TRYPANOSOMIASIS Flashcards
TRYPANOSOMIASIS is caused by
Trypanosoma spp
They are flagellates that live in blood and tissues of their human hosts
Belonging to the phylum: Sarcomastigophora
Class: Mastigophora
AETIOLOGICAL AGENTS
Trypanosoma brucei has three subspecies:
1. Trypanosoma brucei (an animal pathogen)
2. Trypanosoma brucei gambiense
3. Trypanosoma brucei rhodesiense
The last two species cause African trypanosomiasis or sleeping sickness in man
Trypanosoma cruzi causes South American trypanosomiasis or Chagas disease
African Trypanosomiasis
Transmitted by the tsetse fly (Glossina spp.), found across Africa (14°N and 29°S of the equator).
Human African trypanosomiasis (HAT) caused by two subspecies of the extracellular protozoan parasite
HAT: diseases with distinct clinical and epidemiological patterns
1. T. b. gambiense: chronic form in Central and West Africa and represents >95% of all cases
2. T. b. rhodesiense: a more acute disease form in East and Southern Africa
Epidemiology
HAT common in:
Rural areas (suitable habitats for the tsetse fly vector and frequent human– tsetse contact)
Periurban areas (especially where riverine)
People can be infected while farming, fishing, hunting, collecting water or wood (exposes them to insect bite)
All age groups and both sexes are at risk (prevalence is higher in adults, and sex distribution varies in relation to gender-specific at-risk activities)
Reservoir: T. brucei gambiense (human)
T. brucei rhodesiense (domestic and wild animals )
HABITAT: connective tissue spaces of various organs, reticular tissue of the lymph nodes and spleen, intercellular spaces in the brain, lymph channels throughout the body, blood and cerebrospinal fluid
MORPHOLOGY: T. b. gambiense exists as trypomastigote form in the blood of the vertebrate host.
It is said to be polymorphic, occurring in three forms: a long slender form having a flagellum, a short stumpy form without a flagellum and an intermediate form
Vectors
Thirty-one tsetse species and subspecies are classified as forest, riverine, or savannah, according to morphological differences and habitat preference
Transmission of T. b. gambiense is linked to species favoring riverine vegetation (Glossina fuscipes, Glossina palpalis)
T. b. rhodesiense is typically transmitted in wood land savanna habitats (G. fuscipes, G. morsitans, G. pallidipes)
Vector Biology
The vector for HAT is the tsetse fly
Inhabits rural areas
Bites during daytime hours
Both males and females are capable of carrying and transmitting the disease
Clinical features of HAT
These depend on the T. brucei subspecies, host response, and disease stage
Generally, both forms of the disease lead to death if untreated
T. brucei rhodesiense disease is typically acute, progressing to second stage disease within a few weeks, and death within 6 months
T. brucei gambiense disease follows a chronic progressive course
Life Cycle of Trypanosoma brucei gambiense
- When an infected tsetse fly bites a person (or animal), it injects a form of the protozoa that can cause infection (called trypomastigotes) into the skin. The protozoa move to the lymphatic system and bloodstream.
- Inside the person, they change forms and travel to organs and tissues throughout the body, including lymph and spinal fluid.
- The protozoa multiply in the bloodstream and other body fluids.
- They circulate in the bloodstream.
- A fly ingests the protozoa when it bites an infected person.
- Inside the fly, the protozoa change forms and multiply.
7–8. The protozoa travel to the fly’s salivary glands, multiply, and change into trypomastigotes—the form that is injected when the fly bites a person
Stages of T.brucei
Typically 2 stages: haemolymphatic stage followed by meningoencephalitic stage (trypanosomes cross the blood–brain barrier and invade the CNS)
3–4-cm dermal reaction at the site of the tsetse bite (inoculation chancre) appears within 2–3 days (rarely seen in those with T brucei gambiense disease)
Discuss the first stage of T.brucei
Systemic features: Fever, Debility, Headache, Facial oedema, Anaemia (mainly haemolytic), Lymph node enlargement (mainly posterior cervical)
Skin: Rash, Chancre, Pruritis
Gastro-intestinal features: Hepatic dysfunction and hepatomegaly Splenomegaly
Heart: Early tachycardia, Myocarditis, Congestive cardiac failure, Pericarditis
Endocrine dysfunction: Menstrual disorders, sterility and abortion, Premature still births, Loss of skin hair, Loss of libido and impotence, Gynaeacomastia, Testicular atrophy and orchitis
Eye: Iritis, Iridocyclitis, Keratitis, Conjunctivitis, Choroidal atrophy
Discuss the second stage of T.brucei
Psychiatric and mental disturbances: Lassitude and indifference, Anxiety and irritability, Mania and agitation, Violent and suicidal behaviour, Uncontrolled sexual impulses, Hallucinations and delirium
Sleep disturbances: Daytime somnolence, Nocturnal insomnia, Uncontrollable urges to sleep
Motor disturbances: Pyramidal signs, Extrapyramidal (abnormal movements and tremors), Muscle fasciculation, Slurred speech, Cerebellar ataxia, Neuritis and polyneuritis
Sensory disturbances: Pruritis, Paraesthaesia, hyperaesthesia, anaesthesia
Abnormal reflexes: Palmo-mental reflex
Visual involvement: Double vision, Optic neuritis, Optic atrophy, Papilloedema
Principle features
Laboratory diagnosis of HAT
Depends on the demonstration of the trypomastigote forms of the parasite
In blood, lymph node aspirates, sternal bone marrow, cerebrospinal fluid or fluid aspirated from the trypanosomal chancre
By direct microscopic examination of unstained and stained films
Serologic techniques may be employed for mass field surveys
Treatment of HAT
Suramin or Pentamidine isethionate (in primary stage infections that do not involve the CNS)
Melarsoprol (in late secondary CNS stages of trypanosomiasis)
American Trypanosomiasis
Caused by Trypanosoma cruzi
It occurs in Central and South America, causing Chagas disease
Population at risk
Neglected Infection of Poverty (NIP)- impoverished people in the U.S.
