Microbiology Denise Flashcards

1
Q

What congenital infections are currently screened in mothers during pregnancy?

A

Hepatitis B
HIV
Rubella
Syphilis

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2
Q

What congenital infections are currently not screened in mothers during pregnancy but are possible?

A

CMV
Toxoplasmosis
Hepatitis C
Group B Streptococcus

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3
Q

Congenital toxoplasmosis may be asymptomatic at birth but 60% may still go on to suffer long-term sequelae such as….

A

Deafness
Low IQ
Microcephaly

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4
Q

Congenital toxoplasmosis is symptomatic at birth in 40%. What are examples of symptoms?

A
Choroidoretinitis
Microcephaly/hydrocephalus
Intracranial calcifications
Seizures
Hepatosplenomegaly/jaundice
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5
Q

What is the mechanism of congenital rubella syndrome?

A

The mitotic arrest of cells
Angiopathy
Growth inhibitor effect

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6
Q

How does congenital rubella syndrome affect the eyes?

A

Cataracts
Microphthalmia
Glaucoma
Retinopathy

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7
Q

How does congenital rubella syndrome affect the CVS?

A

Patent ductus arteriosis

Atrial/ventricular septal defect

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8
Q

How does congenital rubella syndrome affect the ears?

A

Deafness

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9
Q

How does congenital rubella syndrome affect the brain?

A

Microcephaly
Meningoencephalitis
Developmental delay

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10
Q

What are some other symptoms of congenital rubella syndrome (not including eyes, CVS, ears, brain)?

A
Growth retardation
Bone disease
Hepatosplenomegaly
Thrombocytopenia
Rash
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11
Q

Chlamydia trachomatis is a congenital infection transmitted during delivery. The mother may be asymptomatic but the neonate may show…?

A

Neonatal conjunctivitis
Rarely pneumonia

Treat with erythromycin

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12
Q

What is the neonatal period?

A

First 4-6weeks of life

n.b. if the baby is born early (premature), the neonatal period is longer and adjusted for expected birth date

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13
Q

Which organisms are typically involved with neonatal infections?

A

Group B streptococci
E coli
Listeria monocytogenes

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14
Q

What type bacteria and shape are Group B streptococci?

A

Gram +ve coccus
Catalase -ve
B-haemolytic

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15
Q

In neonates, Group B streptococci causes….?

A

Bacteraemia
Meningitis
Disseminated infection e.g. joint infections

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16
Q

What can E coli lead to in neonates?

A

Bacteraemia
Meningitis
UTI

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17
Q

What are early onset sepsis-risk factors (maternal)?

A
Premature labour
Fever
Foetal distress
Meconium staining
Previous Hx
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18
Q

What are early onset sepsis-risk factors (baby)?

A
Birth asphyxia
Resp distress
Low BP
Acidosis
Hypoglycaemia
Neutropenia
Rash
Hepatosplenomegaly
Jaundice
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19
Q

What are investigations used for suspected sepsis/infections during childhood?

A
FBC
C-reactive protein
Urine
Blood culture
Deep ear swab
Lumbar puncture (CSF)
ET secretions if ventilated
Surface swabs
CXR (full body)
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20
Q

What is the treatment for early onset neonatal sepsis?

A

Supportive mgmt

  • Ventilation
  • Circulation
  • Nutrition
  • Antibiotics e.g. benzylpenicillin and gentamicin
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21
Q

What bacteria are causes of late onset sepsis in neonates (after 48-72 hours)?

A

Coagulase negative staphylococci (CoNS)

(Less commonly:
Group B strep
E coli
Listeria monocytogenes
Staph aureus
Enterococcus sp.
Gram negatives (Klebsiella etc)
Candida)
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22
Q

What are clinical features of late onset sepsis in neonates?

A
Bradycardia
Apnoea
Poor feeding/bilious aspirates/abdo distension
Irritability
Convulsions
Jaundice
Resp distress
Increased CRP
Sudden changes in WCC/platelets
Focal inflammation e.g. umbilicus, drip sites etc
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23
Q

What is the treatment for late onset neonatal sepsis?

A

Treat early
Review and stop Abx if cultures are negative and clinically stable
1st line Abx - cefotaxime and vancomycin
2nd line - meropenem

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24
Q

What is the choice of antibiotics for community acquired late onset neonatal sepsis infections?

