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2 PARA SEM 2 SEM REVISION PARA REVISION (2) PART (2) PART © PW 7 ®@ Ru Contact Information: Official Email: ’ Mobile (Optional): Mobile (O ptional): Academic Hours Academic Hours :: (( Saturday Saturday :: 12:00-2:00 12:00-2:00 pm) pm)  L1 FILARIASIS L1 FILARIASIS L2 MALARIA L2 MALARIA L3 Leishmaniasis L3 Leishmaniasis { NU |) Life cycle: > Life cycle: Www 1. Habitat: 1. Habitat: adult adult in in lymph lymph vessels vessels and and lymph lymph nodes especially that nodes especially that i ai draining lower draining lower part part of of the the body, body, while microfilariae are while microfilariae are in in the the A peripheral blood. peripheral blood. A 2. Definitive host: Man 2. Definitive host: Man 7 RI 3. Intermediate host:. 3. Intermediate host. The The main main vectors are Culex vectors are mosquitoes, Culex mosquitoes, di Ld iù (Anopheles and (Anopheles and Aedes). Aedes). Ri |5.5. Infective Infective stage: stage: infective infective filariform larva is filariform larva is infective infective to to man. man. # | |6. Mode 6. Mode of infection: Humans of infection: Humans get get infection infection by by bite bite of of mosquito mosquito carrying carrying ii / | the the infective infective filariform larvae (L3). filariform larvae (L3).  > Pathogenicity: Pathogenicity: Ni Disease: Bancroftian Disease: Barcroftian filariasis, filariasis, wuchereriasis, wuchereriasis, elephantiasis. elephantiasis. -- The The various pathogenic mechanisms various pathogenic mechanisms of of this this disease disease are are mainly mainly due due to the to the adults, adults, the the microfilariae microfilariae seem seem to to have have no no pathogenic pathogenic manifestations manifestations although although they they have have been been associated associated with with granulomatous inflammation granulomatous inflammation of of the the lung, lung, liver liver and and spleen. spleen. -- It It occurs occurs due due to to blockage blockage of of lymph Ilymph vessels vessels and and lymph lymph nodes nodes by by the the adult worms. adult worms. The The blockage blockage may may be be due due to to mechanical mechanical irritation irritation by by the moving the moving worms worn or or inflammatory inflammatory reaction reaction to to worm worm antigens antigens and and their secretions. their secretions. > Clinical Clinical picture: picture: I- Asymptomatic I- Asymptomatic filariasis: filariasis: this this occurs occurs in in endemic endemic areas, areas, there there is is microfilaria microfilaria in in the blood the blood without clinical manifestations. without clinical manifestations. II- Symptomatic II- Symptomatic (Classical (Classical filariasis): filariasis): The The main main pathological pathological lesions lesions are: are: 1- Acute 1- inflanmatory manifestations: Acute inflammatory monifestations: Due Due to to toxic toxic products products ofof living living or or dead dead adult worms adult worms with with superimposed superinmposed secondary secondary bacterial bacterial infection, infection, it it occurs occurs in in recurrent recurrent attacks and attacks and is is manifested manifested by: by: -Lymphangitis of -Lymphangitis of the the genitalia genitalia (funiculitis, (funiculitis, epididymitis, epididymitis, orchitis orchitis and and scrotal scrotal oedema) with oedema) swelling and with swelling and redness redness of of affected affected parts. parts. -Lymphadenitis especially -Lymphadenitis especially in in the the groin groin and and axilla. axilla. -- Fever, Fever chills, chills, headache, headache, vomiting vomiting and and malaise. malaise. -Leucocytosis and -Leucocytosis and eosinophilia. eosinophilia. 