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Medicine year 2 semester 1 > Case 16- CNS and brain infections > Flashcards

Case 16- CNS and brain infections Flashcards

1
Q

Symptoms of meningitis

A
  • Fever
  • Headache
  • Stiff neck
  • Back rigidity
  • Bulging fontanelle in neonates
  • Photophobia- hate light
  • Altered mental state- confused
  • Unconsciousness, toxic/moribund state
  • Seizures
  • Non-blanching rash
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2
Q

Meningococcal disease

A

Caused by Neisseria meningitidis. Type of meningitis, rare but very serious but biggest cause of bacteria meningitis. Clinical features may be vague and are similar to other non-bacteria causes of meningitis. The disease progresses, children tend to be admitted 24 hours after the illness starts. The diagnosis of meningococcal disease can only be confirmed in secondary care. The definitive test for meningitis is a lumbar puncture with a laboratory examination of the cerebrospinal fluid

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3
Q

MenW

A

A highly virulent strain of meningitis
Characteristic symptoms= Septic arthirits, Severe RTI
Some adults with MenW septicaemia have mainly FI symptoms but without the non-blanching rash, they progressed rapidly to death
Higher mortality

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4
Q

Pneumococcal meninigitis- rash

A

It is not common to have a petechial rash in pneumococcal meningitis

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5
Q

Pneumococcal meninigitis- rash

A

It is not common to have a petechial rash in pneumococcal meningitis

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6
Q

Lyme disease

A

Transmitted from host to host by lxodes spp (deer/sheep ticks)
Causative agent- Borrelia burgdorferi
More common in areas with lots of sheep i.e. the highlands
In order to prevent lyme disease you should remove all ticks using the correct method

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7
Q

Stage 1 of lyme disease

A

Stage 1 or localised disease- the characteristic presentation is an erythema rash which is a circular rash at the site of the infectious tick attachment that radiates from the bite, within 3-36 days. Not always present. Appears as a bullseye (2 circles). The physician should try and rule in or out whether the patient would be exposed to sheep ticks. If you receive antibiotics it should clear up (normally doxycycline)

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8
Q

Stage 2 of lyme disease

A

Stage 2 or Disseminated Lyme disease- if you don’t receive antibiotics at stage 1. Causes a flu like illness. Neurological disorders or neuroborreliosis in 10% of untreated cases. Unilateral or bilateral facial nerve palsies. Meningism and meningitis. Mild encephalitis produces malaise and fatigue. Vague non-specific symptoms

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9
Q

Viral meningites

A

About 3,000 cases in the UK annually. The incidence is probably higher, it’s the most common cause of meningitis. Normally mild and self-limiting. Viral meningitis can be clinically indistinguishable from bacterial meningitis though it tends to be milder and are less likely to have the rash. Treat as if it is bacterial meningitis until you are certain. The young and immunocompromised are the most susceptible.

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10
Q

Treatment for viral meningitis

A

Treatment tends to be supportive, enteroviral meningitis is normally self-limiting. Aciclovir for herpes viral infection. Prognosis is good with complete resolution within 10 days

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11
Q

Difference between meningitis and encephalitis

A

Encephalitis is inflammation of the brain, meningitis is inflammation of the membranes

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12
Q

Major causes of viral encephalitis

A
  • HSV-1 (also HSV-2)
  • VZV
  • Enteroviruses
  • EBV (immunocompromised)
  • CMV (immunocompromised)
  • Measles (1 in 1000 cases)
  • Mumps (1 in 1000 cases)
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13
Q

Herpes simplex encephalitis

A
  • In children older than 3 months and in adults: HSE is usually caused by herpes simplex virus type 1 (HSV-1)
  • In neonates- HSE is usually caused by herpes simplex virus type 2 (HSV-2) acquired at the time of delivery
  • Most common cause is non-epidemic encephalitis and accounts for 5-10% of all cases
  • UK annual incidence of HSE is 0.2-0.2/100,000
  • Its most common and severe in children and the elderly
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14
Q

Symptoms of Herpes simplex encephalitis

A

1) Altered consciousness
2) Focal and generalised seizures
3) Raised intracranial pressure including papilloedema
4) Focal neurological signs and Psychiatric symptoms

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15
Q

Untreated Herpes simplex encephalitis (HSE)

A

Its progressive and often fatal within 7-14 days, 70% mortality in untreated patients. Half of the untreated survivors have severe neurological defects. Among treated patients the mortality rate is 19%

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16
Q

Treatment for Herpes simplex encephalitis (HSE)

A

Intravenous acyclovir as soon as HSE is suspected, do not wait for confirmation. Give for 10 to 21 days

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17
Q

Rabies

A

1) Infection of the CNS
2) Zoonotic disease which often affects domestic and wild animals
3) Spreads through bites from infected animals (dogs, bats)
4) Very rare, last case in 2002
5) Causes Oesophageal spasms

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18
Q

Treatment of rabies

A

Post exposure prophylaxis (vaccine) is given after you are bitten by a bat or a dog, it must be administered before symptoms or rabies is almost always fatal. Immediate wound cleaning.
Vaccine is very effective

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19
Q

The rabies virus

A

Neurotropic- binds to nerves and neurons

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20
Q

Where is rabies most common

A

Deaths mostly in Asia and Africa, thousands a year. Most common in children under 15. Dogs are the source for the majority of human rabies deaths. Immediate wound cleaning and PEP (post exposure prophylaxis) immunisation.

