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Cestodes Flashcards

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1
Q

What phylum and class do cestodes (tapeworms) belong to?

A

Phylum Platyhelminthes (flatworms), Class Cestoidea.

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2
Q

Where do adult cestodes usually live in humans?

A

In the small intestine of vertebrates (humans as definitive hosts for most species).

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3
Q

Where do larval cestodes usually develop?

A

In the tissues of vertebrate or invertebrate intermediate hosts (e.g. fish, cattle, pigs, dogs, humans).

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4
Q

Name the three main anatomical regions of an adult cestode.

A

Scolex (head), neck (germinal region), and strobila (chain of proglottids).

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5
Q

What is the function of the scolex in cestodes?

A

Attachment to the intestinal wall via suckers, grooves and/or hooks.

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6
Q

How do cestodes obtain nutrients?

A

They have no mouth or gut; nutrients are absorbed directly through the tegument.

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7
Q

What does it mean that cestode proglottids are hermaphroditic?

A

Each proglottid contains both male and female reproductive organs.

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8
Q

Define: scolex, rostellum, strobila, proglottid.

A

Scolex = head; rostellum = protrusion at the end of the scolex (may bear hooks); strobila = body of the tapeworm; proglottid = individual segment of the strobila.

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9
Q

What is a metacestode?

A

The larval stage of a cestode found in an intermediate host (e.g. cysticercoid, cysticercus, hydatid cyst).

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10
Q

What is a protoscolex?

A

A young larval scolex within a metacestode, which can develop into an adult scolex if ingested by the definitive host.

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11
Q

Differentiate cysticercoid, cysticercus and hydatid cyst.

A

Cysticercoid: small solid cyst with single evaginated scolex (often in insect IH). Cysticercus: fluid-filled cyst with a single invaginated scolex (Taenia). Hydatid cyst: large fluid-filled cyst containing many protoscolices (Echinococcus).

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12
Q

What is a hexacanth embryo and an oncosphere?

A

Hexacanth embryo: six-hooked larva inside the egg. Oncosphere: the larval stage after the egg is ingested by an intermediate host and activated.

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13
Q

What is an operculum on cestode eggs?

A

A ‘lid-like’ structure on eggs of pseudophyllid cestodes that opens to release the ciliated larva (coracidium).

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14
Q

How does the scolex differ between pseudophyllid and cyclophyllid cestodes?

A

Pseudophyllids: slit-like grooves (bothria). Cyclophyllids: four suckers, often with hooks on a rostellum.

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15
Q

Describe the typical uterus structure in pseudophyllid versus cyclophyllid cestodes.

A

Pseudophyllids: convoluted uterine tubes forming rosette-like uterus. Cyclophyllids: branched uterus with lateral branches.

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16
Q

How do pseudophyllid and cyclophyllid cestodes differ in egg release?

A

Pseudophyllids: eggs released from attached proglottids → eggs in stool. Cyclophyllids: gravid proglottids detach and pass in stool → eggs and proglottids in stool.

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17
Q

How do pseudophyllid and cyclophyllid eggs differ morphologically?

A

Pseudophyllid eggs: operculated, unembryonated, may have abopercular knob and ciliated coracidium develops. Cyclophyllid eggs: non-operculated, thick shell, no ciliated larva.

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18
Q

What is the common name and order of Diphyllobothrium latum?

A

The broad fish tapeworm; a pseudophyllid cestode.

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19
Q

List the definitive and intermediate hosts of Diphyllobothrium latum.

A

Definitive hosts: humans and fish-eating mammals (dogs, cats, foxes, bears). 1st IH: copepods. 2nd IH: freshwater fish (e.g. pike, perch).

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20
Q

How is Diphyllobothrium latum transmitted to humans?

A

By eating raw or undercooked freshwater or marine fish containing plerocercoid larvae.

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21
Q

Describe the adult morphology of Diphyllobothrium latum.

A

Yellow-grey, ribbon-like worm, typically 3–10 m long; scolex with two slit-like grooves (bothria); gravid proglottids with rosette-shaped uterus.

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22
Q

What is the key haematological complication of Diphyllobothrium latum infection?

A

Vitamin B₁₂ deficiency causing megaloblastic (pernicious-like) anaemia due to competition for B₁₂ in the ileum.

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23
Q

What are the main clinical features of Diphyllobothrium latum infection?

A

Often asymptomatic; may cause abdominal pain, diarrhoea, weight loss, and B₁₂ deficiency with anaemia in ~40% of cases.

