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Y1B3 (CVS & IBL) 📘 > Parasitology 🪱 > Flashcards

Parasitology 🪱 Flashcards

1
Q

What is the definition of malaria?

A

Malaria is a life-threatening mosquito-borne blood disease caused by a plasmodium parasite.

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2
Q

What are the species of Plasmodium parasite?

A

Plasmodium vivax: Benign tertian malaria or vivax malaria

Plasmodium ovale: Benign tertian malaria or oval malaria

Plasmodium malariae: Benign quartan malaria or malariae malaria.

Plasmodium falciparum: Tertian or subtertian malignant malaria or falciparum

“Plasmodium malarie causes nephrotic syndrome”

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3
Q

What is a definitive host in the lifecycle of plasmodium?

A

♀ Anopheles

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4
Q

What is intermediate host and the reservoir host in the lifecycle of plasmodium?

A
  • IH: man

- RH: non except P.malaraie monkey

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5
Q

What is the infective stage for both humans and female anopheles mosquito?

A
  • Sporozoites inoculated with mosquito’s saliva at the site of bite.
  • Gametocytes which are present in blood
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6
Q

Where does schizogony occur?

A
  • In I.H (man) asexual multiplication in Liver (exoerythrocytic cycle),& Red cells (erythrocytic cycle).
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7
Q

What are the steps of Exoerythrocytic Schizogony?

A
  • hepatocyte invasion in 30 min, 6-15 days, 1000-40,000 merozoites, no overt pathology
  • The released merozoites, some are histiotropic and infect new liver cells initiating secondary exo-erythrocytic tissue phase (never in mammals, only in bird & lizard), and other merozoites are erythrotropic which invade and infect red blood cells initiating erythrocytic cycle.
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8
Q

Which type of malaria has Hypnozoits?

A
  • Hypnozoite Forms only P. vivax and P. ovale
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9
Q

What are the steps of Erythrocytic phase (asexual erythrocytic schizogony)?

A
  • young trophozoite called ‘ring form’, ingests host hemoglobin by cytostome forming hemozoin (malarial pigment), nuclear division, begin schizont stage (6-40 nuclei)
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10
Q

What are the characteristics of Gametocytogenesis?

A
  • ring but with no vacuolation, increase in size → gametocyte, no pathology, infective stage for mosquito
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11
Q

What is the relation between the merozoites of exo-erythrocytic cycle in liver and merozoites of erythrocytic cycle?

A
  • The merozoites of exo-erythrocytic cycle in liver can invade red cells initiating erythrocytic cycle, but the merozoites of the erythrocytic cycle can’t invade the liver cells.
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12
Q

Where does sorogony cycle occur?

A
  • In female Anopheline mosquito vector
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13
Q

what happens in sorogony cycle?

A
  • occurs in mosquito gut, ‘exflagellation’ 8 microgametes formed,
  • Fertilization →rounded zygote, elongates →ookinete →penetrates between the basement membrane & the elastic layer of the stomach →oocyst →sporocyst
  • The sporocysts ruptures and the released sporozoites (infective stages) migrate to the salivary gland
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14
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to RBCs affected

A

Reticulocytes - mature cells - old & mature - all types” that’s why its dangerous”

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15
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to Cell stippling

A
  • Schuffner’s dots, fine pigments
  • Schuffner’s dots, fine pigments
  • Ziemann’s dots, fine pigments
  • Maurer’s clefts, course pigments
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16
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to ring numbers

A

one - one - one - multiple

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17
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to old trophozoites

A

Amoeboid - compact - band form - compact

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18
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to schizont

A
  • Contains 18 merozoites ,Mature in 2 days
  • 8 merozoites ,Mature in 3 days
  • 8 merozoites ,Mature in 2 days
  • 18 merozoites ,Mature in 2 days
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19
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to gametocytes

A

Rounded - rounded - rounded - crescentic

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20
Q

Compare between P.vivax, P. Ovale, P. Malarie and P. Falciparum acc to stages seen in a blood film

A
  • Ring, trophozoites, schizont, gametocyte
  • Ring, trophozoites, schizont, gametocyte
  • Ring, trophozoites, schizont, gametocyte
  • Ring, Gametocytes only
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21
Q

How is malaria transmitted?

A
  • By the bite of an infected female Anopheles mosquito with sporozoites in its saliva (here there is liver affection).
  • Blood-borne: Blood transfusion, Intravenous injection, Congenital transmission, After organ transplantation. “Merozoites”
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22
Q

What is the immune response against malaria?

A
  • Protective immunity develops after repeated exposure: Fewer parasites in blood stream & Less fever and clinical signs of disease, No strong immunity to malaria due to Ag variation.
  • Immunologic response of the host to parasite Ag & malaria pigments → +++ TNFa and IL-1 release from host cells → clinical picture
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23
Q

Which type of malaria causes fatalities?

A
  • P. falciparum malaria is the cause of virtually all fatalities due to Cytoadherence
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24
Q

What activates the reticuloendothelial system in case of malaria?

A
  • The reticuloendothelial system is activated by the rupture of infected red cells and intravascular release of parasites, malarial pigment, and cellular debris.
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25
Q

What does anoxia stimulate in case of malaria?

A
  • Anoxia stimulate the erythroblastic activity of bone marrow to produce reticulocytes, which are attached principally by P. vivax, so anaemia is marked in this infection.
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26
Q

What causes enlargement of the liver and spleen in case of malaria?

A
  • Enlargement of liver and spleen a result of enhanced phagocytosis of red cell remnants & other debris produced by schizogony.
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27
Q

What is the pathogenesis of malaria?

A
  • Rupture of RBCs are main cause of pathology → Release of merozoites → Reinvasion &↑parasitemia → Release of malarial pigment → Release of HB → Jaundice & Black water fever → Destruction of RBCs → Anemia, Anoxia, & Fatty degeneration of organ → Activation of RES → hepato-spleno-megally
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28
Q

What are the causes of anemia in malaria?

A

1) Obligatory destruction of RBCs in merogeny
2) Complement mediated & autoimmune hemolysis “AB Vs RBCs”
3) Hypersplensim “Affect normal RBCs”
4) Bone marrow suppression by TNF
5) Short RBCs survival
6) Failure to recycle iron in haemozoin

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29
Q

What is cytoadherence?

A
  • RBCs has knobs on surface covered by adhesive protein Lead to adherence to each other “thrombosis” & endothelial cells “infarction”
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30
Q

What are of the clinical pictures of malarial infection?

A
  • Uncomplicated malaria
  • In all 4 species of malaria, human infection is followed by incubation period, then malaria paroxysms include 3 stages: Cold stage “due to VC” , Hot stage & Sweating Stage
  • Hepatosplenomegaly (liver & spenic enlargement), Dysenteric symptoms
  • Hemolytic anemia
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31
Q

What are the symptoms of uncomplicated malarial infection?

A
  • Fever (paroxysm), Anaemia, & splenomegaly

“FAS”

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32
Q

What causes the dysenteric symptoms in malarial infection?

A
  • due to infarctions in large intestine, may occur in P. falciparum
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33
Q

Why is hemolytic anemia more severe in plasmodium falciparum infection?

A

 RBCs of all ages can be invaded by parasites

 Unparasitized RBCs undergo haemolysis

 Parasitaemia is higher than in other malarias → destruction of more red blood cells.

“Affects all RBCs in every way”

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34
Q

What are diseases of complicated falciparum malaria?

A
  • Cerebral malaria: ↓consciousness, convulsions, paralysis. “DUE TO THROMBUS IN CAPPILARIES THAT SUPPLY THE BRAIN”
  • Algid malaria “‏صاعقة”: ↓ Bl. P, peripheral circulatory failure, Acute renal failure & Black water fever
  • Severe malaria: HB <5g/dL, Pulmonary edema,Metabolic acidosis and shock. “PMS”
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35
Q

Why are falciparum infections dangerous?

“They are numerous, furious and fast”

A
  • Highest number of merozoites → ↑parasitemia, Shorest IP, Cytoadherence→ pernicious syndrome, Prediction to all RBCs types
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36
Q

What is relapse in malaria?

A
  • Means recurrence of clinical attacks in patients due to reactivation of hypnozoites in the liver (occurs in P. vivax & P. oval infection) only
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37
Q

What causes recrudescence in malaria?

A
  • is due to persistence of blood forms between attacks
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38
Q

What is recrudescence in malaria?

