To culture Acanthamoeba, scrapings are placed on a non-nutrient agar saline plate seeded with a gram-negative bacteria such as E. coli. If Acanthamoeba are present, they will reproduce readily and become visible on the plate under 10–20 times objective on an inverted microscope. Polymerase chain reaction (PCR) can be used to confirm a diagnosis of Acanthamoeba keratitis, especially when contact lenses are not involved. Confocal microscopy is a non-invasive technique that allows visualization of Acanthamoeba in vivo in cases in which corneal scraping, culture, and cytology do not yield a diagnosis. Treatment
Once Acanthamoeba keratitis is diagnosed, initiation of timely and appropriate treatment will have a significant impact on visual outcomes. Medical therapy aims to eradicate both trophozoite and cystic forms of Acanthamoeba and also control the inflammatory response. Medical therapy
Multiple classes of drugs have been found to be effective in killing the trophozoite form of Acanthamoeba, including anti-bacterial, anti-fungal, anti-protozoal, and anti-neoplastic agents. However, no single therapy has been found to eliminate both trophozoite and cystic forms, and to eradicate corneal infection.One class of medications used in treatment is the biguanides, which include polyhexamethylene biguanide (PHMB) 0.02% to 0.06% drops, and chlorhexidine 0.02 to 0.2% drops. These medications disrupt the cell wall of the trophozoite organism, leading to its death. However, these agents have shown limited efficacy against the cystic forms. Due to the efficacy of these drugs against the Acanthamoeba, as well as their low toxicity to the cornea, they are commonly used as the first line medications in the treatment of AK.
Familial eosinophilia is a rare congenital disorder characterized by the presence of sustained elevations in blood eosinophil levels that reach ranges diagnostic of eosinophilia (i.e. 500-1500/microliter) or, far more commonly, hypereosinophilia (i.e. >1,500/microliter). Although high eosinophil levels are associated with certain diseases and thought to contribute to the tissue destruction found in many other eosinophilia-related diseases (see clonal eosinophilia), clinical manifestations and tissue destruction related to the eosinophilia in familial eosinophilia is uncommon: this genetic disease typically has a benign phenotype and course compared to other congenital and acquired eosinophilic diseases. Presentation
Individuals with familial eosinophilia exhibit hypereosinophilia presumably from birth (earliest documentation at 4 months of age). Elevated blood levels of eosinophils are remarkably stable over time in affected family members. These individuals are generally detected on routine blood cell counts and at the time of diagnosis present without symptoms or at least no symptoms related to their eosinophilia. Their blood cell counts are typically normal except for  eosinophil numbers which range between ~2000 and 5000 cells/microliter (normal <450 cells/microliter). Peripheral blood smears revealed that eosinophils showed normal morphology, a finding distinctly different from many other types of hypereosinophilia in which blood smears commonly shown immature blood cells and eosinophils showing distinctly abnormal areas of cytoplasmic clearing. Ultrastructural changes characteristic of eosinophil activation (e.g. piecemeal degranulation of eosinophils and increases in the number of their lipid bodies), other eosinophil activation markers (e.g.