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Parasitology Flashcards

1
Q

the parasites causing malaria and mention malaria types

A

Plasmodium vivax Benign tertian malaria
Plasmodium ovale Ovale tertian malaria
Plasmodium malariae Quartan malaria
Plasmodium falciparum Malignant tertian malaria

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2
Q

the mode of infection of Plasmodium

A

the anopheles injects the sporozoites into the blood

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3
Q

the infective stage of plasmodium

A

sporozoites

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4
Q

definitive host of plasmodium

A

female anopheles

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5
Q

hypnozoite are related to

A

liver phase of P.vivax and P. ovale

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6
Q

the cycle of the malaria disease (plasmodium)

A

do check it

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7
Q

Rupture of infected red blood cell of plasmodium occurs every

A

3rd day in P. vivax & P.ovale
4th day in P.malarie
irreg. in P.falciprum

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8
Q

diagnostic stages of Plasmodium

A

schizont, late trophozoite, early trophozoite (ring form), gametocytes

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9
Q

pathogenesis of malaria

A
  1. Malaria paroxysms
  2. haemolytic anemia
  3. hepatosplenomegaly
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10
Q

what is the stages of the malaria paroxysms (fever)

A
  1. Cold stage
    The patient has sudden chill, extreme cold and his temperature rises(15minutes)
  2. Hot stage
    The patient has headache, high fever and hot, dry and flushed skin
  3. Sweating stage
    The patient has profuse sweating and temperature falls
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11
Q

why clinical attacks reappear after disappearing?

A
  1. due to Presence of hypnozoites in the liver[Relapse] which occurs in P. vivax and P. ovale
  2. Presence of low-grade parasitaemia when the patient becomes
    immunosuppressed [Recrudescence] which occurs in P.malariae and P. falciparum
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12
Q

ages of RBCs that affect and its specific plasmodium

A
  • Plasmodium vivax & Plasmodium ovale prefer to invade young RBCs
  • Plasmodium malariae prefers toinvade old RBCs
  • Plasmodium falciparum invades RBCs of any age
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13
Q

causes nephrotic syndrome

A

Chronic Plasmodium malariae infection due to deposition of immune complexes on glomerular wall to activate complement cascade leading to kidney tissue damage

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14
Q

complication of chronic P.malariae infection

A

Nephrotic syndrome

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15
Q

Complication of P.falciparum

A
  1. Knob formation on the infected RBCs which adhere to the blood capillaries so decrease blood supply so death of organ tissue
  2. Hyper-reactive malarial splenomegaly (Tropical splenomegaly syndrome)
  3. Black water fever
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16
Q

Lab diagnosis of Malaria

A
  1. Giemsa-stained thin & thick blood film examination to demonstrate the parasite stages
    malaria pigments is a remnant of haemoglobin
    Stippling: degeneration process occurring in Plasmodium infected RBCs
    * Schuffner’s dots of vivax and ovale
    * Ziemann’s dots of malariae
    * Maurer’s clefts of falciparum

2- Detection of circulating parasite antigen using monoclonal antibodies

3- Detection of parasite DNA and RNA in patient’s blood using PCR

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17
Q

Tissue schizonticides of plasmodium

A

pyrimethamine or primaquine

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18
Q

Blood schizonticides of plasmodium

A

chloroquine or mefloquine

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19
Q

Blood gametocytes of plasmodium

A

chloroquine or primaquine

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20
Q

People that are naturally resistant to malaria infection

A
  1. Absence of Duffy antigen
  2. Haemoglobin S (in sickle-cell disease)
  3. Deficiency of G6PD enzyme
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21
Q

causes Microcytic Hypochromic anemia

A

Ancylostoma duodenale
trichuris Trichura

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22
Q

causes rectal prolapse

A

T. Trichura

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23
Q

causes macrocytic hyperchromic anemia

A

Diphyllobothrium Latum

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24
Q

2 morphological forms of Leishmania

A

amastigote intracellulary & promastigote in vector and in culture

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25
Q

species of visceral leishmania

A
  1. L. Donovani
  2. L. Infantum
  3. L. Chagasi
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26
Q

Morphology of Amastigote

A

Vesicular nucleus with large central karyosome
Kinetoplast (= origin of flagellum)

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27
Q

Morphology of promastigote

A

amastigote + free anterior flagellum

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28
Q

man is final host in?

