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TM5559: Clinical Tropical Paediatrics Case Study One: A severe case of relapsing cholera Samantha Leggett: SN 12494652 19/01/2011

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Page 1: Case Study One: A severe case of relapsing cholera · Web viewCholera is an acute diarrhoeal disease resulting from the colonization of the small intestine by the bacteria Vibrio

TM5559: Clinical Tropical Paediatrics

Case Study One: A severe case of relapsing choleraSamantha Leggett: SN 12494652

19/01/2011

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Case Study One

Samantha Leggett

A relapsing case of severe Cholera

Demographic Information

The patient is a young boy who will be identified as W, of approximately eight years of age. His ethnicity is Bamu and he lives in Emeti, a small village on the Bamu River in the Middle Fly district of Western Province, Papua New Guinea (PNG). W lives with his mother, father and two younger siblings and the family are members of the Church of the Latter Day Saints.

Past History

According to his father W had received treatment for severe malaria earlier this year and had suffered from ‘sotwind’ 1since he was a small boy. W appeared fairly under nourished in contrast to his parents and siblings who, unusually compared to the majority of other villagers, appeared relatively well nourished and healthy despite a total absence of health care in the immediate

1 Short wind: shortness of breath.2

Indonesian Border

DARU

SOGERE

BAMU RIVER

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region and a diet largely consisting of sago2. The child’s health record was not available in order for an assessment to be made regarding growth, development and immunisation status.

Background

In the mid afternoon of 29/11/10 during an emergency intervention in response to a cholera outbreak, W was carried into our rudimentary Cholera Treatment Unit (CTU)3 in Sogere village by his father. W had an overnight history of five watery stools with no vomiting or abdominal pain. The family had had to wait for high tide and had then journeyed a number of hours down river in their dugout canoe to the CTU to seek help. W had had little to drink since the onset of the diarrhoea.

Examination and course of admission

On assessment W appeared moderately dehydrated with a palpable radial pulse, sunken eyes, some irritability, a skin pinch return of around two seconds and slightly dry mucous membranes. He was alert and engaged well and drank eagerly when given Oral Rehydration Salts (ORS). At this point I diagnosed him as having cholera with moderate dehydration. Unfortunately W had a large vomit after his first cup of ORS and then refused to drink any more. As a precaution, instead of being assessed on an outpatient basis, W was admitted to the CTU for closer observation. When presented with the choice of having a needle put in his arm or drinking more ORS W chose the oral fluid option. Throughout the afternoon and early evening he drank a litre of ORS with some diarrhoea but no more vomiting. He also managed a small meal of banana and sago at about 8pm. Shortly after this W decided that he wanted to join his mother and siblings outside and took himself off while his father was going to the toilet.

When his father returned I gave him a 600ml bottle of ORS and instructions to ask W to drink at least a third of it before bed and then drink more if he had diarrhoea in the night. I also asked W’s father to bring him back for assessment before he himself went to sleep or before this if W’s diarrhoea increased in frequency or severity.

The two returned at around midnight and W was in good spirits having had only one more episode of watery diarrhoea and no more vomits. He’d managed to drink around 100mls more of ORS. I agreed that he could spend the night with his family but re-iterated to his father that he must return if W became unwell again.

At 5.30am on 30/11/10 W’s father carried him back into the CTU saying that he had started having profuse diarrhoea again over the previous few hours and had not had any more ORS to

2 Sago is devoid of all nutrients apart from carbohydrate (Stanley J. Ulijaszek SJ. Maternal work and childhood nutritional status among the Purari, Papua New Guinea. American Journal of Human Biology 2003; 15 (4): 472-478).

3 I was working as part of a humanitarian medical organisations’ cholera emergency team at this time.3

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drink. Upon assessment W was severely shocked with a non-palpable radial pulse and a thready and rapid brachial pulse, very sunken eyes, a skin pinch return of >4 seconds, and was moribund and freezing cold.

A second and blind attempt at intravenous (IV) cannulation secured tenuous access and I sat with W and his father holding the line in for over an hour while I administered two volumes of resuscitation fluids as rapidly as the IV access would allow. With an estimated weight of 20kg W was given 2 x 600mls of IV Ringer Lactate with 20mls IV Dextrose 50% added to the first 600mls. His family had little in the way of warm clothing or bedding so we covered him with his father’s sweatshirt and some black plastic sheeting. His condition had not improved after the first volume of fluid but after the second he became more responsive and his radial pulse was once again palpable. His IV fluids were then adjusted for rehydration and maintenance and as he became more responsive I encouraged him to begin drinking ORS again. During the resuscitation period W had two more watery stool of a moderate volume. The outcome of this case was a positive one with W being discharged from the CTU two days later eating and drinking well and with no more diarrhoea for the preceding twenty four hours.

