GI Bacteria Flashcards
1
Q
H. pylori
Morphology and Characteristics
A
Helicobacter pylori
- Gram ⊖ helical-shaped rod
- Catalase ⊕
- Oxidase ⊕
- Highly motile with corkscrew motility
- Causes a persistent infection with long-term low-level inflammation
2
Q
H. pylori
Transmission and Epidemiology
A
-
Spreads via human-human contact
- 1° fecal-oral or oral-oral contact
- Humans are the natural reservoir
-
Infects 50% of the world population early in life
- Highest carriage rates in developing countries
- Majority of population infected by age 10
- In developed countries, ~ 40% carriers
- Risk factors for infection: low socioeconomic class & over-crowding
- Risk factors for disease development: smoking, alcohol, NSAIDs
3
Q
H. pylori
Virulence Factors
A
- Flagella and adhesins⇒ colonization and adherence to stomach wall
- LPS ⇒ incites and maintains inflammatory response to persistent infection
- Urease ⇒ produces ammonia and neutralizes gastric acids ⇒ supports long term survival
- Vacuolating cytotoxin (VacA) ⇒ damages cells by producing vacuoles
-
Cytotoxicity associated gene (CagA) ⇒ 30 genes on a pathogenicity island
- Encodes syringe like structure that injects Cag A protein into host epithelial cells
- Interferes with normal cytoskeleton structure
- Induces IL-8 ⇒ attracts PMNs ⇒ release proteases and ROS ⇒ tissue damage
- Not all strains are CagA ⊕
- Encodes syringe like structure that injects Cag A protein into host epithelial cells
4
Q
H. pylori
Clinical Disease and Pathogenesis
A
-
Gastritis
- Chronic inflammation of the stomach
- Infiltration into gastric mucosa by PMNs and MΦ
- Sx include feeling of fullness, N/V
- Can evolve into a gastric ulcer or duodenal ulcer
-
Gastric adenocarcinoma
- Chronic gastritis → destruction of normal mucosa by inflammatory and oxidative damage
- ↑ risk of mutation
- Replacement with fibrosis
- Proliferation of intestinal-like epithelium
- Risk ∆ by host immune system & strain of H. pylori
-
MALT lymphoma
- B cell lymphoma
- Arises due to infiltration of lymphoid tissue into the gastric mucosa
- Can be cured w/ treatment of H. pylori
5
Q
H. pylori
Diagnosis
A
-
Noninvasive
-
Urea breath test
- Ingest radiolabeled urea
- If H. pylori present ⇒ urea → ammonia and CO2
- Radioactive CO2 detected in breath samples
- Very high sensitivity
- Serology
- EIA: sensitive but cannot monitor tx b/c titers fall very gradually
- HpSA: detection of helicobactor Ab in feces, can be used for initial dx and monitoring
-
Urea breath test
-
Invasive
-
Biopsy
- Test for urease
- Culture for organisms
-
Biopsy
6
Q
H. pylori
Treatment
A
- Asymptomatic infections not treated
- Presently, H. pylori disease is tx when pt c/o abd pain or ass. signs and sx
- Pt w/ active duodenal or gastric ulcers tx if infected w/ H. pylori
-
Triple or quadruple therapy:
Triple therapy recommended for eradication of organisms and control of sx-
PPI + β-lactam + macrolide
- Usu. 2 abx to prevent resistance
- Clarithromycin + Amoxicillin or Metronidazole
- Successful in ~90% of cases but antimicrobial resistance ↑
-
H2 Blocker and/or bismuth subsalicylate
- H2 Blocker ⇒ ⊗ histamine which triggers stomach acid
- Bismuth subsalicylate ⇒ coats stomach and protects it from acid
-
PPI + β-lactam + macrolide
- No known immunity
7
Q
H. pylori
Prevention
A
Prevention is limited
No chemoprophylaxis or vaccine
8
Q
Non-invasive, Toxigenic
Enteric Bacteria
A
- Escherichia coli
- Vibrio cholera
- Clostridium difficile
9
Q
Enterobacteriaceae
Characteristics
A
