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MIC3041 Medical Microbiology > Central Nervous System Infections > Flashcards

Central Nervous System Infections Flashcards

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1
Q

How does rabies differ from most CNS infections?

A

Infecting the CNS is an integral part of infection with 2 clear purposes.

  1. Needs to get from bite site to salivary glands
  2. Needs to change behaviour of animal (‘limbic system’)
    - Specifically changes behaviour of cells with limited damage
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2
Q

What occurs in most infections that infect the CNS?

A

Often the result of accidentally infecting the CNS
Typically not a good result for the pathogen
- Damages host
- Moves pathogen to area unlikely to assist transmission
- Disease symptoms of result from host (immune) response and/or cell damage

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3
Q

Why is CNS homeostasis so important?

A

It is a highly sensitive tissue - non-renewable cells
Specialised privileged compartment
Highly metabolically active - solutes, waste products
Control of environment very important

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4
Q

What are the 2 selective gateways that physically separate the CNS from the rest of the body?

A

Blood-brain barrier (BBB)

Blood-Cerebrospinal fluid barrier (BCSFB)

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5
Q

What is the role of the BBB and BCSFB?

A

Protect the brain:

  • Sudden changes in the blood/periphery
  • Inappropriate immunity/inflammation
  • Microbial infection
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6
Q

What type of inflammatory environment is the CNS?

A

An anti-inflammatory environment

- Suppression of immunity

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7
Q

What can be seen as a result of immune responses in the CNS?

A
  • Can remove microbes but can also cause symptoms
  • Major cause of symptoms of many infections
  • Neurons do not regenerate
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8
Q

What are the two outcomes of CNS infections?

A

Meningitis

Encephalitis

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9
Q

What is meningitis?

A

Inflammation of meninges - layers surrounding the brain

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10
Q

What is encephalitis?

A

Inflammation of brain ‘substance’ [tissues/paranchyma]

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11
Q

What types of microbes cause meningitis?

A

Bacteria
Fungi
Protozoa
Viruses

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12
Q

What types of microbes cause encephalitis?

A

Viruses
Prions
Parasites
Bacteria - toxins

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13
Q

What physical feature is the brain protected by?

A

Skull

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14
Q

What physical feature is the spinal cord protected by?

A

Vertebral column

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15
Q

What is the brain surrounded by under the skull?

A

The meninges containing CSF

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16
Q

What is the role of the meninges?

A

Mechanical support, protection and homeostasis

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17
Q

What is the important of having contacts across the barriers?

A

Required for signalling, nutrients, metabolites

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18
Q

What crosses the barriers of the CNS?

A

Blood vessels

Nerves

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19
Q

What is the role of the BBB and BCSFB?

A

Selective regulated exchange
Maintain homeostasis
Protects from immunity
Protect from infection

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20
Q

What is the major route of CNS infection and what pathogens use it?

A

Blood vessels

Bacterial species, Polio virus

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21
Q

What are the 4 routes for CNS infection?

A

Blood vessels
Peripheral nerves
Invasion through ears/sinuses and olfactory nerve
Penetrating injury/surgery

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22
Q

What are 2 pathogens that infect the CNS through peripheral nerves?

A

Rabies

Herpes simplex

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23
Q

How much and where is the CSF contained?

A

Within the subarachnoid space (between the arachnoid mater and pia mater)
140ml

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24
Q

What is the CSF produced by?

A

Produced by choroid plexus

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25
Q

What is the Blood Brain Barrier?

A

Endothelial cells of capillary
Tight junctions between capillary endothelial cells
Thick basement membrane surrounding capillary
“Feet” (processes) of astrocytes in brain surrounding capillary
No fenestrations

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26
Q

What is the BCSFB?

A

Endothelial cells of capillary
Basement membrane
Tight junctions between choroid plexus ependymal (epithelium) cells

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27
Q

What is the difference between BCSFB and BBB?

A 
BCSFB is:
Less tight than BBB
Thinner basement membrane
Looser junctions
Vessel endothelium has fenestrations
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28
Q

Crossing the BBB results in what type of infection?

A

encephalitis

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29
Q

Crossing the BCSFB results in what type of infection?

A

Meningitis

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30
Q

What are 3 mechanisms by which pathogens can cross BBB/BCSFB and cause infection?

A

Transcellular
Pericellular
Trojan Horse

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31
Q

What is the mode of action of the transcellular mechanism?

A
  • Infection (growing across ECs)
  • Passive transport (not infection) through endothelium cells in vacuoles
  • > receptor binding and endocytosis as for physiological cargos
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32
Q

What is the mode of action of the pericellular mechanism?

A

Transport between cells (if tight junctions weakened by inflammation)
-> bystander effect

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33
Q

What is the mode of action of the trojan horse mechanism?

