nightowl
Very Well-Known Member
Here is some information for those of you interested in this subject. This info is taken from the latest edition of "Reptile Medicine & Surgery" by Douglas Mader. I hope it is OK to reproduce the text here because this book is rather expensive and alot of people would not have a copy but the info is a must for herpers if you can understand some of the text! 
Ophidian Paramyxovirus (OPMV) was first isolated in 1973 from a Fer-de-lance (Bothrops moojeni) after an outbreak in a Swiss serpentarium that killed 25% of 431 specimens. Since then, numerous documented outbreaks of Paramyxovirus have been seen in private and zoologic collections. Paramyxovirus has been isolated from all major snake families, including elapids, boids, colubrids and viperids. Crotalids appear to be the most susceptible.
Paramyxovirus is an enveloped RNA virus 120 to 150 μm in diameter that reproduces by budding from cell membranes. Two distinct subgroups have been shown to exist with several intermediate isolates. This grouping does not appear to be species specific, although geographic correlations were found. Recently, a transmission study was carried out in Aruba Island Rattle Snakes and Koch's postulates were fulfilled.
Clinical Signs
There are no pathognomonic signs for the diagnosis of paramyxovirus infection. The disease affects primarily the respiratory system but can present with a tremendous variation of signs, which makes diagnosis difficult for the clinician. The symptoms are divided into three categories.
Acute and Peracute
Often minimal to nonexistent promontory signs are noticed by the keeper or owner; the animals are often just found dead. Anorexia and regurgitation are occasionally seen. The most common symptoms include respiratory compromise, blood in the oral cavity, or neurological involvement such as head tremors, excitement, star gazing, flaccid paralysis, or convulsions. The time from exposure to death can range from 6 to more than 10 weeks. Animals often die of secondary bacterial infections. OPMV should be included in the differential diagnosis in boids with neurological symptoms suspected of Inclusion Body Disease.
The virus may overwhelm the immune system, with death occurring before a detectable antibody response. Improper husbandry and environmental conditions may play a critical role in immunologic incompetence, particularly the absence of a thermal gradient.
Chronic "Poor Doer"
Anorexia, hypophagia, and regurgitation are the earliest signs and have been seen up to seven months before any other signs of disease. Animals exhibit other general signs of debilitation, such as reluctance to move, increased use of heat plates, emaciation and poor muscle tone. Respiratory symptoms include variable degrees of stridor and dyspnea, often developing into secondary bacterial pneumonia. Gastrointestinal signs may include gaseous bowel distention, mucoid diarrhea, malodorous stools and protozoal overgrowth. Directed antiprotozoal and antibacterial treatment increase survival times.
Specimens usually have high titers. However, antibody presence does not prevent viral shedding, as shown by animals able to infect or induce seroconversion in cagemates. These snakes eventually succumb to the disease but actively shed virus and pose the greatest threat to the collection.
Clinically Healthy Animals
Specimens may remain asymptomatic for up to 10 months, although most individuals eventually become chronic "poor doers." Sustained high titers may be indicative of a chronic carrier state and not necessarily immunity. Some specimens have been documented as overcoming a viral encounter and surviving.
In the authors' experience with a paramyxovirus outbreak, the animals with a regular appetite became anorectic, and respiratory compromise developed. They became severely lethargic and died within 1 week of the onset of signs. A few specimens had horizontal head tremors develop that varied from subtle to broad-swinging movements frequently accompanied with star gazing behavior. One specimen, a Bushmaster (Lactesis mutus), did not show any clinical signs despite a seropositive status for 9 months. A Northern Copperhead (Agkistrodin contortrix) placed in an adjacent aquarium did not have a titer or lesions develop after 8 weeks of exposure to the Bushmaster.
Diagnosis
Presumptive diagnosis of Paramyxovirus infection may be based on a history of exposure and clinical signs. Ill animals should be closely monitored. A thorough clinical examination should be performed, including pulmonary auscultation and fecal examination. If abnormal lung sounds are detected, transtracheal washes for cytology and bacterial culture should be performed because both secondary bacterial and verminous pneumonia are common.
If OPMV is suspected, serum should be assayed for the presence of antibody with Hemagglutination inhibition (HI). Titers only reflect exposure, and a rising titer is necessary for diagnosis of active disease. Seroconversion generally takes more than 8 weeks. The laboratory of Dr Elliot Jacobson at the University of Florida, the University of Tennessee and the Texas State Diagnostic Laboratory currently perform HI serologic testing for titers to OPMV. Titer do not necessarily correspond among laboratories because different test antigens are used in each.
