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LECTURE NOTES Degree and Diploma Programs For Health Science Students

Medical ParasitologyDawit Assafa, Ephrem Kibru, S. Nagesh,Solomon ebreselassie, Fetene Deribe, !emal Ali

!imma "ni#ersit$Debub "ni#ersit$"ni#ersit$ of ondar%n collaboration with the Ethiopia Public Health &raining %nitiati#e, &he 'arter 'enter,the Ethiopia (inistr$ of Health, and the Ethiopia (inistr$ of Education

)**+Funded under "SA%D 'ooperati#e Agreement No. -A*****-/0**.

Produced in collaboration with the Ethiopia Public Health &raining %nitiati#e, &he'arter'enter, the Ethiopia (inistr$ of Health, and the Ethiopia (inistr$ of Education.Important Guidelines for Printing and Potocopying1imited permission is granted free of charge to print or photocop$ all pages of thispublication for educational, notforpro2t use b$ health care wor3ers, students orfacult$. All copies must retain all author credits and cop$right notices included in theoriginal document. "nder no circumstances is it permissible to sell or distribute on acommercial basis, or to claim authorship of, copies of material reproduced from thispublication.!"##$ %y &a'it (ssafa) Eprem *i%ru) S+ Nages)) SolomonGe%reselassie) ,etene &eri%e) -emal (li

All rights reser#ed. E4cept as e4pressl$ pro#ided abo#e, no part of this publicationma$be reproduced or transmitted in an$ form or b$ an$ means, electronic ormechanical,including photocop$ing, recording, or b$ an$ information storage and retrie#als$stem,without written permission of the author or authors.

This material is intended for educational use only by practicing health care workers or

students and faculty in a health care field.


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i PREFACEThis lecture note is useful to students of health science, medicine and otherstudents and academicians. It is believed to provide basic knowledge to students

on medical parasitology. It also serves as a good reference to parasitologists,graduate students, biomedical personnel, and health professionals. It aims atintroducing general aspects of medically important parasites prevalent in thetropics and in Ethiopia in particular. It is our belief that this note will contributemuch in alleviating the shortage of Parasitology texts.Students preparing to provide health care in their profession need solidfoundation of basic scientific knowledge of etiologic agents of diseases, theirdiagnosis and management. To face the fast growing trends of scientificinformation, students reuire getting education relevant to what they will be doingin their future professional lives. !ooks that are of manageable si"e areincreasingly important in helping students learn the seemingly overwhelming

amount of information they must absorb.


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ACKNOWLEDGEMENTSThe writers are indebted to the Ethiopian Public #ealth Initiative $EP#I% for

encouragement and financial support. &e thank all who contributed in the writeup of this lecture note and those involved in giving the secretarial service in allcolleges and 'niversities. Included in the acknowledgment are also the reviewersof the draft material, (r. #abtamu and )to )srat #ailu who are currently staffs of

))'*+, +icrobiology, Immunology, and Parasitology department. Theircomments were uiet constructive and well taken up.


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TABLE OF CONTENTSTopic Page

Preface ............................................................................................. ......... i)cknowledgement ............................................................................. ......... iiTable of -ontents .............................................................................. ........ iii

)bout the )uthors ............................................................................. ....... viiist of !oxes and Tables .................................................................. ...... viii

)bbreviations and )cronyms ............................................................ ........ ixUNIT ONE: General Parai!olog" ................................................... ........ /

)ssociation between parasite and host ........................................ ........ /Effect of parasites on the host...................................................... ........ 0!asic concepts in medical parasitology ....................................... ........ 1-lassification of medical parasitology .......................................... ........ 2

3eneral characteristics of medically important parasites ............. ...... //$/% Proto"oa ............................................................................ ...... //$4% #eliminths .......................................................................... ...... /5$5% )rthropods ......................................................................... ...... /0UNIT TWO: Me#ical Pro!o$olog" ................................................... ...... /6Introduction ....................................................................................... ...... /6-lassification of proto"oa .................................................................. ...... 47UNIT T%REE: A&oe'iai .............................................................. ...... 44Introduction ....................................................................................... ...... 44/./. Entamoeba #istolytica .......................................................... ...... 44/.4. 8ther )mebae inhabiting the alimentary canal ..................... ...... 46

/.5. Pathogenic free*living amoebae ............................................ ...... 51UNIT FOUR: Pa!(ogenic Flagella!e ............................................. ...... 56Introduction .................................................................................. ...... 564./ uminal lagellates ................................................................ ...... 56iv

4././. 3iardia amblia .............................................................. ...... 564./.4 Trichomonas vaginalis .................................................... ...... 0/4./.5 (ientamoeba ragilis ...................................................... ...... 054./.0 8ther flagellates inhabiting the alimentary canal ............. ...... 004.4. #aemoflagelates .................................................................... ...... 064.4./ eishmania Species ........................................................ ...... 06

4.4././ 9isceral eishmaniasis ............................................ ...... 064.4./.4 8ld world cutaneous leishmaniasis $8riental sore% . ...... 174.4./.5 :ew world cutaneous and mucocutaneous leishmaniasis144.4.4 Trypanosomiasis ............................................................. ...... 154.4.4./ )frican trypanosomiasis .......................................... ...... 104.4.4.4 )merican trypanosomiasis ...................................... ...... 16UNIT FI)E: Me#icall" i&por!an! cilia!e ........................................ ...... ;/!alantidiasis .................................................................................. ...... ;/


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UNIT SI*: COCCIDIA +SPORO,OA- ............................................... ...... ;50./ +alaria .................................................................................... ...... ;50././ Plasmodium falciparum ................................................... ...... ;;0./.4 Plasmodium vivax ........................................................... ...... ;uestions ......................................................................... ...... 27UNIT SE)EN: Me#ical (e&in!(olog" ............................................. ...... 24UNIT EIG%T: Me#icall" i&por!an! !rea!o#e +Fl./e- .................. ...... 20/./. !lood lukes .......................................................................... ...... 20/././. Schistosomiasis $!ilhar"iasis% ........................................ ...... 20Schistosoma +ansoni .............................................................. ...... 21'rinary Scistosomiasis ............................................................. ...... 21Schistosoma ?aponium ............................................................ ...... 2;Schistosoma Intercalatum ........................................................ ...... 2;

/.4. Intestinal lukes ..................................................................... ...... 2


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5.5.4. Echinococcus multilocularis ........................................... .... /475.0. Taenia Saginata $!eef Tape &orm% ...................................... .... /475.1. Taenia Solium $Pork Tape &orm% .......................................... .... /45vi

5.;. (iphylobotrium atum $ish Tapeworm or !road Tape &orm% ... /40

UNIT ELE)EN: Me#ical En!o&olog" ............................................. .... /46Introduction ................................................................................... .... /46)rthropods ................................................................................... .... /46!iology of )rthopods ................................................................ .... /42(evelopment of )rthropods ..................................................... .... /57Importance of )rthropods in Parasitology ................................ .... /57-lassification of )rthropods ..................................................... .... /54+edical conditions related to arthropods ................................. .... /50

). ly related conditions ...................................................... .... /50!. +osuito related conditions ............................................ .... /51-. lea related conditions ................................................... .... /51

(. ice related conditions .................................................... .... /51E. !ug related conditions .................................................... .... /5;. Tick related conditions .................................................... .... /5;3. +ite related conditions ................................................... .... /5;9ector control measures .......................................................... .... /5;$/% +echanical +ethods ...................................................... .... /5;$4% Ecological control .......................................................... .... /5;$5% -hemical methods ......................................................... .... /56$0% !iological methods ........................................................ .... /56$1% 3enetic control .............................................................. .... /56S.&&ar" ......................................................................................... .... /52Learning Ac!i1i!"

............................................................................. .... /52Re2erence ...................................................................................... .... /52Gloar" .......................................................................................... .... /5parasite relationship, patholog$ and clinical manifestations ofinfection,laborator$ diagnosis, treatment and pre#enti#e>control measures ofparasites. %n thesubse@uent section some of these criteria are brieC$ presented.Morp(olog" 9 includes si7e, shape, color and position of di6erent organelles indi6erent


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parasites at #arious stages of their de#elopment. &his is especiall$ importantinlaborator$ diagnosis which helps to identif$ the di6erent stages ofde#elopment anddi6erentiate between pathogenic and commensal organisms. For e4ample,

Entamoeba histolytica and Entamoeba coli.Geograp(ical #i!ri'.!ion E#en though re#olutionar$ ad#ances intransportation hasmade geographical isolation no longer a protection against man$ of theparasiticdiseases, man$ of them are still found in abundance in the tropics.Distribution ofparasites depends upona. &he presence and food habits of a suitable host5 Host speci2cit$, for e4ample,Ancylostoma duodenale re@uires man as ahost

whereAncylostoma caninum re@uires a dog.5 Food habits, e.g. consumption of raw or undercoo3ed meat or #egetablespredisposes to &aeniasisb. Eas$ escape of the parasite from the host the di6erent de#elopmentalstages of aparasite which are released from the bod$ along with faeces and urine arewidel$distributed in man$ parts of the world as compared to those parasites whichre@uire a #ector or direct bod$ Cuid contact for transmission.c. En#ironmental conditions fa#oring sur#i#al outside the bod$ of the host,i.e.

temperature, the presence of water, humidit$ etc.d. &he presence of an appropriate #ector or intermediate host = parasitesthat do notre@uire an intermediate host :#ector; for transmission are more widel$distributedthan those that do re@uire #ectors.6Bnce we are clear about the geographical distribution and conditionsfa#oring sur#i#al inrelation to di6erent parasites, e6ecti#e pre#enti#e and control measures canmore easil$

be de#ised and implemented.Li2e c"cle o2 parai!e 9 the route followed b$ a parasite from the time of entr$to thehost to e4it, including the e4tracorporeal :outside the host; life. %t can eitherbe simple,when onl$ one host is in#ol#ed, or comple4, in#ol#ing one or moreintermediate hosts. A


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parasite8s life c$cle consists of two common phases one phase in#ol#es theroute aparasite follows inside the bod$. &his information pro#ides an understandingof thes$mptomatolog$ and patholog$ of the parasite. %n addition the method of

diagnosis andselection of appropriate medication ma$ also be determined. &he otherphase, the routea parasite follows outside of the bod$, pro#ides crucial information pertinenttoepidemiolog$, pre#ention, and control.%o! parai!e rela!ion(ip 9 infection is the result of entr$ and de#elopmentwithin thebod$ of an$ inurious organism regardless of its si7e. Bnce the infectingorganism isintroduced into the bod$ of the host, it reacts in di6erent wa$s and this could

result ina. 'arrier state a perfect host parasite relationship where tissue destructionb$ aparasite is balanced with the host8s tissue repair. At this point the parasiteandthe host li#e harmoniousl$, i.e. the$ are at [email protected]. Disease state this is due to an imperfect host parasite relationship wheretheparasite dominates the upper hand. %t can result either from lower resistanceofthe host or a higher pathogenecit$ of the parasite.

c. Parasite destruction = occurs when the host ta3es the upper hand.La'ora!or" #iagnoi = depending on the nature of the parasitic infections,thefollowing specimens are selected for laborator$ diagnosisa; Bloo# = in those parasitic infections where the parasite itself in an$ stageof itsde#elopment circulates in the blood stream, e4amination of blood 2lm formsoneof the main procedures for speci2c diagnosis. For e4ample, in malaria theparasites are found inside the red blood cells. %n ancroftian and (ala$an2lariasis, micro2lariae are found in the blood plasma.

