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ZEB 122 > Chpt 2.26-49 > Flashcards

Chpt 2.26-49 Flashcards

1
Q
  1. Which of the following is the most suitable biopsy material for isolating Toxoplasma gondii? a. Lymph nodes b. Skin c. Mice d. Guinea pigs
A

Explanation: Lymph nodes are a common site of Toxoplasma gondii infection and are therefore the most suitable biopsy material for isolating the parasite.

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2
Q
  1. Which serological test is considered the gold standard for diagnosing toxoplasmosis? a. Complement fixation test b. Sabin-Feldman dye test c. Direct agglutination test d. Fluorescent antibody test
A

Explanation: The Sabin-Feldman dye test is historically considered the gold standard due to its high specificity and sensitivity. However newer molecular techniques are becoming increasingly important.

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3
Q
  1. What is the recommended treatment for both human and animal toxoplasmosis? a. Pyrimethamine and Sulphonamides b. Antibiotics and antivirals c. Vaccination and deworming d. Supportive care and observation
A

Explanation: Pyrimethamine often combined with sulfadiazine or another sulphonamide is a first-line treatment for toxoplasmosis. The specific treatment regimen depends on the severity and location of the infection.

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4
Q
  1. What type of organism causes Leishmaniasis? a. Bacteria b. Virus c. Protozoan d. Fungi
A

Explanation: Leishmaniasis is caused by protozoa of the genus Leishmania.

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5
Q
  1. Which of the following is NOT a clinical manifestation of Leishmaniasis? a. Cutaneous Leishmaniasis b. Muco-cutaneous Leishmaniasis c. Visceral Leishmaniasis d. Cerebral Leishmaniasis
A

Explanation: While Leishmania can sometimes affect the central nervous system cerebral leishmaniasis is rare and not considered a typical clinical manifestation. The other three are well-recognized forms.

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6
Q
  1. What is another name for Visceral Leishmaniasis? a. Oriental sore b. Espundia c. Kala-azar d. Sleeping sickness
A

Explanation: Kala-azar is the common name for visceral leishmaniasis reflecting its devastating effects.

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7
Q
  1. What is the causative agent of Kala-azar? a. Leishmania tropica b. Leishmania braziliensis c. Leishmania donovani or L. infantum d. Trypanosoma brucei
A

Explanation: Leishmania donovani and L. infantum are the main causative agents of visceral leishmaniasis (Kala-azar).

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8
Q
  1. Where is Kala-azar endemic? a. North America b. Europe c. Indian subcontinent d. Australia
A

Explanation: Kala-azar is endemic to parts of the Indian subcontinent as well as other regions in Africa South America and the Mediterranean.

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9
Q
  1. What is the primary mode of transmission for Visceral Leishmaniasis? a. Contact with infected animals b. Contaminated food or water c. Bite of infected sandflies d. Inhalation of spores
A

Explanation: Visceral leishmaniasis is transmitted through the bite of infected female Phlebotomus sandflies.

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10
Q
  1. What is the role of dogs in the transmission of Kala-azar? a. Primary host b. Reservoir host c. Incidental host d. Vector
A

Explanation: Dogs are important reservoir hosts for Leishmania donovani maintaining the parasite’s cycle and contributing to transmission.

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11
Q
  1. What is the name of the flagellar form of Leishmania donovani that develops in the sandfly vector? a. Promastigote b. Amastigote c. Trypomastigote d. Epimastigote
A

Explanation: Promastigotes are the flagellated forms found in the sandfly vector.

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12
Q
  1. What is the name of the non-flagellar form of Leishmania donovani that develops in the mammalian host? a. Promastigote b. Amastigote c. Trypomastigote d. Epimastigote
A

Explanation: Amastigotes are the non-flagellated forms that infect and multiply within the macrophages of the mammalian host.

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13
Q
  1. Where do amastigotes of Leishmania donovani primarily multiply in the human host? a. Bloodstream b. Liver c. Macrophages d. Skin
A

Explanation: Amastigotes reside and multiply inside macrophages (a type of immune cell).