A

Cefotaxime, amoxicillin ± gentamicin

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25
Viral infections are very common during childhood. What are some examples?
Chickenpox (VZV) HSV (coldsores/stomatitis) HHV6, HHV8, EBV, CMV, RSV, enteroviruses etc
26
Bacterial infections may cause secondary infection in childhood after viral illness. An example is....
iGAS disease post-VZV infection
27
What is the most important bacterial cause of paediatric morbidity and mortality?
Meningitis
28
Diagnosis of meningitis in paeds is confirmed by...?
``` Clinical features Blood cultures Throat swab LP for CSF if possible Rapid Ag screen EDTA blood for PCR Clotted serum for serology if needed later ```
29
What can Streptococcus pneumonia cause?
Meningitis Bacteraemia Pneumonia
30
What bacteria is Gram +ve diploccous, a-haemolytic and has >90 capsular serotypes?
Streptococcus pneumoniae
31
Streptococcus pneumoniae has increasing resistance to which drug?
Penicillin
32
What are the bacteria that can cause meningitis at <3 months?
``` Neisseria meningitidis Streptococcus pneumoniae Haemophilus influenzae (if unvaccinated) GBS E coli Listeria sp ```
33
What are the bacteria that can cause meningitis at 3months-5years of age?
Neisseria meningitidis Streptococcus pneumoniae Haemophilus influenzae (if unvaccinated)
34
Respiratory tract infections account for what proportion of childhood illnesses?
1/3 | most viral and upper RTIs
35
What is the most important bacterial cause of RTIs in children?
Streptococcus pneumoniae Most UK strains remain sensitive to penicillin or amoxicillin
36
Mycoplasma pneumonia causes RTIs in which age group?
Older children | >4years
37
What is the choice of treatment for myocplasma pneumonia RTIs in children?
Macrolides | e.g. azithromycin
38
What are some classical presentations of mycoplasma pneumonia RTIs in school age children/young adults?
``` Fever Headache Myalgia Pharyngitis Dry cough Incubation period = 2-3weeks ``` n.b. many are asymptomatic
39
What are the extrapulmonary manifestations of mycoplasma pneumonia?
``` Haemolysis Neurological Cardiac Polyarthralgia Myalgia Arthritis Otitis media Bullous myringitis ```
40
What is the mechanism of haemolysis due to mycoplasma pneumonia?
IgM antibodies bind to the I antigen on erythrocytes | Cold agglutinins in 60% patients occur
41
What are some extra-pulmonary neurological manifestations in patients with mycoplasma pneumonia?
``` Encephalitis (most common) Aseptic meningitis Peripheral neuropathy Transverse myelitis Cerebellar ataxia ```
42
What are the organisms that can cause UTIs?
E coli Other coliforms e.g. Proteus species, Klebsiella, Enterococcus Coagulas negative Staphylococcus
43
How are UTIs diagnosed in children?
Symptoms if child can give clear Hx Pure growth >10^5cfu/ml Pyuria - pus cells on urine microscopy
44
UTIs are common in children and occur in what % in girls and boys by age 11?
Up to 3% girls by age 11 | Up to 1% boys by age 11
45
If treatment for children's RTI for streptococcus pneumoniae and mycoplasma pneumonia fails to respond, we must consider the bacterial cause to be....?
``` Whooping cough (Bordetella pertussis especially if child is not vaccinated) Tuberculosis (including MDRTB and XDRTB) ```
46
What is the mechanism of neurological manifestations due to mycoplasma pneumonia?
The MoA is currently unknown but it is thought that antibodies cross-react with galactocerebroside
47
What are 4 important types of CNS infections?
1. Meningitis 2. Encephalitis 3. Brain abscess 4. Spinal infections
48
What are the 4 routes of entry for CNS infection?
1. Haematogenous spread 2. Direct implantation 3. Local extension 4. PNS into CNS
49
What are the typical signs and symptoms of meningitis?
Fever Headache Stiff neck Vomiting Light aversion Drowsiness Seizures Non-blanching (petechial/purpuric) rash (in 80% of children) 10% mortality rate
50
What are the signs and symptoms of encephalitis?
Disturbance of brain function
51
What are the causative agents of encephalitis?
``` Rabies virus Arboviruses Trypanosoma species Prions Amoeba ```
52
What are the causative agent(s) of myelitis?
Poliovirus
53
What are the signs and symptoms of myelitis?
Disturbance of nerve transmission
54
What region is affected in (i) meningitis, (ii) encephalitis, (iii) myelitis, and (iv) with neurotoxins?
(i) Meninges (ii) Brain (iii) Spinal cord (iv) CNS + PNS
55
What are the signs and symptoms of neurotoxin syndromes?
Paralysis Rigid (tetanus) OR flaccid (botulism)
56
What are the causative agents of neurotoxin syndrome?
Clostridium tetani | Clostridium botulinum
57
What is the difference between meningitis and meningoencephalitis?
Meningitis is the inflammatory process of meninges and CSF. Meningoencephalitis is the inflammation of meninges AND brain parenchyma.
58
What mechanisms does neurological damage occur in meningitis?
Direct bacterial toxicity Indirect inflammation with cytokine release and oedema Shock, seizures and cerebral hypoperfusion
59
In the UK, around 5% meningitis survivors have long-term neurological sequelae, mainly....
Sensorineural deafness
60
What are some common causative agents of acute meningitis?
``` Neisseria meningitidis Strep pneumoniae Haemophilus influenzae Listeria monocytogenes Group B Streptococcus E coli ```
61
How is Neisseria meningitidis transmitted?
Person-to-person Through nasopharyngeal mucosa From asymptomatic carriers
62
Pathogenic strains of Neisseria meningitidis are found in what % of carriers?
1% of N.meningitidis are pathogenic
63
Neisseria meningitidis can cause....
Meningitis (50% cases) Septicaemia (7-10%) Septicaemia AND meningitis (40%) These clinical differences are important for treatment choice for shock vs only increased ICP.
64
What 4 processes produce the clinical spectrum for septicaemia?
1. Capillary leak 2. Coagulopathy 3. Metabolic derangement (namely acidosis) 4. Myocardial failure (i.e. multi-organ failure)
65
How does the capillary leakage process contribute to septicaemia?
Leakage of albumin and other plasma proteins results in hypovolaemia
66
How does the coagulopathy process contribute to septicaemia?
Bleeding and thrombosis occur Due to endothelial injury and platelet-release reactions Protein C pathway and plasma anticoagulants are also involved
67
What is an example of chronic meningitis?
Tuberculous chronic meningitis Commoner in immunosuppressed
68
Which regions does tuberculous chronic meningitis involve?
Meninges and basal cisterns of the brain and spinal cord
69
What can tuberculous chronic meningitis result in?
Tuberculous granulomas Tuberculous abscesses Cerebritis
70
What is the most common infection of the CNS?
Aseptic meningitis PC: headache, stiff neck and photophobia ± rash.
71
What are the causative organism(s) of aseptic meningitis in 80-90% cases?
Coxsackievirus group B Echoviruses (often in children <1yr)
72
How is encephalitis transmitted?
Commonly from person to person | Or through vectors (mosquitoes, lice, ticks)
73
West Nile virus is an international cause of which infection?
Encephalitis
74
What organism can cause bacterial encephalitis?
Listeria monocytogenes n.b. toxoplasmosis can also cause CNS encephalitis
75
What organism(s) can cause amoebic encephalitis?
Naegleria fowleri (lives in warm water) Acanthamoeba Balamuthia mandrillaris These can cause brain abscesses, aseptic or chronic meningitis
76
A focal CNS infection may be indicated by the presence of....?
Brain abscess
77
What are some disorders involved with the pathophysiology of brain abscesses?
1. Otitis media; mastoiditis; paranasal sinuses 2. Endocarditis (haematogenous spread) 3. Tuberculous meningitis
78
What is the most common form of spinal vertebral infection?
Pyogenic vertebral osteomyelitis
79
If pyogenic vertebral osteomyelitis (spinal infection) is left untreated, what can result?
Permanent neurological deficits Significant spinal deformity Death
80
What are some risk factors for spinal infections?
``` Advanced age IV drug use Long-term systemic steroids Diabetes mellitus Organ transplant Malnutrition Cancer ```
81
What investigation is the best for detecting parenchymal abnormalities e.g. abscesses and infarction?
MRI
82
What investigations are useful for CNS infections?
CSF sample Brain tissue MRI (for parenchymal abnormalities e.g. abscesses and infarction)
83
A 20 year old woman presents with headache and neck stiffness. Gram stain shows Gram +ve cocci. What is the causative pathogen?
Strep pneumoniae
84
A 18 year old man present with headache and neck stiffness. Gram stain shows Gram -ve cocci. What is the causative pathogen?
N. meningitidis
85
A 65 year old presents with headache and neck stiffness. Gram stain shows Gram +ve bacillus/rods. What is the causative pathogen?
