Pathogens Causing Cardiovascular Diseases PDF

1 Cardiopulmonary Block Infections: Cardiovascular block: 1 st Lecture: Pathogens Causing Cardiovascular Diseases: Assoc. PROF. DR. MOHAMMED A. A. Al-BAGHDADI  Objectives: ❑At the end of lecture, the students should be ab...

1 Cardiopulmonary Block Infections: Cardiovascular block: 1 st Lecture: Pathogens Causing Cardiovascular Diseases: Assoc. PROF. DR. MOHAMMED A. A. Al-BAGHDADI  Objectives: ❑At the end of lecture, the students should be able to understand the following: 1. List the pathogens causing cardiovascular diseases. 2. Discuss in detail the Properties, Transmission, Clinical findings, Laboratory diagnosis of the organisms: i. Viridians Group Streptococcus (VGS). ii. Epstein bar virus. iii. Trypanosoma. 3. Discuss briefly other pathogens causing CVS disease.  Pathogens Causing CVD: A. Viridians Group Streptococcus (VGS): ▪ Based on Lancefield Classification, which based on C- carbohydrate, they are non-groupable. ❑Viridans Group Streptococci (VGS) include several species, such as: S. sanguinis, S. mutans, S. mitis, S. gordonii, S. salivarius, S. anginosus, S. milleri, and S. intermedius. ❑Non-grouped Streptococci: a) Streptococcus pneumoniae. b) Viridans Group streptococci.  Pathogens Causing CVD: A. Viridians Group Streptococcus (VGS): ▪ They are α-hemolytic; Green zone around the colonies due to bacterial production of Hydrogen peroxide (H2O2) that changes hemoglobin (red color) to biliverdin (green color). Streptococci are spherical gram-positive cocci arranged in chains or pairs. All streptococci are catalase- negative. ▪ VGS are Normal Flora of Oropharynx. ❑Pathogenesis: i. The pathogenesis of S. pneumoniae and the viridans group streptococci is uncertain, as no exotoxins or tissue-destructive enzymes have been demonstrated.  Pathogens Causing CVD: ❑Pathogenesis: ii. The main virulence factor of S. pneumoniae is its antiphagocytic polysaccharide capsule. iii. The main virulence factor of VGS is produce a glycocalyx that enables the organism to adhere to the heart valve causing endocarditis. ❑Viridans Group Streptococci (e.g., S. mutans, S. sanguinis, S. salivarius, and S. mitis) are the most common cause of infective endocarditis. ▪ They enter the bloodstream (bacteremia) from the oropharynx, typically after dental surgery. ▪ Infective endocarditis: It is 100% fatal unless effectively treated with antimicrobial agents.  Pathogens Causing CVD: ❑Signs of endocarditis are fever, heart murmur, anemia, and embolic events such as splinter hemorrhages, subconjunctival petechial hemorrhages, and Janeway lesions. The heart murmur is caused by vegetations on the heart valve. ❑About 10% of endocarditis cases are caused by enterococci, but any organism causing bacteremia may settle on deformed valves. ❑At least three blood cultures are necessary to ensure recovery of the organism in more than 90% of cases.  Pathogens Causing CVD: ❑Viridans streptococci, especially S. anginosus, S. milleri, and S. intermedius, also cause brain abscesses, often in combination with mouth anaerobes (a mixed aerobic–anaerobic infection). Dental surgery is an important predisposing factor to brain abscess because it provides a portal for the viridans streptococci and the anaerobes in the mouth to enter the bloodstream (bacteremia) and spread to the brain. ❑Viridans streptococci are involved in mixed aerobic– anaerobic infections in other areas of the body as well (e.g., lung abscesses and abdominal abscesses,  Subconjunctival petechial hemorrhages. Splinter hemorrhages Janeway Lesion showing as painless, macular, hemorrhagic, irregularly- shaped lesions on patient's palm. Two pronounced lesions are seen at thumb and middle finger. Subungual splinter hemorrhages (arrowhead) are seen at the nail bed of thumb.  Pathogens Causing CVD: ❑Laboratory Diagnosis: 1. Viridans group streptococci (VGS); form α-hemolytic colonies on blood agar and must be distinguished from S. pneumoniae (pneumococci), which is also α- hemolytic. 2. Viridans group streptococci are resistant to lysis by bile and will grow in the presence of optochin, whereas pneumococci will not. 3. The various viridans group streptococci are classified into species by using a variety of biochemical tests.  