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«Name: Medical Reference Manual Table of Contents 1. Chagas Disease 2. Leishmaniasis 3. Malaria 4. Dengue Fever 5. Diarrhea: Evaluation and Treatment ...»

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Name: ____________________

Medical Reference Manual

Table of Contents

1. Chagas Disease

2. Leishmaniasis

3. Malaria

4. Dengue Fever

5. Diarrhea: Evaluation and Treatment

6. Intestinal Parasites

a. Macroscopic parasites (worms)

b. Microscopic parasites (protozoa)

7. Parasites of the Skin

a. Scabies

b. Lice

8. Fungal infections of the skin

9. Eye diseases

a. Pterygium

b. Conjunctivitis

c. Cataracts

10. Iron-deficiency Anemia

11. Pharmacology

12. Home Cures and Popular Beliefs

13. Medicinal Plants

NOTE: Please bring a copy of this document with you on your trip by either printing a copy or by downloading and saving this PDF to your smart-device.

© 2014 International Service Learning Section I: Chagas disease Introduction - Chagas disease, also known as American triponosomiasis, was discovered in 1909 by Carlos Chagas in Brazil. The discovery of this disease is unusual, in that it presents the anomaly that the vector was discovered first, then the etiological agent, and finally the human consequences. Chagas affects the endothelial system and muscular fibers in particular, especially the stretch fibers found in the heart.

The disease is caused by the parasitic flagellate Trypanosoma cruzii. Reduviid bugs, or kissing bugs, are blood-sucking insects that transmit the disease by biting individuals infected with the parasite.

Subsequent individuals may become infected by coming into contact with feces from the reduviid bugs, receiving contaminated blood transfusions, or the disease may be passed in utero from an infected mother to fetus.

Life cycle

Epidemiology The disease is indigenous to the Americas and is distributed from the southern part of North America to every country in Central and South America. Worldwide, it is estimated that 16 to 18 million people are infected with Chagas disease; of those infected, 50,000 will die each year (CDC website).

The reduviid bugs tend to live in cracks and holes of substandard housing, and thus housing made with non lasting materials such as wood, mud, palm leaves and cardboard tend to be at higher risk for infestations. The prevalence in humans is especially high in rural areas, where up to 15% of the population may be infected with this parasite (Chinchilla, 2002) Trypanisoma cruzii is a parasite that has adapted itself to many different animals, and has also been identified in dogs, foxes, marsupials, rats, and racoons. The parasite has a two different cycles: one in the jungle and another around human establishment. The disparate nature of these two locations suggests there may be a mediator animal between both of them, thus forming an intermediate reservoir. The Trypanisoma cruzii is very sensitive to environment changes. However, despite this fragility, it can survive a few days in refrigerated blood, making the serology study for Trypanisoma cruzii obligatory.

Clinical and pathologic aspects

There are three stages of Chagas disease: acute, intermediate, and chronic:

1. Acute stage: Approximately 1% of the people infected with T. cruzi will develop symptoms. In these individuals, the characteristic sign for a Chagas infection is the Romaña sign, in which the person's eye on one side of the face swells, usually at the bite wound or where feces were deposited or accidentally

rubbed into the eye. Other non-specific symptoms seen in association with Chagas disease include:

• Swollen lymph nodes

• Fever

• Enlarged liver or spleen These symptoms may last from 4-8 weeks and then resolve, or a patient may progress to the intermediate and chronic stages.

2. Intermediate stage: Typically occurs 8 to 10 weeks following initial infection. People at the intermediate stage of infection rarely demonstrate symptoms. This stage may last for several years.

3. Chronic stage: In 20-30% of the infected individuals, the disease will progress to its chronic form. Over time, the body produces antibodies against the T. cruzi parasite. In a select number of individuals, these antibodies also recognize epitopes found on healthy cells, leading to an autoimmune reaction. The

chronic stage produces two different pathological aspects:

• Cardiac problems: enlarged heart, arrhythmias, cardiac insufficiency, heart failure

• Development of “megas”: Destruction of nervous fibers around hollow organs, such as the GI tract. Over time, the elastic condition of those organs will be lost, causing decreased peristalsis and excessive expansion of them. This results in megacolon and megaesophagus in affected individuals.

