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Viral DiseasesPart 1

Michael Hohnadel

KCOM

11/25/03

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Herpesvirus Group

• Double stranded DNA virus which replicates in the nucleus.

• Produces latent, lifelong infection.

• Includes:VZV, HSV, CMV, EBV, Human Herpes virus – 6, -7, -8. Animal Virus.

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Herpes Simplex• One of most prevalent infections

worldwide.• 85% of adults are seropositive for HSV-1.• 20% adults seropositive for HSV-2.• More are infected than symptomatic disease

would indicate. – 50% HSV-1 infected individuals asymptomatic.– 20% HSV-2 individuals asymptomatic.

• 60% of others do not recognize symptoms as those of HSV-2.

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Herpes Simplex• Diagnosis

– Tzanck Smear: • 60-90% accurate, 3-13 % false +• Nonspecific (HSV and VZV)• Used on acute vesicular lesions • Multinucleated giant cells jig saw nucleus.

– D. I. F.• More accurate• Identifies virus type.

– Viral culture– PCR– Biopsy with immunoperoxidase

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Tzanck Smear

Multinucleated giant cell

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Herpes Simplex

• Serologic testing– Not used to determine if skin lesion is HSV.

• Only indicates infection, not cause of lesion.

• High background positive.

• Used if need to know if previously infected

– Treatment:• Acyclovir, Valacyclovir.

• Action : Acyclic nucleoside analog of guanosine which inhibits HSV DNA polymerase.

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Orolabial Herpes • 95 % HSV –1• Presentation: Grouped vesicles on an

erythematous base. – May occur anywhere inoculated.– Often prodrome of tingling or itching.– Variable severity of recurrent lesions.– Mild flu like symptoms may be present.– UVB exposure frequent trigger.

• Herpetic Gingivostomatitis– 1 % of infections– Erosions , ulcers in mouth with white base associated

with fever, lymphadenopathy and malaise.

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Orolabial Herpes

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Orolabial Herpes• Treatment:

– Prevention with sun block and UVB avoidance.

– Acyclovir 200mg bid.

– Acyclovir 200mg 5x / day

– Prophylaxis for dermabrasion, chemical peels, laser resurfacing.

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Herpetic Infections• Herpetic Sycosis

– blade shaving after facial herpes induces a slowly spreading folliculitis of the beard with few isolated vesicles.

• Herpes Gladiatorum

• Herpetic whitlow– Herpetic infection of the fingers.– Healthcare workers, children (thumb sucking)– Adults: 2/3 cases HSV-2, Children nearly 100% HSV-1

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Herpetic Infections

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Herpetic Whitlow

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Herpetic Infections

• Herpetic Keratoconjunctivitis– Punctate keratitis or as dendritic ulcers.

– Common cause of vision impairment in the U.S.

– Topical Corticosteroids may cause corneal ulceration.

– Recurrences are common.

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Herpetic Keratoconjunctivitis

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Herpetic Infections• Recurrent Erythema Multiforme Minor

– H.A.E.M. caused by HSV-1 in most cases.

– Presentation: Papules some of which become classic E.M. target lesions of palms, elbows, knees and oral mucosa.

– Atypical lesions: 3% multiple or solitary large red painful plaques, subcutaneous nodules or asymmetric targets.

– Chronic Acyclovir to prevent.

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Erythema Multiforme Minor

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Genital Herpes• Infection of HSV-2 in 85% of cases. • Spread by Skin to Skin contact

– Active lesions are infective– Asymptomatic shedding accounts for the majority of

transmission.

• Prior HSV-1 infection does not protect from HSV-2 infection but may lessen severity of first outbreak.

• Primary infection: – Grouped vesicles which appear for 7-14 days.– Fever, Flu like symptoms, inguinal lymphadenopathy,

proctitis if rectal involvement.

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Genital Herpes

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Genital Herpes

• Recurrent lesions with typical prodrome of burning/itching followed by the formation of grouped vesicles which form erosions and heal without scarring over 7 days.

• HSV-2 facts:– 20% truly asymptomatic, 20% recognize their

lesions, 60% have lesion but don’t recognize them as HSV or don’t notice them at all.

– Recurrences are common (6 / year).

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Genital Herpes - TreatmentPrimary Lesions

Acyclovir 200-400 mg five times/ day. Also, Valacyclovir 1000 mg bid.

Recurrent lesions ( >6 lesions/ year)– Acute lesions

• Acyclovir 200mg 5 times daily. Also, Valacyclovir 500 mg bid.