A
  • recurrence of clinical attacks in patients having low grade parasitaemia when they become debilitated, in all types
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39
Q

How is malaria diagnosed?

A
  1. Clinical findings, History of travel (Imported malaria)
  2. Blood film
  3. Therapeutic test
  4. Serodiagnostic methods
  5. Dipstick test
  6. Polymerase chain reaction (PCR): can be used to detect parasite DNA.
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40
Q

what is the therapeutic test used to diagnose malaria?

A
  • antimalarial, drug if result in disappearance of fever within 6 days
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41
Q

What is serodiagnosis of malaria?

A
  • indirect fluorescent antibody test
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42
Q

What is the dipstick test used for detection of malaria?

A
  • by which parasite antigens are detected by placing a drop of blood on a dipstick impregnated with antibody.
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43
Q

how is malaria treated?

A
  • Treatment in case of 1st trimester of pregnancy: Quinine + Clindamycin
  • Blood schizonticides: destroying the parasitic stages in the blood, so act as a suppressive line of treatment. Ex Chloroquine, Mefloquine, Artimesinin derivatives.,
  • Tissue schizonticides: that destroy parasitic stages in the liver, so act as a prophylactic measure. Ex. Primaquine
  • Transmission blocking: Primaquine has a gametocidal effect
  • Radical treatment: chloroquine & primaquine
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44
Q

How is Uncomplicated falciparum malaria treated?

A
  • Artmesinin combination therapy (ACT) “strongest”
  • Primaquine (gametocidal)
  • Exchange transfusion if parasitemia ≥ 10%.
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45
Q

How are other malaria than falciparum treated?

A
  • Chloroquine
  • Primaquin for prevention of relapse
  • Artmesinin combination therapy (ACT) in case of chloroquine resistance.
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46
Q

How is chemoprophylaxis against malaria done?

A
  • Causal prophylaxis: primaquine

- Suppressive prophylaxis: chloroquine or mefloquine

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47
Q

How is malaria prevented and controlled?

A

Man:- Early diagnosis & treatment

Parasite:- Drugs (prophylactic vs therapeutic use)

Mosquitoes:- Indoor residual spraying & Environmental interventions & Larvicides

Vector-human contact:- Insecticide treated bed nets

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48
Q

Why is malaria such a difficult disease to eliminate?

A

a) Resistance to Drugs “By parasite”
b) Resistance to Insecticides “by insect”
c) Global warming. “inc reproduction”
d) No Malaria Vaccine. “Due to antigen variation”
e) Sustaining funds

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49
Q

What is the definition of Bancroftian filariasis?

A
  • It is caused by a slender “thin” white filarial worm called Wuchereria bancrofti, transmitted by mosquitoes bite, lives in lymphatics, periodically shedding larvae into peripheral bloodstream
  • often causes elephantiasis by blocking lymphatic drainage.
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50
Q

What is the morphology of adult of wuchereria bancrofti?

“Female is double the male”

A
  • Male: 4 cm long, curved posterior end.

- Female: 8 cm long, tapered tail.

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51
Q

What is the morphology of the microfilaria of wuchereria bancrofti?

A
  • About 300 x 10 μ.

- Has lose sheath, rounded anterior end, and tapered posterior end devoid of nuclei.

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52
Q

What is the lifecycle of wuchereria bancrofti?

A
  • Habitat: adults live in lymph vessels and lymph nodes especially those draining lower part of the body, and microfilariae are in peripheral blood.
  • Definitive host (D.H.): man.
  • Intermediate host (I.H., vector): mainly female Culex, also female Anopheles and Aedes mosquitoes.
  • Infective stage: infective filariform larvae in mosquito mouth.
  • Mode of infection: through the skin, during the bite of infected female mosquito.
  • Infected insect bites human→infective filariform larvae actively enter through bite wound→migrate to lymphatics→transform to adult worms.
  • Fertilized females lay microfilariae→migrate to peripheral blood→ sucked by insect vector.
  • In the insect midgut, microfilariae moult “peel” →infective filariform larvae →migrate to the mosquito mouth.
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53
Q

And what causes the clinical manifestations of wuchereria bancrofti?

“Like entamoeba”

A

❑ Results from a complex interplay of:

  1. Pathogenic potential of the parasite.
  2. Tissue response of the host.
  3. External bacterial and fungal infections.
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54
Q

what are the types of pathology caused by wuchereria bancrofti ?

