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Veterinary Medicine - Important Questions

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LONG QUESTIONS

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1. Hemorrhagic Septicemia (HS) - Etiology, Pathogenesis, Clinical Signs, Diagnosis, Treatment

Definition

Etiology

• Causative agent: Pasteurella multocida - a Gram-negative, non-motile, non-spore-forming, encapsulated coccobacillus
• Serotypes responsible:
  • B:2 - responsible for HS in Asia (most common)
  • E:2 - responsible for HS in Africa
• Carter's capsular classification: Type B and E
• The organism is a normal commensal of the upper respiratory tract and becomes pathogenic under stress

Predisposing Factors

• Stress (transportation, heavy work, starvation, overcrowding)
• Extreme weather changes (onset of monsoon)
• Heavy worm burden
• Poor nutrition and husbandry

Pathogenesis

1. Under stress, the organism (carried as a commensal in the nasopharynx) multiplies rapidly
2. Endotoxins and exotoxins are released
3. Hyaluronidase and neuraminidase produced by the organism damage tissue
4. Bacteremia/septicemia occurs - organisms enter the bloodstream
5. Widespread endothelial damage leads to hemorrhages throughout the body
6. Inflammatory exudate accumulates in serous cavities (pleura, pericardium, peritoneum)
7. Severe edematous swelling of head, neck, and brisket develops (due to lymphatic obstruction and increased vascular permeability)
8. Death occurs within 6-24 hours due to toxemia and circulatory failure

Clinical Signs

• Sudden death with no premonitory signs

• High fever (104-107°F / 40-41.5°C)
• Dullness, anorexia, depression
• Profuse salivation, nasal discharge (serous to mucopurulent)
• Characteristic hot, painful, doughy swelling of throat, dewlap (brisket), and neck
• Difficulty in breathing (dyspnea), mouth breathing
• Edema of the tongue and pharynx - may protrude from mouth
• Conjunctivitis, lacrimation
• Constipation followed by diarrhea (sometimes blood-tinged)
• Death within 24-72 hours if untreated

Diagnosis

• History, clinical signs (especially the edematous swelling of head/neck/brisket)
• Blood smear staining: Bipolar staining (safety-pin appearance) with Leishman, Wright, or methylene blue stain
• Blood culture: isolation of Pasteurella multocida
• Passive hemagglutination test, ELISA

• Petechial and ecchymotic hemorrhages on serosal surfaces
• Edematous, gelatinous infiltration of subcutaneous tissue of throat and dewlap
• Pneumonia, splenomegaly
• Hemorrhagic lymphadenopathy

• Isolation and culture on Blood agar - grayish, non-hemolytic colonies
• Biochemical tests (indole +ve, oxidase +ve)
• Mouse inoculation test

Treatment

• Drug of choice: Oxytetracycline (LA) - 20 mg/kg IM
• Alternatives:
  • Penicillin + Streptomycin
  • Sulfonamides (trimethoprim-sulfa combination)
  • Ampicillin
  • Enrofloxacin
• Supportive therapy:
  • Anti-inflammatory drugs (flunixin meglumine)
  • IV fluids (isotonic saline)
  • Antihistamines to reduce edema
  • Vitamins B-complex, C

• Vaccination with HS vaccine (adjuvanted alum-precipitated or oil-adjuvant vaccine)
• Animals should be vaccinated before the monsoon season
• Isolate sick animals
• Avoid stress during transportation and at onset of monsoon

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2. Brucellosis - Etiology, Pathogenesis, Clinical Signs, Diagnosis, Treatment

Definition

Etiology

• Genus: Brucella - Gram-negative, non-motile, non-spore-forming, aerobic coccobacilli
• Species and their hosts:

• In cattle: B. abortus biotype 1 is most common
• Zoonotic importance: B. melitensis is most virulent for humans (causes undulant fever / Malta fever)

Pathogenesis

1. Entry via oral route (ingestion of infected material), conjunctiva, skin abrasions, or venereal route
2. Organism is phagocytosed but survives intracellularly within macrophages (intracellular parasite)
3. The organism has erythritol - a growth factor produced by the fetal trophoblast and chorioallantois; this explains tropism for the placenta
4. Organisms multiply in the reticuloendothelial system - lymph nodes, spleen, liver
5. Bacteremia occurs; organism localizes in gravid uterus (due to erythritol), mammary gland, testicles, epididymis
6. Placentitis (necrotic cotyledons) leads to fetal death and abortion
7. Abortifacient effect: Organisms produce endotoxins that damage placental trophoblasts, causing placental separation and abortion
8. In bulls: orchitis, epididymitis, seminal vesiculitis leading to infertility

