The horse from the Thoopara property, 20 kilometres south of Proserpine, is the second to die from the virus in the last two weeks. Doctor Steven Donohue from Population Health says it is unlikely the group will test positive for the deadly disease as their contact with the horse was minimal. Meanwhile colleagues of a man who was infected with the potentially fatal virus say they are distressed that he has had to be hospitalised for a second time.
The vet contracted the disease after an outbreak in horses at a clinic on Brisbane's bayside last week. He was released from hospital on Tuesday but has since been readmitted and is being closely monitored by infectious disease specialists.
Smith, F. Moore, C. McCall, V. Playford, G. Kung, H. Abstract A recent Hendra virus outbreak at a veterinary clinic in Brisbane, Queensland, Australia, involved 5 equine and 2 human infections. The Outbreak. Patient 1 A year-old man equine veterinarian at the clinic had a 2-day history of an ILI fever, myalgia, and headache in mid-July Figure 1 Figure 1. Patient 2 A year-old woman veterinary nurse at the same clinic was observed 4 days after patient 1 with a 3-day history of an ILI.
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Emerg Infect Dis. Emerging Infectious Diseases. APA Playford, E. However, on day 9, the heart rate continued to rise, and the horse exhibited mild dyspnea with a prolonged expiratory phase. This normally quiet mare also became agitated when approached. The horse was euthanized on the afternoon of day 9, and postmortem examination was conducted.
The horse remained otherwise well until day 6 when its temperature began to rise above baseline. Fever was established by day 7, and a concomitant rise in heart rate was also noted Figure 2.
The serous nasal discharged had resumed, but the horse was otherwise well and eating normally. On day 8, temperature and heart rate were continuing to rise, and small amounts of blood coated in mucus were seen in the feces. The mare exhibited a rigid forelimb stance, alternating with general restlessness and constant shifting of weight from limb to limb, difficulty eating, frequent head shaking, and irritability with attempts to bite her handlers. A panting type of respiration was noted.
The horse was euthanized on the afternoon of day 8. On histologic examination, systemic vasculitis was observed that affected meninges, nasal mucosa, trachea, lung, diverse lymph nodes, spleen, kidney, heart, uterus, ovary, and intestine. Edema, syncytial cells, viral inclusion bodies, and alveolitis were seen in lung sections. Focal necrosis of the adrenal gland was identified, together with glomerulitis and syncytial cell formation in the kidney.
HeV antigen was detected in tissues and organs, including meninges, alveolar walls, lymph nodes, renal glomeruli, and adrenal glands and in blood vessels supplying each of these. In addition, the nasal mucosa, trachea, spleen, heart, uterus, ovary, and intestine showed HeV antigen. Significant gross abnormalities comprised enlarged and edematous submandibular and bronchial lymph nodes and heavy lungs that oozed fluid from the cut surface.
Numerous petechial hemorrhages were found over the surface of the diaphragmatic regions of the lung. The liver was small with an irregular finely nodular surface. Figure 3. Brain vasculitis in horse experimentally infected with Hendra virus, Australia. A Parenchyma and B ovary of horse 2. Figure 4. Lymphadenitis with syncytial cell formation in horse 2 experimentally infected with Hendra virus HeV , Australia. Immunohistochemical staining of HeV N protein showing presence of antigen in red.
On histologic examination, systemic vasculitis was observed that affected meninges, brain Figure 3 , panel A , nasal mucosa, trachea, lung, diverse lymph nodes, spleen, liver, kidney, heart, uterus, ovary Figure 3 , panel B , and intestine.
Focal necrosis and syncytial formation within lymph nodes were identified, together with glomerulitis and syncytial cell formation in the kidney. Acute myocarditis and focal necrosis of corpus luteum tissue were also identified.
HeV antigen was detected in tissues and organs, including meninges, alveolar walls, lymph nodes Figure 4 , renal glomeruli, myocardium, and ovary and in blood vessels supplying each of these. Again, HeV antigen was detected in nasal mucosa, liver, spleen, adrenal gland, uterus, and intestine.
Hepatic amyloidosis was also noted but was considered to be an incidental finding. Figure 5. Dilation of lymphatic vessels and ventral lung lobe margins of horse 3 experimentally infected with Hendra virus, Australia. At postmortem examination, we identified swollen and edematous submandibular, sternal, and bronchial lymph nodes and dilation of lymphatic vessels at ventral lung lobe margins Figure 5. We also found endometrial edema with purplish discoloration of the serosal surface of the uterus.
