PARASITES

01 Learn about the parasites

02 Identify the causative agent for each

parasitic disease

03 Determine how is this transmitted

04 Discuss the treatments

Introduction: What are parasites?

A parasite is an organism that spends a significant portion

1 of its life in or on the living tissue of a host organism and
which causes harm to the host without immediately killing
it.
The parasite is termed:

1 OBLIGATE- when it can live only in association with a host

FACULTATIVE- when it can live both in or on a host as well

2 as in a free form.

Parasites that cause harm to the host are pathogenic parasites

while those that benefit from the host without causing it any harm
are known as commensals.
2 TYPES OF PARASITES

Ectoparasites - live on the outside of the host’s body

1

Endoparasites - live on the inside of the host’s body

2

Parasites are organisms that live on or in other living organisms

called the hosts.
TYPES OF HOST
Intermediate Host - The hosts that harbor the larval and
1 asexual stage. It is the host which harbors the immature
stage of the parasite.
Example: Snails in trematodes
Definitive Host - The hosts which harbors the adult stage
2 of the parasite. The parasite attains sexual maturity in it.
Example: Dog for Ancylostoma caninum
Cattle for Fasciola gigantica

Reservoir Host - Ensure continuity of the parasite's life

3 cycle and act as additional sources of human infection.
- It is a vertebate host in which parasite occurs naturally.
The host harbors the parasite but does not produce harm to
the host.
HELMINTHS
It means parasitic worms.

They are multicellular, eukaryotic organisms in the Kingdom

Animalia.
2 MAJOR DIVISIONS
Nematoda or Nematodes (roundworms)- They are
1 elongated and tapered at both ends, rounds in cross
section, and unsegmented.

-They have only a set of longitudinal muscles, which allows

them to move in a whiplike, penetrating fashion; a complete
digestive system that is well adapted for ingestion of the
host’s gut contents, cells, blood, or cellular breakdown
products

-Most human infections are acquired by ingestion of

the egg or larval stage, but nematode infections can
also be acquired from insect vectors and skin
penetration.
2 MAJOR DIVISIONS
2. Platyhelminthes- flatworms
2 -Flatworms that are dorsoventrally flattened in cross section and
are hermaphroditic

a. Cestodes - tapeworms
-Are flat and have a ribbon-like chain of segments
(proglottids) containing male and female reproductive structures.
-Adult tapeworms have no mouth or gut and absorb their
nutrients directly from their host through their integument.
b. Trematodes - flukes
-Trematodes are typically flattened and leaf shaped with
two muscular suckers.
-Trematodes are hermaphroditic, with the exception of the
schistosomes (blood flukes), which have male and female worms
that exist coupled together within small blood vessels of their
hosts.
3 Major Stages in Helminth Life Cycle

EGG LARVA

ADULT
NEMATODES
INTESTINAL NEMATODES

1 Ascaris lumbricoides

2 Enterobius vermicularis

3 Necator americanus

4 Strongyloides stercoralis

5 Trichuris trichiura
Ascaris lumbricoides
COMMON NAME: Large Intestinal Roundworm
INTERMEDIATE HOST: None
DEFINITIVE HOST: Human
HOW INFECTION IS ACQUIRED: Ingestion of Eggs
HOW INFECTION IS DIAGNOSED:
Observation of eggs in stool specimens (40 to 70 micrometers by
35 to 50 micrometers)
Ascaris lumbricoides
Epidemiology
▪ Affects all ages, more prevalent in the 5 to 9 years, incidence is higher
in poor rural populations
Symptoms
▪ Some people has no symptoms
▪ Others: abdominal pain, weight loss, anorexia, distended abdomen,
intermittent loose stool, occasional vomiting
▪ Heavy infections-block the intestine
▪ Pulmonary stage – cough, wheezing, dyspnea, sub-sternal discomfort
Diagnosis
▪ Microscopic examination of stool
▪ Identification of adult worms in stool or emerging from the nose, mouth, or
rectum
▪ Larvae in sputum (Larvae pulmonary phase)
▪ Chest X-ray: show signs of infiltrates (Larvae pulmonary phase)
▪ Radiographic studies: worm in the GIT
Ascaris lumbricoides

Treatment & Prevention

▪ Albendazole- 400mg PO once
▪ Mebendazole- 100mg 2x/day x3 days
▪ Ivermectin- 150 to 200mcg/kg orally once
▪ Albendazole, mebendazole, and ivermectin may harm the fetus
▪ Before treatment with ivermectin, patients should be assessed for
coinfection with Loa loa if they have lived in areas of central Africa
where Loa loa is endemic because ivermectin can cause severe
reactions in patients with loiasis and high microfilarial levels.
▪ Nitazoxanide-effective for mild infections and not for heavy
infections
▪ Piperazine- once widely used but replaced by less toxic alternatives
▪ Surgery- Obstructive complications
▪ Good hygiene
 Ascaris lumbricoides adult male
and female

An adult Ascaris worm. Diagnostic characteristics: tapered ends;

length 15-35 cm (the females tend to be the larger ones).
This worm is a female, as evidenced by the size and genital girdle
(the dark circular groove at bottom area of image).
Enterobius vermicularis

COMMON NAME: Pinworm

INTERMEDIATE HOST: None
DEFINITIVE HOST: Human
HOW INFECTION IS ACQUIRED: Ingestion of Eggs
HOW INFECTION IS DIAGNOSED: Observation of eggs in “Scotch
Tape Method” or pinworm paddle
Enterobius vermicularis
Enterobius vermicularis
Morphology
• Female - 8 mm x 0.5mm; the male is smaller
• Eggs (60 micrometers x 27 micrometers) are ovoid but
asymmetrically flat on one side.

