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Bacteriology and Mycology > Staphylococcus > Flashcards

Staphylococcus Flashcards

1
Q

What are the general characteristics of Staphylococcus spp.?

A
  • Gram +
  • Cocci in clusters
  • Facultative Anaerobes
  • Grow in HIGH Salt concentrations (7.5 - 10%)
  • Catalase Positive (differentiate from streptococcus)
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2
Q

What disease does S. aureus cause?

A
  • Mastitis in cattle, sheep, and goats
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3
Q

What disease does S. pseudintermedius cause?

A
  • Pyoderma, Otitis externa, endometritis, cystitis in Dogs
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4
Q

What disease does S. hylcus cause?

A
  • Exudative or Exfoliative dermatitis “Greasy pig disease” in Pigs
  • Skin infections in other animals
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5
Q

What are the diagnostic characteristics of Staphylococcus aureus?

A
  • Double Zone hemolysis
  • Ferments Mannitol
    • Turns Mannitol Salt Agar Yellow
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6
Q

Where can S. aureus be found?

A
  • Commensals on the skin and mucous membranes
  • Nostrils are a major site
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7
Q

What are the Virulence Factors of S. aureus?

A
  • Divided in 3 categories:
    • Cell-Associated Components
    • Exoenzymes
    • Exotoxins
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8
Q

What are the Cell-Associated Components of Virulence Factors?

A
  • Surface Proteins:
    • Protein A
    • Adhesins
  • Capsular polysaccharides
  • peptidoglycan and teichoic acid
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9
Q

What does Protein A do?

A
  • Virulence Factor
  • Binds to Fc region of IgG
    • disrupts opsonization and phagocytosis
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10
Q

What do Adhesins do?

A
  • Virulence Factor
  • Surface proteins that promote attachment to the host proteins
    • Fibronectin-binding protein
    • Collagen-Binding protein
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11
Q

What are capsular polysaccharides?

A
  • Serologically distinct capsule types
  • Interfere with host defense mechanisms by inhibiting attachment of antibodies, induce the release of cytokines
  • Mediate cell binding to epithelial and endothelial cells
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12
Q

What does peptidoglycan and teichoic acid do?

A

stimulate cytokine production

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13
Q

What are the Exoenzymes

A
  • Coagulase
  • Lipase
  • Hyaluronidase
  • Proteases
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14
Q

What does Coagulase do?

A
  • Converts fibrinogen to fibrin
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15
Q

What does Lipase do?

A
  • Hydrolyzes lipid molecules that the host produces in response to infections
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16
Q

What does Hyaluronidase do?

A
  • Digests hyaluronic acid present in connective tissue and promotes spread of the infection
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17
Q

What do Proteases do?

A
  • Breakdown antibodies, antimicrobial peptides, tissue proteins
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18
Q

What do Proteases do?

A
  • Breakdown antibodies, antimicrobial peptides, tissue proteins
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19
Q

What are Exotoxins in staphylococcus spp.

A
  • Toxic Shock Syndrome Toxin
  • Enterotoxins
  • Exfoliative or Epidermolytic toxins
  • Hemolysins
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20
Q

What is toxic shock syndrome toxin?

A
  • Act as super-antigens
  • rarely seen in infections
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21
Q

What are Enterotoxins?

A
  • Foodborne infections in humans
  • Act as a super-antigen
  • produced in contaminated food
  • Resistant to proteases and heat stable, hence not inactivated by cooking
  • Toxin is ingested with food d in the stomach the toxin stimulates vagus nerve endings to induce vomiting and abdominal pain
22
Q

What is staphylococcal Food Poisoning?

A
  • Gastroenteritis: Nausea, vomiting, stomach cramps, diarrhea
    • Salty food like ham
    • Contaminated milk and cheeses
    • Contact with food workers who carry the bacteria
  • Fast acting toxins can cause illness in as little as 30 min
  • Symptoms usually develop within 1-6 hours after eating contaminated food
  • Illness usually mild, recovery in 1-3 days
23
Q

What is staphylococcal Food Poisoning?

A
  • Gastroenteritis: Nausea, vomiting, stomach cramps, diarrhea
    • Salty food like ham
    • Contaminated milk and cheeses
    • Contact with food workers who carry the bacteria
  • Fast acting toxins can cause illness in as little as 30 min
  • Symptoms usually develop within 1-6 hours after eating contaminated food
  • Illness usually mild, recovery in 1-3 days
24
Q

What is staphylococcal Food Poisoning?

A
  • Gastroenteritis: Nausea, vomiting, stomach cramps, diarrhea
    • Salty food like ham
    • Contaminated milk and cheeses
    • Contact with food workers who carry the bacteria
  • Fast acting toxins can cause illness in as little as 30 min
  • Symptoms usually develop within 1-6 hours after eating contaminated food
  • Illness usually mild, recovery in 1-3 days
25
Q

What are Exfoliative or Epidermolytic toxins?

A
  • ETA and ETB
  • Cause skin infections
    • Exfoliative dermatitis in pigs: S. hyicus
    • Pyoderma in dogs: S. pseudintermedius
26
Q

What are Exfoliative or Epidermolytic toxins?

A
  • ETA and ETB
  • Cause skin infections
    • Exfoliative dermatitis in pigs: S. hyicus
    • Pyoderma in dogs: S. pseudintermedius
27
Q

What are Exfoliative or Epidermolytic toxins?

A
  • ETA and ETB
  • Cause skin infections
    • Exfoliative dermatitis in pigs: S. hyicus
    • Pyoderma in dogs: S. pseudintermedius
28
Q

What are Hemolysins?

A
  • Protein toxins that lyse RBCs
  • Produced by S. aureus, S. pseudintermedius, NOT a. hyicus
  • S. aureus produced 4 different hemolysins:
    • α, β, γ, δ,
    • Differ antigenically, biochemically, and in their effects on the RBC of animals species
29
Q

What are Alpha Hemolysins

A
  • Membrane-damaging (pore-forming) toxin
  • Produces a zone of complete hemolysis
  • Human platelets and monocytes are also susceptible to the toxin
    • Release of cytokines triggering production of inflammatory mediators
    • Responsible for the symptom of septic shock
30
Q

What are Beta Hemolysins?

A
  • a sphingomyelinase, damages membranes ring in sphingomyelin lipid
  • Incomplete hemolysis of sheep/cattle erythrocytes
  • AKA “Hot-cold hemolysin”
  • Pathogenic role is not known
31
Q

What is Gamma hemolysin?

A
  • AKA “Leukotoxin” “Leukocidin” “Panton-Valentine Leucocidin”
  • Not al S. aureus strains produce
  • pore-forming toxin
  • gene located on a prophage
32
Q

What is the pathogenesis and pathogenic mechanism of staphylococcus spp?

A
  • Cause pyogenic or suppurative lesions
  • Predisposing factors: skin injury or immune suppression
  • Virulence factors promote:
    • Tissue colonization: Protein A and adhesins
    • Immune evasion: Capsular polysaccharide, teichoic acid, protein A, catalase, and coagulase interfere with opsonization ang phagocytosis
    • Spread: hyaluronidase, lipase, proteases
    • Tissue destruction: exotoxins
  • Minor local skin infections to life-threatening septicemic conditions
33
Q

What are the general characteristics of Staphylococcus spp.?

A
  • Gram +
  • Cocci in clusters
  • Facultative Anaerobes
  • Grow in HIGH Salt concentrations (7.5 - 10%)
  • Catalase Positive (differentiate from streptococcus)
34
Q

What diseases does staphylococcus cause

A
  • Mastitis in Dairy Cows
  • Dermatitis and Joint infections in chickens
  • Exudative dermatitis in pigs
  • Pyoderma in Dogs
35
Q

How does staphylococcus cause Mastitis?

A
  • The Route of infection is via the teat
  • Organisms travel through the teat canal to enter the secretory mammary tissue and attach to ductular and alveolar epithelial cells
  • Milk is a good medium for multiplication of staphylococci and production of toxins cause infiltration of the mammary gland by neutrophils
  • Aggregation of neutrophils cause clots in the milk and intravascular edema
  • Neutrophils obstruct the lobules, which begin to involute
  • Accumulation of fibroblast, macrophages, and leukocytes results in the expansion of the intravascular connective tissue
  • Infection can spread from Cow to Cow with contaminated hands/milking machines or through feces
  • Ranges in severity from mild to gangrenous
36
Q

What percentage of mastitic infections are due to staphylococcus spp?

A

25-30%

37
Q

How do you diagnose Bovine Mastitis?

A
  • Isolation of coagulase-positive or -negative staphylococci from bulk tank milk samples
    • Colonies on blood agar with double zone hemolysis
    • Confirmed by additional biochemical tests
  • Herds with subclinical mastitis are diagnosed based on somatic cell count (SCC) or total bacterial count (BCC) in milk samples
  • Increase in somatic cells is because of increased leukocytes
37
Q

How do you diagnose Bovine Mastitis?

A
  • Isolation of coagulase-positive or -negative staphylococci from bulk tank milk samples
    • Colonies on blood agar with double zone hemolysis
    • Confirmed by additional biochemical tests
  • Herds with subclinical mastitis are diagnosed based on somatic cell count (SCC) or total bacterial count (BCC) in milk samples
  • Increase in somatic cells is because of increased leukocytes
38
Q

What is the treatment for Bovine Mastitis?

A
  • Intra-mammary administration of antibiotics
    • B-lactamase-resistant antibiotics, such as Ceftiofur, Cephalosporin (2nd or 3rd gen), or Cloxacillin
  • Systemic antibiotics are employed to achieve effective concentrations of antibiotics in the mammary tissue
  • No vaccines are available
39
Q

What is Dry Cow Therapy?

A

Administration of antibiotics at the beginning of the dry period, to treat or prevent staphylococcus mastitis

40
Q

What diseases does Staphylococcus produce in Poultry

A
  • Dermatitis, osteomyelitis, arthritis, and synovitis, and occasionally bacteremia or septicemia
  • “Bumblefoot”
  • Lameness has a significant economic impact
41
Q

What does S. hyicus cause in pigs?

A
  • Exudative Dermatitis
    • by exfoliative toxin
  • Predisposing factor: breach in epidermis
42
Q

How does Exudative Dermatitis progress?

A
  • Initially. yellowish brown crusts on the face and ears
  • Severe cases:
    • Skin feels greasy and moist, becomes covered in dark brown coating which entraps dirt
  • Crusty lesions heal or progress to increased exudation with crusts becoming more confluent, blackened, and hard with cracks and furrows.
  • Death from dehydration duet to electrolyte and fluid loss
43
Q

How is Exudative Dermatitis diagnosed?

A
  • Characteristic skin lesions
  • Bacterial isolation
44
Q

How is Exudative Dermatitis treated?

A
  • Antibiotics in early stages
    • Ceftiofur, enrofloxacin, lincomycin, or sulfadimethoxizole/trimethoprin
  • Severely affected animals do not respond
  • S. hyicus strains develop resistance, susceptibility testing is recommended
  • Other treatments include spraying pigs with disinfectants (chlorhexidine, iodine, etc) or antibiotics (novobiocin)
45
Q

What is Canine Pyoderma?

A
  • Caused by S. pseudintermedius
  • Dermatitis and folliculitis, rarely systemic
  • Lesions start as papular (small reddened) eruptions progressing to pustules and small intradermal abscesses
  • Deep skin lesions, “furuncles” (large hemorrhagic bullae), may rupture to become fistulous tracts with pus
46
Q

How is Canine Pyoderma treated?

A
  • Beta-lactams
    • Antimicrobial susceptibility testing
    • Amoxicillin plus clavulanic acid
    • Oxacillin
    • Erythromycin
    • Cephalosporins
47
Q

What is Methicillin Resistant S. aureus (MRSA)?

A
  • S. aureus resistant to Beta-lactam antibiotics
    • Penicillins, cephalosporins, and carbapenems
  • No more virulent than other strains
  • Resistance makes it more difficult to treat with standard antibiotics, therefore more serious
48
Q

How is S. aureus resistant to methicillin?

A
  • Resistance is conferred by a gene called, mecA, which encodes for a variant of penicillin-binding protein (PBP), called PBP2a
  • Acquisition of mecA confers resistance to all B-lactam antibiotics in addition to methicillin
49
Q

What contributes to MRSA infections?

A
  • Contributing factors: Close skin-to-skin contact, openings in the skin such as cuts or abrasions, contaminated items and surfaces, crowded living conditions, and poor hygiene.
  • Hospital-Acquired (HA-MRSA) infections: Wound or surgical sites
  • Community-Associated (CA-MRSA) infections: Athletic facilities, Dorms, Military barracks, Correctional facilities, Day care centers
50
Q

Is there MRSA in animals?

A
  • Reported in all animals
    • particularly cattle and pigs
  • Zoonotic transfer from animal to human or humans to animals (Reverse Zoonosis)
  • Livestock-Associated (LA-MRSA) infections

Bacteriology and Mycology (35 decks)

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