E. coli, Salmonella, Shigella, Yersinia
-
Enteric bacilli ⇒ reside or cause infections in the GI tract
- Gram ⊖ rods
- Facultative anaerobes
- Oxidase negative
- All ferment glucose
- Commonly found in soil and GI tract of man and lower animals
- Opportunistic or primary (strict) pathogens
-
Serological classification based on 3 groups of Ag:
- O polysaccharides
- Capsular K antigens
- Flagellar H proteins
- Specific Ab develop in systemic infections but unclear if significant immunity persists
- Secretory IgA ⇒ ⊗ attachment to intestinal mucosa
- Cultivated on ordinary laboratory media
- Kits available for rapid, biochemical ID
10
Q
Enterobacteriaceae
Lab Identification
A
Selective and differential media commonly used include:
-
MacConkey’s Agar
- Contains lactose, Neutral Red (pH indicator) and bile salts (⊗ gram-⊕ organisms)
- Lactose fermenters (i.e. E. coli, Klebsiella, Enterobacter) ⇒ pink to red colonies
- Non-lactose fermenters (i.e. Salmonella, Shigella) ⇒ colorless colonies
-
Eosin-Methylene Blue Agar
- Contains lactose, eosin and methylene blue
- Aniline dyes ⇒ ⊗ some gram-⊕ and fastidious gram-⊖ bacteria; also form a precipitate at acidic pH
- Strong lactose fermenters (i.e. E. coli) ⇒ green-black w/ a metallic sheen
- Other lactose fermenters (i.e. Klebsiella, Enterobacter) ⇒ pink-purple colonies
- Non-lactose fermenters ⇒ colorless transparent colonies
11
Q
Non-Enterobacteriaceae
A
Curved gram-__⊖ rods:
Helicobacter, Vibrio, Campylobacter
Anaerobic, gram-__⊕ rods:
Clostridium difficile
12
Q
E. Coli
Overview
A
- Most common facultative, GNR in normal flora of large intestine
- Lactose & glucose fermenter
- Indole ⊕
- Commonly associated w/ endogenous, opportunistic infections
- UTI
- Neonatal meningitis
- Nosocomial infections, wound infections, secondary PNA, sepsis
- Certain strains may be strict pathogens
13
Q
Pathogenic E. Coli
Classification
A
-
Serological classification:
- O antigens of LPS (serogroup)
- H antigens of flagellum (serotype – O+H)
- Capsular polysaccharide
-
Pathogenicity (pathotype, virotype)
Based on pathogenic capabilities, epidemiology and clinical manifestations of GI disease-
Main types:
- Enterotoxigenic E. coli (ETEC)
- Enteropathogenic E. coli (EPEC)
-
Enterohemorrhagic E. coli (EHEC)
- Shigella toxin-producing E. coli (STEC)
-
Rarer types:
- Enteroaggregative E. coli (EAEC) / Diffuse adherent E. coli (DAEC)
- Enteroinvasive E. coli (EIEC)
-
Main types:
14
Q
E. Coli
Virulence Factors
A
-
Colonization factors, adhesion factors, fimbria, pili
- Attachment to epithelial lining of GI and urinary tract
- May be antiphagocytic
- Enterotoxins
- Cytotoxins
-
Capsule
- Antiphagocytic
- Important in neonatal meningitis due to the K1 strain of E. coli
- Type III Secretion System
- Endotoxin
15
Q
Enterotoxigenic E. coli (ETEC)
Virulence Factors
A
Enterotoxins:
-
LT-1 and LT-2 (heat labile) [A-B toxin]
- B subunit → binds GM1 gangliosides
- A subunit → ADPR transferase
- ⊕ Adenyl cyclase ⇒ cAMP ⇒ secretion of K+, Na+, HCO3- and Cl- ions ⇒ loss of large amounts of water
-
ST toxin (heat stabile)
- Small peptide, proteolytically processed during secretion
- Methanol-soluble (STa) and methanol-insoluble (STb)
- STa ⇒ ⊕ guanyl cyclase ⇒ ↑ cyclic GMP ⇒ ↓ net absorption of Na+ and Cl- ions ⇒ fluid loss
16
Q
Enteropathogenic E. coli (EPEC)
Virulence Factors
A
- Initial loose attachment mediated by bundle forming pili (Bfp)
- Plasmid encoded
-
Type III Secretion System
- Active secretion of virulence factors into epithelial cells
