Microbial Diseases of the Digestive System

Chapter 25: Microbial Diseases of the Digestive System

Learning Objectives

  • Describe 2 common helminthic diseases.
  • Discuss the protozoan that causes giardiasis.
  • Identify the causes of ergot poisoning, aflatoxin poisoning, and their association with fungal diseases.
  • List the causative agents, mode of transmission, and symptoms of mumps and viral gastroenteritis.
  • Discuss bacterial diseases of the lower digestive system.
  • Describe the events that lead to dental caries and periodontal disease.
  • Identify parts of the gastrointestinal tract that normally have microbiota.
  • Name the structures of the digestive system.

Structure and Function of the Digestive System

  • Gastrointestinal (GI) tract or alimentary canal:
    • Components:
    • Mouth
    • Pharynx (throat)
    • Esophagus
    • Stomach
    • Small intestine
    • Large intestine
  • Accessory structures that provide mechanical and chemical support:
    • Teeth
    • Tongue
    • Salivary glands (Parotid)
    • Liver
    • Gallbladder
    • Pancreas

Purpose of the Digestive System
  • Absorbs foods:
    • End products of digestion (nutrients) pass from small intestine into blood or lymph.
    • Food moves to large intestines where water and nutrients are absorbed.
    • Remarkable Fact: 25 tons of food pass through the GI tract in a lifetime.
Intestinal Gas (Flatus)
  • Definition: A mixture of microbially produced gases including nitrogen, carbon dioxide, hydrogen, and methane.
  • Feces (stool): Undigested solids eliminated from the body through the anus.
Immune System Development
  • Development of the immune system is significantly influenced by intestinal microbes (microbiota).
  • Statistic: 70% of immune system cells are located in the intestinal tract.
  • Components of Gut-Associated Lymphoid Tissue (GALT):
    • Lymph nodes
    • Peyer’s patches (similar to lymph nodes; prevent the growth of pathogenic bacteria).

Normal Microbiota of the Digestive System

  • Oral Cavity:
    • Millions of bacteria per milliliter of saliva, supporting a diverse microbial population.
  • Stomach and Small Intestine:
    • Few microorganisms due to HCl acid production and rapid movement through the small intestine.
    • Common microbe: Streptococcus mutans.
  • Small Intestine:
    • Paneth Cells: Granule-filled phagocytic cells that produce defensins and lysozymes to regulate intestinal microbiota.
  • Large Intestine:
    • Contains a vast number of bacteria: anaerobes and facultative anaerobes that assist in degrading food and synthesizing vitamins.
    • Statistic: 100 billion bacteria per gram of feces; 40% of fecal mass is microbial cells. Common microbes include: Bifidobacterium, Lactobacillus, Enterobacteriaceae.

Bacterial Diseases of the Mouth

  • The mouth serves as an entrance to the digestive system, supporting diverse microbial populations.
  • Prevalence: Diseases of the digestive system are the 2nd most common illness in the U.S. resulting from ingesting microbes or toxins in food and water.
  • Transmission: Fecal-oral route; preventable via proper sewage disposal, drinking water disinfection, and careful food preparation/storage.
Dental Caries (Tooth Decay)
  • Plaque Formation:
    • Dental plaque is a biofilm involved in caries formation; consists of microbes and dextran.
    • Around 700 species of bacteria inhabit the oral cavity with Streptococcus mutans being the most significant cariogenic organism.
  • Mechanism:
    • Streptococcus mutans, a Gram-positive coccus, converts sucrose to lactic acid and utilizes glucose to produce dextran (a polysaccharide that forms plaque).
  • Caries Mechanism:
    • Caries penetrate from enamel into dentin caused by local acid production arising from Gram-positive rods and filamentous bacteria.
    • Infection can reach pulp leading to severe complications, such as abscesses.
  • Dietary Impact:
    • Sucrose introduction correlates with increased dental caries.
    • Sugar alcohols (mannitol, xylitol) are non-cariogenic.
Periodontal Disease
  • Gingivitis: Inflammation and infection of the gums caused by various bacteria including streptococci, actinomycetes, and anaerobic Gram-negative bacteria.
  • Periodontitis: A chronic disease caused by inflammation, leading to the destruction of bone and tissue supporting teeth, primarily by Porphyromonas.
  • Acute Necrotizing Ulcerative Gingivitis (Trench Mouth): Caused by Prevotella intermedia; often occurs in tobacco users.
Diseases of the Mouth Summary
DiseasePathogenSymptomsTreatmentPrevention
Dental CariesPrimarily S. mutansDiscoloration or holes in tooth enamelRemoval of decayed areaBrushing, flossing, reducing dietary sucrose
Periodontal DiseaseVarious, primarily Porphyromonas spp.Bleeding gums, pus pocketsRemoval of damaged area; antibioticsPlaque removal
Acute Necrotizing Ulcerative GingivitisPrevotella intermediaPain with chewing, halitosisRemoval of damaged area; antibioticsBrushing, flossing