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14
Q
  1. What is the typical duration of the incubation period for Visceral Leishmaniasis? a. 1-2 weeks b. 1-2 months c. 2 months - 2 years d. 2-5 years
A

Explanation: The incubation period for visceral leishmaniasis is highly variable ranging from a couple of months to several years.

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15
Q
  1. Which of the following is NOT a common clinical feature of Visceral Leishmaniasis? a. Fever b. Splenomegaly c. Lymphadenopathy d. Hepatomegaly
A

Explanation: While hepatomegaly (enlarged liver) can occur splenomegaly (enlarged spleen) is a more consistent and prominent clinical feature of visceral leishmaniasis.

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16
Q
  1. What is the most reliable diagnostic method for Visceral Leishmaniasis in endemic areas? a. Clinical examination b. Microscopic examination of tissue aspirates c. Serological tests d. Complete blood count
A

Explanation: Direct visualization of Leishmania amastigotes in tissue aspirates (e.g.

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17
Q
  1. Which organ provides the highest sensitivity for detecting Leishmania amastigotes in aspirates? a. Liver b. Lymph nodes c. Bone marrow d. Spleen
A

Explanation: Bone marrow aspirates often yield the highest parasite load and thus the greatest diagnostic sensitivity.

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18
Q
  1. What is the major limitation of antibody detection tests for diagnosing Visceral Leishmaniasis? a. High cost b. Low sensitivity c. Antibodies may persist after successful treatment d. Requirement for specialized equipment
A

Explanation: A major limitation is the persistence of antibodies after successful treatment which can lead to false-positive results.

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19
Q
  1. Which of the following is NOT a key factor driving the increase in Visceral Leishmaniasis incidence? a. Improved sanitation b. HIV co-infection c. Malnutrition d. Migration
A

Explanation: Improved sanitation would generally reduce the incidence of vector-borne diseases like visceral leishmaniasis.

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20
Q
  1. What is the recommended first-line treatment for Visceral Leishmaniasis? a. Antimonials b. Amphotericin B c. Pentamidine d. Miltefosine
A

Explanation: Antimonials (e.g. sodium stibogluconate) have historically been the first-line treatment though resistance is emerging and other drugs like liposomal amphotericin B and miltefosine are increasingly used. The best choice depends on local resistance patterns and patient factors.

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21
Q
  1. What is the clinical presentation of the acute form of HAT?a. Fever adenitis and rash b. Hepatosplenomegaly c. Meningoencephalitis d. Coma and death
A

Explanation: The acute stage of HAT (Human African Trypanosomiasis) is characterized by fever swollen lymph nodes (adenitis) and a skin rash.

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22
Q
  1. How is the chronic form of HAT characterized?a. Fever and adenitis b. Meningoencephalitis and wasting c. Hepatosplenomegaly d. Cutaneous lesions
A

Explanation: The chronic stage involves the central nervous system leading to meningoencephalitis (inflammation of the brain and meninges) weight loss (wasting) and ultimately coma and death if untreated.

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23
Q
  1. Where is HAT found?a. Central and South America b. The Mediterranean region c. Sub-Saharan Africa d. Southeast Asia
A

Explanation: HAT is endemic to sub-Saharan Africa.

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24
Q
  1. What is the causative agent of Gambian trypanosomiasis?a. Trypanosoma rhodesiense b. Trypanosoma brucei gambiense c. Leishmania donovani d. Trypanosoma cruzi
A

Explanation: Trypanosoma brucei gambiense is the parasite responsible for the Gambian form of sleeping sickness.

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25
Q
  1. What is the mode of transmission for Gambian trypanosomiasis?a. Contact with infected animals b. Contaminated food or water c. Bite of an infected tsetse fly d. Mother-to-child transmission
A

Explanation: Transmission occurs through the bite of an infected tsetse fly.

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26
Q
  1. What is the primary host for Trypanosoma brucei gambiense?a. Wild animals b. Humans c. Cattle d. Pigs
A

Explanation: Humans are the primary host for T. b. gambiense.