- LEE ⇒ genetic locus for enterocyte effacement
- Pathogenicity island shared by A/E pathogens (E. coli, Salmonella, Shigella, Yersinia)
- Adhesion/attachment molecules, syringe-like injection apparatus, chaperones, effector molecules
- Specific effectors differ between organisms
-
E. coli:
- Attachment/Effacement lesions (A/E lesions)
- Tir (translocated intimin receptor) inserted into epithelial cell membrane
- Tir binds intimin (outer membrane bacterial adhesin on E. coli) → tight binding → signal transduction cascade
- Secreted effectors:
- Disrupt normal microvillus structure
- Mediate rearrangement of host cell actin in the vicinity of adherent bacteria → pedestal formation
17
Q
Enterohemorrhagic E. coli (EHEC)
Virulence Factors
A
-
Type III Secretion System
- A/E lesions ⇒ destruction of intestinal microvillus ⇒ ↓ absorption in large intestine
-
Cytotoxins
- Cytotoxic hemolysins
-
Shiga-like toxins (Stx-1 and Stx-2) [A-B toxin]
- B subunit → binds globotriaosylceramide (GB3) on intestinal villi and renal endothelial cells
- A subunit → cleaved by host furin & calpain upon translocation
- A1 fragment deadenylates a specific 28S rRNA nucleotide
- ⊗ Protein synthesis (chain elongation) by blocking AA-tRNA binding to acceptor site on rRNA
18
Q
E. Coli
Diagnosis
A
-
Culture and isolation on differential/selective media
- MacConkey’s Agar ⇒ pink to red colonies
- Eosin-Methylene Blue Agar ⇒ green-black w/ a metallic sheen
- Identification by biochemical reactions
- Key characteristics: gram-⊖ rod, lactose fermenter, indole ⊕
- Of the KEE organisms, only E. coli is indole ⊕
19
Q
E. Coli
Treatment, Transmission, and Prevention
A
-
Tx:
- Rehydration therapy (oral, IV) for gastrointestinal infections
- Abx used in the very young, pts w/ extra-intestinal infections and pts w/ chronic infections irrespective of location
- Transmission: fecal-oral route, food-borne, endogenous infections
- Prevention: proper sanitation and food handling
20
Q
Vibrionaceae
A
- Vibrio species are common in surface, coastal waters around the world
- Three medically important species: V. cholerae, V. parahemolyticus, V. vulnificus
- All are curved, gram-⊖rods
- Easily cultivated on ordinary lab media
21
Q
Vibrio cholera
Overview
A
-
V. cholerae O1 and 0139 ⇒ Classic epidemic cholera
- Biotypes El Tor and classic
- El Tor ⇒ major cause of human pandemic infection
- Non-O1 V. cholerae ⇒ isolated cases of cholera and small outbreaks of diarrhea
22
Q
Vibrio cholera
Epidemiology and Transmission
A
- V. cholerae caused major pandemics of cholera
- Epidemic disease in South East Asia (esp. India), Northern Africa, Peru, and Brazil
- In the USA, a small endemic focus of disease exists along coastal areas of Louisiana and East Texas
- Transmission is primarily by contaminated water under poor conditions of sanitation
- Infectious dose: 105 organisms
- Carriers important in maintaining and transmitting the organism in the absence of epidemic outbreaks
23
Q
Vibrio cholera
Virulence Factors
A
-
Cholera toxin (“Choleragen”) [A-B toxin] ⇒ potent enterotoxin
- B subunit → bind to the GM1 ganglioside receptor on intestinal mucosal cells
- A subunit → active ADPR-transferase
- ADP ribosylation of GTP-binding protein that regulates adenyl cyclase activity
- Persistent ⊕ of adenyl cyclase ⇒ ↑ cAMP ⇒ hypersecretion of electrolytes and fluid loss
- MOA is the same as E. coli LT
- Enters cells via endosome → Golgi → ER → cytosol → plasma membrane
-
Adhesion factors
