Infectious diseases

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Chapter 41 Infectious diseases

Melinda J. Berry, Mark A. Boyd

EDITOR’S COMMENT

Remember: There is mandatory reporting to your local public health unit of some infectious diseases (see Table 47.2).

ANTIBIOTIC PRESCRIBING

A large volume of antibiotic prescriptions originate from the emergency department. To be responsible in your use of antibiotics, utilise up-to-date antibiotic guidelines and the infectious diseases and/or microbiology services in your hospital.

Antibiotic recommendations in this book are largely based on Therapeutic guidelines.1

Don’t feel pressure to prescribe unnecessary antibiotics—most patients would prefer a thorough assessment and explanation of the medical condition, rather than an unnecessary antibiotic prescription.

Antibiotics are not harmless. They have side effects such as diarrhoea, allergic reactions and drug interactions, and they put pressure on antibiotic resistance in the community. We have already reached the era of untreatable multiresistant organisms and it is likely to get worse.

More often than not, there is sufficient time to discuss your antibiotic prescribing with a more senior emergency department clinician, the infectious diseases service or the hospital team that will be taking over care of your patient. Once an antibiotic is prescribed, it is rarely stopped, no matter how unnecessary it may be.

The antibiotic creed1

M Microbiology guides therapy wherever possible.
I Indications should be evidence-based.
N Narrowest spectrum required.
D Dosage appropriate to the site and type of infection.
M Minimise duration of therapy.
E Ensure monotherapy in most situations.

Remember:

1. Patients on warfarin will need to have their international normalised ratio (INR) closely monitored.
2. Antibiotics can affect the absorption of the oral contraceptive pill (OCP). Recommend relevant patients use another form of contraception that month.
3. Patients are more likely to be adherent to the simplest antibiotic regimen (dosing regimen and pill count).

MULTI-RESISTANT STAPHYLOCOCCUS AUREUS (MRSA)

MRSA is resistant to beta-lactam and one or more other antibiotics. Initially it was only present in the healthcare setting, but now it has independently evolved in the community, hence the use of the term community-acquired MRSA (CA-MRSA) versus hospital-acquired MRSA (HA-MRSA).2 It is all MRSA.

Some MRSA strains are sensitive to antibiotics such as clindamycin, doxycycline or trimethoprim + sulfamethoxazole and are therefore sometimes referred to as non-multi-resistant oxacillin-resistant Staphylococcus aureus (NORSA).2 These strains manifest clinically as subcutaneous abscesses and necrotising pneumonia.

MRSA is now so prevalent in Australia that any staphylococcal infection needs to be thought of as potentially MRSA. Appropriate specimen collection is very important.

Management

Skin abscesses are managed by effective incision and drainage and rarely require antibiotics even when there is some surrounding erythema. If antibiotics are indicated, mild infection can be treated with a beta-lactam such as dicloxacillin while awaiting sensitivity results.1

Severe infection, manifest as organ dysfunction, hypoperfusion or hypotension, needs treatment before sensitivities become available: vancomycin 1 g IV BD (adapted according to estimated glomerular filtration rate, eGFR).

SEPSIS

(See also ‘Septic shock’ in Chapter 11, ‘Shock’.)

• Sepsis is defined as infection with systemic inflammatory response.
• Severe sepsis is defined as sepsis with acute organ dysfunction.
• Septic shock (high mortality ~ 30%) is defined as:

• sepsis with hypotension refractory to initial fluid bolus
or
• evidence of tissue hypoperfusion (lactate > 4 mmol/L).

Early aggressive resuscitation in the emergency department has been shown to improve outcome.3

Management

1. Prompt fluid resuscitation—20–30 mL/kg fluid bolus on diagnosis.
2. Broad spectrum antibiotics within an hour after taking at least two sets of blood cultures simultaneously from different sites:4

• at least one set percutaneously
• at least one set from a vascular access device (if the device has been present > 48 hours)
• culture other sites as clinically indicated.
3. Insert central line and arterial line early.

