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Y2B1 - GIT πŸ“• > Parasitology πŸͺ± > Flashcards

Parasitology πŸͺ± Flashcards

1
Q

what is the morphology of Ascaris lumbricoides (Giant intestinal round worm)?

A
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2
Q

compare between the charachters of Ascaris lumbricoides eggs

A
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3
Q

what is the habitat of Ascaris lumbricoides?

A

Small intestine

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4
Q

what is the definitive host of Ascaris lumbricoides?

A

man

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5
Q

what is the infective stage for Ascaris lumbricoides?

A

Eggs containing second-stage rhabditiform larva

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6
Q

what are the stages of life cycle of Ascaris lumbricoides?

A

egg, larvated egg, larva and adult.

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7
Q

life cycle of Ascaris lumbricoides

A
  • Immature eggs pass in the faeces.
  • Under favorable environmental conditions in the soil (temperature of about 25Β°C, humidity, shady soil and oxygen) a rhabditiform larva develops inside the egg in about two weeks.
  • After one week this larva moults into a second-stage rhabditiform larvae inside the egg.
  • Eggs hatch in the intestine and the rhabditiform larvae penetrate the intestinal wall entering the circulation β†’ the right side of the heart β†’ the lungs where they break out of the pulmonary capillaries into the alveoli.
  • They remain for some days and undergo their second and third moult (Filariform larvae).
  • They then pass up the bronchioles to the bronchi, the trachea, and the epiglottis where they are swallowed to reach their final habitat in the small intestine.
  • They moult for the fourth time and become adults.
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8
Q

what is the mode of infection by Ascaris lumbricoides?

A
  1. Drinking water or eating raw vegetables contaminated with larvated egg.
  2. Through hands contaminated with dirt.
  3. Egg inhalation to nasopharynx.
  4. Egg carried by house flies and cockroaches.
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9
Q

what is responsible for the pathogenecity of Ascaris lumbricoides?

A

I- Migrating larvae
II- Adult worm

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10
Q

what is the clinical picture of affection by migrating larvae of ascaris lumbricoides (in lung)?

A
  • Ascaris pneumonitis or Loeffler’s syndrome: In heavy infection, especially in children.
  • Lobular pneumonitis, cellular infiltration, serous exudates and haemorrhage, cough, bronchial irritation, expectoration with bloodstained sputum and oedema of lips.
  • Microscopically, the larvae may be detected in the sputum, with many eosinophils.
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11
Q

what is the clinical picture of affection by migrating larvae of ascaris lumbricoides (in general circulation)?

A
  • some larvae reach the general circulation and distributed to various organs as lymph nodes, brain, spleen & kidneys leading to abnormal clinical manifestations as a result of visceral larva migrans.
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12
Q

what is the clinical picture of affection by adult worms of ascaris lumbricoides?

A
  1. Traumatic effects (In heavy infection)
  2. Toxic effects
  3. Nutritional impact
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13
Q

Traumatic effects of adult worms of ascaris lumbricoides

A
  • Intestinal obstruction.
  • Obstruction of the bile ducts by the worms β†’ obstructive jaundice.
  • Appendix β†’ appendicitis.
  • Obstruction of ampulla of Vater β†’ acute hemorrhagic pancreatitis.
  • Perforation of intestinal wall β†’ peritonitis.
  • Some worms may ascend via the stomach and esophagus to the nasopharynx, enter the larynx causing suffocation.
  • It may come out of mouth or nose or even go to Eustachian tube from the pharynx resulting in damage of the middle ear

(obstruction - come out through openings)

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14
Q

Toxic effects of adult worms of ascaris lumbricoides

A

Metabolic by-products of living or dead worms: fever, allergic manifestations and nervous irritability.

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15
Q

Nutritional impact of the adult worm of ascaris lumbricoides

A

Loss of appetite: malnutrition, impairment of growth, vitamin A and C deficiency.

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16
Q

How is ascaris lumbricoides diagnosed?

A

Clinical: manifestations of intestinal helminthic infections.

Laboratory:
- Detection of eggs in stool.
- Detection of migrating larvae in sputum or in gastric lavage contents.
- Detection of adults passing out with or without stool or in vomitus

Radiology: Barium meal shows cylindrical filling defect (string sign) as in figure

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17
Q

Treatment of ascaris lumbricoides

A

1- Levamizol hydrochloride (Ketrax) as a single oral dose.

