acute pancreatitis in slender-tailed meerkats (suricata suricatta)

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Acute Pancreatitis in Slender-Tailed Meerkats (Suricatasuricatta)Author(s): Lisa M. Naples, D.V.M., Claude Lacasse, D.V.M., Jennifer A.Landolfi, D.V.M., Dipl. A.C.V.P., Jennifer N. Langan, D.V.M., Dipl. A.C.Z.M.,Jörg M. Steiner, med. vet., Dr. med. vet., Ph.D., Dipl. A.C.V.I.M., Dipl.E.C.V.I.M.-C.A., Jan S. Suchodolski, med. vet., Dr. med. vet., Ph.D., andKathryn C. Gamble, D.V.M., M.S., Dipl. A.C.Z.M.Source: Journal of Zoo and Wildlife Medicine, 41(2):275-286. 2010.Published By: American Association of Zoo VeterinariansDOI: http://dx.doi.org/10.1638/2009-0011R2.1URL: http://www.bioone.org/doi/full/10.1638/2009-0011R2.1

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ACUTE PANCREATITIS IN SLENDER-TAILED MEERKATS

(SURICATA SURICATTA)

Lisa M. Naples, D.V.M., Claude Lacasse, D.V.M., Jennifer A. Landolfi, D.V.M., Dipl. A.C.V.P.,

Jennifer N. Langan, D.V.M., Dipl. A.C.Z.M., Jorg M. Steiner, med. vet., Dr. med. vet., Ph.D., Dipl.

A.C.V.I.M., Dipl. E.C.V.I.M.-C.A., Jan S. Suchodolski, med. vet., Dr. med. vet., Ph.D., and Kathryn C.

Gamble, D.V.M., M.S., Dipl. A.C.Z.M.

Abstract: Four adult, full-sibling slender-tailed meerkats (Suricata suricatta) were diagnosed with acute

pancreatitis. The incident case presented with lethargy, anorexia, abdominal guarding, and a cranial abdominal

mass. Serum was grossly lipemic, with elevated cholesterol and triglyceride concentrations and increased amylase

and lipase activity. An exploratory laparotomy confirmed chylous peritonitis and included excision of a saponified

spleno-duodenal mass, a partial pancreatectomy, and a splenectomy. Histopathology revealed severe, multifocal,

subacute necrotizing and granulomatous pancreatitis. Within 13 days of the incident case, the second meerkat was

identified with essentially identical clinical, surgical, and histologic findings. During subsequent physical

examinations of apparently unaffected cohorts (n 5 12), physical and hematologic findings suggestive of

pancreatitis were identified in the two remaining siblings of the first two cases. The definitive cause for these four

cases is undetermined; however, common risk factors identified were obesity and hyperlipidemia, a change to a

higher-fat diet, and genetic predisposition. To assess its usefulness in the diagnosis of meerkat pancreatitis, serum

canine and feline pancreatic lipase immunoreactivity (cPLI and fPLI) concentrations were measured in serum

samples (n 5 61) from two unrelated meerkat populations. Although these assays are highly sensitive and specific

for the diagnosis of pancreatitis in domestic carnivores, similar correlation was not apparent for meerkats. In

addition, hyperlipidemia was inconsistently present in many meerkats, with no apparent correlation to the

development of clinical illness. Based on these observations, sensitive and specific diagnostic tests for pancreatitis in

meerkats are currently unavailable.

Key words: Hyperlipidemia, meerkat, pancreatic lipase immunoreactivity, pancreatitis, Suricata suricatta.

INTRODUCTION

Pancreatitis is an inflammatory disorder of the

exocrine pancreas in which various stimuli induce

pancreatic autodigestion by prematurely activat-

ed digestive enzymes, followed by an inflamma-

tory reaction.17,19,25,26 The precise mechanisms that

initiate this cascade of reactions are unknown,

but suspected risk factors include a high-fat diet,

obesity, hyperlipidemia, trauma, cholangiohepa-

titis, hepatic lipidosis, neoplasia, infection, in-

flammatory bowel disease, diuretics, antibiotics,

and organophosphate insecticides and other

toxins.1,19,21,22,25,26 Pancreatitis can be categorized

as either acute or chronic and can range in

clinical presentation from asymptomatic to se-

vere, with the latter often being fatal due to

secondary development of shock, hypotension,

pulmonary edema, myocarditis, hepatic lipidosis,

peritonitis, disseminated intravascular coagula-

tion, or multi-organ failure after the systemic

release of vasoactive polypeptides.3,25,26 Patients

that recover from less-severe pancreatitis fre-

quently undergo relapse, or may develop second-

ary complications such as diabetes mellitus,

pancreatic pseudocysts, or exocrine pancreatic

insufficiency.25,26

Antemortem diagnosis of pancreatitis is chal-

lenging, as clinical signs for pancreatitis are often

nonspecific and, in some species, undetect-

able.6,8,9,17 Additionally, many exotic species mask

clinical illness as a defense mechanism, which can

result in marked disease progression prior to

diagnosis. In the past, several serum tests were

used for the diagnosis of pancreatitis in domestic

animals, including serum lipase and amylase

activity, and trypsinogen activation peptide and

From the Chicago Zoological and Aquatic Animal

Residency Program, University of Illinois, College of

Veterinary Medicine, Urbana, Illinois 61802, USA

(Naples); Lincoln Park Zoo, 2001 North Clark Street,

Chicago, Illinois 60614, USA (Gamble, Lacasse);

University of Illinois Zoological Pathology Program,

Loyola University Medical Center, Building 101, Room

0745, 2160 South First Avenue, Maywood, Illinois

60153, USA (Landolfi); College of Veterinary Medi-

cine, University of Illinois and the Chicago Zoological

Society, Brookfield Zoo, 3300 Golf Road, Brookfield,

Illinois 60513, USA (Langan); and the Gastrointestinal

Laboratory at Texas A&M University, College Station,

Texas 77843, USA (Steiner, Suchodolski). Present

addresses (Naples): the John G. Shedd Aquarium, 1200

S. Lake Shore Drive, Chicago, Illinois 60605, USA;

(Lacasse): Australia Zoo, Steve Irwin Way, Beerwah,

Queensland 4519, Australia. Correspondence should be

directed to: Dr. Naples (lnaples@sheddaquarium.

org).

