rash illness training

Rash IllnessRash IllnessPaige Jordan RN, BSNPaige Jordan RN, BSN

Region II Region II EpidemiologistEpidemiologist

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

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 ActionEducate 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).

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)


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 ActionTriage reports of pustular/ vesicular rash illness according to CDC criteria, as follows: High riskHigh risk

Febrile prodrome AND Classic smallpox lesions AND Lesions in same stage of development

Moderate risk Moderate risk Febrile prodrome AND 1 major OR >=4 minor criteria

Low riskLow risk No/mild febrile prodrome Febrile prodrome and < 4 minor criteria

Rash Illness AlgorithmGoal 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.

Varicella TestingOptional

History and ExamHighly Suggestive

of Varicella

Test for VZVand Other Conditions

as Indicated

DiagnosisUncertain

L ow Risk for S m a llpox(see criteria below )

Non-Sm allpoxDiagnosis Confirm ed

Report Results to Infx Control

Cannot R/O Sm allpoxContact Local/State Health Dept

No Diagnosis M adeEnsure Adequacy of Specim en

ID or Derm ConsultantRe-Evaluates Patient

ID and/or Derm ConsultationVZV +/- Other Lab Testing

as indicated

M odera te R isk of S m allpox(see criteria below )

NOT Sm allpoxFurther Testing

SM ALLPOX

Testing at CDC

Sm allpox Response TeamCollects Specim ens andAdvises on M anagem ent

ID and/or Derm ConsultationAlert Infx Control &

Local and State Health Depts

High Risk for S m a llpox(see criteria below )

Institute Airborne & Contact PrecautionsA le rt In fec tion C ontro l on A dm iss ion

Pa tient w ithAcute, G enera lized

Vesicula r or Pustula r R a sh Illness

Evaluating Patients for Smallpox

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.

High Risk of Smallpox Report Report ImmediatelyImmediately


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 Moderate Risk of Smallpox Urgent Urgent EvaluationEvaluation

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 ActionLow Risk of Smallpox Manage as Manage as

Clinically IndicatedClinically Indicated

Assure collection of appropriate clinical samples for testing

SmallpoxChickenpoxMeaslesHerpes simplesMonkeypoxRickettsialpox

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 FeaturesThree stages of disease

IncubationAsymptomatic

ProdromalNonspecific febrile illness, flu-like (may be misdiagnosed or ignored)

EruptiveCharacteristic rash

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

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

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

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 Stage

Macules

Papules

Vesicles

Pustules

Crusts

All crusts separated

Days after Rash Days after Rash onsetonset0-1

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)

Day 1 Day 2 Day 3

Few raised spots (papules)

More papules

appear

Rash more distinctfluid accum. to form vesicles

SMALLPOX - RASH PROGRESSION


Day 4SMALLPOX - RASH PROGRESSION

Day 5 Day 7

Vesicles more distinct

Fluid in vesicles becomes

cloudy to form pustules

Rash characteristic of

smallpox no mistake in diagnosis


SMALLPOX - RASH PROGRESSIONDay 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


Smallpox Rash - Distribution

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 TestingSpecimens 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)

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 laboratory-confirmed and does not have an epi link OR

Atypical presentation not lab confirmed but has an epi link to a confirmed or probable case

Smallpox Surveillance

Common Conditions With Vesicular or Pustular Rashes

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

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

Chickenpox Clinical FeaturesProdrome: 0-1 day of fever, anorexia, headacheRash: 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 14Enanthem: Vesicles and shallow erosions most commonly on the hard palate,

but also on nasal mucosa, conjunctiva, pharynx, larynx, GI tract, urinary

tract, vaginaExanthem: Macules, papules, vesicles, crusts in various stages of evolution

.

Chickenpox on the palate.

Glistening, water-drop characteristic of the chickenpox vesicle on the palate.


Chickenpox vesicle behind the ear.

Classic "dew drop on a rose petal" appearance.


