Volume 46 Number 4 Winter 1999


Hemorrhagic Disease:
Cause of Die-off in White-tailed Deer

Renee Anderson, Gary Mullen, James Wright, Keith Causey, Steve Cotney, George D’Andrea, and Lanqing Li

A significant die-off in a captive research deer herd located in East-Central Alabama occurred during the fall of 1998. The deaths were attributed to hemorrhagic disease and appeared to have involved more than one strain of two closely related viruses.

Die-offs among captive and free-ranging white-tailed deer due to hemorrhagic disease (HD) occurred throughout the central and southeastern United States during the fall of 1998. Hemorrhagic disease is caused by two closely related pathogens, epizootic hemorrhagic disease (EHD) virus and bluetongue (BT) virus. These viruses are transmitted by biting midges (genus Culicoides) and infect both domestic and wild ruminants, including sheep, cattle, and white-tailed deer.

During the fall of 1998, a captive white-tailed deer herd in Lee County experienced an outbreak of HD. The herd had been maintained by the Department of Zoology and Wildlife Sciences (now the School of Forestry and Wildlife Sciences) since 1983. No known clinical disease or deaths due to HD were documented in the research herd prior to the 1998 epizootic, although testing in recent years had demonstrated that active virus transmission was occurring.

Affected deer exhibited classic signs of HD, including general depression and a reluctance to stand. Standing deer had difficulty holding their heads up and often were observed with a swollen tongue protruding from the mouth (Figure 1). They typically exhibited an arched back while standing or walking, due to inflammation of tissues at the base of the hooves that causes pain when weight is put on the hooves (Figure 2). Deer also suffered from emaciation, excessive salivation, facial swelling, labored breathing (Figure 3), hemorrhaging of the inner eyelids, and bloody diarrhea. Both sexes and all age classes were affected.

Figure 1. Acutely ill fawn with characteristic signs of HD: lowered head, protruding tongue, and excessive salivation. 

Figure 2. Deer exhibiting laid-back ears, depression,
and reluctance to stand.


Figure 3. Deer in late-stage of HD, with frothy saliva due to congested lungs and labored breathing.
 

The first death occurred on September 26, 1998. Within 48 hours, 19 deer had died. During the first two weeks of the outbreak, 41 deer died, with four additional deaths in November and three in December. A total of 57 deaths (43% mortality) among a total of 131 deer (90 adult deer and 41 fawns) occurred during the outbreak.

Twenty-nine deer were submitted to the C. S. Roberts State Veterinary Diagnostic Laboratory in Auburn for necropsy (Figure 4). Confirmation of HD was based on gross pathology and detection of positive tissues using PCR (polmerase chain reaction) techniques. Testing of blood samples from 36 deer indicated that the animals had been exposed to several serotypes (strains) of both EHD and BT viruses (see Table 1). All samples showed the presence of EHD virus serotype-2, while more than 70% of the samples also tested positive for BT virus serotype-11.

Figure 4. Lung of deer that has died from hemorrhagic disease
showing internal bleeding and accumulation of fluids in lung tissues. 


Table 1. Serological Monitoring of Captive White-tailed Deer in Lee County, 1998
 

Percent sera with positive antibody response
based on serum testing
 

 BT virus

EHD virus
 Serotype 10 11 13 17 1 2
 Fall 1998   (n=36)  2.8 38.8 77.8 2.8 0.0 5.5 100.0
 Spring    1999
  (n=13)
0.0 33.3 7.7 0.0 0.0 0.0 92.3

Bluetongue virus activity in the deer herd was of special interest given apparent, concurrent BT virus involvement in a beef cattle herd at the AAES’ Piedmont Research Station in Camphill, 15 miles away in Tallapoosa County. The herd experienced significant calving losses in the fall of 1998, with a high level of EHD virus serotype-2 activity.

As a follow-up study to the outbreak in deer, blood samples were obtained from 22 of the captive deer in May 1999 and 13 blood samples have been tested to date (Table 1). There still was a high level of EHD virus serotype-2 activity in the deer in May 1999, whereas indications of BT virus serotype-11 activity had dropped below 10%.

The presence and activity of biting midges at the deer facility were monitored for eight months (October 1998-April 1999). Fourteen species of Culicoides were collected (Table 2). Culicoides variipennis sonorensis was by far the predominant species. This is the principal species of biting midge known to transmit EHD and BT viruses in North America. The presence of this species probably contributed to the spread of these viruses among the deer.

Table 2. Biting Midges (Cullicoides species) Females Collected in Light Traps at Captive White-tailed Deer Facility,
September 30,1998-April 29, 1999
 Species Total Total (pct.)
 C. arboricola 19 (<1)
 C. buguttatus 452 (5.1)
 C. crepuscularis 33 (<1) 
 C. debilipalpis 7 (<1) 
 C. guttipennis 8 (<1)
 C. haematopotus 109 (1.2)
 C. obsoletus-sanguisuga 85 (1.0)
 C. ousairani 10 (<1)
 C. paraensis 9 (<1)
 C. spinosus 6 (<1)
 C. stellifer 424 (4.8)
 C. testudinalis 3 (<1)
 C. variipennis sonorensis 7,555 (85.3)
 C. venustus 110 (1.2)
 Undetermined 32 (<1)
 Total 8,862 (100)

These results indicate that the deer herd was exposed to both EHD and BT viruses and that individual animals were infected with both viruses. The simultaneous infection of deer with more than one serotype of EHD and BT viruses during this outbreak suggests that dual infections with these viruses may contribute to sudden die-offs of deer in areas where EHD and BT viruses are being actively exchanged between white-tailed deer and domestic cattle.

Outbreaks of hemorrhagic disease typically occur in late summer and early fall but are unpredictable from year to year. The HD viruses are well established in deer, cattle, and sheep populations in the southeastern states and are likely to continue to cause future problems. Often the disease is mild with few deaths being reported. In some years, however, outbreaks may be severe enough to warrant the closing of localized hunting seasons. The viruses involved do not pose a health risk to humans, including hunters who may kill and field dress infected deer.

Anderson is Doctoral Graduate Student and Mullen is Professor of Entomology and Plant Pathology; Wright is Associate Professor of Pathobiology; Causey is Professor of Forestry and Wildlife Sciences; Cotney is former Supervisor of Animal Care at the AU Deer Research Facility; and D’Andrea is a Diagnostic Specialist and Li is a Veterinary Microbiology Specialist with the C.S. Roberts State Veterinary Diagnostic Laboratory.


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