Parasitology

Parasitology
Shimelis Teshome (BSc MLS)

Parasite
Protozoa Helminth
 Amoeba  Enterobius
 Giardia  Trichuris
 Malaria  Ascaris
 Leishmania  Taenia
 Trypanosoma  Schistosoma
 etc…  etc…
02/23/2021 Shimelis Teshome (BSc MLS) 2

The Protozoa
 Introduction
The Phylum Protozoa is classified into four
subdivisions according to the methods of locomotion.
• The amoebae :- move by means of pseudopodia.
• The flagellates :-typically move by long, whip like
flagella.
• The ciliates :-are propelled by rows of cilia that beat
with a synchronized wavelike motion.
• The sporozoans :-lack specialized organelles of
motility.

Protozoa….
• Transmission :- mostly person-to-person, via fecal-
oral route; fecally contaminated food or water; other
means include sexual transmission
• Trophozoite: - the motile vegetative stage; multiplies
via binary fission; colonizes host.
• Cyst :- the inactive, non-motile, infective stage
• survives the environment due to the presence of
a cyst wall.
• do not multiply, however, some organisms
divide within the cyst wall

Protozoa….
1. The Amoebae
 General Life cycle
• The definitive host ingests the infective cyst stage
from fecal contamination in environment.
• The cyst passes into the small intestine & excystation
occurs with transformation to the trophozoite stage.
• Trophozoites colonize the host, multiplying asexually
via binary fission.
• They can remain near the lumen (non-pathogens) or
invade the wall of the intestine & multiply
(pathogens).
• Cysts and trophozoites are passed in the feces of the
infected host.
Protozoa….
Life cycle

Protozoa….
 Clinical diseases of E. histolytica
 Amoebic dysentery:- Related to the destruction of the
colonic
– Epithelial cells by the organism.
– Flask shaped ulcerations of the intestinal mucousa
with inflammation
 Secondary bacterial infection
 Symptoms:- Abdominal pain, abdominalcramp,
passage of numerous watery and bloody stools
If untreated patients can die of dehydration

Protozoa….
 Amoeba can invade deeper tissues and enter the
blood circulatory system where they especially infect
the liver as trophozoites are re-moved from blood as
they enter the liver.
– Abscess formation in the liver is common
– Pain in the liver and elevation of the diaphragm

Protozoa….

Treatment and prevention of E. histolytica

Metronidazole:-
–Penetrates deeper tissues and destroys amoeba present in liver,
brain, lungs etc.
•The organism’s metabolism converts the drug into its lethal form

Paromomycin :- is used to eradicate the amoeba present in the
intestinal lumen

Prevention: - When traveling to areas where E. histolytica is
epidemic or endemic
Filter and boil water
Thoroughly wash unpeeled fruits and raw vegetables

Protozoa….
2. Giardia lamblia
• G. lamblia is a flagellate and moves by lashing its
flagella
• G. lamblia attaches to the intestinal villi of
duodenum via an adhesive disk
• Cysts are resistant to the amounts of chlorine put in
municipal water systems
• water systems should also filtrate water

Protozoa….
 G. lamblia life cycle
1. Infection initiated by the ingestion of infectious cysts
(only 10 are required for infection)
2. Acid in the stomach stimulates the release of
trophozoites from the cyst
3. Trophozoites are released in the duodenum and
jejunum where they multiply by binary fission
4. Trophozoites attach to the intestinal villi by means of a
sucking disk
5. Trophozoites can develop into cysts for survival outside
of the host
6. Trophozoites cause an explosive diarrhea such that
cysts are released into
02/23/2021
the environment
Shimelis Teshome (BSc MLS) 11
Protozoa….

Protozoa….
Clinical diseases of G. lamblia
• Symptomatic disease ranges from mild diarrhea to
severe dysentery
• The incubation period before symptomatic disease is
approx. 10 days
• The onset of disease is sudden and consists of
– foul-smelling watery diarrhea (seldom bloody)
– abdominal cramping
– flatulence
• Spontaneous recovery occurs in 2 weeks
– Chronic disease with several relapses may occur.
Protozoa….
 Lab diagnosis of G. lamblia
• With the onset of diarrhea the patient’s stool are
examined for trophozoites and cysts.
• Giardia may appear in stool on a given day and not be
present on the following day
– one stool sample over a period of three days
should be examined before making a negative
diagnosis.
• Samples can be collected through duodenal aspiration
or via biopsy of upper small intestines.