A

Inflammation can allow infected white blood cells to enter CNS

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34
Q

How does Rabies get into the CNS?

A

Rabies viruses -> muscle -> enters peripheral nerves -> travels to CNS

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35
Q

Do peripheral nerves cross the BBB/BCSFB?

A

No they entirely circumvent it

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36
Q

How does HSV get into the CNS?

A

HSV skin lesion -> enters peripheral nerve -> moves to dorsal root ganglia; becomes latent -> on reactivation usually returns to lesion, sometimes enters CNS

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37
Q

How are cellular cargos (sometimes our pathogen) moved from the peripheral nerves to the CNS?

A

Use molecular motors (Dynein) that move along microtubules in neurons toward the CNS

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38
Q

What is the mode of action of invasion via the olfactory route?

A

Nasal passages -> olfactory tract -> mengingitis/encephalitis
e.g. protozoa Naegleria fowleri
amoeba that lives in stagnant water

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39
Q

Which entry pathway does Naegleria fowleri use to enter the CNS?

A

Olfactory route

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40
Q

What is the immune status of normal CNS?

A
  • Quiescent but can mount a response
  • has immune cells but fewer than other tissues
  • protected by immune cells, macrophages (meninges), microglia (brain parenchyma)
  • small number of resident T cells perform immune surveillance
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41
Q

Which immune cell protects meninges?

A

Macrophages

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42
Q

Which immune cell protects brain parenchyma?

A

Microglia

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43
Q

What is the immune status of the CNS during infection?

A

Resident macrophages activate T cells
- pro-inflammatory cytokines released: causing loosening of tight junctions, recruiting immune cells (pericellular)
- more immune cells enter CNS
- large number of immune cells crossing into CNS caue capillaries to become leaky
BBS/BCSFB is compromised

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44
Q

Through which mechanism do immune cells enter the CNS?

A

Pericellular mechanism

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45
Q

Which immune cells are recruited for free living bacteria in the CNS?

A

neutrophils

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46
Q

Which immune cells are recruited for viruses in the CNS?

A

lymphocytes

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47
Q

What are some disadvantages of the immune response?

A
  • Can cause damage to the host

- May develop low blood pressure and/or swelling of the brain within the skull

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48
Q

Compare the immune responses for bacteria vs viruses

A 
Bacteria:
Rapid immune response
Highly inflammatory
Causes a lot of damage
Viruses:
Less rapid
Less inflammatory
Less damage
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49
Q

After recovery from initial infection in CNS, what can occur?

A

autoimmunity, may happen years later

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50
Q

What is the pathogenesis of a CNS infection?

A

It is the combination of pathogen and host immune response

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51
Q

What are the 4 sources of pathogenesis in CNS infection?

A
  1. Cell death/damage
  2. Cellular dysfunction
  3. Immune response
  4. Neurons are non-regenerative - can see permanent damage
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52
Q

What source of pathogenesis does Rabies use?

A

Cellular dysfunction

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53
Q

What source of pathogenesis does Polio use?

A

Cell death/damage - lyses neurons for release

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54
Q

What cell type does rabies infect?

A

Neurons

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55
Q

What cell type does Polio infect?

A

Neurons

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56
Q

What cell type does JC virus infect?

A

Oligodendrocytes

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57
Q

What source of pathogenesis do bacteria tend to incur?

A

Immune response

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58
Q

How do we monitor CNS?

A

Through testing CSF, can provide information on the nature of potential infections of CNS
- Lumbar puncture

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59
Q

What is the gold standard for diagnosis of bacterial meningitis?

A

CSF examination

Positive CSF signs in 80-90% of cases of confirmed bacterial meningitis

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60
Q 
Compare 
normal CSF
aseptic meningitis (viral) and 
pyogenic; bacterial meningitis 
in terms of immune cells
A 
Normal CSF:
- quiescent
- very few WBCs
- all are lymphocytes or monocytes
- NO neutrophils
Viral:
- Increase in lymphocytes (mostly T cells)
- Neutrophils: usually in low numbers
Bacterial:
- Really high numbers of neutrophils (90% of acute cases)
- NOT for TB
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61
Q 
Compare 
normal CSF
aseptic meningitis (viral) and 
pyogenic; bacterial meningitis 
in terms of protein
A 
Normal:
170-550 mg/L
Viral:
Moderately high, 500-1000 mg/L
Bacterial:
High to very high; >1000-5000 mg/L
NOT for TB
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62
Q 
Compare 
normal CSF
aseptic meningitis (viral) and 
pyogenic; bacterial meningitis 
in terms of glucose
A 
Normal:
500-800 mg/L
Ratio of normal CSF/blood - c. 0.6
Viral:
Normal or slight increase
Bacterial:
Low glucose
Ratio CSF/blood c. 0.4
NOT for TB
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63
Q 
Compare 
normal CSF
aseptic meningitis (viral) and 
pyogenic; bacterial meningitis 
in terms of CSF appearance
A

Normal:
clear, no bacterial growth in bacteriological culture
Viral:
Clear, no microscopic evidence, no bacterial growth in bacteriological culture
Bacterial:
often cloudy, bacteria can be observed (microscopy - gram stain) and/or cultured

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64
Q

What accounts for the difference in protein and glucose levels between viral and bacterial CNS infections?

