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K1s Path > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What is the epidemiology of Chlamydia?

A

Worldwide distribution. In UK, 10% of under 25s affected.

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2
Q

How does Chlamydia usually present?

A
  • Asymptomatic in 50% men and 80% women.
  • Can present as urethritis (dysuria/discharge) in men, cervicitis in women.
  • Complications are pelvic inflammatory disease, infertility and ectopic pregnancy in women; epididymitis and orchitis in men.
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3
Q

How is chlamydia infection diagnosed?

A

Can’t be cultured easily as obligate intracellular bacterium.
PCR based methods used which are highly sensitive and specific, plus can be used on non-invasive specimens.

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4
Q

What is the epidemiology of Lymphogranuloma venereum and what is the causative organism?

A

Chlamydia trachomatis serovars L1,L2,L3

Tropical STI but in last 5 years an ongoing outbreak identified in European MSM.

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5
Q

How does Lymphogranuloma venereum present?

A

Painless, non-indurated genital ulcer that heals rapidly +/-painful unilateral (2/3) inguinal buboes that may rupture and heal slowly with scarring.
Progresses to lymphoedema and deformity in some cases. Current UK epidemic in MSM characterised by painful proctitis, with some progressing to bowel strictures if not picked up. PCR diagnosis.

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6
Q

What is the epidemiology of gonorrhoea?

A

Worldwide distribution, in UK particularly seen in core groups (MSM, young people of black ethnicity).

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7
Q

How does gonorrhoea present and what complications are there?

A

Urethral discharge in men, more rarely discharge in women. Asymptomatic in many women.
Complications: PID, epididymo-orchitis. Can disseminate and cause rash.

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8
Q

How is gonorrhoea diagnosed?

A

Neisseria Gonnorrhoeae, gram negative diplococci seen on smear from urethral or cervical discharge. Can be cultured on specific media (fastidious organism). PCR based techniques increasingly used.

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9
Q

What are the two forms chlamydiae organisms exist in?

A

> Elementary bodies: stable, extracellular – infectious

> Reticulate particles: intracellular, metabolically active

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10
Q

What different serovars of chlamydia trachomatis are there and what diseases do they cause?

A

> A, B, C - Trachoma
D to K - genital chlamydia infection, ophthalmia neonatorum
L1, L2, L3 - Lymphogranuloma venereum

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11
Q

What is the epidemiology of syphilis?

A

World wide distribution. Almost disappeared in UK but reappeared in late 1990s in MSM and now endemic again. Unlike most other acute STIs, the burden of syphilis does not fall solely upon young people.

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12
Q

How does syphilis present?

A

> Primary-painless ulcer “chancre” that heals without scarring in 1-3 weeks
Secondary-disseminated infection, with rash, systemic symptoms, alopecia, uveitis, hearing loss, lymphadenopathy, snail track ulcers, condlyomata acuminata.
Tertiary-years later. Cardiovascular, neurological, bone and/or skin (70%) manifestations.

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13
Q

How is syphilis diagnosed?

A

Obligate human parasite Treponema pallidum, a spirochaete, can’t be cultured.
Specific tests: Dark ground microscopy of ulcers/skin lesions can reveal spirochaete.
On blood, EIA for antibody, TPHA/TPPA haemagglutinin assays. PCR recently available for ulcers.
Non-specific tests: RPR (VDRL in past) used to show activity but may be increased in other conditions.

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14
Q

What is the incubation period for syphilis?

A

Primary: 9-90 days
Secondary: 4-8 weeks
Tertiary: 2-40 years

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15
Q

What is the causative organism in chancroid and how does it present?

A

Chancroid is caused by Haemophilus ducreyi (gram -ve coccobacillus) and is diagnosed by microscopy, culture or PCR. It often causes multiple painful ulcers. It is seen in Sub-saharan Africa but incidence has decreased in recent years.

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16
Q

What is the causative organism in donovanosis and how is it diagnosed?

A

Aka Granuloma inguinale is caused by Klebsiella granulomatis (gram -ve bacillus) and is found in Australian aboriginal populations and some other tropical regions. Diagnosis is via visualisation of Donovan bodies on Giemsa staining of a tissue smear, crush preparation or biopsy.

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17
Q

What is the causative organism in trichomoniasis, how does it present and how is it diagnosed?

A 
Trichomonas vaginalis (flagellated protozoan)
Causes discharge in women, asympto or urethritis in men
Diagnosed via wet prep microscopy, culture (rarely done) or PCR
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18
Q

What is bacterial vaginosis?

A

Polymicrobial, altered vaginal flora with raised vaginal pH associated with sex (not transmitted) and hygiene practices e.g. douching. Causes discharge with offensive odour. Diagnosed on gram stain of discharge. Treatment with oral metronidazole.

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19
Q

What is vaginal candidiasis?

A

Usually causes by candida albicans, rarely others.
Presents with itch, soreness and white, thick discharge.
Diagnosed by culture or direct gram stain for spores/hyphae.
Treatment: topical (pessary) antifungals e.g. clotrimazole, or oral e.g. fluconazole.

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20
Q

What serotypes of HPV cause genital warts?

A

HPV 6 and 11.

Types 16 and 18 cause cervical and anal dysplasia and cancer.

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21
Q

What treatment is available for genital warts?

A

Cosmetic/destructive. No curative treatment for virus. Cryotherapy or podophyllotoxin cream/lotion are first line. Vaccine now available for prevention.

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22
Q

What does Molluscum contagiosum cause?

A

Commonly seen in children as lesions on hands/body. In adults often presents with lesions on genitals. Spread via skin to skin contact. Self limiting. Can cause giant lesions in immunosuppressed. Facial lesions in adults are highly suspicious of HIV infection.

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23
Q

What is the treatment for pubic lice?

A

Topical e.g. Malathion lotion, Permethrin lotion, applied to whole body as per instructions.

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24
Q

What are prion diseases?

A

> Protein-only infectious agent
Rare transmissable spongiform encephalopathies in humans + animals
Rapid neuro-degeneration
Currently untreatable

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25
Q

Which chromosome is the prion protein gene?

A

Chr 20, PRNP gene predominantly expressed in the CNS

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26
Q

What are the different structures of the prion protien?

A

Normal PrP > Alpha-helical configuration, protease sensitive

Abnormal PrPSc > Beta-sheet configuration, protease/radiation resistant

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27
Q

How is prion disease classified?

A
  • Sporadic (80%)
  • Acquired (<5%)
  • Genetic (15%)
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28
Q

Examples of genetic prion diseases?

A
  • Gerstmann–Sträussler–Scheinker syndrome
  • Fatal familial insomnia
  • Codon 129 polymorphism MM
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29
Q

What is the commonest form of prion disease?

A

Sporadic CJD

  • Mean age of onset is 65 years old
  • Median survival time is <6 months
  • EEG usually shows periodic complexes
  • CSF markers (S100, 14-3-3) of neuronal damage may be elevated
  • Tonsillar biopsy is NOT diagnostic
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30
Q

How does vCJD differ in presentation to sCJD?

A
  • Younger age of onset (median age 26 yrs)
  • Median survival time longer at 14 months
  • Psychiatric onset before neurological
  • MRI brain = positive pulvinar sign
  • Tonsil biopsy 100% sensitive and specific
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31
Q

What is the etiology of acquired CJD?

A
  • Kuru: Exposure to human prions during cannibalistic feasts
  • Iatrogenic CJD: Accidental inoculation with human prions
  • Variant CJD: Exposure to Bovine spongiform encephalopathy (BSE)-like prion strain
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32
Q

What treatment is available for prion diseases?

A

> Symptomatic: clonazepam – mycolonus, (valproate, levetiracetam, piracetam)
Delaying prion conversion: quinacrine, pentosan (intra-ventricular administration), tetracycline

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33
Q

What is the microscopic appearance of the main causative organisms of community acquired pneumonia?

A
  • Streptococcus pneumoniae: +ve cocci
  • Haemophilus influenzae: -ve cocco-bacilli
  • Moraxella catarrhalis: -ve coccus
  • Staphylococcus aureus: +ve cocci “grape-bunch clusters”
  • Klebsiella pneumoniae: -ve rod, enterobacter
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34
Q

What is the pathology of pneumonia?

