SYSTEMIC BACTERIAL INFECTIONS

Bacteremia

• Bacteremia or Blood-stream infection (BSI) is the presence of viable bacteria in the blood stream.

is a frequent presentation of infection.

• This can be community-acquired or hospital ('nosocomial')

• BSI has an associated mortality of 15-40%, depending on the setting, host and microbial factors.

Common causes of blood-stream infection

(bactremia)Community-acquired• Staph. aureus including MRSA • Strep. pneumoniae • Other streptococci • Escherichia coli

Nosocomial • Staph. aureus including MRSA • Coagulase-negative staphylococci (staph epidermidis)• Enterococci including VRE • Gram-negative bacteria (pseudomonas sp.)• Candida spp.

(MRSA = meticillin-resistant Staph. aureus; VRE = vancomycin-resistant enterococci)

• Primary bacterimia refers to cases in which the site of

infection is unknown; this form 10% of community-acquired cases 30% of nosocomial cases,

• In community-acquired Staph. aureus bacteraemia 20-30% of cases are associated with infectious endocarditis 10% are due to osteomyelitis.

• Peripheral and central venous catheter-related infections are an important source of nosocomial BSI.

Predisposing factors to bacteremia

include

• skin disease• diabetes mellitus• injection drug use• the presence of a central venous, urinary or haemodialysis catheter• surgical procedures, especially involving implantation of prosthetic

materials (in particular, endovascular prostheses). • dental procedures (occasionally including simple tooth brushing)• Colorectal cancer• in oropharyngeal, gastrointestinal and genitourinary infection• Salmonella infection

Physical examination

Physical examination should focus on

• signs of endocarditis• evidence of bone or joint infection (tenderness or

restriction of movement) • abdominal or flank tenderness. • Central venous catheters should be examined for

erythema or thrombophlebitis at the exit site.• fundoscopy should be performed in cases with Candida

spp. infection or suspected infectious endocarditis

Diagnosis

• Bacteremia is most commonly diagnosed by blood culture

• blood is normally sterile • blood cultures must be drawn with great attention to

sterile process. • Occasionally, blood cultures will reveal the

presence of bacteria that represent contamination from the skin

• Blood cultures must be repeated at intervals to determine if persistent bacteremia is present.

blood culture

• Positive blood cultures may be caused by contaminants.

• When isolated from only one bottle or from all bottles from one venesection, coagulase-negative staphylococci (staph epidermidis) often represent contamination.

• Repeated isolation of this organism, however, should raise suspicion of infective endocarditis .

• Streptococci Viridans occasionally contaminate blood cultures

• Bacillus spp. and Clostridium spp. often represent incidental transient bacteraemia or contamination

• chest X-ray. • urine culture . • ultrasound or other imaging of the abdomen.• Imaging should also include any areas of bone

or joint pain and any prosthetic material, e.g. a prosthetic joint or an aortic graft.

• Echocardiography

Initial screening tests should include

Management

• BSI requires antimicrobial therapy and attention to the source of infection, including surgical drainage if appropriate or removing a prosthesis.

• Two weeks of therapy may be sufficient for Staph. aureus BSI from

central and peripheral venous catheter infections when the source is identified and removed, for

uncomplicated skin and soft tissue infections and for

selected cases of uncomplicated right-sided infective endocarditis.

Sepsis

Is blood stream infction with signs of the systemic inflammatory response syndrome (SIRS)

• two of temperature > 38 °C or < 36 °C.• pulse rate > 90 beats per minute.• respiratory rate > 20 per minute or PCO2 < 4.3 kPa

(32.5 mmHg).

• white blood cell count > 12 or < 4 × 109/L-

• evidence of infection.

SEPSIS SYNDROME

Sepsis syndrome is systemic invasion of microbes and their toxins, which results in a disease state characterised by high fever, rigors and tachypnoea, with or without localising signs and the development of shock.

Septic shock

• Septic shock describes sepsis plus hypotension (systolic blood pressure < 90 mmHg systolic or a fall of > 40 mmHg from baseline that is not responsive to fluid challenge).

• It may be complicated by multi-organ failure and requires intensive care unit admission.

Clinical features In severe sepsis,• hypotension unresponsive to fluids• organ dysfunction (septic shock) multi-organ failure.

• encephalopathy (Confusion, delirium and coma )• acute respiratory distress syndrome (ARDS) • Acute renal failure may occur due to acute tubular

necrosis.• Hepatic dysfunction, indicated by hyperbilirubinaemia

and elevated enzyme levels.• Disseminated intravascular coagulation (DIC) is a

frequent complication of severe septicaemia

Investigations• A polymorphonuclear leucocytosis • elevated urea, serum creatinine, bilirubin and hepatic enzymes are

seen. • Progressive thrombocytopenia and other coagulation abnormalities

indicate the presence of DIC.• Arterial blood gas analysis may show alkalosis due to hyperventilation,

but a metabolic acidosis may follow and indicates a poor prognosis. • The chest X-ray may show features of ARDS. • Blood culture multiple cultures are often needed. Blood cultures must be repeated at intervals to determine if

persistent bacteremia is present.• Culture of material from septic foci, if present, should always be

performed.

