Download Citation on ResearchGate | On Mar 5, , Arturo García Valdés and others published AMEBIASIS CUTANEA: PRESENTACION DE UN CASO }. Munive AM, Rojas AM Amebiasis intestinal y cutánea. Rev Med Cos Cen ; 65 (). Language: Español References: Page: PDF: Kb. BackgroundCutaneous amebiasis (CA), which is still a health problem in developing countries, is important Magaña ML Amibiasis cutánea.
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In addition to the age and sex of the patients, the case presentation, associated illness or factors, and method of establishing the diagnosis, clinical pictures and microscopic slides were also analyzed. The ulcers are laden with amebae, which are relatively easy to see microscopically with routine stains. Erythrophagocytosis is an unequivocal sign of CA. Amebae reach the skin via 2 mechanisms: Amebae are able to reach the skin if there is a laceration port of entry and if conditions in the patient are favorable.
Amebae are able to destroy tissues by means of their physical activity, phagocytosis, enzymes, secretagogues, and other molecules. Cutaneous amebiasis CA can be defined as damage to the skin and underlying soft tissues by trophozoites of Entamoeba histolyticathe only pathogenic form for humans. Cutaneous amebiasis may be the only expression of the disease or may involve other organs, usually the gastrointestinal tract.
Other species of Entamoebasuch as Entamoeba hartmanni, Entamoeba coli, and Entamoeba gingivalisare nonpathogenic. Entamoeba moshkovskiiwhich is morphologically indistinguishable from E histolytica and E dispar but biochemically and genetically different, has been considered until recently to be primarily a free-living nonpathogenic ameba.
The early isolates of E moshkovskii were free-living forms found in sewage, but human isolates have now been detected in North America, Africa, Australia, and some parts of Europe. This kind of amebiasis has become more common during the last few years.
Paraffin-embedded blocks that housed skin specimens were recut and stained with hematoxylin-eosin. Slides were prepared to be read under the microscope.
Bacteriologic studies from ulcers and necrotic edges and parasitoscopic analysis from stool samples were performed at the time of amebiadis for care. Results of these tests cutsnea retrieved from patient records. Clinical pictures of all patients were taken before and after treatment. The constant and common clinical denominator of the 4 children was a putrid, painful ulcer, which ranged from 1 to several perineal ulcers. The ulcer measured from a few millimeters to several vutanea Figure 1 and Figure 2.
The 4 pediatric patients were all toddlers using diapers. All these patients had amebic colitis and developed amebic diarrhea. The diaper maintained contact of the trophozoites with the skin. Therefore, the anatomical sites of the ulcers were in the diaper area: Patient 1 has been previously described by 1 of us M.
Diagnosis was clinically suspected and confirmed by skin biopsy. By performing a smear from the edge of the ulcers, we were to show the amebae in 2 of our patients patients 1 and 3.
At amebiaeis 1 ulcer that involved the epidermis and dermis to a variable depth was seen. Often there were wide areas of necrosis, with fine granular and eosinophilic bland material with nuclear debris.
Surrounding the ulcers was a mixed inflammatory infiltrate of neutrophils, lymphocytes, and eosinophils, amebiassis in association with extravasated erythrocytes.
Erythrophagocytosis by amebae was a constant feature in CA and represents a microscopic sign of its pathogenicity.
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No granulomas are seen in amebiasis. In all 4 pediatric patients, microscopic examination of the stool sample showed a cyst of E histolytica ; cultures of the ulcers yielded Staphylococcus epidermidis and Escherichia coli. Cultures from blood and cerebrospinal fluid yielded no growth of bacteria.
In 2 patients patients 1 and 4we were able to perform serologic tests in which amebbiasis enzyme-linked immunosorbent assay reaction was positive for E histolytica.
Chest radiographs from the 4 pediatric patients showed right hemidiaphragm elevation in 2 cutajea them and abdominal radiography confirmed hepatomegaly in those 2, but no other alterations were seen in the 4 pediatric patients. Escharotomy, cleaning, and dressing changes were performed daily for all patients. This regimen produced rapid improvement in days to weeks, with all ulcers healing by the second week of care.
Patient 1, amebiasix had the most severe case of CA, was referred to the plastic surgery service for reconstruction of the vulva and perineum. The other 3 children healed without the need for cutanra. In children CA is rare; when it occurs, it usually, if not always, develops in the anal and perianal area and the genitalia, usually in association with amebic dysentery, as can be deduced from our 4 patients and 9 others mentioned in the literature Table.
Biagi and Martuscelli 22 described 3 patients: A 9-month-old boy with lesions on the abdomen died without treatment—the diagnosis was obtained post mortem. When medical treatment emetine, dehydroemetine, metronidazole, or diiodohydroxyquinoline is initiated, CA responds soon and well; however, because of the destructive character of the disease, surgical repair is often needed.
To better understand the pathogenesis of CA, it is aebiasis to briefly review the life cycle of E histolytica.
It consists of 2 stages: Each cyst gives origin to 8 trophozoites, which live in the lumen of the colon, where they multiply by binary fission and from where they may invade the intestinal wall and eventually penetrate a blood vessel and spread though the bloodstream, most often to the liver, or they may encyst and produce quadrinucleated cysts after 2 successive nuclear divisions.
Direct infestation results with the spread from the colon and rectum to anal, perianal, perineal, pubic, or genital skin, cutajea is the mechanism of CA in infants and is the most common form in adults and thus deserves special mention not only for its rareness but also because all 4 of our pediatric patients share the same clinical picture with those previously described: Cutaneous amebiasis is preceded or accompanied by diarrhea.
Because of these patients wear diapers, trophozoites are able to remain in contact for a longer time with the skin surface and, surely the association of diapers with humidity and ammonia due to urine and bacteria due to feces may play an adjuvant role. However, any other area of the body may be infected via a contaminated hand by scratching.
Although CA is not a common disease, it certainly is still a public health problem in many areas. In Mexico, it was anebiasis frequent from towhen its incidence was estimated to amebiasid 1 of every dermatologic patients children and adults at the Hospital General de Mexico.
Now, it may be less common because metronidazole, emetine, and dehydroemetine are readily and widely available. Amebiasis is an even more important public health problem than CA. There are million individuals infected with Entamoeba.
Amebiasis cutánea: parasitosis emergente y letal – PDF Free Download
Although most people are colonized with E disparwhich is not pathogenic, many of those individuals have E histolyticawith or without symptoms. Malnutrition, poor hygiene, and preexisting disease contribute to the development of CA in infants and toddlers.
Lysis and necrosis of the skin and other tissues are consequences of the interaction between the host and ameba. The necrosis, probably because of the presence of the parasite itself, is specific to this disease and is similar in any tissue: Amebic motility and phagocytosis of erythrocytes are unquestionable histopathologic signs of pathogenicity, 2 seen in all our cases.
Experimentally, phagocytosis has not always been found to be related to virulence of E histolytica.
Cutaneous Amebiasis in Pediatrics. | Dermatology | JAMA Dermatology | JAMA Network
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