Journal of Zoo and Wildlife Medicine 41(2): 275–286, 2010

Copyright 2010 by American Association of Zoo Veterinarians

275

trypsin-like immunoreactivity concentrations.

However, many studies that have focused on

these diagnostic tests have failed to demonstrate

a high sensitivity and specificity for pancreati-

tis.4–6,8,11,15,19,21,22,24,26 Pancreatic biopsy had previ-

ously been considered the most definitive diag-

nostic tool,19 although recent studies have shown

that pancreatic inflammation can be highly

localized, so accurate diagnosis based on a small

sample of the tissue can be difficult.14 Recently,

serum concentrations of pancreatic lipase immu-

noreactivity (PLI) have been shown to be highly

sensitive in patients with pancreatitis and highly

specific in healthy domestic cats (Felis catus) and

dogs (Canis lupus familiaris).5,20,21,23,27 Although

many sources of lipase synthesis and secretion

exist, true pancreatic lipase is solely synthesized

by pancreatic acinar cells. The PLI assays only

measure this serum concentration of pancreatic

lipase, unlike assays for lipase activity, which

potentially also measure extra-pancreatic sources

of lipolytic activity. Serum PLI concentration in

dogs has been shown to not be significantly

affected, clinically, by gastritis, renal failure, or

prednisone administration.19 However, PLI as-

says are species-specific, and tests designed for

species other than domestic felids and canids are

currently unavailable.

Although slender-tailed meerkats (Suricata

suricatta) are classified as carnivores, these

inhabitants of the African deserts typically

consume a predominantly insectivorous diet.

Natural diets, consisting of adult and larval

insects, centipedes, arachnids and, less so, small

rodents, reptiles, birds, eggs, fruit, and plant

matter, are difficult to mimic in the captive

setting. It has been speculated that these difficul-

ties, and the subsequent dietary imbalances, are a

potential cause of several clinical abnormalities

associated with the hyperlipidemia observed in

captive meerkats.2,18

Four cases of pancreatitis and hyperlipidemia

were diagnosed in a sibling cohort within a larger,

captive slender-tailed meerkat population (n 5

14). Although a definitive cause could not be

identified in these meerkats, a dietary etiology,

obesity, and familial relationship were considered

potential factors contributing to the development

of clinical illness.

CASE REPORTS

Dietary history

At the time of the first incident, the meerkat

population consisted of 14 meerkats of mixed, but

related, lineages. Due to the obesity observed in

several individuals, including the affected siblings

discussed in this case series at an age of 8 mo, the

initial diet base of Hills Science DietH Feline

Maintenance dry kibble (Hills Pet Nutrition Inc.,

Topeka, Kansas 66692, USA) was changed to

Hills Science DietH Feline Light dry kibble (Hills

Pet Nutrition Inc.). Based on manufacturer

average nutrient content, analysis revealed a

change from 7.5 to 10 gm/100 kcal for dietary

protein and 5.2 to 2.7 gm/100 kcal for dietary fat.

The meerkat population was maintained on this

second diet for 22 mo, with notable improvement

in body condition for multiple obese members of

the group. All meerkats had begun a gradual

transition to another diet 13 days prior to the first

case of pancreatitis, a diet primarily consisting of

MazuriH ferret chow (Purina Mills Inc., Saint

Louis, Missouri 63367, USA). Other diet items

were continued daily, as before, with limited

quantities of raw meat carnivore diet (Natural

Balance Pet Foods, Inc., Pacoima, California

91331, USA) and produce. Enrichment food

items offered every 48 hr included giant meal

worms, crickets, and egg whites, with monthly

offerings of neonatal mice and chicks, inverte-

brates, and vegetables. The commercial diet

change was done to improve the protein quality

of the ration. Although protein content (9.7 gm/

100 kcal protein) was similar to that of the Feline

Light diet, the fat content was increased to its

original point from 2.7 to 5.6 gm/100 kcal and

caloric intake density was increased from 3.2 to

4.2 kcal/gm metabolizable energy (ME). After

presentation of the second sibling meerkat, the

reduced fat diet was returned to the entire group.

Case 1

A 2.5-yr-old, neutered, female meerkat

(1.44 kg) presented with lethargy and partial

anorexia. The prior medical history of the patient

included hepatopathy and hypercholesterolemia,

first reported at 8 mo of age. Hepatic biopsy

performed at that time revealed moderate hepa-

tocellular hydropic change suggestive of a steroid

hepatopathy. No underlying etiology was appar-

ent. Chronic medical management had included

S-adenosylmethionine (DenosylH, 90 mg tablet,

Nutramax Laboratories, Edgewood, Maryland

21040, USA; 45 mg p.o., s.i.d.) and milk thistle

(10 mg/30 drops, Vitamin ShoppeH, North

Bergen, New Jersey 07047, USA; 15 mg p.o.

s.i.d.) as hepatoprotectants.