Bacterial Diseases of the Lower Digestive System

  • Infection vs. Intoxication:
    • Infection: Growth of pathogens in the intestines; incubation ranges from 12 hours to 2 weeks; generally includes fever.
    • Intoxication: Caused by ingesting preformed bacterial toxins; symptoms appear 1 hour to 48 hours after ingestion; fever is typically not present.
Symptoms and Treatment
  • Both infections and intoxications can lead to diarrhea, dysentery (severe diarrhea with blood and mucus), or gastroenteritis (inflammation).
  • Treatment: Includes fluids and oral electrolyte replacement.
Distinction between Infection and Intoxication
  • Discuss the nuances of bacterial infection versus bacterial intoxication, focusing on causative agents, symptomatic onset, and distinguishing features in clinical appearances.

Staphylococcal Food Poisoning (Staphylococcal Enterotoxicosis)

  • Causative Agent: Enterotoxin produced by Staphylococcus aureus (Gram-positive coccus; Serological type A).
  • Resistance: The toxin is not destroyed by boiling.
  • Toxins are produced when the organism incubates food at room temperature, particularly in high osmotic pressure environments such as cured ham.
Sequence of Events in Outbreak
  1. Food containing protein is cooked, killing bacteria.
  2. Food is contaminated by worker with staphylococci on hands.
  3. Food is left at room temperature, allowing organisms to incubate and release toxins (temperature abuse).
  4. Toxins are ingested.
  5. Onset of staphylococcal intoxication occurs in 1-6 hours.
Comparison of Foodborne Illnesses
  • Consider how bacterial food poisoning differs from foodborne illnesses caused by viruses, focusing on transmission modes.

Shigellosis (Bacillary Dysentery)

  • Causative Agent: Genus Shigella (facultative anaerobic; Gram-negative), specifically four species identified:
    • Shigella dysenteriae: most severe yet least common.
    • Shigella sonnei: mild dysentery; most common.
  • Associated with salad consumption; produces the Shiga toxin leading to symptomatic blood and mucus in stool, abdominal cramps, and fever.
  • Mechanism of Infection: Small infectious dose due to invasion of M cells, damaging the intestinal wall, rarely spreading to the bloodstream.

Salmonellosis (Salmonella Gastroenteritis)

  • Causative Agent: Salmonella enterica (Gram-negative, facultative anaerobe); normal inhabitant of human intestinal tract and various animals.
  • Transmission Associated with:
    • Commercial chicken and egg production (e.g., Salmonella enterica, Typhimurium or Enteritidis).
  • Incubation: 12 to 36 hours leading to symptoms like fever, nausea, cramps, and diarrhea.
  • Statistics: Approximately 1 million cases with 380 annual deaths (mortality <1%).
  • Mechanism of Action: Invades intestinal mucosa and multiplies, utilizing M cells and replicating in macrophages.
Cholera
  • Causative Agent: Vibrio cholerae (slightly curved, Gram-negative rod with a single polar flagellum).
  • Produces the cholera toxin, leading to secretion of electrolytes and water, resulting in severe fluid loss (12 to 20 liters per day).
  • Symptoms: Dehydration, shock, organ failure, and potential death.
  • Treatment includes intravenous fluid replacement.
  • Public Health Concern: Significant risk in areas with compromised sanitation (e.g., Africa, Asia, Haiti).
Preventative Measures for Cholera
  • Strategies include:
    • Oral rehydration solutions.
    • Stockpiling vaccines.
    • Ultimate goal: proper sanitation, including water storage and handwashing practices.