A

Classical filarias

Occult filariasis

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55
Q

Compare between classical filariasis and occult filariasis according to:-

Cause
Lesions
Pathology C/P
MF in blood
Diagnosis

“Adult in lymphatics —–> microfilaria in peripheral blood ——-> infective filariform larva in mosquito midgut”

A

Cause:

  • Adult worm
  • Microfilaria (Microfilaria usually non-pathogenic)

Lesions:

  • LNs & Lymphatics
  • Lung, Liver and Spleen

Pathology C/P:

  • Inflammation, Fibrosis ands classical manifestations
  • esinophilic granuloma, cough, Dyspnea and asthma

MF in blood:

  • Present
  • Pbsent in blood (present in affected tissues)

Diagnosis:

  • Blood film - Serology is less effective
  • Serology
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56
Q

What is the incubation period of wuchereria bancrofti??

A

8 - 16 months

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57
Q

What are the clinical manifestations of wuchereria bancrofti?

A

Asymptomatic filariasis

Symptomatic filariasis

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58
Q

What are the characteristics of asymptomatic Filariasis?

A
  • in people living in endemic areas, and they are source of infection
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59
Q

What are the types of symptomatic filariasis?

A

Acute inflammatory manifestations “in nearly 6 months”

Chronic obstructive manifestations (10-15 years)

Tropical pulmonary eosinophilia (TPE, diffuse filarial lung disease)

60
Q

What are Acute inflammatory manifestations of lymphatic filariasis?

A
  • Lymphangitis
  • Lymphadenitis
  • Filarial fever
61
Q

What are the characteristics of lymphangitis in lymphatic filariasis?

A
  • dilated, inflamed and thickened lymphatic vessels.
62
Q

What are the symptoms of lymphangitis of lymphatic filariasis?

A
  • red, tender & swollen.
63
Q

What are the causes of lymphangitis of lymphatic filariasis?

A

a. Mechanical irritation by moving worms.
b. Metabolites of living worms.
c. Toxic products of living and dead worms.
d. Secondary bacterial infection.

64
Q

What are the symptoms of lymphadenitis of Lymphatic filariasis?

A
  • enlarged, tender and matted lymph nodes
65
Q

What causes lymphadenitis of Lymphatic filariasis?

A
  • due to fibrosis and necrosis & obstruction of proximal lymphatic vessels.
66
Q

What is the site of lymphadenitis of lymphatic filariasis?

A

inguinal lymph nodes.

67
Q

What are the symptoms of filarial fever?

A
  • high fever, chills and excess sweating.
68
Q

What are chronic obstructive manifestations of lymphatic filariasis?

A
  • Dilatation of lymphatic (Varicosity)
  • Lymphorrhagia
  • Lymphedema
  • Elephantiasis
69
Q

Where does dilatation of lymphatics mainly occur?

A
  • occurs mainly in genital organs (hydrocele & lymphatic varices)
70
Q

What causes lymphorrhagia? And what are examples for it?

A
  • rupture of lymph varices release lymph, e.g. chyluria, chylous diarrhea, chylothorax and chyluria.
71
Q

What is lymphedema in lymphatic filariasis?

A
  • abnormal accumulation of lymph in tissues, swelling, mainly of lower limb & genitalia,
72
Q

What are the characteristics of lymphedema of lymphatic filariasis?

A
  • A hard and non-pitting area starts at ankle, then spreads to affect foot & leg.
  • It can also affect scrotum, vulva, arms and breast.
73
Q

What causes lymphedema of lymphatic filariasis?

A
  • dilatation of lymphatic vessels due to inflammation caused by worms.
74
Q

What causes elephantitis of lymphatic filariasis?

A
  • due to obstruction and fibrosis of lymph nodes & lymph vesselS
75
Q

What are the characteristics of the affected parts with elephantitis of lymphatic filariasis?

A
  • Affected parts are edematous & tender
76
Q

What are the characteristics of the skin covering the affected parts by elephantitis of lymphatic filariasis?

A
  • hard, stretched, thick and rough skin covering
77
Q

What are the mainly affected parts with elephantiasis of lymphatic filariasis?

A
  • It mainly affects leg, genitalia, arm and breast.
78
Q

What are the causes of obstruction of lymph flow in lymphatic filariasis?