A

Inflammation of the lung alveoli

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35
Q

What are the commonest causative organisms of community acquired pneumonia in different age-groups 0-30 yrs?

A

0-1 mths- E.coli, GBS, listeria
1-6mths- Chlamydia trachomatis, S aureus, RSV
6mths-5yrs- Mycolpasma, influenza
16-30yrs- M pneumoniae, S pneumoniae

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36
Q

What is the CURB-65 score and how is it used?

A 
Confusion
Urea > 7 mmol/L
RR >30
BP 65 years old
Score 2 = admit, 3-5 = manage as severe
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37
Q

What are the commonest causative organisms of atypical CAP?

A
  • Chlamydia pneumoniae
  • Mycoplasma pneumoniae
  • Legionella
  • Chlamydia psittaci (Psittacosis)
  • Coxiella burnetii (Q fever)
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38
Q

What might suggest legionella CAP?

A

History: travel, air-conditioning, water towers
Extrapulmonary features: hepatitis, low Na, confusion
Growth on buffered charcoal yeast extract

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39
Q

What might suggest Mycoplasma pneumoniae CAP?

A

Young age, prior antibiotics, epidemics every 4-6 years

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40
Q

What might suggest Chlamydia pneumoniae CAP?

A

Long duration of symptoms, headache, epidemics in closed communities

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41
Q

What might suggest Chlamydia psittaci CAP?

A

Exposure to birds, splenomegaly, rash, haemolytic anaemia

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42
Q

What might suggest Coxiella burnetii CAP?

A

Dry cough, high fever, hepatitis, male, farm animal exposure

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43
Q

What is the pathology of bronchitis?

A

Inflammation of medium sized airways

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44
Q

What antibiotics can be used to treat atypical pneumonia?

A

Organisms don’t have cell wall, thus penicillins don’t work
Need agents that work on protein synthesis:
> Macrolides (clarithromycin / erythromycin)
> Tetracyclines (doxycycline)

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45
Q

What is the definition of a hospital acquired pneumonia?

A

Acquired > 48 hours after being in hospital

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46
Q

What are the commonest causative organisms of HAP?

A 
Enterobacteriaciae
Staphylococcus aureus
Pseudomonas spp
Fungi (Candida sp.)
Haemophilus influenzae
Acinetobacter baumanii
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47
Q

What are the features of pneumocystis carinii pneumonia (PCP)?

A

Ubiquitous protozoan aka Pneumocystis jirovecii.
Insidious onset, dry cough, weight loss, SOB, malaise.
Infects immunocompromised hosts esp HIV+
Diagnosed by immunofluorescence on BAL, treatment/prophylaxis with Septrin

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48
Q

What can Aspergillus fumigatus infection cause?

A

Allergic bronchopulmonary aspergillosis
> Chronic wheeze, eosinophilia, bronchiectasis
> Often in patients with asthma or cystic fibrosis
Aspergilloma
> Fungal ball often in pre-existing cavity
> May cause haemoptysis
Invasive aspergillosis
> Immunocompromised
> Rx Amphotericin B

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49
Q

What urine antigen tests are available for severe CAP?

A

S. pneumoniae

Legionella pneumophila

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50
Q

For which organisms are antibody tests useful to identify CAP?

A

organisms that are difficult to culture eg:
Chlamydia
Legionella

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51
Q

What is first-line treatment for hospital-acquired pneumonia?

A

Ciprofloxacin +/- vancomycin

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52
Q

What antibiotic should be used for MRSA pneumonia?

A

Vancomycin

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53
Q

What antibiotic therapy should be used for psudomonas pneumonia?

A

Piptazobactam or Ciprofloxacin +/- gentamicin

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54
Q

What should moderate-severe CAP be treated with?

A

Clarithroycin

+ Co-amoxiclav (augmentin) or cefuroxime

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55
Q

What kind of disease does Mycobacterium avium – intracellulare complex cause?

A

Children: pharyngitis/cervical adenitis
Pulmonary: may invade the bronchial tree, pre-existing areas of bronchiectasis, or old cavities
Disseminated - assoc. Cytotoxics, lymphoma, AIDS etc

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56
Q

What kind of disease does Mycobacterium marinum complex cause?

A

fish tank’ or ‘swimming pool’ granuloma, a localised skin lesion following contamination of an open wound or abrasion with water from fish tanks, swimming pools and natural areas of fresh or salt water

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57
Q

What kind of disease does Mycobacterium ulcerans complex cause?

A

skin lesions in various global areas, including Australia (‘‘Bairnsdale ulcer’’) and Southeast Asia; Uganda and other parts of Africa (‘‘Buruli ulcer’’); and in Central/South America. Infection may lead to a chronic progressive painless ulcer, which can occasionally present in travellers from endemic areas

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58
Q

What is the most common form of extra-pulmonary tuberculosis?

A

Lymphadenitis aka scrofula

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59
Q

What is the first-line treatment regime for TB?

A

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

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60
Q

What second-line drugs are used to treat TB?

A 
Quinolones
Kanamycin
Amikacin
Moxifloxacin
Ethionamide/Prothionamide
Cycloserine
PAS
Linezolid
Clofazamine
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61
Q

What type of virus is influenza?

A

Orthomyxovirus

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62
Q

What is the natural reservoir of influenza A?

A

Ducks

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63
Q

What antivirals are available for influenza?

A

Amantadine (influenza A only) - targets M2 ion channel but single mutation confers resistance
Neuraminidase inhibitors (only effective <48hrs after infection)
- Oseltamivir (tamiflu) oral
- Zanamivir (Relenza) inhaled or iv
- Peramivir iv
- Sialic acid

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64
Q

What antimicrobial agents inhibit cell-wall synthesis?

A

> Beta-lactams (penicillins, cephalosporins and carbapenems)

> Glycopeptides (Vancomycin and Teicoplanin)

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65
Q

How do beta-lactams work?

A
  • Bind to PBPs (Penicillin binding proteins)
  • Bactericidal
  • Active against rapidly-dividing bacteria
  • Ineffective against bacteria that lack peptidoglycan cell walls (e.g. Mycoplasma or Chlamydia)
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66
Q

What are key features of penicillins to remember?

A
  • Relatively non-toxic
  • Renally excreted (so ↓dose if renal impairment)
  • Short t½
  • Will not cross intact blood-brain barrier
  • Cross-allergenic (and approx 10% cross-reactivity with cephalosporins or carbapenems)
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67
Q

Example of a first generation cephalosporin?

A

Cephalexin

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68
Q

Example of a second generation cephalosporin?

A

Cefuroxime

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69
Q

Examples of third generation cephalosporins?

A

Cefotaxime
Ceftriaxone
Ceftazidime

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70
Q

Examples and uses of carbapenems?

A

Imipenem, Meropenem, Ertapenem
Very broad spectrum, used for very sick patients (eg, on ITU), or for patients infected with highly-resistant Gram –ve bacteria.
In general, they can be used against
> all Gram +ves EXCEPT MRSA
> Most Gram –ves except Stenotrophomonas maltophilia

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71
Q

What are key features of glycopeptides to remember?

A
  • Large molecules, unable to penetrate G –ve outer cell wall
  • Active against G +ve organisms
  • Inhibit cell wall synthesis
  • Important for Rx serious MRSA infections (iv only)
  • Oral vancomycin can be used to Rx serious C. difficile infection
  • Slowly bactericidal
  • Nephrotoxic – important to monitor drug levels
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72
Q

What are examples of glycopeptides?

A

Vancomycin and Teicoplanin

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73
Q

What antimicrobial agents inhibit bacterial protein synthesis?

A
  • Aminoglycosides
  • Tetracyclines
  • Macrolides / Streptogramins / Lincosamides – The MSL group
  • Chloramphenicol
  • Oxazolidinones
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74
Q

What are key features of aminoglycosides to remember?

