In individuals assigned female at birth, complications can lead to pelvic inflammatory disease, chronic pelvic pain, vaginitis, mucopurulent cervicitis, and miscarriages. Causes
The disease is classified as either gonococcal urethritis, caused by Neisseria gonorrhoeae, or non-gonococcal urethritis (NGU), most commonly caused by Chlamydia trachomatis, which is accounted for 20-50% of routinely tested cases. NGU, sometimes called nonspecific urethritis (NSU), has both infectious and noninfectious causes. Other causes include:
Mycoplasma genitalium: second most common cause accounting for 15-20% of non-gonococcal urethritis
Trichomonas vaginalis: accounts for 2-13% of cases in the US; infection is mainly asymptomatic in most cases
Adenoviridae
Uropathogenic Escherichia coli (UPEC)
Herpes simplex virus
Cytomegalovirus
Reactive arthritis: urethritis is part of the triad of reactive arthritis, which includes arthritis, urethritis, and conjunctivitis. Ureaplasma urealyticum
Methicillin-resistant Staphylococcus aureus
Group B streptococcus
Irritation of the genital area: for example catheter-induced, physical activity, tight clothing or soaps
Fungal urethritis in immunosuppressed individual
Menopause

Diagnosis
Urethritis is usually diagnosed through collecting history on the individual and through a physical examination. In AFAB individuals, urethritis can be diagnosed with a number of tests including: urine test, blood test, vaginal culture, cytoscopy, or a nucleic acid test. AFAB individuals will also have abdominal and pelvic exams to check for urethral discharge, and tenderness of the lower abdomen or urethra.In AMAB individuals, urethritis is diagnosed by at least one of the following: mucopurulent or purulent urethral discharge on examination,  ≥ 2 white blood cells per oil immersion field from a Gram stain of a urethral swab, or positive leukocyte esterase and/or ≥10 white blood cells per high power field of the first-void urine.
History
AMAN, also known as Chinese Paralytic Syndrome, was first described by a group of Johns Hopkins University and University of Pennsylvania neurologists in collaboration with neurologists from the Second Teaching Hospital of Hebei Medical School and Beijing Childrens Hospital. In 1991, Guy Mckhann, Jack Griffin, Dave Cornblath and Tony Ho from Johns Hopkins University and Arthur Asbury from University of Pennsylvania visited China to study a mysterious epidemic of paralytic syndrome occurring in northern China. Every summer, hundreds of children from rural China developed acute paralysis and respiratory failure. Hospitals were overwhelmed with number of cases and often ran out of ventilators and hospital beds. Examination of these children showed that many of them had acute flaccid paralysis and areflexia but with little or no sensory loss. Electrophysiological testing of these children showed motor axonal loss with occasional conduction block with a lack of demyelinating features and normal sensory potentials. In contrast, the common form of Guillain–Barré syndrome in the West often presents with sensory loss and demyelination on electrophysiology testing and is more common in adults. Later, several autopsies confirmed the focus of the immune attack was at the motor axolemma especially around the nodes of Ranvier. These cases showed deposition of antibody and complement along the motor axolemma and associated macrophage infiltration. References


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