BCSE 15 Days For Test Day Flashcards

Question

A mature goat presents with drooling, left-sided ptosis, a droopy left ear, and positional nystagmus. The goat is also febrile, lethargic, and circling to the left. Which one of the following choices is the best treatment for the presumptive diagnosis? Ponazuril (PO, 28 days), sulfadiazine with pyrimethamine Thiamine (TID, IV 1st dose, then IM), dexamethasone and supportive care Clarithromycin (PO, BID) and rifampin High dose oxytetracycline or penicillin Specific botulinum antitoxin, NSAIDs, and B-lactam antibiotics

Answer 1

Answer: High dose oxytetracycline or penicillin Treat this likely case of listeriosis with high doses of tetracyclines or penicillin. Isolate the goat and take it off silage, +/- IV fluids. Some of the signs are subtle in this image, but classically look for unilateral ipsilateral signs of brainstem and facial nerve dysfunction -swelling of cheek due to accumulation of food in the buccal space, drooling, ptosis (lowered eyelid), drooping ear, collapsed nostril, flaccid lip. Typically listeriosis presents as encephalitis (depressed, fever) with unilateral limb signs (circling, leaning) and unilateral cranial nerve signs as discussed above. Also can see sporadic ABORTIONS with listeriosis at any time in gestation, though more common in 3rd trimester. Listeria is ZOONOTIC. Highest risk is handling aborted fetus or performing necropsy of septicemic animal. With polioencephalomalacia, think opisthotonos, headpressing, blind, 'star-gazing' (dorso-medial strabismus via thiamine deficiency). Caprine arthritis encephalitis (CAE) presents as a polyarthritis in adults, progressive paresis in kids. **Key Information on Listeriosis in Animals** Definitions • Listeriosis: A bacterial infection caused by Listeria monocytogenes, leading to encephalitis, abortion, septicemia. Causative Agent • Organism: Listeria monocytogenes, a gram-positive, motile, nonspore-forming coccobacillus. Epidemiology • Reservoirs: Soil, GI tracts of mammals, silage. • Transmission: Ingestion of contaminated feed, especially spoiled silage; fecal-oral route. Clinical Findings • Ruminants: Encephalitis, asymmetric brain-stem dysfunction (circling, head tilt, facial paralysis), abortion, septicemia. • Other Animals: Septicemia in monogastric animals, abortion in all domestic animals. Diagnosis • Clinical Signs: Asymmetric neurologic signs, abortion without prior symptoms. • Tests: CSF analysis (increased protein, mild pleocytosis), bacterial culture, PCR, immunofluorescence. Treatment • Antimicrobials: High doses of penicillin G, oxytetracycline, ceftiofur, erythromycin. • Supportive Care: Fluids, electrolytes, corticosteroids. Control and Prevention • Silage Management: Avoid feeding spoiled silage, use acidic silage additives. • Vaccination: Efficacy varies; not always recommended. Zoonotic Risk • Human Infection: Handling of contaminated materials; can cause severe illness in immunocompromised individuals. CGPT: Comprehensive Summary on Polioencephalomalacia (PEM) in Ruminants CGPT: Comprehensive Summary on Caprine Arthritis and Encephalitis (CAE)

Answer 2

Answer: Air trapped in the guttural pouch Guttural pouch tympany is trapping of air in the guttural pouch typically seen in foals. Look for a non-painful fluctuant swelling on one or both sides of the throat. Guttural pouch empyema is a bacterial infection of the guttural pouch. It is most often seen with or following strangles infection. Guttural pouch mycosis is a fungal infection of the guttural pouch. Epistaxis is the most common clinical sign. Fracture of the stylohyoid bone within the guttural pouch can be part of a disorder called temporohyoid osteoarthropathy. Comprehensive Summary on Guttural Pouch Tympany in Horses Definition and Etiology Guttural Pouch Tympany (GPT) is a condition characterized by the distension of one or both guttural pouches with air. It primarily affects young horses from birth to 1.5 years of age and is more common in fillies than in colts. The exact cause is often unknown, but it may involve a congenital defect or inflammation affecting the mucosal flap at the pharyngeal orifice. Pathophysiology • Abnormal Air Accumulation: Dysfunction or malformation of the plica salpingopharyngea creates a one-way valve effect, allowing air to enter the pouch but preventing its escape, leading to tympany. • Potential Secondary Causes: In some cases, upper respiratory tract inflammation might contribute to the dysfunction. Clinical Signs • Characteristic Swelling: Nonpainful, fluctuant swelling in the parotid region (behind the jaw). • Unilateral/Bilateral Tympany: Usually unilateral, but bilateral cases can occur. • Respiratory Signs: Stertorous breathing, nasal discharge, and head carriage extension in severe cases. • Complications: Dysphagia, dyspnea, secondary empyema, and aspiration pneumonia in complicated cases. Diagnosis • Clinical Signs: Based on observable swelling and respiratory signs. • Radiographic Examination: X-rays of the skull to confirm the presence of air in the guttural pouch. • Endoscopy: To confirm diagnosis, rule out other conditions, and distinguish between unilateral and bilateral disease. Treatment 1. Conservative Management: • NSAIDs: Nonsteroidal anti-inflammatory drugs to reduce inflammation. • Antibiotics: Broad-spectrum antimicrobials if secondary infection is suspected. 2. Decompression: • Percutaneous Needle/Catheter: Temporary relief by releasing air via a needle or catheter. • Surgical Intervention: • Fenestration: Creating a window between the affected and normal pouch to allow air escape. • Foley Catheters: Long-term placement to remodel the mucosal flap and prevent air trapping. Prognosis • Good Prognosis: Most cases respond well to treatment, particularly if there are no secondary complications. • Surgical Cases: May require repeated procedures, especially for bilateral tympany.

Answer 3

Answer: Functional thyroid adenoma The most common cause of feline hyperthyroidism is a functional thyroid adenoma (adenomatous hyperplasia). In roughly 70% of cases, both thyroid lobes are affected. Thyroid carcinoma is the primary cause of hyperthyroidism in dogs, but it is rare in cats (1-2% of hyperthyroidism cases). Comprehensive Summary on Hyperthyroidism in Animals for BCSE Test Preparation Definition and Etiology Hyperthyroidism is a condition caused by excessive thyroid hormone production, primarily thyroxine (T4) and triiodothyronine (T3). In cats, it is usually due to thyroid adenomas or adenomatous hyperplasia. Thyroid carcinoma is a rare cause in cats but more common in dogs. Pathophysiology • Excessive Hormone Production: Leads to increased metabolic rate. • Adenomatous Hyperplasia: Most common in cats, leading to bilateral thyroid enlargement. • Thyroid Carcinoma: Common in dogs, causing similar clinical signs. Clinical Signs • Common Signs in Cats: • Hyperactivity, excessive vocalization, weight loss despite good appetite. • Vomiting, polyuria, polydipsia, tachycardia, and possible thyroid nodule. • In Dogs: Often associated with thyroid carcinoma; signs include weight loss, increased appetite, and possible palpable thyroid mass. Diagnosis • Clinical Signs and History: Key to initial suspicion. • Serum Thyroid Hormone Testing: Elevated total T4 or free T4 (fT4) concentrations confirm diagnosis. • Additional Tests: CBC, serum biochemistry, urinalysis to assess overall health and rule out concurrent diseases. Treatment 1. Radioiodine Therapy: Preferred curative treatment; selectively destroys hyperactive thyroid tissue. 2. Antithyroid Medications: • Methimazole: Initial dose of 1.25–2.5 mg/cat every 12 hours, adjusted based on T4 levels. • Carbimazole: Similar to methimazole, converted to methimazole in the body. • Propylthiouracil: Not recommended due to severe side effects. 3. Surgical Thyroidectomy: Option for definitive treatment, especially in cases not suited for radioiodine therapy. 4. Iodine-Deficient Diet: Lifelong dietary management to limit iodine intake and reduce hormone production. Medications • Methimazole: Blocks thyroid hormone synthesis; dose adjustment based on response and side effects. • Carbimazole: Prodrug converted to methimazole; used where methimazole is tolerated. • Beta-Adrenoceptor Blockers (Propranolol, Atenolol): Used to control tachycardia and hypertension but do not affect thyroid hormone levels. Monitoring and Follow-Up • Regular Monitoring: Essential to adjust treatment and monitor for side effects or development of hypothyroidism. • Renal Function: Monitor as hyperthyroidism can mask underlying kidney disease.

Answer 4

Answer: Gently cleanse and lubricate the penis; attempt to replace the penis into the prepuce Paraphimosis is a medical emergency; gently cleanse and lubricate the penis and attempt to replace it into the prepuce. Recognize and Tx quickly to prevent permanent damage to the penile and urethral tissue. Tx goals: Reduce swelling, restore normal blood circulation, and replace the penis back into the prepuce. Use cold compresses or topical hypertonic solutions to reduce swelling. Administer sedation/pain medications as indicated. In case such as this where the dog is presented immediately medical therapy may be successful. However, some cases require incision of the preputial skin to examine the preputial cavity and relieve venous obstruction. https://www.merckvetmanual.com/reproductive-system/reproductive-diseases-of-the-male-small-animal/paraphimosis-in-dogs-and-cats

Answer 5

Answer: One-way valves One-way valves help direct gas flow. Expired gasses pass through a CO2 scavenger canister to remove CO2. STRATEGY HINT: See how the word "valve" occurs in 3 choices? Chances are that the correct answer contains this word.

Answer 6

Answer: 1.5 x MAC For most anesthetics and most patients, utilize a dial setting of approximately 1.5 x MAC as a guideline to help the patient reach a surgical plane of anesthesia. Adjust as needed based on how the patient is responding. The minimum alveolar concentration (MAC) of an anesthetic agent is the percent concentration at which 50% of patients would not respond to surgical stimulation. 1.5 x MAC is a guideline only: assess the patient and use the appropriate MAC for the situation depending on the patient's condition and pre-operative medications. It is critical to closely monitor patients under anesthesia and dose the anesthetic "to effect."

Answer 7

Answer: Cornual. Typically a cornual nerve block (branch of the trigeminal- midway between eye and base of horn, just below temporal line) will anesthetize most cows for dehorning. If that is not enough, do a ring block around the base of the horn. In contrast, for goats you need to block BOTH the cornual nerve (caudal ridge, root of zygomatic arch of frontal bone) and infratrochlear nerve (dorsomedial to eye, close to edge of bony orbit) before dehorning. This is because the goat horns lie more rostral on the skull and closer to the bony orbits than the horns of a cow.

Answer 8

Answer: Open and stretch the incisions, systemic NSAIDs, increase exercise. This horse has routine postoperative swelling and the appropriate course of therapy is to open and stretch the incisions using sterile technique, administer systemic NSAIDs, and increase exercise to promote drainage. Scrotal and preputial swelling and edema that peak at day 3-4 and resolve by day 10-12 are the most common complication following castration. In the absence of fever or significant pain/reluctance to move or urinate, the therapy noted above can be performed on the farm. Between 20-38% of geldings experience a complication post-operatively. The 2nd-most common is hemorrhage. The most serious is eventration of intestine through the incision. Additional complications include peritonitis, penile damage, and hydrocele (occurs months to years later). Click here for an excellent article on the complications of castration, courtesy of Dr. Liberty Getman and the AAEP. Intestinal Eventration after castration refers to the prolapse of intestinal contents through the surgical site. This condition is an emergency and is more likely in draft breeds, Tennessee Walking Horses, American Saddlebreds, Standardbreds, and adult stallions due to their larger inguinal rings. Pathophysiology • Post-Surgical Complication: Typically occurs within 4 hours to 6 days post-castration. • Herniation Mechanism: Intestinal loops or omentum protrude through the inguinal canal. Clinical Signs • Visible Prolapse: Intestine or omentum hanging from the surgical site. • Acute Pain: Due to stretching and possible strangulation of the intestine. Diagnosis • Physical Examination: Identification of protruding structures. • Transrectal Palpation: To assess the extent of the prolapse. Treatment 1. Omental Evisceration: • Restraint and Sedation: Ensures the horse remains calm. • Emasculation: Removal of the omentum if involved. • Scrotal Packing and Closure: Sterile gauze and suturing. • Antibiotics and NSAIDs: Prevent infection and manage pain. 2. Intestinal Evisceration: • General Anesthesia: For safe examination and treatment. • Intestinal Lavage: Clean and assess the intestine. • Reduction or Surgical Referral: Depending on the damage, intestine may be reduced or referred for surgical resection. Medications • Broad-Spectrum Antibiotics: To prevent or treat infections. • NSAIDs: For pain and inflammation control. • Tetanus Prophylaxis: To prevent tetanus infection.

