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Diarrhea > Bacterial GI Pathogens > Flashcards

Bacterial GI Pathogens Flashcards

1
Q

Epidemiology of Pediatric Diarrheal Diseases

A

1.7 billion cases of childhood diarrheal diseases each year
Leading cause of malnutrition in children <5 years old
2nd leading cause of mortality in children <5 years old

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2
Q

Secretory Gastroenteritis

A

Proximal small intestine

Watery diarrhea

No fecal leukocytes

Mechanism: enterotoxin (produced in or affecting intestines) or bacterial adherence/invasion causes shift in water and electrolyte excretion/adsorption

Classic pathogens:
Vibrio cholerae
ETEC
Clostridium perfringens
Staphyloccocus aureus
Bacillus cereus
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3
Q

Inflammatory Gastroenteritis

A

Colon (large intestine)

Dysentery

Fecal polymorhonuclear leukocytes

Bacterial invasion or cytotoxins cause mucosal damage that leads to inflammation

Classic pathogens:
Shigella
EHEC
Salmonella (not S. Typhi/Paratyphil)
Campylobacter
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4
Q

Invasive Gastroenteritis

A

Distal small intestine

Enteric fever (Typhoid fever)

Fecal mononuclear leukocytes
(if a patient has diarrhea)

Bacteria penetrate mucosa and invade the reticuloendothelial system

Classic pathogens:
Salmonella S. Typhi/Paratyphil
Yersinia enterocolitica

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5
Q

Enterobacteriaceae

A

Enteric bacteria or Enterics

Ubiquitous (GI, soil, plants): simple nutritional requirements

Primary pathogens
Opportunistic pathogens

Gram-negative rods
Non-sporeforming
Facultative anaerobes
Growth on McConkey agar
Ferment glucose
Reduce nitrate
Catalase-positive
Oxidase-negative

Clinical significance?

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6
Q

Sorbitol MacConkey (SMAC)

A

Used for Gram- enteric rods

Contains bile salts and crystal violet to SUPPRESS Gram+ bacteria

Lactose+ (pink/purple) [E. Coli, Klebsiella]

Lactose- (colorless) [Salmonella, Shigella, Proteus]

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7
Q

Escherichia coli

A

Agent for:
Diarrhea, UTI, meningitis, HUS, septicemia, pneumonia

Different strains associated with different diseases

Serotype classification useful in epidemiology:
Somatic O antigen 
Flagellar H protein
Capsular K antigens 
Ex. E. coli O157:H7

Virotypes based on virulence factors present in a particular strain

Ferments lactose

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8
Q

Etiology and symptoms of HUS

A

Hemolytic Uremic Syndrome

Occurs in 10% of children <10 years old who are infected with EHEC

Death occurs in 3-5% of HUS patients

Toxemia affecting the kidney

  1. Destruction of glomerular endothelial cells
  2. Decreased glomerular filtration
  3. Acute renal function

Anemia, thrombocytopenia, acute renal failure due to microthrombi forming on damaged endothelium

> Mechanical hemolysis > Platelet consumption > Decreased renal flow

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9
Q

Enterohemorrhagic E. coli (EHEC)

A
  1. O157:H7 (colonizes cattle intestinal tract)
    Most common type of serotype in US
  2. Consumption of undercooked Hamburgers, unpasteurized milk, apple cider, municipal water, raw, leafy veggies
  3. Low ID (low inoculum) 100 bacteria is sufficient
  4. Adhere to Large Intestinal Cells
  5. Mild diarrhea 3-4 days after incubation, Hemorrhagic colitis within 2 days after mild diarrhea
  6. Common causative agent for HUS by directly activating platelet aggregation
  7. No antibiotics; electrolyte and fluid maintenance

Hemorrhagic, Hamburgers, HUS

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10
Q

EHEC Virulence Factors

A

Virulence factors transmitted by bacteriophages: take the virulent and spread to non-virulent colonies

