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Biology Year 2 > Parasitology > Flashcards

Parasitology Flashcards

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1
Q

Describe pinworm egg transfer

A

Adult female pinworms lay their eggs on the perianal skin

  • usually during the night
  • eggs are sticky and so adhere to skin

Eggs are easily transferred to the hands and mouth due to scratching of itchy area

  • eggs are then ingested when a person consumes contaminated food, drink or objects
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2
Q

Where do pinworms develop? Describe the process

A
  • Develop in the small intestine
  • after ingestion
  • eggs hatch in small intestine
  • release larvae
  • burrow into the wall of the small intestine
  • where they develop into adult pinworms
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3
Q

When do pinworms migrate to the large intestine?

A

When fully mature and ready to lay eggs

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4
Q

What is the Linnean rank of nematoda?

A

Phylum

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5
Q

How many moults are required for the pinworm to reach adulthood?

A

4

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6
Q

Are pinworms deoicious or monoicious?

A

Deoicious

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7
Q

What is a common diagnostic test for pinworms?

A

Sellotape test
- Tape across anus - place on microscope slide
- Worms or not - diagnostic

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8
Q

Are protozoa micro/macro parasites?

A

Micro

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9
Q

Are worms micro/macro parasites?

A

Micro

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10
Q

Macroparasites cannot generally replicate in the host - what does this mean for the level of infection? Give an example

A
  • levels of infection are determined by the number of infection events and number of infective stages e.g. gut nematodes
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11
Q

Microparasites replicate in the host - what does this mean for the level of infection? Give an example

A

Infection levels can rise rapidly after a single infection event (theoretically from one infectious stage)
- requires fast immune response to combat
- e.g. malaria

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12
Q

Describe the lifecycle of a parasite who is never exposed to the external environment?

A

Infective stage in host
- host eaten (predation or scavenging)
Development in new host
- Reproduction of parasite in host

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13
Q

What is an example of a parasite that’s entire life cycle is spent in internal environments

A
  • Trichinella spiralis (Trichinosis)
  • spiral threadworm (nematode)
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14
Q

Where is the infective stage of Trichinella spiralis (Trichinosis) – the spiral threadworm present?

A
  • Skeletal Muscle
  • Coiled up worm
  • Muscle larvae cyst (encysted larvae)
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15
Q

How does transmission of T. spiralis (Trichinosis) infection occur?

A

Ingestion of infected meat
- when raw or undercooked meat that contains encysted larvae

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16
Q

Where does T. spiralis (Trichinosis) develop?

A
  • Small intestine
  • after digestion larvae are released from their cysts
  • penetrate wall of the intestine to enter the bloodstream
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17
Q

Where does T. spiralis (Trichinosis) migrate after development in the small intestine?

A

Migration to skeletal muscle:

  • larvae travel through the bloodstream and enter the skeletal
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18
Q

What happens to T. spiralis (Trichinosis) after migration into the skeletal muscle?

A
  • Encyst
  • Remain dormant until consumption
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19
Q

Where does reproduction of T. spiralis (Trichinosis) occur?

A

Skeletal muscle cysts

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20
Q

Name the range of human symptoms of trichinosis?

A
  • Fever
  • Muscle pain
  • Gastrointestinal distress
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21
Q

Does T. spiralis (Trichinosis) release eggs or larvae?

A

L1 larvae

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22
Q

Describe the stages of the parasitic cycle which includes two or more host species and no contact with the external environment?

A
  • Reproduction of parasite in host
  • Production of stages infective to vector
  • Uptake of stage by vector
  • Development of infective stages in vector
  • Transmission of infective stages to new host as vector feeds
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23
Q

What is the definitive host?

A

Species where the parasite reaches sexual maturity

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24
Q

What is the intermediate host?

