March 2022   |   Volume 20   |   Issue 2

Step-by-Step Crown Amputation for Tooth Resorption

in this issue

in this issue

Crown Amputation for Tooth Resorption

Top 5 Tips for Interpreting Heartworm Test Results

Ocular Pain & Vision Loss in a Golden Retriever

Systemic Hypertension in Cats

Congenital Portosystemic Shunt in a Dog

Top 5 Antimicrobial Stewardship Practices

Differential Diagnosis: Splenomegaly in Cats

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Top 5 Tips for Interpreting Heartworm Test Results

Andrew R. Moorhead, DVM, MS, PhD, DACVM (Parasitology), University of Georgia

Cassan N. Pulaski, DVM, MPH, PhD, University of Georgia

Parasitology

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Peer Reviewed

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Top 5 Tips for Interpreting Heartworm Test Results

It is commonly believed that heartworm disease can be diagnosed based on a simple positive or negative in-clinic test result; however, this is not always true when testing dogs and is less accurate in cats. Interpretation of a heartworm antigen test is only one component of an accurate heartworm diagnosis; a variety of testing modalities may be required. Testing for the presence of antigens and microfilariae is recommended in dogs; diagnosis in cats usually requires additional testing (eg, antibody testing, radiography; Table).

Following are the top 5 scenarios, according to the authors, encountered when diagnosing heartworm disease in dogs and cats.

1

Microfilariae-Positive; No Antigen Detected

Occult infections (ie, presence of adult worms without circulating microfilariae) can occur in up to 20% of dogs with heartworm disease1 and are likely a result of immune-mediated clearance of microfilariae or drug treatments. Dogs can also be microfilariae-positive but have no detectable antigens. This can occur for various reasons, including infection with a different filarial parasite, blood transfusion from an infected dog, or antigen blocking, in which the heartworm antigen is presumably bound by host antibodies, masking the antigen from antibodies in the testing kit.2 In these patients, a fresh sample should be collected and submitted for further investigation. 

Additional testing may include a modified Knott’s test or molecular modalities to differentiate Dirofilaria immitis from other species (eg, Acanthocheilonema reconditum) or antigen testing with heat-treated serum at a reference laboratory (high heat can break antigen–antibody complexes, leaving free antigens for detection).3 If a microfilariae-positive, antigen-negative dog seroconverts to antigen-positive after heat treatment, then heartworm adulticide therapy is warranted. Because of these phenomena, testing dogs for both antigen and microfilariae is recommended.

TABLE

HEARTWORM DIAGNOSTIC TESTS

Test Species Description Limitations
Microfilariae testing Dog Detects microfilariae via direct examination of a drop of fresh blood or concentration (ie, modified Knott’s test) Direct examination may be insensitive if low microfilariae count; modified Knott’s testing requires formalin and time
Antigen testing Dog, cat Detects antigen produced by adult female worms or dying male and female worms Does not detect larvae or immature worm infections; rarely detects male-only infections; results may be affected by antigen–antibody complex formation
Antibody testing Cat Detects antibodies produced by a cat in response to presence of heartworm larvae, immature adults, or adult worms Studies have shown significant false-negative results
Thoracic radiography Dog, cat Detects vascular enlargement, pulmonary parenchymal inflammation; reliable method of assessing severity of cardiopulmonary disease in dogs Radiographic signs can be subjective and affected by clinical interpretation
Echocardiography Dog, cat Detects echogenic walls of immature or mature worms, providing definitive evidence of heartworm infection; also allows for assessment of cardiac anatomic and functional consequences of disease Not an efficient method of diagnosis, particularly in lightly infected patients; accuracy rate influenced by ultrasonographer experience with heartworm detection
2

Antigen-Positive After Melarsomine Treatment

Although treatment with melarsomine is typically highly effective, a small number of worms may survive and cause the host to remain antigen-positive, despite adherence to the recommended 3-dose adulticidal protocol. In addition, some dogs may have been given a dose that is too small (patient weight and drug dose should be checked before each injection) or an inappropriate melarsomine regimen may have been used (eg, treatment timing was incorrect, 2 doses were given instead of 3). 

Dead and dying worms can release detectable antigens, which can persist for some (unknown) time following treatment.3 The American Heartworm Society (AHS) currently recommends retesting dogs 9 months posttreatment; the 2-dose melarsomine regimen (ie, 2 doses 24 hours apart) is recommended if the patient is still antigen-positive.3

3

Slow-Kill/Salvage Treatment in Antigen-Negative Dogs

Although the AHS treatment protocol using melarsomine is recommended in dogs with heartworm disease, long-term administration of a macrocyclic lactone and doxycycline is an alternative, extra-label adulticidal treatment. The salvage protocol requires a significantly extended treatment timeline compared with the AHS protocol, and, although it can be effective, time needed to kill or eliminate adult worms varies between protocols and can be prolonged.4 It is uncertain when dogs receiving the salvage protocol are considered heartworm-free, as antigens can be bound by the host’s antibodies, resulting in no antigen detected. This has been documented in dogs undergoing a salvage protocol5; however, in a study, no adult worms were found during necropsy in patients in which no antigen was detected after heat treatment of serum.6 No antigens should be detected after heat treatment before patients are considered truly negative.

4

Positive or Negative Heartworm Infection in Cats

Determining heartworm status of a cat can be difficult, and multiple clinical aspects and diagnostic approaches should be considered, including patient history, physical examination, serum chemistry profile, hematology, immunodiagnosis (both antigen and antibody testing), thoracic radiography, and echocardiography.7 Testing for microfilariae is not always helpful or recommended because of the transient nature of microfilaremia in cats; >95% of heartworm infections in cats are occult.8 Heartworm antigen testing in cats has similar (and additional) challenges as with dogs, including reduced test sensitivity and the possibility for antigen–antibody immune complex formation.3 

A combination of antigen (possibly using heat-treated serum if the patient shows clinical signs but results are discordant) and antibody (when available) testing is currently recommended, but a negative antigen test result does not exclude infection, and a positive antibody test result only indicates exposure to heartworms (ie, larvae).7 A positive antigen test result (before or after heat treatment) is a strong indicator of active heartworm infection and may warrant supportive treatment (eg, corticosteroids, antihistamines).9

5

Newly Antigen-Positive

In both dogs and cats, a positive antigen test result should be confirmed prior to diagnosing heartworm disease and beginning treatment. The easiest way to confirm a positive antigen test result is with detection of D immitis microfilariae; however, microfilariae may not be present in a heartworm-positive dog (and are highly unlikely to be present in a heartworm-positive cat). In these patients, additional antigen testing should be pursued for confirmation using a fresh blood sample and an alternative testing platform (eg, different manufacturer, reference laboratory). Heat treatment is not needed in antigen-positive cats. Heat treatment is, however, recommended in cats with clinical signs but no antigen detected or microfilariae-positive and antigen-negative cats.

Conclusion

Diagnosing heartworm disease can be challenging. It is critical to use all resources available and seek continued education on updates to the AHS guidelines.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Systemic Hypertension in Cats

Andrew Sparkes, BVetMed, PhD, DECVIM, MANZCVS, MRCVS, Simply Feline Veterinary Consultancy, Dorset, United Kingdom

Internal Medicine

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Peer Reviewed

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Systemic Hypertension in Cats

ACEI = angiotensin-converting enzyme inhibitor, ARB = angiotensin receptor blocker, BP = blood pressure, CKD = chronic kidney disease, SBP = systolic blood pressure, TOD = target organ damage, UPC = urine protein:creatinine ratio

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Novel Rickettsia Species in Dogs

Susan Little, DVM, PhD, DACVM (Parasitology), Oklahoma State University

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Novel <em>Rickettsia</em> Species in Dogs

In the Literature

Wilson JM, Breitschwerdt EB, Juhasz NB, et al. Novel Rickettsia species infecting dogs, United States. Emerg Infect Dis. 2020;26(12):3011-3015. 


FROM THE PAGE …

Although tick-borne infection is commonly encountered in veterinary medicine, identifying the specific pathogen responsible can be difficult. Emergence of novel agents that can induce similar and, at times, severe disease increases the challenge. Diagnostic tests for tick-borne infection have been developed and validated to identify known, established organisms, but a diverse array of potential pathogens cycle in nature.

This study describes a novel spotted fever group of Rickettsia spp that caused severe disease in 3 dogs infected in the central and southern United States. Although attempts to culture the organism were unrewarding, researchers sequenced identical Rickettsia-specific targets from the blood of the 3 patients. All sequences were identical to each another and unique from other known Rickettsia spp.

The dogs shared a history of tick exposure in a region with heavy tick populations and were presented in the summer with fever, lethargy, and thrombocytopenia, leading to suspicion of tick-borne illness. All 3 patients were seropositive for antibodies reactive to Rickettsia spp on immunofluorescent assay (IFA) testing. One dog also had neutrophilic polyarthritis, which is occasionally reported in dogs with Rocky Mountain spotted fever. 

One dog had protein-losing nephropathy and was euthanized after developing nephrotic syndrome. The remaining 2 dogs recovered after receiving doxycycline, prednisone, and supportive care. The novel organism was identified via PCR and sequencing of Rickettsia-specific nucleic acid targets from the blood of all 3 patients. 

Studies like this are critical to understanding the diversity of tick-borne pathogens that threaten canine health. Spotted fever group Rickettsia spp cause cross-reacting antibodies detected on IFA tests, leading to a suspicion that as-yet-unrecognized agents like the one described here may be widespread. 

Dogs are important sentinels for tick-borne infection risk in humans. The potential zoonotic risk posed by this agent warrants further consideration.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Novel tick-borne agents continue to be described. Recognizing classic clinical signs may allow for a successful outcome, even if the disease is caused by an unrecognized organism.

 

2

Ticks transmit a wide variety of infectious organisms. Focusing on consistent tick preventives and avoiding areas with intense tick populations can help limit risk for disease and protect dogs from infections.

3

Spotted fever group Rickettsia spp also infect humans. Novel infections provide another opportunity to raise awareness among pet owners about the zoonotic risk of tick-borne pathogens.

Suggested Reading

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

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Patient-Side Giardia spp Diagnostics

Lindsay A. Starkey, DVM, PhD, DACVM, (Parasitology), Auburn University

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Patient-Side <em>Giardia</em> spp Diagnostics

In the Literature

Symeonidou I, Gelasakis AI, Miliotou AN, et al. Rapid on-site diagnosis of canine giardiosis: time versus performance. Parasit Vectors. 2020;13(1):544.


FROM THE PAGE …

Giardia spp can be difficult to visualize on fecal flotation or direct smear, as they are very small, may be present only intermittently, and can be confused with other material (eg, yeast, pollen). In addition, some flotation solutions can cause Giardia spp cysts to distort or rupture, hindering recovery and identification. Additional tests (eg, immunoassays, molecular testing) to help accurately detect and diagnose infection have been developed. 

