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Flashcards in Parasitology III Deck (19):
1

Leishmania (New World vs. Old World)

New World
- L. Mexicana - cutaneous, rare mucocutaneous
- L. Braziliensis - cutaneous and mucocutaneous
- L. Chagasi - visceral
Old World
- L. Tropica - cutaneous only
- L. Major - cutaneous only
- L. donovani - visceral
- L. infantum - visceral; S. Europe/Mediterranean

2

Leishmania life cycle

1. Sandfly takes blood meal
2. Promastigotes are phagocytized by macrophages
3. Promastigotes transform into amastigotes inside macrophages
4. Amastigotes multiply in cells (including macrophages) of various tissues
5. Sandfly takes a blood meal (Ingests macrophages)
6. Ingestion of parasitized cell
7. Amastigotes transform in to promastigote in sandfly
8. Divide in midgut and migrate to proboscis

3

Leishmaniasis
Reservoir:
Epidemiology:
Diagnosis:

Reservoir: Domestic and wild animals; In India, humans are reservoir for L. major
Epidemiology: 350 million at risk; 12 million infected; tropical and subtropical
Diagnosis: Biopsy or aspirate the lesion, stain with Giemsa, and look for amastigotes

4

Leishmaniasis Presentations (3)

1) Cutaneous Leishmaniasis - Starts as a bump, then an ulcerative sore at primary site; satellite lesions
2) Mucocutaneous - Ulceration nasopharynx tissues - months to years after primary lesion heals
3) Visceral - onset at 2-12 months; splenomegaly and/or hepatomegaly

5

African Trypanosomiasis (African Sleeping sickness)
3 different organisms:

Trypanosoma brucei brucei - cattle (wild game reservoir)
T. brucei rhodesiense - human, acute (wild game reservoir)
T. brucei gambiense - human, chronic (human reservoir)

6

African Trypanosomiasis (West African)
Agent:
Vector:
Distribution:
Reservoir:
Disease:
Mortality:
At risk:

Agent: T. Brucei gambiense
Vector: Riverine tsetse fly
Distribution: West/central africa
Reservoir: Human
Disease: Chronic (years)
Mortality: 100%
At risk: Rural persons

7

African Trypanosomiasis (East African)
Agent:
Vector:
Distribution:
Reservoir:
Disease:
Mortality:
At risk:

Agent: T. brucei rhodesiense
Vector: Savanna tsetse fly
Distribution: east/south Africa
Reservoir: antelope/cattle
Disease: Rapid progression: 1-4 weeks
Mortality: 100%
At risk: rural, visitors to game reserves

8

African trypanosomes - lifecycle

1) Tsetse fly takes a blood meal
2) Injected metacyclic trypomastigotes transform into bloodstream trypomastigotes
3) Trypomastigotes multiply by binary fission in various body fluids
4) Trypomastigotes in blood
5) Tsetse fly takes a blood meal
6) Bloodstream trypomastigotes transform into procyclic trypomastigotes in tsetse fly's midgut
7) Procyclic trypomastigotes leave the midgut and transform into epimastigotes
8) Epimastigotes multiply in salivary gland - they transform into metacyclic trypomastigotes

9

In only __ sub-Saharan African countries can the tsetse fly transmit disease

36

10

Why has there been an increase in Human African Trypanosomiasis since the 1960s

Colonies and wars decreased healthcare concern

11

African Trypanosomiasis
Epidemiology:
Pathology:
Immunity:
Diagnosis:

Epidemiology: Sub-saharan; endemic in tsetse habitat; 60 million at risk, 5 million under surveillance
Pathology: Self healing chancre; waves of parisitemia with fever, serum IgM 10x normal; winterbottoms sign; CNS infection
Immunity: Immune evasion by antigenic variation
Diagnosis: Direct examination of blood, lymph, and CSF

12

Winterbottom's sign

Enlargement of the posterior cervical lymph nodes

13

Chagas' Disease (South American Trypanosomiasis)
Reservoir:
Location:
Transmission:
Epidemiology:

Reservoir: rats, cats, dogs, opossums...
Location: Blood, lymphatics, and tissues
Transmission: Reduviid bugs
Epidemiology: Endemic in SA; 100 million at risk
- Rural: vector/reservoir in proximity to human dwellings
- Urban: contaminated blood supplies; iv drug use
- Transmission is now occuring in US South

14

Lifecycle of T. cruzi (Chaga's disease)

1) Reduviid bug takes a blood meal
2) Metacyclic trypomastigotes penetrate various cells at bite wound site- transform into amastigotes
3) Amastigotes multiply by binary fission in cells of infected tissues
4) Intracellular amastigotes transform into trypomastigotes then burst out of the cell (can infect other cells and start new infection sites)
5) Reduviid bug takes a blood meal
6) Epimastigote stage in midgut
7) Multiplies
8) Metacyclic trypomastigotes in hindgut

15

Chagas' disease Pathology

Acute:
- 2-4 months fever, chagoma (Romana's sign)
- Hematogenous spread; circulating trypomastigotes
- Severe in children; organ involvement leads to death
Chronic:
- Onset at 10-20 years
- No circulating trypomastigotes; persistent amastigotes
- Damage to nerve/muscle cells of heart, esophagus, colon
- Inflammation and autoimmunity leads to severe tissue damage
- death from sudden heart attack is common

16

Chagas disease - Diagnosis

Acute trypomastigotes in blood
chronic - xenodiagnosis

17

Trichomoniasis
Location:
Lifecycle:
Transmission:
Prevention:

Location: Lumenal; urogenital
Lifecycle: No free living or encysted stages
Transmission: Directed by sexual contact
Prevention: Condom use, not 100%

18

Trichomoniasis
Epidemiology:
Pathology (Male vs. Female)

Epidemiology: Worldwide distribution in the sexually active
- Peak age of contraction 16-35
- Globally 160 million/year; USA 3.7 million/year
Pathology: 70% of people are asymptomatic
Female - vaginitis, burning, itching - frothy vaginal discharge with unusual odor - preterm delivery
Male: Itching or irritation inside penis (usually no symptoms)

19

Trichomoniasis
Immunity:
Diagnosis:

Immunity: None - can be re-infected
Diagnosis: Microscopic observation of motile parasites