A prolonged outbreak of tuberculosis in the North Island

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1 ISSN Volume 8 Number 1 January 2001 A prolonged outbreak of tuberculosis in the North Island Rupthi De Zoysa, Public Health Medicine Registrar, and Phil Shoemack,* Medical Officer of Health, Pacific Health; Ross Vaughan, Medical Laboratory Technologist, and Anne Vaughan, Medical Laboratory Technologist, Tuberculosis Reference Laboratory, Auckland Healthcare This paper reports a prolonged and dispersed outbreak of tuberculosis (TB) in the North Island of New Zealand. The investigation of the outbreak used standard TB case-based follow-up and DNA typing of Mycobacterium tuberculosis isolates when available. The index case was notified in November 1996, and was a sputum-positive case of pulmonary TB diagnosed in a young woman shortly after giving birth. This case was followed by a cluster of four cases in close associates of the index case in the Kawerau District, and a second cluster of cases in the Taupo District. Further cases were notified in another six North Island health districts over a three and a half year period. The outbreak included at least 61 cases, 43 of which were identified as being part of the outbreak by DNA typing of an isolate and 18 by contact history alone. The most recent case was notified in May The majority of the cases were Maori (86.9%) and under 30 years of age (80.3%). Prison incarceration was a common factor linking several of the cases. Control of TB relies on prompt diagnosis and treatment of cases, and swift notification of cases to ensure the identification and follow-up of infected contacts. These measures need to be supported by public health control programmes in prisons and the community to address conditions which foster the transmission of TB. The incidence of tuberculosis (TB) in 1999 (12.6 cases per ) was the highest recorded in New Zealand for 20 years (see Surveillance and control notes section of this issue). This high incidence was due, in part, to two large outbreaks of TB. One of these outbreaks involved an Auckland church group. 1 This article describes the second outbreak, which was initially identified in the Eastern Bay of Plenty and involved predominantly young Maori. Methods Cases of TB disease (TBD) and TB infection (TBI) were defined as described in the Guidelines for tuberculosis control in New Zealand A case was considered part of the outbreak if the case had a history of close contact with *Correspondence: Dr Phil Shoemack, Medical Officer of Health, Pacific Health, Box 2121, Tauranga. philshoe@pacifichealth.co.nz another case linked to the outbreak and/or DNA typing demonstrated an isolate from the case was indistinguishable from the outbreak strain. Cases were described as prison-associated if they were diagnosed while in prison or soon after release, on the assumption Contents A prolonged outbreak of tuberculosis in the North Island 1 Surveillance and control notes 4 Surveillance data 6 Public health abstracts 8 Travel health 8 Page 1 New Zealand Public Health Report Vol. 8 No. 1 January 2001

2 that disease was present during detention. Cases notified subsequent to the index case in November 1996 until June 2000 have been included in this report. DNA typing of Mycobacterium tuberculosis isolates was performed according to an internationally accepted standard method. 3 Isolates from all culture-positive cases were typed. Public health follow-up of each notified TB case was conducted according to the Guidelines for tuberculosis control in New Zealand Follow-up of contacts in the prison setting included all staff and inmates who were in the same unit of the prison at the same time as a case. Inmates on parole were followed up by public health nurses in the relevant health district. Data on each case was extracted from health districts Episurv notifiable disease databases and combined for analysis. Results Outbreak description: Over a three and a half year period (November 1996 to May 2000), 61 cases of TBD were linked to the outbreak (Figure 1). Forty-three of the cases were identified as being part of the outbreak by DNA typing, and the other 18 cases were linked to the outbreak solely by a history of close contact with other outbreak cases. Note: 1 Only 60 of the 61 cases included, as the notification date not known for one case. The index case was a 19 year old woman who presented in November 1996 to Whakatane Hospital with a pleural effusion