Dysentry

COMMUNITY HEALTH NURSING II

A Project Submitted by:

shine Alishba

Registration No. 2018-ACN-0003-UHS

Bachelor of Science in Nursing

Year III

Faculty: Miss.Arfa

ALIGARAH COLLEGE OF NURSING AND ALIED HEALTH SCIENCES

2019-2023

Table of content
Sr.no Contents Page no.

01 Introduction

02 Prevelance

03 Sign & Symptoms

04 Pathophysiology

05 Treatment

06 Objectives

07 Significance
08 Purpose

09 Discussion

10 Conclusion

11 Reference

12 Questionnaire/Performa
Objectives:
 Identify the role of the protozoa Entamoeba histolytica in the etiology of amebiasis.
 Outline the pathophysiology of amebiasis.
 Describe the use of stool microscopy in the evaluation of amebiasis.
 Review the importance of collaboration and communication among the interprofessional team
to improve patients' outcomes affected by amebiasis.

Introduction
Amebiasis or amoebic dysentery is a common parasitic enteral infection. It is caused by any of the
amoebas of the Entamoeba group. Amoebiasis may present with no symptoms or mild to severe
symptoms, including abdominal pain, diarrhea, or bloody diarrhea. Severe complications may include
inflammation and perforation, resulting in peritonitis. People affected may develop anemia.

If the parasite reaches the bloodstream, it can spread through the body and end up in the liver, causing
amoebic liver abscesses. Liver abscesses can occur without previous diarrhea. Diagnosis is typically by
stool examination using a microscope. An increased WBC count may be present. The most accurate test
is specific antibodies in the blood.

Prevention of amoebiasis is by improved sanitation. Two treatment options are possible, depending on
the location. Amoebiasis in tissue is treated with metronidazole, tinidazole, nitazoxanide,
dehydroemetine, or chloroquine. A luminal infection is treated with diloxanide furoate or iodoquinoline.
Effective treatment may require a combination of medications. Infections without symptoms require
treatment, but infected individuals can spread the parasite to others.

Amoebiasis is present all over the world. Each year, about 40000 to 110000 people die from amoebiasis
infection.

E. histolytica is classified as a category B biodefense organism because of its environmental stability,

ease of dissemination, resistance to chlorine, and its ability to easily spread through contaminated food
products. Besides the GI tract, E. histolytica can affect many organ systems.

There are three species of intestinal amoebas. Entamoeba histolytica causes most symptomatic
diseases. Entamoeba dispar is nonpathogenic, and Entamoeba moshkovskii is reported increasingly, but
its pathogenicity is unclear. These organisms are spread via the oral-fecal route. The infected cysts are
often found in contaminated food and water. Rare cases of sexual spread have also been reported.
Prevalence
Amebiasis occurs worldwide but is predominantly seen in developing countries due to decreased
sanitation and increased fecal contamination of water supplies. Globally, approximately 50 million
people contract the infection, with over 100000 deaths due to amebiasis reported annually. The
principal source of infection is ingestion of water or food contaminated by feces containing E. histolytica
cysts. Hence, travelers to developing countries can acquire amebiasis when visiting the endemic region.
Those who are institutionalized or immunocompromised are also at risk. The organism E. histolytica is
viable for prolonged periods in the cystic form in the environment. It can also be acquired after direct
inoculation of the rectum, from anal or oral sex, or from equipment used for colonic irrigation. Despite
the global public health burden, there are no vaccines or prophylactic medications to prevent amebiasis.

Pathophysiology
E. histolytica is a pseudopod-forming, protozoal parasite that causes proteolysis and tissue lysis. Humans
are the natural hosts. Amoebic infection occurs by the ingestion of mature cysts in fecally-contaminated
food or water or from the hands. Excystation of the mature cysts occurs in the small intestine, and
trophozoites are released; the trophozoites then move to the large intestine. The trophozoites increase
by binary fission and produce cysts. Both stages pass in the feces. The cysts can survive days to weeks in
the external environment because of the protection provided by the cyst wall. The cyst is responsible for
further transmission of the parasite. Ingestion of only a small number of organisms can cause disease.

Histology of the intestinal infection is nonspecific. It usually reveals discrete ulcers, mucosal thickening,
and edematous mucosa. Sometimes flask-shaped ulcers may be seen in the submucosal layers. In some
patients, flask-shaped ulcers are seen.

Clinical Features
Although most cases of amebiasis are asymptomatic, many patients with E. histolytica present with a
spectrum of illness. The incubation period from amebiasis is between 2 to 4 weeks.

Symptoms range from mild abdominal cramps and watery diarrhea to severe colitis producing bloody
diarrhea with mucus. Young people tend to have a more severe disease compared to older individuals.
Fulminant colitis can present with bloody diarrhea in some patients. Risk factors include the use of
corticosteroids, poor nutrition, young age, and pregnancy. Toxic megacolon can be a complication and is
associated with very high mortality.

A few patients may develop invasive extraintestinal disease. The most common extraintestinal
manifestations are an amoebic liver abscess. A liver abscess develops in less than 4% of patients and
may occur within 2 to 4 weeks after the initial infection. Liver abscess usually presents with right upper
quadrant pain, fever, and tenderness to palpation.

