Nematodes, Cestodes and Trematodes Flashcards

1
Q
  • Name 5 species of clinically significant Cestodes
A
  1. Taenia saginata - beef tapeworm
  2. Taenia solium - pork tapeworm
  3. Diphyllobothrium latum - broad/fish tapeworm
  4. Hymenolepsis nana - dwarf tapeworm
  5. Echinococcus spp. - hydatid
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2
Q

What are Helminths?

A
  • ‘parasitic worms’
  • 2 phyla
    1. Platyhelminthes - flatworms
      1. Cestodes - tapeworms
        1. Cyclophylidea ‘Land’
          1. Taenidae: T**aenia, Echinococcus
          2. Hymenolepidae: Hymenolepsis
        2. Pseudophyllidea ‘Water
          1. Diphyllobothridae: Diphylobothrium
      2. Trematotodes - flukes
    2. Nematodes - roundworms
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3
Q

What is the Generalised Tapeworm Lifecycle?

A
  • Adults ⇒ definitive hosts
  • Eggs ⇒ external environment
  • Juveniles ⇒ Intermediate host
    • Hymenolepsis nana ⇒ humans
    • Taenia saginata ⇒ cattle
    • Taenia solium ⇒ pigs
    • Diphylobothrum latum ⇒ copepods, fish
    • Hymenolepsis nana ⇒ larvae of cereal meal worms or fleas (rodent reservoir)
    • Hymenolepsis diminula ⇒ fleas or flour beatles
    • Diphylobothrum caninum ⇒ dog or human flea (Ctenocephalides canis or C. felis)
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4
Q

Name 4 species of clinically significant Trematodes.

Etymology

A
  1. Fasciola hepatica - the liver fluke
  2. Paragonimus westermani - the lung fluke
  3. Opisthorchis sinensis - Chinese liver fluke (aka Clonorchis sinensis
  4. Schistosoma mansoni, S. japonicum, S. haematobium - schistosome or bilharzia flukes
  • Etymology: old English word for Flounder
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5
Q

5 species of Clin. significant Nematodes.

What is the etymology?

A
  1. Strongyloides stercoralis - threadworm
  2. Necator americanus & Ancylostoma duodenale - the Hookworms
  3. Ascaris lumbricoides - the Large Roundworm of Man
  4. Tricuris trichuria - the Whipworm
  5. Enterobius vermicularis - the pinworm
  6. Toxocara canis & toxocara cati - Visceral and ocular larva migrans
  • From Greek “nema” or thread
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6
Q

What is this?

Life cycle?

Symptoms?

A
  • Ascaris
  • largest of intestinal soil-transmitted helminths
  • adults live in intestine, eggs passed in feces and contaminate environment, water and food
  • Ascariasis caused by ingeting eggs on soiled hands or consuming fruit or veg that have not been washed or peeled
  • eggs hatch into larva in small intesting, penetrate intestinal wall and migrate through blood and lungs where they may cause symptoms
  • if coughed up and swallowed they return to gut to mature and reproduce
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7
Q

What are these?

A
  • left to right
    • Necator americanus or Cyclostoma duodenalis (hookworm) egg
    • tricuriasis (whipworm) egg
    • fertile ascaris egg
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8
Q

What is this?

Describe it.

A
  • fertile Ascaris egg
  • oval shape, about 60µm long
  • brownish colour
  • thick shell covered by a rough coat stained brown by bile in gut
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9
Q

What is this?

Describe it?

Describe it and what triggers it to dev

A
  • infective Ascaris egg
  • oval, thick wall, contains visible larvum
  • as the fertile egg leaves host, reduction in temperature, oxygen and moisture levels trigger ovum to develop into this infective stage
  • takes 20-40 days to do so
  • if ingested in contaminated food, will hatch in intestine and person will become infected
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10
Q

What is this?

Describe.

A
  • infertile Ascaris egg
  • less common in feces than fertile eggs
  • egg is longer an narrower than fertile ege, as large as 75-90µm long
  • usually very dark in colour with flattened ends
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11
Q

What is this?

Where is it found?

Life cycle?

A
  • adult pinworm (Enterobius)
  • worldwide distribution, commonly affects children
  • female deposits eggs on perianal skin during night, and within a few hours of being laid they contain infected larvae (embryonated eggs)
  • child scratches and autoinoculates self, eggs travel to intestin and hatch
  • sometimes larvae hatch on perinal skin and migrate back to the intestine and mature
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12
Q

What is this?

Describe.

Life Cycle

How diagnosed?

A
  • Enterobius eggs
  • oval in shape, colourless, with clear shell
  • about 55 µm long
  • eggs laid on perianal skin, eggs become infective within few hours, itching causes host to scratch and then reinfects self by swallowing fertile egss, which hatch in the intestine
  • best collected from perianal skin at night “sellotape method” or “Graham swab”, eggs visible under microscope
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13
Q

What is this?

Life Cycle?

Clinical disease?

Complications?

A
  • trichuris (whipworm)
  • round worm of humans found in warm moist climate and poor sanitation
  • may occur in cecum, ileum, appendix and colon of humans
  • ingestion of infective eggs in contaminated food/fingers
  • light infections may cause few symptoms
  • young children severe infections may cause chronic diarrhea, ulceration with blood and mucous passed in stool
  • fe deficiency, wt loss
  • prolapse rectum
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14
Q

What is this?

What other symptoms may occur?

A
  • prolapsed rectum in child
  • caused by whipworm (Trichuris)
  • fe def anemia, wt loss
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15
Q

What is this?

Describe it.

Life Cycle.

How long does egg take to become infective.

A
  • trichuris egg (whipworm)
  • egg barrel-shaped, 50 µm long with clear mucoid plug at either end
  • when passed in feces egg contains undeveloped ovum
  • after about 3 weeks in soil becomes embryonated (infective)
  • infective egg ingested from contaminated food or fingers, larvae hatch and develop in small intestine
  • adult worms bore into wall of the large intestine and embed in anterior part of mucosa
  • secretes digestive fluid into tissues of intestinal wall, liquefying surface, which is then taken up by the worm
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16
Q

What is this?

Describe it?

Size, distinctive characteristics.

A

Trichuris (whipworm) egg.

egg barrel-shaped, 50 µm long with clear mucoid plug at either end

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17
Q

What is this?

A
  • hookworm (Ancylostoma duodenale or Necator americanus)
  • adult parasites live in small intestine, sucking and ingesting blood through intestinal wall
  • male worms 8-9 mm, females 11-12 mm, heads of both males and females are bent dorsally giving “fishing hook appearance”
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18
Q

What is this?

Geographic distribution?

Life Cycle?

Disease?

A
  • Ancylostoma duodenale
  • hookworm
  • worldwide in areas with moist warm climate
  • this species predominant in Middle East, Africa, Southern Europe
  • transdermal entry via hair follicles, also ingested orally ⇒ Wakana syndrome
  • preferred site upper small intestine, but in very heavy infections may extend as far as lower ileum
  • hookworm mouthparts of adult penetrate blood vessels, nourish by sucking blood
  • cause chronic anemia, blood loss
  • differentiate from N. americanus by teeth in buccal cavity. N. americanus has flat cutting plate
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19
Q

What is this?

Geographical distribution?

How distinguished from similar parasite?

A
  • Necator americanus
  • hookworm
  • this species predominates in America and Australia
  • distinguished by flat cutting plates in N. americanus vs teeth in A. duodenale
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20
Q

What is this?

FOBT?

A
  • adult hookworm, either Necator americanus or Ancylostoma duodenale
  • teeth embedded in small intestine wall
  • FOBT usually positive
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21
Q

What is this?

Life Cycle

A
  • Hookwoorm eggs
  • Ancylostoma duodenale and Necator americanus are indistinguishable
  • Size: 57-76 µm, oval or ellipsoidal shape
  • thin shell
  • eggs passed into stool, hatch into rhabditiform larvae, which take about a week to develop into infective stage
  • larvae penetrate skin usually of foot, travel through venous circulation through lungs up to trachea then swallowed, travel to small intestine, attach and mature into adults after feeding on blood
  • female hookworms produce up to 30,000 eggs per day
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22
Q

What is this?

Characteristic features?

A
  • hookworm larvae
  • long buccal cavity at anterior end, which differentiates them from Strongyloides larvae
  • no notch at the tail end
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23
Q

What is this?

sex?

Morphology? Identification

Life Cycle?

A
  • Adults of Strongyloides stercoralis may be found in human host or soil
  • in human host no parasitic males
  • parasitic females are long and slender, measuring 2-3 mm
  • in human host, female lays eggs in intestinal mucosa, larvae hatch almost immediately to only larvae are found in feces
  • larvae similar to first stage Hookworm larve but have shorter mouth cavity and are found in freshly passed feces (hookworm larvae are found in stale faeces)
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24
Q

What is this?

What do the arrows indicate.

A
  • female Strongyloides sterocralis larva passed in fresh species
  • Red arrow indicates short (compared to hookworm larva) cavity and rhabditiform esophagus
  • also differentiated by notch at tail end (not shown here)
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25
Q

What are the specific clinical features/syndromes associated with ascariasis?

Larval migration?

Adult gastrointestinal parasitism?

General features?