Clinical Signs

• Abortion in the last trimester (7th-8th month in cattle)
• Retained placenta (very common post-abortion)
• Metritis, purulent vaginal discharge
• Reduced milk yield
• Transient infertility (repeat breeding)
• Hygroma (fluid-filled swellings over joints - "milk joints")

• Orchitis (unilateral or bilateral), epididymitis
• Seminal vesiculitis
• Infertility, reduced libido

• Abortion, stillbirths
• Epididymo-orchitis in males

• Undulant (intermittent) fever, sweating, malaise, arthralgia

Diagnosis

1. Rose Bengal Plate Test (RBPT) - Rapid screening test (most commonly used)
2. Serum Agglutination Test (SAT) / Standard Tube Agglutination Test - Confirmatory
3. Milk Ring Test (MRT) - Herd screening test using bulk milk
4. Complement Fixation Test (CFT) - Most specific and confirmatory
5. ELISA - Highly sensitive and specific
6. 2-Mercaptoethanol Test - Differentiates IgM from IgG antibodies

• Culture of aborted fetus, placenta, vaginal discharge, milk on Farrell's medium (selective medium)
• Modified Ziehl-Neelsen stain - Brucella appears as red intracellular coccobacilli against blue background

Treatment

• In Animals: Treatment is not recommended - test and slaughter policy is followed
• Infected animals should be permanently eliminated from the herd
• In Humans:
  • Doxycycline + Rifampicin (6 weeks) - first line
  • Doxycycline + Streptomycin - alternative

• Vaccination:
  • Strain 19 vaccine (B. abortus Strain 19) - live attenuated, given to calves 3-6 months of age
  • RB51 vaccine - rough strain, does not interfere with serological tests (advantage over S19)
  • Rev-1 vaccine - for B. melitensis in small ruminants
• Test and slaughter policy for positive reactors
• Quarantine of new animals
• Proper disposal of aborted fetuses and placentas
• Pasteurization of milk
• Brucellosis is a notifiable disease

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SHORT QUESTIONS

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3. White Muscle Disease (Nutritional Muscular Dystrophy)

• Definition: A degenerative disease of skeletal and cardiac muscle in young ruminants caused by deficiency of Selenium (Se) and/or Vitamin E
• Species affected: Calves, lambs, kids, foals (most commonly young animals)
• Etiology: Selenium and/or Vitamin E deficiency; selenium-deficient soils are the main cause
• Pathogenesis:
  • Selenium is a component of glutathione peroxidase (antioxidant enzyme)
  • Vitamin E is a fat-soluble antioxidant
  • Deficiency leads to accumulation of lipid peroxides that damage cell membranes
  • This causes Zenker's degeneration (hyaline degeneration) of striated muscle fibers
  • Both skeletal muscles (locomotor form) and cardiac muscle (cardiac form) are affected
• Clinical Signs:
  • Weakness, stiffness, inability to stand (recumbency)
  • Affected muscles appear pale, chalky-white (chalk-white streaks) on post-mortem
  • Bilateral symmetrical involvement of large muscle groups (hindquarters, tongue, diaphragm)
  • Cardiac form: sudden death due to heart failure in apparently healthy animals
  • Skeletal form: progressive weakness, dysphagia (tongue involvement)
  • Myoglobinuria (dark urine)
• Diagnosis:
  • Elevated serum CK (Creatine Kinase), AST, LDH
  • Low blood selenium levels
  • Low Vitamin E levels
  • Post-mortem: pale chalky streaks in muscles
  • Histopathology: hyaline degeneration and necrosis of muscle fibers
• Treatment:
  • Selenium injection (sodium selenite) - 0.1 mg/kg IM or SC
  • Vitamin E (alpha-tocopherol) supplementation
  • Selenium + Vitamin E combined injection (e.g., E-SE) is the treatment of choice
  • Supportive care (rest, good nutrition)
• Prevention: Selenium supplementation to pregnant animals, selenium-fortified salt licks, selenium-enriched fertilizers on deficient soils

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4. Diseases Caused by Vitamin A Deficiency (Enlist)

