Equidae Flashcards
What order and family are horses in?
Describe the conservation status of these animals.
What are the scientific names of the following animals:
- Przewalski’s Horse
- African Wild Ass
- Asiatic Wild Ass (Kulan, Onanger)
- Kiang
- Cape Mountain Zebra
- Hartmann Mountain Zebra
- Grevy Zebra
- Plain’s Zebra
- General biology:
- Order Perissodactyla (Equidae, tapiridae, rhinocerotidae).
- Distinguished from the family artiodactyla by their foot morphology and digestive system.
- Equidae: Horses, wild asses, zebras.
- IUCN Equid Specialist Group lists 7 species, numerous subspecies under the Equus genus.
- Most spp at risk of extinction.
- Once widespread in grassland and desert habitats through NA, asia, Africa, Europe. Currently eastern and southern Africa, regions of asia.
- Modern equids live in harsh, dry lands/grasslands shared by nomadic peoples.
- Generally polygynous, highly social.
- Order Perissodactyla (Equidae, tapiridae, rhinocerotidae).
Describe the unique anatomy of nondomestic equids.
How do their coats differ?
What is their general dental formula? What type of cheek teeth do they have?
Do they have a gallbladder?
How does nondomestic equid foot anatomy differ from domestic horses?
- Unique anatomy:
- Similar to domestic horse internally, distinguish by external appearance.
- Przewalski horse most noted for horse-like appearance.
- Asian and wild asses - solid and subtle color patterns on body and legs.
- Zebra species - distinct striping patterns, differentiate species and individuals.
- Internal anatomy.
- Bulk-feeding herbivores.
- Dental formula: I3/3, C1/1, PM 3-4/3, M 3/3 total 40-42 teeth.
- Canines vestigial or absent in females.
- Hypsodont cheek teeth.
- GI designed for hindgut fiber fermentation.
- Small stomach, large cecum and colon. All perissodactyls lack a GB.
- Foot posture is unguligrade (bearing weight on one functional digit).
- Third digit is well formed and only weight bearing digit in equidae.
- Minor differences in foot anatomy.
- In general, domestic equids have larger feet with a greater frog:sole ratio vs nondomestic equids.
- Radius and ulna, fibula and tibia are fused.
- Nondomestic horses have smaller feet.
- Przewalski horse hoof is most similar to domestic horse.
- Grevy’s zebra similar to mule or donkey, narrow, more upright.
- Frog to sole ratio is less.
- Mountain zebras have a smaller foot, otherwise similar.
- African wild asses feet are similar to zebras, Asian wild asses more robust structure.
- Similar to domestic horse internally, distinguish by external appearance.
Describe the ideal housing for equids.
What enrironmental and safety considerations need to be considered?
- Special housing requirements:
- Generally hardy, withstand normal to severe temp variations as long as shelter and wind/sun protection is available.
- Gravy zebras are reported to be less cold tolerant.
- Proper food storage, access to fresh water.
- Periodic hoof trimming in some species (mountain zebras and Przewalski horses seem to need more frequent trims, q6-9 months).
- May be violent and aggressive with each other. Infanticide well documented.
- Careful when introducing a male to a new herd or pregnant female to new stallion.
- Stallions aggressive toward new foals and keepers.
Describe the ideal nutrition for equids.
Are they browsers or grazers?
What issues may occur with feeding alfalfa?
What are some common nutritional issues?
- Feeding:
- All are bulk feeding grazers, primarily feed on grass and roughage.
- Wild – 90% grass zebra diet.
- Reportedly eat some browse in wild.
- In general, nondomestic equids have no specialized feeding requirements and may be fed like domestic equines.
- High fiber pellets and grass hay combination recommended.
- In regions where enteroliths are a problem, reducing or eliminating alfalfa in the pellet or hay source is recommended.
- Pellet and hay may be fed at ratio of 50% pellet, 50% hay.
- Intake should be 1.5-3% BW.
- Salt and trace mineral blocks may be used if pellet diet cannot be specially formulated.
- Produce is not recommended. Can use for behavioral training or enrichment.
- No more than 2-5% of the diet on a DM basis.
- Obesity may be a problem in zoos. Encourage exercise, restrict pelleted feed.
- All are bulk feeding grazers, primarily feed on grass and roughage.
Describe a preventative medicine protocol for equids.
- Preventive medicine:
- Preshipment testing recommended for any relocation.
- Including zoo or free ranging transfers such as reintroduction, translocation, relocation from one institution or field site to another.
- Fecal sample for parasites.
- Fecal culture.
- Blood for CBC, chemistry, serum archive.
- Vaccination if indicated regionally i.e. tetanus toxoid, rabies.
- PE.
- Oral and hoof inspections and hoof trims.
- Quarantine.
- Including zoo or free ranging transfers such as reintroduction, translocation, relocation from one institution or field site to another.
