Microbiology Flashcards

Question

Given an exmple of a nitroimidazole

Answer 1

Metronidazole

Answer 2

Anaerobes and protozoa

Answer 3

Rifampicin

Answer 4

Metronidazole

Answer 5

Polymyxin Cyclic lipopeptide

Answer 6

Daptomycin

Answer 7

Gram +ve, MRSA +VRE

Answer 8

Sulfonamides Diaminopyrimidines

Answer 9

Sulphamethoxazole

Answer 10

PCP (with trimethoprim: co-timoxazole)

Answer 11

UTI e.g. Trimethoprim

Answer 12

Co-amoxiclav Tazocin Ciprofloxacin Meropenem

Answer 13

Combination antibotic containing penicllin (piperacillin) and a beta-lactamasae inhibitor tazobactam

Answer 14

Combination antibiotic containing penicllin amoxillin and beta-lactamase inhibitor clavulanic acid

Answer 15

Flucloxacillin, metronidazole, gentamicin

Answer 16

* 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)

Answer 17

Gram +ve organisms e.g. strep, clostridia Broken down by beta-lactamase, prod by S. aureus

Answer 18

Broad spectrum, extends coverage to enterococci and Gram -ve organisms Beta-lactamase produced by S. aureus and many gram negative organisms

Answer 19

Similar to penicllin although less active Stable to beta-lactamase produced by S. aureus

Answer 20

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

Answer 21

Beta-lactamase inhibitors extend coverage of penicllins to include S.aureus, Gram negatives and anaerobes

Answer 22

Increasing activity against gram negative bacilli

Answer 23

Cephalexin

Answer 24

Cefuroxime

Answer 25

Cefotaxime Ceftriaxone Ceftazidime

Answer 26

All cephalosporins regardless of in vitro results

Answer 27

•Stable to many β-lactamases produced by Gram negatives. Similar cover to co-amoxiclav but less active against anaerobes

Answer 28

anti-Pseudomonas

Answer 29

Stable to ESBL enzymes Carbapenemase enzymes becoming more widespread There are multidrug resistant Acinetobacter and Klebsiella species

Answer 30

* 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)

Answer 31

* Large molecules, unable to penetrate Gram –ve outer cell wall * Active against Gram +ve organisms

Answer 32

Oral vancomycin

Answer 33

Nephrotoxic Need to monitor drug levels to prevent accumulation

Answer 34

Gentamicin and tobramycin

Answer 35

* 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

Answer 36

Synergistic

Answer 37

* 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

Answer 38

* 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

Answer 39

•Bind to the 50s subunit of the ribosome 1) Interfere with translocation 2)Stimulate dissociation of peptidyl-tRNA

Answer 40

* Reversibly bind to the ribosomal 30S subunit * Prevent binding of aminoacyl-tRNA to the ribosomal acceptor site, so inhibiting protein synthesis.

Answer 41

) Prevent elongation of the polypeptide chain 2) Cause misreading of the codons along the mRNA

Answer 42

Aplastic anaemia Grey baby syndrome in neonates: inability to metabolise drug

Answer 43

•Chloramphenicol binds to the peptidyl transferase of the 50S ribosomal subunit and inhibits the formation of peptide bonds during translation

Answer 44

* Include the antimicrobial agents metronidazole & tinidazole * Under anaerobic conditions, an active intermediate is produced which causes DNA strand breakage

Answer 45

Compounds related to nitroimidazoles e.g. nitrofurantoin used for UTIs

Answer 46

Monitor LFTs beware interactions with other drugs that are metabolised by the liver Orange secretions

Answer 47

* 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.

Answer 48

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

Answer 49

* 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

Answer 50

Inactivation Altered target Reduced Accumulation Bypass

Answer 51

Beta lactamases Not the mechanism of resistance in penicllin resistant pneumoccoci and MRSA

Answer 52

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

Answer 53

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

Answer 54

Extended spectrum beta lactamases Able to break down cephalosporins, becoming more common Resistant to cephalosporins regardless of in vitro finding

Answer 55

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.

Answer 56

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

Answer 57

Orthomyxovrius

Answer 58

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

Answer 59

Ducks Because the vrius doesn't replicate in the colder URT

Answer 60

8 RNA segements of nucleocaspid protein very prone to mutation

Answer 61

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

Answer 62

H1= HA1 N1= N1

Answer 63

Mutation of HA/NA to give new viral strains

Answer 64

Complete change of HA/NA Reassortment of RNA segments between IFV strains Can only occur in IFVA

Answer 65

Cleavage of HA by clara-tryptase in the lung leads to exteded tropism/grwoth for H5 + H7

Answer 66

Secondary bacterial pneumonia Mutant virus Co morbidity Cytokine storm

Answer 67

Antiviral for IFV IFVA only Targets M2 ion channel but single AA mutation in M2= resistance

Answer 68

Oseltamivir (tamiflu) Zanamivir (relenza) Sialic acid Only effective if given \<48hrs aftern infection

Answer 69

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

Answer 70

Macrophages B-lymphocytes Langerhans DCs

Answer 71

Specific antigent in combination with a cytokine e.g. IL-2

Answer 72

Cell-mediated immune response IL-2 IFN-G TNF

Answer 73

Humoral response IL-4 IL-5 IL-6

Answer 74

Causes agglutination of RBCs/URT cells

Answer 75

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

Answer 76

Expansion Contraction Memory

Answer 77

Choice Host Antimicrobial susceptibilites of the Organism itself and also the Site of the infection

Answer 78

Narrow spectrum Bactericidal Based on local sensitivity Patient characteristics Cost

Answer 79

Serious infection or no PO absorption If need to access deep site or CNS

Answer 80

Age Renal/hepatic function Drug monitoring Allergy

Answer 81

Collect specimens Use a broad-spectrum antibiotic Empirical cover may then be changed to a more specific agent on the basis of culture results

Answer 82

Gram stain: CSF, joint aspirate, Pus Rapid antigen detection: immunofluorescence, PCR

Answer 83

pH Lipid-solubility CNS penetration Special considerations required for Rx of endocarditis or osteomyelitis

Answer 84

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

Answer 85

Concentration-dependant killing and prolonged persistent effects Maximise concentrations Aminglycosides, daptomycin, fluoroquinolines, ketolides

Answer 86

Time-dependant killing and minimal persistent effects Maximise duration of exposure Carabapenems, cephalosporins, erythromycin, linezolid, penicllins

Answer 87

Time-dependent killing and moderate-to prolonged persistent effects Maximise amount of drug Azithromycin, clindamycin, oxazolidinones, tetracyclines, vancomycin

Answer 88

Impetigo, cellulitis, wound infection S.aureusm, beta-haemolytic streptoccoci Fluclox unless penallergic or MRSA

Answer 89

Aggressive and early debridement Antibiotics: adjunctive use of protein synthesis inhibitors esp. clindamycin Use of IVIG

Answer 90

* 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.

Answer 91

Benzyl-pen 10d

Answer 92

Amoxicllin

Answer 93

Co-amoxiclav and clarithromycin

Answer 94

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

Answer 95

N meningitidis S pneumonia +/- Listeria in very young/elderly/immunocompromised Ceftriaxone +/- amoxycilllin if Listeria likely

Answer 96

Cefotaxime + amoxicillin

Answer 97

Used insteead of ceftriaxone as it displaces bilirubin from albumin and can cause biliary sludging

Answer 98

Benzylpen or ceftriaxone/cefotaxime

Answer 99

Trimethoprim

Answer 100

Cephalexin or Augmentin Change under gentamicin cover

Answer 101

Stop offending antibiotic: usually a cephalosporin If severe, RX with PO metronidazole If fails use PO vancomycin

Answer 102

Presence of bacteria in urine Inflammation of the bladder, often caused by infection

Answer 103

Uncomplicated: infection in a structureally and neurologically normal urinary tract Complicated: with functional or structural abnormalities including catheters/calculi

Answer 104

Men Pregnant Women Children Patients who are hospitalised or in healthcare settings

Answer 105

1-3% 40-50%

Answer 106

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

Answer 107

* Proteus mirabilis * Klebsiella aerogenes * Enterococcus faecalis * Staphylococcus saprophyticus * Staphylococcus epidermis

Answer 108

The relative frequency of infections caused by atypical organisms (i.e. not E. Coli) increases greatly

Answer 109

Urine: osmolality, pH, organic acids Urine flow and micturition Urinary tract mucosa: bactericidal activity, cytokines

Answer 110

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

Answer 111

Perpetuation of infection by maintaining a residual pool of infected urine in the bladder after voiding

Answer 112

Frequently a site of abscesses in patients with S aureus bacteremia or both Infection by gram negative bacilli rarely occurs by the haematogenous

Answer 113

Failure to thrive, Vomiting, Fever Frequency, dysuria, abdo or flank pain

Answer 114

* 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.

