Path - Micro - Exam 3 Flashcards
1
Q
- Outline the types of beta-lactam antibiotics and describe their common structural feature.
A
- penicillins
- cephalosporins
- carbapenems
- monobactams
They all contain a beta lactam ring.
2
Q
- Describe the final stage in the production of the bacterial cell wall with emphasis on the role of the transpeptidase enzyme.
A
The peptidoglycan meshwork is assembled in several staged, the final one being the cross linking of the backbone molecules via peptide links. This is done by the enzyme TRANPEPTIDASE.
3
Q
- Describe the mechanism of action of beta-lactam antibiotics and demonstrate understanding of why transpeptidase enzymes are also known as penicillin binding proteins.
A
Cell wall = peptidoglycan surrounding cytoplasmic membrane.
Transpeptidase enzymes are also known as penicillin binding proteins as beta lactam antibiotics bind to them and prevent them from working.
4
Q
. Outline the main ways in which bacteria produce resistance to antibiotics.
A
a) inhibition of ingress of antibiotic
b) enhanced egress of antibiotic
c) enzymatic destruction of antibiotic
d) alteration of antibiotic target
5
Q
Explain the mechanism of action of beta-lactamases.
A
- Beta lactamases are enzymes that destroy beta lactam antibiotics.
- There are many different types produced by gram positive and negative bacteria.
- I.e. penicillinases, cephalosporinases, carbapenemases
- I.e. S. aureus – about 80% resistant to penicillin due to penicillinases
6
Q
Name the penicillinase resistant beta-lactams and explain what the term implies.
A
- methicillin
- flucloxacillin
- dicloxacillin
- cephalexin
Penicillinase resistant beta lactamases.
7
Q
What are two common beta lactamase inhibitors? How do they work? What are some fo the antibiotic names?
A
- clavulanic acid
- tazobactam
The inhibtors are combined with antibiotics, and will inhibit the function of beta lactamase.
Clavulanic acid + amoxicillin = augmentin
Clavulanic acid + ticarcillin = Timentin
Tazobactam + piperacillin = Tazocin
8
Q
Explain the meaning of MRSA and the underlying mechanism.
A
MRSA = methicillin resistant staph aureus.
Mechanism = PBP2a transpeptidase
Instead of producing beta lactamases, it changes the drug target (transpeptidase) so none of the B-lactams can work on it. A genetic alteration makes a new transpeptidase – PBP2a, which the B-lactams have reduced binding for.
Flucloxacillin is what we use now instead of methicillin, but it is still called MRSA. If it is resistant to Flucloxacillin, IT IS MRSA.
9
Q
Name both an oral and an intravenously administered antibiotic that may be used to treat infections with MRSA.
A
Oral – clindamycin
IV - vancomycin
10
Q
Define the meaning of MIC.
A
MIC = minimum inhibitory concentration
The minimum concentration of an antibiotic that inhibits visible growth of bacteria in an in vitro test system.
11
Q
Demonstrate an understanding that strains of a given bacterial species may exhibit a range of MICs to an antibiotic, resulting in degrees of susceptibility or resistance.
A
Routine susceptibility tests are done in simplified form. If the susceptibility measurement is above a chosen MIC called the breakpoint (i.e. the MIC of that bacteria is above the breakpoint), it is RESISTANT, if below the breakpoint, it is SUSCEPTIBLE.
Testing lots of different isolates of bacterial species against a given antibiotic may produce a scatter of different MIC values, with some intermediate degrees of resistance around the break point – i.e you may get a continuum.
12
Q
Use bacterial endocarditis caused by viridans streptococci to illustrate how the range of MICs is clinically relevant.
A
Viridans streptococci, such as S. mitis, exhibit varying degrees of susceptibility to penicillin.
Highly and relatively susceptible, resistant, highly resistant to penicillin.
13
Q
Explain the meaning of antibiotic synergy and describe how this is exploited in the treatment of bacterial endocarditis.
A
Antibiotic synergy occurs when multiple antibiotics are used to treat an infection and their response is stronger or faster than what use of a single antibiotic is. It is opposed to antibiotic antagonism.
Bacterial Endocarditis - could treat highly susceptible viridans strep with:
a) IV penicillin for 4 weeks, OR
b) IV penicillin + IV gentamicin for 2 weeks
14
Q
Demonstrate understanding that there are alternative antibiotics to the beta-lactams and name some of those used to treat a community acquired UTI.
A
For an E. coli UTI…
First line – amoxycillin – a penicillin beta lactam
BUT many are resistant, therefore use augmentin = amoxyxillin + clavulanic acid
If no beta lactamases – nitrofurantoin, trimethoprim, norfloxacin which is exclusively used for UTIs.
15
Q
Demonstrate appreciation that Pseudomonas aeruginosa is inherently resistant to antibiotics and name two antibiotics from each of the following classes to which it may be susceptible: penicillins, cephalosporins, carbapenems, aminoglycosides and quinolones.
A
Pseudomonas aeruginosa has a number of resistance mechanisms.