Symptoms
• Perianal, perineal and vaginal irritation caused by the female
migration
• Itching results in insomnia and restlessness
• Gastrointestinal symptoms (pain, nausea, vomiting, etc.) may
develop

Treatment and Control

• Two doses (10 mg/kg; maximum of 1g each) of Pyrental Pamoate
two weeks apart gives a very high cure rate.
• Mebendazole is an alternative.
• Albendazole
• The whole family should be treated, to avoid reinfection.
• Bedding and underclothing must be sanitized between the two
treatment doses.
• Personal cleanliness
Necator americanus
COMMON NAME: New World Hookworm
INTERMEDIATE HOST: None
DEFINITIVE HOST: Human
HOW INFECTION IS ACQUIRED:Penetration of skin by infective larva
HOW INFECTION IS DIAGNOSED:Observation of eggs in stool
specimens
Necator americanus
PATHOLOGY:
• Adult worms attach to intestinal villi with their buccal teeth and
feed on blood and tissue (can cause severe anemia and iron
deficiency)
• Symptoms: Abdominal discomfort and diarrhea
• Initial skin infection: Ground itch (characterized by erythema and
intense pruritus
• Feet and ankles are common site of infection
due to exposure from walking barefoot
Necator americanus
TREATMENT AND CONTROL
• Mebendazole, 200 mg, for adults and 100 mg for children, for 3
days is effective.
• Sanitary disposal of fecal material
• Avoidance of contact with infected fecal material
Strongyloides stercoralis
COMMON NAME: Threadworm/ Cochin-china diarrhea
INTERMEDIATE HOST: None
DEFINITIVE HOST: Human
HOW INFECTION IS ACQUIRED: Penetration of skin by infective
larva
HOW INFECTION IS DIAGNOSED: Observation of eggs in duodenal
aspirates or stool specimens
Morphology
• parasitic female is larger (2.2 mm x 45 micrometers)
• free-living worm (1 mm x 60 micrometers)
• eggs, when laid are 55 micrometers by 30 micrometers.
Symptoms
• Light infections are asymptomatic.
• Skin penetration causes itching and red blotches.
• During migration, the organisms cause bronchial verminous pneumonia
and, in the duodenum, they cause a burning mid-epigastric pain and
tenderness accompanied by nausea and vomiting.
• Diarrhea and constipation may alternate.
• Heavy, chronic infections - anemia, weight loss and chronic bloody
dysentery.
Treatment and control
• First line therapy: Ivermectin in a single dose 200mcg/kg for 1-2 days
• Alternative: Albendazole 400mg PO 2x/day x7 days
• Thiabendozole was a therapeutic option but was discontinued
• Follow up stool exam (2-4 weeks) after treatment. Retreatment if still positive.
Trichuris trichiura
COMMON NAME: Whipworm
INTERMEDIATE HOST: None
DEFINITIVE HOST: Human
HOW INFECTION IS ACQUIRED: Ingestion of eggs
HOW INFECTION IS DIAGNOSED: Observation of eggs in stool
specimens
Morphology
• female - 50 mm long with a slender anterior (100 micrometer diameter) and a thicker
(500 micrometers diameter) posterior end.
• male is smaller and has a coiled posterior end
• eggs - lemon or football shaped and have terminal plugs at both ends
Symptoms
• Less than 10 worms are asymptomatic
• Heavier infections (e.g., massive infantile trichuriasis) - chronic profuse mucus and
bloody diarrhea with abdominal pains and edematous prolapsed rectum
Treatment and Control
• Drug Dosage for adults and children
Albendazole 400 mg orally for 3 days
Mebendazole 100 mg orally twice a day for 3 days
Ivermectin 200 mcg/kg/day orally for 3 days
Oral albendazole is available for human use in the
United States.
• Improved hygiene
• Sanitary eating habits
 BLOOD AND TISSUE NEMATODES

1 Dracunculus medinensis

2 Trichinella spiralis
Dracunculus medinensis
COMMON NAME: Guinea Worm; Fiery Serpent
INTERMEDIATE HOST: Cyclops (fresh water crustacean)
DEFINITIVE HOST: Human
HOW INFECTION IS ACQUIRED: Ingestion of infected
Cyclops
HOW INFECTION IS DIAGNOSED: Observation of adult worm beneath
the skin or emerging from a blister (ankle or foot)

A & B: The female guinea

worm induces a painful
blister.
(A) after a rupture of the
blister, the worm emerges
as a whitish filament
Morphology
• The adult female worm measures 50-120 cm by 1 mm and the male is half that size.
Symptoms
• If the worm does not reach the skin, it dies and causes little reaction.
• Superficial tissue - inflammatory reaction in the form of a sterile blister with serous
exudation.
• The worm lies in a subcutaneous tunnel with its posterior end beneath the blister,
which contains clear yellow fluid.
• The course of the tunnel is marked with induration and edema.
• Contamination of the blister produces abscesses, cellulitis, extensive ulceration and
necrosis.

