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164 Cards in this Set
- Front
- Back
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ENTAMOEBA HYSTOLYTICA
geographical distribution |
cosmopolitan
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ENTAMOEBA HYSTOLYTICA
morphology of trophozite |
20-60µ
unstained: pseuodopodium, clear ectoplasm, granular endoplasm, ingested erythrocytes are pale greenish refractile bodies. nucleus not visible after staining with iron haematoxylin: ectoplasm clearly differentiated, nucleus is spherical and contains small central karyosome. fine regular chromatin granules line the nuclear membrane RBCS are bluish black discs |
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ENTAMOEBA HYSTOLYTICA
morphology of cysts |
10-20µ
unstained: spherical with hylaine refractile cyst wall, +- visible nuclei or 1-4 hyaline bodies. chromatid bodies (RNA) are rod shaped clear areas in the cytoplasm. stained: nuclear structure similar to trophic. mature cyst: 4 visible nuclei. chromatid bodies: rod shaped, rounded edges, blue black. |
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ENTAMOEBA HYSTOLYTICA
infective stage? |
mature quadrinuclear cysts
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ENTAMOEBA HYSTOLYTICA
life cycle |
mature quadrinuclear cysts --> eight metacystic amoeba --> commensals/ divide by binary fission --> precyst --> mononucleated cyst --> mature quadrinuclear cyst
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ENTAMOEBA HYSTOLYTICA
methods of contamination |
- polluted water
- unwashed raw vegetables - contaminated hands esp food handlers - food contaminated with excreta/ vomitus of flies - human excreta as fertilizer |
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ENTAMOEBA HYSTOLYTICA
factors affecting pathological changes |
- virulence of strain
- host resistence - host nutritional status - bacterial infection of the colon - sluggish parts of the colon: caecum, rt lt colonic flexures, sigmoid colon |
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ENTAMOEBA HYSTOLYTICA
pathogenesis |
pathogenic trophozites secrete lytic enzymes --> small areas of necrosis of lining --> penetrate mucosa, erode into deeper tissue, reach submucosa, spread fan like, multiply --> lytic necrosis
necrotic contents discharged --> flask shaped ulcers may cause: peritonitis, appendicitis, amoeboma, hhg, emboli |
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ENTAMOEBA HYSTOLYTICA
intestinal lesions |
- acute dysentry
- non dystenteric colitis - amoeboma/ amoebic granuloma |
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ENTAMOEBA HYSTOLYTICA
extra intestinal lesions |
- amoebic hepatitis
- amoebic liver abscess - pulmonary amoebiasis - cutaneous lesions - cerebral lesions |
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ENTAMOEBA HYSTOLYTICA
intestinal lab diagnosis |
A) Stool examinations
1- dysenteric stool (fresh saline smears, fixed stool specimens) ---> find trophoites 2- well formed stools ( fresh saline/iodine smears, fixed stool samples) ----> find cysts b) sigmoidoscopy --> ulcers |
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ENTAMOEBA HYSTOLYTICA
hepatic lab diagnosis |
- history, clinical pic
- X ray: upward displacement of diaphragm - Ultrasound, CT scan - aspiration only if large abscess: viscid choco brown thick, no trophozites in pus only in edge of abscess - sputum contains trophozites |
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ENTAMOEBA HYSTOLYTICA
immunologic lab diagnosis |
IHAT
ELISA gel diffusion tests are positive in invasive amoebiasis ie acute amoebic dysentry and amoebic abscess |
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ENTAMOEBA HYSTOLYTICA
treatment of intestinal infection |
A) asymptomatic/ cyst acciers
diloxanide furoate (furamide) 500 mg tds x 10 d SE: GI discomfort CI: preg B) non dysenteric intestinal colitis diloxanide furoate 500 mg tds x 10 + metronidazole 750 mg tds x 10 d ( combo = furazole 2 tab tds x 5-10 d SE: ") c) dystenteric colitis bed rest, fluid + electrolytes, metronidazole, furamide OR furazole |
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ENTAMOEBA HYSTOLYTICA
tt of hepatic abscess |
hospitalization, bed rest, needle aspiration advisable when large
metronidazole 750 mg tds x 10 d SE: N,V, rashes, metallic taste CI: preg, alcohol intake |
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ENTAMOEBA HYSTOLYTICA
prevention and control |
1- proper evironmental sanitaion
2- wash raw vegetables (destroy cysts with 1% phenol or lysol or 5% acetic acid for atleast 30 mins) 3- no human excreta fertilizer 4- protect food from flies 5- ttt cyst passers |
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ENTAMOEBA DISPAR
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trophozites: 20-60/ amoeboid/ well differentiated/ no RBCS/ stained shows central karyosome, fine regular lining with chromatin granules
cysts: 10-15/ rounded/ 4 nuc |
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ENTAMOEBA HARTMANNI
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12-15/ amoeboid/ well differentiated, no RBCs/ karyo central
fine , regular lining cysts: 7-9/ round/ 4 |
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ENTAMOEBA COLI
