Test 2- Poxviradae Flashcards
Properties of Poxviruses
Large, sometimes enveloped, DNA viruses with complex structure (symmetry)
Most poxviruses are pleomorphic, typically brick-shaped.
Possess an irregular surface of projecting tubular or globular structures.
On the other hand, members of the genus Parapoxvirus are ovoid, covered with long thread-like surface tubules, which appear to be arranged in crisscross fashion, resembling a ball of yarn.
top: Orthopoxviruses
bottom: Parapoxviruses
Two distinct infectious poxvirus particles exists:
the intracellular mature virus (IMV) and
the extracellular enveloped virus (EEV). Both forms are infectious.
The extracellular forms (EEV - extracellular enveloped virions)
Envelope
Inner Membrane
has an envelope that they get from the host cytoplasmic membrane- virus comes out via budding
Virions that are released from cells by budding, rather than by cellular disruption,
Virions that are released from cells by budding, rather than by cellular disruption, acquire the extra envelope that contains virus encoded-proteins from host cell membrane.
Intracellular viral particles (IMV - intracellular mature virions)
Intracellular viral particles (IMV - intracellular mature virions) only have an inner membrane. IMV come out by disruption of host cell and have only inner membrane.
does not have a lipid envelope
infectious
Symmetry of Poxviruses
Do not confirm to icosahedral or helical symmetry. Poxviruses have complex symmetry.
The virion outer layer encloses a dumbbell-shaped core and two lateral bodies.
The core contains the viral DNA, together with several proteins.
Poxviruses have more than 200 genes in their genomes, and as many as 100 of these encode proteins that are contained in virions.
genome of poxviruses
The genome of poxviruses consists of a single molecule of linear double-stranded DNA varying in size from 130 kbp (parapoxviruses), to 280 kbp (fowlpox virus), up to 375 kbp (entomopoxviruses).
Poxvirus genomes have cross-links that join the two DNA strands at both ends.
Many proteins encoded by the poxvirus genome are enzymes involved in nucleic acid synthesis and virion structural components.
Also encode proteins that specifically counteract host adaptive and innate immune responses.
Replication of Poxvirdae
Replication of poxviruses occurs predominantly, if not exclusively, in the cytoplasm.
This is possible, because unlike other DNA viruses, poxviruses have evolved to encode the enzymes required for transcription and replication of the viral genome.
Following replication, virions are released by budding (enveloped virions), by exocytosis, or by cell lysis- destruction of the cells(non-enveloped virions).
Most virions are not enveloped and are released by cell lysis.
Both enveloped and non-enveloped virions are infectious.
Enveloped virions are taken up by cells more readily and appear to be more important in the spread of virions through the body of the animal. Thus enveloped are more virulent.
Antigenic Characteristics
All poxviruses share group-specific nucleoprotein (NP) –exposed following alkaline digestion of the virus
Genetic recombination among the viruses within a genus results in extensive serological cross-reactions and cross-protections none between different genera.
Production of a hemagglutinin by only Orthopoxviruses
Stability of Poxviradea
The virion of a poxvirus is an enveloped particle that differs significantly from other enveloped viruses.
Unlike other enveloped viruses, poxviruses show a high environmental stability and remain infectious over a period of several months in an ambient environment.
Due to their low lipid content, they are less sensitive to organic solvents/disinfectants compared to other enveloped viruses.
Poxviruses show an extraordinary high resistance to drying.
Can survive for many years in dried scabs or other virus-laden material.
Transmission of Poxviradea
Poxviruses are transmitted between animals by several routes:
Skin: Poxviruses cannot infect intact skin. Contact of infectious material with broken or lacerated skin is a common route of poxvirus transmission.
Respiratory route: Some poxviruses can be transmitted by the aerosol route. Inhalation of aerosol can result in infection (sheeppox virus).
Mechanically transmitted( no replication in the arthopod) by biting arthropods (Myxoma virus and avipoxviruses).
Pathogenesis and Immunity
Poxviruses are highly Epitheliotropic, causing cutaneous (skin) lesions.
