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Bacteriology and mycology > Block 2 > Flashcards

Block 2 Flashcards

1
Q

Staphylococcus overview
Gram pos
describe

A

cocci in grape-like clusters, facultative anaerobes, non-motile, catalase pos.

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2
Q

Staphylococcus overview
catalase pos.
what is it
what can it be used for?

A

Catalase is an enzyme produced by the bacteria that protects the bacteria against toxic oxygen byproducts

Catalase can be used to tell the different between Staphylococcus and Streptococcus

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3
Q

Staphylococcus overview
Commensals

what are they?
where are they?
why are they opportunistic?
what are the hosts?

A

Commensals (normal residents) of the skin and mucous membranes, which means they are opportunistic pathogens!
* Upper respiratory tract is most important carrier site, especially nose/nares because high concentration of bacteria can be found
* Lower urogenital tract, GI tract
* Opportunistic pathogens are not usually very virulent on their own; environment and host play a role in the level of virulence
* Hosts are humans and animals, and infections cause suppurative or pus filled lesions
*

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4
Q

Staphylococcus overview
Virulence factors: Hemolysins

A

Adhesins: tissue colonization
* Hemolysins: cytologic (kills cells) which destroys tissue

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5
Q

Staphylococcus overview
Virulence factors: enterotoxins

A

Adhesins: tissue colonization

  • Enterotoxins: type of heat stable exotoxin, destroys cells and tissue (food poisoning)
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6
Q

Staphylococcus overview
Virulence factors: Toxic shock syndrome toxins (TSST)

A

Toxic shock syndrome toxins (TSST): superantigen that causes excess cytokine release and results in toxic shock (immune system is in overdrive)

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7
Q

Staphylococcus overview
Virulence factors: coagulase

A
  • Coagulase: coverts fibrinogen to fibrin, fibrin is used to coat/hide the bacteria from phagocytic cells which makes the bacteria more virulent, immune evasion
  • Can do a coagulase test to evaluate virulence of a bacteria (Coagulase + is more virulent)
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8
Q

Staphylococcus overview
Virulence factors: protein A

A
  • Protein A: inhibits opsonization which helps with immune evasion
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9
Q

Staphylococcus overview
Virulence factors: Leukocidin

A
  • Leukocidin: kills leukocytes to aid in immune evasion
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10
Q

Staphylococcus overview
pyrogenic bacteria

A

many of them opportunistic pathogens. range from subclinical to acute and severe infections. some infections can be peracute, severe and life threatening

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11
Q

Staphylococcus overvie
Virulence factors

which colonize?
which deconstruction?
which evasion?

A

colonize=adhesion
deconstruction=hemosins, enterotoxins, toxic shock toxins
evasion=protein a, leukocidin, coagulase

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12
Q

Laboratory diagnosis

Specimens (6)

A

Specimens: exudates, pus from abscesses, mastitic milk, skin scrapings, urine, affected tissues

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13
Q

Laboratory diagnosis
Direct microscopy
what is it
what do you see

A

§ Direct microscopy: Gram-staining
§ Gram + clusters and evidence of inflammation with abundance of neutrophils

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14
Q

Laboratory diagnosis
Isolation (2)

A

Isolation
§ Culturing on (selective) blood agar (hemolysis) and MacConkey agar (absence of growth)
§ Contaminant (esp. CoNS), resident or pathogen? Assess clinical significance!

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15
Q

Staphylococcus aureus
Bovine Contagious Staphylococcal Mastitis

explain

A

Tends to be a chronic subclinical mastitis that can periodically be seen during lactation
* Farmers can experience production loss due to the bacteria not being cleared by the immune system: chronic, low grade or
subclinical mastitis

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16
Q

Staphylococcus aureus
Bovine Contagious Staphylococcal Mastitis
Predisposing factor

A

Predisposing factor: impaired phagocytic function (allows bacteria to survive in the in the cells in the mammary
gland)

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17
Q

Staphylococcus aureus
Bovine Contagious Staphylococcal Mastitis
Transmission:

A

Transmission: infected mammary glad of a cow in the herd is the source of infection
* Milking machine (teat cup liners/udder cloths) or contaminated human/milker hands

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18
Q

Staphylococcus aureus
Bovine Contagious Staphylococcal Mastitis
Prevention & treatment (4)

A

Prevention & treatment:
* Practice good milking hygiene: single use paper towels, gloves, teat dip before & after milking
* Dry cow therapy: antibiotic treatment when the cow is dried off (period of not milking)
* Detect subclinically infected cows: segregate and milk them last, antimicrobial treatment, and cull chronically infected animals
* Prevent introduction of positive cows into the herd

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19
Q

environmental vs. contagious

A

Environmental mastitis: from environment and outside.
Contagious mastitis: inside from one cow to another.

