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BIOL2022 > Host-parasite immune interactions > Flashcards

Host-parasite immune interactions Flashcards

1
Q

What is the definition of a parasite?

A

“An organism which lives in or on another organism (its host) and benefits by deriving nutrients at the other’s expense”

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2
Q

Tell me about an obligate parasite and a facultative parasite

A

An obligate parasite is totally dependent on the host to complete its life cycle, while a facultative parasite is not

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3
Q

What is an endoparasite?

A

“All those that live inside the host (including all parasitic worms)”

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4
Q

Give an example of an endoparasite?

Tell me about the host, carrier and type of disease it causes

A

Eg. 1. Protozoa (known also as microparasites)

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

Protozoa: Trypanosoma brucei (T.brucei)

Host: Man; Cattle; Horses

Carrier: Tsetse fly (Glossina)

Disease: African trypanosomiasis or Sleeping Sickness- Nagana

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5
Q

Whats an ectoparasite?

A

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

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6
Q

Give some examples of ectoparisites?

A
  • Lice, Fleas, Ticks, Leeches, some mites, Biting Flies.
  • Mistletoe!!
  • JUST SCRATCHING THE SURFACE!!!: Epiparasitism… Kleptoparasitism…. Social parasitism …Intraspecific social parasitism…. adelphoparasitism… etc
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7
Q

Give some more examples of endoparasites?

A

Eg2. Helminths (known also as parasitic worms/macroparasites) Inhabiting spaces in the host’s body- NOT ALL INTESTINAL

Tapeworms (Cestodes) e.g., young form of Pork Tapeworm (cysticercus) (reside in brain, eyes, muscles, and skin. Adult in gut

Flukes (Trematodes) e.g., Schistosoma (reside in blood vessels)

Roundworms (Nematodes) e.g., Heartworm (reside in the pulmonary artery)

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8
Q

What do parasitologists study?
What do virologists study?

What do microbiologists study?

A
  • In effect all organisms studied by a parasitologist
  • Virologists study viruses (all are parasites)
  • Microbiologists study bacteria, fungi, (some are parasites)
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9
Q

Name two eukaryotic parasites?

A

Protozoa and Helminths

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10
Q

How are parasitic infections distinguished from bacterial or viral infections?

A

Parasitic infections are distinguished from bacterial or viral infections by their complex life cycles and long duration inside or on the host.

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11
Q

What is the duration of the parasitic infection life cycle due to?

A

This duration is due in part by their ability to evade the immune system and avoid immune destruction

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12
Q

What do most parasites undergo?

In general, what do they not wish to do?

A

Most parasites undergo radical developmental changes throughout their life cycle, are antigenically complex, and host specific

In general, they do not wish to kill their host

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13
Q

Different diseases caused by eukaryotic parasites

A
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14
Q

Tell me some main characteristics of parasite infections?

A
  • Long term
  • Often not lethal to the host (in the short term or in most infections)
  • Not cleared by the host
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15
Q

Perhaps due to the slower lifecycle (cf Bacteria, Virsuses, Fungi) there has had to be more extensive co-evolution. Tell me about this co-evolution

A
  • Due to their close relationship often have lost/ gained metabolic pathways making them dependent upon the host
  • This gives a weak point we can exploit
  • Parasites role in maturation/ control of the immune system
  • Macroparasites and allergy
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16
Q

Tell me diseases have occurred due to parasites

A
  • Directly- damage by the parasite
  • Host immune system induced damage
  • Death of the parasite
  • Immune effects

Pathogenic degeneration eg calcification

  • Other agents carried by the parasite
  • Viruses (ASFV)
  • Bacteria
  • Other parasites e.g. mosquitos and malaria
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17
Q

What type of immunity and most parasites susceptible to?

A

Most parasites are susceptible to both Innate and Adaptive immunity and have produced strategies to escape both Micro and macro endoparasites induce different immune responses

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18
Q

Tell me the drive of a bias of a specific subset of CD4+ T helper cells

A
  • Tho - naive T helper forms the others
  • Th1- intercellular micro-endoparasites
  • Th2- extracellular infective agents- macro-endoparasites
  • Th17
  • Treg
  • Tfh

These alter not only which form of T or B cell response is seen but also, other inflammatory changes

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19
Q

Protozoal infections

A
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20
Q

Most parasites are susceptible to both innate and adaptive immunity and have produced strategies to escape both.

Tell me the immune response to parasitic infection

A
  • Early in infection with intracellular parasites, IL-12 is produced by phagocytic cells and induces the production of IFN-γ by natural killer (NK) cells and T cells.
  • This early production of IFN-γ may activate macrophages and control infection.
  • In addition, IL-12 and IFN-γ favour the development of parasite-specific TH1 cells, Pattern recognition receptors- TLR, ctyper lectin receptors, NOD (nucleotide –binding oligomerisation domain like receptors)
  • NK cells – innate immune cells 3rd class of lymphocyte (B,T,NK)
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21
Q

Tell me the innate immune response to merozoites?

