Taenia saginata

PATHOLOGY

Humans are the sole definitive host. When humans ingest infected raw or incompletely cooked beef,
the cysticercus develops into a reproductive adult in the small intestine in 2 - 3 months. Symptoms
are rare but may include abdominal discomfort and diarrhea. Unlike T. solium, the eggs of T.
saginata are not infectious to humans and their ingestion does not result in cysticercosis.

EPIDEMIOLOGY

Infections with T. saginata occur wherever contaminated raw beef is eaten, particularly in
Eastern Europe, Russia, eastern Africa and Latin America. Taeniasis due to T. saginata is rare in
the United States, except in places where cattle and people are concentrated and sanitation is
poor, such as around feed lots when cattle can be exposed to human feces. Tapeworm infections
due to T. solium are more prevalent in under-developed communities with poor sanitation and
where people eat raw or undercooked pork. Higher rates of illness have been seen in people in
Latin America, Eastern Europe, sub-Saharan Africa, India, and Asia. Taenia solium taeniasis is
seen in the United States, typically among Latin American immigrants. Taenia asiatica is limited
to Asia and is seen mostly in the Republic of Korea, China, Taiwan, Indonesia, and Thailand.

PREVENTION

One way to prevent taeniasis is to cook meat to safe temperatures. A food thermometer should
be used to measure the internal temperature of cooked meat. Do not sample meat until it is
cooked. USDA recommends the following for meat preparation.

For Whole Cuts of Meat (excluding poultry)

Cook to at least 145° F (63° C) as measured with a food thermometer placed in the thickest part
of the meat, then allow the meat to rest* for three minutes before carving or consuming.

For Ground Meat (excluding poultry)

Cook to at least 160° F (71° C); ground meats do not require a rest* time.

LAB DIAGNOSIS

Diagnosis of Taenia tapeworm infections is made by examination of stool samples; individuals

should also be asked if they have passed tapeworm segments. Stool specimens should be
collected on three different days and examined in the lab for Taenia eggs using a microscope.
Tapeworm eggs can be detected in the stool 2 to 3 months after the tapeworm infection is
established.
Taenia solium

PATHOLOGY

Taenia solium infections (taeniasis/cysticercosis) are a major scourge to most developing countries.
Neurocysticercosis, the infection of the human nervous system by the cystic larvae of this parasite, has a
protean array of clinical manifestations varying from entirely asymptomatic infections to aggressive, lethal
courses. The diversity of clinical manifestations reflects a series of contributing factors which include the
number, size and location of the invading parasites, and particularly the inflammatory response of the
host. This manuscript reviews the different presentations of T. solium infections in the human host with a
focus on the mechanisms or processes responsible for their clinical expression.

EPIDEMIOLOGY

T. solium taeniasis/cysticercosis mainly affects the health and livelihoods of subsistence farming
communities in developing countries of Africa, Asia and Latin America. It is common in areas where
animal husbandry practices are such that pigs and cattle come into contact with human faeces. But
imported taeniasis can also lead to cases in the population of countries where T. solium is not considered
a public health problem.

PREVENTION

One way to prevent taeniasis is to cook meat to safe temperatures. A food thermometer should
be used to measure the internal temperature of cooked meat. Do not sample meat until it is
cooked. USDA recommends the following for meat preparation.

For Whole Cuts of Meat (excluding poultry)

Cook to at least 145° F (63° C) as measured with a food thermometer placed in the thickest part
of the meat, then allow the meat to rest* for three minutes before carving or consuming.

For Ground Meat (excluding poultry)

Cook to at least 160° F (71° C); ground meats do not require a rest* time.

LAB DIAGNOSIS

Diagnosis of Taenia tapeworm infections is made by examination of stool samples; individuals

should also be asked if they have passed tapeworm segments. Stool specimens should be
collected on three different days and examined in the lab for Taenia eggs using a microscope.
Tapeworm eggs can be detected in the stool 2 to 3 months after the tapeworm infection is
established. Tapeworm eggs of T. solium can also infect humans, causing cysticercosis. It is
important to diagnose and treat all tapeworm infections.
Diphyllobothrium latum

PATHOLOGY

The life cycle of D. latum, as it relates to humans, begins when un-embryonated eggs are
released into the feces of humans that were infected with the intestinal parasite. These eggs will
become embryonated in water under appropriate conditions, with the process usually lasting 18
to 20 days. During this maturation process, oncospheres, which are the first larval forms of the
tapeworm, materialize within the egg. The oncosphere is then covered by an outer envelope that
contains cilia and is called a coracidium. This coracidium hatches from the egg in the
surrounding water and becomes a free-swimming larval stage that subsequently goes on to attract
the first intermediate host. The free-swimming coracidium is consumed by the first intermediate
host. This is usually an aquatic arthropod, such as crustaceans from the subclass Copepoda.

EPIDEMIOLOGY

Diphyllobothriasis can affect any age group and gender, but the majority of identified cases were
middle-aged men. This parasitic infection can be a public-health issue for residents and travelers
in endemic as well as non-endemic regions. The fish tapeworm, D. latum, has historically been
implicated in human illness for thousands of years. The current state of knowledge regarding
these parasites points to cohabitation with humans since the early Neolithic
period.[2] Epidemiologic studies have concluded that in the 1970s, this infection was estimated
to have affected 9 million individuals globally with newer data estimating 20 million people
currently infected worldwide.[4][5] Additionally, in recent years, certain areas of the world have
seen a re-emergence of diphyllobothriasis thought to be secondary to changes in eating habits as
well as globalization.

PREVENTION

Infection by Diphyllobothrium latum may be prevented by not eating raw or

undercooked fish (for example, sushimi or tasting of fish while cooking).

This parasite is a zoonosis and many species of mammals contibute to the

maintenance of D. latum. Thus, control of this parasite is not likely.

LAB DIAGNOSIS

Diagnosis is made by identification of eggs or segments of the tapeworm in a

stool sample with a microscope. Eggs are usually numerous, but more than one
stool sample may be needed to find them.
Echinococcus granulosus

PATHOLOGY

Foxes, wolves and dogs are definitive hosts. Intermediate hosts include several genera of small
rodents. Human infection occurs in liver, where hydatid develops as an invasive cyst that insinuates
itselfwithin tissue in an alveolar pattern. Although the germinal membrane proliferates in the human
liver, protoscoleces fail to develop.

EPIDEMIOLOGY

E. granulosus is found in Africa, Europe, Asia, the Middle East, Central and South America, and
in rare cases, North America. The parasite is transmitted to dogs when they ingest the organs of
other animals that contain hydatid cysts. The cysts develop into adult tapeworms in the dog.
Infected dogs shed tapeworm eggs in their feces which contaminate the ground. Sheep, cattle,
goats, and pigs ingest tapeworm eggs in the contaminated ground; once ingested, the eggs hatch
and develop into cysts in the internal organs. The most common mode of transmission to humans
is by the accidental consumption of soil, water, or food that has been contaminated by the fecal
matter of an infected dog. Echinococcus eggs that have been deposited in soil can stay viable for
up to a year. The disease is most commonly found in people involved in raising sheep, as a result
of the sheep’s role as an intermediate host of the parasite and the presence of working dogs that
are allowed to eat the offal of infected sheep.

PREVENTION

 Prevent dogs from feeding on the carcasses of infected sheep.

 Control stray dog populations.
 Restrict home slaughter of sheep and other livestock.
 Do not consume any food or water that may have been contaminated by
fecal matter from dogs.
 Wash your hands with soap and warm water after handling dogs, and
before handling food.
 Teach children the importance of washing hands to prevent infection.

LAB DIAGNOSIS

The presence of a cyst-like mass in a person with a history of exposure to

sheepdogs in an area where E. granulosus is endemic suggests a diagnosis of
cystic echinococcosis. Imaging techniques, such as CT scans, ultrasonography,
and MRIs, are used to detect cysts. After a cyst has been detected, serologic tests
may be used to confirm the diagnosis.
Hymenolepis nana

PATHOLOGY

The life cycles consist of adult (tapeworm) stages in the small bowel of humans and rodents, and
also larval tissue stages in insects (cysticercoid). In addition, the cysticercoid stages of H.
nana can also invade and develop in the human intestine thus is capable of completing its entire
life cycle in the human host. H nana can also be transmitted through autoinfection without
having to pass through the insect host.

EPIDEMIOLOGY

Infection is most common in children aged 4-10 years, in dry, warm regions of the developing
world. H nana infection affects millions of people, primarily children, worldwide. Estimated
rates of infection in various regions range from 0.1-58%. It is estimated to have 50-75 million
carriers of H. nana with 5 to 25% prevalence in children worldwide, which can be as high as
50% in children between 1-4 years of age. [7] Regions with high reported infection rates include
Sicily (46%), Argentina (34% of school children), and southern areas of the former Soviet Union
(26%). In contrast, only 0.1% of stools examined at a children's hospital in Calgary were positive
for H nana. Most cases with associated neurologic symptoms have been reported from the
former Soviet Union.

PREVENTION

Good hygiene, public health and sanitation programs, and elimination of infected rats help to prevent
the spread of hymenolepiasis. Preventing fecal contamination of food and water in institutions and
crowded areas is of primary importance. General sanitation and rodent and insect control (especially
control of fleas and grain insects) are also essential for prevention of H. nana infection.

LAB DIAGNOSIS

Stool: The standard O&P examination is the recommended procedure for

recovery and identification of H. nana eggs in stool specimens, primarily from
the wet preparation examination of the concentration sediment. The eggs are
most easily seen on a direct wet smear or a wet preparation of the
concentration sediment.
Adult worms The scolex has four suckers and a short rostellum with hooks.
The adult worm is rarely seen in the stool.
Hymenolepis diminuta

PATHOLOGY

Light infections with H. diminuta are nonpathogenic (Insler and Roberts, 1976). Heavy
infections are rare because primary infection limits the size of the enteric worm population, and
results in strong but short-lived immune resistance to reinfection (Andreassen and Hopkins,
1980). Heavy infection may cause acute catarrhal enteritis or chronic enterocolitis with
lymphoid hyperplasia. However, even mild infections may alter host physiology, including
increased intestinal permeability.

EPIDEMIOLOGY

In humans, infections with Hymenolepis nana are much more common than infections
with Hymenolepis diminuta. H. nana is the most common cause of all cestode infections and is
encountered worldwide. In temperate areas, its incidence is higher in children and
institutionalized groups. H. diminuta is less frequent, but has been reported from various areas of
the world. parasitization rate ranging between .0001 and 5.5%. Isolated cases of H. diminuta
from Spain, Russia, and Eastern Europe have been recently published.
But, a relatively high prevalence of H. nana has been reported in surveys conducted in Europe
and Latin America.

PREVENTION

An effective prevention and control program should include purchase of parasite-free animals,
insect control, and high standards of animal husbandry and facility management.

LAB DIAGNOSIS

Diagnosis is based on finding eggs or proglottids in the feces or the adult worms in the intestine.
Dipylidium caninum

PATHOLOGY

Dipylidiasis in humans occurs through accidental ingestion of the dog or cat flea or the
dog louse infected with cysticercoids (the larval form of D caninum). These fleas and
lice are the intermediate host for D caninum. Cysticercoids develop into adult worms in
the small intestine of the host in about 20 days. The adult worm may attain a length of
10-70 cm and is 2-3 mm in diameter. The worms have a lifespan of less than 1 year.
Pathological changes due to dipylidiasis have not been described.

EPIDEMIOLOGY

Dipylidiasis is distributed worldwide, and human infection has been reported in

Africa, Argentina, Australia, Chile, China, Europe, Guatemala, India, Japan,
and the Philippines.

PREVENTION

There are no controlled trials of treatment for Dipylidium infection, but

infection is likely to respond to regimens used for other tapeworms
The main measure for prevention is treatment of pets for fleas and
tapeworms.

LAB DIAGNOSIS

Stool: The standard O&P examination is the recommended procedure for

recovery and identification of D. caninum eggs in stool specimens, primarily
from the wet preparation examination of the concentration sediment. The eggs
are most easily seen on a direct wet smear or a wet preparation of the
concentration sediment.
Adult worms The mature and gravid proglottids are wider than long, with the
main reproductive structures (mainly the uterus) located in the center of the
gravid proglottid. This configuration of the uterine structure has been called a
rosette.