Review of resp infection Flashcards

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1
Q

What does the URT and LRT consist of?

A

The URT consists of middle ear, mastoid cavity, nasal sinuses, and nasopharynx
The LRT extends from larynx to the lungs
regardless many infections are from infection of throat, may responsible for RTI are from normal flora of naso,oro and laryngopharynx

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2
Q

What are the scientific names for organisms involved in vincents angina?

A

Treponema vincentii are the spirochetes and fusobacterium sp are the GNB which have pointy ends

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3
Q

What do we usually culture a throat swab with?

A

A BA plate with a bacitracin disc to look for B haemolytic strep (mostly group A)

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4
Q

Gram stains of sputum, how to ID M cat? Patient with cystic fibrosis, strep pneumonia, aspergillus

A

squamous cells are contaminants
GNC that are diplococci - M catarrhalis, also sometimes doesn’t decolourise
GPB not long enough to be bacillus and in pairs, V shape, one end slightly wider - ?corynebacteria
cystic fibrosis- GNB inside mucous- serpentine chains
GNC with capsule more likely to be Neiserria
strep pneumoniae- GPC looks elongated, may have halo
aspergillus is red hyphae fungal
Psuedomonas aeurginosa has slime layer seen
small GNB haemophilus sp

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5
Q

Which organisms are GNIDC

A

gram neg intraceullar diplococci include M cat, N meningitidis and N gonorrhea (less likely)

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6
Q

Which genus is a gram negative coccobacillus? (short rod) can also produce cocci. What infections is it associated with

A

Acinetobacter sp.
Skin and wound infections pneumonia, endocarditis, UTI, occasional conjunctivitis
- Second most commonly isolated non-fermenter (no 1 is?)

  • Major cause of Hospital acquired infection - Predominant infection - pneumonia
  • can cause UTI, bacteraemia, wound infections,
  • especially in debilitated patients (burns, ICU, surgery)
  • Hx antibiotic therapy esp. 3GC
  • Problem in respirators (found in tap water)
  • Can survive on fomites for extended periods
  • Capsule, slime production in mixed infections, antibiotic resistance
    Speciation of the main species with MADI-TOF MS is considered to be reasonably good
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7
Q

how do we differentiate between acinetobacter baumannii and a. lwoffii?

A

Baumannii grows at 42 degrees while lwoffii doesn’t. both are OX and motility neg, grows on MAC but baumannii is OF glucose pos while lwoffii is not pos

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8
Q

WHhat are characteristics of acinetobacter sp?

A

GNC/B can look like GPC (retain crystal violet like M cat) in direct blood culture smears
non pigmented colonies convex, some B haemolytic
growth on MAC but all LAC neg - can produce purple pigment
ox neg, non motile, obligate anaerobe, OF oxidative
quite good with commercial kits

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9
Q

What resistance is common for a. baumannii and a lwoffii?

A

lwoffii has large inhibitory zone around AMP, smaller around cephalexin, R to trimethoprim (W) and lack of synergy with sulphonamide (SXT)
baumanii large inhibitory zone around AMC, small around AMP and none around cephalexin (so overall less S)

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10
Q

what are the normal habitats of Pseudomonas, Burkholderia, stenotrophomonas? Are they opportunistic? what are the main pathogens of the 3

A

they are environmental - soil plants water supplies, resp equipment, contact lens sol
yes they are opportunistic pathogens for immunocompromised (young, old, sick) - decreased host defences or access to sterile sites - burns, puncture wounds, aerosols
Intrinsically resistant to a range of antimicrobials and disinfectants
Psuedomonas aeuroginosa, Burkholderia cepacia, stenotrophomonas maltophilia

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11
Q

Which infections do P aeruginosa cause?

A

UTI, Burns, Skin lesions/puncture wounds/trauma
* Lower RTI - cystic fibrosis (mucoid isolates)
* Upper RTI - ear infections, conjunctivitis
- Otitis externa (70% of all OE cases) incl. swimmer’s ear May see a distinctive yellow or green pigments
* Paronychia (infected nails), bacteremia

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12
Q

How to treat P. aeruginosa?

A

Test sensitivity
- Carboxypenicillins (carbenicillin, ticarcillin)
- Ureidopenicillins (mezlocillin, piperacillin)
- Antipseudomonal cephalosporins (ceftazidime)
- Monobactams (aztreonam)
- Carbapenems (imipenem, meropenem)
- Quinolones (ciprofloxacin, levofloxacin)
- Aminoglycosides (gentamicin, tobramycin, amikacin)
* Resistant to:
- All other penicillins and cephalosporins
* Some strains very difficult to treat(ESBLs and metalloβ-lactamases)
-Ceftazidime and cefepime are possible anti-
Pseudomonas cephalosporins. The majority are not suitable (R)

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12
Q

How to diff between the fluoro group of psuedomonas- aeruginosa, fluorescens, putida

A

All pyoverdin pos (yellow), P. aeuroginosa is the only one pyocyanin (green pigment) and only one that grows at 42 degrees
fluorescens is pos for gelatin hydrolysis while putida is neg

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12
Q

Psuedomonas aeruginosa vs stenotrophomonas maltophilia C390

A

P aeruginosa is R, MIC higher than 50 ug/mL and S. maltophilia is S. on MH plates incubate for 18-24hrs, read zone diameter of inhibition zone

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12
Q

Features of Burkholderia cepacia. what can it cause?

A

Not a single phenotype- a complex of 18 species, exposure to contam fluids, dust/environment, also found in hospitals (even disinfectants)
cause pneumonia, uti, endocarditis, conjunctivitis, common in cystic fibrosis patients (measure of worsening disease in lungs, often seen w mucoid P aeuroginosa)
smooth slightly raised colonies grey or yellow pigment, dirt like odour, R to a range of antimicrobial agents
ID with supplement commercial kits with trad biochem tests - PCR or malditof (not perfect- if green pigment not aeromonas)
B. cepacia complex until PCR and RE digest analyse can provide ID

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13
Q

what is B cepacia resistance

A

Test sensitivity to:
- SXT (cotrimoxazole) - drug of choice
- Ureidopenicillins (mezlocillin, piperacillin) - Carbapenems (imipenem, meropenem)
- Cephalosporins (3GC)
* Resistant to:
- Aminoglycosides (gentamicin, tobramycin, amikacin) - Polymyxin B

14
Q

Stenotrophomonas maltophilia characteristics, which infections can it cause? how do virulence factors affect it?

A

Previously Pseudomonas then Xanthomonas maltophilia, now other species have been isolated from soil, sludge, sewage none associated w human infection
widely dist in nature, not part of human NF in healthy humans, common in hospital environment, can colonise skin and RT of long stay patients, clinical sig can be hard to establish
can cause UTI, bacteremia, wound infection, RTI in burns ICU patients- hospital mortality 43%, community infection rare
virulence factor means R to many antimicrobials and disinfectants

15
Q

colony morph of s. maltophilia?

A

GNB with v tiny colonies after 24hrs, yellow on sensi plate, much paler green than burkholderia, more yellow green

16
Q

how to treat stenotrophomonas maltophilia?

A

Test sensitivity to:
- SXT (cotrimoxazole) - drug of choice
* Although rare, can be R to sulphafurazole (see next slide) - Colistin and Polymyxin B
* Likely to be resistant to:
- Ureidopenicillins (mezlocillin, piperacillin) - Carbapenems (imipenem, meropenem)
- Cephalosporins (3GC)
* Intrinsic Resistance to:
- Aminoglycosides (gentamicin, tobramycin, amikacin) - Most B-lactams (penicillins, cephalosporins)

17
Q

S. maltophilia R on plates

A

No inhibitory zone around IPM, pear shape zone of inhibition between trimethoprim -sulfamethoxazol (SXT) and trimethoprim (W) and resistant colonies seen within TIM and ATM zones.

if sulphonamide resistant:
Although we recommend that S. maltophilia be reported resistant to all β-lactam antibiotics (Table 12.4), this can lead to a therapeutic dilemma when the isolate is resistant to sulphafurazole (Plate
11.15.B) or the patient is allergic to sulphonamides. In these difficult, uncommon situations, test aztreonam, ceftazidime, piperacillin, Timentin, Tazocin, ciprofloxacin and moxifloxacin using the criteria set out for Pseudomonas species (susceptibility equals an annular radius of ≥ 6 mm). A warning such as “A combination of antibiotics is necessary for successful therapy” should then be issued with the susceptibility report.

18
Q

What diseases do Haemophilus cause? Which is the main pathogen? What does H. influenza var aegypticus, H. ducreyi cause? which one is not NF in humans? which haemolphilus species are?

A

Haemophilus influenzae is the main pathogen that causes: acute epiglottitis, conjunctivitis, otitis media, pneumonia including septiaemia and meningitis and cellulitis. primarily can be part of oral flora

H influenzae var aegypticus causes acute purulent conjunctivitis (pink eye) and brazilian purpuric fever (meningitis, bacteriamia, rash fever)

H. ducreyi is the non-NF of humans and can cause chancroid (soft sore)

H. haemolyticus, H parainfluenzae, H parahaemolyticus and others are considered NF of URT - can cause infections in/out of the area

19
Q

what are the lab characteristics of haemophilus sp

A

V small GNB- often described as GNCB
grey translucent flat colonies on CHOC from a RESPIRATORY site, NG on selective/diff media (MAC CLED etc), most wont grow on BA or v poorly grows

some Haemophilus sp can prod haemolysin that access X and V factors on BA
S aureus releases NAD - V factor and Strep pyogenes haemolysin lyses RBCs releasing X+V factors

20
Q

What are the types of H influenzae? and which strains are the more virulent?

A

there are types a-f, typing based on specific capsule antigens with type B being the most virulent
Hib vaccine since 90s for children not protective for type a, c-f
encapsulated strains more virulent (infections can be life threatening

21
Q

how can we differentiate haemophilus sp? (X and V factors)

A

H influenzae, H influenzae var aegypticus, H. haemolyticus (haemolytic on BA) = require both X and V factor

H ducreyi (haemolytic on BA) and h aphrophilus require only X factor

Requirement for V factor ONLY
- Haemophilus parainfluenzae
- Haemophilus parahaemolyticus (haemolytic on BA)
- Aggregatibacter (Haemophilus) segnis
- Aggregatibacter (Haemophilus) paraphrophilus
- Haemophilus paraphrophaemolyticus (haemolytic BA)

22
Q

What were the past names of Moraxella catarrhalis? where is it NF?

A

Micrococcus catarrhalis and Neisseria catarrhalis, Branhamella catarrhalis

NF of the URT esp in 50% of healthy children

23
Q

which diseases do M. catarrhalis cause?

A

It is an opportunistic pathogen most commonly associated with RT infection- 15% od cases are otitis media (3rd most common cause in children), pneumonia esp in adults with Chronic Obstructive Pulmonary Disease, sinusitis, chronic bronchitis

can be isolated from wound and eye infections and can cause systemic infection (rare)

24
Q

HOW CAN WE TREAT M. catarrhalis? What is BRO1 and BRO2?

A

more than 70% can produce B lactamases.
bro= branhamella moraxella, enzyme 1 and 2.
both have same activity, encode for R to penicillins 90% are BRO1 strains

therefore test any isolate S to penicillins

can use nitrocefin discs to detect- inc S compared to other methods, suitable for M.cat, H influenza, N gonorrhoea, staph, enterococci. not for enterobacterales or Pseudomonas. moisten disc and add inoculum, pos= pink after 5mins, up to 60mins staph (= produces penicillinases even if isolate is S/produces zone around Pc= m cat/other) S to Pc is rare for M cat

treat w augmentin, 2GC, 3GC, erythromicin

24
Q

What are the lab characteristics of M cat? Which organism can it be confused with on gram stain?
What enzyme can it produce?

A

GNC- some may not decolourise. confuse with pathogenic Neiserria on stain

Hockey puck appearance grey opaque. optimal growth at 35 but also can grow at 22
capnophilic - likes moist conditions
grow on nutrient and BA++

Oxidase pos, cat pos. NG on MAC
Produces butyrate esterase (hydrolyses tributryin)

Neisseria (pathogenic) don’t grow well on BA (need? TM, Gc, NYC)

M cat also cant break down sugars - no result in OF test or in CHO tests

25
Q

How can we tell GNC Neiserria gonorrhoea, n. meningitidis and n lactamica? Growth on BA, (all ng on MAC), all grow on TM, GC, NYC (while M cat is variable), CTA sugars and all neg for TRIB (m cat pos)

A

N. gonorrhoea NG ON BLOOD, only positive for glucose
N. meningitidis has WEAK growth on BA, pos for glucose and maltose
N. lactamica has growth on BA, pos for glucose, maltose and lactose

26
Q

Where is Strep pneumoniae NF, when does serious infections occur? What infections can it cause, what are predisposing factors to infection?

A

NF in URT, serious infection when decrease in circulating Ig (less than 3yrs, greater than 65)
incidence of carriage in 1-3yr olds of 40-60%, in closed populations >60%

cause infections pneumonia, septicaemia, meningitis, sinusitis otitis media

predisposing factors = bronchopulmonary disease, compromised humoral immunity (ab), prior viral infection

27
Q

what are the virulence factors of S pneumonia? (3)

A
  1. polysaccharide capsule- resist opsonisation and phagocytosis, antigenic and the antigen target in vaccine dev
  2. Pseumolysin and alpha haemolysin- both target host cells
  3. Enzymes - hyaluronidase, neuraminidase (cell adherence) IgA1 proteases inactivation assist in invading mucosal surfaces

currently see inc in S pneumonia resistance to Pc worldwide - must determine MIC of isolate to Pc if appears to be Pc sensitive

28
Q

What are S pneumoniae differential features?

A

gram pos diplococci, fastidious only grows on BA and choc alpha haemolytic
either mucoid or draughtsman
not typeable by lancefield but by being optochin sensitive and bile soluble
if appears S to penicillin- determine MIC for penicillin (E test or other)