I have seen this in my canine patients. Have you seen it as well?
Case report: severe, symptomatic hypomagnesemia in acute leptospirosis.
Spichler A, Athanazio DA, Furtado J, Seguro A, Vinetz JM.
We report a case of severe hypomagnesemia in non-oliguric acute renal failure caused by leptospirosis that required large doses of magnesium replacement during the acute phase of disease. Biochemical studies confirmed kidney-related magnesium wasting and the mechanisms of this defect are discussed. Magnesium imbalance with its attendant clinical complications occurs in leptospirosis and should be monitored and treated aggressively in cases of leptospirosis-induced non-oliguric acute kidney injury.
PMCID: PMC2637037
PMID: 19052304 [PubMed - indexed for MEDLINE]
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Monday, June 22, 2009
Monday, June 15, 2009
Evanger's Dog and Cat Food Warning
FDA Suspends Temporary Emergency Permit for Evanger's
Recently the FDA and USDA announced suspension of a permit for Evanger's Dog and Cat Food Company.
In the statement the FDA reports that:
"Evanger's, operating in Wheeling, Illinois, deviated from the prescribed process, equipment, product shipment, and recordkeeping requirements in the production of the company's thermally processed low acid canned food (LACF) products. The deviations in their processes and documentation could result in under-processed pet foods, which can allow the survival and growth of Clostridium botulinum (C. botulinum), a bacterium that causes botulism in some animals as well as in humans."
A recall has not been announced. But please do keep in mind the possibility of Clotridium botulinum infection in cases presenting with flaccid paralysis who have ingested Evanger's canned foods.
Recently the FDA and USDA announced suspension of a permit for Evanger's Dog and Cat Food Company.
In the statement the FDA reports that:
"Evanger's, operating in Wheeling, Illinois, deviated from the prescribed process, equipment, product shipment, and recordkeeping requirements in the production of the company's thermally processed low acid canned food (LACF) products. The deviations in their processes and documentation could result in under-processed pet foods, which can allow the survival and growth of Clostridium botulinum (C. botulinum), a bacterium that causes botulism in some animals as well as in humans."
A recall has not been announced. But please do keep in mind the possibility of Clotridium botulinum infection in cases presenting with flaccid paralysis who have ingested Evanger's canned foods.
What have our consultants been writing?
Christal Pollock, DVM, DABVP (Avian)
Carpenter JW, Pollock CG, Koch DE, Hunter RP. Single- and multiple-dose pharmacokinetics of marbofloxacin after oral administration to rabbits. Am J Vet Res. 2009 Apr;70(4):522-6. PubMed PMID: 19335109.
Pollock CG. West Nile virus in the Americas. J Avian Med Surg. 2008 Jun;22(2):151-7. PubMed PMID: 18689077.
Pollock C. Diagnosis and treatment of avian renal disease. Vet Clin North Am Exot Anim Pract. 2006 Jan;9(1):107-28. Review. PubMed PMID: 16407082.
Michael D. Willard, DVM, MS, DACVIM (Small Animal Internal Medicine)
Willard MD. Endoscopic diagnosis of diseases causing vomiting. Top Companion Anim Med. 2008 Nov;23(4):162-8. Review. PubMed PMID: 19081549.
Farnsworth CC, Herman JD, Osterstock JB, Porterpan BL, Willard MD, Hooper RN, Roussel AJ, Schmitz DG, Fogelberg K, Kochevar DT. Assessment of clinical reasoning skills in veterinary students prior to and after the clinical year of training. J Am Vet Med Assoc. 2008 Sep 15;233(6):879-82. PubMed PMID: 18795847.
Willard M. Therapeutic approach to chronic electrolyte disorders. Vet Clin North Am Small Anim Pract. 2008 May;38(3):535-41, x. Review. PubMed PMID: 18402879.
Chelsea Greenberg, DVM, DACVIM (Oncology)
Greene SN, Lucroy MD, Greenberg CB, Bonney PL, Knapp DW. Evaluation of cisplatin administered with piroxicam in dogs with transitional cell carcinoma of the urinary bladder. J Am Vet Med Assoc. 2007 Oct 1;231(7):1056-60. PubMed PMID: 17916030.
Greenberg CB, Boria PA, Borgatti-Jeffreys A, Raskin RE, Lucroy MD. Phase II clinical trial of combination chemotherapy with dexamethasone for lymphoma in dogs. J Am Anim Hosp Assoc. 2007 Jan-Feb;43(1):27-32. PubMed PMID: 17209082.
Carpenter JW, Pollock CG, Koch DE, Hunter RP. Single- and multiple-dose pharmacokinetics of marbofloxacin after oral administration to rabbits. Am J Vet Res. 2009 Apr;70(4):522-6. PubMed PMID: 19335109.
Pollock CG. West Nile virus in the Americas. J Avian Med Surg. 2008 Jun;22(2):151-7. PubMed PMID: 18689077.
Pollock C. Diagnosis and treatment of avian renal disease. Vet Clin North Am Exot Anim Pract. 2006 Jan;9(1):107-28. Review. PubMed PMID: 16407082.