Listeria monocytogenes
86
A 45 year old presents with headache and neck stiffness. A Ziehl-Neelsen stain was done and was positive. What is the causative pathogen?
Mycobacterium TB
87
A 35 year old presents with headache and neck stiffness. Indian ink stain tests were done and were positive. What is the causative pathogen?
Cryptococcus neoformans Increased risk in HIV patients
88
What is the generic treatment plan for meningo-encephalitis?
Aciclovir 10mg/kg IV tds Ceftriaxone 2g IV bd If >50yrs or immunocompromised add: amoxicillin 2g IV 4hourly
89
Define uncomplicated urinary tract infection
Infection in a structurally and neurologically normal urinary tract
90
Define complicated urinary tract infection
Infection in a urinary tract with functional or structural abnormalities (including indwelling catheters and calculi).
91
Complicated urinary tract infections tend to occur in which groups of patients?
Men Pregnant women Children Patients who are hospitalised/in healthcare associated settings
92
More than 95% of urinary tract infections are caused by a single bacterial species. What is the most frequent infecting organism in acute infection?
E.coli
93
Apart from E.coli causing the majority of UTIs, what other organisms can cause them?
``` Proteus mirabilis Klebsiella aerogenes Enterococcus faecalis Staphylococcus saprophyticus Staphylococcus epidermis ```
94
What are 3 antibacterial host defences in the urinary tract?
1. Urine (osmolality, pH, organic acids) 2. Urine flow and micturition 3. Urinary tract mucosa (bactericidal activity, cytokines)
95
What is the urethra usually colonised with?
BActeria
96
The female urethra is short and in promiximity to what?
The warm and moist vulvar and perianal areas This makes contamination likely. Bacteria is pushed into the female bladder (risk increases during sex)
97
Organisms that cause UTIs in women tend to colonise which regions before the urinary infection results?
Vaginal introitus | Periurethral area
98
Once bacteria is within the bladder, bacteria may multiply and where can it pass up?
Ureters | Especially if vesicoureteral reflux is present, up to the renal pelvis and parenchyma
99
How do renal/urinary tract abnormalities interfere and increase infection risk?
Obstruction inhibits natural urine flow and resulting stasis occurs
100
Name extra-renal causes of obstruction of the renal/urinary tract that can increase UTI risk?
- Valves, stenosis, or bands - Calculi - Extrinsic ureteral compression from a variety of causes - Benign prostatic hypertrophy
101
Name intra-renal causes of obstruction of the renal/urinary tract that can increase UTI risk?
- Nephrocalcinosis - Uric acid nephropathy - Analgesic nephropathy - Polycystic kidney disease - Hypokalemic nephropathy - Renal lesions of sickle cell trait/disease
102
Name neurogenic malfunction causes of obstruction of the renal/urinary tract that can increase UTI risk?
Poliomyelitis Tabes dorsalis, Diabetic neuropathy Spinal cord injury
103
The kidney is frequently the site of abscesses in patients with what infections?
Staphylococcus aureus bacteremia Or endocarditis (Or both. This is by the haematogenous route)
104
Infection of the kidney with which type of bacteria RARELY occurs by the haematogenous route?
Gram-negative bacilli | it is more common with Staph aureus or endocarditis
105
What do the lower urinary tract symptoms result from?
Bacteria causing irritation of urethral and vesical mucosa, causing frequent and painful urination of small amounts of turbid urine
106
What are the lower UTI symptoms present in patients?
``` Frequency Painful urination Small amounts of turbid urine Suprapubic heaviness/pain Grossly bloody urine/bloody tinge at end of micturition ``` (fever tends to be absent in infections limited to the lower tract)
107
What are the upper UTI symptoms present in patients?
Fever (±rigors) Flank pain Frequently lower UTI symptoms too (frequency, urgency, dysuria) - these may occur before the upper tract symptoms by 1-2 days
108
What are the symptoms of UTIs in older/elderly patients?
- Majority are asymptomatic - When they are present, are not diagnostic as many old people have frequency, dysuria, hesitancy, incontinence anyway - Atypical upper UTI symptoms e.g. abdo pain, change in mental status
109
What are the investigations for (i) uncomplicated UTIs/pyelonephritis and (ii) complicated UTIs?
(i) Urine dipstick MSU for urine MC&S Bloods (FBC, U&Es, CRP, inflammatory markers + renal function) (ii) The above investigations but also renal USS and IV urography
110
How can we sample urine for testing in UTIs?
- Midstream clean catch (MSU) - Catherisation - Suprapubic aspiration
111
The presence of white cells (pyuria) in the urine under the microscope indicates what?
Infection
112
The presence of squamous epithelial cells in the urine under the microscope indicates what?
Contamination of the sample
113
What are some causes of sterile pyuria (presence of white cells in urine without any apparent infection)?
- Prior treatment with antibiotics - Calculi - Catheterisation - Bladder neoplasm - TB - Sexually transmitted diseases
114
The treatment for UTIs is empirical therapy, community based for lower UTIs and local guidance. How many days of therapy should be given for UTIs?
- 3 days of therapy with standard doses for treatment of uncomplicated lower UTIs in women - Longer therapy for those with H/O previous UTIs, Abx resistance, >7days symptoms - 7 days of therapy in men
115
What is the treatment for catheter-associated UTIs?
- Remove catheter - Aminoglycosides (e.g. gentamin, amikacin) before catheter removal - Oral fluconazole is NO more effective than no therapy
116
Most UTIs with indwelling catheters are caused by which organism?
Candida fungal infection
117
Oral fluconazole is not given to those with Candida fungal UTIs caused by catheters, except in which patients?
Renal transplant patients | Patients who are about to undergo elective urinary tract surgery
118
The kidney itself is NOT uniformly susceptible to infection. What is the susceptibility in the medulla vs the cortex?
- Few organisms are needed to infect the medulla | - 10,000x are needed to infect the cortex
119
What is pyelonephritis commonly associated with?
Sepsis
120
Pyelonephritis is commonly associated with sepsis so it needs more aggressive treatment such as....?
Co-amoxiclav ±/gentamicin Imaging: calculi, structural cause
121
What are the complications of pyelonephritis?
- Perinephric abscess - Chronic pyelonephritis (scarring, chronic renal impairment) - Septic shock - Acute papillary necrosis
122
What are 3 major pathogens in surgical site infections?
1. Staph aureus (MSSA and MRSA) 2. E.coli 3. Psuedomonas aeruginosa
123
What is the pathogenesis mechanism of surgical site infections?
1. Contamination of wound at operation 2. Pathogenicity and innoculum of microorganisms 3. Host immune response
124
What are the 3 levels of surgical site infection?
1. Superficial incisional - skin and subcutaneous tissue 2. Deep incisional - fascial and muscle layers 3. Organ/space infection
125
The presence of pus with cluster cocci with a surgical site infection is most likely to be which of the organisms: (a) E.coli (b) Enterobacter (c) Neisseria meningitides (d) MRSA
MRSA
126
Diabetes increases the risk of surgical site infection by 2-3x. How can this be managed?
Control blood glucose Aim for HbA1C <7 This is because DM is associated with post-operative hyperglycaemia
127
Rheumatoid arthritis increases the risks of surgical site infections. How can this be managed?
Stop disease modifying agents for 4 weeks pre- and 8 weeks post-operatively.
128
Why is there greater risk of surgical site infection in patients with obesity (BMI>35 have 5-7x greater risk)?
Adipose tissue is poorly vascularised | Poor oxygenation of tissues and functioning of the immune response increases SSI risk
129
Why is there greater risk of surgical site infection in patients who smoke?
Nicotine delays primary wound healing Peripheral vascular disease Therefore encourage tobacco cessation
130
Why is pre-operative showering encouraged?
- Microorganisms colonising skin may contaminate exposed tissues and cause surgical site infections - Patients should wash using soap on operation day or the day before
131
Why is hair removal is not encouraged before operations?
Micro-abrasions caused by shaving with a razor may lead to multiplication of bacteria in surgical site infections (Use electric clippers on the day of surgery with single-use head)
132
Staph aureus contaminates the nasal region in what % of people?
20-30% High RF for surgical site infections
