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Y2B4 - Central Nervous System πŸ“™ > Parasitology πŸͺ± > Flashcards

Parasitology πŸͺ± Flashcards

1
Q

what are parasites that affect CNS?

A
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2
Q

What are free living amoeba?

A
  1. Naegleria fowleri
  2. Acanthamoeba castellani
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3
Q

what is another name for N.fowleri?

A

Brain-eating amoeba

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3
Q

Geographical distribution of N. fowleri

A

Cosmopolitan

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4
Q

Morphology of Ameboid form of N.fowleri

A
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5
Q

Habitat of ameboid form of N.fowleri

A

It inhabits CNS tissues and CSF

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6
Q

Morphology of falgellate form of N.fowleri

A
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7
Q

Habitat of flagellate form of N.fowleri

A
  • Present in warm water.
  • It not presents in tissues.
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8
Q

Morphology of cyst of N.fowleri

A
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9
Q

Habitat of cyst of N.fowleri

A
  • It presents only in soil.
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10
Q

Habitat of N.fowleri

A
  • Soil and warm fresh water.
  • In man it attacks the CNS.
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11
Q

Infective stage of N.fowleri

A

Amoeboid trophozoite.

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12
Q

Mode of infection by N.fowleri

A

Through the nasal route.
1. Swimming or sniffing in contaminated water.
2. Inhalation of contaminated air.

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13
Q

Pathway of N.fowleri after infecting someone

A
  • Amoeboid trophozoites in contaminated water enter the nose, migrate through nasal mucosa β†’ olfactory nerve β†’ olfactory pulp β†’ base of the brain β†’ disseminate to the brain tissue.
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14
Q

Method of N.fowleri ameboid trophozite feeding and division

A

simple binary fission.

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15
Q

what does N.fowleri trophozite change into in soil?

A

transforms into cyst stage

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16
Q

Pathogenesis of N.fowleri

A
  • Naegleria fowleri causes primary amoebic meningo-encephalitis (PAM).
  • Amoeboid trophozoite is neurotropic, feeds on nerve tissue resulting in necrosis –> acute meningoencephalitis.
  • In subarachinoid space: inflammatory cells (Neutrophils)
  • In grey matter: Hemorrhage, necrosis & amoebae
  • In white matter of the brain: demyelination (Due to phospholytic enzyme produced by amoeba)
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17
Q

Course of PAM caused by N.fowleri

A

The clinical course of PAM is dramatic, death usually occurs within a week.

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18
Q

Clinical picture of N.fowleri

A

Stage I: Nausea, vomiting, severe frontal headache, fever, blocked nose with alteration of smell or taste.

Stage II: Signs of meningeal irritation as stiffness of neck (Kernig’s sign), photophobia, seizures, altered mental status, and coma.

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19
Q

Diagnosis of N.fowleri

A
  • Clinical diagnosis
  • Laboratory diagnosis
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20
Q

Clinical diagnosis of N.fowleri

A

C/P with History of swimming or diving in lakes or ponds 2-6 days prior to onset.

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21
Q

Laboratory diagnosis of N.fowleri

A
  • Microscopic examination
  • Culture: non-nutrient agar with Escherichia coli.
  • Molecular diagnosis
  • Mice inoculation
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22
Q

microscopic examination of N.fowleri

A
  • Wet mounts of CSF revealing trophozoites.
  • CSF is purulent but with no bacteria, raised cell count of neutrophils (leucocytosis), elevated protein (> 1gm / L) and low glucose (< 5gm / L).
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23
Q

Treatment of N.fowleri

A
  • Patient must be hospitalized: I.V. Amphotericin-B, Fluconazole and Rifampicin.
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24
Q

Prevention and control of N.fowleri

A
  1. Adequate chlorination of water of swimming pools and public water supplies.
  2. Avoid immersing the head in water during swimming.
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25
Q

Geographical distribution of A. Castellani

A

Worldwide

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26
Q

Morphology of A. Castellani

A
  • Trophozite
  • Cyst
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27
Q

Morphology of A. Castellani trophozoite

A
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28
Q

what characterizes A. Castellani trophozite?

A

multiple small spiky pseudopodia (acanthopodia).

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29
Q

Morphology of A. Castellani cyst

A

Rounded, 20 ΞΌ in size, double wall.