Michael D. Willard, DVM, MS, DACVIM (Small Animal Internal Medicine)
Willard MD. Endoscopic diagnosis of diseases causing vomiting. Top Companion Anim Med. 2008 Nov;23(4):162-8. Review. PubMed PMID: 19081549.
Farnsworth CC, Herman JD, Osterstock JB, Porterpan BL, Willard MD, Hooper RN, Roussel AJ, Schmitz DG, Fogelberg K, Kochevar DT. Assessment of clinical reasoning skills in veterinary students prior to and after the clinical year of training. J Am Vet Med Assoc. 2008 Sep 15;233(6):879-82. PubMed PMID: 18795847.
Willard M. Therapeutic approach to chronic electrolyte disorders. Vet Clin North Am Small Anim Pract. 2008 May;38(3):535-41, x. Review. PubMed PMID: 18402879.
Chelsea Greenberg, DVM, DACVIM (Oncology)
Greene SN, Lucroy MD, Greenberg CB, Bonney PL, Knapp DW. Evaluation of cisplatin administered with piroxicam in dogs with transitional cell carcinoma of the urinary bladder. J Am Vet Med Assoc. 2007 Oct 1;231(7):1056-60. PubMed PMID: 17916030.
Greenberg CB, Boria PA, Borgatti-Jeffreys A, Raskin RE, Lucroy MD. Phase II clinical trial of combination chemotherapy with dexamethasone for lymphoma in dogs. J Am Anim Hosp Assoc. 2007 Jan-Feb;43(1):27-32. PubMed PMID: 17209082.
Neurology Case of the Month
This report is based on video evaluation and conversation with Dr. Smith regarding Fluffy Jones [regarding neurologic signs following ear cleaning].
The video evaluation is as follows: Mentation: BAR, Gait: mild vestibular quality ataxia, occasional stumbling to the right and/or left side, no evidence of UMN involvement or paresis, CN’s: Horner’s syndrome OD-rest NSF and no evidence of spontaneous nystagmus. Postural responses and reflexes were not evaluated. A mild right head tilt was also evident and occasional wide head excursions noted. The patient appears extremely alert and responsive and there does not seem to be evidence of central vestibular disease. However, she is currently on prednisone which may mask some clinical abnormalities.
Denervation hypersensitivity testing should be performed using phenylephrine OU. To confirm that the Horner’s syndrome is indeed a third order Horner’s (i.e. a post ganglionic lesion typically seen with otitis media), phenylephrine drops are used OU and any ocular changes monitored every few minutes. If resolution or near-resolution of the Horner’s occurs in less than 20 minutes, then the lesion is post-ganglionic and would support our presumption that we are dealing with ear disease. If it is between 20-40 minutes, a second order Horner’s must be considered, such as is seen with diseases of the mediastinum. If it takes greater than 40 minutes for resolution, then disease within the cervical spinal cord or midbrain must be considered (which is highly unlikely in this cat).
Since no ototoxic drugs were used to my knowledge, clinical signs likely have resulted from irritation to the sympathetic innervation in the middle ear as well as the vestibulocochlear nerve in the inner ear during the ear cleaning. If so, clinical signs will likely resolve over time but it may take months for the Horner’s syndrome to fully disappear. However, since there is no indication for prednisone in this cat and since prednisone may very well be masking a possible central vestibular disorder, re-evaluation after tapering prednisone is indicated including a full neurologic exam. If signs recur or other signs arise, MRI scanning of the head may be indicated.
Georgina Barone, DVM, DACVIM (Neurology)
The video evaluation is as follows: Mentation: BAR, Gait: mild vestibular quality ataxia, occasional stumbling to the right and/or left side, no evidence of UMN involvement or paresis, CN’s: Horner’s syndrome OD-rest NSF and no evidence of spontaneous nystagmus. Postural responses and reflexes were not evaluated. A mild right head tilt was also evident and occasional wide head excursions noted. The patient appears extremely alert and responsive and there does not seem to be evidence of central vestibular disease. However, she is currently on prednisone which may mask some clinical abnormalities.
Denervation hypersensitivity testing should be performed using phenylephrine OU. To confirm that the Horner’s syndrome is indeed a third order Horner’s (i.e. a post ganglionic lesion typically seen with otitis media), phenylephrine drops are used OU and any ocular changes monitored every few minutes. If resolution or near-resolution of the Horner’s occurs in less than 20 minutes, then the lesion is post-ganglionic and would support our presumption that we are dealing with ear disease. If it is between 20-40 minutes, a second order Horner’s must be considered, such as is seen with diseases of the mediastinum. If it takes greater than 40 minutes for resolution, then disease within the cervical spinal cord or midbrain must be considered (which is highly unlikely in this cat).