Penicillins:
Ticarcillin
Piperacillin
Cephalosporins:
Ceftazidime
Cefepime
Carbapenems:
Imipenem
Meropenem
Aminoglycosides:
Gentamicin
Tobramicin
Quinolones:
Norfloxacin
Ciprofloxacin (Moxifloxacin)
16
Q
Name the four generations of cephalosporins and name an antibiotic from each.
A
*1st generation:
cephalexin
2nd generation
*3rd generation:
ceftriaxone
4th generation:
cefepime
Advanced:
ceftaroline
17
Q
Explain in general terms how the spectra of activity of cephalosporins differ between the generations.
A
*1st generation:
S. aureus
Strep
Some Entero
2nd generation
1 + *H. influenzae
*3rd generation: Strep Entero H. influenzae *P. aeruginosa
4th generation: S. aureus Strep Entero H. influenzae *P. aeruginosa
Advanced:
All of the above + MRSA S. aureus
18
Q
Name the two most significant mechanisms of Gram negative resistance to beta-lactam antibiotics.
A
a) ampC enzyme production (Class I beta lactamase production)
- cephalosporinases
- gene is turned on if exposed to antibiotic
b) ESBL production (Extended Spectrum Beta Lactamase)
- Mutant gene – lactamaseses are capable of destroying 3rd gen
- some active against 4th gen
19
Q
Appreciate the mechanisms of ampC enzyme production and ESBL production confer resistance to 3rd and 4th generation cephalosporins.
A
a) ampC enzyme production – gene if repressed until induced by antibiotic, but mutations in the gene may result in ‘stably de-repressed’ mutant which is a hyperproducer of cephalosporinase. They setroy 3rd generation cephalosporins. Therefore use of 3rd gen selects out these mutants within hospitals.
b) ESBL production – active against 3rd gen and some active against 4th
20
Q
Name the main antibiotic class used to treat gram negative rods with ampC enzyme or ESBL production.
A
Carbapenems
21
Q
Explain why empirical antibiotics must be used against life-threatening infections such as bacterial meningitis. Explain why ceftriaxone is used for this purpose.
A
Don’t have time to test for pathogen and need to cover potential pathogens:
Neisseria meningitides
Streptococcus pneumonia
Haemophilus influenzae
Ceftriaxone covers all of these
22
Q
Describe the epidemiology of N. meningitidis infection, explaining the potential evolution of carriage to invasive disease.
A
Bacteria is in nasopharynx of about 10% of population – carriers. In a small portion of carriers, the bacteria invades the blood or meninges leading to an invasive disease.
23
Q
Discuss the difference between antibiotic eradication of carriage and treatment of invasive infection; list the antibiotics used for each.
A
If people have been exposed to certain infections, prophylaxis is used for eradication of possible carriage.
Treatment of invasive infection: ceftriaxone until antibiotic resistance can be determined. Then switch to best option, i.e. may be IV penicillin for N meningitides.
Prophylaxis:
Adult – ciprofloxacin
Children – rifampicin
Pregnant women – ceftriaxone injection
24
Q
Describe the range of microorganisms causing urethritis.
A
STD: • Chlamydia trachomatis • Neisseria gonorrhoeae • Ureaplasma urealyticum • Mycoplasma genitalium
25
Discuss why empirical treatment of urethritis is often necessary
Culture results may not be available for 24-28 hours but treatment may be needed earlier. People with suspected STDs may be less likely to show up for follow up appointments.
26
Discuss the implications for treatment of detecting N. gonorrhoeae in culture as opposed to PCR.
Resistant to anti-g antibiotics is widespread and increasing, therefore may need to change empiric treatment to one guided by lab susceptibility testing. Culture will tell you what to use.
Gonno:
Empiric choice in rural/remote areas – amoxicillin and probenicid.
Multi resistance is not common here.
Empiric choice metro areas – IMI ceftriaxone (used to be ciprofloxacin)
Overseas strains are more prevalent.
27
State the antibiotic regimen used for the empirical treatment of urethritis and explain why each drug is used.
Empiric choice in rural/remote areas – amoxicillin and probenicid.
Multi resistance is not common here.
Empiric choice metro areas – IMI ceftriaxone (used to be ciprofloxacin)
Overseas strains are more prevalent.
In general:
Gonno – ceftriaxone – can be used for overseas strains as well
Chlamydia – azithromycin - only single dose
28
Explain the term "atypical pneumonia".
* Mycoplasma pneumoniae
* Chlamydophila pneumoniae
* Influenza, depending on season
* Legionella pneumophila
* Legionella longbeachae
* Chlamydophila psitacci
29
Describe a recommended regimen for the treatment of mild community pneumonia and explain why each antibiotic is used.
```
If not atypical:
Oral amoxicillin:
- Strep. Pneumonia
- H. influenzae
If atypical:
- doxocycline po (oral)
- clarithromycin po
- azithromycin po
```
30
Demonstrate appreciation of the grading schemes for pneumonia and describe where information about pneumonia treatment can be found.
