Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Food-Borne Pathogens > Midterm II > Flashcards

Midterm II Flashcards

1
Q

What were the major events of Cronobacter history?

A

1929: First report of a yellow-pigmented coliform
1961: Yellow-pigmented coliforms caused two cases of neonatal meningitis
1977: yellow-pigmented coliform named Enterobacter sakazakii after Japanese microbiologist
2008: Moved to new genus Cronobacter w/ 5 species
Today: Cronobacter has 11 species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the species of Cronobacter?

A
  • C. dublinesis
  • C. muytjensii
  • C. condimenti
  • C. universalis
  • C. helveticus
  • C. zurichenesis
  • C. pulveris
  • C. colletis
    Involved in neonatal infection:
  • C. sakazakii
  • C. turicensis
  • C. malonaticus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the main characteristics of Cronobacter?

A 
Gram -
Non-spore forming
Straight, rod-shaped
Flagellum
Originally yellow-pigmented coliform (unless repeatedly sub-cultured, then loses yellow pigment & cell morphology)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the growth factors of Cronobacter?

A

Nonhalophilic (not salt loving)
Facultative anaerobe
Grows between 6-45C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where is Cronobacter most found?

A

Powdered infant formula (PIF)
- 10-15% of PIF has Cronobacter (very low chance of infection, tho)
Specifically reconstituted PIF
- Intrinsic or extrinsic contaminant during manufacturing under poor good manufacturing practices (GMP) or reconstitution of PIF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the statistics of Cronobacter?

A 
Range from 3 days to 4 years old
- 120 recorded cases (many thought to be undocumented)
- Increases year-to-year
- 19 deaths (40-80% fatality rate)
- 11 countries
Adults
- 20 cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which US State has the largest Cronobacter outbreak?

A

Tennessee
In 2001
10 cases & 1 death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What age group is most at risk of Cronobacter?

A

Infants below 1 year fed PIF
- Neonates (infant below 28 weeks) at greatest risk
Increased risk with:
- Immunocompromised
- Low birth-weight neonates
- Premature infants born below 37 weeks (avg = 40 weeks)
* Most cases in developed world (most likely due to underreporting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why are premature infants at a higher risk for Cronobacter?

A

They secrete less gastric acid than older infants

Increases long-term survival of Cronobacter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Cronobacter likely diagnosed as instead?

A

SIDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What happens to survivors of Cronobacter?

A

Severe neurological & development disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the symptoms of Cronobacter?

A 
Necrotizing enterocolitis (NEC)
Septicemia
Meningitis
Neurological sequelae (aftereffects)
- Brain abscess
- Necrosis of brain tissue
- Liquefaction of white cerebral matter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What food products that don’t cause illness contain Cronobacter?

A 
Milk powder
Cheese
Herbs
Spices
Rice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What clinical sources can contain Cronobacter?

A 
Cerebrospinal fluid
Blood
Intestinal & respiratory tracts
Bone marrow
Skin wounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why can’t Cronobacter be removed from PIF?

A

Would affect organoleptic & nutritional requirements
- PIF is highly regulated for nutritional requirements
Can only be irradiated
- Would deteriorate organoleptic too much
* New approaches = ultrahigh pressure, magnetic fields

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are pathogenesis factors of Cronobacter?

A 
Manufacturer:
- Survival on equipment
- Biofilm formation
- Temperature of processing
Infant:
- Higher stomach pH than adults 
- Lower GI microbiome complexity
- Immunocompromised
Organism:
- Can cross blood-brain barrier (bbb)
- OmpA facilitates invasion of brain cells (not all C. have this)
- Enterotoxins produced (don't know how common)
- Can cross GI barrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do the virulence factors of Cronobacter pathogenesis do?

A

Apical attachment (can attach to epithelial cells)
Invasion (apical & basolateral side)
Disrupt tight junction (causes diarrhea)
Disrupt adheren junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the virulence factors of Cronobacter and their genes?

A
  • Outer membrane proteins (OMPS): ompX, ompA (invade epithelial cells & bbb)
  • Enterotoxin: unknown (heat stable)
  • Outer membrane protease: cpa (protect from immune system
  • Sialic acid utilization: nanAKT (confers in pathogenesis)
  • Iron acquisition system: iuc (Encodes iron-uptake system)
  • Efflux system: ibeB (facilitates invasion of brain cells)
  • Proteolytic enzymes: zpx (deforms & rounds cells)
  • Lipopolysaccharides: chromosomal encoded genes (disrupts epithelial cells
  • Type 3 hemolysin: hly (hemolytic activity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the outer membrane proteins (OMP) of Cronobacter?

A

Critical
On cell surface
Export extracellular virulence factors and anchor the structures that cause adhesion & motility
Gene OmpA: helps cells adhere to GI epithelial cells
- Need to breech bbb (without this gene, the Cronobacter doesn’t get to the brain)
Gene OmpX: helps invade apical side of GI epithelial cells & helps bacterium survive on basolateral side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the outer membrane protease (cpa) of Cronobacter?

A 
Cronobacter plasminogen activator (cpa)
Can cause serum resistance by:
- Cleaving complement components
- Activating plasminogen
- Inactivating a plasmin inhibitor
pESA3 plasmid
- Encodes cpa
- Encodes T6SS (interbacterial antagonists = fight other bacteria)
- Encodes some adhesion factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is sialic acid utilization in Cronobacter?

A

Gene = nanAKT
Found in human milk & infant formula
- In form of sialyloligosaccharides
- Remain undigested in infants, increasing the neonate intestinal microvilli sialic acid levels
Only found in C. sakazakii
- Possible link between sialic acid metabolism & pathogenesis of C. sakazakii

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do you prevent Cronobacter?

A

After preparing PIF, refrigerate at 4C within 1 hr
Prepare PIF in small amounts to reduce “hang time” at room temp before consumption
- Never leave out for more than 4 hrs after prepared
Only use chilled, sterile water for preparation
Discard any remaining PIF after feeding
Use within 4 weeks of opening a can
Sterilize bottles prior to reconsitution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the general characteristics of Vibrio sp?

A 
Non-spore forming
Gram -
Vibrio shaped (looks like a cheeto)
More common in warmer waters
- Increases dramatically above 17C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the most important Vibrio species that cause illness?

A

96 species total (mostly non-pathogenic)
- 40-60% of finfish/shellfish in supermarkets have Vibrio spp.
12 are causative agents in human infection
3 cause most illnesses:
- Vibrio parahaemolyticus
- Vibrio vulnificus
- Vibrio cholera (more waterborne than foodborne)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where is Vibrio sp. found?

A

Estuary waters (between marine & fresh water)
- Predominant here
- Only V. cholerae O1 & O139 are not natural (come from fecal contamination)
Generally associated with seafood consumption or seafood contact
Number differs based on water temp
- More common in warmer waters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the most common Vibrio spp. of infection in Canadian seafood?

A

V. parahaemolyticus
Case study: from oysters after a temperature spike
Colder waters = safer seafood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the general traits of V. parahaemolyticus infection?

