Ebola virus disease

The largest Ebola outbreak ever reported is continuing in West Africa, with on-going transmission reported in Sierra Leone, Liberia and Guinea, and a small number of cases in Nigeria. A new, unrelated Ebola outbreak has also been reported from DRC Congo. In the unlikely event of a case travelling to Australia, the risk of infection to others remains extremely low unless there is direct exposure to the body fluids of an infected person.

NSW Health recently issued information for Emergency Departments to consider Ebola virus disease (EVD) in patients with fever AND a history of travel in affected countries in the 21 days prior to symptom onset.

These patients should be considered to have a High Possibility of EVD if they also have:

  • history of contact with a confirmed EVD case or with EVD-infected blood, tissue or objects (e.g. sharps) or
  • marked vomiting or marked diarrhoea or bruising or bleeding.

For patients considered to have a High Possibility of EVD:

  • isolate the patient in a single room with own bathroom and manage with standard and transmission-based precautions (contact and droplet), including the use of appropriate PPE. The risk of infection is extremely low unless there is direct exposure to the body fluids of an infected person
  • avoid aerosol generating procedures; if necessary use P2 masks and negative pressure
  • standard and transmission based precautions should also be used for environmental cleaning
  • seek urgent advice from infectious diseases / clinical microbiology / Westmead Hospital / ICPMR / local public health unit to discuss the diagnosis, the need for testing and the possible transfer to the Westmead Hospital or Children’s Hospital at Westmead isolation units, and for the management of contacts
  • routine haematology and other tests should be minimised. Tests required for the immediate management of the patient should only be performed in close collaboration with infectious disease physicians, clinical microbiologists, and laboratory staff
  • place suspect patients in a single room and implement standard and transmission-based precautions (contact and droplet).

For other febrile patients with an appropriate travel history where there is a Low Possibility of EVD (i.e. not likely):

  • use standard precautions
  • seek urgent advice from infectious diseases / clinical microbiology / public health unit regarding the diagnosis and testing
  • consider urgent testing for malaria using routine laboratory procedures.

Patients with EVD may also present with other symptoms apart from fever including myalgia, headache, pharyngitis, conjunctival injection, flushing, gastrointestinal symptoms and prostration. EVD complications include bleeding, petechiae, hypotension and shock, oedema and neurologic involvement.

It is important to remember that patients returning from affected areas with a febrile illness are still more likely to have other causes for their illness, particularly malaria.

See the NSW Health Ebola virus disease website for more detailed clinical guidance.

Shiga toxigenic Escherichia coli (STEC) disease

Jane Jelfs, Trainee Public Health Officer, Ministry of Health, NSW
Liz Smedley, Manager, Infectious Diseases Team, Public Health Unit, South Eastern Sydney Local Health District, Randwick, NSW
Craig Shadbolt, Manager, Food Incident Response & Complaints Unit, NSW Food Authority Foodborne Illness Investigation Unit, Newington, NSW

STEC caused a small outbreak of severe disease in southern Sydney in early 2014 (see: NSW Food Authority). Here we provide an overview of the disease and organism that causes it.

Escherichia coli (E.coli) are Gram negative bacteria that are a ubiquitous and essential member of the gut flora in many animals including humans. However, a number of strains of E.coli are pathogenic and one strain, shiga toxigenic E.coli or STEC, is a foodborne pathogen, infrequently detected in Australia.[1] STEC have been isolated from the meat, fluids and faeces of ruminant animals, cattle in particular.[2] Transmission of STEC to people can occur via a number of means, such as the contamination of fruit or vegetable crops through the use of STEC-containing manure fertilisers, contaminated drinking water, cross contamination of food from raw meat, or drinking raw milk. A common culprit is minced meat that is not thoroughly cooked. Minced meat may become contaminated through the mincing process where STEC contamination on the external meat surface is transferred into the internal part of the mince or burger patty. Due to undercooking the STEC are not killed.[2,3]

STEC were first described in 1982 and since that time have been identified as the causative organism in a number of foodborne outbreaks both in Australia and overseas.[1-6] One of the largest outbreaks in recent times in Europe was linked to fenugreek sprouts with over 4000 cases identified.[3,5] The majority of people infected with STEC recover well but some patients will require hospitalisation as a result of abdominal pain and profuse bloody diarrhoea.[2,7] Treatment is generally supportive and antibiotic therapy is not routinely recommended because of an increased risk of increasing toxin release and increasing the risk of developing haemolytic uraemic syndrome.[7] Between 10 to 20% of those infected with STEC may develop haemorrhagic colitis and/or haemolytic uraemic syndrome (HUS).[7] HUS was originally described in 1956 but it wasn’t until 1982 that the link between STEC and HUS was formally described. There are other causes of HUS such as, a complication of pregnancy, in conjunction with certain drug therapies, in association with infections such as Streptococcus pneumoniae or HIV/AIDS, and, a familial genetic predisposition to HUS has also been documented. [8,9]

Everyone is at risk of STEC disease but children aged less than 5 years and the elderly are at greatest risk of developing HUS in conjunction with an STEC infection.[2] Limiting potential STEC exposure by ensuring that minced meat is consumed well cooked, thorough hand washing following the handling of raw meat, avoiding cross contamination of meats and ready to eat foods (such as salads) through careful handling and storage, pasteurisation of milk, treatment of water supplies and the washing of all fruit and vegetables prior to consumption may help minimise the potential for exposure.

