The study of the interaction between parasites and their hosts
Parasitism
The study of important parasites which causes diseases to humans (classification, symptoms, disease, lifecycle, transmission, treatment)
Clinical parasitology
The study of important parasites which causes diseases to humans (classification, symptoms, disease, lifecycle, transmission, treatment)
Taxonomic classification/rank rules
Scientific names are always italicized
The genus is always capitalized
The species is never capitalized, even when it refers to the name of a place or person
In its first use within a particular document, the genus is always written in full. In subsequent uses, the genus can be abbreviated using the first initial and a period
A species name is never used without a genus or genus abbreviation
If you must use a common name, first define it in terms of the scientific name
Major divisions of parasites
Ectoparasite
Protozoa (Phylum)
Helminths
Ectoparasites
Insecta
Arachnida
Insecta ectoparasites
Pediculus humanus (head louse, body louse)
Pthirius pubis (crab louse)
Pulex irritans (human flea)
Arachnida ectoparasites
Sarcoptes scabiei (itch mite)
Demodex folliculorum
Demodex brevis
Protozoa (Phylum)
Ciliata
Sarcodina
Mastigophora
Sporozoa
Apicomplexan
Coccidians
Helminths
Nematoda
Trematodes
Cestodes
Relationships of the medically important parasites
Kingdom Protista
Protozoa
Sarcodina
Sporozoa
Mastigophora
Digenia
Nematoda
Cestoda
Insecta and Arachnida
Medical parasitology
The science that deals with organisms living in the human body (the host) and the medical significance of this host-parasite relationship
Protozoa
Provided with nucleus/nuclei, cytoplasm, outer limiting membrane, and cellular elaborations called organelles
Protozoa
Locomotory apparatus: cilia, flagella and pseudopodia
Require a wet environment for feeding, locomotion, osmoregulation, and reproduction
Protozoan parasite phyla
Sarcomastigophora
Ciliophora
Apicomplexa
Microspora
Apicomplexa
They have a unique organelle called an apicoplast, which is a non-photosynthetic plastid that helps them penetrate host cells. They also have an apical complex structure that contains several rings, including a conoid in some species. They are spore-producing and lack contractile vacuoles and locomotor processes.
Microsporidia
A group of spore-forming unicellular parasites. These spores contain an extrusion apparatus that has a coiled polar tube ending in an anchoring disc at the apical part of the spore. They were once considered protozoans or protists, but are now known to be fungi, or a sister group to fungi.
2. Trophozoites proliferate by binary fission in colon
3. Both cysts and trophozoites passed in feces, but only mature cysts are infective
Entamoeba histolytica
Only amebic species capable of invading tissues and causing disease
Entamoeba histolytica
Pseudopod-forming nonflagellated parasite
Most invasive of the parasites in the Entamoeba family
The only member of the family to cause colitis and liver abscess
Stages in Entamoeba histolytica life cycle
Cyst (infective)
Trophozoite (invasive)
Entamoeba histolytica cyst
Quadrinucleate, resistant to gastric acidity and desiccation, can survive in moist environment for weeks
Entamoeba histolytica transmission
1. Fecal-oral contact
2. Direct colonic inoculation through contaminated enema equipment
Entamoeba histolytica life cycle
1. Ingestion of mature cysts
2. Excystation in small intestine, trophozoites migrate to large intestine
Clinical diseases caused by Entamoeba histolytica
Amebic dysentery
Amebic colitis
Liver abscess
Amebic dysentery
Acute disease characterized by bloody diarrhea with abdominal cramping, invasion of intestinal mucosa leading to ulceration, perforation and peritonitis
Amebic colitis
Mimic ulcerative colitis, less severe than amebic dysentery (may include non-bloody diarrhea, constipation, abdominal cramping, weight loss), develops small, pinpoint mucosal ulcerations that expand within submucosa to form flask-shaped ulcers
Amebic liver abscess
Most common form of extraintestinal amebiasis (5% of patients with history of intestinal amebiasis), symptoms include fever and right upper quadrant pain
Entamoeba histolytica invasiveness
Gal/Gal Nac lectin mediates adherence to host cells
Amebapores form pores in host cell membranes
Cysteine proteinases are cytopathic for host tissues
Immunity to Entamoeba histolytica
Natural immunity (mucin inhibition of amebic attachment to mucosal cells)<|>Systemic circulation (complement-mediated killing of trophozoites)<|>Activated T-cells kill E.histo by direct lysis, cytokine production, and providing helper effect for B cell Ab
Immunosuppression during acute Entamoeba histolytica infection
T cell hyperresponsiveness<|>Suppressed proliferation and cytokine production<|>Depressed delayed type hypersensitivity<|>Macrophage suppression
Entamoeba histolytica diagnosis methods
Microscopic examination of minimum 3 stool specimens
Fresh stool examination within 30 mins (trophozoite identification)
Saline and methylene blue staining
Saline and iodine staining
Formalin ether concentration test (FECT)
Merthiolate iodine formalin concentration test (MIFC)
Morphological structures observed in diagnosis
Size of cyst<|>Number of nuclei<|>Location and appearance of karyosome<|>Appearance of chromatoid bodies<|>Presence of cytoplasmic structures like glycogen vacuole
Laboratories relying on morphology must report as "E. histolytica/E. dispar" if not using immunologic or molecular methods to differentiate