Toxin Mediated Staphylococcal Diseases

An epidemic of TSS in young women in the early 1980s associated with menstruation and the use of high-absorbancy tampons was caused by TSST-1-producing organisms (Dinges, Orwin and Schlievert 2000). Modification in tampon manufacture resulted in a fall in the number of cases in this group. Non-menstrual TSS is associated with a range of S. aureus disease types including invasive S. aureus infection. TSS may also occur in association with influenza and in patients with a wound that is colonized by TSST-1-producing organisms, but where clinical features of wound sepsis are absent.

TSS is a severe disease characterized by high fever, hypotension, diffuse erythematous rash with subsequent desquamation 1-2 weeks later and involvement of three or more organ systems (Dinges, Orwin and Schlievert 2000). Clinical features may include mucous membrane hyperaemia, myalgia, vomiting and diarrhoea, renal and hepatic impairment, altered level of consciousness, coagulopathy and low platelet count. The diagnosis is made on clinical grounds, and the Centers for Disease Control and Prevention (CDC) have devised a clinical case definition (Centers for Disease Control and Prevention 1997). Not all patients with clinical features consistent with TSS meet the CDC diagnostic criteria (Dinges, Orwin and Schlievert 2000). The results of the following laboratory tests may be helpful in reaching a diagnosis in such cases (Parsonnet 1998):

1. isolation of S. aureus from a mucosal or normally sterile body site;

2. production by this organism of TSST-1 or other SAg known to be associated with TSS;

3. absence of antibodies to the relevant toxin at the time of illness;

4. seroconversion to this toxin with detection of antibodies during convalescence.

SSSS primarily affects neonates and young children. This disease results from the action of S. aureus exfoliative toxins on skin epider-midis. Mid-epidermal splitting leads to the development of fragile, thin roofed blisters that rapidly rupture to leave denuded areas (Ladhani etal. 1999). SSSS often follows a localized infection in sites such as the umbilical stump, ear or conjunctiva. Presenting clinical features include fever, lethargy, poor feeding and irritability, followed by a tender red rash that spreads to involve the entire body within a few days. Patients have poor temperature control, suffer large fluid losses and may develop secondary infection. Diagnosis is made on the basis of clinical features, including Nikolsky's sign in which the skin wrinkles on gentle pressure. Culture of blister fluid in SSSS is usually negative since the blisters have developed because of toxin formed by S. aureus at a distant site. Bullous impetigo has been described as a less severe form of disease with localized skin blistering. Culture of blister fluid is often positive for S. aureus. This might indicate that features are caused by local production of bacterial factors.

Staphylococcal food poisoning results from ingestion of preformed SEs (Dinges, Orwin and Schlievert 2000). This occurs when S. aureus is inoculated into food which is then left in conditions that are permissive for bacterial multiplication and toxin secretion before consumption. The mechanism of action of the toxin is still under study, but the initiation of the emetic response is thought to be due to interactions with the emetic reflex located in the abdominal viscera, with subsequent activation of the medullary emetic centre in the brain stem that is stimulated via the vagus and sympathetic nerves (Dinges, Orwin and Schlievert 2000). Nausea and vomiting occur after an incubation period of 2 and 6 h. Abdominal pain and diarrhoea are also common features. Diagnosis is made on clinical grounds. Suspected food may be cultured for the presence of S. aureus.

Bacteraemia and Endocarditis

Around two-thirds of S. aureus bacteraemia cases are attributable to nosocomial sepsis, most of which relate to an intravenous device. The remainder represent community-acquired bacteraemia. Data from the National Nosocomial Infections Surveillance System indicate that rates of S. aureus bacteraemia are increasing (Banerjee etal. 1991). Rates of S. aureus endocarditis have also increased (Sanabria etal. 1990; Watanakunakorn and Burkert, 1993). The use of intravenous catheters may have contributed to this rise. These figures pertain to settings with systems of advanced medical care. Rates of nosocomial S. aureus sepsis are likely to vary considerably depending on the global setting, although there is a paucity of data from many parts of the world.

Readers are referred to an excellent review on S. aureus bacteraemia and endocarditis written by Cathy Petti and Vance Fowler (Petti and Fowler 2003). The general medical condition of cases presenting with S. aureus bacteraemia ranges from the febrile but haemodynamically stable patient, to one who is profoundly shocked and has multiorgan failure with respiratory distress and coagulopathy. All patients with S. aureus bacteraemia require assessment to distinguish between those with uncomplicated versus complicated bacteraemia. Uncomplicated bacteraemia may be defined as S. aureus bacteraemia but no evidence of seeding of bacteria from the bloodstream to other sites (such as heart valves, bone and joint), and complicated bacteraemia is defined as the presence of one or more foci. A study of 724 adult patients presenting to a hospital with S. aureus bacteraemia identified complications in 43% (Fowler etal. 2003). This distinction is important since the presence of complications will determine the length of treatment and the need for investigations and additional intervention. Clinical assessment should be repeated during admission since metastatic complications of bacteraemia may only become evident some time after the initial bacteraemia. However, clinical examination may be inadequate in identifying the complicated case. For example, the absence of signs of endocarditis does not exclude the diagnosis. A study of S. aureus endocarditis over a 10-year period in Denmark reported that the diagnosis was not suspected and was first detected at autopsy in 32% of patients (Roder etal. 1999). Underlying cardiac valvular disease or prosthetic heart valves are risk factors for endocarditis in patients with bacteraemia and should increase clinical suspicion. The Duke criteria should be used in the clinical evaluation of patients suspected of having endocarditis (Durack, Lukes and Bright 1994; Bayer etal. 1998). Cardiac echocardiography has been used widely in many centres because of the clinical difficulty in identifying patients with endocarditis. The sensitivity of transthoracic and transoesophageal echocardiography is around 60% and 90%, respectively (Chamis et al. 1999).

A study of clinical identifiers of complicated S. aureus bacteraemia represents significant progress (Fowler etal. 2003). A scoring system based on the presence or absence of four risk factors (community acquisition, skin examination findings suggesting acute systemic infection, persistent fever at 72 h and positive follow-up blood culture results at 48-96 h) was able to identify accurately complicated S. aureus bacteraemia. The findings of this study allow readily available clinical variables to be used in the identification of patients requiring further investigation and prolonged therapy. Serological testing in its present form is not useful for confirming the diagnosis of S. aureus sepsis or for defining complicated bacteraemia or the extent of disease.

Bone and Joint Sepsis

Staphylococcus aureus is the leading cause of primary septic arthritis and osteomyelitis in all ages except neonates (Baker and Schumacher 1993; Lew and Waldvogel 1997). The route of infection is obvious for individuals with conditions that allow direct bacterial access, including open fractures (where the bone is exposed), surgery involving the bone (including joint replacement or internal fracture fixation) and chronic ulceration down to bone or joint (e.g. in the diabetic foot or in a bed-bound patient with a pressure sore). However, many patients have no obvious predisposing factor and do not have identifiable skin lesions or any other primary focus. In such cases, bacteria presumably gain access to bone and joint because of seeding from the bloodstream. Once present in the bone or joint, they multiply, which triggers a host inflammatory response, the features of which are increased blood flow, increased capillary permeability to fluids and cells and the recruitment of inflammatory cells, initially neutrophil polymorphs. If this immune response is unsuccessful in controlling infection, the result is intense inflammation surrounding an area with high densities of bacteria and the development of an abscess. Figure 5.1 shows the appearance, on magnetic resonance imaging, of osteomyelitis of the femur, with oedema in the bone marrow and a large subperiosteal abscess. Secondary bacteraemia is common at this point in the absence of antibiotic therapy. On presentation, fever is common, but once again the overall condition of the patient may be highly variable, and signs and symptoms will depend on the site affected.

Pulmonary Infections

Infection arises because of inhalation of the organism from a site of colonization (community acquired), via an endotracheal tube in ventilated patients or, more rarely, because of haematogenous spread in a bacteraemic patient. Staphylococcus aureus infection may involve the lung parenchyma (localized abscess or more diffuse pattern), pleural cavity (empyema) or both. No clinical or radiological features are typical of S. aureus pneumonia. Microbiological diagnosis is complicated in that S. aureus is a normal commensal of the upper respiratory tract (predominantly the nose) in a proportion of individuals. As a result, interpretation of S. aureus in sputum culture is difficult, and more invasive procedures such as bronchoscopy and lavage may be necessary. A syndrome of rapidly progressive S. aureus necrotizing pneumonia affecting previously healthy children and young adults has been described (Gillet et al. 2002). The strains responsible were positive for PVL, and pneumonia was often preceded by influenza-like symptoms.

Figure 5.1 Osteomyelitis of the femur. Magnetic resonance imaging demonstrating features indicative of oedema in the bone marrow and a large subperiosteal abscess.

Other Clinical Manifestations

As a generalization, S. aureus may infect any organ or region of the body. Additional deep-site infections such as abscess formation in liver, spleen and kidney usually occur in the setting of a bacteraemic patient who develops seeding to multiple sites. Meningitis is an uncommon primary manifestation and usually occurs because of septic embolization associated with endocarditis.

Staphylococcus aureus is a common cause of skin and soft-tissue infections such as boils, impetigo and cellulitis. Primary infection of muscle is unusual in temperate climatic regions but is reported to be common in the tropical setting where paediatric centres may see several cases requiring surgical drainage each week. The reason for this difference is poorly understood. One possible explanation is that parasitic infection with muscle involvement provides a foreign body nidus that predisposes to infection. Staphylococcus aureus may cause acute otitis media, although is much less commonly found than other pathogens such as S. pneumoniae and Haemophilus influenzae. Staphylococcus aureus may cause urinary tract infection. Patients with S. aureus bacteraemia may also have viable organisms in the urine (Lee, Crossley and Gerding 1978). Whilst the overwhelming majority of patients with S. aureus cultured from the urine will not have bacteraemia, it is useful to bear this in mind as a possibility in those patients presenting unwell to hospital.

Nosocomial Infection

The range of nosocomial or hospital-acquired infections includes surgical wound infection, ventilator-associated pneumonia, bacteraemia associated with intravenous devices and infection associated with other types of prosthetic materials such as cerebrospinal fluid (CSF) shunts, prosthetic joints and vascular grafts. However, any disease manifestation may occur in the hospital setting. Investigation will depend on the nature and severity of infection and requires individual assessment for a given patient. The distinction between community and hospital infection is becoming less clear with the rise in home intravenous therapy and the intravenous device-related bacteraemia that occurs in a proportion of cases.

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