Linsey Shariq
Parasite
Hymenolepis nana and Hymenolepis diminuta
Introduction
Hymenolepiasis is the most common cestode
parasite in the human body. Infections
are seen more often among children. It
is most widespread in warm climates and around unsanitary areas where eggs can
be passed through fecal matter from an infected host to an uninfected person.
Hymenolepiasis is caused by the introduction of either tapeworm species Hymenolepis nana (H. nana) or H. diminuta
(H. diminuta) into the human body. A member of the cestode
class, tapeworms do not have digestive tracts to absorb nutrients, instead
their surface body layer is metabolically active with nutrients and waste
passing in and out continuously. In contrast, the nematodes class, such as hookworms,
have complete digestive tracts and separate orifices for food ingestion and
waste excretion. Although the cestode life cycle requires the cysticercoid,
or larval, phase to be developed in an intermediate host, H. nana does not
follow this observation and can use an intermediate host or auto infect the
human host.
Agent
(classification and taxonomy) [9]
Phylum
- Platyhelminthes
Class
– Cestoidea
Subclass
– Eucestoda
Order
- Cyclophyllidea
Family
- Hymenolepididae
Genus
– Hymenolepis, Rodentolepis
Synonyms [3]
Hymenolepis nana:
Dwarf
tapeworm
Rodentolepis (Hymenolepis) microstoma
Rodentolepsiasis
Vampirolepis nana
Hymenolepis diminuta:
Mathevotaenia
Rat tapeworm
History
of Discovery
H.
nana was first identified as a human parasite by Von Siebold
in 1852. In 1906, Stiles identified an
identical parasite with a rodent host and named it Hymenolepis
fraterna. Later, morphological characteristics were
used for taxonomy identification and H. nana was known to have hooks and linear
reproductive organs. H. diminuta has no hooks and reproductive organs arranged in a
triangular formation. [1]
Clinical
Presentation in Humans
Most
infections do not have many worms and therefore can have no symptoms. Patients with more than 15,000 eggs per gram
of stool may experience cramps, diarrhea, irritability, anorexia, or enteritis
caused by cystercoids destroying the intestinal villi in which they develop. [1]
Transmission
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.[1]Research done in 2000 showed that of 9 pet stores
surveyed in the Connecticut, 75% sold rats, mice or hamsters infected with H.
nana. A serious public health risk could
result from pet store parasite transmissions. [2]
Reservoir
Humans or rodents can be the reservoir of H. nana. H. diminuta, the reservoirs are rodents and insects (specifically flour beetles, Tribulium species). [3,1]
Vector
None
[3]
Incubation
Period
H.
nana’s larval stage occurs either inside an auto infected host’s intestinal villus or an intermediate rat host. In H. diminuta,
this stage occurs only in grain beetles.
It lasts about 5-6 days then the worm matures and attaches itself to the
last part of the small intestine. The
whole time period from egg ingestion until adult worms releasing new fertilized
eggs in stool is 20 to 30 days. [1]
Morphology
H.
nana worms are flat and segmented with skinny necks. They vary in length from approximately
15 to 40 mm and are 1 mm wide.
Adult
Worm Morphology [3], [10]
H.
nana worms are flat and segmented with skinny necks. They vary in length from
approximately 15 to 40 mm and are 1 mm wide.
Each worm has a scolex, which is an anterior
‘head’ segment with a single row of 20-30 retractable hooks (rostellum). Each
worm also has proglottids, which are wider segments
of the tapeworm that contains both male and female reproductive organs. [1, 3] Each mature segment has unilateral genital
pores and 3 testes. When then eggs have
been fertilized the segments are referred to as gravid. These break off from the main portion, the strobila, and deteriorate releasing eggs. The oncospheres, or
embryos, can be from 30-47 hm in diameter and are
covered with a thin hyaline outer membrane and a thicker inner membrane. Embedded in the inner membrane on polar sides
of the oncosphere are a number of hair-like
filaments. [1]
H.
nana Oncosphere and Scolex
[10]
H. diminuta worms are the same shape as H. nana but are much larger, up to 90 cm long and 44 mm wide. Their scolex does not have hooked rostellum like the H. nana species but they do have similar unilateral genital pores and 3 testes per proglottid. The oncospheres of H. diminuta are similar to H. nana’s except they lack hair like filaments embedded in their inner membrane and are two times their size. [1]
H. diminuta Oncosphere and Scolex [10]
Life
Cycle
H.
nana is an auto infecting parasite that does not require an intermediate host.
It can however grow in rats as well. The
fertilized eggs pass in the stool from an infected host. The eggs are then either eaten by an insect
or by a human which mainly occurs through the ingestion of contaminated food or
water. The cysticercoid stage develops either outside
the body in an insect that can then be eaten by a human or a rat, or it
develops in the intestinal villus of an auto infected
human. The adult phase begins with the
growth of the scolex with several hooks. After attaching itself to the intestinal wall
and growing proglottids, fertilized eggs can pass in
the host’s stool as the gravid proglottids
deteriorate and release eggs. [3]
H. diminuta fertilized eggs pass in the stool from an infected
host. The eggs are then eaten by grain
beetles where the cysticerci, or larval stage develops.
Humans then can eat the bug or its mealworm phase in cereal or
flour. The worm matures in the duodenum,
the first portion of the small intestine, and attach to the mucosa lining. Fertilized
eggs can pass in the host’s stool as the gravid proglottids
deteriorate and release eggs. [3]
Diagnostic
Tests
Diagnosis
for Hymenolepiasis is done by examining stool for
eggs. The proglottids
that are disintegrated in the intestine cannot be detected. Egg output could be sporadic so a couple
stool tests a few days apart may need to be done to diagnose the infection.
Management
and Therapy
H.
nana:
For
adults there are 3 options.
Praziquantel given once, 25mg/kg.
Nitazoxanide given at a dose of 500 mg
for 3 days.
Niclosamide given for one day at 2
grams followed by six days at 1 gram.
For
children there are treatment 3 options.
Praziquantel given once, 25mg/kg.
Nitazoxanide given at a dose of 100 mg for 3 days (for children ages
1-3) or 200 mg for 3 days (for children ages 4-11).
Niclosamide given for one day at 1 gram
followed by six days at 0.5 grams. [3]
H. diminuta:
For
adults there are 2 options.
Praziquantel given once, 25mg/kg.
Niclosamide given for one day at 2
grams followed by six days at 1 gram.
For
children there are treatment 2 options.
Praziquantel is given once, 25mg/kg.
Niclosamide given for one day at 1 gram
followed by six days at 0.5 grams. [3]
Epidemiology
Prevalence
in endemic areas can reach from 5-20%. [1]
Prevalence
Maps [3]
H.
nana is the most common cestode in humans with
infection prevalence highest among children and in warm arid climates with poor
sanitation facilities [1]. Results of
case studies completed on each continent suggest that H. nana is a difficult
parasite to eliminate. The prevalence of
H. nana in remote communities in northwest Australia is remarkably high,
55%. The transmission is due mostly from
human to human contact and auto infection [9].
In Bat Dambang Cambodia, middle school students
were found to have a 2.4% prevalence, more than the younger kids at 1.3%,
suggesting children are not learning prevention techniques as they mature[8].
A
study done in Turkey comparing Shantytown schools with Apartment schools showed
a higher prevalence in the Shantytowns,13.6% in males
and 15.0% in females, as opposed to Apartment schools which still had a
significant prevalence of 2.2% in males and 8.4% in females. Children were
presenting with anemia, intestinal worms, and stunted growth raising public
health concerns. Recommendations were
made for schools to administer de-worming medication and provide iron
supplements to the students [7].
In
2006, a study in rural Mexico found that 25% of the children ages 6-10 in
twelve schools were infected with H. nana.
The study indicates that socioeconomic factors and lack of parent
education are strong influences on the high prevalence rate. Recommendations were made to include mother
in de-worming campaigns because drugs alone were not eliminating the parasites [5].
Zimbabwe
children in both small towns and high-density suburbs suffer from H. nana. Infections tend to be more frequent in
younger children who live in urban areas and in older children who live in
rural locations. The study reported an overall
prevalence rate of 24% in urban areas and an 18%
prevalence in rural towns [6].
Six
communities along the banks of Lake Titicaca in Peru were included in a study
to determine the distribution of parasites.
The prevalence of H. nana was found to be 6.6% but the overall intestinal
pathogenic infection prevalence rate was 91.2% with many subjects having up to
5 different types of parasites![4] During
a recent trip to Puno, Peru I took the pictures below of the aeration basin
wastewater treatment facility. The basin
had a permeable soil berm between it and Lake
Titicaca which leaked on the land side as well.
Below sheep are grazing in the algae fields fertilized by human
wastewater.
References
General Information:
1. Schantz, Peter M. (2006). “Tapeworms (Cestodiasis).”
Gastroenterology Clinics of North America. Vol.25, iss.3, p.637-653.
2. Duclos, LM; Richardson, DJ
(2000). “Hymenolepis Nana in Pet
Store Rodents.” Comparative Parasitology.
Vol.67, iss. 2, p.197-201.
3. GIDEON http://web.gideononline.com/web/epidemiology/index.php?gdn_form=ZGlzZWFzZT0xMTE1MA==
Case Studies:
South America
4. Maco Flores, Vicente, Marcos Raymundo, Luis A., Terashima
Iwashita, Angélica et al. (2002) “Distribución
de la Entereoparasitosis en el Altiplano
Peruano: Estudio en 6 comunidades rurales del departamento de Puno, Perú.” Rev.
gastroenterol. Perú, oct./dic. Vol.22, No.4, p.304-309.
North America
5. Luis Quihui, Mauro E Valencia,
David WT Crompton, Stephen Phillips, Paul Hagan, Gloria Morales, Silvia P Díaz-Camacho (2006). “Role of the
employment status and education of mothers in the prevalence of intestinal
parasitic infections in Mexican rural schoolchildren.” BMC Public Health,
Vol.6, p. 225.
Africa
6. Peter R. Mason, Barbara A. Patterson. (1994).
“Epidemiology of Hymenolepis nana Infections in
Primary School Children in Urban and Rural Communities in Zimbabwe.” The Journal of Parasitology. Vol. 80, No. 2, p. 245-250.
Europe
7. Ulukanligil, M. Seyrek, A. (2004). “Anthropometric status, anaemia and
intestinal helminthic infections in shantytown and
apartment schoolchildren in the Sanliurfa province of
Turkey. European Journal
of Clinical Nutrition. Vol. 58, iss. 7, p 1056-1061.
Asia
8. Seung Kyu
Park, Dong-Heui Kim, Young-Kun Deung,
Hun-Joo Kim, Eun-Ju Yang,
Soo-Jung Lim,
Yong-Suk Ryang, Dan Jin,
and Kyu-Jae Lee. (2004). “Status of
intestinal parasite infections among children in Bat Dambang,
Cambodia.” The Korean Journal of Parasitology.
Vol. 42, No. 4, p. 201-203.
Australia
9. Macnish, Marion. (2001).
“Characterization of Community-Derived Hymenolepis in
Australia.” Murdoch University Medical Science Thesis.
10. Grupo de Estadio
para la Formacion y Docencia en Enfermedades Infecciosas