Proliferative glomerulonephritis and chronic active hepatitis with cirrhosis associated with Corynebacterium parvum immunotherapy in a dog

Ivermectin, a broad-spectrum antiparasitic agent, was believed responsible for signs of CNS dysfunction in a dog. Within 2 hours of oral administration of ivermectin, the dog had hind limb ataxia. Neurologic signs progressed rapidly until the dog was in a semicomatose state at admission 20 hours later. The dog improved gradually under supportive care. The ivermectin had been given for suspected endoparasitism. Clinical signs were similar to those reported in dogs with clinical and experimental exposure to ivermectin.     

Adverse reactions suggestive of type III hypersensitivity in six healthy dogs given human albumin

CASE DESCRIPTION:6 healthy dogs given human albumin solution as part of a study were examined following development of an immediate hypersensitivity reaction (1 dog) and signs suggestive of a type III hypersensitivity reaction (all 6 dogs). CLINICAL FINDINGS: All 6 dogs were healthy prior to administration of human albumin solution. One dog developed signs of an immediate hypersensitivity reaction, characterized by vomiting and facial edema, during administration of human albumin solution. All 6 dogs developed signs of a delayed adverse reaction 5 to 13 days after administration of human albumin solution. Initial clinical signs included lethargy, lameness, edema, cutaneous lesions indicative of vasculitis, vomiting, and inappetance. TREATMENT AND OUTCOME: In the dog with signs of immediate hypersensitivity, signs resolved after administration of human albumin solution was discontinued and diphenhydramine was administered. Supportive treatment was provided after dogs developed signs of a delayed adverse reaction. Four dogs recovered, but 2 dogs died despite treatment. All 6 dogs were found to have antihuman albumin antibodies. There was no evidence of contamination of the human albumin solution. CLINICAL RELEVANCE: Findings suggest that administration of human albumin solution in healthy dogs with normal serum albumin concentrations may result in signs of a type III hypersensitivity reaction.     

Acute myelomonocytic leukemia (AML-M4) in a dog with the extradural lesion

A two-year-old dog having presented with neurological signs showed marked leukocytosis and appearance of blast cells in the peripheral blood. Hematological and bone marrow examination showed an increase in blasts having both myeloid and monocytic cells characteristics. The dog was diagnosed with acute myelomonocytic leukemia (AML-M4) on the basis of bone marrow findings. Although the dog was treated with a multi-combination chemotherapy, the neurological abnormalities progressed and the dog was euthanized. Myelographic examination and necropsy revealed the extradural lesion formed by AML-M4 around the cervical spinal cord and this lesion was considered as a cause of the neurological signs.     

Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide

Necrolytic migratory erythema (NME; also known as superficial necrolytic dermatitis) is a syndrome most often associated with certain chronic liver diseases or pancreatic glucagonomas. In humans with glucaconoma‐associated NME, skin lesions usually respond to octreotide, a somatostatin analogue that inhibits glucagon release. In this report an 11‐year‐old golden retriever dog with pancreatic glucononoma and metastasis to the regional lymph nodes, spleen and liver was diagnosed with NME. The dog exhibited erosions, ulcers and crusts on the paws, pressure points, muzzle, periocular area and prepuce. The dog was also anorexic and had difficulty walking. Because metastasis precluded surgery, treatment was initiated with subcutaneous octreotide (2 μg/kg twice daily). Skin lesions and systemic clinical signs improved markedly within 5 days. The dosage was increased to nearly 3 μg/kg twice daily and signs almost completely resolved within 10 days. Anorexia was the major adverse effect observed. During the following month, both dosage (1–3.7 μg/kg) and frequency (two to four times daily) of the octreotide injections were adjusted to permit control of clinical signs while maintaining adequate appetite. Temporary cessation of octreotide administration resulted in the rapid recurrence of skin lesions. Resuming injections led to improvement of clinical signs within 48 h. The dog was later euthanized because of progressive metastatic disease. In conclusion, subcutaneous octreotide injections were beneficial in this dog with glucagonoma‐associated NME. This somatostatin analogue could be a valuable option to treat canine patients with non‐resectable or relapsing pancreatic glucagonoma‐associated NME.     

