ICVA NAVLE Exam Questions

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141.

A three-year-old FS recently-adopted cat presents with mild lesions-comedones on the chin and lower lips. The lesions are mild, and she is otherwise healthy. She is on a flea/tick preventative and is indoors only. However, she presented for her annual wellness, and the owner hadn't even appreciated the change until you pointed it out. On physical, she had black spots and some swelling, primarily on the chin but starting on the lower lips with a few comedones. It doesn't appear to have a secondary infection, but you recommend skin cytology and scraping to be sure. You want to rule out any underlying diseases before confirming your suspicion of feline acne or chin folliculitis/furunculosis to the owner.

Which of the following diagnostics would not be warranted for this disease?

  • Biopsy/histopathology

  • Cytology

  • Culture, bacterial

  • Skin scraping

Correct answer: Biopsy/histopathology

Feline acne is considered a follicular keratinization disorder and can be complicated by secondary bacterial or yeast infections. The exact etiology is unknown and likely multifactorial, related to variable sebum production, stress, grooming habits, and underlying allergies (such as plastic food/water bowls). However, the etiology is still unclear.

Findings may include black follicular casts +/- comedones, crusting on the chin and lip commissures, and erythema. They are usually not painful and not usually itchy. Due to black keratin debris, the chin can look peppered with black. Some cats may also have alopecia.

Lesions (45% or so) may progress to pustular or papular, with severe cases worsening to folliculitis and furunculosis, which will become painful and pruritic. It may, in time, become edematous, mimicking what is seen with an eosinophilic granuloma complex. In severe cases, abscesses can arise. Scars may develop in chronic untreated patients. Systemic signs may develop, but this is rare.

Diagnostics may include:

  1. Dental radiographs to rule out atypical lower canine tooth root abscess
  2. Cytology (Slide impression/tape prep) to rule out yeast or bacterial overgrowth; skin scrapings to rule out Demodex Cati (a differential for folliculitis/furunculosis)
  3. Culture in the case of advanced cases where deep pyoderma is suspected; +/- DTM culture to rule out ringworm (though not usually found in chin lesions)

Biopsy and histopathology are rarely needed but may be beneficial in severe or refractory cases and to differentiate from eosinophilic granulomas.

Treatment can include antiseborrheic topical therapies such as benzoyl peroxide, ethyl lactate, and phytosphingosine. In many cases, a combo of shampoo and Douxo spot-on therapies a few times a week may be sufficient. These likely need to be utilized long-term to prevent a recurrence.

Topical antimicrobials if secondary infections are present. Options may include mupirocin, clindamycin, erythromycin, tetracycline, or metronidazole ointments or gels. However, use appropriate antimicrobial stewardship when selecting your choices.

Compresses/soaks may benefit those with swellings or drainage tracts using warm compresses and Epsom salts to soften the comedones and permit drainage.

Topical retinoids (vitamin A) can be used daily for four weeks, then every other day to twice weekly for prevention.

A topical steroid can be used in patients with significant inflammation and itch.

Systemic therapy may be needed, including antibiotics, with Clavamox or clindamycin being appropriate first-line empiric selections. Oral steroids for those that are very inflamed/pruritic.

Finally, Isotretinoin 2 mg/kg or 5–10 mg/cat/ day for four weeks, then q 24 hours to twice a week. This product helps decrease sebum production and inflammation and reduces follicular hyperkeratosis. This should only be used in confirmed cases refractory to other management modalities because insufficient research supports the use and on side effects and risks.

Some cases may spontaneously resolve, while other patients may have cyclical flares.

142.

A nine-month-old MN European shorthair was adopted from a shelter at 12 weeks of age. He had a history of several URIs before adoption but was otherwise healthy. He is indoor only, unless on a harness outside with the owner. He is UTD on vaccines but he has come in for a visit because he is now PU/PD. No lower urinary tract signs are present, and he is urinating well. Bloodwork showed a moderately elevated globulin level (two times normal), a USG of 1.025, with a negative urine culture. He was still eating but stopped after three days and presented to the local ER. He had mild mature neutrophilia, mild lymphocytosis, and mild eosinophilia confirmed on a blood smear. His globulin remained elevated at just below normal albumin despite dehydration. Serology for Toxoplasma gondii was negative. Chest radiographs showed a mild interstitial pattern, though he had no respiratory abnormalities. Abdominal ultrasound revealed several moderately enlarged mesenteric lymph nodes that, on aspiration, were shown to be reactive. 

The owner declined hospitalization and was sent home on an appetite stimulant (mirtazapine transdermal). He recovered and seemed to be back to his normal self. Fast forward three weeks and the appetite started to decline again. The owner went to a specialty hospital, and the cat now has slight anemia, leukocytosis with mature neutrophilia, lymphocytosis (even higher than before), monocytosis, and eosinophilia. He now has thrombocytosis as well. The total protein was 10.7, with low normal albumin and even more elevated globulins. The hyperglobulinemia was evaluated by electrophoresis and showed a polyclonal gammopathy. Another ultrasound was performed, showing splenomegaly in addition to mesenteric lymphadenopathy. Aspirates were performed, but immunocytochemistry using two different types of FCoV antibodies was negative. Additional diagnostics for infectious diseases were all negative. 

The internist elected to treat with prednisolone on a tapering dose and chlorambucil every three days. After six weeks, all bloodwork parameters were normal, and the cat was still acting normally. He remained on pred (no chlorambucil) maintenance dose for 12 months and was re-evaluated. All parameters were normal, and his physical was nonremarkable. Hence, they elected to decrease the pred to every other day. A month later, his globulin increased, and his FCoV titer (1:400) was now 1:410,000. They increased his steroid dose back up. On a recheck evaluation two months later, he was still clinically fine, but abdominal palpation suggested a mass. An ultrasound now revealed several enlarged lymph nodes in the ileocolic area. Mild retroperitoneal effusion was associated with the right kidney, and the mesentery was hyperechoic in some areas. The pred dose was again increased to the initial starting taper dose, and chlorambucil was added. However, within a week, he became lethargic and anorexic and developed electrolyte abnormalities, tachypnea, a fever, and anemic (16.5%). Radiographs showed significant pulmonary changes, and a tracheobronchial lavage was strongly positive on immunocytochemistry for anti-FCoV antibodies. He then seizured and was euthanized.

What is the only way to definitively diagnose FIP? 

  • Identify FCoV in tissues via immunohistochemistry

  • RT-PCR

  • Rivalta's test on effusions

  • Serology

Correct answer: Identify FCoV in tissues via immunohistochemistry (especially within macrophages)

There are many means to potentially diagnose/aid in diagnosing FIP. However, sensitivity and specificity are very variable, especially premortem. Serology cannot differentiate between exposure to feline coronavirus or FIP infection. Titers can be negative in cats even with FIP, and high titers do not always correlate with disease development. Never euthanize a cat just because of a positive  CoV titer.

Reverse transcriptase polymerase chain reaction can detect FCoV in various samples, including effusions, CSF, tissue, saliva, or feces. Sensitivity is high, but as with serology, we cannot differentiate between FIP and coronavirus. Healthy tests can still test positive with this modality.

Histopathology and immunohistostaining are required for a definitive diagnosis. The hallmark histopathologic lesions include granulomatous to pyogranulomatous areas with vascular orientation and significant vasculitis. Intracellular antigens identified as the FCoV antigen within macrophages in effusions or tissue can confirm the diagnosis. This represents the gold standard.

Rivalta's test can help you take an effusion and determine if it is an exudate or transudate. Fill a test tube with 7–8 ml of distilled water and a single drop of 98% acetic acid. Mix it well. Then place 1 drop of the effusion on top of the solution. A negative occurs when the drop disappears and the fluid remains clear (FIP-negative). A positive test occurs if the drop floats slowly down in a jellyfish-like shape or stays on the surface. A positive means the fluid is exudative in nature. If that fluid is evaluated and the albumin:globulin ratio is < 0.4, this suggests but doesn't confirm FIP. But it isn't definitive, as cats with lymphoma or bacterial peritonitis can also be positive on this test.

This case helps demonstrate the complexity of diagnosis, the disease course path can be challenging, and the use of immunosuppressive drugs or other options is unlikely to change the ultimate clinical course of the disease.

143.

A one-year-old FS DSH recently adopted from a shelter presents with chemosis. On ocular evaluation, signs are consistent with conjunctivitis. The owner only appreciated it in the right eye, but on the physical exam, it is bilateral.

All of the following would be appropriate medications to prescribe, except:

  • Neomycine-bacitracin-polymyxin-B

  • Famciclovir oral q 12 hours

  • 0.5% cidofovir topically q 8 to 12 hours

  • Tetracycline ophthalmic ointment

Correct answer: Neomycine-bacitracin-polymyxin-B

Cats with unilateral or bilateral conjunctivitis often have an underlying infectious cause. Common causes in cats include feline herpesvirus-1, Chlamydia, or mycoplasma infections. Treatment for a viral disease, such as FHV-1, may consist of antivirals such as topical cidofovir or oral famciclovir. Both chlamydia and mycoplasma often respond to topical tetracycline ophthalmic ointments.

Neomycine-bacitracin-polymyxin-B options are usually discouraged in cats as polymixin-B has been associated with anaphylaxis and hypersensitivity reactions. 

144.

You see a cat with a profound plantigrade stance. Before discussing the history or clinical signs with the owner, what is your top differential diagnosis for this patient? 

  • Diabetic peripheral neuropathy

  • Gastrocnemius muscle/Achilles tendon rupture/degeneration

  • Lower motor neuron paresis lesion L6-S1

  • Hypokalemia

Correct answer: diabetic peripheral neuropathy

Cats with a plantigrade stance are easy to spot from across the room. There are only a few causes for this, and they include:

  1. Diabetes Mellitus (most common)
  2. Lower motor neuron paresis lesion L6-S1
  3. Gastrocnemius muscle/Achilles tendon rupture/degeneration - We would likely expect it to be more unilateral than bilateral, but it could be either
  4. Weakness associated with significant hypokalemia may look like this stance, though they also have head weakness and other signs

Bloodwork will help differentiate hypokalemia and identify diabetes. Radiographs may be needed to evaluate for bony/tendon abnormalities, and advanced imaging such as MRI if lower motor neuron disease is expected and to assess the gastrocnemius area.