- Preshipment testing recommended for any relocation.
Describe the restraint of nondomestic equids.
What physical methods can be used? What risks are there to this approach?
What oral sedatives are available?
Describe the diferences in duration and onset of the following neuroleptics: Haloperidol, Zuclopenthixol, Perphenazine.
What drugs are commonly used for immobilization? What ultrapotents do not work in equids?
Describe ideal dart placement for equids.
Describe the monitoring and management of anesthetized equids (intubation, ventilation, monitoring equipment).
- Restraint and handling:
- Hydraulic hugger restraint chutes +/- chemical restraint.
- Startle easily, may bolt into solid obstacles -> fatal head and neck injuries.
- Chemical restraint.
- Acepromazine granules and oral haloperidol effective for oral sedation to aid in transport or acclimation to new housing.
- Injectable short acting sedatives such as xylazine, acepromazine, and butorphanol may be used.
- Long acting neuroleptic sedatives may be used, sometimes in combo to achieve desired length of sedation.
- Haloperidol is short acting, relatively rapid onset of 5-10 minutes. Duration 8-18 hours.
- Zuclopenthixol medium acting. Onset in 1 hour, duration 3-4 days.
- Perphenazine is a long acting. Onset in 12-16 hours and duration of 10 days.
- May occasionally cause extrapyramidal signs i.e. hyperexcitability and incoordination.
- Full immobilization.
- Opiod narcotics.
- Etorphine is most commonly used.
- Often in combination with alpha 2 agonists, ketamine, phenothiazine tranq, or combination.
- Carfentanil has also been used with the Przewalski horse and Hartmann mountain zebras.
- Less consistent, more unpredictable in onagers, kiangs, and somali wild asses.
- Largely ineffective and not a good choice for Grevy zebras.
- Thiafentanil shows promise.
- Opioids generally cause significant muscle rigidity.
- When used alone, animals will often not become recumbent. May require casting.
- May be avoided by using alpha2 agonists prior to or along with opiod.
- Supplemental drugs i.e. guaifenesin or propofol may be used to provide relaxation.
- Several other factors besides chemical agents to consider:
- Obtain accurate body weight.
- Work with experienced or trained support staff.
- Precise dart placement.
- Advantages or disadvantages of pre-anesthetic medications.
- Prevalence of renarcotization in the species
- Soft, appropriate area for recovery.
- Regurgitation is not a risk, food and water should be withheld for 18-24 hours prior to procedure to reduce GI volume. Provide water if hot weather.
- Darting.
- Location ideal in a large muscle mass i.e. gluteals, shoulder, or neck.
- Avoid areas of fat.
- Blindfolds, earplugs.
- Supplemental oxygen.
- Anesthesia monitoring – HR, rhythm, rate and depth of ventilations, pulse ox.
- For prolonged procedures, GA.
- Isoflurane, mechanical ventilation.
- Intermittent IV propofol to extend anesthesia.
- Blind intubation, as in horses.
- Indirect BP may be measured with an appropriate sized cuff around metacarpal or metatarsal area.
- Arterial samples for blood gas from facial artery or IM branch of the caudal auricular artery.
- EtCO2, direct art line for BP, ECG useful for prolonged anesthesia.
- ECG parameters for gravy zebras have been described.
- Hydraulic hugger restraint chutes +/- chemical restraint.
How many equine herpesviruses have been identified?
Which are gammaherpes? Which are alphaherpesviruses?
What are the clinical signs of both groups?
Which viruses lack species specificity?
Equine Herpesvirus Background:
- Herpesviruses are generally host-specific.
- Zoonotic infections are not of general concern.
- However, some cross-species and cross-ordinal infections have been described and severe/fatal.
- i.e. Malignant catarrhal fever (Gammaherpesvirinae) can cause outbreaks with high mortality in mixed-spp collections.
- Equine herpesviruses cause interspecies infections.
- Nine EHVs identified.
- EHV2, EHV5, EHV 7 – Gammaherpesvirinae.
- Most derived from bats and primates.
- Rarely assoc. with dz, except MCF, Epstein-Barr, Kaposi sarcoma-associated herpesviruses.
- EHV1, EHV3, EHV4, EHV6, EHV8, EHV 9 – Alphaherpesvirinae.
- All associated with abortion, neonatal death, respiratory and neurologic disorders in domestic equids.
- EHV1 – one of the most consequential, worldwide.
- Recent discoveries in zoo and wildlife suggest EHV1 and close relative EHV9 lack strong spp specificity, can infect and cause dz in other mammals.
- EHV2, EHV5, EHV 7 – Gammaherpesvirinae.
Describe the diagnosis of equine herpesviral infections.
What are the typical clinical signs?
What tissues and samples should be collected?
What are the typical histologic lesions?
Discuss the benefits fo ELISA over antibody titers or serum neutralization.
