[Discussion] MODULE 1 UNIT 3 Flashcards

1
Q

often cause anemia

A

trypanosomiasis and malaria

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2
Q

can result in bowel obstruction

A

Ascariasis

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3
Q

can cause diarrhea

A

amoebiasis

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4
Q

balance between host and parasite is tipped in favor of the parasite

A

disease

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5
Q

balance shifts in favor of the hosts ability to inhibit the parasite, the it will be damaged and eliminated

A

parasite

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6
Q
  • refers to the number of parasites in or on the host- determines the likelihood of the parasitic disease.
A

Parasite Load

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7
Q
  • the greater the number of parasite infective stages that enter the host, the greater will be the pathological damage.
A

Parasite Load

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8
Q
  • However, a few parasites that have reproductive phase within the host can also have a considerable effect on the host.
A

Parasite Load

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9
Q
  • reflects the ability of a given parasite to infect a specific organ or sets of organs
A

Tissue tropism

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10
Q
  • after entering the host, the parasite migrates to these parts of the body where conditions are suitable for temporary or permanent residence.
A

Tissue tropism

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11
Q

infecting all or most organs

A

tropic

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12
Q

to a given tissue or even to certain tissue niches

A

restricted

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13
Q

Human African trypanosomiasis (HAT) agents

A

T. brucei rhodesiense and T. brucei gambiense

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14
Q

parasite remains in the peripheral blood and lymphatic system

A

First stage of Human African trypanosomiasis (HAT)

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15
Q

parasite crossing into the cerebrospinal fluid and ultimately into the brain parenchyma

A

Second stage of Human African trypanosomiasis (HAT)

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16
Q

refers to the manner of development of a disease

A

PATHOGENESIS

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17
Q

robs the host of essential nutrients and substances

A

Infection

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18
Q

Depleting or denying the host of these leads to (?) and in the process causing damage to surrounding tissues.

A

malnutrition

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19
Q
  • Effects of Malnutrition
A

stunted growth, wasting, hunger, or more specific signs of micronutrient deficiency.

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20
Q

is more likely to occur in individuals with larger burdens of parasites

A

Malnutrition

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21
Q

attach to the intestinal mucosa by means of teeth or cutting plates.

A

Hookworms

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22
Q

Aside from the bleeding at the site of attachment, these parasites ingest human blood, which results in irondeficiency anemia.

A

Hookworms

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23
Q

prevents absorption of nutrients due to it covering the intestinal mucosa

A

Giardia lamblia

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24
Q

Physical trauma, or destruction of cells, tissues or organs brought about by parasite attachment, feeding, blockage, or migration by is common in parasite infections.

A

Traumatic or mechanical damage

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25
Q

Enzymes elaborated by many parasites do not only make it possible for them to digest available food in the immediate environment and to transform this nutrient into their own protoplasm but also to degrade tissues or cells to promote invasion and spread of parasites.

A

Lytic necrosis

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26
Q

vigorous inflammatory response

shares some features with other infectious diseases,

unique aspects of pathophysiology

exacerbate the impact of systemic inflammation on individual organs

A

Malaria

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27
Q

normal secretions and excretions of parasites and the products liberated from dead parasites accumulate in the host tissues

A

Toxic and allergic phenomena

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28
Q

Parasites provoke tissue reaction that consists of cellular proliferation and infiltration at the site of the parasite and may involve increase in certain types of cells – lymphocytes, neutrophils, and macrophages.

A

Stimulation of host’s tissue reaction

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29
Q

consists of a cellular reaction to the presence of parasite which is eventually surrounded by epitheloid cells and multinucleated giant cells and as it dies off

A

Stimulation of host’s tissue reaction

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30
Q

is deposited within the cell

A

calcium

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31
Q

may block fluid flow and lead to necrosis of the surrounding tissues

A

calcium

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32
Q

A parasite may open pathways in the skin or gastrointestinal tract for the entry of other pathogens in the tissues.

A

Secondary invasion

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33
Q

In one documented case, a 3-yr old was found to have a co-infection of Ascaris lumbricoides as well as Vibrio cholerae

A

Secondary invasion

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34
Q

is a distinctive host response to parasitic infections - especially in helminth infections.

A

Eosinophilia

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35
Q

elevated serum IgE leve

A

Eosinophilia

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36
Q

Eosinophils and IgE play a critical role in

A

antibody-dependent cellular cytotoxicity (ADCC)

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37
Q

particularly important mechanism against parasites

A

antibody-dependent cellular cytotoxicity (ADCC)

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38
Q

This immunity with parasitic infections differ significantly from that in viral and bacterial infections.

A

Acquired immunity

39
Q

is much less efficient and not absolute

A

Immunological protection against parasitic infections

40
Q

more antigenically complex

A

Parasite host defense

41
Q

factors contributing to Parasite HD

A

• Large size.
• More complex structure.
• Metabolic diversity.
• Complicated life cycle.
• Have evolved to be closely adapted to the host.

42
Q

This immunity, either complete or partial, may be maintained only while the parasites are present.

A

premunition (or concomitant immunity)

43
Q

parasites inhabit body sites that are inaccessible to immune response.

A

Seclusion

44
Q

parasites persist in the lumen of the GIT, oral cavity, or urinary tract

A

Seclusion

45
Q

Some parasites can avoid exposing themselves to immune response by becoming

A

intracellular

46
Q

inhabit erythrocytes and are able to avoid the effect of antibodies.

A

Plasmodium spp.

47
Q

Unless the integrity of the (?) is breached by injury or inflammation this barrier protects lumen-dwelling parasites, many of which are surrounded by a protective tegument, or (?), from most of the effective humoral and cellular immune mechanisms of the host allowing survival and the opportunity to reproduce.

A

intestinal mucosa
cuticle

48
Q

Those that parasitize (?) possess mechanisms to avoid destruction.

A

macrophages

49
Q

proliferate in macrophages in various organs because they are able to inhibit the fusion of lysosomes with the parasite-containing phagosome.

A

Amastigotes of Trypanosoma cruzi and Leishmania spp.

50
Q

To avoid forces of immune response

A

Antigenic variation

51
Q

It may occur with developmental changes in parasite.

A

Antigenic variation

52
Q

It may occur with developmental changes in parasite.

A

Antigenic variation

53
Q

Even more intriguing is the ability of some parasites to vary the antigenic characteristics of a

A

single developmental stage

54
Q

A number of parasites are able to coat themselves with host molecules. In this way, they are able to hide their own antigenic surface from the immune system.

A

Antigenic disguise

55
Q
  • Resemblance between parasite antigen and host antigen
A

Molecular mimicry

56
Q

Some parasites have the genetic information to synthesize antigens identical to those of its host.

A

Molecular mimicry

57
Q

The larval stage of (?) in the hydatid cyst has been found to carry P blood group antigen

A

Echinococcus granulosus

58
Q

can acquire antigenic molecules from the host.

A

tegument of Schistosoma spp. adult

59
Q

Parasites produce substances that are transported to their tegument that mimic substances naturally found within the host.

A

Molecular mimicry

60
Q

In this case the antigenic determinants of the parasite are so closely related chemically to host (?)components that the immunological cells cannot distinguish between the two and an immune response cannot be raised.

A

“self”

61
Q

Parasites liberate antigenic surface components and, later, regenerating them.

A

Antigen shedding

62
Q

The antigens shed are able to combine with and neutralize antibodies before they reach the target parasite.

A

Antigen shedding

63
Q

Parasites can reduce the immune function by destruction of immunologic mediators.

A

Immunosuppression

64
Q

this means that the host shows depressed immune responses to antigens in general, including those of the infecting pathogen.

A

Immunosuppression

65
Q

produce anticomplementary chemicals

A

Tapeworm larvae

66
Q

splits the Fc component of attached antibodies, rendering it incapable of activating complement

A

Trypanosoma cruzi

67
Q

There are three complement pathways:

A

classic, alternative, and lectin

68
Q

To avoid lysis, (?) relies on molecules which block the initial steps of classic/lectin or alternative pathways, and CRIT, T-DAF, CRP, and host-derived microvesicles that disrupt or block C3 convertase assembly.

A

T. cruzi

69
Q

responsible for African sleeping sickness

induce polyclonal B-cell activation leading to the production of nonspecific immunoglobulins

eventual exhaustion of the antibody-producing capacity of the host

A

Trypanosoma brucei species

70
Q

can absorb vitamin B12

A

Diphyllobothrium latum

71
Q

concave on its ventral surface = suction

A

Giardia lamblia

72
Q

cysteine proteinases (digest cellular materials and the mucosa of the large intestine) = ulcers and abscessed pockets

A
73
Q

Host can resist the large symptoms if few in number

A

Entamoeba histolytica

74
Q

found to carry P blood group antigen

A

Echinococcus granulosus

75
Q

Lysis of the red blood cells in malaria

A

Plasmodium spp

76
Q

inhabit erythrocytes and are able to avoid the effect of antibodies

A

Plasmodium spp

77
Q

pass through several discrete developmental stages, each with its own particular

A

Plasmodium spp

78
Q

can acquire antigenic molecules from the host

A

Schistosoma spp

79
Q

may immunologically hide from the host by masking themselves with host blood group antigens and immunoglobulins

A

adult schistosomes

80
Q

may cause urinary bladder cancer

A

Schistosoma haematobium

81
Q

the migrating larvae may carry viruses and gram-negative bacteria from the intestines to the blood and tissues

A

strongyloidiasis, trichinosis, and
ascariasis

82
Q

Bolus = intestinal/bowel obstruction

A
83
Q

Amoebiasis

A
84
Q

migrate and enter the appendix, ciliary and pancreatic ducts, or the common bile duct, perforate the intestinal wall, or may penetrate the parenchyma of the liver and even the lungs

A

Ascaris lumbricoides

85
Q

responsible for African sleeping sickness

A

Trypanosoma brucei species

86
Q

induce polyclonal B-cell activation leading to the production of nonspecific immunoglobulins

A
87
Q

exhaustion of the antibody-producing capacity of the host

A

Trypanosoma brucei species

88
Q

have the capacity to express more than 100 different surface glycoproteins

A

Trypanosoma brucei species

89
Q

splits the Fc component of attached antibodies, rendering it incapable of activating complement

A

Trypanosoma cruzi

90
Q

proliferate in macrophages in various organs

A

Trypanosoma cruzi and Leishmania spp

91
Q

able to inhibit the fusion of lysosomes with the parasite-containing phagosome

A

Trypanosoma cruzi and Leishmania spp

92
Q

produce anti-complementary chemicals

A

Tapeworm larvae

93
Q

attach to the intestinal mucosa by means of teeth or cutting plates

A

Hookworms

94
Q

iron-deficiency anemia

A

Hookworms