Cats with diabetes can develop potentially irreversible neuropathy, especially if it has been ongoing for a long time before treatment is sought out. They can be weak, have muscle atrophy, or even ataxic and secondary to tibial nerve dysfunction. They often develop a plantigrade stance (standing with their weight directly on the heels/ankles vs. the paws). Prolonged hyperglycemia is thought to trigger the response, including axonal degeneration and/or demyelination with remyelination. Some animals with insulin therapy recover, but the diagnosis is often late in the game, so residual neuropathy may remain.

145.

A four-year-old FS Bloodhound presents to you for a surgical evaluation because of a chronic intermittent history of blepharospasm, pawing at the eyes, and ocular discharge. Vision also seems impaired, and she has recurrent conjunctivitis that no longer seems to respond to medical management. Your veterinarian referred the patient to you for evaluation of her ocular confirmation. You want to evaluate for entropion, which you suspect, given the breed and overall appearance of the skin/eyes.

All of the following may be associated with entropion, except:

  • Comparing the palpebral fissure size to the corneal diameter helps identify entropion

  • Corneal ulcerations

  • Corneal vascularization

  • Eyelid alopecia

Correct answer: Comparing the palpebral fissure size to the corneal diameter helps identify entropion

Entropion, or the inward rolling of eyelid margins, can commonly occur in various breeds and is usually generalized, such as Sharpeis, chow-chows, Rottweilers, English or springer spaniels, bloodhounds, English bulldogs, bassets, Bouvier de Flandres and most giant breed dogs. Other breeds may have only one lid affected. Brachycephalic cats are at risk.

Clinical history includes blepharospasm, pawing at the eyes, and ocular discharge. With chronicity, corneal scarring (pigmentation, vascularization) will develop. Ulcers or conjunctivitis may occur intermittently due to the eyelashes constantly contacting and irritating the corneal surface. Vision can be impaired in severe cases.

Eyelids with entropion may lose fur or color changes because they are always kept moist from tear production.

Pulling the lateral canthus laterally, you can evaluate the palpebral fissure size. Compare this to the corneal diameter as this helps evaluate for macropalpebral fissure and ectropion (outward rolling of the eye), not entropion.

Resolution of clinical signs with the application of topical anesthetic (e.g., proparacaine) suggests a spastic rather than confirmational entropion and isn't surgical. However, for most entropion-related issues, surgery is necessary to fix the problem. Various procedures can be performed, from eyelid tacking (<20 weeks of age) to the modified Holtz-Celsus procedure to a permanent lateral tarsorrhaphy.

For young animals that are still growing, additional surgeries may be needed.

146.

At a regional meeting of a group of farms, you have been asked to review biosecurity protocols with their personnel. You are invited to discuss steps that should be taken with communicable diseases to prevent fomite and mechanical transmission on the farm. You want personnel to be aware that when handling disease outbreaks or even single animals with a known infectious disease, they must presume that any bodily fluid or tissue is potentially contagious and could be transmitted to other animals. You advise them that aborted fetuses, fetal membranes, and discharge from any orifice (feces, urine, nasal discharge, ocular discharge) can all have potentially contagious material in them and should be handled accordingly.

When feasible, you recommend all of the following for personnel handling infected animals on farms, except:

  • If there is insufficient staff to have sick animals tended to by a separate person from healthy animals, then healthy animals should be cared for last.

  • Assigning a specific individual caregiver for the infected animals. That person, ideally, doesn't handle or treat any non-exposed animals.

  • If there is insufficient staff to have sick animals tended to by a separate person from uninfected animals, then healthy animals should be cared for first.

  • Ensure staff wears and properly disposes of appropriate Personal Protective Equipment (PPE) when handling sick animals.

Correct answer: If there is insufficient staff to have sick animals tended to by a separate person from healthy animals, then healthy animals should be cared for last.

Biosecurity protocols should be established on all farms you work with ahead of time. Knowing how to manage infectious diseases in general, what steps to take, and how to prevent contamination of equipment, egress areas, feed, and other materials is paramount to minimizing the spread of disease. While we cannot prepare for all potential outbreaks, disasters, or troubles. However, we can have some basic protocols that all staff know to ensure safety and minimize disease transmission.

Key steps when managing an infectious disease on a farm include:

  1. When feasible, have one or more caregivers assigned only to care for, feed, exercise, muck stalls, and the sick animals. These people should have no contact with healthy or non-clinical animals, including being in the vicinity of those animals while still wearing anything that came in contact with the infected animals. While this is great in a perfect world, not all farms have sufficient staff to achieve this.
  2. For farms where insufficient staff prevents personnel from solely being assigned to care for healthy, exposed, or sick animals, personnel should take care of all healthy animals first. This includes doing all daily required maintenance, feeding, etc., before moving to the next group of animals. The next group to be addressed would be those exposed but not yet showing clinical signs, finishing with those infected and sick. If PPE fails or contamination of shoes or other items occurs with infected materials, these items will be cleaned or disposed of after use and not come in contact with healthy animals.
  3. Ensure proper protective equipment at all times when handling infected/sick animals. This may vary depending on the infectious disease of concern but would include things like disposable gloves, foot coverings, or dedicated shoes that are easily washable and can be disinfected safely. Further, barrier clothing, such as impervious gowns or apparel, is washed immediately after contact with infected animals.
  4. Once the sick animals have been handled, properly disposing of all disposable equipment in the proper receptacles is paramount. Further, hand washing and hygiene remain key to preventing disease transfer and mechanical transmission. 

