• One Health
  • Pain Management
  • Oncology
  • Geriatric & Palliative Medicine
  • Ophthalmology
  • Anatomic Pathology
  • Poultry Medicine
  • Infectious Diseases
  • Dermatology
  • Theriogenology
  • Nutrition
  • Animal Welfare
  • Radiology
  • Internal Medicine
  • Small Ruminant
  • Cardiology
  • Dentistry
  • Feline Medicine
  • Soft Tissue Surgery
  • Urology/Nephrology
  • Avian & Exotic
  • Preventive Medicine
  • Anesthesiology & Pain Management
  • Integrative & Holistic Medicine
  • Food Animals
  • Behavior
  • Zoo Medicine
  • Toxicology
  • Orthopedics
  • Emergency & Critical Care
  • Equine Medicine
  • Pharmacology
  • Pediatrics
  • Respiratory Medicine
  • Shelter Medicine
  • Parasitology
  • Clinical Pathology
  • Virtual Care
  • Rehabilitation
  • Epidemiology
  • Fish Medicine
  • Diabetes
  • Livestock
  • Endocrinology

Challenging cases in internal medicine: An underweight Gordon setter with brittle claws


A 4-year-old, female spayed Gordon setter was evaluated at the Veterinary Medical Teaching Hospital at the University of Wisconsin-Madison because of brittle claws of about one year's duration.

A 4-YEAR-OLD, female spayed Gordon setter was evaluated at the Veterinary Medical Teaching Hospital at the University of Wisconsin-Madison because of brittle claws of about one year's duration. Eighteen months earlier, the referring veterinarian had examined the dog because of a flaky, dry coat that had progressed to abnormal claw integrity. The dog frequently had broken claws requiring cauterization. All four feet were affected at different times throughout the year. The referring veterinarian had performed a premium thyroid panel, consisting of total T4 and T3 concentrations, free T4 and T3 concentrations, the TSH concentration, and T4, T3, and thyroglobulin autoantibody concentrations. The results had been normal with the exception of an increase in thyroglobulin autoantibody (1,159%, normal < 200%). The results of aerobic bacterial and fungal cultures of the claw beds had been negative. The dog had been treated with cephalexin multiple times (dose and duration unknown), and fatty acid supplementation had been initiated.

1. The 4-year-old Gordon setter at presentation. Comparing the dog's size with that of the book illustrates the dog's small stature for its breed.

Physical examination findings and initial diagnostic procedures

On physical examination, the dog was small and thin for its breed ( Figure 1 ), weighing 33 lb (15 kg) (normal = 55 to 66 lb [25 to 30 kg]). The dog's coat was thin, dull, and dry. The claw beds were normal, but the claws on all four feet were brittle and splitting; the hair keratin easily split longitudinally. On further questioning, the owners mentioned that the dog was occasionally lethargic and quiet and intermittently had loose stools and a poor appetite.

Because of this dog's small stature, poor coat, and dry, splitting claws, a systemic disease was suspected rather than a primary claw disorder (e.g. onychomycosis). Primary claw disorders, with no other dermatologic manifestations, are rare in dogs and cats. Most commonly, claw diseases are asymmetric and result from trauma (either physical or chemical) and secondary bacterial infection. Systemic diseases with claw bed involvement include lupoid dermatoses and drug reactions.1 The differential diagnosis list at this point included hypothyroidism, hypoadrenocorticism, and maldigestion or malnutrition secondary to intestinal disease.

The results of a complete blood count and serum chemistry profile were normal. A total T4 concentration was rechecked because increased thyroglobulin autoantibodies can predispose a dog to hypothyroidism. The total T4 concentration was normal. No abnormalities were noted on cytologic examination of claw bed samples.

The patient was discharged, and the owner was instructed to administer fenbendazole (50 mg/kg once a day for three days, repeated in three weeks) and to return in one week for additional diagnostic tests that required fasting.

Further diagnostic testing

One week later, an ACTH stimulation test was performed to rule out hypoadrenocorticism, because the dog had intermittent gastrointestinal signs, lethargy, and depression. The results were normal (cortisol concentration before ACTH administration = 7.4 ng/ml, normal = 2 to 10 ng/ml; cortisol concentration one hour after ACTH administration = 167 ng/ml, normal = 55 to 280 ng/ml). Fasting trypsin-like immunoreactivity and folate and cobalamin concentrations were measured to screen for exocrine pancreatic insufficiency, malabsorption or maldigestion, and small intestinal bacterial overgrowth. The trypsin-like immunoreactivity results were normal. The folate concentration was 3.3 µg/L (normal = 6.5 to 11.5 µg/L), which is consistent with disease affecting the proximal small intestine. The cobalamin concentration was 312 ng/L (normal = 249 to 733 ng/L). The differential diagnosis list now included inflammatory bowel disease (IBD), gastrointestinal lymphoma, and, less likely because of our geographic area, fungal infection (e.g. histoplasmosis). Endoscopy was performed to further evaluate the upper gastrointestinal tract.

On endoscopic examination, the esophagus and fundic region of the stomach looked normal, whereas the pylorus appeared hyperemic. Many areas of the proximal small intestinal mucosa had a cobblestone appearance. Biopsy samples of the stomach and duodenum were submitted for histopathologic examination.