Any animal suspected to have died of OPMV should be necropsied as soon as possible. Blood should be collected, cetrifuged and serum frozen pending histologic findings. Three sets of tissue are recommended to be collected. Special attention should be given to include Lung (cranial, mid and caudal sections), liver, kidney and splenopancreatic tissue in all sets of tissue saved. Garner (Northwest ZooPath, personal communication) also recommends brain and salivary gland.
The first set of tissues should be preserved in 10% neutral buffered formalin for conventional staining and microscopic examination.; the second should be placed in formalin for 48 hours, then removed and placed into 70% ethanol. This improves the likelihood of finding lesions with special staining techniques. A third set of tissues should be frozen and kept for virus isolation, should this be indicated by histopathologic findings.
Gross pathologic lesions range from no visible lesions to clear mucus or blood in the oral cavity, slight pulmonary congestion and a frothy serous or hemorrhagic exudate in the lung and air sacs. Severe cases may exhibit caseous exudative pneumonia that results from the secondary infections.
Histologic lesions in the respiratory system include proliferation of epithelial cells and thickening of the pulmonary septa. Macrophages, heterophils and mononuclear cells often infiltrate the tissue, and moderate amounts of cellular debris, bacterial colonies, and exudate can be found in the primary bronchus and air spaces. Rarely, epithelial cells may contain eosinophilic intracytoplasmic inclusions. If the brain is involved, an encephalitis can be observed, with multifocal areas of gliosis and minimal perivascular cuffing. Moderate ballooning of axon fibres may occur in the brain stem and proximal spinal cord. In many snakes with paramyxoviral lesions in the lung, hepatic pathology also consists of diffuse hepatic necrosis or multifocal pyogranulomatous inflammation. Hyperplasia of pancreatic ducts acinar cells with cystic dilation have also been observed. In the salivary glands, ductular dilation, flattening and crowding of ductular epthelium, and accumulation of cellular debris and secretory material may be noted in the ductular lumina.
Definitive diagnosis of OPMV infection requires isolation of the virus from tissues. Thus far, this has only been achieved with tissue samples harvested at postmortem examination.
Electron microscopy can be used to show virions budding from the apical membranes of type I and type II alveolar cells.
Occasionally, intracytoplasmic inclusions can be observed in affected cells and consisting of paramyxoviral nucleocapsid material.
Immunofluorescence and immunoperoxidase staining techniques have also been developed to show viral antigen in affected tissues. In Situ hybridisation has recently been used to identify paramyxoviral nucleic acid.
Ophidian Paramyxovirus (OPMV) was first isolated in 1973 from a Fer-de-lance (Bothrops moojeni) after an outbreak in a Swiss serpentarium that killed 25% of 431 specimens. Since then, numerous documented outbreaks of Paramyxovirus have been seen in private and zoologic collections. Paramyxovirus has been isolated from all major snake families, including elapids, boids, colubrids and viperids. Crotalids appear to be the most susceptible.
Paramyxovirus is an enveloped RNA virus 120 to 150 μm in diameter that reproduces by budding from cell membranes. Two distinct subgroups have been shown to exist with several intermediate isolates. This grouping does not appear to be species specific, although geographic correlations were found. Recently, a transmission study was carried out in Aruba Island Rattle Snakes and Koch's postulates were fulfilled.
Clinical Signs
There are no pathognomonic signs for the diagnosis of paramyxovirus infection. The disease affects primarily the respiratory system but can present with a tremendous variation of signs, which makes diagnosis difficult for the clinician. The symptoms are divided into three categories.
Acute and Peracute
Often minimal to nonexistent promontory signs are noticed by the keeper or owner; the animals are often just found dead. Anorexia and regurgitation are occasionally seen. The most common symptoms include respiratory compromise, blood in the oral cavity, or neurological involvement such as head tremors, excitement, star gazing, flaccid paralysis, or convulsions. The time from exposure to death can range from 6 to more than 10 weeks. Animals often die of secondary bacterial infections. OPMV should be included in the differential diagnosis in boids with neurological symptoms suspected of Inclusion Body Disease.
The virus may overwhelm the immune system, with death occurring before a detectable antibody response. Improper husbandry and environmental conditions may play a critical role in immunologic incompetence, particularly the absence of a thermal gradient.
Chronic "Poor Doer"
Anorexia, hypophagia, and regurgitation are the earliest signs and have been seen up to seven months before any other signs of disease. Animals exhibit other general signs of debilitation, such as reluctance to move, increased use of heat plates, emaciation and poor muscle tone. Respiratory symptoms include variable degrees of stridor and dyspnea, often developing into secondary bacterial pneumonia. Gastrointestinal signs may include gaseous bowel distention, mucoid diarrhea, malodorous stools and protozoal overgrowth. Directed antiprotozoal and antibacterial treatment increase survival times.
