Acanthamoeba: Biology and Pathogenesis (2nd edition)

Acanthamoeba: Biology and Pathogenesis (2nd edition) | Book

"comprehensive review" (Book News)
"comprehensive handbook ... as well as an invaluable reference" (Fungal Diversity)

Publisher: Caister Academic Press
Author: Naveed Ahmed Khan
Aga Khan University, Karachi, Pakistan
Pages: x + 334
Hardback:
Publication date: January 2015Buy book
ISBN: 978-1-908230-50-8
Price: GB £159 or US $319
Ebook:
Publication date: January 2015Buy ebook
ISBN: 978-1-908230-51-5
Price: GB £159 or US $319
DOI: https://doi.org/10.21775/9781908230508

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A fully comprehensive and up-to-date edition covering all aspects of Acanthamoeba biology. Following the success of the first edition of this book, the author has extensively revised and expanded the text to produce a new volume that includes all the latest research and information on every aspect of this organism. There is a particular emphasis on the Acanthamoeba genome sequence and the novel insights gained from the application of molecular methods to Acanthamoeba developmental and cellular biology in terms of metabolism and morphogenesis, classification, ecology and role in the ecosystem, host-pathogen interactions, virulence factors and immunological basis of pathogenesis, clinical manifestation, diagnosis, treatment, new target development and drug resistance and its interactions with other microbes in the environment.

This new edition is an essential reference text for parasitologists, microbiologists, immunologists, and physicians in the field of basic and medical microbiology, as well as an invaluable reference for new and experienced researchers who wish to understand this organism better. This book is the definitive guide to current research on this increasingly important organism.

Reviews

"... comprehensive review of Acanthamoeba research ... useful to microbiologists, immunologists, and physicians ..." from Book News (2014)

"comprehensive handbook ... useful for students, teachers, parasitologists, microbiologists, immunologists and physicians in the field of basic and medical microbiology, as well as an invaluable reference for new and experienced researchers who wish to understand this organism better." from Fungal Diversity

Table of contents

Section A. Biology and Phylogeny

Pages: 1-66.

