STRONGYLOIDES STERCORALIS Flashcards

1
Q

What’s the common name for strongyloides stercoralis?

A

Threadworm (although in some countries this common name refers to Enterobius vermicularis)

The smallest nematode & is aetiologic agent of Strongylodiasis

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2
Q

Epidemiology of S. stercoralis

A

Warm climates

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3
Q

Habitat of S.stercoralis:

A

①Adults in wall of intestine(duodenum & jejunum)
➁larvae can be found throughout the body
③Parasitic females may invade lung epithelium and reproduce

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4
Q

MORPHOLOGY OF S.STERCORALIS:

A

①Female worms
➁Male worms
③Eggs
④Larvae
Both and male worms have a well developed digestive system.

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5
Q

Female S.stercoralis morphology:

A

Females are thin, transparent & about 2.5 mm long .
*The female reproductive system contains paired uteri, vagina & vulva. Gravid female uteri contain thin­ walled transparent ovoid eggs
*Ovoviviparous with a lifespan of 3 to 4 months, may persist due to autoinfection!

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6
Q

Male S.stercoralis morphology:

A

Male worms are shorter & broader than females measuring 0.6–1 mm in length.
*They have copulatory spicules which penetrate the female during copulation.
*They do not invade the intestinal wall & usually not seen in human infection

Male worms eliminated from the bowel soon after the females begin to oviposit(lay eggs).
However, the majority of females are probably parthenogenetic ( lay fertilized eggs without males).

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7
Q

Egg of S.stercoralis morphology:

A

*Are oval & measure 50–60 µm in length.
*Seen within the uterus of gravid female.
*eggs hatch out to rhabditiform larva (1st stage larva) soon after being layed.
*Hence it is the larva & not the egg which is excreted in feces & detected during stool examination

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8
Q

Larvae of stercoralis morphology:

A

Rhabditiform Larva (L1 stage) and Filariform larva (L3 stage)

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9
Q

Rhabditiform Larva (L1 stage)

A

*Eggs hatch out to form L1 larva in the small intestine.
*Most common form of the parasite found in the feces.
*L1 larva migrates into the lumen of the intestine & excreted in feces.
*Has ‘double bulb’ oesophagus

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10
Q

Filariform Larva (L3 stage)

A

*L1 larva moults twice to become the L3 larva.
*It is the infective stage of the parasite to man
*Has long, slender oesophagus

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11
Q

Life Cycle of S.stercoralis:

A

Has a parasitic cycle & a free-living soil cycle where it can persist for long periods in soil.

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12
Q

Natural host:

A

Man but dogs & cats are found infected with morphologically similar strains

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13
Q

Mode of infection:
.

A
  1. Penetration of skin by filariform larva when a person walks barefoot in contaminated soil.
  2. Internal autoinfection in colon – L3 penetrate mucosa of colon.
  3. External autoinfection: L3 penetrate perianal, and perineal area
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14
Q

In the free-living cycle:

A

①Rhabditiform larvae are passed in the stool of an infected definitive host
➁develop into either infective filariform larvae (direct development)
⑥or free-living adult males and females
③that mate and produce eggs
④from which rhabditiform larvae hatch
⑤and eventually become infective filariform (L3) larvae
⑥The filariform larvae penetrate the human host skin to initiate the parasitic cycle

This second generation of filariform larvae cannot mature into free-living adults and must find a new host to continue the life cycle

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15
Q

Parasitic cycle:

A

⑥Filariform larvae in contaminated soil penetrate human skin when skin contacts soil
⑦and migrate to the small intestine
⑧It has been thought that the L3 larvae migrate via the bloodstream and lymphatics to the lungs, where they are eventually coughed up and swallowed. However, L3 larvae appear capable of migrating to the intestine via alternate routes (e.g. through abdominal viscera or connective tissue).
⑧In the small intestine, the larvae molt twice and become adult female worms . ⑨The females live embedded in the submucosa of the small intestine and produce eggs via parthenogenesis (parasitic males do not exist) , which yield rhabditiform larvae.
①The rhabditiform larvae can either be passed in the stool
⑩or can cause autoinfection

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16
Q

Pathogenicity & Clinical Features

A

①S. stercoralis generally cause benign & asymptomatic disease.
➁Blood eosinophilia & larvae in stool may be the only indications of infn.
③Severe & even fatal disease may occur in those with defective immune response.
④Clinical disease may have skin, pulmonary & intestinal manifestations.

