Category Archives: Microbiology


Seasonal lower respiratory tract infection of young children, typically caused by Respiratory syncytial virus (RSV) but can be others or mixed.

Classically wheezy cough, wheeze and/or crackles, reduced feeding and increased work of breathing.


Clinical. You would probably have to do 133 Chest x-rays before you found something that would change diagnosis – overuse of CXR associated with increased (and inappropriate) use of antibiotics.

Swabbing for virus identification can help with cohorting and avoidance of nosocomial infection, which can be a major problem.


Bacteriuria is not uncommonly seen with bronchiolitis, not always clear if this is true urine infection.


RSV passive immunisation for high risk babies with paluvizimab (Synagis). There’s an important story about the dangers of vaccine development.

HARMONIE trial of Nirsevimab – 83% reduction in RSV hospitalisation, 75% reduction in severe disease. Spain and US doing. Fight for global supply…


See here.


Initial studies did not show any relationship between moulds/damp and health, as there was major confounding with socioeconomic status, and because it is hard to quantify mould exposure (with many different mould species).

Then there is the effect of climate, and the built environment – heating, ventilation, insulation, materials etc.

More recently systemic reviews have made it clear there is a link particularly with development of asthma, particularly in older children, and where there is already a family history of atopy.

Coroner ruled death of 2yr old Awaab Ishak in 2020 from granulomatous tracheobronchitis was due to environmental mould exposure from poor housing.

Longitudinal studies have suggested that there may be protective effects but data is limited.

Similarly there is evidence that higher exposure to moulds leads to more asthma exacerbations.

There are genetic polymorphisms that affect ability to break down the fungal protein chitin, and these have been linked to urgent medical care visits, which suggests a non-immune mechanism may be important.

Dampness is linked to mould growth but also to house dust mite, microbial volatile compounds, mycotoxins and endotoxin.

The most studied mould species are AspergillusPenicilliumAlternaria and Cladosporium.

Limited evidence that interventions to reduce mould make any difference.

[European respiratory review 2018]


eg ciprofloxacin.

Broad spectrum antibiotics.

Block DNA synthesis by bacteria (uniquely among antibiotics).

Good against gram negatives, including Salmonella, Shigella, Neisseria, Pseudomonas (one of the few oral antipseudomonals).

Good intracellular penetration so active against organisms such as Chlamydia, Mycoplasma, Legionella and some Mycobacteria.

Good tissue penetration including central nervous system. 80% of orally administered drug is bioavailable so the IV route is only used when absorption impaired.

But no anti-anaerobic activity, and not very good against common gram positives eg Pneumococcus, Enterococcus, Staphylococcus (in fact, use is associated with MRSA). The newer types (Gatifloxacin, Moxifloxacin, Levofloxacin) have better gram positive activity but would still not be your first line choice, and have less anti-pseudomonal activity.

Not licensed under 1yr.

Only contraindication is previous tendon problem caused by it!

Adverse Effects:

  • Disabling, long-lasting (even irreversible) musculoskeletal and neurological problems reported, v rarely. So only use for severe infections, unless no other antibiotic appropriate. And stop ASAP if symptoms (muscle pain, joint pain, weakness, neuropathy etc)
  • Seizures (+/- predisposing condition)
  • Tendonitis – rupture can occur within 48hrs of starting, but can also be months later! Steroids at same time may increase risk, as may renal impairment and solid organ transplants
  • Arthropathy in immature animals – so avoided in children (except Nalidixic acid) unless extenuating circumstances (only reversible musculoskeletal symptoms have been reported). Arthropathy occurs in CF anyway.
  • Can prolong QT
  • Photosensitivity
  • Valve regurgitation – so caution if preceding valve disease or other risk factor eg connective tissue disorder (Ehlers-Danlos, Marfans), hypertension (!), Turners (!)

Rheumatic fever

Rare in developed world now, still common in underdeveloped world, or at least in underdeveloped communities eg Aboriginal Australians.  Prob also genetic susceptibility.

