MEDICAL PARASITOLOGY

Learning Objectives

At the end of this chapter the student will be able to:

Define common terms used in medical parasitology

Explain host-parasite relationship

Discuss the geographical distribution, mode of transmission, source

of infection, and portal of entry of parasites
Explain the general life cycles of parasites

Discuss pathogenesis mechanism of parasites

Explain host immunity & immuno – evasion mechanisms by

parasites
 Explain different effects of parasites
 Introduction to Medical parasitology

1.1. Definition
Medical parasitology:-

 The study of the parasites of man and their medical consequences or

 it is the study of organisms living in or on the human body (host) and the
Diseases they produce

It is a subject that researches or studies about:

 the biological features of human parasites,

 the relationship between the human being and the parasites,

 the prevention and treatment of the parasitic diseases. 

 Scope of Medical Parasitology
the very broad definition of parasitology,

parasites should include:-

viruses, bacteria, fungi,

protozoa and metazoa (multi-celled organisms) which infect

their host species.
However, for historical reasons the first three have been
incorporated into the discipline of Microbiology. 
 Therefore, Medical parasitology consists of:-
 Protozoa (single celled animals),
 Helminths (worms)
 Arthropods
 Concepts related to medical parasitology

Symbiosis

Any association more or less permanent is called a symbiosis, with each

member a symbiont.

Two different organisms live together and interact,

 one partner lives in or on another one’s body.

3 types:

Mutualism

Commensalism

Parasitism
 Parasite and types of parasites
Parasite:-
are organisms that infect other living beings. They live in or on the
body of another living being (host) and obtain shelter and
nourishment from it.
parasites spend all or parts of their life with host.
In parasitism, parasite is the benefited partner.

In another words
A small organism (Parasite) has the potential to harm a larger
organism (Host), and relies on said host for nutrients and shelter
(a Niche).
The parasite generally has a much higher reproductive capability
compared to its host.
Types of Parasites

Parasite can be Classified

I. According to their habitat
Endoparasite
Lives inside the body of the host
May be just under the surface or deep in the
body
o Tapeworms, flukes, protozoans
Ectoparasite
Stays on outside surface of the host
o Eg., ticks, fleas,
II. Based on dependency on the host
Obligate Parasite
Requires finding and invading the host to complete its
life cycle
Facultative Parasite
May become parasitic if it is given the chance but does
not require a host.
-III. Amount
of time spent
Permanent Parasite
Lives entire adult life stage on or in a host
Usually endoparasites
Temporary Parasite
Spends only a short time on a host
Usually ectoparasites
IV. According to their Pathogenicity:
Pathogenic parasites
Non-Pathogenic (commensal)
Opportunistic parasites
VI. Based on host ranges
Euryxenous parasites:
Those with a broad host range.
Stenoxenous parasites:
Those with a narrow host range;
Other terminology
Aberrant parasite:
Found in locations in the host where they normally do not
occur;
e.g., Ascaris larvae may migrate to the brain
Insidental parasite:
Occurs in hosts where it does not normally occur;
e.g., Fasciola normally does not occur in man but is
incidental if found in man’s liver.
Infective Stage : it is a stage when a parasite can
invade human body and continue to live there.
*Infective Route is the specific entrance through
which the parasite invades the human body.
Hookworms invade human body by skin. Man gets
infection with ascarid by mouth.
Infective Mode means how the parasite invades
human body, such as the cercariae of the blood fluke
actively penetrate the skin of a swimming man and the
infective ascaris eggs are swallowed by man.
Geohelminth
refers to the helminths which complete their life cycles not
requiring the processes of the development in
intermediate hosts.
They have only one host and a simple life cycle, such as
ascarid, hookworm, pinworm and etc.
Biohelminth
refers to the helminths which have to undergo the
development in intermediate hosts to complete their life
cycles, such as filaria, liver fluke, pork tapeworm and so on.
Alternation of Generation:
 In life cycles of some parasites, there is the regular
alternation of sexual and asexual reproductions,
eg.Plasmodium vivax

*Trophozoite is a living stage of protozoa when they

can move, take food and reproduce. (It is usually the
pathogenic stage.)
*Cyst is the resting stage of a protozoa with a
protective wall. It is usually the infective stage. Its
functions are protection, transmission and
multiplication.
Hosts and types of hosts
Host:-Hosts are organism which harbors the
parasite.
In parasitism, it is the injured partner
Types of Hosts: -
Definitive host:-
Intermediate host:-
Reservoir Host
 Any animal that carries a parasite that can cause
infections in humans.
 Even if it is the normal host for that parasite.
Carrier host: -
A person who harbors parasites has no any clinical
symptom. He is an important source of infection in
epidemiology
o e.g. human beings harboring cyst form of
E.histolytica
. Accidental (incidental) host: infection of a host
other than the normal species.
e.g human beings are accidental hosts for
H.dimunita (primarly it is tape worm of rats and
mice )
 Paratenic host: is host that harbors the parasite in a
dormant state of development but the parasite is
capable of continuing its life cycle in a suitable host.
And it serves as a temporal refuge and vehicle for
reaching an obligate host. e.g toxoplasma species in
cattle
 Epidemiology of parasite

Epidimology: The study of the patterns of diseases

within populations
For parasites, this includes:
 Host range – what can it infect?
 Geographic range – where is it?
 Is it a zoonotic agent?
o Can it infect humans?
 Does it have a reservoir?
o A group of vertebrates maintaining the parasite
 Factors
1. Presence of a suitable host
2. Habits of the host
3. Escape from the host
4. Favorable conditions outside of host
5. Economic and social conditions
Sources of Exposure to Parasitic Infections
Contaminated soil:-
 Soils polluted with human excreta is commonly responsible for
exposure to infection with geohelminthes
Contaminated water:-
Water may contain
 (a) viable cysts of Amoeba, flagellates etc,
 (b) cercarial stages of human blood fluke,
 (c) Cyclops containing larva of Dracunculus medinensis
 (d) fresh water fishes which are sources for fish tape
worm, and intestinal flukes infection
 (e) crab or cray fishes that are sources for lung fluke and
 (f ) Water plants which are sources for Fasciolopsis buski.
Cont…
 Raw or Insufficiently cooked meat of pork, beef and fish
 E.g., Trichinella spiralis, Taenia species, D.latum.
Blood sucking arthropods:
Plasmodium - anopheles mosquito,
 Leishmania - sand flies
 Trypanosoma - tsetse fly
 Animals (a domestic or wild animals harboring the parasite),

 e.g, 1. Dogs- the hydatid cyst caused by E. granulosus

F. Human beings:-

 A person his/her clothing, bedding or the immediate environment
that he/she contaminated
 Autoinfection: - e.g., S. stercoralis, E. vermicularis, and T.
solium
 Mode of Transmission

Direct mode of Transmission:-

classified as:
I.Horizontal Direct mode of transmission: Transmission is
mainly effected through:-
Feco-oral route: most intestinal parasites transmitted in this way.
Sexual intercourse
Blood transfusion
Direct skin penetration
II. Vertical Direct Mode of Transmission:
Transmission of the parasite is from the
mother to child through:
Congenital / transplacental
Transmammary (breast milk
 II- Indirect Mode of Transmission:-
 If the parasite
o has complex life cycle
o requires biological vectors and/or
o one or more intermediate hosts
Route of Transmission

I. By ingesting infective stage of parasites:

 In food, water or hands contaminated with faeces,
o E.g. E. histolytica, E. vermicularis, etc.
 In raw or undercooked meat, e.g. T. saginata, T. solium, T.
spiralis
 In raw or undercooked fish, crab, or water vegetation e.g.
intestinal flukes
 Water containing Cyclope e.g., D. medinensis
II. Penetration of Skin When in Contact with:
Faecally polluted soil, e.g., S.stercoralis, Hook worms
Water containing infective stages of the parasite E.g., Cercaria
of Schistosome species .
III. Through Insect Bite,
E.g., filarial worms, Trypanosoma sp, Plasmodium sp. etc.

Sexual Contact, e.g., Trichomonas vaginalis

Transmammary, e.g., S. stercoralis
Inhalation of contaminated air, e.g., E. vermicularis,
Transplacental, e.g., T. gondii
Kissing, e.g., Trichomonas gingivalis, T. tenax
 General Life Cycles of parasites
Describes the cycle of development of the parasite,
This may involve
Passing through a number of developmental stages
& enviroment
Parasitic and non-parasitic stages.
The life of a parasite can be divided into a number of
phases:
Growth and maturation,
Reproductive (sexual and asexual) and
Transmission phases.
All vitally important for the successful survival of the parasite.
Can be simple or complex depending on how many different hosts it
requires to complete its cycle
Simple or Direct Life Cycle (monoxenous)
• only one host is required to complete its cycle
• the parasite often spends most of its life, usually as an adult, and where it
reproduces
• Transmitted from one host to another through the air, by a fomite, or in
contaminated food or water.
 Indirect or heteroxenous life cycles
• requires 2 or more hosts (a vector or intermediate host ) to
reproduce or grow in
• Frequently this may involve passing through a number of
developmental stages & Evt.
 Why study life cycles?

Control.
Treatment.
Epidemiology.
Fundamental research.
 Parasitic Infections & Disease:

 Not all parasitic infections cause disease of clinical

significance.
 Both host and parasitic factors are involved for the
parasitic infection to cause disease or not
 Host Factors
1.Genetic factors, E.g. Black population who lack Duffy
antigen resist P.vivax
2.Age,
3.Sex : e.g., T.vaginalis
4.Level of immunity: natural and acquired immunity
5.Nutrition (malnutrition or under nutrition)
6.Intensity and frequency of infections
7.Presence of co-existing disease or conditions, which
reduces immune response. e.g. Pregnancy, HIV
8.Life style and occupation
Parasite factors

1. Strain of the parasite and adaptation to human host

2. Parasite load ( number of parasite )
3. Site (s) occupied in the body
4. Metabolic processes of the parasite, particularly the
nature of any waste products or toxins produced by
the parasite during its growth and reproduction..
How do Parasites Cause Injury to their Host?

Competition for the host’s nutrients

- Eg. D.latum absorbs vitamin B-12, can cause anemia
- other tapeworms absorb large amounts of proteins and
sugars
Use of host’s fluids
- hookworm ingests blood, can be up to 250 ml/day
Destruction of host tissues
- some injure upon entry, some after established
- eg. Swimmers itch, cercariae penetrate and cause
inflammation
- intestinal worms, after established cause small lesions in
gut, possible secondary infection
- Entamoeba actively digest epithelial cells in large
intestine
Tissue changes
- may cause serious consequences to host
- hyperplasia,. Eg Fasciola
- hypertrophy,
- metaplasia, change of tissue cell type to another
type. Eg. Paragonims (lung fluke)
- neoplasia, growth of cell to form a new structure. Eg.
Tumors
Toxins and secretions
- some may cause pathogenic response, some may inhibit
immune function
- eg. Mosquito saliva
Mechanical interference
- Elephantiasis (filarial worms) blocks lymphatic system
- Tapeworms in large numbers can block intestine
- Plasmodium can cause RBC’s to stick together and clog
capillaries
Host Immunity & Immuno – evasion of the parasite
Host immunity
Nonspecific immunity
Macrophage endocytosis
 Common for bacteria and small protozoa
Inflammation
 Acute – edema and increase of leukocytes
 Subacute – monocytes and lymphocytes present, with fibrocytes
binding parasite with collagen.
 Chronic – plasma cells present and form a granuloma
Hyperplasia – parasite causes host to produce more cells
 Liver fluke simulating enlargement of bile duct
Neoplasia (cancer) – rare parasites have been associated with
cancer, but mechanisms are still unknown.
Host Responses
Specific Immunity
Humeral response: Formation of antibodies or
immunoglobulin s(Ig) by B cells.
IgE fights helminths
IgM and IgG important against protozoans
Cell mediated response: uses T-cells
Cytotoxic T cells inject invading parasites
Also release cytokines, which promote nonspecific
immunity. (interconnected)
 Adaptive immunity to parasites
Parasite Immune response Effector mechanism

TH2 cells --> IL-4, IL-5 Eosinophils kill IgE-coated

Helminths
--> IgE, eosinophils parasites (form of ADCC)

T cells produce IFN-g --> Phagocytes kill parasites

Leishmania
activation of phagocytes living in endosomes

CD8+ T cells --> IFN-g, TNF activate

plasmodium secretion of cytokines macrophages, neutrophils
Role of antibody? to kill parasites
 The role of TH2 responses in defense against helminths

Eosinophils are better at killing helminths than are other

leukocytes; the TH2 response and IgE provide a mechanism
for bringing eosinophils to helminths and activating the cells.
Immune evasion by parasites
 1- Sequestration of Parasite
Means: The location of the parasite that makes it inaccessible to the
immune response.
This can be achieved through:

• Intracellular habitat
e.g. Plasmodium, Toxoplasma, Leishmania
Amastigotes of Plasmodium
Tissue cyst of
Leishmania parasite
Toxoplasma

• Presence of surrounding cyst wall

e.g. Trichinella larva.

Encysted larva of T.spiralis

2- Luminal Habitat
Intestinal parasites: e.g. Ascaris, Enterobius are less
exposed to immune factors present in the mucosa

3- Parasite movement

Adult Ancylostoma: move away from

inflamed tissue to fresh areas.

In larva migrans: Migrating larva escapes

the immune response elicited locally.
 4- Antigenic modification
Antigen variation:
African trypanosomes, malaria parasites.
Antigen disguise:
Parasites cover themselves with host proteins to be considered as
self and will not be attacked by the immune factors e.g. adult
Schistosoma.
Antigen mimicry:
Parasites produce antigens similar to host antigens so they are not
recognized by the host’s immune system e.g. Schistosoma.
Antigen shedding:
Parasites shed their antigens in abundance can neutralize antibody
response at a distance away from the parasite e.g. Schistosoma
mansoni and Plasmodium falciparum.
 5- Inhibition of Immune Factors
• Cleavage of antibodies: parasite produces a protease enzyme that can
cleave immunoglobulin molecule into Fab and Fc portions e.g.
Trypanosoma cruzi.
enzyme
• Inactivation of complement: through: Fab Fc
- Protease activity e.g. Schistosoma larva.
- Acceleration of decay of complement e.g. Trypanosoma cruzi.
- Ejection of membrane attack complex from their surface e.g.
Leishmania.

• Inhibition of macrophages by several inhibitory mechanisms so they

can survive in macrophages e.g. Leishmania, Toxoplasma,

X
Trypanosoma cruzi.
 6- Production of blocking antibodies

Antibodies of little protective effect.

Some helminths produce blocking Abs that combine with
helminths Ags making them unavailable for antibodies
of high protective effect (antibodies involved in ADCC) :
e.g. Schistosoma

7- Immunosuppression
Mediated through Ts cells e.g. Visceral leishmaniasis
Taxonomy and nomenclature of parasites

Taxonomy
 Taxonomic classification of helminths
Sub kingdom Phylum Class Genus – examples

Metazoa Nematodes Ascaris (roundworm)

Round worms; appear Trichuris (whipworm)
round in cross section, they Ancylostoma
have body cavities, a (hookworm)
straight alimentary canal Necator (hookworm)
and an anus
Enterobius (pinworm or
threadworm)
Strongyloides

Platyhelminthes Cestodes Taenia (tapeworm)

Flat worms; dorsoventrally Adult tapeworms are found
flattened, no body cavity in the intestine of their host
and, if present, the They have a head (scolex)
alimentary canal is blind with sucking organs, a
ending segmented body but no
alimentary canal
Each body segment is
hermaphrodite

Trematodes Fasciolopsis (liver fluke)

Non-segmented, usually leaf- Schistosoma (not leaf shaped!)
shaped, with two suckers but no
distinct head
Taxonomic classification of protozoa
Sub kingdom Phylum Sub-phylum Genus- examples Species- examples

Protozoa Sarcomastig- Sarcodina-- - Entamoeba E. histolytica

ophora move by
pseudopodia
further divided into

Mastigophora Giardia G. lamblia

move by flagella

Apicomplexa Plasmodium P. falciparum,

no organelle of P. vivax,
locomotion P. malariae,
P. ovale

Ciliophora Balantidium B. coli

move by cillia

Microspora Enterocyto-zoa E. bienusi

Spore-forming
Nomenclature of parasites

Common name vs scientific name

Parasites named by binomial nomenclature

Genus (capitalized)

Species (not capitalized)

Binimial name underlined or separately italicized

Example: Ascaris lumbricoides, Ascaris lumbricoides
diagnosis
1. Clinical and
2. Laboratory
1. Parasitic (morphological) diagnosis
 Macroscopic
 Microscopic
2. Immunological diagnosis
 Antibody detection
 Antigen detection
3. Molecular diagnosis
4. Culture
5. Animal inoculation
6. Xenodiagnosis
 Control of parasitic disease
A. Prevention
 Blocking transmission
Control of vectors
Reduction of vehicle contamination
Control of animal reservoir
Health education and improved sanitation
Personal hygiene- hand washing
Food handling - covering & Cooking
Using vinegar for green salads for 30 min.
Sewage treatment and waste disposal
Water quality – boiling, treating & Covering
 Control….
B. Treatment :- Early identification and treatment of
infected individuals.

