Bovidae/Antilocapridae

Question 1

What is unique about the family antilocapridae?

Answer 1

Antilocapridae

• Pronghorns are the sole species
• Possess forked horns that shed annually
• Native to North America, found in prairies and deserts
• Fast runners but not agile jumpers - fragmented by fencing
• Extremely fractious - prone to stress hyperglycemia
• Only ungulate to exhibit multiple paternity

Question 2

Describe the taxonomy within Bovidae.

What are the subfamilies - what species are in each of them?

Answer 2

Question 3

Describe the ideal housing of bovids and antilocaprids.

What are some of the difficulties of population management in these species?

Answer 3

Population management (F8)

• Captive populations carry a predicted decline in future space
• Few sustainable bovid populations exist in wild or captivity
• Recommend managing antelope in larger, less intensively managed groups

Special housing requirements

• Pronghorns require wide open spaces, open shelters
  
  • Fractious, compromised by high humidity, novel stimuli, and enclosed spaces
• Fences and bomas should be minimum of 2.5m high with sight barrier (prevent trauma and aggression)
• Desert species risk of frostbite in cold season, get hoof abscesses in muddy conditions
• Forest and cold-adapted species require shade during warm season, benefit from plantings or structures to support hiding

Question 4

What vaccines should be used for bovids?

Question 5

Describe the nutrition of neonatal bovids.

Describe the supplementation of colostrum - which products are preferred?

Describe early GI physiology in neonatal ruminants - how does it change over time?

Answer 5

Feeding the neonate

• Maternal rejection is common and hand rearing is labor intensive
• Acquire immunity through colostrum (IgG) within 24-48 hours
• Ability to absorb antibodies ends 24 hours after the first meal 🡪 FPT after this period
  
  • 1st choice colostrum replacement = fresh or frozen intraspecific colostrum
  • 2^nd choice = low temperature pasteurized cow’s colostrum, commercial freeze-dried cow’s colostrum replacer, or commercial bovine plasma
  • Conspecific plasma or commercial bovine plasma if passive transfer inadequate after 48 hours
• Formula should mimic dam’s milk 🡪 goat milk is a good choice
  
  • May be low in vitamin E, zinc, copper, and iron 🡪 vitamin supplementation
  • Should receive 8-15% of BW every 24 hours
• First 2-3 weeks, milk digestion occurs in abomasum and small intestine
  
  • Deposition into abomasum is facilitated by esophageal groove closure which is stimulated by suckling
  • Force feeding calf with poor suckle response may cause rumenitis and septicemia as milk is deposited into nonfunctional ruminoreticulum
  • Tube feed by passing tube mid-esophagus to stimulate swallowing and closure of esophageal groove
  • 10% sodium bicarbonate or 2-5% copper sulfate may facilitate groove closure
• By 2-3 weeks, ruminal papillae are stimulated and start eating some dry feed

Question 6

Describe the nutrition of adult bovids.

What are some common nutritional problems?

Describe the ideal diet for a grazer.

Describe teh ideal diet for a browser.

How should nutrition be adjusted for a sick bovid?

Answer 6

Feeding the adult

• Many health problems are directly or indirectly related to diet = rumen acidosis, rumenitis, laminitis, hoof overgrowth, periodontal disease
  
  • Partly attributed to historical feeding of domestic cattle diets
• Grazers – consume grass
  
  • Rumen for fermenting high cellulose through prolonged fermentation and particle retention
  • Should be fed commercial herbivore pelleted concentrate containing 12-18% protein and 16-25% acid detergent fiber at 1% BW per day in addition to hay
• Browsers – consume leaves and twigs of woody plants
  
  • Smaller, less muscular rumen compared to grazers
  • Eat less hay and often fed more pelleted concentrate to compensate

§ High levels of easily digested carbohydrates (pelleted concentrates) 🡪 too rapidly fermented in the rumen 🡪 rumen acidosis

· Pelleted diet should include:

§ 1) High fiber forage meal (ex aspen, alfalfa)

§ 2) Contain high pectin, low-sugar energy like beet pulp

§ 3) Limited amounts of grain and corn

· Should be fed 1.5%-2.5% of BW per day of pelleted feed in addition to ad libitum grass or legume hay

• Intermediate – both browse and grass
• Negative energy balance and weight loss from illness or alteration of rumen pH
  
  • Commercial products for boosting caloric intake – Low Odor MEGALAC Rumen Bypass Fat and Wild Herbivore Boost
  • Transfaunation with rumen contents from healthy conspecific also recommended

Question 7

Describe the physical and mechanical restraint of bovids.

How do you restraint small and medium bovids?

What equipment is available for restraint?

Answer 7

Restraint and handling (F8)

• Behavioral restraint – training and desensitization
• Manual capture and restraint
  
  • Small bovids under 5kg
    
    • Can be quickly lifted by a single handler
    • Support the abdomen and spine against handler’s body and restrain head and legs
  • Medium sized bovids
    
    • Catch the head first and quickly push the animal against a wall or floor then placing a knee under the flank
    • Second handler restrains the legs
    • Careful with young animals and those with thin horns prone to horn avulsion
  • Once restrained, place blindfold and ear plugs to minimize stimuli
    
    • Short pieces of hosing over horn tips for safety of handlers
  • Minimize duration to prevent distress and hyperthermia (and subsequent capture myopathy)

Mechanical restraint

• Box chutes - simple pass-through enclosure with front and rear sliding barriers
• Drop-floor chute
  
  • Ramp leading to adjustable V-shaped chute with sliding front and rear doors, once restrained floor drops and animal is suspended by hips/shoulders
  • Procedures should be limited to a few minutes
• Squeeze chutes
  
  • Hydraulic squeeze chutes provide the most flexible manipulation of large numbers of animals
  • Apply pressure to the hips and shoulders of the animal and may lift or close down over the animal to provide a darkened space

Question 8

Describe the role of neuroleptics in bovid restraint.

How do they work?

How long do they take to start working - how long do they last?

Answer 8

o Neuroleptics (butyrophenone and phenothiazine) attenuate stress response

§ Blocking D2 dopamine receptors 🡪 produces state of lucid relief

§ Longer acting formulations have onset of action of 1-3 days, can add shorter acting neuroleptics to produce immediate and long-term tranquilization

§ Overdosing 🡪 tardive dyskinesia (abnormal facial and tongue posture), head pressing, and anorexia

§ TX using low dose xylazine, diazepam or diphenhydramine

Question 9

Describe the chemical restraint of bovids.

How does route of administration change the course of anesthesia?

What are the main classes of anesthetics and sedatives used in these species? What are some pros and cons of each?

Answer 9

Chemical restraint

· Induction of general anesthesia

o IV = decreased induction and recovery time

o IM = rapid/smooth induction and long duration

o Failure to deliver an appropriate dose 🡪 excessive running, capture stress or myopathy

§ Decision to repeat the dose needs to occur within 20 minutes

Question 10

Describe intubation in the following groups of bovids:

Antelope

Bison

Answer 10

Intubation (Antelope)

• Recommend if need to be transported, >1 hour procedure, or spp. prone to regurgitation (giant eland, duiker, roan, addax)
• Ensure adequate plane of anesthesia prior to intubation
• Blind intubation only successful ~50% of time in cattle, not recommended
• Process - visualize larynx w/ laryngoscope, past stylet or ET tube exchanger into trachea, remove laryngoscope and feel stylet through Murphy’s eye of ET tube and pass tube over stylet and into trachea
• IPPV can be used to treat unacceptable hypercarbia (PaCO2 > 60 mmHg)
• Portable batter powered O2 concentrators may be alternative to O2 cylinders in field
  
  • Improved oxygenation in reindeer but not bighorn sheep - more research needed
• Can use lead blower as ventilator is large species - but be cautious of gas-powered d/t potential CO inhalation

Endotracheal Intubation (Bison)

• Often not performed in field settings, but recommended if volatile anesthesia is used
• Sternal recumbency and elevate head, guide tube to epiglottis, displace epiglottis ventrally with a finger and advance tube into glottis
• 24-30 ET tube for mature bison

Question 11

What preanesthetic considerations should be taken into account prior to a procedure on a bovid?

Answer 11

Pre-anesthetic considerations

• Ruminants are prone to ruminal tympany and regurgitation, which can lead to aspiration and subsequent pneumonia
• Animals should be fasted for a period of 18-36h prior to induction
  
  • Authors recommend only removing concentrate and allowing access to hay, grass +/- water
• Water access should be discontinued 8-12 hours prior
• Maintaining the animal in sternal recumbency can reduce the possibility of rumen regurgitation, especially in field conditions, when the animal cannot be fasted
  
  • If sternal recumbency is not possible, the head should be positioned or propped so the mouth and nose are pointed in a downwards direction
• The head and neck should be extended to maintain a patent airway

Question 12

What are the common venipuncture sites in bovids?

What monitoring should be performed during anesthesia?

What are teh concerns with hyperthermia in these species? How can they be managed?

What are typical blood pressures in these species?

Answer 12

Vascular Access Sites and Monitoring

• Common vascular access sites - auricular, jugular, cephalic, medial and lateral saphenous, lateral thoracic
• Arterial access - radial, caudal auricular, and common digital arteries
  
  • Facial artery - palpable but difficult to catheterize
• CV Monitoring - HR, pulse strength, MM color, CRT
  
  • Venous blood color (ear vein) - crude but useful oxygen indicator
  • Resting HR generally unknown but ~80 bpm in cattle, smaller ruminants as high as 110 bpm
  • Pulse pressure can be used in the field for crude estimations

§ If digital pressure on an artery is easily accomplished in diastole - assume pressures low

• Alpha-2 agonists typically make MM pale, and often resolved after 20-30 min or reversal

· Respiratory adequacy - RR, respiratory depth

o Feel breath from nostrils or watch thoracic excursions

· Ocular reflex/eye position often not useful due to remote induction

· Core body temperature monitoring essential

o Rectal typical, but core likely better reflected by esophageal probe

o Hyperthermia and subsequent capture myopathy one of most common anesthetic issues

§ High ambient temps can contribute but can occur in controlled temps as well

§ Hyperthermia may be induced by psychological factors regardless of ambient temps in impala

§ Common causes - prolonged induction, stress, depression of thermoregulation under anesthesia

§ Poor dart placement and underdosing 🡪 excessive running, pacing, capture stress, hyperthermia

§ Study placed data loggers in 15 impala and used 4 induction combinations

§ Extremely high rise in body temp, peaking 20-30 min after reversal of immobilization regardless of drug combo

§ Changes in body temp related to time it took for an animal to become recumbent, not the effect of the drug combo

§ Physiological consequences of capture related to duration of exposure to a stressor (induction) and not the drug pharmacology

· Although shorter time to recumbency had benefit of less stress and body temp changes, were predisposed to hypoxemia, induction apnea (higher doses)

· Authors still prefer quicker inductions w/ anesthetic management of oxygen/resp.

· Common treatment approaches

· Topical water or cold water enemas

· Authors prefer to deepen anesthesia, intubate and place on ventilator (esp. in large species)

§ Allows exchange medium (oxygen, air) to contact large surface area, reduce muscular effort required

§ Paralytics can be used to quickly intubate and reduce resistance against ventilator

§ Moderate fluid therapy and NSAID and steroidal anti-inflammatories can be adjuncts

Additional monitoring if longer procedure

· Pulse oximetry - tongue, ear, vulva, prepuce; reflectance on gingiva, vagina, rectum

· NIBP - commonly tail, distal limbs

· Goats/sheep - 100 mmgHg systolic, 60 mmHg diastolic, mean of 75 mmHg

· Cattle- generally higher

· Good guidelines for small and larger antelope respectively

· Mean of 60 mmHg suggested for zoo bovids

· Addax (carfentanil, acetylpromazine, ketamine) - initial MAP 118 mmHg vs (carfentanil, xylazine) - initial MAP 120.5 mmHg

· Change in BP often sensitive indicator of change in depth

· ECG - base-apex (larger spp.) or standard 3-lead (smaller spp.)

· Premature ventricular contractions (PVCs) most common arrhythmia in ruminants

· Run of 3 PVCs are serious - warrant attention

§ Common causes - hypoxemia, hypercarbia

§ Treatment - lidocaine, correct cause

· Arterial blood gases

Question 13

What are some common anesthetic complications in bovids?

Answer 13

Hyperthermia

Capture myopathy

Ruminal tympany

Hypoxemia

Renarcotization

Question 14

What are some of the advantages of thiafentanil over etorphine or carfentanil?

Answer 14

Fowler 7 Ch 76 - Thiafentanil Oxalate (A3080) in Nondomestic Ungulate Species

Features of thiafentanil oxalate

· opioid, synthetic fentanyl derivative

· MOA → morphine-like analgesic, rapid immobilization following IM injection

Clinical considerations

· reduced induction time (up to 50%) compared w/etoprhine and carfentanil

· more rapidly absorbed and metabolized

· decreased induction time → quicker handling mitigates problems (e.g., trauma, hyperthermia, escape)

· renarcotization less of a problem → escaped wildlife can recover w/o reversal

half-life 50% that of carfentanil

· approved for use in Republic in South Africa

· much knowledge about African spp.

· some knowledge about other spp.

· DOC for American pronghorn antelope

· not that effective for family Equidae (similar to carfentanil)

· has same negative effects as other opioids/opiates

· excitement, tachy- or bradycardia, tachy- or bradypnea, hyper- or hypotension, cyanosis, poikilothermia, reaction to sudden noise

· less repiratory and cardiac depression than others

· typically combined with tranquilizers, sedative, or dissociative agents

· See table pp.591-593 for recommended dosages

Human safety

· same as for the others

Animal studies

Recommended doses for nondomestic hoofstock

· see previous table

· depends on animal and situation

Administration

· IM or IV

Antidote

· naltrexone 10mg per/mg of thiafentanil

Warning

· only use it if you know what you’re doing

Question 15

Describe the following parasite monitoring strategies in nondomestic ruminants:

Modified McMaster’s Fecal Egg Count

Fecal Egg Count Reduction Test

In Vitro Larval Development Assay

Pasture Larval Count

Answer 15

Parasite Monitoring Strategies

Modified McMasters Fecal Egg Count (MMFEC)

• Sensitivity of 50 eggs/g (epg)
• Samples can be refrigerated up to 7 days, but not frozen
• Larval hatch out of fecal matter ~12-24 hrs at room temperature
• Lab technique- SCSRPC; www.scsrpc.org
• Trichostrongyle-type eggs (oval; ~80-90 um) counted on 10 X power
• Other parasites not counted- can make notation of them
• The count (epg) = total number of eggs in both chambers x 50
• More objective to:
  
  • Understand patterns of infection and shedding
  • Success of parasite management
  • When program changes are needed
  • Whether changes are helping
• Annual and biannual fecal egg count for some artiodactylid species
• Higher risk species may need more frequent monitoring
• Monitor trends, use in-house data to establish guidelines

Fecal Larval Culture, Larval Development Assay, and Fecal Egg Count Reduction Test

• Diagnostic options when trichostrongyle species and resistance status are identified:
• In vitro larval development assay (LDA)
• Includes:
  
  • Fecal larval culture (FLC), species ID +/- FLC in combination with fecal egg count reduction test (FECRT)
• 2-year survey of exotic artiodactylid nematode populations in four zoos using FLC:
  
  • Found individual, species, exhibit, and seasonal variability in nematode species
• Nematode species vary in anatomic location of infection, potential for morbidity and mortality, and response to therapy
  
  • FLC can help strategize treatment options

LDA +/- FECRT –

• LDA (DrenchRite)-may identify nematode populations and determine their resistance levels
  
  • Performed in a parasitology diagnostic laboratory
  • May detect resistance to 3 classes in one assay:
    
    • Benzimadazoles, levamisole, and avermectin-milbemycin anthelmintics from a single herd sample
• FECRT (%) = (Pretreatment FEC – post treatment FEC)/ pretreatment FEC x 100
  
  • In-house means of determining if resistance is present
  • FEC sampling done before and 10-14 days following treatment on individual animals
  • An untreated control group should also be included
  • <95% indicates an incomplete therapy response and likely concern for resistance
• FLC and LDA testing can be done monthy or bimonthing for 1^st year, to identify areas of concern, then annually or biannually to monitor for changes in population trends.
• FECRT should be done after every treatment is performed

Pasture Larval Count (PCL)-

• 2-year survey of nematode populations in a Florida zoo using PLC assay found:
• Exhibit, exhibit region, species, and seasonal variability
• Not an in-house test- need a parasitology lab
• Can be done monthy or bimonthing for 1^st year, to identify areas of concern, then annually or biannually to monitor for changes in population trends.

Question 16

Describe the anhelmintic treatment of parasites in bovids.

Is fasting prior to medication administration recommended?

How do cattle, sheep, and goat dosages differ? How does this affect exotic hoofstock dosing?

What anthelmintic has a narrow safety margin?

What is the FAMACHA scoring system?

Answer 16

Parasite Control Strategies:

Drug Treatment-

• Anthelmintics must be used conservatively, not on a rotational basis
• Smart drenching approach-
  
  • Uses information about the parasite, animal, and drugs to maximize effectiveness of treatments and decrease resistance
• Oral dosing in domestic ruminants-
  
  • Duration of drug availability is dependent on flow rate of the rumen
  • For benzimidazole and avermectin classes, fasting animals 24 hrs prior to treatment decreases rumen motility and increased drug efficacy
• Dosing accuracy to minimize resistance challenging in exotic species
• Domestic species:
  
  • Significant differences in dosing of cattle vs small ruminant species
  • Goats metabolize drugs more rapidly than sheep or cattle (1.5-2.0 x higher)
  • Caution- Levamisole has narrow margin of safety, use at no more than 1.5 times dosage
  • In general- anthelmintics most effective orally
  • Moxidectin in goats has superior pharmacokinetics with S.C injection
  • Pour-ons-
  • Poor bioavailablility in nonbovid species
  • Highly variable absorption with different follicular densities and skin lipid characteristics
• Standardized scoring system correlating conjunctival color with level of anemia for control of H. contrortus(FAMACHA; www.ars.usda.gov)

Question 17

Describe animal management strategies to reduce gi parasites in bovids.

What does the term refugia mean?

How can you select to decrease resistance?

How does rotating exhibits (pastures) help?

How should animals be fed to reduce parasite exposure?

What features of an exhibit lead to congregation of animals?

Answer 17

Animal Management-

• Mixed species exhibits combining primary grazers with higher risk browsing species reduce nematode burdens on susceptible species
  
  • Reduces grass length and larval exposure while increasing pass-through species and refugia
• Refugia- population not under selection by drug treatment; includes untreated animals and eggs and larvae present in the pasture
  
  • Refuge of susceptible genes dilutes the frequency of resistant alleles
  • In domestic animal industry, refugia is the key animal strategy to manage drug resistance
• Strategy of selection against resistance- under investigation
  
  • Requires LDA testing in quarantine
  • Susceptible nematodes are added into current population to dilute resistant nematode strains
  • Aggressive, synergistic, multidrug therapy is used against highly resistant nematodes
• Environmental Control-
• Rotating species on exhibit and multispecies populations increase refugia population
• Diet and enrichment items such as elevated browse and grass >3 inches may minimize larval exposure
  
  • Larvae usually migrate 3 to 5 inches up the grass blade
• Tilling exhibits between grazing seasons can help kill larvae
• No chemicals have been proven to be effective in killing larvae on pastures
• Trees can cause congregation of animals and greater exposure to larvae
• Barns and watering areas can also lead to congregation of animals
• Fecal removal recommended if feasible
• Water control measures can limit larval development

Question 18

Describe the non-pharmaceutical methods that are available to control parasites in bovids.

What are copper oxide wire particles? How effective are they? Are there any toxicity concerns?

How do condensed tannins work against parasites?

What nematophagous fungi can be useful? How does that work?

Answer 18

Nonanthelmintic Control and Treatment Strategies

• Limited studies of safety and efficacy in exotic artiodactylids- monitor FEC and possible toxicities.