1. Introduction

1.1. Acanthamoeba: a eukaryotic pathogen

1.2. Protists

1.3. Discovery of pathogenic amoebae

2. Discovery of Acanthamoeba spp.

3. Speciation and genotyping

3.1. Use of 18S rRNA gene sequences (18S rDNA) for Acanthamoeba taxonomy

4. Cell biology

4.1. Nucleus

4.2. Cytoplasm

4.2.1. Cytosol

4.2.2. Organelles (organs of the cell)

4.2.3. Inclusion bodies

4.3. Endoplasmic reticulum

4.4. Ribosomal RNA (rRNA)

4.5. Proteins

4.6. Lipids

4.7. Prostaglandins

4.8. Contractile vacuole and osmoregulation

4.9. Lysosome, peroxisome, and digestive vacuoles

4.10. Plasma membrane

4.11. Surface properties

4.12. Carbohydrates: glycogen storage and cell wall synthesis

4.13. Ionic distribution

4.14. Polyamine

4.15. Adenylate cyclase

4.16. Purine and pyrimidine

4.17. Mitochondria

4.18. ER-mitochondria encounter structure (ERMES)

5. Nuclear genome

6. Mitochondrial genome

7. The complete A. castellanii genome (By Professor Brendan Loftus)

7.1. Genome sequencing strategy

7.2. Genome assembly

7.3. Determination of assembly correctness

7.4. Gene finding

7.5. Transcript coverage for the predicted gene set

7.6. Functional annotation assignments

7.7. Genome analysis

7.7.1. Lateral gene transfer (LGT)

7.7.2. Expression of lateral gene transfer in A. castellanii

7.7.3. Lateral gene transfer introns

7.7.4. Unusual metabolism of A. castellanii

7.7.5. Transcription factors

7.7.6. Kinome of A. castellanii

7.7.7. Phosphotyrosine signalling in A. castellanii

7.7.8. Microbial recognition through pattern recognition receptors

7.7.9. Mannose binding protein

7.7.10. Antimicrobial defence

8. Motility

9. Molecular basis of motility

9.1. Intermediate filaments

9.2. Microtubules

9.3. Microfilaments

9.3.1. Actin polymerization to form actin microfilaments

9.3.2. Regulators of actin polymerization

9.3.2.1. Actin-binding proteins

9.3.2.2. Inositol phospholipids-based regulation of actin microfilaments

9.3.2.3. GTP-binding proteins regulate actin microfilaments

9.3.2.4. Other key regulators

10. Acanthamoeba actin

10.1. Properties of Acanthamoeba actin and its filaments

11. Acanthamoeba myosin

11.1. Myosin-I

11.2. Myosin-II

11.3. Activation of myosin-I and myosin-II

11.4. Localization of Acanthamoeba myosin

11.4.1. Myosin-I

11.4.2. Myosin-II

11.5. Myosins and motility

11.6. Polymerization of Acanthamoeba myosin

11.7. ATPase activity of myosin-I and myosin-II

11.7.1. Myosin-I

11.7.2. Myosin-II

Section B. Life cycle and ecological significance

Pages: 67-116.

1. Ecology

1.1. Distribution in the environment

1.2. Distribution in the man-made environment

1.3. Distribution in clinical settings

2. Ecosystem

3. Life cycle

3.1. Trophozoite stage

3.1.1. Growth cycle

3.1.1.1. G1 phase

3.1.1.2. S phase

3.1.1.3. G2 phase

3.1.1.4. M phase

3.2. Cell division in asynchronous cultures

3.3. Cell division in synchronous cultures

3.4. Stationary phase

3.5. Growth regulators

4. Stress management in cyst-forming pathogenic free-living protists

4.1. Commitrment to encystation in Acanthamoeba

4.2. Encystation

4.2.1. At the morphological-level

4.2.2. At the organelle-level

4.2.3. RNA and protein synthesis

4.2.4. Golgi complex

4.2.5. Phagocytic and pinocytic activity

4.2.6. Respiration

4.2.7. Cytoskeletal proteins

4.2.8. Glycogen

4.2.9. Lipids

4.2.10. Other molecular changes

4.2.11. Calcium-binding sites and encystation

4.2.12. Cell wall synthesis

4.3. Outer cyst wall isolation

4.4. Cyst stage

4.4.1. Effects of environmental conditions on encystation

4.5. Excystation

5. Regulators of the life cycle

6. What stimulates encystation?

6.1. Food deprivation

6.2. High cell density

6.3. Cell surface receptors (hyper- and hypo-osmolarity, extremes in pH)

6.4. Encystation-inducing factors

6.5. DNA synthesis and mitochondrial function in encystation

7. Feeding

7.1. Preferential feeding behaviour of Acanthamoeba is not unusual and commonly observed in other species

7.2. Taste and smell

8. Metabolism

9. Acanthamoeba is a heterotroph (chemo-organotroph)

9.1. Glycolysis pathway (also called Embden- Meyerhof-Parnas pathway)

9.2. Krebs cycle (also called citric acid cycle or tricarboxylic acid cycle)

9.3. Electron transport

10. Hydrogenosomal-type anaerobic ATP generation pathway in A. castellanii

11. Isolation of Acanthamoeba from the environmental samples

11.1. Xenic cultivation (non-nutrient agar plates seeded with Gram-negative bacteria)

11.2. "Axenic" cultivation

11.3. Chemically-defined medium

11.4. Methods of encystation

12. Storage

13. Testing viability of trophozoites and cysts

Section C. Acanthamoeba infections

Pages: 117-152.

