LIFECYCLE OF NEMATODES

Lifecycle
Nematode

Enterobius vermicularis

Gravid adult female Enterobius vermicularis deposit eggs on perianal folds . Infection occurs via self-inoculation
(transferring eggs to the mouth with hands that have scratched the perianal area) or through exposure to eggs in the
environment (e.g. contaminated surfaces, clothes, bed linens, etc.) . Following ingestion of infective eggs, the larvae
hatch in the small intestine and the adults establish themselves in the colon, usually in the cecum . The time
interval from ingestion of infective eggs to oviposition by the adult females is about one month. At full maturity adult
females measure 8 to 13 mm, and adult males 2 to 5 mm; the adult life span is about two months. Gravid females migrate
nocturnally outside the anus and oviposit while crawling on the skin of the perianal area . The larvae contained inside
the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions .
Rarely, eggs may become airborne and be inhaled and swallowed. Retroinfection, or the migration of newly hatched larvae
from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown.

Wuchereria bancrofti

Different species of the following genera of mosquitoes are vectors of W. bancrofti filariasis depending on geographical
distribution. Among them are: Culex (C. annulirostris, C. bitaeniorhynchus, C. quinquefasciatus, and C.
pipiens); Anopheles (A. arabinensis, A. bancroftii, A. farauti, A. funestus, A. gambiae, A. koliensis, A. melas, A. merus, A.
punctulatus and A. wellcomei); Aedes (A. aegypti, A. aquasalis, A. bellator, A. cooki, A. darlingi, A. kochi, A.
polynesiensis, A. pseudoscutellaris, A. rotumae, A. scapularis, and A. vigilax); Mansonia (M. pseudotitillans, M.
uniformis); Coquillettidia (C. juxtamansonia). During a blood meal, an infected mosquito introduces third-stage filarial larvae
onto the skin of the human host, where they penetrate into the bite wound . They develop in adults that commonly
reside in the lymphatics . The female worms measure 80 to 100 mm in length and 0.24 to 0.30 mm in diameter, while
the males measure about 40 mm by .1 mm. Adults produce microfilariae measuring 244 to 296 μm by 7.5 to 10 μm, which
are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked
periodicity. The microfilariae migrate into lymph and blood channels moving actively through lymph and blood . A
mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and some of
them work their way through the wall of the proventriculus and cardiac portion of the mosquito’s midgut and reach the
thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective
larvae . The third-stage infective larvae migrate through the hemocoel to the mosquito’s prosbocis and can infect
another human when the mosquito takes a blood meal .
Ascaris lumbricoides
 Ascaris species are very large (adult females: 20 to 35 cm; adult males: 15 to 30 cm) nematodes (roundworms) that
parasitize the human intestine. A. lumbricoides is the primary species involved in human infections globally,
but Ascaris derived from pigs (often referred to as A. suum) may also infect humans. These two parasites are very closely
related, and hybrids have been identified; thus, their status as distinct, reproductively isolated species is a contentious
topic.
Adult worms live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day,
which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Larvae develop to infectivity
within fertile eggs after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm,
shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried
via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10 to 14 days), penetrate
the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they
develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the
adult female. Adult worms can live 1 to 2 years.

Ancylostoma
duodenale, A.
ceylanicum, and N
ecator americanus Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2 days
and become free-living in contaminated soil. These released rhabditiform larvae grow in the feces and/or the soil ,
and after 5 to 10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective
larvae can survive 3 to 4 weeks in favorable environmental conditions. On contact with the human host, typically bare feet,
the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate
into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the
jejunum of the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small
intestine, typically the distal jejunum, where they attach to the intestinal wall with resultant blood loss by the host .
Most adult worms are eliminated in 1 to 2 years, but the longevity may reach several years.

Intestinal hookworm disease in humans is caused by Ancylostoma duodenale, A. ceylanicum, and Necator
americanus. Classically, A. duodenale and N. americanus were considered the two primary intestinal hookworm species
worldwide, but newer studies show that a parasite infecting animals, A. ceylanicum, is also an important emerging parasite
infecting humans in some regions. Occasionally larvae of A. caninum, normally a parasite of canids, may partially develop
in the human intestine and cause eosinophilic enteritis, but this species does not appear to reach reproductive maturity in
humans.
Trichuris trichiura
 The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced
cleavage stage , and then they embryonate ; eggs become infective in 15 to 30 days. After ingestion (soil-
contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish
themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending
colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to
oviposit 60 to 70 days after infection. Female worms in the cecum shed between 3,000 and 20,000 eggs per day. The life
span of the adults is about 1 year.

Strongyloides
stercoralis
The Strongyloides stercoralis life cycle is complex, alternating between free-living and parasitic cycles and involving
autoinfection. In the free-living cycle: Rhabditiform larvae are passed in the stool of an infected definitive host ,
develop into either infective filariform larvae (direct development) or free-living adult males and females that
mate and produce eggs , from which rhabditiform larvae hatch and eventually become infective filariform (L3)
slarvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . This
second generation of filariform larvae cannot mature into free-living adults and must find a new host to continue the life
cycle.
Parasitic cycle: Filariform larvae in contaminated soil penetrate human skin when skin contacts soil , and migrate to
the small intestine . It has been thought that the L3 larvae migrate via the bloodstream and lymphatics to the lungs,
where they are eventually coughed up and swallowed. However, L3 larvae appear capable of migrating to the intestine via
alternate routes (e.g. through abdominal viscera or connective tissue). In the small intestine, the larvae molt twice and
become adult female worms . The females live embedded in the submucosa of the small intestine and produce eggs
via parthenogenesis (parasitic males do not exist) , which yield rhabditiform larvae. The rhabditiform larvae can either
be passed in the stool (see “Free-living cycle” above), or can cause autoinfection .

Dioctophyma renale
 Unembryonated eggs are shed in the urine of the definitive host and L1 larvae develop inside the egg after about a
month in water . After being eaten by the invertebrate intermediate host (oligochaete worms), the eggs hatch in the
digestive tract and mature into L3 larvae after two molts (usually 2—3 months at 20—30°C). If the intermediate host is
eaten by a paratenic host, the L3 larvae encyst in tissue and do not develop any further . Most commonly, the
definitive host becomes infected after eating a paratenic host with encysted L3 larvae Consuming infected
invertebrate intermediate hosts may also establish infection, but is probably not the major infection route in nature .
After being ingested by the definitive host, the infective larvae migrate through the gastric wall to the liver, and eventually to
the kidney (typically the right kidney). Larvae become adults approximately six months after ingestion by the definitive host.
Humans may also become infected after eating undercooked paratenic hosts . Although humans may serve as
definitive hosts with kidney infections, often the larvae migrate aberrantly, eventually becoming encapsulated in
subcutaneous nodules and ceasing further development.

Trichinella spiralis

Depending on the classification used, there are several species of Trichinella: T. spiralis, T. pseudospiralis, T. nativa, T.
murelli, T. nelsoni, T. britovi, T. papuae, and T. zimbabwensis, all but the last of which have been implicated in human
disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a
definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The
domestic cycle most often involved pigs and anthropophilic rodents, but other domestic animals such as horses can be
involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of
human infection are bear, moose and wild boar.

Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T.
pseudospiralis and T. papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin,
the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms .
Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about four weeks. After 1 week, the
females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on
clinical symptoms, and is confirmed by serology or identification of encysted or non-encysted larvae in biopsy or autopsy
specimens.
Capillaria hepatica
 Capillaria hepatica has a direct life cycle, with no intermediate host. It can develop with only one definitive host, but likely
requires two hosts to complete the life cycle. Adult worms are located deep within the liver parenchyma of the host, and lay
hundreds of eggs in the surrounding parenchymal tissue . The eggs trapped in the parenchyma can not be passed in
the feces of the host, and remain in the liver until the animal dies , or more likely, is eaten by a predator or scavenger
. Eggs ingested by scavengers are unembryonated (not infectious) and are passed in through the digestive tract into
and out in feces, providing an efficient mechanism to release eggs into the environment; this is ecologically the most likely
primary route of transmission . Eggs embryonate in the environment , where they require air and damp soil to
become infective. Under natural conditions, embryonation is slow and may take between 6 weeks and 5 months. The cycle
continues when embryonated eggs are eaten by a suitable mammalian host . Infective eggs hatch in the intestine,
releasing first stage larvae. The larvae penetrate the intestinal wall and migrate via the portal vein to the liver parenchyma
within 3-4 days. Larvae take about 3-4 weeks to mature into adults and mate. Humans are usually infected after ingesting
embryonated eggs in fecally-contaminated food, water, or soil .
Notably, the presence of C. hepatica eggs in human stool during routine ova-and-parasite (O&P) examinations indicates
spurious passage of ingested eggs, and not a true infection. Diagnosis in humans is usually achieved by finding adults and
eggs in biopsy or autopsy specimens.

Brugia malayi

During a blood meal, an infected mosquito (typically Mansonia spp. and Aedes spp.) introduces third-stage filarial larvae
onto the skin of the human host, where they penetrate into the bite wound . They develop into adults that commonly
reside in the lymphatics . The adult worms outwardly resemble those of Wuchereria bancrofti but are smaller. Female
worms measure 43 to 55 mm in length by 130 to 170 μm in width, and males measure 13 to 23 mm in length by 70 to 80
μm in width. Adults produce microfilariae, measuring 177 to 230 μm in length and 5 to 7 μm in width, which are sheathed
and have nocturnal periodicity (in some regions B. malayi may be sub-periodic, and note that microfilariae are usually not
produced in B. pahangi infections). The microfilariae migrate into lymph and enter the blood stream reaching the peripheral
blood . A mosquito ingests the microfilariae during a blood meal . After ingestion, the microfilariae lose their
sheaths and work their way through the wall of the proventriculus and cardiac portion of the midgut to reach the thoracic
muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage larvae .
The third-stage larvae migrate through the hemocoel to the mosquito’s proboscis and can infect another human when
the mosquito takes a blood meal .
Angiostrongylus
cantonensis
 Adult worms of A. cantonensis live in the pulmonary arteries and right ventricle of the normal definitive host . The
females lay eggs that hatch in the terminal branches of the pulmonary arteries, yielding first-stage larvae. The first-stage
larvae migrate to the pharynx, are swallowed, and passed in the feces. They penetrate or are ingested by a gastropod
intermediate host . After two molts, third-stage larvae are produced which are infective to mammalian hosts.
When the infected gastropod is ingested by the definitive host, the third-stage larvae migrate to the brain where they
develop into young adults . The young adults return to the venous system and then the pulmonary arteries where they
become sexually mature. Of note, various animals act as paratenic (transport) hosts: after ingesting the infected snails,
they carry the third-stage larvae which can resume their development when the paratenic host is ingested by a definitive
host. Humans can acquire the infection by eating raw or undercooked snails or slugs infected with the parasite; they may
also acquire the infection by eating raw produce that contains a small snail or slug, or part of one . There is some
question whether or not larvae can exit the infected gastropods in slime (which may be infective to humans if ingested, for
example, on produce). Infection may also be acquired by ingestion of invertebrate paratenic hosts containing L3 larvae
(e.g. crabs, freshwater shrimp). In humans, larvae migrate to the brain, or rarely to the lungs, where the worms ultimately
die . Larvae may develop to fourth or fifth stage in the human host, but seem to be incapable of maturing fully.

Ancylostoma caninum
Ancylostoma Cutaneous larva migrans (also known as creeping eruption) is a zoonotic infection with hookworm species that do not use
braziliense humans as a definitive host, the most common being Ancylostoma braziliense and A. caninum. The cycle in the definitive
Uncinaria stenocephala host is very similar to the cycle for the human species, which involves tracheal migration to the small intestine. Some larvae
become arrested in the tissues and serve as the source of infection for pups via transmammary (and possibly
transplacental) routes. Mature hookworms reproduce in the small intestine, and eggs are passed in the animal definitive
host’s stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2 days. The released
rhabditiform larvae grow in the feces and/or the soil , and after 5 to 10 days (and 2 molts) they become filariform
(third-stage) larvae that are infective . These infective larvae can survive 3 to 4 weeks in favorable environmental
conditions. On contact with the animal host , the larvae penetrate the skin and are carried through the blood vessels
to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and
are swallowed. The larvae reah the small intestine, where they reside and mature into adults. Adult worms live in the lumen
of the small intestine, where they attach to the intestinal wall. Some larvae become arrested in the tissues, and serve as
source of infection for pups via transmammary (and possibly transplacental) routes . Humans become infected when
filariform larvae penetrate the skin . With most species, the larvae cannot mature further in the human host and
migrate aimlessly within the epidermis, sometimes as much as several centimeters a day. Some larvae may become
arrested in deeper tissue after skin migration.

LIFECYCLE OF TREMATODES
Trematode Lifecycle
Clonorchis sinensis

Clonorchis sinensis eggs are discharged in the biliary ducts and in the stool in an embryonated state . Eggs are ingested by
a suitable snail intermediate host . Eggs release miracidia , which go through several developmental stages
(sporocysts , rediae , and cercariae ). The cercariae are released from the snail and, after a short period of free-
swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae
. Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish . After ingestion,
the metacercariae excyst in the duodenum and ascend the biliary tract through the ampulla of Vater . Maturation takes
approximately one month. The adult flukes (measuring 10 to 25 mm by 3 to 5 mm) reside in small and medium sized biliary
ducts.

Fasciolopsis buski
(the largest
intestinal fluke of
humans)

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 cercariae ). The cercariae are released from the snail and encyst as metacercariae on
aquatic plants . The mammalian hosts become infected by ingesting metacercariae on the aquatic plants. After ingestion, the
metacercariae excyst in the duodenum and attach to the intestinal wall. There they develop into adult flukes (20 to 75 mm by
8 to 20 mm) in approximately 3 months, attached to the intestinal wall of the mammalian hosts (humans and pigs) . The adults
have a life span of about one year.
Fasciola hepatica
Facsciola gigantica
 The trematodes Fasciola hepatica (also known as the common liver fluke or the sheep liver fluke) and Fasciola gigantica are
large liver flukes (F. hepatica: up to 30 mm by 15 mm; F. gigantica: up to 75 mm by 15 mm), which are primarily found in
domestic and wild ruminants (their main definitive hosts) but also are causal agents of fascioliasis in humans.

Immature eggs are discharged in the biliary ducts and passed in the stool . Eggs become embryonated in freshwater over
~2 weeks ; embryonated eggs release miracidia , which invade a suitable snail intermediate host . In the snail,
the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ). The cercariae are
released from the snail and encyst as metacercariae on aquatic vegetation or other substrates. Humans and other
mammals become infected by ingesting metacercariae-contaminated vegetation (e.g., watercress) . After ingestion, the
metacercariae excyst in the duodenum and penetrate through the intestinal wall into the peritoneal cavity. The immature
flukes then migrate through the liver parenchyma into biliary ducts, where they mature into adult flukes and produce eggs .
In humans, maturation from metacercariae into adult flukes usually takes about 3–4 months; development of F. gigantica may
take somewhat longer than F. hepatica.

Echinostoma spp.

The trematode family Echinostomatidae includes numerous spiny-collared intestinal flukes known to infect humans. Infections
are documented mostly from members of the genera Echinostoma (E. hortense, E. trivolvis, E. macrorchis, E. revolutum sensu
lato, E. ilocanum, E. cinetorchis, E. echinatum [= lindoense]) and E. fujianensis).

Like many trematodes, echinostomid flukes undergo a multi-host (indirect) life cycle . Unembryonated eggs are passed in feces
of infected definitive hosts and develop in water . Miracidia usually take about 3 weeks to mature before hatching
, after which they swim freely and penetrate the first intermediate host, a snail . The intramolluscan stages include a
sporocyst stage , one or two generations of rediae , and cercariae , which are released from the snail. The
cercariae may encyst as metacercariae within the same first intermediate host or leave the host and penetrate a new second
intermediate host . The definitive host becomes infected after eating metacercariae in infected second intermediate hosts
. Metacercariae excyst in the duodenum and adults reside in the small intestine (for some species, occasionally in the
bile ducts or large intestine) .
Paragonimus
westermani
 More than 30 species of trematodes (flukes) of the genus Paragonimus have been reported which infect animals and humans.
Among the more than 10 species reported to infect humans, the most common is P. westermani, the oriental lung fluke.
The eggs are excreted unembryonated in the sputum, or alternately they are swallowed and passed with stool . In the
external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and
penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae ,
with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host,
a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the
mammalian host . Human infection with P. westermani occurs by eating inadequately cooked or pickled crab or crayfish that
harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall
into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and
develop into adults (7.5 to 12 mm by 4 to 6 mm). The worms can also reach other organs and tissues, such as the brain and
striated muscles, respectively. However, when this takes place completion of the life cycles is not achieved, because the eggs
laid cannot exit these sites. Time from infection to oviposition is 65 to 90 days.

Schistosoma spp.
Schistosomiasis (Bilharziasis) is caused by some species of blood trematodes (flukes) in the genus Schistosoma. The three
main species infecting humans are Schistosoma haematobium, S. japonicum, and S. mansoni.
Schistosoma eggs are eliminated with feces or urine, depending on species . Under appropriate conditions the eggs hatch
and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include
two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae
swim, penetrate the skin of the human host , and shed their forked tails, becoming schistosomulae . The
schistosomulae migrate via venous circulation to lungs, then to the heart, and then develop in the liver, exiting the liver via the
portal vein system when mature, . Male and female adult worms copulate and reside in the mesenteric venules, the
location of which varies by species (with some exceptions) . For instance, S. japonicum is more frequently found in the
superior mesenteric veins draining the small intestine , and S. mansoni occurs more often in the inferior mesenteric veins
draining the large intestine . However, both species can occupy either location and are capable of moving between sites. S.
intercalatum and S. guineensis also inhabit the inferior mesenteric plexus but lower in the bowel than S. mansoni. S.
haematobium most often inhabitsin the vesicular and pelvic venous plexus of the bladder , but it can also be found in the
rectal venules. The females (size ranges from 7–28 mm, depending on species) deposit eggs in the small venules of the portal
and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S. mansoni,S. japonicum, S.
mekongi, S. intercalatum/guineensis) and of the bladder and ureters (S. haematobium), and are eliminated with feces or urine,
respectively .
Opisthorchis
viverrini .
 The adult flukes deposit fully developed eggs that are passed in the feces . After ingestion by a suitable snail (first
intermediate host) , the eggs release miracidia , which undergo in the snail several developmental stages (sporocysts ,
rediae , cercariae ). Cercariae are released from the snail and penetrate freshwater fish (second intermediate host),
encysting as metacercariae in the muscles or under the scales . The mammalian definitive host (cats, dogs, and various fish-
eating mammals including humans) become infected by ingesting undercooked fish containing metacercariae. After ingestion,
the metacercariae excyst in the duodenum and ascend through the ampulla of Vater into the biliary ducts, where they attach
and develop into adults, which lay eggs after 3 to 4 weeks . The adult flukes (O. viverrini: 5 mm to 10 mm by 1 mm to 2
mm; O. felineus: 7 mm to 12 mm by 2 mm to 3 mm) reside in the biliary and pancreatic ducts of the mammalian host, where they
attach to the mucosa.

CESTODES

Lifecycle
Trematode
Diphyllobothrium
latum

Eggs are passed unembryonated in feces . Under appropriate conditions, the eggs mature (approximately 18 to 20 days)

and yield oncospheres which develop into a coracidia . After ingestion by a suitable crustacean (first intermediate

host) the coracidia develop into procercoid larvae . Procercoid larvae are released from the crustacean upon predation by
the second intermediate host (usually a small fish) and migrate into the deeper tissues where they develop into a plerocercoid

larvae (spargana), which is the infectious stage for the definitive host . Because humans do not generally eat these small
fish species raw, the second intermediate host probably does not represent an important source of human infection. However,

these small second intermediate hosts can be eaten by larger predator species that then serve as paratenic hosts . In this
case, the plerocercoid migrates to the musculature of the larger predator fish; humans (and other definitive host species) acquire

the parasite via consumption of undercooked paratenic host fish . In the definitive host, the plerocercoid develops into
adult tapeworms in the small intestine. Adult diphyllobothriids attach to the intestinal mucosa by means of two bilateral groves

(bothria) of their scolex . The adults can reach more than 10 m in length, with more than 3,000 proglottids. Immature eggs
are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces. Eggs appear in the
 feces 5 to 6 weeks after infection.

Taenia solium and

Taenia saginata

Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata or Taenia solium. Humans are the only definitive
hosts for T. saginata and T. solium. Eggs or gravid proglottids are passed with feces ; the eggs can survive for days to
months in the environment. Cattle (T. saginata) and pigs (T. solium) become infected by ingesting vegetation contaminated with
eggs or gravid proglottids . In the animal’s intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the
striated muscles, where they develop into cysticerci. A cysticercus can survive for several years in the animal. Humans become
infected by ingesting raw or undercooked infected meat . In the human intestine, the cysticercus develops over 2 months into
an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside
in the small intestine . Length of adult worms is usually 5 m or less for T. saginata (however it may reach up to 25 m) and 2
to 7 m for T. solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the
anus or are passed in the stool (approximately 6 per day). T. saginata adults usually have 1,000 to 2,000 proglottids, while T.
solium adults have an average of 1,000 proglottids. The eggs contained in the gravid proglottids are released after the proglottids
are passed with the feces. T. saginata may produce up to 100,000 and T. solium may produce 50,000 eggs per proglottid
respectively.

Dipylidium caninum

Gravid proglottids are passed intact in the feces or emerge from the perianal region of the host . In the environment, the

proglottids disintegrate and release egg packets, which are also occasionally found free in the feces . The intermediate
host (most often larval stages of the dog or cat flea Ctenocephalides spp.) ingests egg packets, and the oncosphere within is
released into the larval flea’s intestine. The oncosphere penetrates the intestinal wall, invades the insect’s hemocoel (body

cavity), and develops into a cysticercoid . The cysticercoid remains in the flea as it matures from a larva into an adult

. The vertebrate host becomes infected by ingesting the adult flea containing the cysticercoid . In the small
intestine of the vertebrate host, the cysticercoid develops into the adult tapeworm after about one month. The adult tapeworms
(measuring up to 60 cm in length and 3 mm in width) reside in the small intestine of the host, where they each attach by their

scolex . Gravid, double-pored proglottids detach from the strobila (body) and are shed in the feces.
Humans also acquire infection by ingesting the cysticercoid contaminated flea. Children are most frequently infected, possibly

due to close contact with flea-infested pets .

Hymenolepsis nana

Eggs of Hymenolepis diminuta are passed out in the feces of the infected definitive host (rodents, man) . The mature eggs
are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and
penetrate the intestinal wall of the host , which develop into cysticercoid larvae. Species from the genus Tribolium are
common intermediate hosts for H. diminuta. The cysticercoid larvae persist through the arthropod’s morphogenesis to
adulthood. H. diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the
cysticercoid larvae . Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food
items, and directly from the environment (e.g., oral exploration of the environment by children). After ingestion, the tissue of the
infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of the scoleces
occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small
intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length
. Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms.
The eggs are expelled to the environment in the mammalian host’s feces .

Echinococcus
granulosus
The adult Echinococcus granulosus (sensu lato) (2—7 mm long) resides in the small intestine of the definitive host.

Gravid proglottids release eggs that are passed in the feces, and are immediately infectious. After ingestion by a suitable

intermediate host, eggs hatch in the small intestine and release six-hooked oncospheres that penetrate the intestinal wall
and migrate through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere

develops into a thick-walled hydatid cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the
cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After

ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32
to 80 days.

Humans are aberrant intermediate hosts, and become infected by ingesting eggs . Oncospheres are released in the

intestine , and hydatid cysts develop in a variety of organs . If cysts rupture, the liberated protoscolices may create
secondary cysts in other sites within the body (secondary echinococcosis).
Echinococcus
multilocularis
The adult Echinococcus multilocularis (1.2—4.5 mm long) resides in the small intestine of the definitive host. Gravid

proglottids release eggs that are passed in the feces, and are immediately infectious. After ingestion by a suitable

intermediate host, eggs hatch in the small intestine and releases a six-hooked oncosphere that penetrates the intestinal
wall and migrates through the circulatory system into various organs (primarily the liver for E. multilocularis). The oncosphere

develops into a multi-chambered (“multilocular”), thin-walled (alveolar) hydatid cyst that proliferates by successive
outward budding. Numerous protoscolices develop within these cysts. The definitive host becomes infected by ingesting the

cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the

intestinal mucosa , and develop into adult stages in 32 to 80 days.

Humans are aberrant intermediate hosts, and become infected by ingesting eggs . Oncospheres are released in

the intestine and cysts develop within in the liver . Metastasis or dissemination to other organs (e.g., lungs, brain, heart,
bone) may occur if protoscolices are released from cysts, sometimes called “secondary echinococcosis.”

PROTOZOA

Lifecycle
Protozoon
Giardia duodenalis

Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces
 (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of
cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases
trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the
lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation
occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because
the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals
are infected with Giardia, their importance as a reservoir is unclear.

Chilomastix mesnili

The cyst stage is resistant to environmental pressures and is responsible for transmission of Chilomastix. Both cysts and

trophozoites can be found in the feces (diagnostic stages) . Infection occurs by the ingestion of cysts in contaminated

water, food, or by the fecal-oral route (hands or fomites) . In the large (and possibly small) intestine, excystation releases
trophozoites. Chilomastix resides in the cecum and/or colon; it is generally considered a commensal whose contribution to
pathogenesis is uncertain.

Trichomonas
vaginalis and
Trichomonas tenax

Trichomonas vaginalis resides in the female lower genital tract and the male urethra and prostate , where it replicates by
binary fission . The parasite does not appear to have a cyst form, and does not survive well in the external
environment. Trichomonas vaginalis is transmitted among humans, its only known host, primarily by sexual intercourse .

Trypanosoma
gambiense

During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin

tissue. The parasites enter the lymphatic system and pass into the bloodstream . Inside the host, they transform into

bloodstream trypomastigotes , are carried to other sites throughout the body, reach other body fluids (e.g., lymph, spinal

fluid), and continue the replication by binary fission . The entire life cycle of African trypanosomes is represented by
extracellular stages. The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected

mammalian host , . In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary

fission , leave the midgut, and transform into epimastigotes . The epimastigotes reach the fly’s salivary glands and

continue multiplication by binary fission . The cycle in the fly takes approximately 3 weeks. Rarely, T. b. gambiense may
be acquired congenitally if the mother is infected during pregnancy.

Trypanosoma cruzi

An infected triatomine insect vector (or “kissing bug”) takes a blood meal and releases trypomastigotes in its feces near the site of
the bite wound. Trypomastigotes enter the host through the wound or through intact mucosal membranes, such as the
conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius,
and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into
intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are
released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and
transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The
 bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the
parasites enter another cell or are ingested by another vector. The “kissing bug” becomes infected by feeding on human or animal
blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut
. The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the
hindgut .

Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally (from mother to
unborn baby), and in laboratory accidents.

Leishmania
donovani

Leishmaniasis is transmitted by the bite of infected female phlebotomine sand flies. The sand flies inject the infective stage (i.e.,
promastigotes) from their proboscis during blood meals . Promastigotes that reach the puncture wound are phagocytized by
macrophages and other types of mononuclear phagocytic cells. Promastigotes transform in these cells into the tissue stage
of the parasite (i.e., amastigotes) , which multiply by simple division and proceed to infect other mononuclear phagocytic
cells . Parasite, host, and other factors affect whether the infection becomes symptomatic and whether cutaneous or visceral
leishmaniasis results. Sand flies become infected by ingesting infected cells during blood meals ( , ). In sand flies,
amastigotes transform into promastigotes, develop in the gut (in the hindgut for leishmanial organisms in
the Viannia subgenus; in the midgut for organisms in the Leishmania subgenus), and migrate to the proboscis .

Entamoeba
histolytica

Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically

found in diarrheal stool. Infection with Entamoeba histolytica (and E.dispar) occurs via ingestion of mature cysts from
fecally contaminated food, water, or hands. Exposure to infectious cysts and trophozoites in fecal matter during sexual contact
 may also occur. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large
intestine. Trophozoites may remain confined to the intestinal lumen (A: noninvasive infection) with individuals continuing to pass
cysts in their stool (asymptomatic carriers). Trophozoites can invade the intestinal mucosa (B: intestinal disease), or blood
vessels, reaching extraintestinal sites such as the liver, brain, and lungs (C: extraintestinal disease). Trophozoites multiply by

binary fission and produce cysts , and both stages are passed in the feces . Cysts can survive days to weeks in the
external environment and remain infectious in the environment due to the protection conferred by their walls. Trophozoites
passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric
environment.

Entamoeba coli
and Endolimax
nana

Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic
and reside in the large intestine of the human host . Both cysts and trophozoites of these species are passed in stool and
considered diagnostic . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool.
Colonization of the nonpathogenic amebae occurs after ingestion of mature cysts in fecally-contaminated food, water, or fomites
. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The
trophozoites multiply by binary fission and produce cysts, and both stages are passed in the feces . Because of the protection
conferred by their cell walls, the cysts can survive days to weeks in the external environment and are responsible for
transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive
exposure to the gastric environment.
Naegleria fowleri

Naegleria fowleri has 3 stages in its life cycle: cyst (1), trophozoite (2), and flagellate (3). The only infective stage of the ameba is
the trophozoite. Trophozoites are 10-35 µm long with a granular appearance and a single nucleus. The trophozoites replicate by
binary division during which the nuclear membrane remains intact (a process called promitosis) (4). Trophozoites infect humans
or animals by penetrating the nasal tissue (5) and migrating to the brain (6) via the olfactory nerves causing primary amebic
meningoencephalitis (PAM).

Trophozoites can turn into a temporary, non-feeding, flagellated stage (10-16 µm in length) when stimulated by adverse
environmental changes such as a reduced food source. They revert back to the trophozoite stage when favorable conditions
 return 1. Naegleria fowleri trophozoites are found in cerebrospinal fluid (CSF) and tissue, while flagellated forms are occasionally
found in CSF. Cysts are not seen in brain tissue. If the environment is not conducive to continued feeding and growth (like cold
temperatures, food becomes scarce) the ameba or flagellate will form a cyst. The cyst form is spherical and about 7-15 µm in
diameter. It has a smooth, single-layered wall with a single nucleus. Cysts are environmentally resistant in order to increase the
chances of survival until better environmental conditions occur.

Balantidium coli

Cysts are the stage responsible for transmission of balantidiasis . The host most often acquires the cyst through ingestion

of contaminated food or water . Following ingestion, excystation occurs in the small intestine, and the trophozoites

colonize the large intestine . The trophozoites reside in the lumen of the large intestine and appendix of humans and

animals, where they replicate by binary fission, during which conjugation may occur . Trophozoites undergo encystation to

produce infective cysts . Some trophozoites invade the wall of the colon and multiply, causing ulcerative pathology in the
colon wall. Some return to the lumen and disintegrate. Mature cysts are passed with feces.

Isospora belli

At the time of excretion in stool, the oocyst is immature and usually contains just one sporoblast (sometimes, two) . During
further maturation after excretion, the sporoblast divides in two (the oocyst now contains two sporoblasts); the sporoblasts secrete
a cyst wall, thus becoming sporocysts; and the sporocysts divide twice, resulting in four sporozoites per each of two sporocysts
. Infection occurs by ingestion of mature (fully sporulated) oocysts: the sporocysts excyst in the small intestine and release
their sporozoites, which invade the epithelial cells and initiate schizogony . Upon rupture of the schizonts, merozoites are
released, which invade epithelial cells and continue the cycle of asexual multiplication . Trophozoites develop into schizonts,
which contain multiple merozoites. After a minimum of one week, the sexual stage begins, with the development of male and
female gametocytes . Fertilization results in the development of oocysts, which are excreted in the stool .

Cyclospora
cayetanensis
 When freshly passed in stools, the oocyst is not infective (thus, direct fecal-oral transmission cannot occur; this

differentiates Cyclospora from another important coccidian parasite, Cryptosporidium). In the environment , sporulation
occurs after days or weeks at temperatures between 22°C to 32°C, resulting in division of the sporont into two sporocysts, each

containing two elongate sporozoites . The sporulated oocysts can contaminate fresh produce and water which are

then ingested . The oocysts excyst in the gastrointestinal tract, freeing the sporozoites, which invade the epithelial cells of

the small intestine . Inside the cells they undergo asexual multiplication into type I and type II meronts. Merozoites from
type I meronts likely remain in the asexual cycle, while merozoites from type II meronts undergo sexual development into
macrogametocytes and microgametocytes upon invasion of another host cell. Fertilization occurs, and the zygote develops to an

oocyst which is released from the host cell and shed in the stool . Several aspects of intracellular replication and
development are still unknown, and the potential mechanisms of contamination of food and water are still under investigation.

Toxoplasma gondii

The only known definitive hosts for Toxoplasma gondii are members of family Felidae (domestic cats and their relatives).
Unsporulated oocysts are shed in the cat’s feces . Although oocysts are usually only shed for 1–3 weeks, large numbers may
be shed. Oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature (including
birds and rodents) become infected after ingesting soil, water or plant material contaminated with oocysts . Oocysts transform
into tachyzoites shortly after ingestion. These tachyzoites localize in neural and muscle tissue and develop into tissue cyst
bradyzoites . Cats become infected after consuming intermediate hosts harboring tissue cysts . Cats may also become
infected directly by ingestion of sporulated oocysts. Animals bred for human consumption and wild game may also become
infected with tissue cysts after ingestion of sporulated oocysts in the environment . Humans can become infected by any of
several routes:
Eating undercooked meat of animals harboring tissue cysts .
Consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated
soil or changing the litter box of a pet cat) .
Blood transfusion or organ transplantation .
Transplacentally from mother to fetus .
In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts
may remain throughout the life of the host. Diagnosis is usually achieved by serology, although tissue cysts may be observed in
 stained biopsy specimens . Diagnosis of congenital infections can be achieved by detecting T. gondii DNA in amniotic fluid
using molecular methods such as PCR .

Plasmodium vivax

The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates
sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release
merozoites . (Of note, in P. vivax and P. ovale a dormant stage [hypnozoites] can persist in the liver (if untreated) and cause
relapses by invading the bloodstream weeks, or even years later.) After this initial replication in the liver (exo-erythrocytic
schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect
red blood cells . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites
differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical
manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by
an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle
. While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in
turn become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts
. The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation
of the sporozoites into a new human host perpetuates the malaria life cycle.

Babesia sp.

The Babesia microti life cycle involves two hosts, which include a rodent, primarily the white-footed mouse, Peromyscus
leucopus, and a tick in the genus Ixodes. During a blood meal, a Babesia-infected tick introduces sporozoites into the mouse
host . Sporozoites enter erythrocytes and undergo asexual reproduction (budding) . In the blood, some parasites
differentiate into male and female gametes, although these cannot be distinguished by light microscopy . The definitive host is
the tick. Once ingested by an appropriate tick , gametes unite and undergo a sporogonic cycle resulting in sporozoites .
Transovarial transmission (also known as vertical, or hereditary, transmission) has been documented for “large” Babesia species
but not for the “small” Babesia, such as B. microti .

Humans enter the cycle when bitten by infected ticks. During a blood meal, a Babesia-infected tick introduces sporozoites into the
human host . Sporozoites enter erythrocytes and undergo asexual replication (budding) . Multiplication of the blood-
stage parasites is responsible for the clinical manifestations of the disease. Humans usually are dead-end hosts. However,
human-to-human transmission is well recognized to occur via contaminated blood transfusions .
Blastocystis
hominis
 The life cycle of Blastocystis sp. is not yet understood, including the infectious stage and whether (and which of the) various
morphologic forms of this polymorphic organism that have been identified in stool or culture constitute distinct biologic stages of
the parasite in the intestinal tract of hosts. The cyst form (3–5 µm) is postulated to be an infectious stage, but not confirmed. The
predominant form found in human stool specimens is referred to as the vacuolar (or central body) form and is of variable size
(5–40 µm, occasionally much larger). Replication appears to occur via binary fission. Other morphologic forms (e.g., ameboid and
granular forms) also have been noted in stool samples and/or culture; their biological role and eventual developmental fate
require further investigation.

Sarcocystis
hominis

Both sporulated oocysts (containing two sporocysts) and individual sporocysts can be passed in stool . Sporocysts contain
four sporozoites and a refractile residual body. Sporocysts ingested by the intermediate host (cattle for S. hominis and pigs
for S. suihominis) rupture, releasing sporozoites. Sporozoites enter endothelial cells of blood vessels and undergo schizogony,
resulting in first-generation schizonts. Merozoites derived from the first-generation invade small capillaries and blood vessels,
becoming second-generation schizonts. The second generation merozoites invade muscle cells and develop into sarcocysts
containing bradyzoites, which are the infective stage for the definitive host . Humans become infected when they eat
undercooked meat containing these sarcocysts. Bradyzoites are released from ruptured cysts in the small intestine and
invade the lamina propria of the intestinal epithelium . There, they differentiate into macro- and microgametocytes. Fusion of
male and female gametes results in the formation of oocysts . Oocysts sporulate in the intestinal epithelium and are shed
from the host in feces . Due to the fragile nature of the oocyst wall, individual sporocysts may also be detected in feces.
Vittaforma corneae
The infective form of microsporidia is the resistant spore, which can persist in the environment for months The spore then

germinates, rapidly everting its polar tubule which contacts the eukaryotic host cell membrane . The spore then injects the

infective sporoplasm into the host cell through the polar tubule . Inside the cell, the sporoplasm enters the proliferative

phase marked by extensive multiplication via merogony (binary fission or multiple fission), creating meronts . The location
of this developmental stage within the host cell varies by genus; it can occur either in direct contact with the host cell cytosol
(Enterocytozoon, Nosema), inside a parasitophorous vacuole of unknown origin (Encephalitozoon), in a parasite-secreted
envelope (Pleistophora, Trachipleistophora), or surrounded by the host cell endoplasmic reticulum (Endoreticulatus, Vittaforma)

. Following the proliferative phase, meronts undergo sporogony in which the thick spore wall and invasion apparatus
develop, creating sporonts and eventually mature spores when all organelles are polarized. When the spores increase in number
and completely fill the host cell cytoplasm, the cell membrane is disrupted and spores are released to the surroundings .
These free mature spores can infect new cells thus continuing the cycle.
Mature spores of intestinal-localizing species may be shed in feces, although the route of transmission remains uncertain for
many species. Exposure to spores in water or in soil appears to be a potentially major route, based on the finding of spores in
these sources along with case histories. E. bieneusi and V. corneae have been identified in surface waters, and spores
of Nosema sp. (and likely A. algerae) have been identified in ditch water. Cases of donor-derived microsporidiosis
(Encephalitozoon cuniculi) following bone marrow, kidney, liver, and heart transplantation have been confirmed.