESSION
Day 4
Day 5
Day 7
Vesicles more
distinct
Fluid in vesicles Rash characteristic
becomes
of
cloudy to form smallpox no mistake
pustules
in diagnosis
World Health Organization (WHO)
SMALLPOX - RASH PROGRESSION
Day 8 & 9
Day 10-14
Day 20
Pustules increase in
size
Firm and deeply
embedded
Pustules dry up to
form
dark scabs
Scabs have come off
revealing
depigmented
areas
World Health Organization (WHO)
Smallpox Rash - Distribution
Smallpox Rash - Distribution
World Health Organization (WHO)
Smallpox Rash - Distribution
World Health Organization (WHO)
Smallpox Rash - Distribution
World Health Organization (WHO)
Smallpox Clinical Types

Ordinary smallpox: 90% of cases
 Case-fatality average 30%
 Occurs in non-immunized persons

Modified smallpox
 Milder, rarely fatal
 Occurs in 25% of previously immunized
persons and 2% of non-immunized persons
 Fewer, smaller,more superficial lesions that
evolve more rapidly
Smallpox Clinical Types

Hemorrhagic smallpox: <3% of cases
 Immunocompromised persons and pregnant
women at risk
 Shortened incubation period, severe prodrome
 Dusky erythema followed by petechiae &
hemorrhages into skin and mucous
membranes
 Almost uniformly fatal within 7 days
Hemorrhagic Smallpox
Smallpox Clinical Types


Malignant or flat-type smallpox: 7% of cases
 Slowly evolving lesions that coalesce without
forming pustules
 Associated with cell-mediated immune
deficiency
 Usually fatal
Smallpox – No Rash (Variola sine eruptione)
 Occurs in previously vaccinated persons or
infants with maternal antibodies
 Asymptomatic or mild illness
 Transmission from these cases has not been
documented
Malignant Smallpox
Thomas, D.
Smallpox Laboratory Testing
Specimens
Fluid from vesicles, pustules, or scabs
 Autopsy specimens from major organs
including
skin, spleen, lymph node, liver, lung, kidney,
and
heart
 Tonsillar tissue
 Blood

Laboratory Criteria for Diagnosis of
Smallpox
Isolation of smallpox virus from a clinical
specimen (level D lab only)


PCR identification of Variola DNA in a clinical
specimen, or
Negative stain Electron Microscopy identification
of Variola virus in a clinical specimen (level D lab
or approved level C lab)

Smallpox Surveillance
Clinical Case Definition
An illness with acute onset of fever > 101o F followed by a
rash characterized by firm, deep-seated vesicles or pustules
in the same stage of development without other apparent
cause
Laboratory criteria for confirmation
Isolation of smallpox virus from a clinical specimen, OR
Identification of variola in a clinical specimen by PCR or
electron microscopy
* Initial confirmation of outbreak requires testing in level D lab (I.e CDC)
Smallpox Surveillance
Case classification
Confirmed: laboratory confirmed
Probable: meets clinical case definition & has an epi link to
another confirmed or probable case
Suspected:
Meets clinical case definition but is not laboratoryconfirmed and does not have an epi link OR
Atypical presentation not lab confirmed but has an epi link
to a confirmed or probable case
Common Conditions With Vesicular or Pustular
Rashes



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Varicella (primary infection with VZV)
Disseminated herpes zoster
Impetigo
Drug eruptions and contact dermatitis
Erythema multiforme minor
Erythema multiforme incl. Stevens Johnson syndrome
Enteroviruses incl. Hand, Foot and Mouth disease
Disseminated herpes simplex
Scabies and insect bites
Molluscum contagiosum
CHICKENPOX
(VARICELLA)
Varicella Is the disease
most likely to be
confused with smallpox
Chickenpox Epidemiology
Incubation:
14-16 days (range 10-21 days)
Spread:
Person to person by direct contact with
patients with :

Varicella or Zoster lesions

Airborne spread from respiratory secretions
Infectious Period: two days before the
onset of the rash, until all of the lesions are
crusted over
Chickenpox Epidemiology
Etiology:
Varicella Zoster Virus VZV
Reservoir:
Humans are the only source of infection
Seasonality:
Seasonal transmission of disease
highest during
winter and early spring
Chickenpox Clinical Features
Fever and malaise usually mild in children and more
severe
in adults
 A pruritic skin rash most prominent on chest, back,
shoulders, scalp, or other areas
 Lesions on the mouth, vagina, rectum, eye, or other
mucous
membranes changes to fluid-filled blisters
 Crusting, after the blister breaks
 Crusts become progressively darker with time
 Scabs fall off in about 9 to 13 days
 Itching-- may be severe

