5Chapter1 General Introduction:ParasitologyOral or feco-oral route: It is the mostTRANSMISSIONOFPARASITEScommon mode oftransmission of theIt depends upon:parasites. Infection is transmitted orallySourceorreservoirofinfectionby ingestion offood, water or vegetables:Mode oftransmission.contaminated with feces containing theinfectivestagesoftheparasite. (e.g.,cystsofE.Sources ofInfectionhistolytica,and ova of Ascaris lumbricoides).Man:Manis the source or reservoir forPenetration of the skin and mucousa majority of parasitic infections (e.g.,membranes:Infection is transmittedamoebiasis,enterobiasis,etc.)Theinfectionby the penetration ofthelarval forms oftransmitted from oneinfectedmantothe parasite through unbroken skin (e.g.,anothermaniscalledasanthroponosesfilariform larva of Strongyloides stercoralisAnimal:Theinfection which istransmittedand hookwormcanpenetratethroughfrominfectedanimalstohumansiscalled asthe skin of an individual walking bare-zoonoses.The infection canbetransmittedfootedoverfecallycontaminatedsoil),orbytohumanseitherdirectlyorindirectlyviaintroductionoftheparasitesthroughblood-vectors.(e.g.,cystic echinococcosisfromsucking insect vectors. (e.g.,Plasmodiumdogsandtoxoplasmosisfromcats)species, Leishmaniaspeciesand WuchereriaVectors:Vector is an agent, usuallyanbancrofti)arthropodthattransmitstheinfectionSexual contact: Trichomonas vaginalisfrom one infected humanbeing to another.is the most frequent parasite to beVectorcanbebiological ormechanical.Antransmitted by sexual contact. However,infectedblood suckinginsectcantransmitEntamoeba,GiardiaandEnterobiusarealsothe parasite directly into theblood duringtransmittedrarelybysexualcontactamongits blood meal.homosexualsNote: Vectors have been dealt in detail in MedicalBite of vectors: Many parasitic diseasesEntomology (Chapter 16).are transmitted by insectbite (Table16.2Contaminatedsoilandwater:Soil pollutedin Chapter 16) such as:malaria (femalewithhuman excretacontaining eggsoftheanopheles mosquito), filariasis (Culex),parasites canactas animportant sourceofleishmaniasis(sandfly),Chagas'diseaseinfection,e.g.,hookworm,Ascarisspecies,(reduviidbug)andAfrican sleepingsicknessStrongyloidesspecies and Trichuris species.(tsetse fly)WatercontaminatedwithhumanexcretaVertical transmission: Mother to fetuscontaining cysts of E. histolytica or Giardiatransmission is importantforfewparasiticlamblia,canactassourceofinfectioninfections like Toxoplasma gondii,Raw or under cooked meat:Raw beefPlasmodium spp.and Trypanosomacruzi.containingthelarvaeofCysticercusbovisandBlood transfusion:Certain parasitespork containing Cysticercus cellulosae arelike Plasmodium species,Babesiasomeof the examples whereundercookedspecies,Toxoplasma species,Leishmaniameatactsassourceofinfectionspecies and Trypanosoma species can be?Other sourcesof infection:Fish, crab ortransmitted through transfusion of bloodaquaticplants,etc.orblood productsModesofTransmissionAutoinfection:Few intestinal parasitesmaybe transmitted to the same personThe infective stages of various parasites mayby contaminated hand (external auto-betransmittedfromonehostto another inthefollowingways:infection)orbyreverse peristalsis (inter-
Chapter 1 General Introduction: Parasitology 5 TRANSMISSION OF PARASITES It depends upon: z Source or reservoir of infection z Mode of transmission. Sources of Infection z Man: Man is the source or reservoir for a majority of parasitic infections (e.g., amoebiasis, enterobiasis, etc.) The infection transmitted from one infected man to another man is called as anthroponoses z Animal: The infection which is transmitted from infected animals to humans is called as zoonoses. The infection can be transmitted to humans either directly or indirectly via vectors. (e.g., cystic echinococcosis from dogs and toxoplasmosis from cats) z Vectors: Vector is an agent, usually an arthropod that transmits the infection from one infected human being to another. Vector can be biological or mechanical. An infected blood sucking insect can transmit the parasite directly into the blood during its blood meal. Note: Vectors have been dealt in detail in Medical Entomology (Chapter 16). z Contaminated