Spring 2026 Exam 3 Study Guide FOS4222

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Last updated 6:06 AM on 3/25/26
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55 Terms

1
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Why are Vibrio species associated with seafood and water?

thrives in warmer waters, halophile and tolerates freshwater

2
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What are the three major pathogenic Vibrio species?

V. cholerae

V. vulnificus

V. parahaemolyticus

3
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True or False. ALL subpopulations of Vibrio spp. are virulent.

no, some lack the toxin genes

4
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True or False. The best temperature to isolate Vibrio spp. is 15°C.

no, 15 C is too cold and vibrio thrives as temperatures increase, optimally at 37C aka human body temperature. At 15 C it is likely to go dormant and become VBNC.

5
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True or False. Vibrio spp. require saline environments to grow.

True; V. spp. requires 1-3% salt bc its a halophile

6
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Know the environmental conditions that the highlighted/discussed pathogenic Vibrio spp. can grow in.

Halophile (1-3% salt), optimal growth at 37 C for enteropathogenic vibrio, gram negative, faculatively anaerobic, motile rods

7
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True or False. Risks of Vibrio infections are higher in warmer months.

True; thrives in warmer temperatures

8
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What are common routes for Vibrio transmission.

seafood (raw oyster consumption), contaminated water

9
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What proteins do the two Vibrio chromosomes encode for?

  • Chromosome 1: 3 Mb and encodes essential proteins

  • Chromosome 2: variable sizes amongst species, evolved from plasmids and encodes accessory proteins (but lacks biological activity)

recombination and horizontal gene transfer is important to its evolution

10
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Which Vibrio species can tolerate fresh water and what are the implications?

V. Cholerae tolerates freshwater, can contaminate drinking supply. Direct contact to environmental bacteria via water

11
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What is Vibrio cholerae serotyping based on? What are the serotypes discussed and their virulence factors?

It is based on O, somatic antigens.

  • O1 and O139 serotypes are cholera and produce cholera toxins - life threatening

V. cholerae O1 biotypes

  • classical - historical and caused issues throughout history

  • El Tor - new strain, higher asymptomatic cases, fermentation capabilities for survival

VIRULENCE factors

  • Cholera Toxin (CT) - diarrhea

  • Toxin co-regulated pili - allows for bacterial colonization

  • ToxR - gene regulating CT and determines if it is virulent

12
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How did horizontal gene transfer contribute to the evolution of the seventh pandemic strain of Vibrio cholerae?

Environmental V. cholerae habors genomic islands - genes for colonization, toxin production, and anti-phage defense - uses horizontal gene transfer

caused by O1 biotype El Tor

13
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How is Cholera clinically presented?

Infectious dose 106 - 1011

Susceptible: children, achlorhydria (lack of HCl caused by H. pylori, blood group O (antigens)

Incubation time within hours to 5 days

Symptoms: watery diarrhea, rice water stools (clear water diarrhera), hypotension, vascular collapse, poor skin elasticity = dehydration

14
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Which Vibrio species are most commonly associated with illness in the United States and what foods are linked to infection?

V. vulnificus

  • enters through wounds and septicemia

  • mortality rate >50%

  • associated with Gulf of Mexico oysters (warm environment)

V. parahaemolyticus

  • mild diarrhea

  • 8000 cases/year

  • pacific and atlantic oyster

15
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What are the clinical presentations (symptoms) of V. vulnificus infection?

septic shock

  • fever, bullous lesions, 50% fetal in <24 hr

Wound infections

  • necrostic lesion (flesh eating)

  • debridement, amputation

  • 20% fatal

Diarrhea - rare or co infection

16
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What is V. parahaemolyticus serotyping based on? Does this species correlate to fecal coliforms?

Based on O and K antigens

cases mostly in Japan until pandemic O3:K6

no correlation to fecal coliforms because its not zoonotic

17
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What are the clinical presentations (symptoms) of V. parahaemolyticus infections?

  • short incubation time

  • diarrhea (watery, bloody w/ mucus), cramps, vomiting, fever

  • 3-5 days

  • causes wound infections, septicemia

18
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What are the virulence factors of V. parahaemolyticus?

T3SS is primary factor

Markers:

  • thermostable direct hemolysin (TDH), spore forming

  • TDH related hemolysin (TRH)

  • Presence of either D or R indicates virulence

Species marker of all vibrio - heat labile hemolysin (TLH)

19
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Describe the VBNC state in V. parahaemolyticus.

  • modifications: cell membrane, fatty acid synthesis, morphology, metabolism, gene expression, adhesion and virulence capability

  • rod to coccoid shape, express cytoskeleton genes

  • decreased cell membrane fluidity

  • resistant to thermal, low saline, and acid

20
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Why is Vibrio commonly associated with oysters? What are some tips to cooking shellfish?

Oysters are filter feeding

Cook till shell opens and boil additional 3-5 min

21
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which vibrio species do we need to know for this exam?

Water borne: V. cholerae

Seafood: V. parahaemolyticus, V. vulnificus

22
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characteristics of vibrio?

Gram negative, faculative anaerobe, motile rods, halophile, warm environments

23
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Why is Campylobacter a global concern?

Global cause of diarrheal diseas

  • leading cause of death in children < 5 yrs old bc of dehydration

  • malnutrition, contaminated water, parasites are associated with it

24
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What are characteristics of Campylobacter jejuni?

C. jejuni is the most common strain in USA

Family Campylobacteraceae, gram negative, slender, curve/spirals

non spore forming, non fermenting, motile using flagellum

25
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Which conditions is C. jejuni susceptible to?

  • microaerophilic (low conc O2 tolerant)

  • can’t survive outside host

  • inactivation with heat treatment and survives at low temperatures

  • Sensitive to desiccation (drying bc O2), high oxygen, pH (inactivate at 2.3) → cannot compete w/ other bacterias

26
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What are the reservoirs for Campylobacter?