Since no ototoxic drugs were used to my knowledge, clinical signs likely have resulted from irritation to the sympathetic innervation in the middle ear as well as the vestibulocochlear nerve in the inner ear during the ear cleaning. If so, clinical signs will likely resolve over time but it may take months for the Horner’s syndrome to fully disappear. However, since there is no indication for prednisone in this cat and since prednisone may very well be masking a possible central vestibular disorder, re-evaluation after tapering prednisone is indicated including a full neurologic exam. If signs recur or other signs arise, MRI scanning of the head may be indicated.
Georgina Barone, DVM, DACVIM (Neurology)
Thursday, April 30, 2009
Cool Recent Abstracts
SMALL ANIMAL
Intracranial Arachnoid Cysts in Dogs
from Compendium by Curtis W. Dewey - Veterinary Answers Consultant, Peter V. Scrivani, Ursula Krotscheck, Sofia Cerda-Gonzalez, Kerry Smith Bailey, Dominic J. Marino
Intracranial arachnoid cyst (IAC) is an infrequently reported developmental disorder seen primarily in small-breed dogs. It usually occurs in the caudal fossa, in the region of the quadrigeminal cistern. Although still considered uncommon, IAC is being recognized more frequently in veterinary medicine, coinciding with the increased availability of magnetic resonance imaging. In this article, clinical information from previously reported cases of canine IAC is combined with additional case information from our hospitals. Similar to IAC in people, it is thought that canine IAC is often an incidental finding. When IAC is responsible for neurologic disease in dogs, generalized seizures and cerebellovestibular dysfunction are the most common clinical presentations. Medical therapy of IAC focuses on management of increased intracranial pressure and seizures, if the latter are part of the clinical complaints. Surgical therapy of IAC involves either cyst fenestration or shunting the excess fluid to the peritoneal cavity.
Peripheral Nucleated Red Blood Cells as a Prognostic Indicator in Heatstroke in Dogs
from JVIM by I. Aroch, G. Segev, E. Loeb, Y. Bruchim
Heatstroke in dogs is often fatal and is associated with a high prevalence of secondary complications. Peripheral nucleated red blood cells (NRBC) occur in dogs with heatstroke, but their association with complications and the outcome is unclear. Peripheral NRBC are common in dogs with heatstroke and have prognostic significance. Forty client-owned dogs with naturally occurring heatstroke. Prospective, observational study. Dogs were followed from presentation to discharge or death. Serum biochemistry and coagulation tests were performed at presentation. CBC and evaluation of peripheral blood smears were performed at presentation and every 12 hours. The relative and the absolute NRBC numbers were calculated. Presence of NRBC was observed in 36/40 (90%) of the dogs at presentation. Median relative and absolute NRBC were 24 cells/100 leukocytes (range 0[ndash]124) and 1.48 × 103/[mu]L (range 0.0[ndash]19.6 × 103/[mu]L), respectively. Both were significantly higher in nonsurvivors (22) versus survivors (18) and in dogs with secondary renal failure and DIC versus those without these complications. Receiver operator curve analysis of relative NRBC at presentation as a predictor of death had an area under curve of 0.92. A cut-off point of 18 NRBC/100 leukocytes corresponded to a sensitivity and specificity of 91 and 88% for death. Relative and absolute numbers of peripheral NRBC are clinically useful, correlate with the secondary complications, and are sensitive and specific markers of death in dogs with heatstroke, although they should never be used as a sole prognostic indicator nor should they replace clinical assessment.
Relationships between Low Serum Cobalamin Concentrations and Methlymalonic Acidemia in Cats
from JVIM by C. G. Ruaux, J. M. Steiner, D. A. Williams
Serum cobalamin concentrations below reference range are a common consequence of gastrointestinal disease in cats. Serum cobalamin [le] 100 ng/L is associated with methylmalonic acidemia. To determine the prevalence of cobalamin deficiency, defined by elevated serum methylmalonic acid (MMA), in cats with serum cobalamin [le] 290 ng/L, and the optimum serum cobalamin concentration to predict cobalamin deficiency in cats. Residual serum samples (n = 206) from cats with serum cobalamin [le] 290 ng/L. Retrospective, observational study. Serum cobalamin and folate were measured with automated assays. Serum MMA was determined by gas chromatography-mass spectrometry. Cobalamin deficiency was defined as serum MMA > 867 nmol/L. Sensitivity and specificity of serum cobalamin concentrations [le]290 ng/L for detecting MMA > 867 nmol/L were analyzed using a receiver-operator characteristic curve. There was a negative correlation between serum cobalamin and MMA concentrations (Spearman's r=[minus]0.74, P < 0.0001). The prevalence of MMA [ge] 867 nmol/L in cats with serum cobalamin [le] 290 ng/L was 68.4%. Serum cobalamin [le] 160 ng/L had a 74% sensitivity and 80% specificity for detecting MMA > 867 nmol/L. No significant difference in serum folate concentrations was detected between affected and unaffected cats. Elevated MMA concentrations, suggesting cobalamin deficiency, are common in cats with serum cobalamin [le] 290 ng/L. Cobalamin deficiency is clinically significant, and supplementation with parenteral cobalamin is recommended for cats with gastrointestinal disease and low serum cobalamin concentrations.
For more on MMA in human beings, click here.