A

Species in which larval or non sexual stages develop

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25
Briefly describe the disease cycle of Trichinosis?
- Ingestion of infected meat - Development in the small intestine - Migration to skeletal muscle - Encyst and reproduce - Transmission to predator/scavengers via consumption of meat
26
In malaria what is the definitive host?
Female anopheles mosquito
27
When do female mosquitoes become infected in malaria (Plasmodium)?
- Feed on the blood of plasmodium infected humans
28
What happens to plasmodium after ingestion by mosquitoes?
- development in the mosquito gut - migrates to the mosquito's salivary glands
29
How is plasmodium transmitted to humans?
Infected mosquito bites a human for a blood meal
30
Where does the development of plasmodium occur in humans and what does this cause?
- Liver - Undergo a developmental transformation into liver stage parasites - Multiply rapidly and cause liver damage
31
What occurs after the liver stage of plasmodium development?
Invasion of red blood cells and multiple - Cause the red blood cells to rupture and release new parasites into the bloodstream
32
Briefly describe the 5 steps of plasmodium life-cycle
- Infection of mosquito from bloodmeal - Development in the mosquito - Transmission to humans - Development in liver - Invasion of red blood cells - Cycle repeats
33
Describe direct parasitic life cycle
- Reproduction of parasite in definitive - Release of infective stages (eggs/cysts) into outside environment - Reinfects into same host again
34
Describe features of parasites that have stages that are exposed to the outside environment
- Free living forms relatively inert/inactive - Can be direct life cycle - one host species - Indirect life cycle - intermediate hosts
35
Describe how humans become infected by Ascariasis (Ascaris lumbricoides)?
Ingesting contaminated soil or food that contains eggs
36
Describe the development in the small intestines of humans by Ascariasis (Ascaris lumbricoides)?
- Eggs hatch in the small intestine - Larvae burrow into the walls - Mature into adult worms
37
How long does maturation take and how large is an adult Ascariasis (Ascaris lumbricoides)?
- Reach maturity after about 2-3 months - Up to 40 cm in length - Live in the human small intestine for up to 2 years
38
What happens to eggs produced by adult female Ascariasis (Ascaris lumbricoides)?
Passed out of the body in feces
39
How long does the development of larvae of Ascariasis (Ascaris lumbricoides) in the external environment take?
- Eggs develop into larvae in the soil - Become infective after about 2-3 weeks
40
Briefly describe the life cycle of Ascariasis (Ascaris lumbricoides)
- Egg ingestion from soil by human - Development in small intestine - Maturation of adult worms - Egg production and passing of the eggs in feces - Development of larvae in soil
41
Where do adult (Tapeworms/Cestodes - Taenia) live?
Intestines of the definitive host
42
How are (Tapeworms/Cestodes - Taenia) spread?
Eggs are passed out of the body in feces
43
Describe how Tapeworms/Cestodes (Taenia) enter the intermediate hosts?
- Eggs develop into larvae in the environment - Ingested by intermediate hosts when they consume contaminated food or water
44
What are some examples of intermediate host of Tapeworms (Taenia)?
Cattle, pigs and fish
45
What is the cysticerci of Tapeworms/Cestodes (Taenia)?
- Larvae develop into cycticerci once ingested by intermediate host - Cyst-like structures - Contain tapeworm larvae
46
How do Tapeworm/Cestode larvae (Taenia) enter the definitive host?
- Ingestion of the infected intermediate host - Consumption of raw/undercooked meat
47
Describe the final stage of a Tapeworm infection - after the consumption of the intermediate host by the definitive host?
- Larvae in the cysticerci are released in the intestine - Attaches to the wall of the intestine using scolex - Develop into adult tapeworms - Begins producing eggs
48
How do Tapeworms/Cestodes remain attached to the intestinal wall?
Hooks and Suckers - on scolex
49
Describe tapeworms reproductive strategy?
- Both ovaries and testes - Capable of self fertilisation and cross fertilisation
50
Describe tapeworms egg laying?
Last section drops out with faeces - bag of eggs
51
Where do tapeworms live in the intermediate host and how do they get there?
- Penetrate intestinal wall of host - Live in muscle
52
Describe parasites which are active in external environment
Don't bother
53
Describe the modes of transmission into the definitive host of parasites with a life strategy in which the parasite is active in the external environment
- Ingestion of infective stages from environment - Penetration by infectious stages - Ingestion of infected intermediate host
54
Describe how water becomes contaminated with Schistoma (Blood flukes)?
- excreted from the human host in the feces or urine and end up back in freshwater - eggs hatch in freshwater - miracidia released into water
55
How do Schistoma (Blood flukes) infect the intermediate host?
Miracidia penetrate the skin of snail intermediate hosts
56
What do Schistoma micadia (blood flukes) develop into?
sporocysts in intermediate snail host and multiply
57
How do Schistoma parasites (blood flukes) infect human hosts?
Infective cercariae penetrate the skin of humans in contact with contaminated water
58
Describe the events after a Schistoma parasites (blood flukes) enters a human host?
- Cercariae enter the bloodstream - Mature into adults - Migrate to the blood vessels surrounding the intestines or bladder - Where they lay eggs
59
Briefly describe the lifecycle of Schistoma parasites (blood flukes)
- Release of cercariae into environment from host - Infection of snail intermediate host in water - Release of infectious stage into water - Infection of human host - Development of adult parasites - Egg excretion
60
What is commensalism? Give an example
- No metabolic dependance - e.g. clownfish and sea anemone
61
What is mutualism? Give an example
Obligatory relationship – both benefit - e.g. oxpeckers on cattle in Africa
62
What is parasitism
- One partner benefits - metabolic dependence - may cause harm to host
63
What are the theories for evolution of parasitism?
Loss of otherwise essential genes through mutualistic relationship with bacterial endosymbiont - Gains traits that support manipulation of host Horizontal gene transfer - gain advantageous genes that allow organism to co-opt parasitic way of life Parasitic features evolving under free living conditions - the concept of pre-adaptation - free-living traits co-opted for parasitic lifestyle
64
What is necromeny?
- Consumption of dead organic matter as a primary food source. - necromenous animals do not actively kill their food source - considered a "halfway-house" between parasitic and free-living lifestyles
65
How many times has parasitism evolved in nematodes?
4 groups animal nematode parasites 3 groups of plant nematode parasites - suggests some characteristic of nematodes that favours evolution of parasitism
66
Describe the loss of essential genes in Brugia malayi (Human filarial parasite)
- loss of genes encoding enzymes required for essential biosynthesis pathways - no longer make vital compounds for survival - need external source (parasitism)
67
What are Meloidogyne incognita and M. hapla and what do they cause?
- Plant parasites - Root-knot nematodes - Cause deformities in carrots - Severe infections result in reduced yields - Deformity impacts consumer acceptance
68
Describe horizontal gene transfer (HGT) in Meloidogyne incognita and M. hapla?
- Produce cellulases and xylanases - not found in other animals - most similar to bacterial genes - Horizontal gene transfer from rhizobial bacteria in legume root nodules
69
What are Rhizobia?
bacteria that fix nitrogen after becoming established inside root nodules of legumes
70
Describe how a free living nematode in dung may be pre-adapted for animal parasitism
Conditions in pile of dung is similar to colon - Anaerobic - Toxic enzymes
71
Is there definitive proof of pre-adaptations in parasites
- Nope, hypothetical concept - The pre-parasites of present-day parasites no longer exist
72
Describe how nematode associations with insects may represent pre-adaptation for parasitism
Development of - Phoretic associations - Necromenic associations Neither yet parasitic – metabolic dependence on host develop later
73
What is phoresy?
- Symbiotic relationship - Host organism used for transportation or dispersal purposes
74
What is dauer larvae?
- Larva enters dormant phase - Non feeding stage - Specialised for survival and dispersal - Can survive harsh conditions
75
Do dauer stage larvae use phoresy?
- Some do - Dauer uses insects for transportation - Means of dispersal and finding new food sources
76
Explain the connection between dauer stage larvae and insects
- Dauer associates with insect host in species specific manner (particular beetle species etc) - wait for death then feeds on microbes growing on carcass
77
What features of a dauer larval stage?
- Non aging - Doesn’t feed - Does not grow - Can survive for months
78
What is the evidence for pre-adaptation from dauer larval stage?
- Both have specialised cuticle - Both cannot feed - Both can resume development to 4th larval stage - Where parasitic nematodes use an infective larvae its almost always 3rd stage - Dauer stage larvae are 3rd stage
79
What is the molecular evidence for dauer larval stage being a pre-adaptation for nematode parasitism?
- Molecular similarities - conserved endocrine signalling mechanism involving dafachronic acid (DA) and DAF-12 - controls formation of dauer and infective larvae
80
Describe C. elegans and its development into a the dauer stage
- Free living nematode - L2 has to sense environment (eg temp.) - Can grow (become L3) or arrest (as a Dauer) - Development of dauer is default developmental behaviour - Specified when DAF-12 is not occupied by ligand (DA) - Under inducing conditions - Generate DA which binds to DAF-12 to produce non-dauer larvae
80
Describe Strongyloides papillosus and its development in context of the dauer stage
- Parasitic nematode - Can switch between a free-living stage and a parasitic stage inside a vertebrate host - Halfway house between free living and parasitic lifestyle - During free-living stage - Choice between infective and non-infective larvae - Decision is driven by a signaling molecule called DA - Drives switch from infective to non-infective larvae - Equivalent to C. elegans where DA specifies non dauer larva
81
Where development of L3 is constitutive not facultative can DA turn off formation of infective larvae? What could the potential uses of this be
- Yes, selective ligand modulators of DAF-12 might be used to stop L3 larvae progression - Can DA be used to control nematode transmission?
82
Describe the evidence Pristiochus pacificus provides for pre-adaptation
Necromenic species - Exposed to low oxygen and toxic host enzymes - Increase in detoxifying enzymes compared to C elegans - Not found in any other non-parasitic nematode - Intermediate type of association between C. elegans and true parasites?
83
What would an enlarged spleen suggest about an infection?
- deals with blood-borne infections - potentially malaria
84
What is the malarial vector?
- anopheles mosquito - Females drink blood (Males don't bite)
85
How many plasmodium species can be transmitted to humans?
4
86
Which Plasmodium species is most widespread?
P. falciparum - Tropical Africa, Asia and Latin America
87
What are factors that affect malaria distribution?
- Temperature of >15°C - climate change affects range of malaria carrying mosquitoes - Cannot survive above 3000m
88
What are the 4 phases of the malarial lifecycle?
1 & 2. sexual phase and first asexual phase occur ONLY in Anopheline Mosquitoes. 3. second asexual phase is in the liver 4. Third asexual phase is in the blood (repeated many times)
89
What is the definitive host in malaria?
Anopheles mosquitos
90
What is the test for malaria?
- Blood smear test - Count number of RBCs and infected cells - Calculate percentage parasitaemia
91
What occurs in the 3rd phase of malarial development and what is it called?
- erythrocytic or blood stage - infected red blood cells rupture - releasing new malaria parasites - merozoites invade and infect new red blood cells
92
Describe the sexual phase of malaria
- Anopheles mosquito ingests gametocytes - Activation male gametocyte - Releases osmophilic bodies into RBC - Disrupts RBC membrane - Causing swelling and rupture - Activated gametocytes undergo sexual reproduction - Form zygote
93
How many times is DNA replicated during the development of male gametocyte in malaria?
- Replicated three times - Resulting in a nucleus with eight complete sets of DNA
94
How many kinetosomes are formed during gametogenesis in malaria?
Eight - in a microtubular organizing center during gametogenesis
95
What are kinetosomes?
- Microtubule-based organelles - Crucial role in the generation of the whip-like movements - Base for the formation of cilia and flagella
96
What is the function of the kinetosome in malaria gametogenesis and how many are formed?
- Base and growing point for the flagellum (axoneme) during gametogenesis in malaria - Eight are formed
97
What is exflagellation in malaria?
- Activation of the male gametocyte and the subsequent release of the flagella in malaria - Can then fertilize the female gametes
98
What is the function of the flagellum in malaria?
Male gametocytes actively swims towards female gametocytes for fertilization
99
What happens after fertilization in malaria?
- Zygote develops into an ookinete - Penetrates the inner gut wall of the mosquito
100
What is the next phase of the malaria life cycle after the ookinete stage?
- First asexual phase - Ookinete develops into a sporozoite
101
What is an apicomplexan?
- Group of parasitic protozoans that includes the malaria parasite - All apicomplexans have an apical complex - used for host cell invasion
102
What is a sporozoite? (malaria)
- single-celled form of the malaria parasite - released from a sporocyst during the first asexual phase - migrates to the mosquito's salivary glands - injected into the bloodstream of a new host
103
What is the ookinete? (malaria)
- Product of fertilization between a male and female gametocyte - Enters the mosquito's blood - Develops into single-cellular structure called a sporocyst
104
What and where does the oocyst feed on after development from ookinete? (Malaria)
- Moves into the haemocoel (body cavity) of the mosquito - Feed on the haemoglobin of the mosquito's blood meal
105
What are sporocysts? (malaria)
- Formed inside the oocyst - Inside sporocysts, sporozoites undergo asexual replication - Contains thousands of daughter sporozoite cells
106
Sporozoites burst out of _____ and migrate to salivary gland of mosquito
Sporocysts
107
What cells does malaria enter after leaving the bloodstream? (malaria)
Kupffer cells which line liver capillaries
108
Where do sporozoites go after leaving Kupffer cells and what happens in these cells? (malaria)
Enter hepatocytes - sporozoites rapidly grow - become trophozoites
109
Does an infected person show symptoms during the merozoites phase? (malaria)
Nope
110
What is hypnozoite stage of P. vivax?
- Trophozoites become latent hypnozoite stage (dormant) - Can cause relapses years later
111
What do trophozoites become when they divide? (Malaria)
Schizogony/schizonts - Merozoites
112
Briefly describe the third phase of malaria?
Asexual phase in RBCs - Merozoites burst out of hepatocytes and invade RBCs - Once inside - ingests haemoglobin
113
What are the two steps in Merozoites invasion of RBCs (malaria)?
1. Receptor Recognition and Binding 2. Erythrocyte Deformation
114
Describe RBC structure
- Relatively rigid - Rigidity due to: Cytoskeleton - Difficult to disrupt
115
Describe entry into RBCs by malaria
- Merozoite attachment – anywhere on red cell - Apical complex releases compounds that disrupt rbc membrane - Entry into cell
116
What is the role of MSP-1 in merozoite invasion? (malaria)
Causes parasite rolling around RBC surface for a while during merozoite invasion
117
What are AMA-1 and RON-2, and why are there two with almost identical roles? (Malaria)
Own receptors secreted which bind to RBC - assisting attachment - redundancy (multiple proteins)
