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Dive into the research topics where Susan E. Johnson is active.

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Featured researches published by Susan E. Johnson.


Journal of The American Animal Hospital Association | 2002

Spontaneous gastroduodenal perforation in 16 dogs and seven cats (1982-1999).

Laura E. Hinton; Mary A. McLoughlin; Susan E. Johnson; Steven E. Weisbrode

The records of 23 dogs and cats diagnosed with spontaneous gastroduodenal perforation (GDP) were retrospectively reviewed. Survival was 63% in dogs and 14% in cats. Rottweilers <5 years of age were overrepresented. Clinical evidence of gastrointestinal bleeding was common in dogs but not in cats. Shock was an uncommon presenting condition in dogs and was not closely linked to outcome. In fact, progression of an ulcerating lesion to GDP was not associated with marked changes in symptoms exhibited by many patients in this study. Most GDPs were associated with histopathological evidence of subacute or chronic peritoneal reaction at the time of diagnosis. This suggests that diagnostic methods employed lacked sensitivity in identifying early perforating lesions, and that dramatic signs of acute abdomen following gastroduodenal perforation may not be as common as was previously thought.


Journal of Veterinary Internal Medicine | 2004

Antibiotic‐Responsive Histiocytic Ulcerative Colitis in 9 Dogs

Roger A. Hostutler; Brian J. Luria; Susan E. Johnson; Steven E. Weisbrode; Robert G. Sherding; Jordan Q. Jaeger; W. Grant Guilford

Canine histiocytic ulcerative colitis (HUC) is characterized by colonic inflammation with predominantly periodic acid-Schiff (PAS)-positive macrophages. The inflammation results in colonic thickening, ulcerations, and distortion of normal glandular architecture. Resultant clinical signs consist of chronic large bowel diarrhea, tenesmus, and marked weight loss, and the disease frequently results in euthanasia. Conventional therapy consists of some combination of prednisone, azathioprine, sulfasalazine, and metronidazole. Nine dogs (8 Boxers and 1 English Bulldog) with histologic confirmation of HUC were treated with antibiotic therapy (either with enrofloxacin alone or in combination with metronidazole and amoxicillin). Clinical signs, physical examination findings, laboratory abnormalities, and the histologic severity of the disease were evaluated. Four of the 9 dogs had been treated previously with conventional therapy and had failed to respond favorably; then, these dogs were placed on antibiotic therapy (enrofloxacin, n = 1; enrofloxacin, metronidazole, and amoxicillin, n = 3) and had resolution of clinical signs within 3-12 days. Five dogs were treated solely with antibiotic therapy (enrofloxacin, n = 1; enrofloxacin and metronidazole, n = 1; enrofloxacin, metronidazole, and amoxicillin, n = 3), and clinical signs resolved in 2-7 days. Repeated biopsy specimens were obtained from 5 dogs after treatment, and all showed marked histologic improvement. The increase in body weight after treatment was statistically significant (P = .01). Three dogs currently are not on any treatment and have had resolution of clinical signs for up to 14 months. These observations suggest that an infectious agent responsive to antibiotics plays an integral role in the clinical manifestation of canine HUC, and they support the use of antibiotics in its treatment.


Javma-journal of The American Veterinary Medical Association | 2008

Acid-base and hormonal abnormalities in dogs with naturally occurring diabetes mellitus.

Lawren L. Durocher; Kenneth W. Hinchcliff; Stephen P. DiBartola; Susan E. Johnson

OBJECTIVE To examine acid-base and hormonal abnormalities in dogs with diabetes mellitus. DESIGN Cross-sectional study. ANIMALS 48 dogs with diabetes mellitus and 17 healthy dogs. PROCEDURES Blood was collected and serum ketone, glucose, lactate, electrolytes, insulin, glucagon, cortisol, epinephrine, norepinephrine, nonesterified fatty acid, and triglyceride concentrations were measured. Indicators of acid-base status were calculated and compared between groups. RESULTS Serum ketone and glucose concentrations were significantly higher in diabetic than in healthy dogs, but there was no difference in venous blood pH or base excess between groups. Anion gap and strong ion difference were significantly higher and strong ion gap and serum bicarbonate concentration were significantly lower in the diabetic dogs. There were significant linear relationships between measures of acid-base status and serum ketone concentration, but not between measures of acid-base status and serum lactate concentration. Serum insulin concentration did not differ significantly between groups, but diabetic dogs had a wider range of values. All diabetic dogs with a serum ketone concentration > 1,000 micromol/L had a serum insulin concentration < 5 microU/mL. There were strong relationships between serum ketone concentration and serum glucagon-insulin ratio, serum cortisol concentration, and plasma norepinephrine concentration. Serum beta-hydroxybutyrate concentration, expressed as a percentage of serum ketone concentration, decreased as serum ketone concentration increased. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that ketosis in diabetic dogs was related to the glucagon-insulin ratio with only low concentrations of insulin required to prevent ketosis. Acidosis in ketotic dogs was attributable largely to high serum ketone concentrations.