Treatment
• Extraction of the adult guinea worm
• No drug is effective in killing the worm.
• Protection of drinking water from being contaminated with Cyclops and larvae
 Dracunculus medinensis worm wound around matchsticks.
This helminth is usually withdrawn from the body by winding the stick.
Trichinella spiralis
COMMON NAME: None
INTERMEDIATE/DEFINITIVE HOST: Pig, Bear, Walrus, Human
(dead-end host) and etc.
HOW INFECTION IS ACQUIRED: Ingestion of pork or bear meat with
larva
HOW INFECTION IS DIAGNOSED: Usually not diagnosed or an
incidental finding at autopsy
 Trichinosis Symptomatology

Intestinal mucosa Circulation and muscle Myocardium Brain and meninges

(24-72 hrs) (10-21 days) (10-21 days) (14-28 days)

Chest pain,
Nausea, vomiting Edema, peri-orbital Headache (supraorbital),
tachycardia, EKG
diarrhea, conjunctivitis, photo phobia, vertigo, tinnitus, deafness,
changes, edema of
abdominal pain, fever, chill, sweating, muscle mental apathy, delirium,
extremities, vascular
headache. pain, spasm, eosinophilia. coma, loss of reflexes.
thrombosis.
Morphology
• The adult female measures 3.5 mm x 60 micrometers. The larvae in the tissue (100
micrometers x 5 micrometers) are coiled in a lemon-shaped capsule.

Pathology and Immunology

• Pathogenesis is due the presence of large numbers of larvae in vital muscles and host
reaction to larval metabolites
• Muscle fibers become enlarged edematous and deformed
• Paralyzed muscles are infiltrated with neutrophil, eosinophils and lymphocytes.

Diagnosis
• eating raw or undercooked meat
• laboratory findings (eosinophilia, increased serum creatine phosphokinase and lactate
dehydrogenase and antibodies to T. spiralis).
Treatment and Control

Drug Adult and pediatric dose

Albendazole 400 mg twice a day by mouth for 8 to 14 days
Mebendazole 200 to 400 mg three times a day by mouth for 3
days, then 400 to 500 mg three times a day by
mouth for 10 days
• Steroids - inflammatory symptoms
• Mebendazole - eliminate worms.
• Elimination of parasite infection in hogs
• Adequate cooking of meat
 BLOOD AND TISSUE NEMATODES

1 Brugia malayi and

Wuchereria bancrofti

2 Loa loa
Brugia malayi and Wuchereria bancrofti
COMMON NAME: None
INTERMEDIATE HOST: Various species of mosquitoes.
DEFINITIVE HOST: Human
HOW INFECTION IS ACQUIRED: Injection of infective larvae by
mosquito
HOW INFECTION IS DIAGNOSED: Observation of microfilariae in
stained blood specimens
FILARIASIS / ELEPHANTHIASIS

• The most prominent clinical feature is the development of severe

lymphedema of the limbs (“elephantiasis”) and occasionally
genitalia (hydrocele-a type of swelling in the scrotum that occurs
when fluid collects in the thin sheath surrounding a testicle) due to
dysfunction of lymphatic vessels.
• Affected limbs become grossly swollen; the skin may become thick
and pitted, and secondary infection are frequent due to lymphatic
dysfunction.
• Scrotal hydrocele is also seen in some infected males.
• Lymphangitis, lymphadenopathy, and eosinophilia may accompany
infection in the early stages.
FILARIASIS / ELEPHANTHIASIS
FILARIASIS / ELEPHANTHIASIS

An elderly male with hydrocoele,

elephantiasis of the leg,
hanging groin, leopard skin and
onchocerciasis nodules.
FILARIASIS / ELEPHANTHIASIS

• The MDA (Mass Drug Administration) regimen recommended depends on the co-
endemicity of lymphatic filariasis with other filarial diseases. WHO recommends the
following MDA regimens:
• Albendazole (400 mg) alone twice per year for areas co-endemic with loiasis
• Ivermectin (200 mcg/kg) with albendazole (400 mg) in countries with onchocerciasis
• Diethylcarbamazine citrate (DEC) (6 mg/kg) and albendazole (400 mg) in countries without
onchocerciasis
• Recent evidence indicates that the combination of all three medicines can safely clear
almost all microfilariae from the blood of infected people within a few weeks, as opposed
to years using the routine two-medicine combination.
• WHO now recommends the following MDA regimen in countries without onchocerciasis:
• Ivermectin (200 mcg/kg) together with diethylcarbamazine citrate (DEC) (6 mg/kg) and albendazole
(400 mg) in certain settings
Loa loa
COMMON NAME: Eye Worm
INTERMEDIATE HOST: Chrysops ( Mango Fly).
DEFINITIVE HOST: Human
HOW INFECTION IS ACQUIRED: Injection of infective larvae by
Chrysops
HOW INFECTION IS DIAGNOSED: Observation of adult worm beneath
the skin or in the conjunctiva of the eye
Morphology
▪ cylindrical, has a cuticle with three main outer layers made of collagen and other
compounds which protects the nematodes so they can invade the digestive tract of
animals
▪ adults are small, thin worms ranging 20-70mm long and 350-430 micrometers wide

Ecosystem Roles
▪ an obligate endoparasite, feeding on fluids in the tissues of humans