A
  • larval migration⇒verminous pneumonia
  • adult GI parasitism⇒
    • lactose intolerance
    • vitamin A malabsorption
    • intestinal obstruction
    • hepatopancreatic ascariasis
  • General
    • impaired growth
    • impaired physical fitness
    • impaired cognition
    • reductions in school attendance and performance
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26
Q

What are the specific clinical features/syndromes associated with trichuriasis?

Common name?

Larval migration?

Adult gastrointestinal parasitism?

General features?

A
  • whipworm
  • lm: none
  • adult GI parasitism:
    • colitis
    • trichuris dysentery syndrome
    • rectal prolapse
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27
Q

What are the specific clinical features/syndromes associated with hookworm

parasite name?

Larval migration?

Adult gastrointestinal parasitism?

General features?

A
  • Ancylostoma duodenalis
  • Necator americanis
  • lm:
    • ground itch
    • cough
    • Wakana disease: when A. duodenale transmitted orally, characterized by nausea, vomiting, pharyngeal irritation, cough, hoarseness, dyspnea
  • adult gi parasitism
    • intestinal blood loss
    • fe def anemia
    • protein malnutrition
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28
Q

Describe the lifecycle of Ascariasi lumbricoides.

A
  • infection via fecal-oral transmission
  • embryonated eggs swallowed, first stage larvae (L1) hatch, moult into L2 then penetrate intestinal mucosa and migrate to pulmonary circulation
  • L3 migrate across alveolar wall, ascend tracheobronchial tree to larynx, then to small intestine
  • Adult female A. lumbricoides produce thousands of eggs daily that pass into stool
  • Egg production occurs 2-3 months after infection and worms can live for several years
  • Eggs remain viable in warm moist soil for years
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29
Q

Describe Trichuris trichuria lifecycle.

A
  • embryonated eggs ingested via food or hands, hatch into larvae that moult in small intestine
  • larvae develop into adult worms in cecum and ascending colon
  • female worms lay thousands of eggs daily for several years
  • eggs pass into stool, embryonate over 2-4 weeks in warm, moist soil
  • survive for months
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30
Q

Describe hookworm lifecycle.

Which species?

A
  • Ancyclostoma duodenal and Necator americanus larvae free living in soil
  • infect people by penetrating skin, usually feet
  • larvae migrate to pulmonary capillaries, penetrate alveolare wall, migrate to larynx and are swallowed
  • larvae moult and develop into mature worms in small intestine over 1-2 months
  • can survive for months (A. duodenalis) or years (N. americanus)
  • female worm releases thousands of eggs daily into stool
  • after 5-10 days hatch in warm, moist, sandy soil or feces
  • Rhabditiform larvae (L1) become infective after moulting to L2 & L3 larvae that survive for several weeks
  • A. duodenalis can also be ingested orally and can cause Wakana syndrome (nausea, vomiting, pharyngeal irritation, cough, hoarseness, dyspnea)
  • Zoonotic ancylostoma species can also infect people, causing cutaneous larva migrans (as well as possibly causing pathology similar to a. duodenalis or necator americanus in some people)
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31
Q

What is Wakana syndrome and how does it occur.

A
  • hookworm Ancyclostoma duodenalis can also be ingested orally instead of penetrating skin resulting in Wakana syndrome (nausea, vomiting, pharyngeal irritation, cough, hoarseness, dyspnea)
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32
Q

What causes cutaneous larva migrans?

A
  • infection by zoonotic ancyclostoma species
  • eg dog or cat hookworm
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33
Q

Strongyloides stercoralis lifecycle.

A
  • complex lifecycle, may take multiple routes including complete lifecycle outside human host
  • filariform larvae inject human host orally or percutaneously
  • skin, esp feet ⇒ pulmonary capillaries to alveoli, then larynx to small intestine
  • oral ingestion same route after penetrating intestinal mucosa to lungs etc.
  • female adults penetrate gut wall, lodging in duodenal & jejunal lamina propria, laying up to 50 eggs daily
  • eggs hatch within gut wall, rhabditiform larvae migrate to lumen and are passed with stol
  • larvae might penetrate colonic wall or perianal skin to enter a newy cycle or disseminate to other organs
  • autoinfection may last decades without repeated external exposure
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34
Q

Describe possible clinical presentations with S. stercoralis.

A
  1. commonly assymptomatic in otherwise healthy
  2. pulmonary migration of larvae ⇒ eosinophilic pneumonia with cough, dyspnea, wheezing, hemoptysis
    • in hyperinfection pneumonia may be severe, fatal
  3. chronic strongyloidiasis: asthenia, anorexia, nause, abd pain, diarrhea, abdominal tenderness
  4. larva currens common in chronic infection, serpiginous urticaria, typically over abdomen, torso, buttocks, groin
    • lesions last a few days
  5. rarely reactive arthritis
  6. in immunosupressed strongyloides hyperinfection syndrome leading to pulmonary or intestinal failure
    • disseminated strongyloidiasis to any organ in immune suppressed
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35
Q

How many eggs will a femal ascaris worm produce per day?

A
  • 200,000 sticky resistant eggs/day
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36
Q

Ascaris: how many infections per year?

how many deaths?

A

1 billion infections

20,000 deaths

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37
Q

What kinds of disease can ascaris larvae produce?

A
  • A: pneumonitis
    • seasonal fever, cough, hemoptysis, bronchospasm
    • Dx: Eosinophilia, larvae in sputum, lobular consolidation
  • B: ectopic e.g. brain
  • C: allergy
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38
Q

What are possible effects of ascaris adult worms?

A
  • GI
    • intestinal obstruction, also volvulus, intussusception, gangrene, perforation, rectal prolapse
    • malnutrition, stunting, developmental
    • lactose intolerance
    • vit A deficiency
    • bile duct migration: biliary coli, stones, liver abscess (20 bacterial), pancreatic duct, ascending cholangitis
    • migration to mouth, nose or anus during fever
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39
Q

Eosinophilia means …?

A

Worms

  • predominantly nematodes (roundworms) and trematodes (flukes).
  • non-invasive tapeworms (cestodes) dont usually cause it
    • except Hymenolepsis nana
  • Invasive tapeworms do. i.e. hydatid disease, but often not until rupture
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40
Q

Ascaris treatment?

What about intestinal obstruction?

A
  • mebendazole 100 mg bid x 3 days or
  • albendazole 400 mg one dose
  • deal with the obstruction first, hydratin, ng suction acutely, then deworm
  • may require laparotomy
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41
Q

What aspects of worm population dynamics limit success of mass deworming programs?

A
  • heavy infections concentrated in few individuals
  • worm “crowding” reduces egg output
  • treatment rarely removes all worms
  • surviving worm population compensates by producing mor eggs/worm
  • worm prevalence in human population may diminish acutely but rises rapidly to baseline within a year
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42
Q

Summary of worm treatments:

First and alternative for

Ascaris

trichuris

hookworm

strongyloides

A
  • For Ascaris and hookworm, first line treatments are
    • albendazole 400 mg single dose or
    • mebendazole 500 mg single dose or
    • mebendazole 100 mg bid for 3 days
  • Trichuris needs longer courses:
    • albendazole 400 mg od x 3 days or
    • mebendazole 500 mg od x 3 days or
    • mebendazole 100 mg bid for 3 days
    • ivermectin 200 µgm/kg daily x 3 d
  • Strongyloides needs Ivermectin 200µgm/kg daily x 2 d
    • with long high doses of albendazole as alternatives
  • Of the four, only hookworm cannot be treated with ivermectin
  • This poses a problem for mass deworming campaigns that would then have to include both albendazole and ivermectin in order to target all 4 STH
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43
Q

What are the early clinical features of hookworm disease?

A
  • ground itch: unusual
    • itch, edema, erythema, papulo-vesicular eruptions lasting 1-2 wks
  • pulmonary sx: unusual
    • cough (“foxhole cough” 1st WW), mucoid sputum, wheezing
  • Initial intestinal sx
    • abd pain, diarrhea, steatorrhea
  • Initial eosinophilia
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44
Q

What is this and what is it caused by?

A
  • cutaneous larva migrans
  • cat or dog hookworm larvae
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45
Q

What are the chronic clinical effects of hookworm?

A
  • chronic gi nutritional defects
    • protein loss
    • anemia esp if child has borderline iron intake/stores
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46
Q

What distinguishes hookworm from trichuriasis and ascariasis in terms of worm burden distribution and age.

A
  • hookworm burden increases with age, in contrast with ascaris lumbricoides and trichuris trichiuria, whic are most intense in childhood.
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47
Q

How does skin pallor associated with hookworm respond to deworming.

A
  • skin pallor associated with hookworm disease due to fe deficiency, which recovers quickly after deworming
  • Pallor due to hypoproteinemia is slower to recover
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48
Q

Treatment of hookworm anemia

A
  • oral iron eg Ferrous sulfate 200 mg tid x 3 months after hgb normal
  • folic acid 5 mg daily at least 1 month
  • vit c if not present in diet
  • deworm with albendazole or mebendazole
  • nb NOT ivermectin
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49
Q

What is this?

Outline diagnosis and treatment

A
  • barrel shaped eggs in faeces
  • proctoscopy shows worms in heavy infections
  • treat with mebendazole or albendazole (or thiabendazole) - only moderately effective so REPEAT
  • oral iron, hydration
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50
Q

What are these and how are the species distinguished?