This study* compared an in-clinic Giardia spp immunochromatographic strip test (IST) with double-centrifugal fecal flotation in zinc sulfate. Both tests were then compared with PCR and ELISA testing, which are the gold standards for detection. 

Samples from 100 dogs with diarrhea were analyzed. IST detected 50 positive and 50 negative results. 

Of the IST-positive samples, Giardia spp cysts were detected via flotation in 34 samples. Cysts were not microscopically visible in any of the IST-negative samples. All 50 IST-positive samples also had positive ELISA and PCR results. 

Of the 50 samples that were negative on IST and fecal flotation, 22 had positive PCR results and 15 had positive ELISA results; 8 samples tested positive with both ELISA and PCR.

Although false-negative results occurred with IST and fecal flotation compared with the gold standard tests, IST identified more positive samples than traditional flotation. These findings add to the body of evidence that patient-side immunoassays are valuable clinical tools for aiding in the diagnosis of Giardia spp infection.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Giardia spp can be challenging to detect, but an accurate patient-side diagnostic test can help.

 

2

Fecal flotation remains an important diagnostic tool, as parasites other than Giardia spp can cause or contribute to diarrhea and will not be detectable with a patient-side Giardia spp test.

3

Using a combination of diagnostic tools is more likely to produce an accurate diagnosis.

 

*This study was partially funded by Virbac.

Suggested Reading

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

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Fresh Frozen Plasma Use in Cats

Ashley Allen-Durrance, DVM, DACVECC, University of Florida

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Fresh Frozen Plasma Use in Cats

In the Literature

Lane WG, Sinnott-Stutzman VB. Retrospective evaluation of fresh frozen plasma use in 121 cats: 2009-2016. J Vet Emerg Crit Care (San Antonio). 2020;30(5):558-566.


FROM THE PAGE …

There are extensive guidelines for appropriate use of fresh frozen plasma (FFP) in human medicine, but similar guidelines are not available in veterinary medicine.1-3 Literature on use of FFP in cats is limited, and doses have not been reported, with the exception of nonspecies-specific recommendations of 6 to 20 mL/kg for treatment of coagulopathy.4,5

This retrospective study reported findings on FFP administration in 121 cats. The goal was to document indications for use, doses, and frequency of adverse transfusion reactions. 

Multiple indications for transfusion were recorded in medical records and included suspected coagulopathy (84%), hemorrhage (35%), persistent hypotension (25%), and hypoalbuminemia (5%). Odds of survival to discharge were 2.4 times more likely in cats with improvement in coagulation parameters posttransfusion. Most cats receiving FFP for coagulopathy (58%) and hemorrhage (67%) survived, whereas only 26% of cats with persistent hypotension and 14% of cats with hypoalbuminemia survived. This was likely due to disease severity. 

The median FFP dose (6 mL/kg) was not associated with survival. There was a negative correlation between dose and body weight, likely due to the common practice of administering 1 unit of FFP per cat, causing larger cats to receive a smaller dose. 

Possible adverse transfusion reactions were seen in 16% of cats; increased body temperature and tachypnea were most common. Occurrence of an adverse transfusion reaction was not associated with survival. The rate of FFP transfusion was not significantly different between cats with and without a reaction.  

Indications for FFP use in cats parallel those in dogs and are similar to established guidelines in human medicine. Controversies surrounding use of FFP in human medicine are common, especially for prophylactic use in patients with prolonged clotting times but no clinical bleeding.1,6 This study highlighted similar discrepancies, as approximately one-third of cats received FFP due to prolonged clotting times without clinical bleeding.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Cats with improved pre- and posttransfusion clotting times were 2.4 times more likely to survive. Administering an appropriate starting dose (eg, 6 mL/kg) should therefore be considered in place of the common practice of giving 1 unit per cat, especially in larger cats.

2

Increased temperature and tachypnea were the most common adverse transfusion reactions reported in this study. There was no correlation between adverse transfusion reactions and survival, and there was no difference in FFP transfusion rates between cats with and without an adverse transfusion reaction. Fear of transfusion reaction should not preclude use of FFP in treatment of coagulopathy in bleeding patients.

3

Reduction in hemorrhage has not been consistently shown with prophylactic FFP use in human literature,7,8 and prophylactic use of FFP is controversial in veterinary medicine. Further prospective studies in cats are warranted.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Hypokalemia in Cats Treated with Topical Dorzolamide

Renee Carter, DVM, DACVO, Louisiana State University

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Hypokalemia in Cats Treated with Topical Dorzolamide

In the Literature

Czepiel TM, Wasserman NT. Hypokalemia associated with topical administration of dorzolamide 2% ophthalmic solution in cats. Vet Ophthalmol. 2021;24(1):12-19.


FROM THE PAGE …

Topical carbonic anhydrase inhibitors (CAIs), which do not incite ocular inflammation, are common first-line treatments for feline primary and secondary glaucoma. Cats are uniquely sensitive to the adverse effects (eg, metabolic acidosis, hyporexia, vomiting, lethargy) of systemic CAIs; therefore, use of topical CAIs (eg, dorzolamide, brinzolamide) has largely replaced oral formulations.1,2

CAIs reduce intraocular pressure by inhibiting carbonic anhydrase enzyme activity in the ciliary body epithelium of the uvea, reducing aqueous humor production. Carbonic anhydrase isoenzymes are also present in extraocular sites, including RBCs, kidneys, and the respiratory tract.3 Systemic absorption of topical ocular medications occurs. Given the important metabolic functions of carbonic anhydrase and case reports of clinical signs associated with hypokalemia and metabolic acidosis in cats receiving topical CAIs,4,5 the authors of this study reviewed records of feline glaucoma patients that received topical CAIs and then prospectively evaluated the effect of topical dorzolamide in healthy cats. 

In the retrospective portion of the study, 8 out of 27 (29.6%) cats developed hypokalemia by the first reported screening (median, 67.5 days) after medical treatment was initiated. The degree of hypokalemia varied widely. Information on the development of clinical signs in cats with hypokalemia was limited, but inappetence, anorexia, and vomiting were reported in 4 cats, and alterations in mentation or energy level were reported in 3 cats. Clinical signs occurred in cats with or without concurrent systemic disease and with or without intraocular pressure control; female cats were more commonly affected. The severity of observed clinical signs did not coincide with the degree of hypokalemia identified on blood work.

Prospectively, 10 healthy cats were treated with dorzolamide in both eyes 3 times daily for 6 weeks. Serum potassium values were significantly lower than baseline at all evaluated time points, and serum chloride was significantly increased at weeks 2 and 4; however, all values remained within reference ranges. Adverse effects (including lip licking, hypersalivation, decreased appetite, and local irritation) were reported in half of the study cats. All reported clinical signs were transient and lasted <2 weeks. 

In this study, topical dorzolamide applied to the eyes of healthy cats resulted in a measurable effect on serum electrolytes. Electrolyte changes may be the result of impaired secretion of hydrogen from the kidneys, resulting in distal renal tubular acidosis.4 Further studies evaluating the impact of topical CAIs on systemic health of glaucomatous cats and those with concurrent systemic disease are needed.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Routine electrolyte monitoring is recommended for all cats receiving topical CAIs. After initiating treatment, electrolyte assessment is recommended at 2 weeks and at 2 to 4 months, followed by 6-month intervals for the duration of treatment.

2

Systemic clinical signs of hypokalemia can occur and often do not reflect laboratory values.

 

3

Potassium supplementation and discontinuation of topical CAIs may be required in some patients.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Rescue CB March 2022

Effect of Heat-Treated Lactobacilli on Canine Atopic Dermatitis

William Oldenhoff, DVM, DACVD, ACCESS Specialty Animal Hospital, San Fernando Valley, California

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Effect of Heat-Treated Lactobacilli on Canine Atopic Dermatitis

In the literature

Santoro D, Fagman L, Zhang Y, Fahong Y. Clinical efficacy of spray‐based heat‐treated lactobacilli in canine atopic dermatitis: a preliminary, open‐label, uncontrolled study. Vet Dermatol. 2021;32(2):114-e23.


FROM THE PAGE…

Topical application of heat-killed bacteria (ie, Lactobacillus spp, Vitreoscilla filiformis) has been reported to help in the treatment of atopic dermatitis in humans and mice.1-4 There have been no investigations into the use of a similar product in atopic dogs. 

The current study* evaluated use of a spray containing heat-killed lactobacilli (ie, L rhamnosus, L reuteri) in 10 nonseasonally allergic pet dogs. The spray was applied to the ventrum every 24 hours for 28 days. Clinical scores (ie, canine atopic dermatitis extent and severity index 4 [CADESI-04], pruritus visual analog scale [pVAS]), skin barrier function, and pet owner assessment were obtained on days 0, 14, 28, and 42. The cutaneous microbiota were analyzed on days 0 and 28. There was a significant reduction in CADESI clinical severity scores at each time point as compared with those on day 0 and in pVAS on day 42. Significant changes in cutaneous microbiota and skin barrier function were not observed. Owners reported the spray was easy to apply.


…TO YOUR PATIENTS

Key pearls to put into practice:

1

A spray containing heat-killed Lactobacillus spp may be useful in the treatment of canine atopic dermatitis. This product may appeal to those owners with an increased interest in natural and alternative treatments. Larger-scale, blinded, placebo-controlled studies are needed to confirm the benefit of this product.

2

It is not fully understood why application of a heat-killed bacterial product helps treat allergic patients, but it may be due to an effect on local and systemic immune responses. Bacterial populations can have profound effects on the host’s immune system that may help ameliorate the clinical signs of some diseases (eg, atopic dermatitis). Greater understanding of the relationship between bacterial populations and disease may yield opportunities for new therapeutic options.

3

Treatment for atopic dermatitis is not limited to medication that stops itching. There is a wide range of therapies and products available. The most successful treatment includes a variety of products chosen based on evidence-based rationale. Therapy for clinical signs, allergen-specific immunotherapy, and topical products should be included as part of management in allergic patients.

* This study was funded by DRN srl.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Detecting Canine Intestinal Parasites: An Update

Lindsay A. Starkey, DVM, PhD, DACVM, (Parasitology), Auburn University

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Detecting Canine Intestinal Parasites: An Update

In the literature

Sweet S, Hegarty E, McCrann DJ, Coyne M, Kincaid D, Szlosek D. A 3-year retrospective analysis of canine intestinal parasites: fecal testing positivity by age, U.S. geographical region and reason for veterinary visit. Parasit Vectors. 2021;14(1):173.


FROM THE PAGE…

Adequate detection and treatment of intestinal parasites is important in both veterinary and human medicine, as several intestinal parasites of dogs can pose a zoonotic risk. Proper detection and identification via fecal examination can be challenging because flotation technique and solution, examiner expertise, age of feces, and presence of pseudoparasites can influence results.

