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Infectious diseases I & II > Small ruminants 1/2 > Flashcards

Small ruminants 1/2 Flashcards

1
Q

Alt. name for Orf (disease)

A

Contagious ecthyma

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2
Q

Orf is a highly contagious, zoonotic, disease of sheep and goats, caused by poxvirus, and is characterized by

A

skin lesions on the mouth and muzzle.

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3
Q

Causative agent of Orf.
genus
family
DNA type

A

Genus Parapoxvirus,
family Poxviridae
ds DNA

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4
Q

Orf virus is carried by

A

clinically healthy sheep.

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5
Q

Orf virus survival in the environment.

A

Very resistant to inactivation.
Survives for one month on wool/hides after lesions have healed.

Up to 12 years in lesion crusts.

Disinfectants: e.g. sodium hypochlorite or Virkon. Ethanol is ineffective!

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6
Q

Host range of Orf virus.

A

sheep and goats

Some other ungulates: alpacas, reindeer etc.
Rare cases in dogs and cats.

NB! ZOONOSIS!
But it’s very rare for orf to be passed from one person to another.

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7
Q

Where in the world is Orf found?

A

Found worldwide in all countries that raise sheep

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8
Q

Morbidity of Orf.

A

In unvaccinated flocks it is high,
especially among young animals >1 year old (80%).

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9
Q

Mortality of Orf.

A

Case fatality in uncomplicated cases is low (<1%)

If young animals die of cachexia due to being unable to feed for the ulcers, then case fatality can approach 100%

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10
Q

Transmission of Orf.

A

Excretion: skin lesions and scabs!

Direct contact
Fomites

Route: via skin cuts and abrasions

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11
Q

IP of Orf.

A

IP: 2-3 days

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12
Q

Clinical signs of Orf.

A

Papules, pustules, vesicles on and around the muzzle, mouth and nose.

*Sometimes on the ears, eyelids, feet, perineal region and other sites, inside the mouth; teats and udder.

**Rarely in esophagus, stomach, intestines or respiratory tract.

Develop into thick, friable scabs that bleed easily. Lesions are very painful.

Usually resolves in 1-2 months.
Complications: secondary bacterial infections, maggot or screwworm infestation.

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13
Q

Post mortem signs of Orf.

A

Similar to lesions found in live animals (mouth vesicles etc.).

Histopathology: ballooning degeneration of keratinocytes and eosinophilic cytoplasmic inclusions.

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14
Q

Diagnosis of Orf.

A

Usually diagnosed symptomatically.

Confirmed by electron microscopy of the scabs.

Collected from animals in an early stage of disease.

Orf cannot be distinguished virus from other parapoxviruses!

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15
Q

Methods for diagnosis of Orf.

A

Histopathology
PCR
Serology

Virus isolation is uncommonly used – grows slowly and cannot always be isolated.

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16
Q

Tx of Orf.

A

Tx: supportive care

ABs if secondary infections

Repellents and larvicides to prevent invading the wounds.

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17
Q

Prevention of Orf.

A

Quarantine new animals

Keep equipment/fomites clean

Removal of harsh vegetation from pastures or feed may reduce the risk of cuts in the mouth or on the muzzle.

At fairs/exhibitions: owner opens the mouth themselves.

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18
Q

Control of Orf.

A

Difficult to eradicate

Vaccination – live virus! (not in eesti, is high risk)

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19
Q

Orf in humans.

A

People who handle infected animals or their tissues.

Transmission: contact with infected animals or orf vaccines (live virus)

IP: 3-7 days
Usually single skin lesion. Small, firm papule on the fingers or hands. Eventually covered by crust.

Often resolves spontaneously – self-limiting.

Tx: supportive care, surgery, cryotherapy if needed.

Prevention: wear gloves, wash hands, avoid contact

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20
Q

Maedi-visna is a contagious disease of sheep, caused by Lentivirus, and characterized by

A

wasting and progressive dyspnea (maedi) and neurological signs (visna).

