Malaria in pregnancy poses a great health risk to mother and her fetus and results into complications, such as abortion, still birth, intra uterine growth retardation, and low birth weight. The heavy infiltration of Plasmodium falciparum-infected RBCs in the intervillous spaces of placenta seems to be responsible for all the complications observed. Infected RBCs in the placenta cause an inflammatory environment with increase in inflammatory cells and cytokines which is deleterious to the placenta. Increased inflammatory responses in the infected placenta result into oxidative stress that in turn causes oxidative stress-induced placental cell death. Moreover, heat shock proteins that are produced in high concentration in stressed cells to combat the stress have been reported in fewer concentrations in malaria-infected placenta. Pathologies associated with placental malaria seems to be the effect of a change in immune status from antibody-mediated immune response to cell-mediated immune response resulting into excess inflammation, oxidative stress, apoptosis, and decreased heat shock protein expression. However, we also need to study other aspects of pathologies so that better drugs can be designed with new molecular targets.

Placental malaria is a common clinical complication during pregnancy and is associated with abortion, premature delivery, intrauterine growth retardation and low birth weight. The present study was designed to delineate the underlying mechanism of placental pathology during malarial infection with special reference to oxidative stress and apoptosis. Experimentally, pregnant BALB/c mice were infected with Plasmodium berghei infected red blood cells on gestation day 10. The presence of malarial infection in placenta was confirmed by histopathological studies. It was observation that infected placenta had plugged placental sinusoids with parasitized red blood cells and malarial pigments. Interestingly, we found significant increase in the level of malondialdehyde, the index of oxidative stress and decreased activity of catalase, the antioxidant in infected placenta. Furthermore, in infected placenta the oxidative stress mediated apoptosis was determined by DNA fragmentation assay, ethidium bromide/acridine orange staining and caspase activity. It was observed that oxidative stress begin after second day of malarial infection. Interestingly, it was observed that there was down regulation of anti-apoptotic protein Bcl-2 and up regulation of pro-apoptotic protein Bax in infected placenta, suggesting the involvement of mitochondrial pathway of apoptosis which was further confirmed by activation of caspase 9. However, no change in the expression of Fas gene and caspase 8 activity, indicated the absence of death receptor pathway. Thus, it can be concluded that the placental pathology during malarial infection is mediated by mitochondrial pathway of apoptosis occurring due to augmented lipid peroxidation which may in turn jeopardise the materno-fetal relationship.

Sphingolipids are the major constituent of the mucus secreted by the cells of epithelial linings of lungs where they maintain the barrier functions and prevent microbial invasion. Sphingolipids are interconvertible, and their primary and secondary metabolites have both structural and functional roles. Out of several sphingolipid metabolites, sphingosine-1 phosphate (S1P) and ceramide are central molecules and decisive for sphingolipid signaling. These are produced by enzymatic activity of sphingosine kinase-1 (SK-1) upon the challenge with either biological or physiological stresses. S1P and ceramide rheostat are important for the progression of various pathologies, which are manifested by inflammatory cascade. S1P is a well-established secondary messenger and associated with various neuronal, metabolic, and inflammatory diseases other than respiratory infections such as Chlamydia pneumoniae, Streptococcus pneumoniae, and Mycobacterium tuberculosis. These pathogens are known to exploit sphingolipid metabolism for their opportunistic survival. Decreased sphingosine kinase activity/S1P content in the lung and peripheral blood of tuberculosis patients clearly indicated a dysregulation of sphingolipid metabolism during infection and suggest that sphingolipid metabolism is important for management of infection by the host. Our previous study has demonstrated that gain of SK-1 activity is important for the maturation of phagolysosomal compartment, innate activation of macrophages, and subsequent control of mycobacterial replication/growth in macrophages. Furthermore, S1P-mediated amelioration of lung pathology and disease severity in TB patients is believed to be mediated by the selective activation or rearrangement of various S1P receptors (S1PR) particularly S1PR2, which has been effective in controlling respiratory fungal pathogens. Therefore, such specificity of S1P–S1PR would be paramount for triggering inflammatory events, subsequent activation, and fostering bactericidal potential in macrophages for the control of TB. In this review, we have discussed and emphasized that sphingolipids may represent effective novel, yet dual specific drug targets for controlling pulmonary infections.

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The main objective of the present study was to report the prevalence of methicillin resistant Staphylococcus aureus (MRSA) among bovines used for milk production in Mathura, India. A total of 80 milk samples were collected from clinical and subclinical cases of mastitis from cows (40) and buffalos (40). Milk samples were processed for isolation and identification of S. aureus using standard bacteriological procedures. Staphylococcus aureus were isolated from only 27 samples showing the overall incidence of Staphylococcus aureus in clinical as well as sub clinical mastitis was 33.75%. The incidence of Staphylococcus aureus was higher (50.00%) in clinical mastitis in comparison to that of subclinical mastitis (17.50%). The results revealed that the incidence of Staphylococcus aureus in clinical as well as sub-clinical mastitis was higher in cattle in comparison to buffaloes. Drug sensitivity revealed the 100% resistance against penicillins followed b y vancomycin (88.89%), nalidixic acid (77.78%), cefixime, methicillin, novobiocin (66.67% each), amoxiclav, colistin, pipemidic acid (55.56% each), ofloxacin, streptomycin, sulphamethizole (44.44% each), ampicillin/sulbactam, cefalexin, cefazolin, cefoperazone, enrofloxacin, floxidin, meropenem (33.33% each), cefuroxim, ciprofloxacin, clindamycin, gentamicin, levofloxacin, norfloxacin, tetracycline (22.22% each). Eighteen isolates were found to be methicillin-resistant, while the remaining (09) were methicillin-susceptible. Similarly, twenty four S. aureus isolates were intermediate to vancomycin while three were vancomycin susceptible and no isolate was resistant to vancomycin. Thus, the findings are useful for formulating specific control programs for bovine mastitis caused by S. aureus in this region.