Acute Infection Flashcards
What are the risk factors for patient with Osteomyelitis?
previous osteomyelitis penetrating injury intravenous drug misuse diabetes HIV infection recent surgery distant or local infections sickle cell anaemia rheumatoid arthritis chronic kidney disease immunocompromising conditions upper respiratory tract or varicella infection (in children)
What pathogens can cause meningitis is immunocompromised individuals?
Listeria monocytogenes (unpastureized milk) TB(endemic areas)
What are the risk factors for meningitis?Kernigs and Brudenzski
complement systems defects,hyposplenism,HIV
What investigations should be done in patients suspected of viral mengitis and how are they treated
A polymerase chain reaction (PCR) test for enterovirus, herpes simplex virus 1&2 and varicella zoster virus on the cerebrospinal fluid sample. All patients with meningitis should also be offered a HIV test.
There is no treatment of proven benefit in viral meningitis. Supportive treatment and rest is recommended. Some clinicians advocate using Aciclovir to treat meningitis due to herpes simplex virus but there is no good quality evidence to support this and it results in an increased length of stay in hospital.
Recovery is likely to be slow. Many patients suffer from symptoms including fatigue, headaches, slowed thinking and mental health problems for many months.
How can meningitis be treated and when are steroids given?When is Prophylaxis given?
IV ceftriaxone 2g/12hrs
Pre-hospital
Only in patients with signs of meningococcal sepsis e.g. non-blanching rash
Intramuscular Benzylpenicillin or Ceftriaxone
Hospital
Antibiotics should be given within 1 hour of arrival if meningitis or sepsis are suspected
Ideally, this would be immediately following lumbar puncture and blood cultures
Standard antibiotics recommended for sepsis may not be appropriate
Cefotaxime/ Ceftriaxone (or Chloramphenicol if penicillin allergy)
Duration of antibiotic therapy depends on the causative organism
Modest reduction in mortality in pneumococcal meningitis only
Reduction in risk of hearing loss
Current UK guidelines
Start dexamethasone ideally shortly before but certainly within 12 hours of the first dose of antibiotics
Continue for 4 days only in cases where pneumococcal meningitis is confirmed, or thought probable
Pneumococcal-Signs of meningism present where as meningococcal rash is present
Only recommended for meningococcal infection
Aim - to eradicate nasal carriage of N.meningitidis
Offered to:
Close contacts – living in same house or sharing a kitchen in halls of residence
High risk exposure – exposure to airways secretions e.g. intubation, CPR
Recommended treatment:
Ciprofloxacin oral for a single dose
Rifampicin oral for 2 days
Ceftriaxone intramuscular injection for a single dose
Which factors suggest a poor prognosis from meningitis?
Essentially, these factors reflect the presence of features suggesting the development of complications;
Disseminated intravascular coagulation
Severe sepsis/ septic shock
Raised intracranial pressure
Urgent senior review and critical care assessment is required
What are the complications of meningitis?
Deafness-sensineuronal
Cognitive impairment
Focal neurological deficits
Epilepsy
meningococcal-skin necrosis,amputation,pneumonia,permenant adrenal insufficiency,pericarditis,arthritis,ocular infection
What Vaccinations are given to prevent meningitis
Infants-Capsular group A and B
Quadravent ACWY at age 24 oe high risk travel
What Investigations can be used to diagnose viral encephalitis
Lumbar Puncture
General findings
White blood cells ↑ (lymphocytes)
Protein ↑
Glucose ↔
Specific tests
PCR on cerebrospinal fluid for HSV 1 and 2, VZV and Enteroviruses
Clinical features allow differentiation from viral meningitis
Neuro-imaging
MRI can show evidence of brain parenchyma inflammation
Other tests
EEG – especially to rule out subtle motor seizures or non-convulsive status epilepticus
HIV test – wider investigations are required in immune compromised patients
If relevant travel history – serology and PCR for other neurotropic viruses
What are complication and prognosis of viral encephalitis?
Mortality No treatment ~70% die Treatment - 10-20% die Worse outcomes with delayed treatment >24hrs Acute complications Venous sinus thrombosis Status epilepticus Stroke Aspiration pneumonia
HSV encephalitis is often life-changing
~60% of survivors are left with a permanent neurological disability
Specialist neuro-rehabilitation may be required
Would a negative cerebrospinal PCR test exclude a diagnosis of viral encephalitis?
NO,10% of patients might of a negative serology on initial test, therefore if clinical suspicion remains another PCR should be done 24-48hrs later
To exclude viral Encephalitis -Need to have 2 negative PCR tests done 24 to 48 hours apart and normal MRI
OR
.HSV PCR in the CSF is negative ONCE >72 hours after neurological symptom onset, with unaltered consciousness, normal MRI (performed >72 hours after symptom onset), and a CSF white cell count <5 cells/mm3
What are the Indications and Complications of LP
Indications
Diagnostic
Infection – meningitis (bacterial/ viral/ fungal) or encephalitis
Subarachnoid haemorrhage
Other – multiple sclerosis, malignancy etc.
Therapeutic
Reduce intracranial pressure e.g. idiopathic intracranial hypertension
Spinal epidural
Pain relief (during labour)
Anaesthesia (e.g. lower limb surgery)
Contraindictions
Indications for brain imaging prior to lumbar puncture
Focal neurological signs
Presence of papilloedema
Continuous or uncontrolled seizures
Reduced or fluctuating conscious level
Bleeding risk
Deranged blood clotting or a low platelet count
Taking anticoagulation ( e.g. warfarin if INR >1.4)
Others
Signs of severe sepsis or a rapidly evolving rash
Infection at the site of the lumbar puncture
How can IE be managed?
Antibiotics as soon as blood cultures taken:
4-6 weeks, including at least 2 weeks IV initially.
Empirical treatment-
NVE,indolent-gentamicin+amoxicillin
NVE,severe sepsis no risk factors for entero-psuedomonas-Vancomycin +gentamicin
If risk factor-Vancomycin+meropenem
Empiric therapy and for streptococci: benzylpenicillin (or amoxicillin) + gentamicin.
Staph. aureus: flucloxacillin if native valve, add rifampicin and gentamicin if prosthetic valve.
Enterococcal-Amoxicillin,amoxicillin +gentamicin,
Surgery:
Debridement, repair, or replacement required in 20%.
Indications: refractory HF, persistent sepsis or emboli, or fungal IE.
Prevention
Prophylactic antibiotics for high-risk dental procedures in patients at risk of IE (e.g. prosthetic valves) is controversial: European and American guidelines recommend it, but NICE do not.
How to diagnose prosthetic valve endocarditis?
Diagnosis is more difficult in PVE than in NVE (native valve endocartitis) and is based mainly on the results of echocardiography and blood cultures. However, both are more frequently negative in PVE. Although TOE is mandatory in suspected PVE, its diagnostic value is lower than in NVE. A negative echocardiogram is frequently observed in PVE and does not rule out the diagnosis, but identification of a new periprosthetic leak is a major criterion, in which case an additional imaging modality could be considered (such as CT or nuclear imaging).
How can prothetic valve endocarditis be treated and what complications can develop
A very high in-hospital mortality rate of 20–40% has been reported in PVE.
These patients need aggressive management, consisting of antibiotic therapy and early radical surgery.
Most common causative Organism in prosthetic valve is staph aureus
antibiotics-Vancomycin and rifampicin and gentamicin
If vancomycin resistant-daptomycin
Several factors have been associated with poor prognosis in PVE including older age, diabetes mellitus, healthcare associated infections, staphylococcal or fungal infection, early PVE, HF, stroke and intracardiac abscess
name other signs and symptoms associated with IE?
Fever Roth’s spots Osler’s nodes Murmur Janeway lesion Anaemia Nail haemorrhage Emboli
Infective Endocarditis caused by which pathogens need a colonoscopy?
There have been several studies showing a close association between S. gallolyticus endocarditis and colon cancer, with incidence between 18% and 62%. It has been standard of care to screen the patients with S. gallolyticus endocarditis for colon cancer (eg colonoscopy and/or CT scan).
Strep bovis
When should a trans oesophageal echo be done?
Echo must be performed ASAP (ideally within 24 hours) in all patients with suspected IE (C)
TTE first (C)
If TTE negative but clinical suspicion, repeat TTE/TOE at 7-10 days (C)
SA bacteraemia/Candidaemia should have TTE within first week of treatment or within 24 hours if other evidence of IE (B)
TTE at completion (C)
F/u Echo if cardiac complications or suboptimal response to treatment (B)
Routine repeat Echo whilst on treatment is not required (C)
How many blood cultures need to be done? and what organisms require serology
Blood cultures taken prior to starting treatment in all cases (B)
ANTT when taking blood cultures (B)
If chronic/subacute presentation: 3 optimally filled sets to be taken from peripheral sites with 6 or more hours in between them prior to antibiotics (C)
If septic shock: 2 optimally filled sets at different times within 1 hour prior to antibiotics (C)
Bacteraemia is constant in IE (B)
Paired blood cultures (B)
Coxiella burnetti (Q fever) (B) Bartonella spp (B) Consider: Chlamydia, Legionella, Mycoplasma (C) Brucella if risk of exposure (C) Candida Ab/Ag tests are NOT used
What is the criteria for surgery?
Hf
Controlled infection-access for example
Prevention of embolism
How can IE be managed?
Antibiotics as soon as blood cultures taken:
4-6 weeks, including at least 2 weeks IV initially.
Empirical treatment-
NVE,indolent-gentamicin+amoxicillin
NVE,severe sepsis no risk factors for entero-psuedomonas-Vancomycin +gentamicin
If risk factor-Vancomycin+meropenem
Empiric therapy and for streptococci: benzylpenicillin (or amoxicillin) + gentamicin.
Staph. aureus: flucloxacillin if native valve, add rifampicin and gentamicin if prosthetic valve.
Enterococcal-Amoxicillin,amoxicillin +gentamicin,
2-4% IE caused by fungal Infections(neonates,Iv drug users,prosthetic valve,immunosuppressed)
candida Albicans-25%
Other Candida_25%
Aspergillus-25%
Other-25%
Intial treatment-Echnocandin,Lysosomal AmphoterIcin B
Modified after Organism identidied
For candida combination of Sugical and Medical treatment reccomended
2-4% IE caused by fungal Infections(neonates,Iv drug users,prosthetic valve,immunosuppressed)
Aspergillous-Variconazole
Surgery:
Debridement, repair, or replacement required in 20%.
Indications: refractory HF, persistent sepsis or emboli, or fungal IE.
HACEK Group
Fastidious extracellular Gram negative bacteria
3% of cases
Treatment
Beta lactamases stable cephalosporin or Amoxicillin
Gentamicin for first 2 weeks of therapy
Alternative Ciprofloxacin
Prevention
Prophylactic antibiotics for high-risk dental procedures in patients at risk of IE (e.g. prosthetic valves) is controversial: European and American guidelines recommend it, but NICE do not.
What is the POET STUDY?
- According to guidelines we treat left-sided infective endocarditis with intravenous (IV) antibiotics for up to 6 weeks in hospital (sometimes OPAT when available)-OPAT-Outpatient parenteral antibiotic therapies
- Endocarditis is associated with high in-hospital complication- and mortality rates - but mainly in the early phase
- After stabilisation, the patient may be clinically fit enough for discharge but have to remain an inpatient solely to finish a long course of iv antibiotics, rather than back home and their daily lives.
- Longer inpatient stays are associated with increased risk of complications such as Healthcare Associated Infections
- Therefore there was interest in researching whether using oral antibiotics, was a safe and equally effective alternative to IV.
Conclusion
Efficacy and safety of shifting to oral antibiotic treatment was noninferior to continued intravenous antibiotic treatment
- in stabilized patients with left-sided endocarditis caused by Streptococcus spp, Enterococcus faecalis, Staphylococcus aureus, or coagulase-negative staphylococci
- across co-morbidities, native vs prosthetic valve and surgically vs conservatively Tx
Oral antibiotics may safely be administered during approximately half of the recommended antibiotic treatment period
- potentially as outpatient treatment
- more than 50% of patients with endocarditis may be candidates to partial oral antibiotic treatment
What are the risk factors for IE?What is the modified dude’s criteria?
Risk factors
Increased turbulent flow:
Valve disease.
Prosthetic valves.
Structural disease: unrepaired PDA, VSD, HCM.
Rheumatic heart disease.
Increased pathogen entry and bacteraemia:
IV drug use.
Haemodialysis
Dermatitis
Chronic disease:
Diabetes
Kidney disease.
Duke criteria
Diagnosis requires any 1 of:
2 major.
1 major plus 3 minor.
5 minor.
Major criteria:
+ve blood culture x2 or persistent.
+ve echo: vegetation, abscess, new regurgitation, or prosthetic valve dehiscence.
Minor criteria:
RF +ve.
Fever
Vascular immune-complex signs.
+ve blood culture (x1).
+ve echo for other abnormality.
What are risk factors and organisms responsible for Osteomyelitis?
Risk factors
Portal for pathogen entry:
Trauma: open fracture or orthopedic surgery.
Surgical prostheses.
IVDU
Diseases:
TB
Diabetes
PVD
Immunosuppression.
Alcoholism
Sickle cell disease.
Pathophysiology
Infection can come from direct/contiguous spread (cellulitis, abscess, trauma, surgery prosthesis), or haematogenous spread, which is commoner in kids, patients with urinary catheters, or TB.
Once infected, leukocytes enter bone, releasing enzymes which cause bone lysis and leave necrotic areas known as sequestra. New bone often forms around this.
Chronic osteomyelitis if >6 months of infection.
Pathogens
Staph. aureusis the commonest cause in most patient groups.
Less common pathogens includeStrep. pyogenes(kids),H. influenzae(kids), Gram negative bacilli (elderly), andPseudomonas aeruginosa(IV drug users).
In sickle cell disease,Salmonellais the commonest cause.
What Organisms can cause IE?
The overall causative agents in IE are well documented and have been relatively stable, based on population-based studies over time. The most common pathogens are listed below; these together with any underlying risk factors indicate the most likely causative organism:[2]
Viridans group streptococci Staphylococcus aureus Enterococci Coagulase-negative staphylococci Haemophilus parainfluenzae Actinobacillus Streptococcus bovis Fungi Coxiella burnetii Brucella species Culture-negative Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella species (HACEK). Patients who develop native valve endocarditis in the absence of intravenous drug use commonly present with viridans group streptococci, enterococci, or staphylococci, with other pathogens being less frequent. Intravenous drug users often present with right-sided valvular involvement and are more likely to have S aureus, streptococci, gram-negative bacilli, or polymicrobial infections.[2]
Prosthetic valve endocarditis is most commonly caused by coagulase-negative staphylococci, S aureus, enterococci, or gram-negative bacilli. It should be noted that early prosthetic valve endocarditis is often caused by Staphylococcus epidermidis.[2]
What is the pathophysiology and clinical presentation of bone and joint infection
Bacteria that enter the bloodstream exist in a free-floating planktonic state. Most osteomyelitis is caused by biofilm-forming bacteria. These bacteria express surface components called adhesins that bind to proteins found in host tissues. Once attached, the bacteria produce a polysaccharide extracellular matrix, forming a biofilm.Once sufficient numbers of organisms are present in the biofilm, a complex system of cell-to-cell signalling develops, known as quorum sensing. This controls further development of the mature biofilm. It may also propagate the spread of infection by controlling separation of fragments of this biofilm which seeds to local sites. Some of the organisms in biofilm are able to enter a dormant state with minimal cellular division. In this state, antibiotics that act on cell division are ineffective.
Clinical presentation is highly variable
Septic arthritis tends to present with the rapid onset of pain, swelling and redness in a single joint
Prosthetic joint infection may present with joint pain & evidence of inflammation at the surgical site
Vertebral osteomyelitis presents with back pain & may progress to cause neurological signs
Chronic osteomyelitis often causes a sinus which does not heal
What Investigations can be done for bone and joint infections?
Bedside tests Fever is often absent Blood tests FBC, U&Es, CRP, blood cultures Microbiological tests Joint aspiration, bone biopsy, tissue biopsy, sonication of excised prosthetic material Radiology Plain X-rays, CT scans, MRI scans
How does Disseminated gonococcal infections present?How can they be diagnosed and managed?
Presentation:
- Purulent monoarthritis and/or
- Triad of tenosynovitis, dermatitis (papules, pustules, necrotic lesions) and asymmetric migratory polyarthralgia
- May occur several days to weeks following initial infection
Risk factors:
- Female sex
- HIV infection
- Menses
- Low socioeconomic or educational status
- Pregnancy
- Multiple sexual partners
- SLE
- Complement deficiency
Diagnosis:
- Blood cultures (may be negative)
- Synovial fluid analysis (joint aspirate)
- Gram stain will show inflammatory effusion with neutrophil predominance plus or minus gram negative diplococci
- Culture & sensitivity testing
- NAAT PCR (if available and validated for synovial fluids)
Treatment:
- Intravenous ceftriaxone 2 weeks with appropriate oral switch for further 4 weeks
- Joint drainage for purulent arthritis (may need to be repeated several times)
Of note going back to the original presentation
- Parvovirus B19 infection tends to cause a symmetrical polyarthralgia
- Disseminated gonococcal disease tends to cause an asymmetrical and migratory joint symptoms
- This case highlights the importance of taking a full medical history including sexual history
What Organisms usually cause native and prosthetic joint infections
Native-Stap aureus,strep,clostridium.Neisseria gonorrhea,E-coli
Prosthetic
early-Staph,strep,Enterococci
Late
Coagulase negative staphylococci
How can Acute and Chronic Periprosthetic Infections be differentiated?
Acute-<3 months, acute pain, fever,red swollen joint,Stap,ecoli are the causes
Antibiotics-Courses of antibiotics need to be relatively prolonged
Four weeks for septic arthritis
At least six weeks for vertebral osteomyelitis & prosthetic joint infections
Prolonged courses of iv therapy may be delivered via “OPAT” clinics
Oral therapy may be as effective as iv therapy in many cases
Osteomyelitis-Flucloxacillin
Management-DAIR(Debridement,antibiotics and implant retention)
Chronic-months to years, present with chronic pain, loosening prosthetic, sinus tracts.Causes include coagulase negative staph
Surgical management-Complete removal of prosthesis in stage 1 and 2