a few days after giving birth to a healthy infant. Initial contact tracing identified one Mantoux-positive contact, but this person could not be re-contacted for further follow-up. Over the following 12 months, four of the woman s close family and social contacts in the Kawerau District, including the person who was Mantoux positive on initial contact tracing, presented with respiratory symptoms of TB. Some cases within this cluster in Kawerau had gang associations. One of the cases served a prison sentence during the months following the presentation of the index case. About a year and a half after the diagnosis of the index case, further cases began appearing among an extended family in the Taupo District. These cases are illustrated in Figure 1 by the appearance of sporadic cases in The only documented common exposure among these cases was a tangi at the beginning of DNA typing of M tuberculosis isolates linked this cluster of disease with the Kawerau cluster and with cases subsequently notified in Northland, Auckland, Rotorua, Waikato, Hawkes Bay and Wellington Health Districts. One of the cases in the Taupo cluster served a prison sentence within one month of the tangi and is thought to have been incubating disease at the time of detention. Advanced pulmonary disease was manifest in this case within months of his release. Soon after this, a close prison associate was admitted to Wellington Hospital with TB. These two cases are the prison-associated cases in September and October 1998 in Figure 1. They were in the same central North Island prison as the prisonassociated case in the Kawerau cluster. The prisonassociated case from the Kawerau cluster presented to prison medical staff with a self-diagnosis of TB. Direct cross-infection between the prison-associated case from the Kawerau cluster and the two from the Taupo cluster was unlikely, as their prison terms did not overlap. The appearance of new cases of TB in other parts of the North Island during 1999 coincided with the repatriation of ex-inmates and the known movements of a Whangarei-based ex-inmate from the Taupo cluster of disease. The increase in cases linked to this outbreak during 1999 and 2000 was largely due to 21 Auckland cases who had extensive gang connections. Many of these Auckland cases had a history of recent incarceration in the central North Island prison. The 61 cases were distributed over eight health districts: Northland (9 cases), Auckland (21), Waikato (3), Rotorua (3), Eastern Bay of Plenty (9), Taupo (5), Hawkes Bay (9), and Wellington (2). The annual incidence of sputum smear-positive TB in the Kawerau District averaged 17.0 per during the three years The majority (80.3%) of cases were under 30 years of age. The age range of cases was 1-50 years, and the mean and median age was 20 years. Fifty-three (86.9%) cases were Maori, six (9.8%) were Pacific Islands people, and one was European. The ethnicity of one case was not recorded. Two-thirds (67.2%) of the cases were male. Pulmonary TB was the predominant presentation (86.9%). There were two cases of TB meningitis, two cases of pleural effusions in the absence of intrapulmonary pathology, two cases where pleural and gastric aspirates were diagnostic for disease in the absence of intrapulmonary pathology, one case of peritoneal disease, and one lymph node infection. Fortythree (70.5%) cases were culture positive. In a further Table 1: Cases and contact tracing results in the prison and community setting Notes: Type Total number of contacts Outcome of contact tracing Untraced contacts (%) TBD cases 1 (%) TBI cases 2 (%) Neither TBD or TBI 3 (%) Other cases of TBD 4 Community (0.7) 33 (5.9) 94 (16.9) 425 (76.4) 21 Prison (12.1) 2 (1.0) 25 (12.1) 154 (74.7) 5 Total (3.8) 35 (4.6) 119 (15.6) 579 (76.0) 26 1 TBD, tuberculosis disease 2 TBI, tuberculosis infection only but no disease 3 Among traced contacts only 4 Other cases linked with the outbreak, but not identified through contact tracing 5 Many cases and contacts with a history of imprisonment were not identified as part of the contact tracing that occurred to locate ex-inmates. These cases were identified incidentally as part of community contact tracing or presented in the community with disease and are listed as community cases. New Zealand Public Health Report Vol. 8 No. 1 January 2001 Page 2