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20-30/ sluggish/ not well differentiated/ many food vacuoles, no RBCs/ VISIBLE in unstained/ karyosome ECCENTRIC/ chromatin granules IRREGULAR , COARSE
cysts: 15-30/ rounded/ 8 , similar to veg form/ chromatid bodies like splinters ent. coli in water --> fecal pollution |
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ENTAMOEBA GINGIVALIS
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10-20/ intermed motility/ granular endoplasm w/ many vacuoles and refractile inclusions "salivary corpuscles"/ dot like central karyosome /regular or irregular
mouth cavity in between teeth, esp if with chronic gum disease NO cystic stage direct contact/kissing binary fission |
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NEGLERIA FOWLERI
geographical distribution |
cosmopolitan
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NEGLERIA FOWLERI
habitat |
soil, fresh water, CNS
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NEGLERIA FOWLERI
morphology |
a) Trophozite
amoeboid form: elongate, broad ant, tapering post, 7-20, clear ecto granular endo w/ contractile vacuoles, nucleus, large central karyosome + periph chromatin. single blunt pseudopodium binary fission water @ 27-37 ---> flagellate Flagellate form: pear shaped, 2 flagella at broad end [NO DIVIDE] cysts: nature + agar round, 7-11 single nucleus smooth thick cyst wall |
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NEGLERIA FOWLERI
mode of infection |
swimming/ bathing in contaminated water
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NEGLERIA FOWLERI
infective stage |
FLAGELLATE form
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NEGLERIA FOWLERI
life cycle |
flagellate enters nasal cavity, ---> amoeboid form
penetrates nasal mucosa---> brain via olfactory nerves [amoeboid form is the only form that exists in humans] |
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NEGLERIA FOWLERI
clinical picture |
early sympt: vague respiratory distress, headache, fever, lethargy, N, V
later: mental confusion, signs of meningitis, --> coma "PAM" (primary amoeboid meningoencephalitis) death occurs in 6 days |
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NEGLERIA FOWLERI
diagnosis |
- history, clinical picture
- Direct: examination of CSF by lumbar puncture --> cloudy purulent fluid, +-blood, numerous pus cells, no bacteria. +- motile amoeboid forms [amoeba readily cultured on non nutrient agar seeded with Escherechia coli --> trophozites. cysts seen in old cultures] |
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NEGLERIA FOWLERI
treatment |
amphotericin B
1 mg/Kg/day x 9 days IVI or intrathecal/intraventricular 0.1 mg on alternate days until CSF clear hospitalization SE: GID, myalgia, cardiac arrhythmias CI: heart, kidney diseases |
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ACANTHOMOEBA
geographical distribution |
cosmopolitan
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ACANTHOMOEBA
habitat |
stagnant water, dust, cns, eyes, skin, lung, genitourinary tract
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ACANTHOMOEBA
morphology |
trophozoite: 10-45, large central karyosome, no periph chromatin
endoplasm +- contractile vacuole small spiky pseudopodia "ACANTHOPODIA" cysts: spherical, 20, double wall slightly wrinkled ectocyst roughly polyhedral endocyst |
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ACANTHOMOEBA
infective stage |
trophic/cystic form
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ACANTHOMOEBA
life cycle |
inhalation of trophic/cystic form by inhalation of dust, water/ broken skin/ cornea/GUT
if cysts inhaled--> vegetative forms immediately brain via blood possible from lung, skin, eyes tissue invasion is slow, (+) granuloma formation prefers chronically ill/immunosuppressed (except amoebic keratitis which can occur in healthy) |
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ACANTHOMOEBA
clinical picture |
CNS --> chronic "GAM" (granulomatous amoebic meningoencephalitis)
cornea--> keratitis, cornal ulceration (esp with lenses) skin --> ulcers w/ or w/o trophozoites/cysts aids etc --> fulminant, acute encephalitis |
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ACANTHOMOEBA
diagnosis |
brain biopsy may reveal the organism
NOT present in CSF scrapings from lesions in the corea/skin reveal trophozoites and cysts culture on non nutrient agar. cystic and trophic stages can be observed |
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ACANTHOMOEBA
treatment |
1- amphoterecin B 1 mg/kg/day x 9 days IVI
2- propamidine eyedrops for keratitis |
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ACANTHOMOEBA
prevention and control |
1- health ed, avoid submerging head in warm fresh water
2- fresh water lakes/swimming pools must be examined 3- chlorinate pools 4- sterile contact lenses 5- dont swim with lenses |
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LEISHMANIA
morphology of amastigote |
oval body
2-3 microns Stained with Giemsa stain: pale blue cytoplasm large red nucleus kinetoplast = deep red rod like parabasal body + dot like basal granule axoneme arises from the basal granule |