118
What is the role of PfRh5 in P. falciparum (malaria) RBC invasion?
- Binds to Basigin - Blood group molecule on RBC surface - Essential for the invasion
119
What is the parasitophorous vacuole? (malaria)
- Membrane-bound compartment - Formed around the parasite after invasion of host blood cells - Protective environment for the parasite to develop and replicate within the host cell.
120
What happens to the surface coat upon entry into RBC? malaria
THICK SURFACE COAT NOT ENGULFED - Sloughed off
121
What are the components involved in the invasion of a red blood cell by a malaria parasite?
- forms rhoptries and micronemes - only present in invasive stages. - structures are involved in the secretion of invasion molecules
122
How do rhoptries and micronemes help merozoites get into a cell? (malaria)
- Secretion of invasion molecules e.g. RESA molecule - Enhanced fluidity of RBC membrane
123
What are the changes that occur in the RBC after the entry of the merozoite? malaria
- Development of feeding stage - trophozoites - Production of enzymes that degrade haemoglobin - Development of novel transporter system - Maurer's clefts Changes in the shape and deformability of the RBC - formation of membrane "knobs"
124
What is the role of knobs that form on RBCs during malarial infection?
- Important in the adhesion of parasitized RBCs to blood vessels (deep-seated capillary endothelium) - Knobs keep the parasitized cells away from the spleen, which is the main immune organ that controls malaria.
125
What are the fatal consequences associated with P. falciparum?
Cerebral malaria - sequestration of infected red blood cells in the small capillaries of the brain - Breakdown of BBB Hydrostatic pressure changes - pressure on brain stem causes coma and death
126
What family is Toxoplasma?
Apicomplexa
127
What fraction of the human population does toxoplasma infect?
1/3 of the human population - very prevalent parasite
128
What types of organisms does toxoplasma infect?
Birds and mammals
129
What is the definitive host of toxoplasma?
- Members of the CAT family are the DEFINITIVE host - can only sexually reproduce inside felines
130
Briefly describe toxoplasma
Obligate intracellular protozoan parasite - only lives inside cells
131
How many strains of toxoplasma are there?
Three strains of Toxoplasma I, II, II
132
What is the primary route of infection for felines with the parasite Toxoplasma gondii?
Ingest tissues infected with bradyzoite cysts or oocysts containing sporozoites
133
What happens when bradyzoite cysts or oocysts are ingested by a feline? (toxoplasma)
- Burst due to digestive system - Invade the intestinal epithelium of the feline
134
What can differentiate into male and female gametes in the definitive host and eventually become oocysts containing sporozoites? (Toxoplasma)
Both bradyzoite cysts and oocysts can differentiate into male either and female gametes
135
How are oocysts with sporozoites shed from the feline? (toxoplasma)
- in its feces for up to three weeks - sheds several million oocysts per day
136
What can differentiate into male and female gametes and eventually become oocysts containing sporozoites in the definitive host? (toxoplasma)
Bradyzoites! - Oocysts are ingested by feline - Bradyzoites within oocysts can differentiate into male and female gametes - Leads to formation of new oocysts containing sporozoites
137
What do bradyzoite cysts develop from? (Toxoplasma)
- Tachyzoites invade cells - Develop into bradyzoite cysts
138
What happens if a warm-blooded animal eats infected tissue containing bradyzoite cysts? (toxoplasma)
Bradyzoites are released into the intestine - differentiate into tachyzoites - disseminate throughout the body - become bradyzoite cysts again
139
What occurs when a bradyzoite cyst is ingested by a cat? (Toxoplasma)
- invade the intestinal epithelium - differentiate into male and female gametes - become oocysts again
140
What are bradyzoites? (Toxoplasma)
Slow-dividing forms of the Toxoplasma parasite found in oocysts in infected muscle tissue
141
Where are toxoplasma cysts found in the body of infected animals?
Cysts are found in the muscle tissue of infected animals.
142
What are the potential risks for a pregnant woman if she is infected with Toxoplasma during the early trimester?
- Parasites can cross the placenta and affect the developing baby - potentially causing developmental defects - potentially death
143
Who is at risk for reactivation of latent Toxoplasma infections?
- Immunocompromised individuals - such as organ transplant recipients and HIV
144
What is the potential risk of Toxoplasma in HIV-positive patients?
Toxoplasma encephalitis as the infection can reactivate (from dormancy) and cause severe symptoms
145
What happens when Toxoplasma enters the latent phase?
the infection becomes dormant, and fever may subside
146
What is the rapidly dividing stage of Toxoplasma called?
Tachyzoite stage
147
What are some preventive measures to avoid Toxoplasma infection?
- Avoid cat feces and soil where cats defecate - Cook meat thoroughly
148
What is the asexual stage of the T. gondii life cycle called?
Tachyzoites
149
Which hosts are considered intermediate hosts for T. gondii?
Various warm-blooded animals, including humans
150
Which cells can T. gondii tachyzoites target?
almost any nucleated cell in the body
151
What happens to tachyzoites when they are secreted into the bloodstream? (T. gondii)
tachyzoites actively penetrate into cells, replicate, and then burst out when the host cell die - acute disease - characterized by symptoms such as fever and cold-like symptoms
152
How is the growth of T. gondii tachyzoites limited?
- limited by the immune response of the host - and tachyzoite transformation into cyst-forming bradyzoites.
153
What immune response is responsible for triggering the differentiation of T. gondii into bradyzoite cysts?
Th1 immune response - Specifically the production of interferon-gamma (IFN-g)
154
How does the Th1 immune response contribute to controlling T. gondii infection?
Maintains it in a dormant state within bradyzoite cysts
155
What molecule secreted by T. gondii enhances the Th1 immune response?
- Cyclophilin 18 - establishment of a chronic infection within the host as it promotes dormancy in T. gondii
156
What can T. gondii bradyzoites cause in immunocompromised individuals?
- T. gondii bradyzoites can cause acute encephalitis - inflammation of the brain
157
Where can sporulated oocysts contaminate? (Toxoplasma gondii)
water, soil, food and surfaces - contact with feces
158
How stable are T. gondii oocysts in the environment?
- Very stable - especially in warm and humid environments - enabling them to survive for extended periods outside of the host
159
Where does the sexual stage of T. gondii occur within the definitive host?
Intestine Definitive host - cat
160
Why is the feline the only host that allows sexual reproduction of Toxoplasma?
- Only mammal that lacks enzyme in their small intestines required to break down linoleic acid - Results in an excess of linoleic acid in their intestines - Allows Toxoplasma to develop sexually
161
How can the sexual life cycle of Toxoplasma be induced experimentally in other species?
- Increasing the levels of free linoleic acid - Knocking out the gene for delta-6-desaturase (enzyme that breaks down linoleic acid)
162
What is the significance of inducing the sexual life cycle of Toxoplasma experimentally?
- Study and research without the need for using cats
163
What does the parasite Toxoplasma use to move into host cells?
- Apical complex - Rhoptries and micronemes - Releases chemicals that facilitate its movement into host cells
164
How do Toxoplasma parasites move through their environment?
Glide through the fluid in their environment using a molecular motor
165
How does the parasite Toxoplasma move without projecting pseudopod-like extensions?
- Actomyosin motor system - Located beneath plasma membrane
166
What components are involved in the movement of Toxoplasma?
Actin and myosin - actomyosin motor As well as special "gliding-associated proteins"
167
How does the actomyosin motor system facilitate the movement of Toxoplasma?
- Generates force and pulls itself into host cells
168
What structure does Toxoplasma form to protect itself from the host cytoplasm?
- Forms a parasitophorous vacuole - Acts as a safe compartment for the parasite - Regulating its access to nutrients and waste
169
How does Toxoplasma move by interacting with the extracellular matrix (ECM)?
- Moves by forming and breaking specific interactions with the ECM - When the front of the parasite breaks its attachment, it springs forward
170
Can Toxoplasma be transmitted through blood transfusions?
Yes
171
Who is particularly at risk from Toxoplasma infection?
- dangerous for immunocompromised individuals - fetus of pregnant women
172
Describe the steps in toxoplasma entry into cells
1. Apical structures: rhoptries and micronemes involved in attachment process 2. Moving junction formation: The rhoptries and micronemes form moving junction (MJ) 3. Invasion: tachyzoite enters the host cell through the MJ 4. Rear dragging and front surging: spring-like motion 5. Parasite repeats the cycle of attachment, movement, and release, propelling itself forward
173
What is the rhoptry bulb in apicomplexa?
- Specialized secretory compartment (organelle) - Located at the apical end of the parasite - Contains proteins that are discharged during invasion
174
What is the significance of IgM antibodies in Toxoplasma infection?
- first type of antibodies produced in response to an infection - presence indicates a recent or ongoing infection.
175
What is the recent trend of toxoplasma infection numbers?
substantial rise in the number of people infected
176
What is one factor that has contributed to the high number of toxoplasma infections, particularly in France?
Consumption of rare or undercooked meat is one of the factors that has led to a high number of infections
177
How does Toxoplasma infection influence sex ratios in humans?
Women who are seropositive for Toxoplasma (have antibodies) tend to have more sons than uninfected women
178
Where does Toxoplasma rest in the body?
- Forms microscopic cysts in the brain - Remains in dormant state - These cysts act as a long-term reservoir for the parasite
179
What are the common treatments for Toxoplasma infection?
- Combination of sulfonamides and pyrimethamine - Inhibits growth and replication
180
How is congenital transmission of Toxoplasma reduced?
Spiramycin - often used during pregnancy to reduce the risk of congenital transmission
181
Is there a vaccine available for humans to prevent Toxoplasma infection?
No, currently there is no vaccine available for humans to prevent Toxoplasma infection.
182
Why is it challenging to target encysted bradyzoites with drugs? (Toxoplasma)
Dormant state less susceptible to drug action
183
What could be a potential side effect of targeting bradyzoite cysts in the brain?
- may lead to the release of toxic components - triggering a harmful inflammatory response in the body
184
What are the regions included in the "Old World" for sandflies?
Old World includes Middle East, Europe, Asia, Africa
185
Which regions are considered part of the "New World" for sandflies?
South America, Central America
186
Describe the transformation of Leishmania parasites after injection of metacyclic promastigotes into the host by sandfly
- Invade macrophage - Transform into amastigotes - Amastigotes multiply until lysis - Releasing more parasites that can invade additional macrophages
187
What happens when a sandfly bites an infected host and takes up amastigotes in their bloodmeal? (Leishmania)
Transform into the infective metacyclic promastigotes
188
Why do leishmania parasites produce a substance to block the sandflies mouth
- Sandfly will have to regurgitate to remove the plug - Potentially transmit the parasites to a new host during feeding
189
How do parasites in the midgut create a plug in the fly's mouthparts?
- Produce a proteoglycan gel
190
Describe the morphology of the leishmania parasites in sandflies.
- Promastigote - Single-celled Flagellated organisms - Aids in their movement
191
What is the characteristic feature of cutaneous leishmaniasis?
- Lesions on the surface of the skin - Occurring at sites with a high concentration of infected macrophages
192
What is the infective stage of the parasite in Leishmania?
flagellated metacyclic promastigote
193
What is Lipophosphoglycan (LPG) and what is its role in Leishmania?
- Inositol lipid anchor - Used for adhesion and invasion - Component of glycocalyx
194
What are Glycosylphosphatidylinositol (GPL) anchored glycoproteins and what is their role (Leishmania)
- Surface proteases - Increase in levels during infective metacyclic forms - Helps the metacyclic promastigotes in establishing an effective interaction with host cells - Degrade host immune factors - Degrade components of the extracellular matrix
195
What is the function of complement in opsonization?
Involves coating pathogens with complement proteins - complement-coated pathogens attract immune cells - such as phagocytes - engulf and eliminate them more efficiently
196
What is the function of complement in cell lysis?
formation of a lytic sequence - process involves the buildup of an attack complex that creates pores in the pathogen's membrane - leading to osmotic shock and death
197
What is the function of the complement system in chemotaxis and inflammation?
- Small fragments act as chemoattractants - Attract more immune cells - such as neutrophils and macrophages, to the site of infection or inflammation
198
What is the function of the complement system in chemotaxis and inflammation? - oops did this one twice dont bother
babadook
199
Are complement functions antigen-specific or non-specific?
Non-specific - rapid and generalized immune response
200
What is the role of opsonization in phagocytosis?
- Complement proteins bind to pathogens. - Complement fragments (C3b) act as opsonins. - Opsonins attract phagocytes and macrophages. - Phagocytes and macrophages have receptors for C3b. - Recognition of C3b enhances phagocytosis.
201
How do macrophage-infecting pathogens like Leishmania exploit opsonization and phagocytosis?
Attach to the surface of host cells (macrophages) - using molecules like GP63 - pathogens aim to be pulled inside the host cell - glycocalyx allows complement to stick to it
202
How does the thickness of the surface glycocalyx of Leishmania change during complement interaction and why?
- layer thickens - acts as a protective barrier against the host's immune system - protects against complement-mediated lysis
203
What are strategies deployed by leishmania to survive within host cells?
Thickening of the glycocalyx Shedding of some Lipophosphoglycan (LPG) from surface - removes complement components Increased expression of GP63 (surface protease) - inhibiting the destruction of the parasite by macrophages
204
How does the parasitophorous vacuole of leishmania act on pH to assist in survival with macrophages?
Vacuole maintains a slightly acidic pH - inhibits the activity of lysosomal enzymes - surface protease GP63 functions more efficiently in acidic pH
205
What are scavenger enzymes (leishmania)?
Amastigote form of the parasite produces scavenger enzymes - Help neutralize reactive oxygen species (superoxide and nitric oxide) produced by the macrophage - Protecting the parasite from oxidative damage
206
How does leishmanias inhibition of Protein Kinase C (PKC) benefit the parasite?
PKC - enzyme involved in generating toxic macrophage metabolites - Parasite's Lipophosphoglycan (LPG) inhibits its action - Preventing production of these toxic metabolites
207
What is the first cell type that floods into a wound when the skin is wounded and what is their function?
Neutrophils - Phagocytosis - don’t necessarily move in antigen specific way - as likely to take up bead as parasite
208
What happens when neutrophils take up Leishmania parasites?
- Leishmania survives digestion - Undergo apoptosis - Releasing the parasites into the environment
209
What is the Trojan Horse route of infection?
- Pathogens enter neutrophils and await macrophages for further infection. - macrophages take up apoptosing neutrophils cells as clearance mechanism - take up parasite as well
210
