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BIOL3065 > Lice, Ticks and Lyme disease > Flashcards

Lice, Ticks and Lyme disease Flashcards

1
Q

Where do ticks occur ie their geographical location?

A
  • Distribution of I. ricinus in GBm as recorded by the PHE tick recording scheme and the biologicla records centre
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2
Q

Why do ticks act as a vector for human disease?

A

small organisms such as mosquitoes or ticks that can carry pathogens from animal to person or person to person

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3
Q

Ticks can also cause zoonotic diseases (Zoonoses) what is this?

A

An infectious disease that can be passed between animals and man

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4
Q

Tell me about Lyme disease

A
  • most common human tick-borne disease in the Northern hemisphere
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5
Q

When was lyme diseases first identified?

A

Lyme, connecticut, 1970s

Reported cases of lyme disease in the US in 2014

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6
Q

What is the causative agent of Lyme disease?

A

Borrelia spp. spriochaetes

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7
Q

What are the lyme disease species which are known to be pathogenic to humans?

A

B. burgdorferi sensu stricto: USA, Europe

B. afzelii: Europe, Asia

B. garinii: Europe, Asia

B. spielmanii: Europe

B. bavariensis: Europe

B. mayonii: USA 2015

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8
Q

What species of lyme disease is pathogenicity yet to be proved for?

A

B. valaisiana

B. lusitania

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9
Q

In the UK, what three species cause lyme disease and rank them in order

A

B. garinii > B. afzelii > B. burgdorferi s.s.

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10
Q

Lyme borreliosis transmission cycle

A

generally transmitted by bites of ticks

larvae generally do not cause infection

larvae feed on small organisms and can acquire infection at that stage where it then becomes a nymph

this continues up its development to the adult form

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11
Q

What is the external anatomy of Borrelia spirochaete?

And what are some important proteins?

A

OspA and OspC get turned on/off depending on where the pathogen is

P17 is an ECM protein in many tissues in the body, in particular the joints

P83 protein

P66 protein

VIsE protein

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12
Q

Tell me about the pathogen transmission for the outer surface protein for ticks

A

Tick feeds for at least 12-17 hours – this causes a change in Osp expression

OspC needed to transmit Borrelia to mammalian host, inhibits phagocytosis - OspC binds to tick salivary gland epithelial cells so facilitates infection as more present on saliva

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13
Q

What are the main three stages of lyme disease

A
  1. Early lyme disease
  2. Early disseminated lyme disease
  3. Late disseminated lyme disease
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14
Q

Tell me about what happens in early lyme disease and the symptoms

A

Local infectio: Days to weeks after tick bite

Flu-like symptoms: fever, malaise, myalgias, headaches (1-7d)

Erythema migrans rash (EM) expands around bite site (>7 days)

‘classical’ bulls eye rash

not present in 30-50% cases

Many asymptomatic

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15
Q

Tell me about early disseminated lyme disease, what occurs and the symptoms

A

Disseminated infection

Weeks to months after infection

Through blood or lymphatics

bacteraemia often very low

Multiple secondary Erythema Migrans lesions

Lymphocytoma (esp. children)

Earlobes, nipples, genital area

Neuroborreliosis

Facial / cranial palsy

e.g. Bell‘s palsy

Polyarthralgia or true arthritis

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16
Q

Tell me about Late disseminated lyme disease, when it occurs and the symptoms

A

persistent symptoms- serious as often not obviously related to ticks

Months to years after infection

late Neuroborreliosis

more widespread PNS and CNS involvement; MS-like; encephalopathy; cognitive problems; psychiatric problems

Lyme arthritis

inflammatory ahrthritis; especially knee joints

Lyme Carditis

conduction abnormalities; atrioventricular block

Acrodermatitis chronica atrophicans (ACA)

17
Q

What are the different borrelia species which alter disease?

rank them as well

A

Borrelia garinii

  • No rash in ~30%
  • Neurotropic

Borrelia afzelii

  • Dermatotropic; esp. ACA
  • Neurotropic

Borrelia burgdorferi s.s.

  • Musculoskeletal; esp. arthritis
  • => In USA, B. burgdorferi s.s. predominates, most common late symptom is Lyme arthritis
  • => In Europe, B. garinii and B. azelii predominate, neurological complications

B. garinii > B. afzelii > B. burgdorferi s.s

18
Q

regional variations in genosepcies distribution

A
19
Q

What are the treatment options for those with lyme disease?

A

If treated promptly and adequately, Lyme disease rarely progresses beyond the early, acute stage.

Treat Erythema Migrans empirically (laboratory diagnosis not required) but asymptomatic or flu like presentations may be missed

Oral antibiotics usually adequate for:

  • Early lyme
  • Lyme arthritis
  • Lymphocytoma

Lyme carditis and neuroborreliosis need intravenous antibiotics

20
Q

How is lyme disease diagnosed, what three ways and tell me abit about each one?

A

Clinical diagnosis sufficient for cases of early Lyme presenting with an EM rash

Laboratory diagnosis:

  • Serology is mainstay: but needs confirmatory assay
  • PCR of blood/serum of limited use (low bacteraemia)
  • PCR of Erythema Migrans biopsy or ACA lesion
  • Culture of pathogen is gold-standard, but Borrelia is slow-growing

Alternative tests

  • Lymphocyte transformation tests / EliSpots
21
Q

Tell me about serology tests at PHE

A
22
Q

What does the Ab repertoire increase with?

A

disease progression

23
Q

What are some limitations towards lyme disease?

A

Antibody response slow to develop, false negatives possible in early disease.

IgM appear 2-3 weeks after onset (may persist for months/years)

IgG produced several weeks to months after onset

Antibiotics can suppress antibody development

Known cross reactions:

other spirochaetes

other bacteria with flagella

acute EBV cause polyclonal stimulation of Borrelia antibodies

autoimmune diseases

In late-presenting Lyme, positive serology test does not prove current infection. How to diagnose late Lyme?

24
Q

What is the true incidence of Lyme disease?

A

UK figures are based on laboratory confirmed LD infections

Cases presenting to GPs with EM rash are not centrally recorded

Lyme is not a notifiable disease in UK

–> Figures will be an underestimate of true incidence of LD.

In USA, Lyme is a notifiable disease

Published figures still believed to be an underestimate

30,000 cases => 300,000 cases

25
Q

There is a controversy, that nearly every area of lyme disease knowledge attracts disagreement between medical professions and patients. Give some examples of some disagreements

A
  • Cause of persisting symptoms
  • Incidence and prevalence in the UK
  • Modes of transmission
  • Diagnostic criteria and methodologies
  • Antibiotic treatment duration
  • Role of complementary therapies
  • Role of co-infections
  • Is there chronic Lyme disease?
26
Q

Chronic lyme, post treatment lyme disease?

A

No consistent, agreed definition of ‘Chronic Lyme’

Persistent, untreated active infection e.g., late neuroborreliosis; ACA

Persistent symptoms following treatment for Lyme boreliosis

Post-Lyme disease treatment syndrome (PTLDS)

Patients who have had Lyme disease in past but current

presentation may be unrelated to Borrelia infection

Patients with non-specific symptoms but no evidence of current or past borrelial infection

27
Q

What is the quest for ‘chronic lyme’?

A

Is this chronic Lyme?

patient with non-specific symptoms (fatigue, pain, muscle, or joint pain, ‘brain fog’ etc)

no credible clinical history

negative conventional diagnostic tests

BIOL3065 (23 decks)

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