Bacillus Cereus

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Bacillus cereus

Objectives of study
1. morphology
2. Epidemiology
3. Mode of transmission
4. Life cycle
5. Pathogenesis
6. Clinical features
7. Precaution and treatment.
Introduction.
• Belong to Bacillaceae family.
• Behaves as an opportunistic pathogen to humans.
• Main reservoir is the soil.
• Can colonises mammals and insects.
• Associated with food-borne illnesses.
Morphology.

• Gram positive bacteria


• Rod shaped.
• Motile bacteria- have flagella.
• Uncapsulated.
• Occur singly or in pairs.
• It is a facultative anaerobe.
• Forms endospores that make it resistant to harsh conditions.
Epidemiology and transmission.
• B.cereus is widely distributed in the environment.
• Mostly found in soul and particularly associated with rice- causes fried rice
syndrome.
• Spread by ingestion of contaminated food material – rice, pasta, potatoes,
meat and vegetables.
• Improper food handling, storage and preparation can lead to contamination
and subsequent food poisoning.
• Affects individuals of all ages and backgrounds but causes severe illness in
people with compromised immune systems, the elderly and young children.
• Lacks a specific host- thrive on a wide range of foods that provide nutrients
for growth and toxin production.
• Bacillus cereus is known to cause food poisoning caused by the
enterotoxins it produces.
Involves an emetic syndrome, diarrhoeal syndrome and gastroenteritis.
Pathogenesis.
• When contaminated food is ingested, the bacteria or their spores
enter the digestive system.
• Some of the bacteria and spores survive the acidic conditions in the
stomach allowing them to reach the intestine.
• Once in the intestines, spores germinate under favourable conditions
into vegetative cells and multiply.
• They then produced enterotoxins of two types that are responsible
for the emetic and diarrhoeal syndromes.
• Toxins are of two types:1. heat stable emetic toxin.
2. heat labile diarrheal toxin.
• Emetic toxin- also known as cereulide, interacts with 5-HT3 receptors
in the brain, stimulating the vomiting centre in the brainstem,
triggering the sensation of nausea and vomiting.
the toxin is preformed and ingestion of bacteria is not necessary
inorder to cause emesis.
• Diarrheal toxin- an enterotoxin, produced by vegetative cells. Toxin
binds to specific receptors on intestinal walls, especially the brush
border. It causes increases cyclic AMP levels that activate protein
kinase A. This leads to opening of ion channels that allow electrolytes
to leak out and draw out water leading to the watery diarrhea.
• NOTE: the toxin is not preformed.
Virulence factors.
1. Toxins- two types, heat stable emetic toxin and heat labile diarrheal
toxin. These toxins are central to its pathogenicity as previously
discussed.
2. S- layer- consists of proteins or glycoproteins and play a variety of
roles. Has a role in the adhesion of these bacteria, has anti-
proteolytic properties hence protects against proteolytic enzymes
and also plays a role in promoting increased radiation resistance.
3. Hemolysins- can lyse red blood cells and contribute to tissue
damage and facilitate the spread of the bacterium.
4. Flagella- for motility.
5. Phospholipases- break down phospholipases hence degrading host
cell membranes contributing to both tissue damage and spread of
the bacterium.
6. Beta lactamase- makes the bacteria resistant to penicillins.
Clinical features
1. Food poisoning.- caused by the two toxins produced.
self limiting as symptoms fade after 24hrs.
emetic toxin-causes emetic syndrome
diarrheal toxin- causes diarrheal syndrome.
Emetic syndrome- has a short incubation of about 1-5 hours.
-presents with nausea vomiting and abdominal
cramps.
-short incubation period because of the
preformed heat stable toxin.
Diarrheal syndrome- has a longer incubation period because the
toxin first has to be formed by the vegetatative cells that germinate
from spores. Approximately 8-18 hrs.
-presents with a watery non-bloody diarrhea,
Continuation…
Nausea and abdominal cramps.
Vomiting and fever are less common.

2. Ocular diseases- causes keratitis and panophthalmitis following


trauma.
-also causes endophthalmitis.
3. Systemic disorders such as endocarditis, meningitis and
osteomyelitis.
4.Bactericemia may occur from medical prosthetic devices.
Lab diagnosis.
Specimen: vomitus, stool, blood and csf incase of meningitis.
Microscopy: uncapsulated rod shaped gram positive bacteria.
negative McFaydean’s test-lacks the glutamic acid capsule.
Culture: Blood agar: beta hemolytic colonies.
MYPA medium: colonies have a pink- purple colour surrounded
by pink precipitation.
PEMBA medium: blue colonies.
Biochemical tests: catalase positive
oxidase negative.
coagulase negative.
lecinthinase positive.
Serologic tests: PCR can detect bacterial DNA.
radioimmunoassay and elisa tests by use of polyclonal
and monoclonal antibody tests specific to B. cereus.
MYPA medium. PEMBA medium.
Treatment and prevention.
Treatment:
Resistant to penicillins due to beta lactamase.
Clindamycin and vancomycin should be given during serious infections, with or
without an aminoglycoside.
Also susceptible to erythromycin.

Prevention.
Proper cooking of food at high temperatures to ensure spore death.
Refrigeration
Proper food storage methods.
Practicing hand hygiene.
Use of clean utensils and surfaces to avoid contamination.
Thankyou

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