2- Chronic obstructive 2- Chronic obstructive manifestations: manifestations: Due to Due to fibrosis fibrosis following following the the inflammatory inflammatory process process ,, the the coiled coiled worms worms inside inside Iymphatics and lymphatics and endothelial endothelial proliferation, proliferation, this this may may result result in: in: -- Dilatation Dilatation of of lymphatics |Îymphatics leading leading to to varicosities varicosities especially especially in in genital genital organs organs and abdominal and abdominal wall as hydrocele, wall as hydrocele, scrotal scrotal lymphoedema lymphoedema and and lymphatic Iymphatic variCces. varices. -- Rupture Rupture of of distended distended lymphatics I]ymphatics (varicosities) (varicosities) e.g. in e.g. in urinary urinary passages passages— chyluria, chyluria, the the peritoneal peritoneal cavity cavity — chylous chylous ascitis, ascitis, tunica vaginalis tunica vaginalis of of testis testis— chylocele, chylocele, intestine intestine — chylous chylous diarrhea. diarrhea.  DD i SYLL) A” na 4 du Up E i À : us E n I ni E; Ì Orme ’ pa L ia ; EA di a i: Ì N (ia Aa i FA Ì è ì ' Pa pe i A - ud PI a i e Aeir = i 3 de e NN | y ia ES De i Lia è = Ba 7’ , | ù ANtS e Bsn i 7 i SAP i i a m i | == C P 3 a = NET dpiro 4 = i i v EA a Lee 4 : | =}CID : b a n c r o f t i Nic hereria bancrofti elephantiasis of lower Wuchereria limb ower limb -- Elephantiasis: Elephantiasis: oedema oedema of of the the affected affected part part followed followed by by hypertrophy hypertrophy of the of the skin skin and and subcutaneous subcutaneous connective connective tissue, tissue, the the part part become become hard, hard, tender and tender and the the skin skin becomes becomes thickened, thickened, rough, rough, stretched stretched and and fissured fissured lead to lead to secondary secondary bacterial bacterial infection. infection. -- It It is is common common in in lower lower limbs limbs and and genitalia genitalia (scrotum, (scrotum, penis penis and and vulva) vulva) rare in rare in arms arms and and breasts. breasts. Tropical pulmonary Tropical pulmonary eosinophilia eosinophilia (diffuse (diffuse filarial filarial lung lung disease): disease): -It is -It is caused caused by by immunologic immunologic hyper-responsiveness hyper-responsiveness of of the the host host to to microfilarial microfilarial antigens antigens → — local destruction local destruction of of microfilariae microfilariae in in the the pulmonary pulmonary vascular vascular system system and and diffuse diffuse interstitial interstitial lung disease. lung disease. -Clinically there -Clinically there is is dyspnea, dyspnea, cough, cough, asthmatic asthmatic attacks attacks and and eosinophilia, eosinophilia, which which respond respond well well to treatment to treatment with hetrazan. with hetrazan. -- Blood Blood examination: examination: microfilariae microfilariae are are not not detected detected in in the the peripheral peripheral blood. blood. -- There There is is aa high high level level of of serum serum immunoglobulin immunoglobulin E E (IgE) (IgE) and and filarial filarial antibodies. antibodies. Serological Serological tests with tests with filarial filarial antigen antigen are are usually usually strongly strongly positive. positive.  = E > C Diagnosis: 1- Detection 1- of microfilariae Detection of in peripheral microfilariae in blood peripheral blood Bg, B 2-2- Detection Detection of microfilariae in of microfilariae in chylous chylous urine urine or or from from fluid fluid aspirated aspirated from from hydrocele and hydrocele and peritoneal peritoneal cavities, cavities, as as well well as as urine urine samples samples 3-Detection 3-Detection of of adult adult Nnorms:- worms:- Lymph Lymph node node biopsy. biopsy. -X-ray to -X-ray to detect detect calcified calcified dead dead worm worm 5- Detection 5- of circulating Detection of circulating filarial antibodies using filarial antibodies using the the following following tests; tests; IFAT, IFAT, CFT and CFT and ELISA. ELISA. It It is is used used during during the the incubation incubation period period and and in in late late chronic chronic infections when infections microfilariae are when microfilariae are absert from peripheral absent from peripheral blood. blood.  Treatment >» Treatment: : 7 1. Diethylicarbamazine 1. (Hetrazan) is Diethylcarbamazine (Hetrazan) is the the drug drug of of choice, choice, has has aa lethal action lethal action on on microfilariae. microfilariae. 2. Surgical 2. Surgical treatment: treatment: removal removal of of elephantoid elephantoid tissue. tissue.  