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Bacteriology/ Mycology > Enterococcus, Listeria, Erysipelothryx > Flashcards

Enterococcus, Listeria, Erysipelothryx Flashcards

1
Q

Enterococcus used to be ________ until 1984, when the advent of sequencing such as ____ _____ gene)

A

Streptococcus, 16S rRNA

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2
Q

What kind of bacteria is enterococcus? How does it occur? Is it catalase positive or negative? What is it lancefield group? Does it have a capsule? Is it motile?

A
  • Gram-positive
    • Occur in pairs or short chains like Streptococcus
    • Catalase negative like Streptococcus
    • Lancefield Group D antigen (antibody based serogrouping)
    • Facultative anaerobe
    • Non-capsulate (some species)
    • All non-motile except some species
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3
Q

What media types are used for growing Enterococcus?

A
  1. Blood agar
  2. Media containing up to 40% bile esculin
  3. MacConkey agar
  4. Media containing high salt ( 6.5-10%)
  5. Kenner-fecal agar media
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4
Q

How does enterococcus present on blood agar? Is it hemalytic?

A

Non-hemolytic = gamma

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5
Q

Enterococcus:
Media containing up to 40% bile esculin produces?

A

dark colonies (NB: Streptococcus does not grow on bile)

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6
Q

Enterococcus:
What can you see on MacConkey agar ?

A

ferment lactose, producing small dark-red magenta colonies

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7
Q

Enterococcus:
What do you see on media containing high salt = ?

A

Grow on media containing high salt (6.5-10%) concentration

(unlike Streptococcus)

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8
Q

Enterococcus
What is Kenner-fecal agar media?

A

Selective media for enterococcus

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9
Q

What is this media?

A

Bile Esculin Azide Agar

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10
Q

Enterococcus is a highly ______ organism in ____ even if they
are __-____ forming bacteria

A

resistant, nature, non-spore

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11
Q

Enterococcus:

What conditions are they able to grow in?

A

hypotonic, hypertonic, acidic, or alkaline conditions

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12
Q

Enterococcus:

What factors are they able to withstand?

A

detergents, oxidative stress, desiccation, heavy metals

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13
Q

Enterococcus

What are they resistant to?

A

multiple antimicrobials = member of ESKAPE

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14
Q

Enterococcus:

What are they normal commensals of?

A

Mammals, birds, reptiles, fishes, insects.

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15
Q

Enterococcus: What parts of the body do they live in?

A

Colon and bile tract, Oral cavity, Urethra, Vulva/vagina in humans and animals

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16
Q

Enterococci is the leading ____ and ____ microbiota of animals and humans. Thus, millions of them are _______ with feces daily to the environment

A
  • gut,
  • fecal,
  • excreted
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17
Q

What are the body structures of Enterococci used for adhesion, colonization, and biofilm formation?

A
  1. collagen binding proteins
  2. endocarditis specific antigens (pili)
  3. surface proteins of enterococci
  4. Enterococcal polysaccharide on surface = cell wall carbohydrates serve as a capsular
  5. Aggregation substance = binds to host cells or bacteria-to-bacteria (conjugation)
    - Trafficker of AMR genes by transferring them horizontally to enterococci spp.
    - Acquired broad-spectrum antimicrobial resistance (AMR).
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18
Q

What enzymes do Enterococci use?

A

Gelatinase, Hyaluronidase

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19
Q

What does Gelatinase digests ?

A

Gelatine, elastin, collagen, haemglobin, and other bioactive peptides.

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20
Q

Enterococcus:

What does Hyaluronidase do?

A
  1. Hyaluronidase = destroy blood vessel and mucopolysaccharides of the connective tissue/cartilage
    for spreading of bacteria to the deeper tissue
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21
Q

What toxins or secreted substances do Enterococci use?

A
  1. . Cytolysin/hemolysin (also called bacteriocin or enterocin)
  2. Sex pheromones
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22
Q

Whar is cytolysin/hemolysin? What does it do?

A
  1. Cytolysin/hemolysin (also called bacteriocin or enterocin) =
  2. kills by pore-forming on cell envelope of red and white blood cells 2. kills Gram-negative bacteria competitors = to defend its territory that contributes to niche control
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23
Q

Enterococcus:

What are sex pheromones? What do they do?

