Efficacy of oral supplementation with L-lysine in cats latently infected with feline herpesvirus

OBJECTIVE: To examine the effects of orally administered L-lysine on clinical signs of feline herpesvirus type 1 (FHV-1) infection and ocular shedding of FHV-1 in latently infected cats. ANIMALS: 14 young adult, FHV-1-naive cats. PROCEDURE: Five months after primary conjunctival inoculation with FHV-1, cats were rehoused and assigned to receive 400 mg of L-lysine in food once daily for 30 days or food only. On day 15, all cats received methylprednisolone to induce viral reactivation. Clinical signs of infection were graded, and viral shedding was assessed by a polymerase chain reaction assay throughout our study. Peak and trough plasma amino acid concentrations were assessed on day 30. RESULTS: Fewer cats and eyes were affected by conjunctivitis, and onset of clinical signs of infection was delayed on average by 7 days in cats receiving L-lysine, compared with cats in the control group; however, significant differences between groups were not demonstrated. Significantly fewer viral shedding episodes were identified in the treatment group cats, compared with the control group cats, after rehousing but not following corticosteroid-induced viral reactivation. Mean plasma L-lysine concentration was significantly increased at 3 hours but not at 24 hours after L-lysine administration. Plasma arginine concentration was not significantly altered. CONCLUSIONS AND CLINICAL RELEVANCE: Once daily oral administration of 400 mg of L-lysine to cats latently infected with FHV-1 was associated with reduced viral shedding following changes in housing and husbandry but not following corticosteroid administration. This dose caused a significant but short-term increase in plasma L-lysine concentration without altering plasma arginine concentration or inducing adverse clinical effects.     

Food hypersensitivity in cats: 14 cases (1982-1987)

Food hypersensitivity was diagnosed in 14 cats. Clinical signs varied; pruritus (100%), alopecia (64%), and papules (21%) were the ones most commonly observed. Pruritus was localized principally to the head or to the neck or ear region in 42% of the cats. Diagnosis was made on the basis of resolution of clinical signs when cats were fed a restricted ("hypoallergenic") diet, and recurrence of signs when cats were fed their original diet or other food. The most common allergens (on the basis of dietary challenge exposure) were fish and dairy products. Age or sex predilection was not observed, and 9 (64%) of the cats were domestic shorthairs. Owners could not relate the onset of clinical signs with a recent change in diet. Three cats had concurrent flea bite, inhalant, or flea collar hypersensitivity.     

Acute Hepatic Necrosis And Liver Failure Associated With Benzodiazepine Therapy In Six Cats, 1986–1995.

A retrospective analysis was conducted of all feline necropsies performed during a nine year period to identify cases of sever, acute, centrilobular (periacinar), hepatic necrosis (ACHN). After exclusion of cats with anemia, a series of seven cases of ACHN was identified. In addition, two similar cases were identified from tissue submitted for histopathology following, and eight had bile duct hyperplasia. Seven of the nine cats received diazepam prior to dath, and one received zolazepam. Of the seven cats that received diazepam, five were healthy prior to treatment and received oral diazepam for the treatment of inappropriate urination, intercat aggression, or skin disease. Two cats which received diazepam exhibited other clinical signs: one had chronic vomiting, and the other received diazepam after biochemical evidence of hepatocellular necrosis was present. Onset of clinical sings in cats receiving oral diazepam occurred 7–13 days following the initiation of treatment. Clinical signs and clinical biochemical analysis were compatible with severe hepatocellular necrosis and acute liver failure. All cats had lesions in other organs: five had pancreatic disease, five had cardiac disease, and five had renal disease. All cats died, or were euthanized, within 4 dyas of the onset of clinical signs and 2 days after presentation to a veterinarian. Fatal, acute, centrilobular hepatic necrosis appears to be a serious adverse reaction to diazepam therapy in certain cats.     