3 two cases, the organism was identified from a sputum smear. All isolates were sensitive to the full range of anti-tuberculosis drugs. Contact tracing: The results of contact tracing are summarised in Table 1. A total of 762 contacts were traced and accepted Mantoux testing. Thirty-five cases of TBD and 119 people with TBI were identified through this contact tracing. The other 26 of the total 61 cases of TBD were notified to public health services, rather than identified through contact tracing. Twenty-nine contacts could not be traced. Thirty-six infected contacts were placed on isoniazid chemoprophylaxis. Discussion Unlike most infectious diseases, outbreaks of TB are not immediately evident. The clinical illness itself is often insidious in onset and cases may only notice symptoms once disease is well established. Transmission to others may occur well before a case presents with symptoms. The index case in this outbreak occurred in November 1996, and was followed by related sporadic cases in However, the majority of the outbreak cases were diagnosed in 1999 with a gradual decline in new cases during The features of this outbreak include disease which manifested mainly at pulmonary sites and which was culture positive in over 70% of cases. The cases were predominantly young, male and Maori. The exact role of prison in the transmission of disease has been difficult to elucidate, due to poor information regarding the onset of disease and the unavailability of information on prison detention periods. Infection in inmates may represent a background infection rate in the prison population or prison-acquired infection. During the period of this outbreak, the prison was often functioning at maximum intake capacity. The prison is a low-security facility allowing frequent and prolonged contact between prisoners. The full extent of the outbreak has also been difficult to determine, partly because of the mobile lifestyle of many cases and contacts, and also because of the limited availability of information. It is possible that there were outbreak cases that were not recognised as part of the outbreak. Less than a fifth of all TB isolates cultured over the period were DNA typed. If typing had been more widely used, further cases with the outbreak strain may have been identified. While most TB transmission occurs in the context of sustained contact and crowding, 4 transmission after relatively brief, casual contact has been documented to have occurred on several occasions. 5-8 This underlines the need for early recognition and treatment of infectious cases, as cases pose a risk not only to immediate family and social contacts, but also to others, particularly in confined settings such as prisons which are recognised as potential reservoirs of TB infection The authors recommend that, to improve the detection of serious illnesses such as TB in prisons, the Department of Corrections review the effectiveness of the current protocols for inmate health checks at the time of prison reception and transfer. It is also important to consider the risks posed to the whole community, including inmates, prison staff, visitors and the wider community, by overcrowded or unsuitably designed prison environments. Attention to policies or programmes aimed at improving the health status of people within the prison system is difficult in the absence of better disease characterisation in this population. Development of this capacity requires urgent action, as recently advocated by the World Medical Association. 12 Control of such outbreaks also depends on early identification and treatment of infectious cases in the community. 1,2 Such treatment relies on accessible and acceptable primary healthcare, with ready access to specialist support. Timely and effective contact tracing requires a well resourced public health infrastructure with good community networks. DNA typing has been pivotal in identifying associations among geographically distinct cases in this outbreak and could be usefully applied to all TB isolates obtained in New Zealand. The method is highly discriminatory, with 97 profiles or strains having been identified among M tuberculosis isolates typed to date by the Auckland Healthcare Tuberculosis Reference Laboratory. The profile of the strain involved in this outbreak is unique to cases involved in the outbreak. Outbreaks of this scale should provide an impetus to improve TB prevention programmes. The Guidelines for tuberculosis control in New Zealand 1996 recommend neonatal BCG vaccination be offered in districts where the annual incidence of sputum smear-positive cases has averaged >5 per during the previous three years. 