A 
Serotype:
- O antigen (LPS)
- K antigen (capsular polysaccharide)
- There are regional differences to the serotype (west coast = O4:K12)
Raw or undercooked seafood
At 37C has 8-9min generation time
Symptoms appear within 4-30hrs
- Subside in 3-5 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the generation time of V. parahaemolyticus at 37C?

A

8-9 minutes

Contaminated food becoems highly colonized if temperature abused

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the symptoms of V. parahaemolyticus?

A
  • Appear within 4-30hrs
  • Include diarrhea, abdominal cramps, nausea, vomiting, fever
  • Subside in 3-5 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the characteristics of V. parahaemolyticus?

A

Flagellum:
- 1 at pole of bacterium for swimming
- During growth in semi-solid media, more grow on lateral side for swarming
MAM7:
- Multivalent adhesion protein
- Binds fibronectin & phosphatidic acid to initial attachment
Siderophores:
- Vibrioferrin, ferrichrome, aerobactin, heme
- Scavenge iron from environment, causing haemolysis (red cell rupturing)
- Internalized by different membrane receptors on the OM of bacteria
- Transported to cytoplasm by different ABC complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the virulence factors of V. parahaemolyticus?

A 
Toxins (haemolytic toxins):
- Thermoliable haemolysin (tlh)
- Thermostable direct haemolysin (tdh)
- Thermostable direct-related haemolysin (trh)
T3SS1 Effectors
- VopQ, VopR, VopS
- VPA0450
T3SS2 Effectors
- VopA, VopC, VopL, VopT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How does tdh & trh cause hemolysis or cytotoxicity?

A

Secreted from V. parahaemolyticus
- Two different routes of virulence, but can move between genomes
- Can even move to V. alginolyticus genomes
Needed to cause illness
Form tetrameric pore complexes in host membrane
Pores allow ions to flow freely across host membrane
Leads to hemolysis or cytotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How do T3SS1 effectors of V. parahaemolyticus cause cytotoxicity?

A

Translocated into host cells (allow effectors past membrane)
Cause cytotoxicity in different cell types
- Including macrophages & HeLA cells
* T3SS1 is found in all isolates (even non-pathogenic)
- Means they are important in the environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How do T3SS2 effectors cause enterotoxicity & cytotoxicity?

A

Translocated into host cell (allow effecters past membrane)
Cause either:
- Cytotoxicity of colon epithelial cells
- Enterotoxicity within host
* T3SS2 is found in clinical isolates
- More closely related to a pathogenic lifestyle than T3SS1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the main features of V. vulnificus in infection?

A

Most serious vibrio infection:
- Cause 95% of seafood related deaths in NA
No serotype, but have 3 biotypes:
- Biotype 1: causes human disease
- Biotype 2: causes eel & rarely human disease
- Biotype 3: combination of 1 & 2; found only in Israel
Two distinct syndromes:
- Primary septicemia
- Necrotizing wound infection
Only in warm waters
Symptoms appear 7hrs to multiple days after exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the two V. vulnificus syndromes?

A

Primary septicemia:
- Caused by consuming raw or undercooked seafood
- Raw oysters have 60% fatality rate
Necrotizing wound infection:
- Caused by open wound being exposed to warm seawater or contaminated seafood w/ high conc of bacterium
- 20-25% fatality rate
- Can require surgery to clean infected tissue or even amputation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the symptoms of V. vulnificus?

A 
Appear from 7 hours to several days after exposure
Include:
- Fever
- Chills
- Nausea
- Hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the virulence factors of V. vulnificus?

A

Polysaccharide capsule is required (K antigen)
- Needed, but not understood why
LPS (O antigen)
- Causes high fever, systemic infection, & shock
vvhA
- A heat-stable haemolysin/cytotoxin unique to V. vulnificus
- Plays an unknown role in virulence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the main features of V. cholerae infection?

A

Serotype:
- O antigen (LPS)
O1 & O139 cause epidemics & pandemics (one of few foodborne illnesses to do so)
- Only ones to cause illness from V. cholerae (non-pathogenic otherwise)
- Produce Cholera toxin (CTX) from phages that cause illness (O1 acquired it first)
- Found in US Gulf coast & Australian coasts (warmer waters)
Has VBNC state (cells become ovoid & smaller)
Secrete V. cholerae in feces 1-2 weeks after recovery
Colonizes small intestine using adherence factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What happens to V. cholerae in a VBNC state?

A

Not culturable on any media

If injected into rabbits, can cause ileal loop fluid accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What does the CTX toxin of V. cholerae do?

A

Carried on a phage of O1 (first) or O139
- Needed to make V. cholerae pathogenic (has happened 2 times before, warming waters inc. the likelihood of happening again)
Binds to ganglioside receptors on surface of intestinal epithelium cells
- Internalized by endocystosis & triggers cAMP production
- cAMP activates specific ion channels causing efflux of ions (disrupts ion transports)
- Build of of ions causes osmosis, leads to acute diarrhea
- Results in dehydration that can be fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is interesting about the horizontal gene transfer of V parahaemolyticus?

A

Carries K & O antigen genes in two different clusters
Can rapidly undergo HGT
- Can switch serotypes mid-outbreak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What does V. cholerae do with DNA from the environment?

A

Readily takes up DNA from the environment

- Increases it’s chance of taking up genes that increase its survival & virulence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What can V. cholerae get from V. parahaemolyticus?

A

T3SS2

Would cause V. cholerae to be pathogenic, with symptoms similar to V. parahaemolyticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How can Vibrio infection be prevented?

A

Sensitive to cold
- Freeze, refrigerate, or store seafood in ice
Eat seafood fresh
Properly cooking
Irradiation & high hydrostatic pressure
Food with bactericidal activity: dried spices, herbal oils, tomato sauce, & organic acids (lemon juice)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What effect does depuration have on Vibrio?

A

It is the process that filter-feeding bivalves are purified by pumping through clean water
Does not remove Vibrio
- Does remove Salmonella & E. coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the rare bacterial food-borne infections?

A

Brucellosis
Streptococcus pyogenes
Coxiella burnetii

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What causes human Brucellosis?

A 
Brucella abortus (cattle)
Brucella suis (swine)
Brucella melitensis (goats & sheep)
Brucella canis (dogs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the characteristics of Brucellosis?

A

Gram -
Nonmotile
Non-spore forming
Aerobic
Rods
All species are pathogenic to humans & animals
Most common in northern Africa, the Middle East, and Asia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Where is the bacterium of Brucellosis located in infected animals?

A

Uterus of pregnant animals

Mammary glands of lactating females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the correlation between milk & Brucellosis?

A

Consumption of raw milk can cause brucellosis
Cells survive a long time in milk/milk products
Pasteurization is effective against killing the cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How can Brucellosis be transmitted?

A

Secreted in milk
To people who work with meat
From veterinary care
Vaccination accident, laboratory accident (w/ cultures)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the symptoms of Brucellosis?

A 
Appear 3-21 days after consumption
Include:
- Fever
- Profuse sweats
- Body aches
- Aching joints
- Chills
- Weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the characteristics of Streptococcus pyogenes?

A

Gram +
Has been associated w/ human pharyngitis
Isolated from lactating cows w/ mastitis
- Foodborne cause is consumption of raw milk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the symptoms of Streptococcus pyogenes?

