Section 4: Spirochetes Flashcards

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1
Q

What are Spirochetes

A

They are thin, helical, Gram negative bacteria

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2
Q

What are the 3 genera of spirochetes responsible for human disease

A

Treponema, Borrelia, and Leptospira

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3
Q

What is the more common name for Treponema pallidum

A

Syphilis

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4
Q

What is the epidemiology for Treponema pallidum

A
  • Transmission is by contact with mucous membranes. Sexually transmitted.
  • Microbe can also be transmitted in blood
  • A reportable condition
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5
Q

What is the pathology of Treponema pallidum

A
  • Treponema pallidum enters the body by penetrating mucous membranes
  • Immediately begin moving through body via blood and lymph vessels
  • Incubation period= 2-3 weeks
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6
Q

What is the characteristic of Primary syphilis

A

lesion is a chancre

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7
Q

What is a chancre

A
  • Hard, painless
  • Mostly found on genitals, I 0% not
  • Highly infectious, filled with T. pallidum
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8
Q

What is Secondary Syphilis

A
  • Between 6 weeks to 5 years later the bacteria multiply and spread throughout the body
  • Secondary is systemic; widespread rash, swollen lymph nodes and flu-like symptoms= “great imitator”
  • Most infectious stage, “kissing disease”
  • Skin rash
  • Condylomata lata
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9
Q

What is tertiary syphilis

A

Develops 5-40 years following initial infection in 1/3 oflatent cases

  • Typical presentation= gummas, destructive lesions= necrosis of tissue
  • Painless on skin, painful in organs and bone
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10
Q

What is cardiovascular syphilis (tertiary)

A

Occurs in 10% of patients
• Involves destruction of heart and blood vessels, aneurysms
• Typically inflammation of aorta, valve involvement

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11
Q

What is neurosyphilis

A

Occurs in 8% of patients
• Syphilitic meningitis
• Organisms attack blood vessels in brain and meninges resulting in cerebrovascular occlusions and death of nerve tissue in the brain
• Tabes dorsalis
• General paresis (of the insane)= paralytic dementia

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12
Q

What is Tabes Dorsalis

A
  • Degeneration of the posterior columns of spinal cord and dorsal roots
  • Incoordination (ataxia), sensory difficulty
  • Charcot’s joint-destructive joint disease caused by diminished proprioceptive sensation, with gradual destruction of the joint by repeated subliminal injury
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13
Q

What are other pathologies of Syphilis

A
  • Bone infection
  • Periostitis-inflammation of the periosteum
  • Saber shin = periosteal inflammation of tibia leading to bowing
  • Infection of skin, eyes
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14
Q

What is congenital syphilis

A
  • Infection of the fetus via placenta
  • T pallidum rapidly disseminates throughout fetus
  • T pa/lidum does not cross and damage fetus until the fourth month of gestation, if treated prior, child born free of syphilis
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15
Q

What are possible outcomes of congenital syphilis

A
  • High mortality rate (stillbirth, spontaneous abortion)
  • Infant has secondary syphilis
  • Infant is healthy, develops disease years later
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16
Q

What are symptoms of early congenital syphilis

A
  • Occurs within 2 years of birth
  • Runny nose, “snuffles”
  • “Blueberry muffin” rash= raised vesicles (different then Jim’s muffin top)
17
Q

What are the symptoms of late congenital syphilis

A
  • Similar to adult tertiary syphilis (rarely cardiovascular)
  • Neurosyphilis results in impaired hearing and sight
  • Bone and teeth destroyed-Hutchinson’s teeth
  • Saber shin
  • Saddle nose -no bridge in nose
18
Q

How is syphilis T. Palladium diagnosed

A

Dark-field microscopy
Fluorescent antibody microscopy
Serological Tests for Syphilis (STS

19
Q

What is the Jarisch Herxheimer reaction

A
  • Acute worsening of symptoms after beginning antibiotics
  • Symptoms = fever, chills, headache, malaise
  • Due to the release of endotoxin from killed T. pallidum
  • Self-limiting in 12-24 hours
20
Q

What is Treponema pertenue

A
  • Causative agent ofYaws
  • Restricted to the tropics
  • Transmission occurs through nonsexual human-to-human contact
21
Q

What is the pathology of Treponema pertenue

A
  • Primary lesion, or mother yaw, develops within 2 to 4 weeks at the site of skin entry as a painless erythematous papule or group of papules
  • Treponemes disseminate in 1 to 12 months, secondary lesions appear, similar to the mother yaw
  • Secondary lesions develop initially on the face and moist areas of the body and then spread to the trunk and arms
  • infection of the soles and palms is characteristic
  • Late destructive stage involves treponema! infection of the bones and periosteum, especially the long bones of legs and forearms, and the bones of the feet and hands
22
Q

What is Treponema carateum

A
  • Causative agent of Pinta
  • Purely a skin disease
  • Transmission occurs through human-to-human nonsexual contact
  • Limited to South America
  • Infection is by direct contact, red lesions that tum blue in the sun
  • Lesions then become depigmented, turning white
23
Q

What is Treponema vincentii

A
  • One of the causative agents of Vincent’s angina (aka Trench mouth)
  • Lesions of gingiva (gums)
24
Q

What is another name for Borrelia

A

Relapsing fever

25
Q

How is relapsing fever spread

A

lice and ticks

26
Q

What is the pathology of borrelia

A

Lesions on internal organs (liver, spleen)
-High fever 4-5 days
-Fever disappears, returns 7-10 days later
• Tick borne = relapses average = 3
• Louse borne= more than 10
-Find spirochetes in blood (spirochetemia)

27
Q

What is Borrelia burgdorferi

A

First recognized in 1975 in Lyme, CT

• Borrelia burgdorferi recognized as cause of Lyme disease in 1982

28
Q

What is the epidemiology of Borrelia burgdorferi

A

transnsmitted primarily by the deer tick (Ixodes) in the nymph stage oflife cycle-(black legged hard ticks)
-B. burgdorferi is iJ1jected by the tick in saliva or by regurgitation of tick’s midgut contents .

29
Q

What is the primary stage of Borrelia burgdorferi

A

skin lesion “bulls eye” or target shaped 3 days to 4 weeks following tick bite

30
Q

What is the secondary stage of Borrelia burgdorferi

A

erythema chronicum migrans (ECM)-often appears at the site of the infecting tick bite. It is a red, enlarging rash, flat or slightly raised, and may reach from 4 to 20 inches across

31
Q

What is the tertiary stage of Borrelia burgdorferi

A
  • Meningoencephalitis
  • Myocarditis
  • Musculoskeletal pain
  • Chronic arthritis
32
Q

What is leptospira

A
  • Fine, coiled spirochete
  • Hooked on each end
  • Highly motile
  • Cultured in lab
33
Q

What is the epidemiology of leptospira

A

-Worldwide distribution
-Fewer than 100 cases/year in U.S.
-Reservoirs of infection
• Dogs, rodents, domestic/wild animals
• Bacteria persist in the kidneys of animals, found in urine
• Contaminate soil and water

34
Q

What is the pathology of leptospira

A

-Bacteria penetrate mucous membranes and invade blood and eventually vanous organs
-Experience chills, fever, headache, muscle pain
-Some strains cause Wei!’ s disease or infectious jaundice
• Renal failure, hepatitis with jaundice, mental status change and hemorrhage in various organs.
• Up to 25% mortality