Protozoa….
 Treatment and prevention of G. lamblia
• Metronidazole is active against giardiasis and
alternate drug is tinidazole.
• Boil and filter water taken from lakes and streams
• Municipal water supplies should maintain functioning

filtration Systems since the cysts are resistant to
chlorine and ozone treatment

MALARIA

Introduction
• A major public health problem in more than 109
countries,
• Inhabited by more than 2.4 billion people ( 40% of
the world’s population).
• Estimated to kill a child in every 30 seconds
• Cause up to 600 million new infections worldwide
annually.
2.1 billion people live in MALARIOUS areas

Distribution in Ethiopia
• In Ethiopia, ~75% of the total area is estimated to be
malarious, with 68% of the total population at risk
• Transmission- seasonal (Unstable)
– Mainly depends on rain fall & Temp
• In Ethiopia : A. gambiae, A. funestus, A.nili,
A. arebiansis & A. pharonensis are
main vectors
 A. arabiensis is responsible for most
epidemics in the country
• Two transmission seasons
 Main : September to December
 Minor: April to and May.
• Transmission seasons often coincides with peak

periods of agricultural activity which result a negative
impact on the nation’s economy.
02/23/2021 20 (BSc MLS)

Shimelis Teshome
Malaria Situation…
• P. falciparum and P. vivax are the most dominant
specieses
– P. falciparum accounts 60-70 % of malaria cases,
and P. vivax about 30-40%.
– P. malariae =1%, focal distribution like in Humera
– P. ovale = less than 1% cases , found in Setit Humera
, Gambela & Arbaminch
02/23/2021 21 (BSc MLS)

Shimelis Teshome
Types of plasmodium
5 Plasmodium spp are responsible for human malaria
• P. falciparum
• P. vivax
• P. malariae
• P. ovale
• P. knowlesi

Transmission & life cycle

Clinical features
• Malaria typically produces a string of recurrent attacks, or

paroxysms, each of which has three stages
a cold stage (sensation of cold, shivering) ;
 a hot stage (fever, headaches, vomiting)

 a sweating stage (sweats, return to normal temperature,
tiredness)
• Paroxysms coincide synchronus rupture of schizont
and elevated TNF-alpha

• Tertian Malaria , where paroxysms of malaria is
repeated after 48 hrs or fever occurs every third day.
It is feature of P.falciparum, P.ovale and P.vivax
• Quartan Malaria , where paroxysms occurs after every

72 hour or fever occurs every fourth day.
It is seen in P. malariae

MALALRIA Diagnostics approaches
A. Clinical Diagnosis
Malaria Diagnosis
B. Laboratory diagnosis
Microscopic Molecular
•Thin film Immunological PCR
•Thick film • Ag /enzyme
• QBC etc.
• RDT
• Ab- ELISA

Hemoflagellates
 Leishmania species
Causes three clinical disease

A. Veseral leishmaniasis
B. Cutaneous leishmaniasis
C. Mucocutaneous leishmaniasis
 Morphology
• The species of leishmania exist in two forms, amastigote (aflagellar)

and promastigote (flagellated) in their life cycle.
• They are transmitted by certain species of sand flies (Phlebotomus
& Lutzomyia)
Life cycle of Leishmania species

A. Visceral leishmaniasis
• Cased by Leishmania donovani
• Natural habitat in man is the reticuloendothelial system
of the viscera, in which the amastigote multiplies by
simple binary fission until the host cells are destroyed,
whereupon new macrophages are parasitized.

Pathogenesis
• In visceral leishmaniasis, the organs of the
reticuloendothelial system (liver, spleen and bone
marrow) are the most severely affected organs.
• Reduced bone marrow activity, coupled with cellular
distraction in the spleen, results in anaemia, leukopenia
and thrombocytopenia.
• This leads to secondary infections and a tendency to
bleed.
 Epidemiology
• L. donovani donovani, infection of the classic kala-azar

(“black sickness”) or dumdum fever type occurs in many
parts of Asia, Africa and Southeast Asia.
• The reservoir hosts are primarily dogs, rats, and small
carnivores foxes in sub-Saharan Africa,
• The vector is the Phlebotomus sand fly.

