PROJECT

IN
PARASITOLOGY

Submitted To:
Dr. Ed De Vera
Submitted By:
Francesca Angela Nervar
BSN – 2
 THE
NEMATODES
EnterobiusVermicularis
TrichiurisTrichiura
AscarisLumbricoides
NecatorAmericanus
AncylostomaDuodenale
StrongyloidesStercoralis
TrichinellaSpiralis
DranculusMedinensis
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 Retroinfectiondefined 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
Dientamoebafragilis.
Laboratory Diagnosis:
The specimen of choice for the recovery of E. Vermicularisis 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 whipwormATP
production, causing energy depletion, immobilization, and finally death.
Other drugs that can be usedto 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:
Ascarislumbricoides, 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, mammillatedalbuminous covering, and measures 45 to 75μm in length by 35 to 50 μm in breadth.
Treatment and Prevention:
albendazole, mebendazole, levamisole and pyrantelpamoate. Other effective agents include tribendimidine
and nitazoxanide.Pyrantelpamoate may induce intestinal obstruction in a heavy worm load. Albendazoleis
contraindicated during pregnancy and children under two years of age.Thiabendazole may cause
miPrevention 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 anunembryonated 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 Ancylostomaduodenale 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 Strongyloidesstercoralis 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
DranculusMedinensis. 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. medinensisis 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
FasciolopsisBuski
Fasciola Hepatica
ClonorchisSinensis
HeterophytesHeterophytes
MetagonimusYokogawai
ParagonimusWestermani
SchistosomaMansoni
SchistosomaJaponicum
SchistosomaHaematobium
FASCIOLOPSIS BUSKI:

Life Cycle:
Immature eggs are discharged into the intestine and stool. Eggs become embryonated in water, eggs
release miracidia, which invade a suitable snail intermediate host. In the snail the parasites undergo
several developmental stages (sporocysts, rediae, and cercaria)
Transmission and Pathogenesis:
Transmission of parasite occurs by swallowing the infected aquatic vegetation. When infected plants or its
fruits are peeled with the teeth and swallowed by primary host infection is caused.
The disease caused by F. buski is known as fasciolopsiasis, which is characterized by mild anemia, chronic
diarrhea and asthenia (Lack of strength and energy). The adult worm causes gastro-intestinal irritation,
nausea and vomiting. At the point of attachment of the parasite to the intestinal wall, localized inflammation,
hemorrhage and abscess may occur. Incubation period is 3 to 6 months.
Laboratory Diagnosis:
Microscopic identification of eggs, or more rarely of the adult flukes, in the stool or vomitus is the basis of
specific diagnosis.  The eggs are indistinguishable from those of Fasciola hepatica.
Treatment and Prevention:
Praziquantel is the drug of choice for most intestinal fluke infections, although niclosamide has been
reported to have some in vitro efficacy.
Infection can be prevented by immersing vegetables in boiling water for a few seconds to kill the infective
metacercariae, avoiding the use of untreated feces ("nightsoil") as a fertilizer, and maintenance of proper
sanitation and good hygiene. Additionally, snail control should be attempted.

FASCIOLA HEPATICA:
Life Cycle:
Fasciola hepatica occurs in the liver of a definitive host and its lifecycle is indirect. Definitive hosts of the
fluke are cattle, sheep, and buffaloes. Wild ruminants and other mammals, including humans, can act as
definitive hosts as well. The life cycle of F. hepatica goes through the intermediate host and several
environmental larval stages.
Transmission and Pathogenesis:
Digenean trematodes have indirect life-cycles, involving mammalian definitive hosts and molluscan
intermediate hosts. Transmission between the two hosts occurs within water, via the formation of motile
and encysted larval stages.
Infections have been associated with two types of liver disease in domestic animals: acute or subacute
necrotic disease due to juvenile flukes; and chronic fibrotic disease due to adult flukes. Penetration of the
liver capsule by immature flukes generally does not cause much damage, but their subsequent migration
through the liver parenchyma may cause significant necrosis (liver rot).
Laboratory Diagnosis:
The standard way to be sure a person is infected with Fasciola is by seeing the parasite. This is usually
done by finding Fasciola eggs in stool (fecal) specimens examined under a microscope.
Treatment and Prevention:
Drug of choice are Bithionol or Triclabendazol. Infection by Fasciola hepatica can be preventing by not
consuming raw plants containing metacercariae. This can be accomplishes by inspecting the plants,
especially watercress, very carefully for the metacercariae or more effectively by not eating plants grown in
areas where herbivorous mammals (especially sheep) found. The contamination of water with feces from
infected animals or people in areas where the aquatic plants are use for food should be preventing.