Answer 115

* 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

Answer 116

* 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

Answer 117

Urine Dip MSU for MCS Bloods: FBC, UE, CRP

Answer 118

Renal US IV urography

Answer 119

Squamous epithelial cells

Answer 120

(pus in urine) Prior treatment with antibiotics Calculi Catheterisation Bladder neoplasm TB STI

Answer 121

10^5 cf/mL in infection Patients without infection: \<10^4 cfu/mL

Answer 122

Occurs with indwelling catheters Can be cured by removal of catheter

Answer 123

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

Answer 124

Commonly associated with sepsis and septicaemia Requires more aggressive Rx Broad spectrum bios Co-amoxiclav +/- gent Imaging: calculi, structural cause

Answer 125

Co-amoxiclav +/- gent Cefuorxime +/- gent

Answer 126

Perinephric abscess Chronic pyelonephritis- scarring, chronic renal impairment Septic shock Acute papillary necrosis

Answer 127

E Coli Proteus Klebsiella Staph saprophyticus

Answer 128

Nitrites + leucocytes +ve

Answer 129

Timeothprim or nitrofurantoin

Answer 130

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.

Answer 131

Haematogenous spread Direct implantation (e.g. surgery, LP) Local extension (secondary to established infection) And PNS into CNS (viruses)

Answer 132

Infection of the meninges and CSF Dura mater Pia mater Arachnoid mater

Answer 133

Headache Stiff neck Soome disturbance of brain function

Answer 134

N meningitidis Pneumococcus H influenzae L monocytogenes GBS E Coli Staph aures Treponema pallidum TB Virus Cryptococcus neoformans Candida

Answer 135

N meningitidies

Answer 136

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

Answer 137

Septicaemia in 7-10% Meningitis in 50% Both in 40%

Answer 138

Coagulopathy...

Answer 139

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)

Answer 140

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

Answer 141

Usually bacterial

Answer 142

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

Answer 143

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

Answer 144

80-90% caused by coxsackie virus group B and echoviruses

Answer 145

GI flora: GBS, L monocytogenes, E Coli

Answer 146

GBS Listeria MTB (subacute)

Answer 147

HSV Remember to ask re symptoms of HsV infection

Answer 148

Infection of the brain parenchyma (Meningoencephalitis- inflammation of the meninges and brain parenchyma) Disturbances of brain function

Answer 149

Rabies Arboviruses Trapanasome brucei gambiense TB Prions Amoeba West Nile

Answer 150

SOL on imaging: looks like cancer, needs histopathology to say which Spreads from otitis media, mastoiditis, paranasal sinuses, endocarditis, haematogenously

Answer 151

Streptococci Staph Gram negative (particulalry in neonates) MTB Fungi Parasites Actinomyces Nocardia specias

Answer 152

Infection of the spinal cord

Answer 153

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

Answer 154

Disturbance of nerve transmission Polio

Answer 155

Advanced age IVDU LT-systemic steroids DM Organ transplantation Malnutrition Cancer

Answer 156

Tetanus from C tetani

Answer 157

Botulism C botulinum

Answer 158

Complement deficiency Hyposplenism Hypogammaglobulinameia

Answer 159

Complement deficiency Hyposplenism Immune defect (ETOH) Infection (pneumonia) Entry # Previous head trauma with CSF leak

Answer 160

Strep pneumoniae

Answer 161

Better than CT in detecting parenchymal abnormalities such as abscesses and infarctions

Answer 162

Clinical and blood cultures Throat swabs (neisseria) Serum-Ag EDTA-PCR CSF: WCC, protein, glucose

Answer 163

Colour/clarity WCC/differentaition Protein, glucsoe Culture: blood agar, chocolate agar, sabourand's agar

Answer 164

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

Answer 165

2.2-3.3 (\>50% serum)

Answer 166

Bacterial menintisi ?Meningococcus ?pneumococcus ?Listeria

Answer 167

Aseptic meningitis

Answer 168

MTB or cryptococcal meningitis

Answer 169

Think partiall treated bacterial infection

Answer 170

Cerebral abscesses (Streptococci) Viral encephalitis

Answer 171

ABC Corticosteroids before Abx Ceftriaxone (2g IV BD) for pneumo and meningococcus If elderly/immunocompromsied add amoxicillin or ampicillin to cover for Listeria)

Answer 172

Aciclovir Ceftriaxone If \>50y or immunocompromised add amoxicillin for Listeria cover 2g IV 4 hourly

Answer 173

Give ceftriaxone until you know it is herpes, no aciclovir

Answer 174

10mg/kg IV TDS

Answer 175

2g IV 4 hourly

Answer 176

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

Answer 177

Acute form of childhood protein-energy malnutrition: oedema, anorexia, ulcerating dermatoses and heaptomegaly Insufficient protein consumption but with sufficient calorie intake

Answer 178

Severe malnutrition, charactersied by energy deficiency. Emaciated

Answer 179

Schistosomiasis Hookworm Threadworm Filiarisis

Answer 180

Leishmaniasis Typanosomoiasis Amoebiasis

Answer 181

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

Answer 182

Acute hepatitis, ofetn subclinical, short period 2-6w

Answer 183

Faecal-oral spread Outbreaks associated with occupational risk e.g. sewage workers. Soft fruit, sewage works, shellfish

Answer 184

Recent infection disappears after a few months or vaccine

Answer 185

Previous infection, lifelong or vaccine

Answer 186

dsDNA virus

Answer 187

Vrisu makes an excess of surface antigen Therefore it is a good screening ttest

Answer 188

Acute \<6m Chronic Latent virus can reactivate in immunocompromised

Answer 189

Sexual, vertical, horizontal Blood products

Answer 190

Causes and acute or chronic heaptitis

Answer 191

Over decades leads to scarring and cirrhosis, eventually resulting in HCC. This is accelerated in males and drinkers

Answer 192

Supportive

Answer 193

Pegylated IFn alpha 2a Lamivudine Tenofovir

Answer 194

When liver damage occurs

Answer 195

ALT and AST HbsAg HBeAg (infectivity, changes form +ve to negative) HBcAb (acute- IgM, chronic IgG)

Answer 196

Acute, 80% progress to chronic

Answer 197

Blood products

Answer 198

Genotpyes 1 and 4= 48w 2&3= 24w

Answer 199

ALT Anti-HCV

Answer 200

Cure 54% treated with peg IFN alpha-2b and ribavirin combination therapy.

Answer 201

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

Answer 202

Only infect Hep B patients. Transmitted through contaminated blood

Answer 203

Superinfection and likely to have a very acute hepatitis and develop cirrhosis in 2-3y Treat with prolonged course of IFN

Answer 204

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

Answer 205

Secretory Inflammatory Enteric fever

Answer 206

Toxin production affecting the lumen No fever or a low grade fever No white cells on stool sample

Answer 207

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

Answer 208

Cholera toxin Superantigens from E COli

Answer 209

C jejuni Shigella Atypical salmonella species

Answer 210

Invasion, Peyer's patches, interstitial inflamamtion, monocytes, innate immune response Fever, WBC in stool, can be blood

Answer 211

Typphoidal, salmoneall subtypes, enteropathic Yersinia spp. Brucella spp.

Answer 212

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

Answer 213

Clostriida: botulinum perfringens difficile

Answer 214

Botulism is a descending paralysis

Answer 215

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

Answer 216

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

Answer 217

C perfringens

Answer 218

2 endotoxins (A and B) Causes pseudomembranous colitis Caused by Abx use, usually cephalosporins and fluorguinoloines

Answer 219

PO metronidazole 2nd line Vanco

Answer 220

Cephalosporins/fluoroquinolones

Answer 221

Bacillus cereus S. aureus

Answer 222

Reheated rice, spores gerimnate. Sudden vomiting Superantigen Watery, non bloody diarrhoea

Answer 223

Self-limiting

Answer 224

Prominent vomiting and watery non bloody diarrhoea

Answer 225

Don't treat, self limited

Answer 226

Gram -ve enterobacteriacae (faculative anaerobes, oxidase negative) E. COli

Answer 227

ETEC EIEC EHEC HUS EPEC

Answer 228

Toxigenic E coli, travellers diarrhoea. Food/water contaminated with human faecaes Enterotoxins: Heat labile: stimulates adenyl cyclase and cAMP Heat stable: stimulates guanylate cyclase

Answer 229

Invasive dysentry

Answer 230

Haemorrhagic E Coli: caused by verotoxin

Answer 231

E Coli 01571:H7 toxin Anaemia, thrombocytopenia, renal failure

Answer 232

Infantile diarrhoea

Answer 233

Self-limiting but can treat with ciprofloxacin if needed

Answer 234

Salmonella Shigella Yersinia

Answer 235

Salmonella

Answer 236

Typhi (and paratyphi) Enteritidis Cholearsuis

Answer 237

Transmitted from poultry, eggs, meat Invades small and large bowel Bacteraemia is infrequent Self-limiting **Blood**

Answer 238

Ceftriaxone or ciprofloxacin (if required)

Answer 239

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

Answer 240

Rose spots Enteric (Typhoid) fever

Answer 241

Ceftriaxone or ciprofloxacin

Answer 242

Mainly affects the distal ileum and colon. Infalmmation, fever, pain, bloody diarrhoea Dysentry