2- Mebendazole

3- Flubendazole

4- Surgical treatment of complications e.g. Intestinal obstruction and Appendicitis

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18
Q

how is prevention & control of ascaris lumbricoides done?

A
  1. Mass treatment of infected persons
  2. Health education and cleanliness
  3. washing hands before meal
  4. Sanitary disposal of excreta
  5. Proper washing of green raw vegetables.
  6. Pure water supply
  7. Control of flies and other insects
  8. Stool should not be used as a fertilizer (chemicals or temperature 50Β°C)
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19
Q

what is the morphology of the adult of Enterobius vermicularis (Oxyuris, pinworm or seat-worm)?

A
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20
Q

what is the morphology of the egg of Enterobius vermicularis (Oxyuris, pinworm or seat-worm)?

A
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21
Q

what is the habitat of Enterobius vermicularis?

A

adult worm lives in the caecum, appendix and adjacent parts of small and large intestine.

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22
Q

what is the definitive host of Enterobius vermicularis?

A

man

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23
Q

what is the infective stage of Enterobius vermicularis?

A
  • Fully embryonated eggs containing fully developed larvae.
  • The gravid female migrates to the perianal and perineal area where they lay eggs.
  • The eggs are infectious several hours after deposition.
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24
Q

what is the mode of infection by Enterobius vermicularis?

A
  1. Ingestion of eggs through contaminated food and drink.
  2. Air-borne infection.
  3. Autoinfection: eggs are carried under finger nails to the mouth after scratching of perianal skin (anus to mouth infection).
  4. Retro-infection: eggs hatch on the perianal region and larvae migrate back through the anus to the rectum and caecum.
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25
Q

what is the pathogenesis (clinical picture) of Enterobius vermicularis?

A

Due to migration of the gravid female worm: perianal, perineal and vaginal irritation.

1) Local irritation and discomfort, with nocturnal itching.

2) Vaginitis and salpingitis. Granulomas are formed around eggs or worms.

3) Pruritis ani: due to nocturnal migration of the female worm on the perianal skin with worm like movement, skin sensitization by ruptured worms, striations on the cuticle cause skin irritation and sticky material on the egg causing irritation.

4) Obstructive appendicitis rarely occurs.

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26
Q

how is Enterobius vermicularis diagnosed?

A

1) Clinical: Pinworm infection

2) Laboratory: Detection of adult worms and/or eggs
β–ͺ In stool: (only 5%), when uterus of gravid female ruptures.
β–ͺ In urine of female patients.
β–ͺ On perianal region by swab: this must be done early in the morning before defecation or bathing and should be repeated for several days before the patient is considered free

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27
Q

what are the types of swabs used for diagnosis of Enterobius vermicularis?

A
  • Scotch adhesive tape swab
  • Vaseline swab
  • National Institute of Health (N.I.H.) swab
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28
Q

Scotch adhesive tape swab

A
  • a piece of scotch tape, hold over a tongue depressor is rolled over the perianal skin and removed.
  • The adhesive tape is put on a slide with a drop of toluene and examined for eggs.
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29
Q

Vaseline swab

A
  • the perianal skin is swabbed with a piece of cotton soaked in Vaseline and the swab is put in a mixture of ether and water to dissolve the vaseline.
  • The mixture is centrifuged and the deposit is examined for eggs.
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30
Q

National Institute of Health (N.I.H.) swab

A
  • it is a piece of non-adhesive cellophane fixed to a glass rod.
  • The glass rod is inserted through a perforated stopper in a test tube.
  • The perianal skin is swabbed in the morning by the cellophane paper.
  • The cellophane paper is united, spread between 2 slides with a drop of toluene and examined for eggs.
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31
Q

how is Enterobius vermicularis treated?

A

❖ Mebendazole (Vermox)

❖ Flubendazole (Fluvermol)

❖ Pyrantel pamoate (Combantrin) as a single oral dose and a 2nd dose must be given after 2 weeks to prevent re-infection.

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32
Q

pevention and control of Enterobius vermicularis

A

1) Mass treatment of the whole companions of the infected person.

2) Personal cleanliness.

3) Protection of food and drink from contamination by dust and hands of patients.