How many suckers?

A
  • Taenia saginatum (left) - beef tapeworm
  • Taenia soleum (right) - pork tapeworm
    • ​13-30 primary lateral uterine branches on T. saginatum; 7-13 on T. soleum
    • scolex on both have 4 suckers, but T. soleum has hooks, T. saginatum does not
  • Eggs from both are identical
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51
Q

What are these and how are they distinguished from other species?

A
  • Taenia species ova
    • T. saginatum and T. soleum eggs indistinguishable
    • eggs round, 33 -43 µm with thick radially striated dark brown wall
    • inside each shell an embryonated oncosphere with 3 pairs of hooks
    • egg in figure C still has primary membrane (yolk sac) that surrounds eggs in uterine branches
  • distinguish T. saginatum and T. soleum by presence of hooks on scolex of latter
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52
Q

What are these?

Distinguishing features?

A
  • Diphyllobothrium latum ova
  • egg pale yellow-brown and oval shape
  • 65-70 µm
  • operculum at one end can be hard to see
  • egg contains mass of granulated yolk cells surrounding undeveloped ovum
  • eggs mature and hatch in freshwater and after 1-2 wks hatch to release ciliated coracidium stage
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53
Q

What are these?

How is the diagnosis made?

How long are the eggs infective in the environment?

What are the intermediate hosts?

What are the definitive hosts?

A
  • Eggs of H. nana in an unstained wet mount. Note the presence of hooks in the central oncosphere and polar filaments within the space between the oncosphere and outer shell.

Diagnosis is by identifying the distinctive eggs in faeces: eggs of Hymenolepis nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment.

When eggs are ingested by an arthropod intermediate host (beetles and fleas may serve as intermediate hosts) they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine

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54
Q

What is this?

A

Hydatid Sand

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55
Q

What is this?

A

Hydatid Cyst Cross Section

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56
Q

Name the four main clinically significant species of tissue flukes and their 2nd intermediate hosts.

A
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57
Q

Praziquantel dosing (fix this card)

A

tabs 600 mg, can be broken in 1/4 or have

child dose is 15 mg/kg

use height scale

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58
Q

Describe the lifecycle of Necator americanus.

What are the clinical features of acute infection and the consequences of that infection.

A
  • eggs are passed in the soil and embryonate there, hatching into larvae
  • larvae “quest” on grass or pass through skin from ground, migrate through heart and lungs, coming out through trachea then descending into GI tract
  • In some areas, oral ingestion of cysts is very common⇒Wakana syndrome
  • larvae mature into adults after passing down GI tract to duodenum, anchor there and small intestine consuming blood
  • Syndromes:
    • ground itch
    • cough
    • Wakana disease: when larvae are transmitted orrally, they produce nausea, vomiting, pharyngel irritation, cough, hoarseness, dyspnea
  • Adult GI parasitism in small intestine leads to
    • intestinal blood loss
    • fe def anemia
    • protein malnutrition
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59
Q
  • What is the best initial treatment of a patient with high Loa loa microfilaraemia?
A
  • Albendazole
  • Treatment of individuals with high Loa loa microfilaraemia is associated with a risk of encephalopahty if ivermectin or DEC is used. Albendazole administration for 3 weeks initially reduces the microfilarial load and the risk of encephalopathy. Doxycycline is used in other filarial worms that carry Wolbachia, but this does not apply to Loa loa. Praziquantel is used in other parasitic infections, eg schistosomiasis, taeniasis.
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60
Q
  • How can the differentiation of adult Taenia species in humans most accurately be achieved?
A
  • By examining the scolex
  • The eggs of Taenia solium and T. saginata are identical in morphology and can’t be distinguished. Both may appear in faeces. Microscopy of mature proglottids can indicate species, as T. saginata proglottids have more uterine branches than those of T. solium (12-30 vs. 7-13), but since this is variable it is not very accurate. The scolices (heads) of T. saginata and T. solium are different: T. solium has hooks and suckers, whereas T. saginata has only suckers.
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61
Q
  • A soldier returning from a five year posting in Sierra Leone has suspected onchocerciasis. What, seen on microscopy, would help to confirm diagnosis?
A
  • skin microfilariae without a sheath
  • Onchocerca volvulus microfilariae are found in the skin or eye, not blood. They are unsheathed. Sheathed microfilariae found in blood are W. bancrofti, B. malayi and L. loa. Unsheathed microfilariae found in blood are Mansonella ozzardi, M. perstans.
62
Q
  • A 19 year old student who has returned to Liverpool after a gap year building a school in Cameron visited his GP complaining that two days previously his left eye became very painful and when he looked in a mirror he saw a worm wandering across his eyeball. What is the most likely source of infection?
A
  • A bite of Chrysops silacea
  • This is a clinical description of Loa loa infection. L. loa is transmitted by the bite of Chrysops flies (also known as deerflies, mangrove flies). The flies introduce larvae onto the skin during feeding. Larvae then penetrate into the bite wound and develop as adults in the subcutaneous tissue. Adult worms produce microfilariae with diurnal periodicity.
  • Culex mosquitoes are the main vector of filariae (W. bancrofti); Mansonia may transmit viral infections (Rift Valley fever); Simulium damnosum is the black fly responsible for transmitting onchocerca; Mseocyclops copepods transmit Guinea worm (Dracunculiasis).
63
Q
  • Indoor residual spraying programmes are carried out to control malaria in parts of Africa. The burden of which disease might also be reduced by the same programme?
A
  • Lymphatic filariasis
  • Indoor residual spraying reduces the abundance of indoor biting Anopheles mosquitoes that carry the malaria parasite. In most parts of Africa, lymphatic filariasis is tramsitted by the same Anopheles mosquitoes that transmit malaria. Targeting indoor biting mosquitoes, through IRS will also reduce the burden of LF.
64
Q
  • What is an intermediate host for a parasite?
  • For what disease(s) are humans an intermediate host?
  • What is a definite host?
  • For Taenia saginata, what role does the human play and what role other species of mammal?
  • Taenia soleum?
  • Echinococcus?
A
  • an organism that supports the immature or non-reproductive forms of a parasite.
  • malaria, trypanosomiasis
  • The defninite host of a parasite is defined as that hosting the adult stage. Intermediate hosts would host other, non adult, parasite stages.
  • Taenia saginata is widely known as the beef tapeworm, but is really a human tapeworm, since humans are the definitive host. Taenia solium is also a human tapeworm, with intermediate stages in the pig. Dog tapeworms are the Echinococcus species, with intermediate stages in sheep (or humans, as hydatid disease).
65
Q
  • A crustacean is the second intermediate host of which trematode?
  • What is the first intermediate host for this parasite?
A
  • Paragonimus westermani
  • Crustaceans, such as crabs or crayfish are second intermediate hosts for Paragonimus.
  • The first intermediate hosts are snails. Humans become infected by eating undercooked crustaceans harbouring parasite metacercariae.
66
Q
  • What is the intermediate host for schistosomes?
  • What is the definitive host?
  • Describe the life cycle.
  • For which species of Schistosome do monkeys provide an animal reservoir?
A
  • Snails are the intermediate host
  • humans (and monkeys, which provide a reservoir) for S. hematobium and S. mansoni are the definitive hosts
  1. pair of adults inhabit parts of the venous system of the human host including the terminal venules of the bowel wall in the case of S. mansoni and japonicum; and of the bladder in the case of S. hematobium.
  2. the eggs migrate to the lumen of the bowel or bladder and are released into the environment
  3. in water they hatch to release a miracidium larva, which penetrates the snail intermediate host and multiply to produce mother, then daughter sporocysts that break out of the snail
  4. as cercariae and penetrate human skin, which migrate into the venules, where male and female forms unite and copulate and release eggs and so on …
67
Q
  • What are the preferred anatomic sites of residence for the 4 main species of schistosome causing human disease
A
  • S. mansoni lives in inferior mesenteric veins
  • S. japonicum and S. mekongi live in superior mesenteric veins.
  • S. hematobium almost exclusively in venous plexus draining urinary bladder.
  • S. japonicum also go to choroid plexus, venues around spinal column and other ectopic locations
68
Q
  • For what species of schistosome do animal reservoirs play a significant role in human disease?
A
  • S. japonicum: important reservoirs water buffalo, cattle, pigs
  • S. mansoni also has reservoir in monkeys and baboons, but plays no sig role in human disease.
  • S. hematobium: single mini-epidemic in white-water rafters traced back to monkey
69
Q

Which snails act as intermediate hosts for which species of schistosome?

A
  • S. mansoni intermediate host Biomphalaria snails.
  • S. hematobium, intermediate host snail Bulinus.
  • S. japonicum east Asia, eradicated from Japan. Intermediate host snail Oncomelania.
  • (Lymnea plays a role in transmission of Liver fluke)
70
Q

What are these and for what are they intermediate hosts?

A
  • Bulinus - S. hematobium
  • Biomphalaria - S. mansoni
  • Oncomelania - S. japonicum
  • Lymnea - Fasciola hepaticum (liver fluke)
71
Q

What is this?

A
  • S. mansoni egg, note lateral spine
  • size 150 x 60µm
72
Q

How do the eggs cause their damage?