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LEISHMANIA
morphology promastigote |
spindle shaped
15-20 central nucleus anterior kinetoplast flagellum arises from basal granule |
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LEISHMANIA
infective stage |
promastigote
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LEISHMANIA
life cycle |
man bitten with infected sandfly --> promastigotes --> taken up by macrophages --> amastigotes --> binary fission
sandfly feeds : amastigotes --> promastigotes --> binary fission |
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LEISHMANIA
types |
cutaneous
mucocutaneous visceral or combination of them |
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LEISHMANIA
cutaneous leishmaniasis |
caused by L tropica, L major, L aethiopica
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LEISHMANIA
methods of infection with cutaneous species |
1. bite of an infected sandfly
2. autoinoculation 3. mechanical by bloodsucking flies 4. accidental in the lab |
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LEISHMANIA TROPICA
geographical distribution |
big cities of the mdidle and far east
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LEISHMANIA TROPICA
clinical picture |
incubation period: up to 6 months
small papule that lasts for several months then heals without ulceration dry sore/oriental sore/delhi boil/ bouton d'alep |
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LEISHMANIA MAJOR:
geographical distribtuion |
sinia, souhag, menya
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LEISHMANIA MAJOR
clinical picture |
incubation period: days/weeks
acute infection multiple lesions mature rapidly heal quickly last for months small itchy pauple ---> papery scales first dry then become moist thickened brown forming a crust which covers a shallow oozing ulcer "wet sore" |
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LEISHMANIA AETHIOPICA
geographical distribution |
ethiopia and kenya mainly
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LEISHMANIA AETHIOPICA
clinical picture |
chronic disease
single lesion, spreads slowly till whole body is covered with nodules no ulceration |
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LEISHMANIA AETHIOPICA
cause |
probably failure of immune mechanism of host
and absence of cell mediated immunity |
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CUTANEOUS LEISHMENIASIS
direct method of diagnosis |
1- microscopic examination of material obtained by puncutre of edge of ulcer --> amastigote
2) culture of material on NNN medium --> promastigote |
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CUTANEOUS LEISHMENIASIS
immunological methods of diagnosis |
1) leishmanin/ montenegro test
intradermal test 0.1 ml of suspended promastigotes is injected +ve --> red indurated wheal after 48 hours but negative in diffuse cutaneous leishmaniasis (aethiopica) 2) IFAT is negative |
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CUTANEOUS LEISHMENIASIS
treatment |
1) cutaneous:
antimony sodium gluconate (pentostam) 6 ml daily IV or IM for 10 days SE: GID, hemolytic anemia, EEG changes, impairment of hepatic and renal funciton CI: hepatic and renal diseases 2) mucocutaneous leishmaniasis amphoterecin B |
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CUTANEOUS LEISHMENIASIS
control |
1- cover ulcers to reduce secondary infection and protect from auto inoculation and reduce transmission to houseflies
2- residual insecticides 3- destruction of reservoir hosts 4- protective inoculation with live cultures |
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VISCERAL LEISHMANIASIS
geographical distribution |
el agami
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VISCERAL LEISHMANIASIS
method of infection |
1. bite of a infected sandfly
2. (less common) a) blood transfusion b) direct by nasal secretions c) congenital d) lab a,b,c --> amastigote |
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VISCERAL LEISHMANIASIS
life cycle |
bite of infected sandfly --> amastigote spread to lymph glands then enter the blood stream in the leukocytes and monocytes --> taken up by reticulo endothelial cells
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VISCERAL LEISHMANIASIS
clinical picture |
incubation period : 4-10 months
minute papule may be apparent sudden or gradual onset high fever (remittent or intermittent) oft with double rise BUT no malaise or apathy, has a clean tongue, good appetite, unaware of fever hepatosplenomegaly, lymphadenopathy +- diarrhoea, dysentry skin lesions: primary lesion --> dark colouration ("kala azar/black fever") severe anaemia, leucopenia, thrombocytopenia hhg increase in globulin, decrease in albumin in egypt: affects <5yrs , reservoir host: dog, organism: leishmania donovani infantum |
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VISCERAL LEISHMANIASIS
diagnosis |
1. history, clinical pic (irregular fever, enlarged lymph nodes, spleen, liver, severe anemia , in endemic areas)
2. LAB i) Direct 1- biopsy from bone marrow, spleen, lymph gland 2- blood examination (only in indian) 3- animal inoculation and culture ii) Immunological 1. IFAT 2. ELISA 3. Leishmanin test 3- Formol Gel test |
