Microbiology Flashcards

1
Q

Choice of correct antimicrobial depends on what?

A
CHAOS
Choice
Host characteristics
Antimicrobial susceptibilities of the 
Organism itself and also the
Site of infection
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2
Q

General rules for choice of antimicrobial drug

A
Narrow spectrum if possible
Use bactericidal drugs if poss.
Ideally on bacterial dx but otherwise 'best guess'
Consider local sensitivities
Patient characteristics
Cost

Consider pharmacokinetics, route of administration and dosage

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3
Q

Preliminary identification of infecting organism

A

1) Gram stain
- CSF, joint aspirate, pus
2) Rapid antigen detection
- Immunofluorescence, PCR

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4
Q

Which route for delivery of antimicrobial

A

i.v. : serious or deep seated infection
p.o. :Usually easy but avoid if poor GI function or vomiting
- diff classes of antimicrobials have diff bioavailabilities
i.m. : Not an opotion for long term use. Avoid if bleeding tendency or irritant
Topical: Limited application and may cause local sensitisation

i.v. to p.o. switch recommended in hospital for most infections if patient has stabilised after 48hours i.v. therapy

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5
Q

Adverse effects of aminiglycosides

A

Ottotoxicity and nephrotoxicity

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6
Q

Type 1 antimicrobials

+ 2 examples

A

Concentration dependent killing

Aminoglycosides
Fluoroquinolones

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7
Q

Type 2 antimicrobials

+ examples

A

Time dependent killings + minimal persistent side effects

Penicillins
Carbapenems
Cephalasporins
Linezoid
Erthromycin
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8
Q

Type 3 antimicrobials

A

Time-dependent killing and moderate to prolonged persistent effects

Vancomycin
Azithryomycin
Tetracyclines

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9
Q

Recommended length of antimicrobial therapy for N. meningitides meningitis

A

7 days

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10
Q

Recommended length of antimicrobial therapy for simple cystitis (in women)

A

3 days

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11
Q

Recommended length of antimicrobial therapy for acute osteomyelitis (adult)

A

6 weeks

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12
Q

Recommended length of antimicrobial therapy for bacterial endocarditis

A

4-6 weeks

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13
Q

Recommended length of antimicrobial therapy for Group A streptococcal pharyngitis

A

10 days

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14
Q

Skin infections
Common causative organisms

Antimicrobial choice

A

S. aureus
Beta-haemolytic Streptococci

Flucloxacillin (unless penicillin allergy or MRSA)

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15
Q

iGAS Tx

A

Aggressive and early debridement
Antibiotics adjunctive use of protein synthesis inhibitors esp. clindamycin (good skin and soft tissue penetration
Use of IVIg

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16
Q

What is the eagle effect

A

Eagle effect describes a phenomenon in which bacteria or fungi exposed to concentrations of antibiotic higher than an optimal bactericidal concentration (OBC) have paradoxically improved levels of survival

Applies to beta lactams

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17
Q

Recommended antimicrobial therapy for pharyngitis

A

Benzyl penicillin x10days

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18
Q

Recommended antimicrobial therapy for community acquired pneumonia (mild)

A

Amoxicillin

or
Erythromycin/clarithromycin

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19
Q

Recommended antimicrobial therapy for community acquired pneumonia (moderate - severe)

A

Co-amoxiclav
&
Clarithromycin

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20
Q

Recommended antimicrobial therapy for hospital acquired respiratory tract infections

A

1st line: Ciprofloxacin + Vancomycin

ITU/2nd line: Piptazobactam + Vancomycin
Psuedomonas: Tazacoin or Cirprofloxacin + Gentamicin

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21
Q

Recommended antimicrobial therapy for bacterial meningitis

A

Ceftriaxone (+/- amoxicillin if Listeria likely)

Baby <3 months: Cefatoxamine PLUS amoxicillin (to cover for listeriosis)
- ceftriaxone not used in neonates as displaces bilirubin from albumin and can cause biliary sludging

Neisseria meningitidis: Benzylpenicillin (high dose) or Ceftriaxone/Cefotaxime

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22
Q

Main pathogens in bacterial meningitis

A

N. meningitidis
S. pneumoniae
+/- Listeria in v elderly/young/immunocompromised

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23
Q

Recommended antimicrobial therapy for simple cystitis (community)

