(M) Nematoda: Secernentea: Ascaradida (lecture-based) Flashcards

A. lumbricoides (lesson 1), T. canis, T. cati, Anisakis spp. (lesson 2)

1
Q

Order of subclass

Enumerate all under this subclass: secernentea (5)

A
  • Ascaradida
  • Strongylida
  • Rhabditida
  • Oxyurida
  • Spiruruda
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2
Q

Superfamily of the order Ascaradida

A

Ascaridoidea

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3
Q

Species of the super family Ascaridoidea

A
  • Ascaris lumbricoides
  • Toxocara canis
  • Toxocara cati
  • Anisakis spp.
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4
Q
  • It has a worldwide distribution, (WHO Classification of Helminthes), and is soil transmitted.
  • Incidence of infection among children is greater than adult individuals.
  • Most common helminth infection of man
A

A. lumbricoides

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5
Q

ASCARIS LUMBRICOIDES AKA

A

Giant intestinal roundworm

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6
Q

LIFE CYCLE: ASCARIS LUMBRICOIDES

MOT

A

ingestion of viable, embryonated eggs present in foods and/or drinks

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7
Q

LIFE CYCLE: ASCARIS LUMBRICOIDES

Give the excystation after the egg hatches the small intestine

ano nangyare after

A

larva penetrates the intestinal wall, enters
venous circulation, passes through the liver, and enter the right side of the heart.

intestinal wall -> circulation -> liver -> right side of the heart

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8
Q

LIFE CYCLE: ASCARIS LUMBRICOIDES

It is carried by blood to the lungs and develops into the?

anong stage

A

4th larval stage

blood-lung phase cycle.

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9
Q

LIFE CYCLE: ASCARIS LUMBRICOIDES

The larva breaks through pulmonary capillaries, goes into the air sacs, to the bronchioles, bronchi, trachea, epiglottis, and then?

A

swallowed

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10
Q

LIFE CYCLE: ASCARIS LUMBRICOIDES

Where does the larva in the stomach goes to? to become adult worms

A

small intestine (final habitat)

mainly lumen of the ileum

Mating takes place and females lay eggs, which are discharged into the feces of human host

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11
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

pathogenic to man

A

larva and adults

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12
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

  • where the passage of larvae through liver & lungs provokes no remarkable pathologic symptoms unless the number of larvae is immense.
  • Eosinophilic infiltration & granuloma formation around the path of migrating larvae
  • Fibrosis of the periportal & interlobular spaces
A

larval migration

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13
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

o Migratory larvae in the lungs cause tiny
hemorrhages in the alveoli, which incite cellular
infiltration and consolidation.
o Fever, cough, eosinophilia, dyspnea, and rales may
be present.

A

Ascaris pneumonitis

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14
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

  • Severe pulmonary symptoms
  • Dyspnea, dry productive cough
  • X-ray: scattered, shifting mottled lung infiltration
  • Spontaneously clearing associated w/ marked peripheral eosinophilia: Loffler’s syndrome

reffered to as

A

LOEFFLER’S PNEUMONITIS

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15
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

Adult worms in the small intestine, mainly in the
ileum tend to be well tolerated unless infection is
heavy and/or the patient’s nutrient intake is
inadequate.

A

INTESTINAL ASCARIASIS

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16
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

Children may have intermittent colicky abdominal
cramps, loss of appetite, and protruding abdomen (pot-belly appearance).

A

INTESTINAL ASCARIASIS

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17
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

TOF. Single worm can cause serious disease

A

T

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18
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

Worms may be entangled to each other resulting to a?

A

ball of worms or Ascaris bolus

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19
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

Ascaris bolus may lead to?