Chickenpox Clinical Features
Prodrome:
0-1 day of fever, anorexia, headache
Rash:
 Begins on face and scalp
 Spreading inferiorly to trunk and extremities
 Palms and soles usually spared
 Scabs form as early as day 3 or 4 of rash; fall off by day 14
Enanthem:
Vesicles and shallow erosions most commonly on the hard palate,
but also
on nasal mucosa, conjunctiva, pharynx, larynx, GI tract, urinary
tract, vagina
Exanthem:
Macules, papules, vesicles, crusts in various stages of evolution
Chickenpox Clinical Features
Chickenpox on the
palate.
Glistening, water-drop
characteristic of the
chickenpox vesicle on
the palate.
.
Chickenpox Clinical Features
Chickenpox vesicle
behind the ear.
Classic "dew drop on a
rose petal" appearance.
Chickenpox Clinical Features
© 2001, Johns Hopkins University School of Medicine
Chickenpox Rash
Classic Chickenpox Rash
Superficial lesions
 Not well circumscribed
 Confluence and umblication
uncommon
 Lesions at all stages of development

Chickenpox Rash Evolution
Stages
Macules
Papules
Vesicles
Crusts
Rapid evolution of macules
to papules, vesicles, crusts
All stages simultaneously
present
Lesions superficial,
distribution centripetal
Scabs fall off in 9-13 days
Differentiating Features
Chickenpox Vs Smallpox
Distinguishing Smallpox from Chickenpox
Epi Features that Differ

Smallpox (variola)



Most of the population
expected to be
susceptible

Chickenpox (varicella)

Most cases occur in
children

Expected case fatality
rate 2-3/100,000

Secondary attack rate of
80% among susceptible
household contacts
Expected case fatality
rate averages 30%
Secondary attack rate
~60% in unvaccinated
family contacts
Distinguishing Smallpox from Chickenpox
Clinical Features that Differ
SMALLPOX
FEVER 2-4 DAYS BEFORE
RASH
RASH
SAME STAGE
Appearance
Development
SLOW
CHICKENPOX
AT TIME OF RASH
DIFFERENT STAGES
RAPID
Distribution MORE ON ARMS &
LEGS
MORE ON BODY
On palms & USUALLY PRESENT
soles
USUALLY ABSENT
> 10%
VERY UNCOMMON
DEATH
Distinguishing Smallpox from Chickenpox
Clinical Features that Differ
Classic Smallpox
lesion
Classic Chickenpox
lesion
“Dew drops on a rose
petal”
Rash Distribution
Rash Distribution
Smallpox
Chickenpox
Content Provider: CDC/Dr. John Noble, Jr.
Rash Distribution
Chickenpox
- More pocks on the trunk
Very Few on arms and hands
- Pocks different stages of
development
Smallpox
More pocks on face arms and
thighs
- Pocks same stage of
development
Rash Distribution
Chickenpox
No or few lesions on
the
hands
Smallpox
Pocks usually present
on
the palms of the
hands
Rash Distribution
Smallpox
Many lesions on the
soles
Chickenpox
Few of no lesions
Rash Distribution
Rash Distribution
Smallpox
Chickenpox
Rash Distribution
Smallpox
Chickenpox
Rash Distribution
Smallpox
Rash same stage
of
development
Chickenpox
Several stages of
rash (papules,
vesicles &
pustules)
Rash Distribution
Smallpox
Scabs not yet
formed
Chickenpox
Most lesions
scabbed
Rash Distribution
Smallpox
Scabs beginning to
form
Chickenpox
Most scabs fallen
off
Chickenpox Diagnosis
Rapid diagnostic testing for varicella zoster
virus
(DFA, IFA, PCR)
Laboratory Specimens for Diagnosis
Swab sample from the base of a skin lesion
preferably fresh fluid vesicle
HERPES ZOSTER
(Shingles)
A painful involvement of
cutaneous nerves resulting
from a reactivation of a
dormant varicella zoster
virus
Herpes Zoster Epidemiology
Etiology
DNA virus belonging to herpes group. Same virus that transmits
the chicken pox. Reactivation of varicella infection
Incubation:
There may be latent period of decades before the virus is
reactivated and start spreading along cutaneous nerves.