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20
Q

Staphylococcus aureus
Types of Contagious Mastitis

Peracute Gangrenous Mastitis

A

Black udder
Rare
* Ischemia of the udder resulting in:
* Tissue necrosis and udder
discoloration, swollen quarters,
painful, fever, depression,
anorexia
* In 24 hours you will see blood
from the udder rather than milk

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21
Q

Staphylococcus aureus
Types of Contagious Mastitis
Acute Mastitis

A

Milk color
change or
thickening
* Sever swelling of the affected
gland
* Pus/purulent secretion with fibrin
clots in the milk

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22
Q

Staphylococcus aureus
Types of Contagious Mastitis
Chronic Subclinical Mastitis

A
  • Most common!
  • Elevated somatic cell counts
  • Somatic cells are always present
    in the milk, but when elevated it
    indicates subclinical mastitis
  • Inflammatory response inside the
    udder leads to blockage of ducts
  • Episodes of bacterial shedding
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23
Q

Staphylococcus aureus
Botryomycosis in horses

is it common
what is it
what causes it
why does it occur
Tx
prevention

A

Rare- Chronic granulomatous suppurative disorder
with formation of micro-abscesses
* Cutaneous form has small subdermal granulomas
* Basically causes a chronic inflammatory skin infection
with pus filled abscesses and granulomas
* Predisposed by poor castration hygiene (especially
open castration procedures) Botched surgery
* Tx: long term antibiotics and surgically remove infected
tissue if needed
* Prevention: surgical hygiene, good wound care

*you have notes on the slide but I can’t read them –slide 5

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24
Q

Staphylococcus aureus
Bumblefoot in birds
what is it
who can get it
what does it look like
how does it occur
how do you prevent

A

Bumblefoot in birds

  • Local chronic pododermatitis and tenosynotvitis
  • Can affect the feet of all types of birds
  • Basically dark circular sores/scabs on the feet with
    inflammation lining the tendon sheath
  • Bacteria enters from the environment into an abrasion
    of the skin
  • Nail trimming injuries, rough bedding or roosts
  • CS: will initially notice the birds limping, then they will
    tend to sit/rest more often to avoid the pain
  • Prevention: good bird hygiene and management!
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25
Q

Staphylococcus aureus
Staphylococcal Toxic Shock Syndrome (TSS)
what is it
who gets it
what causes it
CS

A
  • TSS of HUMANS
  • Caused by superantigens entering the bloodstream
    -improper blinding of MHC II molecules–extreme T cell proliferation an drelaeast of cycotine–nausia, vomiting, fever, shock and posibly death
  • CS:
  • Fever, headache, vomiting, diarrhea
  • Reddening of the conjunctiva, hypotension (low blood
    pressure), skin rashes, kidney failure
  • Can ultimately result in death
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26
Q

Staphylococcus aureus
Food poisoning
how do you get it?
CS
Enterotoxins

A

Food poisoning

  • Caused by eating food that Staphylococcus aures has
    multiplied and produced enterotoxins in
    * Enterotoxins: type of heat stable exotoxin, destroys cells
    and tissue (food poisoning)
  • CS: Nausea, vomiting, abdominal cramps, diarrhea,
    sweating
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27
Q

Staphylococcus pseudintermedius

Dogs and cats

is it common?
otitis externa
primary cuases (5)
tx
pyoderma
does it involve other bacteria?
which one?
what causes it
tx
prevention
human carriers?
MRSP

A

Dogs and Cats

  • Most common opportunistic pathogen in dogs that is involved in a wide range of purulent diseases * This bacteria is always “hanging out” on dogs and cats * Pyodermas, otitis externa, wound infections, UTI, vaginitis, balanitis, conjunctivitis, bacteremia, abscesses
  • Otitis externa: bacterial infection is secondary
  • Primary causes: food allergies, parasites, foreign bodies, anatomic/breed predispositions, autoimmune diseases
  • Fix/treat the primary cause first and then treat for the bacteria!
  • Pyoderma: usually due to overgrowth of the normal skin microbiota
    -most always growth negative
  • Can be other bacteria involved, but usually S. pseudintermedius
  • Primary causes: allergies, parasites, foreign bodies, anatomic/breed predispositions, autoimmune diseases
  • Fix/treat the primary cause first and then treat for the bacteria!
  • Tx: antimicrobial shampoo, topical antibiotics, use narrow-spectrum, 2% Mupirocin ointment
  • Prevention: grooming and maintaining the hair coat
  • S. pseudointermedius can be carried on human skin, but is is NOT zoonotic
  • MRSP: Methicillin resistance in S. pseudintermedis
    at.geeapersonisuersinterdermalnsimiartoAncylostoma d
    opportunistic
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28
Q

Staphylococcus pseudintermedius

Dogs and Cats
what is Otitis externa
causes ?
treatment

A

*you have a note on the slide, I cannot read it. slide 7
* Otitis externa: bacterial infection is secondary
* Primary causes: food allergies, parasites, foreign bodies, anatomic/breed predispositions, autoimmune diseases
* Fix/treat the primary cause first and then treat for the bacteria!

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29
Q

Staphylococcus pseudintermedius

Dogs and Cats

what is Pyoderma?
causes?
does it involve other bacteria
TX
prevention

A
  • Pyoderma: usually due to overgrowth of the normal skin microbiota
    -most always growth negative
  • Can be other bacteria involved, but usually S. pseudintermedius
  • Primary causes: allergies, parasites, foreign bodies, anatomic/breed predispositions, autoimmune diseases
  • Fix/treat the primary cause first and then treat for the bacteria!
  • Tx: antimicrobial shampoo, topical antibiotics, use narrow-spectrum, 2% Mupirocin ointment
  • Prevention: grooming and maintaining the hair coat
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30
Q

Staphylococcus pseudintermedius

Dogs and Cats
is
S. pseudointermedius zoonotic?

A

S. pseudointermedius can be carried on human skin, but is is NOT zoonotic

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31
Q

Staphylococcus pseudintermedius

Dogs and Cats
what is
MRSP

A
  • MRSP: Methicillin resistance in S. pseudintermedis
32
Q

Staphylococcus hyicus
GREASY PIG DISEASE
what is it?
who gets it?
who can carry it?
morbidity?
do adult pigs have it?
where?
result?
how do baby pigs get it?
TX
prevention>

A

GREASY PIG DISEASE

  • Highly contagious exudative epidermitis affecting pigs up to 3 mo. of age (suckling
    and weaning aged) adult pigs are carriers but not affected.
  • Excessive sebaceous secretion from skin (greasy looking), anorexia, depression, fever *no pus
  • High morbidity (up to 100%) and high mortality (up to 90%)
  • Normal commensal of adult pigs in the vaginal mucosa and skin of sows or preputial
    diverticulum of boars
  • Does NOT cause disease in adult pigs because they develop immunity with age
  • The bacteria enters the via skin lesions like bite wounds from piglets nipping at each
    other
  • Tx: isolate infected pigs and treat with antibiotics, clean and disinfect contaminated
    building
  • Prevention: clip needle teeth, hygiene and management (soft bedding)
33
Q

Streptococcus overview
Gram Pos
explain

A
  • Gram pos., cocci in chains, catalase neg., facultative anaerobe, non-motile, fastidious growth
34
Q

Streptococcus overview
Catalase

A

Catalase can be used to tell the different between Staphylococcus and Streptococcus

35
Q

Streptococcus overview
Commensals

A

Commensals (normal residents) of the mucous membranes and does not survive well in the environment
* Upper respiratory tract and lower urogenital tract
* Exception: Streptococcus equi subsp. equi is NOT a commensal

36
Q

Streptococcus overview
primary pathogenic?
optortunistic?
how do they present?

A

Primary pathogenic (usually species specific) or opportunistic infections, in humans and animals
* Suppurative or pus filled lesions, systemic infection (septicemia), infections in the adjacent throat/LN, chronic mastitis, or pneumonia

37
Q

Streptococcus overview
Types of hemolysis (3)
classification?
test?

A

Types of hemolysis: BAG
* Beta-hemolytic (complete lysis) , Alpha-hemolytic (partial hemolysis), Gamma-hemolytic (no hemolysis)
* Lancefield classification: ONLY FOR STREPTOCOCCUS SPP.
* Latex bead test or ring precipitation test based on cell wall polysaccharide antigen (groups A-H)

38
Q

Streptococcus overview
Virulence factors

A

Virulence factors: FAME
* Streptokinase and hyaluronidase: invasion of skin (eat away at tissue)
* Protein F: adhesion/attachment
* M protein: evasion
* Exotoxins and lipoteichoic acid

*you have a note on this I can’t read slide 10

39
Q

Streptococcus overview
Pathogenesis:

A

Pathogenesis: bacteria enters into the respiratory tract, multiplication in tonsils/LNs, causes inflammation and abscess formation, and septicemia

40
Q

Antimicrobial resistance

what is antimicrobial resistance (AMR)

what are antimicrobials?

A

substances used to treat a wide variety of infectious diseases in humans and animals. They:
kill micro organisms
stop micro-organisms from growing and multiplying
ex. antibiotics such as ciproflaxacin

41
Q

Antimicrobial resistance

what is antimicrobial resistance (AMR)

what is antimicrobial resistance?

A

the ability of micro-organisms to withstand antimicrobial treatments
ex. MRSA commonly presenton human skin and mucous membranes

42
Q

Antimicrobial resistance

what is antimicrobial resistance (AMR)

whis is resistance growing?
what effect of growing resistance?

A

overuse and misuse of antibiotics.
spread through various routes

treatment may become ineffective
serious risks to public health

43
Q

Antimicrobial resistance
what is b lactamase

A

b lactamase-mediated resistance common in staphylococcal species

44
Q

Antimicrobial resistance
what is methicillin resistance?

A

§ Methicillin resistance in S. aureus (MRSA) and S. pseudintermedius (MRSP)

45
Q

Antimicrobial resistance

what is multi drug resistance

A

Resistance to b-lactam antibiotics often coincides with resistance to other antibacterial drugs (“multidrug
resistance”) e.g. macrolides, aminoglycosides, tetracycline, potentiated sulfa drugs

46
Q

Antimicrobial resistance

how is methicillin resistance mediated?

A

Methicillin resistance is mediated by mecA gene resulting in altered penicillin
binding proteins

47
Q

Antimicrobial resistance

Hospital-acquired (HA)
community acquired (CA)

A

Hospital-acquired (HA) infections (nosocomial) and increasing circulation of
community acquired (CA) infections by MRSA

48
Q

Streptococcus equi subsp. equi
Equine Distemper AKA Strangles

what is it?
reportabe?
morbidity? mortality?
who gets it?
recovery?
how is it transmitted?
incubation period?
CS?
LN Lesions?
what LN is affected?

A

Equine Distemper AKA Strangles

  • Reportable, highly contagious febrile disease involving the upper respiratory tract and causes abscessation of the regional
    LNs
    ISOLATE
  • Called strangles due to the swelling of the LN causing obstruction of the airway that can result in death
  • Enzootic in domestic horses worldwide and all ages are susceptible, but tends to affect yearlings and weanlings (foals are
    protected by the mares antibodies)
  • High morbidity (up to 100%), low mortality (less than 5%)
  • After an infection, most animals recover spontaneously (about 75%) and have immunity
  • NOT a commensal and is transmitted by carriers or currently infected animals
  • Via purulent exudate from the respiratory tract or by pus from the abscesses
  • Direct contact or indirect by contaminated buckets, troughs, stables, flies, grass
  • Incubation period: 3-6 days
  • CS: high fever, depression, anorexia, purulent discharge from the nose and eyes
  • LN lesions: submandibular (1st affected) and retropharyngeal LN’s are affected and will eventually rupture/release purulent
    material that is highly infectious (this pus is what you send to the lab for testing)
    *WHAT LN’s are affected?
49
Q

Streptococcus equi subsp. equi
3 C’s
4 potential complications?
what are they?
what happens?
common?
TX

A

COMMON, CONTAGIOUS, CONTROLABLE
4 potential complications of Stranlges
* Guttural pouch empyema: abscess ruptures in/towards the guttural pouch, secondary to upper respiratory tract infection
* Stiff head carriage, painful swelling around parotid gland, difficult breathing, BAL is necessary, can result in a carrier
* **Bastard strangles: **disseminates or spreads causing abscesses in other organs, very rare
* Purpura hemorrhagica: immune complex mediated vasculitis, very rare
* Asymptomatic carriers: ID and treat ASAP, there can be long term chronic shedders, testing is important (new horses or horses that
were in contact with infected ones)

50
Q

Streptococcus equi subsp. equi
When an animal is infected what do you do?
Dx?
Tx?
Vaccination?
Prevention

A

When an animal is infected, 3 negative cultures taken at weekly intervals is required to be released from quarantine
* Dx: clinical symptoms and culture of pus, ELISA or PCR for M proteins
* Tx: drain abscesses (put Penicillin inside) and relieve pain, can give antibiotics but they are only effective if given before
abscess formation
* Vaccination: not completely effective, give inactive vaccine to pregnant mares and foals to keep high levels of anti-M
antibodies, live intranasal vaccine
* Prevention: stop movement of animals if an infection is suspected, quarantine, hygiene and disinfection

51
Q

Streptococcus suis

what is it?
causes?
who gets it?
who carries it? how?
mortality rate?
how many serotypes? what are serotypes based on?
what is the most common serotype?
what ar ethe predisposing factors?
Tx
Prevention?
what is the future for this and why?
how do humans contract it?
is it zoonotic?

A
  • Causes significant economical losses in the pig industry due to the high fatality rates
  • Meningitis, arthritis, septicemia, bronchpneumonia, and possibly endocarditis, neonatal death, or abortion BAMS
  • Nursery disease: affecting pigs 2-5 weeks post weaning (roughly 5-8 weeks of age) so they are under a high level of stress
  • Nearly all pigs are CARRIERS of the bacterial in their tonsils!
  • Doesn’t often cause disease, but when it does, the mortality rate is high (around 20%)
  • There are 35 different serotypes and their antigenicity is based on the capsular polysaccharide
  • Pigs can carry different serotypes but **serotype 2 **is predominant worldwide (and it has different sequence types)
  • Predisposing factors: STRESS due to changes in housing, temp. changes, poor ventilation
  • Tx: penicillin or ampicillin
  • Prophylaxis: long acting penicillin can be given by injection to sows (1 week before farrowing) and piglets (during the first 2 weeks of
    life)
  • Prevention: hygiene and husbandry, decrease stressful predisposing factors
  • Emerging zoonotic pathogen: underreported and underdiagnosed
  • Most common cause of adult meningitis in Asia and humans are usually infected by consuming raw pork meat or because of occupational hazard

On DIRECT CONTACT

52
Q

Streptocococcus spp. causing mastitis
Bovine Streptococcal Mastitis

Streptococcus agalacticae

is it contagious/envoronmental?
is it chronic/acute/subclinical?
what is it/where is it

A

Streptococcus agalacticae
* CONTAGIOUS MASTITS
* Bacteria will colonize in the milk
ducts (obligate pathogen), which
leads to a persistent infection with
intermittent episodes of acute
mastitis
* Chronic mastitis

-IDK what this says “resovict mammary quarter”

53
Q

Streptocococcus spp. causing mastitis
Bovine Streptococcal Mastitis
Streptococcus dysgalacticae

is it contagious/envoronmental?
is it chronic/acute/subclinical?
what is it/where is it

A

Streptococcus dysgalacticae
* ENVIRONMENTAL MASTITIS
* Bacteria will colonize in the
buccal cavity, genitalia, and skin
of the mammary gland (so not
inside the gland!)
* Acute mastitis

54
Q

Streptocococcus spp. causing mastitis
Bovine Streptococcal Mastitis
Streptococcus uberis

is it contagious/envoronmental?
is it chronic/acute/subclinical?
what is it/where is it

A

Streptococcus uberis
* ENVIRONMENTAL MASTITS
* Linked to straw bedding
* After a night out, “Uber” home
and get in “bed”
* Bacteria will colonize on the skin,
tonsils, and vaginal mucosa
* Subclincal mastitis

55
Q

Streptocococcus spp. causing mastitis
Bovine Streptococcal Mastitis
Tx and prevention
is mastitis multifactorial?

A

teat dip,clean towel, nutrition, reduce teat trauma
Reduce teat injury and trauma
* Mastitis is multifactorial: exposure to microorganisms, host defense mechanisms, environmental conditions

56
Q

Streptococcus spp.
Streptococcus euqi subsp. zooepidemicus

Is it opportunistic?
who gets it?
where is it?
what sort of purulent infections? (5)
what relevance is it as an emerging zoonotic pathogen?

A

Streptococcus euqi subsp. zooepidemicus
* Opportunistic pathogen of many species (horses,
cattle, dogs, lambs, pigs)
* Commensal of mucous membranes
* Purulent infections: respiratory tract infections,
pneumonia, mastitis, navel infections, foal septicemia
* Emerging zoonotic pathogen causing necrotizing
myositis and meningitis (in humans)

57
Q

Streptooccus canis
Streptococcal toxic shock syndrome and necrotizing
fasciitis in dogs and cats
who is most susceptible
where is it?
where can the infection be?
what can it lead to?
what result?

A

Streptococcal toxic shock syndrome and necrotizing
fasciitis in dogs and cats
* Puppies and kittens are the most susceptible
* Don’t confuse with TSS of humans from Staphylococcus
aereus
* Commensal on the skin and mucous membranes
* Can get an infection from vagina or umbilical vein which
will lead to bacteremia
* Septicemia and embolic lesions in heart and lungs

58
Q

Streptococcus pyogenes
who get it?
result?
what does it look like?
what can it cause?
what potential worst results?

A
  • Affects many species, but is mostly associated with humans
  • Can cause anything from a mild superficial skin disease to a life-
    threatening systemic infection
  • Localized skin infection with sores/blisters (impetigo), pharyngitis with
    abscesses on the throat
  • Can cause streptococcal toxic shock: bacterial infection with toxin
    production, destruction of skin/fat/muscles
  • Flesh eating bacteria: necrotizing fasciitis
  • Rare but serious and potentially deadly
  • Rheumatic fever or glomerulonephritis are examples of non-pyogenic
    diseases
59
Q

Enterococcus spp.
where is it tested?
5 characteristics
is it oportunistic?
where is it found?
how is it spread?
is it antimicrobial resistent? explain
what is VRE?

A

Overview

  • Gram pos., diploccoci (PAIRS) facultative anaerobes, catalase neg., can be
    motile (but not many)
  • Enterococcus is tested for in water: drinking, beaches, pools
  • Commensals of the GI tract in animals and humans so they are
    opportunistic! ENTEROCYTES=CELLS OF SI
  • Low grade pathogens found in general wound infections and UTI’s
  • Fecal transmission is the key for spreading
  • Antimicrobial resistance:
  • Naturally resistant to many antimicrobials like cephalosporins for
    examples
  • VRE: Vancomycin resistant enterococcus
  • Acquired resistance
60
Q

Enterococcus spp.

Enterococcus faecalis & Enterococcus

what is it
where is it
who gets it
result?

A

Wound infections
* Secondary mastitis in cattle
* UTI and ear infections in dogs
* Nosocomial infections

-faecalis/faecium-like fecal b/c fecal transition

61
Q

Listeria overview
name 5 characteristics

A

Gram pos., coccobacillary rods (short/thick rods), catalase pos., oxidase neg., facultative anaerobe

62
Q

Listeria overview
Psychrophilic
explain

A

Psychrophilic (grows in cold), most species have tumbling motility at 25oC, tolerate a pH between 5.5-9.6 (acid,
neutral, or basic)

-what psycho likes the cold

63
Q

Listeria overview
Q. When an animal uptakes Listeria, will flagella be present?

A

no, animal is too warm

64
Q

Listeria overview
* Commensals
explain
where is it found/not found? why

A

**Commensals **(normal residents) of the the mammalian **GI tract **in low numbers and found throughout the
environment (especially soil)
* Resistant to harsh environments due to the wide temp. range; can be found in herbage, feces, sewage and water

65
Q

Listeria overview
* Pathogenesis
who is the most susceptible
what are the 2 routes of uptake?
what result?

A

Pathogenesis: ruminants are the most susceptible
* Uptake via inhalation: goes to trigeminal n. and causes encephalitis (most common presentation in ruminants)
* Uptake via ingestion: absorbed through the intestinal wall and into the blood stream, hematogenous spread

66
Q

Listeria overview

Pathogenesis
Encephalitis- who gets it
Septicemia-what is it, how does it present, is it common?
Abortion - relevance

do they overlap?

A

rarely overlap
Encephalitis-seen in very young rumenants
Septicemia (common with monogastrics), multifocal miliary abscesses, can affect multiple organs but we commonly see lesions in the liver
or kidney Most common in rumenants
* Abortion: fetal hepatic necrosis

67
Q

Listeria overview

Virulence factors (5)
explain

A

Virulence factors:
* Internalin A: adhesion to enterocytes
* Internalin B: adhesion to hepatocytes
* Listeriolysin O (LLO): pore formation to break the membrane of the phagosome for escape
* ActA protein: actin-polymerizing protein, pushes bacteria to the side of the cell wall
* Phospholipase C enzymes: helps degrade membranes so Listeria can progress through
cells

*can invade phagocytes and non-phagocytes

68
Q

Listeria overview cont.

Pathogenicity
where can bacteria replicate?
what is fauculative intracellular relevance
how does the bacteria move?

A

Pathogenicity:
* The bacteria can replicate inside ANY cell causing cell death and micro- abscesses to form
* Facultative intracellular persisting in macrophages which allows for the bacteria to move
from one host cell to the next
* The bacteria is up taken by a phagocyte, formation of a phagosome, bacteria will escape
(LLO), multiplication, then the Actin tail pushes the bacteria to the side of the cell and helps
propel it into the adjacent cell via pseudopod
* This process allows the bacteria to travel without being exposed to the humoral defense
mechanisms
escapes phagasome… something about lysome fusion slide 20

69
Q

Listeria monocytogenes

Circling disease or Silage disease

cana farmer cell is infected?

A

yes

-drinking lysterine makes your heart spin ?

70
Q

Listeria monocytogenes
Circling disease or Silage disease

why is it economically important
when is it often occurring? why?
how long until clinical signs show?
transmission?
CS due to CNS lesions result in what?
DX
anti-mortem vs. post mortem
where might you find necrosis?

A

Circling disease or Silage disease

  • Economically important disease causing encephalitis in ruminants due to poor silage quality
  • Mostly seen from winter-spring and is associated with decreased acidic pH of soiled silage which allows for high
    multiplication of bacteria- outbreak and clinical signs usually seen around 10 days after ingestion
  • Transmission: ingestion, inhalation, or through breaks in the oral or nasal mucosa
  • CS due to CNS lesions: anorexia, depression, disorientation, dullness, turning/twisting of the head to one side, walking in
    circles TORWARDS the affected side, UNILATERAL trigeminal and facial n. paralysis     (drooping ear, deviated muzzle,
    droopy eyelid), nystagmus, head pressing, purulent unilateral endophthalmitis
  • Dx: anti-mortem vs. post-mortem
  • Anti-mortem: symptoms and history (new batch of silage?),season, silage quality
  • Post-mortem: look for lesions in the brainstem like micro-abscesses, meningitis, vascular and/or neuronal necrosis
  • Have to use an enrichment culture and histology is important!
  • Q. Will a blood sample be helpful? NO IT IS SHORT LIVED IN THE BLOOD
  • Can potentially see necrosis or inflammation in the liver and spleen, test abomasal content if there was an abortion