A

Trimethopron x 3 days

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24
Q

Recommended antimicrobial therapy for hospital acquired UTI

A

Cephalexin or Augmentin

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25
Recommended antimicrobial therapy for infected urinary catheter
Change under gentamicin cover
26
Recommended antimicrobial therapy for C. difficile colitis
STOP offending antibiotic (usually cephalosporin) p.o. metronidazole 10-14days If above fails, use vancomycin
27
Routes of entry for CNS infection
1) Haematogenous 2) Direct implantation 3) Local extension 4) PNS into CNS
28
Most frequent route of entry for CNS infection
Haematogenous
29
Meningitis Region affected Signs and symptoms Causative agents
Meninges Fever, headache, stiff neck, some brain function disturbance Neisseria meningitidis, Strep pneumonia, Haemophilus influenza, Listeria, group B strep, E. coli
30
Encephalitis Region affected Signs and symptoms Causative agents
Brain Disturbance of brain function Rabies virus, arboviruses, Prions, Amoeba, Trypansoma species
31
Myelitis Region affected Signs and symptoms Causative agents
Spinal cord Disturbance of nerve transmission Poliovirus
32
Neurotoxin Region affected Signs and symptoms Causative agents
CNS and PNS Paralysis, rigid (tetanus) or flaccid (botulism) Clostridium tetani, clostridium botulism
33
What processes produce septicaemia
Capillary leak Coagulopathy Metabolic derangement Myocardial failure... multi-organ failure
34
Aseptic meningitis symptoms | Causative organisms
headache, stiff neck, photophobia. SELF-LIMITED and resolves in 1-2 weeks No inflammatory markers Most freq children <1 Coxackievirus group B and echovirus - responsible for 80-90%
35
Encephalitis transmission
Person to person OR Through vectors (mosquitoes, lice, ticks)
36
Encephalitis causative organisms
Viral - west nile virus etc. Bacterial - listeria monoctogenes Amboeic - naegleria fowleri, acanthamoeba species and Balamunthia mandrillaris Toxoplasmosis
37
Brain abscess - where does the infection come from Causative organisms
Mainly local extension: Ottitis media. mastoiditis/paranasal sinuses Rarely: endocartitis, haematogenoisly ``` Streptococci, staphylocicci Gram -ve organisms (neonates particularly) Mycobacterium tuberculosis Fungi Parasites Actinomyces ```
38
Spinal infections pathogenesis Consequence if untreated
Direct open spinal trauma, from infections in adjacent structures, from haematogenous spread of bacteria to a vertebra Permanent neurological deficits, significant spinal deformity, or death
39
Spinal infections risk factors
``` Advanced age Iv drug use Long term steroids DM Organ transplantation Malnutrition Cancer ```
40
Difference between gram +ve and gram -ve bacteria
Gram+ve - thick peptidoglycan cell wall - Stain purple Gram-ve - outer membrane and thinner peptidoglycan layer - Stain pink
41
Beta-lactams Mechanism Affective against which types of bacteria Ineffective against which types of bacteria
Inactivate enzymes involved in terminal stages of cell wall synthesis (transpeptidases - penicillin binding proteins) - so daughter cells have no peptide cross links and defective/weak peptidoglycan cell walls Active against rapidly dividing bacteria Ineffective against bacteria without peptidoglycan cell wall e.g. mycoplasma or chlamydia
42
Examples of beta-lactams
Penicillin Cephalosporins Carbapenems
43
Penicillin type of antibiotic Organisms used against Broken down by
beta lactam gram +ve Streptococci, Clostridia Broken down by enzyme (beta lactamase) produced by S. aureus
44
Amoxicillin type of antibiotic Organisms used against Broken down by
Beta lactam Broad spectrum penicillin - extends cover to Enterococci and some Gram -ve (esp E.coli) Broken down by beta lactamases produced by S.aureus and many gram -ve organisms
45
Flucloxacillin type of antibiotic Organisms used against
Beta lactam - similar to penicillin but less stable Stable to beta-lactamases produced by S. aureus Mainstay tx for S. aureus
46
What are clavulanic acid and tazobactam?
Beta-lactamase inhibitors. Prevent penicillins from enzymatic breakdown and increase coverage to include S. aureus, Gram negatives and anaerobes
47
What is Augmentin/co-amoxiclav?
Amoxicillin + clavulanic acid
48
What is tazocin?
Piperacillin + tazobactan
49
Piperacillin type of antibiotic Organisms used against Broken down by
Similar to amoxicillin Extends cover to psudomonas and otehr non-enteric gram -ve Broken down by beta lactamase produced by S.aureus and many gram -ver
50
What are cephalopsorins Generations and what does that mean for their activity
Beta-lactam antibiotics - stable to most of beta-lactamases so not broken down 1. Cephalexin 2. Cefuroxime 3. Cefotaxime, ceftriaxone, ceftazidime Later generations v active against gram -ves
51
What is cefuroxime?
2nd gen Cephalosporin Stable to many beta-lactamases produced by gram -ve's Similar cover to co-amoxiclav but less active against anaerobes
52
What is ceftriaxone Active against Limitation
3rd gen cephalosporin V active against pneumococci, N meningitidis, Haemophilus (mainstay of tx for meningitis) Associated with C.difficile infection (limits use)
53
What is ceftazidime Use
3rd gen cephalosporin V active against gram -ve, v little against +ve Anti-psuedomonas
54
What is the limit of cephalosporins
Extended specrtum beta-lactamase (ESBL) producing organisms are resistant to all cephalosporins
55
What are carbapenems? Examples Uses
Beta lactam antibiotics - stable to ESBL enzymes Meropenem, Imipenem, Ertapenem Alternative to penicillins and cephalosporins for ESBLs - last line
56
Key features of beta-lactams
Relatively non-toxic Renally excreted - so reduce dose if renal impairment Short half life - multiple doses in a day Will not cross BBB (can cross inflamed meninges) Cross allergenic (penicillins approx 10% cross reactivity with cephalosporins or carbapenems - don't give if anaphylactic)
57
What are glycopeptides? MOA Active against which organisms? Examples Side effect
Inhibitors of cell wall synthesis - Active against only gram +ve organisms - Stop glycosidic bons and peptide bonds by binding to peptide chain and stopping enzyme from acting - Weakened cell wall and daughter cells will lyse during replication Vancomycin Teicoplanin Nephrotoxic - monitor drug levels and adjust dose
58
Antimicrobial inhibitors of protein synthesis
1) Aminoglycosides 2) Tetracyclines 3) Macrolides 4) Chloramphenicol 5) Oxazolidinones
59
Aminoglycosides mechanism of action Dosage
Concentration dependent bacterial action - prevent elongation of the polypeptide chain - cause misreading of the codons along the mRNA 1 big dose per day
60
Aminoglycosides uses Side effects Inhibited by?
With tazocin for severe pseudomonas With amoxicillin for endocarditis No activity against anaerobes Ototoxic and nephrotoxic Low pH (e.g. abscess needs draining)
61
Tetracyclines limitations
Widespread resistance limits use NOT for children or pregnant women - teratogenic - deposit in growing bones Light sensitive rash - wear sun cream
62
Tetracylines mechanism of action and uses
Reversibly bind to the ribosomal 30s subunit. Prevent binding of aminoacyl tRNA to the ribosomal acceptor site, so inhibiting protein synthesis Broad spectrum activity against intraceullar pathogens and ones that don't have a cell wall (chlamydia, rickettsiea and mycoplasma) + most conventional bacteria and MRSA
63
Macrolides mechanism of action and uses Examples
Binds to 50s subunit of ribosomes. Interferes with translocation. Minimal activity against gram -ve bacteria Useful for mild Staphylococcus or Strep in penicillin allergic patients. + Campylobacter and Legionella Used for community acquired pneumonoa Azithromycin, clarithromycin
64
Chloramphenicol mechanism of action USES