147.

A five-year-old MN toy poodle of adult age presents in respiratory distress. She has had progressive dysphagia over the past days to a week, and the owner feels her tongue seems to move oddly when her mouth is open. She has a bit of strabismus in the left eye and may be slightly swollen below it. Finally, a fluctuant swelling is evident externally under her chin. She is not painful on palpation of the fluctuant swelling. What issue do you suspect is the primary differential diagnosis? 

  • Salivary mucocele(s)

  • Sialadenitis

  • Sialadenosis

  • Dental tooth root abscess

Correct answer: Salivary mucocele(s)

Salivary mucoceles are a collection of saliva that has leaked from a salivary gland or duct that has been damaged. It is surrounded by granulation tissue. 

Cervical mucoceles occur in the intermandibular space's deeper structures, along the jaw's angle, or in the upper cervical area. 

In sublingual mucoceles (ranula), saliva collects in the sublingual tissue, just caudal to the openings of the mandibular and sublingual ducts.

In pharyngeal mucoceles, saliva collects in tissues adjacent to the pharynx. These patients may present in respiratory distress. 

In zygomatic mucoceles, the collection occurs just below the globe. 

Some patients may have complex mucoceles (multiple in one patient).

The exact cause of mucoceles isn't fully elucidated, though blunt trauma, sialoliths, or foreign objects have been suggested. Saliva irritates the tissue and, thus, causes irritation which, in time, leads to granulation tissue. This prevents the saliva from migrating further and forms the collection pocket.

Diagnosis is based on history, physical findings, and cytology. Perform paracentesis aseptically to prevent infection. Salivary mucocele fluid is very ropey, clear to yellowish or blood-tinged, and mucoid with a low cell count. If white cells are also present or elevated white blood cells are found in the blood, one may be dealing with sialoadenitis.

Differentials include infection of the gland (sialoadenitis), non-painful enlargement of the gland (sialadenosis), cancer of the salivary gland(s), sialolith, foreign body, hematoma, lymph nodes (cystic or cancerous), various cysts, or cervical abscess. If the zygomatic area is swollen, differentials also include tooth root abscesses. Histopath is necessary to differentiate these conditions, and treatment is surgical as they rarely resolve without surgical intervention/excision. 

148.

A seven-year-old MN Cocker spaniel presents with acute onset of pupillary dilation, buphthalmia, anisocoria, corneal edema, and scleritis, and he is extremely painful in the right eye. Using tonometry, you assess the intraocular pressures. Which of the following would represent the normal intraocular pressures of dogs?

  • 18.7+/- 5.5  mmHG mean +/- SD

  • 16.6+/- 3.6 mmHg mean +/- SD

  • 22.8 +/-5.5 mmHg mean +/- SD

  • 10.8+/-3.6 mmHg mean +/- SD

Correct answer: 18.7+/- 5.5  mmHG mean +/- SD

The mean IOP with standard deviation for a dog is 18.7+/- 5.5  (generally, we recognize 10–20 mmHg as the normal range for dogs), while for a cat, the normal is 19.7+/-5.6. (with 10–25 mmHg acceptable in cats).

Glaucoma in dogs is usually considered if pressures are greater than 25 mmHg and > 30 in cats.

16.6+/- 3.6 mmHg mean +/- SD represents the normal for llamas and alpacas.

22.8 +/-5.5 mmHg mean +/- SD represents a ferret's normal range.

10.8+/-3.6 mmHg mean +/- SD represents the normal range of owls.

In acute glaucoma, pressures can be elevated in the 50–80 mmHg range. Prompt action is necessary to save vision in acute cases. Still, in chronic cases, while therapy is necessary to protect the eye from further damage, vision is unlikely to be restored. 

149.

Proper nutrition and monitoring of dogs with cirrhosis (end-stage liver disease) is warranted. We need to minimize the work of the liver while at the same time providing the pet with proper nutrition.

All of the following should be included in a cirrhotic dog's diet to lessen the risk of malnutrition, except:

  • High-quality protein in restricted amounts

  • Highly digestible, complex carbohydrates should be fed

  • Diets high in fermentable fiber

  • Vitamin supplementation with E and  K (fat-soluble) and B (water-soluble)

Correct answer: High-quality protein in restricted amounts

While we need to balance metabolism and clinical signs of Hepatoencephalopathy (HE), we must also ensure to minimize malnutrition risk. Thus, we cannot excessively protein restrict these patients as it could cause protein-calorie restriction and lead the body to break down endogenous proteins likely to produce ammonia. Therefore, we actually want to ensure a tasty diet (that they will eat), small meals frequently (four to six times daily) so the body doesn't have to work too hard each meal, lessen the risk of HE signs, and since often appetite is not ideal, to begin with. Further, feeding a high-quality, easily digestible protein in normal amounts when possible.

High-quality soy, or egg, can be added to the diet in dogs who lose weight or develop low albumin.

Animals with chronic hepatitis and cirrhosis may have decreased ability to metabolize carbohydrates. Thus, ensuring the diet has complex, highly digestible carbohydrates is key.

