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Helminths Flashcards

1
Q

What is the classification of Ascaris Lumbricoides

A

Soil transmitted helminth
Nematode

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2
Q

What is the epidemiology of ascariasis

A

Children aged 3-8
800 million people affected
Associated with poor environmental hygiene

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3
Q

What is the lifecycle of Ascaris Lumbricoides

A
  1. Eggs from contaminated vegetables, water, soil are ingested
  2. Eggs hatch within the stomach and small intestine and release larva
  3. The LARVA migrate through the walls of the gut and cause acute ascariasis symptoms
  4. They migrate into the lymphatics and eventually reach the lungs (via liver —> heart) and are coughed up, swallowed and re-enter the digestive tract, where they develop into adults
  5. Female adults produce up to 200000 eggs per day
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4
Q

What are the clinical features of ascariasis?

A

Loefflers syndrome (usually lasts about 10 days)
Anaemia
Eosinophilia
Bowel obstruction
Biliary duct obstruction
Malnutrition and reduced vitamin A

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5
Q

How is ascariasis diagnosed?

A

Stool microscopy via Kato Katz
FLOATAC — stool centrifugación
CXR
Barium swallow
Eosinophilia

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6
Q

How is ascariasis managed?

A

Albendazole 400mg STAT

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7
Q

How is ascariasis prevented?

A

WASH
MDA of albendazole to school aged children

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8
Q

What are the two species of worm which cause Hookworm infections?

A

Necator americanus
Ancylostoma duodenale

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9
Q

What is the clsss of necator americanus and ancylostoma duodenale

A

Hookworms
Soil transmitted helminths
Nematodes

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10
Q

What is the epidemiology of Hookworm infections?

A

Causes 30-40% of maternal anaemia
Found globally
Adults > children (because associated with people who go out and work in fields with Night Soil
600 million people infected globally

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11
Q

What is the lifecycle of hookworms?

A
  1. Hookworm eggs are excreted in the stools of infected hosts
  2. The eggs hatch in warm soil and produce rhabditiform larvae
  3. Under the right condition rhabditiform larvae become filariaform
  4. Mature larvae enter into humans through the skin, either via cuts in the skin or through hair follicles
  5. The worms enter circulation in the lymphatics and venous circulation and travel to the liver — heart — lungs and are swallowed by the host
  6. When swallowed they travel to the small intestine where they mature into adults and attach themselves to the intestinal walls and feed off blood
  7. After 3-5 weeks the worms start to produce eggs
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12
Q

Who is most at risk of symptomatic hookworm infection?

A

Children
Pregnant women
People with underlying anaemia

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13
Q

What are the symptoms of hookworm infection?

A
  1. Asymptomatic
  2. ACUTE: Wakana syndrome, ground itch
  3. CHRONIC: IDA
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14
Q

How are hookworm infections diagnosed?

A

Eosinophilia
IDA
Stool microscopy +/- concentration methods

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15
Q

What is the management of hookworm infection?

A

Albendazole 400mg stat
+/- iron replacement

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16
Q

How is hookworm infection prevented?

A

Improved hygiene and sanitation
MDA of school aged children and childbearing aged women
Wear Shoes
Alternative fertilisers to Night Soil

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17
Q

What is the classification of whip worm?

A

Trichuris trichiura
STH
nematode

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18
Q

What is the epidemiology of whip worm?

A

600 million infections world wide
Warm humid climates

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19
Q

What is the lifecycle of trichuris?

A
  1. Eggs are ingested from contaminated food and water and soil
  2. Eggs pass through the stomach and are de-embryonated within the caecum where they burrow into the mucosa of the large bowel
  3. The worms feed on bowel juices, rather than blood
  4. After several weeks the female worm starts to produce eggs and releases several thousand eggs per day
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20
Q

What is the clinical presentation of Whip worm infection?

A

ASYMPTOMATIC
can occasionally cause symptoms of IBD in heavy worm burdens
Rectal prolapse in children

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21
Q

How is whip worm infection diagnosed?

A

Stool microscopy
Eosinophilia

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22
Q

How is trichuriasis managed?

A

Albendazole 400mg stat

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23
Q

How is whip worm infection prevented?

A

WASH
MDA women and children

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24
Q

What clinical sign is seen in toxocariasis?

A

Visceral larva migrans

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25
Q

How is visceral larval migrans managed?

A

Albendazole 400mg stat

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26
Q

What is strongyloides Stercoralis?

