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SOS Rhino : In the News : Looking for the culprit

Looking for the culprit

  The Star, Malaysia
Tuesday, March, 30, 2004

Wildlife experts and veterinarians huddled together recently to discuss two major concerns: why did all five rhinos at a captive breeding centre die suddenly last year and what should be done to protect the few animals that are left in the Malaysian forests. TAN CHENG LI reports.

WHAT exactly killed all five Sumatran rhinos at the Sungai Dusun captive breeding centre in Selangor late last year? It has been five months since the string of deaths over an 18-day span but the cause of mortality is still being debated.

Veterinarians and pathologists have narrowed down the killer to two: a bacterial and a parasitic infection. But which one played the major role in annihilating the captive population of the critically endangered species is disputed.

Medical staff who treated the sick rhinos and did the post-mortems had said that the animals died of septicaemia (blood poisoning) caused by Escherichia coli bacteria but that view was debunked by an American rhino expert at a recent meeting discussing the rhino deaths. Dr Robin Radcliffe, a consultant to the Sungai Dusun centre who assisted in the captive breeding programme, says it was an infection of the blood parasite Trypano-soma evansi which killed the animals.

Some may argue that the debate on which one played a bigger role ∆ the parasite or the bacteria ∆ is pointless as the animals have all died. But it does matter. If E. coli was the culprit, it hints at husbandry and management problems because the bacteria is associated with poor hygiene.

Insisting that the findings were preliminary, Radcliffe says pathological evidence from two American vets strongly suggests that the animals died from Trypanosomiasis rather than septicaemia. He says the parasite T. evansi was abundant in two of the dead rhinos.

The parasite, found in South-East Asia and South America, is common in cattle and buffaloes but rarely kills them. It is, however, fatal to horses. African rhinos are known to harbour another strain of Trypanosoma but the parasite has never been reported for Sumatran rhinos, until now. This makes rhinos "naive hosts."

"Naive hosts have not adapted to the parasite, so the infection can cause mortality. This was seen in Sungai Dusun where none of the rhinos survived the infection," says Radcliffe, director of animal health at the Fossil Rim Wildlife Centre in Texas.

He highlights other signs pointing to a parasitic infection: the rhinos died during the rainy season which is consistent with outbreaks of T. evansi infection; the breeding centre is infested with Tabanus fly, a known vector of the parasite; and the pattern of the infection is typically that of T. evansi, with a 10-day period between the first and second deaths. This is the "pre-patent period" during which the parasite stays in the intermediate host, the fly, before it is transmitted.

Radcliffe believes the first rhino to die, Seputih, had picked up the parasite from the herd of buffaloes grazing next to the centre. The buffaloes had broken through the centre's fencing several times in the past. When Seputih returned to the paddock, she transmitted the parasite to the other rhinos through the flies.

Radcliffe argues that E. coli infection could have set in after Trypanosomiasis debilitated the rhinos and made them susceptible to other diseases. "We are not eliminating the E. coli finding and it is worthy of closer observation but it is premature to say that it is E. coli which killed the rhinos and that there was negligence in the care of the animals," he says. He stresses that the results on Trypanosomiasis were preliminary and further diagnosis to determine the presence of the parasite in the other rhinos was being done at Murdoch University in Australia.

Radcliffe's stand on T. evansi is supported by Universiti Kebangsaan Malaysia parasitologist Dr Chan Boon Tek who believes parasitic infection was what killed the rhinos. He had found "overwhelming abundance" of T. evansi in two rhinos, Minah and Mas Merah. "It was unusual to see that many parasites in blood samples."

The other view

Vets from Universiti Putra Malayisa (UPM), Zoo Negara and the Department of National Parks and Wildlife Protection (Perhilitan) who had conducted post-mortems on the rhinos, however, maintain that the animals died of septicaemia due to an E. coli outbreak.

While not disputing that T. evansi infection played a role in the deaths, they say it should not be singled out as the major cause of death because high counts of pathogenic bacteria were isolated from all rhino organs. Further-more, there were lesions (changes) in the carcasses, consistent with septicaemia. Samples of nasal fluids and urine from two rhinos when they were still alive also showed high levels of pathogenic E. coli.