Pneumonia Severity Scores, i.e. CURB, SMART-COP and PSI (pneumonia severity index).
Tells you about severity, i.e. risk of death, and treatment advice.
31
Explain what is meant by a polymicrobial infection.
More than one species of microorganism present.
In these infections, the presence of one micro-organism generates a niche for other pathogenic micro-organisms to colonise, one micro-organism predisposes the host to colonisation by other micro-organisms, or two or more non-pathogenic micro-organisms together cause disease.
32
Explain why diabetic foot ulcers are polymicrobial.
They are chronic infections – lots of different microbes will find its way there. Can house aerobic bacteria, anaerobic bacteria and even fungi.
33
List the types of bacteria you would expect to find causing a diabetic foot ulcer.
Gram neg:
- Enterobacteriaceae
- Pseudomonas aeruginosa
Gram positive:
- Staphylococcus aureus
- β-haemolytic streps
- α-haemolytic streps
Anaerobes:
- Bacteroides & others
- Peptococcus spp.
- Peptostreptococcus spp.
34
List the antibiotics with clinically useful activity against anaerobic bacteria.
- augmentin
- clindamycin
- metronidazole
- Timentin IV
- Tazocin IV
35
Describe a typical antibiotic regimen for early diabetic foot infections and explain why each antibiotic is included.
1. If early:
Augmentin po:
- gram +
- entero (not P. aeruginosa)
- anaerobes
Clindamycin po + ciprofloxacin po:
- gram +
- anaerobes
- gram –
- Inclues P. aeruginosa
Cephalexin po + metronidazole po
- gram +
- some entero (not P. aeruginosa or enterococci)
- anaerobes (metro)
2. If deep or bone infection:
Timentin IV, or
Tazocin IV:
- Entero
- P. aeruginosa
- Gram +
- Anaerobes
Meropenem IV:
- very broad
- gram +
- gram –
- P. aeruginosa
- Anaerobes
- NOT MRSA or entero
36
Describe the different types of respiratory tract infections according to anatomical location
- Bronchitis – bronchial tubes
- Pharyngitis - pharynx
- Rhinopharyngitis – nose and pharynx
- Laryngotracheitis – larynx and trachea
- Pneumonia – lung inflammation
- Sinusitis
- Otitis media – middle ear
37
Which viruses cause (most of) the common cold?
- rhinovirus
- coronavirus
- adenovirus
38
Describe the range of symptoms caused by influenza virus
- fever
- headache
- myalgia
- sore throat
- rhinitis
- non productive cough
- otitis media, nausea and vomiting in children
- can lead to pneumonia
39
In relation to influenza, what is an antigenic shift and antigenic drift?
Antigenic drift
- results from mutations in the gene coding for the NA (less frequently the
HA)
- despite the altered NA, the viral subtype remains the same (eg. H3N2
remains H3N2) but the population is less immune
- immunological selection of the new strain takes place in the population and
yearly outbreaks of influenza occur
Antigenic shift
- major antigenic changes in HA or NA
- result from genetic reassortment – exchange of genetic material between
a human influenza virus and an animal influenza virus
- the result is a new HA or NA; eg. H2N2 becomes H3N2
- lack of immunity in the population to the new subtype results in the major epidemics or
pandemics of influenza (1918, H1N1; 1957, H2N2; 1968, H3N2; 1977, H1N1)
40
Why does the influenza have sometimes become epidemic?
1) A novel (new) virus which humans have no immunity
2) The virus causes significant human illness and death
3) The virus can spread easily from person to person (Avian flu does not have this)
41
In what way do influenza viruses represent emerging pathogens?
- avian flu
- swine flu
Antigenic shift – genetic reassortment between a human flu and animal flu
42
Explain briefly why outcomes to the fetus may be different when maternal infection occurs at different stages of pregnancy
Fertilization – week 8 = embryogenesis and organogenesis. Early malformations are usually gross deformities or lethal. Errors in organogenesis often results in errors in developmental processes. More sensitive and greater possibility of maldevelopment.
43
Name the viral infections which may have deleterious effects on the developing fetus
- parvovirus
- CMV
- VZV
- Rubella
- HHV6
- Mumps and measles – increased fetal loss
44
Describe the main features of infection with Rubella in the non-pregnant host
- erythematous maculopapular rash with lymphadenopathy
| - arthritis/arthralgia
45
Describe briefly the potential outcomes to the fetus if infected with rubella.
- intellectual disabilities
- cataracts, glaucoma
- deafness
- cardiac defects
- intrauterine growth retardation
- may be born with haemorrhagic rash
- microcephaly
- inflammatory lesions
46
Describe the main features of infection with Parvovirus B19 in the non-pregnant host
- fever
- headache
- malaise
- erythematous rash of the cheeks
- rash of the trunk and arthritis may occur
47
Describe briefly the potential outcomes to the fetus if infected with parvovirus B19.
