Parasitic Infections: Trypanosoma, Giardia, Leishmania, Plasmodium, Taenia, and More
lab #2protozoa,class fagellatai.Blood flagellates – trypanasomatrypanosoma is a genus inetoplastids (class kinetoplastida),a monophyletic group of unicellular parasitic flagellate protozoa.All trypanosomes R heteroxenous (require more than 1 host
2 complete their life cycle)
.Trypanosomes possess different cell types during their life-cycle stages – amastigote (am),epimastigote (epi),trypomastigote (tryp) african trypanosomiasis – t .B.Gambiense & t .B.Rhodesiense;american trypanosomiasis – t .Cruzi morphology:
trypanosomes R minute,actively motile,fusiform protozoa,flattened from side 2 side.The long,sinuous body hs a tapering anterior & a blunt posterior end.Even in the same species the shape varies.A large oval nucleus,which hs a central karysome,is situated toward the middle of the body .Reproduction takes place by binary longitudinal fission.Trypanosomes fail 2 store carbohydrates & thus require as source of energy the readily available supplies of their host.
1.T rypanosoma bruzei gambiense1.) disease: Gambian trypanosomiasis,mid-african sleeping sickness
2.) morphology:
in the blood t .B.Gambiense is polymorphic,ranging from typical long slender trypanosomes 2 short,stumpy forms.The stumpy forms R in a stationary ,nondividing growth phase & R considered infective 4 thevector fly ,whereas the long,slender trypanosomes R those found dividing in the blood.In the cerebrospinal fluid allsizes & shapes occur .The organisms range from 15 2 35 µ in length & 1,5 2 4,0 µ in width.The variation in sizeand shape of bloodstream trypanosomes is actually less characteristic of t .B.Gambiense than of t .B.Rhodiense.
3.) host:
human is definitiv host,but not the only vertebrate host (pigs & certain wild animals) ;intermediate host,vector is riverine tsetse fly of the palpalis group4.) life-cycle:
when ingested from the blood of an infected mammalian host,the stumpy trypomastigotes migrate posteriorly in the gut of the fly .They either pass through or around the perithropic membrane & migrate anteriorlybetween the membrane & gut wall.Here they transform into epimastigotes multiply ,& migrate 2 the salivaryglands,where they continue 2 multiply & transform into infective metacyclic trypmastigotes.With subsequent bloodmeals the infective forms R transmitted 2 a new host with injected saliva.During a blood meal on the mammalianhost,an infected tsetse fly (genus glossina) injects metacyclic trypomastigotes into skin tissue.The parasites enter thelymphatic system & pass into the bloodstream.Inside the host,they transform into bloodstream trypomastigotes,arecarried 2 other sites throughout the body ,reach other blood fluids (e.G.,lymph,spinal fluid),& continue thereplication by binary fission.The entire life cycle of african trypanosomes is represented by extracellular stages.Thetsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalianhost.In the fly’ s midgut,the parasites transform into procyclic trypomastigotes,multiply by binary fission,leave the
midgut,& transform into epimastigotes.The epimastigotes reach the fly’ s salivary glands & continue multiplicationby binary fission.The cycle in the fly takes approximately 3 weeks.
5.) symptoms:
in the humans the disease varies in severity from a mild type,with few trypanosomes in the blood 2 a severefulminating type resembling that of t .B.Rhodesiense .@ 1st,there may be only mild symptoms.Infected persons mayhave intermittent fevers,headaches,muscle & joint aches,& malaise.Itching of the skin,swollen lymph nodes,andw8 loss can occur .Usually ,after 1-2 years,there is evidence of central nervous system involvement,withpersonality changes,daytime sleepiness with nighttime sleep disturbance,& progressive confusion.T .B.Gambiensecauses chronic infections in west & central africa which can persist up 2 10 years while t .B.Rhodesiense is moreprevalent in eastern africa & mostly results in acute human infections that can be lethal within a few months.
cellular features ofa trypanosomacruzitrypomastigote2.T rypanosoma bruzei rhodesiense
1.) disease:
rhodesian trypanosomiasis,east african sleeping sickness2.) morphology:
t .B.Rhodesiense is morphologically indistinguishable from t .B.Gambiense.
3.) host:
human is definitiv host,antilopes & possibly other wild game & domesticated cattle R reservoir hosts ;intermediate host,vector is woodland tsetse fly glossina moristans,g.Pallidipes & g.Swynnertoni4.) life-cycle:
similar 2 t .B.Gambiense5.) symptoms:
rhodesian trypanosomiasis runs a more rapid & fatal course than does the gambian disease,oftenterminating within a year .The pathologic changes in the acute disease R similar 2 those of gambian sleepingsickness,but the febrile paroxysms R more frequent & severe.Edema,mycarditis,weakness & emaciation aremore prominent.In some patients,a large sore will develop @ the site of the tsetse bite.Most patients develop fever ,headache,muscle & joint aches,& enlarged lymph nodes within 1-2 weeks of the infective bite.Some peopledevelop a rash.After a few weeks of infection,the parasite invades the central nervous system & eventually causes
mental deterioration & other neurologic problems.
6.) diagnosis:
blood smear > similar procedures as 4 t .B.Gambiense R called 4 ,except that trypanosomes aremore frequently found in the blood.
3.T rypanosoma cruzi
1.) disease:
american trypanosomiasis,chagas disease2.) morphology:
in the blood the trypanosomes appear either as long,thin flagellates about 20 µ in length or as short,
stumpy forms about 15 µ in length,width pointed posterior ends.In stained blood smears they have a u or s shape,afree flagellum about 1 3rd of the body length,a deeply staining central nucleus & a large terminal kinetoplast.Inthe tissue the round intracellular amastigotes R found in small groups of cystlike collections.
3.) host:
human is definitiv host;intermediate host,vector is a reduviid bug,of the genera triatoma,panstrongylus,rhodnius an eutriatoma.
4.) life-cycle:
t .Cruzi hs 4 distinct life cycle stages.Within the midgut of the reduviid bug,parasites replicate as flagellated epimastigotes (epi).As epis replicate & increase in number they migrate 2 the hindgut of the bug wherethey differentiate into infective metacyclic trypomastigotes (meta).Metas R discharged in the feces of the bug as they
take a blood meal.Infection results from the contamination of the insect bite or open wounds,mucous membranes orconjunctiva with parasite laden bug feces.1ce in the vertebrate host,the meta,which is unable 2 replicate,mustinvade host cell within which it can differentiate into the replicating amastigote (ama).During invasion the meta isinitially present within a membrane bound vacuole,but it escapes this vacuole & differentiates into the aflagellatedama,which divides in the cytoplasm.After a number of rounds of replication,the amas fill the cytoplasm anddifferentiate into motile trypomastigotes (tryp),which lyse the infected cell & escape 2 infect adjacent cells ordisseminate throughout the body via the bloodstream & lymphatics.Within the vertebrate host,parasites6.) diagnosis:
blood smear > a
definite laboratory diagnosis ismade by finding the trypanosomesin the blood,lymph nodes,andb1 marrow in the early diseaseand in the spinal fluid in the latedisease.Can infect any nucleated cell,but have a predilection 4 muscle,particularly of the heart & gastrointestinal tract.
locally deposited parasites bind 2 & invade host tissue & transform into & replicate as intracellular amastigotes.Trypomastigotes infect cells from a variety of tissues & transform into intracellular amastigotes in new infection sites.Clinical manifestations can result from this infective cycle.The bloodstream trypomastigotes do not replicate (differentfrom the african trypanosomes).Replication resumes only when the parasites enter another cell or R ingested byanother vector .
the 2 hallmarks,usually mutually exclusive,disorders that occur in chronically infected patients R cardiomyopathyand megaorgan syndromes /megacolon.Many people may remain asymptomatic 4 life & never develop chagasrelated symptoms.However ,an estimated 20 – 30% of infected people will develop debilitating & sometimes lifethreatening medical problems over the course of their lives.