1. Medical and surgical

2. Chemotherapy

3. Adequate nutrition
 Medical
Protozoology
What are Protozoa?

proto = first

zoa = animals

single-celled eukaryotic organisms

kingdom Protista

Vary in size (3-2000 micro m).

The cells consist of plasma membrane, cytoplasm, ER, GB,

ribosomes, nuclear membrane, nucleus and chromosomes.
Protozoa…
In addition may possess
pseudopodia,
flagella &
cilia as organ of locomotion.
Single protozoal cell performs all the functions of.
 respiration,
 digestion,
 excretion,
 locomotion and
 reproduction.
Protozoa….
Classification according to morphology and means of
locomotion.

There are 45,000 protozoa species.

 Most species that cause human disease belong to the

phylum
 sarcomastigophora and

 apicomplexa.
 Protozoa….
 Protozoa are found in all moist habitats.

 They are common in sea, in soil & in fresh water.

 These organisms occur generally as a single cell.

 Colonies of protozoa might also occur in which

individual cells are joined by cytoplasmic threads and
form aggregates of independent cells.
 Cont’d….
Reproduction types:
Asexual multiplication:

Simple binary fission-

In this process after division of all the structures, the individual

parasite divides either longitudinally or transversally in to two
more or less equal parts.

Multiple fission or schizogony-

In this process, more than two individuals are produced,

E.g. asexual reproduction in plasmodia.

 Cont’d….
 Sexual reproduction:
Conjugation-
In this process temporary union of two individuals occurs
during which the interchange of nuclear material takes place.
Later on, the two individuals separate.

Syngamy-
In this process, sexually differentiated cells, called gametes,
unite permanently and complete fusion of the nuclear
material takes place.
The resulting product is known as a zygote.
Cont’d….
The protozoa are classified biologically according to
their type of
 locomotory organelles or their habitat in the body of the
host.
Locomotory organelles Habitat
– pseudopodia -Intestinal protozoa
– Flagella -Tissue protozoa
– Cilia - Blood protozoa.
 SARCODINA
Characteristics:

Possess shapeless mass of cytoplasm (ectoplasm and

endoplasm)

Move by means of pseudopodium

Reproduce by simple binary fission

Most species have two stages

Trophozoite and cyst

7 species are found in the intestine and oral cavity

Cont’d….
Six in the large intestine
 E. hystolytica
 E. coli
 E. dispar
 E. hartmanni
 Endolimax nana
 Iodamoeba buetschlii
One species in the oral cavity
 E. gingivalis
Other two species have been found as pathogenic free
living (facultative parasite) amoeba:
Naegleria fowleri and Acanthamoeba cephalus
E. histolytica

 Cause amoebiasis (amoebic dysentery and liver

abscess)
 Only a few strains are pathogenic
Morphology
 Trophozoite:
 Has one nucleus and pseudopodium
The invasive strain possess RBCs
 Cyst:
 Immature cyst possess one or two nucleus and inclusion
bodies
 Mature cyst possess four nuclei
 Cont’d….

Epidemiology:

Distributed worldwide

Incidence is highest in tropical and sub tropical regions

90% of infections are asymptomatic

Transmission and life cycle:

Ingestion of infective cyst in food or water contaminated

with faeces
 Life cycle
After ingestion the cyst passes through the stomach,

where exposure to gastric acid stimulates the release of

pathogenic trophozoite in the duodenum.

 It divide and produce extensive local necrosis in large intestine. Forms

“flask-shaped” or “duct-tube” ulcer.

 Invasion into the deeper mucosa may result extra-

intestinal amoebiasis

 After a period of growth and multiplication, encystations occur in the

cecum and colon.
Pathogenesis and clinical manifestation of amebiasis
 Clinical feature s

About 90% - do not develop clinical symptoms

Some - exhibits amoebic dysentery and/ extra intestinal

amoebiasis in liver, spleen, brain & lungs.

Amoebic dysentery occurs when the trophozoite

invades the intestinal wall.

Symptoms include abdominal pain and dysentery with

blood and mucus.

Multiplication of trophozoite forms ulcer.

Pathogenesis and clinical manifestation of amebiasis

NON-INVASIVE
ameba colony on intestinal mucosa
asymptomatic cyst passer
non-dysenteric diarrhea, abdominal cramps, other GI
symptoms
INVASIVE
necrosis of mucosa  ulcers, dysentery
ulcer enlargement  severe dysentery, colitis,
peritonitis
metastasis  extraintestinal amebiasis
flasked-shaped ulcer’
 Liver abscess
Trophozoite that reach the blood stream are carried to the liver,
lungs, brain & heart and can form ulcer.

The clinical features include:

 pain,

 tenderness in the region of liver,

 wasting and

 fever associated with chills and night sweat.

 Laboratory diagnosis and Rx

1.Stool examination
Examination of a fresh dysenteric fecal specimen
for motile E. histolytica trophozoite.

2.Serologic studies

3.Tissue examination: sigmoidoscopic biopsy, aspiration

Treatment
Tinidazole (drug of choice)
Metronidazole (alternative drug)
 Prevention and control
 Personal hygiene

 Safe water supply or prevents faecally contamination.

 Socking green salads in vinegar for 30’ (kills E. histolytica

cyst)

 Boiling drinking water (cyst killed at 55oC)

 Vegetable should be cooked

 Food handlers should be checked

 Access of flies and cockroach to food must be prevented

 Health education
 Flagellates

• Flagellates are grouped • Intestinal Flagellates:

in to • Giardia lamblia
• Dientamoeba fragilis
1. Luminal (intestinal,
• Chilomastix mesnili
urogenital& oral)
• Trichomonas hominis
flagellates
• Enteromonas hominis
2. Haem(blood & tissue) • Retortamonas intestinalis
flagellates
• Urogenital flagellates
• Trichomonas vaginalis
• Oral flagellates
• Trichomonas tenax
Luminal (intestinal,urogenital& oral) flagellates
General characterstics
Usually posses 2-6 flagella(~ 8 flagella.)
Inhabit the intestinal, urogenital and oral cavity
Direct life cycle/no biological vector
All have trophozoites and cyst stage except the
Trichomonas species
All are comensal/ non-pathogenic/except G.lamblia and T.
vaginalis
worldwide distribution
higher prevalence in tropical or developing countries (20%)
1-6% in temperate countries
most common and easily recognized protozoa in stools
~200 million cases/yr
 Giardia lamblia
Trophozoite stage
Typical Characteristics:
Size range: 8-20 um
Shape: Pear/teardrop
Motility : “Falling leaf”
Appearance: Bilaterally symmetrical
Nuclei: Two ovoidal-shaped, each
with a large Karyosome
No peripheral chromatin
Flagella: Four pairs arising from the ventral
side :
One pair anterior end
One pair posterior end
Two pairs central laterally
 Giardia lamblia
Cyst
• Typical Characteristics:
• Size range: 11-14 um
• Shape: Ovoid ellipsoidal or may
appear round
• Nuclei: -2-4 located at one end
young cyst 2 nuclei,
mature cyst 4 nuclei
- Central Karyosome
- No peripheral chromatin
 Transmission
Giardia is transmitted via the cyst stage

1- ingestion of faecally contaminated food

or water with cyst

2- Person to person

3- sexually among homosexual (feco-oral

contact)
Life Cycle.

1.Life cycle is direct - no intermediate host.

2. When cyst is ingested, the organisms escape from the cyst in
the duodenum.
3. Attach via adhesive disk to microvillar surface of epithelium of
upper two-thirds of the small intestine.
4.They divide by longitudinal fission.
5. Encystment occurs in lower intestinal tract.
6. Freshly passed cysts are infective
7. Trophozoites are found in diarrheic stools; cysts are found in
formed stools.
Cyst survive
cool, moist conditions
for long periods
in cold water:
2 months at 8°C
1month at 21°C
 some cysts can survive –13°C for 2 weeks
relatively resistant to chlorination, particularly if
the water is cold the amount of chlorine in drinking
water is not sufficient to kill G. lamblia
 Pathogenesis
• Epithelial damage
• Villus blunting
• Crypt cell hypertrophy
• Cellular infiltration
• Malabsorption develops
• Enzyme deficiencies
• Lactase (lactose intolerance)
• Steatorhae
• Foul smelling diarrhea
•
Possible Mechanisms
• mechanical irritation
• obstruction of absorption
Clinical Features and Symptoms
one of the more common diarrheal disease seen
among travelers to foreign countries
Outcomes may be
Asymptomatic/latent
Acute short-lasting diarrhea
Chronic/nutritional disorders
 Acute Symptoms

 Develops after an incubation period of 1 to 14 days

(average of 7 days) and usually lasts 1 to 3 weeks
 Sudden explosive, watery diarrhea, bulky, frothy,
greasy, foul-smelling stools, no blood or mucus
 Upper gastro-intestinal uneasiness, bloating, flatulence,
belching, cramps, nausea, vomiting, anorexia
 Usually clears spontaneously (undiagnosed), but can
persist or become chronic
 Irregular excretion of cysts:
 10 days lasting negative phases possible (>1 stool analysis
Subacute/Chronic
recurrent diarrheal episodes
cramps uncommon
sulfuric belching, anorexia, nausea frequent
can lead to weight loss and failure to thrive
The more chronic stage is associated with vitamin
B12 malabsorption, disaccharidase deficiency and
lactose intolerance
stools become steatorrheic (fatty stool) containing
large amount of fats and mucus but no blood
Laboratory Diagnosis:

 Macroscopic
 Stool:
 is usually offensive, bulky, pale, mucoid (fatty), diarrheic
(watery) but
 there is no blood in the stool.
 Microscopy
1.Finding the trophozoite stages in fresh diarrhoeic stool
2.Finding the trophozoite stages in duodenal aspirate
3.Finding cyst stage in formed stool
4.String (entero test
 Immunological methods
 Molecular methods
 Treatment Control
Drug of Choice • avoid fecal-oral transmission
• metronidazole • improve personal hygiene
• 750 mg/tid/5d • especially institutions
• >90% cure rate • treat asymptomatic carriers
• eg, family members
Alternatives • health education
• tinidazole (single dose) • hand-washing
• paromomycin (pregnancy) • sanitation
• quinicrine • food handling
• furazolidone • protect water supply
How to get rid of Giardia in water?:
* boiling (at least 1 minute)
* filtration (1μm pores) 􀀮
* chemical treatment (Iodine, …) 􀀯
 Urogenital flagellates
• General feature
• Inhabit the urogenital TRICHOMONADS
tract of male and female
• Has only trophozoite Human Trichomonas Species
stage T. tenax oral cavity
• Most frequent STD T. hominis* intestine
pathogen
T. vaginalis uro-genital
• longitudinal binary fission
*aka: Pentatrichomonas
 Trichomonas vaginalis
Distribution:-World wide .
Habitat:- uro-genital tract
females: vagina
males: urethra, prostate,
Transmission: trophozoite stage
transmitted during sexual
intercourse
-non-sexual contact possible
-common STD
• co-infection w/other STDs
• more prevalent in at risk groups
• both sexes equally susceptible
• symptoms more common in females
Morphology: Has trophozoite stage only

Trophozoite
• Size 15-25 by 5-12m, is the largest
Trichomonas.
• Shape: pyriform
• Motility: Jerky (on-spot), non-directional
motility .
• undulating membrane :Short extending
along two third of the body.
• In Giemsa/field stain
• Nucleus: Single
• Flagella: 3-5 anterior free flagella
• Axostyle- extends beyond the body
• U.m bordred by flagella
 Clinical manifestations

In females:
ranges from asymptomatic, to mild or moderate irritation, to
extreme vaginitis
• 50-75% abnormal discharge (frothy, yellowish or greenish)
• 25-50% pruritis
• 50% painful coitus
onset or exacerbation often associated with menstruation or
pregnancy
vaginal erythema, ‘strawberry cervix’ (~2%)

In males
• 50-90% are asymptomatic
• Mild dysuria or pruritus
• Minor urethral discharge
 Laboratory diagnosis
Finding the trophozoit in smear of vaginal or uretheral
discharge
Occasionally in urine sediment of men and women

TREATMENT
metronidazole
250 mg (3/d) for 5-7 days
simultaneous treatment of partner! (85-90% cur
PREVENTION
limit number of sexual partners
condoms
 Blood and Tissue flagellates

belonging to the family Trypomastidae

six genera but only two of them are responsible to cause disease to
man
 Genus Leishmania
Genus Trypanosoma
 General Characteristics blood & tissue flagellates

Reproduces by longitudinal binary fission

 biological insect vectors as intermediate hosts & human
as definitive host
The species are morphologically indistinguishable, but
they can be differentiated on the basis of on their
clinical features, geographical distribution,
serologic tests
 Lei…
Leishmania species
Causative agent of Leishmaniasis
obligate intracellular protozoa of the genus Leishmania
Named after Leishman, who first described it in London in May 1903
Human infection is caused by about 21 of 30 species that infect
mammals.  These include:
 L. donovani complex
L. donovani,
 L. infantum,
 L. chagasi;
L. mexicana complex
L. mexicana
 L. amazonensis
 L. venezuelensis;
 Lei…
L. braziliensis complex
L braziliensis
L. Peruviana

L. Guyanensis complex

L. Guyanensis
L. panamensis

L. tropica, L. major & L. aethiopica

 lei…

Leishmaniasis can easily classified clinically as

Visceral leishmaniasis
Cutaneous leishmaniasis
Mucocutaneous leishmaniasis
Diffuse cutaneous leishmaniasis
 lei…

Cutaneous leishmaniasis(CL) caused by

L. tropica
L. major
L. aethiopica
L. panamensis
L. guyanensis
L. peruviana
Visceral leishmaniasis(VL)
Also called Kala azar, Dum- Dum fever, death fever , tropical
spleenomegaly
L. donovani
L. infantum
 L. Chagasi
 lei…

Mucocutaneous leishmaniasis(MCL)
L. panamensis
L. guyanensis
L. bazilliensis
L. aethiopica

Diffuse cutaneous leishmaniasis(DCL)

L. amzonensis
L. aethiopica
 lei…
Geographical distribution

 350 million people are at risk in 88 countries around the world

72 of which are developing countries

an estimated 12 million cases world wide

1.5 to 2 million new cases occur every year

CL form representing 50 to 75% of all new cases
 lei…
Geographical distribution of leishmaniasis is limited by:
The distribution of the sand fly,

Its tendency to take blood from humans or animals only

Its capacity to support the internal development of specific species

of leishmania
In Ethiopia
Four species of Leishmania is found, namely,
L. aethiopica,
L.major
L. tropica
L. donovani
 lei…

Visceral leishmaniasis (VL)

L. donovani
Occurs mainly in arid and semiarid lowlands below 1,300 m
altitude
Important endemic foci include
Gelana focus at lake abaya,
the segen valley (Aba- Roba focus) in Knoso Wereda
 the Omo river plains and
the Metema and Humera plains in north western Ethiopia
 lei…

