A. Amoebae
A1. Acanthamoeba spp.
l. Introduction
2. Discovery of Pathogenic Free-Living Amoebae
3. Acanthamoeba spp.
3.1 Ecological distribution
3.2 Biology
3.3 Motility
3.4 Life cycle
3.5 Feeding
3.6 Acanthamoeba genome
3.7 Methods of isolation
3.8 Methods of encystment
3.9 Storage of Acanthamoeba
3.10 Classification of Acanthamoeba
3.11 Human infections
4. Acanthamoeba Keratitis[...]
A. Amoebae
A1. Acanthamoeba spp.
l. Introduction
2. Discovery of Pathogenic Free-Living Amoebae
3. Acanthamoeba spp.
3.1 Ecological distribution
3.2 Biology
3.3 Motility
3.4 Life cycle
3.5 Feeding
3.6 Acanthamoeba genome
3.7 Methods of isolation
3.8 Methods of encystment
3.9 Storage of Acanthamoeba
3.10 Classification of Acanthamoeba
3.11 Human infections
4. Acanthamoeba Keratitis
4.1 Epidemiology
4.2 Pathophysiology
4.3 CIinical diagnosis
4.4 Host susceptibility
4.5 Risk factors
4.6 Treatment
5. Acanthamoeba Granulomatous Encephalitis
5.1 Epidemiology
5.2 Pathophysiology
5.3 Diagnosis
5.4 Host susceptibility
5.5 Risk factors
5.6 Treatment
6. Cutaneous Acanthamebiasis
7. Pathogenesis
7.1 Contact-dependent factors
7.2 Ecto-ATPases
7.3 Contact-independent factors
8. Indirect Virulence Factors
8.1 Morphology
8.2 Temperature tolerance and osmotolerance
8.3 Growth at different pH
8.4 Phenotypic switching
8.5 Drug resistance
8.6 Ubiquity
8.7 Biofilms
8.8 Host factors
9. Immune Response
9.1 Acanthamoeba keratitis and the immune response
9.2 AGE and the immune response
10. Acanthamoeba and Bacterial Interactions
10.1 Acanthamoeba as bacterial predators
10.2 Acanthamoeba as bacterial reservoirs
10.3 Acanthamoeba as bacterial Trojan horse
1l. Conclusions
12. Acknowledgments
13. References
A2. Balamuthia mandrillaris
1. Introduction
2. Taxonomy
3. Life Cycle
4. Cultivation
4.1 Growth on tissue culture cells
4.2 Axenic growth
5. Ecology
5.1 Isolation from soil
5.2 Are all strains of Balamuthia pathogenic?
5.3 Amoebae as bacteriaI hosts
6. Physiology
7. Molecular Biology of Balamuthia
8. Mechanisms of Pathogenesis
8.1 Cytopathology
8.2 Enzymatic potential
9. Infection and Disease
9.1 Animal model of disease
9.2 Portals of entry
9.3 The Balamuthia paradox
9.4 Groups or individuals at risk
9.5 Immunocompromised versus immunocompetent hosts
9.6 Hispanic Americans
9.7 Disease in animals
10. Balamuthiasis: Nature of the Disease
10.1 Central nervous system disease
10.2 Cutaneous disease
1l. Balamuthiasis at Presentation
11.1 CNS disease
11.2 Cutaneous disease
12. Pathophysiology
13. Epidemiology
13.1 Balamuthia antibodies in humans
13.2 Balamuthiasis in populations
13.3 Prevention
14. Diagnosis
14.1 Gross pathology
14.2 Basic pathology
14.3 Antigen detection: indirect immunofluorescent staining of tissue sections
14.4 Clinical recognition
14.5 Neuroimaging
14.6 Molecular techniques: the polymerase chain reaction
14.7 Cultivation as a diagnostic method
15. Host Response
15.1 Mobilization of the immune system
15.2 Antibody production and detection: fluorescent antibody staining
16. Antimicrobial Therapy
16.1 What works: clinical successes
16.2 What may work: in vitro drug testing
17. Overview, Conclusions and Questions
18. Acknowledgments
19. References
A3. Naegleria fowleri
1. Introduction
2. Morphology of Naegleria
3. Pathogenicity and Virulence Factors
4. Ecology and Methods of Detection from Environmental Sources
5. Clinical Presentation of Primary Amoebic Meningoencephalitis
6. Diagnostic Techniques
7. Treatment and Therapeutic Agents
8. Host-Parasite Interactions
9. Immunity
10. Pathogens Associated with Naegleria
1l. Summary and Conclusions
12. Acknowledgments
13. References
A4. Blastocystis spp.
