MODULE 2 UNIT 2 Flashcards

1
Q

It includes the amoebas, which have no permanent locomotory organs, but move about with the aid of temporary prolongations of the body called

A
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2
Q

It includes those protozoa which possess whip-like structures called

A
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3
Q

Two groups of amoebae are of medical importance.

A
  1. Parasitic amoebae; 2. Pathogenic free-living amebae
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4
Q

three genera of Parasitic amoebae

A

Entamoeba, Endolimax, and Iodamoeba

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5
Q

Parasitic amoebae include

A

Entamoeba histolytica, Entamoeba dispar, Entamoeba coli, Entamoeba hartmanni, Endolimax nana, and Iodamoeba butschlii which are all found in the intestinal lumen, and Entamoeba gingivalis which is found in the mouth

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6
Q

is the only pathogenic species which causes intestinal and extraintestinal amoebiasis.

A

E. histolytica

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7
Q

All the other amaebae species are commensals. They all exist in two forms in the life cycle, trophozoites and cysts, EXCEPT {?} which occurs in the trophozoite stage only

A

E. gingivalis

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8
Q

Several species of free-living amoebae are found in soil and water.

A

Pathogenic free-living amebae

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9
Q

are of clinical interest because they can cause fatal meningoencephalitis and eye infections.

A

(1) Naegleria and (2) Acanthamoeba

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10
Q

Trophozoite Size

A

10-60 µm (ave: 15-20 µm)

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11
Q

Trophozoite Motility and
Pseudopodia

A

Progressive, rapid, unidirectional motility; with hyaline, fingerlike pseudopodia formed rapidly

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12
Q

Trophozoite Nucleus
Number

A

1

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13
Q

Trophozoite Peripheral
chromatin

A

Fine granules, uniform in size and usually evenly distributed; may have beaded appearance

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14
Q

Trophozoite Karyosome

A

Small, compact, centrally located

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15
Q

Trophozoite Linin network

A

The space between the karyosome and the nuclear membrane is traversed by fine thread of linin network giving a radial spokeswheel or cartwheel appearance.

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16
Q

Trophozoite Cytoplasm
Appearance

A

Finely granular, “ground-glass” appearance; clear differentiation into a clear ectoplasm and more granular endoplasm; if present, vacuoles are usually very small

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17
Q

Trophozoite Inclusions

A

RBCs are diagnostic; few ingested bacteria or debris in vacuoles

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18
Q

Cyst Size

A

10-20 µm (12-15 µm)

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19
Q

Cyst Shape

A

Usually spherical

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20
Q

Cyst Nucleus
Number

A

1-4; mature cyst contains 4 nuclei

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21
Q

Cyst Peripheral chromatin

A

Similar to that seen in trophozoite

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22
Q

Cyst Karyosome

A

Similar to that seen in trophozoite

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23
Q

Cyst Cytoplasm
Chromatoidal bodies

A

May be present; usually elongate with blunt, rounded, smooth ends (cigarshaped); may be round or oval.

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24
Q

Cyst Glycogen vacuole

A

May be present, usually diffuse, stains reddish brown with iodine.

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25
Q

is morphologically indistinguishable from E. histolytica and should be reported as E. histolytica/E. dispar unless ingested red blood cells are seen, suggesting E. histolytica infection.

A

Entamoeba dispar

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26
Q

The DNA and ribosomal RNA , and isoenzyme pattern of (?) is different from that of E. histolytica.

A

E. dispar

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27
Q

Unlike E. histolytica, E. dispar is (?).

A

nonpathogenic.

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28
Q

The ratio of E. dispar to E. histolytica in most developing countries can be as high as (?) in a community setting.

A

10:1

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29
Q

The ratio of E. dispar to E. histolytica in most developing countries can be as high as (?) in a community setting.

A

10:1

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30
Q

E. histolytica passes its life cycle in one host and has the following successive stages:

A

cyst, metacyst, metacystic trophozoite, trophozoite, and precyst.

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31
Q

are passed in feces

A

Cysts and trophozoites

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32
Q

Infection with Entamoeba histolytica (and E.dispar) occurs via (?) from fecally contaminated
food, water, or hands.

A

ingestion of quadrinucleated mature cysts

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33
Q

(?) occurs in the cecum or lower part of the ileum, under the influence of neutral or slightly acidic digestive juices.

A

Excystation

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34
Q

A quadrinucleated (?) is liberated from the cyst wall. The nuclei in the metacyst immediately undergo division to form eight nuclei, each of which gets surrounded by its own cytoplasm. The cytoplasm divides into as may parts as there are nuclei.

A

metacyst

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35
Q

(?) are released, which migrate to the large intestine (cecum), their normal habitat.

A

Eight (8) metacystic trophozoites (or amoebulae)

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36
Q

t. In the glandular crypts, they feed and grow and develop into normal (?)

A

trophozoites

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37
Q

The trophozoite discharges undigested food and condenses into a spherical mass, called the (?)

A

precyst

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38
Q

There are 2 types of inclusions in unripe and ripening cysts:

A

chromatoidal bodies and glycogen mass

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39
Q

s. Ripening of cysts of E. histolytica consists of (?) consecutive mitotic divisions of the nucleus to produce (?) nuclei .

A

2; 4

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40
Q

During this process,(?) is expended and the chromatoidal bodies become less conspicuous or completely disappear

A

glycogen

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41
Q

(?) are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool.

