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🐾 CANINE DISTEMPER DISEASE (CDV) — Complete Veterinary Guide

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PART 1 — THE VIRUS ITSELF (Etiology)

What Causes It?

• Family: Paramyxoviridae
• Genus: Morbillivirus
• Type: Single-stranded, negative-sense RNA virus (enveloped)
• Shape: Pleomorphic (not always a fixed shape) — roughly spherical
• Size: 150–250 nm in diameter

• Human Measles Virus (HMV)
• Rinderpest Virus of cattle

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Viral Structure — Know the Proteins

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Viral Lineages

• 17 official lineages have been described worldwide
• An 18th lineage was proposed in India (2019)
• Genetic variation is highest in the H protein gene
• This variation creates challenges for vaccines because old vaccine strains may not perfectly neutralize newer wild strains

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PART 2 — EPIDEMIOLOGY

Who Gets It?

• Domestic dogs (most common)
• Wild dogs, wolves, coyotes, foxes, jackals

• Ferrets (extremely susceptible — often fatal)
• Minks, otters, badgers, wolverines

• Raccoons

• Lions, leopards, tigers, cheetahs — CDV outbreaks have caused mass mortalities in wild lion populations (Serengeti, Tanzania)

• Recent emergence in non-human primates in Brazil (2025 — Santos et al. [PMID: 41287151])

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How Does It Spread? (Transmission)

• Primary route: Direct contact — inhalation of aerosolized respiratory secretions (sneezing, coughing)
• Secondary routes: Contact with infected urine, feces, ocular/nasal discharge
• Virus in environment: CDV is unstable — it dies quickly in the environment at room temperature. However, it survives longer in cold temperatures (below 4°C)
• No insect vectors — only direct animal contact
• Vertical transmission possible: infected pregnant females can pass CDV to puppies (stillbirths, abortions)

• Unvaccinated puppies aged 3–6 months (after maternal antibody wanes)
• Immunocompromised dogs
• Shelter dogs with poor vaccination coverage

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PART 3 — PATHOGENESIS (How CDV Destroys the Body)

Step 1 — Entry and Initial Replication (Days 1–4)

• CDV enters via the respiratory tract (inhaled aerosols)
• The virus uses two main receptors to enter cells:
  • SLAM (Signaling Lymphocyte Activation Molecule) — expressed on immune cells (lymphocytes, macrophages, dendritic cells)
  • Nectin-4 — expressed on epithelial cells of respiratory and GI tracts
• The virus first infects macrophages and dendritic cells in the tonsils and bronchial lymph nodes
• Initial replication = rapid viral multiplication in lymphoid tissue

Step 2 — Primary Viremia (Days 4–6)

• CDV spreads through the bloodstream (inside lymphocytes and monocytes) to all lymphoid organs:
  • Spleen, thymus, lymph nodes, bone marrow, Peyer's patches in the gut
• Severe lymphopenia develops — the virus destroys T and B lymphocytes
• This creates profound immunosuppression — the dog cannot fight CDV or any secondary infection
• Clinical sign at this stage: high fever (40–41°C), lethargy, anorexia

Step 3 — Secondary Viremia (Days 7–14)

• If the dog cannot mount a strong antibody response, the virus escapes lymphoid tissue
• CDV spreads to epithelial cells throughout the body via Nectin-4:
  • Respiratory tract (bronchi, lungs)
  • Gastrointestinal tract
  • Urogenital tract
  • Skin
  • Uvea of the eye
  • Central nervous system

Step 4 — Organ Involvement

• Directly through the olfactory nerve
• Via infected lymphocytes crossing the blood-brain barrier

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The Three Patterns of CDV in the Nervous System

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PART 4 — CLINICAL SIGNS (What You See on Exam)

Phase 1 — Early/Systemic Signs (first 1–2 weeks)

• Biphasic fever — first spike at day 3–6, then returns
• Lethargy and depression
• Loss of appetite (anorexia)
• Serous (watery) nasal discharge → becomes mucopurulent (thick, green-yellow)
• Serous then mucopurulent ocular discharge
• Mild cough
• Lymphopenia on blood work

Phase 2 — Respiratory Signs

• Dry cough → productive moist cough
• Rhinitis, sinusitis
• Bronchopneumonia — crackling lung sounds on auscultation
• Dyspnea (difficulty breathing) in severe cases
• Lung consolidation visible on X-ray

Phase 3 — Gastrointestinal Signs

• Vomiting
• Hemorrhagic or profuse diarrhea
• Dehydration
• Mucous bloody stool in severe cases

Phase 4 — Neurological Signs (can appear weeks to months later)

• Myoclonus (chewing gum seizures) — rhythmic twitching of jaw or limbs — this is PATHOGNOMONIC (unique) for CDV
• Focal or generalized seizures
• Ataxia (wobbly gait, falling)
• Paresis or paralysis (limb weakness)
• Head tilt, circling
• Nystagmus (rapid eye movements)
• Hyperesthesia (increased sensitivity to touch)
• Mental dullness, behavior changes
• Vestibular signs (balance problems)

Clinical pearl: Neurological signs can appear in dogs that seemed to recover from the respiratory phase — this is called "late neurological distemper."

Phase 5 — Other Organ Signs

• Keratoconjunctivitis sicca (dry eye) — CDV destroys the lacrimal gland
• Anterior uveitis (red, painful eye)
• Optic neuritis — sudden blindness
• Chorioretinitis — white/gray lesions visible in the retina on fundoscopy

• Hyperkeratosis of footpads — pads become hard, cracked, dry → this is called "Hard Pad Disease" (old name for CDV)
• Hyperkeratosis of the nose (planum nasale)

• Enamel hypoplasia — permanently pitted, discolored teeth if puppy was infected during tooth development

• Pregnant females: abortion, stillbirths, weak "fading" puppies

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PART 5 — GROSS PATHOLOGY & HISTOPATHOLOGY (What You See at Necropsy)

Gross (macroscopic) Lesions:

• Thymic atrophy — shrunken, pale thymus (especially in puppies)
• Lung consolidation — gray-red firm patches
• Splenomegaly in some cases
• Mucosal erosions in GI tract
• Hard, cracked footpads
• Demyelinating white matter lesions visible in brain cross-sections

Histopathology (Microscopic) Lesions:

• Intranuclear and intracytoplasmic inclusion bodies in epithelial and neuronal cells — CLASSIC finding
  • Lentz inclusion bodies — eosinophilic (pink-staining) inclusions
• Interstitial pneumonia with alveolar infiltration by lymphocytes and macrophages
• Demyelination with gliosis — loss of myelin sheaths in the white matter of the brain and spinal cord
• Perivascular lymphocytic cuffing — cuffs of lymphocytes around blood vessels in the brain
• Meningoencephalitis
• Lymphoid depletion in spleen, thymus, lymph nodes

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PART 6 — DIAGNOSIS

Step 1 — Clinical Suspicion

• Multisystemic signs (respiratory + GI + neurological together)
• Mucopurulent ocular/nasal discharge
• Hard footpads
• Myoclonus (jaw twitching)

Step 2 — Laboratory Testing

Blood Work (CBC + Chemistry)

• Lymphopenia — hallmark finding
• Neutrophilia (if secondary bacterial infection)
• Thrombocytopenia in some cases
• Elevated liver enzymes possible
• Hypoalbuminemia (protein loss through GI)

Specific CDV Tests

Best Samples to Submit:

• Live dog: Conjunctival swab + urine + blood (EDTA) → RT-PCR
• Neurological dog: CSF + blood → RT-PCR
• Dead animal: Tonsil, spleen, lung, brain tissue → IHC + histopathology + FA

Key point: IFA on tissue becomes negative once the dog develops antibodies or if only neurological signs are present. In those cases, CSF RT-PCR is your best tool.

Differential Diagnosis (What Else Could It Be?)

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PART 7 — TREATMENT

1. Keep the dog alive while the immune system fights the virus
2. Control secondary infections
3. Manage neurological and GI signs

Supportive Care

• IV crystalloids (Normal Saline, Lactated Ringer's Solution)
• Correct dehydration, electrolyte imbalances
• Maintain blood pressure
• Rate: based on dehydration percentage + maintenance needs

• Assist feeding if not eating — syringe feeding or nasogastric tube
• High-quality, easily digestible food
• Dogs with GI signs: bland diet (chicken + rice), small frequent meals

• Not to kill CDV (virus is unaffected by antibiotics)
• Target: secondary bacterial pneumonia, urinary tract infections
• Common choices:
  • Amoxicillin-Clavulanate (Clavamox)
  • Enrofloxacin
  • Doxycycline (also anti-inflammatory effects in respiratory tissue)
  • Chloramphenicol (CNS penetration if neuro signs)
• Duration: 7–14 days minimum

• Nebulization with saline ± bronchodilators (Albuterol)
• N-Acetylcysteine (mucolytic) for thick secretions
• Coupage (physiotherapy chest tapping) to mobilize secretions
• Oxygen therapy for dogs with pneumonia (SpO₂ < 94%)

• Anti-emetics: Maropitant (Cerenia), Metoclopramide
• Anti-diarrheal: Metronidazole (also anti-inflammatory)
• GI protectants: Omeprazole, Sucralfate
• Probiotics: help restore normal gut flora

• Phenobarbital — anticonvulsant for seizures (2–5 mg/kg PO BID)
• Potassium bromide — add-on if seizures not controlled
• Diazepam (IV) — for acute status epilepticus
• Methocarbamol — muscle relaxant for severe myoclonus
• For brain edema: Dexamethasone (short-term; controversial due to immunosuppression)

• Artificial tears for keratoconjunctivitis sicca (KCS)
• Antibiotic eye drops (Chloramphenicol, Tobramycin) for secondary bacterial conjunctivitis
• Atropine eye drops for anterior uveitis

• Vitamin A — supports epithelial integrity and immune response
• Vitamin C — antioxidant support
• Vitamin B complex — neurological support

• Ribavirin — shows in vitro activity against CDV, but toxic in dogs (hemolytic anemia, bone marrow suppression). Not routinely used.
• Immunomodulators — Interferon-α (human or feline recombinant): some clinical reports of benefit, especially for neurological CDV. NOT proven in controlled trials.

Isolation Protocol

• ALL suspected CDV cases must be immediately isolated from other dogs
• Barrier nursing: gloves, gown, separate equipment
• CDV is killed by most common disinfectants: bleach (1:32), Virkon, quaternary ammonium compounds
• Virus dies at 50–60°C in minutes

Prognosis

• Dogs that develop myoclonus rarely recover fully — the myoclonus often remains permanent even after the infection resolves
• Overall mortality rate: 50% in dogs showing neurological signs
• Surviving dogs may have permanent neurological deficits, dry eyes, or enamel hypoplasia

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PART 8 — PREVENTION & VACCINATION

Core Vaccine — DHPP / DA2PP

Vaccination Schedule

• First vaccine: 6–8 weeks of age
• Booster: every 3–4 weeks until 16 weeks old (minimum 3 doses)
• Why? — Maternal antibodies (from mother's colostrum) block the vaccine until they wane
• Final puppy dose should be at or after 16 weeks to ensure protection

• Booster: 1 year after last puppy dose
• Then every 3 years (per WSAVA guidelines for MLV vaccines)

• Modified Live Virus (MLV) — most common, most effective. Provides faster and stronger immunity. Risk of post-vaccinal encephalitis is extremely rare but documented.
• Recombinant canary pox-vectored vaccine (e.g., Recombitek) — safer for immunocompromised dogs and wildlife
• Inactivated (killed) vaccines — used less often; require adjuvant; weaker immunity; multiple doses needed
• MLV Measles vaccine — historically used to protect puppies that still have maternal antibodies to CDV; measles virus is antigenically related enough to cross-protect

Vaccine Failure — Why It Happens?

• Vaccination during the "window of susceptibility" when maternal antibodies are too high to allow response but too low to protect
• Inadequate cold chain (vaccine not kept at 2–8°C)
• Dog already infected at time of vaccination
• Antigenic mismatch — increasing concern because wild CDV strains (especially in Asia, Europe, South America) differ significantly from classic Snyder Hill or Lederle vaccine strains in the H protein

Wildlife Control

• In shelters: vaccinate ALL dogs immediately upon intake + booster in 14 days
• Oral bait vaccines are being developed/tested for wild carnivores
• Wildlife populations (lions, wild dogs) remain at high risk because no practical mass vaccination program exists for them

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PART 9 — PRE-SURGICAL ASSESSMENT & POST-SURGICAL CARE IN VETERINARY MEDICINE

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SECTION A — PRE-SURGICAL (Before Surgery)

1. Patient History (Anamnesis)

• Signalment — species, breed, age, sex, weight
• Chief complaint — why is surgery needed?
• Vaccination history — is the dog current on vaccines?
• Medication history — any current drugs? (NSAIDs, anticoagulants, steroids — these affect surgery)
• Previous surgeries — any anesthetic reactions?
• Allergies — to drugs, materials
• Last meal — fasting status
• Reproductive status — intact female? Could be pregnant?
• Diet history, travel history, recent illness

2. Physical Examination (Pre-Op PE)

3. ASA Physical Status Classification (Risk Scoring)

4. Pre-Operative Diagnostic Tests

• CBC (Complete Blood Count): Check for anemia, infection, thrombocytopenia
• Serum Chemistry Panel: Liver (ALT, ALP), kidneys (BUN, creatinine), glucose, electrolytes
• Urinalysis: Kidney function, UTI
• PCV (Packed Cell Volume) + Total Protein: Quick anemia/protein check

• Clotting times (PT, aPTT): If bleeding disorder suspected, or on anticoagulants
• Thoracic X-rays: Lung disease, cardiac size, metastasis check
• Abdominal ultrasound: Organ masses, free fluid
• ECG: Dogs >7 years, or known cardiac disease
• Blood pressure: Hypertensive patients
• Blood type + crossmatch: If major blood loss expected (surgery for splenic rupture, etc.)

