Aura 2016: first Australian report on antimicrobial use and resistance in human health

4.7 Neisseria meningitidis

Health impact

N. meningitidis can cause invasive meningococcal disease (septicaemia and meningitis) or, rarely, more localised disease (such as conjunctivitis, arthritis or pneumonia). Most patients with invasive disease present with nonspecific symptoms, but this is treated as a medical emergency because symptoms can rapidly progress to serious disease and death.

The invasive form of the disease can be associated with outbreaks in environments where there is prolonged close contact, especially within households. Invasive meningococcal disease is very uncommon in Australia because of the availability of vaccines that provide immunity against some strains.

Treatment

Because invasive meningococcal disease is potentially life-threatening, most invasive infection is treated empirically (pending the results of blood cultures and, where necessary, testing of cerebrospinal fluid). The most important antimicrobials for treatment are ceftriaxone (or cefotaxime) and benzylpenicillin. Close contacts of patients with invasive meningococcal disease are given antimicrobial prophylaxis to prevent infection by clearing nasopharyngeal colonisation. The most important antimicrobials for prophylaxis are rifampicin, ciprofloxacin and ceftriaxone.

Types and impact of resistance

There is currently no international consensus on the definition of reduced susceptibility or resistance to benzylpenicillin in this species. In most test systems, wild-type strains (that is, strains with no acquired resistance mechanism) have MICs of 0.25 mg/L or less.

Resistance to benzylpenicillin has been slow to develop in Australia. Ceftriaxone resistance has not yet been documented. Non wild-type strains that have reduced susceptibility to these two agents are now found regularly, but are not yet associated with treatment failure. Occasional strains are found with resistance to rifampicin or reduced susceptibility to ciprofloxacin.

Resistance to benzylpenicillin has been slow to develop in Australia. Ceftriaxone resistance has not yet been documented.

Key findings (national)

In 2014, 169 cases of invasive meningococcal infection were notified nationally (0.7 per 100 000 population). From these cases, 95 isolates were submitted for susceptibility testing. Figure 4.22 shows the national rates of resistance to the four key agents used for treatment or prophylaxis.

Figure 4.22 Neisseria meningitidis resistance to individual antimicrobials used for treatment and prophylaxis, 2014

Note: Decreased susceptibility or resistance to benzylpenicillin: in most test systems, wild-type strains (i.e. with no acquired resistance mechanism) have minimum inhibitory concentrations of ≤0.25 mg/L.

Source: National Neisseria Network (public and private hospitals, and health services)

National trends

During the past 15 years, there has been no change in the (very low or zero) rates of resistance to any of the four key agents (Figure 4.23). In this context, resistance to benzylpenicillin is defined as an MIC of 1 mg/L or more.

Figure 4.23 Fifteen-year trends in resistance in Neisseria meningitidis

Source: National Neisseria Network (public and private hospitals, and health services)

Detailed reports of susceptibility data on N. meningitidis from 1997 to 2013 can be found in the Australian Meningococcal Surveillance Programme annual reports (see Appendix 3).

4.8 Pseudomonas aeruginosa

Health impact

P. aeruginosa is an opportunistic, nosocomial pathogen that primarily affects hospitalised or immunocompromised patients. It is a ubiquitous organism found in moist environments, which act as a reservoir. It is naturally resistant to many chemicals, including most common antimicrobials and some antiseptics. As a consequence, it frequently causes infections in patients who are receiving antimicrobial treatments for other purposes.

P. aeruginosa can cause urinary tract infection in catheterised patients and patients with structural abnormalities of the urinary tract. It is associated with burn and other wound infections, and has a strong propensity to cause airway infection in patients with cystic fibrosis. It also frequently causes septicaemia, especially in neutropenic patients.

Treatment

P. aeruginosa is susceptible to only a limited range of antimicrobials:

specialised β-lactams such as piperacillin (with or without tazobactam), ceftazidime and meropenem

aminoglycosides such as gentamicin and tobramycin

some fluoroquinolones such as ciprofloxacin.

Urinary tract infections can often be managed with oral fluoroquinolones; more serious infections must be treated with β-lactams, which are usually used in combination with aminoglycosides for the most serious infections. The effective β-lactams and the aminoglycosides can only be administered intravenously.

Types and impact of resistance

This species is intrinsically resistant to many antimicrobial classes as a result of the presence of several efflux pumps in its cell wall and cell membrane. It is notorious for its capacity to become resistant during treatment to the limited range of effective agents, mainly due to the upregulation of these efflux pumps. It also has the capacity to become resistant to β-lactams through porin loss and the acquisition of β-lactamases. Multidrug-resistant strains with acquired resistance to two or three of the effective antimicrobial classes will require other treatments, such as the potentially toxic colistin.

Pseudomonas aeruginosa is intrinsically resistant to many antimicrobial classes.

Key findings (Queensland)

Resistance of P. aeruginosa to key antimicrobial agents is shown in Figure 4.24. Only resistance to piperacillin–tazobactam exceeded 10%. Rates of resistance were significantly higher in public hospitals (Figure 4.25), possibly due in part to the influence of isolates from patients with cystic fibrosis who are managed in the public sector. These patients are known to have isolates with higher rates of resistance to all effective agents because they are likely to have been treated multiple times for acute infective exacerbations of cystic fibrosis lung disease.

Figure 4.24 Pseudomonas aeruginosa resistance to individual agents, 2014

CAZ = ceftazidime; CIP = ciprofloxacin; GEN = gentamicin; MER = meropenem; PTZ = piperacillin–tazobactam

Sources: OrgTRx (Queensland); Sullivan Nicolaides Pathology (Queensland and northern New South Wales)

Data table: Figure 4.24

Agent	% resistant
PTZ	10.3
CAZ	4.5
MER	4.0
GEN	5.3
CIP	6.7

Figure 4.25 Pseudomonas aeruginosa resistance, by clinical setting, 2014

CAZ = ceftazidime; CIP = ciprofloxacin; GEN = gentamicin; MER = meropenem; na = not available (either not tested or tested against an inadequate number of isolates); PTZ = piperacillin–tazobactam

Sources: OrgTRx (public hospitals and health services); Australian Group on Antimicrobial Resistance and Sullivan Nicolaides Pathology (SNP) (private hospitals); SNP (community and residential aged care facilities)

Data table: Figure 4.25

Agent	Public hospitals and health services (n = 9,256), % resistant	Private hospitals (n = 2,570), % resistant	Community (n = 8,475), % resistant	Residential aged care facility (n = 1,216), % resistant
PTZ	10.3	na	na	na
CAZ	7.1	4.6	1.8	2.5
MER	6.4	na	0.6	na
GEN	8.9	2.5	2.6	2.5
CIP	9.4	na	2.8	na