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
Where is Vibrio sp. found?
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
26
What is the most common Vibrio spp. of infection in Canadian seafood?
V. parahaemolyticus Case study: from oysters after a temperature spike Colder waters = safer seafood
27
What are the general traits of V. parahaemolyticus infection?
``` 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 ```
28
What is the generation time of V. parahaemolyticus at 37C?
8-9 minutes | Contaminated food becoems highly colonized if temperature abused
29
What are the symptoms of V. parahaemolyticus?
- Appear within 4-30hrs - Include diarrhea, abdominal cramps, nausea, vomiting, fever - Subside in 3-5 days
30
What are the characteristics of V. parahaemolyticus?
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
31
What are the virulence factors of V. parahaemolyticus?
``` 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 ```
32
How does tdh & trh cause hemolysis or cytotoxicity?
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
33
How do T3SS1 effectors of V. parahaemolyticus cause cytotoxicity?
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
34
How do T3SS2 effectors cause enterotoxicity & cytotoxicity?
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
35
What are the main features of V. vulnificus in infection?
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
36
What are the two V. vulnificus syndromes?
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
37
What are the symptoms of V. vulnificus?
``` Appear from 7 hours to several days after exposure Include: - Fever - Chills - Nausea - Hypotension ```
38
What are the virulence factors of V. vulnificus?
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
39
What are the main features of V. cholerae infection?
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
40
What happens to V. cholerae in a VBNC state?
Not culturable on any media | If injected into rabbits, can cause ileal loop fluid accumulation
41
What does the CTX toxin of V. cholerae do?
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
42
What is interesting about the horizontal gene transfer of V parahaemolyticus?
Carries K & O antigen genes in two different clusters Can rapidly undergo HGT - Can switch serotypes mid-outbreak
43
What does V. cholerae do with DNA from the environment?
Readily takes up DNA from the environment | - Increases it's chance of taking up genes that increase its survival & virulence
44
What can V. cholerae get from V. parahaemolyticus?
T3SS2 | Would cause V. cholerae to be pathogenic, with symptoms similar to V. parahaemolyticus
45
How can Vibrio infection be prevented?
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)
46
What effect does depuration have on Vibrio?
It is the process that filter-feeding bivalves are purified by pumping through clean water Does not remove Vibrio - Does remove Salmonella & E. coli
47
What are the rare bacterial food-borne infections?
Brucellosis Streptococcus pyogenes Coxiella burnetii
48
What causes human Brucellosis?
``` Brucella abortus (cattle) Brucella suis (swine) Brucella melitensis (goats & sheep) Brucella canis (dogs) ```
49
What are the characteristics of Brucellosis?
Gram - Nonmotile Non-spore forming Aerobic Rods All species are pathogenic to humans & animals Most common in northern Africa, the Middle East, and Asia
50
Where is the bacterium of Brucellosis located in infected animals?
Uterus of pregnant animals | Mammary glands of lactating females
51
What is the correlation between milk & Brucellosis?
Consumption of raw milk can cause brucellosis Cells survive a long time in milk/milk products Pasteurization is effective against killing the cells
52
How can Brucellosis be transmitted?
Secreted in milk To people who work with meat From veterinary care Vaccination accident, laboratory accident (w/ cultures)
53
What are the symptoms of Brucellosis?
``` Appear 3-21 days after consumption Include: - Fever - Profuse sweats - Body aches - Aching joints - Chills - Weakness ```
54
What are the characteristics of Streptococcus pyogenes?
Gram + Has been associated w/ human pharyngitis Isolated from lactating cows w/ mastitis - Foodborne cause is consumption of raw milk
55
What are the symptoms of Streptococcus pyogenes?
``` Normally - Sore throat - Fever - Chills - Weakness Sometimes: - Nausea - Vomitng - Diarrhea ```
56
How is Streptococcus pyogenes prevented?
Milk pasteurization | People suffering from identified Streptococcus infection should not handle ready-to-eat foods
57
What does Coxiella burnetii cause?
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
58
What are the characteristics of Coxiella burnetii?
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
59
What antibiotics affect the cell wall?
Beta lactam antibiotics Glycopeptides Bacitracin
60
What antibiotics affect the DNA?
Fluoroquinolones Novobiocin Nitroimidazoles Nitrofurans
61
What antibiotics affect the ribosomes?