A

a. Worms blocking the lumen of lymphatic vessels.
b. Endothelial proliferation and thickening of lymphatic vessels.
c. Fibrosis of lymphatic vessels and lymph nodes.
d. Recurrent secondary bacterial lymphangitis.

79
Q

What is the site of tropical pulmonary eosinophilia?

A

lung tissues

80
Q

What is the cause of tropical pulmonary eosinophilia?

A
  • hypersensitivity reaction to microfilarial antigens
81
Q

What is the pathology of tropical pulmonary eosinophilia?

A
  • chronic interstitial fibrosis with destruction of microfilariae in the pulmonary vasculature
82
Q

What is the clinical picture of tropical pulmonary eosinophilia?

A
  • Clinically there is dyspnea, cough & asthma.
83
Q

What is the treatment of tropical pulmonary eosinophilia?

A

Hetrazan

84
Q

How is Wuchereria bancrofti diagnosed?

A

❑ Clinical diagnosis: by good history taking.

❑ Laboratory diagnosis: Direct and indirect

85
Q

What is the direct diagnosis of Wuchereria bancrofti?

A
  1. Detection of microfilariae in peripheral blood
  2. Provocative test
  3. Detection of microfilariae
  4. Detection of adult worms
  5. Immunological tests for detection of filarial antigens
86
Q

What is the indirect diagnosis of Wuchereria bancrofti?

A

1- Immunological tests for detection of filaria-specific antibodies

2- Blood examination

3- X-ray

87
Q

How is Microfilaria detected in peripheral blood?

A

a. Fresh smear.
b. Giemsa-stained thick blood film.
c. Concentration of microfilariae (Knott s method).

88
Q

What are important points that should be concerned about Microfilaria in Peripheral Blood?

A
  • Appear year/s after infection.
  • Rarely found in obstructed lymphatic.
  • More in capillary than venous blood.
  • More in ear lobe than finger blood.
  • Blood must be collected at night (10 PM-2 AM).
89
Q

What is provocative test done to microfilaria?

A
  • 2mg/Kg of diethylcarbamazine are given to the patient microfilaria enters peripheral blood in day time within 30 - 45 min of administration.
90
Q

What are other sites where microfilaria could be detected?

A
  • chylous urine and other chylous fluid.
91
Q

How are adult worms of Wuchereria bancrofti detected?

A

a. Lymph node biopsy.
b. X-ray to detect dead calcified worm.
c. Ultrasonography: can visualize movement of living worms in lymphatics.

92
Q

How is Wuchereria bancrofti treated?

A
  1. Chemotherapy
  2. Surgical
  3. Foot care programme for lymphedema.
93
Q

What is the chemotherapy to Wuchereria bancrofti?

A

a. Diethyl carbamazine citrate (Hetrazan):
- Drug of choice, effective against microfilariae and tropical pulmonary eosinophilia.
- Repeated courses can kill adult worms.

b. Ivermectin: effective against microfilariae, but no effect on tropical pulmonary eosinophilia.
c. Albendazole: efficacy against microfilariae and its action on adults is under research.

94
Q

What is the surgical treatment for Wuchereria bancrofti?

A
  • Hydrocele.

- Elephantiasis.

95
Q

How is lymphedema treated?

A

Foot care programme

96
Q

How is Wuchereria bancrofti prevented and controlled?

A
  1. Detection & treatment of patients.
  2. Vector control.
  3. Health education in endemic areas.
  4. Environmental sanitation.
97
Q

What is indirect diagnosis of wuchereria bancrofti?

A
  1. Immunological tests for detection of filaria-specific antibodies: ELISA, indirect immunofluorescence assay test (IFAT) & complement fixation test (CFT).
  2. Blood examination: for detection of eosinophilia.
  3. X-ray: for diagnosis of tropical pulmonary eosinophilia.
98
Q

What is the definition of visceral leishmaniasis?

A

A chronic and potentially fatal parasitic disease of the viscera (particularly the liver, spleen, bone marrow and lymph nodes) due to infection by Leishmania parasite . Also known as Kala-azar.

99
Q

What is the definition of cutaneous leishmaniasis?

A
  • Cutaneous form of the disease causes skin sores and is usually named for a geographic place (for example, Baghdad, Delhi sore)
100
Q

What are the causative organisms of visceral leishmaniasis?

A

All species of Leishmania donovani complex cause visceral leishmaniasis and are distributed as:

  1. In old world:
    - L. donovani: India, Pakistan, Indonesia, Thailand, Central Africa and Sudan.
    - L. infantum: Mediterranean area, Middle East and China.
  2. In new world:
    - L. chagasi: America (Central and South America).
101
Q

What are the causitive organisms of cutaneous leishmaniasis?

A

L.Major
L.Athiopica
L.Tropica

102
Q

What is the morphology of amastigote “leishman Donovan body” according to:

Site
Size
Shape
Nucleus
Flagellum
Kinetoplast
Significance
A

Site: typically intracellular in macrophages, In reticuloendothelial cells (RECs) all over the human body and reservoir host (vertebrate hosts),

Size: 2-3μ

Shape: ovoid

Nucleus: spherical nucleus (stain red with Giemsa)

Flagellum: Abscent

Kinetoplast: formed of

(a) parabasal body (rod-shaped, deep blue).
(b) Basal granule (blepharoplast), from which arises an intracytoplasmic axoneme (no free flagellum).

Significance: Diagnostic in biopsy

103
Q

What is a morphology of promastigote acc to:

Site
Size
Shape
Nucleus
Flagellum
Kinetoplast
Significance
A

Site: In insect vector (invertebrate host) and culture.

Size: 4×12μ

Shape: fusiform (spindle-shaped)

Nucleus: central vesicular nucleus

Flagellum: anterior free flagellum

Kinetoplast: anterior kinetoplast (no undulating membrane)

Significance: infective stage

104
Q

What is the habitat of visceral leishmaniasis?

A
  • Leishmania amastigotes live intracellular in macrophages of reticuloendothelial ( R.E.S. )tissue., especially spleen, liver, bone marrow, intestinal mucosa and mesenteric lymph nodes.
105
Q

What are other names of visceral Leishmanisis?

A
  • Kala Azar
  • Black fever
  • Dum-Dum fever
106
Q

What is the vector of visceral leishmaniasis?

A
  • Female sand flies of the genus Phelebotomus in the old world, and Lutzomyia in the new world.
107
Q

What is the reservoir host of visceral leishmaniasis?

A

Dogs, rodents, wild and domestic animals.

108
Q

What is the infective stage of visceral leishmaniasis?

A

L.promastigotes.

  • Site: sand fly gut.
109
Q

What are the methods of infection by visceral leishmaniasis?

A

1- regurgitation of promastigotes into bite wound.

2- Rare modes: (by amastigotes):

(a) Blood transfusion.
(b) Transplacental.
(c) Accidental laboratory wound.
(d) Mechanical by blood sucking flies (e.g. Stomoxys).

110
Q

How is visceral leishmaniasis transmitted?

A

Biological cyclo-propagation transmission

111
Q

What is a diagnostic stage for visceral leishmaniasis?

A
  1. L. Amastigote (in tissue smear)

2. L. Promastigote (in culture typically arranged in rosettes)

112
Q

How is visceral leishmaniasis treated?

A

Pentostam

113
Q

What is the lifecycle of leishmania?

A
  • Man acquires the infection when the infected female sand fly attempts a blood meal, where some of the promastigotes in the buccal cavity are regurgitated, and introduced into the skin bite by their motility.
  • Promastigotes are phagocytosed by skin macrophages, where they metamorphose into amastigotes that reproduce by binary fission.
  • Ruptured parasitized cells release large number of amastigotes into circulation
  • Blood monocytes phagocytose the free amastigotes and carry them to the viscera, where they produce generalized infection of the RECs.
  • Amastigotes in blood are taken by the female sand fly during blood meal.
  • In the mid-gut of the sand fly, the amastigotes are metamorphosed into promastigotes and multiplied by binary fission (Cyclo-propagative development), until the lumen of the mid-gut is completely blocked.
  • After 6-9 days, the promastigotes migrate to the pharynx which becomes blocked by the parasites, then to buccal cavity and proboscis.
  • When blocked sand fly attempts subsequent blood meal, some of promastigotes are regurgitated, and introduced into the skin bite and the cycle is repeated.

“Just understand and write on your own words”

114
Q

What is the pathogenesis and clinical picture of a visceral leishmaniasis?

A

” Fever + HS + Pan + DD + Skin”

  1. Fever
  2. Hepatosplenomegaly + generalized lymphadenopathy
  3. Pancytopenia
  4. Diarrhoea or dysentery
  5. Skin changes
115
Q

What is the mechanism of pathogenicity in kala azar?

A
  • Amastigotes multiply in macrophages (rupture + reinvasion) compensatory and reactive hyperplasia of R.E.Cs.
116
Q

What are the characteristics of fever in visceral leishmaniasis?

A

intermittent (40 c, 2 peaks in one day).

117
Q

What are the characteristics of pancytopenia in visceral leishmaniasis?

A

(aplastic anaemia + leucopenia + thrombocytopenia).

118
Q

What are the characteristics of diarrhea and dysentery visceral leishmaniasis?

A
  • ulceration of intestinal mucosa

- amastigote is found in stool

119
Q

What are the causes of diarrhea and dysentery visceral leishmaniasis?

A
  • Invasion of payers patches ——> hyperplasia—-> ischemia —-> ulceration of intestinal mucosa
120
Q

What are the skin changes that happen in visceral leishmaniasis?

A

a) early: hyperpigmentation (circumoral on face – hence the
name: black fever).

(b) PKDL (post kala azar dermal leishmanoids): diffuse depigmented nod

121
Q

How is visceral leishmaniasis diagnosed?

A

Clinical and laboratory

122
Q

What is the laboratory diagnosis of visceral leishmaniasis?

A

Direct and indirect

123
Q

What are the direct methods for diagnosis of visceral leishmaniasis?

A
  1. Microscopic Detection of amastigotes in Leishman or Giemsa-stained smears.
  2. Culture on NNN media
  3. Intraperitoneal Animal inoculation in hamsters by aspirated Specimens

“MCA”

124
Q

What are the indirect methods for diagnosis of visceral leishmaniasis?

A
  1. Immunological diagnosis
    A. Serological tests
    B. Leishmanin skin test. (Montenegro test)
  2. Molecular diagnosis
  3. Blood picture
125
Q

Where is the sample for microscopic detection of amastigote in case of direct diagnosis taken from?

A

Taken from Sample:

  • Peripheral blood
  • Bone marrow.
  • Splenic aspirates.
  • Liver puncture.
  • Enlarged LNs & nodular lesions.
  • Nasopharyngeal secretion, Stool & urine.
126
Q

Describe culture of promastigotes on NNN media

A

Detect Promastigotes in Rosette grouping,can be detected 1-4 weeks after cultivation.

127
Q

What happens in positive cases after intraperitoneal animal inoculation in case of visceral leishmaniasis?

A
  • In positive cases : Amastigotes can be seen in smears taken from ulcers or nodules at site of inoculation or from spleen, weeks post infection.
128
Q

What are the serological tests done to diagnose visceral Leishmaniasis?

A
  • Specific leishmanial antigens prepared from cultures used to delect anti-leishmanial antibodies by IFA, IHA, ELISA, Complement fixation test (CFT), direct agglutination test (DAT) & specific rapid immunochromatographic dipstick (ICT).
129
Q

What is leishmania skin test? (Montenegro test)

A

Delayed hypersensitivity skin test.

130
Q

How is Montenegro test done?

A

0.1 ml Killed promastigotes injected intradermal.

131
Q

What is the result of Montenegro test?

A

Result: induration & erythema within 48-72 h indicate positive test.

  • Positive result indicates past infection & Becomes positive 6-8 weeks after cure.
  • Negative during active infection & PKDL, Why? Due to marked depression of cell-meciated immunity.
132
Q

What is the molecular diagnosis of visceral leishmaniasis?

A

PCR for species identification.

133
Q

What does a blood picture of visceral leishmaniasis show?

A
  • Shows Aplastic anemia : Normocytic normochromic anemia, leucopenia & thrombocytopenia.
  • Serum shows hypergammaglobulinemia & low albumin level. “Inverted A/G ratio”
134
Q

How is visceral leishmaniasis treated?

A

A. Supportive treatment;

  • Diel rich in vitamins, iron & liver therapy.
  • Antibiotics for 2ry bacterial infection.
  • Blood transfusion for severe anemia or bleeding.

B. Specific treatment:

a. Systemic therapy. “Parenteral”.
- Pentostam (Sodium stibogluconate).
- Amphotericin B.
- Interferon-gamma with pentostam effective for relapse.

b. Systemic therapy. “Oral”
: Miltefosine.

135
Q

How is visceral leishmaniasis prevented and controlled?

A
  1. Control of sand flies : by destruction of their breeding grounds near human habitations & by use of residual chlorinated hydrocarbon.
  2. Treatment of infected patients
  3. Control of reservoir hosts will reduce sources of infection
  4. Personal prophylaxis by using :
    - Bed nets
    - Window mesh screen
    - Insect repellents
136
Q

What is the difference between the morphology and lifecycle of causative organism of cutaneous leishmaniasis and L.donovani ?

A
  • The difference is that Leishmania amastigotes remain in skin macrophages without invasion of other organs
137
Q

What is ….. of L. Major?

Habitat
Distribution
D.H
I.H
R.H
Infective Stage
Mode Of Infection
A

Habitat: RES of skin

Distribution: Rural distribution ( near desert : Libya, Egypt”Sohage &Sinai)

D.H: Man

I.H(vector): Female Sandfly “Phelebotomus”.

R.H: Rodents & Desert Gerbil.

Infective Stage: Promastigotes in sandfly midgut & pharynx .

Mode Of Infection:

1) Bite of infected female sandfly & Regurgitation of promastigotes into bite wound.
2) Direct contact.
3) Stable fly (Stomoxys calcitrans) may transmit organisms
mechanically from an open ulcer or through unbroken skin. “No blood amastigote”

138
Q

What is the pathogenicity of cutaneous leishmaniasis?

A
  1. Multiplication of amastigotes in skin macrophages —–> formation of papule, nodule & ulcer.
  2. Ulcer may be single or multiple, that heals over months to years leaving scar.
  3. Recovery from cutaneous leishmaniasis gives a life-long immunity against the Same leishmania species
139
Q

What is the clinical picture of infection with L.major?

A

L. Major : Cause Wet “Moist - Oriental Sore .

Course: acute

Incubation period: SHORT (2-6 WEEKS)

Number: Multiple

Healing: Rapid (3-6 months ).

140
Q

What are the characters of moist ulcer?

A

Starts by: Small itchy erythmatous papule

Site: Located on exposed part of skin “upper limb & L.L”

Edge: Sharp raised edge (volcano sign)

Margin: Red indurated (firm) margin

Floor: Necrotic base

Fate: Heal by depressed depigmented scar in moist type

141
Q

What is a diagnosis of cutaneous leishmaniasis?

A

Clinical and laboratory

142
Q

What is a laboratory diagnosis of cutaneous leishmaniasis?

A

Direct and indirect

143
Q

What is the direct laboratory diagnosis of cutenous leishmaniasis?

A
  1. Microscopic examination of :
    - Smears aspirated or scraped from edge of lesion & stained with Leishman or Giemsa
    - Skin Biopsy stained with H & E.
  2. Culture “NNN media”: Detect Promastigote.
  3. Animal inoculation.
144
Q

What is the indirect laboratory diagnosis of cutaneous leishmaniasis?

A
  1. Leishmanin (Montenegro) skin test :
    - Helpful
    - Becomes positive few days after infection
  2. Serological diagnosis : Of limited value because antibody levels are undetectable.
145
Q

What is the treatment of cutaneous leishmaniasis?

A

Local and systemic measures

146
Q

What are the local meausures followed for treatment of cutaneous leishmaniasis?

A
  • Surgical excision.
  • Scraping (curettage).
  • Plastic surgery for Scars or disfiguring nodules.
    Cleanliness to prevent 2ry bacterial infection.
  • Systemic/local antibiotic : for 2ry infection needs.
  • Local heating of lesion by infra-red rays
  • Freezing therapy by carbon dioxide
    “Cryotherapy”
  • Local injection of 10% atebrine, solution.
  • ID. injection of interferon gamma around lesions promotes healing of ulcers.
147
Q

What are the systemic treatment of cutaneous leishmaniasis?

A

Systemic therapy (parenteral): Pentostam “of choice”.

  • 2 or 3 courses may be needed.
  • If sores 1-3 in number, treatment facilitated by local
    infiltration of drug into edges of ulcers.

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