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27
Q
  1. What is the role of humans in the transmission of Trypanosoma brucei gambiense?a. Vector b. Reservoir c. Incidental host d. Intermediate host
A

Explanation: Humans act as a reservoir maintaining the parasite’s life cycle and enabling its spread.

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28
Q
  1. Which of the following factors does NOT influence the transmission of Trypanosoma brucei gambiense to humans?a. The density of Glossina populations b. Glossina longevity c. Glossina susceptibility to infection d. The presence of other trypanosome species
A

Explanation: While the presence of other trypanosomes might affect the overall dynamics of the ecosystem it’s not a direct factor in T. b. gambiense transmission to humans.

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29
Q
  1. Which form of Human African Trypanosomiasis is considered a zoonosis?a. Gambian trypanosomiasis b. Rhodesian trypanosomiasis c. Both forms are zoonoses d. Neither form is a zoonosis
A

Explanation: Rhodesian trypanosomiasis is considered a zoonosis because the primary reservoir is in animals (wild game).

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30
Q
  1. What is the primary animal reservoir for Trypanosoma rhodesiense?a. Dogs b. Cats c. Cattle d. Rodents
A

Explanation: Various wild animals particularly cattle serve as the primary reservoirs for T. rhodesiense.

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31
Q
  1. Which tsetse fly species is the primary vector for Trypanosoma rhodesiense?a. Glossina palpalis b. Glossina morsitans c. Glossina fuscipes d. Glossina tachinoides
A

Explanation: Different Glossina species are vectors in different regions G. morsitans is prominent for T. rhodesiense.

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32
Q
  1. What is the typical duration of the clinical signs and symptoms of Human African Trypanosomiasis?a. Months to years b. Days to weeks c. Weeks to months d. Years to decades
A

Explanation: The duration can be quite variable depending on the form treatment etc.

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33
Q
  1. What are the initial symptoms of the first stage of Human African Trypanosomiasis?a. Meningoencephalitis b. Chancre and lymphadenopathy c. Hepatosplenomegaly d. Cardiac arrhythmias
A

Explanation: A chancre (sore at the bite site) and swollen lymph nodes (lymphadenopathy) are early signs.

34
Q
  1. What characterizes the second stage of Human African Trypanosomiasis?a. Chancre and lymphadenopathy b.Meningoencephalitis c.Hepatosplenomegaly d. Cardiac arrhythmias
A

Explanation: The second stage involves invasion of the central nervous system leading to meningoencephalitis.

35
Q
  1. What is Winterbottom’s sign?a. Enlarged posterior cervical lymph nodes b. Splenomegaly c. Hepatomegaly d. Skin rash
A

Explanation: Winterbottom’s sign refers to enlarged lymph nodes in the back of the neck.

36
Q
  1. What is the most frequent complaint in the first stage of Human African Trypanosomiasis?a. Headache b. Fever c. Muscle aches d. Lymphadenopathy
A

Explanation: Fever is a very common initial symptom.

37
Q
  1. What is a key feature of the fever experienced in the first stage of Human African Trypanosomiasis?a. Continuous b. Low-grade c. Recurrent d. Absent
A

Explanation: The fever tends to be recurrent or intermittent.

38
Q
  1. What two principles guide the control of Human African Trypanosomiasis?a. Vector control and case detection b. Vaccination and chemotherapy c. Environmental sanitation and health education d. Isolation and quarantine
A

Explanation: Controlling the tsetse fly vector and early diagnosis are crucial for managing HAT.

39
Q
  1. What is the most effective way to reduce man’s exposure to tsetse fly bites?a. Destruction of tsetse fly breeding sites b. Use of personal protective measures c. Treatment of infected individuals d. Vaccination
A

Explanation: Personal protective measures (e.g. protective clothing repellents) are vital in reducing exposure.

40
Q
  1. What is the cornerstone of Human African Trypanosomiasis control?a. Case detection b. Vector control c. Treatment d. Prophylaxis
A

Explanation: Early diagnosis and treatment are essential to preventing progression to the more serious chronic stage.