L1 FILARIASIS L1 FILARIASIS L2 MALARIA L2 MALARIA L3 Leishmaniasis L3 Leishmaniasis > Species: Species: Four species Four species of of Plasmodium Plasmodium cause cause human human malaria: malaria: 1. Plasmodiu 1. Plasmodiummvivax: Benign tertian vivax: Benign tertian malaria. malaria. 2. Plasmodi 2. ovale: Benign um ovale: Plasmodium Benign tertian tertian malaria. malaria. 3. Plasmodi 3. malariae: Benign um malariae: Plasmodium Benign quartan quartan malaria. malaria. 4. Plasmodi 4. umfalcip Plasmodium Tertian or arum Tertian falciparum: or subtertian subtertian malignant malignant malaria. malaria. @ Geographical distribution: Geographical distribution: N Mr -- P.P. vivax: vivax: The The most most widely widely distributed distributed species species found found in in tropical, tropical, subtropical and subtropical and temperate temperate areas. areas. -- P.P. ovale: ovale: West West Africa. Africa. -- P.P. malariae: malariae: Tropical Tropical Africa Africa and and Far Far East. East. -- P.P. falciparumi Africa and falciparum: Africa and Far Far East East > Life Life cycle: cycle: The The life life cycle cycle of of malaria malaria parasites parasites is is heteroxenous heteroxenous (alternation (altemation of of generations between generations between two two hosts), hosts), where an asexual where an asexual cycle cycle occurs occuls in in man man (intermediate host), (intermediate host), and and sexual sexual cycle cycle occurs occurs in in female female Anopheles (definitive host). Anopheles (definitive hosd. 1. Definitive 1. Definitive host: host: Female Female Anopheles mosquito. Anopheles mosquito. 2. Intermediate 2. Intermediate host: host: Man. Man. 3. Reservoir 3. Reservoir host: host: No. No. However, However, in inP.P. malariae, malariae, chimpanzee chimpanzee can can be be affected affected and and act act as aa reservoir as reservoir of of infection. infection.  4. Habitat: 4. Habitat: InIn mosquito: mosquito: Gut, Gut, salivary salivary glands. glands. 7// Inman: In Intracellular inside man: Intracellular inside the the liver liver cells cells and and RBCs. RBCs. 5. Infective 5. Infective stage: stage: a. a. Sporozoites Sporozoites (in(in mosquito-borne mosquito-borne malaria). malaria). b. Merozoites b. Merozoites and/or and/or trophozoites trophozoites (in (in blood-borne blood-borne malaria). malaria). 6. Mode 6. Mode of of infection: infection: 1. Bite 1. Bite of of infected infected female female Anopheles. Anopheles. 2. Blood-borne 2. Blood-bomne transmission: transmission: a. Blood a. Blood transfusion transfusion (whole (whole blood blood and and packed packed RBCs). RBCs). b. Shared b. Shared syringes syringes among among drug drug addicts. addicts. c. Transplacental c. Transplacental transmission. transmission. d. Organ d. Organ transplantation. transplantation.  > Causes Causes of of anaemia anaemia in in malaria? malaria? 1. Obligatory 1. Obligatory destruction destruction of of RBCs RBCs at at merogony. merogorny. 2. Destruction 2. Destruction ofof large large number number of of RBCs RBCs by by complement-mediated complement-mediated and and autoimmune hemolysis. autoimmune hemolysis. 3. Increased 3. Increased clearance clearance of of both both parasitized parasitized and and non-parasitized norn-parasitized RBCs RBCs by by the the spleen. spleen. 4. Decrease 4. Decrease erythropoiesis erythropoiesis in in bone bone marrow marrow due due to to increased increased tumour tumour necrosis necrosis factor factor. 5. Shortened 5. Shortened red red cell cell survival. survival. 6. Failure 6. Failure of of the the host host to to recycle recycle the the iron iron bound bound in in haemozoin haemozoin pigments. pigments. III. Additional III. pathology associated Additional pathology associated with with P.P. falciparum: falcipanum a. Sequestration a. Sequestration of of RBCs: Knobs formation RBCs: Knobs formation on on the the surface surface of of RBCs RBCs infected infected with late stages with late stages of of parasites parasites and and the the resulting resulting increase increase in in rigidity, rigidity, lead lead to to their their adherence to adherence to receptors receptors onon the the endothelium endothelium of of internal internal capillaries, capillaries, aa phenomenon phenomenon termed cytoadherence. termed cytoadherence. -- Also, Also, infected infected