parasitology module in nursing students

1.  Presented by Abdulla Khamis NgwaliPresented by Abdulla Khamis Ngwali
 Module Parasitology in NursingModule Parasitology in Nursing
 22NDND
YEAR, Nurse studentYEAR, Nurse student
 Faculty of health and allied sciencesFaculty of health and allied sciences
 Supervised by Dr. saidSupervised by Dr. said
 Assistance lecture at Zanzibar UniversityAssistance lecture at Zanzibar University

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3. • Explain general information about Protozoa
• Identify epidemiology of Amoeba hystolitica
• Explain morphology of Amoeba hystolitica
• Explain life cycle of Amoeba hystolitica
• Identify mode of infection of Amoeba hystolitica
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4. • Explain pathology of Amoeba hystolitica
• Mention clinical features of the amobiasis
• State diagnostic measures of the amobiasis
• Explain preventive measures of amobiasis
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5. PROTOZOA
 Protozoa are group of organisms that are defined
three common characteristic:-
o They are eukaryotic
o They are unicellular
o They lack a cell wall.
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6.  Many protozoa are free living whereas others are potential
parasites of humans and other animals.
 Notably, immune compromised people are susceptible to
all opportunistic organisms, including Protozoans.
 For the most part, infections caused by Protozoans are
most prevalent in tropical and subtropical nations, but also
occur in temperature region.
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PROTOZOA

7.  Protozoans are unicellular organisms that vary in size
but all require a most environment to survive.
 They consist of a diverse group of microbes and with
the expectation of one subgroup they are motile due to
cilia, flagella and or pseudopodia.
 Most species live in ponds, streams, lakes and oceans
whereas others live in moist soil, beach sand and
decaying organic matter.
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CHARACTERISTICS OF PROTOZOA

8.  Most protozoa are Chemoheterotrophs and obtain their
nutrients from various sources, such as Phagocytizing:-
 Bacteria
 Decaying organic matter
 Other protozoans
 Host tissue
 However some protozoans are Photoautotrophic such as
the Dinoflagellate’s and Euroglenoids.
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CHARACTERISTICS OF PROTOZOA

9.  The Protozoa can have very diverse life cycles with
multiple morphological stages, depending on species.
 Most protozoa have a cyst stage, which is dormant and
highly resistant to environmental stress.
 In the disease-causing species, these cysts are often the
mode of infection, frequently acquired by fecal-oral
contamination.
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LIFE CYCLE OF PROTOZOA

10.  The trophozoite stage is the active, reproductive, and
feeding stage. This stage is typically that causes disease by
pathogenic protozoa.
 Trophozoite can be very specific, infecting only one
species, like humans.
 Some protozoa will produce a protective capsule called a
cyst. A cyst allows the parasite to exist outside of the host
and be the infective stage allowing the parasite to get to
another host.
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LIFE CYCLE OF PROTOZOA

11.  Protozoa separated into four major groups based on
motility and the structures used to generate movement,
those are:-
i. Mastigophora
ii. Sarcodina
iii.Ciliophora
iv.Sporozoa
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GROUPS OF PROTOZOA

12.  Also known as the Flagellates.
 This group swims by waving long, whip-like flagella.
The Protozoal flagellum is structurally different than
the bacterial flagellum.
 Several important disease-causing flagellates are:-
 Trypanosomabrucei:- causes African sleeping sickness,
a disease that kills an estimated 65,000 people in Africa
every year.
 Giardia:- is a common pathogenic flagellate that
causes diarrhea.
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MASTIGOPHORA

13.  Group is commonly known as the Amoebas.
 A huge group with members found in nearly every
environment imaginable.
 These amoebas are characterized by having a trophozoite
stage that is naked, meaning the cell has no structural
components on its membrane that maintain a shape.
 As a result of amorphous it moves by pseudopod
projections.
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SARCODINA

14.  There are many general of Amoebas that live
symbiotically with animals, typically in the oral cavity or
gastrointestinal tract.
 Very few cause disease, but one species in particular,
Entamoeba histolytica, can be quite deadly.
 The disease is acquired by drinking water contaminated
with Entamoeba cysts, usually present in areas with poor
sanitation.
 Entamoeba can cause amoebic dysentery characterized
by painful ulcers in the large intestine and diarrhea.
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SARCODINA

