HOSPITAL ACQUIRED INFECTIONS Flashcards
(76 cards)
1
Q
WHAT IS THE TERM USED FOR INFECTIONS ORIGINATING IN A HOSPITAL?
A
NOSOCOMIAL INFECTIONS
2
Q
OTHER NAMES FOR NOSOCOMIAL INFECTIONS?
A
HOSPITAL ACQUIRED INFECTION (HAI)
HEALTHCARE ASSOCIATED INFECTIONS (HCAI)
3
Q
DEFINITION OF HOSPITAL ACQUIRED INFECTIONS?
A
INFECTIONS THAT ARE NOT PRESENT AT THE TIME OF ADMISSION BUT OCCUR IN A PATIENT DURING ADMISSION TO A HOSPITAL OR HEALTHCARE FACILITY
4
Q
COMMUNITY ACQUIRED INFECTIONS ARE?
A
INFECTIONS CONTRACTED OUTSIDE OF A HOSPITAL, IN THE COMMUNITY
5
Q
ACCORDING TO NICE, HOW MANY PATIENTS EVERY YEAR ACQUIRE AN INFECTION AFTER TREATMENT WITHIN NHS?
A
300 000
6
Q
IN DEVELOPING COUNTRIES, ONE IN HOW MANY HOSPITALISED PATIENTS WILL ACQUIRE A HAI?
A
1/10
7
Q
FINANCIAL BURDEN OF HAI ON THE NHS?
A
1 BILLION POUNDS PER YEAR
8
Q
WHAT KIND OF BACTERIA IS STAPHYLOCOCCUS AUREUS?
A
IT IS A COMMENSAL AND A PATHOGEN, A GRAM POSITIVE COCCUS, SEEN IN TYPICAL GRAPE LIKE (STAPHYLO) CLUSTERS
9
Q
WHICH BACTERIA USUALLY FORMS TYPICAL GRAPE-LIKE CLUSTERS?
A
STAPHYLOCOCCUS AUREUS
10
Q
EXPLANATION OF THE NAME: STAPHYLOCOCCUS AUREUS?
A
STAPHLYO MEANS ‘GRAPE-LIKE’ AND DESCRIBES CLUSTERS THIS BACTERIA USUALLY FORMS
COCCUS MEANS: having a spherical, ovoid, or generally round shape
AUREUS: ADDED TO THE NAME OF THIS SPECIES DUE TO THE GOLDEN (AURUM) PIGMENT IT PRODUCES
11
Q
WHAT IS S. AURUS BASED ON ITS OXYGEN USAGE?
A
A FACULTATIVE ANAEROBE (CAN SURVIVE WITH AND WITHOUT OXYGEN)
12
Q
HOW CAN S. AURUS BE DIFFERENTIATED FROM OTHER STAPHYLOCOCCI?
A
IT PRODUCES COAGULASE (AN ENZYME THAT CAUSES BLOOD CLOTTING), WHILE THE OTHER SC ARE COAGULASE-NEGATIVE
13
Q
DESCRIVE S. AUREUS AS COMMENSAL BACTERIA:
A
S. AUREUS IS A MEMBER OF HUMAN MICROBIOTA; 30% OF POPULATION ARE CARRIERS OF IT AND HAVE IT IN THEIR NARES (NOSTRILS) AND THE SKIN WHERE IT DOESN’T CAUSE INFECTION
14
Q
% OF PEOPLE WITH COMMENSAL S. AUREUS?
A
30%
15
Q
WHAT ARE ADHESINS?
A
PROTEINS THAT AID BACTERIAL ATTACHMENT TO THE HOST CELL SURFACE
16
Q
EXAMPLES OF ADHESINS?
A
FIBRINOGEN BINDING PROTEINS (Fnbp)
CLUMPING FACTOR A
17
Q
HOW DOES FIBRINOGEN BINDING PROTEIN (Fnbp) BIND HOST CELL RECEPTORS?
A
IT BINDS TO INTEGRIN PROTEINS ON HOST EPITHELIAL CELLS
18
Q
SOME OF THE KEY PROCESSES BACTERIA PERFORM DURING INFECTION ARE:
A
- BACTERIAL ADHESION
- TISSUE INVASION
- BIOFILM FORMATION
- INTRACELLULAR SURVIVAL
19
Q
IN WHICH CASES DOES S. AUREUS USUALLY INVADE AND CAUSE INFECTION?
A
WHEN THERE IS A BREACH OF BARRIER, I.E. A CUT IN THE SKIN OR THE SKIN BARRIER OR DAMAGED MUCOSA
20
Q
MECHANISMS NEUTROPHILS USE TO PHAGOCYTE BACTERIA AND KILL THEM?
A
- PRODUCTION OF REACTIVE OXYGEN SPECIES (ROS)
- MYELOPEROXIDASES
- FORMATION OF NEUTROPHIL EXTRACELLULAR TRAPS (NETs)
21
Q
WHAT ARE BIOFILMS?
A
BACTERIAL COMMUNITIES OR AGGREGATES THAT ARE BOUND TOGETHER BY AN EXTRACELLULAR MATRIX
22
Q
WHERE DOES S. AUREUS USUALLY FORM BIOFILMS?
A
- ON TISSUES E.G. WOUNDS
- ON MEDICAL DEVICES LIKE CATHETERS
23
Q
SOME OF THE INFECTIONS CAUSED BY S. AUREUS?
A
- SKIN AND SOFT TISSUE INFECTIONS (SSTI)
- BONE AND JOINT INFECTIONS (E.G. OSTEOMYELITIS)
- INFECTIOUS OF THE HEART VALVES (INFECTIOUS ENDOCARDITIS)
- PULMONARY INFECTIONS, E.G. PNEUMONIA
- MEDICAL DEVICE OR IMPLANT RELATED INFECTIONS
- BACTEREMIA OR BACTERIA IN THE BLOOD
24
Q
INFECTIOUS ENDOCARDITIS IS A LIFE THREATENING INFECTION OF HEART VALVES WHICH CAN BE CAUSED BY HAI RESULTING FROM WHICH PATHOGEN?
A
S. AUREUS
25
SOME ANTIBIOTICS S. AUREUS HAVE DEVELOPED RESISTANCE TO AND EXPLAIN:
- BETA-LACTAM ANTIBIOTIC PENICILIN (S. AUREUS PRODUCED BETA-LACTAMASES THAT INACTIVATED IT)
- BETA LACTAMASE RESISTANT ANTIBIOTICS METHICILIN AND OXACILIN (S. AUREUS DEVELOPED A NEW STRAIN: METHICILIN RESISTANT S. AUREUS AKA MRSA)
- VANCOMYCIN (ANTIBIOTIC USED AGAINST MRSA, NEW STRAIN OF THE BACTERIA DEVELOPED: VANCOMYCIN INTERMEDIATE RESISTANT S. AUREUS AKA VISA OR VANCOMYCIN RESISTANT S. AUREUS AKA VRSA
26
WHAT IS MRSA, WHERE DOES THE NAME COME FROM AND WHAT ARE THE TYPES?
MRSA: METHICILIN RESISTANT S. AUREUS, A TYPE OF S. AUREUS THAT DEVELOPED THE RESISTANCE TO ANTIBIOTIC METHICILIN (METHICILIN WAS USED WHEN S. AUREUS DEVELOPED RESISTANCE TO PENICILIN BY USING BETA-LACTAMASE)
CA-MRSA: COMMUNITY ASSOCIATED
HA-MRSA: HOSPITAL AQUIRED
27
WHAT IS VANCOMYCIN?
A GLYCOPEPTIDE ANTIBIOTIC THAT INHIBITS CELL WALL SYNTHESIS WHICH IS USED AGAINST MRSA
28
WHAT MAKES IT CHALLENGING TO TREAT S. AUREUS INFECTIONS?
- HIGHLY DRUG RESISTANT STRAINS OF THE BACTERIA
| - HIGH RATES OF RECURRENCE THANKS TO BACTERIAL BIOFILM FORMATION WHICH IS HARD TO COMPLETELY 'WASH AWAY'
29
HIGHLY RESISTANT STRAINS OF S AUREUS ARE INCREASING OR DECREASING?
INCREASING
30
NAME SOME S. AUREUS RESISTANCE MECHANISMS AND WHICH ANTIBIOTIC THEY'RE USED AGAINST?
- MODIFICATION OF THE DRUG TARGET (E.G. VANCOMYCIN, BETA LACTAMS LIKE PENICILIN)
- ENZYMATIC INACTIVATION OF THE DRUG (E.G. USING BETA LACTAMASE TO INACTIVE PENICILIN)
- ACTIVE EFFLUX OF THE DRUG (ATP DEPENDENT PUMPING OUT OF UNWANTED SUBSTANCES)
31
HOW TO BETA-LACTAM ANTIBIOTICS (PENICILIN, METHICILIN) WORK?
- THEY INHIBIT BACTERIAL CELL WALL SYNTHESIS BY TARGETING PENICILIN BINDING PROTEINS (PBPs)
- PBPs ARE ESSENTIAL FOR PEPTIDOGLYCAN SYNTHESIS WHICH IS A KEY COMPONENT OF THE GRAM POSITIVE CELL WALL
32
WHAT IS THE TARGET OF BETA-LACTAM ANTIBIOTICS?
PENICILIN BINDINGS PROTEINS (PBPs) WHICH ARE ESSENTIAL FOR SYNTHESIS OF PEPTIDOGLYCAN, WHICH IS A KEY COMPONENT OF CELL WALL IN GRAM POSITIVE BACTERIA
33
BETA LACTAM ANTIBIOTIC PENICILIN WAS USED AGAINST S. AUREUS BY INHIBITING PBPs AND SUBSEQUENTLY THE CELL WALL SYNTHESIS. BUT THE BACTERIA DEVELOPED A STRAIN WHICH HAD ENZYME BETA LACTAMASE THAT INHIBITED THE ANTIBIOTIC. BETA-LACTAMASE ANTIBIOTICS WERE DEVELOPED (LIKE METHICILIN) BUT ANOTHER STRAIN OF S. AUREUS (CALLED MRSA) EMERGED THEN. HOW DOES MRSA INHIBIT METHICILIN ACTIONS?
- MRSA HAVE A MOBILE GENETIC ELEMENT CALLED SCCmec
- SCCmec CONTAINS THE mecA GENE
- THIS GENE ENCODES A VARIANT FORM OF PBP, CALLED PBP2a, WHICH DOESN'T RESPOND TO BETA-LACTAM ANTIBIOTICS (INCLUDING METHICILIN)
- THEREFORE CELL WALL SYNTHESIS IS ABLE TO OCCUR IN MRSA
34
HOW DOES VANCOMYCIN INHIBIT CELL WALL SYNTHESIS?
- IT BLOCKS SPECIFIC D-Ala-D-Ala PEPTIDES AND PREVENTS POLYMERIZATION OF PEPTIDOGLYCAN (KEY COMPONENT OF GRAM POSITIVE CELL WALL)
35
HOW DOES VRSA AVOID EFFECTS OF VANCOMYCIN (I.E. AVOIDS PEPTIDOGLYCAN POLYMERISATION BEING SUPPRESSED)?
- VANCOMYCIN BINDING RESULTS IN BLOCKING OF D-Ala-D-Ala PEPTIDES
- IN VRSA STRAIN THIS PEPTIDE SEQUENCE IS REPLACED BY D-Ala-D-Lac SO VANCOMYCIN DOESN'T AFFECT POLYMERISATION OF PEPTIDOGLYCAN
36
RECURRENCE RATES OF S. AUREUS INFECTIONS?
10-50%
37
IN WHICH INFECTIONS CAUSED BY S. AUREUS IS RE OCCURRENCE MOST COMMON?
- JOINT INFECTIONS
| - SKIN AND SOFT TISSUE INFECTIONS (SSTI)
38
EXAMPLES OF DRUGS TO TREAT MRSA?
- VANCOMYCIN
- LINEZOLID
- DAPTOMYCIN (FOR SKIN AND SOFT TISSUE INFECTIONS)
39
SKIN AND SOFT TISSUE INFECTIONS CAUSED BY MRSA OR MSSA (METHICILIN SENSITIVE S. AUREUS) ARE PREFERABLY TREATED WITH?
DAPTOMYCIN
40
HOW ARE INFECTIONS CAUSED BY METHICILIN SENSITIVE S. AUREUS STRAINS USUALLY TREATED?
- PENICILIN DERIVATIVES LIKE OXACILIN
| - CEPHALOSPORINS (A CLASS OF BETA LACTAM ANTIBIOTICS)
41
2 MAIN WAYS IN WHICH S. AUREUS CAN BE TRANSMITTED IN A HOSPITAL SETTING?
1) ENDOGENOUSLY; IF THE PATIENTS IS ALREADY COLONISED BY S. AUREUS (IS A CARRIER WHO WAS FINE BEFORE), BACTERIA CAN SPREAD TO ANOTHER PART OF THE BODY (APART FROM EYES AND NOSTRILS) WHERE THEY CAN CAUSE INFECTION
2) EXOGENOUS SPREAD; FROM PERSON TO PERSON, USUALLY VIA DIERCT CONTACT WITH SKIN, EQUIPMENT OR OTHER SURFACES + S. AUREUS CAN ALSO BE SHED INTO THE ENVIRONMENT BY SKIN SCALES (EXCESS DEAD SKIN CELLS THAT SHED) OR DUST
42
INFECTION CONTROL MEASURES IN HOSPITAL TO PREVENT MRSA SPREAD:
- PRACTICING HAND HYGIENE
- GENERAL CLEANLINESS OF HOSPITAL PREMISES
- COVERING WOUNDS AND LESIONS
- USING APPROPRIATE PERSONAL PROTECTIVE EQUIPMENT WHEN HANDLING BODY FLUIDS
43
WHAT KIND OF BACTERIUM IS ACINETOBACTER BAUMANNII?
- GRAM NEGATIVE
- ROD SHAPED
- AEROBIC
44
WHERE ARE ACINETOBACTERS GENERALLY FOUND?
IN SOIL AND WATER
45
WHAT ARE ACINETOBACTERS GENERALLY VERY RESISTANT TO?
DESICCATION (REMOVING MOISTURE FROM SOMETHING) AND DRY CONDITIONS
46
WHY WERE ACINETOBACTERS ORIGINALLY CONSIDERED TO BE NON MOTILE?
THEY DO NOT HAVE FLAGELLA
47
WHRE WAS THE NAME 'ACINETOBACTER' DERIVED FROM?
FROM GREEK 'AKINETOS' MEANING NON-MOTILE
48
DESCRIBE MOTILITY OF A. BAUMANNII:
- THE ACINETOBACTERS WERE GENERALLY CONSIDERED TO BE NON MOTILE BECAUSE THEY LACK FLAGELLA
- HOWEVER, A. BAUMANNII DISPLAYS TWITCHING MOTILITY MEDIATED BY PILI AND SURFACE ASSOCIATED MOTILITY WHICH RELIES ON QUORUM SENSING VIA SIGNALING MOLECULES
49
POSSIBLE EXPLANATIONS OF HOW A. BAUMANNII IS ABLE TO ADAPT TO DRY CONDITIONS?
- THE POLYSACCHARIDE CAPSULE OF A.B. CAN RETAIN WATER AND HELP MEDIATE SURVIVAL
- THE DISTINCT LIPID COMPOSITION OF ITS OUTER MEMBRANE ALSO CONTRIBUTES TO WATER RETENTION
50
EXPLAIN RESISTANCE OF A. BAUMANNII TO COMMONLY USED (IN HOSPITAL SETTINGS) DISINFECTANTS (E.G. ANTISEPTIC CHLORHEXIDINE AND ETHANOL)
CHLOREXIDINE: BACTERIA ARE ABLE TO PUMP THIS COMPOUND OUT OF THE CELL THROUGH THE ACINETOBACTER EFFLUX PROTEIN (Ace-1)
ETHANOL: THE BACTERIA CAN SURVIVE IN ETHANOL, LOW CONC OF ALCOHOL CAN EVEN MAKE THESE BACTERIA MORE VIRULENT!!!
51
WHICH OUT OF THESE ISN'T A MAJOR CONTRIBUTOR TO A. BAUMANNII ABILITY TO CAUSE INFECTION:
- SURFACE ADHESINS
- ADAPTATION TO VARIOUS ENVIRONMENTS
- TOXIN PRODUCTION
- SECRETION SYSTEMS AND GLYCOCONJUGATES
TOXIN PRODUCTION
52
BIOFILM FORMATION BY A. BAUMANNII, LOCATIONS AND CONTRIBUTING FACTORS?
- CAN FORM BIOFILMS ON CELLULAR AND ACELLULAR SURFACES
- ON ABIOTIC SURFACES, IMPORTANT CONTRIBUTOR TO BIOFILM FORMATION ARE Csu PILI
- ON HOST SURFACES, IMPORTANT CONTRIBUTOR TO BIOFILM FORMATION IS ADHESIN Ata
+ BIOFILM ASSOCIATED PROTEIN (BAP) IMPORTANT FORM BIOFILM FORMATION AND MATURATION IN GENERAL
53
HOW MANY TYPE OF SECRETION SYSTEMS DOES A. BAUMANNII POSSESS AND WHAT ARE THEY CALLED?
- 5 IN TOTAL
| - TYPES: I, II, IV, V and VI
54
Ata, A SURFACE ADHESIN USED IN BIOFILM FORMATION OF A. BAUMANNII ON HOST SURFACES IS EXPORTED BY THE BACTERIA VIA WHICH SECRETION SYSTEM?
TYPE V
55
BAP (BIOFILM-ASSOCIATED PROTEIN) IMPORTANT FOR A. BAUMANNII BIOFILM PRODUCTION AND MATURATION IS EXPORTED BY THE BACTERIA VIA WHICH SECRETION SYSTEM?
TYPE II
56
ROLE OF TYPE VI SECRETION SYSTEM IN A. BAUMANNII:
IT IS USED FOR COMPETING WITH OTHER BACTERIA IN POLYMICROBIAL INFECTIONS, THROUGH INJECTING TOXIN PROTEINS (EFFECTORS) INTO COMPETING STRAINS
57
% OF HAI CAUSED BY A. BAUMANNII GLOBALLY?
2%
58
WHAT TYPE OF INJURY IS PARTICULARLY SUSCEPTIBLE TO A. BAUMANNII INFECTION?
BURN INJURY
59
WHICH BACTERIA IS A MAJOR CAUSE OF INFECTIONS IN ARMED FORCES IN CONFLICT ZONES (WHERE SKIN AND SOFT TISSUE INFECTIONS ARE USUALLY COMMON)?
A. BAUMANNI
60
RISK FACTORS FOR ACINETOBACTER INFECTIONS?
- DIABETES
- BEING IMMUNOSUPPRESSED
- PROLONGED HOSPITAL STAYS
61
EXAMPLES OF HOSPITAL INFECTIONS CAUSED BY A. BAUMANNI:
- PNEUMONIA (IN HOSPITAL ACQUIRED PNEUMONIA, A. BAUMANNII INFECTIONS USUALLY ASSOCIATED WITH THE USE OF VENTILATORS, CAUSING VENTILATOR-ASSOCIATED PNEUMONIA
- BLOODSTREAM INFECTIONS (A.B. IS ONE OF THE MAIN CAUSES OF BLOODSTREAM INFECTIONS ACQUIRED IN ICU, HIGH MORTALITY)
- UTI (A.B. UTIs USUALLY ASSOCIATED WITH CATHETERS)
62
MORTALITY RATE OF ICU BLOODSTREAM INFECTIONS?
34-46%
63
% OF A. BAUMANNII ISOLATES GLOBALLY THAT ARE MULTIDRUG-RESISTANT (MDR)?
45%
64
THE MULTIDRUG RESISTANCE RATES OF A. BAUMANNII ARE HOW MANY TIMES HIGHER THAN FOR OTHER PATHOGENS LIKE KLEBSIELLA?
4 TIMES
65
DRUGS CALLED CARBAPANEMS ARE USUALLY RESERVED FOR WHICH CASES?
MULTI DRUG RESISTANT INFECTIONS (LAST RESORT)
66
HOW MANY BETA LACTAMASES HAVE BEEN FOUND IN A. BAUMANNII?
MORE THAN 50
67
HOW ARE MOST GENES ENCODING ENZYMES THAT DEGRADE BETA-LACTAM ANTIBIOTICS (BETA LACTAMASES) ACQUIRED IN A. BAUMANNI?
BY HORIZONTAL GENE TRANSFER (NON-SEXUAL MOVEMENT OF GENETIC MATERIAL ACROSS BACTERIA)
68
DRUGS OF LAST RESORT FOR RESISTANT INFECTIONS, EXAMPLES:
- CARBAPANEMS
| - COLISTIN
69
MECHANISMS OF MULTIDRUG RESISTANCE IN A. BAUMANNII, DESCRIBE:
- BETA LACTAM HYDROLYSIS (AGAINST PENICILIN, OXACILIN, CARBAPANEMS..)
- MODIFICATION OF AMINOGLYCOSIDES (ENZYMES THAT ARE ABLE TO MODIFY A RANGE OF AMINO GLYCOSIDE ANTIBIOTICS LIKE GENTAMICIN, TOBRAMYCIN, AMIKACIN..)
- ACTIVE EFFLUX MECHANISMS (CHROMOSOMAL ENCODED EFFLUX PUMPS WHICH CAN PUMP OUT A NUMBER OF ANTIBIOTICS)
- CHANGING THE OUTER MEMBRANE (MODIFYING LIPID A COMPOSITION TO PREVENT BINDING OF COLISTIN, A LAST RESORT DRUG)
70
EXAMPLE OF CHROMOSOMAL PUMP USED BY A. BAUMANNII TO PUMP OUT ANTIBIOTICS?
AdeABC
71
WHAT DO ENZYMES LIKE ACETYLTRANSFERASES DO IN A. BAUMANNII?
THEY MODIFY AND INACTIVATE AMINO GLYCOSIDE ANTIBIOTICS (E.G. GENTAMICIN, TOBRAMYCIN, AMIKACIN..)
72
EXAMPLES OF AMINO GLYCOSIDE ANTIBIOTICS?
GENTAMICIN, TOBRAMYCIN, AMIKACIN..
73
MAIN THERAPEUTIC OPTIONS FOR EXTENSIVELY DRUG-RESISTANT ACINETOBACTER?
- POLYMYXINS (RESISTANCE NOT COMMON)
| - CERTAIN TETRACYCLINES (LIKE TIGECYCLINE, BUT THERE ARE HIGH LEVELS OF RESISTANCE)
74
WHO HAS INCLUDED THE CARBAPANEM RESISTANT A. BAUMANNII AS ONE OF THE TOP PRIORITY PATHOGENS FOR NEW ANTIBIOTIC DEVELOPMENT, TRUE OR FALSE?
TRUE
75
COMBINATION THERAPIES ARE FREQUENTLY USED IN ACINETOBACTER INFECTIONS TO REDUCE THE RISK OF EMERGENT RESISTANCE AND IMPROVE OUTCOMES OF MDR INFECTIONS (NOTE THAT IT IS NOT CERTAIN IF COMBINATION THERAPIES ARE SUPERIOR FOR MONO THERAPIES). NAME SOME EXAMPLES OF OF COMBINATION THERAPIES AGAINST MDR INFECTIONS:
- IMIPENEM AND AMIKACIN
- COLISTIN AND RIFAMPIN
- IMIPENEM, RIFAMPIN, COLISTIN
76
MOST COMMON MODE OF TRANSMISSIO OF A. BAUMANNII IN HOSPITALS?
FROM THE HANDS OF HOSPITAL STAFF (HYGIENE EXTREMELY IMPORTANT)!
