infections Vitamin C and Infections In the early literature, vitamin C deficiency was associated with pneumonia. After its identification, a number of studies investigated the effects of vitamin C on diverse infections. A total of 148 animal studies indicated that vitamin C may alleviate or prevent infections caused by bacteria, viruses, and protozoa. The most extensively studied human infection is the common cold. Vitamin C administration does not decrease the average incidence of colds in the general population, yet it halved the number of colds in physically active people. Regularly administered vitamin C has shortened the duration of colds, indicating a biological effect. However, the role of vitamin C in common cold treatment is unclear. Two controlled trials found a statistically significant dose–response, for the duration of common cold symptoms, with up to 6–8 g/day of vitamin C. Thus, the negative findings of some therapeutic common cold studies might be explained by the low doses of 3–4 g/day of vitamin C. Three controlled trials found that vitamin C prevented pneumonia. Two controlled trials found a treatment benefit of vitamin C for pneumonia patients. One controlled trial reported treatment benefits for tetanus patients. mers paradox Enhanced inflammation in New Zealand white rabbits when MERS-CoV reinfection occurs in the absence of neutralizing antibody we inoculated rabbits with MERS-CoV and monitored the antibody and inflammatory response. Following intranasal infection, rabbits developed a transient dose-dependent pulmonary infection with moderately high levels of viral RNA, viral antigen, and perivascular inflammation in multiple lung lobes that was not associated with clinical signs. The rabbits developed antibodies against viral proteins that lacked neutralizing activity and the animals were not protected from reinfection. In fact, reinfection resulted in enhanced pulmonary inflammation, without an associated increase in viral RNA titers. Interestingly, passive transfer of serum from previously infected rabbits to naïve rabbits was associated with enhanced inflammation upon infection. We further found this inflammation was accompanied by increased recruitment of complement proteins compared to primary infection. However, reinfection elicited neutralizing antibodies that protected rabbits from subsequent viral challenge. Our data from the rabbit model suggests that people exposed to MERS-CoV who fail to develop a neutralizing antibody response, or persons whose neutralizing antibody titers have waned, may be at risk for severe lung disease on re-exposure to MERS-CoV.

scurvy Modern American scurvy - experience with vitamin C deficiency at a large children's hospital. Vitamin C deficiency is not uncommon in large pediatric health care facilities, and it is frequently missed on clinical evaluation and diagnostic imaging. At-risk populations include those with iron overload, neurologic conditions and history of chemotherapy. Scurvy related to dietary deficiency in otherwise normal children was not encountered. When characteristic MRI findings are seen, particularly in children with a predisposing condition for vitamin C deficiency, scurvy should be considered and a serum ascorbic acid level checked to potentially confirm a diagnosis prior to further invasive tests. too much Flu Vaccine—Too Much of a Good Thing? "In one year of the study, it appeared that multiply vaccinated subjects were actually more likely to develop influenza than unvaccinated subjects " "A similar effect was noted during the 2009 influenza A virus subtype H1N1 pandemic when increased rates of pandemic H1N1 were reported in patients who had previously received seasonal H1N1 vaccine in Canada [8]" "The authors speculate that this might be consistent with a disease-enhancing effect of influenza vaccine. Vaccine-enhanced disease has been recognized as a potential problem in other human infectious diseases such as dengue [10] and respiratory syncytial virus [11], and can be a significant obstacle to vaccine development. There is relatively little evidence to support any form of enhanced influenza disease in humans, although disease enhancement by low-avidity antibodies with deposition of immune complexes in the lungs was reported in the 2009 pandemic [12]. "