15.  Commonly known as the Ciliates.
 These protozoa move by waving short cilia that line the
cell.
 The cilia provide great mobility, allowing the ciliates to
move rapidly, stop abruptly, and turn sharply in pursuit
of their prey.
Example
Paramecium and Balantidium coli: which cause
Balantidium dysentery, a condition similar to amoebic
dysentery.
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CILIOPHORA

16.  Are non-motile organisms that live parasitically within
the cell of the host animals.
Example
 Plasmodium vivax, the causal organism of malaria.
http://study.com/academy/lesson/what-are-protozoa-definition-
characteristics-examples.html
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SPOROZOA

17.  Entamoeba histolytica is an anaerobic parasitic
protozoan that feeds on cells in the human colon.
 The word histolytic literally means “tissue
destroyer”.
 It is the cause of ameobic dysentery (bloody diarrhea)
as well as colonic ulcerations (in the large interstine).
 The infection is also referred to as Amoebiasis.
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18.  Amoebiasis is more severe in very young patient and
elderly patient.
 If the organisms spread throughout the body via the
bloodstream they may cause abscesses in the liver or less
frequently on other organs.
 The incubation period is 2- 4 weeks but range from a few
days to years.
 Entamoeba histolytica is mostly occurs in tropical countries
in areas of poor sanitation.
(Cindy Gode, 2010)
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19.  Amobiasis is a disease with distribution in all over the
world, principally in tropical countries with the warm
climate and bad sanitary condition.
 It is more frequent in poorest areas with contaminated
water, bad management of waste and bad drainage
system.
 Approximately 48 million people are infected with
Entamoeba histolytica world wide.
(Diamond & Clark, 1993)
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20.  Reservoirs are human; they spread disease through food
and water contamination.
 Infection is by fecal oral route.
 Food borne out breaks in sanitary handling preparations of
food by infected individuals.
 Human faeces used as fertilizer increase prevalence, Cyst
remain viable and infective for several days in feaces, and
may survive in soil for at least 8 days at 34-380
c.
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21.  Three successive stages occur in the life cycle of
Entamoeba histolytica:-
 Trophozoites
 Pre-cyst
 Cyst
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22.  The trophozoite size ranges from 20 to 40 micrometers in
diameter
 Cytoplasm has an outer clear ectoplasm and inner granula
endoplasm
 Endoplasm contains abundant vesicles which sometimes
contains ingested RBCs in various stages of disintegration.
 Single nucleated
 Nucleus is spherical and measures 3.5 microns with fine
peripheral chromatin and central karyosome
 Trophozoites are actively motile.
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TROPHOZOITES STAGE

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24.  Is the developmental stage between trophozoite and cyst
stages.
 They are colourless, round or oval
 Smaller than trophozoite but larger than cyst.
 They have a rounded single nucleus
 Do not have ingested materials
 No cyst wall.
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PRE-CYST STAGE

25.  The cyst size range from 10 to 20 micrometers in diameter
(mm).
 Is an infective form of the Parasite.
 Round or oval
 Cyst contains four quadrinucleated when mature.
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CYST STAGE