  • GI tract of warm blooded animals → fecal contamination of food and water

  • Zoonotic by poultry

  • Waterborne, in a VBNC state at fridge temps

27
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Describe Campylobacter when present within the natural flora of chickens vs. when introduced into humans.

Present in poultry skin/carcass and muscles. Carcass may be contaminated during slaughter by contact w/ intestines or contaminated environment. Chickens are typically asymptomatic w/ no diarrhea.

  • Natural flora of chickens may enter animal feed/ water supply, and animal byproducts (milk) may contain the pathogen and contaminate humans.

28
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Why would there be higher links of Campylobacter in milk compared to other dairy products?

Milk is neutral pH and a good broth medium for many pathogens growth. Dairy products are often fermented, cooked, and salted so that only beneficial bacteria are present. Campylobacter cannot compete with LAB and other fermenters.

29
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What are the virulence factors for Campylobacter?

  1. flagella allowing motility, secretion of effector proteins via T3SS (virulence injection needle structure in gram neg bacteria)

  2. enterotoxin - cytolethal distending toxin (CDT damages DNA), cholera like toxin

  3. T4SS - translocates DNA and protein, affect Euk and prok

  4. T6SS - releases spikes to kill bacteria and protein

  5. siderophore production - takes iron away from host using transferrin, lactoferrin, hemin, hemoglobin (proteins in the blood).

30
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Which mechanisms are the primary mechanisms for invasion into non-phagocytic host cells? (Select all that apply)

a.     “Binding” mechanism

b.     “Trigger” mechanism

c.     “Zipper mechanism

d. “Engulfment” mechanism

Zipper and Trigger

Zipper - adheres to host receptors, membrane engulfs it, and enters host cell

Trigger - T3SS and T4SS inject effector proteins into host cytoplasm, allowing host to uptake the bacteria; changes cell functionality

31
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How does Campylobacter cause host damage?

  • uses cytolethal distending toxin CDT

    • goes to nucleus and breaks down DNA → cell death

  • Macrophage uptake bacteria

    • dissemination (active spread of bacteria)

    • induces cytokines

    • kills host cells

32
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What is Guillain Barré syndrome?

Autoimmune and humoral immune response triggered by Camplyobacter

  • Camp antibodies recog LPS and nerve tissues

  • immune system attacks peripheral nerves, often triggered by a previous viral or bacterial infection. It causes rapid muscle weakness, numbness, and tingling, which can lead to paralysis or breathing difficulties

33
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How do you control Campylobacter during poultry production? What about at home?

  • HACCP, disinfection, hygiene, security using zoning

  • Nutrition strategy (good food for chickens): probiotics, bacteriocins, bacteriophages, organic and fatty acids in diet (lowers GI pH and boost gut health), using plant feed

  • immune strategy: immunization, vaccination

34
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Understand the difference between total and fecal coliforms.

total - most basic test for bacterial water contamination

fecal - total coliforms present in gut and feces of warm blood animals

35
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characteristics of e.coli

  • Enterobacteriaceae family, very diverse

  • Gram neg, ferments lactose, non sporing

  • found in mammal colons, high numbers in poo

  • successful competitor

36
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What type of coliform is E. coli?

fecal coliform

37
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Why are coliforms used as indicator organisms?

indicates fecal contamination, high amts = high change of enteric pathogens

38
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True or False. All strains of E. coli are pathogenic.

no, only a few

39
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How is E. coli categorized? What is a serogroup? What is a serotype?

  • catagorized based on the antigen present

  • serogroups = shared antigen between organisms

  • serotype = specific antigen like O, K, H

40
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Serotype virulence of E.coli

  • Capsule - K antigen/ Vi in salmonella

  • Somatic - O antigen/cell wall

  • Flagellar - H antigen

41
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Why is E. coli used as an indicator of fecal contamination?

high amts indicates pathogens may be present

42
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List the 6 major categories of  pathogenic E. coli

  1. enterotoxigenic ETEC

  2. enteroinvasive EIEC

  3. Diffuse-adhering DAEC

  4. Enteroaggregative EAggEC

  5. Enteropathogenic EPEC

  6. Enterhemorrhagic EHEC aka Shiga prod and O157:H7

43
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Be able to describe the pathogenic mechanisms of the various pathogenic E. coli.

EPEC and EHEC (ETEC, EAEC)

attach and efface system, uses T3SS

  • EPEC - attach to enterocytes (intestine lining cells) and destroys microvillar. Causes infant diarrhea, vomitting, fever. not invasive, no toxins

  • EHEC - attach and efface lesions in the colon; prod shiga causing severe diarrhea and dmg

  • ETEC - attach to enterocytes, watery diarrhea caused by secretion of heat labile and/or heat stable entertoxins

  • EAEC - adheres to epithelia as a biofilm

  • EIEC invades colon epithelial cell and moves around

  • DAEC - grows long finger projections that wrap around bacteria

44
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E. coli O157:H7 produces what type of toxin?

Why is this serotype important/why do so many researchers focus on this serotype?

45
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What is Hemolytic Uremic Syndrome? Which toxin is associated with this condition

46
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Which food products are associated with pathogenic E. coli strains?

47
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STEC are commonly associated with which food product? What practices may contribute to this?

48
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How is Shigella genetically related to E. coli?

49
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True or false. Shigella is a primary concern for processing plants.

50
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Why is Shigella unique?

51
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What toxin is associated with Shigella?

52
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Does Shigella cause dysentery?

53
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Shigella is generally present in low numbers. Why is this important?

54
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What are the major routes of Shigella transmission?

55
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How do you prevent and treat Shigella?

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