Diagnosis, Treatment and Prevention During the acute stage, Trypanisoma cruzii may be diagnosed by observing the organism in the peripheral blood, detectable by direct observation under a microscope or with Wright or Giemsa stains. If the chronic stage of Chagas is suspected, diagnosis can be made through blood tests, clinical diagnosis, and EKG.

If Chagas is detected during the acute stage, it is possible to treat with benznidazole or nifurtimox (under an Investigational New Drug protocol from the CDC Drug Service). In the chronic stage of this parasite, there are no effective treatments currently approved for use, though a few products are currently being researched.

Prevention consists in eliminate reservoirs, fumigation, and in generalized improvement in the socialeconomic conditions of an affected area.

Section II: Leishmaniasis Introduction - Leishmaniasis is a parasitic infection caused by the bite of a sandfly infected with the intracellular protozoa Leishmania. There are three forms of Leishmaniasis: cutaneous, mucocutaneous, and visceral.

• The cutaneous form of the disease causes skin lesions all over the body, including the arms, legs, and face.

• The mucocutanous form causes potentially disfiguring lesions of the mucous membranes of the nose, throat, and mouth.

• The visceral form affects the internal organs of the body (including the spleen, liver, and bone marrow).

Figure: Leishmaniasis is capable of causing a variety of symptoms, including cutaneous lesions or attack of the visceral organs, depending on the species.

Currently, there are 3 main species of Leishmania that have been identified: L. donovani, L. tropica and L.

braziliensis. L. donovani produces mainly the visceral form of Leishmaniasis, with a tendency to locate itself in the spleen, liver, bone marrow and lymph nodes (reticuloendothelial system). L. tropica and L.

braziliensis tend to cause the mucocutaneous and cutaneous forms of Leishmaniasis.

Epidemiology - Leishmaniasis is currently found in over 88 countries, placing approximately 350 million people at risk for acquiring the disease. Because the sandfly tends to be susceptible to colder climates, the disease is found primarily in tropical and subtropical locations. Current World Health Organization estimates of people affected by Leishmaniasis approaches 12 million.

Approximately 500,000 cases of visceral Leishmaniasis occur annually, with 90% of these cases found in five countries: India, Bangladesh, Nepal, Sudan, and Brazil. Cutaneous Leishmaniasis affects mainly Afghanistan, Brazil, Iran, Peru, Saudi Arabia, and Syria. Mucocutaneous Leishmaniasis appears mainly in Bolivia, Brazil, and Peru.

The distribution of visceral Leishmaniasis.

The insects that transmit this parasite are phlebotomine sand flies. Disease transmission occurs when the flies bite an infected animal or human. The reservoirs for the parasite are different types of wild rodent. The insects tend to be most active in the evening hours, and are about a third of the size of a mosquito. Lifecycle Clinical and pathological aspects Cutaneous Leishmaniasis: lesions occur in places where the sandflies have fed, usually within a few weeks of the initial bite. Over time, the sores take on a volcanic appearance, with a rounded shape, raised edges and a central crater area. Examinations of the crater area may reveal papilla. Swollen lymph nodes may also be present near the site of the lesions.

Mucocutaneous Leishmaniasis: lesions found on the mucous membranes of the mouth, nose, and throat. Over time, these lesions can cause significant disfiguration. The muco-cutaneous lesions can destroy the nasal bone, as well as the soft palate of the mouth, causing deformations in nose and skin around the lips. Due to these complications, Leishmaniasis is sometimes mistaken for leprosy (Hanson’s Disease).

Visceral Leishmaniasis: This form of the disease is also called kala azar. It develops several months after the initial infection, and is characterized by fever, anemia, weight loss, and enlargement of the spleen and liver. Left untreated, visceral Leishmaniasis has a mortality rate of almost 100%. This form of the disease has also recently emerged as a growing problem, as it is increasingly being identified as an opportunistic infection in individuals infected with HIV. In immunosuppressed individuals, such as those with HIV, the disease progresses rapidly to the visceral form. Visceral Leishmaniasis also appears to accelerate the onset of AIDS in HIV positive individuals.