26.  Human is the main reservoir of Entamoeba histolytica.
 The life cycle starts by ingestion of mature
quadrinucleate cyst in infected water and or/ food.
 Cysts are resistant to gastric acid, on ingestion it passes
to the small intestine.
 Amoeba within the Cyst becomes active in the neutral or
alkaline small intestinal environment.
 Cyst wall lysed by intestinal trypsin which liberating a
single trophozoite with four nuclei (excystation).
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27.  Each of the four nuclei in the emerging Entamoeba
histolytica undergoes one round of division, thus forming
eight metacystic trophozoites, smaller than the trophozoites
seen in the colon.
 These trophozoites are carried by peristalsis to the caecum
where they complete their maturation.
 Here they grow and multiply by binary fission. Than they
then colonize the mucosal surfaces.
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28.  Trophozoite colonization is influenced by intestinal
motility, the transit time, the presence or absence of
intestinal flora and diet.
 After colonization, the trophozoites may show different
courses of actions as follows:-
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29. In some individuals, the multiplying trophozoites
produce no or little lesions if any in the tissue.
 They feed only on the starches and mucus secretions on
the surface of the mucosa.
 As trophozoites pass down the colon, they encyst under
the stimulus of desiccation and then are excreted out as
cysts with stool.
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30. In other individuals infected under similar conditions,
the trophozoites may invade the tissue of the large
intestine.
 Factors leading to such invasion are poorly understood.
 Trophozoites produce characteristic lesions in the colon.
 A large number of trophozoites are expected along with
blood and mucus in stool.
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31. In a few cases, erosion of the large intestine may be so
extensive that trophozoites gain entrance into the radicles of
portal vein and are carried away to the liver where they
multiply.
 They produce suppurative amoebic liver abscess proceeded by
non suppurative infection of the liver.
 Cysts in faeces are the infective forms
 They may be viable for weeks or months in suitable
environment.
 They cause infection in other susceptible persons through fecal
contamination of water, vegetables or direct faeco-oral contact
and the cycle is repeated.
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33.  Entamoeba histolytica is spread by the fecal-oral route.
This is achieved through food or water contaminated with
cysts or oral-anal sexual contact.
 The disease is found far more frequently in people from
developing countries or travelers to such areas than in
developed countries.
 Transmission of Entamoeba histolytica from one person
to another occurs due to ingestion of this cyst.
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34. Faecal - oral route.
 In majority of cases infection takes place through intake of
contaminated uncooked vegetables and fruits.
 Insect vectors like flies, cockroaches and rodents act as
agent to carry infective cysts to the food drink.
 Sometimes drinking water supply contaminated with
infected feaces give rise to epidemics.
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35. Oral - rectal contact.
 Sexual transmission by oral rectal contact is also one of
the modes of transmission, especially among male
homosexuals.
(Diamond, 1993)
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36.  The infection of Entamoeba histolytica causes the disease
Amoebiasis.
 E. histolytica infects the digestive tracts of predominantly
humans and other primates.
 E. histolytica can infect dogs and cats, but these animals do
not contribute significantly to transmission since they
usually do not produce cysts.
 Cysts do not invade tissue and are shed with the host's feces.
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37.  The thick protective walls allow the cysts to remain viable
for several weeks in the external environment and the
internal acid content of the stomach.
 After a viable cyst is ingested, it travels to the small intestine
where excystation occurs and it divides into four
trophozoites, which is the active stage of the parasite that
only survives in the host and in fresh feces.
 These trophozoites then mature into adult trophozoites and
colonize the large intestine (particularly the caecum).
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38.  Contact with human cells induces a rapid influx of
calcium into the contacted cell.
 This stops all membrane movement. The internal
organization is disrupted, organelles lyse and the cell
dies.
 The amoeba may ingest the dead cell or intake nutrients
from the cell.
 Presence of trophozoites containing red blood cells is
indicative of tissue invasion by virulent E. histolytica
parasites.
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39.  Ulcers created by trophozoites have a broad base that is
composed of fibrin and cellular debris.
 Trophozoites are found on the surface of ulcers, in the
exudates and in the crater.
 There is little inflammatory response in early ulcers, but as
the ulcer widens there is an accumulation of neutrophils,
lymphocytes, histiocytes, plasma cells and sometimes
eosinophils.
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40.  Occasionally (5%-10%) trophozoites penetrate the