A 
Normally
- Sore throat
- Fever
- Chills
- Weakness
Sometimes:
- Nausea
- Vomitng
- Diarrhea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How is Streptococcus pyogenes prevented?

A

Milk pasteurization

People suffering from identified Streptococcus infection should not handle ready-to-eat foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What does Coxiella burnetii cause?

A

Q fever
Caused by:
- Handling animals, raw milk & meat or drinking raw milk that carry the bacteria
- Animals can carry bacteria w/out symptoms
Symptoms appear after 2-4 weeks & include:
- Fever
- Malaise
- Anorexia
- Muscular pain
- Headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the characteristics of Coxiella burnetii?

A

Most heat resistant bacteria in raw milk

  • Killed by pasteurization at high temperatures for a long time period
  • 62.8C for 30 mins or 71.1C for 15 seconds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What antibiotics affect the cell wall?

A

Beta lactam antibiotics
Glycopeptides
Bacitracin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What antibiotics affect the DNA?

A

Fluoroquinolones
Novobiocin
Nitroimidazoles
Nitrofurans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What antibiotics affect the ribosomes?

A 
Tetracyclines
Aminoglycosides
Lincosamides
Macrolides
Streptogramins
Chloramphenicol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What happens in the absence of beta-lactam antibiotics?

A

Transpeptidases (penicllin binding proteins) catalyze the cross links between glycan changes in the peptidoglycan
Results in covalent bonds between peptide & sugar chains creating a rigid cell wall that protects the bacterial cell from osmotic forces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What do beta-lactams do to transpeptidase?

A

Beta-lactam antibiotics are similar to the natural peptidoglycan subunits that are the substrate for the transpeptidase
- They bind to the active transpeptidase site & stop cell wall synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the natural peptidogylican subunits that are the substrate for transpeptidases?

A

D-Ala-D-ala

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the structure of beta-lactam antibiotics?

A

Core 4-member beta-lactam ring
- Mimics the terminal D-Ala-D-ala peptide sequence (substrate for transpeptidase)
Created by modifying the structure of penicillin
- Created greater spectrums of activity, greater resistance to beta-lactamases, & different pharmacokinetic properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the general resistances to Beta-Lactams?

A

Penetration: intracellular bacteria resistant if in a mammalian cell
Porins: gram - bacteria have the outer cell membrane that protects the peptidoglycan. If porins are small enough, beta-lactams can’t get through
Pumps: gram - bacteria can express ABC transporters to pump out antibiotics
Peptidoglycan is absent: Some bacteria lack a cell wall, making beta-lactams unaffective
- Ex. mycobacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the specific resistances ot Beta-Lactams?

A

Penicillinases: Some bacteria make beta-lactamases that degrade beta-lactam antibiotics before reaching the cell
PBPs: some bacteria can express mutated transpeptidases that have the same enzymatic activity for cell wall synthesis without binding to beta-lactam antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How does antibiotic resistance effect humanity?

A
  • Global health
  • Food security
  • Development/economics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How does antibiotic resistance affect people?

A

Antibiotic resistant infections can affect anyone (no matter age, country, immune status)
Antibiotic overuse has accelerated antibiotic resistance
- Results in multiple infections that are hard/impossible to treat
Will effect:
- Childbirth
- Post-operative care
- Chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How many people will die by 2050 due to antimicrobial resistance (AMR)?

A

10 million (mostly in Asia & Africa)
Will cause unknown financial impacts
Worse than AIDS, Cancer, or COVID-19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Where are antibiotics used?

A

Human medicine
Agricultural production
Food processing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the history of ABR in agriculture?

A

1910: US meat demand outstripped supply
1917: USDA funded research to increase meat production
1928: penicillin was discovered (all S. aureus were susceptible)
1938: Sulphonamides were used in agriculture
1940s: Aureomycin was found to inc. poultry weight gain 1940s: Britain used antibiotics to treat bovine mastitis (increased milk output)
1948: Sulfaquinoxaline was used to prevent coccidiosis in broilers (chicken)
1950s: Antiobitic growth promoters (AGPs) were licensed in US, Britain, Netherlands, & France
Today: North American chickens are given bacitracin & ionophores, beef cattle are given ionophores, dairy cattles are given ceftiofur during lactation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What has happened to agriculture with the use of antibiotics?

A

Decrease of 95% of mastitis infections (with the help of other prevention methods)
AGPs have increased broiler growth by 8% & improved feed efficiency by 5%
- Have decreased chicken deaths from 4.2% to 2.9%
AGPs have increased pig growth by 4.2% & improved feed efficiency by 2.2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

How does WHO combat AMR?

A

Five-pronged approach

  • Improve awareness & understanding of antimicrobial resistance
  • Strengthen surveillance & research
  • Reduce incidence of infection
  • Optimize use of antimicrobial medicines
  • Ensure sustainable investment in countering antimicrobial resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How does Canada combat AMR?

A

Three-pronged approach

  • Surveillance: detect & monitor trends & threats to inform strategies to reduce risks & impacts
  • Stewardship: conserve effectiveness of existing treatments through infection prevention & control guidelines, education & awareness, regulations, & oversight
  • Innovation: create new solutions to counteract the loss in antimicrobial effectiveness through research & development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How does Canada categorize antibiotics?

A

4 categories based on importance to human medicine:

  • Cetegory I (very high importance): preferred treatment of serious human infections; no alternatives available
  • Category II (high importance): preferred treatment; alternatives available (mostly category I drugs)
  • Category III (medium importance): not preferred treatment; alternatives usually available (by category I or II)
  • Category IIII (low importance): not used in human medicine
  • Categories I-III have specific AMR warnings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is Canada’s approach to stewardship against AMR?

A
  • Categorize antiobitics based on importance to human medicine to prioritize risk management options
  • Support microbiological safety evaluation of veterinary antimicrobial drugs (using CIPARS data)
  • Encourage prudent use of antimicrobials
  • Undertake post-market re-evalution of medically important antibiotics over time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What antibiotics are not used in humans but used for other species?

A

Category I antibiotic, Ceftiofur
- Used in dairy cattle before infections
Category II & IV antibiotics
- Used in poultry feed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are cross-reactions in antibiotics?

A

Synercid is used in humans
- Virginiamycin in used in broilers & swine
- Virginiamycin creates resistance to Synercid
MCR-1 creates resistance to colistin & bacitracin
- Bactitracin is used in agriculture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

How does Canada use Surveillance against AMR?

A

2014, ceftiofur was banned in chicken hatchlings

- Response to growing detection of Salmonella & E. coli resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are ways to replace antibiotics?

A 
Improved hygiene
Vaccinations
Bacteriophages
Probiotics
Antibotic derivatives
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the key characteristics for spore forming toxico-infection bacteria?

A

Ingestion of large numbers of live vegetative cells is necessary (usually)
Vegetative cells of sporeformers do not multiply in the digestive tract, but sporulate & release toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What are the key characteristics of gram-negative toxico-infection bacteria?