Binds to 50s ribosomal subunit V broad antibacterial activity - may have use in MDR bacteria - used in anaphylactic penicillin activity for meningitis
65
Chloramphenical limited to use in.. because..
Eye preparations Risk of aplastic anaemia + grey baby syndrome in neonaes
66
Oxalidinones Example Mechanism of action Uses Limitations
Linezolid Binds to 23s component of 50s subunit Highly active against gram +ve organisms, inclusing MRSA and VRE (Not against -ve) Neurotoxic - don't use > 4 weeks Optic neuritis Thrombocytopenia
67
Oxalidinones limitations
Neurotoxic - don't use > 4 weeks Optic neuritis Thrombocytopenia
68
Mechanisms of antimicrobial resistance
1) vBypass antibiotic sensitive step in pathway 2) Enzyme mediated modification/inactivation of the antibiotic 3) Reduced antibiotic Accumulation 4) Modification/replacement of Target
69
Mechanism of resistance to beta lactams
1) Inactivation 2) Altered targets - MRSA + strep pneumoniae 3) Reduced accumulation
70
Reportable GI infections
``` Campylobacter Salmonella Shigella E. Coli 0157 Listeria Norovirus ```
71
Secretory diarrhoea Causative organisms
No fever or low grade. No WBC in stool sample - Vibrio cholera - ETEC - EPEC - EHEC
72
Inflammatory diarrhoea Causative organisms
Fever, WBC in stool (neutrophilia) - Campylobacter jejunia - Shigella - Non typhoidal Salmonella serotypes - EJEC
73
Enteric fever Causative organisms
Fever, WBC in stool sample (mononucleic cells) - Typhoidal salmonella serotypes - Eneteropathogenic - Brucella
74
Mechanism of secretory diarrhoea-toxin production (cholera toxin)
cAMP opens Cl channel at apical membrane of enterocytes --> efflux of Cl to the lumen; loss of H20 and electrolytes
75
Mechanism of secretory diarrhoea-toxin production (superantigens)
Superantigens bind directly to T-cell receptors and MHC molecules OUTSIDE the peptide binding site --> massive cytokine production by CD4 cells i.e systemic toxicity and suppression of adaptive response
76
S. aureus appearance on agar Gram stain
Yellow colonies +ve coccus, clusters
77
S. aureus food poisoning presentation Spread Tx
Enterotoxin in GI tract - releasing IL-1 and Il2 - prominent vomitting and watery non-bloody diarrhoea Skin lesions on food handlers Self limiting
78
Bacillus cereus food poisoning Gram staining Toxins Caused by which food
Gram-positive motile, spore-forming, rod-shaped Heat stabile emetic toxin Heat labile diarrhoeal toxin Reheated rice
79
Bacillius cereus food poisoning presentation Tx
Watery non bloody diarrhoea Rare cause of bacteremia in vulnerable Can cause cerebral abscesses Self limited
80
Clostridia GI infection Gram staining Types (not C.diff)
Large anaerobic, gram-positive, motile rods. ``` 1) Clostridium botulinum: botulism Canned/vacuum packed food Ingestion of preformed toxin Blocks ACh release from peripheral nerve synapses - paralysing Tx : antitoxin ``` 2) Clostridia perfringens: food poisoning Reheated food (meat) Normal flora of colon but not small bowel where the enterotoxin acts (superantigens) Incubation 8-16hrs Watery diarrhoea, cramps, little vomiting lasting 24 - Perfringens is a gram positive bacillus that produces alpha toxin causing gas gangrene in infected wounds
81
Pseudomembranous colitis caused by Related to what Treatment
C. difficile Antibiotic related (any but mainly cephalosporins) PO Metronidazole, vancomycin, stop antibiotics where possible
82
Listeria monocytogenes Source Presentation At risk groups Treatment
Gram +ve, nonspore-forming, motile, facultatively anaerobic, rod - beta haemolytic Refrigerated food i.e. dairy Watery diarrhoea, cramps, headache, fever, little vom Perinatal, immunocompromised Ampicillin
83
E. coli gram stain Source Tx Enterotoxins action
Gram -ve rod Food/water contaminated with human faeces Avoid antibiotics Heat labile stimulates adenyl cyclase and cAMP Heat stabile stimulates guanylate cyclase Act on jejenum, ileum not colon
84
Types of E.coli and characteristics
ETEC: toxigenic - main cause of travellers diarrhoea EPEC: pathogenic - infantile diarrheoa EIEC: invasive, dysentry EHEC: haemorrhagic 0157:H7 EHEC: shiga like verocytotoxin causes HUS
85
Salmonellae gram stain Antigens Species
Gram -ve rods Cell wall O (groups A-I) Flaggellar H Capsular Vi S. typhi S.enteriditis S. cholerasuis
86
Salmonella enteritidis Transmission Presentation Treatment Test
Poultry, eggs, meat Invassion of epi- and sub-epitherlial tissue of SMALL and LARGE bowel. Loose stool, diarrhoea (like cholera) Self limiting and resolves within 3-7days. Bacteremia infrequent, no fever Self limited Stool positivity
87
Salmonella typhi Transmission Presentation Treatment Test
By humans, multiplies in Payer's patches, spreads endoreticular system ``` Enteric fever (typhoid) Slow onset high fever and constipation, splenomegaly, rose spots, anaemia, leucopaenia, bradycardia, haemorrhage and perforation ``` Ceftriaxone IV and then Azithromycin 500mg BD 7 days Blood culture positive
88
Shigella gram stain Antigens Types Tx
Gram -ve rods, non lactose fermenters, non H2S producers, non-motile Cell wall O antigens Polysaccharide (groups A-D) S.dysenteriae, S. flexneri (MSM) Avoid antibiotics
89
Vibrios gram stain Associated with
Curved, comma shaped, gram negative, oxidase positive, late lactose fermenters Seafood raw/undercooked Massive diarrhoeaa (rice water stools without inflammatory cells)
90
Campylobacter gram stain Transmission Presentation tx Complications
Curved, comma gram -ve, oxidase +ve Contaminated food/water with animal faeces Enterotoxin (watery diarrhoea) ?invasion (+/- blood) Watery foul smelling diarrhoea, bloody stool, fever and severe abdo pain Erythromycin or cipro on first 4/5 days Self limiting but can last for weeks Only tx if immunocompromised GBS, reactive arthritis, Reiter's
91
Viral gastroenteritis causes
Norovirus - notifiable Adenovirus <2 non-bloody Rotavirus - dsDNA (by 6 yrs - most have antibodies)
92
Protozoa gastroenteritis causes
Entamoeba histolytica - Killed by boiling water, removed by water filters Flask shaped ulcer, dysentry, flatulence, tenesmus. Chronic wt loss, liver abscess Giardia lamblia 2 nuclei, pear shaped Tx metronidazole Foul smelling, non bloody diarrhoea Cryptosporidium Infects jejenum. Severe in immunocompromised. Profuse watery diarrhoea Tx: reconstitution of immune system
93
Bacteriuria definition Cystitis definition
Bacteria in the urine Inflammation of bladder, often due to infection
94
Classifying UTIs
Uncomplicated - infection in a structurally and neurologically normal urinary tract Complicated - infection in a urinary tract with functional or structural abnormalities (including catheters and calculi)
95
Types of patients that get complicated UTI
Men, pregnant women, children, patients in hospital
96
Most common organism causing UTI
E. coli Others: Proteus, Klebsiella, Pseudomonas, Enterobacter, enterococci, staphylococci
97
Host defences in the urinary tract
Urine (osmolality, pH, organic acids) Urine flow and micturition Urinary tract mucosa
98
Why do females more commonly get UTIs
Female urethra short and is colonised with bacteria | Proximity to warm moist vulvar and perianal areas - contamination likely
99
Why does obstruction of renal tract cause UTIs
Inhibits normal flow of urine. Resulting stasis is important in increasing susceptibility to infection
100
Types of renal tract obstruction
1) Mechanical - Extrarenal: valves, stenosis; calculi; extrinsic ureteral compression from variety of causes;BPH - Intrarenal: nephrocalcinosis, polycystic kidney, uric acid nephropathy, renal lesions of sickle cell trait or disease 2) Neurogenic malformations - Polyomyelitis - Tabes dorsalis - Diabetic neuropathy - Spinal cord injuries
101
What is reflux in the kidney and what can it cause