7b; S!ool = e4amination of the stool forms an important part in the diagnosisofintestinal parasitic infections and also for those helminthic parasites thatlocali7ein the biliar$ tract and discharge their eggs into the intestine.%n proto7oan infections, either tropho7oites or c$stic forms ma$ be detected9the


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former during the acti#e phase and the latter during the chronic phase.E4ample,Amoebiasis, iardiasis, etc.%n the case of helmithic infections, the adult worms, their eggs, or lar#ae arefound in the stool.

c; Urine = when the parasite locali7es in the urinar$ tract, e4amination of theurinewill be of help in establishing the parasitological diagnosis. For e4ample inurinar$ Schistosomiasis, eggs of Schistosoma haematobium are found in theurine. %n cases of ch$luria caused b$ Wuchereria bancrofti, micro2lariae arefound in the urine.d; Sp.!.& = e4amination of the sputum is useful in the following5 %n cases where the habitat of the parasite is in the respirator$ tract, as inParagonimiasis, the eggs of Paragonimus westermani are found.5 %n amoebic abscess of lung or in the case of amoebic li#er abscess burstinginto the lungs, the tropho7oites of E. histolytica are detected in the sputum.

e; Biop" &a!erial #aries with di6erent parasitic infections. For e4amplespleenpunctures in cases of 3alaa7ar, muscle biops$ in cases of '$sticercosis,&richinelliasis, and 'hagas8 disease, S3in snip for Bnchocerciasis.f; Ure!(ral or 1aginal #ic(arge = for Trichomonas vaginalis%ndirect e#idences = changes indicati#e of intestinal parasitic infections area7 Cytological changes in the blood = eosiniphilia often gi#es an indicationof tissue in#asion b$ helminthes, a reduction in white blood cell count isan indication of 3alaa7ar, and anemia is a feature of hoo3worminfestation and malaria.'7 Serological tests = are carried out onl$ in laboratories where special

antigens are a#ailable.8

Trea!&en! = man$ parasitic infections can be cured b$ speci2c chemotherap$.&hegreatest ad#ances ha#e been made in the treatment of proto7oal diseases.For the treatment of intestinal helminthiasis, drugs are gi#en orall$ for directaction onthe helminthes. &o obtain ma4imum parasiticidal e6ect, it is desirable thatthe drugsadministered should not be absorbed and the drugs should also ha#eminimum to4ic

e6ect on the host.Pre1en!ion an# con!rol measures ma$ be ta3en against e#er$ parasiteinfecti#inghumans. Pre#enti#e measures designed to brea3 the transmission c$cle arecrucial tosuccessful parasitic eradication. Such measures includeBGeduction of the source of infection the parasite is attac3ed within thehost, thereb$


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pre#enting the dissemination of the infecting agent. &herefore, a promptdiagnosisand treatment of parasitic diseases is an important component in thepre#ention ofdissemination.

BSanitar$ control of drin3ing water and food.BProper waste disposal = through establishing safe sewage s$stems, use ofscreenedlatrines, and treatment of night soil.B&he use of insecticides and other chemicals used to control the #ectorpopulation.BProtecti#e clothing that would pre#ent #ectors from resting in the surfaceof the bod$and inoculate pathogens during their blood meal.Bood personal h$giene.BA#oidance of unprotected se4ual practices.

CLASSIFICATION OF MEDICAL PARASITOLOG3Parasites of medical importance come under the 3ingdom called protista andanimalia.Protista includes the microscopic singlecelled eu3aro$tes 3nown asproto7oa. %ncontrast, helminthes are macroscopic, multicellular worms possessingwelldi6erentiatedtissues and comple4 organs belonging to the 3ingdom animalia. (edicalParasitolog$ is generall$ classi2ed into5 Me#ical Pro!o$oolog" 9 Deals with the stud$ of medicall$ importantproto7oa.

95 Me#ical %el&in!(olog" 9 Deals with the stud$ of helminthes :worms; thata6ectman.5 Me#ical En!o&olog" 9 Deals with the stud$ of arthropods which cause ortransmitdisease to man.Describing animal parasites follow certain rules of 7oological nomenclatureand eachph$lum ma$ be further subdi#ided as followsSuper class Super family

Pylum Su%pylum Class Order ,amily Genus SpeciesSu%class Su%family10FIGURE 67 CLASSIFICATION OF MEDICALL3 IMPORTANT PARASITESPROTO,OA META,OA +%ELIMINT%S-Sarco#ina +A&oe'ae-: Pla!"(el&in!(e::a; enus, Entameba Tre&a!o#ea:E.g. Entameba histolytica :a; enus Schistosoma


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:b; enus Endolima4 E.g. S. mansoniE.g. Endolima nana :b; enus Fasciola:c; enus %odameba E.g. !. hepaticaE.g. "odameba butchlii Ce!o#a::d; enus Dientmeba :a; enus Diph$lobotrium

E.g. #ientameba fragilis E.g. #. latumMa!igop(ora +Flagella!e-: :b; enus &aenia:a; enus iardia E.g. T. saginataE.g. $. lamblia :c; enus Echinococcus:b; enus &richomonas E.g. E. granulosusE.g. T. vaginalis :d; enus H$menolepsis:c; enus &r$panosoma E.g. H. nanaE.g. T. brucci Ne&a!(el&in!(e::d; enus 1eishmania :a; %ntestinal NematodesE.g. %. donovani E.g.A. lumbricoidesSporo$oa :b; Somatic Nematodes

:


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for storage of food, digestion and e4cretion of waste products. &he nucleusalsofunctions in reproduction and maintaining life.&he proto7oal parasite possesses the propert$ of being transformed from anacti#e

:tropho7oite; to an inacti#e stage, losing its power of motilit$ and enclosingitself withina tough wall. &he protoplasmic bod$ thus formed is 3nown as a c$st. At thisstage theparasite loses its power to grow and multipl$. &he c$st is the resistant stageof theparasite and is also infecti#e to the human host.Repro#.c!ion = the methods of reproduction or multiplication among theparasiticproto7oa are of the following t$pes


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+- %ELIMINT%S:&he heliminthic parasites are multicellular, bilaterall$ s$mmetrical animalsha#ing threegerm la$ers. &he helminthes of importance to human beings are di#ided intothree

main groups with the peculiarities of the di6erent categories described intable ).TABLE 7 DIFFERENTIATING FEATURES OF %ELMINT%ESCESTODE TREMATODE NEMATODE

S(ape&ape li3e, segmented 1eaf li3e, "nsegmented Elongated,'$lindricalSe5e Not separate Not separate Separate.:monoecious; :monoecious; :diecious;E4cept blood Cu3eswhich are dioecious;%ea#; En# Suc3ers with hoo3s Suc3ers no hoo3s No suc3ers, and

hoo3sAli&en!ar" Absent Present Present andcanal but incomplete completeBo#" ca1i!" Absent Absent Present14+


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b$ insects.FIGURE 7 CLASSIFICATION OF ART%ROPODSKingdom AnimaliaPh$lum Arthropoda'lass 'lass 'lass 'lass 'lass

'rustacia Arachnida %nsecta 'hilopoda Pentastomidae.g. Scorpion e.g. &ic3s e.g. (os@uito e.g. 'entipedes e.g. tongue wormsN7B7 'rustacia, Arachnida, and %nsecta are the three most common classes ofarthropods of medical signi2cance, which need closer attention15

SUMMAR3A parasite is an organism which li#es in>on the bod$ of a host. A host is thatwhichharbors the parasite. &here is usuall$ some association such as mutualism,commensalisms, or parasitism between the parasite and the host. &hisassociation

ma$ produce a #ariet$ of e6ects and the host usuall$ tends to react to it."nderstanding the #arious structural and beha#ioral components of parasitesassistsclassi2cation. %n general, the proto7oa, helminthes and arthropods are themostcommonl$ studied and the most important parasites in medical parasitolog$.&he$ arefurther sub classi2ed considering man$ parameters.16RE)IEW =UESTIONS


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At the end of the lesson, the student should be able to5 Discuss the classi2cation of medicall$ important proto7oa.5 Discuss the pathogenesis and clinical aspects of infections.5 Describe the general epidemiological aspects and transmission patterns ofdiseases

caused b$ proto7oa.5 %dentif$ the methods and procedures of laborator$ diagnosis of pathogenicproto7oa inclinical specimens.5 Discuss treatment options for proto7oan infections.5 %mplement the pre#enti#e and control measures of proto7oan infection.

INTRODUCTIONProto7oa :singular, proto7oan;, from the ree3 Lprotos8 and L7oon8 meaningM2rstanimal, are members of eu3ar$otic protists. &he$ ma$ be distinguished fromother

eu3ar$otic protists b$ their abilit$ to mo#e at some stage of their life c$cleand b$ theirlac3 of cell wall.

Occ.rrence o2 pro!o$oaProto7oa are found in all moist habitats. &he$ are common in sea, in soil andin freshwater. &hese organisms occur generall$ as a single cell. 'olonies of proto7oamightalso occur in which indi#idual cells are oined b$ c$toplasmic threads andformaggregates of independent cells.

Howe#er, distinct t$pes of proto7oa, include a resistant c$st :nonmotile;stage tosur#i#e ad#erse en#ironmental conditions, such as desiccation, low nutrientsuppl$, ande#en anaerobiosis. For e4ample, the soil amoeba, Naegleria is a resistantc$st in dr$18weather, a na3ed amoeba in moist soil, and becomes Cagellated whenCooded withwater.