133
Why does mild hypothermia during surgery appear to increase the risk of surgical site infections?
Vasoconstriction Decreased O2 delivery to the wound space Subsequent impairment of neutrophil function therefore peri-operatively give high O2
134
Give 4 bone and joints infections that will increase the risks of surgical site infections?
1. Septic arthritis 2. Vertebral osteomyelitis 3. Chronic osteomyelitis 4. Prosthetic joint infection
135
What are the risk factors for septic arthritis?
- RhA, OA, crystal-induced arthritis - Joint prosthesis - IV drug abuse - Diabetes, chronic renal disease, chronic liver disease - Immunosuppression, steroids - Trauma: intra-articular injection, penetrating injury
136
What is the pathophysiology of septic arthritis?
Organisms adhere to the synovial membrane Bacteria proliferate in synovial fluid and generate a host inflammatory response Joint damage exposes host-derived proteins e.g. fibronectin, to which bacteria adhere
137
Staph aureus has receptors that can recognise selected host proteins. What is an example of a receptor that it has?
Fibronectin binding protein | binds to fibronectin which is a host-derived protein that is exposed from joint damage
138
Kingella kingae is a bacteria that can adhere to the synovial membrane in septic arthritis. How does it adhere?
Bacterial pili
139
Some strains of Staph aureus produce what cytotoxin that has been associated with fulminant infections in septic arthritis?
Cytotoxin PVL | Panton-Valentine Leucocidin
140
What are the causative organisms of septic arthritis?
1. Staph aureus (46%) 2. Coagulase negative staph (4%) 3. Streptococci (22%) - pyogenes, pneumoniae, agalactiae 4. Gram negative organisms - E.coli, HI, Neisseria, § 5. Rare: Lyme, brucellosis, mycobacteria, fungi
141
What are the clinical features of septic arthritis?
- 1-2 week H/O red, painful, swollen restricted joint - Monoarticular in 90% - Knee is involved in 50% - Patients with rheumatoid arthritis may show more subtle signs of joint infection
142
Is septic arthritis polyarticular or monoarticular?
Monoarticular in 90%
143
What signs may be present on imaging of septic arthritis?
USS - joint effusion CT - erosive bone change, periarticular soft tissue extension MRI - effusion, articular cartilage destruction, abscess, contiguous osteomyelitis
144
What is the treatment for septic arthritis?
- Antibiotics (up to 6 weeks therapy can be given) | - Drainage
145
Vertebral osteomyelitis can be classified into which 2 categories?
1. Acute haematogenous | 2. Exogenous - after disc surgery, or implant associated
146
What are the causative organisms of vertebral osteomyelitis?
1. Staph aureus (48.3%) 2. Coagulase negative staph 3. Gram negative rods 4. Strep
147
Where can vertebral osteomyelitis infections be localised to and in what %?
Cervical (10.6%) Cervico-thoraco (0.4%) Lumbar (43.1%)
148
What are the symptoms of vertebral osteomyelitis?
``` Back pain (86%) Fever (60%) Neurological impairment (34%) ```
149
How is vertebral osteomyelitis diagnosed?
MRI - 90% sensitive Blood cultures CT/open biopsy
150
What is the treatment for vertebral osteomyelitis?
6 weeks of treatment (flucocloxacillin usually) | Longer treatment if undrained abscesses or implant associated
151
What are 3 characteristic features of chronic osteomyelitis?
Pain Brodies' abscess Sinus tract
152
How is chronic osteomyelitis diagnosed?
MRI | Bone biopsy for culture and histology
153
What is the treatment for chronic osteomyelitis?
Radical debridement down to living bone Remove sequestra, and remove infected bone and soft tissue
154
What are signs of prothetic joint infections?
Pain Patient complains that the joint was 'never right' Early failure Sinus tract
155
Define sinus tract
A narrow opening or passageway under the skin that can extend in any direction through soft tissue and results in dead space with potential for abscess formation
156
What are the causative organisms for prosthetic joint infections?
- Gram +ve cocci (CoNS, Staph aureus, strep, entero) - Aerobic gram -ve bacilli (entero, pseudomonas) - Anerobes - Polymicrobial - Cultural negative - Fungi
157
How are prosthetic joint infections diagnosed?
- Radiology: loosening - CRP >13.5 (prosthetic knee joint) - CRP >5 (hip joint) - Joint aspiration where WCC >1700/ml (knee) - WCC >4200/ml (hip)
158
What does the 'Endo Klinik single stage revision' treatment for prosthetic joint infection involve?
- Aspirate joint to identify pathogen - Removal of infected tissue, foreign material, dead bone - Re-implant new prosthesis with antibiotic impregnated cement - IV antibiotics
159
What does the 'two stage revision' treatment for prosthetic joint infection involve?
- Remove prosthesis - Take samples for MC+S and histology - 6 weeks IV antibiotics - Stop Abx for 2 weeks - Re-debride and sample at second stage - Re-implant with antibiotic impregnated cement - No further antibiotics if samples clear
160
A 70year old women had a 1994 right total hip replacement, and 1998 revision of acetabular component. X-ray shows lysis around the distal part of the femoral component. H/O diabetes. What is the likely pathogen involved here: (a) Coagulase negative staphylococci (b) Staph aureus (c) E.coli (d) Haemophilus influenzae
Coagulase negative staphylococci Rx: IV vancomycin and oral rifampicin 8 weeks later had second stage revision and cultures showed no growth.
161
How do leucocyte derived proteases and cytokines act as host factors contributing to the pathogenesis of septic arthritis?
Cartilage degradation | Bone loss
162
How does raised intra-articular pressure (a host factor) contribute to the pathogenesis of septic arthritis?
Impaired capillary blood flow | Cartilage and bone ischaemia and necrosis
163
Name 4 host factors involved in the pathogenesis of septic arthritis (n.b. bacterial factors include binding proteins, synovial membrane adherence and cytotoxins)
- Leucocyte derived proteases and cytokines - Raised intra-articular pressure - Genetic deletion of macropage-derived cytokines - Absence of IL-10
164
How does the genetic deletion of macrophage-derived cytokines (a host factor) contribute to the pathogenesis of septic arthritis?
E.g. lymphotoxin-a, TNF-a, IL-1 receptor When present, these reduce host response normally in S.aureus sepsis in animal models. i.e. genetic variation in cytokine expression increases susceptibility to septic arthritis
165
How does the absence of IL-10 (a host factor) contribute to the pathogenesis of septic arthritis?
IL-10 absence in KO mice increases the severity of staphylococcal joint disease i.e. genetic variation in cytokine expression increases susceptibility to septic arthritis
166
Which groups are the most vulnerable to GI infections?
Infants | Elderly
167
What are 6 reportable GI infections?
``` Campylobacter Salmonella Shigella E.coli 0157 Listeria Norovirus ```
168
For Campylobacter, what is the: | a) incubation period (b) duration (days (c) associated risk factors?
(a) 1-10 days (b) 2-20 days (c) Poultry
169
For E.coli 0157, what is the: | a) incubation period (b) duration (days (c) associated risk factors?
(a) 1-5 days (b) 1-4 days (c) HUS, verotoxin
170
For Shigella, what is the: | a) incubation period (b) duration (days (c) associated risk factors?
(a) 12-96hrs (b) 5-7 days (c) Small infective dose, outbreaks
171
For Salmonella (non-typhoidal, what is the: | a) incubation period (b) duration (days (c) associated risk factors?
(a) 8-48hrs (b) 4-7 days (c) Rare cause systemic diagnosis
172
For Vibrio parahaemolyticus, what is the: | a) incubation period (b) duration (days (c) associated risk factors?
(a) 24-72hrs (b) 2-10 days (c) Shellfish
173
For Vibrio cholera, what is the: | a) incubation period (b) duration (days (c) associated risk factors?
(a) 1-5 days (b) Variable (c) 'Ricewater stools', endemic
174
For Bacillus cereus, what is the: | a) incubation period (b) duration (days (c) associated risk factors?
(a) 1-6hrs (b) <1 day (c) Heat stable emetic toxin i.e. rice
175
For Staph aureus, what is the: | a) incubation period (b) duration (days (c) associated risk factors?
(a) 2-7hrs (b) <1 day (c) Preformed toxins
176
What does the mechanism of cholera GI infection involve?
- Cholera (secretory-diarrhoea) toxin - Superantigens - Host responses causing inflammation
177
Describe the mechanism of cholera disease involving cholera toxin (secretory diarrhoea toxin)?
- Cholera toxin binds to proteins - Via cAMP, Cl- channels open at the apical membrane of enterocytes - Cl- efflux into the lumen occurs - H2O and electrolytes are lost
178
Describe the mechanism of cholera disease involving superantigens?
