Ovine & Caprine PowerPages Flashcards by Nellie O'Leary

what disease causes the congenital condition “HAIRY SHAKER DISEASE” in SHEEP?

BORDER DZ caused by a PESTIVIRUS

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BORDER DISEASE…

caused by WHAT kind of virus?

what usually happens when it’s introduced to a flock of SHEEP?

mainly causes problems when sheep is infected WHEN? causing what 2 things?

BORDER DISEASE

PESTIVIRUS

usually >50% LAMBS AFFECTED when first introduced

mainly causes problems when sheep are infected IN EARLY PREGNANCY, then causing…
1. DECREASED PREGNANCY RATE
2. OUTBREAK OF INFERTILITY

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what 3 things does BORDER DISEASE cause in a growing fetus if dam is infected?

DEATH
FETAL RESORPTION
CONGENITAL ABNORMALITIES

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TRUE/FALSE: border disease frequently becomes ENDEMIC

TRUE

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what are 3 CLINICAL SIGNS seen in LAMBS infected with BORDER DISEASE?

UNDERSIZED AT BIRTH
EXCESSIVELY HAIRY or PIGMENTED FLEECE
MUSCLE TREMORS

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what are 3 PATHOLOGIC findings in LAMBS affected with BORDER DISEASE?

CEREBRAL CAVITATIONS
GLIAL CELL HYPERPLASIA
DEMYELINATION OF CNS WHITE MATTER

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is there an effective treatment for BORDER DISEASE?

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DAMS with LAMBS AFFECTED BY BORDER DISEASE should have ___ titers

what do HIGH titers indicate?

what do LOW titers indicate?

ANTIBODY

HIGH Ab titer = SUBSEQUENT IMMUNITY

LOW Ab titer = POSSIBLE PERSISTENT INFECTION

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affected lambs with BORDER DISEASE SHOULD NOT BE USED FOR WHAT?

what CAN they be used for?

lambs affected by BORDER DZ SHOULDN’T be used for BREEDING

BUT AHEAD OF BREEDING SZN they can intermingle with others to help promote IMMUNITY

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CAPRINE CASEOUS LYMPHADENTITIS

mostly associated with WHAT clinical sign?

what is the CAUSATIVE ORGANISM? anaerobic or aerobic?

G+ or -?

CAPRINE CASEOUS LYMPHADENITIS

mostly associated with ABSCESSES in the PERIPHERAL LNs

CORYNEBACTERIUM PSEUDOTUBERCULOSIS which is a FACULTATIVE ANAEROBE

G+

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what does CORYNEBACTERIUM PSEUDOTUBERCULOSIS from CAPRINE CASEOUS LYMPHADENITIS do on BLOOD AGAR?

how LONG does it take to grow?

ZONE OF HEMOLYSIS AROUND THE COLONY

slow-growing and takes 48 hours to GROW

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what are the 3 routes of TRANSMISSION of CAPRINE CASEOUS LYMPHADENITIS?

what makes it particularly hard to get rid of?

3 routes? –> ONCE ABSCESS HAS RUPTURED & SPILLED INTO ENVIRONMENT
1. INHALED
2. INGESTED
3. CROSSES BREAK IN EPIDERMIS

is HARDY in environment and PERSISTS FOR MONTHS

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can we BURN material contaminated with CASEOUS LYMPHADENTITIS

YES

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describe the difference in CLINICAL PRESENTATION for CASEOUS LYMPHADENITIS in GOATS vs. SHEEP

GOATS = peripheral LNs on HEAD, BODY & CHEST usually affected

SHEEP = distribution of abscesses more DIFFUSE & often involves LNs AT HIND END

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how is CASEOUS LYMPHADENITIS often spread in SHEEP herds?

through CONTAMINATED SHEARING EQUIPMENT that can INFECT ANIMALS through BREAKS IN THE SKIN

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specifically for CASEOUS LYMPHADENITIS…

3 LNs affected for GOATS?

2 LNs affected for SHEEP?

GOATS?
1. PAROTID LN
2. SUBMANDIBULAR LN
3. PRESCAPULAR LN

SHEEP?
1. PREFEMORAL LN
2. POPLITEAL LN

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what is the approximate INCUBATION TIME for CASEOUS LYMPHADENITIS?

HOWEVER, clinically DETECTABLE abscesses usually occur over WHAT period?