1. W post-resuscitation fluid

Cholera Overview

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Cholera is an acute diarrhoeal disease resulting from the colonization of the small intestine by the bacteria Vibrio Cholerae of which there are numerous serogroups. Of these, only V. cholerae 01 and V. cholerae 0139 are associated with the epidemiological characteristics and clinical picture of cholera. If V. cholerae breaches the gastric acid defence the vibrios multiply rapidly in the alkaline environment of the small intestine and disease is caused by the exotoxins that they release. Subunit B of the toxin adheres to the intestinal mucosa which permits subunit A entry into the cells. Subunit A then activates cyclic adenosine monophosphate (cAMP) which results in the loss of water, bicarbonate and electrolytes from the cells. The exotoxins effectively act as pumps, moving water from cells in the blood and tissues, into the intestinal lumen [1, 2, 3, 4].

The disease is clinically characterised by an acute onset of profuse painless watery diarrhoea flecked with mucous and epithelial cells (‘rice water stools’) and is often associated with vomiting large amounts of fluid. It can result in rapid dehydration and electrolyte depletion which without prompt recognition and treatment can result in acidosis, cardiovascular collapse and death. In its extreme form cholera is one of the most rapidly fatal illnesses known today [4].

With this in mind, in most cases of cholera (75-80%) the infection is asymptomatic or only causes mild diarrhoea although in both situations it is still possible to transmit the disease. Cholera is a self limiting illness and the diarrhoea usually ceases within a week if the patient survives. Deaths from cholera are largely due to dehydration but can also result from hypoglycaemia and renal failure (although this is commonly as a result of protracted dehydration arising from insufficient fluid replacement) [5]. Without treatment >50% of severe cases will die; with prompt and adequate treatment the Case Fatality Rate (CFR) should be <1%. V. cholerae is a virulent bacterium with a short incubation period of a few hours to five days. Because of this cholera outbreaks can occur quickly and numbers can rise rapidly [1, 2, 3, 4].

Little in-depth information is known about why different individuals have varying pathological responses to V. cholerae infection but prior immunological exposure is highlighted as an important factor [4]. The example of Bangladesh is provided where endemicity translates to a low attack rate in adults. Cholera has never before been seen in Western Province of Papua New Guinea and this may provide an explanation for why the patients we were seeing were so sick. The severity of the illness is also known to be dependent upon the size of the infecting inoculum, blood group, and adequacy of the gastric acid barrier [5].

Humans are the main reservoir of V. cholerae and its spread is directly from person to person via the faecal-oral route, or indirectly via infected food or water; this can be for example, from a lack of hand washing after visiting the toilet or before preparing food or from water contaminated directly by faeces. Funeral ceremonies are a key mode of transmission usually via poor hand hygiene before the preparation of food and drink by family members after handling an infected corpse. Other potential reservoirs are fish and molluscs. Additionally, V. cholerae thrives in saline and brackish conditions and can survive for several months-it is thought that transmission can be maintained from such sources [1, 2, 3]. Humans were long thought to be the natural reservoir of the organism but more recent evidence points to the aquatic environment [4, 6] with climate change, specifically a rise in sea surface temperature and subsequent ocean chlorophyll concentration, being linked to an increasing magnitude of outbreaks [7].

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Cholera remains a global threat to public health affecting the poorest and most vulnerable populations [8] and is a key indicator of a lack of social development [6].

The History of Cholera

During the 19th Century cholera spread across the world from its original reservoir in India-the Ganges delta in the Gulf of Bengal, causing six pandemics which killed millions of people worldwide. The current pandemic (7th) began in South Asia in 1961, reaching Africa in 1971 and the Americas in 1991. Cholera has become endemic in many areas where standards of environmental sanitation and person hygiene are low and where populations are living in crowded conditions and lack access to safe water supplies [1, 9]. Each year it is estimated that there are 3-5 million cases of cholera resulting in 100,000-200,000 deaths although it is acknowledged that due to poor surveillance systems and frequent under reporting, these numbers may only represent 5-10% of the actual annual cases worldwide [6].