– Suppressive therapy• Acyclovir 400 mg bid or tid suppresses 85 % of recurrences.

20 % recurrence free during TX.• Also Valacyclovir 500 mg QD (1000 mg QD if > 10

recurrences / year.)

• After 10 years of suppressive TX, many pts can stop medication and retain a reduction in number of lesions.

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Intrauterine and Neonatal Herpes

• Prevalence 1500 – 2000 cases / year.

• 70 % HSV-2 acquired at time of delivery.

• Intrauterine infection (rare)– Primary lesions of mother– May cause fetal anomalies: skin lesions, scars,

microcephally, microphthalamos, encephalitis, calcifications.

– Almost always permanent sequelae.

• HSV-1 acquired through postnatally by contact with orolabial disease.

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Intrauterine and Neonatal Herpes

• Extent of initial involvement predicts outcome:– Localized: rarely fatal. 10% with long term sequelae

– Disseminated disease fatal 15-20%. If brain dissemination, 50% with long term sequelae.

• Presentations in newborns– 70% present with skin vesicles. Incubation of 3 wks,

vesicles may appear after discharge.

– Disseminated herpes with CNS involvement may occur without skin involvement.

– 20% of cases never have vesicles.

– TX: Acyclovir 250 mg/(m)^2 q8 hours x7 days

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Neonatal Herpes

•

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Neonatal Herpes

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Intrauterine and Neonatal Herpes• Prevention and management:

– 70% of mothers of HSV infected infants are asymptomatic at delivery and have no HX of infection.

– Primary vs secondary infection at time of delivery as well as active lesions important.

• Active recurrent lesion 2-5% risk of HSV infection.

• Active primary lesion 33-50% risk of HSV infection.

– If active lesions at time of delivery then C-section.

– Pregnancy with HSV infection controversial:• Routine cultures not recommended.

• Avoid scalp electrodes.

• HSV-1 more frequently transmitted.

• If primary lesion during pregnancy – Acyclovir during 3rd trimester.

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Disseminated HS infection

• Newborns, premature, malnourished, Immnosup. and children to age 3 years are at risk.

• Presentation: Severe herpetic gingivostomatitis followed by dissemination to viscera esp. the liver, lungs and GI and brain.

• Death possible

• TX Acyclovir

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Eczema Herpeticum

• Also called Kaposi’s Varicelliform eruption.

• Herpes infection in pt with atopic dermatitis results in infection throughout the eczematous areas with hundreds of vesicles.

• Also occurs in: Dariers, pemphigus, pemphigoid, Wiskott-Aldridge or burns.

• Self limited in healthy individuals.

• TX: IV or oral acyclovir in all cases

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Eczema Herpeticum

•

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Eczema Herpeticum

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Herpes Simplex in theImmunocompromised

• Any erosive mucocutaneous lesion should raise suspicion of herpes simples.

• Often less vesicular and more erosive with crusting– Hallmarks: 1.) Pain 2.) active vesicular border 3.)

scalloped periphery.

– Extensive involvement.

• Tzanck smears less valuable (erosions)– DIF is specific and rapid if needed.

• TX: Acyclovir. Consider suppressive therapy– Acyclovir resistance cases: foscarnet

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Immunocompromised

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Immunocompromised

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Varicella

• Infection with Varicella Zoster

• Transmission by contact or respiratory route.

• Initially virus seeds the internal organs at 4-6 days. At 11-20 days the skin eruption occurs.

• Individuals are infectious 4 days before and 5 days after exanthem appears.

• In adults 30.9 / 100,000 death rate.

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Varicella• Presentation: Faint erythematous macules develop

into teardrop vesicles in 24 hours. Fresh crops of vesicles appear for several days on trunk, face or oral mucosa. Vesicles become pustular, umbilicated and crusted. Number of lesions averages about 300.

• Secondary bacterial infection may result in scarring.• Other complications:

– Pneumonia: neonates and adults (1/400)– Reyes syndrome: encephalitis, hepatitis with aspirin use.– Thrombocytopenia– Purpura Fulminans: DIC with low proteins C and S

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Varicella

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Varicella

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Varicella

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Varicella

• Treatment:– Acyclovir for severe cases, high risk

individuals and adults (>13 years).– No Aspirin!!!– Topical Antipruritics– Isolate from immunocompromised.

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Varicella

Prevention:

• Varicella Vaccine– Live attenuated virus– 95% effective

• Those who do contract varicella have mild case.