A

leishmania

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29
Q

infectives stage of leishmania

A

promastigote injected by sandfly

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30
Q

diagnostic stage of leishmania

A

amastigote

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31
Q

intermadiate host of leishmania

A

sandfly
phlebotomus in old world
Lutzomyia in new world

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32
Q

mode of transmission of leishmania

A

1.Bite of female sand fly inoculating metacyclic promastigote.
2. Blood transfusion
3. Organ transplantation
4. Congenital
5. Accidental in lab worker

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33
Q

reservoir host

A

rats and rodents

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34
Q

Pathogenesis of leishmania

A

▪ Papule at site of bite (leishmanioma).
▪ Intermittent fever (double daily rise).
▪ L.N: Lymphadenopathy.
▪ Liver: hepatomegaly, pain and tenderness. reversal of albumin /globulin ratio. Why??????
▪ Spleen: splenomegaly & hypersplenism.
▪ Bone marrow: pancytopenia.
▪ Intestine: diarrhea with dysenteric manifestation d2 ulcers.
▪ Weight loss, cachexia, ascites.
▪ Kidney: renal failure d2 immune complex deposition.
▪ Decrease immunity: 2ry bacterial infections.
▪ Skin manifestations :
a) Dark pigmented erythematous areas (black fever)
b) PKDL(post-kala-azar dermal leishmaniasis) (d2 inadequate treatment).

RES KIIS

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35
Q

name of skin test on leismania

A

Motengro (Leishmanin)

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36
Q

results of Motengro (Leishmanin) skin Test:

A

-ve in active infection
+ve after 2 months of ttt.

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37
Q

Habitat of wuchereria bancrofti

A

the adults lives in lymph vessels and lymph
glands of man

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38
Q

definitive host of wuchereria bancrofti

A

man

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39
Q

vector (intermediate host) of Wuchereria Bancrofti

A

female culex mosquito

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40
Q

life cycle of Wuchereria Bancrofti

A
  • Microfilariae laid by female worm which have smooth body curves, loose sheath and tail end free of nuclei go to lymph vessels then to general circulation through the wall of lymphatics or thoracic duct
  • Microfilariae appear in peripheal blood at night between 10PM-2AM and disappear by day time(nocturnal periodicity)
  • Female Culex mosquito sucks blood containing microfilariae
  • In the stomach of the mosquito microfilariae lose their sheath and penetrate gut wall to the thoracic muscles
  • They moult twice and on 10th day they become infective filariform larvae(1500x20u)then they migrate to the head and labium of the mosquito
    • No multiplication of the larvae in the vector only growth(one microfilariaone infective filariform larvae)i.e Cyclodevelopmental transmission
  • Cycle in the mosquito requires 2-3 weeks

p. 9 lect 5

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41
Q

causes of nocturnal periodicity of wuchereria Bancrofti

A
  1. Adaption
  2. Positive chemotaxis
  3. Decreased oxygen and increased carbon dioxide
  4. Khalils theory:reversal of sleeping hours is followed by reversal of periodicty (effect of gravity)
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42
Q

Pathogenesis of Wuchereria Bancrofti

A
  • Acute inflammatory phase: due to immunological reactions to toxic
    metabolites of adult worms and secondary bacterial infection usually by sterptococci
  • lymphangitis and lymphadenitis
  • Chronic obstructive phase: fibrosis leads to obstrcution of lymphatic vessels leads to leakage of lymph under the skin with high protein content causing proliferation of c.t under the skin
  • non pitting edema
  • Elephantiasis: leg,scrotum,vulva(dependent sites)are usually affected
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43
Q

causes elephantiasis

A

Wuchereria Bancrofti

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44
Q

results of ruptered distended lymphatics

A
  1. Chylothorax(in pleural sac)
  2. Chylous ascites(in peritoneal sac)
  3. Chylocele(in tunica vaginalis of testes)
  4. Chylous diarrhoea(in intestine)
  5. Chyluria(in urinary tract)with passage of microfilariae in urine.
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45
Q

diagnosis of wuchereria bancrofti

A

Detection of microfilariae in blood they are highest at night(10pmto2am)in capillary blood(finger and ear lobe)

Diethylcarbamazine provocative test: microfilariae can be demonsterated at any time of the day

Concentration of microfilariae(knotts technique)
Detection of microfilariae in chylous urine
Detection of adults:ultrasonography,biopsy,lymphangiography
ELISA
EOSINOPHILIA.