A

STH
nematode

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27
Q

What is the only STH that is capable of auto infection?

A

Strongyloides

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28
Q

What is the epidemiology of strongyloides?

A

Unknown.
Tropical climates&raquo_space; but does occur almost worldwide

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29
Q

What are the complications of strongyloides?

A

Hyper infection secondary to immunosuppression, which can lead to death

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30
Q

What virus is associated with strongyloides?

A

HTLV-1

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31
Q

What is the lifecycle of strongyloides?

A
  1. Female worms, which are embedded in the mucosa of the small intestine, produce eggs, which soon hatch and release rhabditiform larvae
  2. Rhabditiform larvae can then become: 
- filariaform within the gut and reinfect by entering into the body at perianal mucosa
-filariaform in good soil conditions, which then eventually infect people through the skin
  3. The worms then migrate through the skin into blood vessels and eventually travel to the lungs, are coughed up and swallowed, where they can then colonise the small intestine
  4. Due to auto infection people can have strongy infection for >40 years
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32
Q

What is the presentation of Strongyloides infection?

A
  • asymptomatic
  • Acute: irritation at infection site, loefflers syndrome, abdo pain and diarrhoea, weight loss
  • Chronic: larva currens, diarrhoea, weight loss
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33
Q

What are the symptoms of hyper infection syndrome in strongyloides?

A

Severe and bloody diarrhoea
Bowel microperforations
Peritonitis
Gram negative septicaemia
Pulmonary exudates and hypoxia
Encephalitis and bacterial meningitis

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34
Q

How is strongyloides infection diagnosed?

A

Eosinophilia (**suspect strongy in any unknown cause High eosinophils)
Stool sample - notoriously difficult to find, even with concentration techniques
Charcoal stool culture
ELISA

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35
Q

how is strongyloides managed?

A

Ivermectin 200ug/kg per day for 2/7

** you need to kill the filarial worms, which is why you need to use ivermectin; its the same theory as ivermectin with Onchocerciasis and Lymphatic FIlariasis (also nematodes)

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36
Q

What are the 4 common tissue flukes?

A

Fasciola Hepatica
Opisthorchis Spp.
Clonorchis
Paragonimus Westermani

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37
Q

What is Fasciola Hepatic

A

A trematode (tissue fluke) which is spread through ingestion of metacercariae on Watercress

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38
Q

What is the epidemiology of Fascioliasis?

A

South American Andes and Bolivia
In these areas prevalence may be >90%

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39
Q

What is the lifecycle of Fasciola Hepatica?

A
  1. Eggs are excreted in host (often human) stool
  2. Miracidia hatch from the eggs after about 2 weeks and find an intermediate host to attach onto (Lymnaeidae snail)
  3. Within the host the miracidia undergo multiple developmental changes to eventually become cercariae
  4. Cercariae leave the snail and encyst as metacercariae onto vegetation.
  5. Vegetation is consumed by final host.
  6. The metacercariae excyst within the duodenum, releasing larvae
  7. The larvae penetrate through the gut wall travelling through the peritoneal cavity to the liver
  8. From the liver the travel to the bile ducts where they mature into adults. Here they can live for up to 10 years.
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40
Q

What is the intermediate host of Fasciola Hepatica

A

Lymnaeidae snail

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41
Q

What are the Clinical Symptoms of Fascioliasis?

A

ACUTE: (symptoms caused by migrating flukes)
- Fever, malaise, weight loss, urticaria
CHRONIC: Recurrent cholangitis, biliary obstruction, fatigue
Has a tendency to cause ectopic infections too

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42
Q

What are the investigations for diagnosing Fascioliasis?

A

Eosinophilia
CT - hypodense lesions (numerous) from fasciola in liver
Serology Tests
Stool Microscopy (Ova) or Bile aspirates (adults or ova)
Fasciola Excretory Secretory Antigen on stool samples

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43
Q

How is fascioliasis managed?

A

THE ONLY FLUKE THAT PRAZY DOESN’T WORK ON!
Triclabendazole 10mg/kg STAT +/- repitiion in 12h
OR
Nitazaxondie 500mg 12h for 7/7

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44
Q

How can fascioliasis be prevented?

A
  1. sheep vaccine
  2. Treatment of plants
  3. Cooking of food before ingestion
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45
Q

What is the Oriental Liver Fluke?

A

Opisthorchis spp. and chlonorchis spp.
Food borne Trematodes

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46
Q

What is the epidemiology of Opisthorchis?