Small Mammals
Single- and multiple-dose pharmacokinetics of marbofloxacin after oral administration to rabbits
From AJVR by James W. Carpenter, MS, DVM; Christal G. Pollock, DVM (VETERINARY ANSWERS CONSULTANT); David E. Koch, MS; Robert P. Hunter, PhD
Objective—To determine the pharmacokinetics of marbofloxacin after oral administration every 24 hours to rabbits during a 10-day period.
Animals—8 healthy 9-month-old female New Zealand White rabbits.
Procedures—Marbofloxacin (5 mg/kg) was administered orally every 24 hours to 8 rabbits for 10 days. The first day of administration was designated as day 1. Blood samples were obtained at 0, 0.17, 0.33, 0.5, 0.75, 1, 1.5, 2, 3, 4, 5, 6, 8, 12, and 24 hours on days 1 and 10 of marbofloxacin administration. Plasma marbofloxacin concentrations were quantitated by use of a validated liquid chromatography–mass spectrometry assay. Pharmacokinetic analysis of marbofloxacin was analyzed via noncompartmental methods.
Results—After oral administration, mean ± SD area under the curve was 10.50 ± 2.00 μg·h/mL and 10.90 ± 2.45 μg·h/mL, maximum plasma concentration was 1.73 ± 0.35 μg/mL and 2.56 ± 0.71 μg/mL, and harmonic mean terminal half-life was 8.0 hours and 3.9 hours for days 0 and 10, respectively.
Conclusions and Clinical Relevance—Marbofloxacin administered orally every 24 hours for 10 days appeared to be absorbed well and tolerated by rabbits. Administration of marbofloxacin at a dosage of 5 mg/kg, PO, every 24 hours is recommended for rabbits to control infections attributable to susceptible bacteria.
EQUINE
Risk Factors for Equine Postoperative Ileus and Effectiveness of Prophylactic Lidocaine
from JVIM by S. Torfs, C. Delesalle, J. Dewulf, L. Devisscher, P. Deprez
Postoperative ileus (POI) is a frequent and often fatal complication of colic surgery. Reliably effective treatments are not available. To determine risk factors and protective factors associated with POI, and to assess the effect of lidocaine IV on short-term survival. One hundred and twenty-six horses that underwent small intestinal colic surgery and that survived for at least 24 hours postoperatively. Retrospective cross-sectional study. The association of 31 pre-, intra-, and postoperative variables with POI and the association of lidocaine treatment with short-term survival were investigated. Associations were evaluated with univariable logistic regression models, followed by multivariable analysis. Significant associations of high heart rate (odds ratio [OR] = 1.05, 95% confidence interval [CI] 1.03[ndash]1.08), the presence of more than 8 L of reflux at admission (OR = 3.02, 95% CI 1.13[ndash]8.02) and the performance of a small intestinal resection (OR = 2.46, 95% CI 1.15[ndash]5.27) with an increased probability of POI were demonstrated. Prophylactic lidocaine treatment was significantly associated with a reduced incidence of POI (OR = 0.25, 95% CI 0.11[ndash]0.56). Lidocaine treatment was also significantly associated with enhanced short-term survival (OR = 0.30, 95% CI 0.09[ndash]0.98). The variables associated with an increased risk of POI can be useful in identifying horses at risk of POI and in providing a more accurate prognosis. The results are supportive for lidocaine IV as an effective prokinetic treatment after small intestinal colic surgery.
Case of the Month - Feline Pemphigus
History
There are ulcerated lesions starting on ear margins, later involving lip margins and periocular area as well as neck. Pruritus started after ulcerated lesions appeared. Skin scraping - neg., DTM - neg., Cytology - PMN's and bacteria, C&S - pending, Dermohistopathology - pending, Bloodwork – normal. She is an outside cat, in a multicat household with no other pets involved. There are no external parasites, owner is not pruritic, no change in diet, on commercial pet food. Gave depo-medrol injection 10 days prior to biopsy. Expect biopsy results in 7 days.
Clinical Consultation
This consultation is based on our phone consultation, submitted history and clinical photos. Thank you for the clinical photos which were helpful. I agree with your suspicion that immune-mediated disease is most likely. Differential diagnoses would include: Erythema multiforme (drug-induced, paraneoplastic, idiopathic) and pemphigus foliaceus (drug-induced, paraneoplastic are possible causes). Lupus erythematosus less commonly occurs in cats so is considered less likely. A cutaneous drug reaction also appears less likely in this case given the cat’s lack of drug history (no medications were being administered prior to the onset of skin disease). Although severe allergic dermatitis can sometimes mimic immune-mediated disease in the cat, the severity of the clinical presentation also makes this less likely. I would also make sure to closely examine mucosal surfaces (perianal, oral)- mucosal surfaces are involved it could indicate vesicular auto-immune disease (pemphigus vulgaris, Stevens-Johnson Syndrome, epidermolysis bullosa acquisita). Immunosuppressive therapy will likely be required to control this disease process. Pending skin biopsies, I would recommend starting this cat on immunosuppressive doses of glucocorticoids (typically 2-3 mg/kg of Prednisolone [over prednisone] divided BID). I start to taper after there has been 75-80% improvement (often within 2 weeks). New lesions should not be developing & older lesions regressing. I would not recommend adding in an additional immunomodulatory agent at this time until after the biopsy results have been reviewed.
