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GI Liver > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Helicobacter Pylori

Microbiology:

A
  1. Slender curve Gram- Rod
  2. Microaerophillic
  3. Survives b/c ecologic niche avoids immunity & mechanical clearance
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2
Q

Helicobacter Pylori

Virulence Factors:

A
  1. Urease: buffers H+
  2. Vacuolating Cytotoxin (VacA) from Pathogenicity-Associated Island (PAI)
  3. Cytotoxin-associated Protein (CagA) from PAI
  4. Pilli: important for attachment & mediated Type III
    Secretion of VacA and CagA
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3
Q

Helicobacter Pylori

Epidemiology:

A
  1. Nearly everyone becomes infected
  2. ↑In low SEC
  3. Elderly&raquo_space; Child
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4
Q

Helicobacter Pylori

Pathogenesis:

A
  1. Source: humans spread disease via fecal-oral (parent-kid) or oral secretions (belching w/GERD)
  2. Bacteria grows in gastric mucosa via urease activity
  3. Host immunity attempts to eliminate Hp, but cannot because bug is not invasive
  4. Immune response –> inflammation –> ulcer
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5
Q

Helicobacter Pylori

Diseases:

A
  1. Duodenal Ulcers (95%) > Gastric Ulcers (70%) (other gastric ulcers from NSAID use)
  2. Gastric Adenocarcinoma / Lymphoma - chronic inflammation.
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6
Q

Diagnosis:

A

Endoscopy with Biopsy + Urease Breath Test + Stool Serology

  • Gram stain for shape: microaerophillic G- curved rod
  • Culture on Campylobacter medium (looks like campylobacter)
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7
Q

Helicobacter Pylori

Treatment:

A
  1. PPI/H2-Blockers will not cure

2. PPI/H2 + 2 Abx = Omeprazole + Metronidizole (impotence) + Clarythromycin

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8
Q

Vibrio Cholerae

Microbiology:

A
  1. Motile (polar flagella)
  2. Gram-, oxidase+ curved bacilli
  3. Grow in ↑pH
  4. Found in aquatic ecosystems
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9
Q

Vibrio Cholerae

Virulence Factors:

A
  1. Phage-encoded cholera toxin (AB Exotoxin)
  2. Toxin-co-regulated-pilus (TCP)
    - Required for GI colonization
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10
Q

Vibrio Cholerae

Epidemiology:

A

Associated with Poor Sanitation/Sewage

  1. 7/8 caused by O1 serogroup (O-antigen on LPS)
  2. 8th caused by O139 serogroup (India)
  3. Cholera big problem in AA refugee camps
  4. SEASONAL: ↑Cholera during warm months
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11
Q

Vibrio Cholerae

Pathogenesis:

A
  1. Source: brackish water (not sea, not fresh), human-feces contaminated water, shell fish, Gulf Coast
  2. Vibrio Cholera attach to small intestine epithelium via TCP (Pilus)
  3. Cholera toxin is produced = NON INVASIVE
    - A2 fragment w/ KDEL mimicks host protein –> retrograde to ER –> looks misfolded –> ejected into cytosol
    - A1 fragment ADP-ribosylates GTP binding protein (Gs) by transferring ADP-ribose from NAD
    - ADP-ribosylated GTP binding protein –> ↑AC –> ↑cAMP –> ↑CFTR –>↑Cl + Na/H2O Follow
    - ↑Secreted ions —> ↑H2O and HCO3- “pulled” into lumen –> Osmotic Diarrhea
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12
Q

Vibrio Cholerae

Disease:

A

Cholera - ABRUPT and SEVERE diarrhea (20 L/Day) & Death from Dehydration (Shock)
- Rice-Water Stool (Mucus Flecks)

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13
Q

Vibrio Cholerae

Diagnosis:

A

TLBS + MacConkey special growth media (fecal material requires different growth media)

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14
Q

Vibrio Cholerae

Treatment:

A

IV Fluids and Electrolytes (+ oral glucose, salts) +/- Antibiotics (Doxy, erythromycin; but not invasive!)

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15
Q

Vibrio Parahaemolyticus:

A

Similar to Vibrio Cholerae but ↑association with raw shellfish & most common in Japan

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16
Q

Vibrio Vulnificus

Microbiology:

A
  1. Free living marine vibrio

2. ↑Association with wound infection in fisherman

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17
Q

Vibrio Vulnificus

Virulence Factors:

A

Fe-Sequestering: great at grabbing iron

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18
Q

Vibrio Vulnificus

Epidemiology:

A
  1. Liver disease (Vit K) / immunocompromised = ↑Risk

2. Gulf Coast in US

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19
Q

Vibrio Vulnificus

Pathogenesis / Disease:

A
  1. Fisherman with Vit K deficiency (liver DZ) with wound comes into contact with Vibrio Vulnificus infected water
  2. Infection –> Severe Septicemia
  3. Develops gastroenteritis ==> vomiting + diarrhea + abdominal cramps
  4. Develops blistering hemorrhagic bullae
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20
Q

Vibrio Vulnificus

Treatment:

A

Aggressive antibiotics for septicemia & wound infection

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21
Q

Campylobacter Jejuni

Microbiology

A
  1. Gram-, Oxidase+ spiral rods (“Seagulls”)
  2. Microaerophilic (grow only in ↓O2)
  3. Grow at 42 C (bird temperature)
  4. Small dose = massive death
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22
Q

Campylobacter Jejuni

Pathogenesis:

A
  1. Source: Raw Meat / Milk with Human-Human Transmission

2. C. Jejuni infects lining of small intestine —> Systemic Spread

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23
Q

Campylobacter Jejuni

Disease:

A
  1. Bloody Diarrhea with Pus after Fever
  2. Guillan Barre Syndrome: symmetric rising paralysis due to x-Reactivity of CJ-Lipo. Oligo Saccharide Abs with myelin protein
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24
Q

Campylobacter Jejuni

Diagnosis:

A

Culture + Gram stain ~ “Sea Gull” Appearance

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25
Q

Campylobacter Jejuni

Treatment:

A

Usually Self limiting (3-7 days) +/- Antibiotics (erythromycin); huge resistance to Fluoroquinolone

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26
Q

Campylobacter Fetus

A

C. Fetus: from contaminated food, rare, & more
likely to cause septicemia & disseminated
infection

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27
Q

Clostridium Perfringens

Microbiology:

A

Gram+ “Boxcar” bacilli

1Found in colon, spores, & on surface of unrefrigerated meats.