1. Acanthamoeba keratitis

1.1. Acanthamoeba binding to worn and unworn contact lenses

1.2. Biofilm formation

1.3. Corneal injury

1.4. Epidemiology

1.5. Pathophysiology

1.6. Is Acanthamoeba keratitis limited to cornea?

1.7. Why is it so painful?

1.8. Diagnosis of Acanthamoeba keratitis

1.8.1. Clinical diagnosis

1.8.2. Laboratory identification and differentiation of Acanthamoeba spp.

1.8.3. Culture of Acanthamoeba

1.8.4. Microscopic identification based on morphological characteristics

1.8.5. Isoenzyme analysis

1.8.6. Antibody-based assays

1.8.6.1. Immunofluorescence assays

1.8.6.2. Flow cytometry

1.8.7. Cellulose-based identification

1.8.8. Polymerase chain reaction

1.8.9. Matrix-assisted laser desorption-ionization time-of-flight mass spectrometry (MALDI-TOF MS)

1.8.10. High-resolution ¹H nuclear magnetic resonance (NMR) spectroscopy in the clinical diagnosis of Acanthamoeba

1.9. T4 genotype is the predominant cause of keratitis and encephalitis

1.10. Host susceptibility

1.11. Species specificity

1.12. Risk factors

1.13. Treatment

1.13.1. Cryosurgery

1.13.2. Chemotherapy

1.13.3. Systemic administration of antimicrobials against stromal Acanthamoeba keratitis

2. Granulomatous amoebic encephalitis due to Acanthamoeba

2.1. Routes of entry into the central nervous system

2.2. Epidemiology

2.3. Pathophysiology of granulomatous ameobic encephalitis due to Acanthamoeba

2.4. Diagnosis: Clinical and laboratory diagnosis

2.5. Host susceptibility

2.6. Species and organ specificity

2.7. Risk factors

2.8. Treatment

2.8.1. Can anesthesia choice affect the clinical outcome of granulomatous amoebic encephalitis due to Acanthamoeba spp.?

3. Cutaneous Acanthamebiasis

4. Multiple sclerosis and Acanthamoeba

Section D. Pathogenesis

Pages: 153-190.

1. Acanthamoeba keratitis

1.1. In vivo models

1.2. Ex vivo models

1.3. In vitro models

2. Granulomatous amoebic encephatlitis due to Acanthamoeba

2.1. In vivo models

2.2. Ex vivo models

2.3. In vitro models

3. Loss and gain of virulence

4. Acanthamoeba: An opportunistic pathogen

4.1. An opportunist with pathogenic potential

5. Crossing of the biological barriers

5.1. Cornea

5.2. Traversal of the blood-brain barrier

6. Direct virulence factors

7. Contact-dependent mechanisms

7.1. Acanthamoeba bind to the extracellular matrix proteins

7.2. Adhesion to the host cells

7.2.1. The structure of MBP

7.2.2. Potential function of the MBP CxCxC repeat region

7.2.3. Evolution of the MBP gene

7.2.4. Other Acanthamoeba adhesin(s) and host cell receptor(s)

7.3. Host intracellular signalling in response to Acanthamoeba

7.4. Phagocytosis

7.4.1. Phagosome formation and fusion with the lysosome

7.5. Acanthamoeba phagocytosis and intracellular signalling

7.5.1. Lysosomal enzymes

7.6. Ecto-ATPases

7.7. Neuraminidase activity

7.8. Superoxide dismutase

7.9. Acanthamoeba-induced plasminogen activation

8. Contact-independent mechanisms

8.1. Hydrolytic enzymes

8.1.1. Elastase

8.1.2. Proteases

8.1.3. A liquid chromatography-based screening methodology for proteolytic enzyme activity.

8.2. Proteases as drug targets

8.3. Phospholipases

8.4. Glycosidases (also called glycoside hydrolases)

8.5. Acanthaporin

9. Indirect virulence factors

9.1. Morphology

9.2. Temperature tolerance, osmotolerance and growth at different pH

9.3. Phenotypic switching

9.4. Chemotaxis

9.5. Ubiquity

9.6. Biofilms

9.7. Effect of cholesterol (or sterol biosynthesis) on Acanthamoeba virulence

9.8. Host factors

Section E. Acanthamoeba and the immune system

Pages: 191-216.

1. Non-specific immune system

1.1. Skin

1.2. Mucosa

1.3. Normal flora

1.4. Recruitment of phagocytes and their mode of killing

1.4.1. Lysosomal-independent mechanism

1.4.2. Lysosomal-dependent mechanism

1.5. Phagocytic call for help (production of cytokines)

1.6. Complement

2. Specific immune system

2.1. Antibodies

3. What are the basic types of parasite immune evasion strategies?

3.1. Non-induction of immune response

3.2. Anatomical seclusion

3.3. Mechanisms of survival in macrophages

3.4. Antigenic variation

3.5. Host mimicry

3.6. Evasion of the complement cascade

3.7. Evasion of antibodies

3.8. Interference with the host immune signalling molecules

4. Acanthamoeba and immune response

4.1. Acanthamoeba keratitis and the immune response

4.1.1. From the contact lens to the cornea

4.1.2. Effect of contact lens wear for extended times on the innate immunity of the ocular surface

4.1.3. Antimicrobial peptides

4.2. Acquired immunity

4.2.1. Immunization using whole Acanthamoeba

4.2.2. Immunization using Acanthamoeba-specific antigens

4.3. Antibody levels in Acanthamoeba patients

4.4. Can cysts evade immune responses?

4.5. Macrophages in vivo

4.6. Neutrophils in vivo

4.7. Macrophages and neutrophils in vitro

4.8. Granulomatous amoebic encephalitis due to Acanthamoeba and the immune response

4.8.1. Complement

4.8.2. Cytokines

4.8.3. T-lymphocytes

4.8.4. Evasion of cytokines

4.8.5. Evasion of antibodies

4.8.6. Evasion of complement

4.8.7. Evasion of macrophages

4.8.8. Acanthamoeba-specific antibodies and activated macrophages, in combination show amoebicidal effects

4.8.9. Evasion of neutrophils

4.8.10. Natural killer cell activity in vivo

5. Effect of immune suppressive component inmarijuana, cannabinoid delta-9-tetrahydrocannabinol on Acanthamoeba encephalitis