Diagnostics:
- Typical clinical signs:
- Neurologic – seizures, encephalopathy (stroke-like syndrome) following endothelial cell infection and vasculitis. Myeloencephalopathy affecting the spinal cord in equids. In other spp, severe seizures
- Abortion.
- Fetal tissues should be frozen.
- Nasal discharge/swabs, blood and serum should be collected from adults.
- In fatal cases – lung, blood, serum, nasal epithelia, and brain tissue should be stored at -80C. Or refrigerate if can be transported to lab within few days.
- Pathologic findings – nonsuppurative encephalitis and gliosis, Barr bodies mostly absent.
- qPCR for pan-herpesvirus or more sensitive EHV-specific quantitative PCR assays.
- Many will be asymptomatic and will clear infection.
- Antibodies may persist long term or lifelong.
- Serology-based approaches measure Ab vs virus or viral antigen.
- Serum neutralization examines whether viral replication can be neutralized by serum of a given animal, indicating Ab are produced by the individual.
- Will not discriminate between closely related viruses because they are antigenically similar.
- Synthetic peptides designed to ID viral epitopes that are distinct are developed for EHV1, 4, and 9 (alphas) (ELISA).
- Can perform on 96 samples in a single plate, allows screening of large number of individuals.
- Peptide antigen coats the plates, then serum applied followed by secondary Ab.
- When secondary Ab binds, initiates enzymatic reaction that can be detected.
- Peptides for EHV1 cross react with EHV9 specific sera.
- However, EHV9 peptide does not react with EHV1 positive sera.
- Substantially more sensitive to low Ab titer vs SNT analysis.
- Application of carnivore sera has not yet been successful, restricting analysis in these spp to SNT.
- Both methods allow for determination of EHV 1 and EHV 9 exposure, whether individual is currently infected or not.
What taxa have been eperimentally infected with Equine Herpesvirus 1 (EHV1)? What clinical signs developed?
What taxa have been experimentally infected with EHV9? What signs developed in those animals?
Experimental Interspecies Infections:
- Like gammaherpesviruses, EHV1 and EHV9 can infect non-equine spp.
- Rabbits infected with EHV1 – resp and neuro signs.
- Mice infected with EHV1 – clear lytic infection but establish latency, depending on EHV1 strain, others produced neuro signs.
- Mice able to clear EHV9 after 72h.
- Lesions induced in hamsters.
- Dogs and cats – neuro signs with EHV9.
- Goats – lethal encephalomyelitis EHV9.
- Pigs – one study saw no CS although neuro lesions were observed, second experiment meningoencephalitis induced.
- Primates – macaques resistant to EHV9, marmosets severe neuro signs.
- EHV1 and EHV9 are able to infect and cause clinical signs in broad mammalian spp, including primates.
What interspecies transmission of equine herpesvirus has been documented in zoos?
What species were susceptible with EHV1? What about EHV9?
What clinical signs developed?
What perisodactyl species is more likely to be seropositive for EHV1 in the wild?
What perisodactyl species is more likely to be seropositive for EHV9 in the wild?
Nonexperimental Interspecies Infections;
- Full susceptibility of species outside of laboratory setting largely unclear.
- Infection in zoological collections and the wild.
- Non-equid spp:
- EHV9 fatal cases in captive Thompson’s gazelles, giraffes, and a polar bear
- Does not appear to be naturally occurring in domestic horses.
- Captive gazelles, antelopes, cattle, alpacas, llamas, and black bears have been infected with EHV1.
- An EHV1 and EHV9 recombinant virus was associated with lethal and nonlethal polar bear encephalitis and with a fatal encephalitis in an Indian rhino.
- EHV9 fatal cases in captive Thompson’s gazelles, giraffes, and a polar bear
- Equid spp:
- Isolated from zebras and other wild equine spp.
- Non-equid spp:
- EHV1 and EHV9 also exhibit cross spp circulation in the wild.
- Black and white rhinos seropositive for both.
- Significant prevalence of EHV1 and 9 in captive and wild black rhino and plains zebra populations.
- Captive zebras have a significantly lower prevalence of seropositivity than wild zebras.
- Zebras in general more likely positive for EHV1 vs EHV9.
- Rhinos more likely seropositive for EHV9 vs EHV1.
- African rhinos may be reservoirs for EHV1 and EHV9.
- Rhinos in captivity could result in cross spp transmission of either virus.
- EHV1 and EHV9 have a broad host range and broad prevalence in perissodactyls.
How is EHV transmitted?
What is the primary transmission between equids?
Cases of interspecies transmission has been what route?
How does EHV persist in the environment?
What role do wild animals or fomites play?
What about the feeding of equine meat?
Modes of Transmission:
- EHV 1 and 9 spread as respiratory smear infection.
- Applies to equids.
- In majority of cross-spp transfers, no obviour physical contact between equids and other spp.
