Microbiology Flashcards
What are the potential targets for antibiotics?
Inhibit cell wall synthesis
Inhibit protein synthesis
Inhibit DNA synthesis
Inhibit RNA synthesis
Cell membrane toxin
Inhibit folate metabolism
Which classes of antibiotics inhibit cell wall synthesis
Beta lactams
Glycopeptides
What are the different types of beta-lactam?
Penicillins e.g. benzylpenicillin
Cephalosporins: ceftriaxone
Carbapenems e.g. meropenem
What are the indications for beta-lactams?
Gram positive
[Gram negative- 3rd generation cephalosporin)
What are some examples of glycopeptides?
Vancomycin, Teicoplanin
What are the indications for glycopeptides?
MRSA, C. Diff
Which classes of antibiotics inhibit protein synthesis?
Aminoglycosides
Tetracyclines
Macrolides
Chloramphenicol
Oxazolidines
Give an example of an aminoglycoside
Gentamicin
Give an example of a tetracycline
Doxcycline
Give an example of a macrolide
Erythromycin
Give an example of a chloramphenicol
Eye drops
Give an example of an Oxazolidinone
Linezolid
What are the indications for aminoglycosides
Gram -ve sepsis
Gram -ve sepsis
Gentamicin
What are the indications for tetracyclines
Intracellular- chlamydia
Rx for chlamydia
Doxycycline
What are the indications for macrolides
Gram +ve in context of Pen Allergic
Rx Gram +ve in context of pen allergic
Erythromycin (macrolide)
What are the indications for chloramphenicol
Bacterial conjunctivitis
Rx bacterial conjunctivitis
Chloramphenicol
What are the indications for oxazolidinones
Gram +ve, MRSA + VRE
Rx for Gram +ve, MRSA + VRE
Linezolid
or
Daptomycin
What classes of antibiotics inhibit DNA synthesis
Fluoroquinolones
Nitroimidazoles
Given an example of a fluoroquinolone
Ciprofloxacin
Given an exmple of a nitroimidazole
Metronidazole
Indications for fluoroquinolones
Gram -ve
Indications for nitroimidazoles
Anaerobes and protozoa
What class of antibiotics inhibits RNA synthesis?
Rifamycin
Given an example of a rifamycin
Rifampicin
Indications for rifamycins
MTB
Rx for anaerobes and protozoa
Metronidazole
What classes of antibiotics act as cell membrane toxins
Polymyxin
Cyclic lipopeptide
Give an example of a polymyxin
Colistin
Give an example of a cyclic lipopeptide
Daptomycin
What are the indications for polymyxins?
Gram -ve
What are the indications for cyclic lipopeptide
Gram +ve, MRSA +VRE
What classes of antibiotics inhibit folate metabolism?
Sulfonamides
Diaminopyrimidines
Give an example of a sulfonamide
Sulphamethoxazole
What are the indications for sulfonamides?
PCP (with trimethoprim: co-timoxazole)
What are the indications for diaminoprimidines?
UTI e.g. Trimethoprim
What are some broad spectrum antibitoics?
Co-amoxiclav
Tazocin
Ciprofloxacin
Meropenem
What is tazocin?
Combination antibotic containing penicllin (piperacillin) and a beta-lactamasae inhibitor tazobactam
What is co-amoxiclav?
Combination antibiotic containing penicllin amoxillin and beta-lactamase inhibitor clavulanic acid
What are some narrow spectrum antibiotics?
Flucloxacillin, metronidazole, gentamicin
Features of beta-lactams
Activity?
Ineffective against?
- Inactivate the enzymes that are involved in the terminal stages of cell wall synthesis (transpeptidases also known as penicillin binding proteins) – β-lactam is a structural analogue of the enzyme substrate
- Bactericidal
- Active against rapidly-dividing bacteria
- Ineffective against bacteria that lack peptidoglycan cell walls (e.g. Mycoplasma or Chlamydia)
Penicllin uses
Broken down by?
Gram +ve organisms e.g. strep, clostridia
Broken down by beta-lactamase, prod by S. aureus
Amoxicillin uses
Broken down by?
Broad spectrum, extends coverage to enterococci and Gram -ve organisms
Beta-lactamase produced by S. aureus and many gram negative organisms
flucloxacillin uses
NB
Similar to penicllin although less active
Stable to beta-lactamase produced by S. aureus
Uses of piperacillin
Similar to amoxicillin, extends coverage to pseudomonas and other non-enteric gram negatives
Broken down by beta-lactamase producing organisms e.g. S. aureus and gram negatives
Clavulanic acid and tazobactam
Beta-lactamase inhibitors extend coverage of penicllins to include S.aureus, Gram negatives and anaerobes
What changes with the generations of cephalosporins?
Increasing activity against gram negative bacilli
What is a 1st generation cephalosporin?
Cephalexin
What is a What is a 2nd generation cephalosporin?
Cefuroxime
What is a 3rd generation cephalosporin?
Cefotaxime
Ceftriaxone
Ceftazidime
What are ESBL organisms resistant to?
All cephalosporins regardless of in vitro results
Use of cefuroxime
•Stable to many β-lactamases produced by Gram negatives. Similar cover to co-amoxiclav but less active against anaerobes
With what is ceftriaxone associated?
C diff
What is the use of ceftazidime?
anti-Pseudomonas
What are the uses of carbapenems?
What is an issue
Stable to ESBL enzymes
Carbapenemase enzymes becoming more widespread
There are multidrug resistant Acinetobacter and Klebsiella species
What are the key points for beta-lactams
- Relatively non-toxic
- Renally excreted (so ↓dose if renal impairment)
- Short half life
- Will not cross intact blood-brain barrier
- Cross-allergenic (penicillins approx 10% cross-reactivity with cephalosporins or carbapenems)
Why are glycopeptides effective against Gram +ve?
- Large molecules, unable to penetrate Gram –ve outer cell wall
- Active against Gram +ve organisms
Rx for MRSA administration
IV only
What is used to treat serious C diff?
Oral vancomycin
What is an issue with glycopeptides?
As a consequence?
Nephrotoxic
Need to monitor drug levels to prevent accumulation
Rx vs P. aeruginosa?
Gentamicin and tobramycin
Features of aminoglycosides
What is significant
- Bind to amino-acyl site of the 30S ribosomal subunit
- Rapid, concentration-dependent bactericidal action
- Require specific transport mechanisms to enter cells (accounts for some intrinsic R)
Ototoxic and nephrotoxic: monitor levels
Combination of beta-lactams and aminoglycosides?
Synergistic
What are the features of tetracyclines
What is significant
Side-effect?
- Broad-spectrum agents with activity against intracellular pathogens (e.g. chlamydiae, rickettsiae & mycoplasmas) as well as most conventional bacteria
- Bacteriostatic
- Widespread resistance limits usefulness to certain defined situations
Do not give to children or pregnant women
Light-sensitive rash
Features of macrolides
- Bacteriostatic
- Minimal activity against Gram –ve bacteria
- Useful agent for treating mild Staphylococcal or Streptococcal infections in penicillin-allergic patients
- Also active against Campylobacter sp and Legionella. Pneumophila
- Newer agents include clarithromycin & azithromycin with improved pharmacological properties
Rx for Campylobacter and L. pneumophila
Macrolide
MOA Macrolides
•Bind to the 50s subunit of the ribosome
1) Interfere with translocation 2)Stimulate dissociation of peptidyl-tRNA
MOA tetracyclines
- Reversibly bind to the ribosomal 30S subunit
- Prevent binding of aminoacyl-tRNA to the ribosomal acceptor site, so inhibiting protein synthesis.
MOA aminoglycosides
) Prevent elongation of the polypeptide chain
2) Cause misreading of the codons along the mRNA
What are the significant adverse effects of chloramphenicol
Aplastic anaemia
Grey baby syndrome in neonates: inability to metabolise drug
MOA chloramphenicol
•Chloramphenicol binds to the peptidyl transferase of the 50S ribosomal subunit and inhibits the formation of peptide bonds during translation
MOA Nitroimidazoles
- Include the antimicrobial agents metronidazole & tinidazole
- Under anaerobic conditions, an active intermediate is produced which causes DNA strand breakage
What are nitrofurans?
Compounds related to nitroimidazoles e.g. nitrofurantoin used for UTIs
Considerations when Rxing rifampicin
Monitor LFTs
beware interactions with other drugs that are metabolised by the liver
Orange secretions
Why should you never use rifampicin as a single agent?
- Except for short-term prophylaxis (vs. meningococcol infection) you should NEVER use as single agent because resistance develops rapidly
- Resistance is due to chromosomal mutation.
- This causes a single amino acid change in the ß subunit of RNA polymerase which then fails to bind Rifampicin.
Features of colistin
Colistin – a polymyxin antibiotic that is active against Gram negative organisms, including Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella. pneumoniae. It is not absorbed by mouth. It is nephrotoxic and should be reserved for use against multi-resistant organisms
Why is sulphonamide and diaminopyrimidine combined Rx useful?
- Act indirectly on DNA through interference with folic acid metabolism
- Synergistic action between the two drug classes because they act on sequential stages in the same pathway
- Sulphonamide resistance is common, but the combination of sulphamethoxazole+trimethoprim (Co-trimoxazole) is a valuable antimicrobial in certain situations (e.g. Treating Pneumocystis. jiroveci pneumonia)
- Trimethoprim is used for Rx community-acquired UTIs
What are the mechanisms of antibiotic resistance?
Inactivation
Altered target
Reduced Accumulation
Bypass
How does resistance to beta-lactams occur?
NB
Beta lactamases
Not the mechanism of resistance in penicllin resistant pneumoccoci and MRSA
How does beta-lactam resistance develop in MRSA?
Altered target: mecA encodes novel PBP (2a) which has a low affinity for binding beta lactams, substitutes for teh essential functions of high affinity PBPs at otherwise lethal concentrations othe antibiotic
How does Strep pneumonia resist Beta lactams?
Altered target: Penicllin is the result of the acquisition of stepwise mutations in PBP genes, lowe rlevel resistance can be overcome by increasing the dose
What are ESBLs?
What can they do?
NB?
Extended spectrum beta lactamases
Able to break down cephalosporins, becoming more common
Resistant to cephalosporins regardless of in vitro finding
What leads to macrolide resistance?
Altered targets:
- Adenine-N6 methyltransferase modifies 23S rRNA
- Modification reduces the binding of MLS antibiotics and results in resistance
- Encoded by erm (erythromycin ribosome methylation) genes.
IFV vaccines in use today
Triaelent or quadrivalent inactivated vaccine: split or subunit HA rich. Given to those at risk. Short term strain specifica immunity mediated by Ab to HA head.
Live attenuated vaccine also quadrivalent or trivalent: cold adapted virus limited to URT, given to children, broader more cross reactive immunity
Features of IFV
Orthomyxovrius
What are the three strains that tend to affect humans each year?
How is this combatted?
IFV: A (H1: peaks begnning of January)
IFV: A (H1N1: peaks end of December)
IFV B: Peaks march
Trivalent vaccine in targetted populations which consists of a purified fraction with HA + NA of inactivated virus
What is the natural resrvoiir of IFV A
Why is these limited human-human transmission
Ducks
Because the vrius doesn’t replicate in the colder URT
What is the structure of IFV
8 RNA segements of nucleocaspid protein very prone to mutation
Outline IFV viral entry
NA (sialidase): cleaves sialic acid residues exposing receptor son host cell disrupting mucin barrier
HA: binds sialic acid receptors-> virus entry. Endosomal-viral envelope fusion= release
How are IFVs named?
H1= HA1
N1= N1
What is antigenic drift?
Mutation of HA/NA to give new viral strains
What is antigenic shift?
Complete change of HA/NA
Reassortment of RNA segments between IFV strains
Can only occur in IFVA
What is the pathogenesis of IFV H5N1
Cleavage of HA by clara-tryptase in the lung leads to exteded tropism/grwoth for H5 + H7
What are the causes of severe outcome in flu?
Secondary bacterial pneumonia
Mutant virus
Co morbidity
Cytokine storm
What is amantadine
Indication
MOA
Issue
Antiviral for IFV
IFVA only
Targets M2 ion channel but single AA mutation in M2= resistance
Give some examples of neuraminidase inhibitors
Oseltamivir (tamiflu)
Zanamivir (relenza)
Sialic acid
Only effective if given <48hrs aftern infection
What are the various issues with the different ROA in vaccines?
Subcute: good, uptake, processing and presentation to Langherans cells
IM: OK
IV Ag: taken to spleen
Orally: good response and local response within GIT
Intranasal: OK but may get allergic response
What are some examples of APCs?
Macrophages
B-lymphocytes
Langerhans
DCs
What does clonal expansion of CD4 cells require?
Specific antigent in combination with a cytokine e.g. IL-2
What response does the TH1 subset mediate
What cytokines are involved?
Cell-mediated immune response
IL-2
IFN-G
TNF
What response does the TH2 mediate?
What cytokines are involved?
Humoral response
IL-4
IL-5
IL-6
Why is it called haemagglutinin?
Causes agglutination of RBCs/URT cells
What are the 2 subsets of memory cells?
Central memory T cells: CCR7+CD62Lhigh: migrate efficiently to peripheral LNs, produce IL-2 but no IFN or perforin
Effector memory T cells: found in other sites, produce high levels of IFN and perforin but no IL-2
What are the three phases of T cell immunological memory?
Expansion
Contraction
Memory
What does the choice of antibiotic depend on?
CHAOS
Choice
Host
Antimicrobial susceptibilites of the
Organism itself and also the
Site of the infection
Choice of drug best features
Narrow spectrum
Bactericidal
Based on local sensitivity
Patient characteristics
Cost
When is IV antibiotic use indicated
Serious infection or no PO absorption
If need to access deep site or CNS
What factors influence antibiotic dose?
Age
Renal/hepatic function
Drug monitoring
Allergy
Principles for empirical treatment with antibiotics:
Collect specimens
Use a broad-spectrum antibiotic
Empirical cover may then be changed to a more specific agent on the basis of culture results
What are thhe preliminary investiations for identification of a bacterial infection
Gram stain: CSF, joint aspirate, Pus
Rapid antigen detection: immunofluorescence, PCR
What are the important factors to consider about the site of the infection?
pH
Lipid-solubility
CNS penetration
Special considerations required for Rx of endocarditis or osteomyelitis
Administration of antibiotics route of choice
IV : serious or deep seated infection
PO: usually easy but differential absorption between different antibiotic classes
IM: not an option for long term use, avoid id bleeding tendency
Topical: limited application that may cause local sensitisation
Generally after a patient has been on IV antibiotc for 48hrs switch to oral if they have stabilised
What is a type 1 pattern of antibiotic activity?
What is the goal of therapy?
Which antibiotics?
Concentration-dependant killing and prolonged persistent effects
Maximise concentrations
Aminglycosides, daptomycin, fluoroquinolines, ketolides
What is a type 2 pattern of antibiotic activity?
Goal of therapy
Antibiotics?
Time-dependant killing and minimal persistent effects
Maximise duration of exposure
Carabapenems, cephalosporins, erythromycin, linezolid, penicllins
What is a type 3 pattern of antibiotic activity?
Goal of therapy
Antibiotics
Time-dependent killing and moderate-to prolonged persistent effects
Maximise amount of drug
Azithromycin, clindamycin, oxazolidinones, tetracyclines, vancomycin
Recommended Rx course for N. meningitides meningitis?
7d
Recommended Rx course for acute adult osteomyelitis?
6w
Recommended Rx course for bacterial endocarditis
4-6w
Recommended Rx course for GpA streoptococcal pharyngitis
10d
Recommended Rx course for simple cystitis
3d
Skin infections common types
Common organism
Rx?
Impetigo, cellulitis, wound infection
S.aureusm, beta-haemolytic streptoccoci
Fluclox unless penallergic or MRSA
Invasive group A strep treatment
Aggressive and early debridement
Antibiotics: adjunctive use of protein synthesis inhibitors esp. clindamycin
Use of IVIG
What is the Eagle effect?
Proposed mechanism?
- Named after Harry Eagle who first described it, originally referred to the paradoxically reduced antibacterial effect of penicillin at high doses, though recent usage generally refers to the relative lack of efficacy of beta-lactam antibacterial drugs on infections having large numbers of bacteria.
- Penicillin is a bactericidal antibiotic that works by inhibiting cell wall synthesis but this synthesis only occurs when bacteria are actively replicating (or in the log phase of growth).
- In cases of extremely high bacterial burden (such as with Group A Strep), bacteria may be in the stationary phase of growth.
- In this instance since no bacteria are actively replicating (presumably due to nutrient restriction) penicillin has no activity.
Rx in pharyngitis?
Benzyl-pen 10d
CAP Rx (mild)
Amoxicllin
CAP Rx (severe)
Co-amoxiclav and clarithromycin
HAI
Rx
Second most common cause of HAI
Associated with highest mortality
Greatest risk associated with tracheal intubation and mechanical ventilation
Cephalosporin, ciprofloxacin, tazocin, if MRSA colonised ris consider addition of vancomycin
What are the main pathogens in bacterial meningitis?
Rx?
N meningitidis
S pneumonia
+/- Listeria in very young/elderly/immunocompromised
Ceftriaxone +/- amoxycilllin if Listeria likely
Meningitis in neonate Rx
Cefotaxime + amoxicillin
Why is cefotaxime used in neonates?
Used insteead of ceftriaxone as it displaces bilirubin from albumin and can cause biliary sludging
N menigitidis treatment
Benzylpen or ceftriaxone/cefotaxime
Rx simple cystitis in community
Trimethoprim
HA-UTI Rx
Infected urinary catheter?
Cephalexin or Augmentin
Change under gentamicin cover
Rx for C diff
Stop offending antibiotic: usually a cephalosporin
If severe, RX with PO metronidazole
If fails use PO vancomycin
Def: bacturia
Def: cystitis
Presence of bacteria in urine
Inflammation of the bladder, often caused by infection
Classification of UTIs?
Uncomplicated: infection in a structureally and neurologically normal urinary tract
Complicated: with functional or structural abnormalities including catheters/calculi
Which patients are generally affected by complicated UTIs?
Men
Pregnant Women
Children
Patients who are hospitalised or in healthcare settings
Prevalence of bacturia in young non-pregnant women?
Incidence of symptomatic UTIs in women?
1-3%
40-50%
What causes 95% of UTIs?
E. coli
•Urinary tract infections are caused by many species of microorganisms, however, only a few serogroups of E. coli, O1, O2, O4, O6, O7, O8, O75, O150, and O18ab, cause a high proportion of infections
What other orangisms cause UTIs?
- Proteus mirabilis
- Klebsiella aerogenes
- Enterococcus faecalis
- Staphylococcus saprophyticus
- Staphylococcus epidermis
What is significant in recurrent UTIs, especially those with structural abnormalities?
The relative frequency of infections caused by atypical organisms (i.e. not E. Coli) increases greatly
What are the antibacterial host defences in the urinary tract?
Urine: osmolality, pH, organic acids
Urine flow and micturition
Urinary tract mucosa: bactericidal activity, cytokines
Causes of renal obstruction
Mecahnical:
Extrarenal: valves, stenosis or bands, cacluli, extrinsic ureteral compression and BPH
Intrarenal: nephrocalcinosis, uric acid nephropathy, analgesic nephropathy, PKD, hypokaelmic nephropathy and the renal lesions of sickle cell trait/disease
Neurogenic:
Polio
Tabes dorsalis
Diabetic neuropathy
SC injuries
What dose vesicoureteral reflux lead to?
Perpetuation of infection by maintaining a residual pool of infected urine in the bladder after voiding
What is significant about infection in the kidney?
Frequently a site of abscesses in patients with S aureus bacteremia or both
Infection by gram negative bacilli rarely occurs by the haematogenous
Symptoms of UTI in neonates/children <2y/o?
>2y/o?
Failure to thrive, Vomiting, Fever
Frequency, dysuria, abdo or flank pain
Lower UTI symptoms?
- The lower tract symptoms result from bacteria producing irritation of urethral and vesical mucosa, causing frequent and painful urination of small amounts of turbid urine.
- Patients sometimes complain of suprapubic heaviness or pain.
- Occasionally, the urine is grossly bloody or shows a bloody tinge at the end of micturition.
- Fever tends to be absent in infection limited to the lower tract.
Upper UTI symptoms
- fever (sometimes with rigors)
- flank pain
- and frequently lower tract symptoms (e.g., frequency, urgency, and dysuria)
- at times, the lower tract symptoms antedate the appearance of fever and upper tract symptoms by 1 or 2 days
- the symptoms described, although classic, may vary greatly
Symptoms of UTI in older patients
- The vast majority of older adult patients with urinary infection are asymptomatic
- Symptoms, when present, are often not diagnostic, because noninfected older adults often experience frequency, dysuria, hesitancy, and incontinence
- Symptoms of upper tract infection are often atypical e.g., abdominal pain, change in mental status
Ix of UTI (uncomplicated):
Urine Dip
MSU for MCS
Bloods: FBC, UE, CRP
Ix of complicated UTI
Renal US
IV urography
What indicates contamination of a urine sample on microscopy?
Squamous epithelial cells
Causes of sterile pyruia?
(pus in urine)
Prior treatment with antibiotics
Calculi
Catheterisation
Bladder neoplasm
TB
STI
What are the differentiating culture forming units/mL in urine sample
10^5 cf/mL in infection
Patients without infection: <10^4 cfu/mL
What is the most common cause of candida infection in UT?
Occurs with indwelling catheters
Can be cured by removal of catheter
Rx of fungal UTI
There is no demonstrated benefit in treatment of asymptomatic infection
Exceptions made for renal transplant patients and patients who are to undergo elective urinary tract Sx
Features of pyelonephritis
Commonly associated with sepsis and septicaemia
Requires more aggressive Rx
Broad spectrum bios
Co-amoxiclav +/- gent
Imaging: calculi, structural cause
Rx of pyelonephritis?
Co-amoxiclav +/- gent
Cefuorxime +/- gent
Cxs of pyelonephritis?
Perinephric abscess
Chronic pyelonephritis- scarring, chronic renal impairment
Septic shock
Acute papillary necrosis
What are the most common causes of UTI
E Coli
Proteus
Klebsiella
Staph saprophyticus
What is the dipstick finding in UTI?
Nitrites + leucocytes +ve
Rx of UTI?
Timeothprim or nitrofurantoin
What is tabes dorsalis?
abes dorsalis, also known assyphilitic myelopathy, is a slow degeneration (specifically,demyelination) of the nerves primarily in the dorsal columns(posterior columns) of the spinal cord (the portion closest to the back of the body). These nerves normally help maintain a person’s sense of position (proprioception), vibration, anddiscriminative touch.
What are the routes of entry for meningitis?
Haematogenous spread
Direct implantation (e.g. surgery, LP)
Local extension (secondary to established infection)
And PNS into CNS (viruses)
Meningitis def:
Infection of the meninges and CSF
Dura mater
Pia mater
Arachnoid mater
Symptoms of meningitis
Headache
Stiff neck
Soome disturbance of brain function
Organsisms causing meningitis
N meningitidis
Pneumococcus
H influenzae
L monocytogenes
GBS
E Coli
Staph aures
Treponema pallidum
TB
Virus
Cryptococcus neoformans
Candida
Grows on chocolate agar, gram negative cocci=
N meningitidies
Transmission of N meningitidis
Person-person from asymptomatic carriers
Pathogenic strain found in only 1% of carriers
Through nasopharyngeal mucosa in susceptible individuals
Causes infection in less than 10 days
Outcome of N meningtiides infection
Septicaemia in 7-10%
Meningitis in 50%
Both in 40%
NB re LP in septicaemia?
Coagulopathy…
Neuropathology of N. meningitis
Direct bacterial toxicity, indirect inflammatory process and cytokine release and oedema
Shock seizures and cerebral hypoperfusion
10% mortality with 5% of survivors having neurological sequelae (predominantly sensorineural deafness)
Clinical spectrum of septicaemia?
Produced by four processes
Capillary leak: albumin, and other plasma proteins leading to hypovolaemia
Coagulopathy: leads to bleeding and thrombosis
Metabolic derangement: acidosis
Myocardial failure and multi-organ failure
Acute meningitis
Usually bacterial
Chronic meningitis
Headaches for months
TB or cryptococcus or spirochetes
More common in immunosuppressed
Involves the meninges and basal cisterns of the brain and SC
Can result in tuberculous granulomas, abscesses or cerebritis
Aspetic meningitis
Usually acute biral, most common CNS infection
Presents with headache, fever, neck stiffness, photophobia
Non-specific rash
Most frequent in children younger than 1y
Self-limiting course that resolves in 1-2w
Most commo organisms causing aseptic meningitis
80-90% caused by coxsackie virus group B and echoviruses
Most common causes of bacterial meningitis in enonates
GI flora: GBS, L monocytogenes, E Coli
Most common cause of bacterial meningitis in elderly
GBS
Listeria
MTB (subacute)
What is another important cause of aseptic meningitis
HSV
Remember to ask re symptoms of HsV infection
Def: encephalitis
Symptoms
Infection of the brain parenchyma
(Meningoencephalitis- inflammation of the meninges and brain parenchyma)
Disturbances of brain function
Organisms causing encephalitis?
Rabies
Arboviruses
Trapanasome brucei gambiense
TB
Prions
Amoeba
West Nile
Features of Brain abscesss
SOL on imaging: looks like cancer, needs histopathology to say which
Spreads from otitis media, mastoiditis, paranasal sinuses, endocarditis, haematogenously
Organisms likely to cause brain abscesses
Streptococci
Staph
Gram negative (particulalry in neonates)
MTB
Fungi
Parasites
Actinomyces
Nocardia specias
Def: myelitis
Infection of the spinal cord
What is a common form vertebral infection?
Spread?
Px?
Pyogenic vertebral osteomyelitis
Direct pen trauma, infections in adjacent structures, from haematogenous spread
If left untreated can lead to permanent neurological deficit, significant spinal deformity or death
Symptoms of myelitis
Significant organism?
Disturbance of nerve transmission
Polio
What are the factors for myelitis
Advanced age
IVDU
LT-systemic steroids
DM
Organ transplantation
Malnutrition
Cancer
Neurotoxin causing rigid paralysis?
Tetanus from C tetani
Neurotoxin causing flaccid paralysis?
Botulism
C botulinum
Risk factors for N meningitis?
Complement deficiency
Hyposplenism
Hypogammaglobulinameia
Risk factors for Strep meningitis?
Complement deficiency
Hyposplenism
Immune defect (ETOH)
Infection (pneumonia)
Entry #
Previous head trauma with CSF leak
Gram -ve cause of meningitis?
Neisseria
Gram +ve cause of meningitis?
Strep pneumoniae
MRI in meningitis
Better than CT in detecting parenchymal abnormalities such as abscesses and infarctions
Meningitis Ix
Clinical and blood cultures
Throat swabs (neisseria)
Serum-Ag
EDTA-PCR
CSF: WCC, protein, glucose
Different types of CSF study
Colour/clarity
WCC/differentaition
Protein, glucsoe
Culture: blood agar, chocolate agar, sabourand’s agar
Limitations of the Ix in meningitis?
MRI oedema pattern and moderate mass effect cannot be differentiated from tumour or stroke or vasculitis
Abx given before culture samples
Amount of CSF
PCR
Methods to detect amoebic infections
CSF:
Clear
0-5 leukocytes
Negative gram stain or Ag test
Protein 0.15-0.4
Glucose 2.2-3.3
Normal
CSF normal WCC
0-5
Protein CSF normal?
0.15-0.4
CSF glucose?
2.2-3.3 (>50% serum)
CSF:
Turbid
100-200 polymorphs
Positive gram stain
0.5-3 on protein (raised)
Reduced glucose
Bacterial menintisi
?Meningococcus
?pneumococcus
?Listeria
CSF: clear or slightly turbid
15-500 lymphocytes
Negative gram stain
0.5-1 protein
Normal glucose
Aseptic meningitis
CSF:
Clear or slighlty turbid
300-500 mixed lymphocytes and polymorphs
Negative gram satin
Raised protein
Reduced glucose
MTB or cryptococcal meningitis
CSF:
Glucose normal
WCC high with polymorphs
Think partiall treated bacterial infection
What CNS infections may show a normal CSF?
Cerebral abscesses (Streptococci)
Viral encephalitis
Mx of bacterial meninigits
ABC
Corticosteroids before Abx
Ceftriaxone (2g IV BD) for pneumo and meningococcus
If elderly/immunocompromsied add amoxicillin or ampicillin to cover for Listeria)
Mx of Meningoencephalitis
Aciclovir
Ceftriaxone
If >50y or immunocompromised add amoxicillin for Listeria cover 2g IV 4 hourly
Mx of aseptic meningitis
Give ceftriaxone until you know it is herpes, no aciclovir
Doses of ceftriaxone?
2g IV BD
Dose of acicvlovir?
10mg/kg IV TDS
Dose of amoxicillin
2g IV 4 hourly
What are the features of the Glasog Meningococcal Septicaemia prognostic score?
Systolic BP
Skin-Rectal T difference
Modified coma scale
Deterioration
Neck stiffness
Extent of purpura
Base deficit
Used as a tool to identify those who may need transfer to a tertiary centre with a PICU
Kwashiorkor?
Acute form of childhood protein-energy malnutrition: oedema, anorexia, ulcerating dermatoses and heaptomegaly
Insufficient protein consumption but with sufficient calorie intake
Marasmus
Severe malnutrition, charactersied by energy deficiency. Emaciated
What are the Helminth diseases?
Schistosomiasis
Hookworm
Threadworm
Filiarisis
What are the protozoal dieases?
Leishmaniasis
Typanosomoiasis
Amoebiasis
Def: Sanitation
The state of being clean and conductive to health
The hygienic separation of human waste form contact. Safe containment, transporation, treatment and disposal of human excreta
Primary barrier to disease transmission
Fluids, fields, flies, fingers and food
Features of Hep A
Acute hepatitis, ofetn subclinical, short period 2-6w
Transmission of Hep A
Faecal-oral spread
Outbreaks associated with occupational risk e.g. sewage workers.
Soft fruit, sewage works, shellfish
anti-HAV IgM
Recent infection disappears after a few months or vaccine
anti-HAV IgG
Previous infection, lifelong or vaccine
Which of the hepatitis vrisuses are RNA?
A
C
D
E
What type of virus is Hep B?
dsDNA virus
What is a good screening test for Hep V and why?
Vrisu makes an excess of surface antigen
Therefore it is a good screening ttest
What is the timefrime for Hep B infection?
Acute <6m
Chronic
Latent virus can reactivate in immunocompromised
Transmission of Hep B
Sexual, vertical, horizontal
Blood products
Clinical picutre for Hep B
Causes and acute or chronic heaptitis
Pathophysiology in Hep B
Over decades leads to scarring and cirrhosis, eventually resulting in HCC. This is accelerated in males and drinkers
Mx of Hep A
Supportive
Mx of Hep B
Pegylated IFn alpha 2a
Lamivudine
Tenofovir
When is Hep B treatment initiated?
When liver damage occurs
Dx of Hep B?
ALT and AST
HbsAg
HBeAg (infectivity, changes form +ve to negative)
HBcAb (acute- IgM, chronic IgG)
Timeframe in Hep C infection
Acute,
80% progress to chronic
Transmission of Hep C
Blood products
How does the Hep C genotype inform treatment?
Genotpyes 1 and 4= 48w
2&3= 24w
Dx of Hep C
ALT
Anti-HCV
Mx of Hep C
Cure 54% treated with peg IFN alpha-2b and ribavirin combination therapy.
Considerations around Peginterferon alpha 2-b
Attacks bone marrow: low WCC, low platelets
Can lead to depression
Care in treating cirrhotic patients as will kill infected hepatocytes
Kidney trransplant is contraindication for IFN
Wariness about treating genotypes 1 and 4 and in elderly patients as there is less chance of a response and treatment is expensive
Hep D features
Only infect Hep B patients.
Transmitted through contaminated blood
Features of Hep B and D infection
Superinfection and likely to have a very acute hepatitis and develop cirrhosis in 2-3y
Treat with prolonged course of IFN
Hep E features
Faeco-oral spread
Mainly seen in tropical areas
Causes GI symptoms e.g. cramps, pain.
High mortality rate, esp in pregnant.
Usually just acute but can cause chronic if untreated
What are the different types of diarrhoea?
Secretory
Inflammatory
Enteric fever
What is the mechanism of secretory diarrhoea
Toxin production affecting the lumen
No fever or a low grade fever
No white cells on stool sample
What is the mechanism for inflammatory diarrhoea
Invasion of bacteria into the lamina propria causing exudative into the lumen or intiaiing an innate immune response mainly through LPS acting on TLR4,5
Fever, WBCs in stool samples, neutrophils +/- blood
What are two common causes of secretory diarrhoea?
Cholera toxin
Superantigens from E COli
What bacteria can cause an inflammatory diarrhoea?
C jejuni
Shigella
Atypical salmonella species
What is the mechanism for enteric fever?
Invasion, Peyer’s patches, interstitial inflamamtion, monocytes, innate immune response
Fever, WBC in stool, can be blood
Causes of enteric fever?
Typphoidal, salmoneall subtypes, enteropathic Yersinia spp. Brucella spp.
What differentiates between inflammatory diarrhoea and enteric fever
Depends on immune status of patient
Both have bacteraemia
If immunocompetenet there is interstitial inflammation aned enteric fever
If they are immunocompromised there is exudative inflamamtion and exudative diarrhoea. This leads to neutrophilia and spetic shock
What are the anaerobic causes of Gi infection
Clostriida:
botulinum
perfringens
difficile
What differentiates between GBS and botulism?
Botulism is a descending paralysis
Treatment of botulism
Antitoxin
C botulinum infeciton
Canned/vacuum packed foods: honey, beans
(ingestion of preformed toxin which would usually be inactivated by cooking0
Blocks Ach from peripheral nerves leading to paralysis
Features of C perfringens
Reheated meats, superantigen enterotoxin leads to massive cytokine production by CD4 leading to systemic toxicitiy
Acts on small bowel
Watery diarrhoe and cramps lasting 24hrs
What bacteria causes gas gangrene?
C perfringens
Features of C difficile
2 endotoxins (A and B)
Causes pseudomembranous colitis
Caused by Abx use, usually cephalosporins and fluorguinoloines
Mx of C diff
PO metronidazole
2nd line Vanco
Which antibiotics are associated with C diff infection
Cephalosporins/fluoroquinolones
What are the aerobic bacteria causing GI infection?
Bacillus cereus
S. aureus
Featuers of B cereus GI infection
Reheated rice, spores gerimnate. Sudden vomiting
Superantigen
Watery, non bloody diarrhoea
Mx of B cereus infection
Self-limiting
Features of S. aureus GI infection
Prominent vomiting and watery non bloody diarrhoea
Main virulence fctor i protein A.
Catalase, coagulase +ve
Appears in tetrads
Clusters on gram stain
Beta haemolytic on blood agar
S aureus
Mx of S. auerus GI infection
Don’t treat, self limited
Lactose fermenting cause of GI infection?
Gram -ve enterobacteriacae (faculative anaerobes, oxidase negative)
E. COli
What are the strains of E Coli causing GI infection?
ETEC
EIEC
EHEC
HUS
EPEC
ETEC
Toxigenic E coli, travellers diarrhoea.
Food/water contaminated with human faecaes
Enterotoxins: Heat labile: stimulates adenyl cyclase and cAMP
Heat stable: stimulates guanylate cyclase
EIEC
Invasive dysentry
EHEC
Haemorrhagic E Coli: caused by verotoxin
HUS
E Coli 01571:H7 toxin
Anaemia, thrombocytopenia, renal failure
EPEC
Infantile diarrhoea
Mx of E Coli
Self-limiting but can treat with ciprofloxacin if needed
Non lactose fermenters causing GI infection
Salmonella
Shigella
Yersinia
O, H, Vi Ag’s
H2S produces
TSI agar
XLD agar
Selenite F broth
Salmonella
What are the three species of Salmonella
Typhi (and paratyphi)
Enteritidis
Cholearsuis
Features of Salmonella Enteritidis
Transmitted from poultry, eggs, meat
Invades small and large bowel
Bacteraemia is infrequent
Self-limiting
Blood
Mx of S. enteritides
Ceftriaxone or ciprofloxacin (if required)
Features of S. Typhi
Human trtansmission
Multiplies in Peyer’s patches
Bactaeremia, 3% become carriers (gallbladder)
Slow onset fever + constipation
Splenomegaly and rose spots
Aneamia and leukopaenia
Haemorrrhage and perforation
Slow onset fever + constipation
Splenomegaly and rose spots
Aneamia and leukopaenia
Haemorrrhage and perforation
S. Typhi

