Organism specific features Flashcards

1
Q

What are the morphologic and culture features of Staphylococcus aureus?

A

Gram-positive cocci
catalase positive
0.5-1.5 µm in diameter, nonmotile, non-spore-forming, facultative anaerobes (with the exception of S. aureus anaerobius)
usually form in clusters.
Many strains produce staphylococcal TOXINS (enterotoxins, the superantigen toxic shock syndrome toxin (TSST-1), and exfoliative toxins)
*unique aspects = coagulase, protein A and species specific teichoic acid

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2
Q

Where is Staph aureus found normally?

A

Staphylococcus aureus are part of human flora, and are primarily found in the nose and skin

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3
Q

How does Staphylococcus aureus cause human disease?

A

Staphylococcus aureus is an opportunistic pathogen that can cause a variety of self-limiting to life-threatening diseases in humans.

  • leading cause of food poisoning, resulting from the consumption of food contaminated with enterotoxins
  • Animal bites can result in local infections, cellulitis, erythema, tenderness, mild fever, adenopathy, and lymphangitis (rarely)
  • Impetigo
  • hydradenitis suppurativa
  • mastitis
  • Scalded skin syndrome is caused by exfoliative toxins secreted on the epidermis and mostly affects neonates and young children
  • Other skin conditions caused by Staphylococcal exfoliative toxins include blisters, skin loss, pimples, furuncles, impetigo, folliculitis, abscesses, poor temperature control, fluid loss, and secondary infection
  • S. aureus can also cause necrotizing fasciitis in immunocompromised individuals, although this is very rare
  • pneumonia (post-viral or post obstruction), empyema, pulm abscess
  • UTI
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4
Q

What are some epidemiological characteristics of Staph aureus?

A

Worldwide distribution.
Staphylococcus aureus is one of the most common causes of skin, soft-tissue, and nosocomial infection
Rates of infection in community settings are increasing
Residents of nursing homes are also at an increased risk of acquiring MRSA
Around 20% of individuals are persistent carriers of Staphylococcus aureus, about 60% are intermittent carriers, and approximately 20% rarely carry it
Children are more likely to be persistent carriers of the bacteria.
Young women are at a higher risk for toxic shock syndrome

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5
Q

What is the infectious dose of staph aureus?

A

For the organism itself to cause illness (as opposed to toxin burden) –> 100,000 organisms

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6
Q

How is disease-causing staph aureus transmitted?

A
  • somewhat trick question as it’s a common colonizer of the human…so usually mucosal breakdown or puncture
  • TOXIN mediated disease = Ingestion of food containing enterotoxins
  • Vertical transmission during vaginal delivery is uncommon
  • Person-to-person transmission occurs through contact with a purulent lesion or with a carrier
  • Unsanitary conditions and crowded community settings increase exposure to S. aureus.
  • Infection may be spread from person-to-person through health care workers or patients
  • Nasal colonization can lead to auto-infection
  • biofilm forming organism so it can be on prosthesis that was implanted or a knife or something
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7
Q

To which drugs is staph aureus normally susceptible?

A

Antibiotics such as cloxacillin and cephalexin are commonly used to treat staph infections.
Vancomycin which is administered intravenously is used to treat MRSA
*the bulky R group penicillins (which are penicillinase-resistant) can treat staph (methicillin, oxacillin, nafcillin, dicloxacillin)
*resistance to these 4 means the strain is resistant to all beta-lactam antibiotics

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8
Q

What different toxins are produced by staph aureus that increase virulence?

A

(main idea) Cytotoxins are integral to colonies of staph aureus causing clinical disease –> they set up infection by secreting death and destruction all around them
*alpha toxin
*beta toxin/sphingomyelinase C
*gamma toxin
*P-V leukocidin
These toxins kill leukocytes, erythrocytes, fibroblasts, platelets, macrophages

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9
Q

(kehl level question) What does catalyse do?

A

catalase is an enzyme that converts hydrogen peroxide into water and oxygen gas. Drop peroxide solution on a colony and bubbles form if catalase is present

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10
Q

What are some other species of staphylococcus that are important to know about for contaminant vs pathogen discussions?

A
Staph capitis (on skin of head and face)
Staph haemolyticus (apocrine gland colonizer)
Staph hominis (apocrine gland colonizer)
***Staph lugdunensis (often a pathogen)
Staph epidermidis
Staph saprophyticus
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11
Q

Why do staph species tend to cluser?

A

Production of coagulase, which will convert fibrinogen to fibrin and form a tiny clot around themselves in serum. Some species don’t have coagulase and are collectively “coag-negative staph”

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12
Q

What diseases are most associated with staph aureus?

A
Toxin mediated diseases (food poisoning, scalded skin syndrome, toxic shock syndrome)
Cutaneus diseases (carbuncles, folliculitis, furuncles, impetigo, wound infections
*other (BLOOD STREAM INFECTIONS, endocarditis, pneumonia, empyema, osteomyelitis, septic arthritis)
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13
Q

What diseases are most associated with staph epidermidis?

A
Bacteremia (be careful --> often contaminant)
endocarditis
surgical wounds
UTI
catheter infections
shunt infections
prosthetic infections
peritoneal dialysates
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14
Q

What dieseases are most associated with staph saprophyticus?

A

UTI (classically young female)

opportunistic infections

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15
Q

What diseases are most associated with staph lugdunensis?

A
(should remember this species as the most important coag negative staph. Recognize it as a pathogen)
Endocarditis
arthritis
bacteremia
opportunistic infections
urinary tract infections
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16
Q

What diseases are most associated with staph haemolyticus?

A
*not often considered a pathogen
Bacteremia
endocarditis
bone and joint infections
UTI
wound infections
opportunistic infections
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17
Q

Can one get colonized by environmental staph aureus?

A

while they live predominantly on the skin of animals, they are rather tough mothers and can live on surfaces for a longer time than you think.

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18
Q

Is there any selective media you could use to recover staph aureus from contaminated or polymicrobial specimens?

A

YES, mannitol-salt agar can be used as staph aureus can survive the salt when other bugs can’t

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19
Q

What is generally thought of the coag negative staph species?

A

Less virulent, still produce the slime layer and biofilm, still stick to surfaces and catheters and prostheses

  • normal human skin flora and mucosa flora
  • live on dry surfaces for a long time (increases contaminant possibility)
20
Q

What is the predominant beta-lactam resistance mechanism for staph species?

A

*If you see mecA –> think MRSA
The mecA gene codes for a special penicillin binding protein, PBP2a, which has low affinity for methicllin and related penicillins and cephalosporins
mecA gene is on the SCCmec cassette chromosome
*there are subtly different flavors of the SCCmec types and show that MRSA is becoming more community based

21
Q

How does the staph aureus superantigen cause problems?

A
The superantigen is the toxic shock syndrome toxin 1 which induces high levels of t-cell proliferation, prompt IL-2 and TNF-alpha release and cause a shock syndrome. 
It does this by binding structural peptides on host T-lymphocyte receptors and macrophage class II histocompatibility antigens, leading to cytokine release.
22
Q

Almost all species of staph are FACULTATIVE anaerobes, but some are strict anaerobes…which ones are strict anaerobes?

A

Staph anaerobius

Staph saccharolyticus

23
Q

There is a protein that staph makes called SSSS…what does that do?

A

SSSS - staph scalded skin syndrome - the exotoxin produced by staph (ET-A and ET-B).

  • both are superantigens in their own right but primarily work in this disease process by being serine proteases on desmoglein 1
  • desmoglein is one of 4 proteins that helps make up desmosomes
  • essentially the serine proteases chew up the proteins that maintain the stratum granulosum and lead to splitting of the epidermis
24
Q

What virulence factors of staph keep it from being destroyed by the immune system?

A

They have a thick polysaccharide capsule that has many different proteins on it

  • recognize the term MSCRAMM
  • essentially they make ‘adhesins’ that stick to surfaces and to the cells of the skin
  • they also make enzymes and secrete them that allow for deeper tissue invasion
  • the capsular polysaccharides themselves protect against complement formation
  • specifically protein A is one of these MSCRAMM things that binds to the Fc portion of IgG and specially protects against opsonization
25
Q

What are some helpful epidemiological numbers for Candida infections to know?

A

Candida spp cause the MAJORITY of fungal infections in the US (and worldwide). While Candida albicans is certainly the most important pathogen (common), non-albicans Candida infections are increasing overall. 75-88% of all fungal infections in teh US are Candida spp.

  • Fungemia is by far most commonly due to candida spp
  • 95% of all cases of Candida are due to 5 spp (in order: albicans, glabrata, parapsilosis, tropicalis, krusei)
  • Thus, it’s best to know the ‘classic’ resistance patterns of the 5 top species)
  • NOTE - Candida auris, should you ever encounter this ID, is scary. It’s pretty resistant and virulent
26
Q

What is fluconazole, and why is it important when discussing Candida spp?

A

Fluconazole is a commonly prescribed antifungal for Candida infections

  • triazole antifungal (often called one of the ‘azoles’)
  • MOA- inhibit the cytochrome P450 enzyme lanosterol demethylase (14alpha-demethylase) encoded by ERG11 gene
  • this inhibition leads to insufficient ergosterol biosynthesis, which is an important yeast cell wall molecule
  • FungiSTATIC (not ‘cidal’) - leading to the desire to use a fungicidal drug first in invasive infection or candidemia
  • another problem with STATIC drugs is increased ‘time’ to create resistance
  • MOST IMPORTANT - different species of candida have different fluconazole susceptibilities
27
Q

Do all spp of Candida respond the same to fluconazole?

A

NO NO NO NO. Identification to the species level is important for this very purpose. Each species has different resistance patterns to the different antifungals

  • important - glabrata = resistant to fluconazole
  • important - lusitania = resistant to amphotericin
28
Q

In regards to fluconazole in particular, what are the main 5 species’ susceptibility patterns?

A
albicans- low incidence of resistance, 0.5-2%
tropicalis - 4-9%
parapsilosis - 2-6%
glabrata - 11-13%
krusei- INNATE resistance
29
Q

What is an echinocandin?

A

Micafungin, anidulafungin, caspofungin

  • TARGET= fungal-specific enzyme glucan synthase
  • results in destruction of the major cell wall polymer
  • fungiCIDAL drug
30
Q

What species of candida is most resistant to echinocandins?

A

GLABRATA
Echinocandin resistance of 8.0%–9.3% was reported by the SENTRY Antimicrobial Surveillance Program for C. glabrata bloodstream isolates from 2006 to 2010 [9], while in a study at Duke hospital over a period of 10 years, echinocandin resistance rose from 2%–3% to >13% in 2009–2010
*at WDL, assume resistance

31
Q

What are the medically important species of Streptococcus?

A
Streptococcus pyogenes (group A)
Streptococcus agalactiae (group B)
Streptococcus pneumoniae
(pyogenic streps): anginosus, constellatus, intermedius
32
Q

Quick overview of streptococcus pyogenes

A

colonizes the oropharynx and skin surface and causes pharyngitis, skin and soft-tissue infections, and non-suppurative infections (rheumatic fever, glomerulonephritis)

33
Q

Quick overview of streptococcus agalactiae

A

colonizes female urogenital tract, also perineal region, causes disease in newborns (sepsis and meningitis) and older patients (also sepsis and meningitis). Can be part of skin/soft tissue infections as well

34
Q

Quick overview of streptococcus pneumoniae

A

colonizes oropharynx and causes pneumonia, sinusitis, otitis media and meningitis

35
Q

Quick overview of important ‘viridans group’ strep

A

anginosus group- abscess former
mitis group - sepsis and endocarditis after mouth operations
salivarius group - sepsis and endocarditis after mouth operations
bovis group - bacteremia in the context of GI cancer

36
Q

Important biochemical properties of the streptococci

A

*catalase NEGATIVE
different and overlapping differential schemes are used for strep
serologic (Lancefield)
hemolytic patters (alpha vs. beta)
biochemical properties
*most simple to think of beta-hemolytic strep as lancefield subdivided and non-beta-hemolytic strep as biochemically subdivided (viridans group)
*often use direct group a antigen testing for rapid diagnosis of the group
*culture or DNA testing for confirmation
*PYR negative (except pyogenes) - mostly PYR to differentiate the enterococci from the staph and most streps
*bacitracin susceptible

37
Q

What toxins and enzymes are important in streptococcus pyogenes?

A

Streptococcal pyrogenic exotoxins (Spe)

  • erythrogenic toxins, similar to c. diphtheriae toxins
  • speA,b,c,f, all act as superantigens
  • these probably involved in nec fasc and strep toxic shock
  • streptolysin…can use to see if exposed
38
Q

what populations should the urine antigen for strep pneumo not be used in ?

A

Pediatric population, less specificity of urine antigen, thus don’t use it in children’s labs.

39
Q

Strep pneumo and bile solubility

A

s. pneumo dissolves readily in bile salts, so it is bile soluble.
Only takes a few minutes to see dissolution
s. pneumo is also optochin susceptible

40
Q

Strep pneumo and optochin

A

SUSCEPTIBLE TO OPTOCHIN (should see a clearing)

41
Q

Brief overview of important stuff with enterococcus

A
  • common UTI agents
  • decently resistant organisms
  • catalase NEGATIVE
  • two main important species: Enterococcus faecalis, Enterococcus faecium
  • less important, but two vanc resistant species are gallinarum and casseliflavus
  • bile salt stable (resistant, don’t dissolve)
  • optochin resistant
42
Q

Brief overview of important stuff for Listeria

A
  • Listeria monocytogenes is the important species
  • gram positive rod (smaller than bacillus)
  • weak beta hemolysis
  • can pair or small chain
  • motile
  • infections are associated with ingestion of contaminated foods (raw veggies or meat or milk)
  • neonatal disease, pregnant women bacteremia, meningitis
43
Q

What are the high yield biochemical properties of the medically important Neisseria species

A

Important species: N. gonorrhoeae and meningitidis
*gram-negative diplococci
*don’t grow easily (need colder temps like 35degrees, humid atmosphere, CO2 supplementation
*oxidase and catalase positive
*glucose oxidation
NOTE: other members of this genus are non-pathogenic normal flora colonizers of upper respiratory tract

44
Q

What toxins does Pseudomonas aeruginosa produce to cause it’s manifestations of disseminated disease?

A

LasA (serine protease)
Las B (zinc metalloprotease)
*both of these proteases are synergistic in their degradation of elastin and result in damage to elastic tissues (like the skin and the lungs), which allows for the hemorrhagic ecthyma gangrenosum lesion and the infiltrative pneumonia destruction picture
Exoenzymes S and T, cytotoxins that are delivered by type III secretion systems
*big problem in burn infections

45
Q

what patient populations are pseudomonas infections almost assumed?

A

cystic fibrosis and burn patients

46
Q

Oxidase in pseudomonas

A

pseudomonas is oxidase positive
(e coli is oxidase negative)
pseudomas is also a non-fermenter

47
Q

What are the properties of pseudomonas on a plate?

A

Oxidase positive
beta-hemolytic (remember some e coli can be too)
non-fermenting
tend to be mucoid, don’t have to be (very mucoid in CF patients