- excess fetal loss
- ascites (causing abdominal swelling)
- pleural effusion
- pericardial effusion
- skin edema
- polyhydramnios (excess amniotic fluid in amniotic sac)
48
Describe the main features of infection with VZV in the non-pregnant host
- chickenpox – rash which progresses from small fluid filled vesicles through to pustules and crusty scabs.
- risk of varicella pneumonitis in adults
- risk of varicella encephalitis in adults
- Zoster – virus in one dermatome
49
Describe briefly the potential outcomes to the fetus if infected with VZV.
- early foetal loss
- foetal varicella syndrome:
- limb atrophy
- skin scarring
- ocular abnormalities
- neurological abnormalities
- shingles early in life
- in utero chickenpox/shingles
50
Describe the main features of infection with CMV in the non-pregnant host
- fatigue
- fever
- mildly enlarged liver and spleen
- hepatitis
- raised lymphocyte count in blood
51
Describe briefly the potential outcomes to the fetus if infected with CMV.
- fetal death
- jaundice
- microcephaly
- intellectual disability
- hepatitis
- thrombocytopaenia
- **deafness
52
List the most clinically important types of blood-borne viral infection.
- HIV,
- HCV (Hep C),
- HBV
53
What are the most clinically important types of Herpesvirus infection?
- VZV
- HSV
- EBV
- CMV
54
What are two types of HIV virus and describe the differences in their geographical distribution
1. HIV 1 - most common cause of HIV
- found throughout the world
2. HIV 2 - it is less transmissible and causes a less severe infection
- much less common than HIV 1
- largley confined to West Africa
In general, over 2/3 of people living with hIV are in Sub-Saharan Africa
55
Outline the lifecycle of the HIV virus in the human host
Lifecycle:
- HIV binds to the CD4 receptor on hosts T helper cell surfaces
- it transcribed its genomic RNA to DNA with reverse transcriptase
- the viral DNA is then integrated into human DNA
- The viral genes encode (transcribe) a variety of proteins, and new virions are produced.
- host cell dies
56
Demonstrate why it is important to understand the HIV lifecycle to appreciate antiretroviral action
- The aim of HIV treatment is to suppress virological replication and allow recovery of the CD4 cell population.
- Antiviral meds include reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors, and fusion inhibitors
57
Describe the routes of transmission of HIV
Fluids that can transmit HIV:
- blood
- semen
- vaginal secretions
- breast milk
These must come in contact with a mucous membrane or damaged tissue, or be directly injected into the blood-stream for transmission to occur.
Most common methods of transmission:
- sexual
- mother to child
- sharing needles
Less common:
- oral sex
- exposure to infected vlood
- transfusion
- organ transplant
58
Describe briefly the time course of HIV infection and the development of AIDS
1. Acute infection
- 0-9 weeks
- peak of HIV RNA copies in plasma, then sudden decrease before latency
- CD4 lymphocyte count decreases and then starts to increase before latency
2. Clinical Latency
- 9wks - 7 years
- HIV RNA copies in plasma increases slowly over time
- CD4 lymphocyte count increases for a bit and then decreases slowly over time
3. Symptomatic Infection
- 7 years +
- HIV RNA copies in plasma increases quicker
- CD4 lymphocyte count continues to decrease
Median period for progression to AIDS is 10 years if not treated
Most infectious in early and late infection
59
Name the main infectious and neoplastic conditions associated with AIDS
1. Opportunistic infections:
- Pneumocystis pneumonia
- tuberculosis
- Progressive Multifocal Leukoencephalopathy
- Cerebral toxoplasmosis
- Cryptococcal infection
- Cryptosporidiosis
- Cytomegalovirus retinitis
- Disseminated MAC (Mycobacterium avid complex)
2. Neoplasia:
- Kaposi's Sarcoma (proliferation of vascular structures within the skin, mucous membranes, and rarely organs.)
- non-Hodgkin's lymphoma
- multiple myeloma
- melanoma
- solid organ cancers
60
What are the stages of VZV (Varicella-Zoster virus)?
a) Primary infection - chicken pox (varicela)
b) Latent infection in dorsal root ganglia
c) Reactivation - shingles (zoster)
61
Describe the pathogenesis and clinical features of shingles
Pathogenesis:
Shingles may occur when the immune system becomes less effective at containing the virus at its site of latency (dorsal root ganglion).
Viruses travel down the corresponding sensory nerve to produce a very painful eruption in the corresponding dermatome.
Clinical features:
Across one dermatome - rash which progresses from small fluid filled vesicles through to pustules and crusty
62
List the viral conditions which commonly produce a rash and arthralgia
- alphaviruses
- flaviviruses
- parvoviruses
- measles
- rubella
- VZV
- HIV
- Seroconversion
- HBV prodrom
63
Define an arbovirus
Any of a group of viruses which are transmitted by mosquitoes, ticks, or other arthropods
64
Outline the main clinical syndromes caused by arboviruses
```
Flaviviruses – e.g.
• Dengue
• Yellow Fever
• Japanese Encephalitis
• Murray Valley Encephalitis
• West Nile Virus
```
Alphaviruses – e.g.