Vesicoureteral reflux - perpetuates infections as residual pool of infected urine in bladder after voiding
102
Symptoms of UTI
Under 2yrs - non specific Failure to thrive Vomiting Fever Over 2 Frequency Dysuria Abdo/flank pain
103
How do we get UTI
Most common: ascending UTI female urethra short and close to vulvar/perianal areas - contamination likely Sexual activity can force bacteria into bladder and multiplies, passes up ureters, particularly if VUR, to renal pelvis and parenchyma
104
Renal tract abnormalities that predispose to UTI
OBSTRUCTION: Intrarenal; renal; neurogenic malformation Reflux - residual pool of urine in bladder Haematogenous route - S.aureus abcess ore endocaditis
105
Renal tract obstruction causes
Extrarenal - valves, stenosis, bands; calculi; extrinsic renal compression; BPH Intrarenal - Nephrocalcinosis, uric acid nephropathy, analgesic nephprhopathy, PKD, hypokalaemic nephropathy, renal lesions of sickle cell Neurogenic malformations - Poliomyelitis; tabes dorsalis; diabetic neuropathy; spinal cord injuries
106
Investigation of UTI
Urine dip MSU urine Bloods: FBC, UE, CRP
107
Interpreting UTI culture result
100,000 CFU /mL Pyuria (10,000/mL) = inflammation - may be absent in children If epithelial cells - indicates perineal containation
108
IVDU hepatitis
B or C
109
Hepatitis transmitted from mother
B more than C
110
Hepatitis transmitted sexually
B more than C
111
Hepatitis related to blood transfusion
C
112
Hepatitis acute only, no chronic infection
``` A sRNA virus Prodromal illness 3-10d then icteric stage for 1-3 weeks ALT rises Faeco-oral transmisison ```
113
Hepatitis food and water contamination
A and E
114
Natural hx of hep B infection
Healthy, hepatic fibrosis, cirrhosis, HCC
115
Elevated serum HBV DNA level (10 000 copies/mL) is a strong risk predictor of what
HCC
116
Chronic Hep B tx
• Interferon alpha - if only boost of own immune system needed • Lamivudine • Adefovir • Tenofovir - - any of 3 for if heading into or got cirrhosis • Entecavir • Emtricitabine Truvada= tenofovir + emtricabine if HIV + too
117
Acute Hep C tx
IFN
118
Define PUO
Pragmatic | Fever of 3 days with no diagnosis despite investigation
119
Initial tests to do for fever
``` FBC U&E Total protein LFTs CRP CXR Blood cultures x 3 Urine culture HIV test - do it!! ``` Extra CK, ANA, ANCA, RhF, Ferritin, Abdo USS/CT, CMV EBV serology, stool cultures and OCP
120
Criteria for dx of infective endocarditis
Dukes criteria 2 major or 1 major and 3 minor or 5 minor Major: Persistent bacteraemia (>2BC +ve) Echo: vegetation Positive serology for Bartonella, Brucella or Coxiellia ``` Minor Predisposition (Murmur, IVDU) Inflammatory markers (fever, CRP high) Immune complexes: splinters, RBC in urine Embolic phenomena: Janeway lesions, CVA Atypical echo 1 +ve BC ```
121
Salmon pink rash | V high ferritin
Adult onset Stills disease | Type of inflammatory arthritis
122
Malignancies associated with fevers
Lymphoma (esp Non-hodgkin) Leukaemia (BM biopsy) Renal cell carcinoma HCC (or any that metastasise to the liver)
123
Unpasteurised milk infections
Brucella, Campylobacter, Cryptosporidium, E. coli, Listeria, and Salmonella.
124
What does HAI stand for
healthcare asociated infections
125
Catheter associated blood stream infection organisms
MRSA MSSA Resistant gram -ve's
126
Surgical site infection organisms
MRSA MSSA Resistant gram -ve's
127
Incidence of HAI in UK
8%
128
Most common syndrome of HAI
``` Pneumococcal pneumonia Then Surg site infections UTI Bloodstream Gastro ```
129
C. difficile gram stain
Gram +ve spore forming anaerobe
130
Why is E. coli bacteraemia increasing
UTI Catheter use Antibiotics Antibiotic resistance
131
What influences surgical site infection risk?
Host defence Wound environment Pathogens - S.aureus most common
132
What is CPE
Carbapenemase producing Enterovacteriaceae
133
Building works organism
aspergillus
134
Water/cooling tower associated organism
Legionella pneumophilia
135
Negative pressure vs positive pressure isolation
Negative pressure - protection of others from an infectious patient with airborne infection Positive pressure - Protection of transplant patients from organisms from outside the room
136
What % of world has TB
33%
137
TB type of bacteria
Aerobic, non-motile rod Cell wall made of long chain fatty acids (structure and staining characteristics) - Acid alcohol fast (resists discolouration with acid) = AAFB
138
Slow growing NTM
M. avium intracellulare - Immunocompetent but propensity for lung abnormalities - Disseminated in immunocompromised M. marinum - in cold water, usually cutaneous M. ulcerans - seen in W Africa, likes cold areas of
139
Rapidly growing NTM
M. absessus M. chelonae M. fortuitum These typically cause skin and soft tissue infection In hospital, isolated from blood cultures. Relatively easier to treat
140
Diagnosis of NTM lung disease
Clinical + microbiological findings + excluding other dx C: pulmonary symptoms, nodular cavities/opacities, bronchiectasis M: 2 sputum cultures or 1 BAL OR + biopsy with granulomata
141
Bacteria causing leprosy
Myobacterium leprae
142
If exposed to a smear +ve pulmonary TB person, what is lifetime risk of developing active TB?
10%
143
What is Ghon focus? What is Ghon complex?
Primary TB - subpleural caseating granuloma Ghon focus + ipsilateral hilar lymphadenopathy
144
Presentation of primary TB
``` usually asymptomatic Ghon focus/complex Limited by cell mediated immunity Rare allergic reactions e.g erythema nodosum Ocassionally dissemination/miliary ```
145
Risk factors for re-activation of TB
Immunosuppression Chronic alcohol use Malnutrition Ageing
146
Post-primary TB presentation
Pulmonary or extra pulmonary >5yrs after primary infection ``` Pulmonary TB Caseating granulomas - lung parenchyma - Mediastinal LN Upper zones ``` Extra-pulmonary - Lymphadenitis (scrofula, cervical) - GI - Peritoneal - Genitourinary - Bone and joint (spinal most common - Pott's disease) - Miliary TB (millet seeds on CXR, increasing due to HIV) - TB meningitis
147
Investigations for TB
CXR ``` Sputum x3 (induced) Bronchoscopy Biopsies EMU Stain for AAFB (smear) Culture NAATT Histology ``` Tuberculin skin test IGRAs - Elispot
148
TB treatment side effects
R: CyP450 inducer, orange secretions I: Peripheral neuropathy (give B6 - pyridoxine), hepatitis P: Hepatotoxicity E: Visual disturbance
149
Length of Tb treatment
RIPE 2 months RI: extra 4 months CNS TB: 10/12 Adherence checked with direct observation or video observed
150
Define MDR TB and worse
MDR: Resistant to R and I XDR: Also resistant to fluroquinolones and at least 1 injectable
151
Causes of MDR TB Treatment of MDR TV
``` Previous TB tx HIV +ve Kniwn contact of MDR TB Failure to respond to conventional Rx >4 months smear positive, >5 months vulture positive ``` 4/5 drug regime, longer duration - Quinolones, aminoglycosides, PAS...
152
Streptococcus pneumoniae gram stain
Gram +ve diplococci Alpha haemolysis (green) + Sensitive to optochin
153
Severe, acute onset pneumonia presenting with fevers, rigors, lobar consolidation. Causative organism Treatment
Streptococcus pneumonia Almost always penicillin sensitive - Check travel hx (resistance in south europe)
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Fever, cough, pleuritic chest pain, SOB Cause and define
Pneumonia - inflammation of lung alveoli
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Pneumonia classification
CAP or HAP
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Main CAP organisms
``` Streptococcus pneumoniae Stapylococcus aureus Hamemophilus influenzae Moraxella catarrhalis Klebsiella pneumoniae ```
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Haemophilus influenzae gram stain
-ve cocco-bacilli | Grow on chocolate agar
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Moraxella catarrhalis gram stain
-ve coccus