Occasionally, poxviruses causes systemic diseases in birds and wild animals.
Many poxviruses are host specific.
However, Orthopoxviruses infect a wide range of species.
Spread of Poxvirus
Following introduction into the body, the poxvirus usually gains access to the systemic circulation via the lymphatic system.
A secondary viremia disseminates the virus back to the skin and to other target organs.
Skin Lesions in Poxvirus Infection
There are degenerative changes in the epithelium.
Rupture of the pustule can predispose to secondary bacterial infection.
Ulceration may develop.
Poxvirus can survive in the dried scabs for many months or years.
Genus: Orthopoxvirus
Cowpox
Distribution: Endemic only in Europe and Asia
Hosts: Cattle, Wild and Domestic Cats, Humans, Zoo Animals, etc.
Reservoir Host: Rodents
Is zoonotic, but most humans get this from cats
Cowpox in Cattle
Transmission:
Transmission from cow to cow in a herd is through infected milker’s hands or teat cups.
Infected farm cats can also transmit the disease.
Rodents serve as the reservoir and can transmit the disease.
Cowpox in Cattle
Economic Importance:
Losses to farmers due to inconvenience in milking because of soreness of teats and mastitis resulting from secondary bacterial infections.
Cowpox in Cattle Clinical Findings:
Clinical Signs
After an incubation period of 3–7 days, during which cows may be mildly febrile, papules appear on the teats and udder. Sucking calves may develop lesions in mouth.
Vesicles may not be evident or may rupture readily, leaving raw, ulcerated areas that form scabs.
Cowpox ulcer on teat
Cowpox in Cats
Transmission:
Usual route of infection in cats is skin inoculation, probably through a bite or skin wound. Rodents are a common source of infection.
Transmission by Oro-Nasal route is also possible.
In exotic felids (cheetahs), viral pneumonia may be evident.
Cowpox in Cats
Clinical Signs:
Primary Lesions:
Most affected cats have a history of a single primary skin lesion, usually on the head, neck, or a forelimb.
The primary lesion can vary from a small, scabbed wound to a large abscess.
Cow pox in a 4-year-old cat, showing blepharitis (inflammation of eye lids).
primary lesion
Cowpox lesion on limb of cat.
primary lesion
Cowpox in Cats
Clinical Signs:
Secondary Lesions:
Approximately 7–10 days after the primary lesion appears, widespread secondary lesions begin to appear.
Throughout 2–4 days, these develop into discrete, circular, ulcerated papules ~0.5–1 cm in diameter.
The ulcers soon become covered by scabs, and healing is usually complete by ~6 wk.
Many cats show no signs other than skin lesions, but ~20% may develop mild coryza or conjunctivitis.
Complications can result from secondary bacterial infections.
Crusting Papular Lesion
secondary lesion
Multiple Papular Lesions on the Trunk
Ulcerative lesions on the upper and lower lip of a cat with poxvirus infection
Cowpox in Humans
Transmission:
Mainly caused by direct contact to ‘‘cuddly’’ cats.
Rarely from rodents and zoo animals.
Virus is not commonly found in cattle, so chances of getting the virus from the cow is very less.
Coxpox in humans
Clinical Signs:
Macropapular lesions first observed on hands and face. Later develop into vesicular, and then ulcerative lesions.
Enlarged painful local lymph nodes.
Patients may report fever, vomiting, and sore throat.
A 16-year-old boy with generalized cowpox
Monkeypox
In Humans:
Monkeypox is a viral zoonosis with symptoms in humans similar to those seen in the past in smallpox patients.
Monkeypox
In Monkeys:
In monkeys, the disease is characterized by generalized skin eruptions, developing to papules on the trunk, face, palms and soles.
Monkeypox
Transmission in Humans:
Primary infection of humans results from direct contact with the blood, bodily fluids, or rashes of infected animals. In Africa, human infections have been documented through the handling of infected monkeys, Gambian rats or squirrels.