soil and water: Soil polluted with human excreta containing eggs of the parasites can act as an important source of infection, e.g., hookworm, Ascaris species, Strongyloides species and Trichuris species. Water contaminated with human excreta containing cysts of E. histolytica or Giardia lamblia, can act as source of infection z Raw or under cooked meat: Raw beef containing the larvae of Cysticercus bovis and pork containing Cysticercus cellulosae are some of the examples where undercooked meat acts as source of infection z Other sources of infection: Fish, crab or aquatic plants, etc. Modes of Transmission The infective stages of various parasites may be transmitted from one host to another in the following ways: z Oral or feco-oral route: It is the most common mode of transmission of the parasites. Infection is transmitted orally by ingestion of food, water or vegetables contaminated with feces containing the infective stages of the parasite. (e.g., cysts of E. histolytica, and ova of Ascaris lumbricoides) z Penetration of the skin and mucous membranes: Infection is transmitted by the penetration of the larval forms of the parasite through unbroken skin (e.g., filariform larva of Strongyloides stercoralis and hookworm can penetrate through the skin of an individual walking barefooted over fecally contaminated soil), or by introduction of the parasites through bloodsucking insect vectors. (e.g., Plasmodium species, Leishmania species and Wuchereria bancrofti) z Sexual contact: Trichomonas vaginalis is the most frequent parasite to be transmitted by sexual contact. However, Entamoeba, Giardia and Enterobius are also transmitted rarely by sexual contact among homosexuals z Bite of vectors: Many parasitic diseases are transmitted by insect bite (Table 16.2 in Chapter 16) such as: malaria (female anopheles mosquito), filariasis (Culex), leishmaniasis (sandfly), Chagas’ disease (reduviid bug) and African sleeping sickness (tsetse fly) z Vertical transmission: Mother to fetus transmission is important for few parasitic infections like Toxoplasma gondii, Plasmodium spp. and Trypanosoma cruzi. z Blood transfusion: Certain parasites like Plasmodium species, Babesia species, Toxoplasma species, Leishmania species and Trypanosoma species can be transmitted through transfusion of blood or blood products z Autoinfection: Few intestinal parasites may be transmitted to the same person by contaminated hand (external autoinfection) or by reverse peristalsis (interChapter-01.indd 5 5/17/2014 5:48:04 PM
6Section1Introductionnal autoinfection).It is observed in Crypto-Table 1.1: Direct/simple life cycleparasites thatneed only one host (man)sporidiumparvum,Taeniasolium,Enterobiusvermicularis, Strongyloides stercoralis andProtozoaHelminthsHymenolepis nana.Entamoeba histolyticaCestodes-Giardia lamblia.HymenolepisnanaLIFECYCLEOFTHEPARASITESTrichomonasvaginalisNematodesThelifecycleoftheparasitemaybedirect:BalantidiumcoliAscarislumbricoides(simple) or indirect (complex).Cryptosporidiumparvum-.HookwormDirect/simplelifecycle:When aparasite：：Cyclospora cayetanensisEnterobiusspp.requires only one host to complete its：Isosporabelli-Trichuristrichiuradevelopment, itis referredas direct/simpleMicrosporidia.Strongyloidesspplife cycle (Table 1.1)Indirect/complex life cycle:When a.PATHOGENESISOFPARASITICparasiterequires twohosts (one definitiveDISEASEShostand anotherintermediatehost)tocomplete its development, it is referredTheparasitescancausedamagetohumansinas indirect/complex life cycle (Table 1.2).various ways.Some ofthe helminths require three hostsMechanical trauma:.(onedefinitivehostandtwointermediateEggs:Trematode eggs being large>hosts) (Table 1.3).in size, can be deposited inside theTable 1.2: Indirect/complex life cycle: parasites requiring one definitive host and one intermediate hostMan acts as definitive hostIntermediatehostParasitesDefinitivehost(man)ManSandflyLeishmaniaspp.ManTrypanosoma cruziReduvid bugsManTsetse flyTrypanosoma bruceiPigManTaenia solium (intestinaltaeniasis)CattleManTaeniasaginataManRat fleaHymenolepis diminutaManSnailSchistosoma spp.ManPigTrichinella spiralisManFilarial wormsMosquito (culex, aedes, anopheles) andflies (blackflies and deerflies)ManDracunculus medinensisCyclopsManacts as intermediatehostParasitesDefinitive hostIntermediatehostPlasmodiumspp.FemaleanophelesmosquitoManTickManBabesiasppManSarcocystis lindemanniCat and dogCatManToxoplasmagondifDogManEchinococcus granulosusManManTaeniasolium (Cysticercosis)
