communicable diseases bulletin - quteprints.qut.edu.au/64729/1/64729.pdfkimberley region received...

Centre for Disease Control

THE NORTHERN TERRITORY

COMMUNICABLEDISEASES BULLETIN

NT

ISSN 1323-8612 Vol. 4, No 3, September 1997

Outbreak of non-sexually transmitted gonococcal conjunctivitis in CentralAustralia and the Kimberley region, 13 February to 27 June 1997

R. Matters,1 I. Wong2 and D. Mak3

1Territory Health Services, 2Western Diagnostic Pathology, Alice Springs,3Kimberley Public Health Unit, Western Australia

Introduction

From 13 February to 27 June 1997, 447 cases ofgonococcal conjunctivitis were identified byCommunicable Disease and Public HealthCentres and Community Clinics in the NorthernTerritory (NT), Western Australia (WA) andSouth Australia (SA). The outbreak involvedAboriginal communities predominantly in CentralAustralia (which included the western AliceSprings region, NT, the Ngaanyatjarra centraldesert area and the Pitjantjatjara Lands of SA)and the Kimberley region in WA. This was thefirst outbreak recorded in the Kimberley region. Itis not yet known whether the Kimberley caseswere part of the larger Central Australianoutbreak or whether they represented a separateand unrelated outbreak.

Gonococcal conjunctivitis causes considerablemorbidity in Aboriginal communities in CentralAustralia during outbreaks.1,2,3,4,5 The disease ischaracterised by acute painful conjunctivitis withrapid non-sexual transmission betweenindividuals caused by person to person contact.

Bushflies may act as a mechanical vector ofNeisseria gonorrhoeae. There have been fivepreviously documented gonococcal conjunctivitisoutbreaks in Central Australia. These aresummarised in Table 1.

ContentsOutbreak of non-sexually transmitted gonococcal conjunctivitisin Central Australia and the Kimberley region, 13 Februaryto 27 June 1997 .............................................................................1Guidelines for the control of gonococcal conjunctivitis ................8Meningococcal disease - 2 NT cases in August 1997 - Theview from CDC............................................................................10El Nino - ? drier wet season, but still expect melioidosisand other “tropical” infections.....................................................13Guidelines for community control of scabies and skin sores.......15Non-communicable diseases update: No. 3. Message:Cholesterol reduction: base your primary preventionstrategy on overall cardiovascular risk, and emphasisenon-drug options first ..................................................................18Acute respiratory illness in 2 Darwin schools .............................21Hepatitis C community awareness campaign ..............................22Immunise Australia......................................................................23NT notifications of diseases by districts 1 April to 30 June1997 and 1996 .............................................................................24Notified cases of vaccine preventable diseases in NT 1 Aprilto 30 June 1997 and 1996............................................................25NT wide notifiable diseases 1 April to 30 June 1997 and 1996 ..25Malaria Notifications, NT April to June 1997 .............................26

EDITOR Vicki Krause PRODUCTION DESIGN Angela Salter & Sue Reid

ASSISTANT EDITORS Fay Johnston, Sue Reid, Angela Merianos, Christine ConnorsPRINTED Forms and Resources

Centre for Disease Control, Block 4, Royal Darwin HospitalPO Box 40596, CASUARINA NT 0811 Phone (08) 8922 8044 Fax (08) 8922 8310

The Northern Territory Communicable Diseases Bulletin Vol. 4 No. 3 September 19972

Table 1 Time and size of reported gonococcalconjuntivitis outbreaks in CentralAustralia

Year of outbreak Cases* Period of outbreak

1934 91 -

1981 35 May to June

1986/87 140+ November to May

1991 432 January to July

1992 62+ April to July

* Includes both clinical and laboratory confirmed cases

Similar environmental factors leading up to andduring previous outbreaks were observed with thisoutbreak. These factors included above averagesummer rainfall preceding the outbreak, summerchanging to winter temperatures, an increase in thepercentage of Haemophilus sp. isolates from eyeswabs and increased fly numbers at the start of theoutbreak. None of the outbreaks werecharacterised by an increase in notifications ofsexually transmitted gonorrhoea in the time periodpreceding the outbreak.

MethodsCase definitionA clinical illness was defined as intenseinflammation of the conjunctivae, copious purulentdischarge with or without periorbital oedema. Aclinical case was confirmed when N. gonorrhoeaewas isolated on culture, detected by PCR or Gramnegative diplococci were seen in microscopy.Unconfirmed clinical cases were included in thisanalysis if there was a laboratory confirmed casenotified from the same community. Date of onsetwas defined as the date on which the eye swabconfirming the diagnosis was taken.

Collection of dataPatient information including age, gender, date ofonset of illness and address was obtained fromDisease Control Centres in Alice Springs NT andAdelaide SA; Goldfields Public Health Services -Boulder, WA; Kimberley Public Health Unit -Derby, WA; Western Diagnostic Pathology - AliceSprings, NT and Pathology - Alice SpringsHospital (ASH), NT. Information on the number ofclinical unconfirmed cases, spread of disease andfly density was obtained from Community HealthClinics in Central Australia. Populationdemographic statistics were obtained fromNganampa Health Council, Ngaanyatjarra Health

Service and Rural Health - Alice Springs, TerritoryHealth Services (THS). Rainfall and temperaturedata were obtained from the Bureau ofMeteorology - Darwin and Alice Springs RegionalOffices NT and WA. Information regarding thenumber of clinical cases was not obtained from theKimberley.

Laboratory InvestigationN. gonorrhoeae strains from Central Australiawere sent to the Prince of Wales Hospital, Sydney,for serotyping, auxotyping and MIC testing andincluded 89 eye, 34 genital and 2 joint isolates.Records at the Pathology Laboratory, ASH, wereexamined to determine the percentage ofHaemophilus sp. identified from eye swabsbetween June 1996 and June 1997 and also thenumber of cases of disseminated gonococcalinfection (DGI) between 1 August 1995 and 18July 1997. DGI was defined as the isolation of N.gonorrhoeae from a sterile site e.g. joint fluid.

ResultsNumber of casesThere were 242 confirmed cases (including 5reinfection cases) and 205 unconfirmed cases ofgonococcal conjunctivitis for a total of 447 cases.Of the confirmed cases 120 were culture positive,53 PCR positive and 69 microscopy positive. TheNT had 121, WA 105 and SA 16 confirmed cases.There appears to have been two epidemics duringthe outbreak (Figure 1). The smaller epidemicpeaked in the Kimberley during March before alarger epidemic, involving many morecommunities in Central Australia, peaked in May.

Figure 1 242 laboratory confirmed cases ofgonococcal conjunctivitis by weekand geographic region, Feb-June ‘97

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The Northern Territory Communicable Diseases Bulletin Vol. 4 No. 3 September 1997 3

Age distribution of casesOver three quarters of the confirmed cases werechildren under 10 years old with the greatestnumber recorded in the 5 to 9 group (Table 2).The youngest child was four months old.

Table 2 Age distribution of confirmed cases

Age group (yrs) Cases % of cases

0 to 4 73 30.2

5 to 9 114 47.1

10 to 14 35 14.5

15 and over 12 4.9

Unknown 8 3.3

Total 242 100.0

Gender

There were 113 males and 129 females withconfirmed infection.

RainfallThe Giles Meteorological Station is in WAapproximately 150 kms North of the junction ofthe WA, NT and SA borders. This station wasone of the closest to the communities whichwere involved in the start of the outbreak. Therainfall at Giles in December was above averageand there was substantial rainfall in January andFebruary preceding the outbreak (Figure 2). Thefirst cases of the outbreak appeared in the middleof February. Alice Springs received 80 mm ofrain in January and 242 mm in February. TheKimberley region received 136 mm of rain inJanuary and 274 mm in February.

Figure 2 Number of cases compared to themonthly rainfall at Giles, January1996 to June 1997

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TemperatureThe mean daily minimum temperature at Giles inFebruary was 24.7°C (Figure 3) at the start of theoutbreak and was below 10°C in June at the endof the epidemic. The mean daily maximumtemperature in February was 36°C at the start ofthe epidemic. Typical summer temperaturespreceded the outbreak.

Figure 3 Number of cases compared to themean daily minimum temperatures atGiles for each month, June 1996 toJune 1997

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Sexually transmitted gonorrhoea in CentralAustraliaThere was no increase in the notifications ofsexually transmitted N. gonorrhoeae preceding theoutbreak. The notification information indicatedthat sexually transmitted disease was endemic atnearly the same level all year round.

Proportion of Haemophilus sp. isolates fromeye swabs received at Alice Springs HospitalUsing Haemophilus sp. as an indicator of theamount of general bacterial/viral eye disease incommunities the total number of Haemophilus sp.


identified each month from eye swabs wasexpressed as a proportion of the monthly totalnumber of eye swabs received. The highestproportion (47%) of Haemophilus sp. during thethirteen months occurred in March 1997. Themean monthly proportion was 33%. There was agradual increase in the proportion of eye diseasein which Haemophilus sp. was isolated at the startof the outbreak.

There is some indication that conjunctivitis causedby Haemophilus sp. is endemic all year andHaemophilus conjunctivitis rises prior and duringgonococcal conjunctivitis outbreaks. This hasbeen observed in every previous outbreak andpossibly due to the same environmental/otherstimuli which promotes the gonococcaltransmission.

Fly densityThirteen Central Australian communities involvedin the epidemic were contacted and asked whenthey thought flies were at their worst and when theflies decreased in number. Five communitieswhere the first gonococcal conjuntivitis indexcases appeared reported the flies were “terrible” inFebruary. Ten communities reported that the flieswere at their worst in March and April. Fourcommunities had their worst flies in May. Flydensity was dramatically reduced in June.