Additional follow-up is requested on this case: biopsy report, response to initial therapeutic recommendations, etc. Addendum comments and additional therapeutic recommendations can be made at that time.
Addendum
Per our phone conversation, the dermatopathology report is consistent with feline pemphigus foliaceus. Pemphigus foliaceus (PF) is a cutaneous auto-immune disease which most commonly occurs in middle aged to older cats. Another consideration would be paraneoplastic pemphigus; I would be suspicious of this if the skin lesions are not responding to appropriate therapy (this is typically more difficult to treat). Treatment for PF is often life-long, however some cats will go into extended periods of remission (without maintenance medications). Immunosuppressive therapy is required to control this disease. I recommend immunosuppressive doses of glucocorticoids (typically 2.2 mg/kg of Prednisolone [over prednisone] divided BID). I start to taper after there has been 75-80% improvement (often within 2 weeks). New lesions should not be developing & older lesions regressing. I often recommend a second immunosuppressive agent to control the disease and allow for lower doses of glucocorticoids to be used. Options include Chlorambucil or Atopica (Cyclosporine). Most commonly chlorambucil (0.1-0.2 mg/kg qd-qod) is used; tapered further over time. Monitor for myelosuppression. Obtain a baseline CBC, Chemistry profile & UA prior to initiating therapy. Recheck CBC values every 2 weeks for the first 6-8 weeks; then every 3-6 months. Although PF is often responsive to therapy, it can be a difficult auto-immune disease to manage. If remission is not initially achievable, I recommend referral to a veterinary dermatologist if possible.
Please contact me if this report is inconsistent with your clinical findings or you have additional questions. Please contact me at PetRays phone number listed below.
Terri Bonenberger, DVM
Diplomate, American College Veterinary Dermatology
3 week Update
The ulcerated lesions have healed and scabs have fallen off. The cat is doing very well.
Labels:
Atopica,
Cat,
Chlorambucil,
Cyclosporine,
DACVD,
Dermatology,
Feline,
Pemphigus,
Prednisolone,
Prednisone,
Terri Bonenberger
Thursday, January 29, 2009
Cool Recent Abstracts
American Journal of Veterinary Research
January 2009, Vol. 70, No. 1, Pages 99-104
Assessment of viremia associated with experimental primary feline herpesvirus infection or presumed herpetic recrudescence in cats
Hans D. Westermeyer, DVM, Sara M. Thomasy, DVM, PhD, Helen Kado-Fong, MS, David J. Maggs, BVSc
Objective—To detect feline herpesvirus type 1 (FHV-1) in blood of cats undergoing experimental primary herpetic disease or with spontaneous disease presumed to be caused by FHV-1 reactivation.
Animals—6 young specific-pathogen–free (SPF) cats and 34 adult cats from a shelter.
Procedures—Conjunctiva and nares of SPF cats were inoculated with FHV-1, and cats were monitored for 21 days. Periodically, blood was collected for CBC, serum biochemical analyses, and detection of FHV-1 DNA via PCR assay. For shelter cats, a conjunctival swab specimen was collected for FHV-1 PCR assay, and blood mononuclear cells were tested via virus isolation (with or without hydrocortisone) and FHV-1 PCR assay.
Results—All SPF cats developed clinical and clinicopathologic evidence of upper respiratory tract and ocular disease only. Via PCR assay, FHV-1 DNA was detected in blood of all SPF cats at least once between 2 and 15 days after inoculation. Feline herpesvirus type 1 DNA was detected in conjunctival swabs of 27 shelter cats; 25 had clinical signs of herpetic infection. However, virus was not isolated from mononuclear cell samples of any shelter cat regardless of passage number or whether hydrocortisone was present in the culture medium; FHV-1 DNA was not detected in any mononuclear cell sample collected from shelter cats.
Conclusions and Clinical Relevance—A brief period of viremia occurred in cats undergoing primary herpetic disease but not in cats undergoing presumed recrudescent herpetic disease. Viremia may be important in the pathogenesis of primary herpetic disease but seems unlikely to be associated with recrudescent disease.
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American Journal of Veterinary Research
January 2009, Vol. 70, No. 1, Pages 16-22
Evaluation of the distribution of enrofloxacin by circulating leukocytes to sites of inflammation in dogs
D. M. Boothe, DVM, PhD, A. Boeckh, DVM, PhD, H. W. Boothe, DVM, MS
Objective—To determine the effect of WBC accumulation on the concentration of enrofloxacin in inflamed tissues in dogs.
Animals—6 adult Bloodhounds.
