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Immunology, infection and inflammation > Parasite infection > Flashcards

Parasite infection Flashcards

1
Q

what is a parasite

A

an organism which lives in or on another organism (its host) and benefits by deriving nutrient sat the others expense

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2
Q

what is an obligate parasite

A

is totally dependent on the host to complete its life cycle

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3
Q

what is a facultative parasite

A

an organism that may resort to parasitic activity, but does not absolutely rely on any host for completion of its life cycle

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4
Q

what are the two main groups of endoparasites

A

Protozoa/ Microparasites

Helminths/ Macroparasite/ Parasitic worms

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5
Q

what are endoparasites

A

all those that live inside the host

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6
Q

what are protozoa/ microparasites

A

Tend to rely on a third organism, which is generally known as the carrier or vector for either transmission or for a maturation set in their life cycle, where the latter this is an intermediate host
(single celled)

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7
Q

what are the infectious species, and primary and secondary carriers that causes sleeping sickness (african trypanosomiasis)

A

Protozoa: Trypanosoma brucei (T.brucei)
Secondary Host: Man; Cattle ; Horses
Primary/ Carrier: Tsetse fly (Glossina )

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8
Q

what are helminths/ macroparasites

A

parasites that inhabit spaces in the hosts body and do not multiply within their definitive host

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9
Q

give three examples of helminths

A

tapeworms (Cestodes)
flukes (Trematodes)
roundworms (Nematodes)

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10
Q

what are ectoparasites

A

Parasites that live on the skin outside of the host either on the skin or the outgrowths of the skin

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11
Q

give examples of ectoparasites

A
  • Lice, Fleas, Ticks, Leeches, Some mites, Biting Flies.

* Mistletoe!!

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12
Q

what are demodex mites

A

mites that naturally live in our hair and on our face feeding off sebum, not a problem until you are immunosuppressed

(benign inhabitants of cutaneous microflora)

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13
Q

what is hyperviviparity

A

A form of viviparity in which young have viviparous young inside them when born
‘russian doll’

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14
Q

what are viviparious parasites

A

development of the embryo inside the body of the parent - parasite that already contains a fully grown embryo in utero

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15
Q

why is treatment of protozoa and helminth infection so hard

A

they are eukaryotic parasites that have evolved with their host and live at their expense

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16
Q

how are parasitic infections distinguished from bacterial and viral infections

A

they have complex life cycles and stay for a long durations in the host (in part due to ability to evade immune system)

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17
Q

why is little money spent on parasitic infections around the globe

A

usually occuring in third world countries and often dont kill the host

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18
Q

why do parasite live long term in the host/ have slower lifecycles

A

because of the more extensive coevolution

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19
Q

how does co evolution give us a weak point to exploit in parasites

A

due to their close relationship with the host, parasites have often lost/gained metabolic pathways making them dependent on the host

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20
Q

what ways can parasites cause disease

A

• Directly – damage due to parasite
• Host immune system induced damages
• Death of the parasite
o Immune effects
o Pathogenic degeneration - eg calcification
• Other agents carried by the parasite – viruses (ASFV), bacteria, other parasites (eg mosquitoes and malaria)

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21
Q

TH1 cells produce an immune response against which type of pathogenic organisms

A

Internal parasites, protozoa, bacteria, viruses

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22
Q

TH2 cells produce an immune response against which type of pathogenic organisms

A

External parasites, Helminths

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23
Q

what immune response is caused by protozoal infection

A

recognition of protozoal antigens by PRRs on macrophages induces production of IFN-y by NK, TH1 and naive CD4 T cells. this activates resting macrophages and controls the infection

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24
Q

what are plasmodium merozoites

A

the small labile invasive stages that invade erythrocytes

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25
Q

what causes the hallmark fever in malaria infections

A

Stimulated macrophages secreting pro-inflammatory cytokines IL-1, IL-6 and TNF-α

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26
Q

what is the main cause of recurrent fever in malaria

A

synchronised release of merozoites from RBC rupture

27
Q

what is the innate immune response to Plasmodium falciparum

A

Stimulation of toll like receptors by binding of TLR2 to GPI from merozoite and TLR9 to dsDNA from merozoite.
Causing activation of IL-12 and so activation of TH1, CD4+ and NK lymphocytes
These release INF-γ that stimulates other macrophages

28
Q

how does acquired immunity get induced by protozoal infections

A

a percentage of the Th-1 cells induced by IL12 and INFγ activate protozoal specific B cells (acquired)
often they preferentially induce IgG2 or IgG3 expression in B cells

29
Q

what is the difference between the immune response towards protozoa vs helminths

A

Protozoa
– TH1 response (IFNγ)
– Inflammatory – IL-12, IFNγ
– Activated macrophages, oxidative burst, NK cells
– Antibody response mainly (+) - IgG2 IgG3
Helminths
• TH2 response (IL4)
• IL10 and TGFβb limit acute inflammation (caused by macrophages
• Basophil and eosinophil activation
• Antibody response mainly (++) – IgG1, IgG4, IgE

30
Q

what is the immune response to helminth infection?

