ABSTRACT
Tsuchitani and Narama 1988, 439-444; Chandler and McClure 1982, 171-180; Doepel, Anver, and Hofing 1980, 505508; Rosenberg, Anderson, and Henrickson 1979, 988-989)
a. Definition: the inflammation of the pancreas (acute or chronic)
b. Causes/pathophysiology: idiopathic, gallstones, ethanol, trauma, steroids, autoimmune, scorpion sting, hypercalcemia, hypertriglyceridemia, hypothermia, drugs (diuretics, azothioprine), pregnancy, irritation during surgery
c. Clinical signs: none, severe upper abdominal pain, nausea and vomiting, ± elevated blood pressure, elevated respiratory rate, elevated heart rate, ileus, subclinical
d. Physical examination/diagnostics: abdominal pain, serum lipase ± amylase more than three times the upper limit of normal
e. Differential diagnoses: liver abnormalities/failure, intussusceptions, strangulated loops of intestines
f. Treatment: supportive care (pain relief; fluid replacement with appropriate electrolyte supplementation; limit oral intake, especially that containing fat)
g. Prevention: none
h. Species differences: macaque, squirrel monkey, baboon
167-170; Sa-Nguanmoo et al. 2009, 73-82; Arankalle and Ramakrishnan 2009, 214-218; Arankalle, Goverdhan, and Banerjee 1994, 125-129; Lanford, Chavez, Barrera, et al. 2003, 7814-7819; Lanford, Chavez, Notvall, et al. 2003, 72-80; Robertson 2001, 233-242; Slighter et al. 1988, 73-81; Montali et al. 1989, 759-765; Lemon et al. 1982, 25-36; Shevtsova et al. 1988, 177-194; Williams-Blangero et al. 1996, 26-30; Burke and Heisey 1984, 940-944; Lankas and Jensen 1987, 340-344; Brown, Jansen, and Lemon 1989, 4932-4937; Eichburg 1980, 541-543)
a. Definition: inflammation of the liver (acute or chronic)
b. Causes/pathophysiology: bacterial, viral (hepatitis A, B, C, D, E, G, TT; callitrichid hepatitis due to lymphocytic choriomeningitis virus in callitrichids and owl monkeys; GBA-A-like flavivirus of tamarins), parasitic (schistosomiasis, trematodiasis, toxoplasma, leptospira), or fungal
c. Clinical signs: none, anorexia, depression, lethargy, fever, vomiting, diarrhea, jaundice
d. Physical examination/diagnosis: based on clinical signs, physical examination, increased liver enzymes
e. Differential diagnoses: hepatic lipidosis, hepatic amyloidosis
f. Treatment: supportive therapy (fluids, pain medication), antibiotics or antiinflammatories if appropriate
g. Prevention: none
h. Species differences: chimpanzee, orangutan, gorilla, gibbon, baboon, macaque, African green monkey, langur, woolly monkey, tamarin, marmoset, owl monkey
2. Hepatic lipidosis (Wolfe-Coote 2005, 621; Christe and Valverde 1999, 12-15; Gliatto and Bronson 1993, 198-202; LaberLaird, Jokinen, and Lehner 1987, 205-209; Bronson et al. 1982, 187-192)
a. Definition: accumulation of lipid within the cytoplasm of the hepatocytes
b. Causes/pathophysiology: rapid weight loss causing a negative energy balance
c. Clinical signs: anorexia, lethargy, weight loss, depression, sudden death
d. Physical examination/diagnosis: clinical signs, physical examination, history (rapid weight loss in an obese animal), laboratory results; ultrasonography reveals a diffuse increased echogenicity, but definitive diagnosis is only made by histopathologic examination of a liver biopsy
e. Differential diagnoses: hepatitis, hepatic amyloidosis
f. Treatment: early diagnosis and aggressive nutritional support to reverse the negative energy balance; if persistent anorexia, force-feed to meet daily caloric requirements; otherwise, consider a PEG (percutaneous endoscopic gastrostomy) tube for long-term nutritional support
g. Prevention: ensure animals do not go 3 days without nutritional intake to prevent negative energy balance
h. Species differences: macaque, African green monkey
3. Hepatic amyloidosis (MacGuire et al. 2009, 168-173; Hukkanen et al. 2006, 119-127; Naumenko and Krylova 2003, 92-95; Hubbard et al. 2001, 260-267; Hubbard et al. 2002, 84-90; Arslan, Nisbet, and Guvenc 2007, 655-659)
a. Definition: tissue deposition of insoluble protein fibrils in a beta sheet configuration; amyloid is most frequently found in the GI tract, liver, spleen, and occasionally kidney
b. Causes/pathophysiology: usually secondary to chronic inflammation (seen with enterocolitis, osteoarthritis, chronic valvular catheterization, and type D retrovirus)
c. Clinical signs: related to the organs involved and extent of the deposition; include weight loss, diarrhea, thickened bowel, hepatomegaly, splenomegaly, enlarged kidneys, poor body condition, sparse hair coat