RBCs RBCs adhere adhere to to uninfected uninfected RBCs, RBCs, resulting resulting in in resetting. resetting. -- Sequestration Sequestration block block blood blood flow, flow, with subsequent infarctions with subsequent infarctions and and haemorrhage, haemorrhage, mainly in mainly in brain brain and and large large intestine. intestine. -- erythrocytic erythrocytic schizogony schizogony takes takes place place in in capillaries capillaries of of internal internal organs organs as as brain, brain, kidney, spleen, kidney, spleen, bone bone marrow, marrow, and and intestine. intestine. -- All these factors All these factors contributing contributing to to the the development development of of severe severe disease disease (malignant (malignant malaria malaria 2. Malarial 2. Malarial paroxysms: paroxysms: The The typical typical picture picture of of malaria malaria consists consists of of series series of of febrile febrile paroxysm, followed paroxysm, followed by by anaemia anaemia and and splenomegaly. splenomegaly. The The febrile febrile paroxysm paroxysm occurs occurs in in 33 successive stages; successive stages; cold, cold, hot hot and and sweating. sweating. a Cold a. Cold stage: stage: Intense Intense cold cold and and uncontrollable uncontrollable shivering shivering for for 15-60 15-60 minutes. minutes. b. Hot b. stage: Intense Hot stage: Intense heat, heat, flushing, flushing, nausea, nausea, vomiting vomiting and and severe severe headache, headache, lasting lasting for for 2-6 2-6 hours. hours. c. Sweating c. Sneating stage: stage: Decreased D ecreased temperature temperature and and profuse profuse sweating, sweating, lasting lasting for for 2- 2- 33 hours. hours. The paroxysm The paroxysm usually usually begins begins in in the the early early afternoon afternoon and and lasts lasts for for 8-12 8-12 hours. hours. -- It It synchronizes synchronizes with with the the erythrocytic erythrocytic schizogony schizogony cycle. cycle. With With aa 48-hour 48-hour cycle, cycle, the the fever fever recurs every recurs every third third day; day, tertian tertian malaria, malaria, and and with with 72-hour 72-hour cycle, cycle, the the fever fever recurs recurs every every fourth fourth day; quartan day; quartan malaria malaria ©@ Recurrence Recurrence of of malarial malarial attack: attack: ul 7 a. Relapse: a. Relapse: It It is is the the recurrence recurrence of of clinical clinical manifestations manifestations of of malaria malaria and and the the reappearance of reappearance of peripheral peripheral parasitaemia parasitaemia months months or or years years after after subsidence subsidence of of aa previous previous attack, attack, in in the the absence absence of of aa new new mosquito mosquito bite. bite. -- Species: Species: Relapse Relapse occurs occurs in in P_vivax and P_ovale P. vivax and (infections last P. ovale (infections last up up to to 44 years). years). -- Cause: Cause: It It is is due due to to activation activation of of the the dormant dormarnt hypnozoites hypnozoites initiating initiating exo- exo- erythrocytic schizogony, erythrocytic schizogony, with with the the production production of of erythrotropic erythrotropic merozoites. merozoites. -- Can Can be be prevented prevented by by giving giving primaquine primaquine to to eradicate eradicate hypnozoites. hypnozoites. b. Recrudescence: b. Recrudescence: It It is is aa recurrence recurrence of of clinical clinical attack attack of of malaria, malaria, few few weeks or weeks or many many years years after after apparent apparernt clinical clinical cure, cure, without without re-infection. re-infection. -- Species: Species: Recrudescence Recrudescence can can occur occur in in all all Plasmodium Plasmodium species, species, but but it it is is more common more common in in falciparum PB. falciparum (up P. (up to to 22 years) years) and andP. malariae P_malariae (up (up to to 40 40 years). years). -- Causes Causes: : It It results results from from the the persistence persistence of of some some erythrocytic erythrocytic parasites parasites at at aa sub-clinical level, sub-clinical level, which start to which start to multiply multiply to to reach reach significant significant numbers. numbers. -causes: a. Incomplete a. Incomplete anti-malarial anti-malarial therapy. therapy. b. Anti-malarial b. Anti-malarial drug drug resistance. resistance. c. Changes c. Changes of of the the surface surface antigens antigens (antigenic (antigenic variation) of variation) of the parasites the parasites resulting resulting in in evasion evasion of of the the host host immune immune response. response. d. Splenectomy d. Splenectomy or or immunosuppression. immunosuppression. -- Can Can be be prevented prevented by by adequate adequate drug drug therapy therapy or or use use of of new antimalarial new antimalarial drugs drugs in in case case of of drug drug resistance. resistance.  > Diagnosis: QD? Diagnosis: I- Clinical diagnosis: I- Clinical diagnosis: In endemic areas, In endemic malaria must areas, malaria must be suspected in be suspected in all all cases of cases of typical typical malarial paroxysm or malarial paroxysm or fever. fever Laboratory diagnosis: II- Laboratory II- diagnosis: 1. Parasi 1. tic diagnosis: Parasitic Examination of diagnosis: Examination of thin thin and/or and/or thick Leishman or thick Leishman or Geimsa stained Geimsa stained blood smears. blood smears. -- All erythrocytic stages All erythrocytic stages can can be detected in be detected peripheral blood in peripheral blood except except in in PP. falciparum, only falciparum, only ring form alone ring form alone or or with gametocytes can with gametocytes can be detected. be detected. 2.2. Therapeutic Therapeutic diagnosis: diagnosis: The The non-subsidence non-subsidence of of the the febrile febrile paroxysms paroxysms after after the administration the administration of of anti-malarial anti-malarial drug drug for for 33 days, days, means means that that the the case case is is not not malaria. malaria. 3. Serodiagnosis: 3. Serodiagnosis: a. Circulating a. Circulating antibodies antibodies can can be be detected detected by by IHA, IHA, IFA IFA and and ELISA. ELISA. b. Circulating b. Circulating antigens antigens can can be be detected detected by by ELISA. ELISA. c. Rapid c. Rapid immunochromatographic immunochromatographic test test for for detection detection of of malaria malaria antigens antigens by by using aa dipstick using dipstick impregnated impregnated with specific monoclonal with specific monoclonal antibodies. antibodies. 4. Molecular 4. Molecular diagnosis. diagnosis. 5. Haematological 5. Haematological diagnosis: diagnosis: Anaemia Anaemia and and reticulocytosis. reticulocytosis. 6. Biochemical 6. Biochemical diagnosis: diagnosis: -- Hypergammaglobulinemia Hypergammaglobulinemia and and low low albumin albumin level. level. -- Hyperglycemia HypergIycemia or or hypoglycemia. hypogIycemia. -- Hyperkalemia. Ayperkalemia.  L1 FILARIASIS L1 FILARIASIS L2 MALARIA L2 MALARIA L3 Leishmaniasis L3 Leishmaniasis li A N e. e e. AO) >» D MU Leishmaniasis Leishmaniasis (e 8997, A-Visceral Leishmaniasis A-Visceral Leishmaniasis (Kala (Kala Azar): Azar): Leishmania Leishmania donovani donovani complex complex Nu In old In old world world -- L. L. donovani: donovani: India, India, Pakistan, Pakistan, In new In new world world Indonesia, Thailand, Indonesia, Thailand, Central Central -- L. L. chagasi: chagasi: America America Africa Africa and and Sudan. Sudan. (Central and (Central and South South America). America). -- L. L. infantum: infantum: Mediterranean Mediterranean area, Middle area, Middle East East and and China. China. B- Cutanous B- Cutanous Leishmaniasis: Leishmaniasis: In In old old world: world: Leishmania Leishmania major major (Old world (Old world cutaneous cutaneous leishmaniasis leishmaniasis (OWCL)); (OWCL)); rural rural distribution distribution (near (near desert: desert: Libya, Egypt: Libya, Egypt: Sinai). Sinai).  Sandflhy Stages Human Stages 1) Sandfiy takes a i blood meal Fromasti (vec prepagate steve pi © iragccyized by i MAI gotes are pa 6 Divide in the gut and — migrate to proboscis # TI of mononuclear pr: phagocytic cells N a Al t— © E lrn ty si A Promastigotes transform into amastigotes GE Amastigotes transform into © promastigote stage in the gut =, e: Poe i - ©A i ©’ i e: gi mastigotes multiphy in cells = "a, e of various tissues and infect rele n Fn, other cells ha © 'nsestion of lee | parasitized cell i [ld i 5) Sandily takes a blood meal fr i Fe (irngests macrophages infecthed i F” Fi 4 with amastigotes} Mai ln A. O da = intective Stage = Diagnostic Stage NZ BAFER-HEALTHIEA- PEOPLE” Life cycle Life cycle of of Leishmania donovani Leishmania donovani 7 Life cycle Life cycle of of Visceral Leishmaniasis Visceral Leishmaniasis e RI Habitat: Leishmania Habitat: amastigotes live Leishmania amastigotes live intracellular intracellular in in macrophages macrophages of of reticuloendothelial (R.E.S.) reticuloendothelial (R.E.S.) tissue, tissue, especially especially spleen, spleen, liver, liver bone bone marrow, marrow, intestinal mucosa intestinal mucosa and and mesenteric mesenteric lymph Iymph nodes. nodes. Pe Man host: Man Definitive host: Definitive - a, Reservoir rodents, wild Dogs, rodents, host: Dogs, Reservoir host: wild and domestic animals and domestic animals. ia as Map Insect vector: Insect vector: Female Female sand sand flies flies of of the the genus genus Phelebotomus in the Phelebotomus in the old old word, world, and Lutzonwia and in the Lutzomyia in the new new world (Cyelo-propagative development). world (Cyclo-propagative development). Infective stage: Infective stage: Leishmania promastigotes in Leishmania promastigotes in female female sand sand fly fly gut. gut. Mode of Mode of infection: infection: 1-Regurigitation of 1-Regurgitation of promastigotes into bite promastigotes into bite wound of infected wound of infected sand sand fly. fly. 2- Rare 2- Rare modes: modes: (by (by amastigotes): amastigotes): (a) Blood (a) Blood transfusion. transfusion. (b) Transplacental. (b) Transplacental. (Cc) Accidental (c) Accidental laboratory laboratory wound. wound. (d) Mechanical (d) Mechanical by by blood blood sucking sucking flies. flies.  Life cycle of Life cycle Leishmaniasis C utanous Leishmaniasis of Cutanous e ul) (7 Habitat: Leishmania Habitat: Leishmania amastigotes inhabits the amastigotes inhabits of skin; RECs of the RECs the skin; the | amastigotes reside amastigotes multiply in and multiply reside and RECs of the RECs in the skin, without the skin, of the without invasion of invasion blood or of blood organs. internal organs. or internal CN Man host: Man. Definitive host: Definitive AN Reservoir host: Reservoir Desert gerbils host: Desert rodents. and rodents. gerbils and ‘e Insect vector: Insect Female sand vector: Female of the flies of sand flies genus Phelebotomus. the genus Phelebotomus. Infective stage: Infective stage: Leishmania promastigotes in Leishmania promastigotes in female female sand sand fly fly gut. gut. Mode of Mode of infection: infection: 1. Bite 1. Bite of of infected infected sand sand fly. fly. 2. Direct 2. Direct contact. contact. 3. The 3. The stable stable fly fly may may transmit transmit the the organisms organisms mechanically mechanically from from an an open ulcer open ulcer or or through through unbroken unbroken skin. skin.  "i Do SI TE AC DÒ @ 4 ZI Ru Sr) A- Visceral Leishmaniasis = Pathogenesis Pathogenesis mm Amastigotes multiply *- Amastigotes multiply in macrophages mm) in macrophages (rupture reinvasion) (rupture ++ reinvasion) mu) compensatory and compensatory and reactive hyperplasia and reactive hyperplasia destruction of and destruction of REES. R.E.Cs. Macrophages as - Macrophages kupffer cells as kupffer cells of littoral cells liver, littoral of liver, of spleen, cells of peyers spleen, peyer's patches of patches intestine, bone of intestine, marrow and bone marrow and lymph nodes. Iymph nodes.  * Multiplication Multiplication of of amastigotes amastigotes in in the the RECs RECs of of liver, liver spleen spleen and and lymph lymph nodes nodes = hepatosplenomegaly and hepatosplenomegaly and lymphadenopathy Iymphadenopathy * The The bone bone marrow marrow mam) pancytopenia pancytopenia * Lymphoid Lymphoid macrophage macrophage cells cells in in intestinal intestinal submucosa submucosa mm) ulceration and ulceration and dysenteric symptoms, dysenteric symptoms, with with leishmanial leishmanial bodies bodies (amastigotes) (amastigotes) inin faeces. faeces. *- Urinary Urinary tract: tract: kidneys, Kidneys, pelvis pelvis and and urinary urinary bladder bladder mmm) break down break down of of mucosa mucosa with leishmanial with leishmanial bodies bodies escape escape in in urine. urine. - Naso-pharyngeal Naso-pharyngeal affection affection m——) mucopurulent discharge mucopurulent discharge containing containing leishmanial bodies. leishmanial bodies.  > Clinical manifestations Clinical manifestations of of Kala Kala azar: azar: (e ul 7 1. fever: 1. fever: intermittent intermittent (40c, (40c, 22 peaks peaks in in one one day, day, twice-daily twice-daily rise). rise). 2. Enlarged 2. Enlarged liver, liver spleen, spleen, lymph Iymph nodes nodes (hepatosplenomegaly (hepatosplenomegaly ++ generalized generalized Iymphadenopathy). lymphadenopathy). 3. Pancytopenia: 3. Pancytopenia: (aplastic (aplastic anaemia anaemia ++ leucopenia leucopenia ++ thrombocytopenia). thrombocytopenia). 4. GIT: 4. GIT: Diarrhoea Diarrhoea or or dysentery dysentery (ulceration (ulceration of of intestinal intestinal mucosa). mucosa). 5. Normocytic 5. Normocytic normochromic normochromic anemia anemia is is aa significant significant feature feature of of kala-azar kala-azar with hemoglobin with hemoglobin levels levels of of 5-10 5-10 g/dl. g/dl. N mu Types causes and and causes Types and of anemia and of Kala-azar: in Kala-azar: anemia in (e ul 7 a a. Normocytic anemia: normochromic anemia: Normocytic normochromic -- Increased sequestration Increased sequestration and destruction of and destruction due to RBCs due of RBCs hyperspleenism. to hyperspleenism. -- Decreased erythropoiesis Decreased infiltration of due infiltration erythropoiesis due marrow by bone marrow of bone parasitized by parasitized macrophages. macrophages. -- Autoantibodies to Autoantibodies red cells to red may cause cells may hemolysis. cause hemolysis. -- Hemorrhage. Hemorrhage. -- Alterations in Alterations RBCs membrane in RBCs permeability. membrane permeability. -- of haemolysin Production of Production haemolysin by the parasites. by the parasites. RW / RN MU (e ul 7 b. Macrocyti b. Macrocytic anemia: Due c anemia: Due to to reticuloendothelial reticuloendothelial hyperplasia hyperplasia and and fatty fatty infiltration infiltration of the of the liver liver leading leading to to deficient deficient storage storage of of vitamin vitamin B12. B 12. c. Microcytic c. anemia: Due Microcytic anemia: Due to to lack lack of of iron iron absorption absorption from from intestine. intestine. (“I 6. Post Post kala-azar kala-azar dermal dermal leishmaniasis leishmaniasis (PKDL): (PKDL): -- ItIt appears appears after after spontaneous spontaneous or or drug drug cure cure (Pentostam) (Pentostam) of of kala-azar kala-azar (6 (6 months months -- 55 ys). ys). -- It It is is common common in in the the Indian Indian and and African African type type of of kala-azar. kala-azar. -- It Itisis due due to to migration migration of of the the parasites parasites from from viscera viscera to to the the skin. skin. -- The The skin skin lesions lesions (diffuse (diffuse depigmented depigmented nodules) nodules) are are chronic, chronic, progressive progressive and and painless hypopigmented painless hypopigmented macules, macules, erythematous erythematous patches, patches, or or yellowish yellowish pink pink non- non- ulcerative granulomatous ulcerative granulomatous nodules. nodules. -- It It is is localized lJocalized in in the the outer outer surface surface of of the the body body mostly mostly the the face face especially especially on on nose, nose, chin, cheeks, chin, cheeks, lips, lips, forehead forehead and and ears, ears, resembling resembling Lepromatous Lepromatous leprosy leprosy or or disseminated cutaneous disseminated cutaneous leishmaniasis. leishmaniasis.  A NATIONAL pp» MANSOURA EA A DN ‘MN; e * N e.. & Ze Wi => OSt kala-azar Post asIs (PKDL) d- aZal dermal leishmaniasis Ru ; E , atoi DI an ZA LF Re sv sl iii va a n E : CT sa > e > i À a N An i i : i è ‘ + ie - P_i le di "N e e LIA. e UN. a > “iaDe LI pre + I e DI i > Diagnosis: : Diagnosis I. Clinical: I. Clinical: Any Any case, case, in in an an endemic endemic area, area, with with fever fever of of more more than than 22 noi weeks, splenomegaly and/or splenomegaly and/or weight weight loss loss is is suspected suspected of of having having kala kala azar