Papua New Guinea in context

Papua New Guinea had not reported a cholera outbreak for around fifty years. However, between July 2009 and June 2010 PNG reported 5039 cases of cholera with 79 deaths across seven provinces representing a CFR of 1.57% [10]. Cases of suspected cholera began to be newly reported in as yet unaffected Western Province in November of this year. During my time in the Middle Fly district of Western Province the WHO / local ministry of health surveillance team were reporting over 4000 known cases of cholera with around 1000 known deaths giving a CFR of 22.5% at that time. Of the 85 villages in the area with radio communication, the WHO and National Department of Health (NDoH) surveillance teams were contacting 36 on a regular basis for situation reports. Many more villages in the Middle Fly are known to be without formal contact and all of the people we were seeing in Sogere came from such places. It may be fair to comment that in this instance, these lesser resourced villages may have perhaps represented some of the worse affected areas and that the statistics that we had were not truly representative of the situation on the ground. It is important to acknowledge that these figures may also have been falsely high due to local surveillance system limitations [11].

Discussion

The main objectives of a response to a cholera outbreak are 1) to reduce cholera related mortality by prompt, appropriate and accessible rehydration treatment and 2) to limit the total number of cholera cases by implementing effective preventive measures; improving access to safe water and optimising sanitation being key (12).

I diagnosed W with cholera using the case definition given in the PNG National Department of Health (NDoH) ‘Guidelines for the Clinical Management of Cholera’ (Appendix A): ...“ anyone with acute watery diarrhoea-at least three watery stools in a 24 hour period”. This differs from the official WHO case definition which states that cholera should be suspected where “ in an area

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where the disease is not known to be present, a patient aged 5 years or more develops severe dehydration or dies from acute watery diarrhoea” [13]. This WHO case definition has been adapted to provide local health care workers a simplified case definition to work with in a country where few people are familiar with cholera (pers. com with MB, Medecins Sans Frontieres PNG Medical Co-ordinator). Further, recent studies demonstrate evidence that suggests the burden of cholera to be highest in young children (<5 years of age) [14] which perhaps highlights a need for the current WHO case definition to be revisited. Although WHO contend that although cholera is known to occur in children under five years of age it cannot be differentiated from other pathologies on clinical grounds [8]. Use of the WHO standard case definition is strongly encouraged in order to ensure global consistency and adherence to a common vocabulary [15]. A case of cholera can currently only be confirmed when V. Cholerae 01 or 0139 is laboratory isolated from any patient with diarrhoea [13].

The differential diagnoses of acute diarrhoea with no fever and an absence of blood in the stool could have been: Food poisoning, viral gastroenteritis or an incomplete bowel obstruction [3], this particularly given the local incidence of Helminthiasis. However, only rarely do other infections produce a similar clinical picture to cholera [2]. Given that W had eaten the same foods as the rest of his family who were not ill, that we were working in the midst of an acute cholera outbreak, that I had visualised W’s classic rice water stools and that his demise was rapid, I was in this instance, confident with my diagnosis of cholera. Caution is advised against the assumption that any patient with diarrhoea has cholera in an outbreak situation [3].Given the remoteness of our location laboratory confirmation of cholera was not possible but in this instance wouldn’t have changed our management as we would not have delayed treatment until confirmation was available.

Within our CTU hydration status was assessed on the presenting clinical condition following WHO guidelines for the assessment of the severity of dehydration [13]. Following this guideline and on his second presentation, W was assessed as severely dehydrated and commenced on IV Ringer Lactate.

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Evidence demonstrates that severe cholera causes massive electrolyte losses and hypoglycaemia, particularly in children [1, 4]. In severe dehydration resulting from infection with V. cholerae Ringer Lactate is recommended as the IV rehydration fluid of choice [13]. Ringer’s is recommended over other IV fluids as it contains enough sodium, some potassium and lactate which is metabolised into bicarbonate and helps to correct the acidosis that results from severe dehydration. It does not contain enough potassium or any glucose and this is why ORS must be commenced as soon as possible [5]. The WHO guidelines detailing the first steps for managing an outbreak of acute diarrhoea [16] dictate that in severely dehydrated children 30mls/kg of IV Ringer Lactate should be given in the first 30 minutes, and repeated if a peripheral pulse does not return during this time with a total of 100mls/kg over a three hour period. Continuous re-assessment is also advocated.