1. Introduction
2. Taxonomy and Speciation
3. Cryptic, Extensive Genetic Diversity
4. Morphology
5. Programmed Cell Death
6. Life Cycle
7. Laboratory Culture
8. Clinical Aspects
8.1 Epidemiology and prevalence
8.2 Infection and disease
8.3 Diagnosis and treatment
9. Concluding Remarks
10. Acknowledgments
1l. References
B. Apicomplexans
B1. Cryptosporidium spp.
1. Introduction
2. An Emerging Disease
3. The Apicomplexa
4. Cryptosporidium spp.
5. Ecological Distribution
6. Life Cycle
7. Cell Biology
8. Methods of Isolation
9. Oocyst Storage
10. Methods for Excystation
1l. Laboratory Cultivation
12. Classification and Genotyping
13. Infection and Disease
13.1 Epidemiology
13.2 Risk factors
13.3 Clinical diagnosis
13.4 Host susceptibility
13.5 Pathophysiology
13.6 Treatment
14. Opportunistic Infections
15. Virulence Factors
16. Host Factors
17. Drug Targets and Development
18. Conclusions
19. References
B2. Toxoplasma gondii
1. Introduction
2. Discovery and Taxonomy
3. Life Cycle
4. Cell Organization
4.1 Trimembrane pellicle
4.2 Cytoskeletal network
4.3 Surface antigens
4.4 Organelles and secretory proteins
4.5 Apicoplast and fatty acid synthesis
5. Differences Between the Infective Stages
5.1 Ultrastructural differences
5.2 Metabolic differences
6. Developmental Processes and Host-Parasite Relationship
6.1 Parasitophorous vacuole
6.2 Tissue cyst
6.3 Oocyst
7. Markers for Identification of Stage
8. Genomic Organization
9. Genetic Diversity, Population Structure and Phylogeny
9.1 Markers and tools for analyzing genetic diversity
9.2 Toxoplasma population structure
10. Epidemiology
10.1 Environmental reservoir
10.2 Animal reservoir
11. Pathogenesis and Immunology of Toxoplasma gondii Infection
11.1 Parasitic factors
11.2 Dissemination into the host
11.3 Immune response
11.4 Relationship between Toxoplasma and the central nervous system
11.5 Conclusions about pathogenesis and immunology
12. Human Toxoplasmosis
12.1 Epidemiology
12.2 Clinical aspects of human toxoplasmosis
13. Diagnosis
13.1 Serological diagnosis
13.2 Parasite detection
14. Treatment
14.1 Anti-Toxoplasma drugs
14.2 Drug Resistance of Toxoplasma gondii
14.3 Conclusions about anti- Toxoplasma drugs
14.4 Therapeutics
15. Conclusions
16. Acknowledgments
17. References
B3. Isospora (Cystoisospora) belli
1. Introduction
2. Classification
3. Life Cycle and Morphology
4. CIinical Disease
5. Pathogenesis
6. Diagnosis
6.1 Key points - laboratory diagnosis
7. Treatment
8. Epidemiology and Prevention
9. References
B4. Babesia microti
1. Introduction
2. Taxonomy
3. Life Cycle
4. Vector Relations
5. Host Relations
5.1 Course of infection
5.2 Resistance mechanisms
5.3 Co-infection and immunomodulation
5.4 Persistence of infection
6. Zoonotic Babesiosis
7. CIinical Manifestations
8. Pathogenesis
9. Diagnostic Features
10. Treatment with Antimicrobials
1l. Epidemiology
11.1 Emergence of the pathogen
11.2 Prevalence
11.3 Neonatal babesiosis
11.4 Geographical distribution
11.5 Molecular epidemiology
11.6 Risk factors for infection
11.7 Risk factors for disease
12. Prevention and Control
13. Conclusions
14. References
Ciliates
Balantidium coli
1. Introduction
2. Classification
3. Life Cycle and Morphology
4. Clinical Disease
5. Pathogenesis
6. Diagnosis
6.1 Key points - laboratory diagnosis
7. Treatment
8. Epidemiology and Prevention
9. References
D. Flagellates
DI. Diplomonadida - Giardia spp.
