Bovidae/Antilocapridae Flashcards
(142 cards)
What is unique about the family antilocapridae?
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
Describe the taxonomy within Bovidae.
What are the subfamilies - what species are in each of them?

Describe the ideal housing of bovids and antilocaprids.
What are some of the difficulties of population management in these species?
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
What vaccines should be used for bovids?
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?
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
- 2nd 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
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?
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
Describe the physical and mechanical restraint of bovids.
How do you restraint small and medium bovids?
What equipment is available for restraint?
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)
- Small bovids under 5kg
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
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?
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

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?
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

Describe intubation in the following groups of bovids:
Antelope
Bison
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
What preanesthetic considerations should be taken into account prior to a procedure on a bovid?
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
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?
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
What are some common anesthetic complications in bovids?
Hyperthermia
Capture myopathy
Ruminal tympany
Hypoxemia
Renarcotization
What are some of the advantages of thiafentanil over etorphine or carfentanil?
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
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
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 1st 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 1st year, to identify areas of concern, then annually or biannually to monitor for changes in population trends.
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?
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)
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?
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
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?
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
What is the scientific name of the barber pole worm?
Describe its light cycle.
What is its prepatent period - why does this matter clinically?
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 4thstomach (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 2nd stage larvae (L2). Second stage larvae (L2) undergo an incomplete moult to become 3rd 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 4th 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

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?
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

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?
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 2nd 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
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?
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
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?
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

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?
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)



