(taken from Parasitic Diseases)

A
  • When the female worm applies her ventral sucker to the endothelial surface, eggs pass through the birth pore located above the ventral sucker, encounter endothelial cells and penetrate into the surrounding connec- tive tissue. The larvae, in the eggs, secrete lytic enzymes facilitating this process. Eggs collect in the sub-mucosa (Fig. 33.7) before lysing their way into the lumen of the small intestine, or, in the case of S. haematobium, the lumen of the bladder.
  • When adult females raise their ventral suckers, eggs inadvertently escape into the circulation, which carries them to the liver via the portal circulation. Nearly 50% of all S. mansoni eggs produced end up in the liver, a dead end for the life cycle. Eggs that reach the lumen of the small intestine are included in the fecal mass. Eggs of S. haematobium must traverse the wall of the bladder (Fig. 33.8) before exiting the host in the urine. In both cases, the egg’s penchant for penetrating tissues causes the infected individual significant pathological consequences.
73
Q

What is this?

A
  • S. japonicum egg (S. mekongi similar)
  • 85x60µm
74
Q

What is this?

A
  • S. hematobium egg - note terminal spine
  • 155x55µm
75
Q
  • What is this?
A
  • Biomphalaria glabrata, major intermediate snail host for S. mansoni
76
Q

What is this?

How long does it live in water after release from snail?

What is the name of the form that infects the snail?

A
  • cercaria (of S. mansoni)
  • about 8 hrs before utilizing glycogen stores (Parasitic Diseases). Beeching says cercariae survive for about 2 days in fresh water.
  • miracidium
  • Cercariae are highly motile, fork-tailed, non-ciliated organisms barely visible to the human eye (200–500 µm long).
  • Cercariae (L-2 or stage-2 larvae) are released each day from infected snails in accordance with a circadian rhythm. Their release is triggered by light and temperature, which act as external cues (zeitgebers).
  • They are especially attracted to shadows, to any water disturbance and, significantly, to the chemicals on human skin.
  • Top part breaks off once penetrates skin, leaving tail behind and becomes schistosomulum.
77
Q

What is this?

A
  • occurs primarily in heavy acute infections with S. mansoni and S. japonicum (Sj>Sm>Sh due to # of eggs and immunogenicity)
  • The symptoms are often dramatic and appear approximately 2-10 weeks after initial exposure, when adult worm pairs begin releasing their eggs in the tissues.
  • Some investigators believe that Katayama fever resembles some of the manifestations of serum sickness: passive production of IgG to first round of egg production
  • There is also a clinical resemblance to typhoid fever.
  • Patients experience hepatosplenomegaly and lymphadenopathy as well as an impressive eosinophilia. The affected individual is frequently febrile and has flu-like symptoms, including cough and headache. At this stage of the illness, schistosome eggs may not yet have appeared in the feces.
  • serology might be positive now, but may need to repeat
  • diff diagnosis:
    • strongyloides stercoralis, trichuris trichuria, capillaris phillipensis - examine stool for eggs of these parasites, though schistosoma eggs my not be seen this early
    • typhoid fever
    • malaria
78
Q
  • Which species of schistosome lead to chronic intestinal schistosomiasis.
  • What are the early clinical features in children?
  • later complciations & comorbidities in children and adults?
A
  • S. mansoni and S. japonicum
  • heavy investations lead to chronic abd pain, sometimes bloody diarrhea, anemia, growth stunting - partly reversible by specific antihelminthic treatment
  • “pipestem portal fibrosis” with relatively prolonged preservation of liver fx until late
  • portal hypertension with hepatosplenomegaly, then development of collateral circulation around liver
  • this leads to eggs from portal circulation being deposited in lungs, inflammatory response leading to pulmonary hypertension, cor pulmonale
  • longstanding infections of all 3 species can lead to deposition of immune complexes in renal basement membrane, nephrotic syndrome
  • S. hematobium leads to extensive GU inflammation and damage, increased susceptibility to HIV
  • hydronephrosis, hydroureter, bladder ca
  • female genital schistosomiasis
  • note Schistosomes in peri-intestinal venules can harbor non-typhoid salmonella, associated with increased risk of non-typhoid salmonellosis
  • rarely S. japonicum and S. hematobium eggs find their way to cns leading to myelitis, encephalopathy
79
Q

How is schistosomiasis diagnosed?

A
  • eggs in stool or urine
  • urine collection best around noon (10am to 2 pm)
  • concentration methods for stool and urine
  • Kato-Katz method for quantification
  • rectal snip for egg identification, “flame cells” eggs containing live miracidia
  • PCR
  • serology +ve 6-12 wks after acute infection, +ve before eggs can be seen in stool or urine
  • role of US, inc bedside US
80
Q
  • How is Schistosomiasis treated?
    • Acute?
    • Chronic?
A
  • Katayama fever treated initially with short course steroids then delayed treatment to allow larvae to mature before treating with praziquantel (active against adults not larvae)
    • treat again with 2nd dose 4-6 wks later
  • Chronic disease also treated with Praziquantel
    • monitor for cns disease - may need steroids
    • may reverse hep fibrosis in kids (Symmer’s fibrosis)
      *
81
Q

What is Symmer’s fibrosis?

A
  • hepatic periportal fibrosis due to chronic schistosomiasis
  • leads to portal hypertension, associated hepatosplenomegaly etc.
82
Q

What is this?

A
  • calcified bladder pathognomonic of S. hematobium infection
83
Q

What is this?

differential diagnosis?

A
  • edema around schistosoma eggs in left hemisphere
  • pml, toxo, tb, lymphoma, glioma
84
Q

What is a schistosomulum?

A
  • A ‘schistosomulum’ is the name given to a cercaria once it has penetrated the skin and lost its tail. It is technically a third stage larva (L-3). After remaining in the skin for several days in search of a post-capillary venule, schistosomula pass to the lungs. S. mansonischistosomula are regarded as slower migrants than others, e.g. S. japonicum. Schistosomula do not multiply in the body.
85
Q

Describe the human phase of the Schistosome lifecycle

A
  • Cercariae pierce unbroken skin but probably prefer to enter via abrasions and hair follicles. As schistosomula they first travel to the lungs and thence in the general circulation to the liver, which they reach in 8–10 days. Here they develop into adults (10 mm long) in 1–3 months. They now couple in an intrahepatic portal vein with the longer slender female lying in the ventral groove of the male. From here the paired worms relocate against the blood flow to the inferior mesenteric veins (S. mansoni, S. japonicum) or the vesical plexus (S. haematobium).

In both cases they induce inflammation and fibrosis so that partial or complete obstruction eventually occurs.

Both sexes are actively motile and appear to mate for life Worm pairs can live from 4–20 years. Males appear to be able to actively compete for paired females by pulling them away from their partners, thus effecting a change of mate.

Eggs are continually being produced with production varying from 300 (S. haematobium) to 3000 (S. mansoni) per day.

After cercarial penetration it takes about 4 weeks for the eggs of S. mansoni to appear in the faeces. In the case of S. haematobium it takes about 12 weeks before eggs appear in the urine. This has important implications for diagnosis and treatment (see below).

The major symptoms of the disease are due to an inflammatory response by the body to circulating egg antigen, and to intact eggs that recirculate to the liver, and to eggs that are in the process of being expelled with the faeces or urine.

86
Q

What is the clinical significance of Hymenolepsis nana?

A
  • dwarf tapeworm, classified as a parasite of minor medical importance
  • occurs worldwide, esp among young children
  • infections usually assymptomatic but abd pain, nausea, vomiting, pruritis ani and diarrhea - sometimes with blood found in heavy infections
  • headache, dizziness, sleep and behavioural disturbances rel frequent, rare convulsions
  • autoinfection common in children, occ in immunosuppressed, rare in adults
  • humans definitive host
  • It is the only cestode that does not require an intermediate host to develop into its infective stage. A common intermediate host, however, is the grain bettle.
87
Q

What is the treatment of choice for intestinal taeniasis?

A
  • praziquantel 1 dose (10–20 mg/kg)
  • albendazole & niclosamide are alternatives
88
Q

What are the principles of treating neurocysticercosis?

A
  • Before therapy is planned, proper characterisation of the specific type and brain involvement of neurocysticercosis is important.42 Therapeutic approaches might include symptomatic therapy, antiparasitic treatment, or surgery (lesion resection or shunt placement), and often more than one of these options are needed)
  • Generally consider whether cysts still viable or calcified - no point in treating dead cysts
  • location: parencymal vs meningeal or intraventricular
  • size of lesion: intraventricular racemose i.e. growing like cluster of a florette, need more aggressive aproach
  • treat with AED’s, pretreat with steroids
  • for multiple active lesions, esp with edema treat with albendazole or praziquentel for 2 weeks.
  • solitary lesions may do as well with short course - 3 days of albendazole or 1 day of praziquantel
  • 1 paper suggesting combined P & A x 10 days for few lesions
89
Q

What is the differential diagnosis for neurocystecercosis on CT?

A
90
Q

What is a hydatid cyst?