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30
Q

habitat of A. Castellani

A

In environment: fresh water, soil and dust

In man: CNS, eye, skin and lungs.

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31
Q

Infective stage of A. Castellani

A
  • Trophozoite and cyst.
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32
Q

Source of infection by A. Castellani

A

Dust, water and contact lens fluid.

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33
Q

Mode of infection by A. Castellani

A
  1. Inhalation of air, aerosol or dust contaminated with trophozoite or cyst.
  2. Direct invasion through skin and mucosal ulcers.
  3. Through the use of contaminated solutions of contact lenses.
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34
Q

pathway of A. Castellani after infecting someone

A
  • After skin lesion entry or inhalation (Reach lungs), Trophozoites thenm invade the CNS through the blood stream
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35
Q

Method of division of A. Castellani

A

simple binary fission

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36
Q

what type of parasite is A. Castellani?

A

It is opportunistic parasite causing severe disease in immuno-compromised persons.

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37
Q

what forms of A. Castellani may exist in tissues of human?

A

Both trophozoite and cyst stages may exist in tissues of Man.

38
Q

Clinical picture of A. Castellani

A
  • Granulomatous amoebic encephalitis (GAE)
  • Amoebic Keratitis
  • Chronic granulomatous skin lesions
39
Q

what is the course of granulamatous amoebic encephalitis (GAE)?

A

The course is chronic, lasting from weeks to years.

40
Q

Clincal picture of GAE

A
  • Hematogenous spread drom the lungs or skin abrasions –> focal granulomas as tumours (Space occupying lesions)
  • Infected tissues contain trophozoites, cysts and multinucleated giant cells.
  • Clinical picture of intracranial space-occupying lesions with headache, seizures, mental deterioration, paresis, nausea and vomiting may also occur.
41
Q

what causes amoebic keratitis?

A
  • Infection occurs by direct contact of the cornea with contaminated water or contact lens.
42
Q

Diagnosis of A. Castellani

A

GAE of CNS:

a. Identification of trophozoites and/or cysts in CSF or brain tissue biopsy by wet mount or after staining with Giemsa, or immunofluorescent technique.

b. Culture.

43
Q

Treatment of A. Castellani (GAE)

A
  • Sulfamethoxazole/Trimethoprim+ Fluconazole and Rifampicin.
  • miltefosine
44
Q

Prevention and control of A. Castellani

A
  1. Health education.
  2. Avoid swimming in stagnant water.
  3. The use of proper contact lens fluid.
45
Q

Species of African Trypanosomes

A

Species:
- Trypanosoma spp, causing African trypanosomiasis are:
a. Trypanosomagambiense.
b. Trypanosoma rhodesiense.

46
Q

what is another name for Trypanosoma gambiense?

A
  • Polymorphic trypanosomes
47
Q

Geographical distribution of Trypanosoma gambiense

A

Central and West Africa.

48
Q

Morphology of Trypanosoma gambiense

A
49
Q

Life cycle of Trypanosoma gambiense

A

It passes in 2 hosts:
- Vertebrate hosts
- Invertebrate hosts

50
Q

DH of Trypanosoma gambiense in vertebrate host

A

Mainly man (D.H.)

51
Q

RH of Trypanosoma gambiense in vertebrate host

A

domestic animals as pigs, goats and dogs (Reservoir hosts).

52
Q

Habitat of Trypanosoma gambiense in vertebrate host

A

Blood, lymph nodes, CNS

53
Q

IH of Trypanosoma gambiense in invertebrate host

A

Both sexes of Glossina palpalis, tsetse fly (I.H.).

54
Q

Infective stage of Trypanosoma gambiense in intervetebrae hosts

A

Metacyclic trypomastigotes.

55
Q

Mode of infection by Trypanosoma gambiense

A
  1. Biological transmission by the bite of infected Glossina.
  2. Blood transfusion.
  3. Congenital.

(Man acquires infection by the bite of Glossina, where the infective metacyclic trypomastigotes (in vector saliva) are inoculated in the skin during a blood meal.)