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33
Q

what is the morphology of Ancylostoma duodenal adult?

A
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34
Q

what is the morphology of Ancylostoma duodenal egg?

A
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35
Q

what is the habitat of Ancylostoma duodenale?

A

Small intestine (Jejunum)

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36
Q

what is the definitive host of Ancylostoma duodenale?

A

man

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37
Q

what is the infective stage of Ancylostoma duodenale?

A

sheathed filariform larvae

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38
Q

what are the life cycle stages of Ancylostoma duodenale?

A

Egg → rhabditiform larva→ infective filariform larva (IFL) → adult

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39
Q

Life cycle of Ancylostoma duodenale

A
  • Adults live in the small intestine of man attached by the mouth capsule to the mucosa. Immature eggs pass in the feces.
  • Under favorable environmental conditions in the soil (moist shaded areas, sandy or loose soil, alkaline and free of salinity, suitable temperature and sufficient oxygen), a rhabditiform larva develops and hatches in about 2 days.
  • It moults again after about 7 days (keeping its skin; ensheathed) to become an infective filariform larva.
  • Filariform larva penetrates human intact skin or mucous membrane of the mouth.
  • The filariform larva is attracted to man by histo-tropism and by warmth of the body (positive thermo-tropism).
  • It shows other tropisms to various factors, e.g. negative geotropism and positive hygro-tropism.
  • The larvae on reaching the blood are carried to the right side of the heart β†’ the lungs β†’ penetrate the capillaries into the alveoli β†’ pass up the tracheal tree, over the epiglottis β†’ swallowed to reach their final habitat in the small intestine.
  • During their migration in the lung they moult giving the adult stage in the small intestine.
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40
Q

compare between rhabditiform larva & Filariform larvae of Ancylostoma duodenale

A
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41
Q

what is the pathology (or clinical picture) of infection with Ancylostoma duodenale?

A

1- Ground itch: local dermatitis caused by FL penetration at the site of entry or contact with soil (feet, buttocks, hands).

2- Cutaneous larvae migrans: caused by FL migration in the skin. Appear as maculopapular rash and itching (Β± pustules due to 2ry infection).

3- Verminous pneumonia (Loffler’s syndrome): caused by FL migration in the lungs. It is presented by fever, cough, dyspnea, haemoptysis and oesinophilia (transient symptoms < 2 weeks).

4- GIT symptoms: colic, vomiting, diarrhea.

5- Chronic iron-deficiency anaemia (hypochromic, microcytic ) due to blood loss.

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42
Q

what are the mechanisms of anemia caused by Ancylostoma duodenale?

A

1.Tear by buccal capsule, curved teeth and cutting plates β†’ ulcer β†’ haemorrhage.
2. Anticoagulant secretion by cephalic glands continued bleeding after detachment.
3. Toxic bone marrow depression.
4. Enteritis (due to 2ry infection) decrease absorption of iron.

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43
Q

how is Ancylostoma duodenal diagnosed?

A

1) Clinical: the clinical picture.
2) Laboratory: finding the eggs in stool.

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44
Q

what is the treatment of Ancylostoma duodenale?

A

1) Mebendazole (Vermox) or Flubendazole.
2) Pyrantel pamoate (combantrin).
3) Supportive treatment: Iron, vitamins and high protein diet.

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45
Q

prevention & control of Ancylostoma duodenale

A
  • Mass treatment of the infected population.
  • Sanitary disposal of human faeces and not to use them as fertilizer.
  • Wearing shoes and gloves for people handling mud or working in mines, gardening, poultry and brick-making.
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46
Q

what is the geographical distribution of Strongyloides stercoralis (Dwarf Thread worm)?

A

Tropical and subtropical areas.

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47
Q

what is the morphology of the adult of Strongyloides stercoralis?

A
  • Parasitic female: 2.2 mm in length with cylindrical oesophagus
  • Male: 0.7 mm in length with ventrally-curved posterior end
  • Free-living female: 1.1 mm in length with rhabditiform oesophagus.
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48
Q

what is the morphology of the egg of Strongyloides stercoralis?

A
  • Seldom found in stool; sub-mucosa or in soil hatches after 2 hours.
  • Size: 55x30 ΞΌ
  • Shape: oval, very thin shell
  • Colour: translucent
  • Contents: mature rhabditiform larva.
49
Q

what is the morphology of the rhabditiform larvae of Strongyloides stercoralis?

