July 17, 2008

Update

Life has been hectic, but I will soon begin posting (in retrospect) the happenings of the last week or so.

Tomorrow is my last day at Zacamil Hospital.

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July 9, 2008

Fast Food

The day I arrived in El Salvador I noticed a ridiculous amount of fast food restaurants. Having visited several times in the past, I can remember when there was only one McDonald´s in San Salvador and I remember what a big deal it was when the first Pizza Hut was opened. Nowadays it´s uncommon to see a street corner without a fast food restaurant. In fact, pizza, hamburger and fried chicken restaurants often sit across the street from another restaurant of the same franchise. Sometimes the United States is criticized for having a coffee shop on every corner, and I can make the same criticism about El Salvador and fast food.

Originally I was planning on designing an informative pamphlet or educational material based on infectious disease, but the staggering amounts of cases of diabetes, hypertension and obesity have led me towards producing a proper-nutrition type of educational material that I will present to the Ministry of Health here in El Salvador.

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July 4, 2008
Entamoeba Histolytica:  After some rummaging through hospital records I found that Amebas and Giardia are the most common of parasitic infections here at Zacamil. Of the amebas, the most common is Entamoeba Histolytica (EH). EH is an ameba and is a common parasite in the large intestine of humans, certain other primates, and some other animals. Three stages of EH are encountered: the active ameba, the inactive cyst, and the intermediate precyst. Infection is caused by a fecal-oral route. EH has several stages (as mentioned above), the most important of which, as concerns pathogenesis, is the trophozoite stage. The trophozoite emerges from the ingested EH cyst after activation of the excystation process in the stomach and duodenum. The metacyst divides rapidly, producing four amebulae (one for each cyst nucleus), each of which divides again to produce eight small trophozoites per infective cyst. These pass to the cecum (entrance to large intestine) and produce a population of lumen-dwelling trophozoites. The trophozoites multiply by binary fission. In the majority of infections the infection remains luminal, and the trophozoites multiply as a bacteria-feeding colony, ultimately encyst, and pass out in the feces (these can be transmitted to other hosts). Active/Symptomatic disease results when the trophozoites of EH invade the intestinal epithelium. Mucosal invasion with the aid of proteolytic enzymes occurs through the crypts of Lieberkühn, forming discrete ulcers with a pinhead-sized center and raised edges, from which mucus, necrotic cells, and amebas pass. Pathologic changes are always induced by trophozoites. Rapid lateral spread of the multiplying amebas follows, undermining the mucosa and producing the characteristic “flask-shaped” ulcer of primary amebiasis: a small point of entry, leading via a narrow neck through the mucosa into an expanded necrotic area in the submucosa. The organisms may travel to the ileocecal valve and terminal ileum, producing a chronic infection. The sigmoid colon and rectum are favored sites for later lesions. An amebic inflammatory or granulomatous tumor-like mass (ameboma) may form on the intestinal wall, sometimes growing sufficiently large to block the lumen. Extraintestinal infection is metastatic and rarely occurs by direct extension from the bowel. By far the most common form is amebic hepatitis or liver abscess, which is assumed to be due to microemboli, including trophozoites carried through the portal circulation. A true amebic abscess is progressive, nonsuppurative (unless secondarily infected), and destructive without compression and formation of a wall. The contents are necrotic and bacteriologically sterile, active amebas being confined to the walls.  Factors that determine invasion of amebas include the following: the number of amebas ingested, the pathogenic capacity of the parasite strain, host factors such as gut motility and immune competence, and the presence of suitable enteric bacteria that enhance amebic growth. Correct and prompt identification of the Entamoeba species remains a critical problem. Currently diagnosis includes diagnostic laboratory tests of stools, serologic blood tests, liver abscess aspirates, and sigmoidoscopy biopsy/scrapings.  Metronidazole (Flagyl) is probably a drug of choice for symptomatic amebiasis even though it is mutagenic in bacteria. For mild to moderate intestinal disease, give metronidazole or tinidazole (Fasigyn) (an excellent drug of low toxicity but not available in the United States). For severe intestinal disease (amebic dysentery), give the regimen described above or, if the other regimens cannot be followed, dehydroemetine (or emetine). For hepatic or other extraintestinal involvement or for ameboma, give metronidazole or tinidazole or dehydroemetine (or emetine). Cysts are usually ingested through contaminated water. In the tropics, contaminated vegetables and food are also important cyst sources; flies have been incriminated in areas of fecal pollution. Asymptomatic cyst passers are the main source of contamination and may be responsible for severe epidemic outbreaks where sewage leaks into the water supply or breakdown of sanitary discipline occurs (as in mental, geriatric, prison, or children’s institutions). A high-carbohydrate, low-protein diet favors the development of amebic dysentery both in experimental animals and in known human cases. Control measures consist of improving environmental and food sanitation.  www.accessmedicine.com - Lang’s Microbiology