Briefly describe the leishmania lifecycle?
- Sand fly blood meal - takes up amastigote - Transforms into infectious metacyclic promastigote - Sandfly bites and passes promastigote to new host - M. Promastigote taken up by macrophage - Transform into amastigotes - Grow and multiply in macrophages
211
How many people are estimated to be infected with Chagas Disease?
Estimated that 16-18 million people
212
How many people die each year from Chagas Disease?
Approximately 50,000 people die annually
213
What is the vector that transmits Chagas Disease?
Triatomine bugs - also known as kissing bugs
214
What are the two ways to combat vector-borne parasites?
- Control the vector (e.g., through insecticide use, habitat modification) - Treat individuals to kill the parasite (e.g., through medication, vaccines)
215
What is Romana's sign?
Marker of acute Chagas disease infection - Swelling and redness that occurs around the eye when a person is infected
216
What happens to the parasite when it is inside the cells of the body? (Chagas Disease)
Parasite loses its flagellum and transforms into amastigote stage
217
What structure binds the flagellum to the surface of a protozoan (trypanosome)?
- Undulating membrane
218
What is the infective stage of Trypanosoma cruzi?
Metacyclic trypomastigote stage
219
What happens when Trypanosoma cruzi enters a cell in the wound site?
- metacyclic amastigotes move into cells and transform into amastigote form - multiplies
220
What happens after the amastigotes burst out of the cells? (Leishmania)
- Transform into trypomastigotes - Flagellated form - Re-infect phagocytes or uptake by sandflies
221
How do Trypanosoma cruzi infect other cells? dont bother
The trypomastigotes infect other cells and transform back into amastigotes. bipbop
222
Where does the multiplication stage of Trypanosoma cruzi occur in the kissing bug and what is the next stage of development?
Occurs in the midgut - Formation of metacyclic trypomastigotes
223
How are Trypanosoma cruzi parasites transmitted by the kissing bug?
Triatomine insects excrete the parasites in their hindgut - the infection can enter the body through rubbing the bug excrement into the eye or through mucosal surfaces
224
Briefly describe the cycle of Trypanosoma cruzi
Triatomine bug takes blood meal - ingests trypomastigotes - transforms into epimastigote - transforms into metacyclic trypomastigote - takes bloodmeal and defecates - passes metacyclic trypomastigote into bite wound or mucosal membrane - M. trypomastigote penetrates various cells at bite site - transforms into amastigotes - transform into trypomastigotes then burst out of cell - ready for uptake by kissing bug or reinfection of cells
225
When do chronic symptoms of Chagas disease typically develop?
Chronic symptoms usually develop after approximately 10-40 years
226
What are some early symptoms of Chagas disease?
Early symptoms may include fever and general malaise.
227
What happens during chronic Chagas disease?
Parasite multiplies in the body over time - Can cause an enlarged heart and may lead to cardiac arrest - (thinning of blood vessel walls and the risk of rupture) - can lead to the enlargement of the esophagus - can cause complete loss of tissue integrity in colon
228
What does molecular analysis suggest about Chagastic patients with parasites in different organs?
Bip bop dont stop!
229
What is the role of Gp85 in T. cruzi attachment and what prevents them from rapid destructions?
- stage-specific surface glycoprotein - Multiple forms of Gp85 are expressed on the surface of the parasite - providing variability to avoid immune destruction while maintaining the ability to attach to host cells
230
What is the function of trans-sialidases in T. cruzi?
Role in the attachment process - Can chop or move sialic acid residues on the surface of the parasite - Allowing it to interact with and attach to host cells
231
How does the variability in Gp85 contribute to T. cruzi's ability to invade cells?
Antigenic variability in Gp85 among different clones of T. cruzi - allowing the parasite to evade the host immune response
232
What is the role of the parasitophorous vacuole in T. cruzi invasion?
Resides in it during invasion of host cells - provides a protected environment for the parasite to survive and replicate
233
How does T. cruzi differ from other protozoans (such as Leishmania) in terms of its invasion mechanism?
- Does not rely on actin-mediated phagocytosis for invasion - Parasitophorous vacuole is not derived from the plasma membrane of the host cell
234
What is the source of the membrane for the parasitophorous vacuole in T. cruzi?
Lysosomal membranes - unlike other protozoans that may use host cell's plasma membrane or surface molecules for vacuole formation
235
Does T. cruzi spend its entire life cycle within the parasitophorous vacuole?
No, while it initially resides in the vacuole, the parasite eventually escapes and replicates in the cytoplasm of the host cell.
236
What molecules does T. cruzi attach to on the cell surface during invasion?
- Receptor Tyrosine Kinases - Protein receptor (TGFβRII) - Act as attachment points for the parasite
237
How does T. cruzi trigger a cellular increase in cellular calcium and the repair process in the host cell?
Attaches to the cell surface Secretion of oligopeptidase B - binds to G protein coupled receptors and activates phospholipase C (PLC) Secretion of Cruzipain - which cleaves kininogen into kinins - bind to cell surface kinin receptors and activate PLC Triggers an increase in intracellular calcium concentration Signals the host cell to initiate a cellular repair process
238
How does T. cruzi deceive the host cell into initiating a cellular repair process?
Attaches to specific molecules on the cell surface - Lysosomes are attracted to the site where T. cruzi attaches to the host cell - Triggers a response in the host cell to repair the "wound"
239
What happens after lysosomes accumulate under the site of T. cruzi attachment?
Lysosomal membranes fuse and create a membrane for the parasitophorous vacuole
240
How does T. cruzi enter the cell during the fusion of lysosomal membranes?
Combination of parasite movement and the "pulling/recovery" of lysosomal membranes along microtubules
241
What triggers the differentiation of T. cruzi from trypomastigote to amastigote?
Low pH
242
What molecule is produced in response to low pH and what is its role? (T. cruzi)
Tc-Tox - disrupts the parasitophorous vacuole and releases the parasite into the cytoplasm of the host cell
243
What molecule does tc-tox resemble in the complement system?
C9 - used by immune system to punch holes in cells
244
Where does T. cruzi replicate within the host cell?
Parasites multiply in cytosol - not synchronous
245
Describe T. cruzi development within host cells
- Trypomastigotes differentiate into Amastigotes - these divide and multiple - then differentiate into intracellular epimastigotes - Before transforming back into trypomastigotes
246
How does T. cruzi spread to new cells or enter the bloodstream? Useless don't bother
bipdopscripscrop
247
What are key features of trypomastigotes in T. cruzi?
- Found in blood - C shaped - Flagellated - Surface proteins essential for pathogenesis
248
What are key features of amastigotes in T. cruzi?
- Intracellular in tissues (esp. muscle) - Rounded - Flagellum not visible, low motility
249
What are the two groups of platyhelminthes?
- Cestodes - Trematodes
250
What are some cestode groups?
- Tapeworms - Planarians
251
What are some trematode groups?
bip bop bad luck
252
What is the common name for the parasitic disease caused by blood flukes?
Schistosomiasis
253
What is the characteristic feature of trematodes (flukes) that distinguishes them from other parasites?
- Trematodes have two prominent suckers - An oral sucker and a ventral sucker
254
What size are blood flukes (trematodes)?
- too big to live inside cells - can reach sizes of about 1 centimeter
255
What is the vector for Schistosomes?
Water snail
256
How do humans become infected with Schistosomes?
Contact with water inhabited by the appropriate species of infected snail
257
Where do Schistosomes mature and reproduce in the human body?
Particularly around the liver
258
How are Schistosome eggs released from the human body?
- Female Schistosomes release eggs into the lumen of blood vessels - Passed out of the body through urination or defecation.
259
What happens to Schistosome eggs in water?
hatch in the water, releasing miracidia, which are free-swimming larvae. - enter water snails
260
How do cercariae, the infective stage of Schistosomes, enter the human body?
Penetrate the skin
261
How are cercariae released from the snail into the water? (Schistosomiasis)
- Released from the snail through physical and enzymatic digestion - Released induced by light shining on snail
262
What happens to the tail of cercariae during penetration? (Schistosomiasis)
Cast off
263
What is the result of incomplete cercarial penetration? (Schistosomiasis)
In some cases, cercariae die in the skin - leading to dermatitis known as "swimmers itch." - occurs when schistosomes of one species try and penetrate the wrong host
264
What do the acetabular glands of cercariae do during penetration? (Schistosomiasis)
Secrete proteases and are involved in the shedding of the glycocalyx - Shed via microvilli - New double unit membrane is formed from membranous vesicle
265
What attracts cercariae to human skin? (Schistosomiasis)
- Gradients of fatty acids released from the skin and L-arginine - As well as warmth
266
How long do schistosome relationships last?(Schistosomiasis)
Mate for life
267
What cues the discharge of the acetabular glands in cercariae? (Schistosomiasis)
Fatty acids which predominate at deeper sites in the skin - Proteases are secreted to help burrow deeper
268
What types of proteases dominate in the secretions of the acetabular glands? (Schistosomiasis)
- Cercarial elastases (serine proteases) - Degrade skin molecules
269
How do we know that acetabular glands are important in invasion? (Schistosomiasis)
- Cercariae without tails can still invade when injected percutaneously - But cercariae without acetabular glands cannot
270
What is the function of enzymes that are released by cercariae when nearing blood vessels? (Schistosomiasis)
Thioredoxin peroxidase and superoxide dismutase - help counteract reactive oxygen species found in the cells of the skin at this level
271
What are two strategies schistosomiasis uses to assist in entry in the bloodstream
Apoptosis of host cells in the skin - may assist in entry Secretion of enzyme that degrades C1 inhibitor - which control vascular permeability - degradation increases permeability - making entry into bloodstream easier
272
What is the characteristic behavior of adult male and female schistosomes in the blood vessels?
Male curls up around the female - groove holds female parasite - female releases eggs
273
In schistosomiasis what would blood in urine suggest about the infection?
Heavy schistosomiasis infection - eggs can pass through the bladder wall - leading to the presence of blood in the urine.
274
What is the role of schistosome eggs in causing pathology?
Can cause damage as they migrate and get lodged in the liver - leading to inflammation and fibrosis
275
How does the host respond to schistosome eggs?
- Tries to wall off the eggs - leading to inflammation and the formation of granulomas
276
What are the long-term effects of schistosome eggs trapped in the body?
Chronic schistosomiasis - Persistent pathology due to the presence of trapped eggs - Ongoing inflammation and fibrosis
277
What are schistosome miracidium?
- Hatch from eggs on contact with water - Penetrate the snail host - Transform into a sporocyst stage
278
How do schistosome miracidia move?
Swim using cilia
279
What triggers the cessation of swimming in schistosome miracidia?
Changes in salt concentration
280
What do miracidia schistosomes differentiate into?
Sporocysts - Undergo asexual reproduction - Produce more daughter sporocysts
281
Where do schistosome cercariae develop?
Form within sporocysts
282
Why do hookworms stunt growth in children?
Drink blood - cause anaemia
283
What is the response of hookworm L3 larvae to thermal gradients?
Migrates to the cutaneous surface of mammals through thermotaxis
284
Where are hookworm larvae typically found in the skin?
Cracked skin, wounds, and hair follicles - they follow the path of least resistance
285
What enzymes do hookworm (Ancylostoma duodenale and Necator americanus) (L3) larvae secrete to help penetrate the skin?
- Secrete hyaluronidase out of their mouthparts - Helps them penetrate the skin by breaking down hyaluronic acid
286
What is the response of hookworm larvae to host-derived chemoattractants?
Move toward the venules (small veins) within the host's circulatory system
287
Where do the larvae of hookworms (Ancylostoma duodenale and Necator americanus) get trapped in the host's body and what does it cause?
Lung capillaries - leading to formation of microhemorrhages in the lung tissue
288
How do hookworm larvae pass through the basement membrane to reach the microvasculature?
- Secrete an alkaline protease - Attacks the basement membrane
289
What do hookworms use to latch on to the small intestine?
Hooks
290
How do hookworms stop clotting during feeding
Secretion of proteases (anticoagulants)
291
What is the function of the efficient pharynx in hookworms?
Constantly drinks blood and pumps out enzymes
292
Where does the final development to adulthood occur in hookworms?
small intestine
293
What is esophageal pumping in hookworms?
Rapid and coordinated contractions of the esophageal muscles - draws in and swallow large amounts of fluid
294
How many people are estimated to be infected with hookworm worldwide?
Approximately 500 million people
295
What is the target of the new hookworm vaccine being developed?
Hookworm aspartic hemoglobinase - a protease that cleaves host hemoglobin - stimulates the production of antibodies against the hookworm aspartic hemoglobinase - leads to starving of the worms
296
What are the stages of infection?
1) Entry into the body 2) Replication and spread 3) Disease manifestation 4) Exit from the body to infect others.
297
What are some of the body's barriers to infection?
Physical barriers - skin - mucous membranes Mechanical barriers - movement of mucus by cilia Chemical barriers - low pH - enzymes Microbiological barriers - normal microbiota
298
What is the difference between cells of the innate and adaptive immune system?
Innate immune system - macrophages and neutrophils - respond quickly to infections but do not have memory Adaptive immune system - B cells and T cells - respond more slowly but possess memory - respond faster upon reinfection
299
What is the common lymphoid progenitor pathway?
Gives rise to B cells and T cells
300
What is the myeloid and granulocyte progenitor?
Gives rise to innate immune cells - Dendritic cells - Macrophages - Granulocytes (neutrophils, eosinophils, and basophils)
301
What are the main functions of macrophages?
Phagocytosis - activation of bactericidal mechanisms
302
What are the main functions of dendritic cells?
- Antigen uptake in peripheral sites - antigen presentation in lymph nodes
303
What are the main functions of neutrophils cells?
Phagocytosis
304
What are the main functions of Eosinophils cells?
Killing of antibody-coated parasites
305
What are the roles of phagocytes in the innate immune system?
- act as effector cells to actively remove infection - Also act as Antigen Presenting Cells (APCs) - contain proteases to create an inflammatory response
306
What are the steps of phagocytosis?
- Attachment of the pathogen to the phagocyte - Ingestion of the pathogen into a phagocytic vacuole - Killing of the pathogen - Degradation of the pathogen
307
What are the key characteristics of the adaptive immune response?
- Acquired (develops after exposure to a pathogen) - Specific (tailored for a particular pathogen) - Memory (the second response is bigger and faster than the first)
308
What are the two main types of lymphocytes in the adaptive immune system, and where are they produced?
B lymphocytes (B cells) - which are produced in the bone marrow T lymphocytes (T cells) - produced in the thymus
309
What are the surface receptors on B cells and T cells called, and what do they recognize?