Cutaneous leishmaniasis
L. aethiopica,L.major L. tropica
Endemic at altitudes 1400 - 2700 m in most administrative regions

Prevalence rates of 5.5 – 40% were reported from villages in

Shewa , Wello and G.Gofa with the highest rate in Ocholo village in
G. Gofa

rock (Procavia habessinica) & tree (Heterhyrax brucei ) hyraxes

serving as reservoir host for L. aethiopica
 lei…

Habitat & morphology

PrPromastigote Amastigote
-Elongated, with flagella -Round (3-7 µm diameter)
(10-20 µm long) -Occurs intracellularly, in
-Occur extracellularly in the mammalian
-insect midgut & in artificial culture -Non-motile
-Motile
 Transmission and life cycle
• Common mode of transmission.
Bite of infected female sandfly
 Phlebotomus in Old world
Lutzomyia in New world

• Uncommon modes of transmission:

Congenital transmission,
Blood transfusion,
Rarely, inoculation of cultures.
 lei…

Mammalian Reservoir Hosts

• Rodents
• Gerbils • Sloths
• Hyraxes • Primates
• Bats • Dogs
• Porcupines • Foxes
• Opossums • Anteaters
• .....
 lei…

General life cycle of Leishmania species

• female sandflies inject promastigotes

stage during blood meals
• about 30 species of sand flies acts a
vector
 lei…

Promastigotes are phagocytized by macrophages & transform

into intracellular amastigotes form
Amastigotes multiply by binary fission, rapture from
macrophages , and infect new cells
 In VL the amastigotes are carried through blood
circulation , then invade and multiply in the macrophages
of spleen, liver, bone marrow, lymph glands
In Cl , MCL – the amasigote multiply in skin macrophages
(histocytes)
lei…
 lei…

Sandflies become infected during blood meals when they ingest

macrophages infected with amastigotes

the host cell break down and releasing the amasigotes which is then
transform to promastigotes

 multiply , fill the lumen of the gut and migrate to the proboscis
lei…
 Pathogenesis  

Entrance into the host and establishment of infection by leishmania is

enhanced by saliva from the vector
Two substances were involved
maxadilin, or maximum dilation molecule: keeps the capillary
bed open at the site of feeding for about 48 hours
 SIP or salivary immunosuppressive protein : restrains the
immune system’s early efforts to eliminate the parasites
 Infective promastigotes entering the blood of the vertebrate are
covered by two key molecules:
the protein gp 63 and
 lipophosphoglycan (LPG)
 Both mediate the uptake of promastigotes by
macrophages
The promastigotes are engulfed & form phagosome
 Con t…
 phagosome fuse with the lysosome to form a phagolysosome

 As the promastigotes transform into amastigotes, which

produce compounds that counter lysosomal enzymes

 The gp 63 molecule inactivates proteolytic enzymes

 LPG protects against other enzymes

 Leishmanial organisms are able to survive the highly acidic
environment of lysosmes by regulating their internal PH
 lei…
Clinical features and pathology
Cutaneous Leishmaniasis

The clinical forms of CL vary according to

 The species of parasite
 Region and
 Response of patient
 lei…
Old World CL
L. Tropica
 SW Asia, N.Africa
• Anthroponotic or dog
reservoir
• dry ,urban ,chronic, old
world oriental sore
• 'dry painless lesion’
• 25-70mm diameter
 lei…

Soldier in Afghanistan
Officer holding Iraqi child with with Leishmania tropica
Leishmania tropica on face on hand
 Leishmaniasis
• multipleRecidivans(LR)
un healing lesions, often on the
face
• Relapsing leishmaniasis
• Often due to inadequate treatment or
allergic state
• Nodular lesions or rash around central
healing
• can last for many years and difficult to
treat
• Untreated LR is destructive and
disfiguring
 L. major
• central Asia, middle East, Africa
• rural (rodent reservoir)
• wet oreintal sore
• Early papules is inflamed (5-
10mm)
• Develop to large uneven ulcer
• Self-healing (3-6mths)
• Protect against reinfection & also
with L.tropica

ulcers are moist or open with

seropurulent exudate
 L. infantum
 Mediterranea, Europe
 dermotrophic strains recently
recognized

• L. aethiopica
 highlands of Kenya and
Ethiopia
 Similar to oreintal sore
 Self-heal 1-3 yrs
 Can cause DCL in patients
• also cause MCL
 lei…

New World CL
L. mexicana)
• Initially, the lesion is a small, red
papule up to 2 cm in diameter

• change in size and appearance

over time
• Chiclero Ulcer (L. mexicana
• chronic ulcerated, papular, or
nodular lesion
• lesion is painless, non-tender,
non-pruritic

Lesions of the body tend to self-healing

but those on the ear may last up to 30
years and entirely destroy the pina of the
ear
Diffuse Cutaneous Leishmaniasis
• caused by L. aethiopica and L.
amazonensis

• Skin lesion develop over large areas

of the body

• Scaly, not ulcerated, nodules

• Chronic and painless

• Numerous parasites in lesions

• Seldom heal despite treatment

Mucocutaneous Leishmaniasis
• Known as espudia
• two stages
• simple skin lesion
• 2o mucosal involvement
• metastasis via blood or lymphatic
systems
• can occur after primary lesion (up to
16 years)
• frequently in naso-pharyngeal
mucosae
• junction of skin and mucosa
• variable types and sizes of
lesions
• chronic and painless
• non-ulcerative type
• local edema (upper lip)
• ulcerative type
• rapid and extensive mutilation
lei…

 Disfiguration is often extreme

with complete destruction of the
 nasal septum, perforation of
the palate and damage of
the tissues of the lips and
larynx
Visceral Leishmaniasis (VL)

Reticulo endothelial system affected

 spleen, liver, bone marrow, lymph nodes
The disease may be asymptomatic and self-resolving but
usually runs a chronic course and may be fatal without
treatment
Untreated VL carries have progressive disease
75-95% mortality
Pneumonia is the common complication
incubation period ,generally 2-6 months ( range 10 days to
years)
Reticulo endothelial system affected
 spleen, liver, bone marrow, lymph nodes

• The disease may be asymptomatic and self-resolving but usually runs a

chronic course and may be fatal without treatment
• . Untreated VL carries have progressive disease
• 75-95% mortality
•Death usually occurs because of severe secondary bacterial infections
in advanced disease
lei…

• fever, malaise, weakness

• wasting despite good appetite
• spleeno- and hepatomegaly, enlarged
lymph nodes
• epistaxis (nose bleeding) and bleeding
of gums

• depressed hematopoiesis
 severe anemia
 leucopenia
 thrombopenia
• A 12-year-old boy
suffering from visceral
leishmaniasis. The boy
exhibits splenomegaly
and severe muscle
wasting
 lei…

Post Kala Azar Dermal leishmaniasis (PKDL)

Cutaneouse form of leishmaniasis, which can occur after

resolution (after treatment and recovery) of VL
 It require expensive and prolonged treatment
characterized by hypo pigmented and raised erythematous patches
on the face, trunk of the body and limbs
may develop in to nodules and resembles those of lepromatous
leprosy, fungi infections or other skin disorders
Occasionally there is ulceration of lips and tongue
 occurs in 1-3% of Indian and 50% of Sudanese VL patients
 lei…

Laboratory Diagnosis of CL, MCL, DCL

suspected because of:

 geographical presence of parasite

 history of sandfly bite

 skin lesion:
o chronic, painless, ‘clean’ ulcer
o nasopharyngeal lesions
o nodular lesions
 lei…

The laboratory diagnosis of CL, MCL & DCL is by

1. Detecting amastigotes from scrapings, biopsy, aspirates

2. Culture from ulcer material
3. Leishmainin test
4. serology
 Diagnosis visceral leishmaniasis

(1) Demonstration of parasite in tissues by

 light microscopic examination of the stained specimen,
 culture
 animal inoculation
(2( Detection of parasite DNA in tissue samples

(3) immunodiagnosis by detection

Antigen detection
 antibody detection
 Cont…
Haematological investigations including:
Measurement of the hemoglobin

Total and differential white cell (leucocytes) count: leucopenic

Platelet (thrombocyte) count: thrombocytopenic

a raised ESR

Plasma albumin levels are greatly reduced

 total protein raised in patients with VL

 lei…

Treatment
Treatment
• Sodium stibogluconate (Pentostam)

• Pentamidine isethionate

• amphotericin B

• cryotherapy and thermotherapy

 lei…
Prevention and control

1. Early detection by serological diagnosis (VL) and treatment of

infected persons

2. Health information dissemination

3. Personal protection from sand fly bites by:

Using insect replants
Avoiding endemic areas especially at times when sand flies are
most active
Use of pyrethroid impregnated bed nets and curtains
 lei…

4. Vector control by the use of light traps or residual insecticide spraying

of houses

5. Destruction of stray dogs and infected domestic dogs

6. Elimination and control of rodents

7. sitting human dwellings away from the habitats of animal reservoir

hosts where sand flies are known to breed
Trypanosoma
 Trypanosoma species

Causative agent trypanosomiasis

 Nagana : animal trypanosomiasis

 Surra: a diseases mainly of camel and horses caused by
T. evansi
 Dourine : equids , T. equiperdum
 Sleeping sickness : African human trypanosomiasis
 Chagas disease : American human trypanosomiasis
Classified in to two groups based on the type of development in the
insect vector and mode of transmission
Two distinct forms occur in humans
African Trypanosomiasis
Trypanosoma brucei gambiense
Trypanosoma brucei rhodesiense
Transmitted by the Tsetse fly
American Trypanosomiasis
Trypanosoma cruzi
Transmitted by the tritomine bug
African Trypanosomiasis
 Human African Sleeping Sickness

There are two clinical forms

Trypanosoma brucei gambiense
Causes a slowly developing disease
Disease: West African or Gambian African
sleeping sickness
Trypanosoma brucei rhodesiense
Causes a rapidly progressing disease
Disease: East African or Rhodesian African
sleeping sickness
 Geographical distribution

Trypanosoma brucei gambiense is found West and western

central Africa, extending from Senegal across to Sudan and
down to Angola

Trypanosoma brucei rhodesiense is found in East Africa,

Central Africa, and Southern Africa, extending from Ethiopia
down to Botswana
In Ethiopia

Animal trypanosomiasis (Nagana or gendi) always has been a

problem in many parts of Ethiopia
T.b. rhodesiense is singled out as the species occurring in
Ethiopia
the Sleeping sickness foci are limited to Gambela
(the areas along Baro, Gilo and Akobo rivers),
Gamo Gofa (from Mursi-Bodi district), Kefa (from
maji), and Welega ( from the settlement area in the
Anger-Didesa valley)
Habitat
Trypomastigotes: In blood vessels
& intercellular spaces of Lymph nodes, spleen,
liver, Brain, CSF
Seen in vertebrate host (human, dog, goat & cattle)
procyclic trypomastigotes: In the mid and fore gut of
the Glossina spp.
Epimastigote & Metacyclic trypomastigotes

seen in the salivary gland of Glossina spp.

Transmission

bite of infected tsetse fly – Glossina spp

In Ethiopia :
 Glossina fuscipes fuscipes , G.tachniodes,
G.pallidipes ,G.moristans sub moristans & G.
longipennis
 congenital
blood transfusion
Humans are the main reservoir for Trypanosoma brucei gambiense. 
Wild game animals are the main reservoir of T. b. rhodesiense
 
Life cycle of African trypanosomiaisis

During a blood meal on the mammalian host, an infected tsetse fly

(genus Glossina) injects metacyclic trypomastigotes into skin tissue

 The parasites enter the lymphatic system and pass in to the blood
stream
o transform into blood stream trypomastigotes , are carried
to other sites throughout the body, reach other body fluids
(e.g., lymph, spinal fluid), and continue the replication by
binary fission  
 The tsetse fly becomes infected with blood stream
trypomastigotes when taking a blood meal on an infected
mammalian host

In the fly’s midgut, the parasites transform into procyclic

trypomastigotes, multiply by binary fission , leave the mid gut, and
transform into epimastigotes

The epimastigotes reach the fly’s salivary glands and continue

multiplication by binary fission and transform into metacyclic
trypomastigotes
 Pathogenesis

 An exact pathogenesis of sleeping sickness is not known, although

immune complexes and inflammation have been suspected to be the
mechanism of damage to tissues

 The immune response against the organism help to eliminate the

parasite but it is not protective

Antigenic variation
Trypanosomes are covered with a glycoprotein surface coat called
variable surface coat glycoprotein (VSG)
VSG is major component ‘surface coat “ covering blood steam
trypomastigotes
Immunoglobulin directed against these VSG recognize the
trypanosomes and destroy it until the organism vary their VSG

Periodically (every 5-7 days ) the parasite will express a

different VSG gene which is antigenically distinct from the
previously expressed VSG

It also causes severe depression of cell mediated and humoral

immunity to other antigens
Results in death
Clinical feature and pathology
Fatigability ,
confusion ,
drowsiness ,
(uncontrollable
urge to sleep day
time which may
alternate with night
time insomnia ),
wasting and
emaciation
 Laboratory diagnosis
1. Microscopy
A. Examination of blood for trypanosomes
B. Examination of lymph gland aspirates
C. Examination of chancre fluid for trypanosomes
D. Examination of CSF for trypanosomes
2. Serology
3. Molecular techniques : polymerase chain reaction
(PCR).
 Other tests
Measurement of haemoglobin : anemia with reticulocytosis
Erythrocyte sedimentation rate (ESR): elevated
Total white blood cells count and differential count :
moderate leucocytoisis with monocytosis, lymphocytosis
and presence of plasma cells
Platelets count : thrombocytopenia
Treatment
Pentamidine isethionate or Suramin
Prevention and Control
1.Detecting and treating human infections at early stage
2.Identifying and killing/ restricting movement of animal
reservoir hosts in endemic areas
3. Health information dissemination
4. Sterile breeding technique
5. Vector control:

By spraying vehicles with insecticide as they enter and

leave the tsetse fly infested area,
By selectively clearing the bush and wood areas especially
around water holes, bridges, and along river blanks
 By using and maintaining insecticide impregnated tsetse
fly traps
American Trypanosomiasis
 American Trypanosomiasis

 Caused by Trypanosoma cruzi

Geographical distribution: Central and S. America
Habitat
Amastigotes: Intracellular forms in the
reticuloendothelial cells and tissues of brain, muscles,
Lymph nodes, liver, Spleen, bone marrow
Epimastigotes: In the mid-gut of the insect vector (bug)
Trypomastigot: In the mid-gut of the
vector and; in the blood circulation &
intercellular spaces of man
Triatomine bug
Metacyclic Trypomastigote: In the mid
gut and in the faeces of the insect vector
Transmission and Life Cycle
 Transmission to human host : An infected triatomine insect
vector (or “kissing” bug) takes a blood meal and releases
metcyclic trypomastigotes in its feces
 Less common transmission :
 blood transfusion ,
 transplacental ,
 organ transplantation or
 accidental ingestion infected insects

 Metacyclic trypomastigotes enter the host, through intact

mucosal membranes, such as the conjunctiva, as the bite wound
is rubbed or scratched
 
 Metacyclic trypomastigotes invade histiocytes & differentiate into
intracellular amastigotes

 The amastigotes multiply by binary fission & differentiate into

trypomastigotes, & then are released into the circulation

 Trypomastigotes infect cells from a variety of tissues and transform

into intracellular amastigotes in new infection sites
   Clinical manifestations can result from this infective cycle 
The “kissing” bug becomes infected by feeding on human or animal
blood that contains circulating parasites

 The ingested trypomastigotes transform into epimastigotes in the

vector’s midgut  

The parasites multiply in the midgut and differentiate into infective

metacyclic trypomastigotes in the hindgut
Clinical feature and Pathology
Chagas' disease can be divided into three

