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Bacteriology and mycology > Block 3 > Flashcards

Block 3 Flashcards

1
Q

Bacillus overview

describe basic features

A

Gram pos., aerobes or facultative anaerobes, catalase pos., oxidase
neg., most are non-pathogenic,** REPORTABLE, zoonotic**

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2
Q

Bacillus overview

what do they look like?

A

Large rectangle/square rods in chains, motile (except B. anthracis),
Medusa head colonies under microscope

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3
Q

Bacillus overview

where are they found? why do they survive there?
what result?

A

Endospore forming and they survive very well in soil (soil
saprophytes)
* Endospores allow the bacteria to have an extremely durable dormant
state
* They are the most durable type of cell found in nature
* Resistant to extreme adverse conditions, and stay viable for long periods
of time

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4
Q

Bacillus overview

what is the most important pathogen? why?

A

B. anthracis is the most important pathogen as it is an obligate
mammalian pathogen
**anthrax=sudden death

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5
Q

Bacillus anthracis

where?

A

Africa, india, china

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6
Q

Bacillus anthracis

source?
waht result with O2 exposure?

A

Source of infection is usually soil that has been contaminated by bacterial spores
* O2 exposure will increase the process of sporulation by the bacteria

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7
Q

Bacillus anthracis

Susceptibility by species from most to least:
what is most resistent and why?

A

Susceptibility by species from most to least: cattle, sheep, horses, goats, dogs, pigs
* Birds are almost completely resistant to anthrax because of their higher body temp.

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8
Q

Bacillus anthracis

Factors that predispose an animal to anthrax infection:
name 4

A
  • History of previous anthrax deaths and/or buried carcasses
  • Alkaline soil that is rich in Ca and N and has a high moisture content
  • Warm temps and repeated flooding/drying
  • Dry/drought conditions that force animals to graze closer to the soil
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9
Q

Bacillus anthracis

Virulence factors: what is needed?

A

both the capsule and tripartite anthrax toxins are needed for full virulence

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10
Q

Bacillus anthracis

  • Virulence factors:
    what is capsule?
A
  • Capsule: polymers of D-glutamic acid will inhibit phagocytosis, only produced in vivo (AKA we will not see a capsule when growing B. anthracis in
    the lab)
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11
Q

Bacillus anthracis

  • Virulence factors:
    Tripartate anthrax toxin:
    name and explain
A

1) Protective antigen (PA): cell binding factor to aid in translocation into host cell (acts like a channel)
2) Edema factor (EF): calmodulin-dependent adenylate cyclase, enter the cell after PA is formed and increases the amount of cyclic AMP, this disrupts water
homeostasis and results in edema, neutrophils are the primary target
3)** Lethal factor** (LF): zinc metalloprotease, also enters via PA, causes cell death and tissue necrosis/hemorrhage

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12
Q

Bacillus anthracis

  • Transmission:
  • IP:
A
  • Transmission: ingestion (main), inhalation, cutaneous
  • IP: hours to days
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13
Q

Bacillus anthracis

  • CS vary by species
  • Ruminants:
    what is it?
    what does it look like?
    what result?
A
  • Ruminants: peracute septicemia (blood disease)
  • Rapidly fatal disease due to respiratory distress and shock
    * Can see bleeding from orifices
  • Post-mortem: blood is dark and unclotted, incomplete rigor mortis (because of increase in cyclic AMP), splenomegaly
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14
Q

Bacillus anthracis

  • CS vary by species
  • Horses:
A
  • Horses: acute septicemia
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15
Q

Bacillus anthracis

  • CS vary by species
  • Pigs & dogs:
A
  • Pigs & dogs: pharyngeal (swelling of the throat area)
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16
Q

Bacillus anthracis

  • Pigs & dogs & humans:
A
  • Pigs & dogs & humans: intestinal
  • Humans by ingestion of an infected animal
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17
Q

Bacillus anthracis

  • CS vary by species
  • Humans (Wool sorters disease):
A
  • Humans (Wool sorters disease): pulmonary
  • Inhalation of spores and can take 2 months to manifest, rare but very deadly
  • Bioterrorism attacks in the US when turning spores into powder form
  • Q. is this contagious from human to human? NO
    **not in lungs
  • Humans (malignant carbuncle): cutaneous
  • Most common but least dangerous, caused by sores getting into wounds, localized necrotic skin
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18
Q

Bacillus anthracis

is it zoonotic?
is it contagious?

A

yes
no

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19
Q

Bacillus anthracis

  • Dx and sampling:
A
  • Do NOT do a field necropsy if anthrax is a possible cause of death- call the state and federal officials
    * Obligate REPORTABLE BSL-3 agent and select agent (potential use as bioterrorism agent)
  • Direct exam of samples:
  • Collect blood from tail vein
  • Look for blue stained bacteria with a pink capsule (McFadyean’s methylene blue)- blood or organ smears
  • Large rectangle/square rods in chains that are encapsulated (gram stain)
  • Aerobic culture on blood agar or PCR
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20
Q

Bacillus anthracis

  • Tx will vary for endemic versus non-endemic regions
    endemic?
    non-endemic?
A
  • Endemic: annual vaccine, long-acting penicillin for valuable livestock (this is very costly) no $
  • Non-endemic: quarantine affected herd, use PPE when handling infected animals and material, long acting antimicrobials,
    observe animals for 2 weeks that have been in contact with infected, vaccinate after AB treatment, incinerate carcasses or
    deep burial of at least 6.5 ft under a layer of quicklime (anhydrous Ca oxide),     disinfect all contaminated materials
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21
Q

Bacillus anthracis

Tx
Q. Why can’t we burn carcasses in the field?

A

b/c endospores don’t die

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22
Q

Acid fast partial bacteria

3 kids what are they?

A

Corynebacterium
* Rhodococcus
* Nocardia

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23
Q

Corynebacterium overview

describe

A

Gram pos., pleomorphic, aerobes or facultative aerobes, non-spore forming, short mycolic
acids in cell wall (hence ACID FAST PARTIAL)

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24
Q

Corynebacterium overview

where?
is it host specific?
where found?
result?

A

Commensals on the mucous membranes (usually host specific) and can also be found in the
environment (soil)
* Opportunistic bacteria causing pyogenic/pus type infections (infection usually follows a trauma)

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25
Q

Corynebacterium overview

  • Virulence factors:
    name 3 and what result
A
  • External lipid coat (mycolic acids): protects bacteria from enzymes in the host phagocytic cells
  • Exotoxin Phospholipase D (PLD): causes damage to the endothelial cells which allows for increased
    vascular permeability
  • Diptheria toxin: interferes with protein synthesis by inhibiting RNA translation
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26
Q

Corynebacterium overview

  • Virulence factors:
    what is causes damage to the endothelial cells which allows for increased
    vascular permeability
A

Exotoxin Phospholipase D (PLD):

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27
Q

Corynebacterium overview

  • Virulence factors:
    what is protects bacteria from enzymes in the host phagocytic cells
A
  • External lipid coat (mycolic acids):
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28
Q

Corynebacterium overview

  • Virulence factors:
    what is interferes with protein synthesis by inhibiting RNA translation
A
  • Diptheria toxin:
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29
Q

Corynebacterium overview

animal has a skin injury that is exposed to purulent material, bacteria enter
and migrate to the LN’s, replicates within phagocytes (facultative intracellular pathogen), and
the result is the formation of abscesses

what is this called?
what is the most common way for bacteria to spread?

A

Pathogenesis:

  • Purulent abscesses is the most common way the bacteria is spread
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30
Q

Corynebacterium pseudotuberculosis

what is it?
who gets it?
what does it look like?
does it hurt?

A

Caseous lymphadenitis (pseudotuberculosis) in sheep and goats
very swollen lymphnodes
not painful

31
Q

Corynebacterium pseudotuberculosis

Chronic pyogranulomatous infection of LN’s that is caused by ?
where found?
result?
example?

A

Chronic pyogranulomatous infection of LN’s that is caused by non-nitrate-reducing biotype of C. pseudotuberculosis
* Infection can be found in superficial or internal LN’s
* Internal abscesses lead to chronic weight loss- Thin Eye Syndrome (LN swelling goes unnoticed due to the wool)

32
Q

Corynebacterium pseudotuberculosis

why is it economically important?

A

Economically important due to: death, condemning carcasses, hide/wool devalued or lost, culling of affected animals

33
Q

Corynebacterium pseudotuberculosis

Transmission:
survival rate of bacteria?

A
  • Transmission: infection is spread by pus from ruptured abscesses, and oral/nasal secretions
  • Bacteria survive for months in the environment
34
Q

Corynebacterium pseudotuberculosis

Pathogenesis:
explain
sheep?
goats?
result?
spread?

A

Pathogenesis: uptake of bacteria results in lymphadenitis with the formation of microscopic multifocal abscesses in the
cortex, the abscesses begin to coalesce and are then encapsulated by fibrous connective tissue (make Tx challenging), and
the LN’s become enlarged
* Sheep: onion skin
* Goats: less dry and not concentrically laminated (not onion-skin)
* Ultimately the result is caseous necrosis- cheese like mass of dead cells
* The bacteria can also spread and affect other organs throughout the body

35
Q

Corynebacterium pseudotuberculosis

  • CS:
    what relevance a low or no titer?
A

CS: abscesses and chronic weight loss (can go unnoticed for a while though due to wool/hair)

low or no titer doesn’t mean no disease

36
Q

Corynebacterium pseudotuberculosis

Dx?
serology?
positive titer?
negative titer?
low or no titer?

A

Dx: CS, culture purulent material, rads and ultrasound to try and detect abscesses (challenging), serology
* Serology: synergistic hemolysin inhibition (SHI) test to detect antibodies against PLD
* Positive titer: past resolved infection, recent exposure, recent vaccine, active lesions
* Can repeat titer in 2-4 weeks to look for an increase- if there is an increase then there is an active infection
* Negative titer: false negative from testing to early after infection, chronic walled off abscesses
* LOW/NO TITER DOES NOT RULE OUT DISEASE and it is difficult to interpret serology in animals under 6 mo. of age

37
Q

Corynebacterium pseudotuberculosis

TX
why is educating an owner important?

A

Tx: **not a ”curable” **disease so educating the owner is important
* Disease is persistent and recurrent making it very hard to get rid of once its on a farm
* Only treat animals that are of value (genetics or emotionally, still no guarantees of success)
* Ideally, cull all infected animals

38
Q

Corynebacterium pseudotuberculosis

Prevention:
does it vary? why?
what about commercial vaccines?

A

Prevention: varies between countries, species-specific commercial vaccines (don’t give to animals/herd that have no history
of this disease), good biosecurity, hygiene and management

39
Q

Corynebacterium pseudotuberculosis

  • Prevention:
    Countries free of ds:
    relevance?
    management?
A

Countries free of ds: only import from countries free of ds., ELISA test before importing, quarantine or slaughter if infected

40
Q

Corynebacterium pseudotuberculosis

Prevention:
* Countries with low ds. prevalence:
relevance?
management?

A

Countries with low ds. prevalence: cull animals with lesions, regular ELISA screening (cull if infected), disinfection, remove lambs from
seropositive dams and raise by hand

41
Q

Corynebacterium pseudotuberculosis

  • Prevention:
    Countries with high ds. prevalence:
    relevance?
    management?
A
  • Countries with high ds. prevalence: strict hygiene measures, vaccinate
42
Q

Corynebacterium pseudotuberculosis

what is it?
who gets it?
what causes it?
common?
economically important? where?

A

Ulcerative lymphangitis AKA Pigeon fever AKA Dry land distemper in horses
Infectious, inflammatory condition of the cutaneous lymphatic system that

affects the lower limbs, ventral and pectoral regions- caused by nitrate-
reducing biotype of C. pseudotuberculosis

* Common and economically important in Texas and California (dry areas)

43
Q

Corynebacterium pseudotuberculosis

  • Transmission:
    how?
    when?
A

Transmission: FLIES (stable flies, horn flies, house flies) as a mechanical
vector that help spread bacteria and then the bacteria enters the horse
through skin abrasions
* More prevalent in fall and early winter (seasonal)

44
Q

Corynebacterium pseudotuberculosis

  • CS:
A

CS: swelling of chest and/or abdomen, deep SQ abscesses, fever,
decreased appetite, lameness (from lower limb swelling)
*normal appetite usually unless lessions inside

45
Q

Corynebacterium pseudotuberculosis

  • Tx:
A

drain abscesses into a catch bucket (purulent material is very
infectious), topical treatment, long term system antibiotics

46
Q

Corynebacterium pseudotuberculosis

Prevention:

A

Prevention: FLY CONTROL, isolate infected horses, sanitation

47
Q

Corynebacterium spp.

Corynebacterium renale group- Contagious Bovine Pyelonephritis

also called?

A

Corynebacterium renale group- Contagious Bovine Pyelonephritis
* C. renale, C. cystiditis, C. pilosum

48
Q

Corynebacterium spp.

Corynebacterium renale group- Contagious Bovine Pyelonephritis
what is it?

A

Inflammatory of the urinary bladder (cystitis) that can extend to the
ureters and kidneys (pyelonephritis)

49
Q

Corynebacterium spp.

Corynebacterium renale group- Contagious Bovine Pyelonephritis
* Reservoir:

A
  • Reservoir: cows carrying bacteria in their vulva and vagina
50
Q

Corynebacterium spp.

Corynebacterium renale group- Contagious Bovine Pyelonephritis
* Possible contributors to infection:

A

Possible contributors to infection: parturition stress, peak lactation,
high protein diet (increases pH of the urine), trauma the
bladder/urethra via catheter

51
Q

Corynebacterium spp.

Corynebacterium renale group- Contagious Bovine Pyelonephritis
* CS:

A

fever, decreased appetite, painful urination, ammonia odor from
urine, kicking at abdomen due to pain, decreased rumen
contractions, decreased milk production

52
Q

Corynebacterium spp.

Corynebacterium kutscheri- Murine
pseudotuberculosis
where?

A

Corynebacterium kutscheri- Murine

pseudotuberculosis
* Suppurative pneumonia (lungs)
* Nodular lesions in the kidney/liver/heart
* Arthritic lesions in the joints
* Hyperplasia of regional LN’s

53
Q

Rhodococcus overview

what is it? describe

A

Gram pos., cocci or rods, aerobic soil saprophyte, non-motile, **envelope rich in mycolic acids **(hence ACID FAST
PARTIAL), unique salmon pink colored colonies on culture

54
Q

Rhodococcus overview

who gets it? why?

A

Opportunistic pathogen of foals less than 6 mo. old that survives in m**acrophages **which results in **granuloma
formation **(facultative intracellular)

55
Q

Rhodococcus overview

Virulence factors:

A

virulence is maintained in horses and foals are the most susceptible (impaired cellular immunity
in the lungs)

56
Q

Rhodococcus overview

  • Virulence factors:
    what is:
  • vapA protein:
  • Capsular polysaccharides and mycolic acids:
A
  • vapA protein: promote survival in non-activated macrophages
  • Capsular polysaccharides and mycolic acids: slow phagocytosis
57
Q

Rhodococcus overview

bacteria is shed from healthy foals in low #’s or shed from diseased foals in high #’s

this is called?

A
  • Pathogenesis:
58
Q

Rhodococcus overview

Pathogenesis:
how does it happen?

A

Bacteria is excreted from the feces and contaminates the dust and the next foal inhales the bacteria and gets suppurative
bronchopneumonia

59
Q

Rhodococcus overview

Pathogenesis:
what are the predisposing factors?

A
  • Predisposing factors: dry weather, high foal/stocking density, poor grass cover

Q: can it be in feces of healthy foal?

60
Q

Rhodococcus equi

what is it?
who gets it?
where in the body?
when do they get it?
what does it look like?

A

Lung abscessation and bronchopneumonia in foals 1-4 months of age (less than 6 mo. old) inhalation
* Infection occurs in the first 2 weeks of life, but we do not see CS until later because its slowly progressive
* 1 mo. old foals with acute disease: fever, anorexia, cough and dyspnea

61
Q

Rhodococcus equi

CS:
why is it difficult to detect?

A

CS: difficult to see due to the slow progression so we don’t typically see CS until they are severe
* Polysynovitis, intestinal/mesenteric abscesses, ulcerative enterocolitis
* *bronchopheumonia

62
Q

Rhodococcus equi

  • Dx:
A

thoracic auscultation/percussion (crackle, wheezing, dull resonance, asymmetrical), ultrasound thorax to look for nodular
lesions, cytology of respiratory secretions (increased WBCs and neutrophils), culture of BAL

63
Q

Rhodococcus equi

  • Tx:
    survival rate?
    why is it economically important?
A

prolonged combination of antimicrobials (4-6 weeks), supportive therapy (IV fluids)
* WITH therapy there is a survival rate of 70-90%,** WITHOUT therapy there is up to 80% case fatality rate
* Economically important due to: mortality, cost of prolonged treatment, surveillance for early detection, expensive prophylactic
treatments

64
Q

Rhodococcus equi

  • Prevention:
    can you vaccinate?
A

Prevention: give hyperimmune serum to foal in the first month of life, good quality/amount of colostrum, dust control *transmitted by inhaling dust
* No vaccine available

65
Q

Nocardia overview

describe

A

Gram pos., pleomorphic cocci or rods with branching
filaments, aerobic, non-motile, mycolic acid in cell wall
(hence ACID FAST PARTIAL)

66
Q

Nocardia overview

is it:
opportunistic?
contagious?

A

Opportunistic and non-contagious, causing
pyogranulomatous to suppurative disease

67
Q

Nocardia overview

where is it found?
is it pathogenic?
who does it affect?

A

Can be found throughout the environment in the soil and
water, and is typically non-pathogenic if immunocompetent
* **Pathogenic spp. **are saprophyte species found in soil and
decaying vegetation, and are usually involved in nosocomial
infections via skin lesions *no cardiac sounds will take you to the hospital
* Affects animals, people, and wildlife
* Dogs and cattle

68
Q

Nocardia spp.

Canine nocardiosis
what causes it?

A
  • Mostly caused by N. astroides
69
Q

Nocardia spp.

Canine nocardiosis
how is it transmitted?

A
  • Transmission: inhalation, ingestion, skin wounds
70
Q

Nocardia spp.

Canine nocardiosis
what do you look for?

A

Look for sulfur granules in the exudate
* Bacteria surrounded by macrophages and neutrophils

71
Q

Nocardia spp.

Canine nocardiosis
* 3 forms
what are they

A

* Thoracic: pneumonia or pyothorax, fibrovascular proliferation of pleura,
sanguinopurulent fluid (peritoneal empyema)
* Cutaneous: abscesses, ulcers, granulomatous swelling, non-specific loctions
* Disseminated: non-specific organ affected and non-specific CS

72
Q

Nocardia spp.

Bovine Nocardial mastitis
what is it?

A

Chronic mastitis with
multifocal fibrosis (scar tissue)
in the affected gland

73
Q

Nocardia spp.

Bovine Nocardial mastitis
when does it occur?
what does it look like?
what are outbreaks associated with?
what results?

A
  • Sporadic outbreak and
    intermittently see white clots
    in the milk
  • Challenging to treat/control
  • Don’t confuse with S. aureus
  • Outbreaks are **ASSOCIATED
    with dry cow therapy, **maybe
    due to contamination
  • Will occasionally cause fever,
    anorexia and depression

Bacteriology and mycology (6 decks)

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