B cells have (BCRs) antibodies or immunoglobulins (Ig) T cells have T cell receptors (TCR) Both BCRs and TCRs recognize foreign molecules
310
What are antigens and antigenic epitopes?
- typically large molecules (usually proteins) that can be recognized by antibodies - parts of antigens recognized by antibodies are called "antigenic epitopes"
311
Describe the structure of an antibody
- Shaped like a 'Y' and is made up of two heavy chains and two light chains - Both light and heavy chains have constant and variable regions - Constant region of the heavy chains is called the Fc portion - Antigens bind at the variable end of the antibody
312
How does the shape of the antigen-binding site contribute to antibody function?
- Different antibodies have differently shaped antigen-binding sites - gives antibodies their specificity
313
What are the effector functions of antibodies in the humoral immune response?
- secreted by plasma cells - can neutralize pathogens and toxins - promote phagocytosis (opsonization)
314
How does Antibody Dependent Cell mediated Cytotoxicity (ADCC) work?
Antibodies bind to antigens on the cell surface - Cells with Fc receptors (NK (neutral killer) cells or macrophages) can bind to the Fc region of these antibodies - Interaction mediates extracellular killing but not phagocytosis
315
What is opsonization?
Opsonins (antibodies and other things) coat pathogen, mark it for destruction and make it easier to engulf
316
How do T cell receptors interact with antigens?
Unlike antibodies, T cell receptors don't recognize antigens directly - Antigens presented to them via Major Histocompatibility Complex (MHC) - Large proteins are broken down into peptides inside cells through a process called antigen processing - these peptides are then associated with MHC molecules inside the cell and expressed on the cell surface
317
What is the Major Histocompatibility Complex (MHC) and what role does it play in antigen presentation?
Unlike antibodies, T cell receptors don't recognize antigens directly - Large proteins are broken down into peptides inside cells - antigen processing - MHC molecules associate with antigenic peptides inside cells and then display these peptides on the cell surface for recognition by T cells.
318
What are Class I MHCs?
presents intracellular antigens (e.g., from viruses) to CD8 cells
319
What are Class II MHCs?
Presents extracellular antigens (e.g., from worms) to CD4 cells
320
What is the difference between MHC class I and class II molecules in terms of their expression and the type of antigens they present?
MHC class I molecules are found on most nucleated cells - present peptides derived from intracellular pathogens MHC class II molecules are expressed on antigen-presenting cells like macrophages, dendritic cells, and B cells - they present peptides from extracellular pathogens.
321
How do CD4 and CD8 T cells interact with MHC molecules?
- T cell receptor binds to both the MHC molecule and the antigenic peptide - Necessary to trigger an immune response
322
What is the role of cytotoxic CD8 T cells in the immune response?
Recognize and kill cells that are infected with pathogens - cells infected with viruses, malaria parasites, or Toxoplasma - Upon recognition, they deliver a death signal to the infected cell
323
How do innate and adaptive immunity cooperate for effective protection?
Antigen-presenting cells of the innate immune system, such as dendritic cells - Pick up antigens from an infection site and activate T cells in the lymph nodes - Activated T cells then return to the site of infection and control innate effector responses through the local secretion of cytokines.
324
What are cytokines?
Cell signalling molecules - Aid in cell-to-cell communication in immune responses
325
What are CD4 T cell subsets and what roles do they play?
Cells can differentiate into several subsets, including Th1, Th2, Th17, and Treg cells, each with its own function.
326
What is the role of Th1 cells?
Produce interferon gamma - which activates macrophages
327
What is the role of Th2 cells?
Produce interleukin 4 - activates cells like eosinophils and basophils
328
What is the role of Th17 cells?
Role in neutrophil activation and inflammatory responses
329
What is the role of Treg cells?
Help suppress the immune response to prevent damage to the body's own cells.
330
What are the key cytokines that drive Th1 cell development?
Interleukin-12 (IL-12)
331
What are the key cytokines that drive Th2 cell development?
Interleukin-4 (IL-4)
332
what are signature cytokines of Th2 response?
Signature cytokines IL-4, IL-5, IL-9, and IL-13
333
What are signature cytokines of Th1 response?
Gamma interferon - IFN-gamma
334
What is the Thp cell?
Unpolarized CD4+ T cell - Can differentiate into either a Th1 or Th2 cell - depending on the cytokines it encounters
335
What is the role of dendritic cells (DC) and macrophages (Mo) in the Th1/Th2 cell development model?
Dendritic cells and macrophages are antigen-presenting cells - They uptake, process, and present antigens to T cells, along with the appropriate cytokines - Drive the differentiation of the T cells - IL-12 produced by these cells can stimulate Th1 cell development, while IL-4 can stimulate Th2 cell development
336
How does the immune response change in chronic vs acute infection according to the Th1/Th2 cell development model?
Acute infection - the immune response tends to be dominated by Th2 cells - activate cells like eosinophils and basophils Chronic infection - the immune response tends to be Th1-dominant - activates macrophages and promotes inflammation.
337
Briefly describe T. muris - resistant and susceptible host immune response?
T. muris is a gut-dwelling nematode parasite - partially invades intestinal epithelial cells In a resistant host - leads to a Th2 response and acute infection Susceptible host - Th1 response is elicited, leading to chronic infection.
338
What are filarial nematodes?
Tissue dwelling nematode parasites
339
What are the two main types of Filariasis?
- Lymphatic filariasis (caused by Wuchereria bancrofti or Brugia malayi) - Onchocerciasis (caused by Onchocerca volvulus).
340
What is the pathology of Onchocerciasis?
- Dermatitis - “river blindness” - damage to cornea in eye.
341
What is the most common feature of Lymphatic filariasis?
Hydrocele - Worms like lymphatics around the scrotum leading to fluid accumulation - In endemic areas, 40-60% of adult males have hydrocoeles
342
How does Onchocerciasis affect the skin and eyes?
Adult worms live over bony prominences - larvae circulate in the skin - causing damage to elasticity, itching, aging, and depigmentation. - If larvae migrate across the cornea, they can cause opacity leading to blindness.
343
Where do the parasites lodge in Lymphatic filariasis?
Lymphatic system
344
How long do the parasites live and what do they produce in Lymphatic filariasis?
- several years within the human lymphatic system. - produce immature larvae called microfilariae - circulate in the bloodstream and lymphatic vessels
345
What is the life cycle of the parasites in Lymphatic filariasis?
Adult females release microfilaria larvae which circulate in blood - Microfilaria is taken up by the mosquito vector penetrates the thoracic muscles of the mosquito - Develops from 1st to 3rd stage larvae in the mosquito - The 3rd stage is released into the human host upon biting
346
Where is Lymphatic filariasis a problem?
Large parts of South America, Africa, and Asia.
347
What is produced by the parasites in Lymphatic filariasis?
millions of microfilariae which circulate in blood.
348
What is the vector of Onchocerciasis?
Simulium (black fly)
349
What causes the suffering and disability in Lymphatic filariasis?
Pathology - adult worms living in lymphatics/sinuses of lymph node causing dysfunction and inflammatory damage Dilation of lymphatics - Thickening of vessel walls, incompetent lymph valves, ultimately blockage of lymphatics (especially on death of the worm)
350
What conditions are caused by filariasis pathology?
- Hydrocoele - Elephantiasis of arms and legs - Local inflammation of lymph nodes (filarial fever)
351
What is the global burden of Lymphatic filariasis?
Total number afflicted is around 120,000,000
352
How does elephantiasis manifest in Lymphatic filariasis?
- Legs become swollen due to dysfunction of lymphatics leading to fluid accumulation - skin becomes cracked - allowing bacteria and fungi to flourish
353
What is chyluria in the context of Lymphatic filariasis?
Worms living in and damaging the lymphatic system - result of hidden internal damage to kidneys and the lymphatic system - intermittent discharge of lymph into urine
354
What is the treatment approach for Lymphatic filariasis?
Interrupt transmission - Eliminate microfilariae from the bloodstream - with drugs (ivermectin) Control morbidity - assisting lymph flow and preventing secondary infections
355
What are the eye manifestations of Onchocerciasis?
Microfilariae migrate to the eye - where they die - causing inflammation, scarring, impaired vision, and potentially blindness - Onchocerciasis is the second leading cause of blindness of infectious origin
356
What are the skin manifestations of Onchocerciasis?
Chronic dermatitis - intense itching - subcutaneous inflammatory response due to dying microfilariae - thickened "lizard skin" - lax skin due to destruction of elastic fibers - potential loss of pigment "leopard skin"
357
What are the levels of antigen-specific IgG and IgE in filariasis?
- Endemic normals make low levels of antibodies across all isotypes. - Elephantiasis individuals produce high levels of antibodies across each isotype. - Microfilaraemics produce high levels of IgG4 and very little IgE - not sure this flashcard is helpful but hay ho
358
Why is the IgG4/IgE ratio important in the immune response in Lymphatic filariasis?
- High IgG4 levels may reduce some pathology - If IgE is needed to get rid of the worm - Excessive IgE-mediated ADCC can contribute to tissue damage and worsen the pathology (antibody-dependent cell-mediated cytotoxicity)
359
What is the role of IgG4 in immune response to lymphatic filariasis?
- high levels of IgG4 antibodies can compete with IgE for binding to the same antigens. - "blocking" of the antigen - preventing IgE-mediated immune response triggering a strong inflammatory reaction - limiting tissue damage
360
What is the characteristic of T cell response in MF+ individuals in lymphatic filariasis?
Poor T cell response - resulting in hyporesponsiveness
361
What is the difference between MF- and MF+ individuals?
- MF- individuals do not have microfilariae (larval stage) in their blood - while MF+ individuals do have microfilariae present
362
What do reduced IFN-gamma and intact IL-4 responses to microfilaria suggest about an MF+ individual?
Reduced IFN-gamma response: - MF+ individuals show a reduced production of interferon-gamma (IFN-gamma) - associated with Th1 immune responses. - suggests an impaired cellular immune response against the filarial parasites Intact IL-4 response: - cytokine associated with Th2 immune response. - IL-4 is involved in promoting antibody production, particularly IgE - plays a role in the immune response against microfilariae.
363
Which type of cytokine is inhibited in MF+ individuals filarial infections?
IFN-gamma - Th1 cytokine response
364
What is the effect of drug treatment on the responsiveness of immune cells in filarial infections?
restore responsiveness to some extent in filarial infections
365
Give an example of a drug used in treatment of filarial infections?
Diethylcarbamazine - kills parasites - partially restores both T cell responses and IFN-gamma production
366
What is the cellular response observed in asymptomatic microfilaraemic individuals with lymphatic filariasis?
Reduced T cell responses - high levels of IL-4, IL-10, and TGF-beta - low levels of IFN-gamma
367
What is the effect of DEC (diethylcarbamazine) treatment on T cell responses and IFN-gamma production in lymphatic filariasis?
EN (endemic normals) and individuals with elephantiasis tend to have low worm numbers but higher IFN-gamma levels.
368
What are the characteristics of Tregs (regulatory T cells) in lymphatic filariasis?
can dampen both TH1 and TH2 responses. They are associated with high levels of IL-10 and TGF-beta.
369
How can the action of activity of Tregs in lymphatic filariasis be countered?
Blocking IL-10 can partially restore proliferation
370
What is a challenge in treating neglected tropical Intestinal dwelling nematodes with drugs?
- developing single nucleotide polymorphisms (SNPs) that confer resistance to the available drugs - leaving few effective options for treatment
371
What are the main species causing human intestinal nematode infections?
- Trichuris trichiura (whipworm) - Ascaris lumbricoides (roundworm) - Necator americanus (hookworm) - Ancylostoma duodenale (hookworm)
372
What is the life cycle of Ascaris lumbricoides (roundworm) and Trichuris trichiura (whipworm)?
- Adults in intestine lay eggs - Develop outside the host (Ascaris - infective L2 stage larvae) (whipworm - infective 1st stage larvae) - ingested by host - larvae hatch in the intestine - migrate through tissues to the lungs - move up trachea then swallowed - Mature into adults in the intestine
373
What is the difference in the life cycle of the Hookworms Necator americanus and Ancylostoma duodenale?
Necator americanus - obligate skin-penetrating hookworm Ancylostoma duodenale - alternate route - infective third-stage larvae (L3) can be swallowed and passed directly to the gut
374
According to WHO, what is the global burden of soil-transmitted helminth infections? What percentage of infections occur in the developing world?
- More than 1.5 billion people (24% of the world population) are infected with soil-transmitted helminths - 70% developing world
375
Why do children born in endemic areas harbor worms for most of their lives? (Intestinal nematode infections)
Repeated exposure and an inability to develop protective immunity against them - Even though immune recognition and attack - Parasites survive - Evolved mechanisms to combat host defence ie. evade/modulate host attack
376
What are the biological features of intestinal nematode infections?
- Long-term persistence - Elicit immunity only after years, or even decades, of exposure - Show an overdispersed distribution
377
What is the common pattern of intestinal nematode infections distribution in communities?
Aggregated (overdispersed) distribution - meaning certain areas carry a higher worm burden
378
What are the clinical syndromes associated with high-intensity intestinal nematode infections?
- Anaemia - Abdominal pain, colitis, diarrhea, dysentery - Growth stunting Rarely - finger clubbing - rectal prolapse
379
Describe the trend in prevalence of intestinal nematode infections in a population?
Reaches 90% and stabilises
380
What is the intensity of infection in the context of helminth infections and what does it tell us?
- Measurement of the number of parasite eggs or worms per gram of feces - provides information about the parasite burden within an individual
381
What can the intensity of infection indicate?
- provides information about the parasite burden within an individual - insights into morbidity and disease severity
382
Explain why the convex age intensity profile is often during childhood (intestinal nematode infections)?
Influenced by Acquired Immunity: resulting from years of exposure to the parasite - repeated exposure lead to development of protective response Differences in Exposure: Children may have higher rates of exposure - due to factors such as environmental conditions, behavior, or cultural practices (hygiene practices & behavioral differences) Susceptibility: due to their developing immune systems - individuals reach adulthood, their immune system matures - leading to decreased susceptibility
383
What does the convex age intensity profile indicate?
Characterized by a peak in infection intensity during a specific age group, often children, indicates several potential factors at play - Children may be more susceptible to infection due to their developing immune systems and reduced ability to mount an effective immune response
384
What is the relationship between worm burden and reacquisition of infection?