A
  1. Sex pheromone = stimulate expression of aggregation substances which results in conjugation;
    thus, it is a means of acquiring and accumulating plasmids
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24
Q

E. faecalis, E. faecium, E. durans occupy which host animals?

A

Multi-host species

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25
Q

E. faecalis, E. faecium, E. durans occupy which habitats?

A

intestinal tract, soil, water, food/feed

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26
Q

E. faecalis, E. faecium, E. durans cause which diseases?

A
  1. Septicemia in poultry
  2. mastitis in cows
  3. endocarditis in cattle & lambs
  4. urinary tract infection in pets
  5. chronic liver diseases (humans)
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27
Q

Overall, 65-95% of the diseases are by __________?

A

E. faecalis

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28
Q
A
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29
Q

What diseases are caused by enterococcus spp. in poultry?

A
  1. E. faecalis affects birds of all ages, but
    exceptionally severe in embryos and young chicks
  2. E. faecalis usually colonizes the intestines first followed by E. faecium, and then E.cecorum
  3. E. cecorum has emerged as a major cause of
    skeletal disease in adult broiler chickens causing
    ✓ osteomyelitis, ✓ femoral head necrosis,
    ✓ Spondylitis (i.e. back & neck pain due to
    inflammation of the vertebrate joints) ✓ arthritis.
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30
Q

What is seen in this image?

A

Spondylitis in broiler chickens (showing it in humans)

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31
Q

Why are enterococci an important zoonotic bacterium of humans?

A

Currently, enterococci rank among the top 3rd leading cause of nosocomial
infection in humans

• In humans in the USA, Enterococcus spp. contributes to:
1. 20% of endocarditis, endodontic and 2. 10-16% urinary infection
• The majority of enterococcal infections are caused by E. faecalis or E. faecium
• E. faecalis accounts for the majority (65-95%) of nosocomial Enterococci infections in humans. • E. faecium constitutes the majority of vancomycin and ampicillin resistant isolates of enterococci
• To a significantly lesser extent, infections are caused by other Enterococci
species such as E. durans, E. avium, E. gallinarum, or E. casseliflavus

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32
Q

In humans in the USA, what do Enterococcus spp. contributes to?

A

In humans in the USA, Enterococcus spp. contributes to:
1. 20% of endocarditis, endodontic and 2. 10-16% urinary infection

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33
Q

What are the majority of enterococcal infections caused by?

A
  • The majority of enterococcal infections are caused by E. faecalis or E. faecium
  • E. faecalis accounts for the majority (65-95%) of nosocomial Enterococci infections in humans.

• E. faecium constitutes the majority of vancomycin and ampicillin resistant isolates of enterococci

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34
Q

To a significantly lesser extent, infections are caused by other Enterococci species such as ?

A

E. durans, E. avium, E. gallinarum, or E. casseliflavus

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35
Q

What are the entry and exit transmission routes of Enterococci?

A 
Entry = oral route: ingestion
Exit = feces from gut (their ecological niche) and other body parts via urine or milk
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36
Q

How much enterococci is excreted in feces daily?

A

➢ Excreted everyday in high concentrations in feces, usually
between 104 and 106 bacteria per gram wet weight

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37
Q

What is enterococcus usually used as an indicator of?

A

• Thus, routinely used as indicator of:
1. fecal contamination and hygienic quality of food, milk, meat,
2. water and environmental contamination/pollution by fecal
materials

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38
Q

What samples are typically taken for isolation and identification for enterococcus?

A
  • feces
  • urine
  • milk
  • blood
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39
Q

Treatment of Enterococci is challenging due to its _____

A

MDR

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40
Q

Relative to the Streptococci, Enterococci are naturally _____
to many commonly used antimicrobial agents such as _____ ______

A

resistant, beta-lactams

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41
Q

Enterococci generously give their AMR genes (_____) to other bacteria species by ______ (_____ _____)

A

plasmid, conjugation, horizontal transfer

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42
Q

MDR is more common in what species of enterococcus?

A

E. faecium, E. faecalis

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43
Q

How do you treat cases of E. faecalis infection?

A

Beta-lactamase

✓ Penicillin
✓ Ampicillin

✓ amoxicillin

Aminoglycosides

✓ Gentamycin
✓ Streptomycin

Their is resistance with vancomycin.

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44
Q

How do you treat cases of E. faecium infection?

A
  • vancomycin.

Resistant to beta lactamases and aminoglycosides.

