The first rat I met in South Vietnam in 1967 was a hairless pup, jiggled by the tail in front of a bawling infant in a clinic we were holding in a refugee camp in sand dunes on the central coast, south of the city of Tuy Hoa. His mother had produced it from inside her shirt for tranquilising purposes, and it did the trick. As his eyes focused, the infant’s larynx relaxed, and everyone began to feel better until stubby hands groped for the rodent. With a twist of the wrist, however, the mother avoided a spectacle that might have lingered in our minds.

I met my second rat later that day. He was a hairy thing, bolting across the sandy road between the barracks, and I wondered what he was doing out in the sun. I was surprised when he came to a sudden stop, and incredulous when he began to move backwards in a limb-whirling shower of sand.

I blinked to clear my eyes of perspiration and found the reason for the rat’s reverse: fishing line connecting a rear leg to the hand of a small boy squatting with friends in the shade beside one of the huts. The rat was being reeled in to be released again, and yet again, by serious captors.

I met more rats when I went into one of the barracks on a “home visit”. The huts were all the same, erected on the sand from corrugated iron and jammed with 30–40 people and their belongings. The inmates had been relocated from war zones for their own “good” and passed their days in idle misery, eating grain delivered by the government and throwing their refuse into open pits.

It was very hot in the barracks — literally like being in an oven because each family cooked its meals over open fires, inside the tin sheds, in the sand dunes, under the blazing sun. The huts were stifling with smoke and humanity.

I made my way to one fire to see what was on for lunch and found a frying pan filled with rats. Denuded, disembowelled and beheaded, they sizzled flank by flank under the care of an older woman in black pyjamas.

Nearby lay the first of my patients: a man who was sick, febrile and immobilised by a large, painful lump in his groin, which was covered by oedematous, bluish skin. An abscess, I thought, and injected the only antibiotic I had, streptomycin, before moving to the next patient, who also had an abscess. And then, another. This seemed odd, but I remembered the holiday I had once endured as a small boy on a waterless farm in Queensland and the crops of boils that had erupted in the nether regions of several of us children after sharing an inch or two of black bath water. I suspected poor hygiene. It never crossed my mind the abscesses might have had something to do with the rats.

But these “boils” were so large, and the people so sick, I aspirated one and sent pus to a nearby United States Air Force laboratory. Returning in a few days for the results, I had barely begun to savour the delicious air conditioning when a door was flung open and the technician announced with great excitement: “It is P. pestis! P. pestis! [Pasteurella pestis; now known as Yersinia pestis]” So what? I wondered, trying to recall any mention of that organism in my recent undergraduate experience at the University of Sydney. The technician informed me that we had discovered an outbreak of plague.

Plague in Vietnam did not begin or end in our refugee camp. It was first recorded in 1898 in Nha Trang, south of Tuy Hoa, and the absence of any local name seemed to confirm its novelty.1 It was assumed it had been transported by ship from Hong Kong, where the Chinese epidemic had reached in 1894.1 In 1906, it was reported in Saigon (now Ho Chi Minh City), where it became endemic and caused about 1000 cases a year until the strict French administration managed to restrict it to about 25 cases a year in the 1930s. It increased again in the 1940s, during World War II.

From 1962, however, the incidence in South Vietnam soared —5000–10 000 cases were reported annually until 1973,1,2 after which it fell. What caused this apparent outbreak? Where did it come from? Why did it stop?

Marshall and colleagues denied an outbreak, stating it had been endemic since importation, and this notable increase merely reflected better identification by the increased numbers of doctors and laboratories associated with the Vietnam War.3 As confirmation of endemicity, they cited outbreaks in refugees and Viet Cong prisoners from regions beyond the reach of allied hospitals.3

Most rejected these denials but, if endemic, where was the fertile reservoir? Rural or town rats? It was argued “if there is no evidence that plague has come from outside sources” it must be based in “local wild rodents”,4 who transmit it either directly to humans, or indirectly, via urban rodents they have infected.

Historically, plague has occasionally been associated with rural disruption. In India in 19945,6 and Algeria in 2003,7 outbreaks were preceded by rural earthquakes. Did burrows of rodents in rural areas collapse, forcing their residents to join — and infect — human refugees? Did broken buildings provide access to more food and permit proliferation? In South Vietnam, during the Vietnam War there were two massive disruptions in rural ecology: the bombing campaign and defoliation.