A
  • a cyst containing larval forms of Echinococcus granulosus or dog tapeworm causes most disease in humans.
  • associated with dog, sheep or cattle contact
  • Infections with Echinococcus multilocularis less common but lesions less capsular and more invasive
  • Hydatid cysts gradually enlarge in liver, each cyst consisting of a mother cyst and daughter cysts. Eventually may become painful or become secondarily infected, or involve the biliary tree.
  • Rupture or leakage can lead to intense allergic reaction or anaphylaxis, or if involving biliary tree, colic, jaundice or ascending cholangitis.
  • Lung cysts usually assymptomatic until they rupture and may be incidental finding, giving characteristic “water-lily” finding on xray.
91
Q

Causes of Eosinophilia

A
  • KEY POINTS

Eosinophilia is an elevation in the total number of bloodstream eosinophils, can be transient or sustained, and can exist in milder versus more significant levels.

Sustained and significant eosinophilia in the 1500 cells/µL or above range, without clear cause, should prompt evaluation.

Processes known to cause modest eosinophilia include allergic disease, parasitic disease, drug allergy, and mastocytosis.

More significant eosinophilia is often caused by drug allergy, aspirin exacerbated respiratory disease, sustained and significant atopic dermatitis, and some parasitic disorders.

If no apparent cause of the eosinophilia is known and levels above 1500 cells/µL exist for greater than 1 month, an exhaustive search guided by clinical presentation should ensue.

Box 1: Causes of allergy associated eosinophilia

Mild degree of eosinophilia

Allergic rhinitis

Asthma

Atopic dermatitis

Eosinophilic esophagitis

Drug allergy

Moderate to severe degree of eosinophilia

Chronic sinusitis (especially polypoid and aspirin-exacerbated respiratory disease)

Allergic bronchopulmonary aspergillosis

Chronic eosinophilic pneumonia

Drug allergy (drug rash with eosinophilia and systemic symptoms [DRESS] syndrome)

Box 2: Commonly implicated pharmaceuticals in drug rash with eosinophilia and systemic symptoms (DRESS) syndrome

Antibiotics: Penicillins, cephalosporins, dapsone, sulfa-based antibiotics

Xanthine oxidase inhibitor: Allopurinol

Antiepileptics: Carbamazepine, phenytoin, lamotrigine, valproic acid

Antiretrovirals: Nevirapine, efavirenz

Nonsteroidal antiinflammatory drugs: Ibuprofen

Box 3: Select parasitic infections that cause eosinophilia

Helminthic infections

Nematodes

Angiostrongyliasis costaricensis

Ascariasis

Hookworm infection

Strongyloidiasis

Trichinellosis

Visceral larva migrans

Gnathostomiasis

Cysticercosis

Echinococcosis

Filariases

Tropical pulmonary eosinophilia

Loiasis

Onchocerciasis

Flukes

Schistosomiasis

Fascioliasis

Clonorchiasis

Paragonimiasis

Fasciolopsiasis

Protozoan infections

Isospora belli

Dientamoeba fragilis

Sarcocystis

  • Fungal Infections: histo, aspergillus, crypto, blasto

Box 4: Eosinophilia associated with connective tissue, rheumatologic, and autoimmune disease

Eosinophilic fasciitis

Eosinophilic granulomatosis with polyangiitis (Churg-Strauss vasculitis)

Dermatomyositis

Severe rheumatoid arthritis

Progressive systemic sclerosis

Sjögren syndrome

Thromboangiitis obliterans with eosinophilia of the temporal arteries

Granulomatosis with polyangiitis (Wegener syndrome)

Systemic lupus erythematosus

Behçet syndrome

IgG4-related disease

Inflammatory bowel disease

Sarcoidosis

Bullous pemphigoid

Dermatitis herpetiformis (celiac disease)

Box 5: Primary eosinophilias

Idiopathic hypereosinophilic syndrome: sustained peripheral eosinophilia at greater than 1500 cells/µL with associated end-organ damage.

Lymphoproliferative hypereosinophilic syndrome: sustained peripheral eosinophilia at greater than 1500 cell/µL, often associated with rash, aberrant T-cell immunophenotypic profile, often steroid responsive.

Myeloproliferative hypereosinophilic syndrome: sustained peripheral eosinophilia at greater than 1500 cell/µL, often features of splenomegaly, heart related complications, and thrombosis. Can have associated FIP1L1-PDGFRA and other mutations and are often steroid resistant. Patients can be considered to have a diagnosis of chronic eosinophilic leukemia.

Episodic eosinophilia associated with angioedema (G syndrome): cyclical fevers, swelling, hives, pruritus, marked eosinophilia, and IgM elevation. Aberrant T-cell phenotypes often associated.

Box 6: Malignancy-associated eosinophilia

Blood-related neoplasms

Acute or chronic eosinophilic leukemia

Lymphoma (T cell and Hodgkin)

Chronic myelomonocytic leukemia

Solid organ–associated neoplasms

Adenocarcinomas of the gastrointestinal tract (gastric, colorectal)

Lung cancer

Squamous epithelium related cancers (cervix, vagina, penis, skin, nasopharynx, bladder)

Thyroid cancer

Box 7: Entities that can be associated with eosinophilia

Rejection of a transplanted solid organ

Graft-versus-host disease after hematopoietic stem cell transplantation

Kimura disease and epithelioid hemangioma

Eosinophilia-myalgia syndrome/toxic oil syndrome

Adrenal insufficiency

Irritation of serosal surfaces

Cholesterol embolus

92
Q

What is this?

What is the lifecycle?

A
  • Echinococcus granulosus or dog tapeworm causes 90% of Hydatid Disease in humans, the remainder being caused by Echinococcus multilocularis.
  • It is 5.5 mm long
  • The zoonotic cycle for E. granulosus involves dogs as the definitive host, sheep or other ungulates as intermediate hosts. Humans are accidental intermediate hosts through accidental ingestion of eggs in dog feces through direct contact with domestic dogs, or through ingestion of contaminated groundberries such as cloudberries (Asia, Arctic).
  • The ingested eggs hatch as oncospheres in the small intestine and penetrate the mucosa and enter the blood stream, most travelling via the portal circulation to the liver, where the oncospheres develop into encysted larvae. Unless the human gets eaten be a dog or wolf it is a dead end cycle for the tapeworm.
  • Indigenous peoples of the Canadian Arctic, especially the Inuit, are infected with a north- ern variant, E. granulosus var. canadensis, acquired in a sylvatic cycle involving moose and caribou (cervids), wolves, and sled dogs.
  • Alveolar Hydatid Disease is caused by E. multilocularis, in which humans become infected by swallowing eggs passed by foxes and other Canidae**, mainly by eating contaminated wild ground fruits such as bilberries, lingonberries and cloudberries, widely eaten in Northern Europe, Canada and highland China.
93
Q

What is this?

A

Dog tapeworm oocyst

Dipylidium caninum

94
Q

What is this?

A
  • Hydatid cyst characteristic calcified rim of mother cyst
95
Q

How are hydatid cysts treated?

Alveolar Echinococcus?

A
  • 2 different diseases with overlapping geographical prevalences

• Cystic hydatid (E granulosus) benign unless large or rupture

– Treat with albendazole and surgery or PAIR

• Alveolar hydatid (E multilocularis) like a malignancy in liver

– Surgery and prolonged albendazole or palliative treatment alone

96
Q

How does alveolar hydatid disease present and how is it treated?

What is the prognosis?

A
  • Alveolar Echinococcus (E. multilocularis)

• TypicallyRUQpain,hepatomegaly/jaundice and palpable mass

• Complications:
– local invasion
– metastatic lesions in 2%

  • Untreated,70-90%ofpatientsdiewithin10 yrs of presentation
  • 70-90%10yrsurvivalpossiblewithearly diagnosis and treatment
97
Q

What are the Taeniid cestodes in humans (metacestodes)

A
  • Tapeworm species causing Disease in humans
    • Echinococcus granulosus
      • Cystic hydatid or echinococcosis (CE)
    • E. multilocularis
      • Alveolar hydatid or echinococcosis (AE)
    • Taenia solium
      • Cysticercosis
98
Q

What is the geographic distribution of Echinococcus?

A
99
Q

What is this?

A
  • Embryonated Echinococcus eggs (Iodine stain)
100
Q

What is this?

A
  • The water-lily sign is seen in hydatid infections when there is detachment of the endocyst membrane which results in floating membranes within the pericyst that mimic the appearance of a water lily.

It is classically described on plain radiographs (mainly chest X-ray) when the collapsed membranes are calcified but may be seen on ultrasound, CT or MRI.

101
Q

How is Cystic Echinococcus treated?

A

Summary of CE management

  • nb. Praziquantel good for tx of intestinal tapeworm in dogs and humans, but albendazole or albendazole + praziquantel needed for tx cysts
  • Calcified inactive asymptomatic: observe – Other asymptomatic ? “watch and wait”
  • Symptomatic or large cysts:
    • Albendazole for 3 month
    • Assess response by ultrasound
    • Surgery for non response or where follow-up difficult
  • single, simple cysts
    • PAIR After albendazole/praziquantel
    • Possible roles for endoscopic surgery
102
Q

What is PAIR?

A
  • PAIR for treatment of echinococcal cysts
    • Puncture under ultrasound control
    • Aspiration of cyst
    • Injection hypertonic saline 20% or EtOH 95%
    • Reaspirate after 20 minutes
  • Patients undergoing surgery or PAIR should receive pre-op albendazole (for 1 – 3 months) +/- praziquantel
103
Q

What is the main palliative treatment for unresectable Alveolar Echinococcus?