1. Night blindness (Nyctalopia) - earliest and most characteristic sign; failure of dark adaptation due to lack of rhodopsin formation in rods
2. Xerophthalmia - dryness and thickening of corneal and conjunctival epithelium
3. Keratomalacia - softening and ulceration of the cornea; can lead to permanent blindness
4. Squamous metaplasia - keratinization of mucous membranes (respiratory, GI, urogenital tracts)
5. Increased susceptibility to infections - loss of mucosal barrier leads to respiratory and enteric infections
6. Reproductive failure - infertility, abortion, stillbirths, birth of weak calves
7. Papilledema and increased CSF pressure - narrowing of optic foramen due to bone remodeling defects; leads to blindness
8. Congenital defects - born blind, hydrocephalus in calves (from deficient dams)
9. Skin changes - thickening, scaliness, rough haircoat (hyperkeratosis)
10. Poor growth and development in young animals
11. Spermatogenesis failure in males
12. Urolithiasis (in pigs) - epithelial changes in urinary tract lead to stone formation

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5. Otitis Externa in Dogs

• Definition: Inflammation of the external ear canal (from the pinna to the tympanic membrane)
• Prevalence: Very common in dogs; especially in breeds with pendulous ears (Cocker Spaniels, Basset Hounds), heavy hair in ear canals (Poodles)

• Altered environment of ear canal (moisture, warmth) promotes microbial overgrowth
• Inflammation leads to hyperplasia of ceruminous glands and epithelium
• Progressive stenosis of canal if chronic

• Head shaking, ear scratching, pawing at ear
• Erythema, edema, swelling of ear canal
• Pain on palpation of ear base
• Foul-smelling discharge (dark brown/waxy = Malassezia; yellow-green purulent = bacterial)
• Head tilt (if otitis media is involved)
• Aural hematoma formation (from head shaking)

• Otoscopic examination
• Cytology of ear discharge (staining - identify organisms, WBCs)
• Culture and sensitivity (for chronic/resistant cases)
• Ear swab culture

• Clean and flush the ear canal (chlorhexidine or saline)
• Topical treatments (most important):
  • Antifungal: Clotrimazole, miconazole (for Malassezia)
  • Antibacterial: Gentamicin, enrofloxacin (for bacteria)
  • Glucocorticoids: Dexamethasone (to reduce inflammation)
  • Combination preparations: Otomax (gentamicin + clotrimazole + betamethasone), Surolan
  • Antiparasitic: Ivermectin drops (for Otodectes)
• Systemic antibiotics for severe or deep infections
• Treat underlying cause (allergies, parasites)
• Surgical options (TECA - Total Ear Canal Ablation) for end-stage chronic otitis

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6. Infectious Bovine Keratoconjunctivitis (IBK) / Pink Eye in Cattle

• Definition: A highly contagious ocular disease of cattle characterized by lacrimation, conjunctivitis, corneal ulceration, and opacity, commonly called "Pink Eye"

• Primary agent: Moraxella bovis - Gram-negative, aerobic diplococcus
• Produces pili (for attachment to corneal epithelium) and hemolysin (cytotoxin)
• Predisposing factors: UV radiation (sunlight), dust, flies (Musca autumnalis - face fly is the main vector), tall grass irritation, concurrent viral infections (IBR)

1. M. bovis is transmitted mechanically by face flies and direct contact
2. Organism attaches to corneal epithelium via pili
3. Hemolysin destroys corneal epithelial cells
4. UV light increases susceptibility by damaging epithelium
5. Neutrophil infiltration causes corneal ulceration
6. Progressive involvement leads to corneal opacity (leukoma)
7. In severe cases: corneal perforation, endophthalmitis, blindness

• Unilateral or bilateral involvement
• Stage 1: Lacrimation, photophobia, blepharospasm, conjunctival hyperemia
• Stage 2: Corneal ulceration (central, white spot), opacity begins
• Stage 3: Deep corneal ulcer, marked opacity (white to yellow)
• Stage 4: Corneal perforation, prolapse of iris (staphyloma), panophthalmitis
• In mild cases: self-limiting (6-8 weeks), complete recovery possible

• Clinical signs (characteristic corneal ulcer)
• Conjunctival swabs for culture on Blood agar
• Isolation of Moraxella bovis
• Fluorescein dye staining - highlights corneal ulcers