A
  • e.g. Gentamicin & tobramycin
  • Bind to amino-acyl site of the 30S ribosomal subunit
  • Rapid, concentration-dependent bactericidal action
  • Require specific transport mechanisms to enter cells
  • Ototoxic & nephrotoxic > must monitor levels
  • Synergistic combination with beta-lactams
  • No activity vs. anaerobes
  • Particularly active vs. Ps. aeruginosa and useful in g -ve sepsis
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75
Q

What are key features of tetracyclines to remember?

A
  • e.g. doxycycline
  • Interfere with initiation step of protein synthesis (30S ribosomal subunit)
  • Broad-spectrum agents with activity against intracellular pathogens (e.g. chlamydiae, rickettsiae & mycoplasmas) as well as most conventional bacteria
  • Bacteriostatic
  • Widespread resistance limits usefulness
  • Do not give to children or pregnant women
  • Light-sensitive rash
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76
Q

What are key features of macrolides to remember?

A
  • Macrolides (erythromycin) / Lincosamides (clindamycin) / Streptogramins (Synercid)
  • Act on 50S ribosome to interfere with mRNA translation
  • Bacteriostatic
  • Minimal Gram –ve activity
  • Useful for mild Staph or Strep infections in penicillin-allergic patients, also active against campylobacter and L. pneumophila
  • Newer agents include clarithromycin & azithromycin
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77
Q

What are key features of chloramphenicol to remember?

A
  • Acts on 50S ribosome to inhibit peptide chain elongation
  • Bacteriostatic
  • Very broad antibacterial activity
  • Rarely used (apart from eye) because risk of aplastic anaemia and grey baby syndrome in neonates
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78
Q

What are key features of oxazolidinones to remember?

A
  • e.g. Linezolid
  • Binds to 50S subunit
  • Highly active against Gram +ve organisms, including MRSA and VRE
  • Not active against most Gram -ves
  • Expensive, may cause thrombocytopoenia and should be used only with consultant Micro/ID approval
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79
Q

What antimicrobial agents inhibit bacterial DNA synthesis?

A
  • (Fluoro)quinolones e.g. Ciprofloxacin, Levofloxacin, Moxifloxacin
  • Nitroimidazoles e.g. Metronidazole & Tinidazole
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80
Q

What are key features of fluoroquinolones to remember?

A
  • Bactericidal: act on DNA gyrase
  • Broad antibacterial activity, esp vs Gram –ves, including Ps. aeruginosa
  • Well absorbed following oral administration
  • Newer agents (e.g. levofloxacin, moxifloxacin) better activity vs G +ves, anaerobes and intracellular bacteria, e.g. Chlamydia spp
  • Use for UTIs, pneumonia, atypical pneumonia & bacterial gastroenteritis
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81
Q

What are key features of Nitroimidazoles to remember?

A
  • e.g. metronidazole & tinidazole
  • Under anaerobic conditions, an active intermediate is produced which causes DNA strand breakage
  • Rapidly bactericidal
  • Active against anaerobic bacteria and protozoa (e.g. Giardia)
  • Nitrofurans are related compounds: nitrofurantoin is useful for Rx simple UTIs
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82
Q

What antimicrobial agents inhibit bacterial RNA synthesis?

A

Rifamycins, e.g. rifampicin & rifabutin

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83
Q

What are key features of Rifamycins to remember?

A
  • Bactericidal
  • Particularly active against Mycobacteria & Chlamydiae
  • Except for short-term prophylaxis should NEVER use as single agent because resistance develops rapidly
  • Monitor LFTs
  • Beware of interactions with other drugs that are metabolised in the liver (e.g oral contraceptives)
  • May turn urine & secretions orange
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84
Q

What antimicrobial agents are cell membrane toxins?

A

Daptomycin – a cyclic lipopeptide with activity limited to G+ve pathogens. It is a recently-licenced antibiotic likely to be used for treating MRSA and VRE infections as an alternative to linezolid and Synercid

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85
Q

What antimicrobial agents are inhibitors of folate metabolism?

A

Sulfonamides

Diaminopyrimidines (e.g. trimethoprim)

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86
Q

What are key features of sulphonamides & diaminopyrimidines to remember?

A
  • Act indirectly on DNA through interference with folic acid metabolism
  • Synergistic action between the 2 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. Rx P. jiroveci pneumonia)
  • Trimethoprim is used for Rx community-acquired UTIs
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87
Q

What different mechanisms of antimicrobial resistance are there in general?

A

BEAT
BYPASS of targeted metabolic or synthetic pathway (e.g. MRSA)
ENZYME inactivation of the antimicrobial (e.g. beta lactamase enzymes)
ACCUMULATION impairment (drug can no longer enter cell, or may be pumped out) e.g., tetracycline resistance
TARGET modification (of the antimicrobial target site) e.g. quinolone resistance

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88
Q

What ~ duration of treatment is needed for N. meningitidis meningitis?

A

7 days

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89
Q

What ~ duration of treatment is needed for acute adult osteomyelitis?

A

6 weeks

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90
Q

What ~ duration of treatment is needed for bacterial endocarditis?

A

4-6 weeks

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91
Q

What ~ duration of treatment is needed for simple cystitis (in women)?

A

3 days

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92
Q

What typical antibiotic would be used to treat a skin infection and what are the typical causative organisms?

A

Flucloxacillin (unless penicillin allergy or MRSA)

Common organisms include S. aureus and beta-haemolytic Streptococci

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93
Q

What typical antibiotic would be used to treat pharyngitis and what are the typical causative organisms?

A

Benzyl penicillin x 10 days

Beta-haemolytic Streptococci

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94
Q

What typical antibiotic would be used to treat mild CAP?

A

Amoxicillin

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95
Q

What typical antibiotic would be used to treat severe CAP?

A

Co-amoxiclav & clarithromycin

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96
Q

What typical antibiotic would be used to treat bacterial meningitis and what are the typical causative organisms?

A

> N. Meningitidis or S. pneumoniae +/- Listeria in the very young/elderly/immuno-compromised
Ceftriaxone (+/- amoxycillin if Listeria likely)

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97
Q

What typical antibiotic would be used to treat a UTI?

A

Community > Trimethoprim x 3 days
Hospital-acquired > cephalexin or nitrofurantoin
Infected urinary catheter: change under gentamicin cover

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98
Q

What typical antibiotics would be used to treat sepsis of unknown cause?

A

Ceftriaxone, Metronidazole, +/- Amikacin

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99
Q

What typical antibiotics would be used to treat neutropenic sepsis of unknown cause?

A

Piperacillin-tazobactam (Tazocin) + gentamicin

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100
Q

What typical antibiotic would be used to treat C. difficile colitis?

A

STOP the offending antibiotic (usually a cephalosporin);
If severe > metronidazole PO
If above fails > vancomycin PO

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101
Q

Examples of human herpes viruses?

A 
Herpes simplex virus (HSV) 1 &amp; 2
Varicella zoster virus (VZV)
Cytomegalovirus (CMV)
Epstein Barr Virus (EBV)
HHV-6
HHV-8
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102
Q

What problems does HSV cause in the immunocompromised?

A

> Most commonly: Cold sores, difficulty swallowing, stomatitis in 85 % of cases, recurrent genital disease (HIV)
Cutaneous dissemination and visceral involvement: oesophagitis, hepatitis, colitis…
HSV encephalitis not increased in frequency

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103
Q

What problems does VZV cause in the immunocompromised?

A

High risk of complications e.g. pneumonitis, hepatitis, 2nd bacterial infection, multi-dermatomal zoster, disseminated infection, purpura fulminans

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104
Q

What problems does CMV cause in the immunocompromised?

A 
Bone marrow suppression
Interstitial pneumonitis
Retinitis
Encephalitis
Hepatitis
Oesophagitis, gastritis, enterocolitis
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105
Q

What problems does EBV cause in the immunocompromised?

A

Post-transplant lymphoproliferative disease
Lymphoma
Oral hairy leukoplakia (in HIV)

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106
Q

What problems does HHV-6 cause in the immunocompromised?

A

Graft failure
Encephalitis
May cause pneumonitis, hepatitis, bone marrow suppression, immunosupression

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107
Q

What problems does HHV-8 cause in the immunocompromised?