A

Bacteria are free-living organisms, they require glucose for metabolism so steal from host lowering the blood glucose, they also multiply and to do that create more protein thus increasing protein levels that can be detected.
Viruses cannot grow independently and survive in host cells. Therefore, they don’t require glucose from the host and the host cells use glucose as normal. In terms of protein more viruses are being produced and viruses have protein components therefore it makes sense that more virions means more protein.

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65
Q

Why are some ‘aseptic’ CSF samples misleading?

A

They may contain slow-growing bacteria/fungi
e.g. TB, partially treated bacteria
Due to low numbers or species of microorganism CSF changes are subtle and/or bacteria/fungi can’t be observed or cultured

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66
Q

How many cases of bacterial meningitis in US each year?

A

100,000

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67
Q

How many cases of bacterial meningitis in Sub-Saharan Africa each year?

A

100-1000 cases per 100,000 people

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68
Q

Can bacterial meningitis be treated?

A

Yes but only with prompt administration of appropriate antibiotics

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69
Q

What are the most common causes of bacterial meningitis in high income countries prior to specific vaccines?

A

Haemophilus influenzae
Streptococcus pneumoniae
Neisseria meningitidis

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70
Q

What are the most common causes of bacterial meningitis in high income countries after specific vaccines?

A 
Streptococcus pneumoniae (many serogroups)
Neisseria meningitidis (different serogroups, geographical)
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71
Q

What is the clinical presentation of acute bacterial meningitis?

A
  1. fever (77% of cases)
  2. stiff neck (83% of cases)
  3. altered mental state (69% of cases)
  4. headache (87% of cases)
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72
Q

What is the classical triad of acute bacterial meningitis?

A

Fever, stiff neck, altered mental state

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73
Q

What causes a stiff neck in acute bacterial meningitis?

A

Body response: rigidity protects subarachnoid space

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74
Q

What is meant by altered mental state in acute bacterial meningitis?

A
  • Nausea/vomiting
  • irritability/excitability
  • decreased level of alertness or consciousness
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75
Q

What percentage of adults present with the classical triad in acute bacterial meningitis?

A

44%

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76
Q

What percentage of adults present with 2 of the 4 signs of acute bacterial meningitis?

A

95%

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77
Q

How do babies/small children present with acute bacterial meningitis?

A

May only be irritable/less alert and look unwell

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78
Q

What percentage of adults show a rash/septicaemia in acute bacterial meningitis?

A

25%

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79
Q

How is acute bacterial meningitis diagnosed?

A

History of patient:
- knowledge of current illness/treatment, living environment and region, vaccination status, contact with children, recent travel
Physical examination:
- skin rash, septicaemia - late stage
Check if blood culture already available:
- 10-15% meningitis cases have septicaemia first
CSF examination

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80
Q

How is CSF examined in acute bacterial meningitis?

A

Look for CSF indicators
PCR to amplify bacterial DNA from CSF sample
Microscopy - gram stain
Positive bacterial culture
- used to identify species and antibiotic susceptibility

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81
Q

How should acute bacterial meningitis be treated?

A

It is a medical emergency
Antibiotics need to be given IMMEDIATELY if meningitis is suspected: before going to hospital, before confirmation, before identification of pathogen

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82
Q

What type of bacteria is Neisseria meningitidis?

A

Gram-negative diplococcus bacterium

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83
Q

What virulence factors does N. meningitidis have?

A

LPS (endotoxin) causes inflammatory response

Thick capsule prevents phagocytosis by immune cells and confers survival in blood

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84
Q

How many serogroups does N. meningitidis have?

A

13

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85
Q

What happens if you don’t treat N. meningitidis?

A

Host immune response (inflammatory cascade) leads to septic shock

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86
Q

What percentage of the population carry N. meningitidis asymptomatically in nasopharynx?

A

20%

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87
Q

Can N. meningitidis infect blood and meninges?

A

Yes but it is rare

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88
Q

Who is most susceptible to N. meningitidis infection?

A

Children >3 months (decreased maternal Ab)

Adolescents with no prior exposure to the infecting serotype (no type-specific immunity)

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89
Q

How is N. meningitidis transmitted?

A

Horizontal (person-to-person)
- via droplets of respiratory/throat secretions
Close contact
- confinement/crowding (prisons, dorms), sneezing/coughing, kissing, sharing utensils or drinks

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90
Q

When are N. meningitidis outbreaks most common in the US?