Fat should be fed in normal quantities unless steatorrhea develops, in which case it may need to be restricted.

Fermentable fiber improves clinical HE. This works by trapping ammonia through the acidification of the colon. Further, this type of fiber increases the amount of nitrogen taken up by gut bacteria and decreases bacterial ammonia production.

Non-fermentable fiber supplementation may also be warned to lessen the risk of constipation. Constipation increases the risk of the development of HE.

Supplementation with various vitamins and minerals may also be needed depending on the type of liver disease, the pet, and the selected diet. Supplementation with zinc, fat, and water-soluble vitamins, including E (antioxidant properties), K (if clotting times are abnormal and before biopsies of any kind), and B vitamins since they may be lost in animals with polyuria. A and D should not be supplemented.

Monitor these patients closely — frequent weight checks, muscle condition scoring, and blood protein levels. 

150.

A farmer is concerned because he hasn't seen any overt signs of heat in his heifers. He wants to be sure he hasn't missed estrus, as he knows that the first cycle can be silent, failing to show signs of vulvar relaxation, behavioral cues, like standing to permit mounting, or vulvar relaxation. He knows he has a narrow window for insemination.

We are more likely to see errors in estrus detection for all of the following reasons, except:

  • Anestrus

  • Silent heat in the first ovulation postpartum or in the first cycle of heifers

  • Lameness or restricted animal movement masking signs of heat

  • Insufficient progesterone priming leads to a lack of estrus behaviors

Correct answer: Anestrus

Cattle may have irregularities in cycling. This can occur because estrus detection fails, such as observers fail to properly note estrus behaviors, a heifer fails to demonstrate normal estrus behaviors (e.g., lameness causing pain or silent heat, as is commonly seen on the first cycle of a heifer), or due to a decreased progesterone levels failing to permit priming of normal estrus behaviors.

Anestrus is the state of lack of estrous behaviors. This occurs during pregnancy, seasonally, or with lactation. Further, it can happen under pathological conditions, such as endometritis, infectious disease, toxicities, neoplasia, and other problems, including husbandry-related concerns such as substrates, heat stress, or other related issues. But given that we are talking about a group of heifers, silent heat (failing to detect heat) is the most likely cause/contributing factor. 

When producers keep appropriate records, have sufficient staff to monitor animal behaviors, and are adept at breeding, most producers know when their animals are expected to show normal periods of anestrus. Subtle changes, such as lack of expressing overt signs of heat (silent heat), lameness, hormonal imbalances, or changes associated with age, or other animal-interrelated mechanisms, are more likely the reason for poor estrus detection. 

151.

A 14-year-old MN DSH was presented for acute blindness. Your ocular exam reveals mydriasis, retinal hemorrhages, partial bullous retinal detachment OD, and complete OS. Given these findings, what diagnostic test do you recommend for this patient? 

  • Peripheral blood pressure

  • Fluorescein stain

  • Tonometry

  • Schirmer tear test

Correct answer: Peripheral blood pressure

While all the answers can be considered correct, systemic hypertension should be front and center on your differential list, given the exam findings. Cats with systemic hypertension often present with the first and only clinical sign as acute blindness, manifesting as a partial or complete retinal detachment, usually bilaterally. Animals will be mydriatic, non-visual, with retinal hemorrhages and obvious retinal detachment. Systolic pressures > 180 mmHg can lead to detachment, though cats often have values exceeding this at the time of diagnosis.

In dogs, we don't often see primary systemic hypertension without an underlying cause. However, cats may have no other underlying cause and still have systemic hypertension.

Underlying etiologies, when present, can include kidney disease (acute/chronic), adrenal tumors such as pheochromocytomas, diabetes mellitus, and feline hyperthyroidism.

Blood pressure assessment should ideally be done after the patient has relaxed with no or minimal restraint (ideally with the owner in a comfy place) for five to ten minutes. Note blood pressure and heart rates at the time of measurement. (Tachycardic patients and elevated blood pressure must be evaluated within context). If the blood pressure remains high, but the patient's heart rate is decreasing, it is less likely secondary to anxiety and likely truly high. Always ensure to take multiple readings and average them. Ensure you wait one to two minutes between measurements to allow the vessel adequate time to refill.

Evaluating intraocular pressures (tonometry) to rule out glaucoma (which can cause acute blindness) is valuable. However, it is less common in cats than in dogs.

Evaluation of tear production (Schirmer tear test), while never wrong in the presence of ocular disease, dry eye doesn't match the clinical picture in this cat, and it is uncommon in cats.

Finally, testing for corneal ulcers via staining is also never wrong, though again, clinical signs do not suggest ulceration.

Bloodwork to rule out underlying disease causes would also be warranted, in addition to assessing the patient's blood pressure.

152.

A five-year-old MN non-brachycephalic mixed-breed dog presents to the surgery service for a rhinoscopy. The pet has had recurrent nasal discharge that failed to respond to antibiotic therapy and now includes intermittent epistaxis. Chest radiographs, and bloodwork, including coagulation evaluations, have been non-remarkable. On rhinoscopy, the surgeon finds cavernous areas due to significant turbinate destruction. Samples are collected for culture, cytology, and histopathology. The surgeon identifies masses that look like inspissated mucus with an odd color.