159
Staphylococcus aureus gram stain
+ve cocci
160
Klebsiella pneumoniae gram stain
-ve rod, enterobacter
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Pneumonia causative organisms based on age of pt
0-1 month: Listeria, E.coli, GBS 1-6months: Chlamydia, S.aureus, RSV 6months-5yrs: Mycoplasma, Influenza 16-30yrs: M. pneumonia, S. pneumoniae
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Atypical causes of CAP
Organisms with no cell wall (don't respond to penicillin Abx. Use macrolides and tetracylcines) Legionella pneumophilia Mycoplasma pneumonia Coxellia burnetti (Q fever) - farm animals, hepatitis Chlamydia psittaci - Bird exposure, splenomegaly, haemolytic anaemia, rash
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How do atypical CAP present differently to typical CAPs
No signs on chest exam or signs not in keeping with CXR. May have extrapulmonary features.
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Low Na, in a hotel, pneumonia picture, hepatitis
Atypical CAP - Legionella
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Systemic symptoms, joint pain, cold agglutin test, erythema multiforme, pneumonia picture
Atypical CAP - Mycoplasma | - Risk factors - SJS, AIHA
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Invesrigations for pneumonia
FBC U+Es CRP (high can indicate S.pneumo - 500ish) Blood culture, sputum (often not sent, often no dx) ABG CXR
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Assessment score for pneumonia
``` Confusion (abbreviated Mental Test score 8 or less, or new disorientation in person, place or time) Urea >7 mmol/litre) RR > 30 BP <90 S, <60 D >65yrs ``` Consider Home if 0-1 Hospital 2 and above ICU 3 and above
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Definition of bronchitis and causative organisms
Inflammation of medium sized airways Viruses, S,pneumoniea, H. influenzae, M.catarrhalis
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CXR in bronchitis
normal
170
Cavitating lesion cxr causes
S. aureus K. pneumoniae TB
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Ddx of failure to improve on pneumonia treatment
``` Empyema/abscess Proximal obstruction (Tumour) Resistant organism (TB) Not receiving/absorbing Abx Immunosuppression ```
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ground glass shadowing cxr bat's wing appearance test to do Treatment
Pneumocystitis jiroveci Walk test - desaturate Immunofluorescence on BAL Silver stain Septrin (co-trimoxazole)
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Neutropenia + on lots of antibiotics | Intersititial change on cxr/ nothing much
Aspergillus (invasive)
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Immunosuppresion (BMT) and LRTI
CMV pneumonitis
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Immunosuppresion (splenectomy)
Encapsulated organisms (NHS), malaria
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Investigations of LRTI
Before antibiotics: Sputum, blood cultures ``` BAl Pleural fluid Antigen tests (urine - one for MCS, one for legionella) Antibody tests Immunofluorescence PCR ```
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Candida diagnosis
Culture - selective agar plate (with antibiotic to kill bacteria) B D glucan assay (serology for component of fungal wall) Imaging e.g. for hepatosplenic candidiasis
178
Candidiasis management
Minimum 2 weeks antifungals from first -ve blood cultures Echo and fundoscopy Enchinicandin empirically and for non albicans Candida Fluconazole for Candida albicans
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Aspergillus spectrums of disease
1) Mycotoxicosis due to ingestion of contaminated food 2) Allergic sequelae - allergic bronchopulmonary aspergillosis - wheeze, eosinophilia, bronchiectasis 3) Colonisation without invasion - aspergilloma 4) Invasion, inflammation, granulomatous disease in lungs - Rx: amphotericin B 5) Disseminated systemic (in immunocompromised)
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Aspergillus dx
Microscopy mainstay - hyphi - Can stain with methenamine silver IgE bloods: to look for allergic response - can look for antigen - galactaman - blood or BAL PCR Histology sample Culture (slow)
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Antifungal agents targets and examples
1) Cell membrane - polyene antibiotics: Amphotericin B, lipid formulations, nystatin (topical) - Azole antifungals: Ketoconazole, itraconazole, fluconazole... 2) DNA synthesis - Pyrimidine analogues, flucytosine 3) Cell wall - Echinocandins
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Azoles mechanism SEs
Target cell membrane of funguses - inhibit fungal P450 enzymes that help synthesise ergosterol (main component of fungal cell membrane) Some cross reactivity with mammalian P450 - Drug interactions esp warfarin - Impairment of steroidneogenesis (keto and itroconazole)
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Echinocandins mechanism
e.g. Anidulafungin Target cell wall of fungus - Specific inhibitors of beta 1 3 glucan synthase (needed for b glucan synthesis - structures in fungal cell wall) Remember cryptococcus is inherently resistant
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Amphotericin B mechanism Active against
Targets cell membrane of fungus - polyene antibiotic - Binds sterols in fungal cell membrane, creates transmembrane channel and electrolyte leak Active against most fungi except aspergillus terreus, Sceedosporium spp Used in cryptococcal meningitis
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Side effects of amphotericin B
Nephrotoxic (delayed toxicity) - Drop in GFR, azotemia (vascular decrease in renal blood flow) - Wasting of K, Na and Mg (distal tubular ischaemia)
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Flucytosine mechanism Indications
Targets fungal DNA synthesis Not really montherapy But used in combinations with amphotericin B or fluconazole for Candidiasis, Cryptococcosis or ?Aspergillosis
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Flucytosine SEs
Liver function, blood disorders, D&V | Blood conc needs monitoring when used in conjunction with Amphotericin B
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Assessment of patient with fever
B symptoms, localising clues Medications Foreign travel - exact, what doing, where, how lonh Unwell contacts, animal expo, Iv drug use, sexual hx Examination - eyes, mouth, palpate back , rash
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V high ferritin caused by
Adult onset stills disease Maacrophage activation syndrome Also infective causes
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Aciclovir mechanism of action
Guanosine analogue - chain terminator of viral DNA - activated by viral thymidine kinase so restricted to virally infected cells - affinity for viral DNA polymerase more than host low drug toxicity. rarely neuro and nephro toxic
191
HSV encephalitis treatment
As soon as suspected 10mg/kg tds aciclovir | 21 days
192
HSV meningitis treatment
Only treat if unwell enough for admission or immunocompromised ACV iv 2-3 days then oral for further 10 days If immunocompromised can use valciclovir to avoid cannula
193
VZV treatment
``` Only for Chicken pox in adults Shingles in adults Immunocompromised Neonatal chickenpox Increased risk of complications ```
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CMV course of infection Histology
latent in blood monocytes and dendritic cells in primary infection Reactivation following immunosuppression Owl's eye inclusions
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CMV risk
``` Immunocompromised. Causes: Marrow suppression Retinitis Pneumonitis Hepatitis Colitis Encephalitis ```
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CMV treatment
