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Principles in Infectious Diseases > Unit 3 > Flashcards

Unit 3 Flashcards

1
Q

What is a parasite?

A

Intimate relationship between two organisms in which one (the parasite) lives at the expense of the other (the host).

The relationship involves:
- Nutritional dependence
- Immunological defence
- Integration of life-cycles

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1
Q

Why are parasites important in veterinary medicine?

A

Parasites may cause:
- Death
- Overt clinical disease
- Sub-clinical disease
—> Less than optimum productivity (farm animal production)

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2
Q

What is less than optimum productivity (LOP)?

A

An Iceberg!
Death + clinical disease is the ‘tip of the iceberg’

Below the sea:
- Sub-clinical disease
Failure of a (production) animal to reach its full genetic potential because of sub-clinical parasitism, e.g. poor weight gain

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3
Q

How do we write parasite names?

A

In scientific papers, books and meetings:

Genus/species names:
- Haemonchus contorts (full name)
- H.contortus (short form used after 1st mention)
- Haemonchus sp. (one un-named species of Haemonchus)
- Haemonchus spp. (more than one species of Haemonchus)

Disease name:
- Haemonchosis

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4
Q

What is commensalism?

A

Two species living together, but no metabolic dependence (e.g. hermit crab and sea anemone)

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5
Q

What is symbiosis?

A

Two species living together, each dependent on the other (e.g. ruminants and ruminal flora)

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6
Q

What are some major parasite groups?

A

Helminths

Arthropods

Protozoa

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7
Q

What are some examples of Helminths?

A

Nematodes (roundworms)

Cestodes (tapeworms)

Trematodes (flukes)

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8
Q

What are some examples of arthropods?

A

Insects (fleas, lice, ticks)

Acarina (mites, ticks)

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9
Q

What are some examples of protozoa?

A

Single-celled organisms

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10
Q

What are morphological features of nematodes?

A

Long (mm to >50cm long)

Tough elastic cuticle

Muscular pharynx

Nerve ring around pharynx and four longitudinal

Separate sexes:
- Female worms (blunt, pointed tail)
- Male worms (spicules +- “bursa” - expansion of cuticle covering male tail in bursate worms; absent in non-bursae nematodes

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11
Q

What is the feeding behaviour of nematodes?

A

Some swallow gut ingesta and/or host secretions

Others suck a plug of mucosa into their buccal cavity (or mouth; plug feeders), leaving a circular ulcer

Others bury their heads deep into the mucosa and suck blood

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12
Q

What is the lifecycle of nematodes?

A

Life cycle:
- Basic life cycle very simple:
Egg –> L1 –> L2 –> L3 –> L4 –> Adult worm (or L5)

Many variations on this theme, e.g. Toxocara Canis:

  1. Egg (in faeces)
  2. Eggs ingested by other dog
  3. Larva
  4. Somatic migration
  5. Final host (dog)
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13
Q

What are the morphological features of cestodes?

A

Chain (strobila) of progressively-maturing independent reproductive units (segments or proglottids)

Anchored to intestinal wall by hold-fast organ (scolex, head-end)

Pseudophyllidean tapeworms - scolex has 4 longitudinal ‘grooves’ (important in tropics/subarctic regions)

Cyclophyllidean tapeworms - scolex often have hooks (armed) (global importance)

Each segment - male and female reproductive organs
- Mature segments drop off adult tapeworm daily
- Mature (gravid) segment >100,000 eggs
- Eggs immediately infective (contain tapeworm larva = oncosphere or hexacanth embryo with 6 hooks)

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14
Q

What is the feeding behaviour of cestodes?

A

No alimentary tract

Absorb nutrients across body surface covered by a tegument (many minute projections, microthreces, increase the surface area)

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15
Q

What is the lifecycle of cestodes?

