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.
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:
1. Macchiavello stain:
- organisms bright red V blue background.
2. Castaneda stain:
- blue organisms V red background.
3. 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.
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.
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.
