Kinetoplastids & Protozoan STDs Flashcards
1
Q
Types of infection w/ diff strains of Leishmaniasis Leishmania mexicana L braziliensis L major (where) L infantum (where)
A
- Leishmania mexicana is cutaneous, rarely mucocutaneous
- L braziliensis is cutaneous and mucocutaneous.
- L major is cutaneous only. Found in India and Europe.
- L infantum is visceral. Found in southern Europe / Mediterranean.
2
Q
Leishmaniasis Location Reservoir Life Cycle Diagnosis Prevention
A
- Location: blood and tissues
- Reservoir – domestic and wild animals (dogs, rodents; zoonosis). Humans are reservoir for L major in India
- Life cycle: Sandfly bites humans to introduce. Flagellated organisms live and multiply in macrophages. Eventually burst out and are taken up by next sandfly. No sexual development in sandfly.
- Diagnosis – biopsy or aspirate lesion, stain w/ Giemsa to look for amastigotes. CDC does DNA tests in US.
- Prevention: vector control, avoid fly habitats
3
Q
Leishmaniasis Transmission
Vector
Endemic areas
A
- Transmission – vector-borne via sandfly. Also vertical transmission.
- Sandflies are common in southern US, but those that transmit to humans are not found in US. Are found in Caribbean, Brazil, Middle East (military)
- Fly → human → fly → human, etc, can occur in urban areas.
4
Q
Leishmaniasis Pathology
Cutaneous
Mucocutaneous
Visceral
A
- Cutaneous: starts as a bump → ulcerative sore at primary site. Satellite lesions may also form. Amastigotes and macrophages are abundant in the lesions. Heal spontaneously but cause scarring.
- Mucocutaneous – L braziliensis is most common. Metastasis months / years after primary lesion heals. Involves ulceration of nasopharynx w/ presence of amastigotes. Scars. Drugs cure and lead to immunity.
- Visceral: onset 2-12 months after infection. Primary skin lesions are rare. Spreads to internal organs. Fever, wasting due to malabsorption, hepatosplenomegaly. Death often due to secondary infection. Drugs cure and lead to immunity.
5
Q
Leishmaniasis Treatment
Cutaneous
Mucocutaneous
Visceral
A
- Cutaneous: typically self-resolves w/ scarring. Fluconazole reduces scarring for L major.
- Mucocutaneous: amphotericin B is DOC but expensive. Antimonials are more often used worldwide but don’t work as well.
- Visceral: miltefosine is DOC. Amphotericin B is alternate.
6
Q
West vs East African Sleeping Sickness Name Vector Distribution Reservoir Timeline Mortality At risk pxs Which is more common?
A
Name: west = Trypanosoma brucei gamiense. East = T brucei rhodesiense
Vector: west = riverine tsetse fly. East = savanna tsetse fly.
Distribution: west: west / central Africa. East: east / south Africa
Reservoir: west = humans. East = antelope / cattle
Timeline: west = chronic (years). east = rapid (1-4 weeks)
Mortality: both are 100% if untreated
At risk: rural persons. Epidemic in areas of civil war / social turmoil (Angola, Congo, Sudan). All Sub-Saharan.
Gambiense (West) is more common / wider spread.
7
Q
African Sleeping Sickness General name Location Transmission Life cycle Immunity Diagnosis (2) Prevention
A
- Trypanosoma brusei
- Location: blood, lymphatics, tissue
- Transmission: vector-borne via tsetse fly which lives near rivers / forests.
- Life cycle: Tsetse fly takes blood meal and infects human. Parasite multiplies via binary fission in multiple human fluids (blood, lymph, CSF). Extracellular. Fly takes another blood meal to spread.
- Immunity: robust initial humoral response but drops off. Evasion by antigenic variation. Changes surface proteins.
- Diagnosis: Direct exam in blood, lymph, or CSF (rhodesiense). Wet mount or geimsa stain. Card agglutination test (not in US b/c not very accurate)
- Prevention – vector avoidance / control, prophylaxis w/ pentamadine. Aggressive tx.
8
Q
Pathology for Gambian (West African) Trypanosoma
Early, Middle, Late
A
- Early: painful self-healing chancre at site of bite. Disseminates through lymphatics to blood.
- Middle (2-3 weeks):
- Waves of parasitemia w/ fever. Serum IgM is 10x normal.
- Winterbottom’s sign: lymphadenopathy of posterior cervical nodes
- Late (6-24 months):
- CNS infection: edema, dementia, sleepy, motor impairment
- Death via coma (hence sleeping sickness) or secondary infection.
- 100% fatal if untreated
9
Q
Pathology for Rhodesian (East African) Trypanosoma
A
Similar to Gambian but w/ accelerated rate. Death in 6-9 months.
10
Q
Chagas Disease Scientific and unscientific names Location Reservoir Prevention
A
- Trypanosoma cruzi / South American Trypanosomiasis
- Location: blood, lymphatics, tissues (intracellular)
- Reservoir: rats, cats, dogs, possums, etc. Huge reservoir b/c there is no specificity.
- Prevention: vector control, good housing, screen blood supply
11
Q
Chagas Transmission
A
- Transmission: vector-borne w/ reduvid bugs, blood transfusion, IV, transplant, vertical. Transplants in US are not tested for Chagas as of now.
- Rural: vector/reservoir in proximity to humans
- Urban: contaminated blood supplies / IV drug use
- Rare disease occurs in southern US. Bug found in most of US but doesn’t carry yet.
12
Q
Chagas Life Cycle
A
- Bug poops on human while feeding and cruzi is rubbed into the skin / eye. Not injected.
- Cruzi enters cells and replicates via binary fission. Burst out of cell to enter blood. Tropism for nerve / muscle cells, especially cardiac cells.
- Bug takes another blood meal to spread.
13
Q
Chagas Pathology (acute vs chronic)
Timeline
Sxs
More severe in which pxs?
A
- Acute infection occurs 2-4 months after bite. Mild.
- Low fever, chagoma at site of entry (Romana’s sign = upper eyelid inflammation)
- Severe in kids though. Organ involvement may cause death. Adults usually control via humoral and cell-mediated immunity.
- Chronic infection occurs 10-20 years later and is more severe.
- No circulating trypomastigotes, but amastigotes are present.
- Damages nerve / muscle cells of heart, esophagus, and colon.
- Heart becomes enlarged and dysfunctional. Death from MI is common.
- Inflammation and autoimmunity → severe tissue damage such as megacolon.
14
Q
Chagas Diagnosis
A
- Diagnosis: acute uses trypomastigotes in blood. Chronic uses xenodiagnosis. Now have strip assay to detect T cruzi Abs.
- Xenodiagnosis: expose possibly-infected tissue to a vector and then examine the vector for presence of microorganism it may have ingested.
15
Q
Trichomoniasis Name How common? Location Life cycle Diagnosis Treatment Prevention
A
- Trichomonas vaginalis
- CDC top 5 due to birth complications. As prevalent as syphilis, gonorrhea, and Chlamydia combined.
- Location: lumenal, urogenital
- Lifecycle: no free living or encysted stages. Only trophozoite that replicates by binary fission, is motile, and aerotolerant.
- Diagnosis - Easy to see on vaginal smear b/c it is moving around. Flagellated, so very motile. DNA test now available. Usually diagnosed after checking for other STDs.
- Treatment: metronidazole is DOC; tinidazole if resistant. Screen sex partners. Check for other STDs.
- Prevention: condoms, don’t share sex toys.