Copper oxide wire particles (COWPs)-

• Success in domestic ruminants well documented
• Good efficacy against Haemonchus spp.
• Can reduce FEC by 60-90% for 21 to 28 days
• COWPs are retained in folds of abomasa, releasing soluble copper ions
• Exact mechanism of action is unknown
• COWP study in four species of exotic artidactylids – species variability
  
  • FECRT >90% in 3 species at 7 days, and 21 days for all species
• Copper doen’t appear to affect intestinal nematodes, FLC critical prior to treatment
• Boluses can be made using copper boluses dosed in gelatin capsules
• Toxicity Cautions-
  
  • Copper accumulates in the liver and can predispose to hepatic disease and anemia
  • Recommended supplemental dose – 0.25 to 0.5 g/kg
  • Limit therapy to no more than once every 6 to 12 months
  • Other factors- dietary sources, other minerals (molybdenum, sulfur, iron, zinc), other environmental sources
  • Do not give COWPs to animals with unknown copper status, those supplemented with other forms of copper, or if have liver disease
  • Copper oxide is not as readily absorbed as copper sulfate, but may stay in the system for a few weeks (copper sulfate is a few days)
  • Concentrations > 1.5% copper sulfate may be caustic

Condensed Tannins-

• Polyphenolic plant compounds that bind proteins and other molecules
• Two main types:
  
  • Hydrolyzable- may be toxic to animals
  • Bioactive condensed tannins (CTs)- found in legumes and other plants
    
    • Table 75-1 (p. 585)– Forage species and g/kg DM CT
    • Sericea lespendeza (Lespedeza cuneata) –
      
      • CT-containing bioactive plant useful in controlling internal parasite infection in sheep and goats fed as pellets
• Exact mechanism of action unknown

Nematophagous Fungi-

• Duddingtonia flagrans- Nematode-trapping fungus
  
  • Parasitizes developing nematode larvae in feces
  • Ubiquitous, found worldwide, normally present in feces at low levels
  • Spores can be added to diet, pass unchanged through digestive tract and concentrate in feces
    
    • Spores germinate after feces deposited onto pasture
  • Used as a preventative, no therapeutic benefits
  • Active against free-living larvae, no effect on adult states in vivo
  • Eventually reduces pasture larval numbers
  • Fungal spores must be fed daily for 2 weeks for full benefit
    
    • Alternate-day feeding shown to have acceptable activity
    • Dose – 250,000 to 500,000 spores/kg BW
    • Larval reduction at 7 to 14 days once treatment starts
    • Feed with dry diet to minimize moisture and premature sporulation
  • No environmental impact studies have been done
    
    • Believed spores survive in feces for 3-4 days
  • Studies in using with COWPs in small ruminants underway
  • No commercial source of spores in US

Other Treatment Strategies-

• Long-term- parasite vaccine
• Increasing protein not recommended in zoo species on high-quality diet
• Nicotine sulfate- nerve-paralyzing toxin- narrow safety margin in host
• Diatomaceous earth-
  
  • Fossilized unicellular marine or fresh water algae used as food ingredient and swimming pool filters
  • Nonfood-grade can have heavy metal contamination
  • Minimal effects in sheep and goats unless high levels given
• Herbal anthelmintics- Various plants- limited investigations or efficacy, some may be toxic
• Garlic or other herbs – Commercial preparations not shown to be effective

Question 19

What is the scientific name of the barber pole worm?

Describe its light cycle.

What is its prepatent period - why does this matter clinically?

Answer 19

Barbers pole worm (Haemonchus contortus) life cycle

· Female barber’s pole are prodigious egg layers and can lay up to 10,000 eggs per day. The adult female in the 4^thstomach (abomasum) lays eggs, which are passed out in the dung.

· If the weather is warm and moist the eggs hatch into first stage larvae (L1). These moult or shed their skin (cuticle) to become 2^nd stage larvae (L2). Second stage larvae (L2) undergo an incomplete moult to become 3^rd stage larvae (L3) which are the infective larvae.

· L3 larvae retain the old L2 cuticle, which provides a protective sheath and nutrients until the larvae are ingested by a sheep. However this cuticle prevents L3 larvae from feeding on bacteria.

· All larval stages (except L3s) feed on bacteria in the dung pellet until they either die or escape from the dung pellet onto the pastures.

· Under ideal environmental conditions, development from egg to L3 takes around seven days, but can be as long as five weeks if conditions depending on warmth and moisture. Heavy dews and rain release the L3 from the dung pellet onto the pasture. L3 larvae increase the chance of being ingested by sheep by responding to light and temperature.

· As the pasture is warmed by sunlight and in the presence of moisture (dew/rain) the L3 migrate up the grass blades where they are most likely to be eaten. On cold nights they move down to the base of the grass. When the L3 are ingested, compounds in the gut of the sheep stimulate the larvae to rapidly (usually within 30 minutes) complete the second moult (exsheathment) and start moving towards the 4^th stomach (abomasum).

· On the way they moult a third time and arrive in the abomasum as an immature worm. When the larvae mature, they mate and the cycle starts all over again.

· It takes around 21 - 28 days from when a sheep ingests the larvae to when worm eggs appear in dung samples. It is important to remember this for 2 reasons:

• If the sheep are treated with a fully effective short acting drench, they can be used to “clean” paddocks for weaners (smart grazing) for the 21 - 28 day period without fear of recontaminating the paddock.
• If the sheep are tested for worms using a worm egg count during the 21 - 28 day period, you may think that the sheep are free of worms when, in fact, they could have a considerable burden of larvae. If you think the sheep could be picking up worms after drenching, tests at about 4 - 6 weeks when egg laying has commenced and you will have a much better idea of the rapidity and scale of the reinfection.

http://www.wool.com/Grow_WormBoss_Know-your-worms_Barbers-pole-worm.htm

Question 20

What is capture myopathy?

What are the four syndomres associated with it?

What bovid species are particularly susceptible?

Are they other risk factors?

How is it prevented?

How is it treated?

Answer 20

Capture myopathy

• Secondary to prolonged pursuit, capture, restraint, high temps
• Exhaustion of ATP, ↓ oxygen delivery to tissues, and ↑ lactic acid production 🡪 muscle necrosis, myoglobulin release, and renal failure
• Characterized by ataxia, metabolic acidosis, muscle necrosis, and myoglobulinuria
• Predisposing factors
  
  • Species (pronghorn, nyala, tsessebe, duiker, roan for example), high temp and humidity, vitamin E or selenium deficiency, pregnant, older
• Prevention
  
  • Less than 3 min pursuit, ↓restraint time, ↓visual and auditory stimulation, avoiding temps >68F, using sedation and anesthesia
• Treatment
  
  • Aggressive fluid therapy and metabolic acidosis treatment ASAP
  • Sodium Bicarbonate bolus (1-2 mEq/kg) and re-administered as indicated
    
    • Lactate should be < 2mmol/L
    • Lactate > 5-6mmol/L = poor prognosis
  • Calcium gluconate as a cardioprotective
  • Insulin and dextrose to stabilize potassium levels
  • Corticosteroids, dimethyl sulfoxide (DMSO), or combination is preferable over NSAID for control of inflammation (due to renal compromise)
  • Keep cool, in quiet area, and monitor renal output (1ml/kg/hr) for several days
  • Death occurs from renal failure

Question 21

Describe the role of calcium and magnesium in the ruminant.

What is the role of magnesium in the body? What are the signs of hypomagenesemia?

What are common dietary sources of magnesium? What causes poor magnesium absorption?

What is the role of calcium in the body? How is it stored? What are the signs of hypocalcemica?

How does hypomagnesemia contribute to hypocalcemia?

Answer 21

Fowler 6 Ch 49 - Hypocalcemia, Hypomagnesemia, Rumenitis in Exotic Ruminants

Introduction

• New feed products and strategies have results in increased prevalence of hypocalcemia and hypomagnesemia = tetany
• Other manifestations of imbalances: chronic laminitis, decreased body condition
• Inverse Ca:phosph ratio is typically seen in animals on “balanced” diet.
• Magnesium is not included in routine analysis, so may be overlooked (not sure if this is blood or feed analysis)
• Persistent hypoCa paired with sudden drop in Mg may lead to tetany
• Species recognized with this syndrome: Nyla, kudu, eland, bongo, giraffe

Review of Mineral Metabolism

• Role of magnesium
  
  • 70% of Mg is found in bone, is not available
  • Mg is the 2^nd most common intracellular cation after K
  • Small Mg pool, therefore Mg must continually be ingested to maintain levels
  • Minimal control over Mg homeostasis
  • Mg plays a roll in muscle contraction, energy metabolism, Ca metabolism, RNA/DNA synthesis
  • “Grass staggers” in domestic ruminants with low Mg
  • Chronic hypoMg:
    
    • Anorexia, abnormal gait, poor growth rate, poor body condition, hyperexcitability, ear twitch, kick abdomen, bruxism, hypersalivation, tetany, seizures, unexpected death
    • Signs often develop with transport, stress, lactation, anorexia
• Role of calcium
  
  • Majority of Ca is stored in skeleton
  • Only 1% is intracellular and in the extracellular fluid
  • Has roll in nerve and muscle function and enzyme processes
  • HypoCa occurs because of:
    
    • Diet deficiency, imbalance /disruption of Ca homeostasis
    • (Can look up elsewhere about Ca metabolism, ex. PTH, vit D)
  • HypoMg may lead to decreased PTH as well as decreased tissue response to PTH, therefore impairs absorption and retention of calcium
  • Hypo Ca signs:
    
    • Muscle stiffness, tetany, decreased rumen motility, death
    • Chronic Ca deficiency:
  • Poor feed intake, poor growth, rickets, osteomalacia, pathologic fractures
• Dietary sources of Mg and Calcium
  
  • Legumes = high Ca and Mg
  • Grains = higher Mg than most forages but lower Ca than legumes.
  • Things that cause poor Mg absorption = lush grasses high in potassium, sudden increase in rumen ammonia, high diet Ca, low diet Na
  • See chapter for details on rumen Mg metabolism

Question 22

How does rumen acidosis and rumenitis contribute to mineral imbalances?

What are some indirect signs of rumenitis and mineral deficiency?

How does this affect immobilization?

How is this treated?

How can this be prevented?

Answer 22

Rumen acidosis and rumenitis

• May be an underlying cause for chronic mineral imbalances in exotic ungulates
• Decreased rumen pH assoc with intake of highly fermentable carbohydrates, decreased effective fiber intake, overall decreased food intake, stress
  
  • Will lead to shift in microflora which may change to acid production instead of normal fermentation
• Acute acidosis results in:
  
  • Loss of normal rumen flora, chemical damage to rumen epithelium, and systemic acidosis
  • This may result in disruption of nutrient absorption, microbial invasion of rumen epithelium which leads to rumenitis.
  • Possible endotoxin release from bacteria or fungi
  • Focal abscess formation, hepatic abscesses and laminitis are possible
• Feeding practices in captivity may change pH and lead to rumen acidosis/rumenitis:
• Indirect evidence of rumenitis and mineral deficiency
  
  • Intermittent lameness, abnormal hoof growth, laminitis, poor hair coat, poor body condition

Clinical syndrome in exotic ungulates

• Clinical signs of HypoMg and Ca may be seen after immobilization. Animals may have trouble rising, they remain recumbent, stagger, tremors. May mistake for renarc. Suspected that these animals have subclinical rumenitis, which causes impaired mineral absorption.
• Other clinical presentations:
• Dystocia, abortion, birth of weak calves
• Diagnosis
  
  • Clinical signs, especially tetany
  • Serum Mg <1.2mg/dl
  • Low CSF Mg level
  • Inverse Ca : Phosph ratio
• Treatment
  
  • IV calcium and Mg. Give SQ if not very severe
  • Dextrose containing fluids are NOT recommended because insulin will dramatically decrease serum Mg
  • Consider treating secondary muscle fasciculation – judicious use of bicarb, diazepam
  • Oral phosphate binders
  • Chronically affected animals – use cattle formulations that have Ca and Mg and buffers (we assume this means a food supplement)
  • Supportive care as needed
  • P3 fractures are commonly seen in these animals, especially kudu
• Prevention
  
  • Addition of buffers, chelated minerals and fiber may ameliorate rumen acidosis and rumenitis
  • Current recommendation: pelleted diets with <3% starch
  • Increase the ADF from 16% to 32% (acid detergent fiber)
  • Fermentable fibers (such as pecten) can be used to improve rumen fermentation

Question 23

What is heartwater caused by? Describe its life cycle.

Where does this disease typically present geographically?

What is the vector? How did this vector spread geographically?

What are the clinical signs of this disease?

Answer 23

Heartwater Disease Definition

• Non contagious tick born disease of domestic ruminants and wildlife
• One of the most devastating livestock diseases in Africa with high mortality (cattle, sheep, goats)
• Present in: Sub-saharan Africa, Madagascar, some Oceanic islands and Caribbean
  
  • NOT in the USA
• Agent: Ehrlichia ruminantium formerly Cowdria
• Obligate intracellular rickettsia
• 3 forms: elementary, intermediate and reticulate
  
  • Elementary body – infectious stage, will enter the cell
  • Within vacuoles in cell, will form reticulate body
  • Reticulate body will become an intermediate body
  • The intermediate body will then become and elementary body
  • The cell ruptures and releases elementary bodies
• Immunity is cell mediated
• Growing concern that Amblyomma will spread Heartwater into naive areas
• Reportable disease

Epidemiology

• Vectors are ticks – Ambylomma genus, 3 host tick
• Two most important ones globally are: A. variegatum and A. hebraeum
• The A. variegatum is the most important on American mainland
  
  • This is how it was introduced into Caribbean
• Transmit: transtadially (btwn life stages) and intrastadially
• Susceptible animals: cattle, sheep, goats, water buffalo (Bubalus bubalus), ferrets
• Many species have had subclinical and clinical infections – see pg 439 for long list
• A long term carrier state possible in cattle, sheep and African buffalos (Syncerus caffer)

Clinical Signs (this info was under diagnosis but we moved it to a separate heading)

• Subclinical cases: mild transient fever
• Peracute: death without premonitory signs
• Acute: rapid onset fever, tachypnea, inappetence, neurologic signs.
• The most common presentation is acute, often results in death

Question 24

Describe the management of heartwater.

How is this disease diagnosed? What are some of the challenges with diagnosis?

What are some of the classic post-mortem findings?

How is this disease treated?

How is this disease prevented and controlled?

Answer 24

Diagnosis

• Lack of reliable and easy antemortem tests because ehrlichia has a predilection for endothelial cells, so not detectable on blood smears
• The only definitive antemortem test is a brain biopsy (!) in order to examine intimal vascular endothelial cells
• Xenodiagnostics – tick transmission studies
• Nothing notable on blood work
• No validated serologic or molecular diagnostic techniques **
  
  • Could cross react with other ehrlichia tests
  • PCR and DNA assays are available for blood or ticks – this was confusing and seemed to contradict above, may not be accurate based on newest literature information. See page 440 for actual text
  • (And in section on prevention, she again says PCR is available)
• Pathophysiology is poorly understood. Parasitizing vascular endothelial cells and neutrophils and macrophages. Increased capillary permeability, excess fluid effusion into tissues and body cavities
• Post mortem findings: pulmonary edema, ascites and hydropericardium (hence the name heartwater), cerebral edema (lead to neuro signs).
• Definitive post mortem diagnosis: brain smear, shows organisms in endothelial cells with Geimsa stain

Treatment

• Mortality is high once clinical signs develop
• Treatment is frequently limited
• Can treat successfully if catch at febrile stage, but not success if treat once neuro or gi signs are present – Sharon Deem’s personal clinical experience
• Long acting oxytetracycline at the time of expected exposure and before clinical signs

Control

• If area is free of Heartwater – need tick control and vaccination (presumably talking Africa)
• Vaccination
• None currently available
• “Vaccinate” by injecting infected blood IV and then treating with antibiotics at start of febrile period

Prevention

• Tick control
• Control animal transportation, treat transported animals from endemic areas with acaricides
• New source: reptiles from Africa which may be carrying the ticks, especially Leopard tortoise (G. pardalis), spurred tortoise (G. sulcata), Bells hinged backed tortoise (Kinixys belliana)
• The only test shown to detect subclinical infection is PCR ( pCS20 ) and is recommended on all animals entering non endemic area
• Ways that Heartwater can enter a non endemic area:
  
  • Infected tick, subclinical carrier animal, infected free ranging wildlife
• The Caribbean situation:
  
  • Infected migratory birds (cattle egrets) have transmitted Heartwater to various islands.
  • Since Heartwater and A variegatum are present in the Caribbean, we have to be watchful of it entering the USA
  • One cattle egret was found in Florida with Amblyomma ticks but no Ehrlichia agent
• Indiscriminate host range of the rickettsia and vectors makes Heartwater a disease of worldwide importance
• The USA has competent Amblyomma tick vectors as well as susceptible species such as white tail deer (experimental)

Question 25

Contact barns are common in many zoological parks. Cryptosporidium is an important zoonotic concern of these exhibits.

What is the most common cryptosporidium in these exhibits? What animals are most susceptible?

What are the typical clinical signs? How about in people?

How is this diease transmitted?

How is it diagnosed?

Answer 25

Fowler 7 Ch 73 - Management of Cryptosporidiosis in a Hoofstock Contact Area

Introduction

• Cryptosporidum spp. are protozoal enteric parasites of many vertebrate groups.
  
  • Zoonotic concern
  • Human cryptosporidiosis linked to public contact with young ruminants
• Cryptosporidium parvum = most common cause zoonotic infections; cattle = host
• Most common in neonates, then juveniles:
  
  • Young calves, often <8wks, are source of almost all zoonotic cases
  • Can also occur in lambs and goat kids.
• Clinical Signs:
  
  • Neonate animals: unformed stool to severe diarrhea, moderate mortality with uncomplicated infections, coinfections or stress may increase morbidity and mortality.
  • No generally accepted specific treatment in US- paromomycin has been used in individual animals, and halofuginone is used in Europe.
• Clinical Signs in People
  
  • Immunocompetent people infected with crypto = self-limiting gastroenteritis
    
    • Children <2yrs: most commonly and severely affected; watery diarrhea, abdominal pain, bloating.
    • Signs typically resolve w/in 3 weeks, but shedding may continue after resolution of signs
  • Immunocompromised people: Severe infections
    
    • Pancreatic duct and gallbladder tree may be involved, intractable diarrhea, chronic diarrhea, severe weight loss
• Transmission: Ingestion of already sporulated oocytes
  
  • Clinical signs usually occur within 1 week of ingestion
  • Oocytes resistant to disinfection and may persist in environment for months

Diagnosis

• Tiny organism (4-6mm? nm?)
• Visualization of oocysts is confirmatory
• Techniques:
  
  • Centrifugal floatation technique – uses Sheather’s sugar solution
  • Acid-fast staining
  • PCR (significant agreement between PCR and flotation technique)
  • IFA – used by most labs
  • Multiple fecal exams are required to i.d. shedding in asymptomatic animals

Question 26

How can a cryptosporidium outbreak in a contact yard be managed?

How is spread of disease between animals contained?

How can visitor safety be secured?

Answer 26

Prevention and Control: Animals

• Prevention is most important since diagnosis, treatment, disinfection are challenge
• Most important = Do not import or exhibit very young dairy calves!
• Screen all incoming ruminants in quarantine
• Routine fecal exams for shedding in contact areas
• Control Plan for positive crypto case in contact area:
  
  • Prevent visitor and caretaker exposure:
    
    • Close yard immediately
    • Limit keeper staff – educate keepers working the area
    • PPE – coveralls, gloves, sanitation practices
    • Foot baths
    • Leave yard empty 6 mo. OR remove top 15cm soil and replace
  • Prevent further contamination
    
    • Isolate any animal with diarrhea in easy to disinfect stall where fecal material cannot reach other animals
    • Divide exposed and non-exposed population
    • Recommend not releasing recovered animal(s) as no way to guarantee they won’t shed in future – consider euthanasia if they can’t retire from contact area (relocating to new owners also taboo)
  • Determine whether infection spread to other contact yard animals
    
    • Screen all animals multiple times
    • Protocol:
      
      • One month after last clinical case move animals in small groups to hospital (or off contaminated area); 3 fecal exams; If clean move to clean yard
      • Exposed animals had individual fecals for crypto at 3 and 9 months after being moved to new enclosure
      • Biannual herd fecals performed thereafter

Visitor Safety

• Risk factors for crypotsporidium infection via animal contact include:
  
  • Hand to mouth contact
  • Failure to wash hands
    
    • Move food stands, drinking fountains, etc away from contact areas
    • Have hand washing stations available
    • Ban smoking, eating, use of pacifiers in or immediately after leaving contact areas
    • Educational materials and signs!

Question 27

A bluetongue outbreak occurred in Europe in the late 2000s.

What is bluetongue?

How is it spread?

Describe the spread of the outbreak through Europe.

Answer 27

Fowler 7 Ch 74 - Bluetongue: Lessons from the European Outbreak 2006-2009

Cause and Epidemiology

Bluetongue-

• Insect-borne disease
• Caused by bluetongue virus (BTV)
• Obrivirus in the family Reoviridae
• DS RNA virus with three concentric structural protein shells
• Variations in proteins of outermost shell determine virus serotype
  
  • Especially variable virus protein 2 (VP2)
  • 24 serotypes, with 25^th proposed
• First described in 1902- thought to be confined to Africa
• Spread to Isreal (1951), US (1952), southern Europe (1956), Asia (1961), Australia (1975)
• Endemic in tropics and subtropics
• Sustained outbreaks in northwest Europe (2006 to 2009)

Sources

• Movement of infected ruminants
• Infected vectors being blown into noninfected areas
• Illegal importation of live attenuated BTV vaccines from Republic of South Africa
• Recent incursions of BTV6 and BTV11
• BTV8 in Belguim in 2006- source unknown
• No previous history of BTV recorded in this country

Transmission-

• Hematophagous female midges- ruminant hosts
• Less than 50 of the known 1500 Culicoides sp. compentent BTV vectors
• Viral distribution dependent on suitable climatologic factors for midges
• Following viral ingestion via a bloodmeal, the virus must infect and replicate within the insect’s midgut cells and again in their salivary gland cells prior to inoculating another ruminant.
• Infection rate of midges increases with warmer temperatures
  
  • Decreased viral multiplication stage within the midge
  • Increased frequency of blood meals taken by midge
• Temperatures <12 C- virus multiplication within midge, and ability to transmit the virus, stops

Outbreak in northwest Europe

• Previously thought that Palaearctic midge species such as C. obsoletus and C. pulicaris could not sustain transmission of BTV in the field due to seasonal temperature fluctuations.
• Found that newly introduced strain (BTV8) had low-grade secondary routes of transmission (ie- transplacental and oral) in addition to suspected latent infection in rumnants and midges
• Able to sustain infection over cold winter months
• Highly seasonal pattern of disease
• Clinical cases in epizootics between July and December

Question 28

Describe the clinical signs associated with blue-tongue infection.

