Chris Reeder, DVM, DACVD
Sometimes no matter how hard we try, a diagnosis of pruritic skin disease is frustrating. There are a few key questions and findings that may make life a little easier in dealing with the itchy dog. The skin as an organ has incredible powers. Not mystical or magical, those are confined to brain along with neurologic pathways to control motion and physiologic/psychologic processes. No, the skin has its own special powers. It acts as a physical barrier providing innate protection against the evils of the environment. Skin stretches and can transition from taut to lose, thick to thin, it controls water loss and temperature regulation, it acts as a sensory organ and to many animals, camouflage to help hide from predators or stalk prey. Skin truly is an incredible organ, though as incredible as it is, an Achilles’ heel does exist…..pruritus.
Pruritus is derived from the Latin prurire meaning to “itch.” It is defined as the desire or reflex to scratch. Itching in the dog is one of the most common presenting complaints from owners to the general practitioner, yet one of the most frustrating and costly as well. There is help, several key questions and findings may provide a starting point or diagnosis as to why a dog is itching. Our first step is the question the owner about the dog’s condition:
– Age of onset of the itching
– Duration of the itching
– Other animals in the household affected
– Housed indoor, outdoor or both
– Travel history
– Current and previously fed diets (including human foods)
– Seasonal history or exacerbations of itching
– Previous medications, what worked and what didn’t work
– Current flea/tick control products (other animals treated)
– Number of bowel movements daily
– Loose, runny stools or any vomiting
Many animals who have a food allergy will present as young dogs (<1 year of age) with loose or runny stools, >3 bowel movements daily and may be refractory to glucocorticoid use. Other household animals are not affected and this is typically non-seasonal with itching as a constant feature. Compare that to the typical dog with atopy (environmental allergies) and we see that most of those dogs present first between 1-4 years of age, have some seasonal pattern, respond to glucocorticoids with a reduction of pruritus and no other animals in the household are affected. The author’s experience, along with many dermatologists, find that atopy is a much more common presentation than food allergy in roughly 90% to 10%, respectively. We also see that food allergic dogs often have some compromise to the gastrointestinal barrier function. This could be a history of intestinal parasites, Parvovirus enteritis, or any other disruption to the gut integrity. What about a dog whose symptoms appears more atopic but is non-seasonal? That could be a dog that is suffering from indoor allergens (dust mites, storage mites, human or cat dander, sheep wool, cotton, etc) which allergy testing may be a helpful tool in order to diagnose.
Scabies can mimic food allergy and atopy very closely. Other animals or even humans in the household may be affected with pruritus. The typical approach to dogs with scabies is to identify a pinnal-pedal reflex. This involves grasping the pinna between the thumb and forefinger of both hands and rubbing the skin together. A positive response would involve the ipsilateral hind leg start scratching vigorously after a few seconds. It has been reported that up to 80% plus of dogs with scabies exhibit a positive pinnal-pedal response and these are cases to empirical treat with an acaracidal therapy (e.g. Advantage-multi® Bayer, Revolution® Pfizer) which is usually an off-label dosing of one treatment every 2 weeks for 3 total doses. Common areas affected with scabies infestation include: hocks, elbows, pinnae, groin and scrotum. All animals in the household should be treated as some may serve as a reservoir even if not itching.
Flea allergy is truly a hypersensitivity response. This appears as a dose-dependent phenomenon with the higher number of flea bites with salivary protein exposure thus resulting in an allergic response. The number of bites to induce an allergic response varies with some animals showing no response even with hundreds of bites. It is important to examine the dog, especially those with long coats, on the rump region. A severe inflammatory response can be seen in dogs with a strong allergic response to fleas with moist pyoderma and excoriations predominantly over the dorsal lumbar region. Another common finding in dogs with flea allergy is the discontinuation of flea control over the winter months. Fleas overwinter indoors and continue to thrive, only at a slower rate than the warm and humid summer months. Continued flea control for all animals in the household is a very effective means of controlling flea allergies. Several topical formulations now have both flea prevention and heartworm prevention in a single dose application (e.g. Advantage-multi® Bayer). Bathing around the time of application of the topical spot-on formulations of flea preventative is another question to ask the owner. Typical recommendations are to wait 48-72 hours after application to bathe a dog or use an oral flea preventative (e.g. Comfortis® or Trifexis® Elanco).
