neonatorum, once common in newborns, is prevented by the application of erythromycin (antibiotic) gel to the eyes of babies at birth as a public health measure. silver nitrate is no longer used in the united states. transmission n. gonorrhoeae is transmitted through vaginal, oral, or anal sex; nonsexual transmission is unlikely in adult infection. it can also be transmitted to the newborn during passage through the birth canal if the mother has untreated genitourinary infection. given the high rate of asymptomatic infection, all pregnant women should be tested for gonorrhea infection. however, communal baths, towels or fabric, rectal thermometers and caregivers hands have been implicated as means of transmission in the pediatric setting. kissing has also been implicated as a theoretical means of transmission in the gay male population, based on a newer study. traditionally, the bacterium was thought to move attached to spermatozoa, but this hypothesis did not explain female to male transmission of the disease. a recent study suggests that rather than "surf" on wiggling sperm, n. gonorrhoeae bacteria use pili to anchor onto proteins in the sperm and move through coital liquid. infection for n. gonorrhoeae, the first step after successful transmission is adherence to the epithelial cells found at the mucosal site that is infected. the bacterium relies on type iv pili that attach and retract, pulling n. gonorrhoeae toward the epithelial membrane where its surface proteins, such as opacity proteins, can interact directly. after adherence, n. gonorrhoeae replicates itself and forms microcolonies. while colonizing, n. gonorrhoeae has the potential to transcytose across the epithelial barrier and work its way in to the bloodstream. during growth and colonization, n. gonorrhoeae stimulates the release of cytokines and chemokines from host immune cells that are pro-inflammatory. these pro-inflammatory molecules result in the recruitment of macrophages and neutrophils. these phagocytic cells typically take in foreign pathogens and destroy them, but n. gonorrhoeae has evolved many mechanisms that allow it to survive within these immune cells and thwart the attempts at elimination. prevention transmission is reduced by using latex barriers (e.g. condoms or dental dams) during sex and by limiting sexual partners. condoms and dental dams should be used during oral and anal sex, as well. spermicides, vaginal foams, and douches are not effective for prevention of transmission. treatment the current treatment recommended by the cdc is an injected single dose of ceftriaxone (a third-generation cephalosporin). sexual partners (defined by the cdc as sexual contact within the past 60 days) should also be notified, tested, and treated. it is important that if symptoms persist after receiving treatment of n. gonorrhoeae infection, a reevaluation should be pursued. antibiotic resistance antibiotic resistance in gonorrhea has been noted beginning in the 1940s. gonorrhea was treated with penicillin, but doses had to be progressively increased to remain effective. by the 1970s, penicillin- and tetracycline-resistant gonorrhea emerged in the pacific basin. these resistant strains then spread to hawaii, california, the rest of the united states, australia and europe. fluoroquinolones were the next line of defense, but soon resistance to this antibiotic emerged, as well. since 2007, standard treatment has been third-generation cephalosporins, such as ceftriaxone, which are considered to be our "last line of defense".recently, a high-level ceftriaxone-resistant strain of gonorrhea called h041 was discovered in japan. lab tests found it to be resistant to high concentrations of ceftriaxone, as well as most of the other antibiotics tested. within n. gonorrhoeae, genes exist that confer resistance to every single antibiotic used to cure gonorrhea, but thus far they do not coexist within a single gonococcus. however, because of n. gonorrhoeae's high affinity for horizontal gene transfer, antibiotic-resistant gonorrhea is seen as an emerging public health threat. serum resistance as a gram negative bacteria, n. gonorrhoeae requires defense mechanisms to protect itself against the complement system (or complement cascade), whose components are found with human serum. there are three different pathways that activate this system however, they all result in the activation of complement protein 3 (c3). a cleaved portion of this protein, c3b, is deposited on pathogenic surfaces and results in opsonization as well as the downstream activation of the membrane attack complex. n. gonorrhoeae has several mechanisms to avoid this action. as a whole, these mechanisms are referred to as serum resistance. history name origin neisseria gonorrhoeae is named for albert neisser, who isolated it as the causative agent of the disease gonorrhea in 1878. galen (130 ad) coined the term "gonorrhea" from the greek gonos which means "seed" and rhoe which means "flow". thus, gonorrhea means "flow of seed", a description referring to the white penile discharge, assumed to be semen, seen in male infection. discovery in 1878, albert neisser isolated and visualized n. gonorrhoeae diplococci in samples of pus from 35 men and women with the classic symptoms of genitourinary infection with gonorrhea – two of whom also had infections of the eyes. in 1882, leistikow and loeffler were able to grow the organism in culture. then in 1883, max bockhart proved conclusively that the bacterium isolated by albert neisser was the causative agent of the disease known as gonorrhea by inoculating the penis of a healthy man with the bacteria. the man developed the classic symptoms of gonorrhea days after, satisfying the last of koch's postulates. until this point, researchers debated whether syphilis and gonorrhea were manifestations of the same disease or two distinct entities. one such 18th-century researcher, john hunter, tried to settle the debate in 1767 by inoculating a man with pus taken from a patient with gonorrhea. he erroneously concluded that both syphilis and gonorrhea were indeed the same disease when the man developed the copper-colored rash that is classic for syphilis. although many sources repeat that hunter inoculated himself, others have argued that it was in fact another man. after hunter's experiment other scientists sought to disprove his conclusions by inoculating other male physicians, medical students, and incarcerated men with gonorrheal pus, who all developed the burning and discharge of gonorrhea. one researcher, ricord, took the initiative to perform 667 inoculations of gonorrheal pus on patients of a mental hospital, with zero cases of syphilis. notably, the advent of penicillin in the 1940s made effective treatments for gonorrhea available.