17
Q

Skin manifestations of Strongyloides infection

A

*Dermatitis with erythema & itching at site of penetration of L3 larva occur.
*In sensitized individuals, there may be an allergic response.
*Pruritus & urticarial lesions particularly around the perianal skin & buttocks are symptoms of chronic strongyloidiasis.
*larva migrans do occur = larva currens or racing larva, 10cm/hour

18
Q

Pulmonary Manifestations of Strongyloidiasis

A

*Small hemorrhages may occur in the alveoli & bronchioles as larva escape pulmonary capillaries .
*Bronchopneumonia may be present, which may progress to chronic bronchitis & asthmatic symptoms in some patients.
*Larva of Stongyloides may be found in the sputum of these patients

19
Q

Intestinal Manifestations of strongyloidiasis

A

*Epigastric pain & hunger pangs in acute stage resembling peptic ulcer or malabsorption syndrome.
*Mucus diarrhea is often present.
*Extensive sloughing of mucosa causing dysenteric stools occur in heavy infn.
*Other manifestations include protein-losing enteropathy and paralytic ileus.

20
Q

Hyperinfection

A

*Refers to extensive internal reinfection leading to large numbers of adult worms in intestines, lungs & larvae in various tissues & organs.
*Common in immunosuppressed persons
*Defective cell-mediated immunity predispose to this condition
*Filariform larvae may enter arterial circulation & lodge in various organs e.g. heart, lungs, brain, kidney, pancreas, liver & lymph nodes.
*CNS involvement lead to brain abscess & meningitis.
*Peritonitis is also a major fatal complications.
*Circulating larvae may carry intestinal bacteria causing septicemia

21
Q

Diagnosis of Strongylodiasis

A
  1. Clinical diagnosis– diarrhoea with epigastric pain,high eosinophilia.
  2. Definitive diagnosis – Microscopy
    *Direct wet mount of stool: Demonstration of L1 larvae in freshly passed stools most important for specific diagnosis.
    *Concentration methods: formol ether concentration method or Baermann’s funnel gauze method.
    *Larvae may be present in sputum, duodenal aspirates & jejunal biopsies.
    *Stool Culture esp when larvae are scanty using Agar plate culture & Charcoal culture method.
    *Serological tests e.g ELISA although has a downside of extensive cross­-reactions with other helminth infns
22
Q

Treatment of Strongyloidiasis

A

All cases whether symptomatic or not need to be treated to prevent severe invasive disease.
*Ivermectin (200 mg/kg daily for 2 days) more effective than Albendazole.
*Disseminated disease need extended treatment with Ivermectin for atleast 5–7 days.
*Absence of eosinophilia is a poor prognostic sign in hyperinfection.

23
Q

Prevention of Strongyloidiasis

A
  1. Sanitary disposal of human excreta
    -long voided feces or surface water specially dangerous.
  2. Treat all cases specifically
  3. Rule out Strongylodiasis before treatment with immunosuppressives.
  4. 30 year old infection in absence of exposure reported – autoinfection.
24
Q

ZOONOTIC STRONGYLOIDIASIS

A

*Wild or domestic animals as definitive /natural hosts.
*Do not cause patient infections.
*Causes cuteneous larva migrans and urticaria in man

25
Q

STRONGYLOIDES FUELLERBORNI

A

*Parasite of Old World monkeys, Zoonotic
*First human case – Zimbabwe
*Papua New Guinea.
*Zambia

Known as SWOLLEN BELLY SICKNESS

26
Q

MORPHOLOGY of S.fuellerborni

A

Eggs in stool, not larvae
Eggs resemble hookworm eggs.
Freeliving female with post vulvar constriction

27
Q

Transmission S.fuellerborni

A

*Similar to S.stercoralis
*Trans-mammary in infants implied –14th day after birth infants develop infection.

28
Q

Pathogenesis of S.fuellerborni

A

*Similar to S.stercoralis (with a very huge egg load)
*Abdominal symptoms with oedema – “swollen belly sickness”as a result of protein loss.
*Respiratory distress and abdominal distension symptoms.

29
Q

Diagnosis of S. fuellerborni

A

*Demonstration of ova in feces
*Copro culture of eggs to adults, and their identification.

30
Q

Treatment of S.fuellerboni

A

*Thiabendazole
*Mebendazole
*Clinical management – in hyperproteinaemia

31
Q

Prevention of S.fuellerborni

A

*Sanitary disposal of human excreta
*Control of monkey populations
*Treat all cases specifically

32
Q

DIPLOSCAPER CORONATA

A
  1. Lives in decaying matter and sewage beds
  2. Facultative parasite of man
  3. Males rarely found – parthenogenesis reproduction
  4. Worms found in human urine and stomach contents
  5. Worms acquired from decaying vegetation.
33
Q

RHABDITIS

A
  1. Resemble free-living Strongyloides
  2. Life cycle free-living – but no fllariform larval form
    3.Can live in ulcerated damaged skin and organs
  3. Contaminators of food and drink
  4. In human larvae found in itching cutaneous papules- resemble craw-craw, female urine.
34
Q

MELOIDOGYNE JAVANICA
Syn Heterodera incognita

A
  1. Plant parasitic Nematodes found in roots and stem of many edible plants
  2. Eggs and larvae in feces after ingestion of infected plants
  3. Eggs thin shelled, elongate ovoid, flattened on one side
  4. Mistaken for infertile eggs of Ascaris or hookworm eggs.