``` Tetracyclines Aminoglycosides Lincosamides Macrolides Streptogramins Chloramphenicol ```
62
What happens in the absence of beta-lactam antibiotics?
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
63
What do beta-lactams do to transpeptidase?
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
64
What are the natural peptidogylican subunits that are the substrate for transpeptidases?
D-Ala-D-ala
65
What is the structure of beta-lactam antibiotics?
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
66
What are the general resistances to Beta-Lactams?
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
67
What are the specific resistances ot Beta-Lactams?
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
68
How does antibiotic resistance effect humanity?
- Global health - Food security - Development/economics
69
How does antibiotic resistance affect people?
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
70
How many people will die by 2050 due to antimicrobial resistance (AMR)?
10 million (mostly in Asia & Africa) Will cause unknown financial impacts Worse than AIDS, Cancer, or COVID-19
71
Where are antibiotics used?
Human medicine Agricultural production Food processing
72
What is the history of ABR in agriculture?
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
73
What has happened to agriculture with the use of antibiotics?
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%
74
How does WHO combat AMR?
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
75
How does Canada combat AMR?
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
76
How does Canada categorize antibiotics?
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
77
What is Canada's approach to stewardship against AMR?
- 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
78
What antibiotics are not used in humans but used for other species?
Category I antibiotic, Ceftiofur - Used in dairy cattle before infections Category II & IV antibiotics - Used in poultry feed
79
What are cross-reactions in antibiotics?
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
80
How does Canada use Surveillance against AMR?
2014, ceftiofur was banned in chicken hatchlings | - Response to growing detection of Salmonella & E. coli resistance
81
What are ways to replace antibiotics?
``` Improved hygiene Vaccinations Bacteriophages Probiotics Antibotic derivatives ```
82
What are the key characteristics for spore forming toxico-infection bacteria?
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
83
What are the key characteristics of gram-negative toxico-infection bacteria?
Live cells can be ingested in moderate numbers Cells rapidly multiply in the digestive tract Many cells die, releasing toxins
84
What is true of all foodborne toxico-infections?
All toxins cause gastroenterititis symptoms
85
What are the names of toxico-infection bacteria?
- Clostridium perfringens - Bacillus cereus Maybe if large number of cells are ingested: - Vibrio cholerae - enterotoxigenic E. coli
86
What are the general characteristics of Clostridium perfringens?
``` 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
How does heat affect Clostridium perfringens?
Pasteurization kills vegetative cells Spores are heat resistant (can survive boiling for several hours) Grow 10-52C - Grow optimally at 45C
88
What does Clostridium perfringens not synthesizing amino acids mean?
Grow more on high-protein foods | - Cooked meat products
89
What are the most important food factors contributing to C. perfringens outbreak?
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
What are the main foods involved in C. perfrignens outbreaks?
``` Beef (26% of outbreaks) Mexican food (12%) Turkey (10%) Chicken (5%) * total number of outbreaks = 12,234 ```
91
Where can vegetative cells of C. perfringens be found in the environment?
Soil Dust Intestines of food-producing animals, animals, & birds Sewage
92
What are the symptoms of C. perfringens?
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
What are the types of toxins of C. perfringens?
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
What is the virulence potential of C. perfringens based on?
The ability to produce a combination of the 15 different toxins & several extracellular hydrolytic enzymes (exoenzymes)
95
What do C. perfringens toxins do?
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
What is Clostridium perfringens Enterotoxin (CPE)?
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
What does Clostridium perfringens Enterotoxin (CPE) do?
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
How can C. perfringens be prevented?
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
What are the general characterstics of Bacillus cereus?
``` 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
How can B. cereus get to cow's udders?
Frequently isoalted from soil & growing plants | From grass to udders to raw milk
101
What are the heat problems of B. cereus?
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
What is the harm of B. cereus in milk on the market?
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
What are the toxins of B. cereus?
Emetic (vomit-inducing) toxin (cyclic peptide) Diarrheal enterotoxin (protein) * most strains only produce one, a few can produce both
104
What are the characterstics of emetic toxin of Bc?
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
What are the characterstics of diarrheal enterotoxin of BC?
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
What are the causes of B. cereus?
Improper holding temperature Contaminated equipment Inadequate cooking Poor personal hygiene
107
How to prevent B. cereus?
