40
Detecting and responding DISEASE AND THE IMMUNE RESPONSE

Disease

Embed Size (px)

Citation preview

Page 1: Disease

Detecting and

responding

DISEASE AND THE

IMMUNE RESPONSE

Page 2: Disease

DISEASE

• What is disease?

• What is a non-infectious disease?

• examples

• What is an infectious disease?

• Examples

• Transmission – methods? –

(see homework)

• Incubation period

Page 3: Disease

Detecting

• Humans, Animals, plants need a way of

detecting when they are “invaded” by

foreign cells or tissue so they can defend

themselves effectively.

• Immune system’s job

Page 4: Disease

Pathogens

• Pathology – study of disease

• Pathogen – disease causing organism or non-cellular agent

• Main groups:• Viruses

• Bacteria

• Fungi

• Protozoans

• Prions

• Multicellular eukaryotic parasites

Page 5: Disease

VIRUSES

• Non cellular infectious agents

• Can only be seen with an e.m.

• Completely parasitic (obligate intracellular

parasites)

• Host relationship is very specific –

glycoproteins on virus interact with

receptors on host cell membrane – e.g.

influenza virus and RBC’s

Page 6: Disease

Size and shape of viruses

Page 7: Disease

How Big?

• http://www.cellsalive.com/howbig.htm

Page 8: Disease

structure

Page 9: Disease

Structure

Page 10: Disease

Viral diseases

DNA viruses RNA viruses

Gastroenteritis Influenza

Respiratory tract infection Polio

Chicken pox Colds

Shingles Rubella

Warts AIDS

Measles

Mumps

diarrhoea

rabies

Page 11: Disease

Transmission Electron Micrograph of an

Influenza A Virus

Page 12: Disease

Transmission Electron Micrograph of HIV-1

Image provided by Dr. Edwin P. Ewing, Jr.Courtesy of the Centers for Disease Control and Prevention

Page 13: Disease

Transmission Electron Micrograph of

Coronavirus

Image provided by Dr. Erskine Palmer.Courtesy of the Centers for Disease Control and PreventionNote the glycoproteins (arrows) on the viral envelope.

Page 14: Disease

Transmission Electron Micrograph of

Poliomyelitis viruses

Image provided by J. J. Esposito and F. A. Murphy.

Courtesy of the Centers for Disease Control and Prevention.

Poliomyelitis viruses are naked viruses.

Page 15: Disease

Polio - symptoms

Page 16: Disease

Hosts

• Can infect all kinds of cells- human, plant,

animal, bacteria

• Many viruses spread by vectors – e.g.

mosquitos Ross River Virus

Page 17: Disease

Reproduction

Page 18: Disease

Treatment

• Antibiotics not effective

• Drugs which interfere with making of viral DNA or RNA might stop reproduction

• Vaccines most effective – inject or swallow inactivated virus into host – initiates the production of antibodies which help fight off the infection when it arrives.

• Rest – fast mutation of coat proteins on some viruses are a huge problem eg AIDS

Page 19: Disease

PRIONS

• See p 137 AM

• PrPc proteins – normal and infectious

versions

• Discovered with Kuru in New Guinea

• E.g. CJD (Creutzfeld Jakob Disease)

• Bovine spongy encephalitis (Mad Cow

disease)

• No cure

Page 20: Disease

Prions

Prions are implicated in BSE (Bovine Spongiform Encephalopathy or Mad Cow Disease) and its human counterpart nvCJD (new variant Creutzfeldt Jakob Disease). These and similar diseases are known as TSEs (Transmissible Spongiform Encephalopathies). TSEs afflict other species, most famously sheep (scrapie).

Page 21: Disease

• Prions are pathogenic variants of proteins that are naturally produced in nerve cells and certain other

cells. The normal "healthy" prions are referred to as PrPc (Prion Protein cellular). The word "prion"

stands for "proteinaceous infectious particle" and so should properly only be applied to the

pathogenic variants. In this picture, the production of PrPc is illustrated from the nucleus at bottom

right. RNA that codes for PrPc is produced in the nucleus and exits via the nuclear pore. The RNA

then passes along ribosomes attached to the rER. PrPc is formed in the rER and then progresses up

through the Golgi. At the upper face of the Golgi, vesicles containing PrPc bud off and travel to the

cell surface. Here, they fuse with the cell membrane and so discharge their cargo at "PrPc". By this

means, the cellular proteins come to sit on the exterior of the cell.