Procedures—Dogs were instrumented bilaterally with tissue chambers. Peripheral WBCs collected from each dog were exposed in vitro to radiolabeled enrofloxacin (14C-ENR). Inflammation was induced with carrageenan in 1 chamber. Ten hours later, treated cells were administered IV to each dog such that 14C-ENR was delivered at a mean ± SD dosage of 212 ± 43 μg. Samples of extracellular fluid from inflammation and control chambers and circulating blood were then collected before (baseline) and for 24 hours after WBCs were administered. Samples were centrifuged to separate WBCs from plasma (blood) or chamber fluid. Radiolabeled enrofloxacin was scintigraphically detected and pharmacokinetically analyzed. Comparisons were made between extra- and intracellular chamber fluids by use of a Student paired t test.
Results—14C-ENR was not detectable in plasma, peripheral WBCs, control chambers, or baseline samples from inflammation chambers. However, 14C-ENR was detected in extra- cellular fluid from inflammation chambers (mean ± SD maximum concentration, 2.3 ± 0.5 ng/mL) and WBCs (maximum concentration, 7.7 ± 1.9 ng/mL). Mean disappearance half-life of 14C-ENR from extracellular fluid and WBCs from inflammation chambers was 26 ± 10 hours and 17 ± 6 hours, respectively.
Conclusions and Clinical Relevance—WBCs were responsible for the transport and release of 14C-ENR at sites of inflammation. Accumulation of drug by WBCs might increase the concentration of drug at the site of infection, thus facilitating therapeutic success.
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Veterinary Patholology 46:63-70 (2009)
Feline Gastrointestinal Eosinophilic Sclerosing Fibroplasia
L. E. Craig, E. E. Hardam, D. M. Hertzke, B. Flatland, B. W. Rohrbach and R. R. Moore
A retrospective study of cases of a unique intramural inflammatory mass within the feline gastrointestinal tract was performed in order to describe and characterize the lesion. Twenty-five cases were identified from archival surgical and postmortem tissues. The lesion most often occurred as an ulcerated intramural mass at the pyloric sphincter (n = 12) or the ileocecocolic junction or colon (n = 9); the remaining cases were in the small intestine. Seven cases also had lymph node involvement. The lesions were characterized by eosinophilic inflammation, large reactive fibroblasts, and trabeculae of dense collagen. Intralesional bacteria were identified in 56% of the cases overall and all of the ileocecocolic junction and colon lesions. Fifty-eight percent of cats tested had peripheral eosinophilia. Cats treated with prednisone had a significantly longer survival time than those receiving other treatments. We propose that this is a unique fibroblastic response of the feline gastrointestinal tract to eosinophilic inflammation that in some cases is associated with bacteria. The lesion is often grossly and sometimes histologically mistaken for neoplasia.
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Journal of Veterinary Internal Medicine
Volume 23 Issue 1, Pages 43 - 49
Clinical Evaluation of a Novel Liquid Formulation of L-Thyroxine for Once Daily Treatment of Dogs with Hypothyroidism
G. Le Traon 1 , S.F. Brennan 2 , S. Burgaud 1 , S. Daminet 3 , K. Gommeren 3 , L.J.I. Horspool 4 , D. Rosenberg 5 , and C.T. Mooney 2
Background: A liquid solution of levothyroxine (L-T4) is available for treatment of canine hypothyroidism.
Hypothesis: Once daily oral administration of a liquid L-T4 solution is effective and safe for controlling hypothyroidism in dogs.
Animals: Thirty-five dogs with naturally occurring hypothyroidism.
Methods: Dogs received L-T4 solution PO once daily at a starting dosage of 20 μg/kg body weight (BW). The dose was adjusted every 4 weeks, based on clinical signs and peak serum total T4 (tT4) concentrations. Target peak serum tT4 and thyroid stimulating hormone (TSH) concentrations, 4–6 hours posttreatment, were 35–95 nmol/L and < 0.68 ng/mL, respectively. Dogs were followed for up to 22 weeks after establishment of the maintenance dose.
Results: Clinical signs of hypothyroidism improved or resolved in 91% of dogs after 4 weeks of L-T4 treatment at 20 μg/kg once daily. The maintenance dose was established in 76, 94, and 100% of dogs after 4, 8, and 12 weeks of treatment, respectively. This was 20 μg L-T4/kg BW for 79% of the dogs, 30 μg/kg BW for 15%, and 10–15 μg/kg BW in the remaining 6%, once daily. Thereafter, median peak tT4 and TSH concentrations were 51 nmol/L and 0.18 ng/mL, respectively, and remained stable during the 22-week follow-up; clinical signs did not recur.
Conclusions and Clinical Importance: All of the hypothyroid dogs had rapid clinical and hormonal responses to supplementation with the PO-administered L-T4 solution. The starting dosage of 20 μg L-T4/kg BW once daily was suitable for 79% of dogs.
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Journal of Small Animal Practice
Volume 50 Issue 1, Pages 9 - 14
Radiographic appearance of cardiogenic pulmonary oedema in 23 cats
L. Benigni, N. Morgan* C. R. Lamb
Objective: To describe the radiographic appearance of pulmonary oedema in cats with cardiac failure.