Rose spots
Enteric (Typhoid) fever
Non-lactose fermenters, non H2S producers, non-motile
Shigella
Mx of Salmonella typhi
Ceftriaxone or ciprofloxacin
Features of Shigella
Mainly affects the distal ileum and colon.
Infalmmation, fever, pain, bloody diarrhoea
Dysentry
Mx of shigella
Avoid Abx, ciprofloxacin if required
Non-lactose fermenting preferring cold temperatures cause of GI infection
Yersinia enteroclitis
Features of Yersinia enterocolitis infection
Enterocolitis, mesenteric adenitis with necrotising granulomas
Associated reactive arthritis and erythema nodosum
Reye’s syndrome
Transmitted via food contaminated with domestic animal excreta
What are the different species of Vibrios
Cholear
Parahaemolyticus
Vulnificus
Curved, comma shaped, late lactose fermenters, oxidase positive
Vibrios
Features of Vibrio cholera
Rice water stool, human faecas
Increased cAMP causes massive diarrhoea without inflammation
O1 group: epidemic
Mx of cholera
Supportive
Features of vibrio parahaemolyticus
Ingestion of raw or undercooked seafoood
Major cause of diarrhoea in Japan or in the carribean
Self-limiting
Features of Vibrio Vulnificus
Cellulitis in shellfish handlers
Fatal septicaemia with D+V in HIV
Mx of vulnificus and parahaemolyticus
Doxy
Features of C jejuni
Drinking unpasteurised milk, food, egg
Prodrome of headache and fever with abdominal cramps
Bloody (foul smelling diarrhoea)
Associated with GBS, reactive arthritis
Mx of C jejnuni
Erythromycin or cipro if first 4-5/7
Curved, S sjaped, microaeriphilic, oxidase positive, motile, sensitive to nalidixic acid
Campylobacter
V or L shaped, beta haemolytic
Aesculin positive with tumbling motility
L monocytogenes
Features of Listeria GI infection
GI watery diarrhoea, cramps, headache, fever, little vomiting
Perinatal infection, immunocompromised patients
Refrigerated foods: unpasteurised dairy, vegetables
Mx of Listeria
Ampicillin
Ceftraixone
Cotrimoxazole
What are the protozoa causing GI infection
Entamoeba histolytica
Giardia lamlia
Cryptosporidium parvum
Protozoa
MSM, food, water, soil
Entamoeba histolytica
Protozoa
Travellers, hikers, MSM, mental hospitals
Giardia
Motile trophozoite in diarrhoea
Non-motle cyst in non-diarrhoeal illness
4 nuclei
Entamoeba histolytica
Flask shaped ulcer on histology
Entamoeaba
Features of Entamoeba infection
Dysentry
Wind
Tenesmus
Chronic weigtht loss and RUQ pain due to liver abscess
Stool microscopy
Mx of entamoeba histolytica
Metronidazole and paramomycin (if luminal disease)
Pear shaped 2 trophozoite with 2 nuclei and trophozoites and cysts in stooll
Giardia
Foul smelling, non-bloody diarrhoea
Giardia
Mx of Giardia
Metronidazole
Features of cryptosporidium
Infects jejunym
Severe diarrhoea in immunocompromised
Oocysts seen in stool by modified Kinyoun acid-fast stain
Mx cryptosporidum
Paromomycin
Nitazoxanide
What are the viruses causeing secretory diarrohea
Rotavirus
Adenovirus
Norovirus
Poliovirus
Enteroviruses (coxsackie, ECHO)
Hepatitis A
Features of rotavirus infection
Secretory diarrhoea with no inflammation
Watery diarrhoea through stimulation of the enteric nervous system
Very common in children <6.
Which types of adenovirus cause non bloody diarrhoea?
Which age group are affected?
Types 40, 41
<2y/o
Gram +ve
Aerobic
Acid alcohol fast
Thick waxy cell wall
Mycobacteria
Mycolic actids
Mycobacteria
Cough +/- haemoptysis
Fever with night sweats
Weight loss
Malaise
Ethnicity
Mycobacteria
Post primary TB occurs in?
Young adults
Features of post-primary TB
?Re-activation/re-infection
Upper lobes- may progress rapidly to cavitation
Caseating granuloma
Miliary spread rare
Healing by fibrosis and calcification
1st line treatment for TB
RIPE
Rifampicin and isoiazid for 6/12
Pyrazinamide and ethambutol for 2/12
Treatment of TB meningitis
Increase isoniazid and rifampicin to 8-10/12
Treatment of latent TB
6/12 isoniazid
Side effects of Rifampicin
Drug interactions (raised transaminases, cytochrome p450 induction)
Orange secretions
Hepatotoxicity
Drug interactions (raised transaminases, cytochrome p450 induction)
Orange secretions
Hepatotoxicity
Rifampicin
Side effects of isoniazid
Peripheral neuropathy (give B6/pyridoxine
Hepatotoxcityi
Peripheral neuropathy (give B6/pyridoxine
Hepatotoxcityi
Isoniazid
Side effects of pyrazinamide
Hyperuricaemia
Hepatotoxicity
Hyperuricaemia
Hepatotoxicity
Pyrazinamide
Side effects of ethambutol
Optic neuritis
Visual disturbance
Optic neuritis
Visual disturbance
Ethambutol
Additional considerations in treating TB
DOTS
Vit D therapy
Why is Vit D therapy important in treatment of TB
Accelerates clinical recovery
Mono resistant TB=
Resistance to one drug only
Prophylaxis of TB
Isoniazid
MDRTB=
Resistance to rifampicin and isoniazid
XDRTB=
Resistance to rifampicin, isoniazid and injectables (kanmycin/amikacin)/ quinolones
Injectables used as 2nd line in TB
Capreomycin
Kanamycin
Amikacin
What are the second line TB treatments
Injectables
Quinolones
Cycloserine
Ethionamide
PAS
Linelozid
Clofazamine
Subacute presentation
Weight loss, fever, neck stiffness
Personality change
Reduced GCS
Focal neurological signs
TB meningitis
Dx if TB meningitis
CT- tubercolmata
LP- lymphocytic
Lymphadenitis
Pericarditis
Peritonitis/ileitis
Genito-urinary, renal testicular
Skin liver etc
(maybe +HIV positive)
Extrapulmonary TB
What is a Ghon focus
A Ghon focus is a primary lesion usually subpleural, often in the mid to lower zones, caused by mycobacterium bacilli (tuberculosis) developed in the lung of a nonimmune host (usually a child).

Ghon focus
Primary TB
Which patient group gets primary TB?
Nonimmunocompetent=
Elderly
Children
HIV
What is progressive primary TB?
Focus or node ulcerates into bronchus-> pneumonia
Cavity formation, bronchiectasis, consolidation, collapse
What is primary complex TB
TB taken by macrophase to LN, generalised lympho-haematogenous spread
Rich foci seen in?
Miliary TB

Miliary TB
Ix in TB
Imaging: CXR (upper lobe cavitation), CT
Culutre: Sputum x3, BAL, urine (EMU), Lowenstein Jensen medium (gold standard)
Sputum microscopy- ZN, auramine staingin: gram +ve, acid fast, aerobic intracellular rods
Tuberculin skin test
IGRA
NAAT
Liquid culture mediums
gram +ve, acid fast, aerobic intracellular rods
TB
Risk factors for contracting TB
Recent migrant
HIV+
Homeless
Drug user
Prison
Close contacts
Young adults/elderly
Risk factors for reactivation of latent TB?
Immunosuppression
Malnutrition
Ageing
Chronic alcohol excess
Fever, sweats, weight loss, back pain
?Spinal TB
Ix of spinal TB
MRI/CT +/- biopsy/aspirate
Treatment of spinal TB
12/12 anti-TB
Pathophysiology of spinal TB
Haematogenous spread
Initial discitis
Vertebral destruciton and collapse +/- anterior extension causing iliopsoas abscess
Potts Disease
Pott disease or Pott’s disease is a form of tuberculosis that occurs outside the lungs whereby disease is seen in the vertebrae. Tuberculosis can affect several tissues outside of the lungs including the spine, a kind of tuberculous arthritis of the intervertebral joints.

Potts Disease
What is the BCG vaccination?
Attenuated strain of M. Bovis
Efficacy of BCG
0-80%
Use of BCG
Bad for pulmonary TB
Good for leprosy, TB meningitis, disseminated TB
Inidications for BCG
Babies born in or with parents/grand parents from areas with incidence ?40/100000
Previously unvaccinated new immigrants from high prevalence countries for TB
HIV and TB
HIV-ve latent TB -> active TB 5-10% lifetime risk
HIV+ve, yearly risk is 5-10%
Hansen’s disease
Leprosy
What are the organisms causing Hansen’s disease
M. Leprae
M. Lepromatosis
Skin: depigmentation, macules, plaques, nodules, trophic ulcers
Nerves: thickened nerves, sensory neuropathy
Keratitis, iridocyclitis
Periostitis aseptic necrosis
Leprosy
Rx in leprosy
Rifampicin, dapsone, clofazimine (if multibacillary)
What is the immunological spectrum of leprosy
Tuberculoid
BT
Borderline
Lepromatous
Tuberculoid leprosy
Paucibacillary
TH1 mediated
Depigmented lesions
BT leprosy
Nerve damageq
BB leprosy
Multiple plaques
Lepromatous leprosy
Multibacillary
Th2 mediated
Neuropathic ulcers
What are the indicators that an infection is being caused by NT Mycobacteria?
Environmental
No person-person transmission
Associated with impaired immunity, poor response to standard anti-TB regime
What is MAIC?
M. avium intracellulare complex
Presentation of MAC in children
Pharyngeal/cervical addenitis
Pulmonary MAC
Underlying lung disease, resembles TB
Disseminated MAC seen in?
Cytotoxics, lymphoma
Features of MAC infection in AIDS?
Disseminated multibacillary infection
Mycobacteraemia
Consider in HIV patients with longstanding diarrhoea
What is fish tank granuloma caused by?
M. Marinarum
Single or clusters of papules/plaques in swimming pool/aquarium owners?
M. Marinarum
What causes Buruli ulcer
M. Ulcerans
Transmission of M. uclerans
By insects, tropics/australia
Treatment of M. Ulcerans
Rifampicin
Streptomycin
Sx
Painless early nodule
Slowly progressive leading to ulceration, scarring and contractures
Seldom fatal but with hideous deformity
Buruli ulcer

Buruli Ulcer
M. Ulcerans
Def: pneumonia
Inflammation of lung alveoli
Can be lobar or bronchopneumonia
Def: bronchitis
Inflammation of medium sized airways, mainly in smokers.
Cough with sputum most days for 3m or 2 or more consecutive years
Organisms in bronchitis
Viruses
S. pneumoniae
H. influenzae
M. catarrhalis
CXR in bronchitis
Often normal
Rx in bronchitis
Bronchodilation, PT +/- Abx
CURB 65
Confusion of new onset (defined as an AMTS of 8 or less)
Blood Urea nitrogen greater than 7 mmol/l (19 mg/dL)
Respiratory rate of 30 breaths per minute or greater
Blood pressure less than 90 mmHg systolic or diastolic blood pressure 60 mmHg or less
Age 65 or older
CURB 0-1
Treat as an outpatient
CURB 2
Consider hospital
CURB 3-5
Hospitalise
?ITU
What are te classical causes of pneumonia
S. Pneumoniae
H. influenzae
M. catarrhalis
S. aureus
K. pneumonia
Pneumonia with:
Rust coloured sputum
Lobar on CXR
S. pneumonia
Pneumonia with:
Smoking/COPD
H. influenza
Pneumonia with:
Smoking
M. catarrhalis
Pneumonia with:
Recent viral infection (post-influenza) and cavitaiton on CXR
Staph aureus
Pneumonia with:
Alcoholic
Elderly
Haemoptysis
Klebsiella
Pneumonia with:
+ve diplococci
Strep pneumoniae
Pneumonia with:
-ve cocci-bacilli
H. infleunza
Pneumonia with:
-ve cocci
M. catarrhalis
Pneumonia with:
+ve cocci in grape bunch clusters
S. aureus
Pneumonia with:
-ve rod, enterobacter
Klebsiella
Atypical pneumonia clinically
No signs or chest XR or signs not in keeping with CXR
May be extrapulmonary signs e.g. hepatitis, hyponatraemia
Causes of atypical pneumonia
Legionella
Mycoplasma
Chalmydia pneumonia
Chlamydia psittaci
Other causes of pneumonia
Bordatella pertussis
TB
Pneumonia with:
Travel, air conditioning, water towers
HEPATITIS
HYPONATRAEMIA
Legionella
Pneumonia with:
Systmic symptoms
Joint pain
Cold agglutination test
Erythema multifrome
RIsk of SJS, AIHA
Mycoplasma
Pneumonia with:
TWAR agent
Chlamydia pneumonia
Pneumonia with:
Birds in hx
Chlamydia psittaci
Pneumonia with:
Whooping cough in unvaccinated
Bordatella pertussis
Pneumonia with:
Poor response to Abx
TB
Causes of pneumonia in patient with:
HIV
PCP
TB
Cryptococcans
Causes of pneumonia in patient with:
Neutropenia
Fungi- aspergillus
Causes of pneumonia in patient with:
BMT
Aspergillus
CMV
Causes of pneumonia in patient with:
Spleenctomy
Encapsulated organisms: H. influenzae, S. pneumonia, N. meningitides
Causes of pneumonia in patient with:
CF
Pseudomonas aeruginosa
Burkholderia cepacia (v. high mortality)

Lobar pneumonia
Strep
Cavitating pneumonia
Staph aureus


Ix in pneumonia
Non microbiological: FBC, U&E, CRP, ABG, CXR
Microbiology: sputum MC+S, blood cultures, effusion aspiration/BAL
Test in severe CAP for S. pneumoniae and Legionella?
Urine antigen tests
What is the use of antibody tests in pneumonia
Paired serum samples at presentation and 10-14/7
Rise in Ab level over time
Useful for difficult to culture (chalmydia, legionella)
Silver stain, boat shaped oragnisms
PCP
Def: HAP
>48 hours into hospital stay without previous infection
What is BAL used for?
To differentiate URT and LRT microbes
CAP
Classical
Mild-moderate
Amoxicillin or macrolide 5-7d
CAP
Classical
Moderate-Severe
Clarithromycin + co-amoxiclav/cefuroxime (2-3w)
CAP
Atypical
(Chlamydia, Mycoplasma)
Macrolide/tetracycline
Clarithromycin
What is consideration re durg interaction of clarithromycin
Increases anticoagulant effect of Warfarin
HAP 1st line
Ciprofloxacin +/- vancomycin
HAP second line/ITU
Piptazobactam + vancomycin
Abx in aspiration pneumonia
Cefuroxime
Metronidazole
Legionella abx
Macrolide + rifampicin
Staph aureus Abx
Fluclox
Pseudomonas Abx
Piperacillin + tazobactam (tazocin) or ciprofloxacin +/- gentamicin
Causative organism in HAP
Coliforms and pseudomonas more likely the longer the stay
Coliform bacteria
Escheria
Klebsiella
Citrobacter
Enterobacter
Causes of ventilator associated pneumonia
P. aeruginosa, acinetobacter, stenotrophomonas maltophilia
Alcoholic, acute SOB, fever, dirty brown sputum, pleuritic
chest pain, malaise, N&V
o Examiniation: tachypnoea, tachycardia, dullness to
percussion, crackles
Pneumococcal pneumonia
Army cadet, 2 week hx, headache, malaise, non-productive cough, examination unremarkable,
normal inflammatory markers
Mycoplasma pneumoniae
Confusion, fever, headache, myalgia, abdominal pain and diarrhoea.
o Low sodium and deranged LFTs
Legionella
MOA aciclovir
Guanosine analogue, blocks viral DNA extension through activation by thymidine kinase present in HSV
NB CMV doesn’t have this enzyme
Indication aciclovir
HSV
Indication ganciclovir
CMB, EBV, HHV-6
MOA ganciclovir
Nucleoside analgoue
SE of ganciclovir
BM suppression
RCHEP
CMV conseuqnecs
Retinitis
Colitis
Hepatitis
Encephalitis
Pneumonitis
Owl eye inclusions=
CMV infected cells

CMV infection
Owl eye inclusions
What is used as an alternative to ganciclovir if resistant/severe side effects
Foscarnet
MOA foscarnet
pyrophosphate analgoue. Inhiits nucleic acid synthesis without requring activation
Foscarnet indication
Used when CMV resistant to ganciclovir
Also used as prophylaxis post organ transplant
MOA Cidofovir
Nuceloside phosphonate
Indications Cidofovir
CMV retinitis
Often used in treatment of non-herpes viral infections in opportunistive post-transplant setting e.g. BK virus for BK nephropathy/BK cystitis/adenovirus/PML (JC virus)
What is a consideration re Foscarnet and cidofovir
Nephrotoxic
Maintain hydration and co=administer probenecid
HSV infection
Act Very Fast
Acyclovir
Valaciclovir
Famciclovir
Foscarnet/cidofovir in herpes infection
If it s resistant
When to treat VZV?
Immunocompromised
Pregnants
Adults with pneumonitis
Treatment of CMV in BMT
Pre-emptive therapy: monitor CMV viral load during high rrisk period
Acute therapy: reduce immunosuppression
1st line: ganciclovir (BM toxicity)
2nd line: foscarnet (+GCV) (nephrotoxic)
3rd line: cidofovir (nephrotoxic)
What determines when to treat HBV
Serum HBV DNA levels (>2000IU)
Serum transaminitis (above normal limit)
Liver biopsy histological grade and stage: moderate-severe active necroinflammation and or fibrosis
Treatment goals in HBV Rx?
Prevent progression to cirrhosis and HCC
Maintain serum HBV DNA as low as possible
Attain histological improvement
ALT normalisation
Loss of HBVeAg and seroconversion to HBVeAb
What are the drugs used in HBV Rx?
Pegylated INF alpha 2a
Nucelos(t)ide analogues
What is the MOA of INFa2a
Direct antiviral effect and upregulates expression of MHC on cell surfaces
(HBV) MOA:
Lamivudine
Inhibitor of viral polymerase
(HBV) MOA:
Adefovir dipivoxil
Inhibitor of viral polymerase
(HBV) MOA:
Entecavir
Inhibitor of viral polymerase (no resistance)
(HBV) MOA:
Telbivudine
Inhibitor of viral polymerase
(HBV) MOA:
Tenofovir
Inhibitor of reverse transcriptase
What is the preferred first line treatment in HBV infection?
Entecavir
PegINF a2a
Tenofovir
What is the treatment goal in HCV?
Sustained virologic response: persistent absence of HCV RNA in serum >6/12 after completing antiviral treatment
Prevent progression to cirrhosis, HCC or decompensated liver disease requiring treatment
MOA Ribavirin
RNA nucleoside analgoue
Major SE of ribavirin
Haemolytic anaemia
Treatment of HCV
PegINF a2a
Ribavirin
Which HCV genotypes have a worse treatment prognosis?
1,4,5,6
Which HCV genotypes have a better treatment outcome
2 and 3
What is the MOA and indication of:
Zanamivir (INH)
IFVA
NA inhibitor
What is the MOA and indication of:
Oseltamavir
IFVA
NA inhibitor
M” cWhat is the MOA and indication of:
Amantidine
M2 Channel
IFVA
What is the MOA and indication of:
Ribavirin
RSV/ parainfluenza
Guanosine analgoue
Live atttenuated vaccines=
MMR
Yellow fever
BCG
OPV
Varicella
Typhoid
Flu
Inactivated vaccines=
Rabies, pertussis, IPV, Hep A, typhoid
Recombinant protein vaccine=
HBV
Subunit vaccines=
Hib
Men C
PCV
Toxoid vaccines=
Tetanus
Diptheria
What causes SSPE?
Subacute sclerosing pancencephalitis
Measles
Special risk groups for vaccines
Pts on CTx, pts <6/12 after BMT, children on high dose steroids +/- cytotoxics
Can HIV patients be given MMR?
Yes if susceptible
What does DTP cause (side effect)
Anaphylaxis
Protracted crying
What does OPV/IPV vaccine cause (side effect)
Poliomyelitis (OPV)
What does measles vaccine cause (side effect)
Thrombocytopenia
What does rubella vaccine cause (side effect)
Acute arthritis
Should HIV patients be given BCG and yellow fever vaccines?
No
Sx: SOB, green sputum, fever. Hypoxic, heavy smoker.
o X ray: shadowing, ground glass changes and hypoxia exacerbated by exercise.
o Immunosuppression – HIV
PCP
Widespread lung fibrosis with ground glass shadowing on histology with a cough
PCP
India ink with halo=
Encapsulated yeast i.e. cryptococcus
Mx of CPC
Co-trimoxazole and oral prednisolone
2nd line= clindamycin and primiquine. IV methylprednisolone
Aerobic gram positive rod with branches
Seen in relatively immunocompromised patients, produces copious amounts of pus in abscess
Commo in alcohlics
Associated with lung abscess or pelvic asbscess
Slow growing and hard to treat
Actinomyces
How does rifampicin help in septic arthritis?
Affects biofilm formation
What are the STIs causing discharge?
Gonorrhoea
Chlamydia
Trichomonas
Candida
BV
What are the STIs causing ulceration?
Syphillis
HSV
LGV
Chancroid
Donovanosis
What are the STIs causing rashes/lumps/growths
Genital warts- HPV
Molluscum contagiosum
Scabies
Pubic lice
Painful genital ulcers=
Herpes
Chancroid
Painless genital ulcers=
Syphillis
Lymphogranuloma venereum
Granuloma inguinale
Obligate intracellular Gram -ve diploccocus causing STI
N. gonorrhoea
Opthalmia neonatorum=
Conjunctivitis that develops if gonorrhoea left untreated when child transfers to birth canal
What happens in N. gonorrhoea infection in patients with complement deficiencies?
Get disseminated gonococcal infection- septicaemia, rash and or arthritis
Dx of Gonorrhoea
Urethral/rectal smears
Culture from these is gold standard
Treatment of gonorrhoea
Ceftriazone IM-250mg one dose
or cefixime PO 400mg single dose
Treatment of resistant gonorrhoea?
Spectinomycin IM 2g single dose
What is the most most common STI in Europe
Non-gonoccocal urethritis
Features of NGU
Mucoid/mucopurulent discharge
What is PGU
Post gonococcal urethritis
Follows gonorrhoea Rx
Can be prevented by concomittant Rx with tetraceline
Rectal prostatitis in gonorrhoeal infection seen in
MSM
Complicated gonorrhoea infectio in men=
Prostatitis
Common manifestation of gonorrhoeal infection in women=
Mucopurulent cervicitis
Erythema and oedema
Urethra from vaginal leakage
What is the most common cause of increased infertility in Europe?
PID
Gram negative obligate intracellular pathogen involved in STIs that cannot be cultured on agar?
Chlamydia trachomatis
Symptoms of C. trachomatis infection
Often assymptomatic (50% men, 80% women)
What is the growth cycle of C. trachomatis?
Exists ion 2 forms
Elementary bodies: stable, extracellular
Reticulate particles: intracellular, metabolically active
What are the A,B.C chlamydia serovars associated with?
Trachoma which can cause blindness
What are the D-K Chlamydia serovars associated with?
Genital chlamydia, opthalmia neonatorum
What are the Cx of chlamydia infection?
PID
Tubal factor infertility
Increased risk of ectopics
Increased risk of endometriosis
Chronic pelvic pain
Epididymitis
Reiters
Adult conjunctivitis
Opthalmia neonatorum
Dx of chlamyydia
NAAT= gold standard
Rx of chlamydia
Azithromycin 1g (4 capsules) STAT
Doxycycline 100mg BD 7/7
Erythromycine 500mg QDS 7/7 or 500mg BD 2/52
SE of doxycycline
N+V
Photosensitivity
C/I in pregnancy
SE of erythromycin
GI upset
What is LGV
Lympho-granuloma venereum
Lymphatic infection with chlamydia trachomatis serovars L1, L2, L3
What is associated with chlamydia infection with serovars L1, 2 and 3
Lymphogranuloma venereum