Answer 9

Answer: Abomasum The abomasum takes up more 50% of the stomach and foregut system in the newborn calf. As the calf is weaned from an all milk diet to roughage, the abomasum shrinks, and the rumenoreticulum system becomes active.

Answer 10

Answer: Damage to cervical sympathetic innervation of the eye. Horner syndrome secondary to brachial plexus avulsion occurs due to damage to the cervical sympathetic innervation to the eye, which originates at T1 - T2 and courses cranially in the sympathetic trunk of the cervical spinal cord. Clinical signs vary depending on lesion severity. Complete spinal nerve avulsion causes flaccid paralysis of the limb, dropped elbow, knuckling, and loss of sensation distal to the elbow. Look also for ipsilateral loss of the cutaneous trunci reflex and ipsilateral Horner syndrome. Tx: Consider limb amputation for complete brachial plexus avulsion to prevent ongoing trauma to the distal limb. In some cases, in which only inflammation of the plexus occurred, clinical signs improve with time. Comprehensive Summary on Intestinal Eventration After Castration for BCSE Test Preparation Definition and Etiology Intestinal Eventration after castration refers to the prolapse of intestinal contents through the surgical site. This condition is an emergency and is more likely in draft breeds, Tennessee Walking Horses, American Saddlebreds, Standardbreds, and adult stallions due to their larger inguinal rings. Pathophysiology • Post-Surgical Complication: Typically occurs within 4 hours to 6 days post-castration. • Herniation Mechanism: Intestinal loops or omentum protrude through the inguinal canal. Clinical Signs • Visible Prolapse: Intestine or omentum hanging from the surgical site. • Acute Pain: Due to stretching and possible strangulation of the intestine. Diagnosis • Physical Examination: Identification of protruding structures. • Transrectal Palpation: To assess the extent of the prolapse. Treatment 1. Omental Evisceration: • Restraint and Sedation: Ensures the horse remains calm. • Emasculation: Removal of the omentum if involved. • Scrotal Packing and Closure: Sterile gauze and suturing. • Antibiotics and NSAIDs: Prevent infection and manage pain. 2. Intestinal Evisceration: • General Anesthesia: For safe examination and treatment. • Intestinal Lavage: Clean and assess the intestine. • Reduction or Surgical Referral: Depending on the damage, intestine may be reduced or referred for surgical resection. Medications • Broad-Spectrum Antibiotics: To prevent or treat infections. • NSAIDs: For pain and inflammation control. • Tetanus Prophylaxis: To prevent tetanus infection.

Answer 11

Answer: Long and lateral digital extensor tendons The long and lateral digital extensor tendons have likely been disrupted. Generally there is minimal affect of extensor tendon injuries on gait; however, in acute phases or with severe injuries may see inability to protract the limb and intermittent knuckling over on the fetlock. Locomotion typically returns to normal after healing of the wound occurs. In some cases trauma to the lateral digital extensor tendon may be associated with the development of stringhalt (exaggerated flexion of the limb at a walk). Comprehensive Summary on Long and Lateral Digital Extensor Tendons for BCSE Test Preparation Definition and Function • Long Digital Extensor Tendon (LDET): Extends the digits and stabilizes the stifle joint. • Lateral Digital Extensor Tendon (LDE): Assists in extending the digits and stabilizing the lower limb. Injury and Pathophysiology • Injuries: Commonly occur due to trauma, such as lacerations or overstretching. • Symptoms: Inability to extend the digit properly, resulting in a dropped fetlock or knuckling over of the limb. Clinical Signs • Lameness: Varying degrees depending on the severity of the injury. • Swelling and Heat: Around the affected tendon. Diagnosis • Physical Examination: Observation of the limb’s position and movement. • Ultrasound: To assess the extent of the damage to the tendons. • Radiography: To rule out concurrent fractures. Treatment 1. Initial Management: • Wound Care: Clean and debride any open wounds. • Stabilization: Bandaging and splinting to prevent further damage. 2. Medical Treatment: • NSAIDs: For pain relief and to reduce inflammation. • Antibiotics: If there’s an open wound or risk of infection. 3. Surgical Intervention: • Repair: Suturing the tendon if necessary. • Rehabilitation: Gradual reintroduction to activity with controlled exercise. Prognosis • Depends on Severity: Early intervention and appropriate management significantly improve outcomes.

Answer 12

Answer: Cranial and caudal superficial epigastric Ligate the cranial and caudal superficial epigastric arteries, the primary blood supply to the mammary glands, during a unilateral mastectomy. For the caudal chain of glands, ligate the caudal superficial epigastric arteries emerging from the external pudendal artery near the inguinal canal. For the cranial chain, ligate the cranial superficial epigastric artery, arising from the internal pudendal artery. The lateral thoracic artery from the axillary artery also supplies the cranial-most mammary gland. Cats usually have four pairs of glands while dogs have five. Mammary gland neoplasia is most common in older intact females; more common in dogs than in cats, but 90% of feline tumors are malignant vs. 45% in dogs.

Answer 13

Answer: Caudal tail fold. Use the intradermal caudal (tail) fold test (CFT) as a preliminary screening test for bovine tuberculosis. The confirmatory test is the comparative cervical test (CCT), done on the neck skin only AFTER a positive CFT. TB is an granulomatous disease caused by Mycobacterium spp. that can cause acute or chronic, debilitating Dz. It is of huge public health and financial concern because it is zoonotic and there are multidrug resistant strains emerging. Test and slaughter is the most common method of handling Dz in North America. The tail fold test is used for diagnosing tuberculosis in cattle, particularly in countries with high TB prevalence. It involves the intradermal injection of a small amount of tuberculin into the skin at the base of the tail. After 72 hours, the injection site is examined for a delayed-type hypersensitivity reaction, such as swelling or thickening of the skin. A positive reaction indicates possible TB infection, necessitating further diagnostic testing and potential culling to prevent disease spread.

Answer 14

Answer: Inability to extrude penis due to constrictions of the preputial orifice Phimosis is an inability to extrude the penis due to constriction at the preputial orifice. It may be congenital (German shepherd, golden retriever) or acquired (trauma, post-surgical). In severe cases urine accumulation within the prepuce results in urine dribbling and balanoposthitis. Tx with surgery to enlarge the preputial opening. Paraphimosis is the inability to retract the penis into the preputial cavity. Balanoposthitis is inflammation of both the penile (balanitis) and preputial (posthitis) mucosa. Priapism is a persistent abnormal erection of the penis in the absence of sexual stimulation, generally accompanied by pain and sensitivity to touch. CGPT: Phimosis in Dogs and Cats CGPT Praphimosis in Dogs and Cats https://www.merckvetmanual.com/reproductive-system/reproductive-diseases-of-the-male-small-animal/balanoposthitis-in-dogs-and-cats

Answer 15

Answer: T12-T13 The dog's lesion is most likely at T12-13. The loss of the cutaneous trunci reflex occurs about 1-4 (usually 2) spinal cord segments CAUDAL to the actual lesion. Another way to think of this is that the actual spinal lesion is generally 2 spinal cord segments in FRONT (cranial) to the line where the cutaneous trunci reflex STOPS. Dorsal cutaneous branches do not exit the spinal cord at around L3-4 so the the loss of the reflex on the left at L3 is normal. The lateral thoracic nerve, which innervates the ipsilateral cutaneous trunci muscle, exits the spinal cord at C7-1. So with a brachial plexus avulsion you may see an ipsilateral loss of the cutaneous trunci twitching while lightly pinching on the skin on the ipsilateral side, however the contralateral side will twitch! Cutaneous Trunci Reflex in Veterinary Neurology Definition The cutaneous trunci reflex is a test to assess the integrity of the spinal cord, particularly the thoracolumbar region. Procedure • Method: Gently squeeze the skin lateral to the spine with a hemostat, starting from the lumbosacral region and moving cranially. • Normal Response: Bilateral contraction of the cutaneous trunci muscles, resulting in a skin twitch over the thorax and abdomen. Clinical Significance • Lesion Localization: Absence of reflex caudal to a lesion, while the reflex remains normal cranial to it. • LMN Involvement: Indicates involvement of the lateral thoracic nerve (C8-T2 spinal segments). Application • Use: Useful for diagnosing spinal cord injuries and differentiating them from peripheral nerve injuries.

Answer 16

Answer: Help blood clot These are thrombocytes (platelets), which help blood clot. Formation of the platelet plug is the first step in hemostasis ("primary hemostasis"). Platelets are also critical in formation of the fibrin plug ("secondary hemostasis"). Follow these links to see clumps of bovine platelets and scattered feline platelets (and rouleaux formation - i.e., stacked up erythrocytes). Res: McCurnin & Bassert, Clin Textbook for Vet Technicians, 9th ed. p. 384. Image courtesy of Dr. Seth Chapman. Platelets in Animals - Key Points for Veterinary Professionals Definition and Function • Platelets: Cell fragments derived from megakaryocytes in the bone marrow. • Role: Form initial hemostatic plug during hemorrhage, source of phospholipid for coagulation factors to form fibrin clots. Physiopathology • Production: Influenced by thrombopoietin, involves megakaryocyte membrane invagination and cytoplasmic fragmentation. • Structure: Dense granules (ATP, ADP, calcium), serotonin, lysosomes, glycogen, mitochondria, intracellular canalicular system. Hemostasis Process 1. Vessel Damage: Exposes collagen and tissue factor. 2. Platelet Adhesion: Via von Willebrand factor. 3. Shape Change: Release of ADP. 4. Aggregation: Forms primary platelet plug. 5. Fibrin Clot Formation: Consolidated by platelet contractile proteins. Disorders • Thrombocytopenia: Low platelet count (<30,000/μL), increased hemorrhage risk. • Causes: Consumption (hemorrhage, DIC), destruction (immune-mediated), sequestration (hypersplenism). • Symptoms: Petechiae, ecchymoses, mucosal bleeding. • Thrombocytosis: Rare, often idiopathic or related to marrow disease. • Thrombocytopathies: Normal count, impaired function (e.g., von Willebrand disease, aspirin-induced thromboxane inhibition). Medications and Management • Treatment for Thrombocytopenia: Address underlying cause, immunosuppressants for immune-mediated cases. • Thrombocytosis: Address primary condition, if identified. • Platelet Function Disorders: Avoid causative drugs, supportive care.

Answer 17

Answer: 33% Normal hemoglobin concentration (Hb, g/dl) is about one-third (33%) of the packed cell volume (PCV) in normal dogs, cats, horses, cows, sheep, goats, and pigs. So, in a cat with a PCV of 30%, the Hb will be roughly 10 g/dl. And in a dog with a PCV of 45%, the Hb will be roughly 15 g/dl. Remember, Hb is a protein in erythrocytes that helps to transport oxygen. Follow this link to see Small and large Animal reference values. One exception to the 33% rule is South American camelids, whose hemoglobin is 40%-45% of the PCV, presumably an adaptation to high altitude, lower oxygen environments. CGPT: Hemoglobin Test in Veterinary Hematology https://www.merckvetmanual.com/special-subjects/reference-guides

Answer 18

Answer: Macrophage Osteoclasts are macrophages that are associated with bone. When circulating monocytes become associated with a tissue they are called resident or tissue macrophages and are often given a new name. Some of the other key tissue-associated resident macrophages are: Kupffer cells, associated with the liver. Histiocytes, associated with connective tissue. Microglial cells, associated with nervous tissue. Pulmonary alveolar macrophages of the lungs. Sinusoidal lining cells of the spleen.

Answer 19

Answer: Immune - mediated thrombocytopenia This is immune-mediated thrombocytopenia (a.k.a. ITP), the most common cause of profound thrombocytopenia in dogs. With ITP look for a platelet count <30,000/L (often <10,000/uL) and normal coagulation parameters. Most commonly idiopathic/primary, but a Dx of exclusion so rule out other causes of thrombocytopenia - e.g., vector-borne Dz, neoplasia. Tx: Immunosuppression (e.g., prednisone, +/- cyclosporine, or other immunosuppressants). Consider one dose of IV vincristine to stimulate platelet release from the bone marrow. Dogs may require blood transfusion if significant blood loss. Note: blood transfusion does not replace circulating platelets. Immune-Mediated Thrombocytopenia (ITP) in Animals Definition • ITP: Immune-mediated destruction of platelets or marrow megakaryocytes. • Also Known As: Idiopathic thrombocytopenic purpura. Causes and Risk Factors • Idiopathic: No identifiable underlying cause. • Risk Factors: Middle-aged, spayed female dogs, especially Cocker Spaniels. Pathophysiology • Mechanism: Immune system targets and destroys platelets or megakaryocytes. • Autoantibodies: Directed against platelet surface antigens. Clinical Signs • Bleeding: Petechiae, ecchymoses, melena, epistaxis. • Severe Thrombocytopenia: Platelet counts <30,000/μL, often <10,000/μL. Diagnosis • Exclusion: Rule out other causes of thrombocytopenia. • Tests: Bone marrow aspirate (rarely needed), platelet count, clinical signs. Treatment • Corticosteroids: High-dose initial treatment, tapered gradually. • Vincristine: 0.01-0.02 mg/kg IV, shortens recovery time. • Transfusion: Fresh whole blood for severe anemia. • Splenectomy: For recurrent cases. • Monitoring: Regular platelet count checks during steroid tapering. • Avoid: Drugs interfering with coagulation.