Safety, pharmacokinetics and use of the novel NK-1 receptor antagonist maropitant (Cerenia) for the prevention of emesis and motion sickness in cats

The present study characterizes the safety, pharmacokinetics, and anti-emetic effects of the selective NK-1 receptor antagonist maropitant in the cat. Safety of maropitant was determined following 15 days of subcutaneous (SC) administration at 0.5–5 mg/kg. Maropitant was well tolerated in cats at doses that exceeded the efficacious anti-emetic dose range of the drug by at least a factor of 10 and adverse clinical signs or pathological safety findings were not noted at any dose.The pharmacokinetics of maropitant in cats were determined following single dose oral (PO), intravenous (IV) and SC administration. Maropitant had a terminal half-life of 13–17 h and a bioavailability of 50 and 117% when administered PO and SC, respectively. Efficacy was determined against emesis induced either by xylazine or by motion. A dosage of 1 mg/kg maropitant administered IV, SC or PO prevented emesis elicited by xylazine. The compound had good oral antiemetic activity and a long (24 h) duration of action. Maropitant (1.0 mg/kg) was highly effective in preventing motion-induced emesis in cats. These studies indicate that the NK-1 receptor antagonist maropitant is well tolerated, safe and has excellent anti-emetic properties in cats.     

Evaluation of complications and prognostic factors associated with administration of total parenteral nutrition in cats: 75 cases (1994-2001)

OBJECTIVE: To determine frequency and types of complications, prognostic factors, and primary diseases affecting clinical outcome associated with administration of total parenteral nutrition (TPN) in cats. DESIGN: Retrospective study. ANIMALS: 75 cats that received TPN for > or = 12 hours. PROCEDURE: Medical records were reviewed, and information was obtained on signalment, history, problems at initial evaluation, physical examination findings, weight and changes in weight while receiving TPN, duration in the hospital before initiation of TPN, the type of TPN catheter used, duration of TPN administration, and final diagnosis. Laboratory results obtained immediately prior to TPN and at 24 and 96 hours following initiation of TPN administration were compared. RESULTS: Reports of weight loss at initial evaluation, hyperglycemia at 24 hours, or diagnosis of chronic renal failure were significantly associated with increased mortality rate. Greater serum albumin concentrations prior to and at 96 hours following TPN administration were significantly associated with decreased mortality rate. Mechanical and septic complications were infrequent and not associated with increased mortality rate. Most cats had multiple diseases. The overall mortality rate was 52%; among 75 cats, 36 recovered, 23 were euthanatized, and 16 died as a result of their primary illness or complications associated with their illness. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated high mortality rate in cats maintained onTPN that had multiple concurrent diseases associated with a poor prognosis. Indicators of poor prognosis included a history of weight loss, hyperglycemia at 24 hours following TPN administration, hypoalbuminemia, and chronic renal failure.     

Preparturient hypocalcemia in four cats.

Preparturient hypocalcemia was identified in 4 cats in a specific pathogen-free colony between 1995 and 1996. All cats had an acute onset of clinical signs, 3 to 17 days prior to parturition. Signs of depression, weakness, tachypnea, and mild muscle tremors were the most common clinical signs, following by vomiting and anorexia. Additional abnormalities included hypothermia, third eyelid prolapse, dehydration, pallor, lethargy, flaccid paralysis, and hyperexcitability. Hematologic abnormalities included leukocytosis with neutrophilia and lymphopenia. Hypocalcemia was documented in each queen. Common serum biochemical abnormalities included high aspartate aminotransferase and creatine kinase activities. All cats responded to IV or SC administration of 10% calcium gluconate. Queens were then given calcium orally prior to and following parturition. The queens did not have additional complications for the duration of the gestational or lactational periods.     

Transient clinical diabetes mellitus in cats: 10 cases (1989-1991)