Morp(olog" o2 pro!o$oaProto7oa are predominantl$ microscopic, ranging in si7e from ) to more than


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3ar$osome, which are useful structures to distinguish proto7oan species fromoneanother based on the shape, si7e and distribution of these structures.

I&por!ance o2 pro!o$oaProto7oa ser#e as an important lin3 in the food chain and ecological balance

of man$communities in wetland a@uatic en#ironments. &he$ are also important inbiologicalsewage treatment, which in#ol#es both anaerobic digestion and>or aeration.%n addition,proto7oa are important laborator$ organisms in research areas, b$ whichtheir ase4ualreproduction enables clones to be established with the same genetic ma3eup. &heseare useful in the stud$ of cell c$cles and nucleic acid bios$nthesis during celldi#ision.

Me#ical concern o2 pro!o$oaProto7oa are ubi@uitous in moist areas, including the human alimentar$canal. From anecological standpoint, proto7oa ma$ be di#ided into freeli#ing forms ands$mbioticforms. Some of the s$mbiotic ones are parasitic and ma$ cause disease.Although most amoebas are freeli#ing, se#eral are found as commensalinhabitants ofthe intestinal tract in humans. Bne of these organisms Entamoeba histolyticama$in#ade tissue and produce disease. &he maorit$ of ciliates are free li#ing and

seldomparasiti7e humans. Flagellates of the genus &r$panosomes and 1eishmaniaarecapable of in#ading the blood tissue of humans, where the$ producese#ere chronicillness. Bthers such as Trichomonas vaginalis and $iardia lamblia, inhabit the19urogenital and gastrointestinal tracts and initiate disease characteri7ed b$mild tomoderate morbidit$ but no mortalit$.Sporo7oan organisms, in contrast, produce two of the most potentiall$ lethal

diseases ofhuman3ind malaria and to4oplasmosis. ith the ad#ent of H%? a new andimportantchapter has been opened9 i.e. Lopportunistic8 parasitosis. (ost of theparasitic incidentsbelong to endocellular proto7oa of di6erent genera or species.

Repro#.c!ion an# regenera!ion o2 pro!o$oa


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As a general rule, proto7oa multipl$ b$ ase4ual reproduction. &his is not tosa$ thatse4ual processes are absent in the proto7oa. Some parasitic forms ma$ ha#eanase4ual phase in one host and a se4ual phase in another host. :refer to page


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Flagellates $iarda lamblia( Trichomonas vaginalis(&r$panosoma spp,1eishmania spp'liliophora 'alantidium coli'occidian "sospora belli( &ryptosporidium parvum, Tooplasma gondii(Plasmodium

speciesProto7oan pathogens can also be grouped according to the location in thebod$ wherethe$ most fre@uentl$ cause disease.21Ta'le96 I&por!an! pa!(ogenic pro!o$oa an# co&&onl" ca.e# #ieae7T"pe an# loca!ion Specie Dieae%ntestinal tractEntamoeba histolytica$iardia lamblia&ryptosporidium parvum

'alantidium coli"sospora belli&yclospora cayentanensisAmbiasisiardiasis'r$ptosporidiosisalantidiasis%sosporiosis'$closporiasis"rogenital tract Trichomonas vaginalis&richomoniasislood and tissue Plasmodium species

Tooplasma gondii&r$panasoma species1eishmania speciesNaegleria speciesAcanthamoeba speciesabesia microti(alaria&o4oplasmosis&r$panosomiasis1eishmaniasisAmoebic (eningoencephalitis

Amoebic (eningoencephalitisabesiosis22

UNIT T%REEAMOEBIASISINTRODUCTION


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Amoebas primiti#e unicellular microorganisms with a relati#el$ simple lifec$cle whichcan be di#ided into two stages5&ropho7oite = acti#el$ motile feeding stage.5 '$st = @uiescent, resistant, infecti#e stage.

&heir reproduction is through binar$ 2ssion, e.g. splitting of the tropho7oiteor throughthe de#elopment of numerous tropho7oites with in the maturemultinucleated c$st.(otilit$ is accomplished b$ e4tension of pseudopodia :Mfalse foot;

6767 En!a&oe'a (i!ol"!icaMorp(ological 2ea!.re+a- Trop(o$oi!e?iable tropho7oites #ar$ in si7e from about


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%n#asion of blood #essels leads to secondar$ e4tra intestinal lesions.raduall$ the e6ect of the parasite on the host is toned down together withconcomitant increase in host tolerance, ma3ing it diQcult for the parasite tocontinueits life c$cle in the tropho7oite phase.

A certain number of tropho7oites come from tissues into lumen of bowel andare 2rsttransformed into prec$st forms.Prec$sts secret a c$st wall and become a uninucleate c$st. E#entuall$,mature@uadrinucleate c$sts form. &hese are the infecti#e forms.oth mature and immature c$sts ma$ be passed in faeces. %mmature c$stscanmature in e4ternal en#ironments and become infecti#e.24Figure< life c$cle of Entamoeba histol$tica

Pa!(ogenei&ropho7oites di#ide and produce e4tensi#e local necrosis in the largeintestine. %n#asioninto the deeper mucosa with e4tension into the peritoneal ca#it$ ma$ occur.&his canlead to secondar$ in#ol#ement of other organs, primaril$ the li#er but alsothe lungs,brain, and heart. E4traintestinal amebiasis is associated with tropho7oites.Amoebasmultipl$ rapidl$ in an anaerobic en#ironment, because the tropho7ites are3illed b$

ambient o4$gen concentration.Epi#e&iolog"E.histolytica has a worldwide distribution. Although it is found in cold areas,theincidence is highest in tropical and subtropical regions that ha#e poorsanitation andcontaminated water. About I*R of infections are as$mptomatic, and theremainingproduces a spectrum of clinical s$ndrome. Patients infected with E.hisolyticapass non25infectious tropho7otes and infectious c$sts in their stools. &herefore, the

main source ofwater and food contamination is the s$mptomatic carrier who passes c$sts.S$mptomatic amebiasis is usuall$ sporadic. &he epidemic form is a result ofdirectpersontoperson faecaloral spread under conditions of poor personalh$giene.Clinical 2ea!.re


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&he outcome of infection ma$ result in a carrier state, intestinal amebiasis,ore4teraintestinal amebiasis. Diarrhoea, Catulence, and cramping arecomplaints ofs$mptomatic patients. (ore se#ere disease is characterised b$ the passing

ofnumerous blood$ stools in a da$. S$stemic signs of infection :fe#er,leu3oc$tosis, rigors;are present in patients with e4traintestinal amebiasis. &he li#er is primaril$in#ol#ed,because tropho7oites in the blood are remo#ed from the blood b$ the portal#eins. &heright lobe is most commonl$ in#ol#ed, thus pain o#er the li#er withhepatomegal$ andele#ation of the diaphragm is obser#ed.I&&.ni!"

E.histolytica elicits both the humeral and cellular immune responses, but it isnot $etclearl$ de2ned whether it modulates the initial infection or pre#entsreinfection.La'ora!or" #iagnoi%n intestinal amoebiasis5 E4amination of a fresh d$senteric faecal specimen or rectal scraping fortropho7oite stage. :(otile amoebae containing red cells are diagnostic ofamoebicd$senter$;.5 E4amination of formed or semiformed faeces for c$st stage. :'$sts indicate

infection with either a pathogenic E.histolytica or nonpathogenic E.dispar.;26Figure ))( E.histolytica tropho7oite :A; E. histolytica '$st :;E5!rain!e!inal a&oe'iai5 Diagnosed b$ the use of scanning procedures for li#er and other organs.5 Speci2c serologic tests, together with microscopic e4amination of theabscessmaterial, can con2rm the diagnosis.Trea!&en!Acute, fulminating amebiasis is treated with metrondia7ole followed b$iodo@uinol, and

as$mptomatic carriage can be eradicated with iodo@uinol, dilo4anide furoate,orparomom$cin. &he c$sticidal agents are commonl$ recommended foras$mptomaticcarriers who handle food for public use.(etronida7ole, chloro@uine, and dilo4anide furoate can be used for thetreatment ofe4tra intestinal amoebiasis.


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Pre1en!ion%ntroduction of ade@uate sanitation measures and education about theroutes oftransmission.A#oid eating raw #egetables grown b$ sewerage irrigation and night soil

27677 OT%ER AMEBAE IN%ABITING T%E ALIMENTAR3 CANAL(ost of these amoebae are commensal organisms that can parasiti7e thehumangastrointestinal tract.Entamoeba hartmanni in all of its life=c$cle stage, E.hartmanni resemblesE.histolyticae4cept in si7e, $et there is a slight o#erlap in the si7e range. &he tropho7oitesdo notingest red blood cells, and their motilit$ is generall$ less #igorous than thatof

E.histolytica. As in other amebae, infection is ac@uired b$ ingestion of food orwatercontaminated with c$stbearing faeces. %denti2cation is based one4amination of smallamebae in unstained or iodinestained preparations. "suall$ no treatment isindicated,measures generall$ e6ecti#e against faecalborne infections will control thisamoebicinfection.Entamoeba coli the life c$cle stages include9 tropho7oite, prec$st, c$st,metac$st, and

metac$stic tropho7oite. &$picall$ the mo#ements of tropho7oites aresluggish, withbroad short pseudopodia and little locomotion, but at a focus the li#ingspecimen cannotbe distinguished from the acti#e trophoto7oite of E.histolytica. Howe#er, thec$sts areremar3abl$ #ariable in si7e. Entamoeba coli is transmitted in its #iable c$sticstagethrough faecal contamination. *.coli as a lumen parasite is nonpathogenicandproduces no s$mptoms. &he mature c$st :with more than four nuclei; is the

distincti#estage to di6erentiate E.coli from the pathogenic E.histolytica. Speci2ctreatment is notindicated since this amoeba is nonpathogenic. &he presence of E.coli in stoolspecimen is e#idence for faecal contamination. Pre#ention depends on betterpersonalh$giene and sanitar$ disposal of human e4creta.