A

Live cells can be ingested in moderate numbers
Cells rapidly multiply in the digestive tract
Many cells die, releasing toxins

84
Q

What is true of all foodborne toxico-infections?

A

All toxins cause gastroenterititis symptoms

85
Q

What are the names of toxico-infection bacteria?

A
  • Clostridium perfringens
  • Bacillus cereus
    Maybe if large number of cells are ingested:
  • Vibrio cholerae
  • enterotoxigenic E. coli
86
Q

What are the general characteristics of Clostridium perfringens?

A 
Gram positive
Motile
Rod shaped
Spore forming
Form small chains
Anaerobic (can tolerate some O2)
Cells sensitive to heat, spores heat resistant
Lack amino acid synthesis ability (grow on high-protein foods)
87
Q

How does heat affect Clostridium perfringens?

A

Pasteurization kills vegetative cells
Spores are heat resistant (can survive boiling for several hours)
Grow 10-52C
- Grow optimally at 45C

88
Q

What does Clostridium perfringens not synthesizing amino acids mean?

A

Grow more on high-protein foods

- Cooked meat products

89
Q

What are the most important food factors contributing to C. perfringens outbreak?

A
  1. cooking large volumes in advance (large amt provides anaerobic environment)
  2. allowing it to cool slowly (allows temperature for spores (which aren’t killed by cooking) to germinate & multiply)
  3. holding for a long period of time
  4. serving without reheating
90
Q

What are the main foods involved in C. perfrignens outbreaks?

A 
Beef (26% of outbreaks)
Mexican food (12%)
Turkey (10%)
Chicken (5%)
* total number of outbreaks = 12,234
91
Q

Where can vegetative cells of C. perfringens be found in the environment?

A

Soil
Dust
Intestines of food-producing animals, animals, & birds
Sewage

92
Q

What are the symptoms of C. perfringens?

A

Appear 8-24 hrs after ingestion of large # of cells
Cause:
- GI infections (food poisoning, antibiotic-associated diarrhea, abdominal pain)
- Tissue infections (necrotic tissue infections, necrotizing enteritis)
- Nausea, vomiting, fever (less common)
- Fatalities are rare (more common in young, elderly, sick)
Symptoms gone after 24 hrs
- Seldom reported

93
Q

What are the types of toxins of C. perfringens?

A

15 different toxins
- Those coding genes are located on mobile genomic elements, meaning several different pathotypes exist
Strains classified into five toxinotypes (A, B, C, D, E) based on four major toxins (alpha (a), beta (B), espilon (E), iota (I))
- Major toxins secreted during the exponential growth phase
Type A associated with food poisonings in humans

94
Q

What is the virulence potential of C. perfringens based on?

A

The ability to produce a combination of the 15 different toxins & several extracellular hydrolytic enzymes (exoenzymes)

95
Q

What do C. perfringens toxins do?

A

Make conditions that favor infection

  • Disrupt host cell membrane to release nutrients for cells
  • Hydrolytic enzymes break down complex nutrients into smaller units that can imported into the cell and used by the bacteria
96
Q

What is Clostridium perfringens Enterotoxin (CPE)?

A

Synthesized by C. perfringens
Responsible for gastrointestinal symptoms
- Bind enterocytes & creates pores releasing large volumes of water & nutrients
- Diarrhea ensures it passes into the environment (ideal for maximum spread & survival)
Heat-liable
Only produced during sporulation
* Only toxin to do this
5% of Type A strains contain CPE gene
- Mostly isolated in outbreaks of food poisoning from livestock (foals, pigs) with diarrhea
Some Types B-E strains can produce CPE

97
Q

What does Clostridium perfringens Enterotoxin (CPE) do?

A

Binds to enterocyte cells
- Binds certain transmembrane tight junction proteins using sequences at the CPE C terminus
Begins forming a “prepare” large-complex formation
- After membrane localization via receptor binding, CPE joins other molecules of CPE to forma highly-stalbe complex
- Needs CPE’s putative transmembrane domain to move past the prepore stage (otherwise it is stuck at the stage & is degraded by proteases)
Need an intact N terminus & putative TMD to undergo conformational changes for insertion into the membrane
- Protects the complex from proteases
- Allows the penetration of the phospholipid bilayer of enterocytes, causing the influx of Ca2+ into the cell
- Ca2+ influx initiates cell death pathways

98
Q

How can C. perfringens be prevented?

A

Keep cell numbers low by:

  • Proper sanitation
  • Cooking food to highest possible temp
  • Food should be cooled quickly & uniformly
  • Food stored for a long time should be reheated quickly & uniformly & kept hot during serving (above 60C)
99
Q

What are the general characterstics of Bacillus cereus?

A 
Gram positive
Spore forming
Rod-shaped
Aerobic
Moderate symptoms similar to other food-borne pathogens (outbreaks are underestimated due to this)
Widespread in nature
- Vegetative cells are not competitive 
Spores can survive pasteurization
Can't grow at refrigerator temperatures
100
Q

How can B. cereus get to cow’s udders?

A

Frequently isoalted from soil & growing plants

From grass to udders to raw milk

101
Q

What are the heat problems of B. cereus?

A

Spores can survive pasteurization
- After can germinate & proliferate, can cause problems in dairy
- Vegetative cells can’t survive
Can’t grow below 10C (fridge temps)
- Phychrotolerant strains can grow as low as 4C

102
Q

What is the harm of B. cereus in milk on the market?

A

Causes one ot two cases (not identified as an outbreak

  • Causes more illness toward the end of the milk’s shelf life
  • Proteases of Bc cause off flavors, preventing consumption of milk
103
Q

What are the toxins of B. cereus?

A

Emetic (vomit-inducing) toxin (cyclic peptide)
Diarrheal enterotoxin (protein)
* most strains only produce one, a few can produce both

104
Q

What are the characterstics of emetic toxin of Bc?

A

Heat stable (like S. aureus toxin)
Acts rapidly (30 mins to 6hrs) after ingestion
- Lasts 6-24 hrs
Produced by cells growing in the food
Stimulates the vagus nerve to initiate vomiting
Dose causing illness = 10^5-8cells/g
Symptoms: nausea, vomiting, malaise
Foods: fried & cooked rice, pasta, pastry, noodles

105
Q

What are the characterstics of diarrheal enterotoxin of BC?

A

Several types of heat-liable toxins
Acts more slowly (6-14hrs)
- Lasts 12-24 hrs
Produced by vegetative cell growth in the small intestine
Mode of action not understood (induces diarrhea by stimulating cAMP system) (like V. cholerae)
Dose causing illness = 10^5-7 cells/g
Symptoms: abdominal pain, watery diarrhea, occasional nausea
Food: meat products, soups, vegetables, puddings, sauces, dairy

106
Q

What are the causes of B. cereus?

A

Improper holding temperature
Contaminated equipment
Inadequate cooking
Poor personal hygiene

107
Q

How to prevent B. cereus?

A

Stop spores from germinating & cells from growing:

  • Uniform quick chilling of food to 4C or holding food above 60C
  • Should not be refrigerated for long periods bc some Bc can grow at 4C
108
Q

What are the differences between B. antracis, B. thuringiensis, & B. cereus on human health?