Virulence is dependent on what factors?

Clinical signs are primarily due to what pathology?

What groups are suceptible to disease?

Answer 28

Clinical Picture and Species Susceptibilities

• All ruminant species and some camelids likely capable of supporting BTV infection
• Clinical disease highly variable, dependent on:
  
  • Viral serotype
  • Species
  • Breed
  • Immunologic status
  • Environmental conditions
  • Individual health status
• Animals indigenous to endemic areas appear to be clinically resistant
  
  • Unknown reason- possible natural or acquired immunity
• Classical clinical signs due to virus-mediated vascular injury:
  
  • Fever, nasal discharge, dyspnea, cyanosis of the tongue, oral lesions and ulcers, edema of the head and neck, lameness, and hyperemia of the coronary band
  • Most frequently seen in sheep- mortality rates >/= 30%
  • Cattle rarely show clinical disease
  • Exception- European BTV8 strain
• Clinical susceptibility of nondomestic species-
  
  • North America-species that can develop severe disease:
    
    • White-tailed deer, prong-horn antelope, desert bighorn sheep
  • Occasional infection in carnivores
    
    • Dogs- abortion and death after injection with BT-contaminated vaccine
    • European lynx- fed infected meat
  • Asymptomatic infection in endemic African carnivores
• Study- survey of 313 European AZA zoos in January, 2008
• Table 74-1 PP. 575-576
  
  • Data collected on clinical disease seen during the 2007 BTV season
  • 49 zoos classified as at risk of infection (confirmed BTV8 cases within 20km)
  • Over 1000 susceptible individuals of 53 different species
  • Seven ruminant families indigenous to Europe, North and South America, Africa, and Asia
  • Clinical disease was seen in 62 individuals, spread among 13 zoos (27% of at-risk collections)
  • Subfamilies bovinae and caprinae were most susceptible of the ruminants to clinical disease
    
    • Four species had morbidity rates higher than 20% and mortality rates higher than 10%
    • Average case-fatality rate for the affected bovinae and caprinae species was 69%
    • All affected ruminant species were indigenous to Europe, Asia, or South America
  • None of the over 200 African ruminant of 20 species had clinical signs of infection
    
    • Consistent with indigenous antelope not developing clinical disease in Africa

Question 29

How was the European outbreak of bluetongue controlled?

What was the safety and efficacy of those efforts? What sort of adverse effects were documented?

Answer 29

Disease Control

• Bluetongue recognized by the OIE as a disease of global importance
• Ability to cause death and debilitating disease across international borders and lack of effective treatment
• Included in the OIE Terrestrial Animal Health Code and Manual of Diagnostic Tests and Vaccines
• 2006-2009 European outbreak-
  
  • Over 80,000 reported outbreaks and 100,000 cases across 14 countries
• OIE is a recognized reference organization by the World Trade Organization (WTO)
  
  • Endemic countries- rear genetically resistant breeds of sheep and cattle in conjunction with vaccination and naturally acquired immunity
  • Countries where disease is rare- Attempt to eradicate the disease to regain disease-free status to engage in free trade
    
    • Members of the European Union (EU)- control and eradication provisions
  • Vector control, restriction to movements of live ruminants, and controlled use of vaccines
• Large economic impact of animal movement restrictions
• Large restriction zones around outbreaks- midges can spread 100km by wind
• Major impact on cooperative breeding programs among European zoos
• Midge preferred breeding sites- moist soil and dung, rather than standing water

Vaccination

• Mainstay of control in areas where BTV has become established
• Mass emergency vaccination campaign objectives:
  
  • Prevent clinical disease
  • Limit regional spread of BT
  • Allow regional and countrywide eradication
  • Permit safe movement of animals between affected and disease-free zones
• Only MLV and inactivated (killed whole virus) vaccines are approved for national disease control programs by the European Commission
  
  • MLV-
    
    • Advantages- Produced quickly (8-10 wks), highly immunogenic, potential long-lasting protection after a single dose
    • Disadvantages- potential for under attenuation, causeing symptomatic disease, milk drop, fetal pathology, and infection of vector population
  • Inactivated Vaccines- *Preferred*
    
    • Disadvantages- 6-8 months to develop, more costly, require regular boosters
• Little or no cross protection between different serotypes of BTV-
  
  • Vaccines produced specifically in response to circulating serotypes and strains
• All vaccines in EU for control of BTV1 and BTV8 are inactivated vaccines that use saponin and aluminum hydroxide as adjuvants (Table 74-2)

Safety

• Vaccine found to be safe in domestic species via trial and field experience:
• Over 60 million doses of BTV8 Vaccine in 12 countries
• Adverse reactions seen in less than 1 in 10,000 animals
  
  • Local vaccine site reactions and non-severe general reactions (ie.- pyrexia and lethargy)
• Vaccine in nondomestic species-
  
  • Survey of all 313 EAZA zoos (February, 2009)
  • Over 2000 individuals of 57 species in 47 institutions in nine European countries:
    
    • Adverse reaction rate of 0.5% (50 in 10,000 animals)
• 50% local vaccine site reactions
• 40% abortions

Efficacy

• Licensed vaccines shown to be efficacious in domestic animals
• Field data from northern European outbreak suggest that when vaccine uptake was high, virus transmission was effectively controlled and number of clinical cases dropped dramatically
• Data from February, 2009 European Zoo Survey:
• Seroconversion post-vaccination:
  
  • 100% seroconversion in the 37 Bovidae and Giraffidae tested
  • 87% seroconversion in the 40 South American camelids tested
  • 50% seroconversion in the nine Cervidae rested
• No animals developed clinical disease postvaccination, despite virus circulating in the area
• Suggest that inactivated BTV8 vaccine is efficacious in bovids, giraffids, and to a lesser extent, camelids.
• Sample size of cervids was too small for definitive conclusions

Conclusions

• BTV can be sustained beyond its traditional tropical and subtropical distribution
• BT poses a significant risk of mortality and morbidity in a variety of naïve nondomestic ruminant species
• Species indigenous to temperate areas of Europe, Asia, and the Americas were most severely affected
• Species indigenous to Africa, the putative source of BTV8, were clinically unaffected
  
  • Suggest that African species carry a degree of genetic resistance to BT
• BTV8 and BTV1 vaccines have been used in many European zoos
  
  • Adverse reactions were rare and in line with those seen in the domestic species they were licensed
• Vaccines appear to be safe in nondomestic ruminants and efficacious in the Bovidae and Camelidae
• Further evaluation in Cervidae is needed

Question 30

What are the benefits of importing semen from nondomestic ruminents?

What sort of risks are involved?

What foreign animal diseases can be transmitted through semen?

What is the current status of importing ruminant semen?

Answer 30

Fowler 7 Ch 78 - Importation of Nondomestic Ruminant Semen for Management of Zoological Populations Using Artificial Insemination

Introduction

• ruminants are diverse group, include some of the most endangered spp., and are a big part of zoo collections
• new genes needed to sustain genetic viability of captive populations
• transporting semen rather than animals is advantageous
  
  • permanent source of wild genetic material
  • decreased disease risk
  • decreased cost
  • enhanced animal welfare
• very difficult to import unfixed/untreated ruminant semen samples into the USA

Status of artificial insemination in ruminant species

• SI techniques modified from those used on cattle
• successful for 7 antelope, 7 cervid, 2 wild cattle, 1 caprid, 1 ovid species
• most of these have been through use of frozen-thawed sperm, which is more pragmatic than fresh

Foreign animal disease and transmission through semen

• see table p. 607
• semen washing may not be effective for FMD
  
  • as few as 10-25 particles needed for transmission
  • washing reduces but does not eliminate viral load

Advantages of semen importation

• less expensive than live import
• no relocation/quarantine animal welfare issues
• no arthropod-transmitted disease risk

Risk assessment of semen versus live animal importation

• risk modeling favors agriculture industry over endangered spp. protection
• risk assessment has limitations
• disease testing before importation in nondomestic animals may not be adequate (no validation in many spp.)
• embryo importation is easier because they can be washed free of etiologic agents

Current status of semen importation

• import protocols for frozen semen from domestic ruminants in FMD-free countries have been established for the USA
• ruminant biologic samples have to have appropriate import/export permits and must undergo disinfection treatment
  
  • not possible for semen, since it renders cells unviable
• tried to use gerenuk as a model for last decade, but regulatory problems prevented it

Question 31

Describe the foot anatomy of ruminants.

What type of limb structure do they have?

Describe the layers of the hoof.

How does the hoof wall develop?

Answer 31

Distinguishing feature of artiodactylids:

• Paraxonic limb structure = symmetry of foot passes between two well developed middle digit
• Third and fourth digits are weight bearing.

Bovine hoof wall anatomy (as prototype)

• Lamina analogous to dermis
  
  • Consists of connective tissue, vasculature, nerves
• Moving outward:
  
  • Basement membrane
  • Germinal epithelium
  • Stratum spinosum
  • Stratum corneum - outer horned layer

Development of hoof wall =

1. Germinal epithelium is the active region of cell proliferation and differentiation.
2. Differentiates into keratinocytes- build keratin protein
3. Keratinocytes undergo cell death and cornification
4. This forms cells of the outer horn.

Question 32

Describe the scoring of lameness in nondomestic ruminants.

Answer 32

Lameness defined = any condition that inhibits or modifies the gait of an animal.

Question 33

Describe hoof disorder in nondomestic ruminants.

What is laminitis? What causes it?

Describe the nomenclature of fissures and cracks - what causes them, how are they managed?

How are worn soles managed?

What are four infectious diseases of the bovid hoof?

How are hoof disorders treated?

Answer 33

Laminitis

• Resulting from metabolic disturbances (rumen acidosis, lactic acidosis)
• Endotoxemia (metritis, retained placenta, mastitis)
• Trauma
  
  • All lead to release of vasoactive substances that intitiate cascade of events to reduce blood flow to lamina by vasoconstriction, thrombosis, ischemia and hypoxia.
  • Results = edema, hemorrhage, necrosis, failure of suspensory function, rotation of P3.

Nutrition

• Biotin, copper, zinc essential for keratin synthesis and hoof health.
• High starch low fiber diets -> rumen acidosis -> laminitis

Sole lesions – full thickness breaks in epidermis, named based on location on sole

• Fissures/Cracks
  
  • Vertical fissures = sand cracks
  • Abnormal production of horn tissue
  • D T poor nutrition, poor conditions, trauma
  • If severe – trimming and wire stents indicated
  • Horizontal fissures = reflect interruption in horn growth
• White line disease
  
  • Separation or avulsion of fibrous junction between sole and wall on the
  • Trim and treat
• Worn soles
  
  • Due to pacing on hard substrates
  • Visual barriers, noise control, neuroleptic agents, soft substrates
• Interdigital hyperplasia
  
  • Proliferative reaction caused by chronic irritation of interdigital skin
  • Rule out infectious diseases similar in appearance.

Infectious hoof disorders

• Infectious pododermatitis
  
  • “foot rot:” - highly contagious
  • Acute to chronic infection and infl of the skin and adjacent soft tissue of the hoof
  • Etiology = Fusobacterium necrophorum and Dichelobacter nodosus and other bacteria
  • Predisposed in wet, muddy poorly drained and fecal contaminated areas.
  • Treatment= trimming, foot soaks, fix the environment or change env.
  • Vaccines currently not effective against all strains, may help reduce transmission.
• Interdigital dermatitis
  
  • = foot scald
  • Mild form of Inf pododerm caused by F. necrophorum
  • Lesions often heal rapidly when foot environment corrected.
• Papillomatous Digital Dermatitis
  
  • Proliferative, highly contagious
  • Plantar aspect of rear foot near interdigital space or heal bulbs.
  • Causative agent – anaerobic spirochete genus Treponema
  • Transmission based on env, host, microbe, husbandry
  • No vaccines

Viral diseases

• Foot and Mouth Disease (FMD)
  
  • Highly contagious, sometimes fatal
  • Swine, goat, sheep, deer water buffalo, bison, antelope, others
  • DDX: bluetongue, bovine viral diarrhea, vesicular stomatitis, contagious ecthyma, malignant catarrhal fever, swine vesicular disease.
  • Virus can remain viable in env for up to one month
  • Erradicated from US in 1929
  • Endemic in Africa, Asia, So America, Europe

Treatment of hoof disorders

• Symptomatic, supportive, proper hoof care and trimming.
• Prevention

Question 34

Describe the perinatal care of female nondomestic bovids.

How should their husbandry be adjusted. How do you know the timing is getting close?

How does dystocia affect bonding with the calf?

What are some common issues with neonatal calves?

Answer 34

Perinatal care

• Neonatal mortality rate often over 30%
• Environmental management
  
  • Provide opportunity for seclusion
  • Strong herd instinct species may be more successful housed with herd
  • Timing of breeding to favor mild-season calving
• Impending parturition
  
  • Energy ration should be increased 1 month prior
  • Signified by teat and udder enlargement (weeks) and vulvar swelling (days)
  • Seek isolation and give birth at night
• Dystocia common
  
  • Especially in species with limited genetic diversity
  • Many dams do not accept offspring following general anesthesia 🡪 FPT and need for hand rearing

Neonatal care

• Weak, unresponsive to stimulation, unable to stand, and failure to nurse 🡪 timely intervention critical
• Maternal neglect is common in inexperienced dams, but neglect from experienced dam may point to underlying problem
• Metabolic acidosis common for up to 48 hours
  
  • Severe acidosis 🡪 weakness, inability to nurse, and FPT
  • IV fluid therapy + Sodium bicarbonate (1-2 mEq/kg) once normal breathing established
• Hypothermia – provide external heat 24 hours following parturition
• Septicemia = hypothermia/hyperthermia, tachycardia, tachypnea, cold extremities, weak pulse, inability to correct hypoglycemia
• Hypoglycemia, dehydration, pneumonia 🡪 all can be rapidly fatal

Question 35

List differentials (Viral, Bacterial, Parasitic, Fungal) for clinical signs associated with the following systems:

Multi-systemic diseases

Respiratory system diseases

GI diseases

Reproductive diseases

Integument/Musculoskeletal Diseases

Nervous System diseases

Circulatory system diseases

Answer 35

Question 36

List the OIE reportable diseases of bovids.

Answer 36

Question 37

What is the scientific name of the Saiga antelope?

What are some recent causes of mass mortalities of this species?

What nutritional deficiency may be playing a role?

Answer 37

Chapter 89 - Mass Mortality Events Affecting Saiga Antelope of Central Asia

• Saiga tatarica introduction
  
  • Keystone species
  • Two subspecies: S. t. tatarica and S. t. mongolica
  • Antelope evolved for semiarid desert steppes – Russia, Kazakhstan, Mongolia
    
    • Copper deficient, high salinity soils
    • Profound temperature fluctuations
  • Anatomy: dense fur, compact body, extended proboscis
  • Annual migration and careful selection of calving sites
    
    • Females and males congregate in May à birthing aggregates producing 1-3 calves
      
      • Females reproduce in the first year of life
      • Highest relative fetal biomass of any mammal
• Mass mortalities
  
  • Poaching with high velocity rifles
    
    • Single most serious cause of premature death in recent decades
    • A million individuals à a few tens of thousands in the early 20^th century
  • Heavy snow or freezing rain (dzhut)
    
    • Sudden weather shifts à low birth weights à poor suckling à predation and death
    • Decreased diet viability à death
  • Infectious disease
    
    • Pasteurellosis – 1981, 1984, 1988, 2015
      
      • Mostly around calving, and repeat events in the same pastures
      • Both P. haemolytica and P. multocida
        
        • 2015: P. multocida serotype B and hemorrhagic septicemia
      • Both 1984,88 were warmer more humid years
    • Peste des petits ruminant virus – 2016
      
      • Spill over from livestock – saiga highly susceptible
      • 54% of a small Mongolian population died
    • Foot and Mouth disease – 1950s and 60s
      
      • Mostly affected calves
• Discussion
  
  • Pasteurella as a common finding in recent MME may be related to modern diagnostics and not emergence
    
    • Pasteurella and Clostridium are commonly isolated from deceased animals
      
      • Pasteurella was isolated from the PPRV outbreak
      • Clostridium was isolated from the pasteurellosis outbreak MME
    • MMEs may actually be multifactorial
      
      • No/less MMEs in regions that have remained dry, whereas climate change has led to wetter conditions in regions that have had Pasteurella outbreaks
  • Spill over from livestock – PPRV and FMD
  • Why so many MMEs in the Kazakh Betpak-Dala population has yet to be answered
    
    • Possible coincidence, good calving location, good vegetation, topography, or other environmental conciderations
  • Low copper may play a role – decreased levels found in deceased animals

Answer 38

• Occurs in both wild and free ranging cervids, bovids, antilocaprids, & tragulids
• Cardiac & skeletal myopathies are most common – oxidative damage can occur in other organs as well
• Gross findings: white or chalky streaks in cardiac/skeletal muscle
• Histo findings: multi-focal polyphasic myofiber degeneration (exertional myopathy is monophasic
• Vitamin E levels – measured as plasma alpha-tocopherol (<3.5 umol/L = deficient)
• Selenium – heavy metal antagonism in Se poor areas

Question 39

Describe primary and secondary copper deficiencies in bovids.

What lesions are commonly present?

What species is particularly susceptible?

How does dermatopathy occur in these cases?

What happens as a result of in utero deficiency?

Deficiency increases suceptibility to what parasites?

Answer 39

• Primary deficiency = lack of dietary copper; Secondary = molybdenum or other antagonism of Cu uptake
• Lesions – anemia, poor bcs, diarrhea, dermatopathy, neonatal degenerative neuropathy with weakness & posterior paresis, cardiovascular or skeletal malformation, reduced fertility and abortions
• Tibetan gazelles – unsteady gait disease – pica, dyskinesia, unsteady gate due to Cu deficiency
• Dermatopathy – impaired tyrosinase activity leads to progressive bleaching and straitening of hairs
• In utero deficiency – neuronal degeneration, malacia of cerebral white matter, Wallerian degeneration in spinal cord
• Increases susceptibility to GI parasitism – especially Haemonchus

Question 40

What lesions are present with osteoporosis in bovids?

What species are particularly susceptible?

Are there any underlying nutritional issues with this disease?

Answer 40

• Free-ranging Bighorn sheep of Southern US, Stiffness of Extremities Disease of Asian Yak & Water buffalo
• Possibly due to copper or magnesium deficiency or increased demand for calcium during pregnancy & lactation
• Mandible, scapulae, sacrum, ilium, ribs – osteoporosis & brittle fragility with thinning of cortical bone and expansion of marrow into epiphyses
• Nonmineralizing expansion of long bone epiphyses, diaphyseal bowing – similar to hypophosphatemic rickets

Question 41

Rumen acidosis is caused by what?

What are teh lesions associated with this disease?

What sequelae may occur as a result?

Answer 41

• Common in all managed ruminants, mostly dominant adult animals getting too much
• Secondary to dietary grain excess
• Lesions – rumen papillary blunting with epithelial hyperplasia and parakeratosis; rumenitis with or without pustules followed by secondary bacterial or fungal rumenitis, hepatic abscessation & necrosis, cerebrocortical necrosis is also observed in deer
• Laminitis common among springbok, deer, and pronghorn
• Neurologic wild pronghorn given access to grain – hemorrhagic foci in thalamus and brainstem with cortical laminar necrosis resembling thiamine-responsive polioencephalomalacia

Question 42

What is the most common site for uroliths to obstruct in ruminants?

What predisposing factors are common?

What are the lesions associated with urolithiasis in ruminants?

What stone types are common? Which species are they common in?

Answer 42

• Mostly managed animals
• Sigmoid urethral flexure and urethral process are common sites in male animals
• Diet, early castration, and dehydration contribute to occurrence similar to domestic ruminants
• Calcium carbonate – giraffe and wildebeest – elevated phosphorus and high concentrate to forage ratios are contributing factors
• Gross & microscopic lesions – irritation, obstruction – hydronephrosis, azotemia, urinary bladder rupture

Question 43

What are the lesions associated with the four syndromes of exertional rhabdomyolysis?

