Case 18- worms Flashcards

1
Q

Parasitic worms epidemiology

A

They are common in unsanitary conditions and spread via the faecal- oral route. Infections in children can cause developmental delays, poor school performance and increased mortality and morbidity. Endemic in Africa, South America, India and the South Pacific.

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2
Q

Helminths

A

Parasitic worms which invade the body, they are a series of eukaryotic macroparasites. Which reside in the GI tract or invade the blood and lymph vessels. Parasites which live within the host are endoparasites. Helminth refers to three worm groupings which differ in morphology and life cycle (Nematodes, trematodes, Cestodes)

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3
Q

Nematodes (roundworm)

A

Includes ascaris, hookworms and whipworms. The head can be distinct from the rest of the body, it contains a ‘mouth’ and tail which may attach to the host

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4
Q

Trematodes (flukes)

A

Include liver and blood flukes which include schitosomes. Flattened body shape (1-6mm) and no digestive tract, they absorb nutrients across their outer surface

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5
Q

Cestodes (tapeworms)

A

Include hyatids, a specialised tapeworm which can cause Echinococcosis, Taenia solium and Taenia saginata. Can grow to extreme lengths i.e. 20 meters.

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6
Q

Soil transmitted Helminths

A

1.5 people at any time are infected with helminths. Four species of nematodes (roundworms) account for the majority of infection:
• Ascaris lumricoides, causative agent of ascariasis
• Trichuris trichiura (whipworm)
• Necator Americanus and Ancylostoma duodenale (hookworms)
Strongyloides stercoralis (threadworm or pinworm) is prevailent and associated with dog faeces.

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7
Q

Ascaris

A

Ascaris lumbricoides (ascaris) causes ascariasis. Largest roundworm (nermatode), grows to 35cm on average. Globally 1 billion people are infected.

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8
Q

Life cycle of ascaris

A

1) Infections occur when ingesting food or water contaminated by eggs, they pass into the intestine.
2) They hatch and release larvae into the gut lumen.
3) They penetrate the gut wall and travel in the circulatory system to the lungs, where further development occurs.
4) The host coughs up the larvae and swallows them, they can mature to the adult form in the gut.
5) The mature worms mate and produce eggs which are expelled in the faeces.

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9
Q

Symptoms of ascaris

A

Normally asymptomatic. When worm burden increases there is an increase in symptoms (lethargy, weight loss, inability to concentrate) due to competition for nutrients. Causes slowed growth in children. Gastrointestinal symptoms i.e. diarrhoea, abdominal pain, malaise and weakness. Can get bowel obstruction and intestinal bleeding.

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10
Q

Complications of ascaris

A

The larvae migrate to the lungs causing respiratory problems due to immune response i.e. eosinophilic pneumonia (Loffler’s syndrome).

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11
Q

Diagnosis and treatment of ascaris

A

Diagnosis- analyse stool sample with light microscopy looking for eggs.
Treatment- mebendazole

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12
Q

Hookworm

A

Widespread and can be concurrent with ascaris infection. Ascaris is a risk factor for hookworm and vice versa.

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13
Q

Hookworm species

A

• Ancylostoma duodenale (Old World hookworm)
• Necator americanus- North American but very rare due to improvements in treatment and sanitation.
Infects dogs- Ancylostoma carinum, can cause skin manifestations in humans but cant complete its life cycle.

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14
Q

Lifecycle of Hookworm

A

The lifecycle is the same as Ascaris but the host doesn’t have to eat the eggs to become infected. The eggs are shed in the environment by an infected individuals i.e. open defecation. The eggs hatch in the soil and the larvae are chemoattracted to the new host and burrow through the skin. Wear shoes to prevent transmission

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15
Q

Symptoms of hookworms

A
  • Cutaneous larva migrans- when hookworms enter the skin, the patient experiences an allergic reaction at the site.
  • Often asymptomatic
  • Hookworm damages the gut wall when it attaches to the gut with its teeth like processes. Causes blood, protein and fluid loss. Leading to malnutrition and hypoproteinaemia
  • Anaemia due to blood loss and iron malabsorption
  • Cardiac complications due to larval forms in circulation
  • Severe acute pulmonary reactions (pneumonia) and gastrointestinal reactions
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16
Q

Ancylostoma caninum

A

Ancylostoma caninum (dog hookworm) is common in UK dogs and spreads to owners if they cant clean up after them. It can get in the skin of humans causing larva migrans no where else, is a dead end host.

