Spirocheates- Borrelia

1. BORRELIA
Dr. V. S. Vatkar
Asso Prof
Microbiology Department
D Y Patil Medical College, Kolhapur

2. Scientific classification
Kingdom: Bacteria
Phylum: Spirochetes
Class: Spirochetes
Order: Spirochaetales
Family: Spirochaetaceae
Genus: Borrelia
Species: Borrelia recurrentis, Borrelia vincentti,
Borrelia burgdorferi

3. MORPHOLOGY
Large , motile, retractile with irregular , wide
open coils
5-30 μm long & 0.3- 0.7 μm wide
Readily stained with ordinary stain, gram negative
Several spp of borrelia are commensales of buccal
cavity
Medically imp spp : Borrelia vincentti along with
fusobacterium it causes Vincents angina, Borrelia
burgdorferi causes Lyme ds , Borrelia recurrentis
causes relapsing fever.

4. BORRELIA REcuRREntIs
Morphology: irregular spirals with one or
both ends pointed.
8-20 μm in length & 0.2-0.4 μm wide
5-10 loose spiral coils
Stained well with Geimsa stain & gram
negative
Cultural characteristics: grow on complex
media: Noguchi’s medium contains: ascitic fl,
rabbit’s kidney, also grow on CAM

5. Giemsa Stain of Borrelia
recurrentis in Blood
Light Microscopy Phase Contrast Microscopy

6. Epidemiology of Borrelia Infections
Borrelia
recurrentis
Borrelia spp.
Borrelia
burgdorferi
Ixodes spp.
Ornithodoros spp.
Pediculus humanus

7. EPIdEMIOLOGY Of RELAPsInG fEvER
Associated with poverty, crowding, and warfare, jails
Arthropod vectors
Louse-borne borreliosis = Epidemic Relapsing Fever
 Transmitted person-to-person by human body lice (vectors)
from infected human reservoir
 Infect host only when louse is injured, e.g., during scratching
 Therefore, a single louse can only infect a single person
 Lice leave host that develops a fever and seek normal
temperature host
Tick-borne borreliosis = Endemic Relapsing Fever
 Sporadic cases
 Transmitted by soft body ticks (vectors) from small mammal
reservoir
 Ticks can multiply and infect new human hosts

8. Pathogenesis of RelaPsing feveR
Relapsing fever : I P: 2-10 days, sudden onset of fever ,this
stage borrelia are seen in pt’s bl
Fever subsides in 3-5 days
Afebrile stage of 4-10 days , borrelia are not seen in pt’s bl
Another bout of fever sets in
Ds ultimately subsides after 3-10 relapses
Epidemic Relapsing Fever = Louse-borne borreliosis
Borrelia recurrentis
Endemic Relapsing Fever = Tick-borne borreliosis
Borrelia spp.

9. lab diagnosis
Drop of bl : wet film examined under dark ground
microscope/phase contrast microscope
Bl smear with Giemsa/Leishman stain
1-2 ml bl injected I/P in mouse, borrelia multiply
& bl is collected from tail vein of the animal
Culture is too difficult & demonstration of Ab are
also too difficult
Agglutinins for proteus: OXK sometimes seen in
higher titre in louse borne relapsing fever

10. Prophylaxis:
Prevention of louse infestation
Tick borne inf: identification of tick infested place
No vaccine available
Treatment:
Tetracyclines, penicillin, erythromycin are effective
antibiotics

12. geneRal ChaRaCteRistiCs
Gram negative
Spirochete
Microaerophilic
Grows slowly - Generation time is 12-24 hours
Motile using an endoflagellum, located in periplasmic
space, causing a corkscrew movement
Juvenile arthritis: named Lyme ds, observed in Lyme
in USA.

13. enviRonment
Obligate parasite, common vector borne inf
Fastidious (requires complex growth medium)
Optimal temperature is 32°C
Adapts readily to environmental changes in different
hosts

14. PathogeniCity
Transmitted by tick bite (Ixodid tick)
Mice are reservoirs for the bacteria
Ticks transmit it to deer, humans, and other mammals
Has a dormant cyst form as well as the active spirochete
form.