A
  • 200 ΞΌ, non-sheathed with short buccal cavity
  • Mature in 2-3 days to filariform larvae.
50
Q

what is the morphology of the filariform larvae of Strongyloides stercoralis?

A
  • 500 ΞΌ, non-sheathed with cylindrical oesophagus (1/2 body length) and notched posterior end.
51
Q

what is the habitat of Strongyloides stercoralis?

A
  • Parasitic adults live in the small intestine (Females embedded in the mucosa, and males live in the lumen of the intestine).
  • Free living adults occur in the soil.
52
Q

what is the definitive host of Strongyloides stercoralis?

A

man

53
Q

what is the infective stage of Strongyloides stercoralis?

A

infective filariform larvae.

54
Q

what is the mode of infection by Strongyloides stercoralis?

A
  • Infective filariform larvae penetrating skin in contact with infected soil.

β€”β€”β€”β€”β€”β€”

  • Autoinfection occurs by the infective filariform larvae that develop in the patient intestine in constipation and intestinal disturbances
  1. Exogenous autoinfection: when infective filariform larvae develop outside the anus and penetrate the perianal skin.
  2. Endogenous autoinfection: infective larvae develop in large intestine and penetrate the mucosa of the intestine.
55
Q

what could auto-infection cause in immunosuppressed patients?

A

hyper-infection

56
Q

when could Strongyloides stercoralis be life-threatining?

A

β–ͺ Are taking corticosteroids (oral or intravenous)

β–ͺ Are infected with the human T-lymphotropic virus type 1 (HTLV-1)

β–ͺ Have hematologic malignancies such as leukemia or lymphoma

β–ͺ Are transplant recipients.

57
Q

Life cycle of Strongyloides stercoralis

A
58
Q

what is the pathogenecity & clinical picture of infection by Strongyloides stercoralis?

A

1- Skin lesions following larvae penetration resembling the ground itch.

2- Pneumonitis may be produced by migrating larvae (Lofflers syndrome)

3- The adult worms in the intestine may cause no symptoms or moderate to severe diarrhea (chronic intermittent painless diarrhea).

4- Malabsorption syndrome with steatorrhea can occur.

5- Hyper-infection may lead to severe debilitation or death and the larvae that are found in virtually all parts of the body may give rise to ectopic strongyloidiasis (in lung or kidney).

59
Q

when do symptoms related to Strongyloides stercoralis usually develop?

A
  • Most people do not know when their exposure occurred.
  • For those who do, a local rash can occur immediately.
  • The cough usually occurs several days later.
  • Abdominal symptoms typically occur approximately 2 weeks later, and larvae can be found in the stool about 3 to 4 weeks later.
60
Q

how is infection by Strongyloides stercoralis by Strongyloides stercoralis diagnosed?

A

Stool analysis
- Demonstration of rhabditiform larvae (or occasionally filariform) in freshly passed stool.
- Eggs may be seen in the stool rarely after purgation or in severe diarrhea.
- Stool culture (to see the larvae and adults).

Duodenal aspiration
- May be done in mild infection (the larvae passed in the stool are few), for detection of eggs and rhabditiform larva.

Blood picture
- May show eosinophilia of 10-40 %

Sputum and bronchoalveolar lavage examination
- Shows the larvae especially if the adults are present in lungs.

61
Q

how is Strongyloides stercoralis treated?

A
  1. Thiabendzole is the drug of choice.
  2. Mebendazole (vermox)

All therapy must be repeated 2 weeks later

62
Q

what is the geoghraphical distribution of Hymenolepis nana?

A

Cosmopolitan (commonest tapeworm in children).

63
Q

what is the morphology of Hymenolepis nana adult?

A
  • 0.5-5 cm (the smallest tapeworm of man).
  • Globular scolex with 4 suckers and a retractile rostellum with a crown of hooks.
  • Broad mature segments
  • Broader gravid segments full of eggs.
64
Q

what is the morphology of Hymenolepis nana egg?

A
  • Oval, 30X50 ΞΌ , colourless, and mature oncosphere, 2 layered shell with bipolar knobs and filaments
65
Q

what is the morphology of Hymenolepis nana cysticercoid?