1st line) Ganciclovir (iv) or valganciclovir (po) 2) Foscarnet 3) Cidofovir 2 and 3 don't need activation by viral kinase but 1 does
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CMV pneumonitis treatment
Ganciclovir (iv) + IVIg
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Ganciclovir indications SE CI
CMV disease in immunocompromised or newborns with congenital CMV BM toxicity Renal toxicity BM suppression (i.e. BM transplant patient)
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Foscarnet indications SE
CMV and occasionally HSV (e.g. if ACV resistance) - GCV CI - CMV retinitis nephrotoxic - need to keep well hydrated and correct electrolytes
200
Cidofovir indications
3rd line tx of CMV in immunocompromised Nephrotoxic - need to keep hydrated and probenicid
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Managing CMV in transplant patients
1) Prophylaxis with GCV - for solid organ transplant. SE - nephrotoxic 2) Pre-emptive therapy: Surveillance - weekly blood CMV PCR, GCV or foscarnet when PCR +ve. mostly for stem cell transplant pts
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Main surface proteins of influenza virus - which one is targeted by anti-influenza drugs
Haemagluttinin | Neuraminidase - inhibited by e.g. oseltamavir (tamiflu) or zanamavir (dry powder inhaler)
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Indications of anti-infleunza drugs MOA Examples
Any pt admitted for flu-like illness In community for at risk groups, within 48 hrs of symptom onset Target neuraminidase Oseltamavir, zanamavir
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Pavilizumab use
Monoclonal Ab against RSV. Can be used in winter months by high risk infant groups as prophylaxis
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BK virus clinical picture
In BMT patients: haemorrhagic cystitis | In renal transplant: BK nephritis and ureteric stenosis
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Treatment of BK haemorrhagic cystitis
Bladder washout and reduce immunosuppression if poss Cidofovir iv + probenicid if significant morbidity Intravsecal cidofovir if nephrotoxic ? future: brincidofovir
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Treatment of BK nephropathy
Reduce immunosuppression if poss IVIg ? future: brincidofovir
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Adenovirus clinical picture Treatment
Paeds transplant recipient - severe multi-organ involvement Tx: Cidofovir + IVIg ? future: brincidofovir
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Brincidofovir MOA
Pro drug of cidofovir. Less toxic. Main potensh is for tx or adenovirus and BK virus in immunocompromised
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Immunodeficiency associated with HSV encephalitis
UNC93B deficiency | TLR3 deficiency
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Immundofeiciency associated with HPV
Epidermodysplasia verruciformis (primary immunodeficiency - EVER1/2)
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neisseria meningitis gram stain
Gram -ve coccus
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Most common causative organism of prosthetic joint infections
1) Coagulase -ve staph | 2) S. aureus
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Hep A epidemuiology
Countries with poor sanitation of water supply | Also MSM and school outbreaks
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Hep A incubation period
2-6 weeks
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HBV transmission
Sexual, blood products and mother to baby
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Hep B incubation period
2-6 months
218
HCV serology
ALT high in acute reaction Anti-HBV may come years after - not in acute phase at all + lag Sooo diagnostic test is HCV RNA
219
HCV treatment
Peginterferon + ribavarin
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Natural reservoir of influenza A virus
Ducks, geese, swans
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Why does influenza virus cause respiratory disease
Needs activation by proteases (human airway tryptase) which cleaves haemagglutinin and this allows virus to leave first infected cell and enter new cell
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Mutation in influenza viruses that can lead to switch to it becoming transmittable in humans - why worry about these?
PB2 627K 627 switch can lead to hypercytokinaemia: MCP, IL-8, IL-10 --> ARDS
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Chicken vaccinations in China for?
H7N9 influenza
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Influenza virus, how does it get through mucuc
Neuraminidase breaks down mucus
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Gene linked with more severe influenza
Loss of IFITM3
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What does seasonal influenza vaccine contain
Purified fraction containing HA and NA of an inactivated virus To children: Live attenuated
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Current screening of mothers during pregnancy
Hep B, HIV, Rubella, Syphillis
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What bacteria is the most common cause of early onset neonatal sepsis?
Group B Strep by far (1/3 of women colonized with) | Then E. coli
229
Most common type of meningococcal disease in UK
Men B (because vaccinated for men c) But now is a men B one
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Most common cause of death WW in children under 5
Prematurity
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Most common cause of congenital deafness in UK
CMV
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Congenital toxoplasmosis presentation
Can cause still birth 60% asymptomatic at birth. May get long-term sequelae - deafness, low IQ, microcepahly 40% symptomatic at birth - choroidoretinitis, microcephaly, hydrocephalus, intracranial calcifications, seizures, hepatosplenomegaly, jaundice
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Congenital rubella presentation
Depends on time of infection. Worst in 1st 12 weeks. 13 - 20 weeks - >15% have deafness and retinopathy Eyes: Retinitis, cataracts, glaucoma Ears: Deafness CVS: PDA; ASD, VSD Ears: Deafness Brain: Microcephaly, meningoencephalitis, DD Other: Bone disease, hepatosplenomegaly, rash, thrombocytopenia Classic triad: Microcephaly, PDA, cataracts
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Early onset sepsis risk factors (maternal)
``` PROM, prem fever Foetal distress Meconium staining PH ``` CAUSE IS: GBS, E.coli, Listeria
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Early onset sepsis in neonate treatment
Ventilation Circulation Nutrition Antibiotics: Benpen (Group B Strep) + Gent (E.coli)
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Late onset sepsis neonate causative organisms
``` By far the most - Coagulase negative staphylococcus. LEG S. aureus Enterococcus Gram -ves - kelbsiella, pseudomonas Candida ```
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Late onset sepsis in neonate treatment | - examples only
1st line: Cefotaxime + Vancomycin 2nd line: Meropenem If community acquired: cefotaxine, amoxicillin+/- geny
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What kind of organism is rubella Congenital rubella moa
RNA virus Stops rate of cell division, decreases no of overall cells, interferes with development of key organs
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Rubella dx
Rubella IgG - 90% +ve antenatally - if -ve, consider aaaa - Seroconversion - Avidity Rubella IgM PCR - blood, resp, urine,
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Pre-natal diagnosis of rubella
Should consider termination in 1st trimester because of congenital rubella syndrome risk