LGV
What are the stages of LGV?
Early LGV Primary
Early LGV Secondary
Late LGV
Current LGV outbreak
What are the features of primary early LGV
3-12/7
Genital ulcer, painless, non-indurated, balantitis, proctitis, cervicitis
Features of secondary early LGV
2-25/52
Inguinal buboes: painful, 2/3rd unilateral
May rupture
Fever, malaise
Rarely (hepatitis, meningo-encephalitis, pneumonitis)
Proctocolitis
Hyperplasia of lymphoid tissue
Features of late LGV
Inguinal lymphadenopathy
Abscess formation
Genital elephantiasis
Genital ulcers
Frozen pelvis
Rectal strictures
Peri-rectal abscesses + fistulae
Lymphorroids
Features of current LGV outbreak
Rectal symptoms- pain, tenesmus, bleeding, mucus discharge
O/E: proctitis
Dx of LGV
NAAT (currently unlicensed)
If positive will be sent to HPA
Confirmation of C trachomatis by RT-PCR on 2 platforms
And identification of L1-3 serovars
Rx LGV
Doxycycline 100mg BD for 21/7
Erythromycin 500mg QDS for 21/7
Azithromycin 3/52 1g weekly
Obligate gram-negatve spriocahete causing STI=
Treponema pallidum (Syphillis)
Epidemiology of syphillis
Majority of cases are in those who are HIV +ve
Patients often co-infected with HCV or another STI
Detection of treponemas
Seen in primary lesions by dark-ground micrscopy
Can be detected with RT-PCR
What are the diagnostic methods for syphillis
- Non-treponemal tests:
Detect nonspecific antigens
VDRL: detects lipoidal antiboddy (can get biological false +ves)
RPR is modified VDRL test, positive is indicative of treponemal infection.
Used in primary syphillis.
Can be used to monitor treatment response.
- Treponemal tests:
Detect Ab against specific Ags from T .pallidum
e.g. EIA, FTA, TPHA, TP-PA
More specfic than non-treponemal test but remains positive after infection treated
What are the phases of syphillis infection
Primary
Secondary
Latent
Tertiary
What are the features of primary syphillis
Macule-> papule-> induracted painless genital ulcer appearing 1-12w following transmission.
Often solitary
May persist for 4-6w= CHANCRE
Clean base with serous exudate
Regional LNadeopathy

Chancre
Syphillis
What are the features of secondary syphillis
Systemic bacteraemia with low grade fever, mailaise
Symmetrical, non-pruritic, maculopapular rash on back, trunk, arms, legs, soles face 1-6/12 following infection
Mucosal lesions, uveitis, choroidoretinitis, elopecia
Snail track oral uclers
Condyloma cuminate
Neurological involvements (aseptic meningitis, cranial nerve palsies, optic neuritis, acute nerve deafness)
What are features of latent syphillis infection
No clinical
Serological infection
What are the features of tertiary syphillis
Gumma (granuloma)- rare. Skin, bonem mucosa, scanty spirochaetes
CV: uncomplicated and complicated aortitis +++ spirochaetes, +++ inflammation
Neurosyphillis: seen in HIV patients. General paresis of the insane, tabes dorsalis, gumma, spirochaetes in CSF, small vessel vasculitis
Argyll Robertson pupil
Argyll Robertson pupil
Prostitute’s pupil
Accomodates but doesn’t react
Syphillis
Rx in Syphillis
Single dose IM benpen (doxy if pen allergic)
Monitor RPR, need to see a 4x reduction to consider tx succesful
What is the Jarisch-Heimer reaction
Fever, headache, myalgia, sometimes and exacerbation of syphillitic symptoms commonly developing within hours of abx administration
Features of congenital syphillis
May occur during pregnancy or birth
Often develops features over the first couple of years including hepatosplenomegaly, rash, fever, neurosyphillis and pneumonitis
Gram negative coccobacillus causing STI
Chanrcoid
Causative organism in Chacnroid
Haemophilus ducreyi
Features of chancroid
Tropical ulcer disease mainly seen in africa
Often multiple ulcers, frequently painful
Chocolate agar
STI
Chancroid
Dx of chancroid
Culture on chocolate agar
PCR

Chancroid
Haemophilus ducreyi
Gram negative bacillus, klebsiella cuasing STI
Donvoanosis: Ganuloma inguinale
Causative organism donovanosis
Klebsiella granulomatis
Features of donovanosis
Africa, India, PNG, Autralian
Large, expanding ulcers starting as a papule or nodule that breaks down with a beefy red appearnce

Donovanosis
Dx of donovanosis
Giemsa stain of biopsy or tissue crush showing Donovan bodies
Rx in donvoanosis
Azithromycin
Enteric pathogens causing STI
(oro-anal contact)
Shigella
Salmonella
Giardia
Occasionally others e.g. Strongyloides
Flagellated protozoan causing STI
Trichomonas
Dx of Trichomonas vaginalis
Wet prep micrscopy, PCR
Symptoms of T. vaginalis infection
Asymptomatic/ urethritis in men
Discharge in women
TV and HIV
Associated with increased risk of HIV acquisition
Rx trichomoniasis
Metronidazole
Features of BV
Abnormal vaginal flora, polymicrobial, discharge, odour
Sexually associated but not transmitted
May be associated with hygiene practices
Dx of BV
Microscopy of gram stain
raised pH
Whiff test
Clue cells
frothy, often unpleasant-smelling discharge
blood spotting in the discharge
itching in and around the vagina
swelling in the groin
the urge to urinate frequently —
- See more at: https://www.plannedparenthood.org/learn/stds-hiv-safer-sex/trichomoniasis#sthash.TuBPPa9G.dpuf
Trichomoniasis
Implications of BV
Associated with preterm delivery
Features of candidasis
Usually candida albicans
If symptomatic: white thick discharge, itching, soreness, redness
Common presentation in women as vulvovaginitis, men as balanitis
Not an STI
Rx candidal genital infection
Clotrimazole or fluconazole (i.e. oral antifungals)
Cause of molluscum contagiousm
Features
Pox virus
Caused by skin to skin contact
In adults causes genital lesions and is spread via sexual contact
Facial molluscum in adult=
HIV until proven otherwise
There are giant lesions in the immunocompromised
Treatment of molluscum contagiosum
If required= destructive cryotherapy
Cause of genital warts?
Human papillmoavirus
Causes of visible genital warts=
HPV6 or 11 (not associated with increased risk of cervical dysplasia)
Incubation time for warts?
3w->8m
Dx of genital warts
Exmaintion: papular, planar, pedunculated, carpet, keratinised, pigmented
Home treatment of genital warts
Podophyllotoxin solution or cream
Can’t be used in pregnant women
Treatment of genital warts in clinic
1st line: cryotherapy
2nd line: Imiquimod
Viral STIs
HAV, HBV, HCV (mainly HIV +ve MSM)
Herpes
HIV
Def: HAI
Infeciton acquired >48h after admission
What is the common HAI of the GIT
C. diff
Transmission of C diff
Spore ingestion
3Cs in C. diff infection
Clindamycin
Cephalosporins
Cprofloxacin
Common HAI UTI
E Coli
Resistance in E COli
ESBeta lactamases
What are the HAIs associated with bacteraemia?
MRSA
Coag negative staph
E Coli
Most prevalent coag negative staph
Staph epidermis
Organisms commonly causing surgical site infection
MRSA
Coag negative Staph
Organisms causing environmental hygiene outbreaks in hospitals
C diff
Norovirus
Acinetobacter
Environmental source:
Cooling towers
Legionella
Environmental source:
Building works
Aspergillus
What infections require negative pressure isolation?
TB, chicken pox, RSV
What is the most common HAI?
UTI> surgical site infection> HA pneumonias
How can HAIs be characterised?
By organism or by syndrome
What are the HAI syndromes
Catheter associated blood stream infection
Urinary catheter associated UTI
Surgical site infeciton
Ventilator associated penumonia
Antibiotic associated diarrhoea
Degree of resistance accumulation in gram negatives
Enterobacter> Klebseilla> E. Coli
ESBLs
Features of superficial incisional SSI
Skin and subcutaenous tissue, red hot and tender
Deep incisional SSI
Down to deep soft tissue, fascia, muscle
Wound may reopen
Organ/space SSI
Organ/space
Reoperation and drainage
Gram positive spore forming anaerobe
C. diff
C diff virulence factors
Toxin A and B: diarrhoea, colitis
Tonxiotype: III/BI/NAP1/027: proinflammatory, cytotoxic, enterotoxic
Pathogenesis of C diff infectoin
Mild colitis-> severe colitis-> pseudomembranous colitis and perforation
Features of severe C Diff infection
Physiologically unstable: PR/ BP/ T/ RR
High WCC >15
Rising or high creatinine > 20
Clinical- peritonism, ileus, obstruction
Radiological: colitis.
Others: age, albumin etc.
Abx vs:
G+ve, narrow
Fluclox
Abx vs:
Gram +ve, community
G-ve anaerobes
Broad
Co-amoxiclav
Abx vs:
Anaerobes
Narrow
Metronidazole
Abx vs:
Hosp G-vem some, G+Ve
Pseudomonas
Broad and antipseudomonal
Tazocin (piperacillin-tazobactam)
Abx vs:
Gram +ve, G-ve, anaerobes (<co-amox>
</co-amox>
Amoxicillin
Abx vs:
Mainly G-ve
Pseudomonal
Broad
Ciprofloxacin
Abx vs:
G-ve
Narrow
Gentamicin
Abx vs:
Hosp G-ve
G+ve
Aeroe
Pseudomonas
Broad
Meropenem
Features of parvovirus B19 infection
Resp/blood-borne infection 6-8d incubation
Fever, malaise, erythema infectiosum, transient aplastic crisis (especially those with sickel cell, spherocytosis)
Implications of parvovirus infection for foetus
Infection <20w assocaited with 30% risk of hydrops foetalis
>20w= no risk
Flu-like symptoms followed by pinpoint-macular papular rash and lymphadenopathy in adults
Diagnosed via serology of saliva swabs
Rubella
Transmission of Rubella
Respiratory
Rubella infection before 10/40
90% develop congeital rubella syndrome
Rubella infection 13-18w
Hearing defects, retinopathy
Rubella infection >20w
No documented rsik
Features of CRS
Cataracts, congenital glaucoma
Deafness
Congeital heart defects
Purpura
Splenogemgaly
mIcroencephaly
Mental retardation
Meningoencephalitis
Implications of influenza infection in pregnancy?
Risk of stillbirth x5
Preterm delivery x3
No congenital malformations
Recommendations for IFV in pregnant women
Vaccination and treatment of pregnant women with antivirals (oseltamivir, zanamivir)
Measles in pregnancy
Can cause IUD/miscarraige, preterm devliery and increased maternal morbidity
Cxs of measles infection
Opportunistic bacterial infections: otitis media, pneumonia, bronchitis
Encepahlits and subacute sclerosing pancencephalitis
Implications of coxsackie infection during pregnancy
Associated with early onset neonatal hepatitis, congenital myocarditis, early onset childhood IDM and abortion of intrauterine death
Gram positive cocci in clusters
Staph
Gram positive cocci in clusters
Coagulase +ve
Staph auerus
Gram positive cocci in clusters
Coagulase negative
Staph epidermis
Gram positive cocci:
Diplocci
Strep
Gram positive cocci in chains
Enterococcus
Gram positive Rods
ABCDL
Actinomyces
Bacillus
Clostridium
Diptheria
Listeria
With what are actinomyces assocaited?
Dental/oral infections
Clostridium=
Difficile, perfringens, botulinum, tetani
Gram positive rods, obligate anaerobes?
Actinomyces
Clostridium
Bacteroides (gram -ve)
Treatment of obligate anaerobes
Metrondiazole, cephamycins
Aminoglycosides vs obligate anaerobes found in GIT
Useless
Gram negative cocci
Neisseria: meningtidis, gonorrhoea
Moraxella catarrhalis
Gram negative rods
E. Coli
Salmonella
Shigella
Klebseilla
Yersinia
Enterobacteriaceae
Gram negative coccobacilli
H. infleunza/ducreyi
Bordatella pertussis
Pseudomonas aeruginosa
Chlamydia trachmoatis
Gram negative spirochaetes
Trep pallidum
Leptospoirosis
Borrelia e.g. Lyme disease
What are the boligate intracellular bacteria
Chalmydia trachomatis
Rickettsia
Coxiella (Q fever)
M leprae
What are the obligate intracellular protozoa?
Toxoplasma
Cryptosporidium
Leishmania spp
PCP intracellular or extracellular microbe?
Obligate intracellular
Congenital infections TORCH
Toxoplasmosis
Other (HIV/HBV)
Rubella
CMV
HSV
Infections screened for in the UK in pregnant women
Rubella
Syphillis
HBV
HIV
Thrombocytopenia
Eyes/ears affected
Cataracts
Choroidoretinitis
Rash
Cerebral abnromality
Hepatosplenomegaly
Classical symptoms of congenital infection
Classical symptoms of congenital infection
TORCH
Thrombocytopenia
Optic, otitic
Rash
Cerebral abnromality
Hepatosplenomegaly
Toxoplasmosis as a congenital infection
60% asymptoamtic at birth but go on to develop LT sequelae: deafness, low IQ, microencephaly
40%: symptomatic at birth: choroidoretinitis, microcephaly, hydrocephalus, intracranial calcificaiton, seizures, jaundice, hepatosplenomeagaly
Why is there a higher incidence in preterm infants
Less maternal Ig
NICU care
Exposure to organisms
Early onset sepsis=
<48h after birth
Causes of early onset sepsis
GBS!!
E. Coli
Listeria
Fever, unwell in neonate <48h
Early onset sepsis
Associations of early onset sepsis
Maternal:
PROM
Fever
Foetal distress
Foetal:
Respiratory distress
Acidosis
Asphyxia
Dx of neonatal sepsis
Septic screen: FBC, CRP, blood cultuie, deep ear swab, CSF, surface swab, CXR
Mx of early onset sepsis
Supprtoive: admission to NICE, ventiulation, circulation, nutrition (TPN)
Benpen and gentamicin (E Coli cover)
Listeria: ampicillin or amoxicillin
Rx for Listeria causing neonatal sepsis
Ampicillin or amoxicillin
Late onset sepsis=
>48h
Causes of late onset sepsis
Coag negative staph
GBS
E COli
Listeria
S. aureus
Enterococci
Gram negatives kleb, enterobacter, pseudomonas
Candida
Clinical presentation of late onset sepsis
Bradycardia
Apnoea
Poor feeding
Irritability
Billious aspirate
Convulsions
Jaundice
Respiratory distress
Ix in late onset sepsis
Septic screen and urine
1st line Abx in late onset sepsi
Fluclox and gentamicin
2nd line abx in late onset sepsis
Tazocin and vancomycin: consider ability to cross BBB if meningitis
2nd line Abx in community acquired late onset sepsis
Cefotazime and amoxicllin +/- getamicin
Causes of bacterial meningitis in children
Neisseria
meningitides
Strep pneumoniae
Hib
Sensitive to optochin
Grown on blood agar
Strep pneumoniae
Causes of meningitis <3/12
N meningitides
S pneumonia
(Hib)
GBS
E Coli
Listeria
Causes of meningitis 3/12- 5y
N meningitidis
S pneumonia
Hib if unvaccinated
Causes of meningitis >6y
N meningitis
S pneumoniae
Organisms causing respiratory infection in children?
Viruses
S pneumoniae
atypica Myocplasma if >4y
Bordatella
MTB
Def UTI
Culture >10^5cfu/ml
Pyuria
Clincal symptoms
Broad spectrum Abx
Co-amoxiclav
Tazoin
Ciprofloxacin
Meropenem
Narrow spectrum Abx
Fluclox
Metronidazole
Gentamicin
BEAT Drug action
Bypass antibiotic sensitive step
Enzyme-mediated drug inactivation
Impairment of drug accumulation
Modification of drug target
Genetics involved in prion disease
Codon 129 polymorphism: MM massively increases the susceptiblity
Specific PRNP mutation
Symptomatic treatment of prion disease
Clonazepam
Myoclonas (valproate, levetiracetam, priacetam
What Rx may be used to delay prion conversion
Quinacrine
Pentosan
Tetracycline
EEG in:
sCJD
Serial EEG shows periodic triphasic changes
EEG in:
vCJD
Non-specifc slow waves
EEG in:
Inherited prion disease
Non-specific changes
MRI in:
sCJD
Normal/highlighting basal ganglia
MRI in:
vCJD
Posterior thalamus highlighted on MRI- T2: pulvinar sign
Pulvinar sign
The pulvinar sign refers to bilateral FLAIR hyperintensities involving the pulvinar thalamic nuclei. It is classically described in variant Creutzfeldt-Jakob disease (vCJD). It is also described in other neurological conditions:
Fabry disease (although the hyperintense signal is seen on T1WI)
bilateral thalamic infarcts
acute disseminated encephalomyelitis
MRI in
Inherited prion disease
Sometimes high signal in BG
CSF analysis in:
sCJD
14-3-3 +ve
CSF analysis in:
vCJD
14-3-3 can be normal
PNRP analysis in:
sCJD
No mutations
PNRP analysis in:
vCJD
No mutations
PNRP analysis in:
iatrogenic CJD
No mutations
PNRP analysis in:
Inherited prion disease
Mutations present and diagnostic
Codon 129 in:
sCJD
Most are MM
Codon 129 in:
vCJD
All MM
Codon 129 in:
iatrogenic CJD
Most homozygous MM and VV
Codon 129 in:
Inherited prion disease
129 codon homozygosity may confer earlier onset
Western blot PrPsc in:
sCJD
Types 1-3
Western blot PrPsc in:
vCJD
Type 4t from tonsillar biopsy (100% sensitive and specific)
Western blot PrPsc in:
Iatrgoneic CJD
Types 1-3
Spongiform vacuolation
PrP amyloid plaques
sCJD
PrPsc 4t detectable in CNS
and lymphoreticular tissue
Florid plaques
vCJD
What is the most common form of prion disease?
sCJD
Aetiology of sCJD
Either somatic PRNP mutation or spontaenous conversion of PRPc to PrPSc
45-75 y/o
Rapid, progressive dementia with myoclonus, cortical blindness, akinetic mutism and LMN signs
sCJD
30y/o
Psychiatric symptoms (anxiety, paranoia, hallucinations)
Followd by development of neurological symptoms (peripheral sensory symptoms, ataxia, myoclonus)
Later symptoms include chorea, ataxia, dementia
vCJD
Causes of acquired CJD
vCJD
Iatrogenic
Kuru
Progressive ataxia initially
Dementia and myoclonus at later stages
Speed of progression depends on route of innoculation
iCJD
Progressive cerebellar syndorme following 45y incubation
Dementia late or absent
Kuru
Causes of inherited CJD
fCJD
GSS
FFI
Various atypical dementias
Insomnia and paranoia progressing to hallucinations and weight loss
Mute period
Death 1-18/12 after start of symptoms
FFI
Inheritance of FFI
AD
Develps between 2-60y
Dysarthria progressing to cerebellar ataxia, ending in dementia
Gesrtmann-Straussler-Scheinker syndrome
Inheritance of GSS
AD
Tonsillar bx in sCJD
Not useful
What to exclude following triphasic EEG in ?CJD
Exclude nonspecific e.g. hepatic encepahlopathy
Lithium toxicity
NB only 2/3rds will have abnormal EEG
Dx of sCJD
14-3-3
Most common pathogen causing surgical site infection
Staph aureus
Pathogens causing surgical site infection
Staph aureus
E Coli
Pseudomonas
Haemolytic strep
Rx in surgical site infection
Fluclox
What are the patient related factors contributing to surgical site infection
DM
Peri-operative hyperglycaemia
Current smoker
Remote infection at time of sx
Obesity
Malnutrition
Low preoperative albumin
Concurrent steroid use
Clean wound=
Sterile site e.g. THR
Common pathogen in clean wounds
S aureus
Clean-contaminated wound=
Post-appendectomy
Contaminated wounds
Perforated bowel
Dirty infected wounds=
Open #
Risk factors for septic arthritis
Abnormal joint (RA/OA/gout/prosthesis)
Immunosuppressed (CLD, steroids)
Bacteraemia (e.g. DM, IVDU)
Trauma/penetrating injury
Causes of septic arthriits
Staph aureus most common
Streptococci 22%
Gram -ve less commonly e.g. E. Coli
Unwell febrile patient with red hot swolllen joint
Unable to weight bear
50% knee
Septic arthritis
Dx of septic arthritis
Blood culturebefore Abx
Joint aspirate (>50,000 cells/ml)
Inflammatory markers
Imaging shows effusion
Mx septic arthritis
IV antibiotics (cephalosporin or fluclox)
MRSA: Vancomycin
Drain joint
Lack of IL-10=
Increased severity of staph infection
Lack of macrophage derived cytokines reduces host protection in
Staph aureus sepsis
Organisms causing septic arthritis
Staph
Strep
Gram negative
Rarely
Staph aureus
Staph epidermis (4%)
Strep pyogenes
Strep pneumonias
Strep agalactiae
E Coli
Hib
Neisseira gonorrhoea
Salmonella
Brucellosis
MTB
Fungi
Brodie abscess
Subacute osteomyleitis which may pesrist for years before converting to frank OM
Pain, fever, local swelling of joint
?OM
Pathogens causing OM
Staph aureus
Dx of OM
MRI
Bone biopsy for culture/histology
Rx in OM
Debride
and remove infected bone and soft tissue
Lautenbach technique
Debridement
After devridement double lumen suction irrigation system is introduced
Abx instilled through central lumen followed by streptokinase
Remains in situ until finishing giving Abx
3w then PO Abx for 6/52
Papineau technique
Complete excision of infected tissue and necrotic bone
Open cancellous grafting of the osseous defect
Skin grafting for wound closure
Risk factors for prostthetic joint infection
Local wound infection
Previous revision
Bilateral athrtoplasty
Wound healing complications
Pain, joint never right, early failure, sinus tract formation
Prosthetic joint infection
Most common organism causing prosthetic joint infection
Coag negative staph
Organisms causing prosthetic joint infection
Staph
Aureus
Strep
Enterococci
Gram negative: enterobacteria, pseudomonas
Anaerobes, fungi etc
Loosening on XR
Prosthetic joint infection
Dx of prosthetic joint infection
XR
Inflammatory markers
Aspirate
CRP in prosthetic knee infection
>13.5
CRP in prosthetic hip infection
>5
WCC in aspirate prosthetic knee infection
>1700
WCC in aspirate prosthetic any joint except knee
>4200
Rx of prosthetic joint infection
Single or two stage revision
Use Abx-impregnated cement
Single stage revision of infected prosthesis
remove all foreign material and dead bone, change gloves and drapes etc re implant
the new prosthesis w/ ABx impregnated cement and give IV antibiotics.
Two stage revision of infected prosthesis
remove prosthesis, take samples for microbiology and histology. Spacer put in place. Period
of IV antibiotics (6 weeks), stop ABx for 2 weeks. Re-debride and sample at second stage. Re-implantation w/
antibiotic impregnated cement. No further ABxs if samples are clear.
Rx in prosthetic joint infection:
Strep, staph, propioni
Clindamycin + Gentamicin
Rx in prosthetic joint infection:
MRSA
Vancomycin, ofloxacin & gentamicin
Rx in prosthetic joint infection:
Enterococci
Vanc
Ampicillin
Gent
Rx in prosthetic joint infection:
Enterobacter and E Coli
Cefotaxime
Ofloxacin
Gent
Rx in prosthetic joint infection:
Pseudomonas
Clindamyinc, gentamicin, cefoperazone
Rx in prosthetic joint infection:
MTB
Amikacin
Streptomycin
Rx in prosthetic joint infection:
Unknown pathogen
Vanc
Clindamycin
Gent
Def: complicateed UTI
Funcitonally or structurally abnormal tract
Rx pyelonephritis
Broad spec IV Abx e.g. co-amoxiclav and gent
or
cefuroxime and gent
Treatment of uncomplicated vs complicated UTI
3d vs 7d
Draw classifciation of abnromalities of the renal tract
Signifcance
One of the main defences is bacterial flushing
Staph aureus renal infection aetiology
Likely to be due to haematogenous spread i.e. staph sepsis
Typical symptoms of UTI
Dysuria
Urgency
Frequency
Polyuria
Suprapubic tenderness
Haematuria
Empirical UTI treatment of uncomplicated female
Trimethoprim
or cephalexin for 3d
NFT for 7d
NB 7d of treatment recommended for women who have had previous UTI
Empirical UTI treatment of breast feeding/pregnant woman
Cephalexin BD for 7d
2nd line: coamoxiclav QDS for 7d
Treatment of fungal UTI
May occur in patients with indwelling catheters
Catheter removal may result in cure
ORal fluconazole is no more effective than therapy, therefore not recommended in asymptomatic infections
What are the stages of PCR
.
.
Denature
Primer annealing
Chain elongation with Taq polymerase
CMV causes what in AIDs?
Retinitis
CMV causes what in BMT?
Pneumonitis
What are the 3 sources of viral infections post-transplant
Reactivation of latent infection e.g. Herpes
Graft brought infection with it e.g. HBV
Exogenous opportunistic infection post-transplant
Dx of viral infection in immunocompromised
Due to immune systems inability to mount a full response serology of limited diagnostic value
Viral detection preferable e.g. PCR
What are he human herpes viruses?
HSV1+2, VZV, CMV, HHV6, 7, 8 EBV
Where are HSV and VZV latent?
Sensory nerve ganglia
Where are CMV and EBV latent?
Leucocytes
Significance of VZV in immunocompromised
As a higher rate of Cx e.g. pneuonitis and hepatitis
Rx in VZV infection
Aciclovir
Prevention of VZV infection
VZIG
When is there are a risk of CMV in solid organ transplant?
Seropositive donor and seronegative recipient due to recipient viral exposure
When is there a risk of CMV reactivation in BMT
Serongetive donor but seropositive recipient due to loss of protective Abs
What causes post-transplant lymphoproliferative disease?
EBV
Rx of CMV in BMT
Pre-emptive treatment with ganciclovir
Mx of PTLD
Reduce immunosuppression
Rixumiab
CTx once it becomes lymphoma
Spindle cells and KSHV proteins when biopsied
HHV8
Castleman’s disease
Castleman disease, also known as giant or angiofollicular lymph node hyperplasia, lymphoid hamartoma, angiofollicular lymph node hyperplasia, is a group of uncommon lymphoproliferative disorders that share common lymph node histological features that may be localized to a single lymph node (unicentric) or occur systemically (multicentric)
Can be associated with HHV8
HHV6 in transplant
Can cause graft rejection
Rx in HHV infection
Ganciclovir
Foscarnet/cidofovir
Implications of adenoviruspost-transplant
Affects paediatric patients
High mortality with disseminated infection
Weekly PCR surveillance
Treated with reduction of immunosuppression and ribavirin
Treatment of measles in immunocompromised
Consider HNIG
BK virus associated with what in BMT
Haemorrhagic cystitis
BK virus associated with what in renal transplant
Ureteric stenosis
Def: endocarditis
Infection of the innermost layer of the heart, usually the valves
PUO
Anorexia, weight loss, amalise, fatigue, rigors, night sweats and weakness
Acutely: SOB, chest tightness, embolic complications
Dental history
PMH: RhF, CHD, cardiac surgery, valve replacemen, LT lines, bcateraemia, GI/bowel
IVDU Hx
Infective endocarditis
Heart murmurs that often change
?Infective endocarditis
Signs of infective endocarditis
Subactue:
Clubbing, splinter haemorrhages, Osler’s nodes, Janeway lesions, Roth spots, splenomegaly, haematuria
Ix in infective endocarditis
FBC (anaemia), U&E, CRP
ESR
3x blood cultures without Abx
Serology if culture negative
CXR
Echo
Dukes criteria: fulfilling endocarditis
2 major
or
1 major + 3 minor
or
5 minor
Duke’s criteria: Major
Persistent bacteraemia (>2 +ve blood cultures)
Echo findings: vegetations
+ve serology for bartonella, coxiella, brucella
Duke’s criteria: Minor
Predisposing risk factor e.g. murmur, IVDU
Fever >38 or raised CRP
Evidnce of immune complex fromation: splinter haemorrhages, haematuria
Vascular phenomena: major arterial emboli
Positive echo that does not meet major criteria
Positive blood culture that does not meet major criteria
Pathogen in subacute endocarditis
Low virulence strep: Strep viridans
Clinical course of subacute endocarditis?
Mild-moderate illness progressing over weeks to months
Decrease propensity haematogenously to seed extracardiac sites
What is the most common cause of prosthetic vavle endocarditis
Coag negative staph
Common cause of acute bacterial endocarditis
S aureus
Clinical course of acute bacterial endocarditis
Fulminant illness d-w
Most common cause of culture -ve infective endocarditis
Cultures taken after abx
Causative organisms in infective endocarditis (culture negative)
HACEK
Haemophilus
Aggregatibacter/Actinobacillus
Cardiobacterium hominis
Eikenella corrodens
Kingella Kingae
Aspergillus, brucella, coxiella, chlamydia, mycoplasma
Empirical treatment of infective endocarditis: prosthetc vavle
Vanc + Gent + Rifampicin
Empirical treatment of infective endocarditis: native valve, acute
Fluclox
Empirical treatment of infective endocarditis: native valve, indolent
Pen and Gent
Treatment of strep viridans causing infective endocarditis
Pen + Gent
Treatment of MSSA endocarditis
Fluclox for 4/52
Treatment of MRSA endocarditis
Vanc + gent/rifamp/fucidin
Treatment of enterococcal endocarditis
Ampiciliin + Gent
What are the indications for surgical intervention in infective endocarditis?
>1 serios sytemic emoblus/high risk
Uncontrolled infection
Significant valve dysfunction
Lack of Abx response
Local suppurative cx e.g. perivavlular abscess
CHF
Prosthetic valve endocarditis
What are the different types of PUO
Classical
Healthcare associated PUO
Neutropaenic PUO
HIV associated PUO
Def: PUO
>38C on several occassions for >3w in spite of at least 1 week of investiagations
Classical PUO
As for PUO oncluding 3/7 in hospital or >3O/P with ambulatory Ix
Causes of classical PUO
Infections
Neoplasms
CTD
Misc conditions: abscesses, endocarditis, TB, complicated UTIs
Undiagnosed conditions
Healthcare associated PUO
Develoops in hospital following >38h in hospital
Causes of PUO in children
Kawasaki’s
JIA
Causes of PUO in elderly
CTD predominant: temporal arteritis, PMR
Infections
Causes of healthcare associated PUO
Sx
Drugs
Medical devices
LRTI
C diff colitis
Immobilisation
Drugs causing PUO
Vancomyin
Penicllins
Serotonergics
Neutropaenic PUO
Fever concomittant with neotrpaenia and subsequent lack of cellular response =
MEDICAL EMERGENCY
Causes of Neutropaenic PUO
Infections
CTx
Haematological malignancies
Look for conditiosn that require neutrophils e.g. fungal infection, bacterial, MTB
GVHD
Drug fever
HIV-associated PUo
HIV +ve patients frequently have PUO
Cause related to CD4 count
Causes of HIV PUO
Seroconversion
TB
Kaposi’s
Bacterial
Disseminated MAI
PCP
CMV
Cryptococcus
Toxoplasmosis
Lymphoma
Histoplasmosis
Drug fever
Ix in PUO
Observe fever, if possible withold therapy until Dx
In febrile neutropaenia, therapy should be witheld until samples have been taklen unless patient is unstable
Vasculitis screen
Bence Jones protein
Dip urine
Familial diseases
Fever in returning traveller
Causes of fever in a returning traveller
Malaria (21%)
Dengue
Typhoid
Rickettsia
Bacterial diarrhoea
UTI
Pneumonia
HIV seroconversion
Viral haemorrhagic fevers
Timing is key
What is the key in fever in a returning traveller?
Timing
Anaerobic gram negative bacillus causing enteric fever
S. typi and paratyphi
Def: tyohiud
Enteric fever infecting Peyers patches, transmitted by food and water
Fever, headache, abdominal pain, diarrhoea or constipation
Rose spots
Relative bradycardia
Hepatosplenomegaly
Typhoid
Consequences of chronic typhoid carriage
Gallstones
Immunosuppression
Dx of typhoid
Hx
Blood cultures
Stool
Mx of typhoid
IV fluids
Oral or IV Abx
HPA notification
Transmission of typhoid
Food or water
What is the most common species of malaria?
Falciparum
What are the organims causing malaria
P. falciparum
P. vivax
P. ovale
P. malariae
Which plasmodium species have a tertian rhythmn?
Falciparum
Vivax
Ovale
(48hr)
Which plasdoium species have a quartan rhythm?
P malariae
Severity and liver stage:
falciparum
V severe
Parasitaemia
Severity and liver stage:
vivax
Chronic liver stage (hypnozoites)
Severity and liver stage:
Ovale
Chronic liver stage
Hypnozoites
Severity and liver stage:
Malariae
Benign
Young trophozoites in the absence of mature trohpozoites and schizonts
Crescent shaped gaemtocytes
P falciparum
Schuffner’s dots
>20 merozoites?schizont
Vivax
Schuffner’s dots
P Ovale
(vivax with merozites)
Ix in malaria
Thick film: parasitaemia
Thin film: species
Various antigen tests
Bloods:
WCC rarely raised
70% have a reduced platelet count
50% have deranged LFTs
30% anaemic
Commonly: Fever. splenomegaly, no signs
Uncommonly:
Focal neurology, reduced GCS/ coma/ shock/hepatomegaly
P falciparum malaria
Fevers and rigors
Flu-like illness
Headache
Back pain
Myalgia
N + V
Uncommonly:
Diarrhoea
Abdominal cramps
Cough
Dark urine
P. falciparum malaria
Treatment of no falciparum malaria
Chloroquine
then
Primaquine if resistant or minimal response
Treatment of mild falciparum malaria
Quinine + doxycylcine/clindamycin
OR malaronie (atovoquone/proguanil)
or RIamet (artemether and lumefantrine)
Treatment of severe falciparum malaria
Artemisinin combination therapy (ACT)
or
IV quinine + doxycycline/clindamycin
What should always be considered in terms of fever in a returning traveller?
HIV
Malaria
TB
Typhoid
Rabies
Fever in returning traveller, incubation:
<10d
ARboviruses: denghue, yellow fever, japanese encephalitis
SARS
Haemorrhagic fevers: lassa, ebola
Meningococcoaemia
Rarely: rabies
Fever in returning traveller, incubation:
10-21d
Flavivirus: tickborune and japanese encephalitis
Typhoid
Toxoplasma
Haemorrhagic fevers
Measles
Rarely: Hep A
Fever in returning traveller, incubation:
>21d
Schistosomiasis
TB
Viral hepatits
Filiarisis
Rarely: EBola/ Lassa
What are the major features of severe or complicated falciparum malaria
Altered consciousness/ seizures
Renal impairment
Acidosis (<7.3)
Hypoglycaemia (<2.2mmol)
Pulmonary oedema/ARDS
Anaemia
Spontaneous bleeding/DIC
Shock
Haemoglobinuria
Parasitaemia >2%
Pregnancy
Vomiting
Algid malaria
Definition: a form of falciparum malaria chiefly involving the gut and other abdominal viscera; gastric algid malaria is characterized by persistent vomiting; dysenteric algid malaria is characterized by bloody diarrheic stools in which enormous numbers of infected red blood cells are found.
What should be used as an alternative to doxy in the treatment of malaria in pregnancy?
Clindmaycin
Dosing structure for complicated malaria
Quinine 20mg/kg loading doese IV over 4h
then 10mg/kg/IV over 4h every 8 hours
+ oral doxy 200mg/clindamycin for 7d.
Taenia solium cysticercosis
infection of the tissues with pork tapeworm larvae
common in all non-Muslim developing countries
commonest cause of adult-onset epilepsy in many countries
e.g. causes 20-30% of adult onset epilepsy in Peru
What are the herpes viruses
HSV
VZV
CMV
EBV
HHV6
HHV8
What are the neurotropic herpes virses?
HSV 1+ 2
VZV
dsDNA
No anoimal reservoir
Persistent latent hpase in DRG
lytic infection of fibroblasts and epithelial cells
Transmitted via mucocutaenous contact
HSV1 and HSV2
dsDNA
Droplet spread
Viral replication in LNs then in liver + spleen
Develops rash 48h post infection
VZV
Oral: Incubation 2-12/7
Severe painful ulceration
Tendency to coalesce
Erythematous base and submandibular lymphadenopathy
Ddx Coxscakie A
HSV infection
Which HSV is predominantly associated with oral herpes
HSV1