A

B. anthracis: cause acute & often lethal disease anthrax
- Toxins = Anthrax, maybe enterotoxins
B. thuringiensis: used as a biological control for insects (able to produce protein crystals w/ insecticidal activity)
- Toxins = Enterotoxins, insecticidal toxins
B. cereus: cause food-borne illness; some strains are biological control against fungal & crop diseases
- Toxins = Enterotoxins, emetic toxin, maybe anthrax
* different phenotypes of all; unknown phylogenetic relationship
- Bt & Bc are essentially the same based on phylogenetic studies; can only tell Ba apart via biochemical tests

109
Q

What is the same between all species of Bacillus?

A

All have enterotoxins (except maybe B. anthracis)

110
Q

What do viruses consist of ?

A

A small segment of nucleic acid encased in a protein shell

Can have more than this (envelope)

111
Q

What is the Baltimore classification scheme of classification of viruses?

A

Classify based on form of nucleic acid present
Positive sense RNA can be immediately translated
- +RNA can directly cause infection (although less infectious than the whole virus particle)
Negative sense RNA must be converted to +RNA by RNA polymerase
- Not infectious itself
- Ambisense ssRNA are grouped under negative sense RNA

112
Q

What is the difference between enveloped & non-enveloped viruses?

A 
Enveloped 
- Lipid bilyaer membrane
- Impermeable barrier between genomes & outside
- Ex. HIV, influenza
Non-enveloped
- No membrane
- No barrier (require tightly packed protein shell to stop damage)
- Ex. poliovirus, papillomavirus
113
Q

What aids viruses in assembly?

A

Being highly symmetrical

114
Q

How do viruses enter cells & uncoat?

A

Binds to surface of receptive host cells
Enters by:
- Inducing conformational changes in the virus that lead to association w/ other receptors, membrane fusion, & penetration
- Transmiting signals through the membrane prepares the cell for invasion
- Inducing the endocytic pathway
Triggers penetration process & enters cytosol
DNA viruses:
- Transported into the nucleus for genome uncoating or replication
- Have different mechanisms to enter nucleus
RNA viruses:
- Can be translated in the cytosol

115
Q

How do viruses replicate?

A

Two ways:
- RNA dependent RNA synthesis (RNA replication)
- RNA dependent DNA synthesis (reverse transcription) then DNA replicaiton & transcription
Make viral proteins by expressing their mRNA early in infection
- Multiple strategies each using different enzymes (enzymes encoded by host or virus)
- mRNA is positive sense RNA & complement of negative sense RNA

116
Q

What is the difference between RNA-dependent RNA polyermase & DNA-dependent DNA polymerase?

A

RdRps & reverse transriptases have an error rate 3x higher than DdDps
RNA viruses evolve much faster than their host due to this
- Error rates impose limits on genome size
- Few are higher than 30kb
- Most are between 5-15kb

117
Q

How are macromolecules of viruses assembled?

A

Macromolecules transported to assembly point inside host cells (different strategies)

  • Most rely on cell for biosynthesis of the macromolecules, intracellular sorting, & delivery to assembly site
  • Macromolecules must have same targeting signals as cell for this to work
118
Q

How are proteins of viruses assembled?

A

Proteins are transported to plasma membrane through the secretory pathway
- Associate with ER & translocated across through proteinaceous pores
- Then move to Golgi complex
- Then to the plasma membrane (unless contain amino acid motifs that move them to a different location)
Occurs in coated vesicles

119
Q

What is the difference in assembly location between enveloped & nonenveloped viruses?

A

Enveloped msut take the lipid bilayer from a host cell membrane
Non-enveloped can assemble in the cytoplasm or nucleus
- Take structural proteins from this location

120
Q

How are non-enveloped viruses assembled?

A

Macromolecules assemble into empty capsids
Viral DNA is inserted into the capsid
- Via packaging sequence at one end of the genome
Precursor core proteins are packaged into the empty capsid
- Proteolytic cleavage of the precursor proteins by proteinase creates mature virions

121
Q

What are the different pathways for enveloped virus assembly?

A
  1. Proteins are transported to plasma membrane & assembly of the capsid & envelop occur at same time
  2. Capsid assembly occurs in cytoplasm then virus buds from plasma membrane (envelope)
  3. Capsid assembly occurs in cytoplasm & envelope comes from ER, then exported via exocytosis
    * Glycoproteisn are transported to location of envelop assembly
    * Viral capsids are developed elsewhere
122
Q

What happens with viral capsid development in enveloped virions during assembly?

A

Nucleic acids are packaged into the capsid & transported in endosomal vesicles to envelop

  • In plasma membrane, induce viral budding
  • In ER, enveloped virion is transported to plasma membrane via transport vesicles
123
Q

What is difficult to humans about foodborne enteric viruses?

A

Difficult to detect
Difficult to recover from contaminated food
- Most are not culturable
Excreted in high numbers

124
Q

What are advantages to humans of foodborne enteric viruses compared to bacteria?

A

Do not multiply in food systems (or anywhere outside the human body)
Some die off rapidly during food storage & preservation
Pastuerization, heat, or irradiation can kill them

125
Q

What are important foodborne viruses?

A

Polio virus
Hepatitis A virus
Norovirus (NoV)
Rota virus

126
Q

Where is poliovirus still endemic?

A

Afghanistan
Nigeria
Pakistan

127
Q

How can poliovirus be transmitted?

A

Dairy
Fecal oral route
- Multiplies in intestine

128
Q

How do you deactivate the poliovirus?

A

Pasteurization above 70C for 30 seconds

129
Q

What is a vaccine of the poliovirus?

A

Inactivated poliovirus vaccine (IPV)

Oral poliovirus vaccine (OPV)

130
Q

What are the statistics of poliovirus?

A

Affects children under 5 mostly
1 in 200 infections lead to irreversible paralysis
- 5-10% of the paralyzed die when breathing muscles are paralyzed
Since 1988, has decreased by 99% (from 350,000 to 74)

131
Q

How does the poliovirus infect?

A 
Multiplies in the intestine
Initial symptoms:
- Fever
- Fatigue
- Headache
- Vomiting
- Stiffness of neck
- Pain in limbs
Invades nervous system
- Causes total paralysis in hours
132
Q

What are the characteristics of the poliovirus?

A 
RNA genome (Group IV: + sense RNA)
Non-enveloped
Protein capsid
Genome = 7500 bp
Order: Picornavirales
Family: Picornaviridae
Species: Enterovirus C
133
Q

What are the serotypes of poliovirus?

A

Each have different capsid proteins (which define cellular receptor specifiticyt & virus antigenicity)
All 3 are extremely infectious
PV1: most common, localized to Pakistan & Afghanistan
PV2: Likely eradicated, last seen in India
PV3: Likely eradicated in 2012, last seen in Nigeria & Pakistan

134
Q

What is the genome of the poliovirus?