Answer 243

Avoid Abx, ciprofloxacin if required

Answer 244

Yersinia enteroclitis

Answer 245

Enterocolitis, mesenteric adenitis with necrotising granulomas Associated reactive arthritis and erythema nodosum Reye's syndrome Transmitted via food contaminated with domestic animal excreta

Answer 246

Cholear Parahaemolyticus Vulnificus

Answer 247

Rice water stool, human faecas Increased cAMP causes massive diarrhoea without inflammation O1 group: epidemic

Answer 248

Supportive

Answer 249

Ingestion of raw or undercooked seafoood Major cause of diarrhoea in Japan or in the carribean Self-limiting

Answer 250

Cellulitis in shellfish handlers Fatal septicaemia with D+V in HIV

Answer 251

Drinking unpasteurised milk, food, egg Prodrome of headache and fever with abdominal cramps Bloody (foul smelling diarrhoea) Associated with GBS, reactive arthritis

Answer 252

Erythromycin or cipro if first 4-5/7

Answer 253

Campylobacter

Answer 254

L monocytogenes

Answer 255

GI watery diarrhoea, cramps, headache, fever, little vomiting Perinatal infection, immunocompromised patients Refrigerated foods: unpasteurised dairy, vegetables

Answer 256

Ampicillin Ceftraixone Cotrimoxazole

Answer 257

Entamoeba histolytica Giardia lamlia Cryptosporidium parvum

Answer 258

Entamoeba histolytica

Answer 259

Entamoeba histolytica

Answer 260

Entamoeaba

Answer 261

Dysentry Wind Tenesmus Chronic weigtht loss and RUQ pain due to liver abscess Stool microscopy

Answer 262

Metronidazole and paramomycin (if luminal disease)

Answer 263

Metronidazole

Answer 264

Infects jejunym Severe diarrhoea in immunocompromised Oocysts seen in stool by modified Kinyoun acid-fast stain

Answer 265

Paromomycin Nitazoxanide

Answer 266

Rotavirus Adenovirus Norovirus Poliovirus Enteroviruses (coxsackie, ECHO) Hepatitis A

Answer 267

Secretory diarrhoea with no inflammation Watery diarrhoea through stimulation of the enteric nervous system Very common in children \<6.

Answer 268

Types 40, 41 \<2y/o

Answer 269

Mycobacteria

Answer 270

Mycobacteria

Answer 271

Mycobacteria

Answer 272

Young adults

Answer 273

?Re-activation/re-infection Upper lobes- may progress rapidly to cavitation Caseating granuloma Miliary spread rare Healing by fibrosis and calcification

Answer 274

RIPE Rifampicin and isoiazid for 6/12 Pyrazinamide and ethambutol for 2/12

Answer 275

Increase isoniazid and rifampicin to 8-10/12

Answer 276

6/12 isoniazid

Answer 277

Drug interactions (raised transaminases, cytochrome p450 induction) Orange secretions Hepatotoxicity

Answer 278

Rifampicin

Answer 279

Peripheral neuropathy (give B6/pyridoxine Hepatotoxcityi

Answer 280

Hyperuricaemia Hepatotoxicity

Answer 281

Pyrazinamide

Answer 282

Optic neuritis Visual disturbance

Answer 283

Ethambutol

Answer 284

DOTS Vit D therapy

Answer 285

Accelerates clinical recovery

Answer 286

Resistance to one drug only

Answer 287

Resistance to rifampicin and isoniazid

Answer 288

Resistance to rifampicin, isoniazid and injectables (kanmycin/amikacin)/ quinolones

Answer 289

Capreomycin Kanamycin Amikacin

Answer 290

Injectables Quinolones Cycloserine Ethionamide PAS Linelozid Clofazamine

Answer 291

TB meningitis

Answer 292

CT- tubercolmata LP- lymphocytic

Answer 293

Extrapulmonary TB

Answer 294

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).

Answer 295

Ghon focus Primary TB

Answer 296

Nonimmunocompetent= Elderly Children HIV

Answer 297

Focus or node ulcerates into bronchus-\> pneumonia Cavity formation, bronchiectasis, consolidation, collapse

Answer 298

TB taken by macrophase to LN, generalised lympho-haematogenous spread

Answer 299

Miliary TB

Answer 300

Miliary TB

Answer 301

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

Answer 302

Recent migrant HIV+ Homeless Drug user Prison Close contacts Young adults/elderly

Answer 303

Immunosuppression Malnutrition Ageing Chronic alcohol excess

Answer 304

?Spinal TB

Answer 305

MRI/CT +/- biopsy/aspirate

Answer 306

12/12 anti-TB

Answer 307

Haematogenous spread Initial discitis Vertebral destruciton and collapse +/- anterior extension causing iliopsoas abscess

Answer 308

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.

Answer 309

Potts Disease

Answer 310

Attenuated strain of M. Bovis

Answer 311

Bad for pulmonary TB Good for leprosy, TB meningitis, disseminated TB

Answer 312

Babies born in or with parents/grand parents from areas with incidence ?40/100000 Previously unvaccinated new immigrants from high prevalence countries for TB

Answer 313

HIV-ve latent TB -\> active TB 5-10% lifetime risk HIV+ve, yearly risk is 5-10%

Answer 314

M. Leprae M. Lepromatosis

Answer 315

Rifampicin, dapsone, clofazimine (if multibacillary)

Answer 316

Tuberculoid BT Borderline Lepromatous

Answer 317

Paucibacillary TH1 mediated Depigmented lesions

Answer 318

Nerve damageq

Answer 319

Multiple plaques

Answer 320

Multibacillary Th2 mediated Neuropathic ulcers

Answer 321

Environmental No person-person transmission Associated with impaired immunity, poor response to standard anti-TB regime

Answer 322

M. avium intracellulare complex

Answer 323

Pharyngeal/cervical addenitis

Answer 324

Underlying lung disease, resembles TB

Answer 325

Cytotoxics, lymphoma

Answer 326

Disseminated multibacillary infection Mycobacteraemia Consider in HIV patients with longstanding diarrhoea

Answer 327

M. Marinarum

Answer 328

M. Marinarum

Answer 329

M. Ulcerans

Answer 330

By insects, tropics/australia

Answer 331

Rifampicin Streptomycin Sx

Answer 332

Buruli ulcer

Answer 333

Buruli Ulcer M. Ulcerans

Answer 334

Inflammation of lung alveoli Can be lobar or bronchopneumonia

Answer 335

Inflammation of medium sized airways, mainly in smokers. Cough with sputum most days for 3m or 2 or more consecutive years

Answer 336

Viruses S. pneumoniae H. influenzae M. catarrhalis

Answer 337

Often normal

Answer 338

Bronchodilation, PT +/- Abx

Answer 339

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

Answer 340

Treat as an outpatient

Answer 341

Consider hospital

Answer 342

Hospitalise ?ITU

Answer 343

S. Pneumoniae H. influenzae M. catarrhalis S. aureus K. pneumonia

Answer 344

S. pneumonia

Answer 345

H. influenza

Answer 346

M. catarrhalis

Answer 347

Staph aureus

Answer 348

Klebsiella

Answer 349

Strep pneumoniae

Answer 350

H. infleunza

Answer 351

M. catarrhalis

Answer 352

Klebsiella

Answer 353

No signs or chest XR or signs not in keeping with CXR May be extrapulmonary signs e.g. hepatitis, hyponatraemia

Answer 354

Legionella Mycoplasma Chalmydia pneumonia Chlamydia psittaci

Answer 355

Bordatella pertussis TB

Answer 356

Legionella

Answer 357

Mycoplasma

Answer 358

Chlamydia pneumonia

Answer 359

Chlamydia psittaci

Answer 360

Bordatella pertussis

Answer 361

PCP TB Cryptococcans

Answer 362

Fungi- aspergillus

Answer 363

Aspergillus CMV

Answer 364

Encapsulated organisms: H. influenzae, S. pneumonia, N. meningitides

Answer 365

Pseudomonas aeruginosa Burkholderia cepacia (v. high mortality)

Answer 366

Lobar pneumonia Strep

Answer 367

Cavitating pneumonia Staph aureus

Answer 368

Non microbiological: FBC, U&E, CRP, ABG, CXR Microbiology: sputum MC+S, blood cultures, effusion aspiration/BAL

Answer 369

Urine antigen tests

Answer 370

Paired serum samples at presentation and 10-14/7 Rise in Ab level over time Useful for difficult to culture (chalmydia, legionella)

Answer 371

\>48 hours into hospital stay without previous infection

Answer 372

To differentiate URT and LRT microbes

Answer 373

Amoxicillin or macrolide 5-7d

Answer 374

Clarithromycin + co-amoxiclav/cefuroxime (2-3w)

Answer 375

Macrolide/tetracycline Clarithromycin

Answer 376

Increases anticoagulant effect of Warfarin

Answer 377

Ciprofloxacin +/- vancomycin

Answer 378

Piptazobactam + vancomycin

Answer 379

Cefuroxime Metronidazole

Answer 380

Macrolide + rifampicin

Answer 381

Piperacillin + tazobactam (tazocin) or ciprofloxacin +/- gentamicin

Answer 382

Coliforms and pseudomonas more likely the longer the stay

Answer 383

Escheria Klebsiella Citrobacter Enterobacter

Answer 384

P. aeruginosa, acinetobacter, stenotrophomonas maltophilia

Answer 385

Pneumococcal pneumonia

Answer 386

Mycoplasma pneumoniae

Answer 387

Legionella

Answer 388

Guanosine analogue, blocks viral DNA extension through activation by thymidine kinase present in HSV NB CMV doesn't have this enzyme