Caused by Group A streptococcus.  Important cause of acquired heart valve disease.  Can recur.

Probably cross reactivity between specific Group A strep M proteins and human tissues.

Erythema marginatum
Erythema marginatum


Jones criteria:

  • Major
    • Carditis eg new murmur.  Mitral most commonly, classically apical blowing pan-systolic.  Aortic next most common.
    • Arthritis esp large joints.  Migratory.
    • Subcutaneous nodules – these are the most uncommon major criterium (in Turkish study of over 1000 cases there were none with nodules).  Typically over extensor surfaces of joints, 0.5-2cm, symmetrical.
    • Sydenhams chorea
    • Erythema marginatum – not specific to rheumatic fever. Seen in 0.4% of Turkish study patients. Serpiginous or annual eruption, can look similar to erythema multiforme. Provoked by warmth eg bath.  Non pruritic.
  • Minor
    • Fever
    • Arthralgia
    • Prolonged PR interval on ECG
    • Elevated CRP/ESR
  • 2 major or 1 major plus 2 minor, plus confirmation of group A streptococcal infection eg positive culture, high ASO titre sufficient for diagnosis. Modified Jones takes into account background incidence.

Note that initial infection may be subclinical eg pharyngitis, erysipelas. Symptoms of rheumatic fever develop 10 days to several weeks later. Chorea can appear months later.  Low threshold for echo as carditis can also be subclinical.

Established criteria for rheumatic valvulitis – Gewitz 2015


Antibiotics – Treat with penicillin,  this does not however affect clinical course but hopefully prevents further spread of that particular bug. Traditionally single dose intramuscular Penicillin G Benzathine.

NSAIDs for joint pain.  Usually dramatic response, if not then reconsider diagnosis!

Valproate for chorea, possibly steroids – see Sydenham’s.

Aspirin and/or Steroids for carditis, but not much evidence.  Diuretics, ACE inhibitors for cardiac failure.

Long term treatment

Recurrence with progression of valve damage is the main concern, and well recognized. Subclinical carditis improves in about 50% but definite risk of progression (mild definite and borderline RHD showed 26% and 9.8% echocardiographic progression respectively).

Regular intramuscular penicillin (benzathine pencillin G) every 2-3 weeks has the lowest recurrence rates but oral penicillin V more acceptable.  Erythromycin or cephalexin if allergic.

WHO recommendations:

  • Rheumatic fever without carditis: 5 years after last attack or until age 18 (whichever is longer)
  • Rheumatic fever with carditis but without residual disease: 10 years after last attack or until age 25 (whichever is longer)
  • Residual valve disease or valve replacement: lifelong

American and Australian heart association guidelines vary slightly:

Penicillin prophylaxis guidelines comparison

Notifiable diseases (Scotland)

Public Health etc Act Scotland 2008

There are notifiable diseases and notifiable organisms:

Notifiable diseases

  • Clinical syndrome due to E.coli O157 infection
  • Haemolytic Uraemic Syndrome (HUS)
  • Necrotizing fasciitis
  • Severe Acute Respiratory Syndrome (SARS)
  • (plus infections caused by organisms below)