2 In accordance with this recommendation, neonatal BCG vaccination is now offered to all babies born in the Kawerau District, where the annual incidence of smear-positive cases averaged 17.0 per during a three year period. Acknowledgements: Julia Carr for assistance with an earlier draft of this paper. References 1 Hill P, Calder L. An outbreak of tuberculosis in an Auckland church group. NZ Public Health Rep 2000; 7: Guidelines for tuberculosis control in New Zealand. Wellington: Ministry of Health; Van Embden J, Cave M, Crawford J, et al. Strain identification of M. tuberculosis by DNA fingerprinting. J Clin Microbiol 1993; 31: Raffali J, Septowitz K, Armstrong D. Community-based outbreaks of tuberculosis. Arch Int Med 1996; 156: Ridzon R, Kent J, Valway S, et al. Outbreak of drug resistant tuberculosis with second generation transmission in a high school in California. J Pediatr 1997; 131: Rao V, Joanes R, Kilbane P, et al. Outbreak of tuberculosis after minimal exposure to infection. BMJ 1980; 281: Mangura B, Napolitano E, Passannante M, et al. Mycobacterium tuberculosis miniepidemic in a church gospel choir. Chest 1998; 113: Cook S, Blair I, Tyers M. Outbreak of tuberculosis associated with a church. Commun Dis Public Health 2000; 3: Stead W. Undetected tuberculosis in prison. Source of infection for community at large. JAMA 1978; 240: Abeles H, Feibes H, Mandel E, et al. The large city prison - a reservoir of tuberculosis. Tuberculosis control among sentenced male prisoners in New York City. Am Rev Respir Dis 1970; 101: Snider D, Hutton M. Tuberculosis in correctional institutions. JAMA 1989; 261: Declaration of Edinburgh on prison conditions and the spread of tuberculosis and other communicable diseases. Ferney- Voltaire, France: World Medical Association; Page 3 New Zealand Public Health Report Vol. 8 No. 1 January 2001

4 Surveillance and control notes Pertussis epidemic update During November 2000, 592 cases of pertussis were notified, the highest monthly total recorded so far during the epidemic (Figure 1). By the end of November, a total of 4768 cases had been notified since the start of the epidemic in June Of these cases, 2149 (45.1%) were laboratory confirmed. There have been 351 hospitalisations (8.2% of cases for whom this information was recorded) and one death reported. Figure 1 records both notified cases and laboratoryreported cases. The laboratory-reported cases are included in Figure 1 so that comparisons can be made with the previous epidemic, which began before pertussis became a notifiable disease in June children aged 5-9 years (414) and 1-4 years (383) (Figure 3). Almost one-half (45.7%) of the cases under one year of age have been hospitalised. The proportion of cases hospitalised was much lower ( 5%) for all other age groups. Given the potential for this outbreak to continue and for a significant increase in cases in parts of New Zealand where there has been relatively little pertussis activity to date, health professionals should continue efforts to achieve high levels of pertussis vaccination in children. During the 18 month period between June 1999 and November 2000, the largest numbers of pertussis cases were notified from the Canterbury Health District (1207), followed by Nelson Marlborough (538), Waikato (482), Southland (349), and Otago (308) Health Districts (Figure 2). Canterbury, Nelson Marlborough, Waikato, and Otago Health Districts also had the highest number of cases in November (refer to the Surveillance data by health district on page 7), whereas cases in Southland peaked early in the epidemic (August 1999) and were low throughout The rate of case confirmation has varied widely between health districts (Figure 2). Rates of pertussis have been highest among infants less than one year of age (768 per ), followed by Tuberculosis in highest number of cases since 1980 In 1999, 450 cases of tuberculosis were notified (12.4 cases per ), a 23.0% increase on the 366 cases notified in 1998 (10.1 per ) and the highest annual case total since 1980 (Figure 4). The number of laboratory-confirmed cases also increased, from 293 (80.1% of cases) in 1998 to 346 (76.9%) in Thirtynine (8.7%) of the cases in 1999 were reactivations, which is similar to the proportion of reactivations in 1998 (7.3%). Rates of tuberculosis above the 1999 national average of 12.4 per were recorded in Central Auckland (28.3), South Auckland (22.5), Northland (19.0), Hutt (18.9), Wellington (17.3), and Hawkes Bay (13.2) Health Districts. New Zealand Public Health Report Vol. 8 No. 1 January 2001 Page 4

