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African and American trypanosomiasis
Jarmila Kliescikova, MD, 1st Faculty of Medicine, Charles University in Prague
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Sleeping sickness
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Sleeping sickness• Kinetoplastida: Salivaria
Trypanosoma brucei gambiense
Western and central Africa (chronic disease)
Trypanosoma brucei rhodensiense
East and SE Africa (acute disease)
Extracellular parasiteVector: tse-tse fly (Glossina)
DRC, Angola, CAR, South Sudan - prevalence up to 50%.
1. or 2. most common cause of death in these countries
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In Africa, patients with sleeping sickness are poor live in remote / poor / unstable / neglected areas
Patient prognosis is dependent on accurate and early diagnosis and staging
The incidence of sleeping sickness has decreased in the most affected countries since 2000 ( elimination ?)
The maintenance of vertical programmes are more difficult to justify and fund integration into existing health structures is the trend practical and cheap diagnostic tools must be used
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Epidemiology
Distribution: tropical Africa (Chad, Congo, Cote de Ivoire, Guinea, Malawi, Uganda, Tanzania, CAR)
Botswana, Swaziland and Namibia – trasmission seems interruped
Connected to the vector distributionPrevalence approximately - 50 mil.
20 – 50 thousand new cases per year
Approximately 55 thousand deaths/year
Belongs to so called neglected diseasesEast African form rarely imported to Europe – infection usually during safari
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Simarro et al., 2010
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The vector = Glossina spp. – both genders able to transmit the disease
T. b. gambiensae
Gl.palpalis/tachinoides – River glossina
The maximum is the end of dry season
Antroponoosis – human is the main reservoir, rarely dog,
swine, sheep, cattle,..
T. b. rhodesiensae
Gl. morsitans/fuscipes Savannah glossina
Zoonosis – reservoir antelope, lions, cattle, sheeps, dogs
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Life cycle
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Pathogenity
CSF Leptomeningitis
Site of inoculation
Lymph, blood
Local inflammation
Chronic inflammation of the lymph system
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Variable Surface Antigens change = The main mechanism of pathogenicity
• Variabile surface coat VSG
(variabile glycoproteins)
• Trypanosomas posses several different genes coding the surface antigens
• VSG protects from phagocytosis and lysis by alternative complement pathway
• Exhaustion of the immune system
• Toxic and end metabolic products of trypanosomas released in the organism
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The surface antigen changes
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Alteration of the human immune response
Malvy and Chappuis, 2011
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Clinical infection: I.Local reaction
IP 6-14 days
Local reaction at inoculation site: oedema, erythema
„chancre“ formation (Grafs chancre) (trypanozomas found in the secret)
Hyperpigmentation of skinIntermitent fever
Loal lymphadenopathy
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Graafs chancre
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Malvy and Chappuis, 2011
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2. Heamolytical stage:
Lymfadenitis
Cervical nodes
Generalisation
• Intermittent fever generalized weakness, headache
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2. Haemolymphatic stage:
Posterior
cervical
lymphadenopathy
Nodes are soft, non dolorous, elastic
Winterbotts sign
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2. heamolymphatic stage
Hepatosplenomegy
Subcutaneous oedemas(face, lids)
Exantema – tripanid
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2. Heamolymphatic stage:
Myocarditis tachycardia (100-140/min); heart failure
AnaemiaPolyneuropathy
sensitive, motoric
Weakness kachexia
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3. Meningoencefalic stage
Periferal polyneuropathy (late hypersteasia after pressure on limbs and muscles, pruritus)
HeadacheInverse sleep
Personality, character changesChorea, atetosis, dyskinesis, tremor, ataxia, tonic-clonic seizures
Sexual behaviour dysfunctions, endocrinne dysregulation
Wasting syndrome
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CT, NMR:
Atrophic changes, hydrocephalus, thickening of meninges
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T.b gambiensae T.b.rhodesiensaeEPIDEMIOLOGY: Middle, West Africa East. Africa
Rezervoir Human, (dog, pig, ..) Antelopes, cattle
Vector River glossina Savannah glossina
Clinical course Chronic Acute
Incubation period 1 – 3 weeks 1 – 3 weeks
Chancre 0, not always present Present, large
Fever Slow onset up to 39°C Acute, chills, > 39°C
Lymph nodes Enlarged Insignificat
Oedemas insignificant Present, esp. In children
Myokarditis Not always Very common
Invasion of CNS After 1 – 2 years after 3-6 months., earliest in 1 month
Inflammatory CNS reaction
High Weak
Fatal without treat. 1-6 years Within 1 year
Rat infection Mild course Fatal
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Laboratory• ESR (> 100 mm/h)
• Blood count• Anaemia: severe, normochromatic• Lymphocytosis and monocytosis with relative
neutropenia• Trombocythopenia
• Serum protein• Total increase• Hypergamaglobulineamia and macroglobulinaemia (↑ IgM)• Elevation of α2-globulins