Specimens usually have high titers. However, antibody presence does not prevent viral shedding, as shown by animals able to infect or induce seroconversion in cagemates. These snakes eventually succumb to the disease but actively shed virus and pose the greatest threat to the collection.
Clinically Healthy Animals
Specimens may remain asymptomatic for up to 10 months, although most individuals eventually become chronic "poor doers." Sustained high titers may be indicative of a chronic carrier state and not necessarily immunity. Some specimens have been documented as overcoming a viral encounter and surviving.
In the authors' experience with a paramyxovirus outbreak, the animals with a regular appetite became anorectic, and respiratory compromise developed. They became severely lethargic and died within 1 week of the onset of signs. A few specimens had horizontal head tremors develop that varied from subtle to broad-swinging movements frequently accompanied with star gazing behavior. One specimen, a Bushmaster (Lactesis mutus), did not show any clinical signs despite a seropositive status for 9 months. A Northern Copperhead (Agkistrodin contortrix) placed in an adjacent aquarium did not have a titer or lesions develop after 8 weeks of exposure to the Bushmaster.
Diagnosis
Presumptive diagnosis of Paramyxovirus infection may be based on a history of exposure and clinical signs. Ill animals should be closely monitored. A thorough clinical examination should be performed, including pulmonary auscultation and fecal examination. If abnormal lung sounds are detected, transtracheal washes for cytology and bacterial culture should be performed because both secondary bacterial and verminous pneumonia are common.
If OPMV is suspected, serum should be assayed for the presence of antibody with Hemagglutination inhibition (HI). Titers only reflect exposure, and a rising titer is necessary for diagnosis of active disease. Seroconversion generally takes more than 8 weeks. The laboratory of Dr Elliot Jacobson at the University of Florida, the University of Tennessee and the Texas State Diagnostic Laboratory currently perform HI serologic testing for titers to OPMV. Titer do not necessarily correspond among laboratories because different test antigens are used in each.
Any animal suspected to have died of OPMV should be necropsied as soon as possible. Blood should be collected, cetrifuged and serum frozen pending histologic findings. Three sets of tissue are recommended to be collected. Special attention should be given to include Lung (cranial, mid and caudal sections), liver, kidney and splenopancreatic tissue in all sets of tissue saved. Garner (Northwest ZooPath, personal communication) also recommends brain and salivary gland.
The first set of tissues should be preserved in 10% neutral buffered formalin for conventional staining and microscopic examination.; the second should be placed in formalin for 48 hours, then removed and placed into 70% ethanol. This improves the likelihood of finding lesions with special staining techniques. A third set of tissues should be frozen and kept for virus isolation, should this be indicated by histopathologic findings.
Gross pathologic lesions range from no visible lesions to clear mucus or blood in the oral cavity, slight pulmonary congestion and a frothy serous or hemorrhagic exudate in the lung and air sacs. Severe cases may exhibit caseous exudative pneumonia that results from the secondary infections.
Histologic lesions in the respiratory system include proliferation of epithelial cells and thickening of the pulmonary septa. Macrophages, heterophils and mononuclear cells often infiltrate the tissue, and moderate amounts of cellular debris, bacterial colonies, and exudate can be found in the primary bronchus and air spaces. Rarely, epithelial cells may contain eosinophilic intracytoplasmic inclusions. If the brain is involved, an encephalitis can be observed, with multifocal areas of gliosis and minimal perivascular cuffing. Moderate ballooning of axon fibres may occur in the brain stem and proximal spinal cord. In many snakes with paramyxoviral lesions in the lung, hepatic pathology also consists of diffuse hepatic necrosis or multifocal pyogranulomatous inflammation. Hyperplasia of pancreatic ducts acinar cells with cystic dilation have also been observed. In the salivary glands, ductular dilation, flattening and crowding of ductular epthelium, and accumulation of cellular debris and secretory material may be noted in the ductular lumina.
Definitive diagnosis of OPMV infection requires isolation of the virus from tissues. Thus far, this has only been achieved with tissue samples harvested at postmortem examination.
Electron microscopy can be used to show virions budding from the apical membranes of type I and type II alveolar cells.
Occasionally, intracytoplasmic inclusions can be observed in affected cells and consisting of paramyxoviral nucleocapsid material.
Immunofluorescence and immunoperoxidase staining techniques have also been developed to show viral antigen in affected tissues. In Situ hybridisation has recently been used to identify paramyxoviral nucleic acid.