A

recognition of helminth antigens by PRRs causes release of IL10 and TGFβ (that limits acute inflammation)
recognition of helminth antigens by naive CD4 T cells causes release of IL-4 which activates TH2. TH2 releases interleukins that activate mast cells/ basophils (IL-4, 9 and 3), eosinophils (IL-5) and B cells (IL-4). B cells produce and release IgE and Ig1&4

31
Q

lymphatic filariasis is caused by which three parasites

A

Wuchereria bancrofti ~106 million cases,
Brugia malayi ~12.5 million.
Brugia timori

32
Q

who discovered the adult form of the nematode causing filariasis

A

Joseph Bancroft in 1876

33
Q

describe the filariasis lifecycle for Wuchereria bancrofti

A

Mosquito takes a blood meal and L3 larvae enter the skin
Adults worms grow in the lymphatics
Adults produce sheathed microfilariae that migrate into lymph and blood channels
Mosquito takes a blood meal and ingests the microfilariae
microfilariae shed sheaths, penetrate into mosquitos’ midgut and migrate to thoracic muscles (L1 larvae)
L3 larvae migrate to the head and mosquitos proboscis - so can infect another man by taking a blood meal

34
Q

what are the hosts of Wuchereria bancrofti and what larval stages develop in each

A

Mosquito is intermediate host (no reproduction) - L1 L2 L3 (6-7days)
Man is definitive host (bcos reproduction occurs) - L3 L4 L5 (6months)

35
Q

what are features of the adult Wuchereria bancrofti worm

A

lives in the human lymph vessels where it mate
produces 5000000 microscopic free living organisms (microfilariae)
can survive up to 7 years

36
Q

who is at the greatest risk of lymphatic filariasis infection

A

People living for a long time in tropical or sub-tropical areas where the disease is common are at the greatest risk for infection. Short-term tourists have a very low risk due to low numbers of parasites transferred per bite.

37
Q

how do microfilariae move around in the body to increase chance of transmission to the nest host

A

show diurnal migratory pattern into tissues - Microfilariae are less active in day blood than in night blood (more likely to be picked p by the nocturnally active mosquitoes

38
Q

what are the most common vectors of lymphatic filariasis in africa and in the americas

A

In Africa, the most common vector is Anopheles

In the Americas, Culex quinquefasciatus.

39
Q

what immune response to the parasite causes the disease lymphatic filariasis

A

Disease caused by fibrosis about the adult in lymphatic vessels and death of microfilarae

40
Q

what is the immune response to Wuchereria bancrofti

A

type 2 immune response - parasitic antigens stimulate dendritic cells (tgfbeta + IL10) and basophils to produce IL4 to activate Th2 cells these activate b cells mast cells and by release of IL5 eosinophils that damage the parasite

41
Q

what are the consequences of the immune response to wuchereria

A

size reduction
fecundity reduction
increased expulsion

42
Q

how does the L3 nematode evade the immune repsonse (filariasis)

A

L3 produces proteins which
A/ block (or don’t activate) TLRs on Langerhans/ Dendritic cells (APC) in skin
B/ inhibit T cell receptor signalling
ES-62 a tetrameric glycoprotein which is attached to phospholipids
and is taken into host T-cells and inhibits the PKC pathway
the TCRs normally induce
C/ Other proteins promote Treg cells so dampen immune response
There is a class switch (IL10 mediated) to IgG4 which has no complement activation and no ADCC activity
IgG4 binds to Fcε receptors and blocks IgE binding without causing Mast cells/ Basophil or Eosinophil degranulation

43
Q

how do L3 namatodes use the immune system to spread

A

Uses the responses to insect bite -mast cell degranulation after bite causes vasodilation + increased vascular permeability
The larvae can move more readily into the blood stream

44
Q

why is is crucial for both parasite and host that immune response is limited

A

Parasite -Immune responses inhibit mating and transmission
Host - A “hyperimmune” response results in pathology
- due to generalised tissue damage (Mast cells and Eosinophils)