A
  • A bladder-like structure, 0.5-1 mm in diameter, having double wall, invaginated everted scolex, and tail-like appendage.
66
Q

what is the habitat of Hymenolepis nana?

A

The small intestine.

67
Q

what is the definitive host of Hymenolepis nana?

A

Man

68
Q

what is the resevoir host of Hymenolepis nana?

A

Rodents (rats and mice).

69
Q

what is the intermediate host of Hymenolepis nana?

A

Man, may be insects like flea larva or grain beetles.

70
Q

what is the infective stage of Hymenolepis nana?

A

Mature eggs and cercocystic cysticercoid.

71
Q

what are the stages of Hymenolepis nana?

A
  • Eggs β†’onchosphereβ†’ cercocystic cysticercoid in (I.H.) β†’ adult in (D. H).
72
Q

what is the mode of infection by Hymenolepis nana?

A
  • Swallowing of infected insects or their larvae containing cysticercoid.
  • Contaminated food, water with eggs.
  • Autoinfection: by ingestion of mature eggs, either from person to person or by external autoinfection or internal autoinfection.
73
Q

Life cycle of Hymenolepis nana

A
74
Q

what is the pathogenecity & clinical picture of Hymenolepis nana?

A

β–ͺ In light infection, usually there are no manifestations.

β–ͺ In heavy infections: ulcerations of the mucosa lead to enteritis. There may be abdominal discomfort, colic and diarrhea with passage of mucus.

β–ͺ Some patients especially children suffer from dizziness and may be convulsion, attributed to neurotoxin product of the worms.

75
Q

how is Hymenolepis nana diagnosed?

A

Stool examination for the characteristic egg.

76
Q

treatment of Hymenolepis nana

A
  • Niclosamide: treatment is prolonged or repeated in 3 weeks to kill worms that emerge from cysticercoids in the submucosa.
  • Praziquantel: a single oral dose after breakfast. It acts on both cysticercoid in the villi and the adult in the lumen of small intestine.
  • All infected members of the family should be treated at the same time.
77
Q

compare between Hymenolepis nana and Hymenolepis diminuta

A
78
Q

what is the geographical distribution of intestinal fluke (heterophyes heterophys)?

A

Common in Egypt in Nile Delta, especially around the lakes of Manzala and Borollos, Turkey, and Far East (Japan, China, Korea, Philippine).

79
Q

what is the morphology of the adult of heterophyes heterophys?

A

βœ“ 3X 0.5 mm, pear shape with 3 suckers (oral, ventral and larger genital sucker).

βœ“ Two oval testes, opposite each other and rounded ovary in between.

80
Q

what is the morphology of the egg of heterophyes heterophys?

A

Size: 30xl5 ΞΌ.

Shape: Oval.

Color: golden yellow.

Shell: Thick with operculum at one pole and a small Knob at the other.

Contents: Full mature embryo (miracidium).

81
Q

what is the habitat of heterophyes heterophys?

A

Adult lives between the villi of the small intestine.

82
Q

what is the definitive host, reservoir host & intermediate host of heterophyes heterophys?

A

DH: Man

RH: Cat, dog, and any fish-eating animals.

IH:
- First is a snail, called Pirenella conica.
- Second is fish, Tilapia (Bolty) and Mugil (Boury).

83
Q

what is the infective stage of heterophyes heterophys?

A

Encysted metacercaria in the muscles of the fish (2nd I. H.).

84
Q

what are the stages of heterophyes heterophys?

A

Egg –> miracidium –> sporocyst –>1st and 2nd generation redialophocercus cercaria –> encysted metacercaria –> adult.

85
Q

what is the mode of infection by heterophyes heterophys?

A

By eating insufficient cooked, roasted or salted fish, staked less than ten days (sweet fesekh), containing the infective stage (encysted metacercariae).

86
Q

life cycle of heterophyes heterophys

A
  • In the small intestine the cyst wall is dissolved, the metacercariae embedded between the villi, maturate and the eggs appear in the stool 2-5 weeks after infection
  • Eggs pass with the stool, to reach to brackish waterβ†’ eggs are ingested by the snail (Pirenella conica) β†’ miracidium hatches into a sporocyst, that gives redia then cercariaβ†’ cercaria penetrates the fish muscle (Boury and Bolty) and becomes encysted metacercaria
87
Q

what is the clinical picture of infection with heterophyes heterophys?

