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Test 2- Poxviradae Flashcards

1
Q

Properties of Poxviruses

A

 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.

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2
Q
A

top: Orthopoxviruses
bottom: Parapoxviruses

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3
Q

Two distinct infectious poxvirus particles exists:

A

the intracellular mature virus (IMV) and

the extracellular enveloped virus (EEV). Both forms are infectious.

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4
Q

The extracellular forms (EEV - extracellular enveloped virions)

A

 Envelope

 Inner Membrane

has an envelope that they get from the host cytoplasmic membrane- virus comes out via budding

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5
Q

Virions that are released from cells by budding, rather than by cellular disruption,

A

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.

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6
Q

Intracellular viral particles (IMV - intracellular mature virions)

A

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

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7
Q

Symmetry of Poxviruses

A

 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.

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8
Q

genome of poxviruses

A

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.

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9
Q

Replication of Poxvirdae

A

 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.

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10
Q

Antigenic Characteristics

A

 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

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11
Q

Stability of Poxviradea

A

 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.

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12
Q

Transmission of Poxviradea

A

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).

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13
Q

Pathogenesis and Immunity

A

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.

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14
Q

Spread of Poxvirus

A

 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.

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15
Q

Skin Lesions in Poxvirus Infection

A

 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.

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16
Q

Genus: Orthopoxvirus

A

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

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17
Q

Cowpox in Cattle

Transmission:

A

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.

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18
Q

Cowpox in Cattle

Economic Importance:

A

 Losses to farmers due to inconvenience in milking because of soreness of teats and mastitis resulting from secondary bacterial infections.

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19
Q

Cowpox in Cattle Clinical Findings:

Clinical Signs

A

 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.

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20
Q
A

Cowpox ulcer on teat

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21
Q

Cowpox in Cats

Transmission:

A

 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.

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22
Q

Cowpox in Cats

Clinical Signs:

A

 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.

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23
Q
A

Cow pox in a 4-year-old cat, showing blepharitis (inflammation of eye lids).

primary lesion

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24
Q
A

Cowpox lesion on limb of cat.

primary lesion

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25
Q

Cowpox in Cats

Clinical Signs:
 Secondary Lesions:

A

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.

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26
Q
A

Crusting Papular Lesion

secondary lesion

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27
Q
A

Multiple Papular Lesions on the Trunk

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28
Q
A

Ulcerative lesions on the upper and lower lip of a cat with poxvirus infection

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29
Q

Cowpox in Humans

Transmission:

A

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.

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30
Q

Coxpox in humans

Clinical Signs:

A

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.

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31
Q
A

A 16-year-old boy with generalized cowpox

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32
Q

Monkeypox

In Humans:

A

Monkeypox is a viral zoonosis with symptoms in humans similar to those seen in the past in smallpox patients.

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33
Q

Monkeypox

In Monkeys:

A

In monkeys, the disease is characterized by generalized skin eruptions, developing to papules on the trunk, face, palms and soles.

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34
Q

Monkeypox

Transmission in Humans:

A

 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.

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35
Q

Monkeypox in Humans

Distribution:

A

 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.

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36
Q

Monkeypox in Humans

Clinical Signs in Humans:

A

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.

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37
Q
A

monkeypox in humans

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38
Q

Other Orthopoxviruses

A

 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)

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39
Q

Pseudocowpox’s genus and nickname

A

Parapoxviruses

This virus can also infect humans and the condition is commonly referred to as milker’s nodule.

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40
Q

Transmission of Pseudocowpox

A

 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

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41
Q

Pseudocowpox is

A

Pseudocowpox is a viral skin disease that causes mild sores on the teats and udders of cattle.

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42
Q

Pathogenesis of Pseudocowpox

A

Lesions are characterized by hyperplasia of squamous epithelium

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43
Q

Clinical Signs of Pseudocowpox

A

 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%.

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44
Q

Acute lesions of Pseudocowpox

A

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!

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45
Q
A

Papule from Pseudocowpox on teat

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46
Q
A

Pseudocowpox teats of cow

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47
Q
A

Horseshoe-shaped ring of Pseudocowpox

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48
Q

Chronic Lesions of Pseudocowpox

A

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

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49
Q

Diagnosis of Pseudocowpox

A

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.

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50
Q

Differential Diagnosis for Pseudocowpox

A

 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)

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51
Q

Pseudocowpox

Treatment:

A

 Removal of scabs
 Burn the scabs to prevent environmental contamination  Application of an emollient ointment before milking
 Application of astringent preparation after milking.

52
Q

SMALLPOX

A

killed Rames IV

53
Q

2 subfamilies in Poxviridae

A

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)

54
Q

Skin lesion pattern in Pox virus

A
  1. macule- flat red lesion
  2. papule- elevated red lesion
  3. vesicle- blister, thin walled sack filled with fluid
  4. pustule-
  5. ulcer- when pustle ruptures- COMPLICATION
  6. or pustule will form a scab and then a scar
55
Q

Pseudocowpox

Prevention:

A

 Disinfection. Use iodophor teat dip.
 Isolation and treatment of infected cows
 Reduce teat trauma, as injuries to skin of teat predisposes to infection.

56
Q

Pseudocowpox in Humans

A

(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.

57
Q
A

Pseudocowpox in Humans (The Milker’s Nodule)

58
Q

Contagious Ecthyma

A

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

59
Q
A

Contagious Ecthyma

60
Q

Contagious Ecthyma

 Transmission:

A

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.

61
Q

Contagious Ecthyma

 Pathogenesis:

A

 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.

62
Q

Contagious Ecthyma

 Clinical signs:

A

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.

