CH 24 - Digestive System Infections Flashcards
Cirrhosis
(definition)
Scarring of liver that interferes with normal liver function
Dental caries
(definition)
Biofilm-mediated process that damages tooth enamel
Dysbiosis
(definition)
Imbalance in normal microbiota
May be caused by taking antimicrobial medications
Dysentery
(definiton)
Serious form of diarrhea characterized by blood, pus, & mucus in feces
Gastroenteritis
(definition)
Acute inflammation of stomach & intestines
Syndrome of nausea, vomiting, diarrhea, abdominal pain
Gingivitis
(definition)
Inflammation of gums
Hemolytic Uremic Syndrome (HUS)
(definition)
Serious condition characterized by RBC breakdown & kidney failure
Hepatitis
(definition)
Inflammation of the liver
Microvilli
(defintion)
Tiny extensions from surfaces of cells such as those lining the intestinal villi
Increase surface area of mucosa
Oral Rehydration Therapy (ORT)
(definition)
Treatment used to replace fluid & electrolytes lost due to diarrhea
Potential Dangers in Thanksgiving Dinner
- Taenia solium (tapeworm)
- Clostridium botulinum
- Salmonella enterica (Campylobacter)
- Staphylococcus aureus
- Escherica coi
- Dental caries (Streptococcus mutans)
Normal Microbiota of the Digestive System:
Esophagus/stomach/duodenum, oral cavity (tongue/teeth), lower small intestine/colon
Esophagus/stomach/duodenum:
- Few resident microbes
Oral cavity (tongue/teeth):
- Viridans streptococci
Lower small intestine & colon:
- Tremendous amount of microbes
- Act as microbial antagonists against transient microbes
Antibiotic-Associated Diarrhea
Microbiota prevent colonization of some pathogenic bacteria
Use of antibiotics disrupts normal microbiota (mild to severe diarrhea)
Toxin-producing bacteria can colonize newly uninhabited intestine
- Damage epithelial cells
- Ex: Clostridium difficile
Dental Caries:
Causative Agent
Streptococcus mutans
- G+ facultative anaerobe
- 10,000 CFU/mL in mouth
Other bacteria participate as well
Streptococcus mutans Virulence Factors:
- Extracellular matrix of glucans from sucrose
- Tolerant to acidic environment
- Produce lactic acid when metabolizing sugars
Dental Caries:
Symptoms
- Toothache
- Discoloration
- Roughening of enamel
- Tooth breakage
Dental Caries:
Pathogenesis
- Attachment of bacteria to enamel & formation of cariogenic plaque
- Addition of sugars (sucrose) to environment causes drop in pH (~5)
- Due to fermentation
- Dissolves calcium phosphate of enamel
Dental Caries:
Prevention
- Good oral hygiene
- Reduce/eliminate sugary foods - Fluoride
- Protects teeth from demineralization caused by acid
- Promotes remineralization
Dental Caries:
Treatment
Drilling of diseased region & filling defect to restore contour of tooth
- Filling of composite or amalgam
Peptic Ulcers:
Causative Agent
Helicobacter pylori
- G-
- Multiflagellated
- Microaerophile
Peptic Ulcers:
Symptoms
- Stomach ache
- Abdominal pain
- Acid reflux
- Regurgitation
- Vomiting
- Belching
- Flatulence
- Nausea
Untreated Helicobacter pylori Infection Can Cause:
- Peptic ulcers (duodenal or gastric)
- Gastroesophageal reflux (GERD)
- Cancers of esophagus & stomach
Peptic Ulcers:
Pathogenesis
- Bacteria invade mucus & attach to gastric epithelial cells
- Helicobacter, its toxins, & inflammation cause layer of mucus to become thin
- Gastric acid destroys epithelial cells & underlying disease
Peptic Ulcers:
Epidemiology (Urease Test)
Conversion of urea into CO2 can be detected in breath
Breakdown of urea by urease enzyme
- Releases ammonia & CO2
Peptic Ulcers:
Treatment
- Proton pump inhibitors (PPIs)
- Reduce acid (heal stomach) - Antibiotics (kill bacteria)
- Clarithromycin
- Amoxicillin
Peptic Ulcers:
Barry Marshall
Drank H. pylori & developed ulcer
Marshall & Warren won Nobel Prize in 2005
Cholera:
Causative Agent
Vibrio cholerae
- G-
- Polar flagellum
Found naturally in aquatic environments (salt & fresh water)
Infects humans upon consumption of contaminated food & water
Cholera:
Symptoms
- Watery diarrhea in large volumes (1-6 L/hr; “rice-water” stool)
- Vomiting
- Muscle cramps
- Organ failure
- Cholera toxin (causes primary symptom)
Cholera:
Epidemiology
1.3-4 million cases/year
- 21-143,000 deaths/year (WHO)
1849 cholera epidemic
- 600 deaths/5000 population (12%)
Cholera:
Dr. John Snow
“Father” of modern epidemiology
Worked to determine source of cholera epidemic in London 1854
- Traced to single water source (water pump)
Cholera:
Pathogenesis
- Bacteria ingested
- Colonize small intestine
- Express cholera toxin (CT)
- Encoded by lysogenic bacteriophage
Cholera:
Cholera Toxin (CT)
B subunit = binding
- Binds to gangliosides on epithelial cell surfaces
A subunit = active
1. Translocated
2. Catalyses ADP-ribosylation of Gs protein
3. Gs activates adenylate cyclase
4. Overproduction of cAMP
5. AMP causes ion channels to open
6. Massive secretion of ions & water into lumen
Cholera:
Treatment
Oral rehydration therapy (ORT)
- Electrolytes to successfully rehydrate pts
IV rehydration (non-responsive pts)
Cholera:
Prevention
Whole cell killed vaccine
- Somewhat protective but short-lived
- Doesn’t work well in small children
Continued search for live vaccine
Shigellosis:
Causative Agent
Shigella
- G-
- Non-flagellated
Fecal-oral contact (primarily young children)
All species cause dysentery
Shigellosis:
Shigella species
- S. flexneri
- S. boydii
- S. sonnei
- S. dysenteriae
Shigellosis:
Pathogenesis
Invades cells in large intestine
- Attaches to epithelial cell of colon
- Triggers endocytosis
- Multiplies in cytosol - Invades neighboring epithelial cells
- Avoids immune defenses
- Abscess forms as epithelial cells killed - Shigella that enters blood = quickly phagocytized & destroyed
Shigellosis:
Shiga Toxin (ST)
A-B toxin
- Carried on lysogenic bacterophage
Inhibits protein synthesis
Can cause hemolytic uremia syndrome (HUS)
- Associated with Enterohemorrhagic Escherichia coli (EHEC) which also carry ST NOT Shigella
Shigellosis:
Epidemiology
Human source of transmission (fecal-oral)
- Transmission occurs most often as result of overcrowding (common in day care)
NOT easily killed by stomach acid
Low infectious dose (as few as 10 organisms)
Shigellosis:
Prevention
Controlled by sanitary measures
NO vaccine
Shigellosis:
Treatment
Fluid & electrolyte replacement
Antibiotics
- Ampicillin & cotrimoxazole (shorten duration)
- 20% of Shigella species resistant
Escherichia coli Gastroenteritis:
Most diarrhea-causing E. coli fall into 4 groups
- Enterotoxigenic E. coli (ETEC)
- Enteroinvasive E. coli (EIEC)
- Enteropathogenic E. coli (EPEC)
- Enterohemorrhagic E. coli (EHEC)
Escherichia coli Gastroenteritis:
Enterotoxigenic E. coli (ETEC)
Most common cause of “traveler’s diarrhea”
Escherichia coli Gastroenteritis:
Enteroinvasive E. coli (EIEC)
Disease closely resembles Shigella species
Escherichia coli Gastroenteritis:
Enteropathogenic E. coli (EPEC)
Causes outbreaks in hospital nurseries in developing countries
Escherichia coli Gastroenteritis:
Enterohemorrhagic E. coli
Often produces severe illness
- Production of Shiga toxin
Shiga toxin encoded on lysogenic bacteriophage
Many infected individuals develop hemolytic uremia syndrome (HUS)
Most common strain = O157:H7
Escherichia coli Gastroenteritis:
Symptoms
Infection depends on virulence of strain
Symptoms range from:
- Vomiting & loose stools
- Profuse diarrhea
- Severe cramps & bloody diarrhea
Recovery usually within 10 days
Escherichia coli Gastroenteritis:
Virulence factors
Depends on type of E. coli
- Capsule
- LPS
- Pili
- Toxins
Salmonellosis:
Causative Agent
Salmonella species
- G-
- Motile
Live in GI tract of animals
- Infect humans through contamination of water & food
Salmonellosis:
Types of Salmonella Associated with Human Diseases
- S. enterica
- S. typhi
Infect humans through contamination of water & food
Salmonellosis:
Symptoms
Gastroenteritis
- Nausea, vom, non-bloody stools
Vary depending on virulence of strain
Typically short-lived& milkd
Salmonellosis:
Pathogenesis
- Ingested in contaminated food/water (chicken eggs)
- Adhere to epithelial cells of small intestine
- Taken up by phagocytsosis (T3SS triggers) - Multiplies within phagosome
- Eventually kills host cells - Inflammatory response increases fluid secretion
- Diarrhea, fever, abdominal cramps - Salmonella shed in feces
Salmonellosis:
Serotype Typhi
Causes typhoid fever
Fecal-oral route
Can enter blood
- Phagocytized but NOT digested
- Phagocytes carry Salmonella to liver, spleen, bone marrow, & gallbladder
Can establish semipermanent in gallbladder
- Carriers can remain infected for years (even with treatment)
Salmonellosis:
Epidemiology
Bacteria survive long periods in environment
Chickens naturally carry (undercooked food source)
Household pets (turtles, iguanas, etc._
Salmonellosis:
Prevention
Cooking kills bacteria
Live attenuated vaccine
- Prevents typhoid fever
- 50-70% effective
Salmonellosis:
Treatment
Antibiotic therapy
Rehydration
Campylobacter jejuni
Pathogen
- G-
- Microaerophilic
Leading bacterial cause of diarrhea in US!!
Campylobacter jejuni:
Symptoms
Watery/foul-smelling diarrhea
Followed by:
- Bloody stools
- Fever
- Severe abdominal pain
Campylobacter jejuni:
Virulence Factors
- Adhesins
- Cytotoxins
- Endotoxin
Campylobacter jejuni:
Major Source/Transmission
Major source = chickens
- 24% of raw chicken contains Campylobacter
- Commensal part of microbiome of chicken (no disease)
Transmitted fecal-oral route
Campylobacter jejuni:
Diagnosis
Based on S/S
Campylobacter jejuni:
Prevention
Proper hygiene after handling raw poultry
Campylobacter jejuni:
Treatment
Most cases resolve without treatment
Campylobacter jejuni:
Guillan-Barre Syndrome
Sequelae
~40% of cases due to Campylobacter
Viral Gastroenteritis:
Causative Agents
- Cailciviruses
- Astroviruses
- Rotaviruses
- Most common cause in small children
- dsDNA
Viral Gastroenteritis:
Symptoms
- Abdominal pain
- Cramping
- Diarrhea
- Nausea
- Vomiting
Viral Gastroenteritis:
Pathogenesis
Rotaviruses infect epithelial cells of small intestine
Damaged lining fails to absorb fluids
- Watery diarrhea
Viral Gastroenteritis:
Epidemiology
More cases occur in winter
Transmitted fecal-oral route
Viral Gastroenteritis:
Treatment
Fluid & electrolyte replacement
Viral Gastroenteritis:
Prevention
Vaccine for rotavirus
Norovirus
ssRNA virus
- Small
- Non-enveloped
- Calicivirus family
Originally caused Norwalk Virus
Norovirus:
Symptoms
- Nausea
- Vomiting
- Watery diarrhea
Symptoms subside in 12-60 hrs
Norovirus:
Pathogenesis
Infects epithelium of upper small intestine
- Epithelial cell death
- Decreases production of digestive enzymes
Epithelium recovers in ~2 weeks
Norovirus:
Epidemiology
23 million cases in US annually
Transmission = fecal-oral route
Outbreaks often occur in institutions, cruise ships, etc.
- Contaminated food/water
Norovirus:
Prevention
Hand washing & disinfectants
NO vaccine
Norovirus:
Treatment
NO proven antiviral med
Viral Hepatitis:
Symptoms
- Jaundice
- Abdominal pain
- Fatigue
- Nausea
- Vomiting
- Appetite loss
Symptoms may occur years after infection
Viral Hepatitis:
Pathogenesis
Hepatitis A virus (HAV)
- Fecal-oral route
Other Hepatitis viruses (HBV, HCV)
- Sexual contact or blood-borne
Host immune system responses = responsible for liver damage`
Viral Hepatitis:
Diagnosis
- Jaundice
- Enlarged liver
- Fluid in abdomen
Most individuals with HAV will be sick for several weeks but recover completely
Viral Hepatitis:
Prevention
Good hygiene
Vaccine against HAV
Giardia Infections:
Causative Agent
Giardia lamblia
- Diarrhea-causing protozoan
1 of most frequent causes of human waterborne disease in US
Giardia Infections:
Transmission (& pathogenesis)
- Ingestion of cyst
- Fecal contaminated food/water, streams
- Chlorination doesn’t kill (boiling & filtration works) - Trophozoite adheres to small intestine via sucking disk
- Interferes with fat absorption
Giardia Infections:
Symptoms
- Non-bloody, foul-smelling diarrhea
- Abdominal cramps
Entamoeba histolytic
(general overview)
Diarrhea
- Ranging from mild asymptomatic to severe dysentery
May invade intestinal mucosa
- Causes erosions
May penetrate portal blood circulation
- Forms abscesses in liver & lung
100,000 deaths worldwide