A

+ssRNA encodes a single polyprotein
5’ non-translated region (NTR) has two domains: cloverleaf & internal ribosome entry site (IRES) that are covalently linked to viral protein VPg
- Cloverleaf regulates replication & initiates translation
- IRES mediates translation
3’NTR is poly-adenlyated
Protein 1 (P1): structural; P2 & P3: non-structural
- All are released from polypeptide chain by proteolytic processing mediated by virally-encoded proteinases
Polyprotein encodes eleven mature viral prteins

135
Q

What is the lifecycle of the poliovirus?

A

Infection begins when poliovirion binds to cell surface receptor
Uncoating occurs by receptor-dependent destabilization of the virus capsid
Viral protein VPg is cleaved by cellular phosphodiesterase
IRES-mediated mechanisms translates viral RNA
mRNA is translated by a long polypeptide
- Proteolytic processing of polyprotein creates mature proteins
+RNA produces dsRNA (the replicative form) & -RNA produces replicative intermediate
- New +RNA molecules are template or associated with capsid precursors to induce cleavage of VP0
Lysis of cells

136
Q

How is the poliovirus assembled?

A

P1 precursor protein is cleaved to yield VP1, VP3, & VP0
The viral proteins are assembled into 5S monomers then 14S pentamers
12 of the pentamers are associated with genomic RNA being transcribed to assemble into immature 150S provision
VP0 is cleaved into VP2 & VP4 resulting in mature virions

137
Q

What are the symptoms of HAV?

A 
Last 8 weeks
90% of children in developing countries have HAV before 10
- Usually asymptomatic
There are ~1.4million symptomatic cases annually w/ 100,000 annual deaths
May cause:
- Nausea
- Vomiting
- Diarrhea
- Jaundice
- Fever
- Abdominal pain
Effect liver
- Acute liver failure can occur in elderly patients
138
Q

How is HAV transmitted?

A

Fecal oral route mostly

Undercooked seafood is vector

139
Q

What is the treatment/vaccine for HAV?

A

Effective agaisnt transmission & recommended for anyone travelling to areas with lower sanitation standards
- After one infection or vaccine, one is immune for life
There is no specific treatment
- Rest
- Medications for nausea & diarrhea
- Liver transplant for liver failure

140
Q

What are the characteristics of the Hepative A Virus?

A 
RNA genome (Group IV: +RNA)
Non-enveloped virus
Protein capsid
Genome = 7500 bp long
Order: Picornavirales
Family: Picornaviridae
Species: Hepatovirus A
141
Q

What are the serotypes/genotypes of HAV?

A

One serotypes
Seven genotypes
- Four human I-III, VII (Six subtypes (IA, IB, IIA, IIB, IIIA, IIIB))
- Three primate IV-VI (exclude VII)

142
Q

What is the HAV genome?

A

Encodes a single polyprotein
- The capsid proteins are coded for at N-terminal
- Remainder of polyprotein encodes a series of nonstructural proteins required for HAV RNA replication
VPg is covalently linked to 5” end
- Serves as protein primer for RNA synthesis

143
Q

Where does viral replication of HAV occur?

A

Produced in the liver

Reaches intestines by secretion from infected hepatocytes via the biliary system

144
Q

What is the lifecycle of HAV?

A

Enters hepatocyte via interaction w/ cellular recpetor
Uncoated releases the +RNA into the cell
Internal ribosome entry site in the 5” NTR mediates cap-independent translation of viral polyprotein
Polyprotein undergoes co-/post-translational proteolytic processing via viral protease
Nonstructural proteins assemble into membrane-bound RNA replicate, bind the 3” end & commence synthesis of -RNA copy
- -RNA used as template for synthesis of new +RNA copies
Some of the new +RNA is recycled for further RNA synthesis or translation
Rest of the +RNA are packaged into viral particles formed by assembly of the structural proteins, followed by cleavage of VP1-2A & maturation cleavage of VP4/VP2
Assembled HAV particles are secreted by the cell across the apical membrane

145
Q

What is the viral load of HAV?

A

Fecal shedding reaches max just before hepatocellular injury where the individual is most infectious
- Causes increased levels of serum alanine aminotransferase (ALT) activity
Accompanied by extended viremia, with slightly lower fecal shedding magnitude
At end of infection, anti-HAV IgM & IgG antibodies are produced
- IgG is lasting immunity
- IgM used to diagnose

146
Q

How is HAV detected in food?

A

Food is collected & suspended in glycine buffer
- Mixed for 15 mins at room temp
- Virus becomes suspended in the buffer
Supernatant from this mixture is centrifused at 170,000g for 60 minutes
- Virus collects in a pellet at bottom of centrifuge tube
- Supernantant can be discarded
The pellet is resuspended in a buffer
- Added to a GIAshredder that breaks the viral capsid & releases RNA
- RNA is precipitated & purified, then used in an RT-qPCR reaction to detect it

147
Q

What is the number of outbreaks of Norovirus/year?

A

300-400 in Canada

More common in fall & winter months

148
Q

How is NoV transmitted?

A

Group setting where people are in close contact (schools, hospitals, childcare facilities, cruise ships…)
Found in stool or vomit
- Always spread via fecal oral route
Infected by:
- Direct contact
- Touching surfaces or objected contaminated
- Eating or drinking contaminated food/water (shellfish may be contaminated by sewage in water
Those infected can be contagious from moment they feel sick to 3 days after recovery
- Sometimes contagious 2 weeks after recovery

149
Q

How is NoV treated?

A

Nothing specific
Rest
Medications for nausea & diarrhea

150
Q

What are the symptoms of NoV?

A 
Occurs withing 24-48 hrs
- Start within 12 earliest
Main symptoms:
- Diarrhea
- Vomiting (usually in children)
- Nausea
- Stomach cramps
Less common symptoms:
- Fever
- Headache
- Chills
- Muscle aches
- Fatigue
Last 3 days
151
Q

What are the characteristics of the Norovirus?

A 
RNA genome (group IV: +RNA)
Non-enveloped
Genome = 7500 bp long
Order: unassigned
Family: Caliciviridae
Genus: Norovirus
Species: Norwalk virus
152
Q

What are the genogroups of NoV?

A 
Five: GI-GV
- GII: most prevalent human genogroup & contains 19 genotypes
- GI, II, IV: infect humans
- GIII: infects bovine
- GV: infects mice
Futher divided into different genotypes
153
Q

What is the genome of NoV?

A

5’ end of Open Reading Fram 1 (ORF1) is a single nonstructural polyprotein
- Cleaved into six mature products by virally encoded protease (Pro)
* other nonstructural proteins = NS1,2,3 (NTPase),4 (p22),5 (VPg),7 (RdRp)
- NoV genomes are covalently linked to VPg & polyadenlyated
ORF2 encodes capsid protein VP1
- Divided into shell (S) & protruding domains (P)
- P domain divided into P1 & P2
ORF3 encodes minor structural protein VP2
ORF4 encodes virulence factor 1 (VF1)

154
Q

What is the life cycle of NoV?

A

Attaches to cell surface using various carbohydrate attachment factors
- Need to bind an unidentified protein receptor to mediate entry
Entry & uncoating occurs with unknown pathways
Genome is translated using VPg
ORF1 polyprotein & co-/post-translationally cleaved via viral protease NS6
Replication complex formed by cellular membrane moving to perinuclear region via NS1,2,4
Replication occurs w/ -RNA intermediate using de novo & VPg- dependent mechanisms
- RNA generated by RdRp
Replicated genomes trnalsted or packaged into VP1
Assembly & exiting occurs (maybe w/ apoptosis)

155
Q

How is NoV cultured?