A
  • The innate immune responses to merozoites occurs by stimulation of toll like receptors, namely TLR2, which binds GPI and TLR9 that binds parasite dsDNA.
  • This cause IL12 activation of Th1 and NK lymphocytes which release INF-γ which stimulates macrophages.
  • Once stimulated they cause secretion of the pro-inflammatory cytokines IL-1, IL-6 and TNF-α that cause fever, the hallmark of malaria infections. (the synchronised release of merozoites from RBC rupture drives this and is the major cause of the recurrent fever in malaria)
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22
Q

Tell me the main events that occur in protozoal infections

A
  • NB We generally have in a MHCII independent activation -so is innate and inflammatory
  • NK cells and Macrophages are the main cell types being expanded
  • However, a small percentage of the Th-1 cells induced by IL12 and INFγ may activate protozoal specific B cells often they preferentially induce IgG2or IgG3 expression in B cells (so innate and adaptive immunity meet here)
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23
Q

Protozoal infections, malaria

A
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24
Q

Is the Helminth a micro or macro endoparasite?

A

Macro endoparasite

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25
Q

Tell me some examples of Helminths

A
  • Tapeworms (Cestodes) e.g., intermediate form of Pork Tapeworm (cysticercus) (reside in brain, eyes, muscles, and skin. - Prevalence in endemic areas can reach from 5-20%
  • Flukes (Trematodes) e.g., Schistosomes (reside in blood vessels) ~ 200,000,000 infected
  • Roundworms (Nematodes) e.g., Heartworm (reside in the pulmonary artery)
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26
Q

Tell me the differences between the immune responses to protozoal and Helminth infections

  • Type of response
  • Whats released
  • Whats activated?
  • Antibody reponse
A
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27
Q

Tell me the Ig subtypes of protozoa and helminth

A
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28
Q

What is the least abundant antibody subtype?

What does it have major roles in?

A

IgE is the least abundant isotype

serum IgE levels ~ 0.05% of the Ig concentration,

Major roles in immunity to helminths and in allergy- has 2 receptors

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29
Q

What are the two types of IgE receptor?

A
  1. High affinity IgE receptor, (FcεRI), or Fc epsilon RI,
  2. CD23, low affinity FcεRII, (lectin)
30
Q

Tell me about the high affinity IgE receptor

  • Where is it expressed?
  • What is it inducible in?
  • Binding?
  • effects?
A
  • constitutively expressed on mast cells and basophils
  • inducible in eosinophils.
  • Binding of antigens to IgE already bound by the FcεRI cells causes cross-linking of the bound IgE and the aggregation of the FcεRI,
  • leads to the degranulation and the release of mediators from the cells.
31
Q

Tell me the importance of the low affinity IgE receptor?

A

important in regulation of IgE levels. Present on mature B cells, macrophages and eosinophils and has a role in regulating IgE levels

32
Q

Tell me about Eosinophils

  • What are they and what do they contain?
  • What do they release?
  • Where they are found and their duration here?
  • When their levels increase?
A

Eosinophils–Generally ~ 1% of all WBCs

  • small granules which contain chemical mediators,
  • IgE/FcεRI mediated release eosinophil peroxidase. (cytotoxic) ribonucleases, deoxyribonucleases, lipase
  • Major basic protein (induces mast cell and basophil degranulation)
  • Eosinophils persist in the circulation for 8–12 hours and can survive in tissue for 8–12 days in the absence of stimulation.
  • Increase in allergic and parasitic settings
33
Q

Tell me about Basophils?

A

Basophils- generally 0.1% of WBCs (with mast cells other cell type with high-affinity IgE receptor)- (Mast cells tissue dwelling cells are from a different lineage but have many similarities to basophils)

34
Q

When activated, what do basophils release?

A
  • pre-formed mediators (from the granules):
  • serine proteases
  • histamine
  • serotonin
  • heparin
  • newly formed lipid mediators (eicosanoids):
  • thromboxane
  • prostaglandin D2
  • leukotriene C4
  • platelet-activating factor
  • cytokines
  • eosinophil chemotactic factor
  • basophils are an important source of interleukin 4
35
Q

What is considered one of the critical cytokines in the development of the production of IgE?

A

Interleukin-4

They increase their numbers in chronic ectoparasite and nematode infection

36
Q

Some key terms…

A
  • Hist- permeability
  • Sero- perm / dilation
  • Thromboxan- vasoconst
  • PGD2- TH2 recuts and vasoduilates
37
Q

What is the cycle of action of FceR1?

