PubMed · 15500898
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
Prakash Manikoth, Mariam George, Avirat Vaishnav, Mohammed Jaffer Sajwani. Omphalitis.. https://doi.org/10.1016/s0140-6736(04)17276-0
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Over the past century, the incidence of cancer rose markedly in developed countries. Many underlying factors are known, but not all of them. Over the same century, advances in public health and hygiene practically eradicated many infectious illnesses, and exposure to some untargeted infectious agents has also declined. There are reasons to suspect that these two trends are linked. Although some viruses and one bacterium are known to be oncogenic, a high percentage of infectious agents, 71% of viruses tested in one study, have shown oncolytic properties. Some of these agents have minimal or no clinical consequences, and some are - or were - quite ubiquitous. Many types of cancer are unusually susceptible to several different agents, sometimes 10-1000 times more susceptible than normal cells. When wild-type or attenuated viruses are used to treat cancer, they are often more effective with smaller tumors, and it may be that nascent, undetectable cancers are especially vulnerable. Environmental exposure to bacteria and viruses may provide natural protection from cancer by attacking it at this stage, or inducing the body to do so. Immunity to an infectious agent can attenuate its oncolytic effect, but generally does not stop it, so both initial and repeated exposures may be protective. As more direct evidence, treatment of animals with selected live virus vaccines has provided protection from cancer, and in humans, exposure to two specific infectious agents is known to correlate with a reduced risk of cancer. The significant decline in exposure to infectious agents over the past century may have inadvertently weakened this naturally protective mechanism, driving cancer rates up. There is considerable research on the impact of oncogenic agents, but surprisingly little regarding the impact of oncolytic agents on cancer rates. An understanding of the relationship between natural infections and the suppression of cancer may lead to prophylactic measures against cancer, improved public health policies regarding vaccination programs and hygiene, and greater insight into cancer treatment as well.
Explore the source record for details and available documents.
The recent literature brings nothing new since it provides only fragmented, though undoubtedly useful, studies which remain within the prevalence interval for the different bacterias. The occurrence of germs varies with time and space; nevertheless, whatever the studied series and the site of the studies, the 3 most frequent causal germs belong to the following five strains: Streptococcus pneumoniae, Influenza A, Mycoplasma pneumoniae, Haemophilus influenzae, and Legionella pneumophila. Thus, 90% of all documented pneumoniae appear to be caused by the following pathogens: Pneumococcus; most frequent in hospitalized patients; Mycoplasma, Chlamydia and respiratory viruses were predominant in outpatients, with great variations; Staphylococcus and enterobacteriace may be encountered, mostly in elderlies with major debilitating diseases; association of germs, generally including pneumococcus, are increasingly identified. Last, in 25% to 50% of cases, the causal agent is not known. Recently, some Staphylococcus meticillin-resistant were identified. The diagnosis of viruses (as well as that of atypical bacterias) seems to have improved, thanks to the use of PCR though the interest of such a diagnosis remains questionable, except for epidemiological studies, as well as the relevance of this type of test in clinical practice. Nothing really new has come out on the epidemiology of acute bronchitis, while in bacterial exacerbation of COPD, attention focused on the colonizing or infective role of H. influenzae in the genesis of bronchus inflammation.