Comparison of mortality and morbidity rates among Iranian pilgrims in Hajj 2004 and 2005.

OBJECTIVE: We compared the incidence of common diseases and accidents among Iranian pilgrims during Hajj 2004 and 2005, and determined the factors affecting the prevalence of each disease. METHODS: We conducted this comparative study on 30037 Iranian pilgrims during Hajj 2004 and 75676 pilgrims during Hajj 2005, in Mecca and Medina in the Kingdom of Saudi Arabia. In this study, 23 types of common illnesses, 8 types of accidents, some important demographic variables, and some probable related factors were investigated. Two-sample tests of proportions in STATA Statistical Software version 8 was used for the data analysis. RESULTS: The most common diseases during the 2 journeys were respiratory diseases and the incidence of these diseases in Hajj 2005 was twice more in the year 2004. The prevalence of cardiovascular diseases among pilgrims in Hajj 2005 was 142 per 10,000 and it was significantly lower than in Hajj 2004 (288 per 10,000). There was no significant difference among gastrointestinal, gynecological, psychological, and other important diseases, in the 2 journeys. Among the 8 types of accidents, the incidence of head and eye injuries during Ramy (one of the components of Hajj rites) in the year 2005, was significantly lower in 2004 (22 per 10,000 against 125 per 10,000). Furthermore, the mortality rate in the year 2005 with 24 deaths per 100000, was significantly lower than the deaths in 2004 (47 per 100000). CONCLUSION: The findings of this study may guide the Hajj managers to estimate the needs of drugs, equipment, manpower, and educational needs for the pilgrims, also to identify and eliminate casual factors of diseases and accidents.

Plasmodium falciparum: an invasion inhibitory human monoclonal antibody is directed against a malarial glycolipid antigen.

A Plasmodium falciparum malaria blood stage antigen was detected using a human monoclonal antibody (MAb A52A6) obtained from a clinically immune donor. Immunofluorescence analysis showed that the MAb reacted with the intracellular parasite throughout the asexual blood stage cycle as well as with gametocytes. The MAb also reacted with the surface of erythrocytes containing late stage P. falciparum parasites. The antigen seen by the MAb was species- but not strain- or isolate-specific. At rupture of the infected erythrocytes, antigenic material was deposited on the membrane of uninfected cells surrounding the parasite. At merozoite invasion MAb reactive material was present on the invaginating erythrocyte membrane, indicating an involvement of the antigen in the invasion process. This was also indicated by the high capacity of the MAb to inhibit merozoite invasion in vitro. The antigen appears to be a phosphoglycolipid, sensitive to phospholipase and present in lipid extracts of P. falciparum-infected erythrocytes.

The effect of tunicamycin on target cell susceptibility to natural killer cell cytotoxicity.

Several sets of data indicate the possibility that carbohydrate moieties on the target cell are important structures in natural killer (NK) cell-mediated lysis. Striking changes in the NK susceptibility of targets can be induced in several systems involving in vitro differentiation of tumour cell lines. The effect on target cells of the glycosylation inhibitor tunicamycin, which acts by blocking the dolichol-dependent asparagine-linked glycosylation pathway was investigated. Using several different tumour cell lines we can conclude that: asparagine-linked carbohydrate chains do not contribute directly to NK susceptibility, induced differentiation may or may not be linked with a change in NK susceptibility, and secondary changes caused by tunicamycin treatment may lead to alterations in the gangliosides, a finding that is positively correlated with decreased NK susceptibility.

The role of myelin lipids in experimental allergic encephalomyelitis. III. Transfer of suppression from guinea pigs recovering from EAE, induced by myelin basic protein--galactocerebroside complexes.