A

Indirect life cycle, e.g. Echinococcus granulosus

  1. Eggs
  2. Eggs ingested by intermediate host, sheep, in faeces
  3. Hydatid cysts form in the liver (and possibly other organs). This is the metacestode stage
  4. Definitive host, the dog, ingests the hydatid cysts from the organs of the sheep
  5. Dog excretes eggs in faeces
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16
Q

What are the examples of epidemiological relationships in cestodes?

A

Predator-prey (e.g. cat eating infected mouse)

Accidental (e.g. horse eating infected pasture mites)

Irritation (e.g. infected flea - swallowed during grooming)

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17
Q

What are the types of metacestode?

A

Vary in the number of developing scolices they carry:
- Cysticerus (one scolex)
- Coenurus (many scolices)
- Hydatid cyst (thousands of scolices)

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18
Q

What are morphological features of trematodes?

A

Typically flat, leaf-like worms (few mms to several cms long)

Oral and ventral suckers

Mouth leads from oral sucker to blind-ending cacao

Most species hermaphrodite, but individuals cross-fertilise

Flukes covered by a metabolically, highly-active tegument - important role in evasion of host immune response

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19
Q

What is the feeding behaviour of trematodes?

A

Suck blood/ingest tissue debris (pumped into cacao)

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20
Q

What is the lifecycle of trematodes?

A

Indirect lifecycle, e.g. Fasciola hepatica

  1. Fluke egg (containing a miracidium)
  2. Mud snail (intermediate host)
  3. Sporocyst, redia, cercaria, metacercaria stages
  4. Sheep - definitive host
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21
Q

What are the morphological features of Arthropods?

A

Great diversity, e.g. insects and acarines

Separate sexes

Insects (3 body divisions, compound eyes, 3 pairs of legs, may have wings)

Acarines (2 body divisions, simple eyes, 4 pairs of legs, no wings, small size)

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22
Q

What is the feeding behaviour of arthropods?

A

Mouthparts show a variety of adaptations:
- Sucking up liquified food
- Sucking blood
- Chewing skin debris
- Not feeding at all

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23
Q

What is the lifecycle of insects?

A

Simple metamorphosis: egg - nymph - adult (e.g. lice)

Complex metamorphosis: egg - larva - pupa - adult (e.g. flies, fleas)

E.g.

  1. Eggs
  2. Larva
  3. Pupa and pupal cases
  4. Adult flea
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24
Q

What is the lifecycle of acarines?

A

Same for mites and ticks:
1. Egg

  1. Larva
  2. Nymph
  3. Adult
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25
Q

What are the morphological features of protozoa?

A

Protozoa are motile, unicellular organisms with a nucleus, endoplasmic reticulum, mitochondria, Golgi body and lysosomes

Great diversity, e.g. Entamoeba Leishmania, Trypanosome

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26
Q

What is the feeding behaviour of protozoa?

A

Pinocytosis (liquid droplets or small particles) or phagocytosis (larger particles)

Eg. bacterium - receptors - phagosome - Lysosome - phagolysosome - soluble debris by exocytosis

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27
Q

What is the lifecycle of protozoa?

A

Variations in:

Complexity:
- Asexual reproduction alone (e.g. simple binary fission, babes)
- Asexual and sexual reproduction (e.g. Eimeria, toxoplasma)

Number of hosts:
- HOMOXENOUS life cycle (= direct), e.g. pultry coccidia (final host, chicken)
- HETEROXENOUS life cycle (=indirect), e.g. Babesia spp (final host, tick; intermediate host, cattle)
- FACULTATIVELY HETEROXENOUS lifecycle (may be >1 host, but not essential), e.g. Toxoplasma (final host, cat; other hosts, any warm-blooded animal)

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28
Q

What is Parasitic Gastro-Enteritis (PGE)?

A

Disease associated with a number of nematode species (singly or in combination)

Characterised by:
- Diarrhoea/weight loss (clinical disease)
- Poor weight gain (sub-clinical disease)
- Seasonal appearance
- Hypoalbuminaemia

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29
Q

What is the economic importance of Parasitic Gastro-enteritis (PGE)?