muscle and serous layers which perforates the intestine.
 Extra intestinal amoebiasis can occur.
 Parasites penetrate portal vessels and embolize to the
liver and form liver abscesses.
 The abscess cavity is sometimes filled with a pasty
chocolate colored material.
 Trophozoites form new cysts which are then excreted in
the stool.
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41.  The symptoms of the disease are often mild, causing
diarrhea and abdominal pain.
 Amebic dysentery - a more severe symptom can occur.
Symptoms of amebic dysentery include severe stomach
pain, blood and mucus in feces and high temperature fever.
 Seldom does the infection invade the liver and cause an
abscess.
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42. Intestinal amoebiasis
 Asymptomatic infection (cyst passers)
 Acute amoebic dysentery characterized by abdominal
pain, tenderness, and tender hepatomegally.
 Non dysenteric colitis.
 Intestinal amoebiasis complicated by: - Toxic megacolon,
fulminant amoebic colitis, amoebic peritonitis and
perianal ulceration.
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43. Extra Intestinal amoebiasis - Amoebic Liver Abscess (ALA)
 10-50% of adults
 Characterized by high fever of gradual onset and right
upper abdominal pain and tenderness.
 Other features include anorexia, nausea, vomiting, fatigue,
and weight loss.
 Mild jaundice in some patients.
 May be complicated by pericarditis and peritonitis
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44. Pleuropulmonary amoebiasis
 Invasion of the pleural cavity of lung parenchyma
commonly due to extension from amoebic liver
abscess.
 Occurs in 15% of patients with Amoebic liver abscess.
 Presents with severe right chest pain radiating to the
right shoulder, dsypnoea and non productive cough.
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45. Cerebral amoebiasis
 Occurs in 1.2 - 2.5% of patients who have amoebiasis
at autops
 Symptoms depend on the site and size of the lesion.
 In 50% of patients death is within 12-72 hrs from
cerebella involvement or rupture.
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46. Genito-urinary amoebiasis
 Kidney and genital organs are affected.
 Punched out painful ulcers with profuse discharge.
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47. Peritoneal amoebiasis
 Caused by the rupture of hepatic liver abscess or
perforation of the caecum.
 Occurs in 2-7% of patients with Amoebic liver abscess
(Left Lobe)
 Characterized by sudden increase in abdominal pain.
 Fever is also a common feature.
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48. Pericardial amoebiasis
 Most serious but rare complication of amoebic liver
abscess.
 Affects less than 1% of Amoebic liver abscess patients
especially of the left lobe.
 Caused by rupture of left lobe abscesses.
 Characterized by chest pain and features of CCF.
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49. Specimens
• Stool
• Rectal exudates
• Rectal ulcer tissue collected using endoscopy
• Pus for Amoebic liver abscess (ALA)
Examination Methods
• Stool and pus microscopy-cyst/trophozoites demonstration
• Stool antigen detection
• Stool culture.
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50. Serodiagnosis.
• Antibodies detected in invasive intestinal amoebiasis.
• Indirect haemoglutination antibodies (IHA)
• Indirect fluorescent antibodies (IFA)
Molecular Diagnosis (DNA Probe).
• Detect E.histolytica
• PCR used to differentiate E.histolytica from E.dispar in
stool specimens
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51. Full Blood Picture
• Leukocytosis (>10,000/cub.mm without oesinophilia)
• Picture for 50% of pts with ALA
• Mild anaemia normocytic normochromic.
Imaging
• Plain x-ray of chest –rt.pleura effusion
• Abdominal ultrasound
• CT - scan and MRI
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52. • Control can be achieved through improvement of living
standards and establishment of adequate sanitary
conditions in endemic countries.
• The methods should include:-
i. Individual prophylaxis
ii. Community prophylaxis
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53.  Improved personal hygiene such as hand washing
before eating and after defecation.
 Making drinking water safe.
 Avoid sexual practices that allow faecal-oral contact
(homosexual).
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INDIVIDUAL PROPHYLAXIS

54.  General sanitation by proper disposal of faeces.
 Prevention of water supplies from faecal
contamination.
 Better management of cases by an early and rapid
detection.
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COMMUNITY PROPHYLAXIS

55.  Diamond, L.S. & Clark, C.G. (1993) A redescription of Entamoeba histolytica
Schaudinn, 1903 (EmendedWalker, 1911) separating it from Entamoeba dispar
Brumpt, 1925. J. Euk. Microbiol. 40: 340-344.
 Espinosa A., Clark D., Stanley S.L.: Entamoebahistolytica alcohol dehydrogenase 2
(EhADH2) as a target for anti-amoebic agents. Journal of Antimicrobial
Chemotherapy 2004.Vol 54 (1): 56-59.
 Loftus B,Anderson I, Davies R,Alsmark UC, Samuelson J,Amedeo P, Roncaglia P,
Berriman M, Hirt RP, Mann BJ et al : The genome of the protist
parasite Entamoebahistolytica. Nature 2005.Volume 433 (7028):865-868.
 The EntamoebaHistolytica Data Base 2000.TIGRThe Institute for Genomeic Research.
29 Aug 2007 www.tigr.org/tdb/edb2/enta/htmls/
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