1.The primary lesion

Chagoma, appearing at the site of infection, within a few hours of a
bite, as slightly raised, flat non-purulent erythematous lesion
usually found on the face, eyelids, cheek, lips or the conjunctiva
Many patients develop conjunctivitis and unilateral edema of the
face and eyelids known as Romana's sign
2.Acute Stage
 appears 7-14 days after insect bite
 characterized by restlessness, sleeplessness, malaise,
chills, fever and bone and muscle pains
 Diffuse myocarditis, sometimes accompanied by
serious pericarditis and endocarditis
 In children, Chagas' disease may cause meningo-
encephalitis and coma
 Death occurs in 5-10 percent of infants
3. Chronic Stage:
 Approximately 10-20% of victims develop a chronic disease
 Many of these cases will be asymptomatic for long period of time
 The symptoms depend on organ affected and the extent of organ
damage
 Myocardial cells are invaded and destroyed leading to
cardiomegaly, myocardial insufficiency
 Destruction of nerves innervating the digestive tract leads to
diminished peristaltic activity and inability to swallow with
gross enlargement of the esophagus (megaesophagus) and
colon(megacolon)
Laboratory Diagnosis

1. Blood film -wet film for motility

-thin and / or thick stained blood films
Trypamastigote stage during acute stage

2. Culture of blood

3. Serological diagnosis to detect anti- T.cruzi antibodies

4. Xenodiagnosis
 in chronic and subacute infections where their number in the blood is
usually very few
uninfected, susceptible, laboratory reared triatomine bugs are starved
for 2 weeks and
 then fed on the patients blood
If trypanosomes are ingested they will multiply and develop into
epimastigotes which can be found 25-30 days later in the faeces
or rectum of the bug
Prevention and Control
Measures reduce contact between the vectors & man
 APICOMPLEXA

Intestinal Blood and tissue

coccidian coccidian
 Apicomplexa (coccidia)

1. Intestinal coccidian

Cryptosporidium
Isospora
Cyclospora
2. Blood and tissue coccidian
Plasmodium
Toxoplasma
Babesia
 Intestinal coccidian
Cryptosporidium ,Isospora ,Cyclospora

General characteristics

• Considered as opportunistic parasite in

immunocompromised person

• Complete entire life cycle in single host

• Within the intestinal epithelial cells of the

host

• Characterized by a thick walled oocyst

excreted in faeces

• Are transmitted by the fecal-oral route

 Cryptosporidium Species:
C. parvum
 A coccidean parasite implicated in intestine
 Disease primarily among immunocompromised patient
 Self-limiting diarrhea in immunocompetent persons
 Profuse, watery diarrhea associated with AIDS (life
threatening
•Geog. Dist.: = Worldwide distribution
•Morphology: = oocyst round or slightly oval-shaped, 4 – 6um
enclosing 4 spindle–shaped sporozoites
Transmission
Mainly through the ingestion and possibly inhalation of
sporulated oocysts
 mainly through contaminated water &
 Occasionally food sources, such as chicken salad
fecal-oral transmission (monoxenous)
anthroponotic transmission
autoinfection
zoonotic transmission
 Transmission
• C. parvum

• human and bovine sources

• infective for mice and calves
• zoonotic & anthroponotic transmission
• waterborne s outbreaks is common

Waterborne Cryptosporidiosis
Human infection usually waterborne and
acquired by fecal-oral route
Highest prevalence of disease in areas with
unreliable water and food sanitation
 Factors Favoring
Waterborne Cryptosporidiosis

• Small size of oocysts (4-5 mm)

• Reduced host specificity and monoxenous development
• Close associations between human and animal hosts
• Large number of oocysts excreted (up to 100 billion per
calf per day)
• Low infective dose (<30)
• Robust oocysts; resistant to chlorine
Life Cycle:
Asexual:
ingestion of oocyst  intestine  release of sporozoite
from contaminated from oocyst
food and water with
feces of man/animal invade the GIT microvilli

developed into tropozoite

schizont (each mature contains)

8 merozoite
merozoite start with
another schizogonic cycle schizogony
(release from host epith. cell)

rupture of schizont
invade microvilli of
intestinal epithelial cell release merozoite
Sexual: = Gametogenesis and Fertilization of male and female
gametocytes  zygote  development of oocyst
 sporogony  4 sporozoites with in oocyst 
passed out in feces

Disease: Cryptosporidiosis

= human infection usually waterborne and acquired by

fecal-oral route
= highest prevalence of disease in areas with unreliable
water and food sanitation
= extraintestinal infection of the respiratory tract, biliary
tract and pancreas may occur.
Clinical Features
Varry from asymptomatic to severe, life-threatening
illness;

infection usually self-limiting diarrhea of 1-2 weeks

duration charactrized by copious watery diarrhea,
vomiting, intense abdominal pain, anorexia and
weakness

among immunocompromised patient (AIDS)  develops

severe chronic diarrhea which may last for months 
malabsorption
Clinical Features….
Incubation period ~ 7 days ( 2 to 10 days). 
In immunocompetent persons,
 Symptoms are usually short lived (1 to 2 weeks)
Persons with AIDS (CD4 counts <200/µl)
 Chronic and more severe lasting for months or even
years
Small intestine- most commonly affected
 the lungs, and possibly conjunctiva may be affected.
 Cyclospora
Species: C. cayetanensis
= was established to cause human diarrhea in 1990
= 1986 cases of prolonged watery diarrhea among
immunocompromised (AIDS) patient has been reported
worldwide
= Species Name C.Cayetanensis was given in 1993
= Initially called ‘cyano-bacteria like body’ (CLB) or large
cryptosporidium
Epidemiology:

= More common in tropical and sub-tropical areas

= Subsequent cases has been reported from most
part of the world
= Infection caused by cyclospora can be acquired
by drinking contaminated water (fecal-oral)
= More associated with food-borne outbreaks( social
events, weddings, etc)
Morphology:
Oocyst spherical-shaped 8-10um dia.
contains membrane bound refractile globules
Mature oocysts contains 2 sporocyst with 2
cresent-shaped sporozoite which fluoresce blue-
green under UV light (cryptosporidium & isospora
do not fluoresce under UV light)
Life cycle:

Life cycle similar to cryptosporodium except that Oocysts mature in

environment (days-weeks)
 Clinical Features

Disease: Cyclosporiasis
= disease is clinically indistinguishable from
cryptosporidiosis and Isosporiasis
= self-limiting, characterized by persistent watery
diarrhea
that ends to recur in a relapsing pattern and last for
3-4 wks,
= associated with abdominal cramps, nausea, vomiting,
low grade fever, weight loss and anorexia
 Isospora

Species: Isospora belli

Epidemiology
• wide geographical distribution (higher
prevalence in warmer climates)
• the least common of the three intestinal
coccidia that infect humans
• transmitted fecally in contaminated
food and drink with oocyst
 Morphology:
=Oocyst elongate ovoidal-shape with moderate constriction
in one end giving a charac. “Bottle with short neck”
appearance
=20 – 33 u L X10 – 19 u W
=Cyst wall double-layered, smooth, thin & colorless
=Unsegmented oocyst contains spherical mass of granule
with visible nucleus
=Mature oocyst has 2 sporocyst and each contains 4
cresent-shaped sporozoites
 Habitat:
intestinal tract probably
in the ileum and cecum

life cycle similar to

Cryptosporodium
except the
oocysts mature in
environment
 Clinical feature
Disease: Isosporosis/Intestinal coccidiosis
often asymptomatic (seldom reported)
symptoms range from mild gastro-intestinal distress
to severe dysentery
mild self-limiting infection charac. by fever, colicky
abdominal pain, severe diarrhea, steatorrhea (fatty
stool) and weight loss.
often self-limiting, but can become chronic (wasting,
anorexia)
symptoms more severe in AIDS patients
Laboratory Diagnosis of Intestinal coccidia

Microscopy
Immunological assay
Molecular methods

Treatment

 paromomycin for Cryptosporidium

-modest benefit

-lowers parasitemia in AIDS

 trimethoprim-sulfamethoxazole for Cyclospora and Isospora

Intestinal Coccidia- Summary

• are opportunistic parasite in immunocompromissed person

Got medical attention after the emergence of HIV/AIDS
Fecal-oral or contaminated food and water are means of
transmission
Requires single host to complete life cycle and reproduce
Sexually and asexually
Infection leads to acute, watery diarrhea; self limiting in
immunocompetent individuals but significant, chronic
illness in the immunosuppressed may occur
oocyst stage :Infective and diagnostic stage
Laboratory dx; finding oocyct in stool specimen
 Blood and tissue coccidian
Found inside blood , blood forming organs or tissues

Blood and tissue sporozoa include

Plasmodium species
Babesia species
Toxoplasma gondii
What is malaria?
Plasmodium ?
 Plasmodium species

Causative agent of Malaria: an acute and/or chronic infection

caused by protozoans of the genus Plasmodium

Four plasmodium species causing human malaria

Plasmodium falciparum (P. falciparum)
P. vivax
 P.malariae
P.ovale
The fith species p.knowlesi
 General feature of Plasmodium species

Intracellular obligate parasites. (liver cell & RBC)

Life cycle,

Alternation of generation ~ alternation of hosts

Requires two hosts:

 Man (IH)

Female Anopheles mosquitoes (DH)

Sexual and asexual reproduction

No animal reservoir host except P.malariae

 Bur. Mal. Eth.

Plasmodium species
P.falciparum =60%
P.vivax = nearly 40%
P.malariae =1% cases ,focal distribution like in Humera
P.ovale = less than 1% cases , found in Setit Humera , Gambela
& Arbaminch
 Epidemiology of Malaria in Ethiopia

The risk of malaria varies highly from season to season and from
place to place
Transmission- seasonal (Unstable)
Mainly depends on rain fall and Temp

Two major transmission periods

Major - September to December after main rainy
season
Minor- April to June following small showers of
rain in autumn.
 Epid…
dega zone(> 2,500 m) mean annual temperature of 10-150C , is
malaria free

weyna dega zone( 1,500 - 2,500 m) mean annual temperatures

range from 15-20o c
malaria most often occurs below 2,000 meters, with short-
lived transmission following the rains

 kolla zone (< 1,500 m), mean annual temperatures are 20-25oc,
malaria transmission is endemic
 Epid…

Endemicity : defined in terms of parasitemia rates or palpable

spleen rates in children 2 to 9 years of age as
hypoendemic (<10%)
 mesoendemic (11 to 50%)
 hyperendemic (51 to 75%)
 holoendemic(>75%)

Hyper and Holoendemic malaria are found in areas of stable

malaria transmission
 Epid…

Hypo and Mesoendemic : are found in areas of unstable malaria

transmission

Characteristics of stable malaria:

~ Constant incidence over several years

Includes seasonal transmission

Immunity and disease tolerance developed by adult

Usually affects children

 Epid…

Characteristics of unstable malaria:

Malaria incidence varies from week to week, month to month, year
to year, day to day.
Communal immunity of the population low.
Makes the region prone to malaria epidemics.
High morbidity and mortality
 Morphological Stages
Sporozoite: develops in the mosquito salivary gland

Hepatic schizont   actively dividing, multinucleated, parasite form in

hepatocytes

Trophozoite: metabolically active form living within the RBC

Sometimes called the ring form

Erythrocytic schizont: multinucleated stage in a RBC resulting from

asexual multiplication of trophozoite
Each schizont contains a species determined number of
merozoites
 Morph…
Merozoite: infective schizont components that break out of
hepatocyte or RBC

Gametocyte: morphologically distinctive sexual (male or female)

form which develops from some trophozoites in RBCs
 Terms in Malaria

Incubation period:
Recurrence:
Relapse:
Recrudescence:
 Inadequate treatment
Drug resistance
Unusual pharmacokinetics
Incomplete dosage
Reinfection:
 Transmission and life cycle
of Malaria
• Principal mode of Transmission

• bites of female anopheles mosquito

60 species of mosquito
sucks the gametocytes during
blood meal
bites between 5 PM and 7 AM,
with maximum intensity at
midnight.

Anopheles
 Tran…
Mosquito transmission depends

 susceptibility of anopheline species

 More than 200 known species of Anopheles , 60 of them

are considered to be vectors of malaria
 feeding habits

 Density
 Longevity

 climatic factors
• temperature, humidity, rainfall, wind, etc
 Tran…
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
Other modes of transmission

1. Blood transfusion (Transfusion malaria):

 This is fairly common in endemic areas
 Following an attack of malaria, the donor may
remain infective for:
o 1-3 years in P. falciparum,
o 3-4 years in P. vivax, and
o 15-50 years in P. malariae
 Most infections occur:
 in blood stored for less than 5 days and

 rare in blood stored for more than 2 weeks

 Frozen plasma is not known to transmit malaria

blood transfusions malaria

Infective stage-trophozoites / merozoites

shorter incubation period, because no exo-erythrocytic

shizogony
 Tran…
no relapses possible (vivax/ovale)

clinical features & management of cases are the

same as naturally acquired infection

Donor blood should be screened

2. Mother to the growing fetus (congenital malaria)
  occurs in 5 % of new borne whose mothers are
infected
 relatively rare although placenta is heavily infected
 Congenital malaria is more common in first
pregnancy, among non - immune populations

3. Needle stick injury:

 Accidental transmission can occur among drug
addicts who share syringes and needles
 Life cycle
• Require two host
• Man:- • Mosquitoes:-
• intermediate host • Definitive host
• Asexual reproduction • Sexual
• Liver cell reproduction
• RBC
• Mosquitoes cycle
• A- Sporogony
• Human cycle
Two phases
B- exo-erythrocytic
schizogony in liver
C- Erythrocytic
schizogony &
gametocytogenesis in
RBC
 Lif…

IN THE MOSQUITO
 During a blood meal on man, female Anopheles mosquito picks
up mature gametocytes

In the mosquito's mid gut, a micro gamete(male) penetrates a

macro gamete(female) and form a zygote

The zygotes inturn become motile and elongated form called

ookinetes
 Lif…

 invade the midgut wall of the mosquito where they develop

into oocysts

The oocysts expanding by asexual multiplication, grow,

rupture, and release motile sporozoites , which make their way
to the mosquito's salivary glands

  Inoculation of the sporozoites into a new human host

perpetuates the malaria life cycle
Lif…
Oocysts seen on the outer wall of the mosquito stomach, view through an electronic
microscope
 Lif…
IN MAN

 During a blood meal, malaria-infected female Anopheles

mosquito inoculates sporozoites and salivary fluid
• The sporozoites remains in the circulating
blood for only 30 minutes

• The kupfer cells of the liver kill and clear many

sporozoites from blood stream
 Lif…

Fraction sporozoites escape destruction are carried rapidly via the

blood stream and invade hepatic parenchymal cells of the liver

 begin their initial asexual replication : Exo- erythrocytic/

Intrahepatic / Pre-erythrocytic schizogony
o within 5-15 days mature into pre-erytrocytice(PE)
schizonts containing 10,000-30,000 merozoites

rupture the swollen liver cells & release merozoites in to blood

stream
 Lif…

P. falciparum
mature and released simultaneously
from liver, no relapse
P. malariae

P .vivax
may remain latent in the liver and relapse
P.ovale
 Lif…
 A proportion of the merozoites are phagocytosed & destroyed

The remaining Enter in to red cells starts erythrocytic schizogony

which to complete takes 36-48 hours (P. falciparum),48 hours (P.
ovale/ vivax) &72 hours (P. malariae).
At this time the intracellular merozoites develop in to
trophozoites (‘ring form’)

When the trophozoites fully developed ,then schizogony

takes place resulting in the formation of schizont
containing 8-32 merozoites
 Lif…

development to erythrocytic schizont in P. falciparum takes place in

the capillaries of deep tissue ,

The mature schizont rapture from red blood cells

releasing merozoites , malaria pigment and toxins in to plasma

Merozoites ,which are not destroyed by host immune system

infect new red blood cells, initiates further cycle of erythrocytic

schizogony with more red blood cells begin destroyed.