6.) diagnosis:
blood smear > the mainstay of diagnosis is detection of trypomastigotes in the blood or the presence oft .Cruzi-specifi c antibodies in serum 2 indicate acute or chronic infection,respectively .Only in the 1st month or 2of the acute disease can t .Cruzi can (tryp) be found by direct examination of fresh anticoagulated blood.A thick andthin blood smear R made & stained 4 visualization of parasites.However ,a blood smear works well only in theacute phase of infection when parasites R seen circulating in blood.After this 1st month exists an other way 2 detect an infection,the xenodiagnosis – by feeding clean reduviid bugswith the blood of an infected patient in the laboratory & examine the low typranosoma concentration in the bugs,aninfection can then be detected.
5.) symptoms: Chagas disease hs an acute & achronic phase.If untreated,infection is
lifelong.Acute chagas disease occursimmediately after infection,may last upto a few weeks or months,& parasitesmay be found in the circulating blood.Infection may be mild or asymptomatic.There may be fever or swelling aroundthe site of inoculation (where theparasite entered into the skin or mucous
membrane).Rarely ,acute infection mayresult in severe inflammation of theheart muscle or the brain & liningaround the brain.Less than 1-3rd ofinfected people developchronic chagas disease.
trypanosoma promastigotes in bloodsmear (giemsa stain)
Ii.Intestinal & luminal flagellates
1.Giardia lamblia
1.) disease: giardiasis2.) morphology:
– trophozoites: binuclear structure (each containing a complete set of genome,4 pairs of flagella,a ventral disc,anda median body .The 2 nuclei R almost identical,have no visible nucleoli,& R arranged in symmetric fashion.-cyst: 7 2 10 um in diameter ,& contains 4 nuclei.
3.) hosts:
humans,mammalian (cats,birds,dogs)
4.) life cylce:
1.Cyst can survive 4 weeks in cold water2.Ingestion of dormant cysts3.Excystation: trophozoite emerge 2 an active state4.Trophozoite undergo asexual replication (binary fission)5.Not every1 exhibit symptoms6.Encystation during transit toward the colon7.Eysts & trophozoites expelled in the feces8.Only cysts can survive outside the host5.) transmission:–
Infection can occur through ingestion of dormant microbial cysts in contaminated water ,food or by the faecal-oralroute (poor hygiene)
6.) symptoms:
diarrhea,malaise,exessive gas (cause the infected person 2 vomit),steatorrhoea,epigastric pain7.) diagnosis:
giardiasis does not spread via the bloodstream,but remains confined 2 the lumen of the small intestine.The presence or absence of cysts (the resistant form of the parasite found in stool) or parasite antigen helps determinewhether or not U have the condition.This test may be repeated several times over several days 2 confirm the presence of the parasite.
8.) prevention:
do not drink or brush yur teeth & wash food or dishes with untreated water from streams,rivers,orlakes,even if they look sparkling clean.Make sure U boil water from these sources before use.Wash yur hands thoroughly with soap & water before & after eating,preparing food,changing diapers,& using
the toilet.Do not send a child who is infected & cannot control his or her bowel movements 2 daycare or school.Avoid swallowing water when swimming in public pools or lakes.Chlorine commonly used in swimming pools will notkill the cysts.Try 2 eat well-cooked hot foods & always peel raw vegetables & fruit.
2.T richomonas vaginalis
1.) disease:
trichomoniasis (sexually transmitted infection)
2.) morphology:
oval,flagellated (5 flagellata),slightly larger than white blood cell,does not have a cyst3.) hosts:
they require a human or animal host.In men,the organism lives in the urinary tract,most commonly theurethra or prostate,where as in women,it is found in the reproductive tract,usually in the vagina.A healthy vagina is asomewhat acidic environment (ph 3.8-4.2).When ph is thrown off & becomes more basic,if t .Vaginalis is present,itcan cause infection.T .Vaginalis is most successful in an enviroment with ph near 6.Nevertheless it can survive up to24h in urine,semen or even wate samples.
4.) life cyle:
1.Trophozoite in vaginal & prostatic secretions & urine2.Multiplies by longitudinal binary fission3.Trophozoite in vagina or orifice of urethra(living ph of trophozoite is 5-6)
5.) symptoms:
infection of the urogenital tractcause in women watery vaginal infection,pain while urinating,eroding of epithelial tissues,itchingcause in men asymptomatic carrier ,acts as a reservoir host 4 femalecause urentraitis & prostatititis,uninary tract problems6.) diagnosis:
classically ,with a cervical smear ,infected women have a transparent “halo” around their superficial cellnucleus.It is unreliably detected by studying a genital discharge or with a cervical smear because of their low sensitivity .The presence of t .Vaginalis can also be diagnosed by pcr,rapid antigen testing & transcription-mediated amplification.
7.) prevention:
health education is mostly important in the community because it is 1 of the sexually transmitted disease.Asymptomatic male carrier must be detected & treated.
Iii.Tissue flagellates1.Leishmania donovani2.Leishmania tropica3.Leishmania braziliensis
1.) disease:
many different kinds;kala – azar2.) morphology:–
Occurs as intracellular amastigotes in vertebrate hosts an das flagellates promastigotes in invertebrate hostamastigotes:
– typical leishmania is small,oval,intracellular organism in vertebrate host- found within phagocytic vacuoles of macrophages & other mononuclear phagomcytes- reproduction occurs by longitudinal binary divisionpromastigotes:- found in sandflies- latter equipped with a long,delicate,anterior flagellum- reproduction occurs by longitudinal binary division3.) life cycle:–
Involves an alternate host (besides human the domestic dog & wild mammals) & aninsect host.- after parasite with blood meal is ingested they form into flagellates andmultiply in the gut of the insect- as stationary growth phase is reached,the organism undergoes biochemicalsurface change & changes as well slightly morphologically & is now infective formammals- when sand fly attempts a blood meal some of the infective promastigotes aredislodged & introduced into the skin- transmission can also occur by contamination of the bite wound & by contact- when introduced into the tissues promastigotes gain access 2 mononuclear phagocytic cells,where they multiply ,cellruptures & provides organism 2 be phagocytosed by other cells & may spread the infection 2 other organs4.) symptoms:
contaneous – causes skin sores,which start out as papules (bumps) or nodules (lumps) andleishmaniasis: may end up as ulcers (like a volcano,with a raised up edge & central crater)- sores can be painless or painfulvisceral – affecting several internal organs & can be life threatening.Leishmaniasis: – affected people usually have fever ,w8 loss,enlargement of spleen andliver ,& low blood count
mucosal – less common formleishmaniasis: – certain type of parasite may spread from the skin & cause sores in themucous membranes of the nose,moth,or throat5.) diagnosis:–