A

Particular problem in AIDS patients:
Kaposi’s sarcoma
Multicentric Castleman’s disease
Primary effusion (body cavity-associated) lymphoma (PEL)

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108
Q

How are HSV and VZV complications prevented in immunocompromised patients?

A

> Aciclovir prophylactic dose (started pre-Tx) mainly to prevent HSV infection
Post-exposure prophylaxis of severe varicella:
- Varicella zoster IG within 10 days of significant contact with chickenpox (airborne) or shingles (direct contact)

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109
Q

What can be seen on a CMV infected biopsy?

A

Characteristic owl’s eye inclusions

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110
Q

What treatments are available for CMV?

A

Ganciclovir (IV) - risk of BM supression
Valganciclovir (oral prodrug of ganciclovir)
Foscarnet (IV) - nephrotoxic
CMV hyperimmunoglobulin

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111
Q

What is the best strategy to manage CMV and HSCT?

A

Preemptive therapy:
> monitor CMV viral load weekly during high risk period
> Treat (GCV) when rises above threshold

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112
Q

What does EBV infection in the normal host cause?

A

Acute: Infectious mononucleosis. EBV infects mainly B cells
Chronic: Lifelong low-grade replication in B lymphocytes with polyclonal activation, kept in check by the cellular immune system (immunosurveillance)

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113
Q

How is post-transplant lymphoproliferative disease managed?

A 
Reduce immunosuppression (regression in < 50%)
Anti-CD20 monoclonal Ab rituximab therapy
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114
Q

What problems does adenovirus cause in BMT patients?

A 
Particularly Paeds BMT
High mortality with disseminated infection
- Fever
- Bone marrow supression
- Haemorrhagic cystitis
- Necrotising pneumonitis
- Hepatitis
- Colitis
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115
Q

What respiratory viruses are particularly associated with high mortality in immunocompromised patients?

A 
Influenza A and B
Parainfluenza 3 and 4
Respiratory Syncitial Virus (RSV) infection
Adenovirus 
Novel coronavirus: MERS coronavirus
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116
Q

What problems does measles infection cause in immunocompromised patients?

A

Severe, life-threatening disease (often without typical rash)
Giant cell pneumonia
Subacute measles encephalitis
No treatment, post-exposure prophylaxis with HNIG

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117
Q

What problems does parvovirus infection cause in immunocompromised patients?

A

Chronic anaemia - treat with human normal immunoglobulin (HNIG) and blood transfusion if necessary

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118
Q

How can hepatitis B be prevented in the immunocompromised?

A

> Nucleoside/nucleotide analogues (eg lamivudine, tenofovir, entecavir)
Hepatitis B immunoglobulin in liver transplant

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119
Q

What are the routes of HSV infection to fetus/neonate?

A

> Direct contact with infected maternal secretions at delivery
Ascending infection if PROM
Primary oral herpes in mother post delivery (kissing baby)
Contact with relatives, hospital staff etc. in babies born to susceptible mothers

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120
Q

When is the greatest risk of HSV transmission to the foetus/neonate and how is that risk managed?

A

Primary genital maternal infection in the third trimester.
Aciclovir offered
C/S recommended to all women presenting with a primary infection at time of delivery or within the 6 weeks proceeding

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121
Q

What problems does neonatal herpes cause?

A

Lesions of skin, eye, mouth 7-12 days
Neurological symptoms +/- SEM 2-6 weeks
Disseminated disease with/without vesicles frequently involving brain 4-11 days

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122
Q

What problems does VZV infection cause in pregnancy?

A

Congenital varicella syndrome:
- 0.4% for maternal infection between 0-12/40
- 2% for maternal infection between 12-20/40
Neonatal varicella: VZV-purpura fulminans
Higher risk of maternal complications:
- pneumonia
- encephalitis

123
Q

What does congenital varicella syndrome cause?

A
  • Dermatotrophic Skin scarring
  • Limb hypoplasia
  • Muscular atrophy
  • Rudimentary digits
  • Cortical atrophy
  • Psychomotor retardation
  • Choreoretinitis
  • Cataracts
124
Q

How is VZV risk managed in pregnancy?

A

VZV Immunoglobulin given to:
- all susceptible pregnant women following VZV exposure
- preterm infants <28 days old born to exposured seroneg mother
Aciclovir given to confirmed VZV infected

125
Q

What are the routes of CMV infection to fetus/neonate?

A

Intrauterine
Perinatally- infected genital secretions
Postnatal- saliva, breastmilk

126
Q

What problems can congential CMV infection cause?

A 
Commonest cause of viral congenital infection: 3/1000 in UK
85-90% asymptomatic at birth
> Hearing defects
> Impaired intellectual performance
> IUGR
> Jaundice
> Hepatosplenomegaly
> Chorioretinitis
> Thrombocytopenia
> Encephalitis
> +/-Microcephaly
127
Q

What problems can EBV infection in pregnancy cause?

A

There are no adverse fetal or maternal outcome described

128
Q

What problems can rubella infection in pregnancy cause?

A

> 90% incidence of fetal defects if infection before 10/40
Up to 20% spontaneous abortion if infection before 8/40
CRS: cataracts, congenital glaucoma, congenital heart disease, loss of hearing, pigmentary retinopathy, purpura, splenomegaly, microcephaly, mental retardation, meningoencephalitis
Infants with CRS may remain infectious for 12/12 or more
Infection 13-18 weeks - hearing defects and retinopathy
Maternal infection after 20 weeks carries no documented risk

129
Q

What problems can measles infection in pregnancy cause?

A 
> Fetal loss (miscarriage, IUD)
> Preterm delivery
> ncreased maternal morbidity
> No congenital abnormalities to fetus
> Measles IG attenuates illness but no evidence it prevents IUD or preterm delivery
130
Q

What problems can parvovirus B19 infection in pregnancy cause?

A

No documented risk of maternal infection after 20/40.
Maternal infection before 20/40:
> 9% risk of infection overall
> 3% risk of hydrops fetalis in infection 9-20/40
> Risk of fetal anomalies less than 1%
> Intrauterine transfusion improves fetal outcome

131
Q

What problems can the enterovirus coxsackievirus infection in pregnancy cause?

A

early onset neonatal hepatitis
congenital myocarditis
early onset childhood insulin dependent diabetes mellitus
abortion or intrauterine death

132
Q

What is the difference between a complicated and uncomplicated UTI?

A

> Uncomplicated UTI = infection in a structurally and neurologically normal urinary tract
Complicated UTI = infection in a urinary tract with functional or structural abnormalities (including indwelling catheters and calculi)
- men
- pregnant women
- children
- patients who are hospitalised or in health care–associated settings

133
Q

What are the most common causative organisms of a UTI?

A 
E. coli = Commonest 
Proteus mirabilis 
Klebsiella aerogenes 
Enterococcus faecalis 
Staphylococcus saprophyticus 
Staphylococcus epidermis
134
Q

What investigations should be ordered for a UTI?

A 
Uncomplicated:
- Urine dipstick
- MSU for urine microscopy, culture and sensitivities
- Bloods: FBC, UE, CRP
Complicated:
- Above plus
- Renal USS
- Intravenous urography
135
Q

What is the differential diagnosis for sterile pyuria?

A 
Prior treatment with antibiotics
Calculi
Catheterisation
Bladder neoplasm
TB
Sexually Transmitted Disease
136
Q

What antibiotics can be used to treat an uncomplicated UTI?

A
  • Amoxicillin (up to 60% resistance, not for Klebsiella)
  • Trimethoprim (up to 30% resistance)
  • Nitrofurantoin
  • Co-amoxiclav
  • Cephalexin
  • Ciprofloxacin
137
Q

How should a Candida UTI be treated?

A

Most Candida UTIs occur in patients with indwelling catheters.
Removal of the catheter may result in cure.
Oral fluconazole is no more effective than no therapy

138
Q

What complications can occur with pyelonephritis?

A 
• Perinephric abscess
• Chronic pyelonephritis
 - Scarring
 - Chronic renal impairment
• Septic shock
• Acute papillary necrosis
139
Q

What antibiotics can be used to treat pyelonephritis?