Juvenile strain 13 guinea pigs were immunized with myelin basic protein (MBP) combined with galactocerebrosides (MBP + GC) or with total myelin lipids without GC [MBP + (TL-GC)] in CFA. Control animals received dinitrophenylated-ovalbumin (DNP-OA) in CFA, CFA or IFA alone. The animals injected with MBP + GC showed a higher rate of recovery from the first EAE episode (83%) than those treated with MBP + (TL-GC) (50%). With the exception of the group treated with IFA alone, all animals were refractory to EAE following rechallenge with MBP in CFA 90 days after the first exposure. The in vitro proliferative response to MBP, of peripheral blood lymphocytes (PBLs) derived from guinea pigs freshly sensitized to MBP in CFA, was drastically suppressed in the presence of PBLs from animals injected with MBP + GC. Upon transfer to normal syngeneic recipients, spleen cells from MBP + GC-treated animals completely suppressed the clinical and histological manifestations of EAE following recipient challenge with MBP in CFA. Cell-free supernatants from PBLs and spleen cells of strain 13 guinea pigs treated with MBP + GC inhibited lymphocyte proliferation to MBP, of allogeneic responder cells, and spleen cell supernatants completely suppressed the induction of EAE upon transfer to allogeneic recipients. Suppression could not be transferred with cells from other treated groups. These results suggest that animals immunized with MBP + galactocerebrosides in CFA develop suppressor cells that may be in part responsible for the recovery from the first EAE episode and for protection against rechallenge with MBP in CFA. Their cell-free supernatants act in an MHC-nonrestricted fashion. These results do not rule out an additional protective mechanism since all animals exposed to CFA were refractory to rechallenge despite lack of demonstrable suppressor cell activity.

The role of myelin lipids in experimental allergic encephalomyelitis. Part 2. Influence on disease production by encephalitogenic doses of myelin basic protein.

Hartley guinea pig CNS myelin lipids (TL) were combined with an encephalitogenic dose (50 micrograms) of myelin basic protein (MBP) and injected together with complete Freund's adjuvant (CFA) into juvenile strain 13 guinea pigs. All the animals developed acute EAE and recovered, but only 50% had a single mild relapse during an observation period of 12 months. To determine the effect of individual myelin lipids on EAE, purified fractions comprising the galactocerebrosides (GC) or gangliosides (GANG) were combined with 50 micrograms MBP together with phosphatidyl choline (PC) and cholesterol (CHOL) and injected with CFA into juvenile Hartley guinea pigs. Control animals received MBP mixed with PC and CHOL or MBP alone, in CFA. The incidence of acute EAE was similar in all groups, but the highest percent recovery (69%) was seen in animals immunized with the MBP-GC combination. All animals that developed acute EAE in the control groups died. Histologically, CNS myelin breakdown was present during the acute attack except in the MBP control group. Parameters of cell-mediated immunity (CMI) showed good correlation with the clinicopathological findings in animals that received MBP-GC or MBP alone. In most animals, serum anti-MBP antibodies were detected as early as 10 days post-immunization (p.i.) whereas anti-lipid antibodies were found at 90 days p.i. Animals that received MBP-PC did not show any positive CMI or serum antibodies although they developed severe disease. The results indicate that myelin lipids, especially the galactocerebrosides, contribute to the development of chronic EAE; however, the mechanism by which this occurs is still obscure.

The role of myelin lipids in experimental allergic encephalomyelitis. Part 1. Influence on disease production by non-encephalitogenic doses of myelin basic protein.

Hartley guinea pig central nervous system (CNS) myelin has been purified and fractionated into its protein and lipid components. Experimental allergic encephalomyelitis (EAE) was induced in juvenile strain 13 guinea pigs with both lyophilized and fresh 'wet' myelin. However, a larger dose of lyophilized myelin was required to induce chronic EAE. Total myelin lipids, galactocerebrosides, gangliosides, phospholipids or proteolipids were combined with a non-encephalitogenic dose of myelin basic protein (MBP) and injected in juvenile Hartley guinea pigs. No clinical or histological manifestations of disease were observed. Parameters of immune functions indicated that the total myelin lipids augmented cell-mediated immune responses as measured by in vitro lymphocyte transformation and by a significant decrease in the percentage of peripheral early T cells. Only the proteolipids elicited delayed hypersensitivity reactions. Animals that received the phospholipid-MBP combination showed no changes when compared to animals injected with MBP alone. The results suggest that although the myelin lipids did not act synergistically with a non-encephalitogenic dose of MBP to induce EAE, they induced immunological changes and potentiated the immune response to MBP.

Isoelectric focusing of cerebrospinal fluid proteins in the diagnosis of multiple sclerosis.

Isoelectric focusing was adapted for analysis of cerebrospinal fluid (CSF) proteins with commercially available materials. CSF from cases of multiple sclerosis or chronic neurologic infections showed abnormal populations of IgG, verified by immunofixation, particularly in the high-alkaline regions (high-alkaline bands). Agarose electrophoresis showed a similar number of abnormal specimens, but patterns were more clearly defined by isoelectric focusing. Despite increased sensitivity, isoelectric focusing is too complex to replace agarose electrophoresis, but it may be useful in clinically difficult cases when agarose electrophoresis patterns are questionable.