- Individuals with high worm burden tend to reacquire high worm burden after treatment, suggesting a predisposition for a specific infection level. - Wormy individuals tend to reacquire similar worm burdens faster compared to those who are less predisposed.
385
Describe typical field study structure for intestinal nematode infections
Select population for study - typically 100-200 people divided into age cohorts. - Estimate current intensity of infection via eggs/g faeces +/or counting worms after anthelmintic treatment - Take blood samples pre and post-treatment - Assess reinfection levels over 1-2 years and take new blood samples Analyse peripheral IRs in relation to - Infection intensity, reinfection levels, worm fecundity +/or weight and look for negative correlations
386
What are potential issues during field studies for intestinal nematode infections?
Compliance – teenagers Compliance – need all stool samples within a certain time period to accurately estimate wb
387
What is the prevalence of Trichuris trichiura infection in the human population?
Approximately 1 in 5 individuals in the human population
388
What is the relationship between IgE levels and infection intensity in Trichuris trichiura infection?
- IgE levels are negatively correlated with infection intensity - High levels of parasite-specific IgE suggest a strong immune response - associated with Th2 immunity
389
What is the evidence for acquired immunity in human trichuriasis?
As infection intensity decreases with age, IgE levels continue to rise - High levels of parasite-specific IgE suggest a strong immune response associated with Th2 immunity
390
What is the role of IL-4 in controlling IgE production (Trichuris trichiura)?
IL-4 is a cytokine associated with Th2 immune responses - very important for making IgE
391
What is a serum biomarker for in Trichuris trichiura?
Th2 immune response - IgE and IL4
392
How many people worldwide are infected with hookworm? and which species is most common?
Approximately 1.3 billion people worldwide - predominantly Necator americanus
393
What is the average worm load in hookworm (Necator americanus and Ancylostoma duodenale) infection?
Approximately 40 worms per infected individual
394
How much blood loss occurs per day due to hookworm infection?
estimated 5.1 million liters of blood loss per day worldwide
394
How much blood loss occurs per day due to hookworm infection?
hookworm infection leads to an estimated 5.1 million liters of blood loss per day worldwide.
395
What cytokine is associated with resistance to hookworm (Ancylostoma duodenale and Necator americanus) reinfection?
- presence of IL-5 - type 2 response - Promotes activation of eosinophils
396
Why do we need laboratory models of intestinal nematode infection?
understand the basis of chronic infection and resistance to infection - provide controlled conditions, defined infection history, and manipulable systems, allowing researchers to study the immune response and effector mechanisms involved in these infections.
397
What are the common features in resistance to intestinal nematode infection?
398
What is the lifecycle of Trichinella spiralis?
Upon digestion of the meat by the new host - larvae are released - Rapid development (L1-L4) and molting occur in the intestine Viviparous females lay live larvae (L1) - muscle larvae then penetrate the intestine - enter blood vessels then migrate to the muscles - where they encyst - muscle larvae develop within the nurse cell complex - muscle larvae remain dormant until the host is eaten
399
How has the key role of CD4+ helper T cells in resistance to Trichinella spiralis been demonstrated?
- Adoptive transfers and in vivo depletions of T cells - shown that mice without CD4+ T cells become susceptible to infection
400
What study on in whipworm showed the importance of T cells in immunity?
Mouse model infected with whipworm (Trichuris muris) showed that nude mice - which lack T cells - unable to expel the parasite
401
What are the CD4+ T helper cell subsets and their regulatory mechanisms?
Th1 cell development - driven by IL-12 - produces interferon gamma (IFN-gamma) Th2 cell development - driven by IL-4 - involved in antibody production and inflammation
402
Why is the lab model of Trichuris muris considered useful?
Mouse whipworm - shares similarities with the human parasite Trichuris trichiura - allows investigation of immune responses involved in both acute infection (resistance) and chronic infection (susceptibility)
403
What is the life cycle of Trichuris muris in mice?
- Ingestion: eggs typically present in contaminated food and water - Egg Hatching: inside intestines, the eggs hatch, releasing larvae - Penetrate the intestinal wall and migrate to the colon where they develop - Larvae mature into adult whipworms within the cecum and colon of the mouse - Produce eggs, passed in the mouse's feces into the environment
404
What response is seen in susceptible mice to Trichuris muris?
Type 1 immune response - characterized by production of IFN-gamma
405
What cytokine responses are associated with resistance to Trichuris muris infection?
Th2 immune response - characterized by production of cytokines such as IL-4, IL-5, IL-9, and IL-13.
406
What is the role of IgG1 and IgG2a antibodies in Trichuris muris infection?
Th2 response - leads to the production of IgG1 antibodies - resistant Th1 response - switch to IgG2a antibodies controlled by gamma interferon - susceptible
407
Which cytokines are associated with rapid expulsion of Trichuris muris in BALB/c mice?
Production of IL-4, IL-9, and IL-13 in the mesenteric lymph nodes.
408
What happens when IL-4R is blocked in BALB/c mice infected with Trichuris muris?
Inhibition of the Th2 immune response - no expulsion of the parasite
409
What happens when IL-4 is knocked out in mice on a resistant background during Trichuris infection?
Susceptible - unable to produce Th2 responses.
410
What happens when IL-13 is knocked out in mice on a resistant background during Trichuris infection?
Delayed Th2 responses - become susceptible to infection
411
What type of T cell response is associated with susceptibility to Trichuris infection?
TH1 type response - lead to chronic infection
412
Which nematode species exhibit a protective immune response involving IL-4 and Th2 cells?
Trichinella, Trichuris, and Heligmosomoides polygyrus
413
What are the common effector mechanisms associated with intestinal helminth infections?
Eosinophils and IgE - Type 1 hypersensitivity response - Their direct role in resistance is difficult to demonstrate
414
Is IL-4 essential for resistance to Nippostrongylus infection?
IL-4 is not essential for resistance to Nippostrongylus infection - there are IL-4 independent mechanisms of expulsion that exist
415
Are eosinophils essential for the expulsion of parasites?
Not essential for the expulsion of parasites. - Depletion of eosinophils or the absence of eosinophils in genetically deficient mice does not prevent the expulsion of parasites
416
Does IL-5 play a role in eosinophil development?
IL-5 is critical for eosinophil development - Depletion of IL-5 leads to a lack of eosinophils.
417
What is the role of mast cells in intestinal helminth infections?
- Non-specific inflammatory responses - Create hostile environment with their proteases
418
What evidence suggests mast cells are not essential for getting rid of helminth worm infections?
- mice depleted of mast cells can still expel Nippostrongylus and Trichuris parasites
419
Are mast cells important in the resistance to Trichinella infection?
Play a role in the resistance to Trichinella infection - suggesting their potential importance in this particular helminth infection.
420
What is mastocytosis?
Characterized by abnormal accumulation and proliferation of mast cells in various tissues of the body
421
What are Antibody's role in resistance to intestinal helminths?
No evidence to support the importance of antibody in resistance.
422
Describe immune serum as a method of producing helminth immunity
Blood serum obtained from individuals who have developed a robust immune response against helminth infections - contains high levels of antibodies specific to the parasite - passively transfer resistance to naïve individuals by administering large volumes of serum - temporary immunity against helminth
423
Describe Interleukin-4 (IL-4) and Interleukin-13 (IL-13)
Th2-type cytokines - can act as effector molecules in immune response against helminth infections.
424
Direct effects of IL-4 and IL-13 on gut epithelial cells
Increase fluid secretion, contractility, and epithelial cell turnover - Effects inhibit feeding and make it harder for helminths to survive in the gut - constantly being expelled along with the shedding of epithelial cells
425
Describe goblet cell hyperplasia
Controlled by Th2 cytokines - promote the expansion and activation of goblet cells - leading to increased mucin production and mucus secretion - defense mechanism against the invading pathogens, trapping and expelling the parasites from the body.
426
What is the significance of Muc5ac in the expulsion of intestinal helminths?
Muc5ac-deficient mice are unable to expel these parasites - crucial role of this mucin in the protective immune response
427
Describe the effector Mechanisms in Protective Immunity to Intestinal Nematodes
Antigen Presentation - Worms burrow in gut epithelial cells and secrete/excrete antigens - Antigens are picked up by antigen-presenting cells (APCs) Antigen Processing and T Cell Activation: - Antigens are processed by APCs and presented to T cells in draining lymph nodes - T cells are exposed to parasitic antigen peptides and become polarized into Th1 or Th2 cells depending on cytokine milieu T Cell Homing and Migration: - T helper cells circulate using homing receptors to follow chemotactic signals and reach the site of infection Cytokine Release: - Th2 cells release IL-13, which can increase gut epithelial cell turnover and facilitate the expulsion of worms from the gut
428
What are the two species of Trypanosoma causing African Trypanosomiasis?
- Trypanosoma brucei gambiense - Trypanosoma brucei rhodesiense
429
Which species of Trypanosoma causes a chronic infection?
Trypanosoma brucei gambiense
430
Which species of Trypanosoma causes an acute infection?
Trypanosoma brucei rhodesiense
431
What is the term for African Trypanosomiasis when found in cattle?
Nagana
432
Which animals have been shown to harbor Trypanosoma brucei rhodesiense?
Bush pigs, zebras, hippos, and warthogs. - wild mammals
433
Which animals have Trypanosoma brucei gambiense been found in?
Cattle and pigs.
434
How are african trypanosomes transmitted to humans?
Tsetse fly bite - genus Glossina
435
How many new cases of trypanosomiasis are reported each year?
300,000 new cases.
436
What factors have contributed to the increase in sleeping sickness cases?
Independence of many countries, civil war, and changes in health policies.
437
Which form of sleeping sickness is more prevalent in West Africa?
The chronic form - Trypanosoma brucei gambiense
438
Is the East African form (Trypanosoma brucei rhodesiense) of sleeping sickness increasing or declining?
Declining
439
What are the initial clinical signs of sleeping sickness?
Fever, weakness, headache, swollen lymph nodes, joint pains.
440
What are the symptoms in the advanced stages of sleeping sickness?
Anaemia, heart problems, oedema, central nervous system invasion leading to concentration difficulties, lethargy, coma, and death.
441
What is the current drug in use for treating sleeping sickness?
Melarsoprol - Arsenic-based drug with serious side effects - 1000 die each year from arsenic encephalopathy DFMO - also known as eflornithine - safer and more efficacious
442
What are the two morphologies of African trypanosomes in blood smears?
Slender form and stumpy form
443
Do African trypanosomes invade cells?
No, they do not invade cells unlike T. cruzi
444
What are the characteristics of African trypanosome morphology?
- free-swimming single-celled protozoans - long, thin body, a flagellum, and an undulating membrane. - kinetoplast at the front
445
What is the role of the stumpy form of African trypanosomes?
- stumpy form is taken up by the tsetse fly and transmits the infection - undergoes development to become the infective metacyclic form in the salivary glands of the tsetse fly
446
What is the infective stage of African trypanosomes?
Metacyclic trypomastigote
447
What happens when a tsetse fly bites an infected mammalian host?
Only the stumpy forms of trypanosomes survive in the tsetse fly - differentiate into procyclic trypomastigote - epimastigote - ending up in the salivary glands as infective metacyclic trypomastigote
448
Different stages in the lifecycle of African Trypanosomes:
- Procyclic stage: Ingested by the tsetse fly and multiplies in the midgut. - Epimastigote stage: Attached to the midgut wall of the tsetse fly vector. - Metacyclic stage: Infective stage in the salivary glands of the tsetse fly. - Slender form: In the bloodstream of the mammalian host, actively dividing. - Stumpy form: Non-dividing, pre-infective form in the bloodstream
449
What is the surface molecule responsible for antigenic variation in Trypanosomes?
Variable Surface Glycoprotein (VSG)
450
What is the composition of VSG in Trypanosomes?
VSG makes up approximately 10% of the dry weight of the organism.
451
What type of forms are dominant in the bloodstream of a mammalian host in African trypanosomes?
Slender forms are the majority, while a few stumpy non-dividing forms are also present.
452
What is the effect of antibodies on trypanosomes expressing the dominant VSG?
kill 99.999% of trypanosomes expressing the dominant VSG - complement fixation and opsonization
453
Why doesn't antibody-mediated killing eliminate all African trypanosomes?
Altering expression of VSG coat - unrecognizable by antibodies - allowing them to continue multiplying
454
How can a slight change in the amino acid isomer on an epitope prevent antibody interaction? (African Trypanosomiasis)
Changing the isomer of an amino acid on an epitope - enough to eliminate antibody interaction with the trypanosome
455
How do antibodies interact with complement to combat trypanosomes? (African Trypanosomiasis)
Antibodies can interact with complement to punch holes in trypanosomes, leading to their destruction. - also cause agglutination, clumping the trypanosomes together, which can then be phagocytosed by macrophages
456
What is the difference between homotype and heterotype in trypanosome VSG expression? (African Trypanosomiasis)
Most slender trypanosomes express one type of VSG - referred to as homotype A small proportion (about 1 in 10,000 to 100,000) have switched to express a different VSG, known as heterotype.
457
Is VSG switching triggered by antibody production? (African Trypanosomiasis)
- No, VSG switching is not caused by antibody production. - It is a timed switch of VSG expression that can occur independently of antibody-mediated immune responses
458
What is the estimated repertoire of VSGs in trypanosomes? (African Trypanosomiasis)
approximately 2,000 to 2,500 different types
459
What is the role of the first 20-30 amino acids in the VSG protein? (African Trypanosomiasis)
constitute a signal peptide that is involved in the movement of the new VSG across the parasite membrane.
460
What is the significance of the next 360 amino acids in the VSG protein? (African Trypanosomiasis)
VSG protein are highly variable between different VSGs and contribute to antigenic variation
461
What is the role of the last 120 amino acids at the C-terminal end of the VSG protein? (African Trypanosomiasis)
relatively conserved and are typically involved in anchoring the protein to the membrane
462
What is the function of the GPI signaling molecule in the VSG protein? (African Trypanosomiasis)
responsible for anchoring the VSG protein into the membrane.
463
Why is there a common structure at the bottom of the VSG? (African Trypanosomiasis)
allows for the efficient removal of the fatty acids by a single enzyme, facilitating the exchange of different VSG variants.
464
How does the trypanosome express one VSG at a time? (African Trypanosomiasis)
- has an expression-linked copy (ELC) of the VSG gene, which is duplicated and translocated to a specific site on the chromosomes called the expression site. - Only the copy of the gene located in the expression site is transcribed, allowing for the expression of a single VSG variant - unique mechanism among single-celled organisms.