Answer 20

Answer: specific gravity Specific gravity compares the density of a substance to that of water. Substances with a specific gravity less than water will float. The fecal flotation test relies on the fact that the specific gravity of the flotation solution used is greater than that of the parasite eggs or oocysts. The eggs or oocysts will float and can be found more easily. A fecal sample is mixed in a vial with a concentrated solution of a salt or sugar in water. The vial is covered with a coverslip and then left undisturbed. The eggs will float to the top and are examined using the low power objective of a microscope.

Answer 21

Answer: Rectal stricture. Salmonella typhimurium is associated with rectal strictures in growing pigs. Caused by an ulcerative proctitis that damages rectal tissue. Can see large numbers of cases. Can see sporadic rectal strictures as a sequelae to rectal prolapse. Intestinal spirochetosis is a post-weaning diarrhea seen in the ABSENCE of Brachyspira (Serpulina) hyodysenteriae (swine dysentery), but similar in presentation to it. This syndrome is being recognized more frequently worldwide. Refs: Ogilve, LA Int Med, pp. 80-4. Link: Rectal Strictures in Pigs https://www.merckvetmanual.com/digestive-system/intestinal-diseases-in-pigs/rectal-strictures-in-pigs Link: Rectal Prolapse in Animals https://www.merckvetmanual.com/digestive-system/diseases-of-the-rectum-and-anus/rectal-prolapse-in-animals?redirectid=31728 Link: Intestinal Spirochetosis in Pigs https://www.merckvetmanual.com/digestive-system/intestinal-diseases-in-pigs/intestinal-spirochetosis-in-pigs Link: Swine Dysentery https://www.merckvetmanual.com/digestive-system/intestinal-diseases-in-pigs/swine-dysentery Rectal Strictures in Pigs - Detailed Veterinary Summary Etiology and Pathogenesis • Causative Agent: Salmonella enterica serotype Typhimurium • Pathogenesis: Fibrosis due to persistent ischemia from ulcerative proctitis Clinical Findings • Symptoms: Bloating, emaciation, history of severe diarrhea • Lesions: Narrowed rectal canal, annular fibrotic ulcers, grossly distended colon filled with gas and green feces Diagnosis • Physical Examination: Resistance to passing index finger into rectum • Postmortem Examination: Confirm distended colon and narrowed rectal canal Treatment and Control • Management: Good housing, sanitation, all-in/all-out system • Surgery: Not economically feasible Prevention • Control of Diarrhea: Early diagnosis and treatment essential Key Points • Strictures result from trauma or infections affecting rectal blood supply • Effective management and sanitation are crucial • Diagnosis involves physical and postmortem examination

Answer 22

A young horse presents with fever, nasal discharge, and mandibular lymphadenopathy. The horse is isolated from the rest of the herd; a sample of the nasal discharge is PCR positive for Streptococcus equi sbsp. equi. You advise the barn manager to check the temperature twice daily on the other horses. Two days later he calls because one of the other horses has spiked a fever. Which one of the following choices is the best recommendation for this new horse with a fever? Isolate this horse immediately Vaccinate this horse against Strep. equisbsp. equi Start on rifampin orally twice a day Apply cold packs to submandibular lymph nodes Call back if it spikes a fever again

Answer 23

Answer: Mycoplasma hyopneumoniae Mycoplasma hyopneumoniae causes enzootic pneumonia in swine. It is common to see a secondary infection on top of a smoldering mycoplasmal cough with Pasteurella multocida. Refs: Jackson and Cockcroft, Handbook of Pig Medicine, 1st ed. pp. 71-4. https://www.merckvetmanual.com/respiratory-system/respiratory-diseases-of-pigs/mycoplasmal-pneumonia-in-pigs Mycoplasmal Pneumonia in Pigs - Comprehensive Information for BCSE Test Definitions and Causative Agents: • Mycoplasmal Pneumonia: Chronic respiratory disease caused by Mycoplasma hyopneumoniae. • Causative Agents: Mycoplasma hyopneumoniae, often complicated by other mycoplasmas, bacteria, and viruses. Epidemiology: • Transmission: Aerosol, direct contact, from dam to piglets. • Age Susceptibility: Pigs of all ages, highest prevalence in pigs 3-5 months old. Clinical Findings: • Signs: Persistent dry cough, reduced growth rate, sporadic severe pneumonia. • Lesions: Gray or purple, consolidated lung areas, primarily in apical and cardiac lobes, histological lymphoid hyperplasia. Diagnosis: • Methods: Clinical signs, histopathology, PCR, serologic tests. • Samples: Tracheal, laryngeal, bronchial swabs, lung tissue. Treatment: • Antibiotics: Effective against Mycoplasma spp (e.g., tetracyclines, macrolides). • Supportive Care: Improved ventilation, reduced stress. Control: • Vaccination: Reduces clinical signs, does not prevent infection. • Management: All-in/all-out practices, gilt acclimation.

Answer 24

Answer: White-tailed deer The normal host of P. tenuis is the white-tailed deer (who do not develop clinical signs). Camelids and small ruminants are aberrant hosts. It is a common disease in camelids, causing high morbidity and mortality. The larvae of P. tenuis migrate through the spinal cord leading to neurological deficits such as ataxia, paralysis, and stiffness. Signs typically begin caudally and progress cranially. Disease progression is variable and can last days to years. Treatment includes deworming, anti-inflammatories, and supportive care. Prognosis depends on the severity and duration of disease.

Answer 25

Answer: Trematode eggs are too heavy to float. The fecal flotation technique relies on eggs being less dense than the float solution used. Most trematode eggs are too dense to float so sedimentation procedures are used to identify trematode eggs. Trematodes are flukes, such as the lung flukes of small animals, Paragonimus westermani and P. kellicotti. Link: Parasitology. https://www.merckvetmanual.com/clinical-pathology-and-procedures/diagnostic-procedures-for-the-private-practice-laboratory/parasitology

Answer 26

Answer: Respiratory disease, limb edema, abortion Equine viral arteritis (EVA) is a contagious viral disease that causes fever, limb edema, abortions, conjunctivitis, and respiratory disease. Stallions can be silent carriers of the disease and transmit it during breeding. There is a vaccine available that can be used during outbreaks except in pregnant mares and young foals. Equine Viral Arteritis https://www.merckvetmanual.com/generalized-conditions/equine-viral-arteritis/equine-viral-arteritis?mredirectid=842 Comprehensive Information on Equine Viral Arteritis for BCSE Test 1. Definitions: • Equine Viral Arteritis (EVA): A contagious viral disease of equids caused by Equine Arteritis Virus (EAV). 2. Causative Agents: • Equine Arteritis Virus (EAV): A small, enveloped, positive-sense, single-stranded RNA virus of the family Arteriviridae. 3. Pathophysiology: • Transmission: Direct contact with respiratory secretions, venereal transmission, and indirectly via fomites. • Infection Mechanism: EAV infects macrophages and endothelial cells, causing widespread vasculitis. It can also cause abortion by infecting the placenta. 4. Clinical Signs: • Respiratory: Fever, nasal discharge, conjunctivitis, and limb edema. • Reproductive: Abortions, usually in the late stages of pregnancy. • Neurologic: Ataxia and encephalitis in severe cases. • Other: Swelling of the limbs and prepuce, subfertility in stallions. 5. Diagnosis: • Laboratory Tests: Virus isolation, RT-PCR, serology, and immunohistochemistry. • Sample Collection: Nasopharyngeal swabs, blood, and tissues from aborted fetuses. 6. Treatment: • Supportive Care: Antipyretics, anti-inflammatory drugs, and diuretics. • Symptomatic Treatment: Reduces fever and swelling. 7. Prevention and Control: • Vaccination: Modified-live vaccines in North America and inactivated vaccines in Europe. • Biosecurity Measures: Isolation of infected animals, disinfection of equipment, and management of breeding programs. 8. Medications: • NSAIDs: Used for reducing fever and inflammation. • Examples: Flunixin meglumine. • Diuretics: To manage edema. • Examples: Furosemide. Summary of Relevant Information: • Causative Agents: Equine Arteritis Virus (EAV). • Symptoms: Fever, nasal discharge, conjunctivitis, limb edema, abortions. • Clinical Changes: Vasculitis, endothelial damage, placental infection. • Assessment: Virus isolation, RT-PCR, serology. • Treatment: Supportive care, antipyretics, diuretics. • Medications: NSAIDs, diuretics.

Answer 27

Answer: Toxoplasma gondii. Toxoplasma gondii is the agent of toxoplasmosis, which causes birth defects in a developing fetus if a mother is infected for the first time in her life while pregnant. It is a zoonotic disease with part of its life cycle in cats. If you are pregnant and you handle cats or clean litter boxes, your developing baby could be at risk if you become infected. If you were already exposed and had antibodies to toxo prior to pregnancy, then the baby is generally protected by maternal immunity. However, unless you get a blood test you will not know, so better to be safe and avoid the risk. Some doctors in the U.S. offer testing. Link: Toxoplasmosis in Animals https://www.merckvetmanual.com/generalized-conditions/toxoplasmosis/toxoplasmosis-in-animals?autoredirectid=14229 Comprehensive Summary on Toxoplasmosis in Animals for BCSE Test Preparation Definition and Etiology: Toxoplasmosis is a zoonotic infection caused by Toxoplasma gondii, an apicomplexan protozoan. It infects all warm-blooded animals, including humans. Cats are the only definitive hosts, shedding oocysts in their feces. Transmission • Ingestion: of sporulated oocysts from contaminated environment or tissue cysts in undercooked meat. • Vertical Transmission: Transplacental transfer from mother to fetus. Pathophysiology Stages of Infection • Tachyzoites: Rapidly multiplying form causing tissue damage. • Bradyzoites: Slow division form in tissue cysts. • Sporozoites: Infectious form in mature oocysts. • Replication: After ingestion, the parasite invades intestinal epithelium, replicates, and disseminates via blood and lymph, causing tissue necrosis. Clinical Findings • General Signs: Often asymptomatic in immunocompetent hosts. • Acute Infection: Fever, diarrhea, cough, dyspnea, icterus, seizures, and death in young or immunocompromised animals. • Reproductive Issues: Abortion, stillbirth in sheep, goats, and pigs. • Chronic Infection: Subclinical with bradyzoites in tissue cysts. Diagnosis • Serologic Testing: Indirect hemagglutination, ELISA, and other serological assays to detect IgM and IgG antibodies. • Histology and PCR: Identification of tachyzoites or bradyzoites in tissues; PCR for definitive diagnosis. Treatment • Anticoccidial Drugs: Sulfadiazine (15–25 mg/kg PO every 12 hours) and pyrimethamine (0.44 mg/kg PO every 12 hours) for 4 weeks. • Combination Therapy: Trimethoprim-sulfamethoxazole (15 mg/kg PO every 12 hours) for 4 weeks. • Clindamycin: Preferred treatment for dogs and cats (10–12.5 mg/kg PO for dogs, 25–50 mg/kg PO for cats every 12 hours for 3-4 weeks). • Other Options: Diaminodiphenylsulfone, atovaquone, spiramycin, toltrazuril, ponazuril, and diclazuril for acute infections and to reduce oocyst shedding in cats. Prevention and Zoonotic Risk • Hygiene: Wash hands thoroughly after handling raw meat or contaminated objects. Clean and disinfect surfaces. • Food Safety: Cook meat to 67°C (152.6°F), avoid raw or undercooked meat, and ensure good kitchen hygiene. • Pet Care: Feed cats commercially prepared food, clean litter boxes daily, and avoid exposure of pregnant women to cat feces.