Ringworm, is neither a ring nor a worm, the saying goes “if it looks like ringworm, it’s probably not” in dogs holds true. Dermatophytosis in dogs usually presents with pruritus, hair loss, erythema and scaling. Rarely does ringworm present as focal, circular patches of alopecia in dogs. Various forms of ringworm can be present in dogs, geophilic, zoophilic, anthrophilic with the geophilic (soil) or zoophilic (animal) forms most common. Microsporum gypseum is a geophilic dermatophyte whereas Microsporum canis is a zoophilic dermatophyte and the most common species seen in the dog and cat. Occasionally multiple animals in the household may be affected and about 10% of humans can also have lesions which are typically pruritic. A dermatophyte test media (DTM) culture is ideal to diagnose and speciate the type of dermatophyte present. Fluconazole (5-10 mg/kg po daily) is the author’s treatment of choice for dermatophytosis. Terbinafine (Lamasil®, 30-40 mg/kg po daily) may also be used for refractory cases.
Pruritus also damages the cutaneous barrier function both as, what we think is, a genetic dysfunction of the intercellular cement along with direct excoriations of the integument. This barrier defect has led to the development of many good products to help control and restore function. Wipes, shampoos, lotions, balms and sprays have all been recently developed an are on the maket to help restore or improve skin barrier function in animals. Shampoos have technology to even prevent bacteria/yeast from adhering to the skin surface (Virbac glycotechnology). Pro-ceramides have been incorporated into sprays and shampoos to help repair damaged skin (phytosphingosine, Douxo® (Sogeval)).
Pruritus may have developed due to an allergic response to food, parasites or the environment and taking the time and understanding what to look for in these cases can make for a much more rewarding treatment outcome. Many dogs need ongoing management for their atopy, need to be on flea prevention every 3-4 weeks ongoing or must be maintained on certain diets if food allergic. Scabies is curable, though we do occasional see reservoirs in other household dogs or wildlife making further questioning an important part of the treatment. Asking the right questions along with a thorough history and physical exam may help increase the correct diagnosis and decrease frustrations levels for the itchy dog.
Could it be Addison’s?
Linda E. Luther, DVM
Diplomate ACVIM (SAIM)
Many cases presented for evaluation of vague symptoms end up having hypoadrenocorticism.
Can you spot the classic cases?
Can you spot the not-so-classic cases?
Hypoadrenocorticism, or “Addison’s” disease, results from atrophy of the adrenal cortex, and often presents as a diagnostic challenge. Clinical signs can vary from subtle signs to acute collapse, and the clinical course is often waxing and waning. Untreated collapsed dogs may die, so identifying dogs affected with this disease early is optimal. Types of hypoadrenocorticism include the ‘classic’ glucocorticoid & mineralocorticoid deficient patient, and the more subtle, glucocorticoid deficient patient.
Clinical signs of classic hypoadrenocorticism may include vomiting, diarrhea, lethargy, collapse, bradycardia, abdominal pain, polyuria, polydipsia, or being “just not right”. Physical examination findings are often nonspecific. Laboratory findings in a classic case may include hyponatremia, hyperkalemia, decreased Na/K ratio, azotemia (with or without an inappropriate specific gravity), hypoalbuminemia, hypoglycemia, hypercalcemia, nonregenerative anemia. The lack of a stress leukogram is common; a normal to elevated lymphocyte count, and normal to elevated eosinophil count in a sick dog are frequent, subtle findings.
The not-so-classic case will often present with more subtle clinical signs. They will have normal electrolytes, and will often have a lack of a stress leukogram. They may also have a low normal hematocrit or a non-regenerative anemia, a low to borderline albumin, hypoglycemia and hypercalcemia. These cases are commonly missed. How can you ensure that you spot these? Look at the CBC carefully. Is there a stress leukogram? Look at the albumin level. Is it decreased or in the low normal range? Consider the history. Consider the lack of other obvious disease, and don’t forget to IGNORE the normal electrolytes. If there are enough consistent findings in a dog with vague symptoms, test for hypoadrenocorticism!