6 Section 1 Introduction nal autoinfection). It is observed in Crypto - sporidium parvum, Taenia solium, Enterobius vermicularis, Strongyloides stercoralis and Hymenolepis nana. LIFE CYCLE OF THE PARASITES Th e life cycle of the parasite may be direct (simple) or indirect (complex). z Direct/simple life cycle: When a parasite requires only one host to complete its development, it is referred as direct/simple life cycle (Table 1.1) z Indirect/complex life cycle: When a para site requires two hosts (one defi nitive host and another intermediate host) to complete its development, it is referred as indirect/complex life cycle (Table 1.2). Some of the helminths require three hosts (one defi nitive host and two intermediate hosts) (Table 1.3). PATHOGENESIS OF PARASITIC DISEASES Th e parasites can cause damage to humans in various ways. z Mechanical trauma: h Eggs: Trematode eggs being large in size, can be deposited inside the Protozoa Helminths • Entamoeba histolytica • Giardia lamblia • Trichomonas vaginalis • Balantidium coli • Cryptosporidium parvum • Cyclospora cayetanensis • Isospora belli • Microsporidia Cestodes • Hymenolepis nana Nematodes • Ascaris lumbricoides • Hookworm • Enterobius spp. • Trichuris trichiura • Strongyloides spp. Table 1.1: Direct/simple life cycle—parasites that need only one host (man) Man acts as defi nitive host Parasites Defi nitive host (man) Intermediate host Leishmania spp. Man Sandfl y Trypanosoma cruzi Man Reduviid bugs Trypanosoma brucei Man Tsetse fl y Taenia solium (intestinal taeniasis) Man Pig Taenia saginata Man Cattle Hymenolepis diminuta Man Rat fl ea Schistosoma spp. Man Snail Trichinella spiralis Man Pig Filarial worms Man Mosquito (culex, aedes, anopheles) and fl ies (blackfl ies and deerfl ies) Dracunculus medinensis Man Cyclops Man acts as intermediate host Parasites Defi nitive host Intermediate host Plasmodium spp. Female anopheles mosquito Man Babesia spp. Tick Man Sarcocystis lindemanni Cat and dog Man Toxoplasma gondii Cat Man Echinococcus granulosus Dog Man Taenia solium (Cysticercosis) Man Man Table 1.2: Indirect/complex life cycle: parasites requiring one defi nitive host and one intermediate host Chapter-01.indd 6 5/17/2014 5:48:05 PM
7Chapter1General Introduction:ParasitologyTable1.3: Indirect/complex lifecycle:parasites requiring onedefinitive host and two intermediate hostsParasitesDefinitive hostFirst intermediate hostSecond intermediatehostFishManDiphyllobothriumspp.CyclopsManSnailAquaticplantFasciolahepaticaManSnailFasciolopsisbuskiAquaticplantManSnailParagonimus spp.Crab and fishManSnailFishClonorchis spp.ManSnailFishOpisthorchis spp.FishGnathostoma spinigerumCat, dog and manCyclopsintestinal mucosa (Schistosoma man-(Plasmodium,LeishmaniaandTrypano-soni),bladder (Schistosoma haemato-soma),produce several enzymes, whichbium),lungs(Paragonimus),livercause digestion and necrosis of host cells(Fasciola hepatica) and can causeE.histolyticaproducesvariousenzymeslikemechanical irritationcysteine proteinases, hydrolytic enzymes>Larvae:Migrationofseveral helminthicandamoebicporeforming protein thatleadlarvae(hookworms, Strongyloides orto destruction ofthetargettissueAscaris)inthelungsproducetraumaticToxins: Some of the parasites producedamageof thepulmonary capillariestoxins, whichmayberesponsibleforpatholeadingtopneumonitisgenesis of the disease, e.g., E. histolytica.