8-9 DAYS

however, clinically DETECTABLE abscesses usually occur over 2-6 MONTHS

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when can FALSE POSITIVES for CASEOUS LYMPHADENITIS occur and WHY? (3)

false positives more common in animals <6 MONTHS due to FPT of Ab against CORYNEBACTERIUM PSEUDOTUBERCULOSIS
animals that are EXPOSED but CLEARED infection
animals previously VACCINATED

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how should we perform SEROLOGY testing for CASEOUS LYMPHADENITIS?

what is a positive result?

PAIRED TITERS collected 2+ WEEKS APART

4X OR MORE RISE IN TITER SHOWS POSITIVE

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SINGLE TITERS for CASEOUS LYMPHADENITIS…

can be useful for SCREENING DISEASE on HERD BASIS or SCREENING NEW INCOMING ANIMALS to the flock

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TRUE/FALSE: we SHOULD lance ABSCESSES of CL as they mature bc otherwise they’ll do it spontaneously

TRUE

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what TYPES of abscesses caused by CL are best for SURGICAL intervention?

WELL-ENCAPSULATED ABSCESSES

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ANTIMICROBIALS for CL need to be treated for WHAT DURATION?

LONG TIME

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what should we do if an animal develops CL in a herd that HAS NOT SEEN THIS DZ BEFORE? 2 options

CULL
ISOLATE until ABSCESSES DEVELOP, are LANCED & HEALED

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is there a VACCINE available for CL? describe the difference in GOATS vs. SHEEP

SHEEP CL vaccine can help DECREASE INCIDENCE OF EXTERNAL ABSCESSES GOAT CL vaccine NOT INDICATED bc usually causes SIGNIFICANT LOCAL INFLAMMATORY RESPONSE at vaccination site

what are 3 clinical signs of SEVERE INTESTINAL PARASITISM (likely secondary to HAEMONCHUS CONTORTUS) in ruminants?

1. WEAKNESS/INABILITY TO STAND 2. BOTTLE JAW = INTRAMANDIBULAR PITTING EDEMA due to LOW BLOOD PROTEIN 3. SYSTEMIC ANEMIA

why is H. CONTORTUS becoming INCREASINGLY RESISTANT to ANTIHELMINTICS?

because it an EXTREMELY LARGE GENETIC POOL that contains NATURALLY OCCURRING RESISTANCE GENES, so animals treated with antihelmintics will have worms that are RESISTANT that can SURVIVE & REPLICATE to pass on resistance

HAEMONCHUS CONTORTUS has very high WHAT? give a numeric example

H. CONTORTUS has very high FECUNDITY a SINGLE WORM can make 5000 EGGS/DAY

what is the AVERAGE WORM BURDEN of H. CONTORTUS in goats?

300 WORMS PER GOAT

what is the BEST way to TREAT FOR H. CONTORTUS since regular deworming is likely to breed resistance

ID animals that have a HIGH WORM BURDEN using things like the FAMACHA score and treat THERAPEUTICALLY

what is REFUGIA? what does this mean in PRACTICE?

= a population of SENSITIVE worms to ANTIHELMINTICS (from NEVER BEING EXPOSED PRIOR) that can be in environment and BREED with RESISTANT WORMS to DECREASE THE LEVEL OF RESISTANT GENES in practice, this means that we must be VERY JUDICIOUS when choosing who to treat; only treat those who are CLINICALLY AFFECTED

SCRAPIE this is a ___ ____ ____ present in WHAT species? how does TRANSMISSION occur and when do CLINICAL SIGNS appear? zoonotic risk?

SCRAPIE this is a TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY present in SHEEP transmitted from EWE --> OFFSPRING via PLACENTA and clinical signs can appear 2-5 YEARS + AFTER EXPOSURE NO ZOONOTIC RISK WITH SCRAPIE

3 clinical signs of SCRAPIE?

1. SCRATCHING/RUBBING against objects 2. HIGH-STEPPING & "BUNNY HOPPING" 3. TREMBLE/CONVULSE in response to NOISE/HANDLING

what are 3 ways to DIAGNOSE SCRAPIE? which one CONFIRMS?

1. BIOPSY of LYMPHOID TISSUES of THIRD EYELID or TONSILS 2. HISTOLOGY OF BRAIN for BILATERALLY SYMMETRIC INTRACYTOPLASMIC VACUOLATION of NEURONS 3. IMMUNOHISTOCHEMISTRY to confirm and see PRION PROTEIN FIBRILS

is there any effective treatment for SCRAPIE?