Answer 28

Answer: Less than 5% Many cows have titers to bovine leukosis virus (BLV) but less than 5% develop lymphosarcoma. Lymphosarcoma is most common in cows 2â6 years old. Tumors can occur in the lymph nodes and tissue almost anywhere in the body. Clinical signs are dependent on tumor location. There is no treatment. Risk is minimized by preventing the transfer of blood (and therefore infected lymphocytes) between cows. Link: Bovine Leukosis https://www.merckvetmanual.com/generalized-conditions/bovine-leukosis/bovine-leukosis?autoredirectid=20435 Bovine Leukosis: Comprehensive Information for BCSE Test Definition • Bovine Leukosis (Bovine Lymphosarcoma): A cancerous disease caused by Bovine Leukemia Virus (BLV), an oncogenic retrovirus. Etiology and Transmission • Causative Agent: Bovine Leukemia Virus (BLV), a C-type oncogenic retrovirus. • Transmission: Primarily horizontal through blood transfer (e.g., contaminated needles, dehorning tools), and rarely vertical (transplacental or via colostrum). Epidemiology • Prevalence: High in US dairy herds (~46.5%) and lower in beef herds (~10.3%). Pathogenesis • Infection Outcomes: • Asymptomatic: Most animals show no signs. • Persistent Lymphocytosis: ~29% develop this benign condition. • Lymphosarcoma: <5% develop cancerous tumors. Clinical Findings • Juvenile Lymphosarcoma: Weight loss, fever, dyspnea, bloat, and posterior paresis. • Thymic Lymphosarcoma: Cervical swelling, dyspnea, bloat, jugular distention, tachycardia. • Cutaneous Lymphosarcoma: Cutaneous plaques, enlarged lymph nodes. Diagnosis • Serology: ELISA and PCR for BLV detection. • Cytology/Histology: Biopsy for diagnosing lymphosarcoma. Treatment and Control • No Treatment: No effective treatment; symptomatic care with corticosteroids. • Control Measures: Testing and culling infected animals, disinfection of equipment, using single-use needles. Prevention • Blood Precautions: Avoiding exposure to blood from infected animals. • Colostrum Management: Using colostrum from seronegative cows. • Farm Practices: Cleaning equipment and facilities, controlling flies. Zoonotic Risk • Human Risk: Potential, but not well-established, zoonotic risk through ingestion of unpasteurized dairy products.

Answer 29

Answer: Poliencephalomalacia This is most consistent with polioencephalomalacia, which can affect all ruminants sporadically or occasionally in herd outbreaks. Remember cortical blindness (i.e., no menace, positive PLR bilaterally) in a ruminant is highly suggestive of polioencephalomalacia. The signs seen with polioencephalomalacia are due to a disruption in cerebral energy metabolism, which causes swelling and necrosis of neurons within the central nervous system. Can be due to thiamine deficiency, sodium/lead/sulfur toxicosis, or water deprivation. Dx usually based on clinical signs and positive response to thiamine administration. Listeriosis may cause similar signs of disorientation/recumbency, but usually also unilateral cranial nerve deficits (e.g., head tilt, ear droop) and continuous salivation and food impacted in the cheek of the affected side. Thrombotic meningoencephalitis (TME) caused by Histophilus somni (formerly Haemophilus somnus) is a common cattle disease in North America which may present with only depression, or sudden death in multiple animals. Histophilosis it is NOT common in sheep though it can occur. Click here to see a report on Histophilus somni in bighorn sheep. Polioencephalomalacia in Ruminants - Comprehensive Study Guide Definition • Polioencephalomalacia (PEM): A neurologic disease in ruminants, characterized by cerebrocortical necrosis. Causative Agents • Primary Causes: Thiamine deficiency and high sulfur intake. • Other Causes: Acute lead poisoning, sodium toxicosis, water deprivation, and toxic plants containing thiaminase. Pathophysiology • Thiamine Deficiency: Thiamine is essential for glucose metabolism in the brain. Deficiency leads to impaired glucose metabolism, energy depletion, and neuronal necrosis. • High Sulfur Intake: Sulfur is reduced to hydrogen sulfide (H2S) in the rumen, which interferes with cellular energy metabolism, particularly in the CNS. Clinical Signs • Acute Form: Blindness, recumbency, seizures, coma, high mortality. • Subacute Form: Separation from group, incoordination, cortical blindness, head pressing, opisthotonos, recumbency, seizures, potentially recovery with minor neurologic impairment. Lesions • Gross Lesions: Brain swelling, gyral flattening, cerebellar coning, yellowish discoloration of cortical tissue, autofluorescent necrotic bands. • Microscopic Lesions: Necrosis of cerebrocortical neurons, cortical spongiosis, vascular hypertrophy and hyperplasia, cavitation of cortical tissue. Diagnosis • Clinical Signs: Blindness, head pressing, seizures. • Necropsy: Autofluorescent bands in the cerebral cortex under UV light. • Histology: Characteristic neuronal necrosis and cavitation. • Differential Diagnoses: Lead poisoning, sodium toxicosis, histophilosis, rabies, vitamin A deficiency, pregnancy toxemia, clostridial enterotoxemia, listeriosis. Treatment • Thiamine Administration: 10 mg/kg IV initially, then IM for 3-5 days. • Supportive Therapy: Dexamethasone or mannitol for cerebral edema, symptomatic therapy for seizures. • Response to Treatment: Improvement usually seen within 24 hours; continued treatment for ≥3 days if no initial response. Prevention • Dietary Management: Thiamine supplementation (3-10 mg/kg feed). • Sulfur Management: Monitor and control sulfur intake from water and feed, especially during hot weather.

Answer 30

Answer: Penicillin is the antibiotic of choice for the treatment of tetanus in ruminants. Additional treatments include tetanus antitoxin, sedation and/or muscle relaxation, and supportive care in a dark, minimally stimulating environment. Penicillin used to be the Tx of choice for tetanus in all species. However, it may have anti-GABA and proconvulsant activities (not ideal in an animal with tetanus!). So, when available, metronidazole is now the Tx of choice HOWEVER it is not legal to use in food animals in North America. Tetanus may occur sporadically within a herd or there can be larger outbreaks following surgical procedures (ear tagging, castration, tail docking (sheep)) or use of contaminated vaccines or injectable dewormers, all of which create an anaerobic environment in the tissues thay may allow spores of Clostridium tetani to release toxin. The neurotoxin (tetanospasmin) blocks the inhibitory function of the interneurons of the spinal cord. Lack of inhibitory muscle tone leads to a stiff gait which progresses to stiffness of the head, neck, extremities and tail. Although animals may recover, death from respiratory paralysis is common. Link: Tetanus in Animals https://www.merckvetmanual.com/generalized-conditions/clostridial-diseases/tetanus-in-animals http://www.farad.org/prohibited-and-restricted-drugs.html Tetanus in Animals - Comprehensive Information for BCSE Test Definitions and Causative Agent: • Tetanus (Lockjaw): A neurological disease caused by the neurotoxin produced by Clostridium tetani, an anaerobic bacterium found in soil and intestines. • Transmission: Introduced through deep puncture wounds, docking, castration, and sometimes through minor or healed wounds. Pathogenesis: • Neurotoxin Mechanism: Inhibits inhibitory neurotransmitters by cleaving synaptobrevin, causing muscle spasms, rigidity, and respiratory failure. • Nerve Pathways: Toxin travels retrograde along motor nerves to the CNS, causing ascending and descending tetanus. Clinical Findings: • Symptoms: Localized stiffness, generalized stiffness, tonic spasms, hyperesthesia, difficulty in prehension and mastication (lockjaw), respiratory failure, cardiac arrhythmias, opisthotonos, “sawhorse” stance in horses. • Incubation Period: Typically 10-14 days. • Species Differences: Horses, lambs, and humans are highly susceptible; dogs and cats are relatively resistant. Diagnosis: • Methods: Clinical signs, recent trauma history, detection of toxin in serum, PCR assay on wound material, gram-stained smears, and anaerobic culture. Treatment and Control: • Medications: • Tetanus Antitoxin: 300,000 IU IV every 12 hours for horses, caution in dogs and cats due to anaphylaxis risk. • Antibiotics: Penicillin or broad-spectrum antimicrobials. • Muscle Relaxants: Curariform agents, tranquilizers, barbiturates, diazepam. • Supportive Care: Wound cleaning, darkened environment, high feeding devices, slings for support. • Vaccination: Tetanus toxoid for active immunization; booster shots for previously immunized animals; vaccination of mares and foals in high-risk areas.

Answer 31

Answer: Fasciola hepatica Lymnaeid snails are the intermediate hosts for trematode flukes like Fasciola hepatica and Fascioloides magna. Link: Fasciola hepatica in Ruminants https://www.merckvetmanual.com/digestive-system/fluke-infections-in-ruminants/fasciola-hepatica-in-ruminants https://www.merckvetmanual.com/multimedia/image/fasciola-hepatica-adult https://en.m.wikipedia.org/wiki/Fascioloides_magna Fasciola hepatica in Ruminants - Comprehensive Study Guide Definition • Fascioliasis: Liver fluke disease caused by Fasciola hepatica, affecting cattle, sheep, alpacas, and llamas. Causative Agent • Fasciola hepatica: A liver fluke causing chronic, subacute, and acute infections, with adults residing in bile ducts. Pathophysiology • Transmission: Ingestion of metacercariae on vegetation. • Life Cycle: Eggs hatch in water, miracidia infect snails, asexual development to cercariae, which encyst on vegetation as metacercariae. After ingestion, young flukes excyst in the duodenum, migrate to the liver, and mature in bile ducts. • Damage: Immature flukes cause hepatic necrosis and hemorrhage, mature flukes cause bile duct fibrosis and calcification. Clinical Signs • Acute Disease: Painful abdomen, anemia, sudden death in sheep. • Subacute Disease: Anemia, hemorrhage, extended survival with hepatic damage. • Chronic Disease: Anemia, weight loss, decreased milk production, submandibular edema, especially in cattle. Lesions • Acute: Enlarged, friable liver with fibrinous deposits. • Chronic: Cirrhosis, enlarged bile ducts, fibrosis, calcification in cattle. Diagnosis • Fecal Sedimentation: Detects eggs. • ELISA: Detects antibodies in serum or milk. • Necropsy: Identifies adult flukes and liver damage. Treatment • Anthelmintics: Triclabendazole, clorsulon, albendazole, nitroxinil, closantel, rafoxanide, oxyclozanide. • Resistance: Documented resistance to albendazole, clorsulon, and triclabendazole. Control • Pasture Management: Reduce snail habitats, avoid grazing high-risk pastures. • Snail Control: Molluscicides (historically used, now mostly banned).

Answer 32

Answer: Maedi-Visna is caused by lentivirus. Maedi-Visna is caused by a lentivirus. It is a slowly progressive disease, usually seen in animals over four years of age. It typically causes pneumonia with respiratory distress. Animals are afebrile and present with weight loss/wasting and ataxia, which progresses to recumbency. Other lentiviruses of veterinary significance include ovine progressive pneumonia, caprine arthritis and encephalitis, and equine infectious anemia, and bovine and feline immunodeficiency viruses. Lentiviruses are RNA viruses (in the family Retrovirus) known for long incubation periods and chronic conditions that do not have a "cure." Louping ill is caused by a flavivirus via tick transmission. Listeriosis is a bacterial encephalitis. Link: Lentivirus Pneumonia in Sheep and Goats https://www.merckvetmanual.com/respiratory-system/respiratory-diseases-of-sheep-and-goats/lentivirus-pneumonia-in-sheep-and-goats?autoredirectid=19855 Link: Caprine Arthritis and Encephalitis https://www.merckvetmanual.com/generalized-conditions/caprine-arthritis-and-encephalitis/caprine-arthritis-and-encephalitis Link: Equine Infectious Anemia https://www.merckvetmanual.com/generalized-conditions/equine-infectious-anemia/equine-infectious-anemia Link: Louping Ill in Animals https://www.merckvetmanual.com/nervous-system/louping-ill/louping-ill-in-animals?redirectid=29133 Lentivirus Pneumonia in Sheep and Goats - Comprehensive Study Guide Definition • Lentivirus Pneumonia: Also known as Ovine Progressive Pneumonia (OPP) or Maedi-Visna, it is a chronic disease in sheep caused by lentiviruses. Causative Agents • Small Ruminant Lentiviruses (SRLVs): Maedi-Visna virus (sheep), Caprine Arthritis Encephalitis virus (goats). Pathophysiology • Transmission: Oral ingestion of colostrum/milk or inhalation of infected aerosol droplets. Persistence in lymphocytes, monocytes, and macrophages. • Infection Mechanism: Virus persists in immune cells, evading elimination and causing a progressive immune response leading to lung and CNS damage. Clinical Signs • Sheep: Weight loss, respiratory distress, coughing, bronchial exudate, lethargy, fever, non-inflammatory mastitis (hard bag), encephalitis, neurologic signs (head tilt, circling, altered mentation, paresis). • Goats: Similar to sheep, including hard bag mastitis and neurologic signs. Lesions • Lungs: Mottled, firm, heavy, with rib indentations and enlarged lymph nodes. Histologic interstitial pneumonia, lymphoid hyperplasia, smooth muscle hypertrophy. • CNS: Meningoencephalitis with demyelination. Diagnosis • Serologic Tests: ELISA, AGID assay. • Advanced Diagnostics: PCR assay, virus isolation, ultrasonography. Control and Prevention • Testing and Culling: Regular serologic screening and removal of infected animals. • Management: Raising lambs/kids from seropositive dams separately, using colostrum/milk from seronegative animals.