Inject shiga toxins

  1. LEE Pathogenicity Island:
    Locus of Enterocyte Effacement
    T3SS (type 3 secretion system)
    Intimin adhesion (A/E factor)
  2. A1B5 toxins
    B subunits bind to Gb3 glycolipid on intestinal villus and renal endothelial cells
    A1 subunit binds to 28s rRNA and disrupts protein synthesis
    {Stx1 = almost identical to Shigella shiga toxin
    Stx2 = associated with HUS}
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11
Q

Enterotoxigenic E. coli (ETEC)

A
  1. From fecally contaminated food or water
  2. Traveler’s diarrhea in adults and potentially fatal diarrhea in children
  3. High ID (have to consume a large amount of contaminated food/water)
  4. Adhere to Small Intestinal mucosa
  5. Cramps, nausea, watery diarrhea, vomiting (rare)
  6. No antibiotics; electrolyte and fluid maintenance
  7. 1-2 day incubation, 3-4 day persistence

Pathogenesis: due to enterotoxins

No histological changes or inflammation

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12
Q

ETEC Virulence Factors (Adhesins and Exotoxins)

A

Type 1 pili
1. Fimbriae:
Colonization factor antigens (CFAs)
Located on plasmids

  1. Heat-labile (LT) {can be altered at high temps} or stable (ST) toxins
    Genes found on same plasmids as CFA genes

LT and ST; LT is 75% similar to cholera toxin, with the same mechanism of action

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13
Q

ETEC Heat-labile toxin

A

Heat-Labile Toxin (LT-1)

A1B5 toxin and homologous to cholera toxin

  1. B subunit binds host GM1 molecule expressed by small intestinal mucosal cells (glycolipid/ganglioside receptor)
  2. A subunit activated by cleavage upon entry
  3. Locks adenylate cyclase in ON state
  4. cAMP levels INCREASE
    Affects transport of Na+ and Cl- and causes ION IMBALANCE
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14
Q

ETEC Heat-stable toxin

A

Methanol-soluble ST (STa)
Family of SMALL PEPTIDE toxins
1. Binds and activates host guanylate cyclase (GC)
2. cGMP levels increase
3. Affects many cellular functions including ion transport

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15
Q

EPEC

A
  1. Watery diarrhea in children <5, fever, nausea, vomiting
    P=pediatrics
  2. Small intestinal cells
    Attachment and effacement like EHEC
    Adheres to apical surface, flattens villi, prevents absorption
  3. No toxins produced
  4. No antibiotics; electrolyte and fluid maintenance
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16
Q

EAEC

A
  1. Persistent diarrhea in children <5
  2. Small intestinal cells
    Autoaggregation “stacked bricks”
    Minimal mucosal damage, bacteria form adherence lesions > deformed vili> malabsorption
  3. Shiga-like toxin, hemolysin
    Mucus secretion > biofilm formation
  4. No antibiotics, electrolyte and fluid maintenance
  5. Contaminated food/water
  6. Diarrhea in developing countries, common in children
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17
Q

DAEC

A
  1. Watery diarrhea in children <5
  2. Small intestinal cells
    Elongation of microvilli
    Adhere over entire surface of epithelial cells -more diffusely (vs stacked bricks like in EAEC)
  3. No antibiotics, electrolyte and fluid maintenance
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18
Q

EIEC

A
  1. Mild form of dysentery
    Fever, cramping, watery diarrhea, blood, mucus
  2. LARGE intestinal cells
    Facultative intracellular pathogen
    Cell to cell spread via actin polymerization

Epithelial cell destruction > inflammatory infiltration > colonic ulceration

  1. VF: Invasion genes on plasmid
  2. No antibiotic

**Related to Shigella, but require higher inoculum because aren’t pH resistant
DO NOT produce Shiga toxin

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19
Q

E. Coli Prevention and Treatment

A

Avoid contaminated foods and water

No medium to rare burgers

Fluid and electrolyte maintenance

HUS: dialysis and blood transfusions

Antibiotics not normally use since infections are mostly self limited (resolved without treatment)