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17
Q

Hookworms- diagnosis/treatment

A

Diagnosis- detection of eggs in stool by a light microsope

Treatment- mebendazole

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18
Q

Schistosoma

A

Causes Schistosomiasis (bilharzia). A tissue resident helminth which invades the body away from the site of primary infection. Two species of trematodes (flukes/flat worms) are associated with the majority of infections, especially in African countries- S.haematobium and S.mansoni, cause 85% of cases in Africa.

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19
Q

Types of schistosoma

A
  • S.haematobium causes urogenital/bladder problems

* S.mansoni and S.japonicum cause intestinal and hepatic disease

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20
Q

Schistosoma life cycle

A
  • Infected human hosts shed eggs into the environment (fresh water).
  • The eggs hatch in the water and the parasites infect freshwater snails.
  • In the snail the parasite matures into an infectious form and is released into water again.
  • The parasites are chemo-attracted to the human host and they penetrate through the skin and enter the circulatory system.
  • They migrate to the liver where they mature into the final worm stage
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21
Q

Where do the different species of Schistosoma migrate to within the body

A

S. haematobium worms migrate to the venous plexus of the bladder and secrete eggs into the bladder and out in the urine
S. mansoni / S. japonicum worms migrate to the mesenteric veins of the intestine and secrete eggs into the GI tract and out via faeces

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22
Q

Swimmers itch

A

When Schistosoma enters via the skin and causes inflammation and itching

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23
Q

Pathology- S.haematobium (urogenital schistosomiasis)

A
  • Haematuria (blood in urine).
  • Fibrosis of the bladder and ureter, sometimes kidney damage
  • Increased risk of squamous cell bladder cancer
  • Women: genital lesions, vaginal bleeding, pain during sexual intercourse and nodules in the vulva
  • Men: damage to the seminal vesicles, prostate and other organs resulting in infertility
  • Rarely: eggs migrate to the spinal cord or brain and can cause seizures, paralysis, or spinal cord inflammation
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24
Q

Pathology- S.mansoni and S.japonicum (hepatic-intestinal schistosomiasis)

A
  • Abdominal pain, diarrhoea, and blood in the stool
  • Hepatomegaly, splenomegaly
  • Ascites, portal hypertension
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25
Q

Diagnosis of Schistosoma

A

Stool or urine samples are examined macroscopically for parasite eggs. Stools for S.mansoni or S.japonicum eggs and urine for S.haematobium eggs.

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26
Q

Treatment for Schistosoma

A

Praziquantel for 1-2 days

27
Q

Cestodes

A

Include tapeworms and hydatid infection. They have a biphasic life cycle, involving non-human hosts and then a human phase.

28
Q

Tapeworms

A

Flat worm, develop in the GI tract. Can be thousands (up to 4000) egg sacs and 20m long. Associated with eating raw or undercooked meat or fish. Includes Taenia solium, Taenia saginata and Taenia asiatica

29
Q

The tapeworms which affect humans

A
  • Taenia solium (pork tapeworm, Worldwide)
  • Taenia saginata (beef tapeworm)
  • Taenia asiatica (pork tapeworm, Asia)
30
Q

Lifecycle of both beef and pork tapeworm

A
  • Eggs or gravid proglottids are in the faeces and passed into the environment
  • Cattle (T.saginata) and pigs (T.solium) become infected by ingesting vegetation contaminated by eggs or gravid proglottids
  • Oncospheres hatch, penetrate the intestinal wall and circulate to musculature
  • Oncospheres develop into cysticerci in muscles
  • Humans are infected by ingesting raw or undercooked infected meat
  • Scolex attach to the intestine
  • Adults in small intestine
31
Q

Difference between definitive and intermediate hosts

A

Intermediate hosts harbour the sexually immature parasite often vectors. Definitive hosts are where the parasite can reach the adult stage.

32
Q

Humans as the definitive host (Taeniasis)- Cestodes

A

Animals i.e. pig or cow (intermediate host) ingest the eggs and cysts develop in the body tissue of the infected animal. The cyst containing meat is ingested by the human (definitive host). The cyst enters the GI tract and forms a worm.

33
Q

Symptoms / Treatment of cestodes when humans are the definitive host

A

Symptoms- largely asymptomatic but heavy infection with multiple worms can cause:
• Weight loss
• Dizziness
• Abdominal pain
• Diarrhoea
• Vitamin B12 deficiency
• Headaches, nausea, constipation, chronic indigestion, loss of appetite
Adult tapeworms can be treated with oral niclosamide.

34
Q

Cestodes- Humans as intermediate hosts

A

The human might ingest the egg directly i.e. by eating food contaminated with the egg. The cysts develop inside the human. If this occurs humans can develop cysticercosis.

35
Q

Symptoms of cystodes when humans are the intermediate host

A
  • Cysts can develop in the muscle- muscle inflammation, fever, eosinophilia, muscle swelling, atrophy and scarring
  • Cysts can die and become calcified
  • Can infect the eyeball, extraocular muscles and conjunctiva causing visual loss
  • Neurocysticercosis- when cysts affect the central nervous system. Symptoms include seizures, headaches, blindness, meningitis and dementia
36
Q

Treatment for Cystodes

A

Specialist treatment with praziquantel or albendazole. Neurocysticercosis may need emergency treatment including steroids, anticonvulsants and neurosurgery.

37
Q

Hydatid infections

A

Caused by Echinococcus tapeworms. Humans are the intermediate host. The four major forms:
• Cystic echinococcosis (CE) also known as hydatid disease or hydatidosis
• Alveolar echinococcosis (AE)
• Neotropical forms
CE and AE are the most common forms. Normally infections are restricted to animals but with accidental exposure humans become infected

38
Q

Hydatid infections intermediate and dead end hosts

A

If a human was to ingest the eggs from food contaminated by egg-containing feces, the human acts as an intermediate host, although in fact is a dead-end host (the cycle ends). Under these conditions, cysts can form in human tissue.

39
Q

Lifecycle of Hydatid

A
  • Ingestion of embryonated eggs in the faeces
  • Oncosphere hatches- penetrates intestinal wall
  • Hydatid cysts in the liver, lungs etc
  • Protoscolex from cyst
  • The Scolex attaches to the intestine, the adult tapeworm is in the intestine
40
Q

Cystoc echinococcosis (CE) i.e. hydatis disease

A

Development of one or more hydatid cysts in the liver and lungs and sometimes other organs. The asymptomatic incubation period of the disease lasts many years until the hydatid cysts grow and exhibit clinical

41
Q

Symptoms of Cystic echinococcosis

A
  • Abdominal pain, nausea and vomiting are commonly seen when hydatids occur in the liver
  • If the lung is affected you get a chronic cough, chest pain and shortness of breath
42
Q

Alveolar echinococcosis (AE)

A

An asymptomatic incubation period of 5-15 years and causes slow development of primary tumour like lesions normally in the liver. Clinical signs include weight loss, abdominal pain, general malaise and signs of hepatic failure. Larvae can spread to organs via the blood or lymphatic system. If left untreated alveolar echinococcosis is progressive and fatal.