Methods: Thoracic radiographs of 23 cats presented to a first opinion practice with signs of cardiac failure were reviewed. All cats had tachypnoea and/or dyspnoea and enlarged left atrium on echocardiography.
Results: Pulmonary oedema was characterised radiographically by an increased opacity associated with a range of patterns and variable distribution. All cats had evidence of a reticular or granular interstitial pattern. This occurred in combination with alveolar pattern in 19 (83 per cent) cats, including six with air bronchograms, with increased diameter of pulmonary vessels in 16 (71 per cent) cats and with bronchial pattern in 14 (61 per cent) cats. The distribution of pulmonary oedema was considered to be diffuse/non-uniform in 14 (61 per cent) cats, diffuse/uniform in four (17 per cent) cats, multi-focal in four (17 per cent) cats and focal in the remaining one (4 per cent). Nine (39 per cent) cats were considered to have a regional distribution of oedema, including five (22 per cent) with a ventral distribution, three (13 per cent) with a caudal distribution and one (4 per cent) cat with a hilar distribution. The distribution of pulmonary opacities was bilaterally symmetrical in five (22 per cent) cats.
Clinical Significance: The variable appearance of feline pulmonary oedema is likely to complicate its radiographic diagnosis.
January 2009, Vol. 70, No. 1, Pages 99-104
Assessment of viremia associated with experimental primary feline herpesvirus infection or presumed herpetic recrudescence in cats
Hans D. Westermeyer, DVM, Sara M. Thomasy, DVM, PhD, Helen Kado-Fong, MS, David J. Maggs, BVSc
Objective—To detect feline herpesvirus type 1 (FHV-1) in blood of cats undergoing experimental primary herpetic disease or with spontaneous disease presumed to be caused by FHV-1 reactivation.
Animals—6 young specific-pathogen–free (SPF) cats and 34 adult cats from a shelter.
Procedures—Conjunctiva and nares of SPF cats were inoculated with FHV-1, and cats were monitored for 21 days. Periodically, blood was collected for CBC, serum biochemical analyses, and detection of FHV-1 DNA via PCR assay. For shelter cats, a conjunctival swab specimen was collected for FHV-1 PCR assay, and blood mononuclear cells were tested via virus isolation (with or without hydrocortisone) and FHV-1 PCR assay.
Results—All SPF cats developed clinical and clinicopathologic evidence of upper respiratory tract and ocular disease only. Via PCR assay, FHV-1 DNA was detected in blood of all SPF cats at least once between 2 and 15 days after inoculation. Feline herpesvirus type 1 DNA was detected in conjunctival swabs of 27 shelter cats; 25 had clinical signs of herpetic infection. However, virus was not isolated from mononuclear cell samples of any shelter cat regardless of passage number or whether hydrocortisone was present in the culture medium; FHV-1 DNA was not detected in any mononuclear cell sample collected from shelter cats.
Conclusions and Clinical Relevance—A brief period of viremia occurred in cats undergoing primary herpetic disease but not in cats undergoing presumed recrudescent herpetic disease. Viremia may be important in the pathogenesis of primary herpetic disease but seems unlikely to be associated with recrudescent disease.
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American Journal of Veterinary Research
January 2009, Vol. 70, No. 1, Pages 16-22
Evaluation of the distribution of enrofloxacin by circulating leukocytes to sites of inflammation in dogs
D. M. Boothe, DVM, PhD, A. Boeckh, DVM, PhD, H. W. Boothe, DVM, MS
Objective—To determine the effect of WBC accumulation on the concentration of enrofloxacin in inflamed tissues in dogs.
Animals—6 adult Bloodhounds.
Procedures—Dogs were instrumented bilaterally with tissue chambers. Peripheral WBCs collected from each dog were exposed in vitro to radiolabeled enrofloxacin (14C-ENR). Inflammation was induced with carrageenan in 1 chamber. Ten hours later, treated cells were administered IV to each dog such that 14C-ENR was delivered at a mean ± SD dosage of 212 ± 43 μg. Samples of extracellular fluid from inflammation and control chambers and circulating blood were then collected before (baseline) and for 24 hours after WBCs were administered. Samples were centrifuged to separate WBCs from plasma (blood) or chamber fluid. Radiolabeled enrofloxacin was scintigraphically detected and pharmacokinetically analyzed. Comparisons were made between extra- and intracellular chamber fluids by use of a Student paired t test.
Results—14C-ENR was not detectable in plasma, peripheral WBCs, control chambers, or baseline samples from inflammation chambers. However, 14C-ENR was detected in extra- cellular fluid from inflammation chambers (mean ± SD maximum concentration, 2.3 ± 0.5 ng/mL) and WBCs (maximum concentration, 7.7 ± 1.9 ng/mL). Mean disappearance half-life of 14C-ENR from extracellular fluid and WBCs from inflammation chambers was 26 ± 10 hours and 17 ± 6 hours, respectively.
Conclusions and Clinical Relevance—WBCs were responsible for the transport and release of 14C-ENR at sites of inflammation. Accumulation of drug by WBCs might increase the concentration of drug at the site of infection, thus facilitating therapeutic success.