A

Cysts

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42
Q

is used clinically to denote all conditions produced in human host by infection with E. histolytica at different areas of invasion.

A

Amoebiasis

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43
Q

E. hislolytica causes 2

A

(1) intestinal and (2) extraintestinal amoebiasis

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44
Q

Adapted by the WHO, intestinal amoebiasis is clinically classified into (a) asymptomatic, and (b) symptomatic infections.

A

Intestinal amoebiasis

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45
Q

intestinal amoebiasis is clinically classified into (?)

A

(a) asymptomatic, and (b) symptomatic infections.

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46
Q

The majority of infections with E. histolytica are

A

Asymptomatic infection

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47
Q

This occurs in approximately 90% of cases especially in endemic communities

A

Asymptomatic infection

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48
Q

There is NO evidence of tissue invasion.

A

Asymptomatic infection

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49
Q

Infected individual passes formed stool with cyst forms. But, there is concern that an infection with E. histolytica may become symptomatic in the intestinal tract or with subsequent extraintestinal invasion.

A

Asymptomatic infection

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50
Q

Only about 10% of amoebiasis are symptomatic

A

Symptomatic infection

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51
Q

(?) is defined as an intestinal infection caused by the presence of E. histolytica exhibiting symptoms occurs when the mucosa is invaded.

A

Amoebic colitis

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52
Q

(?) is defined as an intestinal infection caused by the presence of E. histolytica exhibiting symptoms occurs when the mucosa is invaded.

A

Amoebic colitis

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53
Q

(?) is characterized by gradual or sudden onset, dysentery with 6-10 or more bloodtinged, mucoid, foul-smelling stools per day.

A

Acute amoebic colitis or amoebic dysentery

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54
Q

(?) may resemble bacillary dysentery, but can be differentiated on clinical and laboratory grounds.

A

Amoebic dysentery

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55
Q

(?) does not always result in dysentery.

A

Intestinal amebiasis

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56
Q

(?) is uncommon (only if rectum is involved), low-grade fever or none at all, and mild leukocytosis.

A

Tenesmus

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57
Q

(?), aka nondysenteric amoebic colitis, is characterized by intermittent diarrhea and constipation. i.e., alternating diarrhea and constipation, or abdominal pain.

A

Chronic amoebic colitis

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58
Q

Cysts are found in formed stool while trophozoites are seen during times of diarrhea. This may last for years.

A

Chronic amoebic colitis

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59
Q

(?) got its name through its ability to lyze tissues, initiated by invasion of the colonic mucosa.

A

E. histolytica

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60
Q

There are three pathogenic processes, each of which is facilitated by the expression of virulence factor.

A

Cytoadherence; Cytolysis; Proteolysis

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61
Q

Trophozoite lectins, a group of proteins, bind to specific carbohydrate-containing receptors on host luminal surfaces and mediate adherence.

A

Cytoadherence

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62
Q

Amoebapores are proteins of amoeba capable of inserting into the host cell membrane and form pores causing lysis of the host cells. Trophozoites’ amoeboid movement also contributes to the lysis of mucosal cells.

A

Cytolysis.

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63
Q

Amoebapores are proteins of amoeba capable of inserting into the host cell membrane and form pores causing lysis of the host cells. Trophozoites’ amoeboid movement also contributes to the lysis of mucosal cells.

A

Cytolysis.

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64
Q

Cysteine proteinase enzymes are responsible for further tissue lysis

A

Proteolysis.

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65
Q

(?) by the trophozoites produces discrete ulcers with pinhead center and raised edges. Sometimes, the invasion remains superficial and heals spontaneously.

A

Mucosal penetration

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66
Q

More often, the trophozoites penetrate to submucosal layer and multiplies rapidly, and spread by lateral and downward extension producing a typical (?) in cross section, with mouth and neck being narrow and base large and rounded.

A

flask shaped (or tear drop-shaped) ulcer

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67
Q

The (?) are multiple and are confined to the colon, being most numerous in the cecum and next in the sigmoidorectal region.

A

ulcers

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68
Q

The ulcers generally do not extend deeper than submucosal layer.

A

Colonic perforation.

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69
Q

Occasionally, the ulcers may involve
the muscular and serous coats of the colon, causing perforation
and peritonitis. This occurs in about 60% of fulminant cases.
Blood vessel erosion may cause hemorrhage.

A

Colonic perforation.

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70
Q

Occasionally, a granulomatous mass may develop on the intestinal wall.

A

Amoeboma.

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71
Q

It is the result of cellular responses to a chronic ulcer and often still contains active trophozoites, usually in the cecum or rectosigmoid.

A

Amoeboma.

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72
Q

It produces wall thickening and or constriction of the lumen, the so-called “napkin ring” lesion and may obstruct the bowel.

A

Amoeboma.

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73
Q

This may be mistaken for colon cancer

A

Amoeboma.

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74
Q

Secondary amoebic infection occurs as a result of trophozoites entering portal circulation or by direct extension from the intestinal tissues and becoming lodged in the liver, and other extraintestinal organs such as the lungs, brain, spleen and cutaneous sites.

A

Extraintestinal amoebiasis

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75
Q

Hepatic involvement is the most common extraintestinal complication of amebiasis.

A

Hepatic amoebiasis

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76
Q

The dissemination from the primary site in the colon is primarily by the blood stream.

A

Hepatic amoebiasis

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77
Q

he trophozoites reach the liver through the portal vein.

