Helminths: Pathogenesis and Defenses Flashcards
(70 cards)
1
Q
transmission of infection
A
- accidental ingestion of eggs or larvae
- larvae penetrate skin
- requires intermediate host vector
2
Q
helminths that infect through ingestion
A
- Ascaris
- Echinococcus
- Enterobius
- Trichuris
- Hookworms (larvae)
3
Q
helminths that infect through skin penetration
A
- Hookworms
- Schistosomes
- Strongyloides
4
Q
helminths that infect via intermediate host vector
A
- Filarial worms via arthorpod vectors
- Clonorchis in fish
- tapeworms in meat and fish
- Trichinella in meat
5
Q
Entry of pathogenic helminths
A
- mouth
- bite of insect vector
- penetration
6
Q
entry via mouth
A
eggs or larvae in water, food, or intermediate host
7
Q
entry via bite of insect vector
A
larvae enter skin
8
Q
entry via penetration
A
larvae burrow through skin
9
Q
localization of pathogenic helminths
A
- internal organs
- intestine
- dermal and lymphatic tissues
- blood vessels
10
Q
internal organs
A
- liver
- lungs
- CNS
11
Q
blood vessels
A
around intestine or bladder
12
Q
major factor influencing susceptibility to infection
A
human behavior
13
Q
where is the level of infection directly related to
A
number of infective stages encountered
14
Q
does every exposure result in the development of a mature infection?
A
no
15
Q
what kills infective organisms
A
host’s nonspecific defense mechanism
16
Q
what does the number of worms present represent
A
dynamic balance between:
- rate of infection
- efficiency of defense
17
Q
how do individuals differ in their ability to resist infection
A
genetically
18
Q
what may affect susceptibility
A
changes in diet
19
Q
immunosuppressive therapies
A
- irradiation
- immunosuppressant drugs
20
Q
what offsets the ability of hosts to control infection
A
ability of parasites to avoid host’s defenses and increase their survival
21
Q
worms athat are unaffected by the host’s attempts to limit or destroy them due to them being large and mobile
A
- Ascaris
- hookworms
- hydatid cysts
- Trichuris
- tapeworms
22
Q
where do pathogenic consequences relate to
A
- size
- movement
- longevity of parasites
- host’s exposure to long-term damage and immune stimulation
- sheer physical consequences of being inhabited by large foreign bodies
23
Q
different types of damage
A
- direct damage from worm activity and large helminths
- indirect damage from host response
24
Q
direct damage
A
- blockage of internal organs
- pressure exerted by growing parasites
25
helminths that can physically block the intestine
large Ascaris or tapeworms
26
may also block the bile duct
migrating Ascaris
27
may block blood flow through the liver
granulomas that form around schistosome eggs
28
blockage of lymph flow
adult Wuchereria in lymphatics
29
characteristic of larval tapeworm infections where the parasite grows as a large fluid-filled cyst in the liver, brain, lungs, or body cavity
pressure atrophy
30
hydatid cysts
larva of Echinococcus granulosus
31
caused by Echinococcus granulosus metastasizing within organs and causing necrosis
multilocular hydatid cysts
32
larvae that frequently deveop in the CNS and eyes
Taenia solium
33
actively suck blood from mucosal capillaries
hookworms (Ancylostoma, Necator)
34
can cause vitamin b12 deficiency
Diphyllobothrium latum
35
organs that are most affected by extensive migrations of helminths through body tissues
1. skin
2. lungs
3. liver
4. intestines
36
some of the signs and symptoms produced during migratory phases of helminths
1. petechial hemorrhages
2. pneumonitis
3. eosinophilia
4. urticaria and pruritus
5. organomegaly
6. granulomatous lesions
37
how do cysts cause damage
by mechanical pressure
38
indirect damage from host response
1. hypersensitivity-based inflammatory changes
2. immune-mediated inflammatory changes
3. inflammatory changes become irreversible, producing functional changes in tissues
39
ex. of hypersensitivity-based inflammatory changes
1. Schistosoma infection
2. granulomatous responses to eggs cause physical obstruction to blood flow which leads to liver pathology
3. lymphatic blockage
40
immune-mediated inflammatory chagnes
1. occur in skin, lungs, liver, intestine, CNA, and eyes as worms migrate
2. systemic changes
41
systemic changes
1. eosinophilia
2. edema
3. joint pain
42
example of sturctural change where the small intestine's lining, particularly the finger-like projections called villi, are flattened or damaged
Villous atrophy
43
Indirect damage caused by immunopathologic responses to, for example, Schistosoma
1. adult schistosomes in blood vessels around small intestine
2. eggs laid by female are carried in blood vessels and trapped in liver
3. hypersensitivity to antigens of larva inside egg cause formation of granuloma
4. liver sinusoids become blocked, impending blood flow
5. fibrosis of liver
44
effects of fibrosis of liver
1. raised portal pressure
2. perihepatic shunting of blood
3. hepatomegaly
4. splenomegaly
5. formation of varices
45
inflammatory changes that become irreversible
1. hyperplasia of bile ducts in long-term liver fluke infections
2. extensive fibrosis associated with chronic shistosomiasis
3. skin atrphy associated with onchocerciasis
46
defenses against infection: nonspecific resistance
1. acid stomach
2. environmental conditions of bowel (intestinal microbiota and immune system)
3. penetration into intestinal wall may trigger inflammatory responses
4. worms entering through skin must survive skin secretions, penetrate epidermal layers, and avoid inflammatory trapping in dermis
47
results as the worms become the focus of inflammatory reactions that form trails in the skin
1. dermatitis
2. creeping eruption
48
once in tissues, what do worms need to mature
correct sequence of environmental signals
49
what do absent or incompelte signals constitute
nonspecific resistance that may partially or completely prevent further development
50
may result in pathology from the continuing inflammatory response
prolonged survival
51
defenses against infection: specific acquired immunity
1. antibodies that bind to surface antigens
2. macrophages and eosinophils
3. antibodies block enzymes released by worms
4. inflammatory changes may concentrate effector cells aournd worms
5. encapsulation of trapped worms
52
what do antibodies that bind to surface antigens do
complement- or cell-mediated effectors that can damage worm
53
prime cytotoxic effector cells
1. macrophages
2. eosinophils
54
important immunoglobulins
1. IgM
2. IgG
3. IgE
55
what do antibodies that block enzymes released by the worm interfere
its ability to penetrate tisseus or to feed
56
may disable and kill theworm
release of cellular mediators
57
example of cellular mediators
1. interleukins
2. interferons
58
inflammatory cells that encapsulate worms
1. granulocytes
2. macrophages
3. fibroblasts
59
host defenses: antigen-presenting cells
1. B lymphocytes
2. T-null lymphocytes
3. myeloid cells
60
B lymphocytes
antibody
61
T-null lymphocytes
cytotoxicity
62
myeloid cells
inflammation
63
parasitic escape from antibodies
1. antigenic variation
2. masked antigens
3. shared host antigens
64
parasitic escape from cytotoxicity
1. immunosuppression
2. blocking antibody
3. diversion of immunity
65
parasitic escape from inflammation
1. anti-inflammatory mechanisms
66
how do some worms such as schistosomes avoid host defenses
1. disguise their outer surface by acquiring host molecules which reduce their antigenecity
2. intrinsic membrane changes
67
how do filarial nematode avoid host defenses
acquire serum albumin on their cuticle, acts as disguise
68
effect of substances released by many worms that help avoid host defenses
1. depress lymphocyte function
2. inactivate macrophages
3. digest antibodies
69
how do larval cestodes appear to prolong their survival
produce anticomplement factors which protect their outer layers from lytic attack
70
ways helminths avoid host defenses
1. antigen overload
2. antigenic competition
3. induction of supressor cells
4. production of lymphocyte-specific supressor factors
