Surgical Infectious Disease

Infection continues to be a significant source of mortality and morbidity for children despite improvements in antimicrobial therapy, aseptic surgical technique, and postoperative intensive care. Widespread unchecked antibiotic use has led to the development of more resistant organisms, leading to a rather complex and arduous process of selecting the appropriate antibiotic, especially as newer antibiotics are continually developed. In addition, infections with uncommon organisms are becoming more frequent with diminished host resistance from immunosuppressive states such as immaturity, cancer, systemic diseases, and transplant procedures. Surgical infections, by definition, often require some operative intervention, such as incision and drainage (I&D) of an abscess or removal of necrotic tissue, and often do not respond to antibiotics alone.

Two broad classes of infectious disease processes affect surgeons: those infectious conditions brought to the pediatric surgeon for treatment and cure, and those that arise in the postoperative period as a complication of an operation. Therefore, a good understanding of the infectious process is important.

Pathogenesis of Infection

The evolution of infection involves a complex interaction between the host and the infectious agent. Four components are important: virulence of the organism, size of the inoculum, presence of a nutrient source for the organism, and a breakdown in the host’s defense.

Virulence

The virulence of any microorganism depends on its ability to cause damage to the host. Exotoxins, such as streptococcal hyaluronidase, are digestive enzymes released locally by some organisms that allow the spread of infection by breaking down host extracellular matrix proteins. Endotoxins, such as lipopolysaccharides, are components of gram-negative cell walls that are released only after bacterial cell death. Once systemically absorbed, endotoxins trigger a severe and rapid systemic inflammatory response by releasing various endogenous mediators such as cytokines, bradykinin, and prostaglandins. Surgical infections occasionally may be polymicrobial, involving various interactions among the microorganisms and toxins.

Inoculum

The size of the inoculum is the second important component of an infection. The number of colonies of microorganisms per gram of tissue is the key determinant. Predictably, any decrease in host resistance decreases the absolute number of colonies necessary to cause clinical disease. In general, if the bacterial population in a wound exceeds 100,000 organisms per gram of tissue, an invasive infection is present.

Nutrients

For any inoculum, the environment determines the viability and survival. Therefore, the presence of suitable nutrients for the organism is essential and comprises the third component of any clinical infection. Accumulation of necrotic tissue, hematoma, and foreign matter is an excellent nutrient medium for continued organism growth and spread. Of special importance to the surgeon is the concept of necrotic tissue and infection. When present at an infected site, this tissue often needs to be debrided to restore the host–bacterial balance and lead to effective wound healing. Neutrophils, macrophages, and cytokines can then accumulate in necrotic tissue, initiating a secondary inflammatory response.

Host Defense

Finally, for a clinical infection to arise, the body’s defenses must be overwhelmed. Even highly virulent organisms can be eradicated before clinical infection occurs if the host resistance is intact. Evolution has fortunately equipped humans with numerous mechanisms of defense, both anatomic and systemic.

Defense Against Infection

Anatomic Barriers

Intact skin and mucous membranes provide an effective surface barrier to infection. These tissues barriers are not merely a mechanical obstacle, but rather possess physiologic characteristics that provide an extra layer of protection. In the skin, thermoregulation, the constant turnover of keratinocytes, and acid secretion from sebaceous glands inhibits bacterial cell growth. The mucosal surfaces likewise have developed advanced defense mechanisms to prevent and combat microbial invasion, where specialized epithelial layers provide resistance to infection. In addition, mechanisms such as the mucociliary transport system in the respiratory tract and normal colonic flora in the gastrointestinal tract prevent invasion of organisms. Any alteration in the normal function of these anatomic barriers increases the host’s susceptibility to infection. A skin injury or a burn provides open access to the underlying soft tissues, while antibiotic use disrupts normal colonic flora. Fortunately, such breakdowns in surface barriers are dealt with by the second line of defense, the immune system.

Immune Response

The immune system involves complex pathways and many specialized effector responses. The initial line of defense is the more primitive and nonspecific innate system, which consists primarily of phagocytic neutrophils and the serum-based complement system. The neutrophil is able to rapidly migrate to the source of the infection and engulf and destroy the infecting organisms by phagocytosis. In the complement system, cytokines, low molecular weight proteins including tumor necrosis factor (TNF), and many interleukins that attract and activate neutrophils, play a significant role in mediating the inflammatory response. In addition, the complement system, when activated, initiates a sequential cascade that also enhances phagocytosis and leads to lysis of pathogens. Neonates, particularly premature infants, have an immature immune system and are supported by the protective agents in human breast milk.

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