BLOAT & RUMEN ACIDOSIS 3 risk factors? frothy bloat =? free gas bloat =?

BLOAT & RUMEN ACIDOSIS 3 risk factors? 1. OVEREATING 2. EATING LARGE VOLUMES OF GRAIN 3. not yet ADAPTING TO DIET CHANGE FROTHY bloat = from LEGUME (ALFALFA) forage or GRAIN FREE GAS bloat = ALWAYS FROM GRAIN

how does RUMEN ACIDOSIS occur? (3) AS A RESULT, how can we have bacterial translocation?

1. LARGE AMOUNTS of HIGHLY DIGESTIBLE CARBOHYDRATES ingested 2. rumen pH DROPS 3. LACTOBACILLUS bacteria FURTHER ACIDIFY RUMEN DAMAGED RUMEN EPITHELIUM allows for BACTERIAL TRANSLOCATION

how QUICKLY do clinical signs usually occur for BLOAT & RUMEN ACIDOSIS?

usually 6-36 HOURS AFTER INGESTION

name 3 CLINICAL SIGNS of BLOAT in ruminants

1. ABDOMINAL DISTENSION (particularly LEFT-SIDED) 2. RESPIRATORY DISTRESS from abd distension 3. DEATH

name 4 CLINICAL SIGNS of RUMEN ACIDOSIS in ruminants

1. TOXEMIA 2. DEHYDRATION 3. DIARRHEA 4. DEATH

what is the TREATMENT for BLOAT in ruminants? 3 options

1. if not at risk of IMMEDIATE death = OROGASTRIC TUBE to RELIEVE PRESSURE 2. can give SURFACTANT/OIL via OROGASTRIC tube 3. if in RESP distress, RUMEN TROCARIZATION

what is the TREATMENT for RUMEN ACIDOSIS? (5)

1. CORRECT ELECTROLYTE IMBALANCES / DEHYDRATION WITH FLUIDS 2. NSAIDS 3. RUMEN TRANSFAUNATION 4. ANTIMICROBIALS 5. THIAMINE SUPPLEMENTATION

RUMEN ACIDOSIS has a HIGH RISK of what 3 SECONDARY conditions?

1. POLIOENCEPHALOMALACIA 2. LIVER ABSCESSES 3. LAMINITIS

LISTERIA MONOCYTOGENES usually causes ___ neurological signs what is the RISK FACTOR? especially.. transmission?

LISTERIA MONOCYTOGENES usually causes UNILATERAL neurological signs risk factor = SPOILED or WET feed, especially IMPROPERLY FERMENTED SILAGE transmission = organism CROSSES MUCOSAL SURFACES or INVADES MICROABRASIONS to travel up CNs to cause MICRO-ABSCESSES and FOCAL ENCEPHALITIS

name 3 CLINICAL SIGNS of LISTERIA MONOCYTOGENES

remember --> UNILATERAL NEURO SIGNS 1. UNILATERAL FACIAL PARALYSIS (dropped jaw, dysphagia, drooling) 2. HEAD TILT/CIRCLING 3. FEBRILE

in LISTERIA MONOCYTOGENES, which REFLEX is usually ABSENT?

ABSENT PALPEBRAL REFLEX

besides NSAIDs & FLUID SUPPORT, what are 2 ANTIMICROBIALS you can use to treat LISTERIA?

1. OXYTETRACYCLINE 2. PENICILLIN

CONTAGIOUS ECTHYMA aka called what 2 things? what type of pathogen is this? zoonotic risk?

CONTAGIOUS ECTHYMA aka called 1. ORF 2. SORE MOUTH PARAPOXVIRUS YES ZOONOTIC, can transmit to people through DIRECT CONTACT

CONTAGIOUS ECTHYMA lesions are usually WHAT and SEEN IN WHAT 3 AREAS? 3 diagnostics? which is best?

CONTAGIOUS ECTHYMA lesions are usually SCAB-LIKE 1. LIP COMMISSURES 2. can extend to NASAL OPENINGS 3. also DAM'S TEATS 3 diagnostics? 1. PCR OF CRUSTS (best) 2. ELECTRON MICROSCOPY 3. HISTOPATHOLOGIC CHANGES

CONTAGIOUS ECTHYMA treatment? prognosis? morbidity and mortality?