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
What are the differences between B. antracis, B. thuringiensis, & B. cereus on human health?
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
What is the same between all species of Bacillus?
All have enterotoxins (except maybe B. anthracis)
110
What do viruses consist of ?
A small segment of nucleic acid encased in a protein shell | Can have more than this (envelope)
111
What is the Baltimore classification scheme of classification of viruses?
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
What is the difference between enveloped & non-enveloped viruses?
``` 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
What aids viruses in assembly?
Being highly symmetrical
114
How do viruses enter cells & uncoat?
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
How do viruses replicate?
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
What is the difference between RNA-dependent RNA polyermase & DNA-dependent DNA polymerase?
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
How are macromolecules of viruses assembled?
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
How are proteins of viruses assembled?
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
What is the difference in assembly location between enveloped & nonenveloped viruses?
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
How are non-enveloped viruses assembled?
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
What are the different pathways for enveloped virus assembly?
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
What happens with viral capsid development in enveloped virions during assembly?
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
What is difficult to humans about foodborne enteric viruses?
Difficult to detect Difficult to recover from contaminated food - Most are not culturable Excreted in high numbers
124
What are advantages to humans of foodborne enteric viruses compared to bacteria?
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
What are important foodborne viruses?
Polio virus Hepatitis A virus Norovirus (NoV) Rota virus
126
Where is poliovirus still endemic?
Afghanistan Nigeria Pakistan
127
How can poliovirus be transmitted?
Dairy Fecal oral route - Multiplies in intestine
128
How do you deactivate the poliovirus?
Pasteurization above 70C for 30 seconds
129
What is a vaccine of the poliovirus?
Inactivated poliovirus vaccine (IPV) | Oral poliovirus vaccine (OPV)
130
What are the statistics of poliovirus?
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
How does the poliovirus infect?
``` 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
What are the characteristics of the poliovirus?
``` RNA genome (Group IV: + sense RNA) Non-enveloped Protein capsid Genome = 7500 bp Order: Picornavirales Family: Picornaviridae Species: Enterovirus C ```
133
What are the serotypes of poliovirus?
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
What is the genome of the poliovirus?
+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
What is the lifecycle of the poliovirus?
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
How is the poliovirus assembled?
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
What are the symptoms of HAV?
``` 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
How is HAV transmitted?
Fecal oral route mostly | Undercooked seafood is vector
139
What is the treatment/vaccine for HAV?
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
What are the characteristics of the Hepative A Virus?
``` RNA genome (Group IV: +RNA) Non-enveloped virus Protein capsid Genome = 7500 bp long Order: Picornavirales Family: Picornaviridae Species: Hepatovirus A ```
141
What are the serotypes/genotypes of HAV?
One serotypes Seven genotypes - Four human I-III, VII (Six subtypes (IA, IB, IIA, IIB, IIIA, IIIB)) - Three primate IV-VI (exclude VII)
142
What is the HAV genome?
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
Where does viral replication of HAV occur?
Produced in the liver | Reaches intestines by secretion from infected hepatocytes via the biliary system
144
What is the lifecycle of HAV?
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
What is the viral load of HAV?
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
How is HAV detected in food?
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
What is the number of outbreaks of Norovirus/year?
300-400 in Canada | More common in fall & winter months
148
How is NoV transmitted?
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
How is NoV treated?
Nothing specific Rest Medications for nausea & diarrhea
150
What are the symptoms of NoV?
``` 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
What are the characteristics of the Norovirus?
``` RNA genome (group IV: +RNA) Non-enveloped Genome = 7500 bp long Order: unassigned Family: Caliciviridae Genus: Norovirus Species: Norwalk virus ```
152
What are the genogroups of NoV?
``` 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
What is the genome of NoV?
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
What is the life cycle of NoV?
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
How is NoV cultured?
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
How is NoV detected?
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
How is rotavirus transmitted?
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
How is rotavirus treated?
Oral rehydration Vaccination - US & Canada require - Canada says all children should be vaccinated between 6 weeks & 8 months
159
What are the symptoms of rotavirus?
``` 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
What are the characteristics of Rotavirus?
``` RNA genome (Group III: dsRNA) Non-enveloped virus Genome: 18,550 bp long Order: unknown Family: Reoviridae Genus: Rotavirus ```
161
What is the genome of Rotavirus?