Herpes
Gential:
Incubation 4-2/7
Fever, dysruia, inguinal lymphadenopathy
+++Pain
Vesicular rash
Meningitis 1-2/52 later in 4-8% with primary
HSV infection
What is a potential consequence of genital herpes
Sacral radiculomyelitis leading to urinary retention (self-limiting)
Coxsackie A infection
Herpangina, also called mouth blisters, is the name of a painful mouth infection caused by coxsackieviruses. Usually, herpangina is produced by one particular strain of coxsackie virus A (and the term “herpangina virus” refers to coxsackievirus A)[1] but it can also be caused by coxsackievirus B or echoviruses.[2] Most cases of herpangina occur in the summer,[3] affecting mostly children. However, it occasionally occurs in adolescents and adults. It was first characterized in 1920.
Eyes:
Unilateral/bilateral conjunctivitis and pre-auricular LNs
Ocular herpes infection HSV
What is a consideration in ocular herpes infection
Acute retinal necrosis if immunocompetent
What is seen in herpetic eye infeciton in the immunocompromsied
Progressive Outer Retinal Necrosis (also caused by VZV, EBV, CMV)
Which strain of HSV causes most herpetic encephalitis
HSV-1
Flu-like prodrome 2/52
Focal neurology, fever, confusion, behavioural change, cahgnge in consciousness, seizures, N+V, coma, death
Herpetic encephalitis
Mollaret’s meningitis
Recurrent benign lymphocytic meningitis
What commonly casues Mollaret’s meningitis
HSV-2
CSF: lymphocytic pleiocytosis
Cytology may be normal
N glucose
Raised protein
Herpes encephalitis
Treatment of herpes encephalitis
IV aciclovir STAT
Don’t wait for results
10mg/kg TDS then oral ACV for total of 2-3/52
Scrum pox
Painful blisters, + inguinal lymphadenopathy in rugby players
Herpes gladiatorum
Herpetc whistlow
Painful red finger

Herpetic whitlow
What are the potential skin manifestations of herpes
Gladiatorum
Whitlow
Erythema multiforme
HS dermatitis
Eczema herpeticum
Zosteriform HS (painless)
Fever, malaise, headache followed by dew on rose petal rash
Lesions scab and no longer contagious after 1/52
VZV
Cx of VZV
Scarring
Pneuominitis
Haemorrhage
Eye involvement
Reyes’s syndrome
Neurological
What are the potential neurological manifestations of VZV infection
Acute cerebellar ataxia
GBS
Ramsay hunt syndrome
Encephalitis
Post-herpetic neuralgia
Ramsay Hunt Syndrome
Ramsay Hunt syndrome (RHS) type 2 also known as herpes zoster oticus is a disorder that is caused by the reactivation of pre-existing Varicella zoster virus in the geniculate ganglion, a nerve cell bundle, of the facial nerve.[1]
Ramsay Hunt syndrome type 2 typically presents with inability to move many facial muscles, pain in the ear, taste loss on the front of the tongue, dry eyes and mouth, and the eruption of an erythematous rash.
Dx of VZV
Exam- vesicles
Cytology: Tzanck cells
Immunofluorescnece cytology
PCR: if rash is old, in CNS/ocular disease
Tzanck cells
Multinucleated giant cells found in VZV and HSV infections
VZV vaccien in pregnancy?
CIed as a live vaccine
Shingles
VZV reactivation (DRG) in times of stress/ reduced immunity
Painful, dermatomal rash
When to treat shingles
Symptomatic children
or healthy adult smokes, chronic lung disease
Treatment of shingles
Aciclovir 800mg PO or famciclovir or valaciclovir
Topical eye drops
PEP for immunocompromised
What are the epitheliotropic herpes viruses?
CMV and Roseola virus
What are the lymphotropic herpes viruses?
EBV
HHV8
Possible manifestations of CMV infection
Asymptomatic
Congenital
CMV mononcucleosis
Immunocompromised
What are the consequences of congenital CMV infection
IUGR/Jaundice/hepatosplenomegaly
Chorioretintis
Encephalitis
Microcephaly
Death
Late progressive sensorineural deafness
LD
Cyotmegalic inclusion disese
Manifestations of CMV infection in the immunocompromised?
Fever, heapatitis
Colitis
Retinitis
Pneuopnitis
BM suppression
Addison’s disease
Radiculopathy
Which cells does CMV infect
Macrophages, endothelial cells, B and T lymphocytes
BM cells
What is the cytological test used to diagnose CMV
Paul Bunnel/Monospot
What are the possible manifestations of EBV infection
Infectious mononucleosis
Burkitt’s
Nasopharyngeal Ca
Post-transplant lymphoproliferative disease
Fever, pharyngitis, lymphadenopathy
+ maculopapular rash
Infectious mononucleosis
Rx of HHV8
Gancilcoivr and Foscarnet
When does IFV A peak?
H1` peaks beginning of January each year
When does H1N1 peak?
End of december
When does IFV B peak?
March
H5N1=
Bird flu
H1N1=
Swine flu
SARs caused by
Coronavirus
Effectiveness of antiflu drugs
Only effective if administered within 48h of infection
Zoonoses:
Mice borne
Hantan viruses
Lyme borrelliosis
Erhlichia
Bartonella
Lymphocytic choriomeningtiis
Zoonoses:
Rats
Rabies
Leptospirosis
Lassa fever
Hantan viruses
Plague
Pasterullosis
Haverhill fever
Zoonoses:
Cats
Bartonellosis (cat scratch)
Leptospirosis
Q fever
Toxoplasmosis
Rabies
Ringworm
Toxocariasis
Zoonoses:
Dogs
Hydatid
Leptospirosis
Q fever
Rabies
MRSA
Ringworm
Toxocariasis
Zoonoses:
Small ruminants
Anthrax
Brucellosis
Q fever
Cryptosporidiosis
Enzootic abortion
Louping ill
Orff virus
Rift valley fever
Toxoplasmosis
Zoonoses:
Cattle
Anthrax
Leptopspirosis
Brucella
Bovine TB
Anaplasmosis
Toxoplasmosis
E Coli 0157
Rift valley fever
Ringworm
Zoonoses:
Swine
Brucellosis
Leptospirosis
Erysipeloid
Cysticerosis
Trichinella
HEV
IAV
Streptococcal sepsis
Zoonoses:
Birds
Psitticosis
IFV
Cryptococcus
IAV
Poultry: salmonella
WNV
Zoonoses:
Water sports associated
Leptospirosis
HAV
Giardia
Toxoplasmosis
Mycobacterium marinum/ulcerans
Brukholderia
Pseudomallei
E Coli
Zoonoses:
Water borne
Campylobacter
Salmonella
VTEC 0157
Cryptosporidium
Zoonoses:
Food associated
Listeria
Taenia
Cysticerosis
Toxoplasmosis
Trichinellosis
Yersiniosis
Giardia
Def: zoonosis
Diseases and infections which are transmitted naturally between vertebrate animals and man
Gram negative bacilus (faculative intracellular) zoonosis
Brucellosis
Mode of transport
Brucellosis
Inhalation
Skin or mucus membrane contact
Consumption of contaminated food, (untreated milk/dairy products)
Animal contact or environmental contamination
Also includes labarotory acquired
Brucellosis
Classically undulant fever (peaks in eve, normal by monring)
Malaise
Rigors
Sweating
Myalgia/arthralgia
Tiredness
3-4/52 incubation
Brucellosis
Arthritis
spinal tenderness
Lymphadenopathy
Splenomegaly
Hepatomegaly
Epididymo-orchitis
Rarely:
Jaundice, CNS abnromalities, cardiac murmur, pneumonia
Brucellosis
Ix in Brucellosis
Serology: anti-O-polysaccharide Ab
WCC usually normal
Leucocytosis rare
Signficant number of patients may become neutropaenic
Rx Brucellosis
4-6/52: tetracycline or doxycline combined with streptomycin or PO doxy and rifampicin 8/52
Rhabdovirus affecting warm-blooded animals
Dogs and bats most common vectors
Bullet shaped
Rabies
Negri bodies
Pathognomic for rabies
Prodrome: fever, headache, sore throat
Acute encephalitis (fatal): hyperactive state
Rabies
Ix in Rabies
IFA for rabies antigens in animals brain
Neutralisaiton/ELISA for rabies IgM
Treatment of rabies
Rabies specific Ig post exposure
Gram negative lactose fermenter found in rats
Yersinia pestis
What are the potential manifestations of yersinia infection
Bubonic plague: swollen LNs- dry gangrene
Pulmonary: usually seen during epidemics due to person-person spread
Rx of Yersinia
Streptomycin
Doxy
Gent
Chloramphenicol in meningitis
Gram negative obligate aerobic motile spirochaates
Leptospirosis
Organism in leptospirosis
L. interrogans
Excreted in dog/rat urine
Penetrates broken skin or as a conseuqnce of swimming in contaminated water
Leptospirosis
High siking fever
Headache
Conjuncitval haemorrhages
Jaundice
Malaise
Myalgia
Meningism
Carditis
Renal failure
HA
10-14/7
Leptospirosis
Rx of leptospirosis
Amoxicllin
Erythromycin
Doxy or ampicillin
Rx of anthrax
Ciprofloxacin or doxy
Woolsorters disease
Pulmonary anthrax
Painless round black lesions + rim of oedema
Cutaneous anthrax
Massive lymphadenopathy and mediastinal haemorrhage
Pleural effusion
Respiratory failure
Woodsorter’s disease
Arthropod borne (ixodes tick) spirochaete
Lyme disease (Borrelia burgdorferi)
What are the stages of Lyme disease
Early localised
Early disseminated
Late persistent
Cyclical fevers
Non-specific flu like symptoms
Erythema chronicum migrans (Bullseye rash)
Lyme disease
Malaise, lymphadenopathy, hepatitis, carditis, arthritis
Early disseminated Lyme disease
Arthritis
Focal neurology
Neuropsychiatric disturbance
Acrodermatitis chronic atrophicans
Late persistent lyme disease
Dx of lyme disease
Bx edge of ECM + ELISA for lyme Abs
Treatment of lyme disease
Doxy 2-3/52 (also amoxicillin, cephalosporins)
NB post infection some patients get ME type symptoms
Treatment of Lyme disease with CNS involvement
IV ceftriazone
Causative organism in Q fever
Coxiella burnetii
Fever, dry cough
Fatigue
Pleural effusion
Diarahoea
Looks like atypical pneumonia
NO RASH
Cattle/sheep exposure
Q Fever
Rx Q fever
Doxy
What are the manifestations of Leishmania?
Cutaaneous
Diffuse cutaenous
Muco-cutaenous
Visceral: Kala Azar
Which species cause cutaneous leishmaniasis
L. major
L. tropica
Sandfly bite
Skin ulcer at site of bite
Heals after 1yleaving depigmeneted scar
May be single or multiple painless nodules which grow and ulcerate
T4HS
Cutaenous leishmaniasis
Immunodefieicnt
Nodular skin lesions that do not ulcerate
Especially lots of nodules
Diffuse leishmaniasis
Which speices cause muco-cutaenous leishmaniasis
L braziliensis
Dermal ulcer
Months to yearslater ulcers in mucus membrane of mouth
L. brazilienis (muco-cutaneous)
Which species cause visceral Leishmaniasis?
L donovani
L infantum
L chagasi
Young malnourished child
Abdo discomfort + distension/anorexia/weight loss
Kala Azar
Clinical course of L donovani
Invasion of RES-> hepatosplenomegaly-> BM invasion
Later disfiguring dermal disease PKDL

Acrodermatitis chronic atrophicans
Lym disease
Late persistent
Flu like illness
Lymphadenopathy
Myalgia
Encephalitis
Necrotising retinochoroidits *Trainspotting)
Toxoplasmosis
Causes cysts commonly in the liver
Hydatid disease
Jaundice, conjunctival haemorrhage, canoeing in the US, felt run down
Leptospirosis
Maltese man, headache, fever, slight splenomegaly, small gram negative coccobacilli seen on Castaneda’s medium
Brucellosis
Biology field trip, leg lesion 5cm flat red edge with a dim centre, tired, headaches, fever, irregular heart beat
Lyme disease
India, ulcerating papule on hand, centre is black and necrotic, gram positive rods on blood agar culture, responded to large doses of
penicillin
Anthrax
Arm pain, hypersalivation, twitching, renal failure, death, confusion
Rabies
How can fungal infections be classified?
Yeasts
Dermatophytes
Moulds
What are the yeasts
candida, Cryptococcus, pichia, rhodotorulla, saccharomyces, trichosporon etc
What are hte dermatophytes
epidermophyton, microsporum, trichophyton
What are the moulds
aspergillus, fusarium, mucor, penicillium, rhizopus etc.
How to diagnose superficial fungal infections
Wood lamps
The Tineas
ermatophytes
Pityriasis versicolour
malassezia
Otomycosis
yeasts & moulds. Fungal ear infection
Black piedra
piedraia hortae
White piedra
trichosporon beigelii
What are the different types of tineas?
Capitis: scalp and hair
Corporis: trunk, legs and arms
Cruris: groin and pubic region
Pedis
Manum
Ungium
Pityriasis
Malassezia globosa/furfur
Seborrhoic dermatitis
T. versicolor: depigmentation in those with darker skin

