Micro Chap 22

• a continuously formed coating of micro-organisms and organic matter on tooth surfaces.
• first step in tooth decay & gum disease.

• Tooth decay.
• The chemical dissolution of enamel and deeper parts of teeth.

A combination of gum inflammation and erosion of periodontal ligaments and the alveolar bone that supports teeth.

Mildest form of Periodontal Disease that only affects the gums.

Modst severe form of ginigvitis aka Trench Mounth.

Unchecked Periodontal disease leads to chronic periodontitis which affects the bone and tissue that support the teeth as well as the gums.

The combination of sucrose and the action of S. mutans

• Sugars easily diffuse through plaque to bacteria embeded in it, but acids produced by bacterial fermentation fail to diffuse out.
• The acids gradually dissolve enamel, after which protein-digesting enzymes break down any remaining material.

• Plaque begins as positively charged proteins in saliva adhere to negatively charged enamel surfaces and form a pellicle(film) over the tooth surface.
• Streptococcus mutans and some filamentous bacteria among the normal oral flora microbiota attach to the newly formed pellicle.
• These organisms may hydrolyse sucrose to fructose and gluecose both of which can be metabolized for energy production and growth.

• Staphylococcus aureus.
• Clostridum perfringens.
• Bacillus cereus.

Salmonella (serveral serovars).

Salmonella typhi.

• Shigella dysenteriae (serovar A)
• Shigella flexneri (serovar B)
• Shigella boydii (serovar C)
• Shigella sonnei (serovar D)

Vibrio cholerae. O1 and O139

Pathagenic strains of E. coli.

E. coli O157:H7

Helicobacter pylori.

Enterotoxin A or D (heat stable)

• Enterotoxin=exotoxins that inflame intestines and block water absorption.
• Intoxications rather than infections.

enterotoxin A released only during sporulation

heat labile enterotoxin - function to Diarrheal disease.

Death may result from endotoxin shock

Enterotoxin (cholera toxin) binds to epithelial cells of the small intestine and makes plasma membranes highly permeable to water.

enterotoxigenic strains - have plasmid which encodes for enterotoxin.

Shiga Toxin 1 & 2

• aka LPS (lipopolysaccharide)
• A toxin incorporated in Gram-neg bacterial cell walls and released when the bacterium dies.

An exotoxin that acts on tissues of the gut.

A soluble toxin secreted by microbes into their surroundings, including host tissues.

Any substance that is poisonous to other organisms.

• Extremely fat onset 1-6hrs after injestion.
• Vomiting.
• Nausea.
• Diarrhea.
• self-limiting intoxication 1-3 days.

• Nausea.
• Vomiting w/n 12 hours after injestion.
• Self-limiting, 1-2 days.

• Induces vomiting w/n 12hrs after ingestion.
• short-lived infection.

• Nausea/Vomiting.
• Abdominal pain/Diarrhea.
• Headache.
• Chills.
• Muscular weekness, faintness.
• Mod. Fever/ festlessness and drowsiness.
• 2-3 days.

• Fever 104' due to pyrogens.
• Headach.
• Constipation (normally no diarrhea).
• rash: abdominal rose spots.
• septicemia, bacteria localized in the gall bladder.
• Death may result form endotoxin shock.

An infection caused by rapid multiplcation of pathogens in the blood.

bacillary dysentery (a severe diarrhea that often contains mucus and sometimes blood or pus).

• significant secretion of fluids and chloride ions and inhibition of Na absorption.
• watery diarrhea speckeld with flakes (rice water stool)
• loss of potassium ions results cardiac complicaitons and circulatory failure.
• untreated results in high mortality rates.

• Causes hemorrhagic uremic syndrome.
• Kidney damage and bleeding in the urinary tract.
• Hemolytic uremic syndrome (HUS).
• baby born w/ enlarged liver and spleen Rh- mom.

• lesions of the mucous memberanes lining the esophagus, stomach or duodenum.
• chronic gastritis (stomach inflammation) can produce pain and indigestion.

• Staphylococcus aureus.
• Clostridium perfrigens.
• Bacillus cereus.

• Prompt refrigeration.
• Avoid preparing food with open wounds or skin infections on hands, wrists.
• Proper Hygiene.

• supportive care.
• leftover cooked meat should be refrigerated promptly and reheatd thoroughly before serving (75'C).

• Most are self limiting and will resolve on their own.
• To avoid creating resistant strains.

Antibiotics kill bacteria but the bacteria releases toxins either into host tissue or releases toxins as it dies.

• Staphyloccoccus aureus - BFP
• Clostridium perfringens - BFP

Bacillus cereus.

Mary Mallon: an immigrant, Irish woman who made her way a a cook.

• She was well liked.
• the bacteria was localized in her gall bladder which she refused to have removed.
• She was a cook.

Enteroinvasive strains of E. Coli have plasmid encoded K antigen that allows bacterial cell to invade intestinal mucosal cell.

Enterotoxigenic strains of E.coli have plasmids whcih encode for enterotoxin.

• O refers to the O-antigen (lipopolysaccharide).
• H refers to the H-antigen (flagella)
• Produces Shiga toxins 1 and 2 (may have received these genes from a plasmid from Shigella)

• survives acidic conditions of the stomach by generating ammonia from urea.
• Urea + H20 --> 2NH3 + C02.
• The amonia neutralizes gastric acidity around the cells, allowing the organism to survive and reproduce.
• colonize and multiply in the gastric mucosa directly above the epithelial cell layer of the stomach.

• Hylicobacter Pylori colonize the gastric mucosa.
• Causes sloughing away of dead inflammatory tissue and exposure to acid in the epithelium.
• Lesions eventually result in excavation into the surface of the organ.