A

China, South East Asia

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47
Q

What are the natural hosts of Opisthorchis?

A

Domestic pets

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48
Q

What is the life cycle of Opisthorchis?

A

Eggs are excreted in host (often human) stool
2. Miracidia hatch from the eggs after about 2 weeks and find an intermediate host to attach onto (Bithynia snail)
3. Within the host the miracidia undergo multiple developmental changes to eventually become cercariae
4. Cercariae leave the snail and encyst as metacercariae onto fish.
5. Fish is consumed by final host (raw or undercooked)
6. The metacercariae excyst within the duodenum, releasing larvae
7. The larvae penetrate through the gut wall travelling through the peritoneal cavity to the liver
8. From the liver the travel to the bile ducts where they mature into adults. Here they can live for up to 15 years.

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49
Q

What is the clinical presentation of Oriental Liver Flukes?

A

ASYMPTOMATIC

Vague RUQ pain which most commonly occurs in the mid afternoon when adult worms are most active –> patients may state they feel something moving inside them
Anorexia, Flatulense, diarrhoea, fever
Hepatomegaly
Jaundice

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50
Q

What are the complcations of Oriental Liver Fluke

A

Biliary Cirrhosis
Cholangiocarcinoma (most common cause of liver cancer in SEAsia)

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51
Q

How is Oriental Liver Fluke infection diagnosed?

A

Stool microscopy
BIliary Aspirate Microscopy
USS Liver
Antigen tests under development

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52
Q

How is Opisthorchis/Clonorchis infection managed?

A

Praziquantal 40mg/kg STAT

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53
Q

How can Oriental Liver Fluke be prevented?

A

WASH
MDA with praziquantal
Improved food habits (cook your fish!!)

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54
Q

What is a lung fluke?

A

Trematode (food borne) from cray fish and shellfish caused by Paragonimus Westermani

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55
Q

What is the epidemiology of Paragonimus?

A

Korea, China, India (but cases found in Americas too)

56
Q

What is the lifecycle of Paragonimus?

A

Eggs are excreted in host (often human) stool
2. Miracidia hatch from the eggs after about 2 weeks and find an intermediate host to attach onto (Potodoma Snail)
3. Within the host the miracidia undergo multiple developmental changes to eventually become cercariae
4. Cercariae leave the Potodoma snail and encyst as metacercariae onto crustaceans and crabs.
5. crustaceans and crabs are consumed by final host (raw or undercooked)
6. The metacercariae excyst within the duodenum, releasing larvae
7. The larvae penetrate through the gut wall travelling through the peritoneal cavity to the lungs
8. From the lungs they couple up into pairs as mature adults and hang out there forever, producing eggs (which are coughed up, then ingested)

57
Q

What is the clinical presentation of Paragonimus

A

SIMILAR TO TB
Chronic cough, sputum, haemoptysis, weight loss, breathlessness, chest pain

*like fasciola it can also cause ectopic disease

58
Q

What are the investigations in Paragonimus infections?

A

CXR - peripheral nodules or ring shadows, pleural effusions (± empyema)
Stool or Sputum Microscopy
Broncheolar Lavage
Antigen testing
Eosinophilia

59
Q

How is Paragonimus managed?

A

Praziquantal 75mg/kg/d in three divided doses for 3 days

60
Q

What are the 5 main clinically relevant cestodes?

A

Taenia Saginata
Taenia Solium
Diphyllobothrium Latam
Hymenolepsis Nana
Echinococcus Spp.

61
Q

What are the main anatomical features of cestodes?

A

Length: up to 20m long
Head: Scolex
Body: Proglottids with terminal endings which release eggs
Hermaphroditic
No gut

Adults –> generally asymptomatic
Juveniles (cystercerci) –> cause symptoms

62
Q

What is the general lifecycle in cestodes when the human is the final host?

A
  1. Proglottids are released in the faeces of an infected human, which contain ova
  2. The ova enter into the ecosystem (soil usually) where they are consumed by the intermediate host.
  3. Within the intermediate host the ova (onchocerca) excyst to become metacestodes (juvenile cysticerca) which develop in cysts in the muscles and tissues of the intermediate host
  4. Human eats the intermediate host and ingests the cysticerca
  5. Cysticerca are excysted within the Small intestine, where they latch onto the SI wall and feed off the nutrients that the host is consuming
  6. They develop into adult worms here, with a growing proglottid chain, releasing eggs regularly
63
Q

What is the general management of all cestode infections?