Answer 33

Answer: Giardia lamblia This is a cyst of the flagellate protozoan Giardia lamblia found in the intestinal tracts of humans and most animals. Most infections do not cause clinical signs, but diarrhea and steatorrhea can occur, particularly in puppies and kittens. Giardiasis must be differentiated from exocrine pancreatic insufficiency (EPI) and other malabsorption syndromes. Amebiasis due to Entamoeba histolytica presents as an acute or chronic colitis, with persistent diarrhea or dysentery (mucus, blood in the stool, fever, abdominal pain). More prevalent in tropical and subtropical countries than in North America. Click here to see an image of Entamoeba histolytica. Link: Exocrine Pancreatic Insufficiency in Dogs and Cats https://www.merckvetmanual.com/digestive-system/the-exocrine-pancreas/exocrine-pancreatic-insufficiency-in-dogs-and-cats?redirectid=31744 Link: Malabsorption Syndromes in Small Animals https://www.merckvetmanual.com/digestive-system/diseases-of-the-stomach-and-intestines-in-small-animals/malabsorption-syndromes-in-small-animals Link: Entamoeba histolyticaAmebiasis https://www.merckvetmanual.com/digestive-system/amebiasis/entamoeba-histolytica-amebiasis?autoredirectid=19848 https://www.merckvetmanual.com/multimedia/image/entamoeba-histolytica-cyst https://www.cdc.gov/dpdx/giardiasis/index.html

Answer 34

Answer: Trichophyton verrucosum Trichophyton verrucosum is the primary dermatophyte in cattle, most commonly seen in calves as periocular lesions although it can become generalized. More common among younger animals and is non-pruritic. Tx is not usually required as cattle often spontaneously recover. There are no approved antifungal agents in cattle. Antifungals approved in other animals or humans could be used if a meat and milk withdrawal time can be determined. Microsporum canis is commonly found in dogs and cats, and Trichophyton mentagrophytes in rodents. Link: Dermatophytosis in Cattle https://www.merckvetmanual.com/integumentary-system/dermatophytosis/dermatophytosis-in-cattle Dermatophytosis in Cattle - Comprehensive Veterinary Information Definitions and Terminology: • Dermatophytosis (Ringworm): A fungal infection affecting the skin of cattle. Causative Agents: • Primary: Trichophyton verrucosum. • Others: Trichophyton mentagrophytes, Trichophyton equinum, Microsporum gypseum, Microsporum nanum, Microsporum canis. Physiopathology: • Transmission: Direct contact with infected animals or fomites. • Pathogenesis: Fungi invade keratinized tissues, causing characteristic lesions. Clinical Findings: • Lesions: Discrete, scaling patches of hair loss with gray-white crusts. • Locations: • Calves: Periocular areas. • Cows/Heifers: Chest and limbs. • Bulls: Dewlap and intermaxillary skin. Diagnosis: • Clinical Signs: Visual inspection of characteristic lesions. • Laboratory Tests: Fungal culture, microscopic examination of hair/skin scrapings. Treatment: • Topical Therapy: Lime sulfur (1:16), enilconazole (1:100). • Improving Husbandry: Reducing overcrowding, improving hygiene. • Vaccination: Live-attenuated fungal vaccine (not available in North America). Prevention: • Hygiene: Regular cleaning, burning infective material. • Isolation: Separate infected animals to prevent spread.

Answer 35

Answer: Equine Rhinopneumonitis. If you hear "nasal discharge" in younger horses and then abortion storms four to five months later in late pregnant mares, think equine herpesvirus-1 (EHV-1, equine rhinopneumonitis). It is the most common infectious cause of abortion in mares. Vaccinate pregnant mares at five, seven, and nine months gestation to greatly decrease the risk of abortion. With EVH-1, abortion of a fresh (minimally autolyzed) fetus typically occurs without premonitory signs in the mare. The aborted fetus may have increased thoracic/abdominal fluid, subcutaneous edema, hepatomegaly with numerous white-yellow small foci, and icterus. Link: Abortion in Horses. https://www.merckvetmanual.com/reproductive-system/abortion-in-large-animals/abortion-in-horses Abortion in Horses - Comprehensive Information for BCSE Test Definitions and Etiology: • Abortion: Premature expulsion of the fetus, which can be caused by various infectious and noninfectious agents. Noninfectious Causes: 1. Twinning: Common cause, typically results in abortion at 8-9 months due to placental insufficiency. 2. Umbilical Cord Torsion: Common in Thoroughbreds, diagnosed by localized swelling or hemorrhage. 3. Fescue Grass Toxicosis: Caused by ingestion of Epichloë coenophiala; leads to prolonged gestation, agalactia, and placental separation. Mare Reproductive Loss Syndrome (MRLS): Associated with exposure to eastern tent caterpillars, causes abortions, stillbirths, and weak foals. Pathology includes neutrophilic placentitis and funisitis. Symptoms: Early abortions (40-80 days), late-term abortions (10 months-term), stillbirths, and weak foals. Causes: Associated with ingestion of eastern tent caterpillars, leading to bacteremia and fetal loss. Infectious Causes: 1. Bacterial Abortion: • Common Agents: Streptococcus equi, Escherichia coli, Pseudomonas aeruginosa, Leptospira spp. • Symptoms: Premature udder development, mucopurulent vaginal discharge. • Diagnosis: Isolation from placenta, fetal tissues. • Treatment: Antibiotics, hygiene. 2. Equine Mycotic Placentitis: • Agents: Aspergillus, Mucor, Candida. • Symptoms: Late-term abortion, thickened chorioallantois. • Diagnosis: Presence of hyphae in placenta, fetal tissues. • Treatment: Antifungal therapy. 3. Equine Rhinopneumonitis (EHV-1): • Symptoms: Abortion after 7 months, edematous placenta, jaundice in fetus. • Diagnosis: PCR, virus isolation from fetal tissues. • Prevention: Vaccination at 5, 7, and 9 months gestation. 4. Equine Viral Arteritis (EVA): • Symptoms: Abortion 6-29 days post-infection, fetal arteritis. • Diagnosis: PCR, virus isolation from placenta, fetal tissues. • Prevention: Vaccination, management to prevent viral transmission. Diagnosis and Prevention • Diagnosis: Clinical signs, laboratory tests (culture, PCR, serology). • Prevention: Management practices, vaccination, vector control, and avoiding exposure to known infectious agents.

Answer 36

Answer: Contagious Ecthyma. If you hear "crusty lips/ears" on a goat or sheep, think of contagious ecthyma, also called "orf" or "soremouth." Caused by a parapoxvirus which enters the body through cuts. See papules, pustules, and thick friable scabs on the lips, mouth, nose, ears, and feet; and on the udders of lactating does and ewes. Treatment is supportive. Orf/soremouth is common, very contagious, and zoonotic, so be careful when you handle infected animals, as humans are also at risk of developing crusty sores. In endemic areas, young animals are most susceptible. Goat and sheep-pox are serious, foreign animal diseases. Follow this link to see sheep-pox: NOT found in North America and reportable. For good refs on Foreign Animal Diseases (FADs), download the newly revised 7th edition of The Gray Book (Note- this is a large PDF file, it will take a minute to load), available free online courtesy of the U.S. Animal Health Association. For a fast online search, try the Center for Food Security and Public Health (CSFPH) Zoonosis website. Link: Contagious Ecthyma in Sheeps and Goats. https://www.merckvetmanual.com/integumentary-system/pox-diseases/contagious-ecthyma-in-sheep-and-goats?autoredirectid=21714 https://www.merckvetmanual.com/multimedia/image/sheeppox-lesions Link: Foreign Animal Diseases https://www.usaha.org/upload/Disease Info/FAD.pdf Link: Zoonotic Diseases https://www.cfsph.iastate.edu/zoonoses/ Contagious Ecthyma in Sheep and Goats - Detailed Veterinary Summary Etiology and Pathogenesis • Causative Agent: Parapoxvirus • Transmission: Direct contact, fomites; virus highly resistant in the environment • Pathogenesis: Entry through skin abrasions, viral replication in keratinocytes causing cytoplasmic swelling and degeneration, leading to vesicle formation and subsequent pustules. Clinical Findings • Symptoms: Papules, vesicles, pustules primarily on lips, face, feet, teats, occasionally buccal cavity and feet; anorexia, weight loss, secondary infections • Lesions: Progress from macules to papules, vesicles, pustules, and scabs; most common at mucocutaneous junctions Diagnosis • Tests: • PCR: Gold standard for detecting viral DNA in scabs • Electron Microscopy: Identification of characteristic viral particles • Histopathology: Intracytoplasmic inclusion bodies • Differential Diagnosis: Foot-and-mouth disease, bluetongue, ulcerative dermatosis Treatment and Control • Medications: • Antimicrobials: Prevent secondary bacterial infections • Topical Treatments: Prevent myiasis, soothing ointments for lesions • Vaccination: Live virus vaccines, typically prepared from infected scab material; administered by scarification, providing immunity but with caution due to zoonotic risk Prevention • Hygiene and Management: Regular disinfection of equipment, isolation of infected animals, proper handling of infected materials • Biosecurity: Prevent introduction from new animals, quarantine measures • Environmental Control: Reducing contamination of grazing areas, maintaining dry conditions to minimize virus persistence Key Points • Zoonotic Potential: Can cause orf in humans, characterized by painful pustules, particularly on hands; use of gloves and proper hygiene essential during handling • Resilience: Virus can survive in scabs for years; thorough cleaning and disinfection required to prevent environmental persistence • Public Health Considerations: Inform handlers of zoonotic risk, ensure proper wound care and protection when dealing with infected animals

Answer 37

Answer: Knmidocoptes pilae. This is Knemidocoptes pilae, the scaly face (or leg) mite and this appearance is considered pathognomic. Confirm Dx with facial scraping if indicated. Tx with ivermectin (0.2 mg/kg IM or PO) or moxidectin (0.2 mg/kg PO) repeated in two weeks. Tx is generally curative but beak deformity may persist. In passerine birds (esp. canary, European goldfinch), look more for crusts on legs, digits ("tassel foot"). Do not perform leg scrapings for diagnosis as this can result in excessive hemorrhage. Link: Parasitic diseases of Pet Birds. https://www.merckvetmanual.com/exotic-and-laboratory-animals/pet-birds/parasitic-diseases-of-pet-birds

Answer 38

Answer: Cuterebra. Cuterebra (a.k.a. rabbit botfly larva) is occasionally found in outdoor-roaming cats and dogs. In North America, cases are usually seen during late summer and fall. The visible fistula is a breathing hole for the larva which eventually exits, pupates and becomes a fly. The normal hosts are rabbits, squirrels, chipmunks and mice. Cuterebra flies lay eggs near the nests, burrows, and traffic pathways where they can attach to the body of hosts. The eggs hatch in response to body heat and larvae enter the body via the mouth or nostrils during grooming, but may also enter through a wound. They penetrate the tissues and travel to specific subcutaneous areas where they mature. Extract the larva carefully in one piece to avoid a severe local inflammatory reaction that can result from a ruptured grub. Do not squeeze the area as that might damage the larva. Anaphylaxis in response to rough removal has also been reported anecdotally. If there is only a swelling without an obvious breathing hole (yet), an abscess or foreign body are ruleouts for this lesion. Cattle grubs (Hypoderma spp.) are generally lighter colored with less prominent spines and are rarely found in pets. The larvae that cause cutaneous habronemiasis are tiny - they emerge from infected flies feeding on wounds and invade the damaged tissue. Horse bots (Gasterophilus spp.) live in the stomach and are not known to infect dogs and cats. ies feeding on wounds and invade the damaged tissue. Sheep nose bots (Oestrus ovis) are smaller than cuterebrae larva. They live in the nares and only affect sheep and goats. 1. Cuterebra larvae: seen in outdoor cats/dogs, late summer/fall. 2. Larvae enter through grooming wounds, mature subcutaneously. 3. Extract larvae carefully to avoid severe inflammation, anaphylaxis. Link: Cuterebra infestation in Dogs and Cats. https://www.merckvetmanual.com/integumentary-system/cuterebra-infestation-in-dogs-and-cats/cuterebra-infestation-in-dogs-and-cats Link: Hypoderma spp. https://www.merckvetmanual.com/integumentary-system/cattle-grubs/hypoderma-spp Link: Cutaneous Habronemiasis in Animals. https://www.merckvetmanual.com/integumentary-system/helminths-of-the-skin/cutaneous-habronemiasis-in-animals Link: Gasterophilus spp Infection in Horses https://www.merckvetmanual.com/digestive-system/gastrointestinal-parasites-of-horses/gasterophilus-spp-infection-in-horses?redirectid=27858 Link: Sheep Nasal bot myiasis https://www.merckvetmanual.com/respiratory-system/respiratory-diseases-of-sheep-and-goats/sheep-nasal-bot-myiasis?autoredirectid=19854

