AMEBIASIS HATI PDF

Amebiasis intestinal akut terjadi jika seseorang mengalami gejala yang berat dan berlangsung dalam Tetapi yang paling sering terjadi adalah amebiasis hati. Amebiasis Pleuropulmonal •Terjadi akibat ekspansi langsung abses hati. Amebiasis Hati •Terjadi akibat embolisasi ameba dan dinding usus besar lewat vena. Radiologi Tes fungsi hati Aspirasi abses. Perbedaan disentri ameba dengan disentri basiler (shigellosis) Amebiasis Shigellosis Mulainya Demam.

Author: Tausar Nataxe
Country: Czech Republic
Language: English (Spanish)
Genre: Software
Published (Last): 25 December 2015
Pages: 256
PDF File Size: 9.40 Mb
ePub File Size: 15.85 Mb
ISBN: 376-9-58275-152-3
Downloads: 36514
Price: Free* [*Free Regsitration Required]
Uploader: Duzil

The detection of Entamoeba histolyticathe causative agent of amebiasis, is an important goal of the clinical microbiology laboratory. To assess the scope of E. As more is discovered about the molecular and cell biology of E. Molecular biology-based diagnosis may become the technique of choice in the future because establishment of these protozoa in culture is still not a routine clinical laboratory process. In all cases, combination of serologic tests with detection of the parasite by antigen detection or PCR offers the best approach to diagnosis, while PCR techniques remain impractical in many developing country settings.

The detection of amebic markers in serum in patients with amebic colitis and liver abscess appears promising but is still only a research tool. On the other hand, stool antigen detection tests offer a practical, sensitive, and specific way for the clinical laboratory to detect intestinal E. All the current tests suffer from the fact that the antigens detected are denatured by fixation of the stool specimen, limiting testing to fresh or frozen samples.

This is because amebiasis is presently one of the three most common causes of death from parasitic disease. The World Health Organization reported that E.

The vast majority of these infections are acquired in the developing world. There are at least eight amebas E. However, ameblasis are generally accepted as commensal organisms except for E. In the light of earlier reports about the prevalence of amebiasis in such subjects, interpretation is very difficult because older data did not differentiate between morphologically identical species, one that is noninvasive E.

Laboratory Diagnosis of Amebiasis

It is very important to keep in mind that according to the older data, many E. Each detection test has different advantages and disadvantages. The goals of this review are to describe E. Amebiasis may have been first recognized as a deadly disease by Hippocrates to B.

The early literature of E. Milestones in the study of E.

Laboratory Diagnosis of Amebiasis

A clinical syndrome suggestive of intestinal disease was first widely recognized in the mids, although a parasitic etiology was not determined at that time.

Suggestion of a parasitic etiology was first recorded in from a case where amebas were observed in a stool sample from a child with dysentery in Prague. InFedor Losch isolated E. Leonard Rogers designated emetine as the first effective treatment for amebiasis in InWalker and Sellards demonstrated the infective cyst form of E. InDobell described the life cycle of E. Brumpt proposed that E.

  LOESELIA MEXICANA PDF

Diamond’s first axenic culture of E. InSargeaunt and colleagues reported that E. With the application of a number of new molecular biology-based techniques, tremendous advances have been made in our knowledge of the diagnosis, natural history, and epidemiology of amebiasis. Humans are the primary known reservoir for E.

The main source of transmission is the chronically infected human. Stools infected with the cyst form of the parasite may contaminate fresh food or water. The other common source of transmission is oral-anal sexual contact In addition, there is a suggestion of zoonotic transmission, but this is not clear 2122 Experimental infections with E.

These animals may also acquire human strains as a result of close contact with humans. In one study, E. There may be some animal reservoirs of E. The importance of wildlife primates in zoonotic infections was studied by Jackson et al. However, there are no reports of sporadic zoonotic transmission of cases between infected animals and humans, although E.

Infective cysts may be spread by arthropods such as cockroaches and flies, suggesting that these insects are able to play a rare but important role in transmission 93 The life cycle of E.

