You are on page 1of 26

Parasitic Diseases

Description - Malaria is a mosquito-borne infectious disease caused by a eukaryotic protist of the genus Plasmodium

Cause - The cause of malaria is a parasite of the Plasmodium family, which is transmitted by the bite of a female anopheline mosquito. The parasite infects human red blood cells, resulting in lysis of the red blood cell. The four specific causes of malaria seen most commonly are Plasmodium falciparum, Plasmodium vivax, Plasmodium malariae, and Plasmodium ovale

P. falciparum

P. vivax

P. malariae

P. ovale

- Malaria in humans develops via two phases: an exoerythrocytic and an erythrocytic phase. The exoerythrocytic phase involves infection of the hepatic system, or liver, whereas the erythrocytic phase involves infection of the erythrocytes, or red blood cells. When an infected mosquito pierces a person's skin to take a blood meal, sporozoites in the mosquito's saliva enter the bloodstream and migrate to the liver. Within 30 minutes of being introduced into the human host, the sporozoites infect hepatocytes, multiplying asexually and asymptomatically for a period of 615 days. Once in the liver, these organisms differentiate to yield thousands of merozoites, which, following rupture of their host cells, escape into the blood and infect red blood cells, thus beginning the erythrocytic stage of the life cycle. The parasite escapes from the liver undetected by wrapping itself in the cell membrane of the infected host liver cell.

Within the red blood cells, the parasites multiply further, again asexually, periodically breaking out of their hosts to invade fresh red blood cells. Several such amplification cycles occur. Thus, classical descriptions of waves of fever arise from simultaneous waves of merozoites escaping and infecting red blood cells.

Some P. vivax and P. ovale sporozoites do not immediately develop into exoerythrocyticphase merozoites, but instead produce hypnozoites that remain dormant for periods ranging from several months (612 months is typical) to as long as three years. After a period of dormancy, they reactivate and produce merozoites. Hypnozoites are responsible for long incubation and late relapses in these two species of malaria.

The parasite is relatively protected from attack by the body's immune system because for most of its human life cycle it resides within the liver and blood cells and is relatively invisible to immune surveillance. However, circulating infected blood cells are destroyed in the spleen. To avoid this fate, the P. falciparum parasite displays adhesive proteins on the surface of the infected blood cells, causing the blood cells to stick to the walls of small blood vessels, thereby sequestering the parasite from passage through the general circulation and the spleen. This "stickiness" is the main factor giving rise to hemorrhagic complications of malaria. High endothelial venules (the smallest branches of the circulatory system) can be blocked by the attachment of masses of these infected red blood cells. The blockage of these vessels causes symptoms such as in placental and cerebral malaria. In cerebral malaria the sequestrated red blood cells can breach the blood brain barrier possibly leading to coma.

Although the red blood cell surface adhesive proteins (called PfEMP1, for Plasmodium falciparum erythrocyte membrane protein 1) are exposed to the immune system, they do not serve as good immune targets because of their extreme diversity; there are at least 60 variations of the protein within a single parasite and effectively limitless versions within parasite populations. The parasite switches between a broad repertoire of PfEMP1 surface proteins, thus staying one step ahead of the pursuing immune system. Some merozoites turn into male and female gametocytes. If a mosquito pierces the skin of an infected person, it potentially picks up gametocytes within the blood. Fertilization and sexual recombination of the parasite occurs in the mosquito's gut, thereby defining the mosquito as the definitive host of the disease. New sporozoites develop and travel to the mosquito's salivary gland, completing the cycle. Pregnant women are especially attractive to the mosquitoes, and malaria in pregnant women is an important cause of stillbirths, infant mortality and low birth weight, particularly in P. falciparum infection, but also in other species infection, such as P. vivax

Signs and symptoms

- Symptoms of malaria include fever, shivering, arthralgia (joint pain), vomiting, anemia (caused by hemolysis), hemoglobinuria, retinal damage, and convulsions. The classic symptom of malaria is cyclical occurrence of sudden coldness followed by rigor and then fever and sweating lasting four to six hours, occurring every two days in P. vivax and P. ovale infections, while every three for P. malariae. P. falciparum can have recurrent fever every 3648 hours or a less pronounced and almost continuous fever.

Mode of transmission
-The infection is transmitted by the bite of an infected female mosquito Anopheles. An. culicifecies in Rural area & An. stephensi in urban area. The mosquito usually bites during dawn & dust time. The mosquito becomes infected by biting a patient with malaria infection. When a mosquito bites an infected individual, it sucks the gametocytes, the sexual forms of the parasite, along with blood. These gametocytes continue the sexual phase of the cycle and the sporozoites fill the salivary glands of the infested mosquito. Once the mosquito becomes infected, it remains so far life. The female mosquitoes can survive upto 4 weeks under normal temperature i.e. 28C to 30C and humidity i.e. 60 to 80%. When this female mosquito bites the man for a blood meal, which it needs to nourish its eggs, it inoculates the sporozoites into human blood stream, thus spreading the infection.


- Active malaria infection with P. falciparum is a medical emergency requiring hospitalization. Infection with P. vivax, P. ovale or P. malariae can often be treated on an outpatient basis. Treatment of malaria involves supportive measures as well as specific antimalarial drugs. When properly treated, someone with malaria can expect a complete recovery.