Auxotyping, serotyping and MIC testingfrom Central AustraliaFifty three eye isolates involved in the outbreak,that have been fully typed, belonged toauxotype/serovar class Wt/IB3. Fourteen STDbackground isolates obtained during the outbreakwere typed and included six Wt/IB3 strains aswell as seven other types. Two eye isolates notinvolved in the outbreak, consisted of twodifferent strains which were not Wt/IB3. Twojoint isolates consisted of a Wt/IA4 strain and aIB3 serovar (the Wt/IA4 strain was not involvedin the outbreak but included as a backgroundstrain). The majority of the eye isolates tested sofar have had a penicillin MIC of between 0.125and 0.25 mg/L, with one isolate having apenicillin MIC of 0.5 mg/L. All are classified assensitive to penicillin, but in the less sensitiverange.

Public health responseAn alert was sent by Alice Springs DiseaseControl to Central Australian communities (NT,

WA, SA) in March after several cases had beenreported. This alerted the communities to thepresence of current cases, urged that swabs andcultures be taken and that procaine penicillin oramoxycillin with probenecid be given. A secondalert was sent out in April. In May, with over 40cases reported, a further alert was sent out whichincluded direction to treat household contacts, adirection not explicitly stated in the CentralAustralian Rural Practitioners Association(CARPA) standard treatment manual. An alertalso went to all remote schools telling of theoutbreak and the need for treatment. Theoutbreak, protocol and need to treat allhousehold contacts were discussed both at theCentral Australia Disease Control CoordinatingCommittee (CADCCC) meeting/teleconferenceon 9/5/97 and again at the CARPA Conferenceon 10-11/5/97.

Public Health Unit staff in the Kimberley regionarrived at the affected community within 24hours of the first notification (though notnecessarily the index case) of gonococcalconjunctivitis. They then assisted local staff withscreening and treatment.

DiscussionThe number of cases reported is undoubtedly anunderestimate of the true number of gonococcaleye infections as not all patients presenting withconjunctivitis had an eye swab and smear takenfor laboratory confirmation by either culture,smear or PCR. Direct input from CentralAustralian communities was invaluable inobtaining a more accurate amount of clinicaldisease that was treated. Delays in transportresulted in the death of N. gonorrhoeae inswabs and confirmation of infection could onlybe made from smear and PCR. All theKimberley cases were tested by PCR.

The sharp peak in the number of Kimberleycases in Figure 1 is artefactual. When PublicHealth Unit staff arrived at the communitymany patients had been experiencingsymptoms of conjunctivitis for several days ormore. Cases had been observed during lateJanuary and early February but no swabs hadbeen taken as gonococcal conjunctivitis hadnot been suspected.

Fly counts were not performed in anycommunity and the subjective assessment of flynumbers by staff may be inaccurate but the


survey covered many communities and areasonable picture was obtained. There isstill insufficient evidence to determinewhether flies definitely contribute to thespread of gonococcal conjunctivitis. Recentstudies in WA have shown that Chlamydiatrachomatis can survive in the crop ofbushflies, however, further work is still inprogress to ascertain whether the number oforganisms carried is sufficient to cause trachoma(unpublished work by Dr. Ian Dadour,entomologist).

The environmental factors present in thisoutbreak were similar to previous outbreaks,including: 1) heavy summer rainfall at least onemonth before the first cases appeared, 2) a meandaily minimum temperature above 20°C for thefirst two months of the outbreak, 3) eyeinfections caused by Haemophilus sp. increasedto the highest monthly percentage for the yearand 4) an extremely high fly population occurredin February, March and April. Sexuallytransmitted N. gonorrhoeae cases did notincrease before the outbreak.

Factors which contributed to the outbreakinclude: a) N. gonorrhoeae can only survive inwarm moist conditions and will die rapidly in adry cold atmosphere. Survival of the organismon fomites would have been optimal at the startof the outbreak, rapidly decreasing as thetemperature dropped below 10°C. b) Thebreeding conditions, including humidity andtemperature, for the bushfly were ideal9 just afterthe rainfall in December and then deterioratedmarkedly in June. Bushfly pupae cannot surviveat all when the temperature fluctuates between6°C and 18°C. c) Small adult flies were present(indicating a reduced larval stage) during theoutbreak and there was extreme pressure foravailable protein necessary for the breedingcycle and moisture/food for survival. Flies weretheoretically attracted to moist, pussy eyes andbecame ‘sticky’ flies.

In addition to these factors there is a largereservoir of sexually transmitted N. gonorrhoeaein remote Aboriginal communities in CentralAustralia.7

Injectable penicillin or amoxycillin withprobenecid worked well during this outbreak toeradicate gonococcal conjuntivitis. The highestpenicillin MIC recorded against the isolates ofN. gonorrhoeae causing this outbreak was 0.5mg/L which lies in the less sensitive range.

Another possible site of N. gonorrhoeae, thoughnot necessarily involved in transmission to theeye, is oropharyngeal carriage of the organism.One investigator6 found three asymptomaticoropharyngeal carriers of N. gonorrhoeae in the1991 gonococcal conjuntivitis outbreak. Two ofthese carriers were children under ten years ofage. During the same outbreak three individualshad confirmed gonococcal conjunctivitis as wellas oropharyngeal carriage of N. gonorrhoeae . Itwas thought there was autoinoculation of theoropharynx via the nasolacrimal duct. In onereport gonococci were detected in the saliva ofpharyngeal carriers.10 Autoinoculation may alsooccur from pussy eye to hand to mouth andthroat. There may be conjunctivalautoinoculation to a child’s throat andtransmission via droplet to another child’s eye.The prevalence of pharyngeal carriage inoutbreaks of non-sexually transmittedgonococcal conjunctivitis in Central Australia isunknown.

Oropharyngeal carriage of N. gonorrhoeae ismore difficult to eradicate than uncomplicatedinfections at other mucosal sites.8 Single dosetreatment with less effective antibiotic regimenswill achieve an approximate 70% cure rate. Themost highly effective single dose treatments arelikely to cure at least 80% of pharyngealinfections, although the same treatments will cure> 95% of uncomplicated anogenital gonorrhoeainfections. The failure to eliminate anypharyngeal carriage which may be present hasthree consequences: a) the probability of acontinuing reservoir of infection to further infectthe community; b) the possibility of recurrentinfection in the individual; and c) a possiblesource of disseminated gonococcal infection(DGI) in an individual. DGI in a 3 year old boywas documented as a complication in the 1991epidemic.4 Two cases of DGI were diagnosed atthe ASH in May 1997. N. gonorrhoeae wasisolated from the joint fluid of a 14 year old boyand a 26 year old woman. The isolate from theboy was serovar IB3. Unfortunately the isolatefrom the woman was not kept for testing. Bothof these patients had no history of sexuallytransmitted N. gonorrhoeae at the time and bothlived in communities which were affected by theoutbreak.

There is a great deal of mobility of Aboriginalpeople between communities. This contributes tothe spread of disease. Examination of dates of


onset of disease figures and talking to staff atcommunity clinics has indicated that theoutbreak seemed to have started at the WA/NTborder and moved eastwards into the AliceSprings region as well as down into the top ofSA.

There is the possibility of mini-outbreaks indifferent communities. Auxotyping andserotyping of gonococcal isolates from the1986/87 and 1991 outbreaks identified fourdifferent strains of gonococci in one outbreakand four in the other. So far there has been onlyone strain identified from the Central Australianeye isolates obtained during this outbreak. Therewere no organisms for typing from theKimberley. Two eye background isolates (notcontributing to the outbreak) were tested andfound to be different strains. As has happened inprevious outbreaks there were numeroussexually transmitted N.gonorrhoeae backgroundstrains and eight different strains were detectedin the sample tested preceding and during thisoutbreak. It appears that different strains arepredominant during different times of the yearand any strain is capable of causing agonococcal outbreak.

Control measuresWe have enough information to help predictwhen an outbreak is likely to occur (see table 3)and communities should monitor theirpopulations in these circumstances to detectindex cases. Central Australian outbreaks havebeen occurring approximately every five yearssince 1981. If a case is detected the relevantPublic Health and Disease Control Centresshould be notified immediately. InterstateDisease Control Centres also need to be notifiedso all adjacent communities can be informed of apossible epidemic. Following the collection ofthe specimen, including a direct smear, treatmentshould be given to cases and their close contactsprior to laboratory confirmation as somespecimens, due to transportation availability, cantake up to one week to reach the laboratory.Direct smears are essential for a rapid diagnosis.PCR is more sensitive than either culture orsmear but culture is essential for antibioticsensitivity monitoring.

Once the disease is established contact tracingcan become extremely difficult due to limitedlocal resources. The disease is self limitingwhen it becomes colder and the majority of

clinical cases have been treated, but sporadiccases can still surface (note epidemic curve ofthe Kimberley outbreak) and if conditionsbecome favourable a further epidemic couldeventuate. Treatment failures must be detectedrapidly. Community members must be educatedon the transmission of the disease from eye toeye between children. Poor hygienic practiceshave been observed in previous outbreaks e.g.wiping an infected child’s eyes and then usingthe same material to wipe another child’s face.4

Flies may act as a mechanical vector to establishindex cases from reservoirs of N. gonorrhoeaeand then, along with person to persontransmission, contribute to the spread of thedisease. However, fly control is virtuallyimpossible during the start of the outbreakbecause of the extremely high population offlies.

Early recognition and treatment of index casesand identifying and treating contacts is currentlythe only way of preventing an epidemic.Strategies are in place to detect and treatsexually transmitted N. gonorrhoeae incommunities. Until this reservoir of disease iscontrolled gonococcal conjunctivitis is likely toappear again. The role of oropharyngeal carriageof N. gonorrhoeae has to be evaluated further.

Table 3 Factors which may predictoutbreaks of gonococcalconjunctivitis

1. Heavy above average summer rainfall.2. Mean daily elevated minimum temperature of

20°C following summer rain in earlyautumn.

3. Increase in Haemophilus sp. eye infections.4. Large fly populations.

AcknowledgmentsWe would like to thank Nganampa HealthCouncil, Ngaanyatjarra Health Service andcommunity clinic staff; Western DiagnosticPathology staff and microbiology staff -Pathology Dept, ASH; Virginia Sitzler - DiseaseControl Centre, Alice Springs and John Tapsall,Department of Microbiology, Prince of WalesHospital, Sydney.