Once you suspect hypoadrenocorticism, confirmation historically has been done with an ACTH stimulation test. However, a recent study showed that if a dog had a baseline cortisol level that was greater than 2.0 ug/dL, they were very unlikely to have hypoadrenocorticism. If the baseline cortisol is less than 2.0 ug/dL, hypoadrenocorticism is not ruled out, and an ACTH stimulation test should be done.
But I thought she was in renal failure…
Cases of hypoadrenocorticism can mimic acute renal failure in that clinical signs are similar, and azotemia with an inappropriate urine specific gravity may exist. How does the astute clinician differentiate the two? Questions to ask include: Is there a stress leukogram? Was the resolution of severe azotemia very rapid? Did the patient act like a ‘brand-new dog’ after just a day of fluids?
Let’s compare “Maggie”, a 7-year-old Fs Collie that presented with vomiting and lethargy, to “Bailey”, a 12-yr-old Mn Cocker that presented in lateral recumbancy (see Table 1). Both dogs had severe azotemia with an inappropriate urine specific gravity. “Maggie” lacked a stress leukogram. The electrolyte findings in both dogs were suggestive of hypoadrenocorticism, but this finding is not pathognomonic for the disease. “Maggie” turned out to have hypoadrenocorticism. “Bailey”, did not, and he was diagnosed with renal failure (see Table 3). Because “Maggie” had an abnormal ACTH stimulation test as well as abnormal electrolytes, she had glucocorticoid and mineralocorticoid deficient hypoadrenocorticism.
Therapy for “Maggie” started with intravenous fluid therapy. The hyperkalemia was treated with the fluids, as well as intravenous sodium bicarbonate therapy (1 mEq/kg, slow IV). Glucocorticoids were given, initially using dexamethasone sodium phosphate (0.1-2 mg/kg IV). Chronic glucocorticoid therapy with physiologic dose of prednisone (0.1-0.2 mg/kg/day, doubled when she was stressed) was initiated. She was also given mineralocorticoid therapy using Percorten®-V (Desoxycorticosterone pivalate or DOCP, 2.2 mg/kg IM or SQ q. 25 initially). Florinef ® (fludrocortisone acetate, 0.01-0.02 mg/kg/day initially), which also has glucocorticoid effects, could have been used instead of Percorten®.
Could he be an Addisonian?
Some Addisonian dogs have very subtle symptoms. “Max” is a 7-yr-old Mn Labrador retriever that presented for a blood panel to monitor carprofen therapy that was chronically administered to treat degenerative joint disease (see Table 2).
“Max’s” blood panel revealed significant anemia. Upon further questioning, the owner thought that he had been quieter lately. He really was not all that sick though. Besides the anemia, the blood work showed a lack of a stress leukogram, his electrolytes were normal, and there was no azotemia. An ACTH stimulation test was done (see Table 3), and “Max” indeed was an Addisonian! Since “Max” had normal electrolytes, he had glucocorticoid deficient hypoadrenocorticism, and he was not mineralocorticoid deficient. Chronic glucocorticoid therapy with a physiologic dose of prednisone (0.1-0.2 mg/kg/day, doubled when he was stressed), was started. Mineralocorticoid therapy was not indicated in this dog. Some glucocorticoid deficient cases eventually develop mineralocorticoid deficiency, thus periodic monitoring of electrolytes was indicated.
In summary, hypoadrenocorticism can be a challenging disease to diagnose. Suspicion of the disease in dogs with vague symptoms is recommended, even in dogs that have normal electrolytes.
Disclaimer: Please verify all drug dosages before administering.
Scott-Moncrieff JCR. Hypoadrenocorticism. In Ettinger SJ, Feldman EC (eds.) Textbook of Veterinary Internal Medicine, 7th ed. Saunders Elsevier, St. Louis, 2010, 1847-1857.