V arious laboratory methods can be used 2 diagnose leishmaniasis & the speciesl.Donovani promastigotes (giemsa stain)
—————lab #3protozoa,class sarcodina,class conoidasidaamebasi.Intestinal protozoa,class sarcodina1.Entamoeba histolytica
1.) disease:
amebiasis,amebic dysentery ,amebic hepatitis- caused by e.Histolytica (gastrointestinal infection)habitat: wall & lumen of the colon (especially in cecal & sigmoidorectal regionpresented as: amoebic dysentery ,amoebic liver abscess or asymptomatic
2.) morphology:
– size (microns): 10- 60 –> average: 20- ectoplasm: sharply seperated from endoplasm;wide,clear ,refractile,hyaline- endoplasm: finely granular (contains no bacteria / foreign particles,but sometimes red blood cells)- staining: hematoxylin –> defined nuclear membrane- inner surface: lined with uniform & closely packed granules of chromatin- motility: active progression in definitive direction
– colorless;round/ oval cell- size: precyst < trophozoit,=”” but=”” precyst=””> cyst- round/ oval form,slightly asymmetrical,hyaline bodies- size (microns): 10-20- young cyst: contains –> vacuoles + glycogen;chromatoid bodies(rna,dna);nucleus;karyosome- immature cyst: simple nucleus
– mature cyst: infective form (1-4 nuclei)-general information (morphology & physiology
– reproduction: multiply bei binary fission (nucleus divided by modifiedmitosis);repro.Also takes place via cyst formation- cell organells: no mitochondria,cytochromes- growth: optimal -> 35°- 37° c,ph= 7.0,anaerob condition- survival: decreases rapidly @ very low & very high temperatures (e.G.-28°c (7 h survival);+50°c (5 minutes)
3.) hosts:
definitive host: human(spontaneous natural infections with amebas R also reported in: monkeys,dogs,hogs,rats)
4.) life cycle:
Resistant infective cysts (formed in lumen of the large intestine)pass out in the feces- infection occurs by ingestion of mature cysts (from fecally contaminated food/ water)- excystation occurs in the small intestine à trophozoites R released (migrate 2 large intestine)- trophozoites multiply by binary fission & produce cysts (both stages passed in feces9- cysts R responsible 4 transmission- trophozoits remain confined 2 the intestinal lumen (noninvasive infection)—> therefore asymptomatic carriers- if trophozoites invade the intestinal mucosa àintestinal disease- if trophozoites invade the bloodstream & reach liver ,lung or brain à extraintestinal disease5.) symptoms:–
Common: abdominal discomfort,weakness,diarrhea,abdominal pain,stool contains blood & mucus,fever(38°-39°c)- case of chronic amebiasis: recurrent attacs of dysentery with intervening periods of mild or moderate gastrointestinaldisturbances & constipation- case of hepatic amebiasis (liver abcess or amebic hepatitis): enlarged liver ,pain in the right upperhypochondrium radiating 2 the right shoulder ,fever (difficult 2 diagnose: because of liver function tests.They could be normal or mildlyabnormal)- case of amebic infections of the brain: usual signs/ symptoms of brain abscess or tumor6.) diagnosis:–
Final diagnosis of amebiasis: identification of the parasite in feces or tissues & upon serologic studies- laboratory diagnosis:
microscopic identification of trophozoites & cysts- typical amebic stool à acidic,consists of fecal material,cellular exudate,blood etc.- bacillary dysentery stool: offensive smell,alkaline,consists of fecal material,cellulare exudate,amounts of blood etc.- patients with acute dysentery: identify the trophozoites in the liquid stool- patients with chronic amebiasis: identify the cysts in the formed stool- in fresh,warm feces: trophozoites can be identified by their active,directional,progressive movements (sharply defined ectoplasm)- diagnosis of invasive amebiasis: serologic tests 4 antibodies 2 e.Histo.(e.G.Iha or elisa method)
2.Balantidium coli
1.) disease:
balantidiasis,balantidosis,balantidial dysentery2.) morphology:
– largest intestinal protozoan- trophozoit: size à 60 micrometer (average),shaped like a sac,with contractile vacuoles,food vacuoles,gullet,mouth,macro nucleus & micro nucleus,triangular peristome & cytostome (@ the anterior end)à lined with long cilia (adaptedfor procuring food),excretory opening (posterior end).Lives in the lumen,but also in the mucosa & submucosa of the
large intestine (especially the cecal region & in the terminal portion of the ileum)- cyst: size à 52- 55 (micrometer),only the macronucleus,contractile vacuoles & cilia.Cysts remain viable 4 several
weeks.
3.) hosts:
humans & pigs4.) life cycle:–
Similar 2 the life cycle of entamoeba histolytica
– exception: no multiplication in the cyst- cysts R the infective forms- when ingested by a new host à cyst wall dissolves & liberated trophozoit invades & multiplies in the interstinal wall5.) symptoms & pathology:–
Mucosa/ submucosa invaded & destroyed by multipying organisms- multiplying organisms form nests & small abscesses- acute infections: 6- 15 liquid stools per day (with mucus,blood & pus)
– chronic disease:
diarrhea,constipation,tender colon,anemia,cachexia- many infections R asymptomatic6.) diagnosis:–
Depends on identification of trophozoites in diarrheic stools & less frequently of cysts in formed stools- several stools should be examined,since the discharge of parasites is variable- also identification with sigmoidoscope (if there R patients with simoidorectal infection)
b.Coli,trophozoite –ii.Luminal protozoa,class conoidasida1.T oxoplasma gondii
1.) disease:
t oxoplasmosis2.) morpholoy:–
4 developmental stages R formed: schizonts,tissue cysts,gamonts & oocysts- schizonts appear as small basophilic intracellular bodies which divide rapidly 2 form small collections of tachyzoites- tissue cysts R surrounded by a thin primary cyst wall & contain hundred of basophilic bradyzoites- gamonts exhibit sexual differentiaion- oocyst R small ovoid stages & contain 2 round sporocysts,each containg 4 elongate sporozoites3.) hosts:–
All warm blooded vertebrates,definitive host: cat (4 the sexual stage of the parasite),intermediate host: bird,mice
4.) life cycle:
– oocysts R the main source of transmissionoocyst: – 1st 2 sporoblasts R developing > become sporocysts- ingestion of oocystoocyst releases sporozoites > differentiate into tachyzoites
– invade tissue in the small intestine- encysted stage: bradyzoite > metabolically quiescent
– multiplication: tachyzoites > endodyogeny (2 daughter cells R produced within the mothercell)
– after excystation: bradyzoites penetrate the small intestine (development of macro & microgametes)
5.) symptoms:
– may feel as if U have the „flu“ with swollen lymph glands or muscle aches & pains that last 4 a month or more;fever ,sore throat-reduced vision,blurred vision,pain (with bright light),redness of the eye,tearing-causing damage 2 the brain,eyes or other organs.Severe cases R most likely in individuals who have weak immunesystem.
6.) diagnosis:
Is achieved by serology ,although tissue cysts may be observed in stained biopsy specimens.Diagnosis of congenitalinfections can be achieved by deteching t .Gondii dann in amniotic fluid using molecular methods such as pcr.
