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(A) N. <t>fowleri</t> life cycle and pathogenesis. Free-living trophozoites in warm freshwater penetrate the nasal mucosa during water exposure and migrate through the olfactory epithelium. The organism travels through the cribriform plate, to the olfactory bulbs and cerebrospinal fluid (CSF), leading to central nervous system invasion. B) Trophozoite and (C) cyst observed in N. fowleri cultured from the patient’s CSF. (D) PCR amplification of N. fowleri ITS in CFS from a Healthy Control (HC), patient (P), N. folweri positive control (C+), and negative control (C-). JITS primers are used in the upper panel and NFITS primers in the lower one. (E) Magnetic Resonance Imaging (MRI) of the patient. Small porencephalic lesions located in both thalami, slightly larger on the right side, where they measure approximately 15 mm, without contrast enhancement. Focal lesion, without mass effect, in the left hemipons (less than 1 cm in size, with no contrast enhancement).
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(A) N. <t>fowleri</t> life cycle and pathogenesis. Free-living trophozoites in warm freshwater penetrate the nasal mucosa during water exposure and migrate through the olfactory epithelium. The organism travels through the cribriform plate, to the olfactory bulbs and cerebrospinal fluid (CSF), leading to central nervous system invasion. B) Trophozoite and (C) cyst observed in N. fowleri cultured from the patient’s CSF. (D) PCR amplification of N. fowleri ITS in CFS from a Healthy Control (HC), patient (P), N. folweri positive control (C+), and negative control (C-). JITS primers are used in the upper panel and NFITS primers in the lower one. (E) Magnetic Resonance Imaging (MRI) of the patient. Small porencephalic lesions located in both thalami, slightly larger on the right side, where they measure approximately 15 mm, without contrast enhancement. Focal lesion, without mass effect, in the left hemipons (less than 1 cm in size, with no contrast enhancement).
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(A) N. <t>fowleri</t> life cycle and pathogenesis. Free-living trophozoites in warm freshwater penetrate the nasal mucosa during water exposure and migrate through the olfactory epithelium. The organism travels through the cribriform plate, to the olfactory bulbs and cerebrospinal fluid (CSF), leading to central nervous system invasion. B) Trophozoite and (C) cyst observed in N. fowleri cultured from the patient’s CSF. (D) PCR amplification of N. fowleri ITS in CFS from a Healthy Control (HC), patient (P), N. folweri positive control (C+), and negative control (C-). JITS primers are used in the upper panel and NFITS primers in the lower one. (E) Magnetic Resonance Imaging (MRI) of the patient. Small porencephalic lesions located in both thalami, slightly larger on the right side, where they measure approximately 15 mm, without contrast enhancement. Focal lesion, without mass effect, in the left hemipons (less than 1 cm in size, with no contrast enhancement).
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(A) N. <t>fowleri</t> life cycle and pathogenesis. Free-living trophozoites in warm freshwater penetrate the nasal mucosa during water exposure and migrate through the olfactory epithelium. The organism travels through the cribriform plate, to the olfactory bulbs and cerebrospinal fluid (CSF), leading to central nervous system invasion. B) Trophozoite and (C) cyst observed in N. fowleri cultured from the patient’s CSF. (D) PCR amplification of N. fowleri ITS in CFS from a Healthy Control (HC), patient (P), N. folweri positive control (C+), and negative control (C-). JITS primers are used in the upper panel and NFITS primers in the lower one. (E) Magnetic Resonance Imaging (MRI) of the patient. Small porencephalic lesions located in both thalami, slightly larger on the right side, where they measure approximately 15 mm, without contrast enhancement. Focal lesion, without mass effect, in the left hemipons (less than 1 cm in size, with no contrast enhancement).
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ATCC n fowleri
(A) N. <t>fowleri</t> life cycle and pathogenesis. Free-living trophozoites in warm freshwater penetrate the nasal mucosa during water exposure and migrate through the olfactory epithelium. The organism travels through the cribriform plate, to the olfactory bulbs and cerebrospinal fluid (CSF), leading to central nervous system invasion. B) Trophozoite and (C) cyst observed in N. fowleri cultured from the patient’s CSF. (D) PCR amplification of N. fowleri ITS in CFS from a Healthy Control (HC), patient (P), N. folweri positive control (C+), and negative control (C-). JITS primers are used in the upper panel and NFITS primers in the lower one. (E) Magnetic Resonance Imaging (MRI) of the patient. Small porencephalic lesions located in both thalami, slightly larger on the right side, where they measure approximately 15 mm, without contrast enhancement. Focal lesion, without mass effect, in the left hemipons (less than 1 cm in size, with no contrast enhancement).
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(A) N. fowleri life cycle and pathogenesis. Free-living trophozoites in warm freshwater penetrate the nasal mucosa during water exposure and migrate through the olfactory epithelium. The organism travels through the cribriform plate, to the olfactory bulbs and cerebrospinal fluid (CSF), leading to central nervous system invasion. B) Trophozoite and (C) cyst observed in N. fowleri cultured from the patient’s CSF. (D) PCR amplification of N. fowleri ITS in CFS from a Healthy Control (HC), patient (P), N. folweri positive control (C+), and negative control (C-). JITS primers are used in the upper panel and NFITS primers in the lower one. (E) Magnetic Resonance Imaging (MRI) of the patient. Small porencephalic lesions located in both thalami, slightly larger on the right side, where they measure approximately 15 mm, without contrast enhancement. Focal lesion, without mass effect, in the left hemipons (less than 1 cm in size, with no contrast enhancement).