- i.e. fatal EHV1 infection in polar bear, zebra enclosure was 200 m away. Keepers not shared between. Bears not fed equine meat.
- Direct respiratory transmission from requid to non-equid has NOT been likely in MAJORITY of reported interspecies cases!
- EHV1 has been shown to persist on surfaces such as stall bedding, shavings, and leather (fomites).
- EHV1 remains stable for several weeks in water, even at high temps.
- Possible rodents or birds that move among enclosures in zoos between water sources are exposing multiple enclosures.
- Could also serve as fomites.
- Mode of transmission from environmental sources or IM hosts remains an unsolved mystery.
- Stringent hygiene controls should be applied to prevent spread from equid or rhino enclosures to other areas of the zoo.
- Equid meat should only be fed to carnivores naturally sympatric with equids.
- i.e. lions consume zebras in nature but polar bears do not.
What vaccines are available for equine herpesviruses?
What does the literature say about their efficacy?
What is the role of monitoring of viral shedding in preventing outbreaks and cross-species transmission?
To Vaccinate or Not?
- Horses – commercial live viral vaccine (rhinoimmune) and two inactivated viral vaccines (Pneumabort K-Fort Dodge and Prodigy-Intervet).
- Conflicting evidence for live vs inactivated vaccines lowering incidence of EHV1 induced abortions.
- Majority of publications suggest efficacy.
- Little evidence that vaccination can prevent neuro disease.
- Does not guarantee complete prevention of viral shedding.
- Consistent monitoring of viral shedding, isolation of shedding individuals, and decontamination of areas exposed to shedding animals will be key to managing cross-spp transmission.
- If used regularly, monitoring for shedding can be detected early enough to isolate individual animals and prevent build-up of virus in the environment that would promote transfer.
- Implementation of monitoring is strongly recommended.
What are sarcoids?
What are they caused by?
Where are they typically seen in plain’s zebras? Wat about Somali wild asses?
What about wild Cape mountain zebras?
How are they definitively diagnosed?
- Sarcoids.
- Unencapsulated, poorly demarcated fibroblastic skin tumors.
- Invade locally, may recur after surgery. Not metastatic.
- Overlying epidermis is frequently hyperplastic.
- Equine sarcoid are associated with bovine papilloma virus (BPV) type 1 and 2 infection.
- Reported from sarcoids at the eyelid, nose and inguinal region in captive Burchell’s zebras.
- Sarcoids at the ear, prepuce, and mammary gland in Somali wild asses are thought to be virus-associated.
- Also reported in wild Cape mountain zebra, esp along ventral abdomen and legs, in two reserves in South Africa (53% prevalence).
- Viral DNA has been detected in nuclei of the neoplastic mesenchymal cells of zebra sarcoids.
- Late viral antigens are not found in sarcoids and neutralizing antibodies to the virus are not found in horses.
- Suggests the infection is nonproductive in horses.
- Mechanism of transmission of bovine papilloma virus to the zebras has not been identified.
- Sarcoids do not produce virions.
- Viral DNA and RNA may be detected.
- BPV type 1 and 2 major transforming protein E5 is expressed.
What are some important bacterial diseases of equids?
What conditions predispose animals to anthrax?
What are some clinical signs of salmonellosis in equids?
Strangles is caused by what etiologic agent? How has this affected p horse introductions?
- Anthrax.
- Threat to populations of free ranging Grevy zebras in Africa.
- Both mature and immature animals.
- Drought and other adverse environmental conditions predisposing factors.
- Dry conditions may promote trauma in oral cavity, increases risk of acquiring anthrax spores.
- Widespread vaccination has been used, efficacy has not yet been determined.
- Threat to populations of free ranging Grevy zebras in Africa.
- Salmonellosis – abortion and genital tract infection of equids.
- Clostridial infections – C. welchii with wound infection and septicemia in Somali wild ass.
- Strangles – suppurative lymphadenitis with streptococcus equi.
- Associated with pharynx and resp tract.
- Cluster of deaths in P horses reintroduced to SW Mongolia.
- Association with harsh winter and wolf predation.
Describe fungal disease in equids.
What species appears overly susceptible to coccidioidomycosis? How is this agent transmitted?
How did this impact zoo populations?
Describe phaeohyphomycosis infection in equids? What lesions occurred? What species has this been observed in?
- Coccidioidomycosis has been reported in Przewalski horses in CA, where coccidioides immitus is endemic.
- Usually asymptomatic, resolve spontaneously.
- Transmission by inhalation of arthroconidia.
- Immunosuppression increases risk of disseminated infection in humans and domestic animals.
- Leading cause of death in a population of przewalski horses 1980-2000.
- Disseminated granulomatous lesions/respiratory system.
- More common in males and younger individuals.
- Possibly due to intraspecific aggression and stress in bachelor herds.
- Other species of equid at same facility not affected.
- Disseminated granulomatous lesions/respiratory system.