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46
Q

TREATMENT of Wuchereria Bancrofti

A
  1. Diethylcarbamazine(DEC):lethal to microfilariae,antihistaminics,corticosteroids must
    be added to prevent allergic reactions due to rapid
    destruction of microfilariae .
  2. Ivermectin; kill microfilariae repeated doses can kill adults.
  3. Antibiotics.
  4. Surgical treatment.
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47
Q

what is Occult filariasis

A

It is a syndrome characterized by:
* High eosinophilia
* High titre of antifilarial abs&IgE levels
* Paroxysmal cough(dry)
* Lymphadenopathy
* Low grade fever&wt loss
* The response to DEC is excellent

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48
Q

reservoirs of Brugia Malayi

A

Monkeys&Cats

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49
Q

its vector is mansonia

A

Brugia Malayi

50
Q

vector of Brugia Malayi

A

Mansonia

51
Q

ChronicPlasmodium malariaeinfection is complicated by

A

Nephrotic syndrome

52
Q

ChronicPlasmodium malariaeinfection is complicated by

A

Nephrotic syndrome

53
Q

complication of malignant malaria on affected organs

A

➢ The brain (cerebral malaria) drowsiness, convulsions & coma
➢ The lungs Lung oedema, difficulty in breathing
➢ The liver impaired glycogenolysis Hypoglycaemia
➢ The kidney Acute renal failure
➢ The intestine diarrhoea, dysentery
➢ Circulation (Algid Malaria) hypotension, circulatory collapse & shock

54
Q

causes algid malaria

A

p. falciparum

55
Q

what is algid malaria

A

hypotension,
circulatory collapse
shock

56
Q

cause of the splenomegaly resulted from malignant malaria

A

due to the exaggerated immune response to repeated attacks of malaria so the spleen is marked by increased IgM production

57
Q

clinical picture of black water fever caused by

A

fever and anemia
jaundice
hemoglobinuria

58
Q

people resistant to p. vivax

A

peolpe that dont has duffy antigen

59
Q

people that resistant to P. falciparum

A

Hemoglobin S people has sickle cell disease
Def of G6PD enzyme

60
Q

Radical treatment after clinical attack of malaria

A

Primaquine

61
Q

treatment during attack of malaria

A

Chloroquine

62
Q

Chemoprophylaxis of malaria before entering endemic areas

A

pyrimethamine
primaquine

63
Q

Chemoprophylaxis of malaria after entering endemic areas

A

Chloroquine
mefloquine

64
Q

Other name of loa loa

A

African eye worm

65
Q

Habitat of Loa Loa

A

Subcutaneous tissue

66
Q

Has a diurnal periodicity

A

Micrrofilaria of Loa loa

67
Q

The vector (intermediate host) of Loa Loa

A

Chrysops

68
Q

Where is conversion of microfilaria to infected filariform Larvae

A

Thoracic muscles of chrysops fly

69
Q

Type of transmission and development of Loa Loa in chrysops

A

Cyclodevelopmental

70
Q

Clinical picture of Loa Loa infection

A
  • Acute inflammatory reactions in the form of itching, creeping sensation, redness, oedema, burning pain.
  • Granuloma in chronic stage (according to organ affected)
  • Eye : oedema of the eye lids,pain,redness impaired vision the adult worm may be seen under conjunctiva
71
Q

Associated with calabar swelling

A

Loa Loa

72
Q

What is calabar swelling

A

allergic reaction caused by Loa Loa to worm metabolites
appears as localized hard non pitting subcutaneous
swelling on hands, wrists, elbows and ankle

73
Q

Complication of Loa Loa infection

A

Invasion of the worm to ectopic foci causing orchitis, hydrocele, arthritis, glomerulonephritis
retinopathy, encephalopathy

74
Q

Diagnosis of Loa Loa

A
  • Clinical: eye worm and calabar swellings
  • Laboratory: detection of microfilaria in blood in day time(10am-2pm)
  • Serologic tests e.g ELISA
  • Eosinophilia
75
Q

