Ureaplasma Infection

Ureaplasma urealyticum and Ureaplasma parvum are genital mycoplasmas that colonize the lower genital tract of a significant proportion of sexually active adults asymptomatically, making their role as true pathogens versus incidental colonizers genuinely debated and context dependent.

They are implicated in a subset of cases of non-gonococcal urethritis in men, and have been associated with chorioamnionitis, preterm birth, and neonatal complications (particularly bronchopulmonary dysplasia in very preterm infants) when ascending into the upper genital tract or amniotic cavity in pregnancy.

Most colonized individuals are entirely asymptomatic.

Where symptomatic, presentation in men is typically non-gonococcal urethritis: mild to moderate urethral discharge and dysuria, clinically indistinguishable from chlamydial or other causes of NGU without specific testing.

In pregnancy, ascending infection is associated with preterm labor and, in the neonate born very preterm, has been linked to congenital pneumonia and chronic lung disease.

NAAT testing is available where clinically indicated, though routine screening of asymptomatic individuals is not recommended given the high background colonization rate and uncertain clinical significance of a positive result in this context.

Testing is more appropriately reserved for men with persistent non-gonococcal urethritis symptoms after chlamydia, gonorrhea, trichomonas, and Mycoplasma genitalium have been excluded, or in specific reproductive or neonatal contexts where a causal role is being specifically investigated.

Doxycycline 100 mg PO bd for 7 days is first line where treatment is indicated (symptomatic urethritis with ureaplasma identified as the likely cause after excluding other pathogens)
Azithromycin 1 g PO single dose is an alternative
Macrolide resistance is increasingly recognized, and treatment failure should prompt reconsideration of the diagnosis or a change in agent (a fluoroquinolone such as moxifloxacin may be used in resistant or persistent cases, though evidence specific to ureaplasma is more limited than for Mycoplasma genitalium)
Treatment of asymptomatic colonization is not generally recommended, including in pregnancy, given the lack of clear evidence that treatment improves outcomes and given the very high background prevalence of colonization

Referral: sexual health services for persistent non-gonococcal urethritis; neonatology/infectious disease input where ureaplasma is implicated in a specific neonatal complication.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Tetanus

Tetanus is caused by the neurotoxin (tetanospasmin) of Clostridium tetani, an anaerobic, spore-forming organism introduced through a wound (often minor or unnoticed), with spores germinating in devitalized, anaerobic tissue.

The toxin blocks inhibitory neurotransmitter release (GABA, glycine) at spinal and brainstem synapses, causing unopposed, sustained muscle contraction.

Now rare where vaccination is widespread, but remains significant in unvaccinated populations, particularly neonatal tetanus in settings with unhygienic cord care.

Incubation typically 3 to 21 days, shorter incubation correlating with more severe disease.

Trismus (lockjaw) is usually the presenting feature, followed by risus sardonicus (a fixed, grimacing facial expression from facial muscle spasm), neck stiffness, and progressive generalized muscle rigidity.

Opisthotonus (severe back arching from paraspinal spasm) and painful, reflex-triggered generalized spasms (provoked by minimal stimuli, light, sound, touch) characterize severe disease, with autonomic instability (labile blood pressure, tachycardia, sweating) in the most severe cases. Respiratory failure results from laryngospasm or spasm of respiratory muscles.

Human tetanus immunoglobulin (HTIG) 3,000 to 6,000 units IM, given as soon as possible to neutralize circulating, unbound toxin (does not affect toxin already bound at nerve terminals); some is infiltrated around the wound if identifiable
Wound debridement of all devitalized tissue to eliminate the anaerobic environment favoring further toxin production
Metronidazole 500 mg IV/PO tds for 7 to 10 days (preferred over penicillin, which has a theoretical GABA-antagonist action that could theoretically worsen spasm)
Muscle spasm control: benzodiazepines (diazepam or midazolam, titrated aggressively, often to very high cumulative doses) form the mainstay; magnesium sulfate infusion is used adjunctively to control spasm and autonomic instability; severe cases require neuromuscular blockade and mechanical ventilation in ICU
Autonomic dysfunction managed with labetalol or an alpha/beta blocking approach, and magnesium
Airway protection and early tracheostomy are often needed given the risk of laryngospasm and the prolonged ventilatory support many cases require (weeks)
Active immunization with tetanus toxoid should be given concurrently (at a different site to HTIG), since natural infection does not confer immunity
Minimal stimulation nursing (dark, quiet environment) reduces spasm frequency

Referral: ICU for all moderate to severe cases given the high risk of respiratory compromise and need for prolonged ventilatory support.

Ureaplasma Infection

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management