Serum acute phase proteins in dogs with symptomatic esophageal spirocercosis.

Canine spirocercosis (CS) is a helminthic infection caused by the nematode Spirocerca lupi. The clinical hallmark of the disease is esophageal dysphagia due to parasite-induced esophageal nodules. Currently, there is limited information on the involvement of serum acute phase proteins (APPs) in the symptomatic CS. The objective of this study was to investigate whether C-reactive protein (CRP), serum amyloid A (SAA), haptoglobin (Hp) and albumin are involved in CS, and if their concentrations measured on admission reflect the severity of benign esophageal lesions. Nineteen dogs with spontaneous symptomatic esophageal spirocercosis and 7 clinically healthy dogs were studied retrospectively. The most consistently increased APP in the symptomatic dogs was Hp (95% of the dogs), followed by CRP (68%). The SAA concentrations were infrequently increased (5% of the dogs), while albumin concentrations were decreased in 58% of the affected dogs. The dogs with spirocercosis had significantly higher median concentrations of Hp (p=0.0001) and CRP (p=0.02) compared to healthy dogs. Median albumin concentrations did not differ between the two groups of dogs. The median concentrations of Hp, CRP and albumin did not differ significantly between the dogs having a single or multiple esophageal nodules. The results of this study indicate that in symptomatic CS, Hp and CRP are significantly and consistently increased, while SAA and albumin may be of limited value as diagnostic markers. No association was established between the concentrations of Hp, CRP and albumin measured on admission and the number of esophageal nodules.

Isolated abdominal fat tissue inflammation and necrosis in a cat.

This report describes a rare clinical case of a 4.5-month-old, female domestic shorthair, cat with isolated abdominal fat tissue inflammation and necrosis, resembling human omental panniculitis. Its possible relationship with pancreatitis or bile induced chemical peritonitis is also discussed. The overall clinical course was considered benign. Initial clinical signs were vomiting and anorexia, presumably due to inflammation, followed by mass development. It was speculated that, eventually, the kitten was vomiting because of mechanical pressure from the mass, and that this pressure subsided as the kitten grew. The mass was surgically resected and no relapse was evident during the next 4 years.

Giant hypertrophic gastritis (Menetrier's-like disease) in an Old English sheepdog.

An 11-year-old, male Old English sheepdog was admitted for weight loss and intermittent vomiting of 1 month's duration. A cranioventral abdominal mass, anemia, hypoproteinemia, and hypoalbuminemia were the prominent abnormal findings. Imaging studies identified a remarkably thickened gastric wall with multilobulated folds protruding into the gastric lumen. Gastrotomy revealed the presence of giant cerebriform rugal folds arising from the fundus and body of the stomach. Pronounced gastric glandular hyperplasia and lack of evidence of cellular atypia were suggestive of giant hypertrophic gastritis. The dog was treated with prednisolone, cimetidine, and hyoscine butylbromide, only to experience a short-term remission.

Clinical signs and clinicopathologic abnormalities in dogs with clinical spirocercosis: 39 cases (1996-2004).

OBJECTIVE: To determine clinical signs and clinicopathologic abnormalities in dogs with naturally occurring clinical spirocercosis. DESIGN: Retrospective case series. ANIMALS: 39 dogs with spirocercosis. PROCEDURES: Medical records were reviewed, and information on signalment, residence (rural vs urban), owner complaints, physical examination findings, clinicopathologic abnormalities, radiographic and endoscopic findings, and concurrent systemic diseases was recorded. RESULTS: Hellenic hounds and mixed-breed dogs were overrepresented, compared with a group of 117 control dogs without spirocercosis that were examined because of gastrointestinal tract disease, and mean body weight of dogs with spirocercosis was significantly higher than mean body weight of control dogs. Odynophagia (34 [87%]), regurgitation (24 [62%]), and excessive salivation (14 [36%]) were the most common clinical findings. The most common radiographic abnormalities were a mass in the caudodorsal aspect of the mediastinum (15/35 [43%]) and spondylitis of the caudal thoracic vertebrae (10 [29%]). Parasitic nodules were seen during esophagoscopy in all 39 dogs. Normocytic, normochromic, nonregenerative anemia; neutrophilic leukocytosis; hyperproteinemia; and high alkaline phosphatase activity were significantly more common in dogs with spirocercosis than in a control group of 56 healthy dogs. Concurrent systemic diseases, mainly leishmaniosis, dirofilariosis, and monocytic ehrlichiosis, were documented in 14 (36%) dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that clinical spirocercosis occurs more often in young-adult, large-breed dogs. Nonregenerative anemia, neutrophilic leukocytosis, hyperproteinemia, and high alkaline phosphatase activity may be useful clinicopathologic indicators of this disease.

A comparison between ethanol-induced chemical ablation and ivermectin plus prednizolone in the treatment of symptomatic esophageal spirocercosis in the dog: a prospective study on 14 natural cases.

This study included a total of 14 dogs with spontaneous esophageal spirocercosis. Historical and clinical evidence of esophageal dysphagia, detection of parasitic ova in fecal samples and endoscopic documentation of esophageal nodules were the inclusion criteria. The animals were randomly assigned into two groups: group A (n = 6 ) dogs received two intranodular injections of absolute ethanol (96%) via a through-the-endoscope injector, at weekly intervals; group B (n = 8) dogs were put on ivermectin (600 microg/kg BW, subcutaneously, twice, 14 days apart) and oral prednisolone (0.5mg/kg BW, every 12h, for a total of 3 weeks, tapering the dose accordingly). Clinical and fecal examination as well as endoscopy, were performed on admission and at 20, 60 and 180 days from the beginning of the treatment. One group A dog responded poorly and died of pyothorax during the trial and another developed esophagitis due to accidental intraluminal ethanol infusion, only to experience an uneventful recovery. At different times during the 6-month follow-up period, there was a complete disappearance of the clinical signs in 4/6 group A dogs. However, full nodular regression was achieved only in one dog, and parasitic ova were still found in the feces of 4/6 dogs. At the same period of time in five group B dogs still available for evaluation, resolution of the clinical signs and complete nodular regression were seen in four and five animals, respectively, while negative fecal results were obtained in all dogs (8/8) of the same group 2 months from the beginning of the treatment. No significant difference was found between the groups, regarding the resolution of clinical signs, though group B dogs demonstrated a significantly higher rate of regression of esophageal nodules as well as negative fecal results, compared to group A dogs. The combination of ivermectin and prednizolone may be considered an effective treatment in the symptomatic and evidently asymptomatic esophageal spirocercosis of the dog.

Serum lipase activity in young dogs with acute enteritis or gastroenteritis.

Blood serum lipase activity was determined in 48 young dogs with acute enteritis or gastroenteritis due to canine parvovirus (16 Cases) and presumably to other infectious agents (32 cases). Elevated serum lipase activity (> 500 U/L) was found in 13 dogs (27.1 %) with values ranging from 800 to 2,780 U/L. The hyperlipasemia of these cases may be attributed to acute pancreatitis secondary to acute gastroenteritis or to gastrointestinal upset.