• Topical antibiotics (most effective):
  • Oxytetracycline eye ointment (most commonly used)
  • Cloxacillin eye ointment
  • Penicillin eye drops
• Subconjunctival injection of penicillin or oxytetracycline
• Systemic antibiotics: Oxytetracycline LA - 20 mg/kg IM (most effective systemic treatment)
• Tilmicosin or florfenicol also used
• Eye patch or suture of eyelids (temporary tarsorrhaphy) to reduce UV exposure
• Fly control (insecticide ear tags, pour-ons)
• Move affected animals to shade

• Fly control is key
• Moraxella bovis vaccine (pili-based vaccine)
• Avoid UV exposure
• Isolate affected animals

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7. Black Quarter (Blackleg / Black Leg / Clostridial Myositis)

• Definition: An acute, febrile, highly fatal disease of cattle and sheep characterized by emphysematous, gangrenous myositis, primarily affecting large muscle groups
• Also called: Blackleg, Symptomatic Anthrax (misnomer)

• Causative agent: Clostridium chauvoei (primary cause)
• Also C. septicum (malignant edema) can cause similar lesions
• Gram-positive, spore-forming, anaerobic rod
• Spores persist in soil for decades
• Most commonly affects well-nourished, rapidly growing calves (6 months to 2 years)

1. Spores ingested from contaminated soil/feed
2. Spores absorbed through GI tract and travel to muscle via blood
3. They remain dormant in muscle cells
4. Muscle trauma (even minor) causes local ischemia/reduced O2 tension
5. Anaerobic conditions trigger spore germination and vegetative growth
6. Toxins produced: alpha toxin (lecithinase - most important), beta toxin, gamma toxin, delta toxin, hyaluronidase, neuraminidase
7. Gas (CO2, H2S) produced causes emphysematous swelling
8. Rapid muscle necrosis and systemic toxemia
9. Death due to toxemia within 12-48 hours

• Sudden onset high fever (106-108°F)
• Characteristic hot, painful, crepitant swelling over affected muscles (shoulder, hindquarters, thigh, neck)
• Lameness (affected limb)
• Crepitation (crackling sound on palpation) due to gas production
• Rapid deterioration - animal becomes recumbent
• Death within 12-48 hours
• Post-mortem: affected muscles are dark red-black, dry, spongy with rancid odor
• Crepitus and emphysema in muscle tissue

• Clinical signs (crepitant swelling in young well-nourished animals)
• Post-mortem: characteristic black, dry, frothy lesions in muscle
• Smear from lesion: large Gram-positive rods, often with spores (lemon-shaped spores)
• Fluorescent Antibody Test (FAT) - most rapid confirmatory test
• Culture on Robertson's cooked meat medium (anaerobic)
• Ascoli's thermo-precipitation test (not primary but sometimes used)

• Penicillin G (high doses) - if caught early
• Oxytetracycline
• However, prognosis is grave once clinical signs appear; treatment is usually unsuccessful
• Supportive therapy

• Vaccination is the cornerstone of control:
  • Clostridial vaccines (multivalent - covers 7-8 Clostridial diseases)
  • Blackleg vaccine (alum-precipitated formol vaccine)
  • Primary course: 2 doses, 4-6 weeks apart, then annual booster
  • Vaccinate before 6 months of age
• Avoid grazing on heavily contaminated pastures
• Dispose of carcasses properly (deep burial with lime or burning) - do NOT perform full necropsy (risk of contaminating soil with spores)

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DEFINITIONS

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Night Blindness (Nyctalopia)

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Dermatitis

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Rickets

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McFadyean Reaction (McFadyean's Reaction) in Anthrax

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Aural Hematoma

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Exam Tip: For HS, remember B:2 = Asia, E:2 = Africa. For Brucellosis, the key serological tests in order of use are: RBPT (screening) → CFT (confirmatory). Black Quarter affects well-nourished young cattle (unlike most infections that affect the weak). White Muscle Disease = Selenium + Vitamin E deficiency = Zenker's degeneration.Here is a complete, exam-ready answer for all the questions in the image:

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Veterinary Medicine - Important Questions (Set 2)

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LONG QUESTIONS

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1. Epilepsy in Animals

Definition

Classification

Etiology

• Genetic predisposition - common in specific dog breeds (German Shepherd, Beagle, Golden Retriever, Border Collie, Labrador, Belgian Tervuren)
• No structural lesion found

• Canine Distemper virus encephalitis
• Brain tumors (glioma, meningioma)
• Trauma, hydrocephalus
• Granulomatous meningoencephalitis (GME)
• Toxoplasmosis, Neosporosis