A

Inability to culture was major barrier in research & development of vaccines
Discovered it can be cultured in human bile added to enterocyte cell culture

156
Q

How is NoV detected?

A

Old method:
- Samples suspended in buffer & NoV washed into it
- PCR & RT-qPCR are used to detect presence
New method:
- WGS (expensive)
- determines transmission
- FIlter feces, remove DNA, Collect RNA w/ poly-A-tail, reverse transcribe into cDNA, sequence, check meta-genomic data

157
Q

How is rotavirus transmitted?

A

Fecal-oral route
Most every child gets it before 5
- Immunity develops w/ each infection so adults are rarely affected
1 in 5 cases of gastroenteritis is caused by rotavirus
- 37% of child deaths from diarrhea (215,000 worldwide) occurred in 2013

158
Q

How is rotavirus treated?

A

Oral rehydration
Vaccination
- US & Canada require
- Canada says all children should be vaccinated between 6 weeks & 8 months

159
Q

What are the symptoms of rotavirus?

A 
Appear after 48 hrs
Nausea
Vomiting (begin here)
Watery diarrhea (4-8 days of this)
- Dehydration is common (more common than bacterial pathogens that cause diarrhea): most common cause of death by rotavirus
Fever
160
Q

What are the characteristics of Rotavirus?

A 
RNA genome (Group III: dsRNA)
Non-enveloped virus
Genome: 18,550 bp long
Order: unknown
Family: Reoviridae
Genus: Rotavirus
161
Q

What is the genome of Rotavirus?

A

Segmetned linear dsRNA genome
11 segments that encode 12 viral proteins
Range from 667 to 3302 bp
Lack poly-A-tail
- Have 3/ consensus sequence that terminates translation
Genetic reassortment: individuals may be co-infected with two different rotaviruses at same time cause mixing of viruses

162
Q

What is the structure of rotavirus?

A

VP7 glycoprotein embedded with VP4 spiked attachment protein on outside
Intermediate VP6 layer with thin VP2 core shell
Viral dsRNA line the VP2 shell
Viral polymerase complexes costing of a single subunit of the viral RdRp (VP1) & RNA capping enzyme (VP3) attached to inner surface fo VP2

163
Q

How is the rotavirus gene expressed?

A

Genome is never completely uncoated to prevent activation of antiviral state by cell in response of dsRNA

164
Q

How is rotavirus replicated?

A

Occurs in host-cell cytoplasm
VP4 attaches to host cell & mediates endocytosis of virus
Partially unocated in endosome then penetrates cytoplasm
Transprition done by viral polymerase inside double layered particles so dsRNA isn’t exposed to cytoplasm
+RNA is extruded into cytoplasm for template
Progeny cores are produced w/ replicate activity for transcription
- Coated with VP6 to form immature virions
Bud into ER & gain NSP4 & VP4
- Lose envelop & VP4 & VP7 rearrange to form outside of virus (mature triple-layered particles)
Released after cell death

165
Q

What are teh methods for the rotavirus knowing it has complete dsRNA?

A

Concerted model:
- 11 segments of dsRNA bound by VP1 & VP3
- Undergo assortment via gene-specific interactions among the RNA molecules
- VP2 shell then assembles around the complexes
Core-filling model:
- VP2 shell contains VP1 & VP3 attached to it without nucleic acids
- Each of the 11 dsRNA segments are then individually inserted into the core
- Complete packaging triggers core expansion & initiation of genome replication

166
Q

What are prions?

A

Infectious agents composed of a protein material that can fold multiple abstract ways
- One of these folds is transmissible to other prion proteins, leading to a disease
Prions with the prion protein (PrP) cause transmissible spongiform encephalopathies (TSEs)
- Fatal neurodegenerative diseases in humans & animals
Done by converting cellular prion protein PrPC into aggregation-prone PrPSc

167
Q

What is the definition of a prion isolate?

A

Biological material taht has been obtained through sampling of infected individuals

168
Q

What is the defintion of a prion strain?

A

the term corresponds to a defined prion population isolated from one specified animal

169
Q

What is the definition of a prion type?

A

More particularly to a combination fo biochemical parameters that are independent from the host
- Parameters mainly the size of the unglycosylated PrPSc fragment after proteinase K partial digestion

170
Q

What is transmissible spongiform encephalopathies (TSEs)?

A

Each disease shares the same characteristics:
- Long incubation periods (from years to decades)
- Illness of weeks to months w/ progression to death
- Accumulation in the brain & other tissues of fibrillar amyloid protein aggregates
- Pathologicla changes to the CNS
- Absence of an immune response
There are differences in pathogenesis, transmission, distribution

171
Q

What are the different strains of Transmissible Spongiform Encephalopathies (TSEs)?

A

Scrapie: affects sheep & goats
Chronic wasting disease: affects cervids
Transmissible mink encephalopathy: affects mink
Kuru: Only affects humans (confined to Papua New Guinea cannibals)
- Cannibalism stopped

172
Q

What is the history of Chronis Wasting Disease?

A

1969: first appeared in NA
1978: examined brains of deer showed TSE. Defined CWD

173
Q

What is the progression of CWD?

A

Prolonged incubation periods (2-4 years)
Not restricted to the brain (most PrPSc are)
- Found in extraneural tissues, body fluids, & excreta (urine, feces, saliva)
- Creates horizontal transmission (unique to CWD)
Most contagious TSE

174
Q

What are the driving forces of CWD transmission?

A

Most contagious prion disease
Presence in extraneural tissues
Prion persistanence for years

175
Q

What are the natural hosts of CWD?

A 
Elk
Mule deer
White-tailed deer
Moose
Reindeer
Experimental transmission (interspecies transmission doesn't occur naturally):
- Red deer
- Fallow deer
176
Q

How do cattle get CWD?

A

Intracerebrally

Not orally inoculated

177
Q

How is prion transmission of CWD most effective?

A 
Via the less physiological intracerebral route
Transmitted experimentally to:
- Goats
- Sheep
- Rodents
- Mink
- Ferrets
- Squirrel monkeys (non-human primates)
178
Q

How is CWD controlled?

A

Quarntine
Depopulation of CWD-affected
Persistant (difficult to control)
- Especially in free-ranging animals

179
Q

How is Bovine Spongiform Encephalopathy (BSE) transmitted?

A

Origin & natural routes are not understood
- Sporadic disease may be caused by genetic mutation
Occured mostly due to cows eating the nervous system of other cows
- Once infected once, epidemics occurs from feeding BSE-contaminated meat & bone meal to cattle

180
Q

How well can BSE survive?

A

Stable cuases unusual resistance to destruction
- Heating under pressure at 121C
- Exposure toe dry heat at 600C
- Immersion in .1N NaOH
- Immersion in .5% bleach
- Treated biosolids (persist for years in environment)
To inactivate, need:
- Immersion in 1N NaOH
- Dry heat at 1000C
Impossible to do & still have edible food

181
Q

What are the symptoms of BSE?