Answer 43

Four Syndromes

1. Hyperacute (Capture Shock) - <6 hours after insult
   
   1. Weakness, muscle stiffness, ataxia, hyperthermia, acidosis, shock, sudden death <6 hour after insult
   2. Gross lesions nonspecific, but suggestive of shock
   3. Microscopic lesions – acute coagulative necrosis of skeletal & cardiac myofibers with adjacent foci of microvascular thrombi & necrosis
2. Acute (Ataxic Myoglobinuric) – hours to days after insult
   
   1. Most common presentation
   2. Acute skeletal and cardiac myodegeneration – weakness, ataxia, myoglobinuria leading to renal failure hours to days after insult
   3. Gross lesions – soft, red to black, congested or hemorrhagic muscle bellies with regions of pallor, over time muscles become gritty or chalky; kidneys are swollen and dark brown – more so in the cortex, urine is dark brown
   4. Histo – hemorrhage, myofiber swelling, loss of cross striations, hypereosinophilia, sarcoplasma vacuolation, nuclear pyknosis – all myofibers are affected in severe cases (type II, modified type I primarily); Renal lesions – tubular ectasia, degeneration, necrosis with hypereosinophlic hyaline and granular casts
3. Subacute (Rupture Muscle) – 24-48 hours after insult
   
   1. Rupture of affected muscles and extensive hemorrhage
   2. Typically muscles with greater weight-bearing loads – gastrocnemius is common
   3. Rupture along areas of necrosis, inflammatory and reparative changes may be evident
4. Chronic (Delayed Peracute)
   
   1. Uncommon, animals survive the initial stressor but die suddenly with a subsequent stressor
   2. Few gross lesions, microscopic lesions are similar to the acute syndrome but less severe

Question 45

Polycystic kidney disease is commonin what bovid species?

Answer 45

• Neonatal disease in springbok
• 18% of live births of one springbok population with bilateral nephromegaly
• Cysts mostly in the medulla
• One case also had lysosomal storage disease

Question 46

Describe the dental issues of the following artyriodactyls:

Dall’s & Bighorn Sheep

Giraffe

Hippos

Cervids

Answer 46

• Sheep
  
  • Free-ranging Dall’s & bighorn sheep have high prevalence of dental disease and lumpy jaw
• Giraffe
  
  • Managed giraffe wear their teeth as grazers while wild giraffe wear their teeth as browsers
  • Most wild giraffe have sharp cusps on their teeth where the managed giraffe have rounded and blunted teeth
  • Implicated in acute giraffe mortality syndrome
• Hippos
  
  • Canine and incisors grow continuously – several reports of overgrowth and malocclusion in both species
• Cervids
  
  • Abnormal tooth wear with fluorosis
  • Dental lesions contribute to actinomyces bovis infections

Question 47

What are the dental formulas of the following families?

Bovidae

Antilocapridae

Giraffidae

Tragulidae

Hippopotamidae

Cervidae

Answer 47

Question 48

Laminitis is commonly reported in what ruminant species?

Question 49

Whay is amyloidosis?

What ruminant are particularly susceptible to it?

What lesions are associated with it?

Answer 49

• Accumulation of amyloid, an amorphous hyaline, extracellular proteinaceous material, in various tissues
• Wild and captive caprids, captive gazelles, captive bongo – diagnosed in other bovids as well
• Tissues commonly involved – liver, kidney, spleen, GI lamina propria & submucosa), adrenal glands, thyroid gland, exocrine pancreas, lymph nodes, salivary glands, blood vessels
• Lesions – Liver firm and more prone to fracture or hemorrhage, kidneys pale and waxy, segmental intestinal thickening (ddx Johne’s)
• Histo – HE staining, amyloid is hyaline, pale eosinophilic, and causes atrophy in adjacent tissues, can cause mural thickening in blood vessels, deposited at the space of Dissé and then along the sinusoids, both medullary and glomerularly deposited in the kidneys

Question 50

What are the lesions associated with fat saponification in zoo-housed ruminants?

How do these lesions occur?

Answer 50

• Nondomestic bovids in zoos
• Individual to coalescing masses of necrotic and mineralized fat in the mesentery, retroperitoneum, or omentum
• Histo – necrosis and mineralization of adipocytes – sometimes histiocytic or mixed steatitis
• Rarely osseous metaplasia or extra skeletal osteosarcoma occurs
• Ureteral or GI obstruction can occur secondarily; dystocia also possible if masses are in the pelvic canal
• Lesions can be spontaneous in obese animals – but endophyte-infected fescue is report in cervids

Question 51

What are the etiologic agents of malignant catarrhal fever?

What species are susceptible?

Describe the pathogenesis of this disease.

What are the typical clinical signs? How do they differ between bovids and cervids?

What are the histologic lesions?

How is this disease diagnosed?

Answer 51

• Susceptible Species: multiple bovid species
  
  • Cervids – Pere Davids & WTD highly susceptible, elk, moose, reindeer, roe deer, red deer also susceptible, fallow deer relatively resistant
• Etiology: Macavirus (Herpesviridae, Gammaherpesvirinae) – 10 separate macaviruses
  
  • Ovine Herpesvirus-2 (OvHV-2)
  • Alcelaphine Herpesvirus -1 (AlHV-1)
• Pathogenesis:
  
  • OvHV-2 carried asymptomatically by domestic sheep (sheep associated – SA-MCF), AlHV-1 by wildebeest (wildebeest associated – WA-MCF)
  • Aerosol transmission by reproductive fluids or nasocular secretions
  • Enter oral cavity or tonsillar mucosa leading to viremia leading to lymphoproliferative disease (cytotoxic CD8+ T lymphocytes and NK cells may play a significant role)
• Clinical signs
  
  • Bovids: fever, severe mucopurulent nasal discharge, corneal opacity, diarrhea, lymphadenopathy, neurologic disease, urinary tract lesions are more common in bison and cattle
  • Cervids: hemorrhagic gastroenterocoloitis and oral, nasal, and tracheobronchial lesions (hemorrhagic, ulcerative). The GI form is more common resulting in dehydration and emaciation, generalized cutaneous lesions as well as the classic eye lesions
• Histo Lesions: lymphocytic inflammation around medium-sized arteries and veins with thrombosis, inclusion bodies are not present
• Diagnosis: contact with potential reservoir, detection of viral DNA in tissue – PCR recommended

Question 52

What is the etiologic agent of lumpy skin disease?

What species are susceptible?

Describe the pathogenesis of this disease.

What are the clinical signs?

What are the associated inclusion bodies?

Answer 52

• Susceptible Species:
  
  • Low seroprevalence in African wildlife - impala, giraffe, kudu, waterbuck, reedbuck, springbok
  • African buffalo calves and adult wildebeest were not affected
• Etiology: Capripoxvirus (Poxviridae) – Lumpy Skin Disease Virus (LSDV)
  
  • OIE reportable disease
• Pathogenesis & Epidemiology
  
  • Found in Middle East, Turkey, Greece, Russia, Republic of Georgia
  • Experimental infection in Giraffe and impala calves lead to fatal systemic disease with proliferative and necrotizing dermatitis and panniculitis similar to what occurs in cattle
• Clinical signs & gross lesions
  
  • Large dermal nodules (up to 10 cm) that turn black and rupture releasing serosanguinous fluid
  • Diffuse lymphadenopathy, lingual and oral ulceration leading to emaciation and death
• Histo Lesions
  
  • Epithelial contain intracytoplasmic inclusion bodies, skeletal muscle contains intranuclear inclusion bodies, macrophages contain both
  • Eipdermal proliferation and vacuolar degeneration with neutrophilic panniculitis and myositis and dermal vasculitits

Question 53

What is the etiologic agent of disseminated fibropapillomatosis?

What species are affected?

What is the pathogenesis of this disease?

What are the typical signs and lesions?

Answer 53

• Susceptible Species:
  
  • Nondomestic bovids, giraffe, and pronghorn with disease
  • Chamois and mouflon have tested positive for the virus but without signs
• Etiology: Bovine papillomavirus 1 & 2 (BPV 1, BPV 2)
  
  • Rupicapra papillomavirus 1 (RrupPV 1) caused a proliferative nasolabial tumor in a chamois
• Pathogenesis & Epidemiology
  
  • Benign papilloma induced lesions will regress spontaneously
  • Malignant transformation is not completely understood
• Clinical signs & gross lesions
  
  • Exophytic hyperkeratotic nodules
  • Can result in ulcerations
• Histo Lesions
  
  • Hyperplasia of keratinocytes within strata spinosum and granulosum with cell swelling
  • Occasional amphophilic intranuclear viral inclusion bodies

Question 54

What are the etiologic agents of Bluetongue and Epizootic Hemorrhagic Disease?

What species are susceptible?

How is these diseases transmitted?

What are the pathogeneses?

What are the clinical signs and gross lesions?

What are the histologic lesions?

Answer 54

• Susceptible Species:
  
  • White-tailed deer highly susceptible to both viruses, mild in elk, moose, and hog deer
    
    • Yak & Bighorn sheep have also been documented
  • Most severe disease in sheep, less so in cattle and nondomestic ruminants
  • An outbreak at a zoo affected bison, yak, mouflon, ibex, and muskox
• Etiology: Orbivirus, Reoviridae
  
  • Bluetongue Virus – OIE reportable disease
  • Epizootic Hemorrhagic Disease – primary a cervid disease
• Pathogenesis:
  
  • Transmitted via culicoides midges, replicates in lymph nodes before causing viremia
  • Endotheliotropism in spleen, mononuclear cells, and lymphocytes leads to vascular damage, DIC, fibrosis, and hemorrhage
• Clinical signs & Gross Lesions
  
  • Febrile, ulcers of mouth, muzzle and teats, conjunctivitis, nasal discharge, edema of head and limbs, hyperemia of the coronary band
  • Yak appear to be the only nondomestic caprid that develops the edema of the lips and cyanosis of the tongue after which bluetongue is named
  • Pulmonary edema, pleural and pericardial effusion, and hemorrhage of GI serosa, lymph nodes, and pulmonary artery subintima occurs later in the disease
  • Mule deer with EHDV-2 develop inflammation and hemorrhage of the testes
• Histo Lesions:
  
  • Vascular congestion, hemorrhage, thrombosis, necrosis – GI & heart most commonly but also lung, kidneys, adrenal gland, spleen, thymus & lymph nodes
• Diagnosis:
  
  • Gross lesions, PCR or virus isolation of whole blood or tissue

Question 55

What is the etiologic agent of foot and mouth disease?

What are the susceptible species?

How is this disease transmitted?

What is the pathogenesis?

What are teh clinical signs and gross lesions?

What are the histological lesions?

What are important differentials to consider?

Answer 55

• Susceptible Species:
  
  • Source in Africa is often African buffalo – typically subclinical or mild
  • Mountain gazelles, impala, saiga, blackbuck
• Etiology: Foot and Mouth Disease Virus – Apthovirus – Picornaviridae – OIE Reportable Disease
  
  • 7 serotypes (O, A, C, SAT1, SAT2, SAT3, Asia 1) – infection with one does not provide immunity to others
• Pathogenesis & Epidemiology:
  
  • Transmission is direct contact with body secretions or fluid of infected animals, aerosolization, or fomites – long distance airborne spread has been documented
  • Primary replication occurs within the pharyngeal epithelium then mucosa-associated lymphoid tissue, and finally in pulmonary alveolar epithelium before causing viremia
  • Can also occur via inoculation with breaks in skin and replication in draining lymph nodes
  • Incubation period from 1-2 days to weeks
• Clinical signs
  
  • Gross lesions – mucosal swelling, blanching, or reddening before vesicles form on dental pad, tongue, coronary band, interdigital region and mammary glad
    
    • Lesions on forestomach also seen frequently
  • Sudden death in young animals can be due to myocardial degeneration
  • Sloughing of horns also seen in some specieds
• Histo Lesions: epidermal and mucosal vesicles with intracellular edema (large numbers of virus in fluid)
• Diagnosis:
  
  • Contact lab, then use virus isolation, ELISA, or PCR
  • DDx: vesicular stomatitis, swine vesicular disease, vesicular exanthema of suids, bluetongue/EHDV, malignant catarrhal fever, BVDV

Question 56

What is the etiologic agent of encephalomyocarditis?

What species are susceptible?

Describe the pathogenesis and associated clinical signs.

What is the best method of control?

Answer 56

Encephalomyocarditis Virus - Picornavirus

Susceptible Species:
- Pygmy hippopotamus, Thomson’s gazelle, oryx, addax
- Multiple mammalian taxa

Etiology: Cardiovirus A - Picornaviridae

Pathogenesis:
- Acute to subacute nectotizing to nonsuppurative myocarditis, sometimes with pericardial effusion, pulmonary edema, or other signs of heart failure

Clinical signs: sudden death, heart failure

Rodent control

Question 57

What is the etiologic agent of Peste des Petits Ruminants?

What species are susceptible?

Describe the pathogenesis and clincial signs of this disease.

What are the gross and histologic lesions?

What are the inclusion bodies?

How is this disease diagnosed? What are important differentials?

Answer 57

• Susceptible Species:
  
  • Nondomestic caprids, gazelle, impala, gemsbok, bushbuck, Mongolian saiga, wildebeest
• Etiology: Small Ruminant Morbilivirus - Paramyxoviridae
• Pathogenesis:
  
  • Incubation period of 3-10 days
• Clinical signs
  
  • Animals are febrile with serous to mucopurulent oculonasal discharge often with pneumonia and hemorrhagic diarrhea
  • Gross lesions – oropharyngeal erosion, ulceration, and pseudomembrane formation, hemorrhagic enterocolitis, GALT necrosis, fibrinous peritonitis or pleuritis
• Histo Lesions:
  
  • Necrosis of airway epithelium, type II pneumocyte hyperplasia
  • Eosinophilic, intranuclear and intracytoplasmic viral inclusion bodies in syncytia
• Diagnosis:
  
  • Virus neutrolization, PcR
  • DDx: caprine pluropneumonia, pasteruellosis, bluetongue, BVDv, FMD

Question 58

Rinderpest is an eradicated disease - but what is the etiologic agent?

What species were susceptible?

What wre the clinical signs and lesions associated with this disease?

Answer 58

• Susceptible Species:
  
  • African buffalo, kudu, eland, giraffe
• Etiology: Rinderpest Morbillivirus - Paramyxoviridae
  
  • Eradicated in 2011
• Pathogenesis & Epidemiology:
• Clinical signs
  
  • Diarrhea, oculonasal discharge blindness
  • Mucosal erosion and ulceration
  • Lymph node necrosis
  • Ocular lesions – keratoconjunctivitis, corneal ulceration, uveitis, cataracts
  • Tenosynovitis
• Histo Lesions:
  
  • Syncytial cells with or without intranuclear and intracytoplasmic inclusion bodies
• Diagnosis: hopefully not

Question 59

What is the etiologic agent of bovine tuberculosis?

What species are susceptible?

How is this disease transmitted?

What are the clincial signs and gross lesions?

What are the histologic lesions?

How is this diagnosed?

Answer 59

• Susceptible Species:
  
  • Domestic cattle, many wild ruminants
  • BTB reservoirs: African buffalo (South Africa), lechwe (Zambia), wood bison (Canada), WTD (US)
  • Greater kudu
  • White-tailed deer, elk, fallow deer, and red deer are maintenance hosts, roe deer are spillover hosts
• Etiology: Mycobacterium bovis – OIE reportable disease
  
  • Gram positive (resists staining), acid-fast (Ziehl-Neelson, Fite-Furaco)
  • M. caprae – is in the complex and produces similar disease
• Pathogenesis:
  
  • Respiratory transmission
• Clinical Signs and Gross Lesions
  
  • Subclinical cases may show weight loss, cough, and dull coat
  • Encapsulated granulomas in lungs, and lymph nodes of thorax and head – mediastinal and retropharyngeal nodes in particular
• Histo Lesions: central region of necrotic cellular debris or caseous material surrounded by layers of epithelium and lastly by lymphocytes and collagen capsule
• Diagnosis: culture, PCR

Question 60

What is the etiologic agent of Johne’s disease?

What is the epidemiology of this disease?

What are the typical clinical signs and lesions of this disease?

How is it diagnosed?

Answer 60

• Susceptible Species:
  
  • Variety of domestic and free-ranging ruminants
• Etiology: Mycobacteirum avium ssp paratuberculosis (MAP)
• Pathogenesis & Epidemiology:
  
  • Fecal-oral transmission is the primary route
  • Young animals are much more susceptible than adults
  • In utero infection and neonatal exposure via milk or colostrum are possible
• Clinical Signs & Gross Lesions
  
  • Chronic wasting and diarrhea, submandibular or generalized edema and effusion from hypoproteinemia
  • Serous atrophy of fat. Intestinal mucosa thickening, mesenteric lymphadenomegaly
  • Tuberculoid vs lepromatous forms
• Histo Lesions:
  
  • Granulomatous eteritis, colitis, lymphadenitis with intracellular acid-fast bacilli.
• Diagnosis:
  
  • Fecal culture – possible pass through false positives or failure to catch animals not shedding

Question 61

What is the etiologic agent of clostridial hemorrhagic enteritis?

What species are suceptible?

What are the associated toxins?

How is this disease transmitted?

What are the typical clinical signs?

How is it diagnosed?

Answer 61

• Susceptible Species: variety of nondomestic ruminants, common cause of neonatal morality in hippos
• Etiology: Clostridium perfringens type C – alpha & beta toxins, type A – hemorrhagic enteritis
• Pathogenesis: fecal oral transmission
• Clinical signs: Acute necrotizing enteritis with ulceration and peritonitis
• Diagnosis: clinical signs, isolation of bacteria, toxin ELISA

Question 62

What is the etiologic agent of malignant edema or gas gangrene?

What species are susceptible?

How is this disease transmitted?

What are the clincial signs adn associated lesions?

How is this diagnosed?

Answer 62

• Susceptible Species: Most ruminant species are susceptible
• Etiology: Clostridium septicum, C. novyi
• Pathogenesis: Contamination of skin wounds
• Clinical Signs & Gross Lesions:
  
  • Sudden death, febrile disease
  • Muscle necrosis with or without crepitation
• Histo Lesions: necrosis, gas bubble formation
• Diagnosis: clinical history, signs, bacteria, IFA, culture

Question 63

What is the etiologic agent of blackleg?

What species are susceptible?

How is this disease transmitted?

What are the clinical signs and lesions?

Answer 63

• Susceptible Species: many nondomestic ruminants, unknown in hippos
• Etiology: Clostridium chauvoei
• Pathogenesis: contamination of deep wounds
• Clinical signs: peracude death, sudden onset muscle stiffness, anorexia, depression.
• Gross Lesions: significant regions of muscle necrosis and hemorrhage
• Diagnosis: Culture, Gram stain, IHC, IFA, PCR

Question 64

What is the etiologic agent of anthrax?

What species are susceptible?

Describe the transmission and pathogenesis of this disease.

What are the typical clinical signs and associated lesions?

How is this diagnosed?

Answer 64

• Susceptible Species:
  
  • Woodbison (Alaska), greater kudu, nyala, waterbuck, roan antelope, African buffalo
  • Outbreaks in hippos – possibly due to facultative carnivorous behavior
• Etiology: Bacillus anthracis – OIE reportable disease
  
  • Gram positive, spore-forming, rod-shaped bacteria
• Pathogenesis & Epidemiology:
  
  • Skin or mucous membrane defects, ingestion, or inhalation
  • Rapid replication in regional lymph nodes, bacteremia, & toxemia
  • Exotoxins lead to acute edema, hemorrhage, and terminal shock
• Clinical Signs & Gross Lesions
  
  • Death may occur within hours, carcasses often bloat quickly and leak hemorrhagic fluid (petechiae and eccymoses are also very common)
  • Generalized edema, splenomegaly with soft gelatinous texture, multicavitary effusions
• Diagnosis:
  
  • Bacilli identified on distal tail or ear
  • DON’T perform necropsy unless you have appropriate biosafety

Question 65

What is the etiologic agent of hemorrhagic septicemia?

What serotypes are most virulent?

What species are suceptible?

Describe the pathogenesis of this disease?

What are the typical clinical signs and lesions?

How is this diagnosed?

Answer 65

• Susceptible Species:
  
  • Water buffalo and domestic cattle primarily
  • American bison, cervids – fallow deer, elk, pronghorn, saiga antelope (mass mortality in 2015)
• Etiology: Pasteurella multocida – OIE reportable disease
  
  • Serotypes B2, E2 are primary pathogens causing nearly 100% mortality
  • Gram negative short bacilli – bipolar staining with methylene blue
• Pathogenesis & Epidemiology:
  
  • Occurs in Asia, Africa, Middle East; reported in southern Europe and North America
  • Normal nasopharyngeal flora of many ruminants which acts as opportunistic pathogen
• Clinical Signs & Gross Lesions
  
  • Peracute to acute disease – animals die within 24 hours after initial signs
  • Fever, salivation, dyspnea, recumbency, hemorrhagic diarrhea
  • Petechia, eccymotic hemorrhages on subcutis, endocardium, lymph nodes, muscle; prominent subcutaneous edema – submandibular, cervical, brisket regions; congested lungs with fibrinous pleuritis or pneumonia
• Histo Lesions: hemorrhagic gastroenteritis, fibrinohemorrhagic interstitial pneumonia, pulmonary edema, acute inflammation
• Diagnosis: clinical signs, blood smear bacteremia, serotype ID

Question 66

What are the etiologic agents associated with contagious caprine and bovine pleuopneumonia?