• Hypoglycemia (insulinoma)
• Hepatic encephalopathy (portosystemic shunt)
• Uremia, hyponatremia, hypocalcemia
• Toxins: lead, organophosphates, strychnine, metaldehyde

Pathogenesis

1. Normal brain maintains balance between excitatory (glutamate) and inhibitory (GABA) neurotransmitters
2. In epilepsy, this balance is disrupted - excessive excitation or reduced inhibition
3. A group of neurons (epileptic focus) develops paroxysmal depolarization shifts (PDS)
4. Abnormal discharge spreads to surrounding neurons and eventually throughout the brain
5. This produces the clinical seizure (ictus)
6. Post-ictal phase follows as the brain attempts to restore balance

Phases of a Seizure

1. Prodrome - hours to days before; behavioral change, restlessness
2. Aura (Pre-ictal phase) - minutes before; anxiety, attention-seeking, salivation
3. Ictus (Ictal phase) - the seizure itself (seconds to minutes): tonic-clonic movements, paddling, jaw chomping, salivation, urination, defecation, loss of consciousness
4. Post-ictal phase - after seizure: disorientation, blindness, ataxia, pacing, excessive thirst/hunger (can last minutes to hours)

Status Epilepticus

• Continuous seizure lasting >5 minutes, OR
• Two or more seizures without recovery of consciousness between them
• Medical emergency - can cause hyperthermia, brain damage, death

Clinical Signs

• Sudden loss of consciousness
• Tonic-clonic muscle contractions, paddling of limbs
• Jaw chomping, excessive salivation, frothing
• Involuntary urination and defecation
• Temporary blindness, disorientation post-ictal
• Cluster seizures (multiple within 24 hours)

Diagnosis

• Thorough history: age of onset, frequency, duration, breed
• Minimum database: CBC, biochemistry (BUN, creatinine, glucose, liver enzymes, bile acids), urinalysis - to rule out metabolic causes
• Neurological examination: determine if signs are focal or generalized
• CSF analysis: if encephalitis/meningitis suspected
• MRI/CT scan: most sensitive for structural brain lesions
• EEG (Electroencephalography): detects abnormal electrical activity (less commonly used in veterinary practice)
• Rule out: hypoglycemia, hepatic encephalopathy, toxin exposure

Treatment

1. Diazepam (Valium): 0.5-1 mg/kg IV - drug of choice for acute seizure control
2. If no IV access: Diazepam per rectum (0.5-1 mg/kg)
3. Phenobarbital: 2-4 mg/kg IV if diazepam fails
4. Propofol: IV infusion for refractory status epilepticus
5. General anesthesia (isoflurane) as last resort

• Start when: >1 seizure/month, cluster seizures, or status epilepticus
• Phenobarbital: 2-3 mg/kg PO BID - drug of choice in dogs and cats; monitor liver enzymes
• Potassium Bromide (KBr): 20-30 mg/kg/day - used as add-on in dogs (NOT cats - causes bronchitis)
• Imepitoin (Pexion): licensed for idiopathic epilepsy in dogs (Europe)
• Levetiracetam (Keppra): newer drug, useful adjunct, safe in cats
• Zonisamide, Gabapentin: newer options

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2. Brucellosis, Hemorrhagic Septicemia (HS), and Tetanus

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Tetanus (Lockjaw)

Etiology

• Causative agent: Clostridium tetani
• Gram-positive, strict anaerobe, motile, spore-forming rod
• Spores: terminal, spherical - characteristic "drumstick" / "tennis racket" appearance
• Spores are extremely resistant to heat, disinfectants, and survive in soil for decades
• Portal of entry: Deep penetrating wounds (soil-contaminated), castration, docking, parturition, navel in neonates, surgical wounds

Pathogenesis

1. Spores enter deep anaerobic wounds, germinate into vegetative forms
2. Vegetative bacteria produce two exotoxins:
   • Tetanospasmin (neurotoxin - responsible for clinical signs)
   • Tetanolysin (hemolysin)
3. Tetanospasmin is absorbed at the neuromuscular junction and travels retrograde along motor neurons to the spinal cord and brain stem
4. In the spinal cord, it binds to inhibitory interneurons (Renshaw cells) - blocks release of GABA and glycine (inhibitory neurotransmitters)
5. Loss of inhibition leads to uncontrolled, sustained muscle contraction (spasticity)
6. Autonomic nervous system involvement: increased sympathetic activity