A
38
Q

different WBCs…

A
39
Q

Lecture 1 summary

A
  • Parasites are MAJOR causes of pathology
  • Protozoa and Helminths induce markedly different immune responses
  • Generally, cause long term infections (where the initial immune response is robust they may be destroyed)
  • To survive these the parasite must have immune modulating or evasion strategies
40
Q

Give 2 examples of a parasitic disease

A
  1. Lymphatic filariasis (human disease caused by parasitic worms)
  2. Leishmaniosis (caused by protozoan parasites and transmitted through bites of female sand flies)
41
Q

What two parasites can cause the parasitic disease Lymphatic filariasis?

A

Wuchereria bancrofti with an annual infection rate of ~106 million cases,

Brugia malayi with an annual infection rate of ~12.5 million.

So annual infection ~ 2x that of the UK population

42
Q

What is Filariasis caused by?

A

A Nematode

43
Q

Tell me a history of the disease Filariasis and what type of system it is?

A
  • Known as a disease for ~4000 years. Ancient Egypt (2000 BC)
  • First proper documentation in ancient Greek literature,
  • In 1866, Timothy Lewis, connected between microfilariae and disease,
  • In 1876, Joseph Bancroft discovered the adult form of the worm.
  • In 1877, the lifecycle involving a mosquito vector was theorized by Patrick Manson, who proceeded to demonstrate the presence of the worms in the insect (mosquitoes)
  • So, a two- host system
44
Q

Tell me the life cycle of Wuchereria bancrofti, and filariasis?

A
  • The infection spreads via mosquito bites (mosquito – intermediate host/secondary host as no sexual reproduction occurs here, man- definitive host as sexual reproduction occurs here)
  • The adult worm lives in the human lymph vessels, mates, produces ~ 5,000,000 microscopic free-living offspring (not eggs), microfilariae (an early stage in the life cycle of certain parasitic nematodes)
  • The adults can survive up to 7yrs.
  • Microfilariae circulate in the hosts blood (show diurnal migratory pattern into tissues) and infect the mosquito when it bites a person who is infected.
  • Microfilariae grow and develop in the mosquito.
  • Microfilariae migrate out of gut of insect and into tissues– L1- L2- L3 (6-7days)
  • L3 migrates to the mouthparts and is passed to the host when the mosquito bites another person,
  • Larval worms travel to the lymph vessels.
  • They grow into adult worms, L3-L4-L5 (adult) a process that takes ~ 6 months
  • Then they’ll mate

NB. They go through 5 larval stages and L5 is the adult stage

45
Q

Tell me the common vectors for Filariasis in Africe and America

A
  • In Africa, the most common vector is Anopheles
  • In the Americas, Culex quinquefasciatus
  • 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.
46
Q

Tell me about the immune response to Lymphatic Filariasis

A
47
Q

Tell me how the L3 nematode can modify/ use the immune system

A

1. 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

2. L3 produce proteins which

a. block (or don’t activate) TLR 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 T regulator cell so dampen immune response- T helper 1 and T helper 2 (check) (? Via APC)

3. There is a class switch (IL10 mediated) to IgG4 which has no complement activation and no ADCC (antibody dependent cytotoxicity) activity

4. IgG4 binds to Fcε receptors and blocks IgE binding without causing Mast cells/ Eosinophil or Basophil degranulation

48
Q

What do high levels of IgG4 block?

A

High levels of IgG4 blocks the function of mast cells and eosinophils

49
Q

Why is it crucial for both the parasite and the host that the immune response against the parasite is limited?

A
  • Immune responses inhibit mating and transmission
  • However, a “hyperimmune” response results in pathology
  • due to generalised tissue damage (Mast cells and Eosinophils)
  • Dying worms (adult /microfilarae ) antigens released into the lymphatics causes and caused by a chronic immune response
  • lymphatic swelling and fibrotic blockage and in time produces calcification
50
Q

What is the treatment issues against Filariasis?

A
  • Anthelminthics- kill the microfilaria (toxic!)
  • Don’t kill adults
  • Reduce their fertility
  • Wolbachia- Give symbiotic sensitive to doxycycline
51
Q

Tell me some other filarial worms

A
  • Loa-Loa- Chrysops
  • Oncocerca Volvulus- simulium blackflies
  • River blindness roughly 1M sight impairment
  • Roundly 25M infected
52
Q

Name the protozoa that causes Leishmaniasis?

A

Trypanosomes- Leishmania parasite which are transmitted by the bite of infected female sandflies

Leishmaniosis caused by protozoan of the genus Leishmania and spread by the bite of sandflies

53
Q

What three ways can the disease Leishmaniosis present in humans?

A
  1. Cutaneous (in the skin)
  2. Mucocutaneous (in lips, eyes and nose)
  3. Visceral Leishmaniasis (in the visceral organs- soft internal organs of the body e.g., lungs, heart, digestive system, excretory, reproductive and circulatory systems)
54
Q

Infections in humans are caused by how many species of Leishmania?