Answer 389

CMB, EBV, HHV-6

Answer 390

Nucleoside analgoue

Answer 391

BM suppression

Answer 392

CMV conseuqnecs Retinitis Colitis Hepatitis Encephalitis Pneumonitis

Answer 393

CMV infected cells

Answer 394

CMV infection Owl eye inclusions

Answer 395

pyrophosphate analgoue. Inhiits nucleic acid synthesis without requring activation

Answer 396

Used when CMV resistant to ganciclovir Also used as prophylaxis post organ transplant

Answer 397

Nuceloside phosphonate

Answer 398

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)

Answer 399

Nephrotoxic Maintain hydration and co=administer probenecid

Answer 400

Acyclovir Valaciclovir Famciclovir

Answer 401

If it s resistant

Answer 402

Immunocompromised Pregnants Adults with pneumonitis

Answer 403

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)

Answer 404

Serum HBV DNA levels (\>2000IU) Serum transaminitis (above normal limit) Liver biopsy histological grade and stage: moderate-severe active necroinflammation and or fibrosis

Answer 405

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

Answer 406

Pegylated INF alpha 2a Nucelos(t)ide analogues

Answer 407

Direct antiviral effect and upregulates expression of MHC on cell surfaces

Answer 408

Inhibitor of viral polymerase

Answer 409

Inhibitor of viral polymerase

Answer 410

Inhibitor of viral polymerase (no resistance)

Answer 411

Inhibitor of viral polymerase

Answer 412

Inhibitor of reverse transcriptase

Answer 413

Entecavir PegINF a2a Tenofovir

Answer 414

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

Answer 415

RNA nucleoside analgoue

Answer 416

Haemolytic anaemia

Answer 417

PegINF a2a Ribavirin

Answer 418

IFVA NA inhibitor

Answer 419

IFVA NA inhibitor

Answer 420

M2 Channel IFVA

Answer 421

RSV/ parainfluenza Guanosine analgoue

Answer 422

MMR Yellow fever BCG OPV Varicella Typhoid Flu

Answer 423

Rabies, pertussis, IPV, Hep A, typhoid

Answer 424

Hib Men C PCV

Answer 425

Tetanus Diptheria

Answer 426

Subacute sclerosing pancencephalitis Measles

Answer 427

Pts on CTx, pts \<6/12 after BMT, children on high dose steroids +/- cytotoxics

Answer 428

Yes if susceptible

Answer 429

Anaphylaxis Protracted crying

Answer 430

Poliomyelitis (OPV)

Answer 431

Thrombocytopenia

Answer 432

Acute arthritis

Answer 433

Encapsulated yeast i.e. cryptococcus

Answer 434

Co-trimoxazole and oral prednisolone 2nd line= clindamycin and primiquine. IV methylprednisolone

Answer 435

Actinomyces

Answer 436

Affects biofilm formation

Answer 437

Gonorrhoea Chlamydia Trichomonas Candida BV

Answer 438

Syphillis HSV LGV Chancroid Donovanosis

Answer 439

Genital warts- HPV Molluscum contagiosum Scabies Pubic lice

Answer 440

**Herpes** Chancroid

Answer 441

**Syphillis** Lymphogranuloma venereum Granuloma inguinale

Answer 442

N. gonorrhoea

Answer 443

Conjunctivitis that develops if gonorrhoea left untreated when child transfers to birth canal

Answer 444

Get disseminated gonococcal infection- septicaemia, rash and or arthritis

Answer 445

Urethral/rectal smears Culture from these is gold standard

Answer 446

Ceftriazone IM-250mg one dose or cefixime PO 400mg single dose

Answer 447

Spectinomycin IM 2g single dose

Answer 448

Non-gonoccocal urethritis

Answer 449

Mucoid/mucopurulent discharge

Answer 450

Post gonococcal urethritis Follows gonorrhoea Rx Can be prevented by concomittant Rx with tetraceline

Answer 451

Prostatitis

Answer 452

Mucopurulent cervicitis Erythema and oedema Urethra from vaginal leakage

Answer 453

Chlamydia trachomatis

Answer 454

Often assymptomatic (50% men, 80% women)

Answer 455

Exists ion 2 forms Elementary bodies: stable, extracellular Reticulate particles: intracellular, metabolically active

Answer 456

Trachoma which can cause blindness

Answer 457

Genital chlamydia, opthalmia neonatorum

Answer 458

PID Tubal factor infertility Increased risk of ectopics Increased risk of endometriosis Chronic pelvic pain Epididymitis Reiters Adult conjunctivitis Opthalmia neonatorum

Answer 459

NAAT= gold standard

Answer 460

Azithromycin 1g (4 capsules) STAT Doxycycline 100mg BD 7/7 Erythromycine 500mg QDS 7/7 or 500mg BD 2/52

Answer 461

N+V Photosensitivity C/I in pregnancy

Answer 462

Lympho-granuloma venereum Lymphatic infection with chlamydia trachomatis serovars L1, L2, L3

Answer 463

Lymphogranuloma venereum

Answer 464

Early LGV Primary Early LGV Secondary Late LGV Current LGV outbreak

Answer 465

3-12/7 Genital ulcer, painless, non-indurated, balantitis, proctitis, cervicitis

Answer 466

2-25/52 Inguinal buboes: painful, 2/3rd unilateral May rupture Fever, malaise Rarely (hepatitis, meningo-encephalitis, pneumonitis) Proctocolitis Hyperplasia of lymphoid tissue

Answer 467

Inguinal lymphadenopathy Abscess formation Genital elephantiasis Genital ulcers Frozen pelvis Rectal strictures Peri-rectal abscesses + fistulae Lymphorroids

Answer 468

Rectal symptoms- pain, tenesmus, bleeding, mucus discharge O/E: proctitis

Answer 469

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

Answer 470

**Doxycycline 100mg BD for 21/7** Erythromycin 500mg QDS for 21/7 Azithromycin 3/52 1g weekly

Answer 471

Treponema pallidum (Syphillis)

Answer 472

Majority of cases are in those who are HIV +ve Patients often co-infected with HCV or another STI

Answer 473

Seen in primary lesions by dark-ground micrscopy Can be detected with RT-PCR

Answer 474

1. 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. 2. 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

Answer 475

Primary Secondary Latent Tertiary

Answer 476

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

Answer 477

Chancre Syphillis

Answer 478

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)

Answer 479

No clinical Serological infection

Answer 480

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

Answer 481

Prostitute's pupil Accomodates but doesn't react Syphillis

Answer 482

Single dose IM benpen (doxy if pen allergic) Monitor RPR, need to see a 4x reduction to consider tx succesful

Answer 483

Fever, headache, myalgia, sometimes and exacerbation of syphillitic symptoms commonly developing within hours of abx administration

Answer 484

May occur during pregnancy or birth Often develops features over the first couple of years including hepatosplenomegaly, rash, fever, neurosyphillis and pneumonitis

Answer 485

Haemophilus ducreyi

Answer 486

Tropical ulcer disease mainly seen in africa Often multiple ulcers, frequently painful

Answer 487

Culture on chocolate agar PCR

Answer 488

Chancroid Haemophilus ducreyi

Answer 489

Donvoanosis: Ganuloma inguinale

Answer 490

Klebsiella granulomatis

Answer 491

Africa, India, PNG, Autralian Large, expanding ulcers starting as a papule or nodule that breaks down with a beefy red appearnce

Answer 492

Donovanosis

Answer 493

Giemsa stain of biopsy or tissue crush showing Donovan bodies

Answer 494

Azithromycin

Answer 495

(oro-anal contact) Shigella Salmonella Giardia Occasionally others e.g. Strongyloides

Answer 496

Trichomonas

Answer 497

Wet prep micrscopy, PCR

Answer 498

Asymptomatic/ urethritis in men Discharge in women

Answer 499

Associated with increased risk of HIV acquisition

Answer 500

Metronidazole

Answer 501

Abnormal vaginal flora, polymicrobial, discharge, odour Sexually associated but not transmitted May be associated with hygiene practices

Answer 502

Microscopy of gram stain raised pH Whiff test Clue cells

Answer 503

Trichomoniasis

Answer 504

Associated with preterm delivery

Answer 505

Usually candida albicans If symptomatic: white thick discharge, itching, soreness, redness Common presentation in women as vulvovaginitis, men as balanitis Not an STI

Answer 506

Clotrimazole or fluconazole (i.e. oral antifungals)

Answer 507

Pox virus Caused by skin to skin contact In adults causes genital lesions and is spread via sexual contact

Answer 508

HIV until proven otherwise There are giant lesions in the immunocompromised

Answer 509

If required= destructive cryotherapy

Answer 510

Human papillmoavirus

Answer 511

HPV6 or 11 (not associated with increased risk of cervical dysplasia)