Habitat of Onchocera volvulus

A

Subcutaneous nodules with fibrous tissue capsule

76
Q

The vector transmitting onchocera volvulus

A

Simulium

77
Q

Onchocera volvulus microfilaria migrate to

A

Surrounding skin

78
Q

Location of onchocera nodules

A

bony prominances as scalp, elbow, knee, ribs iliac crests and scapula

79
Q

Cause river blindness

A

Onchocera volvulus

80
Q

Cause sudan blindness

A

Onchocera volvulus

81
Q

Clinical picture of onchocera volvulus

A

Onchocera nodules
Eye lesion (River blindness)
Migration of microdfilaria leads to keratitis,retinitis,chorioditis and optic neuritis with
subsequent fibrosis leads to blindness
Dermatitis:itching and oedema in early stage then
fibrosis in late cases leads to skin atrophy and loss of skin elasticity with wrinkling(premature senility) and hanging groin
* Depigmentation : in black people (leopard skin) or
hyperpigmentation in Yemem(Sowda)

82
Q

Causes blepharospasm

A

Onchocera volvulus

83
Q

Early ocular symptoms of onchocera volvulus

A
  • Photophobia, Lacrimation
  • Blepherospasm
  • F.B sensation
84
Q

Causes leopard skin

A

Onchocera volvulus

85
Q

Complications of onchocera volvulus

A
  • Lymphadenitis: regional lymph nodes may be
    enlarged(immune reaction)
  • Elephantiasis :mainly of external genitalia is seen in some parts of Africa
  • Arthropathy:due to immune complexes
  • Encephalitis and epilepsy:microfilaria may erode skull
86
Q

Diagnosis of onchocera volvulus

A
  • Aspirate of the nodules or bloodless skin snip reveals
    microfilariae
  • Biopsy of the nodules reveals Adults.
  • Eosinophilia
  • Mazzotti test:
  • Patch test
87
Q

What mazzoti test

A

Oral dose of diethylcarbamazine(DEC)
provoke intense pruritis with in a few hours due to
death of microfilaria

88
Q

What is patch test

A

Oral dose of 50mg diethylcarbamazine(DEC)
provoke intense pruritis with in a few hours due to
death of microfilaria

89
Q

mazzoti test is used for

A

diagnosis of onchocera volvulus

90
Q

What are parasites causing anemia

A

Ancylostoma duodenale, Trichuris trichura, Diphyllobothrium latum

91
Q

Life cycle of ancylostoma duodenale

A

Adults in S.i»> Immature eggs in stool moist
warm soil (1-2d)»> hatching & release 1st stage
rhabditiform larva moulting twice within
one week (infective filariform larva )»>
penetrate the skin venules or lymphatics»>
heart lungs (3rd moult) penetrate the
pulmonary capillaries to alveoli migrate up
through the trachea swallowed»> small
intestine 4th moult(adult)

92
Q

Causes Loeffler’s syndrome

A

ancylostoma duodenale

93
Q

What is Loeffler’s syndrome

A

verminous pneumonitis, fever, cough, dyspnea, minute hemorrhage, hemoptysis & eosinophilia

94
Q

Clinical picture of ancylostoma duodenale

A

1)Skin lesions:
ground itch or hookworm dermatitis.
2)Pulmonary lesion: (Loeffler’s syndrome)
verminous pneumonitis, fever, cough, dyspnea, minute hemorrhage, hemoptysis & eosinophilia a
3) Intestinal lesion: hemorrhage due to sucking and producing anticoagulants and attachment of different sites of mucos
Microcytic Hypochromic anemia due to chronic
blood loss & depletion of iron stores
- Subcutaneous edema due to hypo-proteinemia
- Melena & occult blood in stool may occur.
- Gastrointestinal symptoms:
nausea, vomiting, abdominal pain
5)Pica :
habitual ingestion of non-food substances as soil.
6) physical and mental Retardation

95
Q

Laboratory diagnosis of ancylostomata duodenale

A
  1. Stool examination for eggs
  2. Occult blood in stool
  3. Microcytic hypochromic anemia & eosinophilia
96
Q

Treatment of ancylostoma duodenale

A

1- Albendazole
2- Mebendazole
3-Iron supplementation
4- protein rich diet.