5. Fasting (NPO — Nothing by Mouth)

• Food: Withhold for 8–12 hours before surgery
• Water: Can be given up until 2–4 hours before, then withheld
• Purpose: Prevent aspiration of stomach contents under anesthesia (aspiration pneumonia = deadly complication)
• Caution: Neonates and diabetics should NOT be fasted as long — risk of hypoglycemia

6. Pre-Anesthetic Medications (Premedication)

7. IV Catheter Placement

• Place an IV catheter in the cephalic or saphenous vein before induction
• Allows: drug delivery, fluid therapy, emergency drug access

8. Anesthesia Induction

• Propofol IV — most common induction agent in dogs; smooth and controllable
• Alfaxalone — alternative; useful in compromised patients
• After induction: intubate the trachea with an endotracheal tube to:
  • Protect airway from aspiration
  • Deliver inhalant anesthesia (Isoflurane or Sevoflurane)

9. Intraoperative Monitoring

• Heart rate and rhythm (ECG)
• SpO₂ (pulse oximetry) — keep > 95%
• Blood pressure (BP) — keep mean arterial pressure > 60 mmHg
• End-tidal CO₂ (ETCO₂) — keep 35–45 mmHg
• Temperature — keep > 37°C; use warm IV fluids, warming blanket
• Depth of anesthesia — response to stimulus, eye position, jaw tone
• IV fluid rate — maintenance: 5–10 mL/kg/hr during surgery

10. Surgical Site Preparation

• Clip hair widely around the surgical site (at least 5 cm margin)
• Clean with chlorhexidine or povidone-iodine scrub → alternating with sterile saline/alcohol
• Minimum 3 scrub cycles using a spiral-outward motion
• Apply sterile drapes around the surgical field

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SECTION B — TYPES OF VETERINARY SURGERY

• Spay (ovariohysterectomy) and neuter (orchiectomy/castration)
• Lump/mass removal (skin tumors, lipomas)
• GI surgery: foreign body removal, enterotomy, intestinal resection & anastomosis
• Bladder surgery (cystotomy for stones)
• Gastric dilatation-volvulus (GDV) decompression and gastropexy
• Liver/spleen surgery
• Lung lobectomy
• Wound repair and skin grafts
• Hernia repair

• Fracture repair (plates, screws, pins, external fixators)
• TPLO (Tibial Plateau Leveling Osteotomy) for cruciate ligament rupture
• Luxating patella repair
• Femoral head and neck excision (FHO)
• Arthroscopy

• Cherry eye correction
• Enucleation (eye removal)
• Cataract surgery

• Disc surgery (hemilaminectomy for IVDD)

• Tooth extractions, jaw fracture repair

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SECTION C — POST-SURGICAL CARE

1. Recovery Room (Immediate Post-Op — First 1–2 Hours)

• Keep in a quiet, warm, padded area
• Monitor continuously — do not leave alone until fully awake
• Keep in sternal recumbency (chest down, not flat on side) — reduces aspiration risk
• Extubate (remove endotracheal tube) when dog shows swallowing reflexes
• Monitor vital signs every 15 minutes:
  • Temperature (hypothermia is common post-op — keep warm)
  • Heart rate and rhythm
  • Respiratory rate
  • Blood pressure
  • SpO₂
  • Pain score (see below)
• Keep IV catheter in place until dog is stable and alert
• Continue IV fluids until drinking on its own

2. Pain Assessment (Critical Post-Op Skill)

• Glasgow Composite Pain Scale (GCPS) — behavioral indicators
• Colorado State University Acute Pain Scale — visual scale

• Vocalization (whimpering, crying)
• Restlessness, inability to settle
• Hunched posture, guarding the surgical site
• Biting or licking the incision
• Dilated pupils, elevated heart rate
• Aggression when touched near incision

3. Post-Operative Analgesia

4. Wound Care & Incision Monitoring

• Elizabethan collar (E-collar / cone of shame) — must be worn at all times to prevent licking and biting
• Bandaging — especially for orthopedic limb wounds
• Keep incision dry — no bathing until sutures are removed (10–14 days)
• No swimming, no running

5. Activity Restriction

• Strict rest for 10–14 days minimum for soft tissue surgery
• 4–8 weeks for orthopedic surgery
• Short leash walks only for urination/defecation
• No jumping, stairs, rough play
• Baby gates or crate rest to restrict movement

6. Post-Op Medications Typically Prescribed

7. Feeding Post-Surgery

• Withhold food for 2–4 hours after recovery (nausea from anesthesia)
• Offer small amounts of water first
• Gradual return to normal food over 24 hours
• For GI surgery: special liquid diet or easily digestible food for 5–7 days

8. Suture/Staple Removal

• Skin sutures/staples removed at 10–14 days
• Internal (absorbable) sutures dissolve on their own
• At suture removal: reassess wound for complete healing

9. Follow-Up Visits

• 1–3 days post-op: pain check, wound check
• 10–14 days: suture removal
• 4–6 weeks: recheck for orthopedic surgery, healing assessment
• 6–8 weeks: full return to normal activity for major surgery

10. Red Flags — When to Return to the Vet Immediately

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QUICK SUMMARY CARDS

CDV — Key Facts for Exams

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• Jawetz, Melnick & Adelberg's Medical Microbiology 28e (Paramyxoviruses chapter)
• Merck Veterinary Manual — Canine Distemper
• Karki M et al. — Canine morbillivirus (CDV): a review on current status, emergence and diagnostics. Virusdisease 2022 [PMID: 36039286]
• Rivera-Martínez A et al. — Canine Distemper Virus: Origins, Mutations, Diagnosis, and Epidemiology in Mexico. Life 2024 [PMID: 39202744]
• Rendon-Marin S et al. — Safety and Immunogenicity of CDV Vaccines. Viruses 2024 [PMID: 39066240]
• AAHA Anesthesia and Monitoring Guidelines for Dogs and Cats 2020
• VCA Animal Hospitals — Pre-surgical Preparation and Testing
• Preoperative Planning — Veterian Key (veterinary surgery textbook source)

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🐾 CANINE HERPESVIRUS DISEASE (CHV-1) — Complete Veterinary Guide

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PART 1 — THE VIRUS ITSELF (Etiology)

What Causes It?

• Canid Herpesvirus 1 (CaHV-1)
• Varicellovirus canidalpha1 (new official name)

Why Is It Called an Alphaherpesvirus?

1. Fast replication in host cells
2. Wide host cell range — can infect many different cell types
3. Establish latency in nerve ganglia (they hide in the nervous system and never fully leave)

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Viral Structure — Know the Proteins

1. Core — contains the linear dsDNA genome
2. Icosahedral Capsid — protein shell surrounding the genome
3. Tegument — amorphous protein layer between capsid and envelope; contains viral proteins that help take over the host cell immediately after entry
4. Envelope — lipid bilayer (taken from the host cell membrane) studded with glycoproteins

• gB — cell entry (membrane fusion)
• gC — cell attachment to heparan sulfate on host cell surface
• gD — binds specific host entry receptors
• gE and gI — help the virus spread cell-to-cell without being detected by antibodies

• Common disinfectants (bleach, alcohol, iodine, Virkon)
• Detergents and soaps
• Heat above 37°C (very important — this is why temperature management saves neonates)
• Drying (the virus does not survive long outside the host)

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Key Biological Property — Temperature Sensitivity

CHV-1 replicates optimally at 35–36°C (95–97°F)

• Normal adult dog body temperature: 38.5–39.2°C
• This temperature is too high for CHV-1 to replicate effectively — so adult dogs control the infection
• Neonatal puppies CANNOT regulate their own body temperature. Their core body temperature is often 35–36°C — the PERFECT temperature for CHV-1 to multiply
• This is why neonates die and adults survive

• Why only neonates die
• Why warming incubators save puppies
• Why the upper respiratory tract (cooler mucous membranes) and genital tract are the main sites in adults

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PART 2 — EPIDEMIOLOGY

Who Is Affected?

• Domestic dogs — primary and most important host
• Wild canids — wolves, foxes, coyotes, jackals
• Does NOT infect humans, cats, or most other species — host range is restricted to canids

Global Distribution

• In kennels and breeding facilities: 30–100% of dogs — most studies report ~80% seropositive in kennel populations
• In random pet dog populations: 40%+ in European studies; <10% in some US random studies
• The true prevalence is likely underestimated because:
  • Antibody titers drop rapidly after infection (within 1–2 months)
  • Many infections are subclinical
  • Testing is not always done

Who Is Most at Risk?

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PART 3 — TRANSMISSION

How Does CHV-1 Spread?

• Nasal secretions, oral secretions (sniffing, licking, playing)
• Vaginal/preputial secretions (sexual contact, genital licking)
• Urine

• When a puppy passes through an infected birth canal, it is directly exposed to high concentrations of CHV-1 in vaginal secretions
• This is the most common route of infection in neonates

• During acute primary CHV-1 infection in a pregnant bitch
• Virus crosses the placenta and infects the fetuses directly
• Results in: fetal death, abortion, mummification, stillbirth, or premature birth of weak/infected puppies

• Inhalation of infectious aerosols from infected dogs
• Responsible for mild upper respiratory infections in adult dogs

• Via contaminated hands, fomites (equipment, bedding) — but CHV-1 is fragile in the environment, so this is less important than direct contact

• Latently infected adult dogs periodically reactivate and shed virus — often without any visible symptoms
• Triggers for reactivation:
  • Stress (transport, surgery, new environment)
  • Corticosteroid/immunosuppressive drug administration
  • Pregnancy and whelping — the hormonal changes around parturition can reactivate CHV-1 in the mother, exposing her own newborn puppies

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PART 4 — PATHOGENESIS (Step by Step)

In Neonatal Puppies (< 3 weeks)

• Virus enters via the oronasal route (licking the infected mother's mouth/nose), respiratory tract, or during passage through the infected birth canal
• Initial replication in the tonsils and upper respiratory mucosa

• Because the puppy's body temperature (35–36°C) is ideal for CHV-1, the virus replicates explosively
• Virus spreads via the bloodstream to ALL major organs within 24–48 hours

• CHV-1 targets endothelial cells (cells lining blood vessels) and parenchymal cells (working cells of organs)
• The virus causes necrosis (cell death) and hemorrhage in every organ it reaches:
  • Lungs → focal necrosis and hemorrhage → respiratory failure
  • Kidneys (cortex) → necrosis and petechiae
  • Adrenal glands → necrosis
  • Liver → multifocal hepatic necrosis
  • GI tract → hemorrhagic enteritis
  • Lymph nodes → enlargement and necrosis
  • Spleen → splenomegaly and necrosis
  • Brain → meningoencephalitis, cerebellar hypoplasia, necrosis
  • Eyes → retinal necrosis, blindness

• Death usually occurs 24–36 hours after onset of clinical signs
• The incubation period (exposure to first signs) is 4–6 days
• Entire litters can be wiped out within 24 hours

Why Is There No Fever? — CRITICAL EXAM POINT

• There is NO fever (or it is very low-grade)
• Because the puppy's body temperature is already low (35–36°C) — the virus keeps temperature suppressed
• A sick neonatal puppy WITHOUT fever should always raise suspicion for CHV-1
• This is how CHV-1 differs from most other infections

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In Pregnant Bitches (Acute Primary Infection)

• If a bitch has never been exposed to CHV-1 before and gets infected during the last 3 weeks of pregnancy, the virus can:
  • Cross the placenta (transplacental infection)
  • Cause fetal death, mummification, resorption
  • Lead to abortion (spontaneous termination of pregnancy)
  • Cause premature delivery of stillborn or weak, infected puppies
• The bitch herself usually shows no or only mild symptoms (nasal discharge, vaginal discharge)
• If a bitch was previously exposed and has antibodies, she may still reactivate and shed virus during whelping, but her antibodies provide some protection via colostrum to her puppies

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In Adult Dogs (Chronic/Latent Infection)

• After primary infection, CHV-1 retreats to the trigeminal ganglion and becomes latent (dormant)
• The dog's immune system CANNOT eliminate the virus from the ganglion
• Periodically, with stress or immunosuppression → reactivation → virus travels back down the nerve → shedding in oral, nasal, or genital secretions
• This cycle continues for the dog's entire life

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In the Nervous System (Surviving Puppies)

• Puppies aged 3–5 weeks that survive neonatal CHV-1 may develop permanent neurological damage because:
  • The virus damages the developing cerebellum (balance center) → permanent ataxia
  • Damages the optic nerve and retina → permanent blindness
  • Destroys the vestibular apparatus → persistent head tilt, balance problems
  • Causes cerebellar hypoplasia (underdevelopment of the cerebellum)

