spirochetes

Question 1

1. Define the major characteristics of spirochetes? How are they different from other bacteria?

Answer 1

Gram negative corkscrew shaped bacilli. Do NOT have endotoxin (LPS). • They have endoflagella (axial filaments) in their periplasmic space. The endoflagella begin at each end of the organism and wind around it, extending to and overlapping at the midpoint.

Question 2

List the types of spirochetes

Answer 2

From the family treponemataceae: Treponema, Borrelia, and Leptospira.

Question 3

Treponema growth characteristics

Answer 3

Treponema reproduce by transverse fission. • Pathogenic Treponema pallidum (e.g. those that cause syphilis) cannot be cultured continuously on artificial media, in embryonated eggs or in tissue culture. T. pallidum will remain motile for 3-6 days at 25°C in 1-4% oxygen in a special broth medium.

Question 4

Leptospira growth characteristics

Answer 4

Grows aerobically at 28-30C. Uses long chain fatty acids as energy source and urea as nitrogen source

Question 5

List the diseases caused by treponema

Answer 5

T. pallidum subsp pallidum: causes syphilis. T. pallidum subsp pertenue: causes yaws. T. pallidum subsp endemicum: causes endemic syphilis or bejel. T. carateum: causes pinta

Question 6

Pathogenesis of syphilis

Answer 6

3 week incubation period > primary syphilis (2-6 weeks) > asymptomatic period (2-24 weeks) > secondary syphilis (2-6 weeks) > latent syphilis > asymptomatic period (3-30yrs) > tertiary syphilis

Question 7

During which stages of syphilis is the infection transmissble

Answer 7

primary and secondary syphilis are transmissible by blood products and lesions are highly infectious. During latent and tertiary syphilis infection is NOT transmissible by blood and lesions are caused by immune mediated destruction of tissues

Question 8

What percent of pts with syphilis will develop tertiary syphilis and how many of those will die?

Answer 8

30% of untreated patients develop tertiary syphilis and 25% die of this disease

Question 9

Which Sx of syphilis are due to cell mediated hypersensitivity vs invasion

Answer 9

invasion: neurosyphilis, Tabes, and cardiovascular. Cell mediated: gummas in skin bones and liver and cardiovascular syphilis

Question 10

describe primary syphilis

Answer 10

characterized by one or more chancres (ulcers) which may be located anywere on the body, even oral cavity. Regional lyphadenopathy (painless) • Demonstration of T. pallidum in clinical specimens by darkfield microscopy, direct fluorescence antibody (DFA-TP), or equivalent methods. serologic tests may not be positive during early primary syphilis

Question 11

describe development of a chancre

Answer 11

Progresses from macule to papule to ulcer. Typically painless, indurated, and has a clean base. Highly infectious. Heals spontaneously within 3-6 weeks

Question 12

describe secondary syphilis

Answer 12

localized or diffuse mucocutaneous lesions, generalized lymphadenopathy, malaise, alopecia,condylomata lata, liver/kidney involvement possible, splenomegaly possible. primary chancre may still be present. • Demonstration of T. pallidum in clinical specimens by darkfield microscopy, direct fluorescence antibody (DFA-TP), or equivalent methods

Question 13

When are serologic tests for syphilis highest in titer

Answer 13

secondary syphilis

Question 14

describe latent syphilis

Answer 14

A stage of infection in which organisms persist in the body without causing symptoms or signs. Only evidence is a positive serologic test. May occur btw 1 and 2 stages, btw 2 and relapses or after 2 syphilis. Early latent 1 yr

Question 15

describe neurosyphilis

Answer 15

Evidence of central nervous system infection with T. pallidum. Meningitis, ocular involvement and possibly paresis, tabes dorsalis. A reactive serologic test for syphilis and reactive VDRL (Venereal Disease Research Laboratories) in cerebrospinal fluid.

Question 16

describe Late benign syphilis and cardiovascular syphilis

Answer 16

Inflammatory lesions of the cardiovascular system, skin, and bone. Gummatous lesions. Upper and lower respiratory tracts, mouth, eye, abdominal organs, reproductive organs, lymph nodes, and skeletal muscle may be involved. • Demonstration of T. pallidum in late lesions by fluorescent antibody or special stains, although organisms are rarely visualized in late lesions

Question 17

Congenital syphilis

Answer 17

Infection in utero with T. pallidum- hepatosplenomegaly, rash, condyloma lata (wart like lesions on genitals), snuffles, jaundice, pseudoparalysis, anemia or edema (nephrotic syndrome and/or malnutrition) Older children >2 may have stigmata -interstitial keratitis, nerve deafness, anterior bowing of shins, frontal bossing, mulberry molars, Hutchinson teeth, saddle nose, rhagades, or Clutton joints

Question 18

describe stillbirth syphilis

Answer 18

A fetal death that occurs after 20-week gestation or in which the fetus weighs greater than 500 g and the mother had untreated or inadequately treated syphilis

Question 19

syphilis immunology

Answer 19

Humoral response is not very protective but useful for diagnosis. T cell response is important in immunity to reinfection and protection against tertiary syphilis. Probably responsible for some of the damage in 3 syphilis like gummas

Question 20

darkfield examination for syphilis diagnosis

Answer 20

A drop of tissue fluid or exudate is placed on a slide and examined with a light. This is still used for the diagnosis of primary syphilis because the antibody based tests may not yet be positive because it takes about 2 weeks for a person to develop antibodies against an antigen.

