Parasites & People - Host Parasite Relationship - Rumala

Parasites & PeopleHost - Parasite Relationship

Department of ParasitologyFaculty of MedicinePeradeniya

Objectives:

• Define the following terms

Parasite

host,

endoparasite,

ectoparasite, pathogen, commensal, obligatory parasite, facultative parasite, definitive host, intermediate host, reservoir host

Describe the

growth, survival and spread of protozoan and helminth parasites

within and outside the human host

Symbiosis: "life together two organisms live in an association with one another.

RELATIONSHIP BETWEEN HOST AND THE PARASITE

MUTUALISM: Both members of the

association benefit.

Lactobacillin vagina

COMMENSALISM: parasite derives the benefit without causing any injury to the host

PARASITISM:

Parasites derives benefit from the host causing injury to the host

Parasite: An organism that lives in or on and takes its nourishment from another organism. A parasite cannot live independently.

RBC

Parasitized RBC

PARASITISM- association between parasite and host(MAN)

P

P

Ectoparasite (on the host- -skin,hair eg. arthropods)

Endoparasite(inside host-extra cellular/intra cellular)

MAN

ECTOPARASITE

A parasite which lives on the outer surface of the host. Eg : Lice

EndoparasitesParasites which lives within the host

exist in one of two forms:

• Extracellular (inhabiting spaces in the host’s body) or

• intracellular (inhabiting cells in the host’s body)

Intracellular parasite Extracellular parasite

Parasites can also be classified as

OBLIGATORY PARASITE : Parasitic throughout their life cycle. Cannot exist without a parasitic life and totally dependent on the host FACULTATIVE PARASITE: live a parasitic or free-living existence when the opportunity arises ACCIDENTAL PARASITE: A parasite which attaches to a unusual host

HOST:

Organism which harbours the parasite and

provides nourishment and shelter

The hosts are relatively larger in sizein comparison to their parasites

HOSTS

Intermediate host : Asexual reproduction/larvalstages

Definitive host: Sexual reproduction/adult stage

Reservoir host: Vertebrates which harbour the parasites in nature. Act as a sourceof infection.(not affected by parasite)

The host in which the parasite is not usually found

Accidental host:

Infection : The growth of a parasitic

organism within the body.

Pathogen : Parasite that causes

damage to the host

Virulence: Ability of an organism to

cause disease

Multiplication: Like prokaryotes, splits into 2 but more complex All genes copied, each daughter cell receivesa complete duplicate set - mitosisother structures eg. cytoplasm splits as well

into TWO - binary fissioneg. Intestinal protozoa (30 min)

or into several (hundreds) - multiple fissioneg. malaria, other tissue protozoa

ONCE THEY ENTER, WHAT HAPPENS NEXT?

Asexual reproductionmalaria parasite in liver cell

RBC

1 parasite x 60,000 in 5-6 days

No mixing/shuffling of genesBut allows rapid increase in numbers

Methods of multiplication - to allow shuffling of genes

1. Conjugation: cells in intimate contact exchangegenes and later divide

2. Sexual reproduction: cells with 2 sets of genes (Diploid)divide into female and male cells,each with only one set (Haploid) These unite to form the diploid cell = fertilizationResult - a combination from 2 parent cellsIncreased possibility of genetic variationand accelerated evolution

Human host is constantly in contact with microorganisms only few of them are able to establish in human tissues WHY?

RESISTANCE: Ability of host to prevent infection through Defense Mechanisms

Immune evasion - survival strategy of parasites

Successful parasites need to persist in host for transmission - with minimal damage to itself or the host….

These parasites devise strategies of evading the host immune response

HOW DO PARASITES OVERCOME HOST RESISTANCE

unlike prokaryotic microorganisms….

parasites are eukaryotes more complex morphology with multipleorganelles - wide array of Ag diversity

longer generation timemulticellular parasites eg. helminths

some helminths’ life span is 15-20 ynot much less than life span of host

Immune evasion strategies of parasites help in survival within the host

many are common with those adopted by prokaryotes such as bacteria, viruses

at all levels of the immune response both non-specific and specific

but some adapted and exploited successfully by parasites during evolution

Avoidance of recognition Immune modulation (change)

Key strategies

Successful parasites have ‘learnt’ to exploit the fundamental basis of immune response- ‘recognition as foreign’

Mechanisms of avoidance of recognition: antigenic variation

host mimicry

sequestration/intracellular retreat

classic mechanism by which parasites confound the immune systemto promote it’s own survival

Antigenic variation

shown by many blood parasites eg.Trypanosomes, Plasmodium

Switching surface antigensthat have induced protective immune response,to new antigens which are unaffected by that response.

some protozoa adapted to live intracellular inmacrophages

Molecular mimicry

Schistosomes live inside blood vessels for years unaffected by host defense

main strategy: expressing antigens similar/identical to host molecules

Malarial parasite

Invades erythrocytes RED BLOOD CELLS – no organelles,incapable of phagocytic activity,only a food store

Transmission of infection

Successful parasitism requires ability toinfect host and transmission to another host

Simple life cycles: no developmental stage during transmission, resistant stages - spores, cysts

Complex life cycles: some protozoa & all metazoasexual + asexual cycles often in different hosts

PORTALS OF ENTRY- of parasites

SKIN•direct contact•wound infection•injection by vector/human•active penetration by agent

Tissue communicating with outside eg. Resp Tract, GIT, GUT

Placenta - congenital transmission

Blood/ blood products/ tissue /organ transplant

HOW DO PARASITES ENTER INTO HOST?

VECTOR

invertebrate transmitting parasite from one host to another

Biological vector:

Mechanical vector:

development or/andmultiplication of parasite in vector

parasite does not undergo biological change in vector

HP vector

ZOONOSESZOONOSES

“diseases and infections that are naturally transmitted between vertebrate animalsand man”

dynamic From domestic or wild animals Importance depends on human contact

VERTEBRATE ANIMALMAN

Anthropozoonoses

Zooanthroponoses

Amphixenoses

Infections transmitted to man from lower vertebrates

Infections transmitted from man to animals

Infections maintained in both man and lower vertebrates, and may be naturally transmitted in either direction

LIFE CYCLES of parasites

A clear an accurate knowledge of LC’s essential for understanding -

pathogenesis, transmission, diagnosis, treatment, control & prevention of diseases caused by parasites

Protozoans & metazoans: Life cycles have several stages that vary in structure = morphology

Intestinal protozoans- Trophozoite- growing form

Cysts- resistant forms can survive in environment (stage of transmission)

Protozoan life cycles

Tissue protozoans-Trophozoites- various stages,

single/dividing nuclei

Gametocytes = gamete forming cells= sexual forms

Helminthes have complex life cycle

Reproductive stages egg/larva released develop into adults in another host - Intestinal nematodes

Egg/larva has to undergo further development in one or more intermediate hosts

- tape worms & flukes or in insect vector to become adults

- tissue nematodes

Tape worms (Cestodes): Adults in small intestine of vertebrateslive for several years (10-12 y)absorbs nutrients through their integument (wall)

Life cycleAdultIn Man/VertebrateDefinitive host

LarvaInvertebrate/Vertebrate/Man

Egg

Helminthes- multiplication factor

One infective stage one adult

Adult thousands of infective stages during life span

Eg. round worm - 250,000 eggs/day for 6 m

tape worm - 50,000 eggs/day for >10 y

Arthropods:A few have adapted to live as ectoparasites

eg. lice, mites

use humans as source of food - blood / tissue fluid

Many act as vectors of disease

Some are intermediate hosts to parasitesMy grateful thanks to Dr. Devika Iddawela for permission

to use some of her slides