- Exact mechanism by which V. cholera adhere to the microvilli of the small bowel is unclear
- Specific adhesins and a mucinase likely involved
24
Q
Vibrio cholera
Pathogenesis and Clinical Disease
A
-
Cholera is an acute and severe diarrheal disease
- Extensive fluid and dehydration
- Little or no tissue damage
- Initiates infection in the ileum
- Penetrates mucus
- Adheres to mucosal epithelium
- Replicates extracellularly
- May then spread and grow throughout small and large intestines
-
Pathology and symptomatology due exclusively to action of cholera toxin
-
“Rice-water stool” ⇒ hallmark
- Non-bloody watery diarrhea in large volumes
- Contains mucus, epithelial cells and large # of Vibrios
- Loss of fluid and electrolytes ⇒ ± cardiac and renal failure
- If untreated, mortality 40-60%
- Due to profound dehydration and electrolyte imbalanc
-
“Rice-water stool” ⇒ hallmark
25
Q
Vibrio cholera
Diagnosis
A
Fecal specimens
- Culture and isolation on differential/selective media
- TCBS agar
- ID by biochemical reactions and agglutination assays w/ specific antisera
- Key characteristics: gram-⊖, comma-shaped rods, oxidase ⊕, motile
- All Enterobacteriaceae are oxidase ⊖ ⇒ distinguishing feature of Vibrio
26
Q
Vibrio cholera
Immunity
A
- Natural infection → high degree of resistance to reinfection by homologous strains but not to a heterologous strain
- Bactericidal, antitoxin and agglutinating Ab produced but exact role unclear
- Local immunity due to IgA antibodies associated w/ immune state
- Current vaccines provide some short-term protection
27
Q
Vibrio cholera
Treatment and Prevention
A
- Fluid and electrolyte replacement
- Serious cases ⇒ tetracycline, azithromycin, and ciprofloxacin
-
Current vaccines in development but not commercially available in the US
- Oral: heat-killed and genetically attenuated vaccines
- Current vaccines provide some short-term protection
- Ongoing work on subunit vaccines, combinations
- Water purification, sanitation, and elimination of carriers
28
Q
Vibrio parahemolyticus
A
Halophilic marine organism
- Major cause of diarrheal disease in Japan
- Outbreaks of diarrhea in the coastal areas of the USA and on cruise ships
- Ass. w/ ingestion of raw or undercooked seafood
-
Clinical disease:
- Varies from mild to severe watery diarrhea, N/V, abdominal cramps and fever
- Diarrhea is occasionally bloody
- Self-limiting, lasts ~3 days
29
Q
Vibrio vulnificus
A
Halophilic marine organism
- Common in shellfish along Gulf of Mexico coast
- Less common along Atlantic and Pacific
- Severe skin and soft tissue infections in shellfish handlers
-
Rapidly fatal septicemia in immunocompromised hosts
- Chronic liver disease predisposes to severe infection
- 50% fatality rate
30
Q
Clostridium difficile
Characteristics
A
- Large, gram-⊕, spore-forming rod, obligate anaerobe
- Found in soil
- Present in the colon of 2-4% of normal healthy individuals
- Carriage rate for hospital personnel up to 30%
31
Q
Clostridium difficile
Clinical Disease
A
- Major cause of antibiotic-associated diarrhea
- Severe inflammation
- Occasionally lethal
- Almost always ass. w/ intense antibiotic therapy ⇒ imbalance in normal intestinal flora ⇒ overgrowth of resistant organisms (endogenous or exogenous)
- Mild, watery or bloody diarrhea w/ abd cramping
- May progress to pseudomembranous colitis
- Pseudomembrane composed of fibrin, leukocytes and necrotic colonic cells
- Can result in perforations
32
Q
Clostridium difficile
Virulence Factors
A
Two exotoxins (glucosyltransferases) ⇒ ⊗ Ras GTPase (Rho, Rac, Cdc42) ⇒ cell death
-
Toxin A (TcdA) ⇒ enterotoxin
- Causes fluid secretion and hemorrhagic necrosis
- Chemotactic for PMNs, additional release of cytokines
-
Toxin B (TcdB) ⇒ cytotoxin
- Induces actin depolymerization/condensation ⇒ disruption of cellular cytoskeleton
- Loss of cell shape, adherence and tight junctions ⇒ cell rounding
- Subsequent interference w/ protein synthesis
33
Q
Clostridium difficile
Diagnosis
A
-
Detection of toxins in stools
- Toxin B by tissue culture cell cytotoxicity assay
- Toxins A and B by ELISA
- Endoscopy
- Culture and isolation (not routine)
36
Q
Shigella
Overview
A
- Enterobacteriaceae family
- Facultative intracellular pathogens
-
True human pathogen ⇒ no animal reservoir
- 2° attack rates in families up to 40%
-
S. dysenteriae, S. boydii, S. flexneri, S. sonnei
- 15-20k cases of Shigellosis/yr in US
- Developed nations ⇒ S. sonnei and S. flexneri most common
- S. sonnei ⇒ young children and adolescents
-
Bacillary dysentery
- Acute diarrheal disease marked by mucous, blood and tenesmus
37
Q
Shigella
Virulence Factors
A
-
Shiga-toxin [A-B toxin]
- Heat labile, cytotoxic S. dysenteriae exotoxin
- ⊗ Protein synthesis (chain elongation) by blocking AA-tRNA binding to acceptor site on rRNA
- Affects gut, renal endothelial cells, and CNS
- Similar to EHEC verotoxin (Shiga-like toxin)
- Encoded by lysogenic bacteriophage
-
Invasion plasmid antigens
- Type III Secretion System
- Mediate attachment, penetration, escape from phagocytic vesicles, cell-to-cell spread via actin filaments, host cell apoptosis
- Endotoxin
38
Q
Shigella
Pathogenesis
A
- Infectious dose: 100 bacteria
- Infection of small intestine: 1-4 days
- invasion of large intestine: 3 to 4 weeks
- Invasion and penetration of epithelial cells of mucosa
- Penetration into lamina propria
- Can invade resident MΦ
- ⊕ Cytokine secretion or MΦ apoptosis
- Microabscesses and shallow, crater-like ulcers
- Can cause actin rearrangement ⇒ contiguous spread to adjacent epithelial cells
- Invasion into the bloodstream and beyond lamina propria rare
39
Q
Shigella
Clinical Disease
A
- Sx begin w/ fever and abdominal cramps
- Diarrhea common during first 2-3 days
- Afterwards stools are low volume
- In severe cases: frequent, mucoid and bloody stools w/ tenesmus (pain and strain on defecation)
- Except for S. dysenteriae infection, shigellosis is self-limiting w/ low case fatality rates in untreated cases
- Can be acute or chronic
- Can be associated w/ sign. morbidity
- Usu. tx w/ abx
40
Q
Shigella dysenteriae
A
- Found in developing countries
- Produces a potent exotoxin
- Toxic megacolon, intestinal perforation, hemolytic uremic syndrome, severe metabolic alterations
41
Q
Shigella
Diagnosis
A
- Non-specific methylene blue stain for fecal leukocytes
- Culture and isolation on differential/selective media
- MacConkey’s agar
- Eosin methylene blue agar
- Salmonella/Shigella agar
- ID by biochemical reactions
-
Key characteristics:
- Gram-⊖ rod
-
Lactose non-fermenter
- Differentiate from E. coli which is a lactose fermenter
- Urease ⊖
-
H2S ⊖ and non-motile at both 25°C and 37°C
- Differentiate from Salmonella which are H2S ⊕ and motile
43
Q
Salmonella
Classification
A
- Enterobacteriaceae family
-
Historically 3 species recognized
-
Salmonella typhi, Salmonella choleraesuis, Salmonella enteritidis
- Numerous named serotypes of Salmonella enteritidis
- Undergo antigenic variation ⇒ mosaics of genes
- Recombination, ∆ in length, gene duplications, point mucations
-
