Gram positives Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Immune protection to actinobacterial disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

treatment with ABX

A

in vitro, sensitive to many abx.

in vivo, poor response due to intracellular location

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

diseases caused by t. pyogenes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

A. suis

A

Mastitis in pigs due to suckling trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Corynebacterium

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

C. renale group

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

C. renale group

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Diphtheria group

A

C. diphtheria, C. ulcerans, C. pseudotuberculosis

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Cornyebacterium pseudotuberculosis-general characteristics
facultatively anaerobic, non-encapsulated, non-spore forming, non-motile, catalase-positive, non-acid fast
26
2 biotypes of corynebacterium
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
Caseous lymphadenitis
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
Pathogenesis of CLA
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
Virulence factors of C. pseudoTB
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
Diagnosis of C. pseudoTB
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
Prevention strategies of CLA
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
Listeria species
L. monocytogenes: meningoencephalitis, septicemia, abortion, pyogenic infection L. ivanovii: abortion, systemic infection
33
Epidemiology of listeria
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
Listeriosis in Ruminants- symptoms/clinical signs
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
Listeria in pregnant animals
may loclaize in placentomes: cross-over aniotic fluids, multiples; ingested by fetus--> fetal death/abortion
36
Listeria in milking cows
Mammary gland can be involved: subclinical mastitis, contamination of milk, may survive low temp pasteruization inside milking tanks; lengthy survival in nature
37
Modes of access of listeria
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
Pathogenesis of listeria
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
Pathogenic mechanisms
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
Virulence factor of listeria
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
Food products associated with listeria
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
Cutaneous listeriosis in vets
most develop lesions 1-4 days after attending congenitally infected bovines.
43
Erysipelothrix rhusiopathiae- general characteristics
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
E. rhusiopathiae smooth and rough form- diseases caused
Smooth: acute septicemia in pigs, turkeys, sub-acute skin lesions in pigs Rough: chronic arthritis in sheep, endocarditis in pigs
45
Pathogenesis of E. rhusiopathiae
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