Parasitology ๐Ÿชฑ Flashcards

1
Q

what is a Congenital parasitic infection?

A

an infection resulting from the transmission of live parasites from an infected pregnant woman to her fetus that persists after birth.

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2
Q

What do Congenital parasitic infection include and exclude?

A

It includes: prenatal (in utero) and perinatal (at time of delivery) transmission.

It excludes: postnatal transmission of parasites by breast milk and transmission of dead parasites or parasite DNA that may transmit from the maternal to the fetal blood.

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3
Q

what are parasites involved in human congenital infections?

A
  1. Toxoplasma gondii
  2. Trypansoma cruzi (Congenital chagas disease)
  3. Plasmodium spp.
  4. Trichomonas vaginalis
  5. African trypanosomes
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4
Q

Is Congenital transmission of helminths rare?

A

yes, rarely in humans

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5
Q

when does Transmission of Congenital Chagas disease occur?

A

in both acute and chronic forms of Chagas disease.

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6
Q

Vectors control & Congenital Chagas disease

A
  • National programs for vector control and screening of blood donors have limited the occurrence of new cases.
  • The possibility of repeating congenital transmission at each pregnancy remains a risk factor in the absence of vectors.
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7
Q

How does Congenital malaria take place?

A
  • Malaria during pregnancy is characterized by sequestration of Plasmodium falciparum-infected erythrocytes in the inter-villous spaces of the placenta.
  • This results in severe perinatal outcomes e.g. still birth, perinatal mortality, low birth weight, and premature delivery.
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8
Q

what does Maternal-fetal transmission of infected erythrocytes result in?

A

Congenital malaria which may worsen the perinatal outcomes.

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9
Q

when does Congenital African trypanosomiasis occur?

A
  • Occurs in the first lymphatic phase of the human African trypanosomiasis.
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10
Q

what does Congenital African trypanosomiasis cause?

A
  • High rates of spontaneous abortion.
  • Hydrocephalus with severe neurological affection in neonates.
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11
Q

Congenital infection with Trichomonas vaginalis

A
  • Rare cases of vaginal, urinary tract, nasal and respiratory infections with T. vaginalis have been reported in newborns of mothers infected with this parasite.
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12
Q

what is Toxoplasmosis?

A

It is a parasitic infection caused by intracellular protozoan Toxoplasma gondii.

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13
Q

Geographical distribution of Toxoplasma gondii

A

Worldwide

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14
Q

Morphology of Toxoplasma gondii

A

Toxplasma gondii (Phylum Apicomplexa) occurs in 4 forms:

  • Trophozoite (Tachyzoite)
  • Pseudocyst
  • True tissue cyst
  • Oocyst
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15
Q

Shape of Trophozoite (Tachyzoite)

A
  • Crescent in shape, 3X6 ฮผ, with pointed anterior end and rounded posterior end.
  • It has posterior nucleus.
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16
Q

Where is Trophozoite (Tachyzoite) found?

A

It is found in the acute stage of infection.

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17
Q

what is the Trophozoite (Tachyzoite) considered?

A

It is the active multiplying stage

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18
Q

what is Pseudocyst?

A

It is full of rapidly multiplying tachyzoites, has no cyst wall.

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19
Q

where is Pseudocyst found?

A

Localized inside the reticuloendothelial cells (RECs).

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20
Q

Morphology of True tissue cyst

A

Round or oval, 5-50 ฮผ in size, contains bradyzoites and has cyst wall.

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21
Q

Where is True tissue cyst found?

A

It is found in the brain (most common site), skeletal and cardiac muscles, and other organs in chronic stage of infection.

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22
Q

what characterizes the True tissue cyst?

A

Remains viable for years, and immunosuppression causes reactivation of cysts.

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23
Q

where is Oocyst stage found?

A

only present in cats.

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24
Q

Morphology of Oocyst stage

A

Oval, 10 x12 ฮผ with a thick wall.

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25
Q

Characteristcs of Oocyst stage

A
  • Excreted unsporulated (immature) in cat ฬs faecesโ†’sporulates (by sporogony) within 3-5 days โ†’ infectious.
  • Mature, sporulated oocyst contains 2 sporocysts, each containing 4 sporozoites (disporocystic tetrazoic oocyst). It may remain viable in moist shaded soil for a year or more
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26
Q

what is the habitat of T. gondii?