Coincident with the outbreak of plague, 7.5 million tons of bombs (plus other ordnance) were dropped on rural South Vietnam: three times the weight dropped in World War II and with 100 times the combined impact of the atomic bombs dropped on Japan.8 Did these artificially made earthquakes drive rural rodents to the towns? Did they rupture grain stores, allowing access to food sources? Was there a limit to how much even a rat could take?

Did defoliation alter their eating habits, with the same result? In 1962, Operation Ranch Hand was launched to deprive the Viet Cong of food and cover. It peaked in 1968–1969 and ended in 1971, after the spraying of over 6 million acres of rural land.9 Deforestation increases contact between humans and sylvatic sources,5 and Akiev noted that 86% of cases of plague in South Vietnam between 1966 and 1970 occurred in the most defoliated provinces.10 In many of these provinces, plague appeared for the first time.

Although plausible, the theory that rural mammals were the source of plague was contradicted by field studies that found the disease to be surprisingly restricted to town mammals. Although trapping in the countryside was a dangerous pastime in those days, restricting research, Marshall and colleagues found that 99% of infected animals were the town rats, Rattus norvegicus, R. rattus, R. exulans, and the house shrew, Suncus murinus.11 After the war, researchers found that zoonotic foci were restricted to human settlement. Moreover, the flea vector, Xenopsylla cheopis, “exist[ed] only on indoor, commensal rodents”.12 Later, Suntsov and colleagues found only one rare flea to be common to rural and urban rodents, making it unlikely plague would be transferred from one to the other.13

If the rural mammals were not abandoning their homes, humans were. Around 3 million people (10% of the population) were relocated to camps such as ours in Tuy Hoa, and plague has long been recognised as a disease of the poor, crowded in slums where rats proliferate on rubbish.14

Certainly, there was inadequate disposal of rubbish in our camp, but proliferation of the urban rodents may have been even more encouraged by the practice of feeding refugees with grain shipped from central deposits and stored imperfectly in the camps in the provinces.3 This promoted transportation of rats from sites of endemicity and ensured they were well fed for reproduction.

Perhaps eating habits further contributed to disease. Human skinners of infected camels15 and marmots have contracted plague through breaks in the skin, and consumers of undercooked meat have become infected.16 The former are likely to present with axillary buboes and the latter cervical, but our cases were predominantly inguinal, suggesting flea bites on the legs. Also, the rats I saw being cooked were more in danger of being over- than underdone. Fleas quickly abandon the cooling bodies of their dead hosts. I suspect the refugees in our camp were infected as they prepared the corpses for dinner.

The weather affects the incidence of plague and our outbreak occurred in the drier months, as observed elsewhere. It is argued that eggs and larvae of fleas perish in the wet season.17

However, the onset of the wet can hardly explain the pattern of illness, restricted infectivity and low mortality in the outbreaks in Vietnam compared with historical accounts of other epidemics.

In South Vietnam generally, the classic signs of the disease were observed: the bubonic form (after the Greek bubo, for groin), in which lymph nodes draining the infecting bite of the flea are severely affected in association with the usual systemic poisoning by gram-negative bacteria; the septicaemic form, in which the lymph nodes are not prominent; and the pneumonic form, in which bacteria invade the lungs and can be very infectious.3,18 In our outbreak, however, we only recognised the bubonic form, which also seems to have predominated in other regions. Despite the crowding in the barracks, we recognised no pneumonic forms or transference.

Less common features of plague were also observed in Vietnam: asymptomatic pharyngeal carriage;19 pharyngitis and cervical adenopathy;20 and meningitis, particularly if undertreated21 — but we recognised none of these forms.

Vietnam, however, did not conform to the historical concepts of expanding disaster. Many outbreaks were described, but they remained contained in numbers and sites. For example, we only recognised 15–20 patients with plague, and the disease did not spread to nearby camps or the city of Tuy Hoa; nor, mercifully, did any of our team become infected, despite the lack of any preventive measures.

Early diagnosis and treatment was considered “the single most outstanding facet of plague control” in Vietnam, reducing the overall mortality to 1%–5%.3 Our practice of widespread injections of streptomycin, therefore, must have been blindly successful. We did not observe any deaths.