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21
Q

Causative agent of Maedi-Visna.
genus
family
DNA type

A

Genus Lentivirus
family Retroviridae
RNA

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22
Q

Maedi-visna virus is part of what viral group?

A

Part of a groupcalled the small ruminant lentiviruses (SRLVs)

Other virus in this group: caprine arthritis encephalitis virus (CAEV)

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23
Q

What is Maedi-visna called in the US?

A

ovine progressive pneumonia

24
Q

genotypes of Maedi-visna virus?

A

Five genotypes (A-E)

25
Q

Survival of maedi-visna virus in the environment.

A

Survives just few days in the environment.
Does not like hot or dry conditions.

Destroyed by most common disinfectants and low pH (pH <4.2).

26
Q

Host range of maedi-visna.

A

sheep and goats

Classical strains – sheep

Other genotype A variants – sheep and goats.

Wild relatives of small ruminants can be infected by SRLVs from domesticated animals.

(small ruminant lentivirus)

27
Q

Where in the world is maedi-visna found?

A

Widely distributed

MVV has been found in most sheep-raising countries (excluding Iceland -> eradicated!; Australia and New Zealand)

Prevalence <5% to >60%

More common in intensively raised herds or flocks, and in animals housed indoors.

Some breeds more likely to become ill (e.g. Texel, Finnish Landrace).

28
Q

Morbidity & mortality of Maedi-visna?

A

When introduced to new areas: both 20-30%

Endemic MVV:
morbidity <100%, mortality 5%

29
Q

Excretion of Maedi-visna.

A

Excretion: milk, respiratory secretions, feces, semen, female reproductive tract.

Shedding in semen may be intermittent.

30
Q

Transmission mode/route of Maedi-visna.

A

Predominant route is currently unclear!
- Lactogenic transmission
- Direct (close) contact
- Iatrogenic spread
- Fomites

Once infected, virus will be integrated into leukocyte DNA – animal carries the virus for life!

31
Q

IP of Maedi-visna.

A

IP: months to years

Maedi signs typically at 3-4 years of
age.

Visna signs from 2 years of age.

wasting and progressive dyspnea (maedi) and neurological signs (visna).

32
Q

Clinical signs of Maedi.

A

Most infections asymptomatic.

Maedi is the Most common form in sheep.
Affects Adults

Wasting away and progressive dyspnea

Death results from anorexia and secondary bacterial pneumonia.

33
Q

Clinical signs of Visna.

A

Most infections asymptomatic

Visna affects Adult sheep

Subtle neurological signs – hindlimb weakness, trembling of the lips or a head tilt; loss of condition.

Gradually progresses to ataxia, incoordination, muscle tremors, paresis and paraplegia.

Clinical course up to a year -> then death.

34
Q

Post mortem signs of Maedi.

A

Lungs: enlarged, abnormally firm and heavy, fail to collapse when the thoracic cavity is opened.
- Emphysematous and mottled or uniformly discolored, with pale gray to pale brown areas of consolidation.

Nodules around the smaller airways and blood vessels.

Mediastinal and tracheobronchial LNs are enlarged and edematous.

35
Q

Post mortem signs of Visna.

A

Wasting of the carcass

Brain and spinal cord lesions – focal, asymmetric, brownish pink areas in the white matter.

Meningitis: Meninges may be cloudy and the spinal cord may be swollen.

36
Q

Material for diagnosis of Maedi-visna.

A

Blood
Milk
BAL at necropsy

MAEDI: mediastinal LN, spleen

VISNA: brain and spinal cord

37
Q

Lab analyses for diagnosis of Maedi-visna.

A

Antibodies (unpredictable) – ELISA, AGID

PCR and virus isolation (not always successful)

Histology

Suggested: at least two different tests for confirmation due to unpredictability.

38
Q

Tx of Maedi-visna.

A

Supportive therapy – cannot stop the progression of disease.

ABs if secondary bacterial infection (mastitis, pneumonitis).

High-quality, readily digestible feed may delay wasting.