Entamoeba Histolytica: 

After some rummaging through hospital records I found that Amebas and Giardia are the most common of parasitic infections here at Zacamil. Of the amebas, the most common is Entamoeba Histolytica (EH).

EH is an ameba and is a common parasite in the large intestine of humans, certain other primates, and some other animals. Three stages of EH are encountered: the active ameba, the inactive cyst, and the intermediate precyst. Infection is caused by a fecal-oral route.

EH has several stages (as mentioned above), the most important of which, as concerns pathogenesis, is the trophozoite stage. The trophozoite emerges from the ingested EH cyst after activation of the excystation process in the stomach and duodenum. The metacyst divides rapidly, producing four amebulae (one for each cyst nucleus), each of which divides again to produce eight small trophozoites per infective cyst. These pass to the cecum (entrance to large intestine) and produce a population of lumen-dwelling trophozoites. The trophozoites multiply by binary fission. In the majority of infections the infection remains luminal, and the trophozoites multiply as a bacteria-feeding colony, ultimately encyst, and pass out in the feces (these can be transmitted to other hosts). Active/Symptomatic disease results when the trophozoites of EH invade the intestinal epithelium. Mucosal invasion with the aid of proteolytic enzymes occurs through the crypts of Lieberkühn, forming discrete ulcers with a pinhead-sized center and raised edges, from which mucus, necrotic cells, and amebas pass. Pathologic changes are always induced by trophozoites. Rapid lateral spread of the multiplying amebas follows, undermining the mucosa and producing the characteristic “flask-shaped” ulcer of primary amebiasis: a small point of entry, leading via a narrow neck through the mucosa into an expanded necrotic area in the submucosa. The organisms may travel to the ileocecal valve and terminal ileum, producing a chronic infection. The sigmoid colon and rectum are favored sites for later lesions. An amebic inflammatory or granulomatous tumor-like mass (ameboma) may form on the intestinal wall, sometimes growing sufficiently large to block the lumen. Extraintestinal infection is metastatic and rarely occurs by direct extension from the bowel. By far the most common form is amebic hepatitis or liver abscess, which is assumed to be due to microemboli, including trophozoites carried through the portal circulation. A true amebic abscess is progressive, nonsuppurative (unless secondarily infected), and destructive without compression and formation of a wall. The contents are necrotic and bacteriologically sterile, active amebas being confined to the walls. 

Factors that determine invasion of amebas include the following: the number of amebas ingested, the pathogenic capacity of the parasite strain, host factors such as gut motility and immune competence, and the presence of suitable enteric bacteria that enhance amebic growth. Correct and prompt identification of the Entamoeba species remains a critical problem. Currently diagnosis includes diagnostic laboratory tests of stools, serologic blood tests, liver abscess aspirates, and sigmoidoscopy biopsy/scrapings. 

Metronidazole (Flagyl) is probably a drug of choice for symptomatic amebiasis even though it is mutagenic in bacteria. For mild to moderate intestinal disease, give metronidazole or tinidazole (Fasigyn) (an excellent drug of low toxicity but not available in the United States). For severe intestinal disease (amebic dysentery), give the regimen described above or, if the other regimens cannot be followed, dehydroemetine (or emetine). For hepatic or other extraintestinal involvement or for ameboma, give metronidazole or tinidazole or dehydroemetine (or emetine).