Salmonella typhi, Salmonella choleraesuis, Salmonella enteritidis
-
2 species now recognized based on DNA:
- Salmonella enterica (divided into 6 subspecies or serovars, medically relavent group)
- Salmonella bongori
-
Recommended nomenclature:
- Salmonella enterica ser Typhi
- Salmonella enterica ser Enteritidis
- In practice, named serotypes/subspecies referred to as species:
- S. typhi, S. paratyphi A, S. paratyphi B, S. typhimurium, S. enteritidis
44
Q
Salmonella
Virulence Factors
A
- Facultative intracellular pathogens ⇒ able to survive in phagocytic cells
-
Invasins
- Adherence and penetration of intestinal epithelial cells
-
Vi (virulence) antigen
- Antiphagocytic capsular polysaccharide of S. typhi
-
Endotoxin
- LPS w/ specific O polysaccharide chains that contribute to virulence
- Type III Secretion System
45
Q
Salmonella
Pathogenesis and Clinical Disease
A
- 1° enter via oral route
- Infective dose: 106-108 bacteria
- Initiate infection by attaching to epithelium of small intestine
-
Three main types of disease in humans:
-
Typhoid fever
- S. typhi, S. paratyphi A, and S. paratyphi B ⇒ enteric fever (less severe form)
- Enterocolitis
- Bacteremia w/ focal lesions
-
Typhoid fever
46
Q
Typhoid Fever
A
Caused by Salmonella enteric ser Typhi (S. typhi)
Severest form of the disease
Restricted to humans
- Organisms acquired by fecal contamination of water, food or fomites
- Replication starts within salmonella containing vacuoles (SCV)
- Taken up by MΦ and PMNs
- S. typhi penetrates lamina propria → submucosal and serosal layers of intestinal wall → systemic infection
-
First week:
- Lethargy, malaise, fever, aches, pain, constipation
- Multiply in Peyer’s patches in small intestines
- Disseminate to regional lymph nodes, RES, bloodstream, liver and spleen
-
Second week:
- High fever, tender abdomen and ± rose spots on the skin
- ± Diarrhea
- Seeding of bloodstream from different foci of infection
-
Third week:
- Diarrhea; bloody stools may develop
- Infection of biliary system, re-infection of intestines from bloodstream
-
Complications:
- Generalized infection w/ metastasis to bone, joints, liver, and meninges
- Carrier state may develop w/ excretion of organisms in feces for long periods
49
Q
Salmonella
Diagnosis
A
-
Specimens:
-
Enterocolitis
- Stool
-
Typhoid fever
- Blood (1st and 2nd weeks)
- Stool (2nd and 3rd weeks)
- Urine (4th week)
- Bone marrow cultures may be useful in certain circumstances
-
Enterocolitis
- Culture and isolation on differential/selective media
- ID by biochemical reactions and agglutination tests w/ specific sera
-
Key characteristics:
- Gram-⊖ rod
- Lactose non-fermenter
-
H2S ⊕, motile
- Differentiates from Shigella which is H2S ⊖, non-motile
-
Widal test
- Agglutination test for anti-Salmonella Ab in serum
- Paired serum samples must demonstrate rise in titer
51
Q
Campylobacter jejuni
Characteristics
A
- Causes 5-10% of all infectious diarrheas
-
Bimodal peak incidence:
- Infants < 1 y/o
- Adolescents and young adults (15-29 y/o)
- Found in GI tract of wild and domestic animals
- Abx resistant infectious ass. w/ abx used in raising cattle, restricted by FDA
- Transmitted by contaminated food/drink and contact w/ infected animals
- Causes chronic diarrhea in up to 20% of HIV pts
- Two other species: C. fetus and C. intestinalis implicated as a rare cause of systemic infections in immunocompromised hosts
52
Q
Campylobacter jejuni
Pathogenesis and Clinical Disease
A
- Infectious dose: several hundred bacteria
