Infectious Disease -- Bacteria III - Enteric Pathogens Flashcards
Are enteric pathogens very common?
Very deadly?
Yes common
Few kilers
Top three most common food-bourne domestically acquired pathogens
Norovirus
Salmonella
C. perfringens
Top three most common foodbourne illness pathogens requiring hospitalization
Salmonella
Norovirus
Campylobacter
Top five foodbourne illnesses resulting in death
Salmonella Toxoplasma gondii Listeria monocytogenes Norovirus Campylobacter
Based on the bacterial stats name two bacteria that are common contaminants, but do not cause serious disease
Clostridium perfringens
Staph. aureus
List two bacteria who are much less common, but cause fatal disease
E Coli O157:H7
Listeria
Enteric viruses – list three
Norwalk Virus
Enterovirus
Polio Virus
Four enteric parasites
Giardia
Amoebae
Ascaris
Cryptosporiosis
Six more frequently discussed enteropathic bacteria
E Coli Cholera Shigella Salmonella (enteritidis, typhi) Campylobacter Yersnia
Three types of pathogenesis typically seen with enteropathic bacteria
Ingestion of enterotoxins
Infection by colonizing toxigenic organisms
Direct invasion of the gut wall
What happens when enterotoxins are ingested
Absorption of pre-formed toxins
Symptoms in a very short incubation time
What happens with the infection by colonizing toxigenic organisms pathogenesis method
Hypersecretion reaction from bacterial adherence and toxin secretion
Incubation: 1-3 days
Incubation time for the direct invasion of the gu wall pathogenesis
Days-weeks
Three most important traits of virulence factors for enteropathic bacteria
Adherence to mucosal cells
Production of enterotoxin
Capacity of invade
Specific virulence factors involved in adherence to mucosal cells?
Pili
Flagella
Specific virulence factors involved in production of enterotoxins
Prototype secretagogue toxin (cholerae)
Cytotoxins (Shiga toxin – Shigella, O157:H7)
Superantigens (Staph)
Mechanisms involved in for capacity to invade tissue
Intracellular proliferation, cell lysis, cell-to-cell spread
Invasion of cells and lysis causes….
Bloody/Pussy Diarrhea (dysentery)
Predisposing factors for enteropathic bacteria
Fecal contamination of Food Immunosuppression Antispasmodic drugs Antacids Mucosal Disease
Why do antispasmodic drugs and antacids promote enteropathic disease?
Less killed in stomach
Less movement of Intestine–> Overgrowth
Classic Example. Local response to absorbed toxin
Staph food poisoning
Classic Example. Systemic response to absorbed toxin
Botulism, O157:H7
Classic Example. Dysentery
Shigella
Classic Example. Systemic Illness
Typhoid Fever
Classic Example. Secretory Diarrhea
Cholera
Two causes of excess fluid in diarrhea (with example)
Hypersecretion (Cholera) Osmotic Load (Lactose Intolerance)
Dysentery =
Loose Stool + Blood + Leukocytes
Difference between diarrhea and dysentery.
Diarrhea occurs when there is either toxin with no bacteria, superficial colonization+toxin, or superficial colonization + inflammation. Dysentery occurs when the pathology extends deeper to mucosal invasion and necrosis, submucosal invasion, and/or systemic spread.
The detail run down on E Coli
G- Rod
Green Sheet on EMB agar
Coliform
Important Characteristics of E Coli
Watery diarrhea, cramping pain, fever, malaise
Invasive or cytolytic disease - dysyntery
Verotoxin (shigatoxin) – hemolytic uremic syndrome
What happens in hemolytic uremic syndrome
Renal Failure and Anemia
Describe effects of enterotoxic E Coli
Watery Traveler’s Diarrhea
Consumption of food contaminated with enterotoxin-producing strain
Describe the effects of enterohemorrhagic E Coli
Severe bloody colitis from consumption of food contaminated with invasive verotoxin (shiga toxin) strain
(Mainly O157:H7)
Foods assocaited with EHEC?
Hamburger
Dairy Products (unpasteurized)
Fruit Juice
Agricultural products contaminated with manure (spinach)
Which E Coli is primarily pediatric diarrhea in impoverished nations
EAEC (enteroaggregative)
Risk of person-to-person transmission of O157-H7
Low.
Fecal oral transfer sometimes shows up in places like daycare centers.
Relationship of O157:H7 to temperature? Sorbitol?
Won’t ferment sorbitol
Won’t grow at 45 degrees
Mechanism of O157:H7 disease?
Small infectious dose
Bac adhere to cell membrane and colonize LI
Produce shigatoxins which damage endothelial cells
(inhibits mRNA translation, protein synthesis)
Disease course of O157:H7?
Onset 3-4 days after ingestion of the organism
Severe Abdom. cramping, watery diarrhea progressing to bloody in 3-4 days
Occasioanlly Vomiting. Low or No fever.
Average duration – 8 days
Different ways in which O157:H7 might present?
Asymptomatic Mild Illness Dysyntery Hemolytic Uremic Syndrome Thrombotic Thrombocytopenic Purpura (TTP)
Who is most vulnerable to O157:H7 hemolytic uremic syndrome
Children, Elderly
Generic bacteria data for shigella?
G-
Non-motile
Non-coliform
Pathogenesis of Shigella
Fecal/Oral Transmission (Daycares, MSM)
Invasive lesions of colonic mucosa which spreads to LN
Exotoxin causes Mucosal necrosis
Highly Virulent
T or F. Shigella cannot cause bacteremia to distant organs
True
Generic Bacteria information for Vibrio cholerae
Comma-shaped, G-
Alkali tolerant
How is Vibrio cholerae transmitted?
Direct fecal-oral transmission
Asymptomatic Carriers
Pathogenesis of Vibrio cholerae?
Enterotoxin induces the secretion of isotonic fluid
No invasive lesions
Cause of death in Vibrio cholerae?
Dehydration, Hypovolemic Shock
Mechanism of Vibrio cholerae hypersecretion
Subunit A binds with ADP ribosylation factors
Activates GTP-activated adenylate cyclase resulting in cAMP formation
Stimulates secretion of chloride bicarbonate
Generic bacteria info for Salmonella.
G-
Non Coliform
H2S production
Two groupings of Salmonella to separate
S. enteritidis, S. typhimurium
S. typhi
Three forms of Salmonella
Typhoid
Enteric Fever
Salmonella Food Poisoning
Presentation of Salmonella Food Poisoning
Vomiting and Diarrhea (gastroenteritis)
Superficial lesions of colon
Usually self-limiting (except immunocrompromised)
Organisms responsible for Salmonella food poisoning
S. enteritis, S typhimurium
Common origins of Salmonellosis
Eggs, Undercooked Chicken
Contaminated Water
Turtles/Reptiles
Cantaloupes, Mangoes
Who should never own a reptile
IC, Pregnant, Kids Under Five
Salmonella pathologic mechanism
Invasion of Mucosal cells, cause ulceration
No enterotoxin
Multiply in neutrophils+Macrophages
G- Sepsis
Salmonella is a common cause of ______ in children with sickle cell anemia
Osteomyelitis and Sepsis
What is paratyphoid fever (organisms, symptoms)
S. typhinurium, paratyphi or cholera-suis
Fever, Bacteremia, Local Lesions
Ass. w/ sickle cell disease + schistosomiasis
Describe Typhoid Fever symptoms
- Fever with “rose sports” on lower anterior chest and abdomen
- Hepatosplenomegaly
- Typhoid Nodules throughout immune tissues+liver - Diarrhea (rarely with vomiting)
- Ulcerations of Peyer’s Patches
- Neutropenia
Causative organism for Typhoid Fever
Salmonella Typhi
Describe a Typhoid Fever carrier state
3-5% achieve carrier state in Gall Bladder
Bacteria isnt dissolved by bile, so it can move up to stay there
Generic Campylobacter jejuni information
G- Comma shaped
Flagellated
Where does Campylobacter jejuni infection usually come from?
Undercooked Beef
Symptoms of Campylobacter jejuni
Gastritis, Diarrhea, and Dysentery
associated with guilain-barre neuropathies
Risk of ______ in immunocompromised patients with Campylobacter jejuni infection
Sepsis
Transmission of Campylobacter jejuni?
Contaminated Water Sources
Food-Bourne Illness
Improperly cooked chicken/Beef
Pathogenesis of Campylobacter jejuni?
Toxin causes invasive lesions (colonic crypt abscesses) and adherance.
Rarely Septicemia
Causes foul smelling stools with blood/exudate
Who is at highest risk for effects of Yersnia entercolitica
Pediatric Population
Foods assocaited with Yersnia entercolitica
Raw, undercooked Pork
Unpasteurized milk
Does Yersnia entercolitica influence upper or lower GI?
Both
Pathological findings in Yersnia entercolitica?
Ulcerative intestinal lesions (similar to typhoid)
Microabscesses
Granuloma formation
Deeply invasive, potentially tethal
Is Yersnia entercolitica a systemic disease?
No
What’s the deal with Staph Aureus Enterotoxin
Common for pre-formed toxin poisoning
2-4 hours to activity
More Vomiting than Diarrhea
done in 24 hours
Whats the deal with Bacilus cereus toxin
Fried Rice
Vomiting (1-5 hr) and Diarrhea (8-15 hours)
Caused by production of cereulide enterotoxins
So what are Clostridial diseases all about?
G+ sporulating anaerobes
Highly stable in environment
Produce large amount of fermentation products and degradative enzymes
Method of transmission of clostridial diseases
Gut and Soil Cycle – Spores
Contamination of Wounds or Food
Pathologic disease mechanism for Clostridial disease
Local growth –> Absorption and distribution of exotoxin
Spores are difficult to kill, esp. in necrotic tissue/anerobic environment/noncompetitive env.
So what’s the deal with C. tetani?
Common in puncture wounds
Local growht with toxin dissemination
Loss of sympathetic inhibition + inhibitory spinal interneurons
Neurotoxin in C. tetani?
Tetanospasmin
Which Clostridial disease is known for gengrene/necrotizing cellultis?
C. perfringens
Symptoms of C. perfringens
Foul odor, thin/discolored exudate, and wet gangrene at site of infection
Gas gangrene
Hemolytic destruction of RBCs
Myonecrosis
Who gets C. perferingens
Invasion of traumatic/surgical wounds (ex. amputation)
C. perfringens list of extracellular necrotizing enzymes
Phospholipases, Proteinases, Poisons
Describe how clostridial gastroenteritis typically occurs.
Spores survive high temperature preparation and sporulate with cooling. These cooled food are served without reheating (places like catered food).
Symptoms of Clostridial gastroenteritis
Abdominal cramps, watery diarrhea
Incubation period – 6-24 hours
Pseudomembranous colitis is associated with which bacteria
C. difficile
Symptoms of Pseudomembranous colitis
Severe colitis + Pseudomembrane Formation
Diarrhea + Clinical Toxemia
Toxins involved in C. difficile?
Enterotoxin A and Cytotoxin (Toxin B)
Why do people typically get C. difficile?
Disruption of bowel flora by broad spectrum antibiotics
Mechanism of Botulism disease?
Preformed neurotoxin – Cleaves synaptobrevin
Rarely from straight up bacterial infection
Blocks acetylcholine release
Symptoms of botulism infection
Cranial never defects
Loss of muscle contractability
Eventual death from respiratory muscle paralysis
Botulism is typically a disease without colonization. Who is the exception.
Babies eating honey – gives necrotizing enterocolitis.
Symptoms of community acquired C diff
Suppression of Gastric Acid
