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Condition: Primary Amoebic Meningoencephalitis (PAM) is a rare, fulminant, and often fatal brain infection.
Causative Agent: Typically caused by Naegleria fowleri, a free-living amoeba.
Geographical Presence: Naegleria fowleri thrives in warm freshwater environments such as lakes, rivers, hot springs, and poorly maintained swimming pools
Entry Point: N. fowleri enters the central nervous system by penetrating the nasal mucosa and cribriform plate via the olfactory nerves. Trophozoites are found in nerves and perivascular spaces. The amoeba's lytic activity leads to the invasion of gray matter, resulting in purulent meningitis.
Immune Response: Trophozoites are susceptible to complement-mediated lysis, enhanced by agglutinating antibodies to N. fowleri.
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Blood Tests:
Elevated white blood cell (WBC) count with increased neutrophils
Serological tests often not helpful due to rapidity of disease and presence of antibodies in uninfected individuals
Imaging (CT/MRI):
Often unremarkable
CT may show obliteration of cisternae bordering midbrain and subarachnoid space over hemispheres
Cerebrospinal Fluid (CSF) Findings:
Absence of bacteria should lead to consideration of amoeba infection
Fluid may be purulent and greyish to yellowish-white
Red blood cell count may be low early but elevates during disease progression
WBC count ranges from 300 to ≥ 26,000 cells per mm³
Elevated CSF pressure (300-600 mm H₂O)
Elevated protein concentration (100-1,000 mg/100 mL)
Low glucose (≤ 10 mg/100 mL)
Immunofluorescent assays may identify Naegleria in CSF samples
Microscopic Examination:
Wet-mount viewed with phase contrast optics may show active trophozoites
If N. fowleri is suspected, sedimented CSF mixed with sterile water, incubated, and examined for amoebae in the flagella stage
PCR may detect and distinguish amoebae in CSF from as little as one amoeba in 5 hours
Biopsy:
Immunofluorescent assays may identify Naegleria in brain tissues
Only trophozoite form found in the brain
Culture:
CSF or brain tissue can be inoculated onto tissue culture cells or nonnutrient agar coated with bacteria and incubated at 37°C
Amoebae emerge, ingest surrounding cells, and divide; observed by light microscopy
Cardiac Findings:
Cardiac rhythm abnormalities or myocardial necrosis may be present
Premortem diagnosis is rare
Primary Therapy:
Amphotericin B has been the primary therapy in patients who have survived
Adult Dosing: 25-300 mcg intrathecally every 48-72 hours, increasing to 500 mcg as tolerated; 0.25-1.5 mg/kg/day IV
Pediatric Dosing: 25-300 mcg intrathecally every 48-72 hours, increasing to 500 mcg as tolerated; 0.5-0.7 mg/kg/day IV
Treatment duration: 10 days
May be used alone or in combination with rifampin, azithromycin, and/or azole drugs like miconazole or ornidazole
Successful treatments include combinations of amphotericin B, rifampin, fluconazole, azithromycin, miltefosine, and dexamethasone, along with CSF drainage and hyperosmolar therapy
Prognosis: Nearly always fatal without prompt and aggressive treatment. Early diagnosis is critical to improve survival chances
Avoidance:
Avoid swimming in warm freshwater bodies, especially during hot weather.
Use nose clips or avoid submersion in water to prevent water from entering the nasal passages
Water Treatment:
Ensure proper maintenance and chlorination of swimming pools and hot tubs.
Use boiled, distilled, or filtered water for nasal rinsing
For more detailed information on successful treatments of PAM, you can explore the following sources:
Stay informed and vigilant in recognizing and treating PAM to improve patient outcomes