– At present immunity appears to be lasting.– Modified Varicella-like syndrome (MLSV)

• 15 days after exposure to varicella virus.

• 35-50 macules and papules, few vesicles.

• Mild, afebrile course lasting 5 days

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Varicella in Pregnancy• Increased risk of spontaneous abortion (3%

by 20 wks), congenital varicella syndrome and fetal death. Possible increase in pre-term labor.

• Mother at increased risk for varicella pneumonia.

• Congenital Varicella Syndrome– Hypoplastic limbs, scars, ocular and CNS

disease.– F > M– 1-2% risk, highest between weeks 13 and 20.

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Congenital Varicella Syndrome

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Varicella in Pregnancy• Fetal infection may result in Herpes Zoster

early in life (<2 yrs). – Occurs in 1% of VZ complicated pregnancies

with highest risk at wks 25-36 wks gestation.

• Prevention: VZIG for non-immune pregnant mothers within the first 72-96 hours of exposure.– Use only with proven seronegativity. Only

20% of those who relate neg. HX of VAR infection earlier in life are seronegative.

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Varicella in Pregnancy

Neonatal Risk

• Mother who develops varicella 5 days before to 2 days after childbirth places newborn at risk for severe varicella.

• Virus acquired transplacentally before mother has produced antibodies. Newborns immune system is very vulnerable.

• Treatment: VZIG and Acyclovir– No treatment mortality 30%

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Varicella in the Immunocompromised • May result severe and protracted infections.

– Consider in cancer, AIDS and for those on systemic steroids or other immunosuppressive meds.

– More numerous lesions, more necrotic lesions, Large lesions.

– Prior infection is not protective• Non dermatome distribution may indicate

reactivation.

– Before TX available, 1/3 of children with cancer developed complications of varicella and 7% died.

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Varicella in the Immunocompromised• Treatment and Prevention

– VZIG• Given within 96 hours after high risk exposure

– Household contact with VZ, face to face/5 min contact, Indoors with VZ for 1 hour.

• Reduces severity of infection, not frequency.• No proven value once clinical disease develops.

– Varicella vaccination before anticipated immunosuppression is helpful

– Acyclovir• IV acyclovir given until two days after new vesicles stop

appearing. In HIV cases, until vesicles have healed.• Also: Valacyclovir, Famciclovir.• Crucial to give for adequate time in adequate dose to

prevent resistance.

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Herpes Zoster• Reactivation of latent herpes zoster infection from

the dorsal root ganglia– Over 1-5 days new lesions develop. These become

pustular and crust.– Typically along a dermatome with some overflow to

adjacent dermatomes.– Preceded by pain, itching several days

• Duration of the lesion is dependent on:– Age. Young = 2-3wks, Older = 5-6wks– Severity of lesions– Immunosuppression

• Incidence of H.Z. increases with age (esp>50 yrs) and immunosuppression.

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Herpes Zoster

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Herpes Zoster• Heals without scaring in young. Increased

incidence of scaring in elderly and severe eruptions.

• Subtypes of Herpes ZosterDisseminated Zoster

• Defined as >20 vesicles outside dermatome.

• Chiefly elderly or Immunocompromised

• Hemorrhagic/gangrenous lesions with outlying vesicles or bullae.

• Systemic symptoms include fever, H.A., meningeal irritation. Rarely, encephalitis.

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Disseminated Herpes Zoster

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Herpes ZosterZoster Subtypes (Continued)

Ophthalmic Zoster– Involvement of fifth cranial nerve, ophthalmic branch

– Lesion location verses eye involvement:• If tip/side of nose ‘Hutchinson’s sign’, eyeball affected 76 %

vs 34 % if not involved.

• If lid margin affected virtually 100 % involvement.

– Ocular complications:• Uveitis 92 %

• Keratitis 50 %

• Less common: glaucoma, optic neuritis, retinal necrosis

• Other: encephalitis

– Lesions tend to reoccur (as long as ten years).

– Ophthalmology consult.

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Hutchinson’s sign

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Herpes ZosterZoster Subtypes (Continued)

• Ramsay Hunt syndrome– Facial and auditory nerve involvement

with inflammation of geniculate ganglion.

– Zoster of external ear or TM, herpes auricularis, with ipsilateral facial paralysis

– Herpes auricularis, facial paralysis and auditory symptoms.

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Ramsay Hunt syndrome

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Herpes ZosterInflammatory skin lesions following H.Z.