465
Where are the expression sites typically located in the trypanosome genome? (African Trypanosomiasis)
usually found near telomeres, preserving the original VSG gene while allowing for the expression of a specific variant.
466
How is the switch from one VSG gene to another achieved? (African Trypanosomiasis)
degradation of the existing copy of the gene - opens up the expression site for a new VSG gene to be copied and translocated
467
Are all VSG genes expressed by duplicating and translocating them to expression sites near telomeres? (African Trypanosomiasis)
Those already located near telomeres
468
How do trypanosomes achieve a large number of telomeres despite having a relatively normal amount of DNA? (African Trypanosomiasis)
- more telomeres than usual by having an array of different-sized chromosomes - arrangement provides them with numerous telomere sites for the placement of VSG genes and enables the expression of a large repertoire of VSG variants.
469
How can recombination contribute to the generation of variation in VSG genes?(African Trypanosomiasis)
Recombination can occur between telomere-linked genes that code for different segments of a VSG gene - leads to the "joining" of these segments, resulting in the generation of a VSG gene with combined characteristics - novel VSG gene combinations.
470
Why are telomeres considered recombination hotspots in trypanosomes? (African Trypanosomiasis)
highly repetitive stretches of DNA, including short tandem repeats - prone to recombination events
471
What is the significance of the Expression Site Body in trypanosomes? (African Trypanosomiasis)
specialized compartment found in the nucleolus of trypanosomes - site where the expression of a single Variant Surface Glycoprotein (VSG) gene occurs at any given time - sequesters all the necessary molecules required for gene expression, ensuring that only one VSG is expressed - unique feature observed only in African trypanosomes
472
What enzyme is involved in the transcription process within the Expression Site Body and why is it surprising? (African Trypanosomiasis)
RNA polymerase I (Pol I) - Pol I is typically associated with the transcription of ribosomal RNA rather than protein-coding genes.
473
How do trypanosomes control the balance between stumpy and slender forms? (African Trypanosomiasis)
- quorum sensing - population of healthy slender forms reaches a certain threshold - release peptidases that break down host and parasite-derived proteins into oligopeptides. - oligopeptides are reabsorbed by the slender forms - triggering their transformation into the stumpy form.
474
What is the initial step of Leishmania infection in macrophages?
promastigote form of the parasite invades macrophages - subverts the process of phagocytosis to establish a parasitophorous vacuole - provides a protected niche for the parasite to survive and replicate within the host cell
475
What are the two major groups of lymphocytes involved in the adaptive immune response?
T cells and B cells
476
Why are inbred strains of mice used in experiments with Leishmania infection?
- represent a genetically identical population. - better control of host genetics when studying immune responses - facilitates tissue transplantation between animals without rejection.
477
How was the basis for the difference in controlling early Leishmania infection investigated?
- by conducting backcrossing experiments between a resistant strain and a susceptible strain of mice - F1 generation was backcrossed onto the resistant strain, and animals that remained susceptible were selected and further backcrossed - process was repeated several times until mice with all resistant strain genes except for one, which conferred susceptibility, were obtained - response to Leishmania infection in these mice was analyzed and compared to the original resistant strain
478
What was the main finding regarding the control of early Leishmania infection based on the backcrossing experiments?
- control of early Leishmania infection is primarily governed by a single genetic locus - susceptibility or resistance to the infection in mice can be attributed to specific genetic factors.
479
Describe Genetic Susceptibility Study in Leishmaniasis using Backcrossing Experiments
- Select mice: Inbred mouse strains are selected based on their genetic background Infect mice: by injection into the footpad or by exposure to infected sandflies. - Monitor infection: signs of infection, such as swelling of the footpad, weight loss, and parasite load in tissues. - Determine susceptibility: most susceptible strains will show more severe disease symptoms and higher parasite loads than the least susceptible strains. Backcrossing: To study the genetic basis of susceptibility, backcrossing experiments - breed susceptible mice with mice that have a known genetic resistance to leishmaniasis - The resulting offspring will have a mixed genetic background, but will inherit the resistant genes from the resistant parent
480
What is the gene called that controls susceptibility to Leishmania and other macrophage-infecting pathogens?
Lsh (Leishmania susceptibility gene) or N-ramp (natural resistance associated macrophage protein).
481
What is the function of the N-ramp gene? (Leishmania)
encodes a divalent ion transporter molecule, although its exact function is not fully understood.
482
How was the N-ramp gene identified? (Leishmania)
genetic analysis and backcrossing experiments with congenic mice, researchers identified mutations in the N-ramp gene in strains that varied in their ability to control Leishmania infection.
483
What other macrophage-infecting pathogens are controlled by the N-ramp gene? (Leishmania)
implicated in controlling susceptibility to other pathogens, such as Salmonella and Mycobacteria
484
What is the major pathway used by macrophages to deal with intracellular parasites? (Leishmania)
nitric oxide pathway is the major pathway used by macrophages to combat intracellular parasites.
485
How is nitric oxide (NO) produced in macrophages? (Leishmania)
use oxygen and nitric oxide synthase to produce nitric oxide, as well as nitrites and nitrates.
486
What is the role of nitric oxide in killing intracellular pathogens? (Leishmania)
toxic to organic molecules in its vicinity and is used by macrophages to kill intracellular pathogens, along with superoxide.
487
How does nitric oxide enter the parasitophorous vacuole to kill the parasite? (Leishmania)
readily diffuse across lipid membranes
488
How does N-ramp contribute to killing parasites? (Leishmania)
- N-ramp concentrates nitrite ions in the parasitophorous vacuole - converted into nitric oxide (NO) in the acidic pH. - Nitric oxide is toxic to parasites and helps in their elimination.
489
What is the structure of N-ramp? (Leishmania)
- transmembrane molecule with N-terminal and C-terminal regions. - embedded in the membrane and functions as an ion transporter.
490
How can a mutation in N-ramp affect the control of early Leishmania infection?
Certain mutations, such as a glycine to aspartic acid substitution, can alter its ability to transport ions
491
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492
How does the transport activity of Nramp-1 depend on pH? (Leishmania)
faster transport rate observed in more acidic environments
493
What is the role of Nramp-1 in transport? (Leishmania)
- divalent cation transporter - ability to extrude manganese (Mn2+), iron (Fe2+), and zinc (Zn2+) from macrophages at a faster rate in Nramp-1 positive macrophages - starves the parasite of vital cofactors and introduces toxic nitric oxide (NO) - killing of the parasite.
494
What activates macrophages to become effective killers? (Leishmania)
- IFN-γ is produced by CD4+ T cells, specifically Th1 cells. - Interferon-gamma (IFN-γ) activates macrophages
495
Are CD4+ T cells important in leishmaniasis?
- orchestrate aspects of adaptive immunity through cytokine secretion - including the production of IFN-γ, which activates macrophages.
496
What is adoptive transfer of immunity and what can it be used to gain insight into? (Leishmania)
- involves transferring immune cells (such as lymphocytes) from resistant mice into naïvemice to evaluate their impact on infection control - Adoptive transfer of immunity can be tested to understand the importance of specific genes or immune cells.
497
What are the benefits of using inbred mice strains during adoptive transfer studies? (Leishmania)
- done without fear of tissue rejection - allows for the precise investigation of the impact of transferred immune cells on infection outcomes.
498
What were the findings of adoptive transfer studies in leishmaniasis?
- adoptive transfer of CD4+ T cells into naïve animals resulted in faster healing and disease control. - In contrast, recipient animals that received random CD4+ T cells from uninfected mice showed disease progression similar to normal
499
What happened in adoptive transfer studies using BALB/c mice? (Leishmania)
- BALB/c mice, which are poor at controlling leishmaniasis, exhibited worsened disease outcomes in adoptive transfer studies. - CD4+ T cells from infected BALB/c mice were transferred to naïve mice, the infection progressed more rapidly.
500
What is the underlying reason for the difference in adoptive transfer outcomes between C3H and BALB/c mice? (Leishmania)
- attributed to the immune response bias of BALB/c mice - have Th2 bias, which is effective in expelling the gastrointestinal parasite Trichuris muris but ineffective in controlling leishmaniasis
501
What cytokines are produced by Th1 cells? (Leishmania)
Th1 cells produce large amounts of Interferon-gamma (IFN-γ) and IL2. They do not produce IL4, IL5, IL6, IL9, and IL10.
502
What Th1 and Th2 responses both produce? (Leishmania)
IL3 and GM-CSF - mainly remember IL3 not sure where GM-CSF has come from
503
What cytokines are produced by susceptible mice in response to Leishmania infection?
- high levels of IL4 and low levels of Interferon-gamma (IFN-γ) - also produce cytokines such as IL5, IL6, IL9, and IL10. - Characteristcs of Th2 response
504
What cytokines are produced by resistant mice in response to Leishmania infection?
high levels of Interferon-gamma (IFN-γ) and low levels of IL4. Their response is characterized by a Th1 immune profile.
505
How do Interferon-gamma (IFN-γ) and IL4 interact in the immune response to Leishmania?
counter-regulate each other. An Interferon-gamma dominant response suppresses the generation of a Th2 response.
506
What is the effect of neutralizing IFN-γ with antibodies? (Leishmania)
Neutralizing IFN-γ leads to non-cure and exacerbation of the disease.
507
What is the effect of neutralizing IL-4 with antibodies? (Leishmania)
leads to cure and protection against the infection.
508
What does the size of the lesion indicate in the resistant and susceptible mice? (Leishmania)
size of the lesion is larger in susceptible mice compared to resistant mice.
509
Why is it difficult to study Leishmania in humans?
- researchers can only obtain peripheral tissues (e.g., blood) for analysis - individuals may have other infections or illnesses - challenging to assess the number of times a person has been infected and when these infections occurred.
510
What immune parameters can be measured to assess the immune response to Leishmania in humans?
- Delayed type hypersensitivity (DTH) skin tests, which are indicative of Th1 responses, can be performed - presence of strong anti-Leishmania antibody responses in individuals tends to be associated with worse disease - although antibodies themselves do not play a direct role - The antibody response can serve as a proxy for Th2 response, encouraged by interleukin-5 and interleukin-6
511
What type of immune response is associated with mucosal leishmaniasis?
Strong Th1 response.
512
What is associated with a strong Th1 response in mucosal leishmaniasis?
associated with more severe disease manifestations in mucosal leishmaniasis.
513
What is the significance of a balanced response in cutaneous leishmaniasis?
associated with better control of the infection and milder disease symptoms in cutaneous leishmaniasis
514
Diffuse cutaneous leishmaniasis
A severe form of cutaneous leishmaniasis where the infection spreads extensively throughout the skin.
515
Antibody - describe its relevance in leishmania response
Proteins produced by B cells that play a limited role in combating leishmaniasis. In some cases, a strong antibody response may worsen disease outcomes.
516
Which of these is associated with severe diffuse cutaneous leishmaniasis? - Antibodies / DTH (Delayed Type Hypersensitivity) - Parasite Load / Th1 response - Cytotoxicity / Il-10
Antibodies Parasite Load Il-10
517
Which of these is associated with severe mucosal leishmaniasis? - Antibodies / DTH (Delayed Type Hypersensitivity) - Parasite Load / Th1 response - Cytotoxicity / Il-10
DTH (Delayed Type Hypersensitivity) Th1 response Cytotoxicity
518
What is DTH (Delayed Type Hypersensitivity)? (Leishmania)
- immune response that plays a role in cutaneous leishmaniasis. - indicative of a Th1-type response and is characterized by the recruitment of immune cells to the site of infection - localized inflammation and tissue damage
519
What is the vector responsible for transmitting schistosomiasis?
water snail
520
How are humans infected with schistosomiasis?
come into contact with water containing cercariae, which penetrate the skin.
521
What is a fluke?
Trematode worm - Flukes have complex life cycles and often require multiple hosts, including snails and vertebrates. Schistosomes are flukes
522
How many suckers do flukes have?
2
523
Which animals are commonly used as laboratory models for studying schistosomiasis?
Mice, rats, baboons, rhesus monkeys, and cattle.
524
Do animal models show evidence of immunity against schistosomiasis?
Yes, these animal models show evidence of immunity. - Rhesus monkeys exhibit strong immunity to reinfection - rats can terminate primary infection and develop resistance to reinfection
525
Why is it difficult to establish good models of schistosomiasis in the laboratory?
Schistosomes are not natural parasites of rodents, and they have a longer lifespan than mice
526
In early experiments with Rhesus Monkeys infected with S. mansoni, what were the results regarding immunity? (Schistosomes)
- able to destroy worms from a second infection - but did not destroy the adults that had established from the first infection. - Despite this, immunity could be stimulated by both larval and adult stages of the parasite
527
How was immunity stimulated in the monkeys during the experiments? (Schistosomes)
stimulated by either large numbers of irradiated cercariae (which die before maturity) or by transplantation of adult worms.
528
What is the term used to describe the observed immune response in the monkeys? (Schistosomes)
- referred to as "concomitant immunity." - appears to operate most effectively against larval stages - all stages of the parasite can stimulate immunity
529
What is the structure of the schistosome's tegument?
consists of inner and outer plasma membranes. It is represented by two lipid bilayers covering the surface of the schistosome cells.
530
What changes occur in the body surface of the schistosome when it transitions from water to the host body?
- change in its body surface - loses its protective glycocalyx
531
What is the name of the larval stage of the schistosome?
schistosomulum formed from cercariae
532
How do adult schistosomes survive in the host?
- decreased antigenicity - acquire molecules from the host, including blood group antigens, into their tegument. - camouflage and evade recognition by the immune system
533
What was observed in the experiment involving young and older schistosomula and antibodies?
young and older schistosomula were incubated with antibodies specific to host red blood cell (RBC) molecules or schistosome molecules
534
What were the key findings of the experiment on the acquisition of host blood group molecules by schistosomula?
- young schistosomula had schistosome identity on their surface - older schistosomula acquired host blood group molecules onto their surface membranes. - demonstrated young schistosomula initially displayed schistosome molecules on their surface - as they matured over 4 days, they acquired host blood group molecules onto their surface membranes