6. Acanthamoeba and the central nervous system autoimmunity

Section F. Chemotherapeutic strategies against Acanthamoeba infections

Pages: 217-252.

1. Chemotherapeutic agents and Acanthamoeba

2. Membrane-acting agents

2.1. Polyhexamethylene biguanide

2.2. Chlorhexidine

2.3. Alexidine

2.4. Acriflavine hydrochloride and proflavine

2.5. Alkylphosphocholine compounds (phospholipid-like molecules)

2.6. Polymyxin B

2.7. Polymyxin E (colistin)

2.8. Caspofungin

2.9. Ergosterol inhibition

2.9.1. Ketoconazole

2.9.2. Miconazole

2.9.3. Clotrimazole

2.9.4. Fluconazole

2.9.5. Voriconazole

2.9.6. Amphotericin B

2.10. Benzimidazole and Benzotriazole

2.11. Thiazole derivatives

2.12. Statins

2.13. Ceragenins, or cationic steroid antibiotics

3. Inhibitors of DNA synthesis and polyamine metabolism

3.1. Diamidine derivatives

3.2. Methylglyoxal bis (guanyl hydrazone) (MGBG)

3.3. Berenil

3.4. Myristamidopropyl dimethylamine (MAPD)

3.5. Folate biosynthesis inhibitors

4. RNA synthesis inhibition

4.1. Rifampicin

4.2. 5-fluorocytosine

5. Protein synthesis inhibition

5.1. Macrolide compounds

5.1.1. Corifungin

5.1.2. Rokitamycin

5.1.3. Spiramycin

5.2. Aminoglycosides

5.2.1. Paromomycin

5.2.2. Neomycin

5.2.3. Neosporin

5.2.4. N-chlorotaurine

6. Tricyclic neuroleptic agents (calmodulin inhibition)

6.1. Trifluoperazine dihydrochloride and chlorpromazine dihydrochloride (phenothiazine compound)

7. Artesunate

8. Antimicrobial compounds from natural products (in addition to the aforementioned antibiotics)

8.1. Animal-based natural products

8.1.1. Magainins

8.1.2. Alpha-helical and beta-hairpin antimicrobial peptides

8.2. Plant-based natural products (in addition to artemisinin)

8.3. Microbe-based natural products

8.4. Clinically-available drugs against Acanthamoeba

9. Drug targets in Acanthamoeba

10. Drug resistance in Acanthamoeba

11. Disinfectants and Acanthamoeba

11.1. Disinfection agents

11.2. Freeze-thaw

11.3. Heat disinfection

11.4. Microwave irradiation

11.5. Solar disinfection

11.6. Ultraviolet light irradiation

11.7. Gamma irradiation

11.8. Power ultrasound for disinfection

12. Future prospects for treatment

12.1. Antibody-based therapy

12.2. Using a carrier for the drug delivery

12.3. Use of a liposome for drug delivery

12.4. Use of a chitosan for drug delivery

12.5. siRNA-based therapy

12.6. Photodynamic chemotherapy against Acanthamoeba

12.6.1. Photo-inhibition of Acanthamoeba

12.6.1.1. Use of photosensitizers against Acanthamoeba

12.7. "Transcribrial route" for administering antimicrobial compounds in the management of granulomatous amoebic encephalitis as well as primary amoebic meningoencephalitis

Section G. War of the microbial worlds: who is the beneficiary in Acanthamoeba interactions with other microbes.

Pages: 253-278.

1. A host for viruses

1.1. Mimivirus

1.2. Megavirus chilensis

1.2.1. An evolutionary mystery

1.2.2. Adding to complexity: Endosymbiont of Mimivirus

1.2.3. Do endosymbionts contribute to Acanthamoeba infections?

1.3. Courdo11 virus

1.4. Coxsackievirus

1.5. Adenovirus

1.6. Poliovirus, echovirus, enterovirus, or vesicular stomatitis virus