I included bestiality and pedophilia... you complain.
I didn't include heterosexual... you complain.
Might it be better if you write my post?
Hypocritical. Now slanderous. Carry on.
Perhaps you are "Born that way".
You dug through all the "garbage"?
After all that work, you deserve a solid meal.
Here...
I think it's clean.
Sexually Transmitted Diseases in Men Who Have Sex With Men
Men who have sex with men (MSM) have increased rates of human immunodeficiency virus (HIV) infection and sexually transmitted diseases (STDs) compared with demographically matched controls. The reasons for the disproportionate infection burden are complex, including biological, behavioral, and sociocultural factors. HIV and syphilis may often be coprevalent among MSM. ... MSM are at increased risk for viral hepatitis and anal human papillomavirus disease.
Since the last version of the World Health Organization’s Guidelines for the Management of Sexually Transmitted Infections was published in 2004,
sexually transmitted disease (STD) rates among men who have sex with men (MSM) have continued to increase across the United States and abroad.
Enteric diseases of homosexual men
Certain enteric ailments are particularly common among homosexual men. They are primarily infectious diseases and include not only such common venereal diseases as gonorrhea and syphilis but also infections not usually regarded as being sexually transmitted. Among the latter are shigellosis, salmonellosis, giardiasis, and amebiasis. ...Gonorrhea is probably the most common bacterial infection in gay men. Carriage rates as high as 50% have been reported, and extra-genital carriage is common; this necessitates culturing the urethra, rectum, and pharynx.
Shigellosis
Shigellosis is an infection of the intestines caused by Shigella bacteria. Symptoms generally start one to two days after exposure and include diarrhea, fever, abdominal pain, and feeling the need to pass stools even when the bowels are empty. The diarrhea may be bloody. Symptoms typically last five to seven days. Complications can include reactive arthritis, sepsis, seizures, and hemolytic uremic syndrome.
Shigellosis is caused by four specific types of Shigella. These are typically spread by exposure to infected feces.
Shigella
Shigella (/ʃɪˈɡɛlə/) is a genus of gram-negative, facultative aerobic, nonspore-forming, non-motile, rod-shaped bacteria genetically closely related to E. coli. The genus is named after Kiyoshi Shiga, who first discovered it in 1897.
Each of the Shigella genomes includes a virulence plasmid that encodes conserved primary virulence determinants.
The Shigella chromosomes share most of their genes with those of E. coli K12 strain MG1655. Phylogenetic studies indicate Shigella is more appropriately treated as subgenus of Escherichia, and that certain strains generally considered E. coli - such as E. coli O157:H7 - are better placed in Shigella...
Pathogenesis
Shigella infection is typically by ingestion. Depending on the health of the host, fewer than 100 bacterial cells can be enough to cause an infection.
Shigella species generally invade the epithelial lining of the colon, causing severe inflammation and death of the cells lining the colon. This inflammation results in the diarrhea and even dysentery that are the hallmarks of Shigella infection. Some strains of Shigella produce toxins which contribute to disease during infection. S. flexneri strains produce ShET1 and ShET2, which may contribute to diarrhea. S. dysenteriae strains produce the enterotoxin Shiga toxin, which is similar to the verotoxin produced by enterohemorrhagic E. coli. Both Shiga toxin and verotoxin are associated with causing potentially fatal hemolytic-uremic syndrome.
Shigella species invade the host through the M-cells interspersed in the gut epithelia of the small intestine, as they do not interact with the apical surface of epithelial cells, preferring the basolateral side. Shigella uses a type-III secretion system, which acts as a biological syringe to translocate toxic effector proteins to the target human cell. The effector proteins can alter the metabolism of the target cell, for instance leading to the lysis of vacuolar membranes or reorganization of actin polymerization to facilitate intracellular motility of Shigella bacteria inside the host cell. For instance, the IcsA effector protein triggers actin reorganization by N-WASP recruitment of Arp2/3 complexes, helping cell-to-cell spread.
After invasion, Shigella cells multiply intracellularly and spread to neighboring epithelial cells, resulting in tissue destruction and characteristic pathology of shigellosis.
The most common symptoms are diarrhea, fever, nausea, vomiting, stomach cramps, and flatulence. It is also commonly known to cause large and painful bowel movements. The stool may contain blood, mucus, or pus. Hence, Shigella cells may cause dysentery. In rare cases, young children may have seizures. Symptoms can take as long as a week to appear, but most often begin two to four days after ingestion. Symptoms usually last for several days, but can last for weeks. Shigella is implicated as one of the pathogenic causes of reactive arthritis worldwide.
Within-species lateral genetic transfer and the evolution of transcriptional regulation in Escherichia coli and Shigella
The prevalence of recombination breakpoints within regulatory and target gene sets indicates that within-gene transfer has had a significant cumulative effect on the evolution of regulatory interactions in E. coli and Shigella.
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Here we focus on modifications to bacterial TRNs that have arisen via lateral genetic transfer (LGT).
Genomic studies leave no doubt that LGT has played a pervasive role in the evolution of prokaryotic genomes and is a significant source of phenotypic innovation among bacteria. Successful LGT comprises a succession of steps: transfer and physical uptake of foreign DNA into a host new cell; recombination into the main chromosome, or maintenance on an extrachromosomal element; integration into genetic regulatory and biomolecular interaction networks; and finally, establishment in the host population.