– Occur 1-3 months in previously affected dermatome.

– Flat topped or annular papules– Granulomatous histopathology with no viral

genome.– Resolve spontaneously. Topical or intralesional

steroids may be used

• Diagnosis of Herpes Zoster– Tzanck, direct fluorescent antibody, culture,

PCR.

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Herpes Zoster Treatment

• Corticosteriods– Reduce severity of acute pain, returns pt to full

activity sooner.– No evidence that they shorten duration of acute

pain or prevent post herpetic neuralgia when given with an antiviral.

• Acyclovir – May lessen severity of symptoms in acute

outbreak. May lessen incidence of PHN.

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Herpes Zoster

• Postherpetic neuralgia– Persistent pain after cutaneous lesion

heal.

– Age dependant: Rare under 40yrs. 75% over 70 will have pain beyond one month.• Usually gradual improvement• Pain may worsen or persist for years.

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Herpes Zoster

Treatment of Post Herpetic Neuralgia (Quick intervention)• Topical: Capsaicin, topical lidocaine,

aspirin.• Oral analgesics: NSAIDS• Tricyclic antidepressants +/- neurontin• Injected: lidocaine/steriod solutions• Opiates• Nerve blocks can provide long lasting

relief.

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Epstein Barr Virus• Infectious mononucleosis• General: After 3-7 wk incubation period,

bilateral enlargement of cervical and other lymph glands with high fever, malaise and HA, possible enlargement of the spleen. Pharyngitis with hyperplasia of lymphoid tissue are the most frequent signs. Atypical lymphocytosis.

• Cutaneous presentation: edema of eyelids and a macular or morbilliform rash. Macular eruption is located on trunk. Mucous membranes with 5-20 pinhead sized petechiae at junction of soft palate with hard. (Forsheimer spots)– Rarely: scarlatiniform, herpetiform, E.M., purpura.

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Forsheimer spots

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Morbilliform Reaction after Ampicillin

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Epstein Barr Virus

• Lab findings:– WBC count 10,000 to 40,000.– Abnormal large lymphocytes (Downey cells)

are 10% of total leukocyte count.– Heterophile antibodies 1:160 of higher

• EBV is associated with lymphoma esp. Hodgkin's disease.

• Treatment: supportive.

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Infectious mononucleosis

Reactive atypical lymphocytes have pleomorphic reticular nuclei, peripheral basophilia of cytoplasm, and scalloped cell borders

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Oral Hairy Leukoplakia• Associated with chronic shedding of EBV in the

oral cavity.• Presentation: Poorly demarcated, corrugated,

white plaques on lateral aspect of tongue.• Unlike thrush, cannot be removed by scraping.• Occurs with immunosuppression (esp AIDS) and

warrants HIV workup.• Treatment

– No required– If requested: podophyllin and tretinoin are used but

lesions will reoccur.

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Oral Hairy Leukoplakia

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Cytomegalic Inclusion Disease• Infects 50-80% of adults, 1% of newborns.• Newborns:

– 90% asymptomatic– 10% with symptoms. More severe if

mother had a primary infection.• Systemic:

– Jaundice, hepatosplenomegally, calcifications, chorioretinitis, MR, deafness, microcephally.

• Cutaneous: – Petechia, prupura and ecchymosis

– ‘Bluberry muffin baby’ - generlized macular, papular erruption.

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‘Blueberry Muffin’ CMV

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TORCH infant with CMV

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Cytomegalic Inclusion Disease• Symptomatic infection in adults is unusual

and is like that of EBV.– May see morbilliform eruption if ampicillin

given.

• CMV infection of the skin:– Rare, usually immunosuppressed. Identical to

HSV or VZ

– May cause superficial ulcerations or fissures of oral or anal area. Erosive diaper dermatitis

– Pathogenic CMV is present in the dermal vessels, not the epithelium.

– Difficult to determine CMV as causative.

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CMV Ulcerations

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Cytomegalic Inclusion Disease

• Treatment of CMV ulcerations– CMV virus is diagnosis of exclusion.

• Normal skin can shed CMV. Pathogenicity hard to prove. Electron microscopy can’t distinguish among HSV, VZ and CMV.

– Antiherpetic agents: acyclovir, foscarnet, gancyclovir, cidofovir.