A
  • T. gondii is an obligate intracellular parasite, which is found inside the RECs, brain, skeletal and cardiac muscles, and any nucleated cells.
  • It resides inside a parasitophorous vacuole.
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27
Q

Definitive host of T. gondii

A

Cats and other felines.

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28
Q

Intermediate host of T. gondii

A

Man and other mammals (mice, rabbits, goat, sheep, cattle, and pigs), reptiles and birds.

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29
Q

Infective stage of T. gondii

A

All stages are infectious to humans; trophozoites, pseudocysts, true tissue cysts and sporulated oocysts.

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30
Q

What is the mode of infection of T. gondii?

A

Oral route:
- Mature oocysts in contaminated food and drinks.
- Pseudo cysts or true cysts in raw or under cooked contaminated meat.
- Tachyzoites in unpasteurized goatโ€™s and cow ฬs milk.

Inhalation:
- of mature oocysts.

Contamination of skin abrasions:
- during handling and preparation of fresh infected meat, or laboratory workers (accidental inoculation).

Transplacental route:
- tachyzoites from infected pregnant woman to fetus.

Blood transfusion

Organ transplantation

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31
Q

Exoenteric cycle (Asexual cycle) of T.gondii

A
  • It occurs in Man and other intermediate hosts (mammals, reptiles and birds).
  • Sporozoites from oocysts or trophozoites from cysts enter intestinal epithelial cells โ†’tachyzoites multiply by endodyogony
  • Tachyzoites multiply inside macrophages by endodyogony or ectomerogony โ†’form pseudocysts โ†’ruptures.
  • Tachyzoites โ†’spread to organs (e.g. brain, heart, skeletal muscles, eye, liver, spleen) via lymphatic and blood โ†’forming tissue cysts.
  • Bradyzoites remain dormant and get reactivated upon immune suppression.
  • Man acts as blind intermediate host for Toxoplasma.
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32
Q

Enteric cycle (Sexual cycle) of T.gondii

A
  • Enteric cycle occurs in cats (definitive hosts).
  • Cats acquire the infection by true cysts or pseudocysts (from infected rats) or mature oocysts from catโ€™s feces, contaminated food and drinks
  • Trophozoites penetrate intestinal cells, reproduce asexually by schizogony or endopolygony โ†’merozoites โ†’ gametes (gametogony) and zygotes and then immature oocysts to external environment which maturate within 3-5 days to become infective (di-sporocystic tetrazoic).
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33
Q

what are the Forms of asexual multiplication in Toxoplasma gondii?

A

Endodyogeny: Division into two organisms inside the mother cell by internal budding.

Endopolygeny: Division into several organisms at once by internal budding.

Ectomerogony: Simultaneous division into several organisms inside the cyst or pseudocyst by external budding.

34
Q

Pathogenesis of T.gondii

A

In toxoplasmosis, proliferation of tachyzoites in the host cells (intestinal and extra- intestinal), causes cellular death with focal necrosis and surrounding inflammatory cells.

35
Q

Pathogenesis of T.gondii in acute infections

A
  • the outcome of the disease depends on host immune status.

In immunocompetent individuals, tachyzoites disappear from various organs.

In immunocompromised patients, there is dissemination of the parasites through the blood stream to various organs as brain, eyes, lungs, heart, liver, spleen, kidneys, lymph nodes, bone marrow and skeletal muscles, where they form pseudocysts causing severe necrotizing lesions and disease progression.

36
Q

Pathogenesis of T.gondii in chronic infectios

A

true tissue cysts remain viable in tissues for years in resting form. In immunodeficient status, their reactivation cause clinical disease.

37
Q

what causes congenital toxoplasmosis?

A
  • This occurs when the mother get infected for the first time during pregnancy.
  • But, in some woman with chronic infection, reactivation of tissue cysts lead .to liberation of trophozoites, which may infect the fetus.
38
Q

risk and severity of infection by congenital toxoplasmosis

A
  • The risk of fetal infection rises with progress of pregnancy.
  • In contrast, the severity of fetal damage is high, when infection is transmitted in early pregnancy.
39
Q

what is the clinical picture of infection with congenital toxoplasmosis?