 Lif…
After several erythrocytic schizogony cycle , some of the
trophozoites in the red blood cells develop into male female
gametocytes
P. vivax , P. ovale and P. malariae at least two cycle
eryhrocytic schizgony
 P. falciparum ,the asexual parasites in the circulation for
ten days

The gametocytes are now ready to be ingested by an Anopheles

mosquito during a blood meal
 Lif…
Life Cycle:

                                                                    
                  
Comparison of malarial parasites
Pf Pv Po Pm
 

Tissue schizogony 8 - 27 9 - 17
8 - 25 days 15 - 30 days
days days

Erythrocytic phase
48 hours 48 hours 48 hours 72 hours

Red cells affected Reticulocy Reticuloc

All Mature RBC's
tes ytes

Merozoites per
schizont 8 - 32 12 - 24 4 - 16 6 - 12

Relapse from
No, but blood
Hypanozoites
forms can
No Yes Yes
persist up to
30 years
 Clinical Features & pathology
Characterized by acute febrile attacks (malaria
paroxysms)
caused by the release of toxins (when erythrocytic
schizonts rupture) stimulate the secretion of cytokines
from leucocytes and other cells
Manifestations and severity depend on parasite species,
parasitemia and host status, i,e immunity, general health,
nutritional state, genetics

Without treatment, P.vivax, P. ovale, P. malaria ultimately may

result in spontaneous cure
P. falciparum can develop severe complications
 Prodromal Symptoms

Malaria paroxysm preceded by Prodromal period

2-3 days before 1st paroxysm

includes: malaise, fatigue, headache, muscle pain, nausea,

anorexia (i.e., flu-like symptoms)
can range from none to mild to severe
 Febrile Attack (Malaria Paroxysm),
4-8 hr
periodic febrile episodes alternating with symptom-free periods

initially fever may be irregular before developing periodicity

may be accompanied by splenomegaly, hepatomegaly (slight

jaundice), anemia

P. falciparum can be lethal in non-immune

paroxysms comprises of three successive stage: cold stage, hot

stage and sweating stage
cold stage
• feeling of intense cold
• vigorous shivering, rigor
• lasts 15-60 min
hot stage
• intense heat
• dry burning skin
• throbbing headache
• lasts 2-6 hours
sweating stage
• profuse sweating
• declining temperature
• exhausted, weak  sleep
• lasts 2-4 hours
 Malaria Paroxysm
• paroxysms associated with
synchrony of merozoite
release
• between paroxysms
temperature is normal and
patient feels well
• falciparum may not exhibit
classic paroxysms
• continuous fever
• 24 hr periodicity
tertian malaria
quartan malaria
Complication of Acute Malaria
 Malaria caused by P.falciparum
Falciparum/subtertian/malignant malaria

Most pathogenic of all species

Almost all deaths are due to falciparum malaria

 Factors for Malignance of P.falciparum

Rapid multiplication

Infected red blood cells become "stick"

Infects all age group of red blood cells

A single red blood cell can be infected by more than one parasites

Erythrocytic schizogonic reproduction takes place in the deep

capillaries of organs such as brain, lung, heart, spleen, bone-
marrow, placenta, intestine, etc.
 Pathogenecity of P.
falciparum
1.Higher Parasitemia in Falciparum
Malaria
• all erythrocytes invaded
• up to 36 merozoites
• Pv/Po = reticulocytes
• Pm = senescent RBC
P.falciparum.
-Up to 30-40% of RBC
- sever if > 5% RBC are infected.
P.vivax & P.ovale rarely exceeds 2%
P.malariae. Usually < 1%
 2. Cytoadherence of infected
erythrocytes
-trophozoite and schizont
stages
-primarily in brain, heart,
lungs, and gut
complications
• avoidance of -immune evasion (spleen
spleen
• low oxygen avoidance
tensions
• better invasion
 Sequestration
Hypothesis
cytoadherence

cerebral ischemia

hypoxia, metabolic effects

coma

death
 Severe Falciparum Malaria
Features Indicating Poor
Complications Prognosis
cerebral malaria impaired consciousness
blackwater fever repeated convulsions
anemia respiratory distress
hypoglycemia shock
GI and liver syndromes acidosis/hyperlactemia
pulmonary edema hypoglycemia
algid malaria (shock) jaundice or other liver
malfunctions
renal impairment
high parasitemia
(>500,000/mm3)
Predisposing factors for complications of P. falciparum malaria

(1.) Extremes of age.

(2.) Pregnancy, especially in primigravidae and in
2nd half of pregnancy.
(3.) Immunosuppressed - patients on steroids, anti-
cancer drugs, immunosuppressant drugs
(4.) Splenectomy.
(5.) Lack of previous exposure to malaria (non-immune) or
lapsed immunity
(6.) Pre-existing organ failure.
 Cerebral malaria
severe complication of falciparum malaria
 mortality of 30-50%
 associated with sequestration in micro-vasculature of brain

a diffuse encephalopathy with loss of consciousness

 Malaria caused by P. vivax, P. ovale P. malariae

 Plasmodium vivax is referred to as vivax malaria , benign

tertian (BT) malaria

Plasmodium ovale is referred to as ovale malaria, ovale

tertian malaria

Plasmodium malariae is referred to as malariae malaria ,

quartan malaria
 Mal…
Infections caused by P. vivax, P. ovale or P. malariae are rarely life
threatening
 no Cytoadherence of parasitized cells
 parasitic densities are lower
Relapses are a feature of vivax and ovale malaria

Recrudescences are a feature of P. malariae

P. malariae is nephritic syndrome which may progress to renal failure.

 
 Hyper-reactive malaria splenomegaly (Tropical splenomegaly
syndrome)

massive and chronic splenomegaly with

 high levels of IgM ,

 malaria antibody,

 circulating immune complexes

a moderately enlarged liver with hepatic sinusoidal

lymphocytosis
 Hyper…
The patient is usually
anaemic (normocytic)
 low white cell and platelet counts
 Genetic factors That Provide Protection Against
Malaria
1. Nature of hemoglobin
 Hgb S (Sickle cell anemia trait) –p.f
 Thalassemia Hgb-P.f
 Fetal Hgb – all sps
 Hgb E – P.v

2. Enzyme content of erythrocyte

 Glucose-6-phosphate dehydrogenase deficiency ,-P.f

3. Presence or absence of certain factor

 Ovalocytosis -P.f & P.v
 Duffy blood group antigens (i.e., Fya and Fyb) negative RBCs-P.v
Laboratory Diagnosis
MALALRIA Diagnostics approaches

Clinical Diagnosis

Malaria Diagnosis

Laboratory diagnosis

Microscopic Molecular
•Thin film Immunological PCR
•Thick film Ag /enzyme
• QBC •RDT.ICT Malaria Pf etc.
ParaSight F
OptiMAL
Ab- ELISA
 Clinical diagnosis

Based on clinical signs and symptom:

Fever, Chills, perspiration, anorexia, headaches, vomiting, and
malaise
It is inexpensive to perform and requires no special equipment
or supplies.
Are non-specific and symptoms overlap with those of other
febrile illnesses.
A Diagnosis of MAL based on Clinical grounds alone is
therefore unreliable-Over diagnosis
 Treatment
Antimalarial drugs like
Chloroquine
 Widespread resistance has now rendered it virtually
useless against P. falciparum

Artemisinin - active against all Plasmodium species

Pyrimethamine in combination with a sulfonamide

 Effective against all four human malarias

And other can be used

 Prevention and Control

1. Avoid mosquito bites by

Using impregnated bed nets
 Wearing protective clothes
 Using mosquito repellents
screens, house spraying

2. Destroy adult mosquitoes by

Indoor residual regular effective spraying
 Pre…
3.Preventing breeding of mosquitoes by
 environmental modification
 Spraying breeding places with effective larvicides
Biological control
4. Treatment
Active infection
Chemoprophylaxis

5) Health education

6) Blood screening for malaria  

 Babesia species

Causative agent of Babesiosis , piroplasmosis, thick fever, or red

fever

More than 100 species have been reported

 known as parasites of domestic and wild animals

Humans are accidental host

 Bab…
Four species known to infect humans

Name Normal parasite

B. bovis Ox
B. divergens Ox
B. equi Horse
B. microti microtus Rodents
 Transmission and life cycle
Transmission
By bite of infected ixodid or hard –bodied tick (definitive
host )
 blood transfusion

Life cycle
 Lif…
  During a blood meal, a Babesia-infected tick introduces
sporozoites into the mouse host

Sporozoites enter to erythrocytes and undergo asexual

reproduction (budding)

  In the blood, some parasites differentiate into male and

female gametes

The gametes ingested by appropriate tick

 Lif…
gametes unite and undergo a sporogonic cycle resulting in
sporozoites

Babesia-infected tick introduces sporozoites into the human

host during a blood meal

 Sporozoites enter erythrocytes and undergo asexual

replication (budding)
 Humans are, for all practical purposes, dead-end hosts
 Clinical feature

 
Multiplication of the blood stage parasites is responsible for
the clinical features

 chills, sweating, fatigue, hemolytic anemia, jaundice, fever

and hepatomegaly, usually 1-2 weeks after infection

 it is self-limiting disease infection in human

 Laboratory Diagnosis

1. Examination of stained smear

identifying pleomorphic ring like intra-erythrocytic
parasite in Giemsa -stained blood films

The small parasites appearing much like P.falciparum

can be differentiated from malaria parasite by the absence

of pigment in the infected erythrocytes
2. Serologic test: IFA
3. Molecular technique: PCR
Treatment
Clindamycin and quinine or Atovaquone plus Azithromycin
 Prevention and control

1. Tick control through acarcidal treatment ( animal host )

2. Chemotherapy to infected animal and host
3. Avoidance of exposure to tick 
 Toxoplasma gondii
 

Causative agent of toxoplasmosis

Tissue or extraintestinal coccidia

 infects most species of warm blooded animals , including

humans

Epidemiology
World wide
 Toxo…

About 47% of African , more than 50% adult population in

north America and west Europe shows antibodies to T. gondii

Only about 1% of persons showing antibody to T. gondii have

signs and symptoms of diseases

In Ethiopia : few studies indicated the disease found in

Ethiopia
 Toxo…
Habitat
 In the skeletal muscle, heart, lymph nodes, lungs, spleen,
bone marrow, mononuclear leukocytes, brain, CSF, Spleen,
etc. of man, domestic and wild animals

Morphology
 has five main developmental forms
 only trophozoite and cyst stages are found in man
 but all occur in the feline (cats family)
 Toxo…

Toxoplasma (trophozoite):-has two forms

I. Tachyzoite/endozoite
 occurs in the early acute stage of infection
Size: 3m by 7 m
Shape: crescent or oval in shaped, one end is rounded and
the other end is pointed
Content: In Giemsa stain, paranuclear body- stains red,
nucleus stains dark red and cytoplasm stains blue
 Toxo…
Bradyzoites / cryptozoites
Occurs in the chronic stage of infection, develops slowly and
multiplies in the tissues to form a true cyst

Cyst:-10-100m & may contain about 3,000

trophozoites
 Toxo…
Transmission and life cycle
Human infection may be acquired by

A) ingestion of undercooked infected meat

containing Toxoplasma cysts

B) ingestion of the oocyst from fecally

contaminated hands or food

C) organ transplantation or blood transfusion;

D) transplacental transmission;

E) accidental inoculation of tachyzoites

life cycle
 Lif…
Intermediate host : Humans , rodents , chicken , pigs and
other animals
Definitive host:   cat family (Felidae)

 Cats become infected with T. gondii by ingesting tissue cysts

or oocysts

viable organisms are released and invade epithelial cells of the

small intestine where they undergo an asexual cycle followed
by a sexual cycle

Form oocysts which is excreted in faeces

 Lif…
Human ingested cyst and oocyst

Following ingestion of infective oocyst or tissue cyst, the

organism excyst in the intestine, but leave it and develop in other
tissues like lymph node, brain, eye and etc.

 develop quickly and produce tachyzoites then bradyzoites

which form tissue cyst

 These cysts may remain throughout the life of the host

 Clinical Features

 adults acquired infection are often asymptomatic , they can

cause
 fever, rash

 enlargement of lymph gland with lymphocytosis

 occasionally inflammation of the eye (ocular

toxoplasmosis) , myocarditis , menengoencephlitis and

atypical pneumonia.
 Laboratory Diagnosis

1. Identifying toxoplasma in Giemsa stained histological sections,

aspirates of lymphnode, bone-marrow, CSF, pleural fluid, peritoneal
fluids and sputum

2. Serologic tests such as Sabin-feldman dye test, ELISA, IFAT, CFT.

Treatment
Pyrimethamine-sulfadiazine (Fansider) or Spiramycin
Prevention and Control
1. Avoid contamination of hand, food and water with the faeces of
cat
2. Not eating raw or under cooked meat such as pork, beef
3. Screening of blood and organ of individuals for the parasites
4. Treatment and health education
Helminthes
The helminthes are worm like parasites that belongs
to two major groups of animals,
the platy helminthes(flukes and tape worm) and
the round worms or nematodes.

 All are relatively large and some are very large,

exceeding one meter in length.
There bodis are well developed organ system
especially reproductive organs,and
most helminthes are active feeder.
the bodies of flat worms are flatted and covered by
plasma membrane.
The clinically relevant groups are both
hermaphroditics and bisexual species.
the definitive classifications are based on the external
and internal morphology of
egg,
larvae,and
adult
.knowdlege of the different stages in relation to their
growth and development is the bases for
understanding
the epidemiology and
 pathogenesis of helminthes disease as well as
 the diagnosis and treatment of patients harboring
these parasites.
Nematodes
 General features of Nemathelminths

• Round in cross-section
• Unsegmented
• Digestive system complete
 Possess mouth, oesophagus and anus
• Have separate sexes
• Can be oviparous/ovoviviporous/viviparous
• Egg (ova) -Larva(L1-L4)-Adult

Possess a shiny cuticle (smooth/spined/ridged)

Mouth is surrounded by lips or papillae

•High burden
• In the rural villages
• unsanitary overcrowded cities
• 'big three' (Ascaris, Trichuris & Hookworm) is common
•Temperate and cold climates are not spared.
 Intestinal nematodes
General features

• Live in gastro-intestinal tract

• In humans, often spread by poor hygiene related to feces

• Most species are geo-helminths (soil transmited)

• Female worms are oviparous/ovoviviparous

• Humans are the major host of intestinal nematode

• Transmission:

• Ingestion of infective egg

• Larva penetrating skin

• Laboratory diagnosis:

• Egg in faeces ( most often)

• Larva in faeces

• Recovering egg in the skin around the anus

• Occasional adult worms:A.lumricoudes,and . vermicularies

 Cont…
 It includes
Ascaris lumbricoides
Trichuris trichiura
Enterobius vermicularis
Strongyloides stercoralis

Ancylostoma duodenale
Hook worm
Nectator amircanus
 Before becoming adults in their human host, the larvae of A.
lumbricoides, S. stercoralis , and hookworms have heart, lung
migration
 Ascaris lumbricoides

Also known as large intestinal round worm

Epidemiology
 world wide
Habitat
Adult: In the small intestine
Egg: In the faeces
 extremely resistant to adverse environmental
condition and chemicals
 remains viable in soil and dust for up to 10
years
 Transmission and Life Cycle
• Transmission
• A. lumbricoides is spread by faecal pollution of soil
• Infective stage:- egg containing 2nd stage larva
• A person acquire infection by
1- Ingestion of food or water contaminated with infective eggs
2- eating soil(geophge) frequently seen in children
3-putting contaminated finger or toys with infective egg in to
mouth
4- rarely by inhalation of eggs carried in air
 Life cycle
Fully embryonated eggs are swallowed & L2 hatches in
the stomach & penetrate stomach or duodenal mucosa

L2 enter blood stream & leave through alveoli into lung

Then molt several times in the lungs to L3/L4

Then move up and get swallowed

2-3 months after infection the adult worms start laying
eggs (200,000 daily)

Eggs are shed with the feces and embryonate within 2-3
weeks
Pathogenesis:
1. “Verminous” pneumonia, lung tissue damage due to
migratory larvae.

2. Bowel obstruction - too many adult worms.

3. Parasite secretes trypsin inhibitor, prevents host from

digesting proteins.