- Incubation period: 2-6 days
-
Enterocolitis
- Begins as watery, foul smelling diarrhea
- Followed by bloody stools, fever and abdominal pain
-
Locally invasive ⇒ ⊕ for fecal leukocytes
- No known enterotoxins or exotoxins
-
Self-limiting after 5-8 days but sometimes continues for longer
- Not usu. tx w/ abx unless severe or prolonged disease
54
Q
Campylobacter jejuni
Diagnosis
A
- Short, curved, gram-⊖ rods
- Microaerophilic (5-10% O2)
- Grows at 42°C on special media
- Extended culture period (3-4 days, up to 1 wk)
-
Oxidase ⊕
- All Enterobacteriaceae are oxidase ⊖
- Vibrio cholera oxidase ⊕ but have more episodes of diarrhea
58
Q
Enteric Yersinia
Diagnosis and Treatment
A
-
Diagnosis:
- Definitive dx by isolation of Yersinia from stool cultures
- ID by biochemical tests
- Can grow at 4°C
-
Treatment:
- Y. enterocolitica usually self-limiting ⇒ supportive tx
- Disease caused by either species ⇒ Tetracycline, ampicillin, cephalosporins or chloramphenicol
60
Q
Staphylococcus aureus
Characteristics
A
- Gram-⊕ Cocci in Grape-Like Clusters
-
Catalase ⊕
- Differentiates staph (catalase ⊕) from strep (catalase ⊖)
-
Coagulase ⊕
- Differentiates S. aureus (coagulase ⊕) from all other staph (coagulase ⊖)
- Routinely cultured on blood agar plates
- Beta-hemolytic, yellow or golden colonies
61
Q
Staphylococcus aureus
Virulence Factors
A
Enterotoxins
- 18 serologically distinct types of enterotoxin (A-R)
- A-D associated w/ food poisoning
- Heat stable and can resist boiling
- Resistant to gastric enzymes and acidity
- Cytokine release, PMN infiltration, mast cell degranulation
- Loss of brush border
- ⊕ Intestinal peristalsis and diarrhea
- ⊕ Vomit reflex by interacting w/ neural receptors in upper GI tract
- ± Superantigen activity similar to Staph TSST-1 ⇒ excessive cytokine release
64
Q
Bacillus cereus
Characteristics
A
- Aerobic, large gram-⊕ rods
-
Spore-formers (endospores)
- Resistant to adverse chemical and physical environmental changes, withstand dry heat and certain disinfectants
- Survive on grain foods (ex. rice) and in some meat dishes
- Spores germinate when food is kept warm
- B. cereus produces a heat-stable and a heat-labile enterotoxin
68
Q
Clostridium botulinum
Morphology and General Characteristics
A
- Gram-⊕, spore-forming rod
- Obligate anaerobe
- Found in soil, pond and lake sediments
- Germination of spores and growth of vegetative form occur in alkaline foodstuffs (usually home canned) when conditions are anaerobic
- Also found in Alaska following ingestion of home preserved fish
69
Q
Clostridium botulinum
Virulence Factors
A
Neurotoxic exotoxin (botulinum)
⊗ Release of ACh @ peripheral synapses ⇒ flaccid paralysis
8 antigenically distinct subtypes (A-G) of botulinum toxin [A-B toxin]
70
Q
Food-Borne Botulism
A
-
Ingestion of preformed toxin in home canned alkaline vegetables (string beans, mushrooms)
- Not cooked enough to inactivate the toxin
- Acidic foods do not support growth of C. botulinum
- Incubation 12-36 hrs
-
Nausea, vomiting, diarrhea or constipation followed by descending paralysis
- Ocular, pharyngeal, and respiratory muscles involvement → extensive voluntary muscle involvement
- Mortality rate 60% untreated, 10% w/ treatment
73
Q
Clostridium botulinum
Diagnosis
A
- Clinical dx (disease usually an intoxication)
-
Serum and stool samples from all suspected cases
- Stool cultured anaerobically for organism
- Toxin may be identified in serum
-
Samples from suspected contaminated foodstuffs
- Test for both organisms and toxin