A

Considerable economic importance in grazing livestock

Potential welfare problem (especially organic farms)

Losses associated with:
- Replacement stock
- Disruption of breeding programme
- Impaired productivity
- Treatment of clinically affected stock
- Prophylaxis

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30
Q

What are the worm species found in Bovine parasitic gastro-enteritis (PGE)?

A

Abomasum:
- Ostertagia
- Trichostrongylus
- Haemonchus

Small intestine:
- Cooper
- Nematodirus
- Trichostrongylus
- Bunostomum

Large intestine:
- Oesophagostomum
- Chabertia
- Trichuris

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31
Q

What do we know about bovine ostertagiosis?

A

Caused by OSTERTAGIA OSTERTAGI:

Primary pathogen of cattle (temperate regions)

Adult worms 1cm long, cotton-like, brown (when fresh)

In the abomasum (fungus)

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32
Q

What is the Life Cycle of Ostertagia ostertagi?

A
  1. Cow grazes and ingests eggs and larvae
  2. Parasitic stages (larvae and adult worms) in the Abomasum of the cow
  3. Cow excretes the eggs
  4. Eggs and larvae free-living on the pasture
  5. Cow grazes and ingests eggs and larvae

PRE-PATENT PERIOD: 3 weeks to 6+ months

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33
Q

What does the rate of infection depend on?

A

Rate of infection depends on the host appetite and the numbers of infective larvae (L3) on the pasture

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34
Q

Where is ostertagiosis most common, why?

A

In Calves!

Because they are grazing permanent pasture and they are kept at high stocking density

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35
Q

Describe the ostertagiosis disease risk over a year:

A

December to May: Moderate disease risk due to housed animals.

June to July: Low disease risk,
Turnout

August to November: High disease risk due to grazing + eggs in pasture

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36
Q

What do we know about immunity to Ostertagia ostertagi?

A

Slow to develop over whole grazing season

May FALL over winter - re-established upon turnout (2nd grazing season)

Adult cattle solidly IMMUNE (no significant role in disease epidemiology)

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37
Q

What is type 1 vs type 2 disease in Ostertagia ostertagi?

A

Type 1:
Type 1 disease caused by Ostertagia ostertagi refers to a parasitic infection in cattle primarily affecting young, grazing animals.

Type 2:
Type 2 disease caused by Ostertagia ostertagi refers to a condition affecting older cattle, typically over one year of age, and is characterized by a distinct pattern of parasitic infection.

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38
Q

What are the stages of type 2 Ostertagia ostertagi?

A
  1. Calves grazing late in autumn
  2. Pre-type 2 phase: Large numbers arrested development EL4 in abomasal mucosa
  3. Type 2 disease: EL4 resume development and emerge in waves
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39
Q

How can we control type 1 disease?

A

Use clean pasture:
- New leys, pasture not grazed by cattle last year
- BUT not always available

Delay turnout until after spring mortality in L3:
- BUT uneconomical use of pasture, supplementary feeding?

Dose ‘n’ move to aftermath (mid-july)
- BUT will not control early season disease
- Increased anthelmintic resistance risk?

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40
Q

What is dose and move?

A

NORMALLY:
Field A (permanent pasture)
Spring (LOW) - Early summer (LOW) - Late summer (HIGH) - Autumn (HIGH)

Dose and move:
Field A (permanent pasture)
Spring (LOW) - Early summer (LOW)
Move to Field B (Hay/silage)
Late summer (LOW) - Autumn (LOW)

41
Q

If there’s no alternative grazing available what can be done?