• Other variants of L. donovani are also recognized:
– L. donovani infantum has similar geographical
distribution, reservoir host and vector; with L.
donovani donovani.
– L. donovani chagasi is found in South America,
Central America, especially Mexico, and the West
Indies.
• Reservoir hosts are dogs, foxes, and cats, and the
vector is the Lutzomiya sand fly.
 Clinical features
• Symptoms begin with intermittent fever, weakness, and

diarrhea; chills and sweating that may resemble malaria
symptoms are also common early in the infection.
• Untreated visceral leishmaniasis is nearly always fatal as
a result of secondary infection.
 Immunity
• Host cellular and humoral defence mechanisms are
stimulated.
 Laboratory diagnosis
• Examination of tissue biopsy, spleen aspiration, bone

marrow aspiration or lymph node aspiration in properly
stained smear (e.g. Giemsa stain).

 Treatment
• The drug of choice is sodium stibogluconate, a pentavalent
antimonial compound.
• Alternative approaches include the addition of allopurinol
and the use of pentamidine or amphotercin B.
 Prevention
• Prompt treatment of human infections and control of
reservoir hosts.
• Protection from sand flies by screening and insect repellents.

 Trypanosomiasis
 Etiologic agents
1. Trypanosoma brucei complex – African trypanosomiasis (sleeping

sickness)
2. Trypanosoma cruzi – American trypanosomiasis (Chagas’ disease)
 Important features
• These species may have amastigote, promastigote, epimastigote,

and trypomastigote stages in their life cycle.
• In human trypanosomes of the African form, however, the
amastigote and promastigote stages of development are absent.
 African trypanosomiasis
• T. gambiense & T. rhodesiene are causative agents of the

African typanosomiasis
– transmitted by insect bites. The vector for both is the
tsetse fly.

 Pathogenesis
• The trypomastigotes spread from the skin through the blood to the
lymph node and the brain.
• The typical somnolence (sleeping sickness) usually progresses to
coma as a result of demyelinating encephalitis.
• In acute form, cyclical fever spike (approximately every 2 weeks)
occurs that is related to antigenic variation.
– As antibody mediated agglutination and lysis of the
trypomastigotes occurs, the fever subsides.
– With a few remains of antigenic variants new fever spike occurs
and the cycle repeats itself over a long period.
 Epidemiology
• T. burcei gambiense is limited to tropical west and central

Africa, correlating with the range of the tsetse fly vector.
• An animal reservoir has not been proved for this
infection.
• T.burcei rhodeseinse is found primarily in East Africa,
especially the cattle-raising countries, where tsetse flies
breed in the brush rather than along stream banks.

• T. b. rhodeseines also differs from T.b. gambiense in that
domestic animal hosts (cattle and sheep) and wild game
animals act as reservoir hosts.
– This transmission and vector cycle makes the
organism more difficult to control than T.b.
gambiense.
 Clinical features
• Although both species cause sleeping sickness, the

progress of the disease is different.
• T.gambiense induced disease runs a low-grade chronic
course over a few years.
• One of the earliest signs of disease is an occasional ulcer at
the site of the fly bite.
• As reproduction of organisms continues, the lymph nodes
are invaded, and fever, myalgia, arthralgia, and lymph node
enlargement results.
• Swelling of the posterior cervical lymph nodes is
characteristic of Gambian sleeping sickness and is called
winterbottom’s sign.
•Chronic disease progresses to CNS involvement with
lethargy, tremors, meningoencephalitis, mental
retardation, and general deterioration.
•In the final stages, convulsions, hemiplegia, and
incontinence occur.
•Death is the result of CNS damage and other
infections, such as pneumonia.
•In T. rhodesiense, the disease caused is a more acute,
rapidly progressive disease that is usually fatal.
 Immunity
• Both the humoral and cellular immunity involve in these infections.
• The immune responses are faced with antigenic variation
 Laboratory
• Examination of thin and thick films, in concentrated anticoagulated blood

preparations, and in aspiration from lymph nodes and concentrated spinal
fluid.
 Treatment
• For the acute stages of the disease the drug of choice is suramin with
pentamidine as an alternative.
• In chronic disease with CNS involvement, the drug of choice is melarsoprol.