Notifiable organisms

  • Bacillus anthracis (anthrax)
  • Bacillus cereus
  • Bordetella pertussis
  • Borrelia burgdorferi (Lyme disease)
  • Brucella genus
  • Campylobacter genus
  • Chlamydia psittaci
  • Clostridium botulinum (Botulism)
  • Clostridium difficile
  • Clostridium perfringens
  • Clostridium tetani
  • Corynebacterium diphtheriae (toxigenic strains)
  • Corynebacterium ulcerans
  • Coxiella burnetii
  • Crimean-Congo haemorrhagic fever virus
  • Cryptosporidium
  • Dengue virus
  • Ebola virus
  • Echinococcus genus
  • Verocytotoxin-producing E.coli (VTEC)
  • Francisella tularensis
  • Giardia lamblia
  • Guanarito virus
  • Haemophilus influenzae type b (from blood, cerebrospinal fluid or other normally sterile site)
  • Hantavirus
  • Hepatitis A-E virus
  • Influenza virus (all types, including those caused by a new sub-type)
  • Junín virus
  • Kyasanur Forest disease virus
  • Lassa virus
  • Legionella genus
  • Leptospira genus
  • Listeria monocytogenes
  • Machupo virus
  • Marburg virus
  • Measles virus
  • Mumps virus
  • Mycobacterium bovis
  • Mycobacterium tuberculosis complex
  • Neisseria meningitidis
  • Norovirus
  • Omsk haemorrhagic fever virus
  • Plasmodium falciparum, vivax, ovale and malariae (malaria)
  • Polio virus
  • Rabies virus
  • Rickettsia prowazekii
  • Rift Valley fever virus
  • Rubella virus
  • Sabia virus
  • Salmonella (all human types)
  • SARS-associated coronavirus
  • Shigella genus
  • Enterotoxigenic Staphylococcus aureus
  • Staphylococcus aureus (all blood isolates)
  • Methicillin-resistant Staphylococcus aureus (MRSA)
  • Streptococcus pyogenes (from blood, cerebrospinal fluid or other normally sterile site)
  • Streptococcus pneumoniae (from blood, cerebrospinal fluid or other normally sterile site)
  • Toxoplasma gondii
  • Trichinella genus
  • Varicella-zoster virus
  • Variola virus
  • Vibrio cholerae
  • West Nile fever virus
  • Yellow Fever virus
  • Yersinia enterocolitica
  • Yersinia pestis
  • Yersinia pseudotuberculosis

Congenital Syphilis

In US primary, secondary and cong syphilis all surged in the 90s, now focal outbreaks in urban, drug using population. In N Africa, 3% of pregnancies, up to 7% in Carribean. 1 million pregnancies affected worldwide, of which 50% will end in abortion or still birth, and the other 50% will be congenital cases (unlike TORCH).

Clinically, 2/3 affected neonates asymptomatic at birth. Otherwise:

  • “snuffles” (vesicles on upper lip, highly infectious)
  • mucous patches (moist erosions)
  • hepatosplenomegaly and hepatitis
  • anaemia +/- hydrops
  • meningitis, with CSF pleocytosis and high protein
  • pneumonia, +/or fluffy diffuse infitrates on CXR (=pneumonia alba)
  • pseudoparalysis

Years later:

  • Typical facies – frontal bossing, saddle nose, short maxilla, high palate
  • Mulberry Molar (5 blobs in ring shape to tooth, pathognomic!). Hutchinson’s incisors (peg-like) better known.
  • Gummata (rubbery ulcers)
  • Sabre tibia (anterior bowing)
  • Hutchinson’s triad = interstitial keratitis, peg shaped incisors, and sensorineural deafness.


The risk of transmission is very high, particularly for untreated primary (ie a chancre) or secondary (ie multiple lesions, lymphadenopathy) disease. The risk falls to 40% for early latent syphilis (ie test positive but asymptomatic, with infection likely to have occurred in the previous 12 months on the basis of previous tests, symptoms or exposure). A category exists of latent syphilis of unknown duration, which only applies to patients aged 13-35yrs with nontreponemal titre of 32 or more.

Treating syphilis in pregnancy – for early acquired disease (primary, secondary or latent of <1yr) benzathine penicillin 50 000U/kg, with second dose a week later if in third trimester [BNF] but exclude neuro. For late latent syphilis >1yr duration give 3 doses at weekly intervals. For neuro disease benzylpen 50 000U/kg qds for 10-14/7 followed by 3 doses benzathine penicillin as above. If HIV positive also, then there tends to be more CNS disease, treatment failure, and treatment reactions (fever, myalgia, preterm labour – give steroids).