Laboratory confirmation is focused on the detection of STEC from the faeces. E.coli are one of the predominant bacteria found in faeces so it is necessary to screen out the non-pathogenic E.coli, typically using either sorbitol maconkey agar or chromogenic agar plating techniques.

Other laboratory methods utilise the molecular detection of various genes associated with pathogenic E.coli and in the case of STEC, these include the shiga toxin genes (stx1 and stx2).[2]

Both STEC and HUS are notifiable in Australia (Figures 1 and 2). Nationally there have been, on average, approximately 95 notifications of STEC annually over the past 10 years and STEC remains a sporadic cause of foodborne illness in Australia.[1,6] It is important given the serious potential for complications such as HUS following an STEC infection, that faecal samples are screened for STEC when there is clinical suspicion. Whilst serotype O157:H7 has generally been associated with the majority of STEC cases and outbreaks, the 2011 German outbreak of serotype O104:H4 highlighted the pitfalls when limiting detection methods to only serotype O157:H7.[1,3,4,6]

Figure 1: Australian STEC notifications 1999-2014*

*Data up until 26 May 2014
Source: derived from NNDSS May 2014

Figure 2: Australian HUS notifications 1999-2014*

*Data up until 26 May 2014
Source: derived from NNDSS May 2014

It is the responsibility of public health units to receive and to respond to notifications of HUS and STEC. Cases are followed-up urgently, in an attempt to identify possible exposures. If any food premises are implicated, the NSW Food Authority will commence an investigation. There follows close collaboration between the two agencies in an effort to identify the source and to take appropriate action to prevent further cases occurring. A collaborative public health response to a notified STEC and/or HUS case aims to rapidly identify any focal source/s of transmission and to ascertain if there are any other associated cases.[10] Follow-up requires the careful investigation of each case, ensuring that a thorough exposure history is taken, active case-finding occurs by notifying other public health units of cases and a search for common points of exposure is undertaken. Investigation at a food premises will attempt to determine any avenue for cross contamination or undercooking of foods. Depending on levels of evidence and the condition of the premises, immediate action may be taken to prevent sale of foods and further STEC cases until the investigation is finalised.


  1. Bettelheim KA, Goldwater PN. Shigatoxigenic Escherichia coli in Australia: a review. Reviews in Medical Microbiology. 2013;25(1):22-30
  2. Gyles CL. Shiga toxin-producing Escherichia coli: an overview. J Anim Sci. Mar 2007;85(13 Suppl):E45-62.
  3. European Centre for Disease Prevention and Control and European Food Safety Authority. Shiga toxin/ verotoxin-producing Escherichia coli in human, food and animals in the EU/EEA, with special reference to the German outbreak strain STEC O104. Stockholm: ECDC; 2011.
  4. Bettelheim KA. Non-O157 Shiga-toxin-producing Escherichia coli. Lancet Infect Dis. Jan 2012;12(1):12.
  5. Chattaway MA, Dallman T, Okeke IN, Wain J. Enteroaggregative E. coli O104 from an outbreak of HUS in Germany 2011, could it happen again? Journal of Infection in Developing Countries. Jun 2011;5(6):425-436.
  6. Vally H, Hall G, Dyda A, et al. Epidemiology of Shiga toxin producing Escherichia coli in Australia, 2000-2010. BMC Public Health. 2012;12:63.
  7. Goldwater PN, Bettelheim KA. Treatment of enterohemorrhagic Escherichia coli (STEC) infection and hemolytic uremic syndrome (HUS). BMC Med. 2012;10:12.
  8. Ariceta G, Besbas N, Johnson S, et al. Guideline for the investigation and initial therapy of diarrhea-negative hemolytic uremic syndrome. Pediatr Nephrol. Apr 2009;24(4):687-696.
  9. Tostivint I, Mougenot B, Flahault A, et al. Adult haemolytic and uraemic syndrome: causes and prognostic factors in the last decade. Nephrol Dial Transplant. Jul 2002;17(7):1228-1234.
  10. Communicable Diseases NSW Health. Haemolytic Uraemic Syndrome And Shigatoxigenic E. coli Infections. http://www.health.nsw.gov.au/Infectious/controlguideline/Pages/haemo.aspx Accessed 26 May 2014, 2014.
Current as at: Monday 25 August 2014
Contact page owner: Health Protection NSW