63
Q
A

Goat: Raised, crusted lesions around the commissure of the lips

64
Q
A

Goat: Proliferative lesions on lips and mouth

65
Q

Contagious Ecthyma

 Clinical signs:

kits/severe lesions

A

 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.

66
Q
A

Contagious Ecthyma

Lips: Detachment of the Epithelium

67
Q
A

Teat: Erosion & Scabs

Contagious Ecthyma

68
Q
A

Goat: Proliferative lesion; scabs

Contagious Ecthyma

69
Q

Contagious Ecthyma

 Clinical signs:

Secondary Infections:

A

 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.

70
Q

Contagious Ecthyma

 Vaccination:

A

 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.

71
Q

Contagious Ecthyma

 Vaccination

  • when to vaccinate
  • in problem herds
A

 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.

72
Q

Contagious Ecthyma— ORF in Humans

A

 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.

73
Q
A

Contagious Ecthyma ORF in Humans

74
Q

Genus: Capripoxvirus

A

Sheep Pox
 Goat Pox
 Lump Skin Disease (of cattle)

75
Q

Sheeppox and Goatpox distribution and etiology

A

Distribution: Endemic in Africa, Asia and parts of Europe Etiology: Members of Genus Capripoxvirus

76
Q

Sheep pox virus (SPV) and goat pox virus (GPV) were once believed to be

A

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.

77
Q

Most strains of goat and sheeppox are

A

Most strains are host specific and cause severe clinical disease in either sheep or goats, while some strains have equal virulence in both species.

78
Q

Can sheep and goat pox be distinguished from each other?

A

SPV and GPV cannot be distinguished from each other with serological techniques, including viral neutralization.

79
Q

SPV and GPV are also closely related to

A

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.

80
Q

Sheeppox and Goatpox

 Transmission:

A

 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.

81
Q

Sheeppox

 Pathogenesis:

A

 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.

82
Q

Sheeppox: 2 forms of the disease

A

A. Malignantform

B. Benignform

83
Q
A

Necrotizing vasculitis in the ear

84
Q

Sheeppox

A. Malignant form:

A

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%

85
Q

Sheeppox Benign Form:

A

B. Benign form:

 More common in adults and resistant breeds.

 Only skin lesions occur
 No, or a very mild systemic reaction

86
Q
A

Tail of sheep: Sheep Pox lesions

87
Q
A

Sheeppox lesions

88
Q
A

sheepox lesions Lesions on the mucosa of the esophagus

89
Q

Sheeppox

 Prevention & Control:

A

 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.

90
Q

Vaccination for sheepox

A

 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.

91
Q

GoatPox

A

 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

92
Q

Lumpy Skin Disease

A

 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.

93
Q
A

Lumpy Skin Disease

94
Q

Genus: Suipoxvirus

A

Swinepox

95
Q

Swine pox

Etiology, distribution, host, fatality rate

A

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.

96
Q

Swinepox transmission

A

 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.

97
Q

Clinical Signs and control of swine pox

A
  • 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.

98
Q

Swinepox

Erythematous Lesions

A

lead to

99
Q

Synonyms for Contagious Ecthyma

A

Contagious Ecthyma

(Synonyms: ORF, Scabby Mouth, Contagious Pustular Dermatitis, Sore Mouth)

100
Q
A

Congenitally Infected Piglet

Disseminated skin lesions

Swinepox

101
Q

Genus: Avipoxvirus

A

Fowlpox and other avian poxviruses

102
Q

Fowlpox

A

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.

103
Q

Routes of transmission of Fowlpox

A

 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.

104
Q

There are 3 forms of Fowlpox:

A

 The Cutaneous form (The Dry form)

 The Diphtheritic form (The Wet form)

 Ocular form

105
Q

Fowlpox

 The Cutaneous form (The Dry form):

A

 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.

106
Q
A

Cutaneous or dry form of fowlpox

107
Q

Fowlpox

 The Diphtheritic form (The Wet form):

A

 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.

108
Q
A

Fowlpox

 The Diphtheritic form (The Wet form):

109
Q

Ocular Form of Fowlpox

A

Ocular Form of Fowlpox

 Conjunctivitis

 Cheesy exudate accumulates under the eyelids

110
Q
A

Ocular Fowl pox

111
Q

Characterisitic of Avipoxvirus

A

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.

112
Q

Fowlpox Control

 Vaccination:

A

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.

113
Q

Unclassified Poxviruses Ulcerative Dermatosis of Sheep

A

 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.

114
Q

Ulcerative Dermatosis of Sheep

Manifests in two clinical forms:

A

Manifests in two clinical forms:

 Lip and Leg Ulceration:
 Venereal form:

115
Q

Ulcerative Dermatosis of Sheep

 Lip and Leg Ulceration:

A

 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.

116
Q
A

Ulcerative Dermatosis of Sheep

 Lip and Leg Ulceration:

117
Q

Ulcerative Dermatosis of Sheep

 Venereal form:

A

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.

118
Q
A

Balanoposthitis; superficial necrosis of the skin of the mucosa of the prepuce and glans penis

Ulcerative Dermatosis of Sheep

 Venereal form:

119
Q

Diagnosis of Poxviruses

A

-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.

120
Q

Diagnosis of Poxviruses

 Histopathology:

A

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.

121
Q
A

Guarnieri inclusion bodies

122
Q
A

Type-A or ATI inclusion bodies

123
Q

Diagnosis of Poxviruses

 Inoculation in embryonated egg

A

Chorioallantoic membrane [CAM]

Pock lesions

Note: Parapoxviruses do not multiply in chicken embryo

124
Q

Diagnosis of Poxviruses

Molecular

A

 Serological Assays, such as ELISA

 Detection of poxvirus nucleic acid by PCR

125
Q
A
126
Q

Most humans get cowpox from….

A

CATS!

Viro (14 decks)

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