Clinical Signs

• Stiffness of gait, "sawhorse stance" (rigid, extended limbs)
• Trismus ("lockjaw") - inability to open the mouth due to masseter spasm
• Risus sardonicus - sardonic grin due to facial muscle spasm
• Prolapse of third eyelid (nictitating membrane) - classic sign in horses
• Hyperesthesia - exaggerated response to stimuli (sound, light, touch)
• Stiff, erect tail ("pump-handle tail")
• Dysphagia (difficulty swallowing)
• Hyperthermia (from muscle activity)
• Respiratory distress (intercostal and diaphragmatic spasm)
• In severe cases: opisthotonus, convulsions, death

• Bloat (rumen atony due to vagal inhibition)
• Similar rigidity, lockjaw, prolapsed nictitating membrane

Diagnosis

• Primarily clinical - based on history of wound + classic clinical signs
• History of recent surgery, wound, castration, parturition
• No specific lab test widely used clinically
• Bacteriological culture of wound material (anaerobic) - isolation of C. tetani
• Mouse neutralization test (for toxin identification)
• Differential diagnosis: Strychnine poisoning (also causes spasms - differentiate by history), hypocalcemia, polioencephalomalacia

Treatment

1. Eliminate the toxin source:
   • Wound debridement and lavage (H2O2, disinfectants to create aerobic environment)
   • Penicillin G (high dose, 20,000-40,000 IU/kg BID for 7-10 days) - kills vegetative organisms
   • Metronidazole is an alternative (better CNS penetration)
2. Neutralize unbound toxin:
   • Tetanus Antitoxin (TAT): Administer as early as possible
   • Equine: 100,000-200,000 IU IV or IM
   • Give around wound + intrathecal (into subarachnoid space) if possible
   • Note: TAT only neutralizes unbound toxin; cannot reverse already-bound toxin
3. Control muscle spasms:
   • Acepromazine + Chlorpromazine (phenothiazines) - reduce excitability
   • Diazepam (benzodiazepine) - enhance GABA activity
   • Methocarbamol (muscle relaxant) - especially in dogs
   • Magnesium sulfate infusion - reduces acetylcholine release and muscle excitability
   • Place animal in quiet, dark room (minimize sensory stimuli)
4. Supportive care:
   • IV fluids and alimentation (nasogastric tube if dysphagia)
   • Urinary catheterization if urine retention
   • Padding to prevent decubital sores in recumbent animals
   • Prevent aspiration pneumonia

• Toxoid vaccination (tetanus toxoid):
  • Primary: 2 doses 4-6 weeks apart, annual booster
  • Foals: vaccinate at 3-4 months (maternal antibodies wane)
• Wound prophylaxis: TAT (passive immunity - immediate but short-lived, 2-3 weeks)
• Proper wound management, good surgical hygiene

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3. Nephritis and Glomerulonephritis

Nephritis - Definition and Overview

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Glomerulonephritis (GN) - Detailed

Etiology / Causes

• Infectious diseases: Ehrlichia canis, Borrelia burgdorferi (Lyme disease), FeLV, FIV, FIP, Dirofilaria immitis (heartworm), Leishmania, Leptospira
• Neoplasia (lymphoma, multiple myeloma)
• Systemic Lupus Erythematosus (SLE)
• Chronic bacterial infections (pyometra, dental disease, osteomyelitis)
• Idiopathic (most common in cats)

• Antibodies against glomerular basement membrane (GBM)

Pathogenesis

1. Chronic antigen-antibody complex formation (e.g., from persistent infection)
2. Immune complexes deposit in glomeruli (mesangium, subendothelial, or subepithelial)
3. Complement activation (C3, C5a) → neutrophil and monocyte recruitment
4. Inflammatory mediators released → damage to glomerular filtration barrier
5. Loss of podocyte foot processes → loss of size and charge selectivity of filtration
6. Proteinuria (protein loss) → hypoalbuminemia → edema/ascites
7. Loss of antithrombin III → hypercoagulability → thromboembolism
8. Progressive glomerular scarring (glomerulosclerosis) → Chronic Kidney Disease (CKD)

Clinical Signs

• Often subclinical initially - discovered on routine urinalysis
• Proteinuria (frothy urine)
• Edema or ascites (from hypoalbuminemia)
• Weight loss, lethargy, anorexia
• PU/PD (polyuria/polydipsia)
• Hypertension - can cause blindness (retinal detachment), neurological signs
• Thromboembolic events (pulmonary thromboembolism, aortic thromboembolism in cats)
• Signs of uremia in advanced cases (vomiting, oral ulcers, encephalopathy)
• Nephrotic Syndrome: proteinuria + hypoalbuminemia + edema/ascites + hypercholesterolemia