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28
Q

Clostridium Perfringens

Epidemiology:

A

Diabetics

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29
Q

Clostridium Perfringens
Pathogenesis: Based on Disease
Wound Infections =

A

Gas Gangrene (Myonecrosis) + Anaerobic Cellulitis
- C. Perfringens’ toxic hydrolytic enzymes = α-PLC, collagenases, protease –>
chew through tissue –> Gas
- Results in muscle necrosis (myognecrosis) & spread

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30
Q

Clostridium Perfringens

Treatment:

A

(Mainly for Infected Wound): Surgery, Maggots (eat necrosis)

  1. Antibiotics: Penicillin + Protein-Inhibitor (for enzymes)
  2. Hyperbaric Oxygen
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31
Q

Clostridium Tetani

Microbiology

A
  1. G+ “tennis rackets” / “lollipops” / “drum sticks”

2. Found in spores / GI tract

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32
Q

Clostridium Tetani

Virulence Factors:

A
  1. Tetanospasmin = AB Neurotoxin (Plasmid-Encoded)

- Single antigenic type

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33
Q

Clostridium Tetani

Pathogenesis:

A
  1. Spore-contaminated object (Rusty Nail) —> Wounds Patient
    - Wound = inflamed tissues = ↓O2 = ideal for anaerobic spore
    - Wound location is important because can determine time for symptoms (aka time for toxin to reach CNS)
  2. C. Tetani releases Tetanospasmin
    - AB neurotoxin enters NMJ —> transported retrograde to ganglia –> Clips V-Snare via Zn Metalloprotease
    - No V-Snare –> no fusion of vesicle + pre-synaptic neurotransmitter membrane
    - Specifically, no release of GABA + GLYCINE –> no inhibitory neurons –> constant muscular stimuli
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34
Q

Clostridium Tetani

Presentation:

A

1-2 weeks post-exposure = Lockjaw + Risus Sardonicus + Respiratory Failure + Exhaustion

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35
Q

Clostridium Tetani

Treatment and Prevention:

A

Antibiotics Don’t Work = Exotoxin mediated
1. Sedative Treatment: sensitive to stimuli
2. Anti-tetanus Immunoglobin (TIG)
3. Vaccine for wound management
- Even if previously immunized (>3 doses) give vaccine in minor cases if 10+ years since immunization; if severe
wound give if 5+ years since immunization

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36
Q

Clostridium Tetani

Vaccine:

A

Vaccine (**Exam) = Formalin Inactivated Toxin

  1. Initial Immunization (+ Booster every 10 years)
    - Pt < 7 = DTaP
    - Pt 10-64 = Tdap (reduced diphtheria & pertussis)
  2. Wound Management
    - 3 Dose Immunization: xTdap (✓if bad wound)
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37
Q

Clostridium Botulinum

Microbiology:

A
  1. Anaerobic Gram+ spore forming bacilli
  2. Canned food, wound, honey = anaerobic!
  3. 1g = 1 M deaths
  4. 7 Antigenic Types (A-G)
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38
Q

Clostridium Botulinum

Virulence Factors:

A

Botulinum Exotoxin

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39
Q

Clostridium Botulinum

Pathogenesis:

A
  1. Consumption of raw/contaminated canned foods (or honey / carpet for infant cases) / infected wound
  2. Botulinum Toxin = Metalloprotease cleaves V + T-Snares –> ↓AcH Release –> Flaccid Paralysis
    - Classic Food-Borne Adult Botulism (Toxin A)
    - Wound Botulism (Toxin A) = rare, seen in black tar heroin users
    - Infant Botulism (Toxin B > A) = Floppy Baby Syndrome (= This is an infection!)
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40
Q

Clostridium Botulinum

Symptoms:

A

Classic Triad of Symmetric DESCENDING Flaccid Paralysis + NO Fever + Clear Sensorium
- Begins with CN damage (double vision, dysphagia) –> Respiratory Failure

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41
Q

Clostridium Botulinum

Treatment:

A

Ventilation + Horse anti-botulism Ig + Human anti-botulism Ig

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42
Q

Clostridium Difficile

Microbiology:

A

G+ Spore-former in GI normal flora

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43
Q

Clostridium Difficile

Virulence Factors:

A

Toxins A and Toxin B (not AB)
1. Toxin A = Diarrhea
2. Toxin B = Kills Colon Cells
3. Mechanism: Rho-Family GTPase –> damaged
intracellular signaling –> actin/stress fibers
rearranged

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44
Q

Clostridium Difficile

Epidemiology:

A

Nosocomial / Rx-Induced Diarrhea

- Considered “superinfections”

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45
Q

Clostridium Difficile

Pathogenesis:

A
  1. Rx clears out normal flora / polymicrobial environmental —> Free Reign for C. Difficile
    - Rx = Clindamycin + Imipenem + Ceftaxidine + Moxifloxacin
  2. C. Difficile colonizes —> Toxin Mediated Damage (A = Diarrhea; B = kills colon cells)
  3. Toxin –> Water Diarrhea —> Bloody Diarrhea
    - Progression from Watery —> Bloody Diarrhea from pseudomembranous colitis (ulcerative lesion of colon)
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46
Q

Clostridium Difficile

Symptoms:

A

Fever + Watery–>Bloody Diarrhea

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47
Q

Clostridium Difficile

Diagnosis:

A

RADT for Tox A and Tox B in stool (organism rarely found in stool)

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48
Q

Clostridium Difficile

Treatment + Prevention

A
  1. Stop antibiotic –> give metronidazole

2. Prevention: soap > alcohol wipes b/c spores are resistant to alcohol

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49
Q

General Features of Enterobacteriaceae

A
  • Gram- bacilli; faculitative anaerobes
  • Ferment glucose & oxidase negative (vs. Pseudo)
  • Motile/flagella (vs. non-motile Klebsiella & Shigella)
  • Reduce nitrates —> nitrites (diagnostic value with urine dipstick)
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50
Q

E. Coli

Microbiology:

A

• Gram- bacilli, lac+, glucose fermenter w/H2 gas
• Does not produce H2S
• 5 Virotypes Cause Diarrhea
• Opportunists = disease elsewhere (not diarrhea)
• Strains may be inherently enterovirulent; have
additional PAI-encoded genes

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51
Q

E. Coli

Diseases:

A
  1. Diarrhea + Dysentery
  2. # 1 Cause of UTIs
  3. Neonatal Septicemia + Meningitis
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52
Q

E. Coli

Diagnosis:

A
  1. Culture: rule out salmonella (H2S+), shigella
    (H2-), KIA/TSI
    • E. Coli: yellow (Glu/Lac+), no black (xH2S), bottom gap (H2)
    • Shigella: red/yellow (Glu+), no black (xH2S), no bottom gap
    • Proteus: black (H2S)
    • Pseudo: nothing
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53
Q

Enterohemorrhagic E. Coli (EHEC)

Microbiology:

A

• Has O157:H7

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54
Q

Enterohemorrhagic E. Coli (EHEC)

Virulence Factors:

A

• Shiga Toxin (~Stx): phage encoded cytotoxin (AB)
that cleaves 28S RNA of Ribosome
• Locus Enterocyte Effacement (LEE) from PAI
1. Type III Secretion System
2. Intimin: outer-membrane adhesin
3. Tir: secreted receptor to bridge intimin with entero.
4. Attaching/Effacing Lesion: Δhost actin for ↑binding

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55
Q

Enterohemorrhagic E. Coli (EHEC)

Epidemiology:

A

• Reservoir is cattle due to feedlot practices
• Sources of infection: ground beef, bad milk,
drinking/swimming contaminated water
• ↑Risk in childcare centers
• Occasional human-human transmission

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56
Q

Enterohemorrhagic E. Coli (EHEC)

Pathogenesis:

A
  1. Source: raw ground beef / milk / bad veggies or juices / person-person contact (Requires ↓Infectious Dose)
  2. EHEC binds to cell and secretes toxin via LEE/Type III Secretion –> O157:H7 cleaves 28S RNA –> cell death –> Gastroenteritis —> Diarrhea
    • Diarrhea for 1-8 days
  3. Toxin enters blood –> infects endothelium –> endothelial cell injury –> microthrombi –> anemia / renal failure = HUS
    • Progression to HUS in Children (<5) or Elderly
    • Anemia + Acute Renal Failure (+TTP, Nerve/Brain damage)
    • Most common cause AKI in pediatric patients
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57
Q

Enterohemorrhagic E. Coli (EHEC)

Presentation:

A
  1. Sudden onset of abdominal cramps + watery diarrhea
  2. Watery diarrhea —> bloody diarrhea in 24 hours
  3. +/- Fever (102 F)
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58
Q

Enterohemorrhagic E. Coli (EHEC)

Diagnosis:

A

Sorbitol MacConkey Agar
• Like MacConkey; lactose replaced with sorbitol because O157:H7 is sorbitol negative and other E. Coli are positive
• Additional tests: RADT / serotypes / Nucleic Acid test for toxins.

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59
Q

Enterohemorrhagic E. Coli (EHEC)

Treatment:

A

DO NOT TREAT WITH ANTIBIOTICS

• Does not alter colitis; ↑risk for HUS because antibiotic stress simulates lysogenic phage –> ↑Stx Toxin.

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60
Q

Enterotoxigenic E. Coli (ETEC)

Virulence Factors

A
  • LT: heat labile enterotoxin ~ cholera toxin (AB toxin)
  • ST: heat stable enterotoxin –> ↑cGMP ~ ↑cAMP
  • Fimbriae: CFA I/II adhesins for SI enterocytes
  • Non-invasive: secretes exotoxin
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61
Q

Enterotoxigenic E. Coli (ETEC)

Epidemiology:

A

• Leading bacterial cause of diarrhea in 3rd world;
most common cause of Traveler’s Diarrhea
• Waterborne outbreaks/food-related infections

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62
Q

Enterotoxigenic E. Coli (ETEC)

Pathogenesis:

A
  1. Acquired via ingestion of contaminated food + water
  2. Colonizes SI enterocytes via fimbriae
  3. Non-invasive and secretes LT + ST
    • LT (A1B5) binds GM1 gangliosides on cell surface –> ↑GTPase –> AC –> ↑cAMP –> ↑CFTR –> Secretory Diarr
    • ST binds guanylyl cyclase receptor –> ↑cGMP –> ↑PKA –> ↑CFTR –> Secretory Diarrhea
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63
Q

Enterotoxigenic E. Coli (ETEC)

Presentation:

A
  1. Non-inflammatory + ↑↑Volume Diarrhea ~ Cholera
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64
Q

Enterotoxigenic E. Coli (ETEC)

Treatment:

A

ORT

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65
Q

Enteroinvasive E. Coli (EIEC)

Microbiology:

A

Non-motile, NOT lactose fermenter, NOT decarboxylator of lysine

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66
Q

Enteroinvasive E. Coli (EIEC)

Virulence Factors:

A
  • ↑Invade Colonic Tissue: destroys the tissue

* Actually invasive

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67
Q

Enteroinvasive E. Coli (EIEC)

Epidemiology:

A
  • Underdeveloped countries; Traveler’s Diarrhea

* Humans only known reservoir

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68
Q

Enteroinvasive E. Coli (EIEC)

Pathogenesis

A

~ Shigella Toxin
1. Source: acquired via 3rd world person-person contact
• ↑Infectious dose than in children
2. EIEC penetrate and multiply within epithelial cells of colon –> widespread cell destruction
• Actually penetrates = INVASIVE
• Because non-motile, it rearranges the cytoskeleton just behind (Actin Tail) to propel it from enterocyte –> enterocyte
3. Cell death –> Symptoms / Presentation

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69
Q

Enteroinvasive E. Coli (EIEC)

Presentation:

A
  1. Shigella-like dysentery

2. Fever

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70
Q

Enteropathogenic E. Coli (EPEC)

Virulence Factors:

A
  1. EPEP Adherence Factor (EAF): localized binding
  2. Intimin: adherence
  3. LEE: mediates attachment / effacing
    • Like EHEC, LEE allows pedestal formation and
    Attachment / Effacement Lesion
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71
Q

Enteropathogenic E. Coli (EPEC)

Epidemiology:

A

Leading cause of infantile diarrhea
• 3rd world infants
• Transmission: contaminated H2O / meat products
• DAEC: New Mexico + NA

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72
Q

Enteropathogenic E. Coli (EPEC)

Pathogenesis:

A
  1. Acquired via consumption of contaminated water / food
  2. Moderately invasive EPEC strain –> induces inflammatory response (because not toxin-mediated)
  3. Invasive –> intracellular bacterial –> ↓normal cell signaling transduction –> loss of microvilli –> Osmotic Diarrhea
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73
Q

Enteropathogenic E. Coli (EPEC)

Presentation:

A
  1. Profuse watery +/- bloody diarrhea
  2. +/- Inflammation
  3. No fever
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74
Q

Uropathogenic E. Coli (UPEC)

Virulence Factors:

A

• P Fimbria: pyelonephritis associated pili (PAP); P
fimbria because P binds P blood group antigen.
Binds to galactose disaccharides on uroepithelium
• Siderophores: Fe-acquisition
• EC Hemolysin: host cell pore-former = cytotoxic
• K Antigen: ↓immunogenicity

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Perfectly
75
Q

Uropathogenic E. Coli (UPEC)

Epidemiology:

A

90% non-obstructive UTI

• ↑ Female Risk = shorter urethra

76
Q

Uropathogenic E. Coli (UPEC)

Pathogenesis:

A
  1. Bacteria colonize from feces / perianal region —> ascends into urinary tract –> bladder
    • If in sexually active female, could be cystitis propelled up into bladder during sexual intercourse from urethra
  2. Major defense against infection is urine flow
  3. Can progress to Neonatal Meninges (K-Antigen Mediated)
  4. Can progress to SIRS / Shock (Immunocompromised Patients)
77
Q

Uropathogenic E. Coli (UPEC)

Presentation:

A
  1. Dysuria, pyuria, suprapubic pain, cramping, afebrile
78
Q

Uropathogenic E. Coli (UPEC)

Diagnosis:

A

Large number of urinary bacteria
• >10^5/mL in females
• >10^3/mL In males

79
Q

Salmonella Enteritidis, Typhimuium & Non-Typhi Serotype

Microbiology:

A
  • Gram- Frank Pathogen

* Lac-, ferment glucose w/gas + production of H2S

80
Q

Salmonella Enteritidis, Typhimuium & Non-Typhi Serotype

Virulence Factors:

A

PAI Type III Secretion

81
Q

Salmonella Enteritidis, Typhimuium & Non-Typhi Serotype

Epidemiology:

A 
Zoonosis
• Contaminated meat, dairy, poultry, pet reptiles, turtle
• Eggs = S. Enteritidis
• Dissemination rare
• ↑Risk w/AIDs + Hodgkins for Bacteremia
• Sickle Cell for osteomyelitis
• Old/Young
82
Q

Salmonella Enteritidis, Typhimuium & Non-Typhi Serotype

Pathogenesis:

A
  1. Improperly cooked / contaminated food ingestion –> S. Group in gut
  2. Bacteria swim in mucosal layer —> Type III Secretion System Injects M cells —> Ruffles Membrane —> Engulfs Bug
  3. Localized infection (macrophages) in lamina propria –> Gastroenteritis
83
Q

Salmonella Enteritidis, Typhimuium & Non-Typhi Serotype

Presentation:

A

N/V Abdominal cramps + diarrhea ~ 20-72 hours post-eating
• VOMITING*****
• Dissemination rare, but can lead to bacteremia/sepsis, osteomyelitis, endocarditis, renal problems

84
Q

Salmonella Enteritidis, Typhimuium & Non-Typhi Serotype

Diagnosis:

A

Isolation is Mainly Important

1. H. Serotyping for identification

85
Q

Salmonella Enteritidis, Typhimuium & Non-Typhi Serotype

Treatment:

A

Antibiotics may be given; often best not treated

• No vaccine

86
Q

S. Typhi ==> Typhoid + Enteric Fever

Microbiology:

A

Lac-, ferment glucose w/out gas + H2S

87
Q

S. Typhi ==> Typhoid + Enteric Fever

Virulence Factor:

A

• Vi: antigenic capsule inhibits neutrophil uptake
• 2 x Type III: one to inject protein into M-cells for
entry; one to inject proteins into macrophages for
survival.