Pathogens Causing CVD: ❑Treatment: 1. Endocarditis caused by VGS is curable by prolonged penicillin treatment. 2. Enterococcal endocarditis can be eradicated only by a Penicillin or Vancomycin combined with an Aminoglycoside. ▪ Enterococci resistant to multiple drugs (e.g., Penicillins, Aminoglycosides, and Vancomycin) have emerged. ▪ Resistance to vancomycin in enterococci is mediated by a cassette of genes that encode the enzymes that substitute D-lactate for D-alanine in the peptidoglycan. The same set of genes encodes vancomycin resistance in S. aureus.  Pathogens Causing CVD: ❑Treatment: ▪ VREs are now an important cause of nosocomial infections; there is no reliable antibiotic therapy for these organisms. ❑At present, two drugs are being used to treat infections caused by VRE: i. Linezolid (Zyvox) and ii. Daptomycin (Cubicin). Streptococcus pneumoniae Viridans Group streptococci Optochin sensitive Resistant The colonies are Bile Soluble. Not Bile Soluble. Capsulated (Quellung Test +). Non-capsulated (No Quellung Reaction).  Pathogens Causing CVD: B. Epstein–Barr virus (EBV): ❑General Properties: 1. Epstein–Barr virus belongs to the family Herpesviridae. This family is large, second in size to Poxviruses. Enveloped dsDNA viruses, Icosahedral viruses. The envelope derived from nuclear membrane. 2. All herpesviruses have Identical Morphology. All herpesviruses have identical morphology and cannot be distinguished from each other under electron microscopy.  Pathogens Causing CVD: ❑Epidemiology: 1. Route of spread: Epstein–Barr virus is transmitted via saliva and sexual contact, hence the name ‘kissing disease’. Infection is common in younger children and sexually active adolescents. 2. Prevalence: Epstein–Barr virus is ubiquitous virus, which infects 95% of people in the UK before the age of 25 Years. 3. Incubation period: 2–3 weeks. 4. Infectious period: i. Epstein–Barr virus is shed in saliva and genital secretions, and can be present in these for many weeks or months.  Pathogens Causing CVD: ❑Epidemiology: 4. Infectious period: ii. Reactivation of latent infection can occur frequently in some people, especially if they are immunosuppressed, with prolonged shedding of infectious virus, often asymptomatically. 5. At-risk groups: Immunosuppressed persons. ❑Clinical Symptoms: i. Infection can be Asymptomatic. ii. Classical clinical EBV syndrome is Infectious Mononucleosis (IM), but is more commonly referred to as ‘Glandular Fever’, with symptoms of sore throat, hepatitis, lymphadenopathy, fever and malaise.  Pathogens Causing CVD: ❑Clinical Symptoms: iii. Hepatosplenomegaly occurs in about 5–10% of cases. iv. Splenomegaly is more common (50–70%). v. Atypical lymphocytes are present in the peripheral blood, and liver function tests (LVF) are usually with mildly elevated Alanine Aminotransferase (ALT) or Called Serum Glutamic-Pyruvic Transaminase (SGPT).  Laboratory Diagnosis of EBV: Sample Laboratory test Result interpretation EBV IgM Positive result indicates recent EBV infection. Interpret positive results with caution; some will be non-specific. Beware of rheumatoid factor interference. EBV virus capsid antigen Indicates EBV infection at some time. (VCA) Ab Clotted EBV nuclear antigen This antibody is produced about 3 months after blood (EBNA) infection. If positive, it indicates EBV infection more (serum) than 3 months ago. EBNA antibody negative, Suggests recent EBV infection but beware of false VCA antibody positive negative EBNA results, especially in patients >60 years old and immune suppressed patients. Paul Bunnel/Mono-spot Provides a quick diagnosis but can be false positive and test false negative. Not useful for persons under the age of 16 years. EDTA blood EBV DNA molecular The presence of EBV DNA indicates current infection. assays Quantitative PCR is a guide to the severity of infection in immune compromised patients and a guide to management.  Pathogens Causing CVD: ❑Complications: 1. Epstein–Barr virus is a self-limiting disease, and complications are rare. 2. Chronic fatigue – some patients may suffer with tiredness and fatigue for weeks to months post-acute EBV infection; this may or may not be accompanied with Lymphadenopathy. 