Diagnosis

• Urinalysis: persistent proteinuria, hematuria, granular casts
• Urine Protein:Creatinine ratio (UPC): >0.5 in dogs, >0.4 in cats = abnormal; >2 suggests GN
• Serum biochemistry: hypoalbuminemia, azotemia (elevated BUN, creatinine), hypercholesterolemia
• Blood pressure measurement: hypertension common
• Serological tests: rule out underlying causes (Ehrlichia, Leishmania, heartworm antigen test, ANA for SLE)
• Renal biopsy: definitive diagnosis - identifies type of GN (membranous, membranoproliferative, etc.) by light microscopy, electron microscopy, and immunofluorescence (shows immune complex deposits)

Treatment

1. Treat underlying cause (most important - e.g., doxycycline for ehrlichiosis, heartworm treatment)
2. Antiproteinuric therapy:
   • ACE inhibitors (enalapril, benazepril) - reduce glomerular hypertension and proteinuria
   • Angiotensin Receptor Blockers (ARBs) - telmisartan (licensed for cats)
3. Low-protein, low-sodium, omega-3 enriched diet (renal diet)
4. Antithrombotic therapy:
   • Aspirin (low dose) or clopidogrel (Plavix) to prevent thromboembolism
5. Immunosuppressive therapy (controversial; used in immune-mediated cases without infection):
   • Mycophenolate mofetil, cyclosporine
   • Corticosteroids - generally avoided in GN (may worsen proteinuria)
6. Antihypertensive therapy: amlodipine (especially in cats)
7. Manage CKD complications: phosphate restriction, fluid therapy, anti-emetics

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SHORT QUESTIONS

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1. Copper Deficiency - Disease Names

• Primary copper deficiency: Direct dietary deficiency of copper
• Secondary (conditioned) copper deficiency: Normal dietary copper but excess Molybdenum + Sulfate → forms insoluble thiomolybdates → prevents copper absorption (most common cause in ruminants on pasture)

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2. Vitamin A Deficiency - Disease Names

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3. Etiology of Endocarditis (Infective Endocarditis)

• Bacteremia from any source (dental disease, pyometra, skin wounds, IV catheters)
• Pre-existing valvular abnormalities
• Immunosuppression

• Aortic and mitral valves (left-sided) - most common in dogs
• Tricuspid valve - right-sided, associated with IV catheter use

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4. Chronic Kidney Disease (CKD) in Animals

• Glomerulonephritis (immune-mediated)
• Chronic interstitial nephritis (leptospirosis, FIP, chronic bacterial)
• Polycystic kidney disease (PKD - inherited in Persian cats)
• Pyelonephritis (ascending infections)
• Amyloidosis (Abyssinian cats, Shar Pei dogs)
• Renal toxins (aminoglycosides, NSAIDs, lily toxicity in cats, grapes/raisins in dogs)
• Congenital renal dysplasia

• PU/PD (polyuria/polydipsia) - early sign
• Weight loss, muscle wasting, lethargy
• Vomiting, nausea, anorexia
• Uremic signs: oral ulcers (uremic stomatitis), uremic breath (ammonia smell), encephalopathy, seizures
• Anemia (non-regenerative - loss of erythropoietin production)
• Hypertension
• Dehydration
• Pale mucous membranes (anemia)

• BUN, creatinine, SDMA (symmetric dimethylarginine - early marker of GFR decline)
• Urinalysis: isosthenuria (urine SG 1.007-1.015 = loss of concentrating ability), proteinuria, casts
• UPC ratio
• Urinary GGT, retinol-binding protein (tubular markers)
• Renal ultrasound (small, irregular kidneys in CKD)
• Blood pressure
• Phosphorus, potassium levels

1. Renal diet: low protein, low phosphorus, low sodium, omega-3 enriched, increased moisture
2. Phosphate binders: aluminum hydroxide, calcium carbonate (for hyperphosphatemia)
3. IV fluid therapy / subcutaneous fluids (for dehydration)
4. Erythropoietin (darbepoetin): for non-regenerative anemia (CKD-related)
5. Anti-emetics: maropitant (Cerenia), metoclopramide (for nausea/vomiting)
6. ACE inhibitors: enalapril/benazepril (reduce proteinuria, manage hypertension)
7. Amlodipine: for hypertension (especially cats)
8. Potassium supplementation: if hypokalemia
9. H2 blockers/antacids: ranitidine, famotidine (reduce gastric ulcers from uremia)
10. Dialysis/renal transplantation: limited availability; renal transplant used in cats at some centers

