Hippopotamidae Flashcards

1
Q

Describe the unique GI anatomy of the hippopotamus.

A

GI

  • Pseudoruminants – four chambered stomach with ruminant-type digestion but they do not ruminate
  • Cecum and gallbladder are missing

Fowler 8

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2
Q

Describe the unique anatomy & physiology of hippo skin, including the pigments of their blood sweat.

A

Skin

  • Thick, lacks sebaceous glands, few hairs
  • Subepidermal capillary loops – 20 times larger, 3 times more dense than in other animals accomadate high blood pressure for heat transfer to periphery
  • Subdermal mucous glands – blood sweat – protects from water loss, sunburn, & infections
    • Red pigment – hipposudoric acid (bacteirocidal activity vs Pseudomonas & Klebsiella)
    • Orange pigment – Norhipposudoric acid

Fowler 8

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3
Q

Describe the approach to castration in the common hippo.

A

Castration – testes in inguinal canal

  • Dorsal hindleg secured with a rope
  • Testes found on ultrasound, skin incised just ventral to located testes (recheck with US if can’t find)
  • Short spermatic cord – testes can’t be exteriorized, has to be done 20-30 cm inside the surgery site

Fowler 8

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4
Q

Common venipuncture sites of the hippo

A

Venipuncture – ventral tail, sublingual, cephalic, palmar/plantar digital veins, auricular veins

Fowler 8

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5
Q

What are the best injection sites for darting hippos?

A

Injection sites – area caudal to the ear, medal/caudal aspects of hind legs as other areas are very thick

Fowler 8

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6
Q

What are common complications with anesthesia in hippos?

A

Apnea, cyanosis, bradycardia, respiratory arrest, hyperthermia. Drowning is a risk.

Fowler 8

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7
Q

What is the most important infectious disease of wild hippos?

A

Anthrax - Bacillus anthracis

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8
Q

Discuss proper positioning of hippos during anesthesia.

A

Positioning

  • Weight on limbs a concern for neuropathy, compromised perfusion, myopathy
  • Abdominal contents put more pressure on diaphragm if left in sternal (unless there is ventilation)
  • Rolle to lateral if respiratory compromise is suspected

Recovery

  • Leave the hippo in sternal ideally, but recovery in lateral has been performed

West

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9
Q

What are the most common GI issues in managed hippos?

A

Foreign body injestion and small instestinal obstruction

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10
Q

Are cardiovascular disease common in hippos?

What are the most common cardiac diseases?

A
  • 17% of all deaths of captive pygmy hippos are cardiovascular related
  • Encephalomyocarditis virus is the primary cause but DCM, degenerative valve disease, and myocardial degeneration and fibrosis are also documented
  • Encephalomyocarditis Virus aka Cardiovirus A
    • 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
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11
Q

What is the most common renal disease of hippos?

What are the lesions associated with this disease?

What is the common signalment?

A
  • 35% of captive pygmy hippos – mostly adult and geriatric animals, most female but both sexes affected
  • Autosomal dominant inheritance
  • Grossly – cysts efface normal parenchyma composed histologically of ectatic tubules lined with flattened epithelium, dilated bowman’s capsules with membranous glomerulopathy
  • Cysts are surrounded by fibrosis
  • Cysts are also seen in the liver (biliary cysts), duodenum, thyroid, or pancreas in some cases
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12
Q

Describe the multicentric vesicular and ulcerative dermatopathy of hippos.

What is seen on histology?

How is it treated?

