Cases of what is believed to have been rickets have been described since the 1st century, and the condition was widespread in the Roman Empire. The disease was common into the 20th century. Early treatments included the use of cod liver oil. Signs and symptoms
Signs and symptoms of dietary deficiency rickets can include bone tenderness, and a susceptibility for bone fractures, particularly greenstick fractures. Early skeletal deformities can arise in infants such as soft, thinned skull bones – a condition known as craniotabes, which is the first sign of rickets; skull bossing may be present and a delayed closure of the fontanelles. Young children may have bowed legs and thickened ankles and wrists; older children may have knock knees. Spinal curvatures of kyphoscoliosis or lumbar lordosis may be present. The pelvic bones may be deformed. A condition known as rachitic rosary can result as the thickening caused by nodules forming on the costochondral joints. This appears as a visible bump in the middle of each rib in a line on each side of the body. This somewhat resembles a rosary, giving rise to its name. The deformity of a pigeon chest may result in the presence of Harrisons groove. Hypocalcemia, a low level of calcium in the blood can result in tetany – uncontrolled muscle spasms. Dental problems can also arise.An X-ray or radiograph of an advanced patient with rickets tends to present in a classic way: the bowed legs (outward curve of long bone of the legs) and a deformed chest.
The proglottid can copulate with itself, with others in the strobilla, or with those in other worms. When the segment reaches the end of its strobila, it disintegrates en route, releasing eggs in a process called apolysis. Lifecycle
H. nana is the only cestode capable of completing its lifecycle without an intermediate host. It can, however, pass through an intermediate host, as well. The most common intermediate hosts for H. nana are arthropods (e.g. flour beetles). When an egg is ingested by the definitive host, it hatches and releases a six-hook larva called the oncosphere (hexacanth) which penetrates the villi of the small intestine and develops into a cysticercoid. Infection
Transmission of H.nana occurs by the fecal-oral route. It also occurs by accidental ingestion of an insect containing the cysticercoid. Screening for activity against H. nana
H. nana in mice is used because:
Human infection is easily maintained in mice. Its armed scolex is similar to other pathogenic tapeworms. It corresponds to other tapeworms in its sensitivity to standard anthelmintics,Method:
Mature worms are collected from infected mice. Terminal gravid proglottids are removed, crushed under coverslips, and eggs are removed. Eggs containing hooklets (mature) are counted. 0.2 ml stock soln. containing 1000 eggs/ml given to each mouse. Adult worms develop in 15–17 days. The test drug is given orally; mice are necropsied on the third day after treatment. A standard drug is given. The intestines are examined under a dissecting microscope for worms or scolices. The response is measured bt the number mice cleared.