Tinea versicolour
Dx of deep seated candida
Culutre
Mannan
Abs
Pneumonia in immunocompromised
High mortality
Aspergilluis
Meningitis in immunocompromised
Insidious onset in HIV
Cryptoccous
Dx of aspergillus
ELISA
PCR
Beta-blucan test
Dx of crytpococcal meningitis
Cryptococcal antigen in CSF
Halo sign on CT
Ground glass attenuation surrounding a pulmonary nodule
Invasive pulmonary asperigllosis
Hyalohyphomycosis
o Oppourtunistic mycotic infection caused by non-dematiaceous moulds
Dematiaceous moulds: dark coloured, produce melanin
Fusarium, penicillium, paecilomyses, acremonium, scopulariopsis, beauvaria.
o Harmless saprophytic colonisation to acute invasive disease
Saprophytic: organism that lives on dead organic matter.
o Predisposing factors: haematological malignancies, prolonged neutropenia, corticosteroid
therapy and IS supp.
o Only culture and microscopy
Caused by dematiaceous moulds (black/pigmented)
o Localised superficial infections of the stratum corneum, subcutaneous or invasive including brain
infections.
o Organisms: cladophialophora (bantiana), curvularia, exophiala, bipolaris, phialophora,
excerohium, wangiella.
o Detection: culture, microscopy: masson Fontana
Phaeohyphomycosis
Chronic granulomatous, pulmonary and disseminated disease due to blastomyces dermatitidis
o Blastomyces dermatitidis: dimorphic fungi
o Endemic to the Americas and Africa
o Detection: culture and microscopy, serological test, antibody
Blastomycosis
Initially a respiratory infection due to coccidioides immitis, in some patients e.g. HIV, chronic and systemic disease involving
the meninges, bone, joints and other tissues.
o Endemic to south-western USA, north Mexico and part of South America.
o Detection: culture, microscopy, serological test, antibody.
Coccidioidomycosis
Dimorphic
o Intracellular infection of the reticuloendothelial system caused by histoplasma capsulatum
o Can mimic TB
o Endemic to the Americas and Africa - Found in soil enriched with excreta from chickens and bats.
Histoplasmosis
Dimorphic
o Chronic granulomatous disease due to paracoccidioides brasiliensis
o Primary pulmonary, disseminates to form an ulcerative granuloma of the buccal, nasal or GI mucosa.
o Endemic to south and central America.
Paracoccidioidomycosis
Systemic disease in immunocompromised patients, particularly HIV
o Endemic to south east Asia
o Easy to culture in both the yeast and filamentous forms.
Penicillium marneffei
Dimorphic, Sporothrix schenckii
o A chronic infection of the Cutaneous or subcutaneous tissue and the adjacent lymphatics, nodular lesions which may
suppurate and ulcerate
o Spread to articular surfaces, bone and muscle.
Sporotrichosis
Cutaneous or subcutaneous infection resulting in necrotic patches
o Acute rapidly developing, often fatal infection in debilitated or diabetic
patients
o Due to; absidia, cunninghamella, mortierella, mucor, rhizomucor,
rhizopus, and saksenaea.
o Most devastating fungal disease
Mucormycosis
Conidiobolus coronatus
Chronic granulomatous disease of the nasal submucosa,
polyps or palpable masses
Rare: systemic and pulmonary
Seen mainly in the tropics.
o Basidiobolus ranarum
Chronic granulomatous disease limited to limbs, chest, back and buttocks
Seen mainly in the tropics.
Entomophthoromycosis
o Infection due to fungi (eumycetoms) and actinomycetes resulting from traumatic
implantation.
o Cutaneous or subcutaneous tissues and bone of the foot & hand.
o Sinuses discharge serosanguinous fluid containing grains
o Organisms: madurella, acremonium, scedosporium, curvularis, exophiala, leptosphaeria,
fusarium, aspergillus.
Mycetoma
o A slowly progressing cutaneous and subcutaneous infection due to dematiaceous planatedividing
sclerotic bodies resulting from traumatic implantation.
o Associated with wood
o Organisms: cladophialophora, phialophora, fonsecaea etc.
Chromoblastomycosis
Infection of humans and dolphins by unisolated and unclassified yeast like
fungus Loboa loboi- Not grown in the lab yet
o Chronic subepidermal infection - No systemic spread
o Keloidal, verrucoid nodular lesions or vegetating crusty plaques and tumours
o Restricted to the Amazon valley in Brazil.
o Improving culture - dimorphic = extended incubation
Lobomycosis
What are the different classes of antifungals
Polyene
Azole
Terbinafine
Flucytosine
Echinocandin
MOA:
Polyenes
Cell membrane integrity
MOA:
Azoles
Cell membrane synthesis
MOA:
Terbinafine
Cell membrane synthesis
MOA:
Flucytosine
DNA synthesis
MOA:
Echinodcandin
Cell wall
What is used to treat cryptococcal meningitis and invasive fungal infection?
Amphotericin B
What drugs are used to treat yeast infection
Polyenes
Azoles
Echinocandin
E.g. polyene
Amphotericin
E.g. azole
Fluconazole
Eg. echinocandin
Caspofungin
What is used to treat mould infection/dermatophytes
Terbinafine
SE: amphotericin
Permanent renal impairment
Flucytosine used to treat
Candida
Se of flucytosine
Bone marrow suppression
What is the treatment for candidaemia
Fluconazole
Clinical features of HIV infection in children
Systemic symptoms
Skin rashes: extensive follicular rash, disseminated scabies
Oesophageal candidiasis
Kaposi’s sarcoma
Primary zoster
Multidermal zoster infection
Molluscum contagiosum
HIV encephalopathy
Severe
FTT
CMV retinitis
Dramatic lymphadenopathy usuallly accompanied by hepatosplenomegaly and lymphoid intersitital pneumonitits
Sign of immune activation following HIV infection
caused by a threadlike nematode (roundworm) belonging to the superfamily of filarioidea. Transmitted by
clack flies and mosquitoes. Effect the lymph nodes
Filariasis
filariasis, river blindness,
Loa Loa
Classically acquired on a beach holiday because of
hookworm in dog faeces. The conditions in a ropical
holiday are sufficiently sandy, warm and wet to sustain
the life cycle.
o Once acquired the cutaneous larva migrans on the bits of
skin which came into contact with the soil.
o Though the course of the worm can keep wandering, and
cause bullae to form. Very itchy.
Cutaenous larva migrans (ancylostoma braziliense)
Treatment of cutaenous larva migrans
Can do nothingh- may resolve spontaenously
Topical: thiabendazole
Oral: albendazole or ivermectin
Infestation by a fly larvae that feeds on the tissue
o Endemic to tropical
regions of Africe and south of Sahara desert. Eggs are laid on
damp clothing hanging out to dry, when the larvae hatch and
can penetrate a new host. This causes a swelling and takes 8-
12 days to develop through three larval stages. It then leaves
the host, drops to the floor, buries and pupates to emerge as
a fly.
Tumbu fly: cordylobia anthropophagi.
Uses humans as the
host for its larvae. But other vectors such as mosquitoes are
used to deposit larvae in humans. After about 8 weeks they drop out to pupate in the soil after developing in the
subcutaneous tissue. Rare for pts to experience infection unless they kill the larvae without removing it completely. Larvae
can produce antibiotic secretions to help prevent infections while it is feeding. They do not kill the host animal and thus are
true parasites. The fly larvae can only survive the entire 8 weeks if the wound does not become infected.
Human Bot Fly: Dermatobia hominis.
Parasitic arthropod found in tropical climates.
o Is 1mm long, and the smallest know flea
o Burrows head first into the hosts skin, often leaving the caudal top of its
abdomen visible through an orifice in a skin lesion. This orifice allows for the
jigger to breathe and defecate while feeding on blood.
o In the next 2 weeks is abdomen swells up with dozens of eggs which it releases
through the caudal orifice to fall to the ground when ready to hatch.
o The flea then dies and is sloughed off with the hosts skin. Within the next 3-4
days the eggs hatch and mature into adult fleas within 3-4 weeks.
o Infections almost always on the foot, feel like itching or irritation to begin with,
which then passes as the area around the flea calluses and become insensitive.
As the abdomen swells this may cause local pressures.
o Complications- bacterial superinfection, ulceration, nail destruction,
lymphoedema and tetanus.
Tungiasis: Tunga Penetrans / Jigger / Chigoe Flea
The antiviral which is given to untreated pregnant women with HIV to prevent vertical transmission of the virus during childbirth.
.
Zidovudine
B.
Aciclovir
C.
Oseltamivir
D.
Neuraminidase inhibitor
E.
Foscarnet
F.
Nevirapine
G.
Cidofovir
H.
Ganciclovir
I.
Entecevir
J.
Interferon-α (alpha)
K.
Aciclovir triphosphate
L.
Ribavirin
M.
Interferon-b (beta)
N.
Aciclovir monophosphate
O.
Interferon-g (gamma)
ZDV was the first drug for which efficacy was shown. NVP alone has been shown to be more effective than ZDV alone in certain groups (see below). ZDV + 3TC has also been shown to more effective than ZDV alone but efficacy with this regimen falters out by 18 months. Abbreviations ZDV zidovudine, NVP nevirapine, 3TC lamivudine, PLCS prelabour caesarean section PEP post exposure prophylaxis
The drug mechanisms which acts by stopping post-translational cleaving of polyproteins by inhibiting proteases
A.
Nevirapine
B.
Amantadine
C.
Zanamivir
D.
Ganciclovir
E.
Aciclovir
F.
Ribavarin
G.
Interferon
H.
Enfuvirtide
I.
Indinavir
J.
Human normal immunoglobulin
K.
Zidovudine
L.
Human specific immunoglobulin
M.
Efavirenz
Indinavir
The drug which can be delivered by inhalation to treat both influenza A and B.
A.
Nevirapine
B.
Amantadine
C.
Zanamivir
D.
Ganciclovir
E.
Aciclovir
F.
Ribavarin
G.
Interferon
H.
Enfuvirtide
I.
Indinavir
J.
Human normal immunoglobulin
K.
Zidovudine
L.
Human specific immunoglobulin
M.
Efavirenz
Zanamivir
A nucleoside analogue which inhibits reverse transcriptase
A.
Nevirapine
B.
Amantadine
C.
Zanamivir
D.
Ganciclovir
E.
Aciclovir
F.
Ribavarin
G.
Interferon
H.
Enfuvirtide
I.
Indinavir
J.
Human normal immunoglobulin
K.
Zidovudine
L.
Human specific immunoglobulin
M.
Efavirenz
Zidovudine
Common side effects of NRITs?
Lactic acidosis
Main side effects of NNRTIs
Rash
SJS
TEN
Fatal fulminant hepatitis
Main side effects of protease inhibitors
Insulin resistance
Dyslipidaemia
Lipodystrophy
Bleeding in haemophilia
What are the 5 most important p450 substrates?
Warfarin
AEDs
OCP and prednisolone
Ciclosporin A, Tacrolimus
NNRTIs and PIs
Giving rifampicin or chronic alcohol use (or any enzyme inducer) will cause drug levels to fall, with DISASTROUS consequences for the patient and for your career (negligence). The renal transplant patient who catches TB will reject her kidney, the HIV patient will suffer fatal opportunistic infection, the young woman with TB becomes pregnant, the epileptic starts fitting and loses her driving licence for a year and maybe her pregnancy (during the fit), and the patient with a metallic aortic valve strokes out.
An 18 year old trainee clown is being seen in the cystic fibrosis clinic and is found to be colonised with a particularly persistent organism.
A.
Chlamydia psittaci
B.
S. pneumoniae
C.
Anaerobic infection
D.
Burkholderia cepacia
E.
PCP/ P jiroveci
F.
MRSA
G.
MSSA
H.
Legionella pneumophila
I.
M. Catarrhalis
J.
Chlamydia pneumoniae
K.
H. influenzae
L.
MSSA or MRSA
M.
M tuberculosis
Burkholderia
What are the side effects of the macrolides
they are motilin Receptor agonists so increase GI motility: diarrhoea, nausea, vomiting - acute cholestatic hepatitis esp erythromycin estolate (idiosyncratic reaction) - ENZYME INHIBITORS except azithromycin - increase QT interval CONTRA-INDICATED in pregnanc
Rx in VISA or VRSA?
Linezolid
What are VISA
VRSA
VRE
VISA: Staph aureus with intermediate level resistance to vancomycin VRSA: Vancomycin resistant Staph aureus VRE: Vancomycin resistant Enterococcus faecium or Enterococcus faecalis
On your elective in central Africa a 7 year old child comes to your clinic with a large mass on his jaw. You take a biopsy of the lump, which shows EBV positive large cell lymphoma B cells. Histology shows a starry sky appearance (isolated histiocytes on a background of abnormal lymphoblasts). Genetic testing shows the presence of a 14q/8q translocation. The consultant suggests treating with cyclophosphamide and a single dose leads to a spectacular remission.
A.
Chicken Pox
B.
Cytomegaloviruses
C.
Burkitt’s lymphoma
D.
Primary Genital Herpes
E.
Keratitis
F.
Herpes Labialis (Cold sores)
G.
Roseola infantum
H.
Shingles
I.
Glandular fever
J.
HHV 6
K.
HHV 7
Burkitt’s
Which of the above is a naturally occurring cytokine that is able to inhibit HIV fusion to CD4+ T-lymphocytes?
A.
Integrase
B.
CCR5/CXCR4
C.
CD8
D.
Kaposi’s sarcoma
E.
Candidiasis
F.
Viral load (PCR)
G.
Anti-HIV antibody (Western blot)
H.
CD4
I.
CD25
J.
gp120
K.
Reverse transcriptase
L.
Hairy leukoplakia
M.
MIP-1alpha
MIP-1alpha
56 year old male with endocarditis caused by VRE.
A.
Vancomycin
B.
Linezolid
C.
Ciprofloxacin
D.
Erthyromycin
E.
Ceftriaxone
F.
Gentamicin
G.
Metronidazole
H.
Flucloxacillin
I.
Benzyl Penicillin
Ceftriaxone
An 82 yr old gentleman, living at home, develops severe dyspnoea with a productive cough and fever. His PaO2 has fallen below 8kPa, and he is becoming confused.
.
isoniazid
B.
trimethoprim
C.
rifampicin
D.
vancomycin
E.
Ceftriaxone
F.
Amoxicillin
G.
Chloramphenicol
H.
cefuroxime & clarithromycin
I.
no antibiotics required
J.
linezolid
K.
Flucloxacillin
L.
Cefalexin
M.
Erythromycin
cefuroxime & clarithromycin
A 6 month old child whose father has just been diagnosed with tuberculosis.
A.
isoniazid
B.
trimethoprim
C.
rifampicin
D.
vancomycin
E.
Ceftriaxone
F.
Amoxicillin
G.
Chloramphenicol
H.
cefuroxime & clarithromycin
I.
no antibiotics required
J.
linezolid
K.
Flucloxacillin
L.
Cefalexin
M.
Erythromycin
Isoniazid
Treatment of known N menginitides meningitis
Ben Pen
First choice in bacterial meningitis of unknown aetiology
3rd gen cephalosporins
Ceftriaxone
This microbe is spread by faecal-oral route, and often occurs in epidemics. Shellfish from seawater contained by sewage can harbour this microbe.
A.
Entamoeba histolytica
B.
Escherichia Coli
C.
Salmonella
D.
Shigella
E.
Vibrio cholera
F.
Clostridium difficile
G.
Aeromonas
H.
Hepatitis A
I.
Yersinia
HAV
This microbes affects mainly the distal colon, producing acute mucosal inflammation and erosion. It is spread by person-to-person contact, and its clinical features include fever, pain, diarrhoea and dysentery.
A.
Entamoeba histolytica
B.
Escherichia Coli
C.
Salmonella
D.
Shigella
E.
Vibrio cholera
F.
Clostridium difficile
G.
Aeromonas
H.
Hepatitis A
I.
Yersinia
Shigella
This microbe affects the ileum, appendix and colon. Its peyer patch invasion leads to mesenteric lymph node enlargement with necrotising granulomas. Complication can include peritonitis, pharyngitis and pericarditis.
A.
Entamoeba histolytica
B.
Escherichia Coli
C.
Salmonella
D.
Shigella
E.
Vibrio cholera
F.
Clostridium difficile
G.
Aeromonas
H.
Hepatitis A
I.
Yersinia
Yersinia enterocolitica undergoes multiplication in Peyer’s patches following invasion of human epithelial cells and penetration of the mucosa which occurs in the ileum. Complications include diarrhoea, mesenteric adenitis, mesenteric ileitis, or acute pseudoappendicitis, reactive arthritis and erythema nodosum. Ingestion of Entamoeba histiolytica cysts is followed by excystation in the small bowel and trophozite colonisation of the small colon. The trophozyte may then encyst and be excreted in faeces or it may invade the intestinal mucosal barrier, thereby gaining access to the circulation. Complications include amoebic colitis, liver abscesses, pleuropulmonary amoebiasis and cerebral amoebiasis
A 30 year old male is brought into hospital. He is very dehydrated and is feeling very weak. He has had unrelenting diarrhoea, which came on suddenly. He describes the stools as looking like rice water. He has no abdominal pain.
A.
Rotavirus
B.
Tuberculosis of the gut
C.
Clostridium difficile
D.
Bacillus cereus
E.
Verotoxin-producing E.coli
F.
Cholera
G.
Bacterial Dysentry
H.
Stress
I.
Salmonella
J.
Ulcerative colitis
K.
Giardiasis
Cholera
Following a trip to Brazil, a patient develops bloody diarrhoea, with a high fever, sweating and on examination the patient is found to have RUQ pain.
A.
Giardia Lamblia
B.
Entamoeba Histolytica
C.
Camplyobacter Jejuni
D.
Typhoid
E.
Vibrio Cholera
F.
Taenia Saginata
G.
E. coli
H.
Taenia Solium
I.
Shigella
J.
Salmonella
K.
Clostridium Difficile
L.
Laxative abuse
M.
Yersinia Enterocolitica
Entamoeaba histolytica
Following a barbeque, a 41 year old develops watery diarrhoea and vomiting. On retrospect, he wondered whether he should have had that dodgy looking shish kebab.
A.
Giardia Lamblia
B.
Entamoeba Histolytica
C.
Camplyobacter Jejuni
D.
Typhoid
E.
Vibrio Cholera
F.
Taenia Saginata
G.
E. coli
H.
Taenia Solium
I.
Shigella
J.
Salmonella
K.
Clostridium Difficile
L.
Laxative abuse
M.
Yersinia Enterocolitica
Salmonella
A 40 year old homosexual man develops severe flatulence, accompanied by bloating and explosive diarrhoea.
A.
Giardia Lamblia
B.
Entamoeba Histolytica
C.
Camplyobacter Jejuni
D.
Typhoid
E.
Vibrio Cholera
F.
Taenia Saginata
G.
E. coli
H.
Taenia Solium
I.
Shigella
J.
Salmonella
K.
Clostridium Difficile
L.
Laxative abuse
M.
Yersinia Enterocolitica
Giardia
Mr S became ill with nausea, vomiting and watery diarrhoea about 4 hours after eating some ham at a conference buffet lunch. Mr B’s illness was attributed to a heat stable, preformed toxin in the ham. His symptoms resolved within 24hours.
A.
Campylobacter
B.
Salmonella
C.
Rotavirus
D.
Shigella
E.
Escherichia coli
F.
Clostridium botulinum
G.
Entamoeba histolytica
H.
Staphylococcus
I.
Bacillus cereus
Staph
Mr C complained of fever and severe (>10 bowel movements/day) diarrhoea after looking after his neighbours dogs for a few days. Laboratory analysis of Mr C’s stools found the causative organism to be a S-shaped microaerophillic bacteria.
A.
Campylobacter
B.
Salmonella
C.
Rotavirus
D.
Shigella
E.
Escherichia coli
F.
Clostridium botulinum
G.
Entamoeba histolytica
H.
Staphylococcus
I.
Bacillus cereus
Campylobacter
A toxin-mediated organism that does not damage or invade the gastrointestinal epithelium
A.
Giardia lamblia
B.
Shigella
C.
E. coli
D.
Bacillus cereus
E.
Cholera
F.
Staphylococcus aureus
G.
C. difficile
H.
Salmonella
I.
Clostridium botulinum
Cholera
Laryngeal spasm seen in?
Rabies encepalomyelitis
What differentiates between GBS and botulism
GBS is ascending
Inactivated preparations of the bacteria
A.
pneumococcal vaccine
B.
Hepatitis B virus vaccine
C.
tetanus vaccine
D.
BCG vaccine
E.
oral poliomyelitis vaccine
F.
Whole cell typhoid vaccine
G.
Hepatitis A virus vaccine
H.
Hib vaccine
Whole cell typhoid vaccine
A sub-unit / conjugate vaccine
A.
pneumococcal vaccine
B.
Hepatitis B virus vaccine
C.
tetanus vaccine
D.
BCG vaccine
E.
oral poliomyelitis vaccine
F.
Whole cell typhoid vaccine
G.
Hepatitis A virus vaccine
H.
Hib vaccine
A.
pneumococcal vaccine
Vaccine that is made using recombinant DNA technology.
A.
pneumococcal vaccine
B.
Hepatitis B virus vaccine
C.
tetanus vaccine
D.
BCG vaccine
E.
oral poliomyelitis vaccine
F.
Whole cell typhoid vaccine
G.
Hepatitis A virus vaccine
H.
Hib vaccine
Hepatitis B virus vaccine
An antigen assembled in a multimeric form and saponin that provokes a strong serum antibody response.
A.
IFN gamma
B.
Rubella vaccine
C.
Effector memory
D.
Yellow fever vaccine
E.
Immunostimulatory complexes (ISCOMS)
F.
Perforin
G.
Typhoid vaccine
H.
CpG sites
I.
Bacillus Calmette-Guerin
J.
Adjuvant
K.
Rabies vaccine
L.
IL2
M.
MMR vaccine
Immunostimulatory complexes (ISCOMS)
A feature of immunological central memory
A.
IFN gamma
B.
Rubella vaccine
C.
Effector memory
D.
Yellow fever vaccine
E.
Immunostimulatory complexes (ISCOMS)
F.
Perforin
G.
Typhoid vaccine
H.
CpG sites
I.
Bacillus Calmette-Guerin
J.
Adjuvant
K.
Rabies vaccine
L.
IL2
M.
MMR vaccine
IL2Central memory (CM) T cells migrate efficienctly to peripheral LNs and produce IL-2, no IFN-gamma and no perforin. In contrast, effector memory (EF) T cells do not migrate efficiently but are found in other sites such as the liver and lungs. EF T cells produce little IL-2, but high amounts of IFN-gamma and perforin.
Which vaccine is usually given to children at 12-15 months?
A.
Tetanus vaccine
B.
Influenza vaccine
C.
Mycobacterium bovis
D.
Diptheria vaccine
E.
Inactivated
F.
Poliomyelitis vaccine
G.
Mycobacterium tuberculosis
H.
MMR vaccine
I.
Haemophilus influenzae type b vaccine
J.
Varicella-zoster vaccine
K.
Smallpox vaccine
L.
Live attenuated
M.
Typhoid vaccine
MMR
Which vaccine is normally given to infants under the age of 13 months in the form of three doses at monthly intervals to protect against an infection that has symptoms similar to meningitis and predominantly occurs in children < 5 years?
A.
Tetanus vaccine
B.
Influenza vaccine
C.
Mycobacterium bovis
D.
Diptheria vaccine
E.
Inactivated
F.
Poliomyelitis vaccine
G.
Mycobacterium tuberculosis
H.
MMR vaccine
I.
Haemophilus influenzae type b vaccine
J.
Varicella-zoster vaccine
K.
Smallpox vaccine
L.
Live attenuated
M.
Typhoid vaccine
Hib
Conjugate vaccine routinely given to neonates in the UK.
A.
Varicella zoster
B.
HBV
C.
CpG
D.
BCG
E.
Typhoid
F.
IL-2
G.
H. influenzae B
H.
Meningococcal A
I.
Tetanus
J.
Polio (Sabin)
K.
Freund’s
L.
Influenza
M.
Alum
N.
MMR
O.
Rabies
P.
Polio (Salk)
Hib
Agent used in humans that promotes a predominantly antibody response through the release of Il-4 that primes naïve B-cells.
A.
Varicella zoster
B.
HBV
C.
CpG
D.
BCG
E.
Typhoid
F.
IL-2
G.
H. influenzae B
H.
Meningococcal A
I.
Tetanus
J.
Polio (Sabin)
K.
Freund’s
L.
Influenza
M.
Alum
N.
MMR
O.
Rabies
P.
Polio (Salk)
Alum
Live attenuated vaccine that is no longer given as standard in the UK since the rates of reverse mutation are higher than those of active disease
A.
Varicella zoster
B.
HBV
C.
CpG
D.
BCG
E.
Typhoid
F.
IL-2
G.
H. influenzae B
H.
Meningococcal A
I.
Tetanus
J.
Polio (Sabin)
K.
Freund’s
L.
Influenza
M.
Alum
N.
MMR
O.
Rabies
P.
Polio (Salk)
Polio (Sabin)
Subunit vaccine given to the elderly and immunocompromised
A.
Varicella zoster
B.
HBV
C.
CpG
D.
BCG
E.
Typhoid
F.
IL-2
G.
H. influenzae B
H.
Meningococcal A
I.
Tetanus
J.
Polio (Sabin)
K.
Freund’s
L.
Influenza
M.
Alum
N.
MMR
O.
Rabies
P.
Polio (Salk)
Influenza
Vaccination with which of the above prevents a gram negative rod meningitis typically affecting children below 4 years of age?
A.
Rabies vaccine
B.
Influenza vaccine
C.
Polio vaccine
D.
Mumps vaccine
E.
Tetanus vaccine
F.
Hepatitis A vaccine
G.
Hepatitis B vaccine
H.
Rubella vaccine
I.
Diptheria vaccine
J.
BCG
K.
HIB vaccine
HIB vaccine
Which is recommended in all individuals over 65 years of age?
A.
Rabies vaccine
B.
Influenza vaccine
C.
Polio vaccine
D.
Mumps vaccine
E.
Tetanus vaccine
F.
Hepatitis A vaccine
G.
Hepatitis B vaccine
H.
Rubella vaccine
I.
Diptheria vaccine
J.
BCG
K.
HIB vaccine
Pneumococcal and influenza vaccinations are recommended routinely for those over 65 and also for both children and adults in special risk categories.
1) Pneumovax administration:
Routinely given as a one-time dose; administer if previous vaccination history is unknown. However..one-time revaccination is recommended 5yrs later for people at highest risk of fatal pneumococcal infection or rapid antibody loss (e.g., renal disease) and for people >65yrs of age if the 1st dose was given prior to age 65 and >5yrs have elapsed since previous dose
A conjugate vaccine
A.
BCG vaccine
B.
Meningococcal A vaccine
C.
Tetanus vaccine
D.
Hepatitis A virus vaccine
E.
Oral poliomyelitis vaccine
F.
Haemophilus influenzae type B vaccine
G.
Hepatitis B virus vaccine
Haemophilus influenzae type B vaccine
Inactivated vaccine.
A.
BCG vaccine
B.
Meningococcal A vaccine
C.
Tetanus vaccine
D.
Hepatitis A virus vaccine
E.
Oral poliomyelitis vaccine
F.
Haemophilus influenzae type B vaccine
G.
Hepatitis B virus vaccine
Hepatitis A virus vaccine
Excreted in the stools of immunised individuals.
A.
BCG vaccine
B.
Meningococcal A vaccine
C.
Tetanus vaccine
D.
Hepatitis A virus vaccine
E.
Oral poliomyelitis vaccine
F.
Haemophilus influenzae type B vaccine
G.
Hepatitis B virus vaccine
Oral poliomyelitis vaccine
What do these have in common:
Measles, mumps, rubella (German measles), polio (Sabin vaccine), chicken pox, yellow fever, BCG
All live attenuated vaccines
What do these have in common:
Cholera, IFV, HAV, rabies, polio
All inactivated (killed) vaccines)
What type of vaccine is the HBV vaccine?
Subunit vaccine
What type of vaccines are the Hib and pneumococcal vaccine?
Conjugate
This is a vaccine made of recombinant protein.
A.
Freund’s adjuvant
B.
MMR
C.
Mantoux
D.
Live attenuated
E.
Polio
F.
Active immunity
G.
IL-12
H.
HAV
I.
HBV
J.
Conjugate
K.
Passive immunity
L.
Typhoid
M.
Menigococcal
N.
Alum
O.
Inactivated
HBV
A water-in-oil emulsion containing mycobacterial cell wall components that could be used to increase the immune response of a vaccine.
A.
Freund’s adjuvant
B.
MMR
C.
Mantoux
D.
Live attenuated
E.
Polio
F.
Active immunity
G.
IL-12
H.
HAV
I.
HBV
J.
Conjugate
K.
Passive immunity
L.
Typhoid
M.
Menigococcal
N.
Alum
O.
Inactivated
Freund’s adjuvan
A student who presented with two day history of bloody diarrhoea, vomiting, fever, headache and myalgia. He has just returned from camping in the country side near a farm where he had fresh cow’s milk for breakfast everyday.
A.
Brucella abortus
B.
Yersinia pestis
C.
Francisella tularensis
D.
Cryptosporidium parvum
E.
Campylobacter jejuni
F.
Borrelia burgdorferi
G.
Trypanosoma cruzi
H.
Rickettsia prowazekii
I.
Bartonella henselae
J.
Spirillum minus
Campylobacter jejuni
A 2 year old boy living in the slums who has a one day history of profuse watery diarrhoea, fever and abdominal cramps. His family’s main source of water is the river near their squatters.
A.
Brucella abortus
B.
Yersinia pestis
C.
Francisella tularensis
D.
Cryptosporidium parvum
E.
Campylobacter jejuni
F.
Borrelia burgdorferi
G.
Trypanosoma cruzi
H.
Rickettsia prowazekii
I.
Bartonella henselae
J.
Spirillum minus
Cryptosporidium parvum
Cat-scratch disease
Bartonella henselae
A man was bitten by a rat in Asia. Ten days later he complains of fever, malaise, headache and myalgia.
A.
Brucella abortus
B.
Yersinia pestis
C.
Francisella tularensis
D.
Cryptosporidium parvum
E.
Campylobacter jejuni
F.
Borrelia burgdorferi
G.
Trypanosoma cruzi
H.
Rickettsia prowazekii
I.
Bartonella henselae
J.
Spirillum minus
Spirillum minus
A zoonosis associated with hepatitis, jaundice, conjunctival injection and renal impairment. Transmission normally occurs by direct contact with either the urine or tissues of an infected animal.
A.
Rheumatic fever
B.
Leptospirosis
C.
Brucellosis
D.
Tularaemia
E.
Lyme disease
F.
Listeriosis
G.
Meningococcal Septicaemia
Leptospirosis
A 22 year old student, who returned from a holiday in the Mediterranean 3 weeks ago, presents with an undulant fever, malaise, weakness and generalized bone pain. Upon examination lymphadenopathy and hepatosplenomegaly are also noted.
A.
Rheumatic fever
B.
Leptospirosis
C.
Brucellosis
D.
Tularaemia
E.
Lyme disease
F.
Listeriosis
G.
Meningococcal Septicaemia
Brucellosis
A 25 year old Maltese man presented to his GP with lethargy for a month and headaches and fever. On examination, he had a temperature of 39°C and one fingerbreadth splenomegaly. Small Gram-negative coccobacilli were seen on culture in Casteneda’s medium.
A.
Brucella abortus
B.
Rickettsia typhi
C.
Leishmania major.
D.
Yersina pestis
E.
Leptospira interrogans
F.
Rabies
G.
Bacillus anthracis
H.
Borrelia burgdorferi
I.
Brucella melitensis
Brucella melitensis
A tanner on holiday from India presented to hospital with an ulcerating papule on his hand. On inspection of the ulcer, the centre was black and necrotic. Gram-positive rods grew on blood agar culture and responded to treatment with large doses of penicillin.
A.
Brucella abortus
B.
Rickettsia typhi
C.
Leishmania major.
D.
Yersina pestis
E.
Leptospira interrogans
F.
Rabies
G.
Bacillus anthracis
H.
Borrelia burgdorferi
I.
Brucella melitensis
Bacillus anthracis
A 21 year old man presents at his GP complaining of an itchy, scaly rash on the soles of his feet. Skin scrapings are taken and sent away for microscopic examination. Which fungi might be identified?
A.
Corynebacterium minutissimum
B.
Candida albicans
C.
Aspergillus flavus
D.
Epidermophyton floccosum
E.
Cryptococcus neoforms
F.
Pityrosporum orbiculare
G.
Histoplasmosis capsulatum
H.
Pneumocystis carinii
I.
Trichophytum rubrum
richophyton rubrum as it is the commonest fungus from feet. If there was laceration and lots of blisters then it will be Trichophyton interdigitale.
A 55 year old farmer is seen in the Oncology clinic with a diagnosis of hepatocellular carcinoma. He is a lifelong teetotal and his virology has all been negative. Which fungus may have indirectly been a cause of his cancer?
A.
Corynebacterium minutissimum
