Your SlideShare is downloading. ×
Spirochetes
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Spirochetes

506
views

Published on

Published in: Health & Medicine, Technology

0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total Views
506
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
45
Comments
0
Likes
0
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. INFECTIOUS DISEASE OF PATHOLOGY (Bacterial Diseases) Spirochetes Dr. Naila Awal (Postgraduate student)
  • 2. Spirochetes with their diseases 1)Treponema pallidum- Syphilis Non veneral treponemotoses 2)Borellia recurrentis- Relapsing fever Borellia burgdorferi- Lyme disease 3)Leptospira- Leptospirosis
  • 3. Treponema pallidum • Pathogenesis• • • • • Agent- Treponema pallidum Host-Human Disease- Syphilis Reservoir- Patient of syphilis Source of infection- Primary syphilis- Exudate of ulcer containing bacteria Secondary syphilis- Muco cutaneous rash Blood- for both primary & secondary.
  • 4. • Mode of transmission1)Acquired syphilis Sexual contact Blood 2)Congenital syphilis From mother- fetus
  • 5. Primary syphilis • T.pallidum can not penetrate intact skin. They enter into the body through abraded skin invade locally into blood vessels & lymphatics multiply within 3-4 weeks they produce local lesion. Papule macule vesicle (fluid accumulates) vesicle rupture painless ulcer Hard chancre (Hallmark) This is highly contagious stage. Within next 24weeks, ulcer heals spontaneously.
  • 6. Secondary syphilis • It is the disseminated stage of the disease. • 4-8 weeks after healing ulcer, patient develop maculopapular rash involving all over the body including palm & sole ( characteristics) • When the lesion occurs in the moist area, peri anal region condylomata lata ( Hallmark)
  • 7. Tertiary syphilis • It occurs 3-4 yrs after. • Manifestation1) Cardiovascular syphilis- Aneurysm, Aortic regurgitation. 2)Neurosyphilis –Chronic meningovascular disease, tabes dorsalis & generalized paresis. 3) Gumma- Skin, Bone
  • 8. Latent Syphilis • Here the patient is infected with the bacteria but he/she is asymptomatic. The serological test is positive. • Types-2 Latent syphilis Early latent (within 2yrs) Late latent (3-4yrs after) May progress to tertiary syphilis
  • 9. • Clinical significance1)In early latent patient ,patient remains infectious but in late latent patient becomes non- infectious. 2)It is very dangerous condition. • Confirmation1) Patient have no S/S 2)Serological test positive
  • 10. Congenital syphilis • Definition- Syphilis that are transmitted from mother to fetus when mother is attacked byprimary & secondary syphilis rarely in latent syphilis • Transmission occurs after16th weeks of pregnancy b/c of atrophy of syncytiotrophoblast layer.
  • 11. S/s • Infantile syphilsChorioretinitis Desquamating skin rash Viseral & bone changes Osteochondritis, Periostitis Hepatic & pulmonary fibrosis • Late congenitalNotched central incisor teeth Intestitial keratitis Deafness(8th nerve damage) Hutchinson traid
  • 12. Diagnosis • Just after delivery,if mother is untreated with penicillin, both VDRL & TPHA of baby & mother will be done. Mother VDRL- 1:4 TPHA- 1:4 Baby 1:16 1:4 • So 1 month afterVDRL- 1:4 1:4 Comment Baby is infected May be it comes from mother /produced by the baby. 1:8 1:2 Form within the baby Comes from mother.
  • 13. Diagnosis • SampleA)Exudate- from primary chancre B)Serum • Lab procedureA) Exudate1)Dark field microscopyBright ,slender, spiral bacteria with crock-screw & flexion-extension motility 2) Immunofluroscence microscopy
  • 14. 3)Staining a)Silver staining- Fontena’s stain Warthin starry staining b)Immunofluroscence staining- I/F dye is tagged with anti-treponemal Ab.
  • 15. Warthin starry stain
  • 16. B) Serum(serological test) • 1)Non specific testI)VDRL II)RPR (Rapid plasma reagin) • Now-a-daysIII)UST (Unheated serum test) IV)TRUST (Tolludin red Unheated serum test)
  • 17. • SpecificTPHA (Treponema pallidum haemagglutination) TPI (Treponema pallidum immobilization ) IgM FTA-Abs (Fluorescence treponemal Ab absorption test)
  • 18. Histopathology Primary syphilis• Surface of the ulcer- Treponema are visible in warthin starry and Immunofluroscence staining. • Chancre contains infiltration of plasma cells with scattered macrophages & lymphocytes and a proliferative endarteritis.
  • 19. Secondary syphilis • Mucocutaneous lesion shows infiltration of plasma cell & obliterative endarteritis. Tertiary syphilis• GummaCenter- Coagulative necrosis Margin- palisading macrophages & fibroblasts surrounded by mononuclear leukocytes chiefly plasma cells. Treponema are scanty in gumma .
  • 20. VDRL • Advantage1)Very simple 2)Can be done in field level 3)The result may be quantitive & qualitative. 4)The test is sensitive 70% in primary syphilis & 98% in secondary syphilis. 5)Neurosyphilis can be diagnosed. • Disadvantage 1)The Ab against Tp takes about 3-5 weeks times to become appear. So before 3-5 weeks it will show false negative. 2)May give false positive.
  • 21. TPHA • Advantage1)Very simple 2)Can be done in field level 3)The result may be quantitive & qualitative. 4)TPHA is very sensitive 5) It detects specific Ab. 5)Can detect neurosyphilis & latent syphilis. • Disadvantage Once become positive, remains positive for long time even in cured patient.
  • 22. Neurosyphilis • Lab DiagnosisSpecimen- 1)Serum 2)CSF Lab test1)Serum• TPHA- must be positive • VDRL-Reactive/ Non reactive 2)CSF• TPHA- positive • Cell count-lymphocytosis • Protein-Increase.
  • 23. Serological problem in syphilis positive HIV 1)Confusing clinical s/s 2)Lack of serological response 3)VDRL,TPHA- non reactive 4)Due to CD4 & CD4:CD8Tp Ab takes long time to disappear. 5) May be high Ab titer due to B cell activation.