Cysts are usually ingested through contaminated water. In the tropics, contaminated vegetables and food are also important cyst sources; flies have been incriminated in areas of fecal pollution. Asymptomatic cyst passers are the main source of contamination and may be responsible for severe epidemic outbreaks where sewage leaks into the water supply or breakdown of sanitary discipline occurs (as in mental, geriatric, prison, or children’s institutions). A high-carbohydrate, low-protein diet favors the development of amebic dysentery both in experimental animals and in known human cases. Control measures consist of improving environmental and food sanitation. 

www.accessmedicine.com - Lang’s Microbiology

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July 2, 2008

Parasites

I continue to rotate throughout the hospital with various specialists and always enlist the ¨CE¨ as my home base. I´ve been counting and the CE averages 70-80 logged patients a day (from 7am to 3pm). I say logged because not all patients are logged due to human error. This is a huge number of patients to be passing through such a small office, and I´m sure every office and operating room in the hospital is equally as busy.

Lately there have been many patients present with parasites, including two I had not heard of before:

1) Endolimax Nana - The patient is a young girl, about 10 years old. She presented with chronic abdominal pain and weight loss. She came with blood work already done. I cannot recall ever coming across Endolimax in any textbook, but the doctors at Zacamil seemed to be familiar with the culprit. According to Lang´s Microbiology Endolimax is a Sarcodina (an Ameba) and closely related to the two parasites mentioned below. There is no further mention of this bug in Lang. We treated this child with a course of metronidazole for 10 days.

2) Entamoeba Coli - The patient is a young woman, about 20 years old. She presented with chronic diarrhea and she was sent for testing. The results came back as Entamoeba Coli, which was new to me. In medical school we mostly spoke of Entamoeba Histolytica. There is not much mentioned in Harrison´s Online about Entamoeba Coli except that it is closely related to Entamoeba Histolytica, that it is very common, and that it is not a particulary serious infection. We did not give this patient any medication but did refer her to a gastroenterologist.

As a random side note, my grandmother claims to have been born (in Guatemala -  just north of El Salvador) with Malaria. She says she was sick until she was seven and she can remember having fevers every evening and feeling ill. Luckily, this never happened to me.

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June 29, 2008
“ Humanity has but three great enemies: Fever, famine and war; of these by far the greatest, by far the most terrible, is fever.¨ - Sir William Osler

Malaria:

Malaria is a protozoal infection caused by Plasmodium and transmitted by the anopheles mosquito. It is a serious infection and caused 1-3 billion deaths worldwide each year. Four species of the genus Plasmodium cause nearly all malarial infections in humans. These are P. falciparum, P. vivax, P. ovale, and P. malariae. Almost all deaths are caused by falciparum malaria. The life/infection cycle of Plasmodium in humans is complicated and begins with inoculation of sporozoites by a female Anopheles mosquito. These sporozoites travel through the bloodstream and into the liver where they invade hepatic parenchymal cells and begin a period of asexual reproduction. By this amplification process (known as intrahepatic or preerythrocyticschizogony or merogony), a single sporozoite eventually may produce from 10,000 to >30,000 daughter merozoites. The swollen infected liver cell eventually bursts, discharging motile merozoites into the bloodstream. These then invade the red blood cells (RBCs) and multiply six- to twentyfold every 48–72 h. When the parasites reach densities high enough in the blood, the symptomatic stage of the infection begins. In P. vivax and P. ovale infections, a proportion of the intrahepatic forms do not divide immediately but remain dormant for a period ranging from 3 weeks to a year or longer before reproduction begins. These dormant forms, or hypnozoites, are the cause of the relapses that characterize infection with these two species. After entry into the bloodstream, merozoites rapidly invade erythrocytes and become trophozoites. The disease in human beings is caused by the direct effects of RBC invasion and destruction by the asexual parasite and the host’s reaction. After a series of asexual cycles or immediately after release from the liver , some of the parasites develop into morphologically distinct, longer-lived sexual forms (gametocytes) that can transmit malaria. A picture of this life cycle can be seen below:

malaria

The most common form of Malaria in Central America is P. vivax. Initially, the host responds to plasmodial infection by activating nonspecific defense mechanisms. Temperatures of >40°C damage mature parasites; in untreated infections, the effect of such temperatures is to further synchronize the parasitic cycle, with eventual production of the regular fever spikes and rigors that originally served to characterize the different malarias. These regular fever patterns (tertian, every 2 days; quartan, every 3 days) are seldom seen today in patients who receive prompt and effective antimalarial treatment. The geographic distributions of sickle cell disease, ovalocytosis, thalassemia, and glucose-6-phosphate dehydrogenase (G6PD) deficiency closely resemble that of malaria before the introduction of control measures. This similarity suggests that these genetic disorders confer protection against death from falciparum malaria. Chronic complications of malaria include Hyperreactive Malarian Splenomegaly, Quartan Malarial Nephropathy and possibly even Burkitt´s Lymphoma.