A

• Commonly associated with sepsis & septicaemia
• Requires more aggressive treatment
• Treat with broader spectrum intravenous antibiotics
o Co-amoxiclav +/- Gentamicin
o Cefuroxime +/- Gentamicin

140
Q

How does meningitis cause neurological damage?

A

Meningitis = inflammation of meninges and CSF

  • Direct bacterial toxicity
  • Indirect inflammatory process, cytokine release and oedema
  • Shock, seizures, and cerebral hypoperfusion
141
Q

What is the commonest long-term consequence of meningitis in survivors?

A

~ 5% of meningitis survivors have neurological sequelae, mainly sensorineural deafness

142
Q

How is meningitis classified?

A

Acute
Chronic
Aseptic

143
Q

What are the symptoms and causative organism of the most common infection of the CNS?

A

Aseptic meningitis:

  • Headache, stiff neck, and photophobia.
  • A nonspecific rash can accompany these symptoms
  • 80-90% Coxsackievirus group B and echoviruses
144
Q

How is encephalitis transmitted?

A

Transmission is commonly either person to person, or through vectors:

  • Mosquitoes
  • Lice
  • Ticks
145
Q

What is the leading cause of encephalitis worldwide?

A

West nile virus

146
Q

What organisms other than bacterial or viruses causes encephalitis?

A

Naegleria fowleri
Acanthamoeba species
Balamuthia mandrillaris
Toxoplasma gondii

147
Q

What are the risk factors for pyogenic vertebral osteomyelitis?

A 
Advanced age
Intravenous drug use
Long-term systemic steroids
Diabetes mellitus
Organ transplantation
Malnutrition
Cancer
148
Q

What primary infections usually precede a brain abscess?

A 
Otitis media
Mastoiditis
Paranasal sinus infection
Endocarditis
Haematogenous spread from elsewhere
149
Q

What organisms are often implicated in brain abscesses?

A
  • Streptococci (both aerobic and anaerobic)
  • Staphylococci
  • Gram-negative organisms. (particularly in neonates)
  • Mycobacterium tuberculosis
  • fungi
  • parasites
  • Actinomyces and Nocardia species
150
Q

What does normal CSF analysis show?

A 
Clear appearance
Leukocytes 0-5 x10^6/L
-ve stains
0.15-0.4 g/L protein
2.2-3.3 mmol/L glucose
151
Q

What does CSF analysis show in bacterial meningitis?

A 
Turbid appearance
100-2000 x10^6/L neutrophils
\+ve stains
High protein 0.5-3.0 g/L
Low glucose 0-2.2 mmol/L
152
Q

What does CSF analysis show in aseptic meningitis?

A 
Clear or slightly turbid appearance
15-500 x10^6/L lymphocytes
-ve stains
High protein 0.5-1.0 g/L
Normal glucose 2.2-3.3 mmol/L
153
Q

What does CSF analysis show in tuberculous meningitis?

A 
Clear or slightly turbid appearance
30-500 x10^6/L lymphocytes or some polymorphs
-ve stains, scanty acid fast bacilli
V. High protein 1.0-6.0 g/L
Low glucose 0-2.2 mmol/L
154
Q

What does a positive india ink stain suggest?

A

Cryptococcus infection

155
Q

What is the generic therapy for suspected meningitis or meningo-encephalitis?

A 
Meningitis:
- Ceftriaxone 2g iv bd
If >50yrs or immunocompromised add:
- Amoxicillin 2g iv 4 hourly
Meningo-encephalitis:
- As above plus
- Aciclovir 10mg/kg iv tds
156
Q

What causes cutaneous larva migrans?

A
  • Larvae of various nematode parasites of the hookworm family, most commonly Ancylostoma braziliense.
  • Human incidental host, usually live in intestines of dogs, cats and wild animals
  • Causes a red, intensely pruritic, worm-like burrow erruptions susceptible to bacterial superinfection
157
Q

What treatment options are there for cutaneous larva migrans?

A
  • usually heals spontaneously within weeks-months
  • oral Albendazole or Ivermectin
  • topical Thiabendazole
158
Q

What causes cutaneous myiasis?

A

Parasitic infestation of skin by fly larvae (maggots)
e.g. > Cordylobia anthropophaga (Tumbu fly) larvae (Africa)
> Dermatobia hominis (human botfly) (Americas)
Cause painful, slow-developing ulcers or furuncle(boil)-like sores

159
Q

What treatment options are there for cutaneous myiasis?

A

A. Do nothing - larvae will drop out to pupate naturally
B. Operate
C. Asphyxiate - cover breathing hole with Vaseline

160
Q

What is and what causes tungiasis?

A

An inflammatory skin disease caused by infection with the female Tunga penetrans flea (AKA jigger/chigoe/sand flea)
Usually affects feet or hands.
It causes skin inflammation, severe pain, itching, and a lesion characterized by a black dot at the center of a swollen red lesion, surrounded by a white halo.

161
Q

What complications can occur with tungiasis?

A 
bacterial super-infection
ulceration
nail destruction
lymphoedema
tetanus
162
Q

What treatment options are there for tungiasis?

A

Surgical extraction of the flea followed by topical antibiotic due to risk of secondary infection

163
Q

How many children <15 are living with HIV?

A

2.5 million in 2009 - 90% in sub-Saharan Africa

164
Q

How do children contract HIV?

A

> 90% due to mother-to-child transmission

But child sexual abuse and commercial sex work are risk factors for vulnerable children

165
Q

How can HIV infection affect the CNS in children?

A

Basal ganglia calcification
White matter changes
Atrophy
Vasculopathy / Strokes

166
Q

What are the risk factors for mother-to-child transmission of HIV?

A

Maternal plasma viral load = major RF
Risk increases 2% for every hour post-rupture of membranes
Breast feeding increases risk (1L = 1x unprotected sex)

167
Q

What is the global burden of schistosomiasis?

A
  • About 200 million people infected with schistosomiasis (85% of these in Africa)
  • Causes 200,000 deaths in Africa annually
  • Causes 1.7 million DALYs annually
168
Q

What is the main treatment for schistosomiasis?

A
  • Praziquantel
    Treating many people interrupts transmission but reinfection is likely unless exposure is reduced
  • Water supplies and hygiene promotion are viable control measures, sanitation less clear
169
Q

What is the life-cycle of schistosomiasis?

A

Eggs released from infected individuals, hatch in fresh water to release miracidium.
Miracidia infect snails then transform into a sporocysts which produce cercariae > larvae capable of infecting mammals
Cercariae emerge daily from snails to attach and penetrate through human skin.

170
Q

What are important differential diagnoses for fever in the returning traveler?

A
  • Malaria
  • Typhoid
  • Travelers diarrhoea
  • Pneumonia
  • HIV Seroconversion
171
Q

How many cases of malaria are seen in the UK each year and what is the commonest causative organism?

A
  • 2000 cases in UK per annum
  • 75% Plasmodium falciparum
  • 20 deaths per annum
  • Mostly adults
172
Q

What is the global burden of malaria?

A
  • 2 billion cases worldwide per annum

* 1-2 million deaths (90% african children)

173
Q

What are the 4 species of malaria-causing protozoa?

A 
Plasmodium
– falciparum
– malariae
– ovale
– vivax
174
Q

What is the main treatment for malaria?

A

Quinine sulphate +/- Doxycycline

Second-line > Artesunate

175
Q

What is the global burden of typhoid per annum?

A
  • 16 million cases worldwide

* 600,000 deaths

176
Q

What are the causative organisms of typhoid?

A

Salmonella species (gram -ve bacillus)
– typhi
– Paratyphi

177
Q

What are the clinical signs and symptoms of typhoid?

A 
– Fever
– Headache
– Abdominal pain
– Diarrhoea or constipation
– Rose spots (30%)
– Relative bradycardia (non-specific &amp; <50%)
– Hepatosplenomegaly (50%)
178
Q

What can chronic carriage with Salmonella typhi cause?

A

– Gallstones

– Immunosuppression

179
Q

What does TORCH stand for?

A 
Toxoplasmosis
Other – syphilis; HIV; Hepatitis B/C etc
Rubella
CMV (cytomegalovirus)
HSV (herpes simplex virus)
= Screen for congenital infections
180
Q

What problems does congenital toxoplasmosis cause?