7.) prevention:
– don’t eat raw or undercooked meat,wash all fruits & vegetables,don’t drink unpasteurized milk,cover children’ssandboxes,wear gloves when gardening & during any contact with soil or sand because it might be contaminated withcat feces that contain t oxoplasma,wash hands with soap & warm waterinfected mice perit1al macrophages objective 40x
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Lab #4genusplasmodium,class sporozoa
1.) common morphological characteristics:
– earliest form after invasion of red cell: ring of bluish cytoplasm with a dotlike nucleus of red chromatin- growing throphozoite: hemozoin is produced ( darkly staining malarial pigment)- schizont: shows multiple masses nuclear chromatin- gametocytes: compact cytoplasm,no nuclear division2.) hosts:–
Definitive hosts R female anopheles mosquitoes,intermediate hosts R vertebrates3.) life cycle:
schizogony (asexual cycle in vertebrate host):sporozoite is transferred from female anopheles mosquito into bloodstream during bitingafter 30 min,the parasite enters a liver cell,initiating the exoerythrocytic part of life cycleparasite multiplicates,is now called a schizont & produces thousands of merozoites after 8-15 daysparasitized liver cell ruptures,freeing merozoites 2 initiate the erythrocytic cycleinvasion of red cell: recognition by merozoite of a specific receptor site on the red cell;orientation of anterior end of
merozoite,exposing special organelles 2 the red cell surface;deformation of red cell & entering of merozoite throughinvagination of the red cell membranedevelopment through trophozoites,then schizontsrupturing of the cell,reinvasion of new cellssome parasites that invade red cells do not undergo division,but transform into male & female gametocytessporogony (sexual cycle in the mosquito):gametocytes R transferred 2 mosquito during blood mealnucleus of male microgametocytes divides into 6-8 nuclei,migrate 2 periphery of the parasiteexflagellation: uninuclear microgametes R thrust out & detached from the parental cellin meantime,female macrogametocyte hs matured into macrogametefertilization: entry of the microgamete into macrogamete,resulting in the formation of a zygote12-24 hrs.After the blood meal,the zygote changes into the wormlike ookinete;penetrates the gut wall & develops into a spherical oocyst between epithelium & basement membranehere it increases in size & develops thousands of sporozoites insideoocyst ruptures,freeing sporozoites into the body cavitiy;migrate 2 salivary glandswhen the mosquito feeds on human,the sporozoites enter the blood stream & the exoerythrocytic cycle starts againsporogonic cycle takes 10-17 days4.) symptoms:–
Headache,lassitude,vague pains in b1s & joints,chilly sensations,fever ,vomiting,rapid pulse;malarial paroxysms occur in intervals;without treatment,all species of human malaria may ultimately result in spontaneous self-cure,but with p .Falciparum there is a chance of progressively increasing parasitemia & fatal outcome
5.) diagnosis: – microscopic identification of the parasites in blood smear
1.Plasmodium vivaxdisease:
vivax malaria,benign tertian malariamorphology:
enlarged red cell ( partly explained by its affinity 4 the larger reticulocytes)growing signet-ring-appearing trophozoite becomes irregular in shape with ameboid extensions of the cytoplasm;schüffner’ s dots (fine,round,pink or reddish granules) R distributed over the cellafter 36 hrs: parasite fills over half the red cell,nucleus divides (becomes a schizont)after 48 hrs: schizont is segmented into 16 merozoites,each with red nucleus & blue cytoplasmgametocyte: oval,nearly filling the red cell;macrogametocytes with darker blue cytoplasm & more compact nucleusthan microgametocyte2.Plasmodium malariaedisease:
malariae malaria,quartan malariamorphology:
early stage: parasite is smaller ,less irregular ,more compact & cytoplasm deeper blue than p .Vivaxgrowing trophozoite shows dark brown or black granules (may assume a band shape across the cell)infected red cells R normal or even smaller in size (explained by its affinity 4 old cells)after 72 hrs: daisy or rosette mature schizont with 8-10 oval merozoites;mass of greenish black pigments is often located centrally ,surrounded by the merozoites
gametocyte: similar 2 those of p .Vivax but smallerplasmodium falciparumdisease:
falciparum malaria,malignant tertian malariamorphology:
infected red cell is of normal size (infects cells of all ages)only ring forms of early trophozoites & gametocytes R ordinarily seen in peripheral blood,schizonts R seldomfound therering forms: presence of more than 1 ring form in a cell is common,frequently with 2 nucleischizonts: resemble those of p .Vivax,but have smaller & few more merozoites when matureimmature gametocyte: elliptical shape,stretching but remaining inside the cellmature gametocyte: characteristic banana shape,called crescentsometimes maurer’ s dots (irregularly distributed red spots or clefts) appear in cel
——–llab #5class cestoda – t apeworms1.T aenia saginata (beef tapeworm)
1.)
Morphology:
the pyriform scolex of t .Saginata hs 4 hemispherical suckers but no well developed rostellum orhooks.The mature proglottides have irregular alternate lateral genital pores & R different from t .Solium by the morenumerous lateral branches of the uterus.The gravid uterus (which hs no uterine pore) contains about 100.000 eggs.These R completely indistinguishable from t .Solium’s eggs.2.)
Life cycle:
t .Saginata passes its life cycle in 2 hosts.The definitive host is man,who harbors the adult worm.Theintermediate host is cattle.The eggs or gravid segments R passed out with feces on the ground where they R ingestedby cows/buffalos.When the eggs reach the duodenum,the embryo of the egg ruptures & oncospheres R released.
using their hooklets,they penetrate the wall of the intestine & enter the lymphatics or blood vessels.They then reachthe general circulation via the liver ,right & lft side of the heart & lungs.
they R then filtered out in the striated muscles where they develop into bladder worms known as cysticercus bovis.They R ovoid in shape & milky-white.These R frequently found in the muscles of mastication,the cardiac muscle,diaphragm & tongue.The cysticerci can live in cattle 4 about 8 months & can only develop further in humans,which R the definitive host.Humans aquire the infection of t .Saginata by eating raw or undercooked beef containing cysticercus bovis.The larvae
hatch in the small intestine where they exvaginate & attach themselves 2 the mucosal surface using their suckers.After attachment,they start developing 2 adult worms.Here they grow 2 sexual maturity in 2-3 months & lay eggs.Eggs R passed out with feces & the cycle starts over .
2.T aenia solium (pork tapeworm)
1.)
Morphology:
the globular scolex of t .Solium hs 4 cup-shaped suckers & a rostellum with 25-30 hooks.The mature proglottid is roughly square with unilateral genital pores on consecutive segments.The gravid uterus hs 7-12 thicklateral branches on each side of the uterine stem.The gravid proglottid releases about 30.000-50.000 eggs when it ruptures before or after leaving the host.2.)
Life cycle:
t .Solium passes its life cycle in 2 hosts.The definitive host is man.The intermediate host is usuallythe pig but sometimes humans also serve as the intermediate host.The adult worm lives in the small intestine of manand the gravid segments come out with the feces in chains of 5 or 6.Whole segments or eggs R eaten by the pig.After the eggs reach the duodenum,t .Solium hs an almost identical life cycle of t .Saginata.The embryo of the eggsrupture & releases oncospheres inside the pig.Using their hooklets,they penetrate the wall of the intestine & enter
the lymphatics or blood vessels.They then reach the general circulation via the liver ,right & lft side of the heart andlungs.They R then filtered out in the striated muscles where they develop into bladder worms known as cysticercus cellulosae (different from cysticercus bovis of t .Saginata!).The muscles which R most commonly selected R: tongue,neck,shoulder & ham along with cardiac muscle.
man acquires the infection of t .Solium by eating raw or undercooked pork containing cysticercus cellulosae.The larvae hatch in the small intestine where the scolices exvaginate & attach themselves 2 the mucosal surface using theirsuckers & develop into adult worms.They grow 2 sexual maturity in 2-3 months.Gravid segments R passed outwith the feces in chains of 5 or 6 & the life cycle is repeated.Cysticercus cellulosae can also develop in man by ingesting the eggs with contaminated water & food.A man harbouring adult worms can also autoinfect himself by unhygienic personal habits or by reverse peristaltic movements of theintestine.The development 2 cysticercus cellulosae in man is similar 2 that in a pig.Cysticercosis may develop in anyorgan,& usually develop in subucatenous tissues & muscles where they R visible as a type of swelling of the tissue.
3.) diagnosis of t .Saginata/t .Solium:
the diagnosis can be carried out by finding the characteristics of the eggs in the
stool examining fecal smear or by anal swab.Since the eggs R indistinguishable,finding the gravid proglottides orscolices is essential 4 determining species3.Diphyllobothrium latum
1.)
Disease:
fish tapeworm or broad tapeworm2.)