Blood smears are used to diagnose malaria as the parasite can be seen inside of red blood cells via microscopy. The erythrocyte sedimentation rate, plasma viscosity, and levels of C-reactive protein and other acute-phase proteins are high. The platelet count is usually reduced. Findings in severe malaria may include metabolic acidosis, with low plasma concentrations of glucose, sodium, bicarbonate, calcium, phosphate, and albumin together with elevations in lactate, BUN, creatinine, urate, muscle and liver enzymes, and conjugated and unconjugated bilirubin.

Despite recent evidence of chloroquine resistance in P. vivax, chloroquine remains the treatment of choice for the “benign” human malarias (P. vivax, P. ovale, P. malariae) except in Indonesia and Papua New Guinea, where high levels of resistance are prevalent. The treatment of falciparum malaria has changed radically in recent years. In endemic areas, the World Health Organization now recommends artemisinin-based combinations as first-line treatment for uncomplicated falciparum malaria everywhere.

Malarial prevention includes chemoprophylaxis for travelers and erradication of mosquito breeding grounds (which has proved to be difficult). Pregnant women should take extreme care as the disease can be passed through the placenta. Avoidance of mosquitos is crucial and includes use of mosquito nets and care during prime mosquito feeding times of dusk and dawn.

www.accessmedicine.com - Harrison´s Online 

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June 25, 2008
Enteric Fever (Typhoid Fever) Typhoid fever is caused by a species of salmonella named Salmonella typhi. Enteric Fever is common in developing nations and is a significant problem in El Salvador. Infection is of fecal-oral route and often is transmitted by consumption of contaminated food or drink. The incubation period for Typhoid Fever is 5 days to 2 weeks. Enteric Fever is a clinical syndrome characterized by constitutional and gastrointestinal symptoms and by headache. During the early stages there is increasing malaise, headache, cough, and sore throat. These symptoms are also accompanied by abdominal pain and constipation, while the fever ascends in a stepwise fashion. After about 7–10 days, the disease process reaches a plateau and the patient is much more ill, appearing exhausted and often prostrated. There may be marked constipation, especially early (or the patient may have ¨pea soup¨ diarrhea); marked abdominal distention occurs as well.  Usually the patients will slowly improve, although relapse has been known to occur up to two weeks after symptoms have waned. While many patients do improve, Typhoid Fever can often be a deadly disease. Enteric Fever, mostly in untreated patients, can lead to intestinal hemorrhage or intestinal perforation. Appearance of leukocytosis and tachycardia should suggest these complications. Physical findings of the disease include splenomegaly, abdominal distention and tenderness, relative bradycardia, and occasionally meningismus. A rash (rose spots) commonly appears during the second week of disease. The rash is made up of 2-3 mm spots that blanch (fade away with pressure). The rash usually disappears in 3–4 days. Typhoid fever is best diagnosed by blood culture, which is positive in the first week of illness in 80% of patients who have not taken antimicrobials. The rate of positivity declines thereafter, but one-fourth or more of patients still have positive blood cultures in the third week. Several antibiotics including ampicillin, chloramphenicol, and third generation cephalosporins are useful in the treatment of Enteric Fever. Resistance has been documented and in these cases fluoroquinolones are used. Both oral (lasts 5 years) and injected (lasts 2 years) vaccines are available that are approximately 90% effective. Adequate waste disposal and protection of food and water supplies from contamination are important public health measures to prevent salmonellosis. Carriers cannot work as food handlers. www.accessmedicine.com - Current Medical Diagnosis and Treatment

Enteric Fever (Typhoid Fever)

Typhoid fever is caused by a species of salmonella named Salmonella typhi. Enteric Fever is common in developing nations and is a significant problem in El Salvador. Infection is of fecal-oral route and often is transmitted by consumption of contaminated food or drink. The incubation period for Typhoid Fever is 5 days to 2 weeks. Enteric Fever is a clinical syndrome characterized by constitutional and gastrointestinal symptoms and by headache.