CLONORCHIS SINENSIS:
Life Cycle:
The eggs of a C. sinensis are release through the biliary tract, and excreted out along with the feces. The
eggs are embryonated and contain the larvae called miracidia. Unlike most other flukes in which the
miracidia undergo development and swim in water to infect suitable host, the eggs of C. sinensis are simply
deposit in water. The eggs are then eating up by snail.
Transmission and Pathogenesis:
The eggs of Clonorchis are ingesting by freshwater snails. After the eggs hatch, infected snails release
microscopic larvae that then enter freshwater fish. People infected by eating infected raw or undercooked
fish containing the larvae. Clonorchiasis is a food-borne parasitic disease caused by infection
with Clonorchis sinensis (C. sinensis). Mammals are often infected with C. sinensis by consuming raw or
uncooked fish or shrimp containing infectious metacercaria.
Laboratory Diagnosis:
Infection is detected mainly on identification of eggs by microscopic demonstration in feces or
in duodenal aspirate. But other sophisticated methods have been developed such as ELISA, which has
become the most important clinical technique. Diagnosis by detecting DNAs from eggs in feces are also
developed using PCR, real-time PCR, and LAMP, which are highly sensitive and specific. Imaging
diagnosis is studies in depth and is now widely used.
Treatment and Prevention:
Praziquantel(Distocide), the Korean product, was tested for its safety and efficacy in treatment of
Clonorchis sinensis infection during the period from April to September, 1983 in Korea.
Avoid ingestion of fresh water fish.

HETEROPHYTES HETEROPHYTES:
Life Cycle:
The adult flukes live burrowed between the villi of the host's small intestine. It only takes around 4 to 6
hours for H. heterophyes to get to the small intestines in the definitive host and even faster in hosts that it
does not prefer.[6] The eggs that are lay contain a miracidium but do not hatch until they are ingest by
a snail
Transmission and Pathogenesis:
People at high risk for infection are those who live by bay waters including fishermen. Infection is acquire
by eating raw fish, a common food in areas of heavy endemicity. In endemic areas, people who live near
lake or river bank usually have a higher rate and intensity of infection than those living a distance from such
areas. It is possible that inhabitants of these areas eat more low-salted or improperly cooked fish and that
their fish are obtaining from polluted water. Each worm causes a mild inflammatory reaction at its site of
contact with the intestine. In heavy infection that are common causes damages to the mucosa and produce
intestinal pain and mucosa diarrhea. 
Laboratory Diagnosis:
Diagnosis done by stool examination is difficult when adult worms are not present because the eggs are
hard to distinguish from C.sinensis.
Treatment and Prevention:
Praziquantel, a quinolone derivative. The effect of praziquantel on H. heterophyes causes deep lesions on
their teguments, and when exposed to praziquantel over a longer period of time leads to even deeper
lesions.

METAGONIMUS YOKOGAWAI:
Life Cycle:
The life cycle of Metagonimus yokogawai will be examined, however, it should be noted Metagonimus
takahashii and Metagonimus miyatai follow similar life cycle pattern. All three species
are hermaphroditic and capable of self-fertilization. Embryonated eggs are passed into an aquatic
environment (fresh or brackish water) each containing a fully developed larva, called a miracidium.
Transmission and Pathogenesis:
Infection is acquired through the secondary intermediate host, fish, that haven’t been thoroughly cooked.
Metacercariae encyst under the scales or in the flesh of fish from fresh or brackish water. 
Laboratory Diagnosis:
Metagonimiasis is diagnosed by eggs seen in feces.  ELISA tests to diagnose metagonimiasis implied that
simultaneous screening of specific antibodies to several parasite agents are important in serological
diagnosis of acute parasitic disease and more research should be done on the efficacy of these methods of
diagnosis.
Treatment and Prevention:
Praziquantel is recommended in both adult and pediatric cases with dosages of 75 mg/kg/d in 3 doses for 1
day. Praziquantel is a Praziniozoquinoline derivative that alters the calcium flux through the
parasite tectum and causes muscular paralysis and detachment of the fluke. 
One is to control the intermediate host (snails). This can be done through use of molluscidals. Another is to
use education to ensure all people, especially in areas were the disease regularly occurs, fully cook all
fish. 