Diagnosis, Treatment and Prevention Diagnosis of this disease is made via biopsy and subsequent observation of the parasite under microscope, after treating the specimen with Wright, Giemsa or Leishman staining. Further confirmation is sometimes needed through cell culture or animal inoculation. Another laboratory test is the Montenegro reaction, which consists of injecting Leishmaniasis antigen into the dermis of a person suspected to be infected with the parasite. The skin is then examined 48 hours following subdermal injection. Positive results are defined as erythematous (reddened) and swollen area surrounded the site where the antigen was injected.

Treatment is antimony or arsenic products, such as Reprodal and Glucatyme. Both of these drugs are extremely toxic to the liver, and thus therapy must be followed closely by a physician.

Prevention of this disease comes from avoiding exposure to sand flies. Insect repellent, mosquito nets, and insecticide applied to living and sleeping areas can help decrease the risk of exposure. Treatment of patients with Leishmaniasis will also help decrease the number of human reservoirs, as well as eliminate the risk of spread of the disease from blood-borne exposure to infected individuals.

Section III: Malaria Introduction - Malaria is an infection that affects red blood cells and is caused by different species of Plasmodium parasite. From Italian, the name malaria literally means “mal aire” (bad air). Patients suffering from malaria experience periodic attacks of chills, fever, and sweating. Because outbreaks of malaria are associated with areas containing stagnant water, in the past it was assumed that the foul odor of the water was the causative agent of the disease. However, in 1880 Charles Louis Alphonse Laveran, a French army surgeon stationed in Constantine, Algeria, noted the presence of the Plasmodium parasite in a blood smear from a patient suffering from malaria.

Currently, there are two reservoirs present in nature for this parasite: humans and the Anophele mosquito. Malaria is transmitted primarily from human to human transmitted the bites of infected female Anophele mosquitos. The mosquitoes carry the Plasmodium parasite within its salivary glands and inject parasites into humans when it feeds. Transmission may also occur through congenital acquisition or through the transfusion of infected blood products.

Epidemiology - Approximately 41% of the world’s population lives in areas endemic for malaria. Because the Anophele mosquito and the plasmodium parasite require warmer temperatures to survive, malaria is typically found in tropical and subtropical areas. Current figures from the CDC website (www.cdc.gov) estimate that between 700,000 and 2.7 million people die each year from malaria, 75% of them Africa children. Currently, the area most affected by this disease is Sub-Saharan Africa.

The non-human vector responsible for transmission of this disease is the Anophele mosquito. There are different species of the Anopheles, in Central America the most common are A. albimanus and A.

punctimacula. These vectors live in swampy places and some are capable of biting two or three times a day, depending on the feeding habits of a particular species. Both the Anopheles mosquito and the plasmodium parasite are susceptible to climate changes. The malaria parasite is unable to grow and reproduce inside the mosquito vector if temperatures are lower than 16°C or higher than 33°C.

In endemic areas, children are more susceptible to become infected and morbidity among this age group is high. The infectivity rate of malaria decreases proportionally to age increment. In non-endemic areas, the whole population is equally susceptible of getting infected. Occasionally epidemic episodes may be caused by environment or climatic changes, increasing longevity and density of the vector.

Four different species of the Plasmodium parasite cause malaria: P. vivax, P. malariae, P. ovale, and P.

falciparum. P. vivax and P. falciparum cause the majority of infections in the world, especially in Africa. P.

falciparum causes more disease than other species of plasmodium, and tends to have a higher incidence of drug resistant strains. P. vivax infection is uncommon among blacks, as their red blood cells have evolved to eliminate a surface antigen known as the Duffy factor, thus making them resistant to infection.

Life CycleMalaria is spread by mosquitoes of the Anopheles family. (next page)

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