This study* compared parasite recovery from canine feces using centrifugal fecal flotation (zinc sulfate) and coproantigen immunoassay for detection of intestinal parasites. More than 1.9 million tests were performed over a 3-year period. Results were analyzed by age group, US geographic region, and reason for visit (ie, wellness vs other).

When combining flotation and immunoassay results from wellness and other veterinary visits, Giardia spp were detected most frequently (12.2% and 10.8%, respectively); followed by hookworms (4.1% and 4.2%, respectively); roundworms (2.5% and 1.7%, respectively); coccidia (Cystoisospora spp; 1.6% and 1.4%, respectively); whipworms (1.1% and 1.4%, respectively); and tapeworms (0.2% and 0.3%, respectively). During recovery of coccidian oocysts via fecal flotation, Eimeria spp (a pseudoparasite of dogs) were identified more often than Cystoisospora spp.

Dogs 2 to 6 months of age had the highest number of positive results for any intestinal parasite, with Giardia spp, coccidia, and roundworms being most common. The percent of positive tests gradually decreased as age increased. Regardless of geographic region, Giardia spp were most often detected; hookworms were the next most common in all regions except in the west, where roundworms were second most common.

For every parasite detected, coproantigen immunoassay alone detected more positives than fecal flotation alone; furthermore, combined detection using both diagnostics exceeded detection by either diagnostic alone.


…TO YOUR PATIENTS

Key pearls to put into practice:

1

Intestinal parasitism is an ongoing problem. Regardless of patient age, testing for intestinal parasites and use of year-round parasite preventives are recommended.

 

2

Using a combination of fecal diagnostic techniques is more likely to lead to an accurate diagnosis.

 

3

Presence of Eimeria spp oocysts in canine fecal samples may be the result of coprophagy, illustrating the importance of obtaining a thorough patient history regarding diet and lifestyle.

 

*This study was funded by IDEXX Laboratories.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Clinical Outcomes in Dogs with Localized Splenic Histiocytic Sarcoma

Sandra Axiak-Bechtel, DVM, DACVIM (Oncology), University of Florida

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Clinical Outcomes in Dogs with Localized Splenic Histiocytic Sarcoma

In the Literature

Latifi M, Tuohy JL, Coutermarsh-Ott SL, Klahn SL, Leeper H, Dervisis N. Clinical outcomes in dogs with localized splenic histiocytic sarcoma treated with splenectomy with or without adjuvant chemotherapy. J Vet Intern Med. 2020;34(6):2645-2650.


FROM THE PAGE …

Histiocytic sarcoma in dogs can be localized, disseminated, or hemophagocytic; these subtypes and the location of the localized histiocytic sarcoma affect treatment recommendations and prognosis. For example, localized treatment for periarticular, cutaneous, and pulmonary histiocytic sarcoma can lead to prolonged survival times (ie, one year or longer).1-3 Localized histiocytic sarcoma of the spleen in dogs is uncommon, and prognosis after splenectomy with or without chemotherapy has not been clearly characterized. 

The objectives of this retrospective, multi-institutional study were to describe the prognostic clinical factors and patient outcomes of splenectomy with and without adjuvant chemotherapy in dogs diagnosed with localized splenic histiocytic sarcoma. Fourteen dogs were identified for inclusion, and all dogs had splenectomy performed. Two dogs had lymph node metastasis at the time of surgery, and 12 dogs were administered adjuvant chemotherapy that included either lomustine (n = 10) or alternating lomustine and doxorubicin (n = 2). Five dogs developed suspected or confirmed metastatic disease following splenectomy. 

Overall median survival time was 427 days. The median progression-free interval was 205 days. None of the studied clinical variables were predictive of survival; however, this study’s sample size was small. The role of chemotherapy in survival could not be determined, as only 2 dogs did not receive chemotherapy.  

Although this study was retrospective (resulting in variable treatment, staging, and follow-up protocols), results suggest that localized histiocytic sarcoma of the spleen may have a favorable outcome following splenectomy and chemotherapy.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Histiocytic sarcoma in dogs can be disseminated or localized. The most common sites of localized histiocytic sarcoma are periarticular and pulmonary and have a favorable prognosis as compared with disseminated histiocytic sarcoma.

2

Localized splenic histiocytic sarcoma is typically a component of disseminated histiocytic sarcoma. Full staging is recommended prior to considering splenectomy and should include 3-view thoracic radiography, abdominal ultrasonography, and fine-needle aspiration and cytology of any suspicious lesions.

3

Localized splenic histiocytic sarcoma is uncommon. Splenectomy followed by chemotherapy, however, may provide a median survival time of one year.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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KBroVet CB March 2022

Research Note: Ampicillin Use in Healthy & Azotemic Dogs

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Ampicillin is commonly used to treat leptospirosis and pyelonephritis in azotemic dogs. Aminopenicillins are excreted primarily via renal tubular secretion and partially via glomerular filtration and reach high concentrations in the urine of healthy dogs, but drug clearance may be affected in dogs with kidney disease. This study evaluated plasma clearance of a single dose of ampicillin (22 mg/kg IV) in healthy dogs compared with azotemic dogs. Azotemic dogs were found to have 4.55 times higher peak ampicillin concentration, 6.04 times longer plasma half-life, and a significantly lower volume of distribution and clearance as compared with healthy dogs; however, glomerular filtration rates and creatinine levels do not correlate linearly, making dose adjustments difficult. Ampicillin clearance in azotemic dogs in this study suggests once-daily administration may be adequate for the first 48 hours of treatment; however, drug accumulation may occur after 48 hours, increasing the risk for adverse effects.

Source

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Research Note: Effects of Fasting on Serum Markers of Small Intestinal & Exocrine Pancreatic Disease

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Serum cobalamin, folate, canine pancreatic lipase immunoreactivity (cPLI), and canine trypsin-like immunoreactivity (cTLI) are markers for canine small intestinal and exocrine pancreatic disease. Patients are often fasted prior to sampling to avoid theoretical postprandial effects. Guidance on how long food should be withheld is inconsistent, varying from 6 to 12 hours, and recommendations for withholding food are not evidence-based. This study compared serum levels of cobalamin, folate, cPLI, and cTLI in healthy dogs (n = 11) after 12 hours of being fasted, then 1, 2, 4, and 8 hours after being fed. Median serum cobalamin levels were mildly decreased 4 and 8 hours postprandially. Although these results were statistically significant, clinical diagnosis would not be altered. Differences in cPLI, cTLI, and folate were not significant. Postprandial lipemia did not affect serum concentrations of these markers when samples were adequately centrifuged, but withholding food for ≥8 hours was deemed useful for avoiding the centrifugation process required when samples were lipemic.

Source

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Differential Diagnosis: Splenomegaly in Cats

Elijah Ernst, DVM, North Carolina State University

Karyn Harrell, DVM, DACVIM (SAIM), North Carolina State University

Internal Medicine

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Peer Reviewed

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Differential Diagnosis: Splenomegaly in Cats

Following are differential diagnoses for cats presented with splenomegaly.*

  • Infiltrative 
    • Lymphoma
    • Mast cell tumor
    • Multiple myeloma 
    • Leukemia
    • Hypereosinophilic syndrome  
  • Infectious 
    • Cytauxzoonosis 
    • Histoplasmosis
    • Feline infectious peritonitis 
    • Toxoplasmosis 
    • Ehrlichiosis 
    • Bartonellosis
    • Hemotropic mycoplasmosis
  • Congestive
    • Sedation 
    • Right-sided congestive heart failure
    • Splenic vein thrombosis
    • Portal hypertension
  • Reactive/hyperplastic changes (often cause focal enlargement)
    • Extramedullary hematopoiesis (eg, bone marrow failure [myelofibrosis, myelophthisis, toxicity, immune-mediated disease, radiation], tissue inflammation or injury, hypoxia, splenic hematoma, splenic thrombosis)
    • Nodular hyperplasia 
      • Splenic
      • Complex
      • Lymphoid 
  • Focal enlargement due to neoplasia (eg, hemangiosarcoma)
*Splenomegaly refers to diffuse enlargement unless otherwise noted.

Suggested Reading

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Ocular Pain & Vision Loss in a Golden Retriever

Andrew Christopher Lewin, BVM&S, DACVO, Louisiana State University

Ophthalmology

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Peer Reviewed

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Ocular Pain & Vision Loss in a Golden Retriever

Clinical History & Signalment

Trigger, a 6-year-old neutered male golden retriever, was presented for a 48-hour history of blepharospasm, ocular discharge, and excessive tearing in the left eye. His owner reported he had been pawing at the eye and surrounding region over the previous 48 hours. He was lethargic and hyporexic and had bumped into objects several times at home in the previous 24 hours.

Physical Examination

Routine physical examination results were normal, and a complete ophthalmic examination was performed.

Findings in the Right Eye

Menace response, direct pupillary reflex, palpebral reflex, and dazzle reflex were normal. Consensual pupillary reflex was absent. Schirmer tear test was 23 mm/minute (normal, 15-25 mm/minute). Intraocular pressure was 8 mm Hg (normal, 10-20 mm Hg via rebound tonometer). Fluorescein staining was negative for uptake by the cornea.

The cornea was intact with a normal tear film during magnified diffuse and slit-beam examination. Mild conjunctival hyperemia, iridal hyperpigmentation, lenticular nuclear sclerosis, multifocal paraxial regions of pigmentation in a radial arrangement on the anterior lens capsule, and a small amount of visible free pigmented cells in the anterior chamber with mild (trace) aqueous flare (aqueous flare scale, trace to 4+) were also present (Figure 1).

Gonioscopy showed a normal, open iridocorneal angle. Fundoscopy using binocular indirect ophthalmoscopy with a 28-diopter lens revealed a normal fundus.

Conjunctival hyperemia, lenticular nuclear sclerosis, iridal hyperpigmentation, and radially arranged pigmentation visible on the anterior lens capsule in Trigger’s right eye. Image courtesy of Louisiana State University School of Veterinary Medicine Ophthalmology Service
Conjunctival hyperemia, lenticular nuclear sclerosis, iridal hyperpigmentation, and radially arranged pigmentation visible on the anterior lens capsule in Trigger’s right eye. Image courtesy of Louisiana State University School of Veterinary Medicine Ophthalmology Service

FIGURE 1 Conjunctival hyperemia, lenticular nuclear sclerosis, iridal hyperpigmentation, and radially arranged pigmentation visible on the anterior lens capsule in Trigger’s right eye. Image courtesy of Louisiana State University School of Veterinary Medicine Ophthalmology Service

FIGURE 1 Conjunctival hyperemia, lenticular nuclear sclerosis, iridal hyperpigmentation, and radially arranged pigmentation visible on the anterior lens capsule in Trigger’s right eye. Image courtesy of Louisiana State University School of Veterinary Medicine Ophthalmology Service

Findings in the Left Eye

Menace response, direct pupillary reflex (midrange pupil [ie, neither miotic nor mydriatic]), consensual pupillary reflex, and dazzle reflex were absent. Palpebral reflex was normal. Schirmer tear test was >30 mm/minute (normal, 15-25 mm/minute). Intraocular pressure was 58 mm Hg (normal, 10-20 mm Hg via rebound tonometer). Fluorescein staining was negative for uptake by the cornea.