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24
Q

How are Diphyllobothrium latum infections diagnosed?

A

Detection of characteristic operculated eggs or occasionally proglottids in stool, plus low serum B₁₂ if anaemic.

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25
What is the treatment of choice for Diphyllobothrium latum?
Praziquantel 5–10 mg/kg as a single dose; give vitamin B₁₂ supplementation if deficient.
26
How can Diphyllobothrium latum infection be prevented in fish consumers?
Thoroughly cook fish (≥63 °C, opaque flesh) or deep-freeze fish (e.g. −20 °C for at least 24 hours) before consumption.
27
What is sparganosis and which genus causes it?
A tissue infection caused by plerocercoid larvae (spargana) of Spirometra spp. (pseudophyllid cestodes).
28
List three main ways humans acquire sparganosis.
1) Drinking water with infected copepods. 2) Eating raw/undercooked flesh of frogs, snakes, or other 2nd IH. 3) Applying raw infected flesh as poultice to skin or eye.
29
What is the most common clinical presentation of sparganosis?
Migrating subcutaneous swellings ('creeping tumours') caused by motile larvae.
30
Name two serious organ-specific forms of sparganosis.
Ocular sparganosis (eye pain, oedema, visual loss) and cerebral sparganosis (neurological symptoms).
31
What is the mainstay of treatment for sparganosis?
Surgical removal of larvae; anti-helminthic drugs are largely ineffective.
32
Why is Hymenolepis nana epidemiologically important?
It is the most common human cestode infection worldwide and can complete its entire life cycle in humans.
33
What are the definitive and intermediate hosts of Hymenolepis nana?
Definitive hosts: humans and rodents. Optional intermediate hosts: arthropods such as fleas and flour beetles.
34
How is Hymenolepis nana transmitted to humans?
By ingestion of embryonated eggs in contaminated food, water, or hands, or ingestion of infected arthropods containing cysticercoids. Autoinfection can also occur.
35
What is unique about Hymenolepis nana's life cycle compared to other cestodes?
It can complete its entire life cycle within a single human host, allowing autoinfection and heavy worm burdens.
36
Describe the adult morphology of Hymenolepis nana.
A small tapeworm, 15–40 mm long, with a scolex bearing four suckers and a retractable rostellum armed with 20–30 hooks; 100–200 short proglottids.
37
Describe the eggs of Hymenolepis nana.
Oval eggs (40–60 µm) with a thin outer membrane and an inner membrane surrounding the oncosphere; polar thickenings give rise to 4–8 polar filaments (diagnostic).
38
What are the typical clinical features of heavy Hymenolepis nana infection?
Non-specific GI symptoms: abdominal pain, diarrhoea, anorexia; children may have more severe manifestations.
39
How is Hymenolepis nana infection diagnosed and treated?
Diagnosis: characteristic eggs in stool microscopy. Treatment: Praziquantel is effective against adult worms and larvae.
40
What control measures help prevent Hymenolepis nana transmission?
Good personal hygiene, improved sanitation, and control of rodents and insects.
41
What are the definitive and intermediate hosts of Taenia saginata?
Definitive host: humans. Intermediate hosts: cattle and other bovines (cysticercus in muscle).
42
How do humans acquire Taenia saginata infection?
By eating raw or undercooked beef containing cysticerci (Cysticercus bovis) in muscle.
43
Describe the scolex of Taenia saginata.
Small scolex with four muscular suckers and no hooks – an unarmed rostellum.
44
How can Taenia saginata and Taenia solium proglottids be distinguished?
T. saginata gravid proglottids have >15 main lateral uterine branches; T. solium has <15 (typically 7–13).
45
Are Taenia saginata eggs infective to humans?
No. T. saginata eggs are infective only to cattle; humans acquire infection from cysticerci in meat, not from eggs.
46
What are the main clinical features and treatment of Taenia saginata infection?
Usually mild GI symptoms and anal pruritus from motile proglottids. Treat with single-dose praziquantel or niclosamide.
47
What are key control measures for Taenia saginata?
Meat inspection at abattoirs, thorough cooking of beef, and preventing human faecal contamination of grazing land.
48
What are the definitive and intermediate hosts of Taenia solium?
Definitive host: humans. Intermediate hosts: pigs and humans (humans can be both DH and IH).
49
How do humans acquire intestinal Taenia solium (taeniasis)?
By eating undercooked pork containing cysticerci (Cysticercus cellulosae) in muscle.
50
How do humans acquire cysticercosis from Taenia solium?
By ingesting eggs from human faecal contamination (faeco-oral transmission) or via autoinfection from their own intestinal infection.