Adequate antenatal treatment = adequate benzathinepenicillin dose (2.4M Units IM) once weekly x3 – erythromycin is not reliable), 30 days before birth, proven 4x drop in nontreponemal serology.


Syphilis tests are either nontreponemal or treponemal.

  • Nontreponemal viz VDRL, RPR are screening tests, 70% sensitive in primary, 99% in secondary.
    • False positives – lupus, infection, recent immunization, pregnancy, other treponemes.
    • Quantitative – correlate with disease activity: 4x rise in titre early on or in relapse, drop of 4x suggests adequate response to treatment. In secondary, titres are always high ie 1:32.
    • False negative – early? Tertiary – V high levels of antibody! So if high suspicion then do dilutions.
    • Should become negative within 1 yr of treatment in primary, 2 yrs in secondary or congenital, 5 yrs in late.
  • Specific treponemal tests eg TP immobilization (TBI), fluorescent T antibody absorption (FTA-Abs) used to confirm.
    • False positive with non pallidum, Lyme or other borrelia.
    • Remain positive for life, even with treatment.
    • Do not correlate with disease activity.
    • FTA-Abs IgM available for testing baby, but still has false positives/negatives

In newborns, direct microscopy and fluorescent antibody tests can be done from mucous patch, else from placenta (beware non pallidum treponemes in normal flora esp mouth). PCR can be done from lesions too. VDRL more than 2x dilutions richer than mum’s is suggestive. IgM can be negative early esp infection occurring late in pregnancy, not always recommended. False positive VDRL may occur due to transplacental antibodies if high maternal levels.

Where disease is likely, or maternal treatment has been inadequate, further testing is required:

  • FBC, LFTs
  • Lumbar puncture, incl VDRL on CSF (not 100% sensitive so if congenital disease suspected, treat for neuro.)
  • XR long bones to look for destructive lesions. Even in asymptomatic, XR changes seen in 20% esp ankles, knees but also wrists, elbows. Lesions are symmetric, multiple: periostitis, osteitis, osteochondritis.
  • CXR
  • Ophthalmology assessment

For screening adults, 1 step strip test available, and one off oral treatment (Azithro, 1.8g). Antibodies give only partial protection.


For congenital syphilis treat with benzylpen 100-150 000 U/kg/d in bd or tds doses for 10-14/7.

There is concern about CSF levels with procaine or benzathine penicillin, although sometimes these are used for asymptomatic babies with nontreponemal tests less than 4x mum’s, which might occur with inadequate treatment. In this situation, any abnormal finding on evaluation requires full 10/7 course.

If late diagnosis (>4/52), give high dose viz 200-300 000 U/kg/d qds for 10-14/7. If CNS disease is excluded, this could be converted to benzathine penicillin.

Follow up

Monitor to show fall in VDRL at 3-6 months.

(Rana Chakraborty, St George’s)


=methicillin resistant staphylococcus aureus.  Cf methicillin sensitive staph, MSSA.

Methicillin resistance equates with flucloxacillin resistance. mecA is the methicillin resistance gene, which codes for a low affinity PBP (penicillin binding protein) – ie penicillin can’t bind easily. The gene has probably crossed from coag neg staph on at least 5 occasions to create MRSA strains. As with MSSA, different strains exist, carrying a range of different pathogenic genes.

Traditionally MRSA was found in institutions and the elderly, but now can be seen frequently in the young and healthy, causing the same infections that MSSA causes eg skin/soft tissue. It can also be responsible for rarer, more severe diseases eg necrotizing fasciitis. The US Center for Disease Control details criteria for distinguishing hospital acquired and community acquired MRSA infections – community acquired strains are typically SCCmec type IV (this is the cassette that contains mecA), which are sensitive to most non-beta lactam antibiotics, but on the other hand is associated with Panton Valentine Leucocidin (PVL, a cytotoxin associated with necrotizing disease). But again, this distinction is becoming less clear with strains associated with community acquired infection becoming more frequent in hospital acquired cases, and having variable levels of non-beta lactam antibiotic resistance.