Occupational groups
Veterinarians, laboratory personnel
Wildlife handlers
Hunters
Travelers to endemic areas
Discuss Trypanosoma cruzi
Habitat: lives as trypomastigote in the blood and as an amastigote in reticuloendothelial cells and other tissue cells of man and many mammals
Most common locations of the parasite in man are the reticuloendothelial cells of the spleen, liver, lymph nodes, bone marrow and myocardium
two main morphologies
Morphology: two main morphologies are seen in human hosts – trypomastigote forms and amastigote forms
Vector of chagas disease
Triatomine insects: Reduviid bugs, kissing beetle/bug, assassin bug
Clinical features of Chagas disease
Acute phase
Parasites found in blood
Most adults asymptomatic
Chagoma
Localized painless induration
Romaña’s sign
Edema of eyes, conjunctivitis
Usually resolves in weeks to months
Indeterminate phase of Chagas
Indeterminate phase
Asymptomatic phase of varying length
Parasites disappear from blood
Most patients enter chronic phase within 5 to 15 years
Chronic phase of Chagas
Chronic phase
Characterized by organ failure
Heart disease
Most common form of chronic Chagas
Many manifestations may occur
Digestive system abnormalities
Megaesophagus
Megacolon (due to reduced nerve supply to the megacolon)
Laboratory diagnosis of Chagas disease
Microscopic examination – in acute infection, T. cruzi may be found transiently in the peripheral blood by direct microscopy of Giemsa stained and unstained, wet blood film
Culture – blood and other specimens can be inoculated in Novy-MacNeal-Nicolle (NNN) medium
PCR
Animal inoculation
Xenodiagnosis
Immunoassay
Serodiagnosis – for chronic stage
Biopsy – of involved lymph node or muscle may reveal amastigote forms of T. cruzi
Treatment of Chagas disease
Nifurtimox or Benznidazole are used
Prevention of Chagas
Sanitary prophylaxis
Land spray of insecticide, bush clearing and elimination of game animals
Control and eradication of tsetse vector: Insecticides, Sterile male technique, Pheromone baited tsetse traps, Use screens/bed nets when sleeping
Good husbandry of animals at risk and avoid contact with tsetse flies as much as possible
Medical prophylaxis
Drugs such as isometamidium chloride and quinapyramine sulphate can be used as prophylactic during high seasonal parasitic pressure
No vaccines are available
Other Preventive Measures of Chagas
Cook contaminated foods
Screen blood and organ donors
Occupational risk groups
Wear gloves, other PPE
Travelers
Wear thick clothing
Avoid substandard housing
Life Cycle of T. Cruzi
- Trypomastigotes enter takes a blood meal and passes metacyclic trypomastigotes in faeces, the trypomastigotes enter the bite wound or musocal membranes such as the conjunctiva.
- Inside the host, trypomastigotes invade nearby cells, transforming into intracellular amastigotes.
- Amastigotes multiply by binary fission and differentiate into trypomastigotes.
- Trypomastigotes are released into the circulation, infecting cells in various tissues.
- The parasite replicates only within host cells or the insect vector.
- The kissing bug becomes infected by feeding on blood containing circulating parasites.
- Parasites undergo transformation and multiplication within the insect vector, eventually forming infective metacyclic trypomastigotes in the hindgut.
What can affect how chagas is manifested in an individual?
Immunocompromised people can be severely affected
Pregnant women
Congenital infection, premature birth
AIDS patients
Brain abscesses
Higher likelihood of reactivation