• Chikungunya
• Ross River
• Barmah Forest
3. Bunyaviruses – e.g.
• Rift Valley Fever
• Crimean Congo Haemorrhagic fever (ticks)
65
Describe the life cycles of RRV, BFV, chikungunya, MVE and dengue
Ross River Virus:
Mosquito: Culex and Aedes species
Incubation: 7-9 days
Recovery: fully by 3-6 months
Human-mosquito-human
Macropod-mosquito-macropod
Macropod-mosquito-human
Barmah Forest Virus:
Mosquito: Culex and Aedes species
Chikungunya:
Mosquito: Aedes species
Incubation: 1-12 days
Murray Valley Encephalitis:
Mosquito: Culex
Dengue:
Mosquito: Aedes aegypti
Incubation: 4-7 days
66
Describe the natural history and clinical features of EBV infection
Clinical features:
- *severe fatigue
- *fever
- *marked pharyngitis
- lymphadenopathy
- splenomegaly
- subclinical hepatitis - raised
transaminases
- elevates lymphocyte count
(with atypical morphology) in
peripheral blood
- prolonged convalescence
BV is a lifelong, predominantly latent and asymptomatic infection. EBV is spread primarily through saliva, which has led to glandular fever being called the “kissing disease”, although droplet spread and the sharing of food and drink bottles contributes to transmission
67
Name the cancers associated with EBV infection
- *Burkitt’s lymphoma
- *Nasopharyngeal carcinoma
- Post transplant lymphoma
- Hodgkin’s lymphoma
68
Define disinfection.
A process which removes or kills most, but not all, viable (micro)organisms (exception of bacterial endospores and fungal spores)
69
Define Cleaning:
Removal of all foreign material from an object. (eg. soil, organic material)
Water with detergents or enzymatic products.
70
Define Sterilization:
The process of killing or removing ALL (micro)organisms
71
Define Pasteurization:
A form of heat disinfection that eliminates pathogens and reduces the total number of viable organisms
72
2. Distinguish between disinfection and antisepsis
Antiseptics are germicides that can be applied to living tissue and skin.
Disinfectants are germicides applied only to inanimate objects.
73
5. Explain why cleaning of an item must precede disinfection or sterilisation.
Removal or first and secretions that may interfere with sterilization/disinfection.
74
7. Name a type of microorganism that is low in resistance to chemical germicides and one which is high in resistance.
Low: Vegetative bacteria
High: Bacterial Spores
i.e. Clostridium difficile – spores can persist for weeks
75
Explain the terminology applied to medical equipment to describe the level of disinfection or sterilisation it requires.
a) Critical – introduced directly into bloodstream or other sterile site
Requires: sterilization
EG: urinary catheters
b) Semicritical – comes into contact with intact mucous membranes
Requires: high level chemical disinfection (sterilization preferable)
EG: endoscope
c) Noncritical – comes into contact with skin
Requires – cleaning or low level disinfection
EG: BP cuff
76
Name three different antiseptics used on human skin.
- Iodine
- Alcohols
- Hexachlorophane
- Chlorhexidine
77
Name the two broad categories of methods of sterilisation.
- Physical methods (heat)
| - chemical methods
78
Name 4 types of physical sterilisation.
- dry heat
- moist heat
- radiation
- filtration
79
Explain why steam sterilisation is an effective means of heat sterilisation.
- The availability of water allows destruction of enzymes and membranes by disruption of hydrogen bonds
- The provision of heat in gaseous form, under pressure, aids penetration into porous objects
- Features: ease of use, controllability, efficiency, cost
80
State the four parameters governing the effectiveness of steam sterilization.
1. Steam quality
2. Pressure
3. Temp
4. time
81
Describe a biological means by which the effectiveness of steam autoclave function can be assessed.
1. Autoclave tape – shows whether tape has been exposed to a certain temp, but no info on time, steam penetration, pressure etc
2. Biological indicators – contain spores of a heat-resistant bacterium. If autoclave does not reach the right temp, the spores will germinate and their metabolism will change the color of a pH-sensitive chemical.
82
What are the causes of trauma related infections?
- surgical site infections
- bite infections
- specific exposures
83
How significant are the broad consequences of surgical site infections?
- 2nd most common health care associated infection
- 60% of extra hospital days
- >7 days extra in-patient stay
84
What are the classifications of surgical site infections?
a) superficial incisional
= skin + subcut tissue
b) deep incisional
= involving deeper soft tissue
c) organ/space SSI
= involves any part of anatomy other than incision, opened or manipulated during op
85
Which microbes most commonly cause SSI’s?
- *Staph aureus
- coagulase negative staph
- enterobacteriaceae
- anaerobes
86
What are some of the pre-operative SSI predisposing factors?
- elderly
- obesity
- smoking
- diabetes
- steroids
- infection at a distant site
- prolonged hospital stay
- malnutrition
87
What are some of the peri-operative SSI predisposing factors?