Answer 512

Exmaintion: papular, planar, pedunculated, carpet, keratinised, pigmented

Answer 513

Podophyllotoxin solution or cream Can't be used in pregnant women

Answer 514

1st line: cryotherapy 2nd line: Imiquimod

Answer 515

HAV, HBV, HCV (mainly HIV +ve MSM) Herpes HIV

Answer 516

Infeciton acquired \>48h after admission

Answer 517

Spore ingestion

Answer 518

Clindamycin Cephalosporins Cprofloxacin

Answer 519

ESBeta lactamases

Answer 520

MRSA Coag negative staph E Coli

Answer 521

Staph epidermis

Answer 522

MRSA Coag negative Staph

Answer 523

C diff Norovirus Acinetobacter

Answer 524

Legionella

Answer 525

Aspergillus

Answer 526

TB, chicken pox, RSV

Answer 527

UTI\> surgical site infection\> HA pneumonias

Answer 528

By organism or by syndrome

Answer 529

Catheter associated blood stream infection Urinary catheter associated UTI Surgical site infeciton Ventilator associated penumonia Antibiotic associated diarrhoea

Answer 530

Enterobacter\> Klebseilla\> E. Coli ESBLs

Answer 531

Skin and subcutaenous tissue, red hot and tender

Answer 532

Down to deep soft tissue, fascia, muscle Wound may reopen

Answer 533

Organ/space Reoperation and drainage

Answer 534

Toxin A and B: diarrhoea, colitis Tonxiotype: III/BI/NAP1/027: proinflammatory, cytotoxic, enterotoxic

Answer 535

Mild colitis-\> severe colitis-\> pseudomembranous colitis and perforation

Answer 536

Physiologically unstable: PR/ BP/ T/ RR  High WCC \>15  Rising or high creatinine \> 20  Clinical- peritonism, ileus, obstruction  Radiological: colitis.  Others: age, albumin etc.

Answer 537

Co-amoxiclav

Answer 538

Metronidazole

Answer 539

Tazocin (piperacillin-tazobactam)

Answer 540

Amoxicillin

Answer 541

Ciprofloxacin

Answer 542

Gentamicin

Answer 543

Resp/blood-borne infection 6-8d incubation Fever, malaise, erythema infectiosum, transient aplastic crisis (especially those with sickel cell, spherocytosis)

Answer 544

Infection \<20w assocaited with 30% risk of hydrops foetalis \>20w= no risk

Answer 545

Respiratory

Answer 546

90% develop congeital rubella syndrome

Answer 547

Hearing defects, retinopathy

Answer 548

No documented rsik

Answer 549

Cataracts, congenital glaucoma Deafness Congeital heart defects Purpura Splenogemgaly mIcroencephaly Mental retardation Meningoencephalitis

Answer 550

Risk of stillbirth x5 Preterm delivery x3 No congenital malformations

Answer 551

Vaccination and treatment of pregnant women with antivirals (oseltamivir, zanamivir)

Answer 552

Can cause IUD/miscarraige, preterm devliery and increased maternal morbidity

Answer 553

Opportunistic bacterial infections: otitis media, pneumonia, bronchitis Encepahlits and subacute sclerosing pancencephalitis

Answer 554

Associated with early onset neonatal hepatitis, congenital myocarditis, early onset childhood IDM and abortion of intrauterine death

Answer 555

Staph auerus

Answer 556

Staph epidermis

Answer 557

Enterococcus

Answer 558

Actinomyces Bacillus Clostridium Diptheria Listeria

Answer 559

Dental/oral infections

Answer 560

Difficile, perfringens, botulinum, tetani

Answer 561

Actinomyces Clostridium Bacteroides (gram -ve)

Answer 562

Metrondiazole, cephamycins

Answer 563

Neisseria: meningtidis, gonorrhoea Moraxella catarrhalis

Answer 564

E. Coli Salmonella Shigella Klebseilla Yersinia Enterobacteriaceae

Answer 565

H. infleunza/ducreyi Bordatella pertussis Pseudomonas aeruginosa Chlamydia trachmoatis

Answer 566

Trep pallidum Leptospoirosis Borrelia e.g. Lyme disease

Answer 567

Chalmydia trachomatis Rickettsia Coxiella (Q fever) M leprae

Answer 568

Toxoplasma Cryptosporidium Leishmania spp

Answer 569

Obligate intracellular

Answer 570

Toxoplasmosis Other (HIV/HBV) Rubella CMV HSV

Answer 571

Rubella Syphillis HBV HIV

Answer 572

Classical symptoms of congenital infection

Answer 573

Thrombocytopenia Optic, otitic Rash Cerebral abnromality Hepatosplenomegaly

Answer 574

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

Answer 575

Less maternal Ig NICU care Exposure to organisms

Answer 576

\<48h after birth

Answer 577

GBS!! E. Coli Listeria

Answer 578

Early onset sepsis

Answer 579

Maternal: PROM Fever Foetal distress Foetal: Respiratory distress Acidosis Asphyxia

Answer 580

Septic screen: FBC, CRP, blood cultuie, deep ear swab, CSF, surface swab, CXR

Answer 581

Supprtoive: admission to NICE, ventiulation, circulation, nutrition (TPN) Benpen and gentamicin (E Coli cover) Listeria: ampicillin or amoxicillin

Answer 582

Ampicillin or amoxicillin

Answer 583

Coag negative staph GBS E COli Listeria S. aureus Enterococci Gram negatives kleb, enterobacter, pseudomonas Candida

Answer 584

Bradycardia Apnoea Poor feeding Irritability Billious aspirate Convulsions Jaundice Respiratory distress

Answer 585

Septic screen and urine

Answer 586

Fluclox and gentamicin

Answer 587

Tazocin and vancomycin: consider ability to cross BBB if meningitis

Answer 588

Cefotazime and amoxicllin +/- getamicin

Answer 589

Neisseria meningitides Strep pneumoniae Hib

Answer 590

Strep pneumoniae

Answer 591

N meningitides S pneumonia (Hib) GBS E Coli Listeria

Answer 592

N meningitidis S pneumonia Hib if unvaccinated

Answer 593

N meningitis S pneumoniae

Answer 594

Viruses S pneumoniae atypica Myocplasma if \>4y Bordatella MTB

Answer 595

Culture \>10^5cfu/ml Pyuria Clincal symptoms

Answer 596

Co-amoxiclav Tazoin Ciprofloxacin Meropenem

Answer 597

Fluclox Metronidazole Gentamicin

Answer 598

Bypass antibiotic sensitive step Enzyme-mediated drug inactivation Impairment of drug accumulation Modification of drug target

Answer 599

Codon 129 polymorphism: MM massively increases the susceptiblity Specific PRNP mutation

Answer 600

Clonazepam Myoclonas (valproate, levetiracetam, priacetam

Answer 601

Quinacrine Pentosan Tetracycline

Answer 602

Serial EEG shows periodic triphasic changes

Answer 603

Non-specifc slow waves

Answer 604

Non-specific changes

Answer 605

Normal/highlighting basal ganglia

Answer 606

Posterior thalamus highlighted on MRI- T2: pulvinar sign

Answer 607

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

Answer 608

Sometimes high signal in BG

Answer 609

14-3-3 +ve

Answer 610

14-3-3 can be normal

Answer 611

No mutations

Answer 612

No mutations

Answer 613

No mutations

Answer 614

Mutations present and diagnostic

Answer 615

Most are MM

Answer 616

Most homozygous MM and VV

Answer 617

129 codon homozygosity may confer earlier onset

Answer 618

Type 4t from tonsillar biopsy (100% sensitive and specific)

Answer 619

Either somatic PRNP mutation or spontaenous conversion of PRPc to PrPSc

Answer 620

vCJD Iatrogenic Kuru

Answer 621

fCJD GSS FFI Various atypical dementias

Answer 622

Gesrtmann-Straussler-Scheinker syndrome

Answer 623

Not useful

Answer 624

Exclude nonspecific e.g. hepatic encepahlopathy Lithium toxicity NB only 2/3rds will have abnormal EEG

Answer 625

Staph aureus

Answer 626

Staph aureus E Coli Pseudomonas Haemolytic strep

Answer 627

DM Peri-operative hyperglycaemia Current smoker Remote infection at time of sx Obesity Malnutrition Low preoperative albumin Concurrent steroid use

Answer 628

Sterile site e.g. THR

Answer 629

Post-appendectomy

Answer 630

Perforated bowel

Answer 631

Abnormal joint (RA/OA/gout/prosthesis) Immunosuppressed (CLD, steroids) Bacteraemia (e.g. DM, IVDU) Trauma/penetrating injury

Answer 632

Staph aureus most common Streptococci 22% Gram -ve less commonly e.g. E. Coli

Answer 633

Septic arthritis

Answer 634

Blood culturebefore Abx Joint aspirate (\>50,000 cells/ml) Inflammatory markers Imaging shows effusion

Answer 635

IV antibiotics (cephalosporin or fluclox) MRSA: Vancomycin Drain joint

Answer 636

Increased severity of staph infection

Answer 637

Staph aureus sepsis

Answer 638

Staph aureus Staph epidermis (4%) Strep pyogenes Strep pneumonias Strep agalactiae E Coli Hib Neisseira gonorrhoea Salmonella Brucellosis MTB Fungi

Answer 639

Subacute osteomyleitis which may pesrist for years before converting to frank OM

Answer 640

Staph aureus

Answer 641

MRI Bone biopsy for culture/histology

Answer 642

Debride and remove infected bone and soft tissue

Answer 643

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

Answer 644

Complete excision of infected tissue and necrotic bone Open cancellous grafting of the osseous defect Skin grafting for wound closure

Answer 645

Local wound infection Previous revision Bilateral athrtoplasty Wound healing complications

Answer 646

Prosthetic joint infection

Answer 647

Coag negative staph

Answer 648

Staph Aureus Strep Enterococci Gram negative: enterobacteria, pseudomonas Anaerobes, fungi etc

Answer 649

Prosthetic joint infection

Answer 650

XR Inflammatory markers Aspirate

Answer 651

Single or two stage revision Use Abx-impregnated cement

Answer 652

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.