A

Strategic anthelmintic treatment:
- Repeated treatment AFTER mid-July (but temporary control of egg output only; cattle reinfected)
- Strategic treatment BEFORE mid-July, e.g. doramectin by injection at 0+8 weeks post turn out (5 week residual activity vs Ostertagia)

Intra-ruminal anthelmintic devices:
- Minimise pasture contamination –> decrease auto infection peak in L3
- E.g. Autoworm (Schering-Plough), Panacur bolus (intervet)
- BUT expensive

42
Q

How can we control Type 2 disease in Ostertagia ostertagi?

A

Cattle exposed to LOW challenge at pasture in late Autumn:
- UNLIKELY to require treatment at housing

Cattle exposed to MEDIUM/HIGH challenge at pasture in late autumn or cattle of UNKNOWN origin
- Likely to require treatment at housing

43
Q

What is “Control of Worms Sustainably” In cattle?

A

Voluntary, independent experts provide latest, evidence-based information

Advice on tackling roundworms, lungworm, liver and rumen fluke, lice, mites, ticks and flies

Caring for the welfare of cattle as well as for the environment

COWS technical manual updated Sept 2023

44
Q

What is the general importance of ticks?

A

Major cause of disease and production loss (US $7 billion annually worldwide):
- Blood losses (large numbers –> Anaemia)
- Tick worry (prevents animals feeding)
- Disease transmission
- Tick paralysis (ascending motor paralysis)
- Secondary infection/blowfly strike (at bite site)
- Production losses (farm animals)

45
Q

How are ticks grouped?

A

Divided based on their morphology into:

Hard Ticks:
- Important in temperate and warmer climates

Soft Ticks:
- More important in warmer climates

46
Q

How do you identify Hard Ticks?

A

Scutum (hard dorsal covering)

Prominent mouth-parts

Festoons (or notches) may be present

Ornate ticks have coloured patches

Body wall - convoluted to accommodate blood meal (esp. female ticks)

47
Q

How do you identify Soft Ticks?

A

Scutum (hard dorsal covering) - Absent

Mouthparts - Not visible from dorsal surface

Do not swell much (feed little and often)

48
Q

What is the structure of the mouthparts?

A

Palps: Sensory organs

Chelicerae: Puncture skin

Hypostome: Tube for sucking host blood, backward-pointing teeth

49
Q

How does a tick feed?

A

Tick stands upright

Chelicerae cut through the skin –> Pool of blood

Hypostome inserted deep into skin

Mouthparts cemented in place

Tick feeds continuously and injects saliva (contains substances that decrease host inflammatory response, increase permeability of blood vessels –> Free flow of blood)

50
Q

What is the lifecycle of a hard tick?

A
  1. Egg laying
  2. Larva
  3. Larvae
  4. Nymph
  5. Adult tick

Hard ticks are classified according to the number of different hosts to which they attach during their life cycle:

One Host Ticks: Each stage (larva + nymph + adult) feed on one host, e.g. Boophilus

Two host ticks: Larvae + nymphs feed on one host, adult ticks on a second host, e.g. Hyalomma

Three host ticks: Each stage feeds and develops on a different host, i.e. 3 hosts, e.g. Ixodes

Don’t confuse terms “1-,2-, and 3-host ticks” with host specificity

51
Q

What is the lifecycle of a soft tick?

A
  1. Egg laying
  2. Larva
  3. Larvae
  4. Nymph
  5. Adult tick

Not classified like hard ticks. Feed little and often on many hosts

52
Q

What is trans-stadial disease transmission by ticks?

A

Infectious agent ingested during feeding by larva

Passed on from one host to the next (in 2- and 3- host ticks) as tick develops to nymph and adult

Not passed onto the next generation via the egg

Larva –> Nymph –> Adult –> Eggs

53
Q

What is trans-ovarial disease transmission by ticks?

A

Infectious agent is passed from one generation to the next through the egg, e.g. Babesia spp.

Adult –> Eggs –> Larva –> Nymph –> Adult

54
Q

What do we know about hard ticks in the UK?

