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NATURAL HISTORY OF CHAGAS DISEASE/AMERICAN TRYPANOSOMIASIS (Trypanosoma cruzi)

PREPATHOGENESIS PERIOD

AGENT FACTORS:
Protozoan parasite: Trypanosoma cruzi
Susceptible to: disinfectants, direct sunlight, other harsh environments

ENVIRONMENTAL FACTORS:
A. External Environment
Infected feces of triatomine vector
Geographical distribution: Latin America, Central and South America, Mexico, and other European Countries
Poor-quality housing and sanitation eg. adobe or unfinished brick walls and roofs made of thatch
Presence of pets at home

B. Internal Environment
Human: heart, esophagus, colon, and peripheral nervous system
Digestive tract of bug: stomach, HINDGUT, rectum
Low pH

HOST FACTORS
Intermediate Host: Reduviid bug/ Triatomid bug/ Kissing bug/ Assasin bug
Vertebrate Hosts: Humans, domesticated and wild animals
Reservoir: Rodents, opossums, armadillos, raccoons, dogs, cats, guinea pigs, man
Populations at risk: Poor families, veterinarians, laboratory personnel, wildlife handlers, hunters, travelers to endemic areas, immunocompromised
Sleeping habits
Organ transplant and Blood Transfusion
Eating habits eg. Food contaminated with feces from T.cruzi infected bugs

PERIOD OF PATHOGENESIS

NATURAL COURSE OF CHAGAS DISEASE


Clinical Horizon

Metacyclic trypomastigotes enter through the bite wound, intact conjunctiva, or mucous membranes
Phagocytized by macrophage and low lysosomal pH facilitates transformation to amastigotes
Evasion of lysosomal system by escaping into the cytosol.

TISSUE AND PHYSIOLOGIC CHANGES


Increase production of IL-12 and NK cell activity
Intracellular amstigotes express glutathione S-tranferase into the blood stream.

Acute phase parasitemia


Signs and symptoms are mild and nonspecific
o Variable fever, malaise, hepatosplenomegaly, atypical lymphocytosis, lymphadenopathy
o Chagoma (localized inflammation at the site of infection)
o Romaa sign (conjunctivitis and unilateral prolonged eyelid edema)
o Rare and life threatening: myocarditis and meningoencephalitis
o Positive smear, culture, PCR result

Indeterminate phase
o Asymptomatic phase of varying length
o No parasite present in the blood
o Amastigotes nests in muscle tissue
o Anti T.cruzi IgG presebt
o Cardiomyopathy is present but undetectd in ECG and X-ray
o infection)

Indeterminate phase
Asymptomatic phase of varying length
Parasites disappear from blood

PROGRESSION
Increased IL-12 and IFN-
Dysfunction followed by dilation of esophagus, colon or both.
Eg. Constipation

CHRONIC STATE
Sudden death or heart failure caused by progressive destruction of heart muscle and its nervous system
Heart failure caused by progressive destruction of heart muscle and its nervous system
eg. Arrythmias, CHF, ventricular aneurisn

DEATH

HEALTH PROMOTION
Health education focused on:
o Raising awareness and knowledge about Chagas disease and mode of transmission
o Methods of prevention and control
o Good hygiene practices on food preparation, transportation, storage and consumption
Developing patient and provider educational material
Expanding information available online from CDC including information on triatomine bugs

SPECIFIC PROTECTION
Improving quality of human dwellings and peridomestic structures
o Application of long-lasting insecticides eg. pyethrin
o Seal cracks and gaps around walls, roofs and doors
o Remove wood, brush and rock piles near house
o Install screen on doors and windows and repair holes
Use insecticide-treated bed nets with sides tucked in
Applying insect repellent to exposed skin
Wear light-colored, long sleeved shirts and trousers
Protocols for screening pregnant women
Keep pets away from tissues of wild animals
Indoor housing of pets especially at night
Screening of blood and organ donors

EARLY DETECTION AND PROMPT TREATMENT


Diagnostics:
Parasitological Diagnosis
o Microscopy of fresh preparations of anticoagulated blood or buffy coat
o Peripheral blood smear
o Xenodiagnosis
Immunological Diagnosis
o Indirect hemaglutination
o ELISA/IFA
o PCR (Polymerase chain reaction)
o Detecting complement fixation

Case finding
Screening of newborns and other children of infected mothers

Prompt treatment through the following:


Acute phase, congenital infection and reactivation of chronic infection:
Benznidazole
o 12 years: 10 mg/kg/day orally in 2 divided doses x 60 days
o 12 years or older: 5 to 7 mg/kg/day orally in 2 divided doses x 60 days
Nifurtimox
o 10 years: 15 to 20 mg/kg/day orally in 3 or 4 divided doses x 90 days
o 11 to 16 years: 12.5 to 15 mg/kg/day orally in 3 or 4 divided doses x 90 days
o 17 years or older: 8 to 10 mg/kg/day orally in 3 or 4 divided doses x 90 to 120 days
Drugs are obtained from Centers for Disease Control
Indeterminate phase:
Either benznidazole or nifurtimox for children and adolescents through 18 years old with chronic infection
Chronic phase:
No longer curable and will require symptom management and relief

***Vaccines still under study


*** Drugs are obtained from Centers for Disease Control

DISABILITY LIMITATION
Prevention of complications:
Supportive management:
o Cardiopathy: pacemaker placement, medications for irregular heartbeats, surgery, heart transplant, direct stem cell therapy of heart muscle using bone marrow cell
trasplantation
o Megaesophagus or Megacolon: diet modification, medications, corticosteroids, surgery
Monitoring for T. cruzi reactivation

REHABILITATION
Control of patients, contacts and immediate environment
Report to local health authority
Infection control in hospitals
Investigation of contacts and source of infections
National vector control programs
National screening of blood supply
Establish national surveillance to describe prevalence of the disease

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