41
Q
  1. What was considered the gold standard for serological diagnosis of T.b. gambiense in the 1970s? • a. Card agglutination test (CATT) • b. Indirect fluorescent antibody test (IFAT) • c. Enzyme-linked immunosorbent assay (ELISA) • d. Polymerase chain reaction (PCR)
A

Answer: a, Explanation: In the 1970s before the widespread availability and use of ELISA and PCR the CATT was considered the most practical and widely used serological test for diagnosing T.b. gambiense infection due to its simplicity cost-effectiveness and ease of use in resource-limited settings.

42
Q
  1. What is the advantage of the CATT over the IFAT for diagnosing T.b. gambiense? • a. Higher sensitivity • b. Higher specificity • c. Lower cost • d. Ease of use
A

Answer: c, Explanation: While both tests were used the CATT offered a significant advantage in terms of cost-effectiveness making it more suitable for mass screening programs in endemic areas.

43
Q
  1. What type of test is the CATT? • a. Latex agglutination test • b. Indirect fluorescent antibody test • c. Enzyme-linked immunosorbent assay • d. Polymerase chain reaction
A

Answer: a, Explanation: CATT uses latex particles coated with antigens to detect antibodies in the patient’s serum. Agglutination (clumping) indicates a positive result.

44
Q
  1. What is the primary advantage of the card indirect agglutination test (CIAT) for T.b. gambiense? • a. Higher sensitivity • b. Use of smaller volumes of reagents • c. Faster results • d. Higher specificity
A

Answer: c, Explanation: CIAT is a rapid diagnostic test providing results much faster than other serological methods.

45
Q
  1. What is considered the most sensitive and reliable method for diagnosing T.b. gambiense? • a. Serological tests • b. Parasitological methods • c. Clinical examination • d. Molecular methods
A

Answer: d, Explanation: While serological tests are useful molecular methods such as PCR offer superior sensitivity and specificity particularly in detecting low parasitemia and during early stages of infection.

46
Q
  1. Which method provides definitive confirmation of Human African Trypanosomiasis diagnosis? • a. Serological tests • b. Microscopic examination of body fluids • c. Clinical examination • d. Molecular methods
A

Answer: b, Explanation: Direct visualization of the parasite in blood or cerebrospinal fluid (CSF) through microscopy is considered the gold standard for confirming the diagnosis.

47
Q
  1. What is the recommended method for confirming diagnosis in seropositive individuals who are negative by conventional parasitological tests? • a. CATT • b. IFAT • c. Miniature anion-exchange centrifugation technique (mAECT) • d. Polymerase chain reaction (PCR)
A

Answer: d, Explanation: PCR is highly sensitive and can detect the parasite’s DNA even when parasitemia is low making it ideal for confirming cases where conventional microscopy fails to detect the parasite.

48
Q
  1. What was the primary method of vector control for Glossina before the advent of insecticides? • a. Modification of vegetation • b. Use of traps and screens • c. Aerial spraying • d. Biological control
A

Answer: a, Explanation: Before widespread insecticide use clearing vegetation and altering habitats to make them less suitable for tsetse fly breeding and survival was a primary control strategy.

49
Q
  1. What is the standard treatment for early-stage Human African Trypanosomiasis? • a. Pentamidine • b. Melarsoprol • c. Suramin • d. Eflornithine
A

Answer: a, Explanation: Pentamidine is the drug of choice for treating early-stage T.b. gambiense and T.b. rhodesiense infections.

50
Q
  1. What is the standard treatment for late-stage Human African Trypanosomiasis? • a. Pentamidine • b. Melarsoprol • c. Suramin • d. Eflornithine
A

Answer: b, Explanation: Melarsoprol is used to treat late-stage disease though it has significant toxicity. Eflornithine is an alternative less toxic treatment.