Morphology:
adult worm:- it is the longest tapeworm found in man & can have more then 3000 proglottids- it can live 4 several years in host
– it consists of scolex,neck & strobilascolex:- almond shaped or spoon shaped- it hs 2 slit-like grooves demarcated by lateral lip-like folds,1 dorsal & the other ventralneck:- unsegmented & several times the length of the headstrobila:- hs 3000 or more proglottids consisting of immature,mature (broader than long & filled with male & female reproductive organ) & gravid segment- in each segment coiled uterus in compact-rosette form is seen- discharges 1.000.000 eggs daily ,through discharge off eggs,terminal segments dry-up & break off from the bodyegg: – yellowish-brown in color ,oval or elliptical in shape with a operculum @ 1end & a small knob @ the other hand.- eggs not infective 2 manlarval – 1st-stage larva known as coracidium & develops from egg in water
stages: – 2nd-stage larva known as procercoid,develops from coracidium insidesmall copepods ß the 1st intermediate host- 3rd-stage larva known as plerocercoid,develops from procercoid in
freshwater fish ß the secon intermediate host3.)
Life cylcle:
Hs 1 definitive host mainly the man but dogs,cats,foxes,bears & pigs can also be definitive host- hs 2 intermediate host,1 small copepds & the other 1 the freshwater fish- adult worm resides in the small intestine,ileum & jejunum.- inside the egg a spherical ciliated embryo containing 3 pairs hooklets develops
– coracidium egg is ingested by small copepods.Inside the copepods it develops into a procercoid.
– this coracidium is then eaten by a freshwater fish.Inside the fish it develops into a plerocercoid.
– human become infected by eating uncooked,raw or lightly salted meat of freshwater fish.
inside the human it develops into an adult worm & after attaining sexual maturity it starts 2 lay eggs which R passedinto faeces > the cycle repeats again.4.)
Symptoms:
Patient may develop fatigue,weakness,diarrhea & numbness of the extremities- in few cases pernicious anaemia occurs,because d.Latum absorbed vitamin b125.)
Diagnosis:
Laboratory diagnosis can be made by identification of the characteristic operculated eggs or proglottids in the faeces4.Hymenolepis nana
1.)
Disease:
dwarf tapeworm infection2.)
Morphology:
adult worm:- it is the smallest tapeworm infecting humans
– life span is about 2 weeks,but in an infected person 1000 – 8000 worms may be present
– it consists of scolex,neck & strobiliscolex:- hs 4 cup-shaped suckers & a rostellum armed with a single row of 20-30 hookletsneck:- is long & slender & posterior of the scolexstrobila:- hs about 200 proglottids.- genital pores R marginal & situated on the same side- uterus is a transverse sac with lobulated walls & the testes R roundegg:- spherical or oval- smooth,colorless outer shell & an inner membrane,containing a hexacanth embryo3.)
Life cycle:
Only cestode which is capable of completing is life cycle in a single host- adult worm resides in upper 2-thirds of the ileum of man
!Hs 2 life cycles!Direct cycle: – eggs & proglottids with eggs passed in the faeces of infected human
– ingestion of contaminated water or food- in the lumen of small intestine a free oncosphere is liberated from the egg,penetrating into a villus of the anterior part of small intestine & develops intocysticercoid larva- villus ruptures & cysticercoid becomes free in lumen & attaches with it
scolex 2 another villus,developing into an adult worm- strobilization is rapid & in short time eggs & proglottids with eggs willappear in faeces & the cycle is repeatet- in heavy infections eggs may hatch in the intestine resulting in auto infectionindirect cycle: – grain- & floureatin beetles,fleas & moths as intermediate host- infected by ingesting eggs- it develops into cystercoid larva which is infected 2 final host- man is infected by accidentally eating this insects4.)
Symptoms
Infection more common in children- headache,dizziness,anorexia,pruritus of nose & anus,abdominal pain,diarrhea,restlessness5.)
Diagnosis:
Demonstration of characteristic eggs in faeces by direct microscopy
5.Echinococcus granulosus
1.)
Disease:
echinococcosis,hydatid disease,hydatid cyst.2.)
Morphology:
the globular scolex of e.Granulosus hs a prominent rostellum with a double crown of 30-36 hooks
& 4 prominent suckers.Adult worms R small & have a scolex with only 3 attached proglottides.The anteriorproglottide is immature whilst the middle more elongted proglottide contains the fully developed reproductive organs(testes & ovaries) & lastly the posterior proglottide is gravid & hs a median uterus with 12-15 branches distended with 500 eggs.The eggs resemble those of the other taenia.3.)
Life cycle:
the definitive hosts 4 the adult worms R canids (dogs,dingoes,wolves & coyotes) these hosts aquire the adult tapeworm by eating various organs of herbivores (e.G pig & cows) that contain the cyst stage with its numerous protoscolices.Except 4 inflammation of the intestine,it does not hurt the ca9 host.The intermediate host ofthe eggs R omnivorous & herbivorous mammals (humans,domestic animals & wildlife).When the egg is from the
feces of an infected dog is ingested by an intermediate host 4 e.G a person when the dog licks its feces & transmits itto the human,the liberated embryo penetrates the intestinal wall,passes into the lymphatics & or mesenteric venulesand is carried by the bloodstream 2 various parts of the body .It looses its hooklets,undergoes central vesiculation andbecomes a cyst.When the capsule of the fully developed cyst ruptures the protoscolices escape into the hydatid fluid where they & the
brood capsule R known as hydatid sand.Ingested by a dog it would produce a mature adult tapeworm.It is estimatedthat an average fertile cyst contains 2 million protoscolices & when consumed by a dog it is would produce an innumerable amount of adult tapeworms.Hydatids without brood capsules & protoscollies R known as sterile or acephalocysts.The main distribution of cystsin the human is in the liver ,lung,kidneys or b1s.The rupture of a cyst sets free protoscolies,bits of germinal membrane,brood capsules & daughter cysts.These daughter cysts may reach other tissues through the blood or by direct extension & develop into secondary cysts.Rupture of cysts may occur from coughing,muscle strain & aspiration.Theinfection with a metastases like this can be compared 2 cancer .4.)
Symptoms:
the symptoms of the cyst that can be comparable 2 a slowly growing tumor ,depend upon the location ofthe hydatid cyst.In the abdomen they can create discomfort but they do not appear until the cysts have obtained a largesize.Ruptures of cysts may give an irregular fever ,gastrointestinal disturbances,abdominal pain,cyanosis,syncopeand delirium.If a large number of hydatid material enters the bloodstream,anaphylacic shock & death may result.5.)
Diagnosis:
laboratory diagnosis is made by finding the protoscoiles,brood capsules or daughter cysts in the cyst after surgical removal or by finding hydatid fragments from a ruptured cyst in the sputum or in urine.Finding hooklets isalso especially useful in diagnosis.
———lab#7class arthropoda1.Fleas (order siphonaptera)
– blood sucking ectoparasite
1.) v ector of: plague,endemic or murine typhus,dog & rat tapeworms2.)
Morphology:
small,brown,2 – 2,5 mm,all have antennae & suctorial mouth parts,3-segmented thorax with 6legs
2.Family argasidae (soft ticks) – primarily ectoparasites of birds,less often mammals & humans
– coxal glands produce tenacious fluid which contains spirochetes (borrelia) in infected ticks- can be vectors of several diseases simultaneously & may infect patients1.) v ectors of:
lyme disease,rocky mountain spotted fever,relapsing fever,tularemia,tick-borne meningoencephalitis,colorado tick fever,crimean-congo hemorrhagic fever,babesiosis!4 example ixodes damini transmitts borrelia burgdorferi which causes lyme disease in humans2.)
Life cycle:
ticks have 4 life stages > 1.Egg 2.Larva (3 legs & anal pore) 3.Nymph (4 legs & anal pore) 4.Adult (4legs;anal & genital pore on the medial line of the body) !Larva 2 adult also possess 2 pores laterally from the analpore 4 breathing !