Chickenpox Rash

Superficial lesions Not well circumscribed Confluence and umblication uncommon Lesions at all stages of development

Classic Chickenpox Rash

Chickenpox Rash Evolution

StagesStagesMacules

Papules

Vesicles

Crusts

Rapid evolution of macules to papules, vesicles, crusts

All stages simultaneously present

Lesions superficial, distribution centripetal

Scabs fall off in 9-139-13 days

Differentiating FeaturesChickenpox Vs Smallpox

Distinguishing Smallpox from Chickenpox Epi Features that Differ

Chickenpox (varicella)Chickenpox (varicella) Most cases occur in

children

Expected case fatality rate 2-3/100,000

Secondary attack rate of 80% among susceptible household contacts

Smallpox (variola)Smallpox (variola) Most of the population

expected to be susceptible

Expected case fatality rate averages 30%

Secondary attack rate ~60% in unvaccinated family contacts

FEVERFEVER

RASHASHAppearanceAppearance

DevelopmentDevelopment

DistributionDistribution

On palms & On palms & solessoles

DEATHDEATH

SMALLPOXSMALLPOX

AT TIME OF RASH 2-4 DAYS BEFORE RASH

SAME STAGE DIFFERENT STAGES

SLOW

MORE ON ARMS & LEGS

USUALLY PRESENT

> 10%

RAPID

MORE ON BODY

USUALLY ABSENT

VERY UNCOMMON

CHICKENPOXCHICKENPOX

Distinguishing Smallpox from Chickenpox Clinical Features that Differ

Classic Smallpox lesion

Classic Chickenpox lesion

“Dew drops on a rose petal”

Distinguishing Smallpox from Chickenpox Clinical Features that Differ

Rash Distribution

Rash Distribution

Chickenpox

Smallpox

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

SmallpoxMore pocks on face arms and thighs - Pocks same stage of development

Rash DistributionChickenpox

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

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

Rash Distribution

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 EpidemiologyEtiologyDNA 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

HERPES ZOSTERHERPES ZOSTER

Lesions are unilaterallyunilaterally distributed along a dermatome

Lesions at any given time are in different different stages of development (vesicles, pustules, and crusts are in evidence at one time)

SMALLPOXSMALLPOX

Lesions are widely widely distributed

Lesions at any given time are all at the samesame stage of development

Associated with severe constitutional symptoms

Distinguishing Smallpox from Herpes Zoster Clinical Features that Differ

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?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: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 HERPESGenital 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 (ulcersulcers are of similar shape and size)

““The key physical sign of eczema The key physical sign of eczema herpeticum is blisters, pustules, or herpeticum is blisters, pustules, or erosions of a rather uniform size erosions of a rather uniform size and appearance”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

Type of Adverse Event

Age at Vaccination

<1 1-4 5-19 20+

Death (all causes) 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

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 vaccinatumEczema vaccinatumEczema 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 Eczema vaccinatum.vaccinatum.

Eczema vaccinatum.Eczema vaccinatum.

Eczema vaccinatum Eczema vaccinatum in contact to recently in contact to recently vaccinated child. vaccinated child. Recovered without Recovered without sequelae or sequelae or permanent ocular permanent ocular damage.damage.

Eczema vaccinatum in an unvaccinated contact to a Eczema vaccinatum in an unvaccinated contact to a vaccinated sibling. [from Fenner F., Henderson DA, et al. vaccinated sibling. [from Fenner F., Henderson DA, et al. Smallpox and its Eradication. WHO. 1988]. 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

.

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.

This child touched his inoculation site and inoculated his lower lid with vaccinia virus

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 informationDermatology Online Journal tray.dermatology.uiowa.edu/home.html

Internet Dermatology Society www.telemedicine.orgRxDerm-L [email protected]

(email)Tumours of the skin, University of California at Davis

matrix.ucdavis.edu/tumors/tradition/tumors.html

Dermatology online atlas www.derma.med.uni-erlangen.de/index_e.htm

Dermatology atlas www.meddean.luc.edu/lumen/medEd/medicine/dermatology/melton/atlas.htm

Skin cancer and benign tumor image atlas www.meddean.luc.edu/lumen/medEd/medicine/dermatology/content.htm

Dermatology image bank www.tmc.edu.tw/medimage/derma_bank/default_eng.htm

Contact dermatitis www.telemedicine.org/contact.htmDermNet (atlas and information) www.dermnet.org.nz/dna2a.htmlVirtual Dermatology (case directory) erl.pathology.iupui.edu/cases/dermcases/

dermcases.cfmSkindex-case directory (news, reviews, treatment trends, meeting reports, CME, case reports, disease descriptions, atlas, Q&A site)

www.skindex.

rash illness training

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