• PrPc encounter rogue (purple) prions. These are termed PrPsc (sc stands for scrapie, the prion

disease of sheep). The rogue prions seem to force the normal proteins to change shape. Both types

of protein, the PrPc and their corresponding prions, are the same chemical - just different shapes. It

is this shape-flipping which is equivalent to the transmission of infection. Such a conformational shift

or flip could happen at the cell surface or in caveolae (one is shown as a small invagination in the cell

membrane). Residual PrPc might continue to be flipped by contact with the rogue conformations for

some time in these vesicles. Prions polymerise, finally appearing as purple fibrils in the picture at "P".

PrPsc is resistant to degradation by the enzymes contained in the lysosomes that are seen floating

nearby. Consequently, PrPsc accumulates in the cell. PrPsc vesicles may also travel to the Golgi and

intercept PrPc that is being processed there. In this way, PrPc particles could be switched to the

rogue form before they reach the surface of the cell. By such mechanisms, PrPc might be switched to

PrPsc at various points in and on the cell.

• Prions could enter the brain along the axons of neurons. This probably happens by a retrograde flow

of prion filled vesicles. These are shown in the picture as purple spheres ascending the axon like

elevators going up a shaft . Another route of entry could be the blood, probably in immune cells. A

lymphocyte is shown exiting the capillary at bottom left where it could then contact the astrocyte.

Astrocytes and other glial cells also support the production of prions.

Page 22: Disease

BACTERIA

• Prokaryotic cells

•Features?

No nucleus – circular DNA

No membrane bound organelles

Very small

Mostly heterotrophic some autotrophic

Page 23: Disease

Structure

Page 24: Disease

Features

• Shaped – cocci, bacilli, spirilla

• Many are pathogenic, many not

• Cause disease by disrupting host cell’s;

producing powerful toxins; disrupting

host immune system

• Often defined by differential staining

• Gram positive (purple) and Gram

negative bacteria (pink/red)

Page 25: Disease

Diseases

• Tetanus – Clostridium tetani

• Botulism - Clostridium botulinum

• Pneumonia - Pneumococcus

• Diphtheria

• Tuberculosis – Mycobacterium tuberculosis

• Food poisoning – Salmonella typhi, Staphylococcus aureus

• Throat infections - Streptococcus

• Typhoid fever

• Syphilis

• chlamydia

Page 26: Disease

Reproduction

Binary fission

Page 27: Disease

Treatment

• Antibiotics – natural eg penicillin or

synthetic

• Tetracycline

• Work by destroying bacterial structures

or cell membrane

Page 28: Disease

Penicillium and bacterial inhibition

Page 29: Disease
Page 30: Disease

Fungal infections

• Cause many plant diseases e.g. Rust in

wheat

• In animals – ringworm, athletes foot, tinia,

thrush – usually not serious or life

threatening

• Mostly pathogenic in plants

• Transmitted via direct contact

Page 31: Disease
Page 32: Disease
Page 33: Disease

Structure

Page 34: Disease

Cell wall made of chitinNon motile usuallyFilamentous – have hyphaeProduce spores

Yeasts are a sub group –unicellular fungi - thrush

Page 35: Disease

Yeast infection

Page 36: Disease

Life-cycle

Page 37: Disease

Protozoans

• Summarise Malaria parasite from text p

148

• Name pathogen, describe life cycle,

disease and treatment

Page 38: Disease

Multicellular parasites - worms

• Flatworms – platyhelminthes

• Inhabits intestines of humans and other

animals

• May be up to 10m long

• Each segment in chain has

reproductive organs

• Round worms – nematodes

• Thread, pin, hook worms see p 162 text

Page 39: Disease
Page 40: Disease