A
  • Erosive and ulcerative lesions widely distributed over axillary, inguinal, perineal, and limbs
  • Seasonality suggested
  • Histo – dermal edema, epidermal necrosis, neutrophilic dermal vasculitis with thrombosis
  • Bacteria often cultured, but a primary etiology not identified
  • Responds to increased salinity, broad-spectrum antibiotics, and pentoxifylline
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13
Q

Describe the unique anatomy of the hippo including:

The scapula orientation

Skull anatomy

Nares

Testis location

A

Unique Anatomy (Fowler 8)

  • CH Forelimb – scapula is oriented vertically to create a vertical column
    • Pygmy hippo skeleton is built lighter
  • Skull
    • Common hippo – eyes forward, small braincase
    • Pygmy hippo – eyes lateral
  • GI
    • Pseudoruminants – four chambered stomach with ruminant-type digestion but they do not ruminate
    • Cecum and gallbladder are missing
  • Skin
    • Thick, lacks sebaceous glands, few hairs
  • Nares – muscular valves close ears and nostrils during diving
  • Testes – located in the inguinal canal
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14
Q

Describe the housing requirements of hippos

A

Housing Requirements (Fowler 8)

  • Common Hippo
    • Strong barriers
    • Animals are not frost resistant – need heated interior enclosures
    • Interior and exterior pools at least 2.5 m deep for total submersion (extensive filtration required)
  • Pygmy Hippo
    • This species is more aggressive towards people and conspecifics
    • Adequate ability to separate individuals is needed
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15
Q

Describe the feeding of hippos.

What are some common disorder?

How do the diets of the two species differ?

A

Feeding (Fowler 8)

  • GI disorders often attributed to FB ingestion and SI obstruction
  • Common hippo – 30-45 kg of grass, clover, lucerne, maize + various vegetables, can be replaced with hay In the winter
  • Pygmy hippo – wild diet is ferns, herbs, leaves, and fruits, with grass playing a minimal role
  • Both species have low metabolic rates – careful with pellets to reduce obesity
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16
Q

Describe intubation and ventilation of the hippo.

Describe the monitoring of capnography in the hippo.

A

Respiratory Support

  • Some combos (without ultrapotents) result in the dive reflex
  • Nasal insufflation
    • 12 mm ETT for common hippo – isoflurane can be administered that way
  • Intubation
    • Equipment & personnel needed to open the jaws
    • Redundant folds of buccal and oropharyngeal tissue, fleshy tongue, long soft palate can make it difficult to visualize – blind intubation is typically easier
    • ETT size – 24-30mm for common hippos, 14-mm for pygmy hippos
    • Megavertebrate demand ventilator recommended
  • Complications – apnea, hypoventilation, hypoxemia, hypercapnia, respiratory acidosis

Monitoring

  • Capnography
    • First breath after a breath hold often 70-80mmHg, decreases to 40-50 mmHg after a few breaths
    • Should be 35-55 mmHg in regularly ventilated animals
17
Q

How are hippos sexed? Why is it difficult?

When do females mature? How many calves can one animal have?

What is their estrous cycle like?

How long is gestation?

What can they be contracepted with?

A

Reproduction (Fowler 8)

  • Females
    • Sex determination difficult – vulva hidden in perineal folds
    • Sexually mature at 3 years, females can have up to 25 calves in 40 year lifespan
    • Gestation 240 days, post-partum estrus documented
    • Polyestrous with estrous cycle length of 30 days
    • Contraception – MGA in feed (3 mg/day/animal), MPA implants (800 mg q6w)
  • Males
    • Prepuce barely visible on ventral midline
18
Q

What is the most common urolith of the hippopotamus?

A

Calcium oxalate (ZP)

19
Q

What is the dental formula of the hippo?

What are some common dental issues?

A

Dental formulae

Common hippo – 2/2, 1/1, 3-4/3-4, 3/3

Pygmy hippo – 2/1, 1/1, 3/3, 3/3

Dental Attrition & Wear

Canine and incisors grow continuously – several reports of overgrowth and malocclusion in both species

20
Q

What is a common bacterial cause of mortality in neonatal hippos?

How is this disease transmited?

What are the clinical signs?

A
  • Closridial Hemorrhagic Enteritis
    • Susceptible Species: variety of nondomestic ruminants, common cause of neonatal mortality 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
21
Q

What is the most significant bacterial disease of wild hippos?

What is the pathogenesis of this disease?

What lesions does it produce?

How do you safely diagnose it?