The cornea was intact with a normal tear film during magnified diffuse and slit-beam examination. Evidence of epiphora was present at the medial canthus and surrounding facial skin. Marked conjunctival hyperemia, moderate chemosis, severe aqueous flare (3+), mild hyphema obscuring iridal detail, and mild enophthalmos attributed to blepharospasm, leading to elevation of the third eyelid, were also observed (Figure 2).

Intraocular structures were not visible via gonioscopy. Fundoscopy examination using binocular indirect ophthalmoscopy with a 28-diopter lens revealed only the tapetal reflex due to anterior segment abnormalities.

Conjunctival hyperemia, loss of intraocular detail, and elevation of the third eyelid in Trigger’s left eye. Image courtesy of Louisiana State University School of Veterinary Medicine Ophthalmology Service
Conjunctival hyperemia, loss of intraocular detail, and elevation of the third eyelid in Trigger’s left eye. Image courtesy of Louisiana State University School of Veterinary Medicine Ophthalmology Service

FIGURE 2 Conjunctival hyperemia, loss of intraocular detail, and elevation of the third eyelid in Trigger’s left eye. Image courtesy of Louisiana State University School of Veterinary Medicine Ophthalmology Service

FIGURE 2 Conjunctival hyperemia, loss of intraocular detail, and elevation of the third eyelid in Trigger’s left eye. Image courtesy of Louisiana State University School of Veterinary Medicine Ophthalmology Service

DIAGNOSIS:

BILATERAL GOLDEN RETRIEVER PIGMENTARY UVEITIS WITH SECONDARY GLAUCOMA IN THE LEFT EYE

Diagnosis

Based on ocular examination findings and signalment, Trigger was diagnosed with golden retriever pigmentary uveitis (GRPU) in both eyes and secondary glaucoma in the left eye. 

Evidence of uveitis (ie, iridal hyperpigmentation, free pigmented cells in the aqueous humor, mild ocular hypotony, conjunctival hyperemia, aqueous flare) was detected in the right eye, and, although views of intraocular structures were limited in the left eye, most cases of GRPU are bilateral (59%-89%).1,2 In addition, because there was no evidence of goniodysgenesis in the right eye and there were no concurrent physical examination abnormalities or concurrent ocular findings in the left eye, glaucoma in the left eye was believed to be secondary to GRPU. Diffuse hyphema in the left eye was attributed to chronic inflammation associated with GRPU.

Treatment & Management

GRPU in Trigger’s right eye led to uveitis but not glaucoma. Topical and systemic NSAIDs and topical and systemic corticosteroids were considered to control inflammation (see Treatment at a Glance). The eye was initially treated with topical diclofenac 0.1% ophthalmic solution every 8 hours because inflammation in the eye was mild, and topical NSAIDs are typically associated with few adverse effects. 

Topical ocular antihypertensive medications, specialty glaucoma surgery, and surgical salvage were considered for treatment of glaucoma in Trigger’s left eye. Restoration of vision was unlikely given the lack of menace response, pupillary light reflexes, and dazzle reflex. Trigger’s owner decided not to pursue medical management due to the associated poor prognosis for vision and potential for long-term discomfort. The left eye was surgically removed using a closed transpalpebral enucleation technique and submitted for histopathology, which confirmed the diagnosis of GRPU with secondary glaucoma.

TREATMENT AT A GLANCE

  • Treatment options are limited for GRPU, and the underlying disease process is incompletely understood.
  • Standard of care for GRPU is topical and/or systemic anti-inflammatory medications.
  • Long-term treatment is usually required.
  • Medications to control glaucoma should be administered as needed.
  • Salvage procedures (eg, enucleation) should be considered for eyes that are permanently blind and painful.

Prognosis & Outcome

The enucleation site healed uneventfully. Vision was maintained in his right eye, which remained apparently comfortable with normal intraocular pressure (10 mm Hg) 6 months later. Topical diclofenac 0.1% ophthalmic solution every 12 hours in the right eye was the only medication continued at the 6-month follow-up. In most cases, long-term anti-inflammatory treatment is recommended. Long-term anti-inflammatory drugs and routine recheck appointments every 3 to 6 months were recommended for Trigger.

Discussion

GRPU (ie, pigmentary uveitis, golden retriever uveitis) is a common, most likely inherited condition in golden retrievers that can vary in severity (see Take-Home Messages).3 In the United States, ≈5% to 25% of golden retrievers are affected.3 The hallmark of the GRPU phenotype is radially oriented pigment on the anterior lens capsule. Mildly affected patients have a small amount of radially oriented pigment deposition on the anterior lens capsule. Severely affected patients can have radial pigmentation on the lens capsule, fibrinous material in the anterior chamber, and vision- and globe-threatening complications (eg, glaucoma). Affected dogs are most often diagnosed between 4 and 8 years of age.

GRPU diagnosis should be made in golden retrievers when radial pigment is present on the anterior lens capsule, even in the absence of other findings (eg, iridal hyperpigmentation, aqueous flare).3 GRPU is not the only potential cause of uveitis, hyphema, or glaucoma in this breed. Thorough physical and ocular examinations should be supported with appropriate diagnostic testing when the diagnosis is not clear. 

Although not seen in this case, uveal cysts are commonly found in patients with GRPU and are a significant risk factor for development of GRPU in golden retrievers.3 Visualization of uveal cysts is not necessary to diagnose GRPU, as only 13.3% to 42% of eyes with GRPU have this finding on examination.3 When ultrasound biomicroscopy is used, however, 100% of eyes affected with GRPU contain multiple uveal cysts.3,4 This discrepancy is because eyes with GRPU are often affected by miosis, which may prevent complete examination of the posterior chamber. 

GRPU occurs almost exclusively in golden retrievers and is therefore strongly suspected to be inherited. Because of the potential for severe visual impairment and ocular pain, breeding dogs affected with GRPU is not recommended5; however, late onset (ie, 4-8 years) has led to difficulties in preventing breeding of affected dogs.

Treatment for GRPU

Treatment is challenging because underlying pathophysiology is not completely understood. Although it is assumed that GRPU has an inflammatory component, histologic confirmation is not always possible.2 Regardless, topical or systemic anti-inflammatory medications are the standard of care.3

Topical NSAIDs (eg, diclofenac, ketorolac, flurbiprofen) can be used in eyes with mild to moderate intraocular inflammation and should be initially applied every 12 to 24 hours. Frequency can then be tapered to effect. Adverse effects are infrequent, but ocular hypertension may occur.

Systemic NSAIDs (eg, carprofen, meloxicam) can be used in patients with mild to moderate intraocular inflammation. Topical NSAIDs are more often preferred because adverse effects and contraindications are more frequently associated with systemic use.

Topical corticosteroids (eg, dexamethasone, prednisolone) are usually reserved for patients with moderate to severe intraocular inflammation and should be initially applied every 4 to 8 hours. Frequency can then be tapered to effect. Adverse effects include corneal opacification. These drugs are contraindicated in eyes with corneal ulceration.

Systemic corticosteroids (eg, prednisone) are typically reserved for patients with severe intraocular inflammation. Dose recommendations vary, but anti-inflammatory doses (eg, prednisone, 0.5 mg/kg PO every 12 hours, then tapered to effect) are typically used for severe GRPU and tapered to effect. These drugs have numerous adverse effects and contraindications.

Treatment for Glaucoma

Secondary glaucoma and vision loss occur in ≈20% to 45% of eyes with GRPU.1,3,6 Treatment options are limited. There is no difference in disease progression in eyes treated with topical steroids compared with eyes treated with topical NSAIDs, but time between examinations is a significant factor in disease progression.7 Posterior synechiae and fibrinous material in the anterior chamber are significant risk factors for glaucoma development.3,7

Topical ocular antihypertensive medications can be used to treat glaucoma in dogs. Topical dorzolamide 2% ophthalmic solution (typically applied every 8 hours) is preferred for cases of secondary glaucoma. Topical latanoprost 0.005% ophthalmic solution (typically applied every 12 hours) is usually avoided in patients with secondary glaucoma because it can exacerbate underlying uveitis. Topical timolol 0.5% ophthalmic solution (typically applied every 12 hours) is usually inadequate for reduction of severely elevated intraocular pressure.

Specialty glaucoma surgical procedures are another treatment option. Transscleral diode cyclophotocoagulation can be used to control intraocular pressure in some cases.1 A surgical salvage procedure (eg, enucleation) is typically warranted in painful, permanently blind eyes. Elevated intraocular pressure is considered painful.

TAKE-HOME MESSAGES

  • GRPU is a common, inherited ocular disease in golden retrievers.
  • Radial pigment deposition on the anterior lens capsule is the hallmark clinical finding.
  • Many cases of GRPU progress to secondary glaucoma and vision loss.
  • GRPU is most often a bilateral disease.
  • There are numerous causes of uveitis in golden retrievers, and a thorough systemic and ocular diagnostic investigation should be pursued in all cases.
  • Referral to a veterinary ophthalmologist for further assessment is recommended in most cases.
  • Early diagnosis and treatment may help prolong vision.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Top 5 Antimicrobial Stewardship Practices

J. Scott Weese, DVM, DVSc, DACVIM, FCAHS, Ontario Veterinary College, Ontario, Canada

Pharmacology & Medications

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Peer Reviewed
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Web-Exclusive

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Top 5 Antimicrobial Stewardship Practices

Antimicrobial stewardship is a multifaceted approach to responsible antimicrobial use that optimizes clinical outcome, minimize adverse effects, and address the emerging threat of antimicrobial resistance while maintaining good patient care. There are many practical antimicrobial stewardship components that can be used in the clinic.

Following are the author’s top 5 suggested antimicrobial stewardship practices.

1

De-escalation

De-escalation is simple, cost-effective, and based on basic concepts of everyday decision-making that evaluate diagnostic testing and clinical response in order to decrease the number of antimicrobials used and/or the spectrum and duration of antimicrobial treatment. De-escalation depends on daily (or more frequent) reassessment of the patient to determine when to change or stop antimicrobial treatment. For example, broad-spectrum antimicrobials might be indicated when a patient is initially presented; however, based on additional testing and clinical evaluation, treatment could be narrowed by stopping one drug of a combination or by selecting a different drug. 

