1. Babesiosis

• Etiology

  • Canine babesiosis is caused by Babesia spp., a tick-borne protozoal parasite.

  • It can vary in severity, from subclinical to life-threatening disease.

  • The virulence and pathophysiology depend on the Babesia species.

  • Historically, Babesia spp. have been divided into large and small categories based on their intraerythrocytic form.

  • Molecular testing offers more accurate species identification and genetic characterization than traditional morphologic methods.

• Clinical Signs

  • Symptoms can range from mild to severe, depending on the species and individual dog.

  • Common clinical signs include:

    • Lethargy

    • Pale mucous membranes

    • Enlarged spleen (splenomegaly)

    • Fever (waxing and waning)

    • Bounding pulses

    • Lymphadenopathy

    • Weakness and general malaise

    • Jaundice

    • Vomiting (especially with B. conradae infection)

• Pathogenesis

  • Hemolytic anemia in babesiosis is multifactorial:

    • Immune-mediated destruction (both intra- and extravascular)

    • Direct parasitic damage

    • Oxidative stress from parasite activity

  • Thrombocytopenia occurs due to immune-mediated destruction or consumption secondary to endothelial injury.

• Diagnosis

  • Light microscopy (Blood smear):

    • High specificity for detecting Babesia spp. parasites, but low sensitivity.

    • Helps identify parasite forms:

      • Large Babesia spp.: 3–7 µm, tear-drop shapes (single or paired).

      • Small Babesia spp.: 1–3 µm, signet-ring forms.

  • Indirect fluorescent antibody (IFA) test:

    • Can detect exposure but not differentiate among Babesia species.

    • Titers ≥1:64 suggest exposure.

  • Polymerase chain reaction (PCR):

    • Highly sensitive and specific for detecting and identifying species or subspecies.

    • Sensitivity improves with multiple tests over time.

• Treatment​

  • Imidocarb dipropionate:

    • Dosage: 6.6 mg/kg IM once, repeat in 7–14 days.

    • Effective for B. canis vogeli, but ineffective for B. gibsoni or B. conradae.

    • Pretreatment with atropine (0.02 mg/kg SC 30 minutes before imidocarb) to reduce side effects (e.g., salivation, vomiting, tachycardia).

  • Atovaquone + Azithromycin:

    • Atovaquone: 13.3 mg/kg PO every 8 hours.

    • Azithromycin: 10 mg/kg PO once daily.

    • Effective against B. gibsoni and B. conradae.

    • Atovaquone should be administered with a fatty meal for better absorption.

  • Diminazene aceturate:

    • Dosage: 3.5–7 mg/kg SC or IM every 1–2 weeks.

    • Effective for B. canis.

  • Clindamycin:

    • Dosage: 25 mg/kg PO every 12 hours.

    • Used for B. gibsoni, but treatment efficacy is uncertain.

  • Metronidazole:

    • Dosage: 15 mg/kg PO every 12 hours.

    • Used for B. gibsoni, but efficacy is not fully established.

  • Doxycycline:

    • Dosage: 5 mg/kg PO every 12 hours.

    • Associated with B. gibsoni clearance, but true efficacy is unclear.

  • Supportive care includes:​

    • IV fluids for dehydration and hypovolemia.

    • Blood transfusions may be needed for severe anemia (when hematocrit ≤15%).

    • Monitoring for anemia and thrombocytopenia is important during recovery.

• Prevention

  • The primary prevention method is vector control.

    • Tick infestations should be minimized by regularly inspecting dogs for ticks, especially in endemic areas.

    • Use of acaricides (amitraz, fipronil, imidacloprid + permethrin) can reduce tick transmission.

    • Ticks should be removed within 24 hours of detection.

  • Vaccination:

    • Available for B. canis canis in Europe, which reduces the severity of the disease but does not prevent infection.

    • Vaccines do not offer protection against B. gibsoni, B. canis vogeli, or B. canis rossi.

  • Blood transfusion screening: Ensuring donor dogs are free from Babesia to prevent transmission through blood products.

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2. Ehrlichiosis

• Etiology

  • Ehrlichiosis is caused by Ehrlichia canis (the primary species affecting dogs), a tick-borne intracellular bacterium. Ehrlichia canis infects white blood cells, particularly monocytes, and is transmitted through the bite of the brown dog tick (Rhipicephalus sanguineus). Though the disease is widespread globally, it is notably absent in Australia. Other tick-borne diseases, including Babesiosis and Rocky Mountain Spotted Fever, can co-infect dogs, complicating diagnosis and treatment.

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• History and Background

  • Ehrlichia canis was poorly understood until the Vietnam War, where German Shepherd dogs in military service began dying in large numbers due to a severe form of the disease called Tropical Canine Pancytopenia. This condition caused the destruction of all blood cell lines.

  • Ehrlichia ewingii, another species, causes a milder form of the disease and affects granulocytes rather than monocytes. It is transmitted by the lone star tick (Amblyomma americanum) and causes arthritis and mild illness.

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• Clinical Presentation

  • Ehrlichiosis can present in three phases: acute, subclinical, and chronic.

  • Acute Phase (1–3 weeks post-infection):

    • Clinical signs:

      • Fever, lethargy, loss of appetite

      • Enlarged lymph nodes

      • Dropped platelet count and possible immune-mediated platelet destruction

    • This phase is not usually life-threatening and can resolve with early treatment.

  • Subclinical Phase (months to years):

    • The dog appears normal but may show mild blood changes, such as a reduced platelet count or elevated globulin levels.

    • The infection is hidden in the spleen, and the dog may remain in this phase for months or even years without showing symptoms.

  • Chronic Phase (months to years after acute infection):

    • Symptoms:

      • Severe blood abnormalities, including pancytopenia (reduction in all blood cells)

      • Bleeding due to low platelets

      • Uveitis (eye inflammation)

      • Neurological signs in severe cases

      • Glomerulonephritis (kidney inflammation)

    • Dogs in this stage may have an elevated globulin level and low albumin. The disease is more severe, with a high mortality rate.

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• Diagnosis

  • Diagnosis involves two primary methods: PCR testing and antibody testing.

  • PCR Testing:

    • Detects Ehrlichia DNA in the blood and is more sensitive, especially for early or acute cases.

    • A positive result can indicate an active or recent infection, though it may remain positive for weeks even after the infection has resolved.

  • Antibody Testing:

    • Detects antibodies against E. canis in the blood, indicating exposure but not necessarily active infection.

    • Antibodies can be measured using immunofluorescent antibody (IFA) tests or enzyme-linked immunosorbent assays (ELISA).

    • A positive test suggests exposure, but a negative test does not rule out Ehrlichiosis completely, especially in very sick dogs or early infections.

    • Titers typically begin to drop 6 to 9 months after infection.

  • Blood Smear:

    • Ehrlichia organisms can sometimes be seen directly on blood smears, especially in the acute phase, confirming diagnosis.

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• Treatment

  • Doxycycline is the primary treatment and is generally effective, especially when started early.

    • Dosage: 5 mg/kg orally every 12 hours for 28 days.

    • Most dogs show rapid improvement within the first few days of treatment.

    • Post-treatment PCR testing (2 weeks and 2 months after completing doxycycline) is done to confirm eradication of the infection.

  • Chronic Cases:

    • Dogs with chronic infections are harder to treat due to the long-term damage to their immune system and organs.

    • Secondary immune-mediated reactions (e.g., arthritis, platelet destruction) may require corticosteroids like prednisone for management.

    • Blood transfusions may be necessary for dogs with severe anemia or pancytopenia.

  • Alternative Medications:

    • In cases where doxycycline is ineffective, chloramphenicol or imidocarb may be used.

  • Supportive Care:

    • Dogs with severe symptoms may require supportive care, such as blood transfusions, IV fluids, and nutritional support.

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• Prognosis

  • Acute Phase: Most dogs recover fully with early treatment.

  • Chronic Phase: Dogs are more likely to have a poor prognosis, with higher mortality rates due to severe complications like glomerulonephritis, uveitis, and pancytopenia.

  • Reinfection: Immunity against Ehrlichia canis is not lifelong, so dogs can be re-infected if they are exposed again.

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• Prevention

  • Tick Control: Regular tick prevention (acaricides such as fipronil, permethrin, or imidacloprid) is essential, especially in areas where ticks are common.

  • Avoid Tick Habitats: Minimize dogs' exposure to tick-infested environments.

  • Prompt Tick Removal: Remove ticks promptly to prevent the transmission of Ehrlichia and other tick-borne diseases.

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3. Hepatozoonosis

• Etiology

  • Cause: Hepatozoonosis is caused by Hepatozoon canis (and occasionally H. americanum in the southern U.S.).

  • Transmission: Unlike other tick-borne diseases, it is transmitted when a dog ingests an infected tick, rather than through a bite. The tick must first ingest the protozoan from feeding on an infected host (usually rodents).

  • Pathophysiology: The protozoa localize in the dog’s skeletal muscles, where they form cysts. This leads to chronic muscle inflammation (myositis), pain, and in severe cases, muscle atrophy.

• Clinical Signs

  • Acute Signs: Fever, lethargy, muscle pain, and stiffness due to inflammation of the skeletal muscles. Dogs may also show signs of lethargy, anorexia, and weight loss.

  • Chronic Signs: Chronic muscle wasting, particularly of the hind limbs, and recurrent episodes of fever. Some dogs may develop joint issues or difficulty in walking due to inflammation.

  • Secondary Infections: Hepatozoon infections can predispose dogs to other bacterial or viral infections due to immune system suppression.

• Diagnosis

  • Blood Smear: Look for the characteristic Hepatozoon gamonts within neutrophils and monocytes.

  • PCR: Highly sensitive and specific, PCR testing is recommended to detect Hepatozoon DNA.

  • Serology: Antibody tests can confirm exposure but are less useful for acute cases.

  • Muscle Biopsy: For chronic cases, muscle biopsy can show the presence of cysts containing Hepatozoon organisms.

• Treatment

  • Antiprotozoal Therapy: Pyrimethamine, combined with trimethoprim-sulfa and clindamycin, is used for treatment.

  • Chronic Management: Treatment can be prolonged, and dogs with chronic infections may require ongoing therapy to prevent relapses.

  • Supportive Care: Analgesics (NSAIDs or corticosteroids) to control inflammation and pain, along with muscle relaxants.

• Prevention

  • Tick Control: Implement year-round tick prevention measures to avoid ingestion of ticks.

  • Avoidance of Tick Habitats: Dogs should be kept away from environments where ticks are prevalent, such as heavily wooded areas or regions with a high rodent population.

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4. Lyme Disease (Borreliosis)

• Etiology

  • Cause: Borrelia burgdorferi, a spirochete bacterium, causes Lyme disease.

  • Transmission: Transmitted by Ixodes ticks, most commonly Ixodes scapularis (deer ticks) in the U.S.

  • Pathophysiology: The spirochetes disseminate throughout the dog's tissues, including joints and kidneys. They may trigger immune-mediated arthritis, nephritis, and other systemic complications.

• Clinical Signs

  • Acute Signs: Lameness (due to Lyme arthritis), fever, lethargy, and swollen joints.

  • Chronic Signs: Chronic Lyme arthritis, renal damage leading to Lyme nephritis (proteinuria, renal failure), and persistent fever.

  • Systemic Complications: Renal involvement in severe cases can lead to irreversible kidney damage.

• Diagnosis

  • Serology: The SNAP 4Dx test detects antibodies to Borrelia burgdorferi, which is useful for confirming exposure.

  • PCR: Useful in detecting active infections, especially in cases with renal involvement.

  • Urinalysis: Detects proteinuria, which is indicative of Lyme nephritis.

• Treatment

  • Antibiotics: Doxycycline (most commonly used), given for 4 weeks.

  • NSAIDs: For pain management due to arthritis.

  • Renal Support: In cases with Lyme nephritis, renal support may include fluid therapy, ACE inhibitors, and possibly dialysis in severe cases.

• Prevention

  • Tick Control: Routine tick prevention using oral medications (e.g., afoxolaner), topical agents (e.g., fipronil), or collars (e.g., Seresto).

  • Vaccination: Lyme disease vaccination may be considered in endemic areas.

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5. Anaplasmosis

• Etiology

  • Cause: Anaplasma phagocytophilum, a Gram-negative rickettsial bacterium.

  • Transmission: Spread by Ixodes ticks, particularly Ixodes scapularis (deer tick).

  • Pathophysiology: The bacteria infect neutrophils, causing immune-mediated disease and leading to clinical signs like fever, lameness, and thrombocytopenia.

• Clinical Signs

  • Acute Phase: Fever, anorexia, lethargy, lameness, and joint pain.

  • Chronic Phase: Long-term joint pain or intermittent fever may persist.

  • Co-Infection: Dogs infected with Anaplasma often have concurrent infections with other tick-borne pathogens like Ehrlichia or Borrelia.

• Diagnosis

  • Blood Smear: Neutrophilic morulae (round or oval bodies) within neutrophils.

  • PCR: Highly sensitive and the preferred method for confirming active infection.

  • Serology: Antibody detection to confirm exposure but not acute infection.

• Treatment

  • Antibiotics: Doxycycline for 3 weeks, as it is effective in eliminating the bacteria.

• Prevention:

  • Tick Control: Regular administration of tick preventatives, such as oral or topical treatments.

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