 Intestinal Helminthes 2. Cestodes
1. Nematodes (roundworms) (tapeworms)
Ascaris lumbricoides Taenia saginata - The
Beef Tapeworm
Trichuris trichiuria
Taenia solium - The
STH
Pork Tapeworm
Hookworms Hyminlopes spss
3. Trematodes (flukes)
Schistosomiasis -
Bilharzia.
Fasciola hepatica

Nematodes
• Nematodes are cylindrical hence the common name roundworm
• Soil-transmitted helminth (STH) infection is highly endemic in

tropical and subtropical areas of sub-Saharan Africa, Asia and
Latin America
– where up to 2 billion people have active infections.
• Neglected by the global health community because

– most affected are among the most impoverished
– infection causes chronic ill health with insidious clinical
presentations
1. Ascaris lumbricoides
Infection with this roundworm is extremely common
The annual incidence of infection being greater than 1500 million
cases
Morphology
The adults are large white, or pinkish-white, cylindrical
roundworms
The eggs consist of a thick transparent inner shell which is
covered in a thick, warty, albuminous coat.

 Life cycle
• Have a direct life cycle, with no intermediate hosts
• Infection occurs on ingestion of raw food, such as fruit or

vegetables, that is contaminated with these infective
eggs.
• The eggs then hatch in the small intestine, to release the

L2 rhabditiform larvae
• L2 larvae penetrate the intestinal wall, entering the portal

blood stream, and then migrate to the liver, then heart,
then after between 1 to
02/23/2021
7 days, the lungs.
• Here they moult twice on the way to form the L4
larvae
• Out of the blood vessels, entering the bronchiole
• They then enter the throat and are swallowed, finally
ending up in the small intestine where they mature
and mate, to complete their life cycle.
 Pathology of Infection.
1. Pathology Associated with the migration of Larvae

– Simultaneous migration of the larvea through the lungs
may give rise to a severe haemorrhagic pneumonia.

– Often associated with allergic hypersensitivity
reactions such as asthmatic attacks, pulmonary
infiltration and urticaria and oedema of the lips
2. Pathology associated with adult parasites in the Intestine
• The mass of worms may block the intestine and need to
be surgically removed.
• Adult parasites often leave the small intestine to enter
other organs
– Bile duct
• To the appendix, or through the intestinal wall, both
conditions which may cause a fatal peritonitis
• Vomited up or emerging through the nose
• Enter the trachea they may cause suffocation.
Diagnosis
Definitive diagnosis is by demonstration
of
• The characteristic eggs in faecal
samples
• Identifying adult worms passed out
spontaneously by the host.
Unfertilized (left) and fertilized (right) Ascaris lumbricoides eggs.
The unfertilized eggs are longer and narrower than fertilized eggs.
The fertilized eggs have a thick and bumpy outer wall which is stained
golden brown with bile.(SOURCE: PHIL 411/4821 - CDC/Dr. Mae
Melvin)

2. Hookworms
 Ancylostoma duodenale :-Native to parts of Southern
Europe, North Africa and Northern Asia, parts of Western
South America.
 Necator americanus :- Native in Central and Southern
Africa, Southern Asia, Australia and the Pacific Islands.
 It has been estimated that there are 1200 million cases of
hookworm infection in man annually
Symptomatic infections with accompanying anaemia.
 Morphology
• The anterior end of the parasites are formed into a buccal

• Necator have capsules equipped with four cutting plates
on the ventral margins
• Ancylostoma have pairs of teeth on the ventral margin of
the capsule.
• The eggs are bluntly rounded, thin shelled, and are
almost indistinguishable between the different species

Life cycle

 Pathology of Infection.
• Preferred site of infestation is in the upper layer of the
small intestine
• Pathology associated with the presence of the adult
parasite in the intestine
– Hookworm mouthparts penetrate blood vessels, and
the parasites obtain nutrition by sucking blood

– The gross pathology of the disease is very dependent
on the intensity of infection.
– The continuous loss of blood leads to a chronic

anemia
• Severe retardation in growth and development,

both physical and mental, in infected children, and
a general weakness

Diagnosis
•Identify characteristic eggs in feacal samples.