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5. Black Quarter (BQ) - Blackleg

• Agent: Clostridium chauvoei
• Affects: Well-nourished young cattle (6 months - 2 years), sheep
• Key signs: Sudden fever, hot crepitant swelling over muscles (thigh, shoulder), lameness, death in 12-48 hrs
• Post-mortem: Dark red-black, dry, spongy muscles with rancid odor and gas
• Diagnosis: FAT (Fluorescent Antibody Test) is fastest confirmatory test
• Treatment: High-dose Penicillin G (poor prognosis once signs appear)
• Prevention: Clostridial toxoid vaccine annually; avoid opening carcasses

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6. Otitis Externa in Dogs

• Most common cause: Malassezia pachydermatis (yeast) + Staphylococcus pseudintermedius
• Classic presentation: Pruritic, malodorous ear; head shaking; dark waxy discharge
• Treatment: Clean ear + topical combination (antifungal + antibiotic + steroid), e.g., Otomax
• Treat underlying cause (allergy, parasites) to prevent recurrence

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7. Urolithiasis in Dogs

Common Urolith Types in Dogs

Etiology / Risk Factors

• Breed predisposition (genetic metabolic defects)
• Diet - high protein, high mineral intake, low water intake
• Urinary tract infections (UTI) - urease-producing bacteria (Staphylococcus, Proteus) → struvite
• Urine concentration (low water intake)
• Urinary pH
• Metabolic disorders (hypercalcemia → calcium oxalate; portosystemic shunts → urate)
• Dalmatians: defective conversion of uric acid to allantoin (lack functional hepatic uricase) → urate stones

Clinical Signs

• Dysuria (straining to urinate, vocalizing)
• Hematuria (blood in urine) - red/pink urine
• Pollakiuria (frequent small urinations)
• Stranguria (painful urination)
• Obstruction (especially males - narrow urethra):
  • Complete obstruction = urinary emergency - signs of uremia (vomiting, depression, collapse)
  • "Blocked bladder" - palpably distended bladder
• Recurrent UTI
• Incontinence

Diagnosis

• Urinalysis: hematuria, pyuria, crystalluria (crystals may indicate urolith type)
• Urine culture and sensitivity (for concurrent UTI)
• Radiography (plain X-ray):
  • Radiopaque stones: struvite, calcium oxalate, calcium phosphate, silica
  • Radiolucent stones: urate, cystine (require contrast studies or ultrasound)
• Abdominal ultrasound: confirms location, size, number; detects radiolucent stones
• Urolith analysis (quantitative): definitive identification after retrieval (dissolution, surgery, voiding urohydropulsion)
• Blood biochemistry: to check for metabolic causes, renal function

Treatment

• Struvite: Prescription dissolution diet (Hill's s/d or Royal Canin Urinary S/O) + antibiotics for infection
• Calcium oxalate: Increased water intake, low-oxalate diet, potassium citrate, hydrochlorothiazide; NO medical dissolution - must be removed
• Urate (Dalmatians): Low-purine diet, urine alkalinization, allopurinol (xanthine oxidase inhibitor)
• Cystine: Low-protein diet, urine alkalinization (sodium bicarbonate), 2-MPG (2-mercaptopropionylglycine) or D-penicillamine

• Increased water intake (wet food, water fountains)
• Specific dissolution/prevention diets based on stone type
• Regular urinalysis monitoring
• Treat UTI promptly
• Manage predisposing metabolic disorders

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Exam Tips:

• Epilepsy drug of choice: Phenobarbital (long-term); Diazepam IV (acute seizure)
• Tetanus toxin travels retrograde in motor neurons; blocks GABA/glycine at Renshaw cells
• GN diagnosis: renal biopsy is gold standard; treat with ACE inhibitors + treat underlying cause
• Copper deficiency in lambs = Swayback/Enzootic Ataxia; in cattle = Falling Disease
• Dalmatians get urate stones (allopurinol is treatment); Calcium oxalate stones = no medical dissolution
• Most common urolith in dogs = Struvite (infection-induced, alkaline urine)