The meerkat was anesthetized via facemask

using isoflurane (Vet One, MWI, Meridian,

276 JOURNAL OF ZOO AND WILDLIFE MEDICINE

Idaho 83680, USA) in oxygen, 24 hr after the

onset of clinical signs. Physical examination

revealed an obese body condition with a palpably

taught, distended abdomen. Palpation revealed

splenomegaly, hepatomegaly, and a firm, irregu-

lar mass within the left cranial abdominal

quadrant adjacent to the spleen. A jugular venous

blood sample collected was visibly milky prior to

centrifugation, and the separated serum was

grossly lipemic. Hemogram revealed vacuolated

monocytes, toxic neutrophils, and a hematocrit in

the lower reference range. Serum analysis dem-

onstrated a marked elevation in serum cholesterol

and triglyceride concentrations and in amylase

and lipase activities (Table 1). Canine and feline

pancreatic lipase immunoreactivity concentra-

tions were measured, but were nondiagnostic at

this time in the presentation. Radiographs

revealed loss of abdominal visceral contrast and

a soft tissue mass effect in the left cranial

abdomen. Abdominal ultrasound revealed a mass

of mixed echogenicity (9 cm 3 2 cm) adjacent to

the spleen. An exploratory laparotomy was

performed.

The ventral abdomen was aseptically prepared

and then sharply incised for a ventral midline

surgical approach. Abdominal exploration re-

vealed a copious amount of chylous peritoneal

effusion. Fluid analysis revealed a specific gravity

of 1.033, a total protein of 5.7 mg/dl, cholesterol

of 567 mg/dl, and triglycerides of 433 mg/dl.

Continued exploration revealed an enlarged

hyperemic spleen displaced by a white, saponi-

fied, irregular, firm, 9-cm-diameter mass as

observed on radiographs (Fig. 1). A splenectomy

was performed using multiple ligatures with 3-0

polydioxanone (PDSII, Ethicon, Somerville, New

Jersey 08876, USA) and hemoclips (Versa-Clip,

Pitman-Moore Inc., Washington Crossing, New

Jersey 08560, USA) placed on splenic vessels. The

abdominal mass extended along the duodenum

and gastric pylorus, encompassing the left pan-

creatic lobe. Approximately 2 cm of the right

pancreatic lobe was visible and appeared grossly

Table 1. White blood cell counts and results of serum biochemical analyses of clinically affected meerkatsiblings (n 5 4) during pancreatitis case series.a

Test Case 1 Case 2 Case 3 Case 4b Case 4c ISIS no. ISIS mean 6 SD10

WBC 3 103 3.6 2.9 4.1 6.7 5.9 263 6.7 6 3.4

Total protein mg/dl NDd 6.8 7.5 7.7 6.1 209 6.6 6 0.9

Albumin mg/dl NDd 2.9 4.0 3.0 3.3 152 3.3 6 0.5

HCT % 34.0 37.0 35.0 39.0 28.0 266 41.0 6 6.2

Glucose mg/dl 67.0 80.0 218.0 91.0 97.0 215 122.0 6 33.0

BUN mg/dl 33.5 12.0 45.0 37.0 28.0 223 25.0 6 7.0

Creatinine mg/dl 0.6 0.6 1.1 1.1 1.3 196 0.9 6 0.3

Uric acid mg/dl 0.1 0.7 1.7 1.2 0.0 92 0.7 6 0.4

Phosphorus mg/dl 8.4 6.9 8.9 7.5 6.8 157 5.3 6 1.3

Potassium mEq/L 4.0 4.4 5.0 5.1 4.4 153 4.2 6 0.4

AST U/L 209.0 91.0 104.0 69.0 145.0 284 91.0 6 38.0

LDH U/L 679.0 961.0 503.0 390.0 401.0 79 623.0 6 215.0

ALP U/L 5.0 6.0 13.0 5.0 7.0 175 36.0 6 32.0

ALT U/L 240.0 134.0 288.0 99.0 151.0 216 104.0 6 62.0

GGT U/L 4.0 2.0 0.0 2.0 13.0 92 4.0 6 3.0

Total bilirubin mg/dl 0.1 0.3 0.2 0.0 0.0 187 0.3 6 0.2

Cholesterol mg/dl 831.0 1,026.0 1,013.0 656.0 670.0 150 369.0 6 139.0

Triglyceride mg/dl 529.0 1,258.0 1,582.0 NDd 83.0 73 41.0 6 33.0

Amylase U/L 1,492.0 1,157.0 543.0 NDd 1,061.0 82 552.0 6 330.0

Lipase U/L 827.0 795.0 402.0 NDd 357.0 34 81.0 6 63.0

CK U/L 309.0 67.0 29.0 110.0 78.0 122 350.0 6 307.0

Calcium mg/dl 8.7 8.7 10.5 10.5 9.7 182 9.7 6 0.9

Sodium mEq/L 141.0 139.0 135.0 144.0 138.0 154 149 6 5.0

Chloride mEq/L 109.0 105.0 101.0 114.0 109.0 145 114 6 7.0

a All values represent blood values during first signs of clinical illness, with the exception of the column labeled Case 4b. Bolded

values represent results greater than 2 SD from the ISIS mean in 2007.b Case 4 5 blood collected prior to clinical illness during group examinations 13 days after Case 2 became ill.c Case 4 5 blood collected during clinical illness approximately 2 wk after sample displayed in the Case 4b column.d ND 5 not done.

NAPLES ET AL.—PANCREATITIS IN SLENDER-TAILED MEERKATS 277

normal. Excision of the abdominal mass was

performed via sharp dissection, after placement

of serial linear hemoclips parallel to the adjacent

affected duodenal tissue and perpendicular to the

healthy pancreatic tissue. Due to the intimate

communication with the duodenum and the

gastric pylorus, a portion of the mass (2 cm)

was not excised. The right hepatic lobe was

biopsied using hemoclips. The abdomen was

lavaged with warmed, sterile saline multiple times

until evacuated fluid was visibly clear.

All excised and biopsied tissues were sampled

for aerobic bacterial culture; impression smears

were also prepared prior to placement in 10%

neutral-buffered formalin. Histologically, the

biopsied saponified mass was pancreatic tissue.