51
Q
  1. Which of the following is NOT a criterion for diagnosing late-stage trypanosomiasis? • a. Cerebrospinal fluid white cell count > 5/mm3 • b. Presence of trypanosomes in the blood • c. Cerebrospinal fluid protein > 37mg/100ml • d. Presence of trypanosomes in cerebrospinal fluid
A

Answer: c, Explanation: While elevated CSF protein is often seen in late-stage disease a value above 37mg/100ml is not universally considered a definitive criterion. The presence of trypanosomes in the CSF is more critical for diagnosis.

52
Q
  1. What is the goal of control campaigns in endemic foci of Human African Trypanosomiasis? • a. Reduce the vector population • b. Eliminate the parasite • c. Treat all infected individuals • d. Develop a vaccine
A

Answer: a, Explanation: Control campaigns primarily focus on reducing the tsetse fly vector population as eliminating the parasite entirely is currently not feasible.

53
Q
  1. What is the basis for most vector control methods for tsetse flies? • a. Their attraction to specific colors and odors • b. Their sensitivity to insecticides • c. Their preference for certain breeding sites • d. Their susceptibility to biological control agents
A

Answer: a, Explanation: Many control methods including traps and targets exploit the tsetse fly’s attraction to specific visual and olfactory cues.

54
Q
  1. What are the disadvantages of older chemical methods used for tsetse fly control? • a. Low effectiveness and high cost • b. Resistance development in tsetse flies • c. Adverse effects on human health • d. Environmental pollution
A

Answer: d, Explanation: Older chemical methods especially aerial spraying of broad-spectrum insecticides caused significant environmental damage and harm to non-target organisms. All options listed are disadvantages but environmental pollution is arguably the most significant overall.

55
Q
  1. What is the most effective type of trap for tsetse flies in West and Central Africa? • a. Biconical • b. Pyramidal • c. Monoconical • d. Vavoua
A

Answer: c, Explanation: Monoconical traps are widely used and effective in many regions of West and Central Africa.

56
Q
  1. What type of trap is more effective in areas with a high density of vegetation? • a. Biconical • b. Pyramidal • c. Monoconical • d. Vavoua
A

Answer: b, Explanation: Pyramidal traps are designed to be more effective in densely vegetated areas.

57
Q
  1. What is another name for American Trypanosomiasis? • a. Sleeping sickness • b. Kala-azar • c. Chagas disease • d. Espundia
A

Answer: c, Explanation: American Trypanosomiasis is commonly known as Chagas disease.

58
Q
  1. What is the causative agent of American Trypanosomiasis? • a. Trypanosoma brucei gambiense • b. Trypanosoma rhodesiense • c. Trypanosoma cruzi • d. Leishmania donovani
A

Answer: c, Explanation: Trypanosoma cruzi is the causative agent of Chagas disease.

59
Q
  1. The Sabin-Feldman dye test is a highly specific and sensitive test for detecting Toxoplasma gondii antibodies.
A

Answer: True, Explanation: The Sabin-Feldman dye test is a serological test that was historically considered the gold standard for diagnosing toxoplasmosis due to its high sensitivity and specificity. However, it has largely been replaced by more modern methods like ELISA.

60
Q
  1. In cutaneous leishmaniasis, lesions are typically found on internal organs.
A

Answer: False, Explanation: Cutaneous leishmaniasis, as the name suggests, involves lesions on the skin. Visceral leishmaniasis affects internal organs.

61
Q
  1. The spleen is often enlarged (splenomegaly) in patients with visceral leishmaniasis.
A

Answer: True, Explanation: Splenomegaly is a common clinical manifestation of visceral leishmaniasis due to the parasite’s replication in macrophages within the spleen.

62
Q
  1. Dogs are the main reservoir of Leishmania donovani in all endemic areas.
A

Answer: False, Explanation: While dogs can be reservoirs for Leishmania species, including L. donovani, they aren’t the primary reservoir in all endemic areas. The reservoir can vary depending on the geographic location.

63
Q
  1. Leishmania donovani amastigotes replicate within macrophages.
A

Answer: True, Explanation: Amastigotes, the intracellular form of Leishmania, are the replicative stage within the macrophages of the mammalian host.