Spread:
There is no convincing evidence that shingles can be
contracted from another individual.
 The virus remains dormant in dorsal root or cranial nerve
ganglion after the patient recovers from chicken pox.

Herpes Zoster Epidemiology






No airborne droplet spread from cases of shingles.
Direct contact with the blister fluid can cause
chickenpox in a non immune person.
Immunosuppressed individuals - at more risk.
More common in the elderly.
The trigeminal nerve is most commonly involved
cranial nerve.
Overall the thoracic is the most commonly
affected.
Herpes Zoster
Clinical Features


Prodrome: Neuritic pain or paresthesia for 2-3
weeks
Physical examination reveals an eruption, which
is limited to one side of the body and
corresponds to a dermatome.
What is a Dermatome?
American Accreditation HealthCare
Commission (www.urac.org).
Herpes Zoster Rash
Rash
Painful papulovesicular rash
Stages of Rash





Red macule
Papule
Vesicle surrounded by erythema.
The individual vesicles may become confluent
and evolve over the next 2-3 weeks to become
pustular, haemorrhagic and finally scabbed.
Crust formation: days to 2-3 weeks; post-herpetic
neuralgia:months to years
www.niaid.nih.gov/shingles
Herpes Zoster Vesicle

Herpes zoster on the arm.
- Characteristic grouping of
vesicles
Herpes Zoster
Shingles affecting the left side of the chest of an adult male.
- The dermatomes involved are T6 and T7.
Herpes Zoster
HERPES ZOSTER
ON THE FACE
Dermatomal distribution
of the papules, vesicles,
and pustules.
•Groups of vesicles
arranged along the
distribution of a cranial or
spinal nerve
•Cutaneous and visceral
dissemination from the
original dermatome
develops in some
individuals, particularly
immunocompromised
patients
•Associated with localized
or referred pain
Distinguishing Smallpox from Herpes Zoster
Clinical Features that Differ
HERPES ZOSTER
SMALLPOX

Lesions are unilaterally
distributed along a
dermatome

Lesions are widely
distributed

Lesions at any given time
are in different stages of
development (vesicles,
pustules, and crusts are in
evidence at one time)

