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Microbiology (DEN 303) > The spirochaetes > Flashcards

The spirochaetes Flashcards

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1
Q

Definition

A 
Very unusual bacteria:
Gram-negative
Very thin- viewed by dark-field microscopy or EM
Spiral shape
Varied genome size
Many plasmids (large)
Virulence factors poorly understood
Unique method of motility via internal flagella
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2
Q

Properties

A

Anaerobic, fastidious, slow growing

Many difficult to grow or unculturable- T. pallidum

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3
Q

Laboratory diagnosis

A

often relies on serological or immunofluoresence tests

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4
Q

Spirochaete taxonomy

A
  • Recognised by cell shape

- Identification by Sequence analysis of 16s rRNA gene

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5
Q

Cell structure, motility and flagella

A

Inextricably linked
In most bacteria the cell shape is defined by a combination of the peptidoglycan layer and the bacterial cytoskeleton.
For Spirochaetes this is also defined by internal flagella commonly known as axial filaments
Deletion of flagella assembly genes (flaB and flgE) results aflagellate non-motile strains
-these strains are no longer corkscrew-like
-they become straight rod shaped cells.
-occurs for both Treponema denticola and Borrelia burgdoferei

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6
Q

Species identification by 16s rRNA sequencing

A

16s rDNA gene well conserved due to essential function
Acts as molecular clock and species signature as evolves slowly in time
We sequence it to speciate bacteria

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7
Q

How do they swim

A

Counter-rotation of the internal flagella filament bundles results in rotation of the cell body
Rotation of the body results in burrowing motility of spirochaetes

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8
Q

The spirochaete cell surface

A

Cell wall components able to modulate immune response, known as Major sheath proteins (Msp)
No LPS - glycolipids

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9
Q

Spirochaete diseases

A

Leptospira: Weils disease, Leptospirosis
Borrella: Lyme disease, relapsing fever
Treponema: Syphilis, ANUG, periodontitis

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10
Q

Zoonotic infections

A

Both Lyme disease and Weil’s disease are good examples of zoonotic infections (like plague)
They have an animal reservoir of infection that can under certain circumstances infect humans via a zoonotic vector

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11
Q

Zoonotic infections

A

Both Lyme disease and Weil’s disease are good examples of zoonotic infections (like plague)
They have an animal reservoir of infection that can under certain circumstances infect humans via a zoonotic vector

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12
Q

Lyme disease

A

Caused by Borrelia burgdoferi and related sub-species
Most common zoonootic bacterial infection in Europe and North America.
Small spirochete only viewed by EM and Dark-field microscopy
Nutritionally fastidious Anaerobe

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13
Q

Zoonotic reservoir - Lyme disease

A

Transmission via Ixodes spp. Ticks
NOT INSECTS- 8-legs!
Ectoparasites of many vertebrate species: rodents, deer, birds
Three life-cycle stages
Feed once in each stage: 3-5 days per feed
Bacteria live and multiply in midgut of ticks and are transmitted via saliva after biting humans- 36h attachment!

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14
Q

Infection of Humans - lyme disease

A

Rodents –> hard lxodes tick (–> deer)

Tick bite –> infected human, no further spread

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15
Q

Stages of infection of Lyme disease - acute

A

After biting Flu-like symptoms often seen
a localised rash: Erythema migrans present in 30% cases
This is a characteristic bulls-eye rash
Other lesions at sites distal from innoculation occur in 50% of patients

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16
Q

Later stages of lyme disease infection

A

Seen from 1 week to 2 years post-infection:

  • Neurologic: Meningitis, encephalitis, peripheral neuropathy, cranial-nerve (facial) palsies, vision impairment (chronic)
  • Cardiac: myocarditis, blockages
  • Athralgia and arthiritis- may persist for months or years- often debilitating- possible autoimmune component – reactivity to surface proteins (OspA)
17
Q

Causes of later symptoms of lyme disease

A

Caused when bacteria enter sites other than bloodstream - such as neurons and joints

18
Q

Borrelia burgdoferi mechanism/ virulence factors

A

Motility considered a major virulence factor
Invades epithelial cells
Capable of invading many tissue types
No LPS, but numerous Outer membrane lipoproteins OspA-D, expressed at different points in infection cycle. Vls proteins- variable suface proteins- antigenic shift
DbpA- Decorin binding protein, host mimicry?
Copes with low-iron levels by using Manganese instead of iron as an enzyme co-factor

19
Q

Treatment of Lyme disease

A

Long courses of antibiotics
doxycycline
Chronic infections hard to treat since bacteria become metabolically inert and reside in sites refractory to treatment.

20
Q

Prevention of Lyme disease

A

Vaccine:
-to OspA only partly effective: OspA is not expressed by Borrelia in humans, only in the tick.
-some side-effects, also might stimulate autoimmune disease- since many symptoms may be due to autoimmunity
Avoidance of endemic areas
Clothing, DEET based repellents

21
Q

Relapsing fever

A

Borrelia recurrentis
Transmitted via ticks and human body louse
Repeated febrile illness
Initial infection cleared, but antigenic variation by the bacterium starts a new set of symptoms
3-10 episodes
Can infect liver/ spleen

22
Q

How could it relapse?

A

Antigenic variation- surface protein OspC multiple copies- expressed variably in recurring infecitons

23
Q

Prevention and control of relapsing fever

A

CDC: since most cases occur after sleeping in rodent infested cabins- check for mice etc!

24
Q

Leptospirosis and Weils disease

A 
Caused by Leptospira interrogans
Leptos (Gr) – ununusually thin
spira (la)    -   colied, spiral
Two terminal Periplasmic flagella
Present in stagnant water and rivers
Infects many mammals
Dogs and Rats most important zoonotic reservoir (urine)
Enter via broken skin
40- 60 cases/ year in England
Outbreaks in walkers, triathlon runners! (WHY????), but many imported cases
25
Q

Symptoms of leptospirosis and Weil’s disease

A

1-2 week incubation in blood
Leptospirosis: Febrile, flu-like illness with muscle pain, reddening of eyes, and other symptoms such as diarhoea and in some cases meningitis and Hemorrhage in Aqueous humour of eye and CSF
10-15% of cases develop Weil’s disease:
-kidney failure
-jaundice and liver failure
Most symptoms caused by damage to blood vessels

26
Q

Prevention and treatment of leptospirosis and Weil’s disease

A

Rodent control
Doxycycline
Avoid swimming in infected rivers

27
Q

ANUG

A

Acute necrotisinig Ulcerative Gingivitis
‘Trench Mouth’ or Vincents disease
Was common in WW1 soldiers
Thought to be caused by bacterial complex involving oral spirochaete Treponema Vincentii (but not just that)
Treated by metronidazole or Hydrogen peroxide washes

28
Q

Treponema denticola, red complex organisms and periodontitis

A

These three organisms are the most commonly found bacteria in periodontal cases.
-together contribute to the symptoms seen
P gingivales, T. forsythia, T. denticola

29
Q

T. denticola: virulence

A

Adherence to basement membrane proteins via 53 Kda Msp : fibronectin, laminin, fibrinogen, type IV collagen and gelatin
Proteases, sialidases, motility, co-adherence

30
Q

Proteases (T. denticola)

A

In-keeping with other periodontal pathogens
CTLP- Chymotrypsin like Protease (Dentilisin), surface exposed in outer membrane: Cleaves transferrin, fibrinogen, fibronectin, IgA, IgG, gelatin

31
Q

Sialidases (T. denticola)

A

Cleaves surface sialic acid from human cells/ saliva- mutant reduced infection in mice

32
Q

Motility (T. denticola)

A

might also contribute to tissue invasion and disease progression

33
Q

Co-adherence (T. denticola)

A

with other oral bacteria in mixed biofilm also important (i.e. Pg, Tf, and Fuso’s)

34
Q

Syphilis: T. pallidum

A

Major venereal disease for at least last 600 years
Originally known as the ‘french disease’ (morbus gallica) – 1495… french army
Modern name coined by Italian poem in which boy is punished by god
Treatment with Mercury
‘ A night in the arms of Venus leads to a lifetime on Mercury’

35
Q

Other treponemal diseases

A 
Yaws: T. pertenue 
- early skin lesions that clear
- later destrucitive lymph and 	bone
- south america and central africa
Pinta: T. carateum 
- again early skin lesions
- these progress to chronic disfiguring lesions over time
- south and central america
Skin- to- Skin transmission
-treatable with penicillin

Microbiology (DEN 303) (8 decks)

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