Gram positives Flashcards

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1
Q

Actinobacteria- general characteristics

A

related group of gram-positive organisms- form branching structures similar to fungi
non-spore forming, non-motile
ubiquitous in environment (commensals of plants and animals)
pharmacologically active metabolites- found in ABX and MSG
some genera are pathogenic for humans and animals
mycobacterium (TB)
cornyebacterium
truperella
nocardia
rodococcus
actinomyces
All have mycolic acids in cell walls–> resist phagocytosis

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2
Q

Actinobacterial diseases

A

some are opportunistic, some are highly host-adapted pathogens. Pathology is often similar: chronic inflammation, focal lesions or dissemination (within macs); granulomatous lesions (abscessed, pyelonephritis, lymphadenitis, osteomyelitis)

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3
Q

Immune protection to actinobacterial disease

A

CMI is natural host-response to infection; vaccine induced humoral immunity is effective as well.

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4
Q

treatment with ABX

A

in vitro, sensitive to many abx.

in vivo, poor response due to intracellular location

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5
Q

Nocardia

A

Strictly aerobic
aerial hyphae
widely distributed in soil, water, air and sewage
ACID FAST
non-motile, non-spore forming
12 species: pathogenic to a variety of species

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6
Q

Nocardia species

A

N. asteroides: most frequent nocardial pathogens- SQ infections in dogs acquired through environmental contact
N. brasiliensis: pneumonia in horses
N. otitidis caviarum: bovine mastitis (not very frequent cause), ear infection in guinea pigs.
N. farcinica- common isolate (genome)

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7
Q

Nocardia epidemiology

A

Organism are inhaled, ingested or get in via wound
Direct or hematogenous spread
Resist phagocytosis due to acid-fast cell wall.
Chronic invasive pyogenic infections (no production of sulphur granules)
3 clinical forms: cutaneous, respiratory (pyothorax), and systemic (pyrexia, cough, neurological)
Dogs- 3x more common in males
Cats- mainly thoracic infection
Tx is difficult and prolonged (not penicillin–> not great for intracellular infections).

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8
Q

Trueperella (arcanobacterium)

A
T. pyogenes- first described in 1946
commensal but opportunistic
causes non-specific purulent lesions
focal or disseminated abscesses
wound infection
septic arthritis- esp. in pigs
secondary respiratory infections
reproductive impairment: increase frequency in repro tract- big cause of metritis--> perhaps symbiosis with e. coli. 
Often secondary/mixed infections. 
Broad host spectrum
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9
Q

Viruelnce factors of t. pyogenes

A

protease (necrosis/suppuration)
hemolytic exotoxin (dermonecrotic)
neuraminidase- allows it to adhere to host cell
Pyolysin- resembles thiol-activated toxins. Thiol activated toxins have 2 cys residues that form disulfide bridge. PLO doesn’t form bridge. punches a hole between cholesterol residues of cell membrane to allow leakage of cytoplasm resulting in eventual lysis.

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10
Q

diseases caused by t. pyogenes

A

bovine abortion, porcine abscesses (caseous lesions) and porcine polyarthritis.

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11
Q

Actinomyces species

A
A. bovis, A. viscosus, A. suis
Most non-acid fast, branching
Non-motile, Non-spore forming
Microaerophilic or anaerobic
Produce pyogenic, granulomatous reactions with production of sulphur granules.
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12
Q

A. bovis

A

Component of normal mouth flora- anaerobic
Thick, yellow pus (sulphur granules)
Causes actinomycosis/lumpy jaw in cattle
Invasion through wound/rough feed/damaged mucosa- osteomyelitis (granulomas form in bone) animal stops eating
other soft tissue infection- i.e. in GI tract
mastitis: perhaps from suckling damage.