Lesions at any given time
are all at the same stage of
development

Associated with severe
constitutional symptoms
Herpes Zoster Laboratory Diagnosis
 Rapid diagnostic tests for Herpes Zoster
Virus
Direct Fluorescent Antibody (DFA)
- Very sensitive and specific
- Critically dependent on careful
collection of
material from a lesion
Specimen: Vesicle scraping
Polymerase chain reaction
Specimen: body fluid or tissue
What is Herpes?
Herpes is a common viral infection. It causes oral
herpes (cold sores or fever blisters), and genital herpes
(genital sores).
There are two herpes simplex viruses:
•Herpes Simplex Type 1 (HSV-1)
•Herpes Simplex Type 2 (HSV-2)
These viruses look identical under the microscope, and
either type can infect the mouth or genitals. Most
commonly, however, HSV-1 occurs above the waist,
and HSV-2 below.
GENITAL HERPES
Genital herpes is a contagious viral infection
affecting primarily the genitals of men and women.
It is characterized by recurrent clusters of vesicles
and lesions at the genital areas.
It is caused by the Herpes Simplex-2 virus (HSV-2),
one of several strains of the Herpes Simplex Virus
responsible for chickenpox, shingles,
mononucleosis, and oral herpes (fever blisters or
cold sores, HSV-1).
While generally not dangerous, it is a nuisance and
can be emotionally traumatic, as there is no cure.
It has reached epidemic proportions in the U.S.;
500,000 are diagnosed each year.
One in five American adults has herpes, but only
one third of those inflicted are aware that they have
the virus. Many people don’t relate their symptoms
to herpes, since they have either very mild or no
symptoms at all. Over 50 million cases are currently
estimated to exist in either the active or dormant
stage.
Eczema herpeticum (ulcers are of similar shape and size)
“The key physical sign of eczema
herpeticum is blisters, pustules, or
erosions of a rather uniform size
and appearance”
Frequency of Adverse Events Following Primary Smallpox Vaccination
with New York Board of Health Strain Vaccinia, by Age and Type of
Adverse Event
Expected Number of Adverse Events Per Million Vaccines
Age at Vaccination
<1
1-4
5-19
20+
5
0.5
0-5
5 (?)
Post-vaccinial encephalitis
6
2
3
4
Progressive vaccinia
1
0.5
1
10 + (?)
Eczema vaccinatum
14
44
35
30
Generalized rashes
400
9,600
140
250
Accidental implantation
507
577
371
606
Type of Adverse Event
Death (all causes)
Eczema vaccinatum
Eczema vaccinatum is a serious
complication that occurs when people with
eczema or atopic dermatitis get vaccinated.
The lesion spreads to skin that is currently
affected or has recently been affected by
eczema. This complication can occur even if
the eczema or atopic dermatitis is not active
at the time, and requires immediate medical
attention. Prior to 1960, eczema vaccinatum
occurred in 10 to 39 people per 1 million
people vaccinated. Vaccine Immune
Globulin (VIG) is felt to be a useful
treatment for eczema vaccinatum.
Eczema vaccinatum
Eczema vaccinatum is characterized by widespread
vaccinial lesions over the body of patients with
eczema or a history of eczema. These patients are
clinically similar to burn patients, losing fluid, serous
exudate, and electrolytes through their skin. Fatalities
often occurred in patients who were not themselves
vaccinated, but were close household contacts of
recently vaccinated siblings etc. Many patients with
eczema have perfectly normal vaccination responses;
there are no data to show what proportion of eczema
patients develop serious disease, but it is probably
considerably less than half.
While patients with other widespread skin disease can
get superinfection of their rashes, they do not develop
the extensive involvement found with occasional
eczema patients, and essentially never die. Vigorous
therapy with VIG and good supportive care reduced
the fatality rate from about 10% in the pre-VIG era, to
only about 1%.
Eczema vaccinatum
•In the past, it was estimated to occur in 10-39
per million primary vaccinees.* Rates in the
United States today may be higher because
there may be more persons Eczema
vaccinatum is a localized or systemic spread of
vaccinia virus.
•at risk from 1) immune suppression from
cancer, cancer therapy, organ
transplantation, and other illnesses, such
as HIV/AIDS, and 2) eczema or atopic
dermatitis. Rates may be lower for persons
previously vaccinated
•Transfer of vaccinia virus can occur from
autoinoculation or from contact with a
vaccinee whose lesion is in the florid stages.
•Individuals with eczema or atopic dermatitis
are at increased risk. Eczema vaccinatum
can occur regardless of whether the
eczema/atopic dermatitis is active at the time
of vaccination
•Virus implanted in disrupted skin (may be at
multiple sites) spreads from cell to cell
producing extensive lesions dependent on
extent of abnormal skin.
•Treatment should include hospitalization and
urgent treatment with VIG. Mortality has been
prevented in patients treated promptly and
adequately.
•Severe cases and fatalities have been
observed after contact of recently vaccinated
persons with persons who have active
eczema/atopic dermatitis or a history of
eczema/atopic dermatitis.
Eczema
vaccinatum.
Eczema vaccinatum.
Eczema vaccinatum
in contact to recently
vaccinated child.
Recovered without
sequelae or
permanent ocular
damage.