In itself, antibiotic resistance may not translate to increased virulence and pathogenicity – it may just make it harder to treat. Studies have shown that after correcting for other factors eg age and co-morbidity, mortality is not significantly different. However, one important factor is use of inappropriate antibiotics, which of course is more likely with MRSA. Furthermore, in the US many MRSA outbreaks are caused by the USA300 clone, which carries a number of genes (in common with Methicillin sensitive staphylococcus aureus) eg PVL, ACME which are associated with enhanced pathogenicity.

PVL seen in 50% of symptomatic (skin) community MRSA in the US. Now also being reported in hospital acquired MRSA. Prevalence much lower in Europe, but risk of spread. Geographical areas tend to have their own clones (eg type 80 in Europe), with occasional pandemic.


  • MRSA has been shown to survive on sterile packaging for at least 6 months.Journal of hospital infection 2001;49(4):255-61.
  • Basic simple infection control like hand washing works.
  • MRSA prevalence in hospitals is associated with macrolide and 3rd generation cephalosporin use.Clinical microbiology and infection 2007;13(3):269-76.
  • Alcohol hand rub reduces its transmission and hospitals which have introduced a policy of using this between patient contacts reduce their MRSA rate.
  • Isolation and screening work but may be impracticable in emergency admissions or in hospitals with near 100% occupancy.

In the UK, most MRSA are resistant to quinolones and macrolides. Even if sensitive to quinolones, treatment is not recommended as resistance evolves rapidly. Most MRSAs are sensitive to tetracyclines (but not for use under 12yrs), rifampicin, co-trimoxazole, and linezolid, all of which can be given orally. Clindamycin can be effective but beware inducible resistance – see below. No evidence for trimethoprim alone (cf septrin); use in combination with rifampicin? Probably best not to give rifampicin or fusidic acid monotherapy anyway as resistance frequently induced.  See antibiotic classes.

In MRSA skin infections (cellulitis/abscesses), most will get better anyway, esp after I&D, but using the wrong antibiotic increases risk of treatment failure by odds ratio of 2.80 (87% success cf 95% of patients who received an active antibiotic). Topical agents will induce resistance if used for high load infections eg wounds, catheter sites so should be combined with systemic therapy.  About 12% are resistant to topical mupirocin.

For intravenous therapy, gentamicin, vancomycin and teicoplanin are effective, although vancomycin resistance has been described since 2002. Teicoplanin levels can be unpredictable, and treatment failure associated with low levels has been seen; checking levels would make sense (aiming for trough of at least 10, 20 in endocarditis) but is rarely done. In line infections, vancomycin or linezolid should be used if the infection is severe; if milder, then removal of the line and oral therapy may be sufficient.

In bone infection, linezolid is good but should be given for a maximum of 28 days. Fusidic acid and Rifampicin are good adjuncts (rifampicin has in vitro activity against biofilms). Clindamycin and co-trimoxazole have also been used for bone infections. Early surgery (eg within 2/7 of onset of symptoms) is important esp where a prosthesis is present.

Necrotising pneumonia with MRSA post-influenza has mortality up to 75%.

For bacteraemia/endocarditis, vancomycin is the drug of choice, as treatment failures have been described with teicoplanin. Rifampicin or fusidic acid can be considered as adjuncts; there is no evidence for adding an aminoglycoside. A minimum of 14 days treatment is required (although oral treatment may be appropriate for maintenance) but should be extended if vegetations seen on trans-oesophageal echo. Infected pacemakers should be considered the same as orthopaedic prostheses.