Secondary transmission is human-to-human, resulting from close contact with infected respiratory tract excretions, with the skin lesions of an infected person or with recently contaminated objects.
Monkeypox in Humans
Distribution:
Monkeypox occurs primarily in r_emote villages in Central and West Africa,_ near tropical rainforests.
In 2003, it was accidentally introduced in humans into the USA.
Possible source: Rodents from Ghana.
77 Clinical cases, 26% of the patients had to be hospitalized.
Monkeypox in Humans
Clinical Signs in Humans:
Same as smallpox.
First Phase: Invasion period (0-5 days): Fever, intense headache, lymphadenopathy (swelling of the
lymph node), muscle pain.
Second Phase: Skin eruption period: Evolution of the rash from maculo-papules (lesions with a flat bases) to vesicles (small fluid-filled blisters), pustules, followed by crusts.
monkeypox in humans
Other Orthopoxviruses
Variola (Smallpox in humans)
Camelpox virus (Camels)
Ectromelia virus (Mice, Voles)
Horsepox (Horses, Cattle, Humans)
Rabbitpox virus (Rabbits)
Vaccinia virus (Humans, Cattle, Buffalo, Swine, Rabbits)
Uasin Gishu Disease Virus (Horses)
Pseudocowpox’s genus and nickname
Parapoxviruses
This virus can also infect humans and the condition is commonly referred to as milker’s nodule.
Transmission of Pseudocowpox
Source of infection is the infected cattle.
Contaminated milker’s hands, teat cups
Biting insects may transmit the virus
Calves get infected during sucking infected teats(mechnical transmission)
Semen of bulls
Pseudocowpox is
Pseudocowpox is a viral skin disease that causes mild sores on the teats and udders of cattle.
Pathogenesis of Pseudocowpox
Lesions are characterized by hyperplasia of squamous epithelium
Clinical Signs of Pseudocowpox
Infections are generally mild.
Up to 10 lesions on one teat.
Morbidity rate may reach 100%, but at any given time varies between 5% and 10%, and occasionally up to 50%.
Acute lesions of Pseudocowpox
Erythema to Papules to Vesicle or Pustule to Rupture to Thick Scab
The thick scab is 0.5 to 25cm in diameter, becomes elevated due to accumulation of granulation tissue.
- After 7-10 days, the scab drops off, leaving a Horseshoe-shaped ring of small scabs surrounding a small wart-like granuloma.Pox viruses can survive in the scabs in a dry climate for a long time!
Papule from Pseudocowpox on teat
Pseudocowpox teats of cow
Horseshoe-shaped ring of Pseudocowpox
Chronic Lesions of Pseudocowpox
Chronic Lesions:
Commences as Erythema
Yellow-gray, soft scurfy scabs which are rubbed off during milking
Skin is corrugated
No pain- as compared to acute lesions
Lesions may persist for months
Diagnosis of Pseudocowpox
Horseshoe-shaped ring like lesion are pathognomonic for the disease.
Isolation and detection of the virus by various diagnostic laboratory methods from vesicular fluid or from teat skin.
Differential Diagnosis for Pseudocowpox
Cowpox virus
Bovine herpesvirus ulcerative mammilitis
Vesicular stomatitis
Udder impetigo (bacterial dermatitis characterized by the development of small pustules on the skin of the udder and teats).
Teat chaps and frostbite
Black spot (a form of hyperkeratosis)
Pseudocowpox
Treatment:
Removal of scabs
Burn the scabs to prevent environmental contamination Application of an emollient ointment before milking
Application of astringent preparation after milking.
SMALLPOX
killed Rames IV
2 subfamilies in Poxviridae
Subfamily: Chordopoxvirinae (poxviruses of vertebrates)
Genus: Orthopoxvirus
Genus: Parapoxvirus
Genus: Avipoxvirus
Genus: Capripoxvirus
Genus: Leporipoxvirus
Genus: Suipoxvirus
Genus: Molluscipoxvirus (Myxoma virus)
Genus: Yatapoxvirus (Yaba Monkey Tumor Virus)
Subfamily: Entomopoxvirinae (poxviruses of insects)
Skin lesion pattern in Pox virus
- macule- flat red lesion
- papule- elevated red lesion
- vesicle- blister, thin walled sack filled with fluid
- pustule-
- ulcer- when pustle ruptures- COMPLICATION
- or pustule will form a scab and then a scar
Pseudocowpox
Prevention:
Disinfection. Use iodophor teat dip.