A

Hepatic amoebiasis

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78
Q

At times, it may also occur through direct extension from the intestinal ulcer.

A

Hepatic amoebiasis

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79
Q

It covers both amoebic hepatitis and amoebic liver abscess (ALA).

A

Hepatic amoebiasis

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80
Q

In ALA, the trophozoites lyze liver cells and forms abscess filled with necrotic debris described as anchovy sauce or chocolate pus.

A

Hepatic amoebiasis

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81
Q

lt is bacteriologically sterile and free of amoeba.

A

Hepatic amoebiasis

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82
Q

At the periphery, there is almost normal liver tissue, which contains invading trophozoites.

A

Hepatic amoebiasis

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83
Q

(?) ranks next to liver abscess in rate of occurrence.

A

pulmonary amoebiasis

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84
Q

Primary amoebiasis of the lung occurs independently without the presence of hepatic involvement by (?) from the colon wall via the pulmonary circulation into the pulmonary arteries.

A

direct hematogenous spread

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85
Q

But most often it is secondary to hepatic abscess by direct extension through the diaphragm and therefore, the (?) is the usual area affected. The patient presents with pneumonia with
expectoration of anchovy sauce or chocolate sputum.

A

lower part of the right lung

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86
Q

Involvement of distant organs is by hematogenous spread and through lymphatics.

A

Metastatic amoebiasis

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87
Q

Abscesses in kidney, brain, spleen and adrenals have been noticed

A

Metastatic amoebiasis

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88
Q

Spread to brain leads to severe destruction of brain tissue and is fatal.

A

Metastatic amoebiasis

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89
Q

This is a result of damaged skin frequently brought in contact with trophozoites.

A

Cutaneous amoebiasis

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90
Q

It occurs commonly around the perineum or perianal region secondary to amoebic dysentery, also on the skin over the region adjoining the visceral lesion - as in hepatic abscess.

A

Cutaneous amoebiasis

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91
Q

The prepuce and glans are affected in penile amoebiasis which is acquired through anal intercourse.

A

Genitourinary amoebiasis

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92
Q

Similar lesions in females may occur on vulva, vagina, or cervix by spread from perineum.

A

Genitourinary amoebiasis

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93
Q

It is performed for diagnosis of intestinal amoebiasis.

A

Stool examination

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94
Q

It is not of value in the diagnosis of extraintestinal amoebiasis.

A

Stool examination

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95
Q

E. histolytica cyst can be detected in stool in less than 15% cases of amoebic hepatitis.

A

Stool examination

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96
Q

: This is a standard method for routine O & P exam. Trophozoites are primarily recovered from stools that are of soft, liquid, or loose consistency.

A

Direct fecal smear (DFS)

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97
Q

Formed stool specimens are more likely to contain cysts.

A

Direct fecal smear (DFS)

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98
Q

Saline mount of fresh unfixed stool demonstrates motile trophozoites, or cysts while iodine preparation primarily demonstrates the cysts only.

A

Direct fecal smear (DFS)

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99
Q

When patient is suspected of having intestinal amoebiasis, 6 specimens is recommended (however, is rarely requested) and collected on separate days within 14-day period: 3 specimens collected from normal bowel movement and 3 specimens collected after catharsis/purge.

A

Direct fecal smear (DFS)

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100
Q

Bacteria

A

Few, Numerous

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101
Q

Pus cells

A

Scanty, well-preserved; Numerous, degenerated

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102
Q

RBC

A

Often in rouleaux; Unaltered, scattered

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103
Q

Macrophage

A

NOT a feature; May be numerous (may have RBC)

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104
Q

Charcot-Leyden crystals

A

May be present; Absent

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105
Q

Trophozoite

A

Present; Absent

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106
Q

There are two types of concentration procedures:

A

flotation and sedimentation

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107
Q

Cysts may be seen and identified, but trophozoites are not likely to be seen. Therefore, this is recommended for isolation and identification of amoebae in non-diarrheic stool.

A

Stool concentration

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108
Q

It is considered the best practice in the diagnosis of protozoa because it allows examination and recognition of the detailed morphology of the trophozoites or cysts.

A

Permanent staining

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109
Q

It provides contrasting colors for the parasites and the background. The parasite is examined under high magnification by oil-immersion technique.

A

Permanent staining

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110
Q

The parasite is examined under high magnification by (?) technique.

A

oil-immersion

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111
Q

Blue-green, sometimes light pink or with a tinge of purple; Slightly more purple

A

TRICHROME

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112
Q

Blue-gray; Blue-gray

A

IRON HEMATOXYLIN

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113
Q

Red, sometimes with a tinge of purple

A

TRICHROME

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114
Q

Darker than cytoplasm, bluegray to black

A

IRON HEMATOXYLIN

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115
Q

Green, provides nice contrast with the protozoa

A

TRICHROME

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116
Q

Lighter shade of blue-gray

A

IRON HEMATOXYLIN

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117
Q

Scraping obtained by sigmoidoscopy is often contributory.

A

Examination of sigmoidoscopy specimen

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118
Q

Examination method includes a direct wet mount and permanent staining.

A

Examination of tissue aspirates/biopsy

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119
Q

Liver abscess material, may be processed and examined in the same manner. Microscopic examination of pus aspirated from liver abscess may demonstrate trophozoite of E. histolytica in less than 20% cases.