A
40
Q

what is the most affected site in case of toxoplasmosis in immunocompromised patients?

A

In these patients affection of brain is more common

41
Q

clinical picture of toxoplasmosis in immunocompromised patients

A
  • In these patients affection of brain is more common, with meningoencephalitis, and neuropsychiatric manifestations.
  • Pneumonia, myocarditis, chorioretinitis and hepatosplenomegaly may occur.
42
Q

clinical picture of acquired toxoplasmosis in immuno sufficient persons

A
  • It is asymptomatic in 80-90% of healthy hosts.
  • The classical clinical sign of acute acquired toxoplasmosis is lymphadenopathy and the deep cervical lymph nodes are the most commenly affected.
  • The infected lymph nodes are discrete and non-tender.
  • Mild fever, headache, myalgia (Flu-like syndrome), and hepatosplenomegaly are often present.
43
Q

Diagnosis of toxoplasmosis

A

Clinical & Laboratory

44
Q

Laboratory diagnosis of toxoplasmosis

A
  • Direct microscopy
  • Indirect serodiagnosis (Most important)
  • Molecular diagnosis
  • Imaging
  • Animal inoculation
45
Q

Direct microscopy in diagnosis of toxoplasmosis

A

Detection of trophozoites and tissue cysts in lymph node, bone marrow, spleen, placenta & blood stained by Giemsa.

46
Q

indirect serodiagnosis toxoplasmosis

A
47
Q

what does the presence of IgM Ab & rising IgG titre signify?

A

Active infection

48
Q

what do IgG anibodies signify?

A

chronic infection

49
Q

Sabin-Feldman dye test

A

Patientโ€™s serum is mixed with a Toxoplasma trophozoites, and methylene blue is added. If the parasite fails to take the stain, the test is considered posititve (Antibodies exist)

50
Q

molecular diagnosis of toxoplasmosis

A
  • For detection of T. gondii DNA in Blood, CSF, urine and also amniotic fluid (for diagnosis of congenital infection).
51
Q

imaging in diagnosis of toxoplasmosis

A
  • MRI, CT scan and X-ray are used to diagnose CNS involvement
  • Ultrasound of fetus at 20-24 week of pregnancy helps to diagnose congenital toxoplasmosis.
52
Q

treatment of congenital toxoplasmosis

A

Neonates with congenital infection are treated with Pyrimethamine and sulfadiazine with folinic acid for one year.

53
Q

treatment of toxoplasmosis in immunocompetent individuals

A
  • Most healthy people recover from toxoplasmosis without treatment
  • Treated with Pyrimethamine and sulfadiazine plus folinic acid.
54
Q

treatment of toxoplasmosis in immuno compromised individuals

A
  • Continuation of medication as long as they are immunosuppressed is necessary
  • Trimethoprim + Sulfamethoxazole (Cotrimoxazole).
55
Q

treatment of toxoplasmosis in pregnant women

A

Spiramycin help in prevention of congenital infection.

56
Q

prevention and control of toxoplasmosis

A
  • Proper washing of hands, vegetables and fruits before eating.
  • Proper washing of hands and utensils after handling raw meat.
  • Proper freezing and cooking of meat before eating.
  • Avoid contact with cats litter box especially pregnant women and immunocomoromised patients.
  • Raw meat should never be fed to cats.
  • Disposal of litter box daily.
  • Screening for T. gondii antibodies in blood banks.
57
Q

what are Sexually transmitted parasites?

A
  • Trichomonas vaginalis (Trichomoniasis)
  • Phthirus pubis (Pubic Lice)
  • Sarcoptes scabiei (Scabies)
58
Q

what are parasites that cause Genital affection as a complication?

A
  • Schistosomes
  • Enterobius vermicularis
59
Q

what is the definition of Trichomoniasis?

A

It is a parasitic infection caused by urogenital flagellate protozoan Trichomonas vaginalis.

60
Q

Geographical distribution of Trichomonas vaginalis

A

Worldwide ,The most common non-viral sexually transmitted infection in the world.

