GBS

**1. GUILLAIN-BARRÉ SYNDROME (most common meaning)**

*Pathophysiology:* Molecular mimicry follows an infection. The classic trigger is Campylobacter jejuni (the most common; associated with the axonal AMAN variant and anti-GM1 antibodies). Others are CMV, EBV, Zika, HIV, Mycoplasma, recent influenza or other vaccines (rare), and surgery. Autoantibodies and T cells attack peripheral myelin (Schwann cells) or the axon. The result is segmental demyelination of peripheral nerves and nerve roots.

*Clinical:* - Symmetric ascending weakness that starts in the legs over days to weeks, with a nadir by about 4 weeks. - Hypo- or areflexia, with relatively mild sensory findings (paresthesias, back pain). - Autonomic dysfunction: labile BP, arrhythmias, ileus, urinary retention. - Cranial nerve involvement, especially bilateral facial palsy (CN VII). - Respiratory failure from diaphragm weakness. Monitor FVC and negative inspiratory force (NIF). Intubate if FVC is <20 mL/kg or NIF is weaker than −30 cmH2O.

*Diagnosis:* - Clinical diagnosis, supported by LP showing **albuminocytologic dissociation** (↑ protein with normal cell count). This may be normal in the first week. - Nerve conduction studies show slowed conduction, conduction block, and prolonged F-waves. - Check anti-GQ1b antibodies if Miller Fisher is suspected.

*Treatment:* - **IVIG or plasmapheresis**, which are equally effective. Do not combine them. - Supportive care: ventilatory support, DVT prophylaxis, autonomic monitoring. - **Steroids are NOT effective.**

*Variants:* - AIDP: the classic demyelinating form. - AMAN/AMSAN: axonal forms, associated with C. jejuni. - **Miller Fisher:** ophthalmoplegia, ataxia, and areflexia, with anti-GQ1b antibodies.

*Differential:* Acute myelopathy (spinal cord compression has a sensory level, hyperreflexia, and bowel/bladder dysfunction early), myasthenia gravis (fatigable weakness, normal reflexes), botulism (descending paralysis), tick paralysis, polio or West Nile virus (asymmetric, with fever and CSF pleocytosis), hypokalemia, and porphyria.

*Pearls:* Distinguish from CIDP (chronic, progressing over more than 8 weeks, steroid-responsive). Pulmonary function is the key prognostic and management issue. Most patients recover, but some have residual deficits.

**2. GROUP B STREPTOCOCCUS (S. agalactiae)**

*Microbiology:* Gram-positive cocci in chains. It is β-hemolytic, catalase-negative, bacitracin-resistant, hippurate hydrolysis-positive, and CAMP factor-positive. It has a polysaccharide capsule (a virulence factor). It colonizes the vaginal and GI tracts of about 20–30% of women.

*Clinical:* - **Neonatal sepsis, pneumonia, and meningitis.** It is the leading cause of neonatal sepsis and a leading cause of neonatal meningitis. Early-onset disease (<7 days) is acquired by vertical transmission. Late-onset disease (7 days to 3 months) typically presents as meningitis or bacteremia. - Adult infections: UTI and chorioamnionitis in pregnancy, endometritis, and skin and soft tissue infection or bacteremia in diabetics and the elderly.

*Prevention:* Screen all pregnant women with a rectovaginal culture at 36–37 6/7 weeks. Give intrapartum **penicillin G or ampicillin** to colonized women. Give prophylaxis regardless of culture to women with GBS bacteriuria in the current pregnancy, a prior infant with GBS disease, or unknown status with risk factors (preterm labor <37 weeks, ROM ≥18 h, intrapartum fever ≥38 °C). Penicillin-allergic women get cefazolin if the allergy is low-risk, or clindamycin or vancomycin if high-risk, based on susceptibility.

*Treatment:* Penicillin G or ampicillin, plus gentamicin initially for neonatal sepsis.

**Distinguishing the two:** Neurology or weakness vignette: Guillain-Barré. OB or neonatal vignette: Group B Strep. (GBS can also mean Gestational/other terms in rare contexts, but these are the two high-yield ones.)