A

Examination of tissue aspirates/biopsy

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120
Q

In case of liver abscess, when diagnostic aspiration is done, the pus obtained from the center of the abscess may not contain amoeba as they are confined to the periphery.

A

Examination of tissue aspirates/biopsy

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121
Q

The fluid draining after a day or two is more likely to contain the trophozoite. Aspirates from the margins of the abscess would also show the trophozoites.

A

Examination of tissue aspirates/biopsy

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122
Q

Cysts are never seen in extraintestinal lesions. Trophozoite of E. histolytica may be demonstrated in liver biopsy specimen, in case of hepatic amoebiasis or amoebic hepatitis.

A

Examination of tissue aspirates/biopsy

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123
Q

It is a more sensitive method in diagnosing chronic and asymptomatic intestinal amoebiasis.

A

Stool Culture

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124
Q

(?) yields higher positivity for E. histolytica as compared to direct examination.

A

Culture of stools

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125
Q

Media used for polyxenic culture include:

A
  • Boeck and Drbohlav’s biphasic medium - NIH polygenic medium - Craig’s medium - Nelson’s medium - Robinson’s medium - Balamuth’s medium.
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126
Q

Medium for axenic culture:

A
  • Diamond’s medium
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127
Q

Amebic antibodies appear in serum only in late stages of intestinal amebiasis.

A

Antibody detection

128
Q

Test for antibodies in serum help in the diagnosis of mainly extraintestinal infections.

A

ELISA-based assay

129
Q

In reference diagnostic laboratories, molecular analysis by conventional PCR-based assays or real-time PCR is the method of choice for discriminating between E. histolytica and E. dispar

A

Molecular diagnosis

130
Q

X-ray, ultrasonography (USG), computed tomography (CT) scan, or magnetic resonance imaging (MRI) of liver may be found useful in detection of amebic liver abscess.

A

Molecular diagnosis

131
Q

X-ray, ultrasonography (USG), computed tomography (CT) scan, or magnetic resonance imaging (MRI) of liver may be found useful in detection of amebic liver abscess.

A

Radiologic examination

132
Q

Cosmopolitan. Although clinical amoebiasis is more prevalent in the tropics and subtropics than in the temperate zone.

A

Geographical distribution

133
Q

Approximately 1 to 5% worldwide. About 5% in the Philippines, but the true prevalence in not determined yet with the recent redescription of E. histolytica and E. dispar.

A

Prevalence

134
Q

Human is the major reservoir. Dogs, pigs, and monkeys are also implicated.

A

Reservoir

135
Q

Transmission

A

Fecal-oral route.

136
Q

(?) contaminated with feces containing cysts are the most common source of infection.

A

Food and drinks

137
Q

This is associated to poor sanitation particularly from open defecation or night soil practice, or careless plumbing in which sanitary drains were connected to freshwater pipes.

A

Polluted soil/water

138
Q

Transmission of (?) by water is common when people depends on untreated wells, springs, streams, or storage tanks; or by soil when vegetables and fruits are eaten raw and not thoroughly washed.

A

E. histolytica

139
Q

(?) may remain viable in water for 9-30 days and
are not killed by chlorination in strengths used for bacterial
decontamination of public water supply. However, they can be
killed in drinking water by hyperchlorination or by addition of iodine, or by boiling (thermal death point at 50-55 oC).

A

Cysts of E. histolytica

140
Q

In moist soil conditions, they can survive for upto for

A

8 days at 28 to 34°C
40 days at 2 to 6°C
60 days at 0°C

141
Q

Unclean handling of food by infected individuals who are cyst passers or cyst carriers appears to be a very common method.

A

Infected food handlers

142
Q

There are contact carriers - so-called (?) who have never suffered from amoebic dysentery and whose health remains to be unimpaired, and the convalescent carriers who have recovered from a clinical attack of acute amoebic dysentery.

A

“healthy” carriers

143
Q

These serve as mechanical vectors of E. histolytica from feces, then depositing infective cysts on unprotected food. Viable cysts and trophozoites may be recovered from the vomitus or excreta. Cysts remain viable in their excreta for as long as 48 hours after the insect has fed on contaminated feces.

A

Flies, cockroaches, and other insects

144
Q

Ingestion of cyst occurs through hand-tomouth contamination which especially occurs among children and institutionalized individuals (in mental hospitals, prisons, orphanage, daycare).

A

Poor personal hygiene

145
Q

This is related to sexual practices that foster transmission and ingestion of cyst.

A

Sexual transmission

146
Q

Oral-anal contact is a common practice among homosexual men (men who have sex with men, MSM).

A

Sexual transmission

147
Q

It can also occur during oral-genital sex after anal intercourse.

A

Sexual transmission

148
Q

(?) was a medical term first used by Henry L Kazal and colleagues in 1976 to describe a complex of gastrointestinal symptoms associated with sexually transmitted GIT diseases, which had many gay patients.

A

Gay bowel syndrome

149
Q

Accurate identification of commensal amoebae is crucial for the following reasons:

A
  1. They may be confused with Entamoeba histolytica in diagnostic investigations. These amoebae do not cause a disease, therefore treatment is not necessary. 2. Although nonpathogenic, they should still be reported when identified in stool specimens since their presence is an indication of ingestion of fecally contaminated food or water.
150
Q

The three genera of amoeba can be distinguished from each other by the structure of nucleus.

A

Small compact karyosome; Large irregular karyosome; Large circular karyosome

151
Q

(?) central or eccentrically located; nuclear membrane lined with peripheral chromatin.

