Septicemia / bacteremia

Etiology

• Most commonly bacterial infection progressing to large numbers of bacteria in the bloodstream.
• Secondary to septic focus, eg septic arthritis, perforated GI tract, pyelonephritis, pneumonia Pneumonia.
• Bacteria may translocate from the GI tract due to immunosuppression, eg chronic hypothermia Hypothermia due to inadequate husbandry Chelonia husbandry Lizard husbandry Snake husbandry.
• Intravenous or intraosseous catheters can be a source of infection: patient interference with catheters during hospitalization, infrequent changes, lack of disinfection of injection ports
• Pathogen will depend on the location of the septic focus.
• Gram negative infections are common in reptile species.

Predisposing factors

General

• Poor husbandry Chelonia husbandry Lizard husbandry Snake husbandry, eg inadequate temperature gradient, inappropriate humidity.
• Stress, eg overcrowding, excessive handling Handling / restraint, poor group dynamics leading to fighting.
• Immunosuppression, eg underlying disease.
• Poor water quality (aquatic reptiles) due to overstocking, lack of filtration, lack of water changes, leading to bacterial colonization of skin and bloodstream.

Specific

• Viral infection leading to immunosuppression.
• Hypothermia leading to immunosuppression and translocation of gastrointestinal bacteria.
• Any infection can progress to septicemia if untreated.

Pathophysiology

• Bacteremia refers to presence of bacteria in the bloodstream.
• Septicemia or sepsis is a dysregulated inflammatory response to infection (bacterial, viral, protozoal or fungal).
• The release of circulating inflammatory mediators causes signs of systemic inflammatory response syndrome (SIRS) that can range from mild to severe. This can progress to septic shock.
• Septic shock is a subset of sepsis in which profound circulatory, cellular and metabolic abnormalities occur. It is associated with a greater mortality rate than sepsis alone.
• The gram-negative bacterial cell wall contains lipopolysaccharides (LPS) that are potent stimuli for an inflammatory host response. Activation of the inflammatory cascade due to gram positive bacterial can also occur, in response to cell wall components or bacterial DNA. Stimulation of the innate immune system from a variety of pathogen antigens results in the production of inflammatory cytokines.
• The most important cytokines related to sepsis are tumor necrosis factor alpha and interleukins 1,6 and 8. These cytokines attract and activate neutrophils and stimulate other cells in the immune response. Cytokines can cause extensive host tissue damage secondary to the release of reactive oxygen species (ROS) and proteases among others.
• Overproduction of nitric oxide (NO) during sepsis is a major contributing factor to dysregulation of the vasomotor tone (vasoplegia). This vasodilatory state will cause severe hypotension, typically unresponsive to fluid therapy.
• The cumulative effects of these pathways (most particularly systemic inflammation) are responsible for cardiovascular depression, pulmonary hypertension, and arterial hypoxemia.
• These effects can then lead to endotoxin induced decreased tissue perfusion and peripheral hypoxia.
• Eventually perfusion to major organ systems can be compromised and lead to multiple organ dysfunction syndrome (MODS) and death.
• In chelonians, sepsis and bacterial emboli can lead to petechiae and fluid accumulation under the scutes.

Timecourse

• Usually days to weeks.