A
  • longterm albendazole
104
Q

What is this?

Distinguishing features?

Adult morphology?

Lifecycle?

A
  • Operculated egg, with knob, yellow-brown ~70 μm
  • 2–10mlongadult

Bothria – sucking grooves

Segments ‘wider than long’

  • Definitive Host: Human swallows plerocercoid larva, which attach to small intestine and grow, producing proglottids, shed proglottids and eggs in stool
  • (Reservoir Host: Bears)
  • In water, eggs hatch into coracidium (aquatic larvum) that is ingested by
    • 1st Intermediate host: copepod
      • procercoid larvum develops here and is taken up by
    • ​2nd intermediate host
      1. fish, where plerocercoid larvum develops, which is eaten by
  • Definitive or reservoir host and so on …
  • Disease: Fish Tapeworm
105
Q

How do you tell T. soleum from T. saginatum?

A
  • mainly by scolex
  • both have 4 suckers, but only T. soleum has hooks
  • can also tell by examining proglottid microscopically but less reliable. T. saginatum proglottid has approximately twice as many uterine branches
  • 15-32 vs 7-13
106
Q

What is a prepatent period?

What is the prepatent period for D. latum?

A
  • prepatent period. : the period between infection with a parasite and the demonstration of the parasite in the body especially as determined by the recovery of an infective form (as oocysts or eggs) from the blood or feces.
  • D. latum or fish tapeworm PPP is 2-8 wks
107
Q

Describe the lifecycle of the fish tapeworm.

A
  • Definitive Host: Human​ swallows plerocercoid larva, which attach to small intestine and grows, producing proglottids, shed proglottids and eggs in stool
  • (Reservoir Host: Bears)
  • In water, eggs hatch into coracidium (aquatic larvum) that is ingested by
    • 1st Intermediate host: copepod
      • procercoid larvum develops here and is taken up by​
    • 2nd intermediate host

fish, where plerocercoid larvum develops, which is eaten by

  • Definitive or reservoir host and so on …
108
Q

What might this be?

A
  • Echinococcus adult and egg
109
Q

What is this?

How would you distinguish from other clinically relevant cestodes?

A
  • Scolex.
    Rostellum: a knob-like protrusion at the extreme anterior end of a tapeworm, as an extension of the tegument. It is globular, spiny structure when it protrudes, and a circular hollow pit when retracted. It is structurally composed of a number of concentric rows of hooks.
    4 suckers + hooks
  • by size of proglottids: smaller overall and each segment much wider than long
  • scolex: taenia also have 4 suckers, t. soleum has hooks, but only h. nana has rostellum
110
Q

Identify these eggs

A
111
Q

Identify these eggs

A
112
Q

What are the symptoms of trichinellosis aka trichinosis?

A
  • The first symptoms of trichinellosis are gastrointestinal, usually occurring 1-2 days after a person consumes raw or undercooked meat from a Trichinella-infected animal. These symptoms include:

Nausea

Diarrhea

Vomiting

Abdominal pain

  • The classic trichinellosis symptoms often occur within 2 weeks after eating contaminated meat, and can last up to 8 weeks:
    • Muscle pain

Fever

Swelling of the face, particularly the eyes

Weakness or fatigue

Headache

Chills

Itchy skin or rash

Cough

Diarrhea

Constipation

  • Symptoms may range from very mild to severe and relate to the number of infectious worms consumed in the meat. Many mild cases of trichinellosis are never specifically diagnosed because they are assumed to be the flu or other common illnesses. Furthermore, many people with Trichinella infection do not experience any symptoms at all.

If the infection is heavy, persons may have trouble coordinating movements, and have heart and breathing problems. Although rare, death can occur in severe cases. For mild to moderate infections, most symptoms go away within a few months.

113
Q

What is the lifecycle of trichinella?

A
  • one definitive host is man, others in domestic cycle are pigs and rodents: in sylvatic cycle bears, rodents, wild boars act as definitive host
  • there are no intermediate hosts
  • the disease was widespread in 40’s but has been controlled through improved animal husbandry of pigs; still foci of disease in China, Thailand and other parts of Asia where pork is still eaten raw.
  • the worm is not shed via eggs in stool, but passed from one host to another through eating raw or undercooked meat containing nurse cells containing larvae. Capsule is digested by pepsin in stomach, releasing larvae, which mature in intestine, copulate and release a fresh round of larvae which penetrate intestinal mucosa and disseminate via blood stream throughout body causing acute febrile illness 2-8 weeks after ingestion of affected meat associated with fever, diarrhea, abd pain, headache, periorbital edema, occasionally fatal causing death.
  • recovery and development of immunity prevents further reproduction of larvae and expulsion of adults. Larvae which have made it to skeletal muscle penetrate it and take over cellular metabolism to develop protective coat, angiogenesis about larvum to create host-parasite nurse cell that may last decades. Unless the body is consumed raw by another carnivore this is a dead end for the parasite.
114
Q

Discuss life cycle of parasite in relation to clinical syndromes associated with hydatid cysts.

A

Hydatid disease is a zoonosis in which the adult tapeworms (E. granulosus) infest the gut of dogs and other canid hosts such as jackals. The adult is small, only 2-7mm in length and consists of 3 proglottids, an immature one, a mature one and a gravid one full of eggs.

Eggs pass out in the faeces and may be ingested by herbivorous animals such as cows, sheep, horses and goats. Once ingested hooked embryos develop in the duodenum, penetrate the mucosa, and become dispersed throughout the body via the circulation.

As a result, larval cysts (‘hydatid cysts’) form in various tissues with the majority favouring the liver. These cysts contain ‘protoscolices’ or early forms of the head of a new tapeworm. These develop into adult worms when ingested by a dog or similar host.

The condition is perpetuated when animals, especially dogs, ingest contaminated offal with the development of huge numbers of adult worms in the small intestine.

Humans are an incidental host and become infected by the accidental ingestion of eggs from contaminated food or close proximity to infected animals. Turkana in northern Kenya has one of the highest incidences of hydatid disease in the world. Here dogs and man live very closely together and quite often the locals employ ‘nurse dogs’, facilitating echinococcal spread.

Each egg contains an oncosphere, which is liberated in the herbivore intestine, penetrates the gut wall, and travels to distant organs, particularly to the liver and lungs. Ultimately, over the years, the oncosphere (larva) becomes encysted in a typical hydatid cyst. Humans become the secondary host if they ingest eggs due to contamination of food or fingers by dog faeces and ultimately develop cysts in major organs (70% in liver, 20% in lung, 10% elsewhere).

Beware of poorly husbanded sheep rearing areas.

Four echinococcal species cause disease in man, E. granulosus, E. multilocularis, E. oligarthrusand E. vogeli.

E. granulosus is by far the most common.

E. multilocularis is less common but the most virulent. Foxes are the usual primary host for E. multilocularis infections. Rodents are the secondary hosts for the intermediate cyst stages. See Q4 below.

E. vogeli is found mainly in the southern parts of South America and is the rarest form.

A fifth type, E. granulosis, is a tiny dog tapeworm for which it is theoretically possible that humans can act as intermediate hosts with the development of ‘hydatid’ disease.

115
Q

How long does it take Echinococcus oncosphere (larvae) to reach the liver?

Age of diagnosis? Kids?

Male: Female Ratio?

A

The oncosphere usually reaches the liver of man about 3 hours after ingestion of eggs.

Hydatid cysts grow slowly and it is rare to diagnose one before adulthood, unless it happens to be in the cranium, when pressure symptoms appear early even with a small cyst.

The cyst wall consists of an inner nucleated germinal layer and outer laminated one. Brood capsules protrude inwards from the germinal layer. These contain fluid and inwardly projecting protoscolices. When the brood capsules break off to float free in the hydatid cyst they constitute classical ‘hydatid sand’.

If an animal, e.g. a dog, eats a carcass that contains hydatid cysts, then the ingested protoscolices evaginate in the dog’s intestine and mature into adult tapeworms. Thus the cycle is completed.

In humans both sexes are equally affected.

116
Q

What is the difference between Echinococcus multilocularis and granolosus in terms of:

definitive host?

pathophysiology?

disease progression?

A

We acquire infection by swallowing the eggs of E. multilocularis. These eggs are excreted by infected foxes and can contaminate wild ground fruits, wild and cultivated berries and common vegetables to which the expanding fox population has access.

In humans, the cysts are located almost entirely in the liver, in contrast to E. granulosus cysts (liver 75%, lungs 15%, rest of body 10%). They also differ significantly by having daughter cysts that bud outwards instead of inwards. This means a greater invasion into the surrounding local tissues with occasional metastasis to other tissues, notably the lung.

A patient with a liver mass due to E. multilocularis presents as if they have cancer, either primary hepatocellular carcinoma or metastastic spread from other organs. Untreated E. multilocularisdisease carries a very high mortality.

117
Q

What is this?

What kind of host for what kind of parasite?

A
  • Bulimus snail
  • intermediate host for S. mansoni
118
Q

What are the 3 main species of Schistosome causing human disease?

Which snails?

What kind of disease do they cause?

Where are they found?

What is/are the other 3 related minor species causing human disease and where are they found?

A
  1. Schistosoma haematobium
    • causes urogenital schistosomiasis
    • throughout Africa, parts of Arabia, Near East, Madagascar & Mauritius
    • snail Bulinus
  2. S. mansoni
    • bowel and liver primarily
    • Africa, Madagascar
    • exported by slave trade to parts of South America, Caribbean and Arabia where permissive snail intermediate hosts found
    • snail Biomphalaria
  3. S. japonicum
    • bowel and liver primarily
    • China, Phillippines and Sulawesi (now eliminated from Japan)
    • small focus on Mekong river caused by related S. mekongi
    • snail Oncomelania
  4. S. intercalatum and sister species S. guineensis minor species confined to West africa.
    • ​​inhabits veins of lower bowel and produc terminal-spined eggs
119
Q

What is this?

What causes it?

Serology?

A
  • cercarial dermatitis
  • cercarial penetration of skin and entering capillaries
  • acutely in human schistosomal infection, also dead end manifestation of infection by avian schistosome’s (swimmers’ itch).
  • serology will be negative
120
Q

What is the effect of schistosomiasis wrt children’s growth and development?

A
  • causes significant stunting
  • chronic anemia of
    • fe deficiency and
    • chronic disease through interfering with hepcidin
  • related cognitive impairment
  • reversible through treatment
121
Q

What is this?

What are features of this disease on bowel?

On liver?

A
  • polyposis
  • inflammation bowel wall
  • strictures
  • bleeding, overt or occult
  • may screen with FOB, Calprotectin tests
  • periportal fibrosis with relative preservation of liver fx until late, portal hypertension
  • S. japonicum has sl different pattern of fibrosis with normal parenchyma surrounded by “building blocks” of fibrosis, prob related to diff pattern of egg deposition
  • should not usually have ascites or evidence of liver failure, so if you see this, consider comorbidities, eg. alcohol, chronic hepatitis
  • once portal hypertension develops, can get egg deposition in lungs due to egg deposits through portosystemic collaterals ⇒ pulmonary hypertension
  • 17% of children under 10 in Lake Albert Uganda had some degree of liver fibrosis
  • nb can also get spillover of S. eggs into systemic circulation with S. hematobium
122
Q

What is hepcidin?

A
  • Hepcidin is a protein that in humans is encoded by the HAMP gene. Hepcidin is a key regulator of the entry of iron into the circulation in mammals.[4]

In states in which the hepcidin level is abnormally high such as inflammation, serum iron falls due to iron trapping within macrophages and liver cells and decreased gut iron absorption. This typically leads to anemia due to an inadequate amount of serum iron being available for developing red cells.

123
Q

What are possible symptomes of Female Genitourinary Schistosomiasis?

What is the effect on HIV transmission?

A
  • vaginal discharge
  • bloody discharge
  • genital itching
  • dyspaerunia
  • infertility/subfertility
  • pelvic pain during or after intercourse
  • 4-fold increase in HIV transmission
124
Q

Outline an approach to returning traveller with possible eposure to schistosomiasis.

A
125
Q

Can you draw a family tree for Parasitic Worms?

A
126
Q

What are the 4 main groups of food borne trematode diseases?

What are the infectious agents for each disease?

Through consumption of what food?

What is the natural final host for each infection?

A
  • for all, larval stages are ingested as meta-cercariae/cysts
  • adult worms in liver, lungs or gut
  • eggs released harmlessly into lumen of gi tract (unlike schistosomiasis in which eggs are the main component causing harm)
127
Q

What is this? (30µm x 16µm)

Outline the lifecycle.

A
  • Opisthorchis viverrini egg, but it could just as well be Clonorchis sinensis egg as the two are almost identical (also Opisthorcois felineus)
  • Natural definitive hosts include dogs & cats and lifecycles are much the same
  • In this case man is the definitive host
  1. embryonated eggs pass from feces into water
  2. eggs are ingested by snail
  3. free-swimming cercariae penetrate and encyst in skin or flesh of fresh water fish
  4. metacercariae in fish are ingested by human host (or other fish eating mammal)
  5. excyst in duodenum & ascend the biliary tract, where they mature to become
  6. egg producing adults
128
Q

What are the 3 human liver flukes and where are they endemic?

A
129
Q

What is this?

What disease might it transmit?

Where?

A
  • Fresh-water crabs like this one were implicated in a Paragonimus outbreak in January of 2007. Specialty dishes in which shellfish are consumed raw or prepared only in vinegar, brine, or wine without cooking play a key role in the transmission of paragonimiasis. Raw crabs or crayfish are also used in traditional medicine practices in Korea, Japan, and some parts of Africa.
  • Several species of Paragonimus cause most infections;
  • the most important is P. westermani, which occurs primarily in Asia including China, the Philippines, Japan, Vietnam, South Korea, Taiwan, and Thailand.
  • P. africanus causes infection in Africa, and
  • P. mexicanus in Central and South America.
  • Although rare, human paragonimiasis from P. kellicotti has been acquired in the United States, with multiple cases from the Midwest. Several cases have been associated with ingestion of uncooked crawfish during river raft float trips in Missouri
130
Q

What is this?

(It measures 110µm x 60µm)

What disease does it cause?

Describe lifecycle

A
  • Paragonimiasis
    1. The eggs are excreted unembryonated in the sputum, or alternately they are swallowed and passed with stool .
    2. In the external environment, the eggs become embryonated , and
    3. miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues .
    4. Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail.
    5. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host .
    6. Human infection with P. westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite .
    7. The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (7.5 to 12 mm by 4 to 6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycles is not achieved, because the eggs laid cannot exit these sites. Time from infection to oviposition is 65 to 90 days.

Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P. westermani.

131
Q

What are the symptoms of Paragonimiasis?

Treatment?

A
  • Infection with Paragonimus spp. can result in an acute syndrome with cough, abdominal pain, discomfort, and low-grade fever that may occur 2 to 15 days after infection. Persons with light infections may have no symptoms. Symptoms of long-term infection may mimic bronchitis or tuberculosis, with coughing up of blood-tinged sputum.
  • Human paragonimiasis is acquired through ingestion of raw or undercooked crabs or crayfish, and is usually a lung infection. After ingestion, metacercariae excyst in the small intestine and release larvae that penetrate the duodenal wall and enter the peritoneal cavity. The larvae migrate for approximately 1 week, then penetrate the diaphragm, enter the pleural cavity, and migrate directly through lung tissue to reach the bronchi. There they form cystic cavities and develop into adult worms in 5-6 weeks. The adult parasites are reddish brown and ovoid, measuring 7.5-12 mm by 4-6 mm. Adult worms induce an inflammatory response in the lungs, generating a fibrous cyst that contains a purulent, bloody effusion and eggs released by the flukes which are passed into the environment via expectoration, or may be swallowed and passed with feces.
  • Eosinophilia, wide range of CXR findings
  • acid fast stain for TB smear destroys eggs in sputum
  • occ CNS infection, can migrate anywhere
  • occ skin nodules
  • Treatment: praziquantel
132
Q

What is the parasite in fasciolopsis?

Distinguish from?

Treatment.

A
  • usually fasciola hepatica
  • occasionally fasciola gigantica
  • beware, not fasciola buski, which has similar eggs, but is an intestinal fluke and is treated differently - with Praziquantel, which does not work for fasciolopsis.
  • Fasciolopsis is treated with Triclabendazole.
133
Q

What is this?

(size 140µm x 75µm)

What disease?

What is the lifecycle?

A
  • Fasciola hepatica egg
  • Definitive host human (or sheep or cow)
  • Snail is the intermediate host
  1. immature Fasciola eggs are discharged in biliary ducts and in stool
  2. Eggs become embryonated in water and
  3. Invade suitable snail intermediate host, including genera Galba, Fossaria, and Pseudosuccinea.
  4. Undergoes several developmental stages in snail (sporocysts, rediae and cercariae)
  5. Cercaria released from snail
  6. encyst as metacercariae on aquatic plants, esp watercress, where they are ingested by humans, cattle or sheep (or possibly by drinking unfiltered water)
  7. After ingestion the metacercariae excyst in duodenum and
  8. migrate through the intestinal wall, the peritoneal cavity and the liver parenchyma into the biliary ducts where they develop into adult flukes.
  • In humans maturation from metacercariae into adult flukes takes 3-4 months. Adult flukes reside in biliary ducts of mammalian host.
134
Q

Describe clinical features of fascioliasis.

A
  • liver fluke
  • fasciola parasites do not multiply in people so parasite load depends on inoculum
  • acute and chronic phases may be symptomatic or not. non-specific clinical features of both phases include
    • fever, maybe intermittent
    • malaise
    • abd pain: ruq, epigastrium or more diffuse/generalized
    • anorexia, n, v, d, altered bowel habit, wt lossAcute phase
    • hepatomegaly, jaundice
    • eosinophilia, esp in acute phase
    • anemia, esp in kids
    • transaminitis
  • acute phase lasts 2-4 months
  • chronic pahse begins when immature larvae reach bile ducts, mature and start producing eggs
  • comps: cholangitis, biliary obstruction
  • cholecystitis, gallstones
  • pancreatitis, cirrhosis
  • ectopic infection possible
  • Diagnosis: serology may be usefel before egg production begins, or if low level or sporadic egg production, or ectopic infection
  • Treatment: triclabendazole or possible nitazoxanide, NOT PRAZIQUANTEL
135
Q

Outline the generic lifecycle of a FBT

A
136
Q

Outline the general clinical facts about trematodes

A
137
Q

Fascioliasis Treatment

Who to treat?

How?

A
  • Treatment is Triclabendazole 10 mg/kg in single dose (double dose in case of treatment failure)
  • Treat all confirmed cases; in endemic areas treat all suspect cases.
  • Preventive chemotherapy: in areas where cases of fascioliasis appear to be clustered treat all school-age children or all residents q 12 months
138
Q

Clonorchiasis and opisthorchiasis Treatment

Who?

How?

A
  • Praziquantel 25 mg/kg tid for 2-3 days
    • treat all confirmed cases, or in endemic area, all suspect cases
  • Preventive treatment
    • in districts where prevalence > 20% treat all residents q 12 months
    • <20% treat q 24 mo or treat only those reporting habit of eating raw fish q 12 months
  • (Also some evidence that new Chinese drug tribendimidine may provide an alternative)
139
Q

Paragonimiasis: Treatment

Who?

How?

A
  • Individual case managemet: confirmed cases or suspect in endemic areas
    • Triclabendazole 2 x 10 mg/kg in the same day or
    • Praziquantel 25 mg/kd tid x 3 days
  • Preventive Chemo in places where cases appear clustered
    • Triclabendazole 20 mg/kg in single dose
140
Q

Where can you get Paragonomiasis?

What is the Parasite, Definitive and Intermediate Host?

A
  • West Africa: limited to Cameroon & Nigeria
  • China, East and South East Asia
  • Ecuador, Peru
  • Def Host: Human
  • 1st Intermediate: Freshwater Snail
  • 2nd Intermediate: Freshwater Crab or Crayfish
141
Q

What are the causes of Pulmonary Eosinophilia?

A
142
Q

List 7 antiparasitic drugs and some parasites they are effective against.

A
  1. Albendazole
    • 400 mg single dose
      • Roundworm/Ascaris, Hookworm/N.americanus, Pinworm/Enterobius
    • 400 mg daily x 3 days
      • Whipworm/Trichuris
    • 400 mg bid x 3 days
      • Threadworm/Strongyloides
    • Prolonged course +/- Surgery: Echinococcus
  2. Ivermectin: Ascaris, Enterobius, Strongyloides, Filaria
  3. Praziquantel: Schistosomiasis, Paragonomiasis, Clonorchis
  4. Triclabendazole: Fasciolopsis
  5. Metronidazole: Entameba, Giardia
  6. Nitazoxanide most of the above, v broad spectrum
  7. Co-trimoxazole: Isospora belli
143
Q

What is the difference between visceral and cutaneous larva migrans?

What is the similarity?

A
  • Both are conditions in which humans are the accidental host of an animal parasitic worm.
  • Visceral larva migrans is caused by the larvae of animal (usually dog or cat) species of Toxocara Canis or cati. The larva penetrates the intestine and wanders about causing inflammation, usually in the lungs, or liver, sometimes in the eye or csf
  • Cutaneous larva migrans is caused by zoonotic species of Ancylostoma or hookworm. Here the L2 larva penetrates the skin but is only able to proceed a short while before dying, usually causing local inflammation and itching and leaving a serpentiginous rash.
144
Q

How does strongyloides hyperinfection present?

A

Hyperinfection acute or chronic

• Abdo

Weight loss, malabsorption, blood in stool, protein loss, abdo distension

• Chest

As above, also Gram neg sepsis, ARDS/pneumonitis, often post op in ICU

• Skin

Petechial/purpuric rashes, DIC rash
• Eosinophilia absence = poor prognosis

145
Q

Name 5 types of parasitic brain disease and describe briefly how they develop.

A
  • (a) Human African Trypanosomiasis (HAT)
    (b) Neurocysticercosis (tapeworm)
    (c) Neuroschistosomiasis
    (d) Angiostrongylus cantonensis
  • (e) Toxoplasmosis

The correct answer is (a). Any of these conditions may cause stupor/coma. Swollen neck glands (Winterbottom’s sign) are found in African trypanosomiasis and suggest that trypanosomes enter the brain via the lymphatic system. Different stages of coma are seen in this disease from very mild daytime sleepiness to deep coma. HAT (‘sleeping sickness’) is transmitted by the tsetse fly. It occurs in equatorial regions of Africa, notably just north of Lake Victoria.

Humans are the definitive host and ultimate reservoir for pig tapeworm (Taenia solium, Taenia asiatica) and for cattle tapeworm (Taenia saginata). This means that adult tapeworms only develop and produce their eggs in human intestine. One way of acquiring tapeworm infestation (taeniasis) is to ingest eggs via faecally contaminated food or water or via the faeco-oral route. Mostly however infection occurs after eating raw or undercooked ‘measly’ pork or beef that contains encysted tapeworm larvae (cysticerci). In this case the ingested cysts invaginate the mucosa of the small intestine, mature into adults, and, after about 12 weeks, gravid females produce up to 50 000 eggs per day, which are shed in the stool. Adult tapeworms can remain in situ for many years.

When pigs or cattle eat contaminated material it is usual that some eggs turn into oncospheres in the stomach and duodenum, cross the intestinal membrane, and are carried via the vascular system to different parts of the body, where they form larval cysts (cysticerci) 1–2 cm in size.

In the case of man a similar cysticercosis occurs only when oncospheres of T. solium are released. This causes little or no trouble when cysts form in areas such as muscle or subcutaneous tissues, but it can be very serious when they develop in the CNS. Cysts in the CNS may be asymptomatic or cause focal or general neurological symptoms. In many countries neurocysticercosis is by far the commonest cause of seizures.

In short, neurocysticercosis represents an aberrant cystic larval stage of Taenia solium in man in which eggs released in the upper small intestine invade the body and develop into cysts in the CNS (autoinfection).

Neuroschistosomiasis occurs when pairs of adult worms, particularly of S. japonicum, lodge in the CNS instead of in the mesenteric or vesical plexuses. The ensuing granuloma can then produce symptoms if it presses on important structures.

Angiostrongylus cantonensis (rat lung worm) is a parasitic nematode found in the Far East. It is a zoonosis that affects rodents. Humans contract it by eating food (snails, slugs, molluscs) infected with 3rd stage larvae. It is the commonest cause of eosinophilic meningitis.

146
Q

What is Hymenolepsis nana?

Hymenolepsis diminuta?

Disease?

Life Cycle

A
  • rat or dwarf tapeworm
  • Hymenolepis nana, the dwarf tapeworm, occurs worldwide, principally among children. Most infections are asymptomatic, but heavy infections may cause abdominal pain, nausea, vomiting, pruritus ani and diarrhea, sometimes containing blood. Headache, dizziness, sleep and behavior disturbances are frequent. Convulsions have also been reported. Autoinfection is common.

Hymenolepis diminuta, the rat tapeworm, may affect humans who ingest the intermediate host, usually a weevil, flea or cockroach. Most infections are asymptomatic and of short duration.

Dipylidium caninum infection may occur in humans, usually young infants, following accidental ingestion of a flea, the intermediate host of this cestode whose usual host is a dog or other carnivore. Most infections are asymptomatic. Some children experience abdominal pain, diarrhea, pruritus ani and urticaria.

Diagnosis and treatment

Diagnosis is usually made by identification of characteristic eggs or proglottids in feces. There may be a variable eosinophilia, minimal in cases of T. saginata and often reaching 5–10% in hymenolepiasis.

Praziquantel is the drug of choice for all of the above intestinal cestode infections. A single oral dose of 10 mg/kg is usually effective. H. nana requires 25 mg/kg as a single dose.

147
Q

What is the current population burden for

Ascaris

Trichuris

Hookworm

Srongyloides

A
  • Ascaris: 800 mill
  • Trichuris: 440 million
  • Hookworm: 460 million
  • Strongyloides:100 million
148
Q

Visceral larva migrans:

Clinical Features

Blood work

A
  • migrating larvae from toxocara, parasitic roundworms of dogs and cats
  • larva ingested in contaminated soil or food and released in intesting
  • prolonged migration through tissues causing pneumonitis, fever, abd pain, myalgia, lymphadenopathy, hepatosplenomegaly, sleep and behavioural disturbances, focal or generalized convulsions
  • eosinophilia, hypergammaglobulinemia elevated titres of blood group isohemagglutanins.
  • serological dx with ELISA
  • tx albendazole or mebendazole
149
Q

What is Loffler’s syndrome and what causes it?

A
  • it is caused by the migration of helminth larvae through the lungs with the production of eosinophilia and a pneumonic infiltrate. Classically it is ascribed to the passage of Ascaris larvae 7-14 days after egg ingestion.
  • hookworm and strongyloides larva may also cause a mild eosinophilia on transiting the lungs but it is lessed marked.
150
Q

Which hookworm has teeth-like mouthparts and which has a plate.

A
  • Ancylostoma duodenale has teeth
  • Necator americanus does not
151
Q

Flukes treatment

  1. clonorchis and opisthorchis
  2. fasciola
  3. paragonimus
A
  1. praziquantel
  2. triclabendazole
  3. triclabendazole or praziquantel but according to CDC former is simpler, fewer doses hence compliance better