Management

• Prompt antimicrobial therapy Should cover both Gram-negative and Gram-positive once culture and sensitivity reports are available, specific

antibiotics can be chosen.• Correction of metabolic imbalance, ventilatory support• vasopressor agents in hypotension are important

measures in severe sepsis. • Corticosteroids (200-300 mg of hydrocortisone daily for 5

days) may improve survival in patients with septic shock.• Administration of drotrecogin alfa (activated protein C) has been shown to improve survival

in patients with severe sepsis and septic shock.

Necrotising fasciitis

• Cellulitis may rapidly progress to extensive necrosis of subcutaneous tissue and overlying skin.

• In this condition, cutaneous involvement with erythema and oedema progresses to bullae or areas of necrosis. the cutaneous features are often minimal while the pain is severe.

• The infection spreads quickly along the fascial plane. It is a medical emergency, which requires immediate débridement in addition to antimicrobial therapy .

tow types of necrotising fasciitis

• Type 1 necrotising fasciitis is a mixed infection with Gram-negative bacteria and anaerobes, often seen post-operatively in diabetic or immunocompromised hosts. Subcutaneous gas may be present.

• Type 2 necrotising fasciitis is caused by group A or other streptococci.

Approximately 60% of cases are associated with streptococcal toxic shock syndrome .

Necrotising fasciitis• Both types produce a severe, rapidly progressive and destructive

inflammation of the dermis, subcutaneous tissues, subcutaneous fat and tissue planes including the deep fascia.

• associated with profound toxaemia and multisystem failure. • hyperacute, often arising from minor breach in skin integrity. • The affected area is erythematous, hot, shiny and severly tender.,

full-thickness gangrene resembling a thermal burn ensues. The central area of skin involvement becomes anaesthetic due to cutaneous nerve damage.

• Central anaesthesia surrounded by severly tender erythematous skin is pathognomonic of necrotising fasciitis.

• Systemic toxicity develops with high fever, marked leucocytosis and often hypocalcaemia due to subcutaneous fat necrosis.

Treatment

• Empiric treatment is with broad-spectrum agents (e.g. piperacillin-tazobactam plus clindamycin plus ciprofloxacin; OR

meropenem monotherapy; or

third-generation cephalosporin plus metronidazole

• urgent and extensive surgical débridement

• Despite this, mortality is between 30% and 80% and up to 50% may require amputation of affected limbs and/or plastic surgical management.

C. perfringensC. perfringens: cause gas gangrene; food poisoningLarge gram-positive bacilli.

Spores are rarely observed.

Non-motile; capsulated.

Hemolytic and metabolically active.

C. perfringens

Portal of entry: trauma or intestinal tract.

Three types of infections with increasing severity:

• Clostridial anaerobic cellulitis (confined to skin and subcutaneous tissue)

• Fasciitis or suppurative myositis: accumulation of gas in the muscle planes.

• Myonecrosis or gas gangrene: a life-threatening disease.

Gas gangrene • In anaerobic cellulitis, usually due to C. perfringens or other strains

infecting devitalized tissue following a wound,

• the bacteria produce necrotizing toxin and hyaluronidase, which favor the spread of infection, tissue necrosis extends, resulting in increased bacterial growth, hemolytic anemia, then severe toxemia and death..

• Incubation: 1-7 days after infection.

• Symptoms: Crepitation in the subcutaneous tissue and muscle, foul smelling discharge, rapidly progressing necrosis, fever, hemolysis, toxemia, shock, renal failure, and death.

• Prompt surgical débridement of devitalized tissue and therapy with penicillin or clindamycin usually result in an excellent outcome.

(clostridial myonecrosis)

• is defined as acute invasion of healthy living muscle undamaged by previous trauma, and is most commonly caused by C. perfringens.

• In at least 70% of cases it follows deep penetrating injury sufficient to create an anaerobic (ischaemic) environment and allow clostridial introduction and proliferation.

• Severe pain at the site of the injury progresses rapidly over 18-24 hours.

• Skin colour changes from pallor to bronze/purple discoloration and the skin is tense, swollen, oedematous and exquisitely tender.

• Gas in tissues may be obvious with crepitus on clinical examination, or visible on X-ray, CT or ultrasound.

clostridial myonecrosis

• Signs of systemic toxicity develop rapidly, with high leucocytosis, multi-organ dysfunction, raised creatine kinase and evidence of disseminated intravascular coagulation and

haemolysis.

• Antibiotic therapy with high-dose intravenous penicillin and clindamycin is recommended, coupled with aggressive surgical débridement of the affected tissues.