Isolation and treatment of infected cows
Reduce teat trauma, as injuries to skin of teat predisposes to infection.
Pseudocowpox in Humans
(The Milker’s Nodule)
Causes a mild skin lesion known as Milker’s Nodule.
Lesions on the hands of dairy farmers milking teats or vets treating infected cows.
Lesions may vary from multiple vesicles to a single, indurated nodule.
Pseudocowpox in Humans (The Milker’s Nodule)
Contagious Ecthyma
Synonyms: ORF, Scabby Mouth, Contagious Pustular Dermatitis, Sore Mouth
Etiology: Orf virus, Genus Parapoxvirus
Host: Sheep and Goats. Primarily in Lambs and Goat Kids. Morbidity may reach 100% and case fatality rate 5-15%.
Distribution: Worldwide
Contagious Ecthyma
Contagious Ecthyma
Transmission:
Scabs that fall off from the healing lesions contain large number of virus.
Virus are stable in the environment, i.e. remains highly infectious for long periods under dry conditions.
Contaminated instruments, like docking instrument or ear-tagging plier can transmit the virus.
Spread in a flock is very rapid
Virus infects healthy animals primarily through damaged skin.
Oral lesions in lambs or kids result from nursing dams with teat lesions, and vice-versa.
Contagious Ecthyma
Pathogenesis:
Damage of skin is essential to establish infection.
The skin reaction to viral infection consists of a cellular response with necrosis and sloughing of the affected epidermis and underlying stratum papillare of the
dermis.
The cutaneous response to infection includes a delayed-type hypersensitivity
reaction and an influx of inflammatory cells .
The lesions evolve from macule papule vesicle pustule ulcers scab formation.
Immunity is solid, lasts 8 months.
Contagious Ecthyma
Clinical signs:
Contagious Ecthyma
Clinical signs:
The first lesions develop in the mucocutaneous junction and are accompanied by swelling of the lips.
From there, lesions spread to the muzzle and nostrils, surrounding hairy skin and the buccal mucosa.
Animal may find it difficult to take food because of oral lesions: thus - Anorexia and Weight loss.
Goat: Raised, crusted lesions around the commissure of the lips
Goat: Proliferative lesions on lips and mouth
Contagious Ecthyma
Clinical signs:
kits/severe lesions
Affected lambs or kids sucking ewes or goats may result in lesions on teats.
This may predispose to secondary bacterial infection, resulting in mastitis.
Severe cases may show lesions in the genitals, coronets (feet) and ears.
Lesions in feet may result in lameness.
Lesions in scrotum may cause infertility.
Contagious Ecthyma
Lips: Detachment of the Epithelium
Teat: Erosion & Scabs
Contagious Ecthyma
Goat: Proliferative lesion; scabs
Contagious Ecthyma
Contagious Ecthyma
Clinical signs:
Secondary Infections:
Within 1-4 weeks, the scabs drop off and the underlying tissues heal without scarring.
However, complications can result from secondary bacterial infections, or from invasion of lesions by fly larvae.
A malignant form of the disease has also been observed in sheep.
Contagious Ecthyma
Vaccination:
Vaccine is prepared from suspension of scabs in glycerol saline and is painted onto a small area of scarified skin inside the thigh, where a localized lesion develops.
In no circumstances should the vaccine be used on farms that do not have a problem with orf.
You should inspect the lamb 1 week after vaccination for local reactions, which indicates the viability of the vaccine.
Vaccination do not offer long-lasting immunity, ~1-2 years.
Contagious Ecthyma
Vaccination
- when to vaccinate
- in problem herds
In problem flocks/herds, the lambs/kids may need to be vaccinated at 6-8 weeks to help prevent the disease.
