Pediatric bacterial sepsis is a leading killer of children, outpacing deaths from childhood cancer. The hallmark of sepsis includes an abnormal temperature, leukocyte count, tachypnea, and tachycardia. Skin lesions, which can give a clue as to the cause of sepsis, result from direct vascular invasion and occlusion, vasculitis due to immune complex deposition, or the effect of toxins.

Bacterial sepsis in children is usually due to meningococcemia or gram-positive bacteria. Patients that are immunocompromised or have burns, neutropenia, or intravenous (IV) catheters are at higher risk for sepsis. Note: Neonatal sepsis is covered separately, as are many of the individual bacterial and fungal causes of sepsis. See also gonococcemia, Candida sepsis, Trichosporon beigelii sepsis, and septicemic plague.

Meningococcal disease – Meningococcal disease is a rapidly progressive infection caused by Neisseria meningitides, a gram-negative diplococcus bacterium. Symptoms may begin with a nonspecific viral-like illness that rapidly evolves (within hours) into one of two main presentations: meningitis or septicemia. Most cases are acquired through exposure to asymptomatic carriers via respiratory droplets. Children aged younger than 5 years and teenagers aged 15–19 are predominantly affected.

Toxic shock syndrome – In children, toxic shock syndrome (TSS) most commonly follows surgery or skin injuries, but at times can present with no preceding risk factors.

• Staphylococcal TSS is caused by Staphylococcus aureus strains that can produce the TSS toxin-1 (TSST-1). It more commonly has the typical erythrodermic skin findings compared with streptococcal TSS.
• Streptococcal TSS is also caused by exotoxins that cause massive stimulation of T-cells via a superantigen mechanism. Clinically, the most common presenting symptom is severe pain in an extremity with or without underlying soft tissue infection. However, in children, streptococcal TSS may present without an identifiable source of infection. It may also be associated with bacteremia, endocarditis, pneumonia, pleural effusion, and/or osteomyelitis. A prodrome of fever, diarrhea, and myalgias is often seen. The macular exanthem seen in staphylococcal TSS is much less commonly found in streptococcal TSS. Approximately 48-72 hours after the initial onset, shock and multiorgan failure follow. In this form of TSS, risk factors include varicella infection, bites, and lacerations.

Sepsis due to other bacteria may cause skin lesions (such as petechiae or purpura).

• Streptococcus pneumoniae is a common cause of sepsis in young children and children with HIV infection, sickle cell disease, other causes of asplenia, or nephrotic syndrome.
• Sickle cell patients are also at increased risk of sepsis due to Salmonella spp. 
• Pseudomonas aeruginosa sepsis will occasionally present with skin lesions (ecthyma gangrenosum), and neutropenia is a major risk factor for this pathogen. 
• Listeria monocytogenes infection is well documented in neonates, HIV-infected patients, and patients with impaired cellular immunity. In these patients, pneumonia and meningitis dominate the picture, but purpuric skin lesions may occur.
• Patients with complement deficiencies (late phase components C5-C9) including those with nephrotic syndrome are susceptible to N meningitidis.