A

Ixodes spp. (3-host ticks)
- Worldwide
- I.ricinus, most important tick in the UK
- Distribution: Western UK, mainly
- Wide host range
- Vector for HUMAN disease:
—> Lyme disease (humans, dogs)
- Vector for ANIMAL disease:
—> Bovine babesiosis, louping ill, tickborne fever and tick pyaemia
- Paralysis in humans, dogs (warmer climates only)

Other tick species:
Ixodes canisuga
- Dogs (kennels)

Ixodes hexagonus
- Hedgehogs (also cats, dogs, ferrets, weasels etc)

Haemaphylsalis sp.
- Cattle, uncommon (transmits babesia major, non-pathogenic)

Dermacentor sp.
- Rare (SW England, Essex, Wales)

55
Q

What is the epidemiology of the hard tick Ixodes ricinus in the UK?

A

Three host tick

Life cycle: 3 years (range 2-7 years)

Ticks feed for a few days each year

Most of the time - on the ground

Need high Relative Humidity (>90%) - in matted vegetation (e.g. rough grazing, hedgerows)

Tick activity seasonal (e.g. spring and autumn)

Dependent on temperature + relative humidity

56
Q

What are some hard ticks oversees and the diseases they can transmit?

A

Amblyomma spp (3-host tick)
- Warmer climates worldwide
- Vectors for heartwater (cowrie ruminatium, Africa) also Q-fever, Rocky Mountain spotted fever in southern US)

Boophilus spp. (1-host ticks)
- Warmer climates worldwide, except Europe
- Vectors for Babesia and anaplasma spp. in cattle

Dermacentor spp. (3-host ticks)
Vectors for:
- Viral (tickborne encephalitis, colorado tick fever)
- Ricekttsial (rocky mountain spotted fever, bovine anaplasmosis)
- Bacteria (tularaemia) and
- Protozoal (babesiosis diseases)

Hyalomma spp. (2/3-host ticks)
- Warmer climates, old world
- Wide host range
- Vectors for theileria and babesia spp.
- H.aegyptium found on tortoises (Africa, pet shops, UK)

Rhipicephalus spp. (2/3-host ticks):
- Warmer climates worldwide
- Vectors for theirleria parva (east coast fever), Babesia bigemina (ruminants, Africa), B.canis, ehrlichia Canis (canine pancytopenia)
- Paralysis in livestock

57
Q

What do we know about the soft tick Argas spp.?

A

Infect birds in warmer climates (also humans)

A.persicus, poultry tick (or ‘tampan’), lives in crevices in poultry houses

Feeds at night –> production loss and death (large numbers)

Found on migratory birds in temperate regions

58
Q

What is the epidemiology of ticks in tropical/sub-tropical climates?

A

Ticks may be active all year round

If limited vegetation material –> activity influenced by seasonal rainfall and vegetation

59
Q

What are the principles of tick control?

A

Integrated parasite control:
- Parasite control programmes that do not rely solely on drug treatment
- Example: tick control

Kill ticks on ground:
- By altering microclimate: pasture improvement, e.g. cultivation, drainage
- By starving: “spelling” pasture (livestock removed); useful only if ticks don’t feed on other hosts
- By burning; e.g. during dry period before rainy season

Separate host from infection:
- Stock management: remove stock from tick-infected areas when ticks are active
- Fencing: fence off infested pastures

Kill ticks on host:
- Acaricides: dipping, spraying, pour-on formulations

Enhance host resistance

60
Q

How do we enhance host resistance to ticks?

A

Stock hybridisation: e.g. Bos indicus (humped breeds) crossed with Bos taurus (European breeds).
- Heritability of resistance to ticks is higher in humped breeds than European breeds.

Vaccination: A vaccine is now used in Australia for Boophilus microplus control —> raises antibodies against “hidden antigens” in the tick’s gut

61
Q

How does a tick vaccine work?

A
  1. Tick bites and body detects the salivary antigen, the “hidden” antigen
  2. The “hidden” antigen is targeted by the antibody produced by the vaccine
  3. The antibody enters the tick and kills it!
62
Q

What are the common parasites that live in the blood?