15. Pathogenesis of Lyme BorreLiosis
 Lyme disease characterized by three stages: I P 3-30
days
 First stage: unique skin lesion (erythema
chronicum migrans )ECM with general malaise
 ECM not seen in all infected hosts
 Lesions periodically reoccur
 Second stage: fever, headache, malaise,
arthralgia & lymphadenopathy
 Subsequent stage seen in 5-15% of patients with
neurological or cardiac involvement

16.  Third stage : persistent infection sets in months or
yrs, involves migrating episodes of non-
destructive, but painful arthritis, polyneuritis,
encephalitis.
Lab diagnosis: CSF, Bl, skin lesions
 Serology tests: ELISA, CFT, Ab: IgM & IgG within 1-2
mths
 False +ve syphilis serological tests: FTA-ABS +ve &
VDRL neg

17. symPtoms
Fever, headache, fatigue,
and a characteristic skin
rash called erythema
migrans that usually
blooms from the bite mark
Untreated can spread to
joints, heart, and nervous
system
Sometimes causes
paralysis – Bell’s Palsy
Arthritis

18. treatment
Treated with antibiotics
Penicillin
Amoxycillin
Cefuroxime
doxycycline
Rarely resolved without
antibiotics

19. genome
Has a linear genome as opposed to the
usual circular genome.
21 linear and circular plasmids which is the
highest number observed in any bacterial
species.
Virulence likely encoded on plasmids

20. Erythema chronicum migrans of Lyme
Borreliosis
Bullseye rash

21. Diagnosis of Lyme BorreLiosis

22. EpidEmiology of lymE BorrEliosis
Lyme disease was recognized as a syndrome in
1975 with outbreak in Lyme, Connecticut
Transmitted by hard body tick (Ixodes spp.)
vectors
 Nymph stage are usually more aggressive feeders
 Nymph stage generally too small to discern with
unaided eye
 For these reasons, nymph stage transmits more
pathogens
White-footed deer mice and other rodents,
deer, domesticated pets and hard-shelled ticks
are most common reservoirs

23. BorrElia vincEnti
Motile , gram negative
Mouth commensales, but under predisposing
conditions like malnutrition or viral inf ulcerative
gingivostomatitis or oropharangitis (Vincent’s
angina)
B.vincenti along with fusobacterium fusiforme
fusospirocheatosis seen
Large no of borrelia & fusobacteria are seen in
lung abscesses, skin ulcers & gangrenous balanitis,
significance is uncertain
Penicillin, metronedazole

24. nonvEnErEal trEponEmal
disEasEs
Bejel, Yaws & Pinta
Primitive tropical and subtropical
regions
Primarily in impoverished children

25. Treponema pallidum ssp. endemicum
Bejel (a.k.a. endemic syphilis)
 Initial lesions: nondescript oral lesions
 Secondary lesions: oral papules and mucosal patches
 Late: gummas (granulomas) of skin, bones &
nasopharynx
Transmitted person-to-person by contaminated
eating utensils
Primitive tropical/subtropical areas (Africa, Asia &
Australia)

26. Treponema pallidum ssp. pertenue
(T. pertenue)
Yaws: granulomatous
disease
 Early: skin lesions (see on
R.H.S.)
 Late: destructive lesions of
skin, lymph nodes & bones
Transmitted by direct
contact with lesions
containing abundant
spirochetes
Primitive tropical areas (S.
America, Central Africa, SE
Asia)
Papillomatous Lesions of Yaws:
painless nodules widely
distributed over body with
abundant contagious
spirochetes.

27. Treponema carateum
 Pinta: primarily restricted to skin
 1-3 week incubation period
 Initial lesions: small pruritic
papules
 Secondary: enlarged plaques
persist for months to years
 Late: disseminated, recurrent
hypopigmentation or
depigmentation of skin
lesions; scarring &
disfigurement
 Transmitted by direct contact
with skin lesions
 Primitive tropical areas
 (Mexico, Central & South
America)
Hypopigmented Skin Lesions of
Pinta: depigmentation is commonly
seen as a late sequel with all
treponemal diseases

28. THANK YOU