Answer 39

Answer: 0.4 L This goat kid needs 0.4 liters of fluid (~400 ml) to replace its dehydration deficit. The calculation is as follows: Weight in kgs x % dehydration = fluid deficit in liters; 8% dehydration=0.08 12lbs Ã 2.2 kg/lb = 5.45 kg 5.45 kg x 0.08 dehydration = 0.43 liters Replacement fluids should include electrolytes and bicarbonate in kids with diarrhea. Some glucose and potassium support may also be necessary. Fluids can be administered IV with an isotonic solution over 3-4 hours. Kids are notorious for chewing IV lines, so either monitor closely or use an Elizabethan collar. An alternative to isotonic IV fluids for diarrhea is IV hypertonic saline or IV hypertonic sodium bicarbonate with oral electrolytes. This only takes a few minutes and is as just as effective. Link: The Fluid Resuscitation Plan in Animals https://www.merckvetmanual.com/emergency-medicine-and-critical-care/fluid-therapy/the-fluid-resuscitation-plan-in-animals The Fluid Resuscitation Plan in Animals Concepts Fluid resuscitation aims to restore intravascular volume and improve tissue perfusion in animals experiencing shock or severe dehydration. Etiology • Hypovolemic Shock: Often due to hemorrhage, severe dehydration, or third-space fluid losses. Pathogenesis • Shock Response: Compensatory mechanisms, including increased heart rate and vasoconstriction, aim to maintain perfusion but may become exhausted, leading to decompensatory shock and cellular hypoxia. Symptoms • Hypovolemic Shock: Tachycardia, weak pulse, prolonged capillary refill time, pale mucous membranes, altered consciousness. Diagnostic Methods • Clinical Assessment: Heart rate, pulse intensity, mucous membrane color, capillary refill time, blood pressure, rectal temperature. • Laboratory Tests: PCV, total solids, blood lactate, electrolytes, and osmolality. Treatment • Fluid Selection: • Crystalloids: Isotonic solutions (e.g., lactated Ringer’s, 0.9% saline) for interstitial volume replacement. • Colloids: Synthetic or natural colloids (e.g., hydroxyethyl starch, albumin) for intravascular volume expansion. • Fluid Administration Techniques: • Large-Volume Resuscitation: Rapid infusion of isotonic crystalloids followed by colloids for hypovolemic shock. • Small-Volume Resuscitation: Used in cases where large volumes could cause complications (e.g., brain or lung edema). Determination of Resuscitation Endpoints • Clinical Parameters: Restoration of normal heart rate, blood pressure, capillary refill time, and mucous membrane color. • Supplementary Endpoints: Central venous pressure, central venous oxygen saturation, and urine output. Special Considerations • Electrolyte Management: Careful monitoring and adjustment of sodium and potassium levels to avoid complications like cerebral edema or cardiac arrhythmias. • Individualized Approach: Consideration of renal function, ongoing losses, and presence of concurrent diseases (e.g., heart disease, brain injury).

Answer 40

Answer: 8-12 months. Gastrostomy tubes made of silicone can last 8-12 months. Latex tubes do not last more than about 12 weeks as the latex eventually breaks down from exposure to stomach acids. A gastrostomy tube is a feeding tube that passes through the abdominal wall into the stomach. These allow placement of food directly into the stomach and are used when the patient is unable or unwilling to eat normally because of damage to the esophagus, head, or neck. Often called "PEG" (percutaneous endoscopic gastrostomy) tubes because they are placed using an endoscope.

Answer 41

Answer: Serum titer A serum titer (serology.) measures the amount of antibody specific to a particular antigen (or virus) within the blood. It is the most specific way to measure an immune response to a particular virus. Polymerase chain reaction (PCR) looks for particular DNA; it can determine the presence of a virus but NOT the animal's immune reaction to that virus. Changes in the lymphocyte count, neutrophil count, and serum amyloid A all can occur with viral infections but are very nonspecific and are not quantitative.

Answer 42

Answer: Treatment with acetazolamide Treat with acetazolamide PO daily and feed Timothy or Bermuda grass diet to help prevent hyperkalemic periodic paralysis (HYPP) episodes. HYPP is an autosomal dominant trait resulting from a point mutation causing a defect in a voltage dependent skeletal muscle sodium channel. This mutation has been linked to the popular Quarter Horse stallion "Impressive." Affected horses can suffer intermittent episodes of muscular fasciculations and weakness of variable severity. Onset of signs unpredictable, and many triggers: diets high in POTASSIUM (>1.1%, ie: alfalfa hay, molasses, electrolyte supplements, kelp-based supplements). Fasting, anesthesia, heavy sedation, trailer rides, and stress can precipitate clinical signs. Treatment and prevention of HYPP based on DECREASING POTASSIUM in blood. Remember: high K+ SLOWS the HEART (even unto death). Usually (but not always) see INCREASED K+> 5 mEq/L (normal 3-5) during an episode, but normal between episodes. PREVENTION based INCREASING renal excretion of K+ with acetazolamide (carbonic anhydrase inhibitor more assoc. with glaucomaTx) and feeding a low K+ diet (i.e., use Timothy or Bermuda hay, AVOID alfalfa or brome hay). Link: Congenital and Inherited Anomalies of the Musculoskeletal System in Horses https://www.merckvetmanual.com/musculoskeletal-system/congenital-and-inherited-anomalies-of-the-musculoskeletal-system/congenital-and-inherited-anomalies-of-the-musculoskeletal-system-in-horses Link: Hyperkalemia in Ruminants https://www.merckvetmanual.com/metabolic-disorders/disorders-of-potassium-metabolism/hyperkalemia-in-ruminants?autoredirectid=14269 Congenital and Inherited Anomalies of the Musculoskeletal System in Horses Angular Limb Deformities • Etiology: Utero malposition, hypothyroidism, trauma, poor conformation. • Symptoms: Lateral/medial deviation of limbs, lameness, soft-tissue swelling. • Diagnosis: Radiography for physeal, epiphyseal, and carpal bones. • Treatment: Tube casts, splints, surgical correction (hemicircumferential transection, periosteal elevation). Digit Malformation • Types: Polydactyly, hypoplasia, bipartite/tripartite navicular bone. • Treatment: Surgical correction for functional impairment. Dwarfism • Types: Proportionate (growth hormone deficiency) and disproportionate (thyroid hormone issues). • Symptoms: Delayed cuboidal bone development, large head, silky coat. • Diagnosis: Clinical evaluation, hormonal assays. Glycogen Branching Enzyme Deficiency • Etiology: Enzyme deficiency affecting glycogen storage. • Symptoms: Stillbirth, seizures, cardiac/respiratory failure. • Diagnosis: Blood tests for GBE activity, muscle/organ biopsies. • Treatment: No effective treatment, fatal disease. Hernias • Types: Umbilical, diaphragmatic, inguinal. • Symptoms: Scrotal swelling, colic. • Treatment: Surgical repair for larger or symptomatic hernias. Hyperkalemic Periodic Paralysis (HYPP) • Etiology: Genetic mutation in sodium channels. • Symptoms: Paralysis, collapse, sudden death. • Diagnosis: Genetic testing. • Treatment: Manage with diet and medication. Spine Defects • Types: Scoliosis, synostosis, lordosis, kyphosis, torticollis. • Symptoms: Gait abnormalities, back weakness. • Diagnosis: Clinical examination, radiography. • Treatment: Often conservative, severe cases may need management. Tying-up Syndrome • Etiology: Abnormal calcium regulation, polysaccharide storage myopathy (PSSM). • Symptoms: Muscle cramping, stiffness. • Diagnosis: Genetic testing, muscle biopsy. • Treatment: Dietary management, regular exercise.

Answer 43

Answer: Cervical ventroflexion. Cervical ventroflexion can be seen in cats with thiamine deficiency, as well as other neurologic signs like blindness, ataxia, weakness, tremors, seizures and coma. Gl signs are typically seen first. If left untreated, this can be fatal. Deficiency of thiamine (Vitamin B1) is most often seen in cats eating an unbalanced homemade diet; raw seafood contains thiaminases that break down thiamine. Thiamine deficiency, hypokalemia, and taurine deficiency are all possible nutritional causes of cervical ventroflexion in cats. https://www.merckvetmanual.com/nervous-system/diseases-of-the-spinal-column-and-cord/nutritional-disorders-of-the-spinal-column-and-cord-in-animals?autoredirectid=16748#Thiamine-Deficiency_v26305230 Link: Feline Hypokalemic Polymyopathy https://www.merckvetmanual.com/musculoskeletal-system/myopathies-in-small-animals/feline-hypokalemic-polymyopathy **Thiamine Deficiency in Animals** Thiamine (vitamin B1) deficiency is most common in cats; however, it has also been reported in dogs. Causes include inadequately formulated commercial diets, vegetarian diets, food preserved with sulfur dioxide (which destroys thiamine), and raw fish diets (which contain thiaminase). Affected cats typically exhibit brain dysfunction characterized by vestibular signs, head tremor, ataxia, depression, severe ventroflexion of the head, seizures, and death. Clinical signs in dogs include anorexia, depression, paraparesis, seizures, coma, and death. Pathological findings are polioencephalomalacia, most prominent in the midbrain. Diagnosis is based on clinical signs, dietary history, and response to thiamine administration (thiamine hydrochloride, 10-20 mg/cat or 25-50 mg/dog, IM, every 24 hours for 2-4 weeks or until clinical signs abate).

Answer 44

Answer: Phenoxybenzamine Treat urethral spasm, a common complication following treatment of urethral obstruction, with phenoxybenzamine or prazosin. Both drugs reduce urethral sympathetic tone. Use phenylpropanolamine and/or estriol for urethral sphincter mechanism incompetence, a common cause of urinary incontinence in female dogs. Sulfasalazine reduces large bowel inflammation. Sotalol is a non-selective beta blocker and Class III antiarrhythmic used to treat ventricular tachycardia. Link: Obstructive Uropathy in Small Animals https://www.merckvetmanual.com/urinary-system/noninfectious-diseases-of-the-urinary-system-in-small-animals/obstructive-uropathy-in-small-animals Link: Pharmacotherapeutics in Urinary Incontinence in Dogs and Cats https://www.merckvetmanual.com/pharmacology/systemic-pharmacotherapeutics-of-the-urinary-system/pharmacotherapeutics-in-urinary-incontinence-in-dogs-and-cats?autoredirectid=22714#v3333479 Obstructive Uropathy in Small Animals - Comprehensive Study Guide Definition • Obstructive Uropathy: Blockage of urine flow at any point below the kidneys, leading to postrenal azotemia and uremia. Causative Agents • Common Causes: Uroliths (bladder stones) in dogs, matrix-crystalline plugs in young male cats, ureteral uroliths in geriatric cats, tumors, blood clots. Pathophysiology • Mechanism: Obstruction leads to increased hydrostatic pressure in the renal pelvis, causing hydronephrosis, hydroureter, renal parenchyma atrophy, and cystic enlargement. • Acute Complete Obstruction: Rapid onset of azotemia and uremia due to inability to excrete waste. • Partial or Unilateral Obstruction: Compensatory hypertrophy of the nonaffected kidney may mask clinical signs. Clinical Signs • Urethral Obstruction: Pollakiuria, stranguria, hematuria, abdominal pain, distended painful bladder, inability to pass a catheter. • Uremia Signs: Vomiting, dehydration, hypothermia, severe depression. • Severe Hyperkalemia: Bradycardia, cardiac arrhythmias (tall T waves, widened QRS complex). Diagnosis • Clinical Signs and History: Physical examination findings, particularly inability to pass a urethral catheter. • Laboratory Tests: Serum biochemistry (elevated potassium, azotemia), ECG for hyperkalemia. • Imaging: Excretory urography, abdominal ultrasonography to confirm ureteral obstruction. Treatment • Immediate Relief of Obstruction: Urethral catheterization, removal of ureteral obstructions via surgery if necessary. • IV Fluids: Normal saline to improve renal function and correct electrolyte imbalances. • Medications for Hyperkalemia: • Bicarbonate: 0.5 mEq/kg IV over 5 minutes. • Insulin and Dextrose: To drive potassium intracellularly. • Monitoring: Daily assessment of plasma electrolytes, body weight, urine output, hematocrit, and plasma total solids.