References


1. Kirkland W. Endemic and epidemic diseases inthe NT. Report of the National Health andMedical Research Council Sixth Session,Adelaide SA, 24-25 May 1939. Adelaide:Government Printer 1939.

2. Matters R. Non-sexually transmitted gonococcalconjuntivitis in Central Australia. Comm DisIntell 1981; 13:3.

3. Brennan R, Patel M, Hope A. Gonococcalconjuntivitis in Central Australia. Med J Aust1989; 150:48-49.

4. Merianos A, Condon R, Tapsall J, Jayathissa S,Mulvey G, Lane J, Patel M, Rouse I. Epidemicgonococcal conjunctivitis in Central Australia.Med J Aust 1995; 162:178-181.

5. Monger K, Brennan R. Gonococcal conjunctivitisoutbreak in a Northern Territory Aboriginalcommunity. Comm Dis Intell 1992; 16(25):534

6. Condon R. Gonococcal conjuntivitis in theNgaanyatjarra homelands of Western Australia.April-June 1991. Health Department of WesternAustralia Occasional Paper 1991/44, Perth:Health Department of Western Australia, 1991.

7. Skov S, Miller P, Hateley W, Bastian I, Davis J,Tait P. Urinary diagnosis of gonorrhoeae andchlamydia in men in remote Aboriginalcommunities. Med J Aust 1997; 166:468-471.

8. Moran J. Treating uncomplicated Neisseriagonorrhoeae infections: is the anatomic site ofinfection important? Sex Transm Dis 1995;22(1):39-47.

9. Hughes R, Greenham P, Tyndale-Biscoe M, WalkerJ. A synopsis of observations on the biology of theAustralian bushfly (Musca vetustissima Walker). JAust Ent Soc 1972; 11:311-331.

10. Hutt D, Judson F. Epidemiology and treatmentof oropharyngeal gonorrhoeae. Ann Intern Med1986; 104:655-658.

Editorial

The above article is a welcome review ofa recent outbreak of gonococcalconjunctivitis and the discussion raises manypoints regarding the disease, its transmission andtreatment to consider. Most importantly,however, it highlights to health care providersthe fact that childhood conjunctivitis may becaused by Neisseria gonorrhoeae which ishighly contagious and requires systemicantibiotics. This is in contrast to the morecommon causes of conjunctivitis - allergic, viraland the non gonococcal bacterial, ieHaemophilus influenzae, Streptococcuspneumoniae, S. pyogenes and Staphylococcusspecies which are usually treated by topicalantiseptics or in more severe case, topicalcombination antibiotic drops or eye ointment1.So, N. gonorrhoeae does need to beconsidered in conjunctivitis especially inareas where there is endemic highprevalence of venereal gonorrhoeal diseaseand environmental factors which may promotespread to the eyes. Swabs and cultures must betaken to establish the diagnosis. The NT Centrefor Disease Control (CDC) endorsed protocolfor individual management and public healthresponse is provided below. It was beingprepared as the outbreak evolved and it wasformulated after consultation with variouscentres involved in past outbreaks (eg in WA,Alice Springs and Katherine) and after

examining a number of protocols. It generallystill reflects past informal NT CDCcontrol measures.

The paper supports that one notified case of non-sexually transmitted gonococcal conjunctivitisshould be treated as a potential outbreak andresponded to as per the protocol includingtreating household contacts or childcare orschool contacts. Emphasising thorough handand face washing and making sure that there areprovisions for this in affected households orschools is important. Knowing the penicillinMICs for the Central Australian isolates is veryreassuring. Procaine penicillin or amoxycillinwith probenecid are still very adequate to treatthe recurrent gonococcal conjunctivitis beingtransmitted. The knowledge that in generalpenicillinase producing N.gonorrhoeae has notemerged in Central Australia and the NT is alsoreassuring. The isolates fall within the fully orless sensitive range (see Table) and will respondto standard treatment.2 It is prudent, however,to culture and susceptibility test at leastsentinel samples during an outbreak tomonitor MICs. The question of what place,if any, pharyngeal carriage has in acting asa reservoir for transmission, does need to beconsidered but the ability to control outbreakswith penicillin or amoxycillin with probenecidrather than ceftriaxone would make this appearless important. A preparedness to investigate

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this in the event of another outbreak should beconsidered.


Table Penicillin MIC and response totreatment2

• Fully sensitive topenicillin, MIC ≤ 0.03mg/L

• Less sensitive to penicillin,MIC 0.06- 0.5 mg/L

Usually respondto standardtreatment

Usually respondto standardtreatment

• Relatively resistant topenicillin, MIC ≥ 1 mg/L

• Penicillinase producing

N. gonorrhoeae (PPNG)

Usually fail torespond topenicillin

Usually fail torespond topenicillin

References

1. Antibiotic Guidelines 1996-1997. VictorianMedical Postgraduate Foundation TherapeuticsCommittee; 9th edition.

2. Annual report of the Australian GonococcalSurveillance Programme 1996 CDI 1997;21:189-192.

Guidelines for the Control of Gonococcal Conjunctivitis

BackgroundGonococcal conjunctivitis is a highlycontagious eye infection caused by Neisseriagonorrhoeae. It is a notifiable disease. Casesare rarely seen in isolation in the NorthernTerritory (NT) and follow up and treatment ofcontacts is essential.

Case DefinitionClinical features

A clinical illness characterised by intenseinflammation of the conjunctivae, copiouspurulent discharge with or without periorbitaloedema.

Case definition

Neisseria gonorrhoeae detected on culture of aconjunctival specimen.

OR

Positive diagnosis using a molecular techniquesuch as PCR (or LCR).

OR

Clinically compatible illness and either

• gram negative intracellular diplococcivisible on microscopy of a conjunctivalspecimen

OR

• epidemiologically linked to a laboratoryconfirmed case. This includes any otherproven case in a remote Aboriginalcommunity.

Clinical PictureGonococcal conjunctivitis is usually a localisedinfection of the conjunctivae, however cornealulceration, perforation and blindness can occurif treatment is not given promptly. Moredisseminated infection including gonococcalarthritis has been reported in the NT.

Neonatal infection (ophthalmia neonatorum) isa potentially more serious clinical picture thangonococcal infection seen in older children andadults, and the mode of transmission isdifferent, which means that management isdifferent.

Mode of TransmissionIn children and adults transmission is eitherdirect from person to person fromcontaminated fingers, or indirect transmissionfrom contaminated fomites, or from flies.Heavy rains and an increase in fly numbersmay precipitate an outbreak.


Neonatal infection occurs during passagethrough the birth canal.

IncubationUsually 2 to 7 days, but sometimes can belonger.

Period of CommunicabilityMay extend for months in untreated people.Infectivity ceases within hours of appropriateantibiotic therapy. Patients should beisolated/excluded from school for 24 hoursafter treatment.

DiagnosisSwabs should be taken from all patients with adischarging eye for microscopy, culture andsensitivity.

• Wet the swab with sterile normal salineand swab the eye.

• Roll the swab on a slide and let the slideair dry.

• Place the swab in Stuart’s transportmedium.

• Do not refrigerate.

• If there is a delay in receiving thespecimen in the laboratory, culture mayfail to grow Neisseria gonorrhoeae,however gram negative intracellulardiplococci will be visible on microscopy,and is diagnostic.

Management of Cases• Collect a swab as above.

• Irrigate the eyes with saline solution toremove the discharge.

• If possible check visual acuity, andcheck cornea for ulceration. If abnormalrefer to local doctor for management.

• Treat with single dose antibiotics (seebelow).

• Encourage frequent washing of face andhands with warm water and soap.

• Warn families to represent if there ispersisting eye infection, fevers or othersymptoms such as arthritis.

• Exclude from school or child care for 24hours after treatment.

• Report to the Centre for Disease Control(CDC).

• Treat contacts (see below).

• If a neonatal infection, do a full STDscreen on the mother and then treat.

TreatmentStandard

Neonates: < 1 month (ophthalmia neonatorum)

⇒ Admit to hospital urgently for intra-venous antibiotics.

Children and adults:

⇒ Procaine penicillin intramuscularly (IM)as a single dose

50,000 units = 50 mg/kg (to a maximumof 1,500,000 units = 1.5g)

OR

⇒ Amoxycillin plus probenecid as a singledose

Weight Amoxycillin Probenecid

3kg to < 6kg 500 mg nil

6kg to < 10kg 1g nil

10kg to <15kg 1.5g 250mg

15kg to <20kg 2g 500mg

20kg or over 3g 1g

Alternative

For cases who are allergic to penicillin, orwhere the standard treatment has failed, or ifinfection is known to be due to penicillinaseproducing Neisseria gonorrhoeae (PPNG)alternative treatment should be used. Failedtreatment is defined as no substantial decreasein discharge, conjunctival injection or peri-orbital oedema within 24 hours of treatment.

Additionally, if pharyngeal swabs have beentaken and are positive, alternative treatmentshould be given. In an outbreak situation,


pharyngeal swabs are not routinely recommendedunless symptomatic.

The above cases should be treated withceftriaxone:

⇒ Weight ≤ 25 kg: 125 mg dissolved in1% lignocaine hydrochloride, as asingle intramuscular dose.

⇒ Weight > 25 kg: 250 mg dissolved in1% lignocaine hydrochloride, as asingle intramuscular dose.

Note: Infants below 6 weeks of age shouldnot be given ceftriaxone. Refer tohospital.

Management of Contacts

• Treat all household contacts of a casewith a single does of the standardtreatment of procaine penicillin oramoxycillin with probenecid (oralternative treatment as above, ifallergic to penicillin).

• For those with symptoms/signs followthe steps taken for management ofcases.

• If the case attends a child care or school,then those in the same classroom needtreatment.

• Encourage good personal hygiene andregular washing of face and hands withwater and soap.

