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Terms in this set (20)

Pathogen damages human quickly by Exotoxin production
Vibrio cholerae are ingested from contaminated drinking water
They bind to the gut lining
They produce an AB toxin called cholera toxin,
AB toxins a ring of 5 hydrophobic identical B proteins with a single hydrophilic A protein inside them. The A is the toxin the B delivers it to the correct site in the host cell via membrane transport
Toxin acts on the mammalian cell signalling system in gut lining cells, causes high levels of cAMP which it is thought the bacteria metabolise as a benefit.
Bacteria replicate
Gut lining cells lose normal homeostasis and copious diarrhoea results
Replicated bacteria escape the body in the diarrhoea, and go on to infect more hosts by them drinking faecally polluted water.
Many other primary pathogen bacteria employ different exotoxins (such as pathogenic E. coli 0157:H7 and Shigella which use other AB toxins)
Infamous outbreak in Haiti when UN relief workers carrying the bacterium came to aid after earthquake and unwittingly spread V.cholerae in the unsanitary conditions
Vibrio cholerae arrive by chemotaxis in the gut. Bind to gangliosides on the gut villi surface, grow as a biofilm and make an AB toxin
This modifys the host cell ion pumps making them pump out chloride and bicarbonate into the gut lumen. Then the body thinks its eaten a salty meal and pumps out water from the blood stream. Get huge watery "rice water stool" death danger is dehydration
In cholera infections-the body plays a part in its own illness- normal gut physiology/ecology is perturbed
The body gets dehydrated trying to compensate for extra Na+ in the gut caused by the toxin
In cholera infections-the body plays a part in its own illness- normal gut physiology/ecology is perturbed
Support against cholera infection is the supply of ions including K+ (Cl) which can be taken up in place of Na+
Also large amounts of water to drink against dehydration
V. cholerae does not enter human cells it just binds to them and makes them deliver cAMP to it and to distribute it after it replicates, in the large volume of diarrhoea expelled!
The simple small, secreted AB toxin has a huge effect on the human being
Normal ion homeostasis is affected by the bacteria causing the human cells to make more cyclic AMP. This acts on human Na+ transporters shutting them down
Genes for the A/B toxin can be shared by environmental bacteria in polluted water
Damages human quickly with toxins, hides from immune system by capsule, spreads by spores.
•Gram positive, non motile, spore-forming rod shaped bacterium (remember spores from last weeks lecture- seed like resting stages with chromosome in, resist drying out and are wind distributed.).
B. anthracis cells and spores are common in soils and on animal products/coats in tropical areas
Cells have a protective protein S layer ("capsule") around the cell of polymer of D glutamic acid (an amino acid)
Have characteristic sticky white - grey colonies on agar plates. Grows aerobically at 35°C requires simple lab media with egg yolk or similar ingredients
What makes it a pathogen is not so much the genome but the plasmids which are extra genes acquired and shared by environmental bacteria
Virulence plasmids encode the S layer which resists phagocytosis by white blood cells and encode toxins which attach the human body. The and the cap genes on plasmid pXO2 encode the protective "capsule" .Plasmid pXO1 encodes a complex toxin: the paggene product) binds to phagocytes of the immune system blocking their receptors. It then allows the LEF lethal factor to enter the immune system cells and other host cells causing cell death. Thecya gene product is involved in oedema/swelling and fluid retention
B. anthracis causes different diseases of man (also a disease of animals)- depending on site of infection
Moist gut or lung environment allows rapid spread and growth of the bacteria and rapid death. Drier cutaneous skin environment restricts the growth, so time for treatment to take effect
1) Cutaneous anthrax: fairly common in people handling animal products (e.g. woolsorter's disease) in developing countries. B.anthracis spores enter a cut and a black leathery swollen scar develops (anthracite-like black colour- hence the name). Needs a cut in skin to gain access from soil/ contaminated hides of animals.
Can be treated successfully with antibiotics if not treated 20% mortality
2) Gastrointestinal anthrax : very rare caused by eating spores in undercooked putrid meat from an animal with anthrax, blood poisoning and swelling of abdomen & lymph nodes, high mortality but very rare
3) Inhalation or pulmonary anthrax: very rare in normal life but relevant to considerations of bio-warfare. Caused by inhaling B.anthracis spores in dust or air these germinate and release live bacteria expressing toxins into lungs, flu like symptoms in first 2-3 days then difficulty breathing and death
Spirochaetes are Gram negative long helical bacteria, and have internalised flagella, between their inner and outer membranes.
These rotate the outer membrane around the outside of the helical cell, like a corkscrew. They can corkscrew into layers of the body no other bacteria can access
Few surface proteins on outer membrane, and ability to bind activators or the immune system and also plasminogen- allows "cloaking". Evades immune recognition/stimulation and destruction so spirochaete persists
They burrow between tight junctions of mammalian cells. Access normally sterile sites like joint- synovial fluid and cerebrospinal fluid
Feed and multiply slowly in organs & joints. (Lyme disease & syphilis). Cause loss of organ function and arthritis. Can cause autoimmune disease by cross-reactivity of their proteins with ours, when they rarely are attacked by immune system
Replicate slowly keep host alive