Question 21

Syphilis immunofluorescence

Answer 21

Detection of T. pallidum from specimens using fluorescein-labeled anti-treponema serum

Question 22

List the two types of serological tests for syphilis

Answer 22

Nontreponemal antigen tests and Treponemal antibody tests

Question 23

describe the nontreponemal antigen tests

Answer 23

Uses reagin, a mixture of cardiolipin, lecithin, and cholesterol which cross-reacts with IgM and IgA antibodies produced by host if infected with T. pallidum. If the host has been infected with T. pallidum, their antibodies react with reagin causing agglutination. VDRL test is read with microscope and RPR test is visible to naked eye

Question 24

When are antibodies against T. Pallidum found in serum and CSF

Answer 24

antibodies are found in the serum of patients after 2-3 weeks of untreated syphilis infection and in spinal fluid after 4-8 weeks of infection

Question 25

Describe treponemal antibody tests

Answer 25

FTA (fluorescent treponemal antibody): Uses killed treponema organisms to generate anti-human IgG or IgM antibodies which are then added to patient serum.

Question 26

treponema transmission

Answer 26

direct personal contact among humans. An infected person may remain contagious for 3-5 years during early syphilis. Syphilis is very, very unlikely (i.e. it does not happen, except perhaps in someone’s imagination) to spread through contact with toilet seats, doorknobs, swimming pools, hot tubs, bathtubs, shared clothing, or eating utensils.

Question 27

Syphilis rates in US

Answer 27

Has doubled since 2005

Question 28

Syphilis treatment and prevention

Answer 28

condoms. Penicillin is drug of choice, unless pt is allergic then use azithromycin. Some azithromycin resistance is emerging in gay men though

Question 29

Herxheier reaction

Answer 29

Complication of penicillin-fever, headache, sweating, tachycardia, exacerbation of syphilitic lesions occurring ~6-12 hrs after penicillin therapy. due to a cytokine response to the release of treponemal antigens. Its symptoms can be highly variable (very mild to severe)

Question 30

Who gets the Jarisch-herxheimer reaction

Answer 30

­The reaction can be expected in 50% of primary syphilis, 90% of secondary syphilis, and in 25% of early latent infection, but is very rare in late syphilis. It may be more severe in patients with HIV

Question 31

describe Yaws- who gets it, sx, etiology

Answer 31

Caused by T. pallidum subsp pertenue. Endemic in human/tropical countries, esp in children. Ulcerating papule on leg or arms. Scar formation of skin lesions and bone destruction common. Cross immunity btw yaws and syphilis

Question 32

describe Endemic syphilis or Bejel- etiology, sx, who gets it

Answer 32

It is caused by T. pallidum subsp. Endemicum. Prevalent, mostly among children, in Africa, Middle East, and Southeast Asia. Skin lesions

Question 33

Describe Pinta- etiology, sx, who gets it

Answer 33

Caused by T. carateum. Endemic in Mexico, Central and South America, the Philippines. Restricted to dark skinned races. nonulcerating papule, which progress to a flat, hyperpigmented lesion. Depigmentation and hyperkeratosis appear years later

Question 34

Leptospirosis - etiology, Sx

Answer 34

Leptospirosis is caused by Leptospira interrogans. Fever (due to bacteremia). Infect the liver and kidney, producing hemorrhage and necrosis of tissue causing dysfunction of these organs: jaundice, hemorrhage, and nitrogen retention. Second phase when IgM titer rises manifests as aseptic meningitis

Question 35

Leptospirosis transmission

Answer 35

Ingestion of contaminated water or food. Organism is shed in urine and remains viable in stagnant water for weeks. Rarely enters through mucus membranes or breaks in skin

Question 36

Leptospirosis diagnosis

Answer 36

Darkfield examination of a blood smear or urine specimen. Culture of the organism from the blood or urine. Unlike T. pallidum it can be grown on artificial media. Agglutination test – patients serum will agglutinate

Question 37

Leptospirosis treatment

Answer 37

Penicillin and tetracycline have some therapeutic effect, but do not eradicate the infection. Doxycycline has marked prophylactic efficacy