>Adult worms: Adultworms of hook-However,in contrast to bacterial toxin,worm,Strongyloides,AscarisorTaeniaparasitic toxins have minimal role inget adhere to the intestinal wall andpathogenesiscausemechanicaltraumaAllergic manifestations: Many metabolicSpaceoccupyinglesions:Certainparasites.and excretoryproducts oftheparasitesgetproducecharacteristiccysticlesionthatmayabsorbed in the circulation and producecompressthe surroundingtissues ororgans,a varietyof allergic manifestations in thee.g.,hydatid cysts and neurocysticercosissensitizedhostsInflammatoryreactions:Most of theExamples include schistosomes causingparasites induce cellular proliferation andcercarial dermatitis, rupture of hydatidinfiltration atthe siteoftheirmultiplication,cyst producing anaphylactic reactionse.g.,E.histolyticaprovokesinflammationofand occult filariasis (tropical pulmonarythelargeintestineleadingtotheformationeosinophilia)of amoebic granuloma.Adult worm ofNeoplasia:SomeoftheparasiticinfectionsW.bancrofticausesmechanical blockagecancontributetothedevelopmentofandchronicinflammationofthelymphaticsneoplasia (e.g, S. haematobium causesand lymph vessels.Trematode eggs canbladder carcinoma, Clonorchis andinduceinflammatorychanges (granulomaOpisthorchiscausecholangiocarcinoma)formation)surrounding the area of eggSecondary bacterial infections: Seen indepositionEnzyme production and lytic necrosis:somehelminthicdiseases(schistosomiasisand strongyloidiasis).Obligateintracellularparasites of man
Chapter 1 General Introduction: Parasitology 7 intestinal mucosa (Schistosoma mansoni), bladder (Schistosoma haematobium), lungs (Paragonimus), liver (Fasciola hepatica) and can cause mecha nical irritation h Larvae: Migration of several helminthic larvae (hookworms, Strongyloides or Ascaris) in the lungs produce traumatic damage of the pulmonary capillaries leading to pneumonitis h Adult worms: Adult worms of hookworm, Strongyloides, Ascaris or Taenia get adhere to the intestinal wall and cause mechanical trauma z Space occupying lesions: Certain parasites produce characteristic cystic lesion that may compress the surrounding tissues or organs, e.g., hydatid cysts and neurocysticercosis z Inflammatory reactions: Most of the para sites induce cellular proliferation and infi ltration at the site of their multiplication, e.g., E. histolytica provokes infl ammation of the large intestine leading to the formation of amoebic granuloma. Adult worm of W. bancrofti causes mechanical blockage and chronic infl ammation of the lymphatics and lymph vessels. Trematode eggs can induce infl ammatory changes (granuloma formation) surrounding the area of egg deposition z Enzyme production and lytic necrosis: Obligate intracellular parasites of man (Plasmodium, Leishmania and Trypanosoma), produce several enzymes, which cause digestion and necrosis of host cells. E. histolytica produces various enzymes like cysteine proteinases, hydrolytic enzymes and amoebic pore forming protein that lead to destruction of the target tissue z Toxins: Some of the parasites produce toxins, which may be responsible for pathogenesis of the disease, e.g., E. histolytica. However, in contrast to bacterial toxin, parasitic toxins have minimal role in pathogenesis z Allergic manifestations: Many metabolic and excretory products of the parasites get absorbed in the circulation and produce a variety of allergic manifestations in the sensitized hosts Examples include schistosomes causing cercarial dermatitis, rupture of hydatid cyst producing anaphylactic reactions and occult fi lariasis (tropical pulmonary eosinophilia) z Neoplasia: Some of the parasitic infections can contribute to the development of neoplasia (e.g., S. haematobium causes bladder carcinoma, Clonorchis and Opisthorchis cause cholangiocarcinoma) z Secondary bacterial infections: Seen in some helminthic diseases (schistosomiasis and strongyloidiasis). Parasites Defi nitive host First intermediate host Second intermediate host Diphyllobothrium spp. Man Cyclops Fish Fasciola hepatica Man Snail Aquatic plant Fasciolopsis buski Man Snail Aquatic plant Paragonimus spp. Man Snail Crab and fi sh Clonorchis spp. Man Snail Fish Opisthorchis spp. Man Snail Fish Gnathostoma spinigerum Cat, dog and man Cyclops Fish Table 1.3: Indirect/complex life cycle: parasites requiring one defi nitive host and two intermediate hosts Chapter-01.indd 7 5/17/2014 5:48:05 PM