What speceis are susceptible?

What are the typical clinical signs and lesions?

How is it diagnosed?

What is an important differential?

Answer 66

• Susceptible Species:
  
  • CCPP - Domestic goats – mortality in nondomestic caprids (ibex, mouflon), gazelles, Oryx, Tibetan antelope, markhors
  • CBPP – Bos and Bubalas species
• Etiology:
  
  • CCPP - Mycoplasma capricolum capripnumoniae (MCCP)
  • CBPP – Mycoplasma mycoides mycoides
• Clinical Signs & Gross Lesions
  
  • Pleuropneumonia with thick layer of pleural effusion, lungs are dark red to gray with areas of consolidation, fibrinous pericarditis is also present
• Histo Lesions: chronic fibrinonecrotic pleuropneumonia, neutrophilic to lymphocytic interstitial and alveolar infiltrates
• Diagnosis: PCR, culture takes a long time, Mannheima hemolytica is a ddx

Question 67

What is the etiologic agents of brucellosis in ruminant species?

What species are affected by each agent?

How is it transmitted?

What are the typical clinical signs and lesions?

How is this diagnosed?

Answer 67

• Susceptible Species:
  
  • B. abortus – Bison, African buffalo, elk
  • B. suis – muskoxen (serovar 4), caribou knees (hygromas)
  • B. mellitensis – chamois, ibex, yak, sable, Arabian oryx – not found in NA wildlife
• Etiology: Brucella abortus, suis, melitensis, ovis – OIE reportable
• Pathogenesis & Epidemiology:
  
  • Contact with fetal fluids, vaginal exudates, and aborted fetuses
• Clinical Signs & Gross Lesions
  
  • Abortion, stillbirth, infertility in females
  • Orchitis and epididymitis in males
  • Swollen joints and lameness
• Histo Lesions: Gram negative, intracellular bacteria, lymphohistiocytic fibinrosuppurative bronchopneumonia & multisystemic hemorrhages; giant cells and epithelial macrophages
• Diagnosis: bacterial isolation

Question 68

What is the etiologic agent of cowdriosis?

What species are susceptible?

How is it transmitted?

Answer 68

• Susceptible Species:
  
  • Less severe disease in wild ruminants typically, but seen in eland, springbok, steenbok, lechwe, and sitatunga
• Etiology: Erlichia ruminantium – OIE reportable
  
  • Obligate intracellular gram-negative rickettsial bacteria
• Pathogenesis & Epidemiology:
  
  • Endemic throughout sub-Saharan Africa, and the Caribbean
  • Transmitted by Ambylomma ticks

Question 69

What is the etiologic agent of Q fever?

What species are susceptible?

How is it transmitted?

What are the typical clinical signs and lesions?

Answer 69

• Susceptible Species:
  
  • Waterbuck, sable, dama gazelle, Cuvier’s gazelle, bongo, giraffe
  • Likely that all ruminant are susceptible
• Etiology: Coxiella burnettii - OIE Reportable Disease
  
  • Gram negative obligate intracellular bacterium
• Pathogenesis:
  
  • Contact with infective fluids – very low infectious dose in humans
• Clinical signs
  
  • Placentitis, abortion, stillbirth
  • Fetal lesions – fetal distress (alveolar meconium aspiration, increased alveolar squamous cells
  • Placenta may look grossly normal or have pale discolorationor mineralization of cotyledons
• Histo Lesions:
  
  • Necrosis of cotyledonary villi & intercotyldeondary trophoblasts with accumulation of necrotic debris, fibrin, and neutrophils between villi
  • Trophoblasts have aggregates of organisms – stained with modified Ziehl-Neelsan, stamp, Gimenez, or Macchiavello stain

Question 70

What is the etiologic agent of chlamydiosis in ruminants?

What species are affected?

What are the typical clinical signs and lesions?

How is it distinguished from coxiellosis?

Answer 70

• Susceptible Species:
  
  • Multiple reports of several free-ranging ungulates
  • Identified in keratoconjunctivitis lesions in big-horn sheep
• Etiology: Chlamydia (Chlamydophila) abortus
  
  • Gram-negative, obligate, intracellular bacteria
• Clinical Signs & Gross Lesions
  
  • Reproductive loss, infectious keratoconjunctivitis
  • Placentitis and abortion in domestic sheep and goats
• Histo Lesions: vasculitis distinguishes Chlamydiosis from coxeillosis

Question 71

What species are particularly susceptible to Haemonchus?

What nutrient deficiency prediposes them to infestation?

What are the typical clinical signs?

How is it diagnosed?

Answer 71

• Susceptible Species:
  
  • Giraffe, nondomestic caprids, antelope, sable, gazelle, hippopotamus
• Etiology: Haemonchus contortus, H. placei
  
  • Life-cycle - direct, environmental parasite loads build up rapidly
  • Adult females have barber pole appearance (white uterus around blood-filled gut)
• Pathogenesis:
  
  • Larvae and adults are hematophagous
  • Copper deficiency predisposes ruminants to parasitism
• Clinical signs
  
  • Pale mucous membranes, muscles, viscera
  • SC or submandibular edema, hydrothorax, or ascited due to hypoproteinemia
  • May have hemorrhagic abomasla contents
• Diagnosis: Fecal egg count

Question 72

What species cause Osteragiosis in nondomestic ruminants?

What are the typical lesions associated with infestation?

How is this disease diagnosed?

Answer 72

• Susceptible Species: variety of nondomestic ruminants
• Etiology: Ostertagia osteragi (cattle), Teladorsagia circumcincta (sheep), Teladorsagia, Marshallagia, Spiculopteragia, Camelostrongylus
• Clinical Signs & Gross Lesions
  
  • Chronic abomasitis, glandular hyperplasia, mucous metaplasia
  • Emaciated, hypoproteinemic, elevated abomasal pH due to loss of parietal cells
• Diagnosis: fecal examination

Question 73

What is the genus of whipworms?

What are teh clinical signs associated with infestation in ruminants?

What are the histologic lesions?

Answer 73

• Susceptible Species: multiple ruminant species
• Etiology: Trichuris spp
• Clinical signs
  
  • Mucohermorrhagic typhlocolitis and chronic diarrhea, hypoproteinemia, poor BCS
  • Hemorhhagic intestinal contents and worms
• Histo Lesions: worms embedded in mucosa with erosion, glandular hyperplasia, infiltrates, hemorrhage
• Diagnosis: fecal examination

Question 74

What is the natural host of Eleophora?

What are the clinical signs in aberrant hosts? What are some of the typical aberrant hosts?

What are the histologic lesions associated with this disease?

Answer 74

• Susceptible Species:
  
  • Incidental in mule deer and black-tailed deer (natural hosts)
  • Severe disease in aberrant hosts like elk, moose, Barbary and bighorn sheep
• Etiology: Eleaophora schneideri – Filaroidea, Onchocercidae
  
  • Adult nematodes often found in the carotid artery
• Pathogenesis:
  
  • • Clinical Signs & Gross Lesions
  • Severe ulcerative to crusting facial skin lesions, pneumonia, rhinitis, meningomyelitis
• Histo Lesions: eosinophilic to granulomatous inflammation with microfilaria at foci of necrosis
• Diagnosis: fecal examination

Question 75

What is the meningeal worm?

What is the natural host? What are some commonly affected aberrant hosts?

How is it transmitted?

What are the clinical signs and lesions in aberrant hosts?

How is this diagnosed?

Answer 75

• Susceptible Species:
  
  • White-tailed deer is natural host – subclinical infections
  • Disease in black-tailed deer, mule deer, fallow deer, moose, caribou, reindeer, elk, red deer
  • Disease in bighorn sheep, pronghorn, eland, sable, bongo, scimitar horned oryx, blackbuck, bison
• Etiology: Parelaphostrongylus tenuis
• Pathogenesis: fecal oral transmission
• Clinical Signs and Gross Lesions
  
  • Neurological signs (nematode migration) & pneumonia (eggs and developing larvae in lungs)
• Histo Lesions:
  
  • Malacia, hemorrhage, Wallerian degeneration and meningoencephalitis with eosinophilic infiltrate
  • Granulomatous interstitial pneumonia
• Diagnosis: necropsy, fecal examination

Question 76

Besides the meningeal worm, what other Parelophostrongylus species affect ruminants?

What species are susceptible?

What is the pathogenesis and clinical signs of these diseases?

Answer 76

• Susceptible Species:
  
  • Dall sheep, black-tailed deer, mule deer (P. odocolei)
  • White tailed deer (P. andersoni)
• Etiology:
  
  • Parelaphostrongylus odocolei – found in skeletal muscle of various bovids and cervids
  • Parelaphostrongylus andersoni – muscle worm of white-tailed deer
• Pathogenesis:
  
  • Eggs of P. andersoni deposited in vasculature, larvae develop in alveolar capillaries, adults in longissimus dorsi muscle
  • P. andersoni adults found in the connective tissues of muscles, eggs in lungs
• Clinical signs
  
  • Interstitial pneumonia and myositis
• Diagnosis: necropsy, fecal examination

Question 77

What are some ruminant lungworms?

What species are susceptible?

What are the clinical signs and lesions associated with infestation?

Answer 77

• Susceptible Species:
  
  • Component of bighorn sheep pneumonia
  • Found in several nondomestic bovids and cervids
• Etiology: Dictyocaulus, Muellerius, Protostrongylus, Varestrongylus
• Pathogenesis:
  
  • Disease in large numbers
  • Adults in bronchioles or bronchii
• Clinical signs
  
  • Pneumonia
• Histo Lesions: bronchitis and peribronchitis with mucus, neutrophils, mononuclear cells and eosinophils with eggs and larvae in smaller airways

Question 78

What ruminant species are particularly susceptible to babesiosis?

How is this protozoa transmitted?

What are the typical clinical signs and lesions?

How is this diagnosed?

What is another important differential to consider?

Answer 78

• Susceptible Species:
  
  • Sable antelope, chamois, muskox, bighorn sheep, giraffe, reindeer, elk
• Etiology: Babesia spp
  
  • Obligate intracellular, tick-borne, apicomplexan protozoa that infect erythrocytes
• Pathogenesis:
  
  • Ixodid tick transmission
• Clinical signs
  
  • Emaciation, hematuria, anemia, icterus, splenomegaly, hepatomegaly, gall bladder distension,
• Histo Lesions:
  
  • Congestion of capillaries, erythrophagocytosis and hemosiderin accumulation in macrophages
  • Hemoglobin casts, tubular degeneration, tubular epithelial hemosiderosis
  • Centrilobular degeneration and necrosis in the liver
• Diagnosis:
  
  • Blood or impression smears, PCR
  • DDx is anaplasmosis but that does not result in hemolysis

Question 79

What species are susceptible to Theileriosis?

How is this disease transmitted?

What are the typical clinical signs and lesions?

What is seen on histology?

How is this diagnosed?

Answer 79

• Susceptible Species:
  
  • African buffalo, blue wildebeest, tsessebe, waterbuck, Grant’s gazelle, klipspringer, blesbok, reedbuck, bushbuck, nyala, eland, sable, roan, kudu, gray duiker, bison
  • Multiple cervid species – reindeer, white-tailed der, Roe deer, sika deer, red deer
• Etiology: Theileria spp
• Pathogenesis: Ixodid tick transmission, Amblyomma americanum (T. cervi)
• Clinical Signs
  
  • Most disease is subclinical, but real disease most common in roan and sable
  • Depression, fever, anemia, icterus, lymphadenomegaly, dyspnea, diarrhea, neurologic signs
  • Lymphadenopathy, splenomegaly, pulmonary edema, petechial and ecchymotic hemorhage
• Histo Lesions: widespread lymphoid proliferation, infiltration of multiple tissues (PCR of kidney, GI, liver, lung, heart, or brain tissue) by schizont-containing lymphoblasts
• Diagnosis: PCR, intraerythrocytic piroplasms on blood or lymph node impression smears

Question 80

What are the etiologic agents of trypanosomiasis in ruminants?

What species are susceptible?

How is it transmitted?

What are the associated clinical signs and lesions?

How is it diagnosed?

Answer 80

• Susceptible Species:
  
  • Bovids, giraffe, hippopotamus
  • Roe deer, red deer, brocket deer, Axis, sambar deer
• Etiology: Trypanosoma congolense, T. vivax, T. brucei – OIE reportable disease
  
  • Flagellated hemoparasites
• Pathogenesis:
  
  • Spread by Tsetse flies (Glossina spp), Tabanid flies, and Deer keds
  • Trypomastigotes ciculate in peripheral blood and enter macrophages and endothelial system of heart and spleen
• Clinical signs
  
  • Immunosuppression, neurologic diseasef
• Diagnosis: PCR, microscopic evaluation of parasites in blood or impression smears of brain or liver

Question 81

What ungulate species are susceptible to toxoplasmosis?

Describe the pathogenesis of this disease.

What are the typical lesions?

How is it diagnosed?

Answer 81

• Susceptible Species:
  
  • Gazelles, gerenuk, dik dik, saiga, pronghorn, muskox, nilgai
  • Exposure in giraffe and hippopotamus as well based on serology
• Etiology: Toxoplasma gondii
  
  • Coccidian protozoan parasite (Apicomplexa)
• Pathogenesis:
  
  • Cats are definitive hosts
  • Ingestion of oocysts or bradyzoites from tissue cysts
  • Tachyzoites spread to mesenteric lymph nodes and systemically to blood and lymphatics
• Clinical Signs & Gross Lesions
  
  • Abortion, neonatal death, placentitis, pneumonia, or disseminated fatal disease
  • Mesenteric lymphadenopathy, hemorrhagic or catarrhal enteritis, peritoneal effusion, serosal and endocardial petechiae and ecchymoses, pulmonary edema and hemorrhage, pale foci of necrosis on liver, spleen, or kidney
  • Dark red cotyledons with small white foci of necrosis on the placenta
• Histo Lesions: mononuclear to mixed inflammatory cell infiltrates usually centered around blood and lymphatic vessels
• Diagnosis: IHC or PCR

Question 82

What ruminant species is particularly susceptible to Neospora?

What are the clinical signs?

Answer 82

• Susceptible Species:
  
  • Stillbirth in Kudu
  • Detected frequently in serologic surveys of cervids
• Etiology: Neospora caninum
  
  • Obligate intracellular apicomplexan protozoal parasites

Question 83

Describe the general lifecycle of coccidiosis in ruminants.

What demographics are most susceptible?

What are the common clinical signs?

Are there any risk factors?

How is it diagnosed?

Answer 83

• Susceptible Species:
  
  • Multiple cervid and bovid species
• Etiology: Eimeria
  
  • Obligate intracellular parasites, reproduce axexually (merogony) and sexually (gamogony) in the epithelial or endothelial cells of host intestine
• Pathogenesis:
  
  • Ingestion of infected oocysts, exsporulation, and invasion of GI epithelium
  • Younger animals more susceptible
  • High densities, stressful scenarios all play a role in outbreaks
• Clinical signs
  
  • Emaciation, dehydration, watery to bloody diarrhea
• Diagnosis: Fecal examination

Question 84

What nondomestic species are susceptible to bovine spongiform encephalopathy?

What is the typical transmission?

What are the typical clinical signs and lesions?

How is this diagnosed? From what tissues?

Answer 84

• Susceptible Species:
  
  • Nyala, kudu, gemsbok, Arabian oryx, scimitar-horned oryx, eland, Bison
  • Greater kudu appear particularly susceptible
• Etiology: BSE prion
• Pathogenesis:
  
  • Ruminant-derived meat and bone meal in feed
• Clinical signs
  
  • Progressive degeneration of nervous system – temperament, posture, behavior, ataxia, hyperesthesia
• Histo Lesions: neuronal vacuolation of the obex
• Diagnosis: IHC, obex histo, ELISA – no reliable tests in a living animal

Question 85

A recent study evaluated fecal cortisol levels in oryx in managed and semi-free-ranging environments.

Describe the HPA axis.

What factors affect cortisol production?

Why is fecal cortisol measurement better than blood?

What factors were associated with higher cortisol levels?

Were there any differences between the two enclosure types?

Answer 85

Pauling, C. D., Lankford, S. E., & Jackson, V. L. (2017). Fecal cortisol levels in scimitar-horned oryx, Oryx dammah, reveals differences between captive environments. Journal of Zoo and Wildlife Medicine, 48(4), 1049-1057.

Abstract: Due to the intensive management of the scimitar-horned oryx, Oryx dammah, involving both captivity and reintroductions, understanding the stress associated with environmental situations this endangered species might experience would be particularly helpful. Fecal cortisol levels were measured across seasons, between captive management programs, and among varying reproductive states in animals held at Fossil Rim Wildlife Center (FRWC) and Kansas City Zoo (KCZ). A total of 72 samples were collected from FRWC and 69 samples were collected from KCZ. The herd size and sex ratio changed for both locations in the middle of sampling due to translocations and birth. The herd sizes ranged from 25 to 28 individuals at FRWC and 22 to 24 individuals at KCZ. An ELISA was optimized and utilized to investigate fecal cortisol variances across seasons, captive management programs, and among varying reproductive states. Fecal cortisol levels ranged from 68.9 to 668.7 pg/g throughout this study, but key differences were found in response to reproductive status, environmental conditions, and social status. The highest level of fecal cortisol measured (668.7 pg/g) was in a pregnant female 9 days prior to parturition. During winter months, an increase in fecal cortisol levels occurred in both herds (FRWC 160.3 pg/g to 335.1 pg/g and KCZ 118.8 pg/g to 505.0 pg/g). In addition, when intact males were held together in an enclosure, the dominant males had lower fecal cortisol levels compared with submissive males during three of the four sampling periods. Understanding how these data relate to the physiologic stress response will require further study, but these results can be utilized to help establish expected fecal cortisol ranges in multiple environments and can aid current captive scimitar-horned oryx management programs, as well as future reintroduction efforts.

• Release of catecholamine -> activation of hypothalamic-pituitary-adrenal (HPA) axis -> release of adrenocorticotrophic hormone (ACTH) -> glucocorticoids from adrenal cortex.
• Glucocorticoid – metabolized -> liver -> intestinal bacteria -> feces.
  
  • The glucocorticoid most responsive to stressors is cortisol.
    
    • Chronic stress can lead to suppression of reproduction, immune responses, and growth.
    • Cortisol may appear alone or with several other glucocorticoid metabolites, amounts depend on spp.
• Passive collection technique and representation of cortisol over much broader time period makes feces > blood.
• In 2014, prep for large-scale reintroduction effort of Scimitar-horned oryx planned in Chad over 5 years.
  
  • Cortisol measured from animals in two managed herds to establish a baseline.
• Fossil Rim – drive-through wildlife part with free-ranging herd, 100-acre pasture.
• Kansas City Zoo – 7-acre pasture during the day, indoor enclosure during evening. Predominantly indoors during winter.
• First time ELISA has been validated for use in SHO for fecal cortisol levels in a large sample size.
• No relationship between sex and cortisol levels in Fossil Rim herd.
• Increased in winter in both herds.
• In pregnant females, highest individual cortisol in April due to pregnancy establishment.
• Association between high cortisol and pregnancy and parturition, but small sample size.
• In both herds, lower cortisol levels in breeding males vs other males.
  
  • Opposite of what is observed in bison bulls, males higher during rut.
  • Submissive male had the highest cortisol level of all sampled for the males kept indoors.

Question 86

A recent study compared medtomidine-ketamine-butorphanol and etorphin-medetomidine-midazolam protocols followed by a CRI of medetomidine-ketamine-midazolam in impala.

What differences were seen between the two induction protocols?

What are some common side effects with etorphine in impala?

Answer 86

Gerlach, C. A., Kummrow, M. S., Meyer, L. C., Zeiler, G. E., Stegmann, G. F., Buck, R. K., … & Kästner, S. B. (2017). Continuous intravenous infusion anesthesia with medetomidine, ketamine, and midazolam after induction with a combination of etorphine, medetomidine, and midazolam or with medetomidine, ketamine, and butorphanol in impala (Aepyceros melampus). Journal of Zoo and Wildlife Medicine, 48(1), 62-71.

