Bacterial Infections of the GI Tract I

Question 1

How are most/all GI infections transmitted?

Answer 1

Fecal-oral route

Question 2

GI Host Defenses

Answer 2

1. Continuous Epithelium
2. Mucus
3. Low pH (Stomach)
4. Gut Motility
5. Shedding of epithelium
6. Bile
7. Secretory IgA
8. Normal microbiota

Question 3

Which GI host defenses can trigger the expression of bacterial virulence factors?

Answer 3

Mucus and Bile

Question 4

Gastritis

Answer 4

Inflammation of the stomach

Question 5

Gastroenteritis

Answer 5

Inflammation of the stomach and intestines (characterized by nausea, vomiting, diarrhea, and abdominal pain/discomfort)

Question 6

Dysentery

Answer 6

Inflammatory disorder of the GI tract associated with:

1. Diarrhea with BLOOD and PUS in the feces
2. Pain, fever, abdominal cramps
3. Usually results from disease of the LARGE INTESTINE

Question 7

Enteritis

Answer 7

Inflammation of the intestines, especially the SMALL INTESTINE

Question 8

Enterocolitis

Answer 8

Inflammation of the mucosa of the SMALL and LARGE INTESTINES

Question 9

Colitis

Answer 9

Inflammation of the COLON

Question 10

Inflammatory GI Bacteria (Signs)

Answer 10

• More likely to see occult or visible BLOOD
• More likely to see fecal LEUKOCYTES
  e. g. Salmonella spp., Campylobacter jejuni, C. difficile, EHEC, EIEC, Shigella spp., Vibrio parahaemolyticus, Yersinia enterocolitica

Question 11

Non-Inflammatory GI Bacteria (Signs)

Answer 11

• Bacteria passing through the intestine or adherent to intestinal epithelium
• Either:
  1) No known toxins
  2) Produce non-cytotoxic toxin (increase electrolyte and water efflux)
  e. g. EPEC, ETEC, Vibrio cholerae, Listeria monocytogenes

Question 12

General Characteristics of GI Pathogens

Answer 12

• Many can cause disease OUTSIDE of the GI tract
• Fecal-oral transmission
• Varied virulence factors (Toxin production)
• Prevalent infections (Food poisoning and GI infection)

Question 13

Bacterial Food Poisoning (Two Types)

Answer 13

1. Toxins produced by bacteria in the food before the food is consumed
2. Large numbers of spores ingested, spores germinate in intestine and vegetative bacteria produce toxins, there is no implied colonization or adherence to the GI tract

Question 14

Bacterial Food Poisoning (Symptoms and Four Bacterial Causes)

Answer 14

Symptoms: Diarrhea, vomiting, or both. NO FEVER

Bacterial Causes:

1) Staphylococcus aureus
2) Clostridium botulinum
3) Clostridium perfringens
4) Bacillus cereus

Question 15

Staphylococcus aureus (Characteristics)

Answer 15

1. Gram-positive cocci in clusters

2. NOT spore-forming

Question 16

Staphylococcus aureus (Disease)

Answer 16

1. Ingestion of preformed toxin

2. Severe vomiting, diarrhea, and abdominal pain within 1-8 hours after consumption

Question 17

Staphylococcus aureus (Pathogenesis)

Answer 17

HEAT STABLE TOXIN (Can bake food or reheat, but toxin remains stable)

Question 18

Staphylococcus aureus (Treatment)

Answer 18

Supportive Therapy

Question 19

Clostridium botulinum (Characteristics)

Answer 19

1. Gram-positive rod

2. SPORE-FORMING

Question 20

Clostridium botulinum (Disease)

Answer 20

• Botulism mediated by BOTULISM TOXIN (active ingredient in botox)
  1. Early: onset of vomiting, diarrhea, abdominal pain 1-8 hours post ingestion of PREFORMED TOXIN or 8-16 hours post ingestion of SPORS
  2. Late: FLACCID PARALYSIS –> Progressive muscle weakness and respiratory arrest (can lead to death)

Question 21

Clostridium botulinum (Pathogenesis)

Answer 21

Ingestion of:

1. Preformed toxin
2. Large number of spores –> germinate in intestine –> produce toxin

Botulism Toxin:
1. Toxin acts at NEUROMUSCULAR JUNCTIONS, interferes with signaling at synapses (i.e. blocks Acetylcholine release)

Question 22

Where is Clostridium botulinum an especially big issue?