– anteroir portion of legs possess olfactory organ- ticks R not able 2 actively suck blood but rather use the capillary blood pressure 2 feed on blood !If pressure insidethe tick equals the capillary pressure (after about 24 hours) & exchange of possibly infectious body fluids of the tickbecomes possible
breathing siphonculex – mosquito larva3.) how 2 remove a tick:
1) use fine-tipped tweezers 2 grasp the tick as close 2 the skin’s surface as possible.2) pull upward with steady ,even pressure.Don’t twist or jerk the tick;this can cause the mouth-parts 2 break off andremain in the skin.If this happens,remove the mouth-parts with tweezers.If UR unable 2 remove the mouth easilywith clean tweezers,leave it al1 & let the skin heal.3) after removing the tick,thoroughly clean the bite area & yur hands with rubbing alcohol,an iodine scrub,or soapand water .!Do not try 2:smother a tick that is stuck 2 yur skin with petroleum jelly ,nail polish,gasoline,or rubbing alcohol.Burn the tick while it is stuck 2 yur skin.> smothering or burning a tick could make it release fluid—which could be infected—into yur body & increase yourchance of infection.There R some tick-removal devices that U can buy .If UR active outdoors in areas wherethere R a lot of ticks,U may want 2 consider buying such a device.4.)
Symptoms:
itching,swelling,reddening around bitehypostomepores 4 breathing
anal pore4.Lice (order anoplura)
1.)
Disease:
pediculosis,crabsv ectors of: epidemic typhus,trench fever & relapsing fever2.)
Morphology:
relevant members > pediculus humanus capitis (head louse) & pediculus humanus humanus humanus(body louse) & phtirus pubis (crab louse);lice R small,dorsoventrally flattenend wingless insects that haveincomplete metamorphosis,flattenend elongated grayish-white body hs an angular ovoid head,a fused chitinousthorax,& a segmented abdomen.;bears a pair of simple lateral eyes,a pair of short antennae & extensile piercingstylets3.) hosts:
human is definitive host;the head louse & the crab louse have never been incrimiated in diseasetransmission;body louse may transmitt rickettsia prowazekii (gram negative aerobic parasitic bacteria) & borrelia
recurrentis4.) life-cycle:
3 life- stages: larva,nymph & adult parasite;the operculated,white eg
gs 0,6mm 2 0,8mm,called„nits“ R deposited/attached 2 the hairs;eggs hatch in 5 – 11days @ 21°c 2 36°c;nymph develops within the egg caseand emerges through the opened operculum;
average life cycle of the body or head louse covers 18 days & that of the crab louse 15 days,the life span of the adultis approximately 1 month;these lice R exclusively human parasites & have worldwide distributiontransmission of lice through close contact (e.G.Sexual intercourse 4 crab lice) or nits from hair ,clothing etc.- crab louse usually fixed on 1 spot & feed on blood periodically without moving;they use their feed 2 hold on tothe hair & lay the eggs close 2 the base
– hair louse moves around on the head;they lay their eggs (nits) close 2 the peripheral end of the hair
5.) symptoms: Itching,fever6.) diagnosis: Ichting5.Bedbucks / t rue bugs (order cimex)
1.) v ectors of:
role of bedbug in the transmission of human disease is minimal2.)
Morphology:
c.Lectularius (common bedbug) & c.Hemipterus (tropical bedbug);the bedbucks have oval,
dorsoventrallys flattened,chestnut-brown bodies covered with short,stout,simple or serrated hairs,head bearsprominent compound eyes,slender antennae & specialized mouth parts in a long proboscis flexed backward3.) life-cycle:
bedbugs feed @ night preferably on humans,but will feed on various small mammals if human host isnot available.They conceal themselves during the day .The white ovoid egg about 1mm in length,have an obliqueprojecting,collarlike ring with an operculum @ the anterior end & R coated with an adhesive gelatinous substance;hatching takes place in 4 2 10 days,life-span of the adult is 6 2 12 months4.)
Symptoms:
itching,fever5.)
Diagnosis:
itching6.T riatomine or c1-nosed bugs / kissing bug (order reduviid )
1.) v ector of:
trypansoma cruzi & t .Rangeli,
2.)
Morphology:
the triatomid bugs have long,narrow heads with prominent compound eyes,long antennae,a 3segmented,ventrally folded,slender probiscis & an obvious neck.
3.) hosts:
human is definitive host4.) life-cycle:
development by incomplete metamorphosis;the young bug must obtain its 1st blood meal within daysafter hatching & undergoes a lengthy metamorphosis during 6 2 more than 12 months 2 the adult stage,with bloodmeals between each molt5.) symptoms:
skin reactions dependant on individual;several species of the reduviid bug R important vectors oftrypansoma cruzi & of t .Rangeli (appears 2 be nonpathogenic 4 humans);the most important vectors R triatoma
infestans,panstrongylus megistas & rhodnius prolixus7.Cockroaches (order blattodea)
1.) v ectors of: 1.American & german cockroach – hymenolepis diminuta 2.German cockroach – nematodagongyl1ma pulchrum 3.American cockroach – acanthocephalid moniliformis moniliformis by contamination of foodor when eaten by human2.)
Morphology:
many different species – american periplaneta fulginosa,german blattella germanica3.) hosts: human is definitive host;mechanical vectors of pathogenic organisms as well as intermediate host ofhelminthic parasites.
4.) life-cycle:
cockroaches R omnivorous,with a partiality 4 starchy food;development is by incompletemetamorphosis;the nymh passes through 13 molts 2 reach adult stage & the length of the life cycle is 3 2 20 months
depending on species;life-span of the adult is slightly more than 40 days.
———lab#7class arthropoda1.Fleas (order siphonaptera)
– blood sucking ectoparasite
1.) v ector of: plague,endemic or murine typhus,dog & rat tapeworms2.)
Morphology:
small,brown,2 – 2,5 mm,all have antennae & suctorial mouth parts,3-segmented thorax with 6legs
3.)
Life cycle:
hosts R domestic or wild animals,various species tend 2 be host-specific but can infest other hostsadult fleas feed on blood while larvae live on nutritive debris such as dried blood or feces of the adults;eggs R small,ovoid,white 2 cream.Coloured about 0,5 mm in length & laid in the hair or environment of host;theydevelop by complete metamorphosis passing through a larval & a pupal stage until it reaches adulthood;fleas can liveup 2 1 yearhumanity important host 4: pulex irritans,ctenocephalides canis;c.Felis & tunga penetransplague: transmitted by flea from rat 2 human host – mostly by xenopsylla cheopis,also pulex irritanst yphus: endemic or murine typhus from rat 2 human host – mostly x.Cheopis & nosopsyllus fasciatusmiscellaneous diseases: bacterial & viral diseases;ctenocephalides canis,c.Felis & p .Irritans act as intermediatehost of the dog tapeworm;dipylidium caninum & n.Fasciatus,x.Cheopis & leptopsylla segnis intermediate hosts ofrat tapeworm4.)
Symptoms:
bites may cause itching2.Flies (order diptera)
– intermediate hosts or mechanical vectors of bacterial,viral,protozoan & helminthic agents1.)
Morphology:
basic morphology of insects with specialized mouth parts 2 feed from blood,body juices & otherfluidsmosquitos: anopheles – vectors of plasmodium (malaria)!The eggs R suspended on water with 2 floats on either side of them,keeping them from sinking;anopheline larvaeare suspended parallel 2 the water surface & breathe through a pair of spiracles @ the posterior end of the abdomen;culicine larvae hang suspended from the water surface by a prominent posterior breathing siphon with spiracles @ itstip !Some mosquitos carry the filiaris worm (helminth)sand flies: phlebotomus – vectors of leishmaniasis & sand fly fevert se tse fly: glossina – vectors of trypanasoma bruzei rhodesiense & gambiensehousefly: musca domestica – may serve as mechanical vector 4 pathogenic protozoa & helminthic eggs & larvaeespecially of enteric disease organisms3.Ticks (& mites) (order acarina )1.Family ixiodae (hard ticks)
2.Family argasidae (soft ticks) – primarily ectoparasites of birds,less often mammals & humans
– coxal glands produce tenacious fluid which contains spirochetes (borrelia) in infected ticks- can be vectors of several diseases simultaneously & may infect patients1.) v ectors of:
lyme disease,rocky mountain spotted fever,relapsing fever,tularemia,tick-borne meningoencephalitis,colorado tick fever,crimean-congo hemorrhagic fever,babesiosis!4 example ixodes damini transmitts borrelia burgdorferi which causes lyme disease in humans2.)