8Section1IntroductionCertain diseases arecommon in childrenIMMUNOLOGYOFPARASITIClike giardiasis and enterobiasis whileDISEASEScertain infections occurmore commonlyThe immune response against the parasiticin adults likehookworm infection.infections depends ontwofactors:Congenitalinfectionoccurscommonlywith.Host factors: Immune status,age, under-Toxoplasma gondit; whereas newborns arelying disease,nutritional status,geneticprotectedfromfalciparummalariabecauseconstitutionandvariousdefensemechanismsofhighconcentrationoffetalhemoglobinofthehostSex:Certaindiseasesaremorecommonin. Parasitic factors: Size, route of entry,males likeamoebiasis whereas femalesarefrequencyof infection,parasitic load andmorevulnerable todevelopanemia duetohookworminfectionvarious immune evasion mechanisms ofNutritional status: Both humoral andtheparasites.Broadly, the host immunity against thecellular mediated immunity are loweredand neutrophil activityis reduced inparasiticdiseasesmaybe of twotypes:malnutrition1.ProtectiveimmuneresponseGenetic constitution of the individuals:i.InnateimmunityPeoplewithhemoglobinS(sicklecellii.Adaptive/acquiredimmunitydisease),fetal hemoglobin andthalassemia2.Unwanted orharmful immuneresponsehemoglobin areresistant tofalciparum(hypersensitive reactions).malaria where as Duffy blood groupnegativeredbloodcells (RBCs)areresistantProtectiveImmuneResponsetovivaxmalariaBoth innateand acquired immunityplayanComponents ofinnate immunityimportant role in protectingthe hosts againstparasites.Some ofthe parasitic infections can·Anatomic barriers (skin and mucosa):beeliminatedcompletelybythehostimmuneSkinisanimportantbarrierfor theresponses(completeimmunity)while fewparasites that enterbycutaneous routes likeare difficult to eliminate.In some infections,Schistosomes,hookwormandStrongyloidesthe immune defense of the host is sufficientPhysiologic barriers: It includes tempera-to resist further infection but insufficient toture, pH, and various soluble moleculesdestroy the parasite. Immunity lasts till thelikelysozyme,interferonand complement.originalinfectionremainsactiveandpreventsGastric acidity acts as a physiologic barrierfurther infection.This is called as infectionto Giardia and Dracunculusimmunity or premunition or concomitantPhagocytosis:Phagocyteslikemacrophagesimmunityor incompleteimmunity.Thisisandmicrophages(neutrophils,basophilsobserved in malaria, schistosomiasis, trichi-andeosinophils)actasfirstlineofdefensenellosis,toxoplasmosisandChagas'diseaseagainsttheparasitesComplements: They play an important(i)Innate Immunityroleforkillingthe extracellular parasitesInnate immunityis theresistancewhich anbyformingmembraneattack complexes;that leads to the formation of holes in theindividual possesses bybirth, due to geneticparasitemembraneandconstitutionalmake-up.Natural killer cells: Natural killer cellsFactors influencing innate immunity(NKs)areanother importantmediator ofAge of the host: Both the extremes of ageinnate immunity.Theyplay a central rolearemorevulnerabletoparasiticinfections.inkillingfewofthehelminthicparasites
8 Section 1 Introduction IMMUNOLOGY OF PARASITIC DISEASES The immune response against the parasitic infections depends on two factors: z Host factors: Immune status, age, underlying disease, nutritional status, genetic constitution and various defense mechanisms of the host z Parasitic factors: Size, route of entry, frequency of infection, parasitic load and various immune evasion mechanisms of the parasites. Broadly, the host immunity against the parasitic diseases may be of two types: 1. Protective immune response i. Innate immunity ii. Adaptive/acquired immunity 2. Unwanted or harmful immune response (hypersensitive reactions). Protective Immune Response Both innate and acquired immunity play an important role in protecting the hosts against parasites. Some of the parasitic infections can be eliminated completely by the host immune responses (complete immunity) while few are difficult to eliminate. In some infections, the immune defense of the host is sufficient to resist further infection but insufficient to destroy the parasite. Immunity lasts till the original infection remains active and prevents further infection. This is called as infection immunity or premunition or concomitant immunity or incomplete immunity. This is observed in malaria, schistosomiasis, trichinellosis, toxoplasmosis and Chagas’ disease. (i) Innate Immunity Innate immunity is the resistance which an individual possesses by birth, due to genetic and constitutional make-up. Factors influencing innate immunity z Age of the host: Both the extremes of age are more vulnerable to parasitic infections. Certain diseases are common in children like giardiasis and enterobiasis while certain infections occur more commonly in adults like hookworm infection. Congenital infection occurs commonly with Toxoplasma gondii; whereas newborns are protected from falciparum malaria because of high concentration of fetal hemoglobin z Sex: Certain diseases are more common in males like amoebiasis where as females are more vulnerable to develop anemia due to hookworm infection z Nutritional status: Both humoral and cellular mediated immunity are lowered and neutrophil activity is reduced in malnutrition z Genetic constitution of the individuals: People with hemoglobin S (sickle cell disease), fetal hemoglobin and thalassemia hemoglobin are resistant to falciparum malaria where as Duffy blood group negative red blood cells (RBCs) are resistant to vivax malaria. Components of innate immunity z Anatomic barriers (skin and mucosa): Skin is an important barrier for the parasites that enter by cutaneous routes like Schistosomes, hookworm and Strongyloides z Physiologic barriers: It includes temperature, pH, and various soluble molecules like lysozyme, interferon and complement. Gastric acidity acts as a physiologic barrier to Giardia and Dracunculus z Phagocytosis:Phagocytes like macrophages and microphages (neutrophils, basophils and eosinophils) act as first line of defense against the parasites z Complements: They play an important role for killing the extracellular parasites by forming membrane attack complexes; that leads to the formation of holes in the parasite membrane z Natural killer cells: Natural killer cells (NKs) are another important mediator of innate immunity. They play a central role in killing few of the helminthic parasites. Chapter-01.indd 8 5/17/2014 5:48:05 PM
9Chapter1 General Introduction:ParasitologyAgglutinating the parasitic antigens thus(ii)Acquired/AdaptiveImmunitypreventinginvasion (mediated byIgM)Thisis the resistanceacquiredbyan individualComplementactivation (byIgMandIgG):during life following exposure to an agent.Complements bindtotheFcportionofIt is mediated by antibody produced by Bthe antibody coated to the parasitic cells.lymphocytes(humoral immuneresponse)orActivationofthecomplementsleadstobyTcells (cell mediatedimmuneresponse)membranedamageand cell lysisCell mediated immune responseAntibodydependent cell-mediated cytotoxicity (ADCC) is important for killing ofWhenaparasiteenters,theparasiticanti-the helminths.NKs bindtotheFcportion ofgens are processedbythe antigen presentingthe IgG antibody coated to the helminths.cells, (e.g.,macrophages)whichpresentActivationofNKsleadstoreleaseofperforinthe antigenic peptides to T helper cells.andgranazymethatinturncausemembraneThe antigen presenting cells also secretedamageand cell lysisinterleukin-1 (IL-1)that activates the restingMast cell degranulation: IgE antibodiesT helper cells. Activated T helper cellscoated on mast cellswhengetbound todifferentiate into Th-1 and Th-2 cellsparasitic antigens, themast cells becomeT helper cell-1 secrete interleukin-2 (IL-2)activatedandreleaseanumberofmediatorsand interferongamma(IFN-)like serotonin and histamine.>Interleukin-2 activates the cytotoxicTcells and NKs, which are cytotoxic toThe Unwanted or Harmful Immunethetarget parasitic cells.TheyproduceResponsesperforin and granazyme that formpores and lyse the target cellsSometimes immuneresponses maybeexa->IFN-yactivatestherestingmacrophagesggerated or inappropriate in the sensitizedwhichinturnbecomemorephagocyticindividualsonre-exposuretothesameantigen.and release free radicals like reactiveSuchtypeofimmunopathologicreactionsareoxygen intermediate (ROI)and nitriccalled as hypersensitivity reactions that mayoxide (NO)thatkill the intracellularbe harmful tothehosts causingtissuedamage.parasitesThese are of four types (Table 1.4).