241
CMV transmission
Horizontally | Vertically: Transplacental (any stage of pregnancy), during delivery, breastfeeding
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Congenital CMV infection diagnosis
In neonate. Can be smptomless at birth and develop sequelae. Detection of CMV from bodily fluids or tissues within 3 weeks of birth (urine and saliva tested) - PCR best, can do serology
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Congenital CMV treatment
6/12 ganciclovir or valganciclovir Audiology follow up for 6 yrs Opthalmology review
244
Classification of maternal HSV infection and risk
1st episode primary - 57% 1st episode non-primary - 25% Recurrent infection - 2% Symptomatic/asymptomatic
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congenital HSV transmission risks
No maternal neutralising Ab Duration of rupture of membranes Loss of integrity of mucocutaneous barriers Vaginal vs c-section
246
When during pregnancy is HSV infection the greatest risk
``` 3rd trimester (particularly within 6 weeks of delivery) as mum continuously shedding virus - c-section recommended ```
247
HSV congenital disease picture in neonate
SEM - skin, eye and mouth in 45% CNS in 30% - 10d-4weeks post natal Disseminated infection involving multi-organ in 25% - most serious, mortality of 30%
248
Congenital HSV investigations
HSV cultures/PCR of anything blood, CSF, urine | ALT good marker
249
Congenital HSV treatment
IV aciclovir 60mg/kg/day in 3 divided doses - 21 days in CNS or disseminated - 14 days in SEM Monitor neutrophils
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Varicella infection in pregnancy may cause
``` In mother: pneumonia/encephalitis Intrauterine VZV: - congenital varicella syndrome - neonatal varicella - HZ during infancy or early childhood ``` Any pregnant women - 10 days IV aciclovir
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Varicella neonatal infection
Occurs just prior or just after delivery - no time for VZV antibodies to pass May result in: - mild course of infection - disseminated skin lesions - visceral infections - pneumonia
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Congenital varicella syndrome risk
Highest at 13-20 weeks gestation - 2% | 0.4% before
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What type of vaccine is VZV
Live (can't give in pregnancy)
254
VZV exposure in pregnant woman
Determine if contact significant Then do serology, if negative then treat: VZ immune globulin if within 10d of exposure (better <20wk gestation) Aciclovir if 7-14d post exposure (>20 week gestation)
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Measles type of virus Symptoms Complications
RNA Prodrome: Fever, conjunctivitis, Koplik spots Rash on face moving down Pneumonia, bronhcitis, otitis media Encephalitis SSPE
256
Measles exposure by pregnant woman
Measle immunoglobulin within 6 day window of exposure NO CONGEITAL ABNORMALITIES TO FETUS Does cause - Preterm - Fetal loss - Increases maternal morbidity
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Hydrops fatalis if in 1st 20 weeks of pregnancy
Parvovirus B19 Hydrops fetalis - due to severe anaemia After 20 weeks, no documented risk
258
Source animal classification in zoonoses
1) Farm/wild animals: - Cattle, poultry, pigs, goats 2) Companion - Dogs, cats (ticks, mice rodents) - Reptiles - Fish
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UK zoonoses
Farm/wildlife: Camplyobacter + Salmonella Companion: Bartonella, Toxoplasmosis, Ringworm, Psitticosis
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Tropical zoonoses
Farm/wildlife: Brucella, Coxiella, Rabies, VHF Companion: Rabies, tickborn diseases, Spirilum minus
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Diarrhoea bloating cramps after uncooked chicken Investigations Management
Camplyobacter Stool culture Supportive
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Cat at home, bit/licked ot and has fever, night sweats and adenopathy. Cause Treatment
Bartonella henselae - cat scratch disease - In immuncompotent. Can progress to more severe symptoms in 15%. If immunocompromised - bacilliary angiomatosis Skin papules, disseminated and vascular involvement Erythromycine + Doxycycline (+ rifampicin if angiomatosis)
263
Toxoplasmosis treatment
Pregnant: Spiramycin Non-pregnant: Pyramethamine + sulfadiazine
264
Pt from abroad went to cattle/goat farm and milked some cows, drank some unpasteurised milk, mucosal splash, aerolisation/ inhalation. Now has fevers similar to extra-pulmonary TB + back pain, orchitis, focal abscess. Cause Investigation Managament
Brucellosis Blood/pus culture (say suspected brucella) Serology Doxycycline + Gent or rifampicin
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Coxiella burnetti presentation Investigation Treatment
Fever, 'Flu like illness', pneumonia, hepatitis, endocarditis, focal abscesses (paravertebral/discitis) Serology Doxycycline (hydroxychloroquine)
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Rabies presentation Treatment
Seizures, excessive salivation, agitation, confusion, fever, headache Treatment helps before symptomatic stage - Immunoglobulin + vaccine
267
Rat zoonoses
Rat bite fever - fevers, polyarthralgia, maculopapular --> purpuric rash, can get endocarditis Due to spirillum minus and streptobacillus moniformis - penicillin Hentavirus pulmonary syndrome - Resp failure in US, renal failure in SE Asia
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non-falciparum malaria treatment
Chloroquine then primaquine
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19yo male returns from Spain. 4 weeks later hot swollen painful red knee joint. Knee tapped and 20ml cloudy fluid stains as gram -ve intracellulular diplococci
Neisseria gonorrhoea | Most common cause of septic monoarthritis in a 18-30yo who has monarthritis.
270
Meningitis symptoms in 19yo boy. LP reveals gram -ve intraceullar diplococci
Neisseria mengitidis
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6yo meningitis picture. LP reveals gram -ve rods
H. influenzae
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19yo PUO. After 2 months, bloods show gram +ve cocci
``` Endocarditis Signs will slowly appear - Splenomegaly - Splinter heamorrhages - Roth spots - Clubbing - Microscopic haematuria - Janeway lesions ``` Step viridan - chooses aortic valves because higher pressure, already bit of damage there - settles there
273
Iv drug user endocardit
S. aureus. V agressive, lands on first valve and grows there - tricuspid valve - die of septicaemia in 3 weeks. Much quicker disease progression than s.viridans
274
CF with respiratory tract infection | - Organisms responsible
Pseudomonas aeruginosa, Burkholderia
275
HIV respiratory tract infection
Pneumocystitis jiroveci (PCP) TB Cryptococcus neoformans
276
Respiratory tract infection following splenectomy | - responsible organisms
NHS (encapsulated)
277
PCP presentation
Dry cough, weight loss, SOB, malaise
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neutropenic patient develops respiratory tract infection | - causative organism?
Aspergillus spp.
279
Fungal infections
Yeasts - Candida - Cryptociccus - Histoplasma Moulds - Aspergillus - Dermatophytes - Agents of mucormycosis
280
Cryptococcosis diagnosis and management
Presents as meningitis with insidious onset in HIV. Associated with birds, particularly pigeons Diagnosis - detection of cryptococcal antigen in blood/CSF + india ink stain = mainstay - Can often culture but slower (2 days) management - 3/52 amphotericin B +/- flucytosine
281
Classification of PUO
