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year 4 CDM 2 > Case 12: Fever > Flashcards

Case 12: Fever Flashcards

1
Q

Sensitivity testing

A

What antibiotic at what concentration prevents growth? Is it over the threshold value? E tests will show the MIC (minimum value of antibiotic which works)

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2
Q

What do common organisms appear like on gram stain

A
  • Gram positive cocci in clusters: Staph aureus (MSSA and MRSA)
  • Gram positive cocci in pairs: Streptococcus pneumoniae
  • Gram positive cocci in chains: Enterococci, Other streptococci (eg. Group A Strep)
  • Gram positive rods: Clostridium perfringens, Listeria
  • Gram negative cocci: Neisseria gonorrhoea, Neisseria meningitidis
  • Gram negative rods: Pseudomonas aeruginosa, E.Coli, Klebsiella pneumoniae, Salmonella sp, Enterobacter sp.
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3
Q

Culturing bacteria: Agar can have

A
  • Additional growth factors to encourage fussy bacteria: eg. Chocolate agar contains lysed blood which releases NAD (factor V) and haemin (factor X) which Haemophilus influenza requires to grow
  • Antibiotics to inhibit bacteria we are not interested in: eg. NYC agar for N.gonorrhoea contains both vancomycin and colistin to inhibit most gram positives and gram negatives but gonorrhoea is resistant to both of these and so can grow.
  • Colour indicators to help identify bacteria: eg. CLED agar differentiates lactose-fermenting bacteria (eg. E.Coli) from non-lactose fermenting bacteria (eg. Proteus)
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4
Q

Different causes of traveller related infections

A
  • Short Incubation period <10 days: Influenza, Dengue, Yellow fever, Plague
  • Indeterminate (10-21 days): Malaria, viral haemorrhagic fever, Typhoid fever, scrub typhus, African trypanosomiasis
  • Long (>21 days): Malaria, Hepatitis ABCDE, Rabies, Schistosomiasis, Leishmaniasis, Amoebic liver abscess, Tuberculosis
  • Most common: Dengue, Malaria, Mononucleosis, Enteric fever, Rickettsial
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5
Q

Travel history

A
  • Itinerary: Dates, times, routes, modes of transport
  • Accommodation
  • Activities: exposure to standing water
  • Food
  • Water: bottled, sterilised
  • Sexual activity
  • Vaccinations/prophylaxis: insect nets
  • When was the last time you were outside the UK? and before that etc
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6
Q

Investigations for fever in returning traveller

A
  • Bloods: FBC, U&E, LFT, Coag, ABG, Blood culture.
  • Throat/sputum/stool/Urine CSF as appropriate
  • Malaria films
  • Serology – e.g. Rickettsiae, Dengue, HIV, Viral hepatitis, Syphillis
  • PCR – e.g. Dengue (blood), Herpes + enteroviruses for encephalitis (CSF), TB
  • Special stains – ZN/auramine (TB), Grockott (fungi)
  • Special cultures – mycobacterial, fungal
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7
Q

Fever and rash in returning travelling

A
  • Viral: Dengue, HIV seroconversion
  • Bacterial: Meningococcal
  • Rickettsial: Spotted fever
  • Protozoal: Malaria
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8
Q

Enteric fever

A
  • Faecal oral: water and food. Conditions causing low gastric acidity allow for a lower dose to cause infection. Why PPI and H2 antagonists increase infection risk
  • Enteric fever i.e. Typhoid and Paratyphoid
  • Occurs more in Immunocompromised i.e. HIV
  • Incidence is highest in India/South East Asia and other tropical areas
  • Most common in children
  • Is associated with dirty water and food
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9
Q

Pathophysiology of enteric fever

A
  • Salmonellae belong to the Enterobacteriacae family: gram negative enteric organisms
  • Causative agent of typhoid: Salmenella Typhi
  • Two subtypes are S.typhi and S.paratyphi (A,B,C)
  • S.paratyphi (A,B): tend to spread in food where the organism has already multiplied- more predominant N+V
  • S.paratyphi C: causes septicaemia without gut involvement
  • PPI and H2 agonists increase risk of contacting enteric fever as lowers gastric acidity
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10
Q

Structure of S.typhi

A
  • Flagellar (H antigen): helps it move
  • Somatic (O antigen)
  • Capsule (V1 antigen): covers the O antigen and protects it from antibodies
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11
Q

Pathophysiology of typhoid fever

A
  • The organism attach and penetrate the mucosa of the small intestine.
  • Transported by lymphatics to the mesenteric lymph glands.
  • Then enter the blood stream via the Thoracic duct.
  • And travel to the bone marrow, spleen, liver and gallbladder.
  • The bacteria is then re-released into the blood stream causing secondary infection of the bowel. Macrophages accumulate causing necrosis and ulcers. After a week there can be perforation and bleeding
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12
Q

Typhoid fever: where do nodules form

A
  • Secondary bacteraemia causes symptom onset
  • Typhoid nodules can form from Macrophage collections in the liver, spleen, bone marrow and lymph glands
  • Later abscess formation in the bone, brain, liver and spleen
  • Death is be perforation, haemodynamic shock (from bleeding) or Meningitis
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13
Q

Typhoid fever signs and symptoms

A
  • Incubation period:14 days
  • Rash made of small pink spots on the trunk of the body
  • Loss of appetite
  • Constipation (more common) or diarrhoea
  • Exhaustion
  • Confusion
  • Fever: gradual increases day by day, peaks in the evening , no rigors (39-40)
  • Head and muscle aches
  • Stomach pain
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14
Q

Clinical features of typhoid fever by timeline

A
  • 1st week: increasing fever, abdo pain, malaise, headache, constipation, bradycardia
  • End of 1st week: rose spots appear on the upper abdomen, cough, splenomegaly, bronchitis, meningism abdo distension with tenderness, diarrhoea
  • 2nd week: symptoms progress
  • End of 2nd week: delirium, complications, gravely dehydrated, then coma and death (if untreated)
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15
Q

Signs of Typhoid fever

A
  • Rose spots: only seen if fair skinned, found from day >7. Pink macules on the trunk. Fade on pressure
  • Relative Bradycardia: lower heart beat then expected for high fever (<100)
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16
Q

Complications of typhoid fever

A
  • Bowel: perforation (treat with surgery, antibiotics.. Occurs 3rd week onwards), haemorrhage
  • Septicaemic: bone and joint infection, meningitis, Cholcystitis
  • Toxic (resolves with antibiotics): Myocarditis, Nephritis
  • Chronic: Persistent Gallbladder carriage (become chronic carriers, often occurs with gallstones)
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17
Q

Typhoid/Enteric fever- Investigations

A
  • 1st/2nd week; blood culture (first line- need a big sample)
  • Bone marrow
  • Not stool (can identify carriers but not acute infection)
  • Aspirates: rose spots, CSF, Abscesses
  • Widal test (measure antiboidies against Somatic O antigens and flagella H antigens)- wide test, cheap, widely available, low sensitivity, low specificity
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18
Q

Treatment of typhoid fever

A
  • Fluoroquinolones (Ciprofloxacin): 5 – 7 day course. Resistant strains in e.g. India, Vietnam. Nalidixic acid resistance as proxy marker for resistance
  • Third-generation cephalosporins (Ceftriaxone): Effective against MDR strains (resistant strains), severe or complicated disease. Slower response, Expensive
  • Azithromycin: Effective against MDR strains, Growing evidence in severe disease
  • Rise of drug resistance
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19
Q

Carrier state Typhoid/Enteric fever

A
  • Common for several months post-infection- terminates on its own
  • Gallbladder or urinary tract: chronic carriers (3% of cases). May have chronic gallstones or abnormalities in the urinary tract
  • Variable/erratic excretion
  • Ciprofloxacin 750mg BD for 28 days
  • Cholecystectomy: if gallstones
  • Typhoid fever is a notifiable disease
  • Food handlers: may affect employment
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20
Q

Concise complications of Typhoid fever

A
  • osteomyelitis (especially in sickle cell disease whereSalmonellais one of the most common pathogens)
  • GI bleed/perforation
  • meningitis
  • cholecystitis
  • chronic carriage (1%, more likely if adult females)
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21
Q

Encephalitis features

A
  • fever, headache, psychiatric symptoms (personality), seizures, vomiting, reduced conscious level
  • focal features e.g. aphasia
  • peripheral lesions (e.g. cold sores) have no relation to the presence of HSV encephalitis
22
Q

Encephalitis pathophysiology and causes

A
  • HSV-1 causes the majority of the cases then VZV
  • Other causes: Japanese B encephalitis, TB, Acute disseminate encephalomyelitis (ADEM) triggered by infection or vaccination
  • Often cause not identified
  • Typically affects temporal and inferior frontal lobes
  • Inflammation of the brain parenchyma
23
Q

Encephalitis investigations

A
  • Lumbar puncture: elevated lymphocytes, elevated protein. PCR for HSV, VZV and enteroviruses
  • CT: Medial temporal and inferior frontal changes (petechial haemorrhage), normal in 1/3rd of patients
  • MRI: used before CT and shows brain parenchyma inflammation
  • PCR for HSV
  • EEG: lateralised periodic discharges at 2Hz, to rule out seizures
  • HIV test
  • Clinical features differentiate from viral meningitis
24
Q

When would you be concerned that its encephalitis- a patient with fever and headache with

A
  • Seizures
  • Focal neurological signs
  • Neuropsychiatric features (confusion, personality change, agitation, hallucinations)
25
Q

Encephalitis management

A
  • IV acyclovir in all cases of suspected encephalitis 10mg/kg TDS. 14-21 day course
  • Supportive care
26
Q

When can you exclude HSV encephalitis

A
  • LP may originally be negative so repeat in 24-48hrs
  • HSV PCR in the CSF is negative on TWO occasions 24-48 hours apart, and MRI is normal
  • 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 normal WCC in CSF
27
Q

Complications of encephalitis

A
  • Venous sinus thrombosis
  • Status epilepticus
  • Stroke
  • Aspiration pneumonia
  • Without treatment majority of patient die
  • With treatment majority of patients are left with permanent neurological disability- neuro rehab
28
Q

Bacterial meningitis clinical features

A
  • Present similar to viral so have high index of suspicion, often not common in babies
  • Symptoms: headache, fever, Nausea/vomiting, photophobia, drowsiness/confusion, seizures
  • Signs: neck stiffness, purpuric rash
  • Non-blanching rash cause: N meningitides
29
Q

Causes of meningitis

A
  • Viral, bacterial, TB
  • Viral: enterovirus, HSV, VZV (more common then bacterial)
  • Bacterial: strep pneumoniae (most common bacterial), nisseris meningitides. Haemophilia influenza b
  • Group B streptococcus (GBS) and Listeria monocytogenes: particularly in neonates
  • TB: with HIV and worldwide
  • Inflammation of the meninges covering the brain
30
Q

Neisseria meningitidis

A

Gram negative diplococcus. Most common cause of bacterial meningitis. Causes a non-blanching rash

31
Q

Classic signs of meningitis

A
  • Kernig’s sign: pain in back and legs when hip is flexed and the knee is extended
  • Brudzinski’s sign: involuntary hip flexion when the head is flexed
  • Poor sensitivity, good specificity (presence indicates meningitis)
  • Non blanching purpuric rash suggests meningococcal sepsis
32
Q

What factors suggest poor prognosis in meningitis

A
  • Rapidly progressive rash
  • Poor peripheral perfusion, prolonged cap refill, oliguria and systolic BP <90
  • RR <8 or >30
  • Pulse rate <40 or >140
  • Acidosis
  • WBC <4
  • Reduced consciousness
  • Focal neurology
  • Persistent seizures
  • Bradycardia and hypertension
  • Papilloedema
  • Anything which suggest: DIC, septic shock, raised intracranial pressure
33
Q

Investigations for meningitis

A
  • Bloods: FBC, U&E, LFT, CRP, coagulation screen, blood culture, whole-blood PCR
  • blood glucose
  • blood gas
  • Lumbar puncture: gram stain, culture and PCR. Analysis can be affected due to delay or antibiotic treatment
  • Tuberculosis meningitis: Ziehl-Neelson stain, PCR
34
Q

Meningitis- Brain imaging is not required prior to lumbar puncture unless:

A
  • New onset or recent seizures
  • Papilloedema
  • Focal neurological deficit
  • Reduced or deteriorating conscious level (GCS<12)
35
Q

Interpretation of Lumbar puncture: Meningitis

A
  • Bacterial: cloudy appearance, low glucose, high protein, high neutrophils
  • Viral: clear/cloudy appearance, normal glucose, normal protein, high WCC (lymphocytes)
  • Tuberculosis: slightly cloudy, fibrin web, low glucose, high proteins
  • Don’t do LP if signs of raised intracranial pressure
36
Q

Bacterial meningitis treatment by age

A
  • < 3 months: Intravenous cefotaxime + amoxicillin
  • 3 months - 50 years: Intravenous Cefotaxime/Ceftriaxone (Chloramphenicol if penicillin allergic) also give IV dexamethasone to reduce neurological sequelae
  • > 50 years: Intravenous cefotaxime + amoxicillin
  • ABCDE assessment, initiate Sepsis 6. Give antibiotics within 1 hour ideally post LP and blood cultures
37
Q

Meningitis- when should antibiotics be offered in primary care and dose

A

If suspected meningitis and a non blanching rash then IV or IM benzylpenicillin or Ceftriaxone

  • <1 year- 300mg
  • 1-9 years- 600mg
  • > 10 years- 1200mg
38
Q

Meningitis treatment by cause

A
  • Meningococcal meningitis: Intravenous benzylpenicillin or cefotaxime
  • Pneuomococcal meningitis: Intravenous cefotaxime
  • Meningitis caused by Haemophilus influenzae: Intravenous cefotaxime
  • Meningitis caused by Listeria: Intravenous amoxicillin + gentamicin
39
Q

Pneumococcal meningitis (Strep pneumoniae)

A

Has the highest mortality and morbidity. IV dexamethasone reduces mortality and hearing loss.

40
Q

IV Dexamethasone

A
  • ideally given before antibiotics (at least within 12hrs) and should be continues for 4 days if pneumococcal meningitis is confirmed.
  • Reduces mortality and hearing loss
41
Q

Meningitis: Management of contacts

A
  • Prophylaxis offered to household and close contacts and those exposed to respiratory secretions. If contact before 7 days of onset
  • First line: Oral Ciprofloxacin (single dose) or Rifampicin (for two days), Single Ceftriaxone IM
  • When serotype results are available offer vaccine or booster
  • Only for Meningococcal meningitis
  • Guided by local health protection team
42
Q

Complications of meningitis by cause

A
  • Viral: fatigue, headache, slowed thinking, mood disturbance
  • Bacterial: deafness, cognitive impairement, focal neurological deficits, epilepsy
  • Pneumococcal has higher mortality then Pneumococcal
43
Q

Poor prognostic factors for meningitis

A

severe sepsis, DIC, raised ICP

44
Q

Vaccinations meningitis

A
  • For UK infants
  • Haemophilus influenzae b
  • Meningitis ACWY
  • Meningitis B
  • Streptococcus pneumoniae
45
Q

Viral meningitis

A
  • Most common cause of meningitis: Enteroviruses > Herpes Simplex Virus 1 &2 > Varicella zoster virus
  • LP diagnostic: detect virus with PCR
  • Self limiting managed supportively
  • Can cause long term morbidity: fatigue, headaches, slowed thinking
46
Q

Describing a Lumbar puncture and Benefits

A

1.Explain the procedure: A ‘spinal tap’ that involves using a needle to obtain a sample of the fluid surrounding the brain and spinal cord from a space between vertebrae in the lower back. Aseptic technique

2.Describe the likely benefits: To aid diagnosis (therapeutic if raised intracranial pressure)

47
Q

Lumbar puncture- complications and important risks

A

–Common (>5%): back pain, shooting pain down legs at the time of procedure, localised bleeding

–Rare (<1%): persistent headache, infection, lower limb weakness

48
Q

Indications for Lumbar puncture

A

Diagnostic
- Infection: meningitis (bacterial/ viral/ fungal) or encephalitis
- Subarachnoid haemorrhage
- Other – multiple sclerosis, malignancy etc.

Indications for LP Therapeutic: Reduce intracranial pressure e.g. idiopathic intracranial hypertension

49
Q

Indications for LP: spinal epidural

A
  • Pain relief (during labour)
  • Anaesthesia (e.g. lower limb surgery)
50
Q

Contraindications for LP

A
  • Deranged blood clotting or a low platelet count
  • Taking anticoagulants (Warfarin if INR >1.4
  • Signs of sepsis or rapidly evolving rash
  • Infection at lumbar puncture site
  • Raised ICP- concerned brainstem will protrude through the foramen magnum

year 4 CDM 2 (39 decks)

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