3. Rarely, an enlarged spleen may lead to splenic rupture, therefore patients are advised to refrain from contact sports until acute symptoms have subsided.  Pathogens Causing CVD: ❑Complications: 4. Guillain–Barre´ syndrome is a rare post-infectious complication of EBV infection, and presents as an ascending motor paralysis due to an immune-mediated demyelination of the spinal cord. 5. Epstein–Barr virus associated malignancies, such as Burkitt’s lymphoma, Nasopharyngeal carcinoma and Lymphoproliferative disease (LPD)/lymphoma in immunosuppressed patients.  Pathogens Causing CVD: ❑Complications: 6. X-linked lymphoproliferative syndrome (Duncan’s syndrome) is due to a specific X-chromosome-linked recessive genetic defect, which leads to impaired antibody response to EBV alone. It affects the male members of a family who either die of an Excessive EBV infection, or develop Lymphoproliferative malignancies.  Pathogens Causing CVD: ❑Differential diagnosis: Cytomegalovirus, Toxoplasma gondii, Adenovirus. ❑Treatment: 1. There is no evidence that any antiviral drugs are useful in the treatment of EBV infections. 2. In immunosuppressed patients, reducing the amounts of immunosuppression will reduce the severity of disease and the frequency of EBV reactivation. ❑Infection control: ▪ Epstein–Barr virus does not pose any infection-control risks, although sharing drinking vessels and bottles can transmit infection via saliva.  Pathogens Causing CVD: C. Trypanosomes: ❑The medically important haemoflagellates are two genera: 1. Genus: Leishmania 2. Genus: Trypanosoma ❑Trypanosoma: A. African trypanosomes: i. Trypanosoma brucei gambiense. ii. Trypanosoma brucei rhodesiense B. American trypanosome: i. Trypanosoma cruzi  Pathogens Causing CVD: C. Trypanosomes: ❑Haemoflagellates: ▪ They are the flagellated protozoa that are found in peripheral blood circulation. ▪ Infect blood and tissue. ▪ They complete their life cycle in two hosts, i.e. vertebrate host and insect vector.  Haemoflagellates: ❑ African trypanosomiasis: ▪ Disease: Sleeping sickness, ▪ Caused by Trypanosoma brucei and ▪ Transmitted by tsetse flies. ❑South American trypanosomiasis: َّ ‫ذُبَابَةُّتْسيُّتْسيُّأوُّال‬ ‫شذاةُّأوُّالالَّسنَة‬ ▪ Disease: Chagas disease, ‫مرض شاغاس‬ ▪ Chagas disease: also known as American trypanosomiasis is a tropical parasitic disease caused by the Trypanosoma cruzi. It is spread mostly by reduviid insects ‫الحشرات المخففة‬ Family: Triatominae, or "kissing bugs". ‫ البَقُّ ال ُمقَبُّل‬/‫ الفسافس‬/‫البق‬ ‫ُّالبَقُّال ُمقَبل‬/‫ُّالفسافس‬/‫البق‬  Pathogenesis and Clinical Symptoms: ❑The symptoms of hemoflagellate infections: 1. Range from minor symptoms , such as irritation at the infection site with small red papule at the infection site, & intense itching, 2. To Serious Form (comatose state and death). ▪ Secondary bacterial infections, fever, and diarrhea, to kidney involvement, mental retardation, a comatose state, and death. ❑ In some cases, the initial skin lesions spontaneously heal, whereas in others they may remain dormant for months or even years.  Trypanosoma: A. African trypanosomes: 1. Trypanosoma brucei gambiense 2. Trypanosoma brucei rhodesiense ❑Trypanosoma gambiense & Trypanosoma rhodesiense: ▪ They are also known as Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense. ▪ Both Causing African Trypanosomiasis, Sleeping Sickness. ▪ T. b. rhodesiense is found in Eastern and central Africa. ▪ T. b. rhodesiense is a much more virulent organism than T. b. gambiense. ▪ T. b. rhodesiense Cause: East African (Rhodesian) Sleeping Sickness. ▪ T. b. gambiense is found in West & Central Africa.  Trypanosoma: ❑Important Properties: 1. The morphology and life cycle of the two species are similar. 2. The vector for both African trypanosomes is the tsetse fly. 3. Humans are the reservoir for T. gambiense, whereas T. rhodesiense has reservoirs in both domestic animals (especially Sheep & Cattle) and wild animals (e.g., antelopes). ‫الظبي‬ 4. The 3-week life cycle in the tsetse fly begins with ingestion of Blood Trypomastigotes in a blood meal from the reservoir host. i. Bloodstream Trypomastigotes multiply in the insect gut & transform into Procyclic Trypomastigotes.  Trypanosoma: ii. Procyclic Trypomastigotes then migrate to the salivary glands, where they transform into Epimastigote. iii. Epimastigote multiply further in salivary glands, and then form Metacyclic Trypomastigotes, which are transmitted by the tsetse fly bite. 5. The organisms in the saliva are injected into the skin, where they enter the bloodstream, differentiate into blood-form trypomastigotes, and multiply, thereby completing the cycle. ❖Note that these species are rarely found as Amastigotes in tissue, in contrast to T. cruzi and Leishmania species, in which Amastigotes are commonly found.  Trypanosoma: 6. These trypanosomes exhibit remarkable antigenic variation of their surface glycoproteins, with hundreds of antigenic types found. i. One antigenic type will coat the surface of the parasites for approximately 10 days, followed by other types in sequence in the new progeny. ii. This variation is due to sequential movement of the Glycoprotein genes to a preferential location on the chromosome, where only that specific gene is transcribed into mRNA. iii. These antigenic variations allow the organism to continually evade the host immune response.  Trypanosoma: 1. T. brucei gambiense: ▪ Causes slow onset chronic trypanosomiasis in humans. ▪ Most common in central and western Africa, where humans are thought to be the primary reservoir. 2. T. brucei rhodesiense: ▪ Causes fast onset acute trypanosomiasis in humans. ▪ Most common in southern, central, and eastern Africa, where both domestic animals (especially Sheep & Cattle) and wild animals (e.g., antelopes).  Trypanosoma: ❑Life Cycle of T. rhodesiense & T. gambiense are Same: ▪ The only difference in the life cycles of T. b. rhodesiense and T. b. gambiense are the species of tsetse fly vector (Genus: Glossina). 1. The two species of tsetse flies responsible for the transmission of T. b. gambiense are: i. Glossina palpalis and ii. Glossina tachinoides. ▪ There are no known animal reservoir hosts. 2. The two primary species of tsetse fly vectors responsible for transmitting T. b. rhodesiense are: i. Glossina morsitans and ii. Glossina pallidipes.  Trypanosoma: ❑Pathogenesis & Epidemiology: 1. The trypomastigotes spread from the skin through the blood to the lymph nodes and the brain. 2. The typical somnolence (sleeping sickness) progresses to coma as a result of a demyelinating encephalitis. 3. In the acute form, a cyclical fever spike (approximately every 2 weeks) occurs that is related to antigenic variation. ▪ As antibody-mediated agglutination and lysis of the trypomastigotes occur, the fever subsides. ▪ However, a few antigenic variants survive, multiply, and cause a new fever spike. ▪ This cycle repeats itself over a long period. ▪ The lytic antibody is directed against the surface glycoprotein.  Trypanosoma: ❑Pathogenesis & Epidemiology: 4. The disease is endemic in sub-Saharan Africa, the natural habitat of the tsetse fly. ▪ Both sexes of fly take blood meals and can transmit the disease. ▪ T. b. gambiense has also been shown to be acquired through blood transfusion, organ transplantation, and congenital transmission (from pregnant mother to fetus). ▪ The fly is infectious throughout its 2- to 3-month lifetime. o T. gambiense is the species that causes the disease along water courses in west & Central Africa, whereas o T. rhodesiense is found in the arid regions of east & Central Africa. o Both species are found in central Africa.  Trypanosoma: ❑Clinical Findings: ▪Both species cause sleeping sickness, the progress of the disease differs. ▪ T. gambiense–induced disease runs a low-grade chronic course over a few years, whereas ▪ T. rhodesiense causes a more acute, rapidly progressive disease that, if untreated, is usually fatal within several months. 1. The initial lesion is an indurated skin ulcer ("trypanosomal chancre") at the site of the fly bite. 2. After the organisms enter the blood, intermittent weekly fever and lymphadenopathy develop.  Trypanosoma: ❑Clinical Findings: 3. Enlargement of the posterior cervical lymph nodes (Winterbottom's sign) is commonly seen. 4. The encephalitis is characterized initially by headache, insomnia, and mood changes, followed by muscle tremors, ‫كالم غير واضح‬ slurred speech, and apathy that progress to somnolence and coma. 5. Untreated disease is usually fatal as a result of pneumonia.  Trypanosoma: ❑Laboratory Diagnosis: 1. During the early stages, ▪ Microscopic examination of the blood (either wet films or thick or thin smears) reveals trypomastigotes. ▪ An aspirate of the chancre or enlarged lymph node can also demonstrate the parasites. ▪ The presence of trypanosomes in the spinal fluid, coupled with an elevated protein level, pleocytosis, and elevated IgM; indicates that the patient has entered the late encephalitic stage. ▪ Serologic tests, especially the ELISA for IgM antibody, can be helpful.  Trypanosoma: ❑Laboratory Diagnosis: ❑Specimens: ▪ Blood, lymph node aspirations, and CSF are the specimens of choice for diagnosing T. b. gambiense. 1. Giemsa-stained slides of blood and lymph node aspirations from infected patients reveal the typical trypomastigote morphologic forms. 2. CSF: i. Several tests may be performed on CSF— microscopic examination of the sediment for trypomastigotes,  Trypanosoma: ❑Laboratory Diagnosis: 2. CSF: ii. Detection of the presence of immunoglobulin M (IgM), and iii. Detection of the presence of proteins. iv. Infected patients typically have high levels of both IgM and proteins in their CSF. 1. In addition, serum IgM testing may be indicated. 2. The presence of IgM in serum and/or CSF is generally considered diagnostic.  Trypanosoma: ❑Treatment: 1. Treatment must be initiated before the development of encephalitis, because Suramin, the most effective drug, does not pass the blood-brain barrier well. ▪ Suramin will effect a cure if given early. 2. Pentamidine is an alternative drug. 3. If central nervous system symptoms are present, suramin (to clear the parasitemia) followed by Melarsoprol should be given.  Trypanosoma: ❑Prevention: ▪ The most important preventive measure is protection against the fly bite, using: i. Netting and ii. Protective clothing. iii. Clearing the forest around villages. iv. Using insecticides are helpful measures. v. No vaccine is available. ❑Trypanosoma brucei—Trypomastigotes: Arrow points to a trypomastigote (the flagellated form) in the blood.  American Trypanosoma: ❑ Trypanosoma cruzi ❑Disease: Chagas’ disease ▪ Trypanosoma cruzi, the causative agent of Chagas’ disease, was described in 1909 by a young medical student in Brazil named Carlos Chagas. ❑ Epidemiology: ▪ Trypanosoma cruzi is found in southern portions of the United States, Mexico, and Central and South America. Commonly referred to as Chagas’ disease or American trypanosomiasis, ▪ the disease course for this illness often presents itself with cardiac and gastrointestinal distress. ❑Trypanosoma cruzi trypomastigote exhibiting a characteristic full body length undulating membrane (arrow). ❑Trypanosoma cruzi C- shaped Trypomastigoten in a blood smear. ❑Life Cycle of Trypanosoma cruzi: ❑Mode of Transmission of T. cruzi: 1. Transferred to a human host when a reduviid bug vector defecates infective trypomastigotes near the site of its blood meal. 2. The presence of the bite produces an itching sensation in the host. 3. As the host scratches the bite area, the trypomastigotes gain entry into the host by rubbed into the bite wound. 4. Additional routes of transferring T. cruzi include: i. Blood transfusions, ii. Sexual intercourse, iii. Transplacental transmission, and iv. Entry through the mucous membranes when the bug bite is near the eye or mouth.  American Trypanosoma: ❑Life Cycle of Trypanosoma cruzi: 5. Following entry into the host, the trypomastigotes invade surrounding cells, where they transform into Amastigotes. 6. The amastigotes proceed to multiply, destroy the host cells, and then convert back into trypomastigotes. ▪ The resulting trypomastigotes migrate through the blood, penetrate additional cells in the body, and transform back into amastigotes, and the replication and the cycle repeats.  American Trypanosoma: ❑Life Cycle of Trypanosoma cruzi: 7. A number of areas in the body may become infected, including the heart muscle, liver, and brain. i. The T. cruzi trypomastigotes are transmitted back to the reduviid bug when it feeds, via a blood meal, on an infected human. ii. On ingestion, the trypomastigotes transform into Epimastigote in the midgut. iii. Multiplication of the epimastigotes produces thousands of additional parasites that convert back into trypomastigotes when they reach the hindgut. iv. These trypomastigotes are then passed with the feces when the bug defecates near the site of its next blood meal, and thus the cycle begins again. ❑ Epimastigotes: ▪ May rarely be seen in the circulating blood; ▪ however, this form is primarily found only in the arthropod vector. Epimastigote: Parameter Description Size 9-15 μm long Shape Long and slightly wider than promastigote form Nucleus One, located in posterior end Other features Kinetoplast located anterior to the nucleus. Undulating membrane, extending (½) body length Free flagellum, extending from anterior end  Trypomastigote: Parameter Description Size 12-35 μm long by 2-4 μm wide Shape C, S or U shape often seen in stained blood films. Appearance Long and slender Nucleus One, located anterior to the Kinetoplast. Other features Kinetoplast located in the posterior End. Undulating membrane, extending entire body length Free flagellum, extending from anterior end when present ❑Trypomastigotes: ❑Found in blood specimen. ▪ Trypanosoma cruzi ▪ Trypanosoma cruzi C- trypomastigote exhibiting a shaped trypomastigote in characteristic full body length a blood smear. undulating membrane (arrow). Trypomastigote: anterior Undulating membrane posterior  American Trypanosoma: ❑Clinical Symptoms of Trypanosoma cruzi: A. Chagas’ Disease: ▪ Chagas’ disease may be asymptomatic, chronic, or acute in nature. B. Chagoma: ▪ The most common initial symptom is the development of an erythematous nodule, at the site of infection produced by the proliferation of the T. cruzi organisms. ▪ Occurs any where in the body, but it is most frequently located on the face. ▪ Edema as well as a rash around the eyes and face. ▪ The painful chagoma may last 2 to 3 months before subsiding. C. Patients who contract T. cruzi through the ocular mucosa develop a characteristic conjunctivitis and unilateral edema of the eyelids, a condition known as Romana's sign.  American Trypanosoma: ❑Clinical Symptoms of Trypanosoma cruzi: ❑Chagas’ Disease: ▪ Patients suffering from acute Chagas’ disease typically experience fever, chills, fatigue, myalgia, and malaise. ❑An attack of acute infection may result in one of the following scenarios: 1. Recovery; 2. Transition to the chronic stage of disease; or 3. Death, which usually occurs a few weeks after the attack. ❑Chagas’ disease is most commonly seen in children younger than 5 years. ▪ These patients characteristically present with symptoms of CNS. ❑After experiencing an initial acute attack, adults and children older than 5 years usually develop a milder chronic or subacute form of the disease.  Lab. Diagnosis of T. cruzi ❑Specimens: ▪Blood Film, L/N biopsy, Blood for Culture, Serum. 1. Giemsa-stained blood slides are the specimen of choice for detection of the typical T. cruzi trypomastigotes. 2. Epimastigotes may rarely be seen in the circulating blood; however, this form is primarily found only in the arthropod vector. 3. Lymph node biopsy Giemsa-stained slides, as well as blood culture, may reveal the typical amastigotes.  Lab. Diagnosis of T. cruzi 4. A number of serologic tests, including: i. Complement fixation (CF), ii. DAT, and iii. Indirect immunofluorescence (IIF), are also available for diagnostic purposes. 5. The polymerase chain reaction (PCR) and 6. ELISA testing methods are also available for diagnosing infections with T. cruzi; ▪ ELISA is used in blood donor screening to help ensure the safety of transfusable blood and transplantable organs.  Treatment of T. cruzi 1. The treatment of choice for infections with T. cruzi is Nifurtimox (Lampit). 2. Other medications include: ▪Benznidazole, Allopurinol, and ketoconazole (the antifungal agent).  Prevention of T. cruzi 1. The eradication of reduviid bug nests and the construction of homes without open. 2. DDT has proved to be useful, not only to control the reduviid population but also to decrease the incidence of malaria. 3. Educational programs designed to inform people, especially in endemic areas, of the disease, its transmission, and possible reservoir hosts may also prove to be helpful in the fight against T. cruzi transmission. 4. In addition, the prospects for developing a vaccine appear to be promising.