Small ruminants 1/2

Question 1

Alt. name for Orf (disease)

Answer 1

Contagious ecthyma

Question 2

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

Answer 2

skin lesions on the mouth and muzzle.

Question 3

Causative agent of Orf.
genus
family
DNA type

Answer 3

Genus Parapoxvirus,
family Poxviridae
ds DNA

Question 4

Orf virus is carried by

Answer 4

clinically healthy sheep.

Question 5

Orf virus survival in the environment.

Answer 5

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!

Question 6

Host range of Orf virus.

Answer 6

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.

Question 7

Where in the world is Orf found?

Answer 7

Found worldwide in all countries that raise sheep

Question 8

Morbidity of Orf.

Answer 8

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

Question 9

Mortality of Orf.

Answer 9

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%

Question 10

Transmission of Orf.

Answer 10

Excretion: skin lesions and scabs!

Direct contact
Fomites

Route: via skin cuts and abrasions

Question 11

IP of Orf.

Answer 11

IP: 2-3 days

Question 12

Clinical signs of Orf.

Answer 12

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.

Question 13

Post mortem signs of Orf.

Answer 13

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

Histopathology: ballooning degeneration of keratinocytes and eosinophilic cytoplasmic inclusions.

Question 14

Diagnosis of Orf.

Answer 14

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!

Question 15

Methods for diagnosis of Orf.

Answer 15

Histopathology
PCR
Serology

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

Question 16

Tx of Orf.

Answer 16

Tx: supportive care

ABs if secondary infections

Repellents and larvicides to prevent invading the wounds.

Question 17

Prevention of Orf.

Answer 17

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.

Question 18

Control of Orf.

Answer 18

Difficult to eradicate

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

Question 19

Orf in humans.

Answer 19

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

Question 20

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

Answer 20

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

Question 21

Causative agent of Maedi-Visna.
genus
family
DNA type

Answer 21

Genus Lentivirus
family Retroviridae
RNA

Question 22

Maedi-visna virus is part of what viral group?

Answer 22

Part of a groupcalled the small ruminant lentiviruses (SRLVs)

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

Question 23

What is Maedi-visna called in the US?

Answer 23

ovine progressive pneumonia

Question 24

genotypes of Maedi-visna virus?

Answer 24

Five genotypes (A-E)

Question 25

Survival of maedi-visna virus in the environment.

Answer 25

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).

Question 26

Host range of maedi-visna.

Answer 26

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)

Question 27

Where in the world is maedi-visna found?

Answer 27

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).

Question 28

Morbidity & mortality of Maedi-visna?

Answer 28

When introduced to new areas: both 20-30% Endemic MVV: morbidity <100%, mortality 5%

Question 29

Excretion of Maedi-visna.

Answer 29

Excretion: milk, respiratory secretions, feces, semen, female reproductive tract. Shedding in semen may be intermittent.

Question 30

Transmission mode/route of Maedi-visna.

Answer 30

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!

Question 31

IP of Maedi-visna.

Answer 31

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).

Question 32

Clinical signs of Maedi.

Answer 32

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.

Question 33

Clinical signs of Visna.

Answer 33

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.

Question 34

Post mortem signs of Maedi.

Answer 34

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.

Question 35

Post mortem signs of Visna.

Answer 35

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.

Question 36

Material for diagnosis of Maedi-visna.

Answer 36

Blood Milk BAL at necropsy MAEDI: mediastinal LN, spleen VISNA: brain and spinal cord

Question 37

Lab analyses for diagnosis of Maedi-visna.

Answer 37

Antibodies (unpredictable) – ELISA, AGID PCR and virus isolation (not always successful) Histology Suggested: at least two different tests for confirmation due to unpredictability.

Question 38

Tx of Maedi-visna.

Answer 38

Supportive therapy – cannot stop the progression of disease. ABs if secondary bacterial infection (mastitis, pneumonitis). High-quality, readily digestible feed may delay wasting.

Question 39

Prevention & control of Maedi-visna.

Answer 39

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.

Question 40

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

Answer 40

abortions and reproduction failure.

Question 41

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

Answer 41

Brucella melitensis Gram neg. Facultatively intracellular

Question 42

Biovars of Brucella melitensis?

Answer 42

Three biovars Biovar 3 most prominent in the Mediterranean.

Question 43

Survival of Brucella melitensis.

Answer 43

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

Question 44

Host range of ovine/caprine brucellosis.

Answer 44

sheep and goats Occasionally cattle, camels, dogs, horses, pigs. NB! ZOONOSIS!

Question 45

Morbidity of sheep/goat brucellosis.

Answer 45

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

Question 46

Mortality of sheep/goat brucellosis.

Answer 46

Deaths are rare except in fetuses.

Question 47

Transmission of brucellosis.

Answer 47

Excretion: placenta, fetus, fetal fluids, vaginal discharge, milk, semen, feces. Direct contact In utero Fomites Route: through mucous membranes, broken skin

Question 48

Clinical signs of brucellosis in female goats/sheep.

Answer 48

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

Question 49

Clinical signs of brucellosis in male goats/sheep.

Answer 49

Males: acute orchitis and epididymitis, may result in infertility. Arthritis – occasionally in both sexes

Question 50

Epididymitis in rams is typically caused by

Answer 50

Brucella ovis

Question 51

Post mortem signs of brucellosis.

Answer 51

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.

Question 52

Suspect brucellosis when

Answer 52

abortions and stillbirths occur without concurrent illness.

Question 53

Material for diagnosis of brucellosis.

Answer 53

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

Question 54

Lab analyses for diagnosis of brucellosis.

Answer 54

Microscopic examination Culture – for definitive diagnosis Serology PCR

Question 55

Prevention & control of brucellosis.

Answer 55

Eradication: test-and-slaughter or depopulation. Thorough cleaning and disinfection Vaccination Placenta and other contaminated materials to be removed quickly and destroyed.

Question 56

Brucellosis in humans.

Answer 56

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.