Malaria and Bovine Spongiform EncephalitisAHL IB Biology

Option F

Malaria True or False?

Watch this video on malaria and answer the questions on your worksheet

Distribution

• At low altitudes

• During hot seasons

• In places where the Anopheles mosquito is able to breed in fresh water

• Where the environment provides

– water

-vegetation

-optimum temperature

Incidence of Malaria

Incidence of malaria in Mexico

Malaria - parasite• Caused by a protozoan parasite of the genus

Plasmodium• Mainly P. falciparum but other species include

P. vivax, P. ovale and P. malariae• P. knowlesi can cross the species barrier from

monkeys to humans• The parasite lives in subtropical areas of Africa,

Asia and the Americas

ELECTRON MICROGRAPH OF PLASMODIUM PARASITE

RING STAGE OF PLASMODIUM FALCIPARUM

Life Cycle of Plasmodium

You are what you eat!

Arrachera on the barbecue?

Tacos de res?

What´s your favourite?

Calves are fed a “baby formula” made from bovine blood because it is much less expensive than milk, not to mention the comparative resale values of the two liquids.

Adult cows are fed rendered animal protein to aid in “bulking up”.

Rendered Protein Ingredients:Animals unfit for human consumption

such as:

– Sick animals– Horses– Cats and dogs– Zoo animals– Road kill– Frying oil from restaurants

– Brains, spinal cords, feathers, hooves, skins, hair, fur, whiskers, bones, teeth, etc. remaining from slaughterhouses

– Sewage sludge

– Manure

– Sawdust/wood scraps

– Newspaper

– Cement dust

– Maggot infested grains

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Not only is this rendered protein used in the food we feed our pets and food animals, it is in the products we use everyday.

The fat is skimmed off of the top of the vat during the rendering process and used to make “marshmallows and cereal bars, … lipstick and hand lotion and garden fertilizers, tires and yogurt and breath mints.”

Symptoms of Bovine Spongiform Encephalopathy

restlessnessaggressivenessloss of motor

functionloss of appetite

convulsionsblindness

self mutilation

The initial discoveries of BSE…• In April of 1985, the first identified case of BSE was initially believed to be “grass staggers,” a common

illness caused by Magnesium deficiency. The cow was observed as seeming to hallucinate.

• Given an “Unknown” diagnosis, as a possible brain tumor or lead poisoning. The brain autopsy revealed spongiform patterns.

• On March 20, 1996 the UK Department of Health announced that BSE was in fact transmissible to humans.

• The announcement was so devastating to the UK cattle economy that many ranchers were forced into bankruptcy beacuse of the immediate loss of entire herds of potentially contaminated cattle, as well as the immediate consumer boycott of beef and beef products. This downturn was so terrible in fact that there was an epidemic of suicides within the ranching community.

• In June, 1987 John Wilesmith, a veterinarian epidemiologist for the Ministry of Agriculture, Fishers and Food (MAFF) made the link between BSE and cattle feed made from scrapie infected sheep.

• On July 7, 1988, a settlement was offered by British Agriculture of payment for 50% of the worth of the cow if reported to the government.

• This in fact gave the farmers an incentive not to report suspicious cases, as they would make the full profit from sneaking past inspection and selling the meat into the market versus reporting the problem and only receiving 50% compensation.

Causative agent of BSE: What is a Prion?

Prions in the body

Physical Attributes of the affected brain:

– Enlarged astrocytes- Star shaped cells

attached to blood vessels in brain.

– Holes where neurons used to be.

– Amyloid Plaques-flower shaped protein waxy

buildup.

Found in mainly in the brain, spinal cord and nervous tissue, with increasing

research discovering prions in glands and blood as well.

BSE Brain

Scrapie Brain

Prion protein is indestructible

by heat up to 1000° F (350° C)

Hot enough to melt lead.

In 1986, 4.5 million cows were incinerated in the U.K. after the discovery of BSE. The ashes, stored in underground concrete containers, were retested again in 1998 and

found to still be infected with active prions.

So how do these prions affect humans?

Kuru

Creutzfeldt-Jakob Disease (CJD)

New Variant Creutzfeldt-Jakob Disease (vCJD)

Kuru• Cannibal culture of Papua New Guinea.

• Affected mostly women and children, with a

small amount of men. anywhere from 5 to 10

percent of the population died each year from

kuru.

• When loved one died, men ate muscle portions

and women and children were left with the

lesser organs and brain, where we now know

prions tend to cluster.

• The rare male cases occurred because of the

possible 20 to 30 year dormancy period of

prions where the infectious agents were

ingested as children.

Kuru (continued)

• Analyzed by New Yorker Carleton Gajdusek and Lithuanian Dr. Vincent Zigas (both in photo) in 1957.

• Initially believed to be a virus causing encephalitis (swelling of the brain), with the same symptoms as Parkinson's, Alzheimer's, and MS. However these were degenerative, not infectious diseases, and not epidemic as kuru was.

• After autopsy, Gajdusek made the connection of brain damage to recently discovered CJD.

• No treatment was ever found, and when cannibalism was eventually phased out of the culture, so too came the disappearance of kuru.

Creutzfeldt-Jakob Disease (CJD)• Discovered in 1921by Dr. Hans Gerhard

Creutzfeldt and Dr. Alfons Jakob, colleagues at the University of Hamburg Germany.

• Now more common that rabies.

• Physical attributes of the affected brain:– Enlarged astrocytes- Star shaped cells

attached to blood vessels in brain.– Holes where neurons used to be.– Amyloid Plaques-flower shaped protein

waxy buildup.

Microscope slide of brain affected by CJD

CJD Symptoms: (first 7 same as BSE)

• restlessness.• aggressiveness (biting and hitting).• loss of motor function.• loss of appetite.• convulsions.• blindness.• self mutilation.• inability to swallow.

90% of deaths usually occur within one year of diagnosis, difficult to confirm diagnosis until post

mortem.

CJD Transmission:

• Humans can acquire the prion by exposure to meat that has come in contact with the brain or spinal column of the animal.

• Surgical equipment can be unknowingly infected by use on a patient with CJD, and because sterilization techniques do not kill the prion, the are transmitted to the other patients in subsequent procedures.

In common slaughtering practices, the animal is often sliced at least once

through the torso, severing the spinal column and exposing all the the

surrounding flesh to the infectious agent.

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CJDSimilarity to Alzheimer’s disease

• very similar patterns of dementia.

• because of late onset of CJD, both usually occur later in life.

• CJD often misdiagnosed as the more common Alzheimer’s, as only way to differentiate is post mortem brain autopsy (which most families do not agree to.

• However, a 1989 article in the journal Neurology explains that autopsies of 54 dementia patients at the Veterans Medical Center in Pittsburgh, PA revealed that 3 of the had actually died of CJD. Given this figure we can infer than as many as 5% of Alzheimer’s patients are actually suffering from CJD.

As with all TSE’s there is no cure or proven treatment.

New Variant CJD (vCJD)• Much earlier onset but same

symptoms as classic CJD, often with prolonged life expectancy.

• A recent test on surgical equipment used for tonsillectomies in the U.K. revealed that 50% of tools were infected with vCJD, even after sterilization and autoclaving. (The tonsils are one of the major glands where the body stores prions.)

Jonathan was diagnosed with vCJD at 17 and treated with the drug Pentosan polysulphate (PPS) , commonly used as an arthritis treatment for dogs. This extended his life by several years, but did not cure him.