4. Aberrant migration of “irritated” adult worms to:

a. Common duct
b. Liver
c. Pharynx
d. Peritoneum
• With heavier worm loads
a tangled mass of worms
can obstruct the bowel,
or an individual worm
can block a duct
Laboratory Diagnosis
A. Finding and identification of eggs in the stool.
• Direct wet mount
• adequate for detecting moderate to heavy
infections
• concentration technique may be used In light
infection, Sodium chloride floatation technique &
Formolo-ether concentration technique

B. Adult worms occasionally passed in the stool or

through the mouth or nose
Treatment
Mebendazole
Prevention and Control

1.Prevention of infection by
 washing hands before eating & trimming finger

Avoid eating uncooked foods such as vegetables

 3.4.2.Trichuris trichiura
• Common name : whipworm, due to the whip-like form of
the body.
Epidimology
• The third most common round worm of humans
worldwide
• Infections more frequent in areas with tropical weather
and poor sanitation practices, and among children
Habitat
 Adult: large intestine (caecum) and appendix

 Eggs : In the faeces, not infective when passed

Egg:
Size: 50-54m
Shape: "tea tray eggs” or barrel-
shaped with a colorless
protruding mucoid plug at each
end
Transmission and life Cycle
Transmission
Ingestion of embryonated egg in contaminated water ,
food or from contaminated hand

life Cycle
The unembryonated eggs are passed with the stool of
infected individuals
Mature within three weeks of being deposited in soil.
o require a warm, moist environment with plenty of
oxygen to ensure embryonation
o The embryonated eggs are extremely resistant to
environmental conditions
• When embryonated eggs are swallowed larvae are
released into the upper duodenum
• then attach themselves to the villi of small intestine or
invade the intestinal walls
• After 3-10 days they move down to the caecum &
ascending colon where they mature into adult worms
• The adult worms are fixed with the anterior portions
threaded into the mucosa

• The females begin oviposit 60 to 70 days after

infection & shed 3,000 - 20,000 eggs per day

• The life span of the adults is about 1 year

Clinical features
• Are largely determined by the worm burden:

• < 10 worms are asymptomatic (99% asymptomatic)

• Heavy worm burden

• Mechanical damage to the intestinal mucosa

• Chronic profuse mucus and bloody diarrhea with

abdominal pains and edematous prolapsed rectum
Anaemia from blood loss and iron deficiency,
malnutrition, weight loss and sometimes death
o Each adult worm sucks about 0.005 ml of
blood per day

Rarely a child will develop congestive cardiac

failure because of anaemia and fluid retension
hypoproteinemia and oedema
Laboratory diagnosis
1.Finding of characteristics egg in faeces

2. Sigmoidoscopy may enable visualisation of worms

Treatment
Mebendazole
 Treat the iron deficiency anaemia

Prevention and Control : the same as described for A.

lumbricodes
 3.4.3. Enterobius vermicularis
. Common name: “Pin Worm” or “threadworm” or “
seat worm”

Epidimology
occurs world-wide

Children (5-14 years ) are more commonly

infected than adults

Occur in group living together

• Pinworms eggs can be
spread throughout a
house and difficult to
eliminate.
• Small children are most
apt to pick them up
during the “teething
stage.”
Habitat
Adult: Caecum & appendix
Gravid female: Caecum & rectum
Eggs: deposited on perianal skin & occasionally in
faeces

Morphology
Adults: Color: white
Male: Size 2-5mm Coiled tailed
Female: 8-13mm, thin pointed tail
Transmission and Life cycle

Transmission

Person – to - person transmission(ingestion and air

borne)
Eggs remains viable 20 days
Autoinfection

Retro infection
Life cycle
• Ingestion embryonated eggs, usually carried on
fingernails, clothing, bedding or house-dust.

• Eggs hatch in stomach, larvae migrate to caecal region

where they mature into adults

• Copulation takes place in the caecum

• Gravid females migrate nocturnally outside the anus and

oviposit on the perianal area
• 1 pin worm lay over 10,000 -15,000 eggs /day
With in 4-6 hours being laid the egg contain infective
larvae

Perianal itching from the eggs Induces scratching, and

hence the eggs are transmitted to the mouth on the
fingers

Retroinfection, or the migration of newly hatched larvae

from the anal skin back into the rectum

 interval from ingestion of infective eggs to oviposition

by the adult females is about one month

The life span of the adults is about two months

 Clinical features
Nocturnal anal pruritis
• The cause of this is unknown, but may be related to the
intensity of the infestation, and/or an allergic reaction to
parasite
 Sleeplessness, because of the irritation
Vulvovaginitis, and even urethritis may occur in girls when
migrating worms lay their eggs in these sites
 Abdominal pain or appendicitis resulting from the worms
are considered to be very rare
Laboratory Diagnosis
1.Finding eggs from perianal skin using adhesive tape or
swab method

• Done by pressing transparent adhesive tape

("Scotch test", cellulose-tape slide test) on the
perianal skin and then examining the tape placed on
a slide. 
• Alternatively, anal swabs or "Swube tubes" (a paddle
coated with adhesive material) can also be used.
• Collect sample in the morning, before defecation
and washing,  
2. Finding eggs in the faeces
• Eggs can also be found stool, but less frequently

• Less then 10% found in stools, i.e. not a useful

examination;

• occasionally eggs can be found in the urine or

vaginal smears
3. Finding of female worms from perianal skin or
faeces
Adult worms are also diagnostic, when found in
the perianal area, or during ano-rectal or vaginal
examinations
Treatment
 Pyrental Pamoate or Mebendazole

Prevention and Control

1.Treating all members of a family in which infection
has occurred

2. Wearing tight-fitting cotton pants to infected children

3.4.4.Strongyloides stercoralis
• Common name: Dwarf thread worm

Epidemiology
 Found worldwide

• An estimated 50 to 100 million cases

• Favors warmer tropical and subtropical climate

• S. stercoralis show the following characteristics
1. Parasitic males are absent
2. Parasitic females are present in the submocusa of
small intestine which produce egg
parthenogenically
3. Can develop in to free living generation in the soil
out side the human host
4. Has internal and auto infection
Habitat
 Has both free living and parasitic generations
Parasitic Adult females: buried in the mucosal
epithelium of the small intestine of man

Rhabditiform larvae: Passed in the faeces and

external environments

Filariform larvae: soil and water the infective stage

 Transmission and Life cycle

• Transmission
1. Commonly by penetration of skin by filariform larva
2. Ingestion of food or water contaminated with
filariform larva(oral route)
3. Rarely: Transmamary & Organ transplantation
4. Autoinfection with rhabiditi form larva
Life Cycle
 Complex , Two types of cycles exist:
1.Free-living (indirect) cycle
Rhabditiform larvae(stool) molt 4x free-
living adult males and females produce eggs
rhabditiform larvae develop to free living
adult males or females

Filariform larvae(this initiate parasitic life cycle)

2.Parasitic (direct) cycle
Rhabditiform larvae(stool) molt 2x develop
to filarifrom penetrate skin lung Alveolar
space bronchial tree pharynx
swallowed &develop to adult female in small
intestine(molt 2x) produce egg by parthenogenesis
which yield rhabditiform larvae
Autoinfection, the rhabditiform larvae become
infective filariform larvae in the host tissue ,penetrate
 intestinal mucosa (internal autoinfection) or
perianal area (external autoinfection)
Life cycle

Parasitic life cycle

Free-living cycle
Clinical feature
It is usually asymptomatic, in symptomatic cases
People with weaker immune systems
such as elderly people and children
are more susceptible
1.Cutaneous phase
 large number of larva produce itching and erythema at
the site of infection within 24 hours of invasion
2.Pulmonary phase: The migratory larva in the lung
producing bronchopneumonia and full blown
pneumonitis
3. Intestinal phase : Invasion by adult worms may
produce abdominal pain and mucus diarrhea , nausea
vomiting and anemia

Auto- and hyper-infection syndromes

 characterized by massive larval invasion of the lung or
any other organ including CNS, which is fatal

 occurs when the immune status of the host suppressed

by either drugs, malnutrition or the concurrent
diseases
Laboratory Diagnosis
1.Finding the larvae in faeces or in duodenal aspirates
using direct or concentration method by microscopy
 In hyper-infection syndrome the larva may be
found in sputum, urine and in other specimens
o Examination of serial samples may be
necessary because direct stool examination is
relatively insensitive
2. Serological tests
• Antibody Detection

 
Treatment
Ivermectin or thiabendozole

Prevention and Control

1.Sanitary disposal of faeces in latrine
2. avoid use of night soil as a fertilizer

3. Wearing protective footwear

4.Treatment of infected individuals and Health

education
 Properly dispose of
human wastes.

Wear Shoes.

…Don’t eat dirt.

 3.4.5. Hook Worms

Are hematophagous nematodes

Two major species

Ancylomstoma duodenale
Necator americanus

Less important : A. ceylanicum, A. braziliense ,A.

caninum , A.tubaeforme, A. buckleyi
Epidimology
widely distributed throughout the tropics and
subtropics

 more than 1 billion people are infected world-wide

cause daily blood loss

Most commonly infected are children, agricultural

workers and miners
Ancylostoma is found in Europe around the
Mediterranean, on the West coast of South America
and in parts of China and India

Necator is found over much of the western

hemisphere, Africa and South East Asia
In Ethiopia : Necator americanus are more common
than Ancylostoma duodenale
highest infection rates: Ilubabor, Kefa
,Welega
Altitude and moisture is the major factor
affecting their distribution

Hook worm infection is absent in low ,hot dry

areas of Ethiopia and above 2500m alt
Habitat
Adult: Jejunum and less often in the duodenum of
man
Eggs: In the faeces; not infective to man
Rhabditiform and filariform larvae: free in soil and
water
Transmission and life cycle
Transmission
 Penetration of the skin by filariform larvae

 Ingestion
of the filariform larvae present in the soil or
transmammary
 for A. duodenale, but N. americanus requires
transplumonary migration

 Transplacental : rare
Life cycle

• Eggs are passed in the stool, and under favorable

conditions (moisture, warmth, shade),

• rhabditiform larva - larvae hatch in 1 to 2 days in the

feces and/or the soil

• After 5 to 10 days (two molts) they become filariform

(third-stage) larvae that are infective
• larvae can survive 3 to 4 weeks in favorable
environmental conditions. 
• On contact with the human host, the larvae penetrate
the skin and are carried through the veins to the heart
and then to the lungs

• They penetrate into the pulmonary alveoli, ascend the

bronchial tree to the pharynx, and swallowed  

• The larvae reach the small intestine, where they reside

and mature into adults 
• they attach to the intestinal wall with resultant blood
loss by the host
 Symptoms of hookworm infection depending on the site at which the worm is present and the
burden of worms

Table 2. Clinical features of hookworm disease

Site Symptoms Pathogenesis

Cutaneous invasion
Local erythema, macules,
Dermal and subcutaneous
papules (ground itch)
migration of larva
Migration of larvae
Bronchitis, pneumonitis and,
Pulmonary through lung, bronchi,
sometimes, eosinophilia
and trachea

Anorexia, epigastric pain Attachment of adult

Gastro-
and gastro-intestinal worms and injury to
intestinal
hemorrhage upper intestinal mucosa

Iron deficiency, anemia,

Hematolog
hypoproteinemia, edema, Intestinal blood loss
ic
cardiac failure
Laboratory Diagnosis
1.Finding eggs in faeces
A.duodenale and N.americanus eggs morphologically
indistinguishable
Treatment
 Pyrantel pamoate, Mebendazole or Thiabendazole
 if anemic : high protein diet supplemented with
ferrous sulphate, folic acid and vitamin B12

Prevention and control

As described for Strongyloides stercoralis
 Blood and tissue
nematodes
 Blood and tissue nematodes
2 General features:
Adults which live in the tissues of human (lymphatic
system, subcutaneous tissues or muscle)
• Long thread - like worms
Requires two host to complete their life cycle.

Females are viviparous(larvae hatch in the uterus)

The female produce first stage larvae (L1)

The immature L1 stage larva is called Microfilariae
 Small , slender, motile forms

 L1 require blood sucking insects (IH) to develop to infective form (L3)

 No reproduction in the vector, rather development

 Three families/ groups
1. FAMILY FILARIDAE( Filarial worm)
- Common/pathogenic filaria
• Wuchereria bancrofti
• Brugia malayi
• Brugia timori
• Loa loa
• Onchocerca volvulus
• Less/non-pathogenic Filaria
• Mansonella perstance
• Mansonella streptocerca
• Mansonella ozardi
2. FAMILY TRICHINELOIDAE

• Trichinella spiralis

3. FAMILY DRACUNCULIDAE( guinea worm)

• Dracunculus medinensis
 FAMILY FILARIDAE ( Filarial worm)
General features:

 Filariae live as adults in various human tissues

 Agents of LF reside in lymphatic vessels and lymph nodes

 O. Volvulus, Loa loa, M. Ozzardi and M. Streptocerca in subcutaneous

tissues

 M. Streptocerca besides reside in the dermis

 M. Perstans resides in body cavities and surrounding tissues

 Cont ….
 Three of these are responsible for most of the morbidity:

W. bancrofti and B. malayi cause lymphatic filariasis,

and

O. volvulus causes onchocerciasis (river blindness).

Animal reservoirs play no role of significance in most

places, except in sub-periodic B. malayi.

Diagnosis based on Mf findings:
 Morphologic features:
 Size
 Presence or absence of “ sheath”
 Appearance i.e. curvature, kink, coiling etc
 Arrangement of the column of nuclei in the body
 Presence of nuclei at the very tip of the tail

 Other features:
 Periodicity
 Source of specimen
 Factor to be considered when collecting blood

Collect blood at the correct time

Concentration technique recommended
In chronic infection Mf is rarely found in blood
In LF Mf are higher in capillary blood than
venous blood
Mf are higher in capillary blood from the ear lob
Periodicity:-
Mf are found in the blood in greater number in a certain
hours of a day or a night
Corresponds to peak biting times of their insect vector
Nocturnal periodicity: -mf is high in blood
during night hrs
Diurnal periodicity:- mf is high in blood during
day hrs
Nocturnal or diurnal subperiodicity;- mf can
found in blood 24 hrs with slight increase in
number during day or night hrs
Filarial worms Periodicity Main Vector host
(Synonym) (IH)
O. volvulus Non Periodic Black fly (Simulium) Human
(River blindness)

W. bancrofti (LF) Periodic (N) Culex, Anopheles Human

Sub Periodic Aedes Human

B. malayi (LF) Periodic (N) Anopheles Human

Sub Periodic Mansonia Human, Monkey, Cat –

Zoonotic
B. timori (LF) Periodic (N) Anopheles Human
L. loa (Eye worm) Periodic (D) Deer fly Man, Monkeys
M. streptocerca Non Periodic Midge (Culicoides)
M. perstans Sub Periodic Midge (Culicoides)
M. ozzardi Non periodic Midge (Culicoides)
Black fly (Simulium)
Lymphatic Filariasis
Disease caused by filarial worms living in the human
lymphatic system
Causative agents
Wuchereria bancrofti
Brugia malayi
Burigia timori

These worms lodge in the lymphatic system

They live for four to six years, producing millions of
minute larvae that circulate in the blood”
Lymphatic Filariasis
 Large numbers are present in the lymphatics of the:

Lower extremities (inguinal and obturator

groups),
Upper extremities (axillary lymph nodes), and,
Male genitalia (epididymis, spermatic cord,
testicle) - particular for W. bancrofti
Wuchereria bancrofti
Disease: Bancroftian filariasis, Wuchereriasis, elephantiasis

Distribution: tropical and subtropical countries

Morphology:

1. Adult:

Thready,Cylinderical oesophagus,Creamy white in color

Transmission and life cycle
 Cont ....
• Requires two host
• Human-DH
• Mosquitoes-IH

• Transmission
• Bite female mosquitoes (Genera Culex, Aedes, Mansonia)
• Infective larvae deposited onto human
skin during the mosquito's blood meal
• Enter through the mosquito bite puncture
wound or local abrasions.
• In humans:
• Parasites passes to the lymphatic system
• Undergo further molts
• Become adult male and female worms
• Adult female worms produce thousands of sheathed
microfilariae per day

• Mf can be found in blood 9 months after infection

(W.bancrofti) and 3 months (Burigia species)

• Normally found in peripheral circulation in evening.