A

Trypanosomes (African)
- Trypanosomiasis (sleeping sickness)
- Nagana in cattle

Plasmodia
- Malaria

Babesia
- Babesiosis (humans, cattle, dogs, rodents, birds)

Theileria
- East coast fever (cattle)

63
Q

What animals are affected by trypanosoma?

A

T.brucei also causes disease in cattle (nagana) and horses and some wild animals

Different trypanosomes affect other animals such as,
- Amphibians
- Birds
- Horses
- Camels
- Pigs

64
Q

What is trypanosoma disease in humans like?

A

Acute stage:
Fever (cytokine storm)

Chronic:
Sleeping sickness - due to invasion of the brain (but always extracellular)

65
Q

Are all antibodies the same?

A

IgM is produced by naïve B cells on first contain (primary response)

MHC Class 2 secondary responses:
- Helper T cell CD4
- Cytokines
- Memory cells
- Plasma cells
Produce:
—> IgG
—> IgA
—> IgE

66
Q

What do we know about isotypes of antibodies?

A

Different isotopes have different properties:
IgE
IgG
- Similar structures, Y shaped antibodies

IgA
- Double Y shape with a joining chain and secretory proteins

IgM
5 Y shaped antibodies all in a circle held together with a joining chain and disulphide bonds

67
Q

Are all antibodies the same?

A

IgM produced in a T-independent manner, Levels of IgM are not boosted by vaccination or repeated infection (no memory)

Antigen-specific IgG and IgE (T-dependent) increase in concentration after vaccination or repeated infections (specific memory cells)

68
Q

How do antibodies kill parasites?

A

Neutralise essential antigens?

Activate complement (MAC) - lyse targets

Act as opsonins (facilitate phagocytosis)

69
Q

What does IgM do to Trypanosoma brucei?

A

IgM is effective at killing trypanosomes

IgM activates complement (MAC)

IgM doesn’t act as an opsonin

70
Q

What does IgG do to Trypanosoma brucei?

A

IgG and Phagocytes (macrophages/neutrophils) which express Fcy receptors work together against Trypanosoma brucei

IgG is better (than IgM) at clearing Trypanosomes because;
a) higher concentrations in blood
b) Also acts as an opsonin
c) Also activates complement

71
Q

What is IgE important for fighting?

A

Helminths (worms)
IgE is for parasites

Involves Eosinophils/mast cells
Express Fc receptors

NOT Trypanosomes

72
Q

So how does Trypanosoma brucei survive?

A

The surface of the parasite is mostly covered (90% plus) by just 1 protein

This protein is called the variable surface glycoprotein (VSG)

VSGs are approx 60kDa and are densely packed

It is thought that the VSG coat protects more important proteins from the host’s antibodies

Thought to be less efficient at producing IgG to glycoproteins (specifically glycan epitopes) than to proteins

73
Q

What do we know about antibody activity on T brucei?

A

Antibodies do destroy T brucei

Large numbers of parasites are being produced

For a while the replication rate exceeds the ability of the immune system to destroy parasites

Soon the host produce enough antibodies to kill parasites faster than the parasite can replicate

Parasite numbers drop

74
Q

How does trypanosoma brucei escape antibody-mediated killing?

A

Parasites escape antibody-mediated killing by antigenic variation

This is different from antigenic drift or shift

T brucei have multiple copies of same gene producing a variable surface glycoprotein (VSG) which acts as a coat - only expresses one

T brucei switches expression to a different VSG gene (epigenetic)

Antibodies to a previous VSG do not recognise the “new VSG” and the parasite can grow unchecked until new antibodies are produced

75
Q

What role does IgA have in killing Trypanosoma brucei?

A

IgA helps in the defence against Trypanosoma brucei by binding to the parasite, promoting its clearance.

76
Q

What role do cytotoxic T cells (CD8+) play in this infection?