A

Late winter and early spring due to confinement and increased secretions due to respiratory diseases (colds/flu)

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91
Q

Where in the world is the highest rate of N. meningitidis infection?

A

Meningitis belt - Sub-Saharan Africa
During dry season: dust/wind/cold temperature/upper respiratory tract infections are thought to damage the nasopharyngeal mucosa
Pilgrimages and travel markets result in large, confined crowds

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92
Q

Are all N. meningitidis vaccines the same?

A

No, they contain the most prevalent serotypes for their geographical area

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93
Q

What type of bacteria is Streptococcus pneumoniae?

A

Gram-positive coccus, forms chains

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94
Q

What is a virulence factor of S. pneumoniae?

A

Thick polysaccharide capsule, prevents phagocytosis, enables it to survive in blood

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95
Q

How many serogroups of S. pneumoniae are there?

A

> 85

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96
Q

What is the mortality rate of S. pneumoniae infection?

A

20-60%

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97
Q

How is S. pneumoniae diagnosed?

A

Does patient have predisposing factors?

Ear, sinus, or lung infections precede pneumococcal meningitis in ~40% of patients

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98
Q

Who predominately becomes infected with S. pneumoniae?

A

Children <2 and the elderly

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99
Q

Is there a vaccine for S. pneumoniae?

A

Yes, Prevenar which protects against 13 serogroups

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100
Q

Is S. pneumoniae predominant in developed or developing nations?

A

Developed

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101
Q

What type of bacteria is Haemophilus influenzae?

A

Gram-negative coccobacillus

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102
Q

Is H. influenzae predominant is developed or developing nations?

A

Developing

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103
Q

What are some viral factors of H. influenzae?

A

LPS, causes inflammatory response

Capsule, anti-phagocytic

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104
Q

Is H. influenzae carried asymptomatically?

A

Yes in most people in their throat

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105
Q

Is there a vaccine for H. influenzae?

A

Yes, Hib

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106
Q

What is the mortality rate of H. influenzae?

A

5% in treated cases

9% present with sequelae

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107
Q

What is neonatal meningitis?

A

It is meningitis that occurs in newborns up to 4 weeks old.

- They have an immature immune system (brain and periphery)

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108
Q

In adults, what percentage of bacteraemia cases develop into meningitis?

A

<1%

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109
Q

In newborns, what percentage of bacteraemia cases develop into meningitis?

A

33%

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110
Q

What is the mortality rate of neonatal meningitis?

A

10-15%

50% disability (cerebral palsy, epilepsy, mental retardation)

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111
Q

What are the main 3 causes of neonatal meningitis?

A

Group B Streptococcus
E. coli
Listeria monocytogenes

112
Q

If the mother is infected with Group B Streptococcus or E. coli what should be done to prevent neonatal meningitis?

A

Treat the mother with antibiotics

113
Q

What is the best treatment to give a patient with bacterial meningitis intially?

A

3rd generation Cephalosporin as it is broad spectrum

114
Q

What treatment should be given for N. meningitidis bacterial meningitis?

A

3rd gen. cephalosporin or benzylpenicillin for 7 days

115
Q

What treatment should be given for H. influenzae bacterial meningitis?

A

3rd gen cephalosporin for 10 days

116
Q

What treatment should be given for S. pneumoniae bacterial meningitis?

A

3rd gen cephalosporin or benzylpenicillin for 10 days

Since many strains are penicillin resistant, sometimes vancomycin or rifampin are used in combination with cephalosporin

117
Q

What is given to adults and children over 2 years to reduce the inflammatory response in bacterial meningitis?

A

Steroid Dexamethasone

118
Q

Should close contacts of those with bacterial meningitis be treated?

A

Yes

119
Q

Does Mycobacterium tuberculosis meningitis occur alone?

A

Typically there is a focus of infection elsewhere in the body e.g. lungs
However, in 25% of cases there may be no previous evidence of TB disease symptoms

120
Q

Who does meningitis occur in more commonly in TB endemic countries?

A

Children 0-4 years

121
Q

In low TB incidence countries who does meningitis more commonly infect?

A

Adults with pre-disposing factors: HIV, impaired immunity

122
Q

How does TB meningitis present?

A

Gradually over several weeks

Malaise, apathy, anorexia, photophobia, neck stiffness

123
Q

What is CSF like in TB meningitis?

A

Clear
High protein
Low glucose
High WBCs mainly lymphocytes

124
Q

Why is detection of TB meningitis so hard?

A

Low numbers of bacteria:

- large and multiple samples of CSF required to perform acid-fast staining which can detect TB

125
Q

How is TB meningitis treated?

A

It is difficult to treat
Initial treatment at least 2 months with antibiotic combination, isoniazid, rifampin, pyrazinamide, and ethambutol
Treatment needs to be prompt to prevent serious complications
Corticosteroids can also be administered

126
Q

Is there a vaccination to prevent TB meningitis?

A

Yes BCG vaccine

Only 75% effective

127
Q

Does fungal meningitis occur?

A

Yes but it is very rare

128
Q

How do fungi cause meningitis?

A

Enter the lung -> blood -> meningitis

Sometimes from injections of painkillers into CSF in US

129
Q

Who is mainly affected by fungal meningitis?

A

Low birth weight babies

Adults with suppressed cell-mediated immunity

130
Q

Where do the fungi that cause fungal meningitis come from?

A

Bird/Bat droppings

Certain soil types

131
Q

What are the 2 main causes of fungal meningitis?

A

Cryptococcus neoformans

Coccidioides immitis

132
Q

Describe Cryptococcus neoformans

A

Capsulated yeast
Cells visible in CSF stained with India-Ink
Can be cultured

133
Q

What is the progression of meningitis caused by C. neoformans like?

A

Slow over days or weeks

134
Q

What is the treatment for C. neoformans meningitis?

A

Long course/High dose intravenous antifungals

e.g. amphotericin B and flucytosine combination

135
Q

What type of infection do protozoa in the CNS cause?

A

Meningitis and/or encephalitis

136
Q

What is the likelihood of protazoal infection of the CNS?

A

very rare

137
Q

What is the progression of CNS infection caused by protozoa like?

A

Rapid and usually fatal

138
Q

What is the primary cause of amoebic meningoencephalitis?

A

Protozoa

139
Q

Where do free-living amoeba come from?

A

Stagnant fresh water pools and lakes in warm countries

140
Q

How do free-living amoeba infect the CNS?

A

Enter through nose usually during water recreation, travels from olfactory tract directly to meninges

141
Q

Who is infected by Naegleria amoeba?

A

Healthy individuals

142
Q

How is protozoal meningitis treated?

A

Drug treatment is sometimes available but rarely successful

Almost always fatal

143
Q

What is the most common pathogen type to cause meningitis?

A

Viruses

144
Q

Compare bacterial meningitis and viral meningitis in terms of disease?

A

Viral is milder

145
Q

What are the symptoms of viral meningitis?

A

Headache
Fever
Photophobia

146
Q

What is the main group of viruses responsible for viral meningitis?

A

Enteroviruses

e.g. polio, Coxsackie, echo

147
Q

Is viral meningitis seasonal?

A

Yes

148
Q

How is viral meningitis diagnosed?

A

Batteries of PCR specific for each probable infecting virus very important for diagnosis
Each PCR amplifies specific viral nucleic acids

149
Q

How is viral meningitis treated?

A

Few antiviral drugs
Usually complete recovery without drugs
Rest and support (home/hospital)

150
Q

What type of pathogen is the main cause of encephalitis?

A

Viruses

151
Q

Additional to the signs displayed in meningitis, what is seen in encephalitis?

A

Cerebral dysfunction: abnormal behaviour, seizures
Confusion
Focal neurological effects depending on site of infection: loss of sensation, muscle weakness, partial paralysis
Speech/hearing, hallucinations, personality changes
Altered consciousness
Vomiting/nausea
Fever

152
Q

What are 5 groups of virus and an example that can cause viral encephalitis?

A 
Herpesviruses (HSV-1)
Enteroviruses (Polio)
Paramyxoviruses (Mumps)
Rhabdoviruses (Rabies)
Arboviruses (different families Arthropod-borne viruses)
Retroviruses (HIV)
153
Q

How do viruses most commonly enter the CNS?

A

Through the blood

154
Q

What are the steps of pathogenesis of viral encephalitis?

A
  1. ‘free’ virus or virus in blood cell
  2. leaves blood via BBB
  3. infects glial cells such as astrocytes or neurons
  4. causes death/damage/dysfunction
155
Q

What does Polio do in the CNS?

A

Lyses and destroys nerves for release (permanent damage)

156
Q

What is the immune response to viral encephalits?

A

Monocytes, lymphocytes (T cells, B cells/antibodies) move from the blood into the brain
Can clear virus, but also cause immune pathology
Can control primary infection, but cause delayed autoimmune pathology years later

157
Q

How is viral encephalitis managed?

A

Exclude other causes for symptoms displayed (e.g. head injury)
If encephalitis suspected start therapy IMMEDIATELY
Typically give acyclovir (Zovirax) before confirmation.
Acyclovir is a HSV therapy, it is used as most viral encephalitis is caused by HSV
Restrict fluids to lower pressure in brain
Give anti-seizure medication
Ventilation if required

158
Q

What is the most common cause of viral encephalitis?

A

HSV

159
Q

How does HSV cause viral encephalitis?

A

Primary infection: lesion or cold sores
Then enters sensory nerves and travels to dorsal root ganglion (spinal column) or trigeminal ganglion (face) and enters the latent stage
Can be reactivated by stress and/or illness
Ganglion typically returns to lesions; but can travel up nerves to CNS causing encephalitis

160
Q

Which HSV, HSV-1 or HSV-2, typically causes viral encephalitis?

A

HSV-1

161
Q

Who most commonly contracts HSV-1 viral encephalitis?

A

Older children and adults infected with HSV-1

162
Q

Who most commonly contracts HSV-2 viral encephalitis?

A

Neonates and newborns

163
Q

What signs show that the temporal lobe is infected?

A

Speech and understanding affected (aphasia)

May display bizarre behaviour, hallucinations

164
Q

How is HSV viral encephalitis diagnosed?

A

CSF samples may have an increase in lymphocytes, red blood cells also seen
Imaging: CT, EEG or MRI scan (typically of temporal lobe)
PCR on CSF

165
Q

What part of the brain does HSV usually target?

A

Temporal lobe

166
Q

How is HSV viral encephalitis treated?

A

Prompt treatment with acyclovir before diagnosis confirmed

167
Q

What is the mortality rate of HSV viral encephalitis?

A

Untreated = 70% mortality rate

Survivors usually have secondary complications

168
Q

What is the main cause of enterovirus encephalitis?

A

Poliovirus

169
Q

What transmission route do enteroviruses use?

A 
water borne (faecal oral route)
water -> gut -> blood -> brain
170
Q

What was the most common cause of viral encephalitis prior to vaccinations?

A

Poliovirus

171
Q

What percentage of people suffer from encephalitis when infected with Poliovirus?

A

<1%

172
Q

Why is CNS infection unlikely in Poliovirus infection?

A

Because the brain is not a productive/required part of infectious cycle

173
Q

What is the pathogenesis of Poliovirus encephalitis?

A

1-4 days of fever, sore throat
Followed by meningeal symptoms then encephalitis affecting motor neurones.
Destruction of neurons: permanent paralysis

174
Q

How is poliovirs treated?

A

It isn’t

It can only be prevented through vaccine

175
Q

What type of vaccine is the Polio vaccine?

A

Inactivated and then live oral vaccine

Due to this it has been eliminated in most countries

176
Q

Which 2 viruses are the main causes of Hand, Foot and mouth disease?

A

Coxsackie virus

Enterovirus 71

177
Q

Which of Coxsackie and enterovirus 71 is more severe?

A

Enterovirus 71 as it is more likely to be neurological

178
Q

What severity of disease does Enterovirus 71 cause in different demographics?

A

Mild disease: adults and children

Severe disease: young children and immunocompromised adults

179
Q

How is enterovirus 71 resolved?

A

Usually spontaneously

180
Q

What happens in severe enterovirus 71 cases?

A

There is brainstem involvement leading to permanent neurological damage

181
Q

When was there an outbreak of enterovirus 71?

A

1998 in Taiwan, 405 patients, most under 5

Mortality rate 19%

182
Q

Is there a vaccine for enterovirus 71?

A

No

183
Q

What viruses can causes paramyxovirus encephalitis?

A

Mumps virus
Nipah virus
Hendra virus

184
Q

In what percentage of mumps cases does mild meningitis occur?

A

10%

10 days after onset of parotitis (inflammation of salivary gland)

185
Q

What is parotitis?

A

Inflammation of salivary gland

186
Q

What is the outcome of mumps encephalitis?

A

Usually complete recovery but rarely deafness may occur

187
Q

Is there a vaccine for mumps virus?

A

Yes, MMR vaccine

188
Q

What is the case fatality of Nipah/Hendra virus?

A

40-70%

189
Q

Where in the world is Nipah seen?

A

Asia

190
Q

Where in the world is Hendra seen?

A

Australia

191
Q

What is the natural reservoir of Nipah/Hendra?

A

Fruit bats

192
Q

What is the chain of infection for Nipah?

A

Bat -> Pig -> Human

193
Q

How do humans contract Nipah?

A

Eat palm-sap

Human to human

194
Q

Is there a vaccine for Nipah?

A

No

195
Q

How is Nipah infection treated?

A

There are no antivirals

196
Q

Are there outbreaks of Nipah?

A

Yes annually in Asia

197
Q

Are there outbreaks of Hendra?

A

Yes in horses since 1998 in Queensland and New South Wales

198
Q

Has there been horse to human transmission?

A

Yes there have been 4 cases of it, with 7 infected and 4 dead

199
Q

What is the terminal host in Hendra?

A

Humans

200
Q

What is the chain of infection of Hendra?

A

There isn’t one

Although in human infection it has been shown as bat -> horse -> human

201
Q

Is there a vaccine for Hendra?

A

Yes but only for horses

202
Q

What viruses can cause lyssavirus encephalitis?

A

Rabies

Australian Bat Lyssavirus

203
Q

In which animal reservoir can rabies be found?

A

Virus in infected saliva of dogs, foxes, skunk, raccoons, bats

204
Q

Who can rabies infect?

A

All warm-blooded animals

205
Q

What is the fatality rate of rabies?

A

100% in all symptomatic cases

206
Q

What is the terminal host of rabies?

A

Humans

207
Q

What is the chain of infection of rabies?

A

There isn’t one

208
Q

How often do humans die from rabies infection?

A

1 every 10 minutes worldwide

209
Q

What demographic is most commonly affected by rabies?

A

Children

210
Q

Where does rabies rank on the most important global infectious disease chart?

A

7th

211
Q

Can dogs be infectious before they show symptoms?

A

Yes

212
Q

How do humans contract rabies?

A

via bite or saliva or skin abrasion

213
Q

What percentage of rabies cases are caused by unvaccinated dogs per year?

A

99%

214
Q

Which islands have excluded rabies via quarantine?

A

Australia and UK

215
Q

What is the incubation period for rabies?

A

Slow incubation period; 4-13 weeks up to 6 months/years

216
Q

How does rabies travel to the CNS?

A

Virus must first reach peripheral nerves
Travels through peripheral nerves from site of bite to CNS
Peripheral nerves -> CNS -> encephalitis

217
Q

What is the immune response to rabies?

A

There is none as rabies is hidden in muscle/nerve

218
Q

How can we induce active immunity against rabies?

A

Can passively immunise post-exposure with human rabies immunoglobulin together with vaccine

219
Q

What happens to an unvaccinated persons brain when infected with rabies?

A

Virus migrates to brain, spreads from cell to cell, with few cytopathic effects or immune inflammatory response

  • It maintains BBB
  • Causes dysfunction of neurons
220
Q

After rabies has infected the brain what does it do?

A

It spreads back to the body via nerves, including to the salivary glands

221
Q

What are the clinical features of rabies infection?

A

Aggressive behaviour (due to limbic dysfunction)
Flu-like symptoms: sore throat, headache, fever
Spasms, fits, hallucinations, hydrophobia, paralysis, delirium
Coma, respiratory failure

222
Q

What does dysfunction of the limbic system lead to?

A

Aggressive behaviour

223
Q

How is rabies virus diagnosed?

A

Detection of viral antigen by immunofluorescence
or
RT-PCR
- skin biopsies, saliva, CSF
Serology for rabies antibody (blood, CSF)
Intracytoplasmic inclusions called Negri bodies are seen in neurones

224
Q

How is rabies virus treated?

A

Once symptomatic there is not treatment

225
Q

How is rabies prevented?

A

Controlling dogs, wildlife and pets

Human prophylaxis: vaccine

226
Q

How do we prevent rabies in high risk individuals?

A

3 vaccinations, with antibody confirmed

Still need 2 follow up boosters after exposure

227
Q

How to we prevent rabies in non-vaccinated individuals after exposure?

A

Washing wound
If possible, determine rabies status of animal
Prophylactic treatment - immunoglobulin (RIG), 5 vaccinations

228
Q

When was Australian bat lyssavirus first detected?

A

1996 in a flying fox in New South Wales

229
Q

How many cases of Australian bat lyssavirus have there been?

A

3 cases in total, all fatal
1996 women was bitten, died two years later
1996 animal carer was bitten, died within 8 weeks
2013 boy bitten, died 2 and 1/2 months later

230
Q

How to prevent Australian bat lyssavirus infection?

A

Avoid handling bats

Wildlife/bat handlers should be vaccinated

231
Q

What is the treatment for Australian bat lyssavirus?

A

Same as for rabies:

Rabies immunoglobulin and rabies vaccine

232
Q

What is arboviruses short for?

A

Arthropod borne viruses

233
Q

How are arboviruses spread?

A

Spread by mosquito/tick (arthropod) vectors

234
Q

How to control arbovirus spread?

A

Wear protective clothing
Wear insect repellent
Eradicate mosquitos

235
Q

What are 3 main arboviruses that cause encephalitis?

A

Flaviviridae
Togaviridae
Buyaviridae

236
Q

Where can you find Zika virus in the world?

A

Uganda
South east Asia
Pacific islands
Brazil

237
Q

Where can you find Japanese encephalitis virus?

A

Asia with outbreaks worldwide

238
Q

Where can you find Murray Valley encephalitis?

A

Australia

Paupa New Guinea

239
Q

Where can you find Chikungunya virus?

A

Africa
India
South east Asia

240
Q

Where can you find rift valley virus?

A

Africa

241
Q

How can HIV cause encephalitis?

A

Soon after HIV infection, HIV can invade the CNS
First causing mild meningitis
As the disease progresses subacute encephalitis with dementia may occur

242
Q

Define delayed onset encephalitis? (post vaccinial/post infectious encephalitis)

A

Encephalitis after infectious or non-infectious vaccine

Usually immune driven: against virus and host

243
Q

What is a virus that may cause delayed onset encephatlitis?

A

Measles

244
Q

How does measles cause delayed onset encephalitis?

A

Measles is cleared
Influenza-like illness 1-2 weeks later, with encephalitis
Usually no virus recovered from CSF
Most likely an autoimmune response triggered by vaccination/infection

245
Q

What is subacute sclerosing panencephalitis?

A

Infection of CNS by ‘slow virus’ years after infection

246
Q

What virus can cause subacute sclerosing panencephalitis?

A

Measles 5-10 years after initial infection

247
Q

What is encephalopathy?

A

disorder or disease of brain

pathological change, not inflammation

248
Q

What is spongiform encephalopathy?

A

disorder or disease of brain resulting in appearance of gaps in brain tissue

249
Q

What is a disease that causes spongiform encephalopathy?

A

Bovine spongiform encephalopathy (BSE)

250
Q

How do you treat encephalopathy?

A

It is incurable and invariably fatal

251
Q

What causes infectious encephalopathy?

A

prions - proteinaceous infectious agents

252
Q

What is happening inside the brain to cause encephalopathy?

A

Single malfunctioning host protein; misfolded version of PrP (prion protein)
Changes in conformation from normal to dysfunction infectious protein

253
Q

What are the 3 causes of encephalopathy?

A

Genetic (mutation)
Sporadic
Acquired (infectious)

254
Q

What is the incubation period for encephalopathy?

A

Can be up to 50 years before dementia, wasting, lack of motor control

255
Q

What is a disease that infects humans causing encephalopathy?

A

Creutzfeldt-Jakob disease

256
Q

What is Creutzfeldt-Jakob disease?

A

Can be genetically acquired, transmitted via medical treatment, blood transfusion, or ingestion of infected meat

257
Q

What type of pathogen is toxoplasma gondii

A

Parasite

258
Q

Where is Toxoplasma gondii found?

A

Found globally

259
Q

How does Toxoplasma gondii get inside the host?

A

Undercooked meat
Contaminated water
Cat faeces
Objects contaminated by any of the above

260
Q

What is congenital toxoplasmosis?

A

When a newborn acquires toxoplasmosis from the mother.
T. gondii localises in the brain
Causes damage to eyes and hydrocephalus (excess CSF within the skull)

261
Q

What is hydrocephalus?

A

Excess CSF within the skull

262
Q

How does T. gondii typically present?

A

Most disease is latent, with no obvious symptoms

  • may have flu-like symptoms (month or more)
  • sometimes ocular symptoms
263
Q

What happens in T. gondii infection in healthy patients?

A

Usually kept under control

264
Q

What happens in T. gondii infection in immunocompromised patients?

A

encephalitis

265
Q

What disease does Plasmodium falciparum cause?

A

malaria

266
Q

What percentage of cases of malaria develop into cerebral malaria?

A

20-50%

267
Q

What happens in the body during malaria infection?

A

Red blood cells become infected
- become sticky, bind to capillaries in the brain
- block, slow/stop blood flow
Increased cranial pressure and seizures, coma, respiratory arrest

268
Q

What is the mortality rate of malaria?

A

High
one million African children die annually
Of those that survive, 10% have neurological problems

269
Q

What bacteria produces the toxin, tetanospasmin?

A

Clostridium tetani

270
Q

Can Clostridium tetani infect the CNS?

A

No, but the tetanospasmin toxin can cause CNS symptoms

271
Q

What type oxygen conditions does C. tetani require?

A

Anaerobic

272
Q

Where does C. tetani reside in the human body?

A

Deep puncture wounds

Within umbilical stump of newborns

273
Q

What disease does C. tetani cause?

A

tetanus

274
Q

Where does tetanospasmin go in the human body?

A

travels to CNS via retrograde transport up motor neurons to the neurons in the CNS
Binds to neurons and blocks the release of inhibitory mediators

275
Q

What CNS symptoms does C. tetani infection cause?

A

Overactive motor neurons: exaggerated reflexes, muscle rigidity (lock jaw), uncontrolled muscle spasms
Overactive sympathetic nerves: tachycardia and excessive sweating

276
Q

How is C. tetani infection treated?

A

Wound requires thorough cleaning
- excise/open closed wound to enable oxygen to enter to kill C. tetani
Antibiotic treatment
Passive immunisation with tetanus immunoglobulin (antitoxin)
Active immunisation with toxoid (inactivated toxin) vaccine to induce active immunity, lasts 10 years
Muscle relaxants to relieve symtpoms

277
Q

What is the mortality rate of tetanus?

A

50%

MIC3041 Medical Microbiology (11 decks)

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