Spirochaetes

Kingdom II: Bacteria Section XXV: The Spirochetes Phylum X: Spirochetes Class I: Spirochaetes Order I: Spirochaetales Famil I: spirochaetaeceae (9 genus) Genus I: borrelia (30 spp.) Genus IX: Treponema (18 spp) Family III: Leptospiraeceae Genus III: Spirochaeites* Family: Spirochaetaceae Genus Treponema Borrelia Leptospira

Genus: Treponema Spp T.Pallidum ssp. T. Pallidum -> Syphilis - T. Pallidum ssp. Pertenue T. Pertenue -> Yaws - T.pallidum ssp. Endemicum T.Endemicum 0> BEJEL (Endemic syphilis) T. arateum -> Pinta T. Vincentii (Vincent s spirilium) -> Vincent s angina (ulcero membranous gingivitis) Normal flora, but numbers increase in acute necrotizing gingivitis and chronic adult periodontitis (opportunistic) = T. denticola, T. soceanskii, T. Pectinovorum SPIROCHAETES

-

Slender unicellular HELICAL or SPIRAL rods Cytoplasm surrounded by cytoplasmic membrane and peptidoglycan layer -> Rigid shape In treponema spp. Fine cytoplasmic filaments (+) on EM Borvelia : (-)

Both:Motile (very active) Several flagella attached to each pole of cell, wrapped around bacterial cell body Flagella DO NOT PROTRUDE INTO SURROUNDING MEDIUM but enclosed within outer membrane ? Capsule (+) Gram stain: Not stainable! (So we assume them as Gram negative) Pathogenic treponemes do not grow in artificial media (so we subculture in animals)

SYPHILIS Etiology: Teponema pallidum Family: Spirochaetaeae Genus: Treponema Species: T. pallidum ssp. Pallidum Causative agent for SYPHILIS 1905: First isolated from syphilitic lesion Infection: i. Sexual contact = usually ii. Congenital syphilis (vertical transmission) iii. Neonatal syphilis iv. Transfusion (Rarely)

Pathogenesis If left untreated: Primary -> Secondary -> latent -> Tertiary (late) Enter tissue penetrate through abraded skin or intact mucosa --move to-> lumphatics -> disseminated.

- Also hematogenous spread - Initial entry site -> chancre (primary syphilis) i. Usually single, painless ii. with border, [looks clean (Prof Nasa)] iii. base induration

iv. Common sites: foreskin, coronal sulcus, vulva, fourchette, uterine cervis, penile shaft v. 5% ectragenital (lips, mouth, etc.) Incubation period: 18-21 days

-

Chancre usually heals spontaneously within 3-6 weeks SECONDARY SYPHILIS 2-12 weeks later -> Symptoms (+) Highly variable & widespread Usually skin: macular or pustular lesions at trunk or extremities (including palm + soles too!) Serpiginous mouth ulcers Flat warty lesions of perineum (condyloma lata) Sestemic (meningitis, arthritis, patchy alopecia, iritis, retinitis)

LATENT SYPHILIS Period with NO CLINICAL MANIFESTATIONS May persist for years

TERTIARY (LATE) SYPHILIS May occur years/decades after primaty infection 3 most common forms a. Neurosyphilis b. Cardiovascular syphilis ( Bovine heart ) c. Gummatous syphilis Pathogenesis: Autoimmunity??

-

T.PALLIDM - First isolated from syphilitic lesion in 1905 - Causes one of the >30 sexually transmitted diseases - Tightly coiled helical rods - 5-15 microm long x 0.1 0.5 microm in m - highly motile Dx: Direct darkground microscopy IF Serology (serological tests for syphilis Non-Specific: i. VDRL (Venereal disease research laboratory) the antigen used is cardiolypin. Useful as a screening test. A lot of false positive reactions because it is non specific. People

who are pregnant can be VDRL positive. Also, some autoimmune diseases are VDRL positive. After screening, do a more specific test Specific: i. ii. iii. TPHA (T.pallidum haemagglutination test) usually use turkey s RBC because it is a huge cell. FTA-Abs (flourescein treponema antibody absorption test) TPI (treponema pallidum immobilization test) Antibodies will immobilize the moving organism. [ It s a hassle Prof Nasa ]

Rx: Penicllin Allergic Erythromycin, chloramphenicol, tetracycline Procaine peniclline Benzyl penicillin

