Infection Flashcards

1
Q

Features of measles

A

Rash
Think of C’s, conjunctivitis, coryza,
“Koplik spots”.
2 week incubation

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2
Q

Features of meningococcal septicaemia

A

A petechial rash of sudden onset is associated with septicaemia

Treat urgently with antibiotic

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3
Q

Summary of thread worms?

A

Occurs after swallowing eggs in environment

Perianal itching, particularly at night
Girls may have vulval Sx
Asymptomatic in 90%

Apply Sellotape to perianal area send for microscopy to see eggs, but most pt’s treated empirically

Hygiene measures
Single dose of mebendazole for all members of household

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4
Q

Causes of meningitis?

A

<3mnths: GBS, e coli, Gr-, listeria monocytogenes

1mnth-6yrs: Neisseria meningitidis (meningococcus), s pneumonia, h influenzae

> 6yrs: Neisseria meningitidis, s pneumoniae.

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5
Q

Features of meningitis?

A

<3mnths, irritability, general lethargy, poor feeding + fevers.

Seizures

Photophobia, neck stiffness rare, high index of suspicion for meningitis in generally unwell infant

Non-blanching petechial rash.

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6
Q

Investigation for meningitis?

A

CI to LP: any signs of ↑ICP, focal neurological signs, papilledema, bulging of fontanelle, DIC, signs of cerebral herniation. Meningococcal septicaemia.

Blood cultures

PCR

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7
Q

Management of meningitis?

A

<3 mnths: IV amoxicillin + IV cefotaxime. Don’t give steroids.

> 3 mnths: IV cefotaxime/ceftriaxone.

Dexamethasone: if, frankly purulent CSF, CSF WBC >1000/ microlitre, ↑CSF WBCC with protein conc >1g/L bacteria on Gr strain.

Abx prophylaxis of contacts: ciprofloxacin

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8
Q

What is roseola infantum?

A

a common disease of infancy caused by the human herpes virus 6 (HHV6).

It has an incubation period of 5-15 days

typically affects children aged 6 months to 2 years.

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9
Q

Features of roseola infantum?

A

high fever: lasting a few days, followed later by a
maculopapular rash

Nagayama spots: papular enanthem on the uvula and soft palate

febrile convulsions occur in around 10-15%

diarrhoea and cough are also commonly seen

Other possible consequences of HHV6 infection
> aseptic meningitis
> hepatitis

School exclusion is not needed.

Paracetamol + ibuprofen

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10
Q

What is mumps?

A

caused by RNA paramyxovirus

tends to occur in winter and spring

Spread:

  • by droplets
  • respiratory tract epithelial cells → parotid glands → other tissues
  • infective 7 days before and 9 days after parotid swelling starts
  • incubation period = 14-21 day

MMR vaccine: the efficacy is around 80%

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11
Q

Features of mumps?

A

fever

malaise, muscular pain

parotitis (‘earache’, ‘pain on eating’): unilateral initially then becomes bilateral in 70%

fever disappears within 3-4 days

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12
Q

Management of mumps?

A

rest

paracetamol for high fever/discomfort

notifiable disease

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13
Q

Complications of mumps?

A

orchitis - uncommon in pre-pubertal males but occurs in around 25-35% of post-pubertal males. Typically occurs four or five days after the start of parotitis

hearing loss - usually unilateral and transient

meningoencephalitis

pancreatitis

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14
Q

Investigations of mumps?

A

Plasma amylase ↑ = pancreatic involvement

Pos salivary mumps IgM

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15
Q

Management of mumps?

A

No Tx, rest, paracetamol, notifiable disease.

Exclusion from school or work for 5 days of swollen glands

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16
Q

What is measles?

A

RNA paramyxovirus

spread by droplets

infective from prodrome until 4 days after rash starts

incubation period = 10-14 days

rarely seen in developed world following adoption of immunisation programmes

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17
Q

Features of measles?

A

prodromal phase = irritable,
conjunctivitis, fever

Koplik spots = typically develop before the rash, white spots (‘grain of salt’) on the buccal mucosa

rash = starts behind ears then to the whole body, discrete maculopapular rash becoming blotchy & confluent, desquamation that typically spares the palms and soles may occur after a week

diarrhoea occurs in around 10% of patients

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18
Q

Investigations for measles?

A

IgM antibodies can be detected within a few days of rash onset

19
Q

Management of measles?

A

mainly supportive - simple analgesia

admission may be considered in immunosuppressed or pregnant patients

notifiable disease → inform public health

School exlcusion: 4 days after rash develop

20
Q

Complications of measles?

A

otitis media: the most common complication

pneumonia: the most common cause of death
encephalitis: typically occurs 1-2 weeks following the onset of the illness)

subacute sclerosing panencephalitis: very rare, may present 5-10 years following the illness

febrile convulsions

keratoconjunctivitis, corneal ulceration

diarrhoea

increased incidence of appendicitis

myocarditis

21
Q

Managing contacts of measles?

A

if a child not immunized against measles comes into contact with measles then MMR should be offered (vaccine-induced measles antibody develops more rapidly than that following natural infection)

this should be given within 72 hours

22
Q

What is erythema infectiosum?

A

‘slapped cheek syndrome’

Common in children, rarer in adults, but more serious

Only spread to others 3-5 days before rash appears

Parvovirus B19

23
Q

Features of slapped cheek syndrome?

A

↑temp

Runny nose + sore throat

Headache

Bright red rash, both cheeks, look as if been slapped.

Adults don’t usually get rash.

Few days later, lighter rash on chest, arms, legs, skin raised + itchy. Rarely involved palms + soles.

24
Q

Complications of slapped cheek syndrome?

A

Child begins to feel better as rash appears + rash peaks after a wk then fades. For mnths after, bath, sun, heat, fever trigger recurrence of red cheeks + rash.

25
Management of slapped cheek syndrome?
Self limiting, better in 3wks. Paracetamol/ ibruprofen. See GP: pregnant (miscarriage), sickle cell (aplastic crisis, supress erythroporesis for a wk) thalassaemia (severe anaemia), weakned immune system. No school exclusion
26
Other presentations of parvovirus B19?
asymptomatic pancytopenia in immunosuppressed patients aplastic crises e.g. in sickle-cell disease parvovirus B19 suppresses erythropoiesis for about a week so aplastic anaemia is rare unless there is a chronic haemolytic anaemia hydrops fetalis parvovirus B19 in pregnant women can cross the placenta in pregnant women this causes severe anaemia due to viral suppression of fetal erythropoiesis → heart failure secondary to severe anaemia → the accumulation of fluid in fetal serous cavities (e.g. ascites, pleural and pericardial effusions) treated with intrauterine blood transfusions
27
What is Scarlet fever?
a reaction to erythrogenic toxins produced by Group A haemolytic streptococci (usually Streptococcus pyogenes). It is more common in children aged 2 - 6 years with the peak incidence being at 4 years. spread via the respiratory route by inhaling or ingesting respiratory droplets or by direct contact with nose and throat discharges, (especially during sneezing and coughing).
28
Features of scarlet fever?
Incubation period of 2-4 days fever: typically lasts 24 to 48 hours malaise, headache, nausea/vomiting sore throat - can appear 1-2 days after tonsillitis 'strawberry' tongue rash: > fine punctate erythema ('pinhead') which generally appears first on the torso and spares the palms and soles > children often have a flushed appearance with circumoral pallor. The rash is often more obvious in the flexures > it is often described as having a rough 'sandpaper' texture > desquamination occurs later in the course of the illness, particularly around the fingers and toes
29
Diagnosis of scarlet fever?
a throat swab is normally taken but antibiotic treatment should be commenced immediately, rather than waiting for the results
30
Management of scarlet fever?
oral penicillin V for 10 days patients who have a penicillin allergy should be given azithromycin children can return to school 24 hours after commencing antibiotics scarlet fever is a notifiable disease
31
Complications of scarlet fever?
otitis media: the most common complication rheumatic fever: typically occurs 20 days after infection acute glomerulonephritis: typically occurs 10 days after infection invasive complications (e.g. bacteraemia, meningitis, necrotizing fasciitis) are rare but may present acutely with life-threatening illness
32
What is coxsackie virus?
Hand, foot, mouth Caused by intestinal virus of picornaviruses (coxsackie A16 + enterovirus 71). Very contagious typically occurs in outbreaks at nursery
33
Features of hand, foot and mouth disease?
mild systemic upset: sore throat, fever oral ulcers followed later by vesicles on the palms and soles of the feet
34
Management of hand, foot and mouth disease?
symptomatic treatment only: general advice about hydration and analgesia reassurance no link to disease in cattle children do not need to be excluded from school the HPA recommends that children who are unwell should be kept off school until they feel better they also advise that you contact them if you suspect that there may be a large outbreak.
35
What is chicken pox?
caused by primary infection with varicella zoster virus. Shingles is a reactivation of the dormant virus in dorsal root ganglion Highly infectious spread via the respiratory route can be caught from someone with shingles infectivity = 4 days before rash, until 5 days after the rash first appeared* incubation period = 10-21 days
36
Features of chicken pox?
fever initially itchy, rash starting on head/trunk before spreading. Initially macular then papular then vesicular then crust and fall off systemic upset is usually mild more sever in older children/adults
37
Management of chicken pox?
supportive keep cool, trim nails calamine lotion school exclusion: NICE Clinical Knowledge Summaries state the following: Advise that the most infectious period is 1–2 days before the rash appears, but infectivity continues until all the lesions are dry and have crusted over (usually about 5 days after the onset of the rash). immunocompromised patients and newborns with peripartum exposure should receive varicella zoster immunoglobulin (VZIG). If chickenpox develops then IV aciclovir should be considered
38
Complications of chicken pox?
secondary bacterial infection of the lesions -NSAIDs may ^ risk, single infected area/small area of cellulitis, invasive group A streptococcal soft tissue infections may occur > necrotising fasciitis pneumonia encephalitis (cerebellar involvement may be seen) disseminated haemorrhagic chickenpox arthritis, nephritis and pancreatitis may very rarely be seen
39
What is neonatal sepsis?
a serious bacterial or viral infection in the blood affects babies within the first 28 days of life. Neonatal sepsis is categorised into early-onset (EOS, within 72 hours of birth) and late-onset (LOS, between 7-28 days of life) sepsis account for 10% of all neonatal mortality Male:female incidence 1:1 Incidence of neonatal sepsis: 1-5 per 1000 live births Term neonates: 1-2 per 1000 live births Late pre-term infants: 5 per 1000 live births Birth weight <2.5kg: 0.5 per 1000 live births Black race is an independent risk factor for group B streptococcus-related sepsis
40
Causes of neonatal sepsis?
The overall most common causes of neonatal sepsis are group B streptococcus (GBS) and Escherichia coli, accounting for approximately two thirds of neonatal sepsis cases Early-onset sepsis in the UK is primarily caused by GBS infection (75%) Infective causes in early-onset sepsis are usually due to transmission of pathogens from the mother to the neonate during delivery Late-onset sepsis usually occurs via the transmission of pathogens from the environment post-delivery, this is normally from contacts such as the parents or healthcare workers Infective causes are more commonly coagulase-negative staphylococcal species such as Staphylococcus epidermidis, Gram-negative bacteria such as Pseudomonas aeruginosa, Klebsiella and Enterobacter, and fungal species ``` Other less common causes include: Staphylococcus aureus Enterococcus Listeria monocytogenes Viruses including herpes simplex and enterovirus ```
41
Risk factors for neonatal sepsis?
Mother who has had a previous baby with GBS infection, who has current GBS colonisation from prenatal screening, current bacteruria, intrapartum temperature ≥38ºC, membrane rupture ≥18 hours, or current infection throughout pregnancy Premature (<37 weeks): approximately 85% of neonatal sepsis cases are in premature neonates Low birth weight (<2.5kg): approximately 80% are low birth weight Evidence of maternal chorioamnionitis
42
Presentation of neonatal sepsis?
Respiratory distress (85%) = Grunting, Nasal flaring, Use of accessory respiratory muscles, Tachypnoea Tachycardia: common, but non-specific Apnoea (40%) Apparent change in mental status/lethargy Jaundice (35%) Seizures (35%): if cause of sepsis is meningitis Poor/reduced feeding (30%) Abdominal distention (20%) Vomiting (25%) Temperature: not usually a reliable sign as the temperature can vary from being raised, lowered or normal Term infants are more likely to be febrile Pre-term infants are more likely to be hypothermic The clinical presentation can vary from very subtle signs of illness to clear septic shock Frequently, the symptoms will be related to the source of infection (e.g. pneumonia + respiratory symptoms, meningitis + neurological symptoms)
43
Investigations for neonatal sepsis?
Blood culture FBC - abnormal neutrophil count CRP - help to guide management Blood gases - metabolic acidosis is particularly concerning for neonatal sepsis, particularly a base deficit of ≥10 mmol/L Urine MC&S - more useful in LOS, show signs of infection (^ leukocytes, positive culture, haematuria, proteinuria) if urosepsis Lumbar puncture - if suspecting meningitis as source of infection
44
Management of neonatal sepsis?
intravenous benzylpenicillin with gentamicin as a first-line regimen for suspected or confirmed neonatal sepsis - unless local bacterial resistance patterns disagree CRP measured to monitor progress antibiotics can be ceased at 48 hours in neonates who have CRP of <10 mg/L and a negative blood culture at presentation and at 48 hours Normally, in neonates with culture-proven sepsis, duration will be approximately 10 days O2, fluid and elctrolytes severely ill neonates may need volume and/or vasopressor support prevention/management of hypoglycaemia prevention/management of metabolic acidosis