Strains usually resistant to multiple drugs

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20
Q

Salmonella

A
  1. Gram- bacilli in Enterobacteriacea family
    S. typhi and S. parathypi; non-typhoid

Salmonellosis
1. Contaminated food (poultry, eggs) causes S. typhimurium

  1. Very small inoculum
  2. Virulence factors and toxins - mucosal damage
    T3SS
    Flagellin activates TLR5 > inflammation
    LPS activates TLR4 > inflammation
  3. Nausea, vomiting, non bloody diarrhea 6-48 hours after ingestion
    Progression to severe abdominal pain and bloody diarrhea, Gastroenteritis, Septicemia, Enteric fever
  4. Self-limited; Symptoms last 2-7 days before spontaneous resolution

Commensals of a wide variety of domestic and wild animals

Common cause of diarrhea in US

DNA hybridization: strains are closely related

> 2400 O serogroups; variations in the distal end of the LPS

Biochemical tests:
Lactose-negative (in contrast to E. coli; unable to ferment lactose)

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21
Q

Salmonella Typhoid (Enteric) Fever

A
  1. Caused by S. typhi or S. paratyphi
    Encapsulated (by the Vi antigen used in one vaccine formulation)
  2. Humans are the only host
  3. Low ID: person to person spread
  4. Asymptomatic carriers “Typhoid Mary”
  5. Incubation 1-3 weeks
  6. Gradually increasing fever, anorexia, headaches, myalgias (muscle pain), constipation
  7. Systemic disease may precede gastroenteritis
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22
Q

Salmonella Virulence factors

A

Fimbrial adhesions, some encoded by plasmids

Facultative intracellular, replicates in phagosome

2 x T3SS: encoded by two separate pathogenecity islands (SPI-1 internalization, and SPI-2 block of phagosome-lysosome fusion)
Other SPIs - Mg2+ transporter (intravacuolar growth)

Protection against:

  1. Intracellular killing: superoxide dismutase (on lysogenic phage) and catalase
  2. Stomach acid: acid tolerance response (ATR)

Endotoxin

Membrane ruffles

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23
Q

Endotoxins vs endotoxins

A

An exotoxin is a toxin secreted by bacteria. An exotoxin can cause damage to the host by destroying cells or disrupting normal cellular metabolism. They are highly potent and can cause major damage to the host. Exotoxins may be secreted, or, similar to endotoxins, may be released during lysis of the cell.

24
Q

Salmonella: Treatment and prevention

A 
S. Typhoid usually requires antibiotics and vaccines:
1. Antibiotic 
Ciprofloxacin
Levofloxacin
Azithromycin (Asian)
Cefriaxone (Asian)
Carbapenem (critically ill)
  1. Vaccinations
    Heat killed
    Capsular Vi antigen
    Live attenuated strain (TY21a)Proper handling of foods
25
Q

Shigella

A

Four species:
S. sonnei: industrial world
S. flexneri: developing world
S. dysenteriae: most severe infection

  1. Gram- in Enterobacteriaceae family
  2. Contaminated food/water, person to person; fecal oral
  3. Low ID <200 to establish infection (very small inoculum)
  4. Humans are the only reservoir
  5. Invade mucosal cells, proliferate, cause mucosal damage (T3SS) - intracellular growth
  6. Mucosal ulcers may form pseudomembranes
  7. Resistant to gastric acid (survive low stomach pH)
  8. Diarrhea, dysentery, fever, ab pain, prolonged course; common cause of diarrheal death in children
  9. HUS from Shiga toxin
  10. Non-motile, lactose negative
26
Q

Shigella diseases

A
  1. Shigellosis:
    Gastroenteritis incubation 1-3 days
    Watery diarrhea>ab cramps with bloody stools and tenesmus
2. Dysentery:
Mostly caused by S. dysenteriae
Frequent passage of small volume of bloody, mucous stools and tenesmus
Causes seizure in children <2 years
Some strains cause HUS