A
  • Anthrax
    • 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
22
Q

What are two parasites hippos are suscepible to?

A

Parasitic Disease

  • Haemonchosis
    • 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
  • Trypanosomiasis
    • 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 disease
    • Histo Lesions:
      • Diagnosis: PCR, microscopic evaluation of parasites in blood or impression smears of brain or liver
23
Q

A recent study evaluated the genetics of polycystic kidney disease in pygmy hippos.

How common is PCKD in pygmy hippos?

What happens with this disease?

Is it heritable in other species?

Is there a genetic predisposition in pygmy hippos?

A

Flacke, G. L., Tomkins, J. L., Black, R., & Steck, B. (2017). Demographics of polycystic kidney disease and captive population viability in pygmy hippopotamus (Choeropsis liberiensis). Zoo biology, 36(2), 136-151.

Abstract: Polycystic kidney disease (PKD) was previously diagnosed at necropsy in several pygmy hippopotami (Choeropsis liberiensis) from the Smithsonian National Zoo and Zoo Basel, suggesting a threat to the long-term viability of the captive population. We determined the incidence and demographics of PKD in the captive population historically; we tested if the condition is linked to pedigree; we investigated mode of inheritance; we examined effects of PKD on longevity; we conducted survival analysis; and we examined long-term population viability. Thirty-seven percent of 149 necropsied adult pygmy hippos were affected by PKD, and it was more common in females, controlling for the overall female-biased sex-ratio. Prevalence increased significantly with age, but most hippos were beyond their reproductive prime before developing clinical signs; thus fecundity was likely unaffected. PKD was linked to pedigree and may exhibit X-linked dominance, but further research is needed to definitively establish the mode of inheritance. PKD did not affect longevity, overall or within any age class. There was no significant correlation between inbreeding coefficient (F) and PKD, and the prevalence in wild- caught and captive-born animals was similar. Longevity for both captive-born and inbred hippos (F > 0) was significantly shorter than longevity for their wild-caught and non-inbred counter- parts. Demographic projections indicated the extant population will likely experience a slow increase over time, provided there are no space constraints. We conclude that although PKD is an important cause of morbidity and mortality in pygmy hippos, the condition is not a primary concern for overall viability of the captive population.

  • PKD – degenerative condition where cysts replace functional renal tissue – hereditable disease in humans, rodents, bull terriers, and domestic cats
  • PKD served as a clinically significant cause of renal failure & mortality only in 15 of the 56 hippos with PKD

Take Home: PKD should be a primary differential for renal disease in pygmy hippos and is likely a heritable condition (possibly x-linked dominant)

24
Q

A recent case series described bacterial sepsis in pygmy hippo calves.

What bacteria were implicated in these cases?

What precautions should be taken with a pygmy hippo birth?

A

THREE CASES OF ACUTE BACTERIAL SEPSIS IN PYGMY HIPPOPOTAMUS (CHOEROPSIS LIBERIENSIS) CALVE SIBLINGS

Journal of Zoo and Wildlife Medicine 52(2): 755–762, 2021

Abstract: A multiparous pygmy hippopotamus (Choeropsis liberiensis) dam produced three consecutive calves that died acutely at 13–15 wk of age from bacterial sepsis, for which diagnostic and therapeutic intervention was not possible. Streptococcus iniae (Cases 1 and 3), Escherichia coli (Case 2), and an unidentified member of the family Pasteurellaceae (Case 1) were identified in postmortem tissues through bacterial culture followed by standard and molecular identification methods. After the loss of two calves, a series of vaccinations were administered to the dam during the third pregnancy to enhance transplacental and colostral transfer of antibodies to the calf. The third calf did not survive, and the source of the bacterial infection in these three calves was undetermined. Prior to and after the birth of the fourth calf, nutritional and nutraceutical supplements were provided to the dam and calf. Additionally, pest control around the barn was enhanced. The fourth calf survived. Pygmy hippopotamus calves at the age of 13–15 wk may have increased susceptibility to bacterial infection, possibly due to waning maternally derived immunity. The findings in these cases, combined with a previous association of S. iniae in pygmy hippopotamus deaths, suggest that this bacterium is an especially important pathogen of the endangered pygmy hippopotamus.