Medical records of 10 cats with transient clinical diabetes mellitus were reviewed. At the time diabetes was diagnosed, clinical signs included polyuria and polydipsia (10 cats), weight loss (8 cats), polyphagia (3 cats), lethargy (2 cats), and inappetence (1 cat). Mean (+/- SD) fasting blood glucose concentration was 454 +/- 121 mg/dL, mean blood glucose concentration during an 8-hour period (MBG/8 hours) was 378 +/- 72 mg/dL, and glycosuria and trace ketonuria were identified in 10 and 5 cats, respectively. Baseline serum insulin concentration was undetectable (6 cats) or within the reference range (4 cats) and serum insulin concentration did not increase after i.v. glucagon administration in any cat. Insulin-antagonistic drugs were being administered to 5 cats and concurrent disorders were identified in all cats. Management of diabetes included administration of glipizide (6 cats), insulin (3 cats), or both (1 cat), discontinuation of insulin-antagonistic drugs, and treatment of concurrent disorders. Insulin and glipizide treatment was discontinued 4-16 weeks (mean, 7 weeks) after the initial diagnosis of diabetes was confirmed. At the time treatment for diabetes was discontinued, clinical signs had resolved, mean fasting blood glucose concentration was 102 +/- 48 mg/dL, MBG/ 8 hours was 96 +/- 32 mg/dL, glycosuria and ketonuria were not identified in any cat, and concurrent disorders (except mild renal insufficiency in 1 cat) had resolved. Significant (P < .05) increases occurred in postglucagon serum insulin concentrations, insulin peak response, and total insulin secretion, compared with values obtained when clinical diabetes was diagnosed. Histologic abnormalities were identified in pancreatic islets of 5 cats in which pancreatic biopsies were obtained and included decreased number of islets (4 cats), islet amyloidosis (3 cats), and vacuolar degeneration of islet cells (3 cats). Mean beta cell density was significantly (P < .001) decreased in diabetic cats compared with control cats (1.4 +/- 0.7 versus 2.6 +/- 0.5%, respectively). Cells within islets stained positive for insulin, however, the number of insulin-staining cells per islet and the intensity of insulin staining were decreased in 5 and 2 cats, respectively. Clinical diabetes had not recurred in 1 cat after 6 years, in 4 cats lost to follow-up after 1.5, 1.5, 2.0, and 2.5 years, and in 2 cats that died 6 months and 5.5 years after clinical diabetes resolved. Clinical diabetes recurred in 3 cats after 6 months, 14 months, and 3.4 years, respectively. These findings suggest that cats with transient clinical diabetes have pancreatic islet pathology, including decreased beta cell density, and that treatment of diabetes and concurrent disorders results in improved beta cell function, reestablishment of euglycemia, and a transition from a clinical to subclinical diabetic state.     

Hypophosphatemia and Hemolytic Anemia Associated With Diabetes Mellitus and Hepatic Lipidosis in Cats

Hypophosphatemia associated with hemolytic anemia was diagnosed in five cats with diabetes mellitus and in one cat with idiopathic hepatic lipidosis. The hematocrit began decreasing within 24 to 48 hours after documented hypophosphatemia in each case. The anemia resolved in all five surviving cats. Because of the temporal relationship and lack of other detectable causes, hemolytic anemia was presumed to be caused by hypophosphatemia. There were increased Heinz bodies in three of six hypophosphate-mic cats during episodes of hemolysis. Intravenous potassium phosphate administration corrected the hypophosphatemia in four of five cats. The effective dosages of intravenous phosphate ranged from 0.011 to 0.017 mmol of phosphate/kg/h for 6 to 12 hours. Hypocalcemia (5.4 to 8.7 mg/dL) occurred in four of five cats treated with intravenous phosphate; however, only one cat developed clinical signs attributable to hypocalcemia. Based on this retrospective study, we recommend monitoring serum phosphorus concentration every 6 to 12 hours in cats likely to become hypophosphatemic. Treatment of hypophosphatemia in cats is warranted because of the apparent increased susceptibility of cats to hypophosphatemia-induced hemolysis. Cats with severe hypophosphatemia (≤1.5 mg/dL) should be given oral or parenteral phosphate if contraindications do not exist. (Journal of Veterinary Internal Medicine 1993; 7:266–271. Copyright © 1993 by the American College of Veterinary Internal Medicine.)     

Retrospective study: the presence of Malassezia in feline skin biopsies. A clinicopathological study

Malassezia spp. dermatitis, a rare disorder in cats, has previously been associated with immune suppression and internal malignancies. This study evaluates the presence and importance of Malassezia spp. in feline biopsy specimens submitted for histopathological examination. Five hundred and fifty haematoxylin and eosin-stained skin biopsy specimens received for histopathological examination between January 1999 and November 2000 were reviewed. Fifteen (2.7%) submissions contained Malassezia organisms in the stratum corneum of the epidermis or follicular infundibulum. Eleven of 15 cats presented with an acute onset of multifocal to generalized skin lesions. All 11 cats were euthanized or died within 2 months of the onset of clinical signs. Seven cats had dermatopathological changes and clinical signs supportive of paraneoplastic alopecia, and three cats had an interface dermatitis suggestive of erythema multiforme or thymoma-associated dermatosis. Histopathological changes were nonspecific in one cat that was euthanized 2 weeks following onset of severe pruritus and alopecia. In three cats, Malassezia spp. were found in localized sites (two chin, one footpads) and appeared inconsequential to their overall health status. One cat had Malassezia spp. in association with cutaneous demodicosis. These findings suggest that Malassezia yeast in dermatopathological specimens from multifocal or generalized lesions should prompt a thorough clinical work-up for internal neoplasia.     

MICRONODULAR ULTRASOUND LESIONS IN THE COLONIC SUBMUCOSA OF 42 DOGS AND 14 CATS

Micronodular ultrasound lesions have been detected in the colonic submucosa of dogs and cats at our hospital. The lesions had rounded/oval shapes, measured 1–3 mm in size, and exhibited a hypo/anechoic ultrasonographic pattern. To our knowledge, these lesions have not been previously reported in human or veterinary patients. The purpose of this retrospective study was to determine whether micronodular lesions were associated with other abdominal ultrasound abnormalities or clinical findings. Medical records of dogs and cats with sonographic reports describing micronodular lesions within the colonic submucosa were reviewed. Concurrent ultrasonographic abnormalities were recorded and compared with clinical sidgns and follow‐up data. A total of 42 dogs and 14 cats met inclusion criteria. Concurrent sonographic abnormalities included the following: increased colon wall thickness (12.5%); small bowel wall thickening, altered layering, and/or hyperechoic mucosa (45%); abdominal effusion (29%); caudal mesenteric lymphadenopathy (46%); mesenteric lymphadenopathy (27%); and pericolic peritoneal fat reactivity (9%). Fifty of 56 animals presented with diarrhea. Twenty‐seven cases had clinical signs of colitis and ultrasonographic lesions were limited to the colonic submucosa. In nine cases, follow‐up examination at 6–8 weeks showed resolution of clinical and ultrasonographic signs. Ultrasonographic and clinical examinations in 17 patients at 12–18 months and in 20 patients at 18–30 months from initial diagnosis showed resolution of submucosal lesions and clinical signs of enteropathy. The authors propose that micronodular submucosal ultrasound lesions may represent reactive intraparietal lymphoid follicles and may be indicators of colonic inflammatory diseases in dogs and cats.     

The prevalence and significance of hyperglycemia in hospitalized cats

Objective – To report the prevalence of hyperglycemia in cats admitted to a veterinary hospital and to determine if hyperglycemic cats had increased morbidity and mortality when compared with normoglycemic cats.
Design – Retrospective clinical study.
Setting – Community-based referral hospital.
Animals – Nondiabetic cats admitted to the hospital.
Interventions – None.
Measurements and Main Results – The medical records of nondiabetic cats admitted to the hospital over a 1-year period were reviewed. There were 182 cats that met the criteria for inclusion in the study. Information obtained included signalment, length of hospitalization, initial and highest blood glucose measurement, diagnosis, treatment, and final disposition. Sixty-three percent of cats (116/182) were hyperglycemic at the time of presentation. Total incidence of hyperglycemia at any point during hospitalization was 64% (118/182). No association was found between hyperglycemia either initially or at any point during the hospitalization and mortality. However, a significant association was documented between the presence of hyperglycemia and increased length of hospitalization (LOH) ( P =0.04). The duration of LOH was also significantly associated with the degree of hyperglycemia ( P =0.01). A number of different disease processes were represented in the study population. However, the number of cats in each disease category was small and no association could be found between any of them and blood glucose affecting mortality and morbidity.
Conclusion – The prevalence of hyperglycemia in feline patients admitted to a primary referral hospital was 64%. Cats with hyperglycemia had a longer LOH when compared with normoglycemic cats; however, presence of hyperglycemia did not impact mortality in this population of cats.     

Coccidioidomycosis in 48 Cats: A Retrospective Study (1984–1993)

Coccidioidomycosis was diagnosed in 48 cats. Forty-one cases were identified within a period of 3 years. Coccidioides immitis was revealed by cytological or histopathological examinations, or culture in 70% of cats. The remaining 30% of cases were diagnosed by appropriate clinical signs, radiographic lesions, and serological test results. The average age of affected cats was 6.2 years with a median age of 5.0 years. Fifty-four percent (n = 26) were female and 46% (n = 22) were male. Domestic shorthaired and longhaired breeds comprised 89% (n = 41) of affected cats. Sixty-seven percent of cases were diagnosed during the 6-month period of December through May. Cats infected with C immitis were presented for evaluation of dermatologic (56%), respiratory (25%), musculoskeletal (19%), and neurological or ophthalmologic signs (19%). Fever, inappetence, and weight loss were present in 44% of the cats. Duration of clinical signs before diagnosis was less than 4 weeks in 85% (n = 42) of cats, with an average of 3.8 weeks and a median of 2 weeks. Agar gel immunodiffusion tests were positive in all 39 cats tested at sometime during the course of their disease. Hyperproteinemia (greater than 7.9 g/dL) was present in 52% (10/23) of cases. The majority of cats (n = 39) were negative for feline leukemia virus. Antibodies to feline immunodeficiency virus were absent in the 19 cats tested. Ketoconazole was the most common antifungal agent used to treat cats with Coccidioidomycosis. Duration of treatment ranged from less than 1 week to 43 months. Thirty-two cats are currently asymptomatic, with or without treatment. Eleven cats died or were euthanized. Five cats were lost to follow-up. Ketoconazole likely is more suppressive than curative because relapses were common after discontinuing therapy.     

Hypophosphatemia in Cats After Renal Transplantation

Objective— To report the prevalence of hypophosphatemia after renal transplantation in a historical cohort of cats. Design— Case series. Animals— Cats (n=86) that received a renal allograft. Methods— Medical records (January 200–June 2006) were reviewed. Signalment, clinical signs, pre‐ and postoperative diet, pre‐ and postoperative clinicopathologic variables, renal histopathology, and outcome were retrieved. Prevalence, onset, duration, treatment and associated clinical signs of hypophosphatemia were recorded. A χ² test was used to compare hemolysis frequency between cats with normal serum phosphorus concentration or a single spurious low serum phosphorus concentration for <24 hours duration (group 1) and confirmed hypophosphatemia for >24 hours (group 2). A Cox proportional hazards model was used to evaluate the effects of hypophosphatemia on survival while controlling for other potentially confounding variables (age, sex, weight, body condition score, and pre‐ and 24 hours postoperative clinicopathologic variables). Results— Eighty‐six cats (mean age, 7.7 years) were identified. Hypophosphatemia occurred in 32 cats (37%), with a median onset of 2 days and median duration of 4 days. Treatment was initiated in 48 (56%) of hypophosphatemic cats. Survival and hemolysis frequency was not significantly different between groups, and no risk factors were identified. Conclusion— Hypophosphatemia occurs in cats after renal transplantation and does not affect survival. Clinical Relevance— The clinical importance of hypophosphatemia in renal transplant recipients remains unknown.     

Treatment of three cats with hyperviscosity syndrome and congestive heart failure using plasmapheresis

Three cats were evaluated at a veterinary teaching hospital for congestive heart failure (CHF) secondary to hyperviscosity syndrome from plasma cell neoplasia. All cats had severe hyperproteinemia due to hyperglobulinemia. Multiple myeloma or plasma cell neoplasia was diagnosed based on cytopathology and post mortem examination. The cats presented with signs of CHF including acute collapse, tachypnea, increased respiratory effort, and pulmonary crackles. All cats had heart murmurs and echocardiographic signs consistent with hypertrophic cardiomyopathy. An enlarged left atrium was found in all cats and two of three cats also had spontaneous echocardiographic contrast. Plasmapheresis (centrifugal plasma exchange) was performed on all three cats by the removal of whole blood and the infusion of a balanced electrolyte solution while the whole blood was centrifuged and separated. The RBCs were then washed before being readministered to the patient. Plasmapheresis alleviated the clinical signs of CHF (tachypnea) in all three cats. Plasmapheresis should be considered in cases of CHF secondary to hyperviscosity syndrome to rapidly alleviate clinical signs associated with heart failure while diagnosis of the underlying cause is made and appropriate therapy implemented.     

Acetaminophen Toxicosis In 17 Cats

Seventeen cases of acetamninophen intoxication in cats were identified over a 12-year period. Information obtained from the medical records included the signalment, amount acetaminophen ingested, time from ingestion until treatment was initiated, clinical signs, physical examination, clinical pathology, treatment and outcome. The most common cause intoxication was owner administration. In cats that died or were euthanized the dose administered ranged from 10mg/kg to 17Omg/kg, while in cats that survived the dosage ranged from 10mg/kg to 400mg/kg. The most common clinical signs were depression, increased respiratory rate, respiratory distress, pale/muddy mucous membranes, and hypothermia. Twelve cats survived. Ten of these cats had treatment initiated within 14 hours after ingestion. One cat that survived had treatment initiated 24 hours after ingestion, and a second cat that survived had treatment initiated 48 hours after ingestion. Time between ingestion and initiation treatment may be as important if not more important than the actual dosage acetaminophen administered.     