A

Cytotoxic T cells (CD8+) directly attack and kill cells infected with Trypanosoma brucei, limiting the spread of the infection

77
Q

What role do T helper cells (CD4+) play in this infection?

A

T helper cells (CD4+) regulate the immune response by activating other immune cells to combat Trypanosoma brucei infection.

78
Q

What immune responses effectively kill trypanosoma brucei parasites?

A

Effective immune responses against Trypanosoma brucei involve a combination of antibody-mediated responses, cytotoxic T cell activity, and T helper cell activation.

79
Q

How would giving a T cell immunosuppressant (such as cyclosporine) affect the number of T brucei parasites in the blood?

A

Giving a T cell immunosuppressant like cyclosporine would likely lead to an increase in the number of Trypanosoma brucei parasites in the blood due to the suppression of T-cell mediated immune responses, allowing the parasite to proliferate unchecked.

80
Q

What are plasmodia parasites?

A

Single cell apicomplexan (eukaryotic)

Human - P.falciparum and P.vivax

Animals - Apes, reptiles, rodents and birds

Mostly host-specific (not zoonotic)

81
Q

What is parasitaemia?

A

The percentage of erythrocytes that are infected

82
Q

What is malarial disease associated with?

A

Disease is associated only with the asexual blood stage

Mild:
- Fever
- Related to Schizont rupture
- Fever is every 48 hours

Severe (life-threatening):
- Cerebral malaria
- Anaemia

83
Q

What is plasmodia in the human host, Sporozoite?

A

Do not live for any appreciable time in the blood - short period to invade hepatocytes (liver) (in minutes)

Circumsporozoite protein (CSP) main surface antigen

Anti-CSP antibodies block invasion

84
Q

What is the Liver Stage in plasmodia in the human host?

A

Sporozoites infect hepatocytes where they multiply rapidly and develop into merozoites.

Intracellular environment protects them against antibodies

Generate cytotoxic T cells that kill infected liver cells

Vaccine R21/Matrix M

Target is circumsporozoite protein (CSP) which is expressed on sporozoites and liver stages

85
Q

What is the asexual blood stage of malaria?

A
  1. Merozoites released from liver infect red blood cells
  2. Immature trophozoite (ring stage)
  3. Mature trophozoite
  4. Shizont
  5. Ruptured Shizont

OR

  1. Merozoites released from liver infect red blood cells
  2. Immature trophozoite (ring stage)
  3. Gametocytes are ingested by an anopheles mosquito during a blood meal
  4. Mosquito feeds and spreads infection

Invasion - Development - Gametogenesis - Shizont rupture

Development can give rise to 24 daughter merozoites. Potential for very fast growth.

86
Q

What are merozoites?

A

Eukaryotic:
Cell structure is much more complex than either viruses or bacteria

Apical pole:
Gives to name of parasites - Apicomplexa - involved in the invasion of parasite into host cell

Merozoites do not survive in the blood for a long time (die within minutes) - i.e. very different from T.brucei

87
Q

What is the general structure of a merozoite?

A

Rounded teardrop shape, with an apical prominence.

Consists of:
- Nucleus
- Plastid
- Mitochondrion
- Microtubules
- Dense granules
- Microneme
- Polar rings
- Rhoptry
- Pellicular cisterna
- Ribosomes
- Plasma membrane
- Merozoite coat

88
Q

What do we know about binding of parasite to erythrocyte?

A

Binding and invasion are different processes

Binding - specific proteins on both the parasite and the red blood cell (erythrocyte)

Duffy antigen on erythrocytes used by P vivax, rare in West Africa

Essential process required for parasite growth - so a key target for vaccines (RH5 in P.falciparum)

Many proteins on both the parasite and the host erythrocyte are involved - i.e. Needs to form a complex

89
Q

What do we know about invasion of parasite to erythrocytes?