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VISCERAL LEISHMANIASIS
treatment |
miltefosine
2.5 mg/kg per day x 28 days toxicity: vomiting, diarrhoea CI: pregnancy |
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VISCERAL LEISHMANIASIS
prevention and control |
1. diagnosis and treatment of cases
2. sandfly control 3. control of reservoir hosts |
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types of trypanosomes
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1- Salivarian trypanosomes (infect with bite)
2- Stercoranian trypanosomes (infect with feces) |
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Types of salivarian trypanosomes
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trypanosoma brucei gambiense
trypanosoma brucei rhodesiense |
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AFRICAN TRYPANOSOMIASIS
caused by? |
T.b. gambiense
T.b. rhodesiense |
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AFRICAN TRYPANOSOMIASIS
geographical distribution |
north and south of the equator
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AFRICAN TRYPANOSOMIASIS
habitat of trypomastigotes |
early -> EC peripheral blood and lymphatics
later -> EC internal organs eg spleen, liver, bone marrow terminal stages --> CNS, CSF |
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AFRICAN TRYPANOSOMIASIS
morphology of trypomastigotes |
pleomorphic
15-40 central nucleus small terminal kinetoplast single flaggellum arising from blepharoplast, then passes ant to form outer edge of undulating membrane |
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AFRICAN TRYPANOSOMIASIS
infective stage |
metacyclic trypomastigote
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AFRICAN TRYPANOSOMIASIS
life cycle in man |
metacyclic trypomastigote introduced to the tissue during insect bite
multiplies by binary fission at site of inoculation invades lymphatics, gen circulation, internal organs then CNS |
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AFRICAN TRYPANOSOMIASIS
life cycle in glossina fly |
bites man, trypomastigotes are taken up into the midgut
multiply travel to the salivary gland change to epimastogote form and multiply change into metacyclic trypomastigotes |
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AFRICAN TRYPANOSOMIASIS
methods of infection |
1. bite of infected glossina fly
2. mechanical transmission when one blood sucking fly bites an infected person then bites a healthy one immediately 3. blood transfusion |
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AFRICAN TRYPANOSOMIASIS
clinical picture |
incubation period: 6-14 days
local subcutaneous inflammation "TRYPANOSOMA CHANCRE" multiplication in blood stream --> fever, headache, anorexia fever subsides and recurs again dt different surface antigens repeated episodes --> patient becomes anaemic, debilitated spleen enlarges, general lymphadenopathy enlargement of lymph nodes in post triangle of neck "WINTERBOTTOMS SIGN" delayed sensation of pain "KERANDELS SIGN" terminal stages --> symptoms of meningoencephalomyelitis --> coma, death |
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AFRICAN TRYPANOSOMIASIS
diagnosis |
History, clinical picture (fever, enlarged LN in endemic area)
LAB: 1) Direct: - detecting trypanosomes in perhipheral blood, LN aspirate, CSF - intraperitoneal inoculation - culture of aspirates on Weinmans medium --> trypomastigotes 2) Immunological IFAT, ELISA, CFT, CATT |
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AFRICAN TRYPANOSOMIASIS
treatment |
1. Haemolymphatic stage
a- suramin b- pentamidine isethionate c- eflornithine 2. CNS involvement a- melarsoprol b- eflornithine |
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AMERICAN TRYPANOSOMIASIS
(chagas disease) geographical distribution |
central and south america
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AMERICAN TRYPANOSOMIASIS
morphology |
trypomastigote:
15-20 C/S shaped central vesicular nucleus large subterminal kinetoplast free flagellum narrow undulating membrane Amastigote: spherical 1.5-4 |
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AMERICAN TRYPANOSOMIASIS
infective stage |
metacyclic trypomastigote
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AMERICAN TRYPANOSOMIASIS
life cycle |
triatomine bugs infect humans with metacyclic trypomastigotes
scanty in peripheral blood do not multiply in general circulation enter different cells, lose flagellum and undulating membrane --> AMASTIGOTE divide repeatedly by binary fission ---> PSEUDOCYST amastigotes --> epimastigotes --> trypomastigoes. pseudocyst bursts and trypomastigotes are liberated into the blood. Triatomine bugs ingest the blood stream trypomastigotes ---> stomach --> short epimastogtes, multiply --> long epimastigotes --> METACYCLIC TRYPOMASTIGOTES in the insects rectum. shed the infective in its faeces |
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AMERICAN TRYPANOSOMIASIS
reservoir hosts |
wild and domestic animals eg dogs
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AMERICAN TRYPANOSOMIASIS
most common tissue cells which are infected |
RES, fibroblasts, central + peripheral neuroglia, cardiac + smooth + skeletal muscles
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AMERICAN TRYPANOSOMIASIS