88
Q

S. Typhi ==> Typhoid + Enteric Fever

Epidemiology:

A

Not Zoonosis
• Developing nations
• Prophylactic to traveler’s

89
Q

S. Typhi ==> Typhoid + Enteric Fever

Pathogenesis:

A
  1. Parasite of humans —> human/feces contaminated water –> migrant worker/traveler gets illness
  2. Migrates to M folds of small intestine –> lamina propria –> macrophages phogocytose –> not killed
    • Perforations at GI tract at necrotic Peyre’s Patches —> Severe Hemorrhage
  3. Migrates to RES organ (spleen and liver)
  4. Leads to disseminated infection in blood (Sepsis) ===> Insidious Rising Fever + Headache + Abdominal Pain
    • Mental confusion
    • Diarrhea not common
    • Skin rash ~ Rosette Spots
90
Q

S. Typhi ==> Typhoid + Enteric Fever

Diagnosis:

A

culture blood / feces

91
Q

S. Typhi ==> Typhoid + Enteric Fever

Treatment:

A 
aggressive antibiotics (Ceftriaxone)
• Live attenuated oral vaccine
92
Q

Yersinia Enterocolitica

Microbiology:

A

• Gram- coccobacilli ~ Safety Pin (bipolar stain)

93
Q

Yersinia Enterocolitica

Epidemiology:

A
  • Animal reservoir = PIGS
  • Consumption of contaminated milk, water, food
  • Children infected with pet-contact
94
Q

Yersinia Enterocolitica

Presentation:

A
  • Pseudoappendicitis
  • Enterocolitis w/fever, diarrhea & abdominal pain (mesenteric lymphadenitis)
  • May lead to Reiter’s Syndrome
95
Q

Shigella

Three Speciations Based on Disease/Epidemiology

A
  1. S. Dysenteriae
    • South + Central America
    • MDR
    • Produce 1,000x ↑Shiga toxin than others;
    mechanism dysentery unknown
  2. S. Boydii
    • Indian subcontinent
  3. S. Flexneri
    • 2nd most common in US; most common in gay men
  4. S. Sonnei
    • Most common cause of shigellosis in US
    • Mainly dysentery in children (day care where fecaloral transmission is likely to occur)
    • Next seen in mental institutions/jails/gay men (STD)
96
Q

Shigella

Microbiology:

A

Frank Pathogen
• Lac-, no gas, glucose+, non-motile, H2S-
• ~EIEC / EHEC

97
Q

Shigella

Virulence Factors:

A
  • Large Invasion Plasmid: gets into lamina propria

* Shiga Toxin: inhibits eukaryotic 28s rRNA

98
Q

Shigella

Pathogenesis:

A
  1. Source: humans are only source so person-person fecal-oral transmission occurs
    • Very Low Infectious Dose
    • Common food-borne outbreaks do occur
  2. Entry into microfold (M) cells in the gut
  3. Escape from the phagocytic vesicle
  4. Extension to neighboring enterocytes; rarely leaves the GI tract
99
Q

Shigella

Presentation:

A
  1. Begins as water diarrhea + abdominal pain = Small Intestine Involvement
  2. After +/- 1 day, colon is involved –> scant bloody diarrhea with mucus/pus; cramps + tenesmus
  3. Like EHEC, Shigella Dysenteriae —> HUS
100
Q

Shigella

Diagnosis:

A
  1. Fecal leukocytes are prominent; sheets can be seen

2. Gut biopsy - invasion beyond epithelium is rare

101
Q

Shigella

Treatment:

A

Antibiotics & unfortunately resistance (MDR) is a problem

102
Q

Rotavirus (Reoviridae)

Microbiology:

A 
Respiratory Enteric Orphan
• Segmented, ds-RNA
• ↑Antigen diversity (G-P serotypes)
• Non-enveloped: ↑Survival
• 2-3 Concentric icosahedral capsids
103
Q

Rotavirus (Reoviridae)

Epidemiology:

A
  • Most important cause of diarrhea in infants/kids!
  • WInter/Spring Bug (unique season**)
  • Starts in New Mexico / South West
  • REO = spread respiratory / enteric (Fecal/Oral)
  • ↓Deaths effective fluid therapy
104
Q

Rotavirus (Reoviridae)

Management & Treatment:

A

Because only 4 G-P combinations cause majority of disease ===> Ideal for Vaccine

105
Q

Rotavirus (Reoviridae)

Pathogenesis

A

~ Transmission is Fecal / Oral —> Infects Villus Epithelium of Small Intestine

  1. Viral capsid is proteolytically processed outside enterocytes (gut) or intra-enterocyte -> Infectious Virus Particle
  2. Virus taken up via endocytosis –> endosome / lysosome –> penetrates cell
  3. Enzymes within core asymmetrically synthesis mRNA (only + strand is synthesized)
  4. Capped +RNA strands extrude via vertices of capsid and are assembled into “Assortment Complexes”
  5. Capped +RNA strands in assortment complexes serve as template for -RNA strand
  6. Assembly of virus occurs in cytoplasm within Virus Factories —> Shedding & Lysis of Enterocyte
106
Q

Rotavirus (Reoviridae)

Pathogenesis main point:

A

===> Loss of Enterocyte Lining SI / LI —> Functional Loss of Absorption (no AC, cAMP activation like cholera)

107
Q

Rotavirus (Reoviridae)

Manifestation & Diagnosis:

A
  • Nausea, vomiting, diarrhea, fever and dehydration
  • 1-4 day incubation
  • Death of enterocyte —> Diarrhea —> Dehydration —> Death
108
Q

Rotavirus (Reoviridae)

Treatment:

A

Neutralizing antibodies develop to circulating rotavirus + 4 G-P combinations cause 90% of disease = Vaccine
• RotaTeq: live attenuated pentavalent bovine-human reassortant viruses containing G1-G4 + P8
• Rotarix: live attenuated divalent human virus containing Gi, P8

109
Q

Norovirus (Caliciviridae)

Microbiology:

A
  • Non-segmented, +RNA

* Nonenveloped

110
Q

Norovirus (Caliciviridae)

Epidemiology:

A

• Most important cause of foodborne epidemic
acute gastroenteritis in older children & adults
• “Winter Vomiting Disease”
• 50% of community-based (non-bacterial)
gastroenteritis

111
Q

Norovirus (Caliciviridae)

Pathogenesis:

A

~ Transmission is Fecal / Oral —-> Infects Villus Epithelium of Small Intestine

  1. Outbreak usually due to single source (shellfish, cake frosting or Cruse Ship Outbreak)
  2. Replication scheme unknown, but similar to Picornavirus Replication
112
Q

Norovirus (Caliciviridae)

Pathogenesis main point:

A

===> Loss of Enterocyte Lining SI / LI —> Functional Loss of Absorption (no AC, cAMP activation like cholera)

113
Q

Norovirus (Caliciviridae)

Manifestation & Diagnosis:

A
  • Nausea, vomiting, diarrhea, fever & dehydration

* ~1 day incubation (shorter than rotavirus) & vomiting is more severe

114
Q

Norovirus (Caliciviridae)

Management & Treatment:

A

Capsid proteins are ↓antigenic + antigenic drift ===> no vaccine
• Wash hands, disinfect surfaces, & prepare food well

115
Q

Enteroviruses, Coxsackie Virus & Echovirus
(Picronaviruses)
Microbiology:

A

Picorna ~ Pico + RNA
• Small nonenveloped +RNA viruses
• Picorn = polio, insensitive to ether, coxsackie,
orphan virus & rhinovirus
• Enterovirus different from rhinovirus because acid
stable & replication at 37C

116
Q

Enteroviruses, Coxsackie Virus & Echovirus
(Picronaviruses)
Viruses:

A
  1. Poliovirus: cause flaccid paralysis ~ Poliomyelitis
  2. Coxsackievirus: meningoencephalitis, diarrhea,
    muscle pain, myocardial / pericardial inflammation
  3. Echovirus: Enteric Cytopathic Human Orphan
    causing mild gastroenteritis
  4. Hep A
117
Q

Enteroviruses, Coxsackie Virus & Echovirus
(Picronaviruses)
Epidemiology:

A

Humans are only reservoir

• Occur mainly in the summer and fall

118
Q

Enteroviruses, Coxsackie Virus & Echovirus
(Picronaviruses)
Management & Treatment:

A
  1. Other than polio, no vaccines are present
    • Large number of serotypes & asymptomatic
    infection make it difficult to create vaccine
119
Q

Enteroviruses, Coxsackie Virus & Echovirus
(Picronaviruses)
Pathogenesis

A

~ All can be spread by Oral-Fecal Route (Coxsackie also from aerosol on doorknobs, toys, etc)
1. Incubates for 7-14 days
• Initially replicates inside lymphoid tissue in the URT & the gut (looks like measles but don’t be fooled!)
• Can be isolated via throat swab
2. Post-replication Viremia
• Spinal Cord + Meninges + Brain / Heart / Skin
3. Most symptoms come from direct virus-mediated cell damage & tissue necrosis from normal viral replication in a cell
• Myocarditis & nephritis may be more immune complex / cross-reactivity mediated

120
Q

Enteroviruses, Coxsackie Virus & Echovirus
(Picronaviruses)
Manifestation & Diagnosis:

A

Keep in Mind that Infection Period is Asymptomatic
1. Aseptic Meningitis ~ Poliovirus, Coxsackie, & Echovirus
• Fever, malaise, headache, nausea + abdominal pain —> Meningeal Irritation + Vomiting
• Muscle aches occur & maybe confused with polio
2. Pleurodynai (Epidemic Myalgia) ~ Group B Coxsackie
• Abrupt fever + chest + abdominal pain for 2 days-2 weeks
3. Hand, Foot and Mouth ~ Coxsackie A16
• Enanthema: ulcerative lesions of the mouth (especially on tonsils and uvula ~ herpangina)
• Followed by lesions on hands/feet
4. Myocarditis –> Group B
5. Eye Disease –> Coxsackie + Echovirus
6. GI Disease —> Diarrhea, Hepatitis, Pancreatitis
7. Skin Rashes

121
Q

Hepatitis Viruses Classification

Hep A Virus:

A

Enterically transmitted “infectious” hepatitis

122
Q

Hepatitis Viruses Classification

Hep B Virus:

A

Parenterally-transmitted “serum” hepatitis

123
Q

Hepatitis Viruses Classification

Hep C Virus:

A

nonA, nonB PT-transmitted hepatitis

124
Q

Hepatitis Viruses Classification

Hep D Virus:

A

dependent on Hep B co-infection

125
Q

Hepatitis Viruses Classification

Hep E Virus:

A

nonA, nonB ET-transmitted hepatitis

126
Q

Hepatitis Viruses Classification

Hep G Virus:

A

nonA, nonB PT-transmitted hepatitis

127
Q

HAV

Microbiology:

A

Picornaviridae (family), Enterovirus (gen)
• ss-RNA+ non-enveloped icosahedral capsid
• Single serotype, humans known reservoir (vaccine!)