In flocks/herds with severe problems, the vaccine may need to be given when the lamb/kid is just 2-3 days old.
Vaccinate pregnant ewes only 7-8 weeks before lambing, not before.
Contagious Ecthyma— ORF in Humans
Frequent in humans handling sheep and goats, in rural areas.
Macro-papular lesions and large nodular lesions in finger, hand, arm, face and even
the penis .
Duration of lesions: 4-9 weeks
Healing occurs without scarring
Secondary bacterial infections of lesions may cause complications.
Contagious Ecthyma ORF in Humans
Genus: Capripoxvirus
Sheep Pox
Goat Pox
Lump Skin Disease (of cattle)
Sheeppox and Goatpox distribution and etiology
Distribution: Endemic in Africa, Asia and parts of Europe Etiology: Members of Genus Capripoxvirus
Sheep pox virus (SPV) and goat pox virus (GPV) were once believed to be
Sheep pox virus (SPV) and goat pox virus (GPV) were once believed to be strains of the same virus, but genetic sequencing has now demonstrated them to be separate viruses.
Most strains of goat and sheeppox are
Most strains are host specific and cause severe clinical disease in either sheep or goats, while some strains have equal virulence in both species.
Can sheep and goat pox be distinguished from each other?
SPV and GPV cannot be distinguished from each other with serological techniques, including viral neutralization.
SPV and GPV are also closely related to
SPV and GPV are also closely related to lumpy skin disease virus in cattle (LSDV), but there is no evidence LSDV causes disease in sheep and goats.
Sheeppox and Goatpox
Transmission:
Highly contagious viruses
Virus enters by respiratory tract and transmission is commonly by aerosol route
Spread can also occur through mucous membrane or abraded skin, especially by direct contact with contaminated iatrogenic materials (iatrogenic)
Virus is present in nasal and oral secretions for several weeks after infection
Virus can survive in dry scabs for months
Evidence for mechanical transmission by biting arthropods.
Sheeppox
Pathogenesis:
Sheeppox is a systemic disease.
The incubation period is followed by a leukocyte-associated viremia.
Thereafter, the virus localizes in the skin and other internal organs.
Deposition of immune-complexes results in severe necrotizing vasculitis develop in arterioles and postcapillary venules of the skin (Type-III Hypersensitivity reaction).
This results in ischemic necrosis of dermis and overlying epidermis.
Sheeppox: 2 forms of the disease
A. Malignantform
B. Benignform
Necrotizing vasculitis in the ear
Sheeppox
A. Malignant form:
Seen in lambs and susceptible nonnative breeds, eg. Merino.
Incubation period: 4-8 days
Initial signs:
Marked depression and prostration
High fever, salivation, lacrimation
Edema of eyelids
Serous nasal discharge that becomes mucopurulent
Later signs:
1-2 days after, pox lesions develop on the skin and on buccal, respiratory, digestive
and urinary tract mucosae.
In malignant form, pox lesions extend to pharynx, larynx, lungs, vagina, abomasum
& spleen. Secondary pneumonia is common. Abortion is rare.
Cutaneous nodules are distributed widely over the body. The nodules, occasionally
become vesicular, pustular and finally scab.
Lesions heal leaving a star-shaped scar, free of hair or wool.
Mortality rate up to 50%.
Case fatality in lambs up to 100%
Sheeppox Benign Form:
B. Benign form:
More common in adults and resistant breeds.
Only skin lesions occur
No, or a very mild systemic reaction
Tail of sheep: Sheep Pox lesions
Sheeppox lesions
sheepox lesions Lesions on the mucosa of the esophagus
Sheeppox
Prevention & Control:
Notifiable disease in most countries of the world.
Prohibition of importation of animals from infected areas.
In case of outbreaks, ring vaccination, destruction of affected flocks and
quaratine of infected premises should be instituted.
Vaccination for sheepox
A large variety of commercial vaccines are now available, including a subunit
vaccine.