A

Praziquantal 10mg/kg STAT
OR
Niclosamide 2g stat
OR
Albendazole

64
Q

What is the intermediate host of Taenia Saginata?

A

Beef tapeworm, found in cows

65
Q

What is the epidemiology of Taenia Saginata?

A

‘Cosmopolitan’ Areas
Global distribution
Ethiopia has a the widest distribution of Saginata infection

66
Q

What is the presentation of Saginata infection?

A

Typically asymptomatic as humans are only infected wtih adult worms

Mild Abdo bloating

**Can crawl out of your butt and into your bed in the middle of the night. Holy christ.

67
Q

What is the Pre-Patent period of T saginata infection?

A

10-14 weeks

68
Q

How long (segments) can a saginata tape worm be?

A

1000-2000

69
Q

How many eggs per day does T. Saginata and T solium produce?

A

50000

70
Q

How is Taenia Saginata Diagnosed?

A

Stool Microscopy
Proglottid microscopy (15-20 branches)
Copro Antigen in animals
PCR

71
Q

What is Taenia Solium?

A

Pork Tapeworm

72
Q

What are the intermediate and definitive hosts of Taenia Solium?

A

Intermediate: PIGS or HUMANS

Definitive: Humans

73
Q

What is the lifecycle of Taenia Solium when humans are the intermediate hosts?

A
  1. Eggs are released from the proglottids of infected humans
  2. Eggs are ingested by humans
  3. Onchospheres (the fertile bit in the eggs) hatch in the small intestine) and penetrate through the gut wall
  4. Onchospheres travel through the blood where they develop into larva, which can encyst into areas as cysticerci

**Note that because the intermediate form can occur without the consumption of meat, non-meat or non-pork eaters can still get taenia solium infection (cysticercosis)

74
Q

What is the epidemiology of T. Solium

A

Global distribution but endemic in:
Central and South America
Sub-Saharan Africa
South East Asia

75
Q

What is the presentation of T. Solium infection

A
  1. Asymptomatic
  2. Mild abdo symptoms
  3. Cysticercosis
76
Q

What is the pre-patent period of cysticercosis infection?

A

8-12 weeks

77
Q

What is the epidemiology of T. Solium

A

Global distribution but endemic in:
Central and South America
Sub-Saharan Africa
South East Asia

Cysticercosis:
India, Central America

May account for up to 2% of seizure presentations in USA EDs

78
Q

How is Taenia Solium Diagnosed?

A

ELISA: Copro, Ag, Ab
Stool Microscopy (Kato-Katz)

79
Q

What is cysticercosis?

A

The development of cysts throughout the body (usually subcut tissues, muscles and brain) secondary to Taenia Solium infection, when the human is the intermediate host

80
Q

How does Cysticercosis present?

A
  1. Subcut/Muscle: Moveable cysts under the skin, which eventually harden
  2. Neuro presentation: Seizures (number one cause of infective seizures world wide) hydrocephalus
81
Q

Does cysticercosis cause eosinophilia?

A

YES

82
Q

How is cysticercosis diagnosed?

A
  1. X-rays long bones (will show potential plethora of soft tissue hardened cysts)
  2. CTB and MRI Brain
  3. Serology: Immunoblot (EITB); ELISA is not recommended
  4. Screen for latent TB and strongyloides prior to starting steroids
  5. Fundoscopy to check for eye worms (which should be removed surgically prior to starting albendazole)
  6. Check for carriage in family members
83
Q

How is cysticercosis managed?

A
  1. Praziquantal + Albendazole FOR 10-14 days (only 60-70% effective, so repeat courses are required at 6 months)
    - Avoid alb. if raised ICP; surgically manage first
  2. Dexamethasone (Prazi and Albendazole can worsen neuro symptoms, so dex is required to reduce neuro inflammation during treatment)
  3. Anti-epileptic medications
84
Q

How should a NCC patient be followed up at 6 months?

A
  1. Repeat course of Albendazole and Praziquantal (recall only 60-70% elimination)
  2. Repeat MRI Brain
85
Q

What are side effects assocaited with albendazole?

A

Leucopenia
Hepatotoxicity

86
Q

What are the general risk factors for infection from Taenia Spp?

A

Warm, most soil
Poor slaughterhouse conditions and poor animal husbandry
Ingestion of undercooked pork and beef
Poor sewage

87
Q

How can Taenia infections (S+S) be prevented?

A

Vaccination of farm animals against T. Solium and T. Saginata
Cook/Freeze meat adequately
Animal MDA
Coproantigen testing of farm animals

88
Q

What is Diphyllobothrium Latum?

A

Cestode infection that occurs following the consumption of infected raw/undercooked fish

89
Q

What is the lifecycle of DL?

A

**Unlike other cestodes it has 2 intermediated hosts

  1. Adult worms in the definitive host release proglottids, which contain eggs
  2. Eggs enter into fresh water supply and hatch, releasing Coracidium
  3. Coracidium are like little swiming plankton, which are consumed by Copepods
  4. Copepods are then consumed by minnows
  5. Minnows are then consumed by large fish.
  6. Within large fish the coracidia enter into the muscles and tissue and encyst.
  7. These fish and cysts are then consumed by humans (or bears, which act as a reservoir host)
90
Q

How many eggs are produced per day by an adult DL worm?

A

1 million

91
Q

What is the epidemiology of DL?

A

20 million cases globally
Assocaited with lakes and fresh water fish.
Europe: Finland, Estonia, Poland, Ukraine, Russia
USA and Canada
Japan
Argentina and Chile

92
Q

What is the presentation of DL?

A

B12 deficiency –> Macrocytic anaemia
Mild Abdo discomfort

93
Q

What is the Pre-patent period of DL?

A

2-6 weeks

94
Q

How many eggs are produced per day by an adult DL worm?

A

1 million

95
Q

How is DL diagnosed?

A

Stool Microscopy

96
Q

How is DL managed?

A

Praziquantal 10mg/kg STAT

97
Q

What is Hymenolepsis Nana (HN)?

A

Cestode
Dwarfworm

98
Q

What is the intermediate host of HN?

A

IT HAS NONE –> it is the only cestode with no intermediate host

99
Q

What is the epidemiology of HN?

A

Global distribution
Children > Adults

100
Q

What is the presentation of HN infection?

A

General Abdo pain
Pruritus Ani
Diarrhoea
Autoinfection is possible

101
Q

How is HN managed?

A

Praziquantal 25mg/kg STAT (larger dose than all other cestode infections)

102
Q

What is Echinococcus?

A

Tapeworm spp. which can cause Hydatid disease

103
Q

What are the two species of Echinococcus?

A

Echinococcus Multilocularis (Alveolar disease)
E. Granulosis (large hydatid disease)

104
Q

What are the intermediate and definitive hosts of Echinococcus Spp.?

A

Intermediate: Sheep/cattle/rodents/humans
Definitive: Dogs/foxes

105
Q

What is the incubation period of hydatid disease?

A

10-15 years

106
Q

What is the lifecycle of echinococcus granulosis (hydatid cyst disease?)

A
  1. Infected human releases proglottid, which contains infective ova.
  2. Ova are then consumed by herbivorous intermediate hosts. The onchospheres of the ova excyst and enter into the circulation of the animal, where they invaginate into the vessel walls and create ‘Brood Capsules’
  3. Brood capsules are then surrounded by a fibrous tissue, which forms the ‘Hydatid Cyst’
  4. The Brood capsules can grow for years, spawning many daughter cysts.
  5. The capsules can break off from the tissue walls, creating Hydatid sand
  6. When the herbivores are then consumed by a further animal (usually dogs feeding on carcasses) the next host becomes infected, or they eat eggs from stools
107
Q

What is the epidemiology of Hydatid?

A

Global
Canada, UK, Wales (10-20% of dogs are infected), Mexico, SSA

108
Q

What is the clinical presentation of Hydatid Disease?

A

-Hepatic Cyst formation (70%), Right lobe predominant due to circulation
- Lugs (20%)

Symptoms come from mass effect of cyst, secondary bacterial infection or fluid leakage from cyst

109
Q

How is Hydatid Disease diagnosed?

A

Liver USS
CXR –> ‘water lily’ appearance
Serology: ELISA IgG and AgB
Eosinophila (if cyst leaking)

110
Q

How is hydatid disease managed?

A

Surgical removal

Aspiration (careful.. spillage of cyst can be catastrophic and cause seeding throughout the body)
– Percutaneous aspiration under US Guidance is GOLD STANDARD –> PAIR (puncture, aspirate, inject, reaspirate)

Albendazole + Praziquantal for 1-3 months prior to surgical intervention is recommended

111
Q

Which areas of the world have managed to eradicate Hydatid Disease?

A

Iceland
Tasmania
Cyprus
Australia
New Zealand

112
Q

How can hydatid disease be prevented?

A

Recombinant vaccine for animals
Dog control measures
Health education
Animal MDA with praziquantal

113
Q

What is the epidemiology of E. Multilocularis (Alveolar Hydatid Disease)?

A

Northern Hemisphere
- West-Central europe, turkey, russia, West and central china, Japan, Iran, Iraq

10% prevalence in China

114
Q

What are the hosts of E. Multilocularis?

A

Foxes, Dogs

Rodents are intermediate hosts

115
Q

What is the pathophysiology Of e. Multilocularis?

A

Production of daughter cysts through external budding (not internal, like with hydatid), causing progressive invasion into surrounding tissues –> ends up behaving like a malignant tumour for this reason.

116
Q

What is the presentation of E. Multilocularis?

A
  1. RUQ, hepatomegaly, palpable liver mass
117
Q

What is the prognosis of E Multilocularis?

A

Untreated, 90% of patients die within 10 years

**much more deadly and serious than E. Granulosis

118
Q

What are risk factors for disseminated E. Multilocularis disease?

A

HIV co-infection
Immunocompromise

119
Q

How is E. Multilocularis diagnosed?

A

Serology
CT
MRI
Tissue biopsy and histology

120
Q

What is the management of E. Multilocularis

A

Albendazole (for 12 months)± surgical management

121
Q

What are the main strategies for eliminating the Guinea Worm?

Name 5

A

Surveillance-regular reporting from health facilities

Clean water provision and borehole maintenance

Filtering potentially contaminated water

Temephos to kill copepods in water bodies

Health Education/Community and Media

Case containment

Stop any case contaminating water source

Monetary Reward in place/intense surveillance

Rumour registers/follow up within 24 hours

122
Q

Which worm classically causes Vitamin A deficiency?

A

Ascaris

123
Q

How many eggs does a female ascaris produce per day?

A

200000

124
Q

How many eggs does a female hookworm produce per day?

A

A Duodenale: 30000
N. Americanus: <10000

125
Q

What is Wakana Syndrome?

A

An immune response secondary to Hookworm Infection:

resembles an immediate-type hypersensitivity reaction and is characterized by pharyngeal itching, hoarseness, nausea, vomiting, cough, dyspnea, and eosinophilia

126
Q

How many eggs per day are produced by Whipworms?

A

10000-30000

127
Q

What snail is the host of Opisthorchis?

A

Bithynia snail

128
Q

How long can adult opisthorchis live for?

A

up to 15 years

129
Q

What snail is the intermediate host for Paragonimus Westermani?

A

Potodoma Snail

130
Q

What is wakana sundrome

A

In people who have been infected with a large burden of A duodenale through oral ingestion, Wakana syndrome may occur. This syndrome resembles an immediate-type hypersensitivity reaction and is characterized by pharyngeal itching, hoarseness, nausea, vomiting, cough, dyspnea, and eosinophilia

131
Q

What is Gnathostomiasis?

A

Gnathostomiasis is mostly caused by Gnathostoma spinigerum, a zoonotic nematode.

Humans are accidental hosts.

Gnathostomiasis is endemic throughout areas where large amounts of raw or undercooked freshwater fish and crustaceans are consumed, most importantly in East and South-East Asia and Central and South America.

Case reports are emerging from Southern Africa.

132
Q

How does Gnathostomiasis present?

A

**Often presents in clusters of infection

Initial symptoms are non-specific and may include fever, malaise, vomiting and diarrhoea lasting for 2 to 3 weeks.

Within 1 month cutaneous infection may develop, manifesting as non-pitting oedematous migratory swellings that may be pruritic or painful and mainly affect the trunk and the proximal limbs.

133
Q

What are complications of Gnathostomiasis?

A

Visceral symptoms
Meningo-encephalitis –death

134
Q

How do you manage Gnathostomiasis?

A

albendazole 400 mg bid for 21 days
and/or ivermectin 200 μg/kg on two consecutive days.

For CNS infection, adjunctive corticosteroids are considered beneficial.

135
Q

What are 3 risk factors for Strongy hyperinfection?

A
  • HTLV
  • Corticosteroids
  • Solid organ transplant
  • Haematopoietic stem cell transplant (HSCT)
  • Alcohol
  • Malnutrition

**no points for HIV

DTM&H (29 decks)

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