Pathogenesis/Symptoms
▪ Infect human host by travelling from the entry site through the SQ causing
inflammation in the skin (Calabar swelling).
▪ These are localized, inflammatory, pruritic subcutaneous edema seen in joints of
extremities (wrist and ankle) due to allergens and metabolic products released by the
worm.
▪ It can also travel and infect the eye.
▪ In deeper tissues, it can cause encephalitis.
▪ Common symptoms are itching, joint pain, fatigue and death.
Onchocerca volvulus
COMMON NAME: Blinding Worm/ River Blindness
INTERMEDIATE HOST: Simulium (Black Fly).
DEFINITIVE HOST: Human
HOW INFECTION IS ACQUIRED: Injection of infective larvae by
Simulium
HOW INFECTION IS DIAGNOSED: Observation of microfilariae in
“skin snips”

Onchocerca volvulus. A: Palpation of a

subcutaneous nodule. (Reproduced with
permission from WHO/TDR library/Crump.) B:
Nodules that were surgically removed contain
coiled adult worms. (Courtesy of Pathology,
UCSF.)
 CESTODES (TAPEWORMS)

1 Taenia saginata

2 Taenia solium
Taenia saginata
COMMON NAME: Beef Tapeworm
INTERMEDIATE HOST: Cow
DEFINITIVE HOST: Human
HOW INFECTION IS ACQUIRED: Ingestion of infected beef
HOW INFECTION IS DIAGNOSED: Observation of egg or proglottids
in the stool specimen
TREATMENT
• Praziquantel 5 or 10 mg/kg (single oral dose)
• Alternate therapy: Single dose of Niclosamide 2g (not available in the
US) is given as 4 tablets (500mg each) that are chewed one at a time
and swallowed with small amount of water
• Children: Niclosamide-50mg/kg (max dose of 2g) once
• Treatment is successful: no ova in stool for 1-3 months after treatment
• Prevented: cook whole cuts of beef ≥ 63° C (≥ 145° F)
Taenia solium
COMMON NAME: Pork Tapeworm
INTERMEDIATE HOST: Pig
DEFINITIVE HOST: Human
HOW INFECTION IS ACQUIRED: Ingestion of infected pork
HOW INFECTION IS DIAGNOSED: Observation of egg or proglottids
in stool specimen; cysticercosis (CT scans, MRI techniques, x-ray or
immunodiagnostic procedures
Treatment
• For intestinal infection (without neurocysticercosis): Praziquantel or
niclosamide (outside the US)
• Praziquantel 5 to 10 mg/kg orally as a single dose to eliminate
adult worms.
• Alternatively, a single 2-g dose of niclosamide (not available in
the US) is given as 4 tablets (500 mg each) that are chewed one
at a time and swallowed with a small amount of water. For
children, the dose is 50 mg/kg (maximum 2 g) once.
• A stool sample should be repeated three months after therapy is
completed to verify cure
• For neurocysticercosis: Corticosteroids, antiseizure drugs, and
sometimes albendazole or praziquantel and/or surgery
TREMATODES
INTESTINAL TREMATODE
1 Fasciolopsis buski

LIVER TREMATODES
1 Clonorchis sinensis

2 Fasciola hepatica
LUNG TREMATODE
1 Paragonimus westermani

BLOOD TREMATODES
1 Schistosoma haematobium

2 Schistosoma japonicum

3 Schistosoma mansoni
Fasciolopsis buski
COMMON NAME: Giant Intestinal Fluke
INTERMEDIATE HOST: Fresh Water Snails
DEFINITIVE HOST: Human, Dog, Pig, Rabbit
HOW INFECTION IS ACQUIRED: Ingestion of raw or uncooked
plants on which metacercariae are encysted
HOW INFECTION IS DIAGNOSED: Observation of eggs in stool
specimens
Epidemiology
▪ This is a parasite of central and southeast Asia.
Morphology
▪ Elongate oval fluke (2 to 7 cm long) - lives in the small intestine of
man
Life cycle
Man is infected by ingesting water chestnuts contaminated with
metacercaria which find access to the small intestine, attach
themselves to the mucosa and mature in 25 to 30 days. The fluke
eggs are passed in the feces and hatch in fresh water producing
miracidia which must penetrate a suitable snail within hours. The
miracidia in the snail develop into cercaria and enter fresh water
where they attach themselves to water plants (water chestnut) and
encyst to become metacercaria
Symptoms
▪ Epigastric pain, nausea and diarrhea(morning).
▪ Edema and ascites - heavier infections
Pathology
▪ The fluke attaches itself to the intestinal mucosa where
inflammation, ulceration and abscesses occur.