d. Physical examination/diagnosis: based on clinical signs, physical examination, lab results; ultrasonography reveals a diffuse generalized decreased echogenicity, but definitive diagnosis is only made by histopathologic examination of a biopsy
e. Differential diagnoses: hepatitis, hepatic lipidosis
f. Treatment: none; amyloidosis is slowly progressive, and animals can maintain remarkably long after diagnosis depending on the organ involved and the extent of deposition
g. Prevention: none
h. Species differences: chimpanzee, orangutan, baboon, macaque, squirrel monkey, Diana monkey, tree shrew
1. Glomerulonephritis/nephrotic syndrome (White 2011; Adachi et al. 2005, 669-674; Clarke et al. 2008, 42-48)
a. Definition: inflammation of the glomeruli, or small blood vessels in the kidneys
b. Causes/pathophysiology: may occur in conjunction with acute or chronic renal failure, viral or bacterial infection, secondary to liver or intestinal disease
c. Clinical signs: abnormal quantities of urine, discolored urine ± odor, edema, dyspnea
d. Physical examination/diagnostics: hematuria, proteinuria, hypoalbuminemia, hyperlipidemia, generalized edema, hypertension, anemia, dyspnea
e. Differential diagnoses: cardiovascular abnormalities, liver abnormalities, UTI, neoplasia
f. Treatment: supportive care, treat underlying cause (i.e., antibiotics if infection)
g. Prevention: none
h. Species differences: macaque
2. Hydronephrosis/renal cysts (White 2011; Roberts and Wolf 1971, 143-147; Roberts 1976, 1-4; Kessler, Roberts, and London 1984, 147-152; Ooms et al. 2005, 73)
a. Definition: distention and dilation of the renal pelvis calyces, leading to renal atrophy
b. Causes/pathophysiology: usually caused by obstruction of free flow of urine (i.e., kidney stones, neoplastic obstruction, etc.)
c. Clinical signs: depends on chronicity: intense pain (acute) to no pain (chronic), nausea, vomiting, bladder distention, urinary tract infection (UTI) with blood or pus in the urine, kidney failure
d. Physical examination/diagnostics: elevated creatinine, urea, and electrolyte imbalances on blood work, elevated urine pH, enlarged kidneys, may see calculi or mass on ultrasound
e. Differential diagnoses: renal failure, amyloidosis, bacterial/viral infection
f. Treatment: removal of obstruction, treat any concurrent conditions (UTIs)
g. Prevention: feed a well-balanced diet to prevent stone formation
h. Species differences: macaque
3. Urolithiasis and urinary obstruction (White 2011; Burdick et al. 2010, 90; Faltas 2000, 18-19; Ramachandra, Ramesh, and Rao 1995, 778-780; Pryor, Chang, and Raulston 1969, 862865; Matsell, Mok, and Tarantal 2002, 1263-1269; Gaertner, Lytton, and Morgenstern 1991, 1772-1774; Bahnson et al. 1988, 731-733; Caligiuri et al. 1990, 206-214; Cheever and Duvall 1981, 604-608)
a. Definition: urinary calculi formed in the urinary tract, usually in the bladder or urethra
b. Causes/pathophysiology: inflammation of the urinary tract, frequent urinary catheterization, kidney stones migrating through urinary tract, enlargement of prostate in males, nerve dysfunction, side effects of some medications (anticholinergics, antidepressants, cyclooxygenase 2 [COX-2] inhibitors, opiates), schistosoma
c. Clinical signs: frequent, painful, or difficult urination; may observe hematuria
d. Physical examination/diagnostics: pain in the pelvic region, distended bladder, usually occurs when the urine is very concentrated or the patient is dehydrated, ultrasound, radiographs (many calculi are calcium and will be visible), urinalysis, elevated BUN (blood urea nitrogen) and creatinine on blood work
e. Differential diagnoses: UTI, prostate enlargement/obstruction of urethra, urinary tract neoplasia
f. Treatment: fluid load/diurese the patient to flush the stones from the bladder; if calculi do not pass, may need to remove with cystoscope or cystotomy; if urethra is obstructed, pass a urinary catheter
g. Prevention: offer plenty of fluids at all times to prevent formation, change of diet
h. Species differences: males are more susceptible when the prostate is enlarged; macaque, chimpanzee, gibbon
4. Renal failure (White 2011; Barnhart and Bernacky 2008, 52-53; Kalk et al. 1984, 299-306; Steinhausen et al. 1981, 151-156; Clayton, Mylniczenko, and Greenwell 2003, 67-71; Baitchman et al. 2006, 182-185; Garner et al. 2003, 149-152)
a. Definition: Kidneys fail to filter toxins and waste products from the blood adequately (acute or chronic).