- Management strategies that reduce stress may be helpful.
- Phaeohyphomycosis.
- Opportunistic, dematiaceous (pigmented) fungal infection caused by variety of fungal species.
- Ubiquitous in soil and woody plants.
- Systemic infection nis rare.
- Vascular invasion infrequent, often associated with immunosuppression.
- Infection originates in resp system after inhalation.
- Cutaneous disease after wound infection.
- Sudden onset weight loss, lethargy, hypothermia in captive male Grevy’s zebra.
- Focal pyogranulomatous pneumonia, myocarditis, pericardial effusion associated with moniliform fungal hyphae.
- Yeast forms found in heart.
What are the etiologic agents of piroplasmosis in equids?
Where are these diseases endemic?
How are they transmitted?
What clinical signs and lesions to they cause?
What role does translocation play in disease ecology?
What equid species have been affected?
- Piroplasmosis (protozoal disease).
- Possible cause of mortality in reintroduced Przewalski horses in Mongolia.
- Babesia caballi and Theileria equi probably endemic throughout Asia.
- Piroplasmosis.
- Attack and destroy RBCs.
- May occur seasonally with tick vector.
- Translocation may induce dz by spreading pathogens, stress hormones influence immune system and allow proliferation of piroplasms in host.
- Severe regenerative hemolytic anemia, jaundice in acute cases.
- Chronic cases subclinical carriers.
- Pulmonary edema, splenic congestion.
- Renal tubular necrosis, disseminated hemosiderin-laden macrophages.
- Transplacental infection may cause abortion.
- Aborted fetuses have high levels of parasitemia.
- P horses in Mongolia – piroplasmosis cause of death of stallions and a stillborn foal.
- Somali wild ass – diagnose with babesiosis.
- Cograzing donkeys and wild Grevy’s zebra in Kenya – all zebra tested positive for T. equi.
What is the etiologic agent of equine protozoal myeloencephalitis?
What is the definitive host of this organism?
What lesions have been seen as a result of this disease?
- Equine protozoal myeloencephalitis.
- Sarcocystic neurona.
- Opossum Didelphis virginiana definitive host of sarcocystis falcatula and may be definitive host of S. neurona.
- Captive Grant’s zebra acute ataxia, weakness, depression.
- CSF positive for Ab to S. neurona on Western blot.
- Perivascular cuffing with MN cells at brainstem.
- S. neurona ID by IHC staining of merozoites.
A recent study compared opioid based protocols in Grevy’s zebra.
How did etorphine compare to thiafentanil (both with an alpha 2) in terms of induction time?
Did the inclusion of ketamine in these protocols affect induction time?
What about the effect of ketamine on recovery time?
Stuchin, M., Mama, K. R., Zuba, J. R., Oosterhuis, J. E., Lamberski, N., & Olea-Popelka, F. (2019). A comparison of opioid-based protocols for immobilization of captive grevy’s zebra (equus grevyi). Journal of Zoo and Wildlife Medicine, 50(1), 258-261.
Grevy’s zebra (Equus grevyi) is an endangered species often found in zoological collections. Veterinary care for this species often requires immobilization. This study retrospectively evaluated behavioral and physiological parameters from Grevy’s zebra records after three immobilization protocols: etorphine and alpha-2 agonist (EA2; n = 11); etorphine, alpha-2 agonist, and ketamine (EA2K; n = 16); and thiafentanil, alpha-2 agonist, and ketamine (TA2K; n = 6). Median time to working depth was statistically different (P = 0.03; EA2 = 6.5 min, EA2K = 6.3 min, TA2K = 14.5 min) by the Kruskal–Wallis test. When EA2 + EA2K were combined and compared with TA2K (Wilcoxon rank sum test), median recumbency time (P = 0.02) was also significantly longer (15 min compared with 6 min) for TA2K. There were no significant differences between the groups for physiological parameters or recovery time after reversal. Although all protocols produced anesthesia in Grevy’s zebra, increased time to achieve working depth was observed with the alpha-2 and thiafentanil combinations.
- Etorphine and alpha2 agents predictable immobilization in this species.
- This is a retrospective looking at behavioral characteristics and physiological parameters using etorphine and thiafentanil on the basis of immobilization protocols.
- Treatment groups:
- Etorphine and alpha 2
- Etorphine, alpha 2 and ketamine
- Thiafentanil, alpha 2, ketamine
- Reversal with naloxone
- Induction times significantly longer with thiafentanil and alpha 2.
- Inclusion of ketamine in protocol did not have an overall effect on induction time, physiologic parameters, or the need for supplemental drugs.
- Recover was longer.
- Thiafentanil is a viable alternative to etorphine.
A recent study described pituitary pars intermedia dysfunction in nondomestic equids.
How common is PPID in domestic horses?
What are the typical clincial signs?
How is it diagnosed?
How were these animals treated?