Answer 653

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.

Answer 654

Clindamycin + Gentamicin

Answer 655

Vancomycin, ofloxacin & gentamicin

Answer 656

Vanc Ampicillin Gent

Answer 657

Cefotaxime Ofloxacin Gent

Answer 658

Clindamyinc, gentamicin, cefoperazone

Answer 659

Amikacin Streptomycin

Answer 660

Vanc Clindamycin Gent

Answer 661

Funcitonally or structurally abnormal tract

Answer 662

Broad spec IV Abx e.g. co-amoxiclav and gent or cefuroxime and gent

Answer 663

One of the main defences is bacterial flushing

Answer 664

Likely to be due to haematogenous spread i.e. staph sepsis

Answer 665

Dysuria Urgency Frequency Polyuria Suprapubic tenderness Haematuria

Answer 666

Trimethoprim or cephalexin for 3d NFT for 7d NB 7d of treatment recommended for women who have had previous UTI

Answer 667

Cephalexin BD for 7d 2nd line: coamoxiclav QDS for 7d

Answer 668

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

Answer 669

Denature Primer annealing Chain elongation with Taq polymerase

Answer 670

Pneumonitis

Answer 671

Reactivation of latent infection e.g. Herpes Graft brought infection with it e.g. HBV Exogenous opportunistic infection post-transplant

Answer 672

Due to immune systems inability to mount a full response serology of limited diagnostic value Viral detection preferable e.g. PCR

Answer 673

HSV1+2, VZV, CMV, HHV6, 7, 8 EBV

Answer 674

Sensory nerve ganglia

Answer 675

Leucocytes

Answer 676

As a higher rate of Cx e.g. pneuonitis and hepatitis

Answer 677

Seropositive donor and seronegative recipient due to recipient viral exposure

Answer 678

Serongetive donor but seropositive recipient due to loss of protective Abs

Answer 679

Pre-emptive treatment with ganciclovir

Answer 680

Reduce immunosuppression Rixumiab CTx once it becomes lymphoma

Answer 681

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

Answer 682

Can cause graft rejection

Answer 683

Ganciclovir Foscarnet/cidofovir

Answer 684

Affects paediatric patients High mortality with disseminated infection Weekly PCR surveillance Treated with reduction of immunosuppression and ribavirin

Answer 685

Consider HNIG

Answer 686

Haemorrhagic cystitis

Answer 687

Ureteric stenosis

Answer 688

Infection of the innermost layer of the heart, usually the valves

Answer 689

Infective endocarditis

Answer 690

?Infective endocarditis

Answer 691

Subactue: Clubbing, splinter haemorrhages, Osler's nodes, Janeway lesions, Roth spots, splenomegaly, haematuria

Answer 692

FBC (anaemia), U&E, CRP ESR 3x blood cultures without Abx Serology if culture negative CXR Echo

Answer 693

2 major or 1 major + 3 minor or 5 minor

Answer 694

Persistent bacteraemia (\>2 +ve blood cultures) Echo findings: vegetations +ve serology for bartonella, coxiella, brucella

Answer 695

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

Answer 696

Low virulence strep: Strep viridans

Answer 697

Mild-moderate illness progressing over weeks to months Decrease propensity haematogenously to seed extracardiac sites

Answer 698

Coag negative staph

Answer 699

Fulminant illness d-w

Answer 700

Cultures taken after abx

Answer 701

Haemophilus Aggregatibacter/Actinobacillus Cardiobacterium hominis Eikenella corrodens Kingella Kingae Aspergillus, brucella, coxiella, chlamydia, mycoplasma

Answer 702

Vanc + Gent + Rifampicin

Answer 703

Pen and Gent

Answer 704

Pen + Gent

Answer 705

Fluclox for 4/52

Answer 706

Vanc + gent/rifamp/fucidin

Answer 707

Ampiciliin + Gent

Answer 708

\>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

Answer 709

Classical Healthcare associated PUO Neutropaenic PUO HIV associated PUO

Answer 710

\>38C on several occassions for \>3w in spite of at least 1 week of investiagations

Answer 711

As for PUO oncluding 3/7 in hospital or \>3O/P with ambulatory Ix

Answer 712

Infections Neoplasms CTD Misc conditions: abscesses, endocarditis, TB, complicated UTIs Undiagnosed conditions

Answer 713

Develoops in hospital following \>38h in hospital

Answer 714

Kawasaki's JIA

Answer 715

CTD predominant: temporal arteritis, PMR Infections

Answer 716

Sx Drugs Medical devices LRTI C diff colitis Immobilisation

Answer 717

Vancomyin Penicllins Serotonergics

Answer 718

Fever concomittant with neotrpaenia and subsequent lack of cellular response = MEDICAL EMERGENCY

Answer 719

Infections CTx Haematological malignancies Look for conditiosn that require neutrophils e.g. fungal infection, bacterial, MTB GVHD Drug fever

Answer 720

HIV +ve patients frequently have PUO Cause related to CD4 count

Answer 721

Seroconversion TB Kaposi's Bacterial Disseminated MAI PCP CMV Cryptococcus Toxoplasmosis Lymphoma Histoplasmosis Drug fever

Answer 722

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

Answer 723

Malaria (21%) Dengue Typhoid Rickettsia Bacterial diarrhoea UTI Pneumonia HIV seroconversion Viral haemorrhagic fevers Timing is key

Answer 724

S. typi and paratyphi

Answer 725

Enteric fever infecting Peyers patches, transmitted by food and water

Answer 726

Gallstones Immunosuppression

Answer 727

Hx Blood cultures Stool

Answer 728

IV fluids Oral or IV Abx HPA notification

Answer 729

Food or water

Answer 730

Falciparum

Answer 731

P. falciparum P. vivax P. ovale P. malariae

Answer 732

Falciparum Vivax Ovale (48hr)

Answer 733

P malariae

Answer 734

V severe Parasitaemia

Answer 735

Chronic liver stage (hypnozoites)

Answer 736

Chronic liver stage Hypnozoites

Answer 737

P falciparum

Answer 738

P Ovale | (vivax with merozites)

Answer 739

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

Answer 740

P falciparum malaria

Answer 741

P. falciparum malaria

Answer 742

Chloroquine then Primaquine if resistant or minimal response

Answer 743

Quinine + doxycylcine/clindamycin OR malaronie (atovoquone/proguanil) or RIamet (artemether and lumefantrine)

Answer 744

Artemisinin combination therapy (ACT) or IV quinine + doxycycline/clindamycin

Answer 745

HIV Malaria TB Typhoid Rabies

Answer 746

ARboviruses: denghue, yellow fever, japanese encephalitis SARS Haemorrhagic fevers: lassa, ebola Meningococcoaemia Rarely: rabies

Answer 747

Flavivirus: tickborune and japanese encephalitis Typhoid Toxoplasma Haemorrhagic fevers Measles Rarely: Hep A

Answer 748

Schistosomiasis TB Viral hepatits Filiarisis Rarely: EBola/ Lassa

Answer 749

Altered consciousness/ seizures Renal impairment Acidosis (\<7.3) Hypoglycaemia (\<2.2mmol) Pulmonary oedema/ARDS Anaemia Spontaneous bleeding/DIC Shock Haemoglobinuria Parasitaemia \>2% Pregnancy Vomiting

Answer 750

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.

Answer 751

Clindmaycin

Answer 752

Quinine 20mg/kg loading doese IV over 4h then 10mg/kg/IV over 4h every 8 hours + oral doxy 200mg/clindamycin for 7d.

Answer 753

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

Answer 754

HSV VZV CMV EBV HHV6 HHV8

Answer 755

HSV 1+ 2 VZV

Answer 756

HSV1 and HSV2

Answer 757

HSV infection

Answer 758

HSV infection

Answer 759

Sacral radiculomyelitis leading to urinary retention (self-limiting)

Answer 760

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.

