Malignant catarrhal fever
Malignant catarrhal fever
Description, Causes and Risk Factors:
Malignant catarrhal fever is caused primarily by two different herpes viruses, one found in the wildebeest as a reservoir host and one found in sheep as a reservoir host. These reservoir hosts are clinically unaffected by infection with the virus but can serve as a source of infection for susceptible animals such as cattle, deer, bison, water buffalo, and pigs which can die from the infection.
Ovine Herpesvirus 2 (OHV-2): The etiologic agent of sheep-associated MCF remains elusive. Despite numerous isolation attempts and reports, no virus that can be regarded as the causative agent has been isolated either from cases of this form of MCF or from sheep.
A new MCF virus is recognized, causing classic MCF in white-tailed deer.
Caprine Herpesvirus 2 (CHV-2): The virus endemic in domestic goats is closely related to, but distinct from AlHV-1 and OvHV-2, and is pathogenic to some species of deer.
Alcelaphine Herpesvirus 1 (AHV-1): It is characterized as a highly cell-associated, lymphotropic herpesvirus and was classified as a member of the family Herpesviridae, subfamily Gammaherpesvirinae. Members of the herpesviridae are characterized by a core-containing double-stranded DNA and an icosahedral capsid.
Alcelaphine herpesvirus 1 (AHV-1) which causes wildebeast-associated MCF (WA-MCF) and ovine herpesvirus 2 (OHV-2) which causes sheep-associated MCF (SA-MCF). Wildebeast and sheep are natural carriers of the two viruses, respectively. Recently, caprine-associated herpesvirus 2 (CHV-2) has been recognized in domestic goats, and the virus has been associated with MCF in deer. In Africa, WA-MCF occurred in cattle which had been in contact with wildebeast, and AHV-1 was successfully isolated. Though the causative virus of SA-MCF has never been isolated, it is genetically, closely related to AHV-1. It is known that sheep are asymptomatic carriers of OHV-2, shedding the virus and passing it to other ruminants. SA-MCF has been reported in cattle and other ruminants in such locations as the Americas, Europe, and New Zealand. Outbreaks in buffaloes have been recorded in India, New Zealand, Malaysia and Indonesia.
The incubation period in natural cases is not known, but epidemiologic evidence indicates it may be as long as 200 days. Experimentally, the incubation period has varied from 9 to 77 days.
A wide variety of symptoms are seen in this disease.Sudden death may occur; this may be preceded by hours of depression, diarrhea and dysentery, signs of disseminated intravascular coagulation, or dyspnea. In lessacute cases, there may be fever and inappetence. Animals often develop bilateral cornealopacity that begins at the corneoscleral junction and progresses inward. Serous discharges from the eyes and noseare typical; later, these discharges become mucopurulent.The muzzle and nares are usually encrusted, and dyspnea,open-mouthed breathing, and salivation may be seen. Theoral mucosa is often hyperemic and may contain multifocalor diffuse areas of necrosis. Erosions may be found at thetips of the buccal papillae. The skin is sometimes ulcerated,and hardened scabs may develop on the perineum, udder,and teats. In some animals, the horn and hoof coveringsmay be loosened or sloughed. The joints may be swollen,milk production may drop, and the superficial lymph nodesmay be enlarged. Constipation is common, but diarrhea orhemorrhagic gastroenteritis can also be seen. Occasionally,animals have nervous signs including hyperesthesia, incoordination, nystagmus, or head pressing, either with orwithout other characteristic symptoms.
Malignant catarrhal fever should be suspected in susceptible animals with the characteristic clinical signs,particularly if they have been in contact with sheep, goats,Alcelaphine antelope, or wildebeest (especially around theperiod of parturition). The symptoms of typical infectionsinclude sudden death or fever with nasal and lacrimaldischarges, erosions of the mucosa, and bilateral cornealopacity, but other syndromes may be seen. Post mortemlesions that support a diagnosis of malignant catarrhalfever include corneal opacity, enlarged lymph nodes, inflammation and erosions in the nasal passages, gastrointestinal mucosa, and urinary bladder, and prominent tortuous small arteries in the subcutaneous tissue, thorax,and abdomen.
In practice, malignant catarrhal fever is often confirmed by histopathologic demonstration of multisystemlymphoid infiltration, disseminated vasculitis, and degenerative epithelial lesions. However, polymerase chainreaction (PCR) tests are becoming the diagnostic methodof choice. PCR can detect both AHV-1 and OHV-2 viralDNA. AHV-1 infections can also be confirmed by virusisolation. This virus can be recovered from peripheralblood leukocytes, lymph nodes, or spleen. Viable cells arenecessary, as the virus cannot be isolated from dead cells.Virus isolation has not been successful in OHV-2 infections.
Serology can also be helpful. In wildebeest, antibodies to AHV-1 can be detected by virus neutralization, immunoblotting, enzyme-linked immunosorbent assay(ELISA), immunofluorescence, and immunocytochemistry. Ruminants with malignant catarrhal fever rarely develop neutralizing antibodies; in symptomatic cases, immunofluorescence or immunoblotting must be used. Insheep, antibodies to OVH-2 can be found by immunofluorescence or immunoblotting. Immunofluorescence is oftenuseful in cattle infected by OHV-2, but antibodies maynot be found in more acute cases, particularly in deer.
Animals that die peracutely may have few lesions other than hemorrhagic enterocolitis. In the more protractedintestinal and head-and-eye forms, the carcass may be normal, dehydrated, or emaciated. The muzzle is oftenencrusted and raw. Cutaneous lesions sometimes occur as generalized exanthema with exudation of lymph,crusting, and matting of the hair. Hyperemia is apparent in unpigmented skin. These lesions are frequentlyseen in the ventral thorax and abdomen, inguinal region, perineum and loins, and sometimes on the head.Generalized lymphadenopathy is common. Lymphoproliferative changes in the internal organs including CNSare highly suggestive of MCF. Typical herpesvirus inclusion bodies are not present.
There is no consistently effective treatment available. The recent availability of derivatives of acyclovir compounds that inhibit replication of herpesviruses shows promise in potential treatment regimens. A report of inhibition of the replication of the Alcelaphine herpesvirus by using recombinant interferons could be considered in development of a treatment regimen for valuable hoofstock.
An effective vaccine is not available for MCF and, although some viral strains have undergone attenuation in cell cultures, no efficacious vaccines have yet been developed. Since a vaccine does not currently exist, the most effective control is by prevention of contact of susceptible species with reservoir hosts (i.e. wildebeest, other Alcelaphine species, sheep and goats). In mixed species operations, production of MCF virus-free sheep, goats or wildebeest is an alternative for control. Additionally, the introduction of carrier species into game farms or zoological parks should require a quarantine period wherein extensive molecular and serologic testing can be conducted. Precautions should also be taken that water, food, and bedding materials cannot serve to transmit infectious virus among housed species.
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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