CONTAGIOUS ECTHYMA? treatment = NONE, usually SELF-LIMITING and only lasts 1-3 WEEKS but can REMAIN IN HERD FOR YEARS prognosis = GOOD with HIGH MORBIDITY and LOW MORTALITY

OVINE PROGRESSIVE PNEUMONIA (OPP) what TYPE of pathogen is this? transmission? clinical signs are USUALLY what? but give 3 examples

OVINE PROGRESSIVE PNEUMONIA (OPP) RETROVIRUS transmission = to LAMBS via COLOSTRUM clinical signs are usually VAGUE from CHRONIC SUBCLINICAL INFECTION, but 3 examples... 1. PNEUMONIA 2. POOR-DOING (weight loss, febrile) 3. MASTITIS

OVINE PROGRESSIVE PNEUMONIA (OPP) prevalence in ADULTS vs. LAMBS? diagnosis? what does a POSITIVE test mean? treatment?

OVINE PROGRESSIVE PNEUMONIA (OPP) ADULTS > LAMBS diagnosis made on SEROLOGY (antibody test), if POSITIVE means CURRENT DZ because it's LIFELONG treatment = CULL

CAPRINE ARTHRITIS ENCEPHALITIS VIRUS (CAE) what TYPE of virus is this? transmission? clinical signs are usually WHAT? but give 3 examples with some DISEASE NAMES diagnosis? what does a POSITIVE test mean? treatment?

CAPRINE ARTHRITIS ENCEPHALITIS VIRUS (CAE) RETROVIRUS transmission = COLOSTRUM to KIDS clinical signs are usually VAGUE from CHRONIC SUBCLINICAL INFECTION, but can be... 1. POLYARTHRITIS IN ADULTS 2. CHRONIC MASTITIS IN ADULTS (hardbag) 3. ENCEPHALITIS IN KIDS diagnosis made on SEROLOGY (antibody test), if POSITIVE means CURRENT DZ because it's LIFELONG tx = CULL

what makes SHEEP & GOATS more likely to develop UROLITHIASIS? (5)

1. WETHERS CASTRATED <6 MONTHS 2. SMALLER BREEDS 3. more likely at 1-3 YEARS OF AGE 4. HIGH GRAIN DIET/RICH LEGUME HAY 5. IMPROPER MINERAL BALANCE DIET

what part of the RUMINANT URETHRAL TRACT is the most COMMON location for UROLITHS to form? which one is the SECOND MOST COMMON

URETHRAL PROCESS is MOST COMMON SIGMOID FLEXURE is SECOND

what are the 2 most common types of UROLITHS in RUMINANTS?

1. STRUVITE 2. CALCIUM

give 4 options for TREATMENT of UROLITHIASIS in ruminants

1. URETHRAL PROCESS AMPUTATION 2. TUBE CYSTOTOMY 3. PERINEAL URETHROSTOMY 4. URINARY ACIDIFIERS

what does COCCIDIA usually cause? in what AGE ruminants?

COCCIDIA causes PROFUSE DIARRHEA in YOUNG ANIMALS 3-6 MONTHS OLD

what type of PARASITE is H. CONTORTUS?

STRONGYLE

LUNGWORMS in ruminants can cause WHAT clinical sign and are DETECTED HOW?

LUNGWORMS can cause COUGHING diagnosed on BAERMANN exam of FECES

LICE mainly affects WHAT RUMINANT? what 2 clinical signs do we usually see?

LICE mainly affects GOATS PRURITUS & PATCHY ALOPECIA

MANGE MITES mainly affect WHAT RUMINANT? what 2 clinical signs do we usually see? WHERE do they tend to occur what TYPE of mite is COMMON IN US? diagnosed via...

MANGE MITES affect GOATS 2 clinical signs? --> seen on the LEGS 1. ALOPECIA 2. PRURITUS CHORIOPTIC MITE is common in US! diagnosed via SKIN SCRAPE

JOHNE'S DISEASE causative agent? 2 means of TRANSMISSION? animals tend to be ASYMPTOMATIC until WHAT AGE RANGE?

JOHNE'S DISEASE caused by MYCOBACTERIUM AVIUM subsp. PARATUBERCULOSIS 2 means of transmission? 1. CONTAMINATED MILK/FECES 2. TRANSPLACENTAL animals tend to be ASYMPTOMATIC until 2-7 YEARS OLD

JOHNE'S DISEASE BEST choice for diagnosis? treatment?

