Great apes and human diseases: how primatologists hurt and help

A new paper in Current Biology documents the mortality suffered by Taï Forest chimpanzees as a result of common human respiratory ailments during the last ten years. Tissue samples of deceased animals provided information about the pathogens that caused the outbreaks:

Necropsy samples were screened for respiratory pathogens by using different PCR methods. As for most human respiratory cases, a mix of bacterial and viral respiratory pathogens was found in the lungs. The most common bacterium was Streptococcus pneumoniae, which was found in all respiratory outbreaks. In addition, Pasteurella multocida played a role in the 2004 outbreak [10]. All available samples tested positive for one of two paramyxoviruses: human respiratory syncytial virus (HRSV) was diagnosed in two individuals that died in the 1999 north group outbreak and in one adult female (east group) and one infant (south group) who died in the 2006 outbreak, which occurred simultaneously in both groups. The second virus identified was human metapneumovirus (HMPV), detected in three animals that died in the 2004 south group outbreak (Table 1).

Humans have suffered from these respiratory ailments for a long time. The number of human respiratory pathogens almost certainly proliferated greatly during the last 10,000 years, after the advent of agriculture and village life brought the potential of "crowd diseases." For example, human respiratory syncytal virus (HRSV) is closely related to the bovine BRSV and pneumonia virus of mice (PVM). It seems plausible that the human pathogen descended from the mouse or cattle (or sheep) virus, but no one has yet demonstrated this -- and it is after all possible that they got it from us. HRSV is an important cause of lower respiratory tract infections in humans worldwide, especially in children. In an ironic twist, HRSV was first identified in captive chimpanzees as the cause of a respiratory infection with runny nose and sneezing (called coryza) (Blount et al. 1956). It was actually the human RSV virus contracted by the chimpanzees that had caused the infections.

Much the same thing has happened to the wild chimpanzees, but with a high death toll. A 1999 outbreak of HRSV, compounded by Streptococcus pneumoniae, killed 6 out of 32 animals in the affected group, including 5 adults. A 2004 outbreak killed 8 out of 44 animals. These two outbreaks each killed nearly a fifth of the chimpanzees in these groups, and demographic records show that several "multiple mortality events" in the last 24 years are not attributable to poaching or other diseases such as ebola or anthrax (each of which had least one outbreak).

Easily spread respiratory ailments are among the main causes of sickness in contemporary hunter-gatherers, partly because they are able to persist and spread effectively in low-density populations, and partly because they are so common in neighboring groups. Today, respiratory diseases are an important cause of death in these groups -- including adults -- although they count for fewer deaths than gastrointestinal pathogens and parasites. Their ability to infect low-density populations suggests that some human respiratory pathogens surely date to much earlier periods of human evolution.

One thing is certain: humans have undergone thousands of years of selection, in which susceptible individuals have disproportionately been killed by human-infecting respiratory viruses and bacterial strains. Many of these pathogens have adapted very well to humans, including a substantial time or fraction of the population in which they may be present without causing noticeable symptoms.

Chimpanzees lack this history. Relatively minor diseases in humans may have major effects on chimpanzees, and diseases like RSV that cause measurable mortality among human infants may have devastating effects on chimpanzee communities. Together, respiratory illnesses, ebola, and anthrax are having a death toll in the studied chimpanzee groups almost as great as smallpox in post-contact American Indians.

The shocking thing is that this enormous death toll seems likely to have been caused by the researchers themselves, along with ecotourists:

It has long been recognized that respiratory disease is the most important cause of morbidity and mortality among wild great apes habituated to human presence for research or tourism [4], [24], [25], [26] and [27]. However, the etiological agents of such disease have not been documented. Possibly as a consequence of respiratory disease, about half of the long-term chimpanzee research populations have shown major declines [4] and [28]. Our results suggest that the close approach of humans to apes, which is central to both research and tourism programs, represents a serious threat to wild apes (Köndgen et al. 2008:262).

The authors temper this conclusion in two ways. First, they show that the presence of the research station and the tourist site both have significantly decreased the incidence of poaching at and around these areas. Both areas have lots of chimpanzees, but little sign of poachers in contrast to the rest of the protected forest, where poacher sign is common. Poaching accounts for nearly as many documented deaths in the study population as respiratory infection, so this protective effect may be very important.

On the other hand, communicable diseases may well spread beyond a single group, so much of the forest may be at high risk from both poaching and human pathogens. And needless to say, poachers may spend less time around the research and tourist areas, but that hasn't stopped them from killing lots of chimpanzees there. So the protective effect may not be much of a shield.

Second, they provide recommendations that may decrease the risk to the chimpanzees while permitting continued human presence:

In order to reduce the negative effects of research and tourism, strict hygiene protocols, including vaccination requirements for tourists, tourism personnel, park staff, and research personnel against all potentially dangerous diseases for which vaccines are available (e.g., measles, mumps, and rubella), should be implemented [5], [6], [29] and [30]. Only nonsymptomatic visitors and staff should have access to habituated apes. Feces, vomit, and other human debris or wastes should be removed from areas where chimpanzees may come in contact with it or buried at a depth where other animals will not uncover it [29]. Because carriers of human respiratory pathogens are often nonsymptomatic, wearing of masks (e.g., N95 masks as recommended for avian flu) [31] should be mandatory. Human populations living around the parks and reserves should be vaccinated, thereby decreasing the chances of human-pathogen introduction into chimpanzee populations. As in the Taï project, demographic, clinical, and diagnostic monitoring systems should be implemented to objectively document the negative effects of research or tourism. Furthermore, we urge an intensification of research on ways to prevent disease transmission, as well as the development of new methods for vaccine and treatment delivery, to wild apes (e.g., oral baiting) (Köndgen et al. 2008:262-263).

These are necessary precautions, but they are unlikely to be enough. There is no effective or widely available for RSV, or HMPV. S. pneumoniae normally exists in the respiratory tract of 10 percent of healthy adults. There is no way that chimpanzees can hold off these diseases if they are in recurrent contact with people.

References:

Blount RE Jr, Morris JA, Savage RE. 1956. Recovery of cytopathogenic agent from chimpanzees with coryza. Proc Soc Exp Biol Med 92:544-549.

Köndgen S and 17 others. 2008. Pandemic human viruses cause decline of endangered great apes. Curr Biol 18:260-264. doi:10.1016/j.cub.2008.01.012