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PART 5 — CLINICAL SIGNS

A. Neonatal Puppies (< 3 weeks old)

• Persistent, constant crying / vocalization (the puppy cries incessantly — pain from abdominal lesions)
• Anorexia — stops nursing, refuses milk, cannot suckle
• Weakness, depression, lethargy — the puppy becomes limp, soft
• Hypothermia (low body temperature) — cold to touch
• Abdominal pain — abdomen looks distended and painful on palpation
• Nasal discharge — serous to mucopurulent
• Dyspnea / tachypnea — breathing difficulty (lung involvement)
• Soft/yellow-green diarrhea
• Petechiae (pinpoint red hemorrhages) on:
  • Gums (oral mucous membranes)
  • Inner ear flap
  • Conjunctiva (whites of the eyes)
  • Abdomen and skin
• Loss of righting reflex — puppy cannot turn itself over
• No fever (this is pathognomonic — absence of fever in a severely ill neonate)

• Day 0: Exposure (birth or first days of life)
• Day 4–6: First signs appear (crying, not nursing)
• Day 5–7: Rapid deterioration
• Death within 24–36 hours of first visible signs

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B. Puppies 3–5 Weeks Old

• Generally less severe because they can somewhat regulate body temperature
• More likely to survive but with long-term consequences
• Clinical signs:
  • Mild to moderate lethargy, poor growth
  • Mild respiratory signs
  • Some will develop neurological signs as they grow:
    • Ataxia (wobbling, difficulty walking, falling)
    • Blindness (partial or complete)
    • Head tilt (vestibular damage)
    • Deafness (inner ear damage)
    • Cerebellar hypoplasia — puppies that seem "clumsy" even after full recovery

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C. Pregnant Bitches

• Often asymptomatic (no visible illness)
• May show:
  • Mild vaginal discharge (serous or mucopurulent)
  • Mild nasal discharge
  • Lethargy
• Reproductive consequences:
  • Abortion in mid-to-late pregnancy
  • Stillborn puppies
  • Resorption of fetuses (early pregnancy loss)
  • Premature delivery of weak, dying puppies
  • Infertility — repeated pregnancy losses with no other explanation
  • Producing live puppies that rapidly die (fading puppy syndrome)

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D. Adult Dogs (Non-Pregnant)

• Mild upper respiratory infection
• Serous nasal discharge
• Sneezing
• Cough (may be part of "Kennel Cough" / infectious tracheobronchitis complex)
• Tonsillitis
• Usually self-limiting — resolves without treatment

• Females: Vesicular vaginitis — small fluid-filled blisters/vesicles on the vaginal mucosa; reddened, inflamed vaginal lining; mucopurulent vaginal discharge
• Males: Balanoposthitis (posthitis) — vesicles and inflammation of the prepuce and glans penis; discharge from prepuce; dog may lick the area excessively
• Both forms are usually mild and self-limiting

• Conjunctivitis — redness, discharge
• Blepharitis — eyelid inflammation
• Ulcerative keratitis — painful corneal ulcers, often dendritic (branching) pattern — classic herpesvirus corneal ulcer shape
• Non-ulcerative keratitis — corneal cloudiness without open ulcer
• Occurs during primary infection or reactivation
• Particularly important in dogs receiving immunosuppressive drugs (steroids, cyclosporine) — reactivation can cause serious eye disease (Ledbetter, NZ Vet J 2013 [PMID: 23438442]; Soleimani et al. 2025 [PMID: 41259018])

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PART 6 — GROSS PATHOLOGY & HISTOPATHOLOGY

Gross (Macroscopic) Lesions at Necropsy — CLASSIC PICTURE

Disseminated focal necrosis AND hemorrhages throughout multiple organs

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Histopathology (Microscopic Lesions)

• Necrosis in parenchymal cells of affected organs
• Hemorrhage into the adjacent tissue
• Minimal inflammatory reaction — because the immune system is immature and overwhelmed
• Intranuclear inclusion bodies — eosinophilic (pink-staining) inclusions within nuclei of infected cells
  • Cowdry Type A inclusions are typical of herpesviruses
  • Found in epithelial cells of kidneys, liver, lungs, adrenals
• In the brain: meningitis, perivascular cuffing, glial nodules, and neuronal necrosis
• In the eye: retinal necrosis and optic neuritis

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PART 7 — DIAGNOSIS

Step 1 — Clinical Suspicion

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Step 2 — Diagnostic Tests

Post-Mortem (Necropsy) Diagnosis — Most Reliable for Neonates

Ante-Mortem (Live Dog) Diagnosis

• CHV-1 antibody titers drop very quickly — within 1–2 months of infection
• A dog can be actively infected but seronegative (negative antibody test)
• A negative serology does NOT mean a dog is free of CHV-1
• PCR is the preferred diagnostic method for active infection

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Differential Diagnosis — What Else Causes Similar Signs?

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PART 8 — TREATMENT

Critical Reality Check First:

There is no specific licensed antiviral drug approved for CHV-1 treatment in dogs. Treatment is primarily supportive. In neonates, treatment is often unrewarding because the disease progresses within hours.

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Treatment of Neonatal Puppies

1. Warming Therapy — MOST IMPORTANT FIRST STEP

• Raise the puppy's body temperature to 37–38.5°C (98.6–101°F)
• Use:
  • Incubator set to 35°C (95°F) ambient temperature at 50% relative humidity
  • Warming box with a heat lamp
  • Heating pad (be careful — do not burn the puppy; use a towel as a buffer)
• Why it works: CHV-1 cannot replicate efficiently above 37°C. Raising body temperature directly suppresses viral replication.
• This is the single most important intervention in neonatal CHV-1
• Note: Recent evidence suggests warming alone may not fully stop disease progression once signs appear, but it significantly reduces losses in exposed but not-yet-symptomatic littermates

2. Passive Immunization (Hyperimmune Serum)

• Collect serum from a seropositive adult female dog (previously exposed, has antibodies)
• Inject intraperitoneally (IP) into exposed puppies before signs appear
• The maternal antibodies provide passive immunity to neutralize the virus
• This is most effective as prophylaxis (prevention before signs) rather than treatment
• Can also transfer the litter to a seropositive nursing female — her colostrum provides protective antibodies

3. IV/Oral Fluid Therapy

• Dehydration develops rapidly
• Administer warmed fluids:
  • Subcutaneous or intraperitoneal routes in neonates (veins too small for IV in very young pups)
  • Balanced electrolyte solution (Normal Saline or Lactated Ringer's)
  • Add dextrose (glucose) to prevent hypoglycemia
• Rate: Based on hydration status and puppy weight

4. Nutritional Support

• If puppy cannot nurse: tube feeding with puppy milk replacer
• Small, frequent feeds (every 2 hours in neonates)
• Keep warm before and during feeding

5. Antiviral Drugs (Limited Evidence)

• Acyclovir (Zovirax):
  • A nucleoside analogue that inhibits viral DNA polymerase
  • Works well against human herpesviruses
  • In vitro activity against CHV-1 demonstrated
  • Clinical effectiveness in dogs is uncertain — limited studies
  • Can be used as part of treatment but should not be relied upon as the primary intervention
  • Dose: varies; consult a veterinary pharmacologist
  • May be toxic at high doses
• Cidofovir and Ganciclovir — investigated in research settings; not routine clinical use

6. Antibiotics

• CHV-1 is a virus — antibiotics do NOT kill it
• BUT: Use antibiotics to prevent or treat secondary bacterial infections (pneumonia, septicemia) in weakened puppies
• Common choices: Amoxicillin, Ampicillin (IV in neonates)

7. Oxygen Therapy

• For puppies with respiratory distress (lung involvement)
• Use an oxygen cage or flow-by oxygen

8. Supportive Nursing

• Keep puppies clean and dry
• Ensure they are feeding
• Isolate affected puppies from others in the kennel

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Treatment of Adult Dogs

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Prognosis Summary

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PART 9 — PREVENTION & CONTROL

1. Vaccination

• A commercial vaccine exists: Eurican Herpes 205 (Merial/Boehringer Ingelheim)
• Inactivated (killed) CHV-1 vaccine
• Indicated for use in breeding bitches to protect future litters
• Vaccination schedule:
  • First dose: during proestrus/estrus (when the bitch comes into heat)
  • Second dose: 1–2 weeks before expected whelping
  • Revaccinate with every pregnancy
• The vaccine does NOT prevent infection but stimulates high antibody levels in the dam → antibodies passed to puppies in colostrum → passive protection for the litter
• NOT a lifelong vaccine — immunity from CHV-1 antibodies is short-lived (weeks to months), so revaccination with every breeding is necessary

• As of the time of this writing, no licensed CHV-1 vaccine is available in the USA
• Prevention relies on management practices

2. Management Practices (Most Important in Non-Vaccinated Countries)

• Isolate the pregnant bitch for the last 3 weeks of gestation — away from all other dogs
• Keep the dam and puppies isolated for 3 weeks after birth
• This prevents exposure to shedding carrier dogs during the most vulnerable period
• The litter's "safe window" is: from 3 weeks before birth to 3 weeks after birth

• Keep the whelping environment at 29–32°C (84–90°F) ambient temperature for the first 2 weeks
• Puppies should not drop below 35.5°C (96°F) body temperature
• Use a thermometer to check puppy body temperatures regularly
• Incubator, heat lamp, or under-blanket heating mat are acceptable

• Ensure every puppy nurses within the first 12–24 hours of life to receive maternal antibodies via colostrum
• If dam is known seronegative (no antibodies), consider sourcing colostrum from a seropositive female

• Disinfect whelping box and equipment with bleach (1:30 dilution) or Virkon
• Wash hands thoroughly between handling litters
• Do not share equipment between litters

• Test breeding dogs for CHV-1 via PCR (swabs) or serology before breeding
• Paired serology (2 samples 2–3 weeks apart) showing seroconversion confirms recent active infection

• Minimize stress for breeding dogs — stress is the main trigger for viral reactivation
• Avoid transporting pregnant bitches to new environments
• Provide stable, calm whelping environments

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PART 10 — LATENCY AND REACTIVATION (Advanced Concept)

Where Does the Virus Hide?

What Triggers Reactivation?

What Happens During Reactivation?

• Virus travels back down the nerve to the mucosal surface
• Dog begins shedding virus in oral, nasal, or genital secretions
• Often completely asymptomatic — the dog looks healthy but is spreading virus
• This is why CHV-1 persists in dog populations despite vaccination efforts — seroprevalence approaches 80% in kennels because most infected adult carriers shed periodically without owners knowing
• It is biologically impossible to eradicate CHV-1 from a kennel once it is present

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PART 11 — QUICK REFERENCE SUMMARY TABLE

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PART 12 — FREQUENTLY ASKED QUESTIONS (FAQ)

Questions from Pet Owners:

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1. Isolation — keep the pregnant bitch away from all other dogs for the last 3 weeks before whelping
2. Vaccinate (if you are in Europe — Eurican Herpes vaccine with each pregnancy)
3. Whelping box temperature — keep it warm (29–32°C ambient) so puppies maintain a body temperature > 37°C
4. Ensure puppies nurse within 12 hours of birth for colostrum protection

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• Start warming therapy immediately
• Administer hyperimmune serum if available
• Provide fluid and glucose support
• Run PCR testing for confirmation

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• Perform PCR of nasal, oral, and vaginal swabs to check for active shedding
• Run serology (ELISA) to check antibody status
• If seronegative: protect the bitch carefully during breeding and pregnancy from exposure
• If seropositive: she carries the virus; vaccination (where available) before each pregnancy is recommended

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• Merck Veterinary Manual — Canine Herpesvirus Infection
• Decaro N, Martella V, Buonavoglia C — Canine adenoviruses and herpesvirus. Vet Clin North Am Small Anim Pract 2008 [PMID: 18501279]
• Ledbetter EC — Canine herpesvirus-1 ocular diseases of mature dogs. NZ Vet J 2013 [PMID: 23438442]
• Soleimani S et al. — Prevalence and Clinical Impacts of CHV-1 in Dogs: A Review. Vet Med Sci 2025 [PMID: 41259018]
• Dr. Emmanuel Fontaine — Why Is Canine Herpes So Hard to Eliminate? (2026)
• AKC — Canine Herpes Virus: What Breeders Should Know
• Texas A&M Veterinary Medical Diagnostic Laboratory — CHV Case Studies (2024)
• Jawetz, Melnick & Adelberg's Medical Microbiology 28e (Herpesviridae classification)

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Topic map: Veterinary Corneal Ulcers

1. Corneal anatomy and normal healing
   • Epithelium, stroma, Descemet's membrane, endothelium
   • Why corneal ulcers are painful and how they heal
2. Definition and classification
   • Superficial epithelial ulcers
   • Stromal ulcers
   • Deep ulcers, descemetoceles, and corneal perforation
   • Simple, complicated, melting, indolent, infected, and traumatic ulcers
3. Causes and risk factors
   • Trauma, foreign bodies, dry eye, eyelid abnormalities, infection, breed predisposition, chemical injury, and neurologic disease
4. Clinical signs and ophthalmic examination
   • Blepharospasm, epiphora, photophobia, fluorescein staining, Schirmer tear test, tonometry, eyelid examination, and corneal sensation
5. Diagnostics and differential diagnosis
   • Cytology, bacterial culture and susceptibility testing
   • How to differentiate ulceration from uveitis, glaucoma, conjunctivitis, keratitis, herpesvirus disease, and corneal sequestrum
6. Medical treatment
   • Pain relief, topical antimicrobials, anticollagenase therapy, atropine, lubrication, systemic analgesia
   • Safe versus dangerous drugs
   • Drug dose ranges and monitoring principles, species-specific cautions
7. Melting ulcers and emergency management
   • What "melting" means, why it can progress quickly, stabilization, and when referral is urgent
8. Surgical treatment
   • Debridement, diamond burr, grid keratotomy, conjunctival grafts, corneoconjunctival transposition, amniotic membrane, and keratoplasty
   • Indications and complications
9. Species-specific chapters
   • Dogs: including brachycephalic ocular syndrome and indolent ulcers
   • Cats: feline herpesvirus-1, sequestrum, and eosinophilic keratitis
   • Horses and other species if you need them
10. Aftercare, prognosis, prevention, client communication

• Recheck schedule, Elizabethan collar, owner warnings, recurrence prevention

1. Cases, exam questions, and client FAQs

• Case-based decision making from history through treatment
• Interview and viva questions with answers

High-level overview

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🐾 CANINE DISTEMPER DISEASE (CDV) — Complete Veterinary Guide

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PART 1 — THE VIRUS ITSELF (Etiology)

What Causes It?

• Family: Paramyxoviridae
• Genus: Morbillivirus
• Type: Single-stranded, negative-sense RNA virus (enveloped)
• Shape: Pleomorphic (not always a fixed shape) — roughly spherical
• Size: 150–250 nm in diameter

• Human Measles Virus (HMV)
• Rinderpest Virus of cattle

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Viral Structure — Know the Proteins

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Viral Lineages

• 17 official lineages have been described worldwide
• An 18th lineage was proposed in India (2019)
• Genetic variation is highest in the H protein gene
• This variation creates challenges for vaccines because old vaccine strains may not perfectly neutralize newer wild strains

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PART 2 — EPIDEMIOLOGY

Who Gets It?

• Domestic dogs (most common)
• Wild dogs, wolves, coyotes, foxes, jackals

• Ferrets (extremely susceptible — often fatal)
• Minks, otters, badgers, wolverines

• Raccoons

• Lions, leopards, tigers, cheetahs — CDV outbreaks have caused mass mortalities in wild lion populations (Serengeti, Tanzania)

• Recent emergence in non-human primates in Brazil (2025 — Santos et al. [PMID: 41287151])

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How Does It Spread? (Transmission)

• Primary route: Direct contact — inhalation of aerosolized respiratory secretions (sneezing, coughing)
• Secondary routes: Contact with infected urine, feces, ocular/nasal discharge
• Virus in environment: CDV is unstable — it dies quickly in the environment at room temperature. However, it survives longer in cold temperatures (below 4°C)
• No insect vectors — only direct animal contact
• Vertical transmission possible: infected pregnant females can pass CDV to puppies (stillbirths, abortions)

• Unvaccinated puppies aged 3–6 months (after maternal antibody wanes)
• Immunocompromised dogs
• Shelter dogs with poor vaccination coverage

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PART 3 — PATHOGENESIS (How CDV Destroys the Body)

Step 1 — Entry and Initial Replication (Days 1–4)

• CDV enters via the respiratory tract (inhaled aerosols)
• The virus uses two main receptors to enter cells:
  • SLAM (Signaling Lymphocyte Activation Molecule) — expressed on immune cells (lymphocytes, macrophages, dendritic cells)
  • Nectin-4 — expressed on epithelial cells of respiratory and GI tracts
• The virus first infects macrophages and dendritic cells in the tonsils and bronchial lymph nodes
• Initial replication = rapid viral multiplication in lymphoid tissue

Step 2 — Primary Viremia (Days 4–6)

• CDV spreads through the bloodstream (inside lymphocytes and monocytes) to all lymphoid organs:
  • Spleen, thymus, lymph nodes, bone marrow, Peyer's patches in the gut
• Severe lymphopenia develops — the virus destroys T and B lymphocytes
• This creates profound immunosuppression — the dog cannot fight CDV or any secondary infection
• Clinical sign at this stage: high fever (40–41°C), lethargy, anorexia

Step 3 — Secondary Viremia (Days 7–14)

• If the dog cannot mount a strong antibody response, the virus escapes lymphoid tissue
• CDV spreads to epithelial cells throughout the body via Nectin-4:
  • Respiratory tract (bronchi, lungs)
  • Gastrointestinal tract
  • Urogenital tract
  • Skin
  • Uvea of the eye
  • Central nervous system

Step 4 — Organ Involvement

• Directly through the olfactory nerve
• Via infected lymphocytes crossing the blood-brain barrier

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The Three Patterns of CDV in the Nervous System

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PART 4 — CLINICAL SIGNS (What You See on Exam)

Phase 1 — Early/Systemic Signs (first 1–2 weeks)

• Biphasic fever — first spike at day 3–6, then returns
• Lethargy and depression
• Loss of appetite (anorexia)
• Serous (watery) nasal discharge → becomes mucopurulent (thick, green-yellow)
• Serous then mucopurulent ocular discharge
• Mild cough
• Lymphopenia on blood work

Phase 2 — Respiratory Signs

• Dry cough → productive moist cough
• Rhinitis, sinusitis
• Bronchopneumonia — crackling lung sounds on auscultation
• Dyspnea (difficulty breathing) in severe cases
• Lung consolidation visible on X-ray

Phase 3 — Gastrointestinal Signs

• Vomiting
• Hemorrhagic or profuse diarrhea
• Dehydration
• Mucous bloody stool in severe cases

Phase 4 — Neurological Signs (can appear weeks to months later)

• Myoclonus (chewing gum seizures) — rhythmic twitching of jaw or limbs — this is PATHOGNOMONIC (unique) for CDV
• Focal or generalized seizures
• Ataxia (wobbly gait, falling)
• Paresis or paralysis (limb weakness)
• Head tilt, circling
• Nystagmus (rapid eye movements)
• Hyperesthesia (increased sensitivity to touch)
• Mental dullness, behavior changes
• Vestibular signs (balance problems)

Clinical pearl: Neurological signs can appear in dogs that seemed to recover from the respiratory phase — this is called "late neurological distemper."

Phase 5 — Other Organ Signs

• Keratoconjunctivitis sicca (dry eye) — CDV destroys the lacrimal gland
• Anterior uveitis (red, painful eye)
• Optic neuritis — sudden blindness
• Chorioretinitis — white/gray lesions visible in the retina on fundoscopy

• Hyperkeratosis of footpads — pads become hard, cracked, dry → this is called "Hard Pad Disease" (old name for CDV)
• Hyperkeratosis of the nose (planum nasale)

• Enamel hypoplasia — permanently pitted, discolored teeth if puppy was infected during tooth development

• Pregnant females: abortion, stillbirths, weak "fading" puppies

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PART 5 — GROSS PATHOLOGY & HISTOPATHOLOGY (What You See at Necropsy)

Gross (macroscopic) Lesions:

• Thymic atrophy — shrunken, pale thymus (especially in puppies)
• Lung consolidation — gray-red firm patches
• Splenomegaly in some cases
• Mucosal erosions in GI tract
• Hard, cracked footpads
• Demyelinating white matter lesions visible in brain cross-sections

Histopathology (Microscopic) Lesions:

• Intranuclear and intracytoplasmic inclusion bodies in epithelial and neuronal cells — CLASSIC finding
  • Lentz inclusion bodies — eosinophilic (pink-staining) inclusions
• Interstitial pneumonia with alveolar infiltration by lymphocytes and macrophages
• Demyelination with gliosis — loss of myelin sheaths in the white matter of the brain and spinal cord
• Perivascular lymphocytic cuffing — cuffs of lymphocytes around blood vessels in the brain
• Meningoencephalitis
• Lymphoid depletion in spleen, thymus, lymph nodes

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PART 6 — DIAGNOSIS

Step 1 — Clinical Suspicion

• Multisystemic signs (respiratory + GI + neurological together)
• Mucopurulent ocular/nasal discharge
• Hard footpads
• Myoclonus (jaw twitching)

Step 2 — Laboratory Testing

Blood Work (CBC + Chemistry)

• Lymphopenia — hallmark finding
• Neutrophilia (if secondary bacterial infection)
• Thrombocytopenia in some cases
• Elevated liver enzymes possible
• Hypoalbuminemia (protein loss through GI)

Specific CDV Tests

Best Samples to Submit:

• Live dog: Conjunctival swab + urine + blood (EDTA) → RT-PCR
• Neurological dog: CSF + blood → RT-PCR
• Dead animal: Tonsil, spleen, lung, brain tissue → IHC + histopathology + FA

Key point: IFA on tissue becomes negative once the dog develops antibodies or if only neurological signs are present. In those cases, CSF RT-PCR is your best tool.

Differential Diagnosis (What Else Could It Be?)

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PART 7 — TREATMENT

1. Keep the dog alive while the immune system fights the virus
2. Control secondary infections
3. Manage neurological and GI signs

Supportive Care

• IV crystalloids (Normal Saline, Lactated Ringer's Solution)
• Correct dehydration, electrolyte imbalances
• Maintain blood pressure
• Rate: based on dehydration percentage + maintenance needs

• Assist feeding if not eating — syringe feeding or nasogastric tube
• High-quality, easily digestible food
• Dogs with GI signs: bland diet (chicken + rice), small frequent meals

• Not to kill CDV (virus is unaffected by antibiotics)
• Target: secondary bacterial pneumonia, urinary tract infections
• Common choices:
  • Amoxicillin-Clavulanate (Clavamox)
  • Enrofloxacin
  • Doxycycline (also anti-inflammatory effects in respiratory tissue)
  • Chloramphenicol (CNS penetration if neuro signs)
• Duration: 7–14 days minimum

• Nebulization with saline ± bronchodilators (Albuterol)
• N-Acetylcysteine (mucolytic) for thick secretions
• Coupage (physiotherapy chest tapping) to mobilize secretions
• Oxygen therapy for dogs with pneumonia (SpO₂ < 94%)

• Anti-emetics: Maropitant (Cerenia), Metoclopramide
• Anti-diarrheal: Metronidazole (also anti-inflammatory)
• GI protectants: Omeprazole, Sucralfate
• Probiotics: help restore normal gut flora

• Phenobarbital — anticonvulsant for seizures (2–5 mg/kg PO BID)
• Potassium bromide — add-on if seizures not controlled
• Diazepam (IV) — for acute status epilepticus
• Methocarbamol — muscle relaxant for severe myoclonus
• For brain edema: Dexamethasone (short-term; controversial due to immunosuppression)

• Artificial tears for keratoconjunctivitis sicca (KCS)
• Antibiotic eye drops (Chloramphenicol, Tobramycin) for secondary bacterial conjunctivitis
• Atropine eye drops for anterior uveitis

• Vitamin A — supports epithelial integrity and immune response
• Vitamin C — antioxidant support
• Vitamin B complex — neurological support

• Ribavirin — shows in vitro activity against CDV, but toxic in dogs (hemolytic anemia, bone marrow suppression). Not routinely used.
• Immunomodulators — Interferon-α (human or feline recombinant): some clinical reports of benefit, especially for neurological CDV. NOT proven in controlled trials.

Isolation Protocol

• ALL suspected CDV cases must be immediately isolated from other dogs
• Barrier nursing: gloves, gown, separate equipment
• CDV is killed by most common disinfectants: bleach (1:32), Virkon, quaternary ammonium compounds
• Virus dies at 50–60°C in minutes

Prognosis

• Dogs that develop myoclonus rarely recover fully — the myoclonus often remains permanent even after the infection resolves
• Overall mortality rate: 50% in dogs showing neurological signs
• Surviving dogs may have permanent neurological deficits, dry eyes, or enamel hypoplasia

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PART 8 — PREVENTION & VACCINATION

Core Vaccine — DHPP / DA2PP

Vaccination Schedule

• First vaccine: 6–8 weeks of age
• Booster: every 3–4 weeks until 16 weeks old (minimum 3 doses)
• Why? — Maternal antibodies (from mother's colostrum) block the vaccine until they wane
• Final puppy dose should be at or after 16 weeks to ensure protection

• Booster: 1 year after last puppy dose
• Then every 3 years (per WSAVA guidelines for MLV vaccines)

• Modified Live Virus (MLV) — most common, most effective. Provides faster and stronger immunity. Risk of post-vaccinal encephalitis is extremely rare but documented.
• Recombinant canary pox-vectored vaccine (e.g., Recombitek) — safer for immunocompromised dogs and wildlife
• Inactivated (killed) vaccines — used less often; require adjuvant; weaker immunity; multiple doses needed
• MLV Measles vaccine — historically used to protect puppies that still have maternal antibodies to CDV; measles virus is antigenically related enough to cross-protect

Vaccine Failure — Why It Happens?

• Vaccination during the "window of susceptibility" when maternal antibodies are too high to allow response but too low to protect
• Inadequate cold chain (vaccine not kept at 2–8°C)
• Dog already infected at time of vaccination
• Antigenic mismatch — increasing concern because wild CDV strains (especially in Asia, Europe, South America) differ significantly from classic Snyder Hill or Lederle vaccine strains in the H protein

Wildlife Control

• In shelters: vaccinate ALL dogs immediately upon intake + booster in 14 days
• Oral bait vaccines are being developed/tested for wild carnivores
• Wildlife populations (lions, wild dogs) remain at high risk because no practical mass vaccination program exists for them

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PART 9 — PRE-SURGICAL ASSESSMENT & POST-SURGICAL CARE IN VETERINARY MEDICINE

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SECTION A — PRE-SURGICAL (Before Surgery)

1. Patient History (Anamnesis)

• Signalment — species, breed, age, sex, weight
• Chief complaint — why is surgery needed?
• Vaccination history — is the dog current on vaccines?
• Medication history — any current drugs? (NSAIDs, anticoagulants, steroids — these affect surgery)
• Previous surgeries — any anesthetic reactions?
• Allergies — to drugs, materials
• Last meal — fasting status
• Reproductive status — intact female? Could be pregnant?
• Diet history, travel history, recent illness

2. Physical Examination (Pre-Op PE)

3. ASA Physical Status Classification (Risk Scoring)

4. Pre-Operative Diagnostic Tests

• CBC (Complete Blood Count): Check for anemia, infection, thrombocytopenia
• Serum Chemistry Panel: Liver (ALT, ALP), kidneys (BUN, creatinine), glucose, electrolytes
• Urinalysis: Kidney function, UTI
• PCV (Packed Cell Volume) + Total Protein: Quick anemia/protein check

• Clotting times (PT, aPTT): If bleeding disorder suspected, or on anticoagulants
• Thoracic X-rays: Lung disease, cardiac size, metastasis check
• Abdominal ultrasound: Organ masses, free fluid
• ECG: Dogs >7 years, or known cardiac disease
• Blood pressure: Hypertensive patients
• Blood type + crossmatch: If major blood loss expected (surgery for splenic rupture, etc.)

5. Fasting (NPO — Nothing by Mouth)

• Food: Withhold for 8–12 hours before surgery
• Water: Can be given up until 2–4 hours before, then withheld
• Purpose: Prevent aspiration of stomach contents under anesthesia (aspiration pneumonia = deadly complication)
• Caution: Neonates and diabetics should NOT be fasted as long — risk of hypoglycemia

6. Pre-Anesthetic Medications (Premedication)

7. IV Catheter Placement

• Place an IV catheter in the cephalic or saphenous vein before induction
• Allows: drug delivery, fluid therapy, emergency drug access

8. Anesthesia Induction

• Propofol IV — most common induction agent in dogs; smooth and controllable
• Alfaxalone — alternative; useful in compromised patients
• After induction: intubate the trachea with an endotracheal tube to:
  • Protect airway from aspiration
  • Deliver inhalant anesthesia (Isoflurane or Sevoflurane)

9. Intraoperative Monitoring

• Heart rate and rhythm (ECG)
• SpO₂ (pulse oximetry) — keep > 95%
• Blood pressure (BP) — keep mean arterial pressure > 60 mmHg
• End-tidal CO₂ (ETCO₂) — keep 35–45 mmHg
• Temperature — keep > 37°C; use warm IV fluids, warming blanket
• Depth of anesthesia — response to stimulus, eye position, jaw tone
• IV fluid rate — maintenance: 5–10 mL/kg/hr during surgery

10. Surgical Site Preparation

• Clip hair widely around the surgical site (at least 5 cm margin)
• Clean with chlorhexidine or povidone-iodine scrub → alternating with sterile saline/alcohol
• Minimum 3 scrub cycles using a spiral-outward motion
• Apply sterile drapes around the surgical field

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SECTION B — TYPES OF VETERINARY SURGERY

• Spay (ovariohysterectomy) and neuter (orchiectomy/castration)
• Lump/mass removal (skin tumors, lipomas)
• GI surgery: foreign body removal, enterotomy, intestinal resection & anastomosis
• Bladder surgery (cystotomy for stones)
• Gastric dilatation-volvulus (GDV) decompression and gastropexy
• Liver/spleen surgery
• Lung lobectomy
• Wound repair and skin grafts
• Hernia repair

• Fracture repair (plates, screws, pins, external fixators)
• TPLO (Tibial Plateau Leveling Osteotomy) for cruciate ligament rupture
• Luxating patella repair
• Femoral head and neck excision (FHO)
• Arthroscopy

• Cherry eye correction
• Enucleation (eye removal)
• Cataract surgery

• Disc surgery (hemilaminectomy for IVDD)

• Tooth extractions, jaw fracture repair

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SECTION C — POST-SURGICAL CARE

1. Recovery Room (Immediate Post-Op — First 1–2 Hours)

• Keep in a quiet, warm, padded area
• Monitor continuously — do not leave alone until fully awake
• Keep in sternal recumbency (chest down, not flat on side) — reduces aspiration risk
• Extubate (remove endotracheal tube) when dog shows swallowing reflexes
• Monitor vital signs every 15 minutes:
  • Temperature (hypothermia is common post-op — keep warm)
  • Heart rate and rhythm
  • Respiratory rate
  • Blood pressure
  • SpO₂
  • Pain score (see below)
• Keep IV catheter in place until dog is stable and alert
• Continue IV fluids until drinking on its own

2. Pain Assessment (Critical Post-Op Skill)

• Glasgow Composite Pain Scale (GCPS) — behavioral indicators
• Colorado State University Acute Pain Scale — visual scale

• Vocalization (whimpering, crying)
• Restlessness, inability to settle
• Hunched posture, guarding the surgical site
• Biting or licking the incision
• Dilated pupils, elevated heart rate
• Aggression when touched near incision

3. Post-Operative Analgesia

4. Wound Care & Incision Monitoring

• Elizabethan collar (E-collar / cone of shame) — must be worn at all times to prevent licking and biting
• Bandaging — especially for orthopedic limb wounds
• Keep incision dry — no bathing until sutures are removed (10–14 days)
• No swimming, no running

5. Activity Restriction

• Strict rest for 10–14 days minimum for soft tissue surgery
• 4–8 weeks for orthopedic surgery
• Short leash walks only for urination/defecation
• No jumping, stairs, rough play
• Baby gates or crate rest to restrict movement

6. Post-Op Medications Typically Prescribed

7. Feeding Post-Surgery

• Withhold food for 2–4 hours after recovery (nausea from anesthesia)
• Offer small amounts of water first
• Gradual return to normal food over 24 hours
• For GI surgery: special liquid diet or easily digestible food for 5–7 days

8. Suture/Staple Removal

• Skin sutures/staples removed at 10–14 days
• Internal (absorbable) sutures dissolve on their own
• At suture removal: reassess wound for complete healing

9. Follow-Up Visits

• 1–3 days post-op: pain check, wound check
• 10–14 days: suture removal
• 4–6 weeks: recheck for orthopedic surgery, healing assessment
• 6–8 weeks: full return to normal activity for major surgery

10. Red Flags — When to Return to the Vet Immediately

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QUICK SUMMARY CARDS

CDV — Key Facts for Exams

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• Jawetz, Melnick & Adelberg's Medical Microbiology 28e (Paramyxoviruses chapter)
• Merck Veterinary Manual — Canine Distemper
• Karki M et al. — Canine morbillivirus (CDV): a review on current status, emergence and diagnostics. Virusdisease 2022 [PMID: 36039286]
• Rivera-Martínez A et al. — Canine Distemper Virus: Origins, Mutations, Diagnosis, and Epidemiology in Mexico. Life 2024 [PMID: 39202744]
• Rendon-Marin S et al. — Safety and Immunogenicity of CDV Vaccines. Viruses 2024 [PMID: 39066240]
• AAHA Anesthesia and Monitoring Guidelines for Dogs and Cats 2020
• VCA Animal Hospitals — Pre-surgical Preparation and Testing
• Preoperative Planning — Veterian Key (veterinary surgery textbook source)

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🐾 CANINE HERPESVIRUS DISEASE (CHV-1) — Complete Veterinary Guide

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PART 1 — THE VIRUS ITSELF (Etiology)

What Causes It?

• Canid Herpesvirus 1 (CaHV-1)
• Varicellovirus canidalpha1 (new official name)

Why Is It Called an Alphaherpesvirus?

1. Fast replication in host cells
2. Wide host cell range — can infect many different cell types
3. Establish latency in nerve ganglia (they hide in the nervous system and never fully leave)

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Viral Structure — Know the Proteins

1. Core — contains the linear dsDNA genome
2. Icosahedral Capsid — protein shell surrounding the genome
3. Tegument — amorphous protein layer between capsid and envelope; contains viral proteins that help take over the host cell immediately after entry
4. Envelope — lipid bilayer (taken from the host cell membrane) studded with glycoproteins

• gB — cell entry (membrane fusion)
• gC — cell attachment to heparan sulfate on host cell surface
• gD — binds specific host entry receptors
• gE and gI — help the virus spread cell-to-cell without being detected by antibodies

• Common disinfectants (bleach, alcohol, iodine, Virkon)
• Detergents and soaps
• Heat above 37°C (very important — this is why temperature management saves neonates)
• Drying (the virus does not survive long outside the host)

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Key Biological Property — Temperature Sensitivity

CHV-1 replicates optimally at 35–36°C (95–97°F)

• Normal adult dog body temperature: 38.5–39.2°C
• This temperature is too high for CHV-1 to replicate effectively — so adult dogs control the infection
• Neonatal puppies CANNOT regulate their own body temperature. Their core body temperature is often 35–36°C — the PERFECT temperature for CHV-1 to multiply
• This is why neonates die and adults survive

• Why only neonates die
• Why warming incubators save puppies
• Why the upper respiratory tract (cooler mucous membranes) and genital tract are the main sites in adults

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PART 2 — EPIDEMIOLOGY

Who Is Affected?

• Domestic dogs — primary and most important host
• Wild canids — wolves, foxes, coyotes, jackals
• Does NOT infect humans, cats, or most other species — host range is restricted to canids

Global Distribution

• In kennels and breeding facilities: 30–100% of dogs — most studies report ~80% seropositive in kennel populations
• In random pet dog populations: 40%+ in European studies; <10% in some US random studies
• The true prevalence is likely underestimated because:
  • Antibody titers drop rapidly after infection (within 1–2 months)
  • Many infections are subclinical
  • Testing is not always done

Who Is Most at Risk?

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PART 3 — TRANSMISSION

How Does CHV-1 Spread?

• Nasal secretions, oral secretions (sniffing, licking, playing)
• Vaginal/preputial secretions (sexual contact, genital licking)
• Urine

• When a puppy passes through an infected birth canal, it is directly exposed to high concentrations of CHV-1 in vaginal secretions
• This is the most common route of infection in neonates

• During acute primary CHV-1 infection in a pregnant bitch
• Virus crosses the placenta and infects the fetuses directly
• Results in: fetal death, abortion, mummification, stillbirth, or premature birth of weak/infected puppies

• Inhalation of infectious aerosols from infected dogs
• Responsible for mild upper respiratory infections in adult dogs

• Via contaminated hands, fomites (equipment, bedding) — but CHV-1 is fragile in the environment, so this is less important than direct contact

• Latently infected adult dogs periodically reactivate and shed virus — often without any visible symptoms
• Triggers for reactivation:
  • Stress (transport, surgery, new environment)
  • Corticosteroid/immunosuppressive drug administration
  • Pregnancy and whelping — the hormonal changes around parturition can reactivate CHV-1 in the mother, exposing her own newborn puppies

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PART 4 — PATHOGENESIS (Step by Step)

In Neonatal Puppies (< 3 weeks)

• Virus enters via the oronasal route (licking the infected mother's mouth/nose), respiratory tract, or during passage through the infected birth canal
• Initial replication in the tonsils and upper respiratory mucosa

• Because the puppy's body temperature (35–36°C) is ideal for CHV-1, the virus replicates explosively
• Virus spreads via the bloodstream to ALL major organs within 24–48 hours

• CHV-1 targets endothelial cells (cells lining blood vessels) and parenchymal cells (working cells of organs)
• The virus causes necrosis (cell death) and hemorrhage in every organ it reaches:
  • Lungs → focal necrosis and hemorrhage → respiratory failure
  • Kidneys (cortex) → necrosis and petechiae
  • Adrenal glands → necrosis
  • Liver → multifocal hepatic necrosis
  • GI tract → hemorrhagic enteritis
  • Lymph nodes → enlargement and necrosis
  • Spleen → splenomegaly and necrosis
  • Brain → meningoencephalitis, cerebellar hypoplasia, necrosis
  • Eyes → retinal necrosis, blindness

• Death usually occurs 24–36 hours after onset of clinical signs
• The incubation period (exposure to first signs) is 4–6 days
• Entire litters can be wiped out within 24 hours

Why Is There No Fever? — CRITICAL EXAM POINT

• There is NO fever (or it is very low-grade)
• Because the puppy's body temperature is already low (35–36°C) — the virus keeps temperature suppressed
• A sick neonatal puppy WITHOUT fever should always raise suspicion for CHV-1
• This is how CHV-1 differs from most other infections

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In Pregnant Bitches (Acute Primary Infection)

• If a bitch has never been exposed to CHV-1 before and gets infected during the last 3 weeks of pregnancy, the virus can:
  • Cross the placenta (transplacental infection)
  • Cause fetal death, mummification, resorption
  • Lead to abortion (spontaneous termination of pregnancy)
  • Cause premature delivery of stillborn or weak, infected puppies
• The bitch herself usually shows no or only mild symptoms (nasal discharge, vaginal discharge)
• If a bitch was previously exposed and has antibodies, she may still reactivate and shed virus during whelping, but her antibodies provide some protection via colostrum to her puppies

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In Adult Dogs (Chronic/Latent Infection)

• After primary infection, CHV-1 retreats to the trigeminal ganglion and becomes latent (dormant)
• The dog's immune system CANNOT eliminate the virus from the ganglion
• Periodically, with stress or immunosuppression → reactivation → virus travels back down the nerve → shedding in oral, nasal, or genital secretions
• This cycle continues for the dog's entire life

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In the Nervous System (Surviving Puppies)

• Puppies aged 3–5 weeks that survive neonatal CHV-1 may develop permanent neurological damage because:
  • The virus damages the developing cerebellum (balance center) → permanent ataxia
  • Damages the optic nerve and retina → permanent blindness
  • Destroys the vestibular apparatus → persistent head tilt, balance problems
  • Causes cerebellar hypoplasia (underdevelopment of the cerebellum)

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PART 5 — CLINICAL SIGNS

A. Neonatal Puppies (< 3 weeks old)

• Persistent, constant crying / vocalization (the puppy cries incessantly — pain from abdominal lesions)
• Anorexia — stops nursing, refuses milk, cannot suckle
• Weakness, depression, lethargy — the puppy becomes limp, soft
• Hypothermia (low body temperature) — cold to touch
• Abdominal pain — abdomen looks distended and painful on palpation
• Nasal discharge — serous to mucopurulent
• Dyspnea / tachypnea — breathing difficulty (lung involvement)
• Soft/yellow-green diarrhea
• Petechiae (pinpoint red hemorrhages) on:
  • Gums (oral mucous membranes)
  • Inner ear flap
  • Conjunctiva (whites of the eyes)
  • Abdomen and skin
• Loss of righting reflex — puppy cannot turn itself over
• No fever (this is pathognomonic — absence of fever in a severely ill neonate)

• Day 0: Exposure (birth or first days of life)
• Day 4–6: First signs appear (crying, not nursing)
• Day 5–7: Rapid deterioration
• Death within 24–36 hours of first visible signs

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B. Puppies 3–5 Weeks Old

• Generally less severe because they can somewhat regulate body temperature
• More likely to survive but with long-term consequences
• Clinical signs:
  • Mild to moderate lethargy, poor growth
  • Mild respiratory signs
  • Some will develop neurological signs as they grow:
    • Ataxia (wobbling, difficulty walking, falling)
    • Blindness (partial or complete)
    • Head tilt (vestibular damage)
    • Deafness (inner ear damage)
    • Cerebellar hypoplasia — puppies that seem "clumsy" even after full recovery

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C. Pregnant Bitches

• Often asymptomatic (no visible illness)
• May show:
  • Mild vaginal discharge (serous or mucopurulent)
  • Mild nasal discharge
  • Lethargy
• Reproductive consequences:
  • Abortion in mid-to-late pregnancy
  • Stillborn puppies
  • Resorption of fetuses (early pregnancy loss)
  • Premature delivery of weak, dying puppies
  • Infertility — repeated pregnancy losses with no other explanation
  • Producing live puppies that rapidly die (fading puppy syndrome)

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D. Adult Dogs (Non-Pregnant)

• Mild upper respiratory infection
• Serous nasal discharge
• Sneezing
• Cough (may be part of "Kennel Cough" / infectious tracheobronchitis complex)
• Tonsillitis
• Usually self-limiting — resolves without treatment

• Females: Vesicular vaginitis — small fluid-filled blisters/vesicles on the vaginal mucosa; reddened, inflamed vaginal lining; mucopurulent vaginal discharge
• Males: Balanoposthitis (posthitis) — vesicles and inflammation of the prepuce and glans penis; discharge from prepuce; dog may lick the area excessively
• Both forms are usually mild and self-limiting

• Conjunctivitis — redness, discharge
• Blepharitis — eyelid inflammation
• Ulcerative keratitis — painful corneal ulcers, often dendritic (branching) pattern — classic herpesvirus corneal ulcer shape
• Non-ulcerative keratitis — corneal cloudiness without open ulcer
• Occurs during primary infection or reactivation
• Particularly important in dogs receiving immunosuppressive drugs (steroids, cyclosporine) — reactivation can cause serious eye disease (Ledbetter, NZ Vet J 2013 [PMID: 23438442]; Soleimani et al. 2025 [PMID: 41259018])

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PART 6 — GROSS PATHOLOGY & HISTOPATHOLOGY

Gross (Macroscopic) Lesions at Necropsy — CLASSIC PICTURE

Disseminated focal necrosis AND hemorrhages throughout multiple organs

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Histopathology (Microscopic Lesions)

• Necrosis in parenchymal cells of affected organs
• Hemorrhage into the adjacent tissue
• Minimal inflammatory reaction — because the immune system is immature and overwhelmed
• Intranuclear inclusion bodies — eosinophilic (pink-staining) inclusions within nuclei of infected cells
  • Cowdry Type A inclusions are typical of herpesviruses
  • Found in epithelial cells of kidneys, liver, lungs, adrenals
• In the brain: meningitis, perivascular cuffing, glial nodules, and neuronal necrosis
• In the eye: retinal necrosis and optic neuritis

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PART 7 — DIAGNOSIS

Step 1 — Clinical Suspicion

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Step 2 — Diagnostic Tests

Post-Mortem (Necropsy) Diagnosis — Most Reliable for Neonates

Ante-Mortem (Live Dog) Diagnosis

• CHV-1 antibody titers drop very quickly — within 1–2 months of infection
• A dog can be actively infected but seronegative (negative antibody test)
• A negative serology does NOT mean a dog is free of CHV-1
• PCR is the preferred diagnostic method for active infection

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Differential Diagnosis — What Else Causes Similar Signs?

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PART 8 — TREATMENT

Critical Reality Check First:

There is no specific licensed antiviral drug approved for CHV-1 treatment in dogs. Treatment is primarily supportive. In neonates, treatment is often unrewarding because the disease progresses within hours.

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Treatment of Neonatal Puppies

1. Warming Therapy — MOST IMPORTANT FIRST STEP

• Raise the puppy's body temperature to 37–38.5°C (98.6–101°F)
• Use:
  • Incubator set to 35°C (95°F) ambient temperature at 50% relative humidity
  • Warming box with a heat lamp
  • Heating pad (be careful — do not burn the puppy; use a towel as a buffer)
• Why it works: CHV-1 cannot replicate efficiently above 37°C. Raising body temperature directly suppresses viral replication.
• This is the single most important intervention in neonatal CHV-1
• Note: Recent evidence suggests warming alone may not fully stop disease progression once signs appear, but it significantly reduces losses in exposed but not-yet-symptomatic littermates

2. Passive Immunization (Hyperimmune Serum)

• Collect serum from a seropositive adult female dog (previously exposed, has antibodies)
• Inject intraperitoneally (IP) into exposed puppies before signs appear
• The maternal antibodies provide passive immunity to neutralize the virus
• This is most effective as prophylaxis (prevention before signs) rather than treatment
• Can also transfer the litter to a seropositive nursing female — her colostrum provides protective antibodies

3. IV/Oral Fluid Therapy

• Dehydration develops rapidly
• Administer warmed fluids:
  • Subcutaneous or intraperitoneal routes in neonates (veins too small for IV in very young pups)
  • Balanced electrolyte solution (Normal Saline or Lactated Ringer's)
  • Add dextrose (glucose) to prevent hypoglycemia
• Rate: Based on hydration status and puppy weight

4. Nutritional Support

• If puppy cannot nurse: tube feeding with puppy milk replacer
• Small, frequent feeds (every 2 hours in neonates)
• Keep warm before and during feeding

5. Antiviral Drugs (Limited Evidence)

• Acyclovir (Zovirax):
  • A nucleoside analogue that inhibits viral DNA polymerase
  • Works well against human herpesviruses
  • In vitro activity against CHV-1 demonstrated
  • Clinical effectiveness in dogs is uncertain — limited studies
  • Can be used as part of treatment but should not be relied upon as the primary intervention
  • Dose: varies; consult a veterinary pharmacologist
  • May be toxic at high doses
• Cidofovir and Ganciclovir — investigated in research settings; not routine clinical use

6. Antibiotics

• CHV-1 is a virus — antibiotics do NOT kill it
• BUT: Use antibiotics to prevent or treat secondary bacterial infections (pneumonia, septicemia) in weakened puppies
• Common choices: Amoxicillin, Ampicillin (IV in neonates)

7. Oxygen Therapy

• For puppies with respiratory distress (lung involvement)
• Use an oxygen cage or flow-by oxygen

8. Supportive Nursing

• Keep puppies clean and dry
• Ensure they are feeding
• Isolate affected puppies from others in the kennel

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Treatment of Adult Dogs

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Prognosis Summary

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PART 9 — PREVENTION & CONTROL

1. Vaccination

• A commercial vaccine exists: Eurican Herpes 205 (Merial/Boehringer Ingelheim)
• Inactivated (killed) CHV-1 vaccine
• Indicated for use in breeding bitches to protect future litters
• Vaccination schedule:
  • First dose: during proestrus/estrus (when the bitch comes into heat)
  • Second dose: 1–2 weeks before expected whelping
  • Revaccinate with every pregnancy
• The vaccine does NOT prevent infection but stimulates high antibody levels in the dam → antibodies passed to puppies in colostrum → passive protection for the litter
• NOT a lifelong vaccine — immunity from CHV-1 antibodies is short-lived (weeks to months), so revaccination with every breeding is necessary

• As of the time of this writing, no licensed CHV-1 vaccine is available in the USA
• Prevention relies on management practices

2. Management Practices (Most Important in Non-Vaccinated Countries)

• Isolate the pregnant bitch for the last 3 weeks of gestation — away from all other dogs
• Keep the dam and puppies isolated for 3 weeks after birth
• This prevents exposure to shedding carrier dogs during the most vulnerable period
• The litter's "safe window" is: from 3 weeks before birth to 3 weeks after birth

• Keep the whelping environment at 29–32°C (84–90°F) ambient temperature for the first 2 weeks
• Puppies should not drop below 35.5°C (96°F) body temperature
• Use a thermometer to check puppy body temperatures regularly
• Incubator, heat lamp, or under-blanket heating mat are acceptable

• Ensure every puppy nurses within the first 12–24 hours of life to receive maternal antibodies via colostrum
• If dam is known seronegative (no antibodies), consider sourcing colostrum from a seropositive female

• Disinfect whelping box and equipment with bleach (1:30 dilution) or Virkon
• Wash hands thoroughly between handling litters
• Do not share equipment between litters

• Test breeding dogs for CHV-1 via PCR (swabs) or serology before breeding
• Paired serology (2 samples 2–3 weeks apart) showing seroconversion confirms recent active infection

• Minimize stress for breeding dogs — stress is the main trigger for viral reactivation
• Avoid transporting pregnant bitches to new environments
• Provide stable, calm whelping environments

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PART 10 — LATENCY AND REACTIVATION (Advanced Concept)

Where Does the Virus Hide?

What Triggers Reactivation?

What Happens During Reactivation?

• Virus travels back down the nerve to the mucosal surface
• Dog begins shedding virus in oral, nasal, or genital secretions
• Often completely asymptomatic — the dog looks healthy but is spreading virus
• This is why CHV-1 persists in dog populations despite vaccination efforts — seroprevalence approaches 80% in kennels because most infected adult carriers shed periodically without owners knowing
• It is biologically impossible to eradicate CHV-1 from a kennel once it is present

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PART 11 — QUICK REFERENCE SUMMARY TABLE

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PART 12 — FREQUENTLY ASKED QUESTIONS (FAQ)

Questions from Pet Owners:

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1. Isolation — keep the pregnant bitch away from all other dogs for the last 3 weeks before whelping
2. Vaccinate (if you are in Europe — Eurican Herpes vaccine with each pregnancy)
3. Whelping box temperature — keep it warm (29–32°C ambient) so puppies maintain a body temperature > 37°C
4. Ensure puppies nurse within 12 hours of birth for colostrum protection

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• Start warming therapy immediately
• Administer hyperimmune serum if available
• Provide fluid and glucose support
• Run PCR testing for confirmation

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• Perform PCR of nasal, oral, and vaginal swabs to check for active shedding
• Run serology (ELISA) to check antibody status
• If seronegative: protect the bitch carefully during breeding and pregnancy from exposure
• If seropositive: she carries the virus; vaccination (where available) before each pregnancy is recommended

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• Merck Veterinary Manual — Canine Herpesvirus Infection
• Decaro N, Martella V, Buonavoglia C — Canine adenoviruses and herpesvirus. Vet Clin North Am Small Anim Pract 2008 [PMID: 18501279]
• Ledbetter EC — Canine herpesvirus-1 ocular diseases of mature dogs. NZ Vet J 2013 [PMID: 23438442]
• Soleimani S et al. — Prevalence and Clinical Impacts of CHV-1 in Dogs: A Review. Vet Med Sci 2025 [PMID: 41259018]
• Dr. Emmanuel Fontaine — Why Is Canine Herpes So Hard to Eliminate? (2026)
• AKC — Canine Herpes Virus: What Breeders Should Know
• Texas A&M Veterinary Medical Diagnostic Laboratory — CHV Case Studies (2024)
• Jawetz, Melnick & Adelberg's Medical Microbiology 28e (Herpesviridae classification)

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Topic map: Veterinary Corneal Ulcers

1. Corneal anatomy and normal healing
   • Epithelium, stroma, Descemet's membrane, endothelium
   • Why corneal ulcers are painful and how they heal
2. Definition and classification
   • Superficial epithelial ulcers
   • Stromal ulcers
   • Deep ulcers, descemetoceles, and corneal perforation
   • Simple, complicated, melting, indolent, infected, and traumatic ulcers
3. Causes and risk factors
   • Trauma, foreign bodies, dry eye, eyelid abnormalities, infection, breed predisposition, chemical injury, and neurologic disease
4. Clinical signs and ophthalmic examination
   • Blepharospasm, epiphora, photophobia, fluorescein staining, Schirmer tear test, tonometry, eyelid examination, and corneal sensation
5. Diagnostics and differential diagnosis
   • Cytology, bacterial culture and susceptibility testing
   • How to differentiate ulceration from uveitis, glaucoma, conjunctivitis, keratitis, herpesvirus disease, and corneal sequestrum
6. Medical treatment
   • Pain relief, topical antimicrobials, anticollagenase therapy, atropine, lubrication, systemic analgesia
   • Safe versus dangerous drugs
   • Drug dose ranges and monitoring principles, species-specific cautions
7. Melting ulcers and emergency management
   • What "melting" means, why it can progress quickly, stabilization, and when referral is urgent
8. Surgical treatment
   • Debridement, diamond burr, grid keratotomy, conjunctival grafts, corneoconjunctival transposition, amniotic membrane, and keratoplasty
   • Indications and complications
9. Species-specific chapters
   • Dogs: including brachycephalic ocular syndrome and indolent ulcers
   • Cats: feline herpesvirus-1, sequestrum, and eosinophilic keratitis
   • Horses and other species if you need them
10. Aftercare, prognosis, prevention, client communication

• Recheck schedule, Elizabethan collar, owner warnings, recurrence prevention

1. Cases, exam questions, and client FAQs

• Case-based decision making from history through treatment
• Interview and viva questions with answers

High-level overview

Veterinary Corneal Ulcers in Dogs and Cats

Important clinical rule: A painful red eye should be treated as an ophthalmic emergency until a corneal ulcer, glaucoma, anterior uveitis, foreign body, or lens luxation has been excluded. Never prescribe a topical corticosteroid before fluorescein staining.

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1. Corneal Anatomy: Know This Before Treating an Ulcer

Main corneal layers

Why corneal ulcers are painful

• Blepharospasm (forceful eyelid closure)
• Photophobia (avoidance of light)
• Epiphora (excess tearing)
• Reflex anterior uveitis (inflammation inside the front of the eye)
• Miosis (small pupil) due to ciliary-body spasm

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2. Definitions and Classification

A. Superficial corneal ulcer

• Usually stains brightly with fluorescein.
• Often heals in 3 to 7 days if uncomplicated.
• Common causes: trauma, foreign body, dry eye, eyelid hair rubbing the cornea.

B. Stromal ulcer

• More serious because it weakens the cornea.
• May appear as a crater with edema, white cellular infiltration, or a cloudy blue margin.
• Requires careful monitoring and often more aggressive treatment.

C. Deep stromal ulcer

• High risk of rupture.
• Must be considered a veterinary ophthalmic emergency.
• Surgical support is often needed.

D. Descemetocele

• Deep crater
• Clear, shiny, smooth central “bubble”
• Fluorescein stains the ulcer edges but does not stain the exposed Descemet’s membrane itself

E. Corneal perforation

• Sudden collapse or flattening of the anterior chamber
• Iris prolapse through the cornea
• Aqueous humor leakage
• Positive Seidel test: fluorescein dye becomes diluted by aqueous humor leaking from the wound
• Severe uveitis, hyphema (blood in the eye), or endophthalmitis

F. Melting ulcer / keratomalacia

• Bacteria, especially Pseudomonas and beta-hemolytic Streptococcus
• Neutrophils and other inflammatory cells
• Damaged corneal cells

• Yellow-gray or cream infiltrate
• Soft, gelatinous, “soupy,” or liquefied stroma
• Rapid ulcer deepening over hours to days
• Severe pain, discharge, edema, uveitis

G. Indolent ulcer / SCCED

• Usually occurs in middle-aged or older dogs
• Common in Boxers, but can occur in any breed
• Superficial defect that does not heal normally
• Loose, nonadherent epithelial edge
• Minimal stromal inflammation
• Fluorescein often spreads beneath the loose epithelial margin

H. Infected ulcerative keratitis

• Dense white, yellow, or cream infiltrate
• Progressive stromal loss
• Mucopurulent discharge
• Marked conjunctival hyperemia
• Severe edema
• Hypopyon (white blood cells in the anterior chamber)
• Melting or rapid enlargement

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3. Causes of Corneal Ulceration

A. Trauma

• Cat scratch or dog fight
• Plant material or grass awn
• Branch injury
• Grooming accident
• Rubbing against furniture
• Self-trauma from pawing at the eye

B. Foreign body

• Under the upper eyelid
• In the conjunctival sac
• In the cornea
• Behind the third eyelid

C. Eyelid or eyelash abnormalities

D. Brachycephalic ocular syndrome

• Prominent eyes
• Large palpebral fissure (eyelid opening)
• Incomplete blinking
• Medial canthal entropion
• Nasal-fold trichiasis
• Reduced corneal sensation
• Tear-film abnormalities

E. Keratoconjunctivitis sicca (KCS)

• Thick mucoid discharge
• Dull corneal surface
• Conjunctival redness
• Corneal pigmentation and vascularization
• Recurrent or nonhealing ulcers

F. Infectious disease

Dogs

• Staphylococcus spp.
• Streptococcus spp.
• Pseudomonas aeruginosa
• Proteus spp.
• Enterobacteriaceae

Cats

• Dendritic ulcers: branching pattern
• Geographic ulcers: larger irregular lesions
• Concurrent conjunctivitis, sneezing, or nasal discharge may occur
• Can recur after stress or immunosuppression

G. Chemical injury

• Immediate, copious flushing is the priority.
• Alkali injuries are often more severe because alkalis penetrate tissues deeply.
• Do not delay irrigation while searching for medications.

H. Neurotrophic or exposure-related ulceration

• Facial nerve paralysis
• Trigeminal nerve dysfunction
• Brachycephalic anatomy
• Previous surgery or trauma
• Severe chronic ocular-surface disease

I. Systemic or metabolic disease

• Diabetes mellitus
• Hypothyroidism in dogs
• Hyperadrenocorticism
• Immunosuppressive treatment
• Malnutrition
• Severe systemic illness

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4. Risk Factors

• Brachycephalic breed
• Dry eye
• Older Boxer or other dog with SCCED
• Previous ulcer history
• Indoor-outdoor exposure and plant trauma
• Cat fights
• Inadequate blink or facial nerve dysfunction
• Chronic topical corticosteroid use
• Immunosuppressive drugs
• Poor tear-film production
• Environmental irritants
• Poorly fitted Elizabethan collar or bandage contact lens
• Previous corneal surgery

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5. Clinical Signs

• Blepharospasm
• Photophobia
• Epiphora
• Ocular discharge
• Conjunctival hyperemia
• Third-eyelid elevation
• Rubbing face or pawing at the eye
• Corneal haze, edema, or white infiltrate
• Visible corneal indentation or crater
• Miosis from reflex uveitis
• Reduced vision or blindness in severe lesions

Signs that suggest a complicated ulcer

• Cream, yellow, or white stromal infiltrate
• Gelatinous corneal surface
• Progressive ulcer size or depth
• Marked corneal edema
• Hypopyon or hyphema
• Deep stromal loss
• Iris visible near ulcer base
• No improvement within 48 to 72 hours
• Ulcer not healed after 7 to 10 days

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6. Essential Ophthalmic Examination Sequence

Recommended order

1. Observe from a distance before touching the eye.
2. Check vision and menace response, if practical.
3. Examine eyelids, eyelashes, third eyelid, facial symmetry.
4. Perform Schirmer tear test.
5. Collect samples for cytology/culture if indicated.
6. Apply topical anesthetic only after samples if possible.
7. Examine under magnification and focal light.
8. Measure intraocular pressure with tonometry.
9. Apply fluorescein stain.
10. Dilate pupil only if appropriate and only after assessing for glaucoma, lens luxation, and ulcer severity.

A. Schirmer Tear Test (STT)

• Approximately 15 mm/min or more: generally adequate
• 10 to 14 mm/min: borderline, interpret with clinical signs
• Less than 10 mm/min: suspicious for KCS
• Less than 5 mm/min: strongly supportive of KCS

B. Fluorescein stain

• Bright green uptake: epithelial defect or ulcer
• Deep crater with unstained central point: possible descemetocele
• Green dye diluted by fluid streaming: positive Seidel test, indicating leakage from perforation

C. Tonometry

• Low IOP can support anterior uveitis.
• High IOP suggests glaucoma.
• Do not assume every painful red eye is an ulcer.

D. Corneal cytology and bacterial culture

• Deep stromal ulcer
• Melting ulcer
• Large infiltrate
• Severe mucopurulent discharge
• Failure of empirical therapy
• Recurrent infection
• Prior antimicrobial exposure
• Suspected fungal infection

• Neutrophils
• Degenerate neutrophils
• Bacteria
• Fungal hyphae or yeast
• Eosinophils in feline eosinophilic keratitis
• Atypical cells, if neoplasia is possible

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7. Differential Diagnosis

Corneal ulcer versus conjunctivitis

Corneal ulcer versus anterior uveitis

Corneal ulcer versus glaucoma

Corneal ulcer versus corneal sequestrum in cats

• May be associated with chronic irritation, FHV-1, brachycephalic conformation, or tear-film abnormalities.
• It can occur with or without ulceration.
• A dark plaque is not simply “pigmentation.”
• Surgical keratectomy is often required if deep, painful, progressive, or nonhealing.

Corneal ulcer versus eosinophilic keratitis in cats

• Pink-white raised corneal plaques
• Vascularization
• Eosinophils on cytology
• May be associated with FHV-1

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8. Medical Treatment Principles

Core treatment goals

1. Treat or prevent infection.
2. Relieve pain.
3. Stop stromal collagen destruction.
4. Correct the underlying cause.
5. Prevent self-trauma.
6. Reassess frequently.
7. Use surgery before rupture occurs, not after.

A. Elizabethan collar

B. Topical antibiotics

Simple, superficial, noninfected ulcers

Infected or melting ulcers

• Fortified cefazolin plus tobramycin
• A fluoroquinolone where indicated
• Culture-directed antimicrobial treatment

C. Anticollagenase treatment for melting ulcers

D. Atropine for pain from uveitis

• Atropine 1% ophthalmic solution or ointment
• Often one drop once daily, then reduce or stop once adequate pupil dilation and pain control occur
• In dogs, it may last several days
• In cats, use carefully because bitter taste reaching the mouth can cause salivation, vomiting, or reduced appetite

E. Systemic analgesia

• NSAID, if not contraindicated
• Gabapentin
• Opioid analgesia for severe pain
• Sedation or hospital analgesia for deep, infected, or surgical cases

F. Lubricants and tear support

• Preservative-free artificial tears
• Sodium hyaluronate gel
• Lubricating ophthalmic ointment

• Cyclosporine ophthalmic formulation
• Tacrolimus ophthalmic formulation

G. Feline herpesvirus treatment

• Consider systemic famciclovir
• A commonly used clinical range is 40 to 90 mg/kg orally every 8 to 12 hours, with protocol selection based on severity, formulation, renal status, and current feline-ophthalmology guidance.
• Topical cidofovir 0.5% twice daily is used in some settings.

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9. Drugs to Avoid

Never use topical corticosteroids on an ulcerated cornea

• Dexamethasone
• Prednisolone acetate
• Hydrocortisone

• Delays epithelial healing
• Suppresses local immune responses
• Increases risk of bacterial or fungal infection
• Increases collagenase activity
• Can convert a mild ulcer into a melting ulcer or perforation

Avoid topical anesthetics as home treatment

• Proparacaine
• Tetracaine

Do not treat crystalluria-like appearances blindly

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10. Indolent Ulcers / SCCED: Management

Diagnosis

• Adult or older dog
• Superficial ulcer lasting more than 7 to 14 days
• Loose epithelial margins
• No marked infiltrate or melting
• Fluorescein dye tracking under loose epithelium

Treatment

1. Identify and correct cause:
   • KCS
   • entropion
   • ectopic cilia
   • foreign body
   • exposure disease
2. Gentle epithelial debridement:
   • Topical anesthetic applied by veterinarian
   • Loose epithelium removed with sterile cotton-tipped applicator
3. Mechanical stimulation of epithelial attachment:
   • Diamond burr debridement
   • Grid keratotomy
   • Punctate keratotomy

1. Topical antibiotic and pain control.
2. Recheck within several days.

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11. Melting Ulcers: Emergency Protocol

Immediate priorities

1. Confirm ulcer depth and look for leakage.
2. Obtain cytology and culture if possible.
3. Begin frequent topical broad-spectrum antimicrobial therapy.
4. Start anticollagenase treatment.
5. Provide systemic analgesia.
6. Treat uveitis with atropine if no contraindication.
7. Use an Elizabethan collar.
8. Recheck every 12 to 24 hours initially.
9. Plan surgery promptly if deep, progressive, or structurally unstable.

Surgical indications

• Descemocele
• Corneal perforation
• Deep ulcer with progressive stromal loss
• Uncontrolled melting despite aggressive medical therapy
• Ulcer with more than approximately 50% stromal loss
• Iris prolapse
• Large lesion with poor mechanical stability
• Failure to heal despite correct medical management

Surgical options

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12. Dog Versus Cat Differences

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13. Prognosis

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14. Home-Care Instructions for Clients

• Apply every prescribed medicine exactly as directed.
• Wait approximately 5 minutes between different eye drops.
• Apply drops before ointments.
• Keep the Elizabethan collar on all the time.
• Do not let the pet rub the eye.
• Never use human “redness relief” drops.
• Never use old eye drops from a previous problem.
• Never use steroid eye drops unless specifically prescribed after a veterinary eye examination.
• Return urgently if the eye looks cloudier, more painful, more swollen, more yellow/white, or if vision seems reduced.

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15. Quick Clinical Decision Algorithm

Cat or dog with painful red eye

• No: assess glaucoma, uveitis, conjunctivitis, foreign body, dry eye, lens disease.
• Yes: continue.

• Yes: topical prophylactic antibiotic, pain control, E-collar, recheck in 3 to 5 days.

• Yes: cytology/culture, frequent topical therapy, anticollagenase, analgesia, consider hospitalization/referral/surgery.

• Re-examine for SCCED, KCS, entropion, ectopic cilia, FHV-1, foreign body, infection, or systemic disease.

• Investigate and treat for FHV-1; avoid corticosteroids while epithelium is ulcerated.

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16. Important Exam and Interview Questions

1. What stain confirms a corneal ulcer?

2. What is a descemetocele?

3. What is a melting ulcer?

4. Which drugs are contraindicated in corneal ulcers?

5. What does a creamy infiltrate around an ulcer suggest?

6. What causes SCCED?

7. Why is atropine used in a painful corneal ulcer?

8. Why must the Schirmer tear test be done before topical anesthetic or other drops?

9. What is the main viral cause of feline corneal ulceration?

10. What is the immediate priority in a suspected chemical eye injury?

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17. Common Client Questions

“Can a corneal ulcer make my pet blind?”

“Is this ulcer contagious?”

“Why is my pet keeping the eye closed?”

“Can I use my own antibiotic eye drops?”

“Why does my dog need an Elizabethan collar?”

“Why has my cat’s ulcer returned?”

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Key Memory Points

1. Fluorescein-positive defect = corneal ulcer.
2. Never use topical steroids on an ulcerated cornea.
3. Melting ulcer = emergency.
4. Descemetocele or perforation = urgent surgery/referral.
5. SCCED = loose epithelium and poor epithelial adhesion, not simply infection.
6. FHV-1 is a major cause of feline corneal ulcers.
7. KCS, eyelid disease, and brachycephalic anatomy must be identified and corrected.
8. Pain control, E-collar, and scheduled rechecks are part of treatment, not optional extras.

Keratoconjunctivitis Sicca (KCS) in Veterinary Practice

Complete Guide to “Dry Eye” in Dogs and Cats

• Kerato- = cornea
• Conjunctivitis = inflammation of conjunctiva
• Sicca = dry

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1. Normal Tear Film and Why It Matters

Functions of tears

• Lubricate the cornea and eyelids
• Remove dust, debris, bacteria, and inflammatory substances
• Supply oxygen, nutrients, antibodies, growth factors, and antimicrobial proteins
• Maintain a smooth optical surface for clear vision
• Prevent epithelial cells from drying and dying
• Support corneal wound healing

Tear-film components

1. Quantitative KCS: too little aqueous tear production.
2. Qualitative KCS: poor tear quality, despite a possibly normal Schirmer tear test result. For example, lipid or mucin deficiency can cause rapid tear evaporation or poor tear adherence.

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2. Tear-Producing Structures

• 60% of aqueous tears are produced by the main lacrimal gland
• 40% are produced by the gland of the third eyelid or nictitans gland

Clinical principle: A “cherry eye” gland should usually be repositioned, not removed, unless there is a rare compelling reason.

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3. Causes of KCS

A. Immune-mediated KCS: the most common canine cause

Typical patient

• Middle-aged dog
• Bilateral disease
• Chronic thick mucus or mucopurulent discharge
• Red eyes and progressive corneal pigmentation
• Low Schirmer tear test values

B. Breed predisposition

• American Cocker Spaniel
• English Cocker Spaniel
• English Bulldog
• Cavalier King Charles Spaniel
• Shih Tzu
• Lhasa Apso
• West Highland White Terrier
• Pug
• Pekingese
• Miniature Schnauzer
• Yorkshire Terrier
• Bloodhound
• Boston Terrier

C. Drug-induced KCS

• Sulfonamides, particularly trimethoprim-sulfonamide products
• Etodolac
• Some drugs with anticholinergic effects
• Rarely, other drugs that affect autonomic innervation or lacrimal gland function

D. Neurogenic KCS

• Usually unilateral
• Very low or absent tears in one eye
• Dry nostril on the same side, called ipsilateral nasal dryness
• May occur after otitis media/interna, trauma, neurologic disease, or facial/trigeminal/autonomic nerve dysfunction

E. Congenital KCS

F. Infectious KCS

• Canine distemper virus
• Chronic viral conjunctivitis
• Feline herpesvirus-1 in cats

G. Iatrogenic KCS

• Removal of third-eyelid gland
• Radiation therapy affecting lacrimal glands
• Severe ocular surgery
• Damage to nerves during surgery or trauma

H. Systemic and endocrine disease

• Diabetes mellitus
• Hypothyroidism
• Hyperadrenocorticism
• Immune-mediated diseases
• Severe chronic systemic disease

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4. Pathophysiology: How KCS Damages the Eye

1. Immune cells infiltrate the lacrimal gland.
2. Chronic inflammation damages tear-producing acini.
3. Aqueous tear production falls.
4. The cornea and conjunctiva become dry and inflamed.
5. Mucus, bacteria, cellular debris, and inflammatory material accumulate.
6. The epithelial barrier becomes damaged.
7. Corneal ulcers, bacterial keratitis, neovascularization, fibrosis, and pigmentation develop.
8. Chronic damage can impair vision permanently.

Corneal changes in chronic KCS

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5. Clinical Signs

• Thick yellow, cream, green, or gray eye discharge
• Sticky mucus strands
• Red conjunctiva
• Dull, dry-looking corneal surface
• Squinting or blepharospasm (forceful eyelid closure)
• Photophobia (light avoidance)
• Pawing or rubbing the face
• Third-eyelid elevation
• Corneal opacity
• Corneal blood vessels
• Brown-black corneal pigmentation
• Recurrent corneal ulcers
• Reduced vision in chronic severe disease

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6. Diagnosis

A. Schirmer Tear Test I: the key diagnostic test

Correct technique

1. Do the STT before topical anesthetic, fluorescein, irrigation, or most other eye drops.
2. Open the test strip without touching its calibrated portion.
3. Fold at the notch.
4. Place it in the lower conjunctival fornix, usually at the lateral lower eyelid.
5. Leave for 60 seconds.
6. Record millimeters wetted per minute.

Interpretation in dogs

B. Fluorescein stain

• Bright green uptake indicates exposed corneal stroma or epithelial loss.
• KCS-associated ulcers require treatment in addition to tear stimulation.
• Never use topical corticosteroids if a corneal ulcer is present.

C. Tonometry

• KCS can cause painful red eyes, but so can glaucoma and uveitis.
• A low IOP supports uveitis.
• A high IOP supports glaucoma.

D. Tear-film breakup time

E. Rose Bengal or lissamine green staining

F. Cytology and culture

• Corneal ulceration
• Dense white/yellow infiltrate
• Mucopurulent discharge
• Melting ulcer
• Failure of empirical therapy
• Recurrent bacterial keratitis

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7. Important Differentials

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8. Is There a Pathognomonic Sign?

Low Schirmer tear test value + thick mucoid/mucopurulent discharge + chronic corneal surface disease.

Unilateral severe tear deficiency with a dry nostril on the same side.

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9. Treatment Principles

1. Increase natural tear production where possible.
2. Reduce immune-mediated inflammation.
3. Replace missing tears and protect the cornea.
4. Treat ulcers, secondary infection, and eyelid disease.

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10. Topical Immunomodulators and Lacrimostimulants

A. Cyclosporine

• Cyclosporine ophthalmic ointment 0.2%: commonly applied every 12 hours
• Compounded cyclosporine preparations, often 1% or 2%, may be used by ophthalmologists or when commercial products are unsuitable

Expected response

• Improvement in ocular comfort/discharge: often within weeks
• Increase in tear production: may take 4 to 8 weeks or longer
• Some severely chronic cases do not regain normal STT values but still improve clinically

B. Tacrolimus

• Tacrolimus 0.02% to 0.03%, often applied every 12 hours
• Some clinicians use higher concentrations in refractory cases, but formulation and frequency should be selected by a veterinarian or veterinary ophthalmologist

• Cyclosporine response is inadequate
• KCS is severe
• Pigmentary keratitis is prominent
• The patient does not tolerate cyclosporine

C. Pilocarpine for neurogenic KCS

• Vomiting
• Diarrhea
• Salivation
• Reduced appetite
• Bradycardia
• Miosis
• Bronchoconstriction

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11. Artificial Tears and Lubricants

• At the beginning of treatment
• In severe cases
• In nonresponsive cases
• In neurogenic disease
• In cats with qualitative tear deficiency
• When corneal ulceration is present

Options

Practical point

• Drops may need use every 2 to 6 hours in severe dry eye.
• Gels/ointments usually last longer.
• Apply drops first, wait 5 minutes, then apply ointment last.

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12. Treatment of Secondary Infection and Corneal Ulcers

When no ulcer is present

• Chloramphenicol
• Tobramycin
• Triple-antibiotic ophthalmic preparations

When an ulcer is present

• Fluorescein stain at every relevant recheck
• Topical antibiotic
• Pain control
• Lubrication
• E-collar in dogs
• Culture/cytology for deep, infected, or melting lesions
• Do not use topical corticosteroids

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13. What Must Be Avoided

A. Topical corticosteroids if ulcer is present

• Delay epithelial healing
• Promote infection
• Increase collagen breakdown
• Convert an ulcer into a melting ulcer
• Increase risk of perforation

B. Repeated home use of topical anesthetics

C. Stopping immunomodulators when the eye looks better

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14. Surgical Treatment

A. Parotid duct transposition (PDT)

Advantages

• Can provide continuous moisture
• Useful in refractory severe KCS
• Can help preserve comfort and vision

Limitations and complications

• Mineral deposition on cornea
• Wet face/tear overflow
• Duct obstruction
• Sialadenitis
• Corneal irritation
• Continued need for medical treatment in some cases

B. Correct associated eyelid and exposure disease

• Entropion surgery
• Medial canthoplasty
• Nasal-fold resection
• Ectopic cilia removal
• Temporary or permanent tarsorrhaphy in selected exposure cases

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15. KCS in Cats

Feline causes

• FHV-1-associated ocular disease
• Chronic conjunctivitis
• Lacrimal-gland damage
• Brachycephalic conformation
• Corneal sequestrum-associated surface disease
• Qualitative tear-film deficiency
• Drug effects or systemic disease in selected cases

Important feline differences

• FHV-1 is a major differential diagnosis.
• Cats may have a normal or near-normal STT but still have tear-film abnormalities.
• Cats often tolerate or respond differently to lacrimostimulants than dogs.
• Tear replacement and treatment of underlying FHV-1 or chronic ocular-surface disease may be more important than in typical canine immune-mediated KCS.
• Be cautious with atropine because bitter taste may cause hypersalivation and anorexia.

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16. Monitoring and Recheck Plan

Initial monitoring

• Recheck in approximately 2 to 4 weeks after initiating immunomodulator therapy
• Repeat STT before applying drops
• Perform fluorescein stain if pain, discharge, cloudiness, or ulcer risk is present
• Assess corneal pigmentation, vascularization, ulceration, and infection

Long-term monitoring

• Rechecks every 3 to 6 months are often reasonable
• More frequent checks for severe disease, pigmentary keratitis, ulcers, changing STT values, or medication changes

Signs of treatment response

• Less mucus and discharge
• Reduced redness
• Better corneal luster
• Improved STT value
• Reduced ulcer recurrence
• Slower or reduced pigmentation progression
• Improved comfort

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17. Prognosis

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18. Important Clinical Errors to Avoid

1. Diagnosing KCS without doing an STT.
2. Performing STT after topical anesthetic or multiple drops.
3. Missing corneal ulceration.
4. Using a steroid-containing drop in an ulcerated eye.
5. Ignoring eyelid conformation and trichiasis.
6. Treating chronic mucus with antibiotic alone while missing tear deficiency.
7. Expecting cyclosporine or tacrolimus to work immediately.
8. Stopping treatment when the eye appears normal.
9. Failing to investigate unilateral severe KCS for neurologic disease.
10. Ignoring FHV-1 and corneal sequestrum in cats.

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19. Key Exam and Interview Questions

1. What is the most common cause of KCS in dogs?

2. What is the first test in suspected KCS?

3. What STT value strongly supports KCS in a dog?

4. What are the major tear-producing glands in dogs?

5. Why should a prolapsed third-eyelid gland be replaced rather than removed?

6. What treatment is most commonly used for immune-mediated canine KCS?

7. What clue suggests neurogenic KCS?

8. What drug can be used in neurogenic KCS?

9. Why are corticosteroids dangerous in an ulcerated eye?

10. What is a major cause of recurrent corneal ulceration in cats with dry-eye signs?

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20. Common Client Questions and Answers

“Will my dog become blind?”

“Can KCS be cured?”

“Why is there thick green discharge if my dog has dry eye?”

“Can I stop the drops after my dog looks normal?”

“Is KCS contagious?”

“Why does my dog need an Elizabethan collar?”

“Can human artificial tears be used?”

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21. Easy Memory Summary

Think: DRY EYE

• D: Discharge, dryness, dull cornea
• R: Redness, rubbing, recurrent ulcers
• Y: Yellow-green mucus
• E: Evaluate with STT before drops
• Y: Year-round and often lifelong treatment
• E: Exclude ulcer, infection, eyelid disease, and neurologic causes

Main treatment memory

Stimulate tears + replace tears + protect cornea + treat the cause.

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Evidence note