A

May be asymptomatic at birth – 60% but may still go on to suffer long term sequelae – deafness, low IQ, microcephaly
40% symptomatic at birth: chorioretinitis; microcephaly/hydrocephalus; intracranial calcification; seizures; jaundice; hepatosplenomegaly

181
Q

What problems can maternal Chlamydia infection cause at birth?

A

Mother may be asymptomatic,
Infection transmitted during delivery,
Causes neonatal conjunctivitis, or more rarely pneumonia
Treated with erythromycin

182
Q

How is the neonatal period defined?

A

First 6 weeks of life,

If premature, neonatal period is longer as it is adjusted for expected birth date

183
Q

Why is there a higher incidence of infection in the neonatal period than at any other stage of life?

A

> Immature immune system;
Exposure to bacteria and viruses from the mother;
Birth trauma;
Thin skin and open areas e.g. umbilicus, become colonised with bacteria & can invade easily;
+/- overcrowding/understaffing on wards; invasive devices; antibiotic pressure etc.

184
Q

What organisms are associated with early onset neonatal sepsis?

A 
Early onset = within 48 hours of birth
> Group B streptococci
> E. coli
> Listeria
> Others: other streptococci; Haemophilus sp., anaerobes
185
Q

What organisms are associated with late onset neonatal sepsis?

A

Late onset = after first 48 hours of life.
Includes bacteria for early onset plus a large number of “opportunist” pathogens e.g.
> coagulase negative staphylococci;
> Enterococci;
> Staphylococcus aureus;
> coliforms,
> candida etc.

186
Q

What are the microbiological characteristics of Group B strep?

A

Gram positive coccus
Catalase negative
Beta-haemolytic
Lancefield Group B

187
Q

What maternal risk factors are there for early onset neonatal sepsis?

A 
> PROM/prem. Labour
> Fever
> Foetal distress
> Meconium staining
> Previous history
188
Q

What baby risk factors are there for early onset neonatal sepsis?

A 
> Birth asphyxia
> Resp. distress
> Low BP
> Acidosis
> Hypoglycaemia
> Neutropenia
> Rash
> Hepatosplenomegaly
> Jaundice
189
Q

What is the empirical antibiotic treatment for early onset neonatal sepsis?

A

Benzylpenicillin & Gentamicin

190
Q

What is the empirical antibiotic treatment for late onset sepsis in a neonate?

A

If on NICU:
> 1st line: Flucloxacillin & gentamicin
> 2nd line: Pipericillin/tazobactam & vancomycin
If community acquired:
> cefotaxime, amoxicillin +/-gentamicin

191
Q

What are the common causative organisms of bacterial meningitis in children of differnt ages?

A

6 years: N. meningitidis; S. pneumoniae; Mycoplasma pneumoniae

192
Q

What are the common bacterial causes of pneumonia in children?

A

Pneumococcus is an important cause in all ages.
Mycoplasma tends to affect older children (> 4 yrs)
Consider pertussis, mycoplasma and TB if cough fails to resolve quickly.

193
Q

What is the incidence of UTIs in children?

A

Common

Up to 3% girls and 1% boys by age 11

194
Q

Who needs treatment for chickenpox and with what?

A

> Immunocompromised: whenever vesicles present
Pregnant women and adults: within 3 days of rash or with pneumonitits
Acyclovir

195
Q

What can CMV infection cause?

A 
Retinitis
Colitis
Hepatitis
Encephalitis
Pneumonitis
196
Q

What is the global burden of Hep B?

A

> 350-400 million people worldwide have chronic HBV;
1.2 million in US
Up to 1 million deaths/year worldwide due to HBV-related complications of cirrhosis, liver cancer

197
Q

What treatments are available for HBV?

A 
lamivudine (with HBIg in transplants)
Adefovir
Tenofovir
Entecavir
interferon-α
198
Q

What treatments are available for HCV?

A

Interferon-α plus ribavirin

Protease and polymerase inhibitors in clinical trials

199
Q

What is Entecavir?

A

A potent and selective inhibitor of the HBV viral polymerase

200
Q

Examples of HIV nucleoside reverse transcriptase inhibitors?

A 
Zidovudine
lamivudine	
Stavudine
Didanosine
Abacavir
Tenofovir
201
Q

Examples of HIV protease inhibitors?

A 
Saquinavir	
Indinavir			
Ritonavir		
Nelfinavir		
Amprenavir	
Lopinavir		
Tipranavir
Darunavir
202
Q

Examples of HIV non-nucleoside reverse transcriptase inhibitors?

A 
Efavirenz
Etravirine
Nevirapine
Rilpivirine
They are HIV-1 specific
203
Q

Example of an antiviral which should be taken by HIV+ pregnant women?

A 
Zidovudine
- orally ante partum
- IV during delivery
- orally to newborn for 6 weeks
Reduces perinatal transmission form 26% to 8%
204
Q

How effective is post-exposure prophylaxis for HIV?

A

Can reduce risk of transmission by up to 70%
Important to start soon after exposure
Need to take for 4-6 weeks

205
Q

What antiviral treatment is available for Respiratory Syncitial Virus/parainfluenza?

A

Ribavirin

206
Q

What antiviral treatment is available for Picornavirus?

A

Pleconaril

207
Q

What type of drug is Aciclovir?

A

A guanosine analogue antiviral drug.

Used to treat HSV and VZV infections

208
Q

What criteria must an infectious disease meet to possibly be eradicated?

A

> Infection limited to humans with no animal reservoir.
Virus/bacterium should be antigenically stable and have only one or very few strains.
Virus should not persist in the host.
Vaccine must induce a lasting and effective immune response. High coverage is needed for very contagious diseases

209
Q

What serious complications can occur with measles infection?

A

> pneumonia (either direct viral pneumonia or secondary bacterial pneumonia)
otitis media
myocarditis
acute encephalitis
subacute sclerosing panencephalitis (1:1,000,000)
corneal ulceration (leading to corneal scarring)
death (used to kill 13 a year before MMR)

210
Q

What complications can occur with mumps infection?

A 
> Parotitis
> Orchitis 
> Oophortitis.
> Pancreatitis
> Deafness
> Meningitis (used to be commonest cause before MMR)
211
Q

What is the risk of catching measles for an unvaccinated child compared to a vaccinated child?

A

Unvaccinated children 22 times more likely to get measles than vaccinated children.
Herd immunity cannot be relied upon.

212
Q

What route is the BCG vaccine given?

A

Intradermally

213
Q

What is the disease burden of rotavirus in the UK?

A

Infects nearly all children by age 5 years
130,000 GP visits in Engalnd and wales
12,700 hospitalised
4 deaths

214
Q

If which patient groups should live vaccines be avoided?

A

> Patients having chemotherapy for malignancy
Patients Children on high dose steroids +/- cytotoxics
HIV+ should have MMR but not BCG or yellow fever

215
Q

Points to remember about UK vaccines

A

> Do not contain thiomersol (containing mercury).
Contain antigens to a broader range of infectious agents but the total antigen number is lower than with previous vaccine schedules

216
Q

What serotypes of HPV are included in the Gardasil vaccine?

A

6, 11, 16, 18

217
Q

What is the mechanism of action of Cholera toxin?

A

A-B toxin - A subunit activates adenylate cyclase

  • increased cAMP opens Cl channel at the apical membrane of enterocytes
  • efflux of Cl to lumen
  • loss of H2O and electrolytes
218
Q

Example of a superantigen that causes secretory diarrhea?

A

staphylococal enterotoxin (SE)

219
Q

What is the definition of dysentry?

A

Frequent passage of blood and mucus in stools

220
Q

Spores of which organism germinate in re-heated rice and what does it cause?

A

Bacillus cereus

watery non bloody diarrhoea; self limited

221
Q

What is the cause and treatment of botulism?

A

Source: canned or vacuum packed food (honey / infants)
Ingestion of preformed Clostiridium botulinum toxin (inactivated by good cooking..)
Blocks Ach release from peripheral nerve synapses
Treatment with antitoxin

222
Q

What GI problems can Clostiridium pefringens cause?