Meningococcal disease - 2 NT cases in August 1997 - The view from CDCVicki Krause1, Kerry-Ann O’Grady1,2, Jan Bullen3,

1CDC, Darwin, 2NCEPH, MAE Program, ANU, Canberra, 3CDC, Katherine

Case 1On 1 August 1997, the Friday afternoon of thestart of a three day weekend (NT Picnic DayMonday 4 August) a case of suspectedmeningococcal disease was notified to CDCKatherine by an experienced, long serving,local GP.

The patientA 4 year old female vomited the previous dayonce at pre-school and was described by hermother as being “a bit flat”. The childcomplained of a sore elbow, shoulder and leftleg but no headache. She had a fever overnightand vomited 3-4 times. The morning ofadmission, 1 August, she complained of feeling“dizzy” and her head “hurting”. During thecourse of the morning she developed a purplerash on her legs and became comatose duringthe short drive to the hospital.. Over the next 3hours while being resuscitated by EmergencyDepartment staff the rash spread to cover hertrunk, arms and face but became more pink andless typically purpuric There was no neckstiffness and negative Kernig’s signs. Shereceived a stat dose of penicillin and IVceftriaxone She was admitted to hospital underher local GP and placed in respiratoryisolation. Her past history revealed that she

was fully immunised including Hib. Theclinical picture was very suggestive ofmeningococcal disease. One reortedlyinadequate blood culture was obtained prior toantibiotics. A skin lesion aspirate was culturedpost antibiotic. No lumbar puncture wasattempted as within hours the patients wasshowing signs of improvement. Blood and skinlesion cultures showed no growth and urineantigen tests were negative. Of interest, nonasopharyngeal swab was done. The patientmade a full recovery within a week. No serumwas available to send for furthermeningococcal serology investigation.

The public health responseThe NT CDC definition of a contact forinvasive meningococcal or Haemophilusinfluenzae disease is:

1. Any person who has spent 4 hours or morea day for 5 consecutive days or more than24 hours with the index case in the weekprior to the onset of illness.

2. Any person who has significant contactwith the nasopharyngeal secretions of theindex case during the previous week.


The current NH&MRC Guidelines casedefinition of meningococcal meningitisrequires laboratory confirmation. In a smalltown with a public health minded GP, the localDisease Control Unit was promptly notifiedeven before the possibility of laboratoryconfirmation. The case was convincing as ahighly probable meningococcal meningitis.The child had close contacts with children in apre-school setting, neighbourhood playmatesand a long weekend was approaching withchildren likely to disperse and a decision wasneeded. Initially a list of contacts was drawnup. At 24 hours with no growth from bloodcultures or skin and after consultation with theCDC Darwin and RDH Infectious DiseasesSpecialist it was decided to inform the contactsabout meningococcal disease, give out aninformation pamphlet and dispense rifampicinprophylaxis to 22 children and 7 adults andceftriaxone to a pregnant contact. Anewspaper article on meningococcal diseaseappeared in the local paper the following week.At six weeks post this probable meningococcalcase there have been no secondary cases.

Case 2On 12 August 1997 at 1 pm the CDC Darwinwas notified of a suspected case ofmeningococcal disease by the public healthconscious Emergency Department at RoyalDarwin Hospital.

The patientA 14 year old male boarder student at a localDarwin high school became unwell on theevening of 11 August with fever, vomiting,diarrhoea and a headache. He had firstcomplained of headache at 3 pm that afternoon.He was taken to a private hospital at 8 pm witha provisional diagnosis of viral illness anddehydration. IV fluids and paracetamol weregiven and he was sent home. He againpresented at 9 am the following morning, 12August, with persistent fever 38°C, vomiting,photophobia, drowsiness, headache,generalised aches and pains and diarrhoea. Awidespread purpuric rash had developed.There was no neck stiffness and a Kernig’ssign was negative. A provisional diagnosis ofmeningococcal meningitis was made and IMceftriaxone given. He was transferred to theRoyal Darwin Hospital, admitted and placed inrespiratory isolation and commenced on IV

ceftriaxone and penicillin. The patient had nosignificant medical history and no recentillnesses other than a “blocked nose”. He hadnot been out of Darwin since the schoolholidays 5 weeks previously and had only leftthe school on weekends to stay with a friend’sfamily. One member of that family had been illwith fever and mild abdominal cramping thepreceding week which was diagnosed as a viralillness by the family GP. Blood cultures and asmall amount of CSF were obtained afterantibiotic treatment and vesicular fluid from askin lesion associated with the rash wascultured. The patient did not have anasopharyngeal swab. CSF and blood cultureswere negative, however fluid from the skinlesion grew Neisseria meningitidis at 24 hours.The isolate was sent to the National NeisseriaNetwork and serogroup identification is stillpending. The isolate was fully sensitive topenicillin. The patient made a full recoverywithin a week.

The public health response

By 8 pm on the evening of 12 August beforethe isolation of N.meningitidis, 111 people hadbeen identified who had met the above NTCDC definition of a contact for prophylacticrifampicin. These included dormitory residents,house parents, a football team who had sharedwater bottles, the family the patient boardedwith on the weekend and his classmates.Additionally 4 people insisted they beconsidered as contacts despite minimal contactand assurance that their level of risk wasminimal. 20 contacts considered most at riskaccording to the degree of contact weremedicated on the evening of admission. Theseconsisted of the patient’s room mates, thefamily he stayed with on the weekend andhouseparents and others who had come incontact with vomitus etc on the evening of 11August. A decision was made to wait untillaboratory confirmation was obtained beforerifampicin was given to the remaining contacts.Confirmation was received at 10 am 13August. By 4 pm that day, all remainingcontacts had received the first dose ofrifampicin. A letter from CDC, an informationpamphlet on meningococcal disease andrifampicin were provided to all contacts andtheir families. There were numerous calls toCDC and the school nurse from concernedparents, friends and school staff. Information


sessions were held with staff and students atthe school. A notice was prepared for theschool’s newsletter at the principal’s requestand a press release prepared for the localmedia. Staff involved in the public healthresponse included the school nurse, 3pharmacists and 2 CDC staff. It had taken atleast 70 personnel hours in contact tracing,education and medication distribution. Thecost of rifampicin was approximately $3000.

DiscussionThese two cases have raised a few issues inregards to the NH&MRC October 1996endorsed Guildelines for the Control ofMeningococcal Disease in Australia1, whichare generally very thorough and useful. Theissues are also timely as the NT Guidelines forMeningococcal Meningitis/Septicaemia Prophylaxisare currently being revised.

The first issue is the definition of disease.Both the NH&MRC case definition and the NTCDC current definition of meningococcaldisease require laboratory confirmation, ieisolation of N.meningitidis from a normallysterile site or detection of meningococcalantigen in joints, blood or CSF or detection ofgram negative intracellular diplococci in bloodor CSF. There is no provision for probablecases. The USA CDC case classification2

allows for a probable case where there is apositive antigen test in CSF or clinical purpurafulminans in the absence of positive bloodcultures. The UK Meningococcal WorkingGroup3 define meningococcal disease asconfirmed, probable or possible. Confirmeddisease includes microbiological confirmationand probable cases include a clinical diagnosisof meningococcal meningitis/septicaemiawithout microbiological confirmation wherethe Disease Control or Public Health Specialistin consultation with the clinician managing thecase consider that meningococcal disease is thelikeliest diagnosis. Confirmed and probable casesrequire intervention. The first case presented meetsthese definitions of probable meningococcalmeningitis deserving intervention. The currentNH&MRC Guidelines do not address aprobable category and therefore no publichealth intervention is considered. As earlierand appropriate patient treatment occurslaboratory confirmation will be obtained lessfrequently.

When meningococcal infection issuspected, particularly where actual orinsipient shock is evident, immediateimperic therapy in the abscence offormal diagnosis is indicated.Treatment should commenceimmediately before transfer to hospitaland not be withheld untilN.meningitidis or another organism hasbeen identified. This is particularlyimportant with patients with ahaemorrhagic rash.1

There is a need to at least address what to dowhen there is no microbiologic confirmation.

The second issue follows from the first.Even when a probable case category existsemphasis should still be placed onobtaining laboratory evidence. A full rangeof specimens (beyond CSF) for testingshould be taken on every case suspected ofmeningococcal disease. The traditionallumbar puncture to obtain CSF is nowfrequently deferred until therapy andsupportive measures have been established andinvestigations such as a CT have ruled outincreased intracranial pressure. Alternativediagnostic specimens therefore are important.Collection of blood for culture should beattempted prior to antibiotics (but not delayantibiotics) and a throat/nasalpharyngealswab should always be obtainable.Unfortunately on page 1 of the NH&MRCGuidelines, the fifth point reads “There is noindication for use of throat/nasalpharyngealswab in routine management”. This actuallyshould go on to read “in routine contacts” andis misleading. On page 10, under “PatientManagement”, subsection, “DiagnosticStudies” the correct advice is given: “Allpatients with suspected meningococcalinfection should have blood and athroat/nasalpharyngeal swab collected as soonas possible for culture”. The public healthphysician’s role on notification of a case is torecommend to the managing clinician that athroat swab be taken if antibiotics were givento the patient before referral to hospital or ifthe organism has not been cultured from anormally sterile site. Additionally, a collectionof fluid from skin lesions for meningococcalculture or presence of gram positive diplococcishould be encouraged. Routine microbiologicalsurveillance for meningococcal infections


should include the serogroup and antibioticssensitivity of all isolates of N.meningitidis andisolates should be referred to the NationalNeisseria Network (NNN) to confirmidentification, antibiotic sensitivities andprovide further characterisation. As the publichealth response to an outbreak is alsoinfluenced by these findings some timeliness inreporting is expected. This becomes more of anissue when there is more than one case.Participation in projects to explore the utility ofother means of enhancing laboratory diagnosiseg newer or novel tests should be encouraged.

A third issue is the definition of a contact. TheNT definition has historically been the samefor meningococcal and Haemophilus influenzaedisease and differs somewhat from the 8 pointNH&MRC definition on page 33. Possiblythey complement each other.