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Entamoeba polecki arelati#el$ cosmopolitan parasite of hog and mon3e$. %tcan causehuman disease but is rarel$ isolated. &he disease is manifested as mild,transientdiarrhoea. &he diagnosis of E.polec+i infection is con2rmed b$ the

microscopicdetection of c$sts in stool specimens. &reatment is the same as forE.histolyticainfection. Pre#ention is achie#ed b$ good personal h$giene.28

Endolimax nana is a lumen dweller in the large intestine, primaril$ at thececal le#el,where it feeds on bacteria. &he life c$cle is similar to E.histolytica. (otilit$ ist$picall$sluggish :slugli3e; with blunt h$aline pseudopodia, Proects shortl$. Humaninfection

results from ingestion of #iable c$sts in polluted water or contaminated food.&$picalo#oid c$sts of E.nana are con2rmati#e. Gounded c$sts and li#ing tropho7oitesare oftenconfused with E.hartmanni and E.histolytica. No treatment is indicated forthis nonpathogenicinfection. Pre#ention can be achie#ed through personal cleanliness andcommunit$ sanitation.Iodamoeba buetschlii the natural habitat is the lumen of the large intestine,theprincipal site probabl$ being the caecum. &he tropho7oite feeds on enteric

bacteria9 it isa natural parasite of man and lower primates. %t is generall$ regarded as anonpathogeniclumen parasite. No treatment is ordinaril$ indicated. Pre#ention is based ongood personal h$giene and sanitation in the communit$.Entamoeba gingivalis onl$ the tropho7oite stage presents, and enc$stationprobabl$does not occur. E.gingivalis is a commensal, li#ing primaril$ on e4udate fromthemargins of the gums, and thri#es best on unhealth$ gums. No speci2ctreatment is

indicated. Howe#er the presence of E.giingivalis suggests a need for betteroralh$giene. &he infection can be pre#ented b$ proper care of the teeth andgums.Blastocystis hominis is an inhabitant of the human intestinal tract pre#iousl$regardedas nonpathogenic $east. %ts pathogenecit$ remains contro#ersial. &heorganism is


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found in stool specimen from as$mptomatic people as well as from peoplewithpersistent diarrhoea. '.hominis is capable of pseudopodia e4tension andretraction, andreproduces b$ binar$ 2ssion or sporulation. &he classic form that is usuall$

seen in thehuman stool specimen #aries tremendousl$ in si7e, from +*Om. &here arethin =walled c$sts in#ol#ed in autoinfection, and thic3=walled c$sts responsible fore4ternaltransmission #ia the faecaloral route. &he presence of large numbers ofthese parasites:2#e or more per oil immersion microscopic 2eld; in the absence of otherintestinalpathogens indicates disease. &he organism ma$ be detected in wet mountsor trichome

=stained smears of faecal specimens. &reatment with iodo@uinol ormetronida7ole has29been successful in eradicating the organism from intestine and alle#iatings$mptoms.Howe#er, the de2niti#e role of '.hominis in disease remains to bedemonstrated. &heincidence and apparent worldwide distribution of the infection indicatespre#enti#emeasures to be ta3en, which in#ol#e impro#ing personal h$giene andsanitar$

conditions.Parasitolog$

30Ta'le : Morp(olog" o2 Trop(o$i!e o2 in!e!inal A&oe'aeSpecieSi$e +#ia&e!eror leng!(-MotilityN.cle. C"!opla&N.&'er Perip(eralC(ro&a!inKar"oo&alc(ro&a!inAppearance Incl.ionEntamoebahistolytica


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)*Omin#asi#eformProgressi#e withh$aline, 2ngerli3epseudopodsBne not#isible inunstainedpreparationsFine granulesusuall$ e#enl$distributed anduniform in si7eSmall, discreteusuall$ centrall$located, butoccasionall$

eccentricall$ locatedFinel$granularEr$throc$tesoccasionall$nonin#asi#eorganisms ma$contain bacteriaEntamoebahartmanni/


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range, )*)/OmSluggish, nonprogressi#e,with bluntpseudopodsBne often#isible inunstainedpreparations'oarsegranules,irregular insi7e anddistribution1arge, discrete,usuall$ eccentricall$located

'oarse,often#acuolatedacteria $easts,other materials31Entamoebaploec+i


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e#enl$distributed,occasionall$irregularl$arranged,chromatinsometimes inpla@ues orcrescentsSmall, discrete,eccentricall$ locatedoccasionall$ large,di6use, or irregular'oarsel$granular,ma$resemble

E.coli9#acuolatedacteria $eastsEndolimanana


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locatedPresent elongatedbars with bluntl$rounded ends"suall$ di6use

concentratedmass often in$oung c$sts9stains reddishbrown with iodineEntaboebahistolytica/


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Eight inmature c$stoccasionall$,super nucleatec$sts with


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/


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c$stNone 1arge, usuall$eccentricall$located9refractile,

achromaticgranules onranulesoccasionall$present, but bodiesas seen inEntamoebaspecies are not'ompact, wellde2nedmass9stains dar3 brown

with iodine34one side of3ar$osome9indistinct iniodinepreparationspresent3567


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pseudopodia from it. &he tropho7oite ma$ be binucleated. "nli3e mostamoebae thenuclear en#elope brea3s down during mitosis.Naegleria, Acanthamoeba, alamuthia organisms are opportunisticpathogens.

Naegleria fowleri causes acute primar$ amoebic meningoencephalitis.Acantamoeba alamuthia organisms are responsible for granulomatous amoebicencephalitis andsingle or multiple brain abscesses, primaril$ in immunocompromisedindi#iduals.Keratitis :e$e; and s3in infection b$ Acanthamoeba ma$ also occur. For thediagnosisof Naegleria, Acanthamoeba, and alamuthia infections, specimens of nasal36discharge and cerebrospinal Cuid9 and in cases of e$e infections corneal

scrapingshould be collected. &he clinical specimen can be e4amined with salinewetpreparationand %odine stained smear. &reatment of freeli#ing amoebic infections islargel$ ine6ecti#e. &hese infections are rare in Ethiopia.37

UNIT FOURPAT%OGENIC FLAGELLATESINTRODUCTIONFlagellates are unicellular microorganisms. &heir locomotion is b$ lashing a

tailli3eappendage called a Cagellum or Cagella and reproduction is b$ simple binar$2ssion.&here are three groups of Cagellates5 1uminal Cagellates$iardia lamblia#ientmoeab fragilis5 HemoCagellates&r$panosoma species.1eishmania species.5 enital Cagellates

Trichomonas vaginalis767 L.&inal 2lagella!e76767 Giar#ia la&'liaI&por!an! 2ea!.re = the life c$cle consists of two stages,the tropho7oite and c$st. &he tropho7oite is I


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with which it attaches to the intestinal wall. &he o#al c$stis 0


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giardiasis. iardia = speci2c %gA is particularl$ important in both defenseagainst andclearance of parasite.La'ora!or" #iagnoiE4amination of diarrhoeal stool tropho7oite or c$st, or both ma$ be

reco#ered in wetpreparation. %n e4aminations of formed stool :e.g. in as$mptomatic carriers;onl$ c$stsare seen. iardia species ma$ occur in Mshowers, i.e. man$ organisms ma$be presentin the stool on a gi#en da$ and few or none ma$ be detected the ne4t da$.&hereforeone stool specimen per da$ for - da$s is important.40Figure /9 $iardia lamblia tpho7oite :A;, c$st :;%f microscopic e4amination of the stool is negati#e in a patient in whom

giardiasis ishighl$ suspected duodenal aspiration, string test :enterotest;, or biops$ ofthe uppersmall intestine can be e4amined.%n addition to con#entional microscop$, se#eral immunologic tests can beimplementedfor the detection of parasitic antigens.Trea!&en!For as$mptomatic carriers and diseased patients the drug of choice is@uinacrineh$drochloride or metronida7ole.

Pre1en!ion- As$mptomatic reser#oirs of infection should be identi2ed treated.- A#oidance of contaminated food and water.- Drin3ing water from la3esand streams should be boiled, 2ltered and>oriodinetreated.- Proper waste disposal and use of latrine.41

7677 Tric(o&ona 1aginaliI&por!an! 2ea!.re it is a pearshaped organism with a central nucleus andfouranterior Cagella9 and undulating membrane e4tends about twothirds of its

length. %te4ists onl$ as a tropho7oite form, and measured )-Om long /


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gland of men. After introduction b$ se4ual intercourse, proliferation beginswhich resultsin inCammation large numbers of tropho7oites in the tissues and thesecretions. &heonset of s$mptoms such as #aginal or #ul#al pruritus and discharge is often

sudden andoccurs during or after menstruation as a result of the increased #aginalacidit$. &he#aginal secretions are li@uors, greenish or $ellowish, sometimes froth$, andfoulsmelling. %nfection in the male ma$ be latent, with no s$mptoms, or ma$ bepresent asself limited, persistent, or recurring urethritis.42

Epi#e&iolog"&his parasite has worldwide distribution, and se4ual intercourse is the

primar$ mode oftransmission. Bccasionall$, infections can be transmitted b$ fomites :toiletarticles,clothing;, although this transmission is limited b$ liabilit$ of the tropho7oite.Garel$%nfants ma$ be infected b$ passage through the mother8s infected birthcanal. &hepre#alence of this Cagellate in de#eloping countries is reported to be /R =)*R inwomen and )R =


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following massage of the prostate gland.5 'ontamination of the specimen with faeces ma$ confuse T.vaginalis withT.hominis.43Figure 9 Trichomonas vaginalis

Trea!&en!(etronida7ole is the drug of choice. %f resistant cases occur, retreatmentwith higherdoses is [email protected]!ion- oth male female se4 partners must be treated to a#oid reinfection- ood personal h$giene, a#oidance of shared toilet articles clothing.- Safe se4ual practice.767


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Tric(o&ana !ena5 = was 2rst reco#ered from the mouth, speci2call$ in tartarfrom theteeth. &here is no 3nown c$st stage. &he tropho7oite has a p$riform shapeand issmaller and more slender than that of T.hominis. Diagnosis is based on the

reco#er$ ofthe organism from the teeth, gums, or tonsillar cr$pts, and no therap$ isindicated.C(ilo&a!i5 &enli = has both a tropho7oite and c$st stage. %t normall$ li#esin thececal region of the large intestine, where the organism feeds on bacteria anddebris. %tis considered to be a nonpathogenic, and no treatment is recommended.Parasitolog$

45

Ta'le >: Morp(olog" o2 Trop(o$oi!e o2 in!e!inal Flagella!e

Specie Leng!( Shape Mo!ili!" N.&'er o2 N.cleiN.&'er o2Flagella O!(er 2ea!.re#ientamoeba fragilis/


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classi2ed as an amebaTrichomonas hominis0)*Om usualrange,


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#entral surface$iardialamblia


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h$persplenism contributes to the de#elopment of anaemia andl$mphadenopath$also occurs. %ncreased production of globulin results in h$perglobulinemia,andre#ersal of the albumintoglobulin ratio.