5 The proportion of female and male cases was similar: 48.4 and 51.6%, respectively, with sex not reported for four cases. Table 1 shows the age-specific rates of disease by ethnic group. The largest percentage increase in tuberculosis occurred among Maori, with an increase to a rate of 19.1 per in 1999, compared with rates of 12.8 and 11.1 in 1998 and 1997, respectively. Rates among Europeans were fairly stable between 1997 and 1999, while rates among Pacific Islands people rose between 1997 and 1998 (from 27.1 to 46.8) but did not increase further in Rates among people of other ethnicity were fairly stable between 1997 and One of the notable features of tuberculosis in 1999 was an increase in both the number and proportion of New Zealand-born cases. In the five years preceding 1998, the number and proportion of cases born overseas increased from 128 cases (50.0% of all cases) in 1993 to 187 (65.6%) in 1997 (Figure 5). However, in 1998, and particularly in 1999, there was an increase in the number and proportion of New Zealand-born cases: from 98 cases (34.4%) in 1997 to 170 cases (43.0%) in The prolonged outbreak among young Maori males in the North Island, which is reported in the lead article in this issue, made a major contribution to the increase in rates of tuberculosis among Maori in 1999, and the increase in the number and proportion of New Zealand-born cases. Note: 1 Only includes cases for whom place of birth known. The causative organism was identified for 310 cases, and 304 (98.1%) were Mycobacterium tuberculosis and six (1.9%) were M bovis. The antimicrobial susceptibility of 301 isolates (297 M tuberculosis and 4 M bovis) was tested and is shown in Table 2. Two (0.7%) M tuberculosis isolates were multidrugresistant (resistant to at least isoniazid and rifampicin). Like all previous multidrug-resistant M tuberculosis isolated in New Zealand to date, these two isolates were from cases who were born overseas: one in Thailand and one in India. The overall prevalence of resistance to isoniazid, streptomycin, pyrazinamide, rifampicin, and ethambutol was 5.6%, 5.2%, 2.7%, 1.0%, and 0.7%, respectively. Table 2: Resistance patterns of M tuberculosis and M bovis, 1999 Resistance pattern Agent(s) 1 Number of isolates (percent) Resistant to 4 agents HRZE 2 1(0.3) Resistant to 3 agents HZS 1 (0.3) HSE 1(0.3) Resistant to 2 agents HZ 3 3(1.0) HS 4(1.3) HR 2 1 (0.3) RS 1 (0.3) Resistant to 1 agent H 6 (2.0) S 6 (2.0) Z 3 3 (1.0) Fully sensitive (91.0) Notes: 1 H = isoniazid, R = rifampicin, E = ethambutol, S = streptomycin, Z = pyrazinamide 2 Multidrug-resistant cases 3 Includes two M bovis isolates which are intrinsically resistant to pyrazinamide Among the 394 cases for whom the site of disease was recorded, 61.2% (241) had pulmonary disease only, 30.7% (121) had extrapulmonary disease only, and 8.1% (32) had both pulmonary and extrapulmonary disease. Hospitalisation history was recorded for 403 cases, and 67.2% (271) were hospitalised. There were fourteen deaths reportedly due to tuberculosis in 1999 (a casefatality rate of 3.1%). Six outbreaks of tuberculosis, involving 56 cases, were first reported during The largest of these outbreaks was among a Pacific Islands people church group in Auckland (see NZ Public Health Rep 2000; 7: 41-3). The outbreak reported in the lead article in this issue is not included in these outbreak statistics as it was first reported in Prompt diagnosis of cases, thorough contact tracing to detect further cases and infected contacts, and effective treatment of cases and management of infected contacts is the basis of tuberculosis control in New Zealand. Given the ethnicity-specific rates, medical practitioners should have a high level of suspicion for this disease in Pacific Islands people and people who have migrated from areas which have a high prevalence of tuberculosis. Table 1: Tuberculosis notifications by age group and ethnicity, Age group European Maori Pacific Islands people Other ethnicity Unknown ethnicity (years) No. Rate 1 No. Rate 1 No. Rate 1 No. Rate 1 No. No. Rate 1 < Unknown Total Total Note: 1 Crude rate per , based on 1996 census Page 5 New Zealand Public Health Report Vol. 8 No. 1 January 2001