The decision to stop treatment is important, as excessively long treatment durations are common in veterinary patients. This may occur simply because the default is to continue treatment when there is no established stopping point. 

De-escalation has many benefits, including reduced cost, minimized risk for adverse effects, and lowered pressure for antimicrobial resistance selection, as well as allowing for easier transition from inpatient to at-home care. De-escalation may be underused because it is infrequently considered or because of lack of culture or other test results, lack of clinician confidence in narrowing the spectrum, and/or reluctance to change. 

Use of de-escalation can be encouraged via formal approaches (eg, mandatory review points), whereby inpatient antimicrobial regimens should be re-evaluated and treatment orders should be reissued after a specified period (eg, 48 hours). Making continuation of treatment an active decision can facilitate reassessment and transition to narrower spectrum treatment, as opposed to the active step of stopping treatment. Increased discussion and awareness are likely the most important components, prompting thought about the antimicrobial regimen and exercising confidence in making changes.

2

Clinical Guidelines

Clinical guidelines are increasingly available and provide guidance on the approaches recommended for most patients. Available guidelines include those on international disease-specific diagnoses and treatment.1-5 National prescribing guidelines are also available in many countries. Guidelines can assist with key decisions (eg, when to use an antimicrobial, which drug[s] to choose, treatment duration). Easy-to-access online versions are being developed for clinical use.

3

Antimicrobial Tiering

The tiering of antimicrobials raises awareness of the relative importance of different antimicrobials in veterinary and human medicine and the implications of resistance. The emphasis is mostly on the importance of the drug in human medicine and the potential impact of veterinary use on resistance in human pathogens. Antimicrobials can be classified using different systems (eg, those described by the World Health Organization [WHO]6 or the European Medicines Authority [EMA]7; Table). 

Third-generation cephalosporins and fluoroquinolones are the most commonly used higher-tier drugs in veterinary medicine. Use of higher-tier drugs may be appropriate in some patients, but tiering classifications should be considered when choosing an antimicrobial, with the goal of using the appropriate lowest tier drug.

TABLE

COMMONLY USED ANTIMICROBIAL EXAMPLES & CLASSIFICATIONS

Antimicrobial WHO Classification* EMA Classification
Third-generation cephalosporins (eg, cefovecin, cefpodoxime) Highest priority, critically important Restrict
Fluoroquinolones Highest priority, critically important Restrict
Potentiated penicillins (eg, amoxicillin/clavulanic acid) Critically important Caution
First-generation cephalosporins (eg, cephalexin, cefazolin) Highly important Caution
Tetracyclines (eg, doxycycline) Highly important Prudence
Penicillins (eg, amoxicillin) Highly important Prudence
Lincosamides (eg, clindamycin) Highly important Caution
Macrolides (eg, azithromycin) Highest priority, critically important Caution
Metronidazole Important Prudence
Trimethoprim-sulfonamides Highly important Prudence
Carbapenems (eg, meropenem) Critically important Avoid
Chloramphenicol Highly important Caution
*WHO categories include the following: highest priority, critically important; critically important; highly important; important
EMA categories include the following: avoid, restrict, caution, prudence
4

Use & Interpretation of Culture & Susceptibility Results

Culture results should be carefully interpreted, as they can be important for case management, but they can also be misleading, with false-positive or false-negative results (see Potential Explanations For False-Positive & False-Negative Culture Results). Detailed discussion is beyond the scope of this article, but relevance of results depends on whether the isolated organism makes sense for the disease process, the reported level of growth, other test results, and bacteria normally present at the site. 

Not all isolated bacteria need to be targeted. The focus should be on treatment, not test results. Resistant organisms are not more likely to cause disease or require a different treatment approach (apart from drug selection) as compared with their susceptible counterparts, so the susceptibility profile only dictates drug selection, not whether the organism is relevant or whether treatment is needed. Mixed cultures should be interpreted with caution, as they likely represent contamination. 

Prudent use of cultures should also be considered. Specimens should rarely be submitted for culture when there is no realistic need for treatment (eg, urine sample from a clinically normal patient) or when the sample may not be representative (eg, superficial swab of a draining tract).

POTENTIAL EXPLANATIONS FOR FALSE-POSITIVE & FALSE-NEGATIVE CULTURE RESULTS

False-Positive Results

  • Presence of resident microbiota at a normally polymicrobial site
  • Laboratory contamination
  • Contamination during sampling and handling
  • Use of overly sensitive methods (eg, broth enrichment)
  • Sampling incorrect site (eg, necrotic areas, external opening of draining tracts)

False-Negative Results

  • Nonbacterial cause
  • Inadequate or nonrepresentative sample
  • Fastidious organism that died during transportation
  • Poor sample handling, storage, or transportation
  • Organism is not readily grown under routine laboratory conditions
  • Ongoing or recent antimicrobial therapy
  • Poor sampling technique
  • Causative agent not identified because of overgrowth of contaminants
5

Delayed Prescribing

Delayed prescribing targets situations in which antimicrobials are not indicated at the time of examination but might be reasonable later based on the course of disease (determined by clinical signs and/or duration of disease) or pending test results. 

Delayed prescribing provides a specified treatment approach that goes beyond having the pet owner return if there is no improvement. The aim is to balance antimicrobial stewardship and owner satisfaction by indicating to the owner that antimicrobials are not yet recommended but will be made available in certain situations without a need for further examination or additional cost beyond that of the drug. This can consist of providing a postdated prescription or an indication (ideally written and provided to the owner) that if the stated criteria are met, the antimicrobial can be picked up from the clinic or a prescription provided. 

Delayed prescribing has been shown in human medicine to substantially reduce antimicrobial use without impacting patient outcome or complication rates,8 simultaneously leading to greater patient satisfaction as compared with not receiving a prescription at the time of the appointment.9 In veterinary medicine, this method can be considered in patients with acute diarrhea and upper respiratory tract infection. For example, the owner of a dog with acute diarrhea that is otherwise clinically normal can be instructed to manage the patient conservatively (eg, via diet) to provide time for the disease to self-resolve and be informed that an antimicrobial (eg, metronidazole) will be provided if the disease persists for a certain period (eg, >3 days). 

Delayed prescribing should be used with caution or avoided in patients in which the diagnosis is less certain, owner observation or follow-up may be poor, or the patient is likely at higher risk for complications.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Adequan CB March 2022
Clinical Notes: Gut Check

Clinical Notes: Gut Check

Jacqueline C. Whittemore, DVM, PhD, DACVIM (SAIM), University of Tennessee, Animal Emergency and Specialty Center, Knoxville, Tennessee

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Clinical Notes: Gut Check
Sponsored by an Unrestricted Educational Grant from Nutramax Laboratories Veterinary Sciences, Inc.

KEY POINTS

  • Probiotics can be used in the management of a number of GI conditions.
  • Probiotics can help alleviate antibiotic-associated GI signs.
  • When selecting a probiotic, peer-reviewed studies proving efficacy are most important to consider.
  • Evidence increasingly supports the use of probiotics for conditions such as anxiety and CKD, but proven safety and efficacy will remain critical as future uses are explored.

DEFINITIONS

  • Probiotics: Live microorganisms that confer health benefits on the host when administered in adequate amounts.1 Most probiotics are bacteria, but there is at least 1 yeast species (Saccharomyces boulardii) that qualifies as a probiotic as well.
  • Prebiotics: Substrates that selectively promote the growth of microorganisms that confer health benefits2
  • Synbiotics: A mixture of pro- and prebiotics

Pro- and synbiotics, which shift the host’s microbiome and metabolome to achieve local and far-reaching effects,1-2 are being used increasingly to manage GI and extra-GI issues.3-8 This could reflect client demand for natural or alternative management modalities, intolerance of the adverse effects of conventional management, and/or failure of said management options to optimize patient outcomes.

Common Gastrointestinal Applications

Stress & Self-Limiting Gastroenteritis

Universal support of probiotics in managing stress-related GI signs has not been demonstrated. In adequately powered studies, pro/synbiotics decreased feline and canine diarrhea in shelter environments9,10; however, similar efficacy was not demonstrated in weanling kittens,11 working dogs under quarantine,12 or racing Alaskan sled dogs, except during a week-long contagious outbreak.13

Impact on self-limiting gastroenteritis has been more consistently positive. Probiotics decreased the duration of self-limiting diarrhea, alone or with vomiting, by 32% to 41% as compared with controls in multiple randomized trials.14-17 Probiotics have also been found to significantly decrease hyporexia and vomiting,18 the use of rescue antibiotics,15 and study withdrawal for additional medical therapy such as antiemetics or antibiotics.16 In addition, resolution of acute diarrhea significantly correlated with probiotic administration and dietary modification, but not antibiotics, in a large observational study.8

Infectious Gastroenteritis

Probiotics may reduce the severity of clinical signs of infectious gastroenteritis, although adequately powered study results are limited. In a study, dogs with naturally occurring parvovirus enteritis were administered conventional therapy alone or in combination with a high-dose, multistrain probiotic cocktail.19 Dogs administered the probiotic were significantly less sick on days 3 and 5 of hospitalization and had lower mortality than dogs administered supportive care alone. Positive results also were identified for dogs with distemper virus-related diarrhea in a lower-quality trial.20 Although clinical illness scores differed significantly from baseline 1 day earlier in dogs with acute hemorrhagic diarrhea syndrome given probiotics versus placebo, scores were not statistically significant between groups.21 Because scores were clinically equivalent and all dogs responded well to management, the benefit of probiotics in acute hemorrhagic diarrhea syndrome is questionable.

Non-Food–Responsive Chronic Enteropathy

Cats with idiopathic chronic enteropathy (CE) administered a multistrain synbiotic (Proviable®-DC) had significantly lower fecal scores in an open-label trial.22 In another study, 9 out of 10 cats with idiopathic constipation/megacolon administered a high-dose probiotic had resolution of clinical signs, with clinically and statistically significant histologic improvement.23 Clinical activity scores were similarly improved in dogs with large-bowel dysmotility administered probiotics and a hydrolyzed, high-fiber diet.24,25 Clinical activity scores, defecation frequency, and fecal consistency also significantly improved in dogs with CE administered S boulardii versus placebo in addition to conventional management,26 as well as in dogs with colonic polyps given a high-dose multistrain bacterial probiotic.27

Probiotics may also be useful for managing CE in dogs that fail to respond to diet change. In a study, clinical and histologic response rates did not differ for dogs treated with prednisone/metronidazole versus the same probiotic cocktail, with enhanced T regulatory cell function and dysbiosis normalization only in the probiotic group.28 A follow-up study found no difference between dogs administered diet and prednisone alone as compared with the probiotic,29 suggesting probiotic effects may be blunted by prednisone coadministration.

Antibiotic-Associated GI Signs

In the only study assessing the impact of probiotics on antibiotic-associated GI signs (AAGS) secondary to injectable antibiotic use, probiotic administration significantly decreased duration of lincomycin-induced diarrhea and inhibited it from developing when administered concurrently with the antibiotic.30

With regard to oral antibiotics, in one feline study, administration of a probiotic 2 hours prior to administration of amoxicillin/clavulanate did not significantly decrease AAGS.31 In another study, coadministration of a synbiotic with clindamycin also did not decrease diarrhea in cats,32 although vomiting was less common in the synbiotic group. In a follow-up crossover study, administration of a higher-dose synbiotic (Proviable®-Forte) 1 hour after clindamycin administration was associated with significantly increased food intake and decreased vomiting, and cats receiving the synbiotic were more likely to complete the initial phase of the study.33 This suggests that beneficial effects of the synbiotics persisted for ≥6 weeks after administration. Significant differences were also identified for food intake between the initial treatment period and after a 6-week washout, a phenomenon known as period effects (ie, when the washout between treatments is inadequate to prevent carryover effects from the initial treatment). In this case, food intake required to maintain weight was significantly higher at the start of period 2 for cats initially in the placebo group, which was consistent with development of antibiotic-induced CE. Several other placebo cats had persistent diarrhea at the end of the washout period, although period effects were not statistically confirmed.

Based on these results, administration of a synbiotic 1 to 2 hours after oral antibiotic administration has the highest likelihood of minimizing AAGS in cats and dogs.

In another crossover study with an 8-week washout period, derangements in food intake were significantly lower for dogs that received a bacterial/yeast synbiotic combination (Proviable®-Forte with Mycequin®) 1 hour after receiving enrofloxacin/metronidazole as compared with placebo.34 Although vomiting and diarrhea did not statistically differ between groups, both were less severe during the second phase of the study; this suggests support for the synbiotic combination against AAGS. Significant differences in the microbiome and metabolome between groups were also found.2,32,35 Based on these results, administration of a synbiotic 1 to 2 hours after oral antibiotic administration has the highest likelihood of minimizing AAGS in cats and dogs.

Choosing a Probiotic

The most important criterion in product selection is demonstrated efficacy in peer-reviewed literature. Product species, microbial strains, and total microorganisms (colony-forming units) should be considered when scientific data are lacking.

Products containing more colony-forming units and microbial strains are recommended for the management of metabolic and GI disorders based on correlations between dose and efficacy in humans.36-38 Yeast probiotics are not inactivated by antibiotics but can cause serious complications in immunocompromised patients. Products containing pre- and probiotics (ie, synbiotics) are often preferred for GI disorders because they act synergistically to support colonocyte health. Animal protein flavorants can adversely impact patients with food sensitivity. Other selection considerations include administration and storage requirements. Because pro/synbiotics are not regulated as drugs in the United States and less than one-third of evaluated probiotics have been shown to meet or exceed the type and quantity of viable organisms listed on their labels,39 only probiotics that undergo regular evaluations for content and viability should be used.

The Future of Probiotics

Probiotics rarely have adverse effects when appropriately administered, but an evidence-based approach to product selection and administration is essential for maximal benefits. Limited but moderate- to high-quality evidence supports pro/synbiotic administration for management of shelter-induced diarrhea, self-limiting gastroenteritis, parvovirus, intestinal dysmotility, and CE in cats and dogs. Several randomized, blinded placebo-controlled studies support the use of Proviable®-Forte administered alone or in combination with Mycequin® (a yeast-based probiotic) to mitigate AAGS in patients receiving antibiotics.

Evidence also increasingly supports the use of probiotics for some extra-GI issues such as anxiety and CKD.4,7 Results for other disorders such as canine atopy are mixed,3,5,6,40 with positive results found primarily in studies using probiotics with higher colony-forming units.3,5,6 This emphasizes the importance of careful product selection, administration, and attention to details of published research.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Crown Amputation for Tooth Resorption

Jan Bellows, DVM, FAVD, DAVDC, DABVP, All Pets Dental, Weston, Florida

Dentistry & Periodontology

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Crown Amputation for Tooth Resorption

Resorption normally refers to a process in which one part of the body draws in or absorbs another part. Tooth and root resorption involves parts of a tooth being broken down by osteoclasts. Although resorption of internal or external parts of the tooth is possible, the latter is more common, and external root resorption occasionally occurs alongside internal resorption. External tooth resorption often begins on the external surface of the root and progresses inward. In addition to partial hard tissue tooth loss, inflammation of the gingiva is common if the resorption is exposed to the oral cavity.

Common Resorptions

Surface, external inflammatory, and noninflammatory replacement resorption are the most common tooth resorptions in dogs and cats.

Surface Resorption

Surface resorption may occur secondary to release of osteoclast-activating factors at the site of cementum injury triggered by inflammation. Resorption can occur at any location on the root surface and progress into dentin apically and/or coronally. Surface root resorption (Figure 1) is radiographically characterized by one or more shallow voids that affect the cementum, which can extend into dentin located along the margins of the root. The periodontal ligament space and lamina dura may be locally affected. 

When resorption stops, cells from the periodontal ligament proliferate and populate the resorbed area, depositing reparative tissue. Surface resorption is generally self-limiting unless it is exposed to the oral cavity; this is often quite painful because dentin tubules are exposed to heat, cold, and pressure.

Extracted third incisor from a cat with surface external root resorption extending to the oral cavity
Extracted third incisor from a cat with surface external root resorption extending to the oral cavity

FIGURE 1 Extracted third incisor from a cat with surface external root resorption extending to the oral cavity

FIGURE 1 Extracted third incisor from a cat with surface external root resorption extending to the oral cavity

External Inflammatory Resorption

External inflammatory resorption begins in the periodontal ligament apical to the cementoenamel junction and at furcations where dentin is exposed. The etiology is unknown. In early stages, odontoclasts resorb and undermine unsupported enamel or cementum, which subsequently breaks away. As the process continues, deeper and more significant amounts of dental tissue are involved. For resorption that begins near the cementoenamel junction and progresses toward the crown, loss of dentin and enamel near the gingival attachment exposes the defect to the oral environment. Inflammation of surrounding tissues occurs, leading to increased sensitivity. 

On radiographs, voids (ie, radiolucencies) often extend into the pulp cavity and root canal. With external inflammatory resorption, the tooth roots have similar opacity as surrounding teeth, and periodontal ligament space is visible.

Noninflammatory Replacement Resorption

Noninflammatory tooth replacement of unknown etiology occurs in dogs and cats, in which the root fuses to the bone (ie, dentoalveolar ankylosis), and the tooth is eventually resorbed, becoming part of the alveolar bone remodeling process. This process can take years to complete and is considered a form of healing, as the bone integrates dental hard tissue as part of itself, and the tooth becomes involved in normal skeletal turnover. Osteoblasts form bone in the resorbed area when the resorptive process is complete; thus, dental hard tissues are gradually replaced by bone. 

Replacement resorption does not preclude the presence of viable pulp; the pulp can be normal in affected teeth. Lesions sealed below the gingival sulcus may not be painful; however, bacteria can invade the pulp if it is exposed to the oral cavity, leading to painful inflammation. The resorptive process can penetrate the root canal or pulp chamber and, in advanced cases, gradually fill the pulp cavity with new bone. External replacement tooth resorption radiographically appears as a mottled or moth-eaten tooth.

Resorption Classification

Companion animal tooth resorption is often classified by stage and type based on anatomic location and radiographic appearance.1 Stage refers to anatomic loss of dental hard tissue, and type refers to radiographic root opacity and the presence or absence of periodontal ligament space.

Resorption should also be identified as internal or external. Internal resorption takes place in the pulp chamber or root canal and progresses outward; external resorption starts on the outside of the tooth (ie, enamel, cementum) and progresses inward. External resorption should be examined for exposure to the oral cavity and to determine whether roots are significantly replaced with surrounding bone.

STAGES OF TOOTH RESORPTION*

  • Stage 1: mild dental hard tissue loss (ie, cementum or cementum and enamel) 
  • Stage 2: moderate dental hard tissue loss (ie, cementum or cementum and enamel with loss of dentin that does not extend to the pulp cavity)
  • Stage 3: deep dental hard tissue loss (ie, cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth’s integrity is retained
  • Stage 4: extensive dental hard tissue loss (ie, cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth’s integrity is lost
    • Stage 4a: crown and root are equally affected
    • Stage 4b: crown is more severely affected than the root
    • Stage 4c: root is more severely affected than the crown 
  • Stage 5: remnants of dental hard tissue are visible only as irregular radiopacities, and gingival covering is complete

*Adapted from Shope B, Carle D. Tooth resorption in dogs and cats. VetBloom website. February 2, 2017. Accessed December 27, 2021. http://blog.vetbloom.com/dentistry/tooth-resorption-in-dogs-and-cats

Classification by Stage

External tooth resorption stage is a classification system based on affected anatomy. Clinical examination with an explorer and intraoral imaging are used to determine stage (see Stages of Tooth Resorption).

Classification by Type

Tooth resorption type is determined via intraoral radiography based on root opacity and periodontal ligament space (see Types of Tooth Resorption Based on Radiographic Appearance and Figure 2).

Radiograph of a left mandibular molar tooth in a cat with Type 1 resorption (A) in which focal or multifocal radiolucency can be seen with otherwise normal radiopacity and normal periodontal ligament space. Radiograph of mandibular incisors and canine teeth in a cat with Type 2 resorption (B; white arrow) in which narrowing or disappearance of periodontal ligament space is present in at least some areas, and part of the tooth demonstrates decreased radiopacity. Radiograph of the right maxillary third and fourth premolars in a cat with Type 3 resorption (C); the third premolar features Type 1 resorption of the mesial root (arrowhead) and Type 2 resorption of the distal root (dashed arrow) with exposure to the oral cavity.
Radiograph of a left mandibular molar tooth in a cat with Type 1 resorption (A) in which focal or multifocal radiolucency can be seen with otherwise normal radiopacity and normal periodontal ligament space. Radiograph of mandibular incisors and canine teeth in a cat with Type 2 resorption (B; white arrow) in which narrowing or disappearance of periodontal ligament space is present in at least some areas, and part of the tooth demonstrates decreased radiopacity. Radiograph of the right maxillary third and fourth premolars in a cat with Type 3 resorption (C); the third premolar features Type 1 resorption of the mesial root (arrowhead) and Type 2 resorption of the distal root (dashed arrow) with exposure to the oral cavity.

FIGURE 2 Radiograph of a left mandibular molar tooth in a cat with Type 1 resorption (A) in which focal or multifocal radiolucency can be seen with otherwise normal radiopacity and normal periodontal ligament space. Radiograph of mandibular incisors and canine teeth in a cat with Type 2 resorption (B; white arrow) in which narrowing or disappearance of periodontal ligament space is present in at least some areas, and part of the tooth demonstrates decreased radiopacity. Radiograph of the right maxillary third and fourth premolars in a cat with Type 3 resorption (C); the third premolar features Type 1 resorption of the mesial root (arrowhead) and Type 2 resorption of the distal root (dashed arrow) with exposure to the oral cavity.

Radiograph of a left mandibular molar tooth in a cat with Type 1 resorption (A) in which focal or multifocal radiolucency can be seen with otherwise normal radiopacity and normal periodontal ligament space. Radiograph of mandibular incisors and canine teeth in a cat with Type 2 resorption (B; white arrow) in which narrowing or disappearance of periodontal ligament space is present in at least some areas, and part of the tooth demonstrates decreased radiopacity. Radiograph of the right maxillary third and fourth premolars in a cat with Type 3 resorption (C); the third premolar features Type 1 resorption of the mesial root (arrowhead) and Type 2 resorption of the distal root (dashed arrow) with exposure to the oral cavity.
Radiograph of a left mandibular molar tooth in a cat with Type 1 resorption (A) in which focal or multifocal radiolucency can be seen with otherwise normal radiopacity and normal periodontal ligament space. Radiograph of mandibular incisors and canine teeth in a cat with Type 2 resorption (B; white arrow) in which narrowing or disappearance of periodontal ligament space is present in at least some areas, and part of the tooth demonstrates decreased radiopacity. Radiograph of the right maxillary third and fourth premolars in a cat with Type 3 resorption (C); the third premolar features Type 1 resorption of the mesial root (arrowhead) and Type 2 resorption of the distal root (dashed arrow) with exposure to the oral cavity.

FIGURE 2 Radiograph of a left mandibular molar tooth in a cat with Type 1 resorption (A) in which focal or multifocal radiolucency can be seen with otherwise normal radiopacity and normal periodontal ligament space. Radiograph of mandibular incisors and canine teeth in a cat with Type 2 resorption (B; white arrow) in which narrowing or disappearance of periodontal ligament space is present in at least some areas, and part of the tooth demonstrates decreased radiopacity. Radiograph of the right maxillary third and fourth premolars in a cat with Type 3 resorption (C); the third premolar features Type 1 resorption of the mesial root (arrowhead) and Type 2 resorption of the distal root (dashed arrow) with exposure to the oral cavity.

Radiograph of a left mandibular molar tooth in a cat with Type 1 resorption (A) in which focal or multifocal radiolucency can be seen with otherwise normal radiopacity and normal periodontal ligament space. Radiograph of mandibular incisors and canine teeth in a cat with Type 2 resorption (B; white arrow) in which narrowing or disappearance of periodontal ligament space is present in at least some areas, and part of the tooth demonstrates decreased radiopacity. Radiograph of the right maxillary third and fourth premolars in a cat with Type 3 resorption (C); the third premolar features Type 1 resorption of the mesial root (arrowhead) and Type 2 resorption of the distal root (dashed arrow) with exposure to the oral cavity.
Radiograph of a left mandibular molar tooth in a cat with Type 1 resorption (A) in which focal or multifocal radiolucency can be seen with otherwise normal radiopacity and normal periodontal ligament space. Radiograph of mandibular incisors and canine teeth in a cat with Type 2 resorption (B; white arrow) in which narrowing or disappearance of periodontal ligament space is present in at least some areas, and part of the tooth demonstrates decreased radiopacity. Radiograph of the right maxillary third and fourth premolars in a cat with Type 3 resorption (C); the third premolar features Type 1 resorption of the mesial root (arrowhead) and Type 2 resorption of the distal root (dashed arrow) with exposure to the oral cavity.

FIGURE 2 Radiograph of a left mandibular molar tooth in a cat with Type 1 resorption (A) in which focal or multifocal radiolucency can be seen with otherwise normal radiopacity and normal periodontal ligament space. Radiograph of mandibular incisors and canine teeth in a cat with Type 2 resorption (B; white arrow) in which narrowing or disappearance of periodontal ligament space is present in at least some areas, and part of the tooth demonstrates decreased radiopacity. Radiograph of the right maxillary third and fourth premolars in a cat with Type 3 resorption (C); the third premolar features Type 1 resorption of the mesial root (arrowhead) and Type 2 resorption of the distal root (dashed arrow) with exposure to the oral cavity.

FIGURE 2 Radiograph of a left mandibular molar tooth in a cat with Type 1 resorption (A) in which focal or multifocal radiolucency can be seen with otherwise normal radiopacity and normal periodontal ligament space. Radiograph of mandibular incisors and canine teeth in a cat with Type 2 resorption (B; white arrow) in which narrowing or disappearance of periodontal ligament space is present in at least some areas, and part of the tooth demonstrates decreased radiopacity. Radiograph of the right maxillary third and fourth premolars in a cat with Type 3 resorption (C); the third premolar features Type 1 resorption of the mesial root (arrowhead) and Type 2 resorption of the distal root (dashed arrow) with exposure to the oral cavity.

TYPES OF TOOTH RESORPTION BASED ON RADIOGRAPHIC APPEARANCE*

  • Type 1 (T1): focal or multifocal radiolucency in a tooth with otherwise normal radiopacity and normal periodontal ligament space
  • Type 2 (T2): decreased radiopacity in part of a tooth with narrowed or absent periodontal ligament space in at least some areas
  • Type 3 (T3): features of Type 1 and Type 2 in the same tooth; focal or multifocal radiolucency in a tooth and decreased radiopacity in other areas of the tooth with areas of normal and narrow or lost periodontal ligament space

*Adapted from Shope B, Carle D. Tooth resorption in dogs and cats. VetBloom website. February 2, 2017. Accessed December 27, 2021. http://blog.vetbloom.com/dentistry/tooth-resorption-in-dogs-and-cats

Treatment

Treatment for tooth resorption is largely based on stage, type, and internal/external classification (Table). Extraction is the treatment of choice unless resorption appears to minimally affect the tooth and is confined subgingivally (ie, not exposed to the oral cavity). Intraoral radiography has therapeutic clinical significance for diagnosing patients and creating a treatment plan because only Type 2 resorption should be considered for crown amputation (ie, coronectomy) with gingival closure.

Crown Amputation with Gingival Closure

Bone and cementum‐like tissue eventually replace all or part of the periodontal ligament, dentin, and pulp in teeth with Type 2 resorption. Although complete extraction is the generally accepted treatment for resorption, intentional crown amputation with gingival closure can be effective for cases of Stage 2 to 5 with moderate to advanced Type 2 resorptions or Type 2 resorptions exposed to the oral cavity (ie, external noninflammatory replacement resorption).

Crown amputation with gingival closure is an advanced dental procedure involving creation of a mucogingival flap; use of a water-cooled, high-speed delivery system; and closure without tension that should only be performed after intraoral radiography confirms complete root extraction is not possible based on marked decrease in root opacity and absence of periodontal ligament space. The resorption is sealed off from the oral cavity, and the root continues being replaced by bone. 

In teeth affected by Type 3 resorption, roots affected by Type 2 resorption can be treated with crown amputation; the remaining roots should be extracted. Crown amputation typically results in subjectively less trauma and faster healing compared with complete extraction.2 

Contraindications for crown amputation with intentional partial root retention include periodontal disease evidenced by horizontal or vertical bone loss, endodontic disease, radiographic presence of a root canal, and chronic gingivostomatitis. Crown amputation should not be performed if intraoral dental radiography is not possible.

TABLE

CLINICAL RESPONSE TO TOOTH RESORPTION PRESENTATIONS

Presentation Response
Minimal surface external inflammatory resorption not extending into the oral cavity (Type 1 resorption) Monitoring via clinical examination and intraoral imaging every 6 months
Noninflammatory replacement resorption (Type 2 resorption)

Crown amputation with gingival closure

or

Extraction

Noninflammatory replacement resorption affecting only one root (Type 3 resorption) Crown amputation with gingival closure of the root undergoing replacement resorption and extraction of remaining normal root(s) or those affected by Type 1 external resorption

Marked external resorption (Type 1 resorption)

or

External resorption extending into the oral cavity

or

Internal resorption

Complete extraction of crown and all roots

STEP‐BY‐STEP

CROWN AMPUTATION WITH GINGIVAL CLOSURE FOR RADIOGRAPHICALLY CONFIRMED TYPE 2 TOOTH RESORPTION IN A CAT


WHAT YOU WILL NEED

  • #11 scalpel blade and blade handle
  • Fine periosteal elevator
  • High-speed delivery system
  • Tapered crosscut fissure bur
  • #2 round or football diamond bur
  • Suture holder 
  • 4-0 absorbable monofilament or catgut suture on a P-3 needle

STEP 1

Identify clinical (A) and radiographic (B) evidence of Type 2 tooth resorption.

Clinician's Brief
Clinician's Brief

AUTHOR INSIGHT

This patient has Type 2 resorption of the right mandibular canine with extension into the oral cavity.


STEP 2

Use a #11 scalpel blade to make a caudal incision in the gingiva for flap exposure of the coronal root.

Clinician's Brief

AUTHOR INSIGHT

For premolars and molars, either an envelope flap or 1 to 2 vertical and sulcular incisions should be made to expose the root.


STEP 3

Use a fine periosteal elevator (eg, molt elevator) to separate attached gingiva from the alveolar juga.

Clinician's Brief

STEP 4

Use a #2 to #8 sterile round or end‐cutting crosscut fissure bur (A) on a high‐speed, water‐cooled handpiece to remove the tooth crown and 2 to 4 mm of the coronal root apical to the alveolar margin (B).

Clinician's Brief
Clinician's Brief

STEP 5

Remove sharp alveolar margin projections with a #2 round or football diamond bur.

Clinician's Brief

STEP 6

Perform postamputation intraoral radiography to document the result and confirm all dental hard tissue coronal to the alveolar margin has been removed.

Clinician's Brief

AUTHOR INSIGHT

This patient’s left mandibular canine tooth is affected by Stage 5 tooth resorption without exposure to the oral cavity. No treatment is indicated.


STEP 7

Draw the mucoperiosteal flap over the alveolus and place single sutures without tension using 4-0 catgut or absorbable monofilament suture.

Clinician's Brief

STEP 8

Prescribe anti-inflammatory pain relief medication, and recommend feeding soft food for 2 weeks.

AUTHOR INSIGHT

Antimicrobial medication is generally not necessary. The prognosis for complete healing and pain relief is excellent. Surgical site healing and suture dissolution are expected on recheck examination.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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Congenital Portosystemic Shunt in a Dog

Sophie Eiger, VMD, University of Florida

W. Alex Fox-Alvarez, DVM, MS, DACVS-SA, University of Florida

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Congenital Portosystemic Shunt in a Dog

Millie, a 10-month-old spayed Yorkshire terrier, is presented for evaluation of a suspected congenital portosystemic shunt (PSS). She has a history of vomiting and diarrhea, occasional stranguria, polyuria, polydipsia, and postprandial lethargy. Millie was recently spayed, and the referral noted a prolonged anesthetic recovery, prompting further investigation. 

Physical examination is unremarkable, with the exception of a coarse hair coat and BCS of 3/9. CBC reveals a mild microcytic, normochromic, nonregenerative anemia. Serum chemistry profile reveals moderate increases in ALT and AST, mild hypoalbuminemia, mildly decreased BUN, mild hypoglycemia, and mild hypocholesterolemia. Urinalysis demonstrates a urine specific gravity of 1.006 and ammonium biurate crystalluria. Fasting and postprandial serum bile acids are significantly elevated. 

Millie is placed on preoperative medical therapy and a protein-restricted diet and is referred for further diagnostics and surgery.

After 2 weeks, CT angiography is performed, and a splenocaval shunt (Figure 1) and multiple cystoliths are revealed. Exploratory laparotomy is performed, the splenocaval shunt is identified, and an ameroid ring constrictor is placed to achieve gradual occlusion (Figure 2). A liver biopsy is obtained, and a routine cystotomy is performed to remove the cystoliths. All samples are submitted for analysis. 

Postattenuation neurologic signs are seen postoperatively, and Millie has a seizure. Medical intervention is initiated; neurologic signs resolve. She is discharged 2 days postoperatively on continued medical therapy and will return for a 2-week follow-up to have the incision checked. Additional follow-ups to monitor response to therapy are planned 1 and 3 months postoperatively for repeat blood work.

Based on the information provided, how would you grade the following drugs and why?

Do Not Use Proceed with Caution Safe

The following represents the best responses based on drug metabolism, pharmacokinetics, species, diagnostic differentials, clinical and laboratory data, and other pertinent findings.

Levetiracetam

Correct ResponseSafeHepatic encephalopathy is a neuropsychiatric syndrome that occurs if >70% of hepatic function is lost.1,2 In veterinary patients, common signs include lethargy, depression, stupor, head pressing, blindness, seizures, muscle function abnormalities, and coma.3 Because of the hepatic shunting associated with PSS, toxic substances accumulate in systemic circulation and can cause neurologic disturbances.2,4 Antiepileptic medications have previously been used to address hepatic encephalopathy and seizures.

Levetiracetam is a broad-spectrum anticonvulsant that appears to inhibit excitatory neurotransmitter release by binding to SV2A, a synaptic vesicle protein.5-7 Because protein binding is minimal and levetiracetam is primarily eliminated through the kidneys rather than the liver, levetiracetam is safe to use in patients with PSS.8

The use of levetiracetam to prevent postattenuation seizures is controversial. One retrospective study demonstrated that levetiracetam administered preoperatively at 20 mg/kg PO every 8 hours for a minimum of 24 hours significantly decreased the risk for postoperative seizures and death in dogs undergoing surgical attenuation of extrahepatic congenital PSS with ameroid ring constrictors.6 Other studies, however, demonstrated no significant difference in the incidence of postattenuation seizures in dogs that do or do not receive levetiracetam.9,10 Although levetiracetam may not prevent seizures, its liver-sparing metabolic characteristics make it an acceptable antiepileptic medication to use in patients with PSS.

Lactulose

Correct ResponseSafeAmmonia is produced by GI microbiota and is typically converted to urea and glutamine via the urea cycle in the normal liver.4 The abnormal blood flow associated with PSS results in ammonia accumulation.

Lactulose is an ammonia detoxicant, osmotic, and laxative commonly used as an adjunctive treatment to reduce ammonia blood levels associated with hepatic encephalopathy.11,12 Lactulose can be administered orally or via high colonic enemas and is metabolized by colonic bacteria, resulting in the formation of carbon dioxide and lactic, formic, and acetic acids.13 This acidic environment promotes the conversion of ammonia (NH3) to ammonium (NH4+), which is not readily absorbed and becomes ion-trapped and expelled in the feces.

Free fatty acid production also increases osmotic pressure in the bowel, creating a laxative effect and acidifying the colonic microenvironment. Osmotic effects can result in catharsis, reducing fecal transit time and intestinal exposure to bacteria and their ammonia products.4

Metronidazole

Correct ResponseProceed with CautionMetronidazole is a concentration-dependent bactericidal drug commonly used in patients with PSS.11 The goal of antibiotic therapy in patients with PSS is to decrease the intestinal load of urease-producing bacteria.2,4,11 Although metronidazole is often included in the medical management plan for patients with PSS, it is extremely important to adhere to appropriate administration practices and evaluate for signs of toxicity.14,15 Neurologic toxicity may occur after acute high doses of metronidazole, even in healthy dogs, and has been reported at appropriate doses in patients with PSS. Neurologic signs related to metronidazole administration may be difficult to distinguish from hepatic encephalopathy.

Ampicillin

Correct ResponseSafeAmpicillin is a time-dependent, bactericidal agent used to decrease intestinal loads of urease-producing bacteria.16 Although its anaerobic spectrum is not as wide as metronidazole, ampicillin lacks the potential for neurotoxicity. Amoxicillin is also effective, but ampicillin has lower oral bioavailability and is preferrable to minimize systemic absorption. For appropriate antibiotic stewardship, broad-spectrum, potentiated beta-lactams (eg, amoxicillin/clavulanate) should not be used in place of their narrower-spectrum analogs.

Benzodiazepines

Correct ResponseProceed with CautionPostoperative seizures develop in 3% to 18% of dogs after shunt attenuation and are most commonly seen in small-breed dogs with extrahepatic shunts.4,6,9,10,17-21 The cause of postoperative seizures is unknown; however, potential causes include imbalances in excitatory and inhibitory neurotransmitters or decreases in endogenous inhibitory CNS benzodiazepine agonist levels.4,22 Benzodiazepines are generally accepted as first-line treatment for postattenuation status epilepticus.1,23 Intravenous diazepam contains a propylene glycol carrying agent that requires hepatic metabolism; midazolam may be a better choice for acute seizure control than is diazepam.4

Controversy exists regarding the use of benzodiazepines to control seizures in patients with PSS. Intrinsic benzodiazepine-like compounds are hypothesized to be involved in hepatic encephalopathy.3 Accordingly, in humans, flumazenil has been used to improve mental status24; however, potential for similar improvements have not been evaluated in veterinary patients with hepatic encephalopathy. A study also demonstrated elevated concentrations of endogenous benzodiazepine receptor ligands in dogs with congenital PSS when compared with control dogs.1

Although benzodiazepines are clinically effective in patients with PSS that experience seizures, further research is required to determine the role of benzodiazepines in treating hepatic encephalopathy.

Propofol

Correct ResponseSafePropofol is a short-acting, injectable sedative-hypnotic agent frequently used for anesthetic induction in patients with PSS. Many commonly used anesthetic drugs are primarily metabolized by hepatic microsomal enzymes; therefore, hepatic dysfunction with PSS may result in prolonged half-lives and effects of administered anesthetic doses.25

As propofol may have extrahepatic metabolic sites, it is the most commonly used induction agent for patients with hepatic dysfunction25; however, because it is a protein-bound drug, lower total doses may be necessary in patients with PSS that have hypoalbuminemia. In addition, boluses and CRI are useful for the treatment of postattenuation seizures.22,26

Propofol is believed to be beneficial for the treatment of status epilepticus because of its gamma-aminobutyric acid activity at a different site from benzodiazepines.23

Phenobarbital

Correct ResponseProceed with CautionPhenobarbital is an antiepileptic barbiturate used to treat postoperative seizures22,23 that is hepatically metabolized and has been shown to cause hepatic injury after long-term administration in dogs.27 Phenobarbital has a lower lipid solubility and may take up to 30 minutes to reach therapeutic concentrations; therefore, benzodiazepines should be used instead as a first-line treatment for status epilepticus.4

Carprofen

Correct ResponseDo Not UseNSAIDs (eg, carprofen) are commonly used to treat acute and chronic pain. All NSAIDs have the potential to cause hepatic injury (intrinsically or idiosyncratically) and may impair coagulation and hemostasis by impacting platelet aggregation and clot formation.24 NSAIDs are also a risk factor for GI ulceration because of their effect on gastric mucosal integrity and prostaglandin synthesis.28 Because GI signs (eg, vomiting, diarrhea, anorexia, pica, GI bleeding) occur in ≈30% of dogs with PSS, NSAIDs may worsen these signs.4

One study found a 38.5% mortality rate in dogs with intrahepatic shunts treated with NSAIDs perioperatively, compared with 2.4% in dogs not treated with NSAIDs.28 All dogs in the study that died because of confirmed or suspected gastroduodenal ulcerations received NSAIDs postoperatively.28

NSAIDs should be avoided in patients with hepatic dysfunction and PSS because patients with PSS are predisposed to developing gastric ulceration and there are reported increases in mortality.

After successful treatment, NSAIDs can be considered in patients with an extrahepatic PSS but should be used with caution in patients with an intrahepatic PSS, even after surgical correction, due to the lifelong risk for GI ulceration.

Omeprazole

Correct ResponseSafeProton-pump inhibitors (eg, omeprazole) are indicated in dogs with PSS because of the high prevalence of concurrent GI signs. Omeprazole and other substituted benzimidazole proton-pump inhibitors are the most potent antisecretory drugs and are reported to reduce gastric acid secretion by 80% to 95%.29 Studies regarding intrahepatic PSS have demonstrated that up to 21% of dogs have lifelong risk for GI ulceration associated with significantly shorter survival times.30 In dogs undergoing treatment for intrahepatic PSS prior to antacid therapy, 50% of deaths were attributable to GI bleeding; lifelong antacid therapy reduced this rate to 4%.30

Although the reported rates of GI signs in extrahepatic PSS are lower, it is reasonable to use proton-pump inhibitors in patients with extrahepatic PSS that also have a history of ulceration, melena, or GI signs.

S-Adenosyl-Methionine

Correct ResponseSafeS-adenosyl-methionine (SAMe), an endogenous coenzyme, is composed of an adenosine triphosphate and methionine, a sulfur-containing amino acid.12 SAMe is necessary for transmethylation, transsulfuration, and decarboxylation reactions, as well as the production of glutathione, which is a crucial hepatic antioxidant.12,31 Because of the hygroscopic nature of SAMe and known variations in product bioavailability, formulations should be obtained from reputable manufacturers.31 Although there is minimal veterinary evidence-based information to substantiate efficacy of this hepatoprotective supplement, it may be beneficial as adjunctive treatment in dogs with PSS based on its safety profile, anecdotal use, and extensive preclinical studies and use in human hepatic diseases.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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