PROJECT

IN
PARASITOLOGY

Submitted To:
Dr. Ed De Vera
Submitted By:
Francesca Angela Nervar
BSN – 2
 THE
NEMATODES
Enterobius Vermicularis
Trichiuris Trichiura
Ascaris Lumbricoides
Necator Americanus
Ancylostoma Duodenale
Strongyloides Stercoralis
Trichinella Spiralis
Dranculus Medinensis
ENTEROBIUS VERMICULARIS:

Life Cycle:
Humans are the only host of E. Vermicularis. Pinworm infection, which is usually self-limiting. The eggs
migrate through the digestive tract into the small intestine, where they hatch and release young larvae. The
adult worms reside into the colon. These infective eggs may dislodge from the body, caused in part by
intense scratching of the anal area by the infected person. The infective eggs may survive a few days or up
to several weeks under suitable environmental condition. A Retroinfection defined in pinworm eggs that
migrate back into the host body, develop and reproduce rather that becoming dislodged. Autoinfection if
infective pinworm eggs are ingested via hand-to-mouth contamination.
Transmission and Pathogenesis:
Transmission of pinworm occurs by hand-mouth contamination, and responsible for the transmission of
Dientamoeba fragilis.
Laboratory Diagnosis:
The specimen of choice for the recovery of E. Vermicularis is a cellophane tape preparation collected from
the perianal region of the person suspected for the infection
Treatment and Prevention:
Drug of choice are Mebendazole or Pyrantelpamoate. Prevention and control measures include: Practicing
proper personal hygeine particularly handwashing; applying and ointment to and infective perianal area to
help prevent egg dispersal intothe environment and avoid scratching the infected area.
TRICHIURIS TRICHIURA:

Life Cycle:
Eggs are deposit from human feces to soil where, after two to three weeks, they become embryonated and
enter the “infective” stage. These infective embryonated eggs ingested and hatch in the human small
intestine exploiting the intestinal microflora as hatching stimulus. The life cycle from time of ingestion of
eggs to development of mature worms takes approximately three months.
Transmission and Pathogenesis:
Whipworms eggs are pass in the feces of infected persons, and if an infected person defecates outside or if
untreated human feces used as fertilizer, eggs are deposit on soil where they can mature into an infective
stage.
Laboratory Diagnosis:
The best way to diagnose whipworm infection is through the identification of characteristic football shaped
eggs in stool. However, since egg concentration may be low in light infections, the CDC recommends using
a concentration technique to collect eggs.
Treatment and Prevention:
Albendazole is also use to treat for other nematode infections and works by decreasing whipworm ATP
production, causing energy depletion, immobilization, and finally death.
Other drugs that can be used to treat whipworm are mebendazole, which works by selectively and
irreversibly blocking glucose uptake and other nutrients in the intestine where helminths dwell, and oxantel.
Infection is most common in areas with poor sanitation and tropical climates. Improved sanitation is the
most effective way to prevent the spread of whipworm infections.
ASCARIS LUMBRICOIDES:

Life Cycle:
Ascaris lumbricoides, a roundworm, infects humans when an ingested fertilised egg becomes a larval worm
(called rhabditiform larva) that penetrates the wall of the duodenum and enters the blood stream.
Unfertilized eggs may ingested but are not infective.
Transmission and Pathogenesis:
The pathogenesis of ascariasis is related to organ damage and host reactions to larval migration as well as
the number and location of adult worm in the body. Ascaris larvae migrating through the intestinal mucosa,
liver and lungs provoke hypersensitivity reaction in the human host. Some of the larvae may be immobilised
and covered with eosinophils, resulting in the formation of granulomas.
Laboratory Diagnosis:
Each female worm produces a daily output of 200,000 ova and hence direct smear examination of the stool
is sufficient for diagnosis of ascariasis. The fertile ovum is broadly oval, has a thick shell with an outer,
course, mammillated albuminous covering, and measures 45 to 75μm in length by 35 to 50 μm in breadth.
Treatment and Prevention:
albendazole, mebendazole, levamisole and pyrantel pamoate. Other effective agents include tribendimidine
and nitazoxanide. Pyrantel pamoate may induce intestinal obstruction in a heavy worm load. Albendazole is
contraindicated during pregnancy and children under two years of age. Thiabendazole may cause mi
Prevention is by improved access to sanitation which includes the use of properly functioning and clean
toilets by all community members as one important aspect.gration of the worm into the esophagus, so it is
usually combined with piperazine.
NECATOR AMERICANUS:

Life Cycle:
This worm starts out as an unembryonated egg in the soil. After 24–48 hours under favorable conditions,
the eggs become embryonated and hatch. This first juvenile stage 1 is known as 'rhabditiform'. The
rhabditiform larvae grow and molt in the soil, transforming into a juvenile stage 2. This larval form is able to
penetrate human skin, travel through the blood vessels and heart, and reach the lungs. The transformation
from rhabditiform to the filariform usually takes five to 10 days.
Transmission and Pathogenesis:
Once in the lymph nodes, the larvae starts entering the blood, lungs, and intestines. Some larva cannot
readily enter the dermis and remain trapped in the skin, causing skin irritation and cutaneous larva migrans.
Other symptoms include excessive coughing and dyspnea (short of breath) during larvae migration.
Laboratory Diagnosis:
The most common method for diagnosing N. americanus is through identification of eggs in a fecal sample
using a microscope. N. americanus eggs have a thin shell and are oval shaped, measuring roughly 56–74
by 36–40 μm.
Treatment and Prevention:
The most common treatment for N. americanus are benzimidazoles, specifically albendazole and
mebendazole. Benzimidazoles kill adult worms by binding to the nematode’s Beta-tubulin and subsequently
inhibiting microtubule polymerization within the parasite. Infection and transmission of others can be
prevented by not defecating outdoors or using human feces fertilizer. This parasite is not transmittable
directly from person to person.