·T helper cells-2 releaseIL-4,IL-5,IL-6 andParasitic Factors that Evade the HostIL-10 which are involved in activation of BImmuneResponsecellstoproduceantibodies[immunoglobinSometimesthehostsfinditdifficulttocontainE (IgE) by IL-4). IL-5 also acts as chemo-theparasiticinfectionsmainlybecauseoftheattractantfortheeosinophils.Eosinophiliafollowing reasons:is common finding in various helminthic.Large size oftheparasitesinfections..ComplicatedlifecyclesHumoral immuneresponseAntigeniccomplexicity.Th-2response activates the Bcells to produceThereare a number of mechanisms byantibodieswhich in turnhave various roleswhichtheparasites evadethehost immuneagainsttheparasitic infections.They are:responses (Table 1.5).Neutralizationofparasitictoxins(mediated.byIgAand IgG)LABORATORYDIAGNOSISOFPreventing attachment to the gastroPARASITICDISEASESintestinaltract(GIT)mucosa (mediatedbysecretoryIgA)It plays an important role in establishing
Chapter 1 General Introduction: Parasitology 9 (ii) Acquired/Adaptive Immunity This is the resistance acquired by an individual during life following exposure to an agent. It is mediated by antibody produced by B lymphocytes (humoral immune response) or by T cells (cell mediated immune response). Cell mediated immune response z When a parasite enters, the parasitic antigens are processed by the antigen presenting cells, (e.g., macrophages) which present the antigenic peptides to T helper cells. The antigen presenting cells also secrete interleukin-1 (IL-1) that activates the resting T helper cells. Activated T helper cells differentiate into Th-1 and Th-2 cells z T helper cell-1 secrete interleukin-2 (IL-2) and interferon gamma (IFN-g) h Interleukin-2 activates the cytotoxic T cells and NKs, which are cytotoxic to the target parasitic cells. They produce perforin and granazyme that form pores and lyse the target cells h IFN-g activates the resting macrophages which in turn become more phagocytic and release free radicals like reactive oxygen intermediate (ROI) and nitric oxide (NO) that kill the intracellular parasites z T helper cells-2 release IL-4, IL-5, IL-6 and IL-10 which are involved in activation of B cells to produce antibodies [immunoglobin E (IgE) by IL-4]. IL-5 also acts as chemoattractant for the eosinophils. Eosinophilia is common finding in various helminthic infections. Humoral immune response Th-2 response activates the B cells to produce antibodies which in turn have various roles against the parasitic infections. They are: z Neutralization of parasitic toxins (mediated by IgA and IgG) z Preventing attachment to the gastrointestinal tract (GIT) mucosa (mediated by secretory IgA) z Agglutinating the parasitic antigens thus preventing invasion (mediated by IgM) z Complement activation (by IgM and IgG): Complements bind to the Fc portion of the antibody coated to the parasitic cells. Activation of the complements leads to membrane damage and cell lysis z Antibody dependent cell-mediated cytotoxicity (ADCC) is important for killing of the helminths. NKs bind to the Fc portion of the IgG antibody coated to the helminths. Activation of NKs leads to release of perforin and granazyme that in turn cause membrane damage and cell lysis z Mast cell degranulation: IgE antibodies coated on mast cells when get bound to parasitic antigens, the mast cells become activated and release a number of mediators like serotonin and histamine. The Unwanted or Harmful Immune Responses Sometimes immune responses may be exaggerated or inappropriate in the sensitized individuals on re-exposure to the same antigen. Such type of immunopathologic reactions are called as hypersensitivity reactions that may be harmful to the hosts causing tissue damage. These are of four types (Table 1.4). Parasitic Factors that Evade the Host Immune Response Sometimes the hosts find it difficult to contain the parasitic infections mainly because of the following reasons: z Large size of the parasites z Complicated life cycles z Antigenic complexicity. There are a number of mechanisms by which the parasites evade the host immune responses (Table 1.5). LABORATORY DIAGNOSIS OF PARASITIC DISEASES It plays an important role in establishing Chapter-01.indd 9 5/17/2014 5:48:06 PM