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Microbiology > Gram Positives > Flashcards

Gram Positives Flashcards

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Biology 101 flashcards
1
Q

Nocardia spp:

Main characteristics.

A
  • Strictly Aerobic
  • Acid fast (ZN stain)
  • Non motile
  • Non spore forming.
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2
Q

How is Nocarida contracted, spread?

What kind of infections does it form?

A

Infection through contact, inhalation, ingestion.

Direct or hematgoenous spread.

Resists phagocytosis.

Forms chronic invasive pyogenic infections. (no sulphur granules)

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3
Q

What are the 3 clinical forms of Nocardia spp?

What does Nocarida contain in its cell wall to allow it to survive in the phagocyte?

A
  1. Cutaenous
  2. Respiratory (pyothorax)
  3. Systemic (pyrexia, cough, neurological, resembles distemper)
  4. Mycolic acids in its cell wall help its survival in the macrophage. (similar to mycobacterium- resits lysosome digestion)
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4
Q

Nocardia asteroides:

Why is it unique and What does it cause?

A

Most frequent nocardial pathgoen causing subcutaneous infections in dogs.

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5
Q

Arcanobacterium Pyogenes

A.K.A TRUEPERELLA.

A
  • Common organism in abscesses in cattle, sheep and pigs.
  • Shows intense Beta-Hemolysis when cultured.
  • Commensal, Causes non-specific purulent lesions and abscesses
  • Often secondary/ mixed infections:
    1. Summer mastitis with S. dysgalactiae
    2. Foot abscesses in sheep and cattle with F. necrophorum
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6
Q

What are the virulence factors for A. pyogenes?

A
  1. Protease
  2. Hemolytic exotoxin
  3. Neuraminidase- allows adhesion to host cell wall.
  4. **Pyolysin (PLO)- significant virulence factor: **
    - - resembles thiol activated toxins (but not thiol activated)
    - - PLO deficient mutants are avirulent.
    - - the disulphide bridge allows the toxin to be active.
    * *– Punches a hole in the cell membranes containing cholesterol allowing metabolites to leak out and bacteria enters. Cell death. **
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7
Q

Actinomyces spp:

What are the 3 veterinary forms?

What are characteristics of it?

What kind of infections does it cause?

A
  • Actinomyces bovis,
  • Actinomyces viscosus,
  • Actinomyces suis
  • Non acid fast
  • non motile
  • non spore forming
  • microaerophilic or aerobic
  • produce **pyogenic GRANULOMATOUS reactions (contain sulphur granules) (vs. nocardia which produces chronic invasive pyogenic infections with NO SULPHUR GRANULES) **
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8
Q

Actinomyces Bovis:

What disease does it cause in cattle and what disease is it often confused with?

How does it cause infection?

A
  • Component of the normal mouth flora- Anaerobic
  • Thick yellow pus (sulphur granules)
  • Causes actinomycosis (lumpy jaw) in cattle and is often confused with wooden tongue caused by actinobacillus.
  • Invasion through wound/ rough feed/ damaged mucosa- causes osteomyelitis and the animal stops eating causing rapid degeneration.
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9
Q

Actinomyces viscosus

What species does it primarily effect?

Where do they adhere and how?

What kind of infection do they cause?

A

Affects mainly dogs.

Fimbrae adhere to teeth or plaque on teeth

Cause similar lesions to Nocardia however **contains sulphur granules : Localized pyogranulomatous lesions with sulphur granules. **

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10
Q

What are two main conditions caused by Actinomyces viscosus?

A
  1. Thracic lesions (pleural periardial flud, lung lesions)
  2. Osteomyelitis
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11
Q

Actionmyces Suis:

What species does it affect and what disease does it cause?

A

Pigs- causes mastitis. Trauma initiates disease.

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12
Q

Cornyebacterium

A

Small pleomorphic( no real fixed shape) gram positive rods

These guys have snapping division therefore they resemble chinese lettering when examining a gram stain.

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13
Q

What are the Cornyebacterium species of Veterinary interest and what diseases do they cause?

A

C. renale group

  1. C. renale
  2. C.pilosum
  3. C.cytitidis

Diptheria group

  1. C diphtheria
  2. C.ulcerans
  3. C.pseudotuberculosis.
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14
Q

What diseases does the C. renale group cause?

What are the predisposing factors?

A

The C. renale group are opportunistic pathogens.

Cause cytitis, pyelonephritis, balanoposthitis ( inflammation of the glans penis & foreskin)

Predisposing fxs: Pregnancy, parturition, post mating

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15
Q

What are the virulence factors for C. renale group?

A
  1. Pili-adherance
  2. Renalin- cause clots in urine and cell lysis
  3. Urease
  4. Caseinase
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16
Q

What is the pathogenesis associated with C. renale group?

A

Adhere to urogenital mucosa.

Stress

Proliferation

Ascending infection

inflammation

Cysitis/ Pyelonephritis.

17
Q

The diphtheria group requires what to be able to be pathogenic?

A

Beta corynephages (tox +) gene which encodes the diphtheria toxin. Without this gene diphtheria is not pathogenic.

18
Q

Corynebacterium Ulcerans

A

Cat is a reservoir. Organisms isolated from cats with bilateral nasal discharge.

Zoonotic

Potential reservoir for human infection.

19
Q

Corynebacterium pseudotuberculosis

What are the two forms?

A

Facultative anaerobic, non encapsulated, non spore forming, non motile, catalase positive, non acid fast

False tuberculosis “forms similar lesions to tuberculosis”

2 forms:

  1. Ovis- non nitrate reducing (doesn’t produce nitrate), infects sheep, goats (CLA)
  2. Equi- Nitrate reducing, infects horses (produces nitrate)
20
Q

What is Caseous Lymphadenitis?

Pathogenesis?

A

CLA

Fibrous encapsulated lesions.

Caused significant financial/ economic losses.

C. pseudotuberculosis gains entry into host through wounds via shearing or fighting.

Normally transfer of pus via direct contact or flies.

From point of entry drains to local drainage lymph node, and spreads within animal from there.

Lesions tend to be in the head and neck.

21
Q

What are the virulence factors associated with C. pseudotuberculosis & CLA?

A
  1. Phospholipase D (PLD)
    - - produces sphingomyelinase degrades sphingomyelin
  2. Mycolic acid (cell wall lipid)
    - -toxicity, survival within macrophages
  3. Serine protease (Cp40)
  4. Siderophore
    - - Iron uptake from host
22
Q

Listeria monocytogenes:

What disease does it cause?

A

Meningoencephalitis

Septicemia

abortion

pyogenic infection

23
Q

How are cattle/ man infected by Listeriosis?

A
  • Primarily through infected silage.
  • The cattle eats the silage, it get an intestinal colonization, which can cause septicemia. If septicemic will cause abortion, CNS problems, and effect the meat which man will eat.
  • Also from intestinal colonization, cattle will defecate and other cattle will get mastitis from infected feces. Milk will become infected and man will drink the milk.
24
Q

Listeriosis in Ruminants:

Meningoencephalitis

How does infection occur?

A

Common= circling disease (small ruminants)

animals circle in one direction only

unilateral facial paralysis, difficulty swallowing

fever, blindness, headpressing

paralysis, death in 2-3 days.

Infection: Listeria enters wound/ lesion/ cut/ tooth loss in oral cavity, travels through the trigeminal nerve into the brain stem causing meningoencephalitis.

25
Q

Listeriosis transmission from materanl to neonate

mastitis

A

Listeriosis may localize in placentomes and cross over to amniotic fluid, mulitplies, ingested by fetus, causing death/ abortion.

In milking cows, may cause mastitis, contamination of milk

26
Q

Listeriosis Pathogensis:

Meningoencephalitis

Neonatal septicemia

Abortion

A
  • tooth loss/ cutting
  • oral inoculation
  • trigeminal nerve
  • brain stem
  • MENINGOENCEPHALITIS “circling disease”

Naive/ neonatal animal or Pregnancy

epithelial invasion

bacteremia

Neontal septicemia or (Placentitis –> Abortion)

27
Q

Listeria Pathogenic mechanisms:

A

**Facultative intracellular parasites surviving in macropohages and epithelial cells. **

Cell uptake induced by bacterial protein internalin.

Inside the cell they escape the phagolysosome, multiply in the cytoplasm and spread laterally to adjacent cells via actin based motlity

They escape the epithelium and are taken up the PMN and macrophages

These cells are killed and the organism may spread systemically.

28
Q

Listeriosis Virulence factors

A
  • Listeriolysin is a MAJOR virulence factor.
  • -thiol activated toxin
  • -mediates escape from phagocytic vessicle.
  • **Bacteria polymerize actin and form tails. **
  • -bacteria move through cytoplasm, invade adjacent cells.
  • -Secreted acin nucleating factor: ActA
  • -Localized at one end of the bacterium, not found in tail.
29
Q

Describe how both the CAMP test and the CAMP-inhibition test work.

A

CAMP test:

  • Streak S. aureus producing B- hemolysis using Beta-hemolysin (incomplete hemolysis). Perpendicular to this streak you inoculate with Streptococcus agalactiae (Group B strep) which is also B- hemolytic. Synergistically, the Beta hemolysis between the two will form an ‘arrow head’ appearnce zone of complete hemolysis.

CAMP inhibition test:

Same procedure except add an inoculation with Corynebacteria pseudotuberculosis perpendicularly. Due to the phospholipase D virulence factor which produce sphingomyelinase, this will inhibit the synergistic lysis effect between S. aureus and Group B strep. tf

Microbiology (10 decks)

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