Answer 45

Answer: Discontinue phenobarbital in this dog. Discontinue phenobarbital in this dog with neutropenia, thrombocytopenia, and mild anemia. This is a rare side effect of treatment, seen most commonly in the first three months of treatment. Monitor the CBC during this period because changes are typically reversible when detected early. Taper phenobarbital over seven days to reduce the risk of breakthrough seizures, which could result in status epilepticus. Add another anti-epileptic drug (e.g., levetiracetam) in this dog because of continued seizures and the need to discontinue phenobarbital. Monitor liver enzymes and serum phenobarbital concentration every 6 to 12 months in dogs receiving chronic phenobarbital therapy because liver enzyme increase is common. While it does not necessarily indicate hepatic dysfunction, ALT or ALP > 5 x reference range, increased GGT, hyperbilirubinemia, or increased serum bile acid concentration is concerning for phenobarbital-induced hepatic dysfunction. If these chemistry changes occur consider tapering/discontinuing phenobarbital and adding another anti-convulsant. Hepatic dysfunction/failure are typically seen with higher serum phenobarbital concentrations. Other potential side effects of phenobarbital include polyuria/ polydipsia/polyphagia. Phenobarbital can affect the results of thyroid testing and falsely lower total and free T4 and increase TSH. Dogs with these findings do not have hypothyroidism, so do not initiate Tx based on thyroid hormone measurement in patients on phenobarbital. Link: Phrnobarbital https://www.merckvetmanual.com/pharmacology/systemic-pharmacotherapeutics-of-the-nervous-system/maintenance-anticonvulsant-or-antiepileptic-therapy#Phenobarbital:_v4502428 Phenobarbital: Phenobarbital has a long record of safety, efficacy, low cost, and convenience in regard to monitoring serum concentrations. For longterm maintenance in cats and dogs, phenobarbital may be given at 2-4 mg/kg/day, PO, bid. In all species, it takes ~2 wk to approach a steady-state plasma concentration, because oral absorption is extremely variable and the half-life is long. Drug levels are monitored 2 wk after initiation of therapy, 2 wk after any dosage change, and usually every 6-12 mo once seizure control is achieved. Serum therapeutic concentrations are 15-45 mcg/mL. The dosage should be adjusted on the basis of serum level and the history of seizure control. Tolerance to phenobarbital therapy may develop in dogs treated continually for months to years and may result in decreased seizure control; however, an increase (25%) in the dose usually will result in improved seizure control. Phenobarbital causes physical dependence, and thus abrupt withdrawal may cause "barbiturate withdrawal" seizures. Hepatotoxicity and liver failure in dogs have been associated with high serum concentrations (>35 mcg/mL), necessitating the serum level checks every 6-12 mo. Adverse effects such as sedation, polydipsia, polyuria, and polyphagia are common but may decrease within the first few weeks. Other, less common adverse effects are idiosyncratic hyperexcitability, dermatitis, anemia, neutropenia, thrombocytopenia, gingival hyperplasia, and osteomalacia. Phenobarbital has also been used to treat episodic dyscontrol syndrome (rage) in dogs when seizure activity is demonstrable via electroencephalogram recordings. Oral phenobarbital has been used in ruminants at 11 mg/kg/day and in horses at 3-11 mg/kg/day. Serum concentrations should be checked periodically.

Answer 46

Answer: Trimethoprim sulfa, chloramphenicol, enrofloxacin Use of the antimicrobials enrofloxacin, trimethoprim sulfa, and chloramphenicol is considered safe in rabbits and rodents. Avoid penicillins (e.g., amoxicillin) in these species and avoid clindamycin in rabbits. Always review the safety profile and dosing recommendations for drugs in small mammals to ensure safety and efficacy. Rabbits, hamsters, and other rodents are particularly sensitive to enteric dysbiosis +/- enterotoxemia. Antimicrobials may disturb their normal gut flora, particularly the beneficial gram-positive bacteria which digest high-fiber food and keep pathogenic clostridial organisms from over-growing. Remember: Chloramphenicol causes a potentially fatal aplastic anemia in humans, so always use with caution and provide appropriate client information. Link: Clinical Pathology in Rabbits https://www.merckvetmanual.com/exotic-and-laboratory-animals/rabbits/management-of-rabbits#Clinical-Pathology_v3306361 Comprehensive Overview of Rabbit Management for BCSE Test Preparation Definitions and General Management • Housing: Adequate space, proper ventilation, and temperature control are critical. • Diet: High-fiber diet including hay, fresh vegetables, and water. • Breeding: Understanding reproductive cycles and proper care for does and kits. Common Diseases and Conditions • Gastrointestinal Stasis: Symptoms include anorexia, lethargy, and reduced fecal output. • Diagnosis: Clinical signs, radiographs showing gas-filled stomach and intestines. • Treatment: Fluid therapy, motility drugs, and dietary management. • Pasteurellosis: Caused by Pasteurella multocida. • Symptoms: Respiratory signs, abscesses, and otitis media. • Diagnostics: Culture and sensitivity tests. • Treatment: Antibiotics like enrofloxacin or doxycycline. • Urolithiasis: Formation of bladder stones. • Symptoms: Hematuria, dysuria, and abdominal pain. • Diagnostics: Radiographs and urinalysis. • Treatment: Surgical removal, dietary adjustments to reduce calcium intake. Neoplasias in Rabbits • Uterine Adenocarcinoma: Common in older does. • Symptoms: Hematuria, abdominal masses. • Diagnostics: Ultrasound and histopathology. • Treatment: Ovariohysterectomy. • Lymphoma: Affects multiple organ systems. • Symptoms: Weight loss, lethargy, lymphadenopathy. • Diagnostics: Biopsy and immunohistochemistry. • Treatment: Chemotherapy, though prognosis is poor. Clinical Pathology and Diagnostics • Hematology and Biochemistry: Normal values vary slightly from other small animals. • Common Tests: CBC, serum biochemistry, urinalysis. • Interpretations: Specific changes like elevated calcium in renal disease, or changes in liver enzymes in hepatic conditions. • Imaging: Radiographs, ultrasound for internal organ assessment. • Endoscopy: For gastrointestinal and respiratory tract examination. Summary Points for BCSE Test • Housing and Diet: Essential for preventing common diseases. • Disease Management: Identification, diagnosis, and treatment of gastrointestinal stasis, pasteurellosis, and urolithiasis. • Neoplasias: Recognition and management of uterine adenocarcinoma and lymphoma. • Clinical Pathology: Understanding normal values and interpretation of common diagnostic tests.

Answer 47

Answer: Total Parental Nutrition. TPN is Total Parenteral Nutrition, which is giving all the nutrition an animal needs through a route other than the Gl tract (ie: administered via IV route). Animals suffering from severe anorexia may be fed this way. Refs: Bassert and Thomas, McCurnin's Clinical Textbook for Veterinary Technicians, gth ed. p. 334. Link: Nutrition in Disease Management in Small Animals

Answer 48

Answer: Coagulation factor deficiency. Von Willebrand's factor is needed for the first step in clot formation, and animals with von Willebrand's disease are deficient in this factor. In normal animals, von Willebrand’s factor circulates in a complex with coagulation Factor VIlI and facilitates adhesion of platelet to subendothelial surfaces. Suspect von Willebrand's disease in dogs with bleeding disorders with a lab pattern of normal platelet counts and across the board normal coagulation tests. It is the most common inherited coagulation disorder in dogs. Signs include gingival bleeding, epistaxis, and hematuria. Disease may go undetected in a puppy until an excessive bleeding episode after vaccination injection, venipuncture, or surgery (ie: tail docking, dewclaw removal). Chediak-Higashi syndrome, is due to a congenital platelet defect. Associated with dilute hair color-think of smoke-blue Persian cats and beige mice. Not seen in dogs. Pelger-Huet anomaly is a thrombocyte and white cell defect. Granulocytes, especially neutrophils are stuck in band form. A CBC shows an apparent left shift with a normal WBC count. Usually an incidental finding because cell function is normal. Click here for an image of Pelger-Huet anomaly in a dog. https://www.merckvetmanual.com/multimedia/v12762869 Ref: Blackwell's 5-Min. Vet Consult Canine-Feline, 4th ed. pp. 1436-37. Link: Von Willebrand Disease in Animals https://www.merckvetmanual.com/circulatory-system/hemostatic-disorders/platelet-disorders-in-animals#v3258487 Link: Chèdiak-Higashi Syndrome in Animals https://www.merckvetmanual.com/circulatory-system/hemostatic-disorders/platelet-disorders-in-animals#v3258495 Link: Leukogram Abnormalities in Animals Von Willebrand Disease in Animals Definitions: • Von Willebrand Disease (vWD): Inherited bleeding disorder due to defective or deficient von Willebrand factor (vWF). Causative Agents: • Deficient or defective vWF. Physiopathology: • vWF mediates platelet adhesion. • vWF deficiency leads to impaired clotting. Symptoms: • Mucosal bleeding, gingival bleeding, epistaxis, hematuria, prolonged bleeding after surgery. Clinical Changes: • Type 1: Mild to moderate, low vWF concentration. • Type 2: Moderate to severe, loss of high-molecular-weight multimers. • Type 3: Severe, total absence of vWF. Assessment: • Clinical signs, prolonged buccal mucosal bleeding time, PFA-100 closure times. • Laboratory tests: Low vWF concentration, prolonged APTT and ACT in some cases. Treatment: • Avoid drugs that interfere with platelet function. • Transfusion of cryoprecipitate, fresh frozen plasma, or whole blood. • Desmopressin acetate (1 mcg/kg SC 30 minutes before surgery). Medication: • Desmopressin Acetate: Increases vWF release. • Transfusions: Cryoprecipitate, fresh frozen plasma, fresh whole blood. Inheritance: • Autosomal recessive and autosomal dominant patterns. Prevalence: • High in certain dog breeds. Chédiak-Higashi Syndrome in Animals Definitions: • Chédiak-Higashi Syndrome: Autosomal recessive disorder with abnormal granule formation in leukocytes, melanocytes, and platelets. Physiopathology: • Microtubule formation defect; large but reduced granules in cells. Symptoms: • Prolonged bleeding, decreased leukocyte function, diluted coat color. Clinical Changes: • Abnormal granules in various cells, decreased platelet aggregation and storage of adenosine diphosphate and serotonin. Assessment: • Clinical signs, microscopic examination of cells. Prevalence: • Diagnosed in mink, cattle, beige mice, and blue smoke Persian cats. Pelger-Huët Anomaly Definitions: • Pelger-Huët Anomaly: Nuclear hyposegmentation defect of granulocytes. Physiopathology: • Neutrophils appear as bands and metamyelocytes. Symptoms: • None in heterozygotes; lethal in homozygotes. Clinical Changes: • Hyposegmented nuclei in granulocytes. Assessment: • Blood smear analysis showing nuclear hyposegmentation. Prevalence: • Reported in people, cats, rabbits, horses, and dogs.

Answer 49

Answer 40-55mmHg. Capnography measures the amount of expired carbon dioxide (COn) in each breath. This is commonly called'end-tidal CO2! The level should rise to 40-55 mm Hg at peak expiration when under inhalant anesthesia. In awake animals, the level should be 0 mm Hg on inhalation and rise to 35- 45 mm Hg on exhalation. Higher levels of CO, indicate hypoxia and the anesthetist needs to take measures to increase the patient's oxygen intake and decrease the CO levels. Lower levels indicate that the patient is hyperventilating. In this article, Samantha Adshead, VTS (Anesthesia & Analgesia) helps explain capnography, including interpreting the readout on a multiparameter monitor.