method of infection |
1. Rubbing faeces of infective bugs into bite wounds/ conjunctiva
less common: 2. blood transfusion 3. congential 4. lab 5. transmammary |
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AMERICAN TRYPANOSOMIASIS
incubation period |
7-14 days
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AMERICAN TRYPANOSOMIASIS
clinical picture of acute infection |
INFANTS/children
CHAGOMA (local inflammatory reaction) ROMANO'S SIGN (severe usually unilateral palpebral oedema) fever, generalized lymphadenopathy, hepatosplenomegaly child either dies from myocarditis/ meningoencephalitis or enters latent period --> chronic stage |
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AMERICAN TRYPANOSOMIASIS
chronic infection |
ADULTS
depends on organ main target organs: smooth muscles, nerve ganglia, heart, GIT destroyed by toxins of ruptured pseudocysts and autoimmune reaction megaoesophagus --> dysphagia, regurge megacolon --> accum of faeces heart--> AV block, enlargement, bradycardia, HF, sudden cardiac arrest |
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AMERICAN TRYPANOSOMIASIS
diagnosis |
clinically --> endemic + romanos sign
LAB a) direct 1- blood film esp during pyrexia 2. inoculation 3. culture on NNN medium --> epimastigote 4. biopsy of deltoid --> amastigotes 5. xenodiagnosis b) immunological CFT, IHAT, IFAT |
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AMERICAN TRYPANOSOMIASIS
treatment |
nifurtimox
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AMERICAN TRYPANOSOMIASIS
control |
1. increase standard of living
2. insecticides (vector control) |
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TRICHOMONAS VAGINALIS
geographical distribution |
cosmopolitan
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TRICHOMONAS VAGINALIS
habitat |
females: vagina, cervix. parasite causes shift to alkalinity --> more parasitic growth
male: prostate |
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TRICHOMONAS VAGINALIS
morphology |
ONLY AS TROPHOZOITE
7-23 oval 4 anterior flagella, 5th runs along short undulating membrane and protrudes as a caudal spine nucleus vesicular with few chromatin granules |
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TRICHOMONAS VAGINALIS
methods of infection |
DIRECTLY since no cystic stage
1. sexual intercourse 2. contaminated underwear, toilet seats, towels 3. birth |
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TRICHOMONAS VAGINALIS
clinical picture |
females:
vulval and vaginal pruritis frothy seropurulent vaginal discharge males asymptomatic/ persistent urethritis and prostatitis |
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TRICHOMONAS VAGINALIS
diagnosis |
female:
check sedimented urine/vaginal secretion for parasite vaginal smear if wet smear cannot be sampled immediately, air dry fix and stain with giemsa culture NB care should be taken to prevent faecal contamination with T hominis in males: sedimentet urine/ prostatic secretions following massage |
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TRICHOMONAS VAGINALIS
treatment |
1. metronidazole
750 mg tds x 7 days oral or vaginal suppositories 2- tinidazole 2g once toxicity: occasional metallic taste, vomiting, rash 3- clotrimazole 100 mg x 7 days vaginal suppositories [imidazole CI in pregnancy so vaginal suppositories are given.] |
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DIENTAMOEBA FRAGILIS
geographical distribution |
cosmopolitan
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DIENTAMOEBA FRAGILIS
habitat |
mucosal crypts of large intestine
may ingest RBCs, never invades mucosa |
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DIENTAMOEBA FRAGILIS
morphology |
7-12
pseudopodia are hylaine and leaf like active in fresh stools usntained: inconspicuous, nuclei not apparent, food vacuoles may be observed stained w/ iron haematoxylin: two nuclei, no peripheral chromatin, chromatin present in from of 4-8 granules in the center extranuclear spindle may be seen between both nuclei |
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DIENTAMOEBA FRAGILIS
method of infection |
unknown
probably in the egg of entrobius vermicularis |
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DIENTAMOEBA FRAGILIS
clinical picture |
abdominal pain with mucoous diarrhoea
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DIENTAMOEBA FRAGILIS
diagnosis |
fresh saline smears of faecal samples
for verification: examination of fixed stained specimens |
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DIENTAMOEBA FRAGILIS
treatment |
tetracycline
250 mg 4times daily x 7 days |
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GIARDIA LAMBLIA
geographical distribution |
cosmopolitan
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GIARDIA LAMBLIA
habitat |
crypts of the duodenum and the upper jujenum
occasionally in bile ducts and gall bladder |
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GIARDIA LAMBLIA
morphology |
trophozoites:
bilaterally symmetrical pear shaped broad ant tapering post dorsal surface: convex ventral surface: "the sucking disc" ant ovoidal concavity 2 vesicular nuclei in the sucking disc 4 pairs of flagella 2 sausage shaped median bodies multiply by longitudinal binary fission cysts: 4 nuclei parabasal bodies remnants of flagella and axoneme encystation occurs when liquid faeces become dehydrated |