Treatment and Control

▪ Praziquantel
▪ Water chestnuts from contaminated waters should be avoided.
▪ Sewage should be treated before disposal.
Clonorchis sinensis
COMMON NAME: Chinese or Oriental Liver Fluke
INTERMEDIATE HOST: Fresh Water Snails (1st IH); Fresh Water
Fish (2nd IH)
DEFINITIVE HOST: Human, Dog, Cat
HOW INFECTION IS ACQUIRED: Ingestion of infected fresh water
fish
HOW INFECTION IS DIAGNOSED: Observation of eggs in stool
specimens
CLONORCHIASIS
Fasciola hepatica
COMMON NAME: Liver Fluke
INTERMEDIATE HOST: Fresh Water Snails
DEFINITIVE HOST: Human, Cow, Sheep
HOW INFECTION IS ACQUIRED: Ingestion of raw or undercooked
aquatic vegetation (water cress) with metacercariae
HOW INFECTION IS DIAGNOSED: Observation of eggs in stool
specimens
FASCIOLIASIS
Morphology
▪ leaf shaped (1x 3 cm); eggs (80 x 150 µm)
Life cycle
• Humans are infected by the consumption of improperly cooked
watercress that harbors encysted larval metacercariae.
• The larval fluke penetrates the duodenal wall and migrates to the
peritoneal cavity, penetrates the liver capsule and migrates into the
bile duct where it matures.
• The adult fluke passes its eggs in stool that hatch in water to produce
miracidia.
• The miracidium must find an appropriate snail to continue the life
cycle.
• In the snail, the miracidium divides and gives rise to cercariae which
exit the snail and encyst as metacercariae attached to watercress
leaves.
Symptoms
▪ tenderness of the liver and hepatomegaly which results
in upper
quadrant pain, chills and fever accompanied with
eosinophilia. The
toxic secretions cause hepatitis.
▪ bile duct - irritation resulting in hyperplasia of the
epithelium and bile
obstruction. Adult worms may invade the liver and
cause necrotic foci
(liver rot).

Treatment
▪ Triclabendazole
Paragonimus westermani
COMMON NAME: Lung Fluke
INTERMEDIATE HOST: Fresh Water Snails(1ST IH); Crabs or Crayfish
(2ND IH)
DEFINITIVE HOST: Human, Dog, Cat
HOW INFECTION IS ACQUIRED: Ingestion of infected crabs or crayfish
HOW INFECTION IS DIAGNOSED: Observation of eggs in rust colored
sputum (often for TB) or stool specimens

PARAGONIMIASIS
Epidemiology
▪ Lung fluke is most commonly encountered in parts of Asia, Africa and South America.

Morphology
▪ plump reddish brown oval worm (10 by 4 mm.);
▪ ovum (85x55 micrometers)
Life cycle
• Lung fluke infects man (and domestic carnivores) when crabmeat infested with
encysted metacercaria is consumed.
• The metacercaria reach the small intestine, exit their shell and bore their way, as
young flukes, through the intestinal wall, through the thoracic diaphragm and
penetrate the lung.
• There, they become enclosed in 1 to 2 cm cysts and reach maturity.
• The eggs are found in the sputum or, if swallowed, in the feces, 2 to 3 months
after infection.
• The eggs, when introduced in fresh water produce a miracidia which penetrates
the suitable snail.
• In the snail they develop into cercaria which break out in water and penetrate
gills, muscle or viscera of fresh water crabs and become encysted in flesh as
metacercaria
Symptoms
• dry cough, followed by production of blood stained rusty brown
sputum
• Pulmonary pain and pleurisy may develop.
• brain where they lay eggs - granulomatous abscess resulting in
symptoms similar to epilepsy.

Treatment and Control

▪ Praziquantel
▪ Adequate cooking of crustaceans.
▪ Improved sanitary conditions.
Schistosoma species
COMMON NAME: Blood Fluke
INTERMEDIATE HOST: Fresh Water Snails
DEFINITIVE HOST: Human
HOW INFECTION IS ACQUIRED: Penetration of skin by cercariae
present in fresh water
HOW INFECTION IS DIAGNOSED: Observation of eggs in urine
(S. haematobium) or stool (S. japonicum and S. mansoni)

S. haematobium S. japonicum
S. mansoni
Morphology
▪ Adult worms are 10 to 20 mm long; the male has an unusual
lamelliform shape with marginal folds forming a canal in which the
slender female worm resides. Unlike other trematodes, schistosomes
have separate sexes
Symptoms
▪ skin - dermatitis (swimmers' itch),splenomegaly, lymphadenopathy and diarrhea
▪ bladder -granulomatous lesions, hematuria , urethral occlusion.
▪ intestine - polyp formation which, in severe cases, may result in life threatening
dysentery
▪ liver - periportal fibrosis and portal hypertension resulting in hepatomegaly,
splenomegaly and ascites. A gross enlargement of the esophageal and gastric veins
may result in their rupture.
▪ S. japonicum - central nervous system and cause headache, disorientation, amnesia
and coma. Eggs carried to the heart produce arteriolitis and fibrosis resulting in
enlargement and failure of the right ventricle
Life cycle

• Man is infected by cercaria in fresh water by skin penetration.

• The cercaria travel through the venous circulation to the heart, lungs and portal
circulation.
• In about 3 weeks, they mature and reach the mesenteric (S. japonicum and S.
mansoni) or the bladder (S. hematobium) vessels where they live and ovulate
for the duration of the host's life.
• Eggs germinate as they pass through the vessel wall into the intestine or
bladder and are excreted in feces (S. japonicum and S. mansoni) or urine (S.
hematobium).
• In fresh water, the larval miracidium hatches out of the egg and swims about
until it finds an appropriate snail.
• After two generations of multiplication in the snail, the fork-tailed cercariae
emerge into the water and infect another human.
•
Treatment and Control
▪ Praziquantel
▪ Contaminated water should be avoided.
▪ sanitary disposal of sewage and destruction of snails
▪ No vaccine is available.
 The male Schistosoma is much larger
than the female...
Male and female schistosomes.
 A 13-year-old boy with schistosomiasis (bilharziasis).
Hepatosplenomegaly, ascites, muscle atrophy, pyrexia,
anaemiaand haemorrhage from the gastrointestinal tract.
PROTOZOA

* eukaryotic, usually single-celled

•animal-like microorganisms (nutrient needs and
cellular structure
* most of them are free-living organisms found in
soil and water, some live in animal hosts
PROTOZOA

Reproduce asexually by the following means:

1. fission: One cell splits into two.

