aspergillus flavus pharmacognosy

1. ASPERGILUS FLAVUS
GROUP 1
MEMBERS
GREGORY FELIX
BEATUS MALLONGE
BILASA CHUNGA
JAMES BENNO
CALVIN MAAYA
PETRO EMMANUEL

2. INTRODUCTION
Scientific Name: Aspergillus flavus
Common names: Aspergillus boll rot of cotton, Aspergillus corn ear
rot, yellow mold of peanut or storage rot.
Family Trichocomaceae
Aspergillus flavus is saprotrophic and pathogenic fungus, it grows by
producing thread like branching filaments known as hyphae.

3. MAJOR EVENT OF TOXICITY
• In US poisonous food was responsible for killing more than 77 dogs. The
research was done by Cornell university to identify kind of poison present
in pet food.
• They found out that the poison was one of the most deadly natural
substances possibly the carcinogenic substance tested by rat liver assay,
mostly occur in peanut and corn plus other grain food when condition was
favorable.
• USDA came to identify the poison that was a toxic secondary metabolite
produced by a fungus Aspergillus FLAvus hence name the toxin aflatoxin.
• They came out to realize that the corns crops grown in that year had high
prevalence of aflatoxin.

4. DISTRIBUTION
• NORTH AFRICAN COUNTRIES
• In Egypt
• Morocco
• Tunisia
• CENTRAL AFRICAN COUNTRIES
• In Zambia
• EAST AFRICAN COUNTRIES
• Kenya
• Uganda
• Tanzania
• WEST AFRICAN COUNTRIES
• Nigeria
• Ivory cost
• Ghana

5. TOXIC CONSTITUENT
• Aspergillus flavus is an opportunistic pathogen of crops. It is
important because it produces aflatoxin as a secondary metabolite in
the seeds of a number of crops both before and after harvest.
Aflatoxin is a potent carcinogen that is highly regulated in most
countries. In the field, aflatoxin is associated with drought-stressed
oilseed crops including maize, peanut, cottonseed and tree nuts.
Under the right conditions, the fungus will grow and produce
aflatoxin in almost any stored crop seed.

6. MECHANISM OF ACTION
• Aflatoxin is a byproduct of mold that can cause DNA damage. With
prolonged exposure to aflatoxin, cells accumulate DNA mutations and thus
are at increased risk of developing into cancer cells. It forms a reactive
epoxide intermediate, which then forms a covalent bond to the N7 atom of
guanine in site-specific sequences within critical target genes leading to
mutations, altered function, loss of function of those genes. p53 is a major
target for aflatoxin.” “Aflatoxin is probably the best example of a
carcinogen, a human carcinogen that targets p53. There are multiple hot
spots in the p53 gene targeted by different types of carcinogens. Aflatoxin
targets a guanine in codon 249 in the p53 gene. Intermittent sort of
random exposures are not likely to sort of tip the balance and create the
cancer .

7. Aflatoxin Poisoning
• Aflatoxicosis -The technical term for poisoning by aflatoxin mycotoxins is
aflatoxicosis. This usually occurs from eating food contaminated with
aflatoxin mycotoxins.
Aflatoxicosis is not contagious and drugs and antibiotics do little to help.
• Aflatoxicosis damages the liver more than any other organ. Aflatoxin
mycotoxins also suppress the immune system. Aflatoxin mycotoxins are
toxic to humans and even more toxic to animals. They also cause cancer in
humans and animals.
It is believed that eating vegetables like carrots and celery reduces the
carcinogenic effects of aflatoxins.

8. SIGN AND SYMPTOMS
• There are two main ways people are usually exposed to aflatoxins. The first is
when someone takes in a high amount of aflatoxins in a very short time. This can
cause:
Liver damage
• Liver cancer
• Mental impairment
• Abdominal Pain
• Vomiting
• Convulsions
• Edema
• Pulmonary Edema
• Hemorrhaging
• Disruption of food digestion, absorption or metabolism
• Coma
• Death

9. Signs and symptoms cont...
• The other way people suffer aflatoxin poisoning is by taking in small
amounts of aflatoxins at a time, but over a long period. This might
happen if a person's diet has a small amount of aflatoxins, for
example. When this happens it can cause:
Growth and development impairment
• Liver cancer due to DNA mutation caused by aflatoxins

10. DETRIMENTAL EFFECTS
• Chronic granulomatous sinusitis
• Keratitis
• Cutaneous aspergillosis
• Wound infections
• Osteomyelitis following trauma
• hepatocarcinoma