Parasitology Lecture 1: Introduction to Parasitology (PDF)

PARASITOLOGY LECTURE LESSON 1: INTRODUCTION TO PARASITOLOGY HOST DEFINITIVE/FINAL HOST Human Lymphatic filarial worms Elephantiasis, Trypanosomes Anopheles...

PARASITOLOGY LECTURE LESSON 1: INTRODUCTION TO PARASITOLOGY HOST DEFINITIVE/FINAL HOST Human Lymphatic filarial worms Elephantiasis, Trypanosomes Anopheles Plasmodium spp. Malaria INTERMEDIATE HOST Snail Trematodes 1st IH Crabs, Ants Infective larval stage 2nd IH PARATENIC HOST Wild boar Underdeveloped/ arrested state of PH development RESERVOIR HOST Pigs Balantidium coli Additional source of infection PARASITE ACC. TO RELATIONSHIP B/W HOST AND PARASITE Obligate Cannot live without a host Facultative Free-living or commensal or parasitic Temporary Obligatory, free-living Intermittent Visit host during feeding ACC. TO HABITAT Endoparasite Inside; infection Ectoparasite Outside; infestation ADAPTATIONS TO PARASITE Pre-adaptation Changes that make possible existence in an unfavorable environment Pre-adaptive changes Increased resistance to the host Suckers and hooks Special attachment organs that have been developed by parasitic flatworms Body Size Affected by parasitic state - Ascaris: 35 cm - Dracunculus: 1 m Streamlining Loss of metabolic pathway Can’t synthesize cellular components, thus obtain it from its host SPECIALIZED MECHANISMS FOR EFFECTING ENTRANCE Entamoeba histolytica Intestinal amoeba Penetration of the intestinal mucosa Schistosomes Cercarial stage Has penetration glands producing enzymes in digesting the skin Hymenolepis nana Embryonic stage Penetrates the intestinal villi with six hooklets DEFENSE MECHANISMS Immune evasion Location of the parasite Changes in the parasite surface antigen Modification of the host immune response Increased reproductive capacity Chances that an egg will infect a new host are usually very small ALADO  EFFECTS OF THE PARASITE TO THE HOST Depend on the number of worms Immune system of the host Type of injury is due to present, nutritional status of the host affected interferences with the host through secretions, excretions MECHANISMS OF PARASITE INFECTION Fasciolopsis buski Local damage of intestinal wall by its suckers Intestinal obstruction Entamoeba histolytica Erodes intestinal wall by its proteolytic enzyme Plasmodium falciparum Invade and multiple RBC Attach to the walls of smaller blood vessel in the brain producing ischemia - Exoerythrocytic stage - Erythrocytic stage Ascaris lumbricoides Perforate bowel wall; intestinal obstruction Invade the appendix and bile duct Ancylostoma duodenale Human hookworm Microcytic hypochromatic anemia Necator americanus Human hookworm Deprives the host of iron by sucking blood Dibothriocephalus latus Removes vitamin B12 from alimentary tract Producing megaloblastic anemia EFFECTS OF HOST ON THE PARASITE Genetic constitution of the host Duffy null phenotype: Fy (a-b-) resistance to P. vivax Sickle cell trait: increased resistance to P. falciparum Diet or nutritional status of the host High protein diet: intestinal protozoa Low protein diet: amoebiasis Rich carbohydrate diet: tapeworms Malarial resistance Acquired immunity in modifying the severity of disease in endemic areas LIFE CYCLE INFECTIVE STAGE Encysting protozoans Cyst Non-encysting protozoans Trophozoite Egg-laying nematodes Embryonated egg [Vector-Transmitted Parasites] Mechanical vector Passive transfer; no development, fly Biological vector Active, essential in the life cycle; mosquito TYPES OF HOSTS Definitive Host Sexual production Female Anopheles mosquito – DH in Plasmodium spp. Intermediate Host Asexual production Humans – IH in Plasmodium spp. Monoxenous one IH Echinococcus granulosus Heteroxenous More than one IH Fasciola hepatica DIAGNOSTIC STAGE Microscopically Eggs, larvae, cysts, trophozoite Macroscopically Adult forms, proglottids, scolex MODES OF TRANSMISSION Ingestion, skin penetration, organ transplant, direct contact, sexual contact, blood transfusion, vector-bite, inhalation/intranasal, congenital ALADO  TREATMENT ANTIPARASITIC MEDICATION Protozoan Metronidazole Nematodes Mebendazole Trematodes and cestodes Praziquantel THERAPIES Change in diet Vitamin supplements Fluid replacement Blood transfusion Bed rest PARASITE GROUPS PROTOZOAN Phylum Sarcomastigophora Sarcodina: “amoeba”; with pseudopods (false feet) Mastigophora: “flagellate”; with flagellum (whip-like) Phylum Ciliophora Ciliata: “ciliates”; with cilia (hair-like) Multinucleate: marco and micronucleus Balantidium coli Phylum Apicomplexa No locomotor apparatus Schizogony: asexual cycle Sporogony: sexual cycle Micronemes, subpelicullar tubules, conoids Plasmodium spp.: malaria Babesia microti: Nantucket fever Toxoplasma gondii: Toxoplasmosis HELMINTHS Phylum Platyhelminthes Flatworms are hermaphroditic except schistosomes Class Turbellaria Free-living in terrestrial, freshwater, marine With/without suckers Direct development w/out metamorphosis Class Trematoda Flukes Leaf-shaped with attachment organs called suckers Incomplete digestive tract At least one IH (mollusks) Small intestine, liver, pancreas blood vessel Class Cestoda Tapeworm Ribbon-like, segmented with attachment organ called scolex Absent digestive tract May/ may not require IH Small intestine Phylum Nemathelminthes Roundworms are elongate, cylindrical, dioecious Sexes are separate; male smaller than female Copulatory bursa/spicule Complete digestive tract Phylum Acanthocephala Thorny-headed worms; endoparasites Retractable proboscis Absent digestive tract Male smaller than female Moniliformis, Macracanthorhynchus, Bulbosoma Phylum Pentastomida Endoparasites Tongue worm/ linguatulids Phylum Microsporidia Classified with Sporozoa Fungi-related Enterocytozoon and Encephalitozoon Phylum Arthropoda Segmented and bilateral symmetrical Digestive system developed Sexes are separate ALADO  Class Crustacea Aquatic forms thru gills Crabs, shrimps Freshwater crab: IH of Paragonimus westermani Copepods: IH of Dibothriocephalus latus Class Arachnida Spiderlike animals Cephalothorax and abdomen Adults have 4 pairs legs Scorpions, spiders, ticks Ixodes tick: IH of Babesia spp. Class Chilopoda Centipedes First pair of appendages as poison claws Class Insecta Most important of the arthropods Head, thorax, abdomen Anoplura Human lice Hemiptera Cone-nose bugs/reduviids (vector of Trypanosoma cruzi) Coleoptera Grain beetle (IH of Hymenolepsis nana) Flour beetle (IH of Hymenolepsis diminuta) Hymenoptera Ants (IH of Fasciola lanceolata, Eurytrema pancreaticum) Siphonaptera Fleas (IH of Dypilidium caninum) Diptera Mosquitos, flies, gnats EPIDEMIOLOGY Concerns with the occurrence and distribution of disease in Study to the manifestation of any time human population Prevalence Number of cases of a disease present in a particular population at a given time New + old cases Incidence Number of new cases in a given period of time DISTRIBUTION OF DISEASE Endemic Disease population is steady Epidemic Rise in incidence or an outbreak Hyperendemic Prevalence of a disease Sporadic Occurs in few members Pandemic Covers extensive area worldwide ALADO  LECTURE 2: AMOEBA PHYLUM SARCOMASTIGOPHORA Sub-phylum Sarcodina Sub-phylum Mastigophora Class Lobosea Class Class Zoomastigophora Kinetofragminophorea Amoebae Flagellates MORPHOLOGIC FORMS Trophozoite Feeding stage With pseudopods; motile Liquid/watery stools Not stained with iodine Diagnostic stage Mostly 1 nucleus Cyst Non-feeding stage/Inactive Without pseudopods; nonmotile Formed stool Stained with iodine [Lugol and D’Antoni] AMOEBA GENERAL CHARACTERISTICS Intestinal dwellers All amoeba except E. gingivalis, Acanthamoeba, Naegleria