Killed vaccines elicit, at best, temporary protection.
Live attenuated vaccines offer excellent protection > 1 year.
GoatPox
Goatpox occurs in Africa, Asia and Parts of Europe.
Goatpox is a reportable disease.
Disease is clinically similar to sheeppox.
Young kids suffer systemic disease with lesions on skin, respiratory and alimentary
mucosae.
Milder form of disease seen in adults.
A flat hemorrhagic form of capripox is seen in some European goats and this has
a high case fatality.
Lesions in the perineum and scrotum
Lumpy Skin Disease
Etiology: Member of genus Capripoxvirus
Distribution: Enzootic in sub-Saharan Africa and Middle east with recent incursion in Iraq.
Transmission: Arthropod vector (most common). Also direct-contact
Host: Cattle, all ages and types are susceptible
Clinical findings: Fever, multiple nodular lesions on skin and mucous membrane, lymphadenopathy. Morbidity reach 80% during epizootics.
Control: Live attenuated vaccines available. Slaughter of affected and in-contact animals.
Lumpy Skin Disease
Genus: Suipoxvirus
Swinepox
Swine pox
Etiology, distribution, host, fatality rate
Etiology: Member of genus Suipoxvirus
Distribution: Worldwide. Widespread sporadic disease
Host: Pigs.
Generally, benign with low mortality and low morbidity in older pigs.
High case fatality in congenitally infected and very young sucking piglets.
Swinepox transmission
Transmission:
Direct contact associated with skin injury. Virus can survive in scab for years.
Mechanical transmission by pig louse, Haematopinus suis. These lice can carry the virus for weeks or months.
Also mechanical transmission by flies and insects.
There is evidence of transplacental infection of neonatal pigs.
Clinical Signs and control of swine pox
- transient fever
Typical pox lesions (erythematous macule papule vesicle pustule
ulcers scab formation)
Skin lesions may occur anywhere, but are most obvious on skin of the abdomen and inner aspects of thighs.
Exudative epidermitis (greasy pig disease) and secondary bacterial dermatitis occasionally occur as a sequel to swine pox.
In severe infections, especially in congenitally-acquired pox infections (where piglets are born with or develop lesions over the entire body shortly after birth), lesions may occur in upper respiratory and digestive tracts.
Control:
Eradication of lice from piggery.
No commercially available vaccine.
Swinepox
Erythematous Lesions
lead to
Synonyms for Contagious Ecthyma
Contagious Ecthyma
(Synonyms: ORF, Scabby Mouth, Contagious Pustular Dermatitis, Sore Mouth)
Congenitally Infected Piglet
Disseminated skin lesions
Swinepox
Genus: Avipoxvirus
Fowlpox and other avian poxviruses
Fowlpox
Etiology: Member of genus Avipoxvirus.
First virus to be grown in embryonated eggs.
Hosts: Highly infectious disease of poultry and turkeys. Distribution: Worldwide
Transmission:
The virus is:
Extremely resistant to desiccation(dryness)
Can survive in exfoliated scabs for long periods.
Routes of transmission of Fowlpox
Virus can be transmitted within a flock through minor wounds and abrasions in mouth, comb, wattles, or skin as a result of fighting, pecking or other injuries.
Mechanically by mosquitoes, lice, and ticks.
Possibly by aerosol route.
There are 3 forms of Fowlpox:
The Cutaneous form (The Dry form)
The Diphtheritic form (The Wet form)
Ocular form
Fowlpox
The Cutaneous form (The Dry form):
Most common form.
Low mortality.
Probably results from injecting by biting arthropods, or mechanical transmission
to injured or lacerated skin.
Small papules on comb, wattles, and around the beak.
Lesions occasionally develop on legs, feet and around cloaca.
Nodules become yellowish and progress to a thick scab.
Sharp fall in egg production
In uncomplicated cases, affected birds recover in about 4 weeks.
Cutaneous or dry form of fowlpox
Fowlpox
The Diphtheritic form (The Wet form):
The Diphtheritic form (The Wet form):
Probably caused by droplet infection.