We also had supplies of IV Glucose 50% which we administered according to clinical signs of hypoglycaemia and the PNG NDoH ‘Cholera Treatment Guidelines’ (Appendix A). In addition to ORS, locally grown bananas were our only other form of potassium supplementation.

Counting amongst the great triumphs of 20th century medicine should be the discovery that ORS can control mortality associated with cholera and diarrhoeal disease [17]. ORS can dramatically reduce the number of deaths arising from cholera, particularly during an epidemic when given as early as symptoms arise with a 70-80% reduction in IV fluid requirement. ORS cannot influence the infectious process, but corrects dehydration and thus saves lives [17, 18].

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But, what course of action do you take when one’s patients refuse to drink the ORS? Our team encountered widespread reluctance amongst adults to drink ORS as they believed that the cholera sickness was a ‘hot’ disease characterised by a burning feeling in their stomachs. It was a widely held belief that if they put a drink that wasn’t hot into their bodies during a ‘hot’ disease then it would kill them (pers. com with Sr L in Daru hospital CTU). This may have also contributed to parents not encouraging their children to drink despite repeated advocacy for the effectiveness of ORS from the two nurses working in the CTU and the village elders who were our willing assistants twenty four hours a day.

WHO [13] states that IV fluids should only be necessary for the initial resuscitation of severely dehydrated patients and that with early intake of ORS the IV fluid can usually be fairly quickly discontinued. We saw many patients who absolutely required a significant volume of IV fluids over a number of days; children, adults and the elderly. Once IV fluids had been discontinued we saw a number of patients returning in a more dehydrated state than at their initial admission as they had continued to have diarrhoea but were not drinking any ORS as instructed. This delayed recovery may well have been due to their refusal to drink ORS in anything but tiny sips when forced but, could also have been compounded by the fact that due to demographic factors such as distance travelled to the CTU and the time they had to wait while sick for a high tide in order to be able to travel the river, most of the people that presented to us were already moderately to severely dehydrated. An interesting observation was that when the author was later working in the CTU at Daru hospital (the administrative centre of Western Province) the nurses were found to be making patients hot ORS upon request!

A Case Fatality Rate of >1% is generally considered to be high but it is acknowledged that in rural areas with poor accessibility to health care, the rate may be much higher [13]. Effective and timely case management contributes to reducing mortality to less than 1% [18].We treated over 200 people in a five day period and during that time only one person died giving us a CFR of 0.5% despite our location, the length of time it took people to get to us, the paucity of equipment and supplies, the nutritional status and incidence of co-infection in our population and our ORS administration challenges.

Cholera and Helminths

The majority of the population that we met in Sogere appeared chronically malnourished and there was widespread helminthiasis evident by the large number of worms vomited up in the CTU.

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2. Ascariasis evident in vomitus

Helminth infections affect hundreds of millions of people in the developing world in conditions where environmental hygiene is poor. They contribute to a continuous cycle of malnutrition [19, 20], anaemia [21] and subsequently a lowered immunity to other infectious agents [22, 23]. A co-infection of intestinal parasites and cholera may result in a higher rate of mortality and morbidity [23].

Ascaris Lumbricoides is common amongst children in developing countries with peak prevalence and intensity amongst children aged 3-8 years [1, 2] due to their high risk behaviour [24]. Our young case study W falls into this high risk group and although no laboratory diagnostics were available, given the number of large worms being vomited up in the CTU and the accompanying risk factors (e.g. lack of adequate sanitation, high water table, no health care), we could assume that it is highly likely that W was infected not just with A. Lumbricoides but probably Trichuris trichiura and possibly hookworm also [25, 26]. In school aged children intestinal parasites are known to cause subtle forms of morbidity, such as poor growth and poor cognitive performance which help to perpetuate the cycle of poverty into the next generation [9].

There is an obvious interplay between risk factors for cholera and helminth infection and research demonstrates that helminth infection has a significant association with decreased mucosal humoral immune responses to V. Cholerae infection and therefore rationalises the decreased efficacy of live-attenuated V. Cholerae vaccines in helminthiasis/cholera co-infection [27, 28]. In addition to a deleterious effect on both local and systemic immunity to the V Cholerae toxin, co-infection can also exaggerate fluid loss in symptomatic V Cholerae infection [29]. These findings highlight the importance of de-worming programmes in both cholera endemic areas and in cholera preparedness activities and WHO [9] advocate helminth control programmes as a contribution toward poverty reduction.