On histologic examination, systemic vasculitis was observed affecting meninges, nasal mucosa, lung, diverse lymph nodes, tonsil, spleen, liver, kidney, heart, uterus, ovary, and intestine. Focal necrosis and syncytial formation within lymph nodes was identified, together with glomerulitis and syncytial cell formation in the kidney.
Acute myocarditis and focal necrosis of adrenal and corpus luteum tissue was detected. HeV antigen was also detected in tissues and organs including alveolar walls, lymph nodes, tonsil, renal glomeruli, myocardium, and ovary and in blood vessels supplying each of these, as well as in nasal mucosa, liver, spleen, adrenal gland, uterus, and intestine.
Viral genetic material was detected in nasal swabs from 2 days postchallenge Table , only P gene data shown , consistently in 2 of the animals and intermittently in the third. The steady increase in relative copy numbers over time is consistent with viral replication in the upper respiratory tract and shedding into the nasal cavity in nasal secretions.
Viral RNA was first found in the blood of each horse at least 1 day before onset of fever. After onset of fever, but before development of other clinical signs of illness, HeV genome was detected in the oral swabs, urine, and feces of each horse; the rectal swab only of horse 2 was positive. Fecal material on the floor of the pen could have been contaminated by urine containing viral genetic material. In addition, the smaller amount of material collected on the rectal swab could have influenced sensitivity of the test.
Once clinical disease was established, all samples had detectable levels of HeV genome, except the rectal swabs of horses 1 and 3. All samples in which viral RNA was found were examined for live virus by passage in Vero cells. Virus was not reisolated from any sample collected before postmortem examination. Blood samples collected during acute disease, as well as samples of urine and feces, were highly toxic to tissue cultures, and virus might have been present at low titer in some of these samples.
Figure 6. Values are expressed relative to ribosomal 18S copies. Tissue origins Reisolation of virus was attempted for all tissues; tissues from which virus was recovered generally were those with the highest levels of target genes. From horse 1, these tissues were kidney; lung; and submandibular, inguinal, and renal lymph nodes. From horse 2, virus was recovered from the guttural pouch; pharynx; submandibular, inguinal, bronchial, and renal lymph nodes; lung; spleen; kidney; heart; large intestine; spinal cord; brain; and intrathoracic sympathetic chain.
From horse 3, virus was recovered from the guttural pouch; submandibular, inguinal, bronchial, and renal lymph nodes; lung; kidney; heart; adrenal gland; spinal cord; brain; cerebrospinal fluid; and meninges. The mode and critical control points of HeV spillover from flying foxes to horses, along with the risk for transmission of virus from infected horses to other horses and to humans, is poorly understood. In 2 of the 3 animals, HeV RNA was continually detected in nasal swabs over the course of the incubation period, strongly suggesting that systemic spread of virus may be preceded by local viral replication in the nasal cavity or nasopharynx.
These data indicate that nasal secretions of asymptomatic horses may pose a transmission risk during the early phase of disease that precedes viremia, fever, or other discernable clinical signs of HeV infection.
However, the increasing gene copy number recovered over time also suggests that the risk provided by these animals is relatively low, compared with animals in the immediate presymptomatic and symptomatic stages of infection. Duration of exposure also contributes to infection risk because longer contact time increases the potential for acquisition of an infectious dose of virus. Additionally, certain types of contact or procedures may contribute to infection, such as nasal intubation or routine dental procedures, where operator risk is increased even in the preclinical stage of infection.
The febrile, and then symptomatic, horse likely poses a greater transmission risk not only from virus shed in its nasal secretions but also from excretions, such as urine, and blood. However, the activity likely to pose the highest transmission risk is postmortem examination of a horse that has died of acute HeV infection. The potentially high virus load in the animal at this time provides a scenario for gross contamination of operator and assistants with infective material and the associated additional risk inherent in the handling of sharp instruments.
Of the 7 known human HeV infections, 2 have been associated with postmortem examination of affected horses 8 , 9 and the remainder with contact with clinically ill horses in the late incubation period 2 , The early field observations also mention ataxia 10 , 14 and myoclonus 14 , which suggest that neurologic presentations are regularly associated with HeV disease in horses.
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