- shaving the skin surface
- large incisions
- lengthy operations
- poor haemostasis
- dead/devitalised tissue
- foreign bodies
e.g. drains, metalwork
- spillage of micro-organisms
- non scrubbed staff in theatre
88
What are some of the post-operative SSI predisposing factors?
- exposed deep tissues
- persistently moist surfaces
- ischaemia
- haematomas
- foreign bodies e.g. drains
89
How are SSI’s diagnosed?
a) Inspection
- offensive smell or purulent discharge
- fever, raised inflammatory markers (i.e. C-reactive protein, neutrophilia)
b) Microscopy and culture of purulent discharge
90
With what are SSI’s treated?
a) Superficial incisional:
- anti-staph agent
- i.e. flucloxacillin
b) Deep incisional:
- also cover aerobic gram negative bacilli and anaerobes
- i.e. tazocin (pipericillin plus tazobactam)
91
What is the difference between medical and surgical asepsis?
Medical: an practice that helps reduce the number and spread of microorganisms
Surgical: complete removal of microorganisms and their spores from the surface of an object
92
What is cleaning and what do you use?
Removal or all foreign material from an object.
Water with detergents of enzymatic products
93
What is disinfection and what is a disinfectant?
Disinfection – a process that eliminates many or all pathogenic microorganisms on inanimate objects with the exception of bacterial endospores and fungal spores.
Disinfectant – germicide applied only to inanimate object. ANTISEPTICS are applied to living tissue.
94
What is an antiseptic?
Chemical applied to skin or living tissue that prevents of arrests growth or action of microorganisms by inhibiting their activity or destroying them.
95
What is the classification and minimum requirement for equipment that contacts intact skin?
Non-critical
Cleaning or low level infection
96
What is the classification and minimum requirement for equipment that contacts intact mucous membranes?
Semi-critical
High level disinfection (but sterilization preferable)
97
What is the classification and minimum requirement for equipment that contacts a sterile body cavity or is introduced directly into the bloodstream?
Critical
Sterilization
98
How can SSIs be prevented?
- treat infection at distant sites before procedure
- screen and treat s. aureus colonization’s
- avoid shaving of the operation site
- prepare site with antiseptic, i.e. chlorohexidine
- thorough surgical scrub hand washing procedure
- all equipment, sutures, drapes, should be sterile
- good surgical technique
- dressings:
o hand hygiene precautions whenever wound exposed
o aseptic non touch technique
o discard dressings safely
- appropriate attire
- antibiotic prophylaxis
99
Discuss antibiotic prophylaxis In terms of SSI prevention.
- especially high risk patients, i.e. immunosuppressed
- or high risk operations, i.e. joint replacement
- given prior to start of procedure
- initial dose times to peak at time of procedure
- single dose
- prophylactic regimens should not be continued
100
What are some of the non-human and human flora that could cause infections due to dog/cat bites?
- pasteurella
- capnocytophaga canimorsus – usually dogs
- plus staph, strep and anaerobes
101
Discuss the management for dog/cat bites.
- wounds debrided and irrigated
- low threshold for antibiotic treatment
- particularly if:
o delayer presentation (>8 hours)
o puncture wounds that can’t be debrided
o wounds on hands, feet or face
o wounds with underlying bone/joint/tendon involvement
o immunocompromised
- i.e. augmentic (amoxicillin + clavulanic acid)
102
Discuss the management for human bites.
- Eikenella spp, anaerobes
- Fingers, face, ears, genitals are more problematic areas
- Management as per cat/dog bites
- PLUS consider blood borne virus risk
103
What are specific SSIs to watch out for with water/garden injuries?
Fresh water laceration:
- Aeromonas hydrophila
Sea water exposure:
- coral cuts
- beware Vibrio species
Fish tank exposure:
- Mycobacterium marinarum
Garden/soil exposure:
- Nocardia
- Mycobacterium
- Sporothrix schenkii
‘Fish Handlers’ disease
- Erysipelothrix rhusiopathiae – thin/curved gram + bacillus
- Risk factors: handling fish, meat and hides
- Treatment: penicillin
104
Why are diabetics at high risk of foot ulcers?
Diabetes may cause:
- Peripheral neuropathy, compromised sensation
o Reduced sensation in toes
o Reduced sweating, dry and cracked feet
- Vascular disease – compromised blood supply
105
What is charcot’s foot?
A condition causing weakening of the bones in the foot that can occur in people who have significant nerve damage (neuropathy). The bones are weakened enough to fracture, and with continued walking the foot eventually changes shape.
106
Describe the assessment stages of diabetic foot ulcers.
1. determining the extent and severity of infection
2. identifying underlying factors that predispose to and promote infection
3. assessing the microbial aetiology
107
What types of specific assessment are done with diabetic foot ulcers?
- history and examination
b) laboratory assessment
- inflammatory markers
- C-reactive protein
c) radiological assessment
- X-ray
- nuclear scan
- MRI
d) microbiological assessment
108
Describe the microbiology of diabetic foot ulcers.