•Note the eggs of N. americanus and A. duodenale are
morphologically identical.
Egg of Hookworm
02/23/2021 64
Shimelis Teshome (BSc MLS)
 Treatment and Control
• Albendazole
• Mebendazole

3. Trichuris trichiura (whipworm)
• It is distributed worldwide
– More frequent in areas with tropical weather and among
children.
 Morphology
• The thin(whip-like end) is the end that the worm threads
into the mucosa of the colon.
• The widened, pinkish gray region of the body is the
posterior, and it is the end that contains the parasite’s
intestines and reproductive organs.
Eggs contain polar plugs (also known as refractile
prominences) at each end.

Life cycle and transmission
Unembryonated eggs (unsegmented) are passed in the

faeces
In the soil, these eggs develop into a 2-cell stage
(segmented egg) and then into an advanced cleavage
stage
Infective eggs are ingested by way of soil contaminated
hands or food and hatch inside the small intestine,
releasing larvae into the gastrointestinal tract.
 These larvae burrow into a villus and develop into adults
(over 2–3 days).
 They then migrate into the cecum and ascending colon
where they thread their anterior portion (whip-like end)
into the tissue mucosa and reside permanently for their
year-long life span.
 About 60 to 70 days after infection, female adults begin
to release unembryonated eggs

Life cycle of Trichuris trichiura
 Clinical Disease
• Abdominal pain and distention, bloody or mucous-filled

diarrhoea, and in children rectal prolapse may occur
• Tenesmus (feeling of incomplete defecation, generally
accompanied by involuntary straining).
• While damage may be done to the GI tissue and
appendicitis may be brought on

•The embedding of the worms into the ileo-cecal region
may make the host susceptible to bacterial infection.
•Growth retardation, weight loss, nutritional
deficiencies, and anemia

 Lab Diagnosis
• A stool examination reveals the presence of typical whipworm
eggs.
– Typically, the Kato-Katz thick-smear technique is used for
the identification of the Trichuris trichiura eggs in the stool
sample.
• Colonoscopy has been shown to be a useful diagnostic tool,
especially in patients infected by only a few male worms
 Treatmets
• 02/23/2021
Mebendazole Shimelis Teshome (BSc MLS) 73
4. ENTEROBIUS VERMICULARIS (PIN WORM OR
THREAD WORM)
• Small white worm with thread-like appearance.
• The worm causes enterobiasis.
• Infection is common in children.
 Morphology
• Has male and female adult

• Infection is by ingestion of eggs containing larvae with
contaminated raw vegetables.
Mode of infection
 By direct infection from a patient (Fecal-oral route).
 Autoinfection: the eggs are infective as soon as they are
passed by the female worm.
 If the hands of the patient get contaminated with these
eggs, he/she will infect him/herself again and again.
 Aerosol inhalation from contaminated sheets and dust.
 Life cycle
• Adult worm lives in the large intestine.
• After fertilization, the male dies and the female moves out
through the anus to glue its eggs on the peri-anal skin.
• This takes place by night.
• The egg contains larva.
• When the eggs are swallowed, they hatch in the small
intestine and the larvae migrate to the large intestine to
become adult.
Life cycle of E. vermicularis

 Clinical presentation
• The migration of the worms causes allergic reactions around
the anus and during night it causes nocturnal itching
(pruritus ani) and enuresis.
• The worms may obstruct the appendix causing appendicitis.
 Lab Diagnosis
1. Eggs in stool:
– Examination of the stool by direct saline smear to detect
the egg: this is positive in about 5% of cases because
the eggs are glued to
02/23/2021
the peri-anal skin.
2. Peri-anal swab:
– The peri-anal region is swabbed with a piece of
adhesive tape (cellotape) hold over a tongue depressor.
– The adhesive tape is placed on a glass slide and
examined for eggs.
– The swab should be done in the early morning before
bathing and defecation.
 Treatment
– Mebendazole; Piperazine
Morphology of Enterobius vermicularis adult
female
They are small white worms with pointed tail

swollen cuticle at anterior end prominent
esophageal end bulb

Egg of E. vermicularis

Taenia
Taenia species
species
 Geographical Distribution:-
– T. saginata
 World wide distribution where cattle are raised and beef

is eaten raw or under cooked.
 Very common in Ethiopia
– T. solium
• Not widely distributed as T saginata.
• Common in all areas where raw or partially cooked
pork is eaten.
• Not reported from Ethiopia
Taenia saginata
Scolex (head):-
• Quadrate, with four
suckers, no hooks, no
rostellum on scolex
• Size-2mm across