Based on these findings, what is this patient's most appropriate and likely successful therapy?

  • Topical Clotrimazole (Lotrimin)

  • Oral antifungals e.g., azole medications

  • Rhinoscopic debridement of nasal turbinates and surrounding areas

  • Rhinotomy with resection of affected turbinates and soft tissues

Correct answer: Topical Clotrimazole (Lotrimin)

This patient has classic nasal aspergillosis. Unlike systemic aspergillosis, it carries a decent prognosis. It is the second most common cause of chronic nasal discharge in the dog, secondary to neoplasia. This form causes severe nasal turbinate destruction, affecting the nasal cavity or paranasal sinus areas. However, while the prognosis of it can be good, it often occurs secondary to a neoplastic /immunosuppressive illness.

Clinical signs usually include chronic nasal discharge with epistaxis. Sometimes the nasal planum has eroded from the chronicity. Discharge can vary in appearance or type. Animals may also show reverse sneezing, sneezing, less appetite, and depression. CT can detect cortical bone changes, and MRI can better discern differences between fungal colonies vs. thickened secretions/mucosa.

Rhinoscopic changes are as described above. Debridement while in the nose may be helpful. Obvious mats of fungal hyphae may be evident, appearing as fuzzy plaques.

Topical clotrimazole infused into the nasal passages/frontal sinuses is considered the most effective therapy (80–90% success rates) vs. oral antifungals with only 43–70% success rates. Topical may be required once and be curative, though others may require repeat treatment. (Topical may also be accomplished through the oral cavity and nares unless the frontal sinus is the only affected location, and trephination may be needed.)

Careful evaluation before topical therapy to determine if the cribriform plate is intact is warranted before using topical treatment, or serious complications, including death, can arise.

In cases who fail to respond, rhinotomy may be used with surgical plaque debridement and then via infusion of enilconazole.

153.

A beef cattle producer organization has requested you speak to them about the dangers of bovine spongiform encephalopathy. (BSE) They have seen an uptick in the news of another Transmissible Spongiform Encephalopathy (TSE), Chronic Wasting Disease (CWD) in deer, and feel they need to understand prion diseases better and want to understand why we do not have active Creutzfeldt-Jakob Disease (vCJD) in the U.S.

All of the following have prevented BSE from establishing in the U.S., except:

  • Protection against BSE primarily falls to the United States Department of Agriculture

  • 1997 Prohibit the use of mammalian products in ruminant feed

  • 2009 Ban "specified risk materials" (SRM) from feeds, pet foods, fertilizers

  • Human surveillance efforts are the responsibility of the Centers for Disease Control and Prevention (CDC)

Correct answer: Protection against BSE primarily falls to the United States Department of Agriculture

First, you explain that currently, we do not appreciate transmission of CWD to cattle, though experimentally, it can occur. The disease is not of bovine species but of free-range (wildlife) and captive-raised cervids such as reindeer, moose, elk, and deer. However, it is also caused by a prion that causes TSEs like BSE or scrapie (found in sheep/goats). Second, you explain that we do not have BSE in the U.S. due to strict measures from 1997.

In 1997, the U.S. banned the use of any sources of mammals in ruminant feed products. In 2009, the FDA created an enhanced BSE feed ban that extended this ban to the prevention of feeding SRMs which includes nervous tissue which varies with the animal's age but includes tonsils, distal ileum, skull, eyes, brain, spinal cord, trigeminal and dorsal root ganglia and the vertebral column (so no neurological tissue) from entering the food chain.

The USDA provides oversight for food animal meat inspection. Their job is to ensure that the SRMs do not enter the food supply. However, protection from BSE is primarily the responsibility of the Food and Drug Administration (FDA). Research is provided by the National Institute of Health and oversight by the Department of Health and Human Services (DHHS)'s Office of the Secretary. Finally, all human surveillance activities are provided by the CDC.

154.

An owner presents with a recently adopted four-year-old MN DSH who came to the owner severely pruritic about the head and ears. He has a coffee-ground-like discharge in both ears. He is scratching his ears raw and has some alopecia and pruritus of the neck, back, and tail. Ear cytology confirms ear mites, and scrapings in the affected areas on the body also show the mites there. There was no evidence of a secondary otitis externa, so only mite therapy is necessary.

All of the following are appropriate therapies for Otodectes cynotis, except:

  • Otic mineral oil

  • Transdermal macrocylic lactones

  • Otic macrocyclic lactones 

  • Systemic isoxazolines

Correct answer: Otic mineral oil

Treatment for mites, lice, and related critters has come a long way since the advent of newer products, including macrocyclic lactones and the newer systemic isoxazolines.

Before having effective therapies, people used to use topical mineral oil. However, multiple treatments are needed, and it leaves a gross oily film on the pet. Historically, people used otic solutions made from fipronil, lindane, pyrethrin, or rotenone. Still, these were either ineffective or had high toxicity risks. They are no longer recommended.

Current treatment options available for cats and ear mites include: 

  1. Topical preparations of macrocyclic lactones (milbemycin oxime or ivermectin)
  2. Transdermal systemic options such as selamectin or moxidectin
  3. Topical isoxazolines, which are systemically absorbed
  4. Combination of two different types of methods (a topical monthly and a topical ear treatment)

Always make sure you are using a product labeled for use in cats. 

