Severe constipation often follows spinal cord injury. The aim of this study was to evaluate transit of contents through the large bowel in patients with paraplegia after a complete transverse lesion of the spinal cord. Transit through the right colon, left colon, and rectum was evaluated in 11 patients (eight males, 3 females; 17 to 63 years old) and data were compared with that of 37 healthy control subjects. In all patients there was either no, or abnormally low, transit at the level of the left colon and rectum. A minor degree of transit delay at the level of the right colon was also present in eight patients. These data indicate that constipation in patients with paraplegia is due to abnormal transit, mainly at the level of the left colon and rectum, and transection of the spine between the C-4 and T-12 vertebral levels causes alteration of large-bowel motor activity mainly at the level of the segments innervated by the parasympathetic fibers of the sacral outflow.

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Cryptosporidium parvum is a protozoan which causes self-limiting diarrhea in immunocompetent subjects, and severe life-threatening disease in immunocompromised patients. Cryptosporidiosis is more common in developing countries and in infants. In this paper we have evaluated the prevalence of C. parvum in 368 hospitalized children with enteritis, of whom 359 were immunocompetent and 9 HIV-infected. Stool specimens were concentrated by sedimentation and stained with a modified Ziehl-Neelsen method. Cryptosporidium parvum oocysts were found in 7 (1.90%) out of 368 subjects. Six of these were immunocompetent (with an infection rate in this population of 1.67%) and 1 HIV-infected, asymptomatic except for diarrhea. In all children symptoms of enteritis and oocyst excretion cleared within 10 days. These results indicate that the prevalence of C. parvum as a causative agent of diarrheal illness in hospitalized immunocompetent children is rather low in our region (Apulia, South Italy).

A prospective study was performed in 40 chronic uremics which included: (1) the intramuscular administration to all patients of 40 µg of a DNA-recombinant vaccine (Engerix-B) at 0,1,2,6 months; (2) an intramuscular booster dose of 40 µg at 18 months in patients having an anti-HBs titer > 100/ml at the 7th month (group A); (3) a further intramuscular supplementary dose of 40 µg at 12 months (besides that at 18 months) in patients developing an antibody titer < 100 mlU/ml at the 7th months (group B); (4) an intradermal course of 5 µg of vaccine every 2 weeks until the protective titer ( > 10 mlU/ml) was achieved, and then every month for a total of 6 months in patients who did not develop a protective titer even after 19 months (group C). At the end of the study, all patients had developed a protective titer: 77.5% after the 4th intramuscular dose, 12.5% after the 5th and 10% after 3.5 ± 0.5 (mean ± SEM) intradermal inoculations. The mean antibody titers were 1,461 ± 98 mlU/ml in group A, 594 ± 684 in group B and 131 ± 133 in group C. In conclusion, our two-step integrated protocol gives an anti-HBs protective titer in all our patients.

Protozoan parasites of the Leishmania genus are the causative agents of important diseases in humans and animals. During their life cycle in vertebrate hosts, protozoa are able to live and proliferate within phagolysosomes of host phagocytic cells. The capacity to live in this hostile environment is likely due to the cell surface glycoconjugate expression. In particular, lipophosphoglycan (LPG), a major surface glycoconjugate of Leishmania promastigotes, has been reported to play an active role in protecting parasites within phagolysosomes via the impairment of killing mechanisms. In this review, the authors emphasize some novel LPG-mediated escape mechanisms of promastigotes from human phagocyte responses, such as the impairment of oxidative burst and of chemotactic activity. In the light of these findings, the knowledge of biological actions of LPG may be useful in order to prepare a vaccine against human leishmaniasis, using LPG defective avirulent mutant strains.