Abstract: In order to develop a long-term anesthesia for flighty antelope species in field situations, two different protocols for induction and maintenance with an intravenous infusion were evaluated in wild-caught impala (Aepyceros melampus). Ten adult female impala were induced with two induction protocols: one consisted of 0.2 mg/kg medetomidine, 4 mg/kg ketamine, and 0.15 mg/kg butorphanol (MKB) and one consisted of 0.375 mg/kg etorphine, 0.2 mg/kg medetomidine, and 0.2 mg/kg midazolam (EMM). In both treatments, anesthesia was maintained with a continuous intravenous infusion (CII) at an initial dose rate of 1.2 mcg/kg per hr medetomidine, 2.4 mg/kg per hr ketamine and 36 mg/kg per hr midazolam. Partial reversal was achieved with naltrexone (2 : 1 mg butorphanol; 20:1 mg etorphine) and atipamezole (5:1 mg medetomidine). Evaluation of anesthesia included respiratory rate, heart rate, rectal temperature, arterial blood pressure, oxygen saturation, end tidal carbon dioxide tension, and tidal volume at 5-min intervals, palpebral reflex and response to painful stimuli at 15- min intervals, and arterial blood gases at 30-min intervals. Plasma cortisol concentration was determined after induction and before reversal. Duration and quality of induction and recovery were evaluated. EMM caused a faster induction of 9.5 ± 2.9 min compared to 11.0 ± 6.4 min in MKB. Recovery was also quicker in EMM (EMM: 6.3 ± 5.4 min; MKB: 9.8 ± 6.0 min). However, EMM also produced more cardiopulmonary side effects, including hypoxemia and hypercapnia, and calculated oxygenation indices (PaCO2-PETCO2) were worse than in MKB. One animal died after induction with EMM. The CII provided surgical anesthesia in 7 of 10 animals in MKB and in 9 of 9 animals in EMM for 120 min. In conclusion, the MKB induction protocol had advantages for prolonged anesthesia in impala with significantly less cardiopulmonary depression compared to EMM. The comparably decreased anesthetic depth could easily be adjusted by an increase of the CII.

• Quick inductions crucial to prevent exhaustion, hyperthermia, and trauma
• Potent opioids provide rapid induction but lead to poor respiration and muscle rigidity
• Impala are particularly susceptible to etorphine induced respiratory depression – mitigated with administration of butorphanol in other species
• EMM – faster reduction but respiratory depression and chest wall rigidity, all animals developed apnea with the ketamine bolus prior to the CII (could be ketamine or delayed etorphine effects)
• Animals darted once had higher cortisol concentrations than those with two

Take home: MKB better for prolonged procedures, EMM faster induction but poor respiration

Question 87

A recent study evaluated a butorphanol-azaperone-medetomidine protocol against a medetomidine-azaperone-alfaxalone protocol in Nyala.

What is the scientific name of the nyala? What are some of the difficulties immobilizing them?

What are some problems with ultrapotent opioids?

How did the two protocols differ?

What were some common complications in the study?

Answer 87

Black, P. A., Keller, D. L., Burton, M. S., & Martel, C. (2020). EVALUATION OF TWO ANESTHETIC COMBINATIONS IN LOWLAND NYALA (TRAGELAPHUS ANGASII). Journal of Zoo and Wildlife Medicine, 51(2), 290-296.

Abstract: Fourteen lowland nyala (Tragelaphus angasii) in managed care were successfully anesthetized for a total of 17 anesthetic events using either a combination of butorphanol (0.75 ± 0.15 mg/kg), azaperone (0.25 ± 0.05 mg/kg), and medetomidine (0.30 ± 0.06 mg/kg) (BAM) or medetomidine (0.17 ± 0.01 mg/kg), azaperone (0.22 ± 0.02 mg/kg), and alfaxalone (0.52 ± 0.08 mg/kg) (MAA) delivered intramuscularly via dart. Mean time to initial effect, sternal recumbency, lateral recumbency, handling, and intubation were recorded. The nyala were maintained in sternal recumbency with supplemental oxygenation until 60 min after initial injection. Cardiopulmonary effects were recorded every 5 min after handling until reversal. Arterial blood samples were collected every 15 min for analysis. Level of sedation and quality of recovery were scored. Anesthesia was antagonized with atipamezole (at 5 mg per mg of medetomidine) for both protocols and naltrexone (at 2 mg per mg of butorphanol) for the BAM protocol delivered intramuscularly via hand injection. Mean time to extubation, head control, and standing post reversal were recorded. No hyperthermia, acidemia, apnea, or tachycardia occurred; however, animals did display hypoxemia. Two animals in the BAM cohort required supplementation to facilitate handling. These drug combinations provided satisfactory levels of sedation in most cases for safe handling and minor procedures in lowland nyala under managed care.

• Key points:
  
  • Lowland nyala – One of 8 extant spiral horned antelope (genus Tragelaphus).
    
    • High levels of stress-related morbidity and mortality, capture myopathy.
  • Disadvantages to high-potency opioids:
    
    • Respiratory depression, hyperthermia, acidemia, incomplete reversibility, prolonged recovery times, human handling risks.
  • Butorphanol-azaperone-medetomidine (BAM) vs Medetomidine-azaperone-alfaxalone (MAA).
    
    • Immobilized either for habitat moves or medical abnormality evaluation (lacerations, facial abscesses, lameness, hoof overgrowth).
    • Volumes significantly higher for MAA.
    • Two animals in BAM group needed supplemental dart.
    • Only 1 BAM anesthetized animal could be intubated (too light).
    • No extrapyramidal side effects of azaperone or incomplete reversal in either group.
    • All recovered uneventfully, 1 mortality 56 hrs after procedure (osteomyelitis, sepsis, acute myocardial necrosis).
    • No difference between BAM and MAA for induction or recovery times after reversals.
    • No differences between protocols for vital parameters over time.
      
      • BAM significantly higher RR at final time point.
    • Lactate significantly higher in MAA.
    • HCO3- and BE significantly higher/more positive in BAM.
    • No difference at individual time points for any variable aside from BE high at 30 min with BAM, lactate higher at 45 min with MAA.
    • Lactate values were elevated in MAA at all time points.
    • Despite mean SPO2 levels being > 90%, nyala in this study did have low PaO2 indicative of moderate to severe hypoxemia.
      
      • Pulse ox and RR are not really sufficiently reliable measures of oxygenation.
      • Similar hypoxemia reported in other ungulate species.
      • Supplemental O2, intubation, and PPV is recommended when using either of these protocols in nyala.
• Takeaways: BAM and MAA adequate for immobilization of lowland nyala for minor procedures. Higher volume needed for MAA. These are aternative protocols to high-potency opioids. Provide O2.

Question 88

What was observed regarding CBC/chem parameters, cortisol, and other physical parameters for wild impala housed in a boma?

Answer 88

Zeiler, G. E., & Meyer, L. C. (2017). Captive management of wild impala (Aepyceros melampus) during intensive immobilization and general anesthesia study trials. Journal of Zoo and Wildlife Medicine, 48(4), 1058-1071.

Wild impala housed in a boma x 16 wks had no changes in CBC/chem, cortisol, or other physical parameters.

Darting associated with high morbidity and mortality. Cortisol decreased over 120 min while anesthetized but remained unchanged over the 16 wk boma period.

Behavioral changes - decreased antagonistic interactions and reaction to investigators, increased individual and reciprocal allogrooming after 9 wks.

Question 89

What was observed with fecal cortisol levels in oryx between captive environments (Fossil Rm vs Kansas City Zoo)?

Answer 89

Pauling, C. D., Lankford, S. E., & Jackson, V. L. (2017). Fecal cortisol levels in scimitar-horned oryx, Oryx dammah, reveals differences between captive environments. Journal of Zoo and Wildlife Medicine, 48(4), 1049-1057.

Cortisol most common stress-related GC in large mammals.

Fossil rim oryx had higher cortisol in Oct, Apr, July.

Overall, fecal cortisol increased in winter, pregnant females, and submissive males (dominant bulls low cortisol).

Both herds had decreased cortisol in breeding males (opposite of what is observed in bison bulls).

Question 90

Compare TIVA with medetomidine, ketamine, midazolam after induction with etorphine, medetomidine and midazolam or with medetomidine, ketamine, and butorphanol in impala.

Answer 90

Gerlach, C. A., Kummrow, M. S., Meyer, L. C., Zeiler, G. E., Stegmann, G. F., Buck, R. K., … & Kästner, S. B. (2017). Continuous intravenous infusion anesthesia with medetomidine, ketamine, and midazolam after induction with a combination of etorphine, medetomidine, and midazolam or with medetomidine, ketamine, and butorphanol in impala (Aepyceros melampus). Journal of Zoo and Wildlife Medicine, 48(1), 62-71.

Etorphine-medetomidine-midazolam induction was faster, produced more cardiopulmonary side effects - hypoxemia, hypercapnia, high PaCO2-ETCO2.

Etorphine-medetomidine-midazolam also resulted in apnea, one animal died and one animal prolonged recovery after reversal.

Medetomidine-ketamine-butorphanol induction resulted in hyperglycemia at all time points, higher blood pressure.

Both protocols showed hypoxemia, progressive hypercapnia, lactate decreased over time.

Cortisol higher vs impala manually restrained in the field, and higher in animals receiving one dart vs two dart protocol.

Question 91

What was observed with use of detomidine and butorphanol for standing sedation in ungulates?

Answer 91

Bouts, T., Dodds, J., Berry, K., Arif, A., Taylor, P., Routh, A., & Gasthuys, F. (2017). Detomidine and butorphanol for standing sedation in a range of zoo-kept ungulate species. Journal of Zoo and Wildlife Medicine, 48(3), 616-626.

Detomidine-butorphanol commonly used in horses for standing sedation.

Safe to approach when tail and ear swishing stops.

Smooth recovery following reversal, no adverse effects.

Somali wild ass required higher doses vs other equids.

White rhino males more likely to go into sternal vs females. White rhinos in general low resp rate.

Bongo required higher dosages vs other artiodactyls.

Camels rest head back on hump instead of dropping it like other spp.

Question 92

Compare propofol CRI vs isoflurane for anesthesia in Speke’s gazelle.

Answer 92

Kleinschmidt, L. M., Kinney, M. E., Camilo, G. R., Thier, T., Fischer, M., Hanley, C. S., & Padilla, L. R. (2018). Comparison of propofol constant rate infusion and isoflurane for maintenance of anesthesia in speke’s gazelle, gazella spekei. Journal of Zoo and Wildlife Medicine, 49(3), 722-731.

Propofol CRI had lower RR (also decreased over time), higher BP (iso lower), more ataxic recoveries but was manageable without trauma.

Both protocols maintained spontaneous ventilation. No other differences.

Question 93

What was observed with alfaxalone-azaperone-medetomidine vs BAM in lowland nyala?

Answer 93

Black, P. A., Keller, D. L., Burton, M. S., & Martel, C. (2020). Evaluation of two anesthetic combinations in lowland nyala (tragelaphus angasii). Journal of Zoo and Wildlife Medicine, 51(2), 290-296.

Alfaxalone-azaperone-medetomidine caused lower HR, bicarbonate, base excess and higher lactate. Deeper plane of anesthesia, larger volume of injection.

BAM - Lighter (some needed supplementation).

Disadvantages of high potent opioids - respiratory depression, hyperthermia, acidemia, incomplete reversibility, prolonged recovery, human risk.

Question 94

What are some considerations for immobilizing muskox under high arctic conditions?

Answer 94

Grøndahl, C., Andersen-Ranberg, E. U., Mosbacher, J. B., Stelvig, M., Hansen, L. H., & Schmidt, N. M. (2018). Immobilizing muskox (Ovibos Moschatus) under high Arctic conditions. Journal of Zoo and Wildlife Medicine, 49(4), 856-862.

Used etorphine, xylazine, medetomidine, ketamine immobilization. Reliable with minimal pathophysiologic alterations.

Wrapped dart rifle barrel in bubble wrap and hand warmers. Prevented dart freezing by adding ethanol to dart. Supplemental O2 via nasal tube.

All animals reached sufficient anesthesia. 66% needed partial reversal with atipamezole which improved resp depression and bradycardia.

Mild hypertension, mild bradycardia. Cortisol lower vs other studies that used helicopter or gunshot immobilization. Preferred to approach on foot.

Question 95

What is vatinoxan? What was observed with IV vatinoxan in markhors immobilized with IM medetomidine and ketamine?

Answer 95

Sainmaa, S., Mykkänen, A., Adam, M., Jantunen, N., Vainio, O., & Raekallio, M. (2019). INTRAVENOUS VATINOXAN IN MARKHORS (CAPRA FALCONERI HEPTNERi) IMMOBILIZED WITH INTRAMUSCULAR MEDETOMIDINE AND KETAMINE—A PRELIMINARY DOSESCREENING STUDY. Journal of Zoo and Wildlife Medicine, 50(1), 159-166.

Vatinoxan - alpha 2 adrenoreceptor antagonist that mostly affects peripheral receptors (does not cross BBB). Alleviates peripheral cardiovascular and pulmonary effects of medetomidine while sedation is maintained.

Half of the medetomidine-ketamine induced animals were bradycardic and hypertensive. Vatinoxan IV alleviated hypertension but caused bradycardia and hypotension at high doses.

Vatinoxan can reduce hypertension in markhors anesthetized with medetomidine-ketamine.

Question 96

What clinical signs are observed with mycoplasma bovis infection of bison?

What risk factors were associated with mycoplasma bovis-associated disease in farmed bison in Canada?

Answer 96

Bras, A. L., Barkema, H. W., Woodbury, M. R., Ribble, C. S., Perez-Casal, J., & Windeyer, M. C. (2017). Clinical presentation, prevalence, and risk factors associated with Mycoplasma bovis-associated disease in farmed bison (Bison bison) herds in western Canada. Journal of the American Veterinary Medical Association, 250(10), 1167-1175.

Mycoplasma bovis in bison - chronic pneumonia, polyarthritis, mortality.

Compared to cattle with M. bovis, bison are older (>5 yrs), and have higher mortality rates.

Cattle typically are young feedlot animals.

Bison typically adults with low BCS and swollen joints as most common clinical signs.

Question 97

A recent study described interdigital necrobacillosis in Goitered gazelles.

What is the scientific name of this species?

What is the etiologic agent of interdigital necrobacillosis?
- What were secondary effects of this disease in this species?

What are some ways to prevent this in goitered gazelles?

Answer 97

Çeçen, G., Buyukcangaz, E. K., Çalışkan, Ü. G., Cangul, T. I., & Akdesir, E. (2018).
Interdigital necrobacillosis associated with Trueperella pyogenes in goitered gazelles (Gazella subgutturosa).
Journal of Zoo and Wildlife Medicine, 49(2), 429-434.

Key Points:
* Trueperella pyogenes - gram-positive, nonmotile, non spore-forming short rod.
– Interdigital necrobacillosis caused by synergistic bacteria – Fusobacterium, Dichelobacter, Trueperella, Porphyromonas, Prevotella
* In these cases trueperella from foot rot -> disseminated abscesses and death in goitered gazelles.
* Prevention - control biting fly vector populations, reduce contact of udders with water or humid environment, isolate animals with draining abscesses, prevent mechanical damage caused by rough exhibit surfaces.

Question 98

Discuss the seroprevalence of anthrax in mackenzie wood bison (males vs females)?

Answer 98

New, D., Elkin, B., Armstrong, T., & Epp, T. (2017). Anthrax in the Mackenzie wood bison (Bison bison athabascae) population: 2012 anthrax outbreak and historical exposure in nonoutbreak years. Journal of wildlife diseases, 53(4), 769-780.

Anthrax = bacillus anthracis = spore-forming bacteria.

Fatal epizootics in wood bison.

Seroprevalence this study - Males > females. Adults > juveniles.

Seropositivity declines in between outbreaks.

Question 99

What is schmallenberg virus?

What is the vector?

Clinical signs in domestic cattle?

What was the seroprevalence in bison compared to cervids?

Answer 99

Kęsik-Maliszewska, J., Krzysiak, M. K., Grochowska, M., Lechowski, L., Chase, C., & Larska, M. (2018). Epidemiology of Schmallenberg virus in European bison (Bison bonasus) in Poland. Journal of Wildlife Diseases, 54(2), 272-282.

Schmallenberg virus - Arbovirus affecting ruminants in Europe. Orthobunyavirus (family Bunyaviridae).

Vector - Culicoides spp.

CS - Abortion, stillbirths, weak neonates.

Bison seroprevalence 74%, higher vs cervids (40%).

SBV not detected in any fetal tissues and only 3% Culicoides spp were positive in one year.

No change in fecundity of the bison population during this time period.

European bison in Poland havve a high seroprevalence for Schmallenberg virus.

Question 100

A recent study descrbied the introduction of Theileriosis in repatriated mountain bongo.

What species was identified in this outbreak?

What is the vector?

What were the clinical findings?

How was this treated?

Answer 100

Bishop, R. P., Odongo, D. O., Dolan, T. T., Dolan, R. B., Skilton, R. A., & Sayer, P. D. (2019).
Theileriosis in mountain bongo repatriated to Kenya: a clinical and molecular investigation.
Journal of Zoo and Wildlife Medicine, 50(2), 342-349.

Key Points:
* Theileria taurotragi (Rhipicephalus tick vector).
* Heavy tick infestation, necropsy showed splenic enlargement, pulmonary congestion, Theileria schizonts in lymphocytes in LN and blood.
* No additional issues after treating all remaining bongo with buparvaquone and oxytetracycline, one individual remained blind after recovery.

Question 101

A recent study investigated tick and pathogen prevalence in Nilgai in Texas.

What is the scientific name of the Nilgai antelope?

What is the etiologic agent of Texas cattle fever?
- What is the known vectors?

Are white tailed deer reservoirs for this disease?

Answer 101

Olafson, P. U., Thomas, D. B., May, M. A., Buckmeier, B. G., & Duhaime, R. A. (2018).
Tick vector and disease pathogen surveillance of nilgai antelope (Boselaphus tragocamelus) in southeastern Texas, USA.
Journal of wildlife diseases, 54(4), 734-744.

Key Points
* All nilgai were seronegative for Babesia (Theileria) equi and Babesia cabalii.
* All animals were PCR negative for Babesia spp DNA.
* Single animal was seropositive for Babesia bovis and Babesia bigemina.
* Texas cattle fever aka bovine babesiosis. B. bigemina and B. bovis. Vectors Rhipicephalus annulatus and Rhipicephalus microplus.
* WTD NOT a reservoir host.
* Nilgai in southern region very low Rhpicephalus burden vs northern.

Question 102

What happened to cattle fed brain infected with CWD and housed with infected deer and wapiti?

Answer 102

Williams, E. S., O’Toole, D., Miller, M. W., Kreeger, T. J., & Jewell, J. E. (2018). CATTLE (BOS TAURUS) RESIST CHRONIC WASTING DISEASE FOLLOWING ORAL INOCULATION CHALLENGE OR TEN YEARS’NATURAL EXPOSURE IN CONTAMINATED ENVIRONMENTS. Journal of wildlife diseases, 54(3), 460-470.

No cattle developed CWD following oral and environmental exposure.

Cattle are very resistant, only get it if intracranial inoculation. CWD transmitted between deep, wapiti, moose, reindeer.

Risks of CWD transmission to cattle following oral inoculation and prolonged exposure to contaminated environments are low.

Question 103

A recent study described a strange radiographic finding in perparturient Sichuan takin.

What condition was identified?

Did it resolve?

What were the animals other clinical signs?

What differentials should be considered for this condition?

What is its suggested etiology?

Answer 103

Marinkovich, M., Wisner, E. R., & Brenner, D. J. (2019).
Distal limb swelling and periosteal productive reaction in periparturient Sichuan takin (Budorcas taxicolor tibetana): five cases of presumptive hypertrophic osteopathy.
Journal of Zoo and Wildlife Medicine, 50(2), 437-446.

Key Points
- Proliferative periosteal reaction, primarily of metacarpal bones, metatarsal bones, and phalanges consistent with hypertrophic osteopathy secondary to pregnancy in takin.
- After birth the lameness and limb swelling resolved, but bone density changes and extent of periosteal change did not resolve.
- Animals were also lethargic, febrile.
- Ddx for periosteal proliferation – mandibular osteodystrophy, HO, panosteitis, nutritional osteodystrophies i.e. hypervitaminosis A (more likely to affect joints), D, osteomyelitis, trauma, neoplasia, HO.
- Etiology for HO undetermined – Primary pathophysiological changes include increased capillary density, elevated peripheral blood flow, proliferation of vascular connective tissue, and subperiosteal deposition of bone.
– Recent research suggests initiation and expression of vascular endothelial growth factor VEGF appears to play a role.

Question 104

What condition contributed to mortality in a population of pronghorn antelope?
- How prevalent was it?
- How is it detected on histology?
- What other diseases were associated with it?

What is the scientific name of this species?

Answer 104

Martinez, M. E., Zimmerman, D., Seeley, K. E., Zhang, L., Bapodra, P., & Cianciolo, R. E. (2019).
Systemic amyloidosis in a population of pronghorn antelope (Antilocapra americana).
Journal of Zoo and Wildlife Medicine, 50(1), 147-158.

Key Points
* Systemic amyloidosis - 77% prevalence in a group of pronghorn antelope.
* Amyloid detected on histology H&E and Congo red stain.
* Amyloid present in kidneys, spleen, liver, GI, adrenals, thyroid glands.
* Mass spectrometry on renal tissue showed serum amyloid A. SAA levels in blood were normal for all animals.
* Most animals had a clinical history of haemonchosis and many had pneumonia and negative energy balance.
* No significant association between amyloidosis and degree of relatedness in this group.
* Amyloidosis significantly associated with haemonchus infection.