Within submitted sections, approximately 60% of

the pancreatic parenchyma was distorted by

multiple, large, coalescing, pale eosinophilic and

smudged areas, with loss of individual cellular

detail, and karyolysis or karyorrhexis (necrosis).

Necrotic regions frequently contained moderate

to large amounts of eosinophilic fibrillar to

amorphous material (fibrin), numerous degener-

ate neutrophils, and macrophages. Necrosis and

inflammation extended into the adjacent mesen-

teric adipose tissue. Multifocally, pancreatic

interstitial collagen fibers and remaining acini

were separated by large amounts of clear space

and pale eosinophilic homogenous proteinic

material (edema). Pancreatic lobules were widely

separated by necrotic debris and edema. Remain-

ing acinar cells ranged from swollen, with

vacuolated cytoplasm lacking zymogen granuoles

(degeneration), to attenuated, with large vesicular

nuclei and moderate anisokaryosis (regeneration;

Fig. 2). Biopsied sections of liver contained

hepatocellular hydrophic change, lipid deposi-

tion, and multifocal edema.

Intra-operative care included intravenous flu-

ids (LRS, Hospira Inc., Lake Forest, Illinois

60045, USA; 65 ml i.v.), buprenorphine (Bupre-

nex, 0.3 mg/ml, Hospira Inc., 0.028 mg s.c.),

flunixin meglumine (PrevailTM, 50 mg/ml, MWI,

Meridian, Idaho 83680, USA; 1.4 mg i.v.),

famotidine (10 mg/ml, Wockhardt USA Inc.,

Bedminster, New Jersey 07921, USA; 0.7 mg

s.c.), and enrofloxacin (Baytril 100, 100 mg/ml,

Bayer Healthcare, Shawnee Mission, Kansas

66201, USA; 7 mg s.c.). Management of the

patient continued postoperatively with buprenor-

phine (0.028 mg s.c. b.i.d. for 14 days), enro-

floxacin (7 mg s.c. s.i.d for 14 days), LRS (80 ml

s.c. s.i.d for 7 days), milk thistle (20 mg p.o. s.i.d

14 days), and famotidine (0.7 mg p.o. s.i.d for

7 days). S-adenosylmethionine (45 mg p.o. s.i.d)

was continued for hepatic disease, as had been

prescribed prior to pancreatitis. Similar to the

management of domestic pancreatitis cases, oral

alimentation was withheld for 48 hr postopera-

tively. Due to the possible negative social

implications of isolation, this meerkat was

reintroduced to cohorts within 1 wk, and it was

not feasible to continue additional diet restric-

tions.

Figure 1. Intra-operative gross image of abdominal

viscera of a slender-tailed meerkat (Suricata suricatta)

(Case 1) with pancreatitis during exploratory surgery:

A. Saponified mass. B. Spleen. C. Pancreas.

Figure 2. Photomicrograph of a slender-tailed

meerkat (Suricata suricatta) (Case 1) pancreas and

adjacent tissue. Pancreatic lobules (PL) are separated

and distorted by edema and fibrinosuppurative inflam-

mation (I). Adjacent mesenteric adipose (MA) is

necrotic. H&E stain, 3200.


By day 5 after surgery, the meerkat had

recovered clinically, although serial postsurgical

serum biochemical analysis on days 7, 25, and 43

revealed continued increases in serum cholesterol,

triglyceride, and blood urea nitrogen concentra-

tions as well as low-density lipoprotein and lipase

activities. On day 43 after surgery, the meerkat

showed bilateral, rigid hind-limb paresis and

ataxia. The meerkat was anesthetized as previ-

ously described. A hemogram revealed a leuko-

cytosis (15.58 3 103/ml).10 A serum chemistry

profile revealed hyperglycemia (472 mg/dl) and

an elevated alanine aminotransferase (428 U/L).

Although ketoacidosis was not identified on a

performed serum ketone test, a diabetic compli-

cation was suspected; therefore, insulin (Humulin

N, 100 U/ml, Eli Lilly & Co., Indianapolis,

Indiana 46285, USA; 0.28 IU i.m.) was admin-

istered presumptively. Based on chronic and

acute pathologic evidence of hepatic insult,

hepatic encephalopathy was under consideration,

as were secondary shock and lipid embolism, for

an underlying etiology of the neurologic signs.

Therefore, Normosol R (Hospira; 90 ml i.v.),

enrofloxacin (7 mg s.c.), famotidine (0.7 mg s.c.)

and lactulose (10 g/15 ml, Apotex Corp Inc.,

Toronto, Ontario Canada; 0.5 ml p.o.) were

administered. Shortly after recovery from anes-

thesia, the meerkat became obtunded, with pallid

mucous membranes and dyspnea. The animal

went into respiratory arrest and resuscitation was

unsuccessful.

Representative samples of all tissues were

collected postmortem, fixed in 10% neutral

buffered formalin, routinely processed, and

sectioned at 5 mm for light microscopy evalua-

tion. Marked postmortem histopathologic ab-

normalities were lacking. Hepatocellular hydrop-

ic degeneration, suggestive of hepatic insult, was

present. Mild focal chronic mesenteric adipose

necrosis was also noted and considered likely

related to previous pancreatitis. The remaining

pancreas was histologically normal.

Case 2

A 2.5-yr-old, intact, male, (1.4 kg) full-sibling

to the first ill meerkat was found with acute

depression and lethargy 13 days after Case 1. The

meerkat was anesthetized as described for Case 1.

Physical examination of the meerkat revealed

essentially identical findings to Case 1, as did

serum chemistry analysis (Table 1). Gross exam-

ination of a jugular venous serum sample

demonstrated severe lipemia. Radiographs re-

vealed loss of visceral abdominal detail and a

right lateral shift of intestinal gas pattern.