Lennon EM, Boyce TE, Hutchins RG et al. Use of basal serum or plasma cortisol concentrations to rule out a diagnosis of hypoadrenocorticism in dogs: 123 cases (2000-2005). J Am Vet Med Assoc 2007;231:413-416.
Thompson AL, Scott-Moncrieff JC, Anderson JD. Comparison of classic hypoadrenocorticism with glucocorticoid-deficient hypoadrenocorticism in dogs: 46 cases (1985-2005). J Am Vet Med Assoc 2007;230:1190-1194.
|White blood cells, #/μL||12,880||28,290||5,500-16,900|
|Platelets, # x 103/μL||299||431||175-500|
|Urine specific gravity||1.015||1.015|
|Table 2.||“Max”||Normal values|
|White blood cells, #/μL||2,500||5,500-16,900|
|Platelets, # x 103/μL||325||175-500|
|Table 3.||“Maggie”||“Bailey”||“Max”||Normal values|
|Pre-ACTH cortisol, ug/dL||< 0.5||8.0||< 0.5||> 2.0|
|Post-ACTH cortisol, ug/dL||< 0.5||N/A||< 0.5||> 8.0|
|* Note that “Bailey’s” baseline cortisol adequately ruled out hypoadrenocorticism. “Maggie” and “max” had baseline cortisol values < 2.0 ug/dL, thus an ACTH stimulation was needed to rule in the disease.|
C. Scott Bailey, DVM, MS, DACT
Consultant, Veterinary Answers
Veterinarians are often asked to perform pregnancy diagnosis and time a c-section with very little information from the owner. Often, the only information provided is the breeding-dates and occasionally even those are hard to come by. Consequently there is a need for veterinarians to be familiar different with methods of estimating gestational age. This is particularly important when an elective caesarean section is desirable. Elective c-sections can carry an excellent prognosis for maternal and fetal viability when timed correctly and may be less stressful to the bitch, puppies and attending veterinarian than waiting for a potential dystocia. Animals that are particularly good candidates are those with a history of dystocia or a c-section and animals that have small (less than 3 pups) or large (more than 8 pups) litter sizes. Dogs of certain breeds have a known predisposition to dystocia, such as Boxers, Bulldogs, Scottish Terriers, Great Danes and Bernese Mountain Dogs .
A number of factors play critical roles in the ultimate success-rate of elective c-sections, including fetal maturity, patient preparation, selection of anesthesia protocol and surgical technique as well as neonatal care of the pups. In this review we focus on only the first of these – Timing of c-section to maximize fetal maturity.
Three basic methods exist to predict parturition in the bitch:
While the easiest methods for timing involve breeding management, breeding dates provided by owners are notoriously unreliable. Parturition may occur anywhere from 57 to 72 days after a single observed breeding . On the contrary, the easiest and most accurate way to predict whelping is to diagnose or estimate the time of LH surge. Bitches reliably whelp 64-66 days post LH surge [2,3], which can be diagnosed by repeated LH assay (every 12 hours due to the short duration of the LH surge in the bitch). LH-peak may also be estimated by observing serum progesterone levels that achieve 2-3ng/ml and continue to rise thereafter [3,8]. Shortly after this period, vaginal cytology may be used to diagnose the onset of diestrus, occurring approximately 51-60 days before whelping .
Thereafter a variety of measures represent guides to estimate gestational stage within 2-3 days [4-6]. Further, equations have been developed to calculate gestational age in a variety of breeds [6,7].
A brief summary of useful ultrasonographic and radiographic markers of gestational age is listed below:
Ultrasonographic examination [5-8]
The fetal heartbeat is visible at approximately 22-26 days.
Limbuds, fetal movement and a fluid filled stomach may be seen on day 29, 30 and 33.
Fetal length exceeds chorionic width at approximately day 42.
Radiographic examination [5,7,9]
Pregnancy can first be reliably diagnosed radiographically day 45-48 post LH surge. More specific information is also available describing the appearance of specific structures in relation to whelping.
The scapula, humerus and femur are first detectable 17 days (15-18) prepartum.
