Chagas Flashcards
What is the chagas life cycle?
Sylvatic cycle the reduviid bug feeds on animals like possum, an animal which invaes peri-domestic space, causing localised transmission.
In wild strains of reduviid bugs in palm tree, bitten by bug at night, become infected
What are the modes of transmission?
Vector borne transmission and bloodborne transmission with blood products – but lyophilisation will sterilise blood products - 10 to 20% risk
Congenital transmission, risk 1-10% of child being infected by mother during pregnancy
Oral transmission
Transmission from organs during transplantation, 20-30%
How can chagas be orally transmitted?
Sylvatic bugs enter houses and defecate in food
Bugs or bug faeces in food, fruit juices, leads to infection e.g fruits grown in palm trees, bugs can be crushed with fruit
Higher infectious dose and greater morbidity and mortality (8-35%)
Epidemiology of chagas
Number of people infected with american trypanosomiasis varies over the years, currently estimates 8-10 million of people infected in latin america.
Distribution throughout latin america, mainly south and also central america.
Currently 10m infected in endemic areas
- 325,000 cases in USA
- 100,000 cases in europe (87% in spain where people from latin america migrate)
Pathogenesis of chagas
Tissue damage caused by parasite replication and host inflammatory response
Parasite invades cells, host recognises those cells and kills them, resulting in damage to host cells and an inflammatory response around area of damage
Acute illness resolves with effective immune response and parasite sequestration in tissues
- Protective mediated by Th1 cytokines (e.g IFN-g) and NO – requried to clear parasites
Chronic disease caused by progressive low intensity destruction of infected cells like
- Nerves – autonomic nervous system – purkinje fibres in heart, autonomic ganglia in intestine
- Muscle cells – myocytes and intestinal smooth muscle
What is indeterminate chagas?
After acute infection, most people will go to develop indeterminate chagas (20-70%), no clinical signs of illness. During this period there is ongoing immune response against parasite.
Can’t find trypomastigotes on blood slides but they’re still there, just in low numbers, cleared by number of cells like
- NK cells that release TH1 cytokines like IFN-Y, activate macrophages to kill infected cells
- down reg of host immune response/dampening inflammatory response through mechanisms like IL-10, CTLA-4 - so you don’t get damage to nerve and muscle cells whilst immune response slowly kills parasites
What occurs in the intestine during chagas?
Inflammatory lesions in the enteric autonomic nervous system associated with a substantial reduction in the number of neurons – peristalsis becomes less and less effective, gut contents don’t get moved on you and you get ballooning of the gut
Motility disturbances and constipation in large intestine – large intestine unable o expel faeces
Rectum, sigmoid colon and oesophagus most affected with striking luminal enlargement and muscular hypertrophy
What is the acute phase of chagas disease?
Incubation 1-2 weeks after bite
up to months after transfusion, trypanosomes in blood
Occurs within 3 weeks
Generally mild or asymptomatic
- Local inflammatory swelling (Romana)
- Nodule or chagoma
- Fever
- Anorexia
- Lymphadenopathy
1-2% diagnosed
Symptoms last 8-10 weeks
Rarely (young and IS)
- Hepatosplenomegaly
- Acute myocarditis
- Meningoencephalitis
- Fatality <5% of symptomatic
What is the chronic “indeterminate” phase of chagas?
And determinate chronic chagas?
Lifelong infection
Generally trypanosomes not detectable but often positive for parasite DNA
Seropositive
60-70% of infected
Normal ECG and X-rays
Determinate chronic disease – developed over time in people with indeterminant
Seropositive
30-40% of infected 10-30 years after infection
5-10% develop chronic chagas immediately after acute disease – severe damage
Can present as cardiac disease, cardiodigestive or digestive disease
Chronic chagas: Cardiac
Chagas cardiomyopathy there is enlarged heart
Apical aneurysm seen – attenuation of the heart wall and the apex of the left ventricle, may have a thrombus inside.
Enlargement of heart, so heart valves and chambers don’t work effectively
Develops in 20-30% of chronic infections
Abnormalities in conduction system
- Right bundle branch block
- Left anterior fascicular block
- Ventricular premature beats
- ST-T changes
- Q waves
Heart failure
- Right ventricular failure > left ventricular failure
Mural thrombi
- Thromboembolism
Sudden death
- Cause of death (2/3rds)
- VT/VF, complete AV block or SN dysfunction
Chronic chagas digestive
Develops in 10-15% of patients with chronic infections
Esophagus, rectum and sigmoid colon most affected
Megaoesophagus in chronic chagas
and complications
Dysphagia
Salivation
Regurgitation
Chest pain
Parotid hypertrophy
rupture
cancer
aspiration pneumonia
chronic chagas megacolon
Presentation – constipation
Complications
- Faecaloma
- Obstruction
- Sigmoid volvulus
- Ulceration
- Perforation
Chagas in immunosuppressed
May reactive in HIV (2-%)
Transplantation of kidneys/livers
- Reactivation of chronic infection
- Recipients from infected donors
Reactivation following heart transplantation
- In brazil, chagas is 3rd most frequent indication for Tx
Reactivation following chemotherapy for cancer
Presents as fever, myocarditis, skin lesions and meningocenphalities (HIV)
High mortality when unrecognised
Diagnosis of chagas
Thick and thin film (Giemsa)
- Acute disease / reactivation
- Thick film more concentrated blood
- Thin film you smear the blood over a slide so it’s more dispersed
Serology – 2 different tests
- ELISA with specific antigens
- Indirect fluorescent antibody (IFA) test
- Indirect haemagglutination
PCR for T.cruzi DNA
- Acute (90%)
- Chronic (80%)