• Microfilariae ingested during blood meal from infected
person

• Penetrate the mosquito stomach wall

• Enter the body cavity (hemocoel)

• Migrate to the insect's flight muscles for growth.

• After 2 molts, the L3 migrate through the head,

• Reach the proboscis of the mosquito.

Clinical manifestation

Depends on:
Site occupied by adult

Number of worms,

Length of infection and

Immune response of the host

Clinical manifestation
 There may be:

1. Recurrent attacks of lymphangitis(LS)

o Funiculits
o Epididymitis
o Orchitis, etc...
 Lymphadenitis(LN)
 Swelling and redness of affected parts
 Fever, chills, headache, vomiting and malais
 2. Obstructive manifestations –
• Fibrosis following the inflammatory process
• Coiled worms inside lymphatics.
• This may result in:
 Dilatation
 Rupture of distended lymphatics
 In the urinary passage – chyluria
 In the pleura – chylothorax
 In the peritoneal cavity – chylous ascitis
 In the testis – chylocoele
3. Elephantiasis:
 Hard and thick, rough and fissured skin ,Frequently legs
& genitalia (scrotum, penis and vulva)
 Less often arms and breasts.
Clinical ......
4. Tropical pulmonary eosinophilia
 Pulmonary symptoms: cough, dyspnoea, "asthmatic syndrome".

 Chest X-rays: patchy infiltrates

 Splenomegaly

 High ESR & marked eosinophilia

 No microfilariae in the peripheral blood.

 Serological tests strongly positive

 Responds very well to therapy with DEC

 
Diagnosis of W. bancrofti

1. BF (taken at night)

 Thin and thick smears

 Concentration methods

Lyzed capillary blood technique

Tube centrifugation lyzed blood technique

 DEC(Diethyl carbamazine ) provocation test

 
Diagnosis of W. bancrofti
 Mf in:
 Aspirates of hydrocele
 Lymph gland fluid
 Chylous urine

2.Intradermal test (antigen from Dirofilaria immitis)

3.Serological tests as IHA, IFA

4.Antigen detection:

5.DEC provocative test (2mg/Kg): After consuming DEC, mf enters into the peripheral blood in day

time within 30 - 45 minutes

6.Immuno Chromatographic Test (ICT):

 
Treatment of W. bancrofti

 Diethyl carbamazine (DEC)

 General measures:
 Rest, antibiotics, antihistamines, and bandaging

 Surgical measures for elephantiasis

 
Prevention and control of W. bancrofti
Control of mosquitoes

Avoid mosquito bite

Treat patients

Health education

Global LF elimination program strategy

 Mass drug administration

 Care for chronic cases

 
 Loiasis

Caused by filarial worms living in subcutaneous tissue

Causative agents
Loa loa (Eye worm)
Distributed in Rain Forest areas of West Africa and
equatorial Sudan.
 Transmission

• Horse flies (Tabanidae) in genus Chrysops

• Day-feeding & forest-dwelling

• Also called the “deer fly” or mango fly.

Life cycle
 Clinical manifastation

Loiasis is often asymptomatic. 

Calabar swellings (episodic angioedema)

 Itchy, red, and non pitting swollen areas in the skin

 2-10 cm in diameter, Often painful/may be painless

 In any portion of the skin/wrists & ankles most frequent

 Clinical manifastation
Adult worms also migrate in sub-conjunctival tissues. 

They can cause inflammation and irritation but not

blindness
Laboratory diagnosis

Mf in stained BF taken during the daytime

Occasionally the Mf can be found in joint fluid

Differentiation from mansonella required (hematoxylin

staining)
 Onchocerciasis
 Is a filarial disease caused by O. Volvulus
 Commonly known as river blindness
 The world’s second leading infectious cause of
blindness
 WHO estimates the global prevalence is 17.7
million, of whom about 270,000 are blind
• Occurs most widely along the
courses of fast running rivers in
the forests and Savannah areas of
west and central Africa

• Also occurs in the Yemen, Arab

Republic, Central and South
America
Onchocerca volvulus

Transmission:

By the bite of infected vector (simulium species)

Life cycle

During a blood meal, infected blackfly introduces L3

(infective stage) larvae onto the skin of the human

L3 penetrate into the bite wound   

In subcutaneous tissues the larvae develop into adult filariae

Adult commonly reside in nodules in subcutaneous

connective tissues 
Life cycle

The female worms produce Mf for ~ 9 years

Mf have a life span ~ 2 years 
Mf found:
Typically in the skin and in the lymphatics of connective tissues
Occasionally in peripheral blood, urine and sputum
A black fly ingests the Mf during a blood meal

Mf migrate from the blackfly's midgut through the

hemocoel to the thoracic muscles 

Mf develop into L1 larvae and then to L3 

L3  migrate to the blackfly's proboscis

Infection occurs when the fly takes a blood meal

    
Life cycle of Onchocerca volvulus
Clinical feature
Onchocerciasis
Acute onchocerciasis:
Itchy (pruritic)
Erythematous
Papular rash with thickening
of the skin
Clinical feature
Chronic onchocerciasis:
Elephant or lizard skin Hanging groin

Leopard skin River blindness

Clinical feature

 Onchocercomata:
 Upper part of the body (American
onchocerchiasis)
 Pelvic region (African form)
• Nodules surrounded by concentric
bands of fibrous tissue
Laboratory diagnosis
Mf in skin snips

Skin biopsy Skin fragment

Mf in urine, blood & most body fluids (in heavy infection)
Wet mount preparation Staining
Prevention and control

Destruction of Simulium

 Avoiding Simulium bites

Treatment of communities
Treatment

Ivermectin:
Paralysis of worms

Reduces the microfilarial load

Surgical Care:
Nodulectomy

Removes adult worms

Trichinella spiralis
 A tissue nematode

 Zoonotic parasites and the disease is zoonotics

 Disease in humans: Trichinosis, Trichiniasis, Trichinelliasis,

Trichinellosis

 Distribution: Temperate regions where pork is eaten

1. T. Spiralis spiralis – found in temperate regions

2. T. Spiralis nativa – found in the Arctic

3. T. Spiralis nelsoni – found in Africa and S. Europe

 
Trichinella spiralis
 Habitat:
 Adults in the small intestine of man and animals specially pigs and rats
(reservoir hosts).
 Larvae : encysted in muscles

Transmission
Eating flesh of infected pork (raw/undercooked)

 
Life cycle
Life cycle
 The same host (animal/man) act as DH

 After fertilization, males die and are expelled.

 Females penetrate deeply in the mucosa and lay

 Female lays ~ 1500 larvae in its life span (~ 2 months)

 
 Larvae to the circulation
 Passes through pulmonary filter
 Distributed all over the body (esp. diaphragm, tongue, eye, deltoid,
pectoralis, intercostals, etc)
 Larvae coil and encyst in the long axis of muscles
 Pigs become infected by eating infected flesh from other pigs or
ingestion of infected dead pigs and rats
 Rats are infected by eating flesh of dead pigs or rats and by canibalism
 
Life cycle

 Larvae liberated from the cysts in small intestine and

mature to adults

 Larvae start to be deposited by the female

 
Pathogenicity
 Intestinal invasion by adult worms
 Abdominal pain, nausea, vomiting, diarrhoea and colic.

 
 Migration of larvae

 
 Encystment of larvae
 Manifestations depend up
on organs affected.
 > 50 – 100 larvae/gm of
muscle are symptomatic
 < 10 larvae are often
asymptomatic

 
Clinical signs & syptoms
 The main findings are:

o Oedema chiefly orbital

o Muscle pain and tenderness
o Headache, fever, rash, dyspnoea, general weakness
o Death occurs in severe cases from exhaustion, heart
failure (myocarditis), pneumonia, etc.

 
Laboratory diagnosis
1. Immunodiagnosis:
a) Intradermal test (Bachman test)
b) Serological tests:
 Bentonite flocculation (BF)
 Latex agglutination (LA)
 Counter – current electrophoresis (CEP)
 Complement fixation test (CFT)
 IFA and IHA
 
Larvae, freed from Encysted in pressed
their cysts muscle tissue. 
Prevention & control
 Through cooking of pork
 770c or freezing at – 150c for 20 days
 – 180c for 24 hours
 Proper breeding of pigs
 Sterilizing garbage
 Antirat campaign
 Inspection of pork in slaughter houses
 Trichinoscope.

 
Treatment
 Non specific symptomatic treatment:
 Sedatives
 Cortisone and ACTH(adenocortico tropic hormon)
 Supportive treatment:
 Rest, fluids, smooth diet and vitamins
 Thiabendazole
 Mebendazole

 
2.1.3.8. Dracunculus medinenis
“Guinea worm, ”
Dracunculosis

 Synonyms: Dracontiasis, Dracunculosis, Dracunculiasis

 Causative agent
 Scientific name: Dracunculus medinensis
 Common name: Medina worm or Guinea worm

 
Epidemiology

Most common in areas of limited water supply where

individuals acquire water by physically entering water
sources.
“Walk-in well”
Water holes in parts of Africa
Dracunculosis

 Habitat:

 Adults in subcutaneous tissues of

man/reservoir animals

 
Life Cycle of Dracunculus medinensis

Infective larvae
In water, larvae Must be eaten by Copepod
(Crustacean), the IH,
 Life Cycle of Dracunculus medinensis
Once within the copepod, the
infective juvenile larvae moves
into the hemocoel where they
develop into 3rd stage juveniles.

These get consumed when

humans drink water with
infected copepods.
Life cycle of D. medinensis

 Man is infected on drinking water containing cyclops.

 In the small intestine, the cyclops is digested , larvae

liberated and penetrate through the duodenal wall and
migrate to the subcutaneous tissues probably via
lymphatics.

 
 Life cycle .....
 At this point the females are fertilized by the males, and the males
die. 
 The females then migrate to the skin, reach sexual maturity, and
produce juveniles. 
 They tend to go to parts most likely to come in contact with water
as the lower extremities (positive hygrotropism and geotropism)
 Several months (9 or more) elapse between infection and
appearance of the gravid female at the skin surface
Life cycle of D. medinensis
 Male dies after copulation
 The cephalic end of the fertilized female pressing on the
skin, produces a papule that becomes a blister and then
ruptures forming an ulcer
 When the ulcer contacts water, a loop of the uterus
prolapses through a rupture in the anterior end of the
worm and larvae are discharged.
 They penetrate its intestine and settle in the body cavity to
become infective in about 3 weeks.

 
Life Cycle of D. medinensis
Pathogencity of D. medinensis

 Early manifestatiosn are produced when the female worm

approaches the skin.
 It liberates a toxic substance that results in local
erythema, tenderness and pain.

 This is followed by formation of a blister that turns into a

cesicle and ultimately ulcerates

 
 Pathogencity.....
 There may be local or systemic symptoms as urticaria,
pruritus, pain, dyspnoea, nausea and vomiting, which
subside with rupture of the blister
 The ulcer may be secondarily infected producing
cellulitis and induration
 Eosinophilia
Adult worm of D. medinensis
D. medinensis

Blister containing the worm Ruptured blister with filamentous worm

A B
D. medinensis
Diagnosis of D. medinensis

 Laboratory tests to investigate dracunculiasis are limited

because the larvae are normally washed into water

 A diagnosis is usually made when the blister has ruptured

and the anterior end of the female worm can be seen
 
Diagnosis of D. medinensis
 If required, laboratory confirmation of the diagnosis can
be made as follows:
1. Place a few drops of water on the ulcer to
encourage discharge of the larvae

2. After a few minutes collect the water in a plastic

bulb pipette or pasteur pipette

3. Transfer the water to a slide and examine

microscopically using 10x objective – motile larvae
will be observed

 
 Prevention & Treatment

People with an open Guinea worm wound should not

enter ponds or wells used for drinking water.

Water can be boiled, filtered through tightly woven nylon

cloth, or treated with a larvae-killing chemical.

No medication is available to end or prevent infection.

The only treatment is to remove the worm over many weeks by
winding it around a small stick and pulling it out a tiny bit at a
time.
Prevention & Treatment
Sometimes the worm can be pulled out completely within a few
days, but the process usually takes weeks or months.
The worm can be surgically removed before the wound begins to
swell.
 Antihistamines and antibiotics can reduce swelling and ease
removal of the worm.
TREMATODES
 Class Trematoda
 Trematode parasites of man belong to Order Digenea

 Characters:

 Flattened dorsoventrally / leaf like (Schistosomes – cylinderical)

 Bilaterally symmetrical
 Unsegmented
 Has no body cavity
 Cuticle covered with spines (help in fixation)
 Organs of fixation in the form of suckers
Hermaphroditic (A) and Bisexual (B) flukes
Sexes of flukes
Trematodes - schistosomes
 Class Trematoda

 The life cycle is passed in two hosts (alternation of hosts)

1. Final host: harbour the sexual stage of the parasite (adult worm)
 Man (DH)

 Other animals (RH)

2. Intermediate host: harbour the asexual stages of the parasite

 Snail (molluscan host)
General life cycle
 Classification
1. Blood flukes:

1. Schistosoma spp. (S. mansoni, S. hematobium, S. japonicum, S.

intercalatum, S. mekongi)

2. Liver flukes:

1. Clonorchis sinensis, 

2. Opistorchis spp.,

3. Fasciola spp. (F. hepatica, F. gigantica)

3. Lung flukes

1. Paragonimus westermani
 Classification

4. Intestinal flukes

1. Fasciolopsis buski

2. Heterophyes heterophyes
BLOOD FLUKES
 Blood flukes (Schistosomes)

 General feature:

 Develope in the portal venous system (df. Other flukes)

 The adult live in the veins that drain the intestine or the urinary
bladder (species dependent)
 Sexes are separate (Diecious - bisexual)

 Cylinderical

 No redia and metacercaria stages.

Blood flukes (Schistosomes)

 Males broader & females filiform and larger than male

 Male has gynaecophoric canal where the female resides after

mating
 Freshwater snails serve as interemediate host.

 Humans the most significant DHs, cercaria is the infective stage

 The immature stage that migrates in the body after infection by

cercaria is called schistosomulum
 Blood flukes (Schistosomes)

Schistosomiasis is caused by digenetic blood trematodes. 

The three main species infecting humans are Schistosoma

haematobium, S. japonicum, and S. mansoni. 
Two other species, more localized geographically, are S.
mekongi(Southeast Asia) and S. intercalatum (central West Africa). 
 Blood flukes (Schistosomes)

Adult worms reside in venous system

 S. haematobium resides in veins of urinary tract

 S. japonicum in superior mesenteric veins of small intestine

 S. mansoni in inferior mesenteric veins of large intestine

worms move upstream to smaller venules to lay eggs

Eggs traverse tissue to exit in gut or bladder

 S. Mansoni (manson’s blood fluke)
 Distribution: Nile delta, Africa, S. America

 Disease: Intestinal bilharziasis

 Morphology:

 Adults:
 Male: marked tuberculated integument, 6 – 9 testes, intestinal caeca
reunite in the anterior half of the body
 Female: longer and thicker than male, ovary in the anterior half of the
body, lay 100 – 300 eggs/day/female
 S. Mansoni (manson’s blood fluke)

 Egg: oval with one rounded pole and one conical pole, large triangular lateral spine,
contains fully embryonated (developed miracidium) when discharged with feces
S. Hematobium (urinary schistosomiasis)
Also called vesical blood fluke

Distribution: Africa, middle East, S. Europe

 In ethiopia – Awash, Wabeshebele, Asossa

Morphology:

 Adults:
 Male: finely tuberculated integument, 4 – 5 testes, the ventral sucker is larger,
intestinal caeca reunite in the middle body of the worm
S. Hematobium (urinary schistosomiasis)
 Female: ovary in the posterior half of the body, uterus – 20 – 200
ova/day/female, suckers are subequal

Egg: oval with one well rounded pole, terminal spine at one
pole, contains fully developed miracidium when laid
S. Japonicum (intestinal schistosomiasis)
Also called oriental blood fluke

Distribution: China, Phillipins, Indonesia, Thailand

 Not in ethiopia

Morphology:
 Adults:
 Male: non tuberculated (smooth), intestinal caeca reunite in the posterior body of the worm
S. Japonicum (intestinal schistosomiasis)

Female: ovary in the middle part of the body, uterus – 50 or more ova/day/female
 Egg: oval almost round, spine very small hook like spine laterally, contains fully developed
miracidium when laid
 S. Intercalatum
Also called vesical blood fluke

Distribution: West and Central Africa

 Not in Ethiopia

Morphology:
 Adults:
 Male: body covered with tubercules and fine spines, 4 – 6 testes
 Female: ovary lies at the midddle part of the body, uterus – 5– 50ova/day/female

 Egg: resembles S. Hematobium but acid fast positive

General life cycle of Schistosoma spp.