Post infection sequelae: Reiter’s syndrome (arthritis, conjunctivitis, urethritis)

27
Q

Shigella Pathogenesis

A
  1. Orally ingested bacteria survive low stomach pH
  2. Taken up by M cells only (microfold)
  3. Escape from vesicle
  4. Phagocytosis into macrophage
  5. Entry into epithelial cell
  6. Escape from vesicle
  7. Actin transport into next epithelial
28
Q

Shigella Virulence factors and toxins

A
  1. T3SS-mediated invasion (plasmid)
    Important effectors cause macrophage apoptosis, endocytosis, phagosome lysis
  2. Shiga toxin: cause host cell damage and death
    Causes HUS
    B binds GB3, A1 inactivates 60s ribosomal subunit

Hemolysin: vacuolar escape (pore forming toxin)

intracellular spread via actin polymerization (ICS)

29
Q

Shigella Treatment and Prevention

A
  1. Appropriate environment and personal hygiene
  2. Rehydration for mild to moderate shigellosis
  3. Antibiotic treatment for bloody diarrhea and dysentery

DOC:
Ciprofloxacin
Levofloxacin
Ceftriaxone

30
Q

Virbrio cholerae (Cholera)

A

S Asia (indian subcontinent), Gulf of Mexico

Contaminated water; small inoculum

Non-invasive, minimal mucosal changes

Vomiting, watery diarrhea, massive fluid loss

“Rice water stools”

Dehydration, hypovolemic shock, death

Oral rehydration key to recovery

NOt common in US

31
Q

Rotavirus

A
  1. dsRNA virus, encapsulated
  2. Common cause of diarrheal mortality in CHILDREN worldwide
  3. Protection by maternal antibodies in first 6 mo of life
  4. Vaccine available (2 oral)
  5. Contaminated food/water; person to person
    Fecal oral
  6. Small inoculum
  7. Short incubation period
  8. Nausea, vomiting, watery diarrhea, ab pain, low grade fever
  9. Destruction of mature enterocytes with loss of absorptive surface
  10. Infection of mucosal cells of small intestines
32
Q

Norovirus

A
  1. ssRNA of Caliciviridae
  2. MOST common cause of acute gastroenteritis in US; second most common cause in severe diarrhea among children
  3. Contaminated food/water; person to person; fecal oral
  4. Low inoculum
  5. Cruise ships, schools, camps, hospital
  6. Short incubation period
    24-72 hours then recovery
  7. Nausea, vomiting, watery diarrhea, ab pain
    Low grade fever
  8. Mild mucosal abnormalities/bowel
  9. Self-limited, could lead to intermittant diarrhea w nutritional disturbances if not cleared
    No vaccine
33
Q

Salmonella Pathogenesis

A
  1. Attachment (fimbriae), membrane ruffling (SPI-1 T3SS effectors), phagocytosis
  2. Block of phagosome-lysosome fusion (SPI-2 T3SS effectors) and intravacuolar growth
  3. Host cell death and spread to adjacent epithelial cell and lympoid tissue
  4. Inflammatory response, release of prostaglandins, stimulation of cAMP, diarrhea

OR

S. typhi:
3. Taken up by submucosal macrophages

  1. Transported to liver, spleen, bone marrow, replication, release
  2. Gallbladder infection > reinfection of intestines
34
Q

Adenovirus

A
  1. DNA non enveloped virus
  2. Military uses vaccines
  3. Fecal oral or direct inoculation
  4. Attaches to cell then penetrates, uncoats, DNA migrates in; New virions are released with cell lysis
  5. Pharyngitis, respiratory disease, conjuctivitis, hemorrhagic cystitis, nonbloodly diarrhea
35
Q

