When nearly one-half of Kazakhstan’s saiga antelope population died suddenly in May 2015, speculation followed that this unique animal was on the brink of extinction. The immediate cause of death was found to be the bacterial disease hemorrhagic septicemia. But something had to happen to ignite the disease outbreak in the first place, and precious few clues exist as to what this might have been.
The saiga have faced similar mass die-offs in the past and have displayed a remarkable capacity to recover. There is great concern for this critically endangered species, but there is also room for hope. A better understanding of the complex epidemiology of hemorrhagic septicemia in saiga and livestock will reinforce this hope.
Saiga antelope (Saiga tatarica tatarica) inhabit the vast semi-arid grasslands of Kazakhstan. Their peculiar wrinkled, tubular noses are designed to warm frigid winter air and cool sweltering summer air, as well as to filter dust thrown up by thousands of animals on the move.
During the winter mating season, a single male watches over a harem of anywhere from 15 up to 30 females, before the two sexes separate into distinct herds to migrate. The saiga move long distances between their wintering grounds in the south and their summer grazing range in the north, covering up to 50 miles in a day.
On their way north from April to early June, herds of well over 100,000 females gather on calving grounds, nearly all giving birth within a 5-8 day period. Newborns lie motionless in the grass for the first few days, to escape the prying eyes of their nemesis, the gray wolf.
In prehistoric times, the saigas’ range extended from Alaska in the east to what is today Great Britain in the west. But 90% of today’s population, estimated at over 300,000 by early 2015, live for the most part in Kazakhstan (see map).
Cycle of Death
The hapless saiga have experienced severe population swings in recent decades. From over 1 million individuals estimated in the early 1990s, by the year 2000 the saiga population had declined by more than 80%, to an estimated 178,000 individuals. By 2003 their numbers were fewer than 50,000.
The bulk of these declines stemmed from poaching, the result of the economic downturn following the collapse of the Soviet Union in the early 1990s. In addition to supplying meat to hunters, the horns of males are sold in Asian markets as a traditional herbal medicine.
Yet even before poaching, saiga populations were constantly under pressure from other sources. Every few winters, repeated melting and freezing of snow coats pastures with a layer of ice that the saiga cannot penetrate to reach the grass underneath. When following on the heels of a drought the previous summer, the antelope are especially vulnerable. Just such an event led to the starvation of some 400,000 saiga in the winter of 1971-72.
Diseases, too, have taken their toll. One of the more common used to be foot-and-mouth disease (FMD), one outbreak of which killed 50,000 saiga young in 1967. Vaccination campaigns among livestock in Kazakhstan put an end to large FMD outbreaks in the saiga in the 1970s.
The May 2015 Die-off
On or around 10 May 2015, saiga females and their newborn calves began dying in large numbers among the Betpak-Dala population between the Aral Sea and Lake Balkhash (males were relatively unaffected as they do not accompany the females to the calving grounds). Within three weeks, over 150,000 carcasses from a dozen or so herds were scattered across the vast grasslands of central Kazakhstan.
According to Richard Kock of the UK’s Royal Veterinary College, who headed an international team investigating the die-off, mothers fell ill first. They became weak and uncoordinated with labored breathing, followed by bloody diarrhea and frothing from the mouth just before death a few short hours after the onset of illness. Calves died within hours of their mothers, usually with diarrhea.
Necropsy (autopsy on an animal) and laboratory tests showed the immediate cause of death to be the bacterial disease hemorrhagic septicemia. But there are many problems with this diagnosis and its implications for the saiga, as pointed out freely by the investigators themselves.
Hemorrhagic septicemia (HS) is caused primarily by one of two forms of the bacteria Pasteurella multocida: generally the B serogroup in Asia and the E serogroup in Africa. Water buffalo are the main victims of HS, but cattle can also be severely affected and, to a lesser extent, pigs and wild ruminants (such as the saiga).
Southeast Asia suffers the highest number of HS cases, but the disease is enzootic (i.e. endemic in animals) in most countries throughout Asia and Africa and is one of the more costly livestock diseases on both continents.
The bacteria survive well in mud or water and oubreaks are most common during the rainy season. Infection stems from inhaling or ingesting the bacteria.
In a typical livestock outbreak, anywhere from 10% to 50% of the cattle or water buffalo in a herd develop fever, respiratory distress, nasal discharge, frothing from the mouth, swelling from edema at the base of the jaw, and pneumonia. Bacteria spread to the bloodstream, causing the animal to collapse and die shortly afterwards, often within just a few hours. Some animals are affected so severely that they die before any of these outward signs become evident.
Only through antimicrobial treatment at the very earliest sign of illness does the afflicted animal have much hope of surviving. And detection at this early stage is difficult and typically impractical.
Those few animals that survive a bout of HS often become carriers of the bacteria , which set up shop in the animals’ tonsils and generally behave themselves, causing no illness. This has both positive and negative consequences.
The advantage is that this constant exposure of the herd to the bacteria provides a measure of immunity among all the animals, even those not harboring the bacteria.
The disadvantage of carrier animals is that during highly stressful situations, the Pasteurella multocida may multiply precipitously and make their way from inside the tonsils to the throat, where they are shed by the animal into the environment and become a potential source of infection to unprotected individuals. If there are enough susceptible animals in the herd, an outbreak occurs.
Many questions remain regarding the 2015 saiga mass die-off. For one, the saiga have long been exposed to the bacteria that cause HS. Because of this, simply culturing Pasteurella multocida from dead animals is not proof that HS caused those deaths. Many individuals in the herd are healthy carriers of the bacteria and may have died from other causes.
In the case of 2015, however, P. multocida was found associated with every saiga carcass tested. While other potential pathogens were found in some carcasses, no others were found in all of them – highly suggestive that HS was the cause of death.