535
Briefly describe the experiment that showed the importance of host-specific antigens in schistosome infection and its findings
- worms from a mouse were transferred to a normal monkey - worms covered in mouse molecules that were recognized by the monkey's immune system. - camouflaging allowed the worms to evade the immune response - However, when the monkey had pre-formed immunity against the mouse molecules, the worms were killed
536
What are the mechanisms involved in anti-larval immunity against schistosomes?
action of Antibodies, specifically IgG and IgE and cell-mediated cytotoxicity.
537
How are antibodies involved in killing schistosomula?
- bind to the surface of schistosomula, allowing white blood cells (eosinophils and macrophages) to attach to the parasite - release of cytotoxic granules onto the schistosome surface kills parasite
538
What is the role of cell-mediated cytotoxicity in anti-larval immunity against schistosomes?
- Instead of phagocytosing the large schistosome parasite - white blood cells release cytotoxic granules onto the schistosome surface - effectively killing the parasite
539
How do eosinophils contribute to the killing of schistosomes?
- When schistosomula are mixed with eosinophils and schistosome-specific IgE antibodies - the eosinophils attach to the parasite's surface and release cytotoxic granules - The chemicals from these granules destroy the parasite by causing the membranes to bleb and disrupt.
540
What evidence suggests the presence of acquired immunity in schistosome infection?
- higher prevalence of schistosome eggs in the urine of children compared to adults suggests the acquisition of immunity over time - important to consider factors such as water exposure, as schistosome infection occurs through contact with contaminated water
541
What is the purpose of re-infection studies in investigating resistance to schistosomiasis?
- Re-infection studies are conducted to assess the level of resistance or susceptibility to schistosomiasis in individuals who have previously been treated with praziquantel, the drug used to clear the parasites. - By re-infecting individuals after treatment, researchers can evaluate the effectiveness of the drug and monitor the level of re-infection
542
What need to be controlled and what other factors need to be measured in re-infection studies carried out on schistosomiasis?
- controlling for exposure to water, as water contact is a common mode of transmission for schistosomiasis. - measure snail and cercarial densities
543
What drug is used to treat schistosomiasis?
praziquantel
544
What were the findings of the re-infection study regarding acquired immunity in different age groups? (Schistosomiasis in the Gambia)
- Young individuals tend to reacquire infections at similar levels as before treatment. - As individuals get older and develop immunity, they produce more IgE antibodies and have elevated eosinophils. - Children may have antibodies, but they may not effectively activate the cells required to kill the parasites. - Antibody-mediated resistance takes time to develop
545
Which of these is associated with lower re-infection rates in schistosomiasis?
IgE!! - High IgE can decreased re-infection by 10 times - High IgG4 increased re-infection by 10 times
546
What is the main pathogenic stage of schistosomes?
Eggs
547
What happens when schistosome eggs are present in host tissues?
- release histolytic secretions - antigens present on the eggs are recognized by T helper cells (TH) - release lymphokines - leading to the recruitment of inflammatory cells into the granuloma - immune response results in the formation of granulomas around the eggs
548
What are the consequences of severe granuloma formation in S. mansoni infections? (Schistosomes)
- particularly when eggs are washed back into the liver - can lead to hepatosplenomegaly, esophageal varices, and ultimately death
549
What are the consequences of S. haematobium damage to the bladder and ureter? (Schistosomes)
Damage to the bladder and ureter in S. haematobium infections can result in renal failure and ultimately death.
550
How do schistosomes modulate immune responses?
producing eggs that induce granuloma formation and inflammation. The adult worms themselves do not cause illness.
551
What are the chronic issues associated with egg clearance in schistosomiasis?
can lead to the accumulation of granulomas, liver and spleen enlargement, impaired blood flow, increased blood pressure, and the development of complications such as oesophageal varices and renal failure.
552
What is the purpose of the granuloma response? (Schistosomes)
serves to wall off the schistosome eggs and contain the infection. - protective mechanism aimed at reducing pathology and preventing further dissemination of the parasite.
553
How does the immune response to schistosome eggs change over time?
- immune response produces large granulomas in an attempt to contain the eggs - However, as the infection progresses, the immune response is downregulated, resulting in a decrease in the size and intensity of the granuloma response - mechanism to balance the need to contain the eggs with minimizing chronic disease and tissue damage.
554
Where do adult cestodes live in their definitive host?
Adult cestodes live in the intestine of their definitive host - usually a vertebrate animal including humans.
555
How do cestodes attach to the gut of their host?
suckers or hooks located on their scolex (the small head of the tapeworm).
556
What are proglottids?
- Body segments of cestodes - The mature proglottids, known as gravid proglottids, contain eggs and break off from the end of the worm to be passed out of the host's gut into the environment.
557
What are oncospheres?
larval stage of tapeworms that are released from the eggs - penetrate intestinal wall and circulate to musculature - characterized by a six-hooked structure
558
What are cysticerci?
larval stage of tapeworms found in the tissues of intermediate hosts. They form cyst-like structures
559
What is the definitive host for adult tapeworms?
Humans
560
How do cattle and pigs become infected with tapeworms?
Cattle and pigs become infected with tapeworms by ingesting eggs - containing oncospheres
561
What happens to the oncospheres after they hatch from the eggs? (Cestode)
burrow through the gut wall, invade striated muscle, and develop into cysticerci, where they can remain for several years.
562
How do humans become infected with tapeworms?
consuming infected meat containing cysticerci. The tapeworms then develop into adults in the human intestines over a period of two months.
563
What is cysticercosis and where can it occur in the human body? (Cestode)
- condition caused by the encysted larvae of T. solium in humans. - cysticerci can localize in various body organs, including the eye, liver, and brain. In some countries, up to 20% of all neurological cases are attributed to cysticercosis, such as in Mexico.
564
What percentage of neurological cases are attributed to cysticercosis in Mexico? (Cestode)
Up to 20%
565
What causes hydatid disease?
Echinococcus - cestode
566
What is the smallest tapeworm and how long is it?
Echinococcus - only 3-9mm long - has only 3 proglottids.
567
What are the definitive hosts of Echinococcus?
Carnivores - e.g. dogs, foxes etc.
568
What is the distribution of Echinococcus?
Common in Asia, Australia, East Africa, Southern Spain, S America, Northern parts of N. America and Wales!
569
How does the hydatid cyst evade the host immune response? (Echinococcus)
- laminated layer of the cyst becomes coated with Factor H, a complement inhibitory factor from the host - prevents complement from working and helps the metacestode evade immune recognition.
570
What is the life cycle of hydatid disease? (Echinococcus)
Infection occurs when eggs are ingested, and oncospheres hatch in the gut, enter circulation, and migrate to various organs. - develop into cysts, producing protoscolices and daughter cysts, which can grow very large over months or years.
571
What was the cause of sudden death during a football game due to a hydatid cyst? (Echinococcus)
rupture of a hydatid cyst in the liver during a football tackle caused the fluid from the cyst to move into the tissues, triggering a massive allergic reaction that led to the teenager's sudden death.
572
What are the characteristics of the metacestode stage in hydatid disease? (Echinococcus)
- bound by a thin cellular layer called the germinal layer (GL) - fills with fluid to form a cyst - GL buds on the inside to give rise to brood capsules and protoscoleces - outside of the GL forms an acellular extracellular matrix known as the laminated layer - helps maintain the physical integrity of the metacestode and evades the immune response
573
What are brood capsules? (Echinococcus)
- develop within the metacestode stage of certain cestode parasites - budding structures that form on the inner surface of the germinal layer - contain a cluster of protoscoleces
574
What are protoscoleces? (Echinococcus)
- larval forms of cestode parasites found within the brood capsules of the metacestode stage - small, invaginated structures that have the potential to develop into adult worms - equipped with structures such as hooks or suckers that allow them to attach to the intestinal wall of the definitive host upon ingestion.
575
How does the metacestode develop into the adult stage? (Echinococcus)
metacestode develops into the adult stage when it is ingested by the definitive host (carnivore) - attaches to host gut mucosa - develops into adult
576
What is the composition of the laminated layer in Echinococcus metacestodes?
rich in carbohydrates, particularly mucin-like molecules
577
What is the size of Hymenolepis nana?
also known as the dwarf tapeworm measuring less than 40mm in length.
578
How do humans become infected with Hymenolepis nana?
ingesting embryonated eggs from contaminated food, water, or hands.
579
Why are parasite vaccines difficult to develop?
complexity of parasites, their eukaryotic nature, and their intricate life cycles and antigens.
580
How many vaccines are currently available against human parasites?
only one vaccine available against a human parasite.
581
What are some different types of parasite vaccines?
- live vaccines - attenuated vaccines - dead vaccines - extracts - purified antigens recombinant antigens DNA vaccines - RNA vaccines.
582
What factors need to be considered when developing a parasite vaccine?
- target population (e.g., definitive host, disease-bearing host) - type of immunity desired (sterile immunity or disease-controlling immunity)
583
What is sterility immunity?
- complete protection against infection - prevents the infection from establishing in the host - characterized by the complete elimination of the pathogen or its replication within the host
584
What is disease-controlling immunity?
- aims to minimize the severity of the disease rather than completely preventing infection - individual may still become infected, but the immune response induced by the vaccine helps control the infection and reduce the severity of symptoms
585
Which parasite vaccine was the first to be developed and what was it for?
- Dictyocaulus viviparus - a lungworm infection in cattle that causes husk - major problem in the farming industry
586
Can you describe the life cycle of Dictyocaulus viviparus?
- eggs hatching in the host - releasing larvae that pass out with host feces. - larvae are then ingested by the host during feeding - undergo two molts to become infective - migrate to the lungs - moult to juvenile and then to adults - causing infection and disease.
587
How is the lung worm vaccine produced to prevent full infection?
Irradiate L3 larvae - development into L4 then die - prevents them from reaching the lungs - prevents development to adulthood
588
What is the bottleneck to Huskvac production?
Live larvae must be harvested from feces of infected cattle - then washed, and irradiated.
589
Are there human vaccines available for taeniid infections?
No
590
What is the target of immunity (vaccination) against Taenia in the animal model and why?
Target is the onchosphere (great because it is before it gets to muscle).
591
How is immunity achieved in the animal model of taenia?
antibody-mediated
592
Can immunity be achieved by injecting oncosphere antigens alone?
Yes
593
What is the challenge in vaccinating sheep against T. ovis? (Taenia)
Cannot obtain enough oncospheres to vaccinate all the sheep
594
How did researchers overcome the challenge of vaccinating against T. ovis? (Taenia)
- Recombinant antigens were generated using mRNA from oncospheres - cDNA - expressed in E. coli - screened with antibodies from immune sheep - pick correct antigens - Vaccinate
595
What is T. ovis and why is it significant?
species of tapeworm that infects sheep. It is significant because it was the first-ever recombinant parasite vaccine developed. However, it is not currently in commercial use.
596
Describe use of irradiated sporozoites in malarial vaccination
Irradiated Sporozoites - confer sterile protective immunity in humans
597
How many children does malaria?
400,000 in sub-Saharan
598
Why did it take six years to sequence the Malaria genome?
biased base composition - Plasmodium, the parasite that causes malaria, more than 80% of the bases are either adenine (A) or thymine (T) - challenging to determine the overlapping regions
599
Describe the use of immunoglobulin in malaria
Immunoglobulin from immune donors can transfer protection to non-immune people
600
Who are short term immunity vaccines designed for?
Tourists and Soldiers: For short-term protection during travel or deployment to malaria-endemic regions, vaccines aim to provide disease blocking and reduce the risk of infection. - Cost and storage are typically not major concerns in this context.
601
Who are long term immunity vaccines designed for?
Residents of Endemic Areas: vaccines are designed to confer life-long immunity to individuals living in malaria-endemic regions - need to address challenges related to storage, transport, stability, and ease of use.
602
Describe merozoite antigens as a potential vaccine target - what are the antigen targets
- responsible for the symptomatic blood-stage infection Vaccines targeting merozoite antigens - such as Merozoite Surface Protein 1 (MSP-1) and Apical Membrane Antigen 1 (AMA-1) - aim to elicit an immune response against these antigens to prevent or reduce the severity of the disease.
603
What does the RTS,S/AS01/2 do?
Malarial vaccine - induces high levels of CS repeat specific antibody and IFN-γ production (i.e. a Th1 response)
604
What did trials for RTS,S/AS01/2 vaccine find?
- Recipients of the vaccine were 30% less likely to show fever or early signs of the disease at 6 months - Recipients of the vaccine were 60% less likely to show severe symptoms of disease at 6 months - Fourth dose of the vaccine was crucial to maximize its benefits. - Vaccine did not work sufficiently well in younger infants. - Vaccine rollout initiated in areas with high malaria transmission.
605
What is the modified RTS,S vaccine called?
R21.
606
What is the main protein targeted by the R21 vaccine?
circumsporozoite protein (P. falciparum) in Plasmodium falciparum malaria.
607
Describe an indirect life-cycle
Reproduction of parasite in definitive Release of infective stages (eggs/cysts) into outside environment reinfects into same host again - Uptake of stages by intermediate host - Development of infective stages in intermediate host - Transmission to final host by ingestion of infective stages or of intermediate host Cycle continues
608
What causes Lymphatic filariasis?
Wuchereria bancrofti or Brugia malayi
609
What causes Onchocerciasis?
Onchocerca volvulus
610
What is latin name for whipworm?
Trichuris trichiura
611
What is the latin name for roundworm?
Ascaris lumbricoides
612
Name two hookworms
- Necator americanus - Ancylostoma duodenale
613
What are trematodes?
Class of flatworms known as flukes - obligate internal parasites - requiring at least two hosts - includes blood flukes such as schistosomes

Biology Year 2 (4 decks)

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