56
Q

Clinical picture of Trypanosoma gambiense

A
  • Trypanosomal chancre
  • Stage I disease
  • Stage II disease
57
Q

Trypansomal chancre

A
  • at the site of bite, an indurated painful swelling, which lasts for 1-2 weeks.
58
Q

Stage I disease of Trypanosoma gambiense

A
  • Systemic spread of trypomastigotes
  • Irregular fever, headache, joint and muscle pain.
  • Enlargement of posterior cervical lymph nodes (Winterbottom’s sign), or generalized lymphadenopathy and hepatosplenomegaly.
59
Q

Stage II disease of Trypanosoma gambiense

A
  • Invasion of CNS, after several months β€”> Chronic meningoencephalitis. It manifested by behavioral changes, such as a mental apathy, slow speech and involuntary movements. coma followed by death from the disease, or concurrent infections.
60
Q

Diagnosis of Trypanosoma gambiense

A
  • Clinical
  • Laboratory
61
Q

Clinical diagnosis of Trypanosoma gambiense

A

C/P with history of traveling or residence in endemic areas of Africa.

62
Q

Laboratory diagnosis of Trypanosoma gambiense

A
  • Direct demonstration of polymorphic trypomastigotes by Microscopy of wet mount smears or Giemsa-stained smears in: chancre aspirate, blood, lymph node aspirate, bone marrow, and CSF.
  • Culture: on NNN medium.
  • Animal inoculation.
  • Antibody or Antigen detection by ELISA.
  • Molecular diagnosis.
  • Blood examination: Anaemia, thrombocytopenia.
  • Imaging: CT scan and MRI of the brain show cerebral oedema.
63
Q

Treatment of Trypanosoma gambiense

A

In stage I: Pentamedine and Suramin.

In stage II: Melarsoprol as it can pass blood brain barrier.

Treatment of associated medical conditions as anaemia, infections.

64
Q

Prevention & Control of Trypanosoma gambiense

A

1- Protection against vector bite by skin repellents.
2- Treatment of patients.
3- Control of Glossina (vector).

65
Q

Characters of Trypanosoma rhodesiense

A
  • Clinical features of Rhodesian disease are similar to Gambian but they cause severe fatal disease in short duration.
  • Acute course; CNS is involved early and patients usually die rapidly.
66
Q

What is Secondary Amoebic Cerebral Abscess?

A
  • Invasion of brain tissue by Entamoeba histolytica trophozoite (Cyst never detected in tissue).
67
Q

Pathway of E.histolytica to brain

A
  • E.histolytica trophozoite inhabit large intestine then invasion of submucosal blood vessels may lead to spread of amoebae causing extra intestinal amoebiasis e.g. liver, lung, brain
68
Q

Morphology of E.histolytica trophozoite

A
  • Size: 10-60 ΞΌ (average 20 ΞΌ).
  • Shape: Irregular outline with pseudopodia
  • Cytoplasm: outer clear refractile ectoplasm and inner granular endoplasm
  • Nucleus: It has centrally located fine karyosome and peripheral chromatin dots.
69
Q

Mode of infection by E.histolytica

A
  1. Ingestion of mature quadrinucleated E. histolytica cysts in contaminated food or drink, or through infected food handlers.
  2. Mechanical transmission by flies and cockroaches.
  3. Autoinfection: feco-oral route (hand to mouth contact).
70
Q

Pathogenecity of Secondary Amoebic Cerebral Abscess

A
  • Haematogenous spread from amoebic liver abscess or pulmonary amoebiasis usually causes single brain abscess.
71
Q

Clinical picture of Secondary Amoebic Cerebral Abscess

A
  • It results in secondary amoebic meningoencephalitis, with severe destruction of brain tissue.
  • It manifests as a brain tumor (Space-occupying lesion).
72
Q

Diagnosis of Secondary Amoebic Cerebral Abscess

A
  1. Microscopic examination for detection of trophozoites in CSF samples.
  2. Serodiagnosis: The circulating amoebic antigens or antibodies can detected by IHA, IFA or ELISA.
  3. Radiological examination: by ultra-sonography (US), computed axial tomography (CT) or magnetic resonance imaging (MRI).
73
Q

Treatment of Secondary Amoebic Cerebral Abscess

A
  • Tissue amoebicides: They act against the tissue invasive form (trophozoite).
  • Metronidazole.
  • Tinidazole.
74
Q

Definition of NeuroCysticercosis

A
  • invasion of the human tissues by the larval stage of Taenia solium (Cysticercus cellulosa). In this case man acts as an intermediate host.
75
Q

Mode of infection by NeuroCysticercosis

A

it can develop in different ways:

  • Ingestion of food or water contaminated by the eggs of Taenia solium.
  • Auto- infection
76
Q

autoinfection by NeuroCysticercosis

A

External autoinfection (Exogenous):
- the patient harbouring the adult parasite contaminates his fingers with Taenia solium eggs, Feco-oral.