A final issue which has come up in revising theNT Guidelines both for meningococcal and forgonococcal conjunctivitis contacts is the dosingfor ceftriaxone, should this alternative torifampicin be required. The dosage of 5 mg/kgas per the Antibiotic Guidelines4 is impracticalto measure in low doses and the NH&MRCGuidelines are somewhat confusing and basedon age rather than weight.

The simplest rational method would appear tobe to give 250 mg dissolved in 1% lignocainehydrochloride, as a single intramuscular (IM)dose for those over 25 kg and 125 mg dissolvedin 1% lignocaine hydrochloride, as a single IMdose in those 25 kg or under, recognising that itis not to be used in infants below 6 weeks ofage.

The revised NT Guidelines for MeningococcalMeningitis/Septicaemia Prophylaxis will bepublished in the next Bulletin.

References

1. National Health and Medical Research Council(NHMRC). Guidelines for the control ofmeningococcal disease in Australia. AGPS,1996.

2. Centre for Disease Control and Prevention(CDC). Case Definitions for InfectiousConditions Under Public Health Surveillance.MMWR 1997;Vol.46/No.RR-10.

3. Stuart JM, Monk PN, Lewis DA et al.Management of clusters of meningococcaldisease. Communicable Disease Report (CDR)1997;Vol 7 Review No 1:R3-5.

4. Antibiotic Guidelines 1996-1997. VictorianMedical Postgraduate Foundation TherapeuticsCommittee; 9th edition.

El Nino - ? drier wet season, but still expect melioidosisand other “tropical” infections

Bart Currie, Royal Darwin Hospital and Menzies School of Health Research

Melioidosis (disease from infection withBurkholderia pseudomallei) predominantlyoccurs during the wet season. However theamount of rainfall does not definitively predictthe number of melioidosis cases. With therecord wet in 1996/97, between November andApril, there were 24 Top End cases ofmelioidosis with 5 deaths plus an additionalcase of non fatal relapsed melioidosisassociated with non-adherence to eradicationtherapy. From May to August 1997 there havebeen 2 new cases and 2 relapsed cases, all nonfatal.

Over the last eight years the average number ofcases and deaths per year was 23 and 5, with181 cases and 40 deaths overall. Even with thepredicted drier wet season ahead, melioidosis islikely to still be the commonest cause of fatalcommunity-acquired septicaemic pneumonia atRoyal Darwin, Gove and Katherine Hospitals.

It will once again be important for staff new toour Top End hospitals and to urban and ruralhealth centres in the Top End to be made awareof melioidosis and other infectious diseasesuncommonly seen in southern Australia.


Other details on melioidosis1. Apart from pneumonia, other presentations

of melioidosis include skin abscesses orulcers, abscesses in internal organs such asprostate, spleen and liver, fulminantsepticaemia with multi-organ abscesses andunusual neurological illnesses (such asbrainstem encephalitis). Individuals withoutsymptoms or a known history of diseasehave also been found to be serologicallypositive.

2. While melioidosis can occur in children andhealthy adults, almost 40% of cases arediabetic and 40% are excessive alcoholconsumers. Excessive kava drinking alsoappears to be associated with melioidosis.

3. The likelihood of diagnosis is increased byusing selective culture media (modifiedAshdown’s broth), frequent sampling(sputum, throat, rectal and ulcer swabs) andcollection of blood cultures. Cliniciansshould liaise with laboratory staff to ensureselective media are available, including forremote communities.

4. Mortality is decreased by early diagnosisand appropriate antibiotic therapy.

5. Follow up of cases and adherence toeradication therapy (usually at least threemonths of antibiotics after discharge) iscritical to prevent relapse, which can befatal.

6. The Top End empirical treatment protocolfor adult community-acquired pneumonia isdevised to cover both melioidosis inpatients with risk factors, as well as otherimportant pathogens (Table over).

7. Once melioidosis is confirmed the treatmentrecommended is:

Initial INTENSIVE therapy for usually 14days or more of:

- intravenous high dose ceftazidimeplus either

- high dose cotrimoxazoleor

- high dose doxycycline.

This is followed by ERADICATIONtherapy for at least three months of:

- oral monotherapy with either high dosecotimoxazole or doxycycline.

Examples of other infections of particular localinterest include:

i. Scrub typhus from Litchfield Park - theonly known NT focus.

ii. Murray Valley Encephalitis - no casesince 1993, but a nasty disease withmortality over 25% in those withencephalitis - will periodically “break-out”of its endemic northern Western Australia- Top End NT mosquito-animal cycles tocause human cases sporadically or inclusters or a larger epidemic. Mostinfections are actually subclinical.

iii. Barmah Forest Virus - although increasingas a cause of fever, rash and polyarthritisin southern Australia, the first trueepidemic was described from Nhulunbuyin the 1991/92 monsoon.

iv. Cryptococcal meningitis - should beconsidered in anyone with persistentsevere headache, especially in remoteAboriginal communities. The “tropical”variant, Cryptococcus neoformans vargattii, occurs in overtly immunocompetentpeople and may also present as a lungmass(es) on CXR. The connection witheucalypts remains to be sorted out in theNT.

v. Crusted (Norwegian) scabies - often thesource of community or hospital outbreaksof scabies due to the thousands, evenmillions, of mites in the hyperkeratoticskin plaques. Requires intensive therapyand infection control measures.

vi. Community-acquired (“tropical”)Acinetobacter baumannii pneumonia -unusual (1-2 cases/year Top End), usually wetseason and fatal and almost always inalcoholics. Presents as fulminantlobar/total lung pneumonia.

Because of melioidosis and Acinetobacterpneumonia, while recognising thatStreptococcus pneumoniae is the commonestoverall cause of pneumonia (and second tomelioidosis as a documented cause of death inthe Top End), the following is the Top Endprotocol for initial therapy of adult community-acquired pneumonia. With the wet seasonapproaching please make new staff aware ofthis.


Table Initial therapy of adult community-acquired pneumonia in the Top End1

Mild pneumonia Moderate pneumonia Severe pneumonia

No risk factors2 present Penicillin Penicillin Ceftriaxone

Risk factors2 present Penicillin Ceftriaxone plusgentamicin

Ceftriaxone or ceftazidimeplus gentamicin

1. For ‘atypical pneumonia’ consider adding erythromycin.2. Risk factors include: alcohol, diabetes, chronic lung disease, chronic renal failure and steroid therapy.

Guidelines for Community Control of Scabies and Skin Sores

Background

Scabies and skin sores are one of thecommonest problems seen in health centres.

Scabies sores often become infected. Severescabies contributes to malnutrition in children,because their body needs extra energy to healthe skin sores.

The high rates of streptococcal skin sores causeAcute Post Streptococcal Glomerulonephritis(APSGN), which may be severe with swellingof the face, high blood pressure and dark(blood stained) urine. It can also be very mildwith haematuria (blood) found just on urinetest. Research in the Northern Territory (NT)suggests that frequent mild episodes of APSGNin children are contributing to high rates ofkidney disease in adults. High rates of skininfection allow the streptococcus to remaincirculating in communities, leading to theextremely high rates of rheumatic fever andrheumatic heart disease seen in the NT.

Treating individuals, or even whole familiesfor scabies will not be successful in reducingcommunity rates. Up to 50% of children areinfected in some communities and people getreinfected very quickly. This causes continualfrustration for community members and healthstaff.

Community Scabies ProgramA successful community program to controlscabies has occurred in one Top Endcommunity over the past two years.1 This wasbased on a successful program devised tocontrol scabies among Kuna Indians inPanama.2 A simple form of those programs

would help to reduce and control scabies inother communities.

There are three requirements:

1. Community support and education.

2. Single community scabies treatment ofall residents at the same time.

3. Maintenance program involving:

• simple screen of all children lessthan 15 years of age, three times peryear to check skin for scabies andskin sores

• ongoing community education andevaluation of the program

1. Community support and educationTreating all community members at the sametime regardless of whether an individual hasscabies is the only effective method tosignificantly reduce the high prevalence rate.Most communities will need extra staff toassist with community screening and treatment.Although this involves a large commitment oftime and effort by local health staff and thecommunity, it will show results within a shorttime and significantly reduce the clinic workfollowing the scabies program.

Health staff education

Health staff should arrange education sessionsfor themselves:

• to ensure everyone understands the issues

• to ensure staff are confident in diagnosingscabies


• to obtain appropriate educational materialsfor community education

• to organise the community screening andtreatment program

Community support

Discuss issues with key leaders and decisionmakers to enable them to recognise:

• the serious short and long term outcomesof continuing high rates of scabies

• the high rate of success with fullcommunity involvement

Ask council members, community elders,teachers, Health Boards, Arts Centres, CDEPworkers, Woman’s Centre members, outstationresource centres and other appropriate peopleto take the message to their families.

Community education

Education is essential to promote fullparticipation. AHW’s and other local trustedhealth staff are the best people to provide thiseducation. Arrange school and communityeducation sessions and include information onpersonal health practices, such as regular handand face washing, daily bathing, toothbrushingand washing of clothes and linen.

Resources

The issue of resources is currently beinglooked at by CDC, Rural Services, HealthPromotion and Environmental Health. Theplan is to develop educational materials such asposters, videos, booklets and pamphlets toassist community staff in providing thisprogram. Funding will also need to beestablished to cover costs such as the scabiestreatment, publicity materials and transport ofextra staff.

2. Initial screen and communitytreatment

Arrange community screening and treatment.The time taken will depend upon the size of thecommunity and number of outstations.Allocate at least one week.

There are two main reasons for screening:

1. To establish the baseline prevalence ratefor your community which provides acomparison at follow-up screening.

2. To determine which individuals haveinfected sores and need antibiotics.

Who to screen

• Children are the main group that must beseen, as they have the highest rates ofinfected scabies.

• It is desirable but not essential to screenadults, but if adults are not screened it isimportant to ensure that all adults as wellas children are treated.

How to screen

• Organise resources prior to screening (egstaff, scabicide).

• Organise all equipment prior to screeningday.

• Organise appropriate screening area (egschool, clinic, Woman’s Centre).