2. schizogony: A form of asexual reproduction characteristic of
certain protozoa, including sporozoa, in which daughter cells are
produced by multiple fission of the nucleus of the parasite
followed by segmentation of the cytoplasm to form separate
masses around each smaller nucleus.
3. budding: Buds form around a nucleus and pinch off of the
parent cell.
PROTOZOA
PROTOZOA
PROTOZOA
PROTOZOA

* Most are capable of locomotion by:

a) Pseudopods – cell extensions that flow in direction of
travel
b) Cilia – numerous short protrusions that propel
organisms through its environment
c) Flagella – extensions of cells that are fewer, longer
and more whiplike than cilia
Life Cycle Stages
 The stages of parasitic protozoa that actively
feed and multiply are frequently called
trophozoites; in some protozoa, other terms
are used for these stages. Cysts are stages with
a protective membrane or thickened wall.
Protozoan cysts that must survive outside the
host usually have more resistant walls than cysts
that form in tissues.
Entamoeba histolytica
DISEASE: Amebiasis; Amebic Dysentery; Extraintestinal amebic
abscesses
HOW ACQUIRED: Ingestion of cysts in contaminated water and
food
HOW DIAGNOSED: Observation of cysts and/or trophozoites in
fecal specimens; serology; nuclei have sharp central karyosome
and fine chromatin spikes
SIGNS/SYMPTOMS:
- Inverted, flask-shaped lesions in the large intestine with
extension to the peritoneum and liver, lungs, brain, and heart
- Blood and pus in the stools
- Liver abscesses (most severe complications)
Symptoms
Acute: Frequent dysentery with necrotic mucosa and abdominal pain.
Chronic: Recurrent episodes of dysentery with blood and mucus in the
feces. There are intervening gastrointestinal disturbances and
constipation. Cysts are found in the stool. The organism may invade
the liver, lung and brain where it produces abscesses that result in
liver dysfunction, pneumonitis, and encephalitis.
Treatment
Iodoquinol is used to treat asymptomatic infections and metronidazole
is used for symptomatic and chronic amebiasis, including extra-
intestinal disease.
Giardia lamblia (Flagellate)
DISEASE: Giardiasis
- ventral sucking disk attaches to lining of duodenal wall causing a
fatty, foul-smelling diarrhea
- diarrhea - malabsorption

HOW ACQUIRED: ingestion

of cysts in contaminated
water and food

HOW DIAGNOSED:
Observation of cysts and/
or trophozoites in fecal
specimens
Symptoms
▪ Early symptoms - flatulence, abdominal distension, nausea and foul-
smelling bulky, explosive, often watery, diarrhea. The stool contains
excessive lipids but very rarely any blood or necrotic tissue.
▪ Chronic stage is associated with vitamin B12 malabsorption,
disaccharidase deficiency and lactose intolerance.
Pathology
• Covering of the intestinal epithelium by the trophozoite and flattening
of the mucosal surface results in malabsorption of nutrients.
Immunology
▪ There is some role for IgA and IgM and there is increased incidence of
infection in immunodeficient patients (e.g.AIDS).
Morphology
Trophozoite: Giardia is a 12 to 15 micrometer, half pear-shaped organism
with 8 flagella and 2 axostyles arranged in a bilateral symmetry. There are
two anteriorly located large suction discs. The cytoplasm contains two
nuclei and two parabasal bodies
Cyst: Giardia cysts are 9 to 12 micrometer ellipsoidal cells with a smooth
well-defined wall. The cytoplasm contains four nuclei and many of the
structures seen in the trophozoite.
Diagnosis
▪ distinct from other dysenteries due to lack of mucus
and blood in the stool and lack of high fever.

Treatment
• Metronidazole
MASTIGOPHORA
Trichomonas vaginalis (Flagellate)
DISEASE: Trichomoniasis; causes about one-third of cases of
vaginitis
- Abnormal alkalinity of the vagina favors disease
- Asymptomatic
- Frothy, malodorous, yellow-green vaginal discharge
- Inflammation of the vagina (strawberry vagina), vulva, cervix
HOW ACQUIRED: trophozoites; sexual
contact; fomites

HOW DIAGNOSED: Observation of

trophozoites of vaginal or urethral
discharge or prostatic secretions in
methylene blue wet mount
Epidemiology
▪ 5% in normal females and as high as 70% among prostitutes
and prison inmates.
Morphology
▪ trophozoite(15 to 18 micrometers in diameter) and is half pear
shaped with a single nucleus, four anterior flagella and a lateral
flagellum attached by an undulating membrane. Two axostyles are
arranged asymmetrically. The organism does not encyst.