Epi#e&iolog"%. donovani donovani( infection of the classic 3alaa7ar :Mblac3 sic3ness; ordumdum fe#er t$pe occurs in man$ parts of Asia, Africa and Southeast Asia.Kalaa7ar occurs in three distinct epidemiologic patterns. %n (editerraneanbasin:European, Near Eastern, and Africa; and parts of 'hina and Gussia, thereser#oir hosts are primaril$ dogs fo4es9 in subSaharan Africa, rats smallcarni#ores are belie#ed to be the main reser#oirs. %n %ndia and neighboringcountries :and Ken$a;, 3alaa7ar is anthroponosis, i.e. there is no othermammalian reser#oir host other than human. &he #ector is the Phlebotomussand C$. Bther #ariants of %. donovani are also recogni7ed %. donovani

infantumwith similar geographical distribution, reser#oir host and #ector9 with %.donovanidonovani. %. donovani chagasi is found in South America, 'entral America,especiall$ (e4ico, and the est %ndies. Geser#oir hosts are dogs, fo4es, andcats, and the #ector is the 1ut7omi$a sand C$.49

Clinical 2ea!.reS$mptoms begin with intermittent fe#er, wea3ness, and diarrhea9 chills andsweating that ma$ resemble malaria s$mptoms are also common earl$ in theinfection. As organisms proliferate in#ade cells of the li#er and spleen,

mar3edenlargement of the organs, weight loss, anemia, and emaciation occurs. ithpersistence of the disease, deepl$ pigmented, granulomatous lesion of s3in,referred to as post3alaa7ar dermal leishmaniasis, occurs."ntreated #isceral leishmaniasis is nearl$ alwa$s fatal as a result ofsecondar$infection.I&&.ni!"Host cellular and humoral defence mechanisms are stimulated.La'ora!or" #iagnoi5 E4amination of tissue biops$, spleen aspiration, bone marrow aspiration or

l$mph node aspiration in properl$ stained smear :e.g. iemsa stain;.5&he amastigotes appear as intracellular e4tra cellular 1. dono#an :1D;bodies.Figure I9 iemsastained amastigotes :1D bodies;5 'ulture of blood, bone marrow, and other tissue often demonstrates thepromastigote stage of the organisms.5 Serologic testing is also a#ailable.50


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Trea!&en!&he drug of choice is sodium stibogluconate, a penta#alent antimonialcompound.Alternati#e approaches include the addition of allopurinol and the use ofpentamidine or amphotercin .

Pre1en!ion5 Prompt treatment of human infections and control of reser#oir hosts.5 Protection from sand Cies b$ screening and insect repellents.!!"!! %ld &orld Cutaneous $eishmaniasis '%riental sore(Clinical #ieae%.tropica minor ) dr$ or urban cutaneous leishmaniasis%.tropica ma-or wet or rural cutaneous leishmaniasis%.aethiopica cutaneous leishmaniasisI&por!an! 2ea!.re&hese are parasites of the s3in found in endothelial cells of the capillaries ofthe

infected site, nearb$ l$mph nodes, within large mononuclear cells, inneutrophilicleu3oc$tes, and free in the serum e4uding from the ulcerati#e site.(etastasis toother site or in#asion of the #iscera is rare.Pa!(ogenei%n neutrophilic leu3oc$tes, phagoc$tosis is usuall$ successful, but inmacrophages the introduced parasites round up to form amastigote andmultipl$.%n the earl$ stage, the lesion is characteri7ed b$ the proliferation ofmacrophages

that contain numerous amastigotes. &here is a #ariable in2ltration ofl$mphoc$tesand plasma cell. &he o#erl$ing epithelium shows acanthosis andh$per3eratosis,which is usuall$ followed b$ necrosis and ulceration.51Epi#e&iolog"'utaneous leishmaniasis produced b$ %.tropica comple4 is present in man$partsof Asia, Africa, (editerranean Europe and the southern region of the formerSo#iet "nion. &he urban 'utaneous leishmaniasis is thought to be an

anthroponosis while the rural cutaneous leishmaniasis is 7oonosis withhumaninfections occurring onl$ sporadicall$. &he reser#oir hosts in %. ma-or arerodents.%.aethopica is endemic in Ethiopia and Ken$a. &he disease is a 7oonosis withroc3 tree h$ra4es ser#ing as reser#oir hosts. &he #ector for the old worldcutaneous leishmaniasis is the Phlebotomus sand C$.Clinical 2ea!.re


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&he 2rst sign, a red papule, appears at the site of the C$8s bite. &his lesionbecomes irritated, with intense itching, and begins to enlarge ulcerate.raduall$ the ulcer becomes hard and crusted and e4udes a thin, serousmaterial. At this stage, secondar$ bacterial infection ma$ complicate thedisease.

%n the case of the Ethiopian cutaneous leishmaniasis, there are similarde#elopments of lesions, but the$ ma$ also gi#e rise to di6use cutaneousleishmaniasis :D'1; in patients who produce little or no cell mediatedimmunit$against the parasite. &his leads to the formation of dis2guring nodules o#erthesurface of the bod$.I&&.ni!"oth humoral and cell mediated immunit$ :'(%; are in#ol#edTrea!&en!&he drug of choice is sodium stibogluconate, with an alternati#e treatment of

appl$ing heat directl$ to the lesion. &reatment of %.aethopica remains to be aproblem as there is no safe and e6ecti#e drug.52

Pre1en!ion- Prompt treatment eradication of ulcers- 'ontrol of sand Cies reser#oir hosts.!!"!)! New &orld Cutaneous and *ucocutaneous $eishmaniasis+A&erican c.!aneo. lei(&aniai-Clinical #ieae:%eishmania meicana comple 'utaneous leishmaniasis.%eishmania brailiensis comple mucocutaneous or cutaneous leishmaniasis

I&por!an! 2ea!.re:&he American cutaneous leishmeniasis is the same as oriental sore. utsome ofthe strains tend to in#ade the mucous membranes of the mouth, nose,phar$n4,and lar$n4 either initiall$ b$ direct e4tension or b$ metastasis. &hemetastasis isusuall$ #ia l$mphatic channels but occasionall$ ma$ be the bloodstream.Pa!(ogenei&he lesions are con2ned to the s3in in cutaneous leishmaiasis and to themucous

membranes, cartilage, and s3in in mucocutaneous leishmaniasis. Agranulomatousresponse occurs, and a necrotic ulcer forms at the bite site. &he lesions tendtobecome superinfected with bacteria. Secondar$ lesions occur on the s3in aswellas in mucous membranes. Nasal, oral, and phar$ngeal lesions ma$ bepol$poid


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initiall$, and then erode to form ulcers that e4pand to destro$ the soft tissueandcartilage about the face and lar$n4. Gegional l$mphadenopath$ is common.Epi#e&iolog"(ost of the cutaneous mucocutaneous leishmaniasis of the new world

e4ist inen7ootic c$cles of infection in#ol#ing wild animals, especiall$ forest rodents.%eishmania meicana occurs in south 'entral America, especiall$ in theAma7on53basin, with sloths, rodents, mon3e$s, and raccoons as reser#oir hosts. &hemucocutaneous leishmaniasis is seen from the Jucatan peninsula into'entral South America, especiall$ in rain forests where wor3ers are e4posed to sandC$bites while in#ading the habitat of the forest rodents. &here are man$ ungle

reser#oir hosts, and domesticated dogs ser#e as reser#oirs as well. &he#ector isthe 1ut7om$ia sand C$.Clinical 2ea!.re&he t$pes of lesions are more #aried than those of oriental sore and include'hiclero ulcer, "ta, Espundia, and Disseminated 'utaneous 1eishmaniasis.La'ora!or" #iagnoi5 Demonstration of the amastigotes in properl$ stained smears from touchpreparations of ulcer biops$ specimen.5 Serological tests based on Cuorescent antibod$ tests.5 1eishman s3in test in some species.

I&&.ni!"&he humoral and cellular immune s$stems are in#ol#edTrea!&en!&he drug of choice is sodium stibogluconate.Pre1en!ion5 A#oiding endemic areas especiall$ during times when local #ectors are mostacti#e.5 Prompt treatment of infected indi#iduals.777 Tr"panoo&iaiE!iologic agen!Trypanosoma brucei comple = African tr$panosomiasis :sleeping sic3ness;

Trypanosoma crui = American tr$panosomiasis :'hagas8 disease;54I&por!an! 2ea!.re&hese species ma$ ha#e amastigote, promastigote, epimastigote, andtr$pomastigote stages in their life c$cle. %n human tr$panosomes of theAfricanform, howe#er, the amastigote and promastigote stages of de#elopment are


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absent. &$pical tr$panosome structure is an elongated spindleshaped bod$thatmore or less tapers at both ends, a centrall$ situated nucleus, a 3inetoplastposterior to nucleus, an undulating membrane arising from the 3inetoplastand

proceeding forward along the margin of the cell membrane and a single freeCagellum at the anterior end./././.0. African trypanosomiasisTrypanosoma gambiense Trypanosoma rhodesiene are causati#e agents oftheAfrican t$panosomiasis, transmitted b$ insect bites. &he #ector for both isthetsetse C$.Figure


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T.b. gambiense.Clinical 2ea!.reAlthough both species cause sleeping sic3ness, the progress of the disease isdi6erent. T.gambiense induced disease runs a lowgrade chronic course o#era

few $ears. Bne of the earliest signs of disease is an occasional ulcer at thesite ofthe C$ bite. As reproduction of organisms continues, the l$mph nodes arein#aded,and fe#er, m$algia, arthralgia, and l$mph node enlargement results. Swellingof56the posterior cer#ical l$mph nodes is characteristic of ambian sleepingsic3nessand is called winterbottom8s sign.'hronic disease progresses to 'NS in#ol#ement with letharg$, tremors,

meningoencephalitis, mental retardation, and general deterioration. %n the2nalstages, con#ulsions, hemiplegia, and incontinence occur. &he patientbecomesdiQcult to arouse or obtain a response from, e#entuall$ progressing to acomatosestate. Death is the result of 'NS damage and other infections, such aspneumonia.%n T.rhodesiense( the disease caused is a more acute, rapidl$ progressi#ediseasethat is usuall$ fatal. &his more #irulent organism also de#elops in greater

numbersin the blood. 1$mphadenopath$ is uncommon, and earl$ in the infection, 'NSin#asion occurs, resulting in letharg$, anore4ia, and mental disturbance. &hechronic stages described for T.gambiense are not often seen, because inadditionto rapid 'NS disease, the organism produces 3idne$ damage m$ocarditis,leading to death.I&&.ni!"oth the humoral and cellular immunit$ in#ol#e in these infections. &heimmuneresponses of the host to the presence of these parasites, howe#er, is faced

withantigenic #ariation, in which organisms that ha#e changed their antigenicidentit$can escape the host immune response and initiate another disease processwithincreased le#el of parasitemia.La'ora!or"E4amination of thin and thic3 2lms, in concentrated anticoagulated blood


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preparations, and in aspiration from l$mph nodes and concentrated spinalCuid.(ethods for concentrating parasites in blood ma$ be helpful approachesincludingcentrifugation of heparini7ed samples and an ion=e4change chromatograph$.