A

Normal flora of colon but not small bowel, where the enterotoxin acts (superantigen)
Watery diarrhoea, cramps, little vomiting lasting 24hrs

223
Q

What type of antibiotic is associated with C. difficile infection?

A

Cephalosporins

224
Q

How does Clostiridium difficile cause disease?

A

Pseudomembranous colitis
Exotoxins (A,B) glycosylate a G protein, depolymerising actin with loss of the cytoskeleton integrity and death of enterocytes

225
Q

What is the management for C. difficile infection?

A

Prevention

Treatment: (PO) metronidazole, vancomycin if severe, stop antibiotics where possible

226
Q

What microbiological characteristics does Listeria monocytogenes have?

A

V or L shaped,
beta-haemolytic,
aesculin positive,
tumbling motility

227
Q

What is the treatment for Listeria monocytogenes?

A

ampicillin, ceftriaxone, cotrimoxazole

228
Q

What different E. coli toxins cause diarrhoea and how?

A

Heat labile LT stimulates adenyl cyclase and cAMP
Heat stable ST stimulates guanylate cyclase.
Act on the jejeunum, ileum not on colon.
Verocytotoxin causes HUS

229
Q

What are the main strains of E. coli that fcause diarrhoea?

A

Enterotoxigenic (ETEC): main cause of traveller’s diarrhoea
Enteropathogenic (EPEC): infantile diarrhoea
Enteroinvasive (EIEC): invasive, dysentery
Enterohaemorrhagic (EHEC): O157:H7 produces shiga-like verocytotoxin that causes HUS

230
Q

What species of salmonellae are pathogenic?

A
  • S. typhi (and paratyphi) = Typhoid (enteric) fever
  • S. enteritidis = Enterocolitis
  • S. cholerasuis
231
Q

How is S. enteritidis transmitted and what does it cause?

A
  • transmitted from poultry, eggs, meat
  • invades epi- and sub-epithelial tissue of small and large bowel
  • self limited non bloody diarrhoea, usually no treatment (Cipro if required)
232
Q

How is typhoid fever transmitted and what does it cause?

A
  • transmitted only by humans
  • multiplies in Payer’s patches
  • Slow onset, fever and constipation, splenomegaly, rose spots, anaemia, leucopaenia, bradycardia, haemorrhage and perforation
  • Treatment : ceftriaxone, cipro
233
Q

What species of Vibrio are pathogenic and what is the treatment?

A

Vibrio cholerae = cholera
Vibrio parahaemolyticus = major cause of diarrhoea in Japan
Vibrio vulnificus = cellulitis in shellfish handlers and fatal septicaemia with D+V in HIV+
Treat losses and/or doxycycline

234
Q

What are the features of a Campylobacter infection?

A
  • Transmitted via contaminated food and water with animal faeces
  • Watery, foul smelling diarrhoea, bloody stool, fever and severe abdo pain
  • Guillain–Barré syndrome, reactive arthritis, Reiter’s..
  • Treat with erythromycin or cipro if in the first 4-5days
235
Q

What complications can Yersinia enterocolitica cause?

A
  • enterocolitis
  • mesenteric adenitis
  • assoc reactive arthritis, Reiter’s
236
Q

What is a motile trophozoite with 4 nuclei seen in a stool sample?

A

Entamoeba histolytica

237
Q

What complications can entamoeba histolytica cause and how is it treated?

A 
“flask shaped” ulcer in colon
- dysentery, flatulence, tenesmus 
- chronic: wt loss +/- diarrhoea
- liver abscess
Treat: metronidazole + paromomycin in luminal disease
238
Q

What is a motile pear-shaped trophozoite with 2 nuclei seen in a stool sample?

A

Giardia lamblia

No invasion, causes malabsorption of protein and fat

239
Q

What are the symptoms of, diagnosis and treatment for Giardia lamblia?

A

Foul smelling non-bloody diarrhoea, cramps, flatulence, no fever
Diagnosis: stool micro, ELISA, “string test”
Treatment: metronidazole

240
Q

What are the symptoms of, diagnosis and treatment for Cryptosporidium parvum infection?

A
  • Infects the jejunum
  • Severe diarrhoea in the immunocomromised
  • Oocysts seen in stool by modified Kinyoun acid fast stain
  • Treatment : paromomycin, nitazoxamide for children
241
Q

What type of diarrhoea does rotavirus cause?

A
  • Replicates in mucosa of small intestine
  • Secretory diarrhoea, no inflammation
  • 30-40% cause of diarrhoea in children under 3 yrs
242
Q

What main viruses cause diarrhoea?

A 
> Rota virus- children
> Infective hepatitis (Hep A)
> Adenovirus
> Norovirus
> Enteroviruses (coxsackie, ECHO)
243
Q

What vaccines are available for rotavirus?

A

Rotarix : monovalent, 2(PO) doses

Rotateq : pentavalent, 3 (PO) doses

244
Q

What are the common organisms in a wound infection?

A
  1. Staph. aureus
  2. Enterococcus
  3. E.Coli
  4. Haemophilus influenzae
  5. Pseudomonas aeruginosa (surgical site infections)
245
Q

What pre-op interventions are aimed at reducing surgical site infections?

A

> Treat remote sites of infection
Avoid shaving or using razor at operative site
Delay hair removal until time of surgery and remove hair with electric clippers
Ensure timely administration of prophylactic antibiotics
Consider elimination of S.aureus nasal carriage via decolonisation techniques

246
Q

What are the risk factors for septic arthritis?

A

> Rheumatoid arthritis , osteoarthritis, crystal induced arthritis
Joint prosthesis
Intravenous drug abuse
Diabetes, chronic renal disease, chronic liver disease
Immunosuppression- steroids
Trauma- intra-articular injection, penetrating injury

247
Q

What are the commonest causative organisms of septic arthritis?

A

Stap. aureus 46%

Streptococci 22%

248
Q

What is the empirical treatment for septic arthritis?

A

> iv Cephalosporin or Flucloxacillin
add vancomycin if at high risk of MRSA
up to 6 weeks
if gonococcall or gram -ve = iv cefotaxime

249
Q

What are the commonest causative organisms and location of vertebral osteomyelitis?

A

> S.aureus ~ 50%

  • lumbar 43%
  • cervical: 11%
250
Q

How long should antibiotics be given for vertebral osteomyelitis?

A
  • Three months with 6 weeks intravenous

- Longer treatment if undrained abscesses/implant associated

251
Q

What is a Brodies abscess?

A

A subacute osteomyelitis, which may persist for years before converting to a frank osteomyelitis.
Most frequent causative organism is Staphylococcus aureus

252
Q

What are the key points to know about Hep A?

A 
> Acute (2-6 wks incub)
> Faecal-oral transmission
> Subclinical/mild in young, severe in elderly/pre-existing liver disease
> Diagnosed by Anti-HAV IgM
> Safe effective vaccine available
253
Q

What are the key points to know about Hep B?

A

> Acute + chronic (2-6 mths incub)
Parenteral transmission e.g. sexual, vertical, blood
5% risk of chronicity in adult, 95% in neonates, cirrhosis and HCC risk
Diagnosis: high ALT + AST, HBsAg, HBeAg (infectivity), HBcAb (Chronic)
Treatment: Interferon alpha, tenofovir, lamivudine

254
Q

What are the key points to know about Hep C?

A

> Acute, 80% progress to chronic
Blood + needle transmission, also vertical
Risk of cirrhosis and HCC
Diagnosis: ALT, Anti-HCV
Treatment: peginterferon alpha and ribavirin

255
Q

What are the key points to know about Hep D?

A

Requires HBV to replicate

Rapidly progressive liver disease can occur and only a modest response to interferon is reported

256
Q

What are the key points to know about Hep E?

A

Faecal-oral transmission

Acute hepatitis, life-threatening in pregnancy

257
Q

What are the key points to know about Hep G?

A

Appears to cause little liver damage

258
Q

What % of patients get a hospital acquired infection?

A

~10%

~15-30% preventable

259
Q

What are the most common hospital acquired infections?

A
  • Urinary tract infection
  • Surgical site infection
  • Hospital-acquired pneumonia
  • C. difficile colitis
  • Hospital-acquired bacteraemia
260
Q

How is C. difficile transmitted?