Eczema vaccinatum in an unvaccinated contact to a
vaccinated sibling. [from Fenner F., Henderson DA, et al.
Smallpox and its Eradication. WHO. 1988].
Generalized vaccinia
•Generalized vaccinia consists of vesicles or
pustules appearing on normal skin distant from
the vaccination site.
•In the past, it was estimated to occur in 242
per million primary vaccinees.
•It is believed to result from a vaccinia viremia
with skin manifestations.
•Most rashes labeled as generalized vaccinia
produce only minor illness with little residual
damage.
•The rash is generally self-limited and usually
requires only supportive therapy. However,
patients with underlying immunosuppressed
illnesses may have a toxic course and require
Vaccinia Immune Globulin (VIG).
Generalized vaccinia in an apparently normal child. Recovered without
sequelae.
Accidental implantations or
Autoinocculation
This child touched his inoculation
site and inoculated his lower lid
with vaccinia virus
.
More common, but of less concern are accidental implantations, erythematous or
urticarial rashes, and “generalized vaccinia.” Accidental implantation occurs
when a patient scratches his/her vaccination site, and then scratches an eye, the
anus or genitals, or another skin disorder such as poison ivy. This creates a
coprimary lesion distant from the intended vaccination site. When vaccinia infects
the eye, care must be taken to examine for keratitis. About 6% of patients with
vaccinia in the eye develop vaccinial keratitis; VIG is contraindicated in such
patients, because they may get antigen-antibody precipitates in the cornea causing
scarring.
Inadvertent Inoculation
•Successful vaccination produces a lesion at the vaccination site. Beginning
about four days after vaccination, the florid site contains high titers of
vaccinia virus. This surface is easily transferred to the hands and to
fomites, especially since itching is a common part of the local reaction.
•Accidental implantation occurs due to transfer of vaccinia virus from the
primary site to other parts of the body, or to other individuals.
•This is the most frequent complication of smallpox vaccination (529
per million primary vaccinees), accounting for approximately half of all
complications of primary vaccination and revaccination.
•Lesions of inadvertent inoculation can occur anywhere on the body,
but the most common sites are the face, eyelid, nose, mouth, genitalia,
and rectum. Lesions in eczematous skin, in disrupted skin and in the
eye pose special hazards, as the infection can be extensive in skin
lesions and a threat to eyesight in the eye.
•Most lesions heal without specific treatment
Vaccinia keratitis
•Vaccinia keratitis results in lesions of the cornea due to
accidental implantation of vaccinia virus, and is potentially
threatening to eyesight.
•Symptoms appear ten days after transfer of vaccinia virus.
•Left untreated, considerable corneal scarring may result as
lesion heals resulting in significant impairment of vision.
•Topical antiviral agents are the treatment of choice; therapy
should be determined in immediate consultation with an
experienced ophthalmologist.
Progressive vaccinia
•Progressive vaccinia, also known as vaccinia
necrosum, is a severe, potentially fatal illness
characterized by progressive necrosis in the
area of vaccination, often with metastatic
lesions (e.g., lesions at places other than the
vaccination site).
•In the past, it was estimated that progressive
vaccinia occurred in approximately 1 to 2 per
million primary vaccinations, and was almost
always fatal before the introduction of VIG and
antiviral agents.
•Rare in the past, it may be a greater threat
today, given the larger proportion of
susceptible persons in the population and the
greater number with immunocompromise.
Nearly all instances have been in people with
defined cell-mediated immune defect (T-cell
deficiency).
•Prompt hospitalization and aggressive use of
VIG are required.
•Massive doses of VIG are necessary to
control viremia. Up to 10 ml per kg of
intramuscular VIG has been used.
•There is no proven antiviral therapy.
Preliminary studies with cidofovir show some
antiviral effect in vitro; studies in animals are
pending.
•Immediate consultation with the CDC is
recommended to determine if any experimental
antiviral drugs are available.
Electronic sources of dermatological information
Dermatology Online Journal
tray.dermatology.uiowa.edu/home.html
Internet Dermatology Society
RxDerm-L
Tumours of the skin, University of
California at Davis
Dermatology online atlas
Dermatology atlas
www.telemedicine.org
listpro@ucdavis.edu
(email)
matrix.ucdavis.edu/tumors/tradition/tumors
.html
www.derma.med.unierlangen.de/index_e.htm
www.meddean.luc.edu/lumen/medEd/medici
ne/dermatology/melton/atlas.htm
Skin cancer and benign tumor image atlas
www.meddean.luc.edu/lumen/medEd/medici
ne/dermatology/content.htm
Dermatology image bank
www.tmc.edu.tw/medimage/derma_bank/def
ault_eng.htm
www.telemedicine.org/contact.htm
www.dermnet.org.nz/dna2a.html
erl.pathology.iupui.edu/cases/dermcases/der
mcases.cfm
www.skindex.
Contact dermatitis
DermNet (atlas and information)
Virtual Dermatology (case directory)
Skindex-case directory (news, reviews, treatment
trends, meeting reports, CME, case reports,
disease descriptions, atlas, Q&A site)