The bacterium Streptococcus mutans is the primary cause of tooth cavities. S. mutans grows rapidly and produces biofilms in the presence of sugar. The biofilm is a protective layer, and if not removed it will harden through the addition of calcium in the process of calcification, producing tartar. Several other bacteria participate in the progression of decay started by S. mutans, including species of Lactobacillus and Actinomyces. When the buildup of tartar is not removed through regular oral hygiene, the gums become irritated and inflamed (gingivitis), resulting in bleeding and a condition known as periodontal disease. The bacteria associated with periodontal diseases are predominantly anaerobic bacteria and cause the erosion of the enamel and bone surrounding the teeth. Proper hygiene is suggested to prevent the development of cavities, including regular dental cleanings, flossing and brushing at least twice per day, and use of a strong antibiotic mouthwash to kill any remaining bacteria.
Foodborne Infections of the Digestive System
|Causative Agent||Description||Symptoms||Diagnosis and Treatment|
|Bacillus cereus||Soil-dwelling, gram-positive, endospore former; endotoxins released when heated during cooking.||There are two forms. In one, abdominal pain and diarrhea are typical; in the other, nausea and vomiting are typical.||Culture or isolation of bacteria from the contaminated food;
Self-limiting; rehydration and supportive care
|Campylobacter jejuni||Native of avian alimentary canal, gram-negative with variable shape (rod to vibrio to spiral and environmentally dependent) and a single flagella||Abdominal pain, cramps, diarrhea with dehydration, dysentery in severe infections, fever, vomiting; associated with Guillain-Barré syndrome||Not common, culture on selective media and environmental conditions;
Unnecessary, or ciprofloxacin and erythromycin. Resistance to ciprofloxacin is increasing in prevalence.
|Clostridium perfringens||Widely distributed in nature, endospore- and enterotoxin-forming gram-positive rod||Cramps and diarrhea||PCR, toxin detection in stool;
Rehydration—intravenous may be necessary.
|Listeria monocytogenes||Soil-dwelling, food-contaminating, gram-positive rod; along with two closely related species (L. ivanovii, L. grayi), is the causative age of listeriosis||Commonly problematic only for the elderly, immunocompromised, pregnant women, and the young. First symptoms are diarrhea or other alimentary canal symptoms. The pathogen may spread from the intestines to the blood, and confusion, convulsions, fever, headache, and muscle aches can occur. Miscarriage may occur in pregnant women.||Culture from blood or cerebrospinal fluid following spinal tap;
|Salmonella bongori and Salmonella enterica||Commensal in birds and common member of alimentary canal in other vertebrates, gram-negative rod, causative agent of salmonellosis||Abdominal cramps, diarrhea, fever, headache, nausea, vomiting. May (particularly Typhi strains) infect epithelial cells and migrate to the blood and lymph, resulting in systemic infection and exacerbating current symptoms, increasing vascular permeability, altering thermal regulation, decreasing blood volume, and causing septic shock.||Selective culture, PCR;
Often self-limiting. Rehydration alone and antibiotics in serious cases. Ampicillin, cephalosporins, fluoroquinolones. Some strains carry antibiotic resistance, particularly to ciprofloxacin.
|Staphylococcus aureus||Gram-positive cocci, forms clumps, typically found in human nasal passages and on skin||Nausea, vomiting, stomach cramps||Presence of symptoms, blood tests recommended in rare causes;
Plenty of fluids, antibiotics are not effective as toxins are not affected by them
Other Transmitted Infections of the Digestive System
|Causative Agent||Description||Transmission||Symptoms||Diagnosis and Treatment|
|Clostridium difficile||Commensal of the alimentary canal, endospore-forming gram-positive rod. Overgrowth is common following antibiotic therapy.||None or nosocomial||Abdominal pain, appetite suppression, colon inflammation, diarrhea with dehydration, fever. If the colon is perforated, septicemia and death can result.||Colonoscopy, ELISA to toxins, PCR;
Rehydration in mild cases; fidaxomicin, vancomycin
|Vibrio cholerae||Found in brackish aquatic environments, gram-negative comma-shaped rod, causative agent of cholera, susceptible to low pH so large doses are necessary for infection of intestines||Contaminated food or water||Abdominal cramps and vomiting. Extreme diarrhea resulting from enterotoxin-induced osmotic shifts in epithelial cells.||Differential culture from stool sample, Immunoassay
Self-limiting. Rehydration with electrolytes;
Azithromycin, ciprofloxacin, doxycycline, erythromycin, norfloxacin, tetracycline. Many strains have resistance to one or many antibiotics; of note are ampicillin, co-trimoxazole, and sulfamethoxazole-trimethoprim resistance.
|Escherichia coli||Commensal of alimentary canal, gram-negative rod; six pathogenic strains with additional virulence factors including enterotoxin, adhesin compounds that aid in colonization||Fecal-oral, contaminated food or water||Enterohemorrhagic strains: contains verotoxin acquired from Shigella dysenteriae, bloody diarrhea, cramps, may lead to life-threatening hemorrhagic colitis (colon inflammation). Enteroinvasive strains: epithelial cell invasion followed by chills, cramps, diarrhea with dehydration, dysentery, fever. Enteropathogenic strains: diarrhea with dehydration, fever, vomiting. Enterotoxigenic strains: abdominal cramps, diarrhea with dehydration, fever.||Culture and serological typing or PCR diagnosis of toxin genes;
Accurate diagnosis of strain is critical. Following antibiotic therapy, cell lysis of toxin-producing strains releases toxins and worsens conditions.
Self-limiting infections best treated with rehydration and supportive therapy. Antibiotic resistance is common in pathogenic and toxigenic strains, which may be treated with doxycycline, fluoroquinolones, or rifamycin. Antibiotics are not recommended for invasive or hemorrhagic strains.
|Helicobacter pylori||Common resident of the stomach, gram-negative curved rod (helical), causative agent of (peptic) stomach ulcers. Lack of H. pylori increases the risk of some cancers.||Person to person by saliva, fecal contamination of food and water||Appetite suppression, bloating, nausea, stomach inflammation (gastritis), weight loss. If allowed to develop, hemorrhagic ulcers and life-threatening perforation of the stomach can result.||Breath test (detection of radiolabeled CO2 in the breath resulting from treating the stomach with radiolabeled urea), direct detection in stool or stomach biopsy, immunoassay;
Multiple triple treatments are available. Each combines a pair of antibiotics (amoxicillin and clarithromycin, or metronidazole and tetracycline) with an acid-reducing therapy (omeprazole, bismuth subsalicylate, or lansoprazole).
|Shigella species||Found in primate alimentary canal, gram-negative rod, causative agent of shigellosis||Fecal-oral||Abdominal cramps, diarrhea (in some cases with blood or mucus), fever, flatulence, nausea, vomiting. In strains carrying Shiga toxin: hemorrhage of colonic epithelial cells and dysentery, hemolytic uremic syndrome, or reactive arthritis.||Immunoassay, PCR of stool sample;
Azithromycin, ciprofloxacin. Ciprofloxacin resistance occurs in some strains.
|Yersinia enterocolitica||Environmentally widespread gram-negative rod, may produce endotoxins and exotoxins||Zoonotic, fecal-oral||Abdominal cramps, diarrhea, more severe symptoms if spread into blood||Detection in stool;
Self-limiting, rehydration. Aminoglycoside, doxycycline, fluoroquinolones, or sulfamethoxazole-trimethoprim in systemic or blood infections.