The Animal Connection

In the 1970s, it seemed as though the battle against the communicable diseases was won, we had all the weapons we needed to control most of them, all that was required was to have sufficient resources to combat the diseases in the developing world. Smallpox had been eradicated and the development of vaccines promised a similar fate for polio and other immunizable diseases, but then in 1981, there was a rude shock.

In June 1981, CDC in the USA reported five cases of Pneumocystis carinii pneumonia. In the following month, 15 more cases of this normally rare disease were reported as well as 26 cases of Kaposi's sarcoma, an

© R. Webber 2005. Communicable Disease Epidemiology and Control, 2nd edition (Roger Webber)

unusual tumour. The common feature was that all these cases were in homosexual men. By the end of 1981, acquired immune deficiency syndrome (AIDS) as it was called, was also being reported from countries in Europe. In Belgium and France, an AIDSlike illness was observed amongst people originating from Africa. These observations led to investigations in Rwanda and Zaire (now Congo) where many AIDS patients were found. At the same time, an aggressive form of Kaposi's sarcoma was reported from Zambia and a new disease, called slim disease, described in Uganda. These were all found to be manifestations of AIDS. The African infection was transmitted heterosexu-ally, starting its relentless course that has continued unabated until the present time.

The appearance of HIV infection alerted the world to new communicable diseases, several more (e.g. Lassa, Ebola and Marburg), of which have appeared in the last few years. Where had they come from and why were they appearing at this time? The first clue came with the discovery of a virtually identical retrovirus to HIV in simian monkeys called simian immunovirus (SIV), suggesting that HIV originated from a monkey source. Then in 1986, a disease appeared in cattle in England called bovine spongiform encephalopathy (BSE), which was shown to be due to cattle being fed the remains of sheep in their feed, some of which had the similar sheep disease called scrapie. This had not been transmitted from sheep before, so somehow the organism had crossed the species barrier and if this had happened from sheep to cattle, then why not from cattle to humans when they ate infected meat? Sure enough the first case of a new variant Creutzfeldt-Jakob disease (vCJD) appeared linking this condition to the consumption of beef. Since BSE had a 4-5-year incubation period, the potential for human infection was enormous and there was much speculation as to what would happen.

CJD is one of the group of transmissible spongiform encephalopathies (TSEs) which, as well as BSE in cattle and scrapie in sheep, is also found in other animals such as mink, elk and North American mule deer. The only other human disease is kuru, found in the Fore people of Papua New Guinea who traditionally eat the brains of the recently dead in the belief that they will obtain the wisdom and prowess of their ancestors.

The TSEs have been shown to be due to a new kind of organism, a self-replicating protein called a prion, which produces a clinical picture of depression in humans followed by organic brain disease, including cerebella ataxia, cortical blindness, localized weakness and progressive intellectual deterioration. Speech is lost, swallowing becomes difficult and a rigidity of limbs develops as the patient sinks further into a hopeless state of debility and death. Unfortunately, it is difficult to confirm the diagnosis of vCJD (tonsillar biopsy and magnetic resonance scans are useful) until after death, indicating that there had been 142 cases by the end of 2003. This fortunately suggests that the epidemic will not be as large as was feared, and as all offal-based ruminant feeds were banned in Europe in 1994, there should be few if any more cases.

While the public health profession was recovering from BSE and vCJD, another new communicable disease, severe acute respiratory syndrome (SARS) was reported from Vietnam in February 2003. A businessman who had been travelling in China was admitted to hospital in Hanoi with a history of high fever, cough and difficulty in breathing. His condition worsened, so he requested to be transferred to Hong Kong, where despite ventilatory support, he died. In the hospital in Hanoi, several health care workers contracted a similar illness and the attending doctor and a nurse died. Search was made for the organism, which at first was thought to be a new strain of influenza, but subsequently was identified as a corona-virus. An incubation period of 1-14 days, but more commonly 3-5 days and period of communicability of 3-14 days from the start of symptoms was subsequently calculated. Fortunately, the household secondary attack rate was between 6% and 15% in Singapore and Hong Kong, especially low if the initial case was a healthcare worker. This contrasted with hospitals, especially if their barrier nursing was deficient, which were found to be potent sources of transmission.