B.
Candida albicans
C.
Aspergillus flavus
D.
Epidermophyton floccosum
E.
Cryptococcus neoforms
F.
Pityrosporum orbiculare
G.
Histoplasmosis capsulatum
H.
Pneumocystis carinii
I.
Trichophytum rubrum
Aspergillus flavus
A 17 year old Nigerian girl presents at her GP with patches of hypopigmentation on her trunk. After an initial trial of steroid cream, the girl returns complaining that the rash is spreading. Woods lamp examination of the rash produces a yellow fluorescence. What is the causative fungus?
A.
Corynebacterium minutissimum
B.
Candida albicans
C.
Aspergillus flavus
D.
Epidermophyton floccosum
E.
Cryptococcus neoforms
F.
Pityrosporum orbiculare
G.
Histoplasmosis capsulatum
H.
Pneumocystis carinii
I.
Trichophytum rubrum
Pityrosporum orbiculare
Which fungi is normally associated groin infection?
E floccusum is normally associated with GROIN infections, the old joke with Rugby players’ groins
A 23 year old female on a camping holiday used the local rowing club showers nearby. A few days later she noticed an itchy sensation between some her toes. What is the most likely diagnosis?
A.
Pediculosis capitis
B.
Blastomyosis
C.
Zygomycosis
D.
Chromomycosis
E.
Mycetoma (Madura foot)
F.
Tinea cruris
G.
Tinea corporis
H.
Tinea pedis
I.
Candidiasis
J.
Aspergillosis
K.
Cryptococcis
L.
Sporotrichosis
M.
Coccidiodomyosis
Tinea pedis
A 45 year old female whose main hobby was pigeon racing was noted by her GP to an enlarged lymph node in her neck. What is the most likely diagnosis?
A.
Pediculosis capitis
B.
Blastomyosis
C.
Zygomycosis
D.
Chromomycosis
E.
Mycetoma (Madura foot)
F.
Tinea cruris
G.
Tinea corporis
H.
Tinea pedis
I.
Candidiasis
J.
Aspergillosis
K.
Cryptococcis
L.
Sporotrichosis
M.
Coccidiodomyosis
Cryptococcus neoformans, is a pathogenic fungus commonly found in pigeon droppings and pigeon nests (and also soil). The predominant clinical process usually in immunocompromised pts, is a variably subacute meningitis with occasional patients showing features of brain abscess or inflammatory cerebral vasculitis, so the clinical feats are usually - headache, fever, nausea, neck stiffness, feats of raised ICP. Histoplasmosis, is also spread from bird droppings -but apparently not so specific to pigeons. Disseminated histoplasmosis, as you correctly state can cause lymphadenopathy (resembles disseminated TB - fever, weight loss, lymph nodes). PS. Remember India Ink staining for cryptococcus, which is often a clue in questions.
What are the identifiers for the different strains of brucella?
Abortus comes from cattle
Melitensis comes from goats, seen in the Mediterranean region
A 19 year-old student presents to her GP with a macular rash and suboccipital lymphadenopathy. She also complains of pain on moving her hands and wrists.
A.
Tuberculous arthritis
B.
Staphylococcal osteomyelitis
C.
Infectious mononucleosis
D.
Staphylococcal arthritis
E.
Candidiasis
F.
Rubella
G.
Viral hepatitis
H.
Gonococcal arthritis
I.
Lyme disease
J.
Tuberculous osteomyelitis
K.
Brodie’s abscess
Rubella
Mr PD, a 26 year old musician, arrives in A&E with a warm, painful abscess on his inner upper forearm surrounded by puncture marks, he has a low grade fever. He reports no problem in playing his guitar, but does forget lyrics on stage.
A.
Clutton’s joints
B.
Pott’s disease
C.
Osteoporosis
D.
Septic arthritis
E.
Staphylococcus osteomyelitis
F.
Tuberculous osteomyelitis
G.
Painful crisis
H.
Brodie’s abscess
I.
Leukaemia
J.
Paget’s disease
K.
Salmonella osteomyelitis
L.
Lateral epicondylitis
Salmonella osteomyelitis
Salmonella is a very rare cause of osteomyelitis, except in sickle cell disease. If you look up salmonella osteomyelitis, this is striking. It is suggested that the peculiar susceptibility of patients with sickle cell anaemia to salmonella osteomyelitis is due to spread of salmonella from the intestine facilitated by devitalisation of gut caused by intravascular sickling, and that infarcts in bone became infected either by transient bacteraemia or by activation of dormant foci of salmonella in bone marrow when tissues are devitalised. It is further suggested that immunological defects in sicklers may impair host response to infection, while haemolysis and hepatic dysfunction, both of which occur in sickle cell anaemia, favour propagation of salmonellae.
A 10 year old boy presents with moderate pain in his lower leg, little redness and swelling, remitting for 6 months. His mother gives you the X-ray report from the previous episode, which showed “a well defined ovoid shape with a surrounding sclerotic margin but little involucrum in his tibia”.
A.
Clutton’s joints
B.
Pott’s disease
C.
Osteoporosis
D.
Septic arthritis
E.
Staphylococcus osteomyelitis
F.
Tuberculous osteomyelitis
G.
Painful crisis
H.
Brodie’s abscess
I.
Leukaemia
J.
Paget’s disease
K.
Salmonella osteomyelitis
L.
Lateral epicondylitis
Brodie’s abscess
A 30 year old builder develops abdominal pain and diarrhoea 48 hours after having Texa Fried Chicken. Faecal culture shows motile, oxidase-positive colonies and gram stain shows gram-negative rods.
A.
Salmonella typhi
B.
Staphylococcus aureus
C.
Neisseria meningitides
D.
Streptococcus pneumoniae
E.
Haemophilus influenzae
F.
Campylobacter jejuni
G.
Clostridium difficile
H.
Escherichia coli
C jejuni
A 55 year old man comes into A&E complaining of a increasing difficulty in opening is mouth and that the muscles on his face occasionally spasm. On examination you observe that his eyes are partially closed and that the angles of his mouth are stretched outwards and slightly downwards. You also note that he has a very rigid abdomen. Which treatment option should be carried out first for this patient?
A.
Airborne contamination
B.
Heart valve replacement
C.
Escherichia coli
D.
Oral administration of ampicillin
E.
Staphylococcal aureus
F.
Oral administration with penicillin G
G.
Drainage and evacuation of pus
H.
Implantation of a prosthetic hip
I.
Streptococcus pneumoniae
J.
Haemophilus influenzae
K.
I. V. injection of tetanus antitoxin
L.
Oral administration of flucloxacillin
I. V. injection of tetanus antitoxin
Which of the above is an example where prophylactic systemic antibiotic therapy should not be used.
A.
Airborne contamination
B.
Heart valve replacement
C.
Escherichia coli
D.
Oral administration of ampicillin
E.
Staphylococcal aureus
F.
Oral administration with penicillin G
G.
Drainage and evacuation of pus
H.
Implantation of a prosthetic hip
I.
Streptococcus pneumoniae
J.
Haemophilus influenzae
K.
I. V. injection of tetanus antitoxin
L.
Oral administration of flucloxacillin
M.
Removal of a breast carcinoma
Removal of a breast carcinoma
A man is recovering from surgery and inspection of the wound reveals that it has become infected. A swab is taken and the laboratory results show Staphylococcal aureus infection. What is appropriate treatment for this man?
A.
Airborne contamination
B.
Heart valve replacement
C.
Escherichia coli
D.
Oral administration of ampicillin
E.
Staphylococcal aureus
F.
Oral administration with penicillin G
G.
Drainage and evacuation of pus
H.
Implantation of a prosthetic hip
I.
Streptococcus pneumoniae
J.
Haemophilus influenzae
K.
I. V. injection of tetanus antitoxin
L.
Oral administration of flucloxacillin
M.
Removal of a breast carcinoma
Oral administration of flucloxacillin
An 80 year old man returns to his GP two weeks after being prescribed co-trimoxazole for a UTI. His urinary symptoms have now eased, but he is still experiencing a fever. His blood count shows eosinophilia.
A.
Hodgkin’s lymphoma
B.
Hepatitis B
C.
Mycobacterium tuberculosis
D.
Hepatitis C
E.
Escherichia coli
F.
Brucellosis
G.
SLE
H.
Mycobacterium avium complex
I.
Sarcoidosis
J.
Plasmodium malariae
K.
Epstein-Barr virus
L.
Drug induced fever
M.
Hepatitis A
Drug induced fever
A 19 year-old student presents to her GP with a macular rash and suboccipital lymphadenopathy. She also complains of pain on moving her hands and wrists. Why is this Rubella? I thought this is a typical descrption of Infectious Mononucleosis.
The patient is female. Rubella is followed by a reactive polyarthritis in a RA-like distribution (PIP, MCP, wrist) in 50% of women and 6% of men. If she hasn’t had MMR, do a pregnancy test!
Viral causes of reactive arthritis
Rubella
Hep B
Parvovirus B19
Bacterial causes of reactive arthritis
INcludes Reiter’s which can be post-dysentry or post-urethritis
Dysentry: shigella, salmonella, yesrisina, campylobacter (which can also be a precedent of GBS)
Urethritis: CHlamydia, Ureaplasma
Other: GAS, N. gonorrhoea, brucella, TB
Peri-infectious causes of reactive arthritis
Borrelia burdorferia
Rheumatic fever
Poncet’s disease
Reactive arthritis as a consequence of TB infection
Aseptic form of arthritis observed in patients with TB
Brodie’s abscess
A Brodie abscess is a subacute osteomyelitis, which may persist for years before converting to a frank osteomyelitis. Classically, this may present after conversion as a draining abscess extending from the tibia out through the shin.Occasionally acute osteomyelitis may be contained to a localized area and walled off by fibrous and granulation tissue.This is termed as Brodie’s abscess.
Most frequent causative organism is Staphylococcus aureus.
Clutton’s joints
Clutton’s joints is a term describing the finding of symmetrical joint swelling seen in patients with congenital syphilis. It most commonly affects the knees, presenting with synovitis and joint effusions (collections of fluid within the joint capsules) lasting up to a year. It has also been reported affecting the ankles, elbows, wrists and fingers. It is usually painless, although pain in the absence of trauma can occur in a few cases. There is usually no disability associated with the joint swelling, and recovery is usually complete. It occurs between 5 and 20 years of age in both sexes.
These infections are almost invariably associated with functional or anatomical abnormalities of the renal tract. Tip: also causes cavitating pneumonia.
A.
Ceftriaxone
B.
Gentamicin
C.
Staph epidermidis
D.
Ceftazidime
E.
Staph saprophyticus
F.
Trimethoprim
G.
Ciprofloxacin
H.
Escherichia coli
I.
Tuberculosis
J.
Nitrofurantoin
K.
Adenovirus
L.
Candida
M.
Klebsiella
N.
Piperacillin
O.
Ampicillin
P.
Pseudomonas
Klebsiella
The 2nd commonest cause of uncomplicated UTI in young women
A.
Ceftriaxone
B.
Gentamicin
C.
Staph epidermidis
D.
Ceftazidime
E.
Staph saprophyticus
F.
Trimethoprim
G.
Ciprofloxacin
H.
Escherichia coli
I.
Tuberculosis
J.
Nitrofurantoin
K.
Adenovirus
L.
Candida
M.
Klebsiella
N.
Piperacillin
O.
Ampicillin
P.
Pseudomonas
Staph Saprophyticus
an be used as monotherapy for acute pyelonephritis and should always be prescribed orally because its bioavailability is near 100% and iv dosing is 30 times more expensive.
A.
Ceftriaxone
B.
Gentamicin
C.
Staph epidermidis
D.
Ceftazidime
E.
Staph saprophyticus
F.
Trimethoprim
G.
Ciprofloxacin
H.
Escherichia coli
I.
Tuberculosis
J.
Nitrofurantoin
K.
Adenovirus
L.
Candida
M.
Klebsiella
N.
Piperacillin
O.
Ampicillin
P.
Pseudomonas
Ciprofloxacin
Causes haemorrhagic cystitis in children.
A.
Ceftriaxone
B.
Gentamicin
C.
Staph epidermidis
D.
Ceftazidime
E.
Staph saprophyticus
F.
Trimethoprim
G.
Ciprofloxacin
H.
Escherichia coli
I.
Tuberculosis
J.
Nitrofurantoin
K.
Adenovirus
L.
Candida
M.
Klebsiella
N.
Piperacillin
O.
Ampicillin
P.
Pseudomonas
Adenovirus
A cephalosporin used for treating pseudomonal infections in cystic fibrosis
A.
Ceftriaxone
B.
Gentamicin
C.
Staph epidermidis
D.
Ceftazidime
E.
Staph saprophyticus
F.
Trimethoprim
G.
Ciprofloxacin
H.
Escherichia coli
I.
Tuberculosis
J.
Nitrofurantoin
K.
Adenovirus
L.
Candida
M.
Klebsiella
N.
Piperacillin
O.
Ampicillin
P.
Pseudomonas
Ceftazidime
In combination with iv ampicillin, this drug is used iv for very sick patients with obstructed infected upper UTIs and gram negative septicaemia.
A.
Ceftriaxone
B.
Gentamicin
C.
Staph epidermidis
D.
Ceftazidime
E.
Staph saprophyticus
F.
Trimethoprim
G.
Ciprofloxacin
H.
Escherichia coli
I.
Tuberculosis
J.
Nitrofurantoin
K.
Adenovirus
L.
Candida
M.
Klebsiella
N.
Piperacillin
O.
Ampicillin
P.
Pseudomonas
Gentamicin
Given IM as a single shot for gonococcal urethritis
A.
Ceftriaxone
B.
Gentamicin
C.
Staph epidermidis
D.
Ceftazidime
E.
Staph saprophyticus
F.
Trimethoprim
G.
Ciprofloxacin
H.
Escherichia coli
I.
Tuberculosis
J.
Nitrofurantoin
K.
Adenovirus
L.
Candida
M.
Klebsiella
N.
Piperacillin
O.
Ampicillin
P.
Pseudomonas
Ceftriaxone
A 40-year-old Indian male presents to A&E with dysuria and back pain. He has recently noticed blood in his urine and his past medical history reveals that he has had hypertension for 5 years. After some initial reluctance, he admits to having HIV, which was diagnosed on his arrival in the UK 7 years previously.
A.
Inadequately treated UTI
B.
Cystitis
C.
Calculi
D.
Acute Prostatitis
E.
Acute Pyelonephritis
F.
Papillary Necrosis from Analgaesic Overdose
G.
Bladder Tumour
H.
Interstitial Nephritis
I.
Urethral Syndrome
J.
Polycystic Kidney
K.
Intrarenal Abscess
L.
Renal Tuberculosis
M.
Perinephric Abscess
Renal Tuberculosis
A 23-year-old Caucasian women presents to her GP with urinary frequency, urgency and burning. She also complained of slow stream as well as suprapubic pain. She has had several UTIs in the past and analysis of her urine showed no significant bacteruria.
A.
Inadequately treated UTI
B.
Cystitis
C.
Calculi
D.
Acute Prostatitis
E.
Acute Pyelonephritis
F.
Papillary Necrosis from Analgaesic Overdose
G.
Bladder Tumour
H.
Interstitial Nephritis
I.
Urethral Syndrome
J.
Polycystic Kidney
K.
Intrarenal Abscess
L.
Renal Tuberculosis
M.
Perinephric Abscess
Urethral Syndrome
A 42-year-old African American male presents to A&E with severe loin pain that radiates to the groin. He complains of painful urination, interrupted flow and increased urinary frequency. Urine dipstick reveals the presence of leucocytes, nitrites, haematuria and proteinuria. Intravenous uretogram shows a filling defect of the right kidney.
A.
Inadequately treated UTI
B.
Cystitis
C.
Calculi
D.
Acute Prostatitis
E.
Acute Pyelonephritis
F.
Papillary Necrosis from Analgaesic Overdose
G.
Bladder Tumour
H.
Interstitial Nephritis
I.
Urethral Syndrome
J.
Polycystic Kidney
K.
Intrarenal Abscess
L.
Renal Tuberculosis
M.
Perinephric Abscess
Calculi
A 63 year old gentleman has a two day history of fever and rigors with lower back pain and discomfort on passing urine. Urine microscopy and culture revealed 2 x 104 Escherichia Coli per ml urine.
Bacterial prostatitis
A 40 year old lady was previously diagnosed with acute UTI and treated with trimethoprim. Ten days later she returns to her GP with the same symptoms of dysuria and frequency, and urine microscopy reveals a positive culture of the same bacteria.
A relapse of a UTI implies re-infection with the SAME organism. Recurrent UTIs imply infection with DIFFERENT organisms. A sterile pyuria occurs in renal tuberculosis. A urine culture must show >/= 1 x 10^5 colony-forming units (CFU) / mL of mixed bacterial growth with one predominant organism to be diagnostic of a UTI. (OR (for interested persons) 1 x 10^4 if just one organism, or 1 x 10^3 if E.coli or S.saprophiticus).
A 74 year old male is soon to undergo colorectal surgery and hospital procedures of antibiotic prophylaxis is followed.
Cef. & Met. 0-2hrs before incision & no longer than 24 hrs post-surgery
An 18 year old boy with cystic fibrosis recently underwent a knee operation. After a couple of days recovering in the ward he starts to wheeze, becomes breathless and coughs up sputum. He has a fever and blood cultures indicate the presence of gram-negative bacteria.
A.
Hepatitis C
B.
MRSA
C.
Salmonella
D.
Amphotericin B
E.
Clostridium difficile
F.
Urinary Tract Infection
G.
Endocarditis
H.
Aspergillus Fumigatis
I.
Staph. aureus
J.
Toxoplasma gondi
K.
Legionella
L.
Burkholderia cepacia
M.
Pneumocystis pneumonia
Burkholderia cepacia
A 50-year-old man was admitted with acute pancreatitis and underwent emergency pancreatectomy. He was in ITU for four weeks for respiratory support where he remained febrile and septic. Blood cultures and wound swabs grew gram-positive cocci in chains, which grew on MacConkey plate and was aesculin-positive. This isolate was also resistant to the conventional anti-streptococcal antibiotics.
A.
Pseudomonas aeruginosa
B.
Rotavirus
C.
Salmonella enteridis
D.
Vancomycin-resistant enterococcus(VRE)
E.
Respiratory syncytial virus
F.
Herpes Simplex, Type 1
G.
Methicillin-resistant S. aureus (MRSA)
H.
Streptococcus Group A
I.
Klebsiella pneumoniae
J.
Streptococcus viridans
K.
Bacillus subtilis
Vancomycin-resistant enterococcus(VRE)
A patient with 20% burns with open wounds is awaiting skin grafting. The wound swab grew gram-negative bacilli that produced a green pigment and was oxidase-positive. A similar organism was isolated from other patients on the same unit. Bacteriological typing subsequently proved all the isolates were of the same type
A.
Pseudomonas aeruginosa
B.
Rotavirus
C.
Salmonella enteridis
D.
Vancomycin-resistant enterococcus(VRE)
E.
Respiratory syncytial virus
F.
Herpes Simplex, Type 1
G.
Methicillin-resistant S. aureus (MRSA)
H.
Streptococcus Group A
I.
Klebsiella pneumoniae
J.
Streptococcus viridans
K.
Bacillus subtilis
Pseudomonas aeruginosa
Sitting in on your consultant’s GUM clinic, you see a shy 30-year-old woman who admits to losing her virginity a week ago and now is worried about the appearance of insect bite-like marks in her genital region and a concurrent fever. On intense questioning, she reveals that her partner seemed to have a painful sore on his penis.
A.
Chlamidiae Pneumoniae
B.
Chlamydiae Trachomatis
C.
Syphilis
D.
HIV
E.
Non-gonococcal urethritis
F.
HSV type 2
G.
Lymphogranuloma venereum
H.
Gonorrhoea-associated salpingitis
I.
Chlamidiae Psittacosis
J.
Gonococcal conjunctivitis
K.
Disseminated gonococcal infection
L.
Chancroid
HSV 2
On Tuesday, a confident African friend comes to you for advice. He has noticed a painful ulcer on his penis, from which he has helpfully collected exudate. Sneaking into the labs at Chelsea & Westminster late one evening, you culture this. Later, you note the presence of Haemophilus ducreyi.
A.
Chlamidiae Pneumoniae
B.
Chlamydiae Trachomatis
C.
Syphilis
D.
HIV
E.
Non-gonococcal urethritis
F.
HSV type 2
G.
Lymphogranuloma venereum
H.
Gonorrhoea-associated salpingitis
I.
Chlamidiae Psittacosis
J.
Gonococcal conjunctivitis
K.
Disseminated gonococcal infection
L.
Chancroid
Chancroid
NB re Trimethoprim in pregnancy
Trimethoprim is one of the commonly used antibiotics to treat UTIs. However it is contraindicated in early pregnancy because of teratogenic risks (as it is a folate antagonist). Recommendations for the treatment of UTI in pregnancy vary between hospitals. Nitrofurantoin, amoxicillin or cephalexin may be used. Nitrofurantoin should be avoided at term as it may produce neonatal haemolysis.
How do quinacrine and tetracycline delay prion conversion
Both quinacrine and tetracycline have been shown in vitro to directly bind to and prevent polymerisation of prion protein. Therefore these are not acting in the way they work against parasites and bacteria respecitvely, but instead interact directly with the abnormal prion protein.
Mx of meningitis
If you know it is Neisseria- ben pen
If you do not know the answer, broader spectrum therefore ceftriaxone
DDx for ring enhancing lesion
cerebral abscess, tuberculoma, toxoplasmosis and sometimes CNS lymphoma. The ring usually represents vasogenic oedema.
What differentiates between S. haematobium and S. Mansone
The initial histories are liable to be similar - travel, contact with fresh water and associated swimmer’s itch then a period of 3-4 weeks symptom free then fever, rash, myalgia and possible pneumonitis (these more often in travellers than the local population) The only possible difference so far is that you are apparently able to pick up Mansoni infection from trips to the carribean and south america as well as Africa/Middle East unlike Haematobium (Africa/Middle east only) The difference then comes in that Haematobium infection typically migrates to the bladder (strictly, the vesical VEINS) and presents with painless haematuria which then progresses into LUTS and ascending urinary problems and rarely lung and neuro involvement. According to Underwood you can get right sided colon involvement from haematobium but this is less likely. Mansoni however prefers the bowel (strictly, the mesenteric VEINS which are part of the portal circulation) and so presents with bloody diarrhoea, progressive ulceration potentially up to strictures. Involvement is normally left sided but right sided infection does happen. Eggs end up in the liver via the portal circulation and present with a hepatitis and portal hypertension. - So in brief Mansoni - bowel and liver, Haematobium - bladder
A 45 year old female presents with fever. O/E she is pyrexial, has hepatosplenomegaly, lymphadenopathy and a severely swollen eyelid. She returned from Guatemala 2 days ago.
A.
Giardia lamblia
B.
Chagas Disease
C.
Tuberculosis
D.
Schistosomiasis
E.
Plasmodium malariae
F.
Plasmodium vivax
G.
Dengue fever
H.
Mucocutaneous Leishmaniasis
I.
Amoebiasis
J.
Tropical sprue
K.
Plasmodium falciparum
Chagas Disease
A 35 year old male complains of a persistent ulcer in the mucosa of the mouth. When questioned further admits to remembering a small ulcer on his upper arm which healed without treatment when holidaying in Brazil one year ago.
A.
Giardia lamblia
B.
Chagas Disease
C.
Tuberculosis
D.
Schistosomiasis
E.
Plasmodium malariae
F.
Plasmodium vivax
G.
Dengue fever
H.
Mucocutaneous Leishmaniasis
I.
Amoebiasis
J.
Tropical sprue
K.
Plasmodium falciparum
Mucocutaneous Leishmaniasis
A 45 year-old Egyptian male complains of haematuria. On further investigation, cystoscopy reveals a squamous cell carcinomatous lesion.
A.
Mycobacterium leprae
B.
Hepatitis B virus
C.
Trypanosoma brucei rhodesiense
D.
Schistosoma haematobium
E.
Wuchereria bancrofti
F.
Plasmodium falciparum
G.
Salmonella typhi
H.
Schistosoma mansoni
I.
Leishmania donovani
J.
Pneumocystis carinii
K.
Trypanosoma brucei gambiense
Schistosoma haematobium
A 23 year-old female presents with headache and fever 6 weeks after returning from her gap year.
A.
Mycobacterium leprae
B.
Hepatitis B virus
C.
Trypanosoma brucei rhodesiense
D.
Schistosoma haematobium
E.
Wuchereria bancrofti
F.
Plasmodium falciparum
G.
Salmonella typhi
H.
Schistosoma mansoni
I.
Leishmania donovani
J.
Pneumocystis carinii
K.
Trypanosoma brucei gambiense
Plasmodium falciparum
An African woman and her 33 year-old husband come to their doctor because she is worried that he is not as alert as he used to be. On examination, he has non-tender lymphadenopathy, hepatomegaly and marked CNS abnormalities. He is noted to be quite lethargic.
A.
Mycobacterium leprae
B.
Hepatitis B virus
C.
Trypanosoma brucei rhodesiense
D.
Schistosoma haematobium
E.
Wuchereria bancrofti
F.
Plasmodium falciparum
G.
Salmonella typhi
H.
Schistosoma mansoni
I.
Leishmania donovani
J.
Pneumocystis carinii
K.
Trypanosoma brucei gambiense
Trypanosoma brucei gambiense
A thin peripheral blood film from a 59 year-old female demonstrates eosinophilia and microfilariae. On examination, the skin overlying her superficial lymph nodes is streaky red and tender.
A.
Mycobacterium leprae
B.
Hepatitis B virus
C.
Trypanosoma brucei rhodesiense
D.
Schistosoma haematobium
E.
Wuchereria bancrofti
F.
Plasmodium falciparum
G.
Salmonella typhi
H.
Schistosoma mansoni
I.
Leishmania donovani
J.
Pneumocystis carinii
K.
Trypanosoma brucei gambiense
Wuchereria bancrofti
A 43 year-old Asian male with AIDS presents with a prolonged fever, dizziness and a persistent cough. On examination, he is found to have marked splenomegaly and rough, dry skin. Blood results reveal pancytopenia.
A.
Mycobacterium leprae
B.
Hepatitis B virus
C.
Trypanosoma brucei rhodesiense
D.
Schistosoma haematobium
E.
Wuchereria bancrofti
F.
Plasmodium falciparum
G.
Salmonella typhi
H.
Schistosoma mansoni
I.
Leishmania donovani
J.
Pneumocystis carinii
K.
Trypanosoma brucei gambiense
Leishmania donovani
A 5 year-old girl presents unconscious and unrousable. Neck rigidity is not present and kernig’s sign is negative. She dies 3 hours after presentation.
A.
Visceral leishmaniasis (kala-azar)
B.
Giadiasis
C.
Trypanosomiasis
D.
Miliary tuberculosis
E.
Amoebic dysentery
F.
Severe malaria
G.
Cutaneous leishmaniasis
H.
Trichuris trichiura
I.
Chagas disease
J.
Brain worm
K.
Pulmonary tuberculosis
Severe malaria
A 20 year-old man presents with a persisting intermittent fever which began whilst he was travelling in South America the previous week. He has a dry cough and a massively enlarged spleen. Sandfly parasites are detected in a spleen aspirate.
A.
Visceral leishmaniasis (kala-azar)
B.
Giadiasis
C.
Trypanosomiasis
D.
Miliary tuberculosis
E.
Amoebic dysentery
F.
Severe malaria
G.
Cutaneous leishmaniasis
H.
Trichuris trichiura
I.
Chagas disease
J.
Brain worm
K.
Pulmonary tuberculosis
Visceral leishmaniasis (kala-azar)
A 16 yr old boy complains of a one week history of fever, muscle aches, nausea/vomiting/diarrhoea with general malaise following a trip to Zimbabwe visiting relatives. On further questioning he remembers developing an itchy rash on his right thigh following wading in Lake Kariba whilst on holiday. O/E He has generalised lymphadenopathy with hepatosplenomegaly. Initial blood tests reveal raised WCC with eosinophillia.
A.
Loa-Loa
B.
Plasmodium falciparum
C.
Toxoplasma gondii
D.
Entamoeba histolytica
E.
Enchinococcus granulosus
F.
Giardia lamblia
G.
Leishmania donovani
H.
Wucheria bancrofti
I.
Clonorchis sinensis
J.
Trichinella spiralis
K.
Ancylostoma duodenale
L.
Taenia saginata
M.
Schistosoma mansoni
Schistosoma mansoni
A 25 yr old female humanitarian volunteer complaining of swinging fever, profound abdominal pain with severe malaise. On further questioning she reveals a history of self limiting diarrhoeal illness 3/52 ago during which she passed mucus and some blood. You are also informed she recently returned from a humanitarian mission to Ghana 6/52 ago. O/E she is unwell with exquisitely tender hepatomegaly. You also find increased breath sounds and a dull percussion note in the lower region of the right lung.
A.
Loa-Loa
B.
Plasmodium falciparum
C.
Toxoplasma gondii
D.
Entamoeba histolytica
E.
Enchinococcus granulosus
F.
Giardia lamblia
G.
Leishmania donovani
H.
Wucheria bancrofti
I.
Clonorchis sinensis
J.
Trichinella spiralis
K.
Ancylostoma duodenale
L.
Taenia saginata
M.
Schistosoma mansoni
Entamoeba histolytica
A 24 yr old male complaining of 3/52 history of fever/chills with muscular aches and spasms. On further questioning he reveals the he also an episode of diarrhoea/vomiting with a headache lasting 48hrs. This followed his participation in an amateur eating competition 1/12 ago, during which he may have eaten some improperly cooked pork. O/E he has marked periorbital oedema with conjunctivitis. Blood tests reveal a marked eosinophillia, while gastrocnemius biopsy demonstrates the presence of encysted larvae.
A.
Loa-Loa
B.
Plasmodium falciparum
C.
Toxoplasma gondii
D.
Entamoeba histolytica
E.
Enchinococcus granulosus
F.
Giardia lamblia
G.
Leishmania donovani
H.
Wucheria bancrofti
I.
Clonorchis sinensis
J.
Trichinella spiralis
K.
Ancylostoma duodenale
L.
Taenia saginata
M.
Schistosoma mansoni
Trichinella spiralis
An acutely unwell 42 yr old male presents to A&E with high fever accompanied by chills, sweats and vomiting with a 24 hour history. O/E he is clinically jaundiced with cool clammy skin. He is tachypnoeic and tachycardic. You note hepatosplenomegaly and that he is producing small amounts of dark brown urine in his catheter bag. His wife tells you that they recently returned from safari in Tanzania 10 days ago.
A.
Loa-Loa
B.
Plasmodium falciparum
C.
Toxoplasma gondii
D.
Entamoeba histolytica
E.
Enchinococcus granulosus
F.
Giardia lamblia
G.
Leishmania donovani
H.
Wucheria bancrofti
I.
Clonorchis sinensis
J.
Trichinella spiralis
K.
Ancylostoma duodenale
L.
Taenia saginata
M.
Schistosoma mansoni
Plasmodium falciparum
A 32 yr old female complaining of the presence of small pale bodies in her stools on a number of occasions. On further questioning she admits some occasional mild epigastric pain over the past 4/12. O/E she appears clinically well. There is no significant travel history.
A.
Loa-Loa
B.
Plasmodium falciparum
C.
Toxoplasma gondii
D.
Entamoeba histolytica
E.
Enchinococcus granulosus
F.
Giardia lamblia
G.
Leishmania donovani
H.
Wucheria bancrofti
I.
Clonorchis sinensis
J.
Trichinella spiralis
K.
Ancylostoma duodenale
L.
Taenia saginata
M.
Schistosoma mansoni
Taenia saginata
