Escobar syndrome in three male patients of same family.

We describe three male individuals from a consanguineous south Indian family affected with the multiple pterygium syndrome (Escobar syndrome). Common clinical features included short stature, multiple pterygium, skeletal anomalies, and normal intelligence. The first report of this condition was made in 1902 from this same place (Pondicherry) and the disease received its present popular name Escobar syndrome in 1982. The genetic defect for this condition was identified in 2006 as mutation in the fetal acetylcholine receptor.

Alkyl succinate poisoning.

A case of alkyl succinate poisoning is being reported. Oral ingestion of this compound led to gastrointestinal tract involvement and central nervous system manifestatations suggestive of parkinsonism. The patient recovered completely following conservative management without any sequelae.

A clinical and laboratory profile of Cleistanthus collinus poisoning.

AIMS: 1. To study the clinical features in patients with Cleistanthus collinus poisoning, 2.To study in them the effect of Cleistanthus collinus poisoning on the various organ systems and metabolic parameters using standard laboratory investigations. METHODS: All patients admitted to the hospital between September 1998 and April 2000 were studied. Statistical analysis of the results was done using chi-square test, Fisher's exact test and Student's 't' test. RESULTS: Forty six cases were studied, 15 (32%) of whom died. Eighty percent of the patients were in the second to third decade. The female:male ratio was 3:2. Ingestion of the poison as a decoction prepared from the leaves and ingestion of a large number of leaves otherwise were associated with a poor outcome. While survivors remained relatively asymptomatic, fatally poisoned patients presented with significant clinical signs and symptoms, however, laboratory abnormalities such as hypokalaemia, hyponatremia, an elevated AST/LDH/CPK/CPK-MB, nonspecific ST-T changes and QTc prolongation on ECG, metabolic acidosis and hypoxia with widened alveolar-arterial oxygen difference (A-aDO2) were seen in both groups. CONCLUSION: It is a poisoning seen in the young with significant mortality. Cause of death appears to be mainly due to its cardiac and respiratory effects. Metabolic disturbances especially hypokalaemia was a prominent feature. Most deaths occurred on the 3rd day and all within a week. No specific antidote is available.

Amoebic liver abscess in a patient with human immunodeficiency virus infection.

A thirty two years man, heterosexually promiscuous presented with amoebic liver abscess, proven by ultrasonography, aspiration and culture of organism. He was human immunodeficiency virus (HIV) seropositive and had low CD4+ lymphocyte count. He responded to anti-amoebic treatment.

Differential recognition of Brugia malayi antigens by bancroftian filariasis sera.

Individuals residing in an area endemic to Wuchereria bancrofti infection were broadly categorised as endemic normals (EN), microfilaraemics (mf + ve) and elephantoids i.e., chronic lymphatic filariasis (EL). The immune status of these three groups was examined in terms of (i) specific antibody levels; (ii) ability to induce antibody dependent cellular cytotoxicity (ADCC) to microfilariae; and (iii) ability to recognise different microfilarial antigens by immunoblotting. All three groups of endemic residents were indistinguishable in their antibody levels as measured by ELISA with B. malayi microfilarial antigen. Many endemic normal sera and most elephantoid sera exerted strong cytotoxicity against W. bancrofti microfilariae whereas none of the mf + ve sera had any such activity. Immunoblotting studies revealed that a protein with mol. wt of 79 KDa was the only one among the proteins of B. malayi microfilarial extracts that was consistently recognised by sera from all endemic residents. Endemic normal sera and elephantoid sera, which exerted maximum cytotoxicity, together specifically recognised three proteins with molecular weights 25, 58 and 68 KDa and these three proteins could be among the candidate antigens that induce resistance to filarial infection.

Sharing of antigens among filarial species revealed by antibody dependent cell-mediated reactions.

Antisera raised in albino rats against microfilariae of Litomosoides carinii, Brugia pahangi, Brugia malayi and sera from Bancroftian elephantiasis patients promoted rat neutrophil-mediated adherence and cytotoxicity to the microfilariae. Pre-treatment of the immune sera, with microfilarial antigen at a final concentration of 5 and 25 μg per ml blocked cellular adherence and cytotoxicity to the microfilariae indicating the presence of crossreactive antibodies. The heterologous immune sera were effective in eliminating the circulating Litomosoides carinii microfilariae in Mastomys natalensis.

Brugia malayi: serum dependent cell-mediated reactions to microfilariae.

Sheathed and exsheathed microfilariae of Brugia malayi are killed by normal rat cells in the presence of immune serum in vitro. Immune serum heated at 56 degrees C for 1 hour lost this activity which was largely restored by the addition of fresh normal rat serum. EDTA but not EGTA abolished this activity indicating the operation of complement by alternate pathway. Fresh normal rat serum alone promoted cellular adherence without exerting cytotoxicity to the microfilariae. The activity in the immune serum could be removed with Staphylococcus aureus cells containing Protein A or anti-IgG antiserum. The activity could also be absorbed to and eluted from Protein A--sepharose CL-4B suggesting the involvement of IgG. Neutrophils and macrophages participate in the antibody dependent cell-mediated cytotoxicity phenomenon. Eosinophils while adhering to the microfilariae exert cytotoxicity only to the exsheathed parasites.