A 
Infected in first year of life, incubate for 2-8 years
Degeneration of nervous system
- Changes in temperament
- Abnormalities in posture & movement
- Signs of apprehension
- Nervousness & aggression
- Incoordination
- Tremores
- Difficulty standing
Last 2 weeks to 6 months before death
182
Q

What is variant CJD (vCJD)?

A

1996: first recognized (10 years after BSE epidemic began)
- Incubation is 12-15 years
Humans became infected by infected beef
Only a few people were infected
- Due to small “packets” of low-level infectivity that were heterogeneously scattered through meat
- Adolescents were mostly afflicted (sporadic CJD occurs in humans 50-70)
Symptoms:
- Phchiatric disturbance (depression or anxiety)
- Complaints of sensory symptoms (limb pain)
Lasts 14 months
Occurs mostly in NA & Europe

183
Q

How can BSE be controlled?

A
  1. Feed bans: stop cannibilsm in feeding or stop feeding animals other meat
  2. Specified risk material (SRM) bans: highly-infectivity materials (bovine brain & spinal cord) be removed from food & feed chains & destroyed
  3. Regulation of rendering: tools for slaughtering required 20 min autoclave at 133C under 3 bars of pressure
184
Q

What are mycotoxins?

A

Fungal metabolites which cause disease in humans or domestic animals
Multiple mycotoxins can be produced from one species, but mycotoxins are specific to each species (may be a couple species)
Not acute usually, accumulate over time

185
Q

Types of mycotoxins:

A 
Aflatoxins
Ochratoxin A
Fumonisins
Deoxynivalenol
Zearalenone
186
Q

What are the naturally occuring aflatoxins?

A 
B1
B2
G1
G2
* Named based on fluorescence
Excreted by cows as M1 or M2
187
Q

What species produce aflatoxins?

A

Aspergillus flavus
- 40% of strains produce toxin
- Add non-toxic strains to fields to prevent toxic growth (biocontrol)
Aspergillus parasiticus

188
Q

What are the growth factors/control factors of aflatoxins?

A 
A. flavus temp = 10-48C
Aw = depends on temperature
pH = 2.1-11.2
Pasteurization kills cells
- Dry roasting can kill 80% of toxin
- Alkali process to make peanut oil removes 100%
189
Q

Where is Aspergillus found (and by association aflatoxin)?

A 
A. flavus = tropical & warm temperatures
- Peanuts, corn, tree nuts
A. parasiticus = geographically limited
- Peanuts mostly
* Must infect peanuts while growing for high levels of aflatoxins
190
Q

What causes Aspergillus to grow?

A

High spore numbers
- Control via crop rotation & irrigation
Plant stress
High soil temperature

191
Q

What are the effects of aflatoxin?

A

Acute toxicity
Liver carcinogenicity
- If have HBV, 30x more likely to get liver cancer from aflatoxin
- Liver enzymes convert aflatoxin to epoxide
Liver cirrhosis
Immunosuppression
- Decreases phagocytic activity & response to vacciens
Growth retardation in children

192
Q

What does epoxide do the liver?

A

Comes from aflatoxin
Binds liver proteins; leads to liver failure
Binds DNA (precursor to liver cancer)

193
Q

How is aflatoxin controlled?

A

Allowed levels were 5ug/kg

  • Some exporting countries are allowed higher b/c they couldn’t meet the limit
  • Allowed levels is 15ug/kg
194
Q

What are the fungi responsible for ochratoxin A?

A 
Aspergilli that are ocher-colored (clay-colored)
- A. ochraceus
- A. westerdijkiae
- A. steynii
Aspergilli that are black
- A. carbonarius
- A. niger
Penicillium species: (affects people in NA)
- P. verrucosum
- P. nordicum
195
Q

What does ochratoxin A effect?

A

Nephrotoxin (kidneys)
Carcinogenic properties
Circulates in blood for 3 weeks (begins in intestine)

196
Q

What plants are ochratoxin A found?

A

Barley, wheat
Meat (pork)
Beer
Wine, coffee (produced by Aspergillus in tropical regions; low levels)
Cocoa, chocolate
Dried vine fruits
* not in tropical & subtropical regions as much

197
Q

What is a tolerable weekly intake of ochratoxin A?

A

100ng/kg of body weight

In cereals there is 8-17ng/kg usually

198
Q

How is ochratoxin A growth prevented?

A

Fungi are rare & transient, so control needs good management
- Rapid drying to prevent production (difficult)
In wine (due to A. carbonarius):
- Proper irrigation
- Regular pruning (for air flow)
- Use of crop cover
- Fungicide application
- Most removed when solid fractions are removed in winemaking process (ending product has 1-8% of original conc.)
In coffee:
- Sun-drying or mechanical dehydration
- Slow drying is bad
- Temp or roasting can remove 8-98%
In cereal:
- Milling for white flour removes 65% + 10% removed after baking

199
Q

Where are fumonisin toxins from?

A

Fusarium verticillioides
- Corn, sorghum (fusarium always present; toxins produced if plant is stressed)
Aspergillus niger
- Grapes, raisins, coffee

200
Q

What is especially bad about toxins from A. niger?

A

Can produce both fumonisins and ochratoxin A

If produce both at once, very bad

201
Q

What does fumonisins effect?

A 
Sphingolipid metabolism (inhiibts membrane proteins)
Equine leukoencephalomalacia
Pig heart failure
Rat liver cancer
Human esophageal cancer
202
Q

How to control fumonisins?

A

Good agricultural practices (minimize stress)
Breeding fumonisin resistant corn (experimental)
Rapid drying
Testing
Milled
- Wet milled (produces germ, fiber, starch)
- Dry milled (produces bran, germ, corn meal, flour)
- Fumonisins survive best in bran & germ (below 150C)
NIxtamalization
- Corn soaked & cooked in alkaline solution, removes most fumonisins

203
Q

Where is dexynivalenol found?

A

Fusarium graminearum (some)
- Corn (residue corn in fields can be risk for following year)
Fusarium culmorum (all)
- Small grains (wheat, barley)
* These fungi cause gibberella ear rot in corn & fusarium head blight in wheat

204
Q

What does deoxynivalenol effect?

A

Inhibits protein synthesis
Intestinal symptoms
Immunotoxicity

205
Q

What is the control of deoxynivalenol?

A 
USDA allows:
- 1mg/kg for humans
- 10mg/kg for bovine
Fungicides
Forecasting systems to warn producers of wet weather
Crop rotation
206
Q

Where is zearalenone toxin produced?

A

Fusarium graminearum
- Corn
Fulsarium culmorum
- Small grains (wheat, barley)

207
Q

What does zearalenone effect?

A

Agricultural animals (pigs, cattle, sheep)
In pigs:
- Vulvovaginitis (inflammation. of vagini)
- Vaginal & rectal prolapse (move from normal positions)
Estrogenic activity causing early puberty
Hepatotoxic (liver cells)
Hematotoxic (red blood cells)
Immunotoxic
Genotoxic (cancer?)

Food-Borne Pathogens (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions