Infections and Immunity Flashcards

1
Q

What age range is peri-orbital cellulitis most common in?

A

0-15 years with a peak incidence in children younger than 10 years.

It is twice as common in males compared to females.

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2
Q

What time of year is peri-orbital cellulitis most common?

A

There is bi-modal seasonal variation, with peak occurrence in late winter/early spring, attributed to the increased incidence of upper respiratory tract infection and paranasal sinusitis in the same seasons of the year.

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3
Q

Most common cause of peri-orbital cellulitis?

A

Sinus related infections (35% will go on to develop peri-orbital cellulitis). Most commonly ethmoidal.

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4
Q

What are the two forms of peri-orbital cellulitis and pathophysiology?

A

Infection anterior to the septum is pre-septal and posterior is post-septal. The orbital septum is the only barrier impeding spread of infection from the eyelid into the orbit.

Commonly peri-orbital cellulitis occurs as a result of contiguous spread from surrounding periorbital structures such as the paranasal sinuses. Ethmoidal sinusitis is the most common cause of orbital cellulitis, especially in neonates who have not yet formed their frontal sinuses.
Up to 38% of children may have multiple sinus involvement.

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5
Q

Other causes of peri-orbital cellulitis

A

Other causes include:

  • dacrocystitis
  • dental infection
  • endophthalmitis
  • trauma
  • foreign bodies
  • insect bites
  • skin infections (impetigo)
  • eyelid lesions (chalazia, hordeola)
  • iatrogenic causes such as eyelid and oral procedures.
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6
Q

Most common organism causing PO cellulitis:

A

Staphylococcus aureus is usually the most common pathogen.

Organisms are those generally responsible for acute rhinosinusitis, such as Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus, group A streptococcus, and upper respiratory tract anaerobes.

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7
Q

Clinical features of PO cellulitis:

A
  • Acute onset of swelling, redness, warmth and tenderness of the eyelid.
  • Eyelid oedema in the absence of orbital signs such as gaze restriction and proptosis.
  • Fever, malaise, irritability in children.
  • Ptosis.

Important: normal vision, no proptosis and full ocular mobility

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8
Q

Clinical features of orbital cellulitis

A

Orbital features:

  • Proptosis
  • Ophthalmoplegia
  • Decreased visual acuity
  • Loss of red colour vision – first sign of optic neuropathy
  • Chemosis
  • Painful diplopia
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9
Q

What kind of classification can be used in PO cellulitis?

A

Chandler Classification

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10
Q

Investigations in PO cellulitis

A
  • Full neuro, ENT and eye exam
  • Bloods and sepsis screen if necessary
  • VBG if systemically unwell
  • Swab of purulent nose discharge

CT of head can determine if there is orbital involvement if unsure.

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11
Q

Treatment of PO celullitis

A

Mild pre-septal cellulitis in children older than 1 year of age, treatment is typically rendered on an outpatient basis with empiric broad spectrum oral antibiotics,

Children can be initially admitted to hospital, as they should be considered to have orbital cellulitis until proven otherwise (ie repeated examinations normal, good response to antibiotics in the first 24 hours and normal CT scan).

Oral co-amoxiclav may be used both for adults and for children as long as there is no allergy to penicillin. Clinical improvement should occur over 24-48 hours.

Hospital management may involve intravenous therapy (eg, intravenous ceftriaxone until response is seen) and further investigation to confirm preseptal cellulitis (only) and that there are no unusual organisms involved.
The ENT team is generally consulted if sinusitis is present.

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12
Q

Treatment of orbital cellulitis:

A

However, treatment of orbital cellulitis consists of hospital admission (ENT surgeons and optical) IV abx, nasal decongestants, steroid nasal drops and nasal douching.

Intravenous antibiotics are used (eg, cefotaxime and flucloxacillin) with addition of metronidazole in patients over 10 years of age with chronic sinonasal disease . Treatment lasts for 7-10 days.

Optic nerve function is monitored four-hourly (pupillary reactions, visual acuity, colour vision and light brightness appreciation).

Surgery is indicated where there is CT evidence of an orbital collection, where there is no response to antibiotic treatment and where visual acuity decreases.

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13
Q

Complications of PO cellulitis

A

-Progression of infection to orbital cellulitis, especially in young children.
-Unusual complications include:
Lagophthalmos (inability to close the eyelids completely over the globe).
Lid abscess.
Cicatricial ectropion.
Lid necrosis.

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14
Q

Complications of orbital cellulitis:

A
  • Exposure keratopathy (which can lead to visual loss through permanent damage to the cornea).
  • Raised intraocular pressure.
  • Central retinal artery or vein occlusion.
  • Endophthalmitis.
  • Optic neuropathy.

-Orbital abscess: More often associated with post-traumatic orbital cellulitis.
Total loss of vision can occur through direct extension of the infection to the optic nerve.

Intracranial (rare):
Meningitis.
Brain abscess.
Cavernous sinus thrombosis.

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15
Q

Most common ages of glandular fever:

A

1-6 and 18-22.

Most adults are antibody positive by the age of 30 (90%). In 50% of these they won’t have had symptoms.

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16
Q

Infectious organism of glandular fever:

A

EBV in most cases (a human herpes simplex virus)

-10% are cytomegalovirus

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17
Q

What is the transmission mechanism of glandular fever?

A

Droplet transmission. 4-6 week incubation period.

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18
Q

Glandular fever symptoms:

A
  • Low-grade fever, fatigue and prolonged malaise. Fatigue and malaise may persist for several months after the acute infection has resolved.
  • Sore throat; tonsillar enlargement is common, classically exudative and may be massive; palatal petechiae and uvular oedema.
  • Fine macular non-pruritic rash, which rapidly disappears.
  • Transient bilateral upper lid oedema.
  • Lymphadenopathy, especially neck glands.
  • Nausea and anorexia.
  • Also fatigue, photophobia, arthralgia and myalgia can occur

Older adults and elderly patients often have few throat symptoms or signs and have little or no lymphadenopathy.

Later signs include:

  • Mild hepatomegaly and splenomegaly with tenderness over the spleen.
  • Jaundice occurs in fewer than 10% of young adults but in as many as 30% of infected elderly patients.
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19
Q

What would find on examination of a glandular fever patient?

A
  • Enlarged inflamed tonsils, often meeting in the middle and referred to as “kissing tonsils”
  • Significant cervical lymphadenopathy (both anterior and posterior cervical chains)
  • Abdominal tenderness & splenomegaly (in as many as 50%)
  • Hepatomegaly (in as many as 25%)
  • Palatal petechiae
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20
Q

What tests might you do to confirm your diagnosis of glandular fever and what might you see?

A

FBC- lymphocytosis
LFTs- 75% will have elevation of liver enzymes

The monospot test is the primary technique for identifying infection with Epstein-Barr virus. However it relies on the generation of non-specific heterophile IgM autoantibodies, which are not produced immediately following viral infection of B lymphocytes and may take a week to appear.

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21
Q

When might abx be prescribed in glandular fever?

A

When there is bacterial superinfection (can occur in up to 30% of cases). In this case penicillin based abx will be prescribed.

DO NOT give amoxicillin

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22
Q

Possible complications of glandular fever?

A
  • Post viral fatigue
  • Epstein-Barr virus has shown to be associated with the development of a number of different lymphomas (Burkitts, Hodgkins, T Cell) as well as nasopharyngeal carcinoma.
  • Guillan Barre
  • Encephalitis can occur, resulting in fever, seizures, unusual behavior or gait disturbance. It is sometimes preceded by symptoms of glandular fever, but may also occur without preceding symptoms.
  • Splenic rupture: avoid contact sports for 4-6 weeks post symptoms
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23
Q

General glandular fever advice for parents:

A
  • Stay hydrated
  • No need to be excluded from school unless for own wellbeing
  • Advice paracetamol/ibuprofen for fever control
  • Let them know there is no specific therapy
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24
Q

Typical age range of kids and type of kid affected by Kawasaki infection:

A
  • 6 months to 5 years. Peak incidence 18-24 months.
  • East Asian children more likely to be affected
  • Boys more than girls.
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25
Q

Typical features of Kawasaki disease:

A
  • Fever lasting 5 or more days (abrupt onset)

Along with 4/5 of:

  • Erythema, desquamation and swelling of skin of the extremities
  • Bilateral conjunctivitis
  • Inflammation of the lips, tongue “strawberry” and mouth
  • Cervical lymphadenopathy (usually unilateral and non-tender)
  • Polymorphous rash

Often have marked irritability!

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26
Q

What is incomplete Kawasaki?

A

Incomplete Kawasaki disease is the term given to those with fever but without enough other features to fit the diagnostic criteria.

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27
Q

Features of a Kawasaki rash

A
  • Rash (widespread non-vesicular within 3-5 days of fever)
  • It usually begins with nonspecific erythema of the soles, palms and perineum, spreading to involve the trunk and the rest of the extremities.
  • It is often itchy and variable in appearance but is never vesiculo-bullous.
  • It is usually markedly red and may appear macular, morbilliform, papular, scarlatiniform, urticarial, akin to erythema multiforme or be made up of very many tiny micropustules.

Not contagious

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28
Q

Cardiac signs in Kawasakis (not always)

A

Cardiovascular signs are usually nonspecific. Tachycardia, a hyperdynamic precordium, a gallop rhythm or a flow murmur may be present; however, these signs are not unusual in febrile patients without Kawasaki disease. There are occasionally signs of valvular incompetence.

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29
Q

Describe the acute phase of Kawasakis:

A
Highly febrile.
Very irritable.
Toxic-appearing.
Oral changes rapidly following.
Oedema and erythema of feet.
Rash especially common in the perineal area.

1-2 weeks

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30
Q

Describe the subacute phase of Kawasaki:

A
Gradual improvement.
The fever settles.
Desquamation of the perineum, palms, soles.
Arthritis, arthralgia.
Thrombocytosis.
Coronary artery aneurysms.
Myocardial infarction

2-8 weeks

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31
Q

Describe the convalescent phase of Kawasaki:

A
Resolution of remaining symptoms.
Laboratory values return to normal.
Aneurysms may resolve or persist.
Beau's lines.
Cardiac dysfunction and myocardial infarction may still occur.

Months to years

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32
Q

What is Kawasaki disease?

A

Self-limited acute vasculitic syndrome of unknown aetiology

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33
Q

How do you diagnose Kawasaki’s?

A
  • Clinical diagnosis
  • May be deranged bloods e.g. thrombocythaemia, leukocytosis, neutrophilic, elevation of transaminases and bilirubin, raised ESR, CRP.
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34
Q

What is essential to do in Kawasaki’s?

A

ECHO! It can reveal dilatation and aneurysms of the coronary arteries, as well as allowing assessment of the pericardium and left ventricular/valvular function. Serial echocardiography is often needed to detect occult coronary artery disease as the illness evolves.

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35
Q

How do you manage Kawasaki’s?

A
  • Usually cared for on an inpatient basis with cardiology input
  • Aspirin for it’s antiplatelet and antipyretic effect.
  • IV immunoglobulin (antibodies from healthy donor to fight disease). This is specifically gamma globulin. Symptoms should improve in 36 hours, if not a second dose is given
  • Corticosteroids if IG is not working/ at high risk of heart problems

-Need follow up appointment after resolution of symptoms for ECHO. If normal, stop aspirin.

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36
Q

What are the risks of aspirin treatment in under 16s?

A

Reye’s syndrome
persistent vomiting and a lack of energy
Liver and brain damage- can be fatal

37
Q

Cardiac risks in Kawasakis?

A
  • up to 50% show echocardiographic evidence of cardiac impairment and mild mitral regurgitation.
  • 15-25% of untreated patients will experience coronary artery aneurysms but this figure is much lower if early diagnosis and therapy are achieved
  • Most (50-70%) coronary artery aneurysms regress after a period of 1-2 years.
38
Q

How is rubella spread?

A

Respiratory Secretions

39
Q

How long are people with rubella infectious for?

A

1 week before symptoms appear, to 4 days after the onset of the rash.

40
Q

Complications of congenital rubella syndrome:

A

Permanent abnormalities include:

  • Heart and lung defects, for example patent ductus arteriosus, pulmonary artery stenosis, and pulmonary arterial hypoplasia.
  • Eye defects, including cataracts, iris hypoplasia, and retinopathy.
  • Central nervous system defects, such as microcephaly, and mental and psychomotor retardation.
  • Sensorineural deafness.

Developmental and late-onset abnormalities include:

  • Progressive developmental problems
  • Persistent immunological problems.
  • Diabetes mellitus.
  • Progressive panencephalitis (a rare and invariably fatal illness similar to subacute sclerosing panencephalitis seen in measles).
41
Q

Symptoms of rubella prodromal phase:

A

Prodromal phase of lassitude, low-grade fever, headache, mild conjunctivitis and anorexia with rhinorrhoea very similar to a cold. The prodrome may be absent in children and tends to be more noticeable in adults.

42
Q

Describe the rubella rash:

A

After the prodromal phase the rash then develops (it may be absent, especially in young children) - initially, pink discrete macules that coalesce, starting behind the ears and on the face, spreading to the trunk and then the extremities. Lasts 3-5 days.

There may be petechiae on the soft palate (Forchheimer’s sign) but this is not diagnostic for rubella.

43
Q

Other rubella symptoms along with the rash:

A

Cervical, suboccipital and postauricular lymphadenopathy are characteristic and may precede the rash.
Constitutional symptoms are usually mild (can be more prominent in adults).
In older patients, arthralgia is common.

44
Q

Investigations for Rubella:

A
  • Serological and/or polymerase chain reaction (PCR) testing is the gold standard investigation and the local Health Protection Unit (HPU) can provide a testing kit (via mouth fluid sample, bloods)
  • FBC may show a low WBC count with an increased proportion of lymphocytes and thrombocytopenia (usually resolves in a month).

In pregnant women will also test for Parvovirus B19 as can be similar

Clinical diagnosis is unreliable and rash is not diagnostic

45
Q

Management of rubella:

A
  • There is no specific treatment.
  • Keep the child away from school for four days after the rash appears.
  • Use antipyretics for fever
  • Ask about any contact with pregnant women and advise to avoid
  • Notify Public Health
  • Where suspected infection occurs in a pregnant woman, it should be confirmed by investigation, in liaison with a virologist, and counselling should be given about the dangers to the fetus. Management requires referral and expert support. Where non-immunity is found in pregnancy an immunisation after birth offers protection for future pregnancies
46
Q

Complications of Rubella:

A
  • Rubella encephalopathy may occur about six days after the rash (usually there is full recovery in a few days without sequelae).
  • Arthritis and arthralgia can occur in adults (60%)
  • Thrombocytopenia occurs in around 1 in 3,000 cases.
  • Guillain-Barré syndrome/neuritis.
  • Panencephalitis.
47
Q

How common is CRS?

A
  • Before 8–10 weeks’ gestation there is a 90% risk of congenital rubella syndrome (CRS), and a high likelihood of multiple defects. Significant proportion have 1st trimester miscarriage
  • Between 11–16 weeks’ gestation there is a 10–20% risk of CRS, with single defects being most common.
  • Between 16–20 weeks’ gestation there is only a low chance of deafness occurring.
  • Beyond 20 weeks’ gestation there have been no published case reports of CRS.
48
Q

What is counted as a rubella contact?

A

Significant contact means being in the same room for 15 minutes or more, or face-to-face contact, within the previous 3 weeks.
However, if the pregnant woman is known to be susceptible to rubella, contact for less than 15 minutes should be considered a possible exposure

49
Q

How can meningococcal disease present?

A

Meningococcal disease is the leading infectious cause of death in early childhood. It presents as bacterial meningitis (15% of cases), septicaemia (25% of cases), or as a combination of the two presentations (60% of cases)

50
Q

Non specific meningitis signs:

A

-fever, nausea and vomiting, lethargy, irritable or unsettled mood, refusal of food and drink, headache, muscle ache or joint pain, and respiratory symptoms such as a cough.

51
Q

Specific meningitis signs:

A
  • stiff neck
  • altered mental state (confusion, delirium and drowsiness, impaired consciousness)
  • back rigidity
  • bulging fontanelle (in children younger than 2 years of age)
  • photophobia
  • Kernig’s sign (pain and resistance on passive knee extension with hips fully flexed)
  • Brudzinski’s sign (hips flex on bending the head forward)
  • coma, paresis, focal neurological deficit
  • seizures.
52
Q

What is Kernig’s sign?

A

Person unable to fully extend at the knee when hip is flexed

53
Q

What is Brudzinski’s sign?

A

Person’s knees and hips flex when neck is flexed

54
Q

How is meningococcal disease transmitted?

A

Bacterial meningitis and meningococcal diseaseare transmitted through close contact via droplets or secretions from the upper respiratory tract. Transmission usually requires either frequent or prolonged close contact.

Incubation time: 2-7 days

55
Q

What are the common age groups for bacterial meningitis?

A

Although bacterial meningitis can affect all ages, incidence of bacterial meningitis and meningococcal disease is highest in infancy and declines during childhood with a secondary rise in teenagers and young adults.

56
Q

Complications of bacterial meningitis:

A
  • 30–50% of survivors experiencing permanent neurological sequelae
  • death
  • Hearing loss (33.6%)
  • Seizures (12.6%)
  • Motor deficit (11.6%)
  • Cognitive impairment (9.1%)
  • Hydrocephalus (7.1%)
  • Visual disturbance (6.3%)
57
Q

Delayed complications of bacterial meningitis:

A
  • 30–50% of survivors experiencing permanent neurological sequelae
  • death
  • Hearing loss (33.6%)
  • Seizures (12.6%)
  • Motor deficit (11.6%)
  • Cognitive impairment (9.1%)
  • Hydrocephalus (7.1%)
  • Visual disturbance (6.3%)
  • Waterhouse-Friderichsen syndrome (adrenal gland failure due to bleeding into them- usually due to severe infection)
  • Peripheral gangrene.
58
Q

What test must all children that have had bacterial meningitis be booked in for on discharge?

A

Hearing test!

-review with paeds in 4-6 weeks

59
Q

Describe a mening rash

A

Non blanching rash that is either:

  • Scanty petechial rash (red or purple macules smaller than 2 mm in diameter).
  • Purpuric (haemorrhagic) rash (spots larger than 2 mm in diameter) — this may be absent in the early phase of the illness and may initially be blanching or macular in nature.

Need to be careful to examine the whole body for a rash in suspicious cases

60
Q

Prehospital management of bacterial meningitis?

A
  • Immediate administration of benzylpenicillin (unless clear history of penicillin anaphylaxis). This is single IV/IM in a well perfused limb
  • Ambulance transfer to hospital
61
Q

Prehospital management of bacterial meningitis?

A

With non blanching rash: Immediate administration of benzylpenicillin (unless clear history of penicillin anaphylaxis). This is single IV/IM in a well perfused limb
-Ambulance transfer to hospital

Without non blanching rash:

  • ambulance to hospital
  • do not give abx unless transfer to hospital is not available
62
Q

Managing close contacts in bacterial mening

A

-Notify public health and seek advice

Consider abx prophylaxis in:

  • People who have had prolonged close contact with the case in a household-type setting during the 7 days before onset of illness.
  • People who have had transient close contact with a case only if they have been directly exposed to large particle droplets/secretions from the respiratory tract of a case around the time of admission to hospital.

Should be given asap, preferably within 24 hours.
Reassure contacts that are not “close”. Risk is highest in first week.

63
Q

Risk factors for neonatal mening?

A

Risk factors for the development of meningitis include low birth weight (below 2500 g), premature delivery, premature rupture of membranes, traumatic delivery, fetal hypoxia and maternal peripartum infection,GBS positive mother ) abx now given to reduce this risk)

64
Q

Initial presentation of neonatal meningitis?

A

The initial presentation is usually nonspecific with features including raised or unstable temperature, respiratory distress, episodes of apnoea and bradycardia, hypotension, feeding difficulty, irritability and reduced activity. Neonatal jaundice in first 24hours is worrying.

65
Q

Causes of aseptic meningitis?

A
  • Partially treated bacterial meningitis
  • Viral infection/ fungal
  • Kawasaki’s
66
Q

What if it’s viral meningitis?

A

-Can present with less classical patterns. However, if meningitis is suspected treat as bacterial to avoid making a mistake. If clear risk factor (e.g. maternal herpes infection at time of birth) or clinical suspicion can also give acyclovir.

67
Q

Meningococcal septicaemia signs:

A
Shock
Hypotension 
Cold, clammy peripheries
Non-blanching rash
Reduced CRT
Reduced consciousness
68
Q

Investigations in bacterial meningitis:

A
  • Lumbar puncture
  • FBC.
  • CRP.
  • Coagulation screen.
  • Blood culture.
  • Whole-blood polymerase chain reaction (PCR) for N. -meningitidis.
  • Blood glucose.
  • Blood gases.

-Exclusion of other causes of sepsis: e.g. urine dip, chest x-ray, MRI (later for monitoring complications)

69
Q

Lumbar puncture findings:

A

Neutrophils bacterial: Very high
Neutrophils viral: slightly raised initially

Lymphocytes bacterial: slightly raised
Lymphocytes viral: high (but may be normal)

Glucose bacterial: Low
Glucose viral: usually normal

Protein bacterial: High
Protein viral: slightly raised (but may be normal)

70
Q

Initial blind antibiotic choice for bacterial meningitis in a child 3 months or older:

A

Intravenous ceftriaxone as empirical treatment before identification of the causative organism. (IV for at least 7 days)

71
Q

Initial blind antibiotic choice for bacterial meningitis in a child 3 younger than 3 months:

A

Intravenous cefotaxime plus either amoxicillin or ampicillin. NB: ceftriaxone should not be used in premature babies or in babies with jaundice, hypoalbuminaemia or acidosis, as it may exacerbate hyperbilirubinaemia.

72
Q

After culture of CSF and findings of meningococcal culprits what abx do you use to treat meningitis?

A

Intravenous ceftriaxone for at least seven days is usually used..

73
Q

After culture of CSF and findings of pneumococcal culprits what abx do you use to treat meningitis?

A

Vancomycin and a third-generation cephalosporin (either cefotaxime or ceftriaxone) should be used.

-Benzylpenicillin may be given if the organism is penicillin-sensitive but penicillin resistance is becoming an increasing problem.

74
Q

After culture of CSF and findings of haemophilus culprits what abx do you use to treat meningitis?

A

Children aged 3 months and older and young people - intravenous ceftriaxone for 10 days in total unless directed otherwise by the results of antibiotic sensitivities.

75
Q

After culture of CSF and findings of group b streptococcal culprits what abx do you use to treat meningitis?

A

This mainly occurs in babies between the ages of 7-90 days.Intravenous cefotaxime for at least 14 days should be given

76
Q

After culture of CSF and findings of listerial culprits what abx do you use to treat meningitis?

A

For children under the age of 3 months, intravenous amoxicillin or ampicillin for 21 days in total, plus gentamicin for at least the first seven days.

77
Q

Prevention of secondary case of meningococcal meningitis is usually with:

A

rifampicin or ciprofloxacin

78
Q

Immediate complications possible in mening disease:

A

Immediate: septic shock, including disseminated intravascular coagulation, coma with loss of protective airway reflexes, cerebral oedema and raised intracranial pressure, septic arthritis, pericardial effusion and haemolytic anaemia (H. influenzae).

Subdural effusions: reported in 40% of children aged 1-18 months with bacterial meningitis.

Syndrome of inappropriate antidiuretic hormone secretion (SIADH).

Seizures: occur more commonly during the acute stage of the disease. Studies reported that this occurred in 47% of children.

79
Q

Contraindications to LP?

A
-Cardiorespiratory instability
• Focal neurological signs
• Signs of raised intracranial pressure,
e.g. coma, high BP, low heart rate
or papilloedema
• Coagulopathy
• Thrombocytopenia
• Local infection at the site of LP
• If it causes undue delay in
starting antibiotics
80
Q

Clinical features of measles:

A
  • fever
  • cough
  • runny nose
  • conjunctivitis
  • diarrhoea
  • 2-4 day prodrome with the above and koplik spots (white -spots in buccal mucosa in 60-70% of patients)
  • marked malaise
  • maculopapular morbilliform rash (for at least 3 days)
81
Q

Describe a measles rash:

A

Spreads downwards, from behind the ears to the whole of the body. Discrete, maculopapular rash initially, becomes blotchy and confluent. May desquamate in the second week and look brownish.

82
Q

How is measles spread?

A

Very infectious, spread by droplets in the air. incubation period is 10-12 days

83
Q

For how long is a person with measles contagious for?

A

4 days before and after the rash

84
Q

Investigations in measles:

A

Enquire about vaccinations

Lab confirmation required as clinical diagnosis is unreliable:

  • Salivary swab or serum sample for measles-specific immunoglobulin M (IgM) taken within six weeks of onset.
  • RNA detection in salivary swabs or other samples.
85
Q

Management of an individual with measles:

A
  • Uncomplicated measles is usually self-limiting and treatment is mainly symptomatic, with paracetamol or ibuprofen and with plenty of fluids. Patients should remain at home to limit disease spread.
  • Monitor patients carefully for signs of complications and consider hospitalisation if these appear.
86
Q

Public health management of measles:

A
  • Notify public health england. This might prompt a vaccination campaign in the local area
  • If admitted to hospital need to be isolated with appropriate measures put in place
  • Notify vulnerable contacts e.g. pregnant women and immunocompromised for post exposure vaccines
87
Q

Respiratory complications of measles:

A
  • Bronchopneumonia occurs in up to 5% of cases, producing serious respiratory difficulties. The infecting organism is usually Staphylococcus aureus or secondary viral infection with herpes simplex or adenovirus. This is the leading cause of death in measles infection.
  • Giant cell pneumonitis in immunocompromised patients presents 2-3 weeks following infection with measles, with worsening breathing.
88
Q

Neurological complications of measles:

A
  • Acute demyelinating encephalitis - this occurs in 1/1,000 cases of infection. It occurs within two weeks of the rash appearing, usually with seizures often accompanied by fever, irritability, headache and changing consciousness that may progress to coma. It is believed to be a neuro-allergic process. It carries a 10-15% mortality rate and 25% of children have permanent brain damage.
  • Subacute sclerosing panencephalitis - this is a rare complication occurring in 0.001% of infected children in developed countries. It is more common in boys and, where the initial infection occurs before the age of 2, onset is usually 5-10 years after apparently normal measles, with disturbance in intellect and personality, behavioural disorders and worsening school work. This is followed by seizures, signs of extrapyramidal and pyramidal disease and, finally, decerebrate rigidity and death.
  • Measles inclusion body encephalitis - this occurs in the immunocompromised 1-7 months following exposure and is progressive over months. It is largely fatal and, of the approximate 15% of survivors, all will have neurological sequelae
89
Q

Post exposure prophylaxis for measles?

A
  • MMR vaccination may be effective if given to those who are susceptible (over 6 months old), ideally within 72 hours of exposure.
  • As response to MMR in infants is sub-optimal, where the vaccine has been given before 12 months of age, immunisation with two further doses of MMR should be given at the normal ages.
  • Human normal immunoglobulin should be considered within five days of exposure for children and adults with compromised immune systems and potentially pregnant women (but only to susceptible and non-immune women)