What findings were seen on necropsy of these animals?
Shotton, J. C., Justice, W. S., Salguero, F. J., Stevens, A., & Bacci, B. (2018). PITUITARY PARS INTERMEDIA DYSFUNCTION (EQUINE CUSHING’S DISEASE) IN NONDOMESTIC EQUIDS AT MARWELL WILDLIFE: A CASE SERIES. ONE CHAPMAN’S ZEBRA (EQUUS QUAGGA CHAPMANI) AND FIVE PRZEWALSKI’s HORSES (EQUUS FERUS PRZEWALSKII). Journal of Zoo and Wildlife Medicine, 49(2), 404-411.
Abstract: Pituitary pars intermedia dysfunction (PPID), also known as equine Cushing’s disease, is widely reported in middle-aged to older domestic equids but to date reported in only one nondomestic equid, the onager (Equus hemionus onager). This case series reports clinical, hematological, and pathological findings consistent with PPID in two further equid species: one Chapman’s zebra (Equus quagga chapmani) and five Przewalski’s horses (Equus ferus przewalskii). The case series reports basal adrenocorticotropic hormone (ACTH) testing as a method to diagnose and monitor PPID in zoological equids and the use of pergolide mesylate to reduce basal ACTH concentration and reduce clinical signs associated with PPID. Gross and histopathological examinations of the pituitary gland in four of these cases revealed either pars intermedia adenomas or adenomatous hyperplasia, similar to pathological findings in domestic equids affected by PPID. These findings suggest that clinicians working with nondomestic equids should be aware of this condition and consider screening for it routinely, particularly given that improvements in management and veterinary care for exotic animals are resulting in a more aged captive population. Early diagnosis and treatment of PPID may prevent the development of painful clinical sequelae and therefore improve the welfare of zoo equids.
- PPID affects up to 30% of older horses
- Clinical signs include hypertrichosis, laminitis, polyuria, polydipsia, muscle wasting
- Diagnosed with high adrenocorticotropic hormone (ACTH) – normal range < 29 pg/mL
- Other testing options – thyrotropin stimulating hormone or dexamethasone stimulation tests
- Anesthetized with 2.5 mg/kg ketamine + medetomidine 0.1 mg/kg OR 0.05-0.1 mg/kg detomidine + 0.03-0.06 butorphanol
- Treated with pergolide 1 mg daily (3 mcg/kg PO q24h)
- Other clinicopathologic findings – elevated GGT
Take Home: PPID may be playing a role in older non-domestic equids and testing should be done for any showing signs
References:
- Schott H, Andrews F, Durham A, Frank N, Hart K, Kritchevsky J, McFarlane D, Tadros L. Recommendations for the diagnosis and treatment of pituitary pars intermedia dysfunction (PPID) [Internet]. c2017 [cited 5 December 2017]. Available from https://sites. tufts.edu/equineendogroup/files/2017/11/2017-EEG- Recommendations-PPID.pdf
A recent study described gastric ulcers and associated risk factors in wild equids.
What species show a higher disposition for gastric ulceration?
How did age affect the prevalence adn severity of gastric ulcers?
Where were the ulcers located?
What are some risk factors for ulcer development in domestic horses?
What risk factor was found for these wild equids?
Lamglait, B., Vandenbunder-Beltrame, M., Trunet, E., & Lemberger, K. (2017). Description of gastric ulcers and of their suspected, associated risk factors in deceased wild equids at the réserve africaine de sigean, france (2010–2016). Journal of Zoo and Wildlife Medicine, 48(3), 668-674.
Abstract: Gastric ulcers are common in domestic horses and foals, affecting at least 90% of unmedicated racehorses in active training. Despite these high prevalences in domestic horses, literature about this condition in wild equids is almost nonexistent. The presence of gastric ulcers was evaluated at necropsy in six species of wild equids that died at the Re´serve Africane de Sigean, a safari park in the south of France from 2010 to 2016. Among the 55 individuals that died during that period, a description of the gastric mucosa was available in 82% (45/55) of cases. Considering the cases for which a description of the gastric mucosa was available, the prevalence of gastric ulcers was 64% (29/45). The highest prevalences were noted in Grant’s zebra (Equus quagga boehmi) and Hartmann’s mountain zebra (Equus zebra hartmannae) at 83% and 100%, respectively. In contrast to what is reported in domestic foals, gastric ulcerations were only diagnosed in one foal (out of 11 foals necropsied). The higher prevalence was noted in young individuals (3–36 mo old) at 93% (14/15); the lesions observed consisted mainly of single to multiple, superficial lesions, of which, only the mucosa was missing; these superficial lesions are often considered not clinically significant. The prevalence was lower for adults (74%; 14/19), but lesions were deeper or with a hyperemic or inflammatory appearance. All the lesions observed were located in the gastric, nonglandular, stratified squamous mucosa, along the margo plicatus. No statistical correlation could be found between the development of gastric ulcers and an ongoing, chronic pathologic process or a digestive tract pathology. The detection of gastric ulcers was, therefore, significantly greater in wild equids isolated in smaller enclosures. Nevertheless, additional larger-scale research is needed to point out predisposing factors in equids under human care.