CMV

A
  1. DNA enveloped
  2. Saliva, semen, cervical, blood and organ TRANSPLANTation
  3. Oral, esophagus, bowel, liver (mononucleosis syndrome)
  4. Can be asymptomatic
    Enters latent stage in monocytes and can be reactivated
  5. After early protein synthesis, viral DNA polymerase replicates genome, DNA and late protein synthesis start
  6. Structural proteins assemble virion which buds through the nuclear membrane and exits via tubules
  7. Retinitis, esophagitis, mononucleosis, colitis, pneumonitis, systemic disease with fever, BONE marrow suppression
  8. 80% of adults have been infected; acute disease can transmit fetal disease; likely reactivation
36
Q

Mumps

A
  1. RNA enveloped
  2. Vaccination lasts >10 years
  3. Oral (parotitis)
  4. Soluble Ag can be detected by complement fixation
37
Q

EBV

A
  1. Enveloped DNA
  2. Oral (hairy leukoplakia, pharyngitis), liver (mononucleosis syndrome), cervical adenopathy (lymph nodes in neck)
  3. Viral capsid antigen
  4. Infects mainly B lymphocytes and epithelial cells of throat
  5. 90% of Americans have antibody to EBV. Associated with hairy leukoplakia and cancers
38
Q

Coxsackie Virus

A
  1. Fecal oral or respiratory transmission
  2. Oral herpangina
    Hand Foot Mouth
  3. Virion enters cell, uncoats, mRNA translated to large polypeptide cleaved and forms capsid + noncapsid proteins
    Complementary RNA strands formed and RNA is coated with capsid proteins which are released at cell death

A: Herpangina (blistered legions in back of throat), Conjuctivitis

B: Myocarditis, pericarditis, pleurodynia, aseptic meningitis

No vaccine

39
Q

Ancyclovir

A
  1. Anti-herpes
  2. Inhibition of viral Genome Replication
  3. Oral, IV or topical
  4. Guanosine analogue; activted by viral thymidine Kinase (TK)
    Initial phosphorylation requires viral kinase. Acyclovir is substrate for viral polymerase. Incorporation of acyclovir causes chain termination and inhibition of DNA polymerase. TK- viruses resistant
  5. Manage/suppress (cannot cure) HSV 1 and HSV 2. Given to transplant patients for prevention
40
Q

Valacyclovir

A
  1. Anti-herpes
  2. Inhibition of viral Genome Replication
  3. Dosed twice a day instead of 3-5. More expensive
  4. Pro-drug. Cleaved by esterases to yield acyclovir
  5. Treat HSV 1 and HSV 2. Same effect as acyclovir, but more expensive and requires less dosage
41
Q

Ganciclovir

A
  1. CMV Treatment - IV
  2. Inhibition of viral Genome Replication
  3. Myelosuppression (25-40% of patients)- bone marrow suppression
  4. Requires phosphorylation by viral specific enzyme. Doesn’t have thymidine kinase like HSV so acyclovir doesn’t work. CMV gene codes for phosphotransferase that converts ganciclovir to a monophosphate
    Then enzymes in infected cell convert monophosphate to triphosphate that gets high levels in cell and helps stop CMV DNA from elongating.
  5. Treatment for CMV. Not as selective as acyclovir so more toxic.
    Side effects: GI, neuropathies, some CNS, carcinogenic in animals at high doses.
42
Q

Forcarnet

A
  1. CMV and Resistant Herpes Viruses
  2. Not nucleoside analogy - instead pyrophosphate
  3. IV
  4. Binds to and directly inhibits viral polymerases (DNA, RNA and RT)
  5. Treatment:
    Effective against ganciclovir - resistant CMV and acyclovir resistant HSV, VZV
43
Q

Cidofovir

A
  1. Anti-herpes
  2. Cytosine nucleotide analog
  3. IV
  4. Phosphorylated by host kinases (so also active against thymidine kinase deficient HSV) competitive inhibitor of viral DNA synthesis, incorporated into viral DNA
  5. CMV third string drug. If Ganciclovir and forcarnet don’t work
44
Q

Trifluridine

A
  1. Anti-herpes
  2. Competes with TPP at viral polymerase
  3. Topical
  4. Competes with TPP at viral polymerase
    Inhibits DNA synthesis in HSV1 HSV 2 CMV
    Incorporates into both viral and host DNA
  5. Used for HSV 1 and HSV 2 conjuctivitis, epithelial keratitis.