Screening

Scabies:

• Look for small papules and scratch marksaround web spaces between fingers andtoes and around wrists. Children oftenhave scabies papules on elbows, armpitsand trunk. Babies can have widespreadscabies including the head, and pustuleson their palms and feet. Adults mostlyhave lesions in web spaces. Scabies isalmost always itchy. Document if scabiespresent with a simple Yes/No and recordpresence of moderate to severe scabies, asthese people need repeat treatment.

Skin sores:

• Document presence of sores (Yes/No)only for infected sores. Do not includenon-infected cuts, scratches or insect bites.Sores will be moist or have pus, or have ayellow/brown crust. Treat all people withsores with a single intramuscular (IM)dose of benzathine penicillin (orerythromycin for 10 days if allergic topenicillin).

• Permethrin can be applied at the timeantibiotic treatment is given. There is noneed to wait for healing, as permethrin hasvery low skin irritation.


Age groups:

• Young children: check all of skin,including scalp.

• School children: check hands, arms, legs,feet and waist. Only check rest of skin ifscabies or sores noted, or if itching ispresent on other parts of the body.

• Adults: check hands, arms and feet, unlessscabies or sores found.

• Document and offer treatment for otherskin problems (eg ringworm).

Treatment

• Give out scabies treatment to the wholecommunity at the same time.

• Health staff should visit households todemonstrate the correct way to use thecream by treating some young children.

• Use 5% permethrin cream for everyoneolder than 2 months. Permethrin isrecommended because it is simple to useand has low rates of skin irritation. (Forbabies under 2 months, see below).Everyone should treat themselves late inthe afternoon or evening by applyingpermethrin cream from head to toe,ensuring the whole body is covered,avoiding eyes and mouth. Previously weonly treated young children head to toe,but in endemic areas many older childrenand adults have scabies on their head andneck. The cream should be left onovernight (8-12 hours) and washed off inthe morning.

• Repeat scabies treatment in two weeks forall people with moderate to severe scabies.This includes infants with pustules onhands and feet, and other people withmultiple scabies lesions.

• Babies younger than 2 months of age canbe treated with sulphur 5% cream daily for2 to 3 days or crotamiton 10% cream(Eurax) daily for 3 to 5 days, dependingon how quickly they respond. Wash offand reapply the cream once each day. Donot use permethrin as it may be absorbedand cause problems.

People with crusted scabies (Norwegianscabies) are very infectious as they have

thousands of scabies mites on their skin. Thesepeople usually need initial hospital treatmentand their houses need special cleaning (seeCrusted Scabies protocol).

Reducing the high rate of scabies depends upontreating all possible human hosts at the sametime. Cleaning of sheets, blankets and clothesand treatment of mangy dogs is not essentialfor success. However, community membersmay wish to encourage these activities as partof personal health practices and to improve doghealth.

3. Maintenance Program

It is important to continue screening children’sskin regularly over the long term, until endemicscabies has disappeared from Aboriginalcommunities. If health staff don’t continue fourmonthly skin checks, the prevalence of scabieswill slowly increase until it returns to pre-treatment levels.

Screening

• screen all children one month aftercommunity treatment

• then screen all children three times peryear (this can be combined with regularde-worming in the Top End)

• treat any skin sores with penicillin (orerythromycin if allergic) and

• treat any child with scabies AND allfamily members living with them

The clinic and school could decide on threescreening dates at the start of each school year.Ideally, this screening could be done on thesame three dates within a region eg 1st week inFebruary, June and October.

Individual clinics should decide how they willcombine maintenance skin checks with theschool screening program.

Community education

In order to maintain community interest:

• evaluate the success of your program andfeedback the information on a regularbasis to community decision makers suchas Councils, Woman’s Centres,community elders and teachers


• encourage community residents topresent early for treatment of scabies orskin infections

• encourage community residents to refervisitors to health centre for earlytreatment continue positive promotion ofthe benefits of personal health practices;and encourage community councils tolobby for improved “health hardware” ieappropriate housing, showers, toilets,washing machines

References

1. Carapetis JR, Connors C, Yarmirr D, Krause V,Currie BJ. Success of a scabies control programin an Australian Aboriginal community. PediatrInfect Dis J 1997;16:494-9.

2. Taplin D, Porcelain SL, Meinking TL, et al.Community control of scabies: A model basedon the use of permethrin cream. Lancet1991;337:1016-8.

*****************EditorialFollowing discussions at a recent MenziesSchool of Health Research streptococcalsymposium attended by international experts,the recommended treatment of scabies forindividuals has been changed. These newrecommendations will appear in the nextedition of the Antibiotic Guidelines, but allstaff should adopt these changes now. Thechanges are:1. Infected scabies: treat with permethrin and

antibiotics at the same time.Permethrin causes very little irritation onbroken skin, so the 2 day delay is notrequired.

2. Treat all adults and children with scabiesfrom head to toe.In tropical and endemic areas, scabieslesions are frequently found on the scalpand behind ears in adults as well as youngchildren.

3. Retreat people with moderate to severescabies in two weeks.Treating in one week is too early, as someeggs may not have hatched and will not bekilled by the permethrin.

Contact CDC, Darwin on 8922 8044 for a copy ofthe guidelines including Appendices 1-3.

Non-Communicable Diseases Update: No.3Message: Cholesterol reduction: base your primary prevention strategy on

overall cardiovascular risk, and emphasise non-drug options firstTarun Weeramanthri, Community Physician, CDC, Darwin

In the March edition of the CommunicableDiseases Bulletin, the importance of aggressivedrug treatment of hyperlipidaemia in thoseknown to have cardiovascular disease wasstressed. This article looks at the evidence formore aggressive primary prevention strategies(both drug and non-drug) in thoseasymptomatic individuals at risk of, butwithout currently diagnosed, cardiovasculardisease.

The WOSCOP StudyThe results from the West of ScotlandCoronary Prevention Study (WOSCOP) werereported in late 1995.1 The study was restricted

to middle aged men. 6595 men with no historyof myocardial infarction were randomlyassigned to pravastatin or placebo and followedup for an average of 4.9 years. There was anapproximate 30% reduction in definitecoronary events and death from coronary heartdisease in the pravastatin group. The reductionin coronary events was independent of baselinelevels of LDL cholesterol. Overall mortalitywas 22% lower in the pravastatin group, butthis was just short of statistical significance(p=0.051). Strangely, this was not a pureprimary prevention study, since men withangina (5% of the study population) were notexcluded. The results of this trial are


supportive of a more aggressive approach toprimary prevention, but it should beremembered that the study population had ahigh average baseline total cholesterol of 7.0mmol/L and LDL of 5.0 mmol/L. In addition,no women were included. So the study resultscannot be directly extrapolated to the wholepopulation.

A subsequent analysis of six trials of primaryprevention, including WOSCOP, has estimatedthat one would have to treat 53 patients withoutknown atherosclerosis with lipid-loweringdrugs for five years to prevent one additionalnon-fatal infarction or cardiac death, compared toonly 16 patients with known atherosclerosis.2

In the March edition of the Bulletin, it wasnoted that the cost effectiveness of giving lipid-lowering drugs to those with known coronarydisease had been estimated by theScandanavian Simvastatin Survival Studygroup to be $A 12,400 per year of life saved,comparable to bypass grafting for the usualindications. In those without coronary disease,the cost per year of life saved is estimated to beat least four times that amount.3

The Cholesterol Screening DebateThe WOSCOP results, however, have notsettled the issue of who should be screened forhigh cholesterol levels.4 For example in theUnited States, the American College ofPhysicians recommends only limited screening,primarily for middle-aged men, or those withtwo coronary risk factors, whereas the NationalCholesterol Education Program recommendsthat all adults over the age of 20 years knowtheir cholesterol level. The National HeartFoundation (NHF) of Australia has adopted asimilarly aggressive position.5

Proponents of limited screening point out thatclinical trials have not been done in youngadults and that the number of women includedin trials has been small. They are worried aboutthe costs of cholesterol-lowering medicationsand the possibility of over-prescription drivenby a rising consumer demand. For example, theNHF of Australia’s ‘Guide to Plasma Lipidsfor Doctors’ recommends that drug therapy beconsidered in asymptomatic people with a totalcholesterol over 6.5 mmol/L but only if theyhave other risk factors and dietary therapy hasnot worked after 6-8 weeks. How many peoplewould that apply to in Australia? Well, the

1989 NHF Risk Factor Prevalence Study foundthat, in adults aged 20-69 years, 16% of menand 14% of women had levels of 6.5 mmol/Lor more.6 Treating large numbers of peoplewith drugs would be expensive and theopportunity costs would be large. Any benefitsthat could theoretically accrue based on thetrial data would also be lessened in real life, ifthe high discontinuation rates (60% after 12months) seen in one Australian study were toprevail.7

Proponents of widespread screening point outthat knowledge of cholesterol levels does notautomatically lead to drug therapy and thatmeasuring one’s cholesterol may reinforcebehavioural change by focusing attention ondiet, smoking and other cardiac risk factors,although they concede that the magnitude ofany such changes are likely to be modest.8 Inany case, if drug treatment is needed, it canyield as much benefit as the treatment of mildand moderate hypertension, and the numbers inthe population needing treatment are similar tothose with hypertension.

Proponents of widespread screening also stressthat the distinction between primary andsecondary prevention is not especially relevantas those most likely to benefit from primaryprevention are most likely to have advancedbut asymptomatic atherosclerosis at the timetreatment is started. There is a risk in waitingfor symptoms to develop as in approximately25% of patients with atherosclerosis, suddendeath is the first manifestation.

Assessing overall cardiovascular riskAll in all, the approach to primary preventionof cardiovascular disease through lipid-lowering therapy in Australia is changing andbecoming more aggressive. As previouslymentioned, the recently updated NHFguidelines recommend that all adults,excluding pregnant females, should have theirtotal cholesterol, HDL cholesterol andtriglycerides measured, and proposes lowertreatment targets than the PBS guidelines.