Suspected Phenobarbital‐Induced Pseudolymphoma in a Dog

Pseudolymphoma is a drug reaction to anti‐epileptics that is well recognized in humans; it has been reported in one cat but not dogs. In this report, lymphoma‐like clinical signs are suspected to be secondary to phenobarbital administration in a dog. A 2.5‐year‐old male, neutered Shepherd mix presented for a 3‐day history of progressive ataxia, dazed mentation, pyrexia, and lethargy. While hospitalized, the dog developed generalized lymphadenopathy and sustained pyrexia. The dog was receiving levetiracetam and phenobarbital for epilepsy, and serum concentrations of both were within standard therapeutic ranges. Abdominal ultrasound revealed hepatomegaly, splenomegaly, and generalized lymphadenopathy. Cytology of the peripheral lymph nodes was consistent with reactive lymph nodes, and aspirates of the liver and spleen revealed histiocytic‐neutrophilic inflammation. Phenobarbital was discontinued and replaced with zonisamide. Within 24 hours, the dog was normothermic, and other clinical signs resolved within a week. This case highlights a potentially serious yet reversible adverse reaction to phenobarbital in a dog. This idiosyncratic reaction could be mistaken for neoplasia and is an important differential for lymphoma‐like signs in any dog administered phenobarbital.     

Allergic inhalant dermatitis attributable to marijuana exposure in a dog

Exposure to marijuana was believed to be responsible for clinical signs consistent with allergic inhalant dermatitis in a dog. The dog had facial and pedal pruritus associated with bilateral ocular discharge. Clinical signs resolved when the dog was kenneled, but returned when the dog was returned to its home. The results of intradermal skin testing, using a standard tray of 51 inhalant extracts, did not adequately account for the dog's clinical signs. Later, the owners indicated that previous residents of the owners' home had cultivated marijuana intensively inside and outside of the home. Intradermal skin testing with a source of marijuana pollen extract was performed, yielding a positive reaction in the dog and a negative reaction in another dog without clinical or historical evidence of allergic inhalant dermatitis. The affected dog was treated successfully and exclusively by hyposensitization with marijuana pollen extract.     

Chronic primary splenic torsion with peritoneal adhesions in a dog: case report and literature review

Primary splenic torsion in dogs is uncommon and can occur in acute or chronic form. The chronic form is difficult to diagnose because the clinical signs are vague and sometimes intermittent. A dog with a history of diaphragmatic hernia repair two years previously presented with chronic, vague clinical signs and an abdominal mass. The mass was revealed to be spleen on ultrasonography. On exploratory laparotomy, the dog was found to have a splenic torsion of approximately 180 degrees with mature, fibrous adhesions retaining the spleen in a torsed position. A splenectomy was performed, and the dog recovered uneventfully with complete resolution of prior clinical signs. Prognosis for dogs with splenic torsion is good, although complications are relatively common.     

Adipsic hypernatremia in a dog with antithyroid antibodies in cerebrospinal fluid and serum

A 4-year-old, male Labrador retriever, weighing 27 kg, presented with abrupt clinical signs including mental retardation, circling and head pressing. The dog never ingested water by choice. An adipsia of the dog was persisted and developed to hypernatremia with artifactual hyperchloremia. Serial endocrine results and image findings were suggestive of a hypothyroidism. The dog revealed the presence of antithyroid antibodies in the cerebrospinal fluid and serum. With the administration of levothyroxine sodium, his neurologic signs were alleviated within the first week of treatment and adipsia was also resolved.     

Toxic Myopathy in a Dog Associated with the Presence of Monensin in Dry Food

This report describes a case of toxic myopathy in a two year old sheltie dog with clinical signs of profound weakness, myoglobinuria, and muscle enzyme elevations. The clinical signs were likely related to the accidental inclusion of monensin sodium in the dog's food. This food was prepared by a small feed milling company that also prepares cattle and chicken rations. A change of dog food resulted in remission of the clinical signs.     

Magnetic resonance imaging in the diagnosis and surgical management of sacral osteochondrosis in a mastiff dog

The clinical, radiographic, magnetic resonance imaging (MRI), surgical and pathological findings related to an osteochondral lesion of the sacrum in a mastiff dog are described. The dog showed chronic signs of pain in its pelvic limbs. Radiography revealed a triangular mineralised opacity at the craniodorsal aspect of the sacrum consistent with sacral osteochondrosis. A T2-weighted spin-echo MRI revealed dorsal and lateral compression of the cauda equina. The osteochondral fragment was removed via a dorsal laminectomy, and the clinical signs resolved. Histological abnormalities in the fragment were consistent with a diagnosis of osteochondrosis.     