Journal of The American Animal Hospital Association | 2011

Rhinoscopic Diagnosis of Eucoleus boehmi Infection in a Dog

Mieke Baan; Aimee C. Kidder; Susan E. Johnson; Robert G. Sherding

A dog presenting for chronic purulent nasal discharge was diagnosed with an Eucoleus boehmi infection based upon rhinoscopic appearance of the nasal worms in situ, identification of the adult parasites in rhinoscopic nasal biopsies, and ova in the feces. The dog was successfully treated with a 2 wk course of fenbendazole and measures preventing reinfection through coprophagia. Patients with chronic nasal discharge should have a fecal examination performed to rule out infection with E. boehmi.


Digestive Diseases and Sciences | 1983

Postprandial release of gastric inhibitory polypeptide (GIP) and pancreatic polypeptide in dogs with pancreatic acinar atrophy: Correction of blunted GIP response by addition of pancreatic enzymes to a meal

William A. Rogers; Thomas M. O'Dorisio; Susan E. Johnson; Samuel Cataland; Roger Price Stradley; Robert G. Sherding

In order to evaluate the enteropancreatic hormone axis in dogs with pancreatic acinar atrophy, we measured the release of gastric inhibitory polypeptide and pancreatic polypeptide in response to a standard meal and a meal containing pancreatic enzymes in affected dogs and controls. Postprandial release of pancreatic polypeptide was normal in dogs with pancreatic atrophy and was not affected by addition of pancreatic enzymes to the food. Gastric inhibitory polypeptide was not released after a standard meal in affected dogs, but this blunted response was corrected by the addition of pancreatic enzymes to the food. Feeding the enzyme alone did not stimulate a gastric inhibitory polypeptide response. These results, in part, support similar observations previously reported in children with exocrine pancreatic insufficiency associated with cystic fibrosis. We conclude that dogs with idiopathic pancreatic acinar atrophy can be used as an animal model for future study of enteropancreatic hormonal abnormalities that occur in human beings with exocrine pancreatic insufficiency.


Journal of Veterinary Internal Medicine | 2011

Effects of Zinc‐l‐Carnosine and Vitamin E on Aspirin‐Induced Gastroduodenal Injury in Dogs

M. Baan; Robert G. Sherding; Susan E. Johnson

BACKGROUND Nonsteroidal anti-inflammatory drugs frequently cause gastrointestinal (GI) injury. Zinc-L-carnosine has antioxidant, anti-inflammatory, mucosal protective, and healing properties in rodent models and in some human studies of GI injury. HYPOTHESIS The combination of zinc-L-carnosine and vitamin E attenuates aspirin-induced gastroduodenal mucosal injury. ANIMALS Eighteen healthy random-source Foxhound dogs. METHODS In this randomized, double-blinded, placebo-controlled study dogs were treated with placebo (n = 6; 0X group), 30 mg/30 IU (n = 6; 1X group), or 60 mg/60 IU (n = 6; 2X group) zinc-L-carnosine/vitamin E orally every 12 hours for 35 days. Between Day 7 and 35, GI mucosal lesions were induced with aspirin (25 mg/kg p.o. q8h). Mucosal injury lesions (hemorrhage, erosion, and ulcer) were assessed by gastroduodenoscopy on Days 14, 21, and 35 with a 12-point scoring scale. RESULTS At baseline (Day -1) gastroscopy scores were not significantly different between groups (mean ± SD: 0X, 4.4 ± 0.8; group 1X, 4.4 ± 0.6; group 2X, 4.2 ± 0.3; P= .55). Gastroscopy scores increased significantly in all groups between Day -1 and Days 14, 21, and 35 (P < .0001). On Day 35, gastroscopy scores were 29.2 ± 5.2 (0X), 27.3 ± 3.7 (1X), and 28.6 ± 3.3 (2X). Mean gastroscopy scores were not significantly different among treatment groups on any of the days (P = .61). CONCLUSIONS AND CLINICAL IMPORTANCE Administration of the combination of zinc-L-carnosine and vitamin E at 1X or 2X dosing did not attenuate aspirin-induced gastroduodenal mucosal injury.


Journal of The American Animal Hospital Association | 2009

Esophageal diverticulum associated with a trichobezoar in a cat.