Intro

· This case series describes three pygmy hippo calves born to the same dam that died acutely during the juvenile period due to Streptococcus iniae (n ¼ 2) and Escherichia coli (n ¼ 1) infections. The calves were born in succession from an 11-yold dam that had successfully raised two previous offspring

Case reports

· Case 1 – calf was found dead unexpectedly at 15 weeks old – streptococcus iniae isolated, evidence of sepsis on histopath

· Case 2 – Increased zinc in the diet of all hippos. ~ 1 year later the dam had another calf, also found dead unexpectedly at 13 weeks old – sepsis from E. coli

· Case 3 – multiple gestational vaccines were administered prior to the birth of the 3rd calf. Found dead at 13 weeks – sepsis from strep iniae

· Cases 4 – unexpectedly the dam had another calf. When the calf was 5 weeks old the dam began receiving additional nutritional and nutraceutical support (leaf spinach, goat mineral mix to provide higher zinc)

o A nutraceutical mixture of Baptisia sp., Echinacea sp., and Thuja sp. extracts and a commercial protein, vitamin, and mineral supplement formulated for lactating mares were added to the daily feedings.

o Barn hygiene practices were changed to include two to three applications of chlorine bleach (1,200 ppm) prior to washing with water each week and power spraying all surfaces three to four times per month

o In addition, rat and cockroach control applications were increased around the hippo barn immediately after the birth of the calf.

o At the time of writing calf is 1 yo and thriving

Discussion

· Three consecutive pygmy hippo calves, born to the same dam, died from acute bacterial sepsis and endotoxemia due to S. iniae or E. coli infections at 13–15 wk of age.

· Similar pathologic lesions were found in each case, including pneumonia, hepatic necrosis, and tubulointerstitial nephritis

· It is of interest that two of the cases were attributed to S. iniae, which is considered a pathogen primarily of aquatic animals, especially fish.

· A retrospective report of pygmy hippo deaths indicated that of 18 cases in which bacteria were cultured and identified, seven involved Streptococcus sp., of which one was confirmed as S. iniae in a 7-y-old male individual associated with a foot rot lesion.6

· Collectively, these findings suggest that S. iniae is an especially important pathogen of the endangered pygmy hippopotamus.

· These cases highlight that pygmy hippos 3–5 mo of age may have increased susceptibility to bacterial infections and may have special needs

This could include gestational and/or neonatal vaccines, providing additional micronutrients and boosting immune competence via balanced nutrition and nutraceutical supplementation, probiotic supplements, and increased hygiene

25
Q

A recent study described the management of anaplastic sarcoma in a pygmy hippo.

How was this neoplasia treated?

What tumors have been documented in pygmy hippos?

A

Franklinos, L. H., Masters, N., Feltrer, Y., Pocknell, A., Bolt, D. M., Dakin, S., … & Molenaar, F. M. (2017). The management of an oral anaplastic sarcoma in a pygmy hippopotamus (choeropsis liberiensis) using intralesional chemotherapy. Journal of Zoo and Wildlife Medicine, 48(1), 260-264.

Abstract: An adult female captive pygmy hippopotamus (Choeropsis liberiensis) was diagnosed with an oral anaplastic sarcoma. The tumor was surgically debulked and intralesional chemotherapy with mitomycin C (0.4 mg/cm3 of tumor) and cisplatin (1 mg/cm3 of tumor) was administered. Chemotherapeutic treatment proved difficult due to the risks of repeated anesthetics and unknown drug efficacies. Marked proliferation of the mass was observed during estrus, and chemotherapy was repeated as an experimental treatment to slow tumor progression in order for the animal to remain in the species breeding program. Tumor proliferation was detected during the first trimester of pregnancy; however, in the lactation period, the mass became quiescent. No adverse reactions to chemotherapeutic drugs were observed and the animal continues to be monitored for tumor progression. This is the first report of an anaplastic sarcoma and of chemotherapy use in a pygmy hippopotamus and it highlights logistical considerations for treating neoplasia in this species.