The pelvis and 13 pairs of ribs are visible 11 days (9-13) prepartum.
Teeth are visible 4 days (3-8) prepartum.
During the final days of gestation, cortisol is produced and released from the maturing fetal adrenal gland in response to space-constraint and other physiologic stressors. This results in production of prostaglandin F2α in the placenta and endometrium, which in turn induces luteolysis and starts the cascade of events that ultimately result in fetal expulsion . At the same time the cortisol also has critical effects on the fetus, resulting in rapid maturation of vital organ systems, including the musculoskeletal system, gastrointestinal system and lungs. Prior to these final maturation processes, puppy survival may be decreased due to weakness, poor mobility and respiratory distress after removal from the uterus. On the contrary, if these processes have occurred and the bitch experiences a dystocia, survival may also be decreased. Consequently, the goal of gestational timing should be to predict whelping accurately enough to intervene after final maturation has occurred but before the bitch is in active labor. To do this, repeated monitoring of hormone levels during the final week of gestation, in combination with fetal monitoring via ultrasound or tocometry, may improve fetal viability and prevent dystocias [11-13].
Progesterone measures below 2ng/ml indicate imminent parturition within 18-36 hours.
A temperature drop by 1-3F from previous measures occurs in 75-85% of bitches within 8-18 hours prior to parturition.
Fetal heart-rate can accurately diagnose fetal distress during late gestation [12,13]
Normal late pregnancy: 200 beats/min
Fetal Stress: 180 beats/min – Values in this range indicate readiness for parturition
Fetal distress: 150 beats/min – values of 150 or below indicate the urgent need for emergency intervention to save the puppy.
1) Bergström A, Nødtvedt A, Lagerstedt AS, Egenvall A. Incidence and breed predilection for dystocia and risk factors for cesarean section in a Swedish population of insured dogs. Vet Surg 2006 Dec;35(8):786-91.
2) Concannon PW, Whaley S, Leid D, Wissler R. Canine Gestation length: vacioation related to time of mating and fertile life of sperm. Am J Vet Res 1983;44:1819-21.
3) Cohen JA, Holle DM, Meyers-Wallen VN. Accuracy of canine parturition date prediction from LH peak. Clin Theriogenology 2009;1:570
4) Holst PA, Phemister RD. Onset of diestrus in the Beagle bitch: definition and significance. Am J Vet Res 1974;35:401-6
5) Aissi A and Slimani C. Ultrasonographic appearance of the gestational structures throughout pregnancy in bitches. Am J Anim Vet Sciences 2008;3(1):32-35
6) Yeager AE and Concannon PW. Association between preovulatory LH surge and the early ultrasonographic detection of pregnancy and fetal hearteats in beagle dogs. Theriogenology 1990;34:655-665.
7) Lopate C. Estimation of gestational age and assessment of canine fetal marutation using radiology and ultrasonography: A review. Theriogenology 2008;70:397-402
8) Luvoni GC and Beccaglia M. The Prediction of Parturition Date in Canine Pregnancy. Reprod Dom Anim 2006;41:27-32.
9) Rendano VT. Radiographic evaluation of fetal development in the bitch and fetal death in the bitch and queen. In: Current veterinary therapy vol VIII. WB Saunders Co 1983; 947-52
10) Concannon PW, Butler WR, Hansel W, Knight PJ, Hamilton JM. Parturition and lactation in the bitch: serum progesterone, cortisol and prolactin. Biol Reprod 1978 Dec;19(5):1113-8.
11) Verstegen-Onclin K, Verstegen J. Endocrinology if pregnancy in the dog: A review. Theriogenology 2008;70:291-199.
12) Verstegen JP, Silvia LDM, Onclin K, Donnay I. Echocardiographic study of heart rate in dog and cat fetuses in utero. J Reprod Fertil Suppl 1993;47:174-80
13) Zone MA and Wanke MM. Diagnosis of canine fetal death by ultrasonography J. Reprod Fertil 2001;57:215-9.