571e#els of parasitosis #ar$ widel$, and se#eral attempts to #isuali7e theorganismo#er a number of da$s ma$ be necessar$.Figure


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among children in South and 'entral America, where there is directcorrelation59between infected wild animal reser#oir hosts and the presence of infectedbugs

whose nests are found in human dwellings.Clinical 2ea!.re'hagas8 disease ma$ be as$mptomatic acute or chronic disease. Bne of theearliest signs is de#elopment at the site of the bug bite of an er$thematousandindurated area called a chagoma. &his is often followed b$ a rash and edemaaround the e$es and face9 in $oung children fre@uentl$ an acute process with'NSin#ol#ement ma$ occur. Acute infection is also characteri7ed b$ fe#er, chills,malaise, m$algia, and fatigue. &he chronic 'hagas8 disease is characteri7edb$

hepatosplenomegal$, m$ocarditis, and enlargement of the esophagus andcolonas a result of the destruction of ner#e cells :E.g. Auerbach8s ple4us; andothertissues that control the growth of these organs. %n#ol#ement of the 'NS ma$produce granulomas in the brain with c$st formation and ameningoencephalitis.Death from chronic 'hagas8 disease results from tissue destruction in theman$areas in#aded b$ the organisms, and sudden death results from completeheart

bloc3 and brain damage.La'ora!or" #iagnoiE4amine thin or thic3 stained preparations for tr$pomastigotes. etpreparationsshould also be e4amined to loo3 for motile organisms that lea#e the bloodstreamand become diQcult to 2nd. iops$ of l$mph nodes, li#er, spleen, or bonemarrowma$ demonstrate organisms in amastigote stage.Figure


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immune s$stem.Trea!&en!&he drug of choice is nifurtimo4. Alternati#e agents include allopurinol ben7imida7ole.Pre1en!ion

5 ug control, eradication of nests5&reating infected person e4clusion of donors b$ screening blood.5 De#elopment of #accine.61

UNIT FI)EMEDICALL3 IMPORTANT CILIATESBalan!i#iai&he intestinal proto7oan 'alantidium coli is the onl$ member of the ciliategroupthat is pathogenic for humans. Disease produced b$ '. coli is similar to

amebiasis, because the organisms elaborate proteol$tic and c$toto4icsubstances that mediate tissue in#asion and intestinal ulceration.Li2e c"cle&he life c$cle of '. coli is simple, in#ol#ing ingestion of infectious c$sts,e4c$station, and in#asion of tropho7oites into the mucosal lining of the largeintestine, caecum, and terminal ileum. &he tropho7oite is co#ered with rowsofhair li3e cilia that aid in motilit$. (orphologicall$ more comple4 than amebae,'.coli has a funnelli3e primiti#e mouth called a c$tostome, a large :macro;nucleus

and a small :micro; nucleus in#ol#ed in reproduction.Epi#e&iolog"'. coli are distributed worldwide. Swine and :less commonl$; mon3e$s arethemost important reser#oirs. %nfections are transmitted b$ the faecaloralroute9outbrea3s are associated with contamination of water supplies with pigfaeces.Persontoperson spread, including through food handlers, has beenimplicatedin outbrea3s. Gis3 factors associated with human disease include contact

withswine and substandard h$gienic conditions.Clinical 2ea!.reAs with other proto7oan parasites, as$mptomatic carriage of '. coli can e4ist.S$mptomatic disease is characteri7ed b$ abdominal pain, tenderness,tenesmus,62nausea, anore4ia, and water$ stools with blood and pus. "lceration of the


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intestinal mucosa, as with amebiasis, can be seen9 a secondar$ complicationcaused b$ bacterial in#asion into the eroded intestinal mucosa can occur.E4traintestinal in#asion of organs is e4tremel$ rare in balantidiasis.Figure 767 Malaria&here are four species normall$ infecting humans, namel$, Plasmodiumfalciparum( Plasmodium viva( Plasmodium ovale( and Plasmodium malariae.Li2e c"cle&he life c$cle of malaria is passed in two hosts :alternation of hosts; and has

se4ual and ase4ual stage :alternation of generations;.?ertebrate host man :intermediate host;, where the ase4ual c$cle ta3esplace.&he parasite multiplies b$ schi7ogon$ and there is formation of maleand female gametoc$tes :gametogon$;.%n#ertebrate host mos@uito :de2niti#e host; where the se4ual c$cle ta3esplace."nion of male and female gametes ends in the formation of


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sporo7oites :sporogon$;.&he life c$cle passes in four stages&hree in man Pre er$throc$tic schi7ogon$64 Er$throc$tic schi7ogon$

E4o er$throc$tic schi7ogon$Bne in mos@uito Sporogon$"ntroduction into humans when an infecti#e female Anopheles mos@uitobitesman, it inoculates sali#a containing sporo7oites :infecti#e stage;.+re, Erythrocytic schi-ogony sporo7oites reach the blood stream and within-* minutes enter the parench$mal cells of the li#er, initiating a c$cle ofschi7ogon$. (ultiplication occurs in tissue schi7onts, to form thousands oftin$mero7oites. (ero7oites are then liberated on rupture of schi7onts about th =Ith

da$ of the bites and enter into the blood stream. &hese mero7oites eitherin#adethe G'8s or other parench$mal li#er cells. %n case of P. falciparum andpossibl$P. malariae, all mero7oites in#ade G'8s without rein#ading li#er cells.Howe#er,for P. viva and P. ovale, some mero7oites in#ade G'8s and some rein#adeli#er cells initiating further Eo)erythrocytic schi7ogon$, which is responsibleforrelapses. Some of the mero7oites remain dormant :h$pno7oites; becomingacti#e

later on.Er$throc$tic schi7ogon$ :blood phase; is completed in +0 hrs in P. viva( P.ovale( and P. falciparum, and ) hrs in P. malariae. &he mero7oites rein#adefresh G'8s repeating the schi7ogonic c$clesEr$throc$tic mero7oites do not rein#ade the li#er cells. So malariatransmitted b$blood transfusion reproduces onl$ er$throc$tic c$cleGa&e!ogon"Some mero7oites that in#ade G'8s de#elop into se4ual stages :male andfemale gametoc$tes;. &hese undergo no further de#elopment until ta3en b$the

[email protected] 'extrinsic cycle in mos.uito(hen a female Anopheles mos@uito #ector bites an infected person, it suc3sblood containing the di6erent stages of malaria parasite. All stages otherthangametoc$tes are digested in the stomach.&he microgametoc$te undergoes e4Cagellation. &he nucleus di#ides b$


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reduction di#ision into 0 pieces, which migrate to the peripher$. At thesame,time 0 thin 2laments of c$toplasm are thrust out, in each passes a piece ofchromatin. &hese 2laments, the microgametes, are acti#el$ motile andseparate

from the gametoc$te.&he macrogametoc$te b$ reduction di#ision becomes a macrogamete.Fertili7ation occurs b$ entr$ of a micro gamete into the macro gameteforming a7$gote.&he 7$gote changes into a worm li3e form, the oo3inete, which penetratesthewall of the stomach to de#elop into a spherical ooc$st between theepitheliumand basement membrane. &he ooc$stes increase in si7e. &housands ofsporo7oites de#elop inside the ooc$sts. Boc$sts rupture and sporo7oites are

liberated in the bod$ ca#it$ and migrate e#er$where particularl$ to thesali#ar$glands. Now the mos@uito is infecti#e&he sporogonous c$cle in the mos@uito ta3es 0


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causes of signi2cant and widespread epidemics. (oreo#er, drugresistantinfectionof P.falciparum is the commonest challenge in man$ parts of the world. %nEthiopia,e#en though all the four species of plasmodium infecting man ha#e been

recorded,P.falciparum is the one that most causes the epidemic disease and followedb$#i#a4 and malariae. P.ovale is rare. %nfection rates in Ethiopia are *R, +*R,


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the laborator$ reports a mi4ed infection in#ol#ing P.falciparum and P.viva,thetreatment must eradicate not onl$ P.falciparum from the er$throc$tes butalso theli#er stages of P.viva to a#oid relapses pro#ided that the person no longer

li#es ina malaria endemic area.69

/!"!! +lasmodium vivaxP.viva is selecti#e in that it in#ades onl$ $oung immature er$throc$tes.%nfections of P. viva ha#e the following characteristics5 %nfected red blood cells are usuall$ enlarged and contain numerouspin3 granules or schu6ner8s dots.5&he tropho7oite is ringshaped but amoeboid in appearance.5 (ore mature tropho7oites and er$throc$tic schi7onts containing up to)+ mero7oites are present.

5&he gametoc$tes are roundEpi#e&iolog"P. ,iva is the most pre#alent of the human plasmodia with the widestgeographicdistribution, including the tropics, subtropics, and temperate regions.Howe#er, it isthe second most pre#alent in Ethiopia following P. falciparumClinical 2ea!.reAfter an incubation period :usuall$


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'hloro@uine is the drug of choice for the suppression and therapeutictreatment ofP.#i#a4, followed b$ prema@uine for radical cure and elimination ofgamatoc$tes.>767


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are howe#er, fewer relapses with P.o#ale. 1ess than )R of G's usuall$becomeinfected.72Trea!&en!