Characterization of the clinical characteristics, electrolytes, acid–base, and renal parameters in male cats with urethral obstruction

Objective: To characterize the clinical characteristics, electrolyte changes, acid–base changes, and renal parameters in a consecutive population of cats with urethral obstruction. Design: Retrospective clinical study. Setting: University Veterinary Teaching Hospital. Animals: Two hundred and twenty‐three male cats that presented consecutively with urethral obstruction between 1997 and 1999. Interventions: None. Measurements and main results: The medical records of 223 cats with urethral obstruction were reviewed for signalment, previous medical history, indoor/outdoor status, body weight, clinical signs, physical examination findings, renal function tests (blood urea nitrogen and creatinine), and blood gas and electrolyte analysis. The majority of cats were relatively stable without serious metabolic derangements. Only 12% (24/199) of cats had severe hyperkalemia (>8.0 mmol/L). Hyperkalemia did not occur in isolation; the majority of these cats had concurrent acidemia and low ionized calcium concentrations. Potassium was significantly inversely correlated with pH, bicarbonate, pCO₂, sodium, chloride, and ionized calcium, but positively correlated with blood urea nitrogen and creatinine. Ionized calcium was positively correlated with pH and bicarbonate. Of the animals with a potassium concentration greater than 8.0 mmol/L, 75% (18/24) had an ionized calcium concentration of less than 1.0 mmol/L. Seventy‐nine percent (19/24) of cats with a potassium concentration greater than 8.0 mmol/L had a blood pH<7.20. Similarly, 74% (23/31) of cats with a pH<7.20 had an ionized calcium concentration <1.00 mmol/L. Conclusions: The majority of cats with urethral obstruction presented with mild electrolyte and blood gas changes and were relatively stable, although 12% of cats had multiple, life‐threatening metabolic derangements. Of 219 cats in this study, 205 (93.6%), where it could be determined, survived to discharge from the hospital, supporting the fact that most cats with urethral obstruction survive the acute episode with emergency treatment.     

Comparison of classic hypoadrenocorticism with glucocorticoid-deficient hypoadrenocorticism in dogs: 46 cases (1985-2005)

OBJECTIVE: To compare dogs with glucocorticoid-deficient hypoadrenocorticism (GDH) with those with mineralocorticoid- and glucocorticoid-deficient hypoadrenocorticism (MGDH) and determine prevalence, historical and clinicopathologic markers, and outcome of dogs with GDH. DESIGN: Retrospective case series. ANIMALS: 46 dogs with hypoadrenocorticism. PROCEDURES: Records in the veterinary medical database at Purdue University were searched for dogs in which hypoadrenocorticism had been diagnosed at the Veterinary Teaching Hospital from 1985 to 2005. Data pertaining to signalment, history, a minimum clinicopathologic database, treatment, and outcome were collected. Dogs with hypoadrenocorticism were classified as having MGDH if hyponatremia, hyperkalemia, or both were detected and as having GDH if hyponatremia and hyperkalemia were absent. Dogs were excluded if they had ever been treated with mitotane or had been treated with > 1 dose of corticosteroids within a month prior to the ACTH-stimulation test. RESULTS: 35 dogs with MGDH and 11 dogs with GDH met the inclusion criteria. Dogs with GDH were older at the time of diagnosis and had a longer duration of clinical signs prior to diagnosis than those with MGDH. Dogs with GDH were more likely to be anemic, hypoalbuminemic, and hypocholesterolemic than dogs with MGDH. CONCLUSIONS AND CLINICAL RELEVANCE: GDH was more common than reported in a referral hospital population of dogs with primary hypoadrenocorticism. Definitive diagnosis of GDH remains a clinical challenge. Absence of a stress leukogram in dogs with signs of illness (especially relating to the gastrointestinal tract) warrants further investigation. Most dogs with primary cortisol deficiency do not develop mineralocorticoid deficiency.