  • 25-yr-old captive female pygmy hippopotamus (Choeropsis liberiensis)
  • Mass in oral cavity caudal to maxillary R canine tooth 🡪 anaplastic sarcoma of possible smooth or striated muscle origin
  • Treatment – ultimately unsuccessful:
    • Surgical excision
    • Intralesional chemotherapy with mitomycin C (0.4 mg/cm3 of tumor) and cisplatin (1 mg/cm3 of tumor)
      • Minimal systemic effects, including potential teratogenicity
      • Successful use in domestic animals
    • Recurred after multiple treatment attempts
  • Tumors reported in captive pygmy hippos - benign oral osteoma, lymphoblastic leukemia, and uterine leiomyoma, now anaplastic sarcoma
  • Marked growth of the anaplastic sarcoma during estrus and early pregnancy may reflect tumor sensitivity to both estrogen and progesterone
26
Q

A recent study described the treatment of idiopathic dermatitis in a Nile hippopotamus.

Describe the clinical signs associated with this case?

What organisms have been found in hippo derm cases?

How was this treated?

A

Helmick, K. E. (2017). Salt bath as a treatment for idiopathic dermatitis in captive nile hippopotamus (hippopotamus amphibius). Journal of Zoo and Wildlife Medicine, 48(3), 915-917.

Abstract: Ulcerative skin lesions were observed in two captive adult female hippos (Hippopotamus amphibius) from a zoological collection. Lesions appeared as cracking, peeling, or vesicles of the skin affecting the lateral and ventral aspects of the neck, limbs, thorax, and abdomen, dorsum, toes, and perineal region. Some lesions drained blood, serum, or purulent material. Histologic evaluation of sloughed skin consisted of deep dermal collagen with bacterial cellulitis and vasculitis and superficial fungal colonization. No viral pathogens were isolated and no fungal or bacterial pathogen predominated. Minimal response to systemic antibiotics and topical treatment was observed. Commercial cattle food-grade salt was added to the exhibit pool at 2–3 g/L with complete healing of all skin lesions within a 4-mo treatment period. No complications were observed. Patient compliance with salt bath therapy was higher and results more effective compared to topical and oral treatments.

  • Skin lesions first observed in March with recurrence of milder lesions in winter.
  • Cracking, peeling, vesicles progressed to sloughing, erythema, ulcerations.
  • Lethargy, depression, lameness, wt loss in affected hippos.
  • Appeared seasonally over 3 years.
  • Multiple cultures – mixed aerobic population, occ anaerobic or fungal elements.
  • Cytology, biopsy - bacterial cellulitis and vasculitis, superficial fungal dermatitis.
  • Tx – Variety topical antibacterial creams, rinses, sprays. TMS. Amoxicillin. Poor compliance. PB, sugar, pumpkin flavors preferred but skin lesions progressed.
    • Cattle food-grade salt added to exhibit pool beginning at 1ppt, increased to 3 ppt over 1 wk.
    • Dump-and-fill cleaning with re-addition of salt performed every other day.
    • After 30 days decreased to 2 ppt for additional 90 days.
    • Reduction in cost of salt and labor.
    • Symptoms resolved, salt bath continued for several weeks past skin healing.
    • Seasonal recurrence was noted for following years but not severe enough for tx.
  • Dermatitis in hippos:
    • Seasonal dermatitis observed in other captive hippos.
    • Streptococcal spp - significant cause of m+m in captive hippos.
      • Cellulitis, dermatitis, osteomyelitis, placentitis, mastitis, septicemia.
      • No predominant pathogens including strep ID in these cases.

Takeaway: Continuous topical salt bath effective tx for dermatitis in captive hippos, no adverse effects at 2-3 g/L (ppt) for 4 mos.