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45
Q

How do you treat cases of enterococcus that are vancomycin resistant infections? What is the drawback to these infections?

A

These antimicrobials are expensive

  • Linezolid
  • Daptomycin
  • Tigecycline
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46
Q
A
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47
Q

How do you control cases of Enterococcus infection?

A
  1. effective waste treatment of feces/manure and hygiene
  2. Water sanitation to reduce the incidence.
  3. Ensuring proper cleaning and disinfection of the facilities can reduce
    environmental reservoirs of the bacteria.
  4. Preventing immunosuppressive diseases and conditions, because
    enterococcosis often occurs secondary to another disease.
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48
Q

What is the most clinically important strain of listeria?

A

Listeria monocytogenes

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49
Q

What is Listeria ivanovii ?

A
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50
Q

What is the morphology and characteristics of listeria ?( shape, type of bacteria, spore forming? catalase? motility? Hemolytic? growth conditions?)

A

• Gram positive

  • Rod/bacilli
  • Facultative anaerobe
  • Non-spore forming
  • Catalase positive
  • Intracellular pathogen of animals and humans
  • Has flagella for motility and invasion
  • Beta-hemolytic on blood agar
  • Resistant to high salt (7-12%) in the inside host cell
    • Grow at cold (4°C) temperature
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51
Q

Listeria:

What is seen in this image?

A

Tumbling motility or “umbrella” shaped colony growth at
20-28C in a semisold motility media (because of its 1-5
flagella)

actin jet motility inside host cell

Umbrella-shaped subsurface listeria colony growth in semi-solid
motility media.

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52
Q

What are the diverse serotypes of l. monocytogenes? What are they based on?

A

• Has 14 serotypes based on its somatic (O) and flagella (H) antigens
• Of these, 3 serotype are important (virulent) since they cause the
vast majority of clinical case
1.1/2a = the most frequently isolated from food

  1. 1/2b
  2. 4b = causes the majority of human epidemics
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53
Q

What are the two key issues for Isolation of Listeria on a culture media?

A
  1. It require enrichment media as it is fastidious bacteria
  2. It requires prolonged inubationtime for the recovery of stressed Listeria cells.
54
Q

How do you create an enriching media for Listeria?

A
  1. Mullen-Hinton agar with 5% sheep blood as enrichment
  2. Beta-hemolytic colonies on blood agar
  3. Ferments glucose, maltose, lactose …produces acid but no
    gas.
55
Q

How can you recover stressed Listeria cells?

A
  1. Incubation for weeks at 4°C on agar plates until the formation of visible colonies
  2. This method of isolation usually does not allow for the isolation of injured or weak Listeria cells
56
Q
A
57
Q

How can listeria adapt to changing conditions?

A

• Resistant to high salt (7-12%) in the media

• Survive and multiply on inanimate objects
• E.g. silage through the transition processes from one host to another
• adapt to changing temperature (-0.4-45°C),
pH (4.4-9.6)
✓ Can multiply at refrigerator Tm (4°C)

58
Q

What is the habitat listeria lives in?

A

• Grow as saprophytes in soil and decaying vegetation in the environment
✓ Listeria is not commensal rather a real pathogen
✓ Isolated from swage, water, feed, food
• Abundant in cold temperate
✓ EU, North America
✓ Can grow at low temperatures < 4°C

59
Q

What are the host ranges of listeria?

A

• It has diverse host ranges and isolated from:
✓ Humans ✓ 42 species of mammals ✓ 22 species of birds ✓ fish ✓ insects
• It is more common in ruminants (mainly sheep)
✓ It causes seasonal outbreak in ruminants ✓ It is sporadic in pig and horse
• It is one of the well recognized foodborne pathogen in humans

60
Q

Listeria is most common in what species?

A

It is more common in ruminants (mainly sheep)
 It causes seasonal outbreak in ruminants
 It is sporadic in pig and horse

61
Q

_______ is a well recognized food borne pathogen in humans.

A

Listeria

62
Q

What are the points of entry and exit of Listeria?

A

• Entry: It enters the host by ingestion (oral)
1. Livestock: highly associated with feed/feeding of Silage with high iron content is a risk
factor for acquiring Listeria in ruminants
 As you increase iron concentration in silage, it promotes listeria contamination
2. Humans: Consumption of contaminated raw vegetables, meat, and milk
Exit: It exits from the host via feces, vaginal discharge (abortion), milk (mastitis)
 Detected in feces, milk, slurry, soil, feed, water, food

63
Q

What body structures does Listeria possess?