The proposal for universal testing irrespectiveof predicted risk is contentious, but theprinciple of assessment of overall risk prior todrug prescription is now agreed upon and hasbeen incorporated into the PBS guidelines firstpublished in 1994. Paradoxically, in decidingwhether to treat elevated cholesterol levels in


the asymptomatic individual, the level ofcholesterol is not the only or even the mostimportant factor. Instead of treating the isolatedcholesterol level, one should base the decisionto treat on an assessment of the overallcardiovascular risk, taking into account age,gender, family history and other risk factorssuch as diabetes, hypertension and smoking.

There are an increasing number of risk chartsbeing produced to help practitioners calculatethe overall cardiovascular risk for anindividual. For example the Sheffield risk tableidentifies those with a risk of coronary deathover 1.5% per year based on age, gender,cholesterol concentration and the presence ofhypertension, smoking, diabetes and leftventricular hypertrophy on ECG.9 However,there is considerable uncertainty as to how tointegrate such risk tables into routine clinicalpractice and how to incorporate other relevantinformation such as client preferences, cost oftreatment, years of life gained, and probabilityof adverse events.10

In the future, more effective non-drug therapiesare needed that could be applied in populationinterventions to reduce hypercholesterolaemia.Effective population interventions to increaseexercise and activity levels, and to changenational dietary intakes of salt and saturatedfats must be developed. There are alsoemerging options such as using plant sterols,that are known to inhibit cholesterolabsorption, dissolved in margarine.11

We await further trials of primary preventionof coronary heart disease in groups other thanmiddle-aged men. Meanwhile there is a need tofocus on risk factor modification, anddevelopment of expertise in tailoring dietaryand activity advice to an individual’s personalcircumstances and in offering options such assmoking cessation. The preferences and valuesof the patient must be taken into accountwhenever lipid-lowering therapy is considered.Any decision to start and monitor a medication,that may need to be continued over a lifetime,needs to be made jointly.

References

1. Shepherd J, et al. Prevention of coronary heartdisease with pravastatin in men withhypercholesterolemia (WOSCOP). N Engl JMed 1995; 333: 1301-1307.

2. Rembold CM. Number-needed-to-treat-analysis ofthe prevention of myocardial infarction and deathby antidyslipidemic therapy. J Fam Pract 1996; 42:577-86 (abstracted in ACP Journal Club 1997;126: 4).

3. Pharoah PD, Hollingworth W. Cost effectiveness oflowering cholesterol concentration with statins inpatients with and without pre-existing coronaryheart disease: life table method applied to healthauthority population. BMJ 1996; 312: 1443-1448(abstracted in ACP Journal Club 1996; 125: 223).

4. LaRosa JC. Cholesterol Agonistics. Ann InternMed 1996; 124: 505-508.

5. National Heart Foundation. Guide to plasmalipids for doctors (fold-out leaflet). RevisedJanuary 1996.

6. Waters A-M, Bennett S. Risk factors forcardiovascular disease. Canberra: AGPS,1995: 16 (AIHW Cardiovascular DiseaseSeries no. 1).

7. Simons LA, Levis G, Simons J. Apparentdiscontinuation rates in patients prescribedlipid-lowering drugs. Med J Aust 1996; 164:208-211.

8. Hanlon P et al. Health checks and coronaryrisk: further evidence from a randomisedcontrolled trial. BMJ 1995; 311: 1609-1613.

9. Haq IU, Jackson PR, Yeo WW and RamsayLE. Sheffield risk and treatment table forcholesterol lowering for primary prevention ofcoronary heart disease. Lancet 1995; 346:1467-1471.

10. Robson J. Information needed to decide aboutcardiovascular treatment in primary care. BMJ1997; 314: 277-280.

11. Pedersen TR. Lowering cholesterol with drugsand diet. BMJ 1995; 333:1350-1351.


Acute respiratory illness in 2 Darwin schoolsKerry-Ann O’Grady1,2 and Fay Johnston1

1CDC, Darwin, 2NCEPH, MAE Program, ANU, Canberra

Towards the end of May 1997, Darwin Centrefor Disease Control (CDC) received reports ofan illness characterised by a sore throat, runnynose, fever, lethargy, cough and occasionallyvomiting and diarrhoea, affecting largenumbers of staff and students in Darwinschools. An investigation was undertaken ofstaff with the objectives of identifying theillness, establishing if it was an influenzaoutbreak, documenting the impact on the twoschools and determining whether any publichealth action could be taken.A case was defined as a member of staff who hadexperienced a sore throat plus 2 or more of thefollowing symptoms any time since 1 May 1997:fever, runny nose, cough, lethargy, generalisedaches and pains, vomiting, diarrhoea, nausea, chillsor rigors and weakness. People meeting the casedefinition had blood taken for influenza A and B,adenovirus, mycoplasma, respiratory syncytialvirus (RSV) and parainfluenza. If acutely unwell, athroat swab was also collected for influenzacultures.School A (n=26) had 84% and School B (n=47)had 91% of staff participate in the investigation.The remaining staff were on leave at the time.School A had 14 staff (63%) and School B had 26staff (60%) who met the case definition. In additionto the sore throat, a cough, runny nose andweakness were reported most frequently. Feverwas reported by 45% of all staff. The medianlength of illness was 3 days (range: 2-42 days).School A had 43% and School B had 50% ofstaff off work for a median of 2 days (range: 1-12 days). There was a total of 50 days of lostproductivity in staff alone. Student absenteeismin one school ranged from 15-75% throughoutMay. Fifty three percent of all staff had familymembers who had illnesses similar to their ownin the same time period.Blood was collected from 11 staff members inSchool A and 18 in School B. No throat swabswere obtained as no staff were acutely ill at thetime of the investigation. No staff had viraltitres considered diagnostic for acute infection,however levels suggestive of past or earlyinfection were found in 80% of ill staff, with

RSV and parainfluenza 3 being the mostcommon.Unfortunately a specific organism was notidentified, but we are reasonably certain this illnesswas not Influenza A or B. The impact on theschools, however, was significant. There had beenconsiderable disruption to school routine and classprogress. In addition, the attack rates in staff’sfamilies suggest the illness may have beenwidespread in the community.While results were inconclusive, benefits havearisen from this investigation. Firstly, it was anavenue for promoting CDC’s role in outbreakinvestigations, the potential public healthimportance of acute respiratory illness (ARI)outbreaks and the reasons for early notification.School staff are in a position to alert public healthauthorities if an unusual health event occurs so that,when appropriate, immunisations andenvironmental investigations can be implementedand, where possible, the public can be informedand reassured.Secondly, public education regarding theprevention and control of communicable diseaseswas delivered. Inservices were given to providefeedback and answer questions. There was aparticular interest in the modes of transmission ofviral illnesses and in how they could be controlledin the school setting. The sessions provided aforum for discussing the transmission of acuterespiratory illness (ARI), pushing the generalimmunisation message, emphasising the benefits ofhealthy diets, exercise, not smoking, handwashing,covering one’s mouth when coughing or sneezing,staying home when unwell, and for encouragingstaff to alert CDC early whenever they areconcerned about illness in their environment.Active campaigns would be beneficial in theseenvironments at the start of each year. While ARIswill not be eradicated, raising awareness of thepublic health implications of disease may facilitateearly public health initiatives (eg immunisationcampaigns) and encourage institutions to considerstrategies for reducing the impact of these diseasesin their environments. These strategies couldinclude the promotion of handwashing andencouraging staff to stay at home when ill.


Hepatitis C Community Awareness CampaignNaomi Oliver, AIDS/STD Unit, CDC, Darwin

It is thought that hepatitis C is greatlyunderdiagnosed and that the current hepatitis Cnotifications are only the tip of the iceberg. Dr.Alex Wodak (Director, Alcohol and DrugServices, St. Vincent’s Hospital, Sydney)estimates that between 50,000 to 200,000people Australia wide are infected with thevirus. Unlike hepatitis B, only 20% of people,once infected, will eliminate this virus fromtheir body. Currently there is no vaccine orcure and treatment is only effective andavailable for a small percentage of people.Since testing began in 1990 to 26 August 1997,there have been 1,352 notification in the NT -56 in the last two months.

The Hepatitis C Network NT report that manypeople who are hepatitis C positive do feelunsupported by the community and medicalorganisations. Fear of discrimination byemployers, insurance companies and otherswho are ignorant of the facts, is often acomplaint. There are still a lot of unansweredquestions. The results of a small survey showthat whilst most people have heard abouthepatitis C, there is little understanding withinthe community of the virus, its transmissionmodes and its consequences.

In January of this year staff of the AIDS/STDUnit, Alcohol and Other Drugs and other keyorganisations decided to conduct a communityawareness campaign for the purposes ofincreasing knowledge of hepatitis C andproviding the community with an avenuethrough which they could access furtherinformation. Staff working on this project weremindful of the possible stigma which can beassociated with hepatitis C and carefullyplanned materials and media information.

The focus of the campaign was theimplementation of a hepatitis help line using a1 800 number that is available Territory wide.During the first month, when the majority ofthe advertising occurred, the line was staffedfrom 9am - 5.30pm. Calls were monitored andapproximately 50 calls came in within the first

9 days. As was expected, calls have tailed off,and the line is now staffed for two hours perday on an ongoing basis. Members of thepublic can ring between 9am - 11am oralternatively leave a message for their call to bereturned.

Levels of transmission are the highest amongstpeople who have injected drugs. Accuratefigures are difficult to ascertain, but it isestimated that after two years of injectingdrugs, approximately 66% of people will beHepatitis C positive, and 100% after 8 years ofinjecting drugs. Dr. Wodak estimates thatthere is one new hepatitis C infection per hourin Australia amongst people who inject drugs(8,000-10,000 estimated new infections peryear in injecting drug users).

Other high risk groups include young people ingeneral, and prisoners, both possibly reflectinguse and experimentation with injecting drugs.In the southern states a high proportion ofprisoners are convicted for drug related crimes.The percentage in the NT is smaller, but theoverall rate of hepatitis C in NT prisons is stillabout 9 times higher than in the generalcommunity. For these reasons part of thecampaign focuses on the three identifiedgroups. Specifically targeted messages havebeen placed in venues which these risk groupsare likely to frequent, and face to faceeducation is occurring via different agenciesand Territory Health Services (THS).