128
Q

HAV

Disease:

A

Acute ET Hepatitis

129
Q

HAV

Epidemiology:

A
  • 33% of acute hepatitis cases in US each year
  • Nationwide outbreak every decade
  • Noticeable rapid decline w/vaccine (normally slow)
130
Q

HAV

At Risk Patients:

A

Think Memphis Day Care!
• Household/sexual contacts of infected (recall: ET)
• International travelers
• American Indian reservations (West/Southwest)
• Outbreaks (D’s): daycare, dudes, diners, drug-users

131
Q

HAV

Pathogenesis:

A

~ Acute Enterically-Transmitted Hepatitis

  1. HAV spread by fecal-oral route
  2. Replicates in GI tract; incubation period ~ 15-30 days
  3. Transient viremia —> Spreads to liver, kidney & spleen
  4. Virus sheds —> end of shedding signifies jaundice (start of symptoms) aka non-infectious incubation
132
Q

HAV

Presentation:

A
  • Jaundice (end of shedding) with ↑liver enzymes

* ET-Transmitted = acute –> abrupt (12 weeks) icterus with sharp fever

133
Q

HAV

Diagnosis:

A

Isolated from patient’s feces

• ELISA for anti-HAV IgM (see image

134
Q

HAV

Treatment / Control:

A

Hand-washing, Harvrix (killed vaccine) & gamma-globulin

• Vaccination targeted at kids (daycares)

135
Q

HBV

Microbiology:

A

~ Virion = Dane Particle
• Hepadnavirus = Hepatocyte DNA Virus
• dsDNA = L-DNA (full length) vs. S+DNA (smaller)
• Affected individuals have Dane Particle AND trillions of filaments containing HBsAg + P-lipid (no DNA)
• Why disease is chronic; immune system recognizes filaments, but actual virus (DANE) is isn’t there!

136
Q

HBV

Encodes five proteins, key for replication

A
  1. DNA Polymerase with R-T activity
  2. HBsAg: Surface Ag, attachment protein (in filaments)
  3. HBcAg: Core Ag, surface protein
  4. HBeAg: secreted form of HBcAg (imp. for diagnosis)
  5. X-Antigen: regulated gene expression
137
Q

HBV

Disease:

A

PT-Chronic Hepatitis (“Serum” Hepatitis)
• Chronic development depends on AGE
• Younger ( HCC)

138
Q

HBV

Epidemiology:

A

• Endemic to China & sub-Saharan Africa where
infection occurs earlier (not more)
• SE Asia mothers passing on to child
• ↑Incidence b/c Chinese immigration

139
Q

HBV

At Risk Patients:

A

HBV makes a Dane Particle
• Hospital-Workers, Hemopheliacs (H)
• Dudes, Drug Users (D)

140
Q

HBV

Prognosis:

A

25% chronic HBV die liver disease 50s-60s

When to treat?: Liver Injury / fibrosi

141
Q

HBV

Pathogenesis Entry:

A

HBV enters via parenteral-route (Present in semen & vaginal secretions)

142
Q

HBV

Pathogenesis Replication:

A

Replicates primarily within the liver ~ incubation time 45-160 days
• HBV DNA –> nucleus –> completes ds-DNA circle with host machinery (b/c recall that HBV isn’t truly double stranded)
• Host DNA-dependent RNA polymerase –> pre-genomic RNA (looks ~ host mRNA)
• Core protein encapsidates pre-genomic RNA + Viral DNA polymerase (recall has RT activity)
• DNA polymerase RT pre-genomic RNA —> L-DNA (full length)
• Original pre-genomic RNA destroyed except small piece for priming S+DNA strand (incomplete)
• Envelop acquired and virus buds from endoplasmic reticulum - NO CELL LYSIS

143
Q

HBV is opposite of retrovirus?

A

***HBV is opposite of retrovirus (DNA virus using RNA intermediate) except they both share a RT!

144
Q

HBV

Pathogenesis Cellular Damage:

A

NOT Cytolytic –> causes immune-mediated destruction of infected cells

145
Q

HBV

Three Stages of Disease:

A

~ Keep in mind that antiviral therapy can drive seroconversion of HBeAg –> HBeAb
• Immune Tolerance Phase: ↑HBV DNA, HBeAg+; long in childhood infections (no CTL/immune response); skip in adults
• Immune Clearance Phase: seroconversion (HBeAg–>HBe Abs); HBeAg causes CTL tolerance; post-seroconversion activated CTLs (with no more HBeAg) cause liver inflammation & fibrosis (ΔALT levels) ===> results in healthy carriers
• Residual Phase: Post HBeAg seroconversion, ↓HBV DNA + normal ALT; +/- confused with HBeAg mutation

146
Q

HBV

Presentation:

A

Unresolved HBV infection >6 months = chronic
• Chronic cases are asymptomatic until cirrhosis or hepatocellular carcinoma appears
• Chronic HBV cause that suddenly worsens = think HDV superinfection

147
Q

HBV

Diagnosis:

A

~ Screen chronic HBV patients for HBsAg, HBeAg, HBe-Ab, HBV DNA
• HBsAg: acutely infected or carriers = screening test; all chronic cases have this
• Anti-HBs: past infection (resolved) or vaccinated
• HBeAg: active infection, ↑risk of transmission; ↑DNA viral levels
• Anti-HBe: carrier with ↓risk
• Anti-HBc: past infection (notice there is no core capsid marker); this is how you distinguish past infection vs. vaccine
• IgM Anti-HBc: acute infection
• HBV DNA

148
Q

HCV

Microbiology:

A

Flaviviridae -> Hepacivirus
• ss-RNA+ enveloped icosahedral capsid
• Encodes polyprotein cleaved by NS3 protease
• 6 Major Genotypes w/Subtypes (see epidemiology)

149
Q

HCV

Disease:

A

nonA/B PT-Hepatitis –> Chronic Disease

150
Q

HCV

Epidemiology:

A

• Subtypes 1a, 1b, 2a and 2b example of antigen var
• 45-55 year old men
• Untreated patients become chronic carriers
• Hepatocellular carcinoma (HCC) but less than HBV
Time Table
• Chronic hep (10 years), cirrhosis (20), HCC (30)

151
Q

HCV

At Risk Patients:

A

Anyone born between 1945-65
• Hospital-Workers, hemophiliacs, HIV-infected
• Drug users, dialysis
• Alcoholic Liver Disease

152
Q

HCV

Pathogenesis:

A
  1. PT spread with incubation time ~ 7-9 weeks
    • IV drug use > sexual transmission > blood transfusions
  2. NOT Cytolytic –> causes immune-mediated destruction of infected cells (see immune response in HBV)
  3. Cirrhosis —> Liver Cancer –> Liver Failure –> Liver Transplant
153
Q

HCV

Presentation:

A

Compare to HBV
• Patient has multiple bouts of HCV due to reinfection with same or different strains / emergence of different quasispecies
• Subsequent bouts are shorter duration, but each holds equal risk –> chronic disease
• Unlike HBV, antigenic variation facilitates immune escape (mediated by HCV hypervariable region HVR1 near E2 gene)

154
Q

HCV

Diagnosis:

A

~ Screen HCV patients for HCV core antigen + RNA / determine HCV genotype via RT-PCR
• Given patient may have 10 different subtypes of genotypes, but 1 quasispecies predominates
• Difficult to grow in culture
• Screening Test of Choice: HepC Antibody —> HCV RNA PCR —> Biopsy (***Biopsy is to determine severity!)

155
Q

HCV

Treatment:

A

Cure 2 –> 3 –> 4 –> 1 (least curable)
• Screen blood supplies for HCV RNA
• PEG-IFN + Ribavirin + Protease Inhibitors ~ contraindicate: depressed (IFN), liver failure (IFN) & TerX/hem (Ribavirin)

156
Q

HDV

Microbiology:

A

Delta virus = circular ss-RNA

• Contain Delta-Ag + HBsAg

157
Q

HDV

Disease:

A

Co-Infection or Super-infection of HBV patient.

158
Q

HDV

Epidemiology:

A

Only in patients with HBV infection.

159
Q

HDV

Pathogenesis:

A

HDV requires HBV for transmission
• Delta-Ag (polymerase molecule) + HBsAg facilitate hepatocyte infection (replicates in liver)
• Doesn’t produce it’s own receptor; uses HBV
• Can replicate on it’s own; just no transmission

160
Q

HDV

Presentation:

A

If co-infection = acute disease; if super-infection = chronic cause of HBV that suddenly get’s worse

161
Q

HDV

How to diagnose HDV?

A
  • Ab-HDV

* All should have HBsAg!

162
Q

HEV

Microbiology:

A

Calcivirus –> Hepevirus
• ss-RNA+ non-enveloped icosahedral capsid
• Single serotype

163
Q

HEV

Disease:

A

Acute ET Hepatitis

164
Q

HEV

Epidemiology:

A
  • Most prevalent in developing countries***
  • Pregnant women = ↑Fatality Risk***
  • Swine (reservoir) may be important in industrialized countries (Japan)
165
Q

HEV

Pathogenesis:

A

~ HAV ~ makes sense

• Transmitted F/O route –> replicates in GI tract (15-30 days) –> Liver, Kidney, Spleen –> Sheds (jaundice)

166
Q

HEV

Presentation:

A

Jaundice (end of shedding)

167
Q

HEV

Diagnosis:

A

Isolated from patient’s feces

168
Q

HGV

Microbiology:

A

Flaviviridae

• ssRNA+

169
Q

HGV

Disease:

A

nonA/B PT-Hepatitis

• Unsure if it actually causes chronic disease

170
Q

HGV

Epidemiology:

A

Common in blood-donor population

171
Q

Hepatitis Viruses

Which cause cirrhosis?

A

Hepatitis B, D & C

172
Q

Hepatitis Viruses

Which cause acute liver failure?

A

A, E & B

173
Q

Hepatitis Viruses

Which can be cured?

A

HCV NOT HBV

174
Q

Hepatitis Viruses

When should you always be screened for HBV?

A
  • Cancer chemotherapy

* HIV treatment

175
Q

Hepatitis Viruses

What two drugs used for HBV***EXAM?

A
  • Entacavir + Tenofovir

* Need CT scan every 6 months b/c risk for HPC

176
Q

Hepatitis Viruses

What should be vaccinated for?

A

• A & B
Screening
• All HBV should be screened for HepB

177
Q

Acute Hepatitis =

A

Acute Hepatitis = A, E and B

178
Q

Acute Hepatitis

Symptoms:

A

Symptoms: fever, fatigue, abdominal pain

179
Q

Acute Hepatitis

Presentation & Labs:

A
  • Enlarged Liver
  • ↑AST/ALT > 1000
  • ↑PT + ↑Bilirubin
  • During infection: ↑IgM; after infection: ↑IgG
180
Q

Acute Hepatitis

Three Outcomes:

A

Resolution&raquo_space; Progression to Chronic (HBV)&raquo_space;»»> Fulminant Liver Failure (encephalopathy)

181
Q

Chronic Hepatitis =

A

C, B (+D)

182
Q

Chronic Hepatitis

Timeframe:

A

> 6 months infection

183
Q

Chronic Hepatitis

Presentayion:

A
  • Asymptomatic with NORMAL LFTs

* ~ 20 years for liver fibrosis; accelerated by HIV, alcohol + obesity

184
Q

Chronic Hepatitis

Don’t forget 7-8 tests for HBV - what are they?:

A

IgG + IgM Ab-HBcAg, HBsAg, Ab-HBsAg, HBeAg, Ab-HBeAg, HBV DNA

185
Q

Chronic Hepatitis

Epidemiology:

A
  • HepB most common worldwide

* HepC most common US (2.7 M) ~ everyone born between 1945-1965

186
Q

Chronic Hepatitis

Testing:

A
  • HepC test of choice: Ab-HepC —> PCR

* Ab-HepC+ & HCV-RNA+ = acute OR chronic; just Ab-HepC+ = resolution; just HCV-RNA+ = early/acute HCV

187
Q

Clostridium Perfringens
Pathogenesis: Based on Disease
Food Poisoning =

A

Non-Inflammatory Diarrhea for 8-12 Hours

  • Spore germinates on unrefrigerated meats –> ↑Toxin Production
  • Enterotoxin –> Non-inflammatory watery diarrhea; no Vomiting; no Fever

GI Liver (7 decks)

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