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Parasitology [LEC] > Pathophysiology of Parasitic Infections > Flashcards

Pathophysiology of Parasitic Infections Flashcards

1
Q

seeks to explain the functional changes that are occurring within an individual due to a disease or pathologic state. The effects caused by parasitic diseases may be so subtle as to be unrecognizable, or they may be strikingly obvious

A

Pathophysiology

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2
Q

When the balance between host and parasite is tipped in favor of the parasite , a (?) results

A

disease

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3
Q

On the other hand, if the balance shifts in favor of the hosts ability to inhibit the parasite, the (?) will be damaged and eliminated

A

parasite

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4
Q

(?) refers to the ability of an infectious agent to gain entry to the host’s tissues and bring about a physiological or anatomical change, resulting in altered health and leading to disease.

A

Pathogenicity

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5
Q

The factors that contribute to parasite pathogenicity include:

A

parasite load, tissue tropism, and pathogenesis

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6
Q

The (?) (also referred to as worm burden among the helminths) refers to the number of parasites in or on the host.

A

parasite

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7
Q

This determines the likelihood of the parasitic disease.

A

parasite load

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8
Q

Usually, the greater the number of (?) that enter the host, the greater will be the pathological damage.

A

parasite infective stages

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9
Q

However, a few parasites that have (?) within the host can also have a considerable effect on the host

A

reproductive phase

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10
Q

reflects the ability of a given parasite to infect a specific organ or sets of organs

A

Tissue tropism

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11
Q

After entering the host, the parasite migrates to these parts of the body where conditions are suitable for (?).

A

temporary or permanent residence

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12
Q

Some pathogens are broadly (?), infecting all or most organs, while others are restricted to a giventissue or even to
certain tissue niches.

A

tropic

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13
Q

refers to the manner of development of a disease.

A

Pathogenesis

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14
Q

The pathogenic mechanisms of parasites are many and varied, but for the sake of convenience they can be discussed under the headings of:

A

a. Spoliative action
b. Traumatic or mechanical damage
c. Lytic necrosis
d. Toxic and allergic phenomena
e. Stimulation of host’s tissue reaction
f. Secondary invasion

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15
Q

(?) with parasites robs the host of essential nutrients and substances.

A

Infection

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16
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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17
Q

Malnutrition is more likely to occur in individuals with large burdens of parasites. The effects include

A

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

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18
Q

Some parasites compete with the host by (?), others by (?), a variety of nutrients from the host.

A

absorbing
ingesting

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19
Q

The tapeworm (?) can absorb vitamin B12 from the contents of the host’s gut against a concentration gradient.

A

Diphyllobothrium latum

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20
Q

Since (?) is necessary for erythrocyte production and maturation, its deficiency may result in megaloblastic anemia.

A

vitamin B12

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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, hookworms ingest human blood, which results in

A

iron-deficiency anemia.

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23
Q

In other instances, parasites could contribute to malnutrition by

A

decreasing host nutrient intake, increasing nutrient excretion, and/ or decreasing nutrient utilization

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24
Q

The tiny protozoan (?) robs its host in a different way.

A

Giardia lamblia

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25
Q

It is concave on its ventral surface and applies this suction cup to the surface of an intestinal epithelial cell.

A

Giardia lamblia

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26
Q

When many of these parasites are present, they cover so much intestinal absorptive surface that they interfere with the host’s absorption of nutrients. The unused nutrients then pass uselessly through the intestine and are wasted

A

Giardia lamblia

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27
Q

A scanning electron micrograph of the surface of the small intestine of a gerbil infested with Giardia sp. protozoa. The (?) is almost entirely obscured by the attached Giardia trophozoites.

A

intestinal epithelial surface

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28
Q

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

A

Physical trauma

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29
Q

The attachment of hookworms into the host intestinal mucosa by their teeth or cutting plates results into traumatic destruction of the (?) and bleeding at the site of attachment.

A

villi

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30
Q

Large numbers of Ascaris lumbricoides worms form tangled mass called (?) that can lead to intestinal obstruction.

A

bolus

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31
Q

It is also known to 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

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32
Q

Another pathogenic mechanism is by interference with the vital processes of the host through

A

parasitic enzymes.

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33
Q

Enzymes elaborated by many parasites do not only make it possible for them to (?) in the immediate environment and to transform this nutrient into their own protoplasm but also to (?) to promote invasion and spread of parasites.

A

digest available food
degrade tissues or cells

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34
Q

The dysentery amoeba, (?), trophozoites that secrete cysteine proteinases which do digest cellular materials and the mucosa of the large intestine, forming ulcers and abscessed pockets that can cause severe disease.

A

Entamoeba histolytica

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35
Q

typical flaskshaped ulcer

A

intestinal amebiasis

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36
Q

The normal secretions and excretions of parasites and the products liberated from dead parasites accumulate in the host tissues and become toxic to the host, behave like foreign proteins and give rise to various

A

allergic manifestations

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37
Q

Lysis of the red blood cells parasitized by Plasmodium spp. in malaria unleashes large amounts of waste products and cell debris into the blood, to which the host responds with a sharp rise in (?)

A

TNF and other pro-inflammatory cytokines

38
Q

(?) and consequent eruption of TNF accounts for the periodicity of the typical paroxysms of chills and fever in malaria

A

Synchrony of red cell lysis

39
Q

Some manifestations of the immune response are responsible for much of the pathogeneses hosts suffer. Parasites provoke tissue reaction that consists of (?) at the site of the parasite and may involve increase in certain types of cells — (?)

A

cellular proliferation and infiltration

lymphocytes, neutrophils, and macrophages.

40
Q

When (?) are unable to destroy the parasites, since most are too large to be engulfed, one of the end products of an immune response is the formation of (?).

A

neutrophils and macrophages

granuloma

41
Q

This basically 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, calcium is deposited within the cell.

A

Granuloma

42
Q

the physical presence of such structure may block fluid flow and lead to necrosis of the surrounding tissues

A

granuloma

43
Q

A few parasitic infection have been shown to lead to (?).

A

malignancy

44
Q

The liver fluke, (?), may induce bile duct carcinoma

A

Clonorchis sinensis

45
Q

(?) may cause urinary bladder cancer

A

Schistosoma haematobium

46
Q

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

A

Secondary invasion

47
Q

In some helminthic infections, the migrating larvae may carry viruses and gram-negative bacteria from the intestines to the blood and tissues, as in

A

strongyloidiasis, trichinosis, and ascariasis.

48
Q

pathogenic parasites are endowed with special properties that enable them to cause disease if given the right opportunity. Because of the possibility of recovery after a parasitic disease, there is no doubt that a host has protective mechanisms against the parasites.

A

Host Defense

49
Q

two types of host defense:

A

innate and adaptive

50
Q

parasites are well adapted to resisting

A

host innate defenses

51
Q

are critical in attempts by the host to control such infections.

A

Adaptive responses

52
Q

Distinctive host responses to parasitic infections, especially in helminth infections, are (?) - an increase in the number of eosinophils in the blood or tissues, and elevated serum IgE level.

A

eosinophilia

53
Q

Their primary function is considered to be defense against organisms that are too large to be phagocytosed, particularly parasitic helminths.

A

eosinophils

54
Q

Eosinophils and IgE play a critical role in what is known as (?), a particularly important mechanism against parasites.

A

antibody-dependent cellular cytotoxicity (ADCC)

55
Q

bind to the surface antigens of the parasite and eosinophils attach to the Fc portion of the IgE triggering eosinophil degranulation.

A

IgE antibodies

56
Q

The toxic products of the (?) can either kill, damage, or dislodge the parasite as a protective host mechanism.

A

released eosinophil granules

57
Q

(?) with parasitic infections differ significantly from that in viral and bacterial infections.

A

Acquired immunity

58
Q

(?) against parasitic infections is much less efficient and not absolute. It is apparent from the chronic course and recurrences of parasitic infections.

A

Immunological protection

59
Q

(?) provide their human host an intense antigenic challenge because they are more antigenically complex than bacteria or viruses

A

Parasites

60
Q

Several factors may contribute to this:

A

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

61
Q

This immunity, either complete or partial, may be maintained only while the parasites are present—the phenomenon is known as (?) (or concomitant immunity).

A

premunition

62
Q

The parasites remain alive, but its reproduction and other activities are restrained by the (?).

A

host response

63
Q

Once the parasitic infection is completely eliminated, the host becomes again (?) to reinfection.

A

susceptible

64
Q

Parasites could not survive in their hosts if they could not evade the host defenses mounted by immune responses. As noted earlier, parasites have evolved in relation their host. Consequently, they have developed numerous ways to overcome the host’s defense mechanisms.

A

Parasite Immune Evasion Mechanism

65
Q

Many parasites inhabit body sites that are inaccessible to immune response.

A

Seclusion

66
Q

Some parasites persist in the (?) of the gastrointestinal tract, oral cavity, or urinary tract.

A

lumen

67
Q

Unless the integrity of the intestinal mucosa 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

cuticle

68
Q

Some parasites can avoid exposing themselves to immune response by becoming (?).

A

intracellular

69
Q

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

A

Plasmodium spp.

70
Q

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

A

macrophages

71
Q

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

A

Amastigotes of Trypanosoma cruzi and Leishmania spp.

72
Q

One way parasites can avoid forces of immune response is by periodically changing antigens of their surface coat, i.e., to undergo

A

antigenic variation

73
Q

It may occur with developmental changes in parasite.

A

antigenic variation

74
Q

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

A

Plasmodium spp.

75
Q

Immune responses directed at an early developmental stage may be totally (?) against a later stage of the same parasite.

A

ineffective

76
Q

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

A

single developmental stage.

77
Q

have the capacity to express more than 100 different surface glycoproteins. By the time the host has mounted a response against each new antigen, the parasite antigen has changed again.

A

Trypanosoma brucei

78
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

79
Q

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

A

adult schistosomes

80
Q

Resemblance between parasite antigen and host antigen is referred to as

A

molecular mimicry

81
Q

Some parasites have the (?) to synthesize antigens identical to those of its host.

A

genetic information

82
Q

Parasites produce substances that are transported to their (?) that mimic substances naturally found within the host.

A

tegument

83
Q

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

A

host “self” components

84
Q

The larval stage of (?) in the hydatid cyst has been found to carry P blood group antigen, and the tegument of Schistosoma spp. adult can acquire antigenic molecules from the host.

A

Echinococcus granulosus

85
Q

Parasites liberate antigenic surface components and, later, regenerating them. The antigens shed are able to combine with and (?) before they reach the target parasite.

A

neutralize antibodies

86
Q

Parasites can reduce the immune function by destruction of immunologic mediators. This means that the host shows depressed immune responses to antigens in general, including those of the infecting pathogen.

A

Immunosuppression

87
Q

Tapeworm larvae produce

A

anticomplementary chemicals

88
Q

(?) splits the Fc component of attached antibodies, rendering it incapable of activating complement.

A

Trypanosoma cruzi

89
Q

Several protozoa, most notably (?) that are responsible for African sleeping sickness, induce polyclonal B-cell activation leading to the production of nonspecific immunoglobulins and eventual exhaustion of the antibody-producing capacity of the host.

A

Trypanosoma brucei species

90
Q

often cause anemia.

A

trypanosomiasis and malaria

91
Q

can result in bowel obstruction

A

Ascariasis

92
Q

can cause diarrhea.

A

amoebiasis

Parasitology [LEC] (23 decks)

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