Life cycle:
ticks have 4 life stages > 1.Egg 2.Larva (3 legs & anal pore) 3.Nymph (4 legs & anal pore) 4.Adult (4legs;anal & genital pore on the medial line of the body) !Larva 2 adult also possess 2 pores laterally from the analpore 4 breathing !
– anteroir portion of legs possess olfactory organ- ticks R not able 2 actively suck blood but rather use the capillary blood pressure 2 feed on blood !If pressure insidethe tick equals the capillary pressure (after about 24 hours) & exchange of possibly infectious body fluids of the tickbecomes possible
breathing siphonculex – mosquito larva3.) how 2 remove a tick:
1) use fine-tipped tweezers 2 grasp the tick as close 2 the skin’s surface as possible.2) pull upward with steady ,even pressure.Don’t twist or jerk the tick;this can cause the mouth-parts 2 break off andremain in the skin.If this happens,remove the mouth-parts with tweezers.If UR unable 2 remove the mouth easilywith clean tweezers,leave it al1 & let the skin heal.3) after removing the tick,thoroughly clean the bite area & yur hands with rubbing alcohol,an iodine scrub,or soapand water .!Do not try 2:smother a tick that is stuck 2 yur skin with petroleum jelly ,nail polish,gasoline,or rubbing alcohol.Burn the tick while it is stuck 2 yur skin.> smothering or burning a tick could make it release fluid—which could be infected—into yur body & increase yourchance of infection.There R some tick-removal devices that U can buy .If UR active outdoors in areas wherethere R a lot of ticks,U may want 2 consider buying such a device.4.)
Symptoms:
itching,swelling,reddening around bitehypostomepores 4 breathing
anal pore4.Lice (order anoplura)
1.)
Disease:
pediculosis,crabsv ectors of: epidemic typhus,trench fever & relapsing fever2.)
Morphology:
relevant members > pediculus humanus capitis (head louse) & pediculus humanus humanus humanus(body louse) & phtirus pubis (crab louse);lice R small,dorsoventrally flattenend wingless insects that haveincomplete metamorphosis,flattenend elongated grayish-white body hs an angular ovoid head,a fused chitinousthorax,& a segmented abdomen.;bears a pair of simple lateral eyes,a pair of short antennae & extensile piercingstylets3.) hosts:
human is definitive host;the head louse & the crab louse have never been incrimiated in diseasetransmission;body louse may transmitt rickettsia prowazekii (gram negative aerobic parasitic bacteria) & borrelia
recurrentis4.) life-cycle:
3 life- stages: larva,nymph & adult parasite;the operculated,white eg
gs 0,6mm 2 0,8mm,called„nits“ R deposited/attached 2 the hairs;eggs hatch in 5 – 11days @ 21°c 2 36°c;nymph develops within the egg caseand emerges through the opened operculum;
average life cycle of the body or head louse covers 18 days & that of the crab louse 15 days,the life span of the adultis approximately 1 month;these lice R exclusively human parasites & have worldwide distributiontransmission of lice through close contact (e.G.Sexual intercourse 4 crab lice) or nits from hair ,clothing etc.- crab louse usually fixed on 1 spot & feed on blood periodically without moving;they use their feed 2 hold on tothe hair & lay the eggs close 2 the base
– hair louse moves around on the head;they lay their eggs (nits) close 2 the peripheral end of the hair
5.) symptoms: Itching,fever6.) diagnosis: Ichting5.Bedbucks / t rue bugs (order cimex)
1.) v ectors of:
role of bedbug in the transmission of human disease is minimal2.)
Morphology:
c.Lectularius (common bedbug) & c.Hemipterus (tropical bedbug);the bedbucks have oval,
dorsoventrallys flattened,chestnut-brown bodies covered with short,stout,simple or serrated hairs,head bearsprominent compound eyes,slender antennae & specialized mouth parts in a long proboscis flexed backward3.) life-cycle:
bedbugs feed @ night preferably on humans,but will feed on various small mammals if human host isnot available.They conceal themselves during the day .The white ovoid egg about 1mm in length,have an obliqueprojecting,collarlike ring with an operculum @ the anterior end & R coated with an adhesive gelatinous substance;hatching takes place in 4 2 10 days,life-span of the adult is 6 2 12 months4.)
Symptoms:
itching,fever5.)
Diagnosis:
itching6.T riatomine or c1-nosed bugs / kissing bug (order reduviid )
1.) v ector of:
trypansoma cruzi & t .Rangeli,
2.)
Morphology:
the triatomid bugs have long,narrow heads with prominent compound eyes,long antennae,a 3segmented,ventrally folded,slender probiscis & an obvious neck.
3.) hosts:
human is definitive host4.) life-cycle:
development by incomplete metamorphosis;the young bug must obtain its 1st blood meal within daysafter hatching & undergoes a lengthy metamorphosis during 6 2 more than 12 months 2 the adult stage,with bloodmeals between each molt5.) symptoms:
skin reactions dependant on individual;several species of the reduviid bug R important vectors oftrypansoma cruzi & of t .Rangeli (appears 2 be nonpathogenic 4 humans);the most important vectors R triatoma
infestans,panstrongylus megistas & rhodnius prolixus7.Cockroaches (order blattodea)
1.) v ectors of: 1.American & german cockroach – hymenolepis diminuta 2.German cockroach – nematodagongyl1ma pulchrum 3.American cockroach – acanthocephalid moniliformis moniliformis by contamination of foodor when eaten by human2.)
Morphology:
many different species – american periplaneta fulginosa,german blattella germanica3.) hosts: human is definitive host;mechanical vectors of pathogenic organisms as well as intermediate host ofhelminthic parasites.
4.) life-cycle:
cockroaches R omnivorous,with a partiality 4 starchy food;development is by incompletemetamorphosis;the nymh passes through 13 molts 2 reach adult stage & the length of the life cycle is 3 2 20 months
depending on species;life-span of the adult is slightly more than 40 days.
———lab#7class arthropoda1.Fleas (order siphonaptera)
– blood sucking ectoparasite
1.) v ector of: plague,endemic or murine typhus,dog & rat tapeworms2.)
Morphology:
small,brown,2 – 2,5 mm,all have antennae & suctorial mouth parts,3-segmented thorax with 6legs
3.)
Life cycle:
hosts R domestic or wild animals,various species tend 2 be host-specific but can infest other hostsadult fleas feed on blood while larvae live on nutritive debris such as dried blood or feces of the adults;eggs R small,ovoid,white 2 cream.Coloured about 0,5 mm in length & laid in the hair or environment of host;theydevelop by complete metamorphosis passing through a larval & a pupal stage until it reaches adulthood;fleas can liveup 2 1 yearhumanity important host 4: pulex irritans,ctenocephalides canis;c.Felis & tunga penetransplague: transmitted by flea from rat 2 human host – mostly by xenopsylla cheopis,also pulex irritanst yphus: endemic or murine typhus from rat 2 human host – mostly x.Cheopis & nosopsyllus fasciatusmiscellaneous diseases: bacterial & viral diseases;ctenocephalides canis,c.Felis & p .Irritans act as intermediatehost of the dog tapeworm;dipylidium caninum & n.Fasciatus,x.Cheopis & leptopsylla segnis intermediate hosts ofrat tapeworm4.)