39
Q

Prevention & control of Maedi-visna.

A

New additions from seronegative herds (others: quarantine and test).

Do not mix sheep and goats

If virus in the herd:
- Completely depopulate and replace
- Separate lambs or kids permanently from seropositive dams immediately at birth – raise with uninfected milk.
- Tested frequently -> seronegatives and –positives to be kept separately.
- Seropositives should be culled

No vaccines available.

40
Q

Brucellosis is an infectious disease of sheep and goats, caused by Brucella melitensis, and is characterized by

A

abortions and reproduction failure.

41
Q

Causative agent of Brucellosis in sheep and goats.
Gram + or -?

A

Brucella melitensis
Gram neg.
Facultatively intracellular

42
Q

Biovars of Brucella melitensis?

A

Three biovars

Biovar 3 most prominent in the Mediterranean.

43
Q

Survival of Brucella melitensis.

A

Killed by most commonly available disinfectants.

Organic matter and low temperatures decrease the efficacy of disinfectants.

Inactivated by pasteurization

Survives for very short period in meat.

Survives Frozen: years

44
Q

Host range of ovine/caprine brucellosis.

A

sheep and goats

Occasionally cattle, camels, dogs, horses, pigs.

NB! ZOONOSIS!

45
Q

Morbidity of sheep/goat brucellosis.

A

Abortion rate is high on first introduction – usually abort only during the gestation when they are first infected, later they “withstand”.

46
Q

Mortality of sheep/goat brucellosis.

A

Deaths are rare except in fetuses.

47
Q

Transmission of brucellosis.

A

Excretion: placenta, fetus, fetal fluids, vaginal discharge, milk, semen, feces.

Direct contact
In utero
Fomites

Route: through mucous membranes, broken skin

48
Q

Clinical signs of brucellosis in female goats/sheep.

A

Abortions, stillbirths and the birth of weak offspring.

Sheep and goats usually abort only once, but reinvasion of the uterus and shedding of organisms can occur during subsequent pregnancies.

Milk yield is significantly reduced in animals that abort – mastitis is uncommon!

Arthritis – occasionally in both sexes

Non-pregnant: asymptomatic

49
Q

Clinical signs of brucellosis in male goats/sheep.

A

Males: acute orchitis and epididymitis, may result in infertility.

Arthritis – occasionally in both sexes

50
Q

Epididymitis in rams is typically caused by

A

Brucella ovis

51
Q

Post mortem signs of brucellosis.

A

Granulomatous inflammatory lesions may be in the reproductive tract, udder, supramammary lymph nodes etc., and sometimes in joints and synovial membranes .

Necrotizing orchitis, epididymitis, seminal vesiculitis and prostatitis.

Aborted fetus may be autolyzed, normal or have an excess of bloodstained fluid in the body cavities and an enlarged spleen and liver.

Placentitis, with edema and/or necrosis of the cotyledons and a thickened and leathery intercotyledonary region.

52
Q

Suspect brucellosis when

A

abortions and stillbirths occur without concurrent illness.

53
Q

Material for diagnosis of brucellosis.

A

Vaginal swab
Milk
Aborted fetuses, placenta

Spleen, mammary and genital LNs, udder and (late pregnant or early post-parturient) uterus.

Semen, the testis or epididymis

54
Q

Lab analyses for diagnosis of brucellosis.

A

Microscopic examination

Culture – for definitive diagnosis

Serology

PCR

55
Q

Prevention & control of brucellosis.

A

Eradication: test-and-slaughter or depopulation.

Thorough cleaning and disinfection

Vaccination

Placenta and other contaminated materials to be removed quickly and destroyed.

56
Q

Brucellosis in humans.

A

Highly pathogenic to humans!

Occupational exposure to animals and vaccines.

Asymptomatic or symptomatic

Flu-like symptoms; occasionally also other symptoms.

Tx: ABs – but still relapses are seen.

Mortality is low (<5%) but can be due endocarditis, meningitis.

Infectious diseases I & II (33 decks)

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