Description -Amebiasis is an infectious disease caused by a parasitic one-celled microorganism (protozoan) called Entamoeba histolytica. Persons with amebiasis may experience a wide range of symptoms, including diarrhea, fever, and cramps. The disease may also affect the intestines, liver, or other parts of the body.

Cause - Amebiasis causes when person infected with an amoeba called Entamoeba histolytica. It is transmitted when a person eats food or drinks water contaminated by Entamoeba histolytica. It can be spread from infected person to other by stool. Amebiasis occurs because of crowded living condition. In the case of amebiasis infection can also spread through the blood to the liver,brain or other organs.

E. histolytica frequently lives as a commensal within the large intestine with no overt clinical manifestations. However, trophozoites can invade the colonic epithelium and produce ulcers and dysentery. This invasive disease can become progressively worse and lead to a more serious disease. The amebas can also metastasize to other organs and produce anextraintestinal amebiasis. In other words, E. histolytica is a facultative pathogen that exhibits a wide range of virulence

The non-invasive disease is often asymptomatic, but can cause diarrhea or other gastro-intestinal symptoms such as abdominal pain or cramps. This non-invasive infection can persist or progress to an invasive disease in which trophozoites penetrate the intestinal mucosa and kill the epithelial cells. The early lesion is a small area of necrosis, or ulcer, characterized by raised edges and virtually no inflammation between lesions (Figure). The ameba will spread laterally and downward in the submucosa (beneath the epithelium) and kill host cells as they progress. This results in the classic 'flask-shaped' ulcer with a small opening and a wide base. Trophozoites are most numerous at the boundary between the healthy tissue and the necrotic tissue. These invasive ameba are ingesting host cells and trophozoites with ingested erythrocytes are often evident. These hematophagous trophozoites are sometimes found in the dysenteric feces. Cyst production decreases during the invasive stage of the infection and cysts are never found in the tissue lesions.

The ulcerative process may continue to expand laterally or downward. If large numbers of ulcers are present, they may coalesce which could lead to a localized sloughing off of the intestinal wall. Ulcer expansion can also penetrate the serous layer and lead to perforation of the intestinal wall. This perforation can lead to local abscesses or a generalized peritonitis. Amebic ulcers can also become secondarily infected with bacteria which may confuse the clinical picture. In addition, E. histolytica infection can occasionally lead to the formation of an amebic granuloma, also called an ameboma. The ameboma is an inflammatory thickening of the intestinal wall around the ulcer which can be confused with a tumor.

Amebiasis can also progress to a systemic, or extraintestinal infection. Dissemination from the primary intestinal lesion is predominantly via the blood stream, but can also occur by direct extension of the lesion. The liver is the most commonly affected organ and this is probably due to the direct transport of trophozoites from the large intestine to the liver via the hepatic portal vein. Initially the lesions are small foci of necrosis which tend to coalesce into a single abscess as they expand. This hepatic abscess will continue to enlarge as the trophozoites progressively destroy and ingest host cells. The center of the abscess, consisting of lysed hepatocytes, erythrocytes, bile and fat, may liquefy and this necrotic material (sometimes incorrectly called pus) will range in color from yellowish to reddish brown. Secondary bacterial infections in the liver abscess are not common (~2%).

Hematogenous spread of trophozoites to other sites, such as the lungs or brain, is rare, but does occur. The second most common extraintestinal site after the liver is the lungs. Pulmonary infections generally result from a direct extension of the hepatic lesion across the diaphragm and into the pleura and lungs. Cutaneous lesions formed as a result of hepatic or intestinal fistula can also occur, although extremely rare. Other cutaneous lesions include perianal ulcers and involvement of the genitalia, including the penis of homosexuals. These later manifestations are likely due to the skin or mucous membranes coming in contact with invasive trophozoites.

Signs and Symptoms - Abdominal pain with and urge to go to bathroom frequently. Fever and diarrhea which frequently accompanied with blood and/or mucous discharge. Sometimes diarrhea alternates with bouts of constipation, with one occurring for several days, followed by the other. When diarrhea becomes yellow containing neither mucous nor blood but is foamy, this is known as Giardia, an illness brought on by different type of microscopic parasite. When you have fever and bloody diarrhea, the infection is not caused by amoebas, but by bacteria and it is called Shigella

Mode of transmission - Amoebiasis is usually transmitted by the fecal-oral route, but it can also be transmitted indirectly through contact with dirty hands or objects as well as by analoral contact. Infection is spread through ingestion of the cyst form of the parasite, a semi-dormant and hardy structure found in feces. Any non-encysted amoebae, or trophozoites, die quickly after leaving the body but may also be present in stool: these are rarely the source of new infections. Since amoebiasis is transmitted through contaminated food and water, it is often endemic in regions of the world with limited modern sanitation systems, including Mxico, Central America, western South America, South Asia, and western and southern Africa.

Treatment - The choice of drug depends on the type of clinical presentation and the site of drug action (in the intestinal wall versus inside the intestine itself). Drugs may include metronidazole, paromomycin, iodoquinol, or diloxanide furoate. These drugs have side effects that your physician can discuss with you. Occasionally, it may be necessary to drain a liver abscess. Follow-up care includes stool studies 2 to 4 weeks after completing treatment.