6 Surveillance data National surveillance data - November 2000 Disease 1 Current year Previous year Trends - November 2000 Cumulative Cumulative Nov 2000 total Current Nov 1999 total Previous cases year-to-date rate 3 cases year-to-date rate 3 AIDS Campylobacteriosis Cholera Creutzfeldt-Jakob disease Cryptosporidiosis Dengue fever Gastroenteritis 4 Giardiasis H influenzae type b disease Hepatitis A Hepatitis B (acute) 5 Hepatitis C (acute) 5 Hydatid disease Influenza 6 Lead absorption Legionellosis 6 Leprosy Leptospirosis Listeriosis Malaria Measles Meningococcal disease Mumps Paratyphoid Pertussis Rheumatic fever Rubella Salmonellosis Shigellosis Tetanus Tuberculosis Typhoid VTEC/STEC infection Yersiniosis Notes: 1 Other notifiable infectious diseases reported in November: Nil 2 These data are provisional 3 Rate is based on the cumulative total for the current year (12 months up to and including November 2000) or the previous year (12 months up to and including November 1999), expressed as cases per Cases of gastroenteritis from a common source or foodborne intoxication (eg, staphylococcal intoxication or toxic shellfish poisoning) 5 Only acute cases of this disease are currently notifiable 6 Surveillance data based on laboratory-reported cases only 7 Percentage change is the difference between the number of cases in the current year (12 months up to and including November 2000) and the previous year (12 months up to and including November 1999). This difference is expressed as a percentage of the number of cases seen in the previous year. New Zealand Public Health Report Vol. 8 No. 1 January 2001 Page 6

7 Surveillance data Surveillance data by health district - November 2000 Cases this month Current rate 1 Disease Cases for November 2000, 2 and current rate 1,2 by health district 3,4 Northern Midland Central Southern AIDS 3 Campylobacteriosis Cholera Creutzfeldt-Jakob disease Cryptosporidiosis Dengue fever Gastroenteritis Giardiasis H influenzae type b disease Hepatitis A Hepatitis B Hepatitis C Hydatids Influenza 5 Lead absorption Legionellosis 5 Leprosy Leptospirosis Listeriosis Malaria Measles Meningococcal disease Mumps Paratyphoid Pertussis Rheumatic fever Rubella Salmonellosis Shigellosis Tetanus Tuberculosis Typhoid VTEC/STEC infection Yersiniosis Northland NW Auck Central Auck South Auck Waikato Tauranga Eastern BoP Gisborne Rotorua Taupo Taranaki Ruapehu Hawkes Bay Wanganui Manawatu Wairarapa Wellington Hutt Nelson-Marl West Coast Canterbury South Cant Otago Southland Notes: 1 Current rate is based on the cumulative total for the 12 months up to and including November 2000, expressed as cases per These data are provisional 3 AIDS data given by divisions of the Health Funding Authority 4 Further data are available from the local medical officer of health 5 Surveillance data based on laboratory-reported cases only Page 7 New Zealand Public Health Report Vol. 8 No. 1 January 2001

8 Public health abstracts Does child physical abuse continue down the generations? A review found only 10 studies published over the last 35 years which provided information about physical maltreatment in two generations and included a control group. In nine of the studies, children of parents who were themselves abused during childhood were at increased risk of physical abuse. This increased risk was statistically significant in four of the nine studies. The scientific validity of the 10 studies was evaluated based on eight methodological standards, which were derived from a hypothetical randomised-controlled trial. Only one study met all eight standards, and it provided strong evidence for intergenerational abuse transmission (relative risk [RR] 12.6, 95% confidence interval [CI] ). Another study met six of the eight standards, but did not provide strong evidence for abuse transmission (RR 1.1, 95% CI ). The other studies met fewer than six of the standards. The authors suggest their standards should help improve the methodological quality of future studies on the generational continuity of child abuse (Ertem IO, Leventhal JM, Dobbs S. Intergenerational continuity of child physical abuse: how good is the evidence? Lancet 2000; 356: 814-9). Editorial note: New Zealand Health Information Services data record that, in 1997, 12 children (nine under 5 years of age) died of injuries purposely inflicted by others. In the year to the end of June 1998, 122 children (87 under 5 years of age) were hospitalised because of injuries purposely inflicted by others. Over the 9 months October 1999 to June 2000, the Department of Child, Youth and Family Services