Symptoms
T. vaginalis infection is rarely symptomatic in men, although it may
cause mild urethritis or occasionally prostatitis. In women, it is
often asymptomatic, but heavy infections in a high pH environment
may cause mild to severe vaginitis with copious foul-smelling
yellowish, sometimes frothy discharge.
Symptoms:
Women with trichomoniasis may have:
 Vaginal fluid that smells bad and is greenish or yellowish

 Genital itching, burning, redness, or soreness

 Pain when they pee or have sex

 The need to pee more often

 Bleeding after sex

 Men with trichomoniasis may have:

 Itching or irritation inside their penis
 A thin white discharge from the penis
 Pain when they pee or have sex
 The need to pee more often
Treatment
▪ Metronidazole (although teratogenic) is effective in both males and
females.
▪ Vinegar douche may be useful.
▪ Personal hygiene and the use of condoms are helpful.
Trypanosoma brucie
DISEASE: African Trypanosomiasis (African Sleeping Sickness)
HOW ACQUIRED: Injection of the parasite when a Tsetse fly takes a
blood meal
HOW DIAGNOSED: Observation of trypano-mastigotes in blood or
CSF specimens or lymph node aspirates
Symptoms
▪ African trypanosomiasis can be divided into three stages: the bite
reaction (chancre), parasitemia (blood and lymphoid tissues), and
CNS stage.

Bite reaction: A non-pustular, painful, itchy chancre forms 1-3

weeks after the bite and lasts 1-2 weeks. It leaves no scar.
Parasitemia:
• Fever starts 2-3 weeks after the
bite
• Malaise
• Insomnia
• Headache
• Lymphadenopathy
• Edema
CNS Stage
• Changes in character and personality
• Lack of interest and disinclination to work
• Avoidance of acquaintances
• Morose and melancholic attitude alternating with exaltation
• Mental retardation and lethargy
• Low and tremulous speech
• Tremors of tongue and limbs
• Slow and shuffling gait
• Altered reflexes, etc.
• Males become impotent.
• The later stages are characterized by drowsiness and uncontrollable urge
to sleep.
• The terminal stage is marked by wasting and emaciation. Death results
from coma, intercurrent infection or cardiac failure.
Diagnosis
Parasite in the bloodstream, lymph secretions and enlarged lymph
node aspirate provides a definitive diagnosis in early (acute) stages.
The parasite in blood can be concentrated by centrifugation or by the
use of anionic support media. Cerebrospinal fluid must always be
examined for organisms.

Treatment and Control

• Blood stage - Pentamidine isethionate or Suramin but increase the
risk of CNS disease. Cases with CNS involvement should be treated
with Melarsoprol, an organic arsenic compound.
• The most effective means of prevention is to avoid contact with tsetse
flies. Vector eradication is impractical due to the vast area involved.
Immunization has not been effective due to antigenic variation.
Trypanosoma cruzi
DISEASE: American Trypanosomiasis (Chagas’ Disease)
HOW ACQUIRED: Parasites in the feces of a Reduviid (“kissing”) bug
get rubbed into bug bite wound
HOW DIAGNOSED: Observation of trypano-mastigotes in blood or CSF
specimens or lymph node aspirates; tissue biopsy

Trypanosoma cruzi, trypomastigote form,

in a blood smear (Giemsa stain)

Symptoms
• Primary lesion: The primary lesion, chagoma, appearing at the site of
infection, within a few hours of a bite, consists of a slightly raised, flat
non-purulent erythematous plaque surrounded by a variable area of
hard edema.
• It is usually found on the face, eyelids, cheek, lips or the conjunctiva, but may
occur on the abdomen or limbs.
• When the primary chagoma is on the face, there is an enlargement of the pre-
and post- auricular and the submaxillary glands on the side of the bite.
• Infection in the eyelid, resulting in a unilateral conjunctivitis and orbital edema
(Ramana's sign) is the commonest finding.
Acute Stage:
• The acute stage appears 7-14 days after infection.
• It is characterized by restlessness, sleeplessness, malaise, increasing
exhaustion, chills, fever and bone and muscle pains.
• Other manifestations of the acute phase are cervical, axillary and iliac
adenitis, hepatomegaly, erythematous rash and acute myocarditis.
Chronic Stage:
• The acute stage is usually not recognized and often resolves with little
or no immediate damage and the infected host remains an
asymptomatic carrier.
• An unknown proportion (guessed at 10-20%) of victims develop a
chronic disease. They alternate between asymptomatic remission
periods and relapses characterized by symptoms seen in the acute
phase.
• Cardiac arrhythmia is common.
Treatment:
- Nifurtimox or benznidazole
 Leishmania species
DISEASE: Leishmaniasis
HOW ACQUIRED: Injection of the parasite when a Phelobotomus sand fly
takes a blood meal
HOW DIAGNOSED: Observation of parasite in aspirates or biopsy
specimens
Symptoms
Visceral leishmaniasis (kala-azar, dumdum fever):
• L. donovani organisms in visceral leishmaniasis are rapidly eliminated
(rare local lesion)
• Minute papules have been described in children
• One to four months after infection, there is occurrence of fever, with a
daily rise to 102-104 degrees F, accompanied by chills and sweating.
• Spleen and liver enlarged
• With progression of the diseases, skin develops hyperpigmented
granulomatous areas (kala-azar means black disease).
Many children suffering
from visceral leishmaniasis
develop a noticeable
thickening, stiffening and
darkening of the eyelashes
and eyebrows.
Profile view of a teenage boy
suffering from visceral
leishmaniasis. The boy exhibits
A 12-year-old boy suffering from visceral
splenomegaly, distended abdomen
and severe muscle wasting. leishmaniasis. The boy exhibits
splenomegaly and severe muscle wasting.
Jaundiced hands of a visceral leishmaniasis
patient.
Enlarged spleen and liver in an
autopsy of an infant dying of visceral
leishmaniasis.
• Cutaneous leishmaniasis (Oriental sore, Delhi ulcer,
Baghdad boil):
• The organism (L. tropica) multiplies locally, producing of a papule,
1-2 weeks (or as long as 1-2 months) after the bite.
• Painless ulcer
• The center of the ulcer encrusts while satellite papules develop at
the periphery.
• The ulcer heals in 2-10 months, even if untreated but leaves a
disfiguring scar
• Mucocutaneous leishmaniasis (espundia, Uta,
chiclero):
• The initial symptoms of mucocutaneous leishmaniasis are the same
as those of cutaneous leishmaniasis, except that in this disease the
organism can metastasize and the lesions spread to mucoid (oral,
pharyngeal and nasal) tissues and lead to their destruction and
hence severe deformity. The organisms responsible
areL. braziliensis, L. mexicana and L. peruviana.
Diagnosis
• Diagnosis is based on a history of exposure to
sandfies, symptoms and isolation of the organisms
from the lesion aspirate or biopsy, by direct
examination or culture.
• A skin test (delayed hypersensitivity: Montenegro test)
and detection of anti-leishmanial antibodies by
immuno-fluorescence are indicative of exposure.

Treatment and Control

• Sodium stibogluconate (Pentostam) is the drug of
choice.
• Pentamidine isethionate is used as an alternative.
• Control measures involve vector control and avoidance.
• Immunization has not been effective.
NEMATODES
INTESTINAL NEMATODES

1 Plasmodium falciparum

2 Plasmodium malariae

3 Plasmodium ovale

4 Plasmodium vivax
Plasmodium species
DISEASE: Malaria
HOW ACQUIRED: Injection of sporozoites when a female Anopheles
mosquito takes a blood meal
HOW DIAGNOSED: Observation of trophozoites, schizonts, and/or
gametocytes in blood specimens; antigen testing

SCHIZONTS

 STAGES OF INFECTION

1. Infection (Anopheles mosquito):

- Injects sporozoite into blood to liver
2. Liver phase (7-14 days)
- Schizont to merozoite (all)
2*- hypnozoite (P. ovale and P. vivax)
3. RBC phase
3a. Merozoites infects RBC
3b. Trophozoites lyse RBC thus infects RBC
3c. Gametocytes taken up by mosquito
Symptoms
• Incubation period: 10-30 days
• Parasite load becomes significant: headache, lassitude, vague
pains in the bones and joints, chilly sensations and fever.
• Disease progresses: Chills and fever become more prominent.
The chill and fever follow a cyclic pattern (paroxysm) with the
symptomatic period lasting 8-12 hours. In between the
symptomatic periods, there is a period of relative normalcy,
the duration of which depends upon the species of the
infecting parasite.
• Without treatment, all species of human malaria may
ultimately result in spontaneous cure except with P.
falciparum which becomes more severe progressively
and results in death.
• This organism causes sequestration of capillary
vasculature in the brain, gastrointestinal and renal
tissues.
• Chronic malaria results in splenomegaly, hepatomegaly
and nephritic syndromes.

• P. Malariae produces fever every 72 hrs or 3 days which

is the so called Quartan malaria.
• P. vivax and P. Ovale produces fever every 48 hours
hence called the Tertian malaria.
• P. falciparum produces fever every 36-48 hours which
is also known as Malignant tertian malaria.
 TREATMENT AND CONTROL

• Treatment is effective with various quinine derivatives (quinine

sulphate, chloroquine, meflaquine and primaquine, etc.).
• Drug resistance, particularly in P. falciparum and to some extent in P.
vivax is a major problem.
• Control measures are eradication of infected anopheline mosquitos.
• Vaccines are being developed and tried but none is available yet for
routine use.
Toxoplasma gondii
DISEASE: Toxoplasmosis
HOW ACQUIRED: Ingestion of oocysts from cat feces or cysts in
contaminated meat
HOW DIAGNOSED: Immunodiagnostic procedures; tonsil and lymph
gland biopsy
Symptoms
• Congenital infections: Result in miscarriage, serious brain,
eye damage to the fetus, visual handicaps
• Although 58-70% of infected women will give birth to a
normal offspring, a small proportion of babies will develop
active retino-chorditis or mental retardation in childhood or
young adulthood.
• In immunocompetent adults: flu-like symptoms sometimes
associated with lymphadenopathy
• In immunocompromised individuals: generalized
parasitemia involvement of brain, liver lung and other
organs, and often death.
Treatment
• Acute infections benefit from pyrimethamine or
sulphadiazine.
• Spiramycin is a successful alternative.
• Pregnant women are advised to avoid cat litter and to
handle uncooked and undercooked meat carefully.
 Naegleria fowleri
DISEASE: Primary Amebic Meningo-encephalitis
HOW ACQUIRED: Diving into contaminated pond water
HOW DIAGNOSED: Observation of trophozoites in CSF or cysts in
autopsy tissue
 TREATMENT

• The treatment of choice for primary amoebic

meningoencephalitis (PAM), or infection with brain-eating
amoeba (Naegleria fowleri) is the antifungal amphotericin B.
• Some survivors in North America were treated with a
combination of drugs that included amphotericin B, rifampin,
fluconazole and a drug called miltefosine.
• Miltefosine is a drug approved for treating leishmaniasis, a
parasitic disease that’s spread by sandflies.
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