PARAGONIMUS WESTERMANI:
Life Cycle:
Unembryonated eggs are passed in the sputum of a human or feline. Two weeks later, miracidia develop in
the egg and hatches. The miracidia penetrate its first intermediate host (snail). Within the snail mother
sporocyst form and produce many mother rediae, which subsequently produce many daughter rediae
which shed crawling cercariae into fresh water.
Transmission and Pathogenesis:
Transmission of the parasite P. westermani to humans and mammals primarily occurs through the
consumption of raw or undercooked seafood.
Reservoir hosts of Paragonimus spp. include numerous species of carnivores including felids, canids,
viverrids, mustelids, some rodents and pigs. Humans become infected after eating raw freshwater
crabs or crayfish that have been encysted with the metacerciaria.
Laboratory Diagnosis:
Diagnosis is based on microscopic demonstration of eggs in stool or sputum, but these are not present until
2 to 3 months after infection. Radiological methods can be used to X-ray the chest cavity and look for
worms.
Treatment and Prevention:
praziquantel is the drug of choice to treat paragonimiasis.Bithionol is an alternative drug for treatment of
this disease but is associated with skin rashes and urticaria.

SCHISTOSOMA MANSONI:
Life Cycle:
After the eggs of the human-dwelling parasite are emitted in the faeces and into the water, the
ripe miracidium hatches out of the egg. The hatching happens in response to temperature, light and dilution
of faeces with water. The miracidium searches for a suitable freshwater snail belonging to the
genus Biomphalaria.
Transmission and Pathogenesis:
Schistosome eggs, which may become lodged within the hosts tissues, are the major cause of pathology in
schistosomiasis. Some of the deposited eggs reach the outside environment by passing through the wall of
the intestine; the rest are swept into the circulation and are filtered out in the periportal tracts of the liver,
resulting in periportal fibrosis.
Laboratory Diagnosis:
The presence of S. mansoni is detecting by microscopic examination of parasite eggs in stool. A staining
method called Kato-Katz technique is use for stool examination. It involves methylene blue-
stained cellophane soaked in glycerine or glass slides.
Treatment and Prevention:
Avoid swimming or wading in freshwater when you are in countries in which schistosomiasis occurs.
Swimming in the ocean and in chlorinated swimming pools is safe. Drink safe water.
There are two drugs available, praziquantel and oxamniquine, for the treatment of schistosomiasis.

SCHISTOSOMA JAPONICUM:
Life Cycle:
The life cycles of Schistosoma japonicum and Schistosoma mansoni are very similar. In brief, eggs of the
parasite are released in the feces and if they come in contact with water they hatch into free-swimming
larva, called miracidia. The larva then has to infect a snail of the genus Oncomelania such as species
of Oncomelania hupensis within one or two days. 
Transmission and Pathogenesis:
Once the parasite has entered the body and begun to produce eggs, it uses the hosts' immune system
(granulomas) for transportation of eggs into the gut. The eggs stimulate formation of granuloma around
them. The granulomas, consisting of motile cells, carry the eggs to the intestinal lumen. When in the lumen,
granuloma cells disperse leaving the eggs to be excreted within feces.
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.
Treatment and Prevention:
The therapy of choice is praziquantel, a quinolone derivative. Praziquantel is generally administered in an
oral form in one or two doses from 40–60 mg/kg body weight.
Human waste should be hygienically disposed of. Human waste in water with the Oncomelania snail
intermediate host is a major cause to the perpetuation of schistosomiasis. To prevent this from occurring,
human waste should never be used for nightsoiling (fertilization of crops with human waste) and unsanitary
conditions should be improved