- Superantigens bind directly to T-cell receptors and MHC molecules - This occurs OUTSIDE the peptide binding site - Massive cytokine production by CD4 cells occur - This causes systemic toxicity and suppression of adaptive response
179
Describe the host responses in bacteraemia mechanism of disease?
Inflammatory diarrhoea or enteric fever (interstitial inflammation)
180
Staphylococcus aureus can cause food poisoning. What is its method of transmission?
1/3 of the population are chronic carriers, and 1/3 transiently carry it. It is spread by skin lesions on food handlers.
181
What features do Staphylococcus aureus bacteria (that cause food poisoning) show on MC+S?
- Catalase, coagulase positive Gram positive coccus - In tetrads/clusters on Gram stain - Yellow colonies on blood agar
182
Staphylococcus aureus bacteria (that cause food poisoning) produces what toxin, which induces what clinical features?
- An enterotoxin (exotoxin) that can act as a superantigen in the GI tract is produced - Releases IL-1 and IL-2 - Causes prominent vomiting and watery, non-bloody diarrhoea
183
What is the treatment for the prominent vomiting, and watery, non-bloody diarrhoea caused by the enterotoxins and superantigens in Staph aureus food poisoning?
Do not treat | Self-limiting
184
What are gram-positive rods (spore-forming) that cause food poisoning?
Bacillus cereus | spores germinate in reheated fried rice
185
What are the 2 toxins involved in Bacillus cereus?
- Heat stable emetic toxin (not destroyed by reheating rice) | - Heat labile diarrhoeal toxin (food is not cooked to a high enough temperature)
186
What are the clinical features of Bacillus cereus?
Watery, non-bloody diarrhoea (self-limiting) Rare cause of bacteraemia in vulnerable populations Cerebral abscesses (rare)
187
What is a gram-positive anaerobe that can cause botulism and food poisoning?
Clostridia - Clostridium botulinum = botulism - Clostridium pefringens = food poisoning
188
What is the source of clostridium botulinum (botulism)?
Canned or vacuum packed foods Ingestion of preformed toxin (inactivated by cooking) e.g. in honey for infants
189
What is the mechanism of clostridium botulinum gram +ve anaerobe that causes botulism, and the treatment?
- Blockade of ACh release from peripheral nerve synapses | - Treat with antitoxin
190
What is the source of Clostridium pefringens (food poisoning)?
Reheated food (meat)
191
What is the incubation period and clinical features for Clostridium perfringens (food poisoning, Gram +ve anaerobe)?
Incubation = 8-16hours Watery diarrhoea Cramps Little vomiting lasting 24hrs
192
What is the mechanism of clostridium botulism (gram +ve anaerobe) causing food poisoning?
The enterotoxin acts as a superantigen, and affects the colon (but not the small bowel small bowel)
193
Pseudomembranous colitis can occur with Clostridium difficile which is antibiotic-related colitis. This occurs in how many hospitalised patients, and mainly with which antibiotics?
3-30% patients Cephalosporins, cipro and clindamycin are often involved
194
What is the treatment for closteridium difficile?
Metrodinadazole Vancomycin (taken orally) Stop other Abx where possible
195
Listeria monocytogenes presents in a population as...?
Outbreaks of febrile gastroenteritis
196
What does the stain for Listeria monocytogenes show?
Gram-positive rod B-haemolytic Aersculin positive Tumbling motility
197
What is the source for Listeria monocytogenes GI infection?
Refrigerated food (cold enhancement) i.e. unpasteurised dairy Vegetables (Grows at 4 degrees c)
198
What are the clinical symptoms of Listeria monocytogenes?
``` Watery diarrhoea Cramps Headache Fever Little vomiting ```
199
What patient groups are particularly susceptible to Listeria monocytogenes?
``` Perinatal infection (pregnant women) Immunocompromised patients ```
200
What is the treatment for Listeria monocytogenes?
Ampicillin
201
Describe features of enterobacteriacae?
Facultative anerobes Glucose/actose fermenters (LF) Oxidase negative
202
E.coli is also described as traveller's diarrhoea. What is the source of E.coli?
Food/water contaminated with human faeces
203
What are the enterotoxins involved with the mechanism of disease in E.coli and where do they act?
- Heat labile stimulates adenyl cyclase and cAMP - Heat stable stimulates guanylate cyclase These act on jejeunum and ileum, not on colon
204
Name the various types of E.coli that match up with the features: (a) Toxigenic, main cause of traveller's diarrhoea (b) Pathogenic, infantile diarrhoea (c) Invasive, dysentery (d) Haemorrhagic, can cause HUS
(a) ETEC = toxigenic, main cause of traveller's diarrhoea (b) EPEC = pathogenic, infantile diarrhoea (c) EIEC = invasive, dysentery (d) EHEC = haemorrhagic (O157), can cause HUS (H7)
205
What bacteria is a non-lactose fermenter and H2S producer?
Salmonella | tests use TSI agar, XLD agar and selenite F broth
206
What are the 3 species of Salmonellae?
1. S. typhi (and paratyphi) 2. S. enteritidis 3. S. cholerasuis
207
What antigens are produced by Salmonellae?
- Cell wall O (groups A-I) - Flagellar H - Capsular Vi (virulence, anti-phagocytic)
208
How is Salmonella enteritidis (enterocolitis) transmitted?
Poultry Eggs Meat
209
How is Salmonella typhi (typhoid/enteric fever) transmitted?
Only by humans | Multiplies in Payer's patches
210
What regions does Salmonella enteritidis invade to cause enterocolitis?
Epithelial and sub-epithelial tissue of small and large bowel
211
What are the clinical symptoms and signs of enterocolitis (Salmonella enteritidis)?
Non-bloody diarrhoea (self-limiting, no treatment needed) Bacteraemia is rare Stool positivity diagnoses
212
What are the clinical symptoms and signs of typhoid/enteric fever (Salmonella typhi)?
``` Slow onset fever Constipation Splenomegaly Rose spots Anaemia + leukopenia Bradycardia Haemorrhage and perforation ```
213
How is salmonella typhi (typhoid/enteric fever) diagnosed and treated?
Diagnosis is with a positive blood culture Treatment = ceftriaxone
214
What bacteria is a non-lactose fermenter, non-H2S producer and non-motile?
Shigellae
215
What antigens are present with Shigellae?
- Cell wall O antigens | - Polysaccharide (groups A-D): S.sonnei, S.dysenteriae, S.flexneri (MSM)
216
What is the most effective enteric pathogen?
Shigella Due to low infectious dose required (50) n.b. it has no animal reservoir or carrier state
217
Dysentery (caused by Shigellae dysenteriae) involves what processes?
- Invasion of cells of mucosa of distal ileum and colon | - Shiga enterotoxin is produced
218
What is the treatment for Shigellae infections?
Avoid antibiotics | But ciprogloxacin given if required
219
What are some features of Vibrios (cholera) bacteria?
Curved Comma-shaped Late lactose fermenters Oxidase positive
220
What are the types of Vibrio cholera?
- O1 group = endemics, with various biotypes and serotypes | - Non-O1 group = sporadic or non-pathogens
221
How is vibrio transmitted?
Contamination of water and food from human faeces (shellfish, oysters, shrimp)
222
What is the mechanism of action for vibrio cholerae?
Colonisation of small bowel Secretion of enterotoxin with A and B subunit, which persistently stimulate adenylate cyclase and cAMP Opens Cl- channels and causes massive diarrhoea (rice water stool) without inflammatory cells
223
What is the treatment for vibrio cholerae infection?
Treat the losses (i.e. supportive) | ± Doxycycline
224
What are the species of Vibrios?
- Vibrios cholera (O1 and non-O1 group) - Vibrio parahaemolyticus - Vibrio vulnificus
225
How is Vibrio parahaemolyticus transmitted?
Ingestion of raw or undercooked seafood (i.e. oysters) Major cause of diarrhoea in Japan Self-limiting (3days)
226
How is vibrio vulnificus transmitted?
Cellulitis in shellfish handlers In HIV patients, it induces sepsis, D+V.
227
What is the treatment for vibrios pathogens?
Doxycycline
228
What are the features of. Campylobacter bacteria?
``` Curved, comma or S-shaped Micro-aerophilic C.jejuni at 42 degrees C Oxidase positive Motile ```
229
Campylobacter is self-limiting but symptoms can last for weeks (up to 20 days). We only treat campylobacter in which patients and using which treatment?
Only treat if immunocompromised Rx macrolides
230
How is campylobacter transmitted?
Contaminated food and water with animal faeces | poultry, meat, unpasteurised milk
231
What are the clinical features of Campylobacter?
Watery, foul-smelling diarrhoea Bloody stool Fever and severe abdominal pain
232
What are 3 long-term sequelae that may occur post-Campylobacter infection?
GBS syndrome Reactive arthritis Reiter's syndrome
233
What is the treatment for campylobacter?
Erythromycin or ciprofloxacin if infection is in the first 4-5 days
234