- Gastric ulcers common in domestic horses and foals, especially in performance disciplines, recent changes in housing or social interactions, and illness.
- Grant’s and Hartmann’s zebras demonstrated significantly greater proportions of gastric ulcers compared to overall population.
- Low in foals, differs from domestic horses.
- 3-36 mos old significantly more affected. Adults had more severe lesions. Not correlated with severity of CS in this study. Also no correlation between ulcers and other chronic GI conditions.
- All gastric ulcers along the margo plicatus, particularly in the saccus caecus and squamous mucosa (non-glandular) along the lesser and greater curvatures.
- Factors implicated in causing ulcers in horses – fasting, gastric acid clearance (motility and emptying), aggressiveness of gastric acid, pepsin, and volatile fatty acids produced from fermentation of soluble carbohydrates. Anything modifying one or more of those components can lead to EGUS.
- Intermittent feeding with high-grain diets, physical and environmental stress i.e. transport stress and stall conferment, lack of exposure to other conspecifics, chronic administration of NSAIDs. Neonatal domestic foals significant risk for perforating peptic ulcers, gastric mucosa is not full thickness at birth.
- Detection of ulcers significantly greater in wild equids isolated in enclosures < 75 m^2.
Takeaways: Low prevalence in foals, higher in 3-36mos old, more severe in adults, along the margo plicatus in all cases. Associated with individuals isolated in small enclosures.
A recent study evaluated the causes of death in feral horses in Japan.
What type of virus is Japanese encephalitis virus? What are its natural viremic amplifiers?
How commonly were these horses seropositive?
What was the most common pathologic finding in these horses?
Niazmand, M. H., Hirai, T., Ito, S., Habibi, W. A., Noori, J., Hasheme, R., & Yamaguchi, R. (2019). Causes of death and detection of antibodies against japanese encephalitis virus in misaki feral horses (equus caballus) in southern japan, 2015–17. Journal of wildlife diseases, 55(4), 804-811.
ABSTRACT: We performed postmortem examinations on seven Misaki feral horses (Equus caballus) and evaluated Misaki feral horses, Japanese wild boars (Sus scrofa leucomystax), domestic pigs (Sus scrofa), and wild Japanese macaques (Macaca fuscata fuscata) from 2015 to 2017 in Cape Toi, Kushima, Miyazaki Prefecture, southern Japan, for antibodies against Japanese encephalitis virus (JEV). Strongylus vulgaris infection with severe arterial lesions and hemomelasma ilei was present in all necropsied horses. We frequently found intestinal ulcers, perihepatitis filamentosa, and poor body condition. We recorded degenerative arthropathy in metacarpophalangeal joints in two cases and a fracture of the rib with diaphragmatic rupture in one case. A total of 73% (177/242) of horses were seropositive for JEV as tested by hemagglutination inhibition(HI). The HI data also revealed that 74% (59/80) of the wild boars, 67% (60/90) of the pigs, and 29% (22/75) of the wild monkeys were seropositive for JEV. Our findings showed that Strongylus spp. are still a risk to horses in this region, and that environmental factors such as topographic location of the pasture and steep slope may have caused of degenerative arthropathy and bone fracture. Our results showed that JEV is endemic in Japan. The wild boars and pigs were presumed to act as strong amplifiers and sources of infection, with subsequent risk to humans.
- Japanese encephalitis virus (JEV) is transmitted by mosquitoes and severe zoonotic disease with neurologic symptoms - Family Flaviviridae, Genus Flavivirus
- Swine (Sus scrofa) and birds of the family Ardeidae are viremic amplifiers
- N = 7 pathologic findings and N = 242 samples
- Cranial mesenteric arteritis and hemomelasma ilei caused by S. vulgaris larvae infection found in all horses
- Perihepatitis in most horses likely from migration of S. edentates
- Many were emaciated
- Degenerative arthropathy and lameness in 2 horses 🡪 topographic conditions in pastures are predisposing factor
- More common in older horses (>10yr)
- Strongylosis infection rate decreasing due to anthelmintic drugs, but NOT sufficient to break life cycle
- JEV is endemic in Misaki feral horses, wild boars, and domestic pigs 🡪 potential strong amplifiers of JEV
- JEV is endemic in macaques
A recent study compared one versus two dart protocols in Przewalski’s horses.
What were the two different protocols?
How did induction differ?
Did animals need supplementation for intubation?
Compare the three ultrapotent opioids for use in equid anesthesia.
Discuss the pros and cons of a two dart protocol in P horses.
