Parasites 1: Cestodes (fish, beef, pork, hydatid tapeworms) Flashcards
Can you name the different trematodes, cestodes, nematodes and filarial parasites?
What are the different types of cestodes that exist and what is the general structure of a cestode?
Intestinal tapeworms in humans include Taenia saginata (beef tapeworm); Taenia solium (pork tapeworm); Hymenolepis nana (dwarf tapeworm); Diphyllobothrium spp. (fish tapeworm) and the zoonotic tapeworms Hymenolepis diminuta (rat–flea cycle) and Dipylidium caninum (dog–flea cycle)
How is the appearance of beef and pork tapeworm different?
What are the clinical features of taeniasis?
Remember: Taenia saginata does not form cysts in the tissues of human
What are other general differences between saginata and solium?
What is the life-cycle of saginata?
What is the life cycle of solium?
How are the proglottids of saginata and solium different?
What do taenia eggs look like?
Saginata and solium eggs are indistinguishable from one another.
How do we diagnose taeniasis?
- Identification of eggs/proglottid segments in faeces
- Faecal antigen test
- Eosinophilia (T. solium only)
How do we treat taeniasis?
• Praziquantel: kills adult worms but not eggs (therefore faeces highly infective post-treatment)
- If patient also has neurocysticercosis (from solium) then praziquantel should be used with caution because inflammation around dying cysts can cause symptoms such as seizures
- Niclosamide is an alternative given at 2grams once for adults
- After treatment, stools should be examined for three days and then at 1 and 3 months to make sure the infection has gone
How do taenia solium eggs cause cysticercosis?
- Infection by ingestion of solium eggs
- Rare in Islamic countries
- Once the eggs reach the intestines, the egg hatches and the oncospheres penetrate the intestinal wall and blood stream and there it develops into the cystocerci in the tissues (heart, brain, eye, muscle etc.)
- The consequences of cysticercosis are the formation of a lesion and the inflammatory response to it
- Cysticerci can be from a few mm to 10cm
- The largest cysts are found in the ventricles and subarachnoid spaces
- Cysts that are static elicit little immune response
- New, large or degenerating cysts are associated with a much more extensive inflammatory response
- Two types of cysticercosis
- Extraneural cysticercosis
- Neurocysticercosis
- Intraparenchymal -> seizures, generally good prognosis
- Extraparenchymal -> intracranial htn, progressive disease and high mortality. Presents as viable, calcified or degenerating cysts.
- Can be both together
- The morbidity mostly due to CNS or ocular cysts or heart (conduction disturbance)
- Cysts in subcut tissue mostly of cosmetic significance
- Ocular disease:
- Mostly subretinal or in vitreous humour
- Altered vision and blindness
- Important to rule out intraocular cysticercosis before initiating treatment as inflammatory response in eye can severely damage the eye
- Neuro cysticercosis
- Number and distribution as well as degree of inflammation of cysts determines clinical symptoms
- Cognitive impairment also a symptom
- Focal weakness
- Changes in mental state
- Mimics SOL
- In endemic areas often more cysts
- Number and distribution as well as degree of inflammation of cysts determines clinical symptoms
- One of the most common cause of epilepsy in endemic areas
How does neurocysticercosis present?
- Difficult as unspecific presentation
- Even more difficult in places where no CT or MRI or serology present
- Both CT or MRI can present the following:
- Viable or denigrating cysts
- Calcified cysts
- Intraventricular cysts
- MRI is useful for imaging of ventricular cysts
- CT is better for calcified cysts
Further examples of neurocysticercosis scan
How do we treat neurocysticercosis?
- Control of symptoms takes a high priority – be it seizures or intracranial hypertension or hydrocephalus
- This may include surgical intervention
- Anti-helminthic therapy is generally indicated in patient with multiple viable life cysticerci but not for patients with CALCIFIED cysts
- Co-administration of steroids will help to tone down the symptomatic effects of the inflammatory response (dexamethasone)
How do we best prevent the spread of taenia?
Which organism causes fish tapeworm?
Diphyllobothrium latum
- Many different species – mostly in the northern hemisphere
- Up to over 30 feet of length
What is the lifecycle of D. latum?