Lawren L. Durocher; Susan E. Johnson; Eric M. Green

A 9-year-old, castrated male, domestic longhaired cat was evaluated for persistent regurgitation over the previous month. The cat had presented 9 months earlier and was diagnosed with esophageal obstruction secondary to a trichobezoar. The trichobezoar had been removed endoscopically, and the cat was subsequently fed a canned prescription diet. The owners noted only infrequent regurgitation over the following 9 months. After signs recurred, contrast radiography with fluoroscopy revealed an esophageal diverticulum at the thoracic inlet, with an ovoid filling defect. Decreased esophageal motility was noted distal to the diverticulum. Esophagoscopy confirmed the presence of a trichobezoar within an esophageal diverticulum. Following removal of the trichobezoar and therapy to prevent trichobezoar formation, the cat did well for 2 months until it died suddenly with signs of hyperventilation and open-mouth breathing.


Journal of The American Animal Hospital Association | 1998

Physaloptera infection in 18 dogs with intermittent vomiting

Theisen Sk; LeGrange Sn; Susan E. Johnson; Robert G. Sherding; Willard

Physaloptera infections were diagnosed endoscopically in 18 dogs. Each case had vomiting as the primary clinical sign, and four cases had regurgitation as a concurrent sign. Fecal flotations, using magnesium sulfate solution, were performed in 12 of the 18 cases and were negative for Physaloptera eggs. In 12 of the 18 cases, only one worm was seen during endoscopic examination. Fifteen of 18 cases were treated with pyrantel pamoate, and 10 of 12 cases with follow-up had resolution of their vomiting.


International Journal of Behavioral Development | 2017

Toddlers’ Differential Susceptibility to the Effects of Coparenting on Social–Emotional Adjustment

Lauren E. Altenburger; Sarah N. Lang; Sarah J. Schoppe-Sullivan; Claire M. Kamp Dush; Susan E. Johnson

The paper reports on a study which tested whether infants high in negative affectivity are differentially susceptible to observed coparenting behavior in relation to their subsequent social–emotional development. Data came from a longitudinal study of 182 US dual-earner, primiparous couples and their infant children. At nine-months postpartum, child negative affectivity was reported by mothers and fathers and supportive and undermining coparenting behavior were assessed from mother-father-infant observations. At 27-months mothers reported on toddlers’ externalizing behavior and dysregulation using a clinical assessment tool designed to identify competencies and areas of concern in toddlers’ social–emotional development. Hierarchical regression analyses revealed partial support for the differential susceptibility hypothesis. Specifically, infants high in negative affectivity had lower levels of dysregulation when embedded in a more supportive coparenting context, and higher levels of dysregulation when embedded in a less supportive coparenting context. In contrast, supportive coparenting behavior was not relevant for the dysregulation of infants initially low in negative affectivity.


Veterinary Journal | 2016

Proteinuria and lipoprotein lipase activity in Miniature Schnauzer dogs with and without hypertriglyceridemia

Eva Furrow; J.Q. Jaeger; V.J. Parker; Kenneth W. Hinchcliff; Susan E. Johnson; S.J. Murdoch; I.H. de Boer; R.G. Sherding; John D. Brunzell

Spontaneous hyperlipidemia in rats causes glomerular disease. Idiopathic hypertriglyceridemia (HTG) is prevalent in Miniature Schnauzers, but its relationship with proteinuria is unknown. Decreased activity of major lipid metabolism enzymes, lipoprotein lipase (LPL) and hepatic lipase (HL), may play a role in the cyclic relationship between hyperlipidemia and proteinuria. These enzymes have also not been previously investigated in Miniature Schnauzers. The aims of this study were to determine the relationship between HTG and proteinuria in Miniature Schnauzers and to measure LPL and HL activities in a subset of dogs. Fifty-seven Miniature Schnauzers were recruited (34 with and 23 without HTG). Fasting serum triglyceride concentrations and urine protein-to-creatinine ratios (UPC) were measured in all dogs, and LPL and HL activities were determined in 17 dogs (8 with and 9 without HTG). There was a strong positive correlation between triglyceride concentration and UPC (r = 0.77-0.83, P < 0.001). Proteinuria (UPC ≥ 0.5) was present in 60% of dogs with HTG and absent from all dogs without HTG (P < 0.001). Proteinuric dogs were not azotemic or hypoalbuminemic. Dogs with HTG had a 65% reduction in LPL activity relative to dogs without HTG (P < 0.001); HL activity did not differ. Proteinuria occurs with HTG in Miniature Schnauzers and could be due to lipid-induced glomerular injury. Reduced LPL activity may contribute to the severity of HTG, but further assay validation is required.

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