During the early stages there is increasing malaise, headache, cough, and sore throat. These symptoms are also accompanied by abdominal pain and constipation, while the fever ascends in a stepwise fashion. After about 7–10 days, the disease process reaches a plateau and the patient is much more ill, appearing exhausted and often prostrated. There may be marked constipation, especially early (or the patient may have ¨pea soup¨ diarrhea); marked abdominal distention occurs as well.  Usually the patients will slowly improve, although relapse has been known to occur up to two weeks after symptoms have waned. While many patients do improve, Typhoid Fever can often be a deadly disease. Enteric Fever, mostly in untreated patients, can lead to intestinal hemorrhage or intestinal perforation. Appearance of leukocytosis and tachycardia should suggest these complications.

Physical findings of the disease include splenomegaly, abdominal distention and tenderness, relative bradycardia, and occasionally meningismus. A rash (rose spots) commonly appears during the second week of disease. The rash is made up of 2-3 mm spots that blanch (fade away with pressure). The rash usually disappears in 3–4 days.

Typhoid fever is best diagnosed by blood culture, which is positive in the first week of illness in 80% of patients who have not taken antimicrobials. The rate of positivity declines thereafter, but one-fourth or more of patients still have positive blood cultures in the third week.

Several antibiotics including ampicillin, chloramphenicol, and third generation cephalosporins are useful in the treatment of Enteric Fever. Resistance has been documented and in these cases fluoroquinolones are used. Both oral (lasts 5 years) and injected (lasts 2 years) vaccines are available that are approximately 90% effective. Adequate waste disposal and protection of food and water supplies from contamination are important public health measures to prevent salmonellosis. Carriers cannot work as food handlers.

www.accessmedicine.com - Current Medical Diagnosis and Treatment

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June 24, 2008

Chagas

Today I met a man with Chagas Disease (see below). His story is apparently a common one. 8 years ago he attempted to give blood. All blood in El Salvador is screened for Chagas before it is given to a patient due to the possibility of infection. At that time, this man was found to have a positive test and was diagnosed with Chagas. He arrived today, 39 years old, and complaining of extreme exhaustion with any exertion (even talking) and of transient swelling of the thorax, or chest.

The patient was ultimately referred to receive a battery of tests including an EKG, chest x-ray and Chagas ELISA test to verify the diagnosis and rule out any cardiomyopathy. The patient could not recall being told he had Chagas before 8 years ago, which is not uncommon. The doctors at Zacamil Hospital mentioned that Chagas disease is difficult to diagnose in its acute phase and once in its chronic phase the treatment is only symptomatic. For the patients that arrive at this public hospital a heart transplant is out of the question and ultimately they pass away of heart failure. The doctors did note that if acute Chagas is diagnosed the treatment of choice in El Salvador is nifurtimox.

As a final note, this man lived in a house made of adobe with a dried palm thatched roof. Kissing bugs are known for living in these kinds of roofs.

As an even more final note, all health care at public hospitals in El Salvador is free. However, medical supplies, especially medicines and specialized physicians, are in high demand and low supply. Many of these patients that rely on the free care the government provides are victims not of poor diagnosis but of lack of supplies.

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June 23, 2008

First Day

Today was my first official day at Zacamil Hospital. The staff was very helpful and friendly. I spent the day in the ¨Consultas Externas¨ (CE) department, which is similar to an outpatient/triage center. Patients from around San Salvador that have been referred to the hospital first arrive at the CE clinic to be seen and then treated, referred on, or sent home. The reason for the existence of the CE is to ¨weed¨ out unnecessary referrals.

The CE is located in a very small office, about the size of a large walk-in closet. A line forms outside the office at 7am as there are no appointments (first come first serve). In this office, 2-3 doctors reside at a time and patients are seen simulatenously without the luxury of a dividing wall or sheet. If a patient needs to be examined more thoroughly, the other patients are sent out into the hallway.

Although, HIPAA inspectors would have a coronary if they showed up, ultimately, all patients are seen and dealt with in a friendly manner. In fact, the majority have significant issues and are referred to a specialist and seen by said specialist that same day.

I will continue to work in the CE and also rotate through surgery, the emergency department, and internal medicine.

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June 22, 2008
River Blindness (Onchocerciasis) River Blindness is caused by the parasite Onchocerca volvulus. An estimated18 million persons are infected, of whom 3–4 million have skin disease, 500,000 have severe visual impairment, and 300,000 are blinded. While most cases of Onchocerciasis are seen in West Africa, the disease is also prevalent in the Latin America, from Southern Mexico through Northern South America. Onchocerciasis is transmitted by simulium flies (blackflies). These insects breed in fast-flowing streams and bite during the day. After the bite of an infected blackfly, larvae are deposited in the skin, where adults develop over 6–12 months. The disease can be dormant for up to 1-3 years. Eventually the disease produces a red, papular, itchy rash, which may progress to chronic skin thickening and depigmentation. Itching may be severe and unresponsive to medications. In addition, numerous firm, nontender, movable subcutaneous nodules of about 0.5–3 cm, which contain adult worms, may be present. Lymph nodes, especially the inguinal and femoral, can become swollen resulting in a “hanging groin,” with lymph nodes hanging within a sling of atrophic skin. Patients may also have systemic symptoms, with weight loss and musculoskeletal pain. The most well known and significant symptom of Onchocerciasis involves the eyes. Findings include punctate keratitis and corneal opacities, progressing to sclerosing keratitis and blindness. Iridocyclitis, glaucoma, choroiditis, and optic atrophy may also lead to vision loss. The diagnosis of River Blindness is made by identifying microfilariae in skin snips, by visualizing microfilariae in the cornea or anterior chamber by slit-lamp examination, by identification of adult worms in a biopsy or aspirate of a nodule or, uncommonly, by identification of microfilariae in urine. When the diagnosis remains difficult, the Mazzoti test can be used. In this test, a 50-mg dose of diethylcarbamazine is given. A positive test, with exacerbation of skin rash and pruritus, usually within 3 hours, is highly suggestive of the diagnosis. The medicine of choice to treat Onchocerciasis is Ivermectin. While Ivermectin kills microfilariae, it does not kill adult worms, so disease control requires repeat administrations. Treatment is with a single oral dose, but schedules for re-treatment have not been standardized. Protection against Onchocerciasis includes avoidance of biting flies. In fact, major efforts are underway to control insect vectors in Africa. In addition, mass distribution of Ivermectin for intermittent administration at the community level is ongoing, and the prevalence of severe skin and eye disease is decreasing. www.accessmedicine.com - Current Medical Diagnosis and Treatment

River Blindness (Onchocerciasis)

River Blindness is caused by the parasite Onchocerca volvulus. An estimated18 million persons are infected, of whom 3–4 million have skin disease, 500,000 have severe visual impairment, and 300,000 are blinded. While most cases of Onchocerciasis are seen in West Africa, the disease is also prevalent in the Latin America, from Southern Mexico through Northern South America.

Onchocerciasis is transmitted by simulium flies (blackflies). These insects breed in fast-flowing streams and bite during the day. After the bite of an infected blackfly, larvae are deposited in the skin, where adults develop over 6–12 months.

The disease can be dormant for up to 1-3 years. Eventually the disease produces a red, papular, itchy rash, which may progress to chronic skin thickening and depigmentation. Itching may be severe and unresponsive to medications. In addition, numerous firm, nontender, movable subcutaneous nodules of about 0.5–3 cm, which contain adult worms, may be present. Lymph nodes, especially the inguinal and femoral, can become swollen resulting in a “hanging groin,” with lymph nodes hanging within a sling of atrophic skin. Patients may also have systemic symptoms, with weight loss and musculoskeletal pain. The most well known and significant symptom of Onchocerciasis involves the eyes. Findings include punctate keratitis and corneal opacities, progressing to sclerosing keratitis and blindness. Iridocyclitis, glaucoma, choroiditis, and optic atrophy may also lead to vision loss.

The diagnosis of River Blindness is made by identifying microfilariae in skin snips, by visualizing microfilariae in the cornea or anterior chamber by slit-lamp examination, by identification of adult worms in a biopsy or aspirate of a nodule or, uncommonly, by identification of microfilariae in urine. When the diagnosis remains difficult, the Mazzoti test can be used. In this test, a 50-mg dose of diethylcarbamazine is given. A positive test, with exacerbation of skin rash and pruritus, usually within 3 hours, is highly suggestive of the diagnosis.

The medicine of choice to treat Onchocerciasis is Ivermectin. While Ivermectin kills microfilariae, it does not kill adult worms, so disease control requires repeat administrations. Treatment is with a single oral dose, but schedules for re-treatment have not been standardized. Protection against Onchocerciasis includes avoidance of biting flies. In fact, major efforts are underway to control insect vectors in Africa. In addition, mass distribution of Ivermectin for intermittent administration at the community level is ongoing, and the prevalence of severe skin and eye disease is decreasing.

www.accessmedicine.com - Current Medical Diagnosis and Treatment

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June 20, 2008
Chagas Disease (American Trypanosomiasis): Chagas Disease is caused by Trypanosoma cruzi, a protozoan parasite found only in the Americas. It results in about 45,000 deaths annually. The disease is often acquired in childhood. In many countries in Central and South America, American Trypanosomiasis, is the most important cause of heart disease. The parasite is transmitted by reduviid (triatomine) bugs, kissing bugs, infected by ingesting blood from animals or humans who have circulating trypanosomes (it can also be transmitted via blood transfusion or through the placenta). The protozoa are eliminated in feces of the insect and infection in humans occurs when the parasite (from the feces) penetrates the skin through the bite wound, any other wound, mucous membranes, or the conjunctiva.  As many as 70% of infected persons remain asymptomatic. The acute stage is seen principally in children and lasts 1–2 months. The earliest findings are at the site of inoculation. A common site for this to occur is the eye, and results in the Romaña sign, a swelling of the infected eye that appears as a conjunctivits. If infected through the skin a chagoma, swelling with local lymphadenopathy, may occur. Subsequent symptoms include fever, malaise, headache, enlarged spleen, and generalized lymphadenopathy. Acute myocarditis and meningoencephalitis are rare but can be fatal. Chagas Disease can also become chronic manifesting as abnormalities in cardiac and smooth muscle. Cardiac disease includes arrhythmias, congestive heart failure, and embolic disease. Smooth muscle abnormalities lead to megaesophagus and megacolon, with trouble swallowing, regurgitation, aspiration, constipation, and abdominal pain. In immunocompromised patients, such as AIDS patients, Chagas Disease can lead to brain abscesses. In order to diagnose Chagas Disease a blood test for the trypanosomes themselves, culture, or even inoculation of an animal may be used. The treatment of Chagas includes two drugs, nifurtimox and benznidazole. However, these often cause severe side effects and are ineffective against chronic infection. Prevention efforts include improved housing efforts (kissing bugs often live in thatched roofs) and screening before blood transfusion.  www.accessmedicine.com - Current Diagnosis and Treatment

Chagas Disease (American Trypanosomiasis):

Chagas Disease is caused by Trypanosoma cruzi, a protozoan parasite found only in the Americas. It results in about 45,000 deaths annually. The disease is often acquired in childhood. In many countries in Central and South America, American Trypanosomiasis, is the most important cause of heart disease.

The parasite is transmitted by reduviid (triatomine) bugs, kissing bugs, infected by ingesting blood from animals or humans who have circulating trypanosomes (it can also be transmitted via blood transfusion or through the placenta). The protozoa are eliminated in feces of the insect and infection in humans occurs when the parasite (from the feces) penetrates the skin through the bite wound, any other wound, mucous membranes, or the conjunctiva. 

As many as 70% of infected persons remain asymptomatic. The acute stage is seen principally in children and lasts 1–2 months. The earliest findings are at the site of inoculation. A common site for this to occur is the eye, and results in the Romaña sign, a swelling of the infected eye that appears as a conjunctivits. If infected through the skin a chagoma, swelling with local lymphadenopathy, may occur. Subsequent symptoms include fever, malaise, headache, enlarged spleen, and generalized lymphadenopathy. Acute myocarditis and meningoencephalitis are rare but can be fatal.

Chagas Disease can also become chronic manifesting as abnormalities in cardiac and smooth muscle. Cardiac disease includes arrhythmias, congestive heart failure, and embolic disease. Smooth muscle abnormalities lead to megaesophagus and megacolon, with trouble swallowing, regurgitation, aspiration, constipation, and abdominal pain. In immunocompromised patients, such as AIDS patients, Chagas Disease can lead to brain abscesses.

In order to diagnose Chagas Disease a blood test for the trypanosomes themselves, culture, or even inoculation of an animal may be used. The treatment of Chagas includes two drugs, nifurtimox and benznidazole. However, these often cause severe side effects and are ineffective against chronic infection. Prevention efforts include improved housing efforts (kissing bugs often live in thatched roofs) and screening before blood transfusion. 

www.accessmedicine.com - Current Diagnosis and Treatment

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