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21
Q

Rabies incubation

A
  • No symptoms
  • Virus transfers from the periphery to the CNS
  • Variable duration, usually between 3 and 12 weeks but can be up to 19 years
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22
Q

Prodromal stage of rabies

A

Virrus enters the CNS, duration 2 to 10 days, non-specific symptoms (malaise, fatigue). Can develop into two different forms:

  • Furious rabies- the most common form (80%), very agitated, spasms
  • Apathetic rabies- paralytic or dumb, the patient becomes withdrawn (20%)
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23
Q

The 8 different types of herpes

A

All members of the Herpesviridae family have the same basic structure:
Alphaherpes Virus
• Herpes Simplex Virus 1 and 2 (HSV)
• Varicella Zoster Virus (VZV)
Betaherpes Virus
• Cytomegalovirus (CMV/HHV5)
• Human Herpes Virus 6 (HHV6)
• Human Herpes Virus 7 (HHV7)
Gammaherpes Virus
•Epstein Barr Virus (EBV/HHV4)
•Human Herpes Virus 8 (Kaposi’s Sarcoma associated Herpes Virus/HHV8)

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24
Q

4 main componenets of the viral structure

A
  • Viral genome
  • Icosahedral Nucleocapsid- protects the genome, made of proteins
  • Tegument- viral proteins required for replication and evasion of the human immune system
  • Envelope (derived from host nucleus)- in the case of herpes the envelope is derived from the nucleus of the host cells. Contains glycoprotein protrusions, primary function is to bind/fuse with new host cell
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25
Q

Life cycle of herpes virus

A
  • Primary infection- first time virus is encountered
  • Latency- viral DNA persists in specific cell types. Could be lifelong, no replication, immune system has controlled the infection. Dormant virus in nerve cell bodies
  • Reactivation- virus reactivates intermittently, may be symptomatic or asymptomatic. May not ever reactivate, the bacteria sheds and travels through the body. Latent virus starts to actively replicate
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26
Q

Inititial infection

A

The first infection with HSV-1 or HSV-2 in a patient who has already been infected with the other HSV

27
Q

Latency and reactivation of Herpes virus

A

The nucleus goes into the host cell and replicates, primary infection can be asymptomatic. The virus travels up the CNS to the ganglion where it becomes dormant. When it reactivates, it replicates in the ganglion then spreads down the nerves to the skin. It then replicates within the epithelial cells. Can reactivate multiple times or never

28
Q

Why does the virus reactivate?

A 
Not always clear, some potential association (not always sure if correlation?)
• Stress
• Intercurrent illness
• Menstrual Cycle
• Cold temperatures
• Sunlight
• Skin damage 
• Immunosuppression
29
Q

Epidemeology of Herpes

A

Most primary infection occur in childhood (<5 years of age), infections are starting to occur a bit later. Prevalence data: HSV 1 50% (decreasing from 80% high), HSV 2 10-20% (higher in other countries i.e. Bulgaria, Finland).

30
Q

Transmission of herpes

A

Through close contact with mucosal/epithelial surfaces (oral or genital) and fomites. The incubation period is between 4-7 days

31
Q

Primary oral herpes

A

Primary infection with HSV 1 or HSV 2. Usually asymptomatic. May get initial prodrome- fever, sore throat and Lymphadenopathy. Can present with cold sores (vesicular rash on lips and mouth). You may get tingling and burning before the cold sore develops. Lasts 10-14 days. May present as gingivostomatitis in children, can require hospitalisation.

32
Q

Reactivation of oral herpes

A

Nearly all oral reactivation is due to HSV-1. Majority of reactivations are asymptomatic. Clinically manifests as cold sores (crops of vesicles at vermillion border).

33
Q

Genital herpes

A

Primary infection with HSV 2 or HSV 1. Lymphadenopathy in the groin. Reactivation is usually always HSV 2. Primary infections are often more severe:
• May have systemic symptoms e.g. fever, malaise
• LUTSx e.g. dysuria, vaginal/urethral discharge
• Can cause urinary retention
Symptomatic reactivation often not as severe. Primary and reactivation can be asymptomatic.

34
Q

Herpetic Whitlow

A

Herpes rash at non mucosal site i.e. hands

35
Q

Oscular HSV infection

A

Treat with topical antivirals. Usually HSV-1. Usually occurs due to direct contact with orofacial lesions or infected secretions. Can effect different parts of the eye- retina, cornea, iris, conjunctiva and eyelids. Recurrent infections are common. Pain, blurred vision and red eye. Forms a dendritic ulcer on Fluorescein staining. Can lead to scarring and visual loss.

36
Q

HSV encephalitis

A

Commonest cause of viral encephalitis. More then 90% are due to HSV-1, there is a 70% mortality if left untreated. Increased incidence in the elderly. Unilateral temporal/frontal lobe involvement. Symptoms= fever, headache, confusion, reduced GCS, altered behaviour, seizures, focal neurology, can be subtle at the start.

37
Q

Other HSV complications

A

1) Secondary bascterial skin infection

2) HSV meningitis (commonly HSV-2) - self limiting illness, can be recurrent ‘Mollaret’s Meningitis.’

38
Q

People at risk of HSV

A

Immunosuppressed: HIV, transplant patients, primary immunodeficiency, latrogenic (drugs). Causes increased risk of reactivation, increased risk of treatment failure and development of resistance. Can cause disseminated and HSV oesophagitis.

39
Q

Neonatal herpes

A

Neonatal cases are rising. It’s the infection of neonate at birth (contact with vaginal secretions) or shortly after. It causes high mortality and long term neurological sequelae and developmental delays in survivors.

40
Q

Risk factors for neonatal herpes

A
  • Maternal primary or initial genital herpes in late pregnancy- mum doesn’t have time to develop antibodies
  • Family members close contact (kissing baby)- in absence of maternal antibodies
  • Obstetric risk factors- PROM (premature rupture of membranes), prematurity
41
Q

Diagnosis of HSV

A
  • Clinical
  • Serology- not useful in the acute setting. Sometimes used before immunosuppression begins in order to establish need for prophylaxis. Type specific serology can establish what type of herpes, you can then test the blood for antibodies, done to pregnant women with symptoms
  • Molecualar- detection of viral DNA by PCR. You need a sample from swab lesions, CSF or blood. It’s the diagnostic method of choice in acute settings
  • Histological- intranuclear and cytoplasmic inclusion bodies in cells, confirms an acute infection
42
Q

Mangement of HSV

A
  • Supportive care- analgesia, IV fluid, Catheter
  • Antivirals- Aciclovir, Valaciclovir. Aciclovir is more active against HSV then VZV. Reduces duration of disease but not symptoms
43
Q

Herpes- Aciclovir

A
  • Topical, IV, oral
  • Side effects- renal toxicity, neurotoxicity
  • Safe in pregnancy and breast feeding
  • Resistance can develop
  • Competitive DNA polymerase inhibitor leads DNA chain termination
  • Most effective started in the first 24-48 hours of rash onset
  • Topical treatments have limited efficacy
  • Poor oral bioavailability or oral dosing (5x per day dosing)
44
Q

Herpes- Valaiciclovir

A

Pro drug of acyclovir, significantly better oral bioavailability. Converted to acyclovir via first pass metabolism. More expensive

45
Q

Herpes prophylaxis

A

Low dose Aciclovir, prevents reactivation in immunosuppressed patients i.e. post-transplant. Treats recurrent HSV disease.

46
Q

Life cycle of Varicella zoster virus

A
  • Infection via respiratory mucosa / conjunctiva
  • Replication in regional lymph nodes leads to primary viraemia
  • Replication in the liver and spleen causes secondary viraemia
  • Dissemination in the skin causing symptoms of chicken pox
  • Latency in dorsal root ganglion
  • Reactivation causes shingles
47
Q

Wpidemeology of Varicella/chicken pox

A

More then 90% of people have had it by adulthood. Occurs all year round but peaks in late winter/early spring. Household attack rate >90% (likelihood of getting it if someone in your household has it). Normally get it before 5, people are getting it later due to vaccine. Transmission- aerosol, contact.

48
Q

VZV- incubation period and infectious period

A
  • Incubation period = 7-21 days (average 14 days)

* Infectious period = 2 days prior to rash onset until rash fully crusted over (~5 days after onset)

49
Q

Epidemeology of Zoster/shingles

A

25% of people will have an episode of shingles, incidence increases with increasing age, the majority of cases are after 50. Infectious from onset of rash. Transmission to other is via direct contact with vesicle fluid.

50
Q

What is shingles

A

The reactivation of VZV after the patient has already had chickenpox

51
Q

Chickenpox symptoms

A
  • Prodrome- fever, malaise, headaches, fussiness, loss of appetite, nausea, myalgia
  • Rash= centipedal distribution. Goes from Macules -> Papules -> Vesicles -> Pustules. Crops of lesions seen at all stages. Intensely itchy, can get lesions on mucus membranes (shallow painful ulcers in mouth/genitals.
  • Generally benign disease in children
  • Much more severe in adults
52
Q

Chickenpox complications

A
  • Secondary bacterial infections of the skin- more common in children
  • Varicella Pneumonitis- more common in adults, increased risk in smokers, patients often need ventilatory support
  • Other severe but rare complications: Cerebellar ataxia (children)- self limiting, Varicella Encephalitis, Haemorrhagic disease
53
Q

Chickenpox pregnancy

A
  • To the pregnant women- increased risk of severe disease, Pneumonitis, mortality and morbidity
  • To the foetus- congenital varicella syndrome, 2% chance if maternal infection occurs between 13-20 weeks gestationally risk decreases after that. Causes limb shortening, skin scarring, microcephaly and neurological abnormalities
54
Q

Chickenpox- neonates risk

A
  • Increased risk of severe disease in the first year of life
  • Risk of life threatening disease if infected in the first 1-2 weeks of life (particularly those whose mum develops chicken pox 4 days prior to 2 day after birth)
  • Prematurity (<28 weeks) and small babies (<1000kg)
  • Disseminated Haemorrhagic Chickenpox
  • Mortality up to 30% (untreated)
55
Q

Chickenpox- Immunocompromised risk

A
  • Risk of disseminated visceral disease
  • Encephalitis, hepatitis, pneumonitis, DIC
  • May have atypical rash, disease last longer, infectious for longer,
56
Q

Zoster/shingles symptoms

A
  • Prodrome- abnormal sensation in the skin (tingling, burning, pain)
  • Rash- dermatomal, never crosses the midline, vesicular, trunk most commonly affected
  • Can get atypical presentations in older patients and the immunocompromised
  • Recurrent episodes are uncommon
57
Q

Zoster- Postherpetic neuralgia

A
  • Pain that lasts >90 days after rash has resolved
  • Can last for weeks, months, years
  • Risk, severity and duration increase with age (40% of those over 60)
  • High M&M (mortality and morbidity)
58
Q

Herpes Zoster Opthalmicus

A
  • Infection of the Ophthalmic branch of trigeminal nerve- provides sensation to the eye surface, eyelids, forehead and nose
  • More likely if nasocilliary branch involved
  • Can affect the cornea, conjunctiva, sclera
  • Rarely includes the retina
  • Visual disturbance and potential loss if not treated
  • PHN (postherpetic neuralgia) can be significant problem post HZO (Herpes Zoster Opthalmicus)
59
Q

Zoster- other complications

A
  • Secondary bacterial infections
  • Cranial/peripheral nerve palsies- Ramsay hunt syndrome
  • Meningitis/encephalitis
  • Cerebral vasculitis
60
Q

Diagnosis of VZV (varicella zoster virus)

A
  • Serology- not useful in acute settings, used to establish previous infection and immunity
  • Molecular- detection of viral DNA by PCR. Take a sample from lesions, CSF or blood. Diagnostic method of choice in acute settings
61
Q

Managing of chickenpox

A
  • Children very rarely need any treatment - Symptomatic relief (Calamine lotion, Antihistamines, paracetamol)
  • Adults- Antivirals if can be started within 24-48 hours of rash onset. Close monitoring in managing in the community. May need admission to hospital if complicated /pregnancy/ Immunocompromised
  • Aciclovir/valaciclovir- Less effective against VZV than HSV (need 4x dose therefore valaciclovir best oral option). Oral- IV in severe disease
62
Q

Management of shingles

A

All patients should be considered for treatment with antivirals. Start promptly- ideally within 24 hours. Prompt treatment helps to reduce risk of PHN. May need neuropathic pain relief i.e. amitriptyline and pregabalin. If eye involvement suspect, urgent review by ophthalmology.

63
Q

Varicella vaccine

A

Live attenuated vaccine, not everyone can have it. 98% effective in children, only 75% effective in adults. Indication for use in the Uk- susceptible healthcare worker, susceptible household contact of immunosuppressed children. The vaccine is given more routinely in other countries i.e. US.

64
Q

VZV post-exposure prophylaxis

A
  • Given to at risk of groups- pregnant women, neonates, severely immunocompromised. If no immunity to varicella (no VZV IgG detected) and significant exposure. For varicella its face to face contact or same room for 15 minutes for zoster virus its direct contact with exposed rash
  • Varicella zoster immunoglobulins- high concentration of VZV antibodies, given IM
  • Aciclovir

Medicine year 2 semester 1 (53 decks)

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