Abdominal ultrasound revealed a mixed hepatic

echogenicity with a mixed-echogenic mass (4 cm

diameter) adjacent to the spleen. Based on these

clinical findings, pancreatitis was suspected. Due

to the clinical presentation of this animal and its

sibling, and to ultrasonographic findings, a

surgical exploration was elected.

Surgical evaluation of the abdominal viscera

was almost identical to that of the first meer-

kat, with the exception of an apparent invasion

of the spleen by a saponified abdominal mass

(3 cm 3 6 cm) that encompassed the left

pancreatic limb and was adhered to the duode-

num. The spleen was enlarged and hyperemic,

and portions of the mass obscured several large

splenic vessels. Splenectomy, mass excision,

hepatic biopsy, and intraoperative surgical man-

agement were performed as described for Case 1.

Postoperative care and management of the

pancreatitis was employed as for Case 1, with

the exception of a transdermal fentanyl patch

that was applied with 50% skin contact for a 72-

hr postoperative period (25 mcg/hr patch, Jans-

sen Pharmaceutical Products, Titusville, New

Jersey 08560, USA).

The biopsied saponified mass was confirmed

histologically to be pancreatic tissue. Severe,

multifocal to coalescing, subacute, necrotizing

and granulomatous pancreatitis, with regional,

necrotizing, pyogranulomatous mesenteric steati-

tis and peritonitis, were noted, similar to Case 1.

Hepatic biopsy revealed mild hepatic canalicular

bile stasis. Splenic biopsy revealed moderate

congestion.

This meerkat developed lethargy and depres-

sion at 168 days following initial evaluation. On

physical examination, a firm, distended abdomen

with firm, dilated caudal abdominal intestinal

loops was palpated. Anesthesia was performed as

previously described. Abdominal radiographs

revealed a large, impacted colon. A soapy,

warm-water enema was performed and intrave-

nous fluids were administered for treatment of

secondary dehydration. The meerkat was found

dead approximately 16 hr after recovery from

anesthesia.

Postmortem histopathologic changes included

diffuse necrosuppurative colitis, multifocal sup-

purative cholecystitis, and multifocal hepatocel-

lular necrosis with cannicular and ductal bile

stasis. Bronchial and bronchiolar foreign materi-

al, with mild suppurative pneumonia, was sug-

gestive of perimortem aspiration. The remaining

pancreas was histologically normal.


Case 3

Due to the acute presentation of the two

sibling meerkats, described after a dietary change,

the remaining 12 meerkats in the colony were

anesthetized for examination 13 days following

surgical evaluation of Case 2. Anesthesia was

performed on all animals as previously described.

A third full-sibling to the Case 1 and 2 meerkats,

a 2.5-yr-old, intact male (1.4 kg), had a previous

history of obesity, hypercholesterolemia, and

hepatomegaly. Similar to Case 1, hepatic biopsy

had revealed a nonspecific hepatopathy which

had been managed medically. Current physical

examination revealed essentially identical physi-

cal findings to Case 1. Although no abdominal

mass was palpated, splenomegaly was noted.

Gross examination of a jugular venous blood

sample demonstrated severe lipemia. Serum

chemistry analysis suggested acute pancreatitis

(Table 1). Radiographs revealed a loss of visceral

abdominal detail and an enlarged hepatic silhou-

ette. Ultrasonography revealed a mixed echoge-

nicity of the liver and the spleen. Based on the

previous medical history, and similar clinical

findings in the prior two cases, surgical explora-

tion was performed.

A laparotomy was performed as previously

described. Abdominal viscera and omentum were

covered with small amounts of white saponified

fluid, but unlike the prior two cases, minimal

chylous effusion was identified. Further explora-

tion revealed an enlarged hyperemic spleen torsed

approximately 90 degrees. White, saponified

material was identified overlying the mesenteric

border of the proximal duodenum, and was more

intimately involved with the proximal duodenum

than in the previous two cases, so it was not

excised. Splenectomy was performed as in the

first two cases. The left pancreatic lobe was

grossly enlarged, engorged, and dissected for

incisional biopsy. Hepatomegaly with a pale

capsular surface was noted, so a left lateral

hepatic lobe biopsy was performed using hemo-

clips. Intraoperative and postoperative care was

performed as for Case 2.

Histologically, within biopsied sections of

pancreas, acini were widely spaced or absent.

Intervening spaces contained small amounts of

hypocellular, loose, collagen-poor fibrous con-

nective tissue (fibrosis). Hepatic biopsy re-

vealed diffuse, moderate hepatocellular hydropic

change.

Analysis of serial serum samples collected at 1,

1.5, 2.5, 4.5, 7, 7.5, and 8.5 mo postoperatively

revealed persistent increases of serum concentra-

tions of cholesterol and triglycerides, as well as

serum lipase and amylase activities. However,

after the surgical procedure, only infrequent,

brief episodes of mild depression and partial

anorexia were observed. Each of these presenta-

tions resolved quickly with twice daily adminis-

tration of oral buprenorphine (0.028 mg s.c.).

Case 4

The last of the four 2.5-yr-old full-siblings, an

intact (1.4 kg) male, had shown no clinical signs

prior to the date of group physical examinations.

This meerkat also underwent physical examina-

tion with the entire meerkat population 39 days

after the initiation of the diet containing a higher

fat content. Unlike Cases 1 and 3, this individual

had no prior history of hepatic disease or

hypercholesterolemia. On examination, the ani-

mal was obese, but unlike the other cases, showed

no abnormalities in abdominal palpation, radio-

graphs, or ultrasound. A blood sample collected

from the jugular vein, which was grossly lipemic,

was submitted for complete blood count and

serum chemistry analysis. The hemogram was

within the International Species Inventory Sys-

tem (ISIS) reference range for this species.10

However, serum chemistry analysis revealed

hypercholesterolemia. Serum amylase and lipase

activities, and serum triglyceride concentration

were, unfortunately, not measured due to a

laboratory error.

