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6. HDS GI Repro > GI Bacteria > Flashcards

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
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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
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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 ⊕
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4
Q

H. pylori

Clinical Disease and Pathogenesis

A
  1. 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
  2. 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
  3. MALT lymphoma
    • B cell lymphoma
    • Arises due to infiltration of lymphoid tissue into the gastric mucosa
    • Can be cured w/ treatment of H. pylori
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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
  • Invasive
    • Biopsy
      • Test for urease
      • Culture for organisms
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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
  • No known immunity
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7
Q

H. pylori

Prevention

A

Prevention is limited

No chemoprophylaxis or vaccine

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8
Q

Non-invasive, Toxigenic

Enteric Bacteria

A
  • Escherichia coli
  • Vibrio cholera
  • Clostridium difficile
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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
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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
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11
Q

Non-Enterobacteriaceae

A

Curved gram-__⊖ rods:

Helicobacter, Vibrio, Campylobacter

Anaerobic, gram-__⊕ rods:

Clostridium difficile

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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
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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)
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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
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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
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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
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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
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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 ⊕
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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%
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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)
34
Q

Clostridium difficile

Treatment

A
  • Mild cases ⇒ discontinue implicated abx therapy
  • Severe cases ⇒ metronidazole or vancomycin
  • 15-30% relapse or reinfection rate
35
Q

Invasive Enteric Bacteria

A

“Facultative pathogens”

Enterobacteriaceae family ⇒ Salmonella, Shigella, Yersinia

Vibrionaceae ⇒ Campylobacter

  • Attach to and invade epithelial cells
  • Can replicate intracellular & extracellularly
  • Most do not cause disseminated disease
    • Some exceptions
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
42
Q

Shigella

Treatment and Prevention

A
  • Supportive therapy: fluid and electrolyte replacement
  • Abx may be given, particularly to young patient to shorten the duration of disease and carrier state
    • Ciprofloxacin, ampicillin, tetracycline, trimethoprim-sulfamethoxazole
  • Sanitation and personal hygiene to interfere w/ fecal-oral transmission
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
  • 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:
    1. Typhoid fever
      • S. typhi, S. paratyphi A, and S. paratyphi B ⇒ enteric fever (less severe form)
    2. Enterocolitis
    3. Bacteremia w/ focal lesions
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
47
Q

Salmonella

Enterocolitis

A
  • Caused most frequently by S. enteritidis and S. typhimurium
    • Salmonella enterica ser Enteritidis, Salmonella enterica ser Typhimurium
  • Associated w/ contaminated poultry or poultry products
    • Infects ovaries of healthy appearing hens and contaminate eggs before shells are formed
  • Enter via oral route
    • Infectious dose: 105-108 bacteria
  • Organisms invade mucosa of small and large intestines
  • Facultative intracellular pathogen
    • Remains within a membrane bound vacuole ⇒ salmonella containing vacuole (SCV)
    • Bloodstream invasion is rare
  • Nausea, vomiting and diarrhea occur 8-48 hrs after ingestion
  • ± Fever and other constitutional sx
  • Organisms may be isolated from stools
    • ⊕ Fecal leukocytes, not usually bloody
  • Self-limiting, sx last ~1-4 days
    • Not usually treated
  • Similar presentation to Enteroinvasive E. coli (EIEC)
48
Q

Salmonella

Bacteremia w/ Focal Lesions

A
  • 5-10% of Salmonella infections
  • Associated w/ S. choleraesuis (Salmonella enterica ser Cholerasuis) but may involve any NTS serotype
  • Oral ingestion → early invasion of the bloodstream
  • Osteomyelitis, PNA, and meningitis most common manifestations
  • Sickle cell patients at ↑ risk
  • Intestinal symptoms often absent
  • Blood cultures ⊕
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
  • 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
50
Q

Salmonella

Treatment and Prevention

A
  • Enterocolitis
    • Tx: supportive therapy, fluid and electrolyte replacement
    • Prevention: adequate sanitation, immunization of domestic livestock and the proper cooking of poultry products and meat
  • Typhoid fever
    • Tx: chloramphenicol, ampicillin or trimethoprim-sulfamethoxazole
      • Replapses problematic
      • Chronic carrier rates high
    • Prevention: proper sanitation and personal hygiene
      • S. typhi killed and attenuated vaccines available but protection limited
        • Used as traveler’s vaccines
        • Boosters required
      • Potential for vaccination of hens vs non-typhi Salmonella
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
53
Q

Campylobacter and Autoimmunity

A
  • Guillain-Barré Syndrome
    • Autoimmune acute demyelinating neuropathy
    • Symmetical weakness over several days w/ recovery over weeks to months
    • Frequently preceded by infection
      • CMV, Coxsackievirus, echovirus, Flu A, Zika virus, and Camplylobacter
  • ~40% of pts have culture or serologic e/o Camplyobacter infection @ onset of neurologic sx
  • MOA: Ab vs C. jejuni LPS core oligosaccharide cross-react w/ gangliosides of peripheral nerves
    • Molecular mimicry, type II hypersensitivity
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
55
Q

Yersinia

Overview

A

Three species of medical importance:

  • Yersinia pestis
    • Bubonic plague
  • Yersinia enterocolitica and Yersinia pseudotuberculosis
    • GI infections
    • Typhoid fever-like syndromes
56
Q

Enteric Yersinia

Characteristics

A

Yersinia enterocolitica and Yersinia pseudotuberculosis

  • Enterobacteriaceae family ⇒ gram ⊖ rods
  • Found in a wide variety of wild and domestic animals
  • Transmission by contaminated water, food, and milk or by entry via skin break
  • Y. enterocolitica affects mostly children
57
Q

Enteric Yersinia

Pathogenesis and Clinical Disease

A

Y. enterocolitica and Y. pseudotuberculosis

  • Initial infection of the ileum
  • Gastroenteritis (more typical infection)
    • Fever, abd pain and diarrhea
    • Clinically indistinguishable from Shigella or Salmonella gastroenteritis
    • Enterotoxin similar to ST toxin of E. coli
      • May be responsible for fluid loss
    • Usually self-limiting
  • Invasive infection (less common)
    • Mucosal destruction, enlargement of regional mesenteric lymph nodes, ± ulceration
  • Complications:
    • Extraintestinal infection of liver, joints
    • Generalized septicemia
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
59
Q

Staphylococcus

Introduction

A
  • Gram-⊕ cocci in grape-like clusters
  • 3 species of Staphylococcus of clinical importance:
    • S. epidermidis
      • Most commonly associated w/ infections related to cardiovascular and orthopedic prostheses, CSF shunts, vascular grafts and catheters
    • S. saprophyticus
      • Cause 10-20% of urinary tract infections in young, sexually active women
    • S. aureus
      • Normal flora of skin and nares in ~30-40%
    • May cause disease in nearly any tissue
  • Staphylococcal disease divided into 3 general groups:
    1. Skin infections
    2. Infections of hard and soft tissue
    3. Toxic syndromes
  • Virulence factors varied and include:
    • Surface antigens (protein A)
    • Extracellular enzymes (coagulase, lipases, staphylokinase)
    • Exotoxins (enterotoxins, exfoliatin, TSST-1)
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
62
Q

Staphylococcal

Food-Poisoning

A
  • Fairly common food borne illness
  • Caused by ingestion of enterotoxin produced by S. aureus
    • Enterotoxins produced by ~ ½ of all coagulase ⊕ S. aureus strains
  • Ham, processed foods, chicken salad, cottage cheese, etc.
  • Sx onset within 1-6 hours s/p ingestion
  • Nausea, abdominal cramps, vomiting, watery and non-bloody diarrhea, profuse sweating, headache
  • Self-limiting, recovery within 24-48 hours
  • Treatment: fluid replacement; abx not indicated
63
Q

