Septic and toxic shock are complications of infection, rather than representing an infection in themselves. Severe bacterial infection causes a multitude of effects in the body. The body attempts to fight the infection, but sometimes the immune response is amplified to an abnormal degree.
Harmful products can be released by different parts of the body’s immune system (white blood cells, blood vessels, the liver) which lead in turn to fever, low blood pressure, and failure of several of the body’s main organ systems. This is known as “septic shock” and can occur in response to any bacterial infection that is severe.
Products released by the bacteria themselves may also contribute to this cascade of events. Low blood pressure means that vital organs such as the kidney, liver, and brain do not receive enough blood, hence urine flow may stop, and the patient may become drowsy or confused. The lungs may also become inflamed, even if they are not directly involved in the infection. This is known as “shock lung” or ARDS (respiratory distress syndrome), and prevents oxygen from reaching the rest of the body. This will have obvious further consequences for vital organ systems, including the heart, lung, brain, kidney and liver. Blood clotting may also become abnormal, and bruising or bleeding may be seen.
Once in hospital, the priorities are to improve the blood pressure and oxygen intake. Low blood pressure is treated by filling up the blood vessels with intravenous fluids. If this does not work, doctors then have to use powerful drugs to contract blood vessels in order to raise the blood pressure, although the heart may not be able to respond to these drugs properly. This will be particularly true of patients with heart disease already.
Patients may be moved to an intensive care unit where the heart and other organ systems can be monitored more safely. Oxygen intake is improved by giving the patient oxygen to breathe via a mask. If the patient is very drowsy, or if the lung damage is severe, doctors may decide to put a tube into the windpipe (intubation) in order to connect the patient’s lungs to a ventilator.
Other organ systems will be monitored closely and treated if any problems are identified. If the kidneys fail, waste products can be temporarily removed from the body by filtering the blood, similar to methods used in kidney dialysis. Most of these procedures are considered temporary measures, to maintain the rest of the body, whilst the infection is being treated. Occasionally, doctors are unable to save the patient. Sometimes, the lung damage worsens during treatment, such that oxygen just cannot pass from the lungs into the bloodstream.
Alternatively, the fall in blood pressure may be so catastrophic that recovery is impossible. In these circumstances, other organ systems are likely to have failed at the same time.
Bacteria like streps (and also Staphylococcus aureus) make a number of toxins that, on their own, can trigger a huge and potentially harmful inflammatory response in people. Group C and G streps were not thought to be able to do this, but recently it was shown that some of these bacteria can actually make toxins similar to the group A strep. The effects are similar to septic shock: fever, low blood pressure, and failure of several of the body’s main organ systems, though the toxins themselves also appear to cause a characteristic rash or redness (“erythema”) which turns whitish if pressed (“blanching”). This is known as “toxic shock” and really represents a subset of “septic shock”.
Authorised by Dr. Ron Daniels MB, ChB, FRCA, FFICM – UK Sepsis Trust
Staphylococcal Toxic Shock
Streptococcal Toxic Shock
The group A strep produces a family of toxins very similar to those produced by S. aureus, and in the late 1980’s, it was recognised that patients with serious group A strep infections could develop a septic shock illness that has strong resemblance to staph toxic shock. The rash in both conditions was very similar to the rash seen in scarlet fever, a condition known to accompany some cases of strep sore throat. Streptococcal toxic shock is more devastating than staph toxic shock, because the bacteria invariably have entered the bloodstream. Thus, the patient is fighting both septic and toxic shock together. The death rate from strep toxic shock can be high though recovery chances are improved with good intensive care support, and adequate treatment of the underlying infection. Group C and G streps are believed to have caused cases of toxic shock, but these cases are rare.You can find out more about toxic shock at the Toxic Shock Syndrome information service.
Vascular Dysfunction and Ischemic Destruction of Tissue in S. pyogenes Infection – The Role of SLO-induced Platelet/Neutrophil Complexes
Dennis L. Stevens, Amy E Bryant. Infectious Diseases Section, Veterans Affairs Medical Centre, Boise, ID, University of Washington School of medicine,
Streptococcal toxic shock syndrome (StrepTSS) is a severe, invasive group A streptococcal (GAS) infection associated with the sudden onset of shock, acute respiratory distress syndrome, renal failure, bacteremia, and death. Fifty percent of StrepTSS patients develop necrotising fasciitis or myonecrosis which progresses rapidly and requires emergent amputation or extensive surgical debridement to ensure survival.
Necrotising Fasciitis/myonecrosis is characterised by excruciating pain at the site of infection, the onset of which occurs well before shock or organ failure is manifest. The overlying skin becomes erythematous with purple, hemorrhagic bullae – clinical clues indicating that destruction of the deeper tissues is occurring. Histologically, there are large numbers of organisms, massive tissue necrosis and a notable absence of inflammatory cells.
The mechanisms responsible for the early onset of severe pain and the rapid regional destruction of tissues in this infection have not been elucidated. We hypothesized that toxin – induced ischemia contributes to both pain and tissue necrosis. Using Doppler flowmetry. local blood flow at the site of intramuscular injection of exotxins from an invasive M-type 1 GAS was evaluated in a rat model.
GAS exotoxins caused a rapid, dose-dependent decrease in perfusion that was irreversi at the highest toxin concentration tested. Videomicroscopy revealed that blood flow was impeded by occlusive intravascular cellular aggregates. Flow cytometry confirmed that GAS toxins induced the co-aggregation of platlets and neutrophils, that this activity was attributable to streptolysin O (SLO), and that platelet/neutrophil complex formation was largely mediated by platlet P-selectin (CD62P).
Immunotherapeutic stratergies targeting platelet adherence molecules may prevent vascular occlusion, maintain tissue viability, and reduce the need for amputation in necrotising GAS infections.
Reproduced with kind permission from Dennis L Stevens. Speaker at the strepEURO meeting in Lund. 23rd May 06.