A

intestinal obstruction

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20
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

The worm is also able to perforate intestinal wall that
will result to

A

peritonitis

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21
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

The worm in the peritoneum can enter the liver to produce

A

Ascaris liver abscess

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22
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

TOF. Allergic manifestations may appear such as asthma-like symptoms and urticaria

A

T

o Bronchospasm & pulmonary infiltrates
o Pronounced during pulmonary migration
o Asthma & urticaria may continue during intestinal
phase

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23
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

Heavy worm burden may cause

A

protein-calorie malnutrition or impairment of growth

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24
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

Worms that become erratic or restless cause them to enter structures resulting to?

familiarize mo nalang

A

appendicitis, biliary duct, to cause biliary obstruction, or pancreatic duct, causing acute pancreatitis.

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25
Q

PATHOLOGY: ASCARIS LUMBRICOIDES

Erratic worms may go to the epiglottis to cause edema
that may lead to airway obstruction and therefore?

A

asphyxia

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26
Q

DIAGNOSIS: A. LUMBRICOIDES

ENUMARATE

A
  • Sputum
  • gastric washings
  • DFS
  • Abdominal X-ray
  • Barium Swallow
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27
Q

DIAGNOSIS: A. LUMBRICOIDES

o To confirm Ascaris Loeffler’s pneumonitis
o Demonstration of larvae

A

Sputum

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28
Q

DIAGNOSIS: A. LUMBRICOIDES

o To confirm Ascaris Loeffler’s pneumonitis
o Demonstration of eosinophils and Charcot-Leyden
crystals

A

Gastric washings

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29
Q

DIAGNOSIS: A. LUMBRICOIDES

o To confirm intestinal ascariasis
o Highly effective
o Demonstration of eggs (unfertilized or fertilized – not
embryonated in fecal smears)

A

Direct Fecal Smears

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30
Q

DIAGNOSIS: A. LUMBRICOIDES

o X-ray of abdomen may show the so-called “tramway
sign (railroad track-like)”.

A

Abdominal X-ray

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31
Q

DIAGNOSIS: A. LUMBRICOIDES

o Can also be requested and may show the string sign,
wherein the adult worms ingest the contrast material.
o Adult worms that passed out in the anus or in the
mouth can be a sign of erraticism.

A

Barium swallow

32
Q

TREATMENT: A. LUMBRICOIDES

DOG

drug of choice

A

Albendazole and mebendazole

100 mg BID for 1-3 days

33
Q

TREATMENT: A. LUMBRICOIDES

OTHER drugs

A
  • PIPERAZINE CITRATE (75 mg) per kg OD for 2 days
  • PYRANTEL PAMOATE (11 mg) per kg in single dose
34
Q

TREATMENT: A. LUMBRICOIDES

For heavy infestation

A

surgery may be required to remove worms, such as Ascaris bolus and repair damage they’ve caused like intestinal perforations, bile duct blockage, and appendicitis.

35
Q

TREATMENT: A. LUMBRICOIDES

Drainage may also be done for?

A

Liver abscess

36
Q

Prevention: A. LUMBRICOIDES

ANU

A
  • Proper and hygienic methods of human waste disposal
  • Prohibit use of human feces (night soil) as fertilizer in
    vegetable gardens
  • Care for foods and water from contamination with fecal
    material
  • Control of insects that may serve as mechanical
    transmitters, such as flies and cockroaches
  • Provision of safe drinking water
37
Q

SECERNENTEA: UN-ADAPTED WORMS

Identify

A
  1. TOXOCARA CANIS AND CATI
  2. ANISAKIS SPECIES
38
Q

consist of species that are UNABLE TO REACH ADULTHOOD IN THE HUMAN HOST BUT, can cause disease in man.

A

Un-adapted worms

39
Q

SECERNENTEA: UN-ADAPTED WORMS

Disease among humans is labeled as

A

visceral larva migrans

owing to the ability of the larval stages to cause significant and potentially serious pathology in various internal organs

40
Q

SECERNENTEA: UN-ADAPTED WORMS

It is the presence of migrating larval stages of a
particular worm in the visceral organs of the body.