Tracing the case back, it was discovered that there had been a number of cases of a severe and highly contagious pneumonia in Guandong Province (Canton), southern China, in which one in 30 had died. The attending specialist travelled to Hong Kong for a wedding where in the early stages of the illness, he himself infected all the people in a lift in the hotel in which he was staying. One of these persons was the case that came to Hanoi, another was a person from Singapore and the third a lady returning to her home in Toronto, Canada. Hong Kong, southern China, Singapore, Vietnam and Canada then became the centres of epidemics, which demanded strict quarantine measures to contain them. After draconian measures, especially in China, the last case recovered at the end of July 2003. By that time, there had been 8422 cases and 916 deaths.

Coming back to the original question of what was the link between the three epidemics - HIV, BSE/vCJD and SARS - it seems likely that the organism, originally in animals had crossed the species barrier into humans. HIV from simian monkeys, BSE from scrapie-infected sheep and subsequently via beef to humans, while SARS possibly also had an animal connection. Southern China enjoys a culinary custom of eating almost any kind of animal, often held in cages or fish tanks, until required for the table. Such is the close proximity of people to all these animals and the general poor state of hygiene that all methods of transmission are possible. As well as the respiratory route, the SARS virus was found to be excreted in the faeces and urine of patients, possibly up to 23 days after symptoms first started. The original cases in southern China were in food handlers, 66 of whom were found to have antibodies, while of the animals tested masked palm civets, raccoon-dogs, ferret badgers, cyno-molgus macaques, fruit bats, snakes and wild pigs were all found to be positive. Transmission in humans was through close human contact as the infection was in large droplets rather than aerosol, and possibly also via sewage contamination in one area of Hong Kong. Several of these animals are regarded as delicacies and kept in cages so it seems quite possible that either of these methods could have been how the food handlers were infected. After the main epidemic had finished, a new case was found to be strongly associated with the masked palm civet; hence, it seems likely that this could have been how the epidemic started.

Although SARS has declined to negligible limits, its re-appearance must always be considered. It has been suggested that a clustering of pneumonia cases might be an early indicator, while persons of an older age are more likely to transmit infection. While there is no cause to restrict travel, suspect cases are more likely to come from the southern regions of China where there have subsequently been three cases (up to March 2004). Another case came from Henan Province in central China.

The so-called Asian flu epidemic of 1957 was found to have originated in chickens in Guandong province of southern China, followed in 1968 by the Hong Kong influenza epidemic, which also originated from the same area. Although the 1918 epidemic was termed Spanish flu, it is thought that this too might have started originally in southern China. The world waits in dread for the next major epidemic of influenza, possibly of a major antigenic shift (see Section 13.3), will it also originate here? There have been pandemics in 1889, 1918, 1957,1968 and 1977 and the next one seems long overdue!

A recent cause for concern that a major influenza epidemic might be starting was the appearance of avian influenza H5N1 in January 2004. This is an infection predominantly of chickens and ducks, but can also occur in pigs. It is highly infectious and results in an almost 100% mortality of domestic fowl. The infection is probably maintained in wild waterfowl, sea birds and shore birds and can be spread over long distances when they migrate. However, the transport of birds, contaminated clothing and equipment are probably more likely causes, once infection in a fowl population has started. Bird droppings are highly infectious, so humans coming into contact with them or sick birds are at risk of infection. An outbreak occurred in Hong Kong in 1997 with 18 human cases, of which six died. The same virus was identified in fowls in 2002, resulting in a mass slaughter of chickens, but despite this action, there were four more human cases (two of which died) in 2003. In 2004, there was a more serious epidemic in Thailand and Vietnam that spread to domestic fowls in other countries in Southeast and East Asia (Cambodia, China, Indonesia, Japan, Laos and South Korea) with 34 human cases and 23 deaths. The main concern was that the avian flu could acquire genes from the human influenza organism and produce a potent infection that nobody would have any resistance to. Fortunately, this epidemic subsequently declined, but influenza remains the greatest threat of any emergent infection.

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