A

Parasite may take several attempts to bind to erythrocytes

Once tightly bound to the erythrocyte surface the merozoite re-orientates so that the apical end is prominent and begins “invasion”

Rhoptry and micronems - secretory organelles involved in the invasion process

Invasion is an active process that involved calcium fluxes and active actin-myosin “motors”

90
Q

What happens in the development part of the Asexual Blood Stages?

A

Parasites have to modify their environment (erythrocyte)

They undergo differentiation and asexual division

  • Parasite membranes
  • Parasitophorus vacuole with membrane - produced by parasite
  • Parasite tubular network (alimentary canal)
91
Q

How is the development part of Asexual blood stages different to virus replication?

A

Parasite is NOT using the hosts enzymes for replication (how do we know this)

Parasite can produce up to 24 daughter merozoites in 48hrs

Parasite antigens do not appear on the erythrocyte surface during the first 24hrs

92
Q

What do we know about Shizonts and surface proteins in the development part of Asexual blood stages?

A

Surface proteins (PfEMP-1)

Aggregates form knobs that bind to endothelial cells

Binding to endothelial cells (sequestration)

A) May prevent parasitised erythrocytes moving through the spleen (areas of high immune surveillance)

B) May be a cause of cerebral malaria

Shizonts are full of merozoites which are released upon shizont rupture and go on to infect new erythrocytes

Factors released during schizont rupture may cause the cytokine storm - and lead to pathology

93
Q

What do we know about the Asexual blood stages and immunity?

A

Antibodies (IgG) are the main immune response that controls parasite numbers at this stage

Antibodies can help to clear the infected erythrocytes (complement at phagocytosis)

Antibodies can also neutralise (block invasion of new erythrocytes by merozoites)

Plasmodia also uses antigenic variation to avoid destruction - most plasmodium antigens are highly polymorphic

Natural immunity appears to be due to producing antibodies to all the local strains of the parasite

94
Q

Which antibodies are present in the Asexual blood stages?

A

IgM
IgG
IgA
IgE

95
Q

What is the Sexual stage of plasmodia in the blood?

A

Some plasmodia (small %) develop into sexual forms (gametocytes)

Male and female (micro and macro gametocytes) survive in host erythrocytes for several days but die if not taken up by mosquitoes

The antigens involved in plasmodium sex are not expressed in the mammalian host (only expressed in the stomach of the mosquito)

96
Q

What immune responses effectively kill plasmodium parasites?

A

Cellular immune responses, primarily mediated by T cells, effectively kill Plasmodium parasites

97
Q

What are the consequences of producing anti-plasmodium IgE?

A

Producing anti plasmodium IgE can lead to allergic reactions and exacerbate symptoms of malaria

98
Q

Why does an injection of immune sera (sera from somebody resistant to plasmodium) not always cause a reduction of plasmodium parasites in an infected patient?

A

An injection of immune sera may not always reduce Plasmodium parasites in an infected patient due to factors such as the timing of administration, the presence of other immune responses and variations in the patients immune system

99
Q

What is the One Health relevance of topics discussed?

A

Plasmodia infections are a significant cause of mortality and morbidity in wild animals and birds as well as in humans

Wild animals may act as a reservoir of infection that could be difficult to eliminate

Introduction of parasites (or their vectors) to immunologically naïve populations can have devastating effects including extinction.

100
Q

What do we know about plasmodia in the mosquito?

A

Gamete and zygote antigens do not show much antigens do not show much antigenic variation

Little selection pressure

Therefore - good vaccine target

Transmission blocking vaccines

Mosquito takes up antibodies at the same time as the parasite

Antigens necessary for fusion of micro and macro gametes are not expressed to this point

Hosts immune system does not see gametes

Gametocytes mature in response to changes in pH and temperature of the mosquitoes stomach and form gametes

Parasite sex!!! Expression of new proteins allows fusion of micro/macro gametes formation of zygote.

Principles in Infectious Diseases (3 decks)

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