A

Small compact karyosome

152
Q

(?) attached to the nuclear membrane by fibrils radiating to the periphery; no peripheral chromatin.

A

Large irregular karyosome

153
Q

(?) surrounded by refractile achromatic granules called periendosomes; no peripheral chromatin.

A

Large circular karyosome

154
Q

5-12 µm (ave. 8-10 µm)

A

Entamoeba hartmanni

155
Q

10-50 µm (ave. 20-25 µm)

A

Entamoeba coli

156
Q

5-20 µm (ave. 10-15 µm)

A

Entamoeba gingivalis

157
Q

6-15 µm (ave. 8-10 µm)

A

Endolimax nana

158
Q

6-20 µm (ave.12-15 µm)

A

odamoeba butschlii

159
Q

Less progressive motility; with hyaline, fingerlike pseudopodia formed rapidly

A

Entamoeba hartmanni

160
Q

Nonprogressive, sluggish, nondirectional motility; with blunt, usually granular pseudopodia formed slowly

A

Entamoeba coli

161
Q

Moderately active, progressive; with multiple pseudopodia , vary from long, and lobose to short and blunt, often formed rapidly

A

Entamoeba gingivalis

162
Q

Sluggish, moderately progressive; with blunt, hyaline pseudopodia formed slowly

A

Endolimax nana

163
Q

Sluggish, slightly progressive; with blunt or fingerlike, hyaline pseudopodia formed slowly

A

Iodamoeba butschlii

164
Q

Fine granules, uniform in size and usually evenly distributed; may have beaded appearance

A

Entamoeba hartmanni

165
Q

Usually clumped and unevenly arranged on the membrane; may also appear as solid, dark ring with no beads or clumps

A

Entamoeba coli

166
Q

Fine granules, closely packed

A

Entamoeba gingivalis

167
Q

NONE

A

Endolimax nana

168
Q
A

Iodamoeba butschlii

169
Q

Small, compact, centrally located, may be eccentric

A

Entamoeba hartmanni

170
Q

Moderately large, not compact, usually eccentrically located

A

Entamoeba coli

171
Q

Small, welldefined, usually centrally located

A

Entamoeba gingivalis

172
Q

Large, irregularlyshaped,centrally or eccentrically located; may appear “blotlike”; many nuclear variations are common

A

Endolimax nana

173
Q

Large, usually central, surrounded by refractile achromatic granules that are difficult to see

A

Iodamoeba butschlii

174
Q

Finely granular, “ground-glass” appearance; clear differentiation into a clear ectoplasm and more granular endoplasm; if present, vacuoles are usually very small

A

Entamoeba hartmanni

175
Q

Granular, with little differentiation between ectoplasm and endoplasm; with few to numerous vacuoles

A

Entamoeba coli

176
Q

Finely granular, vacuolated

A

Entamoeba gingivalis

177
Q

Granular, vacuolated

A

Endolimax nana

178
Q

Coarsely granular, heavily vacuolated

A

odamoeba butschlii

179
Q

Bacteria and debris; NO RBC

A

Entamoeba hartmanni

180
Q

Bacteria, yeasts and other food materials in vacuoles

A

Entamoeba coli

181
Q

Epithelial cells and leukocytes

A

Entamoeba gingivalis

182
Q

Bacteria and debris

A

Endolimax nana

183
Q

Bacteria and debris

A

Iodamoeba butschlii

184
Q

5-10 µm (ave. 6-8 µm)

A

Entamoeba hartmanni

185
Q

10-35 µm (ave. 15-25 µm)

A

Entamoeba coli

186
Q

NO CYST STAGE

A

Entamoeba gingivalis

187
Q

5-10 µm (ave. 6-8 µm)

A

Endolimax nana

188
Q

5-20 µm (ave. 10-12 µm)

A

Iodamoeba butschlii

189
Q

10-35 µm (ave. 15-25 µm)

A

Entamoeba hartmanni

190
Q

Usually spherical; may be oval, triangular or other shapes

A

Entamoeba coli

191
Q

NO CYST STAGE

A

Entamoeba gingivalis

192
Q

Usually oval, may be spherical or ellipsoidal

A

Endolimax nana

193
Q

May vary from oval to round; cyst may collapse because of large glycogen vacuole space

A

Iodamoeba butschlii

194
Q

Nucleus: 1 to 4

A

Entamoeba hartmanni

195
Q

Nucleus: 1 to 8

A

Entamoeba coli

196
Q

NO CYST STAGE

A

Entamoeba gingivalis

197
Q

Nucleus: 1 to 4

A

Endolimax nana

198
Q

Nucleus: 1

A

Iodamoeba butschlii

199
Q

Peripheral chromatin and Karyosome: Similar to that seen in trophozoite; Similar to that seen in trophozoite

A

Entamoeba hartmanni, Entamoeba coli

200
Q

NO CYST STAGE

A

Entamoeba gingivalis

201
Q

Peripheral chromatin: None

A

Endolimax nana, Iodamoeba butschlii

202
Q

Karyosome: Smaller than karyosome seen in trophozoite, but generally larger than those of the genus Entamoeba

A

Endolimax nana

203
Q

Karyosome: Larger, usually eccentric refractile achromatic granules may be on one side of the karyosome- “basket nucleus”

A

Iodamoeba butschlii

204
Q

Chromatoidal bodies: May be present; usually elongate with blunt, rounded, smooth ends (cigarshaped); may be round or oval

A

Entamoeba hartmanni

205
Q

Chromatoidal bodies: May be present (less frequently than in E. histolytica); splinter-shaped with rough, pointed ends

A

Entamoeba coli

206
Q

Chromatoidal bodies: NO CYST STAGE

A

Entamoeba gingivalis

207
Q

Chromatoidal bodies: Rarely present; occasionally, small spherical or elongated granules or inclusions seen

A

Endolimax nana

208
Q

Chromatoidal bodies: NO chromatoidal bodies present; small granules occasionally present

A

Iodamoeba butschlii

209
Q

Glycogen vacuole: May be present, usually diffuse, stains reddish brown with iodine

A

Entamoeba hartmanni, Entamoeba coli

210
Q

Glycogen vacuole: NO CYST STAGE

A

Entamoeba gingivalis

211
Q

Glycogen vacuole: Usually absent, diffuse, illdefined, brownish

A

Endolimax nana

212
Q

Glycogen vacuole: Large, compact, well-defined mass, stains dark brown with iodine

A

Iodamoeba butschlii

213
Q

was at one time designated as “small race” E. histolytica because of the many similarities between the two

A

Entamoeba hartmanni

214
Q

differentiated from e. histolytica by its smaller size

A

Entamoeba hartmanni

215
Q

Life cycle, epidemiology, and laboratory diagnosis of the intestinal commensal amoebae are similar to that of

A

E. histolytica

216
Q

In single stool examinations of over 30,000 Filipinos, the prevalence of Entamoeba coli was

A

21%

217
Q

In single stool examinations of over 30,000 Filipinos, the prevalence of Endolimax nana

A

9%

218
Q

In single stool examinations of over 30,000 Filipinos, the prevalence of Iodamoeba butschlii

A

1%

219
Q

s lives on the surface of gum and teeth, in gum pockets, and sometimes in the tonsillar crypts

A

Entamoeba gingivalis

220
Q

They are abundant in cases of oral disease.

A

Entamoeba gingivalis

221
Q

Transmission is most probably direct: through kissing, droplet spray, or by sharing utensils.

A

Entamoeba gingivalis

222
Q

may best be made by examining mouth scrapings, particularly from the gingival area

A

Entamoeba gingivalis trophozoites

223
Q

-Elongated with tapered end measuring 7-20 µm

A

Naegleria fowleri Trophozoite

224
Q

-Lobose pseudopodia (lobopodia) are clear initially but fill with granular cytoplasm

A

Naegleria fowleri Trophozoite

225
Q

-Prominent nucleus and dense central karyosome

A

Naegleria fowleri Trophozoite

226
Q

-Finely granular cytoplasm contains a conspicuous clear Nuclear halo and numerous vacuoles (including contractile vacuoles)

A

Naegleria fowleri Trophozoite

227
Q

-Spherical, 8-12 µm in diameter

A

Naegleria fowleri Cyst

228
Q

-Smooth, single-layered wall is pierced by one or two flat, mucus-plugged pores

A

Naegleria fowleri Cyst

229
Q

-Finely granular cytoplasm -Nucleus with a central karyosome

A

Naegleria fowleri Cyst

230
Q

-Pear-shaped

A

Naegleria fowleri Flagellate

231
Q

-Single nucleus

A

Naegleria fowleri Flagellate

232
Q

-Biflagellated

A

Naegleria fowleri Flagellate

233
Q

In their free-living state, trophozoites are found in bodies of warm freshwater, such as lakes, ponds, river, hot springs fresh warm water with temperatures from near 25°C up to 46°C (optimally at 42°C) and also in soil.

A

Naegleria fowleri

234
Q

The trophozoites feed on bacteria.

A

Naegleria fowleri

235
Q

The trophozoites replicate by binary division during which the nuclear membrane remains intact (a process called promitosis).

A

Naegleria fowleri

236
Q

When trophozoites are exposed to a change in ionic concentration, they can turn into temporary non-feeding flagellated forms within a few minutes which usually revert back to the trophozoite stage.

A

Naegleria fowleri

237
Q

Trophozoites encyst due to unfavorable conditions such as food deprivation, crowding, desiccation, accumulation of waste products, and cold temperatures.

A

Naegleria fowleri

238
Q

Trophozoites infect humans or animals by penetrating the nasal tissue during waterrelated activities often in warm or hot freshwater (lakes, rivers, and hot springs) and migrating to the brain via the olfactory nerves causing primary amebic meningoencephalitis (PAM).

A

Naegleria fowleri

239
Q

In tissues, trophozoites phagocytize red blood cells and white blood cells and destroy tissue.

A

Naegleria fowleri

240
Q

PRIMARY AMOEBIC MENINGOENCEPHALITIS (PAM)

A

Naegleria fowleri

241
Q

a rare, rapidly fatal disease with sudden onset (IP 1-7 d) of headache, fever, stiff neck, lethargy, and coma in otherwise healthy people. .

A

PRIMARY AMOEBIC MENINGOENCEPHALITIS (PAM)

242
Q

After the start of symptoms, the disease progresses rapidly and usually causes death within 1 to 12 days.

A

PRIMARY AMOEBIC MENINGOENCEPHALITIS (PAM)

243
Q

Motile trophozoites are demonstrated in wet mounts of fresh sample of CSF or brain tissue specimen.

A

Naegleria fowleri

244
Q

The amebae can also be stained with a variety of stains, such as Giemsa-Wright or a modified trichrome stain, for identification.

A

Naegleria fowleri

245
Q

can be grown on non-nutrient agar plates coated with bacteria.

A

Naegleria fowleri

246
Q

Escherichia coli can be used to overlay the non-nutrient agar plate and a drop of CSF sediment added to it.

A

Naegleria fowleri

247
Q

Plates are then incubated at 37°C and checked daily for clearing of the agar in thin tracks, which indicate that the trophozoites have fed on the bacteria.

A

Naegleria fowleri

248
Q

The plate is microscopically inspected and cysts are identified by their morphology.

A

Naegleria fowleri

249
Q

Confirmation of Naegleria presence can be done by a so-called (?), where the organism is exposed to a hypotonic environment (distilled water).

A

FLAGELLATION TEST

250
Q

in contrast to other amoebae, differentiates within two hours into the flagellar state

A

Naegleria fowleri

251
Q

Pathogenicity can be further confirmed by exposure to high temperature (42°C)

A

Naegleria fowleri

252
Q

is able to grow at this temperature

A

Naegleria fowleri

253
Q

non-pathogenic; not able to grow at this temperature

A

Naegleria gruberi

254
Q

A specific antibody to N. fowleri can be used in conjunction with another antibody that deposits a chemical (?) or glows under specific types of light (?) to directly stain the amebic antigens in tissue.

A

immunohistochemistry [IHC]
indirect immunofluorescence [IIF]

255
Q

Specific molecular tools can amplify DNA from the amebae in CSF or tissue to specifically identify if the amebae are present.

A

Polymerase Chain Reaction (PCR) of Naegleria fowleri

256
Q

Geographical distribution of Naegleria fowleri

A

Cosmopolitan

257
Q

Naegleria fowleribameba can be found in:

A
  • Bodies of warm freshwater, like lakes and river
  • Geothermal (naturally hot) water, like hot springs, and drinking water sources (from water going up the nose)
  • Warm water discharge from industrial plants
  • Also in the soil
258
Q

Humans become infected when water containing the agent enters the nose, usually while swimming.

A

N. fowleri

259
Q

Some factors that might increase risk of Naegleria infection include:

A

Freshwater swimming
Heat waves
Age

260
Q

Most people who become ill have been swimming in a freshwater lake or in swimming pools that are poorly maintained, minimally-chlorinated, and/or un-chlorinated.

A

Freshwater swimming.

261
Q

Causing water temperatures to rise which is favorable for the growth and survival of N. fowleri.

A

Heat waves

262
Q

Children and young adults are the most likely age groups to be affected, possibly because they’re likely to stay in the water longer and are more active in the water.

A

Age

263
Q

Infection has also happened when people use contaminated drinking water to cleanse their nasal passages during religious practices, use a neti pot or other device to rinse their sinuses through the nose, or get the contaminated water up their nose during recreational play.

A

Naegleria fowleri

264
Q

15-45 um

A

Acanthamoeba Trophozoites

265
Q

Spine-like pseudopodia (acanthapodia) – sluggish polydirectional motility

A

Acanthamoeba Trophozoites

266
Q

A single nucleus with a large, dense central nucleolus surrounded by a nuclear clear zone

A

Acanthamoeba Trophozoites

267
Q

Finely granular cytoplasm, as a rule, contractile vacuoles are usually visible in the cytoplasm

A

Acanthamoeba Trophozoites

268
Q

10-25 um

A

Acanthamoeba Cysts

269
Q

Double-walled cysts are generally polygonal, spherical, or star-shaped
- smooth inner wall of the cyst
- wrinkled outer wall at a number of points, forming

A

Acanthamoeba Cysts

270
Q

Nucleus containing a large dense central nucleolus surrounded by a clear nuclear halo

A

Acanthamoeba Cysts

271
Q

have been found in fresh, brackish, and sea water and in the soil.

A

Acanthamoeba

272
Q

has only two stages, cysts and trophozoites , in its life cycle

A

Acanthamoeba

273
Q

The trophozoites replicate by mitosis (nuclear membrane does not remain intact)

A
274
Q

The trophozoites are the infective forms Entry can occur through the eye , the nasal passages to the lower respiratory tract , or ulcerated or broken skin

A

Acanthamoeba

275
Q

When they enters the eye it can cause severe keratitis in otherwise healthy individuals, particularly contact lens users

A

Acanthamoeba

276
Q

When it enters the respiratory system or through the skin, it can invade the central nervous system by hematogenous dissemination causing granulomatous amebic encephalitis (GAE) or disseminated disease , or skin lesions `in individuals with compromised immune systems.

A

Acanthamoeba

277
Q

Its cysts and trophozoites are found in tissue.

A

Acanthamoeba

278
Q

is a rare disease that can affect anyone, but is most common in individuals who wear contact lenses.

A

Acanthamoeba keratitis

279
Q

Symptoms include corneal ulcerations, progressive corneal infiltration and clouding, iritis, scleritis, severe pain, loss of vision.

A

Acanthamoeba keratitis

280
Q

Disseminated infection typically shows up as inflammation of the lungs or sinuses, and/or skin infections but has the potential to spread to the brain.

A

Granulomatous Amebic Encephalitis (GAE)

281
Q

Skin infections caused by Acanthamoeba can appear as reddish nodules, skin ulcers, or abscesses in the skin.

A

Granulomatous Amebic Encephalitis (GAE)

282
Q

Disseminated infection can occur both with and without

A

Granulomatous Amebic Encephalitis (GAE)

283
Q

Granulomatous Amebic Encephalitis (GAE) Symptoms of GAE include:

A
  • Mental status changes
  • Loss of coordination
  • Fever
  • Muscular weakness or partial paralysis affecting one side of the body
  • Double vision
  • Sensitivity to light
  • Other neurologic problems
284
Q

The infection is usually diagnosed by an eye specialist based on symptoms, growth of the amoeba from a scraping of the eye, and/or seeing the amoeba by a process called confocal microscopy.

A

Acanthamoeba keratitis

285
Q

are more difficult to diagnose and are often at advanced stages when they are diagnosed

A

Granulomatous Amebic Encephalitis (GAE) and disseminated infection

286
Q

Tests useful in the diagnosis of GAE include

A

brain scans, biopsies, or spinal taps for detection of trophozoites and/or cysts

287
Q

In disseminated disease, (?) can be useful in diagnosis.

A

biopsy of the involved sites (e.g. , skin, sinuses)

288
Q

For people who wear contact lenses, certain practices can increase the risk of getting Acanthamoeba keratitis:

A

-Storing and handling lenses improperly -Disinfecting lenses improperly (such as using tap water or topping off solutions when cleaning the lenses or lens case) -Swimming, using a hot tub, or showering while wearing lenses
-Coming into contact with contaminated water
-Having a history of trauma to the cornea

289
Q

are very rare forms of Acanthamoeba infection and primarily affect people with compromised immune systems

A

Granulomatous Amebic Encephalitis (GAE) and disseminated infection

290
Q

While unusual, disseminated infection can also affect

A

healthy children and adults

291
Q

Conditions that may increase a patient’s risk for GAE and disseminated infection include:

A

-AIDS
-Organ/Tissue transplant
-Steroids or excessive use of antibiotics
-Diabetes Mellitus
-Cancer
-Disorders in which white blood cells in the lymphatic tissue are overproduced or abnormal
-Disorders in which blood cells or blood clotting mechanisms do not function properly or are abnormal
-Liver cirrhosis
-Lupus

292
Q

has been placed within an informal group, the stramenopiles

A

Blastocystis hominis

293
Q

are defined, based on molecular phylogenies, as a heterogeneous evolutionary assemblage of unicellular and multicellular protists including brown algae, diatoms, chrysophytes, water molds, slime nets, etc

A

Stramenopiles

294
Q

Cavalier-Smith (1998) considers stramenopiles to be identical to infrakingdom (?) under the kingdom (?).

A

Heterokonta
Chromista

295
Q

according to Cavalier-Smith, B. hominis is a

A

heterokontid chromista

296
Q

It was originally described as yeasts, fungi, or ameboid, flagellated, or sporozoan protozoa.

A

B. hominis

297
Q

-Varies greatly in size, with diameters ranging between 2µm and 200µm

A

Blastocystis hominis Vacuolar (or central body) form

298
Q

-Has a large central vacuole surrounded by a thin band of peripheral cytoplasm which contains other organelles

A

Blastocystis hominis Vacuolar (or central body) form

299
Q

-Gives rise to multi-vacuolar (multiple fission) forms

A

Blastocystis hominis Vacuolar (or central body) form

300
Q

Somewhat morphologically similar to the vacuolar forms except that distinct granules are observed in the central vacuole and / or cytoplasm

A

Blastocystis hominis Granular form

301
Q

-Amoeba-like

A

Blastocystis hominis

302
Q

-Exhibit active extension and retraction of pseudopodia

A

Blastocystis hominis Amoeboid form

303
Q

-Mostly oval or circular, or polymorphic

A

Blastocystis hominis Cyst

304
Q

-Varies in size from 6-40 µm

A

Blastocystis hominis Cyst form

305
Q

-Thick-walled cysts are believed to be responsible for external transmission; thin-walled cysts might cause reinfection within the host’s intestinal tract

A

Blastocystis hominis Cyst form

306
Q

is not yet understood, including the infectious stage and whether (and which of the) various morphologic forms of this polymorphic organism that have been identified in stool or culture constitute distinct biologic stages of the parasite in the intestinal tract of hosts

A

Blastocystis

307
Q

The cyst form is postulated to be an infectious stage, but not confirmed.

A

Blastocystis

308
Q

The predominant form found in human stool specimens is referred to as the vacuolar (or central body) form.

A

Blastocystis

309
Q

Replication appears to occur via binary fission.

A

Blastocystis

310
Q

Other morphologic forms (e.g., ameboid and granular forms) also have been noted in stool samples and/or culture; their biological role and eventual developmental fate require further investigation.

A

Blastocystis

311
Q

may be with or without symptoms

A

Blastocystosis

312
Q

Symptoms include watery or loose stools, diarrhea, abdominal pain, anal itching, weight loss, constipation, and excess gas.

A

Blastocystosis

313
Q

Detection of B. hominis in

A

stool

314
Q

Geographical distribution of B. hominis

A

Cosmopolitan

315
Q

B. hominis Prevalence:
(?) in developed countries; upto (?) in developing countries

A

5-10%
50%

316
Q

Possibly by the fecal-oral route through ingestion of contaminated water or food.

A

B. hominis

317
Q

harbor Blastocystis species similar to those found in humans.

A

Farm animals, birds, rodents, reptiles, amphibians, fish, and cockroaches