Goals in the emergency department within 6 hours:4

1. Fluid resuscitation (crystalloid or colloid) to central venous pressure (CVP) 8–12 mmHg.
2. Mean arterial BP > 65 mmHg:

• vasopressor, e.g. noradrenaline, infusion once fluid resuscitated
• low-dose hydrocortisone for resistant hypotension.

3. Central venous oxygen saturation > 70% (sample from central venous catheter, CVC) or mixed venous sample > 65%:

• transfuse blood to haematocrit (HCT) ≥ 30% and/or
• dobutamine infusion (start at 2.5 μg/kg/min).

4. Take appropriate cultures and think about most likely source.
5. Treat the sepsis: broad spectrum antibiotics within an hour (ceftriaxone 2 g IV plus vancomycin 1 g IV if MRSA suspected).
6. Consult early with your infectious diseases service.
7. Source control of infection:

• drainage of abscess, debridement of tissue
• removal of foreign bodies, e.g. vascular access devices etc.

MENINGOCOCCAL INFECTION

Invasive meningococcal disease is life-threatening. The course can be fulminant with patients deteriorating within hours of onset of symptoms.

Neisseria meningitidis is a gram negative diplococcus with many serotypes. Serotypes B and C cause disease in Australia. Serotype C is now on the Australian childhood immunisation schedule. There is no vaccination available for serotype B.

Transmission is via asymptomatic nasal carriage (~ 10% population). Age groups 0–4 years and 15–25 years are most commonly affected by invasive disease with a seasonal peak in winter–spring.

Invasive infection can manifest as meningitis or more commonly as septicaemia (also referred to as meningococcaemia). Meningococcal meningitis has a high mortality rate of around 7%, but the mortality rate is even higher for meningococcal septicaemia at around 19%.

Clinical findings

The classic clinical findings of meningococcaemia are fever with an otherwise unexplained petechial or purpuric rash. However, clinical features can be non-specific early in the course of disease, requiring a high index of suspicion and thorough clinical examination to make the diagnosis.

Early findings can also include:

• maculopapular rash that develops in the first 24 hours of illness
• myalgia which can be very painful
• cold extremities and pallor with fever.

Late signs (12–16 hours) are:

• meningism
• impaired consciousness
• shock.

Management

Prehospital antibiotics in meningococcal sepsis can be life-saving5,6—benzyl penicillin 30 mg/kg up to 1.2 g IM or IV or ceftriaxone 50 mg/kg up to 2 g IM or IV.

1. Ideally, draw blood cultures before giving antibiotics.
2. Antibiotics should be administered as soon as possible and within 30 minutes—ceftriaxone 2 g IV BD.5
3. If bacterial meningitis is suspected, dexamethasone 10 mg IV is recommended except in the patient with septic shock where high-dose steroids can be harmful. Low-dose hydrocortisone (50 mg IV qid) is an option in this situation.7

Investigations

• Send blood for meningococcal polymerase chain reaction (PCR) as well as culture.
• Send skin scrapings of purpuric lesions for gram stain and culture.
• Send cerebrospinal fluid (CSF) for culture and meningococcal PCR.
• Send blood for FBC, coagulation and biochemistry.
• Local public health unit needs to be notified ASAP (< 12 hours) for all cases where invasive meningococcal disease is being considered. Discuss with your infectious diseases service.
• Droplet transmission precautions should be instituted for 24 hours after commencement of antibiotics.

Chemoprophylaxis for meningococcal contacts

This is the role of the public health department.

1. Healthcare workers—the only healthcare workers that require prophylaxis are those who:

• intubated the patient without wearing a mask
• performed mouth to mouth resuscitation.

2. Close contacts—

• main purpose is to eliminate the carrier state
• includes household members and intimate contacts
• outside immediate family, contact tracing and prophylaxis is coordinated by public health authorities.