43
Q

Diagnosis of CE and AE

A

Often by ultrasonography and contrast enhanced MRI

44
Q

Treatment of hydatid disease

A

Cystic echinococcosis is managed with albedazole/mebendazole and surgery to remove the cysts. Surgical treatment can be dangerous, if the cyst ruptures this can trigger anaphylaxis and cause death. Alveolar echinococcosis is more difficult to treat and requires long term medication and surgery.

45
Q

Mebendazole

A

Selectively inhibits the synthesis of microtubules blocking polymerisation of tubulin in the parasites intestinal cells

46
Q

Albendazole

A

Similar action as mebendazole, unable to uptake glucose. Dies due to starvation

47
Q

Levamisole

A

A nicotinic acetylcholine receptor agonist which paralyses the musculature of the sensitive nematodes which unable to maintain their anchorage are expelled by normal peristalsis

48
Q

Ivermectin

A

May cause immediate effect due to the death of the microfilaria (early stage in the life cycle of certain parasitic nematodes). Can be effective in a single dose but works best when repeated at 6-12 month intervals to prevent reactivation of the parasite.

49
Q

Diethylcarbamazine

A

Kills both microfilariae and adult worms. Adverse reaction: fever, headache, anorexia, malaise, urticaria, vomiting and asthmatic attacks following the first dose due to the products produced when the parasite is destroyed. The reactions are minimised due to an increase in dosage over the first 3 days.

50
Q

Niclosamide

A

Blocks glucose uptake, oxidative phosphorylation and anaerobic metabolism in the tapeworm by intestinal tapeworms. Can cause mild GI symptoms.

51
Q

Piperazine

A

Affects neurotransmission (GABA agonist) in worms may cause hypersensitivity reactions. Neurological symptoms (including ‘worm wobble’) and may precipitate epilepsy.

52
Q

Praziquantel

A

Paralyses both adult worms and larvae. It may cause nausea, headaches, dizziness and drowsiness, given in a single dose.

53
Q

Thibendazole

A

Inhibits cellular enzymes of susceptible helminths. Can induce gastrointestinal, neurological and hypersensitivity reaction, liver damage and cystalluria

54
Q

Pyrantel

A

Depolarises neuromuscular junctions of susceptible nematodes which are expelled in the faeces, Single dose. May induce GI disturbances, headaches, dizziness, drowsiness and insomnia.

55
Q

Treatment for tapeworms

A

1) Niclosamide

2) Praziquante

56
Q

Treatment for Hydatid infections

A

Surgery is the preferred method to remove cysts, Albendazole as cover

57
Q

Treatment for roundworms (nermatodes)

A
Ascaris spp- Mebendazole or Levamisole
Hookworms- Mebendazole, Levamisole for <6
Pinworms- Mebendazole
Whipworms- Mebendazole or Albendazole
Cutaneous larva migrans
58
Q

Treatment for Filarial infections

A

Elephantiasis- Diethylcarbamazine

Onchocerciasis (river blindness)- Ivermectin (or Diethylcarbamazine)

59
Q

Treatment for flukes

A

Schistosomiasis (bilharzia)- Praziquantel

60
Q

Treatment for Filariasis/Elephantiasis

A

Instead of Diethylcarbamazine you can use Doxycycline. It targets the symbiotic bacteria which reside in the worm’s reproductive tract (Wolbachia spp). Affects fungal sterility, reduces transmission. 8 week course of treatment.

61
Q

Common side effects of antifungal treatment

A

Nausea, other side effects due to long term use, hepatic involvement.

62
Q

Side effects of Mebendazole

A

Alopecia, dizziness, hepatitis, neutropenia, seizure, severe cutaneous adverse reactions (SCARs), skin reactions

63
Q

Contraindications/ side effects of antifungal medication

A
  • Mebendazole- Pregnancy
  • Ivermectin- Pregnancy, skin reactions
  • Levamisole- contraindicated in blood disorders (anaemia), caution with Epilepsy/Sjogren syndrome (autoimmune). Side effects- vomiting (common). In long term use blood disorders (agranulocytosis), skin disorders/rashes, general malaise