Mass vaccination with live attenuated strains of some 10 million South Vietnamese would have contributed to control, but we did not even know this existed. Our public health management bore no responsibility for the containment of plague in our camp. There was none.

Did the high ambient temperature inhibit spread? Infectivity in the flea is promoted by a “blockage” in the gut, which allows the bacteria to multiply before being regurgitated into the next host, but Cavanaugh and colleagues showed that blockage was reduced when the temperature of the flea exceeds 27.5°C, and I doubt our camp ever got below that temperature.1 Hinnebusch and colleagues found all fleas fail to block at temperatures greater than 30°C and, moreover, that their lifespan at that temperature is severely reduced, arguably due to dehydration.22 Perhaps the hot, dry environment in the camp, especially in the huts where rats were killed and prepared for food, restricted the passage of the disease by its effect on fleas.

The outbreak from 1962 to 1973 was probably due to proliferation of rats and refugees and catalysed by recipes (that involved cooking rodents to prevent starvation), with the bombing and defoliation more a cause of human than rodent displacement. After the war, the reported incidence fell to several hundred cases annually until 1997, and to 22 in 2000.23 No cases have been reported since 2002.24 This progress may reflect better living conditions and patient care in Vietnam, but the natural history of plague has always been episodic, with the disease emerging and disappearing for reasons not understood.7 Pham and colleagues report a reduction in the number of rodents and fleas trapped in central Vietnam from 2000 to 2007, and absence of Y. pestis in both rats and fleas in recent years, and suggest that Vietnam may have entered one of the “silent period[s]” that have historically preceded “sudden explosions of rodent or human plague”.24

Although we did not observe any plague-related deaths in the epidemic in our camp, it might have been close. One night, feeling the need to give a sick child an extra injection (and, it must be confessed, to pursue adventure), three of us set out to visit the camp, which lay on the other side of a wide river, the Song Ba, beyond the security of the town. The road bridge had been destroyed and cars had to traverse the kilometre-long railway bridge on planks of wood that covered the sleepers, about 60 feet above the fast-flowing water. To add to the challenge, no one dared use headlights.

We travelled in our old Land Rover whose gears were as disinclined to engage as the brakes, and whose muffler was as loud and steering as loose as the ladies in the “entertainment” area between the camp and the Air Force base. But when we arrived at the camp, and shut down the roaring engine, we were astonished by the silence and emptiness of the streets. It was a moonless night and we had difficulty in finding the right barrack, searching along the road with increasing dismay. The people were slow to open the door, and stood silently while we gave our needle. Firelight flickered on unsmiling faces. Just how “pacified” were these people? Let’s go!

We held our breath until the car started and hurried back to the bridge to begin the slow, lurching crossing to safety. Then, about a quarter of the way across, a shape loomed from the darkness in front of us and a huge truck ground to a halt, followed by some others. We had run into an American convoy on its way to war. I was driving and, looking up, against the stars I could see the shape of a machine gunner hunched down upon us.

There was a pause, with engines growling like dogs gearing for savagery; then Bruce Hansen, my team leader and good friend, swung open his door, bounded across the sleepers and pounded on the door of the truck, demanding they “back up” because “we were on the bridge first” and we were “Australians”.

The driver of the truck did not take long to respond. A head appeared from above me with a simple message delivered with a southern drawl. Stripped of embellishments it was, “You back up right now, or I will push you off”, and it was confirmed by a roar of his engine and a lurch of his mighty truck.

There were two practical problems with our gears: finding the right one and holding it in place. Crashing through several, I found reverse and, holding it in place, began the long, backward retreat. My leader maintained criticism of my cowardice — but from the safety of the sleepers. The machine gunner maintained his downward menace.

I could have drowned like a rat. Would they have counted me a victim of plague? At least I would have been spared the injections.

Boys in South Vietnam play with a lizard and rats, 1967. Reproduced from the Bruce Hansen Collection with permission of his widow, Miranda Hansen.

The interior of one of the barracks in the refugee camp near Tuy Hoa, South Vietnam, 1967. Reproduced from the Bruce Hansen Collection with permission of his widow, Miranda Hansen.