An amoebic liver abscess may rupture into the pleural cavity or pericardium, presenting as pleural or
pericardial effusion; however, this is a rare occurrence. Rarely, amebiasis may affect the heart, brain,
kidneys, spleen, and skin. One can also develop proctocolitis, toxic megacolon, peritonitis, brain abscess,
and pericarditis. Hence, amebiasis is a leading parasitic cause of death in humans.

Evaluation
Amebiasis can be diagnosed by a demonstration of the organism using direct microscopy of stools or
rectal swabs. However, the organisms are seen in only 30% of patients.

Antigen detection using an enzyme-linked immunosorbent assay and polymerase chain reaction
techniques is often done. However, the most promising detection method is the loop-mediated
isothermal amplification assay because of its rapidity, operational simplicity, high specificity, and
sensitivity. An ultrasound or CT scan evaluates for extraintestinal amebiasis.[5][1]

Cultures can be done from fecal or rectal biopsy specimens or liver aspirates. Cultures are not always
positive, with a success rate of about 60%.

Liver aspiration using CT-guided imaging is often performed when there is a collection in the liver. The
liver aspiration usually reveals a chocolate-like or thick, dark viscous fluid. Liver aspiration is indicated
when the abscess is large, or there is a threat of imminent rupture.

A colonoscopy is done to obtain scrapings of the mucosal surface. It is appropriate when the stool
studies are negative for amebiasis.

Blood tests may reveal the following:

 Elevated WBC
 Eosinophilia
 Elevated bilirubin and transaminase enzymes
 Mild anemia
 Elevated ESR

Imaging studies may be required depending on the presentation. Ultrasound can identify a liver abscess.

Treatment / Management
The primary therapy for symptomatic amebiasis requires hydration and the use of metronidazole and/or
tinidazole. These two agents are dosed as follows:

Metronidazole dosing for adults is 500 mg orally every 6 to 8 hours for 7 to 14 days.

Tinidazole adult dosing is 2 g orally each day for 3 days.

Luminal agents such as paromomycin and diloxanide furoate are also used. An amoebic liver abscess can
be managed by aspiration using CT guidance in combination with metronidazole. Surgery is sometimes
required to treat massive gastrointestinal bleeding, toxic megacolon, perforated colon, or liver abscesses
not amenable to percutaneous drainage.

Complications
 Toxic megacolon
 Fulminant necrotizing colitis
 Rectovaginal fistula
 Ameboma
 Intraperitoneal rupture of liver abscess
 Secondary bacterial infection
 Extension of infection from the liver into the pericardium or pleura
 Dissemination in the brain
 Bowel perforation
 Stricture of the colon
 Gastrointestinal bleeding
 Empyema

Conclusions
Amebiasis is still a big challenge to public health worldwide, especially for children in developing
countries. Several waterborne outbreaks of amebiasis have been documented, and most of them were
caused by water supply contamination. Estimating the global burden of amebiasis is complicated by
limited diagnosis capacities and surveillance in most areas where E. histolytica is endemic (Marie and
Petri Jr., 2014). More investigations related to epidemiology, pathogenesis, diagnosis and treatment

Deterrence and Patient Education

 Avoid drinking contaminated water.
 Use bottled water when traveling.
 Purify water with tetraglycine hydroperiodide.
 Avoid consumption of raw salads and fruits. Peel off the skin of the fruit if possible.
 Thoroughly wash all vegetables before cooking.

Signicifance
Dysentery is an infection of the intestines that causes diarrhoea containing blood or mucus.

Other symptoms of dysentery can include:

 painful stomach cramps

 feeling sick or being sick (vomiting)
 a high temperature

Dysentery is highly infectious and can be passed on if you do not take the right precautions, such as
properly and regularly washing your hands.

References

Saidin S, Othman N, Noordin R. Update on laboratory diagnosis of amoebiasis. Eur J Clin Microbiol Infect
Dis. 2019 Jan;38(1):15-38.

Kumanan T, Sujanitha V, Balakumar S, Sreeharan N. Amoebic Liver Abscess and Indigenous Alcoholic
Beverages in the Tropics. J Trop Med. 2018;2018:6901751.

Shirley DT, Farr L, Watanabe K, Moonah S. A Review of the Global Burden, New Diagnostics, and Current
Therapeutics for Amebiasis. Open Forum Infect Dis. 2018 Jul;5(7):ofy161.

Fleming R, Cooper CJ, Ramirez-Vega R, Huerta-Alardin A, Boman D, Zuckerman MJ. Clinical

manifestations and endoscopic findings of amebic colitis in a United States-Mexico border city: a case
series. BMC Res Notes. 2015 Dec 14;8:781.

Guevara Á, Vicuña Y, Costales D, Vivero S, Anselmi M, Bisoffi Z, Formenti F. Use of Real-Time Polymerase
Chain Reaction to Differentiate between Pathogenic Entamoeba histolytica and the Nonpathogenic
Entamoeba dispar in Ecuador. Am J Trop Med Hyg. 2019 Jan;100(1):81-82.

Burchard GD. [Treatment of diseases acquired abroad]. Internist (Berl). 2014 Sep;55(9):1100, 1012.

https://www.ncbi.nlm.nih.gov/books/NBK519535/