Answer 761

Ocular herpes infection HSV

Answer 762

Acute retinal necrosis if immunocompetent

Answer 763

Progressive Outer Retinal Necrosis (also caused by VZV, EBV, CMV)

Answer 764

Herpetic encephalitis

Answer 765

Recurrent benign lymphocytic meningitis

Answer 766

Herpes encephalitis

Answer 767

IV aciclovir STAT Don't wait for results 10mg/kg TDS then oral ACV for total of 2-3/52

Answer 768

Herpes gladiatorum

Answer 769

Painful red finger

Answer 770

Herpetic whitlow

Answer 771

Gladiatorum Whitlow Erythema multiforme HS dermatitis Eczema herpeticum Zosteriform HS (painless)

Answer 772

Scarring Pneuominitis Haemorrhage Eye involvement Reyes's syndrome Neurological

Answer 773

Acute cerebellar ataxia GBS Ramsay hunt syndrome Encephalitis Post-herpetic neuralgia

Answer 774

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.

Answer 775

Exam- vesicles Cytology: Tzanck cells Immunofluorescnece cytology PCR: if rash is old, in CNS/ocular disease

Answer 776

Multinucleated giant cells found in VZV and HSV infections

Answer 777

CIed as a live vaccine

Answer 778

VZV reactivation (DRG) in times of stress/ reduced immunity Painful, dermatomal rash

Answer 779

Symptomatic children or healthy adult smokes, chronic lung disease

Answer 780

Aciclovir 800mg PO or famciclovir or valaciclovir Topical eye drops PEP for immunocompromised

Answer 781

CMV and Roseola virus

Answer 782

Asymptomatic Congenital CMV mononcucleosis Immunocompromised

Answer 783

IUGR/Jaundice/hepatosplenomegaly Chorioretintis Encephalitis Microcephaly Death Late progressive sensorineural deafness LD Cyotmegalic inclusion disese

Answer 784

Fever, heapatitis Colitis Retinitis Pneuopnitis BM suppression Addison's disease Radiculopathy

Answer 785

Macrophages, endothelial cells, B and T lymphocytes BM cells

Answer 786

Paul Bunnel/Monospot

Answer 787

Infectious mononucleosis Burkitt's Nasopharyngeal Ca Post-transplant lymphoproliferative disease

Answer 788

Infectious mononucleosis

Answer 789

Gancilcoivr and Foscarnet

Answer 790

H1` peaks beginning of January each year

Answer 791

End of december

Answer 792

Coronavirus

Answer 793

Only effective if administered within 48h of infection

Answer 794

Hantan viruses Lyme borrelliosis Erhlichia Bartonella Lymphocytic choriomeningtiis

Answer 795

Rabies Leptospirosis Lassa fever Hantan viruses Plague Pasterullosis Haverhill fever

Answer 796

Bartonellosis (cat scratch) Leptospirosis Q fever Toxoplasmosis Rabies Ringworm Toxocariasis

Answer 797

Hydatid Leptospirosis Q fever Rabies MRSA Ringworm Toxocariasis

Answer 798

Anthrax Brucellosis Q fever Cryptosporidiosis Enzootic abortion Louping ill Orff virus Rift valley fever Toxoplasmosis

Answer 799

Anthrax Leptopspirosis Brucella Bovine TB Anaplasmosis Toxoplasmosis E Coli 0157 Rift valley fever Ringworm

Answer 800

Brucellosis Leptospirosis Erysipeloid Cysticerosis Trichinella HEV IAV Streptococcal sepsis

Answer 801

Psitticosis IFV Cryptococcus IAV Poultry: salmonella WNV

Answer 802

Leptospirosis HAV Giardia Toxoplasmosis Mycobacterium marinum/ulcerans Brukholderia Pseudomallei E Coli

Answer 803

Campylobacter Salmonella VTEC 0157 Cryptosporidium

Answer 804

Listeria Taenia Cysticerosis Toxoplasmosis Trichinellosis Yersiniosis Giardia

Answer 805

Diseases and infections which are transmitted naturally between vertebrate animals and man

Answer 806

Brucellosis

Answer 807

Inhalation Skin or mucus membrane contact

Answer 808

Brucellosis

Answer 809

Brucellosis

Answer 810

Brucellosis

Answer 811

Serology: anti-O-polysaccharide Ab WCC usually normal Leucocytosis rare Signficant number of patients may become neutropaenic

Answer 812

4-6/52: tetracycline or doxycline combined with streptomycin or PO doxy and rifampicin 8/52

Answer 813

Pathognomic for rabies

Answer 814

IFA for rabies antigens in animals brain Neutralisaiton/ELISA for rabies IgM

Answer 815

Rabies specific Ig post exposure

Answer 816

Yersinia pestis

Answer 817

Bubonic plague: swollen LNs- dry gangrene Pulmonary: usually seen during epidemics due to person-person spread

Answer 818

Streptomycin Doxy Gent Chloramphenicol in meningitis

Answer 819

Leptospirosis

Answer 820

L. interrogans

Answer 821

Leptospirosis

Answer 822

Leptospirosis

Answer 823

Amoxicllin Erythromycin Doxy or ampicillin

Answer 824

Ciprofloxacin or doxy

Answer 825

Pulmonary anthrax

Answer 826

Cutaneous anthrax

Answer 827

Woodsorter's disease

Answer 828

Lyme disease (Borrelia burgdorferi)

Answer 829

Early localised Early disseminated Late persistent

Answer 830

Lyme disease

Answer 831

Early disseminated Lyme disease

Answer 832

Late persistent lyme disease

Answer 833

Bx edge of ECM + ELISA for lyme Abs

Answer 834

Doxy 2-3/52 (also amoxicillin, cephalosporins) NB post infection some patients get ME type symptoms

Answer 835

IV ceftriazone

Answer 836

Coxiella burnetii

Answer 837

Cutaaneous Diffuse cutaenous Muco-cutaenous Visceral: Kala Azar

Answer 838

L. major L. tropica

Answer 839

Cutaenous leishmaniasis

Answer 840

Diffuse leishmaniasis

Answer 841

L braziliensis

Answer 842

L. brazilienis (muco-cutaneous)

Answer 843

L donovani L infantum L chagasi

Answer 844

Invasion of RES-\> hepatosplenomegaly-\> BM invasion Later disfiguring dermal disease PKDL

Answer 845

Acrodermatitis chronic atrophicans Lym disease Late persistent

Answer 846

Toxoplasmosis

Answer 847

Hydatid disease

Answer 848

Leptospirosis

Answer 849

Brucellosis

Answer 850

Lyme disease

Answer 851

Yeasts Dermatophytes Moulds

Answer 852

candida, Cryptococcus, pichia, rhodotorulla, saccharomyces, trichosporon etc

Answer 853

epidermophyton, microsporum, trichophyton

Answer 854

aspergillus, fusarium, mucor, penicillium, rhizopus etc.

Answer 855

Wood lamps

Answer 856

ermatophytes

Answer 857

malassezia

Answer 858

yeasts & moulds. Fungal ear infection

Answer 859

piedraia hortae

Answer 860

trichosporon beigelii

Answer 861

Capitis: scalp and hair Corporis: trunk, legs and arms Cruris: groin and pubic region Pedis Manum Ungium

Answer 862

Malassezia globosa/furfur Seborrhoic dermatitis T. versicolor: depigmentation in those with darker skin

Answer 863

Tinea versicolour

Answer 864

Culutre Mannan Abs

Answer 865

Aspergilluis

Answer 866

Cryptoccous

Answer 867

ELISA PCR Beta-blucan test

Answer 868

Cryptococcal antigen in CSF

Answer 869

Invasive pulmonary asperigllosis

Answer 870

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

Answer 871

Phaeohyphomycosis

Answer 872

Blastomycosis

Answer 873

Coccidioidomycosis

Answer 874

Histoplasmosis

Answer 875

Paracoccidioidomycosis

Answer 876

Penicillium marneffei

Answer 877

Sporotrichosis

Answer 878

Mucormycosis

Answer 879

Entomophthoromycosis

Answer 880

Chromoblastomycosis

Answer 881

Lobomycosis

Answer 882

Polyene Azole Terbinafine Flucytosine Echinocandin

Answer 883

Cell membrane integrity

Answer 884

Cell membrane synthesis

Answer 885

Cell membrane synthesis

Answer 886

DNA synthesis

Answer 887

Amphotericin B

Answer 888

Polyenes Azoles Echinocandin

Answer 889

Amphotericin

Answer 890

Fluconazole

Answer 891

Caspofungin

Answer 892

Terbinafine

Answer 893

Permanent renal impairment

Answer 894

Bone marrow suppression

Answer 895

Fluconazole

Answer 896

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

Answer 897

Sign of immune activation following HIV infection

Answer 898

Filariasis

Answer 899

Cutaenous larva migrans (ancylostoma braziliense)

Answer 900

Can do nothingh- may resolve spontaenously Topical: thiabendazole Oral: albendazole or ivermectin

Answer 901

Tumbu fly: cordylobia anthropophagi.

Answer 902

Human Bot Fly: Dermatobia hominis.

Answer 903

Tungiasis: Tunga Penetrans / Jigger / Chigoe Flea

Answer 904

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

Answer 905

Zidovudine

Answer 906

Lactic acidosis

Answer 907

Rash SJS TEN Fatal fulminant hepatitis

Answer 908

Insulin resistance Dyslipidaemia Lipodystrophy Bleeding in haemophilia

Answer 909

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.