• CSF (v II. stage)• Proteinrhachia (up to 10% IgM)• Mononuclear cells
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Diagnostics – direct methods
• Biopsy of ulcus, local lymph nodes
• Blood film, thick film
• Concentration techniques
• CSF examination
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Current diagnostic approach and tools
Sleeping sickness
I. Screening: Serology (CATT, IFI, ELISA) Cervical lymph node palpation
II. Diagnostic confirmation (parasitology): Cervical lymph node puncture Detection of trypanosomes in blood
I. Stage determination: CSF examination (LP): Search for trypanosomes (centrifugation) WBC/mm3 > 5 Raised IgM
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Blood film
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Brun at al., 2010
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Serology
Agglutination tests:
Paper stripes
Only for T.b.gambiense
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THERAPY
T. b. gambiensae
T. b. rhodesiensae
Early phase PentamidinSuramin
Suramin
Late phase (cerebral)
MelarsoprolEflorithineNifurtimox
Melarsoprol
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• Acute trypanosomiasis• Suramin (BAYER 205, ANTRYPOL)
• 5 mg/kg v 5-10 ml H2O slow i.v. 1. day• 10 mg/kg v 10 ml H2O slow i.v. 3. day• 20 mg/kg v 10 ml H2O i.v. 5.,11.,17.,23.and 30. d
• Pentamidin isethionate (PENTACARINATE)• 3-4 mg/kg (150-300 mg)/day i.m. or i.v
Every other day, together 7-10 doses
• Chronic trypanosomiasis• Melarsoprol (MEL B, ARSOBAL)
Strictly i.v. slow injection with increasing dosage, max. 3,6 mg/kg/day in several (3-4) 3-4 day cycles
• Before malarsoprol use suraminem or pentaminidine (Jarisch-Herxheimer reaction)
• High toxicity (5-10% fatal) arsenic encephalopathy• Mannitol i.v. in isotonic glucose á 6 hours.• Prednisolon 50 mg/day, dexametason 6-8 mg/day i.v.EFLORITHINE -2 weeks 4 infusions per day
THERAPY
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Vector control
http://influentialpoints.com/Gallery/Tsetse-flies_Louse-flies_and_Lice.htm
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American trypanosomiasis
Trypanosoma cruzi – Kinetoplastida: Stercoraria
• Vector: Triatoma; Rhodnius• Chagas disease• Rezervoir: human, live stock• Transmission: by vector transfusion/transplantation transplacentary
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Where are we now: 2012
• Transmission by Triatoma infestans halted in 1999 in Uruguay, 1999 in Chile, 2006 in Brazil and 2009 in Guatemala
• Triatoma eliminated also from some parts of Argentina and Paraguay
• Disease now „common“ in non-endemic areas: Europe and USA
• WHO launched an initiative for controlling of disease in non-endemic areas
• USA Food and Drug Administration approved the first serological screening for blood donors
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• Emergence of secondary domestic and peridomestic vectors
• 8-11 mil people infected predominantly in Mexico, Central and South America
• Incidence has dropped from 700 000 new cases per year to 40 000
• The number of deaths has dropped from approximately 45 thousand to 12 500 (chronic kardiomyopathy)
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Europe and Chagas disease
3 periods:
Description of Chagas disease and in 1980 first case description in Europe
Description of non-endemic transmission via transfusion or congenital transmission (southern
Europe, Spain)
Chagas disease recognized as global problem – transmission reported in 28 countries worldwide
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Basile et al, Eurosurveillance, 2009
Estimates of migrant residents from Chagas disease endemic areas in nine studied European countries
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Source: Basile at al, Eurosurvaillence, 2009
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Estimated number of migrants infected with Chagas disease
Basile et al., Eurosurveillance 2009
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Underdiagnosis of Chagas disease in Europe
Basile et al., Eurosurveillance 2009
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Estimated congenital transmission in Europe
Basile et al., Eurosurveillance 2009
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Endemic Chagas disease distribution 2011
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Triatoma/Rhodnius
Blood sucking bed bugsThe parasite is found within
feaces
Actively penetrates the skinTransmitted by adults and progeny
Biting at night
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Typical sites of vector multiplication
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Typical sites of vector multiplication
The vector can live in the crevices that are common in the mud and wood used to build walls and floor
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Chagas Disease in a Domestic Transmission Cycle in Southern Texas, USA
real and predicted distribution of Triatoma gerstaeckeri
Beard et al, 2003 from CDC
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Life cycle
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Trypanosoma cruzi
• Intracellular parasite• Spread by blood to different
organs• Preference: RES heart cells muscle cells neuroglia• In blood the flagellated forms are
found• Intracellulary amastigotes are
found
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Chagas disease has two phases
Acute phase:
Local or diffuse inflammation of myocardium
Chronic phase
Inflammatory fibrotic reaction damaging the cardiac muscle and conduction network and
the enteric nervous system
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Pathofyziology
• Autoimmune mechanisms: molecular mimicry, release of cryptic antigens, polyclonal lymphocyte activation, epitope spread
• But the role is still controversial (immunosuppresion, HIV…)
• The role of Th8 lymphocytes (shift to another population when treated)
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Pathophysiology • Host response can cause tissue damage
(Th8 lymphocytes producing granzymes and other cytokines)
• Progression to symptomatic disease involves imbalance between T-helper 1 and 2 responses
• Heart: conduct system, parasympatic nerve
• Hypertrophy, fibrosis, thinning of the left ventricular wall, aneurysma, thrombes formation
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Clinical symptoms.Primary leasion
• Induration at entry point – inoculative chagoma: local inflammation, amastigotes in lipocytes
• Inudrated erythematous papule (1-3 cm) local lymphadenopathy
• Romaña sign – oedema of lids, conjunctivitis
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French female with Romana sign after visiting her parents
from French Guzana, Source: CDC
http://wwwnc.cdc.gov/eid/article/14/4/07-0489_article.htm
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Indeterminate Chagas disease
• Seropositivity for Ch. disease
• Normal chest radiograph and EKG
• Abscence of clinical signs and symptoms
• One third of patients progresses to symptomatic disease
Some patients: abnormal contractility on Echo, Areas of cardiac fibrosis…
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Acute phase
• ID: 2-3 weeks• Asymptomatic vs symptomatic• Continuous fever 38 C, max evening (38-40 C)• Local vs generalised lymphadenopathy• Morbilliform rash (chest, stomach)• Mild hepatosplenomegaly• Subcutaneous oedema – face, limbs• Myocarditis, endocarditis, pericarditis heart
failure• Meningoencefalitis – mortality less than 5%
(children)• Acute phase will disappear within 2-3 months
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Silva N et al. J Acquir Immune Defic Syndr Hum Retrovirol, 1999.
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Two thirds of patients – cardiac form, one third GIT form
Progression 10-30 years after infection
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Cardiac disease
Early: malaise, palpitations, syncope, abdominal pain (right upper quandrant),
jugular venous distension, peripheral oedema, stroke
Late: Atypical chest pain, syncopal episodes, sudden cardiac death, dyspnoea,
orthopnoea, fatigue, murmurs, stroke
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GIT disease
• Megaoesophagus: dysphagia, regurgitation, odynophagia, oesophagitis, aspiratory pneumonia, hiccups
• Megacolon: chronic constipation, meteorism, chronic abdominal pain, bacterial overgrowth syndrome, malabsorbtion, ileus – toxické megacolon
• Megaureteres
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Congenital disease
• Increased by increased pregnancies, high maternal parasitemia…
• Risk of approximately 5% in endemic and non-endemic areas
• 10-30% babies symptomatic, 10% die within first 2 days without treatment
• Prematurity, low birthweight, hepatomegaly, splenomegaly, jaundice, oedema, RDS, meningoencephalitis
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Transplanation
• Kidney – 20-35%
• Live and haemopoietic cells
• Reactivation after transplantation: heart (20-75%), liver and haemopoietic cells
• Myocarditis, Meningoencephalitis, nodules and plaques on skin
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Chagas disease and HIV+
• Reactivation of latent infection
• CNS – 75% cases
• Hypodense leasions; necrohaemorrhagic leasions,
• Fever, cefalea, seazures, vomiting, focal neurological deficiency
• Treatment must be early and continued for 30-60 days
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PrognosisScore for the progression of cardiac involvement• Age older than 50 years; 2 points• Systolic diameter more than 40 mm; 3 points• Intraventricular conduction disorders; 2 points• Sustained ventricular tachycardia; 3 points• Benznidazole treatment; –2 pointsRisk of progression is• 3 ・ 6% for a score of 0• 6 ・ 9% for a score between 1 and 3• 16% for a score between 4 and 6• 52 ・ 5% for a score above 7Prognostic score for mortality from Chagas disease• New York Heart Association III–IV; 5 points• Cardiomegaly; 5 points• Wall motion disorders; 3 points• Non-sustained ventricular tachycardia; 3 points• Broadened QRS complex; 2 points• Male sex; 2 pointsRisk of death is• 2% at 5 years and 10% at 10 years for a score between 0 and 6 points• 18% at 5 years and 44% at 10 years for a score between 7 and 11 points• 63% at 5 years and 84% at 10 years for a score between 12 and 20 points
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Diagnostics
Acute phaseBlood film
Concentration methods
Biopsy of the lymph nodes, CSF
PCR
Blood culture, xenodiagnostics
Chronic phaseSerology
HIV, congenital, transplantation
such as in acute phase
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Positive skin test T. cruzi
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Chronic phase of infection
XENODIAGNOSTICS
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• Nifurtimox (LAMPIT)• 2,6 – 3,6 mg/kg (children 3-5 mg/kg) p.o. 3x
day 90 days
• Benznidazol (RADANIL)• 2,5 – 3,5 mg/kg (children 5 mg/kg) p.o. 2x
day 60 days• Also effective in early chronic phase
• Allopurinol
• Symptomatic treatment of chronic phase
• Follow up by decline of antibodies levels
Therapy for acute or congenital disease, reactivation or for children
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