Free-Living Amoebae

A primary amoebic meningoencephalitis conditional is an acute central nervous system infection that is fatal in general, and is caused by Naegleria fowleri.

Three main syndromes occur:

Free-living amoebae are protozoa that live independently in soil or water and do not require a human or animal host. They rarely lead to disease – in contrast to the parasitic amoeba Entamoeba histolytica, a common cause of intestinal infections (amebiasis). The pathogenic free-living amoebae the genera Naegleria, Acanthamoeba, Balamuthia and Sappinia include (p pedata was involved in a case of amoebic encephalitis in Texas). Three main syndromes occur: Primary amoebic meningoencephalitis caused granulomatous amoebic encephalitis Amöbenkeratitis Acanthamoeba and Balamuthia can also lead to skin lesions or disseminated disease in immunocompromised individuals; Acanthamoeba can cause an infection of the sinus or lung. The case of S. pedata encephalitis was successfully treated with a combination of azithromycin, pentamidine, itraconazole and flucytosine plus surgical resection of CNS lesion. The addition of miltefosine can be considered. Primary amoebic meningoencephalitis conditional A primary amoebic meningoencephalitis conditional is an acute central nervous system infection that is fatal in general, and is caused by Naegleria fowleri. Naegleria fowleri occur in warm freshwater worldwide. By swimming in contaminated water nasal mucosa is exposed to the pathogen, which may penetrate through the olfactory neuroepithelium and the cribriform plate into the CNS. Most of the patients were previously healthy children or young adults. The symptoms begin – sometimes smell and taste changes – within 1-2 weeks after exposure. It comes to a fulminant meningoencephalitis with headache, neck stiffness and changes in mental status, which leads to death within 10 days, mostly due to cerebral herniation. Few patients have survived. The suspected infection is to anamnestic indications of swimming in fresh water, but the confirmation is difficult because CT and routine cerebrospinal fluid fails nonspecific. However, they are still required to exclude other causes. It should Liquornativpräparate be created, in which mobile amoeboid trophozoites may be visible (that are destroyed at a Gram stain). Immunohistochemistry, amoeba culture and PCR of cerebrospinal fluid and / or brain biopsy are available in specialized laboratories. Optimal therapy is unclear. Appropriate treatment would comprise miltefosine, an experimental antileishmanial substance which has been successfully used for the treatment of granulomatous amoebic encephalitis. Miltefosine is (s CDC. CDC information on Naegleria) through consultation by the Centers for Disease Control and Prevention available. Other drugs that have been used in combination regimens for Naegleria, comprise amphotericin B, rifampicin, an azole (fluconazole, voriconazole or ketoconazole) and azithromycin. Granulomatous amoebic encephalitis A granulomatous amoebic encephalitis is a generally fatal subacute CNS infection in immunocompromised or debilitated hosts caused by Acanthamoeba sp. or Balamuthia mandrillaris is caused. Acanthamoeba sp. and Balamuthia mandrillaris are found in water, soil and dust worldwide. There is often a human exposure, but an infection is rare. Acanthamoebaa infections of the CNS occurs almost exclusively in immunocompromised or debilitated patients for other reasons, but as mandrillaris can also attack healthy hosts. It is believed that the skin or the lower respiratory tract represent the entry gate, with a subsequent hematogenous dissemination in the CNS. The onset is insidious, often with focal neurological manifestations. There are often changes in mental status, seizures and headaches. B. mandrillaris can also cause skin lesions; Patients with B. mandrillaris infection can present with skin lesions and later develop neurological symptoms and signs. Survival is highly unlikely (and only comes in immunocompetent patients), death occurs after the onset of symptoms 7-120 days. The diagnosis is often made only after death. In patients with Acanthamoeba infections CT and MRI, single or multiple lesions with annular contrast enhancement have, most often in the temporal and parietal lobes. The liquor has increased leukocyte count on (mostly lymphocytes), but trophozoites are rarely detected. Visible skin lesions often contain amoebae and should be biopsied; for detection of amoebas they should be cultured and tested for antibiotic susceptibility. A brain biopsy is often positive. In specialized reference laboratories and PCR-based detection methods are available. In patients with a B. mandrillaris infection CT and MRI usually show multiple nodular lesions with annular contrast enhancement. Intralesional hemorrhage is an important radiological clue. The optimal treatment of granulomatous amoebic encephalitis is unclear. Some cases of granulomatous encephalitis respond to drug combinations. Although the number of patients who are treated with miltefosine therapy is small, miltefosine seems to offer a survival advantage. Miltefosine is available directly from the CDCs. To the other substances that have been used in combination to Behandung this syndrome include pentamidine, sulfadiazine or trimethoprim / sulfamethoxazole, flucytosine, an azole (fluconazole, itraconazole or voriconazole) and amphotericin B. albendazole has been used with miltefosine and other medications, to treat the example mandrillaris encephalitis. For all cases of amoebic encephalitis immediate consultation with the CDC recommended is (call the CDC Emergency Operations Center at 770-488-7100 to). By Acanthamoeba sp or B. mandrillaris caused skin infections are usually treated with the same drugs plus surgical debridement. Amöbenkeratitis A Amöbenkeratitis is a corneal infection by Acanthamoeba sp., Which usually occurs in contact lens wearers. Acanthamoeba sp. can cause a chronic and progressive destructive keratitis in normal hosts. The main risk factor (85% of cases) is the wearing of contact lenses, especially when lenses are worn while swimming or when a non-sterile lens cleaning liquid is used. Some infections occur after a Korneaabrasion. The lesions are typically very painful and cause a foreign body sensation. Initially the lesions appear dendriform and reminiscent of a herpes simplex keratitis. Later there will be uneven stromal infiltrates and sometimes a characteristic ring-shaped lesion. Anterior uveitis is usually also. There is a visual impairment. The diagnosis is confirmed by Giemsa or trichrome stained Kornealgeschabsel and by culture on special media. In differenzialdiagnostischem suspected herpes viral culture is carried out. Therapy debridement of the corneal topical propamidine plus a biguanide Possibly systemic fluconazole or itraconazole In the early stages speaks a superficial infection better to therapy. The greatest therapeutic problem, the encysted forms appear to be within the life cycle. Epithelial lesions are debrided and conducted an intensive drug therapy. Topical propamidine isethionate 0.1% plus. Polyhexamethylene either or Biguanidchlorhexidin drop is often the first choice. During the first 3 days, the drugs are given every 1-2 hours. Among the other topical medications that can be used include aminoglycoside, hexamidine diisethionate, miconazole and Neosporin. Also a systemic therapy with fluconazole or itraconazole was applied, especially in patients with anterior uveitis or participation of the sclera. a therapeutic keratoplasty in most cases was unnecessarily through early detection and treatment, but it remains a therapeutic option if drug therapy fails. intensive therapy is required during the first month. According to clinical response is this tapered off, but continued often 6-12 months. In case of early discontinuation of treatment often leads to Rezidiven.Prävention The contact lens solution should be kept clean. Non-sterile, self-made contact lens solutions should not be used. Wearing contact lenses while swimming or showering should be avoided.

Health Life Media Team

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