What can Yersinia enterocolitica cause?
Enterocolitis | Mesenteric adenitis
235
What conditions is Yersinia enterocolitica associated with?
Reactive arthritis | Reiter's syndrome
236
What are some features of Yersinia enterocolitica bacteria?
Non-lactose fermenter | Prefers 4 degrees C i.e. 'cold enrichment'
237
How is Yersinia enterocolitica transmitted?
Via contaminated food with domestic animal faeces
238
What condition is caused by Mycobacteria (M.Tuberculosis, M.Avium Intracellulare)?
Tuberculosis
239
Give 3 examples of protozoa
Entamoeba histolytica Giardia lamblia Cryptosporidium parvum
240
What are the features of the protozoa, entamoeba histolytica, in (i) diarrhoea, and (ii) non-diarrhoeal illness?
(i) Motile trophozoite in diarrhoea (ii) Non-motile cyst in non-dirrhoeal illness 4 nuclei, no animal resevoir
241
How is entamoeba histolytica removed normally?
Killed by boiling or removed by water filters
242
What is the mechanism of action of entamoeba histolytica?
Ingestion of cysts leads to trophozoites in the ileum These colonise the caecum and colon Results in 'flask-shaped' ulcers
243
What are the acute and chronic clinical features of entamoeba histolytrica?
Acute: dysentery, flatulence, tenesmus Chronic: weight loss, ±diarrhoea, liver abscess
244
How is entamoeba histolytica confirmed on diagnosis?
Stool microbiology shows wet mount, iodine and trichrome | Serology confirms in invasive disease
245
What is the treatment for entamoeba histolytica protozoal infection?
Metronidazole and peromomycin in luminal disease
246
What protozoa has the features of a 'pear-shaped' trophozoite, 2 nuclei, 4 flagella and a suction disc?
Giardia lamblia
247
How is giardia lamblia protozoal infection transmitted?
Ingestion of cyst from faecally contaminated water or food
248
What is the mechanism of action of giadia lamblia infection?
Excystation at duodenum Pear-shaped trophozoite attaches No invasion Results in malabsorption of protein and fat
249
What groups of people are likely to suffer from Giardia lamblia infection?
``` Travellers Hikers Day-care Psychiatric hospitals MSM ```
250
What are the clinical features of giardia lamblia?
Foul-smelling, non-bloody diarrhoea Cramps Flatulence No fever
251
How is the diagnosis made for giardia lamblia, and what is the treatment?
Stool MC+S ELISA 'String test' Rx = metronidazole
252
Stool MC+S for using the modified Kinyoun acid fast stain is used for the diagnosis of which infection, and what is shown?
Oocysts are seen in the stool by modified Kinyoun acid fast stain with Cryptosporidium parvum (protozoal infection affecting jejenum)
253
Give 3 reasons why norovirus tends to cause outbreaks?
- Low infectious dose needed (18-1000 viral particles) - Environmental resilience (survives in 0-60 degrees) - No long immunity against it
254
GII.4 is currently the predominant stain of what infection?
Norovirus
255
A dsRNA 'wheel-like' virus refers to which virus?
Rotavirus
256
Rotavirus replicates in which region?
The mucosa of the small intestine
257
What are the clinical features of rotavirus?
- Secretory diarrhoea (with no inflammation) | - Watery diarrhoea (mechanism unknown, but may be caused by stimulation of the enteric nervous system)
258
Rotavirus is common and by age 6 most children globally have antibodies to at least one type. What confers lifelong immunity to rotavirus?
Exposure to natural rotavirus infection twice confers lifelong immunity
259
What types of adenovirus cause non-bloody diarrhoea below 2 years of age?
Types 40 and 41
260
In immunocompromised patients, what types of adenovirus cause non-bloody diarrhoea and infection?
ANY type
261
Using which investigations can we detect and diagnose adenovirus GI infections?
Stool MC+S Antigen detection PCR
262
Poliovirus, enteroviruses (coxsackie, ECHO), hepatitis A are all transmitted via which route?
Faecal-oral route
263
Vaccines for cholera exist for serogroups O1 and O139 in which 2 forms?
(a) Inactivated, whole cell with B-subunit of toxins | (b) Live attenuated, but not recommended
264
Vaccines are available/being tested for which GI infection pathogens?
- Cholera - Campylobacter - ETEC - Salmonella typhi - Rotavirus
265
Bacterial organisms that can cause vertebral oseomyelitis include...
Brucella | Salmonella
266
What two techniques can be used for the surgical treatment of chronic osteomyelitis?
- Modified Lautenbach technique | - Papineau technique (this has a higher success rate)
267
What are the mechanisms that antibiotics target
1. inhibitors of cell wall synthesis 2. inhibitors of protein synthesis 3. inhibitors of DNA, RNA synthesis enzymes (DNA gyrase) 4. inhibitors of folate metabolism 5. cell membrane toxins
268
Which antibiotics are inhibitors of cell wall synthesis?
- B-lactams: penicillins, cephalosporins, carbapenems | - Glycopeptides: vancomycin, teicoplanin
269
B-lactams (cell wall synthesis inhibitors, bactericidal) include
- penicillins e.g. piperacillin - cephalosporins - carbapenems Active against rapidly dividing bacteria. Ineffective against bacteria that lack cell walls (e.g. Mycoplasma + Chlamydia).
270
Glycopeptides (cell wall synthesis inhibitors) include
- Vancomycin | - Teicoplanin
271
B-lactamase inhibitors are useful for protecting penicillins from enzymatic breakdown and include coverage to S.aureus, GRam negatives and anerobes. What are 2 examples?
- Clavulanic acid (given with amoxicillin = co-amoxiclav) | - Tazobactam (given with piperacillin = piptaz)
272
What is a 1st generation cephalosporin?
Cephalexin
273
What is a 2nd generation cephalosporin?
Cefuroxime Active against many b-lactamases produced by Gram negatives. Similar cover to co-amoxiclav but less active against anaerobes.
274
What are three 3rd generation cephalosporins?
- Cefotaxime - Ceftriaxone - Ceftazidime [useful against Psuedomonas].
275
Extended spectrum B-lactamase (ESBL) will produce organisms that are resistant to....
ALL cephalosporins Therefore carbapenems must be used to treat ESBL enzyme infections
276
Carbapenems include...
Meropenem Imipenem Ertapenem Useful for treating ESBL infections
277
Carbapenemase enzymes are seen in which severe infections
Multi-drug resistant Acinetobacter and Klebsiella species
278
How are b-lactams excreted?
Renally excreted Relatively non-toxic with short half-life
279
Glycopeptides are bactericidal and inhibit cell wall synthesis (like b-lactams!). What are 2 examples
Vancomycin [treats MRSA] Teicoplanin n.b. these are nephrotoxic. Active against Gram +ves
280
Which antibiotics are inhibitors of protein synthesis (5 types)?
- Aminoglycosides: gentamicin, amikacin, tobramycin - Tetracyclines - Macrolides: erythromycin, clindamycin - Chloramphenicol - Oxazolidinones: linezolid
281
Aminoglycosides (inhibitors of protein synthesis) examples and side effects
- Gentamicin - Amikacin - Tobramycin Bactericidal. Otoxic and nephrotoxic. Active versus pseudomonas aeruginosa.
282
Tetracyclines (inhibitors of protein synthesis): (a) are useful against which pathogens? (b) what are the side effects?
- Active against most bacteria INCLUDING intracellular pathogens e.g. chlamydia, mycoplasma, rickettsia - Widespread resistance however SE: Light-sensitive rash - Contraindicated in pregnancy and children
283
Macrolides (inhibitors of protein synthesis) examples, and which pathogens are they active against
- Erythromycin - Clarithromycin - Azithromycin Active against staph + strep in those allergic to penicillin. Also active against Campylobacter + Legionella
284
Chloramphenicol (inhibitor of protein synthesis) is a bacteriostatic, with broad anti-bacterial activity, rarely used drug now. Why is it rarely used?
Risk of aplastic anaemia | Grey baby syndrome in neonates
285
Oxazolidinones (inhibitor of protein synthesis) - what is an example and what is it active against?
Linezolid Highly active against gram +ve organisms, including MRSA and VRE. But it is expensive.
286
Linezolid is an oxazolidinone (inhibitor of protein synthesis). It is highly active against gram +ve organisms, including MRSA and VRE. It is expensive and may cause which side effect?
Thrombocytopenia
287
Inhibitors of DNA synthesis antibiotics include...
- Quinolones: ciprofloxacin, levofloaxin, moxifloxacin | - Nitroimidazoles: metronidazole, tinidazole
288
Quinolones (or fluoroquinolones) are inhibitors of DNA synthesis by DNA gyrase. They are bactericidal. What are examples and what are they active against?
- Ciprofloxacin - Levofloxacin Active versus gram -ve including Pseudomonas aeruginosa. Active against gram +ves too and intracellular like chlamydia.
289
Nitroimidazoles are inhibitors of DNA synthesis. Rapidly bactericidal. Examples and what is it active against?