Escherichia coli Strains & Gastroenteritis

  • E. coli Groupings:
    • Enteropathogenic E. coli (EPEC): Diarrhea in developing countries.
    • Enteroinvasive E. coli (EIEC): Causes diarrhea and dysentery (similar to Shigella).
    • Enteroaggregative E. coli (EAEC): Causes watery diarrhea via enterotoxin; common in travelers.
    • Enterohemorrhagic E. coli (EHEC): Produces Shiga-like toxin, often linked to serotype O157:H7, leading to hemorrhagic colitis and hemolytic uremic syndrome.

Viral Diseases of the Digestive System

Mumps
  • Causative Agent: Mumps virus; targets parotid (salivary) glands.
  • Transmission: Enters the body through the respiratory tract, spreads via saliva.
  • Symptoms: Painful swelling occurs 16 to 18 days post-exposure, with possible complications like orchitis, meningitis, ovarian inflammation, and pancreatitis.
  • Prevention: MMR vaccine (Measles, Mumps, Rubella).
Viral Gastroenteritis
  • Causative Agents: Mainly Rotavirus and Norovirus.
    • Rotavirus: Common in children; low mortality rate; incubation of 2 to 3 days; spread via fecal-oral route; prevented by live oral vaccine.
    • Norovirus: Known for cruise ship outbreaks; fecal-oral transmission; low infectious dose; incubation typically 18-48 hours; caused vomiting and diarrhea.

Fungal Diseases of the Digestive System

Ergot and Aflatoxin Poisoning
  • Definition of Mycotoxins: Toxins produced by fungi resulting in various health issues including blood diseases, nervous system disorders, kidney damage, liver damage, and cancer.
    • Produced by Claviceps (fungus) and Aspergillus (mold).
  • Ergot Poisoning:
    • Caused by mycotoxins from Claviceps purpurea, which occur in cereal grains. Results in restricted blood flow (gangrene) and hallucinations.
  • Aflatoxin Poisoning:
    • Caused by mycotoxins from Aspergillus flavus, often found on peanuts, leading to liver cirrhosis and liver cancer.

Protozoan Diseases of the Digestive System

Giardiasis
  • Causative Agent: Giardia intestinalis (flagellated protozoan).
  • Lifecycle: Forms cysts in feces/tap water, develops into trophozoites in the human body; attaches to the intestinal wall.
  • Symptoms: Drinking contaminated water can lead to prolonged diarrhea, malaise, weight loss, flatulence, and cramps with hydrogen sulfide detected in breath/stools.
  • Diagnosis: Microscopic examination of stool samples for cysts.

Helminthic Diseases of the Digestive System

Common Helminths (2015 Data)
  • Prevalence of Human Infections:
    • Trichuris, Ascaris, Hookworms, Schistosomes, Taenia (beef, pork), Flukes (liver, lung) measured in millions of individuals infected.
Nematodes: Whipworm (Trichuris)
  • Causative Agent: Trichuris trichiura, a whipworm that measures 30 to 50 millimeters.
  • Lifecycle: Eggs are ingested, hatch in the intestines, and adult worms feed on cell contents and blood.
  • Symptoms: Causes anemia, malnutrition, and retarded growth.
  • Treatment: Mebendazole or albendazole.
Nematodes: Ascariasis
  • Causative Agent: Ascaris lumbricoides, which can grow up to 30 cm long.
  • Prevalence: Infected 30% of worldwide population; eggs shed in feces and are ingested.
  • Lifecycle: Larvae migrate to the bloodstream, lungs, and back to the intestines to develop into adults. Symptoms can include severe obstruction.
  • Treatment: Mebendazole or albendazole.

Tapeworms
  • How: Contracted via undercooked food.
    • Types include: Beef tapeworm (Taenia saginata), Pork tapeworm (Taenia solium), Fish tapeworm (Diphyllobothrium latum).
  • Taeniasis: Adult tapeworm infects the intestine, with eggs shed in feces.
  • Cysticercosis: Larval stage infection occurs by ingestion of eggs, leading to symptoms including neurocysticercosis.

Conclusion

Group Presentation Guidelines
  • Presentations should be approximately 5 minutes and include:
    • Disease
    • Affected region of the body
    • Cause of the disease
    • Microbe details (classification, description)
    • Public health relevance (affected geographical regions and populations, eradication efforts, vaccines, treatments, and cures).