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GIARDIA LAMBLIA
infective stage |
cysts
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GIARDIA LAMBLIA
life cycle |
man ingests cysts in food/water
excystation occurs in duodenum--> 2 trophozoites mutliply [in frankly diarrhoeic stools its usual to find trophozoites] encystation occurs in the color where stool becomes dehydrated the trophozoites retract their flagella cytoplasm becomes condensed thin cyst wall secreted |
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GIARDIA LAMBLIA
methods of infection |
1- contamination of food and drink
2- direct 3- autoinfection 4- mechanical by houseflies |
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GIARDIA LAMBLIA
clinical picture |
usually asymptomatic
in symptomatic: Incubation perdiod 1-3 wks disease presents itself in diff forms a- diarrhoea b- dyspepsia c- malabsorption |
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GIARDIA LAMBLIA
diagnosis |
Lab
1) Direct a- stool examination diarrhoeic stools --> vegetative forms in saline smears well formed stools --> cysts with lugols iodine solution organisms appear in stools intermittently b- duodenal aspiration c- entero test capsule 2- immunological ELISA |
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GIARDIA LAMBLIA
treatment |
1- metronidazole
250 mg tds x 5-7 days Tox: GID, headache, metallic CI: pregnancy 2- Tinidizazole 2g once tox: GID |
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GIARDIA LAMBLIA
prevention and control |
personal hygeine
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BALANTIDIUM COLI
geographical distribution |
cosmopolitan
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BALANTIDIUM COLI
habitat |
caecum, colon of humans, pigs, guinae pigs, rats etc
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BALANTIDIUM COLI
morphology of trophozoite |
oblong
anterior peristone (oblique depression) in the bottom of which is the cytosome post anal pore "cytopyge" whole body covered with fine cilia arranged in rows one macronucleus in the middle single micronucleus oft hidden from view two contractile vacuoles: one near middle, one post food vacuoles (cell fragments, starch granules, faecal debris, erythrocytes) |
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BALANTIDIUM COLI
morphology of cysts |
ovoid
thick cyst wall micro and macro nuclei can be seen |
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BALANTIDIUM COLI
life cycle |
trophozoite multiplies by binary fission
(conjugation may occur in culture, rare in nature] encystment stimulated by dehydration of faeces in the rectum trophozoites may live up to 10 days [balantidium coli destroyed by ph<5, therefore affects malnourished with low stomach acidity] |
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BALANTIDIUM COLI
infective stage |
cyst
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BALANTIDIUM COLI
method of infection |
contaminated food water
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BALANTIDIUM COLI
pathogenesis |
under ordinary conditions, trophozoite feeds on food in caecum
sometimes produces proteolytic ulcers --> ulcer variable in shape wtih narrow neck leading to sac-like cavity in submucosa colonic ulceration --> lymphocytic infiltration and hhg , +- secondary bact invasion |
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BALANTIDIUM COLI
clinical picture |
may be asymptomatic
majority: dysentry, abd colic, tenesmus fulminating --> perforation rare --> extra intestinal invasion eg liver |
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BALANTIDIUM COLI
diagnosis |
stool examination --> trophozoite +- cyst
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BALANTIDIUM COLI
treatment |
tetracycline
500 mg 4xd x 10 days |
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BALANTIDIUM COLI
control |
avoid contact with pigs
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PLASMODIA
general characteristic |
cycle takes place in one vertebrate and one invertebrate host (ALTERATION OF HOSTS)
has sexual and asexual cycles (ALTERATION OF GENERATION) man --> asexual cycle (schizogony) invertebrate --> sexual/sporogenic and asexual cycle |
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PLASMODIA
malaria of man species |
vivax, ovale, malariae, falciparum
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PLASMODIA
infective stage |
sporozoites
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PLASMODIA
exoerythrocytic cycle |
mosquito bites man, sporozoites injected into skin --> blood stream --> hepatic cells
each sporozoite --> preerythrocytic schizont w/ thousands of merozoites infected liver cell ruptures --> liberating merozoites --> invade RBCs [in vivax and ovale, some sporozoites remain dormant in liver "hypnozoites", become activated weeks/months after primary attakc and reinvade --> relapsing malaria] |
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PLASMODIA
erythrocytic cycle |
merozoites in rbcs --> early trophozoite/ ring stage --> late/mature trophozoite --> schizont/segmenter