It consists of an infective cyst stage and a multiplying trophozoite stage. Humans are infected by ingesting these infective cysts, which travel through the gut lumen to the small intestine terminal ileumwhere each excysts to form eight daughter trophozoites.

The trophozoites are motile forms, which adhere to and invade intestinal epithelial cells which line the gastrointestinal tract. Trophozoites move by extending creeping projections of cytoplasm, called pseudopodia, which pull them along. They also use these projections to surround and engulf food particles. The cytoplasm frequently contains many red blood cells RBCs that have been ingested.

The trophozoites of E. Trophozoites are easily destroyed in the outside environment, degenerating within minutes. The trophozoite of E. The precyst contains aggregates of ribosomes, called chromatoid bodies, as well as food vacuoles that are extruded as the cell shrinks to become a mature cyst. It is the mature cyst that, when consumed in contaminated food or water, is infectious. In the process of becoming tetranucleated, the nucleus of the cyst divides twice.

Chromatoid bodies and glycogen vacuoles cannot be seen at this stage 4664 Cysts are not invasive, but trophozoites can penetrate the gastrointestinal mucosa From there, the trophozoites are able to migrate to other organs, causing extraintestinal infections.

Like other protozoa, E. Biochemical analysis has indicated that glutathione is not present. For this reason, E. It also uses pyrophosphate instead of ATP The cytoplasm of the cyst is vacuolated with numerous glycogen deposits, visible by permanent stains such as iron-hematoxylin, that decrease in size and number as the cyst matures. Also visible are crystalline hahi of aggregated ribosomes in the cytoplasm of the trophozoite 89 The gene organization of E.

  JERRY MANDER FOUR ARGUMENTS FOR THE ELIMINATION OF TELEVISION PDF

Although the structure of E. This sequence has proved quite amebkasis for genotyping of the different enteric amebae 43 Early in the 20th century, Brumpt proposed that E.

Then Sargeaunt et al. Later, Strachan xmebiasis al. Finally, Tannich et al. Successive additions to the data indicating that they are distinct species resulted in the division of E. It is therefore possible to obtain more reliable and correct epidemiological data using molecular, biochemical, and immunological features, and these allow better diagnosis and treatment.

No cases have been documented where intestinal disease and colitis were caused by E. It cannot be forgotten that E.

Diagnosis of most of the previous infections as E. In reality, many of these organisms were probably genetically distinct from E. Currently, there are many molecular tools available to allow the differentiation E.

Commonly, description of Entamoeba species has depended on features of these parasites such as the size of the trophozoites and cysts, the number of nuclei in the mature cyst, the nuclear structure, etc. It belongs to the subphylum Sarcodina, class Lobosea, and family Entamoebidae Drawing of intestinal Entamoeba spp.

All illustrations are adapted from aebiasis sources. Mostly, trophozoites of E. The cyst stage of E. Unstained cysts cannot be differentiated with any certainty from cysts of other species of Entamoeba. The nuclear structure of stained E. Formerly, these parasites were known as a synonym of E. Now they are known to be separate commensal or nonpathogenic parasites, and their infections do not need to hsti treated Trophozoites of ameblasis E.

The incubation period of intestinal amebiasis can vary, ranging from a few days hafi months or years 64, but is generally 1 to 4 weeks The wide spectrum of intestinal infection ranges from asymptomatic to transient intestinal inflammation to a fulminant colitis with an array of manifestations that may include toxic megacolon and peritonitis These patients have normal rectosigmoidoscopic findings, without a history of blood in stool samples.

Cysts and trophozoites lacking ingested RBCs may be visible on microscopy Interestingly, most individuals infected with E. Unlike in Japanwhere E. At present, the diagnosis of intestinal amebiasis anebiasis many countries relies commonly on microscopic examination of stool samples for the presence or absence of E.

qmebiasis

Unfortunately, it is not clear what percentage of patients infected with E. It was thought that asymptomatic infection by E. Estimation of the true prevalence of amebiasis is not easy, because many studies were done with just one microscopic examination of a stool sample 1315 ,