Embryonated egg (urine, feces of DH)

Miracidium - swims (penetrate snail IH)

Sporocyst (two generations in the same snail host & cercaria

released)

Forked cercariae – swims (penetrate DH – sheds the fork)

Schistosomulum (migrate till their residence – veins)

General life cycle of Schistosoma spp.
Adult
S. Mansoni (mesentric vein draining large Intestine)
S. Japonicum (mesentric vein draining small intestine)
S. Hematobium (Venous plexus of bladder)

Females lay eggs in small venules (egg moves to lumen)

Intestinal lumen (mansoni & japonicum) & bladder lumen in
hematobium
Life cycle of Schistosoma species
Pathology
Immunopathology

Host immune response against adult worm is minimal

Eggs induce intense inflammatory reaction ,leading to

granuloma formation
 Granuloma consists of egg at center surrounded by eosinophils ,
macrophages and lymphocytes

Larvae inside the egg produce enzymes that aid in tissue

destruction and allow the eggs to pass through the mucosa and
in to lumen of bowel and bladder
 Clinical feature

Many infections are asymptomatic.

S. mansoni causes

Acute schistosomiasis (Katayama's fever) may occur weeks after the

initial infection, especially by S. mansoni and S. japonicum. 
Manifestations include fever, cough, abdominal pain, diarrhea,
hepatospenomegaly, and eosinophilia. 

There may be irritation & skin rash at the site of cercarial penetration
(swimmer’s itch)
S. haematobium and S. mansoni … Cont’d

• In less than 10% of

cases, granulomas can
cause blockage of blood
flow in liver causing
enlargement of the
spleen and fluid
retention in abdomen.
 Clinical feature

Host reaction to eggs lodged in the intestinal/bladder mucosa leads to

the formation of granulomata, ulceration, thickening of the wall

Occasionally central nervous system lesions occur:

Cerebral granulomatous disease may be caused by ectopic S.

japonicum eggs in the brain, and
Granulomatous lesions around ectopic eggs in the spinal cord from
S. mansoni, and S. haematobium infections may result in a
transverse myelitis with flaccid paraplegia
 Clinical feature

Continuing infection may cause granulomatous reactions and fibrosis

in the affected organs, which may result in manifestations that include:
Colonic polyposis with bloody diarrhea (Schistosoma mansoni
mostly);
Portal hypertension with hematemesis and splenomegaly (S.
mansoni, S. japonicum);
Clinical feature

Cystitis and ureteritis (S. haematobium) with hematuria, which can

progress to bladder cancer;
Pulmonary hypertension (S. mansoni, S. japonicum, more rarely S.
haematobium);
Glomerulonephritis
 Laboratory diagnosis

Microscopic identification of eggs in stool or urine is the most

practical method for diagnosis. 
Stool examination should be performed when infection with S.
mansoni or S. japonicum is suspected, and urine examination
should be performed if S. haematobium is suspected.
Laboratory diagnosis

Eggs can be present in the stool in infections with all Schistosoma

species. 
 The examination can be performed on a simple smear (1 to 2 mg of fecal
material). 
 Since eggs may be passed intermittently or in small amounts, their detection
will be enhanced by repeated examinations and/or concentration procedures
(such as the formalin-ethyl acetate technique). 
Lab…

 In addition, for field surveys and investigational purposes, the egg output
can be quantified by using the Kato-Katz technique (20 to 50 mg of fecal
material).
 Laboratory diagnosis
Antibody detection can be useful in both in clinical management
(e.g., recent infections) and for epidemiologic surveys.
 Prevention and control


Avoid contact with water

Construction of bridges on streams and rivers

Providing safe recreational bathing & swimming sites

Avoid contamination of water with the feces/urine of man

Latrine construction and sanitary disposal of feces and urine

Destroying snail hosts

Treatment of infected individuals

Health education
 Cestodes (Tape worms)

General Characteristics

The body of cestodes is tape like (flat) and is made up of a

head (scolex) and many proglottides (segments) in
which the head attaches the tape worm to its host via suckers
and hooks.

With few exceptions, adults live in the intestinal tract with

some species growing to great length.

The proglottides are formed from behind the head and

progttides which contain eggs are called gravid proglottides.
 Cestodes … Cont’d

In most species, the eggs are released when a gravid

segment becomes detached and ruptured.

In most species of cestodes man is the definitive host e.g.

Taenia saginata, Taenia solium, Hymenolopis nana,
Dyphlobotrium latum.

On the other hand man is accidental host in some species

of cestodes e.g. Echinococcus granulosus (hydatid worm),
Hymenolopis duminuta (rat tape worm), Diplidium caninum
(dog tape worm).
 Cestodes … Cont’d

Their life cycle completes in two hosts (exception H.nana)

Tapeworms are hermaphroditic

Tapeworms do not have a digestive system. Their food is

absorbed from the host’s intestine.

Reproduction can be sexual (Oviporous) or asexual

(sometimes multiplication with in larval forms).
 Hymonelepis nana

Common name: dwarf tape worm

General Features

It is the smallest and most common tape worm

Man acts both as definitive and intermediate host

In addition to man this infects rodents (mice and rats)

Geographical Distribution
 It is worldwide in its distribution, but it is more common in warm
climates than cold climates and fairly common in Ethiopia.
 Children are more commonly infected than adults.
 Hymonelepis nana … Cont’d

Habitat

Adult worm: Small intestine of man (mainly in the upper two-

third of the ileum).

Cysticercoid larvae: In the intestinal villi of man

Eggs: In the faeces

Transmission

Infection with this parasite is mainly transmitted by ingestion of

eggs in contaminated food, water and finger.

Internal autoinfection can also occur

 H. nana … Cont’d

Life cycle: (eggs  cysticercoids  adult). H. nana has a

direct life cycle with a human host serving as both definitive
and intermediate host.

1. Ingestion of eggs by faeco–oral route Or internal

autoinfection

2. Onchosphere larvae is hatched in SI

3. Onchosphere larvae penetrate the intestinal villus and

here develops to cysticerciod larvae
 H. nana … Cont’d

4. Cysticerciod larvae by attaching to the intestinal mucosa

develop to adult worm

5. Eggs are released from the gravid segment in SI

6. Most eggs passed in faeces & some cause auto-infection

7. Faeces containing infective eggs contaminate the

environment
 H. nana … Cont’d

Clinical features and pathology

Most of the time light infection is asymptomatic, but heavy

infection is characterized by clinical symptoms such as abdominal
pain, diarrhea, anorexia, dizziness, headache, eosinophilia,
pruritus of nose and anus, epileptic form convulsions.

Laboratory diagnosis

Finding of their eggs in faeces by direct examination or

concentrations techniques

Sometimes adult worm can be also found in stool

 H. nana … Cont’d

Treatment

Praziquantel (1st line drug)

 Niclosamide (2nd line drug)

Prevention and control

Personal hygiene, washing of hands before eating and after

defecation

Sanitary disposal of faeces in to latrines

Protection of food and drink water from contamination with faeces

Treatment of cases and giving health education

 Taenia species

There are two species of taenia that are mostly medically

important to man. These are
 T. saginata (beef tape worm)

 T. solium (pork tape worm)

Causes a disease called Taeniasis

T. solium in addition to taeniasis it can also cause

cysticercosis.
 Taenia species … Cont’d

Epidemiology/ geographical distribution

Taenia saginata: Has worldwide distribution (common in

beef eating countries) with high prevalence rate in high
lands of Ethiopia, Egypt and Morocco.

Taenia solium: Has worldwide in prevalence (common in

pork eating countries) but it is not common (doubtful for
its presence) in Ethiopia
 Taenia species … Cont’d

Habitat

Adult: Adult worm measures 5-10 meters in length (T.

saginata) and 2-3 meters in length (T. solium) and found
in small intestine (upper jejunum) of man where it may
survive for as long as 25 years.

Larvae: In muscular tissues of pigs (T. solium) and cattle

(T. saginata)

Eggs: In the faeces of man and in gravid segment

 Taenia species … Cont’d

Transmission

Man acquire infection by eating raw or under cooked beef

(in T.saginata) or pork (in T.solium) containing encysted
larval stage.

In case of T. solium infection can also occur by ingestion

of eggs in food or water and by internal auto-infection.
 Taenia species … Cont’d

Life cycle: ( Egg  Cysticercus larvae  Adult)

1. Cysticercus (infective) eaten in raw/under cooked (Beef

meat in T.saginata and Pork meat in T. solium)

2. The scolex of cysticercus inverts and attaches -develop to

cysticercus larvae in tissue to mucosa of small intestine

3. Develop to adult worm in small intestine

4. Free eggs or gravid segment are produced and passed in

stool
 Taenia species … Cont’d

**Exception:- in case of T.solium when the infection is

caused by ingestion of eggs the cysticercus larvae
hatched from the eggs have the ability to penetrate the
intestinal wall and when carried by the blood circulation into
different organ tissue cause a disease called cysticercosis

5. Eggs are eaten by intermediate hosts (Cow in T.

saginata, and pig in T. solium)

6. Onchosphere hatch and penetrate small intestine and via

blood reaches to the tissues and develop to cysticercus.
 Taenia species … Cont’d

Clinical Features and Pathology

T. saginata causes Taeniasis

T. solium causes Taeniasis and Cysticercosis

T. saginata:- Light infection most of the time remains asymptomatic

but in heavy infection it may result in loss of appetite, weight loss,
vomiting, hunger sensation, acute intestinal obstruction and
abdominal discomfort.

T. solium:- The major symptoms of taeniasis are due to the adult
worm and include abdominal pain, loss of appetite, persistent
diarrhea or diarrhea altering with constipation.
 Taenia species … Cont’d

Cysticercosis is caused due to cyst of T. solium and it is

developed in different organs of the body such as lung,
liver, eye and brain. They are usually developed in
subcutaneous tissues and muscles forming visible nodules.

The cysticercosis developed in the brain and eye leading

to epileptic attacks (neurological disorders) and
blindness respectively.
 Taenia species … Cont’d

Laboratory Diagnosis

Detecting (finding) egg in stool specimen

Identifying gravid segments in stool specimen

T. solium (cysticercosis): Finding calcified larvae in

histological or X-rays examination

Treatment

Praziquantel and Niclosomide

 Taenia species … Cont’d

Prevention and Control

Avoid eating raw or insufficiently cooked beef and pork

meat

Inspecting meat for larvae

Treating infected person

Providing health education and adequate sanitary facilities

 Diphlobotrium latum

Common name: Fish tape worm or broad tape worm

Diphlobotrium latum causes diphlobotheriasis

In addition to human this also infects fish eating carnivores

(e.g. cat, dog, pig etc)

Humans are the important definitive host.

It is the longest tape worm found in man.

 Diphlobotrium latum … Cont’d

Epidemiology/ Geographical Distribution

Infection with D. latum is endemic in Europe, Russia,

Japan, tropical Africa, and North and South America.

Habitat

Adult: Found in small intestine (ileum or jejunum) of man

Eggs: Passed in faeces of man

 D. latum … Cont’d

Transmission

Humans become infected when they eat under cooked,

raw or lightly salted meat from infected fresh water fishes.

Life cycle

Diphlobotrium latum have indirect life cycle and requires

three hosts in which the definitive hosts are human and
other carnivores and the two intermediate are
crustacean(Cyclops) and fresh water fish.
 D. latum … Cont’d

Life cycle: (Egg  Coracidia  Procercoid  Plerocercoid

 Adult worm)

Plerocercoid (infective stage) is ingested from fish meat

Plerocercoid develop to adult worm in small intestine

Eggs are produced and passed in faeces

After entering in to water from the eggs coracidia is

hatched and swims in water.
 D. latum … Cont’d

Then coracida is ingested by Cyclops and changed to

procercoid in the cyclops

The Cyclops which contains procercoid are eaten by fresh

water fish and the procercoid is developed to plerocercoids.
Clinical Features and Pathology

The diphylobotheriasis caused by D.latum has gastro intestinal

symptoms such as abdominal discomfort, diarrhea and nausea.

It also causes a megaloblastic Anemia (VB12 uptake)

 D. latum … Cont’d

Laboratory Diagnosis

Finding egg of D. latum in faeces and occasionally segments of

proglottides can be also found in stool specimen

Treatment

Praziquantel and Niclosamide

Prevention and Control

Proper cooking of fish

Prevention of fecal pollution of natural waters

Treatment of identified cases

 Echnococus granulosus

Common name: Hydatid worm

In humans Echnococus granulosus causes hydatid diseases

(zoonosis) or it is also called unilocular echinococcosis.

Normally it is tape worm of carnivores or dogs (definitive

hosts include dog, fox, wolf, and jackal)

Man is an accidental host.

Sheep, cattle, swine are intermediate hosts

 Echnococus granulosus… Cont’d

Epidemiology/geographical distribution

Has worldwide distribution but more common in temperate areas (Europe,

South America, Asia, Australia and also in USA and Canada). The disease
is common in East Africa (highest prevalence is seen in Kenya: 10-15%).

Habitat

Adult: Is found in small intestine of dog and other canine animals, but
not found in man

Larvae (hydatid cyst): In different parts of body (liver, lung, brain etc)
of man and herbivorous animals

Eggs: In faeces of dog, fox etc.

 Echnococus granulosus… Cont’d

Transmission

Human infection follows ingestion of the eggs passed in

faeces of infected dogs.

This may occur by eating raw vegetables or other food

items contaminated with dog faeces, finger contaminated
with the eggs or by kissing pet dogs may cause the eggs
to be transferred directly to the mouth.
 Echnococus granulosus… Cont’d

Life cycle: (Egg Hydatid cyst Adult (but not in man)

I. Man infection is acquired by accidental ingestion of egg in

contaminated food with dog faeces

II. Embryo is hatched from the eggs in small intestine then the
embryo (larvae) penetrates the intestinal wall to be carried into
various organs through the blood circulation. The larvae
embedded in liver, lung, kidney, CNS and elsewhere then it
develops to hydatid cyst in the tissue of the above organs.

N.B: Generally man is the dead end for this parasitic infection
(sometimes called blind infection)
 Echnococus granulosus… Cont’d

Clinical Features and Pathology

Infection may be asymptomatic at all in some cases, or in

most cases the clinical diseases are developed only
several years later (it may range from 5 years to 20
years) when the hydatid cyst has grown big enough to
cause obstructive symptoms and generally the disease
results mainly from pressure effects caused by the
enlarging cysts (can overcrowd organs).
 Echnococus granulosus… Cont’d

In the liver, the cyst may exert pressure on both bile ducts
and blood vessels and creates pain and biliary rupture.

Peribronchial cysts may produce pulmonary abscesses,

cough and chest pains.

Brain cysts produce intracranial pressure and epilepsy.

When the cyst is ruptured in different organs of the body

The contents of a cyst may produce anaphylactic shock
and finally result in death.
 Echnococus granulosus… Cont’d

Diagnosis

Laboratory diagnosis is generally difficult for this hydatid worm.

It involves clinical, radiological and serological methods

Treatment

Surgical removal of the cyst

Using high dose of Albendazole, Mebendazole and Praziquantel

Prevention and Control

Improve personal hygiene

Avoid feeding dogs with slain animals

The end