During the meeting, the vets were clearly disturbed by what appeared to be attempts to dismiss the role of bacterial infection in the rhino deaths despite compelling evidence to the contrary. They objected when Dr Terri Roth of the United States' Cincinnati Zoo who is consultant to Sungai Dusun, proposed a resolution stating that Trypanosoma infection was the primary cause of death and that E. coli infection was only a "possible contributor."

UPM veterinary pathologist Assoc Prof Dr Mohd Hair Bejo says it is improper to reject E. coli infection as a cause of death seeing available evidence. He had even found hardened abscess in Panjang, the third rhino that died. He says this indicated that the animal had long-term bacterial infection. He refutes a claim by Radcliffe that the high E. coli counts in tissue samples were due to contamination and post-mortem overgrowth (proliferation of bacteria after death). He says tissue samples were fresh and the post-mortem adhered to required protocol.

Perhilitan vet Dr Zainal Zahari suggests that the bacterial infection could have weakened the rhinos, thus allowing opportunistic parasites to multiply. If this was the case, then Trypanosomiasis would be a secondary, rather than primary, cause of death.

Deaths preventable?

In Malaysia, Dr Chan of UKM says, T. evansi has been detected in bats, a mousedeer, a slow loris, macaques and rats since 1964. There were two cases of Trypanosoma in humans: in a child in 1933 and in an orang asli in 1974 but both showed no clinical signs.

How life-threatening is T. evansi? A parasitologist from the Veterinary Research Institute in Ipoh, who declined to be named, says the parasite is common in this region and poses little threat to livestock unless the animals suddenly weaken. Then the parasite can multiply and even kill them. She says buffaloes and cattles are routinely screened for the parasite, which is known to infect pigs and dogs too. She says T. evansi is the only Trypanosoma found in Malaysia and it is not as virulent as the African strain, which is transmitted by the tsetse fly and causes the sleeping sickness in humans. But if T. evansi can kill horses, it can possibly kill rhinos too since both are in the same animal order, Perissodactyls, which are ungulates (hooved animals) with odd-numbered toes.

If indeed T. evansi proved to be the major killer of the rhinos, it would be unfortunate because there is a drug to treat the infection. However, parasites were not on the suspect list when the rhinos fell ill, one after another; viruses and bacteria were. The animals also showed general clinical signs and not that of a parasitic infection, says Dr Aidi Mohamed, resident vet of the breeding centre. So they were just treated with broad-spectrum antibiotics.

In hindsight, vets who treated the rhinos say it would have helped if results of drug sensitivity analyses had reached them quicker. But these came only after a week, when all the animals had died. The tests showed that the culprit bacteria was sensitive to only two drugs, neither of which were given during treatment. Similarly, blood tests which indicated T. evansi infection were not relayed to vets on the ground until it was too late. By then, there was little the vets could do for the last two captive animals, Minah and Mas Merah. "The parasite had already attacked the brain and existing drugs for Trypanosoma do not go into brain cells," says Radcliffe.

It is uncertain when and from where the rhinos had contracted the parasite. Blood tests done two years ago found no Trypanosoma in the rhinos. Blood screening is supposedly carried out on the rhinos every month but why this did not pick up the Trypanosoma parasite is anyone's guess. One source says the blood was tested only for blood biochemistry and blood cell count, not parasites.

It is important to determine the source of the parasite to prevent infection of other animals. Dr Chan, however, did not find T. evansi in the neighbouring herd of buffaloes and in a macaque trapped from forests in Sungai Dusun. This is not surprising as the parasite can evade screening if they are few in numbers. Dr Chan suggests further survey of wild and domestic animals in the area as well as entomological investigation on the Tabanus fly.

Regardless of the outcome of these tests and those on T. evansi, the fact remains that something must have triggered the infection in the rhinos, be it bacterial or parasitic. Vets say animals harbour all kinds of bacteria and parasites in their bodies but these cause no harm unless they suddenly proliferate ∆ such as when the animals get stressed up and their immunity is suppressed. Then these bacteria and parasites may cause deadly infections. It is this underlying factor which deserves attention if wildlife experts want to finger the real reason behind the tragic losses of the highly endangered species, and to prevent a recurrence.