45
Q

what causes the characteristic elephantiasis symptoms in lymphatic filariasis

A

Dying worms (adult /microfilariae ) - antigens released into the lymphatics
causes a chronic immune response
lymphatic swelling and fibrotic blockage and in time produces calcification

46
Q

why can killing the microfilariae be bad for you

A

when they die they produce toxic compounds that can drive you into septic shock and kill you

47
Q

what are the problems with Anthelmintics treatment of Wuchereria bancrofi and what have been developed to overcome this

A

Anthelmintics kill the microfilariae which produce toxic compounds that can cause parasitic shock - they dont kill the adult worms only reduce their fertility

Using Wolbachia instead - a gram-negative symbiote that is sensitive to doxycycline - if you apply this to kill the bacteria you can kill the worms slowly so the toxicity isnt so much of a problem

48
Q

what are the three presentations of leishmaniosis

A

cutaneous,
mucocutaneous,
or visceral leishmaniasis.
Due to the part of the body that the parasite ends up

49
Q

what is leishmaniosis caused by

A

more than 20 species of the protozoan genus Leishmania

50
Q

why is leishmaniosis difficult to irradicate

A

– The disease may occur in a number of other animals, including dogs and other mammalian species
and hence difficult to irradicate (reinfection) - If we cure humans there is a reservoir that could reinfect us

51
Q

what are the two forms of leishmania

A

amastigotes and promastigotes

52
Q

what is the lifecycle of leishmania

A

sand fly injects promastigotes into the skin during a blood meal
promastigotes are phagocytosed by neutrophils that are recruited to the bite site
infected neutrophils release the parasites which are then consumed by macrophages
promastigotes transform into amastigotes inside macrophages
amastigotes multiply in cells of various tissues + macrophages
sandfly ingests infected macrophages when it takes a blood meal
ingestion
amastigotes transform into promastigotes in the midgut
promastigotes divide and migrate to the anterior midgut and foregut
sand fly takes a blood meal

53
Q

when are the infective and diagnostic stages of Leishmaniosis

A

Infective stage is the sand fly blood meal injection of promastigotes
Diagnostic stage is the promastigote transformation into amastigotes and subsequent multiplication in macrophages

54
Q

what is a kinetoplast

A

a dense granule of DNA within the large mitochondrion

55
Q

what are the hosts of Leimaniosis

A

Primary host: Sand fly (reproduction)

Secondary host: Humans

56
Q

how does leishmania infection help the spread of itself

A

injection of sand fly saliva when they bite contains promastigotes in a gel that is high chemotactic for neutrophils and macrophages and blocks the gut of the fly increasing its feeding behaviour

57
Q

how does Leimania adapt the immune system to spread

A

Neutrophils phagocytise but parasite prevents fusion of phagocytic vacuoles with tertiary granules (bcos have machinery for superoxide and H+ production)
These cells harbour the parasite in vacuoles for prolonged periods, but in time undergo apoptosis (delayed by the protozoa) and are taken up into Macrophages

the promastigotes produce antioxidants and enzyme inhibitors to neutralize effects of the “toxins” generated by the macrophage phagosome
free Leishmania promastigotes activate complement and become taken up by macrophages.

58
Q

what leads to disease in Leishmania infection

A

induction of T cells to produce inappropriately high Th2 response

59
Q

immunity to leishmania is mediated by what

A

IFN-ɣ- activated macrophages as a part of a specific Th-1 (Il-12) response

(in productive infection IFN-ɣ is suppressed by IL4/IL10 and a Th-2 response)

60
Q

what causes the characteristic symptoms of leishmaniosis

A

The infected macrophage – eg kupffer cells of the liver, recruits CD4 (TH2) and CD8 T cells which leads to fibrosis and granuloma formation
cells recruit those around the to express different transcription factors to start producing fibrotic tissue

61
Q

what is cutaneous leishmaniosis

A

the most common form of leishmaniosis, usually non life thretening.
may develop one or more sores (skin lesions), particularly on exposed parts of the body such as the face, ears and the arms and legs. The lesions form at the site where the bite occurs.

62
Q

what is mucocutaneous leishmaniosis

A

infection of the skin and mucous membranes - leads to partial or total destruction of mucous membranes of the nose, mouth and throat - most common in bolivia, brazil, Ethiopia and Peru

63
Q

what is visceral leishmaniosis

A

affects several internal organs (usually spleen, liver, and bone marrow
fatal if left untreated in over 95% of cases. It is characterized by irregular bouts of fever, weight loss, enlargement of the spleen and liver, and anaemia. Most cases occur in Brazil, East Africa and in India

Immunology, infection and inflammation (8 decks)

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