Acupuncture treatment for idiopathic Horner's syndrome in a dog

A one-year-old female English Cocker Spaniel dog with idiopathic Horner''s Syndrome is described. The specific clinical signs in this specimen were miosis, ptosis, enophthalmos, and prolapsed nictitans for 2 days following sudden onset. According to history taking, ophthalmic, neurological, and radiological examination, the patient was diagnosed with idiopathic Horner''s syndrome. Manual acupuncture treatment was applied to the dog on local points two times in 2 days. The local acupoints were ST-4 (Di Chang) and GB-1 (Tong Zi Liao). The day after the initial acupuncture treatment, clinical signs related to idiopathic Horner''s syndrome had almost disappeared. The day after the second treatment, specific clinical signs were completely absent. During this period, the dog did not receive any orthodox treatment. Thus, it is suggested that manual acupuncture might be an effective therapy for idiopathic Horner''s syndrome.     

Delayed primary surgical treatment in a dog with a persistent right aortic arch

A 5-year-old, 1.36-kg, neutered male Yorkshire terrier was referred for evaluation of a persistent right aortic arch with concurrent megaesophagus. The dog was 3 months old when clinical signs were first noted, 2 years of age when diagnosed with megaesophagus, and 4 years of age when diagnosed with vascular ring anomaly (VRA). Surgical correction of the VRA was performed when the dog was 5 years of age, after gastrostomy tube feeding for 1 year to maintain nutritional requirements and mitigate the degree and duration of the esophageal distention. Thirteen months after surgery, the dog was eating soft dog food with no vomiting or regurgitation.     

Cholangiohepatitis in a dog.

Cholangiohepatitis was diagnosed in a dog with a 4-day history of anorexia, vomiting, fever, and icterus. Additional findings included signs of depression, dehydration, hepatosplenomegaly, and abdominal discomfort. Exploratory laparotomy was performed, and specimens of liver, spleen, and bile were obtained. Histologic evaluation of liver and spleen revealed acute, suppurative cholangio-hepatitis and splenitis, respectively. Cultures of liver and bile yielded Klebsiella sp. The dog responded to rehydration and intravenous administration of chloramphenicol. Although uncommon, cholangiohepatitis should be suspected in dogs with anorexia, fever, vomiting, icterus, and signs of abdominal discomfort. Definitive diagnosis requires bacterial cultures of liver and bile. Administration of an appropriate antibiotic should resolve clinical signs.     

Keratoconjunctivitis sicca and diabetes mellitus in a dog.

Diabetes mellitus and keratoconjunctivitis sicca were diagnosed in a female Poodle. The dog was treated for diabetes and keratoconjunctivitis sicca until blood glucose concentrations were within normal limits. Treatment for keratoconjunctivitis sicca was suspended then, and signs of this disorder did not appear again. Most of the factors known to predispose to keratoconjunctivitis sicca were not applicable to this dog. On the basis of observations made in this dog, we suggest that diabetes mellitus and keratoconjunctivitis sicca may be linked. Clinical signs of the disorders developed simultaneously and resolved when diabetes mellitus was controlled with insulin.     

Cultivation and molecular identification of Ehrlichia canis and Ehrlichia chaffeensis from a naturally co-infected dog in Venezuela

Background: Diagnosis of canine ehrlichiosis in Venezuela is normally performed by examination of buffy coat smears (BCS). Characteristic inclusion bodies are frequently observed in leukocytes and platelets from dogs with clinical signs of the disease. Objective: The purpose of this study was to investigate the co-infection of a dog with Ehrlichia canis and E hrlichia chaffeensis using microbiological and molecular techniques. Methods: Primary cultures of monocytes from a dog showing signs of ehrlichiosis were performed. Ehrlichial inclusions in blood cells were demonstrated by BCS and in cultured cell smears with direct immunofluorescence and Dip Quick staining. Nested PCR analysis was performed with DNA from blood samples and cultures, using primers specific for E. canis and E. chaffeensis. The amplified DNA fragments were sequenced to confirm the specificity of the amplifications. Results: The BCS of the naturally infected dog contained intracellular morulae. Ehrlichial inclusions were observed 9 days after inoculation of the primary cultures. After 3 passages with monocytes from a healthy dog, 65% of infected cells, and cells with >60 morulae were observed. A healthy female German Shepherd dog, seronegative for E. canis and E. chaffeensis antigens and without contact to ticks, was inoculated with an infected culture. The animal developed signs of canine monocytic ehrlichiosis and became seropositive. Nested PCR results and sequencing of amplified DNA fragments demonstrated the simultaneous presence of E. canis and E. chaffeensis in both dogs. Conclusions: This is the first report of E. chaffeensis in dogs in South America. This organism was previously identified in dogs by PCR only in the United States.     