1. Introduction
2. History of Discovery
3. Taxonomy
4. Ecological Distribution
5. Life Cycle
6. Biology
6.1 Organelles
6.2 Nuclei
6.3 Median body and flagella
6.4 Ventral adhesive disk and ventrolateral flange
6.5 Mitosomes
6.6 Lysosome-Iike vesicles (peripheral vesicles)
6.7 Genome
6.8 Transcription
6.9 Giardiavirus
7. MetaboIism
7.1 Purines and pyrimidines
7.2 Amino acids
7.3 Lipids
7.4 Carbohydrate and partial tricarboxyIic acid cycle components
8. Differentiation
8.1 Encystment (encystation)
8.2 Cyst-wall structure
8.3 Cyst-wall synthesis
8.4 Excystation
9. Methods of Isolation and Axenic Cultivation
10. Storage of Giardia
1l. Giardiasis
11.1 Epidemiology
11.2 Pathophysiology and clinical manifestations
11.3 Diagnosis
11.4 Treatment
11.5 Control of waterborne giardiasis
11.6 Antigenic variation and variable surface proteins
11.7 Immune response and therapy
12. Conclusions
13. References
D2. Trichomonas vaginalis
1. Introduction
2. Historical Perspective
3. Morphology and Life Cycle
4. Classification
5. Clinical Symptoms
6. Culture and Detection of T. vaginalis
7. Epidemiology
8. Pathobiology and Models of Host-Parasite Interactions
8.1 Lipids and glycoconjugates
8.2 T. vaginalis lipophosphoglycan
8.3 Other adhesion molecules
8.4 T. vaginalis cytopathogenic effects
8.5 T vaginalis proteases
8.6 T. vaginalis and host-cell apoptosis
8.7 T. vaginalis lipophosphoglycan and cytokine regulation
9. Current Drug Strategies
9.1 Purine metabolism in T. vaginalis
10. Treatment of Infection
1l. Conclusion
12. Acknowledgments
13. References
E. Protozoan Pathogens of Major Medical Importance
l. Entamoeba histolytica
2. Plasmodium spp.
3. Trypanosoma brucei gambiense/Trypanosoma brucei rhodesiense
4. Trypanosoma cruzi
5. Leishmania tropica/Leishmania major
6. Leishmania donovani
F. Protozoan Biology
1. Introduction
2. Cellular Properties
3. Classification
3.1 Phylum Mastigophora
3.2 Phylum Ciliophora
3.3 Phylum Sarcodina
3.4 Phylum Apicomplexa
3.5 Parabasala
3.6 Cercozoa
3.7 Radiolaria
3.8 Amoebozoa
3.9 Alveolata
3.10 Diplomonadid
3.11 Euglenozoa
3.12 Stramenopila
4. Locomotion
4.1 Pseudopodia
4.2 Cilia and flagella
4.3 Gliding movements
4.4 Locomotory proteins
5. Feeding
5.1 Metabolism
6. Reproduction
6.1 Asexual reproduction
6.2 Sexual reproduction
7. Life Cycle
7.1 Plasmodium spp.
7.2 Trypanosoma brucei
7.3 Trypanosoma cruzi
7.4 Leishmania spp.
G. Host Response
1. Human Defense Mechanisms
1.1 Nonspecific immune responses
1.2 Specific immune responses
2. Parasite Strategies of Immune Evasion
2.1 Noninduction of immune responses
2.2 Anatomical seclusion
2.3 Mechanisms of survival in macrophages
2.4 Antigenic variation
2.5 Host mimicry
2.6 Evasion of complement
2.7 Evasion of antibodies
2.8 Interference with host immune signaling molecules
3. Strategies Against Protozoa Pathogens
3.1 Vaccines
3.2 Chemotherapy
3.3 Control measures
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