A
  1. 1-5 Flagella - for motility, adhesion & invasion
  2. Internalin (A, B & C) - for host cell adhesion & invasion
  3. invasion-associated protein (iap) - for host cell adhesion
    & invasion
64
Q

Listeria form _______.

A

Biofilms

65
Q

What cells does listeria multiply in ? What is the benefit of this?

A

Intracellular pathogen and multiply in tissue cells,
monocytes, & macrophages
✓ So hide from the immune patrolling of the host cells,
antibodies & antimicrobials

66
Q

What enzymes does Listeria use?

A
  1. super-oxide dismutase from listeria
  2. Phospholipase
67
Q

What does superoxide dismutase do for listeria?

A
  1. super-oxide dismutase from listeria
    ✓ protects listeria against free radicals from the host phagocyte cells
68
Q

What does phospholipase do for listeria?

A

Pore-forming lysis on endocytosis membrane of 2. Phospholipase
the host to free itself from lysosome (vacuoles) in the cytoplasm of the host cell

69
Q

What toxins or secreted substances does Listeria use?

A
  1. Beta-hemolysin
  2. listeriolysin O
  3. Bacteriocins (listeriolysin S) –
  4. Actin-polymerizing protein (actA)
70
Q

What does Beta hemolysin and listeriolysin O do that benefits listeria?

A

Pore-forming lysis on endocytosis membrane of the host to free itself from lysosome (vacuoles) in the cytoplasm of the host cell

71
Q

Bacteriocins (listeriolysin S) – ____ competing gut microbiota

A

kill

72
Q

What does actin polymerizing protien do for listeria?

A
  1. Actin-polymerizing protein (actA)
    ✓ instructs host cell for deposition of its actin- filaments on the end of Listeria

✓ Then Listeria uses the host actin filaments for propelling to the nearby cells.

✓ Such host actin-based zipper mechanism for propelling and transmission from cell to cell are used by:
✓ Listeria, Rickettsia, and Yersinia pseudotuberculosis

73
Q

Whar are the 4 known barrier of body systems that Listeria enters?

A
  1. Blood-brain barrier
  2. Placental barrier
  3. Intestinal barrier
  4. Cell membrane lipid bilayer barrier (intracellular).
74
Q
A
75
Q

Listeriosis is characterized by ?

A

Febrile gastroenteritis, septicemia/shock, placentitis, brain stem & cranial nerve dysfunction

76
Q
A
77
Q

The two major clinical manifestations of listeriosis are?

A

neural form vs. visceral form

78
Q

Neural form of listeriosis in silage-fed sheep shows?

A

 microabscess in the brain
 Ataxia and ‘circling disease’
 Unilateral facial paralysis
 head tilting to one-side
 ear dropping (one ear)
 tongue protrusion
 salivation

79
Q

Visceral form of listeriosis is linked with septicemia. What can you see in the visceral form?

A

Gastroenteritis
 Septicemia
 Liver and spleen damage
 Fetoplacental tropism (abortion)
 Myocarditis
 Osteomyelitis (bone + bone marrow)
 mastitis

80
Q

____________ is the third leading cause of death from food-borne illnesses in the United States, with approximately 260 deaths annually

A

L. monocytogenes

81
Q
A
82
Q

How do you treat Listeria infections?

A

Treatment : Listeria is a Gram-positive intracellular pathogen
 Ampicillin (200 mg/kg per day, IV)
 Chlortetracycline (10 mg/kg per day for 5 days, IV)
 Penicillin (44,000 U/kg per day for 7 days, IM)
 Trimethoprim-sulphmethoxazole (10 mg/kg per day, IV)

83
Q

How do you control Listeria outbreaks?

A

Its control is difficult as ubiquitously present
Little is known as to its risk factor (except silage) to control
 Control Listeria growth in the feed mainly in silage
Vaccination with live attenuated listeria vaccine (in Norway)
and commercial killed vaccine in some countries

84
Q

Which strain of Erysipelothrix is medically the most important?

A

Erysipelothrix rhusiopathiae

85
Q

What is the Morphology of Erysipelothrix rhusiopathiae?