Non-pathogenic spirochaetes (free living or saprophytes) T. Buccalis Macrodentium Microdentium Genitalis - genitals Pseudopallidum - genitals B.Refringens B. Phagedenis Zuelzerae (free living in mind) Lab strains: (Used in TPI) T. Reiter s strain Boguchi Kroo Nicol BORRELIA Family: Spirochaetaceae

Genus: Borrelia Spp: - Borrelia recurrentis & some other B -> Relapsing fever - B. burgdorferi -> LYME disease RELAPSING FEVER Characterized clinically by recurrent periods of fever and spirochaetaemia 2 forms: 1. EPIDEMIC (louse-norme) Etiology : B. recurrentis Transmitted by body louse (Pediculus humanus) 2. ENDEMIC (tick-borne) Etiology: B. duttoni, B. hermsii, B. parkeri, B. turicatei, etc (at least 15 spp) Transmitted by ticks (soft bodied) = Ornithodorus Relapse: Due to antigenic variation (it keeps on changing its antigenicity, so that new antibodies need to be formed every time)

-

Clinical picture (after 1 week of exposure) Fever Rigors Headache Myalgia/arthralgia Photophobia Cough Resolves in 3-6 days Then relapse resolves relapse, etc

Case fatality: Epidemic RF = 4-40% Endemic RF = 2-5% Causes of fatality: Myocarditis Cerebral hemorrhage Liver failure

Diagnosis: (Thick or thin blood smear) Stained with Giemsa or acridine orange Serological tests are different because of antigenic variation

Treatment: Tetracycline Chloramphenicol Erythromycin Penicillin

Prevention: Avoidance & eradication of arthropod vectors Personal hygiene Delousing

LYME DISEASE (Lyme borreliosis a place in USA. 1975) USA Europe China, Japan, Australia 1975 in Lyme USA: Cluster of ? juvenile rheumatoid arthritis Common factor History of insect bite B. burgdorferi (later isolated from Ixodex tick)

Natural host: wild and domesticated animals Vectors: Ixodes dammini I. pacificus I. ricinus

3 stages of disease I. Early Stage Erythema chronicum migrans (ECM) at site of bite 3-22 days later + malaise, fatigue, headache, rigors, neck stiffness Disseminated infection Abnormalities: Cardiac Neurological Musculoskeletal Late / Persistent Months or years later

II.

III.

Annormalities: Chronic skin Nervous system Joint Congenital infection may be fatal LEPTOSPIRA Genus: Leptospia (12 spp) Species: L. interrogens (parasitic strain) L. biflexa (free-living saprophytes) * both spp. Morphologically indistinguishable * Slender spirals with numerous coils with hooked ends * 6-20 microm x 0.1 microm * mobile rotation and gliding * staining: - Levaditi & Fontana stain - Immunofluorescence Culture
y y y y

Obligate aerobes Optimum temperature: 28 33 C Primart isolation: in fluid medium, pH 7.2, 2-3 weeks Media: EMJH (Ellinghausen & McCollough) L.interrogens require additional animal proteins (serum, BSA)

Serogroups & Serovariants (serovars) L. interrogens: 23 serogroups 218 serovars L. biflexa: 28 serogroups 60 serovaris

LEPTOSPIROSIS (Weil s disease) [German physician 1886]
y y y

Etiology : L interrogens Zoonosis worldwide L. -> infects animals (wild, some domesticated ones also) -> urine -> humans -> acute febrile illness

Pathogenesis
y y y

L-> skin abrasions, nasal mucosa, mouth, eyes -> multiply in blood -> disseminate May begin as influenza-like Can -> meningitis & renal involvement

Leptospirosis 2 forms
y y

Benign (Canicola fever) Severe (Weil s disease) - jaundice - hemorrhage of the eyes (these two symptoms usually due to serovar ictero-hemorrhagiae

Other serovars Australis Andamana Bataiviae Pyrogenes

Carriers: Rodents Small mammals Diagnosis: -History of exposure to animal sources
y y y

Work Recreation Living

-microscopy: blood and urine, dark ground microscopy -Culture: Blood

-

Liquid medium Animal (peritoneum)

-serotype -serology (IgM, IgG) Treatment Antibiotics
y y y y

Benzylpenicilline (7/7 IV), 6-8 mega units Streptomycin Tetracycline Erythromycin

Prevention Human unnatural/end-host Rodents eradicate/control