Diseases caused by spirochaetes develop slowly over years
They aren't rapid pathogens, but can escape detection in the body and develop in normally sterile sites
Sometimes after long periods of infection groups of spirochaetes are broken down and their inner antigens do react with the immune system and a reaction in caused....such as sores on genital tract and skin in syphilis
In Borrelia the damage in Lymes Disease is due to colonisation by the bacteria and some autoimmune responses made when some spirochaetes do burst in the host
Lymes arthritis can develop due to Borrelia living inside the joints of the body- knee, ankle etc
Borrelia is spread by tick bites from animals such as deer infected with the spirochaete in their blood- passed to human by bite always seek rapid GP appointment for antibiotic doxycyclin if you've been walking and have a bulls-eye rash- its from a tick bite. Rash fades as Borrelia evade immune system but they are in your body

Spirochaetes break through tight junctions to get into the blood stream/CNS or joint fluid where they replicate
They don't kill the host quickly so human-human or tick borne transmission from blood. No survival in soil after death of host- obligate pathogen
No/few pathogenicity proteins just get to sterile sites and eat without competition!
Very few transporters or porins in outer membrane so white blood cells have little to recognise = stealth or cloaking
Very hard to culture spirochaetes as they transport food in only slowly and require very rich media- so understudied but widespread problem in environment
Flu virus protein "spikes" on the surface have important roles
They key ones are Hemagglutinin (for which the H1 type is named in "swine flu) and neuraminidase (for which the N1 type is named in swine flu". Different protein sequences for these (caused by altered gene sequences) give different properties and so numbers. The H (or HA) hemagglutinin spikes help the virus attach to respiratory tract cells. They also attach to red blood cells and cause clumping of them in a lab assay - hence the name hemagglutinin. These are of the H1 type in swine flu
The N (or NA) spikes have an enzyme activity called neuraminidase. This acts on a part of the human or animal cell membrane, called sialic acid (a type of neuraminic acid, hence the name), and degrades it. The degrading of this lets the virus assemble and coat itself without having sialic acid in the membrane around it, which would prevent it assembling and working properly. The spikes are of the N1 type in "swine flu"
Past epidemics spike types are recognised by the host immune system and the virus is destroyed, BUT, new variants are not- recognised- this lets the "variant" new flu cause an infection
Because flu virus can swap the genes for its H and N spikes with flu viruses of other animals, and still infect humans, we get waves of new epidemics, such as so-called "swine flu" in 2009
New flu strains can invade an otherwise healthy body as the immune system doesn't recognise and destroy them rapidly
Purified hemagglutinin spikes are used to make flu vaccines and the person injected with them raises antibodies to them. These antibodies recognise the spikes on an invading related virus and cause the immune response to neutralise and destroy the flu virus