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Incidentally, it has been found that cholera prevention measures that are well adhered to have been found to reduce the incidence of helminthiasis in participating communities [26]. Successful de-worming programmes could therefore be assumed to result in a decreased risk of cholera acquisition as the transmission of intestinal parasites and V cholerae are facilitated by the same unhygienic behaviours.

Cholera is, at the current time non-endemic to Papua New Guinea. However, de worming programmes are clearly an important and quite simply actioned public health aspect of cholera preparedness that should be considered by the relevant committee.

Cholera and malnutrition

Malnutrition is one of the most serious and enduring health problems of developing countries [30] with over half of all infectious deaths in children associated with a low weight-for-age [31]. Several micronutrients have immunomodulating and antioxidant functions; Malnutrition and thus a micronutrient deficiency will therefore negatively affect the susceptibility of the individual to infection and to the course and outcome of the disease [32]. The malnourished body provides the perfect environment for the establishment, survival and proliferation of infection [33]. Simply, infection leads to malnutrition and malnutrition increases susceptibility to infection; the immune system becomes ineffective in its protective role.

Malnutrition is a pre-disposing factor to the acquisition of intestinal Helminth infection [33] and in children who eat a poor diet, heavier worm infections can also exacerbate malnutrition [3]; Malabsorption resulting in macro- and micro-nutrient deficiencies is known to arise from intestinal helminth infection, particularly A. lumbricoides [28]. Further, individuals with lower immunity, such as malnourished children are at greater risk of death if infected by cholera [12]. With his marginal nutritional status, poor diet and likely helminthiasis, W, our young case study was always going to be a high risk case in a cholera outbreak. Thankfully, although the course of his illness was a rocky one, his outcome was positive.

Antibiotic therapy and zinc

The use of an antibiotic to which V. cholerae is sensitive is recommended in cases of severe cholera to shorten the duration of diarrhoea and diminish the volume of fluid lost. Such an antibiotic would also decrease the duration that the organisms are found on the stool. [5, 34]. Our stock of antibiotics were on a re-supply boat that had been delayed by the tides and storms, but in reality many of our patients were incredibly nauseous and vomiting too severely during their admission to have tolerated any oral medication. It is important to note that anti-biotic use is not seen as an essential facet of active case management in cholera but as an adjunct to effective rehydration [35].

Micronutrients are also advocated as an adjunctive therapy to ORS in the treatment of cholera [35]. It has been demonstrated that the administration of zinc supplements for 10-14 days reduce

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the duration and severity of the illness and the risk of prolonged diarrhoea thus potentially helping to break the cycle of persistent diarrhoea and malnutrition [17]. An existing zinc deficiency at the time of illness with cholera has also been shown to result in a greater loss of water and electrolytes than in non-deficient individuals [36]. Unfortunately our zinc stocks were also on the re-supply boat, but again, the administration and toleration of oral treatment would have been a challenge.

Cholera, water and sanitation

As one of the ‘classical’ water borne pathogens cholera is responsible for a high burden of water borne disease [37]. Optimising water supply and sanitation status are therefore key issues in outbreak management [8]. The ‘Sphere Humanitarian Charter and Minimum Standards in Disaster Response’ [38] recommends an integrated approach combining safe, sufficient and equitable access to water with adequate sanitation and health education adapted to the sociocultural background of the community.

WHO estimates that 94% of diarrhoea cases could be prevented by interventions to improve sanitation and hygiene and to increase the availability of a clean water supply. 45% of these are estimated to be through effective hand washing alone [39]. These fundamental measures of clean water provision and basic sanitation to control infectious diarrhoea demonstrate how basic science translates into saved lives [17].

Access to potable water in the villages along the Bamu river was variable with some villages having functioning rain water tanks, some having non-functioning rain water tanks and using the safe supply from other villages and others taking water from creeks. For example, Sogere village had a rain water tank that was broken and the villagers had to canoe across the river to an island where there was a functional rain water tank. This could only be done twice a day in accordance with the tides.

The permanent village houses had long drop style latrines but the area of the village we were using had none and the bush was being used as a latrine area with one side for symptomatic patients and the other for non symptomatic individuals. The Bamu River is in a large area of swamp land where the water table is high so even in the advent of latrines it may be assumed that any creek water accessed was at risk of contamination [40].