- Metronidazole - Tinidazole Active versus anaerobes and protozoa e.g. Giardia
290
Nitroimidazoles are inhibitors of DNA synthesis that are rapidly bactericidal e.g. metronidazole. These are related compounds to....
Nitrofurans e.g. nitrofurantoin
291
Inhibitors of RNA synthesis antimicrobials include...
Rifamycins: - rifampicin - rifabutin
292
Rifamycins (inhibit RNA synthesis) are effective vs mycobacteria + chlamydia. What should be monitored, and why shouldn't these be given alone?
- Monitor LFTs - hepatitis - Do not give alone as resistance (Chr mutatio) develops rapidly - RNA polymerase is the target for these bactericidal drugs. - A single amino acid change occurs in the b-subunit of RNA polymerase
293
2 cell membrane toxins used for anti-microbial use are...
- Daptomycin: gram +ve. MRSA and VRE as alternative to linezolid. - Colistin: gram -ve, e.g. psuedomonas, acinetobacter, Klebsiella. basically for multi-resistant infections. nephrotoxic.
294
Inhibitors of folate metabolism antimicrobial drugs examples
- Sulfonamides | - Diaminopyrimidines e.g. trimethoprim
295
Inhibitors of folate metabolism antimicrobial drugs include sulfonamides and diaminopyrimidines e.g. trimethoprim. Combined use of the two is useful for....
Pneumocystis jiroveci pneumonia otherwise, use alone is rare due to common sulphonamide resistance.
296
Methicillin Resistant Staphylococcus aureus (MRSA) mechanism of resistance
- mecA gene encodes a novel penicillin binding protein (2a) | - B-lactams cannot bind to these well. Low affinity for B-lactam binding.
297
What are 3 yeast
- Candida - Cryptococcus - Histoplasma
298
What are 3 moulds?
- Aspergillus - Dermatophytes - Agents of mucormycosis
299
Characteristic 'germ tubes' are produced by which pathogen?
Yeast - candida albicans
300
Which candida is common in patients with indwelling catheters or drug abuse?
Candida endophthalmitis
301
B D Glucan assay serology is useful for diagnosis of which pathogen?
Yeast - candida albicans
302
Treatment of candidasis
- Echinicandin empirically and for non-albicans Candida - Fluconazole for Candida albicans - Ambisome (e.g. CNS) - Fluconazole (e.g. urine) - Voriconazole (e.g. CNS) for organ-based disease
303
Cryptococcosis caused by Cryptococcus neoformans risk is increased in patients with....
impaired T-cell immunity: - AIDS patients who have CD4 T cells usually <200/ml - T cell immunosuppressants post-solid organ transplant
304
Cryptococcus neoformans can cause meningitis and space-occupying lesions in the brain and lung. There is increased resistance to ....
Amphotericin B
305
India ink stain helps to confirm diagnosis of
Cryptococcus neoformans n.b. it grows from Eucalyptus leaves
306
Management of cryptoccocosis
- 3 weeks of Amphotericin B +/- flucytosine - Repeat LP for pressure management - Secondary suppression with fluconazole
307
Methenamine silver (GMS) stain shows fungus balls indicates...
Aspergillus
308
Management of aspergillosis
- Voriconazole - Ambisome (Caspofungin/Itraconazole are less good) At least 6 weeks of therapy
309
Onchomycosis refers to
thickening and discolouration of nails | Can be caused by trichophyton, epidermophyton, microsporum spp
310
Pityriasis versicolor
Fungal infection Reaction to sun Caused be Malassezia furfur Dark/orangey rash patch
311
Mucormycosis is....
Cellulitis of the orbit and face progress with discharge of black pus from the palate and nose. Brain involvement - LOC
312
Mucormycosis - cellulitis of the orbit and face with discharge of black pus from palate and nose. This tends to occur in which patients?
Immunocompromised Poorly controlled DM Caused by rhizopus spp, rhizomucor spp, mucor spp
313
Treatment of mucormycosis
Surgical debridement Amphotericin Posaconazole
314
Gram positive spore forming anaerobe
C-difficile
315
What 3 factors influence SSI risk?
1. host defence 2. wound environment 3. pathogens
316
High ESR, with FDG-PET/CT showing highly increased FDG uptake of the aorta, subclavian arteries, and femoral arteries. What is the likely diagnosis?
Increased FDG = increased glycolysis and inflammation. The inflammation of vessels = large vessel vasculitis. Patient was given corticosteroids and ESR normalised.
317
High ferritin levels are associated with which 2 syndromes
- Adult onset Still's disease | - Macrophage activation syndrome
318
The IGRA test for TB is not good for distinguishing between latent vs active TB. What does IGRA stand for?
IFN gamma release assay
319
HACEK are rare causes of bacterial infective endocarditis which grows a negative blood culture. What does HACEK stand for?
``` Haemophilus Aggregatibacter Cardiovacterium Eikenelia Kingella ```
320
What diagnostic test should be done if there is clinical suspicion of infective endocarditis
Total transthoracic echocardiogram
321
Duke's criteria for infective endocarditis: 2 major or 1 major + 3 minor criteria are needed. What are major criteria?
1. persistent bacteraemia (>2 positive blood cultures) 2. TTE shows vegetation 3. Serology for BArtonella, Coxiella or Brucella
322
Duke's criteria for infective endocarditis: 2 major or 1 major + 3 minor criteria are needed. What are minor criteria?
- Predisposition (murmur, IVDU) - Inflammatory markers - Immune complexes: splinters, RBCs in urine - Embolism - Atypical TTE - 1 positive blood culture
323
Giant cell arteritis criteria
``` Age >50 - most important Headache [not needed for Dx] Jaw claudication ESR >45 Visual changes Ischaemic tongue High risk of stroke/blind ```
324
What is the gold standard test for giant cell arteritis
Temporal biopsy
325
Adult onset stills can present with...
salmon pink rash ferritin is really high DDx: macrophage activation syndrome
326
Malignant causes of fever
- Lymphoma - Leukaemia - BM biopsy - Renal cell carcinoma - HCC/liver mets
327
Treatment of salmonella GI infection
Supportive Ciprofloxacin Azithromycin
328
Treatment of campylobacter GI infection
Supportive | Self-limiting usually
329
Bartonella henselae (gram -ve rod) is found in kittens. it causes 2 diseases
- cat scratch disease | - bacillary angiomatosis [in immunocompromised]
330
Cat scratch disease (caused by Bartonella henselae (Gram -ve rod) presents with a macule at the site of innoculation. It becomes pustular. What is the treatment?
- Erythromycin - Doxycycline [add rifampicin for the disseminated bacillary angiomatosis disease]
331
Bacillary angiomatosis (caused by Bartonella henselae (Gram -ve rod) presents with a as a disseminated multi-organ disease with BV involvement. Skin papules exist. What is the treatment?
- Erythromycin - Doxycycline - Rifampicin n.b. cat scratch disease is not disseminated and also caused by Bartonella. It is treated with erythro + doxy only.
332
Toxoplasmosis treatment
Spiramycin | Pyrimethamine plus sulfadiazine
333
Brucellosis increased risk with
unpasteurised milk/diary
334
Brucellosis treatment
Doxycycline plus: | Gentamicin or rifampicin
335
Unpasteurised diary products can lead to
Brucellosis Coxiella burnetii (Q fever) - milk Listeria
336
Treatment of Coxiella burnetii (Q fever) which is caught from cows/unpasteurised MILK
Doxycycline | hydroxychloroquine
337
Treatment of Lyssa virus (rabies)
Immunoglobulin | Vaccination
338
Treatment of rat bite virus
Penicillins | Rats can also cause hantavirus pulmonary syndrome with has supportive management only.
339
Viral haemorrhagic fever treatment
Supportive
340
What is the resevoir for Lyssa virus (Rabies)
Bats - bat bite with fever, most worrying is rabies i.e. LYSSA virus.
341
Slow-growing mycobacterium examples?
- Mycobacterium avium complex (MAC) or m.avium intracellulare (MAI) - Myobacterium tuberculosis complex: M.bovis BCG, M.tuberculosis - M. marinum - M. ulcerans
342
Rapid-growing mycobacterium tend to cause skin and soft-tissue infections. What are some examples?
- Mycobacterium abscessus - M. chelonea - M. fortuitum
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Ungrouped example of mycobacterium i.e. it is neither rapid nor slow-growing
Mycobacterium leprae
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What kind of vaccine is rubella
Live attenuated
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Mycobacterium avium intracellulare (MAI) a.k.a M. avium complex (MAC) is a slow-growing non-tuberculous mycobacteria. How does it affect those who are: (a) Immunocompetent? (b) Immunosuppressed?
MAI or MAC affects (a) immunocomponent by invading bronchial tree. Usually in those with pre-existing lung disease e.g. bronchiectasis, cavities (b) immunosuppressed by causing disseminated infection.
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M.ulcerans is a non-tuberculous mycobacterium that is slow-growing. It can cause....