Symptoms:
bites may cause itching2.Flies (order diptera)
– intermediate hosts or mechanical vectors of bacterial,viral,protozoan & helminthic agents1.)
Morphology:
basic morphology of insects with specialized mouth parts 2 feed from blood,body juices & otherfluidsmosquitos: anopheles – vectors of plasmodium (malaria)!The eggs R suspended on water with 2 floats on either side of them,keeping them from sinking;anopheline larvaeare suspended parallel 2 the water surface & breathe through a pair of spiracles @ the posterior end of the abdomen;culicine larvae hang suspended from the water surface by a prominent posterior breathing siphon with spiracles @ itstip !Some mosquitos carry the filiaris worm (helminth)sand flies: phlebotomus – vectors of leishmaniasis & sand fly fevert se tse fly: glossina – vectors of trypanasoma bruzei rhodesiense & gambiensehousefly: musca domestica – may serve as mechanical vector 4 pathogenic protozoa & helminthic eggs & larvaeespecially of enteric disease organisms3.Ticks (& mites) (order acarina )1.Family ixiodae (hard ticks)
2.Family argasidae (soft ticks) – primarily ectoparasites of birds,less often mammals & humans
– coxal glands produce tenacious fluid which contains spirochetes (borrelia) in infected ticks- can be vectors of several diseases simultaneously & may infect patients1.) v ectors of:
lyme disease,rocky mountain spotted fever,relapsing fever,tularemia,tick-borne meningoencephalitis,colorado tick fever,crimean-congo hemorrhagic fever,babesiosis!4 example ixodes damini transmitts borrelia burgdorferi which causes lyme disease in humans2.)
Life cycle:
ticks have 4 life stages > 1.Egg 2.Larva (3 legs & anal pore) 3.Nymph (4 legs & anal pore) 4.Adult (4legs;anal & genital pore on the medial line of the body) !Larva 2 adult also possess 2 pores laterally from the analpore 4 breathing !
– anteroir portion of legs possess olfactory organ- ticks R not able 2 actively suck blood but rather use the capillary blood pressure 2 feed on blood !If pressure insidethe tick equals the capillary pressure (after about 24 hours) & exchange of possibly infectious body fluids of the tickbecomes possible
breathing siphonculex – mosquito larva3.) how 2 remove a tick:
1) use fine-tipped tweezers 2 grasp the tick as close 2 the skin’s surface as possible.2) pull upward with steady ,even pressure.Don’t twist or jerk the tick;this can cause the mouth-parts 2 break off andremain in the skin.If this happens,remove the mouth-parts with tweezers.If UR unable 2 remove the mouth easilywith clean tweezers,leave it al1 & let the skin heal.3) after removing the tick,thoroughly clean the bite area & yur hands with rubbing alcohol,an iodine scrub,or soapand water .!Do not try 2:smother a tick that is stuck 2 yur skin with petroleum jelly ,nail polish,gasoline,or rubbing alcohol.Burn the tick while it is stuck 2 yur skin.> smothering or burning a tick could make it release fluid—which could be infected—into yur body & increase yourchance of infection.There R some tick-removal devices that U can buy .If UR active outdoors in areas wherethere R a lot of ticks,U may want 2 consider buying such a device.4.)
Symptoms:
itching,swelling,reddening around bitehypostomepores 4 breathing
anal pore4.Lice (order anoplura)
1.)
Disease:
pediculosis,crabsv ectors of: epidemic typhus,trench fever & relapsing fever2.)
Morphology:
relevant members > pediculus humanus capitis (head louse) & pediculus humanus humanus humanus(body louse) & phtirus pubis (crab louse);lice R small,dorsoventrally flattenend wingless insects that haveincomplete metamorphosis,flattenend elongated grayish-white body hs an angular ovoid head,a fused chitinousthorax,& a segmented abdomen.;bears a pair of simple lateral eyes,a pair of short antennae & extensile piercingstylets3.) hosts:
human is definitive host;the head louse & the crab louse have never been incrimiated in diseasetransmission;body louse may transmitt rickettsia prowazekii (gram negative aerobic parasitic bacteria) & borrelia
recurrentis4.) life-cycle:
3 life- stages: larva,nymph & adult parasite;the operculated,white eg
gs 0,6mm 2 0,8mm,called„nits“ R deposited/attached 2 the hairs;eggs hatch in 5 – 11days @ 21°c 2 36°c;nymph develops within the egg caseand emerges through the opened operculum;
average life cycle of the body or head louse covers 18 days & that of the crab louse 15 days,the life span of the adultis approximately 1 month;these lice R exclusively human parasites & have worldwide distributiontransmission of lice through close contact (e.G.Sexual intercourse 4 crab lice) or nits from hair ,clothing etc.- crab louse usually fixed on 1 spot & feed on blood periodically without moving;they use their feed 2 hold on tothe hair & lay the eggs close 2 the base
– hair louse moves around on the head;they lay their eggs (nits) close 2 the peripheral end of the hair
5.) symptoms: Itching,fever6.) diagnosis: Ichting5.Bedbucks / t rue bugs (order cimex)
1.) v ectors of:
role of bedbug in the transmission of human disease is minimal2.)
Morphology:
c.Lectularius (common bedbug) & c.Hemipterus (tropical bedbug);the bedbucks have oval,
dorsoventrallys flattened,chestnut-brown bodies covered with short,stout,simple or serrated hairs,head bearsprominent compound eyes,slender antennae & specialized mouth parts in a long proboscis flexed backward3.) life-cycle:
bedbugs feed @ night preferably on humans,but will feed on various small mammals if human host isnot available.They conceal themselves during the day .The white ovoid egg about 1mm in length,have an obliqueprojecting,collarlike ring with an operculum @ the anterior end & R coated with an adhesive gelatinous substance;hatching takes place in 4 2 10 days,life-span of the adult is 6 2 12 months4.)
Symptoms:
itching,fever5.)
Diagnosis:
itching6.T riatomine or c1-nosed bugs / kissing bug (order reduviid )
1.) v ector of:
trypansoma cruzi & t .Rangeli,
2.)
Morphology:
the triatomid bugs have long,narrow heads with prominent compound eyes,long antennae,a 3segmented,ventrally folded,slender probiscis & an obvious neck.
3.) hosts:
human is definitive host4.) life-cycle:
development by incomplete metamorphosis;the young bug must obtain its 1st blood meal within daysafter hatching & undergoes a lengthy metamorphosis during 6 2 more than 12 months 2 the adult stage,with bloodmeals between each molt5.) symptoms:
skin reactions dependant on individual;several species of the reduviid bug R important vectors oftrypansoma cruzi & of t .Rangeli (appears 2 be nonpathogenic 4 humans);the most important vectors R triatoma
infestans,panstrongylus megistas & rhodnius prolixus7.Cockroaches (order blattodea)
1.) v ectors of: 1.American & german cockroach – hymenolepis diminuta 2.German cockroach – nematodagongyl1ma pulchrum 3.American cockroach – acanthocephalid moniliformis moniliformis by contamination of foodor when eaten by human2.)
Morphology:
many different species – american periplaneta fulginosa,german blattella germanica3.) hosts: human is definitive host;mechanical vectors of pathogenic organisms as well as intermediate host ofhelminthic parasites.
4.) life-cycle:
cockroaches R omnivorous,with a partiality 4 starchy food;development is by incompletemetamorphosis;the nymh passes through 13 molts 2 reach adult stage & the length of the life cycle is 3 2 20 months
depending on species;life-span of the adult is slightly more than 40 days.