JOHNE'S DISEASE BEST diagnostic = SEROLOGY treatment = NONE, CULL

CAMELIDS are what kinds of breeders?

NON-SEASONAL

how many PERMANENT TEETH do CAMELIDS have?

30-32

CHOANAL ATRESIA mainly occurs in WHAT species? what is it? big clinical sign?

CHOANAL ATRESIA mainly occurs in ALPACAS what is it = OPENING between NASAL & PHARYNGEAL AREA blocked by MEMBRANOUS or BONY TISSUE big clinical sign = DIFFICULTY BREATHING/NURSING

what is the MOST COMMON CONGENITAL defect in CAMELIDS?

CHOANAL ATRESIA

PARAELAPHOSTRONGYLUS TENUIS aka ___ worm what SPECIES usually affected? pathogenesis? (3) what main clinical sign?

PARELAPHOSTRONGYLUS TENUIS aka MENINGEAL worm usually affects LLAMAS pathogenesis? 1. resides in BRAIN of WHITE-TAILED DEER 2. pass in deer FECES and INGESTED BY SNAILS/SLUGS 3. CAMELIDS EAT SNAILS/SLUGS --> migrates to SPINAL CORD & BRAIN clinical sign = HIND END PARESIS

PARELAPHOSTRONGYLUS TENUIS diagnosis? besides SUPPORTIVE CARE, 3 other tx options? how can we PREVENT it?

PARELAPHOSTRONGYLUS TENUIS diagnosis = EOSINOPHILIA on CSF TAP 3 tx? 1. DEWORMING W FENBENDAZOLE > IVERMECTIN 2. NSAIDs 3. CORTICOSTEROIDS prevention = ROUTINE DEWORMING W IVERMECTIN in ENDEMIC AREAS

ADULT CAMELIDS can be PERSISTENTLY INFECTED WITH ___ and can TRANSMIT this disease to ___

BVD, CATTLE

VITAMIN D DEFICIENCY more likely in WHAT 2 TIMES OF YEAR in CAMELIDS? clinical signs mostly appear in WHAT animal/age? what are 2 findings on RADS? what do we need to MONITOR doses of VIT D supplemented for this?

VITAMIN D DEFICIENCY more likely in.. 1. WINTER 2. EARLY SPRING clinical signs mostly appear in CRIAS <6 MONTHS 2 rad findings? 1. GROWTH PLATE WIDENING 2. FAILURE OF OSSIFICATION MONITOR FOR RENAL TOXICITY

MYCOPLASMA HAEMOLAMAE occurs in ___ pathogenesis? many affected are ____ 2 diagnostics? what ANTIBIOTIC can we use to treat?

MYCOPLASMA HAEMOLAMAE occurs in CAMELIDS pathogenesis = BLOOD PARASITE that ATTACHES TO ERYTHROCYTES and causes ANEMIA many affected are ASYMPTOMATIC 2 diagnostics? 1. seen on BLOOD SMEAR 2. PCR antibiotic for SEVERE infections = OXYTETRACYCLINE

ULCERATIVE POSTHITIS aka called "what"? affects species > species? most common in MALES that are.. what is the CAUSATIVE AGENT? G+/-?

ULCERATIVE POSTHITIS aka called "PIZZLE ROT" affects OVINE > CAPRINE/BOVINE most common in MALES that are CASTRATED causative agent = CORYNEBACTERIUM RENALE G +

ULCERATIVE POSTHITIS what is the PATHOGENESIS? dietary factor? what about around the PENIS can make this worse?

ULCERATIVE POSTHITIS pathogenesis = C. RENALE produces UREASE which hydrolyzes UREA to AMMONIA and causes IRRITATION TO PENIS & SKIN dietary factor = HIGH-PROTEIN (>16%) EXCESS HAIR around the penis can RETAIN URINE NEAR THE SKIN

what are 2 ANTIBIOTICS we can use for ULCERATIVE POSTHITIS? what are 2 TOPICAL treatments we can use?

2 ANTIBIOTICS for C RENALE 1. PENCILLIN 2. CEPHALOSPORIN 2 TOPICALS? 1. BACITRACIN 2. COPPER SULFATE

animals in diets HIGH in WHAT 3 THINGS and LOW in WHAT predisposes them to UROLITHS?

HIGH in.. 1. Mg 2. P 3. GRAIN LOW in ROUGHAGE

Ovine & Caprine PowerPages Flashcards

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