We were able, in the initial stages of the emergency response, to implement the following water and sanitation measures: chlorine solutions of varying strengths were made and the principles were taught to the village elders, hand washing bowls containing chlorine solutions were made available at the entrance to the CTU and their use encouraged, solutions for washing soiled clothes were provided and the floors were cleaned with appropriate chlorine solution numerous times a day. Footbaths were also provided. Separate toilet areas were advocated for symptomatic and asymptomatic individuals; the local leaders were educated about cholera and the importance of good hygiene and prompt treatment with ORS, and they in turn carried out daily teaching sessions within the CTU and the Internally Displaced Persons camp, an explanation of which is detailed on later pages.

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3. Leaving Sogere at high tide to fetch water

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4. Sago swamp for as far as the eye can see

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5. Sogere CTU and IDP camp from the air

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6. Chlorine solutions (in the buckets on the left of the picture) in the CTU

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7. Teaching session on the importance of ORS and instructions on how to make it led by the village chief

8. Another day, another lesson

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9. IV fluids and ORS, health education posters, various chlorine solutions and a clean CTU

We encountered an additional potential public health issue in that a small Internally Displaced Persons (IDP) camp formed outside the CTU. When a population is mobile the spread of cholera can be difficult to control [13] due to factors such as the disruption of basic infrastructure, unsanitary and crowded venues and a lack of access to safe water [12]. Additionally, food supplies may be scarce leading to an exacerbation of malnourished states [8]. The camp consisted of the families of the patients we had in the CTU but also the residents of a number of villages where cholera had apparently ravaged. As wantoks4 were becoming sick and rapidly dying, people were abandoning their villages in fear for their lives and moving to Sogere where they knew some kind of health facility had been set up and where they consequently hoped that they had more chance of living should they become sick too.

The camp consisted of around 120 adults plus children, and these numbers put a strain on our and the villages’ already over stretched resources and was a potential infection control risk [5]. After a couple of days of ORS administration and health education, the village elders encouraged the displaced population to return to their own villages.

4 The “wantok” (lit. one talk) system is PNG’s safety net, under which the extended family and clan members are

obligated to support each other. It also functions as an informal country-wide news network (Toft S. Domestic

Violence in Papua New Guinea 1985. Monograph Number 3, Law Reform Commission: Port Moresby).

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10. A corner of the IDP camp

Our health education consisted of the following: basic knowledge about cholera and how it is spread; the importance of good hygiene, sanitation and safe water practices with practical examples of what these might be e.g. using latrines where available, drawing water upstream from any latrines, boiling water before use and appropriate hand washing. We gave out adequate supplies of ORS and placed emphasis on the importance of an adequate fluid intake with diarrhoea of any kind. We also taught that the administration of rice water or the juice from young coconuts is a suitable alternative to ORS should there be no supplies available and the importance of the continuation and increase of breastfeeding in infants and young children with diarrhoea. Finally we provided education around safe funeral practices [16, 35].

Strong community involvement aimed at improving access to safe water, in addition to proper sanitation and hygiene practices can be efficient measures to help curb the incidence of cholera and mitigate high levels of mortality during outbreaks. Sustained development is however, the key to effectively containing and ultimately eradicating outbreaks of the disease [15].

The current WHO/UNICEF [35] recommendations for the management of diarrhoea advocate for better family and community understanding of diarrhoea and its management stating that this group is key in achieving the set WHO goals. In a country where the Prime Minister denies that there is any poverty [41] and pertinent to this case study-in a province of this size where communications are almost entirely absent and little health care or infrastructure exists outside of

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the main administrative centre [10], it is a challenge to imagine how these goals may be achieved within the formal health care system at the present time.

However, anyone who has seen the disease of cholera must realise its formidable power as an instrument for societal fear and change [17]. In the absence of formal public health systems in much of Western Province, it could be hoped that with the health education provided by our team and that of teams of faith based and other ngo river patrols working in the area at the same time as us, the ‘wantok’ system may act as a public health support network and help to save lives in the interim period.

References

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1. Heymann DL. Control of Communicable Diseases Manual. 18th ed. Washington: American Public Health Association; 2004.

2. Gill GV, Beeching NJ. Lecture Notes on Tropical Medicine. 5th ed. Oxford: Blackwell Science; 2004.

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