Involves infection of mucous membranes of mouth, pharynx, larynx, and sometimes trachea.
Lesions, as they coalesce, result in a necrotic pseudomembrane, which may
cause death by asphyxiation. Prognosis is poor.
Fowlpox
The Diphtheritic form (The Wet form):
Ocular Form of Fowlpox
Ocular Form of Fowlpox
Conjunctivitis
Cheesy exudate accumulates under the eyelids
Ocular Fowl pox
Characterisitic of Avipoxvirus
Bollinger bodies: Eosinophilic Granular Intracytoplasmic Inclusion Bodies.
Borrel bodies occur inside Bollinger bodies. Borrel bodies are minute spherical bodies obtained by tryptic digestion of Bollinger bodies.
Fowlpox Control
Vaccination:
Vaccination:
Modified live fowlpox or pigeon pox virus vaccines of chicken embryo or
avian cell culture origin are available commercially.
The use of vaccines is indicated in areas where the disease is endemic, or
on premises where infection has been diagnosed.
Vaccines are applied by scarification of skin of thigh.
One vaccine can be administered in drinking water.
In enzootic areas, vaccinate during the first few weeks of life and then again
8-12 weeks later.
Recombinant fowlpox vectored vaccines have been developed.
Control mosquito population and other biting insects.
Unclassified Poxviruses Ulcerative Dermatosis of Sheep
Etiology: Infectious disease of sheep caused by a virus antigenically similar to the ecthyma virus.
Transmission: Virus infection through damaged skin or by coitus
Clinical forms:
Regardless of location, lesions are usually ulcers with a raw crater that bleeds easily.
Ulcerative Dermatosis of Sheep
Manifests in two clinical forms:
Manifests in two clinical forms:
Lip and Leg Ulceration:
Venereal form:
Ulcerative Dermatosis of Sheep
Lip and Leg Ulceration:
Formation of ulcers around the mouth and nose or on the legs (lip and leg
ulceration).
Face lesions occur on the upper lip, between the border of the lip and the nasal
orifice, on the chin, and on the nose.
Foot lesions are seen anywhere between the coronet and the carpus or tarsus.
Ulcerative Dermatosis of Sheep
Lip and Leg Ulceration:
Ulcerative Dermatosis of Sheep
Venereal form:
Venereal form:
Venereally transmitted ulceration of the prepuce and penis or vulva.
Rarely, the ulcers may extend to the glans penis so that the ram becomes unfit
for natural breeding.
In ewes, edema, ulceration, and scabbing of the vulva have less serious
consequences.
Balanoposthitis; superficial necrosis of the skin of the mucosa of the prepuce and glans penis
Ulcerative Dermatosis of Sheep
Venereal form:
Diagnosis of Poxviruses
-Clinical Signs
Sampling Material: Scrapings from skin lesions, Vesicular fluid, Crusts, Scabs
Electron Microscopy: Characteristic morphology and size of poxviruses. Orthopoxviruses are brick shaped. Parapoxviruses are ovoid.
Diagnosis of Poxviruses
Histopathology:
Presence of characteristic intracytoplasmic inclusion bodies.
Type-B or Guarnieri inclusion bodies: Most poxviruses induce the presence of type-B or Guarnieri inclusion bodies. These are slightly basophilic and composed of viral particles and protein aggregates.
Type-A or ATI inclusion bodies: Some poxviruses (cowpox and ectromelia virus) induce type-A bodies. A-type inclusions are more strongly eosinophilic.
Bollinger and Borrel bodies in avipoxvirus infection.
Guarnieri inclusion bodies
Type-A or ATI inclusion bodies
Diagnosis of Poxviruses
Inoculation in embryonated egg
Chorioallantoic membrane [CAM]
Pock lesions
Note: Parapoxviruses do not multiply in chicken embryo
Diagnosis of Poxviruses
Molecular
Serological Assays, such as ELISA
Detection of poxvirus nucleic acid by PCR
Most humans get cowpox from….
CATS!