SCHISTOSOMA HAEMATOBIUM:
Life Cycle:
S. haematobium completes it life cycle in humans, as definitive hosts, and freshwater snails, as
intermediate hosts, just like other schistosomes. But unlike other schistosomes that release eggs in the
intestine, it releases its eggs in the urinary tract and excrete along with the urine. In stagnant freshwater,
the eggs hatch within 15 minutes into the larvae called miracidia.
Transmission and Pathogenesis:
Normal infection of adults does not produce symptoms. When eggs are released, they sometimes become
permanently stuck in the bladder and cause pathological symptoms. The eggs are initially deposited in
the muscularis propria which leads to ulceration of the overlaying tissue.
Laboratory Diagnosis:
Traditionally, diagnoses has been made by examination of the urine for eggs. In chronic infections, or if
eggs are difficult to find, an intradermal injection of schistosome antigen to form a wheal is effective in
determining infection.
Treatment and Prevention:
The main cause of schistomiasis is the dumping of human waste into water supplies. Hygienic disposal of
waste would be sufficient to eliminate the disease.[28] Water for drinking bathing should be boiled in
endemic regions. Infested water should be avoided.
The therapy of choice is praziquantel, a quinolone derivative. Praziquantel is generally administered in an
oral form in one or two doses from 40–60 mg/kg body weight.
 THE
CESTODES
TaeniaSaginata
TaeniaSolium
HymenolepsisDiminuta
Hymenolepsis Nana
DipylidiumCaninum
DiphyllobothriumLatum
EchinococcusGranulosus

TAENIA SAGINATA:
Life Cycle:
Cattle acquire the embryonated eggs, the oncospheres, when they eat contaminated food. Oncospheres
enter the duodenum, the anterior portion of the small intestine, and hatch there under the influence
of gastric juices. The embryonic membranes are removed, liberating free hexacanth ("six-hooked") larvae.
Transmission and Pathogenesis:
Cows are the intermediate host for T. saginata with the larvae predominantly found in the muscle. Humans
can also act as an intermediate host for T. solium. Cysticercosis results from human ingestion of
T. solium eggs through fecal contamination, reverse peristalsis of gravid proglottids, or autoinfection.
Laboratory Diagnosis:
The basic diagnosis is done from a stool sample. Feces are examined to find parasite eggs.
Treatment and Prevention:
Taenaisis is easily treated with praziquantel (5–10 mg/kg, single-administration) or niclosamide (adults and
children over 6 years: 2 g, single-administration after a light breakfast, follow after 2 hours by a laxative;
children aged 2–6 years: 1 g; children under 2 years: 500 mg). Albendazole is also highly effective for
treatment of cattle infection. Adequate cooking at 56 °C (133 °F) for 5 minutes of beef viscera destroys
cysticerci. Refrigeration, freezing at −10 °C (14 °F) for 9 days or long periods of salting is lethal to
cysticerci. Inspection of beef and proper disposal of human excreta are also important measures.

TAENIA SOLIUM:
Life Cycle:
The life cycle of T. solium is indirect. It passes through pigs or other animals, as intermediate hosts, into
humans, as definitive hosts. In humans the infection can be relatively short or long lasting, and in the latter
case if reaching the brain can last for life. 
Transmission and Pathogenesis:
The pork tapeworm Taenia solium may cause two different infections in humans, intestinal taeniasis (the
intestinal infection with the adult tapeworm), and cysticercosis (a tissue infection with the cystic larvae or
cysticercus). Occurs when humans eat raw or undercooked, infected pork.
Laboratory Diagnosis:
Made by examination of stool samples
Treatment and Prevention:
For intestinal infection: Praziquantel or niclosamide. For neurocysticercosis: Corticosteroids,
anticonvulsants, and sometimes albendazole or praziquantel and/or surgery.
Infection by Taenia solium adults can be prevented by fully cooking pork before eating it. Prevention of
cysticercosis includes the prompt identification and removal of adult infections to eliminate the possibility of
autoinfection.

HYMENOLEPSIS DIMINUTA:
Life Cycle:
The cycle begins as arthropods ingest the eggs. Arthropods are then able to act as the intermediate host.
When ingested, the eggs develop into cysticercoids. As shown in the CDC life cycle, oncospheres hatch
and then penetrate the intestinal wall.
Transmission and Pathogenesis:
As the definitive host (rats) eats an infected arthropod, cysticercoids present in the body cavity transform
into the adult worm. The resulting eggs are then passed through the stool. In recent findings, beetle-to-
beetle transmission of H. diminuta can be seen via the feces.
Laboratory Diagnosis:
Stool:  The standard O&P examination is the recommended procedure for recovery and identification of H.
diminuta  eggs in stool specimens, primarily from the wet preparation examination of the concentration
sediment.
Treatment and Prevention:
Since the infection is acquired from the accidental ingestion of the infected intermediate arthropod hosts,
avoidance of this type of exposure is recommended. Possible situations include swallowing ectoparasites
from the rodent host or accidentally ingesting beetles in precooked cereals. Rat control programs might
also decrease the possibility of human exposure.

HYMENOLEPSIS NANA:
Life Cycle:
Infection is acquired most commonly from eggs in the feces of another infected individual, which are
transferred in food, by contamination. Eggs hatch in the duodenum, releasing oncospheres, which
penetrate the mucosa and come to lie in lymph channels of the villi. An oncosphere develops into a
cysticercoid which has a tail and a well-formed scolex.
Transmission and Pathogenesis:
H. nana eggs are passed through the stool of human hosts. These eggs are then consumed by rats or
humans through contaminated food or water. H. diminuta is thought to be passed to humans most often
through the ingestion of insects in dried grains or cereal.
Laboratory Diagnosis:
Diagnosis for hymenolepiasis is done by examining stool for eggs. The proglottids that are disintegrated in
the intestine cannot be detected. Egg output can be sporadic so a couple of stool tests a few days apart
may be needed to diagnose the infection.
Treatment and Prevention:
The prescription drug Praziquantel is usually prescribed in a single dose to patients suffering from infection
of H.nana.Praziquantel is widely used and preferred due to its high efficacy.

DIPILYDIUM CANIMUM:
Life Cycle:
The definitive host within this lifecycle is primarily canines, and occasionally felines, and in rare cases
young children. The intermediate hosts include fleas (Ctenocephalides spp.) and chewing lice. The first
stage in the lifecycle is when the gravid proglottids are either passed out through fecal matter, or actively
crawl out of the anus of the host. The gravid proglottids once out of the definitive host release eggs. 
Transmission and Pathogenesis:
Dipylidiasis is a common tapeworm infection of dogs and cats caused by Dipylidium caninum. ... Humans
become infected by accidental ingestion of dog or cat fleas that contain D caninum cysticercoids (larva).
The risk of infection to humans is low.
Laboratory Diagnosis:
Scooting behaviour seen in infected dogs is due to anal pruritis caused by motile gravid segments passing
through their anus.
Treatment and Prevention:
As with most tapeworm infections, the drugs of choice are niclosamide or praziquantel. The best way to
prevent human infection is to treat infected animals with products which aid in killing the fleas on the
animal. You can also use oral medication prescribed by a veterinarian.

DIPHYLLOBOTHRIUM LATUM:
Life Cycle:
Adult tapeworms may infect humans, canids, felines, bears, pinnipeds, and mustelids, though the accuracy
of the records for some of the nonhuman species is disputed. Immature eggs are passed in feces of the
mammal host (the definitive host, where the worms reproduce). After ingestion by a suitable
freshwater crustacean such as a copepod (the first intermediate host), the coracidia develop
into procercoid larvae.
Transmission and Pathogenesis:
Approximately four out of five cases are asymptomatic and may go many years without being detected.In a
small number of cases, this leads to severe vitamin B12 deficiency due to the parasite absorbing 80% or
more of the host’s B12 intake, and a megaloblastic anemia indistinguishable from pernicious anemia. The
anemia can also lead to subtle demyelinative neurological symptoms (subacute combined degeneration of
spinal cord). Infection for many years is ordinarily required to deplete the human body of vitamin B-12 to the
point that neurological symptoms appear.
Laboratory Diagnosis:
Diagnosis is usually made by identifying proglottid segments, or characteristic eggs in the feces.
Treatment and Prevention:
The standard treatment for diphyllobothriasis, as well as many other tapeworm infections is a single dose
of Praziquantel, 5–10 mg/kg PO once for both adults and children. An alternative treatment is Niclosamide,
2 g PO once for adults or 50 mg/kg PO once.

ECHINOCOCCUS GRANULOSUS:
Life Cycle:
E. granulosus is ingested and attaches to the mucosa of the intestines in the definitive host and there the
parasite will grow into the adult stages. Adult E. granulosus release eggs within the intestine which will be
transported out of the body via feces. When contaminated waste is excreted into the environment,
intermediate host has the potential to contract the parasite by grazing in contaminated pasture,
perpetuating the cycle.
Transmission and Pathogenesis:
E. granulosus is transmitted from the intermediate host (sheep) to the definitive host (dogs) by frequent
feeding of offal, also referred to as “variety meat” or “organ meat”. Consuming offal containing E.
granulosus can lead to infection; however, infection is dependent on many factors.
Laboratory Diagnosis:
Diagnosis in the definitive host, the dog, may be done by post mortem examination of the small intestine, or
with some difficulty ante mortem by purging with arecoline hydrobromate. Detection of antigens in feces
by ELISA is currently the best available technique.
Treatment and Prevention:
In order to prevent transmission to dogs from intermediate hosts, dogs can be given anthelminthic
vaccinations. In the case of intermediate hosts, especially sheep, these anthelminthic vaccinations do
cause an antigenic response—meaning the body produces antibodi avinash response—however it does
not prevent infection in the host.

ENTAMOEBA HISTOLYTICA:
Life Cycle:
Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water,
or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the
large intestine.
Transmission and Pathogenesis:
The active (trophozoite) stage exists only in the host and in fresh loose feces; cystssurvive outside the host
in water, in soils, and on foods, especially under moist conditions on the latter. The infection can occur
when a person puts anything into their mouth that has touched the feces of a person who is infected with E.
histolytica, swallows something, such as water or food, that is contaminated with E. histolytica, or swallows
E. histolytica cysts (eggs) picked up from contaminated surfaces or fingers.
Laboratory Diagnosis:
Diagnosis is confirmed by microscopic examination for trophozoites or cysts in fresh or suitably preserved
faecal specimens, smears of aspirates or scrapings obtained by proctoscopy, and aspirates of abscesses
or other tissue specimen. A blood test is also available but is only recommended when a healthcare
provider believes the infection may have spread beyond the intestine (gut) to some other organ of the body,
such as the liver. 
Treatment and Prevention:
Intestinal infection: Usually nitroimidazole derivatives (such as metronidazole) are used because they are
highly effective against the trophozoite form of the amoeba. Since they have little effect on amoeba cysts,
usually this treatment is followed by an agent (such as paromomycin or diloxanide furoate) that acts on the
organism in the lumen. Liver abscess: In addition to targeting organisms in solid tissue, primarily with drugs
like metronidazole and chloroquine, treatment of liver abscess must include agents that act in the lumen of
the intestine (as in the preceding paragraph) to avoid re-invasion. Surgical drainage is usually not
necessary except when rupture is imminent.
 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:
The average adult worm lifespan is fifteen years and mature females can produce between 500 and 1,500
microfilariae per day. The normal microfilariae lifespan is 1 to 1.5 years; however, their presence in
the bloodstream causes little to no immune response until death or degradation of the microfilariae or adult
worms.
Transmission and Pathogenesis:
Onchocerciasis, or River Blindness, is a neglected tropical disease (NTD) caused by the parasitic
wormOnchocerca volvulus. It is transmitted through repeated bites by blackflies of the genus Simulium. ...
Worldwide onchocerciasis is second only to trachoma as an infectious cause of blindness.
Laboratory Diagnosis:
Slit lamp eye exam can be used to visualize microfilariae in individuals with eye disease. There are
antibody tests that can assist in the diagnosis ofonchocerciasis, though many are not available outside the
research setting. In general thediagnosis of O. volvulus infection should be made with skin snip.
Treatment and Prevention:
The recommended treatment is ivermectin, which will need to be given every 6 months for the life span of
the adult worms or for as long as the infected person has evidence of skin or eye infection. Ivermectin kills
the larvae and prevents them from causing damage but it does not kill the adults.

MANSONELLA OZZARDI:
Life Cycle:
An arthropod (black fly or biting midge) will take a blood meal from a human and will insert its third-stage
filarial larvae into the human host. The larvae will then become adults and will inhabit the peritoneal spaces
and adjacent locations. The adults will mate and produce unsheathed microfilariae.
Transmission and Pathogenesis:
M. ozzardi is transmitted by two types of arthropods that feed on the blood of humans: biting midges
(genus Culicoides) and blackflies (genus Simulium). In the Caribbean, M. ozzardi uses the biting midge as
its intermediate host. The black fly serves as the intermediate host for the filariae parasite in the Amazon
Basin and mainland South America.
Laboratory Diagnosis:
Microscopic examination is the most practical diagnostic tool used to identify the M. ozzardi microfilariae in
blood samples from infected patients. Blood smears are usually stained with haematoxylin or Giemsa to
visualize the worms under the microscope
Treatment and Prevention:
Ivermectin is the treatment of choice for M. ozzardi infections. It is a potent macrocyclic lactone that binds
to chloride channels, which then open and allow chloride ions to enter the affected cells.

MANSONELLA PERSTANS:
Life Cycle:
During a blood meal, an infected midge (Culicoides grahami and C. austeni) introduces third-stage (L3)
filarial larvae onto the skin of the human host, where they penetrate into the bite wound. Body heat likely
activates the larvas and prompts them to leave the vector and actively penetrate the skin
Transmission and Pathogenesis:
M. perstans is transmitted by the bite of species of Culicoides midges. Only the female midges take blood
meals, because the blood is needed for the maturation of eggs within the female.
Laboratory Diagnosis:
Similar to other filarial parasites, M. perstans is diagnosed by the identification of microfilariae in the
peripheral blood. Because the microfilariae are present in the peripheral blood in almost equal
concentrations during day and night, blood samples can be obtained at any time (unlike other filarial
microfilariae). The microfilariae are short and thin, unsheathed, and have rounded tails with nuclei at the
extremity.
Treatment and Prevention:
M. perstans is one of the most difficult human filarial infections to treat. Effective treatment for
mansonelliasis is lacking, with no consensus among the scientific community on the optimal
approach. Numerous trials evaluating traditional antifilarial drugs such as ivermectin and DEC, as well as
other benzimidazoles such as mebendazole, albendazole, levamisole, and thiabendazole, have been
conducted. Recently, clinical trials assessing the effectiveness of doxycycline to treat M. perstansinfection
have also been documented.

MANSONELLA STREPTOCERCA:
Life Cycle:
The contraction of an M. streptocerca infection can be better understood through an understanding of its
life cycle. The life cycle involves two stages: one involving a midge (genus Culicoides) and another
involving a human host. 
Transmission and Pathogenesis:
It is transmitted to the human host by biting midges (Culicoides spp.). The pathology of streptocerciasis is
both dermal and lymphatic.
Laboratory Diagnosis:
The infection of these roundworms typically causes no symptoms but may sometimes cause a mild
dermatitis of the thorax and shoulders. M. streptocerca infections fortunately do not cause any nodules,
skin disease, or ocular infections like that of Onchocerca volvulus. Due to the absence of nodules,
differentiating between M. streptocerca and O. volvulvus infections are easier to diagnose.
Treatment and Prevention:
Treatment of streptocerciasis includes the use of diethylcarbamazine (DEC) which is reportedly effective
against the microfilarial and adult stage M. streptocerca, but not proven as a method of treatment. Take
preventative measures by using DEET or other insect repellents to ward off midges when traveling into
endemic areas.

DIROFILARIA IMMITIS:
Life Cycle:
Heartworms go throughout several life stagesbefore they become adults infecting the pulmonary artery of
the host animal. The worms require the mosquito as an intermediate stage to complete their lifecycles.
Transmission and Pathogenesis:
Dogs show no indication of heartworm infection during the six-month prepatent period prior to the worms'
maturation, and current diagnostic tests for the presence of microfilariae or antigens cannot detect
prepatent infections. Rarely, migrating heartworm larvae get "lost" and end up in unusual sites, such as the
eye, brain, or an artery in the leg, which results in unusual symptoms such as blindness, seizures,
and lameness, but normally, until the larvae mature and congregate inside the heart, they produce no
symptoms or signs of illness.
Laboratory Diagnosis:
Microfilarial detection was accomplished most commonly in the past by the microscopic identification of
microfilariae on a direct blood smear, above the buffy coat in a microhematocrit tube (or capillary tube),
using the modified Knott test.
Treatment and Prevention:
Prevention of heartworm infection can be obtained through a number of veterinary drugs. The drugs
approved for use in the US are ivermectin (sold under the brand names Heartgard, Iverhart, and several
other generic versions), milbemycin(Interceptor Flavor Tabs and Sentinel Flavor Tabs)
and moxidectin (ProHeart) administered as pills or chewable tablets.