Answer 22

With infants and honey

Question 23

Clostridium botulinum (Epidemiology, Complications, and Treatment)

Answer 23

Epidemiology: often seen in HOME-CANNING (improperly canned food items)

Complications: if patient survives, lingering weakness, dyspnea up to 1 year after primary disease

Treatment: Supportive therapy; IV anti-toxin administration

Question 24

Infant Botulism (i.e. Floppy Baby Syndrome)

Answer 24

Occurs between between birth and 1 year
-Germination of C. botulinum spores in intestins –> growth –> toxin production (often ingested when infants are fed HONEY (tight junctions are not formed enough yet to prevent toxin from coming through until 6+ months old)

***Milder and lower mortality than adult botulism

Question 25

Clostridium perfringens (Characteristics)

Answer 25

Gram-positive rod | SPORE-FORMING

Question 26

Clostridium perfringens (Disease)

Answer 26

1. Mediated by C. perfringens enterotoxin ***NOT endotoxin/LPS*** (Enterotoxin = protein toxins produced within the body) 2. Associated with contaminated meat products/gravies held at below recommended temperatures 3. Onset of diarrhea and abdominal cramps 8-16 hours post-ingestion and lasts for ~24 hours

Question 27

Clostridium perfringens (Treatment)

Answer 27

Supportive therapy

Question 28

Clostridium perfringens (Pathogenesis)

Answer 28

1. C. perfrigens spores survive cooking of food 2. Bacteria grow in food (not kept heated properly) 3. Ingestion of organisms 4. Organisms sporulate in the intestine 5. Sporulation leads to enterotoxin production 6. Toxin alters enterocyte membrane permeability 7. Diarrhea

Question 29

Bacillus cereus (Characteristics)

Answer 29

Gram-positive | SPORE-FORMING

Question 30

Bacillus cereus (Emetic Form: Disease and Pathogenesis)

Answer 30

- Onset of vomiting, nausea, and abdominal cramps 1-8 hours after ingestion of PREFORMED ENTEROTOXIN - Ingestion of preformed-heat stable enterotoxin - Associated with improper storage of COOKED RICE (spore survive cooking --> bacteria multiply --> produce a heat-stable enterotoxin that is not inactivated upon reheated)

Question 31

Bacillus cereus (Diarrheal form: Disease and Pathogenesis)

Answer 31

- Onset of diarrhea, nausea, and abdominal cramps 8-16 hours post-ingestion of food contaminated with organisms - Production of heat-liable enterotoxin in the intestine

Question 32

Bacillus cereus (Treatment)

Answer 32

Supportive Therapy

Question 33

Bacillus cereus (Emetic vs Diarrheal Forms: Food, Cause, Onset of symptoms post-ingestion, Symptoms, Enterotoxin)

Answer 33

Food: Rice vs Meat, Vegetables Cause: Preformed toxin vs Toxin production in the intestine Onset of symptoms post-ingestion: 15 min-8 hours vs 8-16 hours Symptoms: Vomiting, nausea, abdominal cramps vs Diarrhea, nausea, abdominal cramps Enterotoxin: HEAT-STABLE vs Heat Liable

Question 34

Helicobacter pylori (Characteristics)

Answer 34

- Gram-negative, curved rod | - Microaerophilic (5% oxygen)

Question 35

Helicobacter pylori (Disease)

Answer 35

- Ulcers | - Chronic gastritis (***STOMACH CANCERS in <1% of infections, TYPE I CARCINOGEN)

Question 36

Helicobacter pylori (Pathogenesis)

Answer 36

- Not completely understood - Flagella - UREASE - Cytotoxin-VacA - Adhesins

Question 37

Who linked H. pylori to ulcers rather than stress, smoking, and spicy foods?

Answer 37

Barry Marshall and Robin Warren (Marshall ingested H. pylori to prove it then treated with abx)

Question 38

Helicobacter pylori (Stomach: MOA)

Answer 38

1. H. pylori penetrate the mucous layer lining the stomach's epithelium, attracted to the chemotactic substances HEMIN and UREA 2. H. pylori recruit and activate inflammatory cells. It also releases UREASE that cleaves urea, producing NH3 that neutralizes stomach acid in its vicinity 3. H. pylori cytotoxin and the ammonia produced by its urease cause destruction of the mucus-producing cells, exposing the underlying connective tissue to stomach acid

Question 39

Helicobacter pylori (Diagnosis)

Answer 39

1. Urea breath test | 2. Biopsy

Question 40

Helicobacter pylori (Treatment)

Answer 40

1. Only after a POSITIVE test for H. pylori 2. Combination of: Antibiotics and Proton Pump Inhibitor (controls acid/further mucosal damage)

Question 41

Listeria monocytogenes (Small Intestine) (Characteristics)

Answer 41

Gram positive, facultative anaerobe Short rods, sometimes occur in pairs Intracellular pathogen

Question 42

Listeria monocytogenes (Key Survival Traits)

Answer 42

1. Wide growth range (1 to 45 degrees C) ***Psychrophilic = cold-loving*** 2. Resistant to high salt concentrations 3. Wide pH range

Question 43

Listeria monocytogenes (Epidemiology)

Answer 43

- Animal Reservoirs (mammals, birds, fish) - CONTAMINATED FOOD is primary source (ready to eat meats, raw vegetables) - High risk of infection in YOUTH, ELDERLY, IMMUNOCOMPROMISED, and PREGNANT - Human to Human transmission is possible; primarily from MOTHER TO FETUS

Question 44

Listeria monocytogenes (Clinical Manifestation)

Answer 44

-Healthy adults: usually asymptomatic (may have fever, nausea, and/or diarrhea; usually not severe) - Immunocompromised adults: 1) BACTEREMIA- fever, malaise, and chills with no obvious focus 2) MENINGITIS and ENCEPHALITIS- symptoms not distinct from other causes (fever, persistent headache, stiff neck, vomiting, and/or confusion); 20-50% mortality rate, significant neurologic sequelae in survivies

Question 45

Listeria monocytogenes (Clinical Manifestations Continued)

Answer 45

3) Infections in Pregnant Women- may develop nausea, fever, and/or diarrhea; fever with no obvious infection; risk of disease transmission to neonate 4) Neonatal infection- GRANULOMATOSIS INFANTISEPTICA (pyogenic granulomas distributed over the whole body, meningitis, encephalitis) - Earl onset (in utero transmission): can result in premature birth, abortion, or still-birth - Late onset: 2-3 weeks after birth

Question 46

Listeria monocytogenes (Pathogenesis)

Answer 46

1) Adherence and uptake (mediated by Internalin-A (IntA) 2) Internalized in endocytic vacuole 3) Acidification of vacuole/phagosome activates: Listeriolysin O (LLO)- disrupt vacuole membrane to allow for escape to the cytosol 4) Replication in host cell cytosol 5) ActA mediated actin polymerization (Spread to: neighboring cells and bloodstream by PUSHING THROUGH MEMBRANES) 5) Dissemination infection (Liver, Spleen, and CNS)

Question 47

Listeria monocytogenes (Diagnosis)

Answer 47

Microscopy of clinical samples is insensitive (too few bacteria, other gram + bacteria cause bacteremia and infect the CNS) * **Culture of cerebral spinal fluid and blood: - COLD ENRICHMENT SELECTION - Weak B-hemolysis on blood agar - Motility test

Question 48

Listeria monocytogenes (Treatment and Prevention)

Answer 48

Treatment: 1. Beta-Lactam or Trimethoprim-Sulfamethoxazole Prevention: 1. NO VACCINE AVAILABLE 2. Properly cook animal products including ready-to-eat meats, wash raw vegetables (especially if immunocompromised or pregnant)