Effective for acyclovir-resistant HSV

45
Q

Pseudomembranous colitis

A
  1. Antibiotic-associated, usually due to C. diff
  2. C. diff overgrowth due to disruption of normal bowel flora
  3. Pseudomembranes
    Adherent layer of inflammatory cells and debris
  4. Fever, leukocytosis, ab pain, watery diarrhea, dehydration
  5. Major concern in healthcare facilities
46
Q

Giardia

A

Parasite

  1. Non-invasive diarrhea
  2. Treat with oral rehydration and anti-protozoan agents
47
Q

Cryptosporidium

A

Parasite
1. Water borne, spores resistant to chlorine
Spread through pools

  1. Acute self-limited diarrhea or chronic in immunosuppressed host
48
Q

HSV

A
  1. DNA enveloped virus
  2. Bind on cell surface, travel to nucleus to become circular, activates viral immediate early genes by host RNA polymerase and create proteins
    DNA + thymidine kinase
  3. HSV1: Oral>sexual; Very sore mouth gingivostomatitis, herpes labialis on vermillion border, keratitis and encephalitis

HSV2: Sexual>oral; herpes genitalis/labialis, neonatal encephalitis, aseptic meningitis

49
Q

Serotypes

A

IgM = more fast acting than IgG
Core = Actually had the illness
Surface antigen = active disease

No igG or igM = no immunity, never been infected or vaccinated

Surface antibody = shows vaccination or previous manifestation

50
Q

Treatment for HepC

A 
Telaprevir
Simeprevir
Sofosbuvir
Daclatasvir
Velapatasvir

Knowing genotype
Current HepC viral lode
Degree of fibrosis/cirrohosis

Liver biopsy will show cirrhosis

Ultrasound elastography can show fibrosis

Na+ shows prognosis in patients with end stage liver disease

Alpha fetal protein tumor makers helpful with HCC

FibroTest-ActiTest used to stage fibrosis and evaluate for cirrhosis

51
Q

HepA

A

Fecal oral
Acute
2-6 week incubation

Councilman bodies (represents a dying hepatocyte surrounded by normal parenchyma)

52
Q

HepE

A

Fecal oral
Acute
2-8 week incubation

Could only progress to chronic hep in immunocompromised patients

India

No vaccination

53
Q

HepC

A

No vaccination

54
Q

Levels in Data Recommendations

A

The level A suggests that Data is derived from multiple randomized clinical trials, meta-analyses or equivalent.

Level B would be a single randomized trial, nonrandomized studies, or equivalent

Level C would mean Consensus opinion of experts and case studies.

55
Q

Exposure to HepC

A

After needle stick, risk of infection is 1.8%

If HepC is acquired, 15-25% chance of clearing it

Wouldn’t make sense to treat it even though newer medications have better side effect profiles

Baseline testing with follow up 2-3 weeks for Hep RNA

56
Q

Old Hep B/C Treatment

A

Ribavirin with interferon A

57
Q

Campylobacter

A
  1. Common in adults, common cause of traveler’s diarrhea
  2. Contaminated food/water; small inoculum
  3. Mucosal colonization and adherence
  4. Watery diarrhea, dysentery (uncommon); usually self-limited
  5. Arthritis - HLA-B27
    Guillain-Barre syndrome
  6. Curved Gram- rod

Jejuni
1. Symptoms like ulcerative colitis or Crohn’s disease

Diarrhea (3 decks)

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