A COMPARISON OF A SINGLE-DART VERSUS STAGED TWO-DART ANESTHESIA INDUCTION PROTOCOL IN PRZEWALSKI’S HORSES (EQUUS FERUS PRZEWALSKII)
JZWM 2021 52(2) 453–459
Abstract: Przewalski’s horses (Equus ferus przewalskii) are an endangered equid species. Anesthesia administered by remote delivery is often needed to provide medical care. Behavioral and physiologic parameters were prospectively compared in 14 horses (8 females and 6 males, 3–18 yr) after a single-dart or staged two-dart anesthesia induction protocol with intramuscular medetomidine (0.06 mg/kg), butorphanol (0.05 mg/kg), thiafentanil (0.02 mg/kg), and ketamine (1 mg/kg). Seven horses were randomly assigned to receive all drugs in a single dart, and the other seven to receive medetomidine and butorphanol 10 min prior to thiafentanil and ketamine in a second dart. Induction and recovery quality were scored on a scale from 1 to 5 (worst to best), and video recordings were assessed for frequency of specific behaviors. Need for supplemental propofol was recorded. Median induction score was significantly better (P = 0.01) after two darts (4/5) compared to a single dart (3/5). Degree of muscle fasciculation (undesirable) during induction was significantly lower (P = 0.006) with the two-dart protocol. During the transition to recumbency, 71% versus 14% of horses transitioned headfirst (undesirable) after a single dart versus two darts, respectively (P = 0.07). Supplemental propofol administration was necessary in 43% of horses after two darts and in 100% of horses after a single dart (P = 0.10) to facilitate intubation and reach a working depth of anesthesia. Physiologic and recovery parameters were not significantly different between groups. Improved induction quality was observed clinically using a staged two-dart versus a single-dart protocol and should be considered when anesthetizing captive Przewalski’s horses using this drug combination.
Summary:
Intro:
- Wild equid anesthesia – challenging
- non-opioid-based anesthesia techniques have been studied in Przewalski’s horses
- most common - alpha-2 agonist medetomidine (sedation, muscle relaxation) with dissociative anesthetic ketamine
- not all horses successfully immobilized with this combo
- ultrapotent opioid-based techniques reported to induce anesthesia more reliably
- etorphine considered opioid of choice for anesthesia in non-domestic equids
- carfentanil - recently unavailable in US
- rough inductions, increased muscle contraction, significant hypertension in equids
- thiafentanil – newer, info in Przewalski’s horses limited
- respiratory depression
- butorphanol (antagonist of mu opioid receptor) helps mitigate
- respiratory depression
· Objective: study assessed use of thiafentanil as part of a multidrug protocol including medetomidine, butorphanol, and ketamine for anesthesia induction and influence on anesthesia quality following admin of these medications using a single-dart versus a staged two-dart induction protocol
M+M:
· effectiveness and anesthesia quality following single-dart vs staged two-dart anesthesia protocol compared in 14 captive adult Przewalski’s horses
· Drug combo for all horses: butorphanol (0.05 mg/kg), medetomidine (0.06 mg/kg), thiafentanil (0.02 mg/kg), and ketamine (1 mg/kg) IM
· single-dart protocol - all drugs in single dart
· staged two-dart protocol - medetomidine + butorphanol in 1st dart, thiafentanil + ketamine 10 min later in 2nd dart
· supplemental propofol as needed for intubation, etc
· reversal with naltrexone and atipamezole
Results/discussion:
· recumbency achieved in all horses
· induction time longer for two dart protocol
· median time to recumbency of 6 min for single-dart protocol and 15 min for two-dart protocol
· behavioral response to second dart significantly reduced because of sedative effects of first dart
· significant improvement in induction quality with staged two-dart vs single-dart protocol:
· decreased muscle fasciculation, rigidity, incoordination, and reduction in frequency of undesirable (head-first) transitions to recumbency
· when all drugs combined in single dart, first effects are largely those of thiafentanil, as opposed to those of medetomidine combined with butorphanol
· need for supplemental propofol to reach a working depth of anesthesia once recumbent not significantly different between groups
· all horses in single dart group needed propofol supplementation
· physiologic parameters not different between groups
· no significant anesthetic or postanesthetic complications noted in either group
· no difference in recovery scores – all had good to excellent recoveries
· two-dart protocol resulted in longer duration between first dart and reversal
· median duration from first dart to standing was same in both protocols
· time from reversal to standing was shorter with two-dart protocol
Conclusion: study supports use of thiafentanil in combo with butorphanol, medetomidine, and ketamine for anesthesia in Przewalski’s horses and administration of medetomidine and butorphanol prior to thiafentanil administration consistently provided improved sedation and muscle relaxation and minimized negative characteristics associated with potent opioid inductions and need for supplemental propofol; use of staged two-dart protocol provided improvements to anesthesia induction quality and may improve safety of anesthesia in Przewalski’s horses