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
What is the structure of rotavirus?
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
How is the rotavirus gene expressed?
Genome is never completely uncoated to prevent activation of antiviral state by cell in response of dsRNA
164
How is rotavirus replicated?
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
What are teh methods for the rotavirus knowing it has complete dsRNA?
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
What are prions?
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
What is the definition of a prion isolate?
Biological material taht has been obtained through sampling of infected individuals
168
What is the defintion of a prion strain?
the term corresponds to a defined prion population isolated from one specified animal
169
What is the definition of a prion type?
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
What is transmissible spongiform encephalopathies (TSEs)?
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
What are the different strains of Transmissible Spongiform Encephalopathies (TSEs)?
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
What is the history of Chronis Wasting Disease?
1969: first appeared in NA 1978: examined brains of deer showed TSE. Defined CWD
173
What is the progression of CWD?
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
What are the driving forces of CWD transmission?
Most contagious prion disease Presence in extraneural tissues Prion persistanence for years
175
What are the natural hosts of CWD?
``` Elk Mule deer White-tailed deer Moose Reindeer Experimental transmission (interspecies transmission doesn't occur naturally): - Red deer - Fallow deer ```
176
How do cattle get CWD?
Intracerebrally | Not orally inoculated
177
How is prion transmission of CWD most effective?
``` Via the less physiological intracerebral route Transmitted experimentally to: - Goats - Sheep - Rodents - Mink - Ferrets - Squirrel monkeys (non-human primates) ```
178
How is CWD controlled?
Quarntine Depopulation of CWD-affected Persistant (difficult to control) - Especially in free-ranging animals
179
How is Bovine Spongiform Encephalopathy (BSE) transmitted?
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
How well can BSE survive?
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
What are the symptoms of BSE?
``` 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
What is variant CJD (vCJD)?
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
How can BSE be controlled?
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
What are mycotoxins?
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
Types of mycotoxins:
``` Aflatoxins Ochratoxin A Fumonisins Deoxynivalenol Zearalenone ```
186
What are the naturally occuring aflatoxins?
``` B1 B2 G1 G2 * Named based on fluorescence Excreted by cows as M1 or M2 ```
187
What species produce aflatoxins?
Aspergillus flavus - 40% of strains produce toxin - Add non-toxic strains to fields to prevent toxic growth (biocontrol) Aspergillus parasiticus
188
What are the growth factors/control factors of aflatoxins?
``` 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
Where is Aspergillus found (and by association aflatoxin)?
``` 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
What causes Aspergillus to grow?
High spore numbers - Control via crop rotation & irrigation Plant stress High soil temperature
191
What are the effects of aflatoxin?
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
What does epoxide do the liver?
Comes from aflatoxin Binds liver proteins; leads to liver failure Binds DNA (precursor to liver cancer)
193
How is aflatoxin controlled?
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
What are the fungi responsible for ochratoxin 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
What does ochratoxin A effect?
Nephrotoxin (kidneys) Carcinogenic properties Circulates in blood for 3 weeks (begins in intestine)
196
What plants are ochratoxin A found?
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
What is a tolerable weekly intake of ochratoxin A?
100ng/kg of body weight | In cereals there is 8-17ng/kg usually
198
How is ochratoxin A growth prevented?
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
Where are fumonisin toxins from?
Fusarium verticillioides - Corn, sorghum (fusarium always present; toxins produced if plant is stressed) Aspergillus niger - Grapes, raisins, coffee
200
What is especially bad about toxins from A. niger?
Can produce both fumonisins and ochratoxin A | If produce both at once, very bad
201
What does fumonisins effect?
``` Sphingolipid metabolism (inhiibts membrane proteins) Equine leukoencephalomalacia Pig heart failure Rat liver cancer Human esophageal cancer ```
202
How to control fumonisins?
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
Where is dexynivalenol found?
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
What does deoxynivalenol effect?
Inhibits protein synthesis Intestinal symptoms Immunotoxicity
205
What is the control of deoxynivalenol?
``` USDA allows: - 1mg/kg for humans - 10mg/kg for bovine Fungicides Forecasting systems to warn producers of wet weather Crop rotation ```
206
Where is zearalenone toxin produced?
Fusarium graminearum - Corn Fulsarium culmorum - Small grains (wheat, barley)
207
What does zearalenone effect?
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