97
Q

Life cycle of trichuris trichura

A

Adults in caecum immature eggs in faeces
soil 10-21d» embryonated egg (Rhabditiform larvae)» ingestion» hatching in lower part of S.I.&raquo_space;larva» Temporary growth of the larva(1 w)» larva pass to the caecum&raquo_space;Larva attach to mucosa of caecum maturation adult

98
Q

Mode of infection ancylostoma duodenale

A

Filariform larva

99
Q

Mode of infection of Trichuris trichura

A

ingestion of contaminated water, green vegetable
containg embryonated egg or via soil contaminated
hands

100
Q

Clinical picture of Trichuris Trichura

A

b) Dysentery & tenesmus.
c) Chronic blood loss (0.005 ml/ worm/d)due to
oozing from site of worm attachment to
mucosa leading to anemia, nutritional
deficiency & weight loss
d) Anemia: due to
-bleeding microcytic hypochromic anemia.
-Toxic products of the worm macrocytic
hyperchromic anemia (Trichocephalic anemia).
e) moderate eosinophillia
f) Rectal prolapse.
g) Rarely perforation: lead to peritonitis.
h) appendicitis

101
Q

Laboratory diagnosis of Trichuris Trichura

A

a. Stool examination for egg detection.
b- Rectal examination by proctoscopy: in heavy
infection
hyperemic edematous mucosa with hanging worms
from the mucosa.
c- Barium enema: may show translucent adult.
d- cbc:
- Moderate eosinophilia
- Anemia

102
Q

Mode of infection of Diphyllobothrium latum

A

ingestion of improperly cooked fish (fresh water fish
e.g. salmon) containing plerocercoid larva

103
Q

Treatment of Diphyllobothrium latum

A

1-Praziquantel
2-Niclosamide followed by saline purge.
3-Vit. B12 supplementation.

104
Q

Clinical picture of Diphyllobothrium latum

A
  1. Hunger pain, weight loss, vomiting, diarrhea
  2. Pernicious anemia (megaloplastic) due to toxins and B12 def
  3. Neurological manifestation as convulsions and insomnia
  4. Intestinal obstruction due to large number of the worm
  5. Migrating segment can cause cholecystitis and cholangitis
105
Q

Cause cholecystitis
Cause cholangitis

A

Migrating segments of Diphyllobothrium latum
Migrating segments of Diphyllobothrium latum

106
Q

Causes B12 def

A

Diphyllobothrium latum

107
Q

Causes melena

A

Ancylostoma

108
Q

Clinical picture of early intrauterine infection 1st trimester of toxoplasma

A

Spontaneous abortion
Retinochoroiditis
Encephalomyelitis

109
Q

Clinical picture of Late intrauterine infection 3rd trimester of toxoplasma

A

Still birth
Retinochoroiditis due to calcification
Encephalitis due to calcification

110
Q

Clinical picture of neonatal infection of toxoplasma

A

Pneumonitis
Hepatosplenomegaly
Jaundice
Convulsions
Mental retardation
blindness

111
Q

Clincal picture of infection of toxoplasma among immunocomptent

A

Myalgia,extreme fatigue with generalized
lymphadenopathy which mimics infectious
mononucleosis

112
Q

Clinical picture of Infection of toxoplasma among immunocopromized

A

CNS infection» ataxia, convulsions and hemiparesis, with increase antitoxoplasma IgG

113
Q

Habitat of leishmania parasites

A

Reticuloendothelial cells and organs
LN, bone marrow, liver, spleen

114
Q

Visceral leishmania in old world

A
  1. L. Donovani
    2.L. Infantum
115
Q

Visceral leishmania in new world

A

L. Chagasi

116
Q

2 morphological forms of leishmania

A

amastigote intracellulary &
promastigote in vector and in culture

117
Q

Final host, infective, diagnostic, I.H, R.H of leishmania

A

Man,
promastigote,
amastigote,
sandfly (phlebotmus in old and lutzonia in new)
dogs and rodents

118
Q

Mode of transmission of leishmania

A

1.Bite of female sand fly inoculating metacyclic promastigote.
2. Blood transfusion
3. Organ transplantation
4. Congenital
5. Accidental in lab worker

119
Q

We culture in NNN media to diagnose

A

Promastigote of leishmania

120
Q

Diagnose of leishmania

A

*microscopic examination of samples (blood,
liver, L.N, spleen) and stain with giemsa stain.
*Culture on NNN media (promastigote)
*Animal inoculation (amastigote)
*PCR

121
Q

We use motengro test in diagnosis of

A

Leishmania
-ve in active infection,
+ve after 2 months of ttt.

HEN (8 decks)

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