rbc ruptures liberating merozoites in blood gametocyte formation occurs after repeated schizogony --> micro and macrogametes --> taken up by female mosquito initiating the sexual cycle |
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PLASMODIA
life cycle in female anopheles |
microgametocyte in midgut----[exflagellation]----> 4-8 microgametes
macrogametocyte --> macrogamete by reduction division of nucleus Fertilization --> zygote --> elongates into motile ookinete --> oocysts w/ thousands of sporozoites oocyst ruptures --> sporozoites liberated in body cavity --> penetrate salivary gland |
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PLASMODIA
method of infection |
1. bite of female anopheles mosquito [sporozoites]
2. blood transfusion [erythrocytic stages] 3. congenital malaria |
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PLASMODIA
pathogenesis |
exoerythrocytic cycle --> slight enlargement + tenderness of lvier
multiplication w/in RBCS --> haemolytic anemia, metabolic byproducts that ppt malarial attack, pigment and RBC stroma release pigment and rbc stroma --> engulfed by RES --> enlargement of spleen, liver, pigmentation pigment deposition in BM P falciparum is most dangerous ---> malignant malaria : - multiple infections in single RBC - all types of RBCs (severe haemolytic anaemia) - forms electron dense knobs in plasma membranes of parastiized cells --> agglutinate --> malaria w/ pernicious syndromes In P. Malariae --> intense autoimmune reaction --> complex that ppts in mesangial vessels of kidney --> nephrotic syndrome |
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PLASMODIA
clinical picture |
prepatent period = minimum time between entry of sporozoites and first appearance of parasites in RBCs = parasitological incubation period = 6-20d
incubation period = interval between entry of sporozoites and 1st clinical manifestation = 8-24 fever, anaemia, splenomegaly, jaundice |
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PLASMODIA
malarial paroxysms |
rupture of erythrocytic schizonts
premonitory symptoms = malaise, headache, bone aches, lassitude, chilly sensation first irregular, then regular stages: a- cold stage: shivers, temp rises sharply, 0.5 -2 hrs b- hot stage: flushed, high temp, dry skin, congested conjunctiva, 4-6h c- sweating stage: rapid drop of temp, sweating, 2-3h p vivax, ovale --> tertian paroxysm p malariae --> quartan p falcipirum --> subtertian malarial relapse occurs w/ vivax ovale dt hypnozoites recrudescence occurs with the 4 species of malaria |
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PLASMODIA
pernicious sydromes |
p falcipirum
GENERALIZED a- malarial hyperpyrexia b- algid malaria c- black water fever (never give quinine) LOCALIZED cerebral, heaptobiliary, renal, intestinal, cardiopulmonary, placenta |
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PLASMODIA
diagnosis |
DIRECT methods:
1- peripheral blood examination (thick film, thin film) 2- QBC 3- sternal puncutre 4- PCR IMMUNOLOGICAL 1- IHAT, IFAT, ELISA 2- RDT (rapid diagnostic tests) |
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PLASMODIA
guildelines of treatment |
1- PROTECTIVE
a) keeping the number of erythrocytic stages low --> Supressive b) destruction of early stages in the liver --> causal 2- CURATIVE a) drugs acting on erythrocytic stages (Clinical cure) b) drugs acting on hypnozoites (Radical cure) 3- prevention of transmission |
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PLASMODIA
treatment of acute uncomplicated malaria non resistant strain |
a) clinical cure
1- chloroquine resochine 1st d: 2 tab, 1 tab 6 hrs later 2nd, 3rd d: 1 tab SE: headache, NV, blurring cures falciparum, malariae, transfusion malaria w/ relapsing malaria: primaquine also given b) Radical cure primaquine 15 mg x 14 days starting day 4 after chloroquine SE: GED, haemolytic anaemia (esp w/ G6PD deficiency) |
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PLASMODIA
treatment of non resistant severe malaria (pernicious syndromes) |
1. chloroquine disulphate
200mg IM or IV 2. quinine dihydrochloride 20mg/kg loading dose IV in 5% dextrose over 4 hours followed by 10 mg/kg every 8 hours until oral therapy can be started CI: blackwater fever 3. artemether 3.2 mg/kg IM then 1.6 mg/kg daily for one week |
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PLASMODIA
treatment of uncomplicated p falcipirum resistant strain |
1. quinine sulphate
2. mefloquine 3. artemether-lumefantrine (co artem) |
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PLASMODIA
treatment of severe malaria with resistant strains |
1. quinine dihydrochloride
2. artemether |
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PLASMODIA
chemoprophylaxis |
a- for non resistant strains:
chloroquine diphosphate b- for resistant strains: mefloquine |
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PLASMODIA
control of malaria |
1. tt human w/ antimalarial
2. elimination of gametocytes from carriers by giving the already treated patients 4 tablets of primaquine before leaving the hospital 3. control of anopheles mosquitos 4. screening, insect repellants, chemoprophylaxis |