ANCYLOSTOMA DUODENALE:
Life Cycle:
After a filariform "infective" larva penetrates the intact skin – most commonly through the feet – the larva
enters the blood circulation. It is then carried to the lungs, breaks into alveoli, ascends the bronchi and
trachea and is coughed up and swallowed back into the small intestine where it matures. The infective
rhabditiform larvae are able to sense vibrations in the soil from heat or carbon dioxide, and are able to use
dendritic processes similar to cilia. They use these processes as thermosensory, chemosensory, and
mechanosensory receptors in order to migrate towards a host for infection.
Transmission and Pathogenesis:
Transmission of Ancylostoma duodenale is by contact of skin with soil contaminated with larvae. A light
hookworm infection causes abdominal pain, loss of appetite and geophagy. Heavy infection causes severe
protein deficiency or iron deficiency anemia. Protein deficiency may lead to dry skin, edema and potbelly,
while iron deficiency anemia might result in mental dullness and heart failure. Women who are pregnant
and infected should be aware that this parasite is able to infect the fetus and can cause complications such
as low birth weight, maternal anemia, and infant mortality.
Laboratory Diagnosis:
Diagnosis depends on finding characteristic worm eggs on microscopic examination of the stools, although
this is not possible in early infection.
Treatment and Prevention:
The most common treatment for hookworm are benzimidazoles, specifically albendazole and
mebendazole.

STRONGYLOIDES STERCORALIS:
Life Cycle:
The strongyloid's life cycle is heterogonic—it is more complex than that of most nematodes, with its
alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication
within the host. The parasitic cycle is homogonic, while the free-living cycle is heterogonic. The heterogonic
life cycle is advantageous to the parasite because it allows reproduction for one or more generations in the
absence of a host.
Transmission and Pathogenesis:
Adult worms live in the small intestinal epithelial layer. The peculiar biological behavior of Strongyloides
stercoralis with its capacity to autoinfect is of critical importance in determining a successful outcome in the
treatment of strongyloidiasis and it provides the potential for massive, overwhelming strongyloidiasis to
supervene.
Laboratory Diagnosis:
Strongyloides should be considered in any patient with chronic gastrointestinal symptoms and eosinophilia.
The diagnosis is most commonly made by finding the characteristic larvae in stool.
Treatment and Prevention:
The drug of choice is Mebendazole. Prevention requires adherence to good personal hygiene, and
avoidance of contaminated food and water. Avoidance to human feces as fertilizer is necessary to prevent
infection.

TRICHINELLA SPIRALIS:
Life Cycle:
Is an infection of wild domestic mammals, specifically omnivores and carnivores. The pig, bear, cat, dog
and rat are the animals most commonly implicated in infections. Larval forms encyst within the striated
muscle of reservoir hosts and are transmit among host by predation.
Transmission and Pathogenesis:
Trichinosis is acquire by eating raw or undercooked meat containing the Trichinella larvae. The organisms
are liberated from the muscle following digestion of their capsules and go on mature and propagate.
Laboratory Diagnosis
Laboratory examination of muscle biopsy specimens revealing encysted larvae provide a confirmation of
Trichinella Infection.
Treatment and Prevention:
Mebendazole is the drug of choice for the treatment of trichinosis. Thiabendazole has also been use as
alternate therapy. Corticosteroids such as prednisone are beneficial in cases with severe symptomology.

DRANCULUS MEDINENSIS:
Life Cycle:
Human infection is initiating through the ingestion of water contaminated with infected copepods, genus
Cyclops. These tiny crustaceans, also known as water fleas, harbor the infective third stage larvae of
Dranculus Medinensis. Upon release, the larvae migrate through the duodenum wall, develop, mate, and
mature in the loose connective tissue. The entire process takes about a year.
Transmission and Pathogenesis:
Following the ingestion of the infected copepod, few or no clinical symptoms occur until just before the
blister forms. The gravid female worm’s migration to the skin may provoke localizes redness and pain. As
the blister forms there is an onset of fever and generalized allergic symptoms, including urticaria, intense
itching, asthma attacks, periorbital edema, nausea and vomiting.
Laboratory Diagnosis:
X-rays may be use to locate dead calcified worms in subcutaneous tissues.
Treatment and Prevention:
The traditional method for removal of the adult D. medinensis is to slow wind the worm around a stick a rate
of a few centimeters per day. Medical therapy with agents such as metronidazole or thiabendazole has
been limited to the relief of symptoms. Treatment suppresses inflammation and facilities removal of the
worm. Prevention depends on the provision of properly treated, safe, drinking water.
 THE
TREMATODES
Fasciolopsis Buski
Fasciola Hepatica
Clonorchis Sinensis
Heterophytes Heterophytes
Metagonimus Yokogawai
Paragonimus Westermani
Schistosoma Mansoni
Schistosoma Japonicum
Schistosoma Haematobium
FASCIOLOPSIS BUSKI:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
FASCIOLA HEPATICA:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:

CLONORCHIS SINENSIS:
Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:

HETEROPHYTES HETEROPHYTES:
Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:

METAGONIMUS YOKOGAWAI:
Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:

PARAGONIMUS WESTERMANI:
Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
SCHISTOSOMA MANSONI:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
SCHISTOSOMA JAPONICUM:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
SCHISTOSOMA HAEMATOBIUM:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
 THE
CESTODES
Taenia Saginata
Taenia Solium
Hymenolepsis Diminuta
Hymenolepsis Nana
Dipylidium Caninum
Diphyllobothrium Latum
Echinococcus Granulosus
TAENIA SAGINATA:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
TAENIA SOLIUM:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
HYMENOLEPSIS DIMINUTA:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
HYMENOLEPSIS NANA:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
DIPILYDIUM CANIMUM:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
DIPHYLLOBOTHRIUM LATUM:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
ECHINOCOCCUS GRANULOSUS:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
ENTAMOEBA HISTOLYTICA:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
 THE
FILARIAE
Wuchereria Bancrofti
Brugia Malayi and
Brugia Timori
Loa Loa
Onchocerca Volvulus
Mansonella Ozzardi
Mansonella Perstans
Mansonella Streptocerca
Dirofilaria Immitis
WUCHERERIA BANCROFTI:

Life Cycle:
Wuchereria Bancrofti was the first parasitic organism found to have an anthropod vector.
In the human host, infective larvae make their way into the peripheral lymphatics, undergoing two molts
before they mature in the regional lymph nodes and lymphatic vessels.
Transmission and Pathogenesis:
Each symptoms of bacrofian filariasis are fever, chills, lymphagitis, lymphadenitis, and eosinophilia. The
result is lymphedema, with hardening and thickening of the skin known as “elephantiasis”.
Laboratory Diagnosis:
Made by demonstration of characteristic microfilariae in peripheral blood or lymphatic fluid. Thick smears,
with Giemsa, are used for the detection of microfilariae. Centrifugation of fluid mixed in 2% formalin or
Knotts Technqiue.
Treatment and Prevention:
Treatment choice is diethylcabamazine (DEC). Glucocorticosteroids to help control the side effects.
Ivermectin is used to treat River blindness. Surgical procedures may be used for the treat lymphatic
obstruction, hydrocele, and scrotal elephantiasis. The use of personal protection in the form of insect
repellent, protective clothing and bed netting.

BRUGIA MALAYI AND BRUGIA TIMORI:

Life Cycle:
In the human host, infective larvae make their way into the peripheral lymphatics, undergoing two molts
before they mature into the lymph vessels, a process that may take up to 6 to 9 months. Microfilariae
exhibit either a nocturnal periodicity or sub-periodicity depending on geographical distribution.
Transmission and Pathogenesis:
Transmitted by a number of predominantly night feeding mosquitoes. Pathologic changes within the host
are result of the immune response to adult worms and not to the microfilariae.
Laboratory Diagnosis:
A definitive diagnosis are made by detecting the microfilariae in the blood or lymphatic aspirate.
Centrifugation using knott’s technique. Serologic testing, including elevated serum IgE Titers and elevated
antifilarial antibodies, as well as the presence of eosinophilia. Polymerase chain reaction based DNA
testing is also available.
Treatment and Prevention:
Diethylcarbamazine (DEC), usage of corticosteroids. The use of personal protection in the form of insect
repellent, protective clothing and bed netting.

LOA LOA:
Life Cycle:
Human loiasis is initiated by the bite of a number of Chrysops species, commonly known as mango or deer
flies. Microfilariae has a sheath covering and measure 200-300 micrometers in length. One diagnostic
feature for this organism is the presence of body nuclei that are continuous to the tip of microfilarial tail.
Transmission and Pathogenesis:
One characteristic clinical manifestations of loiasis is the development of episodic angioedema known as
calabar swellings the localized inflammatory reactions are by a host response either the worms metabolic
system or the worm itself.
Laboratory Diagnosis:
Examination of blood to determine microfilariae. Blood should be collected between 10AM to 2PM. Thick
and thin smears are prepared with Giemsa. Markedly elevated serum IgE.
Treatment and Prevention:
May be surgical or medical. Removal of surgical worm. Antihistamines and Anti-inflammatory drug to
reduce the side effects of DEC. Ivermectin is a effective microfilaricide.
ONCHOCERCA VOLVULUS:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
MANSONELLA OZZARDI:

Life Cycle:
Transmission and Pathogenesis:
Laboratory Diagnosis
Treatment and Prevention:
MANSONELLA PERSTANS: