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MODULE 4 - Infectious Agents > PARASITOLOGY - Helminths > Flashcards

PARASITOLOGY - Helminths Flashcards

1
Q

What are the three helminth phylums?

A
  • Nematodes (roundworms)
  • Cestodes (flatworms/tapeworms)
  • Trematodes (flukes)
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2
Q

Which phylum does the hookworm helminth belong to?

A

Nematode

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3
Q

How do hookworms infect their hosts?

A

Hookworms infect their hosts through penetration of the skin

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4
Q

What do hookworms produce which allows them to feed on the blood of their hosts?

A

Anti-coagulants

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5
Q

What is Wolbachia and how does it contribute to Dirofilaria (heartworm) treatment?

A

Wolbachia are a bacteria that live within female Dirofilaria parasites and are passed on through generations of Dirofilaria via the eggs produced. Antibiotics that are used to target Wolbachia eventually sterilise the female Dirofilaria and kill the worm

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6
Q

Why is the control of helminths with anthelmintic drugs so challenging (especially in livestock)?

A
  • Limited numbers of anthelmintic drugs
  • Rapid reinfection of the helminths
  • ANTHELMINTIC RESISTANCE
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7
Q

(T/F) There are vaccines developed against helminths

A

FALSE. Helminths are very difficult to develop vaccines against due to being multicellular with very complex genomes

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8
Q

What type of lifecycle do most nematodes have?

A

Direct lifecycle

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9
Q

(T/F) Nematodes have male and female worms

A

TRUE

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10
Q

What does the pre patent period (PPP) mean?

A

The time taken between initial infection of a helminth and the production of eggs by the adult worms

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11
Q

What is a very common canine ascarid?

A

Toxocara Canis

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12
Q

Which phylum does the Toxocara Canis helminth belong to?

A

Nematode

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13
Q

What are the four possible routes of infection for Toxocara Canis?

A
  • Oral (ingestion of eggs containing infectious L3 larvae)
  • Transplacental
  • Transmammary
  • Paratenic hosts
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14
Q

Female Toxocara Canis worms are described to be very fecund. What does this mean?

A

The bodies of the female Toxocara Canis contain lots of ovaries so produce large numbers of eggs

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15
Q

Why does Toxocara Canis affect puppies under three months of age differently to adult dogs?

A

Toxocara Canis affects puppies under three months differently as these puppies are immune-naive whereas adult dogs have a developed immune system to control the infection

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16
Q

What is the infective form of Toxocara Canis?

A

L3 larvae

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17
Q

Describe the lifecycle of Toxocara Canis in puppies under three months old

A
  1. Eggs containing L3 larvae are ingested –>
  2. L3 hatch in the small intestine –>
  3. L3 migrate into the tissues and to the lungs via the liver –>
  4. L3 return to the small intestine via the trachea –>
  5. L3 develop into L4 larvae and then into adults in the small intestine –>
  6. Female Toxocara Canis adults produce eggs which are excreted into the environment in the faeces –>
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18
Q

Describe the lifecycle of Toxocara Canis in adult bitches

A
  1. Eggs containing L3 larvae are ingested –>
  2. L3 hatch in the small intestine —>
  3. L3 migrate to the tissues and go into arrest –>
  4. L3 activate in response to pregnancy (around 3 weeks pre-partum) –>
  5. L3 migrate across the placenta and into the foetal lungs –>
  6. At birth, L3 migrate to the small intestine of the puppy via the trachea –>
  7. L3 develop into L4 larvae and then into adults in the small intestine –>
  8. Female Toxocara Canis adults produce eggs which are excreted into the environment in the faeces –>
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19
Q

What is the pre patent period (PPP) of Toxocara Canis?

A

One month

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20
Q

Which stage in the Toxocara Canis lifecycle ensures 100% transmission of the parasite?

A

Transplacental transmission of L3 larvae into the foetal lungs

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21
Q

What makes Toxocara Canis eggs so challenging to destroy?

A

It has a thick, sticky egg shell that can allow it to survive for years in the environment

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22
Q

Puppies are commonly reinfected with Toxocara Canis at 5 weeks of age. Why is this the case?

A

Some of the T. canis parasites are transmitted 5 weeks later via transmammary transmission. This transmission has no migratory phase and instead adult worms develop in the small intestine directly after transmission

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23
Q

What contributes to the direct pathology and clinical signs of Toxocara Canis in puppies

A
  • The pathology of T. canis is caused by gastrointestinal obstruction of the adult worms causing the puppies to be ‘pot-bellied’
  • The T. canis adult worms also compete with the host for nutrients leading to weight loss
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24
Q

When should anthelmintics be used to treat Toxocara Canis?

A

Anthelmintics 16 days after birth and again at 5 weeks of age

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25
Q

What is a common feline ascarid?

A

Toxocara Cati

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26
Q

What are the three methods of transmission seen in Toxocara Cati?

A
  • Oral (ingestion of eggs containing infectious L3 larvae)
  • Transmammary
  • Paratenic hosts
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27
Q

What does PGE stand for?

A

Parasitic gastroenteritis

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28
Q

What is the term ‘parasitic gastroenteritis (PGE)’ used to describe?

A

Parasitic gastroenteritis (PGE) is a general term used to describe disease caused by gastrointestinal nematodes in livestock

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29
Q

What causes the majority of the production losses associated with livestock gastrointestinal nematode infections?

A

Sub-clinical disease caused by nematode gastrointestinal infections due to the reduction in livestock weight gain

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30
Q

What is the most significant family of nematodes which cause parasitic gastroenteritis (PGE) in grazing ruminants?

A

Trichostrongyloidea (strongyles)

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31
Q

What is a common cause of parasitic gastroenteritis (PGE) in cattle?

A

Ostertagia Ostertagi

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32
Q

Describe the lifecycle of Ostertagia Ostertagi?

A
  1. Female adult worms produce eggs in the abomasum –>
  2. Eggs are excreted in the faeces and into the environment –>
  3. L1 larvae develop –>
  4. L2 larvae develop –>
  5. L3 larvae develop encased in the L2 cuticle –>
  6. L3 larvae are ingested by cattle –>
  7. L3 larvae penetrate the abomasal glands and develop into L4 larvae –>
  8. L4 larvae rupture the abomasal glands and develop into adults –>
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33
Q

The L4 larvae of Ostertagia Ostertagi can undergo hyperbiosis. Why does this occur?

A

The L4 larvae can undergo hyperbiosis (arrest) in the abomasal glands when faced with unideal conditions (i.e. cold winters)

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34
Q

What contributes to the direct pathology of Bovine Ostertagiosis

A

The rupturing of the abomasal glands by the L4 larvae causes hyperplasia and oedema of the abomasal glands. Destruction of the abomasal glands also leads to putrification of the abomasum by secondary bacteria

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35
Q

What is the common appearance of the abomasum in a cow that has been infected with Ostertagia Osteratagi?

A

‘Moroccan leather’ appearance

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36
Q

What is the infectious stage in the lifecycle of Ostertagia Ostertagi

A

L3 larvae

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37
Q

Describe the two clinical forms of Ostertagiosis

A

TYPE 1: Disease seen in first season grazing calves between July and October due to the ingestion of infectious larvae that has developed in pasture

TYPE 2: Disease seen in housed yearlings between March and May due to larvae that were ingested in the previous autumn, that have developed into L4 larvae and been reactivated

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38
Q

What are the clinical signs of type 1 Ostertagiosis?

A
  • Profuse watery diarrhoea
  • Weight loss
  • Submandibular oedema (sometimes)
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39
Q

What are the clinical signs of type 2 Ostertagiosis?

A
  • Intermittent diarrhoea
  • Submandibular oedema (commonly)
  • Weight loss
  • Anorexia
  • Dehydration
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40
Q

How can Ostertagiosis be diagnosed?

A
  • Clinical signs and pasture history
  • Use of diagnostic aids such as faecal egg counts and post-mortems

Ensure diagnosis as a herd, not as individual cattle

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41
Q

How should type 1 Ostertagiosis be treated?

A

Administration of anthelmintics followed by moving the cattle to clean pasture

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42
Q

How should type 2 Ostertagiosis be treated?

A

Administration of more potent anthelmintics such as macrocyclic lactones and pro-benzimidazoles

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43
Q

How can the spread of Ostertagia Ostertagi be controlled?

A
  • Pasture management to reduce exposure to infectious L3 larvae
  • Prophylactic anthelmintic treatments
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44
Q

What is a nematode that can cause Ovine Ostertagiosis in sheep?

A

Teladorsagia Circumcincta

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45
Q

What are the clinical signs of Ovine Ostertagiosis?

A
  • Weight loss
  • Diarrhoea
  • Anorexia
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46
Q

What type of lifecycle do tapeworms have?

A

Indirect lifecycles

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47
Q

Which stage of the tapeworm lifecycle occurs in the final host?

A

The adult stage

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48
Q

Which stage of the tapeworm lifecycle occurs in the intermediate host?

A

The larval stage

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49
Q

(T/F) Tapeworms have male and female worms

A

FALSE. Tapeworms are hermaphrodites so contain both male and female reproductive organs in their proglottids

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50
Q

Describe the anatomical structure of a tapeworm

A

Tapeworms are flat and segmented (proglottids). The proglottids mature from the scolex (head) to the terminal proglottid. Around halfway down the tapeworm, each proglottid contains reproductive organs and the terminal proglottid is gravid (only contains eggs)

51
Q

Tapeworms have an encysted stage in their lifecycle. What do these cysts contain within the intermediate host?

A

The cysts contain scolexes which each contribute to one tapeworm

52
Q

What is the largest tapeworm?

A

Taenia Saginata (5-15m long)

53
Q

List the hosts of the Taenia Saginata tapeworm

A

FINAL HOST: Human
INTERMEDIATE HOST: Bovine

54
Q

What is the encysted form of Taenia Saginata?

A

Cysticercus bovis

55
Q

Describe the lifecycle of Taenia Saginata

A
  1. Adult worm in the human small intestine produces eggs –>
  2. Eggs are passed out of the gravid proglottid and excreted in the faeces –>
  3. Eggs are ingested by cattle –>
  4. The embryo is released from the eggs into the abomasum and penetrates the small intestinal wall –>
  5. Larvae travel into the skeletal muscle and encyst (cysticercus bovis) –>
  6. Larvae mature over 12 weeks and become infectious
  7. Infected meat ingested by humans –>
56
Q

What causes beef to become infected with Taenia Saginata?

A

The use of human sludge to fertilise grazing pasture

57
Q

What causes humans to become infected with Taenia Saginata?

A

The ingestion of undercooked meat

58
Q

How is Taenia Saginata infection diagnosed?

A

Meat inspection at the abattoir
- If there are more than 25 cysts the carcass will be condemned
- If there are less than 25 cysts in one region, the meat has to be frozen for two days before going into the human food chain

59
Q

How can the spread of Taenia Saginatas be controlled?

A
  • Restrict the use of human sludge as fertiliser for grazing pasture
  • Meat inspection
  • Fully cooking meat
60
Q

List the hosts of the Taenia Solium tapeworm

A

FINAL HOST: Human
INTERMEDIATE HOSTS: Pigs, Humans

61
Q

What is the cystic form of Taenia Solium?

A

Cysticercus cellulosae

62
Q

Where in the world is Taenia Solium endemic?

A

Latin America due to close association with man and pig

63
Q

Humans are both final and intermediate hosts for Taenia Solium so can suffer from auto-infection. Describe what this is.

A

Humans can suffer from auto-infection of Taenia Solium via reverse peristalsis where the eggs produced by the adults in the small intestine are moved back into the stomach and rupture. The larvae are activated and migrate through the tissues where they encyst

64
Q

Where do Taenia Solium larvae commonly encyst?

A

Ocular and central nervous system tissue

65
Q

How can the spread of Taenia Solium be controlled?

A
  • Adult tapeworms in humans can be treated
  • Vaccination for pigs (CysVax)
  • Meat inspection
66
Q

What is the morphological difference between Taenia Saginata and Taenia Solium tapeworms?

A

T. solium have both hooks and suckers whereas T. saginata only has suckers

67
Q

List three non-zoonotic Taenia tapeworm species that have a major economic impact on sheep farming in the UK

A
  • Taenia ovis
  • Taenia hydatigena
  • Taenia multiceps
68
Q

List the hosts of T. ovis, T. hydategina and T. multiceps

A

FINAL HOST: Dog
INTERMEDIATE HOST: Sheep

69
Q

List the hosts of Echinococcus granulosus granulosus

A

FINAL HOST: Dogs
INTERMEDIATE HOSTS: Sheep, Humans (accidental hosts)

70
Q

What are the economic and public health impacts of Echinococcus granulosus granulosus infection?

A
  • E. g. granulosus has a major economic impact on the sheep farming industry in the UK
  • E. g. granulosus is zoonotic
71
Q

What is the encysted form of E. g. granulosus?

A

Hydatid cysts

72
Q

Describe the lifecycle of E. g. granulosus

A
  1. Adult worms produce eggs in the dog’s small intestine –>
  2. Eggs shed from the gravid proglottid in the faeces –>
  3. Eggs are ingested by sheep (sometimes humans) –>
  4. Embryo released from the eggs and penetrate the intestinal wall –>
  5. Embryo is encysted in a hydatid cyst in the liver/lungs –>
  6. Hydatid cysts ingested by dogs —>
73
Q

How can dogs (the final host) become infected with E. g. granulosus?

A

By feeding on fallen stock or on offal containing hydatid cysts

74
Q

How can sheep (intermediate hosts) become infected with E. g . granulosus?

A

By the ingestion of eggs from dog faeces

75
Q

How can humans (accidental intermediate hosts) become infected with E. g . granulosus?

A

Close contact with an infectious dog (ingestion of eggs from water, foodstuffs or the coat of the dog)

76
Q

How is E. g . granulosus transmission controlled?

A
  • Regular deworming of dogs (praziquantel)
  • Proper disposal of infected sheep carcasses
  • Hygiene
77
Q

List the hosts of Dipylidium caninum

A

FINAL HOSTS: Dog, Cat, Human
INTERMEDIATE HOSTS: Flea/Louse

78
Q

Describe the lifecycle of D. caninum

A
  1. Adults in the small intestine of the final host produce eggs –>
  2. Gravid proglottids shed from the tapeworm and move out of the host into the environment via the gastrointestinal tract –>
  3. Gravid proglottids rupture in the environment, releasing eggs –>
  4. Eggs are ingested by fleas/lice –>
  5. Cysterceroids are formed in the haemocoel (body cavity) or the flea/louse –>
  6. Dog/cat ingest the infected flea/louse when grooming –>
79
Q

What are the diagnostically significant morphologies of D. caninum that differ from Taenia species of tapeworm. Why is it so important to be able to identify these in practice?

A
  • Motile gravid proglottids
  • Double genital pores in the proglottids
  • Eggs are contained in packets

this is diagnostically significant because when treating D. caninum it is important to treat both the endo- and ectoparasites (motile gravid proglottids)

80
Q

What is the other name used to describe trematodes?

A

Flukes

81
Q

(T/F) Trematodes/flukes are within the phylum platyhelminths (flatworms)

A

TRUE

82
Q

What are the four most important families of flukes?

A

Fasciolidae
Dicrocoeliidae
Paramphistomatidae
Schistosomes

83
Q

What is the most common liver fluke in the UK?

A

Fasciola hepatica

84
Q

What is the common name for Fasciola hepatica?

A

Liver fluke

85
Q

What are the hosts for F. hepatica?

A

FINAL HOST: Most mammals
INTERMEDIATE HOST: Galba truncatula (amphibious snail)

86
Q

What is the name of the disease caused by F. hepatica?

A

Fascioliasis

87
Q

Why is fascioliasis a public health concern?

A

Fascioliasis is a zoonotic disease

88
Q

Describe the lifecycle of F. hepatica

A
  1. Eggs are deposited in the faeces of the final host –>
  2. Embryonisation occurs at 22°C in the presence of moisture –>
  3. Hatching of the miracidium is induced by light opening the operculum (cap) –>
  4. The miracidium penetrate the Galba truncatula (amphibious snail) –>
  5. Miracidum develops into a sporocyst followed by rediae followed by cercaria –>
  6. Cercaria exit from the snail under the right environmental conditions –>
  7. Cercaria lose their tails and develop into metacercariae which encyst on grass –>
  8. Metacercariae are ingested by the final host and enter the small intestine –>
  9. About 4-6 weeks after infection, the metacercariae cross the intestinal wall into the pericardium and through the liver to the biliary ducts where at this point they have developed into juvenile flukes –>
  10. The juvenile flukes develop into adults and produce eggs within the biliary ducts –>
89
Q

What stains F. hepatica eggs and why is this beneficial to the parasite?

A

Quinone stains the eggs giving then a yellowish/brown appearance. Quinone allows the eggs to survive in the environment under sub-optimal conditions

90
Q

What are the three forms of the fascioliasis disease?

A
  • Acute fascioliasis
  • Subacute fascioliasis
  • Chronic fascioliasis
91
Q

When during the year is acute fascioliasis detected?

A

Autumn/early winter

92
Q

What causes the direct pathology of acute fascioliasis?

A

The mass migration of the juvenile flukes through the liver to reach the bile ducts causing liver damage, haemorrhage and often sudden death

93
Q

Describe the appearance of a liver with acute fascioliasis on post-mortem examination

A
  • Enlarged
  • Hyperaemic
  • Necrotic tracts where the juvenile flukes have migrated
  • If the liver is cut open, it is possible to see the juvenile flukes within the tissue
94
Q

When during the year is subacute fascioliasis detected?

A

Late autumn/winter

95
Q

What causes the direct pathology of subacute fascioliasis?

A
  • Migration of the juvenile flukes through the liver to reach the bile ducts causing liver damage and haemorrhagic anaemia
  • Adult flukes feeding on the biliary mucosa within the bile ducts causing damage and inflammation leading to oedema and ascites
96
Q

When during the year is chronic fascioliasis detected?

A

Late winter/early spring

97
Q

What causes the direct pathology of chronic fascioliasis?

A

Adult flukes feeding on the biliary mucosa within the bile ducts resulting is progressive failure to thrive, emaciation, submandibular oedema and ascites

98
Q

Describe the appearance of a liver with chronic fascioliasis on post-mortem examination

A
  • Irregular
  • Pale
  • Firm
  • Heavy fibrosis
  • Thickened, distended bile ducts
  • Squeezing of the liver would cause adult flukes to emerge
99
Q

Why are cattle less susceptible to bovine fascioliasis?

A

Their immune system limits primary infection and inhibits secondary infection

100
Q

What is the economic impact of chronic bovine fascioliasis?

A

Productivity loss

101
Q

What can be used to diagnose ovine fascioliasis?

A
  • Clinical signs
  • Seasonal occurrence
  • Faecal egg count
  • Post-mortem/identification of flukes in the liver
102
Q

What can be used to diagnose bovine fascioliasis?

A
  • Faecal egg counts
  • Liver enzymes
  • ELISA
103
Q

Describe the optimal habitat for Galba truncatula (amphibious snails)

A

Muddy areas/areas with slow moving water with a slightly acidic pH

104
Q

What are the factors required for the presence of F. hepatica metacercardiae in the environment (affecting the epidemiology of the parasite)?

A
  • Galba truncatula (snails) present in their optimal environment
  • Moisture
  • Temperature
105
Q

Describe the ‘summer infection of snails’ with F. hepatica

A

Snails are infected in late spring/summer by miracidium from overwintered eggs or carrier animals

106
Q

Describe the ‘winter infection of snails’ with F. hepatica

A

Snails are infected in autumn when the conditions are sub-optimal so the development of the miracidium is arrested over the winter and resumes again in the spring

107
Q

Which drug can be used to treat acute fascioliasis?