A

Gram positive spore forming anaerobe
Spores transmissible, contaminate environment, persist for long periods
Ingested spores germinate in gut

261
Q

What is Fidaxomicin?

A

A new narrow spectrum macrocyclic antibiotic that is non-systemic, bactericidal, and selectively eradicates pathogenic C. difficile with minimal disruption normal intestinal flora. Super expensive.

262
Q

How is candidasis treated?

A

> At least 2 weeks of antifungals
Fluconazole for Candida albicans
Echinicandin for non-Candida albicans
Ambisome, Fluconazole or Voriconazole for organ-based disease

263
Q

What is the aetiological agent of cryptococcosis and where is it often found?

A 
Cryptococcus neoformans
Eucalyptus tree (C. gattii) and pigeon excreta
264
Q

How is cryptococcosis managed?

A
  • 3/52 Amphotericin B +/- flucytosine
  • Repeat LP for pressure management
  • Secondary suppression with fluconazole
265
Q

What shows up clearly with a methenamine silver (GMS) stain?

A

Fungus in general

266
Q

How is aspergillosis managed?

A 
Voriconazole
Ambisome
Caspofungin/Itraconazole less good
At least 6 weeks of therapy
Duration based on host/radiological/mycological factors
267
Q

What are the major components of fungal cell wall?

A

Glucan, chitin and mannoproteins.

268
Q

What classes of antifungals target the fungal cell membrane?

A 
Polyene antibiotics - for pores in membranes
    - Amphotericin B,
    - lipid formulations
    - Nystatin (topical)
Azole antifungals - target ergosterol production
    - Ketoconazole 
    - Itraconazole 
    - Fluconazole
    - Voriconazole
269
Q

What classes of antifungals target fungal DNA/RNA synthesis?

A

Pyrimidine analogues

- Flucytosine

270
Q

What classes of antifungals target the fungal cell wall?

A 
Echinocandins 
   - Caspofungin acetate (Cancidas)
   - Micafungin
   - Anidulafungin
> Primarily active against candida and aspergillus species
> No coverage of Cryptococcus
> Inhibit glucan synthesis
271
Q

Examples of Water-Soluble Triazoles?

A

Fluconazole

Voriconazole

272
Q

Examples of Lipophilic Triazoles?

A

Itraconazole

Posaconazole

273
Q

What is the definition of pyrexia of unknown origin?

A

Fever higher than 38.3ºC (101ºF) on several occasions, persisting without diagnosis for at least 3 weeks in spite of at least 1 week of intensive investigations

274
Q

How is pyrexia of unknown origin classified?

A
  • Classic PUO
  • Nosocomial PUO
  • Immune deficient PUO
  • HIV-associated PUO
275
Q

What may be the cause of classical PUO?

A
  • Abscesses
  • Endocarditis
  • Tuberculosis
  • Complicated UTI
  • Fever in returning traveller
    Don’t forget
  • HIV
  • Connective Tissue/Vasculitis
  • Neoplasms
276
Q

What are some common cause of fever in an ill returned traveller?

A

Malaria - commonest
Dengue
Typhoid
Rickettsia

277
Q

What is Rickettsia?

A

Tick, mite, flea borne Zoonoses
Small gram negative bacteria
Diagnose on serology
Treat with doxycycline

278
Q

What is the definition of an immune-deficient PUO?

A

Neutropenic fever (of unknown origin): Neutrophils <0.5 total

279
Q

What type of bacteria are Brucella species?

A

Small, Gram-negative, nonmotile, nonspore-forming, facultative intracellular rod-shaped (coccobacilli) bacteria.

280
Q

What is the difference between Osler nodes and Janeway lesions

A

Oslers nodes: small painful nodular lesions

Janeway lesions: haemorrhagic, painless macular lesions

281
Q

How does infective endocarditis differ in IVDUs?

A

> Tricuspid valve is affected in 52.2%
S.aureus is the most common cause
More common in IVDU with HIV
Polymicrobial infection is more common

282
Q

What is the commonest causative organism of infective endocarditis?

A

Streptococcus viridans

Coagulase negative staphylococci (CNS) cause most cases of prosthetic valve endocarditis

283
Q

What is the recommended treatment for strep. viridans endocarditis?

A

benzylpenicillin and gentamicin

284
Q

What is Dukes Criteria for infective endocarditis?

A

Diagnosis = 2 major, or 1 major + 3 minor, or 5 minor
Major criteria:
- Persistent bacteraemia (>2 +ve BCs)
- Echocardiogram: vegetation
- + serology for Bartonella, Coxiella or Brucella
Minor criteria:
- Predisposition (murmur, IVDU)
- Inflammatory markers (fever , CRP high)
- Immune complexes: splinters, RBCs in urine
- Embolic phenomena: Janeway lesion, stroke
- Atypical echocardiogram
- Only 1 positive BC

285
Q

What valves are most commonly affected in infective endocarditis?

A

Mitral + aortic

IVDU = tricuspid

286
Q

What is empirical treatment for prosthetic infective endocarditis?

A

Vancomycin + gentamicin + rifampicin

287
Q

What infections can be acquired from cats?

A 
Bartonellosis (cat scratch)
Leptospirosis
Q-Fever
Toxoplasmosis
Rabies
Ringworm
Toxocariasis
288
Q

What infections can be acquired from dogs?

A 
Hydatid disease
Leptospirosis
Brucellosis
Q-Fever
Rabies
Ringworm
Toxocariasis
289
Q

What infections can be acquired from birds?

A 
Psitticosis
Influenza
Cryptococcus
Influ A
Poultry- salmonella
West Nile Fever
290
Q

What infections can be acquired from mice?

A 
Hantan viruses (via fleas)
Lyme borreliosis
Ehrlichia
Bartonella
Lymphocytic choriomeningitis
291
Q

What infections can be acquired from rats?

A 
Rabies
Leptospirosis
Lassa fever..VHF
Hantan viruses
Plague
Pasteruellosis
Haverhill fever
292
Q

What infections can be acquired from small ruminants?

A

Anthrax
Brucellosis
Q-Fever
Listeria

293
Q

What infections can be acquired from cattle?

A 
Anthrax
Leptospirosis
Brucellosis
Bovine tuberculosis
Anaplasmosis
Toxoplasmosis
Ecoli 0157
294
Q

What infections can be acquired from swine?

A 
Brucellosis
Leptospirosis
Trichinella
Hepatitis E?
Influ A!!!
Jap enceph
295
Q

What infections are associated with water-sports?

A 
Leptospirosis
Hepatitis A
Giardia
Toxoplasmosis
Mycobacterium marinum/ulcerans
Burkholderia pseudomallei
Ecoli
296
Q

What type of virus is rabies and what are the commonest vectors/reservoirs?

A

Rhabdovirus - lyssavirus

Dogs and bats

297
Q

What does rabies infection cause?

A

Virus migrates to CNS
Fatal encephalitis
Negri bodies pathognomonic

298
Q

What are the clinical features of brucellosis?

A

Undulant fever (peaks in eve)
Malaise, rigors, sweats, myalgia, arthralgia
Incubation 3-4 wks
Complications: endocarditis, osteomyelitis, meningoencephalitis

299
Q

What is the treatment for brucellosis?

A

> 4-6 weeks tetracycline or doxycycline combined with streptomycin, or;
8 weeks PO doxycycline + rifampicin

300
Q

What is the treatment for Plague?

A

Streptomycin
Doxycycline
Gentamicin
Chloramphenicol - meningitis

301
Q

What causes tick-borne relapsing fever?

A

Borrelia duttonii

302
Q

What is the vector and agent for lyme disease?

A

Ixodes tick

Borrelia burgdoferi

303
Q

What are the clinical manifestations of lyme borreliosis?

A

Early - erythema migrans, non-specific flu-like illness.
Early Disseminated - secondary EM, palsies, carditis, arthritis.
Late - arthritis, acrodermatitis chronicum atrophocans, encephalopathy

304
Q

What is the managememt for lyme disease?

A

Remove tick

Doxycycline

K1s Path (16 decks)

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