&he treatment regimen, including the use of prima@uine to pre#ent relapsefromlatent li#er stages is similar to that used for P.viva infection.La'ora!or" #iagnoi(icroscopic e4amination of thic3 and thin 2lms of blood is the method ofchoice forcon2rming the clinical diagnosis of malaria and identif$ing the speci2cspeciesresponsible for disease.(alaria parasites in thic3 and thin blood 2lms are best stained at pH .< = .)using a Gomanows3$ stain :contains a7ure d$es and eosin;.

&he thic3 2lm is a concentration method that ma$ be used to detect thepresenceof organisms. &he thin 2lm is most useful for establishing speciesidenti2cation.Serologic procedures are a#ailable but the$ are used primaril$ forepidemiologicalsur#e$s or for screening blood donors.I&&.ni!"&here is e#idence that antibodies can confer hormonal immunit$ againstmalariainfection.

Pre1en!ion5 'hemoproph$la4is and prompt diagnosis and treatment.5 'ontrol of mos@uito breeding5 Protection of insect bite b$ screening, netting and protecti#e clothing5 "se of insect repellents.73Figure 77 O!(er Cocci#ian parai!e>7767 0oxoplasma gondii = causes tooplasmosis. &he de2niti#e host is thedomestic cat and other felines. Humans and other mammals are

intermediatehosts. T.gondii is usuall$ ac@uired b$ ingestion and transplacentaltransmissionfrom an infected mother to the fetus can occur. Human=to=humantransmission,other than transplacental transmission, does not occur. After infection of theintestinal epithelium, the organisms spread to other organs, especiall$ thebrain,


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lungs, li#er, and e$es. (ost primar$ infections in immunocompetent adultsareas$mptomatic. 'ongenital infection can result in abortion, stillbirth, orneonataldisease with encephalitis, chorioretinitis and hepatosplenomegal$. Fe#er,

aundice, and intracranial calci2cations are also seen. For the diagnosis ofacuteand congenital infections, an immunoCuorescence assa$ for detection ofantibod$is used. (icroscopic e4amination of iemsa=stained preparations showscrescent=shaped tropho7oite. '$sts ma$ be seen in the tissue. &reatment iswitha combination of sulfadia7ine and p$rimethamine.Figure )*9 1ife c$cle of Tooplasma gondii75Figure )777 Cyclospora cayetanensis ) is an intestinal proto7oan that causes water$diarrhea in both immunocompetent and immunocompomised indi#iduals. %t isclassi2ed as a member of the 'occidian9 the organism is ac@uired b$ fecal =oraltransmission, especiall$ #ia contaminated water supplies. &here is noe#idence foran animal reser#oir. &he diarrhea can be prolonged and relapsing, especiall$inimmunocompromi7ed patients. %nfection occurs worldwide. &he diagnosis ismademicroscopicall$ b$ obser#ing the spherical ooc$sts in a modi2ed acidfast

stain of astool sample. &here are no serologic tests. &he treatment of choice istrimethoprimsulfametho4a7ole.Figure ))9 Boc$st of cyclospora cayetanensis>77


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b$ 2nding the t$pical ooc$sts in fecal specimens. Serologic tests are nota#ailable.&he treatment of choice is trimethoprimsulfametho4a7ole.Figure )-9 1ife c$cle of "sospora belli.Figure )+9 immature Boc$st of isospora species

77>77>7 Cryptosporidium parvum = causes cr$ptosporidiosis, the main s$mptomof which is diarrhea. %t is most se#ere in immunocompromi7ed patients, e.g.,thosewith A%DS. &he organism is ac@uired b$ faecaloral transmission of Boc$stsfromeither human or animal sources. &he ooc$sts e4c$st in the small intestine,wherethe tropho7oite :and other forms; attach to the gut wall. %n#asion does notoccur.&he eunum is the site most hea#il$ infested. &he pathogenesis of the

diarrhea isun3nown9 no to4in has been identi2ed.'r$ptosporidium causes diarrhea worldwide, for large outbrea3s of diarrheacaused b$ 'r$ptosporidium are attributed to inade@uate puri2cation ofdrin3ingwater. &he disease in immunocompromi7ed patients presents primaril$ as awater$, nonblood$ diarrhea causing large Cuid loss. S$mptoms persist forlongperiods in immunocompromi7ed patients, whereas selflimited inimmunocompetent indi#iduals. Although immunocompromi7ed patientsusuall$ do

not die of cr$ptosporidiosis, the Cuid loss and malnutrition are se#erel$debilitating.Diagnosis is made b$ 2nding ooc$sts in fecal smears when using a modi2edKin$oum acid=fast stain. Serological tests are not a#ailable. &here is noe6ecti#edrug therap$.Figure )/9 life c$cle of 'r$ptosporidium species.78Figure )9 Acidfast stained 'r$ptosporidium ooc$st.Figure )9 Boc$sts of &ryptosporidium parvum :lower left; &yclosporacayetanensis :upper right;. oth stained red with iehlNeelsen stain.

>77@7 Micropori#ia are a group of proto7oa characteri7ed b$ obligateintracellular replication and spore formation. Enterocytooon bienusi andSeptataintestinalis are two important microsporidial species that cause se#ere,persistent,water$ diarrhea in A%DS patients. &he organisms are transmitted from faecaloral


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route. %t is uncertain whether an animal reser#oir e4ists. Diagnosis is madeb$#isuali7ation of spores in stool samples or intestinal biops$ samples9 the drugofchoice is albenda7ole.

Figure )09 rampositi#e spores of (icrosporidia in eunal biops$79Figure )I9 smear of formalin24ed stool specimen showing pin3ish redstained(icrosporidia spores :'hromotrope based stain;80

Re1ie0 =.e!ion


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Pavl &. 'eaver 1 =odney &. 9ung 1 Eddie W. &upp. &linical parasitology.5thed. Philadelphia4 %ea 1 !ebiger( 058>.?enneth 9. =yon. 2edical 2icrobiology( an introduction to infectious disease.3rded. 7SA4 Appleton 1 %ange. 055>

2ichael. 9. Pelcar( E.&.Schan 1 Nocl =. ?rieg. 2icrobiology. @th ed. New #elhi4Tata 2c$rawHill( 058;.Patric+. =. 2urray( ?en. S. =osenthal( $eorge S. ?abayashi( 2ichael A. P.!aller.2edical microbiology >th ed 7SA4 2osby( /


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83-. Domestic or wild animals harboring the parasite :as in echinococcus indogs;.+. Person to person :as in Enterobius vermicularis( Hymenolopis nana;.@. Bneself :autoinfection; as in Enterobius vermicularis.

&he$ enter the bod$ through di6erent routes including mouth, s3in and therespirator$ tract b$ means of inhalation of airborne eggs.&he helminthes are classi2ed into three maor groups. &hese are


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/. Schistosoma me+ongi causes intestinal schistosomiasis. &his seems tocause milder disease in man. %t causes disease in other #ertebrate hosts.85&he 2rst two schistosomes :S. mansoni and S. haematobium; are pre#alent inEthiopia.

SC%ISTOSOMA MANSONI%a'i!a! 9&his species li#es in the #eins of the intestine.Geograp(ical #i!ri'.!ion: %t is found in Africa, South America, (iddle East:some Arab countries; etc. Stream and la3ebased transmission is common.&he snail hosts that harbor S. mansoni are the genera iomphalaria :'.glabrata; and &robicorbis. &hese ha#e o#al shells.Morp(olog"Male:&he male ranges in si7e from


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&his is the rarest and least pathogenic schistosome that matures in man. %t isfound in estern and 'entral Africa. &he dail$ egg output is about -**. &heeggsha#e a terminal spine.LIFE C3CLE OF SC%ISTOSOMES

Adult worms reside in pairs the female l$ing in the g$necophoral canal of themale. After fertili7ation, eggs are passed into the #enules. A lar#al form = themiracidium de#elops within the egg. %ts l$tic en7$mes and the contractionof the#enule rupture the wall of the #enule liberating the egg into the peri#asculartissues of the intestine :S. mansoni; or urinar$ bladder :S. haematobium;.&heeggs pass into the lumens and organs and are e#acuated in the feces :S.mansoni; or the urine :S. haematobium;. Bn contact with fresh water themiracidia hatch from the eggs and swim about until the$ 2nd the appropriatesnail, which the$ penetrate. After two generations of sporoc$st de#elopment

andmultiplication within the snail, the for3tailed cercariae emerge. %nfection tomanta3es place during bathing or swimming. &he cercariae penetrate the s3in,arecarried into the s$stemic circulation and pass through to the portal #essels.ithin the intrahepatic portion of the portal s$stem, the worms feed andgrow tomaturit$.87Fig.re 676. 1ife c$cle of schistosomes

S"&p!o& an# co&plica!ionPatients infected with S. haematobium su6er from terminal haematuria andpainful micturition. &here is inCammation of the urinar$ bladder :c$stitis;,andenlargement of spleen and li#er.Patients infected with S. mansoni su6er from cercarial dermatitis :swimmersitch;and d$senter$ :mucus and blood in stool with tenesmus; as well asenlargementsof the spleen and li#er.S. haematobium causes s@uamous cell carcinoma in the bladder.

La'ora!or" DiagnoiS7 &anoniY (icroscopic e4amination of the stool for eggs after concentration b$sedimentation method. &he egg has characteristic lateral spine.88Y Gectal snipS7 (ae&a!o'i.&:


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Y E4amination of the urine after allowing it to sediment in a conicalurinal$sisglass. A drop from the sediment is ta3en and e4amined for eggs. Egg hasterminal spine.Y iops$ from bladder

Fig.re 67. Eggs of S. mansoni and S. haematobiumTrea!&en!Pra7i@uantel single oral dose of +* mg>3g di#ided into two doses.Pre1en!ion:67 %eal!( e#.ca!ion:A. Bn use of clean latrines and safe water suppl$. A#oid urination and defecation in canals, a#oid contact with canalwater7 Snail con!rol:A. Ph$sical methodsi. Periodic clearance of canals from #egetations.

ii. (anual remo#al of snails and their destruction.. iological methods "se of natural enemies to the snails such as(arisa.89'. 'hemical methods (olluscides are applied in the canals to 3ill thesnails. e.g. Endod677 INTESTINAL FLUKESY 1asciolopsis buski &hese giant intestinal Cu3es :)./ cm in length; arefound in some Asian countries.Y %e!erop("i# (inute Cu3es ac@uired b$ ingestion of raw fresh water 2sh.&he$ are found in Asian countries. Neither are found in Ethiopia.