– Lesions that fail to respond treated as aphthous equivalents

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Human Herpesvirus 6 and 7

• Roseola Infantum (sixth disease)– Presentation: Onset of high fever which

resolves in about 4 days followed by a morbilliform erythema of rose colored macules on neck, trunk and buttocks and sometimes the face and extremities.

• Halo may surround lesions.• Complete resolution in 1-2 days.

• HHV 6 infection is nearly universal.• HHV 7 similar to 6. May occur later.• In adults, may resemble mononucleosis.

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Roseola Infantum

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Roseola Infantum

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Human Herpes Virus 8• HHV-8 is found to be associated with Kaposi’s

Sarcoma in virtually all cases.– Includes AIDs, African and Mediterranean cases.– Seroprevalence correlates with prevalence of KS in a

given population.– Infection predicts and precedes subsequent

development of KS.– HHS-8 is found in KS lesions, saliva, blood and semen

of infected individuals.

• Associated with body cavity based B-cell lymphoma.

• Found in all cases of Castlemans disease assoc with HIV, and a large portion of non-HIV cases.

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Kaposi’s Sarcoma

Plump spindled cells outlining vascular spaces

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Kaposi’s Sarcoma

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B Virus• Herpesvirus Simiae. Infects monkeys with

vesicular lesions similar to HSV on oral mucosa, lips or skin.

• Humans infected by contact.• Within a few days of the bite, vesicles and intense

erythema appear at site of injury with rapid progression to fatal encephalitis in many cases (15 of 22 studied). All survivors of encephalitis had severe neurological sequelae.

• Recurrence is possible in infected individual.• Treatment: Early antiviral HSV.

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B Virus

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B Virus

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Gianotti-Crosti Syndrome• Presentation: Monomorphous eruption of flat

topped, erythematous papules or papulovesicles, 1-5 mm in diameter that erupt suddenly and symmetrically.– Favors face, buttocks and extensors and spares the trunk.– Last 2-4 weeks– Pruritis is variable– Mucous membranes are spared.– May have lymph node enlargement, spleenomegally.

• Affects children 6 mo to 14 yrs.• Association with Hep-B and many other viral

infections.– Acute anicteric Hep-B symptoms occur near time of

onset.

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Gianotti-Crosti Syndrome

•

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Gianotti-Crosti Syndrome

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Hepatitis B infection • Presentations

– Urticaria, arthralgias, GN, vasculitis several days to weeks before onset of clinically apparent liver disease.

• 10-20% of infections.

• Nearly always yields clinical Hep-B.

• Due to Hep-B antigenemia and tracks resolution of antigen.

– PAN may be seen during acute infection or up to 12 years post infection

• Hep-B may be silent.

• 593 dermatologist 15.4% showed evidence of previous Hep-B infection !!!!– Get Vaccinated.

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Hepatitis-C Infection

• 50% infected become chronic, 50% with cirrhosis. Increased hepatocellular carcinoma.

• Presentations:– Necrotizing vasculitis assoc with Type II

cryoglobulin in 84% of cases. Leukocytoclastic vasculitis.

• 2-5% of Hep-C infections.

• Palpable purpura of LE most common presentation.

• Also: Livedo reticularis and Urticaria.

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Hepatitis-C Infection

• Presentations (con’t)– 12-31% of PAN patients Hep-C positive.– PCT associated. 10-95% based on population

studied.• Interferon helps

– 4-38% of Lichen Planus patients have HCV.• Interferon may not help.

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Variola Major‘Small Pox’

• History:– Last reported cases in U.S. 1949 in Texas.– Last Case in world Somalia 1977-80’s ?– Last public U.S. vaccination 1972.

• Spread by respiratory droplets, infected skin contact, shed skin.

• Presentation: – After an incubation of 12 days, sudden onset of fever

and malaise which cease abruptly when exanthem appears.

– In synchrony, erythematous macules become papular then vesicular, pustular and finally crust in two weeks.

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Variola Major• Centrifugal pattern (face arms legs worse).

• Deep seated, large vesicles. Vesicles may occur on palms and soles.

• Crust separate to leave fresh scars, permanent in half of cases.

• Complications: pneumonitits, corneal destruction, encephalitis, jt. effusions, osteitis.

• Contagious period.– Less contagious when fever begins– Most contagious when lesions develop and remains

contagious until the last scab is shed.

• Treatment - supportive

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Variola Major

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Variola Major

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Variola Major

Public Health Bioterrorism Issues• Pre-1972 vaccinations are not considered

protective at present but may reduce severity.• Currently, enough vaccine (diluted) for entire U.S.

population.• Time window to receive vaccination should

outbreaks occur:– If given within 3 days of exposure, vaccination is

protective/greatly reduces severity of infection.

