Rickettsia & chlamydia bls 206
Upcoming SlideShare
Loading in...5

Rickettsia & chlamydia bls 206






Total Views
Views on SlideShare
Embed Views



0 Embeds 0

No embeds


Upload Details

Uploaded via as Adobe PDF

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment

Rickettsia & chlamydia bls 206 Rickettsia & chlamydia bls 206 Presentation Transcript

  • Introduction.• Rickettsiae and Chlamydiae- obligate intracellular organisms.(classif. as bacteria)• Rickettsia General features: -parasites of gut cells of athropods. -transmittion- athropod to animal.
  • 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.
  • Rickettsia.• 3. Coxiella: – (1 spp) obligate parasite –grows preferentially in vacuoles of host cells.• 4. Baartonella – 3 spp - intracellular parasite which attacks the rbc.
  • Fundamental differences btn Chlamydiae and rickettsiae.Rickettsiae ChlamydiaeCytochromes +ve No cytochromesAerobic metabolism Anaerobic metabolism.Multiply by binary fision. Single development cycle.
  • 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.
  • 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.
  • 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.
  • 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.
  • Host defenses• Both Cellular and Humoral immunity may be important.
  • 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.
  • 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.
  • 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).
  • 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.
  • 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).
  • 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.
  • Important Rickettsial diseases of animalsHeartwater:Tropical canine Pancytopenia.Equine and Canine Ehrlichiosis.Q- FeverPotomac horse Fever.Salmon poisoning.
  • Rickettsia of Public health significanceTick-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)
  • Public health…Louse-borne:1. European epidemic typhus (R.prowazekii) -No animal reservoir2. Trench Fever (Bartonella) - No animal reservoir.Flea-borne:1. Endemic murine typhus (R.typhi) -Reservoir- Wild rodents
  • 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 ??
  • Treatment & Control• Chemotherapeutic: – Tetracycline or – Chloramphenicol• Sanitary: – Arthropod and rodent control are possible but difficult.• Immunological: – No vaccines - currently available.
  • 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.
  • 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.
  • 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.
  • Growth and multiplication.
  • 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.
  • 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.
  • 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
  • Host defenses.• Chlamydia induce interferon and are sensitive to it.• During infection, antibodies are synthesized but recovery is not generally protective.
  • 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.
  • 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
  • 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.
  • 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.
  • 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.