Treatment

• Ciprofloxacin 500 mg PO single dose (for adults and children > 12 years of age)

or

• Rifampicin 10 mg/kg (5 mg/kg in neonates) up to 600 mg PO bd for 48 hours (preferred option in children)

or

• Ceftriaxone 250 mg IM single dose (best option in pregnancy)

FEVER

Usually the cause of fever is apparent from other symptoms and signs, allowing focused investigation and management. First-line investigations such as urine culture, blood culture and chest X-ray may reveal an otherwise unapparent infective source.

When there is no apparent cause, a broad differential needs to be considered. Detailed and considered history taking, meticulous examination and tailored investigations are warranted.

Causes of fever can vary according to:

1. Age of patient:

• Elderly—

• Often do not mount much of a fever to a significant infection or may be hypothermic.
• Sepsis may manifest as confusion or decrease in function.
• Urosepsis and respiratory tract sepsis are common, but do not forget other potential sites.

• Paediatric (See Chapter 33, ‘Childhood emergencies’.)

2. Geography and travel history—see the section ‘Fever in the overseas traveller’ below.
3. Patient comorbidities/factors to be considered:

• Immune-deficient, immune-suppressed or immune-compromised
• Hospital inpatient already (or recent discharge within 4 weeks)
• Surgical procedures and indwelling devices
• Injecting drug usage:

• High rates of MRSA.
• Injection sites can be anywhere.
• Septic emboli can lead to abscess in brain, lung, heart, bones, joints, vertebral discs.

• Itinerant lifestyle

• Often immunocompromised due to poor nutrition, poor self-care, drug and alcohol use, lack of medical attention.
• Can be difficult to elicit a clear history.
• High risk of severe sepsis and septic shock.

Pyrexia of unknown origin (PUO)

Classic definition is fever > 38.3°C of unknown cause for 3 weeks despite initial medical consultation.

The decision needs to be made whether the patient requires inpatient or outpatient investigation and management.

Bacterial meningitis

In adults, 80% are Streptococcus pneumoniae or Neisseria meningitidis.

Clinical features

Of adult patients with bacterial meningitis, 95% present with two of the following:6

• fever
• headache
• neck stiffness
• change in mental status (Glasgow Coma Score (GCS) < 14).

Management

Early antibiotics improve outcome.7

1. Take blood cultures.
2. Ideally, perform lumbar puncture (LP) first also, but do not delay antibiotics. In patients where CT head is indicated prior to LP, administer dexamethasone and antibiotics prior to CT.
3. Antibiotics (ceftriaxone 2 g IV BD) should be administered within 30 minutes of clinical assessment.
4. Adjunctive dexamethasone therapy (10 mg IV prior/with antibiotics then q6h for 4 days) reduces mortality in bacterial meningitis, EXCEPT patients with concurrent septic shock where high dose steroids can be harmful. Low-dose hydrocortisone (50 mg qid) is an option.7

Streptococcus pneumoniae

Increasing penicillin/cephalosporin resistance depending on setting.

Management

• Consult microbiology service.
• If gram positive cocci on CSF gram stain, add vancomycin 500 mg IV q6h.

Herpes meningo-encephalitis

This is focal herpes simplex virus (HSV) infection of the cerebral cortex, especially the temporal lobe. Clinically, more neurological changes/seizures than bacterial meningitis.

Meningism is also present.

Request HSV PCR to be performed on CSF.

Treatment

Aciclovir 10 mg/kg IV q8h (adjusted for renal function).

Fever in the overseas traveller

Five important diagnoses to consider:

1. malaria
2. dengue
3. typhoid
4. viral hepatitis
5. HIV (see Chapter 42, ‘The immunosuppressed patient’).

Malaria

Fever in the overseas traveller is malaria until proven otherwise.

Four plasmodium species cause human malaria—falciparum, vivax, ovale and malariae.

Falciparum causes almost all deaths directly related to malaria and is responsible for several million deaths throughout the world each year.

