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Microm 442 > Lecture 17 Spirochete > Flashcards

Lecture 17 Spirochete Flashcards

1
Q

What are all the types of Spirochaetaceae?

A
  • Spirochaeta (water, marsh, springs)
  • Cristispira (mollusks)
  • Treponema (termites)
  • Borrelia (Lyme disease)
  • Leptospira (Free-living)
  • Brachyspira (dysentery in pigs, chickens, human intestine)
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2
Q

What are the families of Spirochetes?

A
  • Spirochaetaceae
  • Leptospiraceae
  • Brachyspiraceae
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3
Q

What are the pathogenic spirochetes?

A
  • Treponema (syphilis, periodontal disease, normal flora)
  • Borrelia (lyme disease, relapse fever)
  • Leptospira (leptospirosis)
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4
Q

What is the structure of spirochetes?

A

• Corkscrew shaped
• The genera vary in terms of length and thickness;
Leptospira have hooked ends
• Lipid-rich outer membrane covering periplasmic flagella; thin peptidoglycan layer covering cytoplasmic membrane

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5
Q

Which pathogenic spirochetes have small genomes?

A

-Borrelia, Treponema pallidum

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6
Q

Borrelia has what type of DNA structures?

A
  • linear chromosome

- linear and circular plasmids

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7
Q

What are Leptosira chromosomes like?

A

-2 circular chromosomes

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8
Q

Which pathogens have high genetic variability?

A
  • Borrelia

- Leptospira

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9
Q

What is unique to Treponema pallidium?

A

Cannot be grown in vitro, has high G+ C in comparison to other spirochetes

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10
Q

Which organisms cause Relapsing fever?

A

–Borreliarecurrentis: louse-borne

–Borreliahermsii: tick-borne

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11
Q

What are the habitats for Relapsing fever causing organisms?

A

–Tick-borne: Reservoirissquirrelsandothersmall
rodents.
– Louse-borne: Person-to-person transmission via louse. No known animal reservoir.

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12
Q

How is relapsing fever transmitted?

A
  • Tick borne (B. hermisii) infects tick tissues, infects human by sailiva or feces during bite
  • Louse borne (human infection) no invasion of louse tissue. Humans are infected by hemolymph when tick is crushed
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13
Q

What is the clinical course of relapsing fever?

A

• Incubation period: 7 days
• Sudden onset of fever (40oC), headache, pain
in muscle, bones, joints
• Recurrent periods of fever (spirochetemia: 107-8/ml blood), interrupted by afebrile periods

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14
Q

What is the pathogenesis of relapsing fever?

A
  • Gene conversion and antigenic variation.
  • New serotypes appear, each new one overgrowing due to the selective advantage against the old serotypes (antibodies made for old)
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15
Q

How do relapssing fevers utilize antigenic variation?

A

• Classic example of antigenic variation of surface variable membrane proteins (21-39 Kd)
• Vmp’s are now divided into Vlp and Vsp; ~30 genes.
They are located on a linear plasmid and are silent, through gene conversion they recombine.

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16
Q

What makes Borrelia so invasive?

A

-It can infect many tissues and organ systems, including the central nervous system (vsp allele)

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17
Q

What is dx and rx of Relapsing fever?

A 
• Clinical features
• Blood films during fever crises - large
numbers of spirochetes in blood 
• Treatment
–Penicillins, tetracyclines
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18
Q

Which organisms cause Lyme disease?

A

◦ Borrelia (Borreliella?) burgdorferi – high heterogeneity in outer surface proteins: OspA, OspB, OspC
◦ Other related Borrelia species identified: B. garini, B. afzeli, B. lonestari (?)

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19
Q

What is the habitat for Lyme disease causing organisms?

A

– Major reservoir in nature is in small rodents,
deer
– Transmitted to humans via tick bite (incidental infection)

20
Q

How is lyme disease transmitted?

A
  • Transmitted by Ixodes ticks
  • Human infection usually occurs by bite of a nymph looking for a blood meal
  • Prevalence of infected ticks: varies by geographic region
21
Q

What is the pathogenesis of lyme disease?

A
  • Injected into skin from tick saliva
  • Slow transmission to mammal—>24 hours
  • Different antigens expressed in tick versus mammal (more OspC in mammals)
22
Q

What occurs once the lyme disease pathogen is in the body?

A

• Organism is very invasive, reaches blood stream and disseminates to many organs, including central nervous system
• Persistent, chronic infection
due to antigenic variation

23
Q

What is the clinical course for Lyme disease?

A
  1. Eyrthema chronicum migrans (ECM) and secondary lesions
  2. Neurologic and cardiac abnormalities (HA, stiff neck, conjunctivitis, muscle pain weeks to months after)
  3. Arthritis (weeks to year, intermittent or chronic)
24
Q

How is Lyme disease dx?

A
  • Physical exam - (ECM or hx)
  • biopsy (cx or staining)
  • serologic test-not reliable
  • DNA detection - PCR
25
Q

How is lyme disease treated?

A
  • Penicillin, ceftriaxone, tetracyclines
  • Treatment of ECM is effective
  • Later treatment may not be successful: chronic inflammation in absence of bacteria (Autoimmunity?)
  • New evidence for persistence of viable Bb after antibiotic treatment
26
Q

What is syphilis?

A

-Disease caused by Treponema pallidum
• Chronic bacterial infection, sexually
transmitted
• Early manifestations involve primarily skin
• Late manifestations involve virtually all organs and tissue sites

27
Q

What is the shape of Treponema pallidum?

A

– Corkscrew-shaped, microaerophilic, noncultivable bacterium, 10-14 μ in length, 0.5 μ in diameter

28
Q

What is the habitat for Syphilis organism?

A

• Habitat

— Human only (? higher primates)

29
Q

What is important about the metabolism of Treponema pallidum?

A

— Highly dependent on host cells
— No pathways for synthesis of fatty acids,
nucleotides, amino acids
— No Kreb’s cycle, no respiratory electron
transport chain

30
Q

How is syphilis transmitted?

A
  • Direct, usually sexual (infectious at 1 or 2 stage)
  • Highly invasive, gains access to blood stream and disseminates (CNS included)
  • May also cross placenta to cause congenital syphilis
31
Q

What is the natural history of untreated syphilis?

A
  • Infection (incubation 2-4 weeks)
  • Primary (heals spontaneously)
  • secondary (rash, enlarged lymph nodes of body
  • Latent (lead to lifetime latency or tertiary)
  • Tertiary (aortic destruction, Gumma, CV syphilis, tabes dorsalis, paresis)
32
Q

What is congenital syphilis?

A
  • infection of fetus during pregnancy

- Results in prematurity, spont abortion, stillbirth, neonatal or death, latent infection

33
Q

What is the pathogenesis of syphilis?

A
  • immune response clears primary and secondary lesions, but not systematically
  • lifelong, chronic if untreated
  • maybe identify surface proteins
  • Some putative OMPs bind fibronectin, laminin, fibrinogen
34
Q

What accounts for the persistent secondary stage of syphilis?

A

-TprK
-7 variable regions
-evade immune system
0antigenic variation by gene conversion
-one expression site, more than 50 variable

35
Q

How is syphilis dx?

A
  • dark field microscopy
  • no cx possible
  • PCR, RT-PCR not commercially available
  • Serological testing
36
Q

How is syphilis treated?

A
  • Penicillin –first line
  • Alternatives: Doxycycline, tetracycline
  • Macrolides – recently discovered resistance
37
Q

What organism causes Leptospirosis?

A

–Leptospira interrogans
–Many strains have been described
–Taxonomy is unclear
–Pathogens considered to be one species with up to 300 serovars

38
Q

What is the habitat of Leptospirosis?

A 
• Most widespread zoonosis in the world
• Animal reservoir
• Both domestic and wild animals
• Infection rate in raccoons, opossums,
skunks ranges from 10-50%
• Change in epidemiology – urban slums with rats
39
Q

How is Leptospirosis transmitted?

A

Leptospirosis: Transmission
• Source of infection is water contaminated with the infected urine of “carrier” animals
• Portal of entry is skin, mucous membranes
• Teenagers, young adults at highest risk of
infection
• Carrier state persists for months to years
• Even in inapparent infection, bacterial load may reach 1010/gram of tissue in kidneys

40
Q

Leptospirosis infection is..

A
  • highly invasive

- disseminates to infect multiple organisms

41
Q

What are clinical outcomes of leptospiral infection?

A

Few- complex, multi-system disease
Some- undifferentiated fever
Most- inapparent infection

42
Q

What are some complex Leptospiral infections?

A 
Aseptic meningitis
Renal failure
Jaundice
Myocarditis
Pulmonary hemorrhage Refractory shock
43
Q

What is the clinical course of Leptospirosis?

A

• 7-10 day incubation period
• Sudden onset of fever (spiking), severe
myalgia, headache
• Bacteria present in blood, CSF, urine
• Usually self-limited, but can be protracted and severe

44
Q

How is Leptospirosis dx?

A

• Culture:
Blood, CSF - Early
Urine - Chronic • PCR is available
• Serology: Useful in later infection

45
Q

How is Leptospirosis treated?

A
  • Penicillin, doxycycline, erythromycin
  • 7% mortality overall, higher in older persons
  • 15-48% mortality for icteric form

Microm 442 (16 decks)

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