Transcript Viral Diseases Part 1 Michael Hohnadel KCOM 11/25/03 Herpesvirus Group • Double stranded DNA virus which replicates in the nucleus. • Produces latent, lifelong infection. • Includes:VZV, HSV,

Viral Diseases
Part 1
Michael Hohnadel
KCOM
11/25/03
1
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.
2
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.
3
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.
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–
–
–
–
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 HSV2 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 - Treatment
Primary 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:
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•
•
•
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 the
Immunocompromised
• 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 46 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 preterm 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 Zoster
Disseminated 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 Zoster
Zoster 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:
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•
•
•
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 Zoster
Zoster 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 Zoster
Inflammatory 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.
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–
–
–
–
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 response
1.
2.
Day 5 – papule then vesicle
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 Necrosum
and Vaccinatum reactions.
– Vaccinia Immune Globulin (VIG) reduced
previous mortality significantly.
– Cidofovir possibly helpful.
100
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
102
Farmyard Pox
•
•
Milker’s nodules and Orf.
Presentation: Similar for both entities.
–
Six stages over six weeks.
1.
2.
Stage 1 / Maculopapular - A red elevated lesion.
Stage 2 / Target - A bulla with an irislike configuration (nodule
with a red center, a white middle ring, and a red periphery).
Stage 3 / Acute - A weeping nodule.
Stage 4 / Regenerative - A firm nodule covered by a thin crust
through which black dots are seen.
Stage 5 / Papillomatous - Small papillomas appear over the
surface.
Stage 6 / Regressive - A thick crust covers the resolving
elevation.
3.
4.
5.
6.
–
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.
104
Milker’s Nodule
105
ORF
Early lesion
Target like lesion.
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Orf
107
Orf
108
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.
109
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.
110
Parapoxvirus from Wildlife
• Several cases of infection from cleaning
deer or camping in area with wild deer.
• Viral particles identified by EM.
111