Transmission and life cycle
– Humans become infected by ingesting raw or
undercooked meat infected with cystcerus larvae:
• Beef- T saginata
• Pork- T.solium

Clinical manifestation
T. saginata
– Taeniasis.
• Usually asymptomatic but may cause dizziness,

abdominal pain, diarrhea, headache and nausea.
– Proglottids obvious in feces.
– Proglottides have a strong tendency to crawl from
the anus during the day when its host is active

 Laboratory Diagnosis
• Detecting eggs in faeces

• Identifying macroscopically
– gravid segments in faeces
– scolex recovered from clothing or passed in faeces.
In addition
• T.saginata-
– ova on perianal skin (cellotape slide)

Egg : T.saginata

Opportunistic Intestinal Parasites

Opportunistic Intestinal Parasites
1. Strongyloides stercoralis
• It is endemic in the southeastern USA, South America, sub-
Saharan Africa, and Southeast Asia
• The geographic range of Strongyloides infections overlap with that
of Hookworm
 Morphology
• Rhabditiform larvae
• Filariform larvae
• Eggs hatch in the intestine (not usually passed in stool specimens).

 Life cycle:-
• Infective third stage filariform larvae penetrate skin, enter
the lymphatics or bloodstream.
• Larvae migrate to the lungs, break out of lung capillaries
into alveoli.
• After maturation, larvae travel to the pharynx, are
swallowed, and return to the intestine.
• Larvae mature to adults and attach to the mucosa of the
small intestine.
• Parthogenetic females only - no parasitic males.
• Females produce viable eggs.
• Eggs hatch in mucosa.
• Larvae: Are passed in feces, live in the soil, mature into a

free-living adult males and females, which produce eggs
• Rhabditiform larvae feed in soil and develop into
infective stage larvae which penetrate the skin; First
stage larvae develop into infective stage larvae in the
intestine (autoinfection).
Opportunistic Intestinal Parasites……
Life cycle

 Major pathology and symptoms:
• Skin – allergic reactions; raised, itchy, red blotches at the

site of larval penetration.
• Lungs – pneumonia.
• Intestinal - abdominal pain, diarrhea, vomiting, weight
loss, anemia, eosinophilia.
• Death occurs in immunosuppressed patients due to
heavy autoinfection.

• Hyperinfection with S. stercoralis results in invasion of larvae
into the
– colonic submucosa,
– lymphatics, and blood vessels, with an associated
mononuclear infiltrate.
– There are many adult worms, larvae, and eggs in the crypts
of the duodenum and ileum.
Worms of all stages may be found in other organs, including skin
and lungs, and may even be found in large numbers in sputum.

Diagnosis:
Recovery and identification of larvae in the feces.
Recovery and identification of eggs in duodenal
drainage
Treatment:-
Thiabendazole

Blood fluke/Schistosomes/
• S. mansoni
• S. hematobium
• S. japonicum
• S. intrecalatum
• S. mekongi
The Schistosomes
• General feature:
– They reside in the blood vessels of the definitive
host.
– The sexes are separate (they are dioecious)
– They are long cylindrical(~ 20mm) and adopted to
life in blood vessel
• Male worm has a split body called the

gynecophoral canal. The female is usually
found within this canal
• She leaves only during the egg laying period.
– Humans are significant host for most of the species
– Snail host is required as intermediate host to
complete their life cycle
– Asexual reproduction takes in the sporocyst stage in
the snail.
– Cercaria is the infective stage to humans in water
– egg with spine
– The eggs are main pathogenic stage.
Epidemology:
• Wide spread species
– Schistosoma haematobium causes urinary schistosomiasis

– Schistosoma mansoni causes intestinal
– Schistosoma japonicum cause intestinal schistosomiasis
• Less wide spread species

– Schistosoma mekongi
– Schistosoma intercalatum
Life Cycle of Schistosoma spp.
Intermediate Hosts of Schistosoma spp.
S. mansoni only infect snails of the genus