The campaign was launched on Wednesday 6August by The Minister for Health, Family andChildren’s Services, The Hon Denis Burke.The event attracted considerable interest fromthe media and was attended by approximately40 people from a number of non governmentorganisations as well as THS personnel.

Future work will focus on education andprevention amongst the target groups specifiedabove.

The help line number is 1 800 353 755

Immunise Australia


Chris Nagy, CDC, Darwin

The Federal Government’s Immunise Australiacampaign was launched on 28 July 1997. Thecampaign aim is to increase the level of ageappropriate immunisation within thecommunity by raising awareness to the benefitsof immunisation and to provide Australianswith the information they need to makeinformed immunisation decisions. In addition,three National Immunisation Days have beendesignated to offer the public immunisation atlocations and times which may be moreaccessible. These dates are three Saturdays, 2August, 4 October and 6 December 1997.

Territory Health Services has participated sofar in the campaign by holding immunisationclinics at Casuarina Community Care Centre,Katherine Health Centre and the PalmerstonShopping Centre on the 2 August. The clinicswere supported by national and localadvertising and shopping centre displays in theweek leading up to the immunisation day.

Attendance and public response to the clinicswas pleasing, with 60 adults and children beingimmunised and many more requestinginformation. Immunisation rates in theNorthern Territory are lowest in the urban andurban satellite areas, hence this is where thecampaign is being focussed. Providing

accessible Saturday clinics should work toimprove coverage in the target groups e.g. thechildren of working parents or parents withtransport difficulties and for adults. Regularweekday baby clinics are provided at theCasuarina Community Care Centre in thenorthern suburbs, however, Saturday clinics arenot usually available. Provision of a Saturdayimmunisation clinic at Katherine Health Centrewas very successful and well attended. AtPalmerston, a vacant shop within the shoppingcentre was transformed into a clinic and it wasby far the busiest clinic on the day. Usersdescribed its convenient location as its mainadvantage. A full report is available from CDCon 8922 8487.

Increasing public awareness to immunisationthrough advertising and taking immunisation tothe public in their preferred locations and timeshould ultimately fulfil the goals of thiscampaign. A full evaluation of the Program isbeing undertaken by the Commonwealth.

Immunisation clinics are planned for 4 Octoberat Gove Infant and Maternal Health Centre,Palmerston Shopping Centre, Tennant Creekand Alice Springs shopping areas. The finalNational Immunisation Day locations are yet tobe finalised.


NT NOTIFICATIONS OF DISEASES BY DISTRICTS1 APRIL TO 30 JUNE 1997 AND 1996

DISEASES ALICESPRINGS

BARKLY DARWIN EASTARNHEM

KATHERINE TOTAL

'97 '96 '97 '96 '97 '96 '97 '96 '97 '96 '97 '96Acute Rheumatic Fever 2 1 0 0 1 8 0 1 0 2 3 12Adverse Vaccine React. 1 2 0 0 2 3 1 1 2 0 6 5Arbovirus infections Barmah Forest Virus 4 1 5 0 7 4 0 2 4 0 20 7 Kunjin Virus 0 0 1 0 0 0 0 0 0 0 1 0 Dengue 0 0 0 0 0 1 0 0 0 0 0 1 Ross River Virus 35 0 10 4 40 17 1 1 6 2 92 24Campylobacter 40 3 1 2 15 51 2 0 4 9 62 65Chlamydia 62 48 11 5 67 53 21 22 8 35 169 163Cong.Syphilis 0 0 0 0 0 0 0 0 0 1 0 1Donovanosis 2 3 0 1 0 0 0 1 0 0 2 5Glomerulonephritis 0 0 0 0 2 0 0 0 0 0 2 0Gonococcal Disease 125 72 13 7 141 29 27 23 34 40 340 171Gonococcal Conjunct. 93 0 2 0 0 0 0 1 0 0 95 1Haemophilus Inf type b 1 0 0 0 0 0 0 0 0 0 1 0Hepatitis A 17 3 3 1 8 10 0 2 13 6 41 22Hepatitis B 1 2 4 0 2 0 0 0 4 1 11 3Hepatitis C (prevalence) 8 9 0 1 65 62 0 0 2 2 75 74Hepatitis D 1 0 0 0 0 0 0 0 0 0 1 0HIV infections 0 0 0 0 2 2 0 0 0 0 2 2HTLV-1 6 9 0 1 0 0 0 0 0 1 6 11Leprosy 0 0 0 0 0 2 0 2 0 0 0 4Malaria 1 1 0 0 11 4 2 0 2 0 7 5Measles 0 0 0 0 0 0 1 0 0 0 1 0Meningococcal Infect. 1 0 0 0 2 1 2 1 0 0 5 2Mumps 0 0 0 0 1 1 0 0 1 0 2 1Pertussis 0 2 0 9 3 0 0 0 0 0 3 11Pneumococcal Disease 9 3 0 2 9 5 1 0 0 2 19 12Rotavirus 3 14 0 5 0 12 0 0 3 6 6 37Rubella 1 0 0 0 1 1 0 0 0 0 2 1Salmonella 22 20 6 11 39 50 3 8 17 18 87 107Shigella 22 9 6 2 3 7 0 4 3 5 34 27Syphilis 32 17 2 0 8 10 7 11 15 11 64 49Tuberculosis 1 2 0 0 10 4 0 0 2 2 13 8Typhoid 1 0 0 0 0 0 0 0 0 0 1 0Yersiniosis 0 0 0 0 1 0 0 0 0 0 1 0Total 491 221 64 51 440 337 68 79 120 143 1183 831

Points to note regarding notifications:

• Australian Encephalitis (MVE,) Amoebiasis, Botulism, Brucellosis, Chancroid, Cholera, Congenital Rubella Syndrome,Diphtheria, Hepatitis C (incidence), Hepatitis E, Hydatid Disease, Legionnaires Disease, Leptospirosis, Listeriosis,Lymphogranuloma venereum, Poliomyelitis, Typhus and Viral Haemorrhagic Fever are all notifiable but had "0"notifications in this period.

• Rotavirus increased in early July 1997 and therefore is not reflected in this quarter.• Arboviruses - The unusual amount and late rain in the Alice Springs and Barkly areas contributed to the highest RRV and

Barmah Forest notifications recorded since 1991. Though not reflected in our notifications due to travel - 1 case of MVEand 3 cases of Kunjin were acquired in these areas during this period. Late rains in the Top End also showed highernumbers in April to June than in previous years.

• Gonococcal disease in Darwin increased due to inclusion of positive results of tampon testing after 1/7/96 and possiblywider PCR screening. For Alice Spriings the increase is due to more screening including improved techniques for antenatalspecimen collection, and opportunistic STD testing.

• Gonococcal conjunctivitis increase shows the outbreak as reported in the first article.• Hepatitis A - A major outbreak in a child care centre in Alice Springs (12 cases) accounts for the increase in notified cases

for this quarter. The increase in Katherine is less clear as all were sporadic unrelated cases except for one family whichresulted in 4 cases.


Notified cases of Vaccine Preventable Diseases in NTby Report Date 1 April to 30 June 1997 and 1996

DISEASES TOTAL No. cases amongchildren aged 0-5years

'97 '96 '97 '96

Congenital rubella syndrome 0 0 0 0

Diphtheria 0 0 0 0

Haemophilus influenzae type b 1 0 1 0

Hepatitis B 11 3 0 0

Measles 1 0 1 0

Mumps 2 1 0 0

Pertussis 3 11 1 2

Poliomyelitis, paralytic 0 0 0 0

Rubella 2 1 1 0

Tetanus 0 0 0 0

• Mumps is largely under-reported.• Hepatitis B increase was across all regions


MALARIA NOTIFICATIONS, NORTHERN TERRITORYApril to June 1997

Compiled by Peter Knibbs and Mervyn Fairley, CDC, Darwin

Seven notifications of malaria were received for the second quarter of 1997. The following tableprovides details about where the infection was thought to be acquired, the infecting agent and whetherchemoprophylaxis was used.

ORIGIN OFINFECTION

REASONEXPOSED

AGENT CHEMO-PROPHY-LAXIS

COMMENTS

PACIFIC

PNG Business visit P.vivax No Travels regularly between NT and PNG

PNG Holiday P.vivax Yes

PNG PNG resident P.falciparum Yes Vague history of chemoprophylaxis. InDarwin for Arafura Games.

ASIA/SE ASIA

Indonesia Illegal immigrant P.falciparum No Travelled by boat from Malaysia toKupang.

Indonesia Indonesian resident P.vivax No Indonesian fisherman detained inAustralian waters.

Indonesia Holiday P.vivax No On Roti for four days. Son diagnosedwith malaria in Adelaide.

Indonesia Diving holiday P.falciparum Yes Symptoms developed 5 weeks afterreturn.

STAFF UPDATES

Sandy Thompson is the new medical officerin the Population Health Unit in Alice Springs,having most recently been working atMacfarlane Burnet Centre for Medical researchin their Epidemiology and Social ResearchUnit. She has a wide range of interests inpublic health, particularly in immunisation andinfectious diseases epidemiology.

Michael Howard recently joined the SexualHealth Unit in Alice springs as theDonovanosis Project Officer. The project aimsto establish a donovanosis register, increasenotification rates and ensure individualsreceive effective treatment and follow-up. Hehas previously worked in Katherine and Utopiaas a Remote Area Nurse.

Angela Merianos has returned to her positionas head of Immunisation and Surveillance,CDC Darwin, after spending 6 months workingon a hepatitis E project in Nepal.

Fay Johnston, who was acting in Angela’sposition has gone on 2 months leave and TaniaWallace, TB/leprosy medical officer, CDC,Darwin has recently commenced 3 monthsmaternity leave. Sarah Huffam (formerly theinfectious diseases and microbiology registrar,RDH) is filling in for Tania for the threemonths.

communicable diseases bulletin - quteprints.qut.edu.au/64729/1/64729.pdfkimberley region received...

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