Rickettsiachlamydia ppt

1. RICKETTSIA & CHLAMYDIA
Hoza, A.S
BLS 206

2. Introduction.
• Rickettsiae and Chlamydiae- obligate
intracellular organisms.(classif. as bacteria)
• Rickettsia General features:
-parasites of gut cells of athropods.
-transmittion- athropod to animal.

3. Genera of the Family Rickettsiaceae:
1.Rickettsia
-11 spp (do not multiply within vacuoles & do
not parasitize wbcs.
2. Ehrlichia:
- 2 spp obligate intracellular parasites
– do not multiply within vacuoles but do
parasitize wbcs.

4. Rickettsia.
• 3. Coxiella:
– (1 spp) obligate parasite
–grows preferentially in vacuoles of host cells.
• 4. Baartonella
– 3 spp
- intracellular parasite which attacks the rbc.

5. Fundamental differences btn Chlamydiae and
rickettsiae.
Rickettsiae Chlamydiae
Cytochromes +ve No cytochromes
Aerobic metabolism Anaerobic metabolism.
Multiply by binary fision. Single development cycle.

6. Similarities
Small, pleomorphic coccobacillary forms
Obligate intracellular parasites.
All contain DNA and RNA.
Susceptible to various antibiotics.
Cell walls resemble those of Gram –ve bacteria.
Require exogenous cofactors from animal cells.
Most grow readily in the yolk sac of embryonated eggs
and in cell cultures.

7. Structure of Rickettsia.
• Typical rickettsia
– Very similar to that of gram-negative bacteria.
• Typical envelope:
– Innermost cytoplasmic membrane, a thin electron
dense rigid cell wall & outer layer
• Cell wall
– Chemically similar to Gram-ve bacteria i.e contains
diamino pimelic acid and no techoic acid.
• No discrete nuclear structure.

8. Metabolism
In dil.buffered salt soln:
– Unstable, losing both metabolic activity and infectivity for
animal cell.
In enriched medium:
– Can survive for may hrs.
Basis for obligate parasitism:
– Require rich cytoplasm to stabilize unusually permeable
cell membrane.
Require exogenous supply of cofactors.

9. Growth and Multiplication.
Transverse binary fission.
Under poor nutrition:
long filamentous forms.
Immediately after division:
– Extensive movements through the cytoplasm of the cell.
NB: C.burnetii:
– Enclosed in a persistent vacuole during growth and
division.
6-10 daughter cells form within the host cell before
ruptures and releases them.

10. Host defenses
• Both Cellular and Humoral immunity may
be important.

11. Epidemiology
• Endemic (murine) typhus:
– primarily maintained in rodent populations.
– transmitted via the flea.
– Humans ( accidental host).
• Spotted fever:
– Found predominantly in animals.
– Transmitted by the tick.
– Humans (accidental hosts).
• Q fever:
– Mostly in animals.
– Humans acquire disease primarily by inhalation of
contaminated aerosols.
• Epidemic typhus and trench fever:
– transmitted from human to human via the louse.

12. Pathogenicity
– Transmittion: via arthropod vectors;
• Q fever :
– via inhalation or ingestion of contaminated milk or food.
• The bacteria enter host endothelial cells via an induced
phagocytosis.
– Phospholipase A may help in penetration.
• Replication of the bacteria causes lysis of the host cell
and consequent spread to other cells.
• Initial replication:
– At the site of entry producing a local lesion.
– Followed by dissemination via the vascular system producing
vasculitis and a skin rash.

13. Pathogenesis...
– The lesions may become necrotic
• Virulence :
– Probably due to many factors including:
• release of endotoxin,
• production of immune complexes
• hypersensitivity reactions.
• A characteristic triad of symptoms include:
– fever,
– headache and
– rash (no rash with Q fever).

14. Diagnosis.
• Clinical:
• These diseases present as:
– febrile illnesses after exposure to arthropods or animal hosts
or aerosols ( endemic areas).
– High mortality from Spotted fever (delayed diagnosis).
• The spread of the rash ( characteristic):
– spread from the trunk to the extremities (centrifugal)- typical
for typhus;
– spread from the extremities to the trunk (centripetal)
-typical for spotted fever.

15. Diagnosis…
Laboratory:
3. Macchiavello stain:
- organisms bright red V blue background.
4. Castaneda stain:
- blue organisms V red background.
5. Giemsa stain:
- bluish purple organisms.
4. Use of immunofluorescent antibodies:
NB: The organism can be inoculated into tissue culture
and grown over 4-7 days (very hazardous to personnel).

16. Diagnosis…
Confirmative diagnosis:
• Serological reaction:(Weil-Felix test):
– The production of serum antibody reactive against
Proteus OX19, OX2 or OXK antigens is determined
• Embryonated eggs.
– (Q- Fever)
• Cell cultures.

17. Important Rickettsial diseases of animals
Heartwater:
Tropical canine Pancytopenia.
Equine and Canine Ehrlichiosis.
Q- Fever
Potomac horse Fever.
Salmon poisoning.

18. Rickettsia of Public health significance
Tick-borne:-
• Rocky mountain spotted fever (R.rickettsii)
– Reservoir (Dog, rodents)
• Q-Fever (C. burnetii)
– Reservoir (cattle, shoat)
• Spotted Fever (R.rhipicephali)
– Reservoir (dogs)
• Ehrlichiosis (E.canis)
– Reservoir (dogs)

19. Public health…
Louse-borne:
• European epidemic typhus (R.prowazekii)
-No animal reservoir
3. Trench Fever (Bartonella)
- No animal reservoir.
Flea-borne:
• Endemic murine typhus (R.typhi)
-Reservoir- Wild rodents

20. Public health….
2.Cat scratch fever/bacillary angiomatosis
(Bartonella henselae) Reservoir (domestic cat)
Mite-borne:
• Scrub typhus(R. tsutsugamushi)reservoir- wild
rodents.
Rickettsialpox (r.akari) reservoir House mice.
•
Fly-borne:
• Oroyo fever/ Verruga peruana (B.
bacilliformis) Reservoir ??

21. Treatment & Control
• Chemotherapeutic:
– Tetracycline or
– Chloramphenicol
• Sanitary:
– Arthropod and rodent control are possible but
difficult.
• Immunological:
– No vaccines - currently available.

22. Chlamydia General characteristics
• Species: trachomatis, psittaci
• The Chlamydia
– Obligate intracellular parasites.
• C. trachomatis
– Trachoma,
– Inclusion conjunctivitis,
– Lymphogranuloma venereum (LGV)
– nongonococcal urethritis (NGU). I.e, oculourogenital
infections.
• C. psittaci produces systemic diseases:
– psittacosis,
– ornithosis and
– pneumonitis.

23. Distinctive properties.
• Have two distinct forms:-
– Infectious elementary bodies and
– Intracellular reticulate bodies.
• Elementary bodies attach and are internalized by
susceptible host cells.
• Once inside, they reorganize into a replicative form (the
reticulate body)
• Over a 24 hour period:
– Reticulate bodies divide and begin to reorganize back into
elementary bodies.

24. Distinctive properties…
• 48-72 hours after infection:
– The cell is lysed and
– numerous infectious elementary bodies released.
• The genome of Chlamydia is only 25% the size
of E. coli (i.e one of the smallest prokaryotes).
• The pathogenic mechanisms employed by
Chlamydia - not well understood.

25. Growth and multiplication.

26. Metabolism.
• No detectable flavoproteins or cytochrome.
• Basis of obligate intracelluar parasitism
– lack of ATP-generating ability
– Obtain ATP from the host cell.
• The cells can synthesize :
– DNA
– RNA and
– Protein.

27. Pathogenesis.
• C. psittaci is acquired from infected birds,
usually via the respiratory route.
• C. trachomatis is spread via the fingers to the
urogenital area and vis versa.
• Trachoma:
– Infection of the epithelial cells of the conjunctiva,
producing inclusion bodies.
– Vascularization and clouding of cornea along with
trichiasis (inward growth of eyelashes) ---- produce
scarring leading to blindness.

28. Pathogenesis….
• Inclusion conjunctivitis
– Milder form,
– Occurs in both children and adults.
• Sexually transmitted nongonococcal urethritis
(NGU):
– Similar to gonorrhea
– Occurs with greater frequency.
• Lymphogranuloma venereum (LGV) involving
inguinal lymphadenopathy ("buboes") can occur
in men

29. Host defenses.
• Chlamydia induce interferon and are sensitive to
it.
• During infection, antibodies are synthesized but
recovery is not generally protective.

30. Epidemiology.
• Trachoma:
– prevalent in Africa and Asia,
– generally in hot and dry areas.
• The organisms are very persistent.
– Their habitat : similar to that of Neisseria and
Haemophilus.
• Infection can occur via:
– swimming in unchlorinated pools,
– sharing towels or
– by passage through the birth canal.

31. Diagnosis
• Clinical:
– Diagnosis of trachoma is usually good.
– Genital vesicles associated with LGV are characteristic.
– NGU can only be suspected in the absence of laboratory
findings.
• Laboratory:
– Iodine stained specimens usually show inclusion bodies.
• Tissue culture:
– Chlamydia can be cultured in tissue culture and appropriate
serological tests performed

32. Diagnosis
Serological diagnosis:
• Micro-immunofluorescent tests in tears of patients
with eye infections for presence of anti-chlamydia
Ab.
• Delayed –type skin rexn (hypersensitivity Type
IV) (Frei-test)
• Rising titer of Ab V chlamydial family Ag in lung
infections.

33. Treatment and Control.
• Chlamydia exhibit low pathogenicity in a compromised
host.
• Chemotherapeutic:
– Tetracycline or erythromycin are drugs of choice.
• Sanitary:
– Good hygiene,
– Treatment of sexual partners and
– Quarantine of birds all reduce the incidence.

34. Treatment and control.
• Immunological:
– No vaccine – available since specific antibodies fail
to neutralize elementary bodies in vivo.
NB:
• Chlamydial d’ses –relatively easy to treat, but:
1.Latency of infection
2.Susceptibility to reinfection.