medical biology 3- sporozoa

Class CILIATA

Balantidium Coli

Only ciliate parasitic to man.

COMMON NAME: Balantidiasis, balantidial dysentery.

PATHOGENESIS: Invasion of intestinal mucosa and submucosa.

GEOGRAPHICAL DISTRIBUTION: Cosmopolitan.

HABITAT: Cecum.

INTERMEDIATE HOST: None.

RESERVOIR HOST: Hogs.

INFECTIVE FORM: Mature cyst.

MODE OF INFECTION: Ingestion.

LABORATORY IDENTIFICATION:

SPECIMEN OF CHOICE: Feces

TROPHOZOITE

SIZE: 40 to 50 by 50 to 70 mcm.

SHAPE: Sac-like.

NUCLEUS: Macronucleus: large, enlongate, kidney-shape (mitotic division);

micronucleus: small, spherical (amitotic).

CYTOPLASM: Cell membrane covered with a delicate pellicle.

CILIA: Locomotion and food procurement; fine hair-like projections.

CYTOPYGE: Excretory pore, posterior.

PULSATING VACUOLES: One or two.

CYST

SIZE: 30 by 55 mcm.

SHAPE: Oval to round.

NUCLEUS: Only the macronucleus is seen.

CYTOPLASM: Double cyst wall; remnants of cilia and gullet.

Balantidium coli life cycle

The trophozoites reside in the lumen of the large intestine of humans and animals, where they replicate by binary fission, during which conjugation may occur. Cysts are formed and passed with feces. The cyst is the infectious stage and is acquired by the host most often through ingestion of contaminated food or water. Following

ingestion, excystation occurs in the small intestine, and the trophozoites colonize the large intestine.

Phylum Apicomlexa

Class Sporozoa

Isospora belli

A B C

Oocysts of Isospora belli. The oocysts are large (25 to 30 µm) and have a typical ellipsoidal shape. When excreted, they are immature and contain one sporoblast (A, B). The oocyst matures after excretion: the single sporoblast divides in two sporoblasts (C), which develop cyst walls, becoming sporocysts, which eventually contain four sporozoites each. Images contributed by Georgia Division of Public Health.

Isospora belli life cycle

This graphic the life cycle of Isospora belli. At time of excretion, the immature oocyst contains usually one sporoblast (more rarely two). In further maturation after excretion, the sporoblast divides in two (the oocyst now contains two sporoblasts); the sporoblasts secrete a cyst wall, thus becoming sporocysts; and the sporocysts divide twice to produce four sporozoites each. Infection occurs by ingestion of sporocysts-containing oocysts: the sporocysts excyst in the small intestine and release their sporozoites, which invade the epithelial cells and initiate schizogony. Upon rupture of the schizonts, the merozoites are released, invade new epithelial cells, and continue the cycle of asexual multiplication. Trophozoites develop into schizonts which contain multiple merozoites. After a minimum of one week, the sexual stage begins with the development of male and female gametocytes. Fertilization results in the development of oocysts that are excreted in the stool. Isospora belli infects both humans and animals.

Clinical Features

Infection causes acute, non bloody diarrhea with crampy abdominal pain, which can last for weeks and result in malabsorption and weight loss. In

immunodepressed patients, and in infants and children, the diarrhea can be severe. Eosinophilia may be present (differently from other protozoan infections).

•Toxoplasma gondii

•The definitive host of T. gondii is the cat , but the parasite can be carried by many warm-blooded animals (birds or mammals). Toxoplasmosis, the disease of which T. gondii is the causative agent, is usually minor and self-limiting but can have serious or even fatal effects on a fetus whose mother first contracts the disease during pregnancy or on an immunocompromised human or cat.

Toxoplasma

gondii

COMMON NAME: None.

GEOGRAPHICAL DISTRIBUTION: Worldwide.

PATHOGENESIS: 30 to 90 percent human infection; acquired: asymptomatic, rarely a severe systemic disease; congenital: acute or chronic; implicated as one of the leading causes of birth defects; primarily diagnosed serologically.

HABITAT: Intracellular parasite; infects any nucleated cell of the body; intestinal epithelium (initially) in felines only: predominance in brain and retina.

Toxoplasma gondii in the bronchoalveolar lavage (BAL) material from an HIV infected patient. Numerous trophozoites (tachyzoites) can be seen, which are

typically crescent shaped with a prominent, centrally placed nucleus. Most of the tachyzoites are free, some are still associated with bronchopulmonary cells.

Toxoplasma gondii oocysts - fecal flotation from a cat. 100X objective, Compare the relative size of Isospora felis to the Toxoplasma oocysts.

INTERMEDIATE HOST: RESERVOIR HOST:

Humans and many Cats and other

other mammals; cats domestic animals

and other felines are (reservoirs for human

definitive hosts infection).

INFECTIVE FORM: Infective oocysts from cat feces; or tissue trophozoites or cysts.

MODE OF INFECTION: Ingestion of oocysts; spread by the blood; placental penetration; ingestion of raw or poorly cooked meat.

LABORATORY IDENTIFICATION: Blood, tissue biopsy.

Malaria

causative agents and vectors

Plasmodium vivax

Anopheles albimanus mosquito feeding on a human arm. This mosquito is a vector of malaria and mosquito control is a very effective way of reducing the incidence of malaria

Anopheles albimanus mosquito feeding on a human arm.

Plasmodium Life Cycle

Different life’s states

Early malarial merozoite infection. The light pink cells are red blood cells (RBCs).

Plasmodium ring stage

Merozoites

Plasmodium vivax - malaria late merozoites (lower object).

Plasmodium vivax - malaria late merozoites

Clinical Features

The symptoms characteristic of malaria include flu-like illness with fever, chills, muscle aches, and headache. Some patients develop nausea, vomiting, cough, and diarrhea. Cycles of chills, fever, and sweating that repeat every one, two, or three days are typical. There can sometimes be vomiting, diarrhea, coughing, and yellowing (jaundice) of the skin and whites of the eyes due to destruction of red blood cells and liver cells.

People with severe P. falciparum malaria can develop bleeding problems, shock, liver or kidney failure, central

nervous system problems, coma, and can die from the infection or its complications. Cerebral malaria (coma, or altered mental status or seizures) can occur with severe P. falciparum infection. It is lethal if not treated quickly; even with treatment, about 15%-20% die.