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Veterinary Patholology 46:63-70 (2009)
Feline Gastrointestinal Eosinophilic Sclerosing Fibroplasia
L. E. Craig, E. E. Hardam, D. M. Hertzke, B. Flatland, B. W. Rohrbach and R. R. Moore
A retrospective study of cases of a unique intramural inflammatory mass within the feline gastrointestinal tract was performed in order to describe and characterize the lesion. Twenty-five cases were identified from archival surgical and postmortem tissues. The lesion most often occurred as an ulcerated intramural mass at the pyloric sphincter (n = 12) or the ileocecocolic junction or colon (n = 9); the remaining cases were in the small intestine. Seven cases also had lymph node involvement. The lesions were characterized by eosinophilic inflammation, large reactive fibroblasts, and trabeculae of dense collagen. Intralesional bacteria were identified in 56% of the cases overall and all of the ileocecocolic junction and colon lesions. Fifty-eight percent of cats tested had peripheral eosinophilia. Cats treated with prednisone had a significantly longer survival time than those receiving other treatments. We propose that this is a unique fibroblastic response of the feline gastrointestinal tract to eosinophilic inflammation that in some cases is associated with bacteria. The lesion is often grossly and sometimes histologically mistaken for neoplasia.
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Journal of Veterinary Internal Medicine
Volume 23 Issue 1, Pages 43 - 49
Clinical Evaluation of a Novel Liquid Formulation of L-Thyroxine for Once Daily Treatment of Dogs with Hypothyroidism
G. Le Traon 1 , S.F. Brennan 2 , S. Burgaud 1 , S. Daminet 3 , K. Gommeren 3 , L.J.I. Horspool 4 , D. Rosenberg 5 , and C.T. Mooney 2
Background: A liquid solution of levothyroxine (L-T4) is available for treatment of canine hypothyroidism.
Hypothesis: Once daily oral administration of a liquid L-T4 solution is effective and safe for controlling hypothyroidism in dogs.
Animals: Thirty-five dogs with naturally occurring hypothyroidism.
Methods: Dogs received L-T4 solution PO once daily at a starting dosage of 20 μg/kg body weight (BW). The dose was adjusted every 4 weeks, based on clinical signs and peak serum total T4 (tT4) concentrations. Target peak serum tT4 and thyroid stimulating hormone (TSH) concentrations, 4–6 hours posttreatment, were 35–95 nmol/L and < 0.68 ng/mL, respectively. Dogs were followed for up to 22 weeks after establishment of the maintenance dose.
Results: Clinical signs of hypothyroidism improved or resolved in 91% of dogs after 4 weeks of L-T4 treatment at 20 μg/kg once daily. The maintenance dose was established in 76, 94, and 100% of dogs after 4, 8, and 12 weeks of treatment, respectively. This was 20 μg L-T4/kg BW for 79% of the dogs, 30 μg/kg BW for 15%, and 10–15 μg/kg BW in the remaining 6%, once daily. Thereafter, median peak tT4 and TSH concentrations were 51 nmol/L and 0.18 ng/mL, respectively, and remained stable during the 22-week follow-up; clinical signs did not recur.
Conclusions and Clinical Importance: All of the hypothyroid dogs had rapid clinical and hormonal responses to supplementation with the PO-administered L-T4 solution. The starting dosage of 20 μg L-T4/kg BW once daily was suitable for 79% of dogs.
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Journal of Small Animal Practice
Volume 50 Issue 1, Pages 9 - 14
Radiographic appearance of cardiogenic pulmonary oedema in 23 cats
L. Benigni, N. Morgan* C. R. Lamb
Objective: To describe the radiographic appearance of pulmonary oedema in cats with cardiac failure.
Methods: Thoracic radiographs of 23 cats presented to a first opinion practice with signs of cardiac failure were reviewed. All cats had tachypnoea and/or dyspnoea and enlarged left atrium on echocardiography.
Results: Pulmonary oedema was characterised radiographically by an increased opacity associated with a range of patterns and variable distribution. All cats had evidence of a reticular or granular interstitial pattern. This occurred in combination with alveolar pattern in 19 (83 per cent) cats, including six with air bronchograms, with increased diameter of pulmonary vessels in 16 (71 per cent) cats and with bronchial pattern in 14 (61 per cent) cats. The distribution of pulmonary oedema was considered to be diffuse/non-uniform in 14 (61 per cent) cats, diffuse/uniform in four (17 per cent) cats, multi-focal in four (17 per cent) cats and focal in the remaining one (4 per cent). Nine (39 per cent) cats were considered to have a regional distribution of oedema, including five (22 per cent) with a ventral distribution, three (13 per cent) with a caudal distribution and one (4 per cent) cat with a hilar distribution. The distribution of pulmonary opacities was bilaterally symmetrical in five (22 per cent) cats.
Clinical Significance: The variable appearance of feline pulmonary oedema is likely to complicate its radiographic diagnosis.
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