Clindamycin resistance is sometimes only 1 mutation away from erythromycin resistance. If the bug is erythromycin sensitive, then there is no issue, and clindamycin is a good choice (and can be given orally). On the other hand, if erythromycin resistance is seen, then the D test should be done: if a D-shaped zone appears around the clindamycin disk when an erythromycin disk is placed nearby, then you have induced resistance and clindamycin should be avoided. The erm gene is responsible for erythromycin-inducible resistance; the mrsA gene also confers resistance to erythromycin but does not affect clindamycin.


Once colonized, about 40% of patients develop persistence – commoner where skin breaks present. Vancomycin does not clear nose, throat or gut.

Eradication of S. aureus nasal colonization eg with 72 hour mupirocin has been successful. However, recolonization usually occurs within a relatively short time, and the Cochrane review did not find much evidence in favour. Use of mupirocin to prevent infection in endemic settings eg dialysis centers have shown conflicting results although metanalysis suggests benefit (but fear of mupirocin resistance). Neomycin is even less effective, but is an alternative where mupirocin resistance is seen.

Combined treatment seems sensible, and recent RCT of 2% chlorhexidine gluconate washes, 2% mupirocin ointment intranasally, oral rifampin and doxycycline for 7 days vs no treatment confirms. At 3 months of follow-up, 74% cf 32% had cleared. Still significant benefit at 8 months (54% of those treated culture negative). On multivariable analysis, having a mupirocin-resistant isolate increased the risk of treatment failure nearly 10 fold. Mupirocin resistance emerged in only 5% of follow-up isolates. Clin Infect Dis. 2007 Jan 15;44(2):178-85.

Other control measures include a combination of active surveillance cultures of high risk patients, improved health care worker hand hygiene, consistent use of contact precautions for colonized/infected patients, and directed treatment of health care workers implicated in transmission. PIDJ January 2005 pp 79-80

Screening patients seems to reduce hospital acquired infection in the Netherlands, but not in Switzerland. UK guidelines say do for high risk only eg previous carriers, transfers, ICU. Standard infection control procedures alone seem to have worked in UK although what do you compare with? Rapid test (PCR) did not help (in crossover trial) except in reducing inappropriate isolation. 3-4x as expensive.

[UK guidelines, J antimicro chemo 2006 PMID 16507559]




Cefalosporins have a broader activity than penicillins, esp 3rd generation eg cefotaxime, ceftriaxone which are effective against most gram positives and gram negatives.

Good for meningitis (penetrate inflamed meninges at high dose) but not effective against pseudomonas, enterococcus, listeria, MRSA, and not that great against normal staphs so beware if possible line infection or neonatal meningitis. Some pneumococci can be resistant (1st line meningitis treatment in US is cef with vanc).

Ceftriaxone is drug of choice for Lyme with complications; it is not recommended for immediate treatment of meningococcal disease as any subsequent calcium containing infusions will reduce its plasma levels.

Ceftriaxone also eradicates meningococcal colonization – since cefotaxime is essentially equivalent, no reason to switch just for this indication.

Contraindications to ceftriaxone:

  • Concomitant treatment with intravenous calcium (including total parenteral nutrition) in premature and full-term neonates—risk of precipitation in urine and lungs (fatal reactions) ;
  • full-term neonates with jaundice, hypoalbuminaemia, acidosis, unconjugated hyperbilirubinaemia, or impaired bilirubin binding—risk of developing bilirubin encephalopathy;
  • premature neonates less than 41 weeks corrected gestational age

Recurrent boils

Potentially symptom of diabetes, chronic granulomatous disease – but more usually just an individual thing, or a nasty strain of staphlycoccus aureus.

GOS says if otherwise well (no other abscesses, no colitis, no weird organisms eg Serratia) then consider eradication with:

  • Naseptin – a medication taken four times a day for a period of 10 day.s
  • Chlorhexidine shower or bath and hairwash every day for a period of 14 days.
  • Keep a separate towel for each member of the family, change for a clean towel every two days and wash the dirty towels on a hot wash cycle.


Antibiotic resistance

Penicillin resistance

Resistance to penicillin is usually due to Beta lactamase enzymes.  Therefore adding a  beta-lactamase inhibitor eg clavulanate (as found in co-amoxiclav) overcomes the resistance and extends the spectrum.

An alternative resistance mechanism however is production of defective Penicillin Binding Proteins – this is the mechanism of resistance in Pneumococci.  Beta lactamase inhibitors therefore do not help.

Macrolide resistance

Variable resistance seen; sometimes effective against penicillin resistant staphylococci including some MRSA, but poor activity against Haemophilus. Variable resistance seen in streptococcus, pneumococcus. Resistant mycoplasma are rare but do exist – try cipro, else tetracycline.

Using Azithromycin probably improves efficacy in Haemophilus (more active) but pneumococci that are resistant to erythromycin (approximately 5 to 20% of strains currently) will also be resistant to azithro, and no difference in in vitro activity between the newer and old macolides against other common respiratory pathogens.

Multiresistant organisms

In theory, you should use a combination of antibiotics (if possible) to treat a multiresistant organism, to prevent resistance developing (as in TB).  However there is no good clinical data to support this, beyond TB treatment (which is slow growing, so probably different).  On the contrary, meta-analyses demonstrate no difference in clinical outcomes between the two treatment strategies (for infections with Gram-negative bacteria), but there are well-documented increased toxicities with combination therapy.

Having said that, given the greater mortality associated with delays in appropriate and effective antimicrobial treatment, starting with combination therapy in critically ill patients seems sensible.

If there is poor response to treatment, rather than simply adding a second agent, consider:

  • dose, frequency – are you achieving adequate time above MIC?  Consider prolonged antibiotic infusion strategy
  • route – give IV if not already
  • duration – extended treatment course?

[doi: 10.1128/CMR.05041-11 Clin. Microbiol. Rev. July 2012 vol. 25 no. 3 450-470]



ESBL – extended spectrum beta lactamase

Scenario 1: lower renal tract infection with ESBL producing Gram negative

Bacteriuria with urinary symptoms but minimal systemic symptoms and no fever

  • Treatment duration 3 days
  • First line – trimethoprim / nitrofurantoin  (not used in under 3 months)
  • Depending on sensitivities and age alternative options include ciprofloxacin, single dose aminoglycoside, pivmecillinam or fosfomycin

Scenario 2: upper renal tract infection with ESBL producing Gram negative

Bacteriuria with urinary symptoms and associated systems symptoms including fever

  • Treatment duration 7-10 days (as per NICE)
  • Always consult with infection management specialist
  • First line – if seriously unwell or under 3 months carbapenem  + consider one dose of aminoglycoside
  • Alternative: tazocin and consider one dose of aminoglycoside (if sensitive and not seriously unwell and after discussion with local microbiologist)
  • OPAT : Ertapenem
  • Daily IVOST review required
  • Potential IVOST options when afebrile, clinically improving, falling CRP and able to take and absorb oral medicines: ciprofloxacin, trimethoprim
  • There was less consensus on the role of pivmecillinam and its ability to penetrate renal tissue. It should be considered only to offer an oral option to finish a course of antibiotics in a clinically improving child

Scenario 3 – infection with ESBL producing Gram negative outside the renal tract (except for meningitis)

  • As per IDSA – carbapenem, meropenem (especially if child unwell)
  • Stepdown co-trimoxazole or ciprofloxacin (would consider fosfomycin on rare occasion)
  • Temocillin not empirical therapy until we understand PK/PD profile better plus expensive and difficult to obtain – consider not including
  • Recommendation would need caveat, how unwell, age of child.  Not experienced discuss with infection specialist. BNFC reference
  • Ertapenem OPAT

Scenario 4 – meningitis complicating ESBL producing Gram negative

  • Carbapenem, limited ability to step down
  • Treatment duration – 3 weeks
  • Lumbar puncture to ensure infection cleared.

[Conor Docherty]