Free-living Naegleria, Acanthamoeba Commensals E. coli, E. hartmanni, E. dispar, E. moshkovskii, E. gingivalis, Endolimax nana, Blastocystis hominis, Iodamoeba butschlii, E. polecki in humans Pathogenic E. histolytica Zoonotic protozoan E. polecki INFECTIVE STAGE Cystic stage (Encystation) Except for E. gingivalis, Acanthamoeba, Naegleria DIAGNOSTIC STAGE Cyst Trophozoite MODE OF TRANSMISSION Ingestion of contaminated water or food Except for Acanthamoeba and Naegleria ENTAMOEBA HISTOLYTICA MORPHOLOGICAL CHARACTERISTICS Trophozoite Movement: progressive, unidirectional, rapid finger-like pseudopodia Karyosome: small and centrally located Cytoplasm: finely granular Cytoplasmic inclusions: “hematophagous” ingested RBC = “erythrophagocytosis” Cyst Shape: spherical Nuclei: 1-4 Cytoplasmic Inclusions: Glycogen mass, chromatoidal bars in young cysts STAGES Infective stage Cyst found in contaminated food and water Diagnostic stage Cyst [formed stool] Trophozoite [diarrheal stool] CLINICAL SYSMPTOMS SYMPTOMATIC INTESTINAL AMOEBIASIS Amoebic colitis Intestinal infection of the colon (large intestine) Abdominal pain/discomfort ALADO  Amoebic dysentery Severe acute form of amoebic colitis Blood and mucus in the stool SYMPTOMATIC EXTRAINTESTINAL AMOEBIASIS Amoebic pneumonitis Liver abscess rupture → Lungs Amoebic liver abscess E. histolytica spread via portal vein and infect the liver Amoebic pericarditis Liver abscess rupture → Pericardium Cutaneous amoebiasis E. histolytica infects the skin via wounds PATHOGENESIS MECHANISM FOR E. HISTOLYTICA VIRULENCE Cysteine proteinase Degrades host proteins and enables attachment to gut Stimulates host cell proteolytic cascades Gal/GalNac-binding lectin Cellular adherence, contact dependent toxicity, cell endocytosis Specific for binding to galactose (Gal) and N-acetylgalactosamine (GalNAc) Amebapore Forms ion channels in the phagocytized eukaryotic cells Cytophagocytes Kills PMNs, monocytes, and macrophages TREATMENT Diloxanide furoate Prevent protein synthesis Disrupting the protozoan’s cellular processes Paramomycin Interferes with protein synthesis by binding to the 30S ribosomal subunit Metronidazole Damage the DNA leading to cell death Amoebic dysentery and amoebic colitis Tinidazole Similar efficacy to metronidazole but has shorter treatment durations PREVENTION 1. Water can be readily disinfected by boiling and treatment with iodine. 2. Avoid usage of human feces as fertilizers. 3. Avoid eating street foods. 4. Avoid consumption of salads and fruits from unreliable food handlers. EPIDEMIOLOGY 1. Sporadic cases of E. histolytica infections occur worldwide. 2. Prevalent in south-east Asia, south-west and east Africa, and central and south America. 3. Varies with the level of sanitation and is higher in the tropics and subtropics. 4. Enteric infections remained one of the causes of mortality worldwide in 2017. 5. In the PH, amoebiasis and diarrheal disease are prevalent. ENTAMOEBA DISPAR AND ENTAMOEBA MOSHKOVSKII Two non-pathogenic that are morphologically similar to Generally asymptomatic; and their presence in stool is E. histolytica benign Entamoeba dispar Nine times more prevalent than E. histolytica Role in causing disease is not established Entamoeba moshkovskii Prevalence is unknown Found in tropical regions, common in areas with poor sanitation Mild gastrointestinal symptoms or diarrhea ENTAMOEBA HARTMANNI “Small race” E. histolytica Non-pathogenic; do not cause infections No morphological difference between E. histolytica, E. Trophozoites are typically smaller than those of E. dispar, and E. hartmanni except for size histolytica and E. dispar ENTAMOEBA COLI Non-pathogenic that resembles E. histolytica Trophozoites and cysts of E. coli are often larger MORPHOLOGICAL CHARACTERISTICS Trophozoite Movement: sluggish nondirectional