Novel gastroretentive controlled-release drug delivery system for amoxicillin therapy in veterinary medicine
Evaluation of orally administered famciclovir in cats experimentally infected with feline herpesvirus type-1
Vet Clin Pathol. 2009 Mar;38(1):113-20.
Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610, USA.
Two young adult dogs with gastrointestinal signs were each found to have an intra-abdominal mass based on physical examination and diagnostic imaging. On exploratory laparotomy, small intestinal masses and mesenteric lymphadenopathy were found in both dogs; a liver mass was also found in dog 1. Cytologic and histologic examination of intestinal and liver masses and mesenteric lymph nodes revealed 2 distinct lymphoid cell populations: lymphoblasts and atypical Mott cells. With Romanowsky stains, the atypical Mott cells contained many discrete, clear to pale blue cytoplasmic inclusions consistent with Russell bodies that were positive by immunohistochemistry for IgM and CD79a in both dogs and for IgG in dog 2. The Mott cells and occasional lymphoblasts stained strongly positive with periodic acid-Schiff. Using flow cytometric immunophenotyping in dog 1, 60% of peripheral blood mononuclear cells and 85% of cells in an affected lymph node were positive for CD21, CD79a, IgM, and MCH II, indicative of B-cells. With electron microscopy, disorganized and dilated endoplasmic reticulum was seen in Mott cells in tumors from both dogs. Antigen receptor gene rearrangement analysis of lymph node and intestinal masses indicated a clonal B-cell population. Based on cell morphology, tissue involvement, and evidence for clonal B-cell proliferation, we diagnosed neoplasms involving Mott cells. To the authors’ knowledge, this is the second report of Mott cell tumors or, more appropriately, B-cell lymphoma with Mott cell differentiation, in dogs. More complete characterization of this neoplasm requires further investigation of additional cases. This lymphoproliferative disease should be considered as a differential diagnosis for canine gastrointestinal tumors.
J Small Anim Pract. 2011 Jan;52(1):32-7
OBJECTIVE: To report clinical findings and outcome in dogs and cats undergoing choledochotomy or primary repair of extrahepatic biliary duct rupture.
METHODS: Retrospective study of dogs (n=7) and cats (n=2) that had choledochotomy or primary bile duct repair.
RESULTS: Extrahepatic biliary obstruction was confirmed at surgery in all cases. The underlying cause in four dogs and both cats was choledocholithiasis, two dogs had gall bladder mucocoeles with associated bile duct rupture, and one dog had inspissated bile obstructing the bile duct secondary to gall bladder carcinoid tumour. Three dogs and both cats had choledochotomies performed to relieve extrahepatic biliary obstruction, and four dogs with bile duct rupture underwent primary repair of the defect. One dog with a bile duct rupture was re-explored four days postoperatively and had suffered dehiscence of the repair; this rupture was re-repaired. All animals were discharged from the hospital, and did not have clinical recurrence of extrahepatic biliary obstruction.
CLINICAL SIGNIFICANCE: Choledochotomy and primary repair of extrahepatic biliary duct rupture were associated with low perioperative morbidity and no mortality in this small cohort of cases. These techniques are reasonable options either alone or in conjunction with other procedures when bile duct patency cannot be re-established by catheterisation or bile duct discontinuity exists.
A third-generation fluoroquinolone, pradofloxacin (PRA), is currently being developed to treat bacterial infections in dogs. The purpose of this study was to assess the clinical efficacy in 20 dogs affected with superficial and deep pyoderma. An initial aerobic skin culture was performed in dogs with superficial pyoderma; aerobic/anaerobic tissue culture was performed in dogs with deep pyoderma; and skin cytology and biopsies were obtained from all dogs. Pradofloxacin (approximately 3 mg/kg per os [PO]) was administered daily to all dogs. Clinical efficacy was recorded at 4 weeks for dogs with superficial pyoderma and at 3 and 6 weeks for dogs with deep pyoderma. At a mean dosage of 3.7 mg/kg PO once daily, PRA treatment resulted in an excellent to good clinical response within 3 to 6 weeks for all 20 dogs with superficial and deep pyoderma.