Anaplasmosis

Pathophysiology & Transmission Dynamics

Causative Organism and Vector

• Pathogen: the bacterium Anaplasma phagocytophilum.
• Vector: the hard ticks Ixodes scapularis (North America) and Ixodes ricinus (Europe). These same ticks carry Lyme disease (Borrelia burgdorferi), so co-infection with anaplasmosis and Lyme disease is fairly common.
• Incubation period: 1–2 weeks after an infected tick attaches and feeds.

How It Invades Granulocytes

• Attachment and entry: A. phagocytophilum uses surface proteins to bind the PSGL-1 receptor (P-selectin glycoprotein ligand-1) on neutrophils and get inside the cell.
• Suppressing the immune response: the bacterium releases factors that blunt the neutrophil's oxidative burst and stop lysosomes from fusing with its vacuole, allowing it to survive and multiply safely inside the host cell.
• Morula formation: the bacteria multiply into mulberry-like clusters (morulae) in the cytoplasm of granulocytes.
• Cell destruction and vascular leak: rapid multiplication ruptures the granulocytes and releases bacteria that trigger inflammatory cytokines. The result is low white cells, low platelets, raised liver enzymes and leaky small vessels in the skin and internal organs.

Clinical Features

Acute Systemic Symptoms

• Sudden onset: high fever (> 39°C), severe chills, intense headache across the forehead or behind the eyes, muscle aches (especially in the back and legs), exhaustion, nausea, vomiting and diarrhea.

Skin Findings

• Uncommon: unlike rickettsial infections or ehrlichiosis, skin lesions are rare in anaplasmosis (fewer than 10% of cases).
• Appearance: when present, usually a nonspecific red maculopapular rash or small pinpoint bleeds (petechiae) from severe thrombocytopenia.
• No eschar: A. phagocytophilum does not cause skin necrosis at the bite site.

Serious Complications in High-Risk Patients

• In older adults, immunocompromised patients or when treatment is delayed, anaplasmosis can progress to:
  • Acute respiratory distress syndrome (ARDS).
  • Myocarditis and acute kidney failure.
  • Hemophagocytic lymphohistiocytosis (HLH).
  • Septic shock and disseminated intravascular coagulation (DIC).

Telling Anaplasmosis Apart From Other Tick-Borne Diseases

Our Diagnostic Approach at Haute-Derma

Exposure History: a tick bite, or hiking, camping or gardening in an area where Ixodes ticks are common, within 1–2 weeks before the fever began.

Giemsa-Stained Peripheral Blood Smear: light microscopy to look for morulae (purple-blue bacterial clusters) inside neutrophils. They are seen in 20%–70% of patients during the first week of illness.

Blood Counts and Chemistry:

• Complete blood count: marked leukopenia and severe thrombocytopenia.
• Blood chemistry: clearly raised liver enzymes (AST and ALT), raised LDH and raised C-reactive protein (CRP).

Molecular (PCR) and Serologic Testing:

• Real-time PCR: detects A. phagocytophilum DNA in whole blood during the acute phase (sensitivity > 85%).
• Indirect immunofluorescence assay (IFA): a fourfold rise in IgG between paired samples taken 2–4 weeks apart.

Treatment and Recovery Plan at Haute-Derma

First-Line Antibiotic Treatment

• Doxycycline (first choice for all age groups):
  • Adult dose: 100 mg twice daily, by mouth or IV.
  • Child dose (< 45 kg): 2.2 mg/kg twice daily.
  • Duration: continue for at least 3 days after the fever has fully resolved and symptoms have improved (usually 10–14 days in total, especially if Lyme co-infection is suspected).
• Rifampin (alternative):
  • Used for: pregnant women or patients with a serious tetracycline allergy.
  • Dose: 300 mg twice daily for 7–10 days.

Monitoring Response and Managing Co-Infection

• Rapid defervescence: anaplasmosis responds very well to doxycycline; fever and headache usually ease within 24–48 hours of the first dose.
• Co-infection: because A. phagocytophilum and Borrelia burgdorferi share the same Ixodes tick, a 14-day course of doxycycline treats both infections at once if the patient also has a bull's-eye rash (EM).