51
Describe the adult scolex of Taenia solium.
Scolex with four suckers and an armed rostellum bearing two concentric rows of hooks.
52
Describe the cysticercus stage of Taenia solium.
A fluid-filled, translucent cyst (5–20 mm) with a thin wall and a single invaginated protoscolex; found in pig or human tissues.
53
Which organs are commonly affected in human cysticercosis?
Subcutaneous tissue, skeletal muscle, eye (ocular cysticercosis), and brain (neurocysticercosis).
54
Can cysticercosis occur in people who do not eat pork?
Yes. Infection is from ingestion of T. solium eggs (human faeces), not from eating pork.
55
What is neurocysticercosis and why is it important?
Infection of the CNS by T. solium cysticerci; it is a leading preventable cause of epilepsy in low- and middle-income countries.
56
How is cysticercosis diagnosed?
Imaging (CT, MRI, X-ray for calcified cysts) plus serology (antibody/antigen detection); lesions evolve from viable to degenerating to calcified.
57
How is neurocysticercosis generally managed?
With albendazole or praziquantel plus corticosteroids, antiepileptic drugs, and sometimes surgery depending on lesion number, location, and symptoms.
58
What are key control strategies to prevent T. solium transmission?
Improved sanitation and hygiene, meat inspection and proper cooking of pork, anthelmintic treatment of pigs (e.g. oxfendazole), and pig vaccination (TSOL18).
59
What are the main species of Echinococcus causing human disease and their clinical syndromes?
E. granulosus causes cystic echinococcosis (hydatid disease); E. multilocularis causes alveolar echinococcosis.
60
What are the usual definitive and intermediate hosts of Echinococcus granulosus?
Definitive hosts: dogs and other canids. Intermediate hosts: sheep and other ungulates; humans are accidental intermediate hosts.
61
How do humans become infected with Echinococcus granulosus?
By ingesting eggs from dog faeces, via direct contact or contaminated food, water, or environment.
62
Describe the hydatid cyst structure in cystic echinococcosis.
A slow-growing fluid-filled cyst with thick laminated outer wall and inner germinal layer producing brood capsules and protoscolices ('hydatid sand'); may contain daughter cysts.
63
Which organ is most commonly affected in cystic echinococcosis and what are the symptoms?
The liver (~75%); symptoms include abdominal pain, mass, and biliary obstruction; lungs and other organs may also be involved.
64
What serious complication can occur if a hydatid cyst ruptures?
Anaphylaxis and dissemination of protoscolices leading to secondary cyst formation.
65
How is cystic echinococcosis treated?
Albendazole ± praziquantel, plus surgical removal or PAIR (puncture–aspiration–injection–reaspiration) when indicated.
66
What are the definitive and intermediate hosts of Echinococcus multilocularis?
Definitive hosts: foxes, coyotes, dogs, cats. Intermediate hosts: rodents; humans are accidental intermediate hosts.
67
How does alveolar echinococcosis differ from cystic echinococcosis in pathology?
E. multilocularis produces poorly defined, multilocular, infiltrative lesions in the liver resembling a malignant tumour, with potential metastasis to other organs.
68
How is alveolar echinococcosis managed?
Early radical surgery plus long-term benzimidazole therapy; advanced disease often requires lifelong medical suppression.
69
List key public health control measures for echinococcosis.
Regular deworming of dogs, safe disposal/cooking of offal, control of stray dogs, improved slaughterhouse hygiene, and washing wild berries/mushrooms in endemic areas.
70
In general, what is the main difference in disease severity between adult and larval cestode infections in humans?
Adult intestinal infections are usually mild; larval tissue infections (e.g. neurocysticercosis, hydatid disease, sparganosis) can be severe or life-threatening.
71
Which human cestode infection is classically associated with vitamin B₁₂ deficiency?
Diphyllobothrium latum (broad fish tapeworm).
72
Which cestode is most commonly acquired via autoinfection and is especially common in children?
Hymenolepis nana.
73
Which cestode infections are mainly controlled by meat inspection and proper cooking?
Taenia saginata, Taenia solium, and to some extent Diphyllobothrium spp.
74
Which cestode larvae cause important CNS disease in humans?
Taenia solium (neurocysticercosis) and Echinococcus multilocularis (alveolar echinococcosis); E. granulosus and Spirometra spp. can also involve the CNS.
75
What is the drug of choice for most adult intestinal cestode infections?
Praziquantel (with niclosamide as an alternative in some cases).
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