received reports of children and young people believed to be at harm due to abuse and neglect. Intergenerational transmission of child abuse has been targeted in the Department s breaking the cycle campaigns. Hereditary factors play a minor role in susceptibility to most cancers A study combining data on pairs of twins listed in the Swedish, Danish and Finnish twin registries found that inherited factors make only a minor contribution to the causation of most types of sporadic cancer. Statistical modelling was used to estimate the relative importance of heritable and environmental factors in causing cancer at 11 anatomical sites. Statistically significant effects of heritable factors were only observed for prostate cancer (42% of the risk may be explained by heritable factors), colorectal cancer (35%), and breast cancer (27%) (Lichtenstein P, Holm NV, Verkasalo PK, et al. Environmental and heritable factors in the causation of cancer. Analyses of cohorts of twins from Sweden, Denmark, and Finland. N Engl J Med 2000; 343: 78-85). Editorial note: This paper emphasises the principal role played by modifiable environmental factors in the causation of cancer, and therefore the combined role of clinicians and public health professionals in cancer prevention. However, the results also indicate there is a relatively large effect of heredity in cancer at a few sites. For individuals and families in New Zealand where the latter is a consideration, genetics services provide the capacity to make detailed investigations and recommendations for management. The Central region service estimates that approximately 10% of cancer cases in New Zealand have a clearly heritable component, and that breast cancer enquiries comprise about two-thirds of the cancer-related referrals they receive. Travel health Malaria risk in pregnancy extends to postpartum period In malaria endemic regions, pregnant women are the main group of adults at risk of malaria. This study followed 71 pregnancies in 38 women living in a village in Senegal where the transmission of malaria is high. During the 8.5 years of follow-up, these women had 58 episodes of clinical Plasmodium falciparum infection. The incidence of malaria increased significantly during the 2nd and 3rd trimesters of pregnancy, and reached a maximum during the first 60 days after delivery. Illness was also significantly more severe during these stages of pregnancy (Diagne N, Rogier C, Sokhna CS, et al. Increased susceptibility to malaria during the early postpartum period. N Engl J Med 2000; 343: ). Editorial note: Because pregnancy is associated with an increased susceptibility to malaria infection, and as malaria in nonimmune pregnant women may be devastating for both the fetus and mother, pregnant women are generally advised to avoid travel to malarious areas. However, if travel is unavoidable, chloroquine and mefloquine can probably be safely used for prophylaxis. The results of this study suggest that women travellers may also be at increased risk during the postpartum period. As this study was conducted in a malaria-endemic area, where women have relatively high levels of acquired immunity, further work is needed to confirm that the findings also apply to women travellers who do not have any immunity. New Zealand Public Health Report is produced monthly by ESR for the Ministry of Health. Internet website: Scientific Editor: Michael Baker, Public Health Physician, ESR Managing Editor: Helen Heffernan, Scientist, ESR Editorial Committee: Sally Gilbert, Senior Advisor, Ministry of Health Douglas Lush, Advisor, Ministry of Health Ian Shaw, Toxicologist, ESR Phone: (04) Fax: (04) Phone: (04) Fax: (04) Reprinting: Articles in the New Zealand Public Health Report may be reprinted provided proper acknowledgement is made to the author and to the New Zealand Public Health Report as source. Contributions to this publication are invited, in the form of concise reports on surveillance, outbreak investigations, research activities, policy and practice updates, or brief review articles. Please send contributions to: Scientific Editor, New Zealand Public Health Report, ESR, PO Box , Porirua, Wellington, New Zealand. Phone: (04) ; Fax: (04) ; michael.baker@esr.cri.nz The content of this publication does not necessarily reflect the views and policies of ESR or the Ministry of Health. New Zealand Public Health Report Vol. 8 No. 1 January 2001 Page 8

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