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SCORPION
morphology |
yellow brown/black
15 cm fused cephalothorax long segmented abdomen telson containing venom glands stinger |
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SCORPION
biology and life cycle |
terrestrial
nocturnal viviparous [carry newly borns on back for 1 week] humans --> accidentally step on them/brush over them and get stung with telson esp preschool age |
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SCORPION
pathology. clinical picture |
immediate intense aching pain, burning sensation from site of bite
lymphadenitis and systemic symptoms --> generalized numbness, throbbing, twitching esp of fingers toes chin earlobes profuse sweating, excess salivation, glossopharyngeal involvement --> difficulty in speech and swallowing, vomiting, muscle spasm of the abdomen, convulsions, mental disturbances, hallucination |
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SCORPION
diagnosis |
clincal pic: aching throbbing pain, inflamed indurated sting site
lymphadenitis, systemic symptoms of ascending motor paralysis |
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SCORPION
treatment |
LOCAL:
ligate limb w/ tourniqet incise freely cover wound w/ potassium permanganate local anaesthetic GENERAL 1. oral analgesic 2. general supportive treatment 3. maintenance of airway, maintenance of BP by IVI of hydrocortisone 4. antivenin IM 5. IVI 5-10% glucose in normal saline 6. insulin if hyperglycemia 7. tt of shock with IV hydrocortisone 8. atropine/barbiturate/diazepam for convulsions, sedation |
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SCORPION
prognosis |
depends on
- age of victim - species of scorpion - amount of venom injected poor prognosis in young children/ old debilitated |
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SCORPION
prevention and control |
1. outdoor spraying of 2% carbaryl, 10% granular diazinon, 0.5% gamma HCH (lindane)
2. indoor hiding places: malathion, lindane 3. raising floor level of house 4. separating entrance steps from foundation 5. removal of debris near houses |
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TICKS
general morphology |
body oval, unsegmented
4 pairs of legs mouth protruded (hand ticks) or hidden ventrally (soft ticks) scutum --> hard ticks develop by incomplete metamorphosis |
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TICKS
diseases caused by hard ticks |
anaemia
dermatosis paralysis otoacariasis |
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TICKS
treatment of diseases caused by hard ticks |
chloroform or ether placed on the tick
then remove by traction |
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TICKS
diseases transmitted by hard ticks |
A. Rickettsial diseases
- rocky mountain spotted fever - boutonneuse fever - q fever bite, faeces, crushing, transovarial in tick B. Bacterial - tularemia (bite, faeces, crushing) - undulant fever/brucellosis (bite, crushing) C. Spirochaetal infection (bite) D. viral (bite, crushing) E. Tick borne protozoal diseases - Babesiosis (bite, crushing, transov) |
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TICKS
diseases caused by soft ticks |
toxic paralysis and skin lesions
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TICKS
diseases transmitted by soft ticks |
A. Spirochaetal diseases
- endemic relapsing fever - persian type of relapsing fever bite/coxal fluid B. Ricketssial diseases - Q fever |
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TICKS
control of ticks |
- spray animal host with residual insecticide
- dip animal host in 0.5% gammaxane suspension - repellants/tick proof clothing - insecticides on floor/cracks - rat proof buildings - tick collars |
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SARCOPTES SCABIEI
morphology |
ovoid contour covered with grey white striated cuticle pierced by bristles and scales
mouth parts are short and poorly developed 4 pairs of legs |
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SARCOPTES SCABIEI
development and life cycle |
fertilized female develops 1-2 eggs
forms cutaneous burrows eggs hatch --> 6 legged larvae migrate to skin surface --> nymphal stage --> adulthood, mate, burrow back |
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SARCOPTES SCABIEI
clinical picture |
faecal pellets --> vesiculations of skin, severe pruritis
warmth at night --> acidic secretion --> intensifies the irritation pustules, 2ry bact infection may complicate the lesion |
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SARCOPTES SCABIEI
diagnosis |
- nocturnal itching
- site and characteristic lesion - recovery of mite after scratching the tunnel with a sharp needle scraped material is cleared in 10% potassium hydroxide and examined by microscope ---> adults, eggs, larvae |
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SARCOPTES SCABIEI
treatment |
infested part thorougly scrubbed by soap and loofa for 5 successive days
sites are rubbed with acaricidal lotion (eg eurax) patients clothes and betsheets should be sterilized by boiling during treatment |
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SARCOPTES SCABIEI
prevention |
- personal hygeine (bathing)
- avoid contact with patients |