A
  • Attachment to mucosal membranes causing inflammation
  • Abdominal colic and discomfort with chronic intermittent diarrhea.
  • The egg may reach the general circulation to different organs:
    βœ“ Parasitic granuloma and fibrosis. Migration of the eggs to the heart sometimes results in potentially fatal myocardial and valvular damage.
88
Q

how is heterophyes heterophys diagnosed?

A

Stool examination for the characteristic eggs.

89
Q

how is heterophyes heterophys treated?

A

βœ“ Praziquantel (Biltricid).
βœ“ Niclosamide (Yomesan).

90
Q

prevention & control of heterophyes heterophys

A
  • Sanitary disposal of feces.
  • Avoid eating raw, insufficient cooked fish or salted fish, salted less than 10 days (sweet fessekh), and proper grilling of fish.
  • Fried fish is safe as temperature needed for frying is high enough to kill metacercariae.
  • Periodic examination of fishermen stool for Heterophyes eggs.
  • Mass treatment of infected cases.
91
Q

geographical distribution of Entamoeba histolytica

A

Worldwide distribution especially in tropical areas and poor communities.

92
Q

what are the stages of Entamoeba histolytica?

A
  • Trophozoite (Vegetative or growing stage)
  • precyst
  • cyst
93
Q

morphology of trophozoite (Vegetative or growing stage) of Entamoeba histolytica

A
  • Size: 10-60 ΞΌ (average 20 ΞΌ).
  • Shape: Irregular outline with finger like pseudopodia.
  • Cytoplasm: containing nucleus, food vacuoles, erythrocytes (RBCs), occasionally bacteria, and tissue debris.
94
Q

morphology of cyst of Entamoeba histolytica

A
  • It is rounded, 10-15 ΞΌ in diameter.
  • Has smooth refractile cyst wall.
  • Immature cysts may be mono- or bi-nucleated.
  • Mature cysts contain 4 nuclei formed by mitotic division.
95
Q

what is the habitat of Entamoeba histolytica?

A

Trophozoite:
- Inhabits the wall and lumen of the large intestine, with extra-intestinal metastases (liver, lung and brain, etc.).

Cyst:
- Inhabits the lumen of the large intestine.

96
Q

what are the hosts of Entamoeba histolytica?

A

Definitive host: Man

Intermediate host: Non

Reservoir host: Dogs, rats and monkeys.

97
Q

what is the infective host (stage) of Entamoeba histolytica?

A

Mature quadrinucleated cyst.

98
Q

what is the mode of infection with Entamoeba histolytica?

A
  • Ingestion of mature quadrinucleated E. histolytica cysts in contaminated food or drink, or through infected food handlers.
  • Mechanical transmission By flies and cockroaches.
  • Autoinfection by Feco-oral route (hand to mouth contact)
99
Q

activities of Entamoeba histolytica in the GIT

A
  • On ingestion, the trophozoites disintegrate in the stomach, while only the mature cysts resist the stomach acidity and pass to the small intestine.
  • The cyst wall is digested By action of trypsin and excystation occurs in the proximal small intestine, where metacystic stage escapes and divides into 8 small amoebae.
  • These trophozoites move down to the ilio-caecal region, multiply by binary fission, and then pass to the lumen of colon, where they may remain, feeding on starch or mucus and pass in liquid stool, or may undergo encystation and cysts pass with formed stool.
  • Also, trophozoite may invade the wall of large intestine by their lytic secretion to invade the host tissues through blood vessels (extra-intestinal invasion).
100
Q

what is the pathogenesis of Entamoeba histolytica?

A

E. histolytica lectin: Attachment to the surface epithelium.

Cytolytic enzymes: Haemolysins and pore-forming enzymes (amoeba pore).

Flask-shaped or crater-like ulcer:
- Irregular, with undermined edge and necrotic base with yellow purulent membrane covering its base
- More common in the ileocecal region followed by the sigmoid-rectal region.

101
Q

what is the clinical picture of infection with Entamoeba histolytica?

A
  • Intestinal amoebiasis
  • Hepatic amoebiasis
  • Pulmonary amoebiasis
  • Amoebic brain abscess
  • Cutaneous amoebiasis
  • Genitourinary amoebiasis
102
Q

what are the types of intestinal amoebiasis?