67


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NEMATODES +ROUND WORMS-All the important human parasites of the Ph$lum Nemathelminthes:Aschelminthes; belong to the 'lass Nematoda.

GENERAL C%ARACTERISTICS OF NEMATODES&he$ are unsegmented, elongated and c$lindrical. &he$ ha#e separate se4es

with separate appearances. &he$ ha#e a tough protecti#e co#ering or cuticle.&he$ ha#e a complete digesti#e tract with both oral and anal openings. &henematodes are free li#ing :(aorit$; or parasites of humans, plants oranimals.T(e parai!ic ne&a!o#e:&he nematodes are generall$ light creamwhite colored. &heir life c$cleincludesegg, lar#ae and adult.T(e parai!ic ne&a!o#e are #i1i#e# in!o:67 In!e!inal ne&a!o#e6767 In!e!inal ne&a!o#e 0i!( !i.e !age

A. Ascaris lumbricoides. Hoo3worms'. Strong$loides stercoralis677 In!e!inal ne&a!o#e 0i!(o.! !i.e !ageA. Enterobius #ermicularis. &richuris trichuira.7 Ti.e an# 'loo# #0elling ne&a!o#e).


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the trachea, descend to the esophagus and 2nall$ reach the small intestinetobecome adult. &he female pass immature eggs which pass to the soil andmaturein ) wee3s.

92Fig.re 67


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Male:&he male measures 0 cm in length. &he posterior end is broadened intoamembraneous copulator$ bursa, which is pro#ided with two long spiculesfuseddistall$.

Fe&ale:&he female measures


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&hiabenda7ole Applied topicall$.'7 )iceral lar1a &igranA s$ndrome caused b$ the migration of parasitic lar#ae in the #iscera of ahost for months or $ears. %t ma$ be caused b$ transient lar#al migration inthe

life c$cles of se#eral parasites such as hoo3worm,Ascaris lumbricoides( T.spiralis( S. strecoralis and other 2larial worms.0oxocariasis&his is a 3ind of #isceral lar#a migrans caused b$Y Toocara canis :Dog ascarid; and97Y Toocara catis B'at ascarid;.&hese cause persistent lar#al migration and thus the #isceral lar#a migrans iscalled to4ocariasis.Morp(olog"Y &he lar#ae of Toocara canis and Toocara catis measure about +** Om in

length.Y &he life c$cle of these parasites in their respecti#e hosts is similar to thatofA.lumbricoides in humans.Epi#e&iolog"?isceral lar#a migrans is cosmopolitan in distribution.Tran&iion:%ngestion of eggs of &o4ocara species in contaminated food or soil or directcontact with infected patients. 'hildren are more at ris3.Clinical 2ea!.re:Y (aorit$ are as$mptomatic.

Y EosinophiliaY 'erebral, m$ocardial and pulmonar$ in#ol#ement ma$ cause death.Diagnoi 9 %denti2cation of lar#ae in tissue.Trea!&en! 9&hiabenda7ole )/ mg>3g twice dail$ for / da$s.C7 In!e!inal lar1a &igran&his is an e4tremel$ rare 3ind of lar#a migrans98

767>7 STRONG3LOIDES STERCORALIS&he worms ma$ be present as parasitic in the host or free li#ing in the soil.Morp(olog":Male:&he male measures< mm in length with cur#ed posterior end and

carriestwo spiculesFe&ale:&he female measures )./ mm in length with straight posterior end.In2ec!ion: follows s3in penetration b$ 2lariform lar#ae.Li2e c"cleAdult male and female worms li#e in the small intestine. After fertili7ation,thefemale penetrates the mucosa of the small intestine and la$ eggs in the


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submucosa. &he eggs hatch and the lar#ae penetrate the mucosa bac3 tothelumen. %f the en#ironmental conditions are fa#orable, the lar#ae will comeoutwith the stool to the soil. &he$ transform into adults, which la$ eggs, and

hatchinglar#ae get transformed to adults and so on. %f the en#ironmental conditionsarenot fa#orable, the lar#ae in the stool will moult and transform into infecti#e2lariform lar#ae, which pierce the intestine :autoinfection;. 1ar#aepenetratingthe s3in from the soil or b$ autoinfection are carried b$ the blood to thelungs,ascend to the trachea, descend to the esophagus and mature in the smallintestine.99

Figure


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5 Autoinfection the eggs are infecti#e as soon as the$ are passed b$the female worm. %f the hands of the patient get contaminated withthese eggs, he>she will infect him>herself again and again.5 Aerosol inhalation from contaminated sheets and dust.Li2e c"cle

Adult worm li#es in the large intestine. After fertili7ation, the male dies andthefemale mo#es out through the anus to glue its eggs on the perianal s3in.&hista3es place b$ night. &he egg is /*4)/ microns, planocon#e4 and containslar#a. hen the eggs are swallowed, the$ hatch in the small intestine andthelar#ae migrate to the large intestine to become adult.Fig.re 67. 1ife c$cle of E. vermicularis102Clinical preen!a!ion

&he migration of the worms causes allergic reactions around the anus andduringnight it causes nocturnal itching :pruritus ani; and enuresis. &he worms ma$obstruct the appendi4 causing appendicitis.DiagnoiY Eggs in stool E4amination of the stool b$ direct saline smear to detect theegg this is positi#e in about /R of cases because the eggs are glued to theperianal s3in.Y Perianal swab &he perianal region is swabbed with a piece of adhesi#etape :cellotape; hold o#er a tongue depressor. &he adhesi#e tape is placedon a glass slide and e4amined for eggs. &he swab should be done in the

earl$ morning before bathing and defecation.Fig.re 676. Egg of E. vermicularisTrea!&en!(ebenda7ole9 Pipera7ine.103777 TRIC%URIS TRIC%IURA +W%IP WORM-&he worm is di#ided into a thin whipli3e anterior part measuring ->/ of thewormand a thic3 Cesh$ posterior part of )>/ the length.Male:&he male measures -+./ cm in length. %ts posterior end is coiled andpossesses a single cubicle.

Fe&ale:&he female measures +/ cm in length. %ts posterior end is straightIn2ec!i1e !age an# &o#e o2 in2ec!ion%nfection is b$ ingestion of eggs containing lar#ae with contaminated raw#egetables.Li2e c"cle:%ngested eggs hatch in the small intestine and the lar#ae migrate to thelarge


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intestine to become adult. After mating, the female la$s immature eggs,whichpass with the stool to the soil and mature in ) wee3s.Fig.re 67667 1ife c$cle of Trichuris trichiura104

S"&p!o&&he patient complains of d$senter$ :blood and mucus in stool together withtenesmus;. Gectal prolapse is also possible.DiagnoiFinding of characteristic eggs. &he egg of trichuris is barrelshaped, /*4)/microns. &he shell is thic3 with a one mucoid plug at each pole.Fig.re 676. Egg of Trichuris trichiuraTrea!&en!(ebenda7ole < tablet twice dail$ for ) da$s.

7


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where the$ de#elop into adult worms. &he micro2lariae are librated into thebloodstream. &he$ remain in the pulmonar$ circulation during da$, emerging intotheperipheral circulation onl$ during night, to coincide with the biting habit of

the#ector. Presence of the adult worms causes l$mphatic bloc3age and grossl$mphedema, which sometimes lead to elephantiasis.Epi#e&iolog": . bancrofti infection is not reported in higher altitudes ofEthiopia, but limited to lowlands of ambella. &he epidemic area co#ers alongdistance along the aro Gi#er.Pa!(ogeneci!" an# clinical 2ea!.re:Y &he adult worm obstructs the Cow of l$mph in the l$mph nodes and thel$mphatic #essels draining the lower limbs and the e4ternal genitalia.Y &he lower limbs and e4ternal genitalia become swollen. &he s3in becomes

thic3 and 2ssured. &he disease is called bancroftian elephantiasis.Y &he maor s$mptoms and 2ndings include l$mphangitis, l$mphedema,fe#er,headache, m$algia, h$drocele and ch$luria.DiagnoiY lood 2lm e4amination after staining b$ iemsa or 1eishman stain todetectmicro2laria. &he 2lm should be ta3en b$ night.107

Fig.re 676>. (icro2laria of . bancrofti in blood smearTrea!&en! 9 Dieth$l carbama7ine :DE'; ) mg>3g -4 dail$ for ) wee3s.

En#e&ic non92ilarial elep(an!iai +Po#oconioi-Non2larial elephantiasis of the lower limbs is common in Ethiopia. Silicon,aluminium and iron particles in the red cla$ soil are absorbed through s3inabrasions in bare footed persons. &he mineral particles cause obstruction ofthel$mphatics.7


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Micro2ilaria(easures -** microns in length. %t is nonsheathed micro2laria. %t is presentinthe subcutaneous tissue Cuids and not in blood.Fig.re 676@. 1ife c$cle of B. #ol#ulus

In2ec!i1e !age an# &o#e o2 in2ec!ion is similar to that of Wuchereria bancrofti.Pa!(ogeneci!" an# clinical &ani2e!a!ion:&he disease, onchocerciasis or ri#er blindness includes5 S3in 2brous nodules :onchocercomata; enclosing female worms. &henodulesare common in nec3, iliac crest and the cocc$4.1095 S3in h$po or h$per pigmentation. Dermatitis is present. %n ad#ancedcases,the s3in becomes thic3ened and wrin3led, showing li7ard or leopard s3inappearance.

5 Elephantiasis of the e4ternal genitalia and corneal opacit$ and opticatroph$ma$ 2nall$ cause blindness.DiagnoiSuper2cial biops$ :s3in snip; is ta3en from the s3in using sharp ra7or blade.&hespecimen is allowed to stand for -* minutes in saline before it is e4aminedmicroscopicall$ for micro2lariae.Fig.re 6767 (icro2laria of D. volvulusTrea!&en!%#ermectin /* mg>3g bod$weight, gi#en e#er$ or


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Adult male worms -*-+ mm in lengthAdult female worms +** mm in lengthPa!(ogenei&he micro2laria ha#e a sheath. &heir diurnal periodicit$ corresponds to thefeeding pattern of the insect #ector, which bites humans from


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about < $ear, female worms in the subcutaneous tissue pro#o3e theformation ofa burning blister in the s3in of the legs. hen in water, the blister bursts, andabout / cm of the worm is e4truded from the resulting ulcer thus releasingman$

thousands of 2rst stage lar#ae. &he lar#ae swim in water and are ingested b$theintermediate host '$clops species within about + da$s. %nside the '$clops,th

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