– Within 4-7 days is likely beneficial to outcome.

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Chickenpox vs Smallpox

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Vaccinia• Not currently available to general public.• Used for immunization after 1 year of age.• Hybrid of Cowpox and Variola• Expected Patterns of Vaccination reactions:

1. Primary response1. Day 5 – papule then vesicle2. Day 9 – Maximal reaction with pustule and regional lymph

node enlargement.

2. Accelerated response in partially immune: Vesicle which involutes by day 10.

3. Immediate reaction in immune: Papule which involutes by 3rd day.

4. Typically heals with scarring.

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Vaccinia - Unimmunized

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Specific Contraindications to Routine Vaccination

See AAD Guidelines.

•Allergy to smallpox vaccine or components

•Heart problems

•Skin conditions

•Weakened immune system

•Pregnancy/breastfeeding

•Infants and children

•Moderate or severe illness

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Vaccinia

Complications of Vaccination:• Generalized Vaccinia

– 4-10 days after vaccination papules become papulovesicles become pustules in crops which involutes over 3 wks.

• Ocular paralysis, retinitis.

• Autoinoculation to other body sites from own vaccination of someone else.

• Eczema Vaccinatum– Widespread lesions in chronic dermatitis

– 1% mortality

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Eczema Vaccinatum

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Vaccinia• Vaccinia Necrosum

– Vesicular involving the skin and mucous membranes which persist for months and become gangrenous resulting in death in 33%.

– TX: Vaccinia immune globulin from red cross.

• Roseola Vaccinia– Extensive, symmetric, morbilliform eruption appearing

2 weeks after vaccination. Vaccination site with crust and large erythematous halo.

• Do not coalesce

• Involutes in several days.

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Vaccinia Necrosum

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Roseola Vaccinia

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Vaccinia Reactions

Treatment for Vaccinia Necrosumand Vaccinatum reactions.

– Vaccinia Immune Globulin (VIG) reduced previous mortality significantly.

– Cidofovir possibly helpful.

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Cowpox• Presentation: Solitary macule/vesicle/pustule

evolution. Becomes blue-purple and hemorrhagic. A 1-3 cm, painful eschar develops after 2-3 wks. – Always painful– Lymphadenopathy. Systemically ill pt.– Heals 6-8 weeks with scarring

• Etiology: Orthopoxvirus restricted to Britain, Europe and Russia.

• Zoonosis. (Small animals are usual source.)

– Domestic cat usual source of infection. Infects cows rarely. (Catpox ??)

• DX: viral culture, Serology.• TX: No treatment.

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Cowpox

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Farmyard Pox• Milker’s nodules and Orf.• Presentation: Similar for both entities.

– Six stages over six weeks.1. Stage 1 / Maculopapular - A red elevated lesion.2. Stage 2 / Target - A bulla with an irislike configuration (nodule

with a red center, a white middle ring, and a red periphery).3. Stage 3 / Acute - A weeping nodule.4. Stage 4 / Regenerative - A firm nodule covered by a thin crust

through which black dots are seen.5. Stage 5 / Papillomatous - Small papillomas appear over the

surface.6. Stage 6 / Regressive - A thick crust covers the resolving

elevation.

– Mild systemic symptoms (compare to cowpox)

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Farmyard Pox• Milker’s nodule

– Occupational disease of vets and milkers transmitted by utters of cows.

– Usually solitary lesions with course as described prev.

• Orf– Sheep farmers. Common affliction. – Transmitted by direct contact or through

fomites since virus is durable.

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Milker’s Nodule

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ORF

Early lesion

Target like lesion.

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Orf

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Orf

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Farmyard Pox

• Histologic features: – Pseudoepitheliomatous hyperplasia.

Keratinocytes with viral inclusion with pale halo and vacuolization. Massive capillary proliferation and dilation.

• Treatment: – Supportive. Shave may shorten duration.– No human to human transmission occurs.

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Bovine Papular Stomatitis

• Presentation: After 5-8 day incubation, a lesion similar to milkers nodule forms lasting about 3 wks.

• Affected cattle may not have evident lesions. (Unlike milker’s nodule)

• DX: virus culture

• TX: Self limited.

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Parapoxvirus from Wildlife

• Several cases of infection from cleaning deer or camping in area with wild deer.

• Viral particles identified by EM.