Question 105

What is the most common neoplasm in thomson’s gazelles?

What were the clinical signs?

What were its histologic characteristics?

What is the scientific name of this species?

Answer 105

French, S. J., Garner, M. M., & Kiupel, M. (2018).
Histopathologic characteristics of thyroid gland neoplasms in thomson’s gazelles (eudorcus thomsonii).
Journal of Zoo and Wildlife Medicine, 49(1), 64-69.

Key Points:
* Thyroid tumors most common neoplasm in thomson’s gazelles.
* CS - palpable mass ventral neck, progressive wt loss.
* Solid thyroid carcinoma most common classification.
* Neoplastic cells positive for thyroid transcription factor 1 and thyroglobulin.
* No evidence of metastatic disease.
* Typically space-occupying, without mets - similar presentation in dogs (coughing), follicular carcinomas.

Question 106

A recent retrospective analyzed mortality in captive bongo.

What is the scientific name of this species?

What were the most common causes of mortality in captive bongo?

Were there differences between males and females?

What diseases were common?

Answer 106

Bartlett, S. L., Arheart, K. L., & Garner, M. M. (2019).
Retrospective analysis of mortality in captive bongo (Tragelaphus eurycerus), 1995–2015.
Journal of zoo and wildlife medicine, 50(2), 303-307.

Key Points:
* Female bongo lived longer.
* Males more likely to die from infectious causes.
– Acid fast organisms detected in respiratory tissues
* Females more likely to die from chronic, noninfectious.
* Amyloidosis common in older bongo. Affected liver, kidneys, adrenals, GI.
* High prevalence of adrenal gland hyperplasia and neoplasia, cystic thyroid glands, aspiration pneumonia.
* Most common cause of anesthetic death was shock/rhabdomyolysis.

Question 107

What were the most common causes of morbidity and mortality in takin?

Answer 107

Jourdan, B., Garner, M. M., Joyner, P. H., Ramer, J., & Zimmerman, D. (2021). Morbidity and mortality of takin (budorcas taxicolor) in north american zoological institutions from 1997 to 2017. Journal of Zoo and Wildlife Medicine, 52(1), 157-165.

Three most frequent causes of morbidity - infectious/inflammatory (lameness, resp signs, diarrhea), degenerative dz (lameness), trauma.

Morbidity in juveniles and adults - ifnectious/inflammatory, mostly endoparasites Eimeria and strongyles.

Lameness most common in males (DJD), forelimbs.

Most common causes of mortality - infectious/inflammatory (sepsis, pneumonia, osteomyelitis, enterocolitis, endocarditis, nephritis - NOT endoparasitism), trauma, DJD.

Males more likely to die of trauma. Females infectious/inflammatory.

Senior animals and adults euthanized due to DJD.

Neonates and juveniles died of trauma.

Question 108

What were clinical signs, antemortem diagnostics, and pathological findings associated with mycobacterium avium subspp paratuberculosis infection in takin?

Answer 108

Naylor, A. D., Richardson, D., Sellar, M., Harley, J., Philbey, A. W., & Girling, S. J. (2018). Clinical Signs, antemortem diagnostics, and pathological findings associated with Mycobacterium avium subspecies paratuberculosis infection in Mishmi Takin (Budorcas taxicolor taxicolor). Journal of Zoo and Wildlife Medicine, 49(2), 412-419.

Marked wt loss over 1-3 mos followed by acute deterioration.

Fecal culture and microscopy failed to ID MAP shedding. Confirmed at necropsy by culture of ileum and mesenteric LN tissues.

Takin appeared to show high MAP susceptibility and a rapid disease course compared with domestic ruminant spp.

All animals had wt loss and behavior changes (isolation, hyporexia).

Some were seropositive on ELISA, but negative on fecal acid fast and culture.

Vaccinated other takin with heat-inactivated MAP vaccine.

Question 109

What is the most sensitive method for diagnosing mycobacterium bovis?

What was the prevalence found in African buffalo?

Answer 109

Katale, B. Z., Fyumagwa, R. D., Mjingo, E. E., Sayalel, K., Batamuzi, E. K., Matee, M. I., … & Mpanduji, D. G. (2017). Screening for bovine tuberculosis in african buffalo (syncerus caffer) in ngorongoro conservation area, northern tanzania: implications for public health. Journal of wildlife diseases, 53(4), 711-717.

Mycobacterium bovis - Found in carnivores i.e. lions that eat buffalo, indigenous cattle, civet, other bovids.

Gamma-interferon blood based ELISA detects cell-based immunity to M. bovis. Higher sensitivity and specificity vs skin testing. Can cross react with other spp of the M. tuberculosis complex.

2% prevalence in African buffalo, suggests M. bovis is endemic.

Most sensitive method for dx M. bovis is detection of CMI response - IFN gamma assay on blood.

IFN gamma test is faster, higher sensitivity in combo with TB skin tests.

SICTT requires a second immobilization to read test.

Question 110

What were the effects of season and postmortem changes on blood analytes in pyrenean chamois?

Answer 110

Tvarijonaviciute, A., Marco, I., Cuenca, R., Lavín, S., & Pastor, J. (2017). Effects of season and postmortem changes on blood analytes in Pyrenean chamois (Rupicapra pyrenaica pyrenaica). Journal of wildlife diseases, 53(4), 718-724.

In food deficient animals - Increased HDL, nonesterified FA, total antioxidant capacity, haptoglobin. Decreased albumin, insulin-like growth factor.

Food deficient animals poor nutrition and negative energy balance.

Live animals - Higher LDL, TG, acetylcholinesterase, nonesterified FA, albumin, IGF1, cortisol, paraoxonase-1 vs dead animals.

Dead animals - Higher haptoglobin.

Capture and manipulation is stressful due to 10x higher cortisol in live animals under physical restraint vs dead animals that were hunted.

Question 111

What was observed in evaluating acute phase protein and serum EPH values for captive vs wild pronghorn?

Answer 111

Tobin, K., Zimmerman, D., Rasmussen, J., Hilton, C. D., Junge, R. E., Armstrong, D., … & Cray, C. (2020).
Establishment of acute-phase protein and serum protein electrophoresis preliminary reference values for Pronghorn (Antilocapra americana).
Journal of Zoo and Wildlife Medicine, 51(2), 321-325.

Key Points:
* Wild pronghorn had lower TP, albumin, A:G ratio, and alpha-1 globulins, SAA. Higher alpha 2 and gamma globulins.
* SAA was undetectable in most wild pronghorn. Captive pronghorn&raquo_space; SAA.
* Pronghorn with facial abscesses had lower A:G, higher TP, beta globulin and haptoglobin. Only 2 individuals had increased SAA.

Question 112

A recent paper evaluated failure of passive transfer in sitatunga.

What parameter was considered useful for identifying failure of passive transfer in sitatunga?

Answer 112

Fraess, G. A., Sander, S., & Bronson, E. (2020).
Parameters for identifying failure of passive transfer in sitatunga (Tragelaphus spekii).
Journal of Zoo and Wildlife Medicine, 51(2), 259-264.

Key Points:
* Ruminant placenta = epitheliochorial (no material Ab transfer in utero). Passive immunity is via IgG of colostrum within hours of birth.
* In sitatunga, TP was the only value lower in FPT calves.
* Sitatunga found to have lower zinc sulfate turbidity test (quantifies serum IgG) normally vs cows.

Question 113

A recent study evaluated pregnancy associated glycoprotein ELISAs for pregnancy diagnosis in okapi, gerenuk, giant eland, and dama gazelles.

What two species did it work best in? What other studies shows it works in as well?

What species did it not work in?

Answer 113

Dvornicky-Raymond, Z. T., Donnelly, K. A., Emerson, J. A., Penfold, L. M., & Citino, S. B. (2021).
Evaluation of a visual enzyme-linked immunosorbent assay (elisa) for pregnancy detection in four ungulate species.
Journal of Zoo and Wildlife Medicine, 51(4), 926-932.

Key Points:
* Pregnancy-associated glycoproteins - PAGs are are produced in trophoblast in mammalian placenta. Blood test, early detection, color change = positive.
* PAG ELISA worked in gerenuk and giant eland with 100% sensitivity and specificity. In other studies also works in barbary sheep and musk oxen.
* PAG ELISA 0% in dama gazelle and okapi.
* Inter-evaluator agreement was consistent for gerenuk, giant eland, and okapi samples.
* Dama gazelle had a faint color change, but inconsistent and poor inter-evaluator agreement.

Question 114

Compare the photometric ELISA vs visual ELISA for PAG evaluation and pregnancy determination in muskoxen.

Answer 114

Greunz, E. M., Stelvig, M., Grøndahl, C., Schmidt, N. M., Mosbacher, J. B., Hansen, L. H., & Bertelsen, M. F. (2018). Evaluation of two enzyme-linked immunosorbent assays measuring pregnancy-associated glycoproteins in the blood of muskoxen (Ovibos moschatus). Journal of Zoo and Wildlife Medicine, 49(3), 798-801.

In pregnant muskoxen, progesterone is not a reliable indicator of pregnancy.

Photometric ELISA more sensitive vs the visual ELISA, but both had high sensitivity and both had 100% specificity.

Photometric ELISA is more reliable but both were specific for pregnancy evaluation using PAGs in muskoxen.

Question 115

What assay can be used for reliable detection of pregnancy in barbary sheep?

Answer 115

Lamglait, B., & Rambaud, T. (2017). Diagnosis of pregnancy in Barbary sheep (Ammotragus lervia) using a bovine assay for pregnancy-associated glycoproteins. Journal of Zoo and Wildlife Medicine, 48(2), 525-528.

Protein-associated glycoprotein ELISA - high sensitivity and specificity in barbary sheep from 32 days gestation to 3 days post partum.

No difference in singlets vs twins (cannot detect the number of kids).

Question 116

A recent retrospective evaluated the use of parenteral nutrition in hospitalized nondomestic ruminants.

What proportion of these animals survived?

What TPN was used?

What metabolic derangements were observed with its use?

Answer 116

Mulreany, L. M., Kinney, M. E., Clancy, M. M., Lamberski, N., & Werre, S. R. (2020).
Retrospective evaluation of the use of parenteral nutrition in hospitalized nondomestic ruminants.
Journal of Zoo and Wildlife Medicine, 50(4), 853-860.

Key Points:
* No clinically significant factors influenced odds of survival.
* 33% animals receiving parenteral nutrition survived. Lower survival with metabolic derangements.
* Ruminant TPN - dextrose + AA + lipids.
* Lipids are added last to minimize contamination. Administer in a line separate from crystalloids.
* Parenteral nutrition can be a viable option for intensive care of hospitalized ruminants.
* Hypokalemia was most common - be prepared for supplementation (excess glucose caused insulin release and intracellular drive of K), hyperphosphatemia was next most common (dehydration), hypophosphatemia - potentially from refeeding

Question 117

What was believed to be associated with moxidectin toxicois in a roan antelope, sable antelope, and arabian oryx?

How was this treated? Was it successful?

What was a predisposing factor in their toxicity?

Answer 117

Swenson, J., Haefele, H. J., & Poppenga, R. H. (2020).
Suspected moxidectin toxicosis in a roan antelope (hippotragus equinus), a sable antelope (hippotragus niger), and an arabian oryx (oryx leucoryx) at a semi-free range zoological park.
Journal of Zoo and Wildlife Medicine, 51(2), 416-425.

Key Points:
* Moxidectin - Causes neuro signs in mammals within 24h; tx IV lipids.
* Used to manage haemonchus in zoo ruminants. Usually administered SC, orally, or topically.
* Moxidectin IM resulted in 3 cases of fatal neuro disease.
* All animals that experienced toxicity had low BCS. Improved clinical signs with lipid therapy but still died. High levels in serum, increased following lipid tx. High levels found in brain tissues.
* Cause of death likely rhabdomyolysis from prolonged recumbency due to neuro toxicosis in these cases, treated same spp in the past without issue. Low BCS in these individuals.

Question 118

Describe the antibody response to epsilon toxin of clostridium perfringens in captive adult springbok, impala, alpaca, and wallaby.

Answer 118

Rousselet, E., Tarin, B., Petit, T., Blanc, B., Ortiz, K., Haelewyn, F., … & Leclerc, A. (2021). Antibody response to epsilon toxin of clostridium perfringens in captive adult springbok (antidorcas marsupialis), impala (aepyceros melampus), alpaca (vicugna pacos), and red-necked wallaby (macropus rufogriseus) over a year. Journal of Zoo and Wildlife Medicine, 52(1), 192-199.

Increase in C. perfringens type D epsilon toxin Ab at 180 d for impalas and springboks and at 360 days for alpacas and wallabies.

Recommendations for the Miloxan vaccine - impala and springbok q 6 mos, wallabies and alpacas q12 mos.

Question 119

What virus was associated with mortality in a moose exposed to goats in a zoo?

Answer 119

Seeley, K. E., Junge, R. E., Jennings, R. N., Cunha, C. W., & Li, H. (2018). Moose (alces alces) mortality associated with caprine herpesvirus 2 (cphv-2) in a zoological collection. Journal of Zoo and Wildlife Medicine, 49(3), 774-778.

Caprine herpesvirus 2 - Moose mortality from asymptomatic goats.

Malignant catarrhal fever - Group of herpesviruses of genus Macavirus (gammaherpesvirus).

Includes ovine herpesvirus 2, alcephaline herpesvirus 1 and 2, caprine herpesvirus 2 and 3.

MCF is frequently fatal in susceptible species. Hallmark is lymphoproliferative inflammatory infiltrates with vasculitis.

Caprine herpesvirus 2 - Endemic, asymptomatic in goats, severe dz in WTD, sika deer, pronghorn antelope.

Moose are dead-end hosts, cannot transmit.

Question 120

A recent paper described chronic pancreatic disease in the lesser kudu.

What is the scientific name of this species?

What are the two forms of chronic pancreatic disease?
- What are some typical causes of pancreatic disease in ruminants?
- What is the suspected etiology in kudu?

What finding on clincial pathology is most suggestive of the disease?

Answer 120

Garner, M. M., Citino, S. B., Suedmeyer, W. K., Rainwater, K. L., Hernandez, J. A., Duarte, G. A., & Stacy, N. I. (2021).
Chronic pancreatic disease in the lesser kudu (tragelaphus imberbis): a report of 16 cases in the united states.
Journal of Zoo and Wildlife Medicine, 52(2), 580-591.

Key Points:
* Chronic pancreatic disease: hereditary or acquired (acute or chronic)
– In ruminants: pancreatoliths, trematodes (Eurytrema coelomaticum), zinc toxicosis
* Chronic pancreatic disease in lesser kudu that originated from an initial founder stock of 12 animals.
* Most had hyperglycemia > 300 mg/dL, small firm or nodular pancreas, fructosamine higher vs control but not statistically significant.
* Early onset in some kudu may support a hereditary etiology. Can be subclinical.

Question 121

A recent study found evidence of EHD in nondomestic ruminants in Florida.

What is the vector for epizootic hemorrhagic disease virus and bluetongue in ruminants?

What are the typical clinical signs?

When do outbreaks typically occur?

Answer 121

Orange, J. P., Dinh, E. T., Goodfriend, O., Citino, S. B., Wisely, S. M., & Blackburn, J. K. (2021).
Evidence of epizootic hemorrhagic disease virus and bluetongue virus exposure in nonnative ruminant species in northern Florida.
Journal of Zoo and Wildlife Medicine, 51(4), 745-751.

Key Points:
* Epizootic hemorrhagic disease virus and bluetongue virus both vectored by Culicoides biting midges.
* Severe clinical signs - hemorrhage, edema, hoof sloughing, oral lesions, death in WTD.
* Outbreaks generally in summer and fall.

Question 122

A recent paper described the eradications of Brucella melitensis from two captive gazelle populations.

What control methods did they use?

What is the significance of latent infections?

Why is this disease so difficult to treat?

Answer 122

Soares, J. F., Desta, F. S., Macasero, W., Butynski, T. M., & Wronski, T. (2019).
Eradication of Brucella melitensis from two captive gazelle populations in Saudi Arabia.
Journal of Zoo and Wildlife Medicine, 50(3), 706-712.

Key Points:
* Control - Relapsing Brucella positive animals were euthanized and incinerated, dirt floored pens were disinfected with calcium oxide and left empty for 2 years, isolation pens were disinfected with bleach and allowed to dry 4x with 3 days apart.
* Brucella - facultative intracellular pathogen, chronic infections. Monotherapies often fail.
* Latent infections are an important problem - Animals will remain negative until first calving, abortion, or other stressful event.

Question 123

A recent study investigated the immunocrit as a diagnostic test for failure of passive transfer in nondomestic wild ruminant neonates.

How does it work?

What are its advantages over other methods?

Which species had the lowest accuracy for the immunocrit as a diagnostic test for failure of passive transfer?

Answer 123

Thompson, K. A., Lamberski, N., Rayburn, M., & Chigerwe, M. (2019).
Validation of immunocrit as a diagnostic test to detect failure of passive transfer of immunity in hand-reared nondomestic ruminant neonates.
Journal of Zoo and Wildlife Medicine, 50(3), 627-633.

Key Points:
* Immunocrit - Involves precipitation of immunoglobulins with known concentration of ammonium sulfate solution.
* Springbok had the lowest accuracy, may require a lower cutoff point.
* Immunocrit accuracy was otherwise > 89% for most ruminant spp tested.
* Advantages are that it is not species specific, results are semiquantitative, test is quick and simple and can be performed at any facility. Also inexpensive and only precipitates immunoglobulins.

Question 124

A recent study described aspiration pneumonia as a complication of anesthesia in Tibetan yaks.

What is the scientific name of this species?

What are some unique parts of Yak anatomy that may make them more predisposed to aspiration than domestic cattle?

What are some strategies to prevent aspiration in domestic cattle?

What organisms should be targeted in nebulization therapy?
- What antibiotics were recommended?

Answer 124

Smith, J. S., Sheley, M., & Chigerwe, M. (2018).
Aspiration pneumonia in two tibetan yak bulls (bos grunniens) as a complication of ketamine-xylazine-butorphanol anesthesia for recumbent castration.
Journal of Zoo and Wildlife Medicine, 49(1), 242-246.

Brief Communication

Abstract: Among members of the genus Bos, aspiration pneumonia has been described in domestic cattle (Bos taurus and Bos indicus). In these species, aspiration pneumonia is most commonly a sequelae to oral administration of fluids or medications, as well as aspiration during procedures under anesthesia. Management of aspiration pneumonia secondary to complications from anesthesia for short duration surgical procedures is minimally reported in the Tibetan yak (Bos grunniens). Although regurgitation under anesthesia has been reported in the yak, there are no reports of aspiration pneumonia treatment. This case report describes the diagnosis and management of aspiration pneumonia in two Tibetan yaks undergoing castration under injectable ketamine-xylazine-butorphanol anesthesia. This case report also describes the gross and pathologic characteristics of anesthesia-induced aspiration pneumonia in one Tibetan yak, as well as successful treatment in another.

Key Points
- Two Tibetan yaks were anesthetized for castration, both regurgitated multiple times under ax.
- Case 1 – Prolonged recovery, bilateral increased harsh lung sounds next day, TUS showed comet-tail lesions in cranioventral lungs.
– Tx – Flunixin, thiamine, tulathromycin, fluids. Nebulized ampicillin, O2.
– Next day continued same tx but ceftiofur instead of ampicillin.
– Euthanized following day, declined.
– Nx – Birefringent plant and other foreign material consistent with asp pneumonia of ruminal contents.
– Culture – proteus mirabilis, serratia rubidaea, klebsiella pneumoniae.
- Case 2 – Uneventful recovery from anesthesia, 1 wk later hyperthermic, tachycardic, tachypnic, clear nasal discharge, harsh lung sounds, US comet-tail lesions, CBC marked leukocytosis, moderate monocytosis, marked neutrophilia, bands, toxic changes, increased fibrinogen.
– Tx – tulathromycin, flunixin, nebulization with ceftiofur.
– Improved, added pantoprazole for bruxism, discharged 9 days later.
- Aspiration pneumonia in ruminants.
– Dx – fever, resp signs, leukocytosis, blood gas, imaging.
– US may be more diagnostic vs auscultation (study in Holstein calves).
– Yak anatomy is unique, may predispose:
– Trachea is shorter, wider than cattle.
– Relatively larger (~200%) rumen relative volume to body size percentage vs cattle.
– Despite having a smaller rumen vs cattle, the rumen is twice the size of cattle when compared to body size.
- Strategies to prevent aspiration in nondomestic cattle:
– Sternal positioning during ax, preoperative fasting.
– In this case, both were fasted 48h.
– Also they didn’t intubate in these cases…interesting choice.
- Nebulization.
– Using ceftiofur in small ruminants, increased likelihood of survival to hosp discharge.
– Protective effect vs pasteurella haemolytica (Mannheimia) type A1 in calves.