Complex:
- Ingestion by humans of raw or undercooked fish
- These fish have to be freshwater fish – adult worm present along the muscle fibres of the fish -> difficult to differentiate
- We eat the larvae which is destined to become an adult
- Goes to small intestine where it is digested by enzymes
- This releases the worms that are destined to become adults
- Attaches to the wall of the intestine by opening up its bothria (grooves)
- Two grooves, one on either side of its scolex
- This tapeworm absorbs some of our feed through its tegument and that’s how it grows
- 3 – 5 months to achieve full length adulthood
- The proglottids are wider than its long (that’s why it is called the broadfish tapeworm)
- The gravid proglottids break off and break up in the large intestine
- Eggs pass out in faeces and MUST enter fresh water
- The Egg contains a larva called coracidium
- This coracidium resembles plankton -> round organism with cilia – free-swimming
- Copepods eat these and act as intermediate hosts
- It penetrates through the stomach of this copepod into muscle tissue and enters first larval stage (procercoid)
- Then ingested by minnow, then releases the procercoid in its own GI tract, which then allows the procercoid to lodge in minnow muscle tissue
- There it grows into last pleural stage
- Minnow can be eaten by a larger fish
How is fish tapeworm infection diagnosed?
How do we treat fish tape worm infection?
Which organisms cause which form of hydatid disease?
- Echinococcus granulosus = dog tapeworm
- According to the WHO, there are four forms of echinococcosis:
Cystic echinococcosis, also known as hydatid disease or hydatidosis, caused by infection with Echinococcus granulises;
Alveolar echinococcosis, caused by infection with E. multilocularis;
Polycystic echinococcosis, caused by infection with E. vogeli;
Unicystic echinococcosis, caused by infection with E. oligarthrus.
How common is hydatid disease and where is it prevalent?
- Risk factors for human cystic echinococcus
- Livestock ownership
- Occupation
- Dog ownership
- Uncontrolled slaughtering and feeding uncooked viscera to dogs
- Poor hygienic living conditions
- Female gender
- Major disease burden
- 1 million people live with these diseases at any one time
- 19 300 deaths and around 871 000 DALY’s globally each year
- Cystic echinococcus: 2.2% mortality after surgery and 6.5% risk of relapse
what are the life cycles of the echinoccocci?
- 10 different genotypes of echinococcus granulosus (with some minor differences between them)
- For both species:
- Carnivores act as definite hosts for the adult-type worms
- Herbivorous prey acts a intermediary host of larvous stage
- For example - cystic:
- The adult tapeworm is about 2-7 cm long
- Small intestine of carnivore host
- Eggs are released from stool
- Intermediary host takes up eggs and they hatch in small intestine
- Intermediate host often sheep:
- Oncopheres hatch and they have 6 hooklings which infiltrate the intestinal wall and migrate to several organs, in particular liver and lungs
- Prevention and control of alveolar echinococcosisis more complex as the cycle involves wild animal species as both definitive and intermediate hosts. Regular deworming of domestic carnivores that have access to wild rodents should help to reduce the risk of infection in humans.
Cystic echinococcosis is less complex to prevent as it involves domestic animal species as definitive and intermediate hosts. Periodic deworming of dogs, improved hygiene in the slaughtering of livestock (including the proper destruction of infected offal), and public education campaigns have been found to lower and, in high-income countries, prevent transmission and alleviate the burden of human disease.
What are the clinical features of echinococcus infection?
- E. granulosus:
- Αbout 70% of cysts develop in the liver, 20% lung and rest brain/bone/spleen/etc.
- Usually asymptomatic unless cysts grow loarge enough to cause mass effect
- Typical presentation is a distending abdomen in an otherwise well pt
- However, can develop secondary bacterial infections. Can rupture and cause hypersensitivity reaction. Liver cysts can seed into the peritoneal cavity.
- E. multilocularis:
- Not a problem in the tropics
- Forms daughter cysts by external budding
- It means it progressively invades surrounding tissue like a malignant tumour
- Not contained in a defined fibrous capsule
- AE affects exclusively the liver
- In humans the incubation period is long (5 – 15 years)
- The initial exposure is often during childhood
- Highly aggressive disease -> leads to liver failure
- Rarely metastasis to lungs and CNS
- Patients can develop symptoms of a failing liver -> up to 90% mortality
Radiographic features of echinococcus 1
Radiographic features of echinococcus 2
Radiographic features of echinococcus 3
Microscopic features echinococcus