Putative peanut allergy-induced urticaria in a dog

A 9-year-old, spayed male schnauzer dog was presented with vomiting, diarrhea, generalized erythema, pruritic urticaria and conjunctival hyperemia after ingestion of peanut. The history, clinical signs, and histopathology of the lesions were compatible with a hypersensitivity reaction. The clinical signs resolved rapidly after treatment with prednisolone and antihistamine. This is the first report of urticaria caused by peanut ingestion in a dog.     

Thiamine deficiency in dogs due to the feeding of sulphite preserved meat

A 6-year-old dog, a 4-year-old dog and three 7-week-old puppies were diagnosed with thiamine deficiency caused by feeding sulphite treated meat. The 6-year-old dog presented with a history of inappetence, weight loss and vomiting that rapidly progressed to signs of multifocal intracranial disease including mental dullness, paresis, seizures, spontaneous nystagmus and strabismus. Thiamine pyrophosphate effect was elevated at 58% and magnetic resonance imaging revealed bilaterally symmetrical hyperintensity of the caudate nucleus and rostral colliculi. The dog recovered with thiamine supplementation. The 4-year-old dog and three 7-week-old puppies also presented with rapidly progressive multifocal central nervous system signs including ataxia, paresis, increased muscle tone, seizures, nystagmus and exophthalmos. The 4-year-old dog made a rapid recovery with thiamine supplementation. Euthanasia and necropsy of a puppy revealed malacia of multiple brainstem nuclei and oedema of the cerebral cortex. These findings were consistent with thiamine deficiency.     

Intestinal Entrapment and Strangulation Caused by Rupture of the Duodenocolic Ligament in Four Dogs

Objective — The purpose of this study was to describe four dogs with intestinal entrapment and strangulation caused by a rupture of the duodenocolic ligament.
Study Design — This case series documents historical findings, physical examination findings, diagnostic workup, surgical intervention, and outcome of four dogs confirmed at surgery with duodenocolic ligament rupture.
Results — Three of four dogs were German shepherds, and two of three German shepherds were intact males. The history, clinical signs, and physical examination findings were not specific for intestinal entrapment. The clinical signs in three of four dogs included chronic vomiting, diarrhea, anorexia, and lethargy. In the remaining dog, the clinical signs were vomiting and peracute collapse. This dog rapidly deteriorated over a few hours because of strangulation of the entrapped intestines. In two of four dogs, abdominal radiographs showed a distended colon displaced to the right side of the abdominal cavity. Surgery involved transection of the remaining ventral remnant of the duodenocolic ligament and replacing the colon into its normal anatomic position. The three dogs with chronic clinical signs were either still alive, or were euthanatized for unrelated problems. The dog with strangulation of the entrapped intestines was euthanatized at the time of surgery.
Conclusions and Clinical Relevance — Duodenocolic ligament rupture with secondary bowel entrapment can occur in dogs. The prognosis for these animals is favorable provided there is no vascular compromise of the entrapped bowel segments. The peracute history, progression of the disease process, and outcome of the fourth dog in this study indicate that surgery should be performed as an emergency procedure.     

Cecal perforation and adrenocortical adenoma in a dog

Cecal perforation was diagnosed in a dog with a history of acute vomiting. The dog also had an adrenocortical adenoma. Intestinal perforation can be a serious complication of cortico-steroid treatment in the dog, but has not been attributable to hyperadrenocorticism. Fever and an inflammatory CBC were not observed, which could have been secondary to adrenal-dependent hyperadrenocorticism. The acute abdominal crisis associated with peritonitis required quick resolution in an attempt to save the dog, but also precluded any further diagnostic procedures for possible hyperadrenocorticism. The signs that suggested hyper-adrenocorticism in this dog included alopecia, lymphopenia, eosinopenia, high liver enzyme activities, hypercholesterolemia, and one large and one small adrenal gland. This latter finding presumably indicated negative feedback suppression and atrophy attributable to a functional adrenocortical adenoma.