61
Q

Morphology of Trichomonas vaginalis

A
  • Urogenital flagellates
  • It is pear-shaped, 17X10 ฮผ in size.
  • It has a single anterior nucleus.
  • It has 4 flagella anteriorly and an axostyle.
  • It has undulating membrane that extends at the anterior 1/3 of body.
62
Q

Suitable pH of Trichomonas vaginalis

A

Suitable vaginal pH for the parasite is 4.5 โ€“ 6 (low acidic).

63
Q

Habitat of Trichomonas vaginalis

A

females: In vagina, cervix and urethra.

males: In urethra and prostate.

64
Q

Definitive host of Trichomonas vaginalis

A

Man

65
Q

Infective stage of Trichomonas vaginalis

A

Trophozoite

66
Q

Multiplication type of Trichomonas vaginalis

A

By longitudinal binary fission.

67
Q

Mode of infection by Trichomonas vaginalis

A
  • Sexual transmission (Direct sexual contact).
  • Non-sexual transmission via contaminated towels or toilet seats.
  • Infection from infected mothers to babies during birth.
68
Q

Pathogenesis of Trichomonas vaginalis

A
  • Cytoadhesion and degradation of target cells.
  • Cytotoxic contact-dependent effects result in cytolysis, disruption of host tissues and hemolysis.
  • Endocytosis and phagocytosis of host cells, bacteria, viruses and fungi.
  • Immune evasion and interaction with vaginal-associated microflora.
69
Q

Is Trichomonas vaginalis related to any cancer?

A

A relationship between trichomoniasis and cervical carcinoma is suggested

70
Q

what does Trichomonas vaginalis cause in females?

A

In female: infection results in vaginitis, cervicitis, urethritis and cystitis.

71
Q

what does Trichomonas vaginalis in males?

A

In male: infection results in urethritis, vesiculitis, epididymitis and prostatitis.

72
Q

what are the predisposing factors for pathogenecity of Trichomonas vaginalis?

A
  1. Change of the normal vaginal bacterial flora and pH.
  2. Decrease in the secretory IgA.
73
Q

Clinical picture of Trichomonas vaginalis in females

A

(Trichomoniais may be asymptomatic in infected males (95%) and females (50%).)

  • Vaginal offensive, profuse leucorrheic discharge.
  • Burning, Itching, frequency of maturation, dysuria and nocturia.
  • On examination: the vaginal wall is red, inflamed with petechial hemorrhages (strawberry mucosa), mucosal erosion and vulval erythema.
74
Q

Clinical picture of Trichomonas vaginalis in males

A

Dysuria, nocturia, and the prostate may be enlarged and tender.

75
Q

Clinical picture of Trichomonas vaginalis in Newborn

A

Respiratory tract infection and conjunctivitis may affect infants during vaginal delivery of an infected mother.

76
Q

Diagnosis of Trichomonas vaginalis

A
  • Clinical
  • Laboratory (Specimen - Direct smear - Culture - Serology - Molecular diagnosis)
77
Q

Specimens used for diagnosis of T. vaginalis

A
  • vaginal discharge in females.
  • Prostatic fluid in males.
  • Urine examination in both; males and females.
78
Q

Wet smear (Diagnosis of T. vaginalis)

A
  • Detection of (Trichomonas trophozoites = diagnostic stage) in: Wet smear or fixed smears (stained with Giemsa)
79
Q

Culture (Diagnosis of T. vaginalis)

A

Diamondโ€™s media or InPouch culture (trophozoite detection).

80
Q

Treatment of T. vaginalis

A
  • Metronidazole or Tinidazole.
  • Both partners must be treated at the same time.
81
Q

Prevention & control of T. vaginalis

A
  • Good personal hygiene.
  • Treatment of both partners simultaneously.
82
Q

Compare between (Pubic liceโ€phthirus pubisโ€ - Sarcoptes sacbiei - Shistosomes - Enterobius vermicularis) in terms of:

  • General characters
  • Transmission
  • Infective stage
  • Diagnostic stage
  • Pathological lesions
  • Epidemology & risk factors
  • Treatment
A

Refer to โ€œ L2: Genital parasitic infectionsโ€