A 25yr old man who had recently returned from travel in Afrcia presented with fever, diarrhoea and hepatoslenomegaly. He also noted skin changes which had developed over the past month.
A.
African trypanosomiasis
B.
Babesiosis
C.
Toxoplasmosis
D.
American trypanosomiasis
E.
Ameobiasis
F.
Giardiasis
G.
Vivax malaria
H.
Visceral Leishmania
I.
Cryptosporidiosis
J.
Trichomoniasis
K.
Falciparum malaria
Visceral Leishmania
A 40 yr old Indian lady who was vacationing in the UK presented with fever which followed no particular pattern, vomiting and the production of brown-black urine.
A.
African trypanosomiasis
B.
Babesiosis
C.
Toxoplasmosis
D.
American trypanosomiasis
E.
Ameobiasis
F.
Giardiasis
G.
Vivax malaria
H.
Visceral Leishmania
I.
Cryptosporidiosis
J.
Trichomoniasis
K.
Falciparum malaria
Falciparum malaria
A 25 year old man presents with weight loss and diarrhoea. He has recently been on holiday in India. On examination of his stool cysts and “tear-drop” shaped trophozoites are present.
A.
Naegleria fowleri
B.
Cryptosporidium parvum
C.
Entamoeba histolytica
D.
Trypanosoma gambiense
E.
Plasmodium falciparum
F.
Leishmania donovani
G.
Trichomonas vaginalis
H.
Trypanosoma cruzi
I.
Giardia lamblia
J.
Toxoplasma gondii
K.
Trypanosoma rhodesiense
Giardia lamblia
A 10 year old girl presents with fever, hepatomegaly, splenomegaly and anaemia. She recently emigrated from the Sudan. Her mother tells you that 6 months ago the girl developed dark patches on her hands and forehead.
A.
Naegleria fowleri
B.
Cryptosporidium parvum
C.
Entamoeba histolytica
D.
Trypanosoma gambiense
E.
Plasmodium falciparum
F.
Leishmania donovani
G.
Trichomonas vaginalis
H.
Trypanosoma cruzi
I.
Giardia lamblia
J.
Toxoplasma gondii
K.
Trypanosoma rhodesiense
Leishmania donovani
An 18 month old girl from Brazil sees you whilst on a short holiday in Britain. Her parents are worried because she appears to have had fever for the last few weeks, seems more tired and out of spirits than usual, has loss of appetite, vomiting and diarrhoea and complains of pains in her legs. On examination she has general lymphadenitis and non-pitting oedema in her legs and feet. Her Machado-Guerreiro test is positive.
A.
Naegleria fowleri
B.
Cryptosporidium parvum
C.
Entamoeba histolytica
D.
Trypanosoma gambiense
E.
Plasmodium falciparum
F.
Leishmania donovani
G.
Trichomonas vaginalis
H.
Trypanosoma cruzi
I.
Giardia lamblia
J.
Toxoplasma gondii
K.
Trypanosoma rhodesiense
Trypanosoma cruzi
An infant is diagnosed with pneumonia in her 5th day of life. Vaginal swabs from the mother as well as umbilical and oral swabs from the neonate showed a Gram positive coccus. The infant is given antibiotics and is monitored in hospital for a period of time until respiration and appetite improve.
A.
Group B Streptococci Syndrome
B.
Chlamydial conjunctivitis in the newborn
C.
Neonatal Herpes Simplex Infection
D.
E.Coli infection
E.
EBV-related infectious mononucleosis
F.
Neonatal Respiratory Tract Infection
G.
Conjunctivitis caused by a blocked tear duct
H.
Neonatal Meningitis
I.
Congenital Rubella Syndrome
J.
Congenital Toxoplasmosis
K.
Neonatal HIV infection
Group B Streptococci Syndrome
A French mother brings her 2 month old daughter with fever to hospital. The infant is shown to have elevated hepatic enzymes and is treated with pyrimethamine, sulphadiazine and folic acid for a year after appropriate investigations are performed.
A.
Group B Streptococci Syndrome
B.
Chlamydial conjunctivitis in the newborn
C.
Neonatal Herpes Simplex Infection
D.
E.Coli infection
E.
EBV-related infectious mononucleosis
F.
Neonatal Respiratory Tract Infection
G.
Conjunctivitis caused by a blocked tear duct
H.
Neonatal Meningitis
I.
Congenital Rubella Syndrome
J.
Congenital Toxoplasmosis
K.
Neonatal HIV infection
Congenital Toxoplasmosis
An infant is born prematurely and subsequently has low birth weight. In addition, he has encephalitis and vesicular skin lesions. Despite being recommended to have a caesarean due to active viral lesions, the mother refuses and the neonate was delivered vaginally. Emperic Acyclovir is given to the neonate.
A.
Group B Streptococci Syndrome
B.
Chlamydial conjunctivitis in the newborn
C.
Neonatal Herpes Simplex Infection
D.
E.Coli infection
E.
EBV-related infectious mononucleosis
F.
Neonatal Respiratory Tract Infection
G.
Conjunctivitis caused by a blocked tear duct
H.
Neonatal Meningitis
I.
Congenital Rubella Syndrome
J.
Congenital Toxoplasmosis
K.
Neonatal HIV infection
Neonatal Herpes Simplex Infection
A 2 week old female had an enlarged liver and spleen and her skin was tinged yellow. She was not eating much nor was she vomiting. She also suffered from regular seizures. Investigation revealed intra-cranial calcification.
A.
Viral meningitis
B.
Congenital toxoplasmosis
C.
Neonatal HSV infection
D.
Congenital rubella syndrome
E.
Listeria
F.
E. coli
G.
Group B streptococci
H.
Hepatitis B
I.
Chlamydial ophthalmia
J.
Bacterial meningitis
K.
Bordetella pertussis
L.
Chickenpoc (VZV)
Congenital toxoplasmosis
A newly born male presented with microphthalmia, deafness and hepatosplenomegaly. His platelet count was 50 x 10^9/L. In addition, rashes were noticed on his body. He suffers from SOB and is unable to finish feeding.
A.
Viral meningitis
B.
Congenital toxoplasmosis
C.
Neonatal HSV infection
D.
Congenital rubella syndrome
E.
Listeria
F.
E. coli
G.
Group B streptococci
H.
Hepatitis B
I.
Chlamydial ophthalmia
J.
Bacterial meningitis
K.
Bordetella pertussis
L.
Chickenpoc (VZV)
Congenital rubella syndrome
The CSF in a neonate showed a raised WCC, consisting mainly of polymorphs. Culture showed pneumococcus.
A.
Viral meningitis
B.
Congenital toxoplasmosis
C.
Neonatal HSV infection
D.
Congenital rubella syndrome
E.
Listeria
F.
E. coli
G.
Group B streptococci
H.
Hepatitis B
I.
Chlamydial ophthalmia
J.
Bacterial meningitis
K.
Bordetella pertussis
L.
Chickenpoc (VZV)
Bacterial meningitis
A prematurely born 1 week old infant presented with microcephaly, chorioretinitis and vesicular skin lesions. He also had non-specific features of fever, irritability and failure to feed.
A.
Viral meningitis
B.
Congenital toxoplasmosis
C.
Neonatal HSV infection
D.
Congenital rubella syndrome
E.
Listeria
F.
E. coli
G.
Group B streptococci
H.
Hepatitis B
I.
Chlamydial ophthalmia
J.
Bacterial meningitis
K.
Bordetella pertussis
L.
Chickenpoc (VZV)
Neonatal HSV infection
Treponemes in dark-ground microscopy is diagnostic
Syphilis
What is a consideration re chancroid?
Patients with a chancroid ulcer are more susceptible to contracting HIV
What treatment should be prescribed for a 25-year old lady complaining of pruritus and a creamy vaginal discharge?
Oral fluconazole
A neonate is referred and presents with skin lesions, lymphadenopathy and failure to thrive.
Syphilis
S. haematobium associated with
SCC of the bladder (5% of all baldder Ca)
If outside the setting of chronic schistosomiasis- TCC
Gram positive cocci
Staph: aureus, epidermis
Strep: pneumoniae, pyogenes
Gram positive bacilli
Bacillus
Clostridium
Cornyebacterium
Listeria
Gram negative bacilli
E Coli
Kleb
Proteus
Salmonella
Shigella
Yersinia
Pseudomonas
Bordatella
Haemophilus
Legionella
Gram negative comma shaped
Vibiro
Campylobacter
Helicobacter
Spiral shaped bacteria
Treponema
Borrelia
Cell-wall defiicient bacteria
Mycoplasma
Quelling reaction
pneumococci
are mixed with anti-serum and methylene blue causes the capsule
to swell can be visualized under the microscope. Optochin-sensitivity
also differentiates pneumococcus from Streptococcus viridans (also
α-haemolytic), which is optochin-insensitve.
What differntiates between strep pneumonia and strep viridans
Strep viridans are optochin insensitivie
What differntaties between staph and strep
Strep are catalse negative
Pontiac fever=
Milder Legionella infection
are aerobic Gram-negative diploccoci. This bacterium
is particularly problematic in patients with chronic lung disease and
causes exacerbations of chronic obstructive pulmonary disorder (COPD).
Other targets of infection include ears, eyes and central nervous system.
Moraxella catarrhalis
are obligate intracellular bacteria which
cause an atypical pneumonia or a mild bronchitis. A cold-agglutinin
test can be used for the diagnosis. In rare cases, infection may lead to
Stevenson–Johnson syndrome.
Mycoplasma pneumoniae
are Gram-negative bacilli that cause influenza
(flu) outbreaks annually. Chocolate agar is used as a culture medium.
Further oxidase and catalase tests are positive.
Haemophilus influenzae
Chlamydia pneumoniae
are obligate intracellular bacteria which
cause an atypical pneumonia. Less commonly, this infection can cause
meningoencephalitis, arthritis, myocarditis and/or Guillain–Barré
syndrome.
is a β-haemolytic anaerobic Gram-positive
rod that may cause outbreaks of non-invasive gastroenteritis. Sources
include refrigerated food and unpasteurized dairy products.
Listeria monocytogenes
are comma-shaped oxidase positive bacteria, causing
profuse watery diarrhoea containing no inflammatory cells on microscopy.
Transmission occurs via the faecal-oral route.
Vibrio cholerae
How does vibrio cholera cause profuse watery diarrhoea
No inflammation
Vibrio cholerae
colonizes the small intestinal section of the gut and secretes enterotoxin
containing subunits A (active) and B (binding). B subunit binds to GM1
ganglioside on the intestinal epithelial cells. Intracellularly, there is activation
of cAMP by A subunit, which causes active secretion of sodium
and chloride ions; as a consequence water is lost due to the osmotic
pull of NaCl.
A 35-year-old woman presents to accident and emergency with fever, diarrhoea
and signs of shock. Her husband mentions that she had attended a work colleague’s
barbeque the previous day. The consultant believes superantigens are
responsible for the patient’s condition.
A Vibrio cholerae
B Staphylococcus aureus
C Enterobacteriaecae
D Listeria monocytogenes
E Salmonella enteritidis
F Shigellae
G Campylobacter jejuni
H Giardia lamblia
I Entamoeba histolytica
Staphylococcus aureus (B) are β-haemolytic Gram-positive cocci
arranged in grape-like clusters. In the gastrointestinal tract, S. aureus
produces the exotoxin TSST-1, which acts as a superantigen causing
non-specific activation of T cells and subsequent release of IL-1, IL-2
and TNF-α. A massive non-specific immune response follows causing
shock and multiple organ failure. Enterotoxin produced by bacteria
causes vomiting and diarrhoea 12–24 hours after the culprit food has
been consumed.
multiplies in
the Peyer’s patches of the small intestine. Clinical features include slow
onset fever, constipation and splenomegaly. Rose spots are pathognomonic.
Salmonella typhi
are oxidase positive, non-motile bacteria.
Transmission occurs via the faecal–oral route, generally due to contamination
by dog faecal matter, causing a watery, foul smelling diarrhoea.
Complications include Guillain–Barré syndrome and Reiter’s syndrome.
Campylobacter jejuni
is a motile trophozite. Ingestion of the cysts
leads to colonization of caecum and colon, which may cause a ‘flaskshaped’
ulcer to develop. Clinical features involve dysentery, chronic
weight loss and liver abscess formation.
Entamoeba histolytica
A tuberculous granuloma that occurs in the cortex of the brain,
subsequently rupturing into the subarachnoid space, is termed a
Rich
focus.
Transmission occurs via contact with animals. xx
are thin aerobic spirochaetes that are tightly coiled. The first stage of
infection is known as the xx phase, during which the patient
suffers non-specific symptoms such as fever, headache, malaise and
photophobia. In the second immune phase, IgM antibodies have formed
and meningitis, liver damage (causing jaundice) and renal failure may
develop. CSF examination will reveal a raised white cell count. The
microscopic agglutination test is considered the gold standard for diagnosing
xx
Leptospirosis
is a Gram-negative diplococcus.
Infants aged 6 months to 2 years are most at risk as well as large
numbers of adults living in close quarters. Virulence factors include its
capsule (antiphagocytic), endotoxin (lipopolysaccharide causes haemorrhage
from blood vessels resulting in characteristic petechiae in meningococcaemia)
and IgA1 protease (destroys IgA).
Neisseria meningitides (meningococcus
Diagnosis is made by examination of CSF; India ink staining reveals
yeast cells with a surrounding halo.
Cryptococcal meningitis
A 35-year-old man presents to an infectious disease specialist with a painful
penile ulcer and associated unilateral lymphadenopathy of the inguinal nodes. A
swab of the ulcer is cultured on chocolate agar
Treponema pallidum
B Klebsiella granulomatis
C Neiserria gonorrhoeae
D Trichomonas vaginalis
E Candidia albicans
F Chlamydia trachomatis
G Bacterial vaginosis
H Haemophilus ducreyi
I Herpes simplex virus 2
Haemophilus ducreyi (H) is a Gram-negative coccobacillus that causes a
tropical ulcer disease (chancroid) and is contracted by sexual transmission.
Chancroid is characterized by a painful genital ulcer that leads to
unilateral painful swollen inguinal lymph nodes. Infected lymph nodes
may rupture releasing pus. The differential diagnosis for genital ulcers
includes syphilis (painless ulcer with bilateral painless lymphadenopathy),
herpes simplex virus 1 and 2 (vesicles that eventually break down)
and lymphogranuloma venereum (slowly developing painless inguinal
lymph nodes). Haemophilus ducreyi can be cultured on chocolate agar.
is a Gram-positive rod that causes the ulcerating
sexually transmitted infection donovanosis. It is diagnosed using
giemsa stain of biopsy, which reveals Donovan bodies
Klebsiella granulomatis
is a flagellated protozoan that causes vaginal
discharge and urethritis in humans. It is otherwise asymptomatic and
can be diagnosed by wet preparation microscopy, culture or PCR.
Trichomonas vaginalis
Superficially, infection causes redness, itching and discharge
from the vagina. In immunocompromised patients, infection can involve
the oesophagus as well as causing xx
Candida albicans
rare side effect of xxx is cholestatic jaundice which
may develop weeks after treatment is stopped.
Fluclox
Side effects of xx include thrombocytopenia, megaloblastic
anaemia and hyperkalaemia (via antagonism of sodium channels
in the distal convoluted tubule of nephrons).
Trimethoprim
acts on 50S ribosomes to inhibit protein synthesis.
It is used in cases of Rocky Mountain spotted fever. Side effects include
aplastic anaemia.
Chloramphenicol
a broad-spectrum carbapenem antibiotic which is
used in the management of severely sick patients, usually in intensive
care. It is resistant to β-lactamase, including extended spectrum
β-lactamase producing bacteria
Meropenem
is a tetracycline antibiotic that interferes with protein
synthesis by binding to the 30S ribosomal subunit. It is used in COPD
exacerbations, sexually transmitted infections (gonorrhoea and chlamydia)
and acne.
Doxycycline
A 38-year-old man presents to his GP with vomiting, mild fever and loss of
appetite. He admits to travelling to sub-Saharan Africa 2 months previously. On
examination the patient is evidently jaundiced.
A Human immunodeficiency virus
(HIV)
B Epstein–Barr virus (EBV)
C Hepatitis B virus
D Cytomegalovirus (CMV)
E Hepatitis D virus
F Varicella zoster virus
G Hepatitis C virus
H Human herpes virus 8
I Influenza virus
Hepatitis B virus (HBV; C) is a double-stranded DNA virus that is prevalent
in sub-Saharan Africa. It is transmitted via sexual contact, contaminated
blood products, intravenous drug use as well as vertical transfer
from mother to child during child birth. The virus has an incubation
period of 2–6 months with 80 per cent of infections remaining acute
and 20 per cent becoming chronic with risk of cirrhosis and hepatocellular
carcinoma. HBV antigens include HBsAg (surface antigen), HBcAg
(core antigen) and HBeAg (soluble antigen).
A 40-year-old man presents to an infectious disease specialist with a 4-month
history of weight loss, fever and malaise. On examination the patient has
lymphadenopathy. His CD4 count is found to be 289 copies/μL. The patient is
started on lamivudine, ritonavir and one other drug.
A Acyclovir
B Oseltamivir
C Interferon-α
D Zidovudine
E Gancylcovir
F Lamivudine
G Efivarenz
H Ritonavir
I Adamantadine
Zidovudine (D) is a nucleoside reverse transcriptase inhibitor (NRTI)
used in the treatment of HIV/AIDS (as well as prevention of vertical
transmission from infected mothers). Treatment is commenced once the
CD4 count falls below 350 copies/μL. Zidovudine works by inhibiting
the action of the enzyme reverse transcriptase, preventing the conversion
of HIV RNA to DNA, which consequently cannot be incorporated
into the host DNA. Side effects include anaemia, neutropenia, hepatic
and cardiac dysfunction as well as myopathy. The standard treatment
regimen involves the use of two nucleoside reverse transcriptase
inhibitors (NRTIs) and a non-nucleoside reverse transcriptase inhibitor
(NNRTI; Efivarenz) or a protease inhibitor (PI; Ritonavir).
A 25-year-old man presents to his GP with a 3-day history of fever, cough,
body aches and severe headaches. The patient is told to rest and drink plenty of
fluids. However, he returns the following week stating his symptoms have not
improved and is started on a drug that acts on viral neuraminidase.
A Acyclovir
B Oseltamivir
C Interferon-α
D Zidovudine
E Gancylcovir
F Lamivudine
G Efivarenz
H Ritonavir
I Adamantadine
Oseltamivir (B) is a viral neuraminidase inhibitor used in the treatment
of influenza. Osteltamivir is in fact a pro-drug; once metabolized in the
liver the active form GS4071 is produced. Once a newly formed influenza
virion is produced, the surface viral protein haemagglutinin is bound
to sialic acid receptors along the upper respiratory tract. Neuraminidase
is normally responsible for cleaving the haemagglutinin–sialic acid
receptor bond, hence facilitating the release of newly formed virions.
Therefore, inhibiting neuraminidase activity prevents further viral
replication.
can cause bone marrow toxicity; it may
therefore be prescribed together with granulocyte-colony stimulating
factor (G-CSF)
Gancyclovir
Mechanism for acyclovir
It is converted to acyclo-guanosine monophosphate by viral thymidine kinase
Acyclo-GMP is further phosphorylated to acyclo-guanosine triphosphate which is then incorportaed into the viral DNA strand
is an M2 ion channel inhibitor preventing the uncoating
of influenza virions and therefore inhibiting entry into susceptible cells.
Amantadine
can lead to severe flu-like
symptoms and can be diagnosed by testing for blood β-D-glucan
Candidaemia
is a chronic fungal infection caused by
Malassezia furfur, characterized by hypopigmentation (in patients with
dark skin tones) and hyperpigmentation (in patients with pale skin tones). Spots affect the back, underarm, arms, legs, chest, neck and rarely
the face. Microscopic investigation of the M. furfur with potassium
hydroxide reveals a ‘spaghetti with meatballs’ appearance. Wood’s light
may also reveal an orange fluorescence in some cases.
Pityriasis versicolor (B)
Infection in pre-formed lung cavities
(for example in TB patients) may lead to a fungal ball visible on
chest X-ray
aspergilloma
is a fungus found in
soil and plants that causes sporotrichosis. A prick by thorns causes nodular
lesions to appear on the surface of the skin. Initially the lesions will
be small and painless; left untreated they become ulcerated. Infection
may also spread to joints, bone and muscle by this route. Inhalation of
spores may lead to pulmonary disease and systemic infection may lead
to central nervous system involvement. Treatment options include itraconazole,
fluconazole and oral potassium iodide.
Sporothrix schenckii
is a fungus transmitted by inhaled spores;
it is highly prevalent in the Mississippi River region. Although mostly
subclinical, a minority of infections will proceed to a chronic progressive
lung disease.
Histoplasma capsulatum
is a copper coloured soil saprophyte found on
rotting wood that causes chromoblastomycosis. Infection is characterized
by a warty lesion resembling a cauliflower
Phialophora verrucosa
is a cutaneous dermatophyte fungal infection of the
scalp leading to scaly red lesions with loss of hair. It primarily affects
children. Infection is characterized by an expanding ring on the scalp.
Tinea capitis (F)
is also known as ringworm. It is a cutaneous dermatophyte
fungal infection affecting the trunk, arms and legs. It is identified
by raised red rings.
Tinea corporis
A 45-year-old man has returned to the UK from a holiday to France. A week
later he presents with flu-like symptoms, drenching sweats, a recurring fever
and is beginning to complain of a lower back pain. He admits to have brought
back some local cheeses on visits to regional farms.
Brucellosis (C) is a Gram-negative rod-shaped bacterium that is harboured
by cattle (Brucella abortus), goats (B. melitensis), pigs (B. suis) and dogs
(B. canis). Brucella spp. are transmitted by inhalation, unpasteurized dairy produce and direct contact with animals. Symptoms include fever,
myalgia, arthralgia, tiredness and in chronic cases may be associated with
depression. Diagnosis is made by blood culture on Castaneda medium.
Complications include granulomatous hepatitis (histology of liver
biopsy demonstrates granulomata), endocarditis, oseteomyelitis and
thrombocytopenia.
A 48-year-old man presents to his GP with flu-like symptoms. On examination
the patient has a maculopapular rash on his trunk. The patient also shows an
area where a vague bite mark is visible.
A Psittacosis
B Rabies
C Brucellosis
D Q fever
E Leptospirosis
F Mycobacterium marinium
G Lyme disease
H Cat scratch disease
I Rocky mountain spotted fever
Rocky Mountain spotted fever (I) is caused by Rickettsia spp. infection,
a Gram-negative genus of bacteria, most prevalent in North and South
America. It is harboured in small wild rodents and domestic animals
(transmitted to humans by ticks). Rickettsia bacteria invade the endothelial
lining of capillaries causing a vasculitis. Clinical features include
headache, fever, myalgia, vomiting and confusion. Late signs include
a rash that is maculopapular and/or petechial on the distal parts of the
limbs which then spreads to the trunk and face. Rocky Mountain spotted
fever may lead to thrombocytopenia, hyponatraemia and/or elevated
liver enzymes.
Human symptoms mainly involve a
severe pneumonia (with or without hepatitis). Although the patient may
report mild symptoms, the X-ray will generally appear to show severe
pathology. Diagnosis is made by visualizing cytoplasmic inclusions on
Giemsa or fluorescent antibody stained sputum or biopsy sample.
Psittacosis
Cerebral Negri bodies (inclusion bodies) are pathognomonic.
Rabies
Transmission occurs by
inhalation of aerosols of urine, faeces or amniotic fluid from infected
livestock.
Q fever
Classically, infection results in tender and swollen
lymph nodes with headache and backache. Atypically, infection may
result in Parinaud’s oculoglandular syndrome
Cat scratch disease (H) is caused by Bartonella
viral respiratory system infection caused by the genus
Morbillivirus. Infection presents with cough, coryza, conjunctivitis and/
or a discrete maculopapular rash
Measles
Long-term complications include saddle-nose
deformity, Higoumenakis’ sign (unilateral enlargement of the clavicle)
and Clutton’s joints (symmetrical joint swelling).
Congenital syphillis
It is an obligate intracellular Gram-negative bacterium
found in farm animals and pets, and is transmitted by aerosol
or contact with animal products like milk or faeces. It manifests as
flu-like symptoms, but can progress to an atypical pneumonia or less
often a granulomatous hepatitis. Typical chest x-ray features include
a ground glass appearance. It does not grow on Lowenstein–Jensen
medium
Coxellia burnetti (Q fever)
A 24-year-old HIV-positive Asian man presents with a cough. A Mantoux test
is performed. After 72 hours, the wheal diameter is measured at 5.8 mm. This
indicates:
A He has never been exposed to TB
B He has been exposed to TB
C He has had a BCG vaccination in the past
D He has latent TB which is now reactivated
E It is not possible to say
1 An induration of 5 mm or more is considered positive in:
• Patients with HIV
• A recent contact of a person with TB disease
• People with fibrotic changes on chest radiograph consistent
with prior TB
• Patients with organ transplants
• People who are immunosuppressed for other reasons (for example
taking the equivalent of >15 mg/day of prednisone for 1
month or longer)
2 An induration of 10 mm or more is considered positive in:
• Recent immigrants (<5 years) from high-prevalence countries
• Intravenous drug users
• Residents and employees of high-risk congregate settings
• Mycobacteriology laboratory personnel
• Persons with clinical conditions that place them at high risk
• Children <4 years of age
• Infants, children, and adolescents exposed to adults in high-risk
categories
3 An induration of 15 mm or more is considered positive in any person,
including those with no known risk factors for TB
Organisation of strep
Can be divided into alpha haemolytic, beta haemolytic and non-haemolytic groups
Alpha= Strep pnuemonia and strep viridans (optochin insensitivie) Beta= Lancefield groups A, B, C, F and G
Non haemolytic strep= enteroccoci
OVeR PS
Optochin- viridans resistance
Pneumonia- sensitive
If you get an HIV patient whose saturations
drop on exertion in a question, think about
Pneumocystis jirovecii
Signs of endocarditis: rules of 2
2 signs in the hands: clubbing and splinter haemorrhages
Two signs in the abdomen: splenomegaly and microscopic haematuria
Two signs elsewhere: New or changing heart murmurs and embolic phenomena
Acute vs subacute infective endocarditis
Acute: tricuspid, staph aureus IVDU
Subacute: mitral and aortic, damaged valves, strep viridans
Culture negative endocarditis
HACEK
Maconkey agar and lactose fermenters
Lactose fermenters turn Maconkey agar pink
Staph saprophytics vs staph aureus
Staph saprophyticus is second most common cause of UTI in young sexually active woman, coagulase positive like other staph but catalase negative unlike Staph aureus
four runners ‘ent-ering’ a race, and the winner
gets a silver flask!
bloody diarrhoea
Entamoeba histolytica
Gram-negative bacterium that is also oxidase positive, but has a corkscrew
rather than a comma appearance
Campylobacter
Oxifase positive organism
PuNCH Me Very Lightly
Pseudomonas
Neisseria
Campylobacter
Helicobacter
Morazella
Vivrio
Legionella
A 35-year-old HIV-positive man presents to his GP complaining of a general
feeling of tiredness, weight loss and night sweats. On examination there is hepatosplenomegaly
and hyperpigmentation of the skin. The most likely diagnosis is:
A Visceral leishmaniasis
B Cutaneous leishmaniasis
C Mucocutaneous leishmaniasis
D Malaria
E Schistosomiasis
Leishmaniasis is transmitted by phlebotomine sandflies and occurs in
Africa, America and the Middle East. Visceral leishmaniasis (A) is also
known as ‘Kala-azar’, and the most common clinical features include
fever and splenomegaly. Hepatomegaly, skin hyperpigmentation and dry
warty skin occur less frequently, and bone marrow invasion can result
in pancytopenia. It can be mistaken for malaria, which is dangerous as
it can be fatal if left untreated. L. donovani and L. infantum are thought
to cause the disease in Africa, Asia and Europe, whilst L. chagasi is
implicated in South America
is transmitted by blood
flukes. An itchy rash, known as ‘swimmer’s itch’, may develop at the
site where the vectors penetrate the skin. They may then migrate to the
liver, causing ‘Katayama fever’ with clinical features such as fever, rash,
myalgia and sometimes hepatosplenomegaly. Following maturation in
the liver, the flukes migrate to either mesenteric veins causing intestinal
xx, or to the urinary tract leading to xx schistosomiasis.
Hepatosplenomegaly can occur, but again the dry warty skin lesions
described are not usually a feature.
Schistosomiasis
A 22-year-old student presents to accident and emergency with a raised, erythematous,
scaly ulcer on his forearm which has not been healing. On examination
he is also found to have lymphadenopathy. He gives a history of recently returning
from a 2-month trek in the rainforests of South America. Tissue is aspirated
from the margin of the ulcer, and the organism is cultured in Novy–MacNeal–
Nicolle medium. The organism implicated is:
A Toxoplasma gondii
B Treponema pallidum
C Leishmania dovani
D Leishmania major
E Leishmania braziliensis
The picture described is consistent with cutaneous leishmaniasis, the