Thirteen days following anesthesia, this meer-

kat presented with vomiting and partial anorexia.

Due to the history of the other siblings, the

meerkat was anesthetized for examination, as

before. Transabdominal palpation revealed

splenomegaly. Abdominal ultrasound was unre-

markable. A serum sample collected was again

grossly lipemic. Due to lack of evidence support-

ing ascites or an abdominal mass, exploratory

surgery was not performed. However, the meer-

kat was treated for presumptive acute pancreati-

tis with supportive care similar to the first three

cases. Despite resolution of vomiting shortly after

treatment initiation, analysis of the second serum

chemistry revealed results similar to the three full-

siblings diagnosed with, or suspected of having,

pancreatitis (Table 1). Medical management of

the presumptive pancreatitis continued with

subcutaneous fluids (LRS 65 ml, s.c., b.i.d. for

7 days), buprenorphine (0.028 mg p.o. b.i.d. for

14 days), famotidine (0.7 mg p.o., s.i.d. for

7 days), and enrofloxacin (7 mg s.c. s.i.d. for

14 days). Due to the possible negative social


implications of isolation from cohorts, this

meerkat was left with the population throughout

the treatment period. As such, the common

practice of withholding oral alimentation while

the pancreas is allowed to heal was not feasible.

Still, vomiting did not recur during the treatment

period. Although serial venous blood samples

submitted at regular intervals after the presenta-

tion of Case 1 revealed elevations in serum

amylase and lipase activities, further episodes of

clinical signs of pancreatitis or gastrointestinal

abnormalities did not develop. Long-term med-

ical management was not needed.

Serum PLI testing

When pancreatitis was first suspected, canine

and feline pancreatic lipase immunoreactivity

(cPLI and fPLI, respectively) assays were per-

formed on serum from the meerkat in Case 1 by

the Gastrointestinal Laboratory of Texas A&M

University (College Station, Texas 77843, USA).

Canine pancreatic lipase immunoreactivity, as

measured by Spec cPLTM (Idexx Laboratories,

Portland, Maine), was 29 mg/L (reference range:

0–200 mg/L, Texas A&M University). Feline

pancreatic lipase immunoreactivity was 14 mg/L

(reference range: 2.0–6.8 mg/L, Texas A&M

University). As the clinical validity of these

assays in exotic carnivores was questionable,

further evaluation of these tests were performed.

Assays of cPLI and fPLI were performed on

serum samples from two distinct populations of

meerkats. The first group (group 1) consisted of

all meerkats in the incident collection at the time

of illness (n 5 14). The second group (group 2) of

individuals tested included meerkats housed for

the entirety of their lives in unrelated collections

(n 5 11). Serum samples (n 5 61) were submitted

and included samples acquired prior to, and

within, 1 yr of the occurrence of pancreatitis in

group 1. All samples were submitted frozen,

thawed for analysis, then analyzed with both a

radioimmunoassay for the measurement of fPLI

and an enzyme-linked immunosorbent assay for

cPL (Spec cPLTM, Idexx Laboratories) using

methods previously described.21,23 In addition to

the PLI testing, serum from both groups was

submitted for chemistry profiles with a focus on

identification of hyperlipidemia (Table 2).

The serum cPL concentration was ,30 and

considered by the laboratory to be at undetect-

able levels in all but four samples. Of the four

samples in which it was detectable, only one was

clinically ill (Case 2), and the value obtained

(38 mg/L) was well within the reference range for

domestic canines. Of the samples that were

analyzed with the fPLI assay, samples that

demonstrated higher values were diluted by a

factor of 10 and retested. However, these

dilutions did not show linearity. Results ranged

from 2.9–28.2 mg/L. Due to this fact, cPLI and

fPLI testing results in meerkats from all popula-

tions were considered nondiagnostic, or spurious,

respectively (Table 3).

DISCUSSION

In dogs and cats, many conditions and

metabolic disturbances have been associated

with a risk of pancreatitis.1,3,17,19,22,26 Bacterial

infection, which is rarely present in small animal

patients with pancreatitis,3,26 was not identified in

any of the four meerkat cases. Although hepatic

abnormalities were diagnosed prior to clinical

presentation for pancreatitis in Cases 1 and 3,

lesions were mild and nonspecific. In addition,

because no documentation of previous pancrea-

titis existed, it is also unknown if the hepatic

abnormalities had a causal relationship with

pancreatitis.

The acute onset of illness after diet alterations

suggests nutrition as the inciting cause of

pancreatitis in these meerkats. Nutritional causes

for this presentation were coincident with clinical

onset of the disease but, without complete

nutrient analysis of those food items, a clear

correlation between diet and pancreatitis is not

possible. Although complete feeds utilized in the

diets are evaluated by their manufacturers,

complete nutritional analysis of those products

may be helpful to fully implicate nutrition as a

cause for the onset of pancreatitis. Comparison

of the ferret chow, introduced prior to illness,

with the later light feline chow diet demonstrated

comparable complex-protein contents, but a

much-higher fat content and caloric intake

density. High fat or inappropriate diets have

been reported as a common cause of pancreatitis

in domestic canines.12,19,26 Research in domestic

canids suggests that abnormal diets not only

cause pancreatitis but may also influence severity

of disease.12 As is evident with the surgical

exploration findings, this etiology was most likely

the case with the meerkats. Dietary indiscretion

more commonly incites acute episodes after

abrupt changes in diet, such as consumption of

garbage or table scraps. Interestingly, in this case,

the meerkat diet change was a gradual transition,

and all affected meerkats did not present

simultaneously. As hyperlipidemia and obesity

were present historically within this collection,


the transition, even though slower, may still have

been sufficient to produce an acute presentation.