A
  • Gram positive • Long filament (rod)…. (causes emboli)
  • Facultative anaerobe • Catalase negative • Oxidase negative • Non-motile • non-spore forming
86
Q

Erysipelothrix rhusiopathiae is shaped like ?
Causes?

A

Long filament (rod)…. (causes emboli)

87
Q

Erysipelothrix rhusiopathiae is Catalase ________

A

Negative

88
Q

Erysipelothrix rhusiopathiae is oxidase ________

A

negative

89
Q

Erysipelothrix rhusiopathiae is ____-motile

A

non

90
Q

Erysipelothrix rhusiopathiae is _____-spore forming.

A

non

91
Q
A

Erysipelothrix rhusiopathiae

92
Q

Erysipelothrix has ____ serotypes based on _____ antigen on the cell wall

A

28, peptidoglycan,

93
Q

The pig is susceptible to at least ___ serotypes of Erysipelothrix.

A

15

94
Q

Field cases of swine erysipelas are predominantly caused by three E.
rhusiopathiae serotypes:

A
  1. 1a
  2. 1b, or
  3. 2
95
Q

In swine, ?% of isolates are classified into serotype 1 or 2

A

75–80

96
Q

What culture media can be used for Erysipelothrix?

A
  • Blood agar (-hemolytic after 24h)
  • Heart infusion + supplemented with sodium azide & crystal violet
  • Nutrient broth + 1% glucose
  • Triple sugar iron
97
Q

How can you achieve nutrient rich media for Erysipelothrix?

A

It require enrichment media
1. Alpha-hemolytic colonies on blood agar
2. Heart infusion agar with sodium azide & crytal violet for plating pig
sample & incubated for 48h
3. Ferments glucose, lactose producing acid but not maltose and mannitol

98
Q

Hydrogen sulfide H2S is produced by 95% of strains of Erysipelothrix species on triple sugar iron (TSI) agar

A
99
Q

Erysipelothrix is unique & probably the only Gram-positive bacillus/rod bacteria that produce H2S (gas)

A
100
Q

What is seen in this image?

A

Triple Sugar Iron

101
Q

What is seen in this image?

A

Blood agar with alpha hemolysis after 24 hours in Erysipelothrix

102
Q

What habitat do Erysipelothrix occupy?

A

Habitat – Tonsils

  • lymphoid tissue of intestinal tracts in carrier animals
  • Detected in the slurry of cattle herds or sewages from abattoirs
103
Q

What is the non-human animal host range of Erysipelothrix?

A

Mammals (pig, horses, cattle), birds (turkey), reptiles, amphibians, fish
Pigs including wild boars (wildlife)
Detected in horses with vegetative endocarditis
Turkey with swollen snood

104
Q

What is the human host range of Erysipelothrix?

A

Humans due to occupational zoonotic disease
• people who have contact with pigs, poultry, fish (vets, abattoir workers, butchers,
farmers)
It causes a purple colored hardened finger swelling in humans
 It may disseminate from skin to cause endocarditis, pneumonia and meningitis.

105
Q

What are the points of entry and exit of Erysipelothrix?

A

Entry: oral route
 enter the host orally to colonize tonsils
 Flies may transmit it
• Exit: fecal route (urine, saliva, nasal
secretion)
 exit from the host mainly with feces to spread
to the environment (effluent) and new host

106
Q

What are the virulence factors of Erysipelothrix?

A

No well known virulence factors except the following surface structures and enzymes

107
Q

How do the structural surfaces of Erysipelothrix cause its virulence?

A
  1. Capsule (lipopolysaccharide, slime or glycocalyx) – for resistance to phagocytosis
  2. Surface protective proteins (spA, B and C antigens) – for biofilm formation,
    adhesion, and to elicit immune response.
    These surface proteins can be used as a protective vaccine
108
Q

What enzymes does Erysipelothrix posess?

A
  1. Neuraminidase (sialidase)
  2. Hyaluronidase
  3. Superoxide dismutase
109
Q

What does Neuroaminidase do in Erysipelothrix?

A

attachment, invasion, destroy
hemorrhage and thrombosis
This can lead to bacterial emboli and infarction in the heart valves (endocarditis), spleen, liver, lung, kidney, and joints (polyarthritis)

110
Q

What does Hyaluronidase do for Erysipelothrix?

A

Hyaluronidase – for spreading via destroying hyaluronic acid and polysaccharides between adjacent cells

111
Q

What does superoxide dismutase do for Erysipelothrix?