Durack and street 1) Classical. >38.3 temp. Lasting >3/52. 3 or more visits/days in hospital - Infection - Malignancy - Collagen vascular disease 2) Nosocomial. >38.3 temp. Hospitalised 24h but no fever on admission. 3 or more days investigation - C. difficile enterocolitis - Drug induced - PE - Septic thrombophlebitis - Sinusitis 3) Immune deficient. >38.3 temp. Neutrophils <500. 3 or more days investigation - Opportunistic bacterial infections - Aspergillosis - Candidiasis - Herpes 4) HIV associated - CMV - PCP - Kaposi/N-H lymphoma
282
How does PET-CT work
Fluoro-D glucose accumulates in cells with an increased rate of glycolysis (all activated leukocytes) - Infection - Inflammation - Cancer Caution in patients with poor glucose control
283
Malaria definition Carried by which mosquito Life cycle
RBCs parasitized --> ineffective --> haemolysis Anopheles mosquito Mosquito stage + human stage. Human stage divided into erythrocytic (in RBCs) and exoerythrocytic. Sometimes a liver stage too (hypnozoite stage) - non-falciparum types sleep in liver (chloraquine doesn't kill liver stage hence need primaquine)
284
Malaria species
5 plasmodium species: 1. P. falciparum - invades erythrocytes of all ages, may be drug resistant and can be life threatening 2. P. vivax 3. P. ovale 4. P. malaria 5. knowlesi
285
Malaria symptoms
``` Fever + rigors Headache Back pain Myalgia N&V ```
286
Severe malaria features
``` Impaired consciousness/seizures Renal impairment Acidosis Hypoglycaemia Pulmonary oedema/ARDS Anaemia DIC/bleeding Shock Haemoglobinuria Parasitaemia >2%, pregnancy, vomiting ```
287
Malaria diagnosis Treatment
Thick and thin blood film x 3 Malaria antigen tests Non-falciparum: - 3 days chloraquine - Primaquine for 14days (hypnozoites) Mild faclciparum (no vomit, parisataemia <2%) - oral malarone 3 days - Oral quinine + doxycycline - artemisinin combination therapies e.g. riamet Severe falciparum - ABC - Correct hypoglycemia - IV artesunate
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Denque cause
Aedes mosquito Fever, headache, myalgia, arthralgia, rash in 50% Usually mild/self limiting Dengue haemorrhagic fever Investigations: Serology (IgM 5-7days), PCR Treatment = supportive
289
Schistosomiasis presentation Treatment
``` Asymptomatic Acute schistosomiasis: - High temp - Blotchy, itchy red rash - Cough - Diarrhoea - Myalgia - Arthralgia ``` Permanent organ damage if not treated Praziquantel
290
Filiarisis
``` Nematode infections spread by blackflies and mosquitoes Classified by location of adult worm - Lymphatic - Subcutaneous - Serous cavity ``` Diagnosis by finding microfilariae (blood films, skin snips), antibodies, finding adults (US)
291
Worm classification
Cestodes (tapeworm) e.g. hyatid, pork/beef tapworms Trematodes (flukes) e. g. lung, liver, intestinatl - schistosomiasis (blood)
292
Cognitive disturbance, personalty change, motor deficits | Demyelination of white matter with neurologial deficits corresponding to areas of brain affected
Progressive multifocal encephalopathy Causd by JC virus - acquired in childhood, latent in BM, circulates to blod Used to mostly be seen in AIDS and patients on natalizumab (for MS) Diagnosis on MRI and PCR of CSF
293
Brown/purple vascular lesions in HIV patient
``` Kaposi sarcoma Characterised by: - Spindle cell proliferation - Neo-angeogenesis - Inflammation and oedema ``` Chemo + initiate antiretroviral therapy
294
HBV sAG +ve HBV core Ab +ve HBV s Ab -ve
Current HBV infection
295
HBV sAG -ve HBV core Ab +ve HBV s Ab +ve
Past HBV infection
296
HBV sAg -ve HBV core Ab -ve HBV s AB +ve
Vaccination against HBV
297
What is prion disease
Protein-only infectious agent. Rare transmissable spongiform encephalopathies in humans and animals --> rapid neurodegeneration and death in months Untreatable Prion protein gene on Chr 20 Normal protein structure PrP. Abnormal PrP^sc abnormally folds --> beta sheet configuration and protease/radiation resistant. PrP^sc promotes irreversible conversion of PrP to insoluble PrP^sc
298
Prion disease classification
Sporadic: trigger for prion disease unknown Acquired - vCJD - kuru - iatrogenic: GH, blood, surgery Genetic: Familial CJD, GSS, Familial fatal insomnia
299
Sporadic CJD cause Presentation Diagnosis
Cause uncertain: – ? somatic PRNP mutation – ? spontaneous conversion of PrPc to PrPsc – ?? Environmental exposure to prions Rapid progressive dementia with - Myocolonus - Cortical blindness - Akinetic mutism - LMN signs Age of onset ~ 45-75 Mean survival = within 6/12 of symptoms starting ``` Diagnosis of sporadic CJD • EEG: periodic, triphasic complexes (non-specific) • MRI: basal ganglia – increased signal • CSF: 14-3-3 protein +ve • Neurogenetics to r/o genetic cause • Tonsillar biopsy NOT useful • Brain biopsy • Autopsy – by experienced pathologist: Spongiform vacuolation, PrP amyloid plaques ```
300
vCJD Cause Presentation Diagnosis
Cause: Exposure to bovine spongiform encephalopathy ``` Younger age of onset than sCJD ~ 26yo Psychiatric onset: anxiety, paranoia, hallucinations Then neurological - peripheral sensory symptoms - ataxia - myoclonus - chorea - dementia ``` Diagnosis of vCJD • EEG – non-specific slow waves • MRI brain - positive pulvinar sign (posterior thalamus highlighted) • CSF – 14.3.3, can be normal • Neurogenetics (almost 100% are MM at codon 129) • Tonsil biopsy 100% sensitive and specific • (Brain biopsy) • Autopsy: PrPSc type 4t detectable in CNS + most lympo-reticular tissues, florid plaques
301
Iatrogrenic CJD Cause
Innoculation with human prions, most commonly from surgery - Progressive ataxia initially - Dementia and myoclonus later - Speed of disease depends on route of innoculation Diagnosis - No mutations
302
Antimicrobial inhibitors of DNA synthesis
Fluoroquinolones e.g. ciprofloxacin. - against gram -ve's Nitroimidazoles - against anaerobes and protozoa (Giardia)
303
Conjugate vaccinations MOA Examples
N. meningitis Haemophilus influenzae Pneumococcal Polysacharide + protein carrier (promotes T cell immunity + therefore enhances B cell/antibody response)
304
Subunit vaccinations MOA Examples
Hep B - made using recombinant DNA HPV Influenza (haemaglutinin + neuraminidase)
305
Live attenuated vaccines MOA Examples
Achieves immunisation with single dose Not suitable for immunocompromised OR PREGNANT ``` MMR BCG Yellow fever Typhoid Oral poliomyelitis Chickenpox ```
306
Inactivated/killed vaccinations
Hep A Cholera Rabies Polio (salk)
307
What is Alum
Induces mild inflammatory response - promotes predominantly antibody response through Il-4 release (eosinophil activation) and (primes naive B cells) Used in - Hep A - Hep B - Hib
308
What is ISCOM
Immune Stimulatory COMplexes | Antigen assembled in multimeric form and saponin that promotes a strong serum antibody response
309
Leptospiriosis
Spiral shaped gram -ve - Urine or tissue of an infected animal. From swimming in contaminated water - Hepatitis, jaundice, conjunctival infections, renal impairment AGGLUTININ TEST = gold standard
310
Bacillus anthralics
Gram +ve rod. Blood agar culture Ulcerating papule - black and necrotic centre Responds to high dose penicillin
311
Vaccine given every 5 years to splenectomy patients
Pneumococcal
312
Inhibitors of RNA synthesis
Rifampicin Watch out for LFTs and orange urine Never use as a single agent because of resistance Used for TB
313
Inhibitors of folate metabolism
Sulphonamides + diaminopridines Sulphonamide e.g. Co-trimoxazole for PCP
314
Painless ulcer, dark brown medium growth Snail tracks in mouth now
Syphilis
315
SSI organisms
MSSA, MRSA E. coli Psesomonas
316
Early neonatal infection in order Late onset sepsis (>48-72h)
Group B streptococci E.coli Listeria CoN Staphyloccous
317
Wet slide prep +ve | Discharge in woman, no other symptoms
Trichomonas. Flagellated protozoa Rx with metronidazole In meny: asymptomatic or urethritis
318
Fever onset 6 weeks after holiday
Vivax malaria Acute hep (B, C, E) TB Amoebic liver abscesses