A

asymptomatic and symptomatic

103
Q

incidence and characters of asymptomatic amoebiasis

A
  • These account for the majority of cases (80-90 %).
  • These patients are cyst passers, and they are called healthy carriers
104
Q

what are the types of symptomatic amoebiasis?

A
  • Acute intestinal amoebiasis (Amoebic dysentery)
  • Chronic amoebic colitis (non-dysenteric colitis)
105
Q

what are the manifestations of acute symptomatic amoebiasis?

A
  • There is severe dysentery (colic + tenesmus + frequency of defecation + blood + mucus and shreds of necrotic mucosa in stool) and abdominal tenderness.
  • The patient is usually afebrile and non-toxic.
106
Q

what are the manifestations of chronic symptomatic amoebiasis?

A
  • Chronic intermittent diarrhea.
  • Abdominal pain and distension (Uncomfortable belly or growling abdomen).
  • Weight loss and weakness.
107
Q

what are the the Complications of symptomatic intestinal amoebiasis?

A

Fulminant amoebic colitis
- The patient is febrile and toxic.

Amoeboma
- It is palpable, firm, painful, movable, chronic nodular lesion occurring mainly in the caecum, sigmoid colon or rectum.

Thick mega-colon and colonic stricture
- associated with obstructive symptoms.
- Appendicitis, intestinal perforation and peritonitis.

Haemorrhage
- Due to erosion of intestinal blood vessels.

Extra intestinal spread
- with manifestations related to the organ affected.

108
Q

what is Diffuse amoebic hepatitis?

A

It is a non-specific reaction of liver to the necrotic debris and toxic materials.

109
Q

what are the manifestations of Diffuse amoebic hepatitis?

A
  • The liver is enlarged and tender with pain in the right hypochondrium.
  • Temperature is usually elevated.
110
Q

what are the manifestations of Amoebic liver abscess?

A
  • The liver is enlarged and tender with pain in the right hypochondrium.
  • Elevation of the right diaphragm with severe pain referred to the right shoulder.
  • Fever, chills, toxemia, anorexia with leukocytosis.
  • Jaundice occurs with multiple lesions or affection of biliary tract.
  • The abscess may extend through the diaphragm to the lung, pericardium, peritoneal cavity or rupture through the abdominal wall.
111
Q

what are the symptoms of Pulmonary amoebiasis?

A

It is characterized by chest pain, cough, dyspnea, chills, fever and leukocytosis.

112
Q

what happens in case of Hepatobronchial fistula with hepatic amoebiasis?

A

Hepatobronchial fistula is usually associated with expectoration of chocolatebrown sputum.

113
Q

Amoebic brain abscess

A

It acts as a brain tumor (Space-occupying lesion).

114
Q

what causes Cutaneous amoebiasis?

A

It results from fistula formation (intestinal, hepatic, or perineal). Lesions can be highly destructive, simulating epithelioma.

115
Q

Genitourinary amoebiasis

A
  • In females, vulva, vagina or cervix can be affected by spread from perineum or fistula formation.
  • The destructive lesions resemble carcinoma
116
Q

diagnos of entamoeba histolytica

A

clinical & laboratory

117
Q

laboratory diagnosis of Entamoeba histolytica

A

Stool examination:
β–ͺ Macroscopy. Dysenteric stool (blood & Mucous).
β–ͺ Microscopy: For identification of cysts and or trophozoites
β–ͺ Stool culture: Using Robinson’s medium, It is a sensitive
method for diagnosing chronic and asymptomatic intestinal
amoebiasis.
β–ͺ Detection of amoebic copro-antigens: By enzyme-linked
immunosorbent assay (ELISA).

Sigmoidoscopic examination:
β–ͺ For detection of trophozoites and associated pathology.

Serodiagnosis β†’ Antibodies to E. histolytica can be detected by indirect hemagglutination (IHA) test, immunofluorescence assay (IFA) test, and ELISA in invasive intestinal amoebiasis.

118
Q

treatment of Entamoeba histolytica

A
  • Metronidazole (Flagyl).
  • Tinidazole (Fasigen).

Y2B1 - GIT πŸ“• (9 decks)

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