Internal autoinfection (Endogenous):
- antiperistaltic movements of the intestine (in case of vomiting or taking emetic drugs) leads to regurgitation of the gravid segments to the stomach.

77
Q

Pathogencity of NeuroCysticercosis

A
  • The cyst produces local cellular reaction and infiltration with neutrophils, eosinophils and lymphocytes.
78
Q

Clinical picture of NeuroCysticercosis

A
  • Neurocysticercosis manifests as a brain tumor (Space-occupying lesion).
  • Cerebral cysticercosis results in severe headache, convulsions and paralysis.
79
Q

Diagnosis of NeuroCysticercosis

A

1- Serological tests may be helpful in diagnosis as I.H.A.T and ELISA.

2- Imaging: Ultrasound, C.T. and MRI.

3- X-ray for calcified cyst.

4- Biopsy for histopathological examination.

80
Q

Treatment of NeuroCysticercosis

A
  1. Surgical removal when possible.
  2. Praziquantel combined with corticosteroids for cerebral oedema.
  3. Albendazole is also effective.
81
Q

Prevention & Control of NeuroCysticercosis

A
  1. Early treatment of infected persons to avoid autoinfection
  2. In infected patients with the adult parasite, no nauseating drugs is given.
  3. Avoid the use of human excreta as fertilizer.
82
Q

Parasites infections affecting the eye

A

Acanthamoeba castellani infection, Taenis solium Cysticercosis & Onchocerca volvulus Onchocercosis

83
Q

what is Onchocerciasis?

A
  • Infection of human skin and subcutaneous tissue by Onchocerca volvulus adult and microfilaria.
84
Q

Mode of infection by Onchocerciasis

A
  • Through inoculation of the infective filariform larva present in the mouth of intermediate host (Simulium fly) into skin bite.
  • Adult worms live in fibrous subcutaneous nodules from the host reaction.
85
Q

Clinical picture of Onchocerciasis

A
  • Ocular manifestations (River or Sudan Blindness)
  • Onchocerca nodule (onchocercoma)
  • Severe dermatitis
  • Disturbed skin pigmentation
86
Q

what is Ocular manifestations (River or Sudan Blindness)?

A
  • This is a serious complication of onchocerciasis resulting in blindness.
87
Q

Charaters of Ocular manifestations (River or Sudan Blindness)

A
  • Common when the nodules are in the scalp, neck and shoulders.
  • The microfilariae have great affinity to the eye tissues.
  • It is characterized by keratitis, iritis, uveitis, choroiditis, retinitis and optical atrophy which end in blindness.
88
Q

Causes of Ocular manifestations (River or Sudan Blindness)

A

1- Hypersensitivity to toxins from living and dead microfilariae.

2- Mechanical action of the moving microfilariae in the eye tissues.

89
Q

Characters of Onchocerca nodule (onchocercoma)

A
  • Smooth firm, painless fibrous nodule in the subcutaneous tissue surrounding one to several adults
90
Q

Characters of Severe dermatitis

A
  • Oedema and inflammatory cellular infiltration of the dermis against microfilaria forming granuloma with subsequent fibrosis.
91
Q

Diagnosis of Severe dermatitis

A
  • Clinical
  • Laboratory
92
Q

Laboratory diagnosis of Severe dermatitis

A
  • Direct detection of microfilaria (Diagnostic stage) or adult in Skin-snip biopsy or aspiration from the nodules or tissue biopsy.
  • Patch skin test: 10% of Hetrazan in lanolin cream is applied to an area of skin. In positive cases; papular eruption develop after 8-24 hours.
93
Q

Treatment of onchoria volvulus

A

1 - Ivermectin against microfilaria.

2- Doxycycline against adult worm.

3- Surgical removal of the nodules.

Y2B4 - Central Nervous System πŸ“™ (8 decks)

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