Histopathologic examination of the gastric biopsy samples showed no marked inflammation. Moderate numbers of large Helicobacter species-like organisms were present within the gastric pits and extended into the gastric glands. The results of a urease test were positive, suggesting the presence of Helicobacter species. The duodenal samples showed moderate to severe lymphocytic-plasmacytic infiltrates within the mucosal lamina propria with mild central lacteal dilatation. This histopathologic report confirmed a diagnosis of IBD.

Treatment and follow-up

The dog was given oral folate supplementation (10 µg/kg) once a day and cobalamin (400 µg) subcutaneously once a week for six weeks and then every other week for six weeks. Folate and cobalamin concentrations were to be evaluated one week after the last cobalamin dose. The clinical importance of Helicobacter species in the stomach of dogs and cats is still controversial. The bacteria may even be a normal inhabitant of the stomach. The Helicobacter species infection was treated in this case because of the gross changes seen on endoscopic examination. This treatment included amoxicillin (20 mg/kg orally b.i.d.), metronidazole (17 mg/kg orally b.i.d.), famotidine (1.3 mg/kg orally once a day), and bismuth subsalicylate (1 ml/kg orally one to three times a day) for two weeks. The dog's diet was also changed to a novel protein diet (Prescription Diet Canine z/d Ultra—Hill's).

The patient did not respond well to therapy initially. After about six weeks, the owner reported that the dog still had a poor coat and poor claw integrity with minimal weight gain. The necessary duration of a novel protein diet is controversial. Clinical improvement may not occur until 10 to 13 weeks after beginning such a diet. However, some clinicians think that substantial improvement should occur within four to six weeks. In one study, 95% of dogs were clinically better within three weeks.2 Prednisone was initiated (2.7 mg/kg/day for four to six weeks, gradually tapered every three or four weeks) because there was no improvement with empirical deworming and six weeks of a diet trial. The metronidazole, famotidine, bismuth subsalicylate, and special diet were continued. The dog quickly improved once it began receiving the prednisone.

Over the subsequent five months, the dog gained weight and had no further claw problems and a much improved coat. The owner reported that the dog was doing great. It was maintained on prednisone (0.6 mg/kg) once a day. The owner was encouraged to continue tapering the prednisone because it is important to find the lowest effective dose.


This case is an interesting example of IBD because the gastrointestinal signs were intermittent and relatively unnoticed by the owner, yet the disease was serious enough to cause malnutrition, which manifested as weak, breaking claws; a poor coat; and stunted growth. IBD is a general term that represents several chronic gastrointestinal disorders characterized by inflammatory infiltrates in the mucosa of the gastrointestinal tract. Diagnosis is based on excluding systemic diseases (e.g. hypoadrenocorticism) and other known causes of intestinal inflammation (e.g. parasites, dietary intolerance or sensitivity) and detecting inflammatory cell infiltrates on histopathologic examination of intestinal biopsy samples. The most common infiltrates are lymphocytes and plasma cells or eosinophils.3

The clinical findings are variable and may include anorexia, intermittent diarrhea, and vomiting in mild cases to intractable small intestinal diarrhea, weight loss, and vomiting in severe cases. The treatment of IBD is based on the severity of clinical and pathologic findings and usually consists of a combination of a novel protein diet, antibiotics, and immunosuppressive therapy. Empirical deworming with a broad-spectrum product (e.g. fenbendazole) and a dietary trial with a highly digestible diet (e.g. Eukanuba Low-Residue Formula—Iams) or a novel protein source should yield results within six weeks if parasites or dietary intolerance or sensitivity is present. Additionally, a therapeutic trial for antibiotic-responsive enteropathy or small intestinal bacterial overgrowth may be warranted.

Immunosuppressive agents are often required in patients that do not respond to these treatments alone or that have hypoproteinemia or moderate to severe infiltrates. Oral prednisone (2 to 4 mg/kg/day orally) is the initial drug of choice. It is important to obtain biopsy samples before immunosuppressive corticosteroid administration. Diagnosis and treatment of lymphoma may be hindered by prior corticosteroid use, and corticosteroids may be fatal in cases of fungal disease.

Kristin Crass, DVM

Department of Medical Sciences

School of Veterinary Medicine

University of Wisconsin

Madison, WI 53706


1. Scott, D.W. et al.: Diseases of eyelids, claws, anal sacs, and ears. Muller & Kirk's Small Animal Dermatology, 6th Ed. W.B. Saunders, Philadelphia, Pa., 2001; pp 1185-1232.

2. Groh, M.; Moser, E.: Diagnosis of food allergy in the non-seasonally symptomatic dog using a novel antigen, low molecular weight diet: A prospective study of 29 cases. J. Vet. Allergy Clin. Immunol. 6 (1):5; 1998.

3. Guilford, W.G. et al.: Idiopathic inflammatory bowel diseases. Strombeck's Small Animal Gastroenterology, 3rd Ed. W.B. Saunders, Philadelphia, Pa., 1996; pp 451-486.


1. Simpson, K.: Chronic enteropathies: How should I treat them? Proc. ACVIM, ACVIM, Lakewood, Colo., 2003.

2. Stone, M.: Is It IBD? Proc. Tufts Animal Expo, Boston, Mass., 2002.

3. Jergens, A.E.: Inflammatory bowel disease in the dog and cat. Proc. WSAVA, World Small Animal Veterinary Association, Granada, Spain, 2002.

Related Videos
Senior Bernese Mountain dog
© 2023 MJH Life Sciences

All rights reserved.