-ONCE ? CAN’T TREAT
NO VALL

71
Q

Erysipelothrix overview

6 CHARACTERISTICS
COMMENSALS?
WHERE IS IT PRESENT THAT OFTEN LEADS TO HUMAN INFECTION?

A
  • Gram pos., small rods or filaments, facultative anaerobes, non-motile, catalase neg., oxidase neg.
  • Commensals (normal residents) of the tonsils and intestines of many animal species
  • Even present in the slime-layer of fish which is a common source for human infection

-Ares is all talk (tonsils) and a slimeball (fish slime)
-same as strep suis

72
Q

Erysipelothrix overview
Pigs
how common? where located?
charachteristics of carrier pigs?
resistent?
how many serotypes, which are most common?
how transmitted?
virulence factors? (4) explain
name 4 things it can cause

A

Pigs: most important reservoir, up to 50% of all healthy pigs will harbor E. rhusiopathiae in their tonsils
* Carrier pigs will excrete bacteria in the feces and/or the oronasal secretions
* Very resistant in the environment and under harsh conditions
* There are 26 serotypes with 1a, 1b, and 2 being common in pigs
* Transmitted: ingestion (fecal-oral route)
* Virulence factors:
* Polysaccharide capsule: allows for intracellular replication and protection against phagocytosis
* Neuraminidase: adhesion and invasion of endothelial cells by cleaving sialic acid
* Leads to vascular damage which leads to thrombus formation
* Hyaluronidase: dissemination or spread of bacteria within tissues
* spaA surface protein: adhesion
* Can cause septicemia, dermatopathy, arthritis, and valvular endocarditis,

73
Q

Erysipelothrix rhusiopathiae

Swine erysipelas AKA Diamond Skin disease

Commensal?
who is most susceptibe?
trigger?
3 forms? what result? what signs?
what does it look like?
Dx (3)
Tx
name 3 resistant drugs
prevention
when do you vaccinate?

A

Commensal of the tonsils, pigs between 3 months and 1 year of age are the most susceptible
* Under 3 months: protected by maternal antibodies
* 1-3 years: building protective active immunity by being exposed to low virulent strains
* STRESS can trigger clinical erysipelas (infection of the top layers of skin)
* 3 forms:
* Acute form: sudden death (within 48 hours), fever, stiff gait/walking on toes, seclusion from the group, anorexia, skin lesions
* Subacute form: inappetence, mild fever, skin lesions
* Chronic form: may follow the subacute form, arthritis, endocarditis, polyarthritis, and skin lesions
* Diamond-shaped skin lesions are pathognomonic for swine erysipelas, so these lesions are diagnostic!
* Dx: skin lesions, culture (difficult to recover bacteria), PCR
* Tx: can treat the acute form if the pig survives by isolation and antimicrobials, cull animals with chronic infection
* Resistance to vancomycin, aminoglycosides, sulfonamides
* Prevention: hygiene and management, vaccination before breeding
* Vaccinate boars every 6 months and sows 3-4 weeks before farrowing

74
Q

Erysipelothrix rhusiopathiae

is this food born?

A

no

75
Q

Erysipelothrix rhusiopathiae

Erysipelothrix rhusiopathiae in turkeys

is this economically significant?
what 2 forms does it take?

A

Erysipelothrix rhusiopathiae in turkeys

  • Economically important disease worldwide that affects
    turkey of all ages
  • 2 forms:
  • Acute form: septicemia, sudden death
  • Chronic form: endocarditis, gradual weight loss
76
Q

Erysipelothrix rhusiopathiae

Erysipelothrix rhusiopathiae in lambs

how does it present?
how is it caused

A
  • Non-suppurative polyarthritis (no pus, arthritis in multiple joints)
  • Bacteria enters through umbilicus, castration wounds,
    or skin abrasions
  • Post-dipping lameness is due to cellulitis and laminitis
    in older lambs
77
Q

Erysipelothrix rhusiopathiae

Erysipelothrix rhusiopathiae in humans

why is it an occupational hazard?
where is it located?
how does it enter?

A

Erysipelothrix rhusiopathiae in humans
* Occupational hazard by working with fish, poultry, and
swine
* Commensal of the slime layer of fish *not eaten
* Enters through skin abrasions and causes localized
cellulitis on fingers, diffuse skin infection, septicemia

Bacteriology and mycology (6 decks)

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