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Flashcards in Chagas Deck (20)
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1
Q

What is the chagas life cycle?

A

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

2
Q

What are the modes of transmission?

A

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%

3
Q

How can chagas be orally transmitted?

A

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%)

4
Q

Epidemiology of chagas

A

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)

5
Q

Pathogenesis of chagas

A

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

6
Q

What is indeterminate chagas?

A

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

7
Q

What occurs in the intestine during chagas?

A

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

8
Q

What is the acute phase of chagas disease?

A

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

9
Q

What is the chronic “indeterminate” phase of chagas?
And determinate chronic chagas?

A

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

10
Q

Chronic chagas: Cardiac

A

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

11
Q

Chronic chagas digestive

A

Develops in 10-15% of patients with chronic infections

Esophagus, rectum and sigmoid colon most affected

12
Q

Megaoesophagus in chronic chagas
and complications

A

Dysphagia
Salivation
Regurgitation
Chest pain
Parotid hypertrophy

rupture
cancer
aspiration pneumonia

13
Q

chronic chagas megacolon

A

Presentation – constipation

Complications
- Faecaloma
- Obstruction
- Sigmoid volvulus
- Ulceration
- Perforation

14
Q

Chagas in immunosuppressed

A

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

15
Q

Diagnosis of chagas

A

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%)

16
Q

Xenodiagnosis

A

Infection free lab strains of reduviid bugs

Allow to feed on patients

Wait 1-2 months for parasite to develop in bugs

Dissect insect hindgut to find parasite

17
Q

Treatment of chagas benznidazole

A

Treatment of choice
Nitroimidazole derivative
Children – 5-10mg/kg/d orally for 60 days – childrn tolerate it better, adults given smaller doses

Adults 5mg/kg/d orally for 60 days

AEs
- Mild to moderate dermatitis in 30%
- Peripheral neuritis up to 40%
- Bone marrow suppression

18
Q

Treatment with nifurtimox

A

5-nitrofluran derivative
Children – 15mg/kg/d orally for 60-90d
Adults – 8-10mg/kg/d orally for 60-90d
Only 50% complete Rx in one study

AEs
- Gastrointestinal (30-70%)
- Mood changes
- Irritability, insomnia
- Peripheral neuropathy

19
Q

Vector control

A

Household spraying with residual pyrethroid insecticides for domestic and peri-domestic vectors

Improved housing

Community education

Screening blood donors in endemic countries

20
Q

Challenges in control

A

Transmission eliminated in Uruguay, southern Brazil and Chile but huge burden of disease remains

Less success in Andean countries
- poorer health access/civili conflic
- different vectors including sylvatic
- large unrecognised problem in many regions