Question 125

A recent study described melanoma in golden and king wildebeests.

What are the two species of wildebeest? What are their scientific names?

Melonoma is commonly found in light coated animals of what species?

Was metastasis documented in these cases?

What markers are used to identify melanoma on histology?

Answer 125

Adetunji, S. A., Krecek, R. C., O’Dell, N., Prozesky, L., Steyl, J., & Arenas-Gamboa, A. M. (2018).
Melanoma in golden and king wildebeests (Connochaetes taurinus).
Journal of Zoo and Wildlife Medicine, 49(1), 134-142.

Key Points:
- Wildebeest – Blue (c. taurinus) and Black (C. gnou)
- Melonoma increased incidence in light coated animals – grey horses, Hereford, Shorthorn, Charolais, simmental cattle, white tigers, rhesus macaques
- Case reports include metastasis to lungs
- Markers to melanocytes – Melan A, PNL2, S100, HMB-45
– Melan A – most consistently expressed by neoplastic melanocytes

Abstract: Pigmentation of the skin is a crucial component in the pathogenesis of melanocytic neoplasms and other skin-related tumors, as melanin is known to function in both the absorbance of ultraviolet radiation and as an antioxidant. Very limited information exists regarding the incidence and metastatic potential of neoplastic conditions of the skin in game animals, especially wildebeests, relative to domestic animals. Four cases of cutaneous melanoma in color-variant golden and king wildebeests (Connochaetes taurinus) (from 2014 to 2015) in South Africa were investigated. Melanoma in these captive animals was characterized using histopathology, transmission electron microscopy, and an immunohistochemistry panel, which consisted of monoclonal antibodies against three melanocytic markers: Melan A, PNL2, and S100. Overall, 2/4 cases (50%) of the melanocytic neoplasms stained strongly positive for all the melanocytic markers, while 4/4 cases (100%) stained positively for at least one of the markers. Cutaneous melanocytic neoplasia has not been reported in wildebeests; the current study suggests that selection of wildebeests for coat color potentially predisposes to this condition.

Question 126

A recent study investigated the pathogen prevalence fo the threatened wood bison population in Yukon Canada.

What is the scientific name of the bison?

What are the main impediements to wood bison restoration?

What pathogens were identified in this isolated population?

Answer 126

Harms, N. J., Jung, T. S., Andrew, C. L., Surujballi, O. P., VanderKop, M., Savic, M., & Powell, T. (2019).
Health status of reintroduced wood bison (Bison bison athabascae): assessing the conservation value of an isolated population in Northwestern Canada.
Journal of wildlife diseases, 55(1), 44-53.

Key Points:
* We found no evidence of exposure to M. bovis or Brucella spp., but antibodies were present to bovine parainfluenza virus 3, bovine coronavirus, Leptospira interrogans, and Neospora caninum, with seroprevalences of 87, 7, 61, and 7% of the tested animals, respectively

Take home points: based on histopathology, bacteriologic culture, and serology results, there is no initial evidence that the Aishihik Herd has been exposed to, or is infected with, Brucella spp. or M. bovis. This is significant because brucellosis and bovine tuberculosis are the main impediments to wood bison restoration

Question 127

A recent study investigated fecal glucocorticoid concentrations in Bison living with or without wolves.

What is the scientific name of the bison?

What is the scientifice name of the wolf?

How did fecal glucocorticoids change with the presence of this predator?

Were sesaonal glucocorticoid fluctuations observed?

Answer 127

Metrione, L. C., Hunter, D., & Penfold, L. M. (2020).
Seasonal Changes in Fecal Glucocorticoid Metabolite Concentrations in Bison (Bison bison) Living with or without Wolves (Canis lupus).
Journal of Wildlife Diseases, 56(1), 175-178.

Key Points:
- Higher FGM concentrations (P<0.001) in samples collected following a wolf encounter compared to other samples collected in the same herd that month demonstrated the presence of an acute adrenal response in the bison.
- further confirmed by measuring a transient increase in FGM in bison that ran through the chute (higher 24h and 1 week after challenge, but not 2 months after)
- Seasonal changes were consistent in the two groups

Question 128

A recent study evaluated the characteristics of various assays in detecting Mycobacterium bovis in African buffalo.

What is the scientific name of the African buffalo?

What was the prevalence this study identified for M bovis?

Which test performed the best?

Answer 128

Bernitz et al.
Test Characteristics of Assays to Detect Mycobacterium bovis Infection in High-Prevalence African Buffalo (Syncerus caffer) Herds
Journal of Wildlife Diseases, 56(2), 2020, pp. 462–465

ABSTRACT: A herd of African buffaloes (Syncerus caffer) was tested for Mycobacterium bovis infection using three cytokine release assays. All animals were subsequently euthanized and mycobacterial culture determined the infection prevalence (52%) and diagnostic characteristics. Sensitivities were lower than previously reported and results provide new insight into the practical utility of these assays.

Key Points:
- the Bovigam IGRA had higher SP than the QFT IPRA and QFT-P and higher SE than the QFT IGRA, so it may be the best test for use in buffaloes

Question 129

A recent study evaluated the preference of ensiled tree leaves to drive in Nyala antelope?

What is the scientific name of this species?

What was the main finding?

Answer 129

Preference of intake of different tree leaves preserved with drying and ensiling by nyala antelope (Tragelaphus angasii)
Zoo Biology. 2020;39:436–442

Takeaway: ensile leaves are comparably palatable to dried leaves, but they may prefer some trees to other

Question 130

A recent study investigated the behavioral and endocrine dominance in female Jackson’s hartebeest.

What is the scientific name of this species?

What was the main finding of this study?

Answer 130

Spratt, K. S., Spratt, J. S., Bauman, J. E., & Chandler, C. R. (2019).
Behavioral and endocrine correlates of dominance in captive female Jackson’s hartebeest (Alcelaphus buselaphus).
Zoo biology, 38(2), 157-166.

Take home: Female hartebeest will maintain a strict linear dominance hierarchy, trauma is likely to result

Question 131

A recent study investigated the presence of schmallenberg virus in European bison.

What is the scientific name of the European bison?

What type of virus is the Schmallenberg virus?
- How is it transmitted?
- What clinical signs does it cause?

How prevalent was this virus in European bison?

Answer 131

Kęsik-Maliszewska, Julia, Krzysiak, Michał K., Grochowska, Maria, Lechowski, Lech, Chase,, Christopher, et. al.
EPIDEMIOLOGY OF SCHMALLENBERG VIRUS IN EUROPEAN BISON (BISON BONASUS) IN POLAND
Journal of Wildlife Diseases, 54(2) 272-282

Key Points:
- Schmallenberg virus (SBV)
– Orthobunyavirus
– emerging arthropod-borne virus in Europe
– transmitted by blood-sucking midges (Culicoides spp.)
– Infection with SBV during susceptible periods of pregnancy may lead to fertility problems in early and fetal malformations in late gestation
- detection of SBV antibodies in almost all European bison populations in Poland and the high seroprevalence (up to 81%) suggest that European bison are highly susceptible to SBV infection

Question 132

A recent study investigated the susceptibility of cattle to Chronic Wasting Disease.

What was their finding?

Answer 132

Williams, Elizabeth S., O’Toole, Donal, Miller, Michael W., Kreeger, Terry J., and Jewell, Jean E.
CATTLE (BOS TAURUS) RESIST CHRONIC WASTING DISEASE FOLLOWING ORAL INOCULATION CHALLENGE OR TEN YEARS’ NATURAL EXPOSURE IN CONTAMINATED ENVIRONMENTS
Journal of Wildlife Diseases, 54(3) : 460-470

Key Points:
* Cows did not develop prion disease – not with oral inoculation or exposure over 10 years in contaminated environments
* No histologic lesions consistent with spongiform encephalopathy were induced in any of the cattle

Question 133

A recent study investigated the GI parasites of the endangered tibetan antelope.

What is the scientific name of this species?

How prevalent were nematodes, cestodes, and coccidia?

What environmental changes were suspected to be causing the increased prevalence?

Answer 133

Journal of Wildlife Diseases, 56(2), 2020, pp. 372–377
PREVALENCE AND PARASITE COMPOSITION OF GASTROINTESTINAL PARASITES IN THE ENDANGERED TIBETAN ANTELOPE (PANTHOLOPS HODGSONII) FROM THE CALVING GROUND OF HOH XIL NATURE WORLD HERITAGE SITE, QINGHAI, CHINA
Yifan Cao, Yuangang Yang, Donald W. Duszynski, Yahui Zhu, Guozhen Shang, Chu Hou, Tongzuo Zhang, and Jianghui Bian

Key Points:
* All fecal samples demonstrated the presence of gastrointestinal parasites: 93% (221/238) had nematodes, 36% (86/238) had cestodes, and 99% (235/238) had coccidian oocysts.
* These results showed that prevalence of Trichostrongylus, Marshallagia, and Eimeria infections in these Tibetan antelopes were high enough to warrant monitoring (higher temps leading to more moisture laden pastures
* Dictyocaulus – significant pulmonary damage and respiratory disease
* Eimeria – destructin of intestinal mucosa leading to diarrhea, weight loss, malabsorption

Question 134

A recent study described deafness in North American Yaks.

What is the scientific name of this species?

What coloration was associated with deafness?

Answer 134

Strain GM, Hardy T.
Deafness associated with pigmentation phenotypes in North American yaks (Bos grunniens).
American Journal of Veterinary Research. 2022;83(10):online

Key Points:
- Deafness found in yaks homozygous for white pigmentation (piebald genus locus), suspected congenital, sensorineural from suppression of strial melanocytes causing stria vascularis degeneration resulting in cochlear hair cell degeneration, can be unilateral or bilateral.

Question 135

A recent study investigated ESR as a potential marker of inflammation in wild African buffalo.

What is the scientific name of this species?

What is ESR?
- What increases it generally?
- What decreases it generally?

What disease states increased ESR?

Answer 135

JWD 2022 58(2):298-308
Exploring the use of the erythrocyte sedimentation rate as an inflammatory marker for free-ranging wildlife: A case study in African buffalo (Syncerus caffer)
Yarborough E, Glidden C, Coon C, et al

ESR measures how quickly RBCs will sediment through plasma due to gravity
* Increased ESR (faster sedimentation) occurs in some inflammatory conditions due to electrostatic forces aggregating erythrocytes into what are called “rouleaux”
* Positive APPs tend to increase ESR, and negative APPs tend to decrease ESR
* Polycythemia and hemoglobinopathies also decrease ESR by hindering rouleaux

POSITIVELY correlated with ESR
* Globulin levels
* BVD virus infection
* M. haemolytica infection
* Parainfluenza virus-3 infection
* A. marginale and A. centrale coinfection

NEGATIVELY correlated with ESR
* RBC and albumin levels
* Adenovirus-3 and parainfluenza virus-3 coinfection
* Parainfluenza virus-3 and bovine herpes virus coinfection
* Anaplasma marginale infection

Question 136

A recent study investigated epizootic mycoplasmosis in wild pronghorn.

What is the scientific name of the pronghorn?

What are some proposed sources of mycoplasma infection to pronghorn?

What is the seasonality of mycoplasmosis in pronghorn?
- What coinfecting pathogens were also observed?
- What conditions prolong the viability of Mycoplasma bovis in the environment during those months?

Answer 136

Johnson M, MacGlover C, Peckham E, Killion H, Allen SE, Creekmore T, Edwards WH, Blaeser M, Davison M, Schwalbe E, Wray AK.
Source and seasonality of epizootic mycoplasmosis in free-ranging pronghorn (Antilocapra americana).
The Journal of Wildlife Diseases. 2022;58(3):524-536.

Background:
* Cattle- subclinical common, clinical disease often triggered by immunosuppression, stress, co-infections
* Bison - can be primary disease, low asymptomatic prevalence (3%)
* Pronghorn diseases: M bovis, lungworm, bovine herpesvirus-1, parainfluenza virus-3, bovine viral diarrhea virus, bovine respiratory syncytial virus, epizootic hemorrhagic disease virus, bluetongue virus, cervid adenovirus
* Mycoplasmas lack a cell wall so are highly susceptible to dessication and heat
– Some conditions (humidity, shade) documented persistent of M bovis up to 8 mo

Key Points:
* Increased number of pronghorn deaths from pulmonary mycoplasmosis in NE WY in 2020 compared to 2019 (6x), none identified in 2021
* Late Feb-late April, both sexes, all age classes
* No cattle or bison identified with respiratory disease in the outbreak region
* Co-infecting respiratory pathogens were consistently detected, Trueperella pyogenes, Mannheimia sp., no respiratory viruses on PCR, lungworms in 75% of cases

Conclusions:
* Seasonally associated, virulent M bovis found in pronghorn suggest livestock are a potential reservoir host, susceptible to spillover to new species
* No evidence of subdivision and minimal evidence of isolation by distance in pronghorn
* Nasal swab PCR were a sensitive and specific test, single unique sequent type in the pronghorn outbreak
* Shade, humidity, and cool temperatures prolong the viability of M bovis in the environment and may contribute to observed seasonality (Feb, March)

Question 137

A recent study investigated the use of a trace element ruminal bolus to address deficiencies in Blesbok.

What is the scientific name of the blesbok?

What clinical signs have been seen with blesbok as the result of copper deficiency?

How well did this bolus work?

Answer 137

EFFECT OF SUSTAINED-RELEASE TRACE ELEMENT RUMINAL BOLUS ON PLASMA TRACE MINERAL PROFILES IN CAPTIVE BLESBOK ANTELOPES (DAMALISCUS PYGARGUS PHILLIPSI)
Journal of Zoo and Wildlife Medicine 53(2): 259–265, 2022

Key Points:
- Mineral deficiencies have been described in a variety of hoofstock
- Bleaching of the hair coat, ataxia, and poor hair quality and body condition have all been described in captive and wild blesbok (Damaliscus pygargus phillipsi) as a result of copper deficiency.
- These results do not support the use of Oligovet ruminal bolus in blesboks as an effective oral supplement
- More broadly, these data call into question the reliability of plasma as a means to monitor trace mineral concentrations.

Question 138

A recent study investigated trazodone on the behavior and cortisol levels in blue wildebeest.

What is the scientific name of the blue wildebeest?

What is trazodone?

Why may trazodone be a better candidate than the long-acting neuroleptics for transports or other stressful events?

What doses were used?

What behavioral changes were seen?

Were cortisol levels significantly different during a single venipuncture event?

Answer 138

Prud’homme Y, Ferrell ST, Haefele H, Swenson J, Beauchamp G, Desmarchelier M.
EFFECTS OF A SINGLE ORAL DOSE OF TRAZODONE ON BEHAVIOR AND SERUM CORTISOL LEVELS IN BLUE WILDEBEEST (CONNOCHAETES TAURINUS).
Journal of Zoo and Wildlife Medicine. 2023;53(4):679-688.

Background
* Trazodone: serotonin antagonist reuptake inhibitor
– Strong antagonism of receptors responsible for primary adverse effects including insomnia and sexual dysfunction
– Absorbed rapidly in goats (polygastric species) with plasma concentrations greater than therapeutic in humans and dogs lasting 6hr
* Long-acting neuroleptics: haloperidol, perphenazine, zuclopenthixol - inhibit movement by dopamine antagonism, no inherent analgesia or antianxiety
– Excessive blockade of dopamine receptors may cause extrapyramidal effects (involuntary movements, tremors, recumbency, altered levels of consciousness)

Key Points
* Pilot study: 15 mg/kg estimated group dosing on pelleted feed had the most noticeable behavior changes
– 12 mg/kg had behavior changes with less effect on food ingestion/ruminating
* Statistically significant differences in posture, time spent resting or sleeping, ingesting or ruminating, moving, and being vigilant
– No difference in grooming or interacting socially
* All remained active and healthy
* Did not result in significant difference in serum cortisol levels during acutely stressful event
* One year cortisol was significantly lower but next year it was higher with trazodone

Conclusions
* Trazodone appeared safe and effective at decreasing activity levels and producing behavioral changes consistent with a more relaxed state in a group treated population of blue wildebeest at an estimated 15 mg/kg dose
* All animals maintained ability to perform usual behaviors
* Systemic absorption was achieved
* No effects on serum cortisol concentrations

Question 139

A recent study investigated the prevalence and risk factors of amyloidosis in Eastern bongo housed in Europe.

What is the scientific name of the bongo?

How prevalent was amyloidosis in this population? How does that compare to the NA population?

What conditions were associated with amyloidosis?

What organs were most commonly affected?

How did SAA correlate with amyloidosis?

Answer 139

JZWM 2022 53(4) 696-704
AMYLOIDOSIS IN CAPTIVE EUROPEAN EASTERN BONGO (TRAGELAPHUS EURYCERUS ISAACI) PREVALENCE, PREDICTIVE FACTORS, ORGAN PREDILECTION, AND SERUM AMYLOID A CONCENTRATIONS

Takeaway:
* A high prevalence of amyloidosis at postmortem examination (36%) was observed in the eastern bongo EEP population, similar to what has been reported in the NA population.
* Appears to be a disease of older animals, liver, kidney and SI most often affected.
* Amyloid AA found in all cases.
* An association between amyloidosis and chronic inflammatory conditions was identified (nephritis, enteritis, pneumonia).
* SAA did not correlate with presence of amyloidosis.

Question 140

A recent case series described a novel fungal pathogen in Eastern bongo.

What is the scientific name of the bongo?

How did these animals present?

Where were lesions identified?
- What was found histologically?

What organism was identified as the suspected etiology?

Answer 140

JZWM 2023 54(1) 102-110
FATAL SYSTEMIC FUNGAL INFECTION IN EASTERN BONGO ANTELOPE (TRAGELAPHUS EURYCERUS ISAACI): SIX CASES
Michael Garner et al

Case Series:
- 4 were found dead, 3 of which had no prior signs, and one had anterior uveitis and weight loss
- 2 euthanized due to unrelated issues
- distribution of mycotic lesions in the examined tissues included heart (six), kidney (six), lung (five), lymph node (five), abomasum (two), pleura (one), and body wall (one)
- The lesions were comprised of histiocytes and multinucleated giant cells admixed with fewer lymphocytes, plasma cells, or neutrophils
- Inflammation often was present within and around blood vessels, extending into the surrounding parenchymal or mesenchymal tissue

Take Home:
* Case series of six bongo with fatal mycosis.
* Heart, kidneys, lung and lymph nodes predominantly affected.
* Cladosporium spp suspected as etiology.

Question 141

A recent study investigated the biting pests of captive Nyala antelope in Vienna, Austria.

What is the scientific name of the nyala?

How do blackflies feed?
- What family are they in?
- What diseases are they known to transmit?
- What is simuliotoxicosis?

How did the nyala present?

What was the identified blackfly in this study?

Answer 141

Ebmer D, Balfanz F, Voracek T, Hering‐Hagenbeck S, Pichler‐Scheder C, Walochnik J, Kniha E.
The Palearctic blackfly Simulium equinum (Diptera: Simuliidae) as a biting pest of captive nyala antelopes (Tragelaphus angasii).
Zoo Biology. 2023;42(1):150-156

Background
* Blackflies - Simuliidae
* Telmophagous (pool-feeding) - cut a hole and suck blood with short proboscis from a pool of blood under the skin
* Transmit Onchocerca vovulus - river blindness in humans and Leucocytozoon in birds
* Simuliotoxicosis - death in cattle and other farm animals from massive biting, acute toxemia, and anaphylactic shock, originally described in reindeer
* Symptoms: intense pruritis, localized swelling, pruritic papules, vesicles, erythematous wheals

Key Points
* Goal: ID causative agent of heavy biting among captive nyala antelope in Vienna Zoo, Austria
* Bite marks found exclusively on both ear pinnae
* Flies caught were Simulium equinum

Conclusions
- Confirmed and grossly characterized blackfly strike on ears of captive nyala in Austria

Question 142

A recent retrospective described the causes of mortality in managed dik-diks in North America.

What is the scientific name of the Kirk’s dik-dik?

What was the leading cause of mortality?

What were the study’s recommendations for future care of this species?

Answer 142

Yuschenkoff D, Bolch C, Phair K, West G, Goe A, Burns RE. RETROSPECTIVE ANALYSIS OF MORTALITY CAUSES IN MANAGED KIRK’S DIK-DIKS (MADOQUA KIRKII) IN NORTH AMERICA FROM 1988 to 2019.
Journal of Zoo and Wildlife Medicine. 2022 Jun;53(2):349-56.

Key Points:
* Age and management related causes of mortality are common in Kirk’s dik-diks under managed care
* Neonatal death (#1), nutritional deficiencies (inanition, Vit E) in juveniles, anesthetic complications, trauma/predation, and exertional myopathy in adults, and degenerative disease in geriatrics
* Incidence of neoplasia was rare
* Recommendations: hand rearing neonates, careful monitoring during weaning, careful planning of anesthesia, animal transfer, and enclosure design, and close quality of life monitoring for geriatric animals