64
Q
  1. Cutaneous leishmaniasis lesions always heal within a few weeks.
A

Answer: False, Explanation: The healing time for cutaneous leishmaniasis lesions can vary greatly depending on the species of Leishmania, the patient’s immune response, and other factors. Some lesions may persist for months or even years.

65
Q
  1. Mucocutaneous leishmaniasis can lead to severe disfigurement of the face.
A

Answer: True, Explanation: Mucocutaneous leishmaniasis, caused by certain Leishmania species, can cause destructive lesions affecting the mucous membranes of the nose, mouth, and throat, leading to significant disfigurement.

66
Q
  1. Tsetse flies transmit Trypanosoma brucei by injecting saliva into their host.
A

Answer: True, Explanation: Trypanosomes are transmitted when an infected tsetse fly takes a blood meal; the parasites are injected with the fly’s saliva.

67
Q
  1. Humans are the only reservoir for Trypanosoma rhodesiense.
A

Answer: False, Explanation: While humans are a significant reservoir for T. rhodesiense, it also circulates in wild animal reservoirs, particularly antelopes.

68
Q
  1. Early diagnosis and treatment are crucial for a good prognosis in Human African Trypanosomiasis.
A

Answer: True, Explanation: Early treatment significantly improves the chances of recovery and prevents the progression of the disease to its more severe and often fatal stages.

69
Q
  1. Describe the life cycle of Leishmania donovani, including the different stages in both the sandfly vector and the human host.
A

Answer: The Leishmania donovani life cycle involves two hosts: a sandfly vector and a mammalian host (human). In the sandfly, promastigotes (elongated, flagellated forms) multiply in the sandfly’s gut. When an infected sandfly feeds, it injects metacyclic promastigotes into the mammalian host. In the human host, metacyclic promastigotes are phagocytosed by macrophages. They transform into amastigotes (non-flagellated forms) and multiply intracellularly within the macrophages. These infected macrophages are transported throughout the body, leading to visceral dissemination. When another sandfly takes a blood meal from an infected human, it ingests macrophages containing amastigotes, which transform back into promastigotes within the sandfly gut, restarting the cycle.

70
Q
  1. List the clinical features of visceral leishmaniasis.
A

Answer: Clinical features of visceral leishmaniasis (kala-azar) include: Fever, Hepatosplenomegaly (enlarged liver and spleen), Anemia, Leucopenia (low white blood cell count), Thrombocytopenia (low platelet count), Weight loss, Cachexia (severe wasting), Lymphadenopathy (swollen lymph nodes).

71
Q
  1. Explain why antibody detection tests may not be reliable for diagnosing visceral leishmaniasis in endemic areas.
A

Answer: Antibody detection tests (like ELISA or IFA) may not be reliable in endemic areas due to: High prevalence of infection: A high proportion of the population may have been exposed to Leishmania and possess antibodies, even if they don’t have active visceral leishmaniasis. This leads to false positives. Cross-reactivity: Antibodies against other related parasites may cross-react, giving false positive results. Low sensitivity in early stages: Antibody detection may be insensitive during early stages of infection before a significant antibody response develops.

72
Q
  1. Outline the different forms of cutaneous leishmaniasis and their respective causative agents.
A

Answer: Cutaneous leishmaniasis can manifest in different forms: Cutaneous leishmaniasis (CL): Caused by various Leishmania species (e.g., L. tropica, L. major, L. braziliensis). Oriental sore (L. tropica and L. major): Characterized by single or multiple papules or nodules which ulcerate. American cutaneous leishmaniasis (L. braziliensis): More variable clinically, can be localized or diffuse, and includes forms like uta (nasal and mucosal involvement).

73
Q
  1. Describe the pathogenesis of mucocutaneous leishmaniasis.
A

Answer: Mucocutaneous leishmaniasis (MCL) is typically caused by Leishmania braziliensis. Parasites spread from an initial cutaneous lesion, likely via lymphatic dissemination. They then invade and destroy the mucous membranes of the nose, mouth, and throat. The pathogenesis involves immune evasion by the parasite and an immune response leading to chronic inflammation and tissue destruction. The exact mechanisms of mucosal invasion are still under investigation.

