In: Nursing
Summarize the case study report you found on pediatric cutaneous amebiasis.What was surprising about the study? What other infection can be confused with cutaneous amebiasis? What new information did you find in the study that was not discussed in class or in your textbook?
Link to case study: https://jamanetwork.com/journals/jamadermatology/fullarticle/420046
SUMMARY OF THE CASE REPORT ON PEDIATRIC CUTANEOUS AMEBIASIS
In this study, retrospective medical record review of 26 patients with CA (22 adults and 4 children) treated from 1955 to 2005 was performed at 2 major hospitals in Mexico City, Mexico.
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.
INTRODUCTION:
Cutaneous amebiasis (CA) can be defined as damage to the skin and underlying soft tissues by trophozoites of Entamoeba histolytica, the only pathogenic form for humans.
Cutaneous amebiasis may be the only expression of the disease or may involve other organs, usually the gastrointestinal tract. The liver, lungs, and especially the central nervous system may also be involved.
Cutaneous amebiasis (CA), which is still a health problem in developing countries, is important to diagnose based on its clinical and histopathologic features.
Cutaneous amebiasis always presents with painful ulcers. The ulcers are laden with amebae, which are relatively easy to see microscopically with routine stains.
Erythrophagocytosis is an unequivocal sign of CA.
MODE OF ENTRY OF THE AMEBAE:
Amebae reach the skin via 2 mechanisms: direct and indirect. 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.
OTHER SPECIES OF ENTAMOEBA
Other species of Entamoeba, such as Entamoeba hartmanni, Entamoeba coli,and Entamoeba gingivalis, are nonpathogenic.
Another species, Entamoeba dispar, identified by Brumpt in 1925, has been recognized as being responsible for many cases of CA in patients previously interpreted as “healthy carriers.”
Entamoeba dispar is morphologically indistinguishable from E histolytica but genetically and serologically different.
Entamoeba moshkovskii, which is morphologically indistinguishable from E histolytica and Edispar but biochemically and genetically different, has been considered until recently to be primarily a free-living (nonpathogenic) ameba.
PATHOGENESIS OF CUTANEOUS AMEBIASIS
Life cycle of E. histolytica.
It consists of 2 stages:
1.The cyst or infective stage and
2.The trophozoites or tissue-invasive stage.
The disease is usually acquired by ingesting food or water contaminated with cysts, which are 10 to 25 μm and have 4 nuclei; they are capable of surviving for days outside the body and are also able to survive the acidic environment of the stomach and excyst in the ileum.
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. Therefore, amebae reach the skin and develop any of the patterns described herein through 2 mechanisms: directand indirect transmission of the trophozoites.
MODE OF TRANSMISSION:
1.Direct infestation results with the spread from the colon and rectum to anal, perianal, perineal, pubic, or genital skin, which is the mechanism of CA in infants . 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.
2.Indirect transmission results when the trophozoites invade the intestinal wall, penetrate a vessel, and reach the liver; rarely, trophozoites invade other organs, such as the lung and/or chest wall, and migrate to the skin. However, any other area of the body may be infected via a contaminated hand by scratching.
CLINICAL PRESENTATION:
In general, all these children presented with dysentery, fever (body temperatures, 39°C-40°C), irritability, weight loss, anemia, and leukocytosis.
TREATMENT:
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.
METHODS
All patients with an unequivocal diagnosis of CA based on the clinical and histopathologic identification of trophozoites were retrieved from our files at the Clinic for Pediatric Dermatology of the Hospital General de México and from the Department of Pathology of the Hospital de Especialidades of the Centro Médico Nacional, IMSS, from 1955 to 2005.
The clinical information was collected from the clinical records and/or by histopathologic request. 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 presentation for care. Results of these tests were retrieved from patient records. Clinical pictures of all patients were taken before and after treatment.
RESULTS
There were 22 adults and 4 children (all <2 years old) identified with CA. The constant and common clinical denominator of the 4 children was a putrid, painful ulcer, which ranged from 1 to several perineal ulcers.
Ulcers showed a gray-white necrotic base, with red edges, that extended rapidly in diameter and depth, during a period of weeks, at the rate of approximately 1 cm/wk. The ulcer measured from a few millimeters to several centimeters).
Diagnosis was clinically suspected and confirmed by skin biopsy. Trophozoites of E histolytica were identified as round or oval unicellular basophilic structures, measuring 20 to 50 μm, often surrounded by a clear halo, which is assumed to be tissue retraction due to dehydration, and with a nucleus measuring 4 to 7 μm .
Ulcers 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. Lysis and necrosis of the skin (and other tissues) are consequences of the interaction between the host and ameba
Surrounding the ulcers was a mixed inflammatory infiltrate of neutrophils, lymphocytes, and eosinophils, generally in association with extravasated erythrocytes. Erythrophagocytosis by amebae was a constant feature in CA and represents a microscopic sign of its pathogenicity. 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 we were able to perform serologic tests in which an enzyme-linked immunosorbent assay reaction was positive for E histolytica.
Chest radiographs from the 4 pediatric patients showed right hemidiaphragm elevation in 2 of them and abdominal radiography confirmed hepatomegaly in those 2, but no other alterations were seen in the 4 pediatric patients.
All these children were treated with dehydroemetine, 1 mg/kg daily for 10 days, and metronidazole, 30 mg/kg daily for 21 days. 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.
One patient, who 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 reconstruction.
What is surprising about this study
The surprising thing in this study is the prevalence of the disease in children under 2 years of age. Out of the 26 patients studied, 4 were children under 2 years of age which means 15.39% of the subjects were young children under 2 years of age.
WHAT INFECTIONS ARE CONFUSED WITH CUTANEOUS AMEBIASIS:
Cutaneous amebiasis is often confused with other infections that cause any ulcer in the diaper area of a child like Staphylococcus, Sterptococcus, Candida.
In areas other than diaper area, such as the abdominal wall (because of a colostomy site, draining of a hepatic abscess, or laparotomy incision) infections due to Pseudomonas aeruginosa, Enterobacter cloacae, E. coli, Morganella morganii, Candida albicans are often confused with Cutaneous Amebiasis.
NEW INFORMATION GAINED IN THIS STUDY
The existence of a variety of Entamoeba species namely Entamoeba hartmanni, Entamoeba coli,and Entamoeba gingivalis, Entamoeba moshkovskii which are all non pathogenic is a new information learnt from this study.
The detailed clinical presentation of the disease, with relevant pictures are well explained in the study.
Also, the detailed prognosis of Pediatric Cutaneous Amebiasis which could not be seen in textbooks is well explained in this study. (All these children were treated with dehydroemetine, 1 mg/kg daily for 10 days, and metronidazole, 30 mg/kg daily for 21 days. 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, who 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 reconstruction).This gives the reader an information that though it is a very serious disease , proper diagnosis and early initiation of treatment can cure it as seen in 3 out of 4 children in the study.