- skin flora
- staph aureus and strep species
- gram negatives including enterobacteriaceae and pseudomonas aeruginosa
- anaerobes
109
Deep swabs required, but results can be confusing (normal flora?)
What is the management for clinically non-infected diabetic foot ulcers?
- debridement and dressings
- close monitoring
110
What is the management for clinically infected diabetic foot ulcers?
- require cultures and antibiotics
- mild, acute wound infections can usually be managed by GPs using oral antibiotics.
- Deep and chronic infections, or infections with systemic toxicity, require immediate referral to hospital
111
Describe the multi-disciplinary management of diabetic foot ulcers.
1. surgical debridement
- vascular surgeons
- procedures to improve vascularity e.g. angioplasty
2. broad spectrum antibiotics via HiTH (home IV)
- e.g. tazocin, ertapenem
3. “off-loading”
- podiatry input very important
- Aircast boots, plaster casts, orthotics
4. good glycaemic control
- better wound healing
- physicians also manage other co-morbidities and risks
112
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If a diabetic presents with:
- high temp
- high pulse
- low BP (septic shock)
- renal failure
- raised CK
- What looks like bloody boils and bruising
What could they have?
```
1. Necrotizing fasciitis
a) type 1: polymicrobial
b) type 2: monomicrobial
2. Clostridial Myonecrosis (‘gas gangrene’)
3. Fournier’s gangrene etc
113
What causes necrotizing fasciitis?
1. polymicrobial infections (1)
- most common, especially if diabetic, elderly or alcoholic
- may follow penetrating injury
2. monomicrobial infections (2)
- less common
- often follows minor trauma (i.e. bruise, muscle strain, or no injury)
- bacteria likely seed area via blood stream
- i.e. GAS or S. aureus
114
Describe the pathogenesis of necrotizing fasciitis.
- bacteria in deep tissues, hence little to see early stages
- swelling, inflammation, thrombosis ischaemia, necrosis
- pus tracks along fascial planes
- spread into lymphatics, blood stream
- patient is now in serious trouble.....
115
How would you know necrotizing fasciitis is a medical emergency?
- systemic toxicity
- pain+++
- BEWARE.... NIL TO SEE EARLY
- swollen discoloured skin
- blistering
- ...then dusky skin
- ...then cutaneous gangrene, wood-hard tissues
You should be highly suspicious if the patient is in pain and is systemically unwell but there is nothing to see.
116
How is necrotizing fasciitis diagnosed?
1. laboratory tests
- neutrophilia
- high CRP
- end organ involvement
- abnormal renal and liver function tests
2. radiology
- computerised tomography - might see black dots = gas formed by bacteria.
3. microbiology
- blood culture
- skin swabs, blister fluid, surgical tissue samples
117
What is the treatment for necrotizing fasciitis?
1. Surgical debridement
- aggressive, repeated surgeries
2. Antibiotics
a) Empiric IV therapy:
- meropenem
- vancomycin
- clindamucin
b) targeted IV therapy:
i. e. GAS – penicillin plus clindamycin
3. Adjunctive therapy
- intensive care
118
What is clostridial myonecrosis and what usually causes it?
Gas gangrene follows penetrating injuries .
More common when soil or faeces contaminated wound, therefore battlefield injuries common.
Usually Clostridium species:
- anaerobes, form spores
- C. perfringens
- C septicum
119
What is involved in the investigation and management of clostridial myonecrosis?
Same as necrotizing fasciitis.
Can see gas in tissues on x-ray
Patient requires:
- surgery
- antibiotics
- supportive care
120
What could cause generalized myositis (inflammation and degeneration of muscle tissue)?
- many viral infections i.e. flu, dengue
| - some bacterial infections, i.e. legionella
121
What is pyomyositis?
A focal bacterial infection within a muscle group.
- most common in tropical countries
- most common in children
- often no obvious portal of entry
- usually Staph aureus
- patients rarely shocked
122
What is Fourniers gangrene?
- Breach in bowel mucosa, leak into perianal area
- scrotum, penis, perineum – abdominal walls, legs
- elderly, diabetics, obese patients, alcoholics
PART 5: Skin and Soft Tissue Infections 3
123
What is a nosocomial infection?
Nosocomial infection is a localized or systemic condition:
```
1. That results from adverse reaction to the presence of an
infectious agent(s) or its toxin(s) and
```
2. was not present or incubating at the time of admission to the hospital
124
Broadly speaking, what are the main consequences of nosocomial infections?
```
- Prolonged hospitalization
o average 11 days per patient with HAI
- Additional morbidity
- Long-term physical & psychosocial sequelae
- Increased cost of hospitalization
o $400 million per year in Australia
o Each BSI costs $10,000 – 50,000
- Death
o Staphylococcus aureus BSI ~25% mortality
```
125
Describe the epidemiology of nosocomial infections.