Journal: medRxiv

Article Title: Primary Amoebic Meningoencephalitis caused by Complement C2 Deficiency

doi: 10.64898/2026.01.31.26345168

Figure Lengend Snippet: (A) N. fowleri life cycle and pathogenesis. Free-living trophozoites in warm freshwater penetrate the nasal mucosa during water exposure and migrate through the olfactory epithelium. The organism travels through the cribriform plate, to the olfactory bulbs and cerebrospinal fluid (CSF), leading to central nervous system invasion. B) Trophozoite and (C) cyst observed in N. fowleri cultured from the patient’s CSF. (D) PCR amplification of N. fowleri ITS in CFS from a Healthy Control (HC), patient (P), N. folweri positive control (C+), and negative control (C-). JITS primers are used in the upper panel and NFITS primers in the lower one. (E) Magnetic Resonance Imaging (MRI) of the patient. Small porencephalic lesions located in both thalami, slightly larger on the right side, where they measure approximately 15 mm, without contrast enhancement. Focal lesion, without mass effect, in the left hemipons (less than 1 cm in size, with no contrast enhancement).

Article Snippet: Naegleria fowleri Carter (ATCC 30894, Manassas, Virginia, USA) trophozoites, a pathogenic strain originally isolated from a human case of primary amoebic meningoencephalitis, were maintained axenically in Nelson’s medium supplemented with 10% fetal bovine serum at 37°C in 75 cm2 tissue culture flasks.

Techniques: Olfactory, Cell Culture, Amplification, Control, Positive Control, Negative Control, Magnetic Resonance Imaging

(A) Immunofluorescence microscopy of N. fowleri stained for C9 (green), DRAQ7 (red, dead), and DAPI (blue, nuclei) when non-treated (NT) or after treatment with normal human serum (NHS), heat-inactivated normal human serum (NHS-HI), or C5-deficient serum (C5D). Scale bar: 100 µm. (B–C) Quantification of cell death and C9 deposition from (A). (D) Scanning electron microscopy images of N. fowleri after normal human serum treatment. Scale bar: 5 μm. (E) Amoebicidal activity of NHS, C2-deficient PAM patient alone or supplemented with purified C2 and serum from C2-deficient patients alone or supplemented with purified C2. Data represent three independent experiments; mean ± SEM. ns: not significant. **P < 0.01; ***P < 0.001 (unpaired t tests). NT: non-treatment; NHS: normal human serum; NHS-HI: normal human serum heat inactivation; C5D: C5 depleted serum

Journal: medRxiv

Article Title: Primary Amoebic Meningoencephalitis caused by Complement C2 Deficiency

doi: 10.64898/2026.01.31.26345168

Figure Lengend Snippet: (A) Immunofluorescence microscopy of N. fowleri stained for C9 (green), DRAQ7 (red, dead), and DAPI (blue, nuclei) when non-treated (NT) or after treatment with normal human serum (NHS), heat-inactivated normal human serum (NHS-HI), or C5-deficient serum (C5D). Scale bar: 100 µm. (B–C) Quantification of cell death and C9 deposition from (A). (D) Scanning electron microscopy images of N. fowleri after normal human serum treatment. Scale bar: 5 μm. (E) Amoebicidal activity of NHS, C2-deficient PAM patient alone or supplemented with purified C2 and serum from C2-deficient patients alone or supplemented with purified C2. Data represent three independent experiments; mean ± SEM. ns: not significant. **P < 0.01; ***P < 0.001 (unpaired t tests). NT: non-treatment; NHS: normal human serum; NHS-HI: normal human serum heat inactivation; C5D: C5 depleted serum

Article Snippet: Naegleria fowleri Carter (ATCC 30894, Manassas, Virginia, USA) trophozoites, a pathogenic strain originally isolated from a human case of primary amoebic meningoencephalitis, were maintained axenically in Nelson’s medium supplemented with 10% fetal bovine serum at 37°C in 75 cm2 tissue culture flasks.

Techniques: Immunofluorescence, Microscopy, Staining, Electron Microscopy, Activity Assay, Purification