most common form of leishmaniasis. An itchy, scaly papule develops
at the bite site and develops into a crusty ulcer with raised edges. Local
lymphadenopathy can also occur, but the lesion usually heals within
8 months leaving a depigmented scar called an oriental sore. The organisms
implicated are Leishmania major (D) and L. tropica. You can
remember this if you picture lots of skin lesions cropping up in travellers
from the ‘major tropics’! It is found in many countries, ranging
from South America to the Middle East. Diagnosis can be by Giemsa
staining of slit skin smears, or from tissue aspirated from the ulcer.The organism can be cultured on Novy–Macneal–Nicolle medium as
described in the question.
Mucocutaneous leishmaniasis can produce
destructive and disfiguring facial lesions, and so is the most
feared form of cutaneous leishmaniasis. It may begin in the same
way as the cutaneous form, but years later ulceration can appear in
mucous membranes leading to mutilation of those areas. It is most
often caused by
L. braziliensis
Visceral leishmaniasis is also known as ‘Kala-azar’, and the
most common clinical features include fever and splenomegaly.
Hepatomegaly, skin hyperpigmentation and dry warty skin occur less
frequently xx are thought
to cause the disease in Africa, Asia and Europe, whilst xx is impicated in South America
L donovani
L infantum
L chagas
Characteristically a CT scan may show ring enhancing lesions with surrounding
oedema.
Toxoplasmosis
Typhoid (E) is caused by Salmonella typhi, and again can present with
non-specific features like brucellosis. However, there are a few unusual
clinical features of typhoid that are worth remembering using the
mnemonic A.B.C.C.D.E:
Abdominal distension, Bradycardia, Cough,
Constipation, Diarrhoea and Erythematous rose spots. Antibiotics of
choice in the treatment of typhoid are the quinolones such as ciprofloxacin
for 2 weeks.
The two forms
of disseminated xxl infection are the septic arthritis form (as
described in this case), and the bacteraemic form. Other clinical features
of the bacteraemic form might include a migratory polyarthralgia and a
vesicular or papular rash.
Gonocchal infection
A 26-year-old squash player is admitted with a red, swollen left knee. He reports
no history of trauma. On examination he has a temperature of 38°C. A joint
aspirate is taken which grows Gram-negative diplococci. What is the antibiotic
treatment regimen of choice for this patient?
A Oral flucloxacillin for 4–6 weeks
B IV flucloxacillin for 4–6 weeks
C IV flucloxacillin for 2–4 weeks
D IV flucloxacillin and vancomycin for 6–8 weeks
E IV cefotaxime for 4–6 weeks
The patient in this question is presenting with septic arthritis, and the
most likely cause given the joint aspiration findings of Gram-negative
diplococci is Neisseria gonorrhoeae. The British National Formulary
(BNF) advises the use of intravenous cefotaxime for 4–6 weeks (E) if
gonococcal arthritis or a Gram-negative infection is suspected. The BNF
is a good source of information for looking up the latest guidelines
regarding antibiotic treatment regimens for common types of infection.
Cefotaxime is a third generation cephalosporin. Cephalosporins are part
of the beta-lactam group of antibiotics which work by inhibiting cell
wall synthesis. The penicillins are also part of this group. There are different
generations of cephalosporins, with those of later generations
having increasing Gram-negative but decreasing Gram-positive cover.
Cefotaxime is also used to treat meningitis and gonorrhoea. Some of the
other commonly used third generation cephalosporins are ceftizoxime
and ceftriaxone – you can remember these because they all have a ‘t’ in
their names, just like in ‘third’ generation.
Hep B
It is the first detectable antigen to appear after
someone has been infected, and can be positive in acute or chronic
disease. Patients who still carry this antigen after 6 months are
termed hepatitis carriers. It is this antigen that is used to make the
hepatitis B vaccine
HBsAg
This is an IgG antibody that appears after the host has
cleared the infection, and indicates recovery. It is also found in a
person who has been vaccinated against hepatitis B
Anti-HBs
HBV
is often used as a marker of infectivity, as
it is only found in the blood when the virus is actively replicating
HBeAg
this indicates that the patient has recently been
infected with hepatitis B, and is a marker of acute infection
Anti-HBc IgM
this is produced in response to the core antigen,
and often persists for life. You can remember this as the ‘c’ standing
for ‘chronicity’, as it is the difference between IgM and IgG antibodies
which can tell you whether the infection is acute or chronic
anti-HBc-Ig
A 79-year old woman is admitted to the hospital for treatment of pneumonia
and is commenced on intravenous antibiotic therapy. Her respiratory symptoms
begin to improve, but 5 days later she develops profuse diarrhoea. The most
appropriate treatment is:
A Oral metronidazole for 7 days
B Oral metronidazole for 14 days
C Isolation and treatment with intravenous fluids
D IV metronidazole for 7 days
E Oral co-amoxiclav for 7 days
First line treatment for infection with C. difficile is oral metronidazole,
with a suggested duration of treatment of 10–14 days (B). Metronidazole
is classified as a nitroimidazole antibiotic, and is particularly useful for
the treatment of anaerobic organisms and protozoa. You can remember
three of the key organisms it is used to treat by remembering that ‘Met
is out to G.E.T you difficult bugs!’ (Giardia, Entamoeba, Trichomonas
and C. difficile). Patients are usually advised to avoid consuming alcohol
whilst taking this antibiotic because of the potential reaction that
can occur characterized by nausea, shortness of breath, flushing and
vomiting.
A 79-year old woman is admitted to hospital for treatment of pneumonia and is
commenced on intravenous antibiotic therapy. Her respiratory symptoms begin
to improve, but 5 days later she develops profuse diarrhoea. After treatment with
oral metronidazole she shows gradual improvement, but the profuse diarrhoea
returns 2 weeks later. The same organism is found to be responsible. The most
appropriate course of action is:
A Oral metronidazole for 7 days
B Oral metronidazole for 14 days
C Isolation and treatment with intravenous fluids
D IV metronidazole for 7 days
E Oral vancomycin for 14 days
As explained previously, a 7-day course of metronidazole (A) is not
considered a sufficient duration of treatment to eradicate the bacterium.
Again, isolation and IV fluid resuscitation (C) is necessary but
not adequate as a single measure in the management of this woman.
Intravenous metronidazole (D) is only needed if a patient is not
responding to vancomycin, the infection is life-threatening, or for
patients with ileus.
Oral vancomycin for 10–14 days (E) is given for:
• Third or subsequent episodes
• Severe infection
• Infection not responding to metronidazole
• patients who cannot tolerate metronidazole
is ‘red man
syndrome’, a reaction to the drug which consists of a sudden onset erythematous,
pruritic rash over the face, neck and upper torso.
Vancomycina rare ADR
A 65-year old retired mechanic is brought by his family to his GP due to their
concern over his recent increase in confusion. This has occurred rapidly over the
past 4 months, and he now struggles to recognize members of his family. His
daughter also reports occasionally seeing intermittent, jerky movements of both
his arms. The GP organizes a CT scan and dementia screen, which are both found
to be normal. Which is the next most useful diagnostic test for the GP to order?
A MRI brain
B Electroencephalogram
C Electrocardiogram
D Ultrasound scan of both carotids
E Tonsillar biopsy
The diagnostic test of choice here is the electroencephalogram (B),
which is abnormal in two-thirds of patients and would classically demonstrate
generalized triphasic sharp wave complexes. Do not confuse
this with an electrocardiogram (ECG) (C), which would not be diagnostic
in this case. An MRI brain (A) may show increased signal in the basal
ganglia, but would not be the best investigation here. An ultrasound
scan of both carotids (D) is a useful test if investigating a transient
ischaemic attack (TIA) to look for carotid stenosis, but this is not
relevant with this patient. Finally, a tonsillar biopsy (E), is a useful
diagnostic test for variant CJD (for which it has 100 per cent sensitivity
and specificity), but not for sporadic CJD.
A 61-year-old patient has recently been diagnosed with sporadic CJD. His GP is
keen to do a lumbar puncture. Which of the following statements is true regarding
this investigation in this situation?
A The lumbar puncture is used to look for the levels of protein, glucose and
polymorphs
B The lumbar puncture is used to look for the levels of a protein called 14-3-3
C A lumbar puncture is the most specific test for variant CJD
D The lumbar puncture is not useful in sporadic CJD, but is an important test
in variant CJD
E A tonsillar biopsy would be a more useful test than a lumbar puncture for
sporadic CJD
The lumbar puncture in CJD is used to analyze the CSF for a protein
named ‘14-3-3’ (B). Note that routine analysis of the cerebrospinal fluid
(CSF) is normal in CJD, therefore looking at levels of protein, glucose
and polymorphs (A) would not be useful to distinguish between possible
causative agents of the clinical features as it is in meningitis
‘14-3-3’ is a term for a large group of proteins which have different
functions in eukaryotic cells, such as in cell signalling. However,
its measurement in CJD is a time consuming process, and as it is a
normal neuronal protein it can be released into the CSF as a result
of many other normal neuronal insults. It is therefore not a specific
finding (C), and the test can be positive in other conditions such as a
recent stroke, viral encephalitis or a subarachnoid haemorrhage. The
14-3-3 protein is present in both variant and sporadic CJD, therefore
(D) is incorrect.
Variant CJD has several important differences from sporadic CJD:
1 It typically occurs in younger patients (median age of onset 26 years)
than sporadic CJD
2 The median survival time is approximately 14 months, compared to
4
months for sporadic CJD
3 Psychiatric features may dominate in the initial stages, before
neurological features such as ataxia, myoclonus, chorea, dementia and
peripheral sensory symptoms appear
4 The MRI in variant CJD shows the ‘positive pulvinar sign’ (enhanced
signal of nuclei in the thalamus)
5 The classical EEG findings are often absent in the variant form
6 A tonsillar biopsy is sensitive and specific in the variant form, but is
not a useful test in the sporadic form (
A 42-year-old alcoholic is admitted with abdominal distension. The shifting
dullness test is positive and he is found to have diffuse abdominal tenderness.
His observations are as follows: pulse 115, blood pressure 116/83, temperature
37.9°C. The next best course of action is:
A Begin therapeutic paracentesis
B Observe, administer analgesia and closely monitor his vital signs
C Commence intravenous spironolactone
D Commence intravenous amoxicillin
E Commence intravenous cefotaxime
The pyrexia and tachycardia, in conjunction with the clinical features of
abdominal tenderness and ascites, make this the most likely diagnosis in
this patient. Other typical clinical features might include nausea, vomiting,
confusion, general malaise or features of hepatic encephalopathy.
In approximately 15 per cent of patients SPB can be asymptomatic.
A prompt diagnostic paracentesis is needed to make the diagnosis, and
SPB is confirmed by the presence of:
1 Ascitic fluid WCC of 500 cells/mm3
2 or Neutrophil count of >250 cells/mm3
Do not confuse a diagnostic paracentesis with a therapeutic paracentesis
(A): in the latter the purpose is to remove the fluid, for example
to relieve abdominal pressure or in the case of respiratory compromise.
This may be appropriate later, but only once SBP has been excluded
from the results of a diagnostic paracentesis or treated.
The most common organisms isolated in patients with SBP include
E. coli, Gram-positive cocci and enterococci. Although local antibiotic
guidelines may differ, of the options listed cefotaxime (E) is one of the
most extensively studied and has been proven to be effective. It is usually
given for at least 5 days. Other third generation cephalosporins
such as ceftriaxone can also be used. Amoxicillin (D) would not provide
sufficient cover against Gram-negative organisms.
Whilst analgesia and close observation are also important measures (B),
the high risk of mortality in SBP necessitates prompt antibiotic treatment.
Spironolactone (C) is used for the treatment of uncomplicated ascites, but
initial antibiotic treatment would take precedence in the case of SBP
A 63-year-old asymptomatic housewife is referred to a gastroenterologist after her
GP found that she had abnormal liver function tests on a routine blood test. A thorough
history reveals that she received a blood transfusion during her pregnancy in
1979. The best test to confirm whether the patient has hepatitis C would be:
A Liver biopsy
B Anti-hepatitis C antibodies
C Alanine aminotransferase levels
D Hepatitis C RNA PCR
E Viral genotyping
There are several different tests which are helpful in investigating the
disease:
1 Hepatitis C RNA PCR (D) – This can be used to differentiate between a
current and past infection. A quantitative test to detect the number of
hepatitis C RNA particles (called the ‘viral load’) can also be performed.
This can be very useful to detect a patient’s response to the anti-viral
treatment. Therefore, this is the best diagnostic test for hepatitis C
2 Anti-hepatitis C antibodies (B) – a positive test would indicate
exposure to the disease, but results should be interpreted with caution
because it cannot distinguish between current or past infection. In
addition, it can take up to 3 months for these antibodies to appear
after exposure, so an initial negative test can be misleading. It has
also been suggested that a weakly positive test might actually be a
false positive, so this is not the best diagnostic test. However, it may
be performed initially, and if the patient has two positive results a
hepatitis C RNA PCR is used to confirm the diagnosis
3 Viral genotyping (E) – this is used to determine the genotype of virus
present. The most common, genotype 1, is less likely to respond to
treatment than genotypes 2 or 3 and requires longer therapy
4 Liver biopsy (A) – this would be the most accurate means of
determining the stage and severity of liver damage caused by the
virus, and may be useful to assess the patient’s likelihood to respond
to treatment. However, it would be performed after the suspected
diagnosis has been confirmed
5 Alanine aminotransferase levels (ALT) (C) – this is not a diagnostic test,
but can be useful aid in the initial stages of confirming the diagnosis.
The ALT to AST (aspartate aminotransferase) ratio is typically <1 in
liver damage caused by hepatitis, whereas if it is >2 this is more
suggestive of alcoholic liver disease. You can remember this because
AST is indicative of Smirnoff drinking, whereas ALT is indicative of
viraL aetiology!
A 33-year-old backpacker visits his GP complaining of feeling weak, lethargic
and feverish since he returned from his trip to South Africa 3 months previously.
He is accompanied by his wife, who reports a change in his behaviour and disturbed
sleeping pattern since his return. On examination, his GP discovers that he
has enlarged cervical lymph nodes, and there is a small chancre on his forearm
that is approximately 2 cm in diameter. The most likely causative organism is:
A Plasmodium falciparum
B Trypanosoma brucei gambiense
C Trypanosoma brucei rhodesiense
D Trypanosoma cruzi
E Leishmania infantum
Human African trypanosomiasis is also known as sleeping sickness, and
is an infection transmitted by the tsetse fly in sub-Saharan Africa. There
are two main types:
1 Trypanosoma brucei gambiense (B) is found in west and central Africa,
is responsible for over 95 per cent of cases, and causes a chronic
infection. It can take months or even years for symptoms to appear.
You can remember this as gambiense causes a gradual infection
2 Trypanosoma brucei rhodesiense (C) is found in south and eastern
Africa, accounts for under 5 per cent of cases, and causes an acute
infection with symptoms appearing over a few weeks or months.
You can remember this as rhodesiense causes a rapid infection. As
this patient’s symptoms appeared 3 months after returning from his
travels, this is more likely to be the causative agent here
A subcutaneous chancre can develop at the site where the tsetse fly
bites, and symptoms such as fevers, weakness, arthralgia and headache
can then appear. Posterior cervical lymphadenopathy can also occur,
especially with T. brucei gambiense. This is known as Winterbottom’s
sign. Later the parasite can cross the blood–brain barrier resulting in
neurological features such as disturbance of the sleep cycle, ataxia,
behavioural changes and psychiatric disturbance. Treatment is with
drugs such as pentamidine and suramin in the early stages.
Plasmodium falciparum (A) is an organism responsible for causing
malaria. Whilst it should be considered in all patients with a fever
returning from an endemic area, the changes in behaviour and sleep
disturbance described in this patient make this a less likely cause.
Trypanosoma cruzi (D) causes Chagas disease which is carried by the
reduviid bug. Chronic infection can appear weeks to years after the
initial infection, affecting the cardiac and gastrointestinal systems.
Leishmania infantum (E) is responsible for leishmaniasis, features of
which can include fever, hepatosplenomegaly and lymphadenopathy.
Again, it is less likely to cause behavioural changes and sleep is unlikely
to be affected.
A 20-year-old student seeks medical attention due to recent difficulty in swallowing,
and severe weight loss. A thorough travel history reveals that he
returned several months ago from a gap year in Brazil. During his trip he
remembers becoming unwell at one point with a fever, diarrhoea, vomiting and
swollen eyelids, but this resolved in approximately 3 weeks with no treatment. A
chest x-ray is ordered as one of his investigations, and this reveals marked dilatation
of his oesophagus. The vector responsible for transmitting this disease is:
A Tsetse fly
B Reduviid bug
C Sandfly
D Aedes mosquito
E Ixodes tick
Trypanosoma cruzi is responsible for causing Chagas disease, a potentially
life-threatening disease which is spread by reduviid bugs (B) in Brazil. These are also known as ‘kissing bugs’. A red nodule, called a
chagoma, can appear at the site of the bite.
There are two forms of the disease: acute and chronic. In the acute phase,
patients may experience non-specific symptoms such as fever, lethargy,
diarrhoea, and vomiting. A characteristic feature, but one which occurs
in less than 50 per cent of cases, is a purplish swelling of the eyelids
(called Romana’s sign). To put this all together, picture Tom Cruise
(Trypanosoma cruzi) starring in a gladiator film as a Roman (Romana’s
sign) wearing purple sunglasses (swollen eyelids) and being kissed
(
kissing bugs) by lots of fans ‘ready with their video cameras’ (reduviid!)
The chronic phase can occur even years after the initial bite, and typically
affects the heart and gastrointestinal tract. You can remember
its effects by thinking of it causing both dilatation and dysfunction in
three organs: in the heart (dilatation = dilated cardiomyopathy, dysfunction
= arrhythmias), in the colon (dilatation = megacolon,
dysfunction = constipation) and in the oesophagus (dilatation = mega
oesophagus, dysfunction = dysphagia). Bennzimidazole or nifurtimox
are effective medications used to treat this disease.
The tsetse fly (A) is responsible for causing human African trypanosomiasis,
also known as sleeping sickness, in sub-Saharan Africa. The
clinical features of this disease can include changes to the sleep–wake
cycle and psychiatric disturbance. The sandfly (C) transmits Leishmania
species in Africa, America and the Middle East. The Aedes mosquito (D)
is a type of mosquito that causes Dengue fever. The Ixodes tick (E), also
known as the ‘deer tick’, transmits the organism responsible for causing
Lyme disease. None of these vectors would cause the spectrum of clinical
features described in this patien
The paralytic phase would
not typically have an ascending pattern of weakness, and fasciculations
prior to paralysis are an important feature.
Polio
A 46-year-old Somalian woman presents to her GP with a dry cough and weight
loss of 5 kg over 3 weeks. She is sent to the hospital, and a chest x-ray reveals
cavitating lung lesions. She is started on a course of anti-tuberculous medication.
Which of the following statements about this regimen is true?
A Liver function tests only need to be checked in those with pre-existing liver
disease
B Ethambutol can cause a peripheral neuropathy
C Pyridoxine should always be given with isoniazid treatment
D Rifampicin can cause optic neuritis
E Ethambutol should be avoided in renal failure
Remember that treatment for pulmonary TB usually consists of two
phases – an initial phase with rifampicin, isoniazid, pyrazinamide and
ethambutol for 2 months, and then a continuation phase with rifampicin
and isoniazid only for 4 months.
Streptomycin and ethambutol are two anti-tuberculous drugs which
should preferably be avoided in patients with renal impairment (
E).
If they have to be used the dosage should be reduced and the plasma
drug concentration closely monitored. A patient’s renal function
should be checked routinely before anti-tuberculous medication is
started.
The side effect that is particularly worrying with the use of ethambutol
is its ocular toxicity, and this is more likely in renal impairment as it is
renally excreted. This can present with changes in visual acuity, colour
blindness and restriction of visual fields. Therefore a patient’s visual
acuity should be assessed with a Snellen chart prior to starting treatment,
and they should be strongly advised to stop the medication and
seek advice if they become aware of any change in their vision. This
side effect does not occur with rifampicin (D).
Liver function should be tested in everyone before starting
antituberculous
therapy, as isoniazid, rifampicin and pyrazinamide are
all hepatotoxic (A). Further checks are not needed unless the patient has
pre-existing liver disease, is alcohol dependent or develops symptoms
of liver disease. Rifampicin can commonly cause a transient disturbance
to liver function tests in the first 2 months, but this does not usually
necessitate any changes to the treatment regimen.
The only common side effect of isoniazid is a peripheral neuropathy.
This can be remembered by ‘isoniazid causes a sensory neuropathy’.
Pyridoxine (vitamin B6) is not given routinely as a prophylactic measure
in patients using isoniazid, but may be given in those with preexisting
risk factors such as diabetes, alcohol dependence and HIV (C).
Ethambutol does not cause a peripheral neuropathy (B).
Quotidian fever malaria
Plasmadoium knowlesi
A young girl returns from visiting her relatives in India, feeling feverish and
with flu-like symptoms. A diagnosis of malaria is suspected. The form of the
malaria parasite which invades erythrocytes is known as a:
A Sporozite
B Schizont
C Merozite
D Hypnozoite
E Gametocyte
1 An infected mosquito injects sporozites (A) from its saliva into a
person’s blood stream when it bites
2 These enter the blood stream and are taken to the liver where they
infect hepatocytes
3 Here they multiply for a varying period of time, and then differentiate
to form haploid merozites (C). These have a ‘signet ring’ appearance.
Schizonts (B) are oval-shaped inclusions that contain the merozoites.
Note that P. vivax and P. ovale sporozoites may not develop into
merozites immediately, but can form hypnozoites (D) that remain
dormant in the liver
4 The merozites escape from the liver into the blood stream and infect
red blood cells – the erythrocytic phase
5 They multiply further in the erythrocytes, and will be released
from them at intervals. The waves of fever the patient experiences
correspond to when the merozites are released from the erythrocytes
6 Some of the merozoites develop into sexual forms of the parasite,
called male and female gametocytes (E). When a mosquito bites an
infected human, it ingests the gametocytes which form gametes inside
the mosquito
7 These then fuse to form oocytes and then sporozites – ready to inject
into a person.
A 55-year-old housewife returns from visiting her relatives in India, with a high
fever and with flu-like symptoms. A diagnosis of uncomplicated falciparum
malaria is confirmed. The most appropriate management plan is:
A Discharge with oral quinine and doxycycline
B Discharge with oral mefloquine and chloroquine
C Admit, give IV paracetemol and observe
D Admit and give IV quinine
E Admit and give oral quinine and doxycycline
All patients with falciparum malaria should be admitted to hospital
initially, so answers (A) and (B) are automatically excluded. Children
should be kept in for at least 24 hours, and infants, pregnant women
and the elderly need to be closely monitored because they can deteriorate
rapidly. The treatment options then depend on whether the malaria
is uncomplicated or complicated.
Uncomplicated malaria can be treated with one of the following:
1 Oral quinine plus doxycycline for 5–7 days (E)
2 Co-artem (artemetherelumefantrine) for 3 days
3 Atovaquone–proguanil (Malarone) for 3 days
Therefore the correct answer here is (E). Giving paracetamol without
anti-malarials would not be adequate, so clearly (C) is not suitable.
Chloroquine and mefloquine (B) are not recommended for the treatment
of falciparum malaria in the UK.
Oral treatment would suffice in an uncomplicated case of falciparum
malaria such as this, but in a severe case the first line anti-malarial
used in the UK is IV quinine (D). IV artesunate may also be considered
in the case of very severe disease instead of or in addition to quinine,
but this is not always widely available.
The treatment for non-falciparum malaria is quite different. In uncomplicated
infection, chloroquine is used initially followed by a 2-week
course of primaquine. The choloroquine treats the parasites in the erythrocytes
only, thus primaquine is still needed to kill the hypnozoites that
remain latent in the liver.
Glucose-6-phosphate dehydrogenase deficiency is an X-linked recessive
hereditary disease, and anti-malarial drugs can cause acute haemolysis
in these patients. The drugs thought to be particularly troublesome are
primaquine and choloroquine, but others may be dangerous at high
doses. For this reason glucose-6-phosphate dehydrogenase levels are
checked in patients before starting anti-malarial treatment.
A 55-year-old housewife returns from visiting her relatives in India, with a
high fever and with flu-like symptoms. thick and thin films are requested, and
Maurer’s clefts are seen under the microscope. The diagnosis is:
A Plasmodium falciparum
B Plasmodium vivax
C Plasmodium ovale
D Plasmodium malariae
E Plasmodium knowlesi
The most reliable way to diagnose malaria is via a blood film, and
traditionally a thick and thin blood film are requested. Most people
remember this fact, but not the reason behind it! Thick films are better
than thin films at picking up lower levels of infection, but thin films
allow the specific species to be identified. Both types of films are used
together to make the diagnosis.
In the erythrocytic life cycle of the malarial parasite, disc-like granulations
can be seen at the edge of the cell using an electron microscope.
These are known as Maurer’s clefts, and are found in falciparum malaria
(A). They are thought to be used by the parasite for protein sorting
and export. They are larger and coarser than the Schuffner’s dots seen
with P. vivax (B) and P. ovale (C). These are punctuate granulations
again seen under the microscope in erythrocytes invaded by the tertian
malaria parasite. These two structures are worth remembering for exam
questions!
P. malariae (D) causes ‘quartan’ malaria, meaning the fever occurs
every fourth day (i.e. days 1, 4, 7 and so on). P. knowleski (E) is much
less common, and mainly occurs in southeast Asia (such as in Borneo).
Maurer’s clefts and Schuffner’s dots would not typically be found in
infection with these species.
Maurer’s clefts
P falciparum
Schuffner’s dots
P vivax
P ovale