A

Visceral Larva Migrans (VLM)

41
Q

SECERNENTEA: UN-ADAPTED WORMS

most common

A

Toxocara canis

42
Q

TOXOCARA CANIS AND CATI

Dog ascarid

A

T. canis

43
Q

TOXOCARA CANIS AND CATI

cat ascarid

A

TOXOCARA CATI

44
Q

TOXOCARA CANIS AND CATI

adult worms inhabit the intestines of?

A

dogs or cats

45
Q

TOXOCARA CANIS AND CATI

TOF. Humans are accidental hosts.

A

T

46
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

Definitive host

A

animals

47
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

What is shed out of the feces?

A

unembryonated eggs

48
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

Where does the eggs will embryonate and become infective?

A

environment

49
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

TOF. The adult worm will be developed and oviposit in the small intestine.

A

T

50
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

MOT

A

fecal-oral route

51
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

Infective stage

A

Embryonated egg

52
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

egg hatches in the small intestine and the larva that escapes from the egg penetrates the intestinal walls to go into the?

A

MESENTERIC VENULES

53
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

larval form reaches different sites through the

A

blood circulation

54
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

Organs invaded

A

liver (most common), lungs, brain, and eyes

55
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

TOF. The larva does not develop into the adult stage in the human body.

A

T

They will become adults in the small intestine of dogs/cats

56
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

If the larva goes into the eyes, the condition is referred to as

A

ocular larva migrans

57
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

TOF. Ocular larva migrans typically occurs only in one eye and can cause irreversible vision loss

A

T

58
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

present in the liver

A

hepatitis

59
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

Main manifestations of toxocariasis

A

VLM and OLM

59
Q

LIFE CYCLE: TOXOCARA CANIS AND CATI

present in the lungs

A

pneumonia

60
Q

PATHOLOGY AND CLINICAL MANIFESTATIONS: T. cati and canis

Migration of larvae causes eosinophilic inflammation that result to

A

granuloma formation

severity of which depends on the number of larvae, the type of tissue invaded, and the duration of the infection

61
Q

PATHOLOGY AND CLINICAL MANIFESTATIONS: T. cati and canis

TOF. most striking clinical feature of human toxocariasis (or VLM) is high, sustained increase of eosinophils (eosinophilia)

A

T

62
Q

PATHOLOGY AND CLINICAL MANIFESTATIONS: T. cati and canis

CHARACTERISTIC TRIAD OF THE INFECTION

A

o Marked eosinophilia
o Hepatomegaly
o Hyperglobulinemia

63
Q

DIAGNOSIS: T. cati and canis

enumerate

A

Microprecipitation test
ELISA (confirmatory)
Tissue biopsy (if present in diff parts of the body)

64
Q

Treatment: T. cati and canis

ENUMERATE

A
  • Drugs used for treatment include thiabendazole and corticosteroids.
  • Albendzole
  • The infection may be prevented through protecting
    children from contact with infected dogs, these animals
    should be de-wormed regularly, and do not allow
    domestic pets to defecate promiscuously.
65
Q

Anisakis species causes?

A

Anisakiasis or Herring Worm Disease

66
Q

Anisakis sp.

MOT

A

Ingestion of 3rd stage larva (L3) in undercooked fish

67
Q

Anisakis sp.

Clinical manifestation

A

instestinal obstructuon

68
Q

Anisakis sp.

Infective stage to definitive host

A

L3 larvae

69
Q

Anisakis sp.

Diagnostic stage

A

Anisakiasis (larva)

70
Q

Anisakis sp.

Adult worm inhibits

A

Stomach of marine mammals

71
Q

Anisakis sp.

Where do they embryonate

A

body of water

the larva stage is developed there

72
Q

Anisakis sp.

When it dies, where does it go?

A

muscle tissues

73
Q

Anisakis sp.

Incidental host

A

Humans

74
Q

Anisakis sp.

Laboratory diagnosis

A
  • serologic
  • gastroscopy (larva)
  • surgery (biopsy)
75
Q

Anisakis spp

Treatment

A

Albendazole and/or surgery