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13
Q

A. viscosus

A

Mainly dogs (but also pigs, goats, cats, cattle and horses)
Virulence factor: fimbriae- adherence to teeth- plaque?
Similar lesions to Nocardia (but nocardia doesn’t produce sulphur granules)
Localized, pyogranulomatous lesions
Two main conditions: thoracic lesions and osteomyelitis

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14
Q

A. suis

A

Mastitis in pigs due to suckling trauma

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15
Q

Corynebacterium

A

diverse genus, small pleomorphic gram positives
look like chinese letters on stain
pyogenic
common commensals

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16
Q

C. renale group

A

C. renale, C. pilosum, C. cystitidis- all cause cystitis and pyelonephritis in cattle

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16
Q

C. renale group

A

C. renale, C. pilosum, C. cystitidis- all cause cystitis and pyelonephritis in cattle

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17
Q

Diphtheria group

A

C. diphtheria, C. ulcerans, C. pseudotuberculosis

cause various diseases of cats, cattle horses, small ruminants and humans

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17
Q

Diphtheria group

A

C. diphtheria, C. ulcerans, C. pseudotuberculosis

cause various diseases of cats, cattle horses, small ruminants and humans

20
Q

C. renale group

A

C. renale most frequently encountered, followed by C. cystitis and c. pilosum
opportunist- highly adapted–>when stressed, cause disease
Causes cystitis, pyelonephritis and balanoposthitis (inflammation of glans and foreskin)
Pre-disposing factors: pregnancy, parturition, post-mating.
90% of bulls have c. cystitidis in prepuce- means by which organism can be transferred.

21
Q

Virulence factors of C. renale group

A

Pili- adherence
Renalin- cell lysis–> causes clots
Urease–> breaks down urea- provides N source for which to grow
Caseinase–> proteolytic enzyme allows organism to obtain nutrients.

22
Q

Pathogenesis of C. renale

A

adhere to urogenital mucoas; proliferation during stress; ascending infection (through bladder into kidney); inflammation; cystitis/pyelonephritis

23
Q

Diphtheria group

A

C. diphtheria, C. ulcerans, C. pseudotuberculosis

24
Q

Diseases caused by diphtheria group

A

C. diphtheria- URI in humans
C. pseudotuberculosis- various pyogenic infections
C. ulcerans- nasal congestion in cats, mastitis in cows

25
Q

Cornyebacterium pseudotuberculosis-general characteristics

A

facultatively anaerobic, non-encapsulated, non-spore forming, non-motile, catalase-positive, non-acid fast

26
Q

2 biotypes of corynebacterium

A

1) ovis: non-nitrate reducing; infects sheep and goats (caseous lymphadenitis)
2) equi: nitrate-reducing; predominantly infects horses.
Evolution of these two strains by horizontal gene transfer (phage)

27
Q

Caseous lymphadenitis

A

Introduced into UK in 1989
Leads to fibrous, encapsulated lesions at various sites.
Significant financial loss to producers- v. chronic disease, doesn’t seem to kill animals outright.
Carcass condemnation at slaughter, decreased wool, milk production, repro performance

28
Q

Pathogenesis of CLA

A

C. pseudotubrculosis gainst entry to host through wounds
Normally transfer of pus (direct contact or flies)
Drains from point of entry to local LN and spreads within animal from there.

29
Q

Virulence factors of C. pseudoTB

A

Phospholipase D: sphingomyelinase- causes vascular permeability, antichemotactic lethal for neutrophils, complement depletion
Mycolic acid (cell wall): toxicity, survival within macrophages
Serine protease: undefined function, possibly survival within macrophages
Siderophore: acquistion of iron from host–> animal tries to decrease iron availability via transferrin and lactoferrin

30
Q

Diagnosis of C. pseudoTB

A

cAMP test: synergistic lysis between S. aureus and group B. strep (strep agalactiae)
cAMP inhibition test: inhibition of synergistic lysis between S. aureus and group B strep

31
Q

Prevention strategies of CLA

A

diagnosis/vax
PLD is found to be a protective antigen.
Diagnosis: ABs against PLD common in infected animals; detection of anti-PLD abs is a marker of infection.

32
Q

Listeria species

A

L. monocytogenes: meningoencephalitis, septicemia, abortion, pyogenic infection
L. ivanovii: abortion, systemic infection

33
Q

Epidemiology of listeria

A

Common commenal (tonsils, intestine) and enviromental organisms. Grow at temps from 4-45 degrees C, ph 6-9.6
Incidence relates to mgmt/husbandry, silage feeding, seasonally
Predisposed by trauma, immunocompromise, hormonal alterations

34
Q

Listeriosis in Ruminants- symptoms/clinical signs

A

Meningoencephalitis
common=circling disease (small rums.)–circles in one direction only
Unilateral facial paralysis, difficult swallowing, fever, blindness, headpressing, paralysis, death in 2-3 days.
Infection happens through cutting of mouth through silage. Bug goes into CN V–> brain.

35
Q

Listeria in pregnant animals

A

may loclaize in placentomes: cross-over aniotic fluids, multiples; ingested by fetus–> fetal death/abortion

36
Q

Listeria in milking cows

A

Mammary gland can be involved: subclinical mastitis, contamination of milk, may survive low temp pasteruization inside milking tanks; lengthy survival in nature

37
Q

Modes of access of listeria

A

entry also by nasal mucosa, conjunctiva
direct access to CNS via dental plates of CN V ganglia
Can survive within macrophages–> can serve as source of infection for humans

38
Q

Pathogenesis of listeria

A

1) tooth loss/cutting–> oral inoculation–> CN V—> brain stem–> meningoencephalitis
2) naive/neonatal animals–> epithelial invasion –> bacteremia–> neonatal septicemia
3) pregnancy –> epithelial invasion –> bactermia –> placentitis –> abortion

39
Q

Pathogenic mechanisms

A

facultative intracellular parasites surviving in macrophage and epithelial cells
cell uptake by bacterial protein internalin
Inside the cell, they escape the phagolysosome, multiply in the cytoplasm and via actin based motility, spread laterally to adjacent cells
Escape epithelium and are taken up by polymorphonuclear neutrophils and macrophages. these cells are killed and the organism may spread systemically.
Listeria is non-motile, but it hijacks the cytoskeleton->polymerizes actin–>forms tail.

40
Q

Virulence factor of listeria

A

Listeriolysin (LLO): thiol-activated toxin; mediates escape from phagocytic vesicle. Bacteria polymerize actin, form tails–> bacteria moves through cytoplasm, invade adjacent cells. Secreted actin nucleating factor (ActA), localized at one of the bacterium

41
Q

Food products associated with listeria

A

raw, unpasteurized milk products
feta, camembert, blue cheese
raw, cooked ready to eat meat and poultry, undercooked hotdogs and chicken
fresh, frozen and processed seafoods.

42
Q

Cutaneous listeriosis in vets

A

most develop lesions 1-4 days after attending congenitally infected bovines.

43
Q

Erysipelothrix rhusiopathiae- general characteristics

A

commensal, widespread in animals and infects man
grows at 4-37 degrees C
infection in pigs, sheep, turkeys and other
smooth and rough forms associated with the disease

44
Q

E. rhusiopathiae smooth and rough form- diseases caused

A

Smooth: acute septicemia in pigs, turkeys, sub-acute skin lesions in pigs
Rough: chronic arthritis in sheep, endocarditis in pigs

45
Q

Pathogenesis of E. rhusiopathiae

A

in Pigs: commensal in tonsils, RES, bone marrow and many other organs
Depression of host defenses
Multiplication of virulent strains (reversion to smooth)
Entry via tonsils or cuts/abrasions
Invades n’phils
Acute: septicemia- fever, anorexia, DIC, hemorrhage, lymphadenitis, fatal
Sub-acute (utricarial form): malaise, fever, DIC, diamond-shaped epidermal lesions
Chronic: arthritis/endocarditis: persistent, erosive, chronic inflammation, ill-thrift