and nonprogressive ALADO  Karyosome: large, irregular-shaped, eccentric Cytoplasm: coarse granulated Cytoplasmic inclusions: vacuoles with bacteria Cyst Shape: spherical Nuclei: 1-8 Cytoplasmic inclusions: Glycogen mass, splinter- shaped chromatoidals IODAMOEBA BUTSCHLII “Iodine-loving amoeba” Trophozoite “basket nucleus” [distinct formation of nuclear granules] Cyst “basket of flowers” [karyosome forming the basket, linin fibril as the stems, and granules as the blossoms] Large glycogen vacuole ENDOLIMAX NANA Most common of the Size range of cysts and trophozoite is same smaller intestinal amoebae with E. hartmanni ENTAMOEBA GINGIVALIS 1st parasitic amoeba describes in humans Close morphological resemblance to E. histolytica Forms no cyst; thus, no cystic stage Found in pyorrheal pockets between teeth and gums Trophozoite Movement: active, blunt pseudopodia Karyosome: centrally located Cytoplasm: finely granular Cytoplasmic inclusions: ingested leukocytes, bacteria NAEGLERIA FOWLERI “Brain-eating amoeba” Family Vahlkamfiidae [ameboflagellates] MORPHOLOGICAL CHARACTERISTICS Trophozoite [Ameboid forms] Movement: sluggish, blunt pseudopodia Karyosome: centrally located Trophozoite [Flagellated forms] Movement: 2 flagella at the broad end; jerky/spinning Cyst Shape: rounded think double wall LIFECYCLE Cyst → Trophozoite (Feeding & Infectious) → Promitosis → Flagellated Form (Temporary) → Trophozoite → Penetrates Nasal Mucosa → Migrates via Olfactory Nerve → Invades Brain → Causes PAM SYMPTOMS AND PATHOGENESIS Primary Amoebic Meningoencephalitis Fatal infection involving CNS Headache, fever, nausea, vomiting, and Kernig’s sign If untreated, death may occur after 3-6 days Chronic Granulomatous Infection Invasion of bone with of the skin and tissues Osteomyelitis TREATMENT Amphotericin B Miconazole Rifampicin PREVENTION 1. Public education awareness 2. Adequate chlorination of public water supplies 3. Use distilled and sterile water EPIDEMIOLOGY 1. 1st reports were recorded from Australia and America 2. Rare disease with worldwide distribution 3. Most cases occur during hot summer months ALADO  ACANTHAMOEBA Ubiquitous and free-living amoeba Cause serious infections in humans MORPHOLOGICAL CHARACTERISTICS Trophozoite Movement: sluggish, spinelike pseudopods Karyosome: large, centrally located Cytoplasm: granular and vacuolated Cyst Round with jagged edges Cytoplasmic inclusion: double cell wall [smooth inner, jagged outer] SPECIMENS CSF Brain Corneal scrapings LIFECYCLE Cyst (Resistant Form) → Trophozoite (Active Feeding Form) → Trophozoite (Binary Fission) → Eyes/Nasal passages/ Skin lesions SYMPOTOMS AND PATHOGENESIS Granulomatous Amoebic Encephalitis Immune cells forming granulomas around the infection 10 SPECIES IDENTIFIES FROM HUMAN INFECTION A. castellanii: most common cause of GAE A. culbertsoni: 2nd most common A. polyphaga: ocular infection Acanthamoeba Keratitis Can enter the eye through contact lenses Acanthamoeba produces proteolytic enzymes that break down corneal tissue EPIDEMIOLOGY 1. 1st case of Acanthamoeba keratitis from Great Britain and USA 2. Linked to wearing contact lenses 3. Not associated with swimming 4. Associated with immunosuppressed patients TREATMENT 1. Combination of dibromopropamide ointment, propamide isethionate drops, and neomycin drops 2. Biguanides and diamidines 3. No drugs specifically approved by FDA PREVENTION 1. Avoid wearing contact lenses while swimming 2. Proper wearing and disinfection of contact lens 3. Avoid using homemade saline solution for contact lens BALAMUTHIA MANDRILLARIS Uncommon and don’t have spikey pseudopodia Causes chronic CNS infection and skin lesions Produces virulence factors that enhances binding and Human to human transmission was noted through solid penetrating to blood brain barrier organ transplantation ALADO