A

Triclabendazole followed by moving the animal to clean pasture

108
Q

Which drugs can be used to treat subacute fascioliasis?

A

Closantel or Nitroxynil followed by moving the animal to clean pasture

109
Q

What can be used to control the spread of F. hepatica?

A
  • Drainage of the land (to reduce snail population)
  • Fence off saturated pasture/move sheep to drier pasture
  • Treat and quarantine any new animals
110
Q

What are the hosts for Dicrocoelium dendriticum?

A

FINAL HOSTS: Most mammals
INTERMEDIATE HOSTS: Land snails and ants

111
Q

What is the name of the disease caused by D. dendriticum?

A

Dicrocoeliosis

112
Q

(T/F) D. dendriticum adults are much larger than F. hepatica adults

A

FALSE. D. dendriticum are much smaller than F. hepatica

113
Q

Describe the lifecycle of D. dendriticum

A
  1. Fully embryonated eggs are excreted in the faeces of the final host –>
  2. Snails ingest the eggs and the miracidium undergo several phases of development within the snail (miracidium -> sporocysts -> cercariae) –>
  3. Cercariae are released from the snail within a slimeball –>
  4. Slimeballs containing cercariae are ingested by ants –>
  5. Cercariae develop into metacercariae within the ant –>
  6. Final hosts ingest ants infected with metacercariae –>
  7. Metacercariae swim up the bile ducts to the liver and the gallbladder where they develop into adults and produce eggs –>
114
Q

Do D. dendriticum metacercariae have a tissue migratory phase?

A

NO. D. dendriticum metacercardiae swim up the bile ducts to reach the liver and the gallbladder

115
Q

Describe how D. dendriticum acts as an enslaver parasite

A

The metacercardiae encyst within the brain of the ant causing the ant to climb to the top of the grass and remain there until ingested by the final host - increasing the chances of transmission

116
Q

Why is it more difficult to control the spread of D. dendriticum compared to F. hepatica?

A

It is more challenging to control D. dendriticum spread as the intermediate hosts of this fluke is not dependent on an aquatic environment

117
Q

What is the common name for Paramphistomum?

A

Rumen fluke

118
Q

What are the hosts for Paramphistomum?

A

FINAL HOSTS: Ruminants
INTERMEDIATE HOSTS: Aquatic snails

119
Q

What is the name of the disease caused by Paramphistomum?

A

Paramphistomiasis

120
Q

Describe the lifecycle of Paramphistomum

A
  1. Eggs are deposited in the faeces of the final host –>
  2. Embryonisation occurs at 22°C in the presence of moisture –>
  3. Hatching of the miracidium is induced by light opening the operculum (cap) –>
  4. The miracidium penetrate the aquatic snail –>
  5. Miracidum develops into a sporocyst followed by rediae followed by cercaria –>
  6. Cercaria exit from the snail under the right environmental conditions –>
  7. Cercaria lose their tails and develop into metacercariae which encyst on grass –>
  8. Metacercariae are ingested by the ruminant –>
  9. Metacercariae encyst in the duodenum where the juveniles develop and attach to the mucosa of the intestinal wall acting as ‘plug feeders’ –>
  10. Adults migrate to the rumen and reticulum where they mature and produce eggs –>
121
Q

What causes the direct pathology of Paramphistomiasis?

A

The juveniles acting as ‘plug feeders’ on the duodenal mucosa causing necrosis, haemorrhage and erosion of the duodenal mucosa resulting in gastroenteritis

122
Q

What are some of the clinical signs of Paramphistomiasis?

A
  • Foetid diarrhoea
  • Anaemia
  • Hypoalbunaemia
  • Intense thirst
  • Anorexia
123
Q

What drug can be used to treat Paraphistomiasis?

A

Oxyclozanide

MODULE 4 - Infectious Agents (20 decks)

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