As only four of the fourteen meerkats became

clinically ill despite this group history, other

factors, in addition to diet, likely contributed to

the onset of pancreatitis. The four affected

meerkats were full siblings of a single litter, with

a variable genetic association to the other

meerkats in the collection. As some breed

predilection is seen with canine pancreatitis,3,25,26

genetics may have contributed to the develop-

ment of pancreatitis in these individuals.

Table 2. Serum biochemistry values commonly associated with pancreatitis, which were analyzed inconjunction with cPLI and fPLI on Suricata suricatta (n 5 61). Samples were collected prior to, and following,the case series of pancreatitis over a 3-yr period. Representative values from individuals with, and without, clinicalillness are listed below. Group 1 refers to meerkats in the incident collection and group 2 refers to meerkats housedin an unrelated collection.a

Meerkat cohortgroup

Clinically affectedYes/No

Cholesterolmg/dl

Triglyceridemg/dl

AmylaseU/L

LipaseU/L

Meerkat reference NAb 369 6 139 SD 41 6 33 SD 552 6 330 SD 81 6 63 SD

Group 1 Yesc 831 529 1,492 827

Group 1 Yesd 600 906 533 330

Group 1 Yese 1,013 1,582 543 402

Group 1 Yese 945 3,660 457 260

Group 1 Yese 1,104 9,643 413 315

Group 1 Yese 1,004 2,217 831 853

Group 1 Yese 1,164 8,960 392 336

Group 1 Yesf 577 2,101 534 155

Group 1 Yesf 471 1,877 368 211

Group 1 Yesf 452 1,943 313 159

Group 1 No 377 71 NDg NDg

Group 1 No 512 530 503 132

Group 1 No 676 1,212 551 155

Group 1 No 783 811 298 181

Group 1 No 438 129 1,226 70

Group 1 No 285 42 426 59

Group 1 No 380 53 895 117

Group 1 No 423 57 NDg NDg

Group 1 No 299 49 642 147

Group 1 No 423 31 861 53

Group 1 No 676 1,212 551 155

Group 1 No 405 40 337 126

Group 1 No 390 38 330 92

Group 1 No 392 22 248 48

Group 1 No 430 45 443 80

Group 2 No 297 73 1,206 329

Group 2 No 340 82 511 154

Group 2 No 311 48 657 100

Group 2 No 309 25 1,191 65

Group 2 No 304 917 888 229

Group 2 No 238 38 1,194 106

Group 2 No 297 12 986 95

Group 2 No 307 9 810 245

Group 2 No 437 9 769 208

Group 2 No 269 9 905 168

Group 2 No 2,112 9 1,300 192

a Bolded values represent values greater than 2 SD from the ISIS mean in 2007.b NA 5 not applicable.c Case 1.d Case 2.e Case 3.f Case 4.g ND 5 not done.


Hyperlipidemia is commonly associated with

pancreatitis in dogs and humans and was seen in

many of these meerkats.4,8,17,25,26 Whether pancre-

atitis is a sequela to, or a cause of, hyperlipidemia

as a result of fat necrosis is unknown.25,26 It is

hypothesized that elevated serum triglycerides

can cause overstimulation of pancreatic lipases,

which then produce fatty acids which are toxic to

the pancreatic tissue.16,19,25 The clinically ill

meerkats had elevations during the acute phase

of illness and during subsequent serial analysis of

blood chemistry profiles following diet changes

back to a lower fat content. Furthermore,

hyperlipidemia was observed randomly in several

of the unaffected meerkats (Table 2). In some

cases, cholesterol and triglyceride concentrations

had exponentially increased between samplings

long after clinical illness, e.g., Case 3 serum

triglyceride concentration 8 mo postoperatively:

8,960 mg/dl. Thus, even without the development

of pancreatitis, hypertriglyceridemia is a problem

which can lead to a variety of other life-

threatening clinical illnesses in this captive

population.2,18 Although infrequently reported in

meerkats suffering fatal illness such as central

nervous system cholesterol granulomas,2,13,18 the

incidence of hyperlipidemia in captive and wild

meerkats is most likely underreported. Fatal,

Table 3. Canine pancreatic lipase immunoreactivity (cPLI) concentration (as measured by Spec cPL) and felinepancreatic lipase immunoreactivity (fPLI) concentration on Suricata suricatta (n 5 61). Group 1 representsmeerkats housed in the incident collection (n 5 14). Group 2 represents individuals housed in an unrelatedcollection (n 5 11). Samples were collected prior to, and following, the case series of pancreatitis over a 3-yr period.Representative samples from individuals with, and without, pancreatitis or hyperlipidemia are listed. The cPLI andfPLI testing results from all individuals were considered nondiagnostic or spurious, respectively, and demonstratedno correlation with any serum markers for pancreatitis or hyperlipidemia.a

Meerkat cohort group Clinically affected Yes/No cPLI mg/L fPLI mg/L Hyperlipidemia Yes/No

Reference values for canines NAb 0–200 NAb NAb

Reference values for felines NAb NAb 2.0–6.8c NAb

Reference values for meerkats NAb NAb NAb NAb

Group 1 Yesd 29 14 Yes

Group 1 Yese 38 QNSf Yes

Group 1 Yesg 29 7.5 Yes

Group 1 Yesh 29 9.9 Yes

Group 1 No 45 2.9 No

Group 1 No 29 4.6 Yes






Group 1 No 29 6.7 Yes





Group 2 No ,30 6.7 NDi

Group 2 No ,30 6.6 No



Group 2 No ,30 2.9 Yes


a Hyperlipidemia was defined by serum cholesterol or triglyceride values greater than 2 SD from the ISIS mean for Suricata

suricatta in 2007.b NA 5 not applicable.c Gastrointestinal Laboratory, Texas A&M University.d Case 1.e Case 2.f QNS 5 quantity not sufficient.g Case 3.h Case 4.i ND 5 not done.


postoperative illnesses developed in two of the

affected meerkats. Early diagnosis and manage-

ment of pancreatitis, or more specifically hyper-

lipidemia, may reduce the risk of similar, life-

threatening complications in other animals.

Acute pancreatitis is a therapeutic challenge for

many reasons in domestic species, and similarly

in meerkats. For example, one important com-

ponent of supportive care is pain management.26

In domestic species, continuous administration of

opioids is often employed. Although difficult to

perform with meerkats, both intramuscular

injection of buprenorphine and transdermal

administration of fentanyl were used. Neither

the half-life nor the efficacy of these drugs is

established for this species, but use of these

medications subjectively appeared to be effective

in all four individuals. In domestic species, mild

to moderate pancreatitis, whether chronic or

recurrent, may persist despite medical treatment

choices.25 This presentation is suspected to be the

case for the two surviving meerkats (Cases 3 and

4) but is speculative based on the lack of

confirmation of relapsing or chronic pancreatitis.

Regardless of the challenges, medical manage-

ment is still the preferred treatment for pancre-

atitis. In domestic species, surgical intervention is

commonly reserved for patients with ascites or

visible abdominal masses.17,25,26 The identification

of these findings in both Cases 1 and 2 was the

impetus for surgical exploration. Case 3 was

surgically explored based on evidence of effusion,

past medical history, and current group presen-

tation. A prognosis for pancreatitis in meerkats is

unknown, so it is uncertain why the first two

meerkats did not survive longer than 6.5 mo after

clinical presentation.

Diabetes mellitus is one of the life-threatening

illnesses reported to develop secondary to pan-

creatitis,26 and in the death of Case 1, was an

important differential for the noted hyperglyce-

mia. Although postmortem histopathology of the

remaining pancreas did not reveal any lesions, a

lack of histologic signs is not uncommon for

diabetes mellitus in other species, and so, does

not rule out functional abnormalities. Although

surgery was a common thread, it is less likely that

it affected prognosis. Case 3 also underwent

surgery with a good outcome. Both currently

surviving animals were treated prior to the

development of clinical illness, which may have

influenced prognosis. In addition, histopathology

for Case 3 was most compatible with the chronic

or suppurative pancreatitis seen in domestic

felids.9 The time course of the disease may also

have contributed to survival. At necropsy, neither

Case 1 nor Case 2 had evidence of peritonitis or

inflammation in the remaining pancreatic tissue,

a finding which may exemplify successful surgical

and postoperative medical management. This

consideration also demonstrates the need for

accurate and early diagnosis of pancreatitis prior

to the development of secondary, life-threatening

disease.

Prevalence of pancreatitis is unknown for

domestics, primarily due to poor diagnostic

tools.6,8,9,17,19 Similarly, the prevalence of pancre-

atitis in both captive and wild meerkats has not

been identified. Only two of the four affected

meerkats demonstrated vague clinical signs,

potentially attributable to a number of disorders.

As with domestics, serum markers for pancrea-

titis, such as amylase and lipase activities, were

found to be poorly sensitive and specific for this

meerkat population.4–6,11,19,20,24,26 Serum cholester-

ol was also an unreliable disease marker, as it was

randomly elevated in apparently healthy individ-

uals (Table 2). Wild meerkat serum cholesterol

concentrations have been assessed as similar to

domestic canine reference values10 and, as com-

pared to captive meerkat populations in 2007,

mean cholesterol concentrations were substan-

tially lower by standard deviation (M. Waters,

unpubl. data). Thus, reference values currently

considered typical for captive meerkats do not

accurately represent healthy values for this

species. It has been hypothesized that higher

serum concentrations of cholesterol in captive

meerkats is an effect of unconventional diets in

captive situations, which causes a continuous

elevation sufficient for clinical illness. Further

investigation into serum cholesterol and triglyc-

eride concentrations, and in liver enzyme activ-

ities, in wild meerkats would be beneficial for the

establishment of appropriate reference ranges

and for the analysis of captive population health.

Serum canine and feline PLI concentrations,

although highly sensitive and specific for the

diagnosis of pancreatitis in domestic dogs and

cats,5,11,20,21,23,27 did not appear to be cross-reactive

in meerkats and were, thus, determined not

clinically useful in this species. Sensitive and

specific diagnostic tests for pancreatitis in meer-

kats are currently unavailable. In addition, the

data from this case series is highly suggestive that

these tests would not be sensitive or specific for

other exotic carnivore species.

Regardless of the underlying cause of pancre-

atitis in these four meerkats, the true prevalence

of hyperlipidemia in captive meerkats, and its


effect on animal health, is unknown. Although

not definitively associated with diet, if meerkats

are presumably similar to domestic carnivores,

hypercholesterolemia is most likely diet induced.

Currently, suggested daily dietary fat content for

meerkats is based on domestic carnivore refer-

ence values, as species-specific guidelines are

unknown. The identification of a proper diet,

and tracking of the impact of diet in captive

meerkats, is therefore extremely important. Pre-

liminary use of insectivore commercial diets in

captive meerkats was useful for weight reduction

in several obese individuals, and it mildly

improved hyperlipidemia.7 Further investigation

of its usefulness in countering captive meerkat

obesity is needed. Until the time a proper captive

meerkat diet has been identified, dietary fat

should be cautiously considered and regulated.

Acknowledgments: The authors thank Dr.

Michael Kinsel and the University of Illinois

Zoological Pathology Program, Lincoln Park

Zoo department of animal care, specifically Jill

Gossett; and the department of veterinary

medicine, specifically Dr. Tawnia Zollinger, John

Pauley CVT, Katrina Scott CVT, and Joel Pond

CVT for their dedication to the health of the

animals in their care; and Sara Reed for her

extensive help with the Texas A&M Gastrointes-

tinal Diagnostic Laboratory.

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Received for publication 21 January 2009


acute pancreatitis in slender-tailed meerkats (suricata suricatta)

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