74
Q
  1. Explain the difference between Gambian and Rhodesian trypanosomiasis, including their causative agents, vectors, and reservoirs.
A

Answer: Gambian trypanosomiasis: Causative agent: Trypanosoma brucei gambiense, Vector: Glossina palpalis and Glossina fusca (riverine tsetse flies), Reservoir: Primarily humans (anthroponotic). Rhodesian trypanosomiasis: Causative agent: Trypanosoma brucei rhodesiense, Vector: Glossina morsitans (bush tsetse flies), Reservoir: Wild mammals (zoonotic), with humans as incidental hosts. The key differences are the causative agent, the vector species, and the primary reservoir. Rhodesian trypanosomiasis progresses more rapidly and is generally more acute than Gambian trypanosomiasis.

75
Q
  1. Discuss the importance of vector control in the management of Human African Trypanosomiasis.
A

Answer: Vector control is critical in managing HAT because it directly targets the transmission pathway. Reducing the tsetse fly population significantly decreases the chance of human infection. Various strategies, including insecticide spraying, targeted traps, and habitat modification, can be employed. Vector control is often crucial in eliminating HAT in endemic areas or to reduce new infections in populations.

76
Q
  1. Describe the different diagnostic methods used for Human African Trypanosomiasis, highlighting their advantages and limitations.
A

Answer: Diagnostic methods for HAT include: Microscopy: Direct examination of blood and cerebrospinal fluid (CSF) for parasites. Advantage: Gold standard for confirmation if parasites are found. Limitation: Low sensitivity, especially in early stages, needs skilled microscopist. Serological tests (e.g., CATT, ELISA): Detect antibodies. Advantage: High sensitivity, useful for screening. Limitation: Can give false positives in endemic areas, doesn’t distinguish between species or stages. PCR: Detects parasite DNA. Advantage: High sensitivity, useful when parasitemia is low. Limitation: More expensive and requires specialized equipment.

77
Q
  1. Outline the treatment options for early-stage and late-stage Human African Trypanosomiasis.
A

Answer: Early-stage: Pentamidine (for both T.b. gambiense and T.b. rhodesiense) or suramin (T.b. rhodesiense). Late-stage: Melarsoprol (for both, but highly toxic), eflornithine (T.b. gambiense only), nifurtimox-eflornithine combination (NECT).

78
Q
  1. Describe the key features of American trypanosomiasis, including its causative agent, vector, and clinical manifestations.
A

Answer: Causative agent: Trypanosoma cruzi, Vector: Triatomine bugs (kissing bugs), Clinical manifestations: Acute phase (often asymptomatic or mild) and chronic phase (cardiomyopathy, megacolon, megaesophagus).

79
Q
  1. What are the three main factors driving the increased incidence of visceral leishmaniasis?
A

“Answer: Three main factors contributing to increased visceral leishmaniasis (VL) incidence are: Immunosuppression: HIV/AIDS and other conditions causing immunosuppression increase susceptibility to VL. Environmental changes: Deforestation, urbanization, and climate change can alter vector habitats and

80
Q

What are the advantages of using traps and screens for tsetse fly control?

A

Targeted approach: Reduces harm to non-target species. Environmentally friendly: No pesticides used. Cost-effective (in some situations): Can be locally produced and maintained. Improved surveillance: Captures provide information about fly populations.

81
Q

List three synonyms for American trypanosomiasis.

A

Chagas disease, American trypanosomiasis, Trypanosoma cruzi infection

82
Q

Describe the mode of transmission for American trypanosomiasis.

A

American trypanosomiasis (Chagas disease) is transmitted primarily through the feces of infected triatomine bugs (kissing bugs). While the bug feeds on blood, it defecates, and the parasite enters the host through breaks in the skin, mucous membranes, or the conjunctiva. Transmission can also occur through blood transfusion, organ transplantation, congenital transmission from mother to child, and consumption of contaminated food.

ZEB 122 (10 decks)

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