- Skin lesions e.g. Bairnsdale ulcer, Buruli ulcer | - Chronic progressive painless ulcer
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M.marinum is a slow growing non-tuberculous mycobacteria that can cause
swimming pool granulomas
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Rapid growing non-tuberculous mycobacteria e.g. m.abscessus, m.chelonea, m.fortuitum can cause ....
skin and soft tissue infections found in hospital settings in patients with vascular catheters/devices
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Treatment of mycobacterium avium complex (MAC) a.k.a intracellular (MAI)
Clarithromycin/azithromycin Rifampicin Ethambutol ± Amikacin/streptomycin
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Treatment of rapid growing non-tuberculous mycobacterium is based on
Susceptibility testing | usually macrolife based e.g. clarithromycin
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2 types of mycobacterium leprae
- paucibacillary tuberculoid | - multibacillary lepromatous
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lifetime risk of developing active TB from latent TB
10%
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What type of vaccine is the m.bovis (bacille calmette-guerin BCG) injection?
Live attenuate M.bovis strain For babies in high prevalence communities. 70-80% efficacy preventing severe childhood TB. Protection wanes over time.
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Ghon focus/complex is typically seen in CXR of..
tuberculosis it is a granuloma in the lungs with ipsilateral lymphadenopathy.
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Rare allergic reactions can occur with TB including which feature
Erythema nodosum occasionally disseminated/miliary
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Risk factors for TB reactivation
- immunosuppression - chronic alcohol excess - malnutrition - ageing
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What is scrofula
Lymphadenitis usually in cervical lymph nodes. abscesses and sinuses can occur. can be present with extra-pulmonary TB.
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Gastrointestinal TB sign
Swallowing of tubercles
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Pott's disease refers to
Spinal TB | haematogenous spread to bones and joints of TB.
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Features of miliary TB
- Millet seeds on CXR - Progressive disseminated haematogenous TB - Increasing due to HIV
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Gold standard for TB
Sputum culture | can take up to 6 weeks.
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The tuberculin skin tests (Mantoux) induces what type of hypersensitivity reaction?
Type 4 delayed hypersensitivity reaction n.b. Does not distinguish between active vs latent infection of TB, only previous exposure. IGRAs are the same in this respect.
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TB management
``` Rifampicin (6 months) Isoniazid (6 months) Pyrazinamide (2 months) Ethambutol (2 months) + pyridoxine ```
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Rifampicin [6 months] side effects
- Raised transaminases - Cytochrome P450 inducer - Orange secretions
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vitamin D given for TB
pyridoxine 10mg OD - helps to prevent peripheral neuropathy, a SE of isoniazid.
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Isoniazid [6months] side effects
- Peripheral neuropathy (pyridoxine 10mg OD helps avoid this) - Hepatotoxicity
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Pyrazinamide [2 months] side effects
hepatotoxicity
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Ethambutol [2 months] side effects
visual disturbance
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If there is CNS tuberculosis, the therapy (RIPE) is given for what time period instead?
10 months | rather than 6 months
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Multi-drug resistant TB (MDR) refers to the resistance to...
rifampicin and isoniazid
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Extremely drug-resistant TB (XDR) refers to the resistance to....
fluoroquinolones and at least 1 injectable
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Treatment for multi-drug resistant TB
4-5 drug regimen combination, longer duration: - Quinolones - injectable aminoglycosides e.g. amikacin - PAS - cycloserine - ethionamide
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Types of helminths
- Cestodes (tape worms) e.g. hydatid - Trematodes (flukes) e.g. schistosomiasis - Nematodes (roundworms) e.g. hookworms, strongyloides
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Hydatid is a dog tapeworm. Complications in humans arise from ....
Hydatid lead to cysts: - Mass effect - Cyst rupture
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Treatment of hydatid tapeworm and cysteicercosis (dying worms and cysts)
Worms - praziquantel | Cysts - PAIR procedure, albendazole, steroids
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Treatment of schistosomiasis (trematodes, a.k.a. flukes)
Praziquantel
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Treatment of roundworms such as stronglyoides
Ivermectin
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Myiasis is the parasitisation of human flesh by...
fly larvae local damage as the maggot eats necrotic flesh.
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Treatment of myiasis
Removal of larva by asphyxiation or surgery
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Shingles occurs as a reactivation of latent VZV in the dorsal root ganglia. What is a complication?
Post-herpetic neuralgia
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Acyclovir action
inhibits DNA synthesis HSV1 > HSV2 >>> VZV
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HSV encephalitis is treated with
IV Acyclovir | for 21 days
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Where does CMV virus remain latent
Blood monocytes and dendritic cells | It becomes reactivated following immunosuppression
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CMV antiviral drugs
Ganciclovir Vanganciclovir Foscarnet Cidofovir
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side effect of ganciclovir (CMV antiviral)
bone marrow toxicity
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side effect of foscarnet and cidofovir (CMV antiviral)
nephrotoxic
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Treatment of post-transplant lymphoproliferative disease (B cell over-activation due to EBV)
- Reduce immunosuppression | - Rituximab (anti-CD20)
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BK virus can lead to lifelong carriage in the kidneys and urinary tract. It can lead to what problems in the immunocompromised?
- Haemorrhagic cystitis - in bone marrow transplant patients | - BK nephritis - in renal transplant patients
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Treatment of BK virus haemorrhagic cystitis
- Bladder washouts - Reduce immunosuppression - Cidofovir (+ probenicid)
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Treatment of BK nephropathy
- Reduce immunosuppresion | - IV Ig
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Treatment of adenovirus
- Cidofovir - IV Ig - Brincidofovir
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HSV resistance to acyclovir usually has mutations in which enyzme?
Viral thymidine kinase (95%) | 5% is DNA polymerase These must be treated with foscarnet or cidofovir.
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CMV resistance to ganciclovir involves which genetic mutation most commonly?
Protein kinase gene Give foscarnet or cidofovir instead
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Immunoglobulin preparations (a) prophylactic (b) post-exposure prophylaxis (c) therapeutic
(a) palivizumab (RSV) (b) VZV Ig, Hepatitis B Ig, human rabies Ig (c) IV Ig for CMV, rituximab for EBV-driven PTLD
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Treatment for non-falciparum malaria (e.g. vivax or ovale)
Chloroquinine | And primaquinine after checking not G6PD deficient
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Treatment for falciparum malaria
IV artesunate | or IV quinine and doxycycline
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Antiviral treatment for chickenpox and shingles (VZV) after acyclovir
- acyclovir 1st line - valacyclovir - acyclovir prodrug - famcyclovir - 2nd line = foscarnet or cidofovir for acyclovir-resistant virus.