How is it diagnosed?

A

20

Diagnosed by seeing the parasites under the microscope.

55
Q

Tell me about number of people infected with leishmania?

A

About 12 million people are currently infected in some 98 countries.

About 2 million new cases and between 20,000 - 50,000 deaths per year.

The disease may occur in a number of other animals, including dogs (may be indirect zoonotic) and hence difficult to irradiate

56
Q

Whats a Zoonotic disease?

A

Zoonotic disease is one which can pass from animals to humans and also humans to animals

57
Q

Some history of Leishmaniosis

A
  • First descriptions of lesions similar to cutaneous leishmaniosis appear in texts of Persian physicians from 1500 to 2500 BC.,
  • Cunningham described the organism in 1885 without relating it to the disease.
  • Borovsky, (1898) published the first accurate description of the causative agent
  • Ronald Ross who proposed that Leishman-Donovan bodies were the intracellular stages of a new parasite, which he named Leishmania donovani
58
Q

WHO and Leishmaniosis

Tell me about the stages of the disease in the sand fly and human

A
  • The World Health Organization estimates there are 1.5 million new cases of cutaneous leishmaniosis and 500,000 new cases of visceral leishmaniosis in the world each year
59
Q

Whats an Amastigote and a Promastigote?

A
  • An amastigote is a protist cell that does not have visible external flagella or cilia. The term is used mainly to describe an intracellular phase in the life cycle of trypanosomes that replicates. These are intracellular
  • Promastigote is the extracellular insect-stage parasite which utilise glucose as the primary energy source
60
Q

Infection with Leishmania is based upon what?

A

Infection with Leishmania is based upon modifying inflammatory pathways

61
Q

Biting by the intermediate host leads to injection of the sandfly saliva which contains promatigotes in a gel which is what…?

A
  1. highly chemotactic for neutrophils and macrophages
  2. blocks the gut of the fly increasing its feeding behaviour
62
Q

What enters once the sand fly has bitten the host?

A

Neutrophils and macrophages enter the bite area and phagocytise the promastigotes then they’re within the primary cells of multiplication

63
Q

Tell me about whats Neutrophils do when they enter the bite area?

A
  • Neutrophils phagocytise but parasite prevents fusion of phagocytic vacuoles with tertiary granules (these contain in their wall the machinery for superoxide and H+ production). These granules aren’t toxic to parasites so parasites live here for long durations
  • These cells harbour the parasite in vacuoles for prolonged periods, but in time undergo apoptosis (believed to be delayed by the protozoa) and are taken up into Macrophages
64
Q

Tell me about the role of Macrophages when they enter the bite area?

A

Macrophages

  1. (free Leishmania promastigotes) activate complement and become taken up by macrophages.
  2. Infected apoptosing neutrophils phagocytosed
65
Q

When the Promastigotes fuse with the cell’s lysosomes what do they produce and what effect does this cause?

A

The promastigotes fuse with the cell’s lysosomes and produce antioxidants and enzyme inhibitors to neutralize effects of the “toxins” generated by the macrophage. Protozoa transferred to the spleen, liver and bone marrow by these macrophages/ monocytes or dendritic cells - multiplying there in the amastigote form

66
Q

Tell me, using mouse data, how a differing host immune response leads to disease

A
  • Most mice strains (C57BL/6) show limited lesions after Leishmania inoculation and then healing and immunity.
  • Other strains have ongoing lethal disease and fail to show healing or immunity (BALB/Cc)
67
Q

Tell me how induction of T cells to produce inapproproate high Th2 response leads to disease?

A
  • Immunity to Leishmania is mediated by IFN-ɣ- activated macrophages as a part of a specific Th-1 (Il-12) response.
  • In Disease (Productive infection) IFN-ɣ is suppressed by IL4 /Il10 and a Th-2 response.
  • Parasite induced disturbance of Th-1 /Th-2 balance occurs with other parasites eg Schistosoma (Bilharzia)
68
Q

Tell me the pathology of the Leishmania disease?

A

The infected macrophage- here Kupffer cells of the liver recruits CD4(Th2) and CD8 T cells these induce CCLs (connective tissue growth factors) and TNFα/ TGFbeta which lead to fibrosis and granuloma formation

69
Q

Tell me the characteristics of parasite infections

A
  • Widespread and very important
  • Range of pathology
  • Often lifelong
  • Regulation of immune response critical for both host and parasite
  • Often don’t kill the host (disadvantageous for the parasite) but can cause long lasting disease
70
Q

Tell me the problems of Leishmaniasis

A
  • Leishmaniasis is caused by over 20 Leishmania species
  • Over 90 sandfly species are known to transmit Leishmania problems
  • Can infect other mammalian species

BIOL2022 (8 decks)

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