A
  1. Superoxide dismutase – for protection from intracellular killing by macrophages
112
Q

Erysipelothrix is the problem of ___, ________, and _____ …. it is also?

A

pigs, ruminants, turkey, zoonotic/humans

113
Q
A
114
Q

What is the diamond shaped skin form of erysiopelothrix?

A

rhomboid urticarial purple/black and hard skin lesion mainly around belly, inside the thighs, throat,
neck, ears

115
Q

What is seen in this image?

A

Swollen snood in acute turkey erysipelas

116
Q

What is seen in this image? Who is at risk?

A
  • E. rhusiopathiae and a characteristic purplish, swollen, painful, hardened rash known as
    erysipeloid…..but Do NOT produce PUS!

Fish handlers, poultry, pig workers, abattoir workers or vets are at risk

117
Q

What is the cardiovascular form of Erysipelas?

A

• Purple/black discoloration of the skin of belly with bluish (cyanotic) of the extremities due to
• septicemia, emboli, infarcts, & vegetative endocarditis that blocks heart valve orifice.
 Erysipelas ranked 2nd next to Sterpt. suis in causing endocarditis in pig industry

118
Q

What is the joint form of Erysipelas?

A

Polyarthritis (swelling joints, lameness and stiffness) mainly elbow, hip, hock, stifle, and knee joints

119
Q

What are the 5 tropisms for erysipelas based on body parts?

A
  • diamond shaped skin form
  • pneumonia
  • cardiovascular form
  • Joint form
  • Uterine form
120
Q

What is the uterine form if Erysipelas?

A

Abortion mainly due to fever, but the bacteria is isolated from fetuses (i.e. congenital/vertical infections
indicating it can pass the placental layers)

121
Q

What are the clinical manifestations of Erysipelothrix?

A

✓ Lacy-skin disease, but it is not a pus forming bacteria
- purple/ red/ black colored diamond shaped skin lesion (pig) is indicator sign

  • Swollen snood ( turkey)
  • Purplish swollen and hardened skin in humans

Systemic Signs:

✓ Septicemia,

✓ fever,

✓ thrombosis,
✓ ischemic necrosis,

✓ abortion
✓ Polyarthritis (lameness of many limbs)

✓ vegetative endocarditis with selective attachment to heart valves

122
Q

What are the differences in the skin presentation between Erysipelothrix vs Staph. hyicus or Strep Suis? Systemic signs?

A

• Erysipelothrix (lace-like or diamond shape skin lesion) - not pus forming

Staphylococcus hyicus = greasy skin

  1. Streptococcus suis = contagious pyoderma

Systemic signs of Erysipelothrix:

Systemic Signs:

✓ Septicemia,

✓ fever,

✓ thrombosis,
✓ ischemic necrosis,

✓ abortion
✓ Polyarthritis (lameness of many limbs)

✓ vegetative endocarditis with selective attachment to heart valves

  • Strep suis is similar , however shape of lesion and pus formation is what is different
123
Q

How can you diagnose Erysipelothrix via bacteriology?

A
  1. Gram positive - Long filamentous (Rod)
  2. Catalase negative
  3. Alpha-hemolytic
  4. H2S in TSI agar
124
Q

How can you diagnose Erysipelothrix via clinical signs?

A

looking for lace like or diamond shaped skin lesions.

125
Q

What is seen in this image?

A

Lace like / diamond skin lesions on swine.

126
Q

What is seen in this image?

A

lace like or diamond patterns

127
Q

How can you diagnose Erysipelothrix via serology?

A

serotyping) - 28 serotypes

128
Q

How do you treat Erysipelothrix infections?

A

Penicillin (50,000U/kg
per day for 3 days, IM)
ampicillin
ceftiofur

129
Q

How do you control Erysipelothrix infections?

A

• Vaccinate pigs > 3 months age with formalin-killed
vaccine bi-annually
 but vaccine fails due to several serotypes i.e. 28
 short duration of immunity i.e. protection lasts less
than 6 months
• Therefore, the feasible control methods are:
1. Remove clinically sick or test positive animals from the
herd immediately (but no reliable test?)
2. Good hygiene (biosecurity): all-in all-out policy followed by
disinfection of the house before restocking

130
Q

Summary Erysipelothrix

A
131
Q

Summary Listeria

A

Bacteriology/ Mycology (19 decks)

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