Bacillus

Overview

A

2 medically important species in the genus Bacillus:

  • Bacillus anthracis ⇒ anthrax (1° a disease of sheep and cattle)
    • Man acquires disease accidentally, usu. in an agricultural or industrial setting
  • Bacillus cereus ⇒ food poisoning in man
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
65
Q

Bacillus cereus

Emetic-type Food Poisoning

A
  • Resembles staph food poisoning
  • Short incubation period (~ 4 hrs)
  • Nausea, vomiting, abdominal cramps and occasional diarrhea
  • Mediated by a heat-stable enterotoxin
  • Contaminated rice and grain dishes
  • Usually self-limitin
66
Q

Bacillus cereus

Diarrheal-type Food Poisoning

A
  • Resembles clostridial gastroenteritis
  • Incubation longer, up to 24 hrs
  • Colonization of GI tract
  • Profuse diarrhea, abd pain and cramps
  • Mediated by heat-labile enterotoxin ⇒ ↑ cAMP production
  • Similar to E. coli and Vibrio cholera
  • Contaminated meat, vegetables and gravy/sauces
  • Generally self-limiting
  • Symptomatic treatment
67
Q

Clostridium

Overview

A

Anaerobic, gram-⊕, spore-forming rods

Most commonly associated w/ human diseases:

  • C. tetani: causative agent of tetanus
  • C. botulinum: food-borne botulism, infant botulism, wound botulism
  • C. perfringens: myonecrosis, gas gangrene, anaerobic cellulitis, food poisoning
  • C. difficile: abx-associated diarrhea, pseudomembranous enterocolitis
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
71
Q

Wound Botulism

A
  • Occasionally organism can multiply in wounds
  • Same clinical picture food-borne w/o GI sx
  • Incubation 4-14 days
72
Q

Infant Botulism

A
  • Most common form of botulism in the US
  • Some ass. w/ feeding infants honey containing C. botulinum spores
    • In many cases, spores from unknown environmental sources
  • Incubation 3-30 days
  • Organism grow in GI tract
  • Produce toxins absorbed through intestinal wall into circulation
  • Babies w/ constipation, weakness and flaccid paralysis (floppy infant syndrome)
  • Infants 1-8 months of age, prior to establishment of normal GI flora
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
74
Q

Clostridium botulinum

Treatment

A
  • Supportive care: nutritional and respiratory
    • Assisted respiration most important determinant of outcome
  • Penicillin is abx of choice, only if organisms present
    • Abx not recommended for infant botulism b/c autolysis of organisms ⇒ ↑ [toxin]
  • Equine antitoxins
    • Trivalent (A, B, and E) and heptavalent (A-G)
    • For food-borne and wound botulism
    • Hypersensitivity rxn in 20%
    • Not recommended in infant botulism
  • BabyBIG®, Botulism Immune Globulin IV (BIG-IV)
    • Human-derived botulism antitoxin Ab for tx of infant botulism types A and B
75
Q

Clostridium botulinum

Prevention & Control

A
  • Education to improve home canning methods, but cases are also restaurant acquired
  • All canned food should be cooked at 100°C for 10 min to inactivate toxin
  • Bulging food containers may contain gas produced by C. botulinum and should be discarded
  • honey should not be given to children under 12 months of age; however most cases of infant botulism are caused by unidentified sources
  • Anti-toxin is not recommended prophylactically in cases of suspected exposure
76
Q

Clostridium perfringens

A

Notable cause of myonecrosis and gas gangrene in contaminated wounds

Food poisoning

  • Ingestion of meat dishes (stew, soup, gravy) contaminated w/ spores of C. perfringens
  • Spores germinate in GI tract
  • Organisms colonize ileum and large intestine
  • Production of heat-labile enterotoxin
  • Onset of sx within 18 hours of ingestion
  • Watery diarrhea w/ abd cramps and little vomiting
  • Usually self-limiting
  • Supportive treatment

6. HDS GI Repro (30 decks)

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