Answer 910

Burkholderia

Answer 911

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

Answer 912

VISA: Staph aureus with intermediate level resistance to vancomycin VRSA: Vancomycin resistant Staph aureus VRE: Vancomycin resistant Enterococcus faecium or Enterococcus faecalis

Answer 913

MIP-1alpha

Answer 914

Ceftriaxone

Answer 915

cefuroxime & clarithromycin

Answer 916

3rd gen cephalosporins Ceftriaxone

Answer 917

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

Answer 918

Entamoeaba histolytica

Answer 919

Salmonella

Answer 920

Campylobacter

Answer 921

Rabies encepalomyelitis

Answer 922

GBS is ascending

Answer 923

Whole cell typhoid vaccine

Answer 924

A. ## Footnote pneumococcal vaccine

Answer 925

Hepatitis B virus vaccine

Answer 926

Immunostimulatory complexes (ISCOMS)

Answer 927

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.

Answer 928

Polio (Sabin)

Answer 929

HIB vaccine

Answer 930

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

Answer 931

Haemophilus influenzae type B vaccine

Answer 932

Hepatitis A virus vaccine

Answer 933

Oral poliomyelitis vaccine

Answer 934

All live attenuated vaccines

Answer 935

All inactivated (killed) vaccines)

Answer 936

Subunit vaccine

Answer 937

Freund's adjuvan

Answer 938

Campylobacter jejuni

Answer 939

Cryptosporidium parvum

Answer 940

Bartonella henselae

Answer 941

Spirillum minus

Answer 942

Leptospirosis

Answer 943

Brucellosis

Answer 944

Brucella melitensis

Answer 945

Bacillus anthracis

Answer 946

richophyton rubrum as it is the commonest fungus from feet. If there was laceration and lots of blisters then it will be Trichophyton interdigitale.

Answer 947

Aspergillus flavus

Answer 948

Pityrosporum orbiculare

Answer 949

E floccusum is normally associated with GROIN infections, the old joke with Rugby players' groins

Answer 950

Tinea pedis

Answer 951

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.

Answer 952

Abortus comes from cattle Melitensis comes from goats, seen in the Mediterranean region

Answer 953

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.

Answer 954

Brodie's abscess

Answer 955

I. V. injection of tetanus antitoxin

Answer 956

Removal of a breast carcinoma

Answer 957

Oral administration of flucloxacillin

Answer 958

Drug induced fever

Answer 959

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!

Answer 960

Rubella Hep B Parvovirus B19

Answer 961

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

Answer 962

Borrelia burdorferia Rheumatic fever

Answer 963

Reactive arthritis as a consequence of TB infection Aseptic form of arthritis observed in patients with TB

Answer 964

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.

Answer 965

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.

Answer 966

Klebsiella

Answer 967

Staph Saprophyticus

Answer 968

Ciprofloxacin

Answer 969

Adenovirus

Answer 970

Ceftazidime

Answer 971

Gentamicin

Answer 972

Ceftriaxone

Answer 973

Renal Tuberculosis

Answer 974

Urethral Syndrome

Answer 975

Bacterial prostatitis

Answer 976

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).

Answer 977

Cef. & Met. 0-2hrs before incision & no longer than 24 hrs post-surgery

Answer 978

Burkholderia cepacia

Answer 979

Vancomycin-resistant enterococcus(VRE)

Answer 980

Pseudomonas aeruginosa

Answer 981

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.

Answer 982

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.

Answer 983

If you know it is Neisseria- ben pen If you do not know the answer, broader spectrum therefore ceftriaxone

Answer 984

cerebral abscess, tuberculoma, toxoplasmosis and sometimes CNS lymphoma. The ring usually represents vasogenic oedema.

Answer 985

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

Answer 986

Chagas Disease

Answer 987

Mucocutaneous Leishmaniasis

Answer 988

Schistosoma haematobium

Answer 989

Plasmodium falciparum

Answer 990

Trypanosoma brucei gambiense

Answer 991

Wuchereria bancrofti

Answer 992

Leishmania donovani

Answer 993

Severe malaria

Answer 994

Visceral leishmaniasis (kala-azar)

Answer 995

Schistosoma mansoni

Answer 996

Entamoeba histolytica

Answer 997

Trichinella spiralis

Answer 998

Plasmodium falciparum

Answer 999

Taenia saginata

Answer 1000

Visceral Leishmania

Answer 1001

Falciparum malaria

Answer 1002

Giardia lamblia

Answer 1003

Leishmania donovani

Answer 1004

Trypanosoma cruzi

Answer 1005

Group B Streptococci Syndrome

Answer 1006

Congenital Toxoplasmosis

Answer 1007

Neonatal Herpes Simplex Infection

Answer 1008

Congenital toxoplasmosis

Answer 1009

Congenital rubella syndrome

Answer 1010

Bacterial meningitis

Answer 1011

Neonatal HSV infection

Answer 1012

Patients with a chancroid ulcer are more susceptible to contracting HIV

Answer 1013

Oral fluconazole

Answer 1014

SCC of the bladder (5% of all baldder Ca) If outside the setting of chronic schistosomiasis- TCC

Answer 1015

Staph: aureus, epidermis Strep: pneumoniae, pyogenes

Answer 1016

Bacillus Clostridium Cornyebacterium Listeria

Answer 1017

E Coli Kleb Proteus Salmonella Shigella Yersinia Pseudomonas Bordatella Haemophilus Legionella

Answer 1018

Vibiro Campylobacter Helicobacter

Answer 1019

Treponema Borrelia

Answer 1020

Mycoplasma

Answer 1021

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.

Answer 1022

Strep viridans are optochin insensitivie

Answer 1023

Strep are catalse negative

Answer 1024

Milder Legionella infection

Answer 1025

Moraxella catarrhalis

Answer 1026

Mycoplasma pneumoniae

Answer 1027

Haemophilus influenzae

Answer 1028

are obligate intracellular bacteria which cause an atypical pneumonia. Less commonly, this infection can cause meningoencephalitis, arthritis, myocarditis and/or Guillain–Barré syndrome.

Answer 1029

Listeria monocytogenes

Answer 1030

Vibrio cholerae

Answer 1031

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.

Answer 1032

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.

Answer 1033

Salmonella typhi

Answer 1034

Campylobacter jejuni

Answer 1035

Entamoeba histolytica

Answer 1036

Rich focus.

Answer 1037

Leptospirosis

Answer 1038

Neisseria meningitides (meningococcus

Answer 1039

Cryptococcal meningitis

Answer 1040

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.

Answer 1041

Klebsiella granulomatis

Answer 1042

Trichomonas vaginalis

Answer 1043

Candida albicans

Answer 1044

Trimethoprim

Answer 1045

Chloramphenicol

Answer 1046

Doxycycline

Answer 1047

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).

Answer 1048

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).

Answer 1049

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.

Answer 1050

Gancyclovir

Answer 1051

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

Answer 1052

Amantadine

Answer 1053

Candidaemia

Answer 1054

Pityriasis versicolor (B)

Answer 1055

aspergilloma

Answer 1056

Sporothrix schenckii

Answer 1057

Histoplasma capsulatum

Answer 1058

Phialophora verrucosa

Answer 1059

Tinea capitis (F)

Answer 1060

Tinea corporis

Answer 1061

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.

Answer 1062

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.

Answer 1063

Psittacosis

Answer 1064

Cat scratch disease (H) is caused by Bartonella

Answer 1065

Congenital syphillis

Answer 1066

Coxellia burnetti (Q fever)

Answer 1067

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

Answer 1068

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

Answer 1069

Optochin- viridans resistance Pneumonia- sensitive

Answer 1070

Pneumocystis jirovecii

Answer 1071

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

Answer 1072

Acute: tricuspid, staph aureus IVDU Subacute: mitral and aortic, damaged valves, strep viridans

Answer 1073

Lactose fermenters turn Maconkey agar pink

Answer 1074

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

Answer 1075

Entamoeba histolytica

Answer 1076

Campylobacter

Answer 1077

Pseudomonas Neisseria Campylobacter Helicobacter Morazella Vivrio Legionella

Answer 1078

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

Answer 1079

Schistosomiasis

Answer 1080

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.

Answer 1081

L. braziliensis

Answer 1082

L donovani L infantum L chagas

Answer 1083

Toxoplasmosis

Answer 1084

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.

Answer 1085

Gonocchal infection

Answer 1086

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.

Answer 1087

Anti-HBc IgM

Answer 1088

anti-HBc-Ig

Answer 1089

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.

Answer 1090

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

Answer 1091

Vancomycina rare ADR

Answer 1092

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.

Answer 1093

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 (

Answer 1094

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

Answer 1095

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!

Answer 1096

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.

Answer 1097

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

Answer 1098

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).

Answer 1099

Plasmadoium knowlesi

Answer 1100

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.

Answer 1101

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.

Answer 1102

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.

Answer 1103

P falciparum

Answer 1104

P vivax P ovale