Helicobacter spp

Moran, A.P., Appelmelk, B.J., Aspinall, G.O. Molecular mimicry of host structures by lipopolysaccharides of Campylobacter and Helicobacter spp. implications in pathogenesis. J Endotoxin Res 3 (1996) 521-531. 

It could be said that Gerald left the best for last. During the 1990s, the fine structural investigations that delved into the complex cell-surface saccharides expressed by the Campylobacter and Helicobacter spp. revealed how these microorganisms exhibited molecular mimicry of the carbohydrate structures of the hosts. These structural findings would later explain many of the clinical features of Campylobacter and Helicobacter spp. infections. 

For millions of years prokaryotes have orchestrated their genetic players to produce survival strategies that overcome almost all ills that bacterial flesh is heir to. Infection of mammalian gastric mucosae by Helicobacter spp. is due to this organism s insistence on habitation of probably the most unfriendly environment in the mammalian body, the inside of the stomach. The eradication of H. pylori for treatment of peptic ulcer disease not associated with nonsteroidal anti-inflammatory drugs (NSAIDs), steroids or severe stress is now accepted as part of medical treatment of this set of illnesses. Whether the infection should always be treated with violence is a point of discussion [1]. 

The urease produced by Helicobacter spp. is a neutral pH optimum enzyme [12] therefore, a fall of cytoplasmic pH is not an adaptive mechanism for this organism. The inhabitation of the gastric mucosa by Helicobacter such as H. pylori requires specialization of properties of this micro-aerophilic bacterial species in order to enable survival and growth on the gastric surface and within antral glands. It should be noted that there are also Helicobacter that do not inhabit the stomach, although why some of them have gastric adapted and some not is as yet unknown [13]. 

Sjostrom JE, Kiihler T, Larsson H (1997) Basis for the selective antibacterial activity in vitro of proton pump inhibitors against Helicobacter spp. Antimicrob Agents Chemother 41 1797-1801... 

We also created a bank of crystaUograms of many other clinically significant microorganisms Staphylococcus spp.. Micrococcus spp., Enterobacter spp., Proteus spp., Klebsiella spp., Serratia spp., Lactobacterium spp., Bacteroides spp.. Streptococcus pneumoniae, Escherichia coli. Pseudomonas aeruginosa. Bacillus subtilis, Helicobacter pylori, etc.). 

Antimicrobial activity of the medication was determined by the agar diffusion method [4, 5]. A wide spectrum of pyogenic microflora (Table 16.1) as well as Candida spp. and Helicobacter pylori were studied as test cultures. 

Active against Malaria, Staphylococcus aureus, Shigella dysenteriae, Haemophilus influenzae, enterobacteria, Escherichia coli. Pseudomonas aeruginosa, Candida albicans, Klebsiella pneumoniae. Salmonella spp., Helicobacter pylori. The essential oil is cfFective against just about every microbe. 

Active against Staphylococcus aureus, Streptococcus spp., enterococcus, Helicobacter pylori. 

Berberine possesses antimicrobial activity against bacterial [13, 94-96], fungal [97], protozoan [98, 99], and viral [100-102] infections. In vitro studies have shown that berberine is effective against Entamoeba histolytica, Giardia lamblia, Trichomonas vaginalis [98, 103], Candida spp. [97, 104], Plasmodium falciparum [99], Staphylococcus aureus [95, 105, 106], influenza virus [100], human immunodeficiency virus (HIV) [107], human cytomegalovirus [101], herpes simplex virus, [102] Chlamydia trachomatis [105], Helicobacter pylori [96], and Leish-mania donovani [99]. 

Salmonella spp. and of the 29 mM capric acid against Escherichia coli. Some reports have shown that lauric acid was the only fatty acid with antimicrobial activity against Helicobacter pylori (Petschow et al., 1996). The susceptibility of Helicobacter pylori to the action of saturated and unsaturated fatty aeids was studied by Bergsson et al. (2001). They showed that 5 mM of lauric, capric and palmitoleic acids decreased the number of viable bacterial cells, after 10 min of incubation at 37°C. Also, they prove the antimicrobial effect of 1.25 mM lauric acid and 0.625 mM of palmitoleic acid against Helicobacter pylori, after 10 minutes of incubation (Bergsson et al., 2002). 

Pena, J.A., Rogers, A.B., Ge, Z., et al. (2005) Probiotic Lactobacillus spp. diminish Helicobacter hepaticus-induced inflammatory bowel disease in interleukin-lO-deficient mice. Infect Immun 73, 912-920. 

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