UNIT-3 DIVERSITY OF SOME UNUSUAL PROKARYOTES

3.1: BACTERIA WITH UNUSUAL MORPHOLOGY

RICKETTSIA:Author:

Gunjan Mehta,Dept. of Biotechnology,

Shree M. & N. Virani Science College, RajkotEmail: gjmehta@vsc.edu.in

Slideshare: http://www.slideshare.net/gunjan_rjt

Rickettsia species

1. Obligate intracellular pathogens

2. Cause spotted fevers and typhus in humans

3. Pathogenesis due to destruction of cells from within

4. All species transmitted to humans via arthropod vectors

5. In some case the vector is also a host, transovarial passage.

Origin

• Howard Taylor Ricketts(1871- 1910) first studied Rocky Mountain Spotted Fever- Bitlerroot Velly, Maxico.

• Rickettsia prowazaki- causative agent

• Ricketts- Vit. D. Deficiency

Rickettsia classification

• Domain: Bacteria• Phylum: Proteobacteria• Class: Alphaproteobacteria• Order: Rickettsiales• Family: Rickettsiaceae• Genus: Rickettsia

Morphology

• Rod shaped/ Pleomorphic• Coccoid• Gram –ve Cell wall• No Flagella/ Non motile• Non sporeforming• Diameter: 0.3- 0.5 µm• Length: 0.8- 2.0 µm

Mode of nutrition and transmission

• Obligate intracellular parasite• Mutualistic• Grow in vertebrate erythrocyte, macrophages, vascular endothelial cells

• Primary and secondary host• Vectors: Blood sucking arthropods- Flies, Ticks, Mites, Lice

• Sometimes vector is primary host.

Metabolism

• Lack Glycolytic pathway• Glucose is not the source of energy• Oxidizes glutamate/ TCA cycle intermediate (Succinate)

• Capability to utilize host ATPs… through adenylate carrier

• Plasma membranecytoplasm has a transport system to facilitate transfer of host cell nutrients/ Enzymes/ Coenzymes

Morphology and composition1. Small, Gram-negative bacteria

2. Slime layer around intracellular growth

3. Both LPS-like and PPG molecules comprise outer coat (variable between strains)

4. Grown in vitro in tissue culture

5. Can produce their own ATP but in limited amounts and will utilize host’s ATP and NAD

Pathogenesis

1. Adhesion

2. Internalization

3. Release from phagosome

4. Intracellular growth

5. Release from infected cell

6. Host cell response to infection

Adhesion

1. In mammals, primarily endothelial cells

2. Low affinity receptors on host cells

3. Rate-limiting step during infection

4. Outer membrane proteins (OmpA & B) are involved

5. Adherence to arthropod cells is unknown

Internalization

1. Induced phagocytosis by non-professional cells

2. Signals unknown

3. Host cell microfilament formation required (cytochalasin inhibits)

4. Requires metabolically active (viable) rickettsias

5. Calcium ion dependent (calmodulin inhibits)

Release from vacuole

1. Taken up in vacuole but cannot survive phagosomal/ lysosomal fusion

2. Induction of bacterial phospholipase A

3. Lysis of vacuolar membrane

4. Release into cytoplasm

Intracellular growth

1. Occurs within host cell cytoplasm

2. Generation time – 9-12 hours

3. Division by binary fission

4. Specific transporters move host molecules into bacteria cell

5. Intracellular spread may occur by process similar to that obserced in Shigella species

6. Actin tails (up to 70 microns) form at bacterial poles

Release from infected cells

1. Usually results in host cell death

2. Cell bursts

3. Mechanism of lysis unknown

4. Two possibilities of intracellular spread:

Extracellular and Intracellular

Host cell response

1. Increase in surface expression of host cell surface markers, e.g. E-selectin, ICAM, etc.

2. Increase in cytokine (IL-1, IL-6, IL-8) expression

3. Varied effects on procoagulant factors, e.g. fibrinogen

4. Effects due to activation of NF-kB

Epidemiology

1. Seasonal incidence in temperate climates in developed countries

2. Endemic in poorer countries associated with overcrowding (e.g. epidemic typhus)

3. In North America, associated with campers, hikers, backpackers, etc.

4. Historically associated with Rocky Mountain states (RMSF) but may now be geographically diverse

Rocky Mountain spotted fever is the most severe and most frequently reported rickettsial illness in the United States.

The disease is caused by Rickettsia rickettsii, a species of bacteria that is spread to humans by ixodid (hard) ticks.

Initial signs and symptoms of the disease are non-specific. If not treated quickly it can be fatal.

Goldberg, M.B. 2001. Microbiol. Mol. Rev. 65:595-262