Biomphalaria
S. japonicum are found in Oncomelania snails
S. haematobium persist in species of Bulinus.
.
• Species differences in Site Preferences of
Adults (male and female in copula)
– S. mansoni –veins of Large Intestine

– S. haematobium – veins of bladder
– S. japonicum – veins of small intestine
Adults can live 20
to 30 years!!
Filari (lymphatic) worms
Reading assignment
02/23/2021 Medical parasitology 106


Parasitology

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Parasitology

Uploaded by

Copyright:

Available Formats

Parasitology

Shimelis Teshome (BSc MLS)

02/23/2021 Shimelis Teshome (BSc MLS) 2

02/23/2021 Shimelis Teshome (BSc MLS) 3

02/23/2021 Shimelis Teshome (BSc MLS) 4

02/23/2021 Shimelis Teshome (BSc MLS) 6

02/23/2021 Shimelis Teshome (BSc MLS) 7

– Abscess formation in the liver is common

– Pain in the liver and elevation of the diaphragm

02/23/2021 Shimelis Teshome (BSc MLS) 8

02/23/2021 Shimelis Teshome (BSc MLS) 9

02/23/2021 Shimelis Teshome (BSc MLS) 10

02/23/2021 Shimelis Teshome (BSc MLS) 12

02/23/2021 Shimelis Teshome (BSc MLS) 14

• Boil and filter water taken from lakes and streams

• Municipal water supplies should maintain functioning

02/23/2021 Shimelis Teshome (BSc MLS) 15

02/23/2021 Shimelis Teshome (BSc MLS) 16

02/23/2021 Shimelis Teshome (BSc MLS) 18

• Transmission seasons often coincides with peak

02/23/2021 20 (BSc MLS)

02/23/2021 21 (BSc MLS)

02/23/2021 Shimelis Teshome (BSc MLS) 22

02/23/2021 Shimelis Teshome (BSc MLS) 23

• Malaria typically produces a string of recurrent attacks, or

 a hot stage (fever, headaches, vomiting)

and elevated TNF-alpha

02/23/2021 Shimelis Teshome (BSc MLS) 25

• Quartan Malaria , where paroxysms occurs after every

02/23/2021 Shimelis Teshome (BSc MLS) 26

02/23/2021 Shimelis Teshome (BSc MLS) 27

Causes three clinical disease

• The species of leishmania exist in two forms, amastigote (aflagellar)

02/23/2021 Shimelis Teshome (BSc MLS) 32

02/23/2021 Shimelis Teshome (BSc MLS) 33

• L. donovani donovani, infection of the classic kala-azar

02/23/2021 Shimelis Teshome (BSc MLS) 35

• Symptoms begin with intermittent fever, weakness, and

• Examination of tissue biopsy, spleen aspiration, bone

02/23/2021 Shimelis Teshome (BSc MLS) 38

02/23/2021 Shimelis Teshome (BSc MLS) 39

1. Trypanosoma brucei complex – African trypanosomiasis (sleeping

• These species may have amastigote, promastigote, epimastigote,

• T. gambiense & T. rhodesiene are causative agents of the

02/23/2021 Shimelis Teshome (BSc MLS) 42

• T. burcei gambiense is limited to tropical west and central

02/23/2021 Shimelis Teshome (BSc MLS) 45

• Although both species cause sleeping sickness, the

• Both the humoral and cellular immunity involve in these infections.

• The immune responses are faced with antigenic variation

• Examination of thin and thick films, in concentrated anticoagulated blood

02/23/2021 Shimelis Teshome (BSc MLS) 49

02/23/2021 Shimelis Teshome (BSc MLS) 50

• Soil-transmitted helminth (STH) infection is highly endemic in

• Neglected by the global health community because

02/23/2021 Shimelis Teshome (BSc MLS) 52

• Infection occurs on ingestion of raw food, such as fruit or

• The eggs then hatch in the small intestine, to release the

• L2 larvae penetrate the intestinal wall, entering the portal

1. Pathology Associated with the migration of Larvae

02/23/2021 Shimelis Teshome (BSc MLS) 54

02/23/2021 Shimelis Teshome (BSc MLS) 57