Presenting symptoms

• Clinical features are protean.
• Spiking fevers up to 40°C.
• Headache, diarrhoea, abdominal pain.
• Can be non-specific ‘flu-like’ symptoms.
• Severe malaria is characterised by:

• altered level of consciousness and/or seizures (cerebral malaria)
• shock
• respiratory distress
• jaundice, anaemia, hypoglycaemia.

Investigations

• Thick blood film for identification of malarial parasites.
• Thin blood film to determine malaria species.

Note: Detectable parasitaemia can lag behind symptoms; should repeat 12-hourly until malaria diagnosed or excluded (usually three negative blood films).

• Other findings include: anaemia, thrombocytopenia, ↑ LDH, ↑bilirubin.
• Rapid detection kits are available; most only detect P. falciparum, not as sensitive as experienced microscopic examination.

Treatment

1. Requires up-to-date knowledge of geographical patterns of drug resistance.
2. Always seek specialist advice.
3. Falciparum malaria can progress to life-threatening complications within hours, even after initiation of treatment. Discuss hospital admission with your infectious diseases service or medical physician/team on call.
4. Severe malaria:

• artesunate 2.4 mg/kg IV (first choice if available)
or
• IV quinine 20 mg/kg over 4 hours.

5. Uncomplicated Falciparum malaria and other malaria species from chloroquine-resistant areas:

• artemether + lumefantrine, 20 + 120 mg tablets (first choice if available), 4 tablets at 0, 8, 24, 36, 48 and 60 hours

or

• mefloquine 750 mg PO then 500 mg PO 6–8 hours later (as long as not the drug used as prophylaxis).

Note: Artemether + lumefantrine is TGA-approved for adults but not children in Australia. Artesunate is not registered for use in Australia, but is available under the special access scheme and is kept in selected hospital pharmacies.

Dengue fever (‘break bone fever’)

• Mosquito-transmitted flavivirus with a short incubation period of 4–7 days.
• Patients usually present with various combinations of fever, myalgia, arthralgia and rash. The rash is fine and sometimes not noticed by the patient. It may involve the palms and soles.
• Thrombocytopenia is almost always present, as is elevated hepatic transaminases.
• Dengue haemorrhagic fever and dengue shock syndrome, due to a sudden increase in vascular permeability, occurs in infants and secondary exposures.8
• Management is supportive.

Typhoid fever

• Faecally-contaminated food or water with Salmonella typhi or paratyphi sub–types.
• Vaccination efficacy is somewhere between 50% and 80%, depending on innoculum, so does not exclude diagnosis.
• Classically, fever and abdominal tenderness initially with constipation.
• May also have confusion, rose spots (faint salmon-coloured maculopapular rash on the trunk), hepatosplenomegaly.
• Relative bradycardia is not very sensitive or specific.
• Untreated infection can lead to intestinal perforation.
• Diagnose by culturing blood and stool.

Treatment

Administer ciprofloxacin 500 mg PO for 5–7 days or ceftriaxone 2 g IV daily.

There is quinolone resistance (e.g. in India and Vietnam), so discussion with infectious diseases services is recommended.

Viral hepatitis

Hepatitis A virus

• Acute self-limiting liver infection is transmitted by the faecal–oral route.
• Endemic in developing countries and immunisation is recommended for travellers.
• Incubation period of 2–7 weeks. Clinical features include flu-like symptoms, fever, fatigue, nausea then jaundice and dark urine. Clinically indistinguishable from other causes of acute hepatitis.
• Serological diagnosis.
• Management is supportive. Does not result in chronic hepatitis. Fulminant hepatitis is a rare complication. Immunoglobulin is used to control outbreaks in developed countries.

Hepatitis B virus (HBV)

This blood-borne virus is transmitted by parenteral or mucosal exposure to blood or bodily fluids.

Incubation period 1–4 months. Acute infection can be subclinical or non-specific hepatitis with flu-like symptoms, fatigue, nausea, right upper abdominal quadrant discomfort and jaundice. Liver transaminases can be elevated over 1000 IU/L. Markedly elevated prothrombin time can indicate development of fulminant liver failure.

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