Answer 50

Answer: In computed tomography (CT) ionizing radiation is used to create an image. During a CT scan, an x-ray beam passes transaxially through the patient. X-ray attenuation (drop off) is measured at sequential sites in a segment of the patient's anatomv. A computer reconstructs the data into a cross-sectional image viewed on a monitor. Computed tomography provides better spatial resolution and radiographic contrast compared to standard radiography. Patients must remain still for a long period of time, necessitating heavy sedation or general anesthesia to achieve proper positioning without motion artifact. Therefore, CT may be too risky in unstable patients. Click here to see a CT image of a lung lobe torsion in a dog (scroll down). https://www.vet.upenn.edu/veterinary-hospitals/ryan-veterinary-hospital/services/radiology-diagnostic-imaging/computed-tomography Link: Computed Tomography in Animals. https://www.merckvetmanual.com/clinical-pathology-and-procedures/diagnostic-imaging/computed-tomography-in-animals

Answer 51

Answer: Acetylcysteine and S-adenosylmethionine. Acetaminophen toxicity in cats usually occurs when owners administer the drug, unaware of its significant potential toxicity in cats. In this case, the cat's clinical signs are most consistent with acetaminophen toxicity based on the Heinz body anemia that is present. Cats can die from oxidative damage and methemoglobinemia within 1-2 days of ingestion. It may also be associated with hepatotoxicity in cats, although this is seen more frequently in dogs. Recall that cats are particularly sensitive to acetaminophen because they have decreased glucuronyl transferase activity which conjugates acetaminophen to glucuronic acid for excretion. As a result, 50-60 mg (a single tablet) may be fatal for a 4-5 kg cat. Treatment should consist of toxin removal if possible by inducing emesis in some cases. As the cat in this case is already vomiting, this may not be necessary. Activated charcoal is controversial and should only be given if ingestion occurred within hours and should be administered very carefully in cats due to the risk of aspiration. The specific antidote is acetylcysteine which binds to some of the reactive metabolites of acetaminophen and increases the availability and synthesis of glutathione. Other treatments may include S-Adenosylmethionine (SAMe) which has hepatoprotective and antioxidant properties. Cimetidine can be given to inhibit the p450 oxidase in the liver and limit formation of toxic metabolites. Ascorbic acid can also be used as an adjunct treatment to bind toxic metabolites. In cats with signs of hypoxemia from severe hemolytic anemia (PCV <20%), a transfusion and further supportive care may be warranted.

Answer 52

Answer: Clumped platelets. Feline platelets (thrombocytes) clump easily. When counting platelets in cat blood, either manually or with an automated cell counter, this must be taken into account. Feline platelets, essential in hemostasis, are produced in the bone marrow and have a typical lifespan of about 5-7 days. They play a crucial role in primary hemostasis, adhering to damaged endothelial cells and forming a platelet plug. In addition, they contribute to secondary hemostasis by providing a surface for coagulation factor activation. Platelets also have functions beyond clot formation, including roles in immune responses and maintaining vascular integrity. Their production, structure, and function are complex, involving various cytokines and cellular processes. For veterinary professionals, understanding the nuances of feline platelet physiology is crucial, particularly in diagnosing and managing hematologic and vascular disorders. Feline platelets no clumping, but normal rouleaux formation is clearly demonstrated. https://www.merckvetmanual.com/multimedia/v4730684 Equine platelets (hard to see-they don't stain well https://www.merckvetmanual.com/multimedia/v4730819 Bovine platelets on a blood smear. https://www.merckvetmanual.com/multimedia/v4730756 Refs: Bassert, Beal and Samples, McCurnin's Clinical Textbook for Velerinary Technicians, gthed, pp. 373. Duncan and Prasse's Clinical Pathology, 4t! ed. p.105. Platelets - Comprehensive Study Guide Definitions and Production • Platelets: Anucleate cell fragments produced in the bone marrow from megakaryocytes, essential for hemostasis. • Production: Stimulated by thrombopoietin from the liver and bone marrow stromal cells. Other cytokines like IL-6, IL-11, GM-CSF also play roles. Physiopathology • Formation: Megakaryocytes undergo endomitosis and cytoplasmic maturation, extending proplatelets into vascular sinuses. • Senescence: Platelets circulate for 5-7 days, undergoing desialylation and apoptosis, removed by liver Kupffer cells and spleen macrophages. Functions • Hemostasis: Platelets adhere to damaged endothelium, aggregate, and form a hemostatic plug. They also release granules containing ADP, thromboxane A2, and other factors to promote coagulation. • Vascular Integrity: Platelet-derived factors maintain endothelial junctions and support angiogenesis. • Immune Roles: Platelets phagocytize pathogens and modulate immune responses. Medications • Thrombopoietin Receptor Agonists: Used in treating refractory thrombocytopenia in humans. Structure • Granules: • Alpha Granules: Contain proteins for adhesion, inflammation, and coagulation. • Dense Granules: Contain ATP, ADP, serotonin, calcium. • Lysosomes: Contain hydrolytic enzymes.

Answer 53

Answer: Atelectasis. Atelectasis can develop in the lungs when an animal is NOT sufficiently ventilated during anesthesia. You can prevent hypoventilation by gently squeezing the manual reservoir bag to inflate the lungs manually once every 2-5 minutes. This is commonly called 'bagging' or 'sighing. Tracheal irritation can occur during intubation if the endotracheal tube is too large for the animal or if the cuff is inflated too much. Laryngospasms occur during induction. Decubital ulcers are secondary to pressure sores over bony prominences in recumbent animals. Phlebitis is inflammation of the veins. Here is a good review on hypoventilation, courtesy of the American Animal Hospital Association (AAHA). Ref: Bassert, Beal and Samples, McCurnin's Clinical Textbook for Veterinary Techni 9th ed. p. 1037. Link: Hypoventilation. https://www.aaha.org/aaha-guidelines/2020-aaha-anesthesia-and-monitoring-guidelines-for-dogs-and-cats/troubleshooting-anesthetic-complications/hypoventilation/ Hypoventilation in Anesthetic Complications (2020 AAHA Guidelines) Definitions and Terminology • Hypoventilation: Inadequate ventilation leading to elevated blood CO2 levels (hypercapnia) and possibly decreased blood oxygen levels (hypoxemia). • Hypercapnia: Increased partial pressure of CO2 in the blood, typically >45 mm Hg. • Hypoxemia: Decreased partial pressure of O2 in the blood, typically <80 mm Hg. Causes of Hypoventilation • Drug Effects: Anesthetic agents (e.g., opioids, propofol, isoflurane) depress respiratory centers in the brain. • Airway Obstruction: Due to mucus, foreign bodies, or anatomical abnormalities. • Mechanical Factors: Improper positioning, equipment malfunction (e.g., ventilator failure), or circuit disconnection. • Disease Conditions: Pre-existing respiratory or neuromuscular diseases affecting ventilation. Pathophysiology • Anesthetic drugs can depress the central respiratory centers, reducing the respiratory rate and tidal volume. • Reduced muscle tone and airway patency can compromise ventilation. • Increased CO2 levels lead to respiratory acidosis, affecting cardiovascular function and reducing oxygen delivery to tissues. • Persistent hypoventilation can result in hypoxemia, leading to tissue hypoxia and potential organ damage. Clinical Changes and Symptoms • Increased CO2 Levels: Tachycardia, increased blood pressure initially, followed by bradycardia and hypotension. • Decreased O2 Levels: Cyanosis, decreased SpO2 readings (<90%). • Altered Blood Gas Values: Elevated PaCO2 (>45 mm Hg), decreased PaO2 (<80 mm Hg). Assessment • Monitoring Tools: Capnography (measuring end-tidal CO2), pulse oximetry (measuring SpO2), blood gas analysis. • Clinical Signs: Respiratory rate and depth, mucous membrane color, and overall patient demeanor. Management Strategies 1. Adjust Anesthetic Depth: • Reduce inhalant anesthetic concentration if excessive. • Use balanced anesthesia techniques (e.g., combining lower doses of multiple agents). 2. Support Ventilation: • Manual or mechanical ventilation to ensure adequate tidal volume and respiratory rate. • Ensure proper positioning to maintain open airways. 3. Treat Underlying Causes: • Clear airway obstructions, correct equipment malfunctions. • Administer reversal agents for opioids (e.g., naloxone) or benzodiazepines (e.g., flumazenil) if necessary. 4. Monitor and Correct Blood Gas Abnormalities: • Supplement oxygen to maintain SpO2 > 95%. • Correct acid-base imbalances with appropriate fluids and medications. Medications • Opioid Reversals: • Naloxone: 0.01-0.04 mg/kg IV, IM, or SC. • Side Effects: Reversal of analgesia, potential for acute pain. • Benzodiazepine Reversals: • Flumazenil: 0.01 mg/kg IV. • Side Effects: Seizures in patients with benzodiazepine dependence. • Supplemental Oxygen: • Delivered via mask, nasal cannula, or endotracheal tube to improve oxygenation. Summary for Veterinary Professionals • Hypoventilation is a critical anesthetic complication requiring prompt recognition and management. • Monitoring tools like capnography and pulse oximetry are essential for early detection. • Management includes adjusting anesthetic depth, supporting ventilation, treating underlying causes, and correcting blood gas abnormalities. • Reversal agents and supplemental oxygen are key treatments.

Answer 54

Answer: Grinding function of similar to teeth. The gizzard (also called the ventriculus), is the muscular stomach that contains grit and small rocks. It helps birds grind up hard seeds and other foods, in effect, acting like teeth. The proventriculus is the glandular stomach in birds. The crop is a diverticulum of the esophagus, used for temporary food storage that empties into the proventriculus. The purpose of the crop is to allow a bird to quickly swallow what food it can, then fly to safety and digest the meal at leisure. In hand fed pediatric birds (usually valuable parrots), there a many potential problems possible with crop burn, crop puncture or proventricular impaction. Click here to see a budgerigar with a full crop. https://en.wikipedia.org/wiki/File:Budgerigar_with_full_crop.jpg Refs: Bassert, Beal and Samples, McCurnin's Clinical Textbook for Veterinary Technicians, 9th ed., p. 775 and Wikipedia online. Link: Pediatric Diseases of Pet Birds https://www.merckvetmanual.com/exotic-and-laboratory-animals/pet-birds/pediatric-diseases-of-pet-birds Pediatric Diseases of Pet Birds 1. Aspiration Pneumonia: Caused by improper feeding, leading to respiratory distress. Treat with oxygen, antimicrobials, and supportive care. 2. Bacterial Disease: Gram-negative infections from unsanitary conditions. Symptoms include crop stasis, poor feeding. Treat with antibiotics, supportive care. 3. Yeast Infection: Candida overgrowth, especially with antimicrobial use. Symptoms include crop stasis, oral plaques. Treat with antifungals. 4. Viral Diseases: Includes polyoma virus, avian bornavirus, and circovirus. 5. Foreign Bodies: Diagnosed via radiographs; may require surgical removal. 6. Crop Stasis: Due to poor husbandry/nutrition. Symptoms include a distended crop. Treat with fluid therapy and adjusted feeding practices. 7. Crop Burns: From overheated formula. Treat with antimicrobials, surgery if severe. 8. Esophageal/Pharyngeal Trauma: From improper feeding techniques. Treat with surgical drainage, antimicrobials. 9. Hepatic Lipidosis: Seen in obese, hand-fed chicks. Treat with nutritional adjustments, fluid therapy. 10. Failure to Thrive: Due to genetic, congenital, or husbandry issues. Provide supportive care, possible antimicrobials. 11. Beak Deformities: Corrective measures include manual correction or prosthetics. 12. Splayleg: Deformities due to nutritional deficiencies or improper substrate. Treat with bandages or surgery. 13. Constricted Toe Syndrome: Circulation impeded by fibrous bands. Treat with debridement, moist dressings. 14. Toe Malposition: Correct with early intervention via bandaging. 15. Cryptophthalmia: Reduced palpebral fissures. Surgical correction if vision is compromised. 16. Choanal Atresia: Blocked choanal opening. Treat with surgical creation of an opening.

Answer 55

Answer: 20 mAs. Together, milliampere-seconds equals mA multiplied by time (mAX sec=mAs), which controls the intensity of an x-ray. In this question, 200 X 1/10= 20 mAs. Milliamperes (mA) are the QUANTITY of electrons produced by the x-ray machine and exposure time (sec) is how LONG you expose the animal to these rays. More mA, or longer exposure time, means a DARKER x-ray. Refs: Bassert, Beal and Samples, McCurnin's Clinical Textbook for Veterinary Technicians, gthed. p. 483 and Mosby's Comprehensive Review for Veterinary Technicians Tighe, Brown, 4th ed. p. 142.

Answer 56

Answer: Grinding. Molars grind food. Incisors are for cutting, nibbling food. Canines grip and tear food. The upper fourth premolar and lower first molar in carnivores are used to shear meat and are called the carnassial teeth.

Answer 57

Answer: 1-3mm Normal depth of the gingival sulcus in dogs is 1-3 mm, and in cats is less than 1 mm. The gingival sulcus is the crevice between the tooth and the gumline where plaque collects. It is important to know that this crevice is not very deep in normal cats when you are cleaning teeth. Dr. Jan Bellows describes the uses of Dental Probes and Explorers https://www.dvm360.com/view/dental-probes-and-explorers-musts-examination