- 10% hospital patients
- most commonly UTIs
- nosocomial pneumonia most often associated with death of the patient
- most frequent microbes:
o MRSA/MSSA
o Pseudomonas aueruginosa
o Klebsiella pneumonia
o Enterococcus faecalis
o Acinetobacter baumannii
o Staph epidermis
o Clostridium difficille
126
What are the risk factors for nosocomial infections?
- duration of stay in hospital
- severity of illness
- number of interventions
127
What are the different sources of these bacteria?
- any permanently moist area
- inanimate surfaces soiled by organic material
- used surgical/anesthetic equipment
- hospital bedding
- protective clothing
- BUT principal source = staff and patients
128
How are nosocomial infections spread?
1. Direct contact
2. Indirect contact, i.e. fomites
3. Air
4. Faecal-oral route
5. Blood and bodily fluid exposure
129
Describe the pathogenesis of nosocomial infections.
a) Endogenous origin – patient’s own resident microbial flora
b) Cross infection – patient-to-patient
c) Assisted by hospital staff
- assistance of medical procedures
- impairment of host defense systems
- invasive medical devices - REMOVE
o breach in epidermis
o in-dwelling device – develops biofilms
130
What is the treatment for nosocomial infections?
Empirical choice based on:
- up to date knowledge of organisms most likely to cause infection
- local antibiotic susceptibility pattern
Need to obtain appropriate diagnostic specimens.
131
How are nosocomial infections prevented?
1. Hand Hygiene – most effective
- before touching patient
- before a procedure
- after procedure or body fluid exposure risk
- after touching a patient
- after touching a patient’s surroundings
2. Infection Control
3. Personal Protective Equipment
Infection control team:
- medical microbiologist/infectious disease cons
- infection control nurse
- member of microbiology lab staff
Infection control doctor/officer – initiated and arranged preventative measures
Reports to infection control committee – regular surveillance, inspection etc
132
What causes nosocomial UTIs?
- urinary catheterization (IUC) or urethral instrumentation
- increased risk with duration
- Bacteria:
o Pseudomonas aeruginosa
o Klebsielle spp
o Enterococcus faecalis
o Coag neg staph
- Introduced during procedure or ascend urethra later
133
How are UTIs prevented?
- aseptic non-touch technique during insertion
- IUC’s should be taped to patients’ inner thigh
- Connect IUC to sterile closed urine collection systems
- IUCs should be used for shortest time possible
- Avoid where an alternative solution is practical
134
What are the risk factors for intravascular cannula infection?
- prolonged use (>48 hrs for peripheral vein cannulas)
- heavy bacterial colonization at insertion site
- diabetes
- neutropenia
- parenteral nutrition
- broad-spectrum antibiotic use
135
Which organisms cause IV cannula infections?
- coag neg staph
- MSSA/MRSA
- Candida albicans
136
How are IV cannula infections diagnosed?
- inspection
- symptoms, pain, blockage, fever, sepsis
- culture of cannula tip once removed OR blood drawn through cannula
137
What is the treatment for IV cannula infections?
- removal
| - antibiotics – flucloxacillin or vancomycin
138
How are IV cannula infections prevented?
Antiseptic non-touch technique
139
What are the risk factors for nosocomial pneumonia?
- prior chest disease
- smokers
- post operative
- ventilated critically ill patients
140
What are the common causes of nosocomial pneumonia?
- pseudomonas aeruginosa
- MSSA/MRSA
- Enterobacteriaceae
- Acinetobacter
- Stenotrophomonas maltophilia
- Legionella
- Respiratory viruses
141
What are the symptoms of nosocomial pneumonia?
- fever
- cough
- raised WCC
- signs CXR
- gradual onset
142
How is nosocomial pneumonia diagnosed?
- sputum sampling?
| - Broncho-alveolar lavage preferred
143
How is nosocomial pneumonia treated?
- empirical therapy to cover organisms mentioned
| - then targeted therapy
144
What are the causes of hospital acquired diarrhea and vomiting?
1. Bacteria
- food poisoning, i.e. listeria
- antibiotic associated, i.e. clostridium difficille infection
2. Viral
- norovirus
- rotavirus
145
How is hospital acquired diarrhea and vomiting transmitted?
- faecal-oral route
| - droplet spread
146
How is hospital acquired diarrhea and vomiting diagnosed?
- serology and molecular testing
| - culture for bacterial causes of gastero
147
What could cause a transfusion associated infection?
1. Bacterial infection
- E.g. Citrobacter, Pseudomonas
- contamination at the time of donation
- contamination of giving equipment
- poor storage
2. Viral infection
- usually due to the presence of viral infection in the donor
- Hepatitis B and C, HIV, CMV, parvovirus
3. Chagas’s disease – “the new AIDS”
148
Which organisms have inducible beta-lactamase activity that is chromosomal mediated?
ESCHAPPM
```
E: Enterobacter spp.
S: Serratia spp.
C: Citrobacter freundii
H: Hafnia spp.
A: Aeromonas spp.
P: Proteus spp. (P. vulgaris)
P: Providencia spp.
M: Morganella morganii
```
Best to treat with carbapenems