For livestock inhabiting regions with HS (i.e. enzootic areas), outbreaks tend to occur at long enough intervals to allow the accumulation of naïve individuals that have never been ill with HS, and thus are highly susceptible to it. When outbreaks erupt in these herds, there are still many carrier animals, all of which should be immune to illness from HS. It is the younger, naive animals that tend to suffer more severely.
This begs the question: If HS survives in a carrier state among the saiga (and we know it does), why did this outbreak have such devastating consequences?
Among the saiga in 2015, the explosive nature of the outbreak resembled what typically happens in animals never before exposed to HS. Essentially every individual in affected herds contracted the disease AND died from it – some 60,000 individuals in one particularly large herd.
A 100% morbidity (percentage of individuals in a herd contracting the disease) and mortality rate are striking and unheard of for any disease I am aware of. Why didn’t at least the carrier animals survive?
Another phenomenon difficult to explain in the 2015 outbreak is the lightning speed with which illness and death spread through affected herds, with the majority of deaths occurring within a period of less than a week.
And HS appeared almost simultaneously in several different herds, some separated by a distance of nearly 200 miles. It is difficult to explain how a disease that is spread directly from one animal to another – and usually not very efficiently – could have spread so far so fast.
And if HS killed the saiga, according to our understanding in livestock, some stressful event must have caused the carrier animals to begin shedding their bacteria into the environment to infect susceptible individuals. Such events can be subtle to the human eye, but hardly the hint of an answer has surfaced to date.
When I worked among Sudanese refugees in South Sudan in 2013-14, HS was a major problem in cattle around the refugee camps. The long, rapid trek undertaken by these cattle, along with much wetter conditions in South Sudan relative to their homeland, was stressful enough to cause many cases of the disease – and many deaths. Those stress factors were easy to recognize. But not so in the saiga.
The dead saiga were generally in good body condition, so food shortages are unlikely to have been a factor. Soil, plant, or water toxins are considered unlikely given the simultaneous deaths across such great distances. And no toxins have been identified that could explain the die-off. Even rocket fuel was ruled out, presumably from a Russian rocket that exploded in the area shortly after launch in 2013.
Some unusually high rainfall and flooding occurred prior to May 2015 in the area, but apparently not enough to cause significant stress on the antelope.
So the mystery remains as to what could have sparked the transition from latent carrier animals to active shedders among these saiga herds, all at the same time and across hundreds of miles.
Not the First Time
Despite its horrific nature, 2015 was not the first time hemorrhagic septicemia struck down thousands of saiga. Mass die-offs involving HS wiped out tens to hundreds of thousands of saiga in the 1970s and 1980s (see Table 2 below), with an apparent lull in the 1990s and early 2000s when poaching took over as the principal threat. Then, like the small tremors foreshadowing a massive earthquake, 1000 saiga died with HS in the Betpak-Dala population in both 2012 and 2013.
While these events were attributed to HS largely due to the isolation of Pasteurella multocida bacteria from the carcasses, the lack of rigorous investigation into the epidemiology and pathology of these earlier outbreaks later raised questions as to the accuracy of the diagnoses.
The May 2015 die-off was particularly devastating because it affected the Betpak-Dala population of central Kazakhstan, which contained about 200,000 saiga, or nearly 80% of the species’ total population. The deaths were a huge blow.
But perhaps because of the harsh conditions they have evolved in, the saiga show an uncanny ability to recover from their frequent disasters. From their low of under 50,000 individuals in the early 2000s, the total saiga population by the spring of 2015 may have been over 300,000.
Rapid population recovery in the past has been aided by the fecundity of the species. Over ¾ of saiga females give birth to twins each year after their first calving season at around a year old.
Males have been little affected by the great spring calving season HS outbreaks. Their vulnerability to poaching has more than made up for the discrepancy with female deaths. But enforcement of anti-poaching regulations appears to be improving, and this should further spur recovery.
But without discovering and addressing the stress event(s) causing these periodic outbreaks, it will be largely ineffective to attempt direct treatment or even prevention of hemorrhagic septicemia in the saiga.
Unlike many bacterial diseases, HS cannot be eliminated through the use of antimicrobials. The drugs that can kill the pathogen do not reach them in the tonsils of carrier animals.
Nor is vaccination of the saiga an option, though effective HS vaccines exist for livestock. Even if it were realistic to round up all the saiga to vaccinate them, the stress of doing so could easily provoke an outbreak of HS in the days before the animals’ immune systems respond adequately to the vaccine. This could end up killing more animals than it saves.
We are far from understanding the hemorrhagic septicemia-associated die-offs in the saiga. This makes it difficult, if not impossible, to predict the threat of extinction to this unique species. But the saiga are resilient and offer hope that they will be around for many more centuries.
Alexandra Aurelia Wolfs S. Assessment of the short-term effects of weather conditions on mass mortality of the saiga antelope (Saiga tatarica tatarica) in Kazakhstan. University of London. 2014-15.
Croke, V. As Antelope Die-Off Ends, The Mystery Deepens. The Wild Life. 5 June 2015.
De Alwis MCL. Haemorrhagic Septicaemia. Australian Centre for International Agricultural Research. 1999. Canberra.
Kock R, Zuther S, Khomenko S, Orynbayev M. Emergency Response to Saiga Mortality Kazakhstan May 2015: Sumary Report 9th May to 11th June 2015. Royal Veterinary College, University of London. 11 June 2015.
Sá Braz Barros D. Background Mortality of Saiga Antelope (Saiga t. tatarica) During Calving Season in Kazakhstan. University of Lisbon, Faculty of Veterinary Medicine. 2016. Dissertation.