Advise the owners that the condition is contagious to other animals in the home and, though rare, could be transmissible to humans in the house. Review environmental contamination and cleanup. Consider a topical monthly preventative if the cat will be going outside.

155.

You are concerned that a patient may have signs of hypothyroidism. However, upon reading the literature and various journal articles and textbooks, you have found that while there are two distinct conditions in neonates/foals consistent with hypothyroidism, it isn’t so clear in adults. You are considering testing an adult gelding patient with hair coat abnormalities, hypohidrosis, decreased exercise tolerance and poor performance, and heat intolerance for hypothyroidism. But you want to make sure none of his current medications or other factors will interfere with the thyroid assays and your ability to interpret the results.

All of the following can lower circulating thyroid hormone concentrations in horses (T3, T4, TSH), except:

  • Exercise

  • Phenylbutazone administration

  • Dexamethasone administration

  • Nutrition-feeding restriction

Correct answer: Exercise

Hypothyroidism in equine patients is not well understood. We do know that congenital hypothyroidism manifests in foals with congenital goiters (weak, poor suckle, poor righting reflex, low body temperatures, and tendon abnormalities). And a second condition in the Western U.S., with an unknown etiology, where foals are born with thyroid gland hypoplasia, have increased gestational lengths, bone/tendon abnormalities, flexural limb deformities, and other abnormalities with signs of dysmaturity. It is suspected to be either a dietary deficiency or a toxin ingested during gestation. It is presumed, however, that primary hypothyroidism is rare in horses, unlike humans and dogs. We appreciate secondary hypothyroidism contributing to clinical issues such as laminitis, anhidrosis, obesity, lower fertility rates, and potentially rhabdomyolysis. However, most of this is anecdotal. Some think horses with abnormal thyroid function testing may have other primary underlying diseases such as PPID or equine metabolic syndrome. This is because various states, medications, and other factors can cause euthyroid sick status or negatively affect thyroid testing, making one falsely assume that function is abnormal.

The following have been known to increase thyroid hormones: exercise, cold weather, carbohydrate and protein feeding, and age (higher naturally in foals than adults). While underlying disease states, dexamethasone administration (single dose for five days), phenylbutazone (single dose for up to ten days), stress, and anorexia/nutrition restrictions all decrease thyroid hormone levels.

156.

Which of the following cells does not play a role in the innate cell defense in mammals?

  • Lymphocytes

  • Neutrophils

  • Natural killer cells

  • Macrophage

Correct answer: Lymphocytes

Neutrophils are the key cells in the innate cell defense that respond immediately. They are very effective in fighting bacterial infections due to their phagocytic and chemotactic properties and their amoeboid-like motion, moving by changing their shape, allowing them to enter infected tissue (diapedesis).

Macrophages are mature monocytes that have left the bloodstream and enter tissues. These are the "big eater" cells. They can phagocytize various things, but unlike neutrophils which dominate in the early, acute phase of infection, these tend to dominate in longer-lasting infections. They, too, work by phagocytosis, but when compared to neutrophils, are better self-protected. They are more efficient killers against bacteria than neutrophils. Further, they can remove dead tissue or dead neutrophils; thus, they have a key role in damaged tissue repair.

Natural killer (NK) cells are a subtype of lymphocyte, but in comparison to other lymphocytes, make up part of the innate immune system. A NK cell's job is to attack, not the body's own cells, but abnormal cells such as virus-infected or cancer cells. These abnormal cells contain different phospholipids and proteins in the cell membrane than that of the host's cells.

Lymphocytes, on the other hand, are part of the adaptive immune system, produce antibodies against invaders, and they tend to be activated later in infection, along with macrophages.

157.

An Appaloosa colt yearling has increased accidents, running into things at night or in low light. It acts oddly, cocking his head at times like star-gazing. He is very clumsy and apprehensive when by himself but almost hyperactive when handled. He has bilateral strabismus and a hint of microphthalmia. Besides the subtle changes in his eyes, his overall physical health is 100% normal. You perform a fundic exam which is normal.

You perform an ERG (electroretinography), and you see what pathognomonic changes for what you suspect to be inherited night blindness?

  • There is a negative A-wave that increases with dark adaptation; lacks or decreased scotopic B-wave

  • There is a negative B-wave that increases with dark adaptation and lacks an A-wave.

  • The ERG is normal

  • Both the A and B-waves are negative

Correct answer: There is a negative A-wave that increases with dark adaptation; lacks or decreased scotopic B-wave

Congenital Stationary Night Blindness (CSNB), a sex-linked recessive trait, is notably attributed to the Appaloosa. However, we can also see it less commonly in the Standardbreds, Thoroughbreds, and Paso Finos. Animals show normal daylight vision with behavioral changes (stress, clumsiness, and hyperactivity/unpredictability) at night. It is not progressive blindness, so daytime vision usually remains normal.

Diagnosis is made by history and clinical signs in conjunction with pathognomonic ERG changes, which include "decreased scotopic b-wave amplitude and a large negative, monotonic a-wave." (AAEP) It is thought to arise due to an abnormality associated with the neurotransmission of the middle retina. There is no treatment, and these animals should not be bred. They should not be exercised in low light or after dark. 

158.

A client in the U.S. has several barn cats. They are outdoor only but intermingle with their indoor/outdoor cats and farm animals. You want to ensure the client protects the cats from fleas/ticks and various intestinal parasites. In addition to the client’s full-time job, the client provides pony rides for special-needs children. She needs to ensure that your property is safe and that the kids won’t pick up any infectious diseases if they play in the fields or areas where the cats frequent. As part of your barn cat herd management, you recommend ensuring that the product(s) they choose to use are active against which potentially zoonotic disease? 

  • Toxocara cati

  • Toxoplasma gondii

  • Bartonella species

  • Tapeworms

Correct answer: Toxocara cati

By ensuring the cats are protected against fleas (the vector for transmitting some types of tapeworms and for Bartonella species), you can help to lessen exposure to these organisms. Toxoplasmosis isn’t preventable with our monthly preventatives as it is an environmental contaminant and can be transmitted via infected meat. However, Toxacara cati, the feline roundworm, which is zoonotic, is paramount to prevent when feasible.

Topical products effective against this organism and/or frequent dewormings a few weeks before visits from kids to ensure no active shedding can help lessen the risk of environmental contamination and human exposure. Ensuring proper hand washing hygiene and sanitation stations are nearby and encouraging kids to use them is also important. 

159.

A 13-year-old FS DMH presents with an acute onset of severe right-sided head tilt, circling (though the owners just called it stumbling, walking funny), and vomiting. They were concerned she was having a seizure. She has been overtly healthy with no previous skin issues, stable stage 1 CKD, and a low grade II/VI heart murmur with no evidence of HCM on echo one year prior. She had been eating well until today. On physical exam, she is mentally appropriate, though distracted. You put her on the floor to watch her walk and appreciate that she is circling to the right, and if she falls, then rolls, trying to right herself. She has horizontal nystagmus with the fast phase to the right. What do you expect to find on the otic examination of this patient? 

  • A ruptured tympanic membrane in the right ear

  • An opaque tympanic membrane in the right ear

  • A normal ear canal, as this represents central vestibular disease

  • Superficial aural discharge and opaque tympanic membrane in the left ear

Correct answer: A ruptured or opaque tympanic membrane in the right ear

In cats with peripheral vestibular disease, they will have normal mentation. Inner and middle ear infections are common in older cats with no history of otitis externa and no previous history of ear issues. However, the reason for this is unclear. The tympanum may be fully ruptured or opaque (suggestive of otitis media). Signs of external ear infection (ceruminous or purulent discharge may be present if there is also an external ear infection, but it doesn’t have to be).

With peripheral vestibular disease, signs may be less obvious when the disease is bilateral. When unilateral, the animals will likely have a head tilt toward the side of the disease and they will circle toward that side. They may have strabismus and nystagmus. The nystagmus can be rotary or horizontal (vertical is more commonly associated with central vestibular problems), and the fast phase is to the unaffected side.

Additional signs can include rolling, struggling to get up (which some owners mistake for seizure activity), vomiting, nausea, and cerebellar ataxia. Hearing may be negatively affected or absent on the affected side. Animals with peripheral vestibular disease will retain normal muscle strength and have normal proprioception. If the animal also has otitis media, we can see Horner’s syndrome as well. The disease can occur bilaterally. One ear may have otitis media and the other interna.

Additional causes of peripheral vestibular disease could include any neoplastic lesion near the vestibular apparatus.

An opaque tympanic membrane suggests middle ear disease. If this extends internally, we can see all the signs discussed here. We may see hearing abnormalities, Horner’s syndrome, facial nerve abnormalities (palsy, paralysis), or dry eye.

However, just because there is the presence of inner or middle ear disease doesn’t mean a superficial ear infection has to be present. Checking with cytology is still indicated to ensure this isn’t the case. However, more commonly than dogs, cats can have no otitis externa yet still develop inner and middle ear infections. 

160.

What is the correct order for disinfection protocols in a hospital regarding disease prevention, management, and control? 

  • Remove organic debris, clean with a detergent, rinse with water, dry, apply to disinfect, rinse with water, dry, repeat if warranted

  • Remove organic debris, disinfect, rinse with water, dry, use detergent, clean with water, dry, repeat if needed

  • Rinse with water, clean organic debris, dry, apply detergent, clean with water, apply disinfectant, dry, repeat if needed

  • Clean organic debris, rinse with water, dry, apply detergent, rinse, dry, apply disinfectant, dry, repeat if needed

Correct answer: Remove organic debris, clean with a detergent, rinse with water, dry, apply to disinfect, rinse with water, dry, repeat if warranted

Multiple steps and repeated steps may be needed. The biggest thing to remember is that you must clean before you disinfect. You must remove all organic material or as much as feasible before attempting to clean. At a minimum, cleaning, and disinfection protocols need to incorporate the following:

  • a detergent